FN Thomson Reuters Web of Science™ VR 1.0 PT J AU RAUB, WF AF RAUB, WF TI OFFICE-OF-SCIENTIFIC-INTEGRITY SO LANCET LA English DT Letter RP RAUB, WF (reprint author), NIH,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 20 PY 1991 VL 337 IS 8747 BP 980 EP 980 DI 10.1016/0140-6736(91)91614-Z PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FH131 UT WOS:A1991FH13100044 PM 1678060 ER PT J AU CAPSON, TL BENKOVIC, SJ NOSSAL, NG AF CAPSON, TL BENKOVIC, SJ NOSSAL, NG TI PROTEIN DNA CROSS-LINKING DEMONSTRATES STEPWISE ATP-DEPENDENT ASSEMBLY OF T4-DNA POLYMERASE AND ITS ACCESSORY PROTEINS ON THE PRIMER-TEMPLATE SO CELL LA English DT Article ID T4 GENE 44-62; ESCHERICHIA-COLI; REPLICATION SYSTEM; III HOLOENZYME; COMPLEX; HYDROLYSIS; PURIFICATION; CLONING AB T4 DNA polymerase, the 44/62 and 45 polymerase accessory proteins, and 32 single-stranded DNA-binding protein catalyze ATP-dependent DNA synthesis. Using DNA primers with cross-linkable residues at specific positions, we obtained structural data that reveal how these proteins assemble on the primer-template. With the nonhydrolyzable ATP analog ATP-gamma-S, assembly of the 44/62 and 45 proteins on the primer requires 32 protein but not polymerase. ATP hydrolysis changes the position and intensity of cross-linking to each of the accessory proteins and allows cross-linking of polymerase. Our data indicate that the initial binding of the three accessory proteins and ATP to a 32 protein-covered primer-template is followed by ATP hydrolysis, binding of polymerase, and movement of the accessory proteins to yield a complex capable of processive DNA synthesis. C1 PENN STATE UNIV,DEPT CHEM,UNIVERSITY PK,PA 16802. RP CAPSON, TL (reprint author), NIDDKD,NUCL ACID BIOCHEM SECT,BIOCHEM PHARMACOL LAB,BLDG 8,ROOM 2A-15,BETHESDA,MD 20892, USA. FU NIGMS NIH HHS [GM 12011, GM 13306] NR 42 TC 86 Z9 86 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD APR 19 PY 1991 VL 65 IS 2 BP 249 EP 258 DI 10.1016/0092-8674(91)90159-V PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FH092 UT WOS:A1991FH09200008 PM 1849797 ER PT J AU HUGIN, AW VACCHIO, MS MORSE, HC AF HUGIN, AW VACCHIO, MS MORSE, HC TI A VIRUS-ENCODED SUPERANTIGEN IN A RETROVIRUS-INDUCED IMMUNODEFICIENCY SYNDROME OF MICE SO SCIENCE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; MURINE LEUKEMIA VIRUSES; T-CELLS; MONOCLONAL-ANTIBODIES; SYNTHETIC PEPTIDES; CLONAL DELETION; C57BL/6 MICE; I-E; MLS; RECEPTOR AB The development of an immunodeficiency syndrome of mice caused by a replication-defective murine leukemia virus (MuLV) is paradoxically associated with a rapid activation and proliferation of CD4+ T cells that are dependent on the presence of B cells. The responses of normal spleen cells to B cell lines that express the defective virus indicated that these lines express a cell surface determinant that shares "superantigenic" properties with some microbial antigens and Mls-like self antigens. This antigen elicited a potent proliferative response that was dependent on the presence of CD4+ T cells and was associated with selective expansion of cells bearing V-beta-5. This response was markedly inhibited by a monoclonal antibody specific for the MuLV gag-encoded p30 antigen. C1 NIAID,IMMUNOPATHOL LAB,BLDG 7,ROOM 304,BETHESDA,MD 20892. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. OI Morse, Herbert/0000-0002-9331-3705 FU NIAID NIH HHS [N01-AI-72622] NR 63 TC 208 Z9 209 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 19 PY 1991 VL 252 IS 5004 BP 424 EP 427 DI 10.1126/science.1850169 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FH103 UT WOS:A1991FH10300038 PM 1850169 ER PT J AU ROSENFELD, MA SIEGFRIED, W YOSHIMURA, K YONEYAMA, K FUKAYAMA, M STIER, LE PAAKKO, PK GILARDI, P STRATFORDPERRICAUDET, LD PERRICAUDET, M JALLAT, S PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF ROSENFELD, MA SIEGFRIED, W YOSHIMURA, K YONEYAMA, K FUKAYAMA, M STIER, LE PAAKKO, PK GILARDI, P STRATFORDPERRICAUDET, LD PERRICAUDET, M JALLAT, S PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI ADENOVIRUS-MEDIATED TRANSFER OF A RECOMBINANT ALPHA-L-ANTITRYPSIN GENE TO THE LUNG EPITHELIUM INVIVO SO SCIENCE LA English DT Article ID CYSTIC-FIBROSIS GENE; INSITU HYBRIDIZATION; DNA; ALPHA-1-ANTITRYPSIN; IDENTIFICATION; EXPRESSION; CELLS; INDIVIDUALS; TYPE-5; ASSAY AB The respiratory epithelium is a potential site for somatic gene therapy for the common hereditary disorders alpha-1-antitrypsin (alpha-1AT) deficiency and cystic fibrosis. A replication-deficient adenoviral vector (Ad-alpha-1AT) containing an adenovirus major late promoter and a recombinant human alpha-1AT gene was used to infect epithelial cells of the cotton rat respiratory tract in vitro and in vivo. Freshly isolated tracheobronchial epithelial cells infected with Ad-alpha-1AT contained human alpha-1AT messenger RNA transcripts and synthesized and secreted human alpha-1AT. After in vivo intratracheal administration of Ad-alpha-1AT to these rats, human alpha-1AT messenger RNA was observed in the respiratory epithelium, human alpha-1AT was synthesized and secreted by lung tissue, and human alpha-1AT was detected in the epithelial lining fluid for at least 1 week. C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. INST GUSTAVE ROUSSY,CNRS,UA 1301,F-94805 VILLEJUIF,FRANCE. TRANSGENE SA,F-67082 STRASBOURG,FRANCE. NR 40 TC 672 Z9 681 U1 3 U2 20 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 19 PY 1991 VL 252 IS 5004 BP 431 EP 434 DI 10.1126/science.2017680 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FH103 UT WOS:A1991FH10300040 PM 2017680 ER PT J AU WATSON, JD AF WATSON, JD TI TOO MANY NOUGHTS SO NATURE LA English DT Letter RP WATSON, JD (reprint author), NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 18 PY 1991 VL 350 IS 6319 BP 550 EP 550 DI 10.1038/350550e0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FH112 UT WOS:A1991FH11200023 PM 2017250 ER PT J AU HENSON, DE BLOCK, G LEVINE, M AF HENSON, DE BLOCK, G LEVINE, M TI ASCORBIC-ACID - BIOLOGIC FUNCTIONS AND RELATION TO CANCER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material C1 NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,BETHESDA,MD 20892. RP HENSON, DE (reprint author), NCI,DIV CANC PREVENT & CONTROL EXECUTIVE PLAZA N,DETECT BRANCH,RM 305,BETHESDA,MD 20892, USA. RI Block, Gladys/E-3304-2010 NR 0 TC 69 Z9 69 U1 0 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 17 PY 1991 VL 83 IS 8 BP 547 EP 550 DI 10.1093/jnci/83.8.547 PG 4 WC Oncology SC Oncology GA FG086 UT WOS:A1991FG08600010 PM 1672383 ER PT J AU BAQUET, CR HORM, JW GIBBS, T GREENWALD, P AF BAQUET, CR HORM, JW GIBBS, T GREENWALD, P TI SOCIOECONOMIC-FACTORS AND CANCER INCIDENCE AMONG BLACKS AND WHITES SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ASSOCIATION; MORTALITY AB Findings from previous studies suggest that differences in socioeconomic status may be responsible for some, if not all, of the elevated incidence of cancer among blacks as compared with whites. Using incidence data from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program, we tested this hypothesis by correlating black and white cancer incidence rates in three US metropolitan areas between 1978 and 1982 with data from the 1980 census on socioeconomic status within individual census tracts. The study analyzed data on the incidence of cancer at all sites combined (> 100 cancer sites) and at seven major sites separately. As in other studies, income and educational levels served as surrogates for socioeconomic status. The present study also used census-tract data on population density as a surrogate factor. Each of these measures of socioeconomic status was analyzed independently. Before correlation with census-tract data, age-adjusted data on cancer incidence showed statistically significant elevated risks among blacks for cancer at all sites combined and at four of the seven separate sites; whites showed an elevated risk for cancer at two sites. Cancer at only one site, the colon, showed no significant association with race. When age-adjusted incidence data were correlated with socioeconomic status, the comparative black-white risks changed: Whites showed an elevated risk of cancer at all sites combined and at three of the seven separate sites; blacks maintained their elevated risk at three sites. These findings suggest that the disproportionate distribution of blacks at lower socioeconomic levels accounts for much of the excess cancer burden among blacks. They also suggest that for both blacks and whites unidentified racial factors, which may be either cultural or genetic and which are not closely linked to socioeconomic status, may play a role in the incidence of some cancers. C1 NCI,DIV CANC PREVENT & CONTROL,SPECIAL POPULATION STUDIES BRANCH,BETHESDA,MD 20892. RP BAQUET, CR (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC CONTROL SCI PROGRAM,BETHESDA,MD 20892, USA. NR 23 TC 208 Z9 209 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 17 PY 1991 VL 83 IS 8 BP 551 EP 557 DI 10.1093/jnci/83.8.551 PG 7 WC Oncology SC Oncology GA FG086 UT WOS:A1991FG08600011 PM 2005640 ER PT J AU PADMANABHAN, R TSURUO, T KANE, E WILLINGHAM, MC HOWARD, BH GOTTESMAN, MM PASTAN, I AF PADMANABHAN, R TSURUO, T KANE, E WILLINGHAM, MC HOWARD, BH GOTTESMAN, MM PASTAN, I TI MAGNETIC-AFFINITY CELL SORTING OF HUMAN MULTIDRUG-RESISTANT CELLS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID GENE; EXPRESSION; TRANSFORMANTS; GLYCOPROTEIN; ANTIBODY; PROTEIN AB We have developed a method for isolating multidrug-resistant cells from a heterogeneous cell population using the magnetic-affinity cell-sorting system. Human KB carcinoma cell lines expressing different amounts of P-glycoprotein have been selected by use of the monoclonal antibody MRK-16 coupled to magnetic particles. This specific, rapid, and sensitive method allows the selection of viable and clonable drug-resistant cells from various drug-resistant human and murine cell populations. This method may prove useful in isolating drug-resistant cells from tumors with heterogeneous P-glycoprotein expression for further analysis. C1 NCI,CELL BIOL LAB,BLDG 37,RM 1B22,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. JAPANESE FDN CANC RES,CTR CANC CHEMOTHERAPY,DIV EXPTL CHEMOTHERAPY,TOKYO 170,JAPAN. NR 19 TC 11 Z9 11 U1 0 U2 1 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 17 PY 1991 VL 83 IS 8 BP 565 EP 569 DI 10.1093/jnci/83.8.565 PG 5 WC Oncology SC Oncology GA FG086 UT WOS:A1991FG08600013 PM 1672384 ER PT J AU BALDISSERI, DM TORCHIA, DA POOLE, LB GERLT, JA AF BALDISSERI, DM TORCHIA, DA POOLE, LB GERLT, JA TI DELETION OF THE OMEGA-LOOP IN THE ACTIVE-SITE OF STAPHYLOCOCCAL NUCLEASE .2. EFFECTS ON PROTEIN-STRUCTURE AND DYNAMICS SO BIOCHEMISTRY LA English DT Article ID MAGNETIC-RESONANCE; HETERONUCLEAR NMR; SPECTROSCOPY; SPECTRA AB It has been shown (Poole et al., 1991) that deletion of residues 44-49 from the sequence of staphylococcal nuclease (E43 SNase) results in an enzyme (E43 DELTA-SNase) that is significantly more active than D43 SNase, an enzyme that differs from the wild-type enzyme by deletion of a single methylene group. In addition, both E43 DELTA-SNase and D43 DELTA-SNase are significantly more stable than their respective parent enzymes. Herein we use high-resolution 2D and 3D NMR spectroscopy to characterize the solution conformations of the four enzymes in order to better understand their differences in stability and activity. The backbone assignments of E43 SNase were extended to the three mutant proteins (uniformly N-15-enriched) by using 2D HSQC, 3D HOHAHA-HMQC, and 3D NOESY-HMQC spectra. The NOE patterns observed for E43 and D43 SNase in solution are consistent with the crystal structures of these proteins. The NOESY data further show that the intact and deleted proteins have essentially the same structures except that (a) the disordered OMEGA-loops in the intact proteins are replaced by tight type II' turns, formed by residues 43-50-51-52, in the deleted proteins and (b) the orientation of the D43 side chain in crystalline D43 SNase differs from that found for D43 DELTA-SNase in solution. Except for regions neighboring the OMEGA-loops, the intact and deleted proteins show nearly identical amide N-15 and H-1 chemical shifts. In contrast, there are widespread, small and similar, chemical shift differences (a) between E43 SNase and D43 SNase and (b) between E43 DELTA-SNase and D43 DELTA-SNase. This observation indicates that deletion of the E43 gamma-methylene group causes small, widespread, and similar changes in the structures of E43 SNase and E43 DELTA-SNase. C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. UNIV MARYLAND,DEPT CHEM & BIOCHEM,COLLEGE PK,MD 20742. FU NIGMS NIH HHS [GM-13211, GM-34573] NR 26 TC 33 Z9 33 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 16 PY 1991 VL 30 IS 15 BP 3628 EP 3633 DI 10.1021/bi00229a006 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG730 UT WOS:A1991FG73000006 PM 2015220 ER PT J AU TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M AF TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M TI GUANINE-NUCLEOTIDE DEPENDENT FORMATION OF A COMPLEX BETWEEN CHOLERAGEN (CHOLERA-TOXIN) A-SUBUNIT AND BOVINE BRAIN ADP-RIBOSYLATION FACTOR SO BIOCHEMISTRY LA English DT Article ID SODIUM DODECYL-SULFATE; CELL-FREE SYSTEM; REGULATORY COMPONENT; ADENYLATE-CYCLASE; HUMAN-NEUTROPHILS; PROTEIN COFACTOR; NADPH OXIDASE; FATTY-ACID; ACTIVATION; RIBOSYLTRANSFERASE AB Cholera toxin activates adenylyl cyclase by catalyzing the ADP-ribosylation of G(s-alpha), the stimulatory guanine nucleotide binding protein of the cyclase system. This toxin-catalyzed reaction, as well as the ADP-ribosylation of guanidino compounds and auto-ADP-ribosylation of the toxin A1 protein (CTA1), is stimulated, in the presence of GTP (or GTP analogue), by 19-21-kDa proteins, termed ADP-ribosylation factors or ARFs. These proteins directly activate CTA1 in a reaction enhanced by sodium dodecyl sulfate (SDS) or dimyristoylphosphatidylcholine (DMPC)/cholate. To determine whether ARF stimulation of ADP-ribosylation is associated with formation of a toxin-ARF complex, these proteins were incubated with guanine nucleotides and/or detergents and then subjected to gel permeation chromatography. An active ARF-toxin complex was observed in the presence of SDS and GTP-gamma-S [guanosine 5'-O-(3-thiotriphosphate)] but not GDP-beta-S [guanosine 5'-O-(2-thiodiphosphate)]. Only a fraction of the ARF was capable of complex formation. The substrate specificities of complexed and noncomplexed CTA differed; complexed CTA exhibited markedly enhanced auto-ADP-ribosylation. In the presence of GTP-gamma-S and DMPC/cholate, an ARF-CTA complex was not detected. A GTP-gamma-S-dependent ARF aggregate was observed, however, exhibiting a different substrate specificity from monomeric ARF. These studies support the hypothesis that in the presence of guanine nucleotide and either SDS or DMPC/cholate, ARF and toxin exist as multiple species which exhibit different substrate specificities. RP TSAI, SC (reprint author), NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892, USA. NR 22 TC 13 Z9 13 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 16 PY 1991 VL 30 IS 15 BP 3697 EP 3703 DI 10.1021/bi00229a015 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG730 UT WOS:A1991FG73000015 PM 1901726 ER PT J AU PHILLIPS, PH LINET, MS HARRIS, EL AF PHILLIPS, PH LINET, MS HARRIS, EL TI ASSESSMENT OF FAMILY HISTORY INFORMATION IN CASE-CONTROL CANCER STUDIES SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Review DE CASE-CONTROL STUDIES; GENETICS, BIOCHEMICAL; NEOPLASTIC SYNDROMES, HEREDITARY ID CUTANEOUS MALIGNANT-MELANOMA; BREAST-CANCER; LUNG-CANCER; ADENOMATOUS POLYPOSIS; MOLECULAR-GENETICS; RISK-FACTORS; CHROMOSOME-5; LEUKEMIA; DISEASE; EPIDEMIOLOGY AB Evidence for the genetic basis of cancer has increased in recent years, and thus, assessing familial aggregation may play an important role in epidemiologic studies. To assess the degree to which family history variables are collected in cancer case-control studies, the authors conducted a literature review of studies published in six journals during 1982-1984. Only 25% of these included a family history component. The authors review some of the literature in favor of inclusion of family information and argue for its routine collection in cancer case-control studies. C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21218. RP PHILLIPS, PH (reprint author), EMMES CORP,11325 7 LOCKS RD,SUITE 214,POTOMAC,MD 20854, USA. NR 64 TC 16 Z9 17 U1 1 U2 1 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 15 PY 1991 VL 133 IS 8 BP 757 EP 765 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA FJ897 UT WOS:A1991FJ89700001 PM 2021142 ER PT J AU MANSOUR, AM CHAN, CC AF MANSOUR, AM CHAN, CC TI RECURRENT UVEITIS PRECEDED BY SWELLING OF SKIN TATTOOS SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Letter ID SARCOIDOSIS C1 NEI,IMMUNOL LAB,BLDG 10,ROOM 6C416,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. UNIV TEXAS,MED BRANCH,DEPT OPHTHALMOL,GALVESTON,TX 77550. NR 5 TC 9 Z9 9 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD APR 15 PY 1991 VL 111 IS 4 BP 515 EP 516 PG 2 WC Ophthalmology SC Ophthalmology GA FF656 UT WOS:A1991FF65600023 PM 2012160 ER PT J AU KORENMAN, J BAKER, B WAGGONER, J EVERHART, JE DIBISCEGLIE, AM HOOFNAGLE, JH AF KORENMAN, J BAKER, B WAGGONER, J EVERHART, JE DIBISCEGLIE, AM HOOFNAGLE, JH TI LONG-TERM REMISSION OF CHRONIC HEPATITIS-B AFTER ALPHA-INTERFERON THERAPY SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID VIRUS-INFECTION; CONTROLLED TRIAL; E-ANTIGEN; HOMOSEXUAL MEN; HBSAG; ANTIBODY; FOLLOW AB Objective: To evaluate whether remissions of chronic hepatitis B induced by alpha-interferon therapy are of long duration. Design: Cohort study. Setting: Clinical Center of the National Institutes of Health, a tertiary referral center. Patients: Sixty-four patients with chronic hepatitis B were treated with alpha-interferon between 1984 and 1986. Main Outcome Measures: Patients were followed with frequent examinations and determinations of serum liver biochemical tests and hepatitis B virus (HBV) markers including hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), and HBV DNA using blot hybridization and polymerase chain reaction. Results: Among 64 patients with chronic hepatitis B who were treated with alpha-interferon, 23 (36%) responded to treatment with loss of HBeAg and improvement in serum aminotransferases. All 23 have been followed for 3 to 7 years (mean, 4.3 years). During follow-up, 3 of 23 patients relapsed, with reappearance of HBeAg and abnormal serum aminotransferases, all within 1 year of therapy. The remaining 20 patients continued to have no detectable HBeAg or HBV DNA (using blot hybridization) in serum and to be asymptomatic for liver disease, although 3 had minimal elevations in serum aminotransferases. Thirteen patients (65%) became negative for HBsAg between 0.2 and 6 years (mean, 3 years) after loss of HBeAg. Although no patient had HBV DNA that was detectable by blot hybridization, the 7 patients who remained HBsAg positive all had HBV DNA in serum detected by polymerase chain reaction, but only 2 of 13 HBsAg-negative patients had viral genome using this method. Testing sequential samples indicated that HBV DNA detected by polymerase chain reaction usually disappeared at or around the time that test results for HBsAg became negative. Conclusions: Remissions in chronic hepatitis B induced by alpha-interferon are of long duration and are followed, in most patients, by the loss of HBsAg and all evidence of residual virus replication. C1 NIDDKD,DIV DIGEST DIS & NUTR,BLDG 31,ROOM 9A23,BETHESDA,MD 20892. NR 22 TC 350 Z9 350 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 15 PY 1991 VL 114 IS 8 BP 629 EP 634 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA FG031 UT WOS:A1991FG03100003 PM 2003708 ER PT J AU FAUCI, AS SCHNITTMAN, SM POLI, G KOENIG, S PANTALEO, G AF FAUCI, AS SCHNITTMAN, SM POLI, G KOENIG, S PANTALEO, G TI IMMUNOPATHOGENIC MECHANISMS IN HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) INFECTION SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material ID CYTO-TOXIC LYMPHOCYTES; IMMUNE-DEFICIENCY SYNDROME; PERIPHERAL-BLOOD LYMPHOCYTES; TUMOR NECROSIS FACTOR; NF-KAPPA-B; T-CELL; SEROPOSITIVE INDIVIDUALS; NATURAL-KILLER; HTLV-III/LAV; MONONUCLEAR PHAGOCYTES AB An understanding of the immunopathogenic mechanisms of infection with human immunodeficiency virus (HIV) is fundamental in developing successful approaches to designing effective therapeutic and vaccine strategies. In this regard, we have investigated the mechanisms by which HIV inserts itself into the human immune system and uses the elaborate cytokine network to its own replicative advantage. We have also shown that the burden of HIV in CD4+ T cells is directly associated with a decline in this cell population in vivo and a progression to disease. Mononuclear phagocytes may play a role in the pathogenesis of HIV infection by serving as reservoirs of the virus. Of note is the fact that monocytes in the peripheral blood of HIV-infected individuals are rarely infected in vivo, whereas infected-tissue macrophages may play a role in organ-specific HIV-related pathogenesis. The role of HIV-specific humoral and cell-mediated immunity in HIV infection is not well understood. However, fine specificity of responses against HIV have been delineated in some in-vitro systems. It is unclear why these responses, particularly HIV-specific cytolytic T-cell responses, diminish over the course of infection and are unable to contain progression of infection. RP FAUCI, AS (reprint author), NIAID,BLDG 31,ROOM 7A03,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Pantaleo, Giuseppe/K-6163-2016 NR 112 TC 270 Z9 271 U1 1 U2 6 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 15 PY 1991 VL 114 IS 8 BP 678 EP 693 PG 16 WC Medicine, General & Internal SC General & Internal Medicine GA FG031 UT WOS:A1991FG03100011 PM 1672248 ER PT J AU SHAPIRA, H WADA, E BATTEY, JF JENSEN, RT COY, DH KUSANO, K AF SHAPIRA, H WADA, E BATTEY, JF JENSEN, RT COY, DH KUSANO, K TI DISTINGUISHING BOMBESIN RECEPTOR SUBTYPES USING THE OOCYTE ASSAY SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID XENOPUS-OOCYTES; NEUROMEDIN-B; CHOLECYSTOKININ; EXPRESSION; AFFINITY; CURRENTS; PROTEIN; CALCIUM C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD 20892. TULANE UNIV,MED CTR,DEPT MED,PEPTIDE RES LABS,NEW ORLEANS,LA 70112. RP SHAPIRA, H (reprint author), NINCDS,NEUROCHEM LAB,BETHESDA,MD 20892, USA. NR 22 TC 11 Z9 11 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 15 PY 1991 VL 176 IS 1 BP 79 EP 86 DI 10.1016/0006-291X(91)90892-B PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FG328 UT WOS:A1991FG32800013 PM 1850273 ER PT J AU SAJI, M IKUYAMA, S AKAMIZU, T KOHN, LD AF SAJI, M IKUYAMA, S AKAMIZU, T KOHN, LD TI INCREASES IN CYTOSOLIC CA++ DOWN REGULATE THYROTROPIN RECEPTOR GENE-EXPRESSION BY A MECHANISM DIFFERENT FROM THE CAMP SIGNAL SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID FRTL-5 THYROID-CELLS; STIMULATION; ACTIVATION; PROTEIN; RELEASE; CALCIUM; CA-2+ RP SAJI, M (reprint author), NIDKDD,BIOCHEM & METAB LAB,CELL REGULAT SECT,BETHESDA,MD 20892, USA. RI Saji, Motoyasu/E-4007-2011 NR 16 TC 41 Z9 41 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 15 PY 1991 VL 176 IS 1 BP 94 EP 101 DI 10.1016/0006-291X(91)90894-D PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FG328 UT WOS:A1991FG32800015 PM 1708253 ER PT J AU KUBOTA, S FRIDMAN, R YAMADA, Y AF KUBOTA, S FRIDMAN, R YAMADA, Y TI TRANSFORMING GROWTH-FACTOR-BETA SUPPRESSES THE INVASIVENESS OF HUMAN FIBROSARCOMA CELLS-INVITRO BY INCREASING EXPRESSION OF TISSUE INHIBITOR OF METALLOPROTEASE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID HUMAN AMNIOTIC MEMBRANE; IV COLLAGENASE; INVASION; FIBROBLASTS; REQUIREMENT; PROTEINASES; SECRETE; TIMP-2 RP KUBOTA, S (reprint author), NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892, USA. NR 21 TC 46 Z9 46 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 15 PY 1991 VL 176 IS 1 BP 129 EP 136 DI 10.1016/0006-291X(91)90899-I PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FG328 UT WOS:A1991FG32800020 PM 1850251 ER PT J AU MILLER, MS JONES, AB CHAUHAN, DP PARK, SS ANDERSON, LM AF MILLER, MS JONES, AB CHAUHAN, DP PARK, SS ANDERSON, LM TI INDUCTION OF CYTOCHROME-P-450IA1 IN FETAL-RAT LIVER BY A SINGLE DOSE OF 3-METHYLCHOLANTHRENE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID HEMATOPOIETIC-CELLS; MOUSE-LIVER; ORGANOGENESIS; GENE; CARCINOGENS; CONCEPTUS; PROTEINS; ENZYMES; FORMS; P-450 C1 NCI,MOLEC CARCINOGENESIS LAB,FREDERICK,MD 21702. RP MILLER, MS (reprint author), NCI,PERINATAL CARCINOGENESIS SECT,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. NR 33 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 15 PY 1991 VL 176 IS 1 BP 280 EP 287 DI 10.1016/0006-291X(91)90921-S PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FG328 UT WOS:A1991FG32800042 PM 1708245 ER PT J AU DANIEL, DG KIM, E KOSTIANOVSKY, D GOLDBERG, TE CASANOVA, MF PICKAR, D KLEINMAN, JE WEINBERGER, DR AF DANIEL, DG KIM, E KOSTIANOVSKY, D GOLDBERG, TE CASANOVA, MF PICKAR, D KLEINMAN, JE WEINBERGER, DR TI COMPUTED-TOMOGRAPHY MEASUREMENTS OF BRAIN DENSITY IN SCHIZOPHRENIA SO BIOLOGICAL PSYCHIATRY LA English DT Article ID SENILE DEMENTIA; CEREBRAL DENSITY; CORPUS-CALLOSUM; CT DENSITY; PATHOLOGY; DEFICITS; ARTIFACT; NUMBERS; VALUES; MATTER AB Although previous studies have reported differences in computed tomography (CT) scan attenuation values between patients with schizophrenia and controls, interpretation of these findings has been hindered by methodological shortcomings such as the failure to control for head size, scanner calibration differences, and other confounding variables. In the present study of CT attenuation values in multiple brain regions in 20 patients with chronic schizophrenia and an equal number of age- and sex-matched normal subjects we controlled for head size and normalized the attenuation values for each scan to an internal standard. No significant differences emerged between the patients with schizophrenia and the controls. However, in the controls only, the mean density of white matter in the left frontal area was significantly higher (t = -2.83, p = 0.01) than that in the right. The results, although possibly suggestive of deviant lateralization in schizophrenia, raise questions about the sensitivity and validity of regional CT attenuation values in detecting subtle anatomic abnormalities in patients with this illness. RP DANIEL, DG (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. NR 46 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 1991 VL 29 IS 8 BP 745 EP 756 DI 10.1016/0006-3223(91)90194-Q PG 12 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA FJ388 UT WOS:A1991FJ38800003 PM 2054449 ER PT J AU HERMAN, R OBARZANEK, E MIKALAUSKAS, KM POST, RM JIMERSON, DC AF HERMAN, R OBARZANEK, E MIKALAUSKAS, KM POST, RM JIMERSON, DC TI THE EFFECTS OF CARBAMAZEPINE ON RESTING METABOLIC-RATE AND THYROID-FUNCTION IN DEPRESSED-PATIENTS SO BIOLOGICAL PSYCHIATRY LA English DT Article ID AFFECTIVELY ILL PATIENTS; EPILEPTIC PATIENTS; WEIGHT-LOSS; NOREPINEPHRINE METABOLISM; ANTICONVULSANT DRUGS; HORMONES; PHENYTOIN; THYROXINE; OBESITY; SERUM AB Resting metabolic rate and thyroid hormone levels were studied in 11 patients with affective disorders before and during treatment with carbamazepine (CBZ). CBZ has been previously reported to reduce thyroid hormones, but the metabolic consequence of this effect has not been explored. During CBZ treatment, thyroid hormones decreased significantly (T4, 7.53 versus 5.74-mu-g/dl, p < 0.001), whereas the resting metabolic rate (RMR) did not (31.6 versus 30.7 kcal/m2/hr). Baseline RMRs were low and the expected positive relationship between RMR and weight was disrupted in females. The extent of previous exposure to tricyclic and monoamine oxidase inhibitors antidepressant treatment was significantly associated with lower baseline RMRs. We conclude that CBZ has no significant effect on RMR despite robust decreases in thyroid function. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02215. NIMH,PREVENT & DEMONSTRAT RES BRANCH,BETHESDA,MD 20892. NR 60 TC 23 Z9 23 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 1991 VL 29 IS 8 BP 779 EP 788 DI 10.1016/0006-3223(91)90197-T PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA FJ388 UT WOS:A1991FJ38800006 PM 2054452 ER PT J AU JACOBSEN, SEW RUSCETTI, FW DUBOIS, CM LEE, J BOONE, TC KELLER, JR AF JACOBSEN, SEW RUSCETTI, FW DUBOIS, CM LEE, J BOONE, TC KELLER, JR TI TRANSFORMING GROWTH-FACTOR-BETA TRANS-MODULATES THE EXPRESSION OF COLONY STIMULATING FACTOR RECEPTORS ON MURINE HEMATOPOIETIC PROGENITOR-CELL LINES SO BLOOD LA English DT Article ID GENE-EXPRESSION; TGF-BETA; BINDING; PROLIFERATION; INTERLEUKIN-3; LEUKEMIA; SURFACE; ROLES; GAMMA C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD 21701. SMITH KLINE BEECHAM,KING OF PRUSSIA,PA. AMGEN INC,THOUSAND OAKS,CA. RP JACOBSEN, SEW (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 39 TC 80 Z9 81 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1991 VL 77 IS 8 BP 1706 EP 1716 PG 11 WC Hematology SC Hematology GA FG728 UT WOS:A1991FG72800011 PM 1707695 ER PT J AU HARRISON, SD PLOWMAN, J DYKES, DJ WAUD, WR GRISWOLD, DP AF HARRISON, SD PLOWMAN, J DYKES, DJ WAUD, WR GRISWOLD, DP TI PRECLINICAL ANTITUMOR-ACTIVITY OF PENCLOMEDINE IN MICE - CROSS-RESISTANCE, SCHEDULE DEPENDENCE, AND ORAL ACTIVITY AGAINST TUMOR XENOGRAFTS IN BRAIN SO CANCER RESEARCH LA English DT Article AB Penclomedine is 3,5-dichloro-2,4-dimethoxy-6-(trichloromethyl)pyridine (NSC 338720), an alpha-picoline derivative with p.o. antitumor activity in preclinical leukemia and solid tumor models. Described here are an in vivo cross-resistance profile of penclomedine, treatment schedule dependence studies, and studies exploring the effects of p.o. drug on human tumors xenografted into mouse brain. The latter studies exploited the apparent facile distribution of penclomedine to the central nervous system. Tumor models used included murine leukemia lines selected in vivo for acquired resistance to various antitumor drugs and the human mammary and lung tumor xenografts MX-1 and H82, respectively. The therapeutic effects of p.o. penclomedine against s.c. MX-1 and H82 xenografts were shown to be independent of treatment schedule. Therapeutic activity was comparable when p.o. and parenteral treatments were compared. Lines of P388 leukemia resistant to melphalan, cyclophosphamide, and carmustine were cross-resistant to penclomedine in vivo. Leukemia lines resistant to antimetabolites, DNA binders/intercalators, and vincristine were not cross-resistant to penclomedine. Intracerebrally implanted MX-1 xenografts retained their sensitivity to p.o. penclomedine, and therapeutic activity was at least comparable to that of carmustine, a drug known for its ability to cross the blood-brain barrier. These results demonstrate attributes of penclomedine that are relatively uncommon among currently available antitumor drugs and that are of interest for the anticipated clinical development of this drug. C1 NCI,COLL CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. RP HARRISON, SD (reprint author), SO RES INST,POB 55305,BIRMINGHAM,AL 35255, USA. FU NCI NIH HHS [N01-CM-73726, P01-CA-34200] NR 17 TC 21 Z9 21 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1991 VL 51 IS 8 BP 1979 EP 1983 PG 5 WC Oncology SC Oncology GA FG082 UT WOS:A1991FG08200002 PM 2009516 ER PT J AU PAN, CJ SARTWELL, AD CHOU, JY AF PAN, CJ SARTWELL, AD CHOU, JY TI TRANSCRIPTIONAL REGULATION AND THE EFFECTS OF SODIUM-BUTYRATE AND GLYCOSYLATION ON CATALYTIC ACTIVITY OF HUMAN GERM-CELL ALKALINE-PHOSPHATASE SO CANCER RESEARCH LA English DT Article ID CHORIOCARCINOMA CELLS; GENE; EXPRESSION; SEQUENCE; ISOZYME; CULTURE; EVOLUTION; SEMINOMA; CLONING; TESTIS AB Human choriocarcinoma cells, the malignant trophoblasts, synthesize germ cell alkaline phosphatase (GCAP) which shares 98% sequence identity with the placental alkaline phosphatase (AP). The two isozymes are immunologically similar but react differentially toward inhibition by L-leucine or EDTA. Administration of sodium butyrate to choriocarcinoma cells greatly increased the transcription rate of the GCAP gene, resulting in an increase in mRNA expression and enzyme biosynthesis. The butyrate-modulated AP induction was blocked by cycloheximide, suggesting that a mediator protein may be involved. Protein sequence deduced from complementary DNA analysis suggests that GCAP contains two potential sites for asparagine (N)-linked glycosylation. The marked increased in GCAP expression by butyrate in choriocarcinoma cells allowed us to study the extent of N-linked glycosylation and its role on GCAP enzyme activity. After limited tunicamycin treatment, M(r) 65,000 (fully processed), M(r) 58,000 (nonglycosylated), and M(r) 62,000 polypeptides were synthesized by these cells in the presence of butyrate. This suggests that the M(r) 62,000 product may be the singly glycosylated GCAP monomer and that both sites are glycosylated in this phosphatase. The glycosylated and nonglycosylated GCAPs, synthesized by butyrate-treated choriocarcinoma cells in the absence or presence of tunicamycin, respectively, were similarly inhibited by L-leucine or EDTA. Moreover, the specific enzyme activity of glycosylated and nonglycosylated GCAP remained unchanged, indicating that AP lacking N-linked oligosaccharide side chains was catalytically active. This is supported by the finding that nonglycosylated GCAP incorporated inorganic phosphate which binds to the active site of AP. Since the active form of AP is a homodimer, our data indicate that the glycan moieties are not required for the dimerization and catalytic activity of GCAP. C1 NICHHD,HUMAN GENET BRANCH,BLDG 10,ROOM 95242,BETHESDA,MD 20892. NR 40 TC 16 Z9 17 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1991 VL 51 IS 8 BP 2058 EP 2062 PG 5 WC Oncology SC Oncology GA FG082 UT WOS:A1991FG08200016 PM 2009524 ER PT J AU LOEFFLER, CM PLATT, JL ANDERSON, PM KATSANIS, E OCHOA, JB URBA, WJ LONGO, DL LEONARD, AS OCHOA, AC AF LOEFFLER, CM PLATT, JL ANDERSON, PM KATSANIS, E OCHOA, JB URBA, WJ LONGO, DL LEONARD, AS OCHOA, AC TI ANTITUMOR EFFECTS OF INTERLEUKIN-2 LIPOSOMES AND ANTI-CD3-STIMULATED T-CELLS AGAINST MURINE MCA-38 HEPATIC METASTASIS SO CANCER RESEARCH LA English DT Article ID ACTIVATED KILLER CELLS; TUMOR-INFILTRATING LYMPHOCYTES; ANTI-T3 ANTIBODY; IDENTIFICATION; MELANOMA; INVIVO; MICE; IMMUNOTHERAPY; AUGMENTATION; CYTOLYSIS AB The stimulation of murine splenocytes with the monoclonal antibody anti-CD3 and interleukin 2 (IL-2) results in propagation of large numbers of cells (T-activated killer; T-AK) which demonstrate high therapeutic efficacy when infused with IL-2 into mice bearing pulmonary metastases. Interleukin 2 infusions are required to maintain the function of the adoptively transferred cells. Recent data demonstrate that the therapeutic efficacy can be enhanced by encapsulating IL-2 in lipsomes. The present work tested the combination of T-AK cells with IL-2 liposomes in an immunotheapy model utilizing the MCA-38 murine colon adenocarcinoma. Expansion of murine splenocytes was achieved with anti-CD3 monoclonal antibody plus IL-2 and was consistently greater than 50-fold during a 9-day culture period. Cytolytic activity of the murine T-AK cells was mediated primarily by Lyt-2+ cells. In vivo results demonstrate synergistic therapeutic efficacy of the combination of IL-2 liposomes and T-AK cells. Evaluation of the in vivo distribution of these T-AK cells utilizing congenic mice demonstrates that Lyt-2+ cells from these in vitro cultures infiltrate hepatic metastases in vivo. The activation of lymphocytes with anti-CD3 monoclonal antibody and IL-2 appears to be a reproducible and convenient method of producing cells capable of producing antitumor effects in models of adoptive immunotherapy. C1 UNIV MINNESOTA,DEPT SURG,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT PEDIAT,MINNEAPOLIS,MN 55455. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT SURG,PITTSBURGH,PA 15260. RP LOEFFLER, CM (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,DYNCORP,BETHESDA,MD 20892, USA. FU NCI NIH HHS [N01-CO-74102, CA 47097]; NIADDK NIH HHS [AM 13083] NR 32 TC 49 Z9 52 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1991 VL 51 IS 8 BP 2127 EP 2132 PG 6 WC Oncology SC Oncology GA FG082 UT WOS:A1991FG08200029 PM 1826232 ER PT J AU HILLMAN, K SHAPIRANAHOR, O BLACKBURN, R HERNANDEZ, D GOLDING, H AF HILLMAN, K SHAPIRANAHOR, O BLACKBURN, R HERNANDEZ, D GOLDING, H TI A POLYMER CONTAINING A REPEATING PEPTIDE SEQUENCE CAN STIMULATE T-CELL-INDEPENDENT IGG ANTIBODY-PRODUCTION INVIVO SO CELLULAR IMMUNOLOGY LA English DT Article ID IMMUNE-RESPONSE; SYNTHETIC POLYPEPTIDES; NUDE MICE; LYMPHOCYTES; IMMUNOGLOBULIN; FREQUENCY; SECRETION; STRAINS; VIRUS C1 NIDR,CBER,FDA,DIV BLOOD & BLOOD PROD,CELL BIOL LAB,BETHESDA,MD 20892. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. RP HILLMAN, K (reprint author), NIDR,DIV VIROL,BETHESDA,MD 20892, USA. NR 35 TC 16 Z9 16 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD APR 15 PY 1991 VL 134 IS 1 BP 1 EP 13 DI 10.1016/0008-8749(91)90326-7 PG 13 WC Cell Biology; Immunology SC Cell Biology; Immunology GA FE026 UT WOS:A1991FE02600001 PM 2013099 ER PT J AU KOFF, WC AF KOFF, WC TI THE PROSPECTS FOR AIDS VACCINES SO HOSPITAL PRACTICE LA English DT Article AB Several vaccine strategies against HIV are under study in phase 1 clinical trials. Many involve recombinant subunit preparations, and the question is which of these components of the virus may be immunogenic. Immune effectors and mediators that protect against HIV are also undefined. Vaccines may ultimately be used to treat as well as prevent AIDS. RP KOFF, WC (reprint author), NIAID,DIV AIDS,VACCINE RES & DEV BRANCH,ROCKVILLE,MD, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 8750-2836 J9 HOSP PRACT JI Hosp. Pract. PD APR 15 PY 1991 VL 26 IS 4 BP 99 EP 106 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FG248 UT WOS:A1991FG24800012 PM 2010483 ER PT J AU CHAMBERS, C RUSSELL, P AF CHAMBERS, C RUSSELL, P TI DELETION MUTATION IN AN EYE LENS BETA-CRYSTALLIN - AN ANIMAL-MODEL FOR INHERITED CATARACTS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GAMMA-CRYSTALLIN; HEREDITARY CATARACT; MESSENGER-RNAS; PHILLY MOUSE; GENE FAMILY; PROTEINS; DNA; LOCUS; SEQUENCE; CDNA AB The most prevalent proteins in the lens of the eye are called crystallins, and it is thought that aberrant crystallins may cause opacification of lens tissue. The Philly mouse, a strain with an inherited cataract, has an abnormal beta-B2-crystallin, the principal beta-crystallin in the mouse. The cDNA that codes for the beta-B2-crystallin protein has been cloned and sequenced from both the normal and the cataractous Philly mouse. The normal mouse beta-B2 cDNA is 756 nucleotides in length with 618 nucleotides of open reading frame. An in-frame deletion of 12 nucleotides has occurred in the Philly mouse cDNA, which results in the loss of 4 amino acids. The sequence of the mutant beta-B2 was analyzed against the reported structure of the normal bovine beta-B2-crystallin determined by x-ray crystallography. The region, in which the deletion of the amino acids occurs near the COOH terminus, is essential for the formation of the tertiary structure of the beta-B2-crystallin. The loss of these residues could explain the alterations that are seen with the Philly beta-B2 protein and may account for the instability of the Philly beta-B2 protein. This abnormal beta-B2-crystallin may be the cause of the cataract in this animal. RP CHAMBERS, C (reprint author), NEI,MECHANISMS OCULAR DIS LAB,BLDG 6,RM 228,BETHESDA,MD 20892, USA. NR 37 TC 98 Z9 101 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 6742 EP 6746 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700018 PM 1707874 ER PT J AU DEVICO, AL COPELAND, TD OROSZLAN, S GALLO, RC SARNGADHARAN, MG AF DEVICO, AL COPELAND, TD OROSZLAN, S GALLO, RC SARNGADHARAN, MG TI INTERACTION OF C-TERMINAL SEQUENCES OF HUMAN-IMMUNODEFICIENCY-VIRUS REVERSE-TRANSCRIPTASE WITH TEMPLATE PRIMER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DEPENDENT DNA-POLYMERASE; COMPLETE NUCLEOTIDE-SEQUENCE; MURINE LEUKEMIA-VIRUS; ROUS-SARCOMA VIRUS; AIDS VIRUS; ESCHERICHIA-COLI; HTLV-III; RNASE-H; POL GENES; EXPRESSION AB We have raised a rabbit monospecific antibody (designated C2003) against a synthetic peptide (CTP66) derived from a conserved sequence in the C-terminal portion of the p66 component of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) (DeVico, A. L., Copeland, T. D., Veronese, F. D., Oroszlan, S., Gallo, R. C., and Sarngadharan, M. G. (1989) AIDS Res. Hum. Retroviruses 5, 51-60). This antibody directly inhibits the polymerase activity of HIV-1 RT and of RTs from a variety of retroviruses. HIV-1 RT is protected from this inhibition by preincubation of the enzyme with template primer prior to treatment with the antibody. Such protection is abrogated when the pretreatment is conducted under conditions of high ionic strength. Kinetic studies showed that the antibody-mediated inhibition is competitive with respect to template primer concentration. These results indicate that C2003 antibody acts to interfere with the template binding function of the enzyme and further indicates that conserved residues recognized by the antibody may be directly involved in this function. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOLEC VIROL & CARCINOGENESIS LAB,FREDERICK,MD 21702. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RP DEVICO, AL (reprint author), ADV BIOSCI LABS,DEPT CELL BIOL,KENSINGTON,MD 20895, USA. FU NCI NIH HHS [N01-CO-74101, N01-CP-73723] NR 36 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 6774 EP 6779 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700023 PM 1707875 ER PT J AU ATTRI, AK LEWIS, MS KORN, ED AF ATTRI, AK LEWIS, MS KORN, ED TI THE FORMATION OF ACTIN OLIGOMERS STUDIED BY ANALYTICAL ULTRACENTRIFUGATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ACANTHAMOEBA PROFILIN; ATP HYDROLYSIS; STEADY-STATE; F-ACTIN; POLYMERIZATION; MECHANISM; PROTEINS; KINETICS; EXCHANGE; INHIBITION AB The small oligomers formed from Mg-G-actin under favorable conditions were studied by sedimentation velocity ultracentrifugation. The critical concentration of actin at pH 7.8 in the presence of 100-mu-M MgCl2 and 200-mu-M ATP was 12.5 +/- 2.8-mu-M. Under these conditions, about 15% of 7.5-mu-M Mg-actin was converted to oligomers of subunit size four to eight in 5 h at 20-degrees-C. In 100-mu-M MgCl2 and no free ATP, the critical concentration was about 6.5-mu-M, and about 22% of 7.5-mu-M Mg-actin was converted to dimers in 80 min. There were no detectable higher oligomers or F-actin present in either case. As determined by the analysis of ATP hydrolysis, most, if not all, of the oligomer subunits contained ATP. When 28.5-mu-M actin was polymerized to steady state in 100-mu-M MgCl2 and 200-mu-M ATP, about 50% of the actin was present as F-actin, consistent with the critical concentration (approximately 12.5-mu-M), about 50% as oligomers as large as seven subunits, and only about 5% as monomers. When solutions containing oligomers were diluted the oligomers dissociated. Alternatively, when the MgCl2 concentration was raised to 1 mM, the solutions containing oligomers polymerized more rapidly than monomeric Mg-G-actin and to the same final steady state. These data are entirely consistent with the condensation-elongation model for helical polymerization proposed by Oosawa and Kasai (Oosawa, F., and Kasai, M. (1962) J. Mol. Biol. 4, 10-21) according to which, under certain conditions, substantial amounts of short linear and helical oligomers should be formed below the critical concentration and linear oligomers should coexist with monomers and F-actin at steady state. C1 NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RP ATTRI, AK (reprint author), NHLBI,CELL BIOL LAB,BETHESDA,MD 20892, USA. RI Korn, Edward/F-9929-2012 NR 40 TC 36 Z9 36 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 6815 EP 6824 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700029 PM 2016296 ER PT J AU DEHERREROS, AG DOMINGUEZ, I DIAZMECO, MT GRAZIANI, G CORNET, ME GUDDAL, PH JOHANSEN, T MOSCAT, J AF DEHERREROS, AG DOMINGUEZ, I DIAZMECO, MT GRAZIANI, G CORNET, ME GUDDAL, PH JOHANSEN, T MOSCAT, J TI REQUIREMENT OF PHOSPHOLIPASE C-CATALYZED HYDROLYSIS OF PHOSPHATIDYLCHOLINE FOR MATURATION OF XENOPUS-LAEVIS OOCYTES IN RESPONSE TO INSULIN AND RAS P21 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BACILLUS-CEREUS; DIACYLGLYCEROL; STIMULATION; PROTEINS; TRANSFORMATION; MICROINJECTION; DIGLYCERIDE; ACTIVATION; RELEASE; CELLS AB Recent studies have demonstrated the activation of phospholipase C-mediated hydrolysis of phosphatidylcholine both by growth factors and by the product of ras oncogene, ras p21. Also, evidence has been presented indicating that the stimulation of this phospholipid-degradative pathway is sufficient to activate mitogenesis in fibroblasts. In Xenopus laevis oocytes, microinjection of transforming ras p21 is a potent inducer of maturation, whereas microinjection of a neutralizing anti-ras p21 antibody specifically inhibits maturation induced by insulin but not by progesterone. The results presented here demonstrate that microinjection of phosphatidylcholine-hydrolyzing phospholipase C is sufficient to induce maturation of Xenopus laevis oocytes. Furthermore, microinjection of a neutralizing anti-phosphatidylcholine-hydrolyzing phospholipase C specifically blocks the maturation program induced by ras p21/insulin but not by progesterone. C1 HOSP GEN GREGORIO MARANON,DR ESQUERDO 46,E-28007 MADRID,SPAIN. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. UNIV TROMSO,INST MED BIOL,N-9001 TROMSO,NORWAY. RI Moscat, Jorge/A-7011-2009; Graziani, Grazia/G-5747-2012; Garcia de Herreros, A/H-3104-2014; Johansen, Terje/N-2971-2015; OI Garcia de Herreros, A/0000-0001-5270-0808; Johansen, Terje/0000-0003-1451-9578; GRAZIANI, GRAZIA/0000-0002-0221-768X NR 32 TC 62 Z9 62 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 6825 EP 6829 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700030 ER PT J AU BURDON, T SANKARAN, L WALL, RJ SPENCER, M HENNIGHAUSEN, L AF BURDON, T SANKARAN, L WALL, RJ SPENCER, M HENNIGHAUSEN, L TI EXPRESSION OF A WHEY ACIDIC PROTEIN TRANSGENE DURING MAMMARY DEVELOPMENT - EVIDENCE FOR DIFFERENT MECHANISMS OF REGULATION DURING PREGNANCY AND LACTATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TISSUE-SPECIFIC EXPRESSION; BETA-CASEIN GENE; HORMONAL-REGULATION; MICE; PROMOTER; MILK; RAT; DIRECTS; GLAND; MOUSE AB Expression of the mouse whey acidic protein (WAP) gene is specific to the mammary gland, is induced several thousand-fold during pregnancy, and is under the control of steroid and peptide hormones. To study developmental regulation of the mouse WAP gene, a 7.2-kilobase (kb) WAP transgene, including 2.6 kb of 5'- and 1.6 kb of 3'-flanking sequences, was introduced into mice. Of the 13 lines of mice examined, 6 expressed the transgenes during lactation at levels between 3 and 54% of the endogenous gene. Although expression was dependent on the site of integration, the transgenes within a given locus were expressed in a copy number-dependent manner and were coordinately regulated. The WAP transgenes were expressed specifically in the mammary gland, but showed a deregulated pattern of expression during mammary development. In all six lines of mice, induction of the WAP transgenes during pregnancy preceded that of the endogenous gene. During lactation, expression in two lines increased coordinately with the endogenous gene, and in three other lines of mice, transgene expression decreased to a basal level. These data indicate that the 7.2-kb gene contains some but not all of the elements necessary for correct developmental regulation. At a functional level it appears as if a repressor element, which inactivates the endogenous gene until late pregnancy, and an element necessary for induction during lactation are absent from the transgene. Complementary results from developmental and hormone induction studies suggest that WAP gene expression during pregnancy and lactation is mediated by different mechanisms. C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE,MD 20705. NR 29 TC 128 Z9 129 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 6909 EP 6914 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700044 PM 2016304 ER PT J AU HIBINO, Y MARIANO, TM KUMAR, CS KOZAK, CA PESTKA, S AF HIBINO, Y MARIANO, TM KUMAR, CS KOZAK, CA PESTKA, S TI EXPRESSION AND RECONSTITUTION OF A BIOLOGICALLY-ACTIVE MOUSE INTERFERON-GAMMA-RECEPTOR IN HAMSTER-CELLS - CHROMOSOMAL LOCATION OF AN ACCESSORY FACTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID VIRUS-INDUCING LOCUS; PROTEIN KINASE-C; IMMUNE INTERFERON; GENE; RECOMBINANT; LINKAGE; SYSTEM; CDNA; SENSITIVITY; BINDING AB In order to localize the chromosome encoding the accessory factor required for function of the murine interferon-gamma (IFN-gamma) receptor, we transfected a cDNA expression vector encoding the receptor into several Chinese hamster x mouse somatic cell hydrids. As mouse Chromosome 10 carries the gene which encodes the interferon gamma-receptor (Ifgr), we used somatic cell hybrids that lack this chromosome. The presence of mouse Chromosome 16 was required to generate a response to murine IFN-gamma as assayed by stimulation of class I major histocompatibility complex antigen expression. These results demonstrate a species-specific accessory factor encoded on mouse Chromosome 16 (termed Ifgt) is necessary for mouse IFN-gamma to stimulate major histocompatibility complex expression through its receptor. C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP HIBINO, Y (reprint author), UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT MOLEC GENET & MICROBIOL,PISCATAWAY,NJ 08854, USA. FU NCI NIH HHS [CA-46465]; NIAID NIH HHS [AI-25914] NR 47 TC 51 Z9 52 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 6948 EP 6951 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700050 PM 1826681 ER PT J AU JONES, JC ZHEN, WP REED, E PARKER, RJ SANCAR, A BOHR, VA AF JONES, JC ZHEN, WP REED, E PARKER, RJ SANCAR, A BOHR, VA TI GENE-SPECIFIC FORMATION AND REPAIR OF CISPLATIN INTRASTRAND ADDUCTS AND INTERSTRAND CROSS-LINKS IN CHINESE-HAMSTER OVARY CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DIHYDROFOLATE-REDUCTASE GENE; PREFERENTIAL DNA-REPAIR; UVRABC EXCISION NUCLEASE; STRAND SPECIFICITY; 6-4 PHOTOPRODUCTS; N-METHYLPURINES; ACTIVE GENE; DHFR GENE; CIS-DIAMMINEDICHLOROPLATINUM(II); MECHANISM AB We have used three methods to study the formation and repair of intrastrand adducts and interstrand cross-links in the DNA of Chinese hamster ovary cells induced by the anticancer drug cis-diamminedichloroplatinum II (cisplatin). Using atomic absorption spectroscopy, we found that 21% of the total genomic cisplatin adducts were removed at 8 h and 42% at 24 h. We use ABC excinuclease digestion, coupled with our previously reported methodology to quantify DNA strand breaks, to detect cisplatin intrastrand adducts in specific genomic regions. These adducts were removed faster in the transcribed dihydrofolate reductase and c-myc genes compared to a noncoding fragment, a region containing the little or nontranscribed c-fos oncogene, and to the overall genome. Interstrand cross-links in specific sequences were quantified by Southern hybridization of denatured-renatured DNA separated on a neutral gel. We found that cross-links were removed more efficiently from the gene regions than intrastrand adducts and, at high levels of cross-linking, removal was similar from transcribed and from nontranscribed regions. C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,MED BRANCH,BETHESDA,MD 20892. UNIV N CAROLINA,SCH MED,DEPT BIOCHEM & BIOPHYS,CHAPEL HILL,NC 27599. FU NIGMS NIH HHS [GM32833] NR 45 TC 167 Z9 168 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 7101 EP 7107 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700072 PM 2016318 ER PT J AU ENCIO, IJ DETERAWADLEIGH, SD AF ENCIO, IJ DETERAWADLEIGH, SD TI THE GENOMIC STRUCTURE OF THE HUMAN GLUCOCORTICOID RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID THYROID-HORMONE RECEPTOR; MINERALOCORTICOID RECEPTOR; NUCLEAR RECEPTORS; RETINOIC ACID; GENE; TRANSCRIPTION; DNA; EXPRESSION; CDNA; ERBA AB We have determined the structure of the human glucocorticoid receptor (hGR) gene after the isolation and characterization of cosmid clones mapping to discrete regions of the cDNA. The gene contains a total of 10 exons and has a minimum size of 80 kilobases. Exon 1 consists solely of 5'-untranslated sequence, and exon 2 encodes the amino-terminal portion of the receptor. The two putative zinc fingers are separately encoded by two exons, and a total of five exons combine to form the cortisol-binding domain. By restriction mapping and sequence analysis of cosmids located on the 3'-end of the gene, we have established that the two receptor isoforms, hGR-alpha and hGR-beta, originate from the same gene by alternative splicing. Each hGR isoform is encoded by nine exons, of which the first eight are identical, whereas the ninth exons are heterologous. Multiple GC boxes and no obvious TATA or CAAT elements have been found in the 5'-flanking region. S1 nuclease analysis yielded one major band, and the transcription start site is localized to the *C residue within TAC*C-CTC. Alignment of sequences around the splice junctions of hGR with those of other members of the steroid receptor superfamily revealed three different splice positions withing the DNA-binding domain. This comparison also permitted the prediction of the positions of the splice sites and the sizes of the putative exons in the human mineralocorticoid receptor. C1 NIMH,CLIN NEUROGENET BRANCH,BLDG 10,RM 3N218,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. OI Encio, Ignacio/0000-0003-1732-1989 NR 40 TC 290 Z9 302 U1 0 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 7182 EP 7188 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700083 PM 1707881 ER PT J AU SAKAGUCHI, K YANAGISHITA, M TAKEUCHI, Y AURBACH, GD AF SAKAGUCHI, K YANAGISHITA, M TAKEUCHI, Y AURBACH, GD TI IDENTIFICATION OF HEPARAN-SULFATE PROTEOGLYCAN AS A HIGH-AFFINITY RECEPTOR FOR ACIDIC FIBROBLAST GROWTH-FACTOR (AFGF) IN A PARATHYROID CELL-LINE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SUBENDOTHELIAL EXTRACELLULAR-MATRIX; CAPILLARY ENDOTHELIAL-CELLS; PROTEIN-TYROSINE KINASE; NUCLEOTIDE-SEQUENCE; BOVINE BRAIN; GLYCOSAMINOGLYCAN CHAINS; PROTEOLYTIC DEGRADATION; MEMBRANE PROTEOGLYCAN; ANGIOGENIC PROTEIN; BINDING-SITES AB We have characterized two high affinity acidic fibroblast growth factor (aFGF) receptors in a rat parathyroid cell line (PT-r). Affinity labeling with I-125-aFGF showed that these two receptors, apparent molecular masses, 150 and 130 kDa, respectively, display higher affinity for aFGF than for bFGF. The 150-kDa receptor bears a heparan sulfate chain(s), demonstrated by a decrease in size of 15-20 kDa with heparitinase digestion after affinity labeling. Heparitinase digestion before affinity labeling markedly reduced the intensity of the 150 kDa species. Scatchard analysis showed two different high affinity binding sites (K(d) of 3.9 pM with 180 sites/cell and K(d) of 110 pM with 5800 sites/cell). The higher affinity site was completely eliminated by digestion with heparitinase before adding labeled aFGF; the lower affinity site was unaffected. In ion exchange chromatography after metabolic labeling of the cells with [H-3]glucosamine and affinity labeling with I-125-aFGF, the larger receptor-ligand complex, 165 kDa, eluted with approximately 0.5 M NaCl, typical eluting conditions for heparan sulfate proteoglycans. Both of the receptor-ligand complexes were smaller on sodium dodecyl sulfate-polyacrylamide gel electrophoresis than two major heparan sulfate proteoglycans, HSPG I and II, which we characterized in this cell line previously (Yanagishita, M., Brandi, M. L., and Sakaguchi, K. (1989) J. Biol. Chem. 264, 15714-15720). Both receptors have similar N-linked oligosaccharide and sialic acid contents, shown by analysis of affinity-labeled receptors upon digestion with glycopeptidase F and with neuraminidase. All together, these results suggest that PT-r cells bear two distinct high affinity receptors for aFGF, a 150-kDa receptor which is a heparan sulfate proteoglycan and another that is a glycoprotein. The heparan sulfate glycosaminoglycan moiety of the 150- kDa receptor is critical for high affinity binding of aFGF. These findings contrast with current concepts derived from other systems, suggesting that heparan sulfate glycosaminoglycans/proteoglycans function as a reservoir source for FGF or as a group of low affinity binding sites. C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. RP SAKAGUCHI, K (reprint author), NIDDK,METAB DIS BRANCH,BLDG 10,RM 9C101,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 74 TC 81 Z9 81 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 7270 EP 7278 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700097 PM 1707883 ER PT J AU FOYT, HL LEROITH, D ROBERTS, CT AF FOYT, HL LEROITH, D ROBERTS, CT TI DIFFERENTIAL ASSOCIATION OF INSULIN-LIKE GROWTH FACTOR-I MESSENGER-RNA VARIANTS WITH POLYSOMES INVIVO SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID 3' UNTRANSLATED REGION; RIBONUCLEIC-ACIDS; 5'-UNTRANSLATED REGIONS; MOLECULAR-CLONING; SCANNING MODEL; PROTO-ONCOGENE; RAT-LIVER; SEQUENCE; GENE; EXPRESSION AB Expression of the rat insulin-like growth factor I (IGF-I) gene results in a number of mature mRNA species that differ in size primarily at the 3' end due to differential polyadenylation site usage. Additionally, alternate splicing in both 5' and 3' regions produces RNAs which have the capacity to encode different IGF-I precursor peptides. We have analyzed total and polysomal RNAs using Northern blot analyses and solution hybridization/RNase protection assays to assess the in vivo translatability of these various IGF-I mRNA species. The results suggest that all of the known splicing variants are found on polysomes and may, therefore, be translated into a number of IGF-I precursors in vivo. One particular 5'-untranslated (UTR) variant is relatively enriched in polysomal RNA, a finding which suggests that removal of some of the 5'-UTR sequences encoded by exon 1 may enhance translatability. Of the IGF-I mRNAs with different lengths of 3'-UTR, only the shorter species were found on polysomes, suggesting that some aspect of the long 3'-UTR may prevent translation. Thus, differential processing of the primary transcript of the IGF-I gene may serve to generate IGF-I mRNA species which specify different precursors as well as to control their relative translatability. C1 NIDDKD,DIABET BRANCH,MOLEC & CELLULAR PHYSIOL SECT,BLDG 10,RM 8S-243,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 44 TC 66 Z9 67 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 7300 EP 7305 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700101 PM 2016330 ER PT J AU SAKAGUCHI, K APPELLA, E OMICHINSKI, JG CLORE, GM GRONENBORN, AM AF SAKAGUCHI, K APPELLA, E OMICHINSKI, JG CLORE, GM GRONENBORN, AM TI SPECIFIC DNA-BINDING TO A MAJOR HISTOCOMPATIBILITY COMPLEX ENHANCER SEQUENCE BY A SYNTHETIC 57-RESIDUE DOUBLE ZINC FINGER PEPTIDE FROM A HUMAN ENHANCER BINDING-PROTEIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR-IIIA; GEL-ELECTROPHORESIS; ESCHERICHIA-COLI; DOMAINS; RECOGNITION; MOTIF AB Two 57-residue peptides containing one pair of "zinc fingers" from a human enhancer binding protein were prepared by solid-phase peptide synthesis. One peptide (MBP-DF) contained the native sequence, while the second peptide ([Abu11]MBP-DF) has an alpha-aminobutyric acid residue substituted for a nonconserved cysteine residue at position 11. The peptides were characterized by several chemical and physical methods, and their DNA binding properties were evaluated using gel retardation experiments. Spectroscopic studies demonstrated that addition of metal ions such as zinc and cobalt resulted in specific conformational changes in both peptides, indicating that cysteine-11 does not appear to be involved in metal chelation. One-dimensional H-1 NMR studies indicate that a stable folded structure is formed upon addition of zinc, and the chemical shift pattern is consistent with that previously observed for one constituent single finger (Omichinski, J., Clore, G. M., Appella, E., Sakaguchi, K., and Gronenborn, A. M. (1990) Biochemistry 29, 9324-9334). Gel retardation experiments demonstrate that the peptides are capable of interacting with a 15-mer oligonucleotide comprising a portion of the major histocompatibility complex enhancer sequence and that the interaction is zinc-dependent. The dissociation constant for the [Abu11]MBP-DF peptide is 1.4 x 10(-7) M with maximal binding occurring at a zinc-to-peptide ratio of 2 to 1. The binding specificity observed with respect to related enhancer sequences exhibits the same relative order as noted previously for the whole protein. Studies with point mutants of the major histocompatibility complex enhancer binding sequence indicate that the last GC base pair in a four-guanine stretch plays a pivotal role in the interaction between the peptide and DNA. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. RP SAKAGUCHI, K (reprint author), NCI,HLTH EDUC LAB,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 26 TC 14 Z9 14 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 7306 EP 7311 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700102 PM 2016331 ER PT J AU AIBA, S KATZ, SI AF AIBA, S KATZ, SI TI THE ABILITY OF CULTURED LANGERHANS CELLS TO PROCESS AND PRESENT PROTEIN ANTIGENS IS MHC-DEPENDENT SO JOURNAL OF IMMUNOLOGY LA English DT Article ID DENDRITIC CELLS; CONTACT HYPERSENSITIVITY; CYTOCHROME-C; IA-ANTIGENS; CLONES; ACTIVATION; RECOGNITION; EXPRESSION; HYBRIDOMAS; MACROPHAGE AB There is controversy regarding the ability of short term (2 to 3 days) cultured epidermal Langerhans cells (cLC) to process and present intact protein Ag to primed T cells. Some studies have shown that cLC are potent APC for both haptens and intact protein Ag, whereas in others cLC have been unable to process and present intact protein Ag. In an attempt to resolve this controversy, we tested the ability of Langerhans cells from several strains of mice to process and present intact protein Ag to T cell clones and T cell hybridomas. We found that both cLC and freshly prepared Langerhans cells from various Ia(k) mice, including BALB.k mice, process and present intact protein antigens (i.e., hen egg lysozyme, cytochrome c, and OVA) to T cells. These functions are retained in cLC cultured for 7 days. In contrast, cLC from Ia(d) mice do not process intact protein Ag, such as hen egg lysozyme and myoglobin, although they can present relevant peptides to specific T cells and are potent stimulators of allogeneic responses. Furthermore, cLC from (Ia(k) x Ia(d))F1 mice process and present intact protein Ag to Ia(k)-restricted T cells, but not to Ia(d)-restricted T cells. Although cLC that processed and presented intact protein Ag to T cells exhibited enhanced class II MHC expression, they were, on a per cell basis, somewhat less efficient than were fresh Langerhans cells. Finally, we found that if Ia(d) Langerhans cells are pulsed with intact protein Ag and then cultured for 3 days, they are then fully capable of inducing Ag- and MHC-specific T cell proliferation. C1 NCI,DERMATOL BRANCH,BLDG 10-12N238,BETHESDA,MD 20892. NR 39 TC 68 Z9 68 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1991 VL 146 IS 8 BP 2479 EP 2487 PG 9 WC Immunology SC Immunology GA FG729 UT WOS:A1991FG72900001 PM 1849934 ER PT J AU KENNY, JJ STALL, AM SIECKMANN, DG LAMERS, MC FINKELMAN, FD FINCH, L LONGO, DL AF KENNY, JJ STALL, AM SIECKMANN, DG LAMERS, MC FINKELMAN, FD FINCH, L LONGO, DL TI RECEPTOR-MEDIATED ELIMINATION OF PHOSPHOCHOLINE-SPECIFIC B-CELLS IN X-LINKED IMMUNE-DEFICIENT MICE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TRANSGENIC MOUSE LINE; PROTEUS-MORGANII; LYMPHOCYTES-B; KAPPA-GENES; MU-GENES; ANTIBODIES; PHOSPHORYLCHOLINE; EXPRESSION; IMMUNODEFICIENCY; AUTOIMMUNE AB The combined expression of the M167-mu/kappa antiphosphocholine (PC) transgenes with the x-linked immunodeficiency gene, xid, results in an almost total failure to develop B cells in the peripheral lymphoid organs of such mice. Although there is no significant difference between the normal transgene positive (TG+) female offspring and the immunodeficient TG+ xid males with respect to the number of B220+ pre-B cells and IgM+B220+ B cells that develop in their bone marrow, the hemizygous xid males have 85% fewer B cells in their spleens than the phenotypically normal heterozygous F1 females. In xid M167-mu-transgenic mice, PC-specific B cells also fail to develop in the spleen; however, numberous B cells bearing the mu-a+V(H)1+-transgene product associated with endogenous kappa-L chains that do not give rise PC-specific antibodies are present. In the phenotypically normal TG+ (B6.CBA/N X-mu-243-4)F1 female mice, PC-specific B cells represent almost 10% of the total B cell population, and these B cells express an M167-Id that has been produced by association of the V(H)1 transgene product with an endogenous V-kappa-24 L chain. B cells expressing the normally dominant T15-Id are not detectable in the spleens of these M167 mu-transgenic mice. Furthermore, M167-Id+B cells are present at a fivefold lower level in the bone marrow of mu-TG+ normal mice than in their spleens. These data suggest that the PC-specific B cells that develop in TG+ xid mice are either clonally deleted via some "IgR-directed" mechanism or they fail to receive the appropriate signals to exit the bone marrow or to enter the peripheral lymphoid tissues. This hypothesis is supported by the finding that TNP-specific B cells develop normally and do not undergo clonal deletion in xid mice carrying the Sp6-mu/kappa-anti-TNP transgenes. C1 STANFORD UNIV,DEPT GENET,STANFORD,CA 94305. USN,MED RES INST,BETHESDA,MD 20814. MAX PLANCK INST IMMUNBIOL,W-7800 FREIBURG,GERMANY. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP KENNY, JJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,BOX B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-23910]; NIAID NIH HHS [AI-24672, AI-21328] NR 38 TC 25 Z9 25 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1991 VL 146 IS 8 BP 2568 EP 2577 PG 10 WC Immunology SC Immunology GA FG729 UT WOS:A1991FG72900012 PM 1901880 ER PT J AU WAYTES, AT MALBRAN, A BOBAK, DA FRIES, LF AF WAYTES, AT MALBRAN, A BOBAK, DA FRIES, LF TI PRE-LIGATION OF CR-1 ENHANCES IGG-DEPENDENT PHAGOCYTOSIS BY CULTURED HUMAN MONOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID IMMOBILIZED IMMUNE-COMPLEXES; COMPLEMENT-RECEPTOR FUNCTION; POLYMORPHONUCLEAR LEUKOCYTES; MEDIATED PHAGOCYTOSIS; C3B RECEPTOR; FC-RECEPTOR; MACROPHAGES; INVITRO; PARTICLES; MECHANISM AB Opsonization of the C3b receptor (CR1) on phagocytic cells with C3b enhances both attachment of targets to the cells and subsequent IgG-dependent ingestion of these targets. To explore mechanisms involved in this increased phagocytosis, we adhered cultured human monocytes to surfaces pre-coated with CR1 ligand or control proteins and quantitated ingestion of sheep E opsonized with IgG alone. Three ligands for CR1 resulted in markedly enhanced phagocytosis of targets when compared individually to a panel of non-ligands, as determined by both the proportion of monocytes ingesting targets (percent phagocytosis) and by the number of targets ingested per 100 monocytes (phagocytic index). The ligands included purified C3b, iC3, and Fab fragments of 1B4, a monoclonal anti-CR1, which resulted in a percent phagocytosis of 56.3 (p < 0.01), 59.0 (p < 0.01), and 54.4 (p < 0.02) and a phagocytic index of 281.2 (p < 0.01), 281.1 (p < 0.01), and 247.1 (p < 0.02), respectively. Control proteins including human serum albumin, hemoglobin, Fab fragments of anti-fibronectin, anti-beta-2 microglobulin, and MOPC 21, and Fc fragments of 1B4 and MOPC 21 produced no significant stimulation of phagocytosis, nor did F(ab')2 fragments of monoclonal anti-CR3, M1/70. CR1-specific augmentation of target ingestion was apparent with monocytes cultured in serum-free medium for 1 to 7 days,but was not seen with freshly elutriated cells. Phagocytosis of unopsonized or IgM-coated targets was minimal. These results suggest that the adherent monocytes are primed by CR1 cross-linking for enhanced FcR-mediated phagocytosis even when the CR1 ligand is not present on the targets. This contrasts with the behavior of CR3, and demonstrated functional divergence between these C3 fragment receptors in the phagocytic process. RP WAYTES, AT (reprint author), NIAID,CLIN INVEST LAB,BLDG 10,ROOM 5N307,BETHESDA,MD 20892, USA. NR 30 TC 6 Z9 6 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1991 VL 146 IS 8 BP 2694 EP 2700 PG 7 WC Immunology SC Immunology GA FG729 UT WOS:A1991FG72900029 PM 1826698 ER PT J AU DESCOTEAUX, A TURCO, SJ SACKS, DL MATLASHEWSKI, G AF DESCOTEAUX, A TURCO, SJ SACKS, DL MATLASHEWSKI, G TI LEISHMANIA-DONOVANI LIPOPHOSPHOGLYCAN SELECTIVELY INHIBITS SIGNAL TRANSDUCTION IN MACROPHAGES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PROTEIN KINASE-C; MURINE PERITONEAL-MACROPHAGES; NECROSIS FACTOR RECEPTORS; MESSENGER-RNA EXPRESSION; MOLECULAR-CLONING; GENE-EXPRESSION; BINDING-SITES; LIPOPOLYSACCHARIDE; FOS; ACCUMULATION AB The effect of purified lipophosphoglycan(LPG) of Leishmania donovani on signal transduction and gene expression in murine bone marrow-derived macrophages was investigated. LPG stimulated the rapid expression of both c-fos and TNF genes within 30 min after exposure, suggesting that the interaction of LPG with its receptor stimulated a specific signal transduction pathway. Macrophages pretreated with LPG for 3 h became unresponsive to subsequent stimulation with LPS and the activators of protein kinase C, 1-oleoyl-2-acetyl-glycerol, and calcium ionophore A23187. Moreover, LPG induced a rapid down-modulation of TNF receptors. In contrast, the ability of macrophages to express the c-fos gene in response to the cAMP analogue, dibutiryl cAMP, was not impaired by LPG. Fragmentation of LPG revealed that the inhibitory activity of LPG required both the repeating phosphorylated disaccharides and the phosphosaccharide core. Collectively, these data demonstrate that LPG selectively impaired signal transduction in macrophages and suggest a role for this molecule in the survival of the parasite within the macrophage. C1 MCGILL UNIV,MACDONALD COLL,INST PARASITOL,21111 LAKESHORE RD,ST ANNE BELLEVUE H9X 1C0,QUEBEC,CANADA. UNIV KENTUCKY,MED CTR,DEPT BIOCHEM,LEXINGTON,KY 40536. NIH,PARASIT DIS LAB,IMMUNOL & CELL BIOL SECT,BETHESDA,MD 20892. FU NIAID NIH HHS [AI209041] NR 48 TC 124 Z9 125 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1991 VL 146 IS 8 BP 2747 EP 2753 PG 7 WC Immunology SC Immunology GA FG729 UT WOS:A1991FG72900037 PM 1707920 ER PT J AU CARDELLINA, JH BOYD, MR AF CARDELLINA, JH BOYD, MR TI INTRAMURAL NATURAL PRODUCT DRUG DISCOVERY RESEARCH AT THE NATIONAL-CANCER-INSTITUTE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FCRDC,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 1 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89302416 ER PT J AU PARSEGIAN, VA RAND, RP AF PARSEGIAN, VA RAND, RP TI ON THE UNLIKELIHOOD OF MOLECULAR PROTRUSION AS THE SOURCE OF HYDRATION FORCES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 BROCK UNIV,ST CATHARINES L2S 3A1,ONTARIO,CANADA. PRINCETON UNIV,PRINCETON,NJ 08544. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 6 EP COLL PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89301027 ER PT J AU TENNANT, RW AF TENNANT, RW TI RELATIONSHIPS BETWEEN MUTAGENICITY, TOXICITY, CARCINOGENICITY, AND CHEMICAL-STRUCTURE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 11 EP CHAS PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300930 ER PT J AU RANDOLPH, JT EMERY, LA BAKER, DC CYSYK, RE AF RANDOLPH, JT EMERY, LA BAKER, DC CYSYK, RE TI SYNTHESIS OF URIDINE DIPHOSPHONATE HEXOSES AS ANALOGS OF URIDINE-DIPHOSPHATE (UDP) HEXOSES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 UNIV TENNESSEE,DEPT CHEM,KNOXVILLE,TN 37996. NCI,BIOL CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 14 EP CARB PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300537 ER PT J AU ELMER, C SIEGEL, S AF ELMER, C SIEGEL, S TI THE VALUE OF ADEQUATE DATA DOCUMENTATION IN HEALTH AND ENVIRONMENTAL SCIENCES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 MONSANTO CO,ST LOUIS,MO 63167. NATL LIB MED,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 27 EP CINF PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300988 ER PT J AU LEWIN, AH RAMACHANDRAN, K LAMB, P MARVIZON, JC PAUL, I WONG, G SKOLNICK, P AF LEWIN, AH RAMACHANDRAN, K LAMB, P MARVIZON, JC PAUL, I WONG, G SKOLNICK, P TI ANALOGS OF GLYCINE IN THE GLYCINE-NMDA-PCP SUPRAMOLECULAR COMPLEX SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 32 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89302447 ER PT J AU SIEGEL, S AF SIEGEL, S TI STRUCTURE OF INFORMATION RESOURCES TO MORE EFFECTIVELY SUPPORT SCIENTIFIC AND REGULATORY DECISION-MAKING SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NATL LIB MED,BETHESDA,MD 20894. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 32 EP CINF PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300993 ER PT J AU WALTERS, DB TRAMMELL, RL KEITH, LH AF WALTERS, DB TRAMMELL, RL KEITH, LH TI PERFORMANCE OF THE NTP CHEMICAL REPOSITORY RELATIVE TO THE NEW OSHA LABORATORY STANDARD SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. RADIAN CORP,AUSTIN,TX 78720. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 42 EP CHAS PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300956 ER PT J AU SEIFRIED, HE LONGFELLOW, DG AF SEIFRIED, HE LONGFELLOW, DG TI THE REFERENCE-STANDARD REPOSITORY CONCEPT AT NCI SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,DIV CANC ETIOL,CHEM & PHYS CARCINOGENESIS BRANCH,BETHESDA,MD 20902. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 44 EP CHAS PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300958 ER PT J AU GROOVER, KH LOMAX, NR AF GROOVER, KH LOMAX, NR TI THE NATIONAL-CANCER-INSTITUTES CHEMOTHERAPEUTIC-AGENTS REPOSITORY SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. ERC BIOSERV CORP,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 45 EP CHAS PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300959 ER PT J AU MARAGOS, CM HRABIE, JA DUNAMS, TM KEEFER, LK WINK, DA BOVE, AA MORLEY, D AF MARAGOS, CM HRABIE, JA DUNAMS, TM KEEFER, LK WINK, DA BOVE, AA MORLEY, D TI COMPLEXES OF .NO WITH NUCLEOPHILES AS AGENTS FOR THE CONTROLLED BIOLOGICAL RELEASE OF NITRIC-OXIDE - VASORELAXANT EFFECTS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FCRDC,FREDERICK,MD 21702. PRI DYNCORP,FREDERICK,MD 21702. TEMPLE UNIV,HLTH SCI CTR,SCH MED,PHILADELPHIA,PA 19140. NR 0 TC 0 Z9 0 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 63 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89302478 ER PT J AU TOMER, KB DETERDING, LJ MOSELEY, MA AF TOMER, KB DETERDING, LJ MOSELEY, MA TI TANDEM MASS-SPECTROMETRY COMBINED WITH NANOSCALE SEPARATION TECHNIQUES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 65 EP ANYL PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300263 ER PT J AU KAY, LE IKURA, M ZHU, G BAX, A AF KAY, LE IKURA, M ZHU, G BAX, A TI 3-DIMENSIONAL AND 4-DIMENSIONAL HETERONUCLEAR TRIPLE RESONANCE NMR-SPECTROSCOPY OF PROTEINS IN SOLUTION SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 74 EP ANYL PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300272 ER PT J AU KROEGERKOEPKE, MB SMITH, RH MICHEJDA, CJ AF KROEGERKOEPKE, MB SMITH, RH MICHEJDA, CJ TI DNA ALKYLATION BY 1-(2-CHLOROETHYL) AND 1-(2-HYDROXYETHYL)-3-CARBOETHOXY-3-METHYLTRIAZENE - RELATIONSHIP BETWEEN CHEMICAL AND BIOCHEMICAL-PROPERTIES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,ABL,BRP,FREDERICK,MD 21702. WESTERN MARYLAND COLL,WESTMINSTER,MD 21157. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 83 EP ORGN PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG894 UT WOS:A1991FG89400186 ER PT J AU HAVLIN, S AF HAVLIN, S TI TRANSPORT AND TRAPPING IN FRACTAL SYSTEMS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 92 EP PHYS PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG894 UT WOS:A1991FG89400597 ER PT J AU FAKINLEDE, KJ COSTA, O GU, ZQ SKOLNICK, P UPASANI, RB FRYER, RI AF FAKINLEDE, KJ COSTA, O GU, ZQ SKOLNICK, P UPASANI, RB FRYER, RI TI BENZODIAZEPINE RECEPTOR (BZR) STUDIES - PYRIDO[3,2-B]INDOLES AS PUTATIVE BZR AGONIST LIGANDS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 RUTGERS STATE UNIV,DEPT CHEM,NEW BRUNSWICK,NJ 08903. NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 126 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89302541 ER PT J AU RIOS, R GU, ZQ SKOLNICK, P FRYER, RI AF RIOS, R GU, ZQ SKOLNICK, P FRYER, RI TI BENZODIAZEPINE RECEPTOR (BZR) STUDIES - CONCERNING POSSIBLE ELECTRON DONATING SITES OF O-METHYL AND N-METHYL PYRAZOLOQUINOLINES AT THE BZR SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 RUTGERS STATE UNIV,DEPT CHEM,NEW BRUNSWICK,NJ 08903. NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 127 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89302542 ER PT J AU ZHANG, PW GU, ZQ SKOLNICK, P FRYER, RI AF ZHANG, PW GU, ZQ SKOLNICK, P FRYER, RI TI BENZODIAZEPINE RECEPTOR STUDIES - COMPARISON OF BIOLOGICAL-ACTIVITY OF NOVEL PYRAZOLOQUINOLINE ANALOGS WITH PREDICTIVE LITERATURE MODELS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 RUTGERS STATE UNIV,DEPT CHEM,NEW BRUNSWICK,NJ 08903. NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 128 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89302543 ER PT J AU CHIA, NC GU, ZQ SKOLNICK, P FRYER, RI AF CHIA, NC GU, ZQ SKOLNICK, P FRYER, RI TI STRUCTURE-ACTIVITY RELATIONSHIP STUDIES AT BZR - STUDIES CONCERNING THE CONFORMATIONAL FIT OF BETA-CARBOLINE AGONIST LIGANDS TO AN IMIDAZO-1,4-BENZODIAZEPINE-3-CARBOXYLATE ESTER TEMPLATE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 RUTGERS STATE UNIV,DEPT CHEM,NEW BRUNSWICK,NJ 08903. NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 129 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89302544 ER PT J AU DEUTSCH, HM EARNHART, LL GLINSKI, JA HERNANDEZ, M HAUGWITZ, RD NARAYANAN, VL ZALKOW, LH AF DEUTSCH, HM EARNHART, LL GLINSKI, JA HERNANDEZ, M HAUGWITZ, RD NARAYANAN, VL ZALKOW, LH TI WATER-SOLUBLE PRODRUGS OF THE BENZENE MALEIMIDE PHOTOADDUCT MITINDOMIDE AS POTENTIAL ANTITUMOR AGENTS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 GEORGIA INST TECHNOL,SCH CHEM & BIOCHEM,ATLANTA,GA 30332. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 139 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89302554 ER PT J AU GRONENBORN, A AF GRONENBORN, A TI APPLICATIONS OF 3D AND 4D NMR SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 14 PY 1991 VL 201 BP 179 EP CHED PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA FG893 UT WOS:A1991FG89300858 ER PT J AU CLEMENS, JD VANLOON, F SACK, DA RAO, MR AHMED, F CHAKRABORTY, J KAY, BA KHAN, MR YUNUS, M HARRIS, JR SVENNERHOLM, AM HOLMGREN, J AF CLEMENS, JD VANLOON, F SACK, DA RAO, MR AHMED, F CHAKRABORTY, J KAY, BA KHAN, MR YUNUS, M HARRIS, JR SVENNERHOLM, AM HOLMGREN, J TI BIOTYPE AS DETERMINANT OF NATURAL IMMUNIZING EFFECT OF CHOLERA SO LANCET LA English DT Note ID VACCINES; BANGLADESH AB To test the hypothesis that clinical Vibrio cholerae O1 infections protect against recurrent cholera, treated cholera episodes in a rural Bangladesh population of 188 153 people who were followed between 1985 and 1988 were analysed. Of the 2214 people with initial episodes of cholera, 7 had a second episode. The incidence of cholera was 61% lower in subjects who had had an earlier episode than in those without such an episode. Whereas initial episodes of classical cholera were associated with complete protection against subsequent cholera, initial episodes of El Tor cholera were associated with negligible protection. C1 INT CTR DIARRHOEL DIS RES,DHAKA,BANGLADESH. JOHNS HOPKINS UNIV,SCH PUBL HLTH,DEPT INT HLTH,BALTIMORE,MD 21218. CTR DIS CONTROL,ENTER INFECT BRANCH,ATLANTA,GA 30333. UNIV MARYLAND,CTR VACCINE DEV,BALTIMORE,MD 21201. GOTHENBURG UNIV,DEPT MED MICROBIOL,S-41124 GOTHENBURG,SWEDEN. RP CLEMENS, JD (reprint author), NICHHD,PREVENT RES PROGRAM,EXECUT PLAZA N BLDG,ROOM 640,BETHESDA,MD 20892, USA. NR 10 TC 46 Z9 46 U1 1 U2 2 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 13 PY 1991 VL 337 IS 8746 BP 883 EP 884 DI 10.1016/0140-6736(91)90207-6 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FG048 UT WOS:A1991FG04800006 PM 1672971 ER PT J AU HOEG, JM AF HOEG, JM TI PHARMACOLOGICAL AND SURGICAL-TREATMENT OF DYSLIPIDEMIC CHILDREN AND ADOLESCENTS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA; LOW-DENSITY-LIPOPROTEIN; LIVER-TRANSPLANTATION; PORTACAVAL-SHUNT; II HYPERLIPOPROTEINEMIA; CARDIOVASCULAR-DISEASE; CHOLESTYRAMINE RESIN; APOLIPOPROTEIN-B; COLESTIPOL RESIN; PLASMA-EXCHANGE RP HOEG, JM (reprint author), NHLBI,BLDG 10,ROOM 7N117,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 53 TC 15 Z9 15 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD APR 12 PY 1991 VL 623 BP 275 EP 284 DI 10.1111/j.1749-6632.1991.tb43737.x PG 10 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FW077 UT WOS:A1991FW07700026 PM 2042836 ER PT J AU CONTRERAS, PC RAGAN, DM BREMER, ME LANTHORN, TH GRAY, NM IYENGAR, S JACOBSON, AE RICE, KC DECOSTA, BR AF CONTRERAS, PC RAGAN, DM BREMER, ME LANTHORN, TH GRAY, NM IYENGAR, S JACOBSON, AE RICE, KC DECOSTA, BR TI EVALUATION OF U-50,488H ANALOGS FOR NEUROPROTECTIVE ACTIVITY IN THE GERBIL SO BRAIN RESEARCH LA English DT Article DE SIGMA-ISCHEMIA; NEUROPROTECTIVE; KAPPA-OPIOID; BENZOMORPHAN U-50,488H ID OPIOID RECEPTOR AGONIST; SPINAL-CORD INJURY; RAT; ISCHEMIA; BRAIN; SIGMA; ANTAGONISTS; PROTECTION; U-50488H AB U-50,488H, a kappa (kappa) opioid ligand with moderate potency at sigma (sigma) receptors, protects against mechanical and ischemia-induced injury. The purpose of this study was to evaluate the possibility that sigma-receptors may be involved in mediating the neuroprotective actions of U-50,488H. This possibility was examined by testing the potential of a series of U-50,488H analogs, which are potent sigma-ligands with minimal activity at kappa-opioid receptors, to protect against ischemia-induced neuronal damage in the gerbil. Like U-50,488H, BD-449 (20 mg/kg), the cis-diastereomer of U-50,488H, protected against ischemia-induced neuronal damage as did BD-737 (50 and 30 mg/kg) and BD-738 (50 mg/kg). All 3 compounds interacted selectively with sigma-receptors. In contrast, BD-601 (50 mg/kg), did not protect against ischemia-induced neuronal damage, although it also interacted potently with sigma-receptors. One difference between the compounds that were neuroprotective and BD-601 is that only BD-601 produced sigma-like behavioral effects in the rat. Thus, it is possible that BD-601 may interact differently or at a different sigma-subtype than BD-449, BD-737 and BD-738 with sigma-receptors. However, these results clearly indicate that an interaction with kappa-opioid receptors is not required for anti-ischemic activity, and that sigma-receptors may play a role in neuroprotection. C1 GD SEARLE & CO,CNSDR,CHESTERFIELD,MO 63198. NIDDKD,MED CHEM LAB,BETHESDA,MD 20892. NR 32 TC 64 Z9 64 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 12 PY 1991 VL 546 IS 1 BP 79 EP 82 DI 10.1016/0006-8993(91)91161-S PG 4 WC Neurosciences SC Neurosciences & Neurology GA FJ655 UT WOS:A1991FJ65500010 PM 1649669 ER PT J AU SAITO, K MARKEY, SP HEYES, MP AF SAITO, K MARKEY, SP HEYES, MP TI CHRONIC EFFECTS OF GAMMA-INTERFERON ON QUINOLINIC ACID AND INDOLEAMINE-2,3-DIOXYGENASE IN BRAIN OF C57BL6 MICE SO BRAIN RESEARCH LA English DT Article DE KYNURENINE PATHWAY METABOLISM; CENTRAL NERVOUS SYSTEM; SYSTEMIC TISSUE; INDOLEAMINE-2,3-DIOXYGENASE; TRYPTOPHAN-2,3-DIOXYGENASE; CELLULAR IMMUNITY; GAMMA-INTERFERON ID INDOLEAMINE 2,3-DIOXYGENASE; KYNURENIC ACID; RAT-BRAIN; TRYPTOPHAN DEGRADATION; QUANTIFICATION; CHROMATOGRAPHY; METABOLITE; INDUCTION; EXPOSURE; SYSTEM AB Chronic infections are associated with increased concentrations of the neuroactive kynurenine pathway metabolite, quinolinic acid (QUIN), in blood and cerebrospinal fluid. In the present study, repeated injections of gamma-interferon (5000 IU, every 3 days for 39 days) to C57BL6 mice were associated with persistent activation of indoleamine-2,3-dioxygenase (IDO), the first enzyme of the kynurenine pathway, in lung and brain, sustained increases in brain QUIN concentration and increases in plasma L-kynurenine and QUIN levels. Mice chronically treated with gamma-interferon offer an animal model to investigate the effects of sustained immune stimulation on kynurenine pathway metabolism. C1 NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BLDG 10,ROOM 3D40,BETHESDA,MD 20892. NR 35 TC 72 Z9 72 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 12 PY 1991 VL 546 IS 1 BP 151 EP 154 DI 10.1016/0006-8993(91)91171-V PG 4 WC Neurosciences SC Neurosciences & Neurology GA FJ655 UT WOS:A1991FJ65500020 PM 1830237 ER PT J AU SCHAUFELBERGER, DE CHMURNY, GN BEUTLER, JA KOLECK, MP ALVARADO, AB SCHAUFELBERGER, BW MUSCHIK, GM AF SCHAUFELBERGER, DE CHMURNY, GN BEUTLER, JA KOLECK, MP ALVARADO, AB SCHAUFELBERGER, BW MUSCHIK, GM TI REVISED STRUCTURE OF BRYOSTATIN-3 AND ISOLATION OF THE BRYOSTATIN-3 26-KETONE FROM BUGULA-NERITINA SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Article ID PHORBOL ESTER RECEPTOR; PROTEIN KINASE-C; ANTINEOPLASTIC AGENTS; BRYOZOA AB Bryostatin 3 and the corresponding 26-ketone 5, which represents a new bryostatin, were isolated from the marine bryozoan Bugula neritina (Bugulidae). Spectroscopic data from 2D NMR studies indicate that the structure of bryostatin 3 (3) has to be revised to structure 4. Bryostatin 3 showed [H-3]phorbol dibutyrate receptor displacement activity similar to that of bryostatin 1, whereas the corresponding 26-ketone 5 was significantly less active. C1 NCI,FREDERICK CANC RES & DEV CTR,DCT,DTP,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. RP SCHAUFELBERGER, DE (reprint author), PRI DYNCORP,CHEM SYNTH & ANAL LAB,FREDERICK,MD 21702, USA. RI Beutler, John/B-1141-2009 OI Beutler, John/0000-0002-4646-1924 NR 19 TC 28 Z9 29 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD APR 12 PY 1991 VL 56 IS 8 BP 2895 EP 2900 DI 10.1021/jo00008a054 PG 6 WC Chemistry, Organic SC Chemistry GA FH238 UT WOS:A1991FH23800054 ER PT J AU TAYLOR, SJ CHAE, HZ RHEE, SG EXTON, JH AF TAYLOR, SJ CHAE, HZ RHEE, SG EXTON, JH TI ACTIVATION OF THE BETA-1 ISOZYME OF PHOSPHOLIPASE-C BY ALPHA-SUBUNITS OF THE GQ CLASS OF G-PROTEINS SO NATURE LA English DT Article ID BOVINE BRAIN; TYROSINE PHOSPHORYLATION AB MANY hormones, neurotransmitters and growth factors, on binding to G protein-coupled receptors or receptors possessing tyrosine kinase activity, increase intracellular levels of the second messengers inositol 1,4,5-trisphophate and 1,2-diacylglycerol. This is due to activation of phosphoinositide-specific phospholipase(s) C (PLC), the isozymes of which are classified into groups, alpha, beta, gamma and delta (refs 1, 2). The beta, gamma and delta-groups themselves contain PLC isozymes which have both common and unique structural domains 3. Only the gamma-1 isozyme has been implicated in a signal transduction mechanism 4. This involves association with, and tyrosine phosphorylation by, the ligand-bound epidermal growth factor and platelet-derived growth factor receptors 5-7, probably by means of the PLC-gamma-1-specific src homology (SH2) domain 8. Because EGF receptor-mediated tyrosine phosphorylation of PLC-gamma-1 stimulates catalytic activity in vitro 9 and G proteins have been implicated in the activation of PLC 10, we investigated which PLC isozymes are subject to G protein regulation. We have purified 11 an activated G protein alpha-subunit that stimulates partially purified phospholipase C and now report that this G protein specifically activates the beta-1 isozyme, but not the gamma-1 and delta-1 isozymes of phospholipase C. We also show that this protein is related to the G(q) class of G protein alpha-subunits 12. C1 VANDERBILT UNIV,MED CTR,SCH MED,HOWARD HUGHES MED INST,DEPT MOLEC PHYSIOL & BIOPHYS,NASHVILLE,TN 37232. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 30 TC 735 Z9 739 U1 1 U2 4 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 11 PY 1991 VL 350 IS 6318 BP 516 EP 518 DI 10.1038/350516a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FG143 UT WOS:A1991FG14300056 PM 1707501 ER PT J AU MCKINNEY, RE MAHA, MA CONNOR, EM FEINBERG, J SCOTT, GB WULFSOHN, M MCINTOSH, K BORKOWSKY, W MODLIN, JF WEINTRUB, P ODONNELL, K GELBER, RD ROGERS, GK LEHRMAN, SN WILFERT, CM AF MCKINNEY, RE MAHA, MA CONNOR, EM FEINBERG, J SCOTT, GB WULFSOHN, M MCINTOSH, K BORKOWSKY, W MODLIN, JF WEINTRUB, P ODONNELL, K GELBER, RD ROGERS, GK LEHRMAN, SN WILFERT, CM TI A MULTICENTER TRIAL OF ORAL ZIDOVUDINE IN CHILDREN WITH ADVANCED HUMAN-IMMUNODEFICIENCY-VIRUS DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; INFECTION; AZT; SURVIVAL; TYPE-1 AB Background and Methods. Zidovudine has been shown to be an effective antiretroviral treatment in adults with human immunodeficiency virus (HIV) infection. We examined the safety of zidovudine and the tolerance of and therapeutic response to the drug in 88 children with advanced HIV disease. During a 24-week outpatient trial, zidovudine (180 mg per square meter of body-surface area per dose) was given by mouth every six hours and serial measurements were made of clinical, immunologic, and virologic indexes. Children who completed 24 weeks of treatment were permitted to continue receiving zidovudine. Results. Of the 88 children (mean age, 3.9 years; range, 4 months to 11 years), 61 completed the initial 24-week trial, and 49 continued to receive zidovudine for up to 90 weeks (median follow-up, 56 weeks). The patients generally tolerated zidovudine well. One or more episodes of hematologic toxicity occurred in 54 children (61 percent) - anemia (hemoglobin level, < 75 g per liter) in 23 children (26 percent) and neutropenia (neutrophil count, < 0.75 X 10(9) per liter) in 42 (48 percent). Many of these abnormalities resolved spontaneously, but 30 children required transfusions or a modification of the dose of zidovudine. Only three children had to stop receiving the drug because of hematologic toxicity. Kaplan-Meier analysis demonstrated that the probability of survival was 0.89 after 24 weeks and 0.79 after 52 weeks. There was marked improvement in weight gain, cognitive function (mainly in children < 3 years old), serum and cerebrospinal fluid concentrations of p24 antigen, and the proportion of cerebrospinal fluid cultures negative for HIV. CD4+ lymphocyte counts (mean at base line, 0.263 X 10(9) per liter) improved during the first 12 weeks, although the improvement was not sustained through the 24th week. Conclusions. Zidovudine in a dose of 180 mg per square meter every six hours can be safely administered to children with advanced HIV disease. The resultant clinical, immunologic, and virologic improvements in children are similar to those reported with zidovudine in adults. C1 BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC 27709. NEW JERSEY CHILDRENS HOSP,NEWARK,NJ. NIAID,DIV AIDS,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,BOSTON,MA 02115. UNIV MIAMI,SCH MED,DEPT PEDIAT,MIAMI,FL 33152. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. NYU,SCH MED,DEPT PEDIAT,NEW YORK,NY 10003. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. RP MCKINNEY, RE (reprint author), DUKE UNIV,MED CTR,SCH MED,DEPT PEDIAT,BOX 3461,DURHAM,NC 27710, USA. NR 23 TC 190 Z9 191 U1 1 U2 3 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 11 PY 1991 VL 324 IS 15 BP 1018 EP 1025 DI 10.1056/NEJM199104113241503 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FF771 UT WOS:A1991FF77100003 PM 1672443 ER PT J AU WALSH, TJ HATHORN, JW SOBEL, JD MERZ, WG SANCHEZ, V MARET, SM BUCKLEY, HR PFALLER, MA SCHAUFELE, R SLIVA, C NAVARRO, E LECCIONES, J CHANDRASEKAR, P LEE, J PIZZO, PA AF WALSH, TJ HATHORN, JW SOBEL, JD MERZ, WG SANCHEZ, V MARET, SM BUCKLEY, HR PFALLER, MA SCHAUFELE, R SLIVA, C NAVARRO, E LECCIONES, J CHANDRASEKAR, P LEE, J PIZZO, PA TI DETECTION OF CIRCULATING CANDIDA ENOLASE BY IMMUNOASSAY IN PATIENTS WITH CANCER AND INVASIVE CANDIDIASIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID LYSIS-CENTRIFUGATION; BLOOD CULTURE; SYSTEMIC CANDIDIASIS; CLINICAL-EVALUATION; ALBICANS; FUNGEMIA; SERA; INFECTIONS; ARABINITOL; ANTIGENS AB Background. Invasive candidiasis is a major nosocomial infection that is difficult to diagnose. Few biochemically defined markers of invasive candidiasis are known. Initial findings suggested that the presence of candida enolase in the blood may be a novel marker for invasive candidiasis. Methods. We tested 170 patients at high risk for invasive candidiasis for candida enolase antigenemia. All the patients had cancer and neutropenia. We detected antigen using a double-sandwich liposomal immunoassay for candida enolase in serially collected serum samples. Invasive candidiasis was proved by finding candida species in deep nonmucosal tissue, blood cultures, or both. Antigen testing was performed with the investigator blinded to tissue or culture diagnosis. Results. Among 24 patients with proved invasive candidiasis, 149 serum samples were tested for enolase antigenemia; 80 were positive and 69 negative (sensitivity per sample, 54 percent). Multiple sampling improved the detection of antigenemia, which was found in 11 of 13 proved cases of deep tissue infection (85 percent) and in 7 of 11 proved cases of fungemia (64 percent). Specificity was 96 percent as measured against control groups including patients with mucosal colonization, bacteremia, and other deep mycoses. Antigenemia was detected in the absence of fungemia in 5 cases of deep tissue candidiasis, but was not detected in 6 cases of fungemia alone. Conclusions. Candida enolase antigenemia is a novel marker for invasive candidiasis. It may be a useful indicator of deep infection in patients with cancer and neutropenia and may complement the diagnostic usefulness of blood cultures. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT LAB MED,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DURHAM,NC 27710. WAYNE STATE UNIV,HARPER HOSP,MED CTR,DETROIT,MI 48202. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. BECTON DICKINSON & CO,ADV DIAGNOST,BALTIMORE,MD. TEMPLE UNIV,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19122. UNIV IOWA HOSP & CLIN,IOWA CITY,IA 52242. RP WALSH, TJ (reprint author), NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,RM 13N-240,BETHESDA,MD 20892, USA. NR 23 TC 190 Z9 201 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 11 PY 1991 VL 324 IS 15 BP 1026 EP 1031 DI 10.1056/NEJM199104113241504 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA FF771 UT WOS:A1991FF77100004 PM 2005939 ER PT J AU SEETHARAM, S SEIDMAN, MM AF SEETHARAM, S SEIDMAN, MM TI MODULATION OF AN ULTRAVIOLET MUTATIONAL HOTSPOT IN A SHUTTLE VECTOR IN XERODERMA CELLS SO NUCLEIC ACIDS RESEARCH LA English DT Article ID MAMMALIAN-CELLS; DNA-POLYMERASE; MUTAGENESIS; SPECTRUM; PLASMID AB Ultraviolet mutagenesis of the shuttle vector plasmid pZ189 in Xeroderma Pigmentosum cells yields a mutational pattern marked by hotspots at photoproduct sites on both strands of the supF marker gene. In order to test the influence of strand orientation on the appearance of hotspots the mutagenesis study was repeated on a vector with the supF gene in the inverted orientation. We recovered a pattern the same as that in the earlier work and conclude that the nature of the DNA polymerase involved in the replication of specific strands is not a primary determinant of hotspot occurrence in this system. One of the hotspots lies in an 8 base palindrome while the corresponding site on the other strand was not a hotspot. These results were obtained with calcium phosphate transfection of the UV treated vector. When DEAE dextran was used as a transfection agent both sites in the palindrome were hotspots. In a mixing experiment the calcium phosphate pattern was recovered. Our data suggest that the sequence determinants of mutational probability at these two sites lie outside the 8 bases of the palindrome and that mutagenesis at one, but not the other, site is sensitive to perturbation of cellular calcium levels. C1 OTSUKA PHARMACEUT CO LTD,9900 MED CTR DR,ROCKVILLE,MD 20850. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 20 TC 19 Z9 19 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 11 PY 1991 VL 19 IS 7 BP 1601 EP 1604 DI 10.1093/nar/19.7.1601 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG762 UT WOS:A1991FG76200035 PM 2027767 ER PT J AU PERRYMAN, SM MCATEE, FJ PORTIS, JL AF PERRYMAN, SM MCATEE, FJ PORTIS, JL TI COMPLETE NUCLEOTIDE-SEQUENCE OF THE NEUROTROPIC MURINE RETROVIRUS CAS-BR-E SO NUCLEIC ACIDS RESEARCH LA English DT Note ID C RNA VIRUS; LEUKEMIA-VIRUS; MICE RP PERRYMAN, SM (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 9 TC 20 Z9 22 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 11 PY 1991 VL 19 IS 7 BP 1707 EP 1707 DI 10.1093/nar/19.7.1707 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG762 UT WOS:A1991FG76200050 PM 1840655 ER PT J AU POLYMEROPOULOS, MH XIAO, H RATH, DS MERRIL, CR AF POLYMEROPOULOS, MH XIAO, H RATH, DS MERRIL, CR TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE HUMAN MHC CLASS-I CD8 ALPHA-CHAIN (LEU-2/T8) GENE SO NUCLEIC ACIDS RESEARCH LA English DT Note RP POLYMEROPOULOS, MH (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,ROOM 131,MARTIN LUTHER KING AVE,WASHINGTON,DC 20032, USA. NR 3 TC 7 Z9 7 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 11 PY 1991 VL 19 IS 7 BP 1718 EP 1718 DI 10.1093/nar/19.7.1718-a PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG762 UT WOS:A1991FG76200064 PM 1902951 ER PT J AU HSIEH, WT BARRICK, JL BERRETTINI, WH CHAN, MMY FONG, D AF HSIEH, WT BARRICK, JL BERRETTINI, WH CHAN, MMY FONG, D TI A PSTI DNA POLYMORPHISM IN THE HUMAN STEFIN-A GENE (STF-1) SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 RUTGERS STATE UNIV,DEPT BIOL SCI,PISCATAWAY,NJ 08855. RP HSIEH, WT (reprint author), NIMH,ADAMHA,CLIN NEUROGENET BRANCH,BLDG 10,RM 3N218,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA49359] NR 2 TC 1 Z9 1 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 11 PY 1991 VL 19 IS 7 BP 1722 EP 1722 DI 10.1093/nar/19.7.1722-a PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG762 UT WOS:A1991FG76200072 PM 1674139 ER PT J AU RAUB, MF CARDELLINA, JH CHOUDHARY, MI NI, CZ CLARDY, J ALLEY, MC AF RAUB, MF CARDELLINA, JH CHOUDHARY, MI NI, CZ CLARDY, J ALLEY, MC TI CLAVEPICTINE-A AND CLAVEPICTINE-B - CYTOTOXIC QUINOLIZIDINES FROM THE TUNICATE CLAVELINA-PICTA SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Note C1 MONTANA STATE UNIV,DEPT CHEM,NATURAL PROD LAB,BOZEMAN,MT 59717. CORNELL UNIV,DEPT CHEM,BAKER LAB,ITHACA,NY 14853. NCI,FREDERICK,MD 21702. RI Choudhary, M. Iqbal/C-8633-2012; chaudhary, Muhammad/E-8638-2015 NR 5 TC 58 Z9 59 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD APR 10 PY 1991 VL 113 IS 8 BP 3178 EP 3180 DI 10.1021/ja00008a060 PG 3 WC Chemistry, Multidisciplinary SC Chemistry GA FG032 UT WOS:A1991FG03200060 ER PT J AU SATHYAMOORTHY, N DECKER, JM SHERBLOM, AP MUCHMORE, A AF SATHYAMOORTHY, N DECKER, JM SHERBLOM, AP MUCHMORE, A TI EVIDENCE THAT SPECIFIC HIGH MANNOSE STRUCTURES DIRECTLY REGULATE MULTIPLE CELLULAR ACTIVITIES SO MOLECULAR AND CELLULAR BIOCHEMISTRY LA English DT Article DE HIGH MANNOSE OLIGOSACCHARIDES; INTERCELLULAR MESSENGERS; PGE2 SYNTHESIS; IL-1 SYNTHESIS; HMP SHUNT ID TUMOR NECROSIS FACTOR; PLATELET-ACTIVATING FACTOR; SPONTANEOUS CYTO-TOXICITY; HUMAN-LYMPHOCYTES; GAMMA-INTERFERON; GLYCOPROTEIN; SWAINSONINE; INHIBITION; CARBOHYDRATE; RECEPTOR AB Previous studies have demonstrated that much of the immunomodulatory activity of the glycoprotein uromodulin can be attributed to attached oligosaccharides. Structural studies of isolated and purified saccharides derived from uromodulin suggest that the structure Man6GlcNAc2-asn can inhibit in vitro assays of antigen driven T cell proliferation. Based on these observations, we isolated a series of high mannose glycopeptides from a variety of natural sources and tested them for biologic activity in a number of assays. We found that purified mannose rich glycopeptides are able to activate the hexose monophosphate (HMP)shunt, induce prostaglandin synthesis, and directly stimulate IL-1 synthesis. These in vitro effects appear to have in vivo counterparts. Thus in a species-restricted fashion, high mannose compounds are able to directly activate a delayed mononuclear cell infiltrate after intradermal injection. Our data suggest that specific mannose oligosaccharides may activate as well as inhibit cellular immune responses at several different levels. These findings support the hypothesis that specific saccharide structures could participate in the physiologic regulation of the immune response. C1 NCI,METAB BRANCH,BLDG 10,RM 6B09,BETHESDA,MD 20892. UNIV MAINE,DEPT BIOCHEM,ORONO,ME 04473. NR 41 TC 22 Z9 23 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0300-8177 J9 MOL CELL BIOCHEM JI Mol. Cell. Biochem. PD APR 10 PY 1991 VL 102 IS 2 BP 139 EP 147 PG 9 WC Cell Biology SC Cell Biology GA FG129 UT WOS:A1991FG12900005 PM 1881387 ER PT J AU BRESNICK, EH JOHN, S HAGER, GL AF BRESNICK, EH JOHN, S HAGER, GL TI HISTONE HYPERACETYLATION DOES NOT ALTER THE POSITIONING OR STABILITY OF PHASED NUCLEOSOMES ON THE MOUSE MAMMARY-TUMOR VIRUS LONG TERMINAL REPEAT SO BIOCHEMISTRY LA English DT Article ID SODIUM-BUTYRATE; GLUCOCORTICOID REGULATION; MMTV PROMOTER; CORE HISTONES; CHROMATIN; ACETYLATION; RECEPTOR; OLIGONUCLEOSOMES; TRANSCRIPTION; BINDING AB Activation of mouse mammary tumor virus transcription by the hormone-bound glucocorticoid receptor results in disruption of a nucleosome that is specifically positioned on the promoter. Limited treatment of cells with the histone deacetylase inhibitor sodium butyrate prevents receptor-dependent promoter activation and nucleosome disruption [Bresnick, E. H., John, S., Berard, D. S., LeFebvre, P., & Hager, G. L. (1990) Proc. Natl. Acad. Sci. U.S.A. 87, 3977-3981]. On the basis of this observation, we undertook a series of experiments to compare the structure of normal and hyperacetylated mouse mammary tumor virus chromatin. Although butyrate prevents hormone-induced restriction enzyme cutting specifically in the B nucleosome region, chromatin containing hyperacetylated histones does not differ from normal chromatin in general sensitivity to restriction enzymes. Indirect end-labeling analysis of micrococcal nuclease digested chromatin reveals that nucleosomes are identically phased on the mouse mammary tumor virus long terminal repeat in normal and hyperacetylated chromatin. A synthetic DNA fragment spanning the B nucleosome region was reconstituted into a monosome by using core particles containing normal or hyperacetylated histones. Analysis of the structure of reconstituted monosomes by nondenaturing polyacrylamide gel electrophoresis, salt stability, thermal stability, restriction enzyme accessibility, and exonuclease III or DNase I footprinting reveals no effect of histone hyperacetylation on monosome structure. These observations suggest that histone hyperacetylation does not induce a major change in the structure of mouse mammary tumor virus chromatin, such as nucleosome unfolding. We propose that inhibition of receptor-dependent nucleosome disruption by butyrate is not dependent upon such a general change in chromatin structure and subtle chromatin modifications may modulate the interaction of glucocorticoid receptor with chromatin-associated recognition sites. C1 NCI,EXPTL CARCINOGENESIS LAB,HORMONE ACT & ONCOGENESIS SECT,BETHESDA,MD 20892. NR 32 TC 36 Z9 36 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 9 PY 1991 VL 30 IS 14 BP 3490 EP 3497 DI 10.1021/bi00228a020 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FF646 UT WOS:A1991FF64600020 PM 1849427 ER PT J AU SACKETT, DL LIPPOLDT, RE AF SACKETT, DL LIPPOLDT, RE TI THERMODYNAMICS OF REVERSIBLE MONOMER DIMER ASSOCIATION OF TUBULIN SO BIOCHEMISTRY LA English DT Article ID MICROTUBULE-ASSOCIATED PROTEINS; NUCLEOTIDE BINDING; DISSOCIATION; POLYMERIZATION; COLCHICINE; SUBUNIT; BRAIN; SUBSTRUCTURE; NUCLEATION; INVITRO AB The equilibrium between the rat brain tubulin alpha-beta-dimer and the dissociated alpha and beta-monomers has been studied by analytical ultracentrifugation with use of a new method employing short solution columns, allowing rapid equilibration and hence short runs, minimizing tubulin decay. Simultaneous analysis of the equilibrium concentration distributions of three different initial concentrations of tubulin provides clear evidence of a single equilibrium characterized by an association constant, K(a), of 4.9 X 10(6) M-1 (K(d) = 2 X 10(-7) M) at 5-degrees-C, corresponding to a standard free energy change on association DELTA-G-degrees = -8.5 kcal mol-1. Colchicine and GDP both stabilize the dimer against dissociation, increasing the K(a) values (at 4.5-degrees-C) to 20 X 10(6) and 16 X 10(6) M-1, respectively. Temperature dependence of association was examined with multiple three-concentration runs at temperatures from 2 to 30-degrees-C. The van't Hoff plot was linear, yielding positive values for the enthalpy and entropy changes on association, DELTA-S-degrees = 38.1 +/- 2.4 cal deg-1 mol-1 and DELTA-H-degrees = 2.1 +/- 0.7 kcal mol-1, and a small or zero value for the heat capacity change on association, DELTA-C(p)-degrees. The entropically driven association of tubulin monomers is discussed in terms of the suggested importance of hydrophobic interactions to the stability of the monomer association and is compared to the thermodynamics of dimer polymerization. RP SACKETT, DL (reprint author), NIDDKD,BLDG 10,ROOM 8N308,BETHESDA,MD 20892, USA. NR 49 TC 49 Z9 50 U1 1 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 9 PY 1991 VL 30 IS 14 BP 3511 EP 3517 DI 10.1021/bi00228a023 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FF646 UT WOS:A1991FF64600023 PM 2012810 ER PT J AU BALDISSERI, DM PELTON, JG SPARKS, SW TORCHIA, DA AF BALDISSERI, DM PELTON, JG SPARKS, SW TORCHIA, DA TI COMPLETE H-1 AND C-13 ASSIGNMENT OF LYS AND LEU SIDE-CHAINS OF STAPHYLOCOCCAL NUCLEASE USING HCCH-COSY AND HCCH-TOCSY-3D NMR-SPECTROSCOPY SO FEBS LETTERS LA English DT Article DE STAPHYLOCOCCAL NUCLEASE; SIDE-CHAIN STRUCTURE; ASSIGNMENT; 3D NMR ID PROTEINS AB Complete proton and carbon sidechain assignments are reported for 22 lysine and 11 leucine residues in staphylococcal nuclease, an enzyme with 149 residues. These assignments are readily obtained in a direct manner from the correlations observed in the 3D'HCCH-COSY and HCCH-TOCSY spectra and the known protein backbone assignments. These assignments open the way to detailed studies of the sidechain structure and dynamics at the active site, in the hydrophobic core and on the surface of the protein. C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. NR 20 TC 5 Z9 5 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD APR 9 PY 1991 VL 281 IS 1-2 BP 33 EP 38 DI 10.1016/0014-5793(91)80352-4 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FH326 UT WOS:A1991FH32600007 PM 1901804 ER PT J AU TOZSER, J BLAHA, I COPELAND, TD WONDRAK, EM OROSZLAN, S AF TOZSER, J BLAHA, I COPELAND, TD WONDRAK, EM OROSZLAN, S TI COMPARISON OF THE HIV-1 AND HIV-2 PROTEINASES USING OLIGOPEPTIDE SUBSTRATES REPRESENTING CLEAVAGE SITES IN GAG AND GAG-POL POLYPROTEINS SO FEBS LETTERS LA English DT Article DE HIV-1 PROTEINASE; HIV-2 PROTEINASE; OLIGOPEPTIDE SUBSTRATE; ENZYME KINETICS; SUBSTRATE SPECIFICITY ID REVERSE-TRANSCRIPTASE; HTLV-III; PROTEASE; VIRUS; EXPRESSION; GENE AB The substrate specificity of the human immunodeficiency virus type 1 (HIV-1) and type 2 (HIV-2) proteinases was compared using oligopeptides corresponding to cleavage sites in the Gag and Gag-Pol polyproteins of both viruses. All peptides mimicking cleavage sites at the junction of major functional protein domains were correctly cleaved by both enzymes. However, some other peptides thought to represent secondary cleavage sites remained intact. The kinetic parameters (K(m) and k(cat)) obtained for the different substrates showed several hundred-fold variation but were similar for the same substrate. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LAB,POB B, FREDERICK, MD 21702 USA. RI Tozser, Jozsef/A-7840-2008; OI Tozser, Jozsef/0000-0003-0274-0056; Tozser, Jozsef/0000-0001-5076-8729 FU NCI NIH HHS [N01-CO-74101] NR 29 TC 128 Z9 128 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 EI 1873-3468 J9 FEBS LETT JI FEBS Lett. PD APR 9 PY 1991 VL 281 IS 1-2 BP 77 EP 80 DI 10.1016/0014-5793(91)80362-7 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FH326 UT WOS:A1991FH32600017 PM 2015912 ER PT J AU YOUNG, AA MOTT, DM STONE, K COOPER, GJS AF YOUNG, AA MOTT, DM STONE, K COOPER, GJS TI AMYLIN ACTIVATES GLYCOGEN-PHOSPHORYLASE IN THE ISOLATED SOLEUS MUSCLE OF THE RAT SO FEBS LETTERS LA English DT Article DE AMYLIN; MUSCLE; GLYCOGEN; PHOSPHORYLASE ID TYPE-2 DIABETES-MELLITUS; GENE-RELATED PEPTIDE-1; SKELETAL-MUSCLE; METABOLISM; INSULIN; EPINEPHRINE; LIVER AB The pancreatic beta-cell hormone amylin acts in isolated rat skeletal muscle to decrease insulin-stimulated incorporation of glucose into glycogen. It also increases blood levels of lactate and glucose in fasted rats in vivo. However, it remained uncertain whether amylin exerts direct effects to stimulate muscle glycogenolysis. We now report that amylin caused a dose-dependent increase in activity of muscle glycogen phosphorylase in isolated rat soleus muscle by stimulating phosphorylase a. Insulin inhibited amylin-stimulated activation of phosphorylase. Effects of amylin to stimulate muscle glycogenolysis are consistent with observed effects of amylin in vivo and could be a major mechanism whereby amylin modulates carbohydrate metabolism. C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. RP YOUNG, AA (reprint author), AMYLIN CORP,DEPT PHYSIOL,9373 TOWNE CTR DR,STE 250,SAN DIEGO,CA 92121, USA. NR 25 TC 68 Z9 69 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD APR 9 PY 1991 VL 281 IS 1-2 BP 149 EP 151 DI 10.1016/0014-5793(91)80380-L PG 3 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FH326 UT WOS:A1991FH32600035 PM 2015885 ER PT J AU CASASFINET, JR HU, S HAMER, D KARPEL, RL AF CASASFINET, JR HU, S HAMER, D KARPEL, RL TI SPECTROSCOPIC CHARACTERIZATION OF THE COPPER(I)-THIOLATE CLUSTER IN THE DNA-BINDING DOMAIN OF YEAST ACE1 TRANSCRIPTION FACTOR SO FEBS LETTERS LA English DT Article DE DNA-BINDING PROTEIN; METAL ION; LUMINESCENT COMPLEX ID METALLOTHIONEIN GENE; MUTANTS; COPPER AB A polypeptide containing the amino-terminal region of ACE1 (residues 1-122; 122*), the activator of yeast Cu-metallothionein gene transcription, shows charge-transfer and metal-centered UV absorption bands, and orange luminescence which are characteristic of Cu-cysteinyl thiolate cluster structures. These spectral features are abolished by the Cu(I) complexing agents CN- and diethyldithiocarbamate or exposure to acid, but not by the Cu(II) chelator, EDTA. Binding of the polypeptide to its specific DNA recognition site, but not to calf-thymus double-stranded DNA, induces quenching of its Tyr and Cu-S cluster luminescence emission. The CD spectrum is characteristic of a tightly folded structure that may be organized around the Cu cluster. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. RP CASASFINET, JR (reprint author), UNIV MARYLAND BALTIMORE CTY,DEPT CHEM & BIOCHEM,BALTIMORE,MD 21228, USA. NR 9 TC 11 Z9 11 U1 2 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD APR 9 PY 1991 VL 281 IS 1-2 BP 205 EP 208 DI 10.1016/0014-5793(91)80394-I PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FH326 UT WOS:A1991FH32600049 PM 2015895 ER PT J AU ABBRUZZESE, A HANAUSKEABEL, HM PARK, MH HENKE, S FOLK, JE AF ABBRUZZESE, A HANAUSKEABEL, HM PARK, MH HENKE, S FOLK, JE TI THE ACTIVE-SITE OF DEOXYHYPUSYL HYDROXYLASE - USE OF CATECHOLPEPTIDES AND THEIR COMPONENT CHELATOR AND PEPTIDE MOIETIES AS MOLECULAR PROBES SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE EUKARYOTIC TRANSLATION INITIATION FACTOR-4D; DEOXYHYPUSYL HYDROXYLASE; METAL BINDING PEPTIDE; PEPTIDE INHIBITOR DESIGN ID INITIATION-FACTOR EIF-4D; IRON TRANSPORT COMPOUNDS; AMINO-ACID; COORDINATION CHEMISTRY; PROLYL 4-HYDROXYLASE; STABILITY-CONSTANTS; HYPUSINE; PROTEIN; CELLS; IDENTIFICATION AB The final step of hypusine formation in the eukaryotic translation initiation factor 4D (elF-4D) is mediated by the enzyme deoxyhypusyl hydroxylase. In an effort to find specific inhibitors for this enzyme, we have studied the effects of two catecholpeptides, N-alpha-acetyl-N-delta-(3,4-dihydroxybenzoyl)-L-Orn-L-Pro-Gly (compound I) and N-alpha-acetyl-N-delta-(2,3-dihydroxybenzoyl)-L-Orn-L-Pro-Gly (compound II). Their structures were designed for anchorage to the enzyme s active site, utilizing the catechol-mediated chelation of a putative, enzyme-bound metal ion. Both compounds were found to strongly inhibit hypusine formation in vitro. Compound I was about seven times more potent than compound II, whereas the component peptide itself showed no intrinsic inhibitory activity even at concentrations as high as 1mM. When used in conjugation with a chelating catechol moiety, however, it gave a 17- and an 8-fold enhancement of the half-maximal inhibition mediated by the chelating moieties per se, i.e. the 3,4- and the 2,3-dihydroxybenzoyl esters, respectively. The mode of inhibition by compound I was competitive with respect to the unhydroxylated precursor of eIF-4D and showed a K(i) value of 32-mu-M +/- 3.4-mu-M. These catecholpeptides are the most efficient peptide antagonists of deoxyhypusyl hydroxylase known at present. They allow an assessment of the enzyme's active site organization and provide the first experimental evidence that a metal ion constitutes an integral part of its catalytic center. C1 RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT PEDIAT,1653 W CONGRESS PARKWAY,CHICAGO,IL 60612. HOECHST AG,PHARM FORSCH SYNTH & BIOCHEM,W-6230 FRANKFURT 80,GERMANY. NAPLES UNIV,FAC MED 1,DIPARTIMENTO BIOCHIM & BIOFIS,I-80138 NAPLES,ITALY. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT MED,DIV ENDOCRINOL,BOSTON,MA 02115. NIDR,BETHESDA,MD 20892. NR 41 TC 33 Z9 33 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD APR 8 PY 1991 VL 1077 IS 2 BP 159 EP 166 DI 10.1016/0167-4838(91)90053-3 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FJ350 UT WOS:A1991FJ35000005 PM 2015290 ER PT J AU ROFFMAN, E FRENKEL, N AF ROFFMAN, E FRENKEL, N TI CHEMILUMINESCENT QUANTITATION OF LYMPHOCYTE SURFACE-ANTIGENS SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Letter ID 1,2-DIOXETANES C1 NIAID,VIRAL DIS LAB,TWINBROOK 2,12441 PKLAWN DR,ROCKVILLE,MD 20852. NR 5 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD APR 8 PY 1991 VL 138 IS 1 BP 129 EP 131 DI 10.1016/0022-1759(91)90073-O PG 3 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA FG310 UT WOS:A1991FG31000016 PM 2019741 ER PT J AU MILLS, JL AF MILLS, JL TI CLOMIPHENE AND NEURAL-TUBE DEFECTS SO LANCET LA English DT Letter RP MILLS, JL (reprint author), NICHHD,DIV PREVENT RES,EPIDEMIOL BRANCH,PEDIAT EPIDEMIOL SECT,BETHESDA,MD 20892, USA. NR 1 TC 2 Z9 2 U1 0 U2 2 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 6 PY 1991 VL 337 IS 8745 BP 853 EP 853 DI 10.1016/0140-6736(91)92562-G PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FF228 UT WOS:A1991FF22800039 PM 1672941 ER PT J AU CORREA, FMA GUILHAUME, SS SAAVEDRA, JM AF CORREA, FMA GUILHAUME, SS SAAVEDRA, JM TI COMPARATIVE QUANTIFICATION OF RAT-BRAIN AND PITUITARY ANGIOTENSIN-CONVERTING ENZYME WITH AUTORADIOGRAPHIC AND ENZYMATIC METHODS SO BRAIN RESEARCH LA English DT Article DE IMMUNOCHEMISTRY; STAPHYLOCOCCAL PROTEIN-A; AUTORADIOGRAPHY; KININASE-II; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS ID SPONTANEOUSLY HYPERTENSIVE RATS; INHIBITOR BINDING ASSAY; BRATTLEBORO RATS; II BINDING; PROTEIN-A; RADIOIMMUNOHISTOCHEMICAL METHOD; DIFFERENTIAL DISTRIBUTION; QUANTITATIVE DISTRIBUTION; STAPHYLOCOCCAL PROTEIN; STRIATONIGRAL PATHWAY AB Angiotensin-converting enzyme (ACE, kininase II, EC 3.4.15.1) was quantified in selected areas of the rat brain by 3 different methods. The enzyme activity was quantified by an enzymatic assay in homogenates of discrete brain areas with the use of the artificial substrate hippuryl-His-Leu-[C-14]glycine. Binding of the specific ACE inhibitor [I-125]351A was quantified after incubation of thin brain section followed by quantitative autoradiography with comparison to [I-125]standards. The antigenic sites of the enzyme were quantified by immunoautoradiography, using a polyclonal antibody to ACE in combination with [I-125]protein A followed by quantitative autoradiography. There was a good correlation between the ACE activity, as determined by the quantitative enzymatic method, and both the enzyme inhibitor binding and the [I-125]protein A binding, as determined by quantitative autoradiography, in brain areas and in anterior and posterior lobes of the pituitary gland. The present data demonstrate that ACE activity and ACE binding can be quantified in discrete tissue areas with different methods in a variety of conditions and with a high degree of accuracy. C1 NIMH,CLIN SCI LAB,PHARMACOL SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2D-45,BETHESDA,MD 20892. UNIV SAO PAULO,SCH MED RIBEIRAO PRETO,DEPT PHARMACOL,BR-14049 RIBEIRAO PRETO,SP,BRAZIL. RI Correa, Fernando /D-1614-2012 OI Correa, Fernando /0000-0003-4067-9524 NR 38 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 5 PY 1991 VL 545 IS 1-2 BP 215 EP 222 DI 10.1016/0006-8993(91)91289-D PG 8 WC Neurosciences SC Neurosciences & Neurology GA FJ128 UT WOS:A1991FJ12800028 PM 1650274 ER PT J AU DECHESNE, CJ HAMPSON, DR GOPING, G WHEATON, KD WENTHOLD, RJ AF DECHESNE, CJ HAMPSON, DR GOPING, G WHEATON, KD WENTHOLD, RJ TI IDENTIFICATION AND LOCALIZATION OF A KAINATE BINDING-PROTEIN IN THE FROG INNER-EAR BY ELECTRON-MICROSCOPY IMMUNOCYTOCHEMISTRY SO BRAIN RESEARCH LA English DT Article DE INNER EAR; KAINATE RECEPTOR; [H-3]KAINATE BINDING; EXICITATORY AMINO ACID; FIBROBLAST; FROG ID POTASSIUM-INDUCED RELEASE; EXCITATORY AMINO-ACIDS; GUINEA-PIG COCHLEA; KAINIC ACID; HAIR-CELLS; AFFERENT TRANSMITTER; GLUTAMATE RECEPTOR; XENOPUS-LAEVIS; AUDITORY-NERVE; LATERAL-LINE AB A kainate binding protein (KBP) was studied in Rana pipiens inner ear using monoclonal and polyclonal antibodies against affinity purified KBP from frog brain. The KBP identified and analyzed in inner ear tissue homogenates, with one- and two-dimensional immunoblots, was similar to the affinity purified KBP and to the antibody-identified frog brain KBP. As brain KBP, inner ear KBP had 5 main components in the molecular weight dimension, centered at M(r) = 48,000; however, inner ear KBP had a greater abundance of the higher molecular weight components. Light and electron microscopy observations showed KBP immunostaining at two locations: (1) in the dendrites of the eight nerve afferent fibers contacting sensory hair cells, with the postsynaptic density being more intensely stained; and (2) on the cytoplasmic membrane of fibroblasts present in the inner ear connective tissue which displayed intense immunostaining. The presence of kainate (KA) binding sites in the inner ear was assessed using in vitro receptor autoradiography. [H-3]KA binding sites were found in connective tissue areas confirming the immunocytochemistry results. The postsynaptic localization of the KBP in afferent endings, strongly supports it as being a component of the KA receptor complex. However, its presence on fibroblasts situated in the inner ear connective tissue makes its function hypothetical. The dual presence of the KBP on non-neuronal cells as well as at postsynaptic membrane sites suggests the existence of a family of proteins involved in KA binding and KA receptors with a complex organization. C1 NIDOCD,MOLEC OTOL LAB,NEUROCHEM SECT,BETHESDA,MD 20892. RP DECHESNE, CJ (reprint author), UNIV MONTPELLIER 2,INSERM,U254,NEUROPHYSIOL SENSORIELLE LAB,PL BATAILLON,F-34095 MONTPELLIER 5,FRANCE. NR 53 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 5 PY 1991 VL 545 IS 1-2 BP 223 EP 233 DI 10.1016/0006-8993(91)91290-H PG 11 WC Neurosciences SC Neurosciences & Neurology GA FJ128 UT WOS:A1991FJ12800029 PM 1650275 ER PT J AU MESCO, ER JOSEPH, JA BLAKE, MJ ROTH, GS AF MESCO, ER JOSEPH, JA BLAKE, MJ ROTH, GS TI LOSS OF D2 RECEPTORS DURING AGING IS PARTIALLY DUE TO DECREASED LEVELS OF MESSENGER-RNA SO BRAIN RESEARCH LA English DT Note DE AGING; MESSENGER RNA; DOPAMINE RECEPTOR ID STRIATAL DOPAMINE-RECEPTORS; RAT STRIATUM; WISTAR RATS; BINDING; AGE; BRAIN; RECOVERY; BLOCKADE; SITES AB Corpora striata of old rats (24-25 months) contain only about half as much mRNA for D2 dopamine receptors as those of young (6 months) counterparts. This reduction can be observed by in situ hybridization of brain slices as well as with Northern and do blot analyses of striatal extracts. Decreased levels of D2 receptor mRNA as described in this study are consistent with reductions in receptor containing neurons (20%) and receptor biosynthesis (40%), as previously observed in this and other laboratories. Thus, age related changes in D2 receptor gene expression appear to be partially responsible for loss of these receptors. C1 NIA,FRANCIS SCOTT KEY MED CTR,GERONTOL RES CTR,DEPT MOLEC GENET,BALTIMORE,MD 21224. RP MESCO, ER (reprint author), NIA,FRANCIS SCOTT KEY MED CTR,GERONTOL RES CTR,BALTIMORE,MD 21224, USA. NR 20 TC 57 Z9 57 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 5 PY 1991 VL 545 IS 1-2 BP 355 EP 357 DI 10.1016/0006-8993(91)91314-Q PG 3 WC Neurosciences SC Neurosciences & Neurology GA FJ128 UT WOS:A1991FJ12800053 PM 1830509 ER PT J AU LEONE, A FLATOW, U KING, CR SANDEEN, MA MARGULIES, IMK LIOTTA, LA STEEG, PS AF LEONE, A FLATOW, U KING, CR SANDEEN, MA MARGULIES, IMK LIOTTA, LA STEEG, PS TI REDUCED TUMOR-INCIDENCE, METASTATIC POTENTIAL, AND CYTOKINE RESPONSIVENESS OF NM23-TRANSFECTED MELANOMA-CELLS SO CELL LA English DT Article ID GENE; NM23; DROSOPHILA; PROTEIN AB Reduced expression of the nm23 gene in certain rodent model systems and human breast tumors has been correlated with high tumor metastatic potential. To investigate the functional effects of nm23 expression, we have transfected a constitutive murine nm23-1 expression construct into highly metastatic K-1735 TK murine melanoma cells. TK clones expressing the exogenous nm23-1 construct exhibited a reduced incidence of primary tumor formation, significant reductions in tumor metastatic potential independent of tumor cell growth, and altered responses to the cytokine transforming growth factor-beta-1 in soft agar colonization assays, compared with control-transfected TK clones. In contrast, nm23-1-transfected TK clones exhibited no significant differences in intrinsic tumor cell growth, i.e., primary tumor size in vivo, anchorage-dependent growth rate in vitro, and anchorage-independent colony formation in soft agar in vitro. The data demonstrate a suppressive effect of nm23 on several aspects of the cancer process, including tumor metastasis. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21740. MOLEC ONCOL INC,GAITHERSBURG,MD 20878. RP LEONE, A (reprint author), NCI,PATHOL LAB,BETHESDA,MD 20892, USA. RI Leone, Alvaro/K-6410-2016 OI Leone, Alvaro/0000-0003-3815-9052 NR 23 TC 533 Z9 556 U1 1 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD APR 5 PY 1991 VL 65 IS 1 BP 25 EP 35 DI 10.1016/0092-8674(91)90404-M PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FF773 UT WOS:A1991FF77300005 PM 2013093 ER PT J AU MONTPIED, P GINNS, EI MARTIN, BM ROCA, D FARB, DH PAUL, SM AF MONTPIED, P GINNS, EI MARTIN, BM ROCA, D FARB, DH PAUL, SM TI GAMMA-AMINOBUTYRIC-ACID (GABA) INDUCES A RECEPTOR-MEDIATED REDUCTION IN GABA-A RECEPTOR ALPHA SUBUNIT MESSENGER-RNAS IN EMBRYONIC CHICK NEURONS IN CULTURE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID GATED CHLORIDE CURRENTS; RAT-BRAIN; BENZODIAZEPINE RECEPTORS; DOWN-REGULATION; EXPRESSION; COMPLEX; CHANNEL; FAMILY; MUSCLE; SHOWS AB Gamma-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in brain, is known to interact with a subclass of receptors that activate a ligand-gated chloride ion channel. Exposure of cultured embryonic chick neurons to physiological concentrations of GABA results in a time-dependent down-regulation of these GABA(A) receptors. To delineate the cellular mechanism(s) responsible for agonist-induced down-regulation of GABA(A) receptors we quantified the levels of GABA(A) receptor alpha-subunit messenger RNAs, which encode the subunit(s) containing agonist recognition site(s), and observed a marked reduction in alpha-subunit mRNAs following exposure of embryonic chick neurons to GABA. Both the down-regulation of GABA(A) receptors and the reduction in alpha-subunit mRNAs induced by GABA were completely antagonized by the specific GABA(A) receptor antagonist SR-95531. These data demonstrate the presence of an agonist-induced receptor-mediated mechanism for regulating the expression of receptor subunit-encoding mRNAs that may be involved in the development of tolerance to the pharmacological actions of drugs known to act via GABA(A) receptors. C1 NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BLDG 10,RM 4N224,BETHESDA,MD 20892. NIMH,CLIN NEUROSCI BRANCH,MOLEC NEUROGENET SECT,BETHESDA,MD 20892. SUNY HLTH SCI CTR,DEPT ANAT & CELL BIOL,BROOKLYN,NY 11203. RI Farb, david/C-7089-2014 OI Farb, david/0000-0002-9050-6480 NR 37 TC 99 Z9 100 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1991 VL 266 IS 10 BP 6011 EP 6014 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE373 UT WOS:A1991FE37300002 PM 1848843 ER PT J AU ADZUMA, K MIZUUCHI, K AF ADZUMA, K MIZUUCHI, K TI STEADY-STATE KINETIC-ANALYSIS OF ATP HYDROLYSIS BY THE B-PROTEIN OF BACTERIOPHAGE-MU - INVOLVEMENT OF PROTEIN OLIGOMERIZATION IN THE ATPASE CYCLE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DNA STRAND-TRANSFER; TRANSPOSITION PROTEIN; ESCHERICHIA-COLI; TARGET IMMUNITY; RECA PROTEIN; RECOMBINATION; PURIFICATION; MECHANISM; SEQUENCE; GENE AB The DNA strand-transfer reaction of bacteriophage Mu requires Mu B protein and ATP for high efficiency. These factors facilitate the capture of target DNA by the donor protein-DNA complex. To understand the mechanism of the Mu B ATPase cycle in the Mu DNA strand-transfer reaction, we undertook a steady-state kinetic analysis of Mu B ATPase. The results reveal complex properties of the ATPase activity; Mu B protein oligomerizes in the presence of ATP, and ATP hydrolysis by the Mu B ATPase is stimulated by the protein oligomerization and shows a positive cooperativity with respect to ATP concentration. Mu B ATPase activity is also modulated by DNA and Mu A protein. DNA alone suppresses the catalytic activity of Mu B ATPase, whereas DNA enhances the apparent binding affinity for ATP. In the presence of Mu A protein together with DNA, however, the catalytic activity is greatly stimulated. Based on these results, we propose a working hypothesis in which oligomerization of Mu B protein plays a key role in its ATPase cycle. RP ADZUMA, K (reprint author), NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 21 TC 44 Z9 44 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1991 VL 266 IS 10 BP 6159 EP 6167 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE373 UT WOS:A1991FE37300027 PM 1826105 ER PT J AU LOMASNEY, JW COTECCHIA, S LORENZ, W LEUNG, WY SCHWINN, DA YANGFENG, TL BROWNSTEIN, M LEFKOWITZ, RJ CARON, MG AF LOMASNEY, JW COTECCHIA, S LORENZ, W LEUNG, WY SCHWINN, DA YANGFENG, TL BROWNSTEIN, M LEFKOWITZ, RJ CARON, MG TI MOLECULAR-CLONING AND EXPRESSION OF THE CDNA FOR THE ALPHA-1A-ADRENERGIC RECEPTOR - THE GENE FOR WHICH IS LOCATED ON HUMAN CHROMOSOME-5 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NUCLEOTIDE REGULATORY PROTEINS; BETA-ADRENERGIC-RECEPTOR; ALPHA-1-ADRENERGIC RECEPTOR; BETA-2-ADRENERGIC RECEPTORS; ALPHA-2-ADRENERGIC RECEPTOR; SMOOTH-MUSCLE; SUBTYPES; BINDING; CHLORETHYLCLONIDINE; PHOSPHORYLATION AB Pharmacological and molecular cloning studies have demonstrated heterogeneity of alpha-1-adrenergic receptors. We have now cloned two alpha-1-adrenergic receptors from a rat cerebral cortex cDNA library, using the hamster alpha-1B-adrenergic receptor as a probe. The deduced amino acid sequence of clone RA42 encodes a protein of 560 amino acids whose putative topology is similar to that of the family of G-protein-coupled receptors. The primary structure though most closely resembles that of an alpha-1-adrenergic receptor, having approximately 73% amino acid identity in the putative transmembrane domains with the previously isolated hamster alpha-1B receptor. Analysis of the ligand binding properties of RA42 expressed in COS-7 cells with a variety of adrenergic ligands demonstrates a unique alpha-1-adrenergic receptor pharmacology. High affinity for the antagonist WB4101 and agonists phenylephrine and methoxamine suggests that cDNA RA42 encodes the alpha-1A receptor subtype. Northern blot analysis of various rat tissues also shows the distribution expected of the alpha-1A receptor subtype with abundant expression in vas deferens followed by hippocampus, cerebral cortex, aorta, brainstem, heart and spleen. The second alpha-1-adrenergic receptor cloned represents the rat homolog of the hamster alpha-1B subtype. Expression of mRNA for this receptor is strongly detected in liver followed by heart, cerebral cortex, brain stem, kidney, lung, and spleen. This study provides definitive evidence for the existence of three alpha-1-adrenergic receptor subtypes. C1 DUKE UNIV,MED CTR,DEPT ANESTHESIOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT CELL BIOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT BIOCHEM,DURHAM,NC 27710. DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DURHAM,NC 27710. NIMH,BETHESDA,MD 20892. YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. RP LOMASNEY, JW (reprint author), DUKE UNIV,MED CTR,DEPT PATHOL,DURHAM,NC 27710, USA. RI Brownstein, Michael/B-8609-2009 FU NHLBI NIH HHS [HL16037] NR 41 TC 449 Z9 453 U1 0 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1991 VL 266 IS 10 BP 6365 EP 6369 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE373 UT WOS:A1991FE37300055 PM 1706716 ER PT J AU SARTOR, O SAMESHIMA, JH ROBBINS, KC AF SARTOR, O SAMESHIMA, JH ROBBINS, KC TI DIFFERENTIAL ASSOCIATION OF CELLULAR PROTEINS WITH FAMILY PROTEIN-TYROSINE KINASES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RETROVIRUS SHUTTLE VECTOR; EXPRESS HIGH-LEVELS; MONOCLONAL-ANTIBODIES; PHOSPHOLIPASE-C; SARCOMA-VIRUS; GENE-PRODUCT; SRC GENE; PP60C-SRC; PHOSPHOTYROSINE; PHOSPHORYLATION AB We have sought to identify candidate substrates for src family protein-tyrosine kinases potentially important for transformation. Transfected NIH/3T3 cells, each overexpressing a normal or activated version of the fyn, fgr, or src translational product, were examined using antibody to phosphotyrosine as a probe. Expression of each cDNA induced similar but distinct patterns of tyrosine phosphorylated cellular proteins, with the extent of phosphorylation being greatest in cells expressing an activated kinase. A 70-kDa tyrosine-phosphorylated protein was found to associate with the activated fyn gene product. A protein designated p130, tyrosine phosphorylated in vitro, and in vivo, was found to physically associate with the activated product of each src family gene examined. Physical interaction of three different highly transforming tyrosine kinases with a common cellular protein suggests that p130 may play an important role in transformation induced by src family kinases. C1 NIDR,CELLULAR DEV & ONCOL LAB,BLDG 30,RM 211,BETHESDA,MD 20892. NR 43 TC 30 Z9 30 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1991 VL 266 IS 10 BP 6462 EP 6466 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE373 UT WOS:A1991FE37300069 PM 2007595 ER PT J AU HOHL, D MEHREL, T LICHTI, U TURNER, ML ROOP, DR STEINERT, PM AF HOHL, D MEHREL, T LICHTI, U TURNER, ML ROOP, DR STEINERT, PM TI CHARACTERIZATION OF HUMAN LORICRIN - STRUCTURE AND FUNCTION OF A NEW CLASS OF EPIDERMAL-CELL ENVELOPE PROTEINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CROSS-LINKED ENVELOPE; INTERMEDIATE FILAMENT SUBUNITS; CORNIFIED ENVELOPE; MOUSE EPIDERMIS; ALPHA-KERATIN; KERATOHYALIN GRANULES; SECONDARY STRUCTURE; GLOBULAR-PROTEINS; MESSENGER-RNA; TRANSGLUTAMINASE AB We have isolated and characterized a full-length cDNA clone encoding human loricrin. Curiously, this protein displays major differences from the recently described mouse loricrin (Mehrel, T., Hohl, D., Nakazawa, H., Rothnagel, J. A., Longley, M. A., Bundman, D., Cheng, C. K., Lichti, U., Bisher, M. E., Steven, A. C., Steinert, P. M., Yuspa, S. H., and Roop, D. R. (1990) Cell 61, 1103-1112). Although both proteins are glycine-serine-cysteine-rich, the sequences have not been conserved. However, analysis of the sequences reveals a common motif of quasi-peptide repeats of an aliphatic or aromatic amino acid residue followed by several glycine and/or serine and cysteine residues. These sequences are interspersed and flanked by short glutamine- or glutamine/lysine-rich peptides. Thus loricrins consist of a family of cell envelope proteins of highly variable sequences that nevertheless retain common structural elements. We show that unlike all other putative protein components of the cell envelope, loricrins are highly insoluble, due at least in part to cross-linking by disulfide bonds. Furthermore, we have isolated four peptides from purified human cell envelopes that contain recognizable loricrin sequences and which are cross-linked by the N-epsilon-(gamma-glutamyl)lysine isodipeptide bond. The presence of such bonds thus affords an explanation for the extraordinary insolubility of loricrin by cross-linking to the cell envelope and can also explain the low steady-state levels of monomeric loricrin in cytoskeletal extracts of epidermis. This study represents the first report of this isodipeptide cross-link in a protein component of the cornified cell envelope. We propose a model for the structure of loricrin in which (i) the unusual glycine-serine-rich sequences adopt a flexible loop conformation, indexed on the recurrent aliphatic residues; (ii) inter- or intramolecular isodipeptide and disulfide cross-links induce or stabilize folding of loricrin so as to form a more compact rosette-like structure; and (iii) the presence of the flexible glycine-rich loops necessarily will impart a flexible character to the cell envelope and entire epithelium. C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NR 71 TC 258 Z9 260 U1 1 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1991 VL 266 IS 10 BP 6626 EP 6636 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE373 UT WOS:A1991FE37300092 PM 2007607 ER PT J AU CELIKEL, R DAVIS, MD DAI, XP KAUFMAN, S XUONG, NH AF CELIKEL, R DAVIS, MD DAI, XP KAUFMAN, S XUONG, NH TI CRYSTALLIZATION AND PRELIMINARY-X-RAY ANALYSIS OF PHENYLALANINE-HYDROXYLASE FROM RAT-LIVER SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Note ID FUNCTIONAL DOMAINS; PROTEIN; PURIFICATION; ACTIVATION; PHOSPHORYLATION; STIMULATION; SEQUENCE; HOMOLOGY; CLONE; CDNA C1 NIMH,NEUROCHEM LAB,BETHESDA,MD 20892. RP CELIKEL, R (reprint author), UNIV CALIF SAN DIEGO,DEPT BIOL,B-017,LA JOLLA,CA 92093, USA. FU NCRR NIH HHS [RR01644] NR 38 TC 12 Z9 12 U1 1 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD APR 5 PY 1991 VL 218 IS 3 BP 495 EP 498 DI 10.1016/0022-2836(91)90694-2 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG422 UT WOS:A1991FG42200005 PM 2016740 ER PT J AU BECKER, ED AF BECKER, ED TI RAMAN-SPECTRA OF ISOTOPIC DERIVATIVES OF PARA-BENZOQUINONE - REVISED VIBRATIONAL ASSIGNMENTS SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID STRUCTURALLY RELATED MOLECULES; FORCE-FIELD AB Raman spectral data are presented of solutions of p-benzoquinone and nine isotopic derivatives (four deuterated species and the five O-18 analogues). The pattern of frequency shifts on isotopic substitution permits the resolution of a longstanding controversy over the assignment of the totally symmetric C = O and C = C stretching vibrations. RP BECKER, ED (reprint author), NIH,BETHESDA,MD 20892, USA. NR 21 TC 39 Z9 39 U1 0 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3654 J9 J PHYS CHEM-US JI J. Phys. Chem. PD APR 4 PY 1991 VL 95 IS 7 BP 2818 EP 2823 DI 10.1021/j100160a035 PG 6 WC Chemistry, Physical SC Chemistry GA FE953 UT WOS:A1991FE95300035 ER PT J AU HSU, IC METCALF, RA SUN, T WELSH, JA WANG, NJ HARRIS, CC AF HSU, IC METCALF, RA SUN, T WELSH, JA WANG, NJ HARRIS, CC TI MUTATIONAL HOTSPOT IN THE P53 GENE IN HUMAN HEPATOCELLULAR CARCINOMAS SO NATURE LA English DT Article ID DNA; EXPOSURE AB HUMAN hepatocellular carcinomas (HCC) from patients in Qidong, an area of high incidence in China, in which both hepatitis B virus and aflatoxin B1 are risk factors 1, were analysed for mutations in p53, a putative tumour-suppressor gene. Eight of the 16 HCC had a point mutation at the third base position of codon 249. The G --> T transversion in seven HCC DNA samples and the G --> C transversion in the other HCC are consistent with mutations caused by aflatoxin B1 in mutagenesis experiments 2,3. No mutations were found in exons 5, 6, 8 or the remainder of exon 7. These results contrast with p53 mutations previously reported in carcinomas and sarcomas of human lung, colon, oesophagus and breast; these are primarily scattered over four of the five evolutionarily conserved domains, which include codon 249 (refs 4-9). We suggest that the mutant p53 protein may be responsible for a selective clonal expansion of hepatocytes during carcinogenesis. C1 NCI,DIV CANC ETIOL,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. CHINESE ACAD MED SCI,INST CANC,BEIJING,PEOPLES R CHINA. QIDONG LIVER CANC INST,JIANGSU,PEOPLES R CHINA. NR 25 TC 1345 Z9 1398 U1 6 U2 41 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 4 PY 1991 VL 350 IS 6317 BP 427 EP 428 DI 10.1038/350427a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FF042 UT WOS:A1991FF04200051 PM 1849234 ER PT J AU SAMUELS, ME KOOP, CE HARTSOCK, PI AF SAMUELS, ME KOOP, CE HARTSOCK, PI TI SINGLE-USE SYRINGES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID INTRAVENOUS DRUG-USERS; RISK C1 NIDA,ROCKVILLE,MD 20857. RP SAMUELS, ME (reprint author), UNIV S CAROLINA,SCH PUBL HLTH,COLUMBIA,SC 29208, USA. NR 10 TC 12 Z9 12 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 4 PY 1991 VL 324 IS 14 BP 996 EP 997 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FE376 UT WOS:A1991FE37600026 PM 2002826 ER PT J AU RAUB, W AF RAUB, W TI INTERFERON-GAMMA PREVENTS INFECTION IN CHRONIC GRANULOMATOUS-DISEASE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP RAUB, W (reprint author), NIH,BLDG 31,ROOM 2B23,BETHESDA,MD 20892, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 3 PY 1991 VL 265 IS 13 BP 1633 EP 1633 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FD659 UT WOS:A1991FD65900006 PM 1900541 ER PT J AU RAUB, W AF RAUB, W TI TAMOXIFEN FOUND TO LOWER GROWTH-FACTOR LEVELS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP RAUB, W (reprint author), NIH,BLDG 31,ROOM 2B23,BETHESDA,MD 20892, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 3 PY 1991 VL 265 IS 13 BP 1633 EP 1633 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FD659 UT WOS:A1991FD65900004 PM 1900541 ER PT J AU RAUB, W AF RAUB, W TI PREDICTORS OF TYPE-II DIABETES IDENTIFIED SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP RAUB, W (reprint author), NIH,BLDG 31,ROOM 2B23,BETHESDA,MD 20892, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 3 PY 1991 VL 265 IS 13 BP 1633 EP 1633 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FD659 UT WOS:A1991FD65900005 PM 1900541 ER PT J AU RAUB, W AF RAUB, W TI THERAPY APPEARS SAFE, EFFECTIVE AGAINST SPONTANEOUS ANIMAL TUMORS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP RAUB, W (reprint author), NIH,BLDG 31,ROOM 2B23,BETHESDA,MD 20892, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 3 PY 1991 VL 265 IS 13 BP 1633 EP 1633 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FD659 UT WOS:A1991FD65900003 PM 1900541 ER PT J AU GWINN, M PAPPAIOANOU, M GEORGE, JR HANNON, WH WASSER, SC REDUS, MA HOFF, R GRADY, GF WILLOUGHBY, A NOVELLO, AC PETERSEN, LR DONDERO, TJ CURRAN, JW AF GWINN, M PAPPAIOANOU, M GEORGE, JR HANNON, WH WASSER, SC REDUS, MA HOFF, R GRADY, GF WILLOUGHBY, A NOVELLO, AC PETERSEN, LR DONDERO, TJ CURRAN, JW TI PREVALENCE OF HIV-INFECTION IN CHILDBEARING WOMEN IN THE UNITED-STATES - SURVEILLANCE USING NEWBORN BLOOD-SAMPLES SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; AIDS; SEROPREVALENCE; INFANTS AB A national, population-based survey was initiated in 1988 to measure the prevalence of human immunodeficiency virus (HIV) infection in women giving birth to infants in the United States. Following standardized procedures, residual dried-blood specimens collected on filter paper for newborn metabolic screening were tested anonymously in state public health laboratories for maternal antibody to HIV. As of September 1990, annual survey data were available from 38 states and the District of Columbia. The highest HIV seroprevalence rates were observed in New York (5.8 per 1000), the District of Columbia (5.5 per 1000), New Jersey (4.9 per 1000), and Florida (4.5 per 1000). Nationwide, an estimated 1.5 per 1000 women giving birth to infants in 1989 were infected with HIV. Assuming a perinatal transmission rate of 30%, we estimate that approximately 1800 newborns acquired HIV infection during one 12-month period. Preventing transmission of HIV infection to women and infants is an urgent public health priority. C1 CTR DIS CONTROL,CTR ENVIRONM HLTH & INJURY CONTROL,DIV ENVIRONM HLTH LAB SCI,ATLANTA,GA 30333. MASSACHUSETTS DEPT HLTH,BOSTON,MA. NICHHD,WASHINGTON,DC. RP GWINN, M (reprint author), CTR DIS CONTROL,DIV HIV AIDS,MAILSTOP E-49,ATLANTA,GA 30333, USA. NR 31 TC 243 Z9 245 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 3 PY 1991 VL 265 IS 13 BP 1704 EP 1708 DI 10.1001/jama.265.13.1704 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA FD659 UT WOS:A1991FD65900026 PM 2002571 ER PT J AU MULLIN, GE AF MULLIN, GE TI FOOD ALLERGY AND IRRITABLE-BOWEL-SYNDROME SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter ID HYPERSENSITIVITY C1 NIAID,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. RP MULLIN, GE (reprint author), JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205, USA. NR 5 TC 5 Z9 5 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 3 PY 1991 VL 265 IS 13 BP 1736 EP 1736 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FD659 UT WOS:A1991FD65900033 PM 2002578 ER PT J AU ROMKES, M FALETTO, MB BLAISDELL, JA RAUCY, JL GOLDSTEIN, JA AF ROMKES, M FALETTO, MB BLAISDELL, JA RAUCY, JL GOLDSTEIN, JA TI CLONING AND EXPRESSION OF COMPLEMENTARY DNAS FOR MULTIPLE MEMBERS OF THE HUMAN CYTOCHROME-P450IIC SUBFAMILY SO BIOCHEMISTRY LA English DT Article ID MEPHENYTOIN 4-HYDROXYLASE; CHROMOSOMAL LOCALIZATION; NUCLEOTIDE-SEQUENCE; PURIFICATION; GENE; PROTEIN; CELLS; POLYMORPHISM; FAMILY; CDNAS AB The present study characterizes the profile of cDNAs from the human P450IIC subfamily in a library from one individual, and it describes three new members of this subfamily (IIC17, IIC18, and IIC19) isolated from two human cDNA libraries. cDNA libraries were constructed from two human livers which differed phenotypically in the hepatic content of P450 HLx (IIC8). The library from the phenotypically low HLx individual was screened by using a cDNA for rat liver P450IIC13 and an oligonucleotide probe for human IIC8. One clone, 254c, was isolated which clearly represents a new member of the human P450IIC subfamily (IIC17). This clone lacked the first 358 nucleotides at the N-terminus but was only 91% homologous in its nucleic acid sequence to IIC9 and 79% homologous to IIC8. Near-full-length clones for IIC9 were also isolated from this library, but no clones for IIC8 were found. Northern blots indicated that the mRNA for IIC8 was low or absent in this individual. A second cDNA library (from a liver phenotypically high in HLx) was then screened. Eighty-three essentially full-length (> 1.8 kb) clones belonging to the IIC subfamily were isolated from this library. These include full-length clones for two additional new members of the IIC subfamily. Clones 29c and 6b appear to be allelic variants (IIC18), differing by one nucleotide (one amino acid change) in the coding region. Clone 11a represents a full-length clone for a third new P450 (IIC19). Both IIC18 and IIC19 are most homologous to IIC17 (87% and 95%, respectively). Full-length clones were isolated for two allelic variants of IIC9 (clones 25 and 65) which differed by three nucleotides, resulting in one amino acid difference. Hybridization analysis and partial sequencing indicated that of the 83 clones in this library, 50 were 1 of the 2 allelic variants of IIC9, 29 were IIC8, 3 were the 2 allelic variants of IIC18, and 1 was IIC19. cDNAs for IIC9, IIC18, and IIC19 were expressed in COS-1 cells. Antibody to IIC9 recognized the proteins in cells transfected with cDNAs for IIC9; however, neither antibody to IIC9 or IIC8 recognized the other two cytochromes, suggesting that these cytochromes differ immunochemically from IIC8 and IIC9. COS-1 cells transfected with IIC18 showed an increase in metabolism of mephenytoin, but no metabolism of mephenytoin was detected in COS-1 cells transfected with IIC9 or IIC19. C1 NIEHS,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709. UNIV NEW MEXICO,COLL PHARM,ALBUQUERQUE,NM 87131. UNIV NEW MEXICO,TOXICOL PROGRAM,ALBUQUERQUE,NM 87131. RI Goldstein, Joyce/A-6681-2012 NR 30 TC 232 Z9 241 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 2 PY 1991 VL 30 IS 13 BP 3247 EP 3255 DI 10.1021/bi00227a012 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE546 UT WOS:A1991FE54600012 PM 2009263 ER PT J AU PASQUALINI, T MCCALLA, J BERG, S POPLACK, DG ROSE, SR NISULA, BC CASSORLA, F AF PASQUALINI, T MCCALLA, J BERG, S POPLACK, DG ROSE, SR NISULA, BC CASSORLA, F TI SUBTLE PRIMARY HYPOTHYROIDISM IN PATIENTS TREATED FOR ACUTE LYMPHOBLASTIC-LEUKEMIA SO ACTA ENDOCRINOLOGICA LA English DT Article ID GROWTH-HORMONE SECRETION; LONG-TERM TREATMENT; THYROID-DYSFUNCTION; BRAIN-TUMORS; CRANIAL IRRADIATION; ENDOCRINE SEQUELAE; CHILDREN; RADIOTHERAPY; CHILDHOOD; PITUITARY AB We evaluated serum thyroid hormone and thyroid antibody levels, the serum TSH response to TRH, and the circadian pattern of serum TSH in 10 children and adolescents after radiation therapy for acute lymphoblastic leukemia. Four patients had received central nervous system preventive cranial irradiation and intrathecal chemotherapy, and the remaining 6 patients were treated with craniospinal irradiation for central nervous system relapse. Serum total T4 and T3 concentrations were within the normal range and thyroid antibodies were negative in all patients. Four patients who had received craniospinal irradiation had low free T4 levels. Prior to TRH administration, the overall mean serum TSH concentration was 5.4 +/- 1.3 mU/l, and the mean peak response to TRH was 33 +/- 6.5 mU/l. Both were significantly increased when compared to the levels observed in our control population (p < 0.05 and < 0.025, respectively). The overall mean nadir diurnal TSH was 3.6 +/- 0.8 mU/l, and the mean peak nocturnal TSH was 6.9 +/- 1.3 mU/l, both significantly elevated when compared to normal children (p < 0.025). The mean nocturnal TSH surge, however, was not significantly different from normal. Four of 6 children treated with craniospinal irradiation, and one of four children treated with cranial irradiation had increased basal and peak serum TSH concentrations in response to TRH. One of the patients treated with cranial irradiation had an abnormal nocturnal TSH surge. We conclude that subtle primary hypothyroidism is relatively common in patients with acute lymphoblastic leukemia, particularly in those who have been treated with craniospinal irradiation. C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NR 27 TC 19 Z9 19 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-5598 J9 ACTA ENDOCRINOL-COP JI Acta Endocrinol. PD APR PY 1991 VL 124 IS 4 BP 375 EP 380 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FM089 UT WOS:A1991FM08900005 PM 1903235 ER PT J AU KIESS, W LIU, LL HALL, NR AF KIESS, W LIU, LL HALL, NR TI LYMPHOCYTE SUBSET DISTRIBUTION AND NATURAL-KILLER-CELL ACTIVITY IN MEN WITH IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM SO ACTA ENDOCRINOLOGICA LA English DT Article ID IMMUNE-SYSTEM; STEROIDS; NK; ESTRADIOL; ANDROGENS; RECEPTOR; THYMUS; MICE AB Sex-related differences in immune responsiveness are mediated at least in part by sex steroid hormones. Lymphocyte subset distribution in peripheral blood and natural killer cell function both have been reported to be under hormonal control. In order to gain more insight into sex steroid hormone action on the immune system, we have measured the lymphocyte subset distribution and natural killer cell activity in 18 men with idiopathic hypogonadotropic hypogonadism before treatment, and after hormonal treatment had normalized plasma testosterone levels. In untreated patients, the mean plasma testosterone concentrations were significantly lower than those in the treated men (3.0 +/- 0.5 nmol/l vs 16 +/- 1.7 nmol/l, p < 0.001). The percentage of peripheral CD3+ lymphocytes, CD8+ cells, the CD4+/CD8+ ratio, and the natural killer cell activity of peripheral mononuclear cells measured in a Cr-51 release assay against target K 562 cells did not differ between patients with idiopathic hypogonadotropic hypogonadism and healthy adults, and most importantly, did not change during hormonal treatment which normalized plasma testosterone levels in the patients. In contrast, the percentage of peripheral CD4+ cells was significantly higher in untreated patients compared with normal adult subjects or patients with idiopathic hypogonadotropic hypogonadism after hormonal treatment that resulted in normal plasma testosterone levels (53 +/- 2 vs 47 +/- 2, p < 0.05). It should be noted that the percentage of peripheral CD16+ cells was significantly lower in untreated men with low plasma testosterone levels than in normal controls. The percentage of CD16+ cells in peripheral venous blood rose significantly after hormonal treatment restored plasma testosterone levels to normal (6 +/- 1 vs 11 +/- 1, p < 0.001). In addition, the percentage of peripheral CD16+ cells correlated significantly with the plasma testosterone levels measured in men with idiopathic hypogonadotropic hypogonadism (r = 0.534, p < 0.001). In conclusion, both the percentage of peripheral CD4+ cells (T-helper lymphocytes) and peripheral CD16+ cells (non-T-non-B cells) are related to the plasma testosterone levels in men with idiopathic hypogonadotropic hypogonadism. These data suggest that in vivo human immune cells are under the regulatory influence of endogenous sex steroids. C1 NCI,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. UNIV S FLORIDA,DEPT PSYCHIAT & BEHAV MED,TAMPA,FL 33620. UNIV S FLORIDA,DEPT MED MICROBIOL & IMMUNOL,TAMPA,FL 33620. RP KIESS, W (reprint author), CHILDRENS HOSP,DEPT PEDIAT ENDOCRINOL,CELL BIOL LAB,LINDWURMSTR 4,W-8000 MUNICH 2,GERMANY. FU NIMH NIH HHS [MH00648]; NINDS NIH HHS [R 01 NS 21210] NR 30 TC 13 Z9 13 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-5598 J9 ACTA ENDOCRINOL-COP JI Acta Endocrinol. PD APR PY 1991 VL 124 IS 4 BP 399 EP 404 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FM089 UT WOS:A1991FM08900009 PM 2031438 ER PT J AU SCHNITTMAN, SM GREENHOUSE, JJ LANE, HC PIERCE, PF FAUCI, AS AF SCHNITTMAN, SM GREENHOUSE, JJ LANE, HC PIERCE, PF FAUCI, AS TI FREQUENT DETECTION OF HIV-1-SPECIFIC MESSENGER-RNAS IN INFECTED INDIVIDUALS SUGGESTS ONGOING ACTIVE VIRAL EXPRESSION IN ALL STAGES OF DISEASE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; PERIPHERAL-BLOOD; T-CELL; LYMPHOID-CELLS; RETROVIRUS; TYPE-1; HIV; LYMPHOCYTES; AMPLIFICATION; TROPISM AB It has been shown that only a small fraction of CD4+ T cells are infected with human immunodeficiency virus type 1 (HIV-1) in vivo, particularly early in the course of infection. An even smaller proportion of cells have been shown to be expressing virus. Recent studies suggest that plasma viremia in asymptomatic HIV-infected individuals, representing active viral replication, is more common than was previously believed (range 23-100% of patients). To determine the in vivo state of HIV expression, samples of peripheral blood of 49 HIV-infected individuals at all stages of disease were examined. All subjects were positive for viral DNA by standard polymerase chain reaction (PCR), and a modified PCR was utilized to detect HIV-specific mRNAs (gag, major splice junction, env, and tat/rev). Patient's plasma was also assayed for p24 antigen and viremia. The results were as follows: [GRAPHICS] Overall, the findings suggest that active viral expression occurs at all stages of HIV infection. In particular, the presence of gag mRNA was determined in only 2 of 14 patients with T4% > 30% but in 20 of 35 patients with T4% less-than-or-equal-to 30% (p < 0.05), demonstrating a direct association between the presence of message for a structural protein, and more advanced immunosuppression. Determination of the expression of certain HIV-specific messagesfrom within a patient's cells adds a new dimension to understanding the pathogenesis of HIV infection. The presence of HIV-specific mRNAs, and in particular gag message, in many healthy seropositives may further argue for early initiation of antiviral therapy. C1 GEORGETOWN UNIV,MED CTR,DEPT INFECT DIS,WASHINGTON,DC 20007. RP SCHNITTMAN, SM (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B-13,BETHESDA,MD 20892, USA. NR 28 TC 98 Z9 98 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1991 VL 7 IS 4 BP 361 EP 367 DI 10.1089/aid.1991.7.361 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA FL683 UT WOS:A1991FL68300001 PM 1676896 ER PT J AU DOMANSKI, MJ CUNNION, RE ROBERTS, WC AF DOMANSKI, MJ CUNNION, RE ROBERTS, WC TI USEFULNESS OF THE SUBAORTIC DIAMETER FOR NORMALIZING LEFT-VENTRICULAR AND LEFT ATRIAL DIMENSIONS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Note C1 NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. RP DOMANSKI, MJ (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B15,BETHESDA,MD 20892, USA. NR 4 TC 3 Z9 3 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD APR 1 PY 1991 VL 67 IS 8 BP 785 EP 786 DI 10.1016/0002-9149(91)90546-W PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FD908 UT WOS:A1991FD90800029 PM 2006636 ER PT J AU VAUGHAN, L ZURLO, F RAVUSSIN, E AF VAUGHAN, L ZURLO, F RAVUSSIN, E TI AGING AND ENERGY-EXPENDITURE SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE ELDERLY PEOPLE; METABOLIC RATE; BODY COMPOSITION; ENERGY EXPENDITURE ID OLDER AMERICANS EAT; FAT-FREE MASS; ELDERLY MEN; BODY-COMPOSITION; WOMEN; AGE; POTASSIUM; HUMANS AB Whether sedentary energy expenditure is normal or lower in elderly people has not yet been clearly established. Twenty-four-hour energy expenditure (24EE) and its different components were measured by use of a respiratory chamber in elderly (17 male, 21 female; 71 +/- 6 y, chiBAR +/- SD; 71.2 +/- 13.5 kg; 32 +/- 8% fat) and young (33 male, 31 female; 24 +/- 4 ys; 84.5 +/- 23.1 kg; 25 +/- 13% fat) subjects. The elderly subjects had lower mean height (P < 0.001), weight (P < 0.01), and fat-free mass (P < 0.001) but higher percent body fat (P < 0.01) than did the young adults. Absolute 24EE, basal metabolic rate (BMR), and sleeping metabolic rate were significantly lower (P < 0.01) in the elderly subjects than in the young subjects. However, after differences in fat-free mass, fat mass, and sex were adjusted for, only BMR was found to be lower in the elderly subjects (P < 0.01). Despite a reduced adjusted BMR in older subjects, sedentary 24EE was decreased only in proportion to their reduced body size, suggesting that the lower energy intake reported in elderly people might be mainly related to lower physical activity in free-living conditions. C1 ARIZONA STATE UNIV,DEPT FAMILY RESOURCES & HUMAN DEV,TEMPE,AZ 85287. RP VAUGHAN, L (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ, USA. NR 34 TC 179 Z9 180 U1 1 U2 7 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1991 VL 53 IS 4 BP 821 EP 825 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA FE153 UT WOS:A1991FE15300003 PM 2008859 ER PT J AU MEDEIROS, LJ LARDELLI, P STETLERSTEVENSON, M LONGO, DL JAFFE, ES AF MEDEIROS, LJ LARDELLI, P STETLERSTEVENSON, M LONGO, DL JAFFE, ES TI GENOTYPIC ANALYSIS OF DIFFUSE, MIXED CELL LYMPHOMAS - COMPARISON WITH MORPHOLOGICAL AND IMMUNOPHENOTYPIC FINDINGS SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE MALIGNANT LYMPHOMA; DIFFUSE MIXED CELL SUBTYPE; IMMUNOPHENOTYPE; GENOTYPE; POLYMERASE CHAIN REACTION; CLONALITY ID NON-HODGKINS LYMPHOMAS; MALIGNANT-LYMPHOMA; DIAGNOSIS; CRITERIA; DNA AB Malignant lymphoma, diffuse, mixed small and large cell type, as defined in the Working Formulation, is heterogeneous both morphologically and immunophenotypically and, in some cases, clonality may be difficult to determine. Because gene rearrangement analysis has been shown to be a sensitive method for determining clonality, the authors genotyped 20 cases and compared the results with histologic and immunophenotypic findings. Immunophenotypic studies demonstrated that all lesions were composed predominantly of T cells. In addition, in eight cases either a monoclonal B-cell population (five lesions) or an aberrant immunophenotype (two T, one B) was detected, supporting a malignant diagnosis. In seven of these eight lymphomas, genotypic analysis confirmed the presence of a population of clonal cells. One case with an an abnormal T-cell phenotype was germline. In 12 cases the immunophenotypic results were uncertain (i.e., no clonal population or abnormal immunophenotype was identified). Genotypic analysis provided evidence of clonality in eight. In four cases with uncertain immunophenotypic results, a clonal population also could not be identified with the use of Southern blot analysis. Thus, the authors conclude that gene rearrangement analysis is a valuable tool in the study of diffuse mixed cell lymphomas and is complementary to immunophenotypic studies. In addition, the authors analyzed the major breakpoint region of the bcl-2 protooncogene on chromosome 18, either by Southern blot analysis and/or with the polymerase chain reaction. The authors identified the t(14;18)(q32;q21) translocation in seven B-cell lymphomas, five of which were not considered to be of follicular center cell type on the basis of morphologic findings. These results suggest that the histologic spectrum of follicular center cell lymphomas is greater than is appreciated in the literature. C1 NCI,MED BRANCH,BETHESDA,MD 20892. RP MEDEIROS, LJ (reprint author), NCI,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,2N108,BETHESDA,MD 20892, USA. NR 24 TC 22 Z9 22 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD APR PY 1991 VL 95 IS 4 BP 547 EP 555 PG 9 WC Pathology SC Pathology GA FE776 UT WOS:A1991FE77600021 PM 2014781 ER PT J AU PETERSEN, DD MCKINNEY, CE IKEYA, K SMITH, HH BALE, AE MCBRIDE, OW NEBERT, DW AF PETERSEN, DD MCKINNEY, CE IKEYA, K SMITH, HH BALE, AE MCBRIDE, OW NEBERT, DW TI HUMAN CYPIAI GENE - COSEGREGATION OF THE ENZYME INDUCIBILITY PHENOTYPE AND AN RFLP SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID ARYL-HYDROCARBON HYDROXYLASE; CULTURED HUMAN-LYMPHOCYTES; MESSENGER-RNA; LUNG-CANCER; CDNA PROBE; DNA; CHROMOSOME-15; SEQUENCE; CYTOCHROME-P1-450; LOCUS AB The human CYP1A1 (cytochrome P1 450) gene encodes an enzyme involved in the activation of procarcinogens, such as benzo[a]pyrene, to the ultimate reactive intermediate. Approximately 10% of the human population exhibit high CYP1A1 inducibility, and Kouri et al. reported that the high-inducibility phenotype might be at greater risk than low-inducibility individuals for cigarette smoke-induced bronchogenic carcinoma. In one 3-generation family of 15 individuals, we show here that the high-CYP1A1-inducibility phenotype segregates concordantly with an infrequent polymorphic site located 450 bases downstream from the CYP1A1 gene. Our findings are consistent with the study of Kawajiri et al., who demonstrated an association between this polymorphism and an increased incidence of squamous-cell lung cancer. Our data suggest that the CYP1A1 structural gene, or a region near this gene, might be correlated with the inducibility phenotype. C1 UNIV CINCINNATI,MED CTR,DEPT ENVIRONM HLTH,CINCINNATI,OH 45267. NICHHD,DEV PHARMACOL LAB,BETHESDA,MD 20892. NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 35 TC 183 Z9 185 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD APR PY 1991 VL 48 IS 4 BP 720 EP 725 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA FK478 UT WOS:A1991FK47800011 PM 1707592 ER PT J AU PINTO, JEB VIGLIONE, P SAAVEDRA, JM AF PINTO, JEB VIGLIONE, P SAAVEDRA, JM TI AUTORADIOGRAPHIC LOCALIZATION AND QUANTIFICATION OF RAT-HEART ANGIOTENSIN CONVERTING ENZYME SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article DE KININASE-II, PEPTIDASES; CORONARY ARTERIES; HEART VALVES AB Quantitative autoradiography with the angiotensin converting enzyme inhibitor [I-125]351A revealed the presence of specific binding for this enzyme in the valve leaflets of the rat heart and in the aortic wall. Branches of the coronary arteries showed binding localized throughout the arterial walls. Binding was also present in the heart atria, where it was four-fold higher than in the heart ventricles. These results support the hypothesis of a physiologic role for angiotensin converting enzyme in peptide metabolism in specific heart structures. C1 NIMH,PHARMACOL SECT,CLIN SCI LAB,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2D-45,BETHESDA,MD 20892. NR 0 TC 44 Z9 44 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD APR PY 1991 VL 4 IS 4 BP 321 EP 326 PN 1 PG 6 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FG949 UT WOS:A1991FG94900006 PM 1647797 ER PT J AU STRIKER, GE AF STRIKER, GE TI 1990 RENAL DATA REPORT PROFILES ESRD IN THE UNITED-STATES SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Editorial Material C1 NIDDKD,DIV HEMATOLOG DIS,BETHESDA,MD 20892. RP STRIKER, GE (reprint author), NIDDKD,DIV KIDNEY UROL,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD APR PY 1991 VL 17 IS 4 BP 488 EP 488 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA FE886 UT WOS:A1991FE88600024 ER PT J AU SMITH, ML PELLETT, OL CAHILL, TC DAVID, DN KASKEL, FJ SMOLIN, LA GREENE, AA WEISSBECKER, K DEAN, M SCHNEIDER, JA AF SMITH, ML PELLETT, OL CAHILL, TC DAVID, DN KASKEL, FJ SMOLIN, LA GREENE, AA WEISSBECKER, K DEAN, M SCHNEIDER, JA TI BIOCHEMICAL AND GENETIC-ANALYSIS OF A CHILD WITH CYSTIC-FIBROSIS AND CYSTINOSIS SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE BARTTER SYNDROME; LINKAGE ANALYSIS; AUTOSOMAL RECESSIVE INHERITANCE ID PROTEIN KINASE-C; BARTTERS-SYNDROME; LINKAGE DISEQUILIBRIUM; CHLORIDE REABSORPTION; AIRWAY EPITHELIA; DNA; CHANNELS; IDENTIFICATION; TRANSPORT; AMPLIFICATION AB We have studied a child with cystic fibrosis (CF), nephropathic cystinosis, and manifestations of Bartter syndrome, a finding reported previously in both of these diseases (CF and cystinosis). The chance of an individual inheriting a mutant allele for both CF and cystinosis from each of his parents by independent segregation is very small. Therefore, other mechanisms of inheritance were investigated, including whether his diseases were caused by a chromosome deletion or rearrangement that caused defects in both genes, whether his phenotype was caused by a new mutation or variant of either disease, or whether both diseases were inherited together due to inheritance of 2 copies of the same chromosome from one of the parents (uniparental disomy). An investigation was made of whether having mutations for both CF and cystinosis resulted in a different phenotype for either disease and whether the child was a heterozygote rather than a homozygote for one of the mutations. The results suggest that neither disease influenced the expression of the defect in the other and that this child inherited a mutant allele for both diseases independently from each parent. C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. SUNY STONY BROOK,SCH MED,DEPT PEDIAT,STONY BROOK,NY 11794. UNIV CONNECTICUT,DEPT MOLEC & CELL BIOL,STORRS,CT 06268. UNIV CALIF LOS ANGELES,SCH MED,DIV MED GENET,LOS ANGELES,CA 90024. PROGRAM RESOURCES INC,FREDERICK CANC RES FACIL,FREDERICK,MD. RP SMITH, ML (reprint author), UNIV CALIF SAN DIEGO,DEPT PEDIAT,LA JOLLA,CA 92093, USA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 FU NICHD NIH HHS [HD 20034]; NIDDK NIH HHS [DK 18434] NR 49 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD APR 1 PY 1991 VL 39 IS 1 BP 84 EP 90 DI 10.1002/ajmg.1320390119 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA FC827 UT WOS:A1991FC82700018 PM 1867269 ER PT J AU FALLOON, J MASUR, H AF FALLOON, J MASUR, H TI THE ERA OF AEROSOL PENTAMIDINE PROPHYLAXIS - THE BEGINNING OR THE END SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material ID PNEUMOCYSTIS-CARINII PNEUMONITIS C1 NIH,DEPT CRIT CARE MED,BLDG 10,ROOM 7043,BETHESDA,MD 20892. NR 10 TC 2 Z9 2 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1991 VL 90 IS 4 BP 415 EP 417 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FG905 UT WOS:A1991FG90500001 PM 2012081 ER PT J AU MOROI, K SAITO, S KURATA, T SATA, T YANAGIDA, M AF MOROI, K SAITO, S KURATA, T SATA, T YANAGIDA, M TI FETAL DEATH ASSOCIATED WITH MEASLES-VIRUS INFECTION OF THE PLACENTA SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE MATERNAL MEASLES; PLACENTAL INFECTION; FETAL DEATH AB A case of fetal death at 25 weeks' gestation, which was associated with maternal measles infection, is described. Immunohistochemical study revealed measles virus antigen in the syncytial trophoblastic cells and decidua but not in the fetus. Results suggest that fetal death was caused by measles virus infection in the placenta. As far as we know, this is the first report in which a measles virus antigen was detected in the placenta by the immunohistochemical method. C1 JUNTENDO UNIV,HOSP MED,DEPT CLIN PATHOL,TOKYO 113,JAPAN. NIH,DEPT PATHOL,BETHESDA,MD 20892. RP MOROI, K (reprint author), TOKYO METROPOLITAN TSUKIJI MATERN HOSP,DEPT OBSTET & GYNECOL,AKASHI CHO 6-24,CHUO KU,TOKYO,JAPAN. NR 2 TC 10 Z9 10 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD APR PY 1991 VL 164 IS 4 BP 1107 EP 1108 PG 2 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA FG945 UT WOS:A1991FG94500027 PM 2014835 ER PT J AU AXIOTIS, CA MONTEAGUDO, C MERINO, MJ LAPORTE, N NEUMANN, RD AF AXIOTIS, CA MONTEAGUDO, C MERINO, MJ LAPORTE, N NEUMANN, RD TI IMMUNOHISTOCHEMICAL DETECTION OF P-GLYCOPROTEIN IN ENDOMETRIAL ADENOCARCINOMA SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Note ID MULTIDRUG-RESISTANCE GENE; DRUG-RESISTANCE; GRAVID UTERUS; CELL-LINES; TISSUES; LOCALIZATION; EXPRESSION; ANTIBODY; CANCER; P170 AB P-glycoprotein (Pgp) has emerged as the central mediator in classic multidrug resistance in model systems in vitro. High levels of Pgp also have been detected in many normal human tissues and tumors; and its role in clinical drug resistance is currently under investigation. Recently significant levels of Pgp were localized to gravid and secretory endometrium; and it was demonstrated that the combination of estrogen and progesterone is sufficient to induce high levels of both Pgp mRNA and Pgp in uterine secretory epithelium. These findings suggest that increased Pgp expression also may be present in hormone-responsive malignancies such as endometrial adenocarcinomas (grade I [n = 17]; grade II [n = 6]; grade III [n = 13]) were investigated retrospectively by the avidin-biotin-complex immuno-histochemical procedure using three murine monoclonal antibodies (MAb) MAb C219, MAb C494, and MAb JSB-1, which recognize spatially distinct cytoplasmic epitopes of Pgp. Seventy-two percent of the tumors showed positive immunostaining with at least one MAb; 67% showed immunostaining with MAb C219, 50% with MAb C494, and 62% with MAb JSB-1. Forty-six percent of tumors were immunoreactive to two and 29% to all three antibodies. Membranous and Golgi/paranuclear type staining patterns were observed. Overall the intensity of immunostaining varied from one sample to another for a given tumor type, and considerable heterogeneity of expression was commonly seen within a given tumor. Strong to moderate immunoreactivity was seen in diffusely infiltrating, adenosquamous, and serous papillary carcinomas. In general, immunoreactivity to MAb C494 was weaker than MAb C219 or MAb JSB-1. Adenomatous and non-neoplastic endometrium adjacent to the tumors displayed strong membranous immunostaining with MAb JSB-1. Endometrial capillaries showed weak-to-moderate immunostaining to all three antibodies. It is concluded that Pgp is commonly expressed in endometrial adenocarcinoma and may be a significant factor responsible for their drug-resistant nature subject to modulation by progesterone. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,DEPT NUCL MED,BETHESDA,MD 20892. RP AXIOTIS, CA (reprint author), NCI,WARREN GRANT MAGNUSON CLIN CTR,OFF DIRECTOR,BLDG 10,ROOM 2N212,BETHESDA,MD 20892, USA. RI Monteagudo, Carlos/H-6555-2016 NR 32 TC 40 Z9 57 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD APR PY 1991 VL 138 IS 4 BP 799 EP 806 PG 8 WC Pathology SC Pathology GA FF067 UT WOS:A1991FF06700003 PM 1707232 ER PT J AU NOGUCHI, S OHBA, Y OKA, T AF NOGUCHI, S OHBA, Y OKA, T TI EFFECT OF SALIVARY EPIDERMAL GROWTH-FACTOR ON WOUND-HEALING OF TONGUE IN MICE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE SALIVA; TONGUE WOUND; SIALOADENECTOMY ID SUBMANDIBULAR-GLAND; FACTOR RECEPTORS; PLASMA; POLYPEPTIDES; LIVER; EGF; RAT AB The role of salivary epidermal growth factor (EGF) in wound healing of the tongue was studied in mice. Sialoadenectomy (removal of the submandibular glands, which are the major source of salivary EGF) or sham operation was performed 2 wk before infliction of wound on the tongue. Salivary EGF levels were 1.98 +/- 0.47 and 0.20 +/- 0.04 (SE) mu-g/ml in sham-operated male and female mice, respectively, whereas sialoadenectomy reduced salivary EGF to undetectable levels in both male and female mice. A circular superficial wound measuring approximately 2 mm in diameter was made in the middle of the tongue by mechanically ablating only the epithelial layer. The rate of wound healing was monitored by a stereomicroscopy. Sialoadenectomized male mice showed a significant delay in wound healing compared with sham-operated controls. Treatment of sialoadenectomized male mice with EGF (1-mu-g/ml in drinking water) restored the rate of wound healing to normal levels. Transforming growth factor (1-mu-g/ml) was as effective as EGF in the promotion of wound healing, whereas nerve growth factor (1-mu-g/ml) was ineffective. Essentially the same results were obtained in female mice. In addition, two classes of EGF binding sites with high and low affinity were demonstrated in the epithelium of the tongue obtained from male and female mice. The maximum binding sites and dissociation constants of the EGF receptors were the same between males and females and were not affected by sialoadenectomy. These results suggest that salivary EGF is involved in the promotion of wound healing of the tongue in both male and female mice. C1 NIDDKD,MOLEC & CELLULAR BIOL LAB,BLDG 8,RM 319,BETHESDA,MD 20892. NR 26 TC 68 Z9 71 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1991 VL 260 IS 4 BP E620 EP E625 PN 1 PG 6 WC Physiology SC Physiology GA FG541 UT WOS:A1991FG54100043 PM 2018126 ER PT J AU MORIYAMA, T GARCIAPEREZ, A OLSON, AD BURG, MB AF MORIYAMA, T GARCIAPEREZ, A OLSON, AD BURG, MB TI INTRACELLULAR BETAINE SUBSTITUTES FOR SORBITOL IN PROTECTING RENAL MEDULLARY CELLS FROM HYPERTONICITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CLONING EFFICIENCY; ALDOSE REDUCTASE; TOLRESTAT; INOSITOL; GLYCEROPHOSPHORYLCHOLINE ID ORGANIC SOLUTES; DIABETIC RATS; SORBINIL; STRESS; NACL AB Renal medullary cells are normally exposed to a variably high extracellular NaCl concentration. They compensate by accumulating large amounts of organic osmolytes, including sorbitol and betaine. The sorbitol is synthesized from glucose, catalyzed by aldose reductase. Previously, inhibition of aldose reductase activity was noted to greatly reduce renal medullary cell survival and growth (measured by cloning efficiency) in tissue cultures of renal medullary cells in hypertonic medium. In contrast, inhibition of aldose reductase and renal medullary sorbitol accumulation is not associated with kidney damage in vivo. In the present experiments we find that addition of betaine to the medium, and its resultant uptake by the cells, largely replaces the decrease in sorbitol caused by aldose reductase inhibitors and restores the cloning efficiency. We presume that in vivo uptake of betaine by renal medullary cells similarly protects them from harm when aldose reductase inhibitors lower sorbitol. The results also demonstrate that one organic osmolyte can substitute for another in protecting cells from hypertonicity, consistent with the compatible osmolytes hypothesis. C1 NHLBI,BLDG 10,RM 6N307,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 17 TC 24 Z9 24 U1 0 U2 4 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1991 VL 260 IS 4 BP F494 EP F497 PN 2 PG 4 WC Physiology SC Physiology GA FG542 UT WOS:A1991FG54200076 PM 1901456 ER PT J AU BLAKE, MJ FARGNOLI, J GERSHON, D HOLBROOK, NJ AF BLAKE, MJ FARGNOLI, J GERSHON, D HOLBROOK, NJ TI CONCOMITANT DECLINE IN HEAT-INDUCED HYPERTHERMIA AND HSP70 MESSENGER-RNA EXPRESSION IN AGED RATS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE HEAT-SHOCK PROTEINS; AGE; INVIVO; STRESS ID SHOCK PROTEIN; BODY-TEMPERATURE; C57BL/6J MICE; COLD STRESS; INDUCTION; CELLS AB An age-related impairment in the induction of heat-shock proteins (HSPs), which are thought to comprise a protective or adaptive response to cellular stress, may contribute to a reduction in thermal tolerance with age. When 5- and 24-mo-old rats were exposed to ambient temperatures of 23, 35, 37.5, or 40-degrees-C for 90 min, a graded increase in the level of HSP70 mRNA expression was observed in brain, lung, and skin of animals from both groups. However, at temperatures above 23-degrees-C, HSP70 expression was less in tissues of older rats when compared with those of young animals. This relative decline of heat-induced HSP70 mRNA levels with age correlated with an attenuated increase in colonic temperature (T(c)) of old rats resulting from heat exposure. In other experiments, it was determined that the duration of hyperthermia was also an important factor in determining the level of HSP70 mRNA expression in vivo. Thus age-related differences in heat-induced HSP70 mRNA expression appear to result from differences in T(c) due to heat stress rather than an impairment in the regulation of HSP70 gene expression. C1 TECHNION ISRAEL INST TECHNOL,DEPT BIOL,IL-32000 HAIFA,ISRAEL. RP BLAKE, MJ (reprint author), NIA,GERONTOL RES CTR,MOLEC GENET LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 32 TC 59 Z9 63 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1991 VL 260 IS 4 BP R663 EP R667 PN 2 PG 5 WC Physiology SC Physiology GA FG542 UT WOS:A1991FG54200048 PM 2012237 ER PT J AU KATZ, A RAZ, I SPENCER, MK RISING, R MOTT, DM AF KATZ, A RAZ, I SPENCER, MK RISING, R MOTT, DM TI HYPERGLYCEMIA INDUCES ACCUMULATION OF GLUCOSE IN HUMAN SKELETAL-MUSCLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE SOMATOSTATIN; ADENOSINE 5'-TRIPHOSPHATE; PHOSPHOCREATINE; HEXOSE MONOPHOSPHATES; ALPHA-D-GLUCOSE 1,6-DIPHOSPHATE; D-FRUCTOSE 2,6-DIPHOSPHATE; CITRATE; LACTATE; GLYCOGEN SYNTHASE; PHOSPHORYLASE; CARBOHYDRATE OXIDATION; FAT OXIDATION ID PERFUSED RAT HINDLIMB; GLYCOGEN-SYNTHASE; INSULIN; HEXOKINASE; OXIDATION; DISPOSAL; KINETICS; ASSAY AB The effect of hyperglycemia on whole body substrate utilization and the metabolic profile of skeletal muscle has been investigated. Eight glucose-tolerant men were infused with somatostatin (S) for 190 min. During the last 120 min of S infusion, glucose was infused to achieve a steady-state plasma level of 26 mmol/l. Biopsies were obtained from the quadriceps femoris muscle immediately before and 35 and 120 min after induction of hyperglycemia. Steady-state glucose disposal during hyperglycemia averaged (+/- SE) 33.8 +/- 3.2-mu-mol.kg fat-free mass-1.min-1, and approximately 70% of the glucose disposal was accounted for by skeletal muscle. Intracellular glucose increased from 0.9 +/- 0.2 mmol/kg dry wt during S to 9.5 +/- 2.5 during hyperglycemia (P < 0.01). It was estimated that approximately 35% of the glucose taken up by muscle during 120 min of hyperglycemia was not phosphorylated. Muscle contents of alpha-D-glucose 1,6-diphosphate, D-glucose 6-phosphate, ATP, ADP, and AMP (both of which are based on the phosphocreatine-to-creatine ratio), which have been shown to inhibit hexokinase in vitro, did not change significantly during hyperglycemia, nor were there any significant changes in any of the other postphosphofructokinase intermediates, D-fructose 2,6-diphosphate, and citrate. Hyperglycemia did not alter the fractional activities of glycogen synthase or phosphorylase, nor total phosphorylase activity. However, hyperglycemia resulted in a 55% increase in glycogen synthase-specific activity (P < 0.01). It is concluded that hyperglycemia results in a marked increase in muscle glucose. It is suggested that the accumulation of glucose in muscle is a consequence of a glucose transport rate that exceeds the rate at which hexokinase phosphorylates glucose in vivo. C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. RP KATZ, A (reprint author), UNIV ILLINOIS,DEPT KINESIOL,906 S GOODWIN AVE,URBANA,IL 61801, USA. NR 32 TC 19 Z9 19 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1991 VL 260 IS 4 BP R698 EP R703 PN 2 PG 6 WC Physiology SC Physiology GA FG542 UT WOS:A1991FG54200054 PM 1672795 ER PT J AU ZATZ, M WANG, HM AF ZATZ, M WANG, HM TI HIGH SALT MIMICS EFFECTS OF LIGHT-PULSES ON CIRCADIAN PACEMAKER IN CULTURED CHICK PINEAL CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MELATONIN; CELL VOLUME; CIRCADIAN RHYTHMS ID N-ACETYLTRANSFERASE ACTIVITY; PHOTOENDOCRINE TRANSDUCTION; MELATONIN RHYTHM; DARK PULSES; PHASE; POTASSIUM; MECHANISMS; INVITRO; OUABAIN; GLAND AB Chick pineal cells in static culture display a persistent photosensitive circadian rhythm of melatonin production and release. Pulses of white light or darkness, in otherwise constant red light, induced phase shifts in subsequent cycles whose magnitude and direction depend on the phase at which the pulse is given. Such "phase-dependent phase shifts" are mediated by effects on the underlying pacemaker. We reported previously that inhibiting the Na+-K+-adenosinetriphosphatase with ouabain evokes phase shifts with the same phase dependence as those induced by pulses of darkness. Two of the consequences of inhibiting the Na+ pump are membrane depolarization and cell swelling. To test the relevance of these effects and to distinguish between them, we exposed chick pineal cells to pulses of high concentrations of added KCl, which should cause both membrane depolarization and cell shrinkage. We also compared the effects of added NaCl, sodium gluconate, and mannitol, which should cause cell shrinkage without comparable depolarization. Each of these hypertonic solutions induced phase shifts in the melatonin rhythm with the same phase dependence as those caused by pulses of light rather than those caused by ouabain or darkness. These results argue strongly against a dominant role for changes in membrane potential in phase shifting the melatonin rhythm. Rather, they suggest that cell swelling may mediate the darklike effects of ouabain on the circadian pacemaker in chick pineal cells and indicate that cell shrinkage mimics the effects of light. RP ZATZ, M (reprint author), NIMH,BIOCHEM PHARMACOL SECT,CELL BIOL LAB,BLDG 36,RM 2A-17,BETHESDA,MD 20892, USA. NR 33 TC 13 Z9 13 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1991 VL 260 IS 4 BP R769 EP R776 PN 2 PG 8 WC Physiology SC Physiology GA FG542 UT WOS:A1991FG54200064 PM 1849378 ER PT J AU OREN, DA BRAINARD, GC JOHNSTON, SH JOSEPHVANDERPOOL, JR SOREK, E ROSENTHAL, NE AF OREN, DA BRAINARD, GC JOHNSTON, SH JOSEPHVANDERPOOL, JR SOREK, E ROSENTHAL, NE TI TREATMENT OF SEASONAL AFFECTIVE-DISORDER WITH GREEN LIGHT AND RED-LIGHT SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID THERAPY AB Objective: This study sought to determine whether an equal photon density of green light is superior to red light in treating seasonal affective disorder. Method: After recruitment through the media, 20 outpatients with seasonal affective disorder participated in a balanced-order crossover trial of 1 week of green light therapy compared with 1 week of red light therapy. Each treatment consisted of 2 hours of daily light treatment at home in the early morning. Ultraviolet light was excluded from both treatment conditions. The photon densities of the two treatments (2.3 x 10(15) photons/sec per cm2) were similar to those used in previous studies of therapy with 2500-lux white light. Fourteen patients completed the study. At least 1 week separated each treatment period to allow time for relapse. Effectiveness of treatment was assessed by analysis of variance of changes in ratings on the Hamilton Rating Scale for Depression. Results: Although patients' expectations of the two treatments were similar, green light induced greater antidepressant effects than red light. A Sequence by Color interaction was also demonstrated. Conclusions: Green light provides a treatment effect superior to that of red light and similar to that seen in previous studies with white light. These results are consistent with the hypothesis that retinal photoreceptors mediate the antidepressant response in seasonal affective disorder. Identifying optimal wavelengths for light treatment is important in optimizing phototherapy efficacy. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT NEUROL,PHILADELPHIA,PA 19107. RP OREN, DA (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,RM 3N228,BLDG 10,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU NIMH NIH HHS [MH-44890] NR 8 TC 40 Z9 40 U1 1 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1991 VL 148 IS 4 BP 509 EP 511 PG 3 WC Psychiatry SC Psychiatry GA FD906 UT WOS:A1991FD90600018 PM 2006698 ER PT J AU GURALNIK, JM LACROIX, AZ BRANCH, LG KASL, SV WALLACE, RB AF GURALNIK, JM LACROIX, AZ BRANCH, LG KASL, SV WALLACE, RB TI MORBIDITY AND DISABILITY IN OLDER PERSONS IN THE YEARS PRIOR TO DEATH SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID FUNCTIONAL STATUS AB Background: A large proportion of the disease and disability which affects older persons occurs in the years just prior to death. Little prospective evidence is available which quantifies the burden of morbidity and disability during these years. Methods: In three community-based cohorts of persons age 65 and older, chronic conditions and disability were evaluated for the three years prior to death in 531 persons who had three annual assessments and then died within one year of the third assessment. Number of chronic conditions, prevalence of disability in activities of daily living (ADLs), and prevalence of disability on a modified Rosow-Breslau scale were determined for these decedents and compared to 8821 members of the cohorts known to have survived. Results: Prevalence rates of disease and disability increased during the follow-up for both decedents and survivors, with decedents generally having higher rates than survivors. Disability rates prior to death, but not the number of diseases, increased with increasing age at death. The odds ratio for disability in ADLs at any of the three assessments for decedents versus survivors ranged from 3.0 to 4.2 in the three communities. In each community the odds ratio for ADL disability was higher in women decedents versus survivors than in men decedents versus survivors. Conclusions: These results have important implications for disability levels in future older populations in which death is projected to occur at increasingly higher ages. C1 GRP HLTH COOPERAT PUGET SOUND,PUGET SOUND,WA. UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195. BOSTON UNIV,SCH MED,DEPT SOCIOMED SCI & COMMUNITY MED,BOSTON,MA 02118. YALE UNIV,SCH MED,DEPT EPIDEMIOL & PUBL HLTH,NEW HAVEN,CT 06510. UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52242. RP GURALNIK, JM (reprint author), NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,7550 WISCONCIN AVE,FED BLDG,BETHESDA,MD 20892, USA. NR 16 TC 112 Z9 113 U1 2 U2 7 PU AMER PUBLIC HEALTH ASSN INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD APR PY 1991 VL 81 IS 4 BP 443 EP 447 DI 10.2105/AJPH.81.4.443 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA FU761 UT WOS:A1991FU76100010 PM 2003621 ER PT J AU JEPSON, C KESSLER, LG PORTNOY, B GIBBS, T AF JEPSON, C KESSLER, LG PORTNOY, B GIBBS, T TI BLACK-WHITE DIFFERENCES IN CANCER PREVENTION KNOWLEDGE AND BEHAVIOR SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note AB Data from the 1987 National Health Interview Survey Cancer Control Supplement were used to estimate multivariate logistic regression models of diet change, mammography utilization, stool blood test utilization, and smoking. Predictor variables included race, sex, age, income, dietary concerns, and four knowledge-related variables: education and three measures of cancer prevention knowledge. When knowledge variables were included in the models, race was not a significant predictor of behavior, with one exception: among women, Blacks were found to smoke less than Whites. C1 NCI,BETHESDA,MD 20892. NR 17 TC 111 Z9 112 U1 0 U2 3 PU AMER PUBLIC HEALTH ASSN INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD APR PY 1991 VL 81 IS 4 BP 501 EP 504 DI 10.2105/AJPH.81.4.501 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA FU761 UT WOS:A1991FU76100026 PM 2003635 ER PT J AU MYERS, C AF MYERS, C TI PEPTIDE GROWTH-FACTORS - THE PARALLEL BETWEEN FETAL DEVELOPMENT AND MALIGNANT TRANSFORMATION SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Article ID RADIOLABELED MONOCLONAL-ANTIBODIES; ANTIIDIOTYPIC ANTIBODIES; THERAPY; EMBRYOGENESIS; DIFFERENTIATION; RECEPTORS; CANCER; DIAGNOSIS AB Normal embryonic development and tissue homeostasis depend upon cell-to-cell and tissue-to-tissue communication. Much of this depends upon the production and release of peptide growth regulators such as fibroblast growth factor, epidermal growth factor, etc. As the molecular basis of malignant transformation has been documented, it is apparent that a common means by which a tumor becomes autonomous of external control is by becoming independent of the need for external growth factor stimulation. This can occur through the cell producing and releasing the growth factors needed for its own growth. A similar end result can occur with growth factor receptor mutants in which the receptor gives a positive signal even when no growth factor is bound to the receptor. One potential therapeutic strategy is to interfere with this autocrine loop. Suramin is presented as an example of a drug capable of blocking such autocrine loops. This drug also reverses malignant transformation due to Platelet Derived Growth Factor and K-fgf/hst oncogenes on this basis. Another potential mechanism to accomplish the same end is through the use of monoclonal antibodies to either the growth factor or its receptor. Examples of this are available for TGF-alpha. We have discussed a range of practical issues involved in developing monoclonal antibodies as therapeutic agents. RP MYERS, C (reprint author), NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892, USA. NR 39 TC 4 Z9 4 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 8755-8920 J9 AM J REPROD IMMUNOL JI Am. J. Reprod. Immunol. PD APR PY 1991 VL 25 IS 3 BP 133 EP 136 PG 4 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA GC163 UT WOS:A1991GC16300010 PM 1930641 ER PT J AU ZEITLIN, PL LU, L RHIM, J CUTTING, G STETTEN, G KIEFFER, KA CRAIG, R GUGGINO, WB AF ZEITLIN, PL LU, L RHIM, J CUTTING, G STETTEN, G KIEFFER, KA CRAIG, R GUGGINO, WB TI A CYSTIC-FIBROSIS BRONCHIAL EPITHELIAL-CELL LINE - IMMORTALIZATION BY ADENO-12-SV40 INFECTION SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID EARLY REGION GENES; PROTEIN KINASE-C; CHLORIDE CHANNELS; AIRWAY EPITHELIA; TRANSFORMATION; KERATINOCYTES; TRANSFECTION; PLASMID; VIRUS; SV40 AB An immortalized cell line was created from a primary culture of bronchial epithelia isolated from a patient with cystic fibrosis. The culture was transformed with a hybrid virus, adeno-12-SV40, which has been used successfully on a number of different human epithelial tissues. The transformed bronchial epithelial cells have the following characteristics. (1) Cyclic adenosine monophosphate (cAMP) is stimulated by beta-adrenergic agonists. (2) Outwardly rectifying C1- channels are present on the apical cell membrane. These channels can be activated by depolarizing voltages but not by protein kinase A or C. (3) Keratin is present by immunofluorescence, and this is consistent with the epithelial origin of the cells. (4) The SV40 large T antigen is present as demonstrated by immunofluorescence. (5) Multiple karyotype analyses show modal chromosome number to be 80 to 90. There are an average of four chromosome 7 per cell. (6) The phenylalanine508 deletion in the gene coding for the cystic fibrosis transmembrane regulator is present on at least one chromosome. The cells can be grown in multiple passages, contain the abnormal regulation of the secretory C1- channel, and should be an appropriate substrate for studies of the mutant cystic fibrosis transmembrane regulatory protein and its interaction with the C1- channel. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT OBSTET & GYNECOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,BALTIMORE,MD 21205. NIH,BALTIMORE,MD. FU NHLBI NIH HHS [HL-40178, K08 HL-02188] NR 18 TC 269 Z9 270 U1 1 U2 2 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD APR PY 1991 VL 4 IS 4 BP 313 EP 319 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA FE903 UT WOS:A1991FE90300004 PM 1849726 ER PT J AU TRAVIS, WD HOFFMAN, GS LEAVITT, RY PASS, HI FAUCI, AS AF TRAVIS, WD HOFFMAN, GS LEAVITT, RY PASS, HI FAUCI, AS TI SURGICAL PATHOLOGY OF THE LUNG IN WEGENERS GRANULOMATOSIS - REVIEW OF 87 OPEN LUNG BIOPSIES FROM 67 PATIENTS SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE VASCULITIS; PULMONARY HEMORRHAGE; WEGENERS GRANULOMATOSIS; LUNG ID CHURG-STRAUSS-SYNDROME; NECROTIZING SARCOID GRANULOMATOSIS; DIFFUSE PULMONARY HEMORRHAGE; LYMPHOMATOID GRANULOMATOSIS; ANTICYTOPLASMIC AUTOANTIBODIES; ALLERGIC GRANULOMATOSIS; THERAPEUTIC EXPERIENCE; SYSTEMIC VASCULITIS; ANGIITIS; CYCLOPHOSPHAMIDE AB We report the pulmonary pathologic features in 87 open lung biopsies from 67 patients with Wegener's granulomatosis (WG) who were treated at a single institution from 1968 to 1990. At the time of open lung biopsy, 48 patients (72%) had classical WG with renal involvement; 19 (28%) had limited WG without renal involvement. The pathologic features were divided into major and minor manifestations. In the 82 specimens demonstrating no infectious organism, the three major pathologic manifestations of classical WG observed were also useful diagnostic criteria and included: (a) parenchymal necrosis, (b) vasculitis, and (c) granulomatous inflammation accompanied by an inflammatory infiltrate composed of a mixture of neutrophils, lymphocytes, plasma cells, histiocytes, and eosinophils. Parenchymal necrosis was found in 84% of biopsy specimens either as neutrophilic microabscesses (65% of specimens) or as large (67%) or small (69%) areas of geographic necrosis. Areas of geographic necrosis were usually surrounded by palisading histiocytes and giant cells. Additional granulomatous lesions consisted of microabscesses surrounded by giant cells (69%), poorly formed granulomas (59%), and scattered giant cells (79%). Sarcoid-like granulomas were uncommon (4%), and in only one specimen (1%) appeared within an inflammatory lesion of WG. Vascular changes were identified in 94% of biopsy specimens. Vascular inflammation was classified as chronic (37% arterial, 64% venous), acute (37% arterial, 29% venous), nonnecrotizing granulomatous (22% arterial, 9% venous), and necrotizing granulomatous (22% arterial, 10% venous). Fibrinoid necrosis was relatively uncommon (11% arterial, 6% venous). Cicatricial changes were found in arteries in 41% of biopsy specimens and in veins in 16%. Capillaritis was present in 31% of specimens. Minor pathologic lesions were commonly observed in biopsy specimens associated with classical WG lesions, but they were usually inconspicuous and not useful diagnostic criteria. These included interstitial fibrosis (26%), alveolar hemorrhage (49%), tissue eosinophils (100%), organizing intraluminal fibrosis (70%), endogenous lipoid pneumonia (59%), lymphoid aggregate (37%), and a variety of bronchial/bronchiolar lesions including acute and chronic bronchiolitis (51% and 64%), follicular bronchiolitis (28%), and bronchiolitis obliterans (31%). These minor lesions were often found at the periphery of typical nodules of WG. However, in 15 specimens (18%) a minor pathologic feature represented the dominant or major finding: pulmonary fibrosis (six specimens, 7%), diffuse pulmonary hemorrhage (six specimens, 7%), lipoid pneumonia (one specimen, 1%), acute bronchopneumonia (one specimen, 1%) and chronic bronchiolitis, bronchiolitic obliterans with organizing pneumonia (BOOP), and bronchocentric granulomatosis (one specimen, 1%). Bronchial stenosis was found in three specimens (4%). In 10 specimens (12%) active vasculitis affecting veins or arteries could not be identified. Diffuse pulmonary hemorrhage associated with capillaritis was the primary finding in three of these specimens. Nodular interstitial fibrosis was the primary finding in six cases, and in three of these specimens cicatricial vascular changes were also present. In the 10th specimen, geographic necrosis, microabscesses, and scattered giant cells were present. This review illustrates the wide variation and broad spectrum of pathologic features that can occur in pulmonary WG and addresses the complicated differential diagnosis that can be encountered in the lung. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP TRAVIS, WD (reprint author), NCI,PATHOL LAB,BLDG 10,RM 2N212,BETHESDA,MD 20892, USA. NR 57 TC 203 Z9 210 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD APR PY 1991 VL 15 IS 4 BP 315 EP 333 DI 10.1097/00000478-199104000-00001 PG 19 WC Pathology; Surgery SC Pathology; Surgery GA FD453 UT WOS:A1991FD45300001 PM 2006712 ER PT J AU SHULDINER, AR TANNER, K SCOTT, LA MOORE, CA ROTH, J AF SHULDINER, AR TANNER, K SCOTT, LA MOORE, CA ROTH, J TI LIGASE-FREE SUBCLONING - A VERSATILE METHOD TO SUBCLONE POLYMERASE CHAIN-REACTION (PCR) PRODUCTS IN A SINGLE DAY SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID SITE-SPECIFIC MUTAGENESIS; ENZYMATIC AMPLIFICATION; GENOMIC SEQUENCES; DNA-POLYMERASE; CLONING; GENES RP SHULDINER, AR (reprint author), NIDDKD,DIABET BRANCH,BETHESDA,MD 20892, USA. NR 17 TC 24 Z9 24 U1 1 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD APR PY 1991 VL 194 IS 1 BP 9 EP 15 DI 10.1016/0003-2697(91)90144-I PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FE430 UT WOS:A1991FE43000002 PM 1651068 ER PT J AU JORDAN, E AF JORDAN, E TI ORGANIZATION AND LONG-RANGE PLAN SO ANALYTICAL CHEMISTRY LA English DT Article RP JORDAN, E (reprint author), NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0003-2700 J9 ANAL CHEM JI Anal. Chem. PD APR 1 PY 1991 VL 63 IS 7 BP A420 EP A423 PG 4 WC Chemistry, Analytical SC Chemistry GA FD917 UT WOS:A1991FD91700006 PM 2053703 ER PT J AU SAKAIRI, M YERGEY, AL SIU, KWM LEBLANC, JCY GUEVREMONT, R BERMAN, SS AF SAKAIRI, M YERGEY, AL SIU, KWM LEBLANC, JCY GUEVREMONT, R BERMAN, SS TI ELECTROSPRAY MASS-SPECTROMETRY - PROTONATED MOLECULE INTENSITIES VERSUS HYDRATION FREE-ENERGIES IN AMINO-ACIDS SO ANALYTICAL SCIENCES LA English DT Article DE ELECTROSPRAY MASS SPECTROMETRY; HYDRATION FREE ENERGY; AMINO ACID; PROTONATED MOLECULE INTENSITY ID ION-SOURCE; EVAPORATION AB We demonstrate a high correlation between the natural logarithms of the relative intensities of protonated molecules of amino acids by electrospray and their standard hydration free energies (r = 0.98). This result means that the solvation free energy is an important physical parameter for interpreting the difference in protonated molecule intensities by electrospray. C1 NICHHD,BETHESDA,MD 20892. NATL RES COUNCIL CANADA,DIV CHEM,OTTAWA K1A 0R9,ONTARIO,CANADA. RP SAKAIRI, M (reprint author), HITACHI LTD,CENT RES LAB,KOKUBUNJI,TOKYO 185,JAPAN. NR 15 TC 3 Z9 3 U1 0 U2 3 PU JAPAN SOC ANALYTICAL CHEM PI TOKYO PA 26-2 NISHIGOTANDA 1 CHOME SHINAGAWA-KU, TOKYO 141, JAPAN SN 0910-6340 J9 ANAL SCI JI Anal. Sci. PD APR PY 1991 VL 7 IS 2 BP 199 EP 202 DI 10.2116/analsci.7.199 PG 4 WC Chemistry, Analytical SC Chemistry GA FH209 UT WOS:A1991FH20900002 ER PT J AU SPEAR, RM YASTER, M BERKOWITZ, ID MAXWELL, LG BENDER, KS NACLERIO, R MANOLIO, TA NICHOLS, DG AF SPEAR, RM YASTER, M BERKOWITZ, ID MAXWELL, LG BENDER, KS NACLERIO, R MANOLIO, TA NICHOLS, DG TI PREINDUCTION OF ANESTHESIA IN CHILDREN WITH RECTALLY ADMINISTERED MIDAZOLAM SO ANESTHESIOLOGY LA English DT Article DE ANESTHESIA, PEDIATRIC; ANESTHETIC TECHNIQUES, RECTAL; ANESTHETICS, RECTAL, MIDAZOLAM; INDUCTION, ANESTHESIA; PREMEDICATION, MIDAZOLAM ID PREMEDICATION; INDUCTION; METHOHEXITONE; DIAZEPAM; SURGERY AB The authors evaluated the efficacy of rectally administered midazolam for preinduction (i.e., premedication/induction) of anesthesia in 67 pediatric patients, ASA physical status 1 or 2, undergoing a variety of elective surgical procedures. In phase 1, 41 children weighing 12 +/- 3 kg (range 7-20 kg) and 31 +/- 16 months (range 8-67 months) of age (mean +/- SD) received midazolam, 0.4-5.0 mg.kg-1, in an attempt to produce unconsciousness. Only one child lost consciousness (4.5 mg.kg-1). However, at all doses, inhalational induction of anesthesia was facilitated because children were tranquil and calmly separated from their parent(s). There were no clinically significant changes in arterial blood pressure, heart rate, oxyhemoglobin saturation, and end-tidal carbon dioxide concentration, 10 min after drug administration. In phase 2, 26 children weighing 17 +/- 4 kg (range 10-26 kg) and 44 +/- 19 months (range 17-84 months) months of age undergoing tonsil and/or adenoid surgery were studied to determine the optimal sedative dose of rectally administered midazolam. Patients received 0.3, 1.0, 2.0, or 3.0 mg.kg-1 of midazolam in a randomized, double-blind fashion. One third (3 of 9) of patients receiving 0.3 mg.kg-1 struggled during mask induction. All patients receiving greater-than-or-equal-to 1.0 mg.kg-1 were adequately sedated (P < 0.008). Discharge from the postanesthesia care unit (PACU), however, was delayed (> 60 min) in children receiving greater-than-or-equal-to 2.0 mg.kg-1 (P < 0.03). Therefore, the authors conclude that rectally administered midazolam in a dose of 1.0 mg.kg-1 is effective for preinduction of anesthesia and does not delay discharge from the PACU. C1 CHILDRENS HOSP SAN DIEGO,SAN DIEGO,CA. UNIV CALIF SAN DIEGO,ANESTHESIA & PEDIAT,SAN DIEGO,CA 92103. NHLBI,CLIN & GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS MED INST,DEPT ANESTHESIOL CRIT CARE MED,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT OTOLARYNGOL,BALTIMORE,MD 21205. NR 21 TC 39 Z9 39 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD APR PY 1991 VL 74 IS 4 BP 670 EP 674 DI 10.1097/00000542-199104000-00009 PG 5 WC Anesthesiology SC Anesthesiology GA FE106 UT WOS:A1991FE10600009 PM 2008948 ER PT J AU POLTORAK, M FREED, WJ AF POLTORAK, M FREED, WJ TI BN RATS DO NOT REJECT F344 BRAIN ALLOGRAFTS EVEN AFTER SYSTEMIC SENSITIZATION SO ANNALS OF NEUROLOGY LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; IMMUNOLOGICAL PRIVILEGE; NEURAL TRANSPLANTS; SUBSTANTIA NIGRA; ANTERIOR-CHAMBER; IMMUNE-RESPONSE; GENETIC-CONTROL; SPINAL-CORD; TISSUE AB Embryonic brain tissue allografts under many circumstances survive transplantation into the brain. It is generally believed that such grafts will not survive if the host animal is systemically sensitized, by skin grafting or other means, to major histocompatibility complex (MHC) antigens of the donor animal. We have found that F344 brain grafts survive in BN hosts even when the host is systemically sensitized to F344 tissue. Embryonic cerebral neocortex from F344 donors was transplanted into BN host rats (n = 95). Subsequently, the host rats were systemically sensitized with donor skin (n = 25), brain tissue (n = 41), or spleen cells (n = 6) and compared with a control group of rats consisting of allografts with no sensitization or sham procedures (n = 23). Rejection of the transplants in BN rat hosts was not provoked by any of the sensitization methods tested. Minor immunological responses that did not result in rejection were, however, present in many host animals. We did not observe infiltration of W3/13+ T cells and OX8+ cytotoxic lymphocytes in any of the groups. Nevertheless, substantial infiltrations of OX6+ antigen-presenting cells and W3/25+ helper T cells were present. There was also an extensive enhancement of MHC class I immunoreactivity in parts of the grafted tissue developing within the third ventricle, but not for the same type of graft in the lateral ventricle. This increase of MHC class I expression was not accompanied by infiltration of cytotoxic T cells. Our findings thus suggest that neural graft rejection depends on general genetic susceptibility to immune reactions, particularly experimental allergic encephalomyelitis and not only on disparity between donor and host antigens encoded by the MHC. Moreover, enhancement of MHC class I and class II expression within transplanted tissue does not predict graft rejection. RP POLTORAK, M (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,PRECLIN NEUROSCI SECT,WASHINGTON,DC 20032, USA. NR 64 TC 29 Z9 30 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1991 VL 29 IS 4 BP 377 EP 388 DI 10.1002/ana.410290408 PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FK134 UT WOS:A1991FK13400007 PM 1929209 ER PT J AU CHABNER, BA AF CHABNER, BA TI THE AMSACRINE STORY - WILL IT CHANGE THE FDA POLICY SO ANNALS OF ONCOLOGY LA English DT Editorial Material RP CHABNER, BA (reprint author), NCI,DIV CANC TREATMENT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD APR PY 1991 VL 2 IS 4 BP 240 EP 241 PG 2 WC Oncology SC Oncology GA FR379 UT WOS:A1991FR37900003 ER PT J AU PLUDA, JM YARCHOAN, R BRODER, S AF PLUDA, JM YARCHOAN, R BRODER, S TI HIV-ASSOCIATED NON-HODGKINS-LYMPHOMAS SO ANNALS OF ONCOLOGY LA English DT Editorial Material ID ACQUIRED IMMUNODEFICIENCY SYNDROME; B-CELL ACTIVATION; TRANSPLANT RECIPIENTS; VIRUS-INFECTION; HOMOSEXUAL MEN; DISORDERS RP PLUDA, JM (reprint author), NCI,BETHESDA,MD 20892, USA. NR 18 TC 5 Z9 5 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-7534 J9 ANN ONCOL JI Ann. Oncol. PD APR PY 1991 VL 2 IS 4 BP 248 EP 249 PG 2 WC Oncology SC Oncology GA FR379 UT WOS:A1991FR37900008 PM 1868019 ER PT J AU ROBERTS, CS ROBERTS, WC AF ROBERTS, CS ROBERTS, WC TI AORTIC DISSECTION WITH THE ENTRANCE TEAR IN THE DESCENDING THORACIC AORTA - ANALYSIS OF 40 NECROPSY PATIENTS SO ANNALS OF SURGERY LA English DT Article ID ANEURYSMS; STENOSIS AB Clinical and necropsy findings are described in 40 patients who had aortic dissection with the entrance tear in the descending thoracic aorta. Their ages at death ranged from 39 to 91 years (mean, 66 years); 24 (60%) were men and 16 (40%) were women. Systemic hypertension was present by history in 33 patients (83%) and the hearts were of increased weight in 78%. Of the 40 patients, 31 (78%) had no operative intervention, while 9 (22%) underwent operation for aortic dissection. Of the 31 patients without operative therapy, the diagnosis of aortic dissection was established in life in 9 patients (29%) and at necropsy in 22 (71%). The interval from aortic dissection to death was 30 days or less in 13 patients (42%); rupture of the false channel was the cause of death in 9 patients (69%), renal failure in 2 (15%), and the cause was unclear in 2 (15%). The interval from aortic dissection to death was more than 30 days in 18 (58%) of the 31 patients without operative therapy. The cause of death in these 18 patients was related to the dissection in 11 (61%) (rupture of the false channel in 5; renal failure from dissection in 3, and rupture of the false channel of a second acute dissection in 3), but in the other 7 patients (39%) death was unrelated to the dissection but a nonfatal complication, specifically stenosis of the true channel from compression by a thrombus-filled false channel, occurred in 4 of these 7 patients. Thus only 3 (10%) of the 31 patients without operative therapy had no complications of aortic dissection. All nine patients who underwent operation had had an aortic dissection within 30 days, and the operation was performed because of a major complication of the dissection. Four patients survived 8 to 84 months after the operation. Thus early operative intervention (before the appearance of complications) appears justified in patients with aortic dissection with the entrance tear in the descending thoracic aorta to prevent rupture of the false channel acutely or after initial healing; to prevent renal failure from compression of renal arteries by an aneurysmal false channel; to prevent true channel stenosis from compression by a thrombus-filled false channel; and possibly to prevent the recurrence of acute dissection. C1 NHLBI,SURG BRANCH,BLDG 10,ROOM 2N258,BETHESDA,MD 20892. NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. NR 21 TC 64 Z9 66 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD APR PY 1991 VL 213 IS 4 BP 356 EP 368 DI 10.1097/00000658-199104000-00011 PG 13 WC Surgery SC Surgery GA FG139 UT WOS:A1991FG13900011 PM 2009018 ER PT J AU BROWN, PS ROBERTS, CS MCINTOSH, CL CLARK, RE AF BROWN, PS ROBERTS, CS MCINTOSH, CL CLARK, RE TI AORTIC REGURGITATION AFTER LEFT-VENTRICULAR MYOTOMY AND MYECTOMY SO ANNALS OF THORACIC SURGERY LA English DT Article ID HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY AB Five hundred twenty-five patients with hypertrophic cardiomyopathy underwent left ventricular myotomy and myectomy (LVMM) from 1960 to 1990. Four hundred ninty-six had nonregurgitant trileaflet aortic valves before LVMM. In 19 (4%) of these patients, aortic regurgitation developed after LVMM. Age of the 19 patients ranged from 10 to 58 years (mean age, 35 +/- 3 years [+/- standard error of the mean]). Seven were male and 12, female. Five patients underwent LVMM followed immediately by aortic valve replacement or valvuloplasty. Aortic regurgitation developed in 14 patients at a later date. The average New York Heart Association functionals class improved from 3.2 +/- 0.1 to 1.3 +/- 0.1 (p < 0.05, Student's t test) after operation. The average peak systolic left ventricular outflow tract gradient at rest and with provocation decreased from 65 +/- 8 to 14 +/- 5 mm Hg (p < 0.05) and 108 +/- 9 to 45 +/- 7 mm Hg (p < 0.05), respectively, 6 to 8 months after operation. Aortic regurgitation occurred in 7 of the 14 patients at 6 months or less after operation, and 3 required operative repair. In the other 7 patients, aortic regurgitation developed 3 years or more after LVMM, and 3 of them also required operative repair. All 12 patients in whom aortic regurgitation developed at operation or within 6 months postoperatively had either a very small aortic annulus (less-than-or-equal-to 21 mm, 5 patients), a low mitral-septal contact lesion (greater-than-or-equal-to 35 mm below the aortic annulus, 3 patients), or both (4 patients). None of the patients in whom aortic regurgitation occurred 3 years or more postoperatively had an aortic annulus of 21 mm or less, and only 1 had a low mitral-septal contact point. A small aortic annulus or a low mitral-septal contact lesion greatly increased the difficulty of the operation and resulted in increased retraction of the aortic valve and annulus (with increased possibility of damage to the valve) to gain exposure to the interventricular septum. We recommend in patients with a very small aortic annulus, a low mitral-septal contact lesion, or both, that caution be exercised when operating through the aortic valve and that the valve be routinely evaluated postoperatively. If LVMM cannot be performed easily in these patients, consideration should be given to using another means of access to the interventricular septum or performing mitral valve replacement. C1 NHLBI,BETHESDA,MD 20892. NR 9 TC 9 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD APR PY 1991 VL 51 IS 4 BP 585 EP 592 PG 8 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA FF788 UT WOS:A1991FF78800012 PM 2012417 ER PT J AU WILLIAMS, DE SWANGO, LJ WILT, GR WORLEY, SD AF WILLIAMS, DE SWANGO, LJ WILT, GR WORLEY, SD TI EFFECT OF ORGANIC N-HALAMINES ON SELECTED MEMBRANE FUNCTIONS IN INTACT STAPHYLOCOCCUS-AUREUS CELLS SO APPLIED AND ENVIRONMENTAL MICROBIOLOGY LA English DT Article ID FREE CHLORINE; INACTIVATION; ACID; DISINFECTION; CHLORAMINE; BACTERIA; WATER AB Two N-halamine compounds, 3-chloro-4,4-dimethyl-2-oxazolidinone and 1,3-dichloro-4,4,5,5-tetramethyl-2-imidazolidinone, were compared with free chlorine as to their effects on selected membrane functions of intact Staphylococcus aureus cells. Free chlorine was found to cause a loss of permeability control, as measured by the efflux of potassium from the cells and a dramatic increase in hydrogen ion permeability, and to affect cell respiration in a nonreversible fashion, as measured by oxygen uptake. The two N-halamines were found to have very little effect on permeability to either potassium or hydrogen ions but were both found to dramatically inhibit respiration in a reversible manner. It is proposed that the first step in the disinfection process by these N-halamines is an inhibition of respiratory enzymes that, if not reversed, ultimately leads to a loss of cell viability. C1 NIEHS,MD D2-03,POB 12233,RES TRIANGLE PK,NC 27709. AUBURN UNIV,COLL SCI & MATH,DEPT CHEM,AUBURN,AL 36849. AUBURN UNIV,COLL VET MED,DEPT PATHOBIOL,AUBURN,AL 36849. RI Williams, David/B-3222-2012 OI Williams, David/0000-0003-4123-5626 NR 27 TC 9 Z9 10 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0099-2240 J9 APPL ENVIRON MICROB JI Appl. Environ. Microbiol. PD APR PY 1991 VL 57 IS 4 BP 1121 EP 1127 PG 7 WC Biotechnology & Applied Microbiology; Microbiology SC Biotechnology & Applied Microbiology; Microbiology GA FF039 UT WOS:A1991FF03900037 PM 2059036 ER PT J AU DUNNY, GM LEE, LN LEBLANC, DJ AF DUNNY, GM LEE, LN LEBLANC, DJ TI IMPROVED ELECTROPORATION AND CLONING VECTOR SYSTEM FOR GRAM-POSITIVE BACTERIA SO APPLIED AND ENVIRONMENTAL MICROBIOLOGY LA English DT Article ID STREPTOCOCCUS-SANGUIS CHALLIS; GENETIC-TRANSFORMATION; PLASMID DNA; RESISTANCE DETERMINANTS; LACTIC STREPTOCOCCI; SHUTTLE VECTOR; RAPID METHOD; FAECALIS; LACTOCOCCUS; MOLECULES AB A protocol for transformation of intact Enterococcus faecalis cells by electroporation was developed through a systematic examination of the effects of changes in various parameters, including (i) growth conditions; (ii) composition of the electroporation solution; (iii) electroporation conditions, such as field strength and resistance; (iv) size, concentration, and purity of DNA used for transformation; and (v) conditions used to select for transformants. Key features of this protocol include the use of exponential-phase cells grown in inhibitory concentration of glycine and the use of an acidic sucrose electroporation solution. Frequencies of > 2 x 10(5) transformants per mu-g of plasmid DNA were obtained for E. faecalis cells, whereas various strains of streptococci and Bacillus anthracis were transformed at frequencies of 10(3) to 10(4) transformants per mu-g of plasmid DNA with the same protocol. A novel Escherichia coli-Streptococcus and Enterococcus shuttle cloning vector, pDL276, was constructed for use in conjunction with the electroporation system. This vector features a multiple cloning site region flanked by E. coli transcription termination sequences, a relatively small size (< 7 kb), and a kanamycin resistance determinant expressed in both gram-positive and gram-negative hosts. Various enterococcal and streptococcal DNA sequences were cloned in E. coli (including sequences that could not be cloned on other vectors) and were returned to the original host by electroporation. The vector and electroporation system was also used to clone directly into E. faecalis. C1 CORNELL UNIV,NEW YORK STATE COLL VET MED,DEPT MICROBIOL,ITHACA,NY 14853. NIAID,MOLEC MICROBIOL LAB,FREDERICK,MD 21701. FU NIAID NIH HHS [AI19310]; NIDCR NIH HHS [DE08915] NR 41 TC 209 Z9 211 U1 0 U2 11 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0099-2240 J9 APPL ENVIRON MICROB JI Appl. Environ. Microbiol. PD APR PY 1991 VL 57 IS 4 BP 1194 EP 1201 PG 8 WC Biotechnology & Applied Microbiology; Microbiology SC Biotechnology & Applied Microbiology; Microbiology GA FF039 UT WOS:A1991FF03900049 PM 1905518 ER PT J AU HAMEL, E LIN, CM KENNEY, S SKEHAN, P AF HAMEL, E LIN, CM KENNEY, S SKEHAN, P TI HIGHLY VARIABLE EFFECTS OF BERYLLIUM AND BERYLLIUM FLUORIDE ON TUBULIN POLYMERIZATION UNDER DIFFERENT REACTION CONDITIONS - COMPARISON OF ASSEMBLY REACTIONS DEPENDENT ON MICROTUBULE-ASSOCIATED PROTEINS, GLYCEROL, DIMETHYL-SULFOXIDE, AND GLUTAMATE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID DARK-FIELD MICROSCOPY; DYNAMIC INSTABILITY; NUCLEOTIDE INTERACTIONS; DIVALENT-CATIONS; GAMMA-PHOSPHATE; GTP HYDROLYSIS; BRAIN TUBULIN; ALUMINUM ION; LIVING CELLS; ZINC C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,PROGRAM DEV RES GRP,BETHESDA,MD 20892. RP HAMEL, E (reprint author), NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,BLDG 37,ROOM 5C25,BETHESDA,MD 20892, USA. NR 39 TC 6 Z9 6 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR PY 1991 VL 286 IS 1 BP 57 EP 69 DI 10.1016/0003-9861(91)90008-7 PG 13 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FA648 UT WOS:A1991FA64800008 PM 1680309 ER PT J AU MORALES, TI AF MORALES, TI TI TRANSFORMING GROWTH FACTOR-BETA-1 STIMULATES SYNTHESIS OF PROTEOGLYCAN AGGREGATES IN CALF ARTICULAR-CARTILAGE ORGAN-CULTURES SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID DERMATAN SULFATE PROTEOGLYCANS; HYALURONIC-ACID; KERATAN SULFATE; BOVINE; BIOSYNTHESIS; METABOLISM RP MORALES, TI (reprint author), NIDR,BONE RES BRANCH,BETHESDA,MD 20892, USA. NR 22 TC 102 Z9 103 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR PY 1991 VL 286 IS 1 BP 99 EP 106 DI 10.1016/0003-9861(91)90013-9 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FA648 UT WOS:A1991FA64800013 PM 1910291 ER PT J AU BLACK, CDV SAMUNI, A COOK, JA KRISHNA, CM KAUFMAN, DC MALECH, HL RUSSO, A AF BLACK, CDV SAMUNI, A COOK, JA KRISHNA, CM KAUFMAN, DC MALECH, HL RUSSO, A TI KINETICS OF SUPEROXIDE PRODUCTION BY STIMULATED NEUTROPHILS SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID SPIN-RESONANCE SPECTROSCOPY; RESPIRATORY BURST; CHEMI-LUMINESCENCE; POLYMORPHONUCLEAR LEUKOCYTES; HYDROGEN-PEROXIDE; MYELOPEROXIDASE; HYDROXYL; OXIDASE; ADDUCTS; OXYGEN C1 NCI,DIV CENT RES,CLIN ONCOL BRANCH,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BACTERIAL DIS SECT,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,SCH MED,IL-91010 JERUSALEM,ISRAEL. RP BLACK, CDV (reprint author), NCI,DIV CENT RES,RADIAT ONCOL BRANCH,BLDG 10,ROOM B3-B69,BETHESDA,MD 20892, USA. NR 39 TC 20 Z9 20 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR PY 1991 VL 286 IS 1 BP 126 EP 131 DI 10.1016/0003-9861(91)90017-D PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FA648 UT WOS:A1991FA64800017 PM 1654777 ER PT J AU KALYANARAMAN, B MOREHOUSE, KM MASON, RP AF KALYANARAMAN, B MOREHOUSE, KM MASON, RP TI AN ELECTRON-PARAMAGNETIC RESONANCE STUDY OF THE INTERACTIONS BETWEEN THE ADRIAMYCIN SEMIQUINONE, HYDROGEN-PEROXIDE, IRON-CHELATORS, AND RADICAL SCAVENGERS SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID DISTINGUISH OH. PRODUCTION; DRIVEN FENTON REACTIONS; HABER-WEISS REACTION; ANTI-TUMOR AGENTS; LIPID-PEROXIDATION; SPIN RESONANCE; STIMULATED SUPEROXIDE; HYDROXYL RADICALS; 4 ASSAYS; ANTHRACYCLINE C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. RP KALYANARAMAN, B (reprint author), MED COLL WISCONSIN,DEPT RADIOL,BIOPHYS SECT,8701 WATERTOWN PLANK RD,MILWAUKEE,WI 53226, USA. FU NCRR NIH HHS [RR-01008]; NIGMS NIH HHS [GM-29035] NR 46 TC 52 Z9 52 U1 1 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR PY 1991 VL 286 IS 1 BP 164 EP 170 DI 10.1016/0003-9861(91)90023-C PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FA648 UT WOS:A1991FA64800023 PM 1654778 ER PT J AU GREENHOUSE, JB STANGL, D KUPFER, DJ PRIEN, RF AF GREENHOUSE, JB STANGL, D KUPFER, DJ PRIEN, RF TI METHODOLOGIC ISSUES IN MAINTENANCE THERAPY CLINICAL-TRIALS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID ILLNESS AB In the early 1980s, the National Institute of Mental Health supported a multicenter, randomized, controlled, clinical trial on unipolar and bipolar disorder to evaluate the comparative efficacies of lithium carbonate, imipramine hydrochloride, a lithium-imipramine combination, and placebo in preventing the recurrence of affective disorders. The objective of this report is to present a reanalysis of the relative efficacies of these treatments in patients with unipolar disorder to focus attention on general issues related to the design and conduct of maintenance therapy trials. We show that the earlier conclusions of that study that imipramine and the combination therapy are more effective than lithium and placebo in preventing the recurrence of depression in unipolar patients can be accounted for by alternative explanations that are a consequence of the design of the study. Our findings have important implications for the design, conduct, and interpretation of results of maintenance therapy clinical trials in general. C1 UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA 15213. NIMH,DIV CLIN RES,ROCKVILLE,MD 20857. RP GREENHOUSE, JB (reprint author), CARNEGIE MELLON UNIV,DEPT STAT,PITTSBURGH,PA 15213, USA. FU NIMH NIH HHS [MH30915, MH15758] NR 19 TC 76 Z9 76 U1 1 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD APR PY 1991 VL 48 IS 4 BP 313 EP 318 PG 6 WC Psychiatry SC Psychiatry GA FE951 UT WOS:A1991FE95100003 PM 1901203 ER PT J AU BENKELFAT, C MURPHY, DL HILL, JL GEORGE, DT NUTT, D LINNOILA, M AF BENKELFAT, C MURPHY, DL HILL, JL GEORGE, DT NUTT, D LINNOILA, M TI ETHANOLLIKE PROPERTIES OF THE SEROTONERGIC PARTIAL AGONIST META-CHLOROPHENYLPIPERAZINE IN CHRONIC-ALCOHOLIC PATIENTS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Letter C1 NIAAA,CTR CLIN,CLIN SCI LAB,10-3D41,BETHESDA,MD 20892. RP BENKELFAT, C (reprint author), NIMH,CTR CLIN,CLIN SCI LAB,10-3D41,BETHESDA,MD 20892, USA. NR 7 TC 73 Z9 73 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD APR PY 1991 VL 48 IS 4 BP 383 EP 383 PG 1 WC Psychiatry SC Psychiatry GA FE951 UT WOS:A1991FE95100016 PM 2009039 ER PT J AU SCHUCKER, B WITTES, JT SANTANELLO, NC WEBER, SJ MCGOLDRICK, D DONATO, K LEVY, A RIFKIND, BM AF SCHUCKER, B WITTES, JT SANTANELLO, NC WEBER, SJ MCGOLDRICK, D DONATO, K LEVY, A RIFKIND, BM TI CHANGE IN CHOLESTEROL AWARENESS AND ACTION - RESULTS FROM NATIONAL PHYSICIAN AND PUBLIC SURVEYS SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID HEART-DISEASE; EDUCATION-PROGRAM; PERSPECTIVE; HYPERCHOLESTEROLEMIA AB The National Heart, Lung, and Blood Institute, Bethesda, Md, sponsored national telephone surveys of practicing physicians and the adult public in 1983, 1986, and 1990 to assess attitudes and practices regarding high serum cholesterol levels. Each time, approximately 1600 physicians and 4000 adults were interviewed. Trends show continuing change in medical practice and public health behavior relating to serum cholesterol. In 1990, physicians reported treating serum cholesterol at considerably lower levels than in 1986 and 1983. The median range of serum cholesterol at which diet therapy was initiated was 5.17 to 5.66 mmol/L(200 to 219 mg/dL) in 1990, down from 6.21 to 6.70 mmol/L (240 to 259 mg/dL) in 1986 and 6.72 to 7.21 mmol/L (260 to 279 mg/dL) in 1983. The median ranges for initiating drug therapy were 6.21 to 6.70 mmol/L (240 to 259 mg/dL) in 1990, 7.76 to 8.25 mmol/L (300 to 319 mg/dL) in 1986, and 8.79 to 9.28 mmol/L(340 to 359 mg/dL) in 1983. The number of adults who reported having had their cholesterol level checked rose from 35% to 46% to 65% in 1983, 1986, and 1990, respectively. Between 1983 and 1990, the number of adults reporting a physician diagnosis of high serum cholesterol increased from 7% to 16%; the number reporting a prescribed cholesterol-lowering diet increased from 3% to 9%. Reports of self-initiated diet efforts reached a high of 19% in 1986 and decreased to 15% in 1990. Two percent of adults reported drug prescriptions in 1990 compared with 1% in earlier years. In 1990, over 90% of physicians reported awareness and use of the recommendations from the Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, and the public reported marked increases in awareness of dietary methods to lower serum cholesterol. These changes suggest educational gains; the data also suggest areas for continued cholesterol educational initiatives. C1 NHLBI,PREVENT & DEMONSTRAT RES BRANCH,BETHESDA,MD 20892. NEW ENGLAND RES INST INC,WASHINGTON,DC. US FDA,CTR FOOD SAFETY & APPL NUTR,DIV CONSUMER STUDIES,WASHINGTON,DC 20204. NHLBI,HLTH EDUC BRANCH,BETHESDA,MD 20892. MARKET FACTS INC,WASHINGTON,DC. RP SCHUCKER, B (reprint author), NHLBI,LIPID METAB ATHEROGENESIS BRANCH,ROOM 401,FED BLDG,BETHESDA,MD 20892, USA. NR 27 TC 118 Z9 118 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD APR PY 1991 VL 151 IS 4 BP 666 EP 673 DI 10.1001/archinte.151.4.666 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FF779 UT WOS:A1991FF77900006 PM 2012446 ER PT J AU WALSH, TJ RUBIN, M HATHORN, J GRESS, J THALER, M SKELTON, J MCKNIGHT, J BROWNE, M MARSHALL, D COTTON, D HIEMENZ, J LONGO, D WESLEY, R PIZZO, PA AF WALSH, TJ RUBIN, M HATHORN, J GRESS, J THALER, M SKELTON, J MCKNIGHT, J BROWNE, M MARSHALL, D COTTON, D HIEMENZ, J LONGO, D WESLEY, R PIZZO, PA TI AMPHOTERICIN-B VS HIGH-DOSE KETOCONAZOLE FOR EMPIRICAL ANTIFUNGAL THERAPY AMONG FEBRILE, GRANULOCYTOPENIC CANCER-PATIENTS - A PROSPECTIVE, RANDOMIZED STUDY SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID FUNGAL-INFECTIONS; ACUTE-LEUKEMIA; INVASIVE ASPERGILLOSIS; IMMUNOCOMPROMISED PATIENTS; NEUTROPENIC PATIENTS; PROPHYLAXIS; PREVENTION; NYSTATIN; TRIAL; COMBINATION AB We compared high-dose ketoconazole (800 mg/kg per day, orally) with amphotericin B (0.5 mg/kg per day, intravenously) for empirical antifungal therapy in a prospective, randomized study of persistenly or recurrently febrile granulocytopenic cancer patients. Among 97 patients eligible for empirical antifungal therapy, 20 (21%) of these patients were ineligible for randomization to ketoconazole treatment because of their inability to tolerate oral medications. Among 72 patients eligible for randomization, 64 were assessable (32 in each arm of the study). Five of six patients with proved fungal infections who were randomized to receive ketoconazole treatment required crossover to amphotericin B treatment because of progressive infection. The conditions of three of these five patients improved after receiving amphotericin B. The frequency of transaminase elevation was higher in those receiving ketoconazole, while the frequency of azotemia was higher in those receiving amphotericin B. Bioavailability of ketoconazole was unpredictable. Amphotericin B remains the drug of choice for empirical antifungal therapy in granulocytopenic patients; whereas, lack of a parenteral formulation, ineffectiveness against proved mycoses, and unreliable bioavailability preclude high-dose ketoconazole from being an appropriate compound for this purpose. C1 NCI,MED BRANCH,BETHESDA,MD 20892. NCI,CLIN ONCOL PROGRAM,INFECT DIS SECT,BETHESDA,MD 20892. RP WALSH, TJ (reprint author), NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA. NR 36 TC 41 Z9 41 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD APR PY 1991 VL 151 IS 4 BP 765 EP 770 DI 10.1001/archinte.151.4.765 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA FF779 UT WOS:A1991FF77900023 PM 2012462 ER PT J AU TAUBENBERGER, JK COLE, DE RAFFELD, M POPLACK, DG JAFFE, ES MEDEIROS, LJ AF TAUBENBERGER, JK COLE, DE RAFFELD, M POPLACK, DG JAFFE, ES MEDEIROS, LJ TI IMMUNOPHENOTYPIC ANALYSIS OF ACUTE LYMPHOBLASTIC-LEUKEMIA USING ROUTINELY PROCESSED BONE-MARROW SPECIMENS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID PARAFFIN-EMBEDDED TISSUE; NON-HODGKINS LYMPHOMA; B-CELL LYMPHOMAS; MONOCLONAL-ANTIBODIES; T-CELL; LYMPHOCYTES-T; SECTIONS; DIAGNOSIS; ANTIGEN; IMMUNOGLOBULIN AB Monoclonal antibodies have been recently developed that react with antigens expressed on T and B lymphocytes in routinely processed, paraffin-embedded lymphoid tissues. In this study, we assessed bone marrow clot and/or core biopsy sections of 19 cases of acute lymphoblastic leukemia (ALL) using routinely decalcified, B5- or formalin-fixed, paraffin-embedded sections and a panel of monoclonal antibodies, including LN1, LN2, L26, Leu-22, UCHL-1, and LCA. Each case had been previously phenotyped using freshly obtained aspirate material and a standard immunophenotypic protocol. Our results demonstrate the utility of the LN2 antibody in differentiating between precursor B-cell (pre-B) and precursor T-cell ALL. The LN2 antibody stained 11 of 12 cases of pre-B ALL and did not react with any of the seven T-cell ALLs. The other antibodies tested were less helpful. The Leu-22 antibody stained both pre-B and T-cell ALLs, while the results with UCHL-1 revealed peculiar nuclear staining of pre-B and T-cell ALLs; this we attributed to processing artifact. The L26 antibody reacted with only one case of pre-B ALL (also CD20 antigen positive), while the LN1 antibody did not react with any pre-B ALLs. Neither L26 nor LN1 stained any cases of T-cell ALL. The LCA antibody stained in only four (21%) of 19 cases, two pre-B and two T-cell ALLs. The results also suggest that this panel of antibodies may be useful in differentiating ALL from mature B-cell and T-cell lymphomas involving the bone marrow. C1 NCI,DIV CANC TREATMENT,PEDIAT BRANCH,BETHESDA,MD 20892. RP TAUBENBERGER, JK (reprint author), NCI,DIV CANC BIOL DIAG,PATHOL LAB,BLDG 10,ROOM 2N 212,BETHESDA,MD 20892, USA. NR 29 TC 15 Z9 15 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD APR PY 1991 VL 115 IS 4 BP 338 EP 342 PG 5 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA FF037 UT WOS:A1991FF03700005 PM 2012494 ER PT J AU JENSEN, JC PASS, HI SINDELAR, WF NORTON, JA AF JENSEN, JC PASS, HI SINDELAR, WF NORTON, JA TI RECURRENT OR METASTATIC DISEASE IN SELECT PATIENTS WITH ADRENOCORTICAL CARCINOMA - AGGRESSIVE RESECTION VS CHEMOTHERAPY SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 43RD ANNUAL CANCER SYMP OF THE SOC OF SURGICAL ONCOLOGY CY MAY 29, 1990 CL WASHINGTON, DC SP SOC SURG ONCOL ID ADRENAL-CORTICAL CARCINOMA; PULMONARY METASTASES; SURGICAL-MANAGEMENT AB In a retrospective, nonrandomized comparison of patients with first recurrence of adrenocortical cancer, 18 patients were treated with chemotherapy (primarily mitotane) and 15 patients were treated with surgical resection plus similar chemotherapy. Surgical resection of recurrent adrenocortical cancer was often extensive, with morbidity in 20% of patients and no mortality. Mitotane therapy was ineffective at controlling tumor growth. Median survival from the time of diagnosis for all patients was only 23 months and no patient was cured. Disease-free interval greater than 12 months was associated with prolonged survival, but it only occurred in six patients (18%), with a similar frequency in both treatment groups. Surgical resection of recurrent disease was associated with prolonged survival from the time of first recurrence. The potential benefit of this resection was evident in the 5 patients (33%) who were able to live greater than 5 years from the time of first recurrence with improvement in symptoms and signs of hypercortisolism. Although no patient with recurrent adrenal cancer could be cured, resection of recurrent disease was associated with a slight prolongation of survival and good palliation of Cushing's syndrome. C1 NCI,SURG BRANCH,SURG METAB SECT,BLDG 10,ROOM 2B07,BETHESDA,MD 20892. NCI,THORAC ONCOL SECT,BETHESDA,MD 20892. NR 27 TC 56 Z9 56 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD APR PY 1991 VL 126 IS 4 BP 457 EP 461 PG 5 WC Surgery SC Surgery GA FE876 UT WOS:A1991FE87600010 PM 1706914 ER PT J AU WINSLOW, JT INSEL, TR AF WINSLOW, JT INSEL, TR TI ENDOGENOUS OPIOIDS - DO THEY MODULATE THE RAT PUPS RESPONSE TO SOCIAL-ISOLATION SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID SEPARATION DISTRESS; BENZODIAZEPINE RECEPTOR; POSTNATAL-DEVELOPMENT; BETA-FUNALTREXAMINE; ISOLATION CALLS; OPIATE; MEDIATION; STRESS; BRAIN; ANALGESIA AB Previous studies with several different species have suggested that opioids and their receptors are involved in the mediation of the infant's vocal response to social isolation. In the case of the rat pup, 2 models have been hypothesized to relate opioids and the ultrasonic call emitted during social isolation. One model views the comforting effects of social contact as opioid mediated and the apparent distress of social isolation as analogous to opiate withdrawal. The 2nd model considers social separation as a stressor that recruits endogenous opioids. This article describes 3 experiments that tested both of these models in 7-10-day-old rat pups. In Experiment 1, morphine (0.04-0.40 mg/kg) decreased the rate of isolation calls in a dose-dependent, naloxone-reversible fashion. However, the decrease in calling rate was observed only at doses that decreased locomotor activity. Administration of the reversible opiate antagonist naloxone (0.05-5.0 mg/kg) did not alter the rate of calls during either 2- or 6-min isolation tests at either 24 or 32-degrees-C. In Experiment 2, the irreversible mu opioid receptor antagonist beta-funaltrexamine (beta-FNA) was administered into the lateral ventricle of 6-day-old pups. Again, no change in the rate of isolation calls was found, although sensitivity to morphine was markedly decreased, and mu (but not delta or kappa) receptors were decreased in selected brain regions by about 40%. In Experiment 3, in vivo receptor binding was used to directly investigate the availability of mu opioid receptors during social contact and social isolation. Pups injected with H-1-diprenorphine showed relatively high levels of specific in vivo binding that followed the regional pattern of in vitro binding, but no effects of social isolation were apparent in the 5 brain regions assayed. Taken together, the consistent negative results with opiate receptor antagonists, as well as the inability to detect an alteration of in vivo binding, suggest that the mu opioid receptor is not an essential part of the rat pup's vocal response to social separation. C1 NIMH,NATL INST HLTH ANIM CTR,POB 289,POOLESVILLE,MD 20837. NR 38 TC 64 Z9 64 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7044 J9 BEHAV NEUROSCI JI Behav. Neurosci. PD APR PY 1991 VL 105 IS 2 BP 253 EP 263 DI 10.1037/0735-7044.105.2.253 PG 11 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA FD819 UT WOS:A1991FD81900005 PM 1645977 ER PT J AU GRANT, KA KNISELY, JS TABAKOFF, B BARRETT, JE BALSTER, RL AF GRANT, KA KNISELY, JS TABAKOFF, B BARRETT, JE BALSTER, RL TI ETHANOL-LIKE DISCRIMINATIVE STIMULUS EFFECTS OF NONCOMPETITIVE N-METHYL-D-ASPARTATE ANTAGONISTS SO BEHAVIOURAL PHARMACOLOGY LA English DT Article DE ETHANOL; ALCOHOL; MK-801; PHENCYCLIDINE; KETAMINE; DRUG DISCRIMINATION; MICE; PIGEONS ID PHENCYCLIDINE-LIKE DRUGS; CENTRAL NERVOUS-SYSTEM; RHESUS-MONKEYS; PHYSICAL-DEPENDENCE; RATS; RECEPTORS; MICE; KETAMINE; PIGEONS; MK-801 AB The discriminative stimulus effects of noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists were investigated in animals trained to discriminate 1.5 g/kg (pigeons) or 1.25 g/kg (mice) ethanol from vehicle. Key-pecking of pigeons and lever responding of mice were maintained under fixed ratio schedules of mixed grain or milk reinforcement, respectively. Phencyclidine (PCP) and ketamine dosedependently substituted for the ethanol stimulus in both species, with PCP being about 10-fold more potent than ketamine. In pigeons, PCP and ketamine fully substituted for ethanol at doses that did not significantly alter rates of responding; with mice, complete substitution was accompanied by response rate-decreasing effects. In pigeons, the highly selective NMDA receptor/ionophore antagonist MK-801 also substituted for ethanol at a dose that was accompanied by reduced response rates. Compounds that did not substitute for the ethanol stimulus were cocaine (both species), the 5-HT1B receptor agonist TFMPP (pigeon), the H-1 receptor antagonist hydroxyzine (mice), and the anticonconvulsants phenytoin and ethosuximide (mice). The present data show that PCP-like drugs that are antagonists of NMDA receptor-mediated neurotransmission share common discriminative stimulus effects with ethanol. C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PHARMACOL & TOXICOL,RICHMOND,VA 23298. UNIFORMED SERV UNIV HLTH SCI,DEPT PSYCHIAT,BETHESDA,MD 20814. RP GRANT, KA (reprint author), NIAAA,SPECIAL PROJECTS UNIT,12501 WASHINGTON AVE,ROCKVILLE,MD 20852, USA. NR 41 TC 105 Z9 106 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8810 J9 BEHAV PHARMACOL JI Behav. Pharmacol. PD APR PY 1991 VL 2 IS 2 BP 87 EP 95 PG 9 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA FU758 UT WOS:A1991FU75800002 ER PT J AU SANNERUD, CA ATOR, NA GRIFFITHS, RR AF SANNERUD, CA ATOR, NA GRIFFITHS, RR TI METHOCARBAMOL - EVALUATION OF REINFORCING AND DISCRIMINATIVE STIMULUS EFFECTS SO BEHAVIOURAL PHARMACOLOGY LA English DT Article DE METHOCARBAMOL; DRUG SELF-ADMINISTRATION; SEDATIVES; DRUG DISCRIMINATION; BABOON; RAT ID SELF-INJECTION; TRAINING CONDITIONS; BABOONS; RATS; DIAZEPAM; BENZODIAZEPINES; LORAZEPAM AB The behavioral effects of methocarbamol, a centrally acting muscle relaxant, were assessed using self-injection procedures in baboons and drug discrimination procedures in baboons and rats. The ability of methocarbamol to maintain self-injection was examined using a drug substitution procedure. Responding was maintained initially by cocaine delivery (0.32 mg/kg/injection, i.v.). Each drug injection was followed by a 3-h timeout allowing a maximum of eight injections per day. Methocarbamol doses or vehicle were substituted for cocaine for a period of 15 or more days each, with re-establishment of responding under cocaine after each substitution. Evaluation of a wide range of methocarbamol doses (1.0-32 mg/kg/injection) showed that this compound maintained rates of self-injection at vehicle control levels, which were below those maintained by cocaine. The discriminative stimulus effects of methocarbamol were studied in baboons trained to discriminate either lorazepam (1.8 mg/kg, p.o.) or pentobarbital (10.0 mg/kg, p.o.) from the no-drug condition and in rats trained to discriminate lorazepam (1.0 mg/kg, i.p.), diazepam (1.0 mg/kg, i.p.), or pentobarbital (10.0 mg/kg, i.p.) from the no-drug condition using a two-lever, food-maintained drug discrimination procedure. Evaluation of a range of doses in baboons (10-180 mg/kg, p.o.) and rats (32-180 mg/kg, i.p.) showed that methocarbamol did not occasion drug-lever responding at any dose. Methocarbamol did not produce changes in response rates in baboons, but higher doses severely suppressed response rates in rats. The present experiments show that the behavioral profile of methocarbamol is clearly distinguishable from that of barbiturates and benzodiazepines. Taken together with analogous studies with other sedative-anxiolytic drugs, these results suggest that methocarbamol has a relatively low likelihood of abuse. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. NIDA,ADDICT RES CTR,BALTIMORE,MD. NR 28 TC 9 Z9 9 U1 1 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8810 J9 BEHAV PHARMACOL JI Behav. Pharmacol. PD APR PY 1991 VL 2 IS 2 BP 143 EP 150 PG 8 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA FU758 UT WOS:A1991FU75800008 ER PT J AU RHEE, SG KIM, H SUH, PG CHOI, WC AF RHEE, SG KIM, H SUH, PG CHOI, WC TI MULTIPLE FORMS OF PHOSPHOINOSITIDE-SPECIFIC PHOSPHOLIPASE-C AND DIFFERENT MODES OF ACTIVATION SO BIOCHEMICAL SOCIETY TRANSACTIONS LA English DT Article; Proceedings Paper CT 637TH MEETING OF THE BIOCHEMICAL SOC CY DEC 18-20, 1990 CL UNIV BIRMINGHAM, BIRMINGHAM, ENGLAND SP BIOCHEM SOC HO UNIV BIRMINGHAM ID GROWTH-FACTOR; TYROSINE PHOSPHORYLATION; PROTEIN-KINASE; BOVINE BRAIN; RECEPTOR; SEQUENCE; GAMMA; ISOZYMES; SRC RP RHEE, SG (reprint author), NHLBI,BIOCHEM LAB,BETHESDA,MD 20892, USA. RI Suh, Pann-Ghill/F-3610-2010 NR 24 TC 91 Z9 91 U1 0 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0300-5127 J9 BIOCHEM SOC T JI Biochem. Soc. Trans. PD APR PY 1991 VL 19 IS 2 BP 337 EP 341 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FQ821 UT WOS:A1991FQ82100023 PM 1653736 ER PT J AU HECKER, G LEWIS, DL RAUSCH, DM JELSEMA, CL AF HECKER, G LEWIS, DL RAUSCH, DM JELSEMA, CL TI NERVE-GROWTH-FACTOR-TREATED AND V-SRC-EXPRESSING PC-12 CELLS - A MODEL FOR NEURONAL DIFFERENTIATION SO BIOCHEMICAL SOCIETY TRANSACTIONS LA English DT Article; Proceedings Paper CT 637TH MEETING OF THE BIOCHEMICAL SOC CY DEC 18-20, 1990 CL UNIV BIRMINGHAM, BIRMINGHAM, ENGLAND SP BIOCHEM SOC HO UNIV BIRMINGHAM C1 NIMH,BETHESDA,MD 20892. MED COLL AUGUSTA,AUGUSTA,GA 30912. RP HECKER, G (reprint author), BAYER AG,RES CTR,W-5600 WUPPERTAL 1,GERMANY. NR 5 TC 7 Z9 7 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0300-5127 J9 BIOCHEM SOC T JI Biochem. Soc. Trans. PD APR PY 1991 VL 19 IS 2 BP 385 EP 386 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FQ821 UT WOS:A1991FQ82100032 PM 1889619 ER PT J AU HUANG, LQ EITZER, B MOORE, C MCGOWN, S TOMER, KB AF HUANG, LQ EITZER, B MOORE, C MCGOWN, S TOMER, KB TI THE APPLICATION OF HYBRID MASS-SPECTROMETRY MASS-SPECTROMETRY AND HIGH-RESOLUTION MASS-SPECTROMETRY TO THE ANALYSIS OF FISH SAMPLES FOR POLYCHLORINATED DIBENZO-PARA-DIOXINS AND DIBENZOFURANS SO BIOLOGICAL MASS SPECTROMETRY LA English DT Article ID GAS-CHROMATOGRAPHY; MS-MS; GC-MS; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN; ISOMERS AB A hybrid mass spectrometer operated in low-resolution selected decomposition monitoring (SDM) mode was used for the analysis of whole fish samples for the 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs). These fish samples were previously analyzed for PCDD/Fs using a high-resolution mass spectrometer following EPA protocols. The hybrid tandem mass spectrometric method using loss of COCl gave similar quantification results to those obtained by high-resolution mass spectrometry and eliminated the interferences attributed to polychlorinated biphenyls that were encountered in the high-resolution mass spectrometric analysis. Comparison of the two methods shows that the high-resolution mass spectrometric method surpasses the tandem mass spectrometric method in other analytical figures of merit, such as detection limit, linearity and reproducibility. C1 KRATOS ANALYT INC,RAMSEY,NJ 07446. NIEHS,RES TRIANGLE PK,NC 27709. RP HUANG, LQ (reprint author), CONNECTICUT AGR EXPT STN,BOX 1106,NEW HAVEN,CT 06504, USA. RI Tomer, Kenneth/E-8018-2013 NR 30 TC 15 Z9 15 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 1052-9306 J9 BIOL MASS SPECTROM JI Biol. Mass Spectrom. PD APR PY 1991 VL 20 IS 4 BP 161 EP 168 DI 10.1002/bms.1200200402 PG 8 WC Biophysics; Spectroscopy SC Biophysics; Spectroscopy GA FH508 UT WOS:A1991FH50800001 PM 2054390 ER PT J AU JASKIW, GE WEINBERGER, DR CRAWLEY, JN AF JASKIW, GE WEINBERGER, DR CRAWLEY, JN TI MICROINJECTION OF APOMORPHINE INTO THE PREFRONTAL CORTEX OF THE RAT REDUCES DOPAMINE METABOLITE CONCENTRATIONS IN MICRODIALYSATE FROM THE CAUDATE-NUCLEUS SO BIOLOGICAL PSYCHIATRY LA English DT Note ID FRONTAL-CORTEX; PROJECTIONS; ACCUMBENS; INVIVO C1 ST ELIZABETH HOSP,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,WAW BLDG,RM 500,WASHINGTON,DC 20032. NIMH,CLIN NEUROSCI BRANCH,WASHINGTON,DC 20032. NR 14 TC 50 Z9 50 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1991 VL 29 IS 7 BP 703 EP 706 DI 10.1016/0006-3223(91)90144-B PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA FG848 UT WOS:A1991FG84800014 PM 1711381 ER PT J AU RAPAPORT, MH MCALLISTER, CG KIRCH, DG PICKAR, D AF RAPAPORT, MH MCALLISTER, CG KIRCH, DG PICKAR, D TI THE EFFECTS OF TYPICAL AND ATYPICAL NEUROLEPTICS ON MITOGEN-INDUCED LYMPHOCYTE-T RESPONSIVENESS SO BIOLOGICAL PSYCHIATRY LA English DT Note ID SCHIZOPHRENIC-PATIENTS C1 UNIV PITTSBURGH,DEPT PSYCHIAT,PITTSBURGH,PA 15260. UNIV PITTSBURGH,DEPT PATHOL,PITTSBURGH,PA 15260. NIMH,SCHIZOPHRENIA RES BRANCH,BETHESDA,MD 20892. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP RAPAPORT, MH (reprint author), UNIV CALIF SAN DIEGO,SCH MED,DEPT PSYCHIAT,LA JOLLA,CA 92093, USA. NR 10 TC 15 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1991 VL 29 IS 7 BP 715 EP 717 DI 10.1016/0006-3223(91)90147-E PG 3 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA FG848 UT WOS:A1991FG84800017 PM 1711382 ER PT J AU GERSHON, ES AF GERSHON, ES TI MARKER GENOTYPING ERRORS IN OLD DATA ON X-LINKAGE IN BIPOLAR ILLNESS SO BIOLOGICAL PSYCHIATRY LA English DT Editorial Material ID MANIC-DEPRESSIVE ILLNESS; CHROMOSOME MARKERS; AFFECTIVE-DISORDER; PEDIGREES; UNIPOLAR; PROBANDS; GENE AB Investigations of linkage markers of the X-chromosome colorblindness region in bipolar manic-depressive illness (BP) have yielded inconsistent results, with linkage accepted in some and rejected in other studies. Although genetic heterogeneity has been proposed as the reason for differences, other possibilities exist, including systematic procedural errors. Statistical evidence for linkage between the markers, Xg and colorblindness, is present in a series of papers on bipolar illness reported in 1972-1975. The linkage implied by this reanalysis is spurious, since the two markers are at opposite ends of the X chromosome. The presumptive reason for this spurious linkage is that it is a result of systematic genotyping errors. The support provided by these data to the X-linkage hypothesis in BP illness is thus diminished. That is, the linkage to illness may depend on systematic errors in marker genotyping. In general, the possible causes of inconsistency between linkage reports may be divided into statistical and systematic causes. Statistical causes would generally consist of chance differences in sampling, such as might occur under genetic heterogeneity. If this occurs, the reports rejecting linkage may be false negatives, or the reports detecting linkage may be false-positive results. Systematic causes of differences among reports could include systematic errors (or variations) in procedures, including ascertainment, diagnosis, genotyping, or analysis. Consistency of the marker map in a particular study with the known marker map is one test for systematic errors in genotyping. RP GERSHON, ES (reprint author), NIMH,CLIN NEUROGENET BRANCH,BLDG 10,ROOM 3N218,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 29 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1991 VL 29 IS 7 BP 721 EP 729 DI 10.1016/0006-3223(91)90149-G PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA FG848 UT WOS:A1991FG84800019 PM 1888383 ER PT J AU SAPERSTEIN, DA NICKERSON, JM AF SAPERSTEIN, DA NICKERSON, JM TI RESTRICTION-FRAGMENT-LENGTH-POLYMORPHISM ANALYSIS USING PCR COUPLED TO RESTRICTION DIGESTS SO BIOTECHNIQUES LA English DT Note ID SICKLE-CELL ANEMIA; ENZYMATIC AMPLIFICATION; DNA; SEQUENCES; MUTATIONS; DIAGNOSIS; IRBP C1 NEI,BLDG 6,ROOM 224,BETHESDA,MD 20892. FU NEI NIH HHS [F32 EY-06177] NR 15 TC 13 Z9 14 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD APR PY 1991 VL 10 IS 4 BP 488 EP 489 PG 2 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG600 UT WOS:A1991FG60000017 PM 1678268 ER PT J AU SHIRAMIZU, B BARRIGA, F NEEQUAYE, J JAFRI, A DALLAFAVERA, R NERI, A GUTTIEREZ, M LEVINE, P MAGRATH, I AF SHIRAMIZU, B BARRIGA, F NEEQUAYE, J JAFRI, A DALLAFAVERA, R NERI, A GUTTIEREZ, M LEVINE, P MAGRATH, I TI PATTERNS OF CHROMOSOMAL BREAKPOINT LOCATIONS IN BURKITTS-LYMPHOMA - RELEVANCE TO GEOGRAPHY AND EPSTEIN-BARR-VIRUS ASSOCIATION SO BLOOD LA English DT Article ID C-MYC-ONCOGENE; UNDIFFERENTIATED LYMPHOMAS; CELL-LINES; TRANSLOCATIONS; LOCUS; EXPRESSION; NEOPLASIA C1 NCI,CLIN ONCOL PROGRAM,PEDIAT BRANCH,BLDG 10 ROOM 13N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. OI neri, antonino/0000-0001-9047-5912 NR 20 TC 199 Z9 200 U1 1 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1991 VL 77 IS 7 BP 1516 EP 1526 PG 11 WC Hematology SC Hematology GA FE374 UT WOS:A1991FE37400016 PM 1849033 ER PT J AU RAGHOEBIER, S VANKRIEKEN, JHJM KLUINNELEMANS, JC GILLIS, A VANOMMEN, GJB GINSBERG, AM RAFFELD, M KLUIN, PM AF RAGHOEBIER, S VANKRIEKEN, JHJM KLUINNELEMANS, JC GILLIS, A VANOMMEN, GJB GINSBERG, AM RAFFELD, M KLUIN, PM TI ONCOGENE REARRANGEMENTS IN CHRONIC B-CELL LEUKEMIA SO BLOOD LA English DT Article ID CHRONIC LYMPHOCYTIC-LEUKEMIA; T(11-14) CHROMOSOME-TRANSLOCATION; HUMAN FOLLICULAR LYMPHOMA; C-MYC ONCOGENE; GENE REARRANGEMENTS; RECIPROCAL PARTNERS; BURKITT-LYMPHOMA; BCL-2 GENE; BREAKPOINT; T(14-18) C1 UNIV LEIDEN,DEPT HEMATOL,2300 RC LEIDEN,NETHERLANDS. UNIV LEIDEN,DEPT HUMAN GENET,2300 RC LEIDEN,NETHERLANDS. NCI,HEMATOPATHOL SECT,PATHOL LAB,BETHESDA,MD 20892. RP RAGHOEBIER, S (reprint author), UNIV LEIDEN,DEPT PATHOL,PATHOL LAB,WASSENAARSWEG 62,POB 9603,2300 RC LEIDEN,NETHERLANDS. RI van Krieken, Joannes/D-4138-2009 OI van Krieken, Joannes/0000-0001-6544-1040 NR 45 TC 88 Z9 88 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1991 VL 77 IS 7 BP 1560 EP 1564 PG 5 WC Hematology SC Hematology GA FE374 UT WOS:A1991FE37400021 PM 2009372 ER PT J AU DIPELLEGRINO, G WISE, SP AF DIPELLEGRINO, G WISE, SP TI A NEUROPHYSIOLOGICAL COMPARISON OF 3 DISTINCT REGIONS OF THE PRIMATE FRONTAL-LOBE SO BRAIN LA English DT Article ID PREFRONTAL UNIT-ACTIVITY; DELAYED-RESPONSE PERFORMANCE; POSTERIOR PARIETAL CORTEX; INFERIOR TEMPORAL CORTEX; SUPPLEMENTARY EYE FIELD; GO/NO-GO DISCRIMINATION; MONKEYS MACACA-MULATTA; SINGLE-CELL-ACTIVITY; PREMOTOR CORTEX; RHESUS-MONKEY AB We examined whether reported physiological distinctions between prefrontal (PF) and premotor (PM) areas reflect true dissimilarity or instead result from technical considerations such as differences among species, individuals, or behavioural, physiological and anatomical techniques. A Rhesus monkey performed a task involving 2 stimulus events on each trial: the first stimulus appeared briefly, then after a delay period, 2 peripheral stimuli appeared simultaneously. The monkey had to delay responding for an additional, self-timed instructed delay period, then contact a touch pad beneath the peripheral stimulus of the colour matching the first stimulus. PM and PF cortex differ in several respects. More PF than PM neurons discharge during the presentation of the first stimulus, and only PF neurons show phasic bursts of activity shortly after that stimulus disappears. During the instructed delay period, cells in PF begin activity earlier than PM neurons, whereas PM neurons continue their activity longer. Similarly, PF cells show greater discharge modulation early in the instructed delay period compared with PM cells, which discharge more intensely later. Cells with apparent selectivity for stimulus characteristics appear only in PF. Thus our results support the view that PM and PF have distinctive physiological properties that cannot be accounted for by technical considerations alone. In addition, we describe the activity cells in a cortical region, here termed the dorsomedial frontal cortex, which has a distinctive dysgranular cytoarchitecture and has physiological properties that ally it with PF. C1 NIMH,NEUROPHYSIOL LAB,POB 289,POOLESVILLE,MD 20837. OI di Pellegrino, Giuseppe/0000-0001-7080-4758 NR 110 TC 80 Z9 81 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0006-8950 J9 BRAIN JI Brain PD APR PY 1991 VL 114 BP 951 EP 978 PN 2 PG 28 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FQ675 UT WOS:A1991FQ67500019 PM 2043959 ER PT J AU GRAFMAN, J THOMPSON, K WEINGARTNER, H MARTINEZ, R LAWLOR, BA SUNDERLAND, T AF GRAFMAN, J THOMPSON, K WEINGARTNER, H MARTINEZ, R LAWLOR, BA SUNDERLAND, T TI SCRIPT GENERATION AS AN INDICATOR OF KNOWLEDGE REPRESENTATION IN PATIENTS WITH ALZHEIMERS-DISEASE SO BRAIN AND LANGUAGE LA English DT Article ID SEMANTIC MEMORY; DEMENTIA; ADULTS C1 GEORGE WASHINGTON UNIV,DEPT PSYCHOL,WASHINGTON,DC 20052. NIMH,GERIATR PSYCHOPHARMACOL UNIT,BETHESDA,MD 20892. RP GRAFMAN, J (reprint author), NINCDS,MED NEUROL BRANCH,COGNIT NEUROSCI SECT,BLDG 10,ROOM 5C422,BETHESDA,MD 20892, USA. OI Grafman, Jordan H./0000-0001-8645-4457 NR 35 TC 31 Z9 31 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0093-934X J9 BRAIN LANG JI Brain Lang. PD APR PY 1991 VL 40 IS 3 BP 344 EP 358 DI 10.1016/0093-934X(91)90134-M PG 15 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA FJ154 UT WOS:A1991FJ15400003 PM 2054591 ER PT J AU MUNDY, WR TANDON, P BARONE, S TILSON, HA AF MUNDY, WR TANDON, P BARONE, S TILSON, HA TI LONG-TERM CHANGES IN PHOSPHOINOSITIDE HYDROLYSIS FOLLOWING COLCHICINE LESIONS OF THE NUCLEUS BASALIS MAGNOCELLULARIS SO BRAIN RESEARCH BULLETIN LA English DT Note DE COLCHICINE; NUCLEUS BASALIS; FRONTAL CORTEX; PHOSPHOINOSITIDE HYDROLYSIS ID INOSITOL PHOSPHOLIPID HYDROLYSIS; CHOLINE-ACETYLTRANSFERASE ACTIVITY; RAT CEREBRAL-CORTEX; MUSCARINIC RECEPTORS; BEHAVIORAL RECOVERY; FOREBRAIN NUCLEI; BRAIN; DISTURBANCES; STIMULATION; DENERVATION AB The effect of bilateral colchicine lesions of the nucleus basalis magnocellularis (NBM) on agonist-stimulated phosphoinositide (PI) hydrolysis was examined in cortical slices 1, 3, or 14 months after surgery. Colchicine lesions resulted in a loss of acetylcholinesterase staining in the cortex which recovered to control levels by 14 months. Choline acetyltransferase activity in the cortex was decreased by 43% one month after lesioning, but returned to control levels by 3 months. In vitro stimulation with carbachol produced a concentration-dependent increase in PI hydrolysis, which was enhanced 3 and 14 months after NBM lesions. Norepinephrine and quisqualate-stimulated PI hydrolysis was also enhanced 14 months after NBM lesions. These results suggest a slow up-regulation of postsynaptic receptor function following presynaptic loss of transmitter. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. E CAROLINA UNIV,SCH MED,DEPT ANAT & CELL BIOL,GREENVILLE,NC 27858. NR 43 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PD APR PY 1991 VL 26 IS 4 BP 657 EP 662 DI 10.1016/0361-9230(91)90112-W PG 6 WC Neurosciences SC Neurosciences & Neurology GA FL893 UT WOS:A1991FL89300027 PM 1651150 ER PT J AU COLLMAN, GW LOOMIS, DP SANDLER, DP AF COLLMAN, GW LOOMIS, DP SANDLER, DP TI CHILDHOOD-CANCER MORTALITY AND RADON CONCENTRATION IN DRINKING-WATER IN NORTH-CAROLINA SO BRITISH JOURNAL OF CANCER LA English DT Article ID LUNG-CANCER; INDOOR RADON; EXPOSURE; RADIATION; LEUKEMIA; ASSOCIATION; DAUGHTERS; DWELLINGS; VICINITY; SMOKING AB We explored the association between groundwater radon levels and childhood cancer mortality in North Carolina. Using data from two state-wide surveys of public drinking water supplies, counties were ranked according to average groundwater radon concentration. Age and sex-adjusted 1950-79 cancer death rates among children under age 15 were calculated for counties with high, medium, and low radon levels. Overall cancer mortality was increased in counties with medium and high radon levels. The strongest association was for the leukaemias, but risks were also suggested for other sites. These associations could be due to confounding or other biases, but the findings are consistent with other recent reports. C1 NIEHS, EPIDEMIOL BRANCH,ENVIRONM & MOLEC EPIDEMIOL SECT, MD A3-05,POB 12233, RES TRIANGLE PK, NC 27709 USA. UNIV N CAROLINA, SCH PUBL HLTH, DEPT EPIDEMIOL, CHAPEL HILL, NC 27514 USA. OI Sandler, Dale/0000-0002-6776-0018 NR 41 TC 32 Z9 32 U1 1 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 EI 1532-1827 J9 BRIT J CANCER JI Br. J. Cancer PD APR PY 1991 VL 63 IS 4 BP 626 EP 629 DI 10.1038/bjc.1991.143 PG 4 WC Oncology SC Oncology GA FH596 UT WOS:A1991FH59600031 PM 2021549 ER PT J AU STONE, M AF STONE, M TI IMAGING THE TONGUE AND VOCAL-TRACT SO BRITISH JOURNAL OF DISORDERS OF COMMUNICATION LA English DT Article; Proceedings Paper CT MEETING OF THE ACOUSTICAL SOC OF AMERICA CY NOV, 1988 CL HONOLULU, HI SP ACOUST SOC AMER, ACOUST SOC JAPAN DE IMAGING; CT; X-RAY; MRI; ULTRASOUND; VOCAL TRACT ID SHAPE; VOWELS RP STONE, M (reprint author), NIH,DEPT REHAB MED,BLDG 10,ROOM 6S235,BETHESDA,MD 20892, USA. NR 4 TC 8 Z9 8 U1 0 U2 1 PU COLLEGE SPEECH & LANGUAGE THERAPISTS PI LONDON PA 7 BATH PLACE, LONDON, ENGLAND EC2A 3DR SN 0007-098X J9 BRIT J DISORD COMMUN PD APR PY 1991 VL 26 IS 1 BP 11 EP 23 PG 13 WC Psychology; Rehabilitation SC Psychology; Rehabilitation GA FL441 UT WOS:A1991FL44100002 PM 1954111 ER PT J AU TRAVIS, LB CURTIS, RE BOICE, JD HANKEY, BF FRAUMENI, JF AF TRAVIS, LB CURTIS, RE BOICE, JD HANKEY, BF FRAUMENI, JF TI 2ND CANCERS FOLLOWING NON-HODGKINS-LYMPHOMA SO CANCER LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; CHRONIC LYMPHOCYTIC-LEUKEMIA; LUNG-CANCER; MALIGNANT-MELANOMA; MYCOSIS-FUNGOIDES; RISK; DISEASE; CYCLOPHOSPHAMIDE; CARCINOMA; SURVIVORS AB The risk of second malignancies following non-Hodgkin's lymphoma (NHL) was estimated in 29,153 patients diagnosed with NHL between 1973 and 1987 in one of nine areas participating in the National Cancer Institute's Surveillance, Epidemiology, and End Results Program. Compared with the general population, NHL patients were at a significantly increased risk of developing second cancers (observed/expected [O/E] = 1.18; O = 1231). The O/E ratio increased significantly with time to reach 1.77 in 10-year survivors. Significant excesses were noted for acute nonlymphocytic leukemia (O/E = 2.88), cancers of the bladder (O/E = 1.30), kidney (O/E = 1.47), and lung (O/E = 1.57), malignant melanoma (O/E = 2.44), and Hodgkin's disease (O/E = 4.16). Chemotherapy appeared related to subsequent acute nonlymphocytic leukemia (ANLL) and bladder cancer, Radiation therapy was associated with ANLL and possibly cancers of the lung, bladder, and bone. Malignant melanoma was not clearly related to initial NHL treatment. C1 NCI,DIV CANC PREVENT & CONTROL,SURVEILLANCE PROGRAM,CANC STAT BRANCH,BETHESDA,MD 20892. RP TRAVIS, LB (reprint author), NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,EXECUT PLAZA N,BETHESDA,MD 20892, USA. NR 44 TC 134 Z9 137 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1991 VL 67 IS 7 BP 2002 EP 2009 DI 10.1002/1097-0142(19910401)67:7<2002::AID-CNCR2820670729>3.0.CO;2-E PG 8 WC Oncology SC Oncology GA FC976 UT WOS:A1991FC97600028 PM 2004317 ER PT J AU AMOS, CI GOLDSTEIN, AM HARRIS, EL AF AMOS, CI GOLDSTEIN, AM HARRIS, EL TI FAMILIALITY OF BREAST-CANCER AND SOCIOECONOMIC-STATUS IN BLACKS SO CANCER RESEARCH LA English DT Article ID COMPLEX SEGREGATION ANALYSIS; HIGH-RISK FAMILIES; HISTORY; RATIO; AGE AB Familial patterns of the occurrence of breast cancer were studied in a population-based case-control series of black women from the Cancer and Steroid Hormone study. The risks of breast cancer among relatives of breast cancer cases were compared to those of controls who were matched for age and locale. Using the term "proband" to indicate either case or control status, significant predictors of risk to the relatives of probands included case/control status of the proband and the number of years of education completed by the proband. Genetic segregation analysis of the case families using external risks generated from SEER data indicated that the familial aggregation was consistent with Mendelian recessive transmission of a single major gene. The use of internally estimated risks, which are much less stable than the SEER risks, no longer permitted discrimination among the major locus models examined. To avoid possible reporting bias, we also performed segregation analysis on families of probands who had completed at least 12 years of education. The results from this analysis reflected the results from the entire data. C1 JOHNS HOPKINS UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21205. RP AMOS, CI (reprint author), NCI,FAMILY STUDIES SECT,SUITE 439,EXECUT PLAZA N,BETHESDA,MD 20892, USA. FU PHS HHS [3-Y01-8-1037] NR 37 TC 20 Z9 20 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1991 VL 51 IS 7 BP 1793 EP 1797 PG 5 WC Oncology SC Oncology GA FE041 UT WOS:A1991FE04100007 PM 2004364 ER PT J AU MAHMOUD, S STALEY, J TAYLOR, J BOGDEN, A MOREAU, JP COY, D AVIS, I CUTTITTA, F MULSHINE, JL MOODY, TW AF MAHMOUD, S STALEY, J TAYLOR, J BOGDEN, A MOREAU, JP COY, D AVIS, I CUTTITTA, F MULSHINE, JL MOODY, TW TI [PSI13,14] BOMBESIN ANALOGS INHIBIT GROWTH OF SMALL-CELL LUNG-CANCER INVITRO AND INVIVO SO CANCER RESEARCH LA English DT Article ID GASTRIN-RELEASING PEPTIDE; SWISS 3T3 CELLS; RECEPTOR ANTAGONISTS; CLONAL GROWTH; CARCINOMA; LINES; EXPRESSION; CALCIUM; BINDING; POTENT AB Bombesin/gastrin releasing peptide (BN/GRP) functions as an autocrine growth factor in small cell lung cancer (SCLC). Previously, this autocrine growth cycle was disrupted by a monoclonal antibody which binds to the carboxyl terminal of BN and neutralizes the peptide so that it is unable to interact with the BN/GRP receptor. Here a series of BN analogues were synthesized which have a reduced peptide bond near the carboxyl terminal. The analogues inhibited specific binding of I-125-GRP to SCLC cell line NCI-H345 in a dose-dependent manner and the analogue [D-Nal6, Psi13,14, Phe14] BN6-14 was approximately 6-fold more potent than was (Psi13,14, Leu14)BN with a 50% inhibition concentration value of 5 nM. [DNal6, Psi13,14, Phe14]BN6-14 and [Psi13,14, Leu14]BN had no effect on the cytosolic Ca2+ levels but antagonized the increase in cytosolic Ca2+ caused by 10 nM BN. [Psi13,14, Leu14]BN (1-mu-M) inhibited the growth of SCLC in vitro using a clonogenic assay by approximately 70% Also, injection of [Psi13,14, Leu14]BN (10-mu-g, s.c.) inhibited the growth of SCLC xenografts in nude mice in vivo by approximately 50%. These data suggest that the autocrine growth cycle of BN/GRP in SCLC may also be disrupted by peptide antagonists which bind to the BN receptor. C1 GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,DEPT BIOCHEM & MOLEC BIOL,WASHINGTON,DC 20037. BIOMEASURE INC,HOPKINTON,MA 01748. TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. USN HOSP,NCI,NCI NAVY MED ONCOL BRANCH,BETHESDA,MD 20814. FU NCI NIH HHS [CA-53477, CA-45153, CA-48071] NR 32 TC 163 Z9 165 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1991 VL 51 IS 7 BP 1798 EP 1802 PG 5 WC Oncology SC Oncology GA FE041 UT WOS:A1991FE04100008 PM 1848479 ER PT J AU WARD, FT KELLEY, JA ROTH, JS LOMBARDO, FA WEISS, RB LEYLANDJONES, B CHUN, HG AF WARD, FT KELLEY, JA ROTH, JS LOMBARDO, FA WEISS, RB LEYLANDJONES, B CHUN, HG TI A PHASE-I BIOAVAILABILITY AND PHARMACOKINETIC STUDY OF HEXAMETHYLENE BISACETAMIDE (NSC-95580) ADMINISTERED VIA NASOGASTRIC TUBE SO CANCER RESEARCH LA English DT Article ID DIFFERENTIATING AGENT; LEUKEMIA-CELLS; METABOLITES; INDUCTION; INFUSION; INDUCERS; PLASMA; TRIAL; LINE AB A Phase I clinical trial and pharmacological study of nasogastrically administered hexamethylene bisacetamide, a polar-planar compound with in vitro differentiating activity, was conducted in 14 adult patients with refractory cancer. Hexamethylene bisacetamide was administered as a 5% (w/v) solution via a nasogastric or gastrostomy tube every 4 h for 5 days, followed in 21 days by a 5-day continuous i.v. infusion at the same daily dose. Parenteral drug administration was then continued at the same interval in the absence of disease progression or unacceptable toxicity. Three patients each were treated at doses of 12 and 24 g/m2/day, while eight patients received a dose of 30 g/m2/day. Toxicity was comparable for both routes of drug administration at the above doses. Nasogastrically administered hexamethylene bisacetamide was well tolerated at the lower doses, whereas neurotoxicity and nausea and vomiting were the major, but manageable, toxicities at 30 g/m2/day. Metabolic acidosis, renal dysfunction, mucositis, and thrombocytopenia were the other commonly observed drug toxicities at this dose. No objective tumor responses were observed. Hexamethylene bisacetamide was rapidly absorbed from the gastrointestinal tract with a mean measured bioavailability of 99 +/- 15%. Pharmacokinetic parameters for hexamethylene bisacetamide and plasma concentrations of the two major metabolites, N-acetyl-1,6-diaminohexane and 6-acetamidohexanoic acid, were similar for either route of administration in individual patients. Hexamethylene bisacetamide exhibited apparent monoexponential plasma elimination after either nasogastric or parenteral administration with 27 to 60% of the administered dose being excreted in the urine as parent compound. Based on its demonstrated complete bioavailability and tolerability, nasogastric administration of hexamethylene bisacetamide can be directly and safely substituted for the comparable i.v. dose. C1 WALTER REED ARMY MED CTR,DEPT MED,HEMATOL ONCOL SERV,WASHINGTON,DC 20307. NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,INVEST DRUG BRANCH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NR 24 TC 13 Z9 13 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1991 VL 51 IS 7 BP 1803 EP 1810 PG 8 WC Oncology SC Oncology GA FE041 UT WOS:A1991FE04100009 PM 2004365 ER PT J AU VONHOFE, E SCHMEROLD, I NIMS, RW KEEFER, LK REIST, EJ KLEIHUES, P AF VONHOFE, E SCHMEROLD, I NIMS, RW KEEFER, LK REIST, EJ KLEIHUES, P TI BETA-DEUTERATION OF N-NITROSOETHYLMETHYLAMINE CAUSES A SHIFT IN DNA METHYLATION FROM RAT-LIVER TO ESOPHAGUS SO CARCINOGENESIS LA English DT Article ID HYDROXYLATED NITROSAMINES; F344 RATS; DEUTERIUM; NITROSOMETHYLETHYLAMINE; NITROSODIMETHYLAMINE; CARCINOGENICITY; METABOLISM; INVIVO; ALKYLATION; POSITIONS AB While N-nitrosoethylmethylamine (NEMA) is carcinogenic primarily for the liver, its beta-trideuterated derivative, N-nitroso([2-D3]ethyl)methylamine (NEMA-d3), also produces a high incidence of tumors in the esophagus. To determine whether this shift in organ specificity is associated with an altered pattern of DNA alkylation, [methyl-C-14]- and [1-ethyl-C-14]-labeled NEMA-d3 were administered to adult male Fischer 344 rats as a single i.p. dose (0.05 mmol/kg; 4 h survival). Levels of methylated and ethylated purines in the DNA of various organs were determined by radiochromatography on Sephasorb-HP columns. When compared to previous data using undeuterated NEMA, 7-methylguanine levels were found to be reduced by approximately 30% in liver and kidney, but were 160% greater in esophagus. This resulted in a decrease in the 7-methylguanine ratio for liver/esophagus from 109 to 29. O6-methylguanine was diminished in liver and kidney, but levels in lung and esophagus were too low for quantitative detection. Similarly, deuteration led to an 18% decrease of 7-ethylguanine in hepatic DNA. The observed increase in esophageal DNA methylation correlates with the increased carcinogenicity of NEMA-d3 relative to undeuterated NEMA in that organ. Since pharmacokinetic studies have shown that beta-trideuteration of NEMA does not alter its bioavailability, the data suggest that the observed shift in target organ results from isotopically-induced changes in the balance among competing metabolic pathways in different rat tissues. C1 UNIV ZURICH,INST PATHOL,NEUROPATHOL LAB,CH-8091 ZURICH,SWITZERLAND. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,CHEM SECT,FREDERICK,MD 21702. SRI INT,DIV LIFE SCI,MENLO PK,CA 94025. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 NR 21 TC 2 Z9 2 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1991 VL 12 IS 4 BP 545 EP 549 DI 10.1093/carcin/12.4.545 PG 5 WC Oncology SC Oncology GA FG197 UT WOS:A1991FG19700001 PM 1901522 ER PT J AU MATSUKURA, N WILLEY, J MIYASHITA, M TAFFE, B HOFFMANN, D WALDREN, C PUCK, TT HARRIS, CC AF MATSUKURA, N WILLEY, J MIYASHITA, M TAFFE, B HOFFMANN, D WALDREN, C PUCK, TT HARRIS, CC TI DETECTION OF DIRECT MUTAGENICITY OF CIGARETTE-SMOKE CONDENSATE IN MAMMALIAN-CELLS SO CARCINOGENESIS LA English DT Article ID BRONCHIAL EPITHELIAL-CELLS; WILMS TUMOR; HUMAN CHROMOSOME-11; TUMORIGENIC EXPRESSION; HUMAN CANCER; GENETICS; MUTAGENESIS; FORMALDEHYDE; GENOTOXICITY; FIBROBLASTS AB Mutagenicity of cigarette smoke condensate (CSC) and the acidic, basic and neutral fractions of CSC was examined in the A(L) hybrid cell, a Chinese hamster ovary cell containing one human chromosome 11. Since the human chromosome 11 is not necessary for survival of the A(L) cells, mutations involving large deletions and chromosomal loss by non-dysjunction are non-lethal events that are detectable by loss of human cell surface antigens (a1, a2 and a3) encoded by genes on chromosome 11p (a1 and a3) and 11q (a2) through an antibody-complement lysis assay. Exposure of A(L) cells to CSC without exogenous metabolic activation caused a dose-dependent cytotoxicity and mutagenicity. Mutagenicity also increased with time of incubation up to 3 h with a maximum of 300 a1- mutants/10(5) survivors (250% above background; P < 0.0005) after incubation with 100-mu-g/ml CSC. Cytotoxicity and mutagenicity of CSC were inversely proportional to cell density. Fifty percent lethal doses for the acidic, basic and neutral fractions of CSC after 3 h of incubation were 30, 100 and 240-mu-g/ml respectively, and the acidic fraction at a concentration of 25-mu-g/ml induced 350 a1-mutants/10(5) survivors (230% above background; P < 0.0005); the basic and neutral fractions were less mutagenic. These results indicate that CSC and fractions of CSC can directly produce a spectrum of mutations, through both deletional and non-dysjunctional mechanisms of a kind known to lead to inactivation of tumor suppressor genes. C1 NCI,DIV CANC ETIOL,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. AMER HLTH FDN,NAYLOR DANA INST DIS PREVENT,VALHALLA,NY 10595. ELEANOR ROOSEVELT INST CANC RES,DENVER,CO 80262. NR 39 TC 12 Z9 12 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1991 VL 12 IS 4 BP 685 EP 689 DI 10.1093/carcin/12.4.685 PG 5 WC Oncology SC Oncology GA FG197 UT WOS:A1991FG19700021 PM 2013132 ER PT J AU RAY, PE CASTREN, E RULEY, EJ SAAVEDRA, JM AF RAY, PE CASTREN, E RULEY, EJ SAAVEDRA, JM TI DIFFERENT EFFECTS OF CHRONIC NA+, CL-, AND K+ DEPLETION ON BRAIN VASOPRESSIN MESSENGER-RNA AND PLASMA VASOPRESSIN IN YOUNG-RATS SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE EXTRACELLULAR CELL VOLUME; SUPRAOPTIC NUCLEUS; PARAVENTRICULAR NUCLEUS; DEVELOPMENT; VASOPRESSIN FORMATION; VASOPRESSIN RELEASE; INSITU HYBRIDIZATION ID RELEASE; ANGIOTENSIN AB 1. We studied the effects of selective chronic dietary sodium, chloride, or potassium depletion in young rats on vasopressin mRNA levels in the supraoptic and paraventricular nuclei, an index of vasopressin formation, and in plasma vasopressin levels, and index of vasopressin release. 2. All diets significantly increased plasma renin activity, contracted the extracellular fluid volume, and decreased serum osmolarity. 3. In the supraoptic nucleus, vasopressin mRNA levels were significantly decreased in the low-sodium group but were not significantly affected by chloride depletion. 4. There were no significant changes in vasopressin mRNA in the paraventricular nucleus after sodium or chloride dietary depletion. 5. After 2 weeks of potassium depletion, vasopressin mRNA levels were decreased in the supraoptic nucleus. When potassium depletion was prolonged for 3 weeks, vasopressin mRNA levels increased in both supraoptic and paraventricular nuclei. 6. Plasma vasopressin levels were high in animals subjected to dietary chloride depletion or to 3 weeks of potassium depletion. Dietary sodium depletion or 2 weeks of dietary potassium depletion did not significantly affect plasma vasopressin. 7. Our results show that chronic sodium, chloride, or potassium depletion differentially affect brain vasopressin mRNA and vasopressin release in young rats. 8. The effect of these diets may be mediated through changes in the extracellular fluid volume, serum osmolarity, and/or renin angiotensin system. C1 NIMH,CLIN SCI LAB,PHARMACOL SECT,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,CHILDRENS NATL MED CTR,DEPT NEPHROL,WASHINGTON,DC 20052. GEORGE WASHINGTON UNIV,DEPT PEDIAT,WASHINGTON,DC 20052. RI Castren, Eero/A-4618-2010 NR 25 TC 9 Z9 9 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD APR PY 1991 VL 11 IS 2 BP 277 EP 287 DI 10.1007/BF00769040 PG 11 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA EZ379 UT WOS:A1991EZ37900005 PM 2029728 ER PT J AU TSUTSUMI, K SAAVEDRA, JM AF TSUTSUMI, K SAAVEDRA, JM TI INCREASED DITHIOTHREITOL-INSENSITIVE, TYPE-2 ANGIOTENSIN-II RECEPTORS IN SELECTED BRAIN-AREAS OF YOUNG-RATS SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Note DE DEVELOPMENT OF ANGIOTENSIN-II RECEPTORS; NUCLEUS OF THE SOLITARY TRACT; AREA POSTREMA; INFERIOR OLIVE ID BINDING-SITES; SUBFORNICAL ORGAN; PARAVENTRICULAR NUCLEUS; ANTERIOR-PITUITARY; AUTORADIOGRAPHY; SUBTYPES; GLAND AB 1. Angiotensin II receptors have been studied by quantitative autoradiography in selected brain areas of young (2-week-old) and adult (8-week-old) rats. 2. In young rats, angiotensin II receptors were present in brain areas which did not express receptors in the adult brain, such as thalamic nuclei, cortical areas, and the cerebellum. 3. Young rats had more angiotensin II receptors in the subfornical organ than adult rats. In the inferior olive, the number of angiotensin receptors in young animals was 10 times higher than that in adult rats. Angiotensin II binding in the inferior olive was insentive to incubation in the presence of dithiothreitol. 4. Conversely, the number of angiotensin II receptors in the nucleus of the solitary tract was lower in young rats compared to adults. Incubation in the presence of dithiothreitol resulted in a more than 90% inhibition of angiotensin II binding in the nucleus of the solitary tract. 5. Our results indicate the presence of two types of angiotensin II receptor in brain, one sensitive (type 1) and one insensitive (type 2) to the reducing agent dithiothreitol. 6. The expression of type 2 angiotensin II receptors, insensitive to dithiothreitol, is more marked in young rats, indicating a role for this type of angiotensin receptors in brain development. C1 NIMH,CLIN SCI LAB,PHARMACOL SECT,BLDG 10,ROOM 2D-45,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 21 TC 24 Z9 24 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD APR PY 1991 VL 11 IS 2 BP 295 EP 299 DI 10.1007/BF00769042 PG 5 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA EZ379 UT WOS:A1991EZ37900007 PM 2029730 ER PT J AU BERAUD, E LORBERBOUMGALSKI, H CHAN, CC FITZGERALD, D PASTAN, I NUSSENBLATT, RB AF BERAUD, E LORBERBOUMGALSKI, H CHAN, CC FITZGERALD, D PASTAN, I NUSSENBLATT, RB TI IMMUNOSPECIFIC SUPPRESSION OF ENCEPHALITOGENIC-ACTIVATED LYMPHOCYTES-T BY CHIMERIC CYTOTOXIN IL-2-PE40 SO CELLULAR IMMUNOLOGY LA English DT Article ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; ANTI-INTERLEUKIN-2 RECEPTOR ANTIBODY; INTERLEUKIN-2 RECEPTOR; MULTIPLE-SCLEROSIS; EFFECTOR-CELLS; RHEUMATOID-ARTHRITIS; MONOCLONAL-ANTIBODY; DIABETIC INSULITIS C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RP BERAUD, E (reprint author), NEI,IMMUNOL LAB,BETHESDA,MD 20892, USA. NR 49 TC 15 Z9 16 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD APR 1 PY 1991 VL 133 IS 2 BP 379 EP 389 DI 10.1016/0008-8749(91)90112-O PG 11 WC Cell Biology; Immunology SC Cell Biology; Immunology GA FA011 UT WOS:A1991FA01100010 PM 1707763 ER PT J AU KOCHANSKA, G AF KOCHANSKA, G TI PATTERNS OF INHIBITION TO THE UNFAMILIAR IN CHILDREN OF NORMAL AND AFFECTIVELY ILL MOTHERS SO CHILD DEVELOPMENT LA English DT Article ID BEHAVIORAL-INHIBITION; YOUNG-CHILDREN; DEPRESSION; CHILDHOOD; DISORDER; PARENTS; INFANT RP KOCHANSKA, G (reprint author), NIMH,DEV PSYCHOL LAB,BLDG 15K,BETHESDA,MD 20892, USA. NR 45 TC 98 Z9 99 U1 0 U2 4 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0009-3920 J9 CHILD DEV JI Child Dev. PD APR PY 1991 VL 62 IS 2 BP 250 EP 263 DI 10.1111/j.1467-8624.1991.tb01529.x PG 14 WC Psychology, Educational; Psychology, Developmental SC Psychology GA FE582 UT WOS:A1991FE58200003 PM 2055122 ER PT J AU ENGEL, BT TALAN, MI AF ENGEL, BT TALAN, MI TI CARDIOVASCULAR-RESPONSES AS BEHAVIOR SO CIRCULATION LA English DT Article; Proceedings Paper CT SYMP ON MENTAL STRESS AS A TRIGGER OF CARDIOVASCULAR EVENTS CY OCT, 1989 CL VERUNO, ITALY SP CLIN LAVORO FDN PAVIA, BOEHRINGER INGELHEIM DE EXERCISE; NERVOUS SYSTEM, CENTRAL; AUTONOMIC BLOCKADE ID HEART-RATE; LEARNED CONTROL; OPERANT; MONKEYS AB Exercise is a ubiquitous, biologically and clinically significant behavior. Although the somatomotor responses are generally regarded as "behavior," the cardiovascular adjustments that accompany these responses are generally considered to be reflexes that are elicited by neurally mediated stimuli and metabolites arising from working muscles. We report experimental evidence that monkeys can be trained to exercise, to slow heart rate, and to combine these two skills. Furthermore, some animals will emit more physical work at slower heart rates (at comparable levels of cardiac output) and lower left ventricular work during the combined condition relative to an exercise-only condition. Thus, these findings show that the cardiovascular and somatomotor responses of exercise can be dissociated and that both sets of responses should be considered behaviors. Also included are results that show these animals can perform these behaviors during sympathetic or vagal blockade. These findings are further evidence that the cardiovascular adjustments to exercise are, in part, learned behaviors because they show that the behavior - attenuation of the tachycardia of exercise - is not a reflex that is specifically tied to any neuroeffector system; rather, this behavior is emitted to achieve a contingent reward, and the nervous system will use whatever mechanisms are available to attain that consequence. RP ENGEL, BT (reprint author), NIA,GERONTOL RES CTR,NEUROBIOL LAB,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 22 TC 10 Z9 10 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR PY 1991 VL 83 IS 4 SU S BP 9 EP 13 PG 5 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FH047 UT WOS:A1991FH04700003 ER PT J AU DILSIZIAN, V SMELTZER, WR FREEDMAN, NMT DEXTRAS, R BONOW, RO AF DILSIZIAN, V SMELTZER, WR FREEDMAN, NMT DEXTRAS, R BONOW, RO TI THALLIUM REINJECTION AFTER STRESS-REDISTRIBUTION IMAGING - DOES 24-HOUR DELAYED IMAGING AFTER REINJECTION ENHANCE DETECTION OF VIABLE MYOCARDIUM SO CIRCULATION LA English DT Article DE MYOCARDIAL VIABILITY; CORONARY ARTERY DISEASE; THALLIUM; MYOCARDIAL ISCHEMIA ID CORONARY-ARTERY DISEASE; PERSISTENT DEFECTS; TL-201; EXERCISE; SCINTIGRAPHY; PERFUSION; REST; ELECTROCARDIOGRAPHY; REVASCULARIZATION; SPECT AB Background. Thallium reinjection immediately after conventional stress-redistribution imaging improves the detection of viable myocardium, as many myocardial regions with apparently "irreversible" thallium defects on standard 3-4 hour redistribution images manifest enhanced thallium uptake after reinjection. Because the 10-minute period between reinjection and imaging may be too short, the present study was designed to determine whether 24-hour imaging after thallium reinjection provides additional information regarding myocardial viability beyond that obtained by imaging shortly after reinjection. Methods and Results. We studied 50 patients with chronic stable coronary artery disease undergoing exercise thallium tomography, radionuclide angiography, and coronary arteriography. Immediately after the 3-4-hour redistribution images were obtained, 1 mCi thallium was injected at rest, and images were reacquired at 10 minutes and 24 hours after reinjection. The stress, redistribution, reinjection, and 24-hour images were then analyzed qualitatively and quantitatively. Of the 127 abnormal myocardial regions on the stress images, 55 had persistent defects on redistribution images by qualitative analysis, of which 25 (45%) demonstrated improved thallium uptake after reinjection. At the 24-hour study, 23 of the 25 regions (92%) with previously improved thallium uptake by reinjection showed no further improvement. Similarly of the 30 regions determined to have irreversible defects after reinjection, 29 (97%) remained irreversible on 24-hour images. These findings were confirmed by the quantitative analysis. The mean normalized thallium activity in regions with enhanced thallium activity after reinjection increased from 57 +/- 13% on redistribution studies to 70 +/- 14% after reinjection but did not change at 24 hours (71 +/- 14%). In regions with irreversible defects that were unaltered by reinjection, mean regional thallium activity did not differ from the reinjection to the 24-hour studies (57 +/- 17% and 58 +/- 17%, respectively). Twenty-four-hour imaging after reinjection showed improvement in only four of 35 irreversible regions (involving three of the 50 patients). Conclusions. These data indicate that thallium reinjection at rest after 3-4 hours of redistribution provides most of the clinically relevant information pertaining to myocardial viability in regions with apparently irreversible thallium defects. Hence, thallium reinjection may be used instead of 24-hour imaging in most patients in whom a persistent thallium defect is observed on conventional redistribution images. C1 NIH,DEPT NUCL MED,BETHESDA,MD 20892. RP DILSIZIAN, V (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 18 TC 78 Z9 79 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR PY 1991 VL 83 IS 4 BP 1247 EP 1255 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FF419 UT WOS:A1991FF41900008 PM 2013145 ER PT J AU GOEDERT, JJ GAIL, MH AF GOEDERT, JJ GAIL, MH TI PREDICTING AIDS ONSET FOR INDIVIDUAL PATIENTS SO CLINICAL CHEMISTRY LA English DT Editorial Material ID HUMAN IMMUNODEFICIENCY VIRUS; IMMUNE-DEFICIENCY SYNDROME; HOMOSEXUAL MEN; SAN-FRANCISCO; INFECTION; HEMOPHILIA; MARKER; NEOPTERIN; COUNT; HIV RP GOEDERT, JJ (reprint author), NCI,6130 EXECUT BLVD,EPN 434,ROCKVILLE,MD 20892, USA. NR 28 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD APR PY 1991 VL 37 IS 4 BP 486 EP 487 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA FH316 UT WOS:A1991FH31600003 PM 2015659 ER PT J AU HUANG, CM KRAFT, HG GREGG, RE AF HUANG, CM KRAFT, HG GREGG, RE TI MODIFIED IMMUNOBLOTTING TECHNIQUE FOR PHENOTYPING LIPOPROTEIN(A) SO CLINICAL CHEMISTRY LA English DT Note DE APOLIPOPROTEINS; POPULATION STUDIES ID LP(A) GLYCOPROTEIN PHENOTYPES; MYOCARDIAL-INFARCTION; APOLIPOPROTEIN-B; RISK FACTOR; PLASMA AB We describe a modified immunoblotting method for phenotyping lipoprotein(a) [Lp(a)]. This immunoblotting procedure uses commercially available reagents that have a long shelf life. The method is sensitive and takes only 18-mu-L of sera. Lp(a) phenotyping can be performed on sera stored at 4-degrees-C for as much as a week or at -80-degrees-C for as long as a year. In a study of 145 unrelated healthy subjects, we found Lp(a) allelic frequencies of Lp(F) = 1.8%, Lp(B) = 2.6%, Lp(S1) = 5.1%, Lp(S2) = 14.8%, Lp(S3) = 35.9%, Lp(S4) = 11.6%, and Lp0 = 28.0%. C1 NIH,BETHESDA,MD 20892. NR 13 TC 14 Z9 15 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD APR PY 1991 VL 37 IS 4 BP 576 EP 578 PG 3 WC Medical Laboratory Technology SC Medical Laboratory Technology GA FH316 UT WOS:A1991FH31600023 PM 2015675 ER PT J AU WILDER, RL CROFFORD, LJ AF WILDER, RL CROFFORD, LJ TI DO INFECTIOUS AGENTS CAUSE RHEUMATOID-ARTHRITIS SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID EPSTEIN-BARR VIRUS; HEAT-SHOCK PROTEIN; SYNOVIAL-FLUID; DISEASE; PEPTIDOGLYCAN; MYCOBACTERIA; PATHOGENESIS; ANTIGENS; CHAIN AB Although rheumatoid arthritis (RA) has been widely suspected to have an infectious etiology, this hypothesis has remained difficult to prove. Epstein-Barr virus, parvoviruses, and retroviruses are considered by some investigators to be the primary candidates. An increasing body of data, on the other hand, appears to implicate bacteria or their products in the syndrome. Important evidence has surfaced in support of this view. Lyme arthritis, a disease caused by a bacterium, can mimic RA. Bacteria and their products have been conclusively linked to many forms of inflammatory "reactive" arthropathies. RA-like diseases can be induced in certain inbred strains of rats with bacterial cell-wall fragments, e.g., streptococcal and other bacterial peptidoglycans. Immunologic relationships between host and bacterial peptidoglycans, relevant to RA, have been well documented, e.g., heat shock proteins, bacterial IgG Fc binding proteins, and rheumatoid factors. These data not only support the hypothesis that bacteria may play an important role in RA but also indicate that current concepts of infection and autoimmune disease are broadening and overlapping. RP WILDER, RL (reprint author), NIAMSD,ARTHRITIS & RHEUMAT BRANCH,BLDG-10,ROOM 9N240,BETHESDA,MD 20892, USA. RI Crofford, Leslie/J-8010-2013 NR 36 TC 12 Z9 12 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD APR PY 1991 IS 265 BP 36 EP 41 PG 6 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FE787 UT WOS:A1991FE78700005 PM 2009675 ER PT J AU MOSS, RB SOSULSKI, R AF MOSS, RB SOSULSKI, R TI EARLY MENINGITIS SO CLINICAL PEDIATRICS LA English DT Article ID CHILDREN; CONVULSIONS C1 UNIV HOSP STONY BROOK,DEPT PEDIAT,STONY BROOK,NY 11790. RP MOSS, RB (reprint author), NIAID,NATL INST HLTH BLDG 10,RM11S242,BETHESDA,MD 20892, USA. NR 11 TC 1 Z9 1 U1 0 U2 0 PU WESTMINSTER PUBL INC PI GLEN HEAD PA 708 GLEN COVE AVE, GLEN HEAD, NY 11545 SN 0009-9228 J9 CLIN PEDIATR JI Clin. Pediatr. PD APR PY 1991 VL 30 IS 4 BP 229 EP 230 DI 10.1177/000992289103000406 PG 2 WC Pediatrics SC Pediatrics GA FM129 UT WOS:A1991FM12900006 PM 2025987 ER PT J AU LEE, TH OGNIBENE, FP SCHWARTZ, JS AF LEE, TH OGNIBENE, FP SCHWARTZ, JS TI CORRELATES OF EXTERNAL RESEARCH SUPPORT AMONG RESPONDENTS TO THE 1990 AMERICAN FEDERATION FOR CLINICAL RESEARCH SURVEY SO CLINICAL RESEARCH LA English DT Article ID INVESTIGATORS AB To identify correlates of external funding for research, a mail survey of the membership of the American Federation for Clinical Research was conducted. Data were collected from 2,642 respondents on research training environment, current work environment, current sources and amounts of external research support, and probability of remaining in research. Respondents reported that they worked 62.4 +/- 20.4 hours per week, and that their dominant activities were research (37% of time), clinical responsibilities (20%), teaching (15%), and administration (13%). Nearly two-thirds reported some external research funding, including 1,371 (52%) individuals who received support as principal investigators from federal agencies. In multivariate analyses, the probability of having federal or nonprofit foundation support was positively correlated with the number of hours per week devoted to research, the number of grants submitted in the previous two years, the amount of research training during fellowship, and the presence of PhD degree recipients in the research training environment; and negatively correlated with the number of hours per week of clinical, teaching, and administrative activities, and having a PhD degree. In contrast, corporate support was positively correlated with the number of hours of total work per week, but negatively correlated with the amount of time currently devoted to research. Respondents who reported that their probability of remaining in research was decreasing had fewer months of research training, greater clinical responsibilities, and less external research support. We conclude that federal and nonprofit foundation support but not corporate support are positively correlated with the adequacy of research training and the amount of time currently devoted to research, and negatively correlated with clinical responsibilities. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV GEN MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,DIV CLIN EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,DIV GEN MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. NIH,WARREN G MAGNUSON,CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892. UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,GEN MED SECT,PHILADELPHIA,PA 19104. RP LEE, TH (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,DIV CLIN EPIDEMIOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 9 TC 19 Z9 19 U1 0 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP 135 EP 144 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300001 PM 2044345 ER PT J AU AIBA, S BOOKMAN, M KATZ, SI AF AIBA, S BOOKMAN, M KATZ, SI TI LANGERHANS CELLS PROCESS AND PRESENT TUMOR-ASSOCIATED ANTIGENS TO T-HELPER CELL CLONES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A497 EP A497 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302024 ER PT J AU AMAGAI, M KLAUSKOVTUN, V STANLEY, JR AF AMAGAI, M KLAUSKOVTUN, V STANLEY, JR TI SOUTHERN ANALYSIS OF THE 230-KD BULLOUS PEMPHIGOID ANTIGEN (BPA) GENE IN ANIMALS, NORMAL HUMANS AND JUNCTIONAL EPIDERMOLYSIS-BULLOSA (JEB) PATIENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A476 EP A476 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301901 ER PT J AU BALLA, T SIM, SS IIDA, T RHEE, SG CATT, KJ AF BALLA, T SIM, SS IIDA, T RHEE, SG CATT, KJ TI ROLE OF INOSITOL (1,3,4,5)-TETRAKISPHOSPHATE IN CALCIUM SIGNAL GENERATION - STUDIES IN FIBROBLASTS TRANSFECTED WITH INS-P3-KINASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A470 EP A470 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301868 ER PT J AU BATISTA, M CARTLEDGE, TC MERINO, M AXIOTIS, C LORIAUX, DL NIEMAN, L AF BATISTA, M CARTLEDGE, TC MERINO, M AXIOTIS, C LORIAUX, DL NIEMAN, L TI DELAYED ENDOMETRIAL MATURATION INDUCED BY THE ANTIPROGESTIN RU 486 - A POTENTIAL NEW CONTRACEPTIVE STRATEGY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A324 EP A324 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301041 ER PT J AU BERNSTEIN, EF HARISIADIS, L SALOMON, G NORTON, J GLASS, J TALBOT, T SOLLBERG, S UITTO, J BURESH, C GLATSTEIN, E RUSSO, A MITCHELL, JB AF BERNSTEIN, EF HARISIADIS, L SALOMON, G NORTON, J GLASS, J TALBOT, T SOLLBERG, S UITTO, J BURESH, C GLATSTEIN, E RUSSO, A MITCHELL, JB TI TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) IMPROVES HEALING OF RADIATION-IMPAIRED WOUNDS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,SURG BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A510 EP A510 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302104 ER PT J AU BERZOFSKY, JA PENDLETON, CD CLERICI, M AHLERS, J LUCEY, DR PUTNEY, SD SHEARER, GM AF BERZOFSKY, JA PENDLETON, CD CLERICI, M AHLERS, J LUCEY, DR PUTNEY, SD SHEARER, GM TI PEPTIDES CONTAINING MULTIDETERMINANT CLUSTERS OF HUMAN-IMMUNODEFICIENCY-VIRUS ENVELOPE INDUCE MURINE AND HUMAN T-CELL RESPONSES IN DIVERSE HISTOCOMPATIBILITY TYPES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A282 EP A282 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300821 ER PT J AU BLOK, B TAYLOR, RS GONZALEZ, A SIMON, M KING, C SOLOMON, W ELLIS, C JAFFE, H COOPER, KD AF BLOK, B TAYLOR, RS GONZALEZ, A SIMON, M KING, C SOLOMON, W ELLIS, C JAFFE, H COOPER, KD TI PERIPHERAL-BLOOD LEUKOCYTE SUBSETS IN ATOPIC-DERMATITIS - EFFECT OF GAMMA INTERFERON SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MICHIGAN,DEPT DERMATOL,ANN ARBOR,MI 48109. ALLEN PK VET ADM HOSP,ALLEN PK,MI. NIH,BETHESDA,MD 20892. GENENTECH INC,SAN FRANCISCO,CA 94080. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A498 EP A498 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302031 ER PT J AU BURCH, RM MAHAN, LC AF BURCH, RM MAHAN, LC TI OLIGONUCLEOTIDES ANTISENSE TO MESSENGER-RNA FOR INTERLEUKIN-1 RECEPTORS BLOCK THE EFFECTS OF INTERLEUKIN-1 IN CELL-CULTURE AND INVIVO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NOVA PHARMACEUT CORP,BALTIMORE,MD. NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A314 EP A314 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300987 ER PT J AU BURKE, EM YOON, SC MARTIN, GR AF BURKE, EM YOON, SC MARTIN, GR TI ALTERED TRANSCRIPTIONAL REGULATION OF COLLAGENASE IN HUMAN DERMAL FIBROBLASTS FROM OLDER DONORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,NIH,GRC,MOL GENET LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A200 EP A200 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300345 ER PT J AU BUTRYNSKI, JE SPIEGEL, AM AF BUTRYNSKI, JE SPIEGEL, AM TI TRANSIENT EXPRESSION AND SUBCELLULAR-LOCALIZATION OF PHOSDUCIN AND THE BETA AND GAMMA SUBUNITS OF G-PROTEINS IN COS CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,MOLEC PATHOPHYS BRANCH,BETHESDA,MD. HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,COCONUT GROVE,FL 33133. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A353 EP A353 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301195 ER PT J AU CARTER, RH PARK, DJ RHEE, SG FEARON, DT AF CARTER, RH PARK, DJ RHEE, SG FEARON, DT TI TYROSINE PHOSPHORYLATION OF PHOSPHOLIPASE-C INDUCED BY MEMBRANE IGM IN B-LYMPHOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A294 EP A294 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300882 ER PT J AU CHEN, G FOLK, JE HOLADAY, J NIGRA, T AF CHEN, G FOLK, JE HOLADAY, J NIGRA, T TI A NEW CLASS OF INHIBITORS TO TRANSGLUTAMINASE - THE ISOTHIOCYANATES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MEDICIS PHARMACEUT CORP,NEW YORK,NY. NATL INST DENTAL RES,BETHESDA,MD. WASHINGTON HOSP CTR,DEPT DERMATOL,WASHINGTON,DC 20010. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A538 EP A538 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302270 ER PT J AU CID, M KLEINMAN, H GRANT, D FAUCI, AS HOFFMAN, GS AF CID, M KLEINMAN, H GRANT, D FAUCI, AS HOFFMAN, GS TI ESTRADIOL INCREASES LEUKOCYTE ADHESION TO TNF-STIMULATED ENDOTHELIAL-CELL MONOLAYERS - IMPLICATIONS FOR THE PATHOGENESIS OF TAKAYASU ARTERITIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A224 EP A224 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300476 ER PT J AU CIZZA, G BRADY, LS CHROUSOS, GP GOLD, PW AF CIZZA, G BRADY, LS CHROUSOS, GP GOLD, PW TI THE STEADY-STATE MESSENGER-RNA OF CORTICOTROPIN-RELEASING HORMONE IN THE PARAVENTRICULAR NUCLEUS OF THE HYPOTHALAMUS AND PROOPIOMELANOCORTIN IN THE ANTERIOR-PITUITARY IS PROGRESSIVELY DECREASING IN AGING MALE 344 FISCHER RATS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. NATL INST CHILD HLTH & DEV,DEV ENDOCRINOL BRANCH,BETHESADA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A392 EP A392 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301418 ER PT J AU COBB, JP NATANSON, C SOLOMON, MA KOEV, LA HOFFMAN, WD BANKS, SM DANNER, RL AF COBB, JP NATANSON, C SOLOMON, MA KOEV, LA HOFFMAN, WD BANKS, SM DANNER, RL TI NG-AMINO-L-ARGININE, AN INHIBITOR OF NITRIC-OXIDE SYNTHASE, INCREASES LETHALITY IN CANINE ENDOTOXIC-SHOCK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A321 EP A321 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301025 ER PT J AU COHEN, PJ KATZ, SI AF COHEN, PJ KATZ, SI TI CULTURED HUMAN LANGERHANS CELLS CAN PROCESS AND PRESENT INTACT PROTEIN ANTIGENS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A531 EP A531 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302232 ER PT J AU DIGIOVANNA, JJ TURNER, ML PECK, GL ABANGAN, DL AF DIGIOVANNA, JJ TURNER, ML PECK, GL ABANGAN, DL TI RECOMBINANT INTERFERON GAMMA TREATMENT OF BASAL-CELL CARCINOMA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A504 EP A504 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302065 ER PT J AU DLUGOSZ, AA KNOPF, JL YUSPA, SH AF DLUGOSZ, AA KNOPF, JL YUSPA, SH TI MESSENGER-RNA ENCODING PROTEIN-KINASE-C ALPHA, DELTA, EPSILON, AND ZETA IS EXPRESSED IN NORMAL AND NEOPLASTIC MOUSE KERATINOCYTES INVITRO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. GENET INST,CAMBRIDGE,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A485 EP A485 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301953 ER PT J AU DOBRZANSKI, DJ CORJAY, M KAUR, G WORLAND, PJ SAUSVILLE, EA BATTEY, J AF DOBRZANSKI, DJ CORJAY, M KAUR, G WORLAND, PJ SAUSVILLE, EA BATTEY, J TI NEUROMEDIN-B INDUCED INCREASE IN INRACELLULAR CALCIUM IN H345 CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NINCDS,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A357 EP A357 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301213 ER PT J AU EICHACKER, PO FARESE, A HOFFMAN, W BANKS, SM WAISMAN, Y DANNER, RL MACVITTIE, T NATANSON, C AF EICHACKER, PO FARESE, A HOFFMAN, W BANKS, SM WAISMAN, Y DANNER, RL MACVITTIE, T NATANSON, C TI ALVEOLAR NEUTROPHILS ARE MAXIMAL DURING RECOVERY OF PULMONARY-FUNCTION IN A CANINE MODEL OF HUMAN SEPTIC SHOCK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A453 EP A453 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301782 ER PT J AU EICHACKER, PO WAISMAN, Y HOFFMAN, W BANKS, SM RICHMOND, S MACVITTIE, T AF EICHACKER, PO WAISMAN, Y HOFFMAN, W BANKS, SM RICHMOND, S MACVITTIE, T TI EFFECTS OF PENTOTHAL ANESTHESIA ON OXYGEN DELIVERY AND CONSUMPTION IN A CANINE MODEL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. ARMED FORCES RADIOBIOL RES INST,DEF NUCL AGCY,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A265 EP A265 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300717 ER PT J AU EICHENHOLZ, PW EICHACKER, PQ HOFFMAN, WD DANNER, RL BANKS, SM PARRILLO, JE NATANSON, C AF EICHENHOLZ, PW EICHACKER, PQ HOFFMAN, WD DANNER, RL BANKS, SM PARRILLO, JE NATANSON, C TI INCREASING DOSES OF TUMOR-NECROSIS-FACTOR PRODUCE DIFFERENT PATTERNS OF ACUTE AND SUBACUTE MYOCARDIAL DYSFUNCTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. ARMED FORCES RADIOBIOL RES INST,DEF NUCL AGCY,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A321 EP A321 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301023 ER PT J AU ELGART, GW AMAGAI, M STANLEY, JR AF ELGART, GW AMAGAI, M STANLEY, JR TI 5' EXTENSION CLONING OF BULLOUS PEMPHIGOID (BP) CDNA BY RAPID AMPLIFICATION OF CDNA ENDS (RACE) WITH POLYMERASE CHAIN-REACTION (PCR) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A478 EP A478 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301909 ER PT J AU FABRY, ME COSTANTINI, F PACHNIS, A HOFRICHTER, J CHRISTOPH, GW FACTOR, S NAGEL, RL AF FABRY, ME COSTANTINI, F PACHNIS, A HOFRICHTER, J CHRISTOPH, GW FACTOR, S NAGEL, RL TI A TRANSGENIC MOUSE LINE EXPRESSING A HIGH-LEVEL OF HBS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10461. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT PATHOL,BRONX,NY 10461. NIH,CHEM PHYS LAB,WASHINGTON,DC. COLUMBIA UNIV COLL PHYS & SURG,DEPT GENET,NEW YORK,NY 10032. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A267 EP A267 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300730 ER PT J AU FALANGA, V SU, WQ DANIELPOUR, D KATZ, MH ROBERTS, AB SPORN, MB AF FALANGA, V SU, WQ DANIELPOUR, D KATZ, MH ROBERTS, AB SPORN, MB TI TGF-BETA-1 MESSENGER-RNA AND PROTEIN-SYNTHESIS BY HUMAN DERMAL FIBROBLASTS ARE CONTROLLED BY OXYGEN-TENSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,DEPT DERMATOL,MIAMI,FL 33152. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A561 EP A561 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302408 ER PT J AU FALLOON, J ONEILL, D LAFON, S ROGERS, M TUAZON, C FEUERSTEIN, I MASUR, H AF FALLOON, J ONEILL, D LAFON, S ROGERS, M TUAZON, C FEUERSTEIN, I MASUR, H TI 566C80 FOR THE TREATMENT OF PNEUMOCYSTIS PNEUMONIA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A216 EP A216 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300433 ER PT J AU FINZI, E SKOUGE, J CELANO, P BLAKE, M AF FINZI, E SKOUGE, J CELANO, P BLAKE, M TI CELLULAR-LOCALIZATION OF RETINOIC ACID RECEPTOR-GAMMA IN NORMAL AND NEOPLASTIC SKIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,DEPT DERMATOL ONCOL,BALTIMORE,MD 21218. NIA,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A486 EP A486 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301958 ER PT J AU FISHER, WR ZECH, LA STACPOOLE, PW AF FISHER, WR ZECH, LA STACPOOLE, PW TI CONTROL OF APOLIPOPROTEIN-B METABOLISM IN FAMILIAL HYPERCHOLESTEROLEMIA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV FLORIDA,COLL MED,GAINESVILLE,FL 32611. NCI,MATH BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A146 EP A146 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300029 ER PT J AU FLANAGAN, JR BECKER, KG OZATO, K AF FLANAGAN, JR BECKER, KG OZATO, K TI A CLONED DNA-BINDING PROTEIN-SPECIFIC FOR A NEGATIVE REGULATORY REGION OF MURINE LEUKEMIA VIRUS-RELATED RETROVIRUSES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV IOWA,DEPT INTERNAL MED,IOWA CITY,IA 52242. NICHHD,LDMI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A255 EP A255 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300659 ER PT J AU FRIEDMAN, E GORDELADZE, JO GEJMAN, PV AF FRIEDMAN, E GORDELADZE, JO GEJMAN, PV TI HYPERTROPHIC CARDIOMYOPATHY - FAILURE TO DEMONSTRATE EITHER ACTIVATING MUTATIONS IN GS ALPHA GENE OR MUTATIONS IN THE CARDIAC BETA MYOSIN HEAVY-CHAIN GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIMH,MOLEC PATHOPHYS BRANCH,BETHESDA,MD 20892. NIMH,NIDDK & NEUROGENET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A256 EP A256 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300668 ER PT J AU FRITZ, S DALE, J GOULD, B STROBER, W STRAUS, SE AF FRITZ, S DALE, J GOULD, B STROBER, W STRAUS, SE TI LYMPHOCYTE PHENOTYPE ANALYSIS SUGGESTS CHRONIC IMMUNE STIMULATION IN PATIENTS WITH THE CHRONIC FATIGUE SYNDROME SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LCI,BETHESDA,MD 20892. NCI,FREDERICK CANC RES FACIL,DYN COI,FREDERICK,MD 21701. DYNCORP,PRI,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A435 EP A435 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301673 ER PT J AU GAN, SQ MARKOVA, N KORGE, B KIM, IG STEINERT, P AF GAN, SQ MARKOVA, N KORGE, B KIM, IG STEINERT, P TI THE CORRECT EXPRESSION OF A HUMAN MINI PROFILAGGRIN GENE IN TRANSGENIC MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A561 EP A561 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302412 ER PT J AU GOEDERT, JJ ODONNELL, M CARRINGTON, M ALFORD, WG MANN, DL AF GOEDERT, JJ ODONNELL, M CARRINGTON, M ALFORD, WG MANN, DL TI INFLUENCE OF HLA ON DISEASE PROGRESSION AND OUTCOME IN HIV-1 INFECTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,PROGRAM RESOURCES INC,DATA MANAGEMENT SERV INC,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A462 EP A462 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301827 ER PT J AU GREENBERG, AS EGAN, JJ WEK, SA TAKEDA, T LONDOS, C KIMMEL, AK AF GREENBERG, AS EGAN, JJ WEK, SA TAKEDA, T LONDOS, C KIMMEL, AK TI PERILIPIN, A LIPID DROPLET-ASSOCIATED, ADIPOCYTE SPECIFIC PROTEIN - CDNA CLONING AND EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 3 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A287 EP A287 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300844 ER PT J AU GREENBERG, AS CALVO, JC RONDINONE, CM KIMMEL, AR NORDAN, RP LONDOS, C AF GREENBERG, AS CALVO, JC RONDINONE, CM KIMMEL, AR NORDAN, RP LONDOS, C TI INHIBITION OF ADIPOCYTE DIFFERENTIATION BY INTERLEUKIN-6, A POSSIBLE MEDIATOR OF TUMOR-NECROSIS-FACTOR ACTIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NATL INST DIABET & DIGEST & KIDNEY,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A225 EP A225 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300485 ER PT J AU GRIFFITHS, C ROSENTHAL, D LEACH, K WANG, T YUSPA, S VOORHEES, J FISHER, G AF GRIFFITHS, C ROSENTHAL, D LEACH, K WANG, T YUSPA, S VOORHEES, J FISHER, G TI HUMAN EPIDERMAL TRANSGLUTAMINASE ACTIVITY AND IMMUNOSTAINING ARE INCREASED INVIVO AND DECREASED IN KERATINOCYTES INVITRO BY RETINOIC ACID TREATMENT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MICHIGAN,DEPT DERMATOL,ANN ARBOR,MI 48109. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A524 EP A524 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302193 ER PT J AU HALABAN, R FUNASAKA, Y RUBIN, J YARDEN, Y WILLIAMS, D LYMAN, S BIRNBAUM, D AF HALABAN, R FUNASAKA, Y RUBIN, J YARDEN, Y WILLIAMS, D LYMAN, S BIRNBAUM, D TI GROWTH-FACTORS AND TYROSINE PROTEIN-KINASES IN NORMAL AND MALIGNANT MELANOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT DERMATOL,NEW HAVEN,CT 06510. NCI,CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. WEIZMANN INST SCI,DEPT CHEM IMMUNOL,IL-76100 REHOVOT,ISRAEL. IMMUNEX CORP,SEATTLE,WA. INST J PAOLI I CALMETTES,F-13009 MARSEILLE,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A487 EP A487 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301964 ER PT J AU HALLFRISCH, J SINGH, VN MULLER, DC BALDWIN, H BANNON, ME ANDRES, R AF HALLFRISCH, J SINGH, VN MULLER, DC BALDWIN, H BANNON, ME ANDRES, R TI HIGH PLASMA VITAMIN-C ASSOCIATED WITH INCREASED PLASMA HDL-CHOLESTEROL AND HDL2-CHOLESTEROL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,NIH,GERONTOL RES CTR,BALTIMORE,MD. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A203 EP A203 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300358 ER PT J AU HEROLD, KC BLUESTONE, JA PARIHAR, A WEIGNER, A FITCH, FW HIRSCH, R AF HEROLD, KC BLUESTONE, JA PARIHAR, A WEIGNER, A FITCH, FW HIRSCH, R TI PREVENTION OF AUTOIMMUNE DIABETES WITH A NON-ACTIVATING FORM OF ANTI-CD3 MONOCLONAL-ANTIBODY (MAB) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. UNIV CHICAGO,DEPT PATHOL,CHICAGO,IL 60637. NCI,EXPT MM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A211 EP A211 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300404 ER PT J AU HOFFMAN, WD POLLACK, M BANKS, SM KOEV, L SOLOMON, MA DANNER, RL KOLES, N GUELDE, G YATSIV, I MOUGINIS, T ELIN, RJ HOSSEINI, JM PORTER, JC NATANSON, C AF HOFFMAN, WD POLLACK, M BANKS, SM KOEV, L SOLOMON, MA DANNER, RL KOLES, N GUELDE, G YATSIV, I MOUGINIS, T ELIN, RJ HOSSEINI, JM PORTER, JC NATANSON, C TI A CONTROLLED TRIAL OF IGG MONOCLONAL ANTIENDOTOXIN ANTIBODIES IN A CANINE MODEL OF HUMAN SEPTIC SHOCK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,AFFRI,DEPT MED,DEF NUCL AGENCY,BETHESDA,MD 20814. NR 0 TC 5 Z9 5 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A164 EP A164 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300136 ER PT J AU HOLBROOK, KA UNDERWOOD, RA DALE, BA THACHE, SM WUEPPER, KD BANKSSCHLEGEL, S AF HOLBROOK, KA UNDERWOOD, RA DALE, BA THACHE, SM WUEPPER, KD BANKSSCHLEGEL, S TI CORNIFIED CELL-ENVELOPE (CCE) IN HUMAN FETAL SKIN - INVOLUCRIN, KERATOLININ, LORICRIN AND TRANSGLUTAMINASE EXPRESSION AND ACTIVITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. UNIV WASHINGTON,SCH MED,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,DEPT BIOL STRUCT,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,DEPT ORAL BIOL,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,DEPT PERIODONT,SEATTLE,WA 98195. UNIV WASHINGTON,SCH DENT,SEATTLE,WA 98108. TEXAS A&M UNIV SYST,DEPT MED BIOCHEM,COLLEGE STN,TX 77843. UNIV OREGON,HLTH SCI CTR,DEPT DERMATOL,EUGENE,OR 97403. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A524 EP A524 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302196 ER PT J AU HORGAN, KJ TANAKA, Y SHAW, S AF HORGAN, KJ TANAKA, Y SHAW, S TI PAUCITY OF NAIVE CD4+ T-CELLS IN INTESTINAL LYMPHANGIECTASIA MAY REFLECT SELECTIVE SUBSET LOSSES FROM GUT LYMPHATICS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,EIB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A213 EP A213 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300418 ER PT J AU HUANG, SZ RODGERS, GP ZENG, FY SCHECHTER, AN ZENG, YT AF HUANG, SZ RODGERS, GP ZENG, FY SCHECHTER, AN ZENG, YT TI IDENTIFICATION OF BETA-THALASSEMIA CARRIERS USING CDNA AMPLIFICATION OF RETICULOCYTE MESSENGER-RNA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 SHANGHAI INST MED GENET,SHANGHAI,PEOPLES R CHINA. NIH,CHEM BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A171 EP A171 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300180 ER PT J AU HUFF, CA ROSENTHAL, DS YUSPA, SH ROOP, DR AF HUFF, CA ROSENTHAL, DS YUSPA, SH ROOP, DR TI IDENTIFICATION AND CHARACTERIZATION OF A COMPLEX REGULATORY ARRAY 3' TO THE GENE ENCODING HUMAN KERATIN-1 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. BAYLOR UNIV,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A487 EP A487 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301968 ER PT J AU IMMERMAN, KL LUCAS, C HARVEY, J NOEL, G AF IMMERMAN, KL LUCAS, C HARVEY, J NOEL, G TI TEACHING THE CAGE - STUDENTS CAN DO BETTER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NATL INST ALCOHOL ABUSE & ALCOHOLISM,BETHESDA,MD. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A618 EP A618 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302750 ER PT J AU JAFFE, HA LONGENECKER, G ROSENFELD, MA MCELVANEY, NG LEMARCHAND, P GANT, TW THORGEIRSSON, SS STRATFORDPERRICAUDET, LD PERRICAUDET, M JALLAT, S PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF JAFFE, HA LONGENECKER, G ROSENFELD, MA MCELVANEY, NG LEMARCHAND, P GANT, TW THORGEIRSSON, SS STRATFORDPERRICAUDET, LD PERRICAUDET, M JALLAT, S PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI ADENOVIRAL MEDIATED TRANSFER AND EXPRESSION OF A NORMAL HUMAN ALPHA-1-ANTITRYPSIN CDNA IN PRIMARY RAT HEPATOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. INST GUSTAVE ROUSSY,F-94805 VILLEJUIF,FRANCE. INST G ROUSSY,TRANSGENE,FRANCE. INST G ROUSSY,STRASBOURG,FRANCE. RI McElvaney, Noel/A-6809-2010 NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A302 EP A302 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300924 ER PT J AU JANE, SM NEY, PA NIENHUIS, AW AF JANE, SM NEY, PA NIENHUIS, AW TI COMPETITION BETWEEN THE GAMMA-GLOBIN AND BETA-GLOBIN PROMOTERS FOR THE LOCUS-CONTROL REGION SITE-2 ENHANCER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A344 EP A344 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301147 ER PT J AU JU, WD TAYEBI, N VELU, TJ VASS, WC LOWY, DR AF JU, WD TAYEBI, N VELU, TJ VASS, WC LOWY, DR TI AUTOCRINE SYNTHESIS OF TGF-ALPHA INDUCES FOCAL TRANSFORMATION WHICH CAN BE SUPPRESSED BY PARACRINE TREATMENT WITH TGF-ALPHA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A488 EP A488 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301972 ER PT J AU KAELIN, WG PALLAS, DC DECAPRIO, JA KAYE, FJ LIVINGSTON, DM AF KAELIN, WG PALLAS, DC DECAPRIO, JA KAYE, FJ LIVINGSTON, DM TI CELLULAR PROTEINS THAT INTERACT SPECIFICALLY WITH THE RETINOBLASTOMA GENE-PRODUCT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NCI,BETHESDA,MD 20892. RI kaye, frederic/E-2437-2011 NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A339 EP A339 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301117 ER PT J AU KALOGERAS, KT GLOWA, JR SAFOS, G SAFOS, P CHROUSOS, GP GOLD, PW AF KALOGERAS, KT GLOWA, JR SAFOS, G SAFOS, P CHROUSOS, GP GOLD, PW TI HYPOTHALAMIC-PITUITARY-ADRENAL AXIS RESPONSES TO BENZODIAZEPINE WITHDRAWAL - POTENTIAL ROLE OF CRH IN THE WITHDRAWAL SYNDROME SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIMH,CNE,BETHESDA,MD 20892. NICHHD,DEB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A324 EP A324 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301038 ER PT J AU KELLY, JF MORRIS, PP KAYE, JA MIDHA, KK RAPOPORT, SI SONCRANT, TT AF KELLY, JF MORRIS, PP KAYE, JA MIDHA, KK RAPOPORT, SI SONCRANT, TT TI HALOPERIDOL PHARMACODYNAMICS IN HEALTHY-YOUNG VERSUS ELDERLY HUMAN-SUBJECTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A393 EP A393 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301421 ER PT J AU KENNEY, RT MALECH, HL ROBERTS, RL GALLIN, JI LETO, TL AF KENNEY, RT MALECH, HL ROBERTS, RL GALLIN, JI LETO, TL TI AMNIOCENTESIS DIAGNOSIS OF A NORMAL FETUS IN A FAMILY WITH P67PHOX DEFICIENT CHRONIC GRANULOMATOUS-DISEASE USING A POLYMORPHIC GENE MARKER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LCI,BACTERIAL DIS SECT,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,DEPT PEDIAT,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A274 EP A274 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300776 ER PT J AU KERN, JA GAZDAR, A FENDLY, B SHEPARD, M AF KERN, JA GAZDAR, A FENDLY, B SHEPARD, M TI AN ANTI-P185HER2 ANTIBODY HAS ANTIPROLIFERATIVE EFFECTS ON LUNG-CANCER CELL-LINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV IOWA,DEPT MED,IOWA CITY,IA 52242. NCI,BETHESDA,MD 20892. GENENTECH INC,SAN FRANCISCO,CA 94080. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A279 EP A279 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300800 ER PT J AU KHAN, WA WETSEL, WC MERCHENTHALER, I RIVERA, H NEGROVILAR, A HANNUN, Y AF KHAN, WA WETSEL, WC MERCHENTHALER, I RIVERA, H NEGROVILAR, A HANNUN, Y TI DIFFERENTIAL TISSUE DISTRIBUTION OF PROTEIN-KINASE-C ISOENZYMES - ENDOCRINE LOCALIZATION OF PKO-ZETA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. NIEHS,MOLEC & INTEGRATED NEUROSCI LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A451 EP A451 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301771 ER PT J AU KING, CL NUTMAN, TB AF KING, CL NUTMAN, TB TI REGULATION OF IGE AND IGG4 RESPONSES BY INTERLEUKIN-4 AND INTERFERON-GAMMA IN HUMAN HELMINTH INFECTIONS - ASSESSMENT BY B-CELL PRECURSOR FREQUENCY-ANALYSIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A289 EP A289 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300854 ER PT J AU KLEINBERG, ME MITAL, D ROTROSEN, D MALECH, HL AF KLEINBERG, ME MITAL, D ROTROSEN, D MALECH, HL TI CHARACTERIZATION OF CYTOCHROME B558 91 KDA SUBUNIT CARBOXYTERMINAL PEPTIDES THAT INHIBIT THE PHAGOCYTE NADPH OXIDASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MARYLAND,SCH MED,DEPT MED,BALTIMORE,MD 21201. NIAID,BACTERIAL DIS SECT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A175 EP A175 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300200 ER PT J AU KOPP, JB WEEKS, BS MARINOS, NJ BRYANT, JL DICKIE, P NOTKINS, AL KLOTMAN, PE AF KOPP, JB WEEKS, BS MARINOS, NJ BRYANT, JL DICKIE, P NOTKINS, AL KLOTMAN, PE TI NEPHROPATHY IN HIV-TRANSGENIC MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,LDBA,BETHESDA,MD 20892. NIDR,LOM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A312 EP A312 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300976 ER PT J AU KORGE, B GAN, SQ KIM, IG MISCHKE, D STEINERT, P AF KORGE, B GAN, SQ KIM, IG MISCHKE, D STEINERT, P TI POLYMORPHISMS OF THE HUMAN KERATIN-10 GENE ARE DUE TO VARIABLE NUMBERS OF GLYCINE LOOPS IN THE END DOMAINS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. FREE UNIV BERLIN,RUDOLF VIRCHOW MED CTR,INST EXPTL ONCOL & TRANSPLANTAT MED,W-1000 BERLIN 33,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A564 EP A564 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302427 ER PT J AU KOVACS, JA BOENNING, C DAVEY, RT WALKER, RJ POLIS, MA FALLOON, J GALETTO, G SEIDEL, E DAVEY, V METCALF, J FAUCI, AS MASUR, H LANE, HC AF KOVACS, JA BOENNING, C DAVEY, RT WALKER, RJ POLIS, MA FALLOON, J GALETTO, G SEIDEL, E DAVEY, V METCALF, J FAUCI, AS MASUR, H LANE, HC TI PHASE I-II TRIAL OF DIDEOXYINOSINE WITH INTERFERON-ALPHA IN THE TREATMENT OF HIV-INFECTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NIH,CCMD,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A220 EP A220 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300454 ER PT J AU KOVACS, JA GREGORY, F BOARMAN, D ALLEGRA, CJ AF KOVACS, JA GREGORY, F BOARMAN, D ALLEGRA, CJ TI INHIBITION OF PNEUMOCYSTIS-CARINII DIHYDROPTEROATE SYNTHASE BY PARAACETAMIDOBENZOIC ACID MAY EXPLAIN THE ACTIVITY OF ISOPRINOSINE IN HIV-INFECTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CCMD,BETHESDA,MD. NCI,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A143 EP A143 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300012 ER PT J AU KWONG, CH MALECH, HL LETO, TL AF KWONG, CH MALECH, HL LETO, TL TI 3-CYTOSOLIC PROTEINS ARE NECESSARY AND SUFFICIENT FOR RECONSTITUTING NADPH OXIDASE IN NEUTROPHIL MEMBRANE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A273 EP A273 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300766 ER PT J AU LICINIO, J WONG, ML ALTEMUS, ME BERNAT, A DEMITRACK, M GOLD, PW AF LICINIO, J WONG, ML ALTEMUS, ME BERNAT, A DEMITRACK, M GOLD, PW TI INTERLEUKIN-1-ALPHA - LOCALIZATION IN BRAIN AND ASSESSMENT OF CENTRAL AND PERIPHERAL LEVELS IN BULIMIA-NERVOSA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06510. NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RI Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A290 EP A290 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300859 ER PT J AU LIPSCHIK, GY GILL, VJ ANDRAWIS, V NELSON, N KOVACS, JA AF LIPSCHIK, GY GILL, VJ ANDRAWIS, V NELSON, N KOVACS, JA TI DETECTION OF PNEUMOCYSTIS-CARINII BY POLYMERASE CHAIN-REACTION IN INDUCED SPUTUM AND BRONCHOALVEOLAR LAVAGE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. NIH,MICROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A144 EP A144 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300014 ER PT J AU LOWREY, CH SORRENTINO, BP NEY, PA BODINE, DM MCDONAGH, KT NIENHUIS, AW AF LOWREY, CH SORRENTINO, BP NEY, PA BODINE, DM MCDONAGH, KT NIENHUIS, AW TI MECHANISM OF NUCLEASE HYPERSENSITIVE SITE FORMATION IN THE GLOBIN LOCUS-CONTROL REGION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A251 EP A251 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300638 ER PT J AU LUCEY, DR MCGUIRE, SA CLERICI, M HENDRIX, CW HALL, K BENTON, J BUTZIN, CA WARD, WW SHEARER, GM BOSWELL, RN AF LUCEY, DR MCGUIRE, SA CLERICI, M HENDRIX, CW HALL, K BENTON, J BUTZIN, CA WARD, WW SHEARER, GM BOSWELL, RN TI SPINAL-FLUID BETA2-MICROGLOBULIN IN 163 NEUROLOGICALLY ASYMPTOMATIC ADULTS WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 WILFORD HALL USAF MED CTR,SAN ANTONIO,TX. NCI,BETHESDA,MD 20892. RI Hendrix, Craig/G-4182-2014 OI Hendrix, Craig/0000-0002-5696-8665 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A145 EP A145 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300025 ER PT J AU MACK, J STEINERT, P AF MACK, J STEINERT, P TI THE MECHANISM OF INTERACTION OF FILAGGRIN WITH KERATIN INTERMEDIATE FILAMENTS - THE IONIC ZIPPER HYPOTHESIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A527 EP A527 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302203 ER PT J AU MAHANTY, S ABRAMS, JS LIMAYE, AP KING, CL NUTMAN, TB AF MAHANTY, S ABRAMS, JS LIMAYE, AP KING, CL NUTMAN, TB TI PARALLEL REGULATION OF IL-4 AND IL-5 IN HUMAN HELMINTH INFECTIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. DNAX RES INST MOLEC & CELLULAR BIOL INC,PALO ALTO,CA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A304 EP A304 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300933 ER PT J AU MANGANIELLO, V TAIRA, M MEACCI, E MOOS, M SMITH, C DEGERMAN, E BELFRAGE, P AF MANGANIELLO, V TAIRA, M MEACCI, E MOOS, M SMITH, C DEGERMAN, E BELFRAGE, P TI ACTIVATION OF A SPECIFIC ADIPOCYTE CAMP PHOSPHODIESTERASE (PDE) IS AN IMPORTANT COMPONENT IN THE ANTILIPOLYTIC ACTION OF INSULIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV LUND,S-22101 LUND,SWEDEN. RI Moos, Malcolm/F-3673-2011 OI Moos, Malcolm/0000-0002-9575-9938 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A382 EP A382 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301364 ER PT J AU MAUVIEL, A REDIN, F PUJOL, JP EVANS, CH AF MAUVIEL, A REDIN, F PUJOL, JP EVANS, CH TI MODULATION OF HUMAN DERMAL FIBROBLAST EXTRACELLULAR-MATRIX METABOLISM BY THE LYMPHOKINE LEUKOREGULIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. CHU CAEN,BIOCHIM TISSUE CONJONCTIF,F-14033 CAEN,FRANCE. NIH,DIV CANC ETIOL,BIOL LAB,TUMOR BIOL SECT,BETHESDA,MD 20892. RI REDINI, Francoise/K-7981-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A513 EP A513 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302119 ER PT J AU MCDONAGH, KT BODINE, DM BYRNE, E AGRICOLA, B NIENHUIS, AW AF MCDONAGH, KT BODINE, DM BYRNE, E AGRICOLA, B NIENHUIS, AW TI LONG-TERM, MULTILINEAGE RECONSTITUTION OF PRIMATES WITH HEMATOPOIETIC STEM-CELLS TRANSDUCED BY A RECOMBINANT RETROVIRUS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A326 EP A326 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301050 ER PT J AU MEIER, CA MCCLASKEY, JH USALA, SJ DICKSTEIN, BM MUCHMORE, P BERCU, BB SAMUELS, HH WEINTRAUB, BD AF MEIER, CA MCCLASKEY, JH USALA, SJ DICKSTEIN, BM MUCHMORE, P BERCU, BB SAMUELS, HH WEINTRAUB, BD TI DOMINANT NEGATIVE POTENCY OF MUTANT T3 RECEPTORS FROM 2 KINDREDS WITH GENERALIZED THYROID-HORMONE RESISTANCE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. E CAROLINA UNIV,GREENVILLE,NC 27834. NYU MED CTR,NEW YORK,NY 10016. UNIV S FLORIDA,TAMPA,FL 33620. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A293 EP A293 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300878 ER PT J AU MIXSON, AJ PARRILLA, R USALA, SJ RANSOM, SC MCCLASKEY, JH MCPHERSON, JA WEINTRAUB, BD AF MIXSON, AJ PARRILLA, R USALA, SJ RANSOM, SC MCCLASKEY, JH MCPHERSON, JA WEINTRAUB, BD TI DIVERSE PHENOTYPES OF 11 KINDREDS WITH GENERALIZED THYROID-HORMONE RESISTANCE AND NOVEL MUTATIONS IN THE GENE ENCODING THE T3-BETA RECEPTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. E CAROLINA UNIV,GREENVILLE,NC 27834. RI Parrilla, Roberto/B-6307-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A293 EP A293 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300877 ER PT J AU MOVSESIAN, MA SMITH, CJ KRALL, J BRISTOW, MR MANGANIELLO, VC AF MOVSESIAN, MA SMITH, CJ KRALL, J BRISTOW, MR MANGANIELLO, VC TI SARCOPLASMIC RETICULUM-ASSOCIATED CYCLIC-AMP PHOSPHODIESTERASE ACTIVITY IN NORMAL AND FAILING HUMAN HEARTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV UTAH,MED CTR,DIV CARDIOL,SALT LAKE CITY,UT 84112. NIH,CELL METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A159 EP A159 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300105 ER PT J AU MURTAGH, JJ MOWATT, MR LEE, CM MISHIMA, K TAKADA, T NASH, TE MOSS, J VAUGHAN, M AF MURTAGH, JJ MOWATT, MR LEE, CM MISHIMA, K TAKADA, T NASH, TE MOSS, J VAUGHAN, M TI GUANINE NUCLEOTIDE-DEPENDENT SIGNALING PATHWAYS IN THE INTESTINAL PARASITE GIARDIA-LAMBLIA - ISOLATION OF A GENE ENCODING A 20-KDA ADP-RIBOSYLATION FACTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A156 EP A156 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300085 ER PT J AU NAKAMURA, H YOSHIMURA, K MCELVANEY, NG CHANGSTROMAN, Z BIRRER, P AF NAKAMURA, H YOSHIMURA, K MCELVANEY, NG CHANGSTROMAN, Z BIRRER, P TI NEUTROPHIL ELASTASE IN CYSTIC-FIBROSIS LUNG EPITHELIAL LINING FLUID INDUCES INTERLEUKIN-8 GENE-EXPRESSION IN BRONCHIAL EPITHELIAL-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. RI McElvaney, Noel/A-6809-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A292 EP A292 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300870 ER PT J AU OBRIEN, MC MITSUYA, H AF OBRIEN, MC MITSUYA, H TI ACTIVATION OF HUMAN IMMUNODEFICIENCY VIRUS-1 (HIV-1) BY DNA DEMETHYLATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A220 EP A220 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300452 ER PT J AU OGNIBENE, FP LEVINE, SJ SHELHAMER, JH FEUERSTEIN, IM GILL, VJ MASUR, H AF OGNIBENE, FP LEVINE, SJ SHELHAMER, JH FEUERSTEIN, IM GILL, VJ MASUR, H TI DIAGNOSTIC YIELD FOR PNEUMOCYSTIS-CARINII PNEUMONIA (PCP) IN AIDS PATIENTS INCREASES WITH MULTIPLE STAINING TECHNIQUES AND RADIOGRAPHICALLY DIRECTED BRONCHOALVEOLAR LAVAGE (BAL) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,CTR CLIN,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A217 EP A217 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300435 ER PT J AU OPARA, EC HUBBARD, VS BURCH, WM AKWARI, OE AF OPARA, EC HUBBARD, VS BURCH, WM AKWARI, OE TI LINOLEATE BUT NOT PALMITATE STIMULATES GLUCAGON-SECRETION BY ISOLATED PERIFUSED ISLETS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. NIDDKD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A449 EP A449 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301755 ER PT J AU PAAR, D SAVARESE, B BURKE, RL MARGOLIS, D MEIER, J MARKOFF, L ASHLEY, R COREY, L ADAIR, S DEKKER, C STRAUS, SE AF PAAR, D SAVARESE, B BURKE, RL MARGOLIS, D MEIER, J MARKOFF, L ASHLEY, R COREY, L ADAIR, S DEKKER, C STRAUS, SE TI ABILITY OF A RECOMBINANT HERPES-SIMPLEX VIRUS TYPE-2 GLYCOPROTEIN-D VACCINE TO INDUCE ANTIBODY-TITERS COMPARABLE TO THOSE FOLLOWING GENITAL HERPES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LCI,BETHESDA,MD 20892. UNIV WASHINGTON,SEATTLE,WA 98195. CHIRON CORP,EMERYVILLE,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A216 EP A216 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300429 ER PT J AU PARMER, RJ PETZ, LN RIETOW, MG HELMAN, LJ OCONNOR, DT AF PARMER, RJ PETZ, LN RIETOW, MG HELMAN, LJ OCONNOR, DT TI HUMAN CHROMOGRANIN-A IS TARGETED TO AND RELEASED FROM REGULATED SECRETORY VESICLES IN RAT PHEOCHROMOCYTOMA CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,DEPT MED,SAN DIEGO,CA 92161. UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A172 EP A172 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300183 ER PT J AU PARRIS, CN KRAEMER, KH AF PARRIS, CN KRAEMER, KH TI CELLULAR-TRANSFORMATION ALTERS ULTRAVIOLET MUTAGENESIS IN XERODERMA-PIGMENTOSUM CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A483 EP A483 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301942 ER PT J AU PAULY, RR CHENG, L LAKATTA, EG PASSANITI, A AF PAULY, RR CHENG, L LAKATTA, EG PASSANITI, A TI VASCULAR SMOOTH-MUSCLE CELLS INVADE RECONSTITUTED BASEMENT-MEMBRANE IN RESPONSE TO PDGF SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A254 EP A254 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300655 ER PT J AU PERLISH, JS CONTARD, P FISHER, LW MACDONALD, ED JACOBS, L TERMINE, TD FLEISCHMAJER, R AF PERLISH, JS CONTARD, P FISHER, LW MACDONALD, ED JACOBS, L TERMINE, TD FLEISCHMAJER, R TI INVIVO AND INVITRO DEMONSTRATION OF DECORIN INTERACTING WITH HUMAN INTERSTITIAL COLLAGEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CUNY MT SINAI SCH MED,NEW YORK,NY 10029. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A514 EP A514 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302125 ER PT J AU PETERSON, J SANTAMARINAFOJO, S HAYDEN, M DEEB, S BRUNZELL, J AF PETERSON, J SANTAMARINAFOJO, S HAYDEN, M DEEB, S BRUNZELL, J TI FUNCTIONAL-EVALUATION OF MUTANT LIPOPROTEIN-LIPASE CONTAINING MISSENSE MUTATIONS ENCODED BY EXON-5 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV WASHINGTON,SEATTLE,WA 98195. NIH,BETHESDA,MD 20892. UNIV BRITISH COLUMBIA,VANCOUVER V6T 1W5,BC,CANADA. RI Hayden, Michael/D-8581-2011 OI Hayden, Michael/0000-0001-5159-1419 NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A276 EP A276 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300787 ER PT J AU PETTY, KJ NIKODEM, VM AF PETTY, KJ NIKODEM, VM TI CLONING OF THE CDNA FOR A FACTOR THAT BINDS CACCC BOXES FROM THE PROMOTERS OF THE RAT MALIC ENZYME AND HUMAN C-FOS GENES (CBBF) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A344 EP A344 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301144 ER PT J AU PETTY, KJ RAPTIS, A NIKODEM, VM AF PETTY, KJ RAPTIS, A NIKODEM, VM TI CHARACTERIZATION OF NUCLEAR FACTORS BINDING TO A CIS-REGULATORY ELEMENT OF THE RAT MALIC ENZYME (ME) GENE PROMOTER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A207 EP A207 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300381 ER PT J AU PRICE, SR TSAI, SC STEVENS, LA MISHIMA, K MOSS, J VAUGHAN, M AF PRICE, SR TSAI, SC STEVENS, LA MISHIMA, K MOSS, J VAUGHAN, M TI MAJOR TUMOR NECROSIS FACTOR-STIMULATED MYRISTOYLATED PROTEINS IN HUMAN FIBROBLASTS ARE THE ALPHA 20-KDA GUANINE NUCLEOTIDE-BINDING ADP-RIBOSYLATION FACTORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,NATL HEART LUNG & BLOOD INST,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A208 EP A208 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300386 ER PT J AU PUNNONEN, K YUSPA, SH AF PUNNONEN, K YUSPA, SH TI EFFECTS OF UVB IRRADIATION ON THE FORMATION OF MEMBRANE LIPID DERIVED MEDIATORS OF SIGNAL TRANSDUCTION IN MURINE KERATINOCYTES IN CULTURE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A549 EP A549 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302340 ER PT J AU RESZKA, K MIYAKE, Y ALENA, F JIMBOW, K AF RESZKA, K MIYAKE, Y ALENA, F JIMBOW, K TI GENERATION OF RADICAL SPECIES FROM MELANOCYTOTOXIC AGENTS, PHENOLIC THIOETHER AMINES UPON TYROSINASE ACTIVATION - AN ESR STUDY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIEHS,MOLEC BIOL LAB,RES TRIANGLE PK,NC 27709. HOKKAIDO UNIV,DEPT POLYMER SCI,SAPPORO,HOKKAIDO 060,JAPAN. UNIV ALBERTA,DIV DERMATOL & CUTANEOUS SCI,EDMONTON T6G 2E1,ALBERTA,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A541 EP A541 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302290 ER PT J AU ROSENFELD, MA YOSHIMURA, K STIER, LE TRAPNELL, BC STRATFORDPERRICAUDET, LD PERRICAUDET, M DALEMANS, W JALLAT, S MERCENIER, A PAVIRANI, A LECOCQ, JP GUGGINO, WB CRYSTAL, RG AF ROSENFELD, MA YOSHIMURA, K STIER, LE TRAPNELL, BC STRATFORDPERRICAUDET, LD PERRICAUDET, M DALEMANS, W JALLAT, S MERCENIER, A PAVIRANI, A LECOCQ, JP GUGGINO, WB CRYSTAL, RG TI INVIVO TRANSFER OF THE HUMAN CYSTIC-FIBROSIS GENE TO THE RESPIRATORY EPITHELIUM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. INST GUSTAVE ROUSSY,F-94805 VILLEJUIF,FRANCE. TRANSGENE SA,STRASBOURG,FRANCE. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NR 0 TC 3 Z9 3 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A311 EP A311 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300975 ER PT J AU ROSENTHAL, J CUSACK, N THURMAN, G PETERSON, V MALECH, H AMBRUSO, D AF ROSENTHAL, J CUSACK, N THURMAN, G PETERSON, V MALECH, H AMBRUSO, D TI NEUTROPHILS FROM BURN PATIENTS DEMONSTRATE A QUANTATIVE DEFICIENCY OF THE 47KDA PHOSPHOPROTEIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV COLORADO,DEPT PEDIAT,DENVER,CO 80202. UNIV COLORADO,DEPT SURG,DENVER,CO 80202. UNIV COLORADO,DEPT MED,DENVER,CO 80202. BONFILS BLOOD CTR,DENVER,CO. NIAID,BACTERIAL DIS SECT,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A274 EP A274 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300771 ER PT J AU RUSSO, TA GUENTHER, JE FRANK, MM AF RUSSO, TA GUENTHER, JE FRANK, MM TI COMPLEMENT RESISTANCE DETERMINANTS IN ESCHERICHIA-COLI SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,BETHESDA,MD. DUKE UNIV,DURHAM,NC 27706. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A241 EP A241 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300577 ER PT J AU SARRET, Y KLEINMAN, HK WOODLEY, DT AF SARRET, Y KLEINMAN, HK WOODLEY, DT TI THE PEPTIDE (CSIKVAVS-NH2) NEAR THE AMINO TERMINUS OF THE LAMININ A CHAIN MARKEDLY INHIBITS HUMAN KERATINOCYTE LOCOMOTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 STANFORD UNIV,STANFORD,CA 94305. NIH,NATL INST DENT RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A514 EP A514 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302128 ER PT J AU SCHAEFER, JR RADER, DJ GREGG, RE FAIRWELL, T ZECH, LA KINDT, MR DAVIGNON, J BREWER, HB AF SCHAEFER, JR RADER, DJ GREGG, RE FAIRWELL, T ZECH, LA KINDT, MR DAVIGNON, J BREWER, HB TI INVIVO METABOLISM OF APOLIPOPROTEIN A-I IN FAMILIAL HYPERCHOLESTEROLEMIA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A333 EP A333 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301088 ER PT J AU SCHNITTMAN, SM SINGER, KH GREENHOUSE, JJ STANLEY, SK WHICHARD, LP HAYNES, BF FAUCI, AS AF SCHNITTMAN, SM SINGER, KH GREENHOUSE, JJ STANLEY, SK WHICHARD, LP HAYNES, BF FAUCI, AS TI THE ROLE OF THE THYMIC MICROENVIRONMENT IN THE PATHOGENESIS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 (HIV 1) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. DUKE UNIV,DURHAM,NC 27706. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A220 EP A220 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300451 ER PT J AU SEDMAN, SA BARBOSA, MS HUBBERT, NL VASS, WC SCHILLER, JT LOWY, DR AF SEDMAN, SA BARBOSA, MS HUBBERT, NL VASS, WC SCHILLER, JT LOWY, DR TI THE FULL LENGTH E6 PROTEIN OF A HIGH-RISK HPV IS MORE ACTIVE THAN E6 FROM A LOW-RISK HPV SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A557 EP A557 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302386 ER PT J AU SEIAOKI, S KLEINER, DE CHANDRA, R YARCHOAN, R HUSSON, R PIZZO, PA BRODER, S MITSUYA, H AF SEIAOKI, S KLEINER, DE CHANDRA, R YARCHOAN, R HUSSON, R PIZZO, PA BRODER, S MITSUYA, H TI QUANTITATIVE-ANALYSIS OF HIV-1 DNA AND MESSENGER-RNA IN VARIOUS TISSUES FROM PATIENTS WITH AIDS OR ARC BY POLYMERASE CHAIN-REACTION (PCR) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CLIN CTR,BETHESDA,MD. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A283 EP A283 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300826 ER PT J AU SHENKER, A GOLDSMITH, P UNSON, CG SPIEGEL, AM AF SHENKER, A GOLDSMITH, P UNSON, CG SPIEGEL, AM TI THE G-PROTEIN COUPLED TO THE THROMBOXANE A2 RECEPTOR IN HUMAN PLATELETS IS A MEMBER OF THE NOVEL GQ FAMILY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NATL INST DIABET & DIGEST & KIDNEY,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD. ROCKEFELLER UNIV,DEPT BIOCHEM,NEW YORK,NY 10021. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A343 EP A343 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301138 ER PT J AU SHIMADA, T NIENHUIS, AW AF SHIMADA, T NIENHUIS, AW TI TARGETED GENE-TRANSFER INTO CD4 EXPRESSING CELLS USING A RECOMBINANT HIV RETROVIRAL VECTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A283 EP A283 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300824 ER PT J AU SOLOMON, MA ALEXANDER, HR BALABAN, RS COBB, JP HOFFMAN, WD KOEV, LA CUNNION, RE YATSIV, I BANKS, SM KIM, DK DANNER, RL ROBERTS, WC NATANSON, C AF SOLOMON, MA ALEXANDER, HR BALABAN, RS COBB, JP HOFFMAN, WD KOEV, LA CUNNION, RE YATSIV, I BANKS, SM KIM, DK DANNER, RL ROBERTS, WC NATANSON, C TI MYOCARDIAL CYTOSOLIC PHOSPHORYLATION POTENTIAL IN A CANINE SEPSIS MODEL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,CARDIAC ENERGET LAB,SURG BRANCH,BETHESDA,MD 20892. NIH,DEPT PATHOL,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A164 EP A164 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300138 ER PT J AU SOLOMON, MA CORREA, R HOFFMAN, WD CUNNION, RE COBB, JP DANNER, RL FERRANS, VJ NATANSON, C AF SOLOMON, MA CORREA, R HOFFMAN, WD CUNNION, RE COBB, JP DANNER, RL FERRANS, VJ NATANSON, C TI ULTRASTRUCTURAL AND HISTOLOGIC-CHANGES ASSOCIATED WITH MYOCARDIAL DEPRESSION IN A CANINE MODEL OF SEPTIC SHOCK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,DEPT CRIT CARE MED,ULTRASTRUCT SECT,PATHOL BRANCH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A321 EP A321 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301026 ER PT J AU STANLEY, SK SCHNITTMAN, SM GREENHOUSE, JJ HATCH, WC LYMAN, WD FAUCI, AS AF STANLEY, SK SCHNITTMAN, SM GREENHOUSE, JJ HATCH, WC LYMAN, WD FAUCI, AS TI CHARACTERIZATION OF AN EARLY THYMOCYTE CELL-LINE WHICH IS CHRONICALLY INFECTED WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,IMMUNREGULAT LAB,BETHESDA,MD 20892. ALBERT EINSTEIN MED SCH,DEPT PATHOL,BRONX,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A216 EP A216 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300431 ER PT J AU STEINERT, P MACK, J KORGE, B GAN, SC KIM, JG YONEDA, K IDLER, W HAYNES, S STEVEN, A AF STEINERT, P MACK, J KORGE, B GAN, SC KIM, JG YONEDA, K IDLER, W HAYNES, S STEVEN, A TI STRUCTURE AND POSSIBLE FUNCTIONS OF THE GLYCINE LOOP MOTIF ON EPIDERMAL STRUCTURAL PROTEINS - THE VELCRO HYPOTHESIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NIAMS,STRUCT BIOL RES LAB,BETHESDA,MD. NICHHD,MOLEC GENET LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A530 EP A530 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302223 ER PT J AU TANG, A UDEY, MC AF TANG, A UDEY, MC TI ULTRAVIOLET B RADIATION MODULATES ICAM-1 (CD54) EXPRESSION BY LANGERHANS CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,DERM BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A194 EP A194 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300309 ER PT J AU TENNENBAUM, T YUSPA, SH KNOX, BM SOBEL, ME CASTRONOVO, V YAMADA, Y DE LUCA, LM AF TENNENBAUM, T YUSPA, SH KNOX, BM SOBEL, ME CASTRONOVO, V YAMADA, Y DE LUCA, LM TI ALTERATIONS IN ATTACHMENT TO LAMININ AND LOCALIZATION OF LAMININ BINDING-PROTEINS DURING DIFFERENTIATION OF PRIMARY MOUSE KERATINOCYTES INVITRO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI, BETHESDA, MD 20892 USA. NIDR, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A495 EP A495 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302015 ER PT J AU THIRMAN, MJ ALBRECHT, JH HAAS, MA ERICKSON, RR CHERWITZ, DL PARK, SS GELBOIN, HV HOLTZMAN, JL AF THIRMAN, MJ ALBRECHT, JH HAAS, MA ERICKSON, RR CHERWITZ, DL PARK, SS GELBOIN, HV HOLTZMAN, JL TI METABOLISM OF BENZO(A) PYRENE BY AORTAS OF INDUCED RATS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MINNESOTA,DEPT MED,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT PHARMACOL,MINNEAPOLIS,MN 55455. VET ADM MED CTR,MINNEAPOLIS,MN 55417. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A406 EP A406 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301500 ER PT J AU VAMVAKOPOULOS, NC MARGIORIS, AN CHROUSOS, GP AF VAMVAKOPOULOS, NC MARGIORIS, AN CHROUSOS, GP TI FUNCTIONAL-ANALYSIS OF A DISTAL PROMOTER-LIKE STRUCTURE OF THE HUMAN CORTICOTROPIN RELEASING HORMONE GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,PEDIAT ENDOCRINOL SECT,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A460 EP A460 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301818 ER PT J AU VANDERVORT, AL STEUTZ, P DANNER, RL AF VANDERVORT, AL STEUTZ, P DANNER, RL TI 3-AZA-LIPID X-4-PHOSPHATE (ALXP) SPECIFICALLY ANTAGONIZES ENDOTOXIN-INDUCED PRIMING OF HUMAN NEUTROPHILS INDEPENDENT OF CYTOSOLIC CALCIUM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A164 EP A164 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300135 ER PT J AU WAISMAN, Y MACVITTIE, TJ FARESE, A BANKS, SM HOFFMANN, WD SOUZA, L NATANSON, C EICHACKER, PQ AF WAISMAN, Y MACVITTIE, TJ FARESE, A BANKS, SM HOFFMANN, WD SOUZA, L NATANSON, C EICHACKER, PQ TI A CONTROLLED TRIAL OF GRANULOCYTE COLONY STIMULATING FACTOR IN A CANINE MODEL OF HUMAN BACTERIAL SEPSIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT EXPTL HEMATOL,BETHESDA,MD 20892. NIH,AFRRI,BETHESDA,MD 20892. NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,CTR EMERGENCY MED TRAUMA,WASHINGTON,DC. AMGEN INC,THOUSAND OAKS,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A165 EP A165 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300139 ER PT J AU WALSH, CE LIU, JM YOUNG, NS NIENHUIS, AW SAMULSKI, RJ AF WALSH, CE LIU, JM YOUNG, NS NIENHUIS, AW SAMULSKI, RJ TI GENE-TRANSFER AND HIGH-LEVEL EXPRESSION OF A HUMAN GAMMA GLOBIN GENE MEDIATED BY A NOVEL ADENOASSOCIATED VIRUS (AAV) VECTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,CHB,BETHESDA,MD. UNIV PITTSBURGH,DEPT BIOL SCI,PITTSBURGH,PA 15260. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A325 EP A325 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301045 ER PT J AU WONDISFORD, FE STEINFELDER, HJ WEINTRAUB, BD RADOVICK, S AF WONDISFORD, FE STEINFELDER, HJ WEINTRAUB, BD RADOVICK, S TI THE PITUITARY SPECIFIC FACTOR (PIT-1) OR A CLOSELY RELATED PROTEIN MEDIATES CAMP AND TRH RESPONSIVENESS OF THE HUMAN THYROTROPIN BETA-SUBUNIT (HTSH-BETA) GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CASE WESTERN RESERVE UNIV,SCH MED,CLEVELAND,OH 44106. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A206 EP A206 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300375 ER PT J AU WONG, M GORELICK, DA AF WONG, M GORELICK, DA TI CARDIAC RESPONSES TO ABSTINENCE AND DRINKING IN ALCOHOL-DEPENDENT MALES - SERIAL OBSERVATIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,LOS ANGELES,CA. NIDA,ARC,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A408 EP A408 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301509 ER PT J AU WRIGHT, JJ KENNISON, J KASSIS, J KELLY, K SIEBENLIST, U AF WRIGHT, JJ KENNISON, J KASSIS, J KELLY, K SIEBENLIST, U TI DROSOPHILA HOMOLOG OF ZINC FINGER TRANSCRIPTIONAL FACTOR INDUCED BY HUMAN RETROVIRUSES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. US FDA,BETHESDA,MD 20014. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A169 EP A169 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300167 ER PT J AU YASUMURA, S KIEBZAK, GM GOTHELF, T SHORT, L SPEERS, R DILMANIAN, FA JONES, K SPANNE, P SCHIDLOVSKY, G GLAROS, D HEYMSFIELD, S AF YASUMURA, S KIEBZAK, GM GOTHELF, T SHORT, L SPEERS, R DILMANIAN, FA JONES, K SPANNE, P SCHIDLOVSKY, G GLAROS, D HEYMSFIELD, S TI BODY-COMPOSITION IN AGING MALE-RATS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 SUNY HLTH SCI CTR,BROOKLYN,NY. BROOKHAVEN NATL LAB,UPTON,NY 11973. ST LUKES ROOSEVELT HOSP,NEW YORK,NY 10025. NIA,GRC,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A657 EP A657 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302981 ER PT J AU YATSIV, I KOEV, LA HOFFMAN, WD SOLOMON, MA DANNER, RL DOLAN, D BANKS, SM NATANSON, C AF YATSIV, I KOEV, LA HOFFMAN, WD SOLOMON, MA DANNER, RL DOLAN, D BANKS, SM NATANSON, C TI A CONTROLLED TRIAL OF CONTINUOUS ARTERIAL-VENOUS HEMOFILTRATION FAILS TO IMPROVE OUTCOME IN A CANINE MODEL OF HUMAN SEPTIC SHOCK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A264 EP A264 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300716 ER PT J AU YONEDA, K MCBRIDE, W IDLER, W HOHL, D STEINERT, P AF YONEDA, K MCBRIDE, W IDLER, W HOHL, D STEINERT, P TI STRUCTURE OF THE HUMAN LORICRIN-GENE - LINKAGE AT 1Q21 WITH PROFILAGGRIN AND INVOLUCRIN GENES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,BIOCHEM LAB,BETHESDA,MD 20892. CHU VAUDOIS,SERV DERMATOL,CH-1011 LAUSANNE,SWITZERLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A496 EP A496 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302021 ER PT J AU YOSHIMURA, K NAKAMURA, H TRAPNELL, BC DALEMANS, W MERCENIER, A PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF YOSHIMURA, K NAKAMURA, H TRAPNELL, BC DALEMANS, W MERCENIER, A PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI TRANSCRIPTIONAL MODULATION OF HUMAN CYSTIC-FIBROSIS GENE-EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULMONARY BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A192 EP A192 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300296 ER PT J AU ZHENG, ZS POLAKOWSKA, RR JOHNSON, AC GOLDSMITH, LA AF ZHENG, ZS POLAKOWSKA, RR JOHNSON, AC GOLDSMITH, LA TI REGULATION OF EPIDERMAL GROWTH-FACTOR RECEPTOR GENE-TRANSCRIPTION BY RETINOIC ACID SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV ROCHESTER,DEPT DERMATOL,ROCHESTER,NY 14627. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A497 EP A497 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302023 ER PT J AU BERGER, MP RODBARD, D AF BERGER, MP RODBARD, D TI A PHARMACODYNAMIC APPROACH TO OPTIMIZING INSULIN THERAPY SO COMPUTER METHODS AND PROGRAMS IN BIOMEDICINE LA English DT Article DE DIABETES MANAGEMENT; INSULIN OPTIMIZATION; MATHEMATICAL MODELING; SIMULATION ID COMPUTER-SIMULATION; BLOOD-GLUCOSE; SENSITIVITY; ADJUSTMENT; DOSAGE; MODEL AB We have developed a program for simulation and optimization of insulin therapy in patients with insulin-dependent diabetes. The program, denoted GLUCOJECT, is based on a physiologic model of minimal complexity, which describes the pharmacokinetics of absorption and clearance of subcutaneous insulin and the dynamics of glucose utilization as dependent on both prevailing glucose and insulin levels. With self-monitored glucose values and insulin doses collected with one of several commercially available memory meters, GLUCOJECT reconstructs an average or 'typical' daily plasma glucose and insulin profile and displays them in a graph. The program then calculates the expected rate of glucose utilization, which permits calculation of the rate of glucose entry into plasma from both endogenous (hepatic) and exogenous (dietary) sources. In turn, this allows one to calculate an 'ideal' plasma insulin profile required to maintain a relatively constant 'ideal' plasma glucose level. GLUCOJECT can evaluate several different insulin regimens involving various combinations of short-, intermediate- and long-acting insulins, and select the one(s) most closely approximating the ideal or optimal insulin profile, using a least-squares criterion. For any optimized insulin regimen, GLUCOJECT calculates and displays the predicted time course of plasma glucose. These features make the program attractive as an educational tool for both patients and health care professionals and could potentially assist in the management of patients with insulin-dependent diabetes. C1 NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NR 15 TC 11 Z9 11 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0169-2607 J9 COMPUT METH PROG BIO JI Comput. Meth. Programs Biomed. PD APR PY 1991 VL 34 IS 4 BP 241 EP 253 DI 10.1016/0169-2607(91)90107-5 PG 13 WC Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Engineering, Biomedical; Medical Informatics SC Computer Science; Engineering; Medical Informatics GA FT263 UT WOS:A1991FT26300001 PM 1873991 ER PT J AU PALMER, EA HARDY, RJ DAVIS, BR STEIN, JA MOWERY, RL TUNG, B PHELPS, DL SCHAFFER, DB FLYNN, JT PHILLIPS, CL AF PALMER, EA HARDY, RJ DAVIS, BR STEIN, JA MOWERY, RL TUNG, B PHELPS, DL SCHAFFER, DB FLYNN, JT PHILLIPS, CL TI OPERATIONAL ASPECTS OF TERMINATING RANDOMIZATION IN THE MULTICENTER TRIAL OF CRYOTHERAPY FOR RETINOPATHY OF PREMATURITY SO CONTROLLED CLINICAL TRIALS LA English DT Article DE CLINICAL TRIALS; TERMINATION OF ENROLLMENT; MULTICENTER CLINICAL TRIALS; RANDOMIZED CONTROLLED TRIAL; RETINOPATHY OF PREMATURITY; TERMINATION ID TERM CLINICAL-TRIALS; HEART ATTACK TRIAL; AID AB The Multicenter Trial of Cryotherapy for Retinopathy of Prematurity (CRYOROP) is a randomized clinical trial sponsored by the National Eye Institute (NEI) designed to test whether cryotherapy applied to eyes of premature infants with a specified extent of stage 3+ ROP significantly decreases the incidence of an unfavorable outcome. An unfavorable outcome is defined as either retinal detachment or a retinal fold and was determined at 3 months posttreatment by the use of a masked photographic system. Enrollment into the trial was terminated on recommendation of the Data and Safety Monitoring Committee 9 months before the scheduled closing date for enrollment because of demonstrated treatment benefit. The purpose of this article is to discuss the operations involved in the orderly termination of enrollment and dissemination of results from this trial. These activities included preparation of trial participants and staff, release of trial information, continuing patient care, data collection and coding, and publication of trial results. C1 UNIV MIAMI,CORAL GABLES,FL 33124. UNIV ROCHESTER,ROCHESTER,NY 14627. UNIV PENN,PHILADELPHIA,PA 19104. UNIV TEXAS,AUSTIN,TX 78712. NEI,BETHESDA,MD 20892. RP PALMER, EA (reprint author), OREGON HLTH SCI UNIV,DEPT OPHTHALMOL,L467,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. FU NEI NIH HHS [5 U01 EY05874] NR 23 TC 8 Z9 8 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD APR PY 1991 VL 12 IS 2 BP 277 EP 292 DI 10.1016/0197-2456(91)90025-H PG 16 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA FE793 UT WOS:A1991FE79300002 PM 1645640 ER PT J AU RUTTIMANN, UE POLLACK, MM AF RUTTIMANN, UE POLLACK, MM TI OBJECTIVE ASSESSMENT OF CHANGING MORTALITY RISKS IN PEDIATRIC INTENSIVE-CARE UNIT PATIENTS SO CRITICAL CARE MEDICINE LA English DT Article DE PEDIATRICS; MORTALITY; SEVERITY OF ILLNESS INDEX; PATIENT OUTCOME ASSESSMENT; EFFICIENCY; LOGISTIC REGRESSION; RECEIVER OPERATING CHARACTERISTIC ANALYSIS; PATIENT OUTCOME ASSESSMENT; INTENSIVE CARE UNIT; PROGNOSIS ID ORGAN SYSTEM FAILURE; TRAUMA SCORE; APACHE-II; CRITERIA; SEVERITY; PREDICTION; CHILDREN; SURVIVAL; INFANTS; INDEX AB Objective: To develop and validate a mortality risk predictor based on physiologic data that estimates daily the probability of a patient dying within the next 24 hrs as that probability changes with disease and recovery. Setting: Nine pediatric ICUs in tertiary care centers. Patients: Data from 1,401 patients (116 deaths, 5,521 days of care) were used for predictor development, and 1,227 patients (105 deaths, 4,597 days of care) provided data for predictor validation. Methods: The predictor was developed by logistic regression analysis using the Pediatric Risk of Mortality scores of all previous days as potential predictor variables. Performance was measured by the area under the receiver operating characteristic curve (A(z)), and by the comparison of the daily predicted vs. observed patient status in five mortality risk groups (< 0.01, 0.01 to 0.05, 0.05 to 0.15, 0.15 to 0.3, > 0.3) using chi-square goodness-of-fit tests. Measurements and Main Results: Only the most recent and the admission day Pediatric Risk of Mortality scores (with a weighting ratio of 3:1) contributed significantly (p < .05) to the prediction. The overall prediction attained an accuracy of A(z) = 0.904. The daily number and distribution of survivors and nonsurvivors in the five mortality risk groups were well predicted in the total sample (CHI-2[5 degrees of freedom] = 2.51; p > .75), and each ICU separately (CHI-2[5 degrees of freedom] range 2.41 to 7.96; all p > .15). This dynamic predictor improved (p < .01) ICU outcome prediction over an admission-day predictor and, in the opinion of the authors, is essential for pediatric ICU efficiency analysis. Conclusions: The predictor is valid for assessing the 24-hr mortality risk in pediatric ICU patients hospitalized in other tertiary care institutions, different from those used for predictor development. The predicted mortality risks allow prospective patient stratification into risk groups. The ability of this predictor to follow risk changes over time expands its applicability over static predictors by enabling the charting of patient courses, and permitting ICU efficiency analysis. C1 CHILDRENS HOSP,NATL MED CTR,DEPT CRIT CARE MED,111 MICHIGAN AVE,WASHINGTON,DC 20010. NIDR,DIAGNOST SYST BRANCH,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,SCH MED,DEPT ANESTHESIOL,WASHINGTON,DC 20052. GEORGE WASHINGTON UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20052. FU PHS HHS [MCJ-110527] NR 38 TC 23 Z9 24 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD APR PY 1991 VL 19 IS 4 BP 474 EP 483 DI 10.1097/00003246-199104000-00004 PG 10 WC Critical Care Medicine SC General & Internal Medicine GA FH611 UT WOS:A1991FH61100004 PM 2019132 ER PT J AU WISTOW, G ROQUEMORE, E KIM, HS AF WISTOW, G ROQUEMORE, E KIM, HS TI ANOMALOUS BEHAVIOR OF BETA-B1-CRYSTALLIN SUBUNITS FROM AVIAN LENSES SO CURRENT EYE RESEARCH LA English DT Article ID BETA-CRYSTALLIN; CHICKEN LENS; EYE LENS; STRUCTURAL PROTEIN; DELTA-CRYSTALLIN; POLYPEPTIDE; ENZYME; EXPRESSION; SEQUENCE; INVITRO AB In soluble extracts of bird lenses, crystallin subunits of apparent sizes between 30kDa and 40kDa show considerable variability in both abundance and mobility in sodium dodecyl sulfate polycrylamide gel electrophoresis (SDS PAGE). This is only partly due to the taxon-specific distribution of lactate dehydrogenase-B (LDH-B)/epsilon-crystallin. Here we show that, in spite of high conservation in primary sequence, beta-B1-crystallin subunits of avian lenses have a markedly slower migration in SDS PAGE than those of mammals and that the apparent subunit size of beta-B1-crystallin varies among birds. This may be at least partly due to unusual post-translational modifications, since beta-B1-crystallins of adult birds react strongly in a glycan detection procedure. No other crystallins in birds or mammals share this strong reaction. Modification of beta-B1-crystallin could have interesting consequences for the formation of high molecular weight beta-crystallin aggregates in bird lenses. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205. RP WISTOW, G (reprint author), NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA42486] NR 36 TC 10 Z9 10 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD APR PY 1991 VL 10 IS 4 BP 313 EP 319 DI 10.3109/02713689108996337 PG 7 WC Ophthalmology SC Ophthalmology GA FM937 UT WOS:A1991FM93700005 PM 2070640 ER PT J AU ROBINSON, WG MCCALEB, ML FELD, LG MICHAELIS, OE LAVER, N MERCANDETTI, M AF ROBINSON, WG MCCALEB, ML FELD, LG MICHAELIS, OE LAVER, N MERCANDETTI, M TI DEGENERATED INTRAMURAL PERICYTES (GHOST CELLS) IN THE RETINAL CAPILLARIES OF DIABETIC RATS SO CURRENT EYE RESEARCH LA English DT Article ID ALDOSE REDUCTASE INHIBITOR; GALACTOSE-FED DOGS; BB WISTAR RAT; CORPULENT RAT; MURAL CELLS; RETINOPATHY; SUCROSE; PREVENTION; MODEL; COMPLICATIONS AB One of the earliest histopathological signs of diabetic retinopathy is a selective loss of intramural pericytes from retinal capillaries. In the present study, the retinal vessels of rats with streptozotocin-induced diabetes (STZ Wistar) and rats with genetically-induced insulin dependent diabetes mellitus (BB Wistar) and non-insulin dependent diabetes mellitus (SHR/N-corpulent) were examined after 6 to 8 months duration for diabetes-related retinal microangiopathies. The SHR/N-corpulent (cp) rats were fed a 54% sucrose diet, whereas the STZ Wistar and BB Wistar rats were fed laboratory chow for 32 to 36 weeks. In all the diabetic rats, the retinal capillaries in enzyme-digested flat mounts exhibited an increase in periodic-acid-Schiff (PAS) staining and loss of pericytes compared to their respective euglycemic controls. Pericyte "ghosts", like those defined in human diabetes as intramural pockets lacking normal cell contents, were documented by high resolution micrographs in all the diabetic rats. Endothelial cell proliferation, capillary dilation, and varicose loop formation were noted in some of the diabetic rats. Hence, similar capillary lesions were found in very different groups of diabetic rats. The findings suggest that a chronic high tissue concentration of glucose is the underlying factor which triggers pathogenesis in the pericyte. Hyperglycemia-induced activation of endogenous aldose reductase of the polyol pathway is probably the initial insult, but other factors such as advanced glycosylation products may affect the final outcome. C1 WYETH AYERST RES,METAB DISORDERS,PRINCETON,NJ. CHILDRENS HOSP,DIV NEPHROL,BUFFALO,NY 14222. SUNY BUFFALO,SCH MED & BIOMED SCI,DEPT OPHTHALMOL,BUFFALO,NY 14260. USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,BELTSVILLE,MD 20705. RP ROBINSON, WG (reprint author), NEI,BLDG 10,ROOM 10N-105,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 40 TC 57 Z9 58 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD APR PY 1991 VL 10 IS 4 BP 339 EP 350 DI 10.3109/02713689108996340 PG 12 WC Ophthalmology SC Ophthalmology GA FM937 UT WOS:A1991FM93700008 PM 1829996 ER PT J AU McCormick, A Campisi, J AF McCormick, Anna Campisi, Judith TI Cellular aging and senescence SO CURRENT OPINION IN CELL BIOLOGY LA English DT Article AB Differentiated eukaryotic cells have only a finite capacity for cell division. This limitation is thought to be a cellular manifestation of organismal aging, and a restraint to tumor progression. The molecular basis for cellular senescence is not known, but a molecular framework for understanding this phenomenon has recently been established. C1 [McCormick, Anna] NIA, Biol Aging Program, Bethesda, MD 20892 USA. [Campisi, Judith] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Div Cell & Mol Biol, Berkeley, CA 94720 USA. RP McCormick, A (reprint author), NIA, Biol Aging Program, Bethesda, MD 20892 USA. NR 30 TC 53 Z9 54 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0955-0674 EI 1879-0410 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD APR PY 1991 VL 3 IS 2 BP 230 EP 234 DI 10.1016/0955-0674(91)90144-N PG 5 WC Cell Biology SC Cell Biology GA V39FX UT WOS:000209398000011 PM 1883615 ER PT J AU KRUISBEEK, A RAJEWSKY, K AF KRUISBEEK, A RAJEWSKY, K TI LYMPHOCYTE DEVELOPMENT - EDITORIAL OVERVIEW SO CURRENT OPINION IN IMMUNOLOGY LA English DT Editorial Material C1 UNIV COLOGNE,INST GENET,W-5000 COLOGNE 41,GERMANY. RP KRUISBEEK, A (reprint author), NIH,DEPT HLTH & HUMAN SCI,BLDG 10,RM 12N-226,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD APR PY 1991 VL 3 IS 2 BP 169 EP 170 DI 10.1016/0952-7915(91)90045-3 PG 2 WC Immunology SC Immunology GA FK593 UT WOS:A1991FK59300001 ER PT J AU SPANGRUDE, GJ AF SPANGRUDE, GJ TI HEMATOPOIETIC STEM-CELL DIFFERENTIATION SO CURRENT OPINION IN IMMUNOLOGY LA English DT Article ID COLONY-FORMING CELLS; BONE-MARROW TRANSPLANTATION; GROWTH-FACTOR; C-KIT; W-LOCUS; T-CELL; PROTO-ONCOGENE; STROMAL CELLS; SI-LOCUS; MOUSE AB Hematopoietic stem cells can be identified and isolated from hematopoietic tissues of mammalian hosts. Assay systems that solely reflect hematopoietic stem cell activity are being developed, and new cytokines that influence hematopoietic stem-cell proliferation and differentiation have been described. Differentiation pathways that lead to lymphoid stages of hematopoiesis have also been suggested. RP SPANGRUDE, GJ (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 54 TC 26 Z9 27 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD APR PY 1991 VL 3 IS 2 BP 171 EP 178 DI 10.1016/0952-7915(91)90046-4 PG 8 WC Immunology SC Immunology GA FK593 UT WOS:A1991FK59300002 PM 2069744 ER PT J AU COHEN, DI LANE, HC AF COHEN, DI LANE, HC TI NEW UNDERSTANDING OF THE BIOLOGY OF HIV SO CURRENT OPINION IN INFECTIOUS DISEASES LA English DT Article AB Knowledge regarding the in vivo and in vitro properties of human immunodeficiency virus replication is rapidly expanding. In particular, studies into the mechanism of action of three genes essential for virus growth, the gag gene encoding the p24 viral core protein, the rev gene required for the export of human immunodeficiency virus envelope RNA from the nucleus to the cytoplasm of infected cells, and the tat gene responsible for transcriptional and translational viral activation, have led to the discovery of mutations capable of dominantly disrupting the function of each of these three genes. Culturing the plasma of human immunodeficiency virus-infected individuals for transmissible virus has emerged as a sensitive and potentially predictive assay for disease progression. Both primate and murine models have been refined by the isolation of molecular clones capable of inducing acquired immunodeficiency syndrome in rhesus monkeys and by the demonstration that human immunodeficiency virus-infected mice treated with zidovudine exhibit retardation of viral spread. RP COHEN, DI (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B09,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 0951-7375 J9 CURR OPIN INFECT DIS JI Curr. Opin. Infect. Dis. PD APR PY 1991 VL 4 IS 2 BP 179 EP 184 DI 10.1097/00001432-199104000-00010 PG 6 WC Infectious Diseases SC Infectious Diseases GA FK411 UT WOS:A1991FK41100010 ER PT J AU SAWCHUK, WS AF SAWCHUK, WS TI ANCILLARY DIAGNOSTIC-TESTS FOR DETECTION OF HUMAN PAPILLOMAVIRUS INFECTION SO DERMATOLOGIC CLINICS LA English DT Article C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8635 J9 DERMATOL CLIN JI Dermatol. Clin. PD APR PY 1991 VL 9 IS 2 BP 277 EP 286 PG 10 WC Dermatology SC Dermatology GA FK673 UT WOS:A1991FK67300008 PM 1647906 ER PT J AU GLICK, AB MCCUNE, BK ABDULKAREM, N FLANDERS, KC LUMADUE, JA SMITH, JM SPORN, MB AF GLICK, AB MCCUNE, BK ABDULKAREM, N FLANDERS, KC LUMADUE, JA SMITH, JM SPORN, MB TI COMPLEX REGULATION OF TGF-BETA EXPRESSION BY RETINOIC ACID IN THE VITAMIN-A-DEFICIENT RAT SO DEVELOPMENT LA English DT Article DE TGF-BETA; RETINOIC ACID; VITAMIN-A DEFICIENCY ID TRANSFORMING GROWTH-FACTOR; TRACHEAL EPITHELIAL-CELLS; TERMINAL DIFFERENTIATION; KERATINOCYTES; RECEPTOR; FACTOR-BETA-2; RNA; IDENTIFICATION; PROLIFERATION AB We report the results of a histochemical study, using polyclonal antipeptide antibodies to the different TGF-beta isoforms, which demonstrates that retinoic acid regulates the expression of TGF-beta in the vitamin A-deficient rat. Basal expression of TGF-beta-2 diminished under conditions of vitamin A deficiency. Treatment with retinoic acid caused a rapid and transient induction of TGF-beta-2 and TGF-beta-3 in the epidermis, tracheobronchial and alveolar epithelium, and intestinal mucosa. Induction of TGF-beta-1 expression was also observed in the epidermis. In contrast to these epithelia, expression of the three TGF-beta isoforms increased in vaginal epithelium during vitamin A deficiency, and decreased following systemic administration of retinoic acid. Our results show for the first time the widespread regulation of TGF-beta expression by retinoic acid in vivo, and suggest a possible mechanism by which retinoids regulate the functions of both normal and pre-neoplastic epithelia. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. NR 46 TC 113 Z9 115 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD APR PY 1991 VL 111 IS 4 BP 1081 EP & PG 0 WC Developmental Biology SC Developmental Biology GA FK576 UT WOS:A1991FK57600022 PM 1879351 ER PT J AU WODA, BA HANDLER, ES GREINER, DL REYNOLDS, C MORDES, JP ROSSINI, AA AF WODA, BA HANDLER, ES GREINER, DL REYNOLDS, C MORDES, JP ROSSINI, AA TI LYMPHOCYTE-T REQUIREMENT FOR DIABETES IN RT6-DEPLETED DIABETES-RESISTANT BB RATS SO DIABETES LA English DT Article ID NATURAL-KILLER CELLS; BREEDING WORCESTER RAT; MONOCLONAL-ANTIBODIES; LYMPHOPENIA; SUBSETS; PREVENTION; MELLITUS; ANTIGEN AB Diabetes-prone (DP) BB rats develop spontaneous autoimmune insulin-dependent diabetes mellitus (IDDM). The cell populations involved in the expression of diabetes are not precisely known but probably include natural killer (NK) cells, macrophages, and T lymphocytes. Because the DP rat has few lymphocytes of the CD5+/CD+ phenotype, cytotoxic T lymphocytes (T(c)) are not believed to be important in the process. Diabetes-resistant (DR) BB rats that are depleted of RT6+ T lymphocytes also become diabetic and provide an additional model of IDDM. We report that diabetes in DR rats depleted of RT6+ T lymphocytes is prevented by the concomitant depletion of either the CD5+ or the CD8+ population. In contrast, coadministration of anti-asialoganglioside(M1) (alpha-ASG(M1)), an antiserum that principally recognizes NK cells, failed to prevent hyperglycemia in RT6-depleted rats. We propose that the initiation of diabetes in both DP and RT6-depleted DR rats is T-lymphocyte dependent. However, the final common pathway leading to autoimmune beta-cell destruction in IDDM may be different in these models. The RT6-depleted DR rat requires a cell that is sensitive to anti-CD8 (possibly a T(c)), whereas the DP rat requires an anti-ASG(M1)-sensitive cell. C1 UNIV MASSACHUSETTS,MED CTR,DEPT MED,WORCESTER,MA 01605. UNIV CONNECTICUT,CTR HLTH,DEPT PATHOL,FARMINGTON,CT 06032. NCI,FREDERICK CANC RES FACIL,BIOL RESOURCES BRANCH,FREDERICK,MD 21701. RP WODA, BA (reprint author), UNIV MASSACHUSETTS,MED CTR,DEPT PATHOL,55 LAKE AVE N,WORCESTER,MA 01655, USA. FU NIDDK NIH HHS [DK-36042, DK-41235, DK-36024] NR 42 TC 9 Z9 9 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD APR PY 1991 VL 40 IS 4 BP 423 EP 428 DI 10.2337/diabetes.40.4.423 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FE091 UT WOS:A1991FE09100003 PM 1707018 ER PT J AU LAURIE, GW STONE, CM YAMADA, Y AF LAURIE, GW STONE, CM YAMADA, Y TI ELEVATED 32-KDA LBP AND LOW LAMININ MESSENGER-RNA EXPRESSION IN DEVELOPING MOUSE CEREBRUM SO DIFFERENTIATION LA English DT Article ID MESSENGER-RNA; ADHESION MOLECULES; BASEMENT-MEMBRANES; PERIPHERAL-NERVE; BINDING-PROTEIN; CELL MIGRATION; IV COLLAGEN; RECEPTOR; NEURONS; BRAIN AB Several laminin receptors have been identified, originally a high-affinity 67-kDa laminin binding protein ('LBP-67'), and later galactosyltransferase and the low-affinity but functionally potent integrin receptors. Attempts at obtaining cDNA for LBP-67, although unsuccessful, have given rise to a full-length cDNA coding for an interesting 32-kDa protein, tentatively referred to as '32-kDa LBP', whose relationship to LBP-67 is unclear. Since no information is available on the in vivo expression of 32-kDa LBP mRNA nor of the three laminin chains during CNS development, appropriate S-35-antisense and -sense RNA probes were applied to developing mouse cerebral wall at embryonic day (E)10-16, birth and 1-3 weeks after birth. Expression was examined using Northern blot analysis and in situ hybridization. The 32-kDa LBP mRNA was found to be elevated during the embryonic and perinatal period, and then rapidly declined. At the cellular level, 32-kDa LBP mRNA was distributed throughout the embryonic cerebral wall and became concentrated during the perinatal period in the proliferative ventricular zone and in the cortical plate. By comparison, laminin B1, B2, and A chain mRNA expression was relatively low at all times examined, in keeping with the punctate distribution of laminin antigenicity previously observed by others in developing brain parenchyma. Whereas the functional characterization of 32-kDa LBP and the nature of its laminin and proposed nonlaminin ligands is incomplete, the elevated and unique distribution of 32-kDa LBP mRNA raises interesting questions of the role of 32-kDa LBP mRNA in CNS development. C1 NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. RP LAURIE, GW (reprint author), UNIV VIRGINIA,DEPT ANAT & CELL BIOL,CHARLOTTESVILLE,VA 22908, USA. RI Laurie, Gordon/A-5244-2008 FU NCRR NIH HHS [RR05431-28]; NIDDK NIH HHS [DK 38941-03] NR 48 TC 9 Z9 9 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD APR PY 1991 VL 46 IS 3 BP 173 EP 179 DI 10.1111/j.1432-0436.1991.tb00879.x PG 7 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA FN392 UT WOS:A1991FN39200005 PM 1833253 ER PT J AU FRUCHT, H MATON, PN JENSEN, RT AF FRUCHT, H MATON, PN JENSEN, RT TI USE OF OMEPRAZOLE IN PATIENTS WITH ZOLLINGER-ELLISON SYNDROME SO DIGESTIVE DISEASES AND SCIENCES LA English DT Review DE GASTRIC HYPERSECRETION; GASTRIC CARCINOID TUMORS; GASTRINOMA ID GASTRIC-ACID SECRETION; ENTEROCHROMAFFINLIKE CELL ACTIVATION; ARGYROPHIL CARCINOID-TUMORS; LONG-TERM TREATMENT; PERNICIOUS-ANEMIA; ENDOCRINE-CELLS; ANTISECRETORY TREATMENT; HYPERSECRETORY STATES; ANTRECTOMIZED RATS; PLASMA GASTRIN AB Omeprazole, a substituted benzimdazole, has been shown to be a potent inhibitor of gastric acid secretion in patients with Zollinger-Ellison syndrome (ZES). We review our experience, as well as the published data on 210 patients with ZES who have required omeprazole for control of gastric acid hypersecretion over the past seven years. The dose of omeprazole required in individual patients ranged from 10 to 180 mg/24 hr with 20-60% requiring a split dosage regimen. Omeprazole was effective in approximately 99% of the patients over a period ranging from 0.5 to 54 months. Twenty-four percent of patients required an increase in omeprazole dose, while 26% required a decrease in dose. Adverse effects atributable to omeprazole were reported in 2% of patients, and in all cases, they were mild (ie, rash, constipation, headache). There was no effect of omeprazole on serum gastrin concentration or on gastric endocrine cells in three studies. Although one patient with multiple endocrine neoplasia, type-I syndrome (MEN-I) in this series developed a gastric carcinoid while taking omeprazole, evidence is presented that suggests the presence of MEN-I per se may be important in determining the development of gastric carcinoid in patients with ZES. It is concluded that omeprazole is safe and effective in patients with ZES, and in these patients, it is the drug of choice for the management of gastric acid hypersecretion. However, yearly assessment is indicated to clearly evaluate the long-term risk of gastric carcinoid as well as therapy directed at the gastrinoma itself. C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD. NR 78 TC 65 Z9 65 U1 0 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD APR PY 1991 VL 36 IS 4 BP 394 EP 404 DI 10.1007/BF01298865 PG 11 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FF467 UT WOS:A1991FF46700002 PM 2007355 ER PT J AU FUHR, P COHEN, LG ROTH, BJ HALLETT, M AF FUHR, P COHEN, LG ROTH, BJ HALLETT, M TI LATENCY OF MOTOR EVOKED-POTENTIALS TO FOCAL TRANSCRANIAL STIMULATION VARIES AS A FUNCTION OF SCALP POSITIONS STIMULATED SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE MOTOR EVOKED POTENTIALS; CORTICAL STIMULATION; MAGNETIC STIMULATION; MOTOR CORTEX; CORTICOSPINAL TRACT; PERIPHERAL NERVE STIMULATION ID MAGNETIC BRAIN-STIMULATION; MULTIPLE-SCLEROSIS; ELECTRICAL-STIMULATION; UNIT RESPONSES; CONDUCTION; CORTEX; HUMANS; COIL; PATHWAYS; MUSCLES AB We recorded motor evoked potentials (MEP) to transcranial magnetic stimulation from abductor pollicis brevis (APB), flexor carpi radialis (FCR), biceps brachii and deltoid muscles at rest and during slight voluntary activation. An 8-shaped coil connected to a Cadwell MES-10 magnetic stimulator was positioned over different scalp positions 1 cm apart. At least 24 stimuli were delivered at each location. Latencies of MEPs were compared with those obtained by electrical and magnetic stimulation during muscle activation. Progressively longer MEP latencies were obtained in 5 groups depending on the type and position of stimulation. The shortest latencies were obtained with (1) electrical stimulation during muscle contraction and (2) non-focal magnetic stimulation during muscle contraction; magnetic stimulation at rest produced longer latencies with stimulation of (3) an optimal position, (4) a suboptimal position, and (5) a non-optimal position. Mean latency differences between successive groups were 1.9, 2.0, 1.6, and 2.6 msec for APB. Similar latency differences were found for the other arm muscles. The results are compatible with the hypothesis that the different latencies evoked by stimulation at different scalp locations are determined by the summation at spinal motoneurons of excitatory postsynaptic potentials generated by successive numbers of I waves. C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NIH,DIV RES SERV,BIOMED ENGN & INSTRUMENTAT BRANCH,BETHESDA,MD 20892. RI Roth, Bradley/A-4920-2008 NR 34 TC 80 Z9 82 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD APR PY 1991 VL 81 IS 2 BP 81 EP 89 DI 10.1016/0168-5597(91)90001-E PG 9 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA FL782 UT WOS:A1991FL78200001 PM 1708718 ER PT J AU ORBAN, L CHRAMBACH, A AF ORBAN, L CHRAMBACH, A TI DISCONTINUOUS BUFFER SYSTEM FOR POLYACRYLAMIDE AND AGAROSE-GEL ELECTROPHORESIS OF DNA FRAGMENTS SO ELECTROPHORESIS LA English DT Article ID SUBCELLULAR PARTICLES; SIZE STANDARDS; FERGUSON PLOT; PLANT-VIRUSES; DSDNA; HLGE; PH AB DNA fragments up to 9 kb in size were stacked and separated by polyacrylamide gel electrophoresis, and those up to 50 kb in size by agarose gel electrophoresis, using a discontinuous buffer system. Polyacrylamide gels at pH 8.9, 2-degrees-C, 0.01 M ionic strength, yielded sharp bands with DNA loads of 8-mu-g/cm2 of gel of a mixture of 19 DNA fragments in the size range of 72-23130 bp, while agarose gels at pH 8.5, 25-degrees-C, provided well-resolved, unperturbed bands at 0.04 M ionic strength with DNA loads of 1-mu-g/cm2 of the same mixture. Note that the ionic strength of the agarose gels is comparable to the conventionally used 0.5 x TBE (Tris-borate-EDTA) buffer, while that successfully applied to polyacrylamide is seven-fold less than the ionic strength of conventionally used 1 x TBE buffer, with a substantially shorter duration of electrophoresis as a result. The application of a discontinuous buffer system to the gel electrophoresis of DNA results in (i) B and identification by R(f), the migration distance relative to a sharply defined "buffer front" (moving boundary). This is sufficiently labor saving, compared to determining absolute mobilities, so as to render practical the expression of bands as numbers, with benefits for data storage, statistical manipulations and physico-chemical exploitation of mobility data. The use of R(f)'s also circumvents loss of precision in mobility measurement resulting from progressive band spreading of dye bands used as a front. (ii) A uniformly and highly concentrated starting zone, beneficial to resolution, is obtained, without the losses by which separate concentration steps are usually burdened. (iii) The degree of dilution of the DNA sample becomes unimportant. C1 NICHHD,MACROMOLEC ANAL SECT,THEORET & PHYS BIOL LAB,BLDG 10,RM 6C101,BETHESDA,MD 20892. AGR BIOTECHNOL CTR,INST MOLEC GENET,GODOLLO,HUNGARY. RI Orban, Laszlo/A-3030-2009 OI Orban, Laszlo/0000-0001-5435-5948 NR 24 TC 20 Z9 20 U1 1 U2 3 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD APR PY 1991 VL 12 IS 4 BP 233 EP 240 DI 10.1002/elps.1150120402 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FM086 UT WOS:A1991FM08600001 PM 2070779 ER PT J AU ORBAN, L CHRAMBACH, A AF ORBAN, L CHRAMBACH, A TI INFORMATION ON DNA CONFORMATION DERIVED FROM THE FERGUSON PLOT OF DNA FRAGMENTS OF UP TO 9KB IN SIZE, USING POLYACRYLAMIDE-GEL ELECTROPHORESIS IN A DISCONTINUOUS BUFFER SYSTEM SO ELECTROPHORESIS LA English DT Article ID AGAROSE GELS; DEOXYRIBONUCLEIC-ACID; LOAD LEVEL; PARTICLES; DEPENDENCE; COMPUTER; MOBILITIES; APPARATUS; STANDARDS AB The Ferguson plot in polyacrylamide gel electrophoresis (PAGE) (15 %C(DATD), moving boundary electrophoresis buffer system operative at pH 8.9, 4-degrees-C, 8 mA/cm2 of gel) of DNA fragments up to 9.4 kb in size was found to exhibit a linear segment at polyacrylamide concentrations starting at 3 %T and undergoing a gradual transition into a concave segment at higher gel concentrations, confirming previous findings by Stellwagen [1]. The larger the DNA, and the higher the gel concentration, the less extended the linear and the more extended the concave segment of the plot. The lowest %T of the linear range for DNA in polyacrylamide remains unknown since mobilities at nongelling concentrations below 3%T have not as yet been measured. As previously suggested [1,2], the transition from the linear to the concave segment corresponds to that from the randomly oriented DNA to the anisotropically stretched, "reptating" DNA. For a DNA of 9.4 kb in size, the end of the linear range of the Ferguson plot can be extended from 3.5 to 5 %T when 15 % DATD rather than 2.5 % Bis is used to crosslink the polyacrylamide. Increasing the temperature of PAGE from 4-degrees-C to 25 and 50-degrees-C widens the linear segment progressively, indicating an increasingly random orientation with rising temperature. When current density is increased from 8 to 40 mA/cm2, the concave curvature of the Ferguson plot of DNA 1 to 9.4 kb in size decreases, suggesting a transition from a "reptating" to a randomly distributed molecule, due to increased Joule heat. Increasing the ionic strength from 0.01 to 0.04 M similarly appears to lead to a relative linearization of the Ferguson plot, suggesting a similar effect of Joule heat. Prestaining of DNA with ethidium bromide results in a decrease of both its size and its free mobility. This effect is exacerbated as the size of DNA increases from 0.1 to 9.4 kb. C1 NICHHD,MACROMOLEC ANAL SECT,THEORET & PHYS BIOL LAB,BLDG 10,RM 6C101,BETHESDA,MD 20892. AGR BIOTECHNOL CTR,INST MOLEC GENET,GODOLLO,HUNGARY. OI Orban, Laszlo/0000-0001-5435-5948 NR 32 TC 22 Z9 22 U1 0 U2 1 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD APR PY 1991 VL 12 IS 4 BP 241 EP 246 DI 10.1002/elps.1150120403 PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FM086 UT WOS:A1991FM08600002 PM 1712721 ER PT J AU POSPICHAL, J VICCHIO, D CHRAMBACH, A AF POSPICHAL, J VICCHIO, D CHRAMBACH, A TI FREE MOBILITY DETERMINATION BY ELECTROPHORESIS IN POLYACRYLAMIDE CONTAINING AGAROSE AT A NONRESTRICTIVE CONCENTRATION SO ELECTROPHORESIS LA English DT Article ID GEL-ELECTROPHORESIS; FERGUSON PLOTS; SIZE STANDARDS; PARTICLES; DNA; DEPENDENCE; APPARATUS AB In the determination of the free mobility, related to the surface net charge, by quantitative gel electrophoresis, the previous arbitrary extrapolation of Ferguson plots from the lowest gel concentrations that give a mechanically stable gel to 0 %T has recently been replaced by measurement of mobilities across that concentration range, using the addition of 0.5 % agarose to polyacrylamide at the various low concentrations in application to a DNA fragment 155 bp in size (Orban, L. et al., in preparation). The present study applies that approach to several proteins and DNA fragments smaller than 1300 bp, using 0.4 % agarose in polyacrylamide gels of varying concentration. The intercepts of the plots with the mobility axis provide experimental data by which the free mobility in polyacrylamide gel electrophoresis can be estimated for molecules not significantly retarded in their migration at the agarose concentration admixed to polyacrylamide. Across the gel concentration range below 3 %T, in the presence of agarose, the Ferguson plots of proteins and DNA fragments are convex. It was shown by mass spectrometry that this convex curvature of the plots in the mixed polymer is not significantly due to low polymerization efficiency in the concentration range of liquid polyacrylamide (below 3 %T). C1 NICHHD,MACROMOLEC ANAL SECT,THEORET & PHYS BIOL LAB,BLDG 10,RM 6C101,BETHESDA,MD 20892. NICHHD,METAB ANAL & MASS SPECTROMETRY SECT,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NR 29 TC 8 Z9 8 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD APR PY 1991 VL 12 IS 4 BP 247 EP 253 DI 10.1002/elps.1150120404 PG 7 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FM086 UT WOS:A1991FM08600003 PM 2070780 ER PT J AU PETERKOFSKY, B PALKA, J WILSON, S TAKEDA, K SHAH, V AF PETERKOFSKY, B PALKA, J WILSON, S TAKEDA, K SHAH, V TI ELEVATED ACTIVITY OF LOW-MOLECULAR-WEIGHT INSULIN-LIKE GROWTH FACTOR-BINDING PROTEINS IN SERA OF VITAMIN-C-DEFICIENT AND FASTED GUINEA-PIGS SO ENDOCRINOLOGY LA English DT Article ID IGF-I; MESSENGER-RNA; COLLAGEN-SYNTHESIS; DIABETIC RATS; SOMATOMEDIN; EXPRESSION; CARTILAGE; SEQUENCE; ACID; BIOSYNTHESIS AB We have previously reported that scorbutic and fasted guinea pig sera contain an insulin-like growth factor-I (IGF-I)-reversible inhibitor of collagen, proteoglycan, and DNA synthesis in cultured cells. Here we report that IGF-binding protein (IGFBP) activity is increased in serum containing the inhibitor. [I-125]IGF-I or -II bound to these sera was eluted in the 30- to 50-kDa region of an S200 gel column. [I-125]IGF-I affinity cross-linking analysis revealed that a 38-kDa cross-linked species increased markedly in fasted and scorbutic sera, with a lesser increase in a 34-kDa species, while scorbutic sera also yielded a 44-kDa species. Gel filtration of unlabeled sera showed a 10-fold increase in the activity of two proteins in the 30- to 50-kDa region from the experimental sera. Their activity correlated with their ability to inhibit binding of [I-125]IGF-I to its cellular receptor, suggesting that they have the potential to inhibit IGF-I-dependent functions. Ligand blotting showed that 29- and 35-kDa IGFBPs were almost undetectable in normal serum, but were dramatically induced by scurvy and fasting, so that they accounted for close to 40% of the total circulating BPs. Total IGFBP-3 in the experimental sera was increased about 30%, while there was little effect of scurvy or fasting on the level of BP-3 activity isolated by acid extraction of the high mol wt region of the S200 column. An IGF-I analog with normal affinity for the 30- to 50-kDa BPs from fasted and scorbutic sera, but with reduced affinity for the cell receptor, was equivalent to IGF-I in reversing the inhibition of collagen synthesis by scorbutic guinea pig serum in human fibroblasts. Thus, reversal of inhibition appears to require initial saturation of IGFBPs. The overall results suggest that two circulating IGFBPs with unoccupied binding sites are induced in vitamin C-deficient or fasted guinea pigs and may be responsible for inhibition of IGF-I-dependent functions by sera from these animals. RP PETERKOFSKY, B (reprint author), NCI,BIOCHEM LAB,BLDG 37,ROOM 4C-18,BETHESDA,MD 20892, USA. NR 39 TC 52 Z9 52 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1991 VL 128 IS 4 BP 1769 EP 1779 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD869 UT WOS:A1991FD86900012 PM 1706259 ER PT J AU LIANG, CT BARNES, J SACKTOR, B TAKAMOTO, S AF LIANG, CT BARNES, J SACKTOR, B TAKAMOTO, S TI ALTERATIONS OF DUODENAL VITAMIN-D-DEPENDENT CALCIUM-BINDING PROTEIN-CONTENT AND CALCIUM-UPTAKE IN BRUSH-BORDER MEMBRANE-VESICLES IN AGED WISTAR RATS - ROLE OF 1,25-DIHYDROXYVITAMIN-D3 SO ENDOCRINOLOGY LA English DT Article ID DIETARY CALCIUM; ABSORPTION; METABOLISM; INTESTINE; RECEPTORS; CELLS AB Previously we reported that uptake of Ca2+ in cells isolated from rat duodenum declined in senescence. In this paper we examined the possible mechanisms for this age-related defect. Duodenal vitamin D-dependent calcium-binding protein decreased steadily from 3-12 months (mo), followed by a minimal decline at 24 mo. On the contrary, Ca2+ uptake was not different in 3-, 6-, and 12-mo-old rats. A significant decline of Ca2+ uptake was observed at 24 mo. ATP contents in duodenal cells from 6- and 24-mo-old rats were not different. This suggests that the metabolic status of the duodenal cells was not the cause of the change in Ca2+ uptake. Ca2+ uptake activity was significantly lower in brush border membrane vesicles isolated from 24-mo-old rats than in those from 6-mo-old rats. The decrease in Ca2+ uptake activity in old rats was not due to a change in the Ca2+ -binding capacity of the membranes. Kinetic analysis shows that the V(max), the apparent maximum uptake capacity of membrane vesicles, decreased in senescent rats, whereas the K(m), the apparent affinity to Ca2+, was unchanged. Since duodenal Ca2+ influx at the brush border was regulated by 1,25-dihydroxy-vitamin D3 [1,25-(OH)2D3], we tested the effect of 1,25-(OH)2D3 administration on the uptake activity in isolated membrane vesicles. After 1,25-(OH)2D3 treatment, Ca2+ uptake activity in brush border membranes prepared from senescent rats was only slightly lower than that in membranes from adult rats. We conclude that the decline in the influx of Ca2+ at the brush border membrane was the main cause of the decrease in duodenal Ca2+ uptake activity in aging. This defect was probably due to the low serum 1,25-(OH)2D3 concentration and not the result of impaired response to 1,25-(OH)2D3. RP LIANG, CT (reprint author), NIA,GERONTOL RES CTR,BIOL CHEM LAB,4940 EASTERN AVE,BETHESDA,MD 20892, USA. NR 21 TC 7 Z9 8 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1991 VL 128 IS 4 BP 1780 EP 1784 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD869 UT WOS:A1991FD86900013 PM 2004601 ER PT J AU METZGER, DA CURTIS, S KORACH, KS AF METZGER, DA CURTIS, S KORACH, KS TI DIETHYLSTILBESTROL METABOLITES AND ANALOGS - DIFFERENTIAL LIGAND EFFECTS ON ESTROGEN-RECEPTOR INTERACTIONS WITH NUCLEAR MATRIX SITES SO ENDOCRINOLOGY LA English DT Article ID ACCEPTOR SITES; BINDING-SITES; PROBES; PHARMACOLOGY; ANTIESTROGEN; RESPONSES; DOMAINS AB Estradiol (E), diethylstilbestrol (DES), and three structurally similar DES derivatives and analogs, consisting of racemic mixtures of indenestrol-A (IA; rac), indenestrol-B (IB; rac), and the Z-isomer of pseudo-DES (PD) were used as probes to determine the effect of ligand on receptor-nuclear acceptor site interactions. IA (rac), IB (rac), and Z-PD have been previously shown to interact with the mouse uterine estrogen receptor with high affinity (K(d), approximately 1.5-2.2 x 10(-10) M), occupy similar levels of receptor in the nucleus in vivo, and have nuclear retention times similar to those of E and DES. However, in spite of these similarities, they differentially stimulate estrogenic responses that were previously thought to be interrelated and obligatory for full estrogenic action. In an attempt to elucidate the mechanism of differential stimulation of estrogen-regulated responses, the temporal pattern of KCl-resistant receptor sites was examined after a single injection of E, DES, IA (rac), IB (rac), Z-PD, or saline. Z-PD displayed lower levels of KCl-resistant receptor than the other compounds, whereas IA (rac) and IB (rac) had patterns similar to those of E and DES. In cell-free binding assays, all of the different receptor-ligand complexes were equally effective at competitively inhibiting the binding of receptor-[H-3]E complexes to mouse uterine nuclear matrix with a K(i) of 1.1 x 10(-10) M. Direct binding analysis showed no difference in the number of nuclear binding sites (range, 40.4-63.9 fmol/100-mu-g DNA) or K(d) (range, 1.3-1.8 x 10(-10) M) among the different receptor-ligand complexes. Dissociation studies performed at 4 C showed no differences among the different complexes. In contrast, Z-PD-receptor complexes dissociated much faster from matrix sites at 22 C than any of the other complexes. Significant differences were noted in the proportion of complexes that were resistant to extraction with 0.6 M KCl. Forty-three percent of receptor-E complexes and 44% of receptor-DES complexes were resistant of KCl extraction, while 61% of receptor-IA and 29% of receptor-PD complexes were resistant to extraction, paralleling their activity in eliciting some estrogenic responses. In contrast, no difference was seen by gel shift assays in the ability of the ligand-receptor complexes to bind to a specific PS2 estrogen-responsive DNA sequence. These results demonstrate that the ligand may significantly affect the interaction of the estrogen receptor with nuclear acceptor sites. C1 NIEHS,REPROD & DEV TOXICOL LAB,POB 12233,RES TRIANGLE PK,NC 27709. DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DIV REPROD ENDOCRINOL & INFERTIL,DURHAM,NC 27710. OI Korach, Kenneth/0000-0002-7765-418X NR 30 TC 16 Z9 16 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1991 VL 128 IS 4 BP 1785 EP 1791 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD869 UT WOS:A1991FD86900014 PM 2004602 ER PT J AU ROBCIS, HL CALDES, T DEPABLO, F AF ROBCIS, HL CALDES, T DEPABLO, F TI INSULIN-LIKE GROWTH FACTOR-I SERUM LEVELS SHOW A MIDEMBRYOGENESIS PEAK IN CHICKEN THAT IS ABSENT IN GROWTH-RETARDED EMBRYOS CULTURED EXOVO SO ENDOCRINOLOGY LA English DT Article; Proceedings Paper CT 72ND ANNUAL MEETING OF THE ENDOCRINE SOC CY JUN 20-23, 1990 CL ATLANTA, GA SP ENDOCRINE SOC ID SHELL-LESS CULTURE; GENE-EXPRESSION; SOMATOMEDIN; FETAL; RADIOIMMUNOASSAY; DIFFERENTIATION; SECRETION; ONTOGENY; PEPTIDE; INVITRO AB Insulin-like growth factor-I (IGF-I) is the primary mediator of GH action after birth, but its role as a regulator of prenatal growth is unclear. In a previous study we showed that IGF-I mRNA was expressed in chicken embryos beginning at the blastoderm stage (day 0, newly laid egg). Here we present the ontogeny of serum IGF-I in normal and growth-retarded chicken embryos. Serum samples were pooled from multiple embryos starting on day 4 of development in ovo until hatching (day 21). Extracts of day 2 and 3 whole embryos were also studied. IGF-binding proteins were removed by filtration on Sep-Pak C-18 cartridges. IGF-I was quantitated by a heterologous RIA validated for chicken species. Embryonic IGF-I showed a HPLC profile similar to that of adult chicken serum IGF-I. Serum IGF-I was measurable on day 6 of development (approximately 0.04 ng/ml), reached a peak on day 15 (18 ng/ml), and decreased to a low concentration (0.2 ng/ml) the day before hatching. Embryos cultured ex ovo showed progressive growth retardation after day 10 of development, and by day 20 their weight was 50% of normal. The serum IGF-I concentration of ex ovo cultured embryos was normal on day 10, but remained low until day 21, without the midembryogenesis rise observed in normal embryos. These results support the concept that IGF-I may have a role in general embryonic growth in addition to any paracrine/autocrine action in individual tissues. C1 NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,BLDG 10,ROOM 85-243,BETHESDA,MD 20892. NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. NR 42 TC 22 Z9 23 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1991 VL 128 IS 4 BP 1895 EP 1901 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD869 UT WOS:A1991FD86900030 PM 1706261 ER PT J AU BOWERS, CY SARTOR, AO REYNOLDS, GA BADGER, TM AF BOWERS, CY SARTOR, AO REYNOLDS, GA BADGER, TM TI ON THE ACTIONS OF THE GROWTH HORMONE-RELEASING HEXAPEPTIDE, GHRP SO ENDOCRINOLOGY LA English DT Article ID PERIFUSED PITUITARY-CELLS; ADULT MALE-RATS; (GH)-RELEASING PEPTIDES; SYNTHETIC HEXAPEPTIDE; INVIVO ACTIVITY; INVITRO; HIS-D-TRP-ALA-TRP-D-PHE-LYS-NH2; SECRETION; CULTURE AB GH-releasing peptide (His-DTrp-Ala-Trp-DPhe-Lys-NH2 or GHRP) releases GH by a unique and complementary dual site of action on the hypothalamus and pituitary. These effects are mediated via non-GH-releasing hormone (non-GHRH) and nonopiate receptors in rats. Select types of opiates are known to release GH by a hypothalamic site of action, and thus, the dermorphin heptapeptide and benzomorphan opiate agonist 2549 used in this study presumably act on the hypothalamus to release GH. Neither dermorphin nor 2549 release GH or augmented the GH responses of GHRP or GHRH in vitro by a direct pituitary action, while GHRH antiserum inhibited the GH response of both dermorphin and 2549 in vivo (see below). Evidence indicates that these opiates and GHRP administered together synergistically release GH, demonstrating the independent action(s) of GHRP and the opiates. Present data indicate that one of the major differences in the actions of dermorphin, 2549, and GHRP is the inhibition of somatostatin (SRIF) release by the opiates but not by GHRP. Although the actions of dermorphin, 2549, and GHRP on GH release are GHRH dependent, release of endogenous GHRH does not explain how GH is released synergistically by the combination of these peptides. It is proposed that dermorphin/2549 synergistically release GH with GHRP or GHRH because these opiates inhibit SRIF release. Since the GHRP plus GHRH synergistic GH release was not explained by inhibition of SRIF or stimulation of GHRH, an alternative mechanism is proposed to explain how GHRP synergistically releases GH in combination with GHRH. The complementary, rather dramatic synergistic interaction of GHRP, GHRH, and dermorphin or GHRP, GHRH, and 2549 in releasing GH again strongly supports the independent actions of these compounds. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. UNIV ARKANSAS MED SCI HOSP,DEPT PEDIAT,LITTLE ROCK,AR 72205. RP BOWERS, CY (reprint author), TULANE UNIV,SCH MED,DEPT MED,ENDOCRINOL & METAB SECT,1430 TULANE AVE,NEW ORLEANS,LA 70112, USA. FU NIDDK NIH HHS [DK-40202] NR 32 TC 312 Z9 314 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1991 VL 128 IS 4 BP 2027 EP 2035 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD869 UT WOS:A1991FD86900045 PM 2004615 ER PT J AU DEDIEGO, JG GORDEN, P CARPENTIER, JL AF DEDIEGO, JG GORDEN, P CARPENTIER, JL TI THE RELATIONSHIP OF LIGAND RECEPTOR MOBILITY TO INTERNALIZATION OF POLYPEPTIDE HORMONES AND GROWTH-FACTORS SO ENDOCRINOLOGY LA English DT Article ID CULTURED HUMAN-LYMPHOCYTES; INSULIN-RECEPTOR; RAPID MICROAGGREGATION; MEDIATED ENDOCYTOSIS; OCCUPIED RECEPTORS; KINASE-ACTIVITY; COATED PITS; SURFACE; CELLS; I-125 AB Polypeptide hormones and growth factors bind to cell surface receptors and are internalized by receptor-mediated endocytosis. Both [I-125]insulin and [I-125]epidermal growth factor (EGF) are internalized to a much greater extent than [I-125]glucagon in freshly isolated rat hepatocytes. All three ligands bind initially and preferentially to the microvillous surface of the hepatocyte, but only [I-125]insulin and [I-125]EGF undergo significant redistribution to the nonvillous surface of the cell. Thus, the degree of lateral mobility of the ligand receptor complex is strongly correlated with the extent of internalization of the ligand. Since the beta-subunit of the insulin and the EGF receptors span the plasma membrane only once and both receptors are autophosphorylated, it is possible that these are important determinants of the receptor mobility. C1 UNIV GENEVA,MED CTR,INST HISTOL & EMBRYOL,CH-1211 GENEVA 4,SWITZERLAND. NIDDKD,DIABET BRANCH,BETHESDA,MD 20205. NR 22 TC 14 Z9 14 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1991 VL 128 IS 4 BP 2136 EP 2140 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD869 UT WOS:A1991FD86900060 PM 1848511 ER PT J AU NOGUCHI, S OHBA, Y OKA, T AF NOGUCHI, S OHBA, Y OKA, T TI PRETRANSLATIONAL ENHANCEMENT OF EPIDERMAL GROWTH-FACTOR RECEPTOR BY DIRECT EFFECT OF TESTOSTERONE IN MOUSE-LIVER SO ENDOCRINOLOGY LA English DT Article ID ISOLATED RAT HEPATOCYTES; AMINO-ACID-TRANSPORT; SEXUAL DIMORPHISM; HORMONE SECRETION; RIBONUCLEIC-ACID; PRIMARY CULTURES; MICE; GENE; EGF; STIMULATION AB The effects of testosterone on the levels of epidermal growth factor receptor (EGFR) in mouse liver were studied. Orchiectomy resulted in 39% and 41% reductions in the levels of EGFR mRNA and EGF binding, respectively, within 2 weeks. Treatment of orchiectomized mice with a sc injection of testosterone propionate (TP; 100-mu-g/mouse.day) for 1 week restored these values to normal male levels. The hepatic levels of EGFR mRNA and EGF binding in females were 37% and 36% of those in males, respectively, and were not affected by ovariectomy, whereas treatment of females with TP (100-mu-g/mouse.day) increased EGFR to normal male levels within 1 week. On the other hand, neither orchiectomy nor androgen treatment affected levels of mRNAs for EGFR in the kidney or mRNAs for the structural protein beta-actin in the liver. To examine whether testosterone directly increased EGFR levels in the liver, TP (1.0 mg) pellets were implanted into the spleen of orchiectomized mice, so that testosterone released from the pellets reached the liver through the portal vein but did not enter the systemic circulation due to rapid clearance by the liver. The hepatic levels of EGFR mRNA and EGF binding in orchiectomized mice were restored to normal male levels by intrasplenic implantation of TP (1.0 mg) pellets. This treatment also increased the hepatic levels of EGFR mRNA and EGF binding in female mice by 61% and 68%, respectively. In addition, sialoadenectomy, which reduced plasma EGF, as well as EGF antiserum treatment did not affect the androgen-dependent increase in EGFR levels in the liver, suggesting that endogenous EGF is not involved in the androgenic regulation of hepatic EGFR levels. These results suggest that hepatic EGFR levels are at least in part regulated at a pretranslational level by direct effects of androgens on the liver. C1 NIDDKD,MOLEC & CELLULAR BIOL LAB,BLDG 8,ROOM 304,BETHESDA,MD 20892. NR 43 TC 16 Z9 16 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1991 VL 128 IS 4 BP 2141 EP 2148 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD869 UT WOS:A1991FD86900061 PM 2004618 ER PT J AU SHORES, EW SHARROW, SO SINGER, A AF SHORES, EW SHARROW, SO SINGER, A TI PRESENCE OF CD4 AND CD8 DETERMINANTS ON CD4-CD8- MURINE THYMOCYTES - PASSIVE ACQUISITION OF CD8 ACCESSORY MOLECULES SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID COMBINED IMMUNE-DEFICIENCY; MONOCLONAL-ANTIBODIES; LYMPHOCYTES-T; MOUSE; DIFFERENTIATION; PRECURSORS; MICE; EXPRESSION; CELLS AB In the present study we have examined the possibility that CD4 and CD8 accessory molecules can be passively acquired by thymocytes. We initially observed that most thymocytes contained within the CD4-CD8-subset actually possess low levels of CD4 and CD8 on their cell surface. However, the detection of CD4 and CD8 on CD4-CD8- cells was dependent on the presence of other CD4+/CD8+ thymocytes which were actively synthesizing CD4 and CD8. These initial findings suggested that the appearance of CD4/CD8 on "double-negative" thymocytes was due to the passive acquisition of these accessory molecules from CD4+/CD8+ cells present within the thymus. To investigate this possibility directly, we made both in vivo and in vitro mixes of thymocytes possessing different alleles of CD8 (Ly-2.1 and Ly-2.2). Under these experimental conditions, we detected Ly-2.2 on the surface of thymocytes that were genetically Ly-2.1+ and incapable of synthesizing Ly-2.2. These data indicate that thymocytes can express cell surface CD8 molecules which they have not produced but have acquired from other cells in their environment. Thus, the present study indicates that low-level surface expression of cell surface CD4/CD8 differentiation molecules does not necessarily identify distinct thymocyte subpopulations. RP SHORES, EW (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM 4B17,BETHESDA,MD 20892, USA. NR 24 TC 17 Z9 17 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD APR PY 1991 VL 21 IS 4 BP 973 EP 977 DI 10.1002/eji.1830210417 PG 5 WC Immunology SC Immunology GA FJ284 UT WOS:A1991FJ28400016 PM 1902181 ER PT J AU DAVIS, CM PAPADOPOULOS, V JIA, MC YAMADA, Y KLEINMAN, HK DYM, M AF DAVIS, CM PAPADOPOULOS, V JIA, MC YAMADA, Y KLEINMAN, HK DYM, M TI IDENTIFICATION AND PARTIAL CHARACTERIZATION OF LAMININ BINDING-PROTEINS IN IMMATURE RAT SERTOLI CELLS SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID EXTRACELLULAR-MATRIX COMPONENTS; AMINO-ACID SEQUENCE; SYNTHETIC PEPTIDE; ENDOTHELIAL-CELLS; CARCINOMA-CELLS; MESSENGER-RNA; A-CHAIN; RECEPTOR; INTEGRIN; ADHESION C1 GEORGETOWN UNIV,SCH MED,DEPT ANAT & CELL BIOL,3900 RESERVOIR RD NW,WASHINGTON,DC 20007. NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. OI Papadopoulos, Vassilios/0000-0002-1183-8568 FU NICHD NIH HHS [HD-16260] NR 58 TC 29 Z9 29 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD APR PY 1991 VL 193 IS 2 BP 262 EP 273 DI 10.1016/0014-4827(91)90095-C PG 12 WC Oncology; Cell Biology SC Oncology; Cell Biology GA FB960 UT WOS:A1991FB96000003 PM 2004643 ER PT J AU DENNIS, EA RHEE, SG BILLAH, MM HANNUN, YA AF DENNIS, EA RHEE, SG BILLAH, MM HANNUN, YA TI ROLE OF PHOSPHOLIPASES IN GENERATING LIPID 2ND MESSENGERS IN SIGNAL TRANSDUCTION SO FASEB JOURNAL LA English DT Article DE SIGNAL TRANSDUCTION; LIPID 2ND MESSENGERS; PHOSPHOLIPASES; PHOSPHOLIPASE-A1; PHOSPHOLIPASE-C; SPHINGOMYELINASE ID PROTEIN-KINASE-C; VENOM PHOSPHOLIPASE-A2; CELLULAR-REGULATION; COMPLETE CDNA; BOVINE BRAIN; SEQUENCE; INHIBITION; ACID; PURIFICATION; MANOALIDE AB Many lipids or lipid-derived products generated by phospholipases acting on phospholipids in membranes are implicated as mediators and second messengers in signal transduction. Our current understanding of the primary sequence relationships within the class of extracellular phospholipase A2's and among the numerous forms of the mammalian phosphatidylinositol-specific phospholipase C's is reviewed. New results suggesting roles for these phospholipases as well as other phospholipases such as phospholipase C and D acting on phosphatidlycholine in generating arachidonic acid for eicosanoid biosynthesis, inositol phosphates for Ca2+ mobilization, and diglyceride for protein kinase C activation through receptor-mediated processes, are discussed. In addition, the possible role of phospholipases acting on sphingolipids such as sphinglomyelinase in generating lipid mediators is considered. C1 UNIV CALIF SAN DIEGO,CTR MOLEC GENET,LA JOLLA,CA 92093. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. SCHERING PLOUGH CORP,BLOOMFIELD,NJ 07003. DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT CELL BIOL,DURHAM,NC 27710. RP DENNIS, EA (reprint author), UNIV CALIF SAN DIEGO,DEPT CHEM,LA JOLLA,CA 92093, USA. OI Dennis, Edward A/0000-0003-3738-3140 FU NICHD NIH HHS [HD 26171]; NIGMS NIH HHS [GM 20501] NR 51 TC 534 Z9 541 U1 1 U2 13 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR PY 1991 VL 5 IS 7 BP 2068 EP 2077 PG 10 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FF442 UT WOS:A1991FF44200009 PM 1901288 ER PT J AU UCHINO, R CARDINALI, M CHUNG, SI AF UCHINO, R CARDINALI, M CHUNG, SI TI REGULATION OF EXTRAVASCULAR FIBRINOLYSIS BY FACTOR-XIII SO FIBRINOLYSIS LA English DT Article DE EXTRAVASCULAR FIBRINOLYSIS; FACTOR-XIII; WOUND HEALING; LEUKOCYTE ELASTASE ID STABILIZING FACTOR; EPSILON-(GAMMA-GLUTAMYL)LYSINE CROSSLINK; DEGRADATION PRODUCTS; PLASMIC DEGRADATION; FIBRINOGEN; TRANSGLUTAMINASES; PROTEASES; ELASTASE; LINKING AB The stability of fibrin clots in the extravascular compartment was examined using samples of I-125-labelled fibrin implanted subcutaneously into Balb/c mice. These samples of I-125-labelled fibrin were prepared in vitro. Crosslinking of fibrin in the presence of a high level of factor XIIIa resulted in complete conversion of gamma-chain monomers to gamma-gamma-dimers and extensive covalent polymerisation of the alpha-chain monomers. This fibrin, categorised as fully crosslinked (FXL), showed a 50% clot lysis time (LT-50) of 9.6 +/- 0.8 days. In contrast, fibrin, termed as partially crosslinked (PXL), prepared with a low level of Factor XIIIa, had all of its gamma-chain monomers converted to gamma-gamma-dimers, but only a portion of its alpha-chain monomer polymerised. This PXL fibrin showed an LT-50 of 4.8 +/- 1.1 days. Non-crosslinked (NXL) fibrin displayed an LT-50 of 5.2 +/- 1.2 days. Fibrin produced by the addition of thrombin to plasma was of the PXL type and gave an LT-50 of 4.2 +/- 1.0 days. Fibrin produced by the addition of thrombin to whole blood, on the other hand, was found to be FXL and showed an LT-50 of 13.0 +/- 2.0 days. Western blot analysis of fibrin samples prepared from plasma and whole blood with the use of antibody to alpha-2-plasmin inhibitor (alpha-2-PI) provided evidence that this inhibitor was covalently crosslinked to fibrin from both sources. FXL fibrin proved far more stable than either PXL fibrin or NXL fibrin to fibrinolysis by leukocyte elastase in vitro (p < 0.001). Inclusion of the specific elastase inhibitor Elastatinal in the implanted NXL fibrin clot extended the LT-50 from 5 to 11.7 days (p < 0.001), whereas a plasmin inhibitor, epsilon-amino caproic acid caused no change in lysis time. These results suggest that extravascular fibrinolysis is mediated chiefly by leukocyte proteases and that factor XIIIa-catalysed alpha-chain crosslinking is essential for protection of extravascular clots against fibrinolysis by these proteases. C1 NIDR,CELLULAR DEV & ONCOL LAB,BLDG 30,ROOM 202,BETHESDA,MD 20892. NR 37 TC 13 Z9 13 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0268-9499 J9 FIBRINOLYSIS JI Fibrinolysis PD APR PY 1991 VL 5 IS 2 BP 93 EP 98 DI 10.1016/0268-9499(91)90049-A PG 6 WC Hematology SC Hematology GA FG492 UT WOS:A1991FG49200005 ER PT J AU WILLIAMS, J PRICE, CJ SLEET, RB GEORGE, JD MARR, MC KIMMEL, CA MORRISSEY, RE AF WILLIAMS, J PRICE, CJ SLEET, RB GEORGE, JD MARR, MC KIMMEL, CA MORRISSEY, RE TI CODEINE - DEVELOPMENTAL TOXICITY IN HAMSTERS AND MICE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID ZERO DOSE CONTROL; DRUGS; MALFORMATIONS C1 US EPA,REPROD & DEV TOXICOL BRANCH,OHEA,WASHINGTON,DC 20460. NIEHS,NATL TOXICOL PROGRAM,DEV & REPROD TOXICOL GRP,RES TRIANGLE PK,NC 27709. RES TRIANGLE INST,CTR LIFE SCI & TOXICOL,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [N01-ES-55080] NR 35 TC 8 Z9 9 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1991 VL 16 IS 3 BP 401 EP 413 DI 10.1016/0272-0590(91)90081-E PG 13 WC Toxicology SC Toxicology GA FE983 UT WOS:A1991FE98300002 PM 1855614 ER PT J AU DRAGAN, YP RIZVI, T XU, YH HULLY, JR BAWA, N CAMPBELL, HA MARONPOT, RR PITOT, HC AF DRAGAN, YP RIZVI, T XU, YH HULLY, JR BAWA, N CAMPBELL, HA MARONPOT, RR PITOT, HC TI AN INITIATION PROMOTION ASSAY IN RAT-LIVER AS A POTENTIAL COMPLEMENT TO THE 2-YEAR CARCINOGENESIS BIOASSAY SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID ALTERED HEPATOCYTE FOCI; HEPATIC FOCI; FEMALE RATS; MULTISTAGE HEPATOCARCINOGENESIS; CHEMICAL CARCINOGENESIS; N-NITROSODIETHYLAMINE; PHENOTYPIC STABILITY; TUMOR PROMOTION; POSITIVE FOCI; DIETHYLNITROSAMINE C1 UNIV WISCONSIN,MCARDLE LAB CANC RES,SCH MED,1400 UNIV AVE,MADISON,WI 53706. NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. FU NCI NIH HHS [CA-45700, CA-22484, CA-07175] NR 82 TC 42 Z9 42 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1991 VL 16 IS 3 BP 525 EP 547 DI 10.1016/0272-0590(91)90093-J PG 23 WC Toxicology SC Toxicology GA FE983 UT WOS:A1991FE98300014 PM 1855624 ER PT J AU DUBOIS, A TARNAWSKI, A NEWELL, DG FIALA, N DABROS, W STACHURA, J KRIVAN, H HEMANACKAH, LM AF DUBOIS, A TARNAWSKI, A NEWELL, DG FIALA, N DABROS, W STACHURA, J KRIVAN, H HEMANACKAH, LM TI GASTRIC INJURY AND INVASION OF PARIETAL-CELLS BY SPIRAL BACTERIA IN RHESUS-MONKEYS - ARE GASTRITIS AND HYPERCHLORHYDRIA INFECTIOUS-DISEASES SO GASTROENTEROLOGY LA English DT Article ID CAMPYLOBACTER-PYLORI INFECTION; HELICAL-SHAPED BACTERIA; GNOTOBIOTIC PIGLETS; SERUM GASTRIN; STOMACH; ORGANISMS; MUCOSA; SECRETION; IDENTIFICATION; COLONIZATION C1 ARMED FORCES RADIOBIOL RES INST,DEPT PHYSIOL,BETHESDA,MD 20814. ARMED FORCES RADIOBIOL RES INST,DEPT VET MED,BETHESDA,MD 20814. VET ADM MED CTR,LONG BEACH,CA 90822. UNIV CALIF IRVINE,IRVINE,CA 92717. PUBL HLTH LAB SERV,CTR APPL MICROBIOL & RES,SALISBURY SP4 0JG,WILTS,ENGLAND. NIH,STRUCT BIOL LAB,BETHESDA,MD 20892. BIOCARB INC,GAITHERSBURG,MD. RP DUBOIS, A (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT MED,DIV DIGEST DIS,GASTROINTESTINAL & LIVER STUDIES LAB,BETHESDA,MD 20814, USA. NR 37 TC 72 Z9 73 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1991 VL 100 IS 4 BP 884 EP 891 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FB642 UT WOS:A1991FB64200005 PM 2001827 ER PT J AU JANOFF, EN ORENSTEIN, JM MANISCHEWITZ, JF SMITH, PD AF JANOFF, EN ORENSTEIN, JM MANISCHEWITZ, JF SMITH, PD TI ADENOVIRUS COLITIS IN THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO GASTROENTEROLOGY LA English DT Article ID HOMOSEXUAL MEN; AIDS; INFECTIONS; GASTROENTERITIS; PREVALENCE; PATHOGENS; VIRUS C1 NIDR,CELLULAR IMMUNOL SECT,IMMUNOL LAB,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20037. US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD 20014. RP JANOFF, EN (reprint author), UNIV MINNESOTA,VET AFFAIRS MED CTR,SCH MED,DEPT MED,INFECT DIS SECT,1 VET DR,MINNEAPOLIS,MN 55417, USA. NR 16 TC 70 Z9 69 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1991 VL 100 IS 4 BP 976 EP 979 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FB642 UT WOS:A1991FB64200017 PM 2001834 ER PT J AU EVERHART, JE RENAULT, PF AF EVERHART, JE RENAULT, PF TI IRRITABLE-BOWEL-SYNDROME IN OFFICE-BASED PRACTICE IN THE UNITED-STATES SO GASTROENTEROLOGY LA English DT Article ID FUNCTIONAL GASTROINTESTINAL DISORDERS; QUESTIONNAIRE; IDENTIFY; DISEASE RP EVERHART, JE (reprint author), NIDDKD,DIV DIGEST DIS & NUTR,ROOM 106,FED BLDG,7550 WISCONSIN AVE,BETHESDA,MD 20892, USA. NR 28 TC 196 Z9 202 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1991 VL 100 IS 4 BP 998 EP 1005 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FB642 UT WOS:A1991FB64200020 PM 2001837 ER PT J AU ALLEN, JD LINTS, T JENKINS, NA COPELAND, NG STRASSER, A HARVEY, RP ADAMS, JM AF ALLEN, JD LINTS, T JENKINS, NA COPELAND, NG STRASSER, A HARVEY, RP ADAMS, JM TI NOVEL MURINE HOMEO BOX GENE ON CHROMOSOME-1 EXPRESSED IN SPECIFIC HEMATOPOIETIC LINEAGES AND DURING EMBRYOGENESIS SO GENES & DEVELOPMENT LA English DT Article DE HEMATOPOIESIS; EMBRYOGENESIS; HOMEO BOX EVOLUTION; GENE MAPPING ID TRANSCRIPTION FACTOR; ANTENNAPEDIA-COMPLEX; SEQUENCE-ANALYSIS; ENGRAILED GENE; B-CELLS; DROSOPHILA; MOUSE; HOMEODOMAIN; ORGANIZATION; MACROPHAGES AB We describe here a new murine homeo box gene, denoted Hlx, which is expressed within specific hematopoietic lineages. The cDNA sequence indicates that Hlx differs markedly from known vertebrate homeo box genes, and linkage analysis of an interspecific murine backcross showed that it resides at a novel homeo box locus on the distal portion of mouse chromosome 1. The Hlx homeo domain is most similar to that of the Drosophila H2.0 gene, but outside this region the two polypeptides are related only within a few short segments, the most notable being a motif (denoted Hep) also partially conserved in the engrailed and invected homeo proteins and possibly related to an octapeptide in certain paired box proteins. The presence of an intron within the Hlx homeo box at the same position as in several divergent Drosophila genes (H2.0, labial, Distal-less, probosipedia, Abdominal-B, NK-1) suggests an ancient evolutionary relationship between these genes. RNA analysis of 67 murine hematopoietic cell lines and normal hematopoietic cells revealed Hlx expression throughout the myeloid/macrophage lineage and at early stages of B lymphocyte development but not in T lymphocytes, erythroid cells, or mast cells. Hence, Hlx is a candidate regulator of hematopoietic lineage commitment and maturation. It probably also functions outside the hematopoietic system, however, because Hlx mRNA could be detected in diverse adult tissues and in embryos from as early as day 8 of development. C1 NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,FREDERICK,MD 21701. RP ALLEN, JD (reprint author), ROYAL MELBOURNE HOSP,WALTER & ELIZA HALL INST MED RES,PARKVILLE,VIC 3050,AUSTRALIA. RI Lints, Thierry/K-4408-2012; Strasser, Andreas/C-7581-2013; Adams, Jerry/E-1199-2013 FU NCI NIH HHS [CA 12421]; NICHD NIH HHS [HD26024]; PHS HHS [N01-C0-74101] NR 64 TC 104 Z9 109 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD APR PY 1991 VL 5 IS 4 BP 509 EP 520 DI 10.1101/gad.5.4.509 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA FF004 UT WOS:A1991FF00400001 PM 1672660 ER PT J AU OLSON, S WANG, MG CARAFOLI, E STREHLER, EE MCBRIDE, OW AF OLSON, S WANG, MG CARAFOLI, E STREHLER, EE MCBRIDE, OW TI LOCALIZATION OF 2 GENES ENCODING PLASMA-MEMBRANE CA2+-TRANSPORTING ATPASES TO HUMAN-CHROMOSOMES 1Q25-32 AND 12Q21-23 SO GENOMICS LA English DT Article ID ION MOTIVE ATPASES; INSITU HYBRIDIZATION; CA-2+ PUMP; CA-2+-TRANSPORTING ATPASE; REGULATORY DOMAIN; MOLECULAR-CLONING; DNA-SEQUENCES; CDNA CLONING; CALCIUM-PUMP; LINKAGE MAP C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. SWISS FED INST TECHNOL,BIOCHEM LAB,CH-8092 ZURICH,SWITZERLAND. RI Carafoli, Ernesto/K-5192-2016 OI Carafoli, Ernesto/0000-0002-7826-0094 NR 53 TC 58 Z9 60 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1991 VL 9 IS 4 BP 629 EP 641 DI 10.1016/0888-7543(91)90356-J PG 13 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA FB629 UT WOS:A1991FB62900010 PM 1674727 ER PT J AU KOZAK, CA DYMECKI, SM NIEDERHUBER, JE DESIDERIO, SV AF KOZAK, CA DYMECKI, SM NIEDERHUBER, JE DESIDERIO, SV TI GENETIC-MAPPING OF THE GENE FOR A NOVEL TYROSINE KINASE, BLK, TO MOUSE CHROMOSOME 14 SO GENOMICS LA English DT Note ID LINKAGE C1 JOHNS HOPKINS UNIV,SCH MED,DEPT SURG,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,HOWARD HUGHES MED INST,BALTIMORE,MD 21205. RP KOZAK, CA (reprint author), NIAID,MOLEC BIOL LAB,BLDG 4,ROOM 324,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA16519] NR 16 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1991 VL 9 IS 4 BP 762 EP 764 DI 10.1016/0888-7543(91)90372-L PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA FB629 UT WOS:A1991FB62900026 PM 2037301 ER PT J AU GEJMAN, PV WEINSTEIN, LS MARTINEZ, M SPIEGEL, AM CAO, Q HSIEH, WT HOEHE, MR GERSHON, ES AF GEJMAN, PV WEINSTEIN, LS MARTINEZ, M SPIEGEL, AM CAO, Q HSIEH, WT HOEHE, MR GERSHON, ES TI GENETIC-MAPPING OF THE GS-ALPHA SUBUNIT GENE (GNAS1) TO THE DISTAL LONG ARM OF CHROMOSOME 20 USING A POLYMORPHISM DETECTED BY DENATURING GRADIENT GEL-ELECTROPHORESIS SO GENOMICS LA English DT Note ID LINKAGE C1 NIDDK,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892. RP GEJMAN, PV (reprint author), NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892, USA. RI Weinstein, Lee/I-5575-2015; Martinez, Maria/B-3111-2013 OI Martinez, Maria/0000-0003-2180-4537 NR 13 TC 59 Z9 61 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1991 VL 9 IS 4 BP 782 EP 783 DI 10.1016/0888-7543(91)90377-Q PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA FB629 UT WOS:A1991FB62900031 PM 1674732 ER PT J AU ZUNICH, KM LANE, HC AF ZUNICH, KM LANE, HC TI IMMUNOLOGICAL ABNORMALITIES IN HIV-INFECTION SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID HUMAN IMMUNODEFICIENCY VIRUS; ACQUIRED IMMUNE-DEFICIENCY; AIDS-RELATED COMPLEX; TUMOR NECROSIS FACTOR; DELAYED-TYPE HYPERSENSITIVITY; PERIPHERAL-BLOOD MONOCYTES; INTRAVENOUS DRUG-ABUSERS; CELL-MEDIATED-IMMUNITY; HOMOSEXUAL MEN; LYMPHOCYTE-T C1 NIAID,IMMUNOREGULAT LAB,9000 ROCKVILLE PIKE,BLDG 10,ROOM 11B13,BETHESDA,MD 20892. NIAID,DIV ALLERGY IMMUNOL & TRANSPLANTAT,TRANSPLANTAT SECT,BETHESDA,MD 20892. NR 121 TC 16 Z9 17 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1991 VL 5 IS 2 BP 215 EP 228 PG 14 WC Oncology; Hematology SC Oncology; Hematology GA FD961 UT WOS:A1991FD96100003 PM 2022591 ER PT J AU PLUDA, JM MITSUYA, H YARCHOAN, R AF PLUDA, JM MITSUYA, H YARCHOAN, R TI HEMATOLOGIC EFFECTS OF AIDS THERAPIES SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID ACQUIRED IMMUNODEFICIENCY SYNDROME; COLONY-STIMULATING FACTOR; PNEUMOCYSTIS-CARINII PNEUMONIA; IMMUNE-DEFICIENCY SYNDROME; RECOMBINANT INTERFERON-ALPHA; EPIDEMIC KAPOSIS SARCOMA; PLACEBO-CONTROLLED TRIAL; LEUKOCYTE-A INTERFERON; BONE-MARROW TOXICITY; HOMOSEXUAL MEN C1 NCI,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,9000 ROCKVILLE PIKE,BLDG 10,ROOM 13N 248,BETHESDA,MD 20892. NR 122 TC 35 Z9 35 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1991 VL 5 IS 2 BP 229 EP 248 PG 20 WC Oncology; Hematology SC Oncology; Hematology GA FD961 UT WOS:A1991FD96100004 PM 1708759 ER PT J AU ENSOLI, B BARILLARI, G GALLO, RC AF ENSOLI, B BARILLARI, G GALLO, RC TI PATHOGENESIS OF AIDS-ASSOCIATED KAPOSIS-SARCOMA SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID COLONY-STIMULATING FACTORS; YOUNG HOMOSEXUAL MEN; GROWTH-FACTOR; CELLS; PREVALENCE; LESIONS; INVITRO; UGANDA; ORIGIN; SKIN RP ENSOLI, B (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,RM GA09,BETHESDA,MD 20892, USA. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 53 TC 94 Z9 95 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1991 VL 5 IS 2 BP 281 EP 295 PG 15 WC Oncology; Hematology SC Oncology; Hematology GA FD961 UT WOS:A1991FD96100007 PM 2022594 ER PT J AU BAKER, BL DIBISCEGLIE, AM KANEKO, S MILLER, R FEINSTONE, SM WAGGONER, JG HOOFNAGLE, JH AF BAKER, BL DIBISCEGLIE, AM KANEKO, S MILLER, R FEINSTONE, SM WAGGONER, JG HOOFNAGLE, JH TI DETERMINATION OF HEPATITIS-B VIRUS-DNA IN SERUM USING THE POLYMERASE CHAIN-REACTION - CLINICAL-SIGNIFICANCE AND CORRELATION WITH SEROLOGICAL AND BIOCHEMICAL MARKERS SO HEPATOLOGY LA English DT Article ID CHRONIC LIVER-DISEASE; SURFACE-ANTIGEN; CARRIERS AB Sera from 98 patients with various stages of chronic hepatitis B virus infection were studied to determine the clinical significance of hepatitis B virus DNA in serum detected by the polymerase chain reaction. Patients were divided into three groups according to their HBsAg and HBeAg status. Group I (n = 31) had detectable HBsAg and HBeAg, group II (n = 46) had HBsAg but not HBeAg and group III (n = 21) consisted of patients who were once chronic hepatitis B virus carriers but had lost HBsAg during follow-up. Group I patients usually had significant liver disease (raised serum aminotransferases), had higher titers of HBsAg and had been infected with hepatitis B virus for a shorter period than patients in the other two groups. All patients in group I had hepatitis B virus DNA detectable by polymerase chain reaction and 94% had sufficient hepatitis B virus DNA present for detection by dot-blot hybridization. Group II patients had lower mean serum aminotransferase activities and titers of HBsAg than those in group I. Serum hepatitis B virus DNA was detectable by polymerase chain reaction in 78% but in only 30% of group II patients by dot-blot hybridization. Group II patients who did not have hepatitis B virus DNA detectable by polymerase chain reaction had mean serum aminotransferase levels within the normal range and had a younger mean age than those with hepatitis B virus DNA. Group III patients generally had no evidence of active liver disease. Of five patients in this group seropositive for hepatitis B virus DNA by polymerase chain reaction on initial testing, all eventually became negative for hepatitis B virus DNA on subsequent testing. There was a tendency for those patients in group III with hepatitis B virus DNA detectable by polymerase chain reaction to have elevated serum aminotransferase levels (40% vs. 25%); however, these differences were not statistically significant. Taken together, these data show that the presence of hepatitis B virus DNA in serum as detected by polymerase chain reaction appears to be a good marker of the level of viremia, can be correlated with aminotransferase levels and parallels the presence of HBsAg in serum. C1 NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892. RP BAKER, BL (reprint author), NIDDKD,LIVER DIS SECT,BLDG 10,ROOM 4D-52,BETHESDA,MD 20892, USA. NR 12 TC 62 Z9 62 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1991 VL 13 IS 4 BP 632 EP 636 DI 10.1016/0270-9139(91)92556-N PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FG399 UT WOS:A1991FG39900003 PM 2010158 ER PT J AU DIEHL, AM BISGAARD, HC KREN, BT STEER, CJ AF DIEHL, AM BISGAARD, HC KREN, BT STEER, CJ TI ETHANOL INTERFERES WITH REGENERATION-ASSOCIATED CHANGES IN BIOTRANSFORMING ENZYMES - A POTENTIAL MECHANISM UNDERLYING ETHANOLS CARCINOGENICITY SO HEPATOLOGY LA English DT Article ID POST-TRANSCRIPTIONAL REGULATION; GLUTATHIONE S-TRANSFERASES; RAT SERUM-ALBUMIN; ASIALOGLYCOPROTEIN RECEPTOR; MONOCLONAL-ANTIBODIES; LIVER-MICROSOMES; CYTOCHROME-P-450; EXPRESSION; SEQUENCE; HEPATOCARCINOGENESIS AB The effects of chronic ethanol consumption on enzyme systems involved in carcinogen activation and detoxification were studied in a rat model of liver regeneration. In control rats, steady-state messenger RNAs of cytochrome P450j decreased 12 to 24 hr after partial hepatectomy but were fully recovered by 48 to 72 hr. In contrast, messenger RNA levels of cytochrome P450b and P450d did not vary significantly during that period. Steady-state messenger RNA levels for the placental form of glutathione S-transferase decreased within 30 min after partial hepatectomy but fluctuated until levels returned to normal by 48 hr. Preliminary nuclear run-on analyses suggest that the regulation of cytochrome P450j and the placental form of glutathione S-transferase messenger RNA levels involves posttranscriptional control in these animals. In ethanol-fed rats, as in controls, expression of cytochrome P450j and the placental form of glutathione S-transferase decreased transiently after partial hepatectomy. However, compared with control values, messenger RNA levels for cytochrome P450j were greater in ethanol-fed rats at each time point. Similar results were noted for placental glutathione S-transferase levels from 12 to 48 hr after partial hepatectomy. Ethanol feeding had no apparent effect on steady-state messenger RNA levels of cytochrome P450d, P450b or the multidrug-resistant gene. In both ethanol and control rats, only prehepatectomy levels of cytochrome P450 transcripts correlated with levels of the respective P450 isoenzymes. These data indicate that liver regeneration selectively decreases the steady-state messenger RNA expression of certain isoenzymes of cytochrome P450 and glutathione S-transferase. Chronic ethanol consumption induces basal messenger RNA expression of cytochrome P450j and blunts regeneration-associated decreases in cytochrome P450j and glutathione S-transferase expression. These alterations may be involved in ethanol's ability to function as a co-carcinogen in liver. C1 VET AFFAIRS MED CTR,DEPT MED,WASHINGTON,DC 20422. NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20814. NR 37 TC 39 Z9 40 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1991 VL 13 IS 4 BP 722 EP 727 DI 10.1016/0270-9139(91)92571-O PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FG399 UT WOS:A1991FG39900018 PM 2010167 ER PT J AU DIBISCEGLIE, AM AF DIBISCEGLIE, AM TI TREATMENT OF HEPATOCELLULAR-CARCINOMA SO HEPATOLOGY LA English DT Note ID CHEMOTHERAPY; THERAPY AB This study reports the results of resection in 72 cirrhotic patients with hepatocellular carcinoma from Europe. One and 3 year survival rates were 68% and 51% respectively. Survival was significantly higher in Child's class A than in class B or C patients. Patients with a thickly encapsulated tumor lived longer than those with an infiltrating tumor and also had a significantly lower recurrence rate. There was no relationship between the size of the tumor or the presence of symptoms and survival. These data suggest that good results can be achieved by resection of hepatocellular carcinoma in European cirrhotic patients. A thickly encapsulated tumor and good liver function are the main determinants of low cancer recurrence and high survival. RP DIBISCEGLIE, AM (reprint author), NIDDKD,LIVER DIS SECT,BETHESDA,MD 20892, USA. NR 12 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1991 VL 13 IS 4 BP 802 EP 804 DI 10.1016/0270-9139(91)92585-V PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FG399 UT WOS:A1991FG39900030 PM 1849116 ER PT J AU OSHER, FC AF OSHER, FC TI DUAL DIAGNOSIS - COUNSELING THE MENTALLY-ILL SUBSTANCE-ABUSER - EVANS,K, SULLIVAN,JM SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Book Review RP OSHER, FC (reprint author), NIMH,OFF PROGRAMS HOMELESS MENTALLY ILL,ROCKVILLE,MD 20857, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD APR PY 1991 VL 42 IS 4 BP 431 EP 432 PG 2 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA FD969 UT WOS:A1991FD96900028 ER PT J AU LERMAN, MI LATIF, F GLENN, GM DANIEL, LN BRAUCH, H HOSOE, S HAMPSCH, K DELISIO, J ORCUTT, ML MCBRIDE, OW GRZESCHIK, KH TAKAHASHI, T MINNA, J ANGLARD, P LINEHAN, WM ZBAR, B AF LERMAN, MI LATIF, F GLENN, GM DANIEL, LN BRAUCH, H HOSOE, S HAMPSCH, K DELISIO, J ORCUTT, ML MCBRIDE, OW GRZESCHIK, KH TAKAHASHI, T MINNA, J ANGLARD, P LINEHAN, WM ZBAR, B TI ISOLATION AND REGIONAL LOCALIZATION OF A LARGE COLLECTION (2,000) OF SINGLE-COPY DNA FRAGMENTS ON HUMAN CHROMOSOME-3 FOR MAPPING AND CLONING TUMOR SUPPRESSOR GENES SO HUMAN GENETICS LA English DT Article ID RENAL-CELL CARCINOMA; VONHIPPEL-LINDAU DISEASE; LINKAGE MAP; LUNG-CANCER; SHORT ARM; LIBRARIES; PROBES; CONSTRUCTION; DELETION; ACID AB A collection of 2,000 lambda phage-carrying human single-copy inserts (> 700 bp) were isolated from two chromosome-3 flow-sorted libraries. The single-copy DNA fragments were first sorted into 3p and 3q locations and about 700 3p fragments were regionally mapped using a deletion mapping panel comprised of two human-hamster and two-human-mouse cell hybrids, each containing a chromosome 3 with different deletions in the short arm. The hybrids were extensively mapped with a set of standard 3p markers physically localized or ordered by linkage. The deletion mapping panel divided the short arm into five distinct subregions (A-E). The 3p fragments were distributed on 3p regions as follows: region A, 26%; B, 31%; C, 4%; D, 4% and E, 35%. We screened 300 single-copy DNA fragments from the distal part of 3p (regions A and B) with ten restriction endonucleases for their ability to detect restriction fragment length polymorphisms (RFLPs). Of these fragments 110 (36%) were found to detect useful RFLPs: 35% detected polymorphisms with frequency of heterozygosity of 40% or higher, and 25% with frequency of 30% or higher. All polymorphisms originated from single loci and most of them were of the base pair substitution type. These RFLP markers make it possible to construct a fine linkage map that will span the distal part of chromosome 3p and encompasses the von Hippel-Lindau disease locus. The large number of single-copy fragments (2,000) spaced every 100-150 kb on chromosome 3 will make a significant contribution to mapping and sequencing the entire chromosome 3. The 300 conserved chromosome 3 probes will increase the existing knowledge of man-mouse homologies. C1 PROGRAM RESOURCES INC,FREDERICK CANC RES FACIL,FREDERICK,MD 21701. NCI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV MARBURG,INST HUMAN GENET,W-3550 MARBURG,GERMANY. USN HOSP,NCI,MED ONCOL BRANCH,BETHESDA,MD 20814. NCI,SURG BRANCH,UROL ONCOL SECT,BETHESDA,MD 20892. RP LERMAN, MI (reprint author), NCI,FREDERICK CANC RES FACIL,IMMUNOBIOL LAB,BLDG 560,ROOM 12-71,FREDERICK,MD 21701, USA. RI Takahashi, Takashi/I-7262-2014 NR 61 TC 63 Z9 57 U1 1 U2 6 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD APR PY 1991 VL 86 IS 6 BP 567 EP 577 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA FH810 UT WOS:A1991FH81000006 PM 1673958 ER PT J AU MONTEAGUDO, C MERINO, MJ LAPORTE, N NEUMANN, RD AF MONTEAGUDO, C MERINO, MJ LAPORTE, N NEUMANN, RD TI VALUE OF GROSS CYSTIC-DISEASE FLUID PROTEIN-15 IN DISTINGUISHING METASTATIC BREAST CARCINOMAS AMONG POORLY DIFFERENTIATED NEOPLASMS INVOLVING THE OVARY SO HUMAN PATHOLOGY LA English DT Article DE OVARIAN METASTASES; BREAST CARCINOMA; GCDFP-15; IMMUNOHISTOCHEMISTRY ID GCDFP-15; CANCER; LOCALIZATION C1 NCI,PATHOL LAB,BLDG 10,ROOM 2N212,BETHESDA,MD 20892. NCI,DEPT NUCL MED,BETHESDA,MD 20892. RI Monteagudo, Carlos/H-6555-2016 NR 24 TC 67 Z9 68 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD APR PY 1991 VL 22 IS 4 BP 368 EP 372 DI 10.1016/0046-8177(91)90084-3 PG 5 WC Pathology SC Pathology GA GJ450 UT WOS:A1991GJ45000009 PM 2050370 ER PT J AU SCHMITT, JM WEBBER, RL WALKER, EC AF SCHMITT, JM WEBBER, RL WALKER, EC TI OPTICAL DETERMINATION OF DENTAL-PULP VITALITY SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING LA English DT Article ID TOOTH AB In this preliminary study, we explored the feasibility of employing photoplethysmography and pulse oximetry to assess the status of the blood circulation in the dental pulp. A simple photometer that measures diffuse light transmission at 575 nm was built to record tooth plethysmograms, and the ability to distinguish vital from surgically devitalized teeth of a dog using plethysmography was demonstrated. As an extension of the photoplethysmographic technique, red infrared pulse oximetry applied to the measurement of the oxygen saturation (SO2) of blood in the pulp was also examined using an in vitro test setup. Results suggest that the measurement of relative SO2 changes is feasible, but standard dual-wavelength pulse oximetry does not enable determination of SO2 independent of tooth geometry and sensor placement. C1 NIDR,DIAGNOST SYST BRANCH,BETHESDA,MD 20892. RP SCHMITT, JM (reprint author), NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,DIV RES SERV,LASERS & MODERN OPT GRP,BETHESDA,MD 20892, USA. NR 13 TC 24 Z9 24 U1 0 U2 1 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0018-9294 J9 IEEE T BIO-MED ENG JI IEEE Trans. Biomed. Eng. PD APR PY 1991 VL 38 IS 4 BP 346 EP 352 DI 10.1109/10.133229 PG 7 WC Engineering, Biomedical SC Engineering GA FP653 UT WOS:A1991FP65300008 PM 1855796 ER PT J AU UNSER, M AF UNSER, M TI CLASSIFICATION OF NATURAL TEXTURES BY MEANS OF 2-DIMENSIONAL ORTHOGONAL MASKS - COMMENTS SO IEEE TRANSACTIONS ON SIGNAL PROCESSING LA English DT Letter AB The correspondence of Cohen et al. describes a texture analysis method that is a special use of the approach reported in [3]. Moreover, the derivation of the optimum set of masks presented by these authors is based on an incorrect assumption; the correct solution should be the local Karhunen-Loeve transform which is generally different from a 2 x 2 Hadamard transform (2 x 2 DHT). However, this error has relatively minor effects from a practical point of view since the ability of the 2 x 2 DHT to decorrelate real texture images is usually excellent. RP UNSER, M (reprint author), NIH,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 1053-587X J9 IEEE T SIGNAL PROCES JI IEEE Trans. Signal Process. PD APR PY 1991 VL 39 IS 4 BP 1005 EP 1006 DI 10.1109/78.80939 PG 2 WC Engineering, Electrical & Electronic SC Engineering GA FD675 UT WOS:A1991FD67500042 ER PT J AU BLUESTONE, JA CRON, RQ BARRETT, TA HOULDEN, B SPERLING, AI DENT, A HEDRICK, S RELLAHAN, B MATIS, LA AF BLUESTONE, JA CRON, RQ BARRETT, TA HOULDEN, B SPERLING, AI DENT, A HEDRICK, S RELLAHAN, B MATIS, LA TI REPERTOIRE DEVELOPMENT AND LIGAND SPECIFICITY OF MURINE TCR-GAMMA-DELTA CELLS SO IMMUNOLOGICAL REVIEWS LA English DT Review ID MAJOR HISTOCOMPATIBILITY COMPLEX; DENDRITIC EPIDERMAL-CELLS; INTESTINAL INTRAEPITHELIAL LYMPHOCYTES; ANTIGEN RECEPTOR GENES; T-CELLS; SELF-TOLERANCE; HEAT-SHOCK; MONOCLONAL-ANTIBODIES; LIMITED DIVERSITY; FETAL THYMOCYTES C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. UNIV CHICAGO,DEPT PATHOL,COMM IMMUNOL,CHICAGO,IL 60637. UNIV CALIF SAN DIEGO,DEPT BIOL,LA JOLLA,CA 92093. RP BLUESTONE, JA (reprint author), UNIV CHICAGO,BEN MAY INST,BOX 424,CHICAGO,IL 60637, USA. OI Cron, Randy/0000-0003-2661-3086 NR 79 TC 76 Z9 76 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0105-2896 J9 IMMUNOL REV JI Immunol. Rev. PD APR PY 1991 VL 120 BP 5 EP 33 DI 10.1111/j.1600-065X.1991.tb00585.x PG 29 WC Immunology SC Immunology GA FL991 UT WOS:A1991FL99100001 PM 1650760 ER PT J AU ACCOLLA, RS AUFFRAY, C SINGER, DS GUARDIOLA, J AF ACCOLLA, RS AUFFRAY, C SINGER, DS GUARDIOLA, J TI THE MOLECULAR-BIOLOGY OF MHC GENES SO IMMUNOLOGY TODAY LA English DT Article AB Antigenic peptides become associated with major histocompatibility complex (MHC) class I and class II surface antigens, are then presented to T cells and thereby elicit an antigen-specific cellular or humoral immune response. MHC molecules are genetically heterogeneous and polymorphic; their structure is therefore relevant to modulation of the immune system. The selective pressure resulting from this modulation is in turn the main driving force for the evolution of the complex genetic system. The density of MHC molecules on the cell surface is another parameter that influences immune responsiveness. The study of the evolution and regulation of MHC genes is, therefore, of great interest. These and other themes were discussed at the Third IIGB Workshop* which was recently held in Capri. C1 INST EMBRYOL CELLULAIRE & MOLEC,F-94736 NOGENT SUR MARNE,FRANCE. INT INST GENET & BIOPHYS,I-80125 NAPLES,ITALY. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP ACCOLLA, RS (reprint author), UNIV VERONA,POLICLIN BORGO ROMA,IST SCI IMMUNOL,I-37100 VERONA,ITALY. OI Accolla, Roberto/0000-0003-2493-7378 NR 2 TC 22 Z9 22 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD APR PY 1991 VL 12 IS 4 BP 97 EP 99 DI 10.1016/0167-5699(91)90090-G PG 3 WC Immunology SC Immunology GA FH078 UT WOS:A1991FH07800001 PM 1676269 ER PT J AU GRANT, DS LELKES, PL FUKUDA, K KLEINMAN, HK AF GRANT, DS LELKES, PL FUKUDA, K KLEINMAN, HK TI INTRACELLULAR MECHANISMS INVOLVED IN BASEMENT-MEMBRANE INDUCED BLOOD-VESSEL DIFFERENTIATION INVITRO SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY LA English DT Article DE ENDOTHELIUM; BASEMENT MEMBRANE; LAMININ; DIFFERENTIATION; BLOOD VESSEL; MECHANISMS ID HUMAN-ENDOTHELIAL CELLS; EXTRACELLULAR-MATRIX INTERACTIONS; CAPILLARY-LIKE STRUCTURES; FIBROBLAST GROWTH-FACTOR; ANGIOGENESIS INVITRO; DNA-SYNTHESIS; LAMININ; SURFACE; CULTURE; IDENTIFICATION AB The extracellular matrix, particularly basement membranes, plays an important role in angiogenesis (blood vessel formation). Previous work has demonstrated that a basement membranelike substrate (Matrigel) induces human umbilical vein endothelial cells to rapidly form vessel-like tubes (Kubota, et al., 1988; Grant et al., 1989b); however, the precise mechanism of tube formation is unclear. Using this in vitro model, we have investigated morphologic changes occurring during tube formation and the cytoskeletal and protein synthesis requirements of this process. Electron microscopy showed that endothelial cells attach to the Matrigel surface, align, and form cylindrical structures that contain a lumen and polarized cytoplasmic organelles. The cytoskeleton is reorganized into bundles of actin filaments oriented along the axis of the tubes and is located at the periphery of the cells. The addition of colchicine or cytochalasin D blocked tube formation, indicating that both microfilaments and microtubules are involved in this process. Cycloheximide blocked tube formation by 100%, indicating that the process also required protein synthesis. In particular, collagen synthesis seems to be required for tube formation because cis-hydroxyproline inhibited tube formation, whereas either the presence of ascorbic acid or the addition of exogenous collagen IV to the Matrigel increased tube formation. Our results indicate that endothelial cell attachment to Matrigel induces the reorganization of the cytoskeleton and elicits the synthesis of specific proteins required for the differentiated phenotype of the cells. C1 UNIV WISCONSIN,DEPT MED,CELL BIOL LAB,MILWAUKEE,WI 53201. RP GRANT, DS (reprint author), NIDR,DEV BIOL & ANOMALIES,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 54 TC 92 Z9 92 U1 0 U2 2 PU SOC IN VITRO BIOLOGY PI COLUMBIA PA 8815 CENTRE PARK DRIVE SUITE 210, COLUMBIA, MD 21045 SN 0073-5655 J9 IN VITRO CELL DEV B PD APR PY 1991 VL 27 IS 4 BP 327 EP 336 PG 10 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA FT918 UT WOS:A1991FT91800011 PM 1856158 ER PT J AU TAMISLEMONDA, CS BORNSTEIN, MH AF TAMISLEMONDA, CS BORNSTEIN, MH TI INDIVIDUAL VARIATION, CORRESPONDENCE, STABILITY, AND CHANGE IN MOTHER AND TODDLER PLAY SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE PLAY; INDIVIDUAL DIFFERENCES; MOTHER-INFANT INTERACTION; STABILITY ID SYMBOLIC PLAY; LANGUAGE; ATTENTION; BEHAVIOR; INFANCY; PERIOD C1 NICHHD,CHILD & FAMILY RES SECT,BETHESDA,MD 20892. RP TAMISLEMONDA, CS (reprint author), NYU,INFANCY STUDIES PROGRAM,6 WASHINGTON PL,NEW YORK,NY 10003, USA. NR 35 TC 66 Z9 66 U1 0 U2 4 PU ABLEX PUBL CORP PI NORWOOD PA 355 CHESTNUT ST, NORWOOD, NJ 07648 SN 0163-6383 J9 INFANT BEHAV DEV JI Infant Behav. Dev. PD APR-JUN PY 1991 VL 14 IS 2 BP 143 EP 162 DI 10.1016/0163-6383(91)90002-A PG 20 WC Psychology, Developmental SC Psychology GA FX951 UT WOS:A1991FX95100002 ER PT J AU NASH, TE MERRITT, JW CONRAD, JT AF NASH, TE MERRITT, JW CONRAD, JT TI ISOLATE AND EPITOPE VARIABILITY IN SUSCEPTIBILITY OF GIARDIA-LAMBLIA TO INTESTINAL PROTEASES SO INFECTION AND IMMUNITY LA English DT Article ID EXCRETORY-SECRETORY PRODUCTS; ANTIGENIC VARIATION; LECTIN AB The surface antigens of Giardia lamblia differ. To determine whether the unique surface antigens found in variants and isolates could differentially protect the parasite from digestion by intestinal proteases, G. lamblia clones WB-2X (WB), GS/M-H7 (GS/M), and B6, each of which expresses a unique surface variant antigen, were exposed to alpha-chymotrypsin and trypsin at concentrations up to 20 mg/ml in culture medium. The number of surviving trophozoites and morphologic changes were assessed over time. After 24 h, there was a significant decrease in the number of surviving trophozoites of WB (80.5 and 94.2% for trypsin and alpha-chymotrypsin treatments, respectively, compared with controls) and B6 (78.9 and 95.5% for trypsin and alpha-chymotrypsin treatments, respectively, compared with controls) at 10 mg of enzyme per ml compared with culture medium alone. Cytotoxicity was prevented by the presence of soybean trypsin inhibitor, indicating the effects were due to protease activity. In contrast, there was no significant cytotoxicity after exposure of GS/M to either enzyme at the same enzyme concentration. After exposure to alpha-chymotrypsin, susceptible G. lamblia became rounded and then lysed, but after exposure to trypsin, G. lamblia appeared plastered onto the surface of the well and was interwined and surrounded by finely granular material. Effects were concentration and time dependent; at least 6 h of treatment was required to observe changes 12 to 18 h later. Trophozoites surviving alpha-chymotrypsin or trypsin exposure became stably resistant to protease treatment. In vitro, the variant surface antigen of GS/M, but not those of WB or B6, resisted digestion by trypsin or alpha-chymotrypsin, suggesting that the variant surface antigens impart susceptibility or resistance to digestion. The initial surface variant antigens of WB and B6 were replaced in resistant cultures. Trophozoites differ in their ability to survive after exposure to intestinal proteases, which may enable certain G. lamblia isolates or isolates possessing certain surface variant antigens to survive in the small intestine. RP NASH, TE (reprint author), NIAID,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 21 TC 47 Z9 47 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1991 VL 59 IS 4 BP 1334 EP 1340 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FD915 UT WOS:A1991FD91500018 PM 1706319 ER PT J AU BURNS, DL GOULDKOSTKA, JL KESSEL, M ARCINIEGA, JL AF BURNS, DL GOULDKOSTKA, JL KESSEL, M ARCINIEGA, JL TI PURIFICATION AND IMMUNOLOGICAL CHARACTERIZATION OF A GROEL-LIKE PROTEIN FROM BORDETELLA-PERTUSSIS SO INFECTION AND IMMUNITY LA English DT Article ID 2-DIMENSIONAL IMMUNOELECTROPHORESIS; ANTIGENIC ANALYSIS; COMMON ANTIGEN; BINDING; CELLS; IDENTIFICATION; CHLAMYDIAE; ANTIBODIES; ARTHRITIS AB A GroEL-like protein from Bordetella pertussis was purified. This protein was found to have the tetradecameric subunit structure typical of the GroEL family of proteins and to contain epitopes similar to those of other members of this family, including a human GroEL-like protein. Active immunization of neonatal mice with the B. pertussis GroEL-like protein provided little protection against an aerosol challenge with B. pertussis. Antibodies to this protein were elicited in mice by a standard diphtheria-tetanus-pertussis (DTP) vaccine but not by an experimental acellular pertussis vaccine. Since the Bordetella GroEL-like protein was found to contain epitopes similar to those on the mammalian analog, the potential exists that vaccination with standard DTP vaccines may induce antibodies which react with the mammalian GroEL analog. C1 NIAMSD,STRUCT STUDIES RES LAB,BETHESDA,MD 20892. RP BURNS, DL (reprint author), NIAMSD,CTR BIOL EVALUAT & RES,DIV BACTERIAL PROD,BETHESDA,MD 20892, USA. NR 39 TC 20 Z9 21 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1991 VL 59 IS 4 BP 1417 EP 1422 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FD915 UT WOS:A1991FD91500029 PM 2004820 ER PT J AU MACRINA, FL JONES, KR ALPERT, CA CHASSY, BM MICHALEK, SM AF MACRINA, FL JONES, KR ALPERT, CA CHASSY, BM MICHALEK, SM TI REPEATED DNA-SEQUENCE INVOLVED IN MUTATIONS AFFECTING TRANSPORT OF SUCROSE INTO STREPTOCOCCUS-MUTANS V403 VIA THE PHOSPHOENOLPYRUVATE PHOSPHOTRANSFERASE SYSTEM SO INFECTION AND IMMUNITY LA English DT Article ID SUCROSE-6-PHOSPHATE HYDROLASE; 6-PHOSPHATE HYDROLASE; GENE; PLASMID; LACTIS; SCRB AB Mutants of Streptococcus mutans V403 defective in the intracellular sucrose-6-phosphate hydrolase (product of the scrB gene) are sensitive to sucrose because of the intracellular accumulation of the phosphorylated sugar. Using a scrB mutant prepared by allelic exchange, we have isolated and characterized a number of sucrose-resistant revertants. One such mutant was found to lack the ability to transport sucrose into the cell via the phosphoenolpyruvate-dependent sucrose phosphotransferase system (PTS). Genetic analysis of this strain revealed this lesion to be linked to the scrB gene. This was corroborated by the physical demonstration of an insertion mutation very near scrB. Taken together with DNA sequence information (Y. Sato, F. Poy, G. R. Jacobson, and H. K. Kuramitsu, J. Bacteriol. 171:263-271, 1989), our results indicated that all of the mutations characterized were located in the adjoining scrA gene which encodes the membrane-associated, sugar-specific enzyme II (EII(sucrose)) component of the sucrose PTS in S. mutans. Biochemically, such a genetic lesion disables the sucrose PTS and prevents sucrose from entering the cell by this system. In this paper, we detail the nature of two independent insertion mutations and conclude them to be the result of duplicative transposition events into the scrA gene. This region of the chromosome was amplified and purified in large quantities by using polymerase chain reaction. Examination of the amplified and purified in large quantities by using the polymerase chain reaction. Examination of the amplified DNA revealed that the two independent insertion mutations were composed of sequences that were indistinguishable by size and by restriction site endonuclease maps. Their insertion points in the scrA gene were approximately 200 bp apart. The amplified DNA fragment was also used as a probe to demonstrate the presence of five copies of this element on the S. mutans V403 chromosome. A second strain, S. mutans V310, also was found to carry similarly arranged, multiple copies of this sequence on its chromosome, suggesting a clonal origin of V403 and V310. The small size of this sequence, its presence in multiple copies on the V403 chromosome, and its ability to duplicate itself semiconservatively into remote sites argue compellingly that it is an insertion sequence element. One such insertion mutant, with a defective sucrose PTS, was tested for virulence in rats and was found to cause caries at levels similar to those of the wild-type strain. C1 NIDR,MICROBIOL & IMMUNOL LAB,BETHESDA,MD 20892. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. RP MACRINA, FL (reprint author), VIRGINIA COMMONWEALTH UNIV,DEPT MICROBIOL & IMMUNOL,RICHMOND,VA 23298, USA. FU NIDCR NIH HHS [DE08182, DE04224, DE09035] NR 34 TC 20 Z9 20 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1991 VL 59 IS 4 BP 1535 EP 1543 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FD915 UT WOS:A1991FD91500044 PM 2004831 ER PT J AU MULLAN, H AF MULLAN, H TI INHERENT MORAL PRACTICE IN GROUP-PSYCHOTHERAPY SO INTERNATIONAL JOURNAL OF GROUP PSYCHOTHERAPY LA English DT Article C1 GEORGETOWN UNIV,SCH PSYCHIAT,GRP PSYCHOTHERAPY TRAINING PROGRAM,WASHINGTON,DC. NIH,BIOETH PROGRAM,LIAISON GRP,BETHESDA,MD 20892. NR 17 TC 4 Z9 4 U1 0 U2 0 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0020-7284 J9 INT J GROUP PSYCHOTH JI Int. J. Group Psychother. PD APR PY 1991 VL 41 IS 2 BP 185 EP 197 PG 13 WC Psychology, Clinical SC Psychology GA FV208 UT WOS:A1991FV20800004 PM 2040543 ER PT J AU KINSELLA, TJ DELUCA, AM BARNES, M ANDERSON, W TERRILL, R SINDELAR, WF AF KINSELLA, TJ DELUCA, AM BARNES, M ANDERSON, W TERRILL, R SINDELAR, WF TI THRESHOLD DOSE FOR PERIPHERAL NEUROPATHY FOLLOWING INTRAOPERATIVE RADIOTHERAPY (IORT) IN A LARGE ANIMAL-MODEL SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE INTRAOPERATIVE RADIOTHERAPY; PERIPHERAL NEUROPATHY ID RADIATION-THERAPY; RETROPERITONEAL; TOLERANCE AB Radiation injury to peripheral nerve is a dose-limiting toxicity in the clinical application of intraoperative radiotherapy, particularly for pelvic and retroperitoneal tumors. Intraoperative radiotherapy-related peripheral neuropathy in humans receiving doses of 20-25 Gy is manifested as a mixed motor-sensory deficit beginning 6-9 months following treatment. In a previous experimental study of intraoperative radiotherapy-related neuropathy of the lumbo-sacral plexus, an approximate inverse linear relationship was reported between the intraoperative dose (20-75 Gy range) and the time to onset of hind limb paresis (1-12 mos following intraoperative radiotherapy). The principal histological lesion in irradiated nerve was loss of large nerve fibers and perineural fibrosis without significant vascular injury. Similar histological changes in irradiated nerves were found in humans. To assess peripheral nerve injury to lower doses of intraoperative radiotherapy in this same large animal model, groups of four adult American Foxhounds (wt 20-25 kg) received doses of 10, 15, or 20 Gy to the right lumbo-sacral plexus and sciatic nerve using 9 MeV electrons. The left lumbo-sacral plexus and sciatic nerve were excluded from the intraoperative field to allow each animal to serve as its own control. Following treatment, a complete neurological exam, electromyogram, and nerve conduction studies were performed monthly for 1 year. Monthly neurological exams were performed in years 2 and 3 whereas electromyogram and nerve conduction studies were performed every 3 months during this follow-up period. With follow-up of greater-than-or-equal-to 42 months, no dog receiving 10 or 15 Gy IORT shows any clinical or laboratory evidence of peripheral nerve injury. However, all four dogs receiving 20 Gy developed right hind limb paresis at 8, 9, 9, and 12 mos following intraoperative radiotherapy. These experimental data suggest that intraoperative doses of < 20 Gy may not result in clinically significant peripheral nerve injury with follow-up of 3.5 years. Longer (5 yrs) follow-up with planned sacrifice of the remaining dogs is scheduled to assess any late peripheral nerve damage. C1 INDIANA UNIV,SCH MED,TERRE HAUTE,IN. NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,SURG BRANCH,BETHESDA,MD 20892. UNIV WISCONSIN,CTR CLIN CANC,DEPT HUMAN ONCOL,MADISON,WI 53792. NR 13 TC 66 Z9 69 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD APR PY 1991 VL 20 IS 4 BP 697 EP 701 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FC806 UT WOS:A1991FC80600008 PM 2004946 ER PT J AU FERRICK, MR THURAU, SR OPPENHEIM, MH HERBORT, CP NI, M ZACHARIAE, COC MATSUSHIMA, K CHAN, CC AF FERRICK, MR THURAU, SR OPPENHEIM, MH HERBORT, CP NI, M ZACHARIAE, COC MATSUSHIMA, K CHAN, CC TI OCULAR INFLAMMATION STIMULATED BY INTRAVITREAL INTERLEUKIN-8 AND INTERLEUKIN-1 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE INTERLEUKIN-8; NEUTROPHIL CHEMOTAXIS; INTERLEUKIN-1; ANTERIOR UVEITIS; OCULAR INFLAMMATION ID NEUTROPHIL CHEMOTACTIC FACTOR; TUMOR NECROSIS FACTOR; LEWIS RATS; PROTEIN; ARTHRITIS AB Interleukin-8 (IL-8), a cytokine with neutrophil chemotactic and activating properties, is known to be stimulated by IL-1. Fischer rats are more resistant to inflammation than Lewis rats probably due to a higher corticosteroid stress response. To determine the role of IL-8 in ocular inflammation, the effect of intravitreal injection of IL-8 was compared with that of IL-1 in both Lewis and Fischer rats. The IL-8, IL-1-alpha, or sterile balanced salt solution (control) was injected into one eye of each animal. Both IL-8 and IL-1-alpha caused inflammation in the eye of both strains, as detected by leukocyte counts of the anterior chamber and histopathologic examination. The eyes of animals injected with a cytokine had significantly higher numbers of leukocytes compared with eyes of control animals. Histopathologic examination confirmed these findings. The IL-1-alpha induced inflammation more consistently and more severely than the most effective dose of IL-8. This finding agreed with the concept of IL-1 initiating a cascade of inflammatory mediators including IL-8, which acts more specifically on a smaller population of leukocytes. A contralateral response was observed in the uninjected eye of experimental and control animals. The contralateral response in animals receiving the cytokines was significantly greater than that in controls. Lewis rats show a higher inflammatory response to the injections than do the Fischer rats. These data suggest that IL-8 may be active as one component in neutrophil-mediated ocular inflammation. C1 NEI,HOWARD HUGHES MED INST,BLDG 10,ROOM 10N206,BETHESDA,MD 20892. NEI,IMMUNOL LAB,BETHESDA,MD 20892. NCI,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 19 TC 81 Z9 83 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD APR PY 1991 VL 32 IS 5 BP 1534 EP 1539 PG 6 WC Ophthalmology SC Ophthalmology GA FH197 UT WOS:A1991FH19700015 PM 2016135 ER PT J AU TAO, RV TAKAHASHI, Y KADOR, PF AF TAO, RV TAKAHASHI, Y KADOR, PF TI EFFECT OF ALDOSE REDUCTASE INHIBITORS ON NAPHTHALENE CATARACT FORMATION IN THE RAT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE NAPHTHALENE-INDUCED CATARACT; ALDOSE REDUCTASE INHIBITOR; SLIT-LAMP MICROSCOPY; HISTOLOGIC STUDY; RATS ID PREVENTION AB Naphthalene feeding can result in cataract formation in rats and rabbits due to specific metabolites of naphthalene. The concomitant administration of the aldose reductase inhibitor Al1576 to naphthalene-fed rats was proven to prevent cataract formation. To determine whether this effect was directly linked to the ability of Al1576 to inhibit enzyme aldose reductase, a variety of structurally diverse aldose reductase inhibitors, including the carboxylic acids tolrestat, Ponalrestat, and FK366, and the spirohydantoins, sorbinil and Al1576, were investigated for their ability to inhibit naphthalene-induced cataracts. Brown Norway rats, administered naphthalene by gavage, were fed normal rat chow containing these aldose reductase inhibitors at levels known to inhibit sugar cataract formation. The lens changes in these rats were monitored over a 90-day period by portable slit-lamp microscopy and histologic study. Al1576 showed a dose-dependent reduction in naphthalene-induced cataract formation, with no naphthalene-associated deposits seen in toluidine blue-stained lens sections. Sorbinil also reduced lens changes, whereas tolrestat, Ponalrestat, and FK366 had no effect. These results suggest that inhibition of naphthalene-induced cataract formation by structurally diverse aldose reductase inhibitors was not linked to the inhibition of aldose reductase. C1 NEI,BETHESDA,MD 20892. RP TAO, RV (reprint author), UNIV ILLINOIS,COLL MED,LIONS ILLINOIS EYE RES INST,DEPT OPHTHALMOL,1905 W TAYLOR ST,CHICAGO,IL 60612, USA. FU NEI NIH HHS [EY-01792, EY-01821] NR 17 TC 16 Z9 16 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD APR PY 1991 VL 32 IS 5 BP 1630 EP 1637 PG 8 WC Ophthalmology SC Ophthalmology GA FH197 UT WOS:A1991FH19700028 PM 1901836 ER PT J AU ZAHN, TP KRUESI, MJP RAPOPORT, JL AF ZAHN, TP KRUESI, MJP RAPOPORT, JL TI REACTION-TIME INDEXES OF ATTENTION DEFICITS IN BOYS WITH DISRUPTIVE BEHAVIOR DISORDERS SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article ID SUSTAINED ATTENTION; CHILDREN; HYPERACTIVITY; LIMITATIONS; INTERVIEW C1 NIMH,PSYCHOL & PSYCHOPATHOL LAB,BETHESDA,MD 20892. NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. NR 38 TC 41 Z9 41 U1 1 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0091-0627 J9 J ABNORM CHILD PSYCH JI J. Abnorm. Child Psychol. PD APR PY 1991 VL 19 IS 2 BP 233 EP 252 DI 10.1007/BF00909980 PG 20 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA FG315 UT WOS:A1991FG31500006 PM 2056165 ER PT J AU WHITE, MV PHILLIPS, RL KALINER, MA AF WHITE, MV PHILLIPS, RL KALINER, MA TI NEUTROPHILS AND MAST-CELLS - NEDOCROMIL SODIUM INHIBITS THE GENERATION OF NEUTROPHIL-DERIVED HISTAMINE-RELEASING ACTIVITY (HRA-N) SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; EXERCISE-INDUCED ASTHMA; MONONUCLEAR-CELLS; BASOPHIL; SECRETION; CROMOGLYCATE; ACTIVATION; PLACEBO; TILADE; IL-3 AB The effect of nedocromil sodium on the generation of neutrophil-derived histamine-releasing activity (HRA-N) from human peripheral blood neutrophils and on the secretory effects of HRA-N and anti-IgE on rat basophil leukemia (RBL) cells was studied. Nedocromil sodium caused dose-related inhibition of HRA-N generation by human neutrophils (10(-7) to 10(-4) mol/L; inhibitory concentration of 50%, 1.5 x 10(-8) mol/L). In contrast, the presence of nedocromil sodium had no effect on HRA-N-mediated serotonin release from RBL cells. In five experiments, with one crude and four partially purified HRA-N preparations, serotonin release from RBL cells exposed to native HRA-N or HRA-N in the presence of nedocromil sodium (10(-4) mol/L) was 28% +/- 6% and 26% +/- 5%, respectively. Similar results were found with all concentrations of nedocromil sodium studied. Preincubation of RBL cells with nedocromil sodium (10(-4) mol/L) for 0 to 60 minutes also did not affect HRA-N-mediated serotonin release. Likewise, nedocromil sodium (10(-7) to 10(-4) mol/L) had no effect on anti-IgE-induced serotonin release from RBL cells. In 10 experiments, anti-IgE alone or in the presence of nedocromil sodium (10(-4) mol/L) induced 32% +/- 6% and 32% +/- 5% serotonin release, respectively. Preincubation of RBL cells with nedocromil sodium before anti-IgE exposure had no further effect. This is the first study of pharmacologic manipulation of the generation of a histamine-releasing factor. It is hypothesized that one possible mechanism whereby nedocromil sodium protects against asthma and allergic rhinitis is through inhibition of HRA-N generation. RP WHITE, MV (reprint author), NIAID,BLDG 10,ROOM 11C207,BETHESDA,MD 20892, USA. NR 29 TC 13 Z9 13 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD APR PY 1991 VL 87 IS 4 BP 812 EP 820 DI 10.1016/0091-6749(91)90127-A PG 9 WC Allergy; Immunology SC Allergy; Immunology GA FG059 UT WOS:A1991FG05900010 PM 1707428 ER PT J AU GARRIGA, MM BERKEBILE, C METCALFE, DD AF GARRIGA, MM BERKEBILE, C METCALFE, DD TI A COMBINED SINGLE-BLIND, DOUBLE-BLIND, PLACEBO-CONTROLLED STUDY TO DETERMINE THE REPRODUCIBILITY OF HYPERSENSITIVITY REACTIONS TO ASPARTAME SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID IMMEDIATE ADVERSE REACTIONS; ORAL FOOD CHALLENGE; ADULT PATIENTS; HEADACHE; SAFETY AB Aspartame is an O-methyl ester composed of phenylalanine and aspartic acid. After its final approval as a sweetner in 1981, a number of reports of adverse reactions to aspartame appeared in the literature. To explore the pathogenesis of such reactions, we initiated a study in July 1986 to identify subjects with hypersensitivity reactions to aspartame with blinded challenge procedures. The study was closed after 32 months. During that time, we advertised in local newspapers and worked closely with the local community of allergists and dermatologists in an attempt to recruit subjects with hypersensitivity reactions to aspartame. A total of 61 self-referrals and physician referrals were screened, with 20 referrals evaluated in clinic. After this evaluation, 12 patients underwent single- and double-blind challenge with up to 2000 mg of aspartame. No subject with a clearly reproducible adverse reaction to aspartame was identified. In summary, we found that it is difficult to recruit study subjects with a history of hypersensitivity reactions to aspartame and that subjects who believed themselves allergic to aspartame did not have reproducible reactions. C1 NIAID,CLIN INVEST LAB,MAST CELL PHYSIOL SECT,BETHESDA,MD 20892. NR 17 TC 33 Z9 33 U1 0 U2 4 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD APR PY 1991 VL 87 IS 4 BP 821 EP 827 DI 10.1016/0091-6749(91)90128-B PG 7 WC Allergy; Immunology SC Allergy; Immunology GA FG059 UT WOS:A1991FG05900011 PM 2013676 ER PT J AU BUESCHER, PC PEARSE, DB PILLAI, RP LITT, MC MITCHELL, MC SYLVESTER, JT AF BUESCHER, PC PEARSE, DB PILLAI, RP LITT, MC MITCHELL, MC SYLVESTER, JT TI ENERGY-STATE AND VASOMOTOR TONE IN HYPOXIC PIG LUNGS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE HYPOXIA; ANOXIA; CYANIDE; PULMONARY ARTERIAL PRESSURE; ADENOSINE 5'-TRIPHOSPHATE; P-31 NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY ID RAT LUNGS; OXYGEN-TENSION; METABOLISM; VASOCONSTRICTION; RESPONSES; INHIBITORS AB To evaluate the role of energy state in pulmonary vascular responses to hypoxia, we exposed isolated pig lungs to decreases in inspired PO2 or increases in perfusate NaCN concentration. Lung energy state was assessed by P-31 nuclear magnetic resonance spectroscopy or measurement of adenine nucleotides by high-pressure liquid chromatography in freeze-clamped biopsies. In ventilated lungs, inspired PO2 of 200 (normoxia), 50 (hypoxia), and 0 Torr (anoxia) did not change adenine nucleotides but resulted in steady-state pulmonary arterial pressure (Ppa) values of 15.5 +/- 1.4, 30.3 +/- 1.8, and 17.2 +/- 1.9 mmHg, respectively, indicating vasoconstriction during hypoxia and reversal of vasoconstriction during anoxia. In degassed lungs, similar changes in Ppa were observed; however, energy state deteriorated during anoxia. An increase in perfusate NaCN concentration from 0 to 0.1 mM progressively increased Ppa and did not alter adenine nucleotides, whereas 1 mM reversed this vasoconstriction and caused deterioration of energy state. These results suggest that 1) pulmonary vasoconstrictor responses to hypoxia or cyanide occurred independently of whole lung energy state, 2) the inability of the pulmonary vasculature to sustain hypoxic vasoconstriction during anoxia might be associated with decreased energy state in some lung compartment, and 3) atelectasis was detrimental to whole lung energy state. C1 JOHNS HOPKINS MED INST,DEPT MED,DIV PULM & CRIT CARE MED,600 N WOLFE ST,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT MED,DIV GASTROENTEROL,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,CELLULAR & MOLEC BIOL LAB,BALTIMORE,MD 21224. FU NHLBI NIH HHS [HL-10342] NR 29 TC 47 Z9 47 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD APR PY 1991 VL 70 IS 4 BP 1874 EP 1881 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA FF832 UT WOS:A1991FF83200059 PM 2055866 ER PT J AU ROBERGE, FG CASPI, RR CHAN, CC NUSSENBLATT, RB AF ROBERGE, FG CASPI, RR CHAN, CC NUSSENBLATT, RB TI INHIBITION OF LYMPHOCYTE-T PROLIFERATION BY RETINAL GLIAL MULLER CELLS - REVERSAL OF INHIBITION BY GLUCOCORTICOIDS SO JOURNAL OF AUTOIMMUNITY LA English DT Article ID MYELIN BASIC-PROTEIN; HELPER LYMPHOCYTES; LEWIS RATS; HORMONES; ANTIGEN; UNRESPONSIVENESS; EXPRESSION; ACTIVATION; RECEPTORS; INDUCTION C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 27 TC 9 Z9 9 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0896-8411 J9 J AUTOIMMUN JI J. Autoimmun. PD APR PY 1991 VL 4 IS 2 BP 307 EP 314 DI 10.1016/0896-8411(91)90026-9 PG 8 WC Immunology SC Immunology GA FQ140 UT WOS:A1991FQ14000010 PM 1831985 ER PT J AU EGWUAGU, CE CHOW, C BERAUD, E CASPI, RR MAHDI, RM BREZIN, AP NUSSENBLATT, RB GERY, I AF EGWUAGU, CE CHOW, C BERAUD, E CASPI, RR MAHDI, RM BREZIN, AP NUSSENBLATT, RB GERY, I TI T-CELL RECEPTOR BETA-CHAIN USAGE IN EXPERIMENTAL AUTOIMMUNE UVEORETINITIS SO JOURNAL OF AUTOIMMUNITY LA English DT Article ID MYELIN BASIC-PROTEIN; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MAJOR HISTOCOMPATIBILITY COMPLEX; RETINOID-BINDING PROTEIN; RAT; DETERMINANT; EXPRESSION; IMMUNODOMINANT; IMMUNIZATION; RECOGNITION RP EGWUAGU, CE (reprint author), NEI,IMMUNOL LAB,BLDG 10,ROOM 10B10,BETHESDA,MD 20892, USA. NR 25 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0896-8411 J9 J AUTOIMMUN JI J. Autoimmun. PD APR PY 1991 VL 4 IS 2 BP 315 EP 324 DI 10.1016/0896-8411(91)90027-A PG 10 WC Immunology SC Immunology GA FQ140 UT WOS:A1991FQ14000011 PM 1652969 ER PT J AU TOKESON, JPE GARGES, S ADHYA, S AF TOKESON, JPE GARGES, S ADHYA, S TI FURTHER INDUCIBILITY OF A CONSTITUTIVE SYSTEM - ULTRAINDUCTION OF THE GAL OPERON SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; CYCLIC-AMP; REPRESSOR BINDING; GALACTOSE OPERON; CLONING VEHICLES; 2 PROMOTERS; OPERATOR; GENE; TRANSCRIPTION; EXPRESSION AB In wild-type Escherichia coli, expression of the gal operon is negatively regulated by the Gal repressor and is induced 10- to 15-fold when the repressor is inactivated by an inducer. In strains completely deleted for galR, the gene which encodes the Gal repressor, the operon is derepressed by only 10-fold without an inducer. But this derepression is increased further by threefold during cell growth in the presence of an inducer, D-galactose or D-fucose. This phenomenon of extreme induction in the absence of Gal repressor is termed ultrainduction-a manifestation of further inducibility in a constitutive setup. Construction and characterization of gene and operon fusion strains between galE and lacZ, encoding beta-galactosidase as a reporter gene, show that ultrainduction occurs at the level of transcription and not translation. Transcription of the operon, from both the cyclic AMP-dependent P1 and the cyclic nucleotide-independent P2 promoters, is subject to ultrainduction. The wild-type galR+ gene has an epistatic effect on ultrainducibility: ultrainduction is observed only in cells devoid of Gal repressor protein. Titration experiments show the existence of an ultrainducibility factor that acts like a repressor and functions by binding to DNA segments (operators) to which Gal repressor also binds to repress the operon. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 35 TC 17 Z9 17 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD APR PY 1991 VL 173 IS 7 BP 2319 EP 2327 PG 9 WC Microbiology SC Microbiology GA FE184 UT WOS:A1991FE18400026 PM 2007555 ER PT J AU KERNS, RD HAYTHORNTHWAITE, J ROSENBERG, R SOUTHWICK, S GILLER, EL JACOB, MC AF KERNS, RD HAYTHORNTHWAITE, J ROSENBERG, R SOUTHWICK, S GILLER, EL JACOB, MC TI THE PAIN BEHAVIOR CHECK LIST (PBCL) - FACTOR STRUCTURE AND PSYCHOMETRIC PROPERTIES SO JOURNAL OF BEHAVIORAL MEDICINE LA English DT Article DE CHRONIC PAIN; PAIN BEHAVIORS; PAIN ASSESSMENT; SELF-REPORT ID LOW-BACK-PAIN; CONSTRUCT; SCALE C1 YALE UNIV,SCH MED,NEW HAVEN,CT 06510. NIA,BALTIMORE,MD 21224. UNIV CONNECTICUT,SCH MED,FARMINGTON,CT 06032. RP KERNS, RD (reprint author), VET ADM MED CTR,PSYCHOL SERV,W HAVEN,CT 06516, USA. NR 19 TC 68 Z9 69 U1 0 U2 4 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0160-7715 J9 J BEHAV MED JI J. Behav. Med. PD APR PY 1991 VL 14 IS 2 BP 155 EP 167 DI 10.1007/BF00846177 PG 13 WC Psychology, Clinical SC Psychology GA FP980 UT WOS:A1991FP98000005 PM 1880794 ER PT J AU LINDHOLM, PF MARRIOTT, SJ GITLIN, SD BRADY, JN AF LINDHOLM, PF MARRIOTT, SJ GITLIN, SD BRADY, JN TI DIFFERENTIAL PRECIPITATION AND ZINC CHELATE CHROMATOGRAPHY PURIFICATION OF BIOLOGICALLY-ACTIVE HTLV-I TAX1 EXPRESSED IN ESCHERICHIA-COLI SO JOURNAL OF BIOCHEMICAL AND BIOPHYSICAL METHODS LA English DT Article DE HLTV-I TAX1; PURIFICATION ID VIRUS TYPE-I; HUMAN IMMUNODEFICIENCY VIRUS; NF-KAPPA-B; METAL-LINKED DIMER; RESPONSIVE ELEMENT; GENE-EXPRESSION; TAT PROTEIN; ACTIVATION; TRANSCRIPTION; BINDING AB A protocol which involves sequential ammonium sulfate precipitation and zinc chelate chromatography to purify the HTLV-I Tax1 protein expressed in E. coli is described. The final Tax1 product is greater than 90% pure and the yield is approximately 1 mg per liter of liquid culture. The purified Tax1 protein is biologically active in indirect in vitro DNA binding assays and cellular NF-kB induction experiments. RP LINDHOLM, PF (reprint author), NCI,MOLEC VIROL LAB,BETHESDA,MD 20892, USA. NR 24 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-022X J9 J BIOCHEM BIOPH METH JI J. Biochem. Biophys. Methods PD APR PY 1991 VL 22 IS 3 BP 233 EP 241 DI 10.1016/0165-022X(91)90071-4 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FG109 UT WOS:A1991FG10900005 PM 1865054 ER PT J AU DUBAND, JL DUFOUR, S YAMADA, SS YAMADA, KM THIERY, JP AF DUBAND, JL DUFOUR, S YAMADA, SS YAMADA, KM THIERY, JP TI NEURAL CREST CELL LOCOMOTION INDUCED BY ANTIBODIES TO BETA-1 INTEGRINS - A TOOL FOR STUDYING THE ROLES OF SUBSTRATUM MOLECULAR AVIDITY AND DENSITY IN MIGRATION SO JOURNAL OF CELL SCIENCE LA English DT Article DE CELL LOCOMOTION; CELL ADHESION; INTEGRIN RECEPTORS; FIBRONECTIN ID FIBRONECTIN RECEPTOR COMPLEX; EXTRACELLULAR-MATRIX; VERTEBRATE EMBRYO; MONOCLONAL-ANTIBODIES; CULTURED FIBROBLASTS; SULFATE PROTEOGLYCAN; NERVOUS-SYSTEM; GROWTH CONES; ADHESION; CONTACTS AB Migration of neural crest cells depends on direct, transient interactions between fibronectin molecules and their corresponding Arg-Gly-Asp integrin receptors. We have previously suggested that the moderate-avidity interaction between integrin receptors and fibronectin may be critical for the transient association of the cells with their substratum. In order to test this hypothesis, we have examined the in vitro locomotory behavior of neural crest cells on substrata of differing apparent avidities for integrin receptors. As substrata, we used a variety of monoclonal and polyclonal antibodies to the integrin beta-1 subunit that were characterized for their respective relative apparent avidities for the receptor. Neural crest cells were able to migrate on these antibodies and exhibited an organization of substratum-adhesion sites and of cytoskeletal elements virtually identical to that observed on fibronectin, indicating that they can at least partially mimic the migration-promoting activity of fibronectin. However, the number of migrating cells as well as their morphology and their speed of locomotion varied significantly with both the concentration of the antibody substratum and its relative avidity for the receptor. Thus, on high-avidity monoclonal antibodies and on polyclonal divalent antibodies at high concentrations only a limited number of cells escaped from the neural tube, and the rate of their migration was reduced compared to that on fibronectin (23 +/- 5-mu-m h-1 versus 65 +/- 10-mu-m h-1). In addition, cells were unusually flattened and cohesive. Time-lapse videomicroscopy revealed that, on high-avidity substrata, neural crest cells were able to extend cell processes that adhered to the substratum, but showed a dramatically reduced capability of breaking pre-existing substratum contacts. In contrast, the same antibodies at low concentrations produced neural crest cell migration at rates very similar to those on fibronectin at the same concentrations. Low-avidity monoclonal antibodies and polyclonal monovalent antibodies at all concentrations tested permitted extensive migration of neural crest cells, which exhibited the same morphology and locomotory behavior as on fibronectin. These results indicate that both the avidity of receptors for the substratum and the number of receptors bound to the substratum are critical in regulating the locomotory behavior of neural crest cells in vitro, and therefore might help to regulate the directionality of migration and final localization pattern of neural crest cells in vivo. C1 ECOLE NORM SUPER,CNRS,PHYSIOPATHOL DEV LAB,F-75230 PARIS 05,FRANCE. NCI,MOLEC BIOL LAB,MEMBRANE BIOCHEM SECT,BETHESDA,MD 20892. NR 63 TC 92 Z9 92 U1 0 U2 2 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD APR PY 1991 VL 98 BP 517 EP 532 PN 4 PG 16 WC Cell Biology SC Cell Biology GA FK589 UT WOS:A1991FK58900010 PM 1713595 ER PT J AU WEEKS, BS PAPADOPOULOS, V DYM, M KLEINMAN, HK AF WEEKS, BS PAPADOPOULOS, V DYM, M KLEINMAN, HK TI CAMP PROMOTES BRANCHING OF LAMININ-INDUCED NEURONAL PROCESSES SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID RAT SYMPATHETIC NEURONS; CENTRAL NERVOUS-SYSTEM; PROTEIN KINASE-C; NEURITE OUTGROWTH; MORPHOLOGICAL-DIFFERENTIATION; TISSUE-CULTURE; PHORBOL ESTER; GROWTH-FACTOR; CELLS; FIBRONECTIN AB Laminin is a potent stimulator of neurite outgrowth. We have examined the signal transduction events involved in the neuronal cell response to laminin. Cyclic nucleotides, calcium, and sodium-proton exchange do not appear to be required for the transduction of the laminin signal during neurite outgrowth. Direct measurement of cAMP and cGMP levels shows no changes in NG108-15 cells when cultured on laminin. Exogenous cAMP alone had no effect on either the rate of process formation or process length, but did alter the morphology of laminin-induced neurites. A four-fold increase in the number of branches per neurite and a two-to-three-fold increase in the number of neurites per cell were observed in both NG108-15 and PC12 cells cultured on laminin when either 8-BrcAMP or forskolin was added. The cAMP-induced branching was also observed when PC12 cells were cultured on a laminin-derived synthetic peptide (PA22-2), which contains the neurite-promoting amino acid sequence IKVAV. By immunofluorescence analysis with axonal or dendritic markers, the PC12 processes on laminin and PA22-2 were axonal, not dendritic, and the cAMP-induced morphological changes were due to axonal branching. These data demonstrate that changes in cAMP are not involved in laminin-mediated neurite outgrowth, but cAMP can modulate the effects of laminin. C1 GEORGETOWN UNIV,SCH MED,DEPT ANAT & CELL BIOL,WASHINGTON,DC 20007. RP WEEKS, BS (reprint author), NIDR,DEV BIOL LAB,BETHESDA,MD 20892, USA. OI Papadopoulos, Vassilios/0000-0002-1183-8568 NR 33 TC 27 Z9 31 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD APR PY 1991 VL 147 IS 1 BP 62 EP 67 DI 10.1002/jcp.1041470109 PG 6 WC Cell Biology; Physiology SC Cell Biology; Physiology GA FP691 UT WOS:A1991FP69100008 PM 1645363 ER PT J AU FERRIOLA, PC EARP, HS DIAUGUSTINE, R NETTESHEIM, P AF FERRIOLA, PC EARP, HS DIAUGUSTINE, R NETTESHEIM, P TI ROLE OF TGF-ALPHA AND ITS RECEPTOR IN PROLIFERATION OF IMMORTALIZED RAT TRACHEAL EPITHELIAL-CELLS - STUDIES WITH TYRPHOSTIN AND TGF-ALPHA ANTISERA SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; TYROSINE KINASE-ACTIVITY; MESSENGER-RNA; EGF-RECEPTOR; SIGNAL TRANSDUCTION; TRANSGENIC MICE; FACTOR-BETA; NEOPLASTIC PROGRESSION; GENE-EXPRESSION; CARCINOMA AB We have shown in the present study and in studies reported previously that preneoplastic and neoplastic rat tracheal epithelial (RTE) cell lines express TGF-alpha and do so regardless of the mechanism by which they were transformed. In order to determine whether TGF-alpha is an autocrine growth regulator of immortalized RTE cells, we have examined the function of TGF-alpha/EGF receptors and the growth requirements for TGF-alpha in these cells. The level of immunoprecipitated TGF-alpha/EGF receptor protein in immortalized RTE cells was similar to or less than levels in primary RTE cells, indicating that chemically induced transformation of RTE cells does not involve overexpression of TGF-alpha/EGF receptors. Scatchard analysis of TGF-alpha/EGF receptors in the neoplastic EGV5T cell line revealed the presence of high-affinity (Kd = 0.4nM) and low-affinity (Kd = 9.8nM) binding sites. A tyrphostin TGF-alpha/EGF receptor tyrosine kinase inhibitor decreased in a dose-dependent manner the proliferation as well as EGF-induced autophosphorylation of the TGF-alpha/EGF receptor of transformed RTE cells. The inhibitory effect of tyrphostin on proliferation and receptor kinase activity was attenuated in late log and plateau phase cultures. The phosphotyrosine content of several other EGF-dependent and independent phosphoproteins was also decreased by the tyrphostin. Proliferation of transformed RTE cells was also inhibited when TGF-alpha antisera was added to the media of growing cells. These data are consistent with the hypothesis that proliferation of transformed RTE cells involves autocrine regulation by TGF-alpha and its receptor. C1 NIEHS,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,CANC RES CTR,CHAPEL HILL,NC 27599. RP FERRIOLA, PC (reprint author), NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709, USA. NR 66 TC 23 Z9 23 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD APR PY 1991 VL 147 IS 1 BP 166 EP 175 DI 10.1002/jcp.1041470121 PG 10 WC Cell Biology; Physiology SC Cell Biology; Physiology GA FP691 UT WOS:A1991FP69100020 PM 2037620 ER PT J AU PAGE, RE METCALF, RA METCALF, RL ERICKSON, EH LAMPMAN, RL AF PAGE, RE METCALF, RA METCALF, RL ERICKSON, EH LAMPMAN, RL TI EXTRACTABLE HYDROCARBONS AND KIN RECOGNITION IN HONEYBEE (APIS-MELLIFERA L) SO JOURNAL OF CHEMICAL ECOLOGY LA English DT Article DE HONEYBEE; APIS-MELLIFERA; HYMENOPTERA; APIDAE; HYDROCARBONS; KIN RECOGNITION; GENETIC RELATEDNESS ID NESTMATE RECOGNITION; DISCRIMINATION CUES; BEES; ONTOGENY; SISTERS; FULL; WAX AB Hydrocarbons of worker honeybees of known pedigree were extracted and analyzed using gas chromatography and mass spectrometry. Variability in hydrocarbon extracts of individual workers is determined at least in part genetically. Correlations in hydrocarbon composition of extracts were highest among more closely related individuals. Individuals maintained in groups exchange hydrocarbons but still maintain enough self-produced compounds to retain genetically determined individual characteristics. These results demonstrate that extractable hydrocarbons of bees provide sufficiently reliable genetic information to function as labels for use during kin recognition. C1 NCI,LHC,BETHESDA,MD 20817. UNIV ILLINOIS,DEPT ENTOMOL,URBANA,IL 61801. USDA,ARS,CARL HAYDEN BEE RES UNIT,TUCSON,AZ 85719. RP PAGE, RE (reprint author), UNIV CALIF DAVIS,DEPT ENTOMOL,DAVIS,CA 95616, USA. NR 37 TC 78 Z9 78 U1 0 U2 6 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0098-0331 J9 J CHEM ECOL JI J. Chem. Ecol. PD APR PY 1991 VL 17 IS 4 BP 745 EP 756 DI 10.1007/BF00994197 PG 12 WC Biochemistry & Molecular Biology; Ecology SC Biochemistry & Molecular Biology; Environmental Sciences & Ecology GA FH769 UT WOS:A1991FH76900006 PM 24258919 ER PT J AU BAIRD, DD WEINBERG, CR WILCOX, AJ MCCONNAUGHEY, DR MUSEY, PI COLLINS, DC AF BAIRD, DD WEINBERG, CR WILCOX, AJ MCCONNAUGHEY, DR MUSEY, PI COLLINS, DC TI HORMONAL PROFILES OF NATURAL CONCEPTION CYCLES ENDING IN EARLY, UNRECOGNIZED PREGNANCY LOSS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HUMAN CHORIONIC-GONADOTROPIN; HUMAN MENOPAUSAL GONADOTROPIN; INVITRO FERTILIZATION; IMPLANTATION; WOMEN; RADIOIMMUNOASSAY; OVULATION; ABORTION; FAILURE; PHASE AB Loss of a conceptus early in development can be detected by very sensitive assays specific for hCG. We examined 20 menstrual cycles ending in early loss of a conceptus in order to identify hormonal correlates of loss. Each loss cycle was compared to a successful conception cycle in the same woman, using daily concentrations of urinary estrone-3-glucuronide and pregnanediol-3-glucuronide (PdG). The estrone-3-glucuronide and PdG profiles in cycles of early pregnancy loss were very similar to those in successful conception cycles until late in the luteal phase. Early pregnancy loss was not related to a midluteal deficiency in PdG. hCG tended to be detected later in cycles of early pregnancy loss than in successful conception cycles, presumably indicating later implantation. Ten of the early pregnancy losses implanted after luteal-day-10; only one of the successful pregnancies implanted that late. The corpus luteum responded to the conception in only 2 of the 10 loss cycles with late implantation. In contrast, the corpus luteum responded in 8 of 10 loss cycles with normally timed implantation. The similarity of preimplantation hormonal profiles in cycles of early pregnancy loss and in cycles with successful conceptions suggests that most early losses in reproductively normal women do not result directly from deficiencies in ovarian steroid production. C1 EMORY UNIV, SCH MED, DECATUR, GA 30033 USA. VET ADM MED CTR, DECATUR, GA 30033 USA. CLARK ATLANTA UNIV, DEPT BIOL SCI, ATLANTA, GA 30314 USA. NIEHS, DIV BIOMETRY & RISK ASSESSMENT, STAT & BIOMATH BRANCH, RES TRIANGLE PK, NC 27709 USA. RP BAIRD, DD (reprint author), NIEHS, DIV BIOMETRY & RISK ASSESSMENT, EPIDEMIOL BRANCH, A3-05, POB 12233, RES TRIANGLE PK, NC 27709 USA. OI Wilcox, Allen/0000-0002-3376-1311; Baird, Donna/0000-0002-5544-2653 NR 26 TC 52 Z9 52 U1 0 U2 5 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1991 VL 72 IS 4 BP 793 EP 800 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD877 UT WOS:A1991FD87700010 PM 2005203 ER PT J AU BRUCE, J TAMARKIN, L RIEDEL, C MARKEY, S OLDFIELD, E AF BRUCE, J TAMARKIN, L RIEDEL, C MARKEY, S OLDFIELD, E TI SEQUENTIAL CEREBROSPINAL-FLUID AND PLASMA SAMPLING IN HUMANS - 24-HOUR MELATONIN MEASUREMENTS IN NORMAL SUBJECTS AND AFTER PERIPHERAL SYMPATHECTOMY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID URINARY 6-HYDROXYMELATONIN EXCRETION; SERUM; CORTISOL; DRAINAGE; CYCLE AB Simultaneous measurements of plasma and cerebrospinal fluid (CSF) melatonin and urinary excretion of 6-hydroxymelatonin were performed in four normal volunteers and one patient before and after upper thoracic sympathectomy for the control of essential hyperhidrosis. For normal individuals, hourly 24-h melatonin concentrations in plasma and CSF exhibited similar profiles, with low levels during the day and high levels at night. Peak plasma levels varied from 122-660 pmol/L, and the peak CSF levels from 94-355 pmol/L. The onset of the nocturnal increase in melatonin did not occur at the same time for each individual. Urinary 6-hydroxymelatonin levels also exhibited a daily rhythm, with peak excretion at night. The individual with the lowest nocturnal levels of circulating melatonin also had the lowest excretion of 6-hydroxymelatonin. In the patient with hyperhidrosis, a prominent melatonin rhythm was observed preoperatively in the CSF and plasma. After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished. These results provide direct evidence in humans for a diurnal melatonin rhythm in CSF and plasma as well as regulation of this rhythm by sympathetic innervation. C1 NIMH, CLIN SCI LAB, BETHESDA, MD 20892 USA. NINCDS, SURG NEUROL BRANCH, BETHESDA, MD 20892 USA. RP BRUCE, J (reprint author), COLUMBIA UNIV COLL PHYS & SURG, INST NEUROL, DEPT NEUROSURG, BOX 122, NEW YORK, NY 10032 USA. NR 27 TC 36 Z9 37 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1991 VL 72 IS 4 BP 819 EP 823 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD877 UT WOS:A1991FD87700014 PM 2005207 ER PT J AU COONEY, KA NICHOLS, WC BRUCK, ME BAHOU, WF SHAPIRO, AD BOWIE, EJW GRALNICK, HR GINSBURG, D AF COONEY, KA NICHOLS, WC BRUCK, ME BAHOU, WF SHAPIRO, AD BOWIE, EJW GRALNICK, HR GINSBURG, D TI THE MOLECULAR DEFECT IN TYPE-IIB VONWILLEBRAND DISEASE - IDENTIFICATION OF 4 POTENTIAL MISSENSE MUTATIONS WITHIN THE PUTATIVE GPLB BINDING DOMAIN SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE VONWILLEBRAND FACTOR; THROMBOCYTOPENIA; RISTOCETIN-INDUCED PLATELET AGGREGATION; POLYMERASE CHAIN REACTION; DIDEOXY SEQUENCING ID SPONTANEOUS PLATELET-AGGREGATION; VON WILLEBRAND FACTOR; GLYCOPROTEIN-IB; 52/48-KDA FRAGMENT; GENE; THROMBOCYTOPENIA; LOCALIZATION; COLLAGEN; HEPARIN; SITES AB Type IIB von Willebrand Disease (vWD) is characterized by the selective loss of large von Willebrand Factor (vWF) multimers from plasma, presumably due to their increased reactivity with platelets and subsequent clearance from the circulation. Using the PCR, one of a panel of four potential missense mutations was identified in each of the 14 patients studied from 11 unrelated families. None of these substitutions was encountered in a large panel of normal DNAs. These changes all represent C --> T transitions at CpG dinucleotides, proposed "hot spots" for mutation in the human genome. The four resulting amino acid substitutions, Arg543 --> Trp, Arg545 --> Cys, Val553 --> Met, and Arg578 --> Gln, are all clustered within the GpIb binding domain of vWF. Disruption of this latter functional domain may explain the pathogenesis of Type IIB vWD. By sequence polymorphism analysis, the Arg543 --> Trp substitution was shown to have occurred as at least two independent mutational events. This latter observation, along with the identification of mutations in all 14 patients studied and their localization to the GpIb binding domain, all strongly suggest that these substitutions represent the authentic defects responsible for Type IIB vWD. This panel of mutations may provide a useful diagnostic tool for the majority of patients with Type IIB vWD. C1 UNIV MICHIGAN,MED CTR,SCH MED,HOWARD HUGHES MED INST,4520 MSRBI,1150 W MED CTR DR,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,ANN ARBOR,MI 48109. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. INDIANA UNIV,MED CTR,INDIANAPOLIS,IN 46202. NIH,HEMATOL SERV,BETHESDA,MD 20892. SUNY STONY BROOK,DEPT MED,STONY BROOK,NY 11794. FU NHLBI NIH HHS [5R01 HL-39693-02] NR 38 TC 112 Z9 113 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1991 VL 87 IS 4 BP 1227 EP 1233 DI 10.1172/JCI115123 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FE722 UT WOS:A1991FE72200015 PM 1672694 ER PT J AU VARMA, A KWONCHUNG, KJ AF VARMA, A KWONCHUNG, KJ TI RAPID METHOD TO EXTRACT DNA FROM CRYPTOCOCCUS-NEOFORMANS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note ID CAPSULAR POLYSACCHARIDE; PROTOPLASTS AB A rapid and easy method for the extraction of total cellular DNA from Cryptococcus neoformans is described. This procedure modifies and considerably simplifies previously reported methods. Numerous steps were either eliminated or replaced, including preincubations with cell wall permeability agents such as beta-mercaptoethanol and dithiothreitol. The commercially available enzyme preparation Novozyme 234 was found to contain a potent concentration of DNases which actively degrade DNA. Degradation and loss of DNA was prevented by maintaining a high concentration of EDTA in the lysing solution. This procedure resulted in high yields (150 to 200-mu-g of DNA from 100 ml of culture) of good-quality (undegraded), high-molecular-weight DNA which was readily digested by restriction endonucleases, making it suitable for use in various molecular applications. RP VARMA, A (reprint author), NIAID,CLIN INVEST LAB,BETHESDA,MD 20892, USA. NR 9 TC 49 Z9 50 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1991 VL 29 IS 4 BP 810 EP 812 PG 3 WC Microbiology SC Microbiology GA FC919 UT WOS:A1991FC91900026 PM 1909713 ER PT J AU SATO, S BALISH, M MURATORE, R AF SATO, S BALISH, M MURATORE, R TI PRINCIPLES OF MAGNETOENCEPHALOGRAPHY SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY LA English DT Article DE MAGNETOENCEPHALOGRAPHY; INSTRUMENTATION; EEG; EVOKED RESPONSES; EPILEPSY ID HUMAN AUDITORY-CORTEX; CEREBRAL MAGNETIC-FIELDS; TEMPORAL-LOBE EPILEPSY; INTRACRANIAL LOCALIZATIONS; HUMAN-BRAIN; TONOTOPIC ORGANIZATION; NEUROMAGNETIC EVIDENCE; SOMATOSENSORY CORTEX; CURRENT DIPOLE; RESPONSES AB Magnetoencephalography (MEG) is a new, noninvasive functional test equivalent to EEG. It has been used to localize the sources of evoked responses and interictal and ictal epileptiform discharges and to study patients with psychiatric illnesses, cerebrovascular accidents, and migrane. In epilepsy research, it is hoped that MEG will provide information similar to that yielded by depth or subdural electrode recording, or that the combination of these methods will provide more information than either one alone. The application of MEG appears to be widening, although it is not yet a routine clinical diagnostic tool. The utility of MEG is limited by technological problems, but new and more efficient systems are becoming available. Within several years, advances in the technology and understanding of MEG may modify the course of its application. C1 NINCDS,MED NEUROL BRANCH,NEUROPHYSIOL UNIT,BETHESDA,MD 20892. NR 98 TC 30 Z9 30 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0736-0258 J9 J CLIN NEUROPHYSIOL JI J. Clin. Neurophysiol. PD APR PY 1991 VL 8 IS 2 BP 144 EP 156 DI 10.1097/00004691-199104000-00003 PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FK455 UT WOS:A1991FK45500003 PM 2050815 ER PT J AU MOSTOW, EN BYRNE, J CONNELLY, RR MULVIHILL, JJ AF MOSTOW, EN BYRNE, J CONNELLY, RR MULVIHILL, JJ TI QUALITY-OF-LIFE IN LONG-TERM SURVIVORS OF CNS TUMORS OF CHILDHOOD AND ADOLESCENCE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID BRAIN-TUMORS; CANCER-PATIENTS; CHILDREN; SEQUELAE; LEUKEMIA; SIBS C1 NCI,BIOMETRY BRANCH,BETHESDA,MD 20892. RP MOSTOW, EN (reprint author), NCI,CLIN EPIDEMIOL BRANCH,CANC CONTROL APPLICAT,BETHESDA,MD 20892, USA. NR 34 TC 133 Z9 133 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1991 VL 9 IS 4 BP 592 EP 599 PG 8 WC Oncology SC Oncology GA FD863 UT WOS:A1991FD86300008 PM 2066756 ER PT J AU GOORIN, AM SHUSTER, JJ BAKER, A HOROWITZ, ME MEYER, WH LINK, MP AF GOORIN, AM SHUSTER, JJ BAKER, A HOROWITZ, ME MEYER, WH LINK, MP TI CHANGING PATTERN OF PULMONARY METASTASES WITH ADJUVANT CHEMOTHERAPY IN PATIENTS WITH OSTEOSARCOMA - RESULTS FROM THE MULTIINSTITUTIONAL OSTEOSARCOMA STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID OSTEOGENIC-SARCOMA; SURVIVAL; THORACOTOMY; RESECTION C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. CHILDRENS HOSP MED CTR, BOSTON, MA 02115 USA. NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. STANFORD UNIV, MED CTR, SCH MED, STANFORD, CA 94305 USA. CHILDRENS HOSP STANFORD, PALO ALTO, CA 94304 USA. FU NCI NIH HHS [CA-31566, CA-29139, CA-41573] NR 14 TC 95 Z9 103 U1 0 U2 1 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1991 VL 9 IS 4 BP 600 EP 605 PG 6 WC Oncology SC Oncology GA FD863 UT WOS:A1991FD86300009 PM 2066757 ER PT J AU DUTCHER, JP GAYNOR, ER BOLDT, DH DOROSHOW, JH BAR, MH SZNOL, M MIER, J SPARANO, J FISHER, RI WEISS, G MARGOLIN, K ARONSON, FR HAWKINS, M ATKINS, M AF DUTCHER, JP GAYNOR, ER BOLDT, DH DOROSHOW, JH BAR, MH SZNOL, M MIER, J SPARANO, J FISHER, RI WEISS, G MARGOLIN, K ARONSON, FR HAWKINS, M ATKINS, M TI A PHASE-II STUDY OF HIGH-DOSE CONTINUOUS INFUSION INTERLEUKIN-2 WITH LYMPHOKINE-ACTIVATED KILLER-CELLS IN PATIENTS WITH METASTATIC MELANOMA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID RECOMBINANT HUMAN INTERLEUKIN-2; ADOPTIVE IMMUNOTHERAPY; ADVANCED CANCER; THERAPY C1 MONTEFIORE MED CTR,ALBERT EINSTEIN CANC CTR,NCI,IL2LAK EXTRAMURAL WORKING GRP,BRONX,NY 10467. CITY HOPE CANC RES CTR,DUARTE,CA. LOYOLA UNIV,MED CTR,MAYWOOD,IL 60153. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111. NCI,BETHESDA,MD 20892. FU NCI NIH HHS [N01-CM-73703, N01-CM-73704, N01-CM-73702] NR 29 TC 78 Z9 78 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1991 VL 9 IS 4 BP 641 EP 648 PG 8 WC Oncology SC Oncology GA FD863 UT WOS:A1991FD86300014 PM 2066760 ER PT J AU ADAMSON, PC BALIS, FM MCCULLY, CL GODWIN, KS BACHER, JD WALSH, TJ POPLACK, DG AF ADAMSON, PC BALIS, FM MCCULLY, CL GODWIN, KS BACHER, JD WALSH, TJ POPLACK, DG TI RESCUE OF EXPERIMENTAL INTRATHECAL METHOTREXATE OVERDOSE WITH CARBOXYPEPTIDASE-G2 SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; PRIMATE MODEL; INTRACRANIAL-PRESSURE; CEREBROSPINAL-FLUID; ENZYMATIC CLEAVAGE; ADMINISTERED DRUGS; LONG-TERM; PHARMACOKINETICS; INTOXICATION; FRAGMENTS C1 NCRR,VET MED & SURG BRANCH,BETHESDA,MD. RP ADAMSON, PC (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 25 TC 36 Z9 37 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1991 VL 9 IS 4 BP 670 EP 674 PG 5 WC Oncology SC Oncology GA FD863 UT WOS:A1991FD86300018 PM 2066764 ER PT J AU SIEGEL, JP PURI, RK AF SIEGEL, JP PURI, RK TI INTERLEUKIN-2 TOXICITY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID ACTIVATED KILLER CELLS; TUMOR NECROSIS FACTOR; HIGH-DOSE INTERLEUKIN-2; VASCULAR LEAK SYNDROME; COLONY-STIMULATING FACTOR; RECOMBINANT INTERLEUKIN-2; CANCER-PATIENTS; ENDOTHELIAL-CELLS; HUMAN-LYMPHOCYTES; CLINICAL-TRIAL C1 US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,CELLULAR IMMUNOL LAB,BETHESDA,MD 20205. RP SIEGEL, JP (reprint author), NIH,BLDG 29A,ROOM 2B-24,HFB-820,8800 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 83 TC 369 Z9 377 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1991 VL 9 IS 4 BP 694 EP 704 PG 11 WC Oncology SC Oncology GA FD863 UT WOS:A1991FD86300021 PM 2066765 ER PT J AU CALOGERO, AE LIAPI, C CHROUSOS, GP AF CALOGERO, AE LIAPI, C CHROUSOS, GP TI HYPOTHALAMIC AND SUPRAHYPOTHALAMIC EFFECTS OF PROLONGED TREATMENT WITH DEXAMETHASONE IN THE RAT SO JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION LA English DT Article DE DEXAMETHASONE; CORTICOTROPIN-RELEASING HORMONE; ARGININE VASOPRESSIN; ADRENOCORTICOTROPIN; BETA-ENDORPHIN; HYPOTHALAMUS; HIPPOCAMPUS; CEREBRAL CORTEX; AND CEREBELLUM ID CORTICOTROPIN-RELEASING HORMONE; INTERMEDIATE-POSTERIOR PITUITARY; GLUCOCORTICOID RECEPTOR; SECRETION INVITRO; MINERALOCORTICOID RECEPTOR; PARAVENTRICULAR NUCLEUS; CORTISOL TREATMENT; MEDIAN-EMINENCE; ACTH-SECRETION; MESSENGER-RNA AB Corticosteroid type I and II receptors mediate the negative feedback effects of these hormones at various central nervous system sites involved in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis. To examine the effects of chronic treatment with dexamethasone (DEX), a type 2 receptor agonist, on the regulation of this axis, male Sprague-Dawley rats weighing 200-250 g were given daily injections of DEX for 1,2,3, and 4 weeks or were treated with a subcutaneously implanted DEX-releasing minipump for one week. At the end of treatment, the animals were weighed and brains and truncal blood were collected. Daily intermittent DEX treatment reduced the body weight of the rats in a time-dependent fashion, but had little or no effect on their wet brain weight. Plasma ACTH and corticosterone, measured by RIA, were fully suppressed after one week of intermittent treatment and did not show any further reduction in rats treated for longer periods. In these animals, the content of immunoreactive corticotropin-releasing hormone (iCRH), arginine vasopressin (AVP), ACTH and beta-endorphin (beta-EP) in the hypothalamus, hippocampus, cerebral cortex and cerebellum and pituitary ACTH content did not show any difference compared to vehicle-treated rats. In contrast, continuous DEX treatment increased iCRH content in thecortex, reduced AVP content in the cerebellum, increased ACTH content in the hippocampus, decreased ACTH and beta-EP content in the hypothalamus, and reduced pituitary ACTH content. Hypothalami explanted from rats treated with DEX for one week released lower basal amounts of iCRH in vitro and did not respond to a maximally stimulatory concentration of serotonin (5-HT), a known CRH secretagogue. Continuous DEX administration suppressed also potassium chloride-induced iCRH release. Interestingly, hypothalami explanted from rats receiving daily injection of vehicle, but not from unhandled, untreated controls, did not respond to 5-HT with an increase of iCRH release in vitro. In conclusion, prolonged and continuous, but not intermittent, administration of DEX had a strong effect on brain neuropeptide content. Both regimens of DEX reduced the hypothalamic iCRH responsiveness to stimuli in vitro. Chronic handling also decreased the responsiveness of the hypothalamus to a stimulatory neurotransmitter and may confound the interpretation of data pertinent to inhibitory mechanisms. RP CALOGERO, AE (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N262,BETHESDA,MD 20892, USA. NR 41 TC 20 Z9 20 U1 0 U2 2 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0391-4097 J9 J ENDOCRINOL INVEST JI J. Endocrinol. Invest. PD APR PY 1991 VL 14 IS 4 BP 277 EP 286 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FL751 UT WOS:A1991FL75100004 PM 1650804 ER PT J AU CHAN, SH PERUSSIA, B GUPTA, JW KOBAYASHI, M POSPISIL, M YOUNG, HW WOLF, SF YOUNG, D CLARK, SC TRINCHIERI, G AF CHAN, SH PERUSSIA, B GUPTA, JW KOBAYASHI, M POSPISIL, M YOUNG, HW WOLF, SF YOUNG, D CLARK, SC TRINCHIERI, G TI INDUCTION OF INTERFERON-GAMMA PRODUCTION BY NATURAL-KILLER-CELL STIMULATORY FACTOR - CHARACTERIZATION OF THE RESPONDER CELLS AND SYNERGY WITH OTHER INDUCERS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID HUMAN PERIPHERAL-BLOOD; TUMOR NECROSIS FACTOR; HUMAN T-CELLS; IMMUNE INTERFERON; LYMPHOCYTE-ACTIVATION; ACCESSORY FUNCTION; MONONUCLEAR-CELLS; DENDRITIC CELLS; PHORBOL ESTER; NK CELLS AB We previously reported that natural killer cell stimulatory factor (NKSF), a heterodimeric lymphokine purified from the conditioned medium of human B lymphoblastoid cell lines, induces interferon-gamma (IFN-gamma) production from resting peripheral blood lymphocytes (PBL) and synergizes with interleukin 2 in this activity. In this study, we show that human NKSF induces IFN-gamma-production from both resting and activated human PBL and from freshly isolated murine splenocytes. Human T and NK cells produce IFN-gamma in response to NKSF, but resting PBL require the presence of nonadherent human histocompatibility leukocyte antigens DR+ (HLA-DR+) accessory cells to respond to NKSF. The mechanism(s) by which NKSF induces IFN-gamma-production results in accumulation of IFN-gamma mRNA, is insensitive to cyclosporin A, and synergizes with those mediated by phytohemmagglutinin, phorbol diesters, anti-CD3 antibodies, and allogeneic antigens, but not by Ca2+ ionophores. The ability of NKSF to directly induce IFN-gamma-production and to synergize with other physiological IFN-gamma-inducers, joined with the previously described ability to enhance lymphocyte cytotoxicity and proliferation, indicates that this lymphokine is a powerful immunopotentiating agent. C1 WISTAR INST,3601 SPRUCE ST,PHILADELPHIA,PA 19104. GENET INST,CAMBRIDGE,MA 02140. CZECHOSLOVAK ACAD SCI,INST MICROBIOL,PRAGUE 4,CZECHOSLOVAKIA. NCI,FREDERICK CANC RES & DEV CTR,DCT,EXPTL IMMUNOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA-20833, CA-32898, CA-10815] NR 48 TC 966 Z9 976 U1 0 U2 8 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1991 VL 173 IS 4 BP 869 EP 879 DI 10.1084/jem.173.4.869 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FE128 UT WOS:A1991FE12800010 PM 1672545 ER PT J AU WAHL, SM ALLEN, JB MCCARTNEYFRANCIS, N MORGANTIKOSSMANN, MC KOSSMANN, T ELLINGSWORTH, L MAI, UEH MERGENHAGEN, SE ORENSTEIN, JM AF WAHL, SM ALLEN, JB MCCARTNEYFRANCIS, N MORGANTIKOSSMANN, MC KOSSMANN, T ELLINGSWORTH, L MAI, UEH MERGENHAGEN, SE ORENSTEIN, JM TI MACROPHAGE-DERIVED AND ASTROCYTE-DERIVED TRANSFORMING GROWTH-FACTOR-BETA AS A MEDIATOR OF CENTRAL-NERVOUS-SYSTEM DYSFUNCTION IN ACQUIRED-IMMUNE-DEFICIENCY-SYNDROME SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; NECROSIS FACTOR-ALPHA; ACCOMPANIES VIRAL TRANSFORMATION; HTLV-III; MONONUCLEAR PHAGOCYTES; CEREBROSPINAL-FLUID; BRAIN-TISSUE; CELLS; AIDS; EXPRESSION AB The multifunctional cytokine, transforming growth factor beta (TGF-beta), was identified by immunocytochemistry in the brain tissues of four patients with acquired immune deficiency syndrome (AIDS), but not in control brain tissue. The TGF-beta staining was localized to cells of monocytic lineage as well as astrocytes, especially in areas of brain pathology. In addition, the brain tissues from the AIDS patients contained transcripts for human immunodeficiency virus 1 (HIV-1) by in situ hybridization, suggesting a correlation between the presence of HIV-1 in the brain and the expression of TGF-beta. However, the expression of TGF-beta was not limited to HIV-1-positive cells, raising the possibility of alternative mechanisms for the induction of TGF-beta in these AIDS patients' brains. To investigate these mechanisms, purified human monocytes were infected in vitro with HIV-1 and were shown to secrete increased levels of TGF-beta. In addition, HIV-1-infected monocytes released a factor(s) capable of triggering cultured astrocytes that are not infected with HIV-1 to secrete TGF-beta. The release of TGF-beta, which is an extremely potent chemotactic factor, may contribute to the recruitment of HIV-1-infected monocytic cells, enabling viral spread to and within the central nervous system (CNS). Moreover, TGF-beta augments cytokine production, including cytokines known to be neurotoxic. The identification of TGF-beta within the CNS implicates this cytokine in the immunopathologic processes responsible for AIDS-related CNS dysfunction. C1 COLLAGEN CORP,CONNECT TISSUE RES LABS,PALO ALTO,CA 94303. GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20037. RP WAHL, SM (reprint author), NIDR,CELLULAR IMMUNOL SECT,IMMUNOL LAB,BLDG 30,RM 326,BETHESDA,MD 20892, USA. NR 57 TC 286 Z9 287 U1 1 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1991 VL 173 IS 4 BP 981 EP 991 DI 10.1084/jem.173.4.981 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FE128 UT WOS:A1991FE12800021 PM 2007861 ER PT J AU MARTICH, GD DANNER, RL CESKA, M SUFFREDINI, AF AF MARTICH, GD DANNER, RL CESKA, M SUFFREDINI, AF TI DETECTION OF INTERLEUKIN-8 AND TUMOR-NECROSIS-FACTOR IN NORMAL HUMANS AFTER INTRAVENOUS ENDOTOXIN - THE EFFECT OF ANTIINFLAMMATORY AGENTS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID PENTOXIFYLLINE; NEUTROPHILS; INHIBITION; CACHECTIN; SHOCK AB Interleukin 8 (IL-8), a potent activator of neutrophils, may be important in the early host response to serious Gram-negative infections. IL-8 was measured with other acute phase cytokines (tumor necrosis factor-alpha [TNF-alpha], IL-6, and IL-1-beta) in 25 normal humans randomized to receive either intravenous endotoxin alone or endotoxin after oral administration of ibuprofen or pentoxifylline, agents that alter some of the inflammatory responses induced by endotoxin in vitro. TNF immunoreactivity was maximum at 1.5 h, and total TNF (area under the curve) was 4.2- and 4.5-fold greater in subjects given endotoxin/ibuprofen compared to subjects given endotoxin alone (p = 0.026) or endotoxin/pentoxifylline (p = 0.004), respectively. IL-6 levels were maximum at 2-3 h and did not differ among the three groups. No IL-1-beta was detected in any subject. IL-8 levels peaked at 2 h in subjects given either endotoxin alone or endotoxin/pentoxifylline, falling towards baseline by 5 h. Subjects given endotoxin/ibuprofen had a more sustained rise in IL-8 with peak levels 2.8- and 2.5-fold higher at 3 h compared to endotoxin alone (p = 0.048) or endotoxin/pentoxifylline (p = 0.023), respectively. Differences in total IL-8 release among groups approached statistical significance (ANOVA, p = 0.07). This trend reflected the increased release of IL-8 by the subjects receiving ibuprofen compared to pentoxifylline (1.9-fold higher; p = 0.024). This suggests that cyclooxygenase products may provide important negative feedback loops for cytokine production in vivo. Increases in circulating IL-8 are part of the acute inflammatory response of humans to endotoxin. Altered cytokine responses caused by antiinflammatory therapy may have important implications for both host defense and injury during septicemia. C1 SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. RP MARTICH, GD (reprint author), NIH,DEPT CRIT CARE MED,BLDG 10,10-D048 CC,BETHESDA,MD 20892, USA. NR 25 TC 401 Z9 406 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1991 VL 173 IS 4 BP 1021 EP 1024 DI 10.1084/jem.173.4.1021 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FE128 UT WOS:A1991FE12800025 PM 2007851 ER PT J AU ALEXANDER, HR DOHERTY, GM BURESH, CM VENZON, DJ NORTON, JA AF ALEXANDER, HR DOHERTY, GM BURESH, CM VENZON, DJ NORTON, JA TI A RECOMBINANT HUMAN RECEPTOR ANTAGONIST TO INTERLEUKIN-1 IMPROVES SURVIVAL AFTER LETHAL ENDOTOXEMIA IN MICE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID TUMOR NECROSIS FACTOR; PASSIVE-IMMUNIZATION; CACHECTIN; BACTEREMIA; SHOCK; ANTIBODIES; APPEARANCE; CYTOKINES; RABBITS; INJURY AB Interleukin 1 (IL-1) is an endogenously produced cytokine that mediates a variety of physiological effects that may be beneficial or deleterious to the host. C57Bl/6 mice treated intravenously with a recently characterized human recombinant receptor antagonist protein to IL-1 (IL-1ra) had improved survival when treated after a lethal Escherichia coli endotoxin (lipopolysaccharide [LPS]) challenge. IL-1ra was effective when treatment was initiated after LPS, and intravenous administration every 4 h for 24 h was required. Serum levels of tumor necrosis factor (TNF) activity after LPS and in vitro TNF cytotoxicity were not altered by treatment with IL-1ra. These experiments provide direct evidence that the lethal effects of LPS may be mediated through the action of IL-1 and that the IL-1ra can provide a new treatment strategy for disease processes mediated via this cytokine. C1 NCI,SURG BRANCH,SURG METAB SECT,BLDG 10,ROOM 2B07,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 19 TC 296 Z9 297 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1991 VL 173 IS 4 BP 1029 EP 1032 DI 10.1084/jem.173.4.1029 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FE128 UT WOS:A1991FE12800027 PM 1826127 ER PT J AU SALTINI, C KIRBY, M BISETTI, A CRYSTAL, RG AF SALTINI, C KIRBY, M BISETTI, A CRYSTAL, RG TI THE LUNG EPITHELIAL IMMUNE-SYSTEM SO JOURNAL OF IMMUNOLOGICAL RESEARCH LA English DT Editorial Material ID ACTIVE PULMONARY SARCOIDOSIS; LOWER RESPIRATORY-TRACT; T-CELL SUBSET; PROTEIN TYROSINE PHOSPHATASE; LYMPHOCYTE HOMING RECEPTOR; CHRONIC BERYLLIUM DISEASE; BRONCHOALVEOLAR LAVAGE; HYPERSENSITIVITY PNEUMONITIS; ALVEOLAR MACROPHAGES; HELPER-INDUCER C1 UNIV ROME LA SAPIENZA,IST TISOL & MALATTIE APPARATO RESP,I-00185 ROME,ITALY. NHLBI,PULM BRANCH,BETHESDA,MD 20892. RP SALTINI, C (reprint author), UNIV MODENA,IST TISIOL & MALATTIE APPARATO RESP,VIA POZZO 71,I-41100 MODENA,ITALY. NR 69 TC 6 Z9 6 U1 0 U2 2 PU PENSIERO SCIENTIFICO EDITOR PI ROME PA VIA BRADANO 3/C, 00199 ROME, ITALY SN 1120-3765 J9 J IMMUNOL RES PD APR-JUN PY 1991 VL 3 IS 2 BP 43 EP 48 PG 6 WC Immunology SC Immunology GA FU006 UT WOS:A1991FU00600001 ER PT J AU HAKIM, FT SHARROW, SO PAYNE, S SHEARER, GM AF HAKIM, FT SHARROW, SO PAYNE, S SHEARER, GM TI REPOPULATION OF HOST LYMPHOHEMATOPOIETIC SYSTEMS BY DONOR CELLS DURING GRAFT-VERSUS-HOST REACTION IN UNIRRADIATED ADULT F1-MICE INJECTED WITH PARENTAL LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ALLOHELPER-T-CELLS; MONOCLONAL-ANTIBODY; BONE-MARROW; MUTUAL RECOGNITION; HYBRID RESISTANCE; IMMUNE-DEFICIENCY; EFFECTOR-CELLS; KILLER CELLS; GVH REACTION; DISEASE AB The graft-vs-host reaction (GVHR) generated by the injection of parental lymphocytes into unirradiated immune-competent F1 hosts is characterized by an acute loss of immune functions, an attack on host tissues, and a gradual recovery of function. Flow cytometric analysis of the donor- and host-derived splenic populations during the course of acute dysfunction and gradual recovery revealed a complex pattern of changes in lymphoid and myeloid populations that resulted in the repopulation of the host with donor-derived cells. Initially, donor-derived T cell populations expanded, particularly CD8+ T cells. Next, host T cell and B cell populations disappeared. Finally, donor-derived cells repopulated the lymphohematopoietic system in the sequence myeloid populations, B cells, and, after a protracted period, T cells. The recovery of immune functions following GVHR-induced immune deficiency was associated with this repopulation of the spleen by donor-derived cells. Donor repopulation of the host lymphohematopoietic system required the presence of both CD4 and CD8 cells in the original donor inoculum. Depletion of donor CD4 populations precluded development of GVHR or any donor engraftment; depletion of CD8 cells resulted in engraftment solely of donor CD4 populations. RP HAKIM, FT (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B17,BETHESDA,MD 20892, USA. NR 37 TC 62 Z9 64 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2108 EP 2115 PG 8 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700006 PM 1672343 ER PT J AU SNAPPER, CM HOOLEY, JJ URBAN, JF FINKELMAN, FD AF SNAPPER, CM HOOLEY, JJ URBAN, JF FINKELMAN, FD TI LACK OF FC-EPSILON-RII EXPRESSION BY MURINE B-CELLS AFTER INVIVO IMMUNIZATION IS DIRECTLY ASSOCIATED WITH IG SECRETION AND NOT IG ISOTYPE SWITCHING SO JOURNAL OF IMMUNOLOGY LA English DT Article ID STIMULATORY FACTOR-I; LYMPHOCYTES-B; MONOCLONAL-ANTIBODY; NIPPOSTRONGYLUS-BRASILIENSIS; FLOW MICROFLUOROMETRY; POLYCLONAL ACTIVATION; MOLECULAR-STRUCTURE; SURFACE-RECEPTORS; INVITRO SYNTHESIS; MYELOMA PROTEINS AB The "low affinity" Fc receptor for IgE (Fc-epsilon-RII) has been reported to be absent from normal murine and human B cells that express a membrane (m)Ig isotype other than mIgM or mIgD in vivo. This would suggest that Fc-epsilon-RII expression is specifically lost after in vivo Ig isotype switching. We demonstrate that during a murine immune response to the bacterium Brucella abortus, to goat anti-mouse IgD (G-alpha-M-delta) antibody, or to infection with the nematode parasites Nippostrongylus brasiliensis or Heligmosomoides polygyrus, Fc-epsilon-RII expression is low or absent on virtually all B cells secreting IgM, IgG1, IgG2a, and IgE. However, up to 50% of B cells that express mIgG1 after G-alpha-M-delta injection continue to express Fc-epsilon-RII. These mIgG1+Fc-epsilon-RII+ cells secrete little, if any, IgG1 when placed in vitro, in contrast to their mIgG1+Fc-epsilon-RII- counterparts. The mIgG1+Fc-epsilon-RII+ cells may be a transitional cell population, because they undergo substantial loss of Fc-epsilon-RII in culture, unlike mIgM+Fc-epsilon-RII+ cells, which maintain constant levels of Fc-epsilon-RII throughout a comparable culture period. Thus, low or absent expression of Fc-epsilon-RII after immunization in vivo is directly associated with B cell differentiation to Ig production in the presence or absence of Ig isotype switching. However, all post-switched B cells may eventually lack Fc-epsilon-RII expression, independently of their differentiative state. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. USDA ARS,BELTSVILLE AGR RES CTR,HELMINTH DIS LAB,BELTSVILLE,MD 20705. RP SNAPPER, CM (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT PATHOL,4301 JONES BRIDGE RD,BETHESDA,MD 20814, USA. FU NIAID NIH HHS [R01-AI21328] NR 59 TC 12 Z9 12 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2161 EP 2168 PG 8 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700013 PM 1826019 ER PT J AU CLERICI, M LANDAY, AL KESSLER, HA ZAJAC, RA BOSWELL, RN MULUK, SC SHEARER, GM AF CLERICI, M LANDAY, AL KESSLER, HA ZAJAC, RA BOSWELL, RN MULUK, SC SHEARER, GM TI MULTIPLE PATTERNS OF ALLOANTIGEN PRESENTING STIMULATING CELL DYSFUNCTION IN PATIENTS WITH AIDS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; IMMUNE-DEFICIENCY SYNDROME; T-LYMPHOTROPIC VIRUS; MIXED LYMPHOCYTE-REACTION; CLASS-II ANTIGENS; MONOCYTE FUNCTION; HTLV-III/LAV; INFECTION; MACROPHAGES; EXPRESSION AB The APC/stimulating cell (APC/SC) potential of PBMC from Walter Reed stage 1 and 2 patients and patients with AIDS was tested by using these PBMC as stimulators in an allogeneic MLR. The responding cells were PBMC from unrelated, HIV- donors that were either unfractionated or depleted of APC by plastic and nylon wool adherence. Using this approach, we observed no defect in the APC/SC potential of PBMC from Walter Reed stage 1 and 2 patients. However, PBMC from AIDS patients used as allogeneic stimulators exhibited three different patterns of APC/SC function: 1) no defect in alloantigen (ALLO) APC/SC potential; 2) a defect in ALLO APC/SC function that was detected only if the responder cells were depleted of APC (presenting cell defect); and 3) a defect in ALLO APC/SC function, irrespective of whether the responder cells were depleted of APC (stimulating cell defect). These results indicate that in addition to Th cell defects associated with AIDS, the PBMC from AIDS patients can also exhibit a defect in APC/SC function. This study provides an approach that permits the testing of Ag-presenting function in all AIDS patients, and is therefore not limited to testing patients for whom HIV-, HLA-identical T cells and APC are available. C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B-17,BETHESDA,MD 20892. RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT IMMUNOL MICROBIOL & MED,CHICAGO,IL 60612. WILFORD HALL USAF MED CTR,HIV UNIT,LACKLAND AFB,TX 78236. NR 36 TC 30 Z9 30 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2207 EP 2213 PG 7 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700019 PM 1672347 ER PT J AU CLERICI, M LUCEY, DR ZAJAC, RA BOSWELL, RN GEBEL, HM TAKAHASHI, H BERZOFSKY, JA SHEARER, GM AF CLERICI, M LUCEY, DR ZAJAC, RA BOSWELL, RN GEBEL, HM TAKAHASHI, H BERZOFSKY, JA SHEARER, GM TI DETECTION OF CYTOTOXIC LYMPHOCYTES-T SPECIFIC FOR SYNTHETIC PEPTIDES OF GP160 IN HIV-SEROPOSITIVE INDIVIDUALS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL ANTIGENIC SITES; AIDS VIRUS; INFECTION; VACCINE; RECOGNITION; MOLECULE; SEQUENCE; PROTEIN; EPITOPE AB Four synthetic peptides corresponding to the IIIB sequence of gp160 of HIV were recently reported to stimulate Th cell function by PBL from HIV-infected, asymptomatic patients. In the present report, we used these same peptides to demonstrate CTL activity in a similar patient population. EBV-transformed B-cell lines from asymptomatic, HIV seropositive and seronegative control donors were pre-incubated with the peptides. Fresh PBL from 19 (76%) of 25 HIV seropositive donors lysed autologous targets pulsed with at least one of the four peptides. Autologous targets pulsed with two non-immunogenic peptides were not lysed. PBL from none of the eight HIV seronegative controls lysed peptide-preincubated autologous targets. The CTL activity was mediated by T cells, was predominantly MHC class I restricted, and was increased by in vitro restimulation of PBL with the peptides. HLA A-2 was identified as a restricting element for all four peptides in different patients, and for three of the peptides in the same donor. HLA-A1 or -B8 may also present some of the peptides. Thus, the same peptides can be recognized by human Th cells and class I MHC-restricted CTL. C1 NCI, EXPTL IMMUNOL BRANCH, BLDG 10, ROOM 4B-17, BETHESDA, MD 20892 USA. NCI, METAB BRANCH, BETHESDA, MD 20892 USA. WILFORD HALL USAF MED CTR, HIV UNIT, LACKLAND AFB, TX 78236 USA. RUSH PRESBYTERIAN ST LUKES MED CTR, DEPT IMMUNOL & MICROBIOL, CHICAGO, IL 60612 USA. NR 31 TC 174 Z9 174 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2214 EP 2219 PG 6 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700020 PM 1826020 ER PT J AU DEMARIA, A PANTALEO, G SCHNITTMAN, SM GREENHOUSE, JJ BASELER, M ORENSTEIN, JM FAUCI, AS AF DEMARIA, A PANTALEO, G SCHNITTMAN, SM GREENHOUSE, JJ BASELER, M ORENSTEIN, JM FAUCI, AS TI INFECTION OF CD8+ LYMPHOCYTES-T WITH HIV - REQUIREMENT FOR INTERACTION WITH INFECTED CD4+ CELLS AND INDUCTION OF INFECTIOUS VIRUS FROM CHRONICALLY INFECTED CD8+ CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; PERIPHERAL-BLOOD; AIDS VIRUS; RECEPTOR; REPLICATION; RETROVIRUS; ANTIGEN; COMPLEX; INVITRO; TYPE-1 AB In this study, we have investigated the basic requirements for HIV-1 infection of CD8+ lymphocytes in vitro. Unfractionated PBL obtained from healthy HIV-1 seronegative donors were activated with PHA and infected in vitro with HIV-1LAV. Based on immunofluorescent labeling, the vast majority of cells (85 to 97%) surviving peak virus replication belonged to the CD8+ subset and only a small percentage (0.5 to 1.5%) were CD4+. Amplification of HIV-1 proviral sequences by polymerase chain reaction performed on the sorted surviving CD8+ cells demonstrated that CD8+ cells harbored HIV-1 proviral DNA. In addition, stimulation of these HIV-1-infected, CD8+-sorted cells either with PHA or anti-CD2 mAb resulted in induction of virus replication, as measured by reverse transcriptase activity. Electron microscopic analysis of CD8+ cells chronically infected with HIV-1 and stimulated with PHA showed typical virions budding from, and associated with, the surface of cells immunolabeled with gold beads directed toward the CD8 molecule. Infection of CD8+ cells with HIV-1 occurred only when CD4+ cells were present in the PHA-activated lymphocyte population exposed to HIV-1 at the beginning of the culture or when sorted CD8+CD4- lymphocytes were cocultured with autologous sorted CD8-CD4+ cells that had been previously infected with HIV-1. Coculture of these cells with PHA-blasts and incubation of their supernatants with a CD4+ cell line showed that these chronically infected CD8+ cells could spread HIV-1 infection to uninfected CD4+ cells after stimulation with PHA or anti-CD2 mAb. Therefore, these results suggest that the minimal requirement for in vitro infection of CD3+CD8+CD4- lymphocytes is the presence of infected CD4+ cells and that infected CD8+ T lymphocytes can further spread the infection to CD4+ cells. C1 PROGRAM RESOURCES INC,FREDERICK,MD. GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20052. RP DEMARIA, A (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 11B-13,BETHESDA,MD 20892, USA. RI de maria, andrea/F-7116-2016; Pantaleo, Giuseppe/K-6163-2016 OI de maria, andrea/0000-0001-5782-333X; FU NCI NIH HHS [N01-CO-74102.778] NR 31 TC 54 Z9 54 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2220 EP 2226 PG 7 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700021 PM 1706390 ER PT J AU GOTLIEB, WH DURUM, SK GREGORIO, TA MATHIESON, BJ AF GOTLIEB, WH DURUM, SK GREGORIO, TA MATHIESON, BJ TI SELECTIVE STIMULATION OF THYMOCYTE PRECURSORS MEDIATED BY SPECIFIC CYTOKINES - DIFFERENT CD3+ SUBSETS ARE GENERATED BY IL-1 VERSUS IL-2 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL RECEPTOR; MAJOR HISTOCOMPATIBILITY COMPLEX; MONOCLONAL-ANTIBODY; ANTIGEN RECEPTOR; IMMATURE THYMOCYTES; GENE-EXPRESSION; SURFACE-ANTIGEN; LYMPHOCYTES-T; GAMMA-CHAIN; ALPHA-BETA AB The sequence of activation signals that stimulate proliferation, differentiation, and selection of mature T cell subsets from immature, dull-CD5+/CD4-, CD8- double negative (bCD5), (dCD5/DN) thymocytes are still unclear. However, it is likely that cytokines play integral roles in these events. Here we report that IL-1, in the presence of Con A, supports the proliferation and differentiation of highly purified dCD5/DN precursors into bright-CD5+ DN, CD2- lymphocytes with an apparently mature phenotype. These cells express CD3 and preferentially express the products of two TCR gene families, V-beta-8 and V-beta-6, whose expression is dependent on the allelic expression of the Mls-1 locus. Experiments, using DN thymocytes mixed with purified dCD5 subset of DN cells from a congenic strain of mice (i.e., expressing two different alleles of CD5) have shown that the cells that are stimulated by IL-1 and comitogen are derived from the immature dCD5 subset and not from the mature bCD5 cells contained within the DN subset. In contrast, IL-2 with the co-mitogen stimulates three-to fourfold higher levels of proliferation, from the same purified immature precursor population, and nearly a twofold increase in cell yield. However, the cells that were generated from precursor thymic cells stimulated with IL-2 represent a completely different T cell subset compared to IL-1-generated cells; these IL-2-stimulated cells express comparable levels of CD3, but also express substantial levels of CD2 and the TCR-gamma/delta, and a subset expresses CD8. These data suggest that these two TCR-alpha/beta and TCR-gamma/delta subsets of mature thymocytes use different cytokines and therefore possibly different stromal interactions to initiate differentiation. C1 NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD 21701. NCI,FREDERICK CANC RES FACIL,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21701. NCI,FREDERICK CANC RES FACIL,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. FU NCI NIH HHS [N01-CO-74102] NR 80 TC 6 Z9 6 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2262 EP 2271 PG 10 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700027 PM 1706392 ER PT J AU KEEGAN, AD BECKMANN, MP PARK, LS PAUL, WE AF KEEGAN, AD BECKMANN, MP PARK, LS PAUL, WE TI THE IL-4 RECEPTOR - BIOCHEMICAL-CHARACTERIZATION OF IL-4-BINDING MOLECULES IN A T-CELL LINE EXPRESSING LARGE NUMBERS OF RECEPTORS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID STIMULATORY FACTOR-I; RESTING B-CELLS; GROWTH-FACTOR; SURFACE RECEPTOR; CROSS-LINKING; BETA-CHAIN; MURINE-T; INTERLEUKIN-4; IGE; LIPOPOLYSACCHARIDE AB Cross-linking of I-125-IL-4 to the surface of cells expressing IL-4R yields as the major IL-4-binding molecules, polypeptide chains with inferred m.w. of approximately 70,000 (p70) and approximately 120,000 to 140,000 (p120-p140). The demonstration that the functional product of the IL-4R cDNA clone has m.w. of approximately 140,000 and that no p70 product is detected in transfected COS-7 cells has led to an uncertainty regarding the nature of p70. To study this issue, we examined the relationship of the IL-4-binding molecules p120 and p70 and, in parallel, attempted to immunoprecipitate p70 from surface and internally labeled cells using IL-4 and two anti-IL-4R antibodies (M1 and M2), bound to Affigel 10, as ligands. Cross-linked complexes containing I-125-IL-4 and p70 or p120 were isolated and digested with chymotrypsin or with V8 protease. Three distinct IL-4-binding peptides could be compared; these were indistinguishable for cross-linked p70 and p120, strongly implying that p70 and p120 were structurally related. Furthermore, immunoprecipitates made with IL-4 or anti-IL-4R-Affigel did not contain p70. This led us to conclude that p70 is a breakdown product of p120. A second IL-4-binding molecule of 40,000 Da (p40) expressing the M1 and M2 epitopes of the IL-4R was detected and appears to be the product of an mRNA coding for the soluble form of the receptor. mRNA for p40 was detected in both the T cell line CT.4R and the mast cell line CFTL.12 using polymerase chain reaction primers unique to this species of message. Pulse-chase studies of IL-4R in [S-35] methionine-labeled cells indicates that p40 is derived from a 42,000-Da precursor that is detectable at the end of the pulse period, and thus, further argue that p40 is an independently translated molecule and not a degradation product of p120. Although p40 has been previously shown to be a soluble, truncated form of the receptor, we failed to observe secretion of p40 into the medium by internally labeled CT.4R cells. C1 NIAID,IMMUNOL LAB,BLDG 10,RM 11N311,BETHESDA,MD 20892. IMMUNEX CORP,SEATTLE,WA 98101. NR 42 TC 35 Z9 35 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2272 EP 2279 PG 8 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700028 PM 2005396 ER PT J AU WONG, RA ALEXANDER, RB PURI, RK ROSENBERG, SA AF WONG, RA ALEXANDER, RB PURI, RK ROSENBERG, SA TI INVIVO PROLIFERATION OF ADOPTIVELY TRANSFERRED TUMOR-INFILTRATING LYMPHOCYTES IN MICE SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE TUMOR-INFILTRATING LYMPHOCYTES; ADOPTIVE IMMUNOTHERAPY; INTERLEUKIN-2; MICE; METASTATIC MELANOMA ID HIGH-DOSE INTERLEUKIN-2; RECOMBINANT INTERLEUKIN-2; T-CELLS; THERAPEUTIC EFFICACY; IMMUNOTHERAPY; MIGRATION; CANCER; LOCALIZATION; LEUKEMIA; IMMUNIZATION AB The adoptive transfer of tumor-infiltrating lymphocytes (TILs) in conjunction with interleukin-2 (IL-2) administration can mediate a reduction in established pulmonary and hepatic metastases of a variety of murine tumors as well as in patients with metastatic melanoma. To characterize further the fate of adoptively transferred TILs, the uptake of the thymidine analog 5-[I-125]iodo-2-deoxyuridine ([I-125]UdR) into the DNA of dividing cells was used to study the in vivo proliferation and migration patterns of transferred TILs in C57BL/6N mice. Animals received 500 rad of total body irradiation prior to cell transfer to separate incorporation of radiolabel into endogenous lymphoid cells from that into transferred TILs. Mice were subsequently treated with i.v. injections of TILs or no cells followed by i.p. injections of Hanks' balanced salt solution or IL-2. At various time points, mice received [I-125]UdR, and 20 h later tissues were removed and counted on a gamma analyzer. A proliferation index (PI) was calculated by dividing the mean cpm of organs of experimentally treated mice by the mean cpm of organs of control mice. Animals receiving TILs alone demonstrated small increases in [I-125]UdR in the lungs, liver, and spleen of saline-treated controls (PI = 1.4, 1.6, and 1.7, respectively, on day 4), while animals treated with 50,000 U of IL-2 alone showed greater increases in the lungs, liver, kidneys, and spleen (PI = 3.9, 6.1, 3.3, and 15.8). Mice receiving TILs plus IL-2 demonstrated the highest levels of radiolabel incorporation in the same organs (PI = 10.5, 19.4, 10.2, and 22.4). Over a period of 10 days, TIL plus IL-2 treated animals continued to incorporate significantly greater amounts of [I-125]UdR for as long as high-dose IL-2 was administered. Animals treated with TILs demonstrated increased incorporation of radiolabel with increasing doses of IL-2. Injection of irradiated TILs did not result in an increased uptake of [I-125]UdR into these tissues, thus confirming that TIL proliferation is responsible for the radiolabel uptake in animals receiving TILs alone or TILs plus IL-2. Additionally, fluorescein-labeled anti-Thy-1.1 antibody identified proliferating TILs derived from congenic B6.PL Thy 1a/CY (Thy-1.1) animals in the lungs, spleen, and liver of recipient C57BL/6N (Thy 1.2) mice. In summary, we have demonstrated that adoptively transferred TILs distribute widely after i.v. injection and can proliferate in various tissues especially under the influence of exogenous IL-2. C1 NCI,SURG BRANCH,BLDG 10,ROOM 2B56,BETHESDA,MD 20892. US FDA,CBER,DIV CYTOKINE BIOL,CELLULAR IMMUNOL LAB,BETHESDA,MD 20014. NR 39 TC 22 Z9 22 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD APR PY 1991 VL 10 IS 2 BP 120 EP 130 DI 10.1097/00002371-199104000-00006 PG 11 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA FD715 UT WOS:A1991FD71500006 PM 2043592 ER PT J AU HEIMBROOK, DC STIRDIVANT, SM AHERN, JD BALISHIN, NL PATRICK, DR EDWARDS, GM DEFEOJONES, D FITZGERALD, DJ PASTAN, I OLIFF, A AF HEIMBROOK, DC STIRDIVANT, SM AHERN, JD BALISHIN, NL PATRICK, DR EDWARDS, GM DEFEOJONES, D FITZGERALD, DJ PASTAN, I OLIFF, A TI BIOLOGICAL-ACTIVITY OF A TRANSFORMING GROWTH FACTOR-ALPHA - PSEUDOMONAS EXOTOXIN FUSION PROTEIN INVITRO AND INVIVO SO JOURNAL OF INDUSTRIAL MICROBIOLOGY LA English DT Article DE EPIDERMAL GROWTH FACTOR; EXOTOXIN; CANCER ID TOXIN; RECEPTOR AB Transforming growth factor-alpha (TGF-alpha)-pseudomonas exotoxin-40 (PE40) is a chimeric protein consisting of an N-terminal TGF-alpha domain fused to a C-terminal 40-kDa segment of the pseudomonas exotoxin A protein. TGF-alpha-PE40 exhibits the receptor binding activity of TGF-alpha and the cell killing activity of PE40. In the current study, we report that a modified TGF-alpha-PE40 derivative significantly prolongs the survival of nude mice bearing tumors derived from cell lines which express the epidermal growth factor receptor (EGFR). In addition, the therapeutic benefit of this protein is mediated by specific binding to the EGF receptor. These results indicate that a therapeutic window exists in vivo for the use of some growth factor - toxin fusion proteins as anticancer agents. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. MERCK SHARP & DOHME LTD,DEPT CANC RES,W POINT,PA 19486. NR 7 TC 1 Z9 1 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0169-4146 J9 J IND MICROBIOL JI J. Indust. Microbiol. PD APR PY 1991 VL 7 IS 3 BP 203 EP 207 DI 10.1007/BF01575884 PG 5 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA FK692 UT WOS:A1991FK69200007 PM 1367127 ER PT J AU ASHORN, P ENGLUND, G MARTIN, MA MOSS, B BERGER, EA AF ASHORN, P ENGLUND, G MARTIN, MA MOSS, B BERGER, EA TI ANTI-HIV ACTIVITY OF CD4-PSEUDOMONAS EXOTOXIN ON INFECTED PRIMARY HUMAN-LYMPHOCYTES AND MONOCYTE MACROPHAGES SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; SOLUBLE CD4; AIDS VIRUS; HYBRID PROTEIN; CELLS; INVITRO; INFECTIVITY; FORM; MOLECULES; RECEPTOR AB CD4(178)-PE40 is a recombinant protein consisting of a portion of human CD4 linked to active domains of Pseudomonas aeruginosa exotoxin A. In previous experiments with human T cell lines, the hybrid toxin was found to selectively kill cells infected with human immunodeficiency virus type 1 (HIV-1), and to inhibit HIV-1 spread in mixtures of infected and uninfected cells. CD4(178)-PE40 inhibits HIV-1 spread in cultured primary human lymphocytes. Moreover, the hybrid toxin selectively kills HIV-1 chronically infected monocyte/macrophage cell lines and inhibits HIV-1 spread in primary macrophage cultures. Control experiments indicate that the protective effects of CD4(178)-PE40 against HIV-1 spread are due to selective killing of the infected cells rather than simply to neutralization by the CD4 moiety. Thus, for the major cell types susceptible to HIV infection in vivo, surface envelope glycoprotein is expressed at sufficient levels to enable binding and internalization of CD4(178)-PE40 and consequent selective cell killing. C1 NIAID,VIRAL DIS LAB,BLDG 4,RM 232,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 30 TC 27 Z9 28 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1991 VL 163 IS 4 BP 703 EP 709 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA FD939 UT WOS:A1991FD93900004 PM 2010626 ER PT J AU EDWARDS, KM KING, JC STEINHOFF, MC THOMPSON, J CLEMENTS, ML WRIGHT, PF MURPHY, BR AF EDWARDS, KM KING, JC STEINHOFF, MC THOMPSON, J CLEMENTS, ML WRIGHT, PF MURPHY, BR TI SAFETY AND IMMUNOGENICITY OF LIVE ATTENUATED COLD-ADAPTED INFLUENZA-B/ANN ARBOR/1/86 REASSORTANT VIRUS-VACCINE IN INFANTS AND CHILDREN SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID B-VIRUS; A-VIRUS; SERONEGATIVE CHILDREN; YOUNG-CHILDREN; INFECTIONS; COMMUNITY; EPIDEMIC; HAMSTERS; HOUSTON; ADULTS AB A cold-adapted (ca) influenza B reassortant vaccine consisting of two genes encoding the hemagglutinin and neuraminidase from wild-type influenza B/Ann Arbor/1/86 virus and the six internal RNA segments from influenza B/Ann Arbor/1/66 ca virus was evaluated in 18 seropositive and 57 seronegative infants and children. The ca reassortant was infectious in seronegative vaccinees, with an estimated 50% human infectious dose of 10(2.5) TCID50. Nasal wash specimens from vaccinees retained the temperature-sensitive phenotype, indicating that the virus was phenotypically stable after replication in fully susceptible children. The vaccine was highly immunogenic in the seronegative vaccinees; 54% of the seropositive vaccines also developed an increase in serum antibody. The ca vaccine was well tolerated, with only a mild increase in upper respiratory tract symptoms seen in the seronegative vaccinees. These studies indicate that the B/Ann Arbor/1/86 ca reassortant is safe, immunogenic, and phenotypically stable in infants and children. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,CTR IMMUNIZAT RES,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. RP EDWARDS, KM (reprint author), VANDERBILT UNIV,MED CTR,SCH MED,DEPT PEDIAT,DIV INFECT DIS,D-7226 MCN,NASHVILLE,TN 37232, USA. FU NCRR NIH HHS [RR-00095]; NIAID NIH HHS [AI-02645, AI-62515] NR 35 TC 43 Z9 44 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1991 VL 163 IS 4 BP 740 EP 745 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA FD939 UT WOS:A1991FD93900010 PM 2010627 ER PT J AU REX, JH BENNETT, JE GALLIN, JI MALECH, HL DECARLO, ES MELNICK, DA AF REX, JH BENNETT, JE GALLIN, JI MALECH, HL DECARLO, ES MELNICK, DA TI INVIVO INTERFERON-GAMMA THERAPY AUGMENTS THE INVITRO ABILITY OF CHRONIC GRANULOMATOUS-DISEASE NEUTROPHILS TO DAMAGE ASPERGILLUS HYPHAE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article AB During the recently completed double-blind, placebo-controlled, randomized trial of recombinant interferon-gamma (rIFN-gamma) therapy in chronic granulomatous disease (CGD), a metabolic assay of neutrophil damage to Aspergillus fumigatus hyphae was used to monitor neutrophil function before and during therapy. In this assay, 5 x 10(4) conidia that had germinated into hyphae were exposed to 5 X 10(5), 15 X 10(5) or 50 X 10(5) CGD neutrophils. By analysis of variance, neutrophils from patients on rIFN-gamma were found to produce significantly more damage to hyphae than those from the placebo group (P < .01). In subgroup analysis, this effect was best seen in the hyphae exposed to 50 x 10(5) CGD neutrophils, where neutrophils from patients receiving rIFN-gamma produced significantly more damage to the hyphae than those from the placebo group (P < .05). In vivo rIFN-gamma therapy improves the ability of CGD neutrophils to damage Aspergillus fumigatus hyphae in an in vitro assay. RP REX, JH (reprint author), NIAID,CLIN INVEST LAB,BLDG 10,ROOM 11N107,BETHESDA,MD 20892, USA. NR 7 TC 101 Z9 104 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1991 VL 163 IS 4 BP 849 EP 852 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA FD939 UT WOS:A1991FD93900028 PM 1901332 ER PT J AU HOHL, D LICHTI, U BREITKREUTZ, D STEINERT, PM ROOP, DR AF HOHL, D LICHTI, U BREITKREUTZ, D STEINERT, PM ROOP, DR TI TRANSCRIPTION OF THE HUMAN LORICRIN GENE INVITRO IS INDUCED BY CALCIUM AND CELL-DENSITY AND SUPPRESSED BY RETINOIC ACID SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID HUMAN EPIDERMAL-KERATINOCYTES; CULTURED HUMAN KERATINOCYTES; TERMINAL DIFFERENTIATION; TRANSGLUTAMINASE ACTIVITY; ENVELOPE COMPETENCE; CROSS-LINKING; EXPRESSION; RNA; HYBRIDIZATION; LOCALIZATION AB We have previously shown that loricrin is a major component of the cornified cell envelope (CE) expressed late in epidermal differentiation in the granular layers of normal skin. Normal human keratinocytes were cultured under various conditions and loricrin mRNA levels were assessed at various time points. Only Ca++ concentrations above 0.1 mM Ca++ were permissive for the expression of lori- crin mRNA. Maximal mRNA levels were found at 0.35 mM Ca++ and a critical cell density appeared to be required for optimal accumulation of loricrin transcripts. Retinoic acid (RA) at 10(-7) to 10(-9) M completely blocked Ca++-induced loricrin mRNA synthesis when applied simultaneously. Furthermore, addition of RA to cultures already exposed to higher Ca++ levels resulted in the complete loss of loricrin mRNA within 48-72 h. So far, no other components of the CE have been shown to be suppressed by RA. However, similar patterns of expression were reported for filaggrin, a matrix protein also expressed late in epidermal differentiation. Therefore, we compared the mRNA levels of loricrin and filaggrin and found them to change in parallel in response to the various culture conditions. These results suggest that Ca++, cell density, and RA are crucial regulators of loricrin expression in vitro and that the transcriptional control of loricrin and filaggrin expression in the epidermis are closely coordinated. C1 UNIV HOSP ZURICH,CH-8091 ZURICH,SWITZERLAND. NCI,SKIN BIOL LAB,BETHESDA,MD 20892. NIAMS,BETHESDA,MD. BAYLOR UNIV,DEPT CELL BIOL,HOUSTON,TX 77030. BAYLOR UNIV,DEPT DERMATOL,HOUSTON,TX 77030. GERMAN CANC RES CTR,DIV DIFFERENTIAT & CARCINOGENESIS INVITRO,W-6900 HEIDELBERG 1,GERMANY. GERMAN CANC RES CTR,INST BIOCHEM,W-6900 HEIDELBERG 1,GERMANY. FU NIAMS NIH HHS [AR 40240] NR 41 TC 139 Z9 140 U1 1 U2 4 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 414 EP 418 DI 10.1111/1523-1747.ep12469779 PG 5 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100003 PM 2007780 ER PT J AU AIBA, S BOOKMAN, M KATZ, SI AF AIBA, S BOOKMAN, M KATZ, SI TI LANGERHANS CELLS PROCESS AND PRESENT TUMOR-ASSOCIATED ANTIGENS TO T-HELPER CELL CLONES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 533 EP 533 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100035 ER PT J AU GAN, SQ MARKOVA, N KORGE, B KIM, IG STEINERT, P AF GAN, SQ MARKOVA, N KORGE, B KIM, IG STEINERT, P TI THE CORRECT EXPRESSION OF A HUMAN MINI PROFILAGGRIN GENE IN TRANSGENIC MICE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 534 EP 534 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100038 ER PT J AU SEDMAN, SA BARBOSA, MS HUBBERT, NL VASS, WC SCHILLER, JT LOWY, DR AF SEDMAN, SA BARBOSA, MS HUBBERT, NL VASS, WC SCHILLER, JT LOWY, DR TI THE FULL LENGTH E6 PROTEIN OF A HIGH-RISK HPV IS MORE ACTIVE THAN E6 FROM A LOW-RISK HPV SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 534 EP 534 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100039 ER PT J AU ELGART, GW AMAGAI, M STANLEY, JR AF ELGART, GW AMAGAI, M STANLEY, JR TI 5' EXTENSION CLONING OF BULLOUS PEMPHIGOID (BP) CDNA BY RAPID AMPLIFICATION OF CDNA ENDS (RACE) WITH POLYMERASE CHAIN-REACTION (PCR) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 535 EP 535 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100047 ER PT J AU AMAGAI, M KLAUSKOVTUN, V STANLEY, JR AF AMAGAI, M KLAUSKOVTUN, V STANLEY, JR TI SOUTHERN ANALYSIS OF THE 230-KD BULLOUS PEMPHIGOID ANTIGEN (BPA) GENE IN ANIMALS, NORMAL HUMANS AND JUNCTIONAL EPIDERMOLYSIS-BULLOSA (JEB) PATIENTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 540 EP 540 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100077 ER PT J AU SARRET, Y KLEINMAN, HK WOODLEY, DT AF SARRET, Y KLEINMAN, HK WOODLEY, DT TI THE PEPTIDE (CSIKVAVS-NH2) NEAR THE AMINO TERMINUS OF THE LAMININ-A CHAIN MARKEDLY INHIBITS HUMAN KERATINOCYTE LOCOMOTION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 STANFORD UNIV,DEPT DERMATOL,STANFORD,CA 94305. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 540 EP 540 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100079 ER PT J AU KORGE, B GAN, SQ KIM, IG MISCHKE, D STEINERT, P AF KORGE, B GAN, SQ KIM, IG MISCHKE, D STEINERT, P TI POLYMORPHISMS OF THE HUMAN KERATIN-10 GENE ARE DUE TO VARIABLE NUMBERS OF GLYCINE LOOPS IN THE END DOMAINS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. FREE UNIV BERLIN,MED CTR RUDOLF VIRCHOW,INST EXPTL ONCOL & TRANSPLANTAT MED,W-1000 BERLIN 33,GERMANY. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 541 EP 541 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100082 ER PT J AU YONEDA, K MCBRIDE, W IDLER, W HOHL, D STEINERT, P AF YONEDA, K MCBRIDE, W IDLER, W HOHL, D STEINERT, P TI STRUCTURE OF THE HUMAN LORICRIN GENE - LINKAGE AT 1Q21 WITH PROFILAGGRIN AND INVOLUCRIN GENES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,BIOCHEM LAB,BETHESDA,MD 20892. CHU VAUDOIS,SERV DERMATOL,CH-1011 LAUSANNE,SWITZERLAND. NR 0 TC 5 Z9 5 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 541 EP 541 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100081 ER PT J AU HOLBROOK, KA UNDERWOOD, RA DALE, BA THACHER, SM WUEPPER, KD BANKSSCHLEGEL, S AF HOLBROOK, KA UNDERWOOD, RA DALE, BA THACHER, SM WUEPPER, KD BANKSSCHLEGEL, S TI CORNIFIED CELL-ENVELOPE (CCE) IN HUMAN FETAL SKIN - INVOLUCRIN, KERATOLININ, LORICRIN AND TRANSGLUTAMINASE EXPRESSION AND ACTIVITY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV WASHINGTON,SCH MED,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,DEPT BIOL STRUCT,SEATTLE,WA 98195. UNIV WASHINGTON,SCH DENT,DEPT ORAL BIOL,SEATTLE,WA 98195. UNIV WASHINGTON,SCH DENT,DEPT PERIODONT,SEATTLE,WA 98195. TEXAS A&M UNIV SYST,DEPT MED BIOCHEM,COLLEGE STN,TX 77843. OREGON HLTH SCI UNIV,DEPT DERMATOL,PORTLAND,OR 97201. NHLBI,BETHESDA,MD 20892. NR 0 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 542 EP 542 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100091 ER PT J AU JU, WD TAYEBI, N VELU, TJ VASS, WC LOWY, DR AF JU, WD TAYEBI, N VELU, TJ VASS, WC LOWY, DR TI AUTOCRINE SYNTHESIS OF TGF-ALPHA INDUCES FOCAL TRANSFORMATION WHICH CAN BE SUPPRESSED BY PARACRINE TREATMENT WITH TGF-ALPHA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 543 EP 543 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100096 ER PT J AU FALANGA, V SU, WQ DANIELPOUR, D KATZ, MH ROBERTS, AB SPORN, MB AF FALANGA, V SU, WQ DANIELPOUR, D KATZ, MH ROBERTS, AB SPORN, MB TI TGF-BETA-1 MESSENGER-RNA AND PROTEIN-SYNTHESIS BY HUMAN DERMAL FIBROBLASTS ARE CONTROLLED BY OXYGEN-TENSION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,DEPT DERMATOL,MIAMI,FL 33152. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 544 EP 544 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100100 ER PT J AU STEINERT, P MACK, J KORGE, B GAN, SQ KIM, IG YONEDA, K IDLER, W HAYNES, S STEVEN, A AF STEINERT, P MACK, J KORGE, B GAN, SQ KIM, IG YONEDA, K IDLER, W HAYNES, S STEVEN, A TI STRUCTURE AND POSSIBLE FUNCTIONS OF THE GLYCINE LOOP MOTIF ON EPIDERMAL STRUCTURAL PROTEINS - THE VELCRO HYPOTHESIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NIAMS,STRUCT BIOL RES LAB,BETHESDA,MD. NICHHD,MOLEC GENET LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 545 EP 545 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100104 ER PT J AU ZHENG, ZS POLAKOWSKA, RR JOHNSON, AC GOLDSMITH, LA AF ZHENG, ZS POLAKOWSKA, RR JOHNSON, AC GOLDSMITH, LA TI REGULATION OF EPIDERMAL GROWTH-FACTOR RECEPTOR GENE-TRANSCRIPTION BY RETINOIC ACID SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV ROCHESTER,DEPT DERMATOL,ROCHESTER,NY 14627. NCI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 546 EP 546 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100112 ER PT J AU FINZI, E SKOUGE, J CELANO, P BLAKE, M AF FINZI, E SKOUGE, J CELANO, P BLAKE, M TI CELLULAR-LOCALIZATION OF RETINOIC ACID RECEPTOR-GAMMA IN NORMAL AND NEOPLASTIC SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,DEPT DERMATOL,BALTIMORE,MD 21218. NIA,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 547 EP 547 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100119 ER PT J AU HUFF, CA ROSENTHAL, DS YUSPA, SH ROOP, DR AF HUFF, CA ROSENTHAL, DS YUSPA, SH ROOP, DR TI IDENTIFICATION AND CHARACTERIZATION OF A COMPLEX REGULATORY ARRAY 3' TO THE GENE ENCODING HUMAN KERATIN-1 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. BAYLOR UNIV,HOUSTON,TX 77030. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 550 EP 550 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100134 ER PT J AU DLUGOSZ, AA KNOPF, JL YUSPA, SH AF DLUGOSZ, AA KNOPF, JL YUSPA, SH TI MESSENGER-RNA ENCODING PROTEIN-KINASE-C ALPHA, DELTA, EPSILON, AND ZETA IS EXPRESSED IN NORMAL AND NEOPLASTIC MOUSE KERATINOCYTES INVITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. GENET INST,CAMBRIDGE,MA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 566 EP 566 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100233 ER PT J AU TENNENBAUM, T YUSPA, SH KNOX, BM SOBEL, ME CASTRONOVO, V YAMADA, Y DE LUCA, LM AF TENNENBAUM, T YUSPA, SH KNOX, BM SOBEL, ME CASTRONOVO, V YAMADA, Y DE LUCA, LM TI ALTERATIONS IN ATTACHMENT TO LAMININ AND LOCALIZATION OF LAMININ BINDING-PROTEINS DURING DIFFERENTIATION OF PRIMARY MOUSE KERATINOCYTES INVITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI, BETHESDA, MD 20892 USA. NIDR, BETHESDA, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 566 EP 566 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100230 ER PT J AU DIGIOVANNA, JJ TURNER, ML PECK, GL ABANGAN, DL AF DIGIOVANNA, JJ TURNER, ML PECK, GL ABANGAN, DL TI RECOMBINANT INTERFERON GAMMA TREATMENT OF BASAL-CELL CARCINOMA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 569 EP 569 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100250 ER PT J AU CHEN, G FOLK, JE HOLADAY, J NIGRA, T AF CHEN, G FOLK, JE HOLADAY, J NIGRA, T TI A NEW CLASS OF INHIBITORS TO TRANSGLUTAMINASE - THE ISOTHIOCYANATES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MEDICIS PHARMACEUT CORP,NEW YORK,NY. NIDR,BETHESDA,MD 20892. WASHINGTON HOSP CTR,DEPT DERMATOL,WASHINGTON,DC 20010. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 581 EP 581 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100322 ER PT J AU RESZKA, K MIYAKE, Y ALENA, F JIMBOW, K AF RESZKA, K MIYAKE, Y ALENA, F JIMBOW, K TI GENERATION OF RADICAL SPECIES FROM MELANOCYTOTOXIC AGENTS, PHENOLIC THIOETHER AMINES UPON TYROSINASE ACTIVATION - AN ESR STUDY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIEHS,MOLEC BIOL LAB,RES TRIANGLE PK,NC 27709. HOKKAIDO UNIV,DEPT POLYMER SCI,SAPPORO,HOKKAIDO 060,JAPAN. UNIV ALBERTA,DIV DERMATOL & CUTANEOUS SCI,EDMONTON T6G 2E1,ALBERTA,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 581 EP 581 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100320 ER PT J AU PUNNONEN, K YUSPA, SH AF PUNNONEN, K YUSPA, SH TI EFFECTS OF UVB IRRADIATION ON THE FORMATION OF MEMBRANE LIPID DERIVED MEDIATORS OF SIGNAL TRANSDUCTION IN MURINE KERATINOCYTES IN CULTURE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 590 EP 590 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100375 ER PT J AU PARRIS, CN KRAEMER, KH AF PARRIS, CN KRAEMER, KH TI CELLULAR-TRANSFORMATION ALTERS ULTRAVIOLET MUTAGENESIS IN XERODERMA-PIGMENTOSUM CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 597 EP 597 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100417 ER PT J AU BLOK, B TAYLOR, RS GONZALEZ, A SIMON, M KING, C SOLOMON, W ELLIS, C JAFFE, H COOPER, KD AF BLOK, B TAYLOR, RS GONZALEZ, A SIMON, M KING, C SOLOMON, W ELLIS, C JAFFE, H COOPER, KD TI PERIPHERAL-BLOOD LEUKOCYTE SUBSETS IN ATOPIC-DERMATITIS - EFFECT OF GAMMA-INTERFERON SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV MICHIGAN,DEPT DERMATOL,ANN ARBOR,MI 48109. VET ADM MED CTR,ALLEN PK,MI. NIH,BETHESDA,MD 20892. GENENTECH INC,SAN FRANCISCO,CA 94080. NR 0 TC 7 Z9 7 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 604 EP 604 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100459 ER PT J AU PERLISH, JS CONTARD, P FISHER, LW MACDONALD, ED JACOBS, L TERMINE, TD FLEISCHMAJER, R AF PERLISH, JS CONTARD, P FISHER, LW MACDONALD, ED JACOBS, L TERMINE, TD FLEISCHMAJER, R TI INVIVO AND INVITRO DEMONSTRATION OF DECORIN INTERACTING WITH HUMAN INTERSTITIAL COLLAGEN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 CUNY MT SINAI SCH MED,DEPT DERMATOL,NEW YORK,NY 10029. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 605 EP 605 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100465 ER PT J AU BERNSTEIN, EF HARISIADIS, L SALOMON, G NORTON, J GLASS, J TALBOT, T SOLLBERG, S UITTO, J BURESH, C GLATSTEIN, E RUSSO, A MITCHELL, JB AF BERNSTEIN, EF HARISIADIS, L SALOMON, G NORTON, J GLASS, J TALBOT, T SOLLBERG, S UITTO, J BURESH, C GLATSTEIN, E RUSSO, A MITCHELL, JB TI TRANSFORMING GROWTH-FACTOR-BETA (TGF-BETA) IMPROVES HEALING OF RADIATION-IMPAIRED WOUNDS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,SURG BRANCH,BETHESDA,MD 20892. HAHNEMANN UNIV,PHILADELPHIA,PA 19102. THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 606 EP 606 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100473 ER PT J AU MAUVIEL, A REDINI, F PUJOL, JP EVANS, CH AF MAUVIEL, A REDINI, F PUJOL, JP EVANS, CH TI MODULATION OF HUMAN DERMAL FIBROBLAST EXTRACELLULAR-MATRIX METABOLISM BY THE LYMPHOKINE LEUKOREGULIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT DERMATOL,PHILADELPHIA,PA 19107. CHU CAEN,BIOCHEM TISSUE CONJONCT LAB,F-14033 CAEN,FRANCE. NIH,DIV CANC ETIOL,BIOL LAB,TUMOR BIOL SECT,BETHESDA,MD 20892. RI REDINI, Francoise/K-7981-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 607 EP 607 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100479 ER PT J AU MACK, J STEINERT, P AF MACK, J STEINERT, P TI THE MECHANISM OF INTERACTION OF FILAGGRIN WITH KERATIN INTERMEDIATE FILAMENTS - THE IONIC ZIPPER HYPOTHESIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 615 EP 615 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100526 ER PT J AU GRIFFITHS, C ROSENTHAL, D LEACH, K WANG, T YUSPA, S VOORHEES, J FISHER, G AF GRIFFITHS, C ROSENTHAL, D LEACH, K WANG, T YUSPA, S VOORHEES, J FISHER, G TI HUMAN EPIDERMAL TRANSGLUTAMINASE ACTIVITY AND IMMUNOSTAINING ARE INCREASED INVIVO AND DECREASED IN KERATINOCYTES INVITRO BY RETINOIC ACID TREATMENT SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV MICHIGAN,DEPT DERMATOL,ANN ARBOR,MI 48109. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 620 EP 620 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100557 ER PT J AU COHEN, PJ KATZ, SI AF COHEN, PJ KATZ, SI TI CULTURED HUMAN LANGERHANS CELLS CAN PROCESS AND PRESENT INTACT PROTEIN ANTIGENS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 624 EP 624 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100580 ER PT J AU DECOSTA, BR BOWEN, WD AF DECOSTA, BR BOWEN, WD TI SYNTHESIS AND CHARACTERIZATION OF OPTICALLY PURE [H-3] (+)-AZIDOPHENAZOCINE ([H-3](+)-AZPH), A NOVEL PHOTOAFFINITY LABEL FOR SIGMA-RECEPTORS SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE [H-3](+)-CIS-N-(2-(4-AZIDOPHENYL)ETHYL)-2'-HYDROXY-2,6-DIMETHYL-6,7-BENZ OMORPHA; NOVEL BENZOMORPHAN-BASED PHOTOAFFINITY LABEL; SIGMA-RECEPTORS; OPTICALLY PURE (+)-NORMETAZOCINE ID OPIATE RECEPTORS; OPIOID RECEPTOR; RAT; CELLS; PHENCYCLIDINE; AFFINITY; BRAIN; SITE AB [H-3](+)-cis-N-(2-(4-Azidophenyl)ethyl)-2'-hydroxy-2,6-dimethyl-6,7-benzomorphan ([H-3]1) ([H-3](+)-AZPH), a novel high affinity and high selectivity benzomorphan based photoaffinity label for sigma receptors was synthesized in 4 steps starting with optically pure (+)-normetazocine and 2-(p-azidophenyl)ethyl methanesulfonate ester. Condensation of these compounds in DMF in the presence of NaHCO3 afforded 1 in 77% yield. The tritiation precursor (+)-cis-N-(2-(4-azidophenyl)ethyl)-2'-hydroxy-1',3'-dibromo-2,6-dimethyl-6,7-benzomorphan (4) for medium specific activity [H-3]1 was obtained in 96% yield by bromination of 1 with 2 equivalents of bromine. The sequence of catalytic tritiation of 4, treatment of the resulting aniline ([H-3]5) (13.5% radiochemical yield, specific activity 22.9 Ci/mmol) with nitrous acid followed by sodium azide afforded the target compound in 78% chemical yield. C1 BROWN UNIV,DIV BIOL & MED,BIOCHEM SECT,PROVIDENCE,RI 02912. RP DECOSTA, BR (reprint author), NIDDKD,MED CHEM,BETHESDA,MD 20892, USA. NR 25 TC 2 Z9 3 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0362-4803 J9 J LABELLED COMPD RAD JI J. Label. Compd. Radiopharm. PD APR PY 1991 VL 29 IS 4 BP 443 EP 453 DI 10.1002/jlcr.2580290409 PG 11 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA FH418 UT WOS:A1991FH41800007 ER PT J AU CHILDERS, WE SILVERTON, JV KELLIS, JT VICKERY, LE ROBINSON, CH AF CHILDERS, WE SILVERTON, JV KELLIS, JT VICKERY, LE ROBINSON, CH TI INHIBITION OF HUMAN PLACENTAL AROMATASE BY NOVEL HOMOLOGATED 19-OXIRANYL AND 19-THIIRANYL STEROIDS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID 10-BETA-THIIRANYL STEROIDS; CYTOCHROME-P-450; 4-HYDROXY-4-ANDROSTENE-3,17-DIONE; AROMATIZATION; PURIFICATION; INACTIVATION; MICROSOMES AB Novel homologated 19-oxiranyl- and 9-thiiranylandrost-4-ene-3,17-diones (8a,b and 9a,b, respectively) have been synthesized. The configuration and conformation of compound 8a have been established by X-ray crystallographic analysis. All four compounds have been shown to be competitive inhibitors of human placental aromatase. The thiiranes were more potent inhibitors than the corresponding oxiranes, and the 2'S isomers (8b and 9b) were better inhibitors than the 2'R (8a and 9a) diastereomers in each series. Spectroscopic studies with purified human placental aromatase suggest that the oxiranyl oxygen and thiiranyl sulfur of 2'S compounds 8b and 9b coordinate to the enzyme's heme iron. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205. NHLBI,CHEM LAB,BETHESDA,MD 20892. UNIV CALIF IRVINE,DEPT PHYSIOL & BIOPHYS,IRVINE,CA 92717. FU NICHD NIH HHS [HD-11840]; NIDDK NIH HHS [DK-37551] NR 25 TC 12 Z9 12 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR PY 1991 VL 34 IS 4 BP 1344 EP 1349 DI 10.1021/jm00108a016 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA FG776 UT WOS:A1991FG77600016 PM 2016709 ER PT J AU LAZARUS, LH SALVADORI, S SANTAGADA, V TOMATIS, R WILSON, WE AF LAZARUS, LH SALVADORI, S SANTAGADA, V TOMATIS, R WILSON, WE TI FUNCTION OF NEGATIVE CHARGE IN THE ADDRESS DOMAIN OF DELTORPHINS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID DELTA-OPIOID RECEPTOR; SOLID-PHASE SYNTHESIS; ENKEPHALIN-RELATED PEPTIDES; NUCLEAR MAGNETIC-RESONANCE; HIGH-AFFINITY; BIOLOGICAL-ACTIVITY; DERMORPHIN ANALOGS; OPIATE RECEPTOR; BINDING-SITES; MU-OPIATE AB Deltorphins A, B, and C exhibit high delta-affinities (K(i) = 0.12-0.31 nM) and very high delta-receptor binding selectivities (K(i)mu/K(i)delta = 1800-4100). A study of the delta-receptor binding properties of 15 deltorphin analogues focused primarily on the influence of the anionic group in the C-terminal tetrapeptide. Amidation of the beta-carboxyl groups of [Asp7], [Glu4], or [Asp4] in deltorphins A, B, and C, respectively, yielded peptides with enhanced mu-receptor affinities and minor changes in delta-affinities (K(i)delta = 0.20-0.65 nM), but 5-8-fold diminished delta-selectivities. A free C-terminal carboxyl group markedly reduced delta-affinities andand decreased delta-selectivities 6-11-fold; thus, the C-terminal amide group critically facilitates delta-affinity. Modifications in the anionic charged group or hydrophobic residues in the C-terminal tetrapeptide address domain of deltorphin A altered spatial distributions critical for delta-affinity and selectivity; e.g., [Nle6]deltorphin A enhanced mu-affinity and lowered delta-selectivity by two-thirds; the progressive, step-wise repositioning of Asp in deltorphin C (from position 4 to 7) was accompanied by linear decreases in delta-affinities and -selectivities, and increased mu-affinities of these peptides; enhancement of the charge density to -2, in [Asp6,Asp-OH7]deltorphin A, decreased delta-affinity and -selectivity, while [Asp4,5,His7]deltorphin A bound to neither mu- nor delta-sites. These results demonstrate that while an anionic group may occassionally facilitate high delta-receptor affinity, it represents an absolute requirement for the high delta-binding selectivity of these peptides. The locations of the charged groups relative to hydrophobic residues in the address domain of the peptide are also critical determinants for both delta-affinity and -selectivity. C1 UNIV FERRARA,DEPT PHARMACEUT SCI,I-44100 FERRARA,ITALY. RP LAZARUS, LH (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,PEPTIDE NEUROCHEM SECT,POB 12233,RES TRIANGLE PK,NC 27709, USA. OI SALVADORI, Severo/0000-0002-8224-2358 NR 100 TC 68 Z9 68 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR PY 1991 VL 34 IS 4 BP 1350 EP 1355 DI 10.1021/jm00108a017 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA FG776 UT WOS:A1991FG77600017 PM 1849997 ER PT J AU SCHULMAN, SP LAKATTA, EG WEISS, RG WOLFF, MR HANO, O GERSTENBLITH, G AF SCHULMAN, SP LAKATTA, EG WEISS, RG WOLFF, MR HANO, O GERSTENBLITH, G TI CONTRACTILE, METABOLIC AND ELECTROPHYSIOLOGIC EFFECTS OF ETHANOL IN THE ISOLATED RAT-HEART SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE ETHANOL; EXCITATION CONTRACTION COUPLING; HIGH ENERGY PHOSPHATES; CALCIUM; LEFT VENTRICULAR FUNCTION ID MAXIMAL CA-2+-ACTIVATED FORCE; NUCLEAR MAGNETIC-RESONANCE; SARCOPLASMIC-RETICULUM; AUTONOMIC BLOCKADE; HUMAN MUSCLE; CALCIUM; P-31; ACETALDEHYDE; ALCOHOL; CELLS C1 JOHNS HOPKINS UNIV, SCH MED, DEPT MED, DIV CARDIOL, BALTIMORE, MD 21205 USA. NIA, GERONTOL RES CTR, BALTIMORE, MD 21224 USA. FU NHLBI NIH HHS [P-50-HL17655-16] NR 38 TC 22 Z9 22 U1 0 U2 3 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD APR PY 1991 VL 23 IS 4 BP 417 EP 426 DI 10.1016/0022-2828(91)90166-J PG 10 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA FR984 UT WOS:A1991FR98400005 PM 1942079 ER PT J AU DRISCOLL, BF LAW, MJ CRANE, AM AF DRISCOLL, BF LAW, MJ CRANE, AM TI CELL-DAMAGE ASSOCIATED WITH CHANGING THE MEDIUM OF MESENCEPHALIC CULTURES IN SERUM-FREE MEDIUM IS MEDIATED VIA N-METHYL-D-ASPARTATE RECEPTORS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE MESENCEPHALIC CULTURES; DOPAMINERGIC NEURONS; SERUM-FREE MEDIUM; MEDIUM CHANGE; EXCITATORY AMINO ACIDS; GLUTAMATE ID EPILEPTIFORM ACTIVITY; POTENT; ACID; NEUROTOXICITY; ANTAGONIST; GLUTAMATE; SLICES; MK-801 AB Dopaminergic neurons from embryonic rat mesencephalon were grown in simple serum-free media. The cells develop over a period of several weeks in vitro, particularly between day 14 and day 23. Removing the culture medium and replacing it with fresh medium during this interval caused severe damage to the cultures; this damage is mediated by excitatory amino acids acting through glutamate receptors. Damage could be completely prevented by antagonists of the N-methyl-D-aspartate subtype of glutamate receptor. As expected, medium that contains glutamate (i.e., Ham's F-12 medium) caused damage; however, medium that contains no glutamate or aspartate (i.e., Dulbecco's modified Eagle medium) also caused severe damage, and most of the damage was dependent on the presence of glutamine in the medium. The presence of the antibiotics penicillin and streptomycin greatly enhanced damage caused by medium change. RP DRISCOLL, BF (reprint author), NIMH,CEREBRAL METAB LAB,BLDG 36,ROOM 1A05,BETHESDA,MD 20892, USA. NR 15 TC 43 Z9 43 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD APR PY 1991 VL 56 IS 4 BP 1201 EP 1206 DI 10.1111/j.1471-4159.1991.tb11411.x PG 6 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA FB656 UT WOS:A1991FB65600014 PM 1672142 ER PT J AU TUOMINEN, RK HUDSON, PM MCMILLIAN, MK YE, H STACHOWIAK, MK HONG, JS AF TUOMINEN, RK HUDSON, PM MCMILLIAN, MK YE, H STACHOWIAK, MK HONG, JS TI LONG-TERM ACTIVATION OF PROTEIN-KINASE-C BY ANGIOTENSIN-II IN CULTURED BOVINE ADRENAL-MEDULLARY CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE PROTEIN KINASE-C; ANGIOTENSIN-II; 2ND MESSENGERS; ADRENAL MEDULLA; CELL CULTURE ID CHROMAFFIN CELLS; RAT-BRAIN; IMMUNOCHEMICAL CHARACTERIZATION; CATECHOLAMINE SECRETION; INOSITOL TRISPHOSPHATE; PHORBOL ESTER; CALCIUM; BINDING; PHOSPHORYLATION; DIACYLGLYCEROL AB Previous studies from our laboratory suggest that protein kinase C (PKC) is involved in the angiotensin II (AII)-induced increase in the expression of genes encoding proenkephalin and catecholamine biosynthesizing enzymes in primary cultured bovine adrenal medullary (BAM) cells. The purpose of this study was to examine the effects of [Sar1]-AII (S1-AII), an AII agonist, on PKC activity in BAM cells. Thirty-minute incubation with S1-AII produced a dose-dependent activation of PKC. The particulate PKC activity was significantly increased by 2 nM S1-AII after both 30 min and 12 h of incubation. A high concentration of S1-AII (200 nM) caused an increase in particulate PKC activity after 30 min of incubation and this increase was still observed after 18 h of continuous incubation. [Sar1,Thr8]-angiotensin II (S1,T8-AII) (100-mu-M), an AII antagonist, inhibited the effect of S1-AII (20 nM) on PKC activity, suggesting a specific AII receptor-mediated effect. An increase in BAM cell particulate PKC immunoreactivity after 18 h of S1-AII treatment was observed in Western blot analysis of PKC-immunoreactive protein (82 kDa). The persistent activation of PKC seen in this study is consistent with our hypothesis that PKC may mediate the S1-AII-induced increase in the expression of genes encoding proenkephalin and catecholamine synthesizing enzymes in BAM cells. C1 NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,NEUROPHARMACOL SECT,POB 12233,RES TRIANGLE PK,NC 27709. FU PHS HHS [4066] NR 43 TC 37 Z9 37 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD APR PY 1991 VL 56 IS 4 BP 1292 EP 1298 DI 10.1111/j.1471-4159.1991.tb11424.x PG 7 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA FB656 UT WOS:A1991FB65600027 PM 2002341 ER PT J AU BAER, SM RINZEL, J AF BAER, SM RINZEL, J TI PROPAGATION OF DENDRITIC SPIKES MEDIATED BY EXCITABLE SPINES - A CONTINUUM THEORY SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID PURKINJE-CELLS; ACTIVE MEMBRANE; STIMULATION; MECHANISM; CALCIUM; INVITRO; NEURONS AB 1. Neuroscientists are currently hypothesizing on how voltage-dependent channels, in dendrites with spines, may be spatially distributed or how their numbers may divide between spine heads and the dendritic base. A new cable theory is formulated to investigate electrical interactions between many excitable and/or passive dendritic spines. The theory involves a continuum formulation in which the spine density, the membrane potential in spine heads, and the spine stem current vary continuously in space and time. The spines, however, interact only indirectly by voltage spread along the dendritic shaft. Active membrane in the spine heads is modeled with Hodgkin-Huxley (HH) kinetics. Synaptic currents are generated by transient conductance increases. For most simulations the membrane of spine stems and dendritic shaft is assumed passive. 2. Action-potential generation and propagation occur as localized excitatory synaptic input into spine heads causes a few excitable spines to fire, which then initiates a chain reaction of spine firings along a branch. This sustained wavelike response is possible for a certain range of spine densities and electrical parameters. Propagation is precluded for spine stem resistance (R(ss)) either too large or too small. Moreover, even if R(ss) lies in a suitable range for the local generation of an action potential (resulting from local synaptic excitatory input), this range may not be suitable to initiate a chain reaction of spine firings along the dendrite; success or failure of impulse propagation depends on an even narrower range of R(ss) values. 3. The success or failure of local excitation to spread as a chain reaction depends on the spatial distribution of spines. Impulse propagation is unlikely if the excitable spines are spaced too far apart. However, propagation may be recovered by redistributing the same number of equally spaced spines into clusters. 4. The spread of excitation in a distal dendritic arbor is also influenced by the branching geometry. Input to one branch can initiate a chain reaction that accelerates into the sister branch but rapidly attenuates as it enters the parent branch. In branched dendrites with many excitable and passive spines, regions of decreased conductance load (e.g., near sealed ends) can facilitate attenuating waves and enhance waves that are successfully propagating. Regions of increased conductance load (e.g., near common branch points) promote attenuation and tend to block propagation. Nonuniform loading and/or nonuniform spine densities can lead to complex propagation characteristics. 5. Some analytic results of classical cable theory are generalized for the case of a passive spiny dendritic cable. New expressions for electrotonic length and input resistance reflect the cumulative effect of having many passive spines, and they depend explicitly on spine density nBAR and individual spine electrical parameters. As nBAR increases, the electrotonic length increases proportionally to square-root nBAR, whereas the input resistance decreases reciprocally with square-root nBAR, i.e., higher spine density means more membrane available for current loss. If R(ss) is increased the electrotonic length decreases, and the input resistance increases. However, in the expected parameter range, where the spine head resistance R(sh) substantially exceeds R(ss), the effect of changing R(ss) is negligible. 6. The initiation of a chain reaction by synaptic input in spines depends on whether the voltage-dependent channels are located in the spine heads or in the dendrite; direct activation of more synapses is needed when the channels are distributed along the dendritic shaft than when they are isolated in the heads. On the other hand, an established propagating wave is little influenced by the location of the channels. Also, the minimal number of synapses required for initiation and the wave's peak dendritic potential are much more sensitive to changes in R(ss) for the case of spine head channels than for dendritic channels. 7. With the continuum theory, different morphologies and distributed physiological properties may be represented explicitly and compactly by just a few differential equations. The equations may be integrated with standard finite difference methods adapted to treat branching geometries. The theory is general so that idealized or complex kinetic models may also be adapted. These features mean that models are easily communicated, that computations can be readily reproduced by other investigators, and that spines can and should be taken into account where appropriate. C1 NIDDKD,MATH RES BRANCH,BLDG 31,RM 4B-54,BETHESDA,MD 20892. NR 47 TC 76 Z9 77 U1 0 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD APR PY 1991 VL 65 IS 4 BP 874 EP 890 PG 17 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA FF973 UT WOS:A1991FF97300010 PM 2051208 ER PT J AU STANLEY, EF GOPING, G AF STANLEY, EF GOPING, G TI CHARACTERIZATION OF A CALCIUM CURRENT IN A VERTEBRATE CHOLINERGIC PRESYNAPTIC NERVE-TERMINAL SO JOURNAL OF NEUROSCIENCE LA English DT Article ID CHICK SENSORY NEURONS; SQUID GIANT SYNAPSE; SYMPATHETIC NEURONS; CILIARY GANGLION; PERIPHERAL NEURONS; CA-2+ CHANNELS; TRANSMISSION; INFLUX; SYNAPTOSOMES; SENSITIVITY AB Calcium currents were recorded from a cholinergic presynaptic nerve terminal in the chick ciliary ganglion using the whole-cell voltage-clamp technique. The presynaptic element of this synapse is in the form of a calyx that envelops the postsynaptic ciliary neuron. A method was developed to isolate the ciliary neuron, expose the calyx, and apply patch-clamp electrodes under visual control. The presynaptic Ca current activated at +30 mV with a fast time constant of about 1.5 msec and deactivated at -80 mV with a time constant of about 0.5 msec, values that are consistent with a role in action-potential-dependent transmitter release. The calyx Ca current was blocked by 0.1 mM Cd or 2-mu-M omega-conotoxin and was resistant to voltage-dependent inactivation. The presynaptic Ca channel exhibits similarities to the N-type group but differs from these by the minimal voltage-dependent inactivation. This type of channel, designated Ca(N-PT) (N-like, presynaptic terminal), may play a key role in transmitter release at many vertebrate fast-transmitting synapses. C1 NIDDK,CELL BIOL & GENET LAB,BETHESDA,MD 20892. RP STANLEY, EF (reprint author), NINCDS,BIOPHYS LAB,BLDG 9,ROOM 1E124,BETHESDA,MD 20892, USA. NR 46 TC 126 Z9 126 U1 0 U2 2 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1991 VL 11 IS 4 BP 985 EP 993 PG 9 WC Neurosciences SC Neurosciences & Neurology GA FG030 UT WOS:A1991FG03000014 PM 2010819 ER PT J AU GERFEN, CR MCGINTY, JF YOUNG, WS AF GERFEN, CR MCGINTY, JF YOUNG, WS TI DOPAMINE DIFFERENTIALLY REGULATES DYNORPHIN, SUBSTANCE-P, AND ENKEPHALIN EXPRESSION IN STRIATAL NEURONS - INSITU HYBRIDIZATION HISTOCHEMICAL ANALYSIS SO JOURNAL OF NEUROSCIENCE LA English DT Article ID IMMUNO-CYTOCHEMICAL LOCALIZATION; PROENKEPHALIN MESSENGER-RNA; ANTI-SCHIZOPHRENIC DRUGS; CENTRAL NERVOUS-SYSTEM; RAT-BRAIN; BASAL GANGLIA; HORSERADISH-PEROXIDASE; MICROSCOPIC LOCALIZATION; INTRACELLULAR INJECTION; IMMUNOREACTIVE NEURONS AB Dopamine regulation of the levels of dynorphin, enkephalin, and substance P messenger RNAs in rat striatal neurons was analyzed with in situ hybridization histochemistry (ISHH). Relative levels of peptide mRNA expression in the patch and matrix compartments of the dorsolateral striatum were compared among control rats, rats treated for 10 d with apomorphine, rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal dopaminergic system, and rats with nigrostriatal dopaminergic lesions followed 2 weeks later by 10 d of apomorphine treatment. Image analysis of ISHH labeling demonstrated that the number of neurons expressing each peptide mRNA remained constant, whereas the relative level of peptide mRNA per neuron changed significantly, depending on the experimental treatment. Dynorphin mRNA expression increased following chronic apomorphine treatment: striatal patch neurons increased to an average of 100% above control values, whereas striatal matrix neurons showed only a 25% increase. Dynorphin mRNA expression decreased following 6-OHDA lesions: patch neurons showed an average 75% reduction in expression, whereas matrix neurons showed no significant change. In animals with 6-OHDA lesions followed by apomorphine treatment, both patch and matrix neurons showed an average increase in dynorphin expression of 300% above control levels. Changes in dynorphin mRNA levels with these treatments were matched by qualitative changes in dynorphin immunoreactivity both in the striatum and in striatonigral terminals in the substantia nigra. Neither substance P nor enkephalin mRNA levels showed a significant difference between the striatal patch and matrix compartments in any experimental condition (in the dorsolateral striatum). Substance P mRNA expression was increased an average of 50% after 10 d of apomorphine treatment and showed an average decrease of 75% following 6-OHDA lesions of the mesostriatal system. There was no significant change in the expression of substance P mRNA in striatal neurons compared to control values in rats with combined 6-OHDA lesion and apomorphine treatment. Enkephalin mRNA expression was not significantly altered by chronic apomorphine treatment but showed an average increase per cell of some 130% above control levels following 6-OHDA-induced lesions of the mesostriatal system. In animals with a 6-OHDA lesion and apomorphine treatment, enkephalin mRNA was also elevated but not significantly above the levels produced by the lesions alone. These data show that the expression of dynorphin, enkephalin, and substance P is differentially regulated by the mesostriatal dopaminergic system and, further, suggests that the mechanisms by which this regulation occurs may be different for the 3 peptide families. C1 E CAROLINA UNIV,SCH MED,DEPT ANAT & CELL BIOL,GREENVILLE,NC 27858. RP GERFEN, CR (reprint author), NIMH,CELL BIOL LAB,BLDG 36,ROOM 2D-10,BETHESDA,MD 20892, USA. RI Young, W Scott/A-9333-2009 OI Young, W Scott/0000-0001-6614-5112 NR 61 TC 410 Z9 417 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1991 VL 11 IS 4 BP 1016 EP 1031 PG 16 WC Neurosciences SC Neurosciences & Neurology GA FG030 UT WOS:A1991FG03000017 PM 1707092 ER PT J AU WEBSTER, MJ UNGERLEIDER, LG BACHEVALIER, J AF WEBSTER, MJ UNGERLEIDER, LG BACHEVALIER, J TI CONNECTIONS OF INFERIOR TEMPORAL AREAS TE AND TEO WITH MEDIAL TEMPORAL-LOBE STRUCTURES IN INFANT AND ADULT MONKEYS SO JOURNAL OF NEUROSCIENCE LA English DT Article ID POSTNATAL-DEVELOPMENT; CORTICAL PROJECTIONS; CALLOSAL CONNECTIONS; RHESUS-MONKEY; STRIATE CORTEX; VISUAL-CORTEX; COLLATERAL ELIMINATION; TRANSIENT PROJECTIONS; ENTORHINAL CORTEX; PYRAMIDAL TRACT AB As part of a long-term study designed to examine the ontogeny of visual memory in monkeys and its underlying neural circuitry, we have examined the connections between inferior temporal cortex and medial temporal-lobe structures in infant and adult monkeys. Inferior temporal cortical areas TEO and TE were injected with WGA conjugated to HRP and tritiated amino acids, respectively, or vice versa, in 1-week-old and 3-4-yr-old Macaca mulatta, and the distributions of labeled cells and terminals were examined in both limbic structures and temporal-lobe cortical areas. In adult monkeys, inferior temporal-limbic connections included projections from area TEO to the dorsal portion of the lateral nucleus of the amygdala and from area TE to the lateral and lateral basal nuclei; inputs to both areas TEO and TE included those from the lateral, lateral basal, and medial basal nuclei of the amygdala and to area TE from the accessory basal nucleus. Additional limbic inputs to both areas TEO and TE arose from the posterior portion of the presubiculum. In infant monkeys, we found, in addition to these adultlike connections, a projection from area TEO to the lateral basal nucleus of the amygdala. Inferior temporal cortical connections in adult monkeys included projections from area TEO to area TE and, in turn, from area TE to area TG and perirhinal area 36, as well as from area TE back to area TEO; inputs to both areas TEO and TE included those from area TG, perirhinal areas 35 and 36, and parahippocampal areas TF and TH. All of these adultlike connections were also observed in infant monkeys, but, in addition, the infants showed projections from area TE to perirhinal area 35 as well as to parahippocampal areas TF and TH, and from area TEO to area TF. Moreover, in infants, the projection from area TE to perirhinal area 36 was considerably more widespread than in adults, both in areal extent and in laminar distribution. The results therefore indicate the existence of projections in infant monkeys from inferior temporal areas to the amygdala, perirhinal cortex, and parahippocampal cortex that are either totally eliminated in adults or more refined in their distribution. Both elimination and refinement of projections thus appear to characterize the maturation of axonal pathways between the inferior temporal cortex and medial temporal-lobe structures in monkeys. C1 NIMH,NEUROPSYCHOL LAB,BLDG 9,ROOM 1N107,BETHESDA,MD 20892. NR 81 TC 181 Z9 181 U1 0 U2 2 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1991 VL 11 IS 4 BP 1095 EP 1116 PG 22 WC Neurosciences SC Neurosciences & Neurology GA FG030 UT WOS:A1991FG03000024 PM 2010806 ER PT J AU STOLL, J GOLDMAN, D AF STOLL, J GOLDMAN, D TI ISOLATION AND STRUCTURAL CHARACTERIZATION OF THE MURINE TRYPTOPHAN-HYDROXYLASE GENE SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE TRYPTOPHAN HYDROXYLASE; GENE STRUCTURE; PROMOTER SEQUENCE; EVOLUTIONARY RELATIONSHIP ID TYROSINE-HYDROXYLASE; FUNCTIONAL DOMAINS; MESSENGER-RNAS; RAT-BRAIN; GLUCOCORTICOIDS; SEQUENCE; ORGANIZATION; EVOLUTION; INDUCTION; CLONING AB The mouse tryptophan hydroxylase gene was isolated and its intron/exon boundaries and putative regulatory sequences identified. To isolate the gene a mouse mastocytoma cDNA clone encoding tryptophan hydroxylase was used to identify and isolate ten overlapping DNA fragments from a mouse genomic library. Restriction mapping and sequence analysis of the clones revealed that the gene contains 11 exons and covers a region of DNA of approximately 21 kb. The transcription initiation site was mapped and the major site of initiation yields an untranslated leader sequence of 124 nucleotides. A minor initiation site is located 9 nucleotides 3' of the major site. The 5' untranslated sequence is interrupted by the first intron. Analysis of the sequence upstream of the initiation site showed the presence of several putative promoter and regulatory sequences. Nine of the ten intron/exon boundaries of tryptophan hydroxylase are conserved with tyrosine hydroxylase and phenylalanine hydroxylase, further delineating the evolutionary relationship of these three genes. C1 NIAAA,CLIN STUDIES LAB,BETHESDA,MD. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 36 TC 41 Z9 41 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR PY 1991 VL 28 IS 4 BP 457 EP 465 DI 10.1002/jnr.490280402 PG 9 WC Neurosciences SC Neurosciences & Neurology GA FJ248 UT WOS:A1991FJ24800001 PM 1714508 ER PT J AU SIMPSON, DL DICKENS, G DOLL, S KOIZUMI, S TOCCO, M OKUDA, O OSHIMA, M RUDKIN, BB BRIGHTMAN, M GUROFF, G AF SIMPSON, DL DICKENS, G DOLL, S KOIZUMI, S TOCCO, M OKUDA, O OSHIMA, M RUDKIN, BB BRIGHTMAN, M GUROFF, G TI DIFFERENTIATION OF PC12 CELLS WITH K-RAS - COMPARISON WITH NERVE GROWTH-FACTOR SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE K-RAS; PC12; NERVE GROWTH FACTOR; DIFFERENTIATION; ONCOGENE ID EXTERNAL NILE GLYCOPROTEIN; FACTOR-INDUCED INCREASE; PHEOCHROMOCYTOMA CELLS; MORPHOLOGICAL-DIFFERENTIATION; NEURONAL DIFFERENTIATION; FACTOR RECEPTOR; V-SRC; PROTEIN; EXPRESSION; BINDING AB The cell line PC12, derived from a rat pheochromocytoma, has served as a model for studies on the mechanism of action of nerve growth factor, as well as for the exploration of neuronal differentiation in general. When treated with nanomolar concentrations of nerve growth factor, these neoplastic chromaffin-like cells stop dividing and acquire, for all intents and purposes, the phenotype of mature sympathetic neurons. This phenotype is characterized by the extensive outgrowth of electrically excitable neurites, the ability to form functional synapses, and the acquisition of a number of biochemical markers. Treatment of PC12 cells with retroviral vectors encoding the K-ras, the N-ras, or the v-src oncogenes also produces a marked morphological differentiation very similar to that seen upon treatment with nerve growth factor. Treated cells stop dividing and develop an extensive network of neurites. It has recently been shown that PC12 cells differentiated with v-src, while resembling, morphologically, those treated with nerve growth factor, differ substantially in the biochemical characteristics normally associated with nerve growth factor-induced differentiation. Cells infected with K-ras also develop a neurite network similar to that seen after treatment with nerve growth factor. In addition, such cells develop tetanus toxin-binding sites and saxitoxin-binding sites, as do cells treated with nerve growth factor. Decreases in the binding of epidermal growth factor and in the activity of calpain also occur and these, as well, are characteristic of nerve growth factor-treated cells. But the adhesive properties of cells infected with K-ras are different than those of nerve growth factor-treated cells, and the former do not show an increase in the NILE glycoprotein. Finally, K-252a, an inhibitor of the actions of nerve growth factor on PC12 cells, has no effect on the neurite outgrowth produced by infection with K-ras. Thus, many of the key markers of nerve growth factor-induced differentiation of PC12 cells also appear upon differentiation with K-ras, but there are, nevertheless, some crucial differences in the properties of these two sets of cells. C1 NICHHD,GROWTH FACTORS SECT,BETHESDA,MD 20892. RP SIMPSON, DL (reprint author), NINCDS,BRAIN STRUCT PLAST SECT,BETHESDA,MD 20892, USA. NR 42 TC 9 Z9 9 U1 1 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR PY 1991 VL 28 IS 4 BP 486 EP 496 DI 10.1002/jnr.490280405 PG 11 WC Neurosciences SC Neurosciences & Neurology GA FJ248 UT WOS:A1991FJ24800004 PM 1651400 ER PT J AU JUCKER, M KLEINMAN, HK INGRAM, DK AF JUCKER, M KLEINMAN, HK INGRAM, DK TI FETAL-RAT SEPTAL CELLS ADHERE TO AND EXTEND PROCESSES ON BASEMENT-MEMBRANE, LAMININ, AND A SYNTHETIC PEPTIDE FROM THE LAMININ-A CHAIN SEQUENCE SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE FETAL SEPTAL CHOLINERGIC NEURONS; NEURITE OUTGROWTH; CELL SUBSTRATUM ADHESION; EXTRACELLULAR MATRIX ID NEURITE OUTGROWTH; CHOLINERGIC NEURONS; HEPARIN-BINDING; ATTACHMENT; SURVIVAL; GROWTH; FIBRONECTIN; BRAIN; DIFFERENTIATION; NEUROGENESIS AB Responses of rat embryonic septal cells to reconstituted basement membrane, laminin, and laminin A chain-derived synthetic peptides were studied in culture. Dissociated fetal E16/17 septal cells were grown for three days on differently coated plastic substrata. Reconstituted basement membrane (Matrigel), laminin, and a 19-amino acid synthetic peptide CSRARKQAASIKVAVSADR-NH2 (PA22-2) from the laminin A chain sequence mediated cell-substratum adhesion and promoted neurite outgrowth. In contrast, cells did not attach to or form processes on uncoated plastic or on plastic substrata coated with synthetic, laminin-derived control peptides. Polyethylenimine (PEI) supported the adhesion and survival of fetal septal cells; however, when laminin was added to the medium during cell plating or 18 hr afterward, a dose-dependent increase was observed in neurite outgrowth of cells attached to this substratum. Cells grown for 6 days on PEI in the presence of laminin showed a determined increase in the number of cholinergic neurons as marked by acetylcholinesterase staining. These data suggest that the subpopulation of cholinergic septal neurons present in the septal cells studied here were also responding to laminin. The results of this in vitro study suggest potential uses for basement membrane, laminin, or synthetic peptides, such as PA22-2, in fetal septal grafts to enhance regeneration in the damaged septo-hippocampal system. C1 NIA,GERONTOL RES CTR,NATHAN W SHOCK LABS,CELLULAR & MOLEC BIOL LAB,BALTIMORE,MD 21224. NIDR,DEV BIOL & ANOMALIES LAB,BETHESDA,MD 20892. NR 51 TC 51 Z9 51 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR PY 1991 VL 28 IS 4 BP 507 EP 517 DI 10.1002/jnr.490280407 PG 11 WC Neurosciences SC Neurosciences & Neurology GA FJ248 UT WOS:A1991FJ24800006 PM 1870155 ER PT J AU WADHWANI, KC MURPHY, VA RAPOPORT, SI AF WADHWANI, KC MURPHY, VA RAPOPORT, SI TI TRANSFER OF CA-45 AND CL-36 AT THE BLOOD-NERVE BARRIER OF THE SCIATIC-NERVE IN RATS FED LOW OR HIGH CALCIUM DIETS SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE ELECTROLYTES; MANNITOL; HYPOCALCEMIA; HYPERCALCEMIA; BRAIN; PERIPHERAL NERVE; PERMEABILITY; HOMEOSTASIS; DIFFUSION; RAT ID PERIPHERAL-NERVE; CEREBROVASCULAR PERMEABILITY; FROG; PLASMA; BRAIN AB Unidirectional fluxes of Ca-45, Cl-36, and of [H-3]mannitol from blood into the sciatic nerve and cerebral cortex were determined from 5- and 15-min uptakes of these tracers after an intravenous (i.v.) bolus injection in awake rats. Rats were fed diets for 8 wk, that had either a low (0.01% wt/wt), normal (0.67%), or high (3%) Ca content. Plasma [Ca] was 32% less and 11% more in rats fed low (LOCA) and high Ca diets (HICA), respectively, than in rats fed a normal Ca diet (CONT). The mean permeability-surface area product (PA) of Ca-45 at the blood-nerve barrier was about eightfold higher than at the blood-brain barrier in the same animals and did not differ significantly between groups (> 0.05). Mean PA ratios of Ca-45/Cl-36 for the blood-nerve and blood-brain barriers in CONT rats, 0.52 +/- 0.04 and 0.40 +/- 0.02, respectively, were not significantly different from corresponding ratios in LOCA and HICA groups, and corresponded to the aqueous limiting diffusion ratio (0.45). Our results show no evidence for concentration-dependent transport of Ca over a plasma [Ca] range of 0.8-1.4 mmol/liter at the blood-nerve barrier of the rat peripheral nerve, and suggest that Ca and Cl exchange slowly between nerve and blood via paracellular pathways. RP WADHWANI, KC (reprint author), NIA,NEUROSCI LAB,BETHESDA,MD 20892, USA. NR 22 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR PY 1991 VL 28 IS 4 BP 563 EP 566 DI 10.1002/jnr.490280413 PG 4 WC Neurosciences SC Neurosciences & Neurology GA FJ248 UT WOS:A1991FJ24800012 PM 1908025 ER PT J AU NARIAI, T DEGEORGE, JJ GREIG, NH RAPOPORT, SI AF NARIAI, T DEGEORGE, JJ GREIG, NH RAPOPORT, SI TI INVIVO INCORPORATION OF [9,10-H-3]-PALMITATE INTO A RAT METASTATIC BRAIN-TUMOR MODEL SO JOURNAL OF NEUROSURGERY LA English DT Article DE FATTY ACID; PALMITIC ACID; BRAIN METABOLISM; LIPID; TUMOR MARKER ID PLASMA C-14 PALMITATE; GLUCOSE-UTILIZATION; BLOOD-FLOW; UNANESTHETIZED RATS; FATTY-ACIDS; ADULT-RAT; METABOLISM; CELLS; AWAKE; PHOSPHOLIPIDS AB Lipid metabolism of an intracerebrally implanted brain tumor and normal brain was investigated in awake Fischer 344 rats using intravenously injected [9,10-H-3]-palmitate as a probe. A suspension of Walker 256 carcinosarcoma cells (250 cells in 5-mu-l medium), with or without 1% low-melting-point agar, was implanted into the caudate nucleus of rats 8 to 9 weeks old. Control animals received an intracerebral injection without tumor cells. Seven days after implantation, awake rats were infused intravenously for 5 minutes with [9,10-H-3]-palmitate (6.4 mCi/kg). The rats were killed 20 minutes after initiation of the infusion and coronal brain slices were obtained for quantitative autoradiography and light histological study. Tumor cell masses were histologically well demarcated from the surrounding brain tissue. Tumor tissue incorporation of [9,10-H-3]-palmitate was heterogeneous, ranging on average from 3.1- to 6.1-fold greater than in the corresponding contralateral brain. In addition, incorporation corresponded to regional tumor cell density. The incorporation rate constant of [9,10-H-3]-palmitate in tumor was significantly increased compared to control brain and was independent of tumor size. Necrotic areas within tumors showed no incorporation of radiolabeled palmitate. Brain surrounding the tumors and control injection sites showed reactive gliosis, and possessed 30% greater incorporation of [9,10-H-3]-palmitate than contralateral normal brain. These results suggest that [9,10-H-3]-palmitate can be used to image brain tumors in vivo, measuring turnover and/or synthesis of tumor and brain lipid. C1 NIA,NEUROSCI LAB,BLDG 10,ROOM 6C-103,BETHESDA,MD 20892. NR 42 TC 13 Z9 13 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD APR PY 1991 VL 74 IS 4 BP 643 EP 649 DI 10.3171/jns.1991.74.4.0643 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA FC951 UT WOS:A1991FC95100017 PM 2002379 ER PT J AU RAPOPORT, SI AF RAPOPORT, SI TI MICROINFARCTION - OSMOTIC BBB OPENING OR MICROCRYSTALS IN INFUSATE SO JOURNAL OF NEUROSURGERY LA English DT Letter ID BLOOD-BRAIN-BARRIER RP RAPOPORT, SI (reprint author), NIA,BETHESDA,MD 20892, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD APR PY 1991 VL 74 IS 4 BP 685 EP 685 PG 1 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA FC951 UT WOS:A1991FC95100026 PM 1900529 ER PT J AU PIEDMONT, RL MCCRAE, RR COSTA, PT AF PIEDMONT, RL MCCRAE, RR COSTA, PT TI ADJECTIVE CHECK LIST SCALES AND THE 5-FACTOR MODEL SO JOURNAL OF PERSONALITY AND SOCIAL PSYCHOLOGY LA English DT Article ID NEO PERSONALITY-INVENTORY; VALIDITY; CONSTRUCT C1 NIA,GERONTOL RES CTR,4940 EASTERN AVE,BALTIMORE,MD 21224. NR 38 TC 109 Z9 109 U1 2 U2 10 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0022-3514 J9 J PERS SOC PSYCHOL JI J. Pers. Soc. Psychol. PD APR PY 1991 VL 60 IS 4 BP 630 EP 637 DI 10.1037//0022-3514.60.4.630 PG 8 WC Psychology, Social SC Psychology GA FE171 UT WOS:A1991FE17100014 ER PT J AU JACKSON, AJ ZECH, LA AF JACKSON, AJ ZECH, LA TI EASY AND PRACTICAL UTILIZATION OF CONSAM FOR SIMULATION, ANALYSIS, AND OPTIMIZATION OF COMPLEX DOSING REGIMENS SO JOURNAL OF PHARMACEUTICAL SCIENCES LA English DT Article AB Complex dosing regimens simulated in the literature using a universal dosing regimen were calculated with a general dosing program developed using the program CONSAM. The program provides a rapid method of calculating nonuniform dosing regimens for up to n = 3 compartments for any linear model. Subject data can also be curve fitted with the program to obtain individual subject estimates to allow for dosage optimization, which is important in a clinical setting. Examples are presented to show the use of the program in optimizing a theophylline regimen, as well as estimation of a new parameter, C(uneq)(T), which is defined as the average non-steady-state drug concentration at time t for a drug with an irregular dosing interval. C1 NIH,MATH BIOL LAB,BETHESDA,MD 20892. RP JACKSON, AJ (reprint author), CTR DRUG EVALUAT & RES,DIV BIOEQUIVALENCE,ROCKVILLE,MD 20857, USA. NR 9 TC 3 Z9 3 U1 0 U2 0 PU AMER PHARMACEUTICAL ASSN PI WASHINGTON PA 2215 CONSTITUTION AVE NW, WASHINGTON, DC 20037 SN 0022-3549 J9 J PHARM SCI JI J. Pharm. Sci. PD APR PY 1991 VL 80 IS 4 BP 317 EP 320 DI 10.1002/jps.2600800406 PG 4 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA FF977 UT WOS:A1991FF97700005 PM 1865330 ER PT J AU TORRESLABANDEIRA, JJ DAVIGNON, P PITHA, J AF TORRESLABANDEIRA, JJ DAVIGNON, P PITHA, J TI OVERSATURATED SOLUTIONS OF DRUG IN HYDROXYPROPYLCYCLODEXTRINS - PARENTERAL PREPARATION OF PANCRATISTATIN SO JOURNAL OF PHARMACEUTICAL SCIENCES LA English DT Article ID GAMMA-CYCLODEXTRIN; COMPLEXATION; DERIVATIVES; DISSOLUTION AB The effect of 15 cyclodextrin derivatives (polar-electroneutral, cationic, anionic, and lipophilic) and of three 2-hydroxypropyldigitonins on the solubility of pancratistatin, an anticancer drug, was evaluated. The direct solubilizations into aqueous solution were invariably low (0.1-1.2 mg/mL compared with 50-mu-g/mL in water). Complexes of pancratistatin with hydroxypropyl-beta-cyclodextrin were more stable (K(app) 153 M-1) than those with hydroxypropyl-gamma-cyclodextrin (K(app) 108 M-1). Acceptable preparations were made by dissolution of pancratistatin in a large excess (50x) of hydroxypropylcyclodextrin by ammonia and then freeze drying to ammonia-free preparations. In these preparations, both the inclusion and interdispersion phenomena were operative, and the preparations dissolved rapidly forming clear solutions of pancratistatin of concentrations up to 9 mg/mL. These solutions were oversaturated and while those based on hydroxypropyl-beta-cyclodextrin precipitated within 1 h; those based on hydroxypropyl-gamma-cyclodextrin were stable for at least 4 h when kept in a plastic container (i.e., time sufficient for potential use in parenteral preparations). C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NCI,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 19 TC 20 Z9 22 U1 0 U2 1 PU AMER PHARMACEUTICAL ASSN PI WASHINGTON PA 2215 CONSTITUTION AVE NW, WASHINGTON, DC 20037 SN 0022-3549 J9 J PHARM SCI JI J. Pharm. Sci. PD APR PY 1991 VL 80 IS 4 BP 384 EP 386 DI 10.1002/jps.2600800421 PG 3 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA FF977 UT WOS:A1991FF97700020 PM 1865341 ER PT J AU OSTROWSKI, NL CAGGIULA, AR AF OSTROWSKI, NL CAGGIULA, AR TI CORRELATION BETWEEN LOCOMOTOR STIMULATION AND THE ELECTROPHYSIOLOGICAL EFFECTS OF LOW-DOSES OF MORPHINE ON SUBSTANTIA-NIGRA DOPAMINE NEURONS .1. ACUTE DRUG ADMINISTRATION SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID VENTRAL TEGMENTAL AREA; STRIATAL OPIATE RECEPTORS; EXTRACELLULAR ELECTROPHYSIOLOGY; RAT STRIATUM; ENKEPHALIN; LOCALIZATION; AMPHETAMINE; BRAIN; HISTOFLUORESCENCE; ACTIVATION AB Parallel experiments were done to determine whether the behavioral effects of low doses of morphine correlated with changes in the electrophysiological activity of two subpopulations of mesencephalic dopamine neurons in rats. Acute administration of morphine sulfate (0.01 or 0.20 mg/kg i.v.) produced a naloxone antagonizable increase in locomotion and a corresponding increase in the discharge rates of Type A dopamine neurons. Morphine sulfate led to a relatively long-latency (120-200 sec) loss of spontaneous discharge activity in the majority of Type B dopamine neurons and this was blocked by a high dose of naloxone (5.0 mg/kg). Naloxone (0.10 or 5.0 mg/kg i.v.), combined with morphine, led to a paradoxical behavioral suppression. These data suggest that morphine produces opposite effects on two functionally distinct subtypes of neurons in the substantia nigra pars compacta and that behavioral output may reflect an interaction between these changes in discharge activity in mesencephalic dopamine pathways. C1 NIMH,CEREBRAL METAB LAB,CLIN BRAIN IMAGING SECT,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT PSYCHOL,PITTSBURGH,PA 15260. FU PHS HHS [5219] NR 64 TC 10 Z9 10 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1991 VL 257 IS 1 BP 72 EP 81 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FH240 UT WOS:A1991FH24000010 PM 2020010 ER PT J AU BRACKETT, LE DALY, JW AF BRACKETT, LE DALY, JW TI RELAXANT EFFECTS OF ADENOSINE-ANALOGS ON GUINEA-PIG TRACHEA INVITRO - XANTHINE-SENSITIVE AND XANTHINE-INSENSITIVE MECHANISMS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID SMOOTH-MUSCLE CELLS; ADENYLATE-CYCLASE; RECEPTOR; ANTAGONISTS; AGONISTS; BRONCHOCONSTRICTION; PHOSPHODIESTERASE; CONTRACTION; NUCLEOSIDE; AFFINITIES AB Adenosine analogs were tested for their ability to relax carbachol-contracted trachea in vitro. The rank order of potency was: 5'-N-ethylcarboxamidoadenosine (NECA) > 2-chloroadenosine (2-CIADO) > 5'-chloroadenosine = N6-R-1-phenyl-2-propyladenosine (R-PIA) > N6-cyclohexyladenosine > 2-phenylaminoadenosine (CV1808) > 5'-methylthioadenosine (MTA). The rank order of potency for NECA, 2-ClADO and R-PIA is characteristic of an A2 subtype of adenosine receptor. 8-Para-sulfophenyltheophylline (8-p-ST) and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), were used to antagonize tracheal relaxation elicited by adenosine analogs. 8-p-ST antagonized the 2-ClADO, N6-cyclohexyladenosine, R-PIA and 5'-chloroadenosine responses, but had little or no effect on the CV1808 and MTA responses. 8-p-ST antagonized responses to NECA at concentrations of NECA up to approximately 30-mu-M, but had no effect on responses to higher concentrations of NECA. The differences in antagonist potency of 8-p-ST and the clear biphasic response of NECA are indicative of at least two mechanisms of adenosine analog action leading to, tracheal relaxation. One mechanism is mediated through a xanthine-sensitive site, at which NECA acted in a potent manner, whereas the other mechanism or mechanisms are insensitive to blockade by xanthines and account for the effects of action of MTA and CV1808, as well as for NECA at high concentrations. The low potency of the A1-selective antagonist DPCPX indicates that the xanthine-sensitive site is an A2 type receptor. MTA is known to be an antagonist at A2-adenosine receptors that stimulate adenylate cyclase activity, yet MTA did not antagonize the NECA-induced relaxation of trachea. Thus, the A2-type adenosine receptors in smooth muscle appear different from the A2-adenosine receptors that are linked to adenylate cyclase in other tissues. RP BRACKETT, LE (reprint author), NIDDKD,BIOORGAN CHEM LAB,BLDG 8A,ROOM 1A-1S,BETHESDA,MD 20892, USA. NR 33 TC 36 Z9 37 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1991 VL 257 IS 1 BP 205 EP 213 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FH240 UT WOS:A1991FH24000027 PM 2019986 ER PT J AU WU, XZ BELL, JA SPIVAK, CE LONDON, ED SU, TP AF WU, XZ BELL, JA SPIVAK, CE LONDON, ED SU, TP TI ELECTROPHYSIOLOGICAL AND BINDING-STUDIES ON INTACT NCB-20 CELLS SUGGEST PRESENCE OF A LOW AFFINITY SIGMA-RECEPTOR SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID GUINEA-PIG BRAIN; ETORPHINE-INACCESSIBLE SITES; HYBRID NEUROTUMOR CELLS; ANTIPSYCHOTIC-DRUGS; RAT-BRAIN; PHENCYCLIDINE RECEPTORS; -LABELED SKF-10047; OPIATE RECEPTORS; OPIOID BINDING; VAS-DEFERENS AB Whole cell voltage clamp studies were performed on NCB-20 cells to examine physiological responses to drugs possessing affinities for sigma receptors. Those drugs [haloperidol, alpha-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperazinebutanol (BMY-14802), pentazocine, N-allylnormetazocine (SKF-10047), 3-(3-hydroxyphenyl)-N-(1-propyl)piperidine (3-PPP), phencyclidine, 1-[1-(2-thienyl)cyclohexyl]piperidine (TCP), (+)-5-methyl-10,11-dihydro-5H-dibenzo-[a,d]cyclohepten-5,10-imine maleate (MK-801)] caused an apparent inward current, which was due to blockade of a tonic, outward potassium current. The rank order of drug potencies in producing this effect generally resembled the rank orders of sigma-receptor affinities for the drugs, except that a reverse stereoselectivity was observed for several drugs. [H-3] (+)-SKF-10047 labeled two sites in intact NCB-20 cells (K(d) = 49 nM, B(max) = 1.0 pmol/mg protein and K(d) = 9.6-mu-M, B(max) = 69 pmol/mg protein). The high affinity site was similar pharmacologically to the sigma receptor assayed in membrane fragments from NCB-20 cells. However, the low affinity site showed a slightly different profile, highlighted by a reverse stereoselectivity. The rank order of drug potencies was as follows at the low affinity site: haloperidol > BMY-14802 > (-)-pentazocine > (+)-pentazocine > (-)-SKF-10047 > (-)-3-PPP > (+)-SKF-10047 > (+)-3-PPP > phencyclidine > TCP > MK-801. Drug potencies at the low affinity site correlated well with those observed in voltage clamp studies as well as those obtained in a guinea pig vas deferens bioassay (r = 0.93 and 0.84, respectively, Spearman rank correlation). Although reverse stereoselectivity was observed at these sites for some drugs, the rank order of the potencies of several key sigma drugs at the two sites did not differ. Therefore, the two sigma binding sites (the high affinity site and the low affinity site) may be related. C1 NIDA,ADDICT RES CTR,NEUROPHARMACOL LAB,POB 5180,BALTIMORE,MD 21224. NR 44 TC 79 Z9 80 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1991 VL 257 IS 1 BP 351 EP 359 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FH240 UT WOS:A1991FH24000047 PM 1850471 ER PT J AU LEE, HS LEE, CI LI, SSL AF LEE, HS LEE, CI LI, SSL TI COMPARISON OF THE ANTIGENIC PEPTIDES BETWEEN HUMAN PROSTATIC AND LYSOSOMAL ACID-PHOSPHATASES SO JOURNAL OF PROTEIN CHEMISTRY LA English DT Note DE ACID PHOSPHATASE; PROSTATE; LYSOSOME; ANTIGENIC PEPTIDES ID CLONING AB The relative antigenicity (capacity to bind antibodies raised against the intact prostatic acid phosphatase) of the selected peptides from human prostatic and lysosomal acid phosphatases was evaluated in a competitive assay. Both prostatic and lysosomal acid phosphatases were shown to possess similar antigenic determinants on both terminal regions, along with more similarity on NH2-terminal peptide than COOH-terminal site. At least one additional antigenic site is present at the internal region of prostatic acid phosphatase, since the mixture of both amino- and carboxyl-terminal peptides exhibited only 70% inhibition. C1 NIEHS,GENET LAB,RES TRIANGLE PK,NC 27709. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT DIAGNOST IMMUNOL RES & BIOCHEM,BUFFALO,NY 14263. NR 11 TC 4 Z9 4 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0277-8033 J9 J PROTEIN CHEM JI J. Protein Chem. PD APR PY 1991 VL 10 IS 2 BP 253 EP 256 DI 10.1007/BF01024789 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FN776 UT WOS:A1991FN77600014 PM 1718311 ER PT J AU SCHUSTER, CR AF SCHUSTER, CR TI THE NATIONAL-INSTITUTE-ON-DRUG-ABUSE AND METHADONE-MAINTENANCE TREATMENT SO JOURNAL OF PSYCHOACTIVE DRUGS LA English DT Article RP SCHUSTER, CR (reprint author), NIDA,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 0 TC 8 Z9 8 U1 0 U2 0 PU HAIGHT-ASHBURY PUBL PI SAN FRANCISCO PA 409 CLAYTON ST, SAN FRANCISCO, CA 94117 SN 0279-1072 J9 J PSYCHOACTIVE DRUGS JI J. Psychoact. Drugs PD APR-JUN PY 1991 VL 23 IS 2 BP 111 EP 112 PG 2 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA GH554 UT WOS:A1991GH55400004 PM 1765885 ER PT J AU RADER, JS ROSENZWEIG, BA SPIRTAS, R PADLECKAS, R JAVAHERI, G GERARDO, L LAIMINS, LA AF RADER, JS ROSENZWEIG, BA SPIRTAS, R PADLECKAS, R JAVAHERI, G GERARDO, L LAIMINS, LA TI ATYPICAL SQUAMOUS CELLS - A CASE-SERIES STUDY OF THE ASSOCIATION BETWEEN PAPANICOLAOU SMEAR RESULTS AND HUMAN PAPILLOMAVIRUS DNA GENOTYPE SO JOURNAL OF REPRODUCTIVE MEDICINE LA English DT Article ID CERVICAL-CARCINOMA; INTRAEPITHELIAL NEOPLASIA; GENITAL CANCER; SEQUENCES; LINES; PREVALENCE; CYTOLOGY; TYPE-16 AB Thirty women with "atypical" squamous cells but not cervical intraepithelial neoplasia (CIN) on their Papanicolaou smears were tested for the presence of human papillomavirus (HPV) with the Southern blot hybridization technique. The Papanicolaou smears were reviewed for the presence of atypical squamous cells according to Patten's criteria. Comparison groups consisted of 30 patients with normal, 29 patients with CIN I and 24 patients with CIN II Papanicolaou smears. Ten of the 30 women (33%) with atypical cells on Papanicolaou smears were positive for HPV DNA as compared to 17% with normal and 59% with CIN I or II Papanicolaou smears. HPV 16 was present in 70-80% of the HPV DNA-positive patients in each Papanicolaou smear group. Concurrent CIN was also identified on colposcopically directed biopsies in 27% of the patients with squamous atypia. Patients with atypical squamous cells on Papanicolaou smears had coexisting HPV infection and CIN in about one-third of the cases. Colposcopy and further follow-up are recommended for such patients. C1 UNIV CHICAGO,HOWARD HUGHES MED INST,DEPT MOLEC GENET & CELL BIOL,920 E 58TH ST,CHICAGO,IL 60637. MICHAEL REESE HOSP & MED CTR,DEPT OBSTET & GYNECOL,CHICAGO,IL 60616. MICHAEL REESE HOSP & MED CTR,DEPT PATHOL,CHICAGO,IL 60616. NIH,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892. NR 24 TC 20 Z9 20 U1 0 U2 0 PU SCI PRINTERS & PUBL INC PI ST LOUIS PA P.O. DRAWER 12425 8342 OLIVE BLVD, ST LOUIS, MO 63132 SN 0024-7758 J9 J REPROD MED JI J. Reprod. Med. PD APR PY 1991 VL 36 IS 4 BP 291 EP 297 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA FH069 UT WOS:A1991FH06900010 PM 1649307 ER PT J AU GITTERMAN, M HAVLIN, S WEISS, GH AF GITTERMAN, M HAVLIN, S WEISS, GH TI EFFECTS OF AN OSCILLATING FIELD ON A DIFFUSION PROCESS IN THE PRESENCE OF A TRAP SO JOURNAL OF STATISTICAL PHYSICS LA English DT Article DE BROWNIAN MOTION; STOCHASTIC RESONANCE; TRAPPING PROCESSES ID STOCHASTIC RESONANCE; BROWNIAN-MOTION; CLIMATIC-CHANGE; DENSITIES; BOUNDARY; SYSTEM AB Consider a diffusion process on an infinite line terminated by a trap and modulated by a periodic field. When the frequency is equal to zero the mean time to trapping will be finite or infinite, depending on the sign of the field. We ask whether this behavior can be changed by an oscillatory field, and show that it cannot for pure Brownian motion. We suggest that transition can appear when the signal propagation velocity is finite as for the telegrapher's equation. We further suggest that the asymptotic time dependence of the survival probability is proportional to t-12 just as in the case of ordinary diffusion. The same conclusion is shown to hold for a system whose dynamics is governed by the equation x = xv(t)/.L, where L is a constant. C1 BAR ILAN UNIV,DEPT PHYS,IL-52100 RAMAT GAN,ISRAEL. RP GITTERMAN, M (reprint author), NIH,BETHESDA,MD 20892, USA. NR 18 TC 1 Z9 1 U1 0 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0022-4715 J9 J STAT PHYS JI J. Stat. Phys. PD APR PY 1991 VL 63 IS 1-2 BP 315 EP 322 DI 10.1007/BF01026607 PG 8 WC Physics, Mathematical SC Physics GA FM523 UT WOS:A1991FM52300019 ER PT J AU THOMAS, L KOCSIS, E COLOMBINI, M ERBE, E TRUS, BL STEVEN, AC AF THOMAS, L KOCSIS, E COLOMBINI, M ERBE, E TRUS, BL STEVEN, AC TI SURFACE-TOPOGRAPHY AND MOLECULAR STOICHIOMETRY OF THE MITOCHONDRIAL CHANNEL, VDAC, IN CRYSTALLINE ARRAYS SO JOURNAL OF STRUCTURAL BIOLOGY LA English DT Article ID RAT-LIVER MITOCHONDRIA; NEUROSPORA-CRASSA MITOCHONDRIA; OUTER-MEMBRANE CHANNEL; TRANSMISSION ELECTRON-MICROSCOPE; HEXOKINASE-BINDING PROTEIN; METAL-SHADOWED SPECIMENS; PORE PROTEIN; PURIFICATION; IDENTIFICATION; BACTERIORHODOPSIN C1 NIAMSD,STRUCT BIOL RES LAB,BETHESDA,MD 20892. NIH,DIV COMP RES & TECHNOL,COMP SYST LAB,BETHESDA,MD 20892. USDA,BELTSVILLE AGR RES CTR,BELTSVILLE,MD 20705. RP THOMAS, L (reprint author), UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742, USA. RI Colombini, Marco/A-1540-2014 NR 61 TC 49 Z9 49 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1047-8477 J9 J STRUCT BIOL JI J. Struct. Biol. PD APR PY 1991 VL 106 IS 2 BP 161 EP 171 DI 10.1016/1047-8477(91)90085-B PG 11 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FM766 UT WOS:A1991FM76600008 PM 1725124 ER PT J AU GOMELLA, LG STEINBERG, SM ELLISON, MF REEVES, WW FLANIGAN, RC MCROBERTS, JW AF GOMELLA, LG STEINBERG, SM ELLISON, MF REEVES, WW FLANIGAN, RC MCROBERTS, JW TI ANALYSIS OF I-125 INTERSTITIAL THERAPY IN THE TREATMENT OF LOCALIZED CARCINOMA OF THE PROSTATE SO JOURNAL OF SURGICAL ONCOLOGY LA English DT Article DE RADICAL RETROPUBIC PROSTATECTOMY; PROGRESSION RATE; SURVIVAL; RADIATION THERAPY; PROSTATE CANCER ID EXTERNAL BEAM RADIATION; PELVIC LYMPHADENECTOMY; DEFINITIVE TREATMENT; I-125 IMPLANTATION; CANCER; COMPLICATIONS; RADIOTHERAPY; BIOPSY AB Definitive treatment of localized carcinoma of the prostate has included radical surgery, external beam radiation therapy, and interstitial radiation therapy. The interstitial agent most commonly used is Iodine-125. Forty-eight patients were treated with interstitial radiation therapy using Iodine-125 implants with a median follow-up of 55 months. Forty-three percent of the evaluable patients had progressive disease with approximately 50% progressing at 5 years by Kaplan-Meier analysis. Overall actuarial survival in the group was 80% at 5 years. This and several other studies suggest that control of prostate cancer with Iodine-125 seeds may be suboptimal as compared with other treatment modalities, especially the radical retropubic prostatectomy. Analysis of treatment parameters is presented along with a discussion of the current status and future prospects for treatment of localized carcinoma of the prostate with interstitial radiation therapy. C1 UNIV KENTUCKY,MED CTR,DEPT SURG,DIV UROL,LEXINGTON,KY 40506. NCI,BIOSTAT & DATA MANAGEMENT,BETHESDA,MD 20892. NR 24 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0022-4790 J9 J SURG ONCOL JI J. Surg. Oncol. PD APR PY 1991 VL 46 IS 4 BP 235 EP 240 PG 6 WC Oncology; Surgery SC Oncology; Surgery GA FE959 UT WOS:A1991FE95900005 PM 2008089 ER PT J AU SERRANO, H SCOTTO, J SHORNICK, G FEARS, TR GREENBERG, ER AF SERRANO, H SCOTTO, J SHORNICK, G FEARS, TR GREENBERG, ER TI INCIDENCE OF NONMELANOMA SKIN-CANCER IN NEW-HAMPSHIRE AND VERMONT SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID CARCINOMA; MELANOMA; RISK AB A survey of skin cancer occurrence between June 1979 and May 1980 among residents of New Hampshire and Vermont identified 277 cases of squamous cell carcinoma and 1761 cases of basal cell carcinoma. The age-adjusted incidence rates for squamous cell carcinoma (32 per 100,000 in men, 8 per 100,000 in women) and for basal cell carcinoma (159 per 100,000 in men, 87 per 100,000 in women) were similar to those reported in other populations in the northern United States. Skin cancer incidence was particularly high among men more than 70 years of age and a large proportion (> 30%) of patients 55 years or older had a history of at least one previous skin cancer. C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,HINMAN BOX 7927,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,NORRIS COTTON CANC CTR,HANOVER,NH 03756. NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,LOS ANGELES,CA 90024. FU NCI NIH HHS [CA23108, N01CP91030] NR 17 TC 34 Z9 35 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD APR PY 1991 VL 24 IS 4 BP 574 EP 579 DI 10.1016/0190-9622(91)70086-H PG 6 WC Dermatology SC Dermatology GA FD903 UT WOS:A1991FD90300010 PM 2033134 ER PT J AU MORGAN, DL JOKINEN, MP HASEMAN, JK ULLAND, BM PARKER, GA LEMEN, JK MENNEAR, JH AF MORGAN, DL JOKINEN, MP HASEMAN, JK ULLAND, BM PARKER, GA LEMEN, JK MENNEAR, JH TI CARCINOGENICITY OF 3,3'-DIMETHYLBENZIDINE DIHYDROCHLORIDE GIVEN IN DRINKING-WATER TO F344/N RATS SO JOURNAL OF THE AMERICAN COLLEGE OF TOXICOLOGY LA English DT Article ID BENZIDINE; TESTS; 3,3'-DIMETHOXYBENZIDINE; MUTAGENICITY; METABOLITES; CHEMICALS; BIOASSAY; MODELS AB 3,3'-Dimethylbenzidine dihydrochloride (DMB) was evaluated for toxicity and carcinogenicity because of the potential for human exposure during production and use of bis-azobiphenyl dyes and because benzidine, a structurally related chemical, is a known human carcinogen. Two studies (9 and 15 months) were conducted by administering 0, 30, 70, or 150 ppm DMB (approx. 99% pure) in drinking water to F344/N rats. In the 15-month studies, 60 rats of each gender were used in the control group, 45 in the low-dose, 75 in the mid-dose, and 60 in the high-dose group. After exposure for 9 months, chemical-related neoplastic lesions were observed in the skin, Zymbal's gland, preputial gland, clitoral gland, liver, oral cavity, large and small intestines, and lung. Although designed for 24 months these studies were terminated after 15 months because significant numbers of treated rats were dying with tumors or were killed in moribund condition. Chemical-related nonneoplastic lesions included cystic degeneration and foci of alteration in the liver; exacerbation of nephropathy; hyperplasia of Zymbal's gland, preputial and clitoral glands, and alveolar epithelium. After exposure for 15 months, significantly increased incidences of neoplasms were observed at many organ sites: skin, Zymbal's gland, preputial and clitoral gland, liver, oral cavity epithelium, small and large intestines, mammary gland, lung, and mesothelium of treated rats. It is concluded that DMB is clearly carcinogenic for male and female F344/N rats. C1 HAZELTON LABS AMER INC,VIENNA,VA 22180. CAMPBELL UNIV,BUIES CREEK,NC. RP MORGAN, DL (reprint author), NIEHS,MD 14-08,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 35 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0730-0913 J9 J AM COLL TOXICOL JI J. Am. Coll. Toxicol. PD APR PY 1991 VL 10 IS 2 BP 255 EP 267 PG 13 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA GN779 UT WOS:A1991GN77900005 ER PT J AU CHAI, CY LIN, AMY SU, CK HU, SR YUAN, C KAO, LS KUO, JS GOLDSTEIN, DS AF CHAI, CY LIN, AMY SU, CK HU, SR YUAN, C KAO, LS KUO, JS GOLDSTEIN, DS TI SYMPATHOADRENAL EXCITATION AND INHIBITION BY LOWER BRAIN-STEM STIMULATION IN CATS SO JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM LA English DT Article DE NOREPINEPHRINE; EPINEPHRINE; SYMPATHETIC NERVOUS SYSTEM; CATECHOLAMINE; PARAMEDIAN RETICULAR NUCLEUS; MEDULLA; NUCLEUS OF THE SOLITARY TRACT; BRAIN-STEM; GLUTAMATE; VAGOTOMY; ADRENALECTOMY ID ROSTRAL VENTROLATERAL MEDULLA; PLASMA-CATECHOLAMINES; TEGMENTAL FIELD; ADRENAL-MEDULLA; RAT; NUCLEUS; VASOPRESSIN; RESPONSES; PRESSURE; NEURONS AB Effects of stimulation of brainstem sites on hemodynamics and plasma catecholamine levels were assessed in cats under chloralose-urethane anesthesia. Pressor areas of the dorsal medulla (DM) and ventrolateral medulla (VLM) and the depressor area of the paramedian reticular nucleus (PRN) were stimulated electrically using a monopolar electrode, or chemically using sodium glutamate microinjection. Plasma levels of norepinephrine (NE) and epinephrine (EPI) were measured in caval blood above the adrenal veins. Electrical stimulation of the DM and VLM produced increases in blood pressure and in plasma NE and EPI levels that were enhanced after acute vagotomies. The NE and EPI responses were attenuated after acute, bilateral adrenalectomies, confirming augmented adrenomedullary secretion, whereas the pressor responses were intact. Injection of sodium glutamate into the same pressor regions of the DM or VLM also produced pressor responses and elevated plasma catecholamine levels, indicating that the responses resulted from activation of neuronal perikarya. Stimulation of the PRN attenuated pressor and catecholamine responses during stimulation of the DM and VLM. The results indicate that pressor responses during stimulation of the DM and VLM are due at least partly to activation of perikarya in these regions, are associated with but not dependent on adrenomedullary activation, and are enhanced after vagotomy; and that neurons of the PRN exert inhibitory modulation of the pressor and adrenomedullary responses during stimulation of the VLM and DM. C1 TAICHUNG VET GEN HOSP,DEPT MED RES,TAICHUNG,TAIWAN. NHLBI,HYPERTENS ENDOCRINE BRANCH,BETHESDA,MD 20892. RP CHAI, CY (reprint author), ACAD SINICA,INST BIOMED SCI,TAIPEI 11529,TAIWAN. OI Su, Chun-Kuei/0000-0002-5211-3520 NR 39 TC 22 Z9 22 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-1838 J9 J AUTONOM NERV SYST JI J. Auton. Nerv. Syst. PD APR PY 1991 VL 33 IS 1 BP 35 EP 46 DI 10.1016/0165-1838(91)90016-V PG 12 WC Neurosciences SC Neurosciences & Neurology GA FK194 UT WOS:A1991FK19400004 PM 1869769 ER PT J AU BURGIO, KL ENGEL, BT LOCHER, JL AF BURGIO, KL ENGEL, BT LOCHER, JL TI NORMATIVE PATTERNS OF DIURNAL URINATION ACROSS 6 AGE DECADES SO JOURNAL OF UROLOGY LA English DT Article DE URINATION; AGE FACTORS; SEX FACTORS ID WOMEN AB The patterns and frequency of diurnal urination were studied in 412 male and 244 female participants in the Baltimore Longitudinal Study of Aging. Men urinated less often (mean 4.8 voids per day) than women (mean 5.6 voids per day). There was no main effect for age decade. However, an age by sex interaction showed that voiding in men increased across the decades and in women it decreased. The highest frequency was found in women in their 30s (mean 6.2) and the lowest was in men in their 30s (mean 4.3). Men and women in the 70 and older age group had the same voiding frequency (mean 5.0). In men frequency of urination was related to benign prostatic enlargement and 2 of 4 symptoms of urinary obstruction (change in the force of the urinary stream and having to urinate again shortly after voiding). In women frequency was related negatively to a history of pregnancy complications but not to parity. In both sexes frequency was unrelated to the reported daily ingestion of coffee, tea or diuretics, and no relationships were found with a history of an anxiety disorder. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP BURGIO, KL (reprint author), UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261, USA. NR 8 TC 29 Z9 30 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD APR PY 1991 VL 145 IS 4 BP 728 EP 731 PG 4 WC Urology & Nephrology SC Urology & Nephrology GA FE597 UT WOS:A1991FE59700010 PM 2005688 ER PT J AU KAELBLING, M EDDY, R SHOWS, TB COPELAND, NG GILBERT, DJ JENKINS, NA KLINGER, HP OHARA, B AF KAELBLING, M EDDY, R SHOWS, TB COPELAND, NG GILBERT, DJ JENKINS, NA KLINGER, HP OHARA, B TI LOCALIZATION OF THE HUMAN GENE ALLOWING INFECTION BY GIBBON APE LEUKEMIA-VIRUS TO HUMAN-CHROMOSOME REGION 2Q11-Q14 AND TO THE HOMOLOGOUS REGION ON MOUSE CHROMOSOME-2 SO JOURNAL OF VIROLOGY LA English DT Article ID HUMAN GENOME; RECEPTOR; PROTEIN; CELLS; T4; SUSCEPTIBILITY; ORGANIZATION; REPLICATION; ENCODES; COMPLEX AB Retrovirus receptors remain a largely unexplored group of proteins. Of the receptors which allow infection of human and murine cells by various retroviruses, only three have been identified at the molecular level. These receptors include CD4 for human immunodeficiency virus, Rec-1 for murine ecotropic virus, and GLVR1 for gibbon ape leukemia virus. These three proteins show no homology to one another at the DNA or protein level. Therefore, work to date has not shown any general relationship or structural theme shared by retroviral receptors. Genes for two of these receptors (CD4 and Rec-1) and several others which have not yet been cloned have been localized to specific chromosomes. In order to assess the relationship between GLVR1 and other retroviral receptors, we mapped the chromosome location of GLVR1 in human and mouse. GLVR1 was found to map to human chromosome 2q11-q14 by in situ hybridization and somatic-cell hybrid analysis. This location is distinct from those known for receptors for retroviruses infecting human cells. Glvr-1 was then mapped in the mouse by interspecies backcrosses and found to map to chromosome 2 in a region of linkage conservation with human chromosome 2. This mouse chromosome carries Rec-2, the likely receptor for M813, a retrovirus derived from a feral Asian mouse. These data raise the interesting possibility that Rec-2 and Glvr-1 are structurally related. C1 AMER CYANAMID CO,LEDERLE LABS,MOLEC BIOL RES SECT,PEARL RIVER,NY 10965. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,FREDERICK,MD 21701. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MOLEC GENET,BRONX,NY 10461. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT HUMAN GENET,BUFFALO,NY 14263. FU NCI NIH HHS [CA16720, N01-CO-74101, CA43951] NR 28 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1991 VL 65 IS 4 BP 1743 EP 1747 PG 5 WC Virology SC Virology GA FC031 UT WOS:A1991FC03100011 PM 1672162 ER PT J AU LAL, RB RUDOLPH, DL GRIFFIS, KP KITAMURA, K HONDA, M COLIGAN, JE FOLKS, TM AF LAL, RB RUDOLPH, DL GRIFFIS, KP KITAMURA, K HONDA, M COLIGAN, JE FOLKS, TM TI CHARACTERIZATION OF IMMUNODOMINANT EPITOPES OF GAG AND POL GENE-ENCODED PROTEINS OF HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I SO JOURNAL OF VIROLOGY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; LEUKEMIA-VIRUS; HTLV; INFECTION; GENOME; ANTIBODIES; PREDICTION; ENVELOPE; DONORS; REGION AB A series of synthetic peptides derived from the corresponding regions of the gag, pol, and env proteins of human T-cell lymphotropic virus types I (HTLV-I) and II (HTLV-II) were used in an enzyme immunoassay to map the immunodominant epitopes of HTLV. Serum specimens from 79 of 87 (91%) HTLV-I-infected patients reacted with the synthetic peptide Gag-1a (amino acids [a.a.] 102 to 117) derived from the C terminus of the p19gag protein of HTLV-I. Minimal cross-reactivity (11%) was observed with serum specimens from HTLV-II-infected patients. Peptide Pol-3, encoded by the pol region of HTLV-I (a.a. 487 to 502), reacted with serum specimens from both HTLV-I- and HTLV-II-infected patients (94 and 86%, respectively). The antibody levels to Pol-3 were significantly higher (P < 0.01) in patients with HTLV-I-associated myelopathy/tropical spastic paraparesis than in either adult T-cell leukemia patients or HTLV-I-positive asymptomatic carriers. None of the other peptides studied demonstrated significant binding to serum specimens obtained from HTLV-I- or HTLV-II-infected individuals. While Gag-1a did not react with serum specimens from normal controls, Pol-3 demonstrated some reaction with specimens from seronegative individuals (11.4%). The antibodies to Gag-1a and Pol-3 in serum specimens from HTLV-I-infected patients could be specifically inhibited by the corresponding synthetic peptides and by a crude HTLV-I antigen preparation, indicating that these peptides mimic native epitopes present in HTLV-I proteins that are recognized by serum antibodies from HTLV-I- and -II-infected individuals. C1 NATL INST HLTH,AIDS RES CTR,TOKYO 141,JAPAN. NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20894. RP LAL, RB (reprint author), CTR DIS CONTROL,DIV VIRAL & RICKETTSIAL DIS,RETROVIRUS DIS BRANCH,ATLANTA,GA 30333, USA. NR 30 TC 35 Z9 35 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1991 VL 65 IS 4 BP 1870 EP 1876 PG 7 WC Virology SC Virology GA FC031 UT WOS:A1991FC03100027 PM 2002547 ER PT J AU PORTIS, JL PERRYMAN, S MCATEE, FJ AF PORTIS, JL PERRYMAN, S MCATEE, FJ TI THE R-U5-5' LEADER SEQUENCE OF NEUROVIRULENT WILD MOUSE RETROVIRUS CONTAINS AN ELEMENT CONTROLLING THE INCUBATION PERIOD OF NEURODEGENERATIVE DISEASE SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; EMBRYONAL CARCINOMA-CELLS; C RNA VIRUS; NEUROTROPIC RETROVIRUS; EXPRESSION; INFECTION; REGION; MICE; TRANSMISSION; PARALYSIS AB The wild mouse ecotropic retrovirus CasBrE causes a spongiform neurodegenerative disease after neonatal inoculation, with an incubation period ranging from 2 to 12 months. We previously showed that introduction of long terminal repeat (LTR) and gag-pol sequences from a strain of Friend murine leukemia virus (FB29) resulted in a dramatic acceleration of the onset of the disease. The chimeric virus FrCas(E), which consisted of the FB29 genome containing 3' pol and env sequences from the wild mouse virus, induced a highly predictable, lethal neurodegenerative disease with an incubation period of only 16 days. Here we report that the sequences which are primary determinants of the length of the incubation period are located in the 5' end of the viral genome between a KpnI site in the R region of the LTR and a PstI site immediately 5' of the start codon for pro65gag (R-U5-5' leader). This region contains the tRNA primer binding site, splice donor site for the subgenomic env mRNA, and the packaging sequence. Computer-assisted sequence analysis failed to find evidence of a consensus sequence for a DNA enhancer in this region. In addition, sequences within a region of the genome between a ClaI site at the 3' end of env to the KpnI site in the R region of the LTR (inclusive of U3) also influenced the incubation period of the disease, but the effect was distinctly weaker than that of the R-U5-5' leader sequence. This U3 effect, however, appeared to be independent of the number of direct repeats, since deletion of one of two duplicated 42-base repeats containing consensus sequences of nuclear-factor binding domains had no effect on the incubation period of the disease. On the basis of Southern blot analysis of total viral DNA in the tissues, the effect of these sequences on the incubation period appeared to be related to the level of virus replication in the central nervous system. All of the chimeric viruses analyzed, irrespective of neurovirulence, replicated to comparable levels in the spleen and induced comparable levels of viremia. RP PORTIS, JL (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 26 TC 24 Z9 24 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1991 VL 65 IS 4 BP 1877 EP 1883 PG 7 WC Virology SC Virology GA FC031 UT WOS:A1991FC03100028 PM 2002548 ER PT J AU EARL, PL MOSS, B DOMS, RW AF EARL, PL MOSS, B DOMS, RW TI FOLDING, INTERACTION WITH GRP78-BIP, ASSEMBLY, AND TRANSPORT OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE PROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID INFLUENZA HEMAGGLUTININ TRIMERS; CHAIN BINDING-PROTEIN; ENDOPLASMIC-RETICULUM; MONOCLONAL-ANTIBODIES; OLIGOMERIC STRUCTURE; INTRACELLULAR-TRANSPORT; TRANSMEMBRANE PROTEIN; MEMBRANE-FUSION; GOLGI PROTEINS; BREFELDIN-A AB A detailed kinetic and quantitative analysis of the early and late biosynthetic events undergone by the human immunodeficiency virus type 1 envelope protein expressed by a recombinant vaccinia virus was performed. Early folding events that occurred in the endoplasmic reticulum included disulfide bond formation (t1/2 almost-equal-to 10 min), folding of envelope protein into a form competent to bind CD4 (t1/2 almost-equal-to 15 min), and specific and transient association and dissociation with GRP78-BiP (t1/2 almost-equal-to 25 min). After initial folding, envelope protein monomers formed noncovalently associated dimers with high efficiency (t1/2 almost-equal-to 30 min). Studies with brefeldin A, a compound that inhibits endoplasmic reticulum-to-Golgi transport, suggested that assembly occurred in the endoplasmic reticulum while cleavage of gp160 into gp120/gp41 subunits occurred in a post-endoplasmic reticulum compartment. Transport to the Golgi was monitored by modification of N-linked sugars to forms partially resistant to endoglycosidase H. The kinetics of endoglycosidase H resistance were nearly identical to the kinetics of gp160 cleavage (t1/2 almost-equal-to 80 min). Cleavage efficiency was strongly cell type dependent, ranging from 13 to 70%. By contrast, approximately 50% of the gp120 generated by the cleavage event was shed (t1/2 almost-equal-to 120 min) regardless of the cell type used. The results are discussed in terms of the overall biosynthetic pathway of the envelope protein and provide a framework with which to assess the effects of mutations on structure and function. C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 52 TC 266 Z9 267 U1 1 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1991 VL 65 IS 4 BP 2047 EP 2055 PG 9 WC Virology SC Virology GA FC031 UT WOS:A1991FC03100048 PM 1900540 ER PT J AU SUSMAN, EJ DORN, LD CHROUSOS, GP AF SUSMAN, EJ DORN, LD CHROUSOS, GP TI NEGATIVE AFFECT AND HORMONE LEVELS IN YOUNG ADOLESCENTS - CONCURRENT AND PREDICTIVE PERSPECTIVES SO JOURNAL OF YOUTH AND ADOLESCENCE LA English DT Article ID BIOCHEMICAL MANIFESTATIONS; DEVELOPMENTAL PROCESSES; DEPRESSIVE-DISORDERS; CHRONOLOGIC AGE; PUBERTAL STAGE; STRESS; TESTOSTERONE; NEUROBIOLOGY; BEHAVIOR; CORTISOL C1 NIMH,BETHESDA,MD 20892. RP SUSMAN, EJ (reprint author), PENN STATE UNIV,DEPT HUMAN DEV & FAMILY STUDIES,314 HLTH & HUMAN DEV E,UNIVERSITY PK,PA 16802, USA. NR 50 TC 105 Z9 105 U1 0 U2 2 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0047-2891 J9 J YOUTH ADOLESCENCE JI J. Youth Adolesc. PD APR PY 1991 VL 20 IS 2 BP 167 EP 190 DI 10.1007/BF01537607 PG 24 WC Psychology, Developmental SC Psychology GA FR929 UT WOS:A1991FR92900005 PM 24265005 ER PT J AU SUOMI, SJ AF SUOMI, SJ TI ADOLESCENT DEPRESSION AND DEPRESSIVE SYMPTOMS - INSIGHTS FROM LONGITUDINAL-STUDIES WITH RHESUS-MONKEYS SO JOURNAL OF YOUTH AND ADOLESCENCE LA English DT Article ID FAMILY ENVIRONMENT; SEPARATION; MOTHER RP SUOMI, SJ (reprint author), NICHHD,COMPARAT ETHOL LAB,BETHESDA,MD 20892, USA. NR 33 TC 15 Z9 15 U1 0 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0047-2891 J9 J YOUTH ADOLESCENCE JI J. Youth Adolesc. PD APR PY 1991 VL 20 IS 2 BP 273 EP 287 DI 10.1007/BF01537612 PG 15 WC Psychology, Developmental SC Psychology GA FR929 UT WOS:A1991FR92900010 PM 24265010 ER PT J AU STRIKER, LJ PETEN, EP ELLIOT, SJ DOI, T STRIKER, GE AF STRIKER, LJ PETEN, EP ELLIOT, SJ DOI, T STRIKER, GE TI MESANGIAL CELL TURNOVER - EFFECT OF HEPARIN AND PEPTIDE GROWTH-FACTORS SO LABORATORY INVESTIGATION LA English DT Review ID SMOOTH-MUSCLE CELLS; TUMOR NECROSIS FACTOR; IMMUNE-COMPLEX GLOMERULONEPHRITIS; FACTOR-I; TRANSGENIC MICE; FACTOR-BETA; ENDOTHELIAL-CELLS; GLOMERULAR CELLS; GENE-EXPRESSION; PROLIFERATIVE GLOMERULONEPHRITIS RP STRIKER, LJ (reprint author), NIDDK,MDB,RENAL CELL BIOL,BETHESDA,MD 20892, USA. NR 129 TC 192 Z9 197 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD APR PY 1991 VL 64 IS 4 BP 446 EP 456 PG 11 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA FH171 UT WOS:A1991FH17100002 PM 2016850 ER PT J AU SCHAUFELBERGER, DE CHMURNY, GN KOLECK, MP AF SCHAUFELBERGER, DE CHMURNY, GN KOLECK, MP TI H-1 AND C-13 NMR ASSIGNMENTS OF THE ANTITUMOR MACROLIDE BRYOSTATIN-1 SO MAGNETIC RESONANCE IN CHEMISTRY LA English DT Article DE BRYOSTATIN-1; NMR DATA; STRUCTURE ID LEUKEMIA-CELLS; SPECTROSCOPY; DIFFERENTIATION; SEPARATION; PROTEINS; AGENTS; PHASE; COSY AB During a large-scale isolation of bryostatin 1, NMR measurements indicated that parts of the published C-13 and H-1 NMR assignments had to be revised. These reassignments were based on extensive homonuclear and heteronuclear one- and two-dimensional NMR techniques performed at 500 MHz. These independently obtained assignments are also in good agreement with the revised assignments and structure of bryostatin 3. RP CHMURNY, GN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PRI DYN CORP,CHEM SYNTH & ANAL LAB,POB B,FREDERICK,MD 21702, USA. NR 23 TC 4 Z9 4 U1 2 U2 3 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0749-1581 J9 MAGN RESON CHEM JI Magn. Reson. Chem. PD APR PY 1991 VL 29 IS 4 BP 366 EP 374 DI 10.1002/mrc.1260290414 PG 9 WC Chemistry, Multidisciplinary; Chemistry, Physical; Spectroscopy SC Chemistry; Spectroscopy GA FJ545 UT WOS:A1991FJ54500013 ER PT J AU EVANS, CH HOOKS, JJ DETRICK, B AF EVANS, CH HOOKS, JJ DETRICK, B TI LEUKOREGULIN - A NEW BIOTHERAPEUTIC CYTOKINE IN THE SEARCH FOR MORE EFFECTIVE ANTIVIRAL PHARMACOLOGICAL AGENTS SO MILITARY MEDICINE LA English DT Article AB This investigation examines whether cytokines, as exemplified by leukoregulin, with their immense potential for biorecognition and target cell modulation as a result of their complex three-dimensional structure, have the potential to provide new directions for biotherapy of infectious disease. Leukoregulin is a naturally occurring immunologic cytokine, secreted by stimulated lymphocytes, which increases membrane permeability and drug uptake in tumor but not in normal cells. This study demonstrates that leukoregulin also increases the plasma membrane permeability of cells acutely infected with herpes simplex type 1 virus and that the increase in membrane permeability is accompanied by a 10- to 100-fold increase in the ability of acyclovir to inhibit the release of infectious virus when the cells are treated with leukoregulin 3 hours after infection with the virus. This is the first demonstration that a cytokine, alone or in combination with anti-viral chemotherapy, can effectively inhibit virus replication in human cells following acute virus infection, which indicates that combination immunotherapy and chemotherapy have the potential to completely inhibit the production of infectious virus by acutely infected human cells. RP EVANS, CH (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ASSN MILITARY SURG US PI BETHESDA PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0026-4075 J9 MIL MED JI Milit. Med. PD APR PY 1991 VL 156 IS 4 BP 155 EP 159 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA FG528 UT WOS:A1991FG52800002 PM 1851546 ER PT J AU KLION, AD RAGHAVAN, N BRINDLEY, PJ NUTMAN, TB AF KLION, AD RAGHAVAN, N BRINDLEY, PJ NUTMAN, TB TI CLONING AND CHARACTERIZATION OF A SPECIES-SPECIFIC REPETITIVE DNA-SEQUENCE FROM LOA-LOA SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE LOA-LOA; REPETITIVE DNA; FILARIASIS ID ONCHOCERCA-VOLVULUS; BRUGIA-MALAYI; IDENTIFICATION; MICROFILARIAE; PROBE; ACID AB A genomic DNA library of Loa loa was constructed in lambda-gt11 using EcoRI-digested DNA from microfilariae isolated from two West African patients. Screening with labeled L. loa DNA yielded several potential repetitive DNA clones. An Mbol fragment of one of these, LL3M9, was identified and characterized. Sequence analysis of LL3M9 revealed an 839-bp fragment with an unusual 356-bp region containing 37 copies of the hexamer CTTAGG, many of which are arranged in repeated motifs of 12, 27 and 63 bp. This region shares many of the characteristics of eukaryotic satellite DNA. A synthetic oligonucleotide corresponding to the 27-bp repeated motif, LL3M9REP, was found to be both sensitive and species-specific by dot hybridization. Species specificity of LL3M9REP was confirmed by amplification of the repetitive region using genomic DNA as a template in the polymerase chain reaction. RP KLION, AD (reprint author), NIH,PARASIT DIS LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. OI Klion, Amy/0000-0002-4986-5326 NR 26 TC 20 Z9 20 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-6851 J9 MOL BIOCHEM PARASIT JI Mol. Biochem. Parasitol. PD APR PY 1991 VL 45 IS 2 BP 297 EP 306 DI 10.1016/0166-6851(91)90098-Q PG 10 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA FC458 UT WOS:A1991FC45800014 PM 2038361 ER PT J AU KATZAV, S CLEVELAND, JL HESLOP, HE PULIDO, D AF KATZAV, S CLEVELAND, JL HESLOP, HE PULIDO, D TI LOSS OF THE AMINO-TERMINAL HELIX-LOOP-HELIX DOMAIN OF THE VAV PROTOONCOGENE ACTIVATES ITS TRANSFORMING POTENTIAL SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MYC GENE FAMILY; DNA-BINDING; DROSOPHILA-MELANOGASTER; NUCLEAR-LOCALIZATION; ENHANCER BINDING; N-MYC; C-MYC; SEQUENCES; TRANSCRIPTION; PROTEINS AB vav, a novel human oncogene, was originally generated in vitro by replacement of its normal 5' coding sequences with sequences from pSV2neo DNA, cotransfected as a selectable marker (S. Katzav, D. Martin-Zanca, and M. Barbacid, EMBO J. 8:2283-2290, 1989). The vav proto-oncogene is normally expressed in cells of hematopoietic origin. To determine whether the 5' rearrangement of vav or its ectopic expression in NIH 3T3 cells contributes to its transforming potential, we isolated murine and human proto-vav cDNA clones as well as human genomic clones corresponding to the 5' end of the gene. Normal proto-vav was poorly transforming in NIH 3T3 cells, whereas truncation of its 5' end greatly enhanced its transforming activity. The relative failure of full-length proto-vav cDNA clones to transform NIH 3T3 cells indicates that the transforming activity of vav is not simply due to ectopic expression. Analysis of the predicted amino terminus of the vav proto-oncogene shows that it contains a helix-loop-helix domain and a leucine zipper motif similar to that of myc family proteins, though it lacks a basic region that is usually found adjacent to helix-loop-helix domains. Loss of the helix-loop-helix domain of proto-vav, either by truncation or by rearrangement with pSV2neo sequences, activates its oncogenic potential. C1 NCI, FREDERICK CANC RES FACIL, BRI BASIC RES PROGRAM, FREDERICK, MD 21701 USA. RP KATZAV, S (reprint author), ST JUDE CHILDRENS RES HOSP, DEPT BIOCHEM, 332 N LAUDERDALE, MEMPHIS, TN 38101 USA. FU NCI NIH HHS [P30 CA21765] NR 52 TC 159 Z9 162 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1991 VL 11 IS 4 BP 1912 EP 1920 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FC852 UT WOS:A1991FC85200017 PM 2005887 ER PT J AU FAZIOLI, F KIM, UH RHEE, SG MOLLOY, CJ SEGATTO, O DIFIORE, PP AF FAZIOLI, F KIM, UH RHEE, SG MOLLOY, CJ SEGATTO, O DIFIORE, PP TI THE ERBB-2 MITOGENIC SIGNALING PATHWAY - TYROSINE PHOSPHORYLATION OF PHOSPHOLIPASE-C-GAMMA AND GTPASE-ACTIVATING PROTEIN DOES NOT CORRELATE WITH ERBB-2 MITOGENIC POTENCY SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PDGF RECEPTOR; KINASE-ACTIVITY; NEU ONCOGENE; GROWTH; CELLS; EGF; GENE; TRANSDUCTION; TRANSFORMATION; ANTIBODIES AB The erbB-2 gene product, gp185erbB-2, unlike the structurally related epidermal growth factor (EGF) receptor (EGFR), exhibits constitutive kinase and transforming activity. We used a chimeric EGFR/erbB-2 expression vector to compare the mitogenic signaling pathway of the erbB-2 kinase with that of the EGFR, at similar levels of expression, in response to EGF stimulation. The EGFR/erbB-2 chimera was significantly more active in inducing DNA synthesis than the EGFR when either was expressed in NIH 3T3 cells. Analysis of biochemical pathways implicated in signal transduction by growth factor receptors indicated that both phospholipase C type-gamma (PLC-gamma) and the p21ras GTPase-activating protein (GAP) are substrates for the erbB-2 kinase in NIH 3T3 fibroblasts. However, under conditions in which activation of the erbB-2 kinase induced DNA synthesis at least fivefold more efficiently than the EGFR, the levels of erbB-2- or EGFR-induced tyrosine phosphorylation of PLC-gamma and GAP were comparable. In addition, the stoichiometry of tyrosine phosphorylation of these putative substrates by erbB-2 appeared to be at least an order of magnitude lower than that induced by platelet-derived growth factor receptors at comparable levels of mitogenic potency. Thus, our results indicate that differences in tyrosine phosphorylation of PLC-gamma and GAP do not account for the differences in mitogenic activity of the erbB-2 kinase compared with either the EGFR or platelet-derived growth factor receptor in NIH 3T3 fibroblasts. C1 NCI,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RI Di Fiore, Pier Paolo/K-2130-2012; Molloy, Christopher/A-6821-2013 OI Di Fiore, Pier Paolo/0000-0002-2252-0950; Molloy, Christopher/0000-0003-2964-6166 NR 45 TC 99 Z9 99 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1991 VL 11 IS 4 BP 2040 EP 2048 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FC852 UT WOS:A1991FC85200033 PM 1672440 ER PT J AU BATRA, JK FITZGERALD, DJ CHAUDHARY, VK PASTAN, I AF BATRA, JK FITZGERALD, DJ CHAUDHARY, VK PASTAN, I TI SINGLE-CHAIN IMMUNOTOXINS DIRECTED AT THE HUMAN TRANSFERRIN RECEPTOR CONTAINING PSEUDOMONAS EXOTOXIN-A OR DIPHTHERIA-TOXIN - ANTI-TFR(FV)-PE40 AND DT388-ANTI-TFR(FV) SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID MUTANT PROTEINS; CLEAVAGE; FRAGMENT; DOMAINS; CYTOSOL AB Two single-chain immunotoxins directed at the human transferrin receptor have been constructed by using polymerase chain reaction-based methods. Anti-TFR(Fv)-PE40 is encoded by a gene fusion between the DNA sequence encoding the antigen-binding portion (Fv) of a monoclonal antibody directed at the human transferrin receptor and that encoding a 40,000-molecular-weight fragment of Pseudomonas exotoxin (PE40). The other fusion protein, DT388-anti-TFR(Fv), is encoded by a gene fusion between the DNA encoding a truncated form of diphtheria toxin and that encoding the antigen-binding portion of antibody to human transferrin receptor. These gene fusions were expressed in Escherichia coli, and fusion proteins were purified by conventional chromatography techniques to near homogeneity. In anti-TFR(Fv)-PE40, the antigen-binding portion is placed at the amino terminus of the toxin, while in DT388-anti-TFR(Fv), it is at the carboxyl end of the toxin. Both these single-chain immunotoxins kill cells bearing the human transferrin receptors. However, anti-TFR(Fv)-PE40 was usually more active than DT388-anti-TFR(Fv), and in some cases it was several-hundred-fold more active. Anti-TFR(Fv)-PE40 was also more active on cell lines than a conjugate made by chemically coupling the native antibody to PE40, and in some cases it was more than 100-fold more active. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 26 TC 73 Z9 75 U1 0 U2 5 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1991 VL 11 IS 4 BP 2200 EP 2205 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FC852 UT WOS:A1991FC85200050 PM 2005905 ER PT J AU DICHEK, DA AF DICHEK, DA TI RETROVIRAL VECTOR-MEDIATED GENE-TRANSFER INTO ENDOTHELIAL-CELLS SO MOLECULAR BIOLOGY & MEDICINE LA English DT Article ID TISSUE PLASMINOGEN-ACTIVATOR; LOW-DENSITY-LIPOPROTEIN; ADENOSINE-DEAMINASE; FUNCTIONAL-ANALYSIS; EXPRESSION INVIVO; ARTERIAL-WALL; B-CELLS; PROMOTER; INFECTION; THERAPY RP DICHEK, DA (reprint author), NHLBI,MOLEC HEMATOL BRANCH,BLDG 10,ROOM 7D-18,BETHESDA,MD 20892, USA. NR 42 TC 21 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0735-1313 J9 MOL BIOL MED PD APR PY 1991 VL 8 IS 2 BP 257 EP 266 PG 10 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA HG664 UT WOS:A1991HG66400010 PM 1806767 ER PT J AU ERICKSON, JD TROJANOWSKI, JQ EIDEN, LE AF ERICKSON, JD TROJANOWSKI, JQ EIDEN, LE TI REGIONAL DISTRIBUTION AND PARTIAL MOLECULAR CHARACTERIZATION OF CD4-RELATED MESSENGER-RNA IN HUMAN BRAIN AND PERIPHERAL-TISSUES SO MOLECULAR BRAIN RESEARCH LA English DT Article DE CD4; 5'-TRUNCATED CD4; MESSENGER RNA EXPRESSION; MACROPHAGE MICROGLIA; HUMAN IMMUNODEFICIENCY VIRUS TYPE-1 (HIV-1); ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS); AIDS DEMENTIA COMPLEX ID HUMAN IMMUNODEFICIENCY VIRUS; CENTRAL NERVOUS-SYSTEM; HTLV-III INFECTION; LYMPHOCYTE-T; GLIAL-CELLS; CD4 ANTIGEN; AIDS VIRUS; RECEPTOR; HIV; EXPRESSION AB We purified human poly(A)+ RNA from 11 individuals to assess the regional distribution of CD4 and CD4-related mRNA transcripts in human brain and in peripheral tissues by Northern blot hybridization. A 3.0 kb CD4 mRNA transcript was expressed in all brain areas and several peripheral tissues examined. A second CD4-related 1.8 kb mRNA species showed an uneven distribution in the brain with cortical regions possessing highest levels and basal ganglia, thalamus, cerebellum and spinal cord containing relatively lower amounts. Messenger RNA transcripts for CD8, a T cell specific marker, were not detectable in human brain by Northern analysis, yet were as abundant as CD4 in spleen. The expression of the 1.8 kb mRNA was tissue specific as it was not observed in peripheral tissues such as spleen, adrenal, colon, or lung, nor was it found in the choroid plexus, dorsal root ganglion and human neuronal (SY5Y) or astroglial (N132N1) cell lines. Blot hybridization and S1 nuclease protection analysis of poly(A)+ RNA with selective probes derived from CD4 indicated that the 1.8 kb mRNA transcript is truncated, lacking the extracellular protein coding region of CD4, and may in fact be a unique transcript from the CD4 gene locus rather than an alternatively spliced or processed CD4 mRNA. C1 UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. RP ERICKSON, JD (reprint author), NIMH,ADAMHA,MOLEC & CELLULAR NEUROBIOL UNIT,CELL BIOL LAB,BLDG 36,BETHESDA,MD 20892, USA. NR 43 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD APR PY 1991 VL 10 IS 1 BP 23 EP 31 DI 10.1016/0169-328X(91)90052-Y PG 9 WC Neurosciences SC Neurosciences & Neurology GA FF074 UT WOS:A1991FF07400003 PM 1676132 ER PT J AU BACH, MA SHENORR, Z LOWE, WL ROBERTS, CT LEROITH, D AF BACH, MA SHENORR, Z LOWE, WL ROBERTS, CT LEROITH, D TI INSULIN-LIKE GROWTH FACTOR-I MESSENGER-RNA LEVELS ARE DEVELOPMENTALLY REGULATED IN SPECIFIC REGIONS OF THE RAT-BRAIN SO MOLECULAR BRAIN RESEARCH LA English DT Article DE INSULIN-LIKE GROWTH FACTOR-I; INSULIN-LIKE GROWTH FACTOR-I RECEPTOR; BRAIN DEVELOPMENT ID CENTRAL NERVOUS-SYSTEM; NEURO-BLASTOMA CELLS; SOMATOMEDIN-C; AUTORADIOGRAPHIC LOCALIZATION; IGF-I; RIBONUCLEIC-ACIDS; BETA-SUBUNITS; GLIAL-CELLS; HUMAN-FETAL; RECEPTORS AB The expression of mRNAs encoding insulin-like growth factor I (IGF-I) and the IGF-I receptor in the developing rat brain from embryonic day 16 to postnatal day 82 was analyzed using solution hybridization-RNase protection assays. Four distinct developmental patterns in the steady-state levels of IGF-I mRNA were seen. Specifically, the olfactory bulb showed a high perinatal level of IGF-I mRNA which declined dramatically by postnatal day 8. In contrast, cerebral cortex displayed maximal levels of IGF-I mRNA at postnatal day 8 and 13, which subsequently declined to adult levels (P82). A third developmental pattern was seen in the hypothalamus, where IGF-I mRNA increased from E16 up to postnatal day 3 and remained elevated thereafter. Finally, IGF-I mRNA levels in brainstem and cerebellum remained unchanged throughout the time period studied. We conclude that there are specific regional patterns of IGF-I gene expression in the developing rat brain. In contrast, IGF-I receptor gene expression did not exhibit any region-specific developmental changes. The developmental patterns of IGF-I gene expression seen in this study further substantiate the potential role of IGF-I in normal brain development. C1 NIDDK,DIABET BRANCH,MOLEC & CELLULAR PHYSIOL SECT,BLDG 10,ROOM 85243,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. VET ADM MED CTR,DEPT INTERNAL MED,IOWA CITY,IA 52246. UNIV IOWA,COLL MED,IOWA CITY,IA 52246. NR 41 TC 78 Z9 79 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD APR PY 1991 VL 10 IS 1 BP 43 EP 48 DI 10.1016/0169-328X(91)90054-2 PG 6 WC Neurosciences SC Neurosciences & Neurology GA FF074 UT WOS:A1991FF07400005 ER PT J AU MEZEY, E PALKOVITS, M AF MEZEY, E PALKOVITS, M TI TIME-DEPENDENT CHANGES IN CRF AND ITS MESSENGER-RNA IN THE NEURONS OF THE INFERIOR OLIVE FOLLOWING SURGICAL TRANSECTION OF THE OLIVOCEREBELLAR TRACT IN THE RAT SO MOLECULAR BRAIN RESEARCH LA English DT Article DE CORTICOTROPIN-RELEASING FACTOR MESSENGER RNA; INSITU HYBRIDIZATION; CORTICOTROPIN-RELEASING FACTOR IMMUNOCYTOCHEMISTRY; INFERIOR OLIVE; SURGICAL TRANSECTION ID CORTICOTROPIN-RELEASING FACTOR; INSITU HYBRIDIZATION HISTOCHEMISTRY; PARAVENTRICULAR NUCLEUS; HYPOGLOSSAL NUCLEUS; NERVE TRANSECTION; GENE-EXPRESSION; ADRENALECTOMY; ORGANIZATION; INCREASE; BRAIN AB Changes in corticotropin-releasing factor (CRF) immunostaining and CRF mRNA in neurons of the inferior olive were compared following unilateral surgical transections of the olivocerebellar tract. Alterations in CRF immunoreactivity could not be observed earlier than 24 h after surgery. The difference - an accumulation in the contralateral side - was most pronounced at 3 days, and disappeared by the 7th postoperative day. On the other hand, changes in mRNA could be observed as early as 5-30 min after the transection. The most significant accumulation was present at 3 h after the cut and no difference could be observed from the 3rd day following surgery. The results suggest that changes in mRNA levels by axotomy may occur at an earlier time point than previously thought. C1 DEPT ANAT 1,BUDAPEST,HUNGARY. RP MEZEY, E (reprint author), NIMH,CELL BIOL LAB,BLDG 36,ROOM 3A17,BETHESDA,MD 20892, USA. RI Palkovits, Miklos/F-2707-2013 NR 22 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD APR PY 1991 VL 10 IS 1 BP 55 EP 59 DI 10.1016/0169-328X(91)90056-4 PG 5 WC Neurosciences SC Neurosciences & Neurology GA FF074 UT WOS:A1991FF07400007 PM 1647483 ER PT J AU LIN, KH PARKISON, C MCPHIE, P CHENG, SY AF LIN, KH PARKISON, C MCPHIE, P CHENG, SY TI AN ESSENTIAL ROLE OF DOMAIN-D IN THE HORMONE-BINDING ACTIVITY OF HUMAN BETA-1 THYROID-HORMONE NUCLEAR RECEPTOR SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID ESTROGEN-RECEPTOR; C-ERBA; IDENTIFICATION; SUPERFAMILY; PROTEIN; ELEMENT AB By analogy with steroid receptors, human placental thyroid hormone nuclear receptor (hTR-beta-1) could be divided into four functional domains: A/B (Met1-Leu101), C (Cys102-Ala170), D (Thr171-Lys237), and E (Arg238-Asp456). The E domain was thought to bind thyroid hormone. To evaluate whether domain E alone is sufficient to bind T3 or requires the presence of other domains for functional T3-binding activity, a series of deletion mutants was constructed. The mutants were expressed in Escherichia coli, and the expressed proteins were purified. Analysis of the T3-binding affinity and analog specificity of the purified truncated hTR-beta-1 indicated that domain E alone did not have T3-binding activity. Extension of the amino-terminal sequence of domain E to include part of domain D yielded a mutant (Lys201-Asp456) with a K(a) for T3 of 0.5 +/- 0.2 x 10(9) M-1. Further extension to include the entire domain D (Met169-Asp456) yielded a mutant with T3-binding activity with a K(a) of 0.8 +/- 0.1 x 10(9) M-1. Further extension of the amino-terminal sequence to include domain C increased the affinity for T3 by nearly 2-fold (K(a) = 1.5 +/- 0.4 x 10(9) M-1). The K(a) for the wild-type hTR-beta-1 is 1.5 +/- 0.2 x 10(9) M-1. Furthermore, mutant (Met169-Asp456) binds to 3',5',3-triiodo-L-thyropropionic acid, D-T3, L-T4, and L-T3 with 307%, 37%, 7%, and 0.1%, respectively, of the activity of L-T3. This order of analog affinity is similar to that of the wild-type hTR-beta-1. These results indicate that domain D is essential for hormone-binding activity. In contrast, the A/B domain is not required for T3-binding activity. Domain C has modulation activity for domains D and E. Deletion of the last eight carboxyl amino acids completely abolishes the T3-binding activity of the mutant (Met169-Asp456). Thus, domain D is essential for domain E to function as a hormone-binding domain. C1 NCI,MOLEC BIOL LAB,BLDG 37,ROOM 4B09,BETHESDA,MD 20892. NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 28 TC 52 Z9 52 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD APR PY 1991 VL 5 IS 4 BP 485 EP 492 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FK114 UT WOS:A1991FK11400004 PM 1922081 ER PT J AU WASHBURN, RG BRYANTVARELA, BJ JULIAN, NC BENNETT, JE AF WASHBURN, RG BRYANTVARELA, BJ JULIAN, NC BENNETT, JE TI DIFFERENCES IN CRYPTOCOCCUS-NEOFORMANS CAPSULAR POLYSACCHARIDE STRUCTURE INFLUENCE ASSEMBLY OF ALTERNATIVE COMPLEMENT PATHWAY C3 CONVERTASE ON FUNGAL SURFACES SO MOLECULAR IMMUNOLOGY LA English DT Article ID SIALIC-ACID; COMPONENTS; ACTIVATION; PHAGOCYTOSIS; MACROPHAGES; BREAKDOWN; BINDING; SYSTEM; YEAST AB Binding of complement component C3 and Factor B to Cryptococcus neoformans serotypes A through D via the alternative complement pathway was measured in a system containing fresh nonimmune human serum. Serotypes B and C (C. neoformans var. gattii) bound approximately half as many molecules of both complement components as serotypes A and D (C. neoformans var. neoformans). In contrast, removal of xylosyl and glucuronyl side chains from the mannan main chain of capsular polysaccharide by the Smith degradation procedure resulted in binding of similar quantities of C3 to each of the four serotypes. We conclude that the relatively high degree of side chain substitution of capsular polysaccharide from C. neoformans variety gattii contributes to inefficient surface assembly of the alternative pathway C3 convertase. Inefficient binding of alternative pathway complement components to serotypes B and C may contribute to the relative difficulty in successfully treating infections caused by these organisms. C1 NIAID,CLIN MYCOL SECT,BETHESDA,MD 20892. RP WASHBURN, RG (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT MED,INFECT DIS SECT,300 S HAWTHORNE RD,WINSTON SALEM,NC 27103, USA. FU NIAID NIH HHS [R29 AI 25037] NR 26 TC 30 Z9 30 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD APR-MAY PY 1991 VL 28 IS 4-5 BP 465 EP 470 DI 10.1016/0161-5890(91)90160-L PG 6 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA FW027 UT WOS:A1991FW02700020 PM 2062324 ER PT J AU PADLAN, EA AF PADLAN, EA TI A POSSIBLE PROCEDURE FOR REDUCING THE IMMUNOGENICITY OF ANTIBODY VARIABLE DOMAINS WHILE PRESERVING THEIR LIGAND-BINDING PROPERTIES SO MOLECULAR IMMUNOLOGY LA English DT Article ID 3-DIMENSIONAL STRUCTURE; ANTIGEN COMPLEX; RESOLUTION; PROTEINS; LYSOZYME; SOLVENT; CELLS; MICE AB It is proposed to reduce the immunogenicity of allogeneic antibody variable domains, while preserving ligand-binding properties, by reducing their antigenicity through replacement of the exposed residues in the framework regions which differ from those usually found in host antibodies. The results of a comparison of representative murine antibody sequences with those of human origin suggest that the number of residues that need to be replaced to "humanize" those antibodies could be small. RP PADLAN, EA (reprint author), NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 23 TC 108 Z9 114 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD APR-MAY PY 1991 VL 28 IS 4-5 BP 489 EP 498 DI 10.1016/0161-5890(91)90163-E PG 10 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA FW027 UT WOS:A1991FW02700023 PM 1905784 ER PT J AU BERGER, SP MARTENSON, RE LAING, P THURKAUF, A DECOSTA, B RICE, KC PAUL, SM AF BERGER, SP MARTENSON, RE LAING, P THURKAUF, A DECOSTA, B RICE, KC PAUL, SM TI PHOTOAFFINITY-LABELING OF THE DOPAMINE REUPTAKE CARRIER PROTEIN WITH 3-AZIDO[H-3]GBR-12935 SO MOLECULAR PHARMACOLOGY LA English DT Note ID RAT-BRAIN SYNAPTOSOMES; H-3 GBR-12935 BINDING; UPTAKE SITES; GBR-12935 BINDING; TRANSPORT COMPLEX; STRIATAL MEMBRANES; PARKINSONS-DISEASE; NEURONAL DOPAMINE; COCAINE RECEPTORS; HUMAN-PLATELETS AB A high affinity tritiated azido-diphenylpiperazine derivative, 3-azido[H-3]GBR-12935, was synthesized as a potential photoaffinity probe of the dopamine transporter. Initially, the reversible binding of 3-azido[H-3]GBR-12935 to crude synaptosomal membranes from the rat striatum was characterized. Specific binding was sodium dependent and inhibited by a variety of drugs that are known to potently inhibit dopamine uptake. Other neurotransmitter uptake inhibitors, as well as cis-flupenthixol, a potent inhibitor of [H-3]GBR-12935 binding to piperazine binding sites, failed to inhibit specific binding at concentrations of less-than-or-equal-to 10-mu-M. A good correlation was observed between the relative potencies of these drugs in inhibiting dopamine uptake into synaptosomes and in inhibiting specific 3-azido[H-3]GBR-12935 binding to rat striatal membranes (r = 0.95, p < 0.01). These data suggest that 3-azido[H-3]GBR-12935, like other diphenylpiperazines such as [H-3]GBR-12935 and [H-3]GBR-12909, binds primarily to the dopamine transporter under defined assay conditions. After UV photolysis of crude synaptosomal membranes preincubated with 3-azido[H-3]GBR-12935 (1-2 nM), a single radiolabeled polypeptide with an apparent molecular mass of 80 kDa was observed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fluorography. Photoincorporation of 3-azido[H-3]GBR-12935 into this polypeptide was inhibited selectively by compounds that inhibit the uptake of dopamine (but not other biogenic amines) and was completely dependent on the presence of Na+. No photolabeled proteins were observed when cerebellar membranes were substituted for striatal membranes. Essentially complete adsorption of the radiolabeled 80-kDa polypeptide to wheat germ agglutinin and elution with N-acetyl-D-glucosamine strongly suggest that the dopamine transporter polypeptide photolabeled by 3-azido[H-3]GBR-12935 is glycosylated. C1 NIMH,CLIN NEUROSCI BRANCH,MOLEC PHARMACOL SECT,BLDG 10,ROOM 4N224,BETHESDA,MD 20892. NIADDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 35 TC 24 Z9 24 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 1991 VL 39 IS 4 BP 429 EP 435 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FG918 UT WOS:A1991FG91800001 PM 2017146 ER PT J AU CLARK, GC BLANK, JA GERMOLEC, DR LUSTER, MI AF CLARK, GC BLANK, JA GERMOLEC, DR LUSTER, MI TI 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN STIMULATION OF TYROSINE PHOSPHORYLATION IN LYMPHOCYTES-B - POTENTIAL ROLE IN IMMUNOSUPPRESSION SO MOLECULAR PHARMACOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; PROTEIN-KINASES; GENE HCK; CELLS; DIFFERENTIATION; MOUSE; RAT; PROLIFERATION; ACTIVATION; MEMBRANES AB The prototype halogenated aromatic hydrocarbon 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is carcinogenic and toxic in experimental animals. At the cellular level, TCDD toxicity is often expressed as an inhibition or alteration in normal cell maturation. In this respect, we and others have demonstrated that exposure of experimental animals to TCDD causes immunosuppression, including inhibition of B lymphocyte maturation and antibody synthesis. Although the immunological effects of TCDD are well described, little is known about its mechanism of action. In the present studies, it was found that TCDD increases membrane protein phosphorylation, which is, in part, associated with tyrosine-specific phosphorylation in B lymphocytes. This increase in phosphorylation occurred within minutes following TCDD treatment and was not associated with protein kinase C. The increase in tyrosine kinase by TCDD appears to be primarily due to de novo synthesis of new protein, because the protein synthesis inhibitors puromycin and cycloheximide, as well as the transcriptional inhibitor actinomycin D, partially inhibited the effect, although increased activity of preexisting protein cannot be fully dismissed. The dose response for increased phosphorylation by TCDD was identical to that we previously reported for inhibition of antibody synthesis, suggesting that immunosuppression by TCDD may be expressed through alterations in regulatory processes controlled by tyrosine kinases. These studies are discussed in terms of the potential role of TCDD-induced tyrosine phosphorylation in immunosuppression. C1 NIEHS,NATL TOXICOL PROGRAM,SYST TOXICOL BRANCH,RES TRIANGLE PK,NC 27709. NR 32 TC 44 Z9 44 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD APR PY 1991 VL 39 IS 4 BP 495 EP 501 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FG918 UT WOS:A1991FG91800012 PM 1850092 ER PT J AU SHEN, RL WARD, RD DASILVA, PP NISHIOKA, D AF SHEN, RL WARD, RD DASILVA, PP NISHIOKA, D TI LOCALIZATION OF WHEAT-GERM-AGGLUTININ AND ANTIBODY-BINDING SITES ON THE PLASMA-MEMBRANES OF SEA-URCHIN SPERM HEADS AS REVEALED BY LABEL-FRACTURE AND FRACTURE-FLIP SO MOLECULAR REPRODUCTION AND DEVELOPMENT LA English DT Article DE ACROSOME; IMMONUGOLD CYTOCHEMISTRY; INTRAMEMBRANE PARTICLES; CELL SURFACE; SPERM SURFACE ANATOMY ID ACROSOME REACTION; SURFACE-ANTIGENS; STRONGYLOCENTROTUS-PURPURATUS; MAMMALIAN SPERMATOZOON; CHANGING LOCALIZATIONS; MONOCLONAL-ANTIBODY; CYTO-CHEMISTRY; EGGS; FERTILIZATION; ORGANIZATION AB Freeze-fracture electron microscopy reveals that intramembrane particles are concentrated in a band encircling the posterior portion of the acrosome of Strongylocentrotus purpuratus sperm. Two colloidal gold labeling methods, label-fracture and replica-staining fracture-flip, were employed to show that the plant lectin wheat germ agglutinin, which recognizes a 210 kDa sperm surface glycoprotein, binds to this localized band of intramembrane particles. Monoclonal antibody J18/2, which also recognizes the 210 kDa surface glycoprotein, shows this localized binding in almost-equal-to 20% of the sperm observed in this study. The majority of sperm displayed a uniform distribution of receptor sites for monoclonal antibody J18/2. Since wheat germ agglutinin and monoclonal antibody J18/2 are known to agglutinate Strongylocentrotus purpuratus sperm but not sperm of another sea urchin, Lytechinus pictus, similar determinations were made for the latter species. Lytechinus pictus sperm are not labeled with wheat germ agglutinin and are only sparsely labeled with monoclonal antibody J18/2. The acrosomal localizations of wheat germ agglutinin and monoclonal antibody J18/2 receptors in Strongylocentrotus purpuratus sperm are consistent with the involvement of the 210 kDa surface glycoprotein in an egg jelly-induced sperm acrosome reaction. Low-temperature post-embed labeling of thin sections with wheat germ agglutinin and monoclonal antibody J18/2 show concentrations of label within the acrosomal vesicle of Strongylocentrotus purpuratus sperm, suggesting the presence of an intracellular storage site for the 210 kDa glycoprotein. C1 GEORGETOWN UNIV,DEPT BIOL,WASHINGTON,DC. RP SHEN, RL (reprint author), NCI,FREDERICK CANC RES & DEV CTR,MEMBRANE BIOL SECT,MATH BIOL LAB,BLDG 538,ROOM 104,FREDERICK,MD 21702, USA. RI Shen, Rulong/E-4079-2011 FU NICHD NIH HHS [HD-19054] NR 40 TC 3 Z9 3 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1040-452X J9 MOL REPROD DEV JI Mol. Reprod. Dev. PD APR PY 1991 VL 28 IS 4 BP 410 EP 418 DI 10.1002/mrd.1080280414 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology GA FD133 UT WOS:A1991FD13300013 PM 2064784 ER PT J AU BISHOP, JB RUTLEDGE, J ARONSON, J GENEROSO, WM AF BISHOP, JB RUTLEDGE, J ARONSON, J GENEROSO, WM TI MUTATIONAL CONSEQUENCES OF MOUSE ZYGOTE EXPOSURE SO MUTATION RESEARCH LA English DT Meeting Abstract C1 UNIV WASHINGTON,SEATTLE,WA 98195. NIEHS,RES TRIANGLE PK,NC 27709. OAK RIDGE NATL LAB,OAK RIDGE,TN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD APR PY 1991 VL 252 IS 2 BP 188 EP 188 DI 10.1016/0165-1161(91)90061-C PG 1 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA FE677 UT WOS:A1991FE67700051 ER PT J AU CASPARY, W DASTON, D RUDD, C LEE, P AF CASPARY, W DASTON, D RUDD, C LEE, P TI ESTIMATION OF INDUCED MUTATION FREQUENCIES IN MAMMALIAN-CELLS SO MUTATION RESEARCH LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. SRI INT,MENLO PK,CA 94025. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD APR PY 1991 VL 252 IS 2 BP 204 EP 205 DI 10.1016/0165-1161(91)90093-N PG 2 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA FE677 UT WOS:A1991FE67700083 ER PT J AU DALY, JW NISHIZAWA, Y EDWARDS, MW WATERS, JA ARONSTAM, RS AF DALY, JW NISHIZAWA, Y EDWARDS, MW WATERS, JA ARONSTAM, RS TI NICOTINIC RECEPTOR-ELICITED SODIUM FLUX IN RAT PHEOCHROMOCYTOMA PC12 CELLS - EFFECTS OF AGONISTS, ANTAGONISTS, AND NONCOMPETITIVE BLOCKERS SO NEUROCHEMICAL RESEARCH LA English DT Article DE ACETYLCHOLINE RECEPTORS; NICOTINE; DESENSITIZATION ID ADRENAL-MEDULLARY CELLS; ION CHANNEL COMPLEX; ACETYLCHOLINE-RECEPTOR; CHOLINERGIC RECEPTOR; NERVE-CELL; CATECHOLAMINE SECRETION; PIPERIDINE-DERIVATIVES; MUSCARINIC RECEPTORS; TORPEDO ELECTROPLAX; HIGH-AFFINITY AB Nicotinic agonists stimulate Na-22 flux in rat pheochromocytoma PC12 cells. The stimulatory effect of carbamylcholine is maximal at 1 mM, while the stimulatory effect of nicotine and anatoxin maximize at the same level at 100-mu-M and 10-mu-M, respectively. The tertiary amines arecolone and isoarecolone have no effect on flux at 100-mu-M, while the methiodides at 100-mu-M stimulate flux to an extent similar to 1 mM carbamylcholine. Dihydro and alcohol analogues of isoarecolone methiodide have markedly smaller effects on flux. A preincubation for 2 to 20 min with carbamylcholine (2 mM), nicotine (300-mu-M), anatoxin (30-mu-M) or isoarecolone methiodide (100-mu-M) causes marked desensitization to a subsequent carbamylcholine-elicited stimulation of flux. d-Tubocurarine, mecamylamine, hexamethonium, and chlorisondamine inhibit carbamylcholine-elicited flux with IC50 values of 1.0, 0.8, 43, and 0.020-mu-M, respectively. Atropine has no effect at 1-mu-M, but reduces the response to carbamylcholine by 50% at 8.6-mu-M, presumably as a noncompetitive blocker. Other noncompetitive blockers of nicotinic acetylcholine-receptors, such as histrionicotoxins, gephyrotoxin, pumiliotoxin C, phencyclidine, bupivacaine and piperocaine, inhibit carbamylcholine-elicited stimulation of Na-22 flux with IC50 values from 0.3 to 1.8-mu-M. In contrast to d-tubocurarine, which inhibits carbamylcholine-elicited desensitization, and mecamylamine, which has no apparent effect on desensitization, chlorisondamine and certain noncompetitive blockers appear to enhance desensitization. The effects of agonists, antagonists and noncompetitive blockers at the neuronal nicotinic acetylcholine receptor-channel of PC12 cells are compared to their effects on binding of [I-125]alpha-bungarotoxin to agonist-recognition sites and of [H-3]perhydrohistrionicotoxin to noncompetitive blocker sites of the nicotinic acetylcholine receptor-channel of electric ray (Torpedo) electroplax membranes. There are marked differences in relative potencies for the two types of nicotinic acetylcholine receptor-channel. C1 MED COLL GEORGIA,DEPT PHARMACOL & TOXICOL,AUGUSTA,GA 30912. RP DALY, JW (reprint author), NIH,BIOORGAN CHEM LAB,BLDG 8,ROOM 1A17,BETHESDA,MD 20892, USA. NR 62 TC 56 Z9 56 U1 0 U2 4 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0364-3190 J9 NEUROCHEM RES JI Neurochem. Res. PD APR PY 1991 VL 16 IS 4 BP 489 EP 500 DI 10.1007/BF00965571 PG 12 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA GC145 UT WOS:A1991GC14500011 PM 1922660 ER PT J AU DUBINSKY, RM HALLETT, M DICHIRO, G FULHAM, M SCHWANKHAUS, J AF DUBINSKY, RM HALLETT, M DICHIRO, G FULHAM, M SCHWANKHAUS, J TI INCREASED GLUCOSE-METABOLISM IN THE MEDULLA OF PATIENTS WITH PALATAL MYOCLONUS SO NEUROLOGY LA English DT Article ID INFERIOR OLIVE; SPINAL-CORD; STIMULATION; ROOT; RAT C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NINCDS,DIV INTRAMURAL RES,NEUROIMAGING SECT,BETHESDA,MD 20892. NR 25 TC 38 Z9 43 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1991 VL 41 IS 4 BP 557 EP 562 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA FG377 UT WOS:A1991FG37700018 PM 2011257 ER PT J AU FENGER, M AF FENGER, M TI PROCESSING OF PRO-OPIOMELANOCORTIN-DERIVED AMIDATED JOINING PEPTIDE AND GLYCINE-EXTENDED PRECURSOR IN MONKEY PITUITARY SO NEUROSCIENCE LETTERS LA English DT Article DE PROOPIOMELANOCORTIN; JOINING PEPTIDE; MONKEY; PRIMATE; AMIDATION; GLYCINE-EXTENDED; PITUITARY; ACTH ID (POMC)-DERIVED PEPTIDES; PROOPIOMELANOCORTIN; ENDORPHIN; CELLS; FORMS; ACTH AB The molecular forms of proopiomelanocortin (POMC) derived amidated and C-terminal glycine-extended joining peptide from monkey (Macaca mulatta) pituitary were determined. The predominant forms of joining peptide found were the low molecular peptides POMC(76-105) and POMC(76-106), respectively. Significant amounts of N-terminally truncated POMC(78-105) and POMC(78-106) were also detected in the posterior-intermediate lobe. No N-terminal extended froms were detected. The relative amount of amidated joining peptide to total joining peptide was 6-35%. It is concluded that not only is the primary sequence of monkey and human POMC extremely conserved, but also the processing patterns are similar. The monkey therefore serves as a suitable model for studying regulation of the processing of POMC and the hypothalamus-pituitary-adrenal axis in man. C1 UNIV MICHIGAN,MENTAL HLTH RES INST,ANN ARBOR,MI 48109. NIH,BETHESDA,MD 20892. NR 17 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD APR 1 PY 1991 VL 124 IS 2 BP 190 EP 194 DI 10.1016/0304-3940(91)90091-7 PG 5 WC Neurosciences SC Neurosciences & Neurology GA FG004 UT WOS:A1991FG00400013 PM 2067719 ER PT J AU WAKISAKA, S KAJANDER, KC BENNETT, GJ AF WAKISAKA, S KAJANDER, KC BENNETT, GJ TI INCREASED NEUROPEPTIDE-Y (NPY)-LIKE IMMUNOREACTIVITY IN RAT SENSORY NEURONS FOLLOWING PERIPHERAL AXOTOMY SO NEUROSCIENCE LETTERS LA English DT Article DE AXOTOMY; DORSAL ROOT GANGLION; NEUROPEPTIDE-Y; NERVE INJURY; SPINAL CORD ID DORSAL-ROOT GANGLION; SPINAL-CORD; NERVE SECTION; BRAIN PEPTIDE; SUBSTANCE-P; HORN; VIP; LAMINAE; INJURY; CELLS AB The effects of peripheral axotomy (sciatic nerve transection) on the presence and distribution of neuropeptide Y (NPY) in rat dorsal root ganglion (DRG) and spinal grey matter were examined using immunocytochemistry. In normal rats and on the sham-operated side of experimental rats. NPY-like immunoreactivity (NPYir) was observed in all laminate of the lumbar spinal cord, with an especially dense concentration of immunostained axons and axonal varicosities in laminae I-II of the dorsal horn. There was no detectable NPYir in L4-L5 DRG cells from normal rats or from the sham-operated side of experimental rats. At 14 days after axotomy, there was a large ipsilateral increase in the density of NPYir axons and varicosities in the lumbar spinal cord on the side of the nerve injury; this was especially apparent in laminae III-V. In the same rats, NPYir was observed in many small, medium, and large neurons in the L4-L5 DRGs on the side of the severed nerve. C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 30,ROOM B-20,BETHESDA,MD 20892. NR 24 TC 284 Z9 286 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD APR 1 PY 1991 VL 124 IS 2 BP 200 EP 203 DI 10.1016/0304-3940(91)90093-9 PG 4 WC Neurosciences SC Neurosciences & Neurology GA FG004 UT WOS:A1991FG00400015 PM 1712437 ER PT J AU DEGUCHI, Y MORONEY, JF WILSON, GL FOX, CH WINTER, HS KEHRL, JH AF DEGUCHI, Y MORONEY, JF WILSON, GL FOX, CH WINTER, HS KEHRL, JH TI CLONING OF A HUMAN HOMEOBOX GENE THAT RESEMBLES A DIVERGED DROSOPHILA HOMEOBOX GENE AND IS EXPRESSED IN ACTIVATED LYMPHOCYTES SO NEW BIOLOGIST LA English DT Article DE DNA-BINDING PROTEINS; EMBRYOGENESIS; HEMATOPOIESIS; HOMEOBOX GENES; LYMPHOCYTES ID TRANSCRIPTION FACTOR; ANTIGENIC ANALYSIS; SEGMENTATION GENE; T-CELLS; PROTEINS; HOMEODOMAIN; SEQUENCE; DOMAIN; REPRESSION; RNA C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT GASTROENTEROL & NUTR,CAMBRIDGE,MA 02138. OI Kehrl, John/0000-0002-6526-159X NR 56 TC 42 Z9 43 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4674 J9 NEW BIOL PD APR PY 1991 VL 3 IS 4 BP 353 EP 363 PG 11 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA GK719 UT WOS:A1991GK71900008 PM 1676597 ER PT J AU RON, D ZANNINI, M LEWIS, M WICKNER, RB HUNT, LT GRAZIANI, G TRONICK, SR AARONSON, SA EVA, A AF RON, D ZANNINI, M LEWIS, M WICKNER, RB HUNT, LT GRAZIANI, G TRONICK, SR AARONSON, SA EVA, A TI A REGION OF PROTO-DBL ESSENTIAL FOR ITS TRANSFORMING ACTIVITY SHOWS SEQUENCE SIMILARITY TO A YEAST-CELL CYCLE GENE, CDC24, AND THE HUMAN BREAKPOINT CLUSTER GENE, BCR SO NEW BIOLOGIST LA English DT Article DE PROTO-DBL; CDC24; BCR ID ACUTE LYMPHOBLASTIC-LEUKEMIA; SACCHAROMYCES-CEREVISIAE; PHILADELPHIA-CHROMOSOME; ABL-ONCOGENE; PHOSPHOLIPASE-C; TERMINAL REGION; PRODUCT; LOCALIZATION; MORPHOGENESIS; LYMPHOMA C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. UNIV CALIF SANTA CRUZ,DEPT BIOL,SANTA CRUZ,CA 95064. NIADDKD,BIOCHEM PHARMACOL LAB,BETHESDA,MD 20892. NATL BIOMED RES FDN,WASHINGTON,DC 20007. RI Lewis, Michael/A-9572-2009; Graziani, Grazia/G-5747-2012; Zannini, Mariastella/I-1735-2012; Eva, Alessandra/J-8268-2016; OI Eva, Alessandra/0000-0003-2949-078X; GRAZIANI, GRAZIA/0000-0002-0221-768X FU NCI NIH HHS [CA 40474] NR 40 TC 160 Z9 163 U1 1 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4674 J9 NEW BIOL PD APR PY 1991 VL 3 IS 4 BP 372 EP 379 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA GK719 UT WOS:A1991GK71900010 PM 2065022 ER PT J AU JU, WD VELU, TJ VASS, WC PAPAGEORGE, AG LOWY, DR AF JU, WD VELU, TJ VASS, WC PAPAGEORGE, AG LOWY, DR TI TUMORIGENIC TRANSFORMATION OF NIH 3T3 CELLS BY THE AUTOCRINE SYNTHESIS OF TRANSFORMING GROWTH FACTOR-ALPHA SO NEW BIOLOGIST LA English DT Article DE AUTOCRINE GROWTH; CELL TRANSFORMATION; GENE TRANSFER; GROWTH FACTORS; TRANSFORMING GROWTH FACTOR-ALPHA ID TGF-ALPHA; FACTOR RECEPTOR; EGF-RECEPTOR; TRANSGENIC MICE; PRECURSOR; EXPRESSION; OVEREXPRESSION; INDUCTION; PROTEIN; INTERNALIZATION C1 NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 35 TC 23 Z9 23 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4674 J9 NEW BIOL PD APR PY 1991 VL 3 IS 4 BP 380 EP 388 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA GK719 UT WOS:A1991GK71900011 PM 2065023 ER PT J AU LAROCHELLE, WJ GIESE, N ROBBINS, KC AARONSON, SA AF LAROCHELLE, WJ GIESE, N ROBBINS, KC AARONSON, SA TI VARIANT PDGF LIGANDS AND RECEPTORS - STRUCTURE-FUNCTION-RELATIONSHIPS SO NEWS IN PHYSIOLOGICAL SCIENCES LA English DT Article AB Platelet-derived growth factor (PDGF) is a connective tissue cell mitogen comparised of two related chains encoded by distinct genes. Properties that distinguish these ligands include greater transforming potency of the B and more efficient secretion of the A chain. By generating immunochemical probes, as well as PDGF A and B chimeras, these properties were mapped to distinct domains. Increased transforming efficiency segregated with the ability to activate both alpha-and beta-PDGF receptors. RP LAROCHELLE, WJ (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,ROOM 1E24,BETHESDA,MD 20892, USA. NR 0 TC 4 Z9 4 U1 0 U2 1 PU NEWS IN PHYSIOLOGICAL SCIENCES PI BALTIMORE PA C/O WILLIAMS & WILKINS, PO BOX 1496, BALTIMORE, MD 21203 SN 0886-1714 J9 NEWS PHYSIOL SCI JI News Physiol. Sci. PD APR PY 1991 VL 6 BP 56 EP 60 PG 5 WC Physiology SC Physiology GA FH634 UT WOS:A1991FH63400002 ER PT J AU VEECH, RL AF VEECH, RL TI THE METABOLISM OF LACTATE SO NMR IN BIOMEDICINE LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; RAT-LIVER; INVIVO; HEPATOCYTES; GLYCOGEN; ASSAY; C-13 AB Lactate contents of tissues can vary during normal physiological conditions in mammals from 0.5 to over 5 mM, and higher in pathological states, suitable for measurement by NMR. Lactate itself is a dead-end metabolite, metabolized only by lactate dehydrogenase. The extent and direction of that reaction is determined by the free [NAD+]/[NADH][H+] ratio of cytoplasm with which lactate and pyruvate are in near-equilibrium. Pyruvate is a crossroads of most of the major degradative and synthetic pathways, but present in about one-tenth the amount of lactate. Information on the content of both lactate and its redox partner pyruvate is likely to provide more information on the metabolic state of tissue than are measurements of lactate alone. RP VEECH, RL (reprint author), NIAAA,METAB & MOLEC BIOL LAB,12501 WASHINGTON AVE,ROCKVILLE,MD 20850, USA. NR 32 TC 65 Z9 66 U1 0 U2 3 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0952-3480 J9 NMR BIOMED JI NMR Biomed. PD APR PY 1991 VL 4 IS 2 BP 53 EP 58 DI 10.1002/nbm.1940040204 PG 6 WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA FL486 UT WOS:A1991FL48600003 PM 1859786 ER PT J AU MALLOY, MH ONSTAD, L WRIGHT, E AF MALLOY, MH ONSTAD, L WRIGHT, E TI THE EFFECT OF CESAREAN DELIVERY ON BIRTH OUTCOME IN VERY-LOW-BIRTH-WEIGHT INFANTS SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID PERIVENTRICULAR INTRAVENTRICULAR HEMORRHAGE; OBSTETRIC FACTORS; VAGINAL DELIVERY; 1,500 GRAMS; SECTION; LESS; SURVIVAL; RATES; GM AB To determine whether cesarean delivery is associated with a better outcome than vaginal delivery for infants weighing less than 1500 g (very low birth weight), we examined neonatal mortality and the incidence of intraventricular hemorrhage (IVH) in 1765 very low birth weight inborn infants admitted to seven neonatal intensive care centers. The cesarean rate was 32.5% for infants weighing 501-750 g and 52.4% for infants weighing 751-1000 g. The neonatal death rate was 53.1% for infants weighing 501-750 g delivered by cesarean, compared with 64.3% for vaginally born infants (P = .046). However, for infants weighing 1001-1250 g, the neonatal death rate for infants delivered by cesarean was 14.4%, compared with 7.8% for infants born vaginally (P = .02). The incidence of IVH was significantly lower in infants born by cesarean than in those born vaginally only in the 1251-1500-g birth weight interval (11.8 versus 18.9%; P = .03). Compared with women delivering vaginally, those delivered by cesarean were more likely to attain a higher mean gestation, to have preeclampsia, and to have a breech presentation, and less likely to be in labor. After adjusting by logistic regression for gestational age, preeclampsia, breech presentation, presence or absence of labor, and for center effects, the odds ratio for neonatal death was 1.00 (95% confidence interval 0.71-1.41); for IVH, the odds ratio was 0.85 (95% confidence interval 0.61-1.19). These data suggest that after accounting for certain maternal and fetal factors, cesarean delivery is not associated with a lower risk of either mortality or IVH. C1 GEORGE WASHINGTON UNIV,DEPT BIOSTAT,WASHINGTON,DC 20052. RP MALLOY, MH (reprint author), NICHHD,DIV PREVENT RES,EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 640,BETHESDA,MD 20892, USA. NR 20 TC 86 Z9 86 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD APR PY 1991 VL 77 IS 4 BP 498 EP 503 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA FD561 UT WOS:A1991FD56100002 PM 2002969 ER EF