FN Thomson Reuters Web of Science™ VR 1.0 PT J AU STEINBERG, AD AF STEINBERG, AD TI CONCEPTS OF PATHOGENESIS OF SYSTEMIC LUPUS-ERYTHEMATOSUS SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID RECOMBINANT INBRED LINES; NZB MICE; DEFECTIVE TOLERANCE; AUTOIMMUNE MOUSE; MURINE LUPUS; BONE-MARROW; INDUCTION; DNA; IMMUNE; ASSOCIATION RP STEINBERG, AD (reprint author), NIAMSD,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD 20892, USA. NR 36 TC 18 Z9 18 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 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1992 VL 63 IS 1 BP 19 EP 22 DI 10.1016/0090-1229(92)90087-5 PG 4 WC Immunology; Pathology SC Immunology; Pathology GA HK772 UT WOS:A1992HK77200008 PM 1591877 ER PT J AU LECCIONES, JA LEE, JW NAVARRO, EE WITEBSKY, FG MARSHALL, D STEINBERG, SM PIZZO, PA WALSH, TJ AF LECCIONES, JA LEE, JW NAVARRO, EE WITEBSKY, FG MARSHALL, D STEINBERG, SM PIZZO, PA WALSH, TJ TI VASCULAR CATHETER ASSOCIATED FUNGEMIA IN PATIENTS WITH CANCER - ANALYSIS OF 155 EPISODES SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID HOSPITAL-ACQUIRED CANDIDEMIA; CENTRAL VENOUS CATHETERS; BLOOD-STREAM INFECTIONS; ONCOLOGY PATIENTS; CANDIDIASIS; THERAPY; FREQUENCY; COMPLICATIONS; PREVENTION; MANAGEMENT AB We reviewed all 155 episodes of central venous catheter-associated fungemia among inpatients at the National Cancer Institute during a 10-year period. Candida species accounted for 98% of episodes. Fungemia was documented by culture of blood drawn through catheters in 50% of cases and by culture of both catheter-drawn and peripheral blood in 39%; mortality and the rate of dissemination were similar for these two groups. Four management strategies were used: catheter removal, antifungal therapy (with amphotericin B), both, or neither; indications for the use of both modes of treatment included fever, neutropenia, long-term indwelling catheterization, positive cultures of both catheter-drawn and peripheral blood, isolation of Candida tropicalis, and fungal isolation from two or more blood cultures. Disseminated fungal infection was documented in 82% of cases with these features but also in 35% of the less severe cases treated only with catheter removal. In addition, nine (82%) of 11 cases managed only with antifungal therapy had a negative outcome (either death from disseminated infection or the recurrence of fevers and/or fungemia), a finding suggesting that intravascular catheters should be removed in fungemia. Virtually all cases of catheter-associated fungemia in patients with cancer are clinically significant and require prompt therapy with amphotericin B. C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,ROOM 13N-240,BETHESDA,MD 20892. NCI,CLIN ONCOL PROGRAM,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT CLIN PATHOL,MICROBIOL SERV,BETHESDA,MD 20892. NR 42 TC 241 Z9 245 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD APR PY 1992 VL 14 IS 4 BP 875 EP 883 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HL304 UT WOS:A1992HL30400012 PM 1576282 ER PT J AU ADELBERG, S PARRIS, CN KRAEMER, KH AF ADELBERG, S PARRIS, CN KRAEMER, KH TI MUTAGENESIS BY 295NM UV-B RADIATION OF A PLASMID VECTOR REPLICATED 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 1992 VL 40 IS 2 BP A537 EP A537 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102309 ER PT J AU AHUJA, SK OZCELIK, T FRANCKE, U MURPHY, PM AF AHUJA, SK OZCELIK, T FRANCKE, U MURPHY, PM TI CHARACTERIZATION OF THE HUMAN INTERLEUKIN-8 RECEPTOR GENE FAMILY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. STANFORD UNIV,MED CTR,HOWARD HUGHES MED INST,STANFORD,CA 94305. STANFORD UNIV,MED CTR,DEPT GENET,STANFORD,CA 94305. STANFORD UNIV,MED CTR,DEPT PEDIAT,STANFORD,CA 94305. 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 1992 VL 40 IS 2 BP A184 EP A184 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100281 ER PT J AU AMAGAI, M KARPATI, S PRUSSICK, R KLAUSKOVTUN, V STANLEY, JR AF AMAGAI, M KARPATI, S PRUSSICK, R KLAUSKOVTUN, V STANLEY, JR TI AUTOANTIBODIES AGAINST THE CADHERIN-LIKE HOMOPHILIC BINDING REGION OF PEMPHIGUS-VULGARIS ANTIGEN (PVA) CAUSE ACANTHOLYSIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,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 1992 VL 40 IS 2 BP A447 EP A447 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101771 ER PT J AU BACH, LA PERDUE, JF HUDGINS, WR RECHLER, MM AF BACH, LA PERDUE, JF HUDGINS, WR RECHLER, MM TI TUMOR HYPOGLYCEMIA IS NOT DUE TO ABNORMAL BINDING OF INSULIN-LIKE GROWTH FACTOR-II PRECURSOR TO INSULIN-LIKE GROWTH-FACTOR BINDING PROTEIN-2 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. AMER RED CROSS,BETHESDA,MD 20814. 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 1992 VL 40 IS 2 BP A166 EP A166 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100177 ER PT J AU BELLANTONI, MF HARMAN, SM VITTONE, JL BRYANT, L BASS, KM COTRELL, E COPLEY, CJ BLACKMAN, MR AF BELLANTONI, MF HARMAN, SM VITTONE, JL BRYANT, L BASS, KM COTRELL, E COPLEY, CJ BLACKMAN, MR TI ANDROID BODY HABITUS IS ASSOCIATED WITH DECREASED GROWTH-HORMONE SECRETION IN POSTMENOPAUSAL WOMEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,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 1992 VL 40 IS 2 BP A196 EP A196 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100346 ER PT J AU BERNSTEIN, EF HARISIADIS, L SALOMON, G NORTON, J TALBOT, T MITCHELL, JB AF BERNSTEIN, EF HARISIADIS, L SALOMON, G NORTON, J TALBOT, T MITCHELL, JB TI RADIATION-IMPAIRED MODELS OF WOUND-HEALING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NIH,SURG BRANCH,BETHESDA,MD 20892. NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,BETHESDA,MD 20892. HAHNEMANN UNIV,DIV DERMATOL,PHILADELPHIA,PA 19102. 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 1992 VL 40 IS 2 BP A480 EP A480 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101966 ER PT J AU BIRO, S FU, YM YU, ZX EPSTEIN, SE AF BIRO, S FU, YM YU, ZX EPSTEIN, SE TI ANTISENSE OLIGODEOXYNUCLEOTIDES TARGETING THE MESSENGER-RNA ENCODING C-MYC INHIBITS SMOOTH-MUSCLE CELL-PROLIFERATION AND MIGRATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,CARDIOL 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 1992 VL 40 IS 2 BP A192 EP A192 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100324 ER PT J AU BISWAS, P POLI, G KINTER, AL JUSTEMENT, JS ORENSTEIN, JM FAUCI, AS AF BISWAS, P POLI, G KINTER, AL JUSTEMENT, JS ORENSTEIN, JM FAUCI, AS TI DIFFERENTIAL ROLES OF INTERFERON-GAMMA AS A MODULATOR OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) EXPRESSION IN CHRONICALLY INFECTED-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC 20052. 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 1992 VL 40 IS 2 BP A227 EP A227 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100519 ER PT J AU BLACK, DE MICHAELIS, OE SERVETNICK, DA HANSEN, CT TULP, OL AF BLACK, DE MICHAELIS, OE SERVETNICK, DA HANSEN, CT TULP, OL TI THE CAPACITY FOR NONSHIVERING THERMOGENESIS IN WKY/N-CP RATS - A CONGENIC MODEL OF OBESITY+NIDDM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 DREXEL UNIV,PHILADELPHIA,PA 19104. NIH,VRB,BETHESDA,MD 20892. USDA,BHNRC,BELTSVILLE,MD 20705. 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 1992 VL 40 IS 2 BP A413 EP A413 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101583 ER PT J AU BODENNER, DL MCCLASKEY, JH WEINTRAUB, BD AF BODENNER, DL MCCLASKEY, JH WEINTRAUB, BD TI THE PROTOONCOGENES C-FOS AND C-JUN MODULATE THYROID-HORMONE INHIBITION OF THE HUMAN THYROTROPIN-BETA SUBUNIT GENE (HTSH-BETA) IN OPPOSITE DIRECTIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 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 1992 VL 40 IS 2 BP A301 EP A301 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100953 ER PT J AU BOLLINGER, RC QUINN, TC LIU, AY HAMMOND, SA STANHOPE, PE SILICIANO, RF AF BOLLINGER, RC QUINN, TC LIU, AY HAMMOND, SA STANHOPE, PE SILICIANO, RF TI CYTOKINE PRODUCTION BY HIV-SPECIFIC HUMAN CYTOLYTIC LYMPHOCYTE-T FROM RECIPIENTS OF CANDIDATE AIDS VACCINES - POTENTIAL EFFECTS ON HIV-1 REPLICATION AND THE CLEARANCE OF INFECTED-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. NIAID,IMMUNOREGULAT 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 1992 VL 40 IS 2 BP A245 EP A245 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100628 ER PT J AU BOLUYT, M ONEILL, L TANTINI, B LAKATTA, EG CROW, M AF BOLUYT, M ONEILL, L TANTINI, B LAKATTA, EG CROW, M TI DECREASE IN PREPROENKEPHALIN GENE-EXPRESSION DURING CARDIAC-HYPERTROPHY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,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 1992 VL 40 IS 2 BP A149 EP A149 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100070 ER PT J AU BOULETTHIEBOUT, A MILES, D BOHAK, Z CHAIT, B SCHNEIDER, K MANNING, J RODGERS, GP AF BOULETTHIEBOUT, A MILES, D BOHAK, Z CHAIT, B SCHNEIDER, K MANNING, J RODGERS, GP TI PATTERN OF HEMOGLOBIN INDUCTION IN SICKLE-CELL PATIENTS TREATED WITH HYDROXYUREA AND ERYTHROPOIETIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. ROCKEFELLER UNIV,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 1992 VL 40 IS 2 BP A283 EP A283 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100852 ER PT J AU BRADY, RO DAMBROSIA, JM BARTON, NW AF BRADY, RO DAMBROSIA, JM BARTON, NW TI EFFECTIVENESS OF LOW-DOSE ENZYME REPLACEMENT THERAPY IN GAUCHERS-DISEASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 3 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 1992 VL 40 IS 2 BP A144 EP A144 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100043 ER PT J AU BRANTLY, ML HILDESHEIM, J LAUBACH, V RUNDQUIST, B PAUL, L AF BRANTLY, ML HILDESHEIM, J LAUBACH, V RUNDQUIST, B PAUL, L TI ALPHA-1-ANTITRYPSIN NULL NEW HOPE - NATURAL CONVERSION OF THE ALPHA-1-ANTITRYPSIN DEFICIENCY Z-VARIANT INTO A NULL VARIANT BY THE ADDITION OF 2ND AMINO-ACID SUBSTITUTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. PARK NICOLLET MED CTR,DEPT PULM,ST LOUIS PK,MN. RI Laubach, Victor/E-8818-2015 OI Laubach, Victor/0000-0001-9673-5383 NR 0 TC 4 Z9 4 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 1992 VL 40 IS 2 BP A328 EP A328 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101098 ER PT J AU BRESSLER, P BROWN, K TIMMER, W BOURS, V SIEBENLIST, U FAUCI, AS AF BRESSLER, P BROWN, K TIMMER, W BOURS, V SIEBENLIST, U FAUCI, AS TI MUTATIONAL ANALYSIS OF THE NF-KAPPA-B P50 PROTEIN AND INHIBITION OF NF-KAPPA-B ACTIVITY BY TRANSDOMINANT MUTANTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1992 VL 40 IS 2 BP A245 EP A245 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100625 ER PT J AU BRODY, SL JAFFE, HA HAN, SK PASSANITI, A MARTIN, GR KRATZKE, RA KAYE, FJ PERRICAUDET, M STRATFORDPERRICAUDET, L CRYSTAL, RG AF BRODY, SL JAFFE, HA HAN, SK PASSANITI, A MARTIN, GR KRATZKE, RA KAYE, FJ PERRICAUDET, M STRATFORDPERRICAUDET, L CRYSTAL, RG TI DIRECT INVIVO GENE-TRANSFER TO MALIGNANT-CELLS USING ADENOVIRUS VECTORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NIA,BALTIMORE,MD 21224. INST GUSTAVE ROUSSY,F-94805 VILLEJUIF,FRANCE. 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 1992 VL 40 IS 2 BP A211 EP A211 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100429 ER PT J AU BURKE, LP FIBACH, E RODGERS, GP SCHECHTER, AN NOGUCHI, CT AF BURKE, LP FIBACH, E RODGERS, GP SCHECHTER, AN NOGUCHI, CT TI HYDROXYUREA INCREASES FETAL HEMOGLOBIN IN AN ERYTHROID LIQUID CULTURE SYSTEM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DIV HEMATOL,IL-91010 JERUSALEM,ISRAEL. NIDDK,CHEM BIOL LAB,BETHESDA,MD. RI Burke, Lillian/A-7334-2008 NR 1 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 1992 VL 40 IS 2 BP A243 EP A243 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100614 ER PT J AU CANESSA, LM PORTER, C FELDER, CC MOURADIAN, MM ROBILLARD, JE JOSE, PA AF CANESSA, LM PORTER, C FELDER, CC MOURADIAN, MM ROBILLARD, JE JOSE, PA TI DISTRIBUTION OF THE ALPHA-1B ADRENERGIC-RECEPTOR IN NEPHRONS OF NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RAT (SHR) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV IOWA,MED CTR,DEPT PEDIAT,IOWA CITY,IA 52242. GEORGETOWN UNIV,MED CTR,DEPT PEDIAT,WASHINGTON,DC 20007. NINCDS,NIMH,BETHESDA,MD 20892. NR 1 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 1992 VL 40 IS 2 BP A388 EP A388 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101441 ER PT J AU CENCIARELLI, C HOHMAN, R GUSOVSKY, F WEISSMAN, AM AF CENCIARELLI, C HOHMAN, R GUSOVSKY, F WEISSMAN, AM TI PHOSPHORYLATION OF THE T-CELL RECEPTOR ZETA-SUBUNIT - GTP BINDING-PROTEIN INVOLVEMENT IN TYROSINE PHOSPHORYLATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,EXPTL IMMUNOL 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 1992 VL 40 IS 2 BP A153 EP A153 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100095 ER PT J AU CHORZELSKI, TP STEFANATO, CM BEUTNER, E STANLEY, JR KORMAN, NJ OLSZEWSKA, M MACIEJOWSKA, E JABLONSKA, S AF CHORZELSKI, TP STEFANATO, CM BEUTNER, E STANLEY, JR KORMAN, NJ OLSZEWSKA, M MACIEJOWSKA, E JABLONSKA, S TI ERYTHEMA ANNULARE-LIKE ACANTHOLYTIC DERMATOSIS (EAAD) ASSOCIATED WITH EPIDERMAL SPECIFIC ANTIBODIES - A NEW ENTITY OR NONBULLOUS PEMPHIGUS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 WARSAW ACAD MED & HOSP,DEPT DERMATOL,WARSAW,POLAND. SUNY BUFFALO,DEPT DERMATOL,BUFFALO,NY 14260. NCI,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 1992 VL 40 IS 2 BP A449 EP A449 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101779 ER PT J AU CHU, CS TRAPNELL, BC CURRISTIN, SM CUTTING, GR CRYSTAL, RG AF CHU, CS TRAPNELL, BC CURRISTIN, SM CUTTING, GR CRYSTAL, RG TI MOLECULAR-BASIS FOR VARIABLE EXON 9 SPLICING OF CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) MESSENGER-RNA TRANSCRIPTS IN THE HUMAN AIRWAY EPITHELIUM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. NR 1 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 1992 VL 40 IS 2 BP A338 EP A338 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101149 ER PT J AU CIZZA, G GOLD, PW CHROUSOS, GP WILDER, RL STERNBERG, EM AF CIZZA, G GOLD, PW CHROUSOS, GP WILDER, RL STERNBERG, EM TI INFLAMMATORY DISEASE-SUSCEPTIBLE LEWIS (LEW/N) RATS SHOW A RELATIVE PRIMARY HYPOTHYROIDISM COMPARED TO INFLAMMATORY DISEASE-RESISTANT FISCHER (F344/N) RATS 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 1992 VL 40 IS 2 BP A280 EP A280 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100834 ER PT J AU CIZZA, G GLOWA, JR GOLD, PW AF CIZZA, G GLOWA, JR GOLD, PW TI NEUROENDOCRINE CORRELATES OF BEHAVIORAL-EFFECTS OF ALPRAZOLAM IN AGED FISCHER RATS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIMH,CLIN NEUROBIOL 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 1992 VL 40 IS 2 BP A226 EP A226 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100513 ER PT J AU COBB, JP NATANSON, C KOEV, CA HOFFMAN, WD GRIFFITH, OW KILBOURN, RG GROSS, SS LEVI, R AKIN, G BANKS, S LODATO, R DANNER, RL AF COBB, JP NATANSON, C KOEV, CA HOFFMAN, WD GRIFFITH, OW KILBOURN, RG GROSS, SS LEVI, R AKIN, G BANKS, S LODATO, R DANNER, RL TI THE CARDIOVASCULAR EFFECTS OF N-INFINITY-METHYL-L-ARGININE, A NITRIC-OXIDE SYNTHASE INHIBITOR IN ENDOTOXEMIC AND NORMAL CANINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. CORNELL UNIV,DEPT BIOCHEM & PHARMACOL,ITHACA,NY 14853. UNIV TEXAS,DEPT MED ONCOL & PULM & CRIT CARE MED,AUSTIN,TX 78712. 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 1992 VL 40 IS 2 BP A267 EP A267 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100755 ER PT J AU COHEN, PJ COHEN, PA ROSENBERG, SA KATZ, SI MULE, JJ AF COHEN, PJ COHEN, PA ROSENBERG, SA KATZ, SI MULE, JJ TI MURINE EPIDERMAL LANGERHANS CELLS (LC) AND SPLENIC DENDRITIC CELLS (DC) PROCESS AND PRESENT TUMOR-ANTIGENS TO PRIMED T-CELLS 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 1992 VL 40 IS 2 BP A497 EP A497 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102070 ER PT J AU COITINHO, DC LEAO, MM RECINE, E SICHIERI, R EVERHART, JE AF COITINHO, DC LEAO, MM RECINE, E SICHIERI, R EVERHART, JE TI CHANGES IN THE PREVALENCE OF UNDERWEIGHT AND OVERWEIGHT IN BRAZIL - COMPARISON OF THE 1974 AND 1989 NATIONWIDE SURVEYS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,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 1992 VL 40 IS 2 BP A625 EP A625 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102822 ER PT J AU COON, HG HENKIN, RI AF COON, HG HENKIN, RI TI CONTINUOUS CULTURE OF HUMAN PAROTID-GLAND CELLS SECRETE THE MAJOR SALIVARY PROTEINS - AMYLASE, GUSTIN, AND LUMICARMINE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. SMELL CLIN,WASHINGTON,DC. 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 1992 VL 40 IS 2 BP A261 EP A261 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100718 ER PT J AU CROFFORD, LJ SANO, H KARALIS, K CHROUSOS, G WILDER, RL AF CROFFORD, LJ SANO, H KARALIS, K CHROUSOS, G WILDER, RL TI LOCAL SECRETION OF IMMUNE CORTICOTROPIN-RELEASING HORMONE IN EXPERIMENTAL ARTHRITIS IN LEW/N AND F344/N RATS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Crofford, Leslie/J-8010-2013 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 1992 VL 40 IS 2 BP A359 EP A359 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101265 ER PT J AU CROFFORD, LJ SANO, H KARALIS, K REMMERS, EF CHROUSOS, G WILDER, RL AF CROFFORD, LJ SANO, H KARALIS, K REMMERS, EF CHROUSOS, G WILDER, RL TI IMMUNE CORTICOTROPIN-RELEASING HORMONE LOCALIZED IN THE JOINTS OF PATIENTS WITH RHEUMATOID-ARTHRITIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Crofford, Leslie/J-8010-2013 NR 1 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 1992 VL 40 IS 2 BP A298 EP A298 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100933 ER PT J AU CROW, MT PAULY, RR PAPADOPOULOS, N PASSANITI, A LAKATTA, EG AF CROW, MT PAULY, RR PAPADOPOULOS, N PASSANITI, A LAKATTA, EG TI THE EXTRACELLULAR-MATRIX SURROUNDING VASCULAR SMOOTH-MUSCLE CELLS CONTROLS THEIR PROLIFERATION AND GENE-EXPRESSION 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 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 1992 VL 40 IS 2 BP A345 EP A345 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101186 ER PT J AU DEBINSKI, W KARLSSON, B LINDHOLM, L SIEGALL, CB WILLINGHAM, MC FITZGERALD, D PASTAN, I AF DEBINSKI, W KARLSSON, B LINDHOLM, L SIEGALL, CB WILLINGHAM, MC FITZGERALD, D PASTAN, I TI MONOCLONAL-ANTIBODY C242 - PSEUDOMONAS EXOTOXIN-A - A SPECIFIC AND POTENT IMMUNOTOXIN WITH ANTITUMOR-ACTIVITY ON A HUMAN COLON XENOGRAFT IN NUDE-MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,LMB,BETHESDA,MD 20892. PHARMACIA CANAG,GOTHENBURG,SWEDEN. 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 1992 VL 40 IS 2 BP A211 EP A211 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100430 ER PT J AU DECLUE, JE PAPAGEORGE, AG VASS, WC JOHNSON, MR LOWY, DR AF DECLUE, JE PAPAGEORGE, AG VASS, WC JOHNSON, MR LOWY, DR TI ABNORMAL REGULATION AND PHARMACOLOGICAL CORRECTION OF THE RAS ONCOGENE PROTEIN IN MALIGNANT SCHWANNOMAS FROM PATIENTS WITH VONRECKLINGHAUSENS NEUROFIBROMATOSIS 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 1992 VL 40 IS 2 BP A545 EP A545 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102358 ER PT J AU DEGUCHI, Y WILSON, GL KEHRL, JH AF DEGUCHI, Y WILSON, GL KEHRL, JH TI A HUMAN HOMEOBOX GENE, HB24, IS IMPORTANT IN THE PROLIFERATION AND LINEAGE COMMITMENT OF HEMATOPOIETIC PROGENITOR CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1992 VL 40 IS 2 BP A350 EP A350 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101215 ER PT J AU DEGUCHI, Y KEHRL, JH AF DEGUCHI, Y KEHRL, JH TI INDUCTION OF T-CELL ACTIVATION AND IL-2 RECEPTOR EXPRESSION FOLLOWING EXPRESSION OF A HUMAN HOMEOBOX GENE, HB24, IN JURKAT CELLS AND IN TRANSGENIC MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1992 VL 40 IS 2 BP A251 EP A251 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100662 ER PT J AU DICHEK, HL PARROTT, C BREWER, HB SANTAMARINAFOJO, S AF DICHEK, HL PARROTT, C BREWER, HB SANTAMARINAFOJO, S TI FUNCTIONAL-CHARACTERIZATION OF A CHIMERIC PROTEIN GENETICALLY ENGINEERED FROM HUMAN LIPOPROTEIN-LIPASE AND HUMAN HEPATIC LIPASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,MOLEC DIS 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 1992 VL 40 IS 2 BP A312 EP A312 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101010 ER PT J AU DLUGOSZ, AA YUSPA, SH AF DLUGOSZ, AA YUSPA, SH TI ACTIVATION OF PROTEIN-KINASE-C REGULATES KERATIN-1 AND KERATINOCYTE TRANSGLUTAMINASE MESSENGER-RNA IN OPPOSITE DIRECTIONS 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 1992 VL 40 IS 2 BP A489 EP A489 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102022 ER PT J AU DUGAN, EM LINTON, JT KATZ, SI AF DUGAN, EM LINTON, JT KATZ, SI TI GRAFT VERSUS HOST-DISEASE (GVHD) - CORRELATION OF IMMUNE AND HISTOLOGICAL EVENTS AND ATTEMPTED PREVENTION WITH PUVA-TREATED LYMPHOCYTES 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 1992 VL 40 IS 2 BP A498 EP A498 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102076 ER PT J AU DULIEGE, AM GOEDERT, JJ AMOS, CI FELTON, S BIGGAR, RJ AF DULIEGE, AM GOEDERT, JJ AMOS, CI FELTON, S BIGGAR, RJ TI THE INTERNATIONAL REGISTRY OF HIV-EXPOSED TWINS - HIGH-RISK OF HIV-1 INFECTION FOR 1ST-BORN TWINS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. GENENTECH INC,S SAN FRANCISCO,CA. NCI,ROCKVILLE,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 1992 VL 40 IS 2 BP A246 EP A246 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100634 ER PT J AU ENK, AH KATZ, SI AF ENK, AH KATZ, SI TI IDENTIFICATION AND INDUCTION OF KERATINOCYTE-DERIVED INTERLEUKIN-10 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,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 1992 VL 40 IS 2 BP A499 EP A499 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102080 ER PT J AU ERZURUM, SC CHU, CS DANEL, C TRAPNELL, BC CRYSTAL, RG AF ERZURUM, SC CHU, CS DANEL, C TRAPNELL, BC CRYSTAL, RG TI INVIVO ANTIOXIDANT GENE-EXPRESSION IN HUMAN AIRWAY EPITHELIUM OF NORMAL INDIVIDUALS EXPOSED TO 100-PERCENT OXYGEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 1992 VL 40 IS 2 BP A318 EP A318 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101044 ER PT J AU FLACK, MR BENNET, AP FROEHLICH, J ANASTI, JN NISULA, BC AF FLACK, MR BENNET, AP FROEHLICH, J ANASTI, JN NISULA, BC TI SELECTIVE-INHIBITION OF FSH GLYCOSYLATION BY SITE-DIRECTED MUTAGENESIS - EFFECTS ON SECRETION AND BIOLOGIC ACTIVITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,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 1992 VL 40 IS 2 BP A206 EP A206 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100404 ER PT J AU FOLI, A YARCHOAN, R AF FOLI, A YARCHOAN, R TI MONOCYTE MACROPHAGES (M/M) PRODUCE INTERLEUKIN-6 (IL-6) AND TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA) IN RESPONSE TO GRANULOCYTE-MACROPHAGE COLONY STIMULATING FACTOR (GM-CSF) BUT NOT TO HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) ALONE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,MED 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 1992 VL 40 IS 2 BP A227 EP A227 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100518 ER PT J AU GALLIN, JI DECARLO, E KUHNS, DB AF GALLIN, JI DECARLO, E KUHNS, DB TI DECREASED INTERFERON-GAMMA AND INCREASED TNF-ALPHA IN SKIN BLISTERS OF PATIENTS WITH THE HYPERIMMUNOGLOBULIN E-RECURRENT INFECTION (JOBS) SYNDROME SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PRI,FREDERICK,MD 21702. 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 1992 VL 40 IS 2 BP A343 EP A343 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101176 ER PT J AU GARTENHAUS, RB LUNARDIISKANDAR, Y BERNEMAN, Z REITZ, M GALLO, RC KLOTMAN, ME AF GARTENHAUS, RB LUNARDIISKANDAR, Y BERNEMAN, Z REITZ, M GALLO, RC KLOTMAN, ME TI SOLUBLE RECOMBINANT HTLV-I TAX PROTEIN IS RELEASED FROM AND TAKEN UP BY CELLS-INVITRO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 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 1992 VL 40 IS 2 BP A169 EP A169 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100192 ER PT J AU GRAZIOSI, C PANTALEO, G KOTLER, DP FAUCI, AS AF GRAZIOSI, C PANTALEO, G KOTLER, DP FAUCI, AS TI DISSOCIATION BETWEEN HIV EXPRESSION IN PERIPHERAL-BLOOD VERSUS LYMPHOID ORGANS OF THE SAME PATIENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,NEW YORK,NY. ST LUKES ROOSEVELT HOSP,NEW YORK,NY 10025. RI Pantaleo, Giuseppe/K-6163-2016 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 1992 VL 40 IS 2 BP A333 EP A333 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101124 ER PT J AU HALLFRISCH, J MULLER, DC ANDRES, R AF HALLFRISCH, J MULLER, DC ANDRES, R TI TYPES AND SOURCES OF CARBOHYDRATE IN DIETS OF ADULT MEN AND WOMEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,CARBOHYDRATE NUTR LAB,BELTSVILLE,MD 20705. NIA,GERONTOL RES CTR,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 1992 VL 40 IS 2 BP A629 EP A629 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102848 ER PT J AU HAUN, RS SERVENTI, IM TSAI, SC LEE, CM CAVANAUGH, E STEVENS, L MOSS, J VAUGHAN, M AF HAUN, RS SERVENTI, IM TSAI, SC LEE, CM CAVANAUGH, E STEVENS, L MOSS, J VAUGHAN, M TI CHARACTERIZATION OF MAMMALIAN GENES ENCODING ADP-RIBOSYLATION FACTORS, 20-KDA GUANINE NUCLEOTIDE-BINDING PROTEIN ACTIVATORS OF CHOLERA-TOXIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB 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 1992 VL 40 IS 2 BP A248 EP A248 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100645 ER PT J AU HAUSER, P ZAMETKIN, AJ VITIELLO, B MARTINEZ, P MIXSON, AJ WEINTRAUB, BD AF HAUSER, P ZAMETKIN, AJ VITIELLO, B MARTINEZ, P MIXSON, AJ WEINTRAUB, BD TI ATTENTION-DEFICIT HYPERACTIVITY DISORDER IN 18 KINDREDS WITH GENERALIZED RESISTANCE TO THYROID-HORMONE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. 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 1992 VL 40 IS 2 BP A338 EP A338 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101151 ER PT J AU HAWK, ST BOUJOUKOS, AJ SUFFREDINI, AF AF HAWK, ST BOUJOUKOS, AJ SUFFREDINI, AF TI HIGH OUTPUT STATES IN PATIENTS WITH NONHODGKINS LYMPHOMA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,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 1992 VL 40 IS 2 BP A412 EP A412 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101578 ER PT J AU HIRUMA, H NOGUCHI, CT UYESAKA, N SCHECHTER, AN RODGERS, GP AF HIRUMA, H NOGUCHI, CT UYESAKA, N SCHECHTER, AN RODGERS, GP TI QUANTITATION OF THE EFFECTS OF INTRACELLULAR HEMOGLOBIN-S POLYMERIZATION ON ERYTHROCYTE FILTERABILITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,CHEM BIOL LAB,BETHESDA,MD. NIPPON MED COLL,DEPT PHYSIOL,TOKYO 113,JAPAN. 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 1992 VL 40 IS 2 BP A422 EP A422 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101633 ER PT J AU HOFFMAN, WD KOEV, CA BANKS, SM SOLOMON, MA NATANSON, C AF HOFFMAN, WD KOEV, CA BANKS, SM SOLOMON, MA NATANSON, C TI PHENYLEPHRINE DECREASES CANINE CARDIAC-PERFORMANCE BY EFFECTS ON DIASTOLIC FUNCTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,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 1992 VL 40 IS 2 BP A372 EP A372 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101344 ER PT J AU HOU, D JENSEN, JP CENCIARELLI, C DEAN, M WEISSMAN, AM AF HOU, D JENSEN, JP CENCIARELLI, C DEAN, M WEISSMAN, AM TI CROSS-SPECIES ANALYSIS OF THE T-CELL RECEPTOR ETA-SUBUNIT - LACK OF CONSERVATION OF AN ALTERNATIVE SPLICE OF THE ZETA-TRANSCRIPT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,EXPTL IMMUNOL 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 1992 VL 40 IS 2 BP A153 EP A153 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100094 ER PT J AU HSU, VW SHAH, N KLAUSNER, RD AF HSU, VW SHAH, N KLAUSNER, RD TI A BREFELDIN A-LIKE PHENOTYPE IS INDUCED BY THE OVEREXPRESSION OF A HUMAN ERD2-LIKE PROTEIN, ELP-1 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB 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 1992 VL 40 IS 2 BP A191 EP A191 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100322 ER PT J AU HULTSCH, T HOHMAN, RJ AF HULTSCH, T HOHMAN, RJ TI RAPAMYCIN INHIBITS IL-3 DEPENDENT PROLIFERATION OF MAST-CELLS AND OTHER HEMATOPOIETIC-CELLS - FK506 ANTAGONIZES THE EFFECT OF RAPAMYCIN 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 1992 VL 40 IS 2 BP A468 EP A468 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101898 ER PT J AU IKEWAKI, K RADER, DJ SAKAMOTO, T SCHAEFER, J THOMAS, F ISHIKAWA, T NAGANO, M ZECH, LA BREWER, HB AF IKEWAKI, K RADER, DJ SAKAMOTO, T SCHAEFER, J THOMAS, F ISHIKAWA, T NAGANO, M ZECH, LA BREWER, HB TI ABNORMAL INVIVO METABOLISM OF APOLIPOPROTEIN-B-100 IN HUMANS WITH CHOLESTEROL ESTER TRANSFER PROTEIN-DEFICIENCY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 1992 VL 40 IS 2 BP A291 EP A291 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100899 ER PT J AU JAFFE, HA DANEL, C LONGENECKER, G METZGER, M SETOGUCHI, Y ROSENFELD, MA GANT, TW THORGEIRSSON, SS STRATFORDPERRICAUDET, LD PERRICAUDET, M PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF JAFFE, HA DANEL, C LONGENECKER, G METZGER, M SETOGUCHI, Y ROSENFELD, MA GANT, TW THORGEIRSSON, SS STRATFORDPERRICAUDET, LD PERRICAUDET, M PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI INVIVO GENE-TRANSFER TO LIVER - ADENOVIRUS-MEDIATED TRANSFER AND EXPRESSION OF EXOGENOUS GENES IN NORMAL RAT-LIVER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. INST GUSTAVE ROUSSY,F-94805 VILLEJUIF,FRANCE. TRANSGENE SA,STRASBOURG,FRANCE. 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 1992 VL 40 IS 2 BP A252 EP A252 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100668 ER PT J AU JIANG, H ROBEY, FA GEWURZ, H AF JIANG, H ROBEY, FA GEWURZ, H TI IDENTIFICATION OF A SPECIFIC SEQUENCE IN THE COLLAGEN-LIKE REGION OF THE CLQ A-CHAIN AS THE BINDING-SITE FOR DNA, HEPARIN, FIBRONECTIN AND C-REACTIVE PROTEIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 RUSH MED COLL,CHICAGO,IL 60612. 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 1992 VL 40 IS 2 BP A299 EP A299 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100941 ER PT J AU JU, WD VASS, WC TAYEBI, N SCHILLER, JT LOWY, DR AF JU, WD VASS, WC TAYEBI, N SCHILLER, JT LOWY, DR TI TGF-ALPHA ENHANCES MOTILITY AND INDUCES MORPHOLOGICAL-CHANGES IN KERATINOCYTES 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 1992 VL 40 IS 2 BP A469 EP A469 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101902 ER PT J AU JUDD, JT TAYLOR, PR LONGCOPE, C JONES, DY NAIR, PP CAMPBELL, WS AF JUDD, JT TAYLOR, PR LONGCOPE, C JONES, DY NAIR, PP CAMPBELL, WS TI INFLUENCE OF TYPE AND AMOUNT OF DIETARY-FAT ON PLASMA-HORMONE LEVELS IN PREMENOPAUSAL WOMEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 USDA,BELTSVILLE HUMAN NUTR RES CTR,BELTSVILLE,MD 20705. 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 1992 VL 40 IS 2 BP A631 EP A631 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102858 ER PT J AU JUSTICE, J HAUN, RS AVIGAN, J MURTAGH, JJ MOSS, J VAUGHAN, M AF JUSTICE, J HAUN, RS AVIGAN, J MURTAGH, JJ MOSS, J VAUGHAN, M TI HYDROPHOBIC DOMAINS OF THE HETEROTRIMERIC GUANINE NUCLEOTIDE-BINDING PROTEINS EXAMINED BY PHASE PARTITIONING - PARTICIPATION OF THE AMINO AND CARBOXY TERMINI OF TRANSDUCIN ALPHA-SUBUNIT IN MEMBRANE INTERACTIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 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 1992 VL 40 IS 2 BP A223 EP A223 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100493 ER PT J AU KAHN, ML LEE, SW DICHEK, DA AF KAHN, ML LEE, SW DICHEK, DA TI DEVELOPMENT AND USE OF A PROTOCOL TO OPTIMIZE RETROVIRAL VECTOR-MEDIATED GENE-TRANSFER INTO BOVINE AORTIC ENDOTHELIAL-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,MOLEC 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 1992 VL 40 IS 2 BP A365 EP A365 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101301 ER PT J AU KARPATI, S AMAGAI, M CEHRS, K KLAUSKOVTUN, V STANLEY, JR AF KARPATI, S AMAGAI, M CEHRS, K KLAUSKOVTUN, V STANLEY, JR TI IGG LOCALIZES TO THE CORE OF SPLIT DESMOSOMES IN BLISTERS INDUCED BY PEMPHIGUS-VULGARIS (PV) ANTIBODIES IN NEONATAL MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,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 1992 VL 40 IS 2 BP A478 EP A478 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101957 ER PT J AU KATZ, P WHALEN, G KEHRL, JH AF KATZ, P WHALEN, G KEHRL, JH TI GERMINAL CENTER LYMPHOCYTES-B DIFFERENTIALLY EXPRESS A NOVEL PROTEIN-KINASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 GEORGETOWN UNIV,WASHINGTON,DC 20057. NIAID,BETHESDA,MD 20892. NR 1 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 1992 VL 40 IS 2 BP A295 EP A295 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100917 ER PT J AU KENNEY, RT MALECH, HL LETO, TL AF KENNEY, RT MALECH, HL LETO, TL TI STRUCTURAL CHARACTERIZATION OF THE P67PHOX GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF 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 1992 VL 40 IS 2 BP A261 EP A261 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100716 ER PT J AU KIM, LG MCBRIDE, OW WANG, M KIM, SY IDLER, WW STEINERT, PM AF KIM, LG MCBRIDE, OW WANG, M KIM, SY IDLER, WW STEINERT, PM TI STRUCTURE AND ORGANIZATION OF THE HUMAN TRANSGLUTAMINASE-1 (TGM-1) GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,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 1992 VL 40 IS 2 BP A490 EP A490 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102027 ER PT J AU KIM, MK MCCLASKEY, JH WEINTRAUB, BD AF KIM, MK MCCLASKEY, JH WEINTRAUB, BD TI REPRESSION OF THE EXPRESSION OF THE HUMAN THYROTROPIN-BETA (HTSH-BETA) GENE IN NON-THYROTROPIC CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,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 1992 VL 40 IS 2 BP A310 EP A310 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100998 ER PT J AU KING, CL MAHANTY, S KUMARASWAMI, V ABRAMS, JS RAGUNATHAN, J JAYARAMAN, K OTTESEN, EA NUTMAN, TB AF KING, CL MAHANTY, S KUMARASWAMI, V ABRAMS, JS RAGUNATHAN, J JAYARAMAN, K OTTESEN, EA NUTMAN, TB TI TOLERANCE IN HUMAN LYMPHATIC FILARIASIS - PREFERENTIAL INDUCTION OF A REGULATORY TH2 LYMPHOCYTE SUBSET SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. NIH,PARASIT DIS LAB,BETHESDA,MD 20892. ANNA UNIV,MADRAS,INDIA. DNAX RES INST MOLEC & CELLULAR BIOL INC,PALO ALTO,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 1992 VL 40 IS 2 BP A199 EP A199 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100367 ER PT J AU KLEINBERG, ME MALECH, HL MITAL, D LETO, TL AF KLEINBERG, ME MALECH, HL MITAL, D LETO, TL TI P47-PHOX IS THE 1ST CYTOSOL PROTEIN TO PARTICIPATE IN FORMATION OF THE PHAGOCYTE NADPH OXIDASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MARYLAND,SCH MED,DEPT MED,BALTIMORE,MD 21201. VET ADM MED CTR,BALTIMORE,MD 21218. NIAID,HOST DEF 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 1992 VL 40 IS 2 BP A351 EP A351 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101219 ER PT J AU KLEMPNER, MS SCHWAN, TG AF KLEMPNER, MS SCHWAN, TG TI ANTIBODIES TO A 39 KDA ANTIGEN OF BORRELIA-BURGDORFERI ARE A SPECIFIC MARKER OF LATE BUT NOT EARLY HUMAN LYME-DISEASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NEW ENGLAND MED CTR HOSP,BOSTON,MA 02111. NIH,ROCKY MT LABS,HAMILTON,MT. 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 1992 VL 40 IS 2 BP A214 EP A214 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100443 ER PT J AU KLOTMAN, ME BERNEMAN, ZN VAUGHNS, J GALLO, RC AF KLOTMAN, ME BERNEMAN, ZN VAUGHNS, J GALLO, RC TI DETECTION AND QUANTITATION OF ALTERNATIVELY SPLICED PX MESSENGER-RNA IN HTLV-1 INFECTED-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 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 1992 VL 40 IS 2 BP A169 EP A169 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100193 ER PT J AU KOPP, JB ROONEY, JF WOHLENBERG, C DORFMAN, N MARINOS, NJ BRYANT, JL NOTKINS, AL KLOTMAN, PE AF KOPP, JB ROONEY, JF WOHLENBERG, C DORFMAN, N MARINOS, NJ BRYANT, JL NOTKINS, AL KLOTMAN, PE TI HYPERKERATOTIC SKIN DISORDERS IN HIV-TRANSGENIC MICE ARE ASSOCIATED WITH INCREASED TRANSGENE EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,LDB,LOM,BETHESDA,MD 20892. NIDR,ACU,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 1992 VL 40 IS 2 BP A309 EP A309 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100993 ER PT J AU KORGE, B GAN, SO YONEDA, K COMPTON, JG VOLZ, A STEINERT, PM ZIEGLER, A MISCHKE, D AF KORGE, B GAN, SO YONEDA, K COMPTON, JG VOLZ, A STEINERT, PM ZIEGLER, A MISCHKE, D TI PHYSICAL MAPPING OF THE EPIDERMAL DIFFERENTIATION MARKERS LORICRIN, PROFILAGGRIN AND INVOLUCRIN ON CHROMOSOME 1Q21 BY PULSED FIELD ELECTROPHORESIS 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 1992 VL 40 IS 2 BP A490 EP A490 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102028 ER PT J AU KOZLOW, EJ HONG, JX WILSON, GL KEHRL, JH AF KOZLOW, EJ HONG, JX WILSON, GL KEHRL, JH TI ISOLATION AND CHARACTERIZATION OF GENES WHICH ARE SPECIFICALLY EXPRESSED IN LYMPHOCYTES-B SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1992 VL 40 IS 2 BP A197 EP A197 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100352 ER PT J AU KULKARNI, AB BECKER, D LYGHT, M HUH, CG GEISER, A KARLSSON, S AF KULKARNI, AB BECKER, D LYGHT, M HUH, CG GEISER, A KARLSSON, S TI MOUSE CHIMERAS WITH A DISRUPTED TRANSFORMING GROWTH FACTOR-BETA-1 GENE OBTAINED BY GENE TARGETING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NINCDS,DEV & METAB NEUROL BRANCH,MOLEC & MED GENET SECT,BETHESDA,MD 20892. NCI,CHEMOPREVENT 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 1992 VL 40 IS 2 BP A295 EP A295 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100920 ER PT J AU KUNA, P REDDIGARI, SR RUCINSKI, D OPPENHEIM, JJ SCHALL, TJ KAPLAN, AP AF KUNA, P REDDIGARI, SR RUCINSKI, D OPPENHEIM, JJ SCHALL, TJ KAPLAN, AP TI CHARACTERIZATION OF HUMAN HISTAMINE RELEASING FACTORS (HRF) AS A GROUP OF CYTOKINES BELONG TO THE INTERCRINE CYTOKINE FAMILY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 SUNY STONY BROOK,DEPT MED,STONY BROOK,NY 11794. NCI,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21701. GENENTECH INC,SAN FRANCISCO,CA 94080. 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 1992 VL 40 IS 2 BP A228 EP A228 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100527 ER PT J AU LARSON, DE RISING, R ANDERSON, TE FERRARO, R FONTVIEILLE, AM RAVUSSIN, E AF LARSON, DE RISING, R ANDERSON, TE FERRARO, R FONTVIEILLE, AM RAVUSSIN, E TI SPONTANEOUS OVERFEEDING WITH A CAFETERIA DIET - EFFECTS ON 24-H ENERGY-EXPENDITURE AND SUBSTRATE OXIDATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ. 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 1992 VL 40 IS 2 BP A632 EP A632 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102865 ER PT J AU LEE, ES KATZ, SI JU, WD NECKERS, L AF LEE, ES KATZ, SI JU, WD NECKERS, L TI TRANSFORMING GROWTH FACTOR-ALPHA (TGF-ALPHA) IS AN AUTOCRINE GROWTH-FACTOR FOR HUMAN DERMAL FIBROBLASTS AND NIH/3T3 CELLS 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 1992 VL 40 IS 2 BP A470 EP A470 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101908 ER PT J AU LEE, MM LAMBERT, WC ANDREWS, A KRAEMER, KH AF LEE, MM LAMBERT, WC ANDREWS, A KRAEMER, KH TI THE ROLE OF ULTRAVIOLET-RADIATION IN HUMAN-MELANOMA AND NONMELANOMA SKIN-CANCER - STUDIES OF XERODERMA-PIGMENTOSUM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CMDNJ,DEPT DERMATOL,NEWARK,NJ. NCI,DEPT DERMATOL,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. COLUMBIA UNIV,DEPT DERMATOL,NEW YORK,NY 10027. 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 1992 VL 40 IS 2 BP A458 EP A458 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101837 ER PT J AU LEE, SC KIM, IG MCBRIDE, OW COMPTON, JG OKEEFE, E STEINERT, PM AF LEE, SC KIM, IG MCBRIDE, OW COMPTON, JG OKEEFE, E STEINERT, PM TI THE HUMAN TRICHOHYALIN GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT DERMATOL,CHAPEL HILL,NC 27514. 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 1992 VL 40 IS 2 BP A490 EP A490 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102029 ER PT J AU LEE, SW KAHN, ML DICHEK, DA AF LEE, SW KAHN, ML DICHEK, DA TI APICAL EXPRESSION OF ENZYMATICALLY ACTIVE ANCHORED UROKINASE IN BOVINE AORTIC ENDOTHELIAL-CELLS INVITRO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,MOLEC 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 1992 VL 40 IS 2 BP A192 EP A192 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100326 ER PT J AU LEMARCHAND, P JAFFE, HA DANEL, C CID, M KLEINMAN, HK STRATFORDPERRICAUDET, LD PERRICAUDET, M PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF LEMARCHAND, P JAFFE, HA DANEL, C CID, M KLEINMAN, HK STRATFORDPERRICAUDET, LD PERRICAUDET, M PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI ADENOVIRUS-MEDIATED TRANSFER AND EXPRESSION OF EXOGENOUS GENES TO HUMAN ENDOTHELIAL-CELLS IN INTACT HUMAN BLOOD-VESSELS EXVIVO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NIDR,BETHESDA,MD 20892. INST GUSTAVE ROUSSY,F-94805 VILLEJUIF,FRANCE. TRANSGENE SA,STRASBOURG,FRANCE. 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 1992 VL 40 IS 2 BP A226 EP A226 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100510 ER PT J AU LETO, TL GARRETT, MC AF LETO, TL GARRETT, MC TI SRC-LIKE (SH3) DOMAINS OF P67-PHOX ARE NOT ESSENTIAL FOR CELL-FREE RECONSTITUTION OF NADPH OXIDASE ACTIVITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF 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 1992 VL 40 IS 2 BP A175 EP A175 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100229 ER PT J AU LEVY, DD GROOPMAN, JD LIM, SE SEIDMAN, MM KRAEMER, KH AF LEVY, DD GROOPMAN, JD LIM, SE SEIDMAN, MM KRAEMER, KH TI MUTAGENIC SPECTRUM OF AFLATOXIN-B1 EPOXIDE INDUCED DNA ADDUCTS IN A SHUTTLE VECTOR PLASMID FOLLOWING REPLICATION IN XERODERMA-PIGMENTOSUM AND DNA-REPAIR PROFICIENT HUMAN FIBROBLASTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. OTSUKA PHARMACEUT CO LTD,ROCKVILLE,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 1992 VL 40 IS 2 BP A547 EP A547 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102367 ER PT J AU LEVYTOLEDANO, R ACCILI, D TAYLOR, SI AF LEVYTOLEDANO, R ACCILI, D TAYLOR, SI TI DELETION OF C-TERMINAL 113 AMINO-ACIDS OF HUMAN INSULIN-RECEPTOR IMPAIRS RECEPTOR AUTOPHOSPHORYLATION AND INTERNALIZATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DIABET 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 1992 VL 40 IS 2 BP A321 EP A321 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101062 ER PT J AU LI, L KRUSZEWSKI, FH PUNNONEN, K YUSPA, SH HENNINGS, H TUCKER, RW AF LI, L KRUSZEWSKI, FH PUNNONEN, K YUSPA, SH HENNINGS, H TUCKER, RW TI THE MECHANISM OF STRONTIUM INDUCED TERMINAL DIFFERENTIATION IN CULTURED MOUSE KERATINOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV HOSP,CTR ONCOL,BALTIMORE,MD 21205. 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 1992 VL 40 IS 2 BP A515 EP A515 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102180 ER PT J AU LICHTI, U WEINBERG, WC GOODMAN, L LEDBETTER, S DOOLEY, T MORGAN, D YUSPA, SH AF LICHTI, U WEINBERG, WC GOODMAN, L LEDBETTER, S DOOLEY, T MORGAN, D YUSPA, SH TI IMMORTALIZED DERMAL PAPILLA CELLS SUPPORT HAIR-GROWTH IN A MINIMAL COMPONENT NUDE-MOUSE GRAFT MODEL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT,BETHESDA,MD 20892. UPJOHN CO,CANC RES,KALAMAZOO,MI 49001. RI Weinberg, Wendy/A-8920-2009 NR 1 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 1992 VL 40 IS 2 BP A443 EP A443 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101748 ER PT J AU LIU, ZY SCHECHTER, AN NOGUCHI, CT AF LIU, ZY SCHECHTER, AN NOGUCHI, CT TI EXPRESSION OF THE HUMAN ERYTHROPOIETIN RECEPTOR GENE IN TRANSGENIC MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,CHEM BIOL LAB,BETHESDA,MD. NR 1 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 1992 VL 40 IS 2 BP A350 EP A350 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101214 ER PT J AU MAHANTY, S KING, CL ABRAMS, JS KUMARASWAMI, V RAGUNATHAN, J JAYARAMAN, K OTTESEN, EA NUTMAN, TB AF MAHANTY, S KING, CL ABRAMS, JS KUMARASWAMI, V RAGUNATHAN, J JAYARAMAN, K OTTESEN, EA NUTMAN, TB TI PARASITE ANTIGENS SELECTIVELY EXPAND A TH2-LIKE CELL-POPULATION IN HELMINTH-INFECTED INDIVIDUALS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. DNAX RES INST MOLEC & CELLULAR BIOL INC,PALO ALTO,CA. TB RES CTR,MADRAS,INDIA. ANNA UNIV,MADRAS,INDIA. 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 1992 VL 40 IS 2 BP A329 EP A329 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101105 ER PT J AU MANGELS, AR MORRIS, VC BLOCK, G LEVANDER, OA TAYLOR, PR AF MANGELS, AR MORRIS, VC BLOCK, G LEVANDER, OA TAYLOR, PR TI URINARY MALONDIALDEHYDE (MDA) IN ADULT MEN DURING ASCORBIC-ACID (AA) DEPLETION AND REPLETION WITH AND WITHOUT IRON SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 USDA,BELTSVILLE HUMAN NUTR RES CTR,BELTSVILLE,MD 20705. NCI,BETHESDA,MD 20892. RI Block, Gladys/E-3304-2010 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 1992 VL 40 IS 2 BP A633 EP A633 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102872 ER PT J AU MAUVIEL, A REITAMO, S REMITZ, A CESKA, M BAGGIOLINI, M WALZ, A EVANS, CH UITTO, J AF MAUVIEL, A REITAMO, S REMITZ, A CESKA, M BAGGIOLINI, M WALZ, A EVANS, CH UITTO, J TI LEUKOREGULIN IS A POTENT INDUCER OF IL-8 GENE-EXPRESSION IN HUMAN SKIN FIBROBLASTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,DEPT DERMATOL,PHILADELPHIA,PA 19107. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. THEODOR KOCHER INST,BERN,AUSTRIA. NCI,BIOL LAB,TUMOR BIOL SECT,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 1992 VL 40 IS 2 BP A471 EP A471 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101913 ER PT J AU MAUVIEL, A KAHARI, VM KURKINEN, M EVANS, CH UITTO, J AF MAUVIEL, A KAHARI, VM KURKINEN, M EVANS, CH UITTO, J TI TRANSCRIPTIONAL ACTIVATION OF FIBROBLAST STROMELYSIN-1 GENE-EXPRESSION BY A NOVEL LYMPHOKINE, LEUKOREGULIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT DERMATOL,PHILADELPHIA,PA 19107. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,PISCATAWAY,NJ 08854. NCI,BIOL LAB,TUMOR BIOL SECT,BETHESDA,MD 20892. NR 1 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 1992 VL 40 IS 2 BP A307 EP A307 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100985 ER PT J AU MCAREAVEY, D BARTLETT, T FANANAPAZIR, L AF MCAREAVEY, D BARTLETT, T FANANAPAZIR, L TI SYNCOPE IN PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY - ETIOLOGY AND LONG-TERM OUTCOME FOLLOWING CORRECTION OF HEMODYNAMIC AND ELECTROPHYSIOLOGIC ABNORMALITIES 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 1992 VL 40 IS 2 BP A403 EP A403 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101525 ER PT J AU MOFENSON, LM BETHEL, J MOYE, J AF MOFENSON, LM BETHEL, J MOYE, J TI EFFECT OF INTRAVENOUS IMMUNOGLOBULIN (IG), PCP PROPHYLAXIS (PRO) AND AZT ON PREVENTION OF INFECTIONS IN HIV-INFECTED CHILDREN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,PAMA,BETHESDA,MD. WESTAT CORP,ROCKVILLE,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 1992 VL 40 IS 2 BP A380 EP A380 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101389 ER PT J AU MURAYAMA, T TSAI, SC ADAMIK, R MOSS, J AF MURAYAMA, T TSAI, SC ADAMIK, R MOSS, J TI ROLE OF HOST FACTORS IN ADAPTATION OF CHOLERA-TOXIN TO PHYSIOLOGICAL TEMPERATURES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,CELLULAR 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 1992 VL 40 IS 2 BP A289 EP A289 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100884 ER PT J AU MURTAGH, JJ LEE, FJS LEE, CM MOSS, J VAUGHAN, M AF MURTAGH, JJ LEE, FJS LEE, CM MOSS, J VAUGHAN, M TI CHARACTERIZATION OF MULTIGENE FAMILIES OF GUANINE NUCLEOTIDE-BINDING PROTEINS - BIOTIN-ENHANCED POLYMERASE CHAIN-REACTION STRATEGIES FOR RAPID SEQUENCING AND CLONING OF ADP-RIBOSYLATION FACTORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 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 1992 VL 40 IS 2 BP A223 EP A223 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100495 ER PT J AU NIEMAN, L DOPPMAN, J TRAVIS, W CHROUSOS, G NORTON, J CUTLER, GB AF NIEMAN, L DOPPMAN, J TRAVIS, W CHROUSOS, G NORTON, J CUTLER, GB TI MASSIVE MACRONODULAR ADRENAL DISEASE - A RARE CAUSE OF CUSHING SYNDROME SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. NCI,BETHESDA,MD 20892. NIH,BETHESDA,MD 20892. NR 1 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 1992 VL 40 IS 2 BP A206 EP A206 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100402 ER PT J AU OSHEA, JJ MCVICAR, DW BAILEY, TL BURNS, C SMYTH, MJ AF OSHEA, JJ MCVICAR, DW BAILEY, TL BURNS, C SMYTH, MJ TI ACTIVATION OF HUMAN PERIPHERAL-BLOOD T-CELLS BY PHARMACOLOGICAL INDUCTION OF PROTEIN TYROSINE PHOSPHORYLATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,FCRDC,BRMP,LEI,LCBS,FREDERICK,MD 21701. NCI,FCRDC,DYNCORP,PRI,BCDP,FREDERICK,MD 21701. 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 1992 VL 40 IS 2 BP A153 EP A153 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100097 ER PT J AU OSULLIVAN, MJ BOYER, P SCOTT, G PARKS, W WELLER, S BLUM, MR BALSLEY, J GILLESPIE, S MITCHELL, C BRYSON, YJ AF OSULLIVAN, MJ BOYER, P SCOTT, G PARKS, W WELLER, S BLUM, MR BALSLEY, J GILLESPIE, S MITCHELL, C BRYSON, YJ TI A PHASE-I STUDY OF THE PHARMACOKINETICS AND SAFETY OF ZIDOVUDINE IN 3RD TRIMESTER HIV-1 INFECTED PREGNANT-WOMEN AND THEIR INFANTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MIAMI,DEPT OBSTET,MIAMI,FL 33152. UNIV MIAMI,DEPT PEDIAT,MIAMI,FL 33152. UNIV CALIF LOS ANGELES,MED CTR,LOS ANGELES,CA 90024. NYU,DEPT PEDIAT,NEW YORK,NY 10003. NYU,DEPT OBSTET,NEW YORK,NY 10003. BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC 27709. NIAID,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 1992 VL 40 IS 2 BP A333 EP A333 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101126 ER PT J AU OTANI, H LEONARD, WJ AF OTANI, H LEONARD, WJ TI THE TYROSINE KINASE INHIBITOR, HERBIMYCIN-A, AND THE CALCIUM IONOPHORE, A23187, HAVE OPPOSING EFFECTS ON APOPTOSIS IN 32D CELLS TRANSDUCED WITH THE HUMAN IL-2 RECEPTOR BETA-CHAIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD. NICHHD,MOLEC GENET LAB,BETHESDA,MD. NHLBI,IRP,OD,PULM & MOLEC IMMUNOL SECT,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 1992 VL 40 IS 2 BP A295 EP A295 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100918 ER PT J AU PANTALEO, G TREBAI, N GRAZIOSI, C LANE, HC SEKALY, RP FAUCI, AS AF PANTALEO, G TREBAI, N GRAZIOSI, C LANE, HC SEKALY, RP FAUCI, AS TI PERTURBATION OF THE T-CELL RECEPTOR V-BETA REPERTOIRE IN PERIPHERAL-BLOOD T-CELLS OF HIV INFECTED INDIVIDUALS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID, IMMUNOREGULAT LAB, BETHESDA, MD 20892 USA. INST RECH CLIN MONTREAL, IMMUNOL LAB, MONTREAL H2W 1R7, QUEBEC, CANADA. RI Pantaleo, Giuseppe/K-6163-2016 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 1992 VL 40 IS 2 BP A253 EP A253 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100671 ER PT J AU PARRIS, CN KRAEMER, KH AF PARRIS, CN KRAEMER, KH TI THE CONTRIBUTION OF UV INDUCED CYCLOBUTANE PYRIMIDINE DIMERS AND OTHER DNA PHOTOPRODUCTS TO MUTAGENESIS IN A SHUTTLE VECTOR REPLICATED IN COCKAYNE SYNDROME 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 1992 VL 40 IS 2 BP A542 EP A542 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102340 ER PT J AU PATCHEV, VK KALOGERAS, K ZELAZOWSKI, P WILDER, RL CHROUSOS, GP AF PATCHEV, VK KALOGERAS, K ZELAZOWSKI, P WILDER, RL CHROUSOS, GP TI INCREASED VASOPRESSIN SYNTHESIS AND SECRETION IN INFLAMMATORY DISEASE-SUSCEPTIBLE LEWIS RATS - POTENTIAL PATHOPHYSIOLOGIC IMPLICATIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. NIAMDD,ARB,BETHESDA,MD 20892. NIMH,CNB,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 1992 VL 40 IS 2 BP A269 EP A269 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100766 ER PT J AU PAULY, RR SOLLOTT, S MONTICONE, R WEINSTEIN, C BURNETT, M BALASUBRAMANIAN, S CROW, M PASSANITI, A LAKATTA, EG AF PAULY, RR SOLLOTT, S MONTICONE, R WEINSTEIN, C BURNETT, M BALASUBRAMANIAN, S CROW, M PASSANITI, A LAKATTA, EG TI VASCULAR SMOOTH-MUSCLE CELL INVASION BUT NOT CHEMOTAXIS IS INHIBITED BY BUFFERING INTRACELLULAR CALCIUM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,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 1992 VL 40 IS 2 BP A345 EP A345 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101190 ER PT J AU PEREIRA, GMB ESQUENAZI, DA FELIPEDASILVA, MCS GALLO, MEN SARNO, EN SHEVACH, EM AF PEREIRA, GMB ESQUENAZI, DA FELIPEDASILVA, MCS GALLO, MEN SARNO, EN SHEVACH, EM TI RECONSTITUTION OF SEVERE COMBINED IMMUNODEFICIENT MICE WITH MONONUCLEAR-CELLS FROM PATIENTS WITH LEPROSY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. UNIV ESTADO RIO DE JANEIRO,FCM,FDN OSWALDO CRUZ,RIO DE JANEIRO,BRAZIL. SECRETARIA SAUDE,BELO HORIZONTE,MG,BRAZIL. 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 1992 VL 40 IS 2 BP A288 EP A288 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100882 ER PT J AU PETRIDES, JS MUELLER, GP KALOGERAS, KT CHROUSOS, GP DEUSTER, PA AF PETRIDES, JS MUELLER, GP KALOGERAS, KT CHROUSOS, GP DEUSTER, PA TI EXERCISE-INDUCED ACTIVATION OF THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS - DIFFERENTIAL SENSITIVITY TO GLUCOCORTICOID SUPPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PHYSIOL,BETHESDA,MD 20814. UNIFORMED SERV UNIV HLTH SCI,DEPT MIL MED,BETHESDA,MD 20814. 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 1992 VL 40 IS 2 BP A374 EP A374 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101355 ER PT J AU POLI, G KINTER, AL FAUCI, AS AF POLI, G KINTER, AL FAUCI, AS TI N-ACETYL-L-CYSTEINE (NAC) IS A POTENT SUPPRESSOR OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) TRANSCRIPTION IN PERSISTENTLY INFECTED-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1992 VL 40 IS 2 BP A333 EP A333 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101121 ER PT J AU POMMERENKE, F ACKERMAN, S AF POMMERENKE, F ACKERMAN, S TI THE USE OF LOCAL MORTALITY STATISTICS TO TARGET CANCER CONTROL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. CTR DIS CONTROL,ATLANTA,GA 30333. 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 1992 VL 40 IS 2 BP A609 EP A609 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102737 ER PT J AU QUEZADO, ZMN NATANSON, C BANKS, SM ALLING, DW KOEV, CA DANNER, RL ELIN, RJ HOSSEINI, JM POLLACK, M BACHER, JD DOLAN, DP HOFFMAN, WD AF QUEZADO, ZMN NATANSON, C BANKS, SM ALLING, DW KOEV, CA DANNER, RL ELIN, RJ HOSSEINI, JM POLLACK, M BACHER, JD DOLAN, DP HOFFMAN, WD TI A HUMAN-IGM MONOCLONAL-ANTIBODY (MAB) AGAINST ENDOTOXIN (HA-1A) DECREASED SURVIVAL IN A CANINE MODEL OF GRAM-NEGATIVE BACTERIAL SEPTIC SHOCK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 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 1992 VL 40 IS 2 BP A286 EP A286 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100867 ER PT J AU QUON, MJ CAMA, A TAYLOR, SI AF QUON, MJ CAMA, A TAYLOR, SI TI POST-BINDING STUDIES OF 5 NATURALLY-OCCURRING MUTATIONS IN THE HUMAN INSULIN-RECEPTOR GENE - ABNORMAL INSULIN-STIMULATED C-JUN EXPRESSION AND THYMIDINE INCORPORATION DESPITE NORMAL RECEPTOR AUTOPHOSPHORYLATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,DIABET BRANCH,BETHESDA,MD. RI Quon, Michael/B-1970-2008 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 1992 VL 40 IS 2 BP A321 EP A321 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101060 ER PT J AU RAY, PE HORIKOSHI, S BRUGGEMAN, LA KLOTMAN, PE AF RAY, PE HORIKOSHI, S BRUGGEMAN, LA KLOTMAN, PE TI ANGIOTENSIN-II (AII) INCREASES FIBRONECTIN EXPRESSION IN CULTURED HUMAN FETAL MESANGIAL CELLS (HFMC) BY BINDING TO TYPE-I AII-RECEPTORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,LDB,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,WASHINGTON,DC. 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 1992 VL 40 IS 2 BP A353 EP A353 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101229 ER PT J AU REINCKE, M KARL, M TRAVIS, W CHROUSOS, G AF REINCKE, M KARL, M TRAVIS, W CHROUSOS, G TI NO EVIDENCE OF CONSTITUTIVELY ACTIVATING POINT MUTATIONS IN THE STIMULATING AND INHIBITING G-PROTEIN IN HUMAN ADRENAL NEOPLASMS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,CTR CLIN,DEV ENDOCRINOL BRANCH,BETHESDA,MD. NR 2 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 1992 VL 40 IS 2 BP A436 EP A436 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101715 ER PT J AU RESZKA, K SALOPEK, TG JIMBOW, K CHIGNELL, CF AF RESZKA, K SALOPEK, TG JIMBOW, K CHIGNELL, CF TI PHOTOLYSIS OF PHEOMELANIN, ITS PRECURSOR 5-CYSTEINYLDOPA AND A EUMELANIN METABOLITE, 5-HYDROXY-6-METHOXYINDOLE-2-CARBOXYLIC ACID WITH UV-LIGHT ABOVE 300 NM - AN EPR AND SPIN TRAPPING STUDY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. 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 1992 VL 40 IS 2 BP A543 EP A543 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102344 ER PT J AU RISING, R LARSON, DE RAVUSSIN, E AF RISING, R LARSON, DE RAVUSSIN, E TI DO OBESE EAT FASTER THAN LEAN SUBJECTS - FOOD-INTAKE STUDIES IN PIMA-INDIANS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,PHOENIX,AZ. 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 1992 VL 40 IS 2 BP A636 EP A636 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102892 ER PT J AU ROACH, P ARAKAKI, RF ACCILI, D TAYLOR, SI GORDEN, P AF ROACH, P ARAKAKI, RF ACCILI, D TAYLOR, SI GORDEN, P TI EXTREME INSULIN RESISTANCE ASSOCIATED WITH DECREASED TYROSINE KINASE-ACTIVITY - MUTATION IN THE INSULIN-RECEPTOR BETA-SUBUNIT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,DIAB BRANCH,BETHESDA,MD. NR 1 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 1992 VL 40 IS 2 BP A311 EP A311 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101007 ER PT J AU ROCKEN, M URBAN, J SHEVACH, EM AF ROCKEN, M URBAN, J SHEVACH, EM TI CD4+ T-CELLS FROM ANIMALS TOLERIZED TO STAPHYLOCOCCAL ENTEROTOXIN-B(SEB) CAN ACT AS T-HELPER-2 (TH2) EFFECTOR-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. USDA,BELTSVILLE,MD 20705. 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 1992 VL 40 IS 2 BP A505 EP A505 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102115 ER PT J AU RODGERS, GP HUANG, SZ LU, ZH REN, ZR SCHECHTER, AN ZENG, YT AF RODGERS, GP HUANG, SZ LU, ZH REN, ZR SCHECHTER, AN ZENG, YT TI HYDROXYUREA THERAPY IN BETA-THALASSEMIA-INTERMEDIA - IMPROVEMENT IN HEMATOLOGICAL PARAMETERS DUE TO ENHANCED BETA-GLOBIN SYNTHESIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. INST MED GENET,SHANGHAI,PEOPLES R CHINA. 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 1992 VL 40 IS 2 BP A282 EP A282 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100844 ER PT J AU ROMAN, DG DANCIS, A ANDERSON, GJ KLAUSNER, RD AF ROMAN, DG DANCIS, A ANDERSON, GJ KLAUSNER, RD TI THE FERRIC REDUCTASE GENE OF SCHIZOSACCHAROMYCES-POMBE - TRANSCRIPTIONAL CONTROL BY IRON AND SEQUENCE SIMILARITY WITH HUMAN PHAGOCYTE NADPH OXIDASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. RI Anderson, Gregory/G-4148-2013 OI Anderson, Gregory/0000-0002-8814-5866 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 1992 VL 40 IS 2 BP A168 EP A168 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100186 ER PT J AU ROONEY, JF MANNIX, ML DUMOIS, J WOHLENBERG, CR ALLING, D STRAUS, SE NOTKINS, AL AF ROONEY, JF MANNIX, ML DUMOIS, J WOHLENBERG, CR ALLING, D STRAUS, SE NOTKINS, AL TI SUPPRESSION OF FREQUENTLY RECURRENT HERPES LABIALIS BY DAILY ORAL ACYCLOVIR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,ORAL MED LAB,BETHESDA,MD 20892. 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 1992 VL 40 IS 2 BP A319 EP A319 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101048 ER PT J AU ROSENBERG, HF GALLIN, JI AF ROSENBERG, HF GALLIN, JI TI NEUTROPHIL SPECIFIC GRANULE DEFICIENCY INCLUDES EOSINOPHILS AND LIKELY IS A DEFECT OF TRANSCRIPTIONAL REGULATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 2 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 1992 VL 40 IS 2 BP A283 EP A283 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100848 ER PT J AU ROSENFELD, MA ROSENTHAL, ER WERSTO, RP YONEYAMA, K YOSHIMURA, K STRATFORDPERRICAUDET, LD PERRICAUDET, M DALEMANS, W PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF ROSENFELD, MA ROSENTHAL, ER WERSTO, RP YONEYAMA, K YOSHIMURA, K STRATFORDPERRICAUDET, LD PERRICAUDET, M DALEMANS, W PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI ADENOVIRUS-MEDIATED TRANSFER OF THE NORMAL HUMAN CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) CDNA TO FRESHLY ISOLATED NORMAL AND CYSTIC-FIBROSIS 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. NR 1 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 1992 VL 40 IS 2 BP A317 EP A317 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101039 ER PT J AU ROTROSEN, D YEUNG, CL LETO, TL MALECH, HL KWONG, CH AF ROTROSEN, D YEUNG, CL LETO, TL MALECH, HL KWONG, CH TI ANALYSIS OF NADPH OXIDASE ACTIVATION IN A CELL-FREE SYSTEM COMPRISED OF PURIFIED PROTEIN-COMPONENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 1 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 1992 VL 40 IS 2 BP A351 EP A351 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101218 ER PT J AU SCHNITTMAN, SM DAVEY, RT HANEIWICH, S FAUCI, AS LANE, HC AF SCHNITTMAN, SM DAVEY, RT HANEIWICH, S FAUCI, AS LANE, HC TI A PHASE-I STUDY OF ALPHA-INTERFERON (IFN-ALPHA) IN COMBINATION WITH INTERLEUKIN-2 (IL-2) IN PATIENTS WITH HIV-INFECTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,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 1992 VL 40 IS 2 BP A246 EP A246 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100630 ER PT J AU SEKHSARIA, S GALLIN, JL KUHNS, DB MALECH, HL AF SEKHSARIA, S GALLIN, JL KUHNS, DB MALECH, HL TI ENDOTOXIN INCREASES MYELOID PRECURSORS IN PERIPHERAL-BLOOD SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD 21701. 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 1992 VL 40 IS 2 BP A287 EP A287 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100874 ER PT J AU SHULKIN, DJ GLICK, H KINOSIAN, B GLENPUSCHETT, C SIRO, C AF SHULKIN, DJ GLICK, H KINOSIAN, B GLENPUSCHETT, C SIRO, C TI EXPLAINING COST VARIATIONS USING SEVERITY OF ILLNESS MEASURES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV PENN,PHILADELPHIA,PA 19104. 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 1992 VL 40 IS 2 BP A591 EP A591 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102624 ER PT J AU SICHIERI, R LOLIO, CA EVERHART, JE AF SICHIERI, R LOLIO, CA EVERHART, JE TI GEOGRAPHICAL VARIATION OF CARDIOVASCULAR-DISEASE AND CANCER MORTALITY IN BRAZIL - AN ECOLOGIC STUDY OF SELECTED DIETARY FACTORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MARINGA,NUPENS,MARINGA,BRAZIL. NIDDK,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 1992 VL 40 IS 2 BP A640 EP A640 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102912 ER PT J AU SIRIO, CA KNAUS, WA WAGNER, DP ZIMMERMAN, JE AF SIRIO, CA KNAUS, WA WAGNER, DP ZIMMERMAN, JE TI PREDICTING PATIENT LENGTH OF STAY (LOS) IN THE INTENSIVE-CARE UNIT (ICU) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,INTENS CARE UNIT RES UNIT,WASHINGTON,DC 20052. NIH,DEPT CRIT CARE MED,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 1992 VL 40 IS 2 BP A303 EP A303 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100963 ER PT J AU SMITH, CJ KRALL, J MEACCI, E MANGANIELLO, VC MOVSESIAN, MA AF SMITH, CJ KRALL, J MEACCI, E MANGANIELLO, VC MOVSESIAN, MA TI PHOSPHORYLATION OF MYOCARDIAL CGMP-INHIBITED CAMP PHOSPHODIESTERASE BY CAMP-DEPENDENT PROTEIN-KINASE - COMPARISON OF CYTOSOLIC AND SARCOPLASMIC RETICULUM-ASSOCIATED ENZYMES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV UTAH,SALT LAKE CITY,UT 84112. 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 1992 VL 40 IS 2 BP A257 EP A257 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100695 ER PT J AU STEINERT, PM STEVEN, AC AF STEINERT, PM STEVEN, AC TI PROTEIN-COMPOSITION OF THE EPIDERMAL CORNIFIED CELL-ENVELOPE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NIAMS,STRUCT BIOL RES 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 1992 VL 40 IS 2 BP A520 EP A520 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102206 ER PT J AU TAYLOR, PR JUDD, JT JONES, DY NAIR, PP CAMPBELL, WS AF TAYLOR, PR JUDD, JT JONES, DY NAIR, PP CAMPBELL, WS TI INFLUENCE OF TYPE AND AMOUNT OF DIETARY-FAT ON PLASMA ESTRADIOL (E2) IN PREMENOPAUSAL WOMEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. USDA,BELTSVILLE HUMAN NUTR RES CTR,BELTSVILLE,MD 20705. 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 1992 VL 40 IS 2 BP A642 EP A642 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102924 ER PT J AU TENNENBAUM, T MROZ, A BROWN, LJ WILDNAUER, T DE LUCA, LM YUSPA, SH GORDON, JS AF TENNENBAUM, T MROZ, A BROWN, LJ WILDNAUER, T DE LUCA, LM YUSPA, SH GORDON, JS TI RETINOIC ACID INDUCES EARLY CHANGES IN THE DISTRIBUTION OF ALPHA-6-BETA-4 INTEGRIN AND KERATIN-13 EXPRESSION IN HAIRLESS MOUSE SKIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH, LCCTP, BETHESDA, MD 20892 USA. JOHNSON & JOHNSON CONSUMER PROD INC, SKILLMAN, NJ 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 1992 VL 40 IS 2 BP A520 EP A520 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102209 ER PT J AU THEVENIN, C RIECKMANN, P KOZLOW, E WILSON, GL KEHRL, JH AF THEVENIN, C RIECKMANN, P KOZLOW, E WILSON, GL KEHRL, JH TI ANALYSIS OF THE CD20 PROMOTER - IDENTIFICATION OF A DIVERGED OCTAMER BINDING-SITE IMPORTANT IN LYMPHOCYTE-B SPECIFIC EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT 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 1992 VL 40 IS 2 BP A300 EP A300 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100946 ER PT J AU THOMAS, DL FACTOR, SH CARELLA, AV MOSS, MW QUINN, TC AF THOMAS, DL FACTOR, SH CARELLA, AV MOSS, MW QUINN, TC TI HEPATITIS-B AND HEPATITIS-C INFECTION AMONG HEALTH-CARE PROVIDERS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NIAID,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 1992 VL 40 IS 2 BP A248 EP A248 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100643 ER PT J AU THOMAS, PM SAMELSON, LE AF THOMAS, PM SAMELSON, LE TI ASSOCIATION OF THE PROTEIN TYROSINE KINASE P60(FYN) WITH THE MURINE SURFACE-MOLECULE THY-1 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB 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 1992 VL 40 IS 2 BP A198 EP A198 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100356 ER PT J AU TIMMERS, K RECANT, L CUSHMAN, SW AF TIMMERS, K RECANT, L CUSHMAN, SW TI DECREASED ABUNDANCE OF GLUCOSE TRANSPORTER PROTEIN (GLUT2) IN ISLETS OF GENETICALLY OBESE-HYPERINSULINEMIC RATS WITH AND WITHOUT DIABETES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,DIABET RES LAB,WASHINGTON,DC 20422. NIDDK,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 1992 VL 40 IS 2 BP A311 EP A311 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101006 ER PT J AU TINAJERO, J FABBRI, A DUFAU, ML AF TINAJERO, J FABBRI, A DUFAU, ML TI SEROTONERGIC ACTIONS OF PROPRANOLOL - EVIDENCE FOR INHIBITORY EFFECTS ON LEYDIG-CELL FUNCTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,MOLEC ENDOCRINOL SECT,BETHESDA,MD. 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 1992 VL 40 IS 2 BP A263 EP A263 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100731 ER PT J AU TOLEDANO, MB DELAHUNTY, M LIN, JX LEONARD, WJ AF TOLEDANO, MB DELAHUNTY, M LIN, JX LEONARD, WJ TI DIFFERENTIAL DNA-BINDING SPECIFICITY OF NF-KAPPA-B P50 AND P65 IS CONFERRED BY A SHORT N-TERMINAL DNA-BINDING DOMAIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM & MOLEC IMMUNOL SECT,BETHESDA,MD 20892. NICHHD,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 1992 VL 40 IS 2 BP A301 EP A301 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100950 ER PT J AU TSAI, SC ADAMIK, R HAUN, RS MOSS, J VAUGHAN, M AF TSAI, SC ADAMIK, R HAUN, RS MOSS, J VAUGHAN, M TI GUANINE NUCLEOTIDE-BINDING PROTEINS IN PROTEIN TRAFFICKING - SELECTIVE ASSOCIATION OF ADP-RIBOSYLATION FACTORS WITH GOLGI SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 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 1992 VL 40 IS 2 BP A191 EP A191 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100321 ER PT J AU UDEY, MC TANG, A AF UDEY, MC TANG, A TI DOSES OF UV-RADIATION THAT MODULATE ICAM-1 EXPRESSION AND INHIBIT ACCESSORY CELL-FUNCTION ARE CYTOTOXIC FOR MURINE LANGERHANS CELLS (LC) 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 1992 VL 40 IS 2 BP A506 EP A506 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102124 ER PT J AU URABE, K TSUKAMOTO, K KAMEYAMA, K HEARING, VJ AF URABE, K TSUKAMOTO, K KAMEYAMA, K HEARING, VJ TI THE TYROSINASE GENE FAMILY - INTERACTIONS OF MELANOGENIC PROTEINS TO REGULATE MELANOGENESIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,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 1992 VL 40 IS 2 BP A530 EP A530 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102269 ER PT J AU VANDERVORT, AL MADARA, PJ COBB, JP CORRIVEAU, CC TROPEA, MM DANNER, RL AF VANDERVORT, AL MADARA, PJ COBB, JP CORRIVEAU, CC TROPEA, MM DANNER, RL TI THE EFFECTS OF NITRIC-OXIDE (NO) ON ENDOTOXIN (LPS)-INDUCED TNF TRANSCRIPTION AND TRANSLATION IN HUMAN NEUTROPHILS (PMN) 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 1992 VL 40 IS 2 BP A306 EP A306 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100978 ER PT J AU VARMA, VM GROLLMAN, EF DAI, WL HENKIN, RI AF VARMA, VM GROLLMAN, EF DAI, WL HENKIN, RI TI TASTE LOSS AFTER I-131 TREATMENT FOR THYROID-CANCER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,TASTE & SMELL CLIN,WASHINGTON,DC 20052. 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 1992 VL 40 IS 2 BP A417 EP A417 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101605 ER PT J AU VOLAREVIC, S NIKLINSKA, BB BURNS, CM YAMADA, H JUNE, CH DUMONT, FJ ASHWELL, JD AF VOLAREVIC, S NIKLINSKA, BB BURNS, CM YAMADA, H JUNE, CH DUMONT, FJ ASHWELL, JD TI THE CD45 TYROSINE PHOSPHATASE REGULATES T-CELL PHOSPHOTYROSINE HOMEOSTASIS AND ACTIVATION-INDUCED CALCIUM OSCILLATIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BIOL RESPONSE MODIFIERS PROGRAM,BETHESDA,MD 20892. USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20814. MERCK SHARP & DOHME LTD,DEPT IMMUNOL RES,RAHWAY,NJ 07065. 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 1992 VL 40 IS 2 BP A322 EP A322 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101064 ER PT J AU WAISMAN, Y EICHACKER, PQ BANKS, SM HOFFMAN, WD MACVITTIE, TJ NATANSON, C AF WAISMAN, Y EICHACKER, PQ BANKS, SM HOFFMAN, WD MACVITTIE, TJ NATANSON, C TI COMPARISON OF PREDICTION MODELS TO QUANTIFY ACUTE BLOOD-LOSS IN CANINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. ARMED FORCES RADIOBIOL RES INST,BETHESDA,MD 20814. EMERGENCY MED TRAUMA,WASHINGTON,DC. 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 1992 VL 40 IS 2 BP A372 EP A372 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101342 ER PT J AU WANG, BH RIEGER, A KILGUS, O OCHIAI, K FODINGER, D OSTERHOFF, B KINET, JP STINGL, G AF WANG, BH RIEGER, A KILGUS, O OCHIAI, K FODINGER, D OSTERHOFF, B KINET, JP STINGL, G TI EPIDERMAL LANGERHANS CELLS FROM NORMAL HUMAN SKIN BIND MONOMERIC IGE VIA FC-EPSILON-RI SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV VIENNA,SCH MED,DEPT DERMATOL 1,DIV CUTANEOUS IMMUNOBIOL,A-1010 VIENNA,AUSTRIA. NIAID,MOLEC ALLERGY & IMMUNOL SECT,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 1992 VL 40 IS 2 BP A507 EP A507 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102127 ER PT J AU WELSH, CF MOSS, J VAUGHAN, M AF WELSH, CF MOSS, J VAUGHAN, M TI ADP-RIBOSYLATION FACTOR, A GUANINE NUCLEOTIDE-BINDING PROTEIN ACTIVATOR OF CHOLERA-TOXIN, IS ISOLATED IN AN ACTIVATED STATE WHEN EXPRESSED AS A FUSION PROTEIN IN ESCHERICHIA-COLI SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,LCM,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 1992 VL 40 IS 2 BP A215 EP A215 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100449 ER PT J AU WILSON, WH BRYANT, G BATES, S FOJO, T WITTES, R CHABNER, DA AF WILSON, WH BRYANT, G BATES, S FOJO, T WITTES, R CHABNER, DA TI EPOCH CHEMOTHERAPY +/- R-VERAPAMIL FOR RELAPSED LYMPHOMAS - INFUSIONAL ETOPOSIDE (E), VINCRISTINE (O), ADRIAMYCIN (H) WITH CYCLOPHOSPHAMIDE (C) AND PREDNISONE (P) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,MED 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 1992 VL 40 IS 2 BP A170 EP A170 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100201 ER PT J AU YATSIV, I QUEZADO, ZMN HOFFMAN, WD KOEV, LA WINKELSTEIN, JA CORK, LC EICHACKE, PQ BANKS, SM NATANSON, C AF YATSIV, I QUEZADO, ZMN HOFFMAN, WD KOEV, LA WINKELSTEIN, JA CORK, LC EICHACKE, PQ BANKS, SM NATANSON, C TI THE 3RD COMPONENT OF COMPLEMENT (C3) IS NECESSARY FOR THE FEBRILE RESPONSE AFTER ENDOTOXIN CHALLENGE IN DOGS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,DEPT CRIT CARE,BETHESDA,MD 20892. CHILDRENS HOSP,NATL MED CTR,DEPT CRIT CARE,WASHINGTON,DC 20010. JOHNS HOPKINS UNIV,DEPT PEDIAT,BALTIMORE,MD 21218. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 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 1992 VL 40 IS 2 BP A163 EP A163 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100156 ER PT J AU YOKOYAMA, WM SMITH, HRC DANIELS, BF RIBAUDO, RK KARLHOFER, FM AF YOKOYAMA, WM SMITH, HRC DANIELS, BF RIBAUDO, RK KARLHOFER, FM TI MOLECULAR-BASIS OF MAJOR HISTOCOMPATIBILITY COMPLEX-ASSOCIATED RESISTANCE TO NATURAL KILLING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV CALIF SAN FRANCISCO,DEPT MED,ROSALIND RUSSEL ARTHRITIS RES LAB,SAN FRANCISCO,CA 94143. NIH,IMMUNOL 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 1992 VL 40 IS 2 BP A342 EP A342 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101173 ER PT J AU YONEDA, K KORGE, B MCBRIDE, OW STEINERT, PM AF YONEDA, K KORGE, B MCBRIDE, OW STEINERT, PM TI THE HUMAN LORICRIN GENE IS POLYMORPHIC SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,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 1992 VL 40 IS 2 BP A494 EP A494 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102054 ER PT J AU YOSHIMURA, K ROSENFELD, MA NAKAMURA, H SCHERER, EM DALEMANS, W PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF YOSHIMURA, K ROSENFELD, MA NAKAMURA, H SCHERER, EM DALEMANS, W PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI INVIVO INTRATRACHEAL PLASMID-MEDIATED TRANSFER OF THE HUMAN CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR GENE TO THE MOUSE LUNG SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. TRANSGENE SA,STRASBOURG,FRANCE. 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 1992 VL 40 IS 2 BP A339 EP A339 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101156 ER PT J AU USDIN, K AF USDIN, K TI HYPERCARD-BASED DATA MANAGEMENT TOOLS FOR MOLECULAR BIOLOGISTS SO COMPUTER APPLICATIONS IN THE BIOSCIENCES LA English DT Article ID DNA; SEQUENCE; AMPLIFICATION; PROGRAM; INVITRO AB I have designed a Macintosh data management system for molecular biologists. This system, called DataMinder, can be used to store information about oligonucleotides, nucleic acid or protein sequences, recombinant DNA clones, cells, reagents and protocols. DataMinder is not limited to data storage. A number of utilities for data analysis are provided, including those for the evaluation of oligonucleotides for use as hybridization probes or primers for DNA synthesis, and a variety of sequence editing features. Context-sensitive help is available on-line. DataMinder is simple to use and to customize and allows for sharing of database information across a computer network. RP USDIN, K (reprint author), NIDDKD, BLDG 8, ROOM 202, BETHESDA, MD 20892 USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0266-7061 J9 COMPUT APPL BIOSCI JI Comput. Appl. Biosci. PD APR PY 1992 VL 8 IS 2 BP 107 EP 111 PG 5 WC Computer Science, Interdisciplinary Applications SC Computer Science GA HP526 UT WOS:A1992HP52600002 PM 1591605 ER PT J AU KONOPKA, AK AF KONOPKA, AK TI SEQUENCES, CODES AND FUNCTIONS SO COMPUTERS & CHEMISTRY LA English DT Editorial Material RP KONOPKA, AK (reprint author), NCI,DCBDC,MATH BIOL LAB,BLDG 1052,RM 237,FREDERICK,MD 21702, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD APR PY 1992 VL 16 IS 2 BP 83 EP 84 DI 10.1016/0097-8485(92)80032-U PG 2 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA JA657 UT WOS:A1992JA65700001 ER PT J AU GRIBSKOV, M AF GRIBSKOV, M TI THE LANGUAGE METAPHOR IN SEQUENCE-ANALYSIS SO COMPUTERS & CHEMISTRY LA English DT Article ID PROMOTER SEQUENCES; STRUCTURAL UNITS; CODON PREFERENCE; PROTEIN; GENES; DNA; EXPRESSION; INFORMATION; PATTERNS; REGIONS AB The metaphors of language and coding have provided a powerful framework for organizing molecular biology. Many techniques developed in the analysis of text and other communication channels hasve been successfully applied to macromolecular sequences with little or no change. However, a number of properties, such as long-range interactions, structural dynamics and the importance of sequence variation in modulation of function, are poorly modelled by the language metaphor. It is not necessary to abandon the power of the language metaphor, but it is suggested that a conscious effort to set aside this compelling metaphor and examine other viewpoints is likely to be useful. RP GRIBSKOV, M (reprint author), NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, POB B, FREDERICK, MD 21702 USA. OI Gribskov, Michael/0000-0002-1718-0242 NR 31 TC 5 Z9 5 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD APR PY 1992 VL 16 IS 2 BP 85 EP 88 DI 10.1016/0097-8485(92)80033-V PG 4 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA JA657 UT WOS:A1992JA65700002 ER PT J AU CLAVERIE, JM AF CLAVERIE, JM TI SEQUENCE SIGNALS - ARTIFACT OR REALITY SO COMPUTERS & CHEMISTRY LA English DT Article AB I first review the concept of molecular sequence signal and the various forms it can take in the literature. I then comment on the limitation of this concept on the grounds that sequence signals are neither independent of a subjective representation, nor complete and/or verifiable correlates of the associated biological phenomena. RP NIH, NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA. NR 9 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD APR PY 1992 VL 16 IS 2 BP 89 EP 91 DI 10.1016/0097-8485(92)80034-W PG 3 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA JA657 UT WOS:A1992JA65700003 ER PT J AU SALAMON, P KONOPKA, AK AF SALAMON, P KONOPKA, AK TI A MAXIMUM-ENTROPY PRINCIPLE FOR THE DISTRIBUTION OF LOCAL COMPLEXITY IN NATURALLY-OCCURRING NUCLEOTIDE-SEQUENCES SO COMPUTERS & CHEMISTRY LA English DT Article; Proceedings Paper CT WORKSHOP ON OPEN PROBLEMS IN COMPUTATIONAL MOLECULAR BIOLOGY Y CY JUN 02-08, 1991 CL TELLURIDE, CO ID DNA AB A maximum entropy principle (MEP) governing the distribution of complexity of short oligonucleotides from large collections of functionally equivalent sequences is presented. The principle is seen to work well in both translated regions (exons and bacterial genes) and introns from various genomes. It also works in cases of sample sequences from various genomes and even a representative sample of the entire GenBank. This suggests that all naturally occurring DNA sequences are likely to follow the MEP described in this report. The linear trend of surprisal as a function of complexity is systematically characterized by remarkably different slope values for introns and translated regions of genes from all eukaryotic genomes studied (primates, rodents, other mammals, other vertebrates, invertebrates, organella, plants and viruses). This fact may be used as a criterion for discriminant analysis. C1 NCI,DCBDC,MATH BIOL LAB,FREDERICK,MD 21702. RP SALAMON, P (reprint author), SAN DIEGO STATE UNIV,DEPT MATH SCI,SAN DIEGO,CA 92182, USA. NR 19 TC 21 Z9 22 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD APR PY 1992 VL 16 IS 2 BP 117 EP 124 DI 10.1016/0097-8485(92)80038-2 PG 8 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA JA657 UT WOS:A1992JA65700007 ER PT J AU SELL, SM AF SELL, SM TI V(D)J RECOMBINASE PRECURSORS AND CODING STRUCTURE OF SIGNAL SEQUENCE DIRECTED REARRANGEMENT SO COMPUTERS & CHEMISTRY LA English DT Article; Proceedings Paper CT WORKSHOP ON OPEN PROBLEMS IN COMPUTATIONAL MOLECULAR BIOLOGY Y CY JUN 02-08, 1991 CL TELLURIDE, CO ID DNA TOPOISOMERASE-II; T-CELL; SACCHAROMYCES-CEREVISIAE; JUNCTIONAL SEQUENCES; GENE REARRANGEMENTS; JOINING MECHANISM; RECEPTOR; EXPRESSION; SEGMENTS; ORGANIZATION AB In order to increase our understanding of the complex process of immunoglobulin and T-cell receptor signal sequence directed rearrangements in vertebrates, an evolutionary approach was designed to (1) assess structural motifs important for rearrangement, (2) discuss evidence for precursors of recombinase candidates and (3) characterize a putative example of a recombinase mediated translocation in a human tumor of non-hematologic origin. Genomic reorganization occurs as a normal, developmentally regulated process in a variety of organisms. In the vertebrates, recombination signal sequence directed V(D)J rearrangement operates during the development of both T- and B-cells to generate mature T-cell receptor and immunoglobulin variable region genes, respectively. It is argued that this type of signal sequence directed rearrangement event probably evolved from a primitive rearrangement system, and it is proposed that novel rearranging gene families exist in other terminally differentiating tissues. RP SELL, SM (reprint author), NIDDKD,4212 N 16TH ST,PHOENIX,AZ 85016, USA. NR 62 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PD APR PY 1992 VL 16 IS 2 BP 125 EP 133 DI 10.1016/0097-8485(92)80039-3 PG 9 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA JA657 UT WOS:A1992JA65700008 ER PT J AU QUEZADO, ZN KEISER, HR PARKER, MM AF QUEZADO, ZN KEISER, HR PARKER, MM TI REVERSIBLE MYOCARDIAL DEPRESSION AFTER MASSIVE CATECHOLAMINE RELEASE FROM A PHEOCHROMOCYTOMA SO CRITICAL CARE MEDICINE LA English DT Article DE CARDIOMYOPATHY; PHEOCHROMOCYTOMA; CATECHOLAMINES; VASCULAR RESISTANCE; INTENSIVE CARE UNIT; MYOCARDIAL DEPRESSION; DOPAMINE; NOREPINEPHRINE; EPINEPHRINE; HEART ID CARDIOMYOPATHY; CRISIS C1 NHLBI,DEPT CRIT CARE MED,BETHESDA,MD 20892. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 10 TC 40 Z9 41 U1 0 U2 0 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 1992 VL 20 IS 4 BP 549 EP 551 DI 10.1097/00003246-199204000-00022 PG 3 WC Critical Care Medicine SC General & Internal Medicine GA HP191 UT WOS:A1992HP19100022 PM 1559374 ER PT J AU ROBERGE, FG XU, DH CHAN, CC AF ROBERGE, FG XU, DH CHAN, CC TI A NEW EFFECTIVE AND NON-HARMFUL CHEMICAL ADJUVANT FOR THE INDUCTION OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS SO CURRENT EYE RESEARCH LA English DT Article ID BLOCK POLYMER SURFACTANTS; S-ANTIGEN; EXPRESSION; COPOLYMER; UVEITIS; RATS AB The induction of T cell mediated disease models in animals is usually dependent on the use of complete Freund's adjuvant (CFA). In order to avoid the painful side effects of CFA on the animals, we tested the capacity to induce experimental autoimmune uveoretinitis (EAU) with Hunter's adjuvant (HA). This new adjuvant makes use of nonionic copolymer surfactants, and does not cause deleterious effects to animals. We have found that EAU could be efficiently induced in rats with low doses of S-Ag (10-mu-g) in very small quantity of HA (10-mu-l). The biologic parameters of EAU induction showed a potent stimulation of lymphocytes proliferation maximal 11 days after immunization, as well as high levels of antibody production. C1 UNIV MONTREAL,NOTRE DAME HOSP,DEPT OPHTHALMOL,MONTREAL,QUEBEC,CANADA. NEI,BETHESDA,MD 20892. NR 22 TC 4 Z9 4 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 1992 VL 11 IS 4 BP 371 EP 376 DI 10.3109/02713689209001790 PG 6 WC Ophthalmology SC Ophthalmology GA HT219 UT WOS:A1992HT21900009 PM 1526167 ER PT J AU KAISERKUPFER, MI BOUZAS, EA AF KAISERKUPFER, MI BOUZAS, EA TI OCULAR MANIFESTATIONS OF METABOLIC DISORDERS SO CURRENT OPINION IN OPHTHALMOLOGY LA English DT Article AB Papers published between October 1990 and September 1991 on the ocular manifestations of metabolic diseases are reviewed. In this period, the correlation and heterogeneity of the clinical features of albinism in 13 members of a family were presented. Linkage studies in a six-generation family with Aland eye disease have assigned the gene locus to Xq22. The phenotypic variability of the clinical findings in one familv was discussed. Misrouting of the visual pathwavs was found to be specific for albinism and absent in congenital nystagmus in a comparative study, based on visual evoked potential. The pattern of hypopigmentation of the fundus in six carriers of X-linked ocular albinism was presented with a provocative discussion of its explanation. An extensive linkage analysis of oculocutaneous albinism in 47 South African black families was begun. The first ocular histopathologic study of a vitamin B6-responsive gyrate atrophy patient was reported. The ocular findings and symptoms in nephropathic cystinosis showed evidence of clinical variability. The ocular tissue obtained at autopsy from a patient with type 1 primary hyperoxaluria revealed oxalate deposits in the outer plexiform and nuclear layers. The clinical findings of a family with autosomal dominant crystalline dystrophy were presented; transmission electron microscopy of circulating lymphocytes demonstrated crystals and an unknown amorphous material, findings thought to be similar to those seen in cholesterol ester storage disease. Unesterified cholesterol deposits have all extracellular localization in Schnyder's corneal crystalline dystrophy. A mutation responsible for the fish eye disease has been identified in the lecithin-cholesterol acyltransferase gene in two affected brothers. Kayser-Fleischer ring is an especially important clinical finding in the neurologic form of Wilson's disease. Occasionally, it may be seen as a sign in other forms of liver disease. Strabismus and retinitis pigmentosa are frequently found in the disialotransferrin developmental deficiency syndrome. The first histopathologic report of a case of late-infantile galactosialidosis showed diminished numbers of swollen ganglion cells with abnormal deposits throughout the retina. Mucopolysaccharide deposition in the trabecular meshwork may be responsible for the development of glaucoma in older patients with Morquio syndrome. The ocular findings of Fabry's disease in affected male patients and carrier female patients without angiokeratosis were reported. Type IV amyloidotic polyneuropathy (Meretoja syndrome), a dominant disorder, has ocular manifestations that include lattice corneal dystrophy, open-angle glaucoma, blepharochalasis, and cranial nerve neuropathy. The discovery of light-fixed pupils led to the first antemortem diagnosis of neuronal intranuclear hyaline inclusion disease. Electroretinography confirmed central nervous system dysfunction. RP KAISERKUPFER, MI (reprint author), NEI,OPHTHALM GENET & CLIN SERV BRANCH,9000 ROCKVILLE PIKE,10-10N226,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 1040-8738 J9 CURR OPIN OPHTHALMOL PD APR PY 1992 VL 3 IS 2 BP 221 EP 227 DI 10.1097/00055735-199204000-00013 PG 7 WC Ophthalmology SC Ophthalmology GA HT337 UT WOS:A1992HT33700013 ER PT J AU CHOYKE, PL AF CHOYKE, PL TI MAGNETIC-RESONANCE-IMAGING OF THE GENITOURINARY TRACT SO CURRENT OPINION IN RADIOLOGY LA English DT Article AB Advances have occurred in practically all aspects of MR imaging of the genitourinary tract. Fat-suppressed T1 weighting and dynamic-enhanced imaging are two new methods for evaluating renal and adrenal masses. MR angiography techniques are beginning to depict anatomy with sufficient detail to be considered clinical tools. Bladder cancers can be better staged with enhanced high-resolution images, especially when combined with surface coils. Endorectal surface coils continue to provide dramatic images of the prostate and have significantly improved local staging with MR imaging. MR imaging is proving superior to all other techniques in staging endometrial and cervical cancers, and high-resolution, fat-suppressed, fast spin-echo techniques will undoubtedly further improve the diagnostic utility of this modality. RP CHOYKE, PL (reprint author), NIH,DEPT RADIOL,BLDG 10,ROOM 1 C660,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 1040-869X J9 CURR OPIN RADIOL PD APR PY 1992 VL 4 IS 2 BP 24 EP 31 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HH803 UT WOS:A1992HH80300005 PM 1554584 ER PT J AU TURNER, MLC MARINOFF, SC AF TURNER, MLC MARINOFF, SC TI GENERAL-PRINCIPLES IN THE DIAGNOSIS AND TREATMENT OF VULVAR DISEASES SO DERMATOLOGIC CLINICS LA English DT Article RP TURNER, MLC (reprint author), NIH,DERMATOL BRANCH,BLDG 10,ROOM 12N238,BETHESDA,MD 20892, USA. NR 0 TC 3 Z9 4 U1 0 U2 1 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 1992 VL 10 IS 2 BP 275 EP & PG 0 WC Dermatology SC Dermatology GA HN082 UT WOS:A1992HN08200002 PM 1606759 ER PT J AU SAWCHUK, WS AF SAWCHUK, WS TI VULVAR MANIFESTATIONS OF HUMAN PAPILLOMAVIRUS INFECTION SO DERMATOLOGIC CLINICS LA English DT Article C1 NIH,DERMATOL BRANCH,BETHESDA,MD 20892. NR 0 TC 6 Z9 6 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 1992 VL 10 IS 2 BP 405 EP & PG 0 WC Dermatology SC Dermatology GA HN082 UT WOS:A1992HN08200011 PM 1318813 ER PT J AU TURNER, MLC AF TURNER, MLC TI VULVAR MANIFESTATIONS OF SYSTEMIC-DISEASES SO DERMATOLOGIC CLINICS LA English DT Article RP TURNER, MLC (reprint author), NIH,DERMATOL BRANCH,BLDG 10,ROOM 12N238,BETHESDA,MD 20892, USA. NR 0 TC 4 Z9 4 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 1992 VL 10 IS 2 BP 445 EP & PG 0 WC Dermatology SC Dermatology GA HN082 UT WOS:A1992HN08200015 PM 1606770 ER PT J AU TURNER, MLC MARINOFF, SC AF TURNER, MLC MARINOFF, SC TI VULVAR DISEASES - PREFACE SO DERMATOLOGIC CLINICS LA English DT Editorial Material RP TURNER, MLC (reprint author), NIH,DERMATOL BRANCH,BLDG 10,ROOM 12N238,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 1 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 1992 VL 10 IS 2 BP R6 EP R6 PG 1 WC Dermatology SC Dermatology GA HN082 UT WOS:A1992HN08200001 ER PT J AU THORP, BH ANDERSON, I JAKOWLEW, SB AF THORP, BH ANDERSON, I JAKOWLEW, SB TI TRANSFORMING GROWTH FACTOR-BETA-1, FACTOR-BETA-2 AND FACTOR-BETA-3 IN CARTILAGE AND BONE-CELLS DURING ENDOCHONDRAL OSSIFICATION IN THE CHICK SO DEVELOPMENT LA English DT Article DE ENDOCHONDRAL OSSIFICATION, CARTILAGE; TGF-BETA; BONE; CHICKEN; TYPE-II COLLAGEN; CHONDROCYTE; OSTEOBLAST; OSTEOCLAST ID FACTOR-BETA; TGF-BETA; CHONDROCYTES; EXPRESSION; PURIFICATION; REGULATOR AB The localization of TGF-beta-1, -beta-2 and -beta-3 was studied in the growth plate, epiphysis and metaphysis of the tibiotarsus of three-week-old chicks. The different TGF-beta-isoforms were localized to hypertrophic chondrocytes, chondroclasts, osteoblasts and osteoclasts using immunohistochemical staining analysis with specific TGF-beta-antibodies. TGF-beta-s in osteoclasts and chondroclasts were restricted to those cells located on the respective matrices. TGF-beta-3 localization was mainly cytoplasmic in the transitional (early hypertrophic) chondrocytes, but nuclear staining was also detected in some proliferating chondrocytes. The cell-specific localization of these TGF-beta-isoforms supports the hypothesis that TGF-beta has a role in the coupling of new bone formation to bone and cartilage matrix resorption during osteochondral development and suggests that TGF-beta may be a marker of chondrocyte differentiation. TGF-beta-localization preceded a marked increase in type II collagen mRNA expression in transitional chondrocytes, suggesting a role for TGF-beta in the induction of synthesis of extracellular matrix. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP THORP, BH (reprint author), AFRC,INST ANIM PHYSIOL & GENET,EDINBURGH RES STN,ROSLIN EH25 9PS,MIDLOTHIAN,SCOTLAND. NR 33 TC 123 Z9 125 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 0950-1991 J9 DEVELOPMENT JI Development PD APR PY 1992 VL 114 IS 4 BP 907 EP 911 PG 5 WC Developmental Biology SC Developmental Biology GA HR732 UT WOS:A1992HR73200012 PM 1618152 ER PT J AU FLUCHER, BE PHILLIPS, JL POWELL, JA ANDREWS, SB DANIELS, MP AF FLUCHER, BE PHILLIPS, JL POWELL, JA ANDREWS, SB DANIELS, MP TI COORDINATED DEVELOPMENT OF MYOFIBRILS, SARCOPLASMIC-RETICULUM AND TRANSVERSE TUBULES IN NORMAL AND DYSGENIC MOUSE SKELETAL-MUSCLE, INVIVO AND INVITRO SO DEVELOPMENTAL BIOLOGY LA English DT Article ID SLOW CALCIUM CURRENT; MUSCULAR DYSGENESIS; DIHYDROPYRIDINE RECEPTOR; CA-2+ CHANNEL; ALPHA-ACTININ; CONTRACTION; PROTEINS; SYSTEM; TITIN; MICE C1 NHLBI,BIOCHEM GENET LAB,BETHESDA,MD 20892. SMITH COLL,DEPT BIOL SCI,NORTHAMPTON,MA 01063. RP FLUCHER, BE (reprint author), NINCDS,NEUROBIOL LAB,BETHESDA,MD 20892, USA. NR 51 TC 43 Z9 43 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD APR PY 1992 VL 150 IS 2 BP 266 EP 280 DI 10.1016/0012-1606(92)90241-8 PG 15 WC Developmental Biology SC Developmental Biology GA HK696 UT WOS:A1992HK69600005 PM 1551475 ER PT J AU BARBETTI, F GEJMAN, PV TAYLOR, SI RABEN, N CAMA, A BONORA, E PIZZO, P MOGHETTI, P MUGGEO, M ROTH, J AF BARBETTI, F GEJMAN, PV TAYLOR, SI RABEN, N CAMA, A BONORA, E PIZZO, P MOGHETTI, P MUGGEO, M ROTH, J TI DETECTION OF MUTATIONS IN INSULIN-RECEPTOR GENE BY DENATURING GRADIENT GEL-ELECTROPHORESIS SO DIABETES LA English DT Article ID POLYMERASE CHAIN-REACTION; EPIDERMAL GROWTH-FACTOR; TYROSINE KINASE DOMAIN; IMPAIRS TRANSPORT; MUTANT ALLELES; POINT MUTATION; MESSENGER-RNA; ALPHA-SUBUNIT; ACID-SEQUENCE; RESISTANCE AB Denaturing gradient gel electrophoresis (DGGE) has been used to screen for mutations in the insulin receptor gene. Each of the 22 exons was amplified by the polymerase chain reaction (PCR). For each exon, one of the two PCR primers contained a guanine-cytosine (GC) clamp at its 5' end. The DNA was analyzed by electrophoresis through a polyacrylamide gel containing a gradient of denaturants. Two geometries for the gels were compared; the gradient of denaturants was oriented either parallel or perpendicular to the electric field. The sensitivity of the technique was evaluated by determining whether DGGE succeeded in detecting known mutations and polymorphisms in the insulin receptor gene. With parallel gels, 12 of 16 sequence variants were detected. The use of perpendicular gels increased the sensitivity of detection so that all 16 sequence variants were successfully detected when DNA was analyzed by a combination of perpendicular and parallel gels. Furthermore, DGGE was used to investigate a patient with leprechaunism whose insulin receptor genes had not previously been studied. Two mutant alleles were identified in this patient. The allele inherited from the father had a mutation substituting alanine for Val-28; in the allele inherited from the mother, arginine was substituted for Gly-366. C1 NIDDKD,DIABET BRANCH,BLDG 10,ROOM 85235,BETHESDA,MD 20892. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. UNIV VERONA,OSPED POLICLIN,DEPT METAB DIS & PEDIAT,I-37100 VERONA,ITALY. OI BONORA, Enzo/0000-0003-1074-5164 NR 41 TC 41 Z9 43 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 1992 VL 41 IS 4 BP 408 EP 415 DI 10.2337/diabetes.41.4.408 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HK692 UT WOS:A1992HK69200002 PM 1607067 ER PT J AU HORTON, WE WANG, LQ BRADHAM, D PRECHT, P BALAKIR, R AF HORTON, WE WANG, LQ BRADHAM, D PRECHT, P BALAKIR, R TI THE CONTROL OF EXPRESSION OF TYPE-II COLLAGEN - RELEVANCE TO CARTILAGE DISEASE SO DNA AND CELL BIOLOGY LA English DT Article ID PROCOLLAGEN GENE COL2A1; SPONDYLOEPIPHYSEAL DYSPLASIA; MILD CHONDRODYSPLASIA; 1ST INTRON; IDENTIFICATION; ENHANCER; PROMOTER; PROTEIN; FAMILY; DOMAIN AB Cartilage is a unique tissue containing only one cell type, the chondrocyte, surrounded by an extensive extracellular matrix. One of the principal components of the cartilage matrix is type II collagen. The gene coding for type II collagen is relatively large and contains several distinct sequences that function to both up-regulate and down-regulate expression by interacting with chondrocyte transcription factors. Also, there appears to be regulation of collagen II expression by differential splicing of the collagen II mRNA to form different forms of the protein. Finally, the gene is a target for mutations that result in diseases of cartilage such as chondrodysplasias and some forms of osteoarthritis. RP HORTON, WE (reprint author), NIA,GERONTOL RES CTR,BIOL CHEM LAB,BALTIMORE,MD 21224, USA. NR 21 TC 13 Z9 13 U1 0 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD APR PY 1992 VL 11 IS 3 BP 193 EP 198 DI 10.1089/dna.1992.11.193 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA JG734 UT WOS:A1992JG73400004 PM 1567552 ER PT J AU MUKHERJEE, AB CORDELLAMIELE, E MIELE, L AF MUKHERJEE, AB CORDELLAMIELE, E MIELE, L TI REGULATION OF EXTRACELLULAR PHOSPHOLIPASE-A2 ACTIVITY - IMPLICATIONS FOR INFLAMMATORY DISEASES SO DNA AND CELL BIOLOGY LA English DT Article ID ANTIINFLAMMATORY PEPTIDES ANTIFLAMMINS; PORCINE PANCREATIC PHOSPHOLIPASE-A2; PLATELET-ACTIVATING-FACTOR; C2221 CRYSTAL FORM; CYTOSOLIC PHOSPHOLIPASE-A2; OXIDIZED UTEROGLOBIN; LIPOCORTIN-I; CELL-LINE; RELEASE; TRANSGLUTAMINASE AB Phospholipases A2(PLA2s; E.C. 3.1.1.4) are a family of esterases that are involved in myriads of physiological and pathological processes. The involvement of these enzymes, especially the extracellular PLA2S, in the generation of proinflammatory lipid mediators makes them a very important target for investigation. These PLA2s have been suggested to be involved in the pathogenesis of several human inflammatory diseases. Thus, delineating the mechanism(s) of regulation of the activity of these enzymes may provide a better understanding of the pathophysiology of these diseases and allow the rational design and development of novel therapeutic agents. In this article, we provide a brief description of PLA2S in general with a special emphasis on extracellular enzymes, their mechanism(s) of action, and possible role in the pathogenesis of inflammatory diseases. Additionally, we describe: (i) a novel mechanism of activation of extracellular PLA2s by transglutaminases and (ii) the development of one class of antiinflammatory agents, antiflammatory, derived from the active site structure of endogenous PLA2-inhibitory proteins. RP MUKHERJEE, AB (reprint author), NICHHD, HUMAN GENET BRANCH, DEV GENET SECT, BLDG 10, ROOM 95242, BETHESDA, MD 20892 USA. NR 58 TC 60 Z9 60 U1 0 U2 1 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD APR PY 1992 VL 11 IS 3 BP 233 EP 243 DI 10.1089/dna.1992.11.233 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA JG734 UT WOS:A1992JG73400010 PM 1567556 ER PT J AU GOURLEY, MF KISCH, WJ MOJCIK, CF KING, LB KRIEG, AM STEINBERG, AD AF GOURLEY, MF KISCH, WJ MOJCIK, CF KING, LB KRIEG, AM STEINBERG, AD TI MOLECULAR ASPECTS OF SYSTEMIC LUPUS-ERYTHEMATOSUS - MURINE ENDOGENOUS RETROVIRAL EXPRESSION SO DNA AND CELL BIOLOGY LA English DT Article ID RECOMBINANT INBRED LINES; B-CELL ACTIVATION; NZB MICE; AUTOIMMUNE MOUSE; LEUKEMIA-VIRUS; ASSOCIATION; GENES; LPR AB Systemic lupus erythematosus is an immune-mediated disease in which the etiology is unknown. Full-length (8.4 kb), type C, modified polytropic (Mpmv) retroviral transcripts from the thymus are characteristic of murine lupus. Reciprocal bone marrow transplantation studies determined that this thymic expression maps to the pre-T bone marrow stem cell. In vitro and in vivo oligonucleotide antisense work suggest that type C retroviruses play a role in immune activation. This paper summarizes our studies of endogenous retroviruses in murine lupus. RP GOURLEY, MF (reprint author), NIAMS,ARB,CELLULAR IMMUNOL SECT,BLDG 10,ROOM 9N-218,BETHESDA,MD 20892, USA. NR 23 TC 5 Z9 5 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD APR PY 1992 VL 11 IS 3 BP 253 EP 257 DI 10.1089/dna.1992.11.253 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA JG734 UT WOS:A1992JG73400012 PM 1567558 ER PT J AU HIGGINS, ST PRESTON, KL CONE, EJ HENNINGFIELD, JE JAFFE, JH AF HIGGINS, ST PRESTON, KL CONE, EJ HENNINGFIELD, JE JAFFE, JH TI SUPERSENSITIVITY TO NALOXONE FOLLOWING ACUTE MORPHINE PRETREATMENT IN HUMANS - BEHAVIORAL, HORMONAL AND PHYSIOLOGICAL-EFFECTS SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE ACUTE PHYSICAL DEPENDENCE; OPIOIDS; MORPHINE; NALOXONE; HORMONES; PROLACTIN; CORTISOL; BEHAVIOR; HUMANS ID OPIOID PHYSICAL-DEPENDENCE; PROLACTIN; CORTISOL; SECRETION; INTERVAL; RATS AB The effects of naloxone (10 mg/70 kg) given 6 h following acute exposure to morphine (4, 8, 16 mg/70 kg) were assessed in 5 opiate-abusing volunteers who were not physically dependent upon entering the study. Naloxone increased cortisol plasma levels more following morphine than placebo pretreatment. Naloxone reversed the effects of morphine on pupil diameter and oral temperature and decreased skin temperature as a function of morphine pretreatment. Subjects' ability to detect the effects of naloxone, their scores on an opiate-withdrawal questionnaire, and their visual-analog ratings of 'bad effects', 'chills', 'confused' and 'restlessness' increased when naloxone followed pretreatment with 8 and 16 mg, but not 4 mg, of morphine. Performance on the Digit Symbol Substitution Test was not discernibly affected under any of the dose conditions. Overall, results from the present study provide further evidence in humans that the administration of naloxone shortly following acute morphine pretreatment increases naloxone sensitivity, produces signs and symptoms typical of opiate withdrawal and that these effects are dependent on the dose of morphine administered. C1 NIDA,ADDICT RES CTR,BOX 5180,BALTIMORE,MD 21224. RI Preston, Kenzie/J-5830-2013 OI Preston, Kenzie/0000-0003-0603-2479 NR 42 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD APR PY 1992 VL 30 IS 1 BP 13 EP 26 DI 10.1016/0376-8716(92)90031-7 PG 14 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA HU063 UT WOS:A1992HU06300002 PM 1591977 ER PT J AU GRANT, BF CHOU, SP PICKERING, RP HASIN, DS AF GRANT, BF CHOU, SP PICKERING, RP HASIN, DS TI EMPIRICAL SUBTYPES OF DSM-III-R ALCOHOL DEPENDENCE - UNITED-STATES, 1988 SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE ALCOHOL DEPENDENCE; DSM-III-R; DEPENDENCE SYMPTOMS; SUBTYPES OF DEPENDENCE; VALIDATION OF PSYCHIATRIC DIAGNOSES AB The purpose of the present study was to quantify the degree of heterogeneity of the DSM-III-R alcohol dependence category by comparing the number of potential subtypes of dependence to those empirically observed in a general population survey. Forty-one percent (n = 189) of the 466 potential subtypes of DSM-III-R alcohol dependence were observed, indicating that the category is indeed heterogeneous, but not as heterogeneous as theoretically predicted. Variations in the number, percent and configuration of empirical subtypes of dependence are discussed in terms of coincident morbidity, premature death from alcoholism or death from other competing causes, reporting biases and differences in drinking patterns. The predominance of the 'tolerance' 'withdrawal' and 'impaired control over drinking' criteria among the empirically observed subtypes of dependence are examined within the context of the physiological dependence subtype proposed for the DSM-IV category of alcohol dependence and difficulties encountered in operationalizing these diagnostic criteria. The relevance of study findings to the validation of diagnostic categories in psychiatry is also highlighted. C1 COLUMBIA UNIV,NEW YORK,NY 10032. NEW YORK STATE PSYCHIAT INST & HOSP,DEPT RES ASSESSMENT & TRAINING,NEW YORK,NY 10032. RP GRANT, BF (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,ROOM 14C-26,5600 FISHERS LANE,ROCKVILLE,MD 20852, USA. NR 14 TC 20 Z9 20 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD APR PY 1992 VL 30 IS 1 BP 75 EP 84 DI 10.1016/0376-8716(92)90039-F PG 10 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA HU063 UT WOS:A1992HU06300010 PM 1591982 ER PT J AU UNGER, T NAU, MM SEGAL, S MINNA, JD AF UNGER, T NAU, MM SEGAL, S MINNA, JD TI P53 - A TRANSDOMINANT REGULATOR OF TRANSCRIPTION WHOSE FUNCTION IS ABLATED BY MUTATIONS OCCURRING IN HUMAN CANCER SO EMBO JOURNAL LA English DT Article DE ACTIVATION DOMAIN; LUNG CANCER; P53; TEMPERATURE SENSITIVITY; TRANSACTIVATION ACTIVITY ID CELL LUNG-CANCER; MAMMALIAN-CELLS; WILD-TYPE; GENE; PROTEIN; MUTANT; DNA; TRANSFORMATION; EXPRESSION; ACTIVATION AB Gal4-p53 fusion constructs demonstrate that wild type p53 is a potent transactivator in human lung cancer cells with the transactivation domain for p53 residing in amino acids 1-42. Strikingly, a variety of lung cancer derived p53 mutations occurring outside this domain disrupt this activity. Temperature sensitive conformational shifts of p53 mutant proteins to the wild type form exist and, with a temperature downshift, several mutants become transcriptionally active. Wild type p53 protein is known to form oligomers with mutant p53 and cotransfection of wild type and mutant genes shows that p53 acts in a transdominant manner that is independent of the DNA binding specificity. Transcription is either increased or decreased depending on whether the wild type is more or less abundant than the mutant form. Finally, lung cancers differ in their ability to support the transactivation related functions, providing evidence of other abnormalities of the p53 system in human cancer. C1 UNIFORMED SERV UNIV HLTH SCI,USN,NCI,MED ONCOL BRANCH,BETHESDA,MD 20889. UNIV TEXAS,SW MED CTR,SIMMONS CANC CTR,DALLAS,TX 75235. NR 41 TC 295 Z9 297 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR PY 1992 VL 11 IS 4 BP 1383 EP 1390 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HM836 UT WOS:A1992HM83600017 PM 1314165 ER PT J AU MARKS, MS HALLENBECK, PL NAGATA, T SEGARS, JH APPELLA, E NIKODEM, VM OZATO, K AF MARKS, MS HALLENBECK, PL NAGATA, T SEGARS, JH APPELLA, E NIKODEM, VM OZATO, K TI H-2RIIBP (RXR-BETA) HETERODIMERIZATION PROVIDES A MECHANISM FOR COMBINATORIAL DIVERSITY IN THE REGULATION OF RETINOIC ACID AND THYROID-HORMONE RESPONSIVE GENES SO EMBO JOURNAL LA English DT Article DE DIMERIZATION; GENE REGULATION; HORMONE RECEPTORS; RETINOIC ACID; THYROID HORMONE ID CLASS-I GENE; EMBRYONAL CARCINOMA-CELLS; DNA-BINDING; ESTROGEN-RECEPTOR; NUCLEAR-PROTEIN; NEGATIVE REGULATION; INDUCIBLE ENHANCER; ELEMENT; SEQUENCE; EXPRESSION AB H-2RIIBP (RXR-beta) is a member of the nuclear hormone receptor superfamily that activates transcription of NHC class I genes in response to retinoic acid (RA). Using chemical cross-linking, co-immunoprecipitation, gel mobility shift and streptavidin - biotin DNA precipitation assays, we show that H-2RIIBP formed heterodimers with thyroid hormone (T3) and RA receptors (T3R-alpha and RAR-alpha). H-2RIIBP heterodimer formation required a conserved sub-domain of its C-terminal region, occurred independently of target DNA and was much more efficient than either T3R-alpha/RAR-alpha heterodimer or H-2RIIBP homodimer formation. Heterodimers displayed enhanced binding to target DNA elements and contacted DNA in a manner distinct from that of homodimers. A functional role for heterodimers in vivo was demonstrated by synergistic enhancement of MHC class I transcription following co-transfection of H-2RIIBP with T3R-alpha or RAR-alpha. We provide biochemical evidence that H-2RIIBP formed heterodimers with several naturally occurring nuclear proteins. The results suggest that H-2RIIBP, by virtue of its ability to heterodimerize, enhances combinatorial diversity and versatility in gene regulation mediated by nuclear hormone receptors. C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NCI,CELL BIOL LAB,BETHESDA,MD 20892. OI Marks, Michael/0000-0001-7435-7262 NR 81 TC 457 Z9 457 U1 0 U2 4 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR PY 1992 VL 11 IS 4 BP 1419 EP 1435 PG 17 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HM836 UT WOS:A1992HM83600021 PM 1314168 ER PT J AU SAMUEL, SK HURTA, RAR KONDAIAH, P KHALIL, N TURLEY, EA WRIGHT, JA GREENBERG, AH AF SAMUEL, SK HURTA, RAR KONDAIAH, P KHALIL, N TURLEY, EA WRIGHT, JA GREENBERG, AH TI AUTOCRINE INDUCTION OF TUMOR PROTEASE PRODUCTION AND INVASION BY A METALLOTHIONEIN-REGULATED TGF-BETA-1 (SER223, 225) SO EMBO JOURNAL LA English DT Article DE CATHEPSIN-L; COLLAGENASE; INVASION; MOTILITY; TGF-BETA ID GROWTH-FACTOR-BETA; PLASMINOGEN-ACTIVATOR INHIBITOR; HUMAN-LUNG FIBROBLASTS; METASTATIC PHENOTYPE; MESSENGER-RNA; FACTOR-BETA-1 GENE; RAT FIBROBLASTS; COLLAGEN GELS; CELL INVASION; FACTOR-ALPHA AB An expression vector was constructed in which TGF-beta-1 was placed under the control of the metallothionein promoter. Cys223 and Cys225 in the TGF-beta-1 propeptide were converted to serines, mutations which result in dissociation of the pro-peptide and secretion of bioactive TGF-beta-1 [Brunner,A.M., Marquardt,H., Malacko,A.R., Lioubin,M.N. and Purchio,A.F. (1989) J. Biol. Chem., 264, 13660-13664]. A fibrosarcoma was transfected with this plasmid and a clone (17.18) was selected in which TGF-beta-1 mRNA was able to be induced six-fold following zinc sulphate treatment. These cells increased the secretion of bioactive TGF-beta-1 14-fold and exhibited a coincidental increase in jun-B mRNA expression, suggesting that secreted TGF-beta-1 was acting to induce this early response gene by autocrine activation. Following zinc sulphate induction, the tumor cells became progressively more motile and able to invade collagen gels. In contrast to parental tumor not bearing the TGF-beta-1 expression vector, zinc sulphate stimulation of clone 17.18 enhanced collagenase IV and procathepsin L mRNA levels and enhanced the secretion of many collagenolytic proteases into the medium. Since the action of TGF-beta generally decreases proteolysis by suppression of protease transcription, we compared the response of normal parental fibroblasts to ras-transformed fibrosarcomas and confirmed that TGF-beta could greatly enhance collagenase IV and procathepsin L mRNA levels while having little effect on non-transformed fibroblasts. These experiments indicate that induction of TGF-beta secretion can enhance motility and protease production through autocrine activation, thus increasing the invasion potential of fibrosarcomas. C1 MANITOBA INST CELL BIOL,100 OLIVIA ST,WINNIPEG R3E 0V9,MANITOBA,CANADA. NIH,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 49 TC 129 Z9 131 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR PY 1992 VL 11 IS 4 BP 1599 EP 1605 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HM836 UT WOS:A1992HM83600039 PM 1314170 ER PT J AU KAMILARIS, TC JOHNSON, EO CALOGERO, AE KALOGERAS, KT BERNARDINI, R CHROUSOS, GP GOLD, PW AF KAMILARIS, TC JOHNSON, EO CALOGERO, AE KALOGERAS, KT BERNARDINI, R CHROUSOS, GP GOLD, PW TI CHOLECYSTOKININ-OCTAPEPTIDE STIMULATES HYPOTHALAMIC-PITUITARY-ADRENAL FUNCTION IN RATS - ROLE OF CORTICOTROPIN-RELEASING HORMONE SO ENDOCRINOLOGY LA English DT Article ID PARAVENTRICULAR NUCLEUS; AREA POSTREMA; CORTISOL SECRETION; ADRENOCORTICAL SYSTEM; VASOPRESSIN RELEASE; OXYTOCIN SECRETION; DOSE-RESPONSE; ANTERIOR; CONNECTIONS; CAPSAICIN AB Peripherally-administered cholecystokinin (CCK) is a profound suppressor of food intake, can promote anxiety, and causes the acute release of ACTH into plasma. Centrally administered corticotropin-releasing hormone (CRH), on the other hand, not only represents the principal stimulus to the pituitary corticotroph cell, but also has been shown to suppress appetite and to be profoundly anxiogenic. Because of the overlap in the effects of peripherally administered CCK and of centrally administered CRH, we report here a study to determine whether sulphated CCK octapeptide (CCK-8) could induce the release of CRH within the central nervous system. To accomplish this task, we first assessed the dose-related effects of CCK-8 on ACTH release. Graded doses of CCK-8 (0.1-10-mu-g/kg BW) given in an iv bolus to freely moving male rats, resulted in a dose-dependent increase of plasma immunoreactive (IR)-ACTH (ED50: 1-10-mu-g/kg BW). The lowest maximal stimulatory dose of CCK-8 (5-mu-g/kg BW) was used in all subsequent experiments. To evaluate whether CCK-induced ACTH secretion was mediated by a peripheral CCK receptor, an iv bolus injection of vehicle or L-364,718 (1 mg/kg BW), a specific, highly potent peripheral CCK receptor antagonist, was given before the iv administration of CCK-8 or vehicle. Plasma IR-ACTH response to CCK-8 was significantly attenuated by L-364,718. A role for the vagal afferents that contain CCK receptors in peripherally administered CCK-mediated hypothalamic-pituitary-adrenal (HPA) axis activation was examined in animals that had been pretreated with capsaicin, a potent neurotoxin that destroys vagal afferents. Plasma IR-ACTH and IR-corticosterone responses in capsaicin-treated animals were significantly lower than those in vehicle treated rats. In subsequent in vivo experiments, pituitary stalk-transected and sham-operated animals were used to evaluate whether CCK-8 stimulates the HPA axis via a centrally mediated mechanism. IR-ACTH and IR-corticosterone responses to iv CCK-8 were significantly reduced in the pituitary stalk-transected compared to sham-operated animals. In further effort to determine whether the central nervous system was involved in the plasma IR-ACTH response to the peripheral administration of iv CCK-8, we compared the effects of the iv administration of CRH antisera vs. normal rabbit serum on this parameter. IR-ACTH and IR-corticosterone responses to iv CCK-8 were significantly reduced in the context of pre-treatment with CRH antisera compared to the administration of normal rabbit serum. We also showed that the intracerebroventricular administration of CCK-8 (250 ng) resulted in the significant stimulation of IR-ACTH release compared to vehicle, indicating a direct central effect of CCK. To further examine the locus of the effects of CCK-8 on HPA axis stimulation, we also investigated the in vitro response of graded concentrations of CCK-8 on hypothalamic IR-CRH and pituitary IR-ACTH release. Although CCK-8 stimulates hypothalamic CRH secretion in a dose-dependent fashion, it had no effect, regardless of the dose, on IR-ACTH secretion by dispersed rat anterior pituicytes. We conclude that the HPA axis activation following the peripheral administration of CCK involves CCK-mediated CRH release occurring in part, via activation of CCK receptors on peripherally located vagal afferents. We also conclude that CCK in the central nervous system may cause the direct release of CRH from the paraventricular nucleus. These data suggest that CCK effects on pituitary-adrenal function, and perhaps food intake and anxiety, may be mediated, at least in part, via CRH. These data are of potential clinical relevance in the light of data linking both CCK and CRH to the pathogenesis and symptom complex of both eating and anxiety disorders. C1 NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. RP KAMILARIS, TC (reprint author), NIMH, CLIN NEUROENDOCRINOL BRANCH, BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA. OI bernardini, renato/0000-0002-4765-0663 NR 54 TC 90 Z9 91 U1 0 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1992 VL 130 IS 4 BP 1764 EP 1774 DI 10.1210/en.130.4.1764 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL122 UT WOS:A1992HL12200003 PM 1312423 ER PT J AU TINAJERO, JC FABBRI, A DUFAU, ML AF TINAJERO, JC FABBRI, A DUFAU, ML TI REGULATION OF CORTICOTROPIN-RELEASING FACTOR SECRETION FROM LEYDIG-CELLS BY SEROTONIN SO ENDOCRINOLOGY LA English DT Article ID PITUITARY-TESTICULAR AXIS; RAT HYPOTHALAMUS INVITRO; 5-HT2 RECEPTORS; RESTRAINT STRESS; BRAIN; BINDING; ANTAGONISTS; INHIBITION; VARICOCELE; SUBTYPES AB CRF is produced in the Leydig cells and acts as a negative autocrine regulator of Leydig cell function. To clarify the hormonal control of CRF secretion by Leydig cells, we evaluated the participation of serotonin (5HT) and serotonin agonists in the release of CRF from Leydig cells and their effects on hCG-induced cAMP generation and steroidogenesis. Serotonin stimulated CRF secretion up to 4-fold above basal levels and inhibited basal and hCG-stimulated cAMP generation and testosterone production (ID50, 1 nM). The inhibitory action of 5HT was prevented by a CRF antibody and the alpha-helical CRF-(9-41) antagonist. The selective 5HT2 receptor agonist (+/-)1-[2,5-dimethoxy-4-iodophyryl]2-amino propane hydrochloride (DOI) also stimulated CRF secretion and inhibited hCG-stimulated cAMP generation and testosterone production to control levels (ID50, 7-mu-M). Serotonergic 5HT1A, 5HT1B/1C, 5HT1D, and 5HT3/5HT2 agonists were less effective inhibitors of hCG-stimulated cAMP and testosterone production, while agonists for the 5HT3 receptor had no effect. [I-125]DOI binding studies in Leydig cells demonstrated two sets of receptors with K(d) values in the nanomolar and micromolar range, with low and high capacities, respectively. The low affinity site differed from that of brain receptors (K(d), 4.2 nM) and displayed higher binding capacity (50-fold). The selective 5HT2 receptor antagonist ketanserin prevented CRF stimulation and blocked the inhibitory actions of 5HT and DOI, while the alpha(1)-adrenergic antagonist prazosin had no effect. Also, treatment of cells with ketanserin increased sensitivity to hCG and raised maximal cAMP and testosterone production. 5HT was a more effective stimulus than hCG in stimulating CRF secretion, and gonadotropin-induced CRF release was inhibited by ketanserin. Inhibitory effects of exogenous CRF were demonstrable after blockade of 5HT action by ketanserin. The inhibitory actions of 5HT were unaffected by pertussis and cholera toxins and were reversed by the addition of 8-bromo-cAMP. These results demonstrate that 5HT acts on 5HT2 receptors in Leydig cells that are distinct from those in the brain to stimulate CRF secretion through a pertussis toxin-insensitive G-protein. This action of 5HT is predominantly mediated by the low affinity 5HT2-binding site and requires full occupancy for maximal CRF stimulation, indicating the absence of spare receptors. 5HT-stimulated CRF inhibits basal and hCG-induced cAMP generation and steroidogenesis. Furthermore, 5HT mediates the stimulatory action of LH/hCG on CRF secretion from Leydig cells and, thus, participates in a negative autoregulatory loop to limit the testosterone response to the gonadotropic stimulus. C1 NICHHD, ENDOCRINOL & REPROD RES BRANCH, MOLEC ENDOCRINOL SECT,BLDG 10, ROOM 8C-407, BETHESDA, MD 20892 USA. NR 46 TC 48 Z9 50 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1992 VL 130 IS 4 BP 1780 EP 1788 DI 10.1210/en.130.4.1780 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL122 UT WOS:A1992HL12200005 PM 1312425 ER PT J AU SELTZER, A VISWANATHAN, M SAAVEDRA, JM AF SELTZER, A VISWANATHAN, M SAAVEDRA, JM TI MELATONIN-BINDING SITES IN BRAIN AND CAUDAL ARTERIES OF THE FEMALE RAT DURING THE ESTROUS-CYCLE AND AFTER ESTROGEN ADMINISTRATION SO ENDOCRINOLOGY LA English DT Article ID GUANINE-NUCLEOTIDES; GONADAL-HORMONES; RECEPTORS; AUTORADIOGRAPHY; GLUCOCORTICOIDS; PROGESTERONE; MODULATION; ESTRADIOL; AFFINITY; CATIONS AB Melatonin-binding sites were studied by quantitative autoradiography in brain and caudal (tail) arteries and in selected brain areas of cycling female rats, ovariectomized rats, and ovariectomized rats treated with estradiol. In the caudal artery, the number of melatonin-binding sites was significantly lower during proestrus, estrus, and metestrus than during diestrus. In ovariectomized rats, melatonin binding to the caudal artery was similar to that found during proestrus, estrus, and metestrus, and a further decrease in the receptor number was produced by estradiol replacement. Similarly, melatonin binding in anterior cerebral arteries was higher during diestrus than at other stages of the estrous cycle. In ovariectomized rats, estradiol replacement also resulted in decreased melatonin binding in anterior cerebral arteries. Conversely, no changes in the number of melatonin-binding sites were observed in the suprachiasmatic nucleus or the area postrema during the estrous cycle, in ovariectomized rats, or after estradiol replacement. The present results suggest that in the female rat, reproductive hormones modulate the expression of cerebral and caudal arterial melatonin-binding sites. RP SELTZER, A (reprint author), NIMH, CLIN SCI LAB,PHARMACOL SECT,9000 ROCKVILLE PIKE, BLDG 10, ROOM 2D-45, BETHESDA, MD 20892 USA. NR 28 TC 67 Z9 67 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1992 VL 130 IS 4 BP 1896 EP 1902 DI 10.1210/en.130.4.1896 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL122 UT WOS:A1992HL12200021 PM 1547717 ER PT J AU LOPEZ, FJ DONOSO, AO NEGROVILAR, A AF LOPEZ, FJ DONOSO, AO NEGROVILAR, A TI ENDOGENOUS EXCITATORY AMINO-ACIDS AND GLUTAMATE RECEPTOR SUBTYPES INVOLVED IN THE CONTROL OF HYPOTHALAMIC LUTEINIZING-HORMONE-RELEASING HORMONE-SECRETION SO ENDOCRINOLOGY LA English DT Article ID N-METHYL-D; CENTRAL-NERVOUS-SYSTEM; QUINOLINIC ACID; ASPARTIC-ACID; HOMOCYSTEIC ACID; MEDIAN-EMINENCE; ARCUATE NUCLEUS; NMDA RECEPTORS; FEMALE PUBERTY; INVITRO AB These studies were designed to evaluate the actions and relative potencies of different endogenous and excitatory amino acid (EAA) selective analogs on EAA-induced neuropeptide secretion as well as to analyze the receptor subtypes involved. For this purpose, different glutamate agonists were tested for their ability to evoke release of the hypothalamic neuropeptide LHRH from arcuate nucleus-median eminence (AN-ME) fragments incubated in vitro. Different glutamate agonists, i.e. 3-amino-3-hydroxy-5-methyl-isoxazole-4-propionic (AMPA), kainic, quisqualic, homocysteic (HCA), quinolinic (QUIN), N-methyl-D-aspartic (NMDA), and pyroglutamic (PYR) acids, elicited LHRH release from AN-ME fragments in vitro. Further evaluation of the range of activity of several of these compounds, both in terms of the dose inducing a half-maximal response and the LHRH-releasing effect at that particular dose, indicated that AMPA > HCA > QUIN > PYR, suggesting that non-NMDA receptors are primarily involved in EAA-induced LHRH release at the level of the AN-ME. Evaluation of the receptor types involved using two specific antagonists for NMDA and non-NMDA receptors, D,L-2-amino-7-phosphoheptanoic acid and 6,7-cyanoquinoxaline-2,3-dione, respectively, showed that the effects of AMPA and HCA on LHRH release can be completely blocked by 6,7-cyanoquinoxaline-2,3-dione, whereas QUIN activity was blocked by D,L-2-amino-7-phosphoheptanoic acid. The effects of PYR on LHRH release were abolished by both receptor blockers. The metabotropic receptor agonist trans-1-amino-cyclopentyl-1,1,3-dicarboxylic acid was not active in eliciting LHRH secretion. The data indicate that endogenous substances active at EAA receptor sites, such as HCA, QUIN, and PYR, can significantly increase the secretion of the neuropeptide LHRH and, thus, may participate in the physiological regulation of the activity of this important neuroendocrine neuronal system. In addition, the results suggest that non-NMDA receptor sites may be preferentially activated at lower ligand concentrations, although NMDA receptors may also be involved in the response to certain endogenous agonists. RP LOPEZ, FJ (reprint author), NIEHS, MOLEC & INTEGRAT NEUROSCI LAB, REPROD NEUROENDOCRINOL SECT, RES TRIANGLE PK, NC 27709 USA. NR 46 TC 90 Z9 92 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1992 VL 130 IS 4 BP 1986 EP 1992 DI 10.1210/en.130.4.1986 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL122 UT WOS:A1992HL12200032 PM 1312433 ER PT J AU OSHIMA, H SIMONS, SS AF OSHIMA, H SIMONS, SS TI MODULATION OF GLUCOCORTICOID INDUCTION OF TYROSINE AMINOTRANSFERASE GENE-EXPRESSION BY VARIATIONS IN CELL-DENSITY SO ENDOCRINOLOGY LA English DT Article ID MAMMARY-TUMOR VIRUS; TISSUE-CULTURE CELLS; RAT HEPATOMA-CELLS; GROWTH FACTOR-BETA; DEXAMETHASONE 21-MESYLATE; AGONIST ACTIVITY; CYCLIC MODEL; RECEPTOR; BINDING; ACTIVATION AB Glucocorticoids induce tyrosine aminotransferase (TAT) in hepatoma cells. We have previously shown that both the concentration of the agonist dexamethasone (Dex) required for half-maximal induction (EC50) and the amount of agonist activity produced by the antagonist dexamethasone 21-mesylate (Dex-Mes), expressed as a percentage of maximum induction achieved by Dex, are different in Fu5-5 and HTC cells. Furthermore, both activities vary over several weeks in each cell line in an apparently random manner, but, nevertheless, are correlated by a linear semilog plot. We now find that this long term and previously unpredictable variation in both the Dex EC50 and the amount of Dex-Mes agonist activity for the induction of TAT enzyme activity can be made to occur reproducibly in 40 h or less by changing the cell density and/or amount of medium in the tissue culture plates. Thus, a higher cell density and/or a lower volume of medium produced both higher amounts of Dex-Mes agonist activity and lower EC50 values for Dex. Experiments with cells at different densities but exposed to the same medium indicated that cell density was the dominant determinant. A qualitatively identical modulation was seen at the level of TAT mRNA, but not mouse mammary tumor virus RNA. We are not aware of any previous report of cell growth conditions altering either the level of agonist activity of an antisteroid or the EC50 of a full agonist. These results further indicate that extrachromosomal parameters, such as cell-cell contact and/or a diffusable factor(s), can modulate the basic features of glucocorticoid induction of some, but not all, glucocorticoid-inducible genes. C1 NIDDKD, MOLEC & CELLULAR BIOL LAB,STEROID HORMONES SECT, BLDG 8,ROOM B2A-07, BETHESDA, MD 20892 USA. NR 44 TC 34 Z9 33 U1 1 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1992 VL 130 IS 4 BP 2106 EP 2112 DI 10.1210/en.130.4.2106 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL122 UT WOS:A1992HL12200048 PM 1347740 ER PT J AU LAITINEN, JT VISWANATHAN, M VAKKURI, O SAAVEDRA, JM AF LAITINEN, JT VISWANATHAN, M VAKKURI, O SAAVEDRA, JM TI DIFFERENTIAL REGULATION OF THE RAT MELATONIN RECEPTORS - SELECTIVE AGE-ASSOCIATED DECLINE AND LACK OF MELATONIN-INDUCED CHANGES SO ENDOCRINOLOGY LA English DT Article ID GUANINE-NUCLEOTIDES; BINDING-SITES; INVITRO AUTORADIOGRAPHY; SUPRACHIASMATIC NUCLEI; AREA POSTREMA; PITUITARY; BRAIN; LOCALIZATION; MODULATION; AFFINITY AB To gain some understanding of the factors regulating high affinity melatonin (MT) receptors in the rat, we conducted a series of studies using quantitative autoradiography of [2-I-125]iodo-MT binding in vitro with validated assay conditions. MT receptor status and the relative protein content of the autoradiographic sections were assessed in the anterior pituitary gland, the area postrema, the caudal (tail) artery (CA), the anterior cerebral artery (ACA), and the suprachiasmatic nuclei (SCN) of 9-, 96-, and 306-day-old Wistar rats. When age-associated changes in protein content were taken into account, MT receptor expression in the area postrema and the SCN remained relatively constant between 9-306 days of age. On the contrary, a dramatic loss of MT receptors was observed in the arteries of 306-day-old rats (98% and 89% loss compared to the 9-day-old rats in the ACA and CA, respectively). In the anterior pituitary gland, MT receptors were expressed only in the 9-day-old rats. The above changes reflected major changes in binding capacity and minor changes in binding affinity. Neither removal of endogenous circulating MT (acute light exposure for 24 h, pinealectomy, or superior cervical ganglionectomy) nor MT injections (1 mg/kg for 10 days 6 h after lights on) affected MT receptor status in the ACA, CA, area postrema, or SCN. Our data suggest that MT receptor expression is differentially regulated during development and that permanent alterations in MT levels do not affect rat MT receptor status. C1 NIMH, CLIN SCI LAB, PHARMACOL SECT, BLDG 10, ROOM 2D-45, BETHESDA, MD 20892 USA. UNIV OULU, DEPT PHYSIOL, SF-90220 OULU, FINLAND. NR 25 TC 53 Z9 55 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1992 VL 130 IS 4 BP 2139 EP 2144 DI 10.1210/en.130.4.2139 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL122 UT WOS:A1992HL12200053 PM 1312446 ER PT J AU ESKAY, RL EIDEN, LE HSU, CM AF ESKAY, RL EIDEN, LE HSU, CM TI INTERLEUKIN-1-ALPHA AND TUMOR-NECROSIS-FACTOR-ALPHA DIFFERENTIALLY REGULATE ENKEPHALIN, VASOACTIVE INTESTINAL POLYPEPTIDE, NEUROTENSIN, AND SUBSTANCE-P BIOSYNTHESIS IN CHROMAFFIN CELLS SO ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING-FACTOR; NEURONAL DIFFERENTIATION; GENE-EXPRESSION; PHORBOL ESTER; SOMATOSTATIN; ACTIVATION; SECRETION; CALCIUM; BRAIN AB The pattern of expression of at least four neuropeptides contained in adrenomedullary chromaffin cells is altered by exposure to the cytokines interleukin-1-alpha (IL-1-alpha) and tumor necrosis factor-alpha (TNF-alpha), alone or in combination with stimulation of other second messenger pathways. Vasoactive intestinal polypeptide (VIP) was elevated 2- to 3-fold by 1 nM IL-1-alpha within 48 h of exposure, while neurotensin and substance P synthesis were unaffected, and met-enkephalin levels were decreased 25-35%. Stimulation of VIP and substance P biosynthesis by forskolin was markedly enhanced by IL-1-alpha, while forskolin stimulation of enkephalin and neurotensin biosynthesis was unaffected. IL-1-alpha amplified the effect of phorbol myristate acetate to increase the VIP content of chromaffin cells, but antagonized phorbol ester-induced elevation of neurotensin levels. TNF-alpha also demonstrated a neuropeptide-specific pattern of modulation of second-messenger effects on chromaffin cell neuropeptide levels similar to those seen with IL-1-alpha. The neuroendocrine actions of IL-1-alpha described above, unlike IL-1 action in the immune system, do not appear to be mediated through IL-2 as this cytokine did not affect VIP or enkephalin expression in the presence or absence of protein kinase stimulation. Neither IL-1-alpha nor TNF-alpha affected the calcium-coupled stimulation of neuropeptide secretion and biosynthesis that occurs in response to cell depolarization in these and other neuroendocrine cells in vitro and in vivo. These data provide a functional demonstration of IL-1 and TNF receptors in chromaffin cell cultures and suggest a physiological role for cytokine production in the adrenal medulla. Since both the magnitude and direction of neuropeptide synthesis modulation by IL-1-alpha and TNF-alpha are highly peptide-specific, it appears that these cytokines do not merely augment second messenger pathways that affect neuropeptide synthesis, but potentially regulate the activity of factors controlling the pattern of neuropeptide gene expression in chromaffin cells. C1 NIMH, CELL BIOL LAB, BLDG 36, ROOM 3A-17, BETHESDA, MD 20892 USA. NIAAA, CLIN STUDIES LAB, BETHESDA, MD 20892 USA. NIMH, MOLEC & CELLULAR NEUROBIOL UNIT, BETHESDA, MD 20892 USA. OI Eiden, Lee/0000-0001-7524-944X NR 29 TC 55 Z9 55 U1 0 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1992 VL 130 IS 4 BP 2252 EP 2258 DI 10.1210/en.130.4.2252 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL122 UT WOS:A1992HL12200068 PM 1372239 ER PT J AU SHIVER, T FAMILARI, M AGUILERA, G AF SHIVER, T FAMILARI, M AGUILERA, G TI REGULATION OF INTERMEDIATE PITUITARY CORTICOTROPIN-RELEASING HORMONE RECEPTORS BY DOPAMINE SO ENDOCRINOLOGY LA English DT Article ID MESSENGER-RNA LEVELS; RAT PITUITARY; GLAND; LOBE; RESPONSES; BRAIN; CRF AB It has been shown that chronic cold exposure results in selective CRH receptor up-regulation in the intermediate pituitary. Since the intermediate pituitary is under dopaminergic control, the participation of a dopaminergic mechanism in the effect of cold stress was studied in rats treated with dopaminergic agonists and antagonists. CRH receptors were measured by the binding of radioiodinated Tyr-ovine (o) CRH to neurointermediate pituitary membranes of slide-mounted sections. Cold exposure for 60 h caused the expected increase in CRH binding in neurointermediate lobe membranes. Administration of the dopaminergic agonist bromocriptine did not prevent the effect of cold stress, but increased CRH binding in control rats. The dopaminergic antagonist metoclopramide decreased intermediate pituitary CRH binding in control and cold-exposed rats. Bromocriptine administration for 1-8 days caused a progressive increase in the binding of [I-125]Tyr-oCRH in neurointermediate pituitary membranes, despite atrophy of the intermediate zone. Scatchard analysis of the binding data indicated that the changes were due to variations in receptor concentration, without changes in affinity. No changes in anterior pituitary CRH receptors were observed with agonist or antagonist treatment. Autoradiographic analysis of CRH binding after 3 days of treatment with bromocriptine or haloperidol confirmed the results observed in membranes and demonstrated that changes in binding were confined to the intermediate lobe. The functional consequences of the changes in CRH binding were studied by analysis of adenylate cyclase activity in cells and homogenates of intermediate pituitaries of rats treated with bromocriptine. In 18-h cultured intermediate pituitary cells from rats treated with bromocriptine for 3 days, CRH-stimulated cAMP production, measured in the presence of phosphodiesterase inhibitors, was increased to levels only slightly higher than those in cells from control rats. Likewise, CRH-stimulated adenylate cyclase, measured by conversion of [P-32]ATP to [P-32] cAMP, was not significantly different in homogenates from microdissected intermediate lobes from control and bromocriptine-treated rats. The lack of parallel changes in adenylate cyclase responsiveness suggests only partial receptor coupling, probably reflecting an inhibitory effect of dopamine on components of the adenylate cyclase. This study demonstrates that in contrast to the recognized inhibitory effect on cell division and POMC mRNA expression, dopamine causes up-regulation of CRH receptors in the intermediate pituitary. The qualitatively similar and nonadditive effects of cold stress and dopaminergic agonists suggest that a dopaminergic mechanism may be involved in intermediate pituitary CRH receptor regulation during chronic cold stress. RP SHIVER, T (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, ENDOCRINE PHYSIOL SECT, BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA. NR 24 TC 12 Z9 12 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1992 VL 130 IS 4 BP 2299 EP 2304 DI 10.1210/en.130.4.2299 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL122 UT WOS:A1992HL12200075 PM 1347742 ER PT J AU BERTRAND, R OCONNOR, PM KERRIGAN, D POMMIER, Y AF BERTRAND, R OCONNOR, PM KERRIGAN, D POMMIER, Y TI SEQUENTIAL ADMINISTRATION OF CAMPTOTHECIN AND ETOPOSIDE CIRCUMVENTS THE ANTAGONISTIC CYTOTOXICITY OF SIMULTANEOUS DRUG ADMINISTRATION IN SLOWLY GROWING HUMAN COLON-CARCINOMA HT-29 CELLS SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID DNA TOPOISOMERASE-II; CYTO-TOXICITY; STRAND BREAKS; REPLICATION; INHIBITORS; 4'-(9-ACRIDINYLAMINO)METHANESULFON-META-ANISIDIDE; INVOLVEMENT; RESISTANCE; NOVOBIOCIN; POISONS AB We compared the cytotoxicity of simultaneous and sequential combination chemotherapy with camptothecin and etoposide, in slowly growing human colon carcinoma, HT-29 cells. Simultaneous treatments of HT-29 cells with etoposide and camptothecin produced no marked enhancement of cytotoxicity over single agent administration. This finding demonstrates antagonism of one drug's cytotoxicity over the other. When these studies were repeated in sequential treatment protocols, we observed that antagonism could be circumvented if the period between individual drug administration was separated by 6-8 h. The cytotoxicity that was observed with this approach was never more than additive and the order of camptothecin or etoposide administration did not significantly affect the extent of combined cytotoxicity observed. The protective effect of simultaneous camptothecin and etoposide exposure was not due to reduced formation or alterations in the rate of cleavable complex reversal, and protection persisted for a considerably longer period of time than DNA strand breaks. Protection correlated with the kinetics of DNA and RNA synthesis inhibition produced by either drug. Remarkably, full cytotoxic protection could be afforded by one drug over the other, in the presence of only partial inhibition of DNA or RNA synthesis (50-60%). Our findings suggest that sequential rather than simultaneous administration of topoisomerase I and II inhibitors in future cancer chemotherapy schedules will enhance cytotoxicity over single-agent administration. C1 NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,BLDG 37,ROOM 5C27,BETHESDA,MD 20892. NR 28 TC 108 Z9 112 U1 0 U2 8 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD APR-MAY PY 1992 VL 28A IS 4-5 BP 743 EP 748 DI 10.1016/0959-8049(92)90107-D PG 6 WC Oncology SC Oncology GA HV130 UT WOS:A1992HV13000009 PM 1326304 ER PT J AU REED, E COOPER, MR LAROCCA, RV BOSTICKBRUTON, F MYERS, CE AF REED, E COOPER, MR LAROCCA, RV BOSTICKBRUTON, F MYERS, CE TI SURAMIN IN ADVANCED PLATINUM-RESISTANT OVARIAN-CANCER SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID AGENT AB 10 patients with ovarian cancer, whose disease had progressed while receiving platinum-based therapy, were entered onto a phase II clinical trial of the antiproliferative agent suramin. Suramin was administered in a fashion that is associated with durable objective disease response in patients with hormonally resistant metastatic prostate cancer. No individual had an objective response to therapy in this study, but 3 of 9 evaluable patients (33%) experienced disease stabilisation and subjective clinical improvement for periods ranging from 2 to 5 months. Disease stabilisation was associated with prolonged periods of comparatively high plasma levels of drug, which appeared to be determined primarily by reduced drug clearance. We conclude that suramin has potential activity in platinum-resistant ovarian cancer, and we have initiated a second clinical trial using pharmacological information derived from this study. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. RP REED, E (reprint author), NCI,MED BRANCH,BLDG 10,ROOM 12N226,BETHESDA,MD 20892, USA. NR 13 TC 26 Z9 26 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD APR-MAY PY 1992 VL 28A IS 4-5 BP 864 EP 866 DI 10.1016/0959-8049(92)90135-O PG 3 WC Oncology SC Oncology GA HV130 UT WOS:A1992HV13000037 PM 1524910 ER PT J AU GOLDSMITH, HF BELL, RA WARHEIT, G AF GOLDSMITH, HF BELL, RA WARHEIT, G TI INDIRECT NEEDS ASSESSMENT FOR MENTAL-HEALTH-SERVICES PLANNING - INTRODUCTION TO THIS SPECIAL ISSUE SO EVALUATION AND PROGRAM PLANNING LA English DT Editorial Material C1 UNIV LOUISVILLE,DEPT PSYCHIAT & BEHAV SCI,LOUISVILLE,KY 40292. UNIV MIAMI,DEPT SOCIOL,CORAL GABLES,FL 33124. RP GOLDSMITH, HF (reprint author), NIMH,STAT RES BRANCH,APPL DEMOG PROGRAM,BETHESDA,MD 20892, USA. NR 8 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0149-7189 J9 EVAL PROGRAM PLANN JI Eval. Program Plan. PD APR-JUN PY 1992 VL 15 IS 2 BP 111 EP 113 DI 10.1016/0149-7189(92)90002-C PG 3 WC Social Sciences, Interdisciplinary SC Social Sciences - Other Topics GA HZ791 UT WOS:A1992HZ79100002 ER PT J AU GARRISON, HH HERMAN, SS LIPTON, JA AF GARRISON, HH HERMAN, SS LIPTON, JA TI COLLABORATIVE RELATIONSHIPS IN DENTAL MATERIALS RESEARCH - MEASURING THE VOLUME AND OUTCOMES SO EVALUATION REVIEW LA English DT Article ID UNIVERSITY AB Data from a survey of dental materials researchers were used to assess collaborative relationships involving researchers and resources from government, industry, and academia. The examination of research project organization yielded a higher estimate of collaboration (and industry collaboration in particular) than data on the most common research outcome, publications. The vast majority of the research outcomes reported by the survey respondents were publications. Only a small number of patents, products or processes were noted; however, these commercially oriented outcomes were far more likely than the publications to have involved collaborative research relationships with industry. C1 NIDR,OFF PLANNING EVALUAT & DATA SYST,BETHESDA,MD 20892. RP GARRISON, HH (reprint author), ASPEN SYST CORP,962 WAYNE AVE,SILVER SPRING,MD 20910, USA. NR 14 TC 1 Z9 1 U1 0 U2 0 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0193-841X J9 EVALUATION REV JI Eval. Rev. PD APR PY 1992 VL 16 IS 2 BP 184 EP 197 DI 10.1177/0193841X9201600205 PG 14 WC Social Sciences, Interdisciplinary SC Social Sciences - Other Topics GA HM744 UT WOS:A1992HM74400005 ER PT J AU RAO, PV ZIGLER, JS AF RAO, PV ZIGLER, JS TI MUTANT ZETA-CRYSTALLIN FROM GUINEA-PIG HEREDITARY CATARACTS HAS ALTERED STRUCTURAL AND ENZYMATIC-PROPERTIES SO EXPERIMENTAL EYE RESEARCH LA English DT Letter ID LENS; PROTEINS RP RAO, PV (reprint author), NEI,MECHANISMS OCULAR DIS LAB,9000 ROCKVILLE PIKE,BLDG 6,RM 237,BETHESDA,MD 20892, USA. NR 11 TC 18 Z9 18 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD APR PY 1992 VL 54 IS 4 BP 627 EP 630 DI 10.1016/0014-4835(92)90142-F PG 4 WC Ophthalmology SC Ophthalmology GA HT421 UT WOS:A1992HT42100017 PM 1623948 ER PT J AU KHAN, MA WORTHAM, JW WATZMAN, N GREEN, JG AF KHAN, MA WORTHAM, JW WATZMAN, N GREEN, JG TI THE NATIONAL-INSTITUTES-OF-HEALTH IS GOING HIGH-TECH IN PEER-REVIEW SO FASEB JOURNAL LA English DT Article RP KHAN, MA (reprint author), NIH,DIV RES GRANTS,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 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 1992 VL 6 IS 7 BP 2384 EP 2385 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA HP030 UT WOS:A1992HP03000002 PM 1563590 ER PT J AU CARAGAY, AB AF CARAGAY, AB TI CANCER-PREVENTIVE FOODS AND INGREDIENTS SO FOOD TECHNOLOGY LA English DT Article C1 ARTHUR D LITTLE INC,FOOD IND SECT,CAMBRIDGE,MA 02140. RP CARAGAY, AB (reprint author), NCI,EXPTL FOOD PROGRAM,ACORN PK,CAMBRIDGE,MA 02140, USA. NR 10 TC 158 Z9 164 U1 0 U2 2 PU INST FOOD TECHNOLOGISTS PI CHICAGO PA SUITE 300 221 N LASALLE ST, CHICAGO, IL 60601-1291 SN 0015-6639 J9 FOOD TECHNOL-CHICAGO JI Food Technol. PD APR PY 1992 VL 46 IS 4 BP 65 EP 68 PG 4 WC Food Science & Technology SC Food Science & Technology GA HN961 UT WOS:A1992HN96100003 ER PT J AU WEINER, RI WETSEL, W GOLDSMITH, P DELAESCALERA, GM WINDLE, J PADULA, C CHOI, A NEGROVILAR, A MELLON, P AF WEINER, RI WETSEL, W GOLDSMITH, P DELAESCALERA, GM WINDLE, J PADULA, C CHOI, A NEGROVILAR, A MELLON, P TI GONADOTROPIN-RELEASING-HORMONE NEURONAL CELL-LINES SO FRONTIERS IN NEUROENDOCRINOLOGY LA English DT Review DE GONADOTROPIN-RELEASING HORMONE; NEURONAL CELL LINES; TRANSGENIC MICE; NEUROSECRETORY NEURONS; PEPTIDE PROCESSING ID GNRH-ASSOCIATED PEPTIDE; RAT HYPOTHALAMUS; MESSENGER-RNA; IMMUNOCYTOCHEMICAL LOCALIZATION; LIQUID-CHROMATOGRAPHY; PYROGLUTAMYL-PEPTIDES; MOLECULAR-FORMS; TRANSGENIC MICE; PREOPTIC AREA; PRECURSOR AB Gonadotropin-releasing hormone (GnRH) cell lines were developed by genetically targeted tumorigenesis in transgenic mice. The cell lines designated GT1 cells have a neuronal phenotype, express neuronal but not glial markers and express the GnRH gene at high levels. The GnRH prohormone is processed in the cells to multiple molecular forms including biologically active GnRH and GnRH-associated peptide. Basal secretion of GnRH from the cells is regulated in part by fast Na+ channels necessary for propagated action potentials. In many instances, basal GnRH release is pulsatile with an interpulse frequency similar to that seen in castrated rodents, suggesting that GnRH neurons are the pulse generator and are capable of synchronizing their secretion in vitro. The secretion of GnRH is stimulated by depolarization and by the neurotransmitter norepinephrine. In related studies we have demonstrated that expression of Simian virus 40 T antigen in GnRH neurons of transgenic mice leads to hypothalamic hypogonadism due to the inability of GnRH nerve terminals to organize in the median eminence. These findings support the use of genetically-directed tumorigenesis to establish highly differentiated GnRH neuronal cell lines that are a valuable model to study the cell biology and regulation of thc neurons. C1 UNIV CALIF SAN FRANCISCO,CTR REPROD ENDOCRINOL,SAN FRANCISCO,CA 94143. SALK INST BIOL STUDIES,REGULATORY BIOL LAB,LA JOLLA,CA 92037. NATL INST ENVIRONM HLTH,MOLEC INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC. OI Windle, Jolene/0000-0001-6690-385X NR 70 TC 100 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 0091-3022 J9 FRONT NEUROENDOCRIN JI Front. Neuroendocrinol. PD APR PY 1992 VL 13 IS 2 BP 95 EP 119 PG 25 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA JE234 UT WOS:A1992JE23400001 PM 1468602 ER PT J AU CHHABRA, RS EUSTIS, S HASEMAN, JK KURTZ, PJ CARLTON, BD AF CHHABRA, RS EUSTIS, S HASEMAN, JK KURTZ, PJ CARLTON, BD TI COMPARATIVE CARCINOGENICITY OF ETHYLENE THIOUREA WITH OR WITHOUT PERINATAL EXPOSURE IN RATS AND MICE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID CHILDHOOD-CANCER; PARENTS; TESTS; TOXICOLOGY; INDUCTION; CHEMICALS; SMOKING; TUMORS; CELLS C1 BATTELLE MEM INST,COLUMBUS,OH 43201. RP CHHABRA, RS (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 45 TC 40 Z9 40 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 1992 VL 18 IS 3 BP 405 EP 417 DI 10.1016/0272-0590(92)90139-9 PG 13 WC Toxicology SC Toxicology GA HN393 UT WOS:A1992HN39300010 PM 1597265 ER PT J AU YUAN, JH JAMESON, CW GOEHL, TJ ELWELL, MR LEININGER, JR THOMPSON, MB CORNIFFE, G CARLTON, T AF YUAN, JH JAMESON, CW GOEHL, TJ ELWELL, MR LEININGER, JR THOMPSON, MB CORNIFFE, G CARLTON, T TI APPLICATION OF MOLECULAR ENCAPSULATION FOR TOXICOLOGY STUDIES - COMPARATIVE TOXICITY OF PARA-CHLORO-ALPHA,ALPHA,ALPHA-TRIFLUOROTOLUENE IN ALPHA-CYCLODEXTRIN VEHICLE VERSUS CORN-OIL VEHICLE IN MALE AND FEMALE FISCHER 344 RATS AND B6C3F1 MICE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID PROLIFERATIVE LESIONS; EXOCRINE PANCREAS; F344/N RATS; DOSE LEVELS; ALPHA-2U-GLOBULIN; GAVAGE C1 NIEHS,POB 12233,RES TRIANGLE PK,NC 27709. NR 37 TC 5 Z9 5 U1 1 U2 2 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 1992 VL 18 IS 3 BP 460 EP 470 DI 10.1016/0272-0590(92)90144-7 PG 11 WC Toxicology SC Toxicology GA HN393 UT WOS:A1992HN39300015 PM 1375921 ER PT J AU FRIED, MW SHINDO, M FONG, TL FOX, PC HOOFNAGLE, JH DIBISCEGLIE, AM AF FRIED, MW SHINDO, M FONG, TL FOX, PC HOOFNAGLE, JH DIBISCEGLIE, AM TI ABSENCE OF HEPATITIS-C VIRAL-RNA FROM SALIVA AND SEMEN OF PATIENTS WITH CHRONIC HEPATITIS-C SO GASTROENTEROLOGY LA English DT Article ID NON-B HEPATITIS; NON-A; VIRUS-INFECTION; RISK C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. RP FRIED, MW (reprint author), NIDDKD,LIVER DIS SECT,BLDG 10,ROOM 4D 52,BETHESDA,MD 20892, USA. NR 11 TC 137 Z9 138 U1 3 U2 3 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 1992 VL 102 IS 4 BP 1306 EP 1308 PN 1 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HK976 UT WOS:A1992HK97600026 PM 1312976 ER PT J AU SHINDO, M DIBISCEGLIE, AM HOOFNAGLE, JH AF SHINDO, M DIBISCEGLIE, AM HOOFNAGLE, JH TI ACUTE EXACERBATION OF LIVER-DISEASE DURING INTERFERON ALFA THERAPY FOR CHRONIC HEPATITIS-C SO GASTROENTEROLOGY LA English DT Note ID NON-A-HEPATITIS; NON-B-HEPATITIS; CONTROLLED TRIAL; ALPHA-INTERFERON; VIRUS RP SHINDO, M (reprint author), NIDDKD,DIGEST DIS BRANCH,LIVER DIS SECT,BLDG 10,ROOM 4D52,BETHESDA,MD 20892, USA. NR 11 TC 95 Z9 97 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 1992 VL 102 IS 4 BP 1406 EP 1408 PN 1 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HK976 UT WOS:A1992HK97600043 PM 1551549 ER PT J AU KOVACS, A KOVACS, G AF KOVACS, A KOVACS, G TI LOW CHROMOSOME-NUMBER IN CHROMOPHOBE RENAL-CELL CARCINOMAS SO GENES CHROMOSOMES & CANCER LA English DT Note ID TUMORS AB Cytogenetic analysis revealed low chromosome number, telomeric association, and pulverisation of chromosomes in three chromophobe renal cell carcinomas. One fully karyotyped and a previously published case showed the common loss of chromosomes 1, 2, 6, 10, 13, 17, and 21. C1 UNIV FREIBURG,INST PATHOL,W-7800 FREIBURG,GERMANY. NCI,FREDERICK CANC RES & DEV CTR,INC DYN CORP,PROGRAM RESOURCES,BETHESDA,MD 20892. FU NCI NIH HHS [N01-CO-74102] NR 6 TC 100 Z9 100 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 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD APR PY 1992 VL 4 IS 3 BP 267 EP 268 DI 10.1002/gcc.2870040313 PG 2 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA HT014 UT WOS:A1992HT01400012 PM 1382570 ER PT J AU BRUDER, JT HEIDECKER, G RAPP, UR AF BRUDER, JT HEIDECKER, G RAPP, UR TI SERUM-INDUCED, TPA-INDUCED, AND RAS-INDUCED EXPRESSION FROM AP-1/ETS-DRIVEN PROMOTERS REQUIRES RAF-1 KINASE SO GENES & DEVELOPMENT LA English DT Article DE RAF-1; V-HA-RAS; PROTOONCOGENE; SIGNAL TRANSDUCTION ID COMPLETE CODING SEQUENCE; SIGNAL TRANSDUCTION; C-FOS; REGULATORY DOMAIN; TRANSFORMED CELLS; PROTO-ONCOGENE; A-RAF; ACTIVATION; GENE; PROTEINS AB Raf-1 serine-threonine protein kinase has the hallmarks of a critical switch that connects growth factor receptor activation at the cell membrane with transcriptional events in the nucleus. We show by use of Raf-1 dominant-negative mutants that Raf-1 is required for serum-, TPA-, and Ras-induced expression from the oncogene-responsive element in the polyomavirus enhancer. The minimal region of Raf-1 that displays this dominant-negative phenotype (Raf-C4) contains a cysteine finger motif. Raf-C4 appears to function by titrating out a Raf-1-activating factor that is induced by Ras following serum or TPA treatment of NIH-3T3 cells. In addition, we show that Raf-1 and Ras cooperate in trans-activation through the oncogene-responsive element and that the cysteine-rich region is necessary for this effect. RP BRUDER, JT (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. NR 54 TC 464 Z9 465 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 1992 VL 6 IS 4 BP 545 EP 556 DI 10.1101/gad.6.4.545 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA HP038 UT WOS:A1992HP03800003 PM 1313769 ER PT J AU MARTINCAMPOS, JM COMERON, JM MIYASHITA, N AGUADE, M AF MARTINCAMPOS, JM COMERON, JM MIYASHITA, N AGUADE, M TI INTRASPECIFIC AND INTERSPECIFIC VARIATION AT THE Y-AC-SC REGION OF DROSOPHILA-SIMULANS AND DROSOPHILA-MELANOGASTER SO GENETICS LA English DT Article ID RESTRICTION-MAP VARIATION; ACHAETE-SCUTE REGION; NATURAL-POPULATIONS; GENE-COMPLEX; PHENOTYPIC VARIATION; MOLECULAR EVOLUTION; DNA POLYMORPHISM; YELLOW LOCUS; X-CHROMOSOME; ENDONUCLEASES AB A 2.2-kb region including the ac gene of Drosophila simulans has been sequenced. Interspecific divergence between Drosphila melanogaster and D. simulans was estimated as 0.0695 and 0.0558 for silent and for all sites, respectively. Estimated silent site divergence for the ac region is comparable to that estimated for other regions of the genome between these species, indicating that silent sites of the ac region are not under significantly stronger functional constraint. Intraspecific variation in both species was also investigated. Restriction-site and length polymorphism in the ac region of D. simulans has been investigated for 103 X chromosome lines sampled from three natural populations in Spain using eight four-cutter restriction enzymes. Neither restriction-site nor length variation was detected in the three populations surveyed. In D. melanogaster restriction-site and length polymorphism in all major transcription units of the y-ac-sc region (23.1-kb region) has been studied using four four-cutter restriction enzymes for 245 X chromosome lines sampled from 10 natural populations (seven from Europe, two from North America and one from Japan). Fourteen restriction-site and 28 length polymorphisms were detected. There was some indication of population subdivision for North American vs. European samples of D. melanogaster. The frequency spectrum of restriction-site polymorphisms in European populations was skewed toward rarer frequencies than predicted by the neutral theory. Comparison of silent site variation at this telomeric region with that in the Adh 5'-flanking region showed a reduced level of heterozygosity in the y-ac-sc region. Since interspecific silent divergence is not reduced in the y-ac-sc region as compared to other regions, the reduction in standing levels of variation at this telomeric locus in both D. simulans and D. melanogaster is most easily explained by a hitchhiking effect of linked selected substitutions. C1 NIEHS, GENET LAB, RES TRIANGLE PK, NC 27709 USA. RP MARTINCAMPOS, JM (reprint author), UNIV BARCELONA, FAC BIOL, DEPT GENET, BARCELONA 7, SPAIN. RI Comeron, Josep/G-6630-2012; OI Martin-Campos, Jesus Maria/0000-0003-0414-037X NR 43 TC 61 Z9 62 U1 0 U2 2 PU GENETICS SOC AM PI BETHESDA PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA SN 0016-6731 J9 GENETICS JI Genetics PD APR PY 1992 VL 130 IS 4 BP 805 EP 816 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA HL490 UT WOS:A1992HL49000010 PM 1582559 ER PT J AU DANCIGER, M CHAKRABORTI, A FARBER, DB KOZAK, CA AF DANCIGER, M CHAKRABORTI, A FARBER, DB KOZAK, CA TI LOCALIZATION OF THE GENE FOR A 3RD G-PROTEIN BETA-SUBUNIT TO MOUSE CHROMOSOME-6 NEAR RAF-1 SO GENOMICS LA English DT Article ID BINDING REGULATORY PROTEINS; RETINAL DEGENERATION; MOLECULAR-CLONING; RHODOPSIN GENE; RD MOUSE; ONCOGENE; IDENTIFICATION; POLYPEPTIDE; SEQUENCES; FRAGMENTS C1 UNIV CALIF LOS ANGELES,SCH MED,JULES STEIN EYE INST,100 STEIN PLAZA,LOS ANGELES,CA 90024. NIAID,BETHESDA,MD 20892. FU NEI NIH HHS [EY 00331, EY 02651] NR 31 TC 14 Z9 14 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 1992 VL 12 IS 4 BP 688 EP 692 DI 10.1016/0888-7543(92)90295-4 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HJ574 UT WOS:A1992HJ57400011 PM 1572642 ER PT J AU POWNALL, S KOZAK, CA SCHAPPERT, K SARKAR, M HULL, E SCHACHTER, H MARTH, JD AF POWNALL, S KOZAK, CA SCHAPPERT, K SARKAR, M HULL, E SCHACHTER, H MARTH, JD TI MOLECULAR-CLONING AND CHARACTERIZATION OF THE MOUSE UDP-N-ACETYLGLUCOSAMINE - ALPHA-3-D-MANNOSIDE BETA-1,2-N-ACETYLGLUCOSAMINYLTRANSFERASE-I GENE SO GENOMICS LA English DT Article ID LEUKEMIA INHIBITORY FACTOR; CELLS C1 UNIV BRITISH COLUMBIA, DEPT MED GENET, VANCOUVER V6T 1Z3, BC, CANADA. UNIV BRITISH COLUMBIA, DEPT BIOCHEM, VANCOUVER V6T 1Z3, BC, CANADA. NIAID, MOLEC MICROBIOL LAB, BETHESDA, MD 20892 USA. HOSP SICK CHILDREN, RES INST, TORONTO M5G 1X8, ONTARIO, CANADA. UNIV TORONTO, DEPT BIOCHEM, TORONTO M5G 1X8, ONTARIO, CANADA. RP POWNALL, S (reprint author), UNIV BRITISH COLUMBIA, BIOMED RES CTR, VANCOUVER V6T 1Z3, BC, CANADA. NR 21 TC 65 Z9 66 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 EI 1089-8646 J9 GENOMICS JI Genomics PD APR PY 1992 VL 12 IS 4 BP 699 EP 704 DI 10.1016/0888-7543(92)90297-6 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HJ574 UT WOS:A1992HJ57400013 PM 1533386 ER PT J AU CUTTING, GR CURRISTIN, S ZOGHBI, H OHARA, B SELDIN, MF UHL, GR AF CUTTING, GR CURRISTIN, S ZOGHBI, H OHARA, B SELDIN, MF UHL, GR TI IDENTIFICATION OF A PUTATIVE GAMMA-AMINOBUTYRIC-ACID (GABA) RECEPTOR SUBUNIT RHO(2) CDNA AND COLOCALIZATION OF THE GENES ENCODING RHO(2) (GABRR2) AND RHO(1) (GABRR1) TO HUMAN-CHROMOSOME 6Q14-Q21 AND MOUSE CHROMOSOME-4 SO GENOMICS LA English DT Article ID ALPHA-SUBUNIT; BETA-SUBUNIT; ASSIGNMENT; LINKAGE; ARM; MAP C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL & NEUROSCI,BALTIMORE,MD 21205. BAYLOR COLL MED,DEPT PEDIAT,HOUSTON,TX 77030. BAYLOR COLL MED,INST MOLEC GENET,HOUSTON,TX 77030. STANFORD UNIV,DEPT BIOL SCI,STANFORD,CA 94305. DUKE UNIV,SCH MED,DEPT MED,DIV RHEUMATOL IMMUNOL,DURHAM,NC 27706. DUKE UNIV,SCH MED,DEPT MICROBIOL,DURHAM,NC 27706. NIDA,ADDICT RES CTR,MOLEC NEUROBIOL LAB,BALTIMORE,MD. RP CUTTING, GR (reprint author), JOHNS HOPKINS UNIV,SCH MED,CTR MED GENET,BALTIMORE,MD 21205, USA. FU NHGRI NIH HHS [HG00373, HG001D1]; NINDS NIH HHS [NS27699] NR 32 TC 191 Z9 193 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 1992 VL 12 IS 4 BP 801 EP 806 DI 10.1016/0888-7543(92)90312-G PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HJ574 UT WOS:A1992HJ57400028 PM 1315307 ER PT J AU CLAVERIE, JM AF CLAVERIE, JM TI IDENTIFYING CODING EXONS BY SIMILARITY SEARCH - ALU-DERIVED AND OTHER POTENTIALLY MISLEADING PROTEIN SEQUENCES SO GENOMICS LA English DT Note ID TOOL RP CLAVERIE, JM (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894, USA. NR 10 TC 24 Z9 24 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 1992 VL 12 IS 4 BP 838 EP 841 DI 10.1016/0888-7543(92)90321-I PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HJ574 UT WOS:A1992HJ57400037 PM 1572661 ER PT J AU BRANT, LJ GERMAN, PS ROVNER, BW BURTON, LC PEARSON, JD CLARK, RD AF BRANT, LJ GERMAN, PS ROVNER, BW BURTON, LC PEARSON, JD CLARK, RD TI A LONGITUDINAL APPROACH TO MODELING OUTCOMES IN A NURSING-HOME STUDY SO GERONTOLOGIST LA English DT Article; Proceedings Paper CT SYMP ON MENTAL MORBIDITY IN THE NURSING HOME AT THE 43RD ANNUAL SCIENTIFIC MEETING OF THE GERONTOLOGICAL SOC OF AMERICA CY NOV, 1990 CL BOSTON, MA SP GERONTOL SOC AMER DE ADAPTATION; INDIVIDUAL VARIABILITY; INSTITUTIONAL CARE; PREDICTIVE OUTCOME AB Recent developments in longitudinal statistical methodology have improved our ability to model dynamic processes such as adaptation to nursing homes. Longitudinal observations provide information on individual patterns of change and factors affecting them. However, longitudinal analyses are often complicated by unequal periods of observation and individual variability in patterns of change. This paper demonstrates the use of a linear mixed-effects model to study adaptation in a longitudinal nursing home study with different numbers of repeated measurements for each individual becase of discharges, transfers, and mortality. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT HLTH POLICY & MANAGEMENT,BALTIMORE,MD 21218. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. RP BRANT, LJ (reprint author), NIA,GERONTOL RES CTR,LONGITUDINAL STUDIES BRANCH,BALTIMORE,MD 21224, USA. NR 8 TC 9 Z9 9 U1 0 U2 1 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD APR PY 1992 VL 32 IS 2 BP 159 EP 163 PG 5 WC Gerontology SC Geriatrics & Gerontology GA HM995 UT WOS:A1992HM99500005 PM 1577309 ER PT J AU BURTON, LC GERMAN, PS ROVNER, BW BRANT, LJ CLARK, RD AF BURTON, LC GERMAN, PS ROVNER, BW BRANT, LJ CLARK, RD TI MENTAL-ILLNESS AND THE USE OF RESTRAINTS IN NURSING-HOMES SO GERONTOLOGIST LA English DT Article; Proceedings Paper CT SYMP ON MENTAL MORBIDITY IN THE NURSING HOME AT THE 43RD ANNUAL SCIENTIFIC MEETING OF THE GERONTOLOGICAL SOC OF AMERICA CY NOV, 1990 CL BOSTON, MA SP GERONTOL SOC AMER DE MENTAL DISORDERS; DEMENTIA; ACTIVITIES OF DAILY LIVING ID MECHANICAL RESTRAINTS; PHYSICAL RESTRAINTS; MEDICAL WARDS; MANAGEMENT; FREEDOM; NURSES AB Using data from 441 newly admitted nursing home residents, we examined whether the diagnoses of mental illnesses, as well as other resident characteristics, were associated with use of physical restraints in both high restraint and low restraint use homes. Predictors of restraint use during both the first month and the first year of admission were inability to transfer and having a combination of severe ADL and cognitive impairment. Other predictors were wandering, inability to dress, symptoms of depression, and severity of cognitive impairment. C1 THOMAS JEFFERSON UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PHILADELPHIA,PA 19107. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP BURTON, LC (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT HLTH POLICY & MANAGEMENT,624 N BROADWAY,BALTIMORE,MD 21205, USA. FU NIA NIH HHS [AGO6765] NR 36 TC 40 Z9 40 U1 0 U2 1 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0016-9013 J9 GERONTOLOGIST JI Gerontologist PD APR PY 1992 VL 32 IS 2 BP 164 EP 170 PG 7 WC Gerontology SC Geriatrics & Gerontology GA HM995 UT WOS:A1992HM99500006 PM 1577310 ER PT J AU POTTER, M AF POTTER, M TI PERSPECTIVES ON THE ORIGINS OF MULTIPLE-MYELOMA AND PLASMACYTOMAS IN MICE SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Article ID HUMAN-BONE-MARROW; C-MYC ONCOGENE; MOUSE PLASMACYTOMAS; PLASMA-CELLS; B-CELLS; INTERLEUKIN-6; DIFFERENTIATION; PROLIFERATION; TRANSLOCATION; PRECURSORS RP POTTER, M (reprint author), NCI,GENET LAB,DCDBC,BETHESDA,MD 20892, USA. NR 66 TC 26 Z9 28 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 1992 VL 6 IS 2 BP 211 EP 223 PG 13 WC Oncology; Hematology SC Oncology; Hematology GA HQ380 UT WOS:A1992HQ38000002 PM 1582969 ER PT J AU RIEDEL, DA POTTERN, LM AF RIEDEL, DA POTTERN, LM TI THE EPIDEMIOLOGY OF MULTIPLE-MYELOMA SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID ZEALAND-CANCER-REGISTRY; SWEDISH AGRICULTURAL-WORKERS; WELL-DEFINED POPULATION; UNITED-STATES; SOCIOECONOMIC-STATUS; RUBBER WORKERS; C-MYC; LYMPHOPROLIFERATIVE DISORDERS; PROPORTIONATE MORTALITY; ANKYLOSING-SPONDYLITIS RP RIEDEL, DA (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 418,BETHESDA,MD 20892, USA. NR 187 TC 100 Z9 103 U1 1 U2 5 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 1992 VL 6 IS 2 BP 225 EP 247 PG 23 WC Oncology; Hematology SC Oncology; Hematology GA HQ380 UT WOS:A1992HQ38000003 PM 1582971 ER PT J AU BURKE, TR RUSS, PL MARQUEZ, VE AF BURKE, TR RUSS, PL MARQUEZ, VE TI A NEW SYNTHETIC METHOD FOR THE SYNTHESIS OF HYDROXYLATED ISOQUINOLINES - PREPARATION OF METHYL 6,7-DIHYDROXY-ISOQUINOLINE-3-CARBOXYLATE AND 7,8-DIHYDROXY-ISOQUINOLINE-3-CARBOXYLATE, POTENTIAL PROTEIN-TYROSINE KINASE INHIBITORS SO HETEROCYCLES LA English DT Article AB Synthesis of potential protein-tyrosine kinase inhibitors (6c) and (6e) is presented as a general procedure for the preparation of polyhydroxylated isoquinolines. Key features of the method include selective hydroxyl protection of tetrahydroisoquinolines by O-acylation followed by aromatization using MnO2. Quantitative deprotection of resulting O-acylisoquinolines is achieved using methanolic HCl. RP BURKE, TR (reprint author), NCI, DIV AUTOMAT CONTROL, MED CHEM LAB, DEV THERAPEUT PROGRAM, BETHESDA, MD 20892 USA. RI Burke, Terrence/N-2601-2014 NR 16 TC 9 Z9 9 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0385-5414 J9 HETEROCYCLES JI Heterocycles PD APR 1 PY 1992 VL 34 IS 4 BP 757 EP 764 PG 8 WC Chemistry, Organic SC Chemistry GA HU390 UT WOS:A1992HU39000016 ER PT J AU ANDERSON, WF AF ANDERSON, WF TI THE NIH HUMAN GENE-THERAPY SYMPOSIUM SO HUMAN GENE THERAPY LA English DT Editorial Material RP ANDERSON, WF (reprint author), NHLBI,MOLEC HEMATOL BRANCH,BLDG 10,7D-18,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD APR PY 1992 VL 3 IS 2 BP 127 EP 128 DI 10.1089/hum.1992.3.2-127 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA HU417 UT WOS:A1992HU41700001 PM 1391031 ER PT J AU FONG, D CHAN, MMY HSIEH, WT MENNINGER, JC WARD, DC AF FONG, D CHAN, MMY HSIEH, WT MENNINGER, JC WARD, DC TI CONFIRMATION OF THE HUMAN CATHEPSIN-B GENE (CTSB) ASSIGNMENT TO CHROMOSOME-8 SO HUMAN GENETICS LA English DT Article ID INSITU HYBRIDIZATION; ACID AB Human cathepsin B gene (CTSB) has been mapped to two locations: 8p22 and 13q14. Here we confirm the chromosome 8 assignment by three independent methods: (1) analysis of human-hamster somatic cell hybrid DNA by polymerase chain reaction; (2) comparison of hybridization signals to cathepsin B in interphase nuclei of normal fibroblasts and fibroblasts with a chromosome 8 deletion; and (3) fluorescence in situ hybridization to metaphase spreads using cathepsin B cosmid clones. Our results indicate that human CTSB is located at 8p22-p23.1. C1 UNIV ALABAMA,DEPT BIOL,BIRMINGHAM,AL 35294. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. RUTGERS STATE UNIV,DEPT BIOL SCI,PISCATAWAY,NJ 08855. RP FONG, D (reprint author), RUTGERS STATE UNIV,DEPT BIOL SCI,PISCATAWAY,NJ 08855, USA. FU NCI NIH HHS [CA49359]; NHGRI NIH HHS [HG00272, HG00246] NR 21 TC 32 Z9 33 U1 0 U2 0 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 1992 VL 89 IS 1 BP 10 EP 12 DI 10.1007/BF00207033 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA HQ684 UT WOS:A1992HQ68400002 PM 1577456 ER PT J AU POLYMEROPOULOS, MH XIAO, H MERRIL, CR AF POLYMEROPOULOS, MH XIAO, H MERRIL, CR TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE HUMAN C-MYC ONCOGENE LOCUS (MYC) SO HUMAN MOLECULAR GENETICS LA English DT Article ID REGION; GENE C1 ST ELIZABETH HOSP, NIMH, CTR NEUROSCI, WASHINGTON, DC 20032 USA. NR 4 TC 9 Z9 9 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1992 VL 1 IS 1 BP 65 EP 65 DI 10.1093/hmg/1.1.65 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA JN240 UT WOS:A1992JN24000015 PM 1301140 ER PT J AU FUTREAL, PA BARRETT, JC WISEMAN, RW AF FUTREAL, PA BARRETT, JC WISEMAN, RW TI DINUCLEOTIDE REPEAT POLYMORPHISM IN THE THRA1 GENE SO HUMAN MOLECULAR GENETICS LA English DT Article C1 UNIV N CAROLINA, DEPT PATHOL, CHAPEL HILL, NC 27599 USA. NIEHS, MOLEC CARCINOGENESIS LAB, RES TRIANGLE PK, NC 27709 USA. NR 3 TC 17 Z9 17 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1992 VL 1 IS 1 BP 66 EP 66 DI 10.1093/hmg/1.1.66-a PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA JN240 UT WOS:A1992JN24000018 PM 1301142 ER PT J AU DAVIS, BR OBERMAN, A BLAUFOX, MD WASSERTHEILSMOLLER, S HAWKINS, CM CUTLER, JA ZIMBALDI, N LANGFORD, HG AF DAVIS, BR OBERMAN, A BLAUFOX, MD WASSERTHEILSMOLLER, S HAWKINS, CM CUTLER, JA ZIMBALDI, N LANGFORD, HG TI EFFECT OF ANTIHYPERTENSIVE THERAPY ON WEIGHT-LOSS SO HYPERTENSION LA English DT Article DE MILD HYPERTENSION; WEIGHT LOSS; DIET; DIURETIC THERAPY; ADRENERGIC BETA-RECEPTOR BLOCKADERS; SYMPATHOLYTICS ID ESSENTIAL-HYPERTENSION; BLOOD-PRESSURE; PROPRANOLOL; TRIAL; MECHANISM; BLOCKADE; RENIN; OBESE AB We report the effect on weight changes of the type of antihypertensive medication prescribed in a trial of the relative efficacy of drug and dietary measures in mild hypertension. The Trial of Antihypertensive Interventions and Management studied 878 mildly hypertensive individuals randomly assigned, in a 3 x 3 design, to no diet change, weight loss, or a low sodium-high potassium diet and to placebo, 25 mg chlorthalidone, or 50 mg atenolol. The type of drug prescribed affected weight change with all diets. The drug effect on weight change, present in all groups at 6 months, was most pronounced in those randomly assigned to the weight loss diet, where the placebo group lost 4.4 kg, the atenolol group lost 3.0 kg, and the chlorthalidone group lost 6.9 kg. The group differences were attenuated but persisted at 24 months. We suggest that the antihypertensive drug prescribed affects the success of a conjoint weight loss program and speculate that the difference between the drugs may be due to their intrinsic effects on the sympathetic nervous system and related metabolic changes. C1 UNIV ALABAMA,DIV GEN & PREVENT MED,BIRMINGHAM,AL. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT NUCL MED,BRONX,NY 10461. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT EPIDEMIOL & SOCIAL MED,BRONX,NY 10461. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. UNIV MISSISSIPPI,MED CTR,DEPT MED,JACKSON,MS 39216. RP DAVIS, BR (reprint author), UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,COORDINATING CTR CLIN TRIALS,1200 HERMAN PRESSLER ST,HOUSTON,TX 77030, USA. FU NHLBI NIH HHS [HL-24369, HL-30171, HL-30163] NR 25 TC 33 Z9 33 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD APR PY 1992 VL 19 IS 4 BP 393 EP 399 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HM354 UT WOS:A1992HM35400015 PM 1555871 ER PT J AU HAGMANN, MJ LEVIN, RL CALLOWAY, L OSBORN, AJ FOSTER, KR AF HAGMANN, MJ LEVIN, RL CALLOWAY, L OSBORN, AJ FOSTER, KR TI MUSCLE-EQUIVALENT PHANTOM MATERIALS FOR 10-100 MHZ SO IEEE TRANSACTIONS ON MICROWAVE THEORY AND TECHNIQUES LA English DT Note ID DIELECTRIC-PROPERTIES; BIOLOGICAL-MATERIALS; THERMAL-PROPERTIES; HYPERTHERMIA; TISSUES AB New tissue-simulating materials are described which are aqueous solutions. Glycine is used to obtain the large permittivity of muscle at frequencies below 100 MHz. The lack of suspended solids simplifies preparation, and ensures the dielectric properties are homogeneous, stable and reproducible. The solutions are transparent, facilitating placement of probes for measuring temperature or electric field. The optical clarity of the phantom mixtures may also be desirable in a quick assessment of RF applicators by the use of liquid crystalline display sheets. Long-term stable gelling, with no measurable change in dielectric properties, can be obtained with 1 to 2 percent of agarose or carrageenan. C1 NIH,DIV RES SERV,BIOMED ENGN & INSTRUMENTAT BRANCH,BETHESDA,MD 20892. RP HAGMANN, MJ (reprint author), FLORIDA INT UNIV,DEPT ELECT & COMP ENGN,MIAMI,FL 33199, USA. NR 31 TC 6 Z9 6 U1 0 U2 3 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0018-9480 J9 IEEE T MICROW THEORY JI IEEE Trans. Microw. Theory Tech. PD APR PY 1992 VL 40 IS 4 BP 760 EP 762 DI 10.1109/22.127527 PG 3 WC Engineering, Electrical & Electronic SC Engineering GA HL985 UT WOS:A1992HL98500021 ER PT J AU YUAN, Q KOZAK, CA JIANG, WM HOLLANDER, D WATSON, JD KRISSANSEN, GW AF YUAN, Q KOZAK, CA JIANG, WM HOLLANDER, D WATSON, JD KRISSANSEN, GW TI GENETIC-MAPPING OF THE GENE CODING FOR THE INTEGRIN-BETA-7 SUBUNIT TO THE DISTAL PART OF MOUSE CHROMOSOME-15 SO IMMUNOGENETICS LA English DT Note ID INSITU HYBRIDIZATION; MURINE PLASMACYTOMAS; SYNTHETIC PEPTIDE; MYC ONCOGENE; RECEPTORS; LEUKEMIA; MICE; TRANSLOCATIONS; LOCALIZATION; LYMPHOCYTES C1 UNIV AUCKLAND,SCH MED,DEPT MOLEC MED,AUCKLAND,NEW ZEALAND. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. UNIV CALIF IRVINE,DEPT MED,IRVINE,CA 92717. NR 34 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD APR PY 1992 VL 35 IS 6 BP 403 EP 407 PG 5 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA HN882 UT WOS:A1992HN88200008 PM 1349587 ER PT J AU MUKAIDA, N GUSSELLA, GL KASAHARA, T KO, Y ZACHARIAE, COC KAWAI, T MATSUSHIMA, K AF MUKAIDA, N GUSSELLA, GL KASAHARA, T KO, Y ZACHARIAE, COC KAWAI, T MATSUSHIMA, K TI MOLECULAR ANALYSIS OF THE INHIBITION OF INTERLEUKIN-8 PRODUCTION BY DEXAMETHASONE IN A HUMAN FIBROSARCOMA CELL-LINE SO IMMUNOLOGY LA English DT Article ID NEUTROPHIL CHEMOTACTIC FACTOR; TUMOR NECROSIS FACTOR; GENE-EXPRESSION; GLUCOCORTICOID RECEPTOR; MEDIATED INHIBITION; MAMMALIAN-CELLS; LYMPHOCYTES-T; MESSENGER-RNA; DNA-BINDING; ACTIVATION AB In order to analyse the effects of glucocorticoids on interleukin-8 (IL-8) production more precisely, we examined the effects of dexamethasone on IL-8 production at the molecular level in a human fibrosarcoma cell line, 8387, which IL-1 induces to express IL-8 messenger RNA (mRNA) and to secrete IL-8. Over a wide dose range, dexamethasone inhibited IL-8 production induced by IL-1-alpha stimulation. Northern blotting analysis showed that dexamethasone also inhibited the IL-8 mRNA accumulation in a similar dose-related manner. Nuclear run-off assay revealed that dexamethasone decreased the transcription of the IL-8 gene and the degree of inhibition of transcription correlated well with the inhibition of IL-8 production, suggesting that the action of glucocorticoids is mainly at the transcriptional level. Furthermore, transfection with chloramphenicol acetyl transferase (CAT) expression vectors inserrted with the 5'-deleted IL-8 gene demonstrated that the 5'-flanking region which contains the glucocorticoid response element (GRE) was mainly involved in the dexamethasone-induced repression of the IL-8 gene. These data suggest that the inhibition of the IL-8 gene transcription by glucocorticoids occurs through the interaction of the glucocorticoid receptor complex with GRE in the 5'-flanking region of the IL-8 gene. C1 JICHI MED SCH,DEPT MED BIOL & PARASITOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. INC DYN CORP,PROGRAM RESOURCES,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,FREDERICK,MD 21701. KANAZAWA UNIV,CANC RES INST,DEPT PHARMACOL,TAKARA,JAPAN. RP MUKAIDA, N (reprint author), JICHI MED SCH,DEPT CLIN PATHOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN. RI Mukaida, Naofumi/D-7623-2011 OI Mukaida, Naofumi/0000-0002-4193-1851 NR 39 TC 79 Z9 79 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD APR PY 1992 VL 75 IS 4 BP 674 EP 679 PG 6 WC Immunology SC Immunology GA HP551 UT WOS:A1992HP55100020 PM 1592440 ER PT J AU WITKOP, B AF WITKOP, B TI REMEMBERING RAMACHANDRAN,ELKAY SO INDIAN JOURNAL OF BIOCHEMISTRY & BIOPHYSICS LA English DT Item About an Individual C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU COUNCIL SCIENTIFIC INDUSTRIAL RESEARCH PI NEW DELHI PA PUBL & INFO DIRECTORATE, NEW DELHI 110012, INDIA SN 0301-1208 J9 INDIAN J BIOCHEM BIO JI Indian J. Biochem. Biophys. PD APR PY 1992 VL 29 IS 2 BP U97 EP U97 PG 1 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HR449 UT WOS:A1992HR44900002 ER PT J AU SCHNEIDER, ML SUOMI, SJ AF SCHNEIDER, ML SUOMI, SJ TI NEUROBEHAVIORAL ASSESSMENT IN RHESUS-MONKEY NEONATES (MACACA-MULATTA) - DEVELOPMENTAL-CHANGES, BEHAVIORAL STABILITY, AND EARLY EXPERIENCE SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE MACACA-MULATTA; RHESUS MONKEY; NEONATAL BEHAVIOR; ENRICHMENT; NEUROMOTOR MATURITY; TEMPERAMENT; VISUAL ORIENTING; NURSERY REARING; STABILITY; INDIVIDUAL DIFFERENCES ID ENVIRONMENTAL ENRICHMENT; INFANTS; MODEL AB This prospective study documented developmental changes, individual stability, and the effects of early experience on the neurobehavioral repertoire of nursery-reared rhesus monkey neonates (Macaca mulatta) tested repeatedly across the first month of life. Thirty-six infants were tested three times weekly on a substantially modified version of the Neonatal Behavioral Assessment Scale. The infants were reared under several conditions in which their exposure to animate and inanimate objects varied. Eleven infants were reared with only a cloth, 8 were reared with an upright cloth-covered surrogate, 7 were reared with an upright movable cloth-covered surrogate, and 10 were reared with an upright movable cloth-covered surrogate and regular exposure to peers and novel toys. Infants reared with a movable surrogate demonstrated superior motor maturation in comparison to those reared with only a cloth or cloth-covered surrogate. However, infants reared with a movable surrogate as well as exposure to peers and novel toys showed not only greater motor maturation than cloth-reared infants but also greater responsiveness on orientation items and lower ratings of fearfulness when compared to infants in the three other conditions. Furthermore, the data indicate that behavioral stability of individual differences can be demonstrated in individuals undergoing rapid developmental change regardless of rearing conditions. C1 UNIV WISCONSIN,MADISON,WI 53706. NICHHD,BETHESDA,MD 20892. NR 33 TC 91 Z9 91 U1 0 U2 7 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 1992 VL 15 IS 2 BP 155 EP 177 DI 10.1016/0163-6383(92)80021-L PG 23 WC Psychology, Developmental SC Psychology GA JH522 UT WOS:A1992JH52200002 ER PT J AU MANGAN, DF WAHL, SM SULTZER, BM MERGENHAGEN, SE AF MANGAN, DF WAHL, SM SULTZER, BM MERGENHAGEN, SE TI STIMULATION OF HUMAN MONOCYTES BY ENDOTOXIN-ASSOCIATED PROTEIN - INHIBITION OF PROGRAMMED CELL-DEATH (APOPTOSIS) AND POTENTIAL SIGNIFICANCE IN ADJUVANTICITY SO INFECTION AND IMMUNITY LA English DT Note ID POLYCLONAL ACTIVATOR; LYMPHOCYTES; EXPRESSION; MITOGEN AB Mononuclear phagocytes are essential for adjuvant activity and polyclonal immunoglobulin synthesis induced by endotoxin-associated protein (EP) from Salmonella spp. To define the mechanisms of EP-mediated immunostimulation, we evaluated monocyte functions central to adjuvanticity following exposure to Salmonella typhimurium EP. In this study, we show that EP promotes the survival of monocytes by blocking programmed cell death (apoptosis), enhancing the production of the immunostimulatory cytokine interleukin-1 (IL-1) and stimulating the increased expression of HLA-DR and IL-2 receptors, which are cell membrane proteins that facilitate antigen presentation and IL-2 regulation, respectively. These results indicate that, like lipopolysaccharide, EP is a potent activator of human monocytes and suggest that EP-induced immunostimulation may be mediated, in part, by enhanced monocyte survival, cytokine release, and receptor expression. C1 SUNY HLTH SCI CTR,MORSE INST MOLEC GENET,DEPT MICROBIOL & IMMUNOL,BROOKLYN,NY 11203. RP MANGAN, DF (reprint author), NIDR,IMMUNOL LAB,CELLULAR IMMUNOL SECT,BETHESDA,MD 20892, USA. FU NIAID NIH HHS [AI28526]; NIDCR NIH HHS [DE05576] NR 22 TC 23 Z9 24 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 1992 VL 60 IS 4 BP 1684 EP 1686 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HK753 UT WOS:A1992HK75300057 PM 1548091 ER PT J AU BHATTACHARYA, A GHILDYAL, R PRASAD, J BHATTACHARYA, S DIAMOND, LS AF BHATTACHARYA, A GHILDYAL, R PRASAD, J BHATTACHARYA, S DIAMOND, LS TI MODULATION OF A SURFACE-ANTIGEN OF ENTAMOEBA-HISTOLYTICA IN RESPONSE TO BACTERIA SO INFECTION AND IMMUNITY LA English DT Note ID PROTEINS; CULTIVATION; AMEBIASIS AB Changes in the cell surface of Entamoeba histolytica, a human intestinal parasite and the causative agent of amebic dysentery, were examined with a monoclonal antibody, 2D7.10, which selectively recognizes carbohydrate epitopes in some axenic amebic strains. While high-level expression of this epitope was observed in axenic amebae, it was either absent or present only in small amounts in xenic amebae. Furthermore, reassociation of the axenic amebae with intestinal flora resulted in loss of the 2D7.10 epitope. Our data suggest that surface antigens of E. histolytica can be modulated in response to bacteria and may provide an explanation for the observed influence of bacteria on amebic virulence. C1 NIAID, PARASIT DIS LAB, BETHESDA, MD 20892 USA. JAWAHARLAL NEHRU AGR UNIV, SCH LIFE SCI, NEW DELHI 110067, INDIA. JAWAHARLAL NEHRU AGR UNIV, SCH ENVIRONM SCI, NEW DELHI 110067, INDIA. NR 27 TC 13 Z9 14 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 EI 1098-5522 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1992 VL 60 IS 4 BP 1711 EP 1713 PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HK753 UT WOS:A1992HK75300064 PM 1548096 ER PT J AU SWANSON, CA MAO, BL LI, JY LUBIN, JH YAO, SX WANG, JZ CAI, SK HOU, Y LUO, QS BLOT, WJ AF SWANSON, CA MAO, BL LI, JY LUBIN, JH YAO, SX WANG, JZ CAI, SK HOU, Y LUO, QS BLOT, WJ TI DIETARY DETERMINANTS OF LUNG-CANCER RISK - RESULTS FROM A CASE-CONTROL STUDY IN YUNNAN PROVINCE, CHINA SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID TIN MINERS; POPULATION; VEGETABLES; HAWAII; WOMEN AB The relation between diet and lung cancer was studied among male residents of a mining community in Yunnan Province. After obtaining food frequency data from subjects or proxies, we compared diets of 428 cases, aged 35-74 years, and 1,011 age-matched controls. Cases tended to consume slightly more rice, but less protein-rich foods (i.e., bean curd, meat, eggs) and vegetables than did controls. The relative risks of lung cancer across increasing quartiles of meat (i.e., pork) consumption, for example, were 1.00, 0.67, 0.72 and 0.46 (p for trend < 0.01). The relative risks of lung cancer across increasing quartiles of consumption of dark-green, leafy vegetables were 1.00, 0.62, 0.52 and 0.41 (p for trend < 0.01). Although specific dietary constituent(s) responsible for the protective effect of vegetable consumption could not be identified, carotenoids other than beta-carotene, or compounds in cruciferous or Allium vegetables, are possibilities. C1 YUNNAN TIN CORP,INST LABOR PROTECT,GEJIU,PEOPLES R CHINA. CHINESE ACAD MED SCI,INST CANC,DEPT EPIDEMIOL,BEIJING,PEOPLES R CHINA. DEPT CANC PREVENT & CONTROL,GEJIU,PEOPLES R CHINA. RP SWANSON, CA (reprint author), NCI,DCF,EPIDEMIOL & BIOSTAT PROGRAM,6130 EXECUT BLVD,EPN ROOM 430,ROCKVILLE,MD 20852, USA. NR 23 TC 60 Z9 60 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 1 PY 1992 VL 50 IS 6 BP 876 EP 880 DI 10.1002/ijc.2910500609 PG 5 WC Oncology SC Oncology GA HM006 UT WOS:A1992HM00600008 PM 1555887 ER PT J AU HALL, P BERG, G BJELKENGREN, G BOICE, JD ERICSSON, UB HALLQUIST, A LIDBERG, M LUNDELL, G TENNVALL, J WIKLUND, K HOLM, LE LINDBERG, S CEDERQUIST, E WICKLUND, H LARSSON, LG AF HALL, P BERG, G BJELKENGREN, G BOICE, JD ERICSSON, UB HALLQUIST, A LIDBERG, M LUNDELL, G TENNVALL, J WIKLUND, K HOLM, LE LINDBERG, S CEDERQUIST, E WICKLUND, H LARSSON, LG TI CANCER MORTALITY AFTER I-131 THERAPY FOR HYPERTHYROIDISM SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID A-BOMB SURVIVORS; BREAST-CANCER; TUBERCULOSIS; WOMEN; I-131; RISK; DS86 AB Cancer mortality was studied in 10,552 Swedish hyperthyroid patients treated with I-131 between 1950 and 1975. The patients were matched with the Swedish Cause-of-Death Register and the cases of 977 patients who died from cancer or leukemia were studied. The patients had been followed up for an average of 15 years (range 0 to 35 years), and the overall standardized mortality ratio (SMR) was 1.09 [95% confidence interval (CI) = 1.03 to 1.16], with a higher risk for women. The highest mortality was seen during the first year after exposure (SMR = 1.15) and decreased for the following 9 years (SMR = 1.04). The risk of dying from a cancer in the digestive tract and respiratory organs was significantly elevated more than 10 years after exposure, as was the overall cancer mortality (SMR = 1.14). No increased risk was seen for leukemia, bladder cancer or breast cancer. Younger patients and those receiving I-131 at higher activity had higher SMRs than older patients and those receiving lower activity. Patients with toxic nodular goiter had higher risk than those with Graves' disease. The lack of increasing mortality over time and with increasing activity of I-131 administered argues against a carcinogenic effect of I-131. However, in the case of cancers of the stomach, the I-131 exposure could have contributed to the excess mortality from these cancers. C1 SAHLGRENS UNIV HOSP,DEPT GEN ONCOL,S-41345 GOTHENBURG,SWEDEN. MALMO GEN HOSP,DEPT GEN ONCOL,S-21401 MALMO,SWEDEN. NCI,DIV CANC ETIOL,BETHESDA,MD 20892. MALMO GEN HOSP,DEPT OBSTET & GYNECOL,S-21401 MALMO,SWEDEN. UNIV LUND HOSP,DEPT GEN ONCOL,S-22185 LUND,SWEDEN. KAROLINSKA INST,RADIUMHEMMET,DEPT CANC EPIDEMIOL,S-10401 STOCKHOLM 60,SWEDEN. KAROLINSKA INST,RADIUMHEMMET,DEPT CANC PREVENT,S-10401 STOCKHOLM 60,SWEDEN. SAHLGRENS UNIV HOSP,DIV NUCL MED,S-41345 GOTHENBURG,SWEDEN. UNIV HOSP UPPSALA,DEPT GEN ONCOL,UPPSALA,SWEDEN. UMEA UNIV HOSP,S-90185 UMEA,SWEDEN. RP HALL, P (reprint author), KAROLINSKA INST,RADIUMHEMMET,DEPT GEN ONCOL,S-10401 STOCKHOLM 60,SWEDEN. RI Tennvall, Jan/F-8760-2014 FU NCI NIH HHS [N01-CP-51034] NR 29 TC 74 Z9 75 U1 0 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 1 PY 1992 VL 50 IS 6 BP 886 EP 890 DI 10.1002/ijc.2910500611 PG 5 WC Oncology SC Oncology GA HM006 UT WOS:A1992HM00600010 PM 1555888 ER PT J AU SPITZER, RL DEVLIN, M WALSH, BT HASIN, D WING, R MARCUS, M STUNKARD, A WADDEN, T YANOVSKI, S AGRAS, S MITCHELL, J NONAS, C AF SPITZER, RL DEVLIN, M WALSH, BT HASIN, D WING, R MARCUS, M STUNKARD, A WADDEN, T YANOVSKI, S AGRAS, S MITCHELL, J NONAS, C TI BINGE EATING DISORDER - A MULTISITE FIELD TRIAL OF THE DIAGNOSTIC-CRITERIA SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Article ID BEHAVIORAL TREATMENT; DOUBLE-BLIND; BULIMIA; OBESITY; WEIGHT; EATERS AB Diagnostic criteria have been developed for a new eating disorder, binge eating disorder (BED), to describe the many individuals who have problems with recurrent binge eating but do not engage in the characteristic compensatory behaviors of bulimia nervosa, vomiting, or use of laxatives. The results of a multisite field trial involving 1,984 subjects indicate that the disorder is common (30.1%) among subjects attending hospital-affiliated weight control programs, but is relatively rare in the community (2.0%). The disorder is more common in females than in males and is associated with severity of obesity and a history of marked weight fluctuations. Based on these results, the DSM-IV Work Group on Eating Disorders has recommended that the disorder be considered for inclusion in DSM-IV, either as an official category or in an appendix of categories requiring further study. C1 COLUMBIA UNIV,DEPT PSYCHIAT,NEW YORK,NY 10027. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261. UNIV PENN,PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,PSYCHOL PSYCHIAT,PHILADELPHIA,PA 19104. NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. STANFORD UNIV,MED CTR,SCH MED,STANFORD,CA 94305. UNIV MINNESOTA,DEPT PSYCHIAT,MINNEAPOLIS,MN 55455. UNITED WEIGHT CONTROL CORP,PROGRAM DEV,NEW YORK,NY. NR 20 TC 511 Z9 520 U1 5 U2 32 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD APR PY 1992 VL 11 IS 3 BP 191 EP 203 DI 10.1002/1098-108X(199204)11:3<191::AID-EAT2260110302>3.0.CO;2-S PG 13 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA HN399 UT WOS:A1992HN39900001 ER PT J AU MAVALANKAR, DV GRAY, RH TRIVEDI, CR AF MAVALANKAR, DV GRAY, RH TRIVEDI, CR TI RISK-FACTORS FOR PRETERM AND TERM LOW-BIRTH-WEIGHT IN AHMEDABAD, INDIA SO INTERNATIONAL JOURNAL OF EPIDEMIOLOGY LA English DT Article ID LOW-BIRTH-WEIGHT; INTRAUTERINE GROWTH-RETARDATION; INFANT-MORTALITY; PRENATAL-CARE; FETAL GROWTH; DETERMINANTS; PREMATURITY; SOCIETIES; DELIVERY; LABOR AB To identify and quantify risk factors for preterm and term low birthweight (LBW) we conducted a hospital-based case control study, linked with a population survey in Ahmedabad, India. The case-control study of 673 term LBW, 644 preterm LBW cases and 1465 controls showed that low maternal weight. poor obstetric history, lack of antenatal care, clinical anaemia and hypertension were significant independent risk factors for both term and preterm LBW. Short interpregnancy interval was associated with an increased risk of preterm LBW birth while primiparous women had increased risk of term LBW. Muslim women were at a reduced risk of term LBW, but other socioeconomic factors did not remain significant after adjusting for these more proximate factors. Estimates of the prevalence of risk factors from the population survey was used to calculate attributable risk. This analysis suggested that a substantial proportion of term and preterm LBW births may be averted by improving maternal nutritional status, anaemia and antenatal care. C1 NICHHD,BLDG FDN,KM 640,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21205. NHL MUNICIPAL MED COLL,AHMEDABAD 380006,INDIA. NR 36 TC 52 Z9 53 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0300-5771 J9 INT J EPIDEMIOL JI Int. J. Epidemiol. PD APR PY 1992 VL 21 IS 2 BP 263 EP 272 DI 10.1093/ije/21.2.263 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JB206 UT WOS:A1992JB20600010 PM 1428479 ER PT J AU WEINSTEIN, JN VANOSDOL, W AF WEINSTEIN, JN VANOSDOL, W TI THE MACROSCOPIC AND MICROSCOPIC PHARMACOLOGY OF MONOCLONAL-ANTIBODIES SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article; Proceedings Paper CT 5TH INTERNATIONAL CONF ON IMMUNO-PHARMACOLOGY CY MAY 26-30, 1991 CL TAMPA, FL SP INT SOC IMMUNOPHARM ID LYMPH-NODE METASTASES; MODELING ANALYSIS; DOSE DEPENDENCE; TUMOR SPHEROIDS; HUMAN-MELANOMA; HUMAN-COLON; THERAPY; DELIVERY; BINDING; IMMUNOLYMPHOSCINTIGRAPHY AB When monoclonal antibodies directed against tumor-associated antigens are injected intravenously, they sometimes fail to distribute uniformly in the substance of a tumor. To understand the possible reasons, it is necessary to consider both macroscopic and microscopic features of the pharmacology. We have analyzed antibody penetration into microscopic primary tumors and metastases by melding together information on the global pharmacokinetics, convective and diffusive transport across the blood capillary wall, diffusion through the tumor interstitial space, antigen-antibody interaction, metabolism, and lymphatic outflow. This analysis predicts that the very fact of successful binding will decrease the homogeneity of distribution. We believe that this "binding site barrier" constitutes major challenges to the molecular design of next-generation antibodies and also to the design of many other types of ligands for use in treatment of solid tumors. RP WEINSTEIN, JN (reprint author), NCI,DCBDC,MATH BIOL LAB,THEORET IMMUNOL SECT,BLDG 10,RM 4B-56,BETHESDA,MD 20892, USA. NR 45 TC 21 Z9 21 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PD APR PY 1992 VL 14 IS 3 BP 457 EP 463 DI 10.1016/0192-0561(92)90176-L PG 7 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA HU498 UT WOS:A1992HU49800017 PM 1618598 ER PT J AU KREITMAN, RJ FITZGERALD, D PASTAN, I AF KREITMAN, RJ FITZGERALD, D PASTAN, I TI TARGETING GROWTH-FACTOR RECEPTORS WITH FUSION TOXINS SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Article; Proceedings Paper CT 5TH INTERNATIONAL CONF ON IMMUNO-PHARMACOLOGY CY MAY 26-30, 1991 CL TAMPA, FL SP INT SOC IMMUNOPHARM ID ACTIVATED LYMPHOCYTES-T; PSEUDOMONAS EXOTOXIN; FACTOR-ALPHA; RECOMBINANT IMMUNOTOXIN; INTERLEUKIN-6 RECEPTOR; CELL-GROWTH; TUMOR-CELLS; ANTI-TAC; PROTEIN; EXPRESSION AB Recombinant toxins which bind to growth factor receptors have been prepared and used to kill cells responsible for malignant or autoimmune disease. Our strategy has been to genetically fuse ligands to different forms of Pseudomonas exotoxin which due to mutations or deletions do not bind to normal cells. The resulting recombinant chimeric toxins, in concentrations often less than 1 ng/ml, selectively kill cells expressing the appropriate growth factor receptor. The ligand may be a growth factor, such as transforming growth factor alpha (TGF-alpha), interleukin 6 (IL6) or interleukin 2 (IL2), or single chain antigen binding proteins, such as the variable heavy and light regions of the monoclonal antibody anti-Tac. These chimeric toxins kill not only established cell lines but also fresh tumor cells from patients and display anti-tumor activity toward human malignant tumors in nude mice. While clinical trials are beginning with some of these agents, work continues to improve the effectiveness of recombinant chimeric toxins, and to widen the scope of disorders which might be treated by this approach. RP KREITMAN, RJ (reprint author), NCI,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 48 TC 16 Z9 16 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PD APR PY 1992 VL 14 IS 3 BP 465 EP 472 DI 10.1016/0192-0561(92)90177-M PG 8 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA HU498 UT WOS:A1992HU49800018 PM 1319965 ER PT J AU SICHIERI, R EVERHART, JE HUBBARD, VS AF SICHIERI, R EVERHART, JE HUBBARD, VS TI RELATIVE WEIGHT CLASSIFICATIONS IN THE ASSESSMENT OF UNDERWEIGHT AND OVERWEIGHT IN THE UNITED-STATES SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE BLACKS; BODY MASS INDEX; HISPANICS; MORBIDITY; MORTALITY; PREVALENCE; UNITED-STATES; WHITES ID BODY-MASS INDEX; FINNISH MEN; MORTALITY; DISABILITY; LONGEVITY; IMPACT AB We compared five recent relative weight classifications based on body mass index for their estimates of prevalence of underweight and overweight in the adult population of the United States and for their ability to predict subsequent morbidity and mortality. The sources of the classifications were: the 1990 Dietary Guidelines for Americans of the US Departments of Agriculture and Health and Human Services, the National Academy of Sciences, the National Center for Health Statistics, the World Health Organization, and the Canadian Minister of National Health and Welfare. These classifications were applied to the body mass index distributions of the second National Health and Nutrition Examination Survey (1976-1980) and to the Hispanic Health and Nutrition Examination Survey (1982-1984). Depending on classification, a wide range of prevalence for the total population was found: 9-17% of the US population were categorized as underweight, and 25-45% were categorized as overweight. White women had the highest prevalence of underweight in all but the National Center for Health Statistics classification. Black and Mexican American women had the highest prevalence of overweight under all classifications (range: 38.4-58.6%). Associations with health outcomes were determined using all cause hospitalization and mortality in the 1971-1987 follow-up of the first National Health and Nutrition Examination Survey. Underweight and overweight as defined by the National Academy of Sciences classification had the highest population attributable risk for hospitalization and death: 5.0% of hospitalizations and 11.0% of deaths among men and 4.2% of hospitalizations and 11.4% of deaths among women were associated with weights outside the healthy range. Under this classification a greater proportion of both hospitalizations and mortality were associated with overweight than underweight. For all classifications, a higher proportion of hospitalizations were associated with overweight than underweight. All classifications performed better at predicting death than hospitalization. C1 NIDDK,DIV DIGEST DIS & NUTR,MPH,ROOM 3A-10,WESTWOOD BLDG 5333 WESTBARD AVE,BETHESDA,MD 20892. UNIV ESTADUAL MARINGA,CTR CIENCIAS BIOL & SAUDE,MARINGA,PARANA,BRAZIL. NR 37 TC 44 Z9 45 U1 0 U2 4 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD APR PY 1992 VL 16 IS 4 BP 303 EP 312 PG 10 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA HQ662 UT WOS:A1992HQ66200009 PM 1318285 ER PT J AU JOLESZ, FA SHTERN, F AF JOLESZ, FA SHTERN, F TI THE OPERATING-ROOM OF THE FUTURE - REPORT OF THE NATIONAL CANCER INSTITUTE WORKSHOP, IMAGING-GUIDED STEREOTAXIC TUMOR-DIAGNOSIS AND TREATMENT SO INVESTIGATIVE RADIOLOGY LA English DT Editorial Material C1 NCI,DIAGNOST IMAGING RES BRANCH,ROCKVILLE,MD. RP JOLESZ, FA (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,DEPT RADIOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 0 TC 58 Z9 59 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD APR PY 1992 VL 27 IS 4 BP 326 EP 328 DI 10.1097/00004424-199204000-00016 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HK992 UT WOS:A1992HK99200011 PM 1601626 ER PT J AU ANGUIANO, A OATES, RD AMOS, JA DEAN, M GERRARD, B STEWART, C MAHER, TA WHITE, MB MILUNSKY, A AF ANGUIANO, A OATES, RD AMOS, JA DEAN, M GERRARD, B STEWART, C MAHER, TA WHITE, MB MILUNSKY, A TI CONGENITAL BILATERAL ABSENCE OF THE VAS-DEFERENS - A PRIMARILY GENITAL FORM OF CYSTIC-FIBROSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID POLYMERASE CHAIN-REACTION; GRADIENT GEL-ELECTROPHORESIS; POLYMORPHIC DNA MARKER; SINGLE-BASE CHANGES; ABNORMAL DISTRIBUTION; POINT MUTATIONS; GENE; IDENTIFICATION; LOCALIZATION; MISMATCHES AB Objective. - Almost all males with cystic fibrosis (CF) have absent vasa deferentia. It has been suggested that otherwise healthy males with congenital bilateral absence of the vas deferens (CBAVD), previously considered a distinct genetic entity, have an increased frequency of CF gene mutations. This study examined the genetic commonality of these two disorders. Design. -We typed six common CF gene mutations in 25 patients with CBAVD. Additional rare mutations were sought using single-stranded conformation polymorphisms and direct DNA sequencing. When rare mutations were found, they were sought in a large sample of both CF patients and obligate CF carriers to exclude them as polymorphisms. Setting. - All the patients presented to a male infertility clinic of a teaching hospital. Subjects.-Twenty-five unselected, unrelated azoospermic men with CBAVD, most of them of Northern European ancestry. Results. - Sixteen (64%) of the 25 men with CBAVD had at least one detectable CF mutation, 16 times the expected frequency (P < .001). Moreover, we have thus far determined that three of these 16 men are compound heterozygotes, one of whom has a mutation not previously described. Analyses continue on patients who have yet to yield a detectable mutation. Conclusions. - Some, if not all, otherwise healthy men with CBAVD reflect a newly recognized, primarily genital, phenotype of CF. Prior to sperm aspiration to remedy infertility, CF mutation analysis should be recommended for them and their partners, as well as for their relatives. C1 BOSTON UNIV,SCH MED,CTR HUMAN GENET,80 E CONCORD ST,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT UROL,BOSTON,MA 02118. BOSTON UNIV HOSP,BOSTON,MA 02218. BOSTON CITY HOSP,BOSTON,MA 02118. NCI,VIRAL CARCINOGENESIS LAB,BETHESDA,MD 20892. PROGRAM RESOURCES INC,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 FU NCI NIH HHS [N01-CO-74102] NR 54 TC 393 Z9 395 U1 2 U2 4 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 1 PY 1992 VL 267 IS 13 BP 1794 EP 1797 DI 10.1001/jama.267.13.1794 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HK672 UT WOS:A1992HK67200029 PM 1545465 ER PT J AU INOFFGERMAIN, G NOTTELMANN, ED RADKEYARROW, M AF INOFFGERMAIN, G NOTTELMANN, ED RADKEYARROW, M TI EVALUATIVE COMMUNICATIONS BETWEEN AFFECTIVELY ILL AND WELL MOTHERS AND THEIR CHILDREN SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article ID MANIC-DEPRESSIVE PARENT; YOUNG-CHILDREN; SEX-DIFFERENCES; PSYCHIATRIC-DISORDER; AFFECTIVE-ILLNESS; RISK; AGGRESSION; CHILDHOOD; PSYCHOPATHOLOGY; ADOLESCENCE AB Earlier research suggests that the natural verbal discourse of mothers with their children can be important in clarifying, verifying, and evaluating the behavior in which a child is engaged, in attributing qualities to the child, and in influencing the child's self-perceptions. We investigated the potential influences of parental affective illness (bipolar affective disorder and unipolar depression in contrast to no history of psychiatric illness) on such "labeling" behavior in a sample of 61 mothers and their older (school-age) and younger (preschool-age) children. It was hypothesized that the dispositions characterizing affective illness (specifically, negativity and disengagement) would be reflected in the labeling statements of mothers with a diagnosis as they interacted with their children. Based on videotaped interactions during a visit to a home-like laboratory apartment, labeling statements were identified in terms of speaker and person being labeled ("addressee") and coded (positive, negative, mixed, or neutral) for judgmental and affective quality of the statement and reaction of the addressee. Data were analyzed (a) by family unit and (b) my mother to child statements. The general pattern of findings indicated, in relative terms, an excess of negativity on the part of family members in the bipolar group and a dearth of negative affect for mothers in the unipolar group. Negativity in the bipolar group appeared to be especially likely when the setting involved mothers and two male children. Additionally, findings are discussed in terms of sex differences in vulnerability to depression. RP INOFFGERMAIN, G (reprint author), NIMH,BLDG 15K,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 57 TC 21 Z9 21 U1 2 U2 5 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 1992 VL 20 IS 2 BP 189 EP 212 DI 10.1007/BF00916548 PG 24 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA HT097 UT WOS:A1992HT09700004 PM 1593026 ER PT J AU STEINBERG, AD KRIEG, AM TAKASHI, T GOURLEY, MF AF STEINBERG, AD KRIEG, AM TAKASHI, T GOURLEY, MF TI TIMING OF IMMUNOSUPPRESSION IN THE NATURAL-HISTORY OF AUTOIMMUNE-DISEASES SO JOURNAL OF AUTOIMMUNITY LA English DT Article; Proceedings Paper CT 2ND CONGRESS OF IMMUNOINTERVENTION IN AUTOIMMUNE DISEASES CY MAY 13-16, 1991 CL PARIS, FRANCE ID THERAPY; MICE RP STEINBERG, AD (reprint author), NIAMS,ARB,CELLULAR IMMUNOL SECT,BLDG 10,ROOM 9N-218,BETHESDA,MD 20892, USA. NR 6 TC 2 Z9 2 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 1992 VL 5 SU A BP 197 EP 203 DI 10.1016/0896-8411(92)90034-N PG 7 WC Immunology SC Immunology GA HP721 UT WOS:A1992HP72100022 PM 1503612 ER PT J AU NUSSENBLATT, R AF NUSSENBLATT, R TI THE EXPANDING USE OF IMMUNOSUPPRESSION IN THE TREATMENT OF NONINFECTIOUS OCULAR DISEASE SO JOURNAL OF AUTOIMMUNITY LA English DT Article ID CYCLOSPORINE-A; VERNAL KERATOCONJUNCTIVITIS; TOPICAL CYCLOSPORINE; AUTOIMMUNE UVEITIS; PENETRATION; EYE; NEPHROTOXICITY; THERAPY; REJECTION; EYEDROPS RP NUSSENBLATT, R (reprint author), NEI, IMMUNOL LAB, BLDG 10, ROOM 10N202, BETHESDA, MD 20892 USA. NR 36 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0896-8411 J9 J AUTOIMMUN JI J. Autoimmun. PD APR PY 1992 VL 5 SU A BP 247 EP 257 DI 10.1016/0896-8411(92)90040-W PG 11 WC Immunology SC Immunology GA HP721 UT WOS:A1992HP72100028 PM 1503617 ER PT J AU PARKER, CT KLOSER, AW SCHNAITMAN, CA STEIN, MA GOTTESMAN, S GIBSON, BW AF PARKER, CT KLOSER, AW SCHNAITMAN, CA STEIN, MA GOTTESMAN, S GIBSON, BW TI ROLE OF THE RFAG AND RFAP GENES IN DETERMINING THE LIPOPOLYSACCHARIDE CORE STRUCTURE AND CELL-SURFACE PROPERTIES OF ESCHERICHIA-COLI K-12 SO JOURNAL OF BACTERIOLOGY LA English DT Article ID CAPSULAR POLYSACCHARIDE SYNTHESIS; GRAM-NEGATIVE BACTERIA; SALMONELLA-TYPHIMURIUM; OUTER-MEMBRANE; NEISSERIA-GONORRHOEAE; MUTAGENESIS; PROTEIN; REGION; BIOSYNTHESIS; INSERTION AB Deletions which removed rfa genes involved in lipopolysaccharide (LPS) core synthesis were constructed in vitro and inserted into the chromosome by linear transformation. The deletion DELTA-rfa1, which removed rfaGPBI, resulted in a truncated LPS core containing two heptose residues but no hexose and a deep rought phenotype including decreased expression of major outer membrane proteins, hypersensitivity to novobiocin, and resistance to phage U3. In addition, DELTA-rfa1 resulted in the loss of flagella and pili and a mucoid colony morphology. Measurement of the synthesis of beta-galactosidase from a cps-lacZ fusion showed that the mucoid phenotype was due to rcsC-dependent induction of colanic acid capsular polysaccharide synthesis. Complementation of DELTA-rfa1 with rfaG+ DNA fragments resulted in a larger core and restored the synthesis of flagella and pili but did not reverse the deep rough phenotype or the induction of cps-lacZ, while complementation with a fragment carrying only rfaP+ reversed the deep rough phenotype but not the loss of flagella and pili. A longer deletion which removed rfaQGPBIJ was also constructed, and complementation studies with this deletion showed that the product of rfaQ was not required for the functions of rfaG and rfaP. Thus, the function of rfaQ remains unknown. Tandem mass spectrometric analysis of LPS core oligosaccharides from complemented DELTA-rfa1 strains indicated that rfaP+ was necessary for the addition of either phosphoryl (P) or pyrophosphorylethanolamine (PPEA) substituents to the heptose I residue, as well as for the partial branch substitution of heptose II by heptose III. The substitution of heptose II is independent of the type of P substituent present on heptose I, and this results in four different core structures. A model is presented which relates the deep rough phenotype to the loss of heptose-linked P and PPEA. C1 ARIZONA STATE UNIV,DEPT MICROBIOL,TEMPE,AZ 85287. LOUISIANA STATE UNIV,MED CTR,DEPT MICROBIOL IMMUNOL & PARASITOL,NEW ORLEANS,LA 70112. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT PHARMACEUT CHEM,SAN FRANCISCO,CA 94143. FU NCRR NIH HHS [RR-01614]; NIGMS NIH HHS [GM-39087] NR 53 TC 163 Z9 164 U1 1 U2 3 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 1992 VL 174 IS 8 BP 2525 EP 2538 PG 14 WC Microbiology SC Microbiology GA HM899 UT WOS:A1992HM89900016 PM 1348243 ER PT J AU WETSEL, WC KHAN, WA MERCHENTHALER, I RIVERA, H HALPERN, AE PHUNG, HM NEGROVILAR, A HANNUN, YA AF WETSEL, WC KHAN, WA MERCHENTHALER, I RIVERA, H HALPERN, AE PHUNG, HM NEGROVILAR, A HANNUN, YA TI TISSUE AND CELLULAR-DISTRIBUTION OF THE EXTENDED FAMILY OF PROTEIN-KINASE-C ISOENZYMES SO JOURNAL OF CELL BIOLOGY LA English DT Article ID PHORBOL ESTER RECEPTOR; RAT-BRAIN; IMMUNOCYTOCHEMICAL LOCALIZATION; DIFFERENTIAL EXPRESSION; ISOZYMES; ACTIVATION; HETEROGENEITY; CEREBELLUM; MULTIPLE; BINDING AB Polyclonal isoenzyme-specific antisera were developed against four calcium-independent protein kinase C (PKC) isoenzymes (delta, epsilon, epsilon', and zeta) as well as the calcium-dependent isoforms (alpha, beta(I), beta(II), and gamma). These antisera showed high specificities, high titers, and high binding affinities (3-370 nM) for the peptide antigens to which they were raised. Each antiserum detected a species of the predicted molecular weight by Western blot that could be blocked with the immunizing peptide. PKC was sequentially purified from rat brain, and the calcium-dependent forms were finally resolved by hydroxyapatite chromatography. Peak I reacted exclusively with antisera to PKC-gamma, peak II with PKC-beta(I) and -beta(II), and peak III with PKC-alpha. These same fractions, however, were devoid of immunoreactivity for the calcium-independent isoenzymes. The PKC isoenzymes demonstrated a distinctive tissue distribution when evaluated by Western blot and immunocytochemistry. PCK-delta was present in brain, heart, spleen, lung, liver, ovary, pancreas, and adrenal tissues. PKC-epsilon was present in brain, kidney, and pancreas, whereas PKC-epsilon' was present predominantly in brain. PKC-zeta was present in most tissues, particularly the lung. brain, and liver. Both PKC-delta and PKC-zeta showed some heterogeneity of size among the different tissues. PKC-alpha was present in all organs and tissues examined. PKC-beta(I) and -beta(II), were present in greatest amount in brain and spleen. Although the brain contained the most PKC-gamma immunoreactivity, some immunostaining was also seen in adrenal tissue. These studies provide the first evidence of selective organ and tissue distributions of the calcium-independent PKC isoenzymes. C1 DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT CELL BIOL,DURHAM,NC 27710. RP WETSEL, WC (reprint author), NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709, USA. FU NCI NIH HHS [CA 47741]; NHLBI NIH HHS [HL-43707] NR 56 TC 411 Z9 414 U1 0 U2 7 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1992 VL 117 IS 1 BP 121 EP 133 DI 10.1083/jcb.117.1.121 PG 13 WC Cell Biology SC Cell Biology GA HL818 UT WOS:A1992HL81800011 PM 1556149 ER PT J AU SANDBERG, K JI, H IIDA, T CATT, KJ AF SANDBERG, K JI, H IIDA, T CATT, KJ TI INTERCELLULAR COMMUNICATION BETWEEN FOLLICULAR ANGIOTENSIN RECEPTORS AND XENOPUS-LAEVIS OOCYTES - MEDIATION BY AN INOSITOL 1,4,5-TRISPHOSPHATE-DEPENDENT MECHANISM SO JOURNAL OF CELL BIOLOGY LA English DT Article ID ADRENAL GLOMERULOSA CELLS; INTRINSIC MUSCARINIC RESPONSES; CALCIUM RELEASE; INTRACELLULAR CALCIUM; GAP-JUNCTIONS; TRISPHOSPHATE RECEPTOR; MYOINOSITOL 1,4,5-TRISPHOSPHATE; HEMISPHERIC-ASYMMETRY; MOBILIZES CALCIUM; OVARIAN FOLLICLES AB In Xenopus laevis oocytes, activation of angiotensin II (AII) receptors on the surrounding follicular cells sends a signal through gap junctions to elevate cytoplasmic calcium concentration ([Ca2+]i) within the oocyte. The two major candidates for signal transfer through gap junctions into the oocyte during AII receptor stimulation are Ins(1,4,5)P3 and Ca2+. In [H-3]inositol-injected follicular oocytes, AII stimulated two- to fourfold increases in phosphoinositide hydrolysis and production of inositol phosphates. Injection of the glycosaminoglycan, heparin, which selectively blocks Ins(1,4,5)P3 receptors, prevented both AII-stimulated and Ins(1,4,5)P3-induced Ca2+ mobilization in Xenopus follicular oocytes but did not affect mobilization of Ca2+ by ionomycin or GTP. These results indicate that the AII-regulated process of gap junction communication between follicular cells and the oocyte operates through an Ins(1,4,5)P3-dependent mechanism rather than through transfer of Ca2+ into the ooplasm and subsequent Ca2+-induced Ca2+ release. RP SANDBERG, K (reprint author), NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892, USA. NR 60 TC 29 Z9 29 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1992 VL 117 IS 1 BP 157 EP 167 DI 10.1083/jcb.117.1.157 PG 11 WC Cell Biology SC Cell Biology GA HL818 UT WOS:A1992HL81800014 PM 1556150 ER PT J AU FENTON, RG KUNG, HF LONGO, DL SMITH, MR AF FENTON, RG KUNG, HF LONGO, DL SMITH, MR TI REGULATION OF INTRACELLULAR ACTIN POLYMERIZATION BY PRENYLATED CELLULAR PROTEINS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID GAMMA SUBUNITS CONTAIN; MEVALONIC ACID; CARBOXYL-METHYLATION; LAMIN-B; CELLS; FLUORIDE; ALUMINUM; CYSTEINE; P21RAS; IDENTIFICATION AB Posttranslational modification by covalent attachment of polyisoprene intermediates to a carboxy-terminal CAAX-box motif is required for the biologic function of proteins such as p21ras, the supergene family of ras-related proteins, nuclear lamins, and subunits of heterotrimeric G-proteins. Cells grown in the presence of lovastatin, which inhibits HMG-CoA reductase and prevents synthesis of intermediates required for protein prenylation, develop a round, refractile morphology. Our data indicate that this is due to the selective loss of actin cables without gross changes in the microtubular lattice or intermediate filament structure. Microinjection of a competitive peptide inhibitor of protein prenyltransferases into the cytoplasm of cells induces an identical change in morphology with loss of actin cables. Mevalonate (MVA) reverses the lovastatin-induced morphologic change by inducing a rapid repolymerization of actin cables with coincident reversion to the flat morphology. Furthermore, microinjection of farnesyl-pyrophosphate or geranylgeranyl-pyrophosphate into lovastatin-treated cells also results in rapid morphologic reversion. The morphologic reversion induced by MVA requires the presence of serum, and is independent of extracellular calcium. The addition of cycloheximide to the growth medium prevents lovastatin-induced loss of actin cables, and causes morphologic reversion of lovastatin-treated cells by a mechanism that is independent of MVA. AlF4- induces morphologic reversion in a manner indistinguishable from MVA. These data indicate that prenylated protein(s) play a critical role in regulating the state of intracellular actin, and that GGPP can rescue the lovastatin-induced morphologic phenotype in the absence of upstream intermediates of cholesterol biosynthesis. We have begun to dissect the signaling events that mediate this pathway. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RP FENTON, RG (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,BIOCHEM PHYSIOL LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 38 TC 114 Z9 114 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1992 VL 117 IS 2 BP 347 EP 356 DI 10.1083/jcb.117.2.347 PG 10 WC Cell Biology SC Cell Biology GA HP037 UT WOS:A1992HP03700010 PM 1560030 ER PT J AU LAFLAMME, SE AKIYAMA, SK YAMADA, KM AF LAFLAMME, SE AKIYAMA, SK YAMADA, KM TI REGULATION OF FIBRONECTIN RECEPTOR DISTRIBUTION SO JOURNAL OF CELL BIOLOGY LA English DT Article ID CELL-ADHESION; CYTOSKELETAL ORGANIZATION; INTERLEUKIN-2 RECEPTOR; PLASMA FIBRONECTIN; CYTOPLASMIC DOMAIN; FOCAL CONTACTS; CSAT ANTIGEN; INTEGRIN; FIBROBLASTS; SEQUENCE AB To determine the role of each intracellular domain of the fibronectin receptor in receptor distribution, chimeric receptors were constructed containing the human interleukin-2 receptor (gp55 subunit) as the extracellular and transmembrane domains, in combination with either the alpha-5 or beta-1 intracellular domain of the fibronectin receptor as the cytoplasmic domain. These chimeric receptors were transiently expressed in normal fibroblasts, and their localization on the cell surface was determined by immunofluorescence using antibodies to the human interleukin-2 receptor. The alpha-5 chimera was expressed diffusely on the plasma membrane. The beta-1 chimera, however, colocalized with the endogenous fibronectin receptor at focal contacts of cells spread on fibronectin. On cells spread in the presence of serum, the beta-1 chimera colocalized both with the fibronectin receptor at sites of extracellular fibronectin fibrils and with the vitronectin receptor at focal contacts. The beta-1 intracellular domain alone, therefore, contains sufficient information to target the chimeric receptor to regions of the cell where ligand-occupied integrin receptors are concentrated. The finding that the beta-1 chimeric protein behaves like a ligand-occupied receptor, even though the beta-1 chimera cannot itself bind extracellular ligand, suggests an intracellular difference between occupied and unoccupied receptors, and predicts that the distribution of integrin receptors can be regulated by ligand occupancy. We tested this prediction by providing a soluble cell-binding fragment of fibronectin to cells spread on laminin. Under conditions preventing further ligand adsorption to the substrate, this treatment nevertheless resulted in the relocation of diffuse fibronectin receptors to focal contacts. Similarly, a redistribution of diffuse vitronectin receptors to focal contacts occurred on cells spread on laminin after the addition of the small soluble peptide GRGDS. We conclude that the propensity for receptor redistribution to focal contacts driven by the beta-1 cytoplasmic domain alone is suppressed in heterodimeric unoccupied fibronectin receptors, and that ligand occupancy can release this constraint. This redistribution of integrin receptors after the binding of a soluble substrate molecule may provide a direct means of assembling adhesion sites. RP LAFLAMME, SE (reprint author), NIDR,DEV BIOL LAB,BETHESDA,MD 20892, USA. OI Yamada, Kenneth/0000-0003-1512-6805 NR 52 TC 276 Z9 276 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1992 VL 117 IS 2 BP 437 EP 447 DI 10.1083/jcb.117.2.437 PG 11 WC Cell Biology SC Cell Biology GA HP037 UT WOS:A1992HP03700018 PM 1373145 ER PT J AU BOGARDUS, C LILLIOJA, S AF BOGARDUS, C LILLIOJA, S TI PIMA-INDIANS AS A MODEL TO STUDY THE GENETICS OF NIDDM SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE DIABETES-MELLITUS; GENETICS; PIMA INDIANS; INSULIN RESISTANCE ID INVIVO INSULIN ACTION; DEPENDENT DIABETES-MELLITUS; IMPAIRED GLUCOSE-TOLERANCE; ENERGY-EXPENDITURE; IDENTICAL-TWINS; RECEPTOR GENE; POLYMORPHISM; RESISTANCE; ASSOCIATION; OBESITY AB More than half the Pima Indians over 35 years of age have non-insulin dependent diabetes mellitus (NIDDM). They have been the focus of prospective epidemiologic and metabolic studies for over two decades and the data collected during these studies are now proving invaluable in efforts to find genetic markers for NIDDM in humans. The Pima Indian model of this disease affords two major advantages. The population is genetically homogeneous compared to Caucasian populations, and therefore the causes of NIDDM are less heterogeneous, simplifying genetic linkage studies. Equally important, based on results from metabolic studies, two pre-diabetic phenotypes have been identified in the Pimas: insulin resistance and a low metabolic rate. Use of these phenotypes in genetic linkage analyses should greatly improve chances of finding genetic markers for NIDDM since these phenotypes may be more closely related to the putative abnormal gene products, and actual disease genes, than is the hyperglycemia of the fully developed phenotype of NIDDM. RP BOGARDUS, C (reprint author), NIDDK,CLIN DIABET & NUTR SECT,4212 NORTH 16TH ST,ROOM 541,PHOENIX,AZ 85016, USA. RI Lillioja, Stephen/A-8185-2012; OI Lillioja, Stephen/0000-0001-5333-5240 NR 35 TC 28 Z9 28 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR PY 1992 VL 48 IS 4 BP 337 EP 343 DI 10.1002/jcb.240480402 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HQ017 UT WOS:A1992HQ01700001 PM 1577873 ER PT J AU LOTAN, R PIENIAZEK, J GEORGE, MD JETTEN, AM AF LOTAN, R PIENIAZEK, J GEORGE, MD JETTEN, AM TI IDENTIFICATION OF A NEW SQUAMOUS-CELL DIFFERENTIATION MARKER AND ITS SUPPRESSION BY RETINOIDS SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID TRACHEAL EPITHELIAL-CELLS; TRANSFORMING GROWTH-FACTOR; CHOLESTEROL SULFOTRANSFERASE ACTIVITY; HUMAN EPIDERMAL-KERATINOCYTES; TRANSGLUTAMINASE ACTIVITY; TERMINAL DIFFERENTIATION; CARCINOMA-CELLS; LEUKEMIA-CELLS; ACID-BINDING; INHIBITOR AB Rabbit tracheobronchial epithelial cells (RbTE) can undergo squamous cell differentiation under defined culture conditions and, therefore, have been used as a model to study the regulation of squamous cell differentiation markers. In the present study, we identified a 20-kDa protein, designated rSQ20, in the serum-free growth medium conditioned by RbTE cells undergoing squamous cell differentiation. The protein was also found in extracts of squamous differentiated cells. rSQ20 was labeled by cells incubated with [S-35]methionine but not with [H-3]glucosamine, suggesting that it is not a glycoprotein. Undifferentiated cells did not produce this protein. rSQ20 was detected in the conditioned medium of RbTE cells after they reached a confluent and growth-arrested state, and thereafter its level increased markedly and concurrently with an increase in type I (epidermal) transglutaminase, an established marker of squamous cell differentiation. rSQ20 found in concentrated conditioned medium of squamous differentiated RbTE cells was eluted from a gel filtration column as a protein of 20 kDa, similar to that found by gel electrophoresis under denaturing conditions, suggesting that it is not a multimeric protein. A protein with an apparent molecular weight of 16 kDa (rSQ16), probably the product of partial proteolysis of rSQ20, was often found in various amounts in the conditioned medium of differentiated RbTE cells. Beta-All-trans retinoic acid and other vitamin A analogues (retinoids), which suppress squamous cell differentiation, inhibited the expression of rSQ20 in RbTE cells. RbTE cells immortalized by transfection with SV40 large T antigen as well as malignantly transformed derivatives obtained from the immortalized cells by further transfection with v-Ha-ras secreted SQ20 and SQ16 when grown to high cell densities although their squamous differentiation was impaired. An analogous protein with an apparent molecular weight of 16 kDa, designated hSQ16, was detected in the medium of differentiated normal human bronchial epithelial (NHBE) cells and normal human epidermal keratinocytes (NHEK). No such protein could be detected in the medium in which undifferentiated NHBE or NHEK cells were grown. These results suggest that rSQ20 and hSQ16 are new markers of squamous cell differentiation. C1 NIEHS,PULM PATHOBIOL LAB,CELL BIOL SECT,RES TRIANGLE PK,NC 27709. RP LOTAN, R (reprint author), UNIV TEXAS,DEPT TUMOR BIOL,MD ANDERSON CANC CTR,HOUSTON,TX 77030, USA. OI Jetten, Anton/0000-0003-0954-4445 NR 50 TC 9 Z9 9 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 1992 VL 151 IS 1 BP 94 EP 102 DI 10.1002/jcp.1041510114 PG 9 WC Cell Biology; Physiology SC Cell Biology; Physiology GA HM960 UT WOS:A1992HM96000013 PM 1348511 ER PT J AU ROACH, ES SMITH, M HUTTENLOCHER, P BHAT, M ALCORN, D HAWLEY, L AF ROACH, ES SMITH, M HUTTENLOCHER, P BHAT, M ALCORN, D HAWLEY, L TI REPORT OF THE DIAGNOSTIC-CRITERIA COMMITTEE OF THE NATIONAL-TUBEROUS-SCLEROSIS-ASSOCIATION SO JOURNAL OF CHILD NEUROLOGY LA English DT Editorial Material C1 UNIV CALIF IRVINE,IRVINE,CA 92717. UNIV CHICAGO,CHICAGO,IL 60637. NIDR,BETHESDA,MD 20892. STANFORD UNIV,STANFORD,CA 94305. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. RP ROACH, ES (reprint author), UNIV TEXAS,HLTH SCI CTR,SW MED SCH,DEPT NEUROL,5323 HARRY HINES BLVD,DALLAS,TX 75235, USA. NR 6 TC 170 Z9 179 U1 0 U2 0 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD APR PY 1992 VL 7 IS 2 BP 221 EP 224 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA HM083 UT WOS:A1992HM08300019 PM 1573244 ER PT J AU FRANK, JW REED, DM GROVE, JS BENFANTE, R AF FRANK, JW REED, DM GROVE, JS BENFANTE, R TI WILL LOWERING POPULATION-LEVELS OF SERUM-CHOLESTEROL AFFECT TOTAL MORTALITY - EXPECTATIONS FROM THE HONOLULU-HEART-PROGRAM SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE CHOLESTEROL; CORONARY HEART DISEASE (PREVENTION); MORTALITY (ALL CAUSE); CANCER; HEMORRHAGIC STROKE ID FACTOR INTERVENTION TRIAL; RISK FACTOR MODIFICATION; MIDDLE-AGED MEN; FOLLOW-UP; CANCER MORTALITY; LIFESTYLE CHARACTERISTICS; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; PLASMA-CHOLESTEROL; PRIMARY PREVENTION AB Major campaigns now underway to reduce the serum cholesterol levels of entire national populations have not given serious consideration to the high rates of non-cardiovascular disease and death associated with low cholesterol levels (< 190 mg/dl). To explore this problem, the relationships between serum cholesterol levels, measured in 1965-1968 in 7478 Japanese American men in Hawaii, and subsequent total and cause-specific mortality through 1985, were analyzed by multivariate Cox regression to control for potential confounders. Total mortality rates for 1648 deaths showed a U-shaped curve by baseline cholesterol level, with significant inverse trends (p < 0.03) for deaths due to hemorrhagic stroke, all cancer, benign liver disease, chronic obstructive lung disease and "unknown cause". Only the inverse trends for cancer and benign liver disease showed flattening when 227 deaths in the first 5 years of follow-up were deleted from the analysis. Simulation models using three different strategies of cholesterol reduction in this cohort revealed that none of these approaches had any substantial impact on predicted total mortality over 15 years. However, the population-based approach might theoretically increase mortality for 60% of the cohort with baseline cholesterol levels less than 225 mg/dl. C1 UNIV TORONTO,DEPT PREVENT MED & BIOSTAT,TORONTO M5S 1A1,ONTARIO,CANADA. UNIV TORONTO,DEPT FAMILY & COMMUNITY MED,TORONTO M5S 1A1,ONTARIO,CANADA. NHLBI,BETHESDA,MD 20892. CANADIAN INST ADV RES,POPULAT HLTH GRP,TORONTO,ONTARIO,CANADA. KUAKINI MED CTR,HONOLULU,HI 96822. UNIV HAWAII,SCH PUBL HLTH,HONOLULU,HI 96822. HONOLULU HEART PROGRAM,HONOLULU,HI 96817. FU NHLBI NIH HHS [HC-02901] NR 86 TC 84 Z9 85 U1 2 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD APR PY 1992 VL 45 IS 4 BP 333 EP 346 DI 10.1016/0895-4356(92)90034-K PG 14 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA HR886 UT WOS:A1992HR88600002 PM 1569429 ER PT J AU DEAN, J AF DEAN, J TI BIOLOGY OF MAMMALIAN FERTILIZATION - ROLE OF THE ZONA-PELLUCIDA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article ID SPERM RECEPTOR ACTIVITY; OOCYTE-SPECIFIC EXPRESSION; O-LINKED OLIGOSACCHARIDES; ACROSOME REACTION; DNA-BINDING; DEVELOPMENTAL REGULATION; EGG INTERACTION; MOUSE OOCYTES; ZP3; PROTEINS RP DEAN, J (reprint author), NIDDKD,CELLULAR & DEV BIOL LAB,BLDG 6,ROOM B1-26,BETHESDA,MD 20892, USA. NR 37 TC 58 Z9 59 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1992 VL 89 IS 4 BP 1055 EP 1059 DI 10.1172/JCI115684 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HL840 UT WOS:A1992HL84000001 PM 1556174 ER PT J AU PAULAIS, M TURNER, RJ AF PAULAIS, M TURNER, RJ TI BETA-ADRENERGIC UP-REGULATION OF THE NA+-K+-2CL- COTRANSPORTER IN RAT PAROTID ACINAR-CELLS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE EXOCRINE GLAND; FLUID SECRETION; LOOP DIURETIC; CHLORIDE SECRETION; XEROSTOMIA ID CL TRANSPORT; RECEPTOR STIMULATION; CHLORIDE TRANSPORT; AMMONIUM TRANSPORT; CA-2+ MOBILIZATION; MEMBRANE-VESICLES; PROTEIN SECRETION; GLAND; CALCIUM; ADRENOCEPTOR AB We used the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6')-carboxyfluorescein to monitor the recovery of the intracellular pH (pH(i)) of rat parotid acini from an NH4+-induced alkaline load. This recovery was markedly inhibited by the loop diuretic bumetanide and by Cl- removal, indicating that it is largely due to NH4+ entry via the basolateral Na+-K+-2Cl- cotransporter. The rate of recovery of pH(i) was enhanced threefold by pretreatment (37.5 s) with isoproterenol (K1/2 = 21.5 nM) or norepinephrine (in the presence of phentolamine), and blocked by the beta(1)-specific antagonist atenolol, indicating an upregulation of cotransport activity by beta(1)-adrenergic stimulation. The effect of isoproterenol was prevented by protein kinase inhibitors and mimicked by cAMP analogues, and by maneuvers known to increase cytosolic cAMP levels in these cells, consistent with the involvement of protein kinase A. Physiologically, such an upregulation of the acinar Na+-K+-2Cl- cotransporter would lead to an increase in acinar chloride uptake across the basolateral membrane, and consequently, an increase in overall chloride and fluid secretion. Prevention of this upregulation by beta-blockers and possibly by other commonly used clinical agents may account for the dry mouth and dry eyes experienced by some patients taking these medications. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BLDG 10,RM 1A06,BETHESDA,MD 20892. RI Paulais, Marc/E-5623-2017 NR 36 TC 68 Z9 69 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1992 VL 89 IS 4 BP 1142 EP 1147 DI 10.1172/JCI115695 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HL840 UT WOS:A1992HL84000012 PM 1313447 ER PT J AU CARDINALI, M SARTOR, O ROBBINS, KC AF CARDINALI, M SARTOR, O ROBBINS, KC TI SURAMIN, AN EXPERIMENTAL CHEMOTHERAPEUTIC DRUG, ACTIVATES THE RECEPTOR FOR EPIDERMAL GROWTH-FACTOR AND PROMOTES GROWTH OF CERTAIN MALIGNANT-CELLS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE EPITHELIAL MALIGNANCY; SURAMIN; AUTOCRINE GROWTH; TYROSINE PHOSPHORYLATION; TRANSFORMING GROWTH FACTOR-ALPHA ID FACTOR-ALPHA; TGF-ALPHA; EGF-RECEPTOR; A431 CELLS; PROTEIN; TRANSFORMATION; INHIBITION; MECHANISM; MEMBRANES; BINDS AB Previous studies have shown that suramin is capable of disrupting autocrine growth involving coexpression of platelet-derived growth factor and its receptors in a fibroblast model for mesenchymal oncogenesis. Suramin is currently in use as an experimental drug for the treatment of patients with epithelial cell tumors. In the present study, we have investigated the efficacy of suramin in a carcinoma model system. Our findings demonstrate that suramin enhances cell surface signaling in A431 cells by activating an autocrine loop involving the receptor for epidermal growth factor (EGFR). The mechanism of suramin action was shown to be indirect, not affecting the ability of ligand to bind and activate the EGFR. Instead, suramin induced the release of membrane-bound transforming growth factor alpha, thereby increasing its potential to activate cell surface EGFRs. Since suramin potently blocks tyrosine phosphorylation induced by platelet-derived growth factor but can activate the growth pathway regulated by the EGFR, biological responses of tumor cells to suramin treatment may differ dramatically. C1 NIDR,CELLULAR DEV & ONCOL LAB,BLDG 30,ROOM 211,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 25 TC 51 Z9 51 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1992 VL 89 IS 4 BP 1242 EP 1247 DI 10.1172/JCI115708 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HL840 UT WOS:A1992HL84000025 PM 1556185 ER PT J AU SCHWAN, TG GAGE, KL KARSTENS, RH SCHRUMPF, ME HAYES, SF BARBOUR, AG AF SCHWAN, TG GAGE, KL KARSTENS, RH SCHRUMPF, ME HAYES, SF BARBOUR, AG TI IDENTIFICATION OF THE TICK-BORNE RELAPSING FEVER SPIROCHETE BORRELIA-HERMSII BY USING A SPECIES-SPECIFIC MONOCLONAL-ANTIBODY SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID EPIZOOTIC BOVINE ABORTION; MICE PEROMYSCUS-LEUCOPUS; LYME-DISEASE SPIROCHETE; SURFACE PROTEIN; BURGDORFERI; CULTIVATION; AGENT; EPITOPE AB Borrelia hermisii causes a relapsing fever in humans and is one of several species of tick-borne spirochetes known to occur in the western United States. Spirochetes observed in the peripheral blood of patients acutely ill have been presumptively identified in the past by the geographic location of exposure and the probable species of tick vector. We describe a monoclonal antibody (H9826) that bound to the flagellar protein of B. hermisii but not to those of any of the other species tested, which included B. parkeri, B. turicatae, B. coriaceae, B. anserina, B. burgdorferi, and Leptospira interrogans serovar ballum. This antibody bound efficiently to B. hermsii in an indirect immunofluorescence assay and was used to rapidly detect and identify this spirochete in the peripheral blood of experimentally infected mice and in the central ganglia of Ornithodoros hermsi ticks. H9826 can rapidly confirm the identification of B. hermsii to increase our understanding concerning the geographic distribution, vector specificity, and epidemiological significance of this zoonotic human pathogen. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,SAN ANTONIO,TX 79284. RP SCHWAN, TG (reprint author), NIAID,ARTHROPOD BORNE DIS SECT,VECTORS & PATHOGENS LAB,ROCKY MTN LABS,HAMILTON,MT 59840, USA. RI Barbour, Alan/B-3160-2009 OI Barbour, Alan/0000-0002-0719-5248 NR 38 TC 19 Z9 19 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 1992 VL 30 IS 4 BP 790 EP 795 PG 6 WC Microbiology SC Microbiology GA HJ487 UT WOS:A1992HJ48700007 PM 1572965 ER PT J AU GAYDOS, CA QUINN, TC EIDEN, JJ AF GAYDOS, CA QUINN, TC EIDEN, JJ TI IDENTIFICATION OF CHLAMYDIA-PNEUMONIAE BY DNA AMPLIFICATION OF THE 16S RIBOSOMAL-RNA GENE SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID STRAIN TWAR; TRACHOMATIS; INFECTION; PSITTACI; ORGANISM AB Chlamydia pneumoniae is an important cause of respiratory disease in humans, but diagnosis of C. pneumoniae is hindered by difficulties in the in vitro growth of the organism. In order to improve detection and identification, we recently developed a polymerase chain reaction (PCR) assay which uses oligonucleotide primers specific for C. pneumoniae. The nucleic acid sequence was determined for the 16S rRNA of C. pneumoniae, and regions in which C. pneumoniae differed from both Chlamydia psittaci and Chlamydia trachomatis were identified. Oligonucleotide primers corresponding to these unique regions were then synthesized and used in a PCR for the detection of C. pneumoniae. The C. pneumoniae-specific primers permitted the identification of six isolates of C. pneumoniae, but no reaction was observed with the 15 serovars of C. trachomatis or two strains of C. psittaci. PCR should prove to be valuable in confirming the identification of C. pneumoniae and in the diagnosis of C. pneumoniae infections. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,DIV INFECT DIS,BALTIMORE,MD 21205. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP GAYDOS, CA (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV INFECT DIS,BALTIMORE,MD 21205, USA. RI Gaydos, Charlotte/E-9937-2010; Quinn, Thomas/A-2494-2010 NR 28 TC 164 Z9 171 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 1992 VL 30 IS 4 BP 796 EP 800 PG 5 WC Microbiology SC Microbiology GA HJ487 UT WOS:A1992HJ48700008 PM 1374077 ER PT J AU WHETSELL, AJ DREW, JB MILMAN, G HOFF, R DRAGON, EA ADLER, K HUI, J OTTO, P GUPTA, P FARZADEGAN, H WOLINSKY, SM AF WHETSELL, AJ DREW, JB MILMAN, G HOFF, R DRAGON, EA ADLER, K HUI, J OTTO, P GUPTA, P FARZADEGAN, H WOLINSKY, SM TI COMPARISON OF 3 NONRADIOISOTOPIC POLYMERASE CHAIN REACTION-BASED METHODS FOR DETECTION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID HOMOSEXUAL MEN; DNA AMPLIFICATION; HIV-1 DNA; INFECTION; INFANTS; ANTIBODY; NEONATE; COHORT; AIDS AB Three nonradioisotopic polymerase chain reaction (PCR)-based detection techniques were evaluated for sensitivity and specificity in detecting human immunodeficiency virus type 1 (HIV-1) proviral DNA in peripheral blood mononuclear cells. The Roche prototype HIV-1 PCR assay, the Du Pont enzyme-linked oligonucleotide sandwich assay (ELOSA), and the Gen-Probe hybridization protection assay (HPA) were compared with a standard radioisotopic oligonucleotide solution hybridization (OSH) technique. A panel of 111 well-characterized clinical samples that included peripheral blood mononuclear cells from 48 healthy, low-risk, HIV-1 antibody-negative subjects, 24 antibody-positive subjects with stable CD4 counts of less than 200/mm3, and 39 antibody-positive subjects with stable CD4 counts of greater than 800/mm3 were studied. Each method demonstrated good specificity, ranging between 96 and 100%; those of the OSH and ELOSA (Du Pont) were 100%, those of the HPA (Gen-Probe) were 100% with one probe and 96% with the other probe, and that of the HIV-1 PCR assay (Roche) was 96%. Sensitivities ranged from 96 to 100% for the low-CD4-count group, with the OSH, the HIV-1 PCR assay (Roche), and the HPA (Gen-Probe) all attaining a sensitivity of 100%. For the high-CD4-count group, sensitivities ranged from 69 to 97%, with the OSH attaining a sensitivity of 97% and the HPA attaining sensitivities of 97% with one probe and 95% with the other probe. These data indicate that the nonradioisotopic techniques are sensitive and specific for the detection of HIV-1 proviral DNA in clinical samples. C1 NORTHWESTERN UNIV,CHICAGO,IL 60611. NIAID,BETHESDA,MD 20892. ROCHE DIAGNOST SYST,FAIR LAWN,NJ 07410. DUPONT CO,N BILLERICA,MA 01862. UNIV PITTSBURGH,PITTSBURGH,PA 15261. JOHNS HOPKINS UNIV,BALTIMORE,MD 21205. RI Wolinsky, Steven/B-2893-2012 FU NIAID NIH HHS [N01-AI-32535, N01-AI-72632, N01-AI-72634] NR 23 TC 82 Z9 82 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 1992 VL 30 IS 4 BP 845 EP 853 PG 9 WC Microbiology SC Microbiology GA HJ487 UT WOS:A1992HJ48700016 PM 1572969 ER PT J AU SUBBARAO, EK KAWAOKA, Y RYANPOIRIER, K CLEMENTS, ML MURPHY, BR AF SUBBARAO, EK KAWAOKA, Y RYANPOIRIER, K CLEMENTS, ML MURPHY, BR TI COMPARISON OF DIFFERENT APPROACHES TO MEASURING INFLUENZA-A VIRUS-SPECIFIC HEMAGGLUTINATION INHIBITION ANTIBODIES IN THE PRESENCE OF SERUM INHIBITORS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note ID ANTIGENIC SITES; ACID; GLYCOPROTEINS; RECEPTOR AB The A/Los Angeles/2/87 (H3N2) (A/LA/2/87) virus is sensitive to inhibitors of hemagglutination present in certain human sera. It was found that the effect of these inhibitors could be removed by treating sera with high-concentration receptor-destroying enzyme or trypsin-periodate or by using inhibitor-resistant viruses in the hemagglutination inhibition (HAI) test. Inhibitor-resistant viruses were not effective for detecting rises in antibody titers in the sera of volunteers infected with the A/LA/2/87 wild-type virus, while rises in antibody titer were readily detected in sera treated with trypsin-periodate and tested against A/LA/2/87 wild-type virus in an HAI test. It is therefore suggested that chemical or enzymatic methods be used to inactivate serum inhibitors and that standard virus be used in the HAI test for the currently circulating H3N2 viruses. C1 ST JUDE CHILDRENS RES HOSP, DEPT VIROL & MOLEC BIOL, MEMPHIS, TN 38101 USA. UNIV TENNESSEE CTR HLTH SCI, DEPT PEDIAT, MEMPHIS, TN 38163 USA. JOHNS HOPKINS UNIV, SCH HYG & PUBL HLTH, CTR IMMUNIZAT RES, BALTIMORE, MD 21205 USA. JOHNS HOPKINS UNIV, SCH MED, BALTIMORE, MD 21205 USA. RP SUBBARAO, EK (reprint author), NIAID, RESP VIRUSES SECT, INFECT DIS LAB, BETHESDA, MD 20892 USA. NR 16 TC 20 Z9 20 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1992 VL 30 IS 4 BP 996 EP 999 PG 4 WC Microbiology SC Microbiology GA HJ487 UT WOS:A1992HJ48700044 PM 1572989 ER PT J AU RAPOPORT, JL SWEDO, SE LEONARD, HL AF RAPOPORT, JL SWEDO, SE LEONARD, HL TI CHILDHOOD OBSESSIVE-COMPULSIVE DISORDER SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT SYMP ON OBSESSIVE COMPULSIVE DISORDER : INTEGRATING THEORY AND PRACTICE HELD AT THE 144TH ANNUAL MEETING OF THE AMERICAN PSYCHIATRIC ASSOC CY MAY 11-16, 1991 CL NEW ORLEANS, LA SP AMER PSYCHIAT ASSOC ID PROSPECTIVE FOLLOW-UP; LA-TOURETTES SYNDROME; PSYCHIATRIC-DISORDERS; CHILDREN; EPIDEMIOLOGY; ADOLESCENCE; PREVALENCE; SYMPTOMS; CHOREA; RAT AB Childhood obsessive compulsive disorder has recently been recognized as being more common than previously believed, supporting epidemiologic studies in adults that found rates far higher than clinical studies have suggested. Clinically, presentation is generally similar to that for adult patients, but compulsions may occur in the absence of obsessions although both obsessions and compulsions are common. Symptoms typically change over time, but almost all subjects at some time experienced excess washing as one of their symptoms. There is an increased rate of obsessive compulsive disorder and of motor tics in the relatives of children with obsessive compulsive disorder. As with Tourette's disorder, partial voluntary control of symptoms is usual. Prospective follow-up studies show continued disability from obsessive compulsive disorder and continued comorbidity with affective disorders. Obsessive compulsive symptoms are selectively associated with several childhood onset neurologic disorders such as Tourette's disorder and Sydenham's chorea, both presumed to be basal ganglia disorders. The implication of this association is that there may be hard-wired complex behaviors subsumed by basal ganglia frontal cortical pathways that are inappropriately released in obsessive compulsive disorder. RP RAPOPORT, JL (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20895, USA. NR 43 TC 42 Z9 42 U1 1 U2 2 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD APR PY 1992 VL 53 SU S BP 11 EP 16 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA HQ741 UT WOS:A1992HQ74100003 PM 1564053 ER PT J AU JACOBSEN, FM AF JACOBSEN, FM TI FLUOXETINE-INDUCED SEXUAL DYSFUNCTION AND AN OPEN TRIAL OF YOHIMBINE SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID INDUCED ANORGASMIA AB Background. Reports of fluoxetine-induced sexual dysfunction have described orgasmic and erectile difficulties but have neglected possible changes in sexual desire. This prospective study was undertaken to determine the percentages of patients experiencing different types of sexual dysfunction after successful antidepressant treatment with standard doses of fluoxetine. Additionally, an open trial of the alpha-2-adrenoceptor blocker yohimbine as a potential treatment for fluoxetine-induced sexual dysfunction was conducted in nine patients. Method. Over a 2-year period, outpatients who had fulfilled DSM-III-R criteria for major depression and subsequently responded to treatment with fluoxetine 20-40 mg were asked to report and describe changes in sexual function. A small number of consecutive nongeriatric patients complaining of new onset sexual dysfunction were invited to participate in an open trial of yohimbine 5.4 mg t.i.d. Results: Fifty-four (34%) of 160 outpatients reported the onset of sexual dysfunction after successful treatment with fluoxetine: 16 (10%) of the 160 patients reported decreased libido, 21 (13%) patients reported decreased sexual response, and 17 (11%) patients reported declines in both areas. Eight of nine patients reported improvement in sexual function with yohimbine, although five patients reported side effects that led to discontinuation in two cases. Conclusion: These findings suggest that (1) fluoxetine-induced sexual dysfunction may include decreased sexual desire as well as decreased physical functioning and may occur more frequently than previously appreciated and (2) fluoxetine-induced sexual dysfunction may be treatable with yohimbine. C1 NIMH,CLIN SCI LAB,WASHINGTON,DC 20032. GEORGE WASHINGTON UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20052. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC 20057. RP JACOBSEN, FM (reprint author), TRANSCULTURAL MENTAL HLTH INST,1301 20TH ST NW,SUITE 711,WASHINGTON,DC 20036, USA. NR 13 TC 156 Z9 156 U1 0 U2 1 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD APR PY 1992 VL 53 IS 4 BP 119 EP 122 PG 4 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA HQ267 UT WOS:A1992HQ26700001 PM 1564046 ER PT J AU ARANGO, V TRASKMANBENDZ, I MANN, JJ LINNOILA, M STANLEY, M MONTGOMERY, DB AF ARANGO, V TRASKMANBENDZ, I MANN, JJ LINNOILA, M STANLEY, M MONTGOMERY, DB TI NEUROBIOLOGY AND PHARMACOTHERAPY OF SUICIDAL-BEHAVIOR - DISCUSSION SESSIONS SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Discussion C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT PSYCHIAT,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT PHARMACOL,NEW YORK,NY 10032. NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,BETHESDA,MD. UNIV LUND HOSP,DEPT PSYCHIAT,S-22185 LUND,SWEDEN. ST MARYS HOSP,ACAD DEPT PSYCHIAT,LONDON W2 1NY,ENGLAND. RP ARANGO, V (reprint author), UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,NIMH,DEPT PSYCHIAT,PITTSBURGH,PA 15213, USA. RI Arango, Victoria/K-9377-2015 OI Arango, Victoria/0000-0001-8811-400X NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1992 VL 12 IS 2 SU S BP S32 EP S34 PG 3 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA HM610 UT WOS:A1992HM61000008 ER PT J AU LINNOILA, M VIRKKUNEN, M AF LINNOILA, M VIRKKUNEN, M TI BIOLOGIC CORRELATES OF SUICIDAL RISK AND AGGRESSIVE BEHAVIORAL TRAITS SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT 5TH WORLD CONGRESS OF BIOLOGICAL PSYCHIATRY : NEUROBIOLOGY AND PHARMACOTHERAPY OF SUICIDAL BEHAVIOR CY JUN 10, 1991 CL FLORENCE, ITALY ID ALCOHOL AB The authors' own and other key studies on alcoholism, impulse control, violent behavior, and suicidality and their biochemical concomitants are included in this mini-review. C1 NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,BETHESDA,MD. UNIV HELSINKI,DEPT PSYCHIAT,SF-00100 HELSINKI 10,FINLAND. NR 7 TC 41 Z9 41 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1992 VL 12 IS 2 SU S BP S19 EP S20 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA HM610 UT WOS:A1992HM61000005 PM 1374432 ER PT J AU MANN, JJ ARANGO, V AF MANN, JJ ARANGO, V TI INTEGRATION OF NEUROBIOLOGY AND PSYCHOPATHOLOGY IN A UNIFIED MODEL OF SUICIDAL-BEHAVIOR SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT 5TH WORLD CONGRESS OF BIOLOGICAL PSYCHIATRY : NEUROBIOLOGY AND PHARMACOTHERAPY OF SUICIDAL BEHAVIOR CY JUN 10, 1991 CL FLORENCE, ITALY ID TRITIATED IMIPRAMINE BINDING; CSF MONOAMINE METABOLITES; DEPRESSED-PATIENTS; FRONTAL-CORTEX; RECEPTOR-BINDING; POST-MORTEM; HUMAN-BRAIN; CEREBROSPINAL-FLUID; VICTIMS; OXIDASE AB Suicidal behavior is the result of a combination of factors that span the domains of psychopathology, genetics, early life experience, family interactions, social stress, physical illness, and neurobiology. To develop predictive and explanatory models of suicidal behavior it is necessary to consider all of these domains. A stress-diathesis model is proposed that classifies risk factors for suicidal behavior into those that are trait-dependent and those that are state-dependent. The timing of suicidal behavior is determined by state-dependent factors. The relationship of psychopathologic factors such as severity of depression or anxiety to suicide will be discussed. Biologic changes that correlate with suicide may be either state- or trait-dependent. Particular emphasis will be given to changes in the serotonin system and how these may represent a constitutional risk factor as opposed to a state-dependent risk factor for suicidal behavior. RP MANN, JJ (reprint author), UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,NIMH,DEPT PSYCHIAT,PITTSBURGH,PA 15213, USA. RI Arango, Victoria/K-9377-2015 OI Arango, Victoria/0000-0001-8811-400X FU NIMH NIH HHS [MH40210, MH46745] NR 59 TC 55 Z9 55 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1992 VL 12 IS 2 SU S BP S2 EP S7 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA HM610 UT WOS:A1992HM61000002 PM 1374433 ER PT J AU GUSSIO, R POU, S CHEN, JH SMYTHERS, GW AF GUSSIO, R POU, S CHEN, JH SMYTHERS, GW TI A PSEUDORECEPTOR DOCKING STUDY OF 4,5-ALPHA-EPOXYMORPHINANS WITH A RANGE OF DIELECTRIC-CONSTANTS SO JOURNAL OF COMPUTER-AIDED MOLECULAR DESIGN LA English DT Article DE PSEUDORECEPTOR MODELING; OPIATE MOLECULAR MODELING; QUANTITATIVE STRUCTURE-ACTIVITY RELATIONSHIPS; QSAR; DIELECTRIC CONSTANTS; DOCKING ID MOLECULAR-ORBITAL CALCULATIONS; OPIATE RECEPTOR INTERACTIONS; CLASTIC BINDING; ANTAGONISTS; AGONISTS; DNA AB Thirteen 4,5-epoxymorphinan mu-agonists with established analgesic action were docked into an Asp-Lys-His-Phe pseudoreceptor complex under a range of distance-dependent dielectric conditions. The number of compounds with potential energies of the docked complexes that agreed in rank order with corresponding analgesic potencies was determined for each condition. Two dielectric conditions, n-decane (1.991) and ethanol (24.3), enabled the greatest number of compounds to relate to their pseudoreceptors with each having 9 and 8 successes respectively. Both of these conditions demonstrated unique influences on the types of structures that were successfully docked. For example, the morphine stereoisomer alpha-isomorphine, the geometric isomer B/C trans-morphine, and the 8-position-substituted gamma-isomorphine were successes in the n-decane condition, whereas the ethanol condition produced the substituted codeine derivatives dihydrocodeinone and dihydroxycodeinone. These findings emphasize the importance of dielectric influence when developing force-field modeled quantitative structure-activity relationships for a closely related homologous series. C1 UNIV MARYLAND,SCH PHARM,DEPT PHARMACOL & TOXICOL,BALTIMORE,MD 21201. RP GUSSIO, R (reprint author), NCI,PRI DYNCORP,FREDERICK CANC RES DEV CTR,ADV SCI COMP LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 29 TC 5 Z9 5 U1 0 U2 0 PU ESCOM SCI PUBL BV PI LEIDEN PA PO BOX 214, 2300 AE LEIDEN, NETHERLANDS SN 0920-654X J9 J COMPUT AID MOL DES JI J. Comput.-Aided Mol. Des. PD APR PY 1992 VL 6 IS 2 BP 149 EP 158 DI 10.1007/BF00129425 PG 10 WC Biochemistry & Molecular Biology; Biophysics; Computer Science, Interdisciplinary Applications SC Biochemistry & Molecular Biology; Biophysics; Computer Science GA HU525 UT WOS:A1992HU52500004 PM 1320664 ER PT J AU COLE, PM PUTNAM, FW AF COLE, PM PUTNAM, FW TI EFFECT OF INCEST ON SELF AND SOCIAL FUNCTIONING - A DEVELOPMENTAL PSYCHOPATHOLOGY PERSPECTIVE SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY LA English DT Review ID BORDERLINE PERSONALITY-DISORDER; CHILDHOOD SEXUAL ABUSE; CHRONIC PELVIC PAIN; CHEMICAL DEPENDENCY; ADOLESCENT GIRLS; SUBSTANCE ABUSE; PHYSICAL ABUSE; CHILDREN; WOMEN; VICTIMIZATION AB The effects of child sexual abuse have become a leading concern of mental health service providers. Despite an explosion of studies, one major difficulty in this research is the lack of a developmentally sensitive model for conceptualizing short- and long-term effects and continuity and discontinuity of effects over time. This article proposes a model based in the perspective of developmental psychopathology. It is argued that incest has its unique negative effects in the domains of self and social functioning, specifically in jeopardizing self-definition and integration, self-regulatory processes, and a sense of security and trust in relationships. Studies with clinical samples indicate that diagnostic conditions associated uniquely with a history of incest reflect serious self- and social impairments. A review of the developmental literature on self and social development summarizes each major developmental transition from infancy to middle adulthood, and the implications for the negative effects of incest on development are discussed. Finally, implications for developmentally sensitive research are discussed. RP COLE, PM (reprint author), NIMH,BLDG 15K,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 127 TC 260 Z9 263 U1 4 U2 18 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0022-006X J9 J CONSULT CLIN PSYCH JI J. Consult. Clin. Psychol. PD APR PY 1992 VL 60 IS 2 BP 174 EP 184 DI 10.1037//0022-006X.60.2.174 PG 11 WC Psychology, Clinical SC Psychology GA HM682 UT WOS:A1992HM68200004 PM 1592946 ER PT J AU PROSKIN, HM CHILTON, NW KINGMAN, A AF PROSKIN, HM CHILTON, NW KINGMAN, A TI INTERIM-REPORT OF THE AD-HOC-COMMITTEE FOR THE CONSIDERATION OF STATISTICAL CONCERNS RELATED TO THE USE OF INTRAORAL MODELS IN SUBMISSIONS FOR PRODUCT CLAIMS APPROVAL TO THE AMERICAN-DENTAL-ASSOCIATION SO JOURNAL OF DENTAL RESEARCH LA English DT Editorial Material AB Subsequent to the American Dental Association Symposium on Intra-oral Studies, held in Chicago in September, 1990, the Council on Dental Therapeutics decided that further consideration should be given to statistical issues relating to intra-oral models. The authors accepted the request of Council staff to assist in the development of Guidelines concerning the validity, reliability, and combinability of data obtained from these models. The ensuing work in this area, which began in the fall of 1990 and has continued to date, has thus far focused on the issue of validity. The purpose of the present paper is to provide the interested community at large with an update on the progress made thus far, and to provide some perspective as to where all of the work in this area may eventually be leading. It is anticipated that a more comprehensive and definitive report will be produced at the completion of this process. C1 TASK FORCE DESIGN & ANAL INC,LAWRENCEVILLE,NJ 08648. COLUMBIA UNIV,SCH PUBL HLTH,DIV BIOSTAT,NEW YORK,NY 10027. NIDR,EODPP,BETHESDA,MD 20814. RP PROSKIN, HM (reprint author), EASTMAN DENT CTR,DIV BIOSTAT & COMP,625 ELMWOOD AVE,ROCHESTER,NY 14620, USA. NR 1 TC 14 Z9 15 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD APR PY 1992 VL 71 SI SI BP 949 EP 952 PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HX273 UT WOS:A1992HX27300031 PM 1592992 ER PT J AU LASH, RW DESAI, RK ZIMMERMAN, CA FLACK, MR YOSHIDA, T WONDISFORD, FE WEINTRAUB, BD AF LASH, RW DESAI, RK ZIMMERMAN, CA FLACK, MR YOSHIDA, T WONDISFORD, FE WEINTRAUB, BD TI MUTATIONS OF THE HUMAN THYROTROPIN-BETA SUBUNIT GLYCOSYLATION SITE REDUCE THYROTROPIN SYNTHESIS INDEPENDENT OF CHANGES IN GLYCOSYLATION STATUS SO JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION LA English DT Article DE THYROTROPIN; TSH; GLYCOPROTEIN HORMONES; GLYCOSILATION; SITE-DIRECTED MUTAGENESIS; RECOMBINANT HORMONES ID HUMAN CHORIONIC-GONADOTROPIN; THYROID-STIMULATING HORMONE; TRANSIENT EXPRESSION; LINKED OLIGOSACCHARIDES; GENE; CLONING; MUTAGENESIS; TSH; DEGLYCOSYLATION; CARBOHYDRATE AB In recent studies, site-directed mutagenesis has been used to alter the tripeptide glycosylation recognition sequences of glycoprotein hormone subunits, thereby affecting their structure and function. However, it is not known whether these effects result from changes in glycosylation status, amino acid sequence, or both. We therefore studied the synthesis of wild-type and mutant recombinant human thyrotropins produced by transient transfection of a human cell line. Mutating the TSH-beta-subunit glycosylation recognition sequence, Asn-Thr-Thr (codons 23-25), to either Gln-Thr-Thr or Asn-Thr-Tyr abolished subunit glycosylation, as demonstrated by the inability to incorporate H-3-carbohydrates. However, a third mutation (Asn-Thr-Ser) contained an intact glycosylation recognition sequence site, and was shown to retain glycosylation. The mutations that abolished TSH-beta-subunit glycosylation resulted in greater than 90% decreases in TSH synthesis. However, the glycosylation recognition sequence mutant that retained beta-subunit glycosylation exhibited a 70% decrease in TSH production. These decreases were not attributable to the intracellular accumulation of TSH or its free beta-subunit. We also engineered two TSH-beta-subunit mutations that did not alter the glycosylation recognition sequence. A glycine to arginine mutation adjacent to the glycosylation recognition sequence, in a region thought to be critical for heterodimer formation, abolished TSH production. In contrast, shortening the TSH-beta-subunit carboxyterminus by six amino acids increased TSH synthesis. In summary, a series of mutations within and adjacent to the TSH-beta-glycosylation recognition sequence significantly reduced TSH production, whether or not they abolished subunit glycosylation. These findings emphasize the dual roles of the TSH glycosylation recognition sequence; as the signal for the addition of carbohydrate, and as an amino acid sequence necessary for the efficient synthesis of the TSH dimer. C1 NIH,MOLEC CELLULAR & NUTR ENDOCRINOL BRANCH,BETHESDA,MD 20892. NIH,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP LASH, RW (reprint author), UNIV MARYLAND,SCH MED,DIV ENDOCRINOL,22 S GREENE ST,BALTIMORE,MD 21201, USA. NR 29 TC 12 Z9 12 U1 0 U2 3 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 1992 VL 15 IS 4 BP 255 EP 263 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HX248 UT WOS:A1992HX24800002 PM 1512415 ER PT J AU ALEXANDER, HR WONG, GGH DOHERTY, GM VENZON, DJ FRAKER, DL NORTON, JA AF ALEXANDER, HR WONG, GGH DOHERTY, GM VENZON, DJ FRAKER, DL NORTON, JA TI DIFFERENTIATION FACTOR LEUKEMIA INHIBITORY FACTOR PROTECTION AGAINST LETHAL ENDOTOXEMIA IN MICE - SYNERGISTIC EFFECT WITH INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID SUPEROXIDE-DISMUTASE; STIMULATING FACTOR; MONOCYTIC CELLS; EXPRESSION; CACHECTIN; CLONING; INJURY; RATS AB Differentiation factor (D factor), also called leukemia inhibitory factor (LIF), is a glycoprotein that has been increasingly recognized to possess a wide range of physiological activities. We examined the possibility that the administration of D factor may confer beneficial effects and enhance host resistance against lethal endotoxemia. A single intravenous dose of recombinant human D factor completely protected C57/B16 mice from the lethal effect of Escherichia coli endotoxin (lipopolysaccharide [LPS]). The protective effects were dose dependent and observed when administered 2-24 h before LPS. Previous work has shown that interleukin 1 (IL-1) and tumor necrosis factor (TNF) also protect against a subsequent LPS challenge in a dose-dependent manner. When human D factor was combined with sub-protective doses of IL-1-beta or TNF-alpha, there was dramatic synergistic protection against a subsequent lethal LPS challenge. C1 NCI,DATA MANAGEMENT SECT,BETHESDA,MD 20892. GENENTECH INC,DEPT MOLEC BIOL,SAN FRANCISCO,CA 94080. RP ALEXANDER, HR (reprint author), NCI,SURG BRANCH,SURG METAB SECT,BLDG 10,ROOM 2B01,BETHESDA,MD 20892, USA. RI Venzon, David/B-3078-2008 NR 24 TC 47 Z9 49 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1992 VL 175 IS 4 BP 1139 EP 1142 DI 10.1084/jem.175.4.1139 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HL014 UT WOS:A1992HL01400029 PM 1552284 ER PT J AU COLLINS, PL MOTTET, G AF COLLINS, PL MOTTET, G TI OLIGOMERIZATION AND POSTTRANSLATIONAL PROCESSING OF GLYCOPROTEIN-G OF HUMAN RESPIRATORY SYNCYTIAL VIRUS - ALTERED O-GLYCOSYLATION IN THE PRESENCE OF BREFELDIN-A SO JOURNAL OF GENERAL VIROLOGY LA English DT Article ID HERPES-SIMPLEX VIRUS-GC-1; CELL-INDUCED DIFFERENCES; TRANS-GOLGI CISTERNAE; LINKED OLIGOSACCHARIDES; ENDOPLASMIC-RETICULUM; SUBGROUP-A; G-PROTEIN; COMPLEX; POLYPEPTIDES; SEQUENCE AB The post-translation maturation of the attachment G glycoprotein of human respiratory synctial virus (RSV) was investigated. The G protein formed homo-oligomers which sedimented in sucrose gradients at the same rate as the fusion F protein tetramer. Oligomerization of the G protein was insensitive to carbonylcyanide m-chlorophenylhydrazine, showing that this step occurs in the endoplasmic reticulum prior to O-glycosylation which initiated in the trans-Golgi compartment. The sedimentation of the G protein oligomer was essentially unchanged by the subsequent addition of O-linked sugars. This indicated that their contribution to the M(r) of the G protein is less than that estimated by electrophoretic mobility. It also suggested that O-glycosylation is not an important determinant of G protein oligomerization and, by implication, of polypeptide folding. The G protein is palmitylated. In short labelling pulses, the G protein accumulated as two species of 48K and 50K which contained only N-linked sugars, whose difference in M(r) was due solely to an N-linked sugar, which both assembled into oligomers, but which differed in the rate of subsequent O-glycosylation. The G protein was not detectably O-glycosylated in the presence of monensin, confirming previous work. In the presence of brefeldin A (BFA), it accumulated as a partially O-glycosylated species (BFA-G) of 68K to 78K. But further analysis by chase incubations following BFA-washout, by lectinbinding, and by glycosidase treatment suggested that BFA-G was not a fully authentic processing intermediate. In particular, some of the O-linked side-chains of the BFA-G protein were found to be sialylated. Rather than being a normal step in processing, this sialylation probably was due to altered distribution or activity of sialytransferases during BFA treatment and may have resulted in the premature termination of elongation of some of the O-liked side-chains. Thus, these studies (i) indicate that O-glycosylation of the G protein begins in the trans-Golgi compartment and (ii) suggest that O-glycosylation is completed in as a subsequent compartment, but this latter suggestion is complicated by the evidence that the BFA-G protein is not a fully authentic intermediate. Finally, an additional species of 48K to 60K was detected under standard conditions of infection and was found to differ in several ways from the 48K and 50K precursors described above: it was detected only following long labelling periods, it was detected only following long labelling periods, it was found in monomers rather than oligomers, and it contained a high content of O-linked sugars. Also, antibodies raised against a peptide from the G ectodomain reacted with the 48K, 50K and mature G proteins but did not react with the 48K to 60K species. This indicated that the latter contained differences in conformation or O-glycosylation which masked that part of the ectodomain. The 48K to 60K species was not detected in virions or secreted from infected cells. Thus, it appeared to be a dead-end by-product rather than a true processing intermediate. RP COLLINS, PL (reprint author), NIAID,INFECT DIS LAB,BLDG 7,ROOM 100,BETHESDA,MD 20892, USA. NR 46 TC 69 Z9 71 U1 0 U2 0 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1317 J9 J GEN VIROL JI J. Gen. Virol. PD APR PY 1992 VL 73 BP 849 EP 863 DI 10.1099/0022-1317-73-4-849 PN 4 PG 15 WC Biotechnology & Applied Microbiology; Virology SC Biotechnology & Applied Microbiology; Virology GA HM861 UT WOS:A1992HM86100012 PM 1634876 ER PT J AU SETTE, A OSULLIVAN, D SIDNEY, J GAETA, FCA ARRHENIUS, T COLON, SM APPELLA, E GREY, HM AF SETTE, A OSULLIVAN, D SIDNEY, J GAETA, FCA ARRHENIUS, T COLON, SM APPELLA, E GREY, HM TI MULTIPLE AMINO-ACID SUBSTITUTIONS AS A STRATEGY TO IMPROVE CLASS-II BINDING-CAPACITY OF PEPTIDE MOLECULES SO JOURNAL OF IMMUNOLOGICAL RESEARCH LA English DT Article DE CLASS-II MHC; MULTIPLE ANALOGS; PEPTIDE AFFINITY ID T-CELL; MHC BINDING; IA; ANTIGEN; RECOGNITION; RESIDUES; EPITOPE AB In the present study, we describe a simple procedure to generate high affinity, specific class II binding peptides. According to this method, each residue of a known class II binding peptide is replaced by one of several different single amino acid substitutions. The panel of peptides thus generated is tested for binding, and then a second generation of analogs is made by combining, at each position, substitutions positively affecting binding. This approach has been tested in two different experimental systems (Ova 323-336/IA(d) and HEL 107-116/DR2w2). In both cases, high affinity, specific binders were identified, thus demonstrating the validity of this approach in at least two different class II MHC types. C1 NCI,BETHESDA,MD 20892. RP SETTE, A (reprint author), CYTEL,3525 JOHN HOPKINS COURT,SAN DIEGO,CA 92121, USA. NR 20 TC 3 Z9 3 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 1992 VL 4 IS 2 BP 56 EP 60 PG 5 WC Immunology SC Immunology GA HY876 UT WOS:A1992HY87600002 ER PT J AU FRANCIS, ML RYAN, J JOBLING, MG HOLMES, RK MOSS, J MOND, JJ AF FRANCIS, ML RYAN, J JOBLING, MG HOLMES, RK MOSS, J MOND, JJ TI CYCLIC AMP-INDEPENDENT EFFECTS OF CHOLERA-TOXIN ON B-CELL ACTIVATION .2. BINDING OF GANGLIOSIDE-GM1 INDUCES B-CELL ACTIVATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID KINASE-C ACTIVATION; ANTI-IG ANTIBODIES; SURFACE-IMMUNOGLOBULIN; MEMBRANE GANGLIOSIDES; MONOCLONAL-ANTIBODIES; BACTERIAL TOXINS; CROSS-LINKING; FREE CALCIUM; PROLIFERATION; RECEPTOR AB Although the physiologic function of gangliosides is unknown, evidence suggests they play a role in the regulation of cell growth. The binding of ganglioside G(M1) by recombinant B subunit of cholera toxin (rCT-B) inhibited mitogen-stimulated B cell proliferation without elevating intracellular cAMP. CT-B paradoxically enhanced the expression of MHC class II (Ia) molecules and minor lymphocyte-stimulating determinants without altering the expression of some other immunologically relevant B cell surface Ag. Increased expression of Ia was not detected until 4 h after stimulation, kinetics similar to those seen when B cells are stimulated with anti-Ig antibody or IL-4, suggesting that the enhancement was not the result of redistribution of existing cell surface markers but rather the result of a new metabolic event. Both the inhibitory and stimulatory effects of CT-B could be blocked by incubation of CT-B with ganglioside G(M1). Furthermore, enhancement of the CT-B-mediated effect was seen when additional ganglioside G(M1) was incorporated into the B cell membrane. rCT-B with a mutation that interfered with its binding to ganglioside G(M1) did not enhance Ia expression. Taken together, these results indicate that the observed effects of CT-B were most likely mediated through the binding of cell surface ganglioside G(M1). CT-B-mediated stimulation of la expression provides a potential explanation for the previously described ability of CT-B to act as an immunoadjuvant. These results suggest that the binding of ganglioside G(M1) has multiple B cell growth-regulating effects. C1 UNIFORMED SERV UNIV HLTH SCI, DEPT MED, ROOM A3060, 4301 JONES BRIDGE RD, BETHESDA, MD 20814 USA. UNIFORMED SERV UNIV HLTH SCI, DEPT MICROBIOL, BETHESDA, MD 20814 USA. USN, MED RES INST, BETHESDA, MD 20814 USA. NHLBI, CELLULAR METAB LAB, BETHESDA, MD 20892 USA. FU NIAID NIH HHS [AI24273, AI27465] NR 59 TC 72 Z9 73 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 EI 1550-6606 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1992 VL 148 IS 7 BP 1999 EP 2005 PG 7 WC Immunology SC Immunology GA HJ596 UT WOS:A1992HJ59600005 PM 1312102 ER PT J AU WONG, HL LOTZE, MT WAHL, LM WAHL, SM AF WONG, HL LOTZE, MT WAHL, LM WAHL, SM TI ADMINISTRATION OF RECOMBINANT IL-4 TO HUMANS REGULATES GENE-EXPRESSION, PHENOTYPE, AND FUNCTION IN CIRCULATING MONOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID STIMULATORY FACTOR-I; HUMAN PERIPHERAL-BLOOD; ACTIVATED KILLER ACTIVITY; HIGH-DOSE INTERLEUKIN-2; TUMOR NECROSIS FACTOR; HUMAN FC-RECEPTORS; DIFFERENTIATION FACTOR; HYDROGEN-PEROXIDE; HUMAN-LYMPHOCYTES; CANCER-PATIENTS AB As a multifunctional cytokine that can augment certain T cell responses, IL-4 is being evaluated currently as a possible therapeutic agent in the treatment of cancer patients. In this report, PBMC were isolated from such patients before and after IL-4 therapy and were analyzed for phenotypic and functional alterations. Differential blood counts showed that the relative percentages of lymphocytes and, to a lesser degree, monocytes decreased after treatment with IL-4. However, when phenotypically analyzed by FACS, monocyte numbers generally increased, whereas there was a decrease in lymphocyte numbers. Monocytes taken from patients before therapy and cultured with and without LPS exhibited normal patterns of monokine-specific (IL-1-beta and TNF-alpha) mRNA expression, as well as secretion of peptide. The addition of rIL-4 to these cultures, however, resulted in the down-regulation of both gene expression and peptide release. Although monocytes taken from post-therapy patients also displayed normal patterns of monokine gene expression and cytokine release after stimulation with LPS, they were no longer inhibited by the addition of exogenous rIL-4 in vitro. These data suggest that monocytes become refractory to the inhibitory effects of IL-4 after in vivo exposure to this cytokine. However, when these monocytes were examined for expression of CD14, CD32, and CD64, exogenous IL-4 was observed to decrease markedly the appearance of these markers, regardless of whether the cells were obtained before or after therapy. Furthermore, monocytes from post-therapy patients exhibited reduced production of PGE2 and superoxide anion, compared with cells obtained before therapy. This effect persisted in culture independent of the further addition of exogenous IL-4. These data suggest a dichotomy between the IL-4-dependent mechanisms that regulate monokine production and those that regulate certain other monocyte functions. The exact mechanisms that govern these two pathways are not known. These results have important clinical implications for the use of IL-4 as an immunotherapeutic agent, as well as providing insight into the physiologic role of IL-4. C1 NCI,SURG BRANCH,BETHESDA,MD 20892. RP WONG, HL (reprint author), NIDR,IMMUNOL LAB,BLDG 30,ROOM 334,BETHESDA,MD 20892, USA. NR 53 TC 68 Z9 68 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 1992 VL 148 IS 7 BP 2118 EP 2125 PG 8 WC Immunology SC Immunology GA HJ596 UT WOS:A1992HJ59600023 PM 1531998 ER PT J AU COLAMONICI, OR PFEFFER, LM DALESSANDRO, F PLATANIAS, LC GREGORY, SA ROSOLEN, A NORDAN, R CRUCIANI, RA DIAZ, MO AF COLAMONICI, OR PFEFFER, LM DALESSANDRO, F PLATANIAS, LC GREGORY, SA ROSOLEN, A NORDAN, R CRUCIANI, RA DIAZ, MO TI MULTICHAIN STRUCTURE OF THE IFN-ALPHA RECEPTOR ON HEMATOPOIETIC-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN INTERFERON-ALPHA; HUMAN-LYMPHOBLASTOID CELLS; CROSS-LINKING; BINDING-SITES; EXPRESSION; SUBUNIT; GENE AB The structure of IFN-alpha receptor was studied by 1) developing antibodies against the receptor, and 2) screening a number of cell lines by affinity cross-linking to identify cells that express different IFN-alpha-2 receptor structures. We report that two different patterns of IFN-alpha-2 receptor are observed in human cells of hematopoietic origin. The predominant form of the IFN-alpha receptor is a multichain structure in which IFN-alpha-2 forms complexes of 110 and 130 kDa (alpha-subunit). A high M(r) complex of 210 kDa results from the association of alpha-subunit and other receptor components. In contrast, another form of the receptor has been identified in the IFN-alpha-resistant U-937 cell line and in some cases of acute leukemia. This form of the IFN-alpha receptor is characterized by the presence of the alpha- subunit, and the absence of the 110- and 210-kDa bands. Also a novel 180-kDa complex and a more prominent 75-kDa band are observed. Functional studies performed in U-937 cells showed that this cell line is not only partially resistant to the antiproliferative and antiviral effects of IFN-alpha, but also fails to down-regulate the alpha-subunit of the IFN-alpha receptor upon IFN-alpha binding. C1 NCI,MED BRANCH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NINCDS,NEUROPHYSIOL LAB,BETHESDA,MD 20892. UNIV TENNESSEE,CTR HLTH SCI,COLL MED,DEPT PATHOL,MEMPHIS,TN 38163. RP COLAMONICI, OR (reprint author), UNIV CHICAGO,DEPT MED,HEMATOL ONCOL SECT,MC2115,CHICAGO,IL 60637, USA. FU NCI NIH HHS [CA42557, CA49133]; NIGMS NIH HHS [GM 36716] NR 32 TC 76 Z9 76 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 1992 VL 148 IS 7 BP 2126 EP 2132 PG 7 WC Immunology SC Immunology GA HJ596 UT WOS:A1992HJ59600024 PM 1531999 ER PT J AU ROVIN, BH YOSHIUMURA, T TAN, L AF ROVIN, BH YOSHIUMURA, T TAN, L TI CYTOKINE-INDUCED PRODUCTION OF MONOCYTE CHEMOATTRACTANT PROTEIN-1 BY CULTURED HUMAN MESANGIAL CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN ENDOTHELIAL-CELLS; EXPERIMENTAL GLOMERULONEPHRITIS; MACROPHAGES; EXPRESSION; INTERLEUKIN-1; PURIFICATION; GLOMERULI; IL-1; JE AB The infiltration of the glomerulus by monocyte-derived macrophages is an important step in the pathogenesis of glomerular injury. The factors regulating glomerular leukocyte traffic remain unknown. We postulated that the glomerular mesangial cell (MC) may participate in the development of glomerular inflammation through the production of the monocyte-specific chemotactic factor, monocyte chemoattractant protein-1 (MCP-1). Using a cell culture system, we found that human MC produced a basal level of monocyte chemotactic activity, which was significantly increased by the inflammatory cytokines IL-1-beta and TNF-alpha. This increase in bioactivity correlated with the increased expression of MCP-1 mRNA by cytokine-conditioned MC. The total chemotactic activity of MC-conditioned supernatants was reduced by more than 80% after immunoadsorption with a specific anti-MCP-1 antibody. Thus, MC could play a role in inflammatory glomerular conditions through the production of MCP-1. C1 OHIO STATE UNIV,DEPT MED,DIV NEPHROL,COLUMBUS,OH 43210. NCI,FREDERICK,MD 21702. NR 37 TC 196 Z9 202 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 1992 VL 148 IS 7 BP 2148 EP 2153 PG 6 WC Immunology SC Immunology GA HJ596 UT WOS:A1992HJ59600027 PM 1532001 ER PT J AU ATKINSON, TP KALINER, MA HOHMAN, RJ AF ATKINSON, TP KALINER, MA HOHMAN, RJ TI PHOSPHOLIPASE C-GAMMA-1 IS TRANSLOCATED TO THE MEMBRANE OF RAT BASOPHILIC LEUKEMIA-CELLS IN RESPONSE TO AGGREGATION OF IGE RECEPTORS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; HISTAMINE-RELEASE; TYROSINE PHOSPHORYLATION; INOSITOL PHOSPHATES; MEDIATED ACTIVATION; CHOLERA-TOXIN; BOVINE BRAIN; MAST-CELLS; C-GAMMA; STIMULATION AB Aggregation of the high affinity receptor for IgE (Fc-epsilon-RI) on the surface of mast cells results in the rapid hydrolysis of membrane inositol phospholipids by phospholipase C (PLC). Although at least seven isoenzymes of PLC have been characterized in different mammalian cells, the isoenzyme involved in Fc-epsilon-RI-mediated signal transduction and the mechanism of its activation have not been demonstrated. We now report that PLC-gamma-1 is translocated to the membrane of mast cells after aggregation of Fc-epsilon-RI. Activation of rat basophilic leukemia cells, a rat mast cell line, with oligomeric IgE resulted in an increase in PLC activity in washed membrane preparations in a cell free assay containing exogenous [H-3]phosphatidylinositol (PI). The increase in PLC activity has the same dose-response to oligomeric IgE as receptor mediated hydrolysis of inositol lipids (PI hydrolysis) in intact cells. Analysis by Western blot probed with anti-PLC-gamma-1 antibody revealed that there is a three- to fourfold increase in PLC-gamma-1 in membranes from activated cells. The increase in PLC activity is augmented a further 20% by the addition of orthovanadate to the incubation medium suggesting that a tyrosine phosphatase is involved in the down-regulation of this phenomenon. These findings demonstrate translocation of PLC-gamma-1 to the membrane following activation of a receptor which does not contain intrinsic tyrosine kinase activity. Activation of PLC-gamma-1 by this pathway may account for Fc-epsilon-RI-mediated PI hydrolysis. C1 NIAID,BLDG 10,ROOM 11C215,BETHESDA,MD 20892. NR 39 TC 50 Z9 50 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 1992 VL 148 IS 7 BP 2194 EP 2200 PG 7 WC Immunology SC Immunology GA HJ596 UT WOS:A1992HJ59600035 PM 1312104 ER PT J AU NAKAJIMA, K SMITH, CV MIXON, A SYKES, M GUZZETTA, PC SPITZER, TR ECKHAUS, MA SACHS, DH AF NAKAJIMA, K SMITH, CV MIXON, A SYKES, M GUZZETTA, PC SPITZER, TR ECKHAUS, MA SACHS, DH TI INVITRO AND INVIVO EFFECTS OF RECOMBINANT HUMAN INTERLEUKIN-2 IN NAIVE MINIATURE SWINE SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE INTERLEUKIN-2; LYMPHOKINE-ACTIVATED KILLER CELLS; MINIATURE SWINE ID BONE-MARROW TRANSPLANTATION; MAJOR HISTOCOMPATIBILITY COMPLEX; PURIFIED HUMAN INTERLEUKIN-2; KILLER CELLS; HALF-LIFE; DISEASE; AUGMENTS; TOXICITY; CANCER AB Recent data in mice have shown that early administration of recombinant human interleukin-2 (rIL-2) provides significant protection from lethal graft-versus-host disease. Because of the potential clinical importance of these findings, it will be important to assess the effectiveness of this therapy in a large animal preclinical bone marrow transplantation model. We report here our initial studies of the in vitro and in vivo effects of rIL-2 in miniature swine. In vitro 4-day cultures of pig peripheral blood lymphocytes (PBL) in complete medium containing rIL-2 at 1,000 U/ml resulted in optimal proliferation and generation of lymphokine-activated killer (LAK) cells. A pig-mouse hybridoma cell line was found to be highly sensitive as a LAK cell target. Two naive pigs received 20,000 U/kg and 2 pigs received 100,000 U/kg of rIL-2 intravenously twice a day for 4 days. No clinical symptoms were seen during or after administration at the lower dose while both high dose-treated animals showed generalized erythema from days 2 to 4, and one showed mild diarrhea during this period. The disappearance of IL-2 activity from the serum showed two components: (1) an initial fast component with a half-time of approximately 10 min and (2) a slow component with a half-time of approximately 60 min. LAK cell precursors disappeared from the peripheral circulation by 6 min after rIL-2 administration and began to recover by 6 h in the low dose recipients and only after 12 h in the high dose recipients. These data indicate that the effects of rIL-2 in vivo in miniature swine are very similar to those previously demonstrated in humans, and suggest that these animals should provide an excellent preclinical model for studies of the effects of rIL-2 on graft-versus-host disease. C1 MASSACHUSETTS GEN HOSP,TRANSPLAT BIOL RES CTR,SURG SERV,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. CHILDRENS HOSP,NATL MED CTR,DEPT SURG,WASHINGTON,DC 20010. GEORGE WASHINGTON UNIV,DEPT CHILD HLTH & DEV,WASHINGTON,DC 20052. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. NIH,DIV RES SERV,VET RESOURCES BRANCH,BETHESDA,MD 20892. NR 21 TC 7 Z9 7 U1 0 U2 0 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 1992 VL 11 IS 3 BP 169 EP 175 DI 10.1097/00002371-199204000-00003 PG 7 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA HK543 UT WOS:A1992HK54300003 PM 1515421 ER PT J AU DAY, C SCHWARTZ, B LI, BL PESTKA, S AF DAY, C SCHWARTZ, B LI, BL PESTKA, S TI ENGINEERED DISULFIDE BOND GREATLY INCREASES SPECIFIC ACTIVITY OF RECOMBINANT MURINE INTERFERON-BETA SO JOURNAL OF INTERFERON RESEARCH LA English DT Article ID ESCHERICHIA-COLI; PROTEIN STABILITY; M13 VECTORS; PURIFICATION; MUTAGENESIS; EXPRESSION; GENE AB Unlike other species of interferon-beta (IFN-beta) mouse (Mu) IFN-beta has no naturally occurring intramolecular disulfide bond. When expressed in Escherichia coli, MuIFN-beta appears to exhibit instability and low activity. To increase its activity, we engineered a pair of cysteines into recombinant MuIFN-beta to test whether this change would improve its antiviral activity. In the absence of detailed structural data, the optimal placement of cysteines was determined by sequence comparison with other species of IFN-beta. While MuIFN-beta has only a single cysteine (at position 17), other species of IFN-beta have three cysteines, at positions 17, 31, and 141 (numbering based on consensus sequence), a disulfide bond being formed between the latter two residues. Thus, we introduced cysteines into MuIFN-beta at positions 29 and 136, which correspond to positions 31 and 141 of the consensus sequence. When the variant form of MuIFN-beta was expressed in bacteria and purified, we found that the additional cysteines greatly increased the antiviral activity. Further improvement was obtained by replacement of the Cys-17 with a serine. In this manner a specific activity approximately 15-fold that of the wild-type recombinant molecule was achieved. C1 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT MOLEC GENET & MICROBIOL,PISCATAWAY,NJ 08854. NIAID,ROCKVILLE,MD 20852. ACAD SINICA,SHANGHAI INST BIOCHEM,SHANGHAI 200031,PEOPLES R CHINA. FU NCI NIH HHS [CA-46465]; NIAID NIH HHS [AI-25914] NR 35 TC 13 Z9 13 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0197-8357 J9 J INTERFERON RES JI J. Interferon Res. PD APR PY 1992 VL 12 IS 2 BP 139 EP 143 DI 10.1089/jir.1992.12.139 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT118 UT WOS:A1992HT11800010 PM 1578187 ER PT J AU LISBY, G REITZ, MS VEJLSGAARD, GL AF LISBY, G REITZ, MS VEJLSGAARD, GL TI NO DETECTION OF HTLV-I DNA IN PUNCH SKIN BIOPSIES FROM PATIENTS WITH CUTANEOUS T-CELL LYMPHOMA BY THE POLYMERASE CHAIN-REACTION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID ENZYMATIC AMPLIFICATION; LEUKEMIA AB In this study we have tried to take advantage of the high genetic homology between conserved regions of human T-cell lymphotropic virus (HTLV) types I and II, hoping that a possible retrovirus in patients with cutaneous T-cell lymphoma (CTCL) would have regions with homology to types I/II. DNA was extracted from punch skin biopsies from 21 patients and subjected to the polymerase chain reaction (PCR), using primer sets designed to match conserved regions in the HTLV-I/II genome. The PCR products were subjected to agrose gel electrophoresis with subsequent Southern blotting and hybridization to an HTLV-I probe. No bands of exogenous origin were seen on the agarose gel or by hybridization. If a retrovirus is present in the skin in CTCL patients, it is either not related to HTLV-I/II, present at a copy number below the PCR detection limit, or has been cleared from the skin before the clinical symptoms appear. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RIGSHOSP,DEPT DERMATOL,DK-2100 COPENHAGEN,DENMARK. RP LISBY, G (reprint author), HERLEV HOSP,DEPT CLIN MICROBIOL,DK-2730 HERLEV,DENMARK. NR 14 TC 38 Z9 38 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 1992 VL 98 IS 4 BP 417 EP 420 DI 10.1111/1523-1747.ep12499842 PG 4 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600004 PM 1548426 ER PT J AU BOEHNCKE, WH TAKESHITA, T BERZOFSKY, JA GERMAIN, RN AF BOEHNCKE, WH TAKESHITA, T BERZOFSKY, JA GERMAIN, RN TI PEPTIDE BINDING-STUDIES DEMONSTRATE PROMISCUOUS RATHER THAN SELECTIVE CHARACTER OF MHC RESTRICTION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV ULM,DEPT DERMATOL,W-7900 ULM,GERMANY. 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 1992 VL 98 IS 4 BP 506 EP 506 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600033 ER PT J AU LI, L KRUSZEWSKI, FH PUNNONEN, K YUSPA, SH HENNINGS, H TUCKER, RW AF LI, L KRUSZEWSKI, FH PUNNONEN, K YUSPA, SH HENNINGS, H TUCKER, RW TI THE MECHANISM OF STRONTIUM INDUCED TERMINAL DIFFERENTIATION IN CULTURED MOUSE KERATINOCYTES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV HOSP,CTR ONCOL,BALTIMORE,MD 21205. 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 1992 VL 98 IS 4 BP 559 EP 559 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600315 ER PT J AU STEINERT, PM STEVEN, AC AF STEINERT, PM STEVEN, AC TI PROTEIN-COMPOSITION OF THE EPIDERMAL CORNIFIED CELL-ENVELOPE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,STRUCT BIOL RES LAB,BETHESDA,MD. NR 0 TC 2 Z9 2 U1 1 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 1992 VL 98 IS 4 BP 559 EP 559 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600314 ER PT J AU TENNENBAUM, T MROZ, A BROWN, LJ WILDNAUER, T DE LUCA, LM YUSPA, SH GORDON, JS AF TENNENBAUM, T MROZ, A BROWN, LJ WILDNAUER, T DE LUCA, LM YUSPA, SH GORDON, JS TI RETINOIC ACID INDUCES EARLY CHANGES IN THE DISTRIBUTION OF ALPHA-6-BETA-4 INTEGRIN AND KERATIN-13 EXPRESSION IN HAIRLESS MOUSE SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH, LCCTP, BETHESDA, MD 20892 USA. JOHNSON & JOHNSON CONSUMER PROD INC, SKILLMAN, NJ USA. 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 1992 VL 98 IS 4 BP 561 EP 561 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600325 ER PT J AU LEE, ES KATZ, SI JU, WD NECKERS, L AF LEE, ES KATZ, SI JU, WD NECKERS, L TI TRANSFORMING GROWTH FACTOR-ALPHA (TGF-ALPHA) IS AN AUTOCRINE GROWTH-FACTOR FOR HUMAN DERMAL FIBROBLASTS AND NIH/3T3 CELLS 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 1992 VL 98 IS 4 BP 563 EP 563 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600342 ER PT J AU AMAGAI, M KARPATI, S PRUSSICK, R KLAUSKOVTUN, V STANLEY, JR AF AMAGAI, M KARPATI, S PRUSSICK, R KLAUSKOVTUN, V STANLEY, JR TI AUTOANTIBODIES AGAINST THE CADHERIN-LIKE HOMOPHILIC BINDING REGION OF PEMPHIGUS-VULGARIS ANTIGEN (PVA) CAUSE ACANTHOLYSIS 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 1992 VL 98 IS 4 BP 566 EP 566 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600358 ER PT J AU URABE, K TSUKAMOTO, K KAMEYAMA, K HEARING, VJ AF URABE, K TSUKAMOTO, K KAMEYAMA, K HEARING, VJ TI THE TYROSINASE GENE FAMILY - INTERACTIONS OF MELANOGENIC PROTEINS TO REGULATE MELANOGENESIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 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 1992 VL 98 IS 4 BP 566 EP 566 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600360 ER PT J AU DECLUE, JE PAPAGEORGE, AG VASS, WC JOHNSON, MR LOWY, DR AF DECLUE, JE PAPAGEORGE, AG VASS, WC JOHNSON, MR LOWY, DR TI ABNORMAL REGULATION AND PHARMACOLOGICAL CORRECTION OF THE RAS ONCOGENE PROTEIN IN MALIGNANT SCHWANNOMAS FROM PATIENTS WITH VONRECKLINHAUSENS NEUROFIBROMATOSIS 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 1992 VL 98 IS 4 BP 567 EP 567 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600364 ER PT J AU LICHTI, U WEINBERG, WC GOODMAN, L LEDBETTER, S DOOLEY, T MORGAN, D YUSPA, SH AF LICHTI, U WEINBERG, WC GOODMAN, L LEDBETTER, S DOOLEY, T MORGAN, D YUSPA, SH TI IMMORTALIZED DERMAL PAPILLA CELLS SUPPORT HAIR-GROWTH IN A MINIMAL COMPONENT NUDE-MOUSE GRAFT MODEL SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. UPJOHN CO,CANC RES,KALAMAZOO,MI 49001. RI Weinberg, Wendy/A-8920-2009 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 1992 VL 98 IS 4 BP 567 EP 567 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600365 ER PT J AU KIM, IG MCBRIDE, OW WANG, M KIM, SY IDLER, WW STEINERT, PM AF KIM, IG MCBRIDE, OW WANG, M KIM, SY IDLER, WW STEINERT, PM TI STRUCTURE AND ORGANIZATION OF THE HUMAN TRANSGLUTAMINASE-1 (TGM-1) GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,BIOCHEM 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 1992 VL 98 IS 4 BP 569 EP 569 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600373 ER PT J AU KORGE, B GAN, SO YONEDA, K COMPTON, JG VOLZ, A STEINERT, PM ZIEGLER, A MISCHKE, D AF KORGE, B GAN, SO YONEDA, K COMPTON, JG VOLZ, A STEINERT, PM ZIEGLER, A MISCHKE, D TI PHYSICAL MAPPING OF THE EPIDERMAL DIFFERENTIATION MARKERS LORICRIN, PROFILAGGRIN AND INVOLUCRIN ON CHROMOSOME-1Q21 BY PULSED FIELD ELECTROPHORESIS 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 1992 VL 98 IS 4 BP 569 EP 569 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600377 ER PT J AU JU, WD VASS, WC TAYEB, N SCHILLER, JT LOWY, DR AF JU, WD VASS, WC TAYEB, N SCHILLER, JT LOWY, DR TI TGF-ALPHA ENHANCES MOTILITY AND INDUCES MORPHOLOGICAL-CHANGES IN KERATINOCYTES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,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 1992 VL 98 IS 4 BP 570 EP 570 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600380 ER PT J AU MAUVIEL, A REITAMO, S REMITZ, A CESKA, M BAGGIOLINI, M WALZ, A EVANS, CH UITTO, J AF MAUVIEL, A REITAMO, S REMITZ, A CESKA, M BAGGIOLINI, M WALZ, A EVANS, CH UITTO, J TI LEUKOREGULIN IS A POTENT INDUCER OF IL-8 GENE-EXPRESSION IN HUMAN SKIN FIBROBLASTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,DEPT DERMATOL,PHILADELPHIA,PA 19107. SANDOZ GMBH,A-1235 VIENNA,AUSTRIA. THEODOR KOCHER INST,BERN,SWITZERLAND. NCI,BIOL LAB,TUMOR BIOL SECT,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 1992 VL 98 IS 4 BP 571 EP 571 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600386 ER PT J AU ENK, AH KATZ, SI AF ENK, AH KATZ, SI TI IDENTIFICATION AND INDUCTION OF KERATINOCYTE-DERIVED INTERLEUKIN-10 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 1992 VL 98 IS 4 BP 578 EP 578 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600428 ER PT J AU KARPATI, S AMAGAI, M CEHRS, K KLAUSKOYTUN, V STANLEY, JR AF KARPATI, S AMAGAI, M CEHRS, K KLAUSKOYTUN, V STANLEY, JR TI IGG LOCALIZES TO THE CORE OF SPLIT DESMOSOMES IN BLISTERS INDUCED BY PEMPHIGUS-VULGARIS (PV) ANTIBODIES IN NEONATAL MICE 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 1992 VL 98 IS 4 BP 580 EP 580 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600441 ER PT J AU CHORZELSKI, TP STEFANATO, CM BEUTNER, E STANLEY, JR KORMAN, NJ OLSZEWSKA, M MACIEJOWSKA, E JABLONSKA, S AF CHORZELSKI, TP STEFANATO, CM BEUTNER, E STANLEY, JR KORMAN, NJ OLSZEWSKA, M MACIEJOWSKA, E JABLONSKA, S TI ERYTHEMA ANNULARE-LIKE ACANTHOLYTIC DERMATOSIS (EAAD) ASSOCIATED WITH EPIDERMAL SPECIFIC ANTIBODIES - A NEW ENTITY OR NONBULLOUS PEMPHIGUS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MED ACAD WARSAW,DEPT DERMATOL,PL-02032 WARSAW,POLAND. SUNY BUFFALO,DEPT DERMATOL,BUFFALO,NY 14260. 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 1992 VL 98 IS 4 BP 586 EP 586 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600476 ER PT J AU COHEN, PJ COHEN, PA ROSENBERG, SA KATZ, SI MULE, JJ AF COHEN, PJ COHEN, PA ROSENBERG, SA KATZ, SI MULE, JJ TI MURINE EPIDERMAL LANGERHANS CELLS (LC) AND SPLENIC DENDRITIC CELLS (DC) PROCESS AND PRESENT TUMOR-ANTIGENS TO PRIMED T-CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,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 1992 VL 98 IS 4 BP 594 EP 594 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600524 ER PT J AU DUGAN, EM LINTON, JT KATZ, SI AF DUGAN, EM LINTON, JT KATZ, SI TI GRAFT VERSUS HOST-DISEASE (GVHD) - CORRELATION OF IMMUNE AND HISTOLOGICAL EVENTS AND ATTEMPTED PREVENTION WITH PUVA-TREATED LYMPHOCYTES 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 1992 VL 98 IS 4 BP 594 EP 594 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600523 ER PT J AU UDEY, MC TANG, A AF UDEY, MC TANG, A TI DOSES OF UV-RADIATION THAT MODULATE ICAM-1 EXPRESSION AND INHIBIT ACCESSORY CELL-FUNCTION ARE CYTOTOXIC FOR MURINE LANGERHANS CELLS (LC) 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 1992 VL 98 IS 4 BP 594 EP 594 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600526 ER PT J AU ROCKEN, M URBAN, J SHEVACH, EM AF ROCKEN, M URBAN, J SHEVACH, EM TI CD4+ T-CELLS FROM ANIMALS TOLERIZED TO STAPHYLOCOCCAL ENTEROTOXIN-B(SEB) CAN ACT AS T-HELPER-2 (TH2) EFFECTOR-CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 USDA,BELTSVILLE,MD 20705. NIAID,LI,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 1992 VL 98 IS 4 BP 598 EP 598 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600551 ER PT J AU LEE, MM LAMBERT, WC ANDREWS, A KRAEMER, KH AF LEE, MM LAMBERT, WC ANDREWS, A KRAEMER, KH TI THE ROLE OF ULTRAVIOLET-RADIATION IN HUMAN-MELANOMA AND NONMELANOMA SKIN-CANCER - STUDIES OF XERODERMA-PIGMENTOSUM SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. HARVARD UNIV,DEPT DERMATOL,CAMBRIDGE,MA 02138. COLUMBIA UNIV,DEPT DERMATOL,NEW YORK,NY 10027. CMDNJ,DEPT DERMATOL,NEWARK,NJ. NR 0 TC 1 Z9 1 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 1992 VL 98 IS 4 BP 603 EP 603 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600582 ER PT J AU HULTSCH, T HOHMAN, RJ AF HULTSCH, T HOHMAN, RJ TI RAPAMYCIN INHIBITS IL-3 DEPENDENT PROLIFERATION OF MAST-CELLS AND OTHER HEMATOPOIETIC-CELLS - FK506 ANTAGONIZES THE EFFECT OF RAPAMYCIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,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 1992 VL 98 IS 4 BP 609 EP 609 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600614 ER PT J AU BERNSTEIN, EF HARISIADIS, L SALOMON, G NORTON, J TALBOT, T MITCHELL, JB AF BERNSTEIN, EF HARISIADIS, L SALOMON, G NORTON, J TALBOT, T MITCHELL, JB TI RADIATION-IMPAIRED MODELS OF WOUND-HEALING SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BIOMED ENGN & INSTRUMENTAT BRANCH,BETHESDA,MD 20892. NIH,SURG BRANCH,BETHESDA,MD 20892. NIH,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. HAHNEMANN UNIV,DIV DERMATOL,PHILADELPHIA,PA 19102. 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 1992 VL 98 IS 4 BP 625 EP 625 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600712 ER PT J AU LEE, SC KIM, LG MCBRIDE, OW COMPTON, JG OKEEFE, E STEINERT, PM AF LEE, SC KIM, LG MCBRIDE, OW COMPTON, JG OKEEFE, E STEINERT, PM TI THE HUMAN TRICHOHYALIN GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,BIOCHEM LAB,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT DERMATOL,CHAPEL HILL,NC 27514. 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 1992 VL 98 IS 4 BP 626 EP 626 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600719 ER PT J AU YONEDA, K KORGE, B MCBRIDE, OW STEINERT, PM AF YONEDA, K KORGE, B MCBRIDE, OW STEINERT, PM TI THE HUMAN LORICRIN GENE IS POLYMORPHIC SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,BIOCHEM 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 1992 VL 98 IS 4 BP 626 EP 626 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600716 ER PT J AU DLUGOSZ, AA YUSPA, SH AF DLUGOSZ, AA YUSPA, SH TI ACTIVATION OF PROTEIN-KINASE-C REGULATES KERATIN-1 AND KERATINOCYTE TRANSGLUTAMINASE MESSENGER-RNA IN OPPOSITE DIRECTIONS 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 1992 VL 98 IS 4 BP 627 EP 627 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600726 ER PT J AU RESZKA, K SALOPEK, TG JIMBOW, K CHIGNELL, CF AF RESZKA, K SALOPEK, TG JIMBOW, K CHIGNELL, CF TI PHOTOLYSIS OF PHEOMELANIN, ITS PRECURSOR 5-CYSTEINYLDOPA AND A EUMELANIN METABOLITE, 5-HYDROXY-6-METHOXYINDOLE-2-CARBOXYLIC ACID WITH UV-LIGHT ABOVE 300 NM - AN EPR AND SPIN TRAPPING STUDY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. UNIV ALBERTA,DIV DERMATOL CUT 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 1992 VL 98 IS 4 BP 657 EP 657 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600905 ER PT J AU ADELBERG, S PARRIS, CN KRAEMER, KH AF ADELBERG, S PARRIS, CN KRAEMER, KH TI MUTAGENESIS BY 295NM UV-B RADIATION OF A PLASMID VECTOR REPLICATED IN XERODERMA-PIGMENTOSUM CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,MOLEC CARCINOGENESIS 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 1992 VL 98 IS 4 BP 658 EP 658 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600907 ER PT J AU LEVY, DD GROOPMAN, JD LIM, SE SEIDMAN, MM KRAEMER, KH AF LEVY, DD GROOPMAN, JD LIM, SE SEIDMAN, MM KRAEMER, KH TI MUTAGENIC SPECTRUM OF AFLATOXIN-B1 EPOXIDE INDUCED DNA ADDUCTS IN A SHUTTLE VECTOR PLASMID FOLLOWING REPLICATION IN XERODERMA-PIGMENTOSUM AND DNA-REPAIR PROFICIENT HUMAN FIBROBLASTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. OTSUKA PHARMACEUT CO LTD,ROCKVILLE,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 1992 VL 98 IS 4 BP 661 EP 661 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600925 ER PT J AU LI, J WETZEL, MG OBRIEN, PJ AF LI, J WETZEL, MG OBRIEN, PJ TI TRANSPORT OF N-3 FATTY-ACIDS FROM THE INTESTINE TO THE RETINA IN RATS SO JOURNAL OF LIPID RESEARCH LA English DT Article DE ALBUMIN; CHYLOMICRONS; DOCOSAHEXAENOIC ACID; LINOLENIC ACID; LIPOPROTEIN; PHOTORECEPTOR; RETINAL DEBRIS; ROD OUTER SEGMENTS; VERY LOW DENSITY LIPOPROTEIN ID PERFORMANCE LIQUID-CHROMATOGRAPHY; DOCOSAHEXAENOIC ACID; BRAIN; LIPIDS; PHOSPHOLIPIDS; LIPOPROTEINS; METABOLISM; MEMBRANE; LIVER AB This study was undertaken to determine the mode of transport of the essential (n-3) fatty acids docosahexaenoic acid 22:6(n-3) and linolenic acid 18:3(n-3). Male weanling. Sprague-Dawley rats received a mixture of corn oil and [C-14]18:3(n-3) or [C-14]22:6(n-3) by gavage. At periods of 1 to 4 days after the injection, four rats per time point were killed and samples of blood were taken via heart puncture and the livers and retinas were collected. Blood lipoproteins and plasma proteins were separated by ultracentrifugation and analyzed by HPLC. Lipids were extracted and saponified and the fatty acids were converted to phenacyl esters for separation of individual fatty acids. After 1 and 2 h, radioactivity from 18:3(n-3) and 22:6(n-3) was observed primarily in the chylomicron/very low density lipoprotein fraction. By 4 h, radioactivity in the lipoprotein fraction was greatly decreased, with a small amount of radioactivity associated with albumin in the soluble protein fraction. After 24 h, the total amount of radioactivity associated with lipoprotein was further reduced, with more than half of the remaining label occurring in association with albumin and another unidentified protein. In the liver, 22:6(n-3) was concentrated in triacylglycerols (40.7%) and phospholipids (51.1%), with a maximum specific activity at 4 h. In the rod outer segments (ROS), the specific activity of [C-14]22:6(n-3) increased to a maximum at 24 h and maintained a high level even at 4 days. These data suggest that after injection, 18:3(n-3) and 22:6(n-3) are esterified to triglyceride and phospholipid by the intestinal absorptive cells and transported in chylomicrons to the liver. After conversion of 18:3(n-3) to 22:6(n-3) in the liver, the retina accumulates 22:6(n-3) which may be transported from the liver via albumin and another unidentified protein, and is retained by the rod outer segments. RP LI, J (reprint author), NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 37 TC 53 Z9 53 U1 0 U2 0 PU LIPID RESEARCH INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD APR PY 1992 VL 33 IS 4 BP 539 EP 548 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR224 UT WOS:A1992HR22400009 PM 1527477 ER PT J AU WEISS, GH KIEFER, JE FERRETTI, JA AF WEISS, GH KIEFER, JE FERRETTI, JA TI ACCURACY AND PRECISION IN THE ESTIMATION OF INTERNUCLEAR DISTANCES FOR STRUCTURE DETERMINATIONS SO JOURNAL OF MAGNETIC RESONANCE LA English DT Article ID SEQUENTIAL RESONANCE ASSIGNMENTS; NUCLEAR MAGNETIC-RESONANCE; MINIMIZATION; SPECTRA; ERRORS; ENERGY C1 NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. RP WEISS, GH (reprint author), NHLBI,PHYS SCI LAB,DIV COMP RES & TECHNOL,BETHESDA,MD 20892, USA. NR 8 TC 12 Z9 12 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 0022-2364 J9 J MAGN RESON JI J. Magn. Reson. PD APR PY 1992 VL 97 IS 2 BP 227 EP 234 DI 10.1016/0022-2364(92)90309-U PG 8 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA HL675 UT WOS:A1992HL67500001 ER PT J AU KAY, LE NICHOLSON, LK DELAGLIO, F BAX, A TORCHIA, DA AF KAY, LE NICHOLSON, LK DELAGLIO, F BAX, A TORCHIA, DA TI PULSE SEQUENCES FOR REMOVAL OF THE EFFECTS OF CROSS-CORRELATION BETWEEN DIPOLAR AND CHEMICAL-SHIFT ANISOTROPY RELAXATION MECHANISM ON THE MEASUREMENT OF HETERONUCLEAR T1 AND T2 VALUES IN PROTEINS SO JOURNAL OF MAGNETIC RESONANCE LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; NMR-SPECTROSCOPY; BACKBONE DYNAMICS; C-13; POLYPEPTIDE; ASSIGNMENT; SYSTEMS; TENSOR; TIMES; H-1 C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NR 34 TC 527 Z9 528 U1 3 U2 39 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-2364 J9 J MAGN RESON JI J. Magn. Reson. PD APR PY 1992 VL 97 IS 2 BP 359 EP 375 DI 10.1016/0022-2364(92)90320-7 PG 17 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA HL675 UT WOS:A1992HL67500012 ER PT J AU MOONEN, CTW VANGELDEREN, P VUISTER, GW VANZIJL, PCM AF MOONEN, CTW VANGELDEREN, P VUISTER, GW VANZIJL, PCM TI GRADIENT-ENHANCED EXCHANGE SPECTROSCOPY SO JOURNAL OF MAGNETIC RESONANCE LA English DT Note ID WATER-SUPPRESSION; NMR-SPECTROSCOPY C1 DELFT UNIV TECHNOL,DEPT APPL PHYS,DELFT,NETHERLANDS. NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. RP MOONEN, CTW (reprint author), NCRR,BEIP,INVIVO NMR RES CTR,BLDG 10,ROOM B1D-125,BETHESDA,MD 20892, USA. RI van Zijl, Peter/B-8680-2008; Moonen, Chrit/K-4434-2016 OI Moonen, Chrit/0000-0001-5593-3121 NR 9 TC 45 Z9 45 U1 1 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-2364 J9 J MAGN RESON JI J. Magn. Reson. PD APR PY 1992 VL 97 IS 2 BP 419 EP 425 DI 10.1016/0022-2364(92)90327-4 PG 7 WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Biochemistry & Molecular Biology; Physics; Spectroscopy GA HL675 UT WOS:A1992HL67500019 ER PT J AU SMOLEN, P KEIZER, J AF SMOLEN, P KEIZER, J TI SLOW VOLTAGE INACTIVATION OF CA2+ CURRENTS AND BURSTING MECHANISMS FOR THE MOUSE PANCREATIC BETA-CELL SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE BETA-CELL; BURSTING; CALCIUM INACTIVATION; VOLTAGE INACTIVATION; K-ATP CHANNEL; INSULIN SECRETION ID INDUCED ELECTRICAL-ACTIVITY; INSULIN-SECRETING CELLS; SENSITIVE K+ CHANNELS; B-CELLS; POTASSIUM CHANNEL; CALCIUM CURRENTS; GLUCOSE; CA-2+; OSCILLATIONS; MODEL AB Recent whole-cell electrophysiological data concerning the properties of the Ca2+ currents in mouse beta-cells are fitted by a two-current model of Ca2+ channel kinetics. When the beta-cell K+ currents are added to this model, only large modifications of the measured Ca2+ currents will reproduce the bursting pattern normally observed in mouse islets. However, when the measured Ca2+ currents are modified only slightly and used in conjunction with a K+ conductance that can be modulated dynamically by ATP concentration. reasonable bursting is obtained. Under these conditions it is the K-ATP conductance. rather than the slow voltage inactivation of the Ca2+ current, that determines the interburst interval. We find that this latter model can be reconciled with experiments that limit the possible periodic variation of the K-ATP conductance and with recent observations of intracellular Ca2+ bursting in islets. C1 UNIV CALIF DAVIS,INST THEORET DYNAM,DAVIS,CA 95616. UNIV CALIF DAVIS,DEPT CHEM,DAVIS,CA 95616. RP SMOLEN, P (reprint author), NIDDKD,MATH RES BRANCH,BETHESDA,MD 20892, USA. NR 31 TC 59 Z9 59 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD APR PY 1992 VL 127 IS 1 BP 9 EP 19 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA HR292 UT WOS:A1992HR29200002 PM 1328645 ER PT J AU FIEDLER, JL POLLARD, HB ROJAS, E AF FIEDLER, JL POLLARD, HB ROJAS, E TI QUANTITATIVE-ANALYSIS OF DEPOLARIZATION-INDUCED ATP RELEASE FROM MOUSE-BRAIN SYNAPTOSOMES - EXTERNAL CALCIUM DEPENDENT AND INDEPENDENT PROCESSES SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE ATP SECRETION; SYNAPTOSOMES; NERVE ENDINGS; CALCIUM INDEPENDENT; CALCIUM DEPENDENT ID 1,4,5-TRISPHOSPHATE-INDUCED CA-2+ RELEASE; ADENOSINE-TRIPHOSPHATASE-ACTIVITY; MEDULLARY CHROMAFFIN CELLS; TORPEDO ELECTRIC ORGAN; NERVE-TERMINALS; CHOLINERGIC SYNAPTOSOMES; INOSITOL 1,4,5-TRISPHOSPHATE; SARCOPLASMIC-RETICULUM; ACETYLCHOLINE-RELEASE; CRUSTACEAN MUSCLE AB We and others have shown previously that ATP is secreted from mouse brain synaptosomes following depolarization of the membrane by high [K+]O and the time course can be monitored accurately by measuring the light emitted from luciferin-luciferase included in the reaction medium. In the present work we have evaluated the relative importance of [Ca2+]O and membrane potential on the ATP secretion process by modelling the time course of ATP release under different conditions. After correction of the records for destruction of released ATP by synaptosomal ecto-ATPase activity, we found that ATP secretion occurs by an apparent first order process. We also established that, in addition to the classical [Ca2+]O-dependent mode, ATP secretion also occurred in the absence of extracellular calcium ([Ca2+]O < 1-mu-m). Upon lowering the extracellular Ca2+ concentration, both the rate and the extent of ATP secretion decreased. To assess the contribution of membrane potential to the release rate we measured ATP secretion at membrane potentials determined by extracellular [K+]O, (or [Rb+]O) as defined by the distribution of the carbocyanine dye, diSC3(5). Rate constants computed from measured secretion curves revealed that this parameter was essentially independent of membrane potential in the absence of [Ca2+]O. Noise analysis of the light signal showed that the variance increased upon stimulation by high [K+]O, suggesting that both modes of secretion are quantal. Thus, we conclude that the rate of ATP secretion from nerve terminals depends upon Ca2+ entry but not on membrane potential, per se. RP FIEDLER, JL (reprint author), NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. RI Fiedler, Jenny/I-5617-2016 NR 36 TC 7 Z9 7 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD APR PY 1992 VL 127 IS 1 BP 21 EP 33 PG 13 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA HR292 UT WOS:A1992HR29200003 PM 1357181 ER PT J AU HUYNEN, MA KONINGS, DAM HOGEWEG, P AF HUYNEN, MA KONINGS, DAM HOGEWEG, P TI EQUAL G-CONTENT AND C-CONTENT IN HISTONE GENES INDICATE SELECTION PRESSURES ON MESSENGER-RNA SECONDARY STRUCTURE SO JOURNAL OF MOLECULAR EVOLUTION LA English DT Article DE HISTONE GENES; CODON USAGE; NUCLEOTIDE FREQUENCIES; MESSENGER RNA SECONDARY STRUCTURE ID CODON USAGE PATTERN; UNTRANSLATED REGION; ESCHERICHIA-COLI; DNA-REPAIR; H-4 GENES; GENOME; SEQUENCES; TRANSCRIPTION; DEGRADATION; EVOLUTION AB Protein-specific versus taxon-specific patterns of nucleotide frequencies were studied in histone genes. The third positions of codons have a (well-known) taxon-specific G + C level and a histone type-specific G/C ratio. This ratio counterbalances the G/C ratio in the first and second positions so that the overall G and C levels in the coding region become approximately equal. The compensation of the G/C ratio indicates a selection pressure at the mRNA level rather than a selection pressure or mutation bias at the DNA level or a selection pressure on codon usage. The structure of histone mRNAs is compatible with the hypothesis that the G/C compensation is due to selection pressures on mRNA secondary structure. Nevertheless, no specific motifs seem to have been selected, and the free energy of the secondary structures is only slightly lower than that expected on the basis of nucleotide frequencies. C1 NCI,FCRDC,MATH BIOL LAB,FREDERICK,MD 21701. RP HUYNEN, MA (reprint author), UNIV UTRECHT,BIOINFORMAT GRP,PADUALAAN 8,3584 CH UTRECHT,NETHERLANDS. RI Hogeweg, paulien/D-1242-2011; Huynen, Martijn/A-1530-2014 NR 52 TC 25 Z9 27 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2844 J9 J MOL EVOL JI J. Mol. Evol. PD APR PY 1992 VL 34 IS 4 BP 280 EP 291 DI 10.1007/BF00160235 PG 12 WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity GA HL389 UT WOS:A1992HL38900003 PM 1569583 ER PT J AU CHMURNY, GN HILTON, BD BROBST, S LOOK, SA WITHERUP, KM BEUTLER, JA AF CHMURNY, GN HILTON, BD BROBST, S LOOK, SA WITHERUP, KM BEUTLER, JA TI H-1-NMR AND C-13-NMR ASSIGNMENTS FOR TAXOL, 7-EPI-TAXOL, AND CEPHALOMANNINE SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID TAXUS-BREVIFOLIA; SPECTROSCOPY; TAXANES AB The H-1- and C-13-nmr spectra of taxol [1], 7-epi-taxol [2], and cephalomannine [3] were assigned using modern 1D and 2D nmr methods. Preliminary conformational information was obtained by nOe spectroscopy. RP CHMURNY, GN (reprint author), NCI,FREDERICK CANC RES FACIL,CHEM SYNTH & ANAL LAB,DYNCORP INC,PRI,POB B,FREDERICK,MD 21702, USA. RI Beutler, John/B-1141-2009 OI Beutler, John/0000-0002-4646-1924 FU NCI NIH HHS [N01-CO-74102] NR 8 TC 98 Z9 100 U1 4 U2 10 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD APR PY 1992 VL 55 IS 4 BP 414 EP 423 DI 10.1021/np50082a002 PG 10 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA HM447 UT WOS:A1992HM44700002 PM 1355110 ER PT J AU WHEELER, NC JECH, K MASTERS, S BROBST, SW ALVARADO, AB HOOVER, AJ SNADER, KM AF WHEELER, NC JECH, K MASTERS, S BROBST, SW ALVARADO, AB HOOVER, AJ SNADER, KM TI EFFECTS OF GENETIC, EPIGENETIC, AND ENVIRONMENTAL-FACTORS ON TAXOL CONTENT IN TAXUS-BREVIFOLIA AND RELATED SPECIES SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID CHROMATOGRAPHIC-SEPARATION; PINUS-CONTORTA; AGENT AB The demand for taxol, a promising cancer chemotherapeutic agent, far exceeds supply. Presently, taxol is derived from the bark of the Pacific yew, Taxus brevifolia, a small, slow-growing evergreen tree native to the northwestern United States. Knowledge of the distribution and magnitude of genetic and non-genetic sources of variation in taxol content in the genus Taxus is necessary if supply issues are to be met through plant harvesting. Analytical determinations of taxol, cephalomannine, and baccatin III in more than 200 trees representing several populations of T. brevifolia and other yew taxa indicate that (1) significant variation in taxane content exists among and within populations and species, (2) taxol levels exceeding those reported for T. brevifolia bark were found in shoots of individual trees from most taxa studied, and (3) the season in which samples are collected and handling procedures can influence taxane content. C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21702. NCI,DCT,DTP,NAT PROD BRANCH,FREDERICK,MD 21702. RP WHEELER, NC (reprint author), WEYERHAEUSER RES CTR,505 N PEARL ST,CENTRALIA,WA 98531, USA. FU NCI NIH HHS [N01-CO-74102] NR 18 TC 107 Z9 115 U1 0 U2 13 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD APR PY 1992 VL 55 IS 4 BP 432 EP 440 DI 10.1021/np50082a005 PG 9 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA HM447 UT WOS:A1992HM44700005 PM 1355111 ER PT J AU SMITH, MC MOLLICA, RF AF SMITH, MC MOLLICA, RF TI ISSUES OF MEMORY IN THE DIAGNOSTIC INTERVIEW SCHEDULE - COMMENTARY SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Editorial Material ID TRAUMATIC STRESS DISORDER; GENERAL-POPULATION C1 HARVARD UNIV,SCH PUBL HLTH,PROGRAM REFUGEE TRAUMA,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,NIMH,TRAINING PROGRAM PSYCHIAT EPIDEMIOL,BOSTON,MA 02115. ST ELIZABETH HOSP,INDOCHINESE PSYCHIAT CLIN,BRIGHTON,MA 02135. NR 11 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD APR PY 1992 VL 180 IS 4 BP 225 EP 226 DI 10.1097/00005053-199204000-00003 PG 2 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA HN906 UT WOS:A1992HN90600003 ER PT J AU FREED, WJ WILLINGHAM, G HEIM, R AF FREED, WJ WILLINGHAM, G HEIM, R TI EFFECTS OF ADRENAL-MEDULLA AND SCIATIC-NERVE COGRAFTS IN RATS WITH UNILATERAL SUBSTANTIA-NIGRA LESIONS SO JOURNAL OF NEURAL TRANSPLANTATION & PLASTICITY LA English DT Article DE PARKINSONS DISEASE; ADRENAL MEDULLA; GRAFTS; BRAIN GRAFTS; TRANSPLANTATION; SUBSTANTIA-NIGRA; CHROMAFFIN CELLS ID CHROMAFFIN CELLS; PERIPHERAL-NERVE; GROWTH-FACTOR; DENERVATED STRIATUM; ROTATIONAL BEHAVIOR; PARKINSONS-DISEASE; CAUDATE-NUCLEUS; FOLLOW-UP; COGRAFTS; ENHANCE AB Major limitations of adrenal medulla transplantation in animal models of Parkinson's disease have been the relatively small behavioral effects and the poor or inconsistent graft survival. Transplantation of fragments of sural nerve in combination with adrenal medulla has been reported to increase the survival of chromaffin cells in adrenal medulla grafts in primates. In the present study, the possibility was tested that peripheral nerve co-grafts would increase the functional effects of adrenal medulla grafts in a 6-hydroxydopamine-lesioned rat model. Animals received unilateral substantia nigra lesions, and subsequently received intraventricular grafts of adrenal medulla, sciatic nerve, adrenal medulla plus sciatic nerve, or sham grafts consisting of medium only. Functional effects of the grafts were tested using apomorphine-induced rotational behavior. The sciatic nerve co-grafts did not increase the survival of TH-immunoreactive chromaffin cells. The co-grafting treatment also did not augment the overall effect of adrenal medulla grafts on rotational behavior. In the animals with substantial numbers of surviving chromaffin cells, however, the animals with sciatic nerve co-grafts showed greater decreases in rotational behavior as compared to the animals with adrenal medulla grafts alone, even though the number of surviving cells was not increased. C1 USN,NATL NAVAL MED CTR,DEPT NEUROSURG,BETHESDA,MD 20889. RP FREED, WJ (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032, USA. NR 38 TC 8 Z9 8 U1 0 U2 0 PU FREUND PUBLISHING HOUSE PI LONDON PA STE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA SN 0792-8483 J9 J NEURAL TRANSP PLAS JI J. Neural Transplant. Plast. PD APR-SEP PY 1992 VL 3 IS 2-3 BP 159 EP 167 PG 9 WC Neurosciences; Transplantation SC Neurosciences & Neurology; Transplantation GA JF330 UT WOS:A1992JF33000010 PM 1355367 ER PT J AU MCMILLIAN, MK TUOMINEN, RK HUDSON, PM SUH, HH HONG, JS AF MCMILLIAN, MK TUOMINEN, RK HUDSON, PM SUH, HH HONG, JS TI ANGIOTENSIN-II RECEPTORS ARE COUPLED TO OMEGA-CONOTOXIN-SENSITIVE CALCIUM INFLUX IN BOVINE ADRENAL-MEDULLARY CHROMAFFIN CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE ANGIOTENSIN-II; CALCIUM INFLUX; OMEGA-CONOTOXIN GVIA; BOVINE ADRENAL MEDULLARY CHROMAFFIN CELLS ID CYTOSOLIC CA-2+; INOSITOL PHOSPHATES; CHANNELS; RESPONSES; IDENTIFICATION; BRADYKININ; SECRETION; CULTURES; MOBILIZATION; PURIFICATION AB The contribution of an omega-conotoxin GVIA (omega-Cgtx)-sensitive Ca2+ influx pathway to the effects of angiotensin II (AII) receptor activation was examined in bovine adrenal medullary (BAM) cells. Pretreatment of BAM cells with 10(-6) M omega-Cgtx blocked stimulation of exocytosis by the degradation-resistant analogue, sarcosine1-angiotensin II (S1-AII). In contrast, omega-Cgtx had no effect on basal secretion, nor did it inhibit [H-3]norepinephrine and [P-32]ATP release in response to bradykinin, another phospholipase C-linked receptor agonist. Similarly, omega-Cgtx pretreatment inhibited the stimulation of Ca-45(2+) uptake by S1-AII, but did not affect the response to bradykinin. This selective inhibition did not appear to be due to blockade of AII receptors by omega-Cgtx, as the accumulation of H-3-labeled inositol phosphates in response to S1-AII was not inhibited. The peak S1-AII-stimulated increase in the intracellular free Ca2+ concentration (Ca(i)) in fura 2-loaded BAM cells also was not significantly reduced by omega-Cgtx (or by stimulating in nominally Ca2+-free buffer), indicating that this response is dependent on intracellular Ca2+ pools. However, a small omega-Cgtx-sensitive Ca(i) response was detected after depletion of intracellular Ca2+ pools with ionomycin. This study shows that AII receptors, but not bradykinin receptors, are linked to an omega-Cgtx-sensitive Ca2+ influx pathway in BAM cells. RP MCMILLIAN, MK (reprint author), NIEHS,NEUROPHARMACOL SECT,MD14-06,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 37 TC 23 Z9 23 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 1992 VL 58 IS 4 BP 1285 EP 1291 DI 10.1111/j.1471-4159.1992.tb11340.x PG 7 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HK061 UT WOS:A1992HK06100013 PM 1548465 ER PT J AU MCMILLIAN, MK HE, XP HONG, JS PENNYPACKER, KR AF MCMILLIAN, MK HE, XP HONG, JS PENNYPACKER, KR TI DOPAMINE STIMULATES [H-3] PHORBOL 12,13-DIBUTYRATE BINDING IN CULTURED STRIATAL CELLS SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE DOPAMINE; [H-3]PHORBOL 12,13-DIBUTYRATE; STRIATAL CELLS; NOREPINEPHRINE; RAT ID RECEPTOR SUBTYPES; RAT STRIATUM; EXPRESSION; D1; ENKEPHALIN; DYNORPHIN; INCREASES; NEURONS; AGONIST; BRAIN AB The effect of dopamine (DA) on the binding of [H-3]phorbol 12,13-dibutyrate ([H-3]PdBu) in cultured rat striatal cells was examined. DA maximally increased specific [H-3]PdBu binding by 70 +/- 10%, an increase comparable to that observed with norepinephrine (NE). This finding suggests that DA activates protein kinase C in cultured striatal cells, because increases in [H-3]PdBu binding reflect translocation of protein kinase C. Half-maximal stimulation was observed with 10(-6) M DA. The peak response was observed at 2-3 min after addition of 10(-4) M DA, but [H-3]PdBu binding was still increased above basal at 30 min. DA was not acting via an adrenergic receptor. Prazosin (10(-6) M) blocked the response to NE, suggesting mediation by an alpha-1-adrenergic receptor, but had little effect on the response to DA. Conversely, the D1 receptor antagonist SCH-23390 (10(-6) M) blocked the response to DA, but only partially inhibited the response to NE. Morphine (10(-6) M) inhibited the response to DA by 46 +/- 14%, but did not affect significantly the response to NE. The DA effect on [H-3]PdBu binding is apparently independent of the increase in cyclic AMP seen on D1 receptor activation. Forskolin, apomorphine, and the D1 agonist SKF-38393 all increased cyclic AMP in striatal cells, but were less effective than DA in stimulating [H-3]PdBu binding. The D2 agonist quinpirole was ineffective in stimulating either cyclic AMP or [H-3]PdBu binding. RP MCMILLIAN, MK (reprint author), NIEHS,NEUROPHARMACOL SECT,MD14-06,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Pennypacker, Keith/I-5092-2012 NR 20 TC 16 Z9 16 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 1992 VL 58 IS 4 BP 1308 EP 1312 DI 10.1111/j.1471-4159.1992.tb11343.x PG 5 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HK061 UT WOS:A1992HK06100016 PM 1312574 ER PT J AU SMITH, QR NAGURA, H TAKADA, Y DUNCAN, MW AF SMITH, QR NAGURA, H TAKADA, Y DUNCAN, MW TI FACILITATED TRANSPORT OF THE NEUROTOXIN, BETA-N-METHYLAMINO-L-ALANINE, ACROSS THE BLOOD-BRAIN-BARRIER SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE NEURODEGENERATIVE DISEASE; EXCITATORY AMINO ACID; AMYOTROPHIC LATERAL SCLEROSIS; PARKINSONS DISEASE; BLOOD-BRAIN BARRIER; TRANSPORT ID AMYOTROPHIC LATERAL SCLEROSIS; AMINO-ACID TRANSPORT; MOTOR NEURON DISEASE; PARKINSONISM-DEMENTIA; CEREBROVASCULAR TRANSPORT; PARTITION-COEFFICIENTS; PERFUSION TECHNIQUE; CORTICAL-NEURONS; CYCAD USE; GUAM AB Beta-N-Methylamino-L-alanine (BMAA) is a neurotoxic plant amino acid that has been implicated in the pathogenesis of the high incidence amyotrophic lateral sclerosis and related parkinsonism dementia of the western Pacific. Previous studies have demonstrated that BMAA is taken up into brain following intravenous or oral administration. To examine the kinetics and mechanism of brain transfer, BMAA influx across the blood-brain barrier was measured in rats using an in situ brain perfusion technique. BMAA influx was found to be saturable with a maximal transfer rate (V(max)) of 1.6 +/- 0.3 x 10(-3) mu-mol/s/g and a half-saturation constant (K(m)) of 2.9 +/- 0.7 mM based on total perfusate BMAA concentration. Uptake was sodium independent and inhibitable by excess L-leucine, but not by L-lysine, L-glutamate, or methylaminoisobutyric acid, indicative of transfer by the cerebrovascular large neutral amino acid carrier. L-BMAA competitively reduced brain influx of L-[C-14]leucine, as expected for cross-inhibition. The results demonstrate that BMAA is taken up into brain by the large neutral amino acid carrier of the blood-brain barrier and suggest that uptake may be sensitive to the same factors that affect neutral amino acid transport, such as diet, metabolism, disease, and age. C1 NINCDS,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892. RP SMITH, QR (reprint author), NIA,NEUROCHEM & BRAIN TRANSPORT SECT,NEUROSCI LAB,BLDG 10,ROOM 6C-103,BETHESDA,MD 20892, USA. NR 46 TC 47 Z9 50 U1 0 U2 5 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 1992 VL 58 IS 4 BP 1330 EP 1337 DI 10.1111/j.1471-4159.1992.tb11346.x PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HK061 UT WOS:A1992HK06100019 PM 1548467 ER PT J AU HUNTER, C WENTHOLD, RJ AF HUNTER, C WENTHOLD, RJ TI SOLUBILIZATION AND PURIFICATION OF AN ALPHA-AMINO-3-HYDROXY-5-METHYLISOXAZOLE-4-PROPIONIC ACID BINDING-PROTEIN FROM BOVINE BRAIN SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE EXCITATORY AMINO ACIDS; ALPHA-AMINO-3-HYDROXY-5-METHYLISOXAZOLE-4-PROPIONIC ACID (AMPA) RECEPTOR; QUISQUALATE RECEPTOR; DETERGENT SOLUBILIZATION; BOVINE CORTEX ID RAT-BRAIN; GLUTAMATE RECEPTOR; QUANTITATIVE AUTORADIOGRAPHY; SYNAPTIC-MEMBRANES; NERVOUS-SYSTEM; SITES; LOCALIZATION; EXPRESSION; CEREBELLUM; IDENTIFICATION AB alpha-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) is a selective ligand for an excitatory amino acid receptor subtype in mammalian brain. We have solubilized an AMPA binding protein from bovine brain membranes with 1% Triton X-100 in 0.5 M phosphate buffer and 20% glycerol at 37-degrees-C and purified the stable binding sites using a series of chromatographic steps. Scatchard analysis of the purified preparation showed a curvilinear plot with dissociation constants of 10.6 and 323 nM and B(max) values of 670 and 1,073 pmol/mg of protein for the high- and low-affinity sites, respectively. Inhibition constants for several excitatory amino acid analogues were similar to those obtained for other membrane and solubilized preparations. Gel filtration of the soluble AMPA binding protein showed a single peak of [H-3]AMPA binding activity at M(r) approximately 500,000. With sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the purified AMPA binding protein showed a single major band at M(r) = 110,000. Previously, we have shown that a monoclonal antibody (KAR-B1) against a frog brain kainate binding protein selectively recognizes an unknown protein in mammalian brain migrating at M(r) approximately 100,000. We now show that this antibody recognizes the major component of the purified AMPA binding protein, supporting a structural similarity between the frog brain kainate binding protein and the mammalian AMPA binding protein. RP HUNTER, C (reprint author), NIDOCD, NEUROTRANSMITTER RECEPTOR BIOL, NEUROCHEM LAB, BLDG 36, ROOM 5D08, BETHESDA, MD 20892 USA. NR 40 TC 20 Z9 20 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 1992 VL 58 IS 4 BP 1379 EP 1385 DI 10.1111/j.1471-4159.1992.tb11353.x PG 7 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HK061 UT WOS:A1992HK06100026 PM 1312575 ER PT J AU MUNOZ, DP WURTZ, RH AF MUNOZ, DP WURTZ, RH TI ROLE OF THE ROSTRAL SUPERIOR COLLICULUS IN ACTIVE VISUAL FIXATION AND EXECUTION OF EXPRESS SACCADES SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Note ID FRONTAL EYE FIELDS; REACTION-TIMES; RHESUS-MONKEY; NEURONS; MOVEMENTS; LOCALIZATION; STIMULATION; RESPONSES; TARGETS; SYSTEM AB 1. In the rostral pole of the monkey superior colliculus (SC) a subset of neurons (fixation cells) discharge tonically when a monkey actively fixates a target spot and pause during the execution of saccadic eye movements. 2. To test whether these fixation cells are necessary for the control of visual fixation and saccade suppression, we artificially inhibited them with a local injection of muscimol, an agonist of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). After injection of muscimol into the rostral pole of one SC, the monkey was less able to suppress the initiation of saccades. Many unwanted visually guided saccades were initiated < 100 ms after onset of a peripheral visual stimulus and therefore fell into the range of express saccades. 3. We propose that fixation cells in the rostral SC form part of a fixation system that facilitates active visual fixation and suppresses the initiation of unwanted saccadic eye movements. Express saccades can only occur when activity in this fixation system is reduced. C1 NEI,SENSORIMOTOR RES LAB,BLDG 10,ROOM 10C101,BETHESDA,MD 20892. NR 22 TC 211 Z9 213 U1 3 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 1992 VL 67 IS 4 BP 1000 EP 1002 PG 3 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA HQ250 UT WOS:A1992HQ25000018 PM 1588382 ER PT J AU DUNCAN, MW MARINI, AM WATTERS, R KOPIN, IJ MARKEY, SP AF DUNCAN, MW MARINI, AM WATTERS, R KOPIN, IJ MARKEY, SP TI ZINC, A NEUROTOXIN TO CULTURED NEURONS, CONTAMINATES CYCAD FLOUR PREPARED BY TRADITIONAL GUAMANIAN METHODS SO JOURNAL OF NEUROSCIENCE LA English DT Article ID AMYOTROPHIC LATERAL SCLEROSIS; MESENCEPHALIC DOPAMINERGIC-NEURONS; PARKINSONISM-DEMENTIA; UNLIKELY CAUSE; ACID BMAA; DISEASE; GUAM; CELLS; GLUTAMATE; RECEPTOR AB We have used cultured ventral mesencephalic and cerebellar granule cells to test the toxicity of extracts of cycad seeds (genus Cycas) and cycad-derived flours traditionally prepared in Guam. There was no significant difference in the toxicity of extracts prepared from the female gametophyte tissue of C. circinalis, C. revoluta, and C. media, common wheat flour, and 13 of 17 cycad flour samples. However, extracts prepared from 4 of 17 Guamanian flour samples exhibited marked dose-dependent neurotoxicity to mesencephalic and granule cell cultures. There was no correlation between toxicity and 2-amino-3-(methylamino)-propanoic acid (BMAA) content, and the concentration of BMAA in the medium arising from these extracts was far below that required to be neurotoxic. Toxicity of extracts was not blocked by the NMDA receptor antagonist MK-801 or the non-NMDA receptor antagonist 6-cyano-7-dinitroquinoxaline-2,3-dione, indicating that toxicity was not mediated by excitatory amino acid receptors. Analysis of the four toxic processed flour samples indicated high zinc content. Zinc produced a concentration-dependent neurotoxic response in mesencephalic and granule cell cultures that paralleled the calculated concentrations of zinc in the cultures derived from the four toxic flour samples. When sliced C. circinalis gametophyte tissue was "processed" in our laboratory by soaking in a galvanized container, there was a time-dependent increase in zinc content. C1 NINCDS,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892. NATL INST STANDARDS & TECHNOL,GAITHERSBURG,MD 20899. NIMH,ANALYT BIOCHEM SECT,BETHESDA,MD 20892. NR 36 TC 59 Z9 59 U1 0 U2 3 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1992 VL 12 IS 4 BP 1523 EP 1537 PG 15 WC Neurosciences SC Neurosciences & Neurology GA HM363 UT WOS:A1992HM36300030 PM 1556606 ER PT J AU NIKODIJEVIC, B GUROFF, G AF NIKODIJEVIC, B GUROFF, G TI NERVE GROWTH FACTOR-STIMULATED CALCIUM-UPTAKE INTO PC12 CELLS - UNIQUENESS OF THE CHANNEL AND EVIDENCE FOR PHOSPHORYLATION SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE RADIOACTIVE CALCIUM; BK-8644 ID PHEOCHROMOCYTOMA CELLS; RAT PHEOCHROMOCYTOMA; CHROMAFFIN CELLS; FACTOR INCREASES; FIBER OUTGROWTH; LINE; NEURONS; RESPOND; RELEASE AB Nerve growth factor stimulates.the uptake of radio-active calcium into PC12 cells. This stimulation is inhibited by low concentrations of dideoxyforskolin or staurosporine, and by high concentrations of nifedipine or cadmium. On the other hand, neither dideoxyforskolin nor staurosporine inhibited the stimulation of calcium uptake caused by BK-8644 or adenosine triphosphate (ATP). Nickel inhibited only the effect of ATP on calcium uptake, and actually stimulated the effects of either BK-8644 or nerve growth factor. Down-regulation of L-calcium channels by BK-8644 blocked the subsequent stimulation of calcium uptake by this agent, but not the stimulation by nerve growth factor. Conversely, pre-treatment of the cells with nerve growth factor inhibited the subsequent stimulation of calcium uptake by nerve growth factor, but not the stimulation by BK-8644. The effects of BK-8644 and nerve growth factor on calcium uptake were additive, as were the effects of nerve growth factor and ATP. Phosphatase 2A inhibited the effect of nerve growth factor on calcium uptake, but did not influence the action of BK-8644. On the other hand, calcineurin inhibited the effect of BK-8644 on calcium uptake, but potentiated the action of nerve growth factor. Calmidazolium or fluphenazine also inhibited the effect of nerve growth factor on calcium uptake, but okadaic acid stimulated it. A comparison of the effects of these inhibitors on the actions of various calcium channel agonists shows that the channels on which the action of nerve growth factor is exerted are different than either the L-type calcium channels or the ATP-activated calcium channels. These data also indicate that the action of nerve growth factor is mediated by phosphorylation of some component of the nerve growth factor-sensitive calcium channel. C1 NICHHD,GROWTH FACTORS SECT,BETHESDA,MD 20892. NR 31 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 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR PY 1992 VL 31 IS 4 BP 591 EP 599 DI 10.1002/jnr.490310402 PG 9 WC Neurosciences SC Neurosciences & Neurology GA HM080 UT WOS:A1992HM08000001 PM 1374475 ER PT J AU POWERS, WF CLEMENS, J AF POWERS, WF CLEMENS, J TI RISK-FACTORS FOR BRONCHOPULMONARY DYSPLASIA SO JOURNAL OF PEDIATRICS LA English DT Letter RP POWERS, WF (reprint author), NICHHD, DIV EPIDEMIOL STAT & PREVENT RES, EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD APR PY 1992 VL 120 IS 4 BP 667 EP 667 DI 10.1016/S0022-3476(05)82520-X PN 1 PG 1 WC Pediatrics SC Pediatrics GA HN861 UT WOS:A1992HN86100047 PM 1552420 ER PT J AU PIZZO, PA AF PIZZO, PA TI MANAGEMENT OF THE FEBRILE PATIENT WITH CANCER AND NEUTROPENIA - REPLY SO JOURNAL OF PEDIATRICS LA English DT Letter RP PIZZO, PA (reprint author), NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD APR PY 1992 VL 120 IS 4 BP 669 EP 670 DI 10.1016/S0022-3476(05)82525-9 PN 1 PG 2 WC Pediatrics SC Pediatrics GA HN861 UT WOS:A1992HN86100052 ER PT J AU AZORLOSA, JL HEISHMAN, SJ STITZER, ML MAHAFFEY, JM AF AZORLOSA, JL HEISHMAN, SJ STITZER, ML MAHAFFEY, JM TI MARIJUANA SMOKING - EFFECT OF VARYING DELTA-9-TETRAHYDROCANNABINOL CONTENT AND NUMBER OF PUFFS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID TETRAHYDROCANNABINOL CONTENT; PERFORMANCE; PROFILES; BEHAVIOR; CANNABIS; ALCOHOL; HUMANS; USERS AB The purpose of this study was to determine marijuana dose-effects on subjective and performance measures over a wider dosage range than previously reported using technology which allowed for specification of both the volume and DELTA(9)-tetrahydrocannabinol (THC) content of smoke delivered, and to relate these effects to plasma THC levels. Seven male community volunteers, who were moderate users of marijuana, smoked 4, 10 or 25 puffs from cigarettes containing either 1.75 or 3.55% THC on 6 separate days. Postsmoking plasma THC levels were systematically related to both number of puffs and cigarette THC content. Maximal THC levels occurred immediately after smoking and ranged from 57 to 268 ng/ml. These plasma levels provided a measure of systemic delivery when a known volume and THC content of marijuana smoke was inhaled. Orderly dose-related increases were also observed for heart rate, expired air carbon monoxide and subjective report of drug effects. The 25-puff, 3.55%-THC condition produced greater plasma THC levels than previously reported and reliably impaired performance on a battery of psychomotor and cognitive tasks with substantial individual differences noted in the degree of performance impairment. Puff number/THC content combinations producing comparable plasma THC levels resulted in similar subjective effects and performance impairment. This study provided a comprehensive assessment of the pharmacological effects of smoked marijuana over a wider and more precisely controlled dosage range than has been accomplished previously. The study showed that subjective measures were more sensitive to marijuana effects than were performance measures at mean plasma THC levels of 170 ng/ml or lower and that large individual differences in extent of performance impairment were apparent at higher plasma THC levels. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21205. NIDA,ADDICT RES CTR,CLIN PHARMACOL BRANCH,BALTIMORE,MD. FU NIDA NIH HHS [DA-07209, DA-05880] NR 31 TC 71 Z9 74 U1 1 U2 3 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 1992 VL 261 IS 1 BP 114 EP 122 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HN733 UT WOS:A1992HN73300016 PM 1313866 ER PT J AU TAKADA, K BARRETT, JE ALLEN, MS COOK, JM KATZ, JL AF TAKADA, K BARRETT, JE ALLEN, MS COOK, JM KATZ, JL TI PUNISHMENT OF SCHEDULE-CONTROLLED BEHAVIOR WITH BETA-CARBOLINE INJECTIONS - ANTAGONISM AND COMPARISONS WITH OTHER COMPOUNDS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID ACID ETHYL-ESTER; SQUIRREL-MONKEYS; INVERSE AGONIST; BENZODIAZEPINE RECEPTORS; CHLORDIAZEPOXIDE; SUPPRESSION; RO-15-1788; ETHANOL; COCAINE; RATS AB Squirrel monkeys were trained to press a key under a multiple schedule of food presentation. In the presence of either green or red stimulus lights, the 30th response produced a food pellet (fixed-ratio schedule). In the presence of the red stimulus lights (punishment component), the first response of each fixed-ratio produced either an i.v. injection of histamine [30.0-100.0-mu-g/kg/injection (inj)] or saline, accompanied by a 200-msec presentation of amber stimulus lights. Sessions in which histamine was injected alternated with sessions in which saline was injected. Another group of subjects was studied under identical schedule conditions except that electric shock was scheduled with the 200-msec stimulus light. During alternate sessions, electric shock at a high or low intensity with the stimulus, or the stimulus alone was scheduled. When performances stabilized, histamine or high intensity electric shock selectively suppressed responding in the punishment component; saline, low intensity electric shock or the stimulus light alone had no effects. Subsequently, different doses of histamine, l-nicotine, cocaine or beta-carboline-3-carboxylic acid ethyl ester (beta-CCE) were substituted for histamine during single sessions. Histamine (17.8-100-mu-g/kg/inj), l-nicotine (32-mu-g/kg/inj) and beta-CCE (10-56-mu-g/kg/inj), but not cocaine (10.0-100.0-mu-g/kg/inj), produced a dose-related selective suppression of responding similar to that obtained with electric shock, suggesting that the drugs were functioning as punishers. Punishment by beta-CCE was antagonized with the benzodiazepine antagonist, flumazenil. Injections of beta-CCE before sessions increased the effectiveness of low intensity shock. However, the effectiveness of beta-CCE depended on the intensity of electric shock. The punishing effects of beta-CCE were mediated by benzodiazepine receptor mechanisms and were reliably obtained when the drug was administered as a consequence of operant behavior. C1 NIDA,ADDICT RES CTR,PSYCHOBIOL LAB,POB 5180,BALTIMORE,MD 21224. CIEA,PRECLIN RES LABS,KAWASAKI,KANAGAWA,JAPAN. ELI LILLY & CO,LILLY RES LABS,LILY CORP CTR,INDIANAPOLIS,IN 46285. UNIV WISCONSIN,DEPT CHEM,MILWAUKEE,WI 53201. FU NIDA NIH HHS [DA-02873]; NIH HHS [NH-36644] NR 30 TC 11 Z9 11 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 1992 VL 261 IS 1 BP 138 EP 145 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HN733 UT WOS:A1992HN73300019 PM 1560359 ER PT J AU STONE, M FABER, A RAPHAEL, LJ SHAWKER, TH AF STONE, M FABER, A RAPHAEL, LJ SHAWKER, TH TI CROSS-SECTIONAL TONGUE SHAPE AND LINGUOPALATAL CONTACT PATTERNS IN [S], [INTEGRAL], AND [1] SO JOURNAL OF PHONETICS LA English DT Article ID ASYMMETRIES; HANDEDNESS; MOVEMENT; ANATOMY; BASE C1 HASKINS LABS INC,NEW HAVEN,CT 06511. NIH,DEPT RADIOL,BETHESDA,MD 20892. RP STONE, M (reprint author), NIH,DEPT REHABIL MED,BETHESDA,MD 20892, USA. NR 30 TC 56 Z9 57 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0095-4470 J9 J PHONETICS JI J. Phon. PD APR PY 1992 VL 20 IS 2 BP 253 EP 270 PG 18 WC Linguistics; Language & Linguistics SC Linguistics GA HP651 UT WOS:A1992HP65100006 ER PT J AU SU, H KOZAK, CA VEERHUIS, R LAU, YFC WIBERG, U AF SU, H KOZAK, CA VEERHUIS, R LAU, YFC WIBERG, U TI ISOLATION OF A PHYLOGENETICALLY CONSERVED AND TESTIS-SPECIFIC GENE USING A MONOCLONAL-ANTIBODY AGAINST THE SEROLOGICAL H-Y-ANTIGEN SO JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Article DE HISTOCOMPATIBILITY Y-ANTIGEN; GENE ISOLATION; SPERMATOGENESIS; TESTIS-ENHANCED EXPRESSION; PHYLOGENETIC CONSERVATION ID MOUSE; CELLS; TISSUES; ACID AB Several cDNA clones of a gene termed male-enhanced antigen-2 (Mea-2), have been isolated from a mouse testicular expression cDNA library using a monoclonal histocompatability Y (H-Ys) antibody which detects specific protein(s) present in the mouse testis but not the ovary. The Mea-2 gene is phylogenetically conserved among various mammalian species examined, and is expressed at high levels in adult mouse testis. The expression pattern of Mea-2 is very similar to that of another gene, the male-enhanced antigen-1 (Mea-1), previously isolated using a polyclonal H-Ys antibody. Northern blotting and RT-PCR analyses demonstrated that Mea-2 is also expressed in other adult and fetal mouse organs at low levels. The testis-enhanced expression of this gene is associated with germ cell development at mid- to latemeiotic stages of spermatogenesis. Analysis of an intersubspecies mouse backcross has assigned this gene to chromosome 5, between the loci Gus and Hnf-1. C1 UNIV CALIF SAN FRANCISCO,VET AFFAIRS MED CTR,DEPT MED,DIV CELL & DEV GENET,4150 CLEMENT ST,SAN FRANCISCO,CA 94121. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RES INST ANIM PROD SCHOONOORD,3700 AM ZEIST,NETHERLANDS. UNIV FREIBURG,INST HUMAN GENET & ANTHROPOL,W-7800 FREIBURG,GERMANY. OI Lau, Yun-Fai /0000-0002-9119-7050 FU NICHD NIH HHS [HD24384, HD27392] NR 35 TC 22 Z9 23 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-0378 J9 J REPROD IMMUNOL JI J. Reprod. Immunol. PD APR PY 1992 VL 21 IS 3 BP 275 EP 291 DI 10.1016/0165-0378(92)90031-X PG 17 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA HM663 UT WOS:A1992HM66300005 PM 1522559 ER PT J AU BLUESTONE, JA SPENCER, C HIRSCH, R AF BLUESTONE, JA SPENCER, C HIRSCH, R TI THE T-CELL RECEPTOR IN AUTOIMMUNE-DISEASES SO JOURNAL OF RHEUMATOLOGY LA English DT Article; Proceedings Paper CT 3RD PARK CITY PEDIATRIC RHEUMATOLOGY MEETING : PEDIATRIC RHEUMATOLOGY INTO THE 90S CY MAR 02-06, 1991 CL PARK CITY, UT SP SHRINERS HOSP CRIPPLED CHILDREN, BUR MATERNAL & CHILD HLTH, HABILITAT SERV BRANCH, DIV SERV CHILDREN SPECIAL, HLTH NEEDS, BAXTER HEALTHCARE, HYLAND DIV, CIBA GEIGY, HOME INTENS CARE, LEDERLE LABS, MCNEIL CONSUMER PROD, MCNEIL PHARM, SYNTEX LABS, UPJOHN CO DE T-CELL RECEPTOR; AUTOIMMUNITY ID OKT3 MONOCLONAL-ANTIBODY; PREDOMINANT EXPRESSION; ENCEPHALOMYELITIS; INVIVO; MICE; TRANSPLANTATION AB Autoimmunity is likely the cause of a variety of diseases including systemic lupus erythematosus, rheumatoid arthritis and diabetes. Normally, the body's immune system serves as a defense against a variety of conditions, including, injury, infection and neoplasm. However, for reasons that are currently unclear, the normal regulation of the immune system can breakdown resulting in autoaggressive responses. T cells, especially CD4+ cells, appear to play a predominant role in most autoimmune diseases. We summarize our workshop which focussed on the role of the T cells in autoimmune diseases; the T cell receptor in autoantigen recognition (emphasizing the role of selective T cell receptor V regions in the autoimmune response); and a discussion of possible therapeutic interventions. C1 UNIV CHICAGO,DEPT PEDIAT,CHICAGO,IL 60637. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP BLUESTONE, JA (reprint author), UNIV CHICAGO,DEPT PATHOL,COMM IMMUNOL,5841 S MARYLAND AVE,BOX 424,CHICAGO,IL 60637, USA. NR 19 TC 1 Z9 1 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD APR PY 1992 VL 19 SU 33 BP 75 EP 77 PG 3 WC Rheumatology SC Rheumatology GA HT052 UT WOS:A1992HT05200018 ER PT J AU POGREBNIAK, HW MATTHEWS, W PASS, HI AF POGREBNIAK, HW MATTHEWS, W PASS, HI TI ALTERATIONS IN MACROPHAGE FREE-RADICAL AND TUMOR-NECROSIS-FACTOR PRODUCTION BY A POTASSIUM CHANNEL ACTIVATOR SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE ASSOC FOR ACADEMIC SURGERY CY NOV 00-23, 1991 CL COLORADO SPRINGS, CO SP ASSOC ACAD SURG ID PROTEIN KINASE-C; FACTOR-ALPHA; PERITONEAL-MACROPHAGES; CACHECTIN; ENDOTOXIN; INJURY; CELLS; NICORANDIL; ISCHEMIA; INVITRO RP POGREBNIAK, HW (reprint author), NCI,SURG BRANCH,THORAC ONCOL SECT,BETHESDA,MD 20892, USA. NR 28 TC 14 Z9 15 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 0022-4804 J9 J SURG RES JI J. Surg. Res. PD APR PY 1992 VL 52 IS 4 BP 395 EP 400 DI 10.1016/0022-4804(92)90122-G PG 6 WC Surgery SC Surgery GA HW809 UT WOS:A1992HW80900018 PM 1534387 ER PT J AU QUYYUMI, AA PANZA, JA DIODATI, JG DILSIZIAN, V CALLAHAN, TS BONOW, RO AF QUYYUMI, AA PANZA, JA DIODATI, JG DILSIZIAN, V CALLAHAN, TS BONOW, RO TI RELATION BETWEEN LEFT-VENTRICULAR FUNCTION AT REST AND WITH EXERCISE AND SILENT-MYOCARDIAL-ISCHEMIA SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; MILDLY SYMPTOMATIC PATIENTS; MEDICALLY TREATED PATIENTS; RADIONUCLIDE ANGIOGRAPHY; PROGNOSTIC VALUE; EJECTION FRACTION; HEART-DISEASE; STABLE ANGINA; INFARCTION; MORTALITY AB The prognostic value of radionuclide measures of left ventricular function at rest and exercise is well established. Some studies have suggested that the frequency and duration of silent ischemia during ambulatory monitoring provide similar prognostic information; however, studies comparing these two techniques have not been performed. This study examines the relation between left ventricular function at rest and exercise-induced ischemia assessed by radionuclide ventriculography with myocardial ischemia during ambulatory electrocardiographic (ECG) monitoring. Of the 155 patients with coronary artery disease studied, 88% had left ventricular dysfunction with exercise, defined as failure of the ejection fraction to increase by > 4% with exercise, and 33% of patients had left ventricular dysfunction at rest (ejection fraction < 45%); 52% had transient episodes of ST segment depression during 48-h ambulatory ECG monitoring. Exercise-induced left ventricular dysfunction during radionuclide ventriculography was extremely sensitive (94%) in detecting patients with ischemic episodes during ambulatory ECG monitoring; however, only 55% of patients with exercise-induced left ventricular dysfunction had ST segment depression during ambulatory monitoring. Moreover, patients with left ventricular dysfunction at rest had a lower prevalence of transient episodes of ST segment depression (31%) than did patients with normal left ventricular function at rest (62%) (p = 0.008). The relation between prognostically important variables during exercise radionuclide ventriculography and the number and duration of transient episodes of ST depression was examined. By multivariate regression analysis only the change in left ventricular ejection fraction with exercise was independently related to the number and duration of episodes of ST depression, but these correlations were weak (r2 = 0.04, p < 0.01 and r2 = 0.03, p = 0.05, respectively). Thus, myocardial ischemia during daily life detected by ST segment monitoring correlates poorly with radionuclide ventriculographic measures of ischemia. This is particularly evident in patients with left ventricular dysfunction at rest in whom episodes of transient ST segment depression are infrequent. Ambulatory ST segment monitoring must be used with caution in risk stratification of patients with coronary artery disease, especially in patients with left ventricular dysfunction after myocardial infarction. RP QUYYUMI, AA (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 35 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1992 VL 19 IS 5 BP 962 EP 967 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HL273 UT WOS:A1992HL27300015 PM 1552120 ER PT J AU LAWRENCE, JB PREVOSTI, LG KRAMER, WS SMITH, PD BONNER, RF LU, DY LEON, MB AF LAWRENCE, JB PREVOSTI, LG KRAMER, WS SMITH, PD BONNER, RF LU, DY LEON, MB TI PULSED LASER AND THERMAL ABLATION OF ATHEROSCLEROTIC PLAQUE - MORPHOMETRICALLY DEFINED SURFACE THROMBOGENICITY IN STUDIES USING AN ANNULAR PERFUSION CHAMBER SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID LUMINAL CORONARY ANGIOPLASTY; GLYCOPROTEIN-IIB-IIIA; PERIPHERAL ARTERY OCCLUSIONS; ASSISTED BALLOON ANGIOPLASTY; ADHESIVE PROTEIN-BINDING; BLOOD-CELL DEFORMABILITY; PLATELET-ADHESION; SHEAR RATE; VONWILLEBRAND-FACTOR; THROMBUS FORMATION AB Although clinical trials using laser and thermal angioplasty devices have been underway, the effects of pulsed laser and thermal ablation of atherosclerotic plaque on surface thrombogenicity are poorly understood. This study examined the changes in platelet adherence and thrombus formation on freshly harvested atherosclerotic aorta segments from Watanabe-heritable hyperlipidemic rabbits after ablation by two pulsed laser sources (308-nm xenon chloride excimer and 2,940-nm erbium:yttrium-aluminum-garnet [YAG] lasers) and a prototype catalytic hot-tip catheter. Specimens were placed in a modified Baumgartner annular chamber and perfused with citrated whole human blood, followed by quantitative morphometric analysis to determine the percent surface coverage by adherent platelets and thrombi in the treated and contiguous control areas. Pulsed excimer laser ablation of plaque did not change platelet adherence or thrombus formation in the treated versus control zones. However, photothermal plaque ablation with a pulsed erbium:YAG laser resulted in a 67% reduction in platelet adherence, compared with levels in control areas (from 16.7 +/- 2.2% to 5.5 +/- 1.8%; p < 0.005). Similarly, after plaque ablation using a catalytic thermal angioplasty device, there was a 74% reduction in platelet adherence (from 29.2 +/- 5.1% to 7.7 +/- 1.6%; p < 0.005) and a virtual absence of platelet thrombi (from 8.6 +/- 2.3% to 0.03 +/- 0.03%; p < 0.005). This reduced surface thrombogenicity after plaque ablation with either an erbium: YAG laser or a catalytic hot-tip catheter suggests that thermal modifications in the arterial surface ultra-structure or thermal denaturation of surface proteins, or both, may be responsible for reduced platelet adherence. These in vitro findings indicate that controlled thermal plaque ablation by catheter-based techniques may elicit endovascular responses that can reduce early thrombus formation during angioplasty procedures. C1 NHLBI,DEPT CLIN PATHOL,SERV HEMATOL,BETHESDA,MD 20892. NHLBI,CARDIOL BRANCH,CLIN CTR,BETHESDA,MD 20892. NIH,DIV RES SERV,BIOMED ENGN & INSTRUMENTAT BRANCH,BETHESDA,MD 20892. RP LAWRENCE, JB (reprint author), CASE WESTERN RESERVE UNIV,INST PATHOL,2085 ADELBERT RD,CLEVELAND,OH 44106, USA. RI Bonner, Robert/C-6783-2015 NR 68 TC 14 Z9 14 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1992 VL 19 IS 5 BP 1091 EP 1100 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HL273 UT WOS:A1992HL27300037 PM 1552100 ER PT J AU BRAUNWALD, E KNATTERUD, G PASSAMANI, E AF BRAUNWALD, E KNATTERUD, G PASSAMANI, E TI THE RT-PA VERSUS STREPTOKINASE CONTROVERSY .2. SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Letter ID ACUTE MYOCARDIAL-INFARCTION; TISSUE PLASMINOGEN-ACTIVATOR; INTRAVENOUS STREPTOKINASE; THROMBOLYTIC THERAPY; RANDOMIZED TRIAL; ANGIOPLASTY; IMMEDIATE C1 MARYLAND MED RES INST,BALTIMORE,MD 21210. NHLBI,BETHESDA,MD 20892. RP BRAUNWALD, E (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 19 TC 1 Z9 1 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1992 VL 19 IS 5 BP 1116 EP 1119 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HL273 UT WOS:A1992HL27300042 PM 1552103 ER PT J AU LENFANT, C AF LENFANT, C TI THE RT-PA VERSUS STREPTOKINASE CONTROVERSY .1. SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Letter RP LENFANT, C (reprint author), NHLBI,BETHESDA,MD 20892, USA. NR 4 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1992 VL 19 IS 5 BP 1116 EP 1116 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HL273 UT WOS:A1992HL27300041 PM 1348064 ER PT J AU LYNESS, JM CONWELL, Y NELSON, JC AF LYNESS, JM CONWELL, Y NELSON, JC TI SUICIDE ATTEMPTS IN ELDERLY PSYCHIATRIC-INPATIENTS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID DELIBERATE SELF-HARM; COMPLETED SUICIDE; LATE LIFE; AGE 50; DEPRESSION; ONSET; RISK AB Objective: To describe the psychopathological characteristics of elderly suicide attempters admitted to an inpatient psychiatric unit. Design: Retrospective chart review. Patients: All 168 patients age 60 years and over treated on the adult psychiatric inpatient unit of Yale-New Haven Hospital from 1979 to 1984. Twenty-five made a suicide attempt. Main Outcome Measures: Presence and severity of suicide attempts were rated and compared with demographic, clinical, and functional data. Results: (1) Eighty percent of the attempters had a major depressive syndrome; (2) among patients with affective disorders, presence of an attempt was significantly associated with a later age of onset; (3) patients who had made more severe attempts were more likely to be diagnosed as psychotic depression, although this trend was not significant; (4) substance abuse and dementia were uncommon diagnoses; (5) symptomatic and functional outcome of hospitalization was as favorable for the attempters as for the entire elderly cohort. Conclusions: Affective illness, especially late-onset major depression, was the major association with suicide attempts. C1 YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06510. RP LYNESS, JM (reprint author), UNIV ROCHESTER,MED CTR,SCH MED & DENT,DEPT PSYCHIAT,NIMH,CLIN RES CTR STUDY PSYCHOPATHOL ELDERLY,ROCHESTER,NY 14642, USA. FU NIMH NIH HHS [T32 MH18911, P50 MH40381] NR 43 TC 60 Z9 60 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 1992 VL 40 IS 4 BP 320 EP 324 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA HM369 UT WOS:A1992HM36900003 PM 1556358 ER PT J AU SCHNELLE, JF NEWMAN, DR WHITE, M VOLNER, TR BURNETT, J CRONQVIST, A ORY, M AF SCHNELLE, JF NEWMAN, DR WHITE, M VOLNER, TR BURNETT, J CRONQVIST, A ORY, M TI REDUCING AND MANAGING RESTRAINTS IN LONG-TERM-CARE FACILITIES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID PHYSICAL RESTRAINTS; HEALTH-CARE AB Objective: To evaluate a management system designed to improve staff adherence to a federal regulation that stated restrained residents should be released, exercised, and repositioned every 2 hours. Design: A delayed intervention, controlled, cross-over design with three phases. During phase one, baseline, the length of intervals that residents remained in restraints was monitored. The intervention was implemented at site A in Phase two while site B remained in baseline. During Phase three, the intervention was replicated at site B. Setting: Two long-term care proprietary nursing facilities. Patients: Sixty-three physically restrained residents in the two facilities. Intervention: The intervention was a system of restraint release using colored pads corresponding to specific hours. The management rule was that the resident should be on a different colored pad every 2 hours. Staff had to lift residents to place the pad, and the colors made the system easy for supervisors to check. Main Outcome Measures: Checks by research personnel by black light and invisible ink, to detect movement of the knot tying the restraints. Results: During the baseline phase, the majority of residents at both sites were inappropriately restrained longer than 2 hours (site A: 54.1%; site B: 60.1%). The percentage of residents restrained over 2 hours was significantly reduced during the intervention phase to 13.9% (site A) and 19.4% (site B). Three weeks after the end of the intervention, inappropriate use of restraints remained low, 14.2%, but rose to 47.7% after another 3 weeks. Conclusion: The management system is an effective way to increase the consistency with which nursing-home staff release and reposition restrained residents. C1 MIDDLE TENNESSEE STATE UNIV,MURFREESBORO,TN 37130. VANDERBILT UNIV,SCH NURSING,NASHVILLE,TN 37240. NIH,BETHESDA,MD 20892. RP SCHNELLE, JF (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,DIV GERIATR MED & GERONTOL,10833 LE CONTE AVE,CHS 32-144,LOS ANGELES,CA 90024, USA. FU NIA NIH HHS [5 U01 AG05270-02] NR 14 TC 26 Z9 26 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 1992 VL 40 IS 4 BP 381 EP 385 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA HM369 UT WOS:A1992HM36900013 PM 1556366 ER PT J AU LITVAK, J BLATTNER, W BLOT, W BRINTON, L CORREA, P FONAROFF, A RESTREPO, H AF LITVAK, J BLATTNER, W BLOT, W BRINTON, L CORREA, P FONAROFF, A RESTREPO, H TI WORKSHOP ON CANCER-EPIDEMIOLOGY IN LATIN-AMERICA AND THE CARIBBEAN SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material C1 NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. LOUISIANA STATE UNIV,MED CTR,DEPT PATHOL,NEW ORLEANS,LA 70112. NIH,FOGARTY INT CTR,BETHESDA,MD 20892. NCI,DIV CANC ETIOL,ENVIRONM BRANCH,BETHESDA,MD 20892. RP LITVAK, J (reprint author), NCI,NUFFIELD DEPT INT AFFAIRS,BLDG 31,RM 4B-55,BETHESDA,MD 20892, USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 0 TC 2 Z9 2 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 1 PY 1992 VL 84 IS 7 BP 484 EP 488 DI 10.1093/jnci/84.7.484 PG 5 WC Oncology SC Oncology GA HM284 UT WOS:A1992HM28400013 PM 1312175 ER PT J AU DYKES, DJ HARRISON, SD MAYO, JG GRISWOLD, DP AF DYKES, DJ HARRISON, SD MAYO, JG GRISWOLD, DP TI EXCISION ASSAY FOR INITIAL EVALUATION OF ANTITUMOR DRUG ACTIVITY IN MICE BEARING HUMAN TUMOR XENOGRAFTS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Note ID CELL-LINES C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,FREDERICK,MD 21701. RP DYKES, DJ (reprint author), SO RES INST,POB 55305,BIRMINGHAM,AL 35255, USA. FU NCI NIH HHS [CM-97553] NR 14 TC 3 Z9 3 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 1 PY 1992 VL 84 IS 7 BP 528 EP 530 DI 10.1093/jnci/84.7.528 PG 3 WC Oncology SC Oncology GA HM284 UT WOS:A1992HM28400022 PM 1545443 ER PT J AU HENDERSON, LE BOWERS, MA SOWDER, RC SERABYN, SA JOHNSON, DG BESS, JW ARTHUR, LO BRYANT, DK FENSELAU, C AF HENDERSON, LE BOWERS, MA SOWDER, RC SERABYN, SA JOHNSON, DG BESS, JW ARTHUR, LO BRYANT, DK FENSELAU, C TI GAG PROTEINS OF THE HIGHLY REPLICATIVE MN STRAIN OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 - POSTTRANSLATIONAL MODIFICATIONS, PROTEOLYTIC PROCESSINGS, AND COMPLETE AMINO-ACID-SEQUENCES SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; TANDEM MASS-SPECTROMETRY; STRUCTURAL PROTEINS; HTLV-III; RETROVIRUSES; MUTANTS; AIDS; MORPHOGENESIS; INFECTIVITY; CLEAVAGE AB The MN strain of human immunodeficiency virus type 1 was grown in H9 cells, concentrated by centrifugation, and disrupted, and proteins were purified by reversed-phase high-pressure liquid chromatography. Complete amino acid sequences were determined for the mature Gag proteins, showing natural proteolytic cleavage sites and the order of proteins (p17-p24-p2-p7-p1-p6) in the Gag precursors. At least two sequence variants of p24 and eight sequence variants of p17 were detected. The two most abundant variants of p24 and p17 represented at least 50% +/- 5% and 20% +/- 5% of their totals, respectively. These data suggest heterogeneity in the virus population, with 50% of the total virus containing the most abundant forms of p17 and p24 and 20% of the virus containing the second most abundant forms. The Gag precursors of these suggested viruses differ from each other by only 3 amino acid residues but differ from the precursors predicted by the published MN proviral DNA sequence by 10 residues. Electrospray ionization mass spectrometry analysis of the purified p24 forms showed that the measured molecular weight of the protein was 200 +/- 50 atomic mass units greater than the calculated molecular weight. The source of additional mass for the p24 forms was not determined, but the observation is consistent with previous suggestions that the protein is phosphorylated. Greater than 98% of the total recovered p17 was myristylated at the N-terminal glycine residue, and the measured molecular weights (as determined by electrospray ionization mass spectrometry) of the most abundant forms were within 3 atomic mass units of the calculated molecular weights (15,266). C1 UNIV MARYLAND,DEPT CHEM & BIOCHEM,CATONSVILLE,MD 21228. RP HENDERSON, LE (reprint author), NCI,FREDERICK CANC RES & DEV CTR,INC DYNCORP,PROGRAM RESOURCES,AIDS VACCINE PROGRAM,FREDERICK,MD 21702, USA. RI Bess, Jr., Julian/B-5343-2012 FU NCI NIH HHS [N01-CO-74102] NR 36 TC 261 Z9 262 U1 0 U2 5 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 1992 VL 66 IS 4 BP 1856 EP 1865 PG 10 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400004 PM 1548743 ER PT J AU DAVIES, MV ELROYSTEIN, O JAGUS, R MOSS, B KAUFMAN, RJ AF DAVIES, MV ELROYSTEIN, O JAGUS, R MOSS, B KAUFMAN, RJ TI THE VACCINIA VIRUS K3L-GENE PRODUCT POTENTIATES TRANSLATION BY INHIBITING DOUBLE-STRANDED-RNA-ACTIVATED PROTEIN-KINASE AND PHOSPHORYLATION OF THE ALPHA SUBUNIT OF EUKARYOTIC INITIATION FACTOR-II SO JOURNAL OF VIROLOGY LA English DT Article ID INTERFERON-INDUCED RESISTANCE; VESICULAR STOMATITIS-VIRUS; MESSENGER-RNAS; INFECTED CELLS; FACTOR-II; GENE; EXPRESSION; DELETION; RESCUE; DNA AB Interferon resistance of vaccinia virus is mediated by specific inhibition of phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF-2-alpha) by the double-stranded-RNA-activated (DAI) protein kinase. Vaccinia virus encodes a homolog of eIF-2-alpha, K3L, the deletion of which renders the virus sensitive to interferon treatment. We have studied the mechanism by which this protein product elicits interferon resistance in a transient DNA transfection system designed to evaluate regulators of eIF-2-alpha phosphorylation. In this system, translation of a reporter gene mRNA is inefficient because of eIF-2 phosphorylation mediated by the DAI protein kinase. Cotransfection of the K3L gene enhances translation of the reporter mRNA in this system. The K3L protein inhibits eIF-2-alpha phosphorylation and DAI kinase activation, apparently without being phosphorylated itself. Inhibition of protein synthesis, elicited by expression of a mutant Ser-51 --> Asp eIF-2-alpha designed to mimic a phosphorylated serine, is not relieved by the presence of K3L, suggesting that K3L cannot bypass a block imposed by eIF-2-alpha phosphorylation. The results suggest that K3L acts as a decoy of eIF-2-alpha to inhibit DAI kinase autophosphorylation and activation. Another vaccinia virus gene product, K1L, which is required for growth of vaccinia virus on human cells, does not enhance translation in this assay. C1 GENET INST, 87 CAMBRIDGE PK DR, CAMBRIDGE, MA 02140 USA. NIAID, VIRAL DIS LAB, BETHESDA, MD 20892 USA. UNIV MARYLAND, CTR MARINE BIOTECHNOL, BALTIMORE, MD 21202 USA. NR 44 TC 166 Z9 166 U1 0 U2 2 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 1992 VL 66 IS 4 BP 1943 EP 1950 PG 8 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400014 PM 1347793 ER PT J AU CARROLL, R PETERLIN, BM DERSE, D AF CARROLL, R PETERLIN, BM DERSE, D TI INHIBITION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TAT ACTIVITY BY COEXPRESSION OF HETEROLOGOUS TRANS ACTIVATORS SO JOURNAL OF VIROLOGY LA English DT Article ID LONG TERMINAL REPEAT; HIV-1 TAT; MUTATIONAL ANALYSIS; GENE-EXPRESSION; RESPONSIVE REGION; PROTEIN; RNA; TRANSACTIVATION; SEQUENCE; INVITRO AB We examined the mechanism of Tat-mediated trans activation through competition experiments employing Tat proteins of human immunodeficiency virus type 1 (HIV-1) and equine infectious anemia virus (EIAV). EIAV Tat, as well as chimeric EIAV/HIV-1 Tat proteins, inhibited HIV-1 Tat-mediated trans activation in a cell-type-dependent fashion. Furthermore, these proteins inhibited trans activation by Tat-bacteriophage R17 coat protein chimeras. Inhibition resulted from competition between activation domains of effectors and competitors for a limiting cellular cofactor. The context in which competitor activation domains were expressed contributed to the extent of inhibition. In transfected cells, EIAV Tat and all chimeric competitors were located primarily in the cytoplasm, whereas HIV-1 Tat was primarily located in the nucleus. These data are consistent with a model for trans activation in which the activation domain of Tat associates with and conveys a cellular factor to the transcription complex via the trans-acting-responsive element (TAR). C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT MICROBIOL & IMMUNOL,SAN FRANCISCO,CA 94143. NR 43 TC 77 Z9 77 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 1992 VL 66 IS 4 BP 2000 EP 2007 PG 8 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400021 PM 1312617 ER PT J AU KADAN, MJ STURM, S ANDERSON, WF EGLITIS, MA AF KADAN, MJ STURM, S ANDERSON, WF EGLITIS, MA TI DETECTION OF RECEPTOR-SPECIFIC MURINE LEUKEMIA-VIRUS BINDING TO CELLS BY IMMUNOFLUORESCENCE ANALYSIS SO JOURNAL OF VIROLOGY LA English DT Article ID MEDIATED GENE-TRANSFER; ENVELOPE GLYCOPROTEIN; RETROVIRAL VECTORS; MAMMALIAN-CELLS; MOUSE CELLS; SUSCEPTIBILITY; FIBROBLASTS; ENTRY; LINES; GP71 AB Four classes of murine leukemia virus (MuLV) which display distinct cellular tropisms and bind to different retrovirus receptors to initiate virus infection have been described. In the present study, we describe a rapid, sensitive immunofluorescence assay useful for characterizing the initial binding of MuLV to cells. By using the rat monoclonal antibody 83A25 (L. H. Evans, R. P. Morrison, F. G. Malik, J. Portis, and W. J. Britt, J. Virol. 64:6176-6183, 1990), which recognizes an epitope of the envelope gp70 molecule common to the different classes of MuLV, it is possible to analyze the binding of ecotropic, amphotropic, or xenotropic MuLV by using only a single combination of primary and secondary antibodies. The MuLV binding detected by this assay is envelope receptor specific and matches the susceptibility to infection determined for cells from a variety of species. The binding of amphotropic MuLV to NIH 3T3 cells was shown to be rapid, saturable, and temperature dependent. Chinese hamster ovary (CHO-K1) cells normally lack the ability to bind ecotropic virus and are not infectible by ecotropic vectors. Expression of the cloned ecotropic retrovirus receptor gene (Rec) in CHO-K1 cells confers high levels of ecotropic virus-specific binding and confers susceptibility to infection. Characterization of MuLV binding to primary cells may provide insight into the infectibility of cells by retroviruses and aid in the selection of appropriate vectors for gene transfer experiments. C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. RP KADAN, MJ (reprint author), GENET THERAPY INC,GENE TRANSFER LAB,GAITHERSBURG,MD 20878, USA. NR 41 TC 66 Z9 66 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 1992 VL 66 IS 4 BP 2281 EP 2287 PG 7 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400054 PM 1312632 ER PT J AU GESSAIN, A GALLO, RC FRANCHINI, G AF GESSAIN, A GALLO, RC FRANCHINI, G TI LOW DEGREE OF HUMAN T-CELL LEUKEMIA LYMPHOMA VIRUS TYPE-I GENETIC DRIFT INVIVO AS A MEANS OF MONITORING VIRAL TRANSMISSION AND MOVEMENT OF ANCIENT HUMAN-POPULATIONS SO JOURNAL OF VIROLOGY LA English DT Article ID TROPICAL SPASTIC PARAPARESIS; NUCLEOTIDE-SEQUENCE ANALYSIS; HTLV-I; AFRICAN PATIENTS; HUMAN RETROVIRUS; ENVELOPE GENE; C RETROVIRUS; PROVIRAL DNA; MYELOPATHY; INFECTION AB We have studied the genetic variation of human T-cell leukemia/lymphoma virus type I (HTLV-I) isolates in the same individuals over time, as well as of HTLV-I isolates from various parts of the world. The viral DNA fragment studied encodes the carboxy terminus of gp46 and almost all of gp21, both of which are envelope glycoproteins. Samples were obtained from native inhabitants of five African countries, two South American countries, China, the French West Indies, and Haiti and included 14 patients with tropical spastic paraparesis/HTLV-I-associated myelopathy, 10 patients with adult T-cell leukemia, 1 patient with T-cell non-Hodgkin's lymphoma, and 3 healthy HTLV-I-seropositive individuals. DNA analyses of HTLV-I sequences demonstrated that (i) little or no genetic variation occurred in vivo in the same individual or in different hosts from the same region carrying the same virus, regardless of their clinical statuses; (ii) changes in nucleotide sequences in some regions of the HTLV-I genome were diagnostic of the geographical origin of the viruses; (iii) HTLV-I sequences from West African countries (Mauritania and Guinea Bissau) and some from the Ivory Coast and Central African Republic were virtually identical to those from the French West Indies, Haiti, French Guyana, and Peru, strongly suggesting that at least some HTLV-I strains were introduced into the New World through infected individuals during the slave trade events; and (iv) the Zairian HTLV-I isolates represent a separate HTLV-I cluster, in which intrastrain variability was also observed, and are more divergent from the other HTLV-I isolates. Because of the low genetic variability of HTLV-I in vivo, the study of the proviral DNA sequence in selected populations of infected individuals will increase our knowledge of the origin and evolution of HTLV-I and might be useful in anthropological studies. C1 NCI, TUMOR CELL BIOL LAB, BETHESDA, MD 20892 USA. NR 50 TC 216 Z9 219 U1 0 U2 2 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 1992 VL 66 IS 4 BP 2288 EP 2295 PG 8 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400055 PM 1548762 ER PT J AU VANDEPOL, SB HOWLEY, PM AF VANDEPOL, SB HOWLEY, PM TI THE BOVINE PAPILLOMAVIRUS CONSTITUTIVE ENHANCER IS ESSENTIAL FOR VIRAL TRANSFORMATION, DNA-REPLICATION, AND THE MAINTENANCE OF LATENCY SO JOURNAL OF VIROLOGY LA English DT Article ID E2 GENE-PRODUCT; HPV18 REGULATORY REGION; CARBOXY-TERMINAL DOMAIN; LONG CONTROL REGION; OPEN READING FRAME; TRANSCRIPTIONAL REGULATION; PLASMID MAINTENANCE; TRANS-ACTIVATION; TYPE-11 ENHANCER; BINDING-PROTEIN AB Bovine papillomavirus type 1 (BPV-1) has served as the prototype papillomavirus for the study of viral transcription, DNA replication, and latency. However, no cis essential transcription control regions which are necessary for both transformation and replication of BPV-1 or any other papillomavirus have yet been defined. We have found that BPV-1 mutants with deletions in the long control region were defective for transformation and replication, with the essential region in the 5' long control region corresponding to the previously defined BPV-1 constitutive enhancer (S. B. Vande Pol and P. M. Howley, J. Virol. 64:5420-5429, 1990). BPV-1 mutants deleted of the constitutive enhancer could be complemented in trans by the full-length virally encoded E2 transactivator and replication factor (E2TA) and in cis by the simian virus 40 enhancer. The constitutive enhancer induced the production of E2TA by activating all the major viral early promoters upstream of the E2 open reading frame. Complementation experiments using a temperature-sensitive E2TA mutant indicated that the constitutive enhancer was necessary for the maintenance of viral DNA replication within latently infected cells and implied that viral transcription under the regulation of the constitutive enhancer may be controlled during the cell cycle. The constitutive enhancer is a master regulatory control region for establishing and maintaining BPV-1 latency, and its characteristics reveal some analogies with cell type-specific enhancer elements recognized in the human papillomaviruses. RP VANDEPOL, SB (reprint author), NCI,TUMOR VIRUS BIOL LAB,BLDG 41,ROOM D506,BETHESDA,MD 20892, USA. NR 59 TC 23 Z9 23 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 1992 VL 66 IS 4 BP 2346 EP 2358 PG 13 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400062 PM 1312634 ER PT J AU PHELPS, WC MUNGER, K YEE, CL BARNES, JA HOWLEY, PM AF PHELPS, WC MUNGER, K YEE, CL BARNES, JA HOWLEY, PM TI STRUCTURE-FUNCTION ANALYSIS OF THE HUMAN PAPILLOMAVIRUS TYPE-16 E7 ONCOPROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID RETINOBLASTOMA GENE-PRODUCT; TRANSCRIPTION FACTOR-IIIA; ZINC-BINDING DOMAINS; ADENOVIRUS E1A GENE; MUTATIONAL ANALYSIS; HUMAN KERATINOCYTES; TRANSFORMING GENE; SEPARATE DOMAINS; TRANS-ACTIVATION; DNA-SYNTHESIS AB The E7 gene of human papillomavirus type 16 encodes a multifunctional nuclear phosphoprotein that is functionally and structurally similar to the adenovirus (Ad) E1A proteins and the T antigens of other papovaviruses. E7 can cooperate with an activated ras oncogene to transform primary rodent cells, trans activate the Ad E2 promoter, and abrogate transforming growth factor beta-mediated repression of c-myc. Recent studies suggest that these functions may in part be a consequence of the ability of E7 to associate with the product of the retinoblastoma tumor suppressor gene (pRB). In this study, a series of site-specific mutations of the human papillomavirus type 16 E7 gene product were constructed and assessed for their effects on intracellular protein stability, ras cooperativity, transcriptional trans activation, pRB association, and phosphorylation. The results of these studies indicate that the transforming and trans-activating domains extensively overlap within a region of the protein analogous to conserved region 2 of Ad E1A, suggesting that pRB binding is necessary for both activities. Deletion of sequences in conserved region 1 abrogates cellular transformation but has only a marginal effect on trans activation. These data suggest that E7 trans activation and cellular transformation are interrelated but separable functions. C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. RP PHELPS, WC (reprint author), BURROUGHS WELLCOME CO,DIV VIROL,RES TRIANGLE PK,NC 27709, USA. OI Munger, Karl/0000-0003-3288-9935 NR 58 TC 187 Z9 196 U1 0 U2 2 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 1992 VL 66 IS 4 BP 2418 EP 2427 PG 10 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400069 PM 1312637 ER PT J AU SHARPLESS, NE OBRIEN, WA VERDIN, E KUFTA, CV CHEN, ISY DUBOISDALCQ, M AF SHARPLESS, NE OBRIEN, WA VERDIN, E KUFTA, CV CHEN, ISY DUBOISDALCQ, M TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TROPISM FOR BRAIN MICROGLIAL CELLS IS DETERMINED BY A REGION OF THE ENV-GLYCOPROTEIN THAT ALSO CONTROLS MACROPHAGE TROPISM SO JOURNAL OF VIROLOGY LA English DT Note ID CENTRAL NERVOUS-SYSTEM; CD4 ANTIGEN; HIV-1; AIDS; INFECTION; GP120; SEQUENCE; RECEPTOR; TISSUE; DOMAIN AB Human immunodeficiency virus type 1 (HIV-1), the agent of AIDS, frequently infects the central nervous system. We inoculated adult human brain cultures with chimeric viruses containing parts of the env gene of a cloned primary isolate from brain tissue, HIV-1 JRFl, inserted into the cloned DNA of a T-cell-tropic strain. A chimeric virus containing the carboxy-terminal portion of HIV-1 JRFl env did not replicate in these brain tissue cultures, while a chimera expressing an env-encoded protein containing 158 amino acids of HIV-1 JRFl gp120, including the V3 loop, replicated well in brain microglial cells, as it does in blood macrophages. Infection of brain microglial cells with such a chimera was blocked by an antibody to the V3 loop of gp120. Thus, env determinants in the region of gp120, outside the CD4-binding site and comprising the V3 loop, are critical for efficient viral binding to and/or entry into human brain microglia. C1 NINCDS,VIRAL & MOLEC PATHOGENESIS LAB,BETHESDA,MD 20892. NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. NIH,HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,BETHESDA,MD 20814. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,JONSSON COMPREHENS CANC CTR,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,JONSSON COMPREHENS CANC CTR,DEPT MED,LOS ANGELES,CA 90024. OI Verdin, Eric/0000-0003-3703-3183 NR 37 TC 109 Z9 110 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 1992 VL 66 IS 4 BP 2588 EP 2593 PG 6 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400095 PM 1548785 ER PT J AU ROBBINS, J BLONDEL, BJ GALLAHAN, D CALLAHAN, R AF ROBBINS, J BLONDEL, BJ GALLAHAN, D CALLAHAN, R TI MOUSE MAMMARY-TUMOR GENE-INT-3 - A MEMBER OF THE NOTCH-GENE FAMILY TRANSFORMS MAMMARY EPITHELIAL-CELLS SO JOURNAL OF VIROLOGY LA English DT Note ID CYCLE CONTROL PROTEINS; YEAST HO GENE; PROVIRAL INSERTION; GROWTH-FACTORS; DROSOPHILA; ONCOGENE; INT-2; HOMOLOGY; SEQUENCE; PRODUCT AB Expression of a 2.3-kb RNA species is induced in mammary tumors as a consequence of insertional mutagenesis at the int-3 locus by the mouse mammary tumor virus. The nucleotide sequence and biological activity of this mammary tumor-specific int-3 RNA species were determined. It contains an open reading frame which encodes a 57-kDa protein. The translated protein possesses six nearly contiguous 32-amino-acid repeats which are related to a similar motif in the Saccharomyces cerevisiae cdc-10-encoded cell cycle protein. In addition, the int-3 cdc-10 repeats are bounded by the PEST amino acid sequence motif which is commonly found in proteins having a rapid turnover and may represent sites for phosphorylation. The int-3 cdc-10 repeat sequences are 50% identical to a portion of the intracellular domain of the neurogenic Drosophila notch gene product. Activation of expression of a recombinant int-3 genomic DNA fragment encoding the 2.3-kb RNA species in HC11 mouse mammary epithelial cells in vitro induces anchorage-independent growth in soft agar. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NR 42 TC 223 Z9 225 U1 0 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 1992 VL 66 IS 4 BP 2594 EP 2599 PG 6 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400096 PM 1312643 ER PT J AU ROY, MJ WALSH, TJ AF ROY, MJ WALSH, TJ TI HISTOPATHOLOGIC AND IMMUNOHISTOCHEMICAL CHANGES IN GUT-ASSOCIATED LYMPHOID-TISSUES AFTER TREATMENT OF RABBITS WITH DEXAMETHASONE SO LABORATORY INVESTIGATION LA English DT Article DE CORTICOSTEROIDS; MUCOSAL IMMUNITY; M-CELLS; DOME EPITHELIUM ID DOME EPITHELIUM; CORTICOSTEROID ACTION; PEYERS PATCHES; SUBPOPULATIONS; HYDROCORTISONE; LYMPHOCYTES; MECHANISMS; MIGRATION; IGA AB Corticosteroids cause impaired cell-mediated immunity which may encourage development of gastrointestinal and respiratory infections. In order to better understand the effects of corticosteroids on gastrointestinal immunity, immunological and histological changes in gut-associated lymphoid tissues were examined after intravenous administration of dexamethasone to rabbits. In treated animals, lymphoid domes and follicles were considerably reduced in size, and the dome epithelial layer was markedly depleted of M cells and lymphocytes. There were numerous open lesions at the luminal surface of dome epithelium, consistent with necrosis of M cells, and a striking depletion of follicular B cells in treated animals. These immunologic and histologic effects of corticosteroids could have found profound, deleterious effects on mucosal immune responses and host resistance to microbial infections. C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,RM 13N-240,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,DEPT EXPTL PATHOL,WASHINGTON,DC 20307. NR 26 TC 14 Z9 16 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 1992 VL 66 IS 4 BP 437 EP 443 PG 7 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HP263 UT WOS:A1992HP26300005 PM 1583884 ER PT J AU FIAT, D LIGETI, L LYON, RC RUTTNER, Z PEKAR, J MOONEN, CTW MCLAUGHLIN, AC AF FIAT, D LIGETI, L LYON, RC RUTTNER, Z PEKAR, J MOONEN, CTW MCLAUGHLIN, AC TI INVIVO O-17 NMR-STUDY OF RAT-BRAIN DURING O-2(17) INHALATION SO MAGNETIC RESONANCE IN MEDICINE LA English DT Note C1 NIAAA,ALCOHOL DRUG ABUSE & MENTAL HLTH ADM,METAB & MOLEC BIOL LAB,ROCKVILLE,MD 20852. RI Moonen, Chrit/K-4434-2016 OI Moonen, Chrit/0000-0001-5593-3121 NR 12 TC 40 Z9 41 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD APR PY 1992 VL 24 IS 2 BP 370 EP 374 DI 10.1002/mrm.1910240218 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HM149 UT WOS:A1992HM14900017 PM 1569875 ER PT J AU NASH, TE MOWATT, MR AF NASH, TE MOWATT, MR TI CHARACTERIZATION OF A GIARDIA-LAMBLIA VARIANT-SPECIFIC SURFACE PROTEIN (VSP) GENE FROM ISOLATE GS/M AND ESTIMATION OF THE VSP GENE REPERTOIRE SIZE SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE ANTIGENIC VARIATION; GIARDIA-LAMBLIA; CYSTEINE-RICH PROTEIN ID EXPERIMENTAL HUMAN INFECTIONS; EXCRETORY-SECRETORY PRODUCTS; ANTIGENIC VARIATION; DNA; FAMILY AB Giardia lamblia undergoes surface antigenic variation. The variant-specific surface proteins (VSPs) of isolate WB are cysteine-rich, can vary dramatically in size, contain Cys-X-X-Cys motifs, and are differentially expressed. GS/M(H7) is a Giardia clone from a different isolate which expresses a VSP epitope not found in WB. The VSP gene encoding this epitope was selected by differential hybridization using radiolabeled cDNA from H7 and variant sibling trophozoite lines from the same isolate that express other VSPs. The VSPH7 gene probe detects an 1800 nucleotide transcript abundant in H7 but undetectable in variant siblings. Primer extension directly from RNA was used to complete the gene sequence which predicted a protein with a molecular weight of 56 832. The protein showed many of the characteristics of 2 previously sequenced WB VSPs including many Cys-X-X-Cys tetrapeptides and a conserved carboxy-terminal region. Genomic Southern analysis indicated the presence of 2 distinct VSPH7 genes in H7. An oligonucleotide from the conserved region was used in combination with one specific for the VSPH7 gene to estimate the VSP repertoire size at between 133 and 151. VSPs, even from isolates expressing unique epitopes, constitute a family of related proteins. RP NASH, TE (reprint author), NIAID,PARASIT DIS LAB,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. NR 25 TC 66 Z9 68 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 1992 VL 51 IS 2 BP 219 EP 227 DI 10.1016/0166-6851(92)90072-R PG 9 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA HK169 UT WOS:A1992HK16900006 PM 1574080 ER PT J AU WALKERJONAH, A DOLAN, SA GWADZ, RW PANTON, LJ WELLEMS, TE AF WALKERJONAH, A DOLAN, SA GWADZ, RW PANTON, LJ WELLEMS, TE TI AN RFLP MAP OF THE PLASMODIUM-FALCIPARUM GENOME, RECOMBINATION RATES AND FAVORED LINKAGE GROUPS IN A GENETIC CROSS SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE PLASMODIUM-FALCIPARUM; MALARIA; CHROMOSOME MAPPING; LINKAGE ANALYSIS; GENETIC RECOMBINATION ID ELECTRIC-FIELDS; DNA-MOLECULES; MALARIA; CHROMOSOMES; SEPARATION AB We report a genetic linkage map of the Plasmodium falciparum genome, using the inheritance patterns of nearly 90 RFLP markers in a genetic cross. Markers were assigned to polymorphic loci on all 14 nuclear chromosomes. Genetic recombination between parental markers was detected in each of the progeny, indicating that progeny from cross-fertilization events were favored over progeny from self-fertilization of either parent alone. Inheritance patterns among the markers suggested that certain parental linkage groups on chromosomes 2, 3, 12 and 13 were favored in the cross. Recombination frequencies on five chromosomes indicated an approximate map unit size of 15-30 kb per centiMorgan for P. falciparum. C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 23 TC 82 Z9 82 U1 0 U2 1 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 1992 VL 51 IS 2 BP 313 EP 320 DI 10.1016/0166-6851(92)90081-T PG 8 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA HK169 UT WOS:A1992HK16900015 PM 1349423 ER PT J AU MARAIA, RJ CHANG, DY WOLFFE, AP VORCE, RL HSU, K AF MARAIA, RJ CHANG, DY WOLFFE, AP VORCE, RL HSU, K TI THE RNA POLYMERASE-III TERMINATOR USED BY A B1-ALU ELEMENT CAN MODULATE 3'-PROCESSING OF THE INTERMEDIATE RNA PRODUCT SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ALPHA-FETOPROTEIN GENE; TRANSCRIPTION TERMINATION; ALU FAMILY; REPEATED SEQUENCES; SUCCESSIVE WAVES; LINEAGE HISTORY; XENOPUS-LAEVIS; EXPRESSION; DNA; FIXATION AB The dispersion of short interspersed elements (SINEs) probably occurred through an RNA intermediate. B1 is a murine homolog of the human SINE Alu; these elements are composed of 5' G+C-rich regions juxtaposed to A-rich tracts and are flanked by direct repeats. Internal promoters direct RNA polymerase III to transcribe B1 and Alu elements and proceed into the 3' flanking DNA until it reaches a (dT)4 termination signal. The resulting transcripts contain 3'-terminal oligo(U) tracts which can presumably base pair with the A-rich tract to form self-primed templates for reverse transcriptase and retrotransposition. Nuclear extracts from mouse tissue culture cells contain an RNA processing activity that removes the A-rich and 3'-terminal regions from purified B1 RNAs (R. Maraia, Nucleic Acids Res. 19:5695-5702, 1991). In this study, we examined transcription and RNA processing in these nuclear extracts. In contrast to results with use of purified RNA, nascent transcripts synthesized in nuclear extract by RNA polymerase III are not processed, suggesting that the transposition-intermediate-like RNA is shielded from processing by a protein(s). Alteration of an AATTTT TAA termination signal to a GCTTTTGC signal activated processing by > 100-fold in coupled transcription/processing reactions. A similar difference was found when expression was compared in frog oocytes. No difference in processing was found if the transcripts were made by T7 RNA polymerase in the presence of the nuclear extract, indicating that the different processing effects of the two terminators were dependent on synthesis by polymerase III. The modulation of processing of B1-Alu transcripts and the potential for retrotransposition of B1 and Alu DNA sequences are discussed. C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. RP MARAIA, RJ (reprint author), NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892, USA. NR 38 TC 34 Z9 34 U1 0 U2 0 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 1992 VL 12 IS 4 BP 1500 EP 1506 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HK751 UT WOS:A1992HK75100011 PM 1549107 ER PT J AU HOLBROOK, NJ CARLSON, SG CHOI, AMK FARGNOLI, J AF HOLBROOK, NJ CARLSON, SG CHOI, AMK FARGNOLI, J TI INDUCTION OF HSP70 GENE-EXPRESSION BY THE ANTIPROLIFERATIVE PROSTAGLANDIN PGA2 - A GROWTH-DEPENDENT RESPONSE MEDIATED BY ACTIVATION OF HEAT-SHOCK TRANSCRIPTION FACTOR SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CELL-CYCLE PROGRESSION; CYCLOPENTENONE PROSTAGLANDINS; DURABLE SYNTHESIS; STRESS PROTEIN; INHIBITION; MECHANISM; SITE; STIMULATION; EUKARYOTES; ARREST AB Prostaglandins (PG) of the A series are potent inhibitors of cell proliferation. Recently, it was shown that PGA2-induced growth arrest was associated with the increased synthesis of stress proteins encoded by the HSP70 gene family. In this study, we have examined the molecular basis for this increased HSP70 expression. Northern (RNA) blot analysis and nuclear run-on assays demonstrated that induction of high levels of HSP70 mRNA results from an increase in the rate of transcription. High-level induction is specific to the HSP70 family of heat shock proteins and is rapid, reversible, dose dependent, and specific for PGs capable of growth-arresting HeLa cells. In addition, the response was found to be highly dependent on the growth state of the cells, as induction occurs in growing but not in confluent nongrowing cell populations. Induction is dependent on the activation of heat shock factor. Cycloheximide pretreatment, which inhibits the antiproliferative effects of PGA2, prevents activation of the heat shock factor and induction of HSP70 mRNA by PGA2. These results support a role for HSP70 in mediating the antiproliferative effects of PGA2. C1 JOHNS HOPKINS MED INST, DIV PULM & CRIT CARE, BALTIMORE, MD 21224 USA. RP NIA, MOLEC GENET LAB, BALTIMORE, MD 21224 USA. NR 44 TC 69 Z9 69 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 EI 1098-5549 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1992 VL 12 IS 4 BP 1528 EP 1534 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HK751 UT WOS:A1992HK75100014 PM 1549109 ER PT J AU CARRIER, F OWENS, RA NEBERT, DW PUGA, A AF CARRIER, F OWENS, RA NEBERT, DW PUGA, A TI DIOXIN-DEPENDENT ACTIVATION OF MURINE CYP1A-1 GENE-TRANSCRIPTION REQUIRES PROTEIN KINASE-C-DEPENDENT PHOSPHORYLATION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID XENOBIOTIC RESPONSIVE ELEMENTS; EPIDERMAL GROWTH-FACTOR; CYTOCHROME P-450C GENE; AH RECEPTOR COMPLEX; HEPATOMA-CELL LINE; RAT-LIVER; DNA INTERACTIONS; AROMATIC-HYDROCARBONS; NUCLEOTIDE-SEQUENCE; CAUSES INCREASES AB Transcriptional activation of the murine Cyp1a-1 (cytochrome P(1)450) gene by inducers such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (dioxin) requires the aromatic hydrocarbon (Ah) receptor and the interaction of an inducer-receptor complex with one or more of the Ah-responsive elements (AhREs) located about 1 kb upstream from the transcriptional initiation site. We find that treatment of mouse hepatoma Hepa-1 cells with 2-aminopurine, an inhibitor of protein kinase activity, inhibits CYP1A1 mRNA induction by TCDD as well as the concomitant increase in CYP1A1 enzyme activity. Formation of DNA-protein complexes between the Ah receptor and its AhRE target is also inhibited by 2-aminopurine, as determined by gel mobility shift assays. Phosphorylation is required for the formation of Ah receptor-specific complexes, since in vitro dephosphorylation of nuclear extracts from TCDD-treated Hepa-1 cells abolishes the capacity of the Ah receptor to form specific complexes with its cognate AhRE sequences. To determine whether any one of several known protein kinases was involved in the transcriptional regulation of the Cyp1a-1 gene, we treated Hepa-1 cells with nine other protein kinase inhibitors prior to induction with TCDD; nuclear extracts from these cells were analyzed for their capacity to form specific DNA-protein complexes. Only extracts from cells treated with staurosporine, a protein kinase C inhibitor, were unable to form these complexes. In addition, staurosporine completely inhibited CYP1A1 mRNA induction by TCDD. Depletion of protein kinase C by prolonged treatment with phorbol ester led to the complete suppression of CYP1A1 mRNA induction by TCDD. We conclude that (i) phosphorylation is necessary for the formation of a transcriptional complex and for transcriptional activation of the Cyp1a-1 gene; (ii) the phosphorylation site(s) exists on at least one of the proteins constituting the transcriptional complex, possibly the Ah receptor itself; and (iii) the enzyme responsible for the phosphorylation is likely to be protein kinase C. C1 NICHHD,DEV PHARMACOL LAB,BETHESDA,MD 20892. RI Puga, Alvaro/B-7676-2008; Carrier, France/C-3063-2008 FU NIEHS NIH HHS [5F32 ESO5360 BI-7] NR 77 TC 157 Z9 158 U1 0 U2 0 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 1992 VL 12 IS 4 BP 1856 EP 1863 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HK751 UT WOS:A1992HK75100049 PM 1312672 ER PT J AU BARGON, J TRAPNELL, BC CHU, CS ROSENTHAL, ER YOSHIMURA, K GUGGINO, WB DALEMANS, W PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF BARGON, J TRAPNELL, BC CHU, CS ROSENTHAL, ER YOSHIMURA, K GUGGINO, WB DALEMANS, W PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI DOWN-REGULATION OF CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR GENE-EXPRESSION BY AGENTS THAT MODULATE INTRACELLULAR DIVALENT-CATIONS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PROTEIN-KINASE-C; AIRWAY EPITHELIA; CHLORIDE CHANNELS; IDENTIFICATION; CALCIUM; DIFFERENTIATION; TRANSPORT; DISEASE; CA-2+ AB In cystic fibrosis (CF), epithelial cells are unable to normally up-regulate apical membrane Cl- secretion in response to agents which increase cyclic AMP, but they do increase Cl- secretion in response to increases in intracellular Ca2+. Since intracellular divalent cations regulate the expression of many genes, we hypothesized that mobilization of intracellular Ca2+ and/or other divalent cations might modulate not only Ca2+-dependent Cl- channels but also cystic fibrosis transmembrane conductance regulator (CFTR) gene expression. To evaluate this concept, HT-29 human colon carcinoma cells were cultured under various conditions designed to manipulate intracellular divalent cation concentrations and CFTR gene expression was quantified at the levels of transcription, mRNA accumulation, mRNA half-life, and protein. Exposure to the divalent cation ionophores A23187 and ionomycin (agents which increase intracellular divalent cation concentrations) caused dose- and time-dependent reductions of CFTR mRNA levels, which could be blocked by the use of Ca2+- and Mg2+-free media. Ionophore-induced CFTR gene modulation was also observed with T84 human colon carcinoma cells and freshly isolated normal human bronchial epithelial cells. Incubation of HT-29 cells with thapsigargin, an agent that releases Ca2+ from intracellular stores, or in medium containing increased extracellular concentrations of Ca2+ or Mg2+ also caused down-regulation of CFTR mRNA levels. Transcription run-on analysis showed that, parallel with the decrease in CFTR mRNA levels, A23187 reduced the rate of transcription of the CFTR gene, while CFTR mRNA transcript half-life was unaffected. Consistent with the down-regulation of CFTR gene expression, CFTR protein levels also decreased after exposure to A23187. Thus, despite the independence of Ca2+-dependent Cl- channels and cyclic AMP-dependent CFTR-related Cl-channels in epithelial cells, increases in intracellular divalent cation concentrations down-regulate the expression of the CFTR gene at the transcriptional level, with consequent decreases in CFTR mRNA and protein. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,BALTIMORE,MD 21205. NHLBI,PULM BRANCH,BETHESDA,MD 20892. TRANSGENE SA,STRASBOURG,FRANCE. FU NHLBI NIH HHS [HL 47122, HL 40178] NR 41 TC 31 Z9 31 U1 0 U2 1 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 1992 VL 12 IS 4 BP 1872 EP 1878 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HK751 UT WOS:A1992HK75100051 PM 1372390 ER PT J AU TAKEMURA, M DONOVAN, DM UHL, GR AF TAKEMURA, M DONOVAN, DM UHL, GR TI PRIMARY AFFERENT STIMULATION ACTS THROUGH A 193 BASE PAIR PROMOTER REGION TO UP-REGULATE PREPROENKEPHALIN EXPRESSION IN DORSAL HORN OF TRANSGENIC MICE SO MOLECULAR BRAIN RESEARCH LA English DT Article DE PREPROENKEPHALIN; TRANSGENIC MOUSE; PAIN; TRIGEMINAL NERVE; TRANSSYNAPTIC REGULATION; ELECTRIC STIMULATION; ARTHRITIS; DORSAL HORN ID NUCLEUS CAUDALIS NEURONS; RAT SPINAL-CORD; GENE-EXPRESSION; PROENKEPHALIN GENE; MESSENGER-RNA; CYCLIC AMP; HYBRIDIZATION; INDUCTION; ELEMENT; PROTEIN AB The expression of the principal opioid peptide gene, preproenkephalin A, is exquisitely regulated by primary afferent inputs to the spinal and medullary dorsal horns. This regulated expression in response to neural synaptic activity has been referred to as trans-synaptic regulation. To define which DNA regions could mediate this trans-synaptic regulation, transgenic 'HEC' mice whose genomes include 193 bp of the human preproenkephalin A promoter fused to a chloramphenicol acetyltransferase (CAT) reporter gene were studied. Mice received unilateral electrical stimulation of the trigeminal ganglion or adjuvant injection into the hindpaw, stimuli known to regulate dorsal horn proenkephalin expression in vivo. CAT activity conferred by this promoter displayed trans-synaptic upregulation with both stimuli. Although the level of the upregulation was 2- to 3-fold higher than the change in the wild type gene, several features of this induction paralleled aspects of the behavior of the wild-type gene: the rapidity of responses to trigeminal ganglion stimulation, the stimulation intensity dependence of responses to trigeminal ganglion stimulation and the time course of upregulation noted following adjuvant injection. Regulatory proteins binding to this restricted promoter region are thus likely to mediate aspects of dorsal horn enkephalin regulation by pain and other somatic stimuli. C1 NIDA,ARC,MOLEC NEUROBIOL LAB,POB 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21224. NR 24 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 1992 VL 13 IS 3 BP 207 EP 212 DI 10.1016/0169-328X(92)90028-A PG 6 WC Neurosciences SC Neurosciences & Neurology GA HN030 UT WOS:A1992HN03000004 PM 1317494 ER PT J AU PAN, CJ SHELLY, LL RABIN, DS CHOU, JY AF PAN, CJ SHELLY, LL RABIN, DS CHOU, JY TI INHIBITION OF TYROSINE AMINOTRANSFERASE GENE-EXPRESSION BY RETINOIC ACID SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID MESSENGER-RNA STABILITY; LIVER-CELL LINE; PHOSPHOENOLPYRUVATE CARBOXYKINASE; RESPONSIVE ELEMENT; RECEPTOR; RAT; IDENTIFICATION; TRANSCRIPTION; DIFFERENTIATION; INDUCTION AB Regulation of tyrosine aminotransferase (TAT) gene expression was examined in RALA255-10G, a simian virus-40 tsA mutant-immortalized adult rat hepatocyte line. At the nonpermissive temperature (40 C), these hepatocytes exhibited a differentiated phenotype and actively expressed the TAT gene, but only in the presence of dexamethasone (DEX). The glucocorticoid-mediated TAT expression was inhibited by cycloheximide, a protein synthesis inhibitor, and by RU486, a glucocorticoid antagonist, suggesting that glucocorticoid induction requires protein synthesis and may be mediated through hormone receptors. (Bu)2cAMP (Bt2cAMP) or retinoic acid, individually or in combination, failed to increase TAT mRNA levels. However, Bt2cAMP greatly potentiated the induction by DEX, whereas retinoic acid inhibited the induction by DEX or DEX/Bt2cAMP. Nuclear run-on assays demonstrated that the induction of TAT expression by DEX or DEX/Bt2cAMP in RALA255-10G cells is regulated primarily at the transcriptional level. In contrast, retinoic acid antagonized the DEX- or DEX/Bt2cAMP-mediated induction without affecting the rate of TAT gene transcription. Instead, retinoic acid destabilized TAT mRNA. The half-life values of TAT mRNA in DEX/Bt2cAMP- and DEX/Bt2cAMP/retinoic acid-treated cells were approximately 235-270 min and 90-100 min, respectively. Our results indicate that inhibition of TAT expression by retinoic acid was regulated primarily at the posttranscriptional level. C1 NICHHD,HUMAN GENET BRANCH,BLDG 10,ROOM 95242,BETHESDA,MD 20892. NR 54 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 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD APR PY 1992 VL 6 IS 4 BP 572 EP 580 DI 10.1210/me.6.4.572 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HQ337 UT WOS:A1992HQ33700010 PM 1350056 ER PT J AU SHIMADA, S CUTTING, G UHL, GR AF SHIMADA, S CUTTING, G UHL, GR TI GAMMA-AMINOBUTYRIC-ACID A-RECEPTOR OR C-RECEPTOR - GAMMA-AMINOBUTYRIC-ACID RHO-1 RECEPTOR RNA INDUCES BICUCULLINE-INSENSITIVE, BARBITURATE-INSENSITIVE, AND BENZODIAZEPINE-INSENSITIVE GAMMA-AMINOBUTYRIC-ACID RESPONSES IN XENOPUS OOCYTES SO MOLECULAR PHARMACOLOGY LA English DT Article ID OPTIC TECTUM INVITRO; ALPHA-SUBUNIT; FUNCTIONAL EXPRESSION; SYNAPTIC TRANSMISSION; ION CHANNELS; GABAA; PHARMACOLOGY; BRAIN; HETEROGENEITY; POTENTIATION AB Xenopus oocyte expression of the recently cloned gamma-aminobutyric acid (GABA) rho-1 receptor subunit cDNA yields a pharmacologic profile characteristic of the GABAc responses described by Johnston [Benzodiazepine/GABA Receptors and Chloride Channels. Receptor Biochemistry and Methodology (R. W. Olsen and J. C. Venter, eds.), Vol. 5. Alan R. Liss, New York, 57-71 (1986)] and the responses to retinal mRNA recently reported in the Xenopus expression system [Proc. Natl. Acad. Sci. USA 88:4318-4322 (1991)]. A rationale for defining GABA rho-1 as forming a GABAc receptor is discussed. C1 NIDA,ARC,MOLEC NEUROBIOL LAB,BOX 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT GENET,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. NR 33 TC 217 Z9 220 U1 0 U2 1 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 1992 VL 41 IS 4 BP 683 EP 687 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HP405 UT WOS:A1992HP40500014 PM 1314944 ER PT J AU SCHULTE, PA BOENIGER, M WALKER, JT SCHOBER, SE PEREIRA, MA GULATI, DK WOJCIECHOWSKI, JP GARZA, A FROELICH, R STRAUSS, G HALPERIN, WE HERRICK, R GRIFFITH, J AF SCHULTE, PA BOENIGER, M WALKER, JT SCHOBER, SE PEREIRA, MA GULATI, DK WOJCIECHOWSKI, JP GARZA, A FROELICH, R STRAUSS, G HALPERIN, WE HERRICK, R GRIFFITH, J TI BIOLOGIC MARKERS IN HOSPITAL WORKERS EXPOSED TO LOW-LEVELS OF ETHYLENE-OXIDE SO MUTATION RESEARCH LA English DT Article DE ETHYLENE OXIDE; BIOLOGIC MARKERS ID SISTER-CHROMATID EXCHANGES; CHROMOSOME-ABERRATIONS; OCCUPATIONAL EXPOSURE; HEMOGLOBIN ADDUCTS; RABBIT LYMPHOCYTES; INHALATION; MICRONUCLEI; MORTALITY; INDUCTION; CELLS AB Operators of hospital sterilizers that use ethylene oxide were studied to determine if there was a relationship between exposure and a battery of biological markers. A total of 73 workers from nine hospitals in the United States (U.S.) and one hospital in Mexico City was evaluated for ethylene oxide exposure during four months prior to collection of peripheral blood. The frequency of hemoglobin adducts (p = 0.0006) and sister-chromatid exchanges (SCEs) (p = 0.002) increased with cumulative exposure to ethylene oxide in U.S. subjects when controlling by regression analysis for various confounding factors, including cigarette smoking. Hemoglobin adducts, but not SCEs, were also increased in Mexican subjects (p = 0.0012). Chromosomal micronuclei showed no consistent relationship with exposure. The U.S. study participants were classified by four-month cumulative exposure levels of 0 ppm-h (n = 8), greater than 0 to 32 ppm-h (n = 32) and greater than 32 ppm-h (n = 11) of ethylene oxide exposure. The group with an exposure of greater than 32 ppm-h had an increased frequency of hemoglobin adducts (p = 0.002) and SCEs (p = 0.0001) compared to the nonexposed group. The estimated mean of the 8-h time-weighted average (8-h TWA) exposure levels for the highest U.S. exposure group (> 32 ppm-h) was 0.16 +/- 0.007 ppm (mean +/- SD). A similar exposure-related differential was observed in the Mexican subjects for hemoglobin adducts (p = 0.04) but not for SCEs. The latter finding may have been due to longer shipping times for the specimens in the cytogenetic assays. The estimated mean of the 8-h TWA exposure levels for the highest Mexican exposure group (> 32 ppm-h) was 0.48 +/- 0.08 ppm, This study is the third to suggest that exposures less than the U.S. OSHA standard of 1 ppm 8-h TWA result in biochemical and biologic changes. It is not known whether these changes may be indicative of increased risk of disease; however, they do appear to reflect exposure to relatively low levels of ethylene oxide. The exact meaning of these changes is unknown. C1 NIDA,LEXINGTON,KY 40583. ENVIRONM HLTH RES & TESTING INC,RES TRIANGLE PK,NC. LOS ANGELES CTY DEPT HLTH SERV,LOS ANGELES,CA. US EPA,WASHINGTON,DC 20460. RP SCHULTE, PA (reprint author), NIOSH,IND WIDE STUDIES BRANCH,4676 COLUMBIA PKWY,MS R42,CINCINNATI,OH 45226, USA. NR 49 TC 32 Z9 33 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD APR PY 1992 VL 278 IS 4 BP 237 EP 251 PG 15 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HN037 UT WOS:A1992HN03700003 PM 1373860 ER PT J AU DASTON, D HINES, K RUDD, C CASPARY, W AF DASTON, D HINES, K RUDD, C CASPARY, W TI EXPRESSION OF CHEMICALLY-INDUCED MUTATIONS IN MAMMALIAN-CELLS USING AN INSITU PROCEDURE 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 1992 VL 271 IS 2 BP 152 EP 153 DI 10.1016/0165-1161(92)91174-P PG 2 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HN597 UT WOS:A1992HN59700092 ER PT J AU KLIGERMAN, AD ALLEN, JW BRYANT, MF CAMPBELL, JA COLLINS, BW DOERR, CL EREXSON, GL KWANYUEN, P MORGAN, DL AF KLIGERMAN, AD ALLEN, JW BRYANT, MF CAMPBELL, JA COLLINS, BW DOERR, CL EREXSON, GL KWANYUEN, P MORGAN, DL TI CYTOGENETIC STUDIES OF MICE EXPOSED TO STYRENE BY INHALATION SO MUTATION RESEARCH LA English DT Meeting Abstract C1 ENVIRONM HLTH RES & TESTING INC,RES TRIANGLE PK,NC. US EPA,RES TRIANGLE PK,NC 27711. NIEHS,RES TRIANGLE PK,NC 27709. 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 1992 VL 271 IS 2 BP 173 EP 173 DI 10.1016/0165-1161(92)91223-E PG 1 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HN597 UT WOS:A1992HN59700141 ER PT J AU DILLON, DM MCGREGOR, DB COMBES, RD ZEIGER, E AF DILLON, DM MCGREGOR, DB COMBES, RD ZEIGER, E TI OPTIMAL CONDITIONS FOR DETECTING BACTERIAL MUTAGENICITY OF SOME ALDEHYDES AND PEROXIDES SO MUTATION RESEARCH LA English DT Meeting Abstract C1 INVERESK RES INT LTD,TRANENT,SCOTLAND. NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 1 Z9 1 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 1992 VL 271 IS 2 BP 184 EP 184 DI 10.1016/0165-1161(92)91253-N PG 1 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA HN597 UT WOS:A1992HN59700172 ER PT J AU SELTZER, A PINTO, JEB VIGLIONE, PN CORREA, FMA LIBERTUN, C TSUTSUMI, K STEELE, MK SAAVEDRA, JM AF SELTZER, A PINTO, JEB VIGLIONE, PN CORREA, FMA LIBERTUN, C TSUTSUMI, K STEELE, MK SAAVEDRA, JM TI ESTROGENS REGULATE ANGIOTENSIN-CONVERTING ENZYME AND ANGIOTENSIN RECEPTORS IN FEMALE RAT ANTERIOR-PITUITARY SO NEUROENDOCRINOLOGY LA English DT Article DE RENIN-ANGIOTENSIN SYSTEM; REPRODUCTIVE HORMONES; KININASE-II; HYPOPHYSIS; ESTRADIOL; ESTROUS CYCLE; OVARIES; QUANTITATIVE AUTORADIOGRAPHY ID QUANTITATIVE AUTORADIOGRAPHIC DETERMINATION; II BINDING-SITES; PROLACTIN-RELEASE; BRATTLEBORO RATS; ADRENAL-GLANDS; DISCRETE AREAS; KININASE-II; BRAIN; RENIN; MODULATION AB We studied the effects of the estrous cycle, ovariectomy and estrogen replacement on angiotensin-converting enzyme (ACE) (kininase II, EC 3.4.15.1) and angiotensin II (AT) receptors in the pituitary gland of the female rat. Quantitative autoradiography, with the use of consecutive pituitary sections, allowed for simultaneous determination of changes in binding and in the potential AT synthetic ability of individual pituitaries, and for a correlation between these two phenomena. In the anterior pituitary, ACE activity and binding of the ACE inhibitor [I-125]-351A were not changed during the estrous cycle. Ovariectomy produced a significant increase in ACE activity and binding, and both of these parameters returned to normal after estrogen replacement. There were no changes in ACE activity or binding in the posterior pituitary during the estrous cycle or after ovariectomy or hormone replacement. AT receptors were characterized as of the AT1 type, since they were displaced by the selective AT1 antagonist DuP 753 and not by the AT2 competitor PD 123177. There were marked changes in the concentration of AT1 receptors during the estrous cycle, with highest numbers in metestrus, lower in estrus and diestrus, and lowest during proestrus. Estrogen replacement in ovariectomized rats decreased AT1 receptor number in the anterior pituitary. Our results indicate a dual effect of estrogen on anterior pituitary AT, physiologically on AT receptor expression and pharmacologically on ACE activity. C1 UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL,SAN FRANCISCO,CA 94143. RP SELTZER, A (reprint author), NIMH,CLIN SCI LAB,PHARMACOL SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2D-45,BETHESDA,MD 20892, USA. RI Correa, Fernando /D-1614-2012 OI Correa, Fernando /0000-0003-4067-9524 NR 47 TC 67 Z9 70 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD APR PY 1992 VL 55 IS 4 BP 460 EP 467 DI 10.1159/000126157 PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA HL372 UT WOS:A1992HL37200014 PM 1314339 ER PT J AU DRAVET, C JULIAN, C LEGRAS, C MAGAUDDA, A GUERRINI, R GENTON, P SOULAYROL, S GIRAUD, N MESDJIAN, E TRENTIN, G ROGER, J AYME, S AF DRAVET, C JULIAN, C LEGRAS, C MAGAUDDA, A GUERRINI, R GENTON, P SOULAYROL, S GIRAUD, N MESDJIAN, E TRENTIN, G ROGER, J AYME, S TI EPILEPSY, ANTIEPILEPTIC DRUGS, AND MALFORMATIONS IN CHILDREN OF WOMEN WITH EPILEPSY - A FRENCH PROSPECTIVE COHORT STUDY SO NEUROLOGY LA English DT Article ID ANTICONVULSANT DRUGS; FACIAL CLEFTS; TERATOGENICITY; PREGNANCY; EXPOSURE; DEFECTS; HEART; RISK AB We conducted a prospective study of teratogenic effects of antiepileptic drugs (AEDs) in pregnant women with epilepsy in southeast France, comparing malformation rates with those collected by a birth defects registry. We evaluated isolated microcephalies separately. Malformations were seen in 7% of infants of mothers with epilepsy (IME) and in 1.36% of the general population. No significant relationship was found between type and severity of epilepsy and occurrence of malformations or isolated microcephaly. Valproate and phenytoin were the most teratogenic (all malformations). None of the malformations observed in IME whose mothers received valproate, phenytoin, or phenobarbital was seen in IME not exposed to the respective AEDs. Phenytoin plus phenobarbital was more teratogenic than phenobarbital alone. Benzodiazepines, prescribed only in combinations, had a borderline, nonspecific effect on microcephaly. C1 NIH,MED RES,CTR ST PAUL,BETHESDA,MD 20892. NIH,U 242 CTR GENET MED,BETHESDA,MD 20892. UNIV MESSINA,INST NEUROL & NEUROSURG SCI,1ST NEUROL CLIN,MESSINA,ITALY. UNIV PISA,INST CHILD NEUROL & PSYCHIAT,I-56100 PISA,ITALY. PORTO ALEGRO UNIV CTR,PORTO ALEGRE,BRAZIL. OI magaudda, adriana/0000-0001-9862-8493 NR 50 TC 61 Z9 62 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1992 VL 42 IS 4 SU 5 BP 75 EP 82 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA HT750 UT WOS:A1992HT75000012 PM 1574181 ER PT J AU MULLOL, J RIEVES, RD BARANIUK, JN LUNDGREN, JD MERIDA, M HAUSFELD, JH SHELHAMER, JH KALINER, MA AF MULLOL, J RIEVES, RD BARANIUK, JN LUNDGREN, JD MERIDA, M HAUSFELD, JH SHELHAMER, JH KALINER, MA TI THE EFFECTS OF NEUROPEPTIDES ON MUCOUS GLYCOPROTEIN-SECRETION FROM HUMAN NASAL-MUCOSA INVITRO SO NEUROPEPTIDES LA English DT Article ID GENE-RELATED PEPTIDE; VASOACTIVE-INTESTINAL-PEPTIDE; GASTRIN-RELEASING PEPTIDE; PERIPHERAL NORADRENERGIC NEURONS; HUMAN AIRWAYS INVITRO; SUBSTANCE-P; GLYCOCONJUGATE; COEXISTENCE; VASODILATOR; POLYPEPTIDE AB The role of neuropeptides in the regulation of macromolecule secretion from human nasal mucosa is incompletely understood. Previous in vitro explant culture studies have demonstrated the effects of neuropeptides on lactoferrin release from serous cells and H-3-glucosamine labeled respiratory glycoconjugate secretion from mucus-containing cells. The generation of a new monoclonal antibody, 7F10, has led to the development of an ELISA for high molecular weight respiratory mucous glycoproteins (MGP). This ELISA was used to measure the ability of sensory, parasympathetic and sympathetic neuropeptides to stimulate MGP release from human nasal mucosal fragments in short term explant culture in vitro. Significant MGP release was stimulated by the sensory neuropeptides gastrin releasing peptide (10-mu-M GRP: 10.6% +/- 2.4% increase, n = 8, P < 0.01 vs. control), substance P (1-mu-M SP: 12.5% +/- 5.4%, n = 11, P < 0.05), neurokinin A (1-mu-M NKA: 17.8 +/- 4.3%, n = 6, P < 0.01), while calcitonin gene related peptide (CGRP) was without effect. Vasoactive intestinal peptide (VIP), a neurotransmitter from parasympathetic nerves, induced significant dose dependent MGP secretion, but had no additive or inhibitory interaction with methacholine-induced secretion. Neuropeptide Y (NPY), present in sympathetic nerves, had no effect on MGP secretion. These observations correlate with the effects of neuropeptides on serous cell lactoferrin secretion, and the presence of specific GRP, SP, and VIP binding sites on human nasal submucosal glands that have been detected by autoradiography. GRP and tachykinins (SP and NKA) from sensory nerves, and VIP released during parasympathetic reflexes may signficantly stimulate mucous and serous cell secretion from human nasal mucosa in vivo. C1 NIAMDD,CLIN INVEST LAB,ALLERG DIS SECT,BLDG 10,ROOM 11-C-205,BETHESDA,MD 20892. NIH,CLIN CTR,DEPT CRIT CARE,BETHESDA,MD 20892. OI Lundgren, Jens/0000-0001-8901-7850 NR 54 TC 29 Z9 30 U1 0 U2 2 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0143-4179 J9 NEUROPEPTIDES JI Neuropeptides PD APR PY 1992 VL 21 IS 4 BP 231 EP 238 DI 10.1016/0143-4179(92)90027-T PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA HN424 UT WOS:A1992HN42400005 PM 1381497 ER PT J AU ERICKSON, JD LLOYD, R TROJANOWSKI, JQ IACANGELO, A EIDEN, E AF ERICKSON, JD LLOYD, R TROJANOWSKI, JQ IACANGELO, A EIDEN, E TI SITES OF SYNTHESIS OF CHROMOGRANIN-A AND CHROMOGRANIN-B IN THE HUMAN BRAIN SO NEUROPEPTIDES LA English DT Article ID CENTRAL NERVOUS-SYSTEM; NEURO-ENDOCRINE CELLS; HUMAN ADRENAL-MEDULLA; MESSENGER-RNA; IMMUNOHISTOCHEMICAL LOCALIZATION; REGIONAL DISTRIBUTION; CHROMAFFIN GRANULES; SECRETOGRANIN-I; IMMUNOLOGICAL CHARACTERIZATION; BOVINE ENDOCRINE AB The sites of synthesis of the chromogranins A and B, and their potential processed peptides, were examined by quantitating the levels of chromogranin A and B mRNA in various regions of the human brain by Northern blot analysis. Chromogranin A and B mRNA expression in the brain is region-specific and confined to grey matter. In situ hybridization histochemistry detected chromogranin A and B mRNA in pyramidal neurons of human cerebral cortex. Cell-specific expression in subpopulations of cerebrocortical neurons suggest that chromogranin A and B gene products may play a role in central neuronal function. C1 UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109. UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. RP ERICKSON, JD (reprint author), NIMH,ADAMHA,CELL BIOL LAB,MOLEC & CELLULAR NEUROBIOL UNIT,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA36245]; NIA NIH HHS [AG09215] NR 46 TC 20 Z9 20 U1 0 U2 1 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0143-4179 J9 NEUROPEPTIDES JI Neuropeptides PD APR PY 1992 VL 21 IS 4 BP 239 EP 244 DI 10.1016/0143-4179(92)90028-U PG 6 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA HN424 UT WOS:A1992HN42400006 PM 1518561 ER PT J AU DURCAN, MJ LISTER, RG LINNOILA, M AF DURCAN, MJ LISTER, RG LINNOILA, M TI THE EFFECTS OF 2 DIFFERENT INHIBITORS OF PNMT AND THEIR INTERACTIONS WITH ETHANOL SO NEUROREPORT LA English DT Article DE PHENYLETHANOLAMINE-N-METHYLTRANSFERASE (PNMT); ETHANOL; LOCOMOTION; EXPLORATION; ATAXIA ID PHENYLETHANOLAMINE-N-METHYLTRANSFERASE; EPINEPHRINE NEURONS; ADRENALIN NEURONS; RAT-BRAIN AB THE effects of two structurally different inhibitors of phenylethanolamine-N-methyltransferase, LY 134046 and CGS 19281A were investigated in a holeboard test of directed exploration and locomotor activity. Both compounds dose-dependently reduced exploratory head-dipping without affecting locomotor activity. The interaction of each drug with ethanol was also studied by testing the ataxia. Administration of these compounds had differential effects in a test of ethanol-induced ataxia. LY 134046 significantly attenuated ethanol-induced ataxia whereas CGS 19281A was without effect or (at 50 mg kg-1) potentiated ethanol's effect. These results suggest that the ethanol attenuating properties of LY 134046 may not solely be due the inhibition of PNMT and that its alpha(2)-adrenoceptor blocking properties may be playing a role. RP DURCAN, MJ (reprint author), NIAAA,DICBR,CLIN STUDIES LAB,BLG 10 RM 3C218,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 14 TC 3 Z9 3 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD APR PY 1992 VL 3 IS 4 BP 349 EP 352 DI 10.1097/00001756-199204000-00015 PG 4 WC Neurosciences SC Neurosciences & Neurology GA HP935 UT WOS:A1992HP93500015 PM 1515594 ER PT J AU LONG, EO AF LONG, EO TI ANTIGEN PROCESSING FOR PRESENTATION TO CD4+ T-CELLS SO NEW BIOLOGIST LA English DT Review DE ANTIGEN PROCESSING; ENDOCYTOSIS; INVARIANT CHAIN; MHC CLASS-II MOLECULES; LYMPHOCYTES-T ID MHC CLASS-II; MAJOR HISTOCOMPATIBILITY COMPLEX; PEPTIDE-BINDING-PROTEIN; HEN EGG LYSOZYME; HLA-DR MOLECULES; INVARIANT CHAIN; INFLUENZA-VIRUS; RESTRICTED PRESENTATION; ENDOPLASMIC-RETICULUM; ENDOGENOUS ANTIGEN RP LONG, EO (reprint author), NIAID,IMMUNOGENET LAB,MOLEC IMMUNOL SECT,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. RI Long, Eric/G-5475-2011 OI Long, Eric/0000-0002-7793-3728 NR 87 TC 30 Z9 30 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 1992 VL 4 IS 4 BP 274 EP 282 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR312 UT WOS:A1992JR31200002 PM 1535789 ER PT J AU REIN, A LEVIN, JG AF REIN, A LEVIN, JG TI READTHROUGH SUPPRESSION IN THE MAMMALIAN TYPE-C RETROVIRUSES AND WHAT IT HAS TAUGHT US SO NEW BIOLOGIST LA English DT Review DE RETROVIRUSES; TRANSLATIONAL SUPPRESSION; PSEUDOKNOTS; SUPPRESSOR TRANSFER RNAS ID MURINE LEUKEMIA-VIRUS; TOBACCO MOSAIC-VIRUS; RIBOSOMAL FRAMESHIFTING SIGNAL; UGA TERMINATION CODONS; GLUTAMINE TRANSFER-RNA; POL FUSION PROTEIN; GENE AMBER CODON; NUCLEOTIDE-SEQUENCE; TRANSLATIONAL READTHROUGH; ESCHERICHIA-COLI C1 NICHHD, MOLEC GENET LAB, BETHESDA, MD 20892 USA. RP REIN, A (reprint author), NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N01-CO-74101] NR 56 TC 13 Z9 13 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 1043-4674 J9 NEW BIOL PD APR PY 1992 VL 4 IS 4 BP 283 EP 289 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR312 UT WOS:A1992JR31200003 PM 1320396 ER PT J AU WOLFFE, AP TAFURI, S RANJAN, M FAMILARI, M AF WOLFFE, AP TAFURI, S RANJAN, M FAMILARI, M TI THE Y-BOX FACTORS - A FAMILY OF NUCLEIC-ACID BINDING-PROTEINS CONSERVED FROM ESCHERICHIA-COLI TO MAN SO NEW BIOLOGIST LA English DT Review ID XENOPUS-LAEVIS OOCYTES; SINGLE-STRANDED DNA; FILAMENTOUS BACTERIOPHAGE IKE; HISTONE-LIKE PROTEINS; TRANSCRIPTION FACTOR; MESSENGER-RNA; 5S RNA; DEVELOPMENTAL REGULATION; MAGNETIC-RESONANCE; MOLECULAR-CLONING RP WOLFFE, AP (reprint author), NICHHD,MOLEC EMBRYOL LAB,BLDG 6,ROOM 131,BETHESDA,MD 20892, USA. NR 75 TC 258 Z9 263 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 1992 VL 4 IS 4 BP 290 EP 298 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR312 UT WOS:A1992JR31200004 PM 1622927 ER PT J AU HOROWITZ, JA HARFORD, JB AF HOROWITZ, JA HARFORD, JB TI THE SECONDARY STRUCTURE OF THE REGULATORY REGION OF THE TRANSFERRIN RECEPTOR MESSENGER-RNA DEDUCED BY ENZYMATIC CLEAVAGE SO NEW BIOLOGIST LA English DT Article DE IRON METABOLISM; RNA DEGRADATION; RNA STRUCTURE ID IRON-RESPONSIVE ELEMENT; 3' UNTRANSLATED REGION; CYTOSOLIC PROTEIN; STABILITY; BINDING; TRANSLATION; DETERMINANT; PREDICTION RP HOROWITZ, JA (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 19 TC 11 Z9 11 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 1992 VL 4 IS 4 BP 330 EP 338 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR312 UT WOS:A1992JR31200010 PM 1320397 ER PT J AU TAFURI, SR WOLFFE, AP AF TAFURI, SR WOLFFE, AP TI DNA-BINDING, MULTIMERIZATION, AND TRANSCRIPTION STIMULATION BY THE XENOPUS-Y BOX PROTEINS INVITRO SO NEW BIOLOGIST LA English DT Article DE PROTEIN MOTIFS; TRANSCRIPTION; XENOPUS; Y-BOX ID HISTONE-LIKE PROTEINS; RNA-POLYMERASE; REGULATORY ELEMENTS; MOLECULAR-CLONING; ESCHERICHIA-COLI; NUCLEOSOME CORE; HSP70 GENE; PROMOTER; SHOCK; EXPRESSION C1 NICHHD,MOLEC EMBRYOL LAB,BLDG 6,ROOM 131,BETHESDA,MD 20892. NR 41 TC 94 Z9 96 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 1992 VL 4 IS 4 BP 349 EP 359 PG 11 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR312 UT WOS:A1992JR31200012 PM 1622930 ER PT J AU DONIGER, J LANDSMAN, D GONDA, MA WISTOW, G AF DONIGER, J LANDSMAN, D GONDA, MA WISTOW, G TI THE PRODUCT OF UNR, THE HIGHLY CONSERVED GENE UPSTREAM OF N-RAS, CONTAINS MULTIPLE REPEATS SIMILAR TO THE COLD-SHOCK DOMAIN (CSD), A PUTATIVE DNA-BINDING MOTIF SO NEW BIOLOGIST LA English DT Article ID FILAMENTOUS BACTERIOPHAGE IKE; NUCLEAR MAGNETIC-RESONANCE; ESCHERICHIA-COLI; SECONDARY STRUCTURE; MOLECULAR-CLONING; CRYSTAL-STRUCTURE; Y-BOX; PROTEIN; SEQUENCE; COMPLEX C1 NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BLDG 38A, ROOM 8N807, BETHESDA, MD 20894 USA. GEORGETOWN UNIV, MED CTR, DEPT OBSTET & GYNECOL, WASHINGTON, DC 20007 USA. NCI, FREDERICK CANC RES & DEV CTR,DYN CORP, PROGRAM RESOURCES INC,CELL & MOLEC STRUCT LAB, FREDERICK, MD 21702 USA. RI Landsman, David/C-5923-2009; OI Landsman, David/0000-0002-9819-6675 FU NCI NIH HHS [N01-CO-74102] NR 38 TC 27 Z9 29 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 1043-4674 J9 NEW BIOL PD APR PY 1992 VL 4 IS 4 BP 389 EP 395 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR312 UT WOS:A1992JR31200016 PM 1622933 ER PT J AU VINSON, CR GARCIA, KC AF VINSON, CR GARCIA, KC TI MOLECULAR-MODEL FOR DNA RECOGNITION BY THE FAMILY OF BASIC HELIX LOOP HELIX ZIPPER PROTEINS SO NEW BIOLOGIST LA English DT Article ID C-MYC PROTEIN; LEUCINE-ZIPPER; BINDING PROTEINS; MOTIF; DOMAIN; REGION; MYOD; TRANSCRIPTION; PREFERENCES; ACTIVATION C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOPHYS & BIOPHYS CHEM,BALTIMORE,MD 21205. RP VINSON, CR (reprint author), NCI,BIOCHEM LAB,BETHESDA,MD 20892, USA. NR 34 TC 47 Z9 47 U1 1 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 1992 VL 4 IS 4 BP 396 EP 403 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR312 UT WOS:A1992JR31200017 PM 1622934 ER PT J AU BOGUSKI, MS MURRAY, AW POWERS, S AF BOGUSKI, MS MURRAY, AW POWERS, S TI NOVEL REPETITIVE SEQUENCE MOTIFS IN THE ALPHA AND BETA SUBUNITS OF PRENYL-PROTEIN TRANSFERASES AND HOMOLOGY OF THE ALPHA SUBUNIT TO THE MAD2 GENE-PRODUCT OF YEAST SO NEW BIOLOGIST LA English DT Letter ID PEPTIDE-BINDING; RAS PROTEINS; SNAP HELIX; FARNESYLTRANSFERASE; EXPRESSION; ALIGNMENT; DNA; CLONING; MITOSIS; CELLS C1 UNIV MED & DENT, ROBERT WOOD JOHNSON MED SCH, DEPT BIOCHEM, PISCATAWAY, NJ 08854 USA. UNIV CALIF SAN FRANCISCO, DEPT BIOCHEM & BIOPHYS, SAN FRANCISCO, CA 94143 USA. UNIV CALIF SAN FRANCISCO, DEPT PHYSIOL, SAN FRANCISCO, CA 94143 USA. RP NIH, NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA. NR 33 TC 31 Z9 33 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 1043-4674 J9 NEW BIOL PD APR PY 1992 VL 4 IS 4 BP 408 EP 411 PG 4 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA JR312 UT WOS:A1992JR31200019 PM 1622936 ER PT J AU WOODWORTH, CD CHENG, ST SIMPSON, S HAMACHER, L CHOW, LT BROKER, TR DIPAOLO, JA AF WOODWORTH, CD CHENG, ST SIMPSON, S HAMACHER, L CHOW, LT BROKER, TR DIPAOLO, JA TI RECOMBINANT RETROVIRUSES ENCODING HUMAN PAPILLOMAVIRUS TYPE-18 E6 AND E7 GENES STIMULATE PROLIFERATION AND DELAY DIFFERENTIATION OF HUMAN KERATINOCYTES EARLY AFTER INFECTION SO ONCOGENE LA English DT Article ID HUMAN EPIDERMAL-KERATINOCYTES; HUMAN FORESKIN KERATINOCYTES; SERUM-FREE MEDIUM; EPITHELIAL-CELLS; TERMINAL DIFFERENTIATION; CERVICAL-CARCINOMA; GENITAL CANCER; GROWTH; DNA; TRANSFORMATION AB Human papillomavirus (HPV) DNAs are detected in most genital dysplasias and cancers, suggesting that these viruses perturb epithelial growth and differentiation. The E6 and E7 genes of HPV type 18 induce immortality in keratinocytes cultured from genital tract epithelia, and the immortal cell lines display aberrant squamous differentiation. To examine whether the E6 and E7 proteins directly alter keratinocyte growth and differentiation, high-titer recombinant retroviruses were constructed for efficient transfer and expression of HPV-18 genes E6, E6* and E7 in cultures of normal human keratinocytes. Infection with retroviruses encoding E6 and E7 stimulated cell proliferation, reduced the requirement for bovine pituitary extract and induced immortality. E6 and E7 also delayed but did not prevent the onset of terminal squamous differentiation. The magnitude of effects on growth and differentiation of cultured cells was directly related to levels of E7 protein expression. Thus, expression of the HPV-18 E6 and E7 genes stimulates cell proliferation and delays differentiation of keratinocytes in vitro. C1 UNIV ROCHESTER,SCH MED,DEPT BIOCHEM,ROCHESTER,NY 14642. RP WOODWORTH, CD (reprint author), NCI,BIOL LAB,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA36200] NR 57 TC 72 Z9 73 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1992 VL 7 IS 4 BP 619 EP 626 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HQ682 UT WOS:A1992HQ68200002 PM 1314365 ER PT J AU SELS, FT LANGER, S SCHULZ, AS SILVER, J SITBON, M FRIEDRICH, RW AF SELS, FT LANGER, S SCHULZ, AS SILVER, J SITBON, M FRIEDRICH, RW TI FRIEND MURINE LEUKEMIA-VIRUS IS INTEGRATED AT A COMMON SITE IN MOST PRIMARY SPLEEN TUMORS OF ERYTHROLEUKEMIC ANIMALS SO ONCOGENE LA English DT Article ID MOUSE MYELOBLASTIC LEUKEMIAS; PUTATIVE ONCOGENE; THYMIC LYMPHOMAS; CELL-LINES; DNA; ACTIVATION; SPI-1; PROGRESSION; EXPRESSION; POLYMERASE AB A common proviral integration site was identified and characterized in erythroleukaemias induced by Friend murine leukaemia virus (F-MuLV). Using inverse polymerase chain reaction, we found a proviral integration site common to at least 90% of 20 primary tumours tested. This site was identical to Fli-1, a locus recently reported by others to be rearranged in 75% (9/12) of cell lines established from spleens of erythroleukaemic mice and to code for a member of the ets gene family. Our data suggest that about half of the F-MuLV-induced erythroleukaemias contained more than one cell clone with a proviral integration in Fli-1, with different individual integration sites within Fli-1 in each cell clone. All proviruses were found to be integrated in the same transcriptional orientation with respect to flanking cellular DNA. We discuss these findings in relation to multistage models of neoplasm. C1 UNIV GIESSEN,INST MED VIROL,FRANKFURTER STR 107,W-6300 GIESSEN,GERMANY. HOP COCHIN,INSERM,U152,ICGM,IMMUNOL & ONCOL MALADIES RETROVIRALES LAB,F-75674 PARIS 14,FRANCE. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RI Sitbon, Marc/A-6771-2010 OI Sitbon, Marc/0000-0003-3616-2338 NR 39 TC 23 Z9 23 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1992 VL 7 IS 4 BP 643 EP 652 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HQ682 UT WOS:A1992HQ68200005 PM 1565463 ER PT J AU THOMPSON, PA GUTKIND, JS ROBBINS, KC LEDBETTER, JA BOLEN, JB AF THOMPSON, PA GUTKIND, JS ROBBINS, KC LEDBETTER, JA BOLEN, JB TI IDENTIFICATION OF DISTINCT POPULATIONS OF PI-3 KINASE-ACTIVITY FOLLOWING T-CELL ACTIVATION SO ONCOGENE LA English DT Article ID PROTEIN-TYROSINE KINASE; FACTOR-I RECEPTOR; PHOSPHATIDYLINOSITOL KINASE; SIGNAL TRANSDUCTION; HUMAN PLATELETS; ANTIGEN RECEPTOR; CD4 RECEPTOR; PDGF RECEPTOR; RAT-LIVER; ASSOCIATION AB Activation of mature CD4+ T lymphocytes by antigen-presenting cells involves engagement of the CD3/T-cell antigen receptor complex along with the CD4 surface glycoprotein and the phosphorylation of cellular proteins on tyrosine residues leading to stimulation of a variety of cellular second-messenger systems. Several recent studies have implicated non-receptor protein tyrosine kinases of the src family, especially p56lck and p59fyn, in mediating at least a portion of these tyrosine phosphorylation events. In the present study we have examined the involvement of one type of second-messenger system, phosphatidylinositol-3 kinase (PI-3 kinase), in signal transduction during antibody-induced activation of normal resting human CD4+ T cells. We demonstrate that PI-3 kinase activity is increased following co-approximation of CD4 with the T-cell receptor and that PI-3 kinase activity co-precipitates with the CD4-p56lck complex. We also show that following T-cell activation a complex containing PI-3 kinase activity can be demonstrated in CD3-epsilon-immunoprecipitates which is distinct from that which interacts with p56lck. C1 BRISTOL MYERS SQUIBB PHARMACEUT RES INST,DEPT MOLEC BIOL,POB 4000,PRINCETON,NJ 08543. NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121. RI Gutkind, J. Silvio/A-1053-2009 NR 59 TC 60 Z9 60 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1992 VL 7 IS 4 BP 719 EP 725 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HQ682 UT WOS:A1992HQ68200014 PM 1373484 ER PT J AU BODNER, SM MINNA, JD JENSEN, SM DAMICO, D CARBONE, D MITSUDOMI, T FEDORKO, J BUCHHAGEN, DL NAU, MM GAZDAR, AF LINNOILA, RI AF BODNER, SM MINNA, JD JENSEN, SM DAMICO, D CARBONE, D MITSUDOMI, T FEDORKO, J BUCHHAGEN, DL NAU, MM GAZDAR, AF LINNOILA, RI TI EXPRESSION OF MUTANT P53 PROTEINS IN LUNG-CANCER CORRELATES WITH THE CLASS OF P53 GENE MUTATION SO ONCOGENE LA English DT Note ID CELLULAR TUMOR-ANTIGEN; FREE DEFINED MEDIUM; TRANSFORMED-CELLS; SIMIAN VIRUS-40; SV40-TRANSFORMED CELLS; MONOCLONAL-ANTIBODIES; ACTIVATING MUTATIONS; CLINICAL SPECIMENS; T-ANTIGEN; ONCOGENE AB We investigated the immunocytochemical staining and immunoblotting characteristics of 33 different p53 mutant proteins identified in lung cancer cell lines (18 small-cell lung cancer and 15 non-small-cell lung cancer) using monoclonal antibodies pAbs 240, 421 and 1801. The p53 mutants studied were representative of those found in lung cancer and included three deletions, four nonsense, seven splicing and 19 missense lesions. Control cell lines included six B-lymphoblastoid cell lines and two lung cancer cell lines without p53 mutations. Immunocytochemistry demonstrated 16 cell lines (48%) with definite overexpression of p53 protein (the high-expresser group of mutants), while in the remainder of cases either no p53 expression or low levels of p53 protein expression were found (the low-expresser group of mutants). The type of p53 mutation correlated with the expresser group. High expresser's all had p53 missense mutations in exons 5-8, and immunocytochemistry identified 16/17 (94%) of these mutants. Several classes of p53 mutations occur in the low-expresser groups: deletions, splicing mutants, nonsense mutants and missense mutations outside of exons 5-8 all resulted in very low or undetectable levels of p53 protein. We conclude that there are low- and high-expression groups of p53 mutants in lung cancer and that the detection of protein expression in tumor cells by immunocytochemistry and immunoblotting is dependent upon the type of mutation of the p53 tumor-suppressor gene. C1 UNIV TEXAS, SW MED CTR, SIMMONS CANC CTR, DALLAS, TX 75235 USA. RP NATL NAVAL MED CTR, NCI,NAVY MED ONCOL BRANCH,BLDG 8,RM 5101, 8901 WISCONSIN AVE, BETHESDA, MD 20889 USA. OI Mitsudomi, Tetsuya/0000-0001-9860-8505 NR 59 TC 318 Z9 321 U1 2 U2 6 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 EI 1476-5594 J9 ONCOGENE JI Oncogene PD APR PY 1992 VL 7 IS 4 BP 743 EP 749 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HQ682 UT WOS:A1992HQ68200017 PM 1565469 ER PT J AU SITHANANDAM, G DRUCK, T CANNIZZARO, LA LEUZZI, G HUEBNER, K RAPP, UR AF SITHANANDAM, G DRUCK, T CANNIZZARO, LA LEUZZI, G HUEBNER, K RAPP, UR TI B-RAF AND A B-RAF PSEUDOGENE ARE LOCATED ON 7Q IN MAN SO ONCOGENE LA English DT Note ID COMPLETE CODING SEQUENCE; GAUCHER DISEASE; HUMAN HOMOLOGS; X-CHROMOSOME; MIL ONCOGENE; A-RAF; C-RAF; V-RAF; GENE; FAMILY AB The B-raf gene was lozalized to human chromosome region 7p11-7qter by Southern blot analysis of its segregation in a panel of rodent-human hybrids, using a B-raf cDNA clone. Chromosomal in situ hybridization refined the localization to 7q33-36. Analysis of genomic B-raf clones identified a B-raf pseudogene in addition to the active gene. Based on the chromosomal mapping data we conclude that the pseudogene is located near the active gene. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. PRI DYNCORP,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. TEMPLE UNIV,HLTH SCI CTR,SCH MED,FELS INST CANC RES & MOLEC BIOL,PHILADELPHIA,PA 19140. FU NCI NIH HHS [N01-CO-74102] NR 39 TC 25 Z9 26 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1992 VL 7 IS 4 BP 795 EP 799 PG 5 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HQ682 UT WOS:A1992HQ68200026 PM 1565476 ER PT J AU LARGAESPADA, DA KAEHLER, DA MISHAK, H WEISSINGER, E POTTER, M MUSHINSKI, JF RISSER, R AF LARGAESPADA, DA KAEHLER, DA MISHAK, H WEISSINGER, E POTTER, M MUSHINSKI, JF RISSER, R TI A RETROVIRUS THAT EXPRESSES V-ABL AND C-MYC ONCOGENES RAPIDLY INDUCES PLASMACYTOMAS SO ONCOGENE LA English DT Note ID MURINE LEUKEMIA-VIRUS; DROSOPHILA-MELANOGASTER ABL; ABELSON VIRUS; MOUSE PLASMACYTOMAS; NUCLEOTIDE-SEQUENCE; FIBROBLAST LINES; MAMMALIAN-CELLS; BALB/C MICE; H-RAS; GENE AB ABL-MYC, a murine retrovirus that encodes the v-abl and c-myc oncogenes, was constructed from Abelson murine leukemia virus (A-MuLV) in order to assess the biological consequences of co-expression of these genes in lymphoid cells. When inoculated into mice this retrovirus induced plasmacytomas in up to 100% of infected mice and less frequently induced pre-B lymphomas. Both tumor types contained genome-length proviruses in one or a few chromosomal locations, were mono- or oligoclonal as judged by immunoglobulin gene rearrangement and had unrearranged endogenous c-myc loci. The type of tumor induced depended upon the age and strain of mouse, and whether helper virus was present in the inoculated virus pool. ABL-MYC induced plasmacytomas with or without helper virus, with or without pretreatment of the mice with pristane, and in strains of mice resistant to pristane-induced plasmacytomas. Pristane treatment prior to ABL-MYC infection shortened the latent period of plasmacytomagenesis and produced mostly IgM-secreting tumors rather than IgA-secreting tumors, which predominantly arose in the absence of pristane. Control viruses for ABL-MYC with either a deletion in v-abl or a frameshift mutation in c-myc caused predominantly monocyte/macrophage tumors and pre-B-cell lymphomas respectively. Histopathological analysis of ABL-MYC-infected mice showed foci of transformed plasma cells as early as 14 days after infection. These results indicate that v-abl and c-myc act synergistically to transform mature B cells with high efficiency. C1 NCI,GENET LAB,BETHESDA,MD 20892. RP LARGAESPADA, DA (reprint author), UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706, USA. RI Largaespada, David/C-9832-2014 FU NCI NIH HHS [T32-CA09135, CA 41302] NR 52 TC 37 Z9 37 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR PY 1992 VL 7 IS 4 BP 811 EP 819 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HQ682 UT WOS:A1992HQ68200029 PM 1565479 ER PT J AU THOMAS, DA OLIVERAS, JL MAIXNER, W DUBNER, R AF THOMAS, DA OLIVERAS, JL MAIXNER, W DUBNER, R TI SYSTEMIC MORPHINE ADMINISTRATION ATTENUATES THE PERCEIVED INTENSITY OF NOXIOUS HEAT IN THE MONKEY SO PAIN LA English DT Article DE OPIOIDS; NOCICEPTION; PSYCHOPHYSICS; DETECTION; BEHAVIOR; (MONKEY) ID MEDULLARY DORSAL HORN; THERMAL DISCRIMINATION TASK; TOOTH-PULP SENSATIONS; NEURONAL-ACTIVITY; PAIN; STIMULATION; RESPONSES; NUCLEUS AB We examined the ability of systemic morphine to diminish the sensory discriminative features of noxious heating. Monkeys were trained to perform a thermal detection task, and the time until their detection of small increases in heating was used as a measure of the perceived intensity of pain. Relatively small doses of morphine sulfate (0.1, 0.3 and 1.0 mg/kg, i.m.) increased the time until detection of graded temperature increases (0.4-1.0-degrees-C) from a noxious 46-degrees-C baseline. These effects were generally dose-dependent, reversed by systemic naloxone, and did not result from changes in attentional, motivational or motoric aspects of the monkeys' behavior. Furthermore, the effects of morphine were more pronounced on detection of temperature shifts that were near threshold. These findings indicate that doses of morphine in the therapeutic dose range for humans alter the perceived intensity of noxious heat in monkeys. RP THOMAS, DA (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 30,ROOM B20,BETHESDA,MD 20892, USA. NR 30 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD APR PY 1992 VL 49 IS 1 BP 129 EP 135 DI 10.1016/0304-3959(92)90199-L PG 7 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA HR533 UT WOS:A1992HR53300020 PM 1594274 ER PT J AU VERMUND, SH SHEON, AR AF VERMUND, SH SHEON, AR TI THE WORLDWIDE IMPACT OF HIV AIDS ON CHILD SURVIVAL - A REVIEW OF THE MODEL OF BENNETT AND ROGERS SO PEDIATRIC AIDS AND HIV INFECTION-FETUS TO ADOLESCENT LA English DT Editorial Material RP VERMUND, SH (reprint author), NIAID,DIV AIDS,CLIN RES PROGRAM,VACCINE TRIALS & EPIDEMIOL BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1045-5418 J9 PEDIATR AIDS HIV INF JI Pediatr. AIDS HIV Infect.-Fetus Adolesc. PD APR PY 1992 VL 3 IS 2 BP 49 EP 52 PG 4 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA HU490 UT WOS:A1992HU49000001 ER PT J AU ORCUTT, TA GODWIN, CR PIZZO, PA OGNIBENE, FP AF ORCUTT, TA GODWIN, CR PIZZO, PA OGNIBENE, FP TI AEROSOLIZED PENTAMIDINE - A WELL-TOLERATED MODE OF PROPHYLAXIS AGAINST PNEUMOCYSTIS-CARINII PNEUMONIA IN OLDER CHILDREN WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO PEDIATRIC INFECTIOUS DISEASE JOURNAL LA English DT Article DE AEROSOLIZED PENTAMIDINE; PNEUMOCYSTIS-CARINII PROPHYLAXIS; HUMAN IMMUNODEFICIENCY VIRUS INFECTION ID SYNDROME AIDS; CHEMOPROPHYLAXIS; PATIENT AB Aerosolized pentamidine has been recommended as an alternative mode of antipneumocystis prophylaxis in human immunodeficiency virus-infected children with trimethoprim-sulfamethoxazole intolerance. However, there have been no definitive data concerning the most appropriate dose and the tolerance of aerosolized pentamidine in children. In the present study, we assessed the tolerance of aerosolized pentamidine in older children using a regimen similar to the one recommended in adults. A 300-mg dose of pentamidine was administered to our human immunodeficiency virus-infected patients monthly using the Respirgard II(R) nebulizer. Patients were assessed for their heart rate, respiratory rate, breath sounds and oxygen saturations during and after pentamidine aerosolization. During a 21-month period (August, 1989, to May, 1991), 22 patients (mean age, 9.8 +/- 0.6 years; range, 3 to 15 years) received a total of 185 treatments. Patients complained of either a bitter taste (16 of 22) or developed short periods of coughing (15 of 22) during the aerosol. Five patients developed reversible bronchospasm requiring bronchodilators; no patients developed oxygen desaturation. None of the patients developed Pneumocystis carinii pneumonia during the limited protocol follow-up (mean, 9.8 months). Thus aerosolized pentamidine for antipneumocystis prophylaxis is well-tolerated in older children. However, more comprehensive investigations of efficacy are indicated. C1 NCI,WARREN G MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BLDG 10,ROOM 7D-43,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NR 27 TC 16 Z9 16 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0891-3668 J9 PEDIATR INFECT DIS J JI Pediatr. Infect. Dis. J. PD APR PY 1992 VL 11 IS 4 BP 290 EP 294 DI 10.1097/00006454-199204000-00006 PG 5 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA HN497 UT WOS:A1992HN49700006 PM 1565553 ER PT J AU ARDITI, M OSTROVE, JM SHULMAN, ST AF ARDITI, M OSTROVE, JM SHULMAN, ST TI ACUTE MEASLES COMPLICATED BY FATAL ADENOVIRUS PNEUMONIA WITH BONE-MARROW FAILURE - LACK OF EVIDENCE FOR DIRECT VIRAL INVASION OF THE BONE-MARROW SO PEDIATRIC INFECTIOUS DISEASE JOURNAL LA English DT Article DE MEASLES; ADENOVIRUS PNEUMONIA; BONE MARROW; APLASTIC ANEMIA ID HUMAN TRIGEMINAL GANGLIA; HERPES-SIMPLEX VIRUS; NON-B HEPATITIS; APLASTIC-ANEMIA; NON-A; INFECTION; HEMATOPOIESIS; CONSEQUENCES; SUPPRESSION; INVITRO C1 NORTHWESTERN UNIV,CHILDRENS MEM HOSP,SCH MED,DIV INFECT DIS,CHICAGO,IL 60614. NIAID,CLIN INVEST LAB,MED VIROL SECT,BETHESDA,MD 20892. NR 23 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0891-3668 J9 PEDIATR INFECT DIS J JI Pediatr. Infect. Dis. J. PD APR PY 1992 VL 11 IS 4 BP 327 EP 330 DI 10.1097/00006454-199204000-00013 PG 4 WC Immunology; Infectious Diseases; Pediatrics SC Immunology; Infectious Diseases; Pediatrics GA HN497 UT WOS:A1992HN49700014 PM 1565559 ER PT J AU YANOVSKI, SZ YANOVSKI, JA MALLEY, JD BROWN, RL BALABAN, DJ AF YANOVSKI, SZ YANOVSKI, JA MALLEY, JD BROWN, RL BALABAN, DJ TI TELEPHONE TRIAGE BY PRIMARY CARE PHYSICIANS SO PEDIATRICS LA English DT Article DE TELEPHONE; PRIMARY CARE; PEDIATRICS; FAMILY PRACTICE; MANAGEMENT; TRIAGE; DECISION MAKING ID MANAGEMENT AB To determine if experienced primary care physicians are more likely to reach correct decisions on the telephone than their less experienced colleagues, we asked 31 first-year and 29 third-year residents, 21 faculty, and 36 private practitioners in pediatrics and family practice to evaluate three pediatric patients via a telephone interview with a simulated mother and to decide whether each patient needed to be seen that evening. Compared with first-year residents, the third-year residents, faculty and private practitioners decided less frequently to see children who were not severely ill (P < .05) or injured (P < .01); however, less than half obtained histories considered adequate to rule out potential serious illnesses. Faculty did better than either residents or private practitioners in managing a severely dehydrated child; 100% of the faculty, but less than 60% of the residents or private practitioners, chose to see the patient promptly (P < .001). More than one third of all residents and private practitioners reached inappropriate management decisions despite obtaining information that should have altered their decisions. In these simulations, experience in private practice was not associated with improved telephone management of very sick children. Faculty physicians appeared to be better able to identify severely ill children without inappropriately evaluating those who were less ill. In all three simulations, attainment of the correct decision appeared to be determined not by the number or type of questions asked, but rather by the physician's interpretation of the information collected. C1 THOMAS JEFFERSON UNIV,GREENFIELD RES CTR,DEPT FAMILY MED,PHILADELPHIA,PA 19107. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA. NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. NR 19 TC 44 Z9 44 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD APR PY 1992 VL 89 IS 4 BP 701 EP 706 PN 2 PG 6 WC Pediatrics SC Pediatrics GA HM253 UT WOS:A1992HM25300003 PM 1557265 ER PT J AU NAGOSHI, CT WALTER, D MUNTANER, C HAERTZEN, CA AF NAGOSHI, CT WALTER, D MUNTANER, C HAERTZEN, CA TI VALIDATION OF THE TRIDIMENSIONAL PERSONALITY QUESTIONNAIRE IN A SAMPLE OF MALE DRUG-USERS SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article ID VENTURESOMENESS; IMPULSIVENESS; AGGRESSION; VERSION; ADULTS; STATES; ABUSE AB One hundred seventy-three male drug using volunteers for drug-related studies completed the Cloninger Tridimensional Personality Questionnaire (TPQ), with most of these Ss also completing the Eysenck Personality Questionnaire, the Eysenck I.7, the Buss-Durkee Hostility Inventory, the Symptom Check List 90, the Elliot-Huizinga Lifetime Criminality Measure, the Diagnostic Interview Schedule for DSM-III, and the Personality Disorders Questionnaire. TPQ novelty seeking was correlated with impulsivity, aggression, and criminality, TPQ harm avoidance was correlated with introversion, neuroticism, low venturesomeness, and high psychological distress, while TPQ reward dependence was correlated with extraversion, low psychoticism, and empathy. With the possible exception of novelty seeking, the TPQ scales did not, as predicted by Cloninger, correlate with specific personality disorders or alcohol and drug abuse. The rationale for the construction of the TPQ scales was generally not supported in the present sample. C1 UNIV PENN,TREATMENT RES CTR,DATA MANAGEMENT UNIT,PHILADELPHIA,PA 19104. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21205. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. RP NAGOSHI, CT (reprint author), ARIZONA STATE UNIV,DEPT PSYCHOL,TEMPE,AZ 85287, USA. RI Muntaner, C/A-5043-2010 NR 33 TC 38 Z9 38 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0191-8869 J9 PERS INDIV DIFFER JI Pers. Individ. Differ. PD APR PY 1992 VL 13 IS 4 BP 401 EP 409 DI 10.1016/0191-8869(92)90067-Y PG 9 WC Psychology, Social SC Psychology GA HM245 UT WOS:A1992HM24500002 ER PT J AU DABESTANI, R SIK, RH MOTTEN, AG CHIGNELL, CF AF DABESTANI, R SIK, RH MOTTEN, AG CHIGNELL, CF TI SPECTROSCOPIC STUDIES OF CUTANEOUS PHOTOSENSITIZING AGENTS .17. BENZANTHRONE SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID SINGLET OXYGEN; RADICALS; SUPEROXIDE; SOLVENT AB The photochemistry of benzanthrone (7H-benz[de]-anthracene-7-one) has been studied using electron paramagnetic resonance (EPR) in conjunction with the spin trapping technique and the direct detection of singlet molecular oxygen luminescence. Irradiation (lambda(ex) = 394 nm) of benzanthrone (BA) in aerated ethanol, dimethylsulfoxide or benzene resulted in the generation of superoxide (O is approximately equal to 2) which was trapped by 5,5-dimethyl-1-pyrroline-N-oxide. The ethoxyl radical was also detected in ethanol. Photolysis of BA in deaerated basic ethanol led to the formation of BA anion radical, BA is approximately equal to, which was detected directly by ESR. This radical anion decayed back to BA with a unimolecular rate constant of 1.5 x 10(-3) s-1. The 1O2 quantum yields (lambda(ex) > 345 nm) for BA in ethanol, 90% ethanol and basic ethanol (0.1N NaOH) were 0.89, 0.88 and 0.28 respectively relative to Rose Bengal. The lower yield of 1O2 in basic ethanol may be attributable to the reaction of oxygen with BA is approximately equal to (which is generated in higher yield at alkaline pH) to give O2 is approximately equal to. These findings suggest that on exposure to light BA can generate active oxygen species which may be responsible for the photocontact dermatitis caused by BA in industrial workers exposed to this chemical. RP DABESTANI, R (reprint author), NIEHS,MOLEC BIOPHYS LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 21 TC 8 Z9 8 U1 0 U2 1 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD APR PY 1992 VL 55 IS 4 BP 533 EP 539 DI 10.1111/j.1751-1097.1992.tb04275.x PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HK374 UT WOS:A1992HK37400010 PM 1320277 ER PT J AU MASOLIVER, J PORRA, JM WEISS, GH AF MASOLIVER, J PORRA, JM WEISS, GH TI THE CONTINUUM-LIMIT OF A 2-DIMENSIONAL PERSISTENT RANDOM-WALK SO PHYSICA A-STATISTICAL MECHANICS AND ITS APPLICATIONS LA English DT Article ID HEAT WAVES; DIFFUSION; MODEL AB We consider a two-dimensional persistent random walk in which the motion consists of alternative steps along one of two vectors, a and b. It is shown that the continuum limit of the evolution equation is not a two- but rather a one-dimensional telegrapher's equation. C1 NIH, DIV COMP RES & TECHNOL, BETHESDA, MD 20892 USA. RP UNIV BARCELONA, DEPT FIS FONAMENTAL, DIAGONAL 647, E-08028 BARCELONA, SPAIN. RI Masoliver, Jaume/F-7198-2016 OI Masoliver, Jaume/0000-0002-5810-879X NR 15 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4371 EI 1873-2119 J9 PHYSICA A JI Physica A PD APR 1 PY 1992 VL 182 IS 4 BP 593 EP 598 DI 10.1016/0378-4371(92)90023-J PG 6 WC Physics, Multidisciplinary SC Physics GA HQ368 UT WOS:A1992HQ36800007 ER PT J AU BRESNAHAN, EL WISER, PR MUTH, NJ INGRAM, DK AF BRESNAHAN, EL WISER, PR MUTH, NJ INGRAM, DK TI DELAYED MATCHING-TO-SAMPLE PERFORMANCE BY RATS IN A NEW AVOIDANCE-MOTIVATED MAZE - RESPONSE TO SCOPOLAMINE AND FIMBRIA-FORNIX LESIONS SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE LEARNING; MEMORY; HIPPOCAMPUS; CHOLINERGIC SYSTEM; AGING; ANTICHOLINERGICS ID SHORT-TERM-MEMORY; PROACTIVE-INTERFERENCE; HIPPOCAMPAL-FORMATION; IMPAIRMENT; PRODUCE; MONKEYS AB A new avoidance-motivated detour-maze in which memory for an immediately preceding sample event could be assessed was evaluated by testing seven 6-month-old male F-344 rats with a delayed matching-to-sample (DMTS) paradigm. Rats first received extensive pretraining with this paradigm over several months and after a minimum of 1,390 choice-trials demonstrated great proficiency in this maze. Studies were then conducted to establish cholinergic and hippocampal involvement in the DMTS task by using drug manipulations (scopolamine and physostigmine), and after lesions to the fimbria-fornix (FF) pathway. A high dose (1.0 mg/kg) of scopolamine but not a low dose (0.3 mg/kg) significantly interfered with choice accuracy as measured by errors and trials to criterion; physostigmine (0.01 and 0.03 mg/kg) had no significant effect; and fimbria lesions significantly disrupted both choice accuracy and runtime performance. Disruption was most pronounced on difficult problems (different paths to the goal). After lesions only, considerable within-trial perseverative errors occurred during the early postlesion weeks on four difficult problems from among the 18 tested. Results were discussed in terms of (a) specificity of this disruption, (b) indications of proactive interference effects, and (c) the movement-related excitation component of maze learning. The present results accord with earlier findings of disruption by scopolamine and FF lesions in a 14-unit T-maze, both mazes having similar performance requirements of shock avoidance and multiple 90-degree turns along the paths to the goal. The present results affirm that this new detour maze provides a viable approach for assessing cognitive performance in a within-subjects design and thereby offers new possibilities for testing various aspects of cognitive processing, particularly for aged rodent models, in a complex aversive situation. C1 FRANCIS SCOTT KEY MED CTR,NIH,GERONTOL RES CTR,NATHAN W SHOCK LABS,MOLEC PHYSIOL & GENET SECT,BALTIMORE,MD 21224. NR 30 TC 9 Z9 9 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD APR PY 1992 VL 51 IS 4 BP 735 EP 746 DI 10.1016/0031-9384(92)90110-N PG 12 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA HR331 UT WOS:A1992HR33100011 PM 1594672 ER PT J AU RIPAMONTI, U MA, SS REDDI, AH AF RIPAMONTI, U MA, SS REDDI, AH TI INDUCTION OF BONE IN COMPOSITES OF OSTEOGENIN AND POROUS HYDROXYAPATITE IN BABOONS SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID EXTRACELLULAR-MATRIX; DIFFERENTIATION; PROTEIN AB A major goal of the combined effort of basic scientists and plastic and reconstructive surgeons is the development of novel bone substitutes based on osteogenic growth and differentiation factors with optimal delivery systems for skeletal repair. Osteogenin is a protein initiator of bone differentiation. The present study examined the osteogenic potential of osteogenin in combination with porous hydroxyapatite replicas obtained after hydrothermal conversion of calcium carbonate exoskeletons of corals. Bovine osteogenin, with an apparent molecular weight of 28 to 42 kDa, purified by hydroxyapatite-Ultrogel adsorption chromatography, heparin-Sepharose affinity chromatography, and HR Sephacryl S-200 molecular sieve chromatography, was delivered into rods of nonresorbable and resorbable hydroxyapatite replicas with an average porosity of 600-mu-m. A total of 48 rods were bioassayed for osteogenic activity by intramuscular implantation into eight adult baboons (Papio ursinus) as a prerequisite for clinical trials in humans. Bovine osteogenin fractions reconstituted with baboon insoluble collagenous bone matrix were implanted in an additional four adult baboons. Specimens were harvested at 30 and 90 days after implantation and subjected to histomorphometry and alkaline phosphatase activity determination. Differentiation of bone occurred in nonresorbable hydroxyapatite rods, both osteogenin-treated and controls. However, no bone formation was observed in resorbable rods, even in the presence of osteogenin. These results demonstrate that the surface and chemical characteristics of the substratum, independent of the osteogenic stimulus, have a profound influence on the morphogenesis of bone. The demonstration of bone induction in nonhuman primates with porous nonresorbable hydroxyapatite replicas and baboon insoluble collagenous bone matrix reconstituted with bovine osteogenin establishes the therapeutic potential of the principle of bone induction in craniofacial, periodontal, and orthopedic reconstructive surgery. C1 NIDR,BONE CELL BIOL SECT,BETHESDA,MD 20892. RP RIPAMONTI, U (reprint author), UNIV WITWATERSRAND,DENT RES INST,MRC,PO WITS 2050,JOHANNESBURG 2001,SOUTH AFRICA. NR 26 TC 68 Z9 68 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD APR PY 1992 VL 89 IS 4 BP 731 EP 739 DI 10.1097/00006534-199204000-00025 PG 9 WC Surgery SC Surgery GA HL494 UT WOS:A1992HL49400025 PM 1312241 ER PT J AU KANG, CY NARA, P CHAMAT, S CARALLI, V CHEN, A NGUYEN, ML YOSHIYAMA, H MORROW, WJW HO, DD KOHLER, H AF KANG, CY NARA, P CHAMAT, S CARALLI, V CHEN, A NGUYEN, ML YOSHIYAMA, H MORROW, WJW HO, DD KOHLER, H TI ANTIIDIOTYPE MONOCLONAL-ANTIBODY ELICITS BROADLY NEUTRALIZING ANTI-GP120 ANTIBODIES IN MONKEYS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANTIIDIOTYPE ANTIBODY; NEUTRALIZING ANTIBODY; HUMAN IMMUNODEFICIENCY VIRUS VACCINE ID MICE AB Murine monoclonal antibodies (mAbs) were raised against human, polyclonal, anti-gp120 antibodies (Ab1) and were selected for binding to broadly neutralizing anti-gp120 antibodies in sera positive for human immunodeficiency virus (HIV). One anti-idiotype mAb (Ab2), 3C9, was found to be specific for human anti-gp120 antibodies directed against an epitope around the conserved CD4 attachment site of gp120. The 3C9 reactive human anti-gp120 antibodies (3C9+ Ab) neutralized MN, IIIB, RF, and four primary isolates of HIV type 1 (HIV-1). Cynomolgus monkeys were immunized with 3C9 in adjuvant to test whether this anti-idiotype mAb could induce neutralizing anti-gp120 antibodies. The results show that purified anti-anti-idiotype antibodies (Ab3) from 3C9 immune sera bind to an epitope around the CD4 attachment site of gp120SF and gp120IIIB. Furthermore, purified gp120-specific Ab3 neutralize MN, IIIB, and RF isolates. These results demonstrate that primates immunized with an anti-idiotype mAb produce broadly neutralizing anti-HIV-1 antibodies. Since this anti-idiotype mAb was selected by identifying a clonotypic marker, its biological activity can be explained as the result of clonotypic B-cell stimulation. C1 NCI,FREDERICK,MD 21701. AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10016. RP KANG, CY (reprint author), IDEC PHARMACEUT CORP,11099 N TORREY PINES RD,LA JOLLA,CA 92037, USA. RI Yoshiyama, Hironori/D-7902-2012; OI Yoshiyama, Hironori/0000-0001-7588-278X FU NIAID NIH HHS [1R43AI31310] NR 23 TC 30 Z9 30 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2546 EP 2550 DI 10.1073/pnas.89.7.2546 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600008 PM 1557358 ER PT J AU NEVILLE, DM SCHARFF, J SRINIVASACHAR, K AF NEVILLE, DM SCHARFF, J SRINIVASACHAR, K TI INVIVO T-CELL ABLATION BY A HOLO-IMMUNOTOXIN DIRECTED AT HUMAN CD3 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DIPHTHERIA TOXIN; RECEPTOR; IMMUNOSUPPRESSION ID BONE-MARROW TRANSPLANTATION; VERSUS-HOST DISEASE; DIPHTHERIA-TOXIN; A-CHAIN; MONOCLONAL-ANTIBODIES; HODGKINS-DISEASE; LYMPHOCYTES; MUTATIONS; RECEPTOR; EFFICACY AB We have evaluated the in vivo efficacy of anti-CD3-CRM9, a holo-immunotoxin constructed with a diphtheria toxin binding-site mutant. Eighty percent of established human T-cell subcutaneous tumors in nude mice completely regressed following intraperitoneal injection of immunotoxin at a dose set at half the minimum lethal dose assayed in toxin-sensitive animals. Similar regressions produced by a Cs-137 source required a dose in excess of 500 cGy. The high degree of in vivo T-cell ablation produced by this immunotoxin is apparently due to maintenance of the toxin translocation function provided by CRM9 and a necessary intracellular routing function supplied by CD3. This immunotoxin may be useful in treating conditions caused by pathologic oligoclonal T-cell expansion such as graft-versus-host disease, autoimmune diseases, and possibly AIDS. RP NEVILLE, DM (reprint author), NIMH,MOLEC BIOL LAB,BIOPHYS CHEM SECT,BETHESDA,MD 20892, USA. NR 37 TC 55 Z9 55 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2585 EP 2589 DI 10.1073/pnas.89.7.2585 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600016 PM 1372981 ER PT J AU POLI, G KINTER, AL JUSTEMENT, JS BRESSLER, P KEHRL, JH FAUCI, AS AF POLI, G KINTER, AL JUSTEMENT, JS BRESSLER, P KEHRL, JH FAUCI, AS TI RETINOIC ACID MIMICS TRANSFORMING GROWTH-FACTOR-BETA IN THE REGULATION OF HUMAN-IMMUNODEFICIENCY-VIRUS EXPRESSION IN MONOCYTIC CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MACROPHAGE; CYTOKINES; U1-CELLS; U937-CELLS; PHORBOL 12-MYRISTATE 13-ACETATE ID CYTOKINE PRODUCTION; TGF-BETA; DIFFERENTIATION; FACTOR-BETA-1; INFECTION; LEUKEMIA; HIV-1; MECHANISMS; PROTEIN; LINES AB Retinoic acid (RA) exerts potent suppressive and upregulatory effects on human immunodeficiency virus (HIV) expression in mononuclear phagocytes, strikingly similar to the effects of the cytokine transforming growth factor beta (TGF-beta). RA significantly inhibited phorbol ester-mediated, but not tumor necrosis factor alpha-mediated, induction of HIV transcription in the chronically infected promonocytic U1 cell line. RA and TGF-beta also completely suppressed the induction of virus production in U1 cells by interleukin 6 alone or in combination with glucocorticoids, which predominantly upregulate virus expression at the posttranscriptional level. Despite the close parallel to TGF-beta-induced effects, no evidence was obtained that RA mediated its effect by inducing secretion of active TGF-beta-1, -beta-2, or -beta-3. As with chronically infected U1 cells, similar inhibitory effects were also observed in primary monocyte-derived macrophages previously infected with HIV and then exposed to either RA or TGF-beta. In contrast, stimulation of monocyte-derived macrophages or U937 cells (the parental cell line of U1) with either RA or TGF-beta prior to in vitro infection resulted in the enhancement of virus production. Given the already successful use of retinoids in the treatment of several malignancies and the present demonstration of their capability of blocking the induction of HIV expression in infected mononuclear phagocytes, it would be of interest to pursue the potential role of this class of compounds in the development of strategies aimed at the pharmacologic regulation of HIV expression. RP NIAID, IMMUNOREGULAT LAB, BLDG 31, ROOM 7A03, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 47 TC 74 Z9 74 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2689 EP 2693 DI 10.1073/pnas.89.7.2689 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600037 PM 1372988 ER PT J AU GERWIN, BI SPILLARE, E FORRESTER, K LEHMAN, TA KISPERT, J WELSH, JA PFEIFER, AMA LECHNER, JF BAKER, SJ VOGELSTEIN, B HARRIS, CC AF GERWIN, BI SPILLARE, E FORRESTER, K LEHMAN, TA KISPERT, J WELSH, JA PFEIFER, AMA LECHNER, JF BAKER, SJ VOGELSTEIN, B HARRIS, CC TI MUTANT-P53 CAN INDUCE TUMORIGENIC CONVERSION OF HUMAN BRONCHIAL EPITHELIAL-CELLS AND REDUCE THEIR RESPONSIVENESS TO A NEGATIVE GROWTH-FACTOR, TRANSFORMING GROWTH FACTOR-BETA(1) SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CARCINOGENESIS; TUMOR SUPPRESSOR GENE; HEAT SHOCK PROTEIN ID LARGE-T-ANTIGEN; FACTOR-BETA; WILD-TYPE; SQUAMOUS DIFFERENTIATION; SV40-TRANSFORMED CELLS; P53 PROTEIN; INHIBITION; GENE; SV40; TRANSCRIPTION AB Loss of normal functions and gain of oncogenic functions when the p53 tumor suppressor gene is mutated are considered critical events in the development of the majority of human cancers. Human bronchial epithelial cells (BEAS-2B) provide an in vitro model system to study growth, differentiation, and neoplastic transformation of progenitor cells of lung carcinoma. When wild-type (WT) or mutant (MT; codon 143Val-Ala) human p53 cDNA was transfected into non-tumorigenic BEAS-2B cells, we observed that (i) transfected WT p53 suppresses and MT p53 enhances the colony-forming efficiency of these cells, (ii) MT p53 increases resistance to transforming growth factor beta(1), and (iii) clones of MT p53 transfected BEAS-2B cells are tumorigenic when inoculated into athymic nude mice. These results are consistent with the hypothesis that certain mutations in p53 may function in multistage lung carcinogenesis by reducing the responsiveness of bronchial epithelial cells to negative growth factors. C1 NCI,HUMAN CARCINOGENESIS LAB,BLDG 37,ROOM 2C05,BETHESDA,MD 20892. NESTLE SA,GENET TOXICOL SECT,VEVEY,SWITZERLAND. JOHNS HOPKINS UNIV,SCH MED,CTR ONCOL,BALTIMORE,MD 21213. NR 56 TC 140 Z9 144 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2759 EP 2763 DI 10.1073/pnas.89.7.2759 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600052 PM 1557382 ER PT J AU OTANI, H SIEGEL, JP ERDOS, M GNARRA, JR TOLEDANO, MB SHARON, M MOSTOWSKI, H FEINBERG, MB PIERCE, JH LEONARD, WJ AF OTANI, H SIEGEL, JP ERDOS, M GNARRA, JR TOLEDANO, MB SHARON, M MOSTOWSKI, H FEINBERG, MB PIERCE, JH LEONARD, WJ TI INTERLEUKIN (IL)-2 AND IL-3 INDUCE DISTINCT BUT OVERLAPPING RESPONSES IN MURINE IL-3-DEPENDENT 32D CELLS TRANSDUCED WITH HUMAN IL-2 RECEPTOR BETA-CHAIN - INVOLVEMENT OF TYROSINE KINASE(S) OTHER THAN P56(LCK) SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID COLONY-STIMULATING FACTOR; SIGNAL TRANSDUCTION; MONOCLONAL-ANTIBODIES; MOLECULAR-CLONING; T-CELLS; GENE; PHOSPHORYLATION; EXPRESSION; INTERNALIZATION; CDNA AB We have established IL-3-dependent 32D myeloid progenitor cells stably expressing the human IL-2 receptor beta-chain (IL-2R-beta). Whereas parental 32D cells proliferated only in response to IL-3, the transduced cells also proliferated in response to IL-2. Transduced cells expressed high- and intermediate-affinity IL-2Rs, resulting from expression of human IL-2R-beta and murine IL-2R alpha-chain (IL-2R-alpha). IL-2 induced phenotypic changes not induced by IL-3, including the upregulated expression of endogenous murine IL-2R-alpha and IL-2R-beta and an increase in cell size. Therefore, the transduced IL-2R-beta was not merely coupling with the IL-3 signaling pathway. IL-3 augmented several IL-2-induced responses including the up-regulation of IL-2R-alpha. Both IL-2- and IL-3-induced proliferation and IL-2 induced IL-2R-alpha expression were inhibited by the tyrosine kinase inhibitor herbimycin A. Thus, both IL-2- and IL-3-mediated effects required tyrosine kinase activity. The identity of the tyrosine kinase(s) mediating the IL-2 signals in these cells is not known but cannot be p56lck, a tyrosine kinase found in T cells, since 32D-IL-2R-beta cells do not express p56lck. C1 US FDA,CTR BIOL EVALUAT & RES,DIV CYTOKINE BIOL,CELLULAR IMMUNOL LAB,BETHESDA,MD 20892. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. NHLBI,INTRAMURAL RES PROGRAM,OFF DIRECTOR,PULM & MOLEC IMMUNOL SECT,BETHESDA,MD 20892. RP OTANI, H (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 45 TC 61 Z9 61 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2789 EP 2793 DI 10.1073/pnas.89.7.2789 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600058 PM 1557384 ER PT J AU YAMASHITA, S WADA, K HORIKOSHI, M GONG, DW KOKUBO, T HISATAKE, K YOKOTANI, N MALIK, S ROEDER, RG NAKATANI, Y AF YAMASHITA, S WADA, K HORIKOSHI, M GONG, DW KOKUBO, T HISATAKE, K YOKOTANI, N MALIK, S ROEDER, RG NAKATANI, Y TI ISOLATION AND CHARACTERIZATION OF A CDNA-ENCODING DROSOPHILA TRANSCRIPTION FACTOR-TFIIB SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE TRANSCRIPTION INITIATION; INVITRO TRANSCRIPTION; DIRECT REPEAT; BASIC REPEAT; SIGMA-SEQUENCE SIMILARITY ID RNA POLYMERASE-II; BOX-BINDING-FACTOR; TATA-BOX; INITIATION-FACTOR; PREINITIATION COMPLEX; GAL4 DERIVATIVES; YEAST; ACTIVATION; PROTEIN; PROMOTER AB A Drosophila cDNA encoding a human transcription factor TFIIB homologue was isolated by PCR methods. The deduced amino acid sequence indicates 85% sequence similarity with human TFIIB, and the corresponding cDNA product expressed in Escherichia coli is interchangeable with human TFIIB for both basal and GAL4-VP16-induced transcription. Structural motifs including the direct repeats, basic repeats, and sigma-sequence similarities are well conserved among Drosophila, human, and Xenopus TFIIB. However, the N-terminal region of each direct repeat is less conserved among the three species, suggesting the presence of two structural subdomains in the direct repeat. Moreover, the amino acid changes in the N-terminal subdomain produce altered positions of the conserved amino acids between the direct repeats. An overall similarity in general structural features between TFIIB and TFIID-tau (the TATA-binding subunit of TFIID) was previously noted. However, in contrast to the sequence divergence reported for the N-terminal domains of TFIID-tau from different species, the N-terminal sequence of TFIIB was highly conserved among the species. This suggests that TFIIB has a more rigid structure, consistent with its function as a "bridging" protein between TFIID and RNA polymerase II. Further implications of the TFIIB structure are discussed. C1 NINCDS,MOLEC BIOL LAB,BLDG 36,ROOM 3D02,BETHESDA,MD 20892. NIDCD,NEUROCHEM LAB,BETHESDA,MD 20892. ROCKEFELLER UNIV,BIOCHEM & MOLEC BIOL LAB,NEW YORK,NY 10021. FU NCI NIH HHS [CA42567]; NIAID NIH HHS [AI27397]; NIGMS NIH HHS [GM13244] NR 44 TC 41 Z9 42 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2839 EP 2843 DI 10.1073/pnas.89.7.2839 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600068 PM 1557390 ER PT J AU DOI, T VLASSARA, H KIRSTEIN, M YAMADA, Y STRIKER, GE STRIKER, LJ AF DOI, T VLASSARA, H KIRSTEIN, M YAMADA, Y STRIKER, GE STRIKER, LJ TI RECEPTOR-SPECIFIC INCREASE IN EXTRACELLULAR-MATRIX PRODUCTION IN MOUSE MESANGIAL CELLS BY ADVANCED GLYCOSYLATION END-PRODUCTS IS MEDIATED VIA PLATELET-DERIVED GROWTH-FACTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MULTIDOMAIN PROTEIN; TRANSGENIC MICE; GLOBULAR DOMAIN; CHAIN; GLOMERULOSCLEROSIS; SEQUENCE; DISEASE AB Renal disease is one of the most common and severe complications of diabetes mellitus. The hallmark of the disease, glomerulosclerosis, is characterized by an accumulation of extracellular matrix in the mesangial areas, leading to progressive obliteration of the vascular spaces. The role of the metabolic derangements of diabetes mellitus in the development of these lesions is incompletely understood. One of the consequences of hyperglycemia is the formation of advanced glycosylation end products (AGEs), which result from a series of rearrangements secondary to nonenzymatic reaction of glucose with proteins. Specific receptors for proteins modified by AGEs, present in several cell types, were recently described in human and rat mesangial cells. Furthermore, exposure of mesangial cells to AGEs was followed by an increase in fibronectin production. In the present study we show evidence that mouse mesangial cells exhibit an increase in collagen type IV mRNA and peptide synthesis after exposure to AGEs. Antibodies to AGE receptors prevent this increase, indicating that the response is AGE-receptor-mediated. In addition, anti-platelet-derived growth factor abrogates the AGE response, suggesting that platelet-derived growth factor acts as an intermediate factor. Transcription assay reveals that the elevated mRNA levels are due to an increase in the transcription rate, rather than to an increase in the stability of the message. Finally, the mRNAs coding for laminin and heparan sulfate proteoglycan are also increased after exposure to AGE, whereas glyceraldehyde 3-phosphate dehydrogenase mRNA levels remain constant. The increase in extracellular matrix mRNAs seen in the current study suggests that AGE formation in vivo may be one of the metabolic events leading to the development of diabetic glomerulosclerosis. C1 NIDDKD,METAB DIS BRANCH,RENAL CELL BIOL SECT,BETHESDA,MD 20892. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. PICOWER INST MED RES,MANHASSET,NY 11030. RI Kirstein, Martina/L-9247-2014 OI Kirstein, Martina/0000-0001-8716-2309 FU NIA NIH HHS [AG-8245, AG-6943] NR 29 TC 326 Z9 333 U1 0 U2 4 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2873 EP 2877 DI 10.1073/pnas.89.7.2873 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600075 PM 1313571 ER PT J AU NAZARALI, A KIM, Y NIRENBERG, M AF NAZARALI, A KIM, Y NIRENBERG, M TI HOX-1.11 AND HOX-4.9 HOMEOBOX GENES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HOX-4.3; HOX-4.2; HOMEOBOX NUCLEOTIDE SEQUENCES ID HOMEOTIC GENES; BOX GENE; EXPRESSION; DROSOPHILA; MURINE; ORGANIZATION; HOMEODOMAIN; CHROMOSOME; SEQUENCE; COMPLEX AB Mouse Hox-1.11 and Hox-4.9 genes were cloned, and the nucleotide sequences of the homeobox regions were determined. In addition, nucleotide sequence analysis of the homeobox regions of cloned Hox-4.3 and Hox-4.2 genomic DNA revealed some differences in nucleotide sequences and in the deduced homeodomain amino acid sequences compared with the sequences that have been reported. C1 NHLBI,BIOCHEM GENET LAB,BLDG 36,ROOM 1C-06,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 28 TC 19 Z9 23 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2883 EP 2887 DI 10.1073/pnas.89.7.2883 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600077 PM 1348361 ER PT J AU SCHNIERLE, BS GERSHON, PD MOSS, B AF SCHNIERLE, BS GERSHON, PD MOSS, B TI CAP-SPECIFIC MESSENGER-RNA (NUCLEOSIDE-O(2)'-)-METHYLTRANSFERASE AND POLY(A) POLYMERASE STIMULATORY ACTIVITIES OF VACCINIA VIRUS ARE MEDIATED BY A SINGLE PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MESSENGER RNA PROCESSING; METHYLATION; POLYADENYLYLATION; POXVIRUS ID EARLY TRANSCRIPTION FACTOR; GENE D12L ENCODES; CAPPING ENZYME; NUCLEOTIDE-SEQUENCE; LARGE SUBUNIT; HELA-CELLS; GUANYLYLTRANSFERASE; PURIFICATION; VIRIONS; IDENTIFICATION AB The vaccinia virus gene for S-adenosyl-L-methionine:mRNA (nucleoside-O2'-)-methyltransferase, an enzyme required for the formation of the 5' cap structure of mRNA, was identified. Protein sequence analysis revealed that this cap-specific methyltransferase is derived from the same open reading frame as that previously shown to encode VP39, a M(r) 39,000 dissociable subunit of poly(A) polymerase that stimulates the formation of long poly(A) tails. Consistent with this finding, methyltransferase activity was associated with the heterodimeric poly(A) polymerase, which is composed of VP55 and VP39 subunits, as well as with monomeric VP39 protein isolated from vaccinia virions. In addition, cap-specific nucleoside-O2'-methyltransferase activity is associated with recombinant VP39, which was purified to near homogeneity from mammalian cells. From these data, we concluded that the same protein functions as a methyltransferase and a poly(A) polymerase stimulatory factor to modify the 5' and 3' ends of mRNA, respectively. RP SCHNIERLE, BS (reprint author), NIAID,VIRAL DIS LAB,BETHESDA,MD 20892, USA. NR 41 TC 87 Z9 88 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2897 EP 2901 DI 10.1073/pnas.89.7.2897 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600080 PM 1313572 ER PT J AU REINLIB, L JEFFERSON, DJ MARINI, FC DONOWITZ, M AF REINLIB, L JEFFERSON, DJ MARINI, FC DONOWITZ, M TI ABNORMAL SECRETAGOGUE-INDUCED INTRACELLULAR FREE CA(2+) REGULATION IN CYSTIC-FIBROSIS NASAL EPITHELIAL-CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ION-TRANSPORT; TRACHEAL EPITHELIUM; CHLORIDE TRANSPORT; SECRETORY RESPONSE; CYTOSOLIC CALCIUM; AIRWAY EPITHELIA; CHANNELS; PROTEIN; NEUTROPHILS; CHILDREN AB These studies identify a further abnormality in cystic fibrosis (CF). The increase in intracellular free calcium concentration ([Ca2+]i) after exposure to histamine and PGE1 is demonstrated to be abnormally low in nasal cells, studied in short-term culture, from patients with CF compared with control subjects. [Ca2+]i is measured by using the Ca2+-sensitive fluorescent dye fura-2 and a fluorescence microscope imaging system. The percentage of CF cells that increase [Ca2+]i in response to histamine is decreased compared with controls, and, even in those CF cells that increase [Ca2+]i, the magnitude of the increase in [Ca2+]i in response to histamine is smaller than in controls. When exposed to PGE1, a similar number of control and CF cells responded with an increase in [Ca2+]i, but again the magnitude of the response was smaller in the CF cells. The mechanism of the PGE1-induced increase in [Ca2+]i is not mediated by cAMP, since 8-bromo-cAMP failed to increase [Ca2+]i in these cells. This abnormality in [Ca2+]i response did not apply to all secretagogues, with the response to carbachol being similar in CF and normal cells. How the abnormal CF gene product accounts for the abnormality in intracellular Ca2+ response to some but not all secretagogues is unknown. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV GASTROENTEROL,GASTROINTESTINAL UNIT,ROSS 9N,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,GASTROINTESTINAL UNIT,BALTIMORE,MD 21205. TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. NEW ENGLAND MED CTR HOSP,DEPT MED,BOSTON,MA 02111. NEW ENGLAND MED CTR HOSP,DEPT PEDIAT,BOSTON,MA 02111. NIAAA,DIV INTRAMURAL CLIN & BIOL RES,ROCKVILLE,MD 20852. RI Marini, Frank/L-8018-2016 FU NIDDK NIH HHS [R01 DK AM26523, P30 DK 34928] NR 34 TC 20 Z9 20 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2955 EP 2959 DI 10.1073/pnas.89.7.2955 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600092 PM 1557401 ER PT J AU VERES, Z TSAI, L SCHOLZ, TD POLITINO, M BALABAN, RS STADTMAN, TC AF VERES, Z TSAI, L SCHOLZ, TD POLITINO, M BALABAN, RS STADTMAN, TC TI SYNTHESIS OF 5-METHYLAMINOMETHYL-2-SELENOURIDINE IN TRANSFER-RNAS - P-31 NMR-STUDIES SHOW THE LABILE SELENIUM DONOR SYNTHESIZED BY THE SELD GENE-PRODUCT CONTAINS SELENIUM BONDED TO PHOSPHORUS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SELENOPHOSPHATE; SELENO-TRANSFER RNAS ID ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; METABOLISM; NUCLEOSIDE AB An enzyme preparation from Salmonella typhimurium catalyzes the conversion of 5-methylaminomethyl-2-thiouridine in tRNAs to 5-methylaminomethyl-2-selenouridine when supplemented with selenide and ATP. Similar preparations from a Salmonella mutant strain carrying a defective selD gene fail to catalyze this selenium substitution reaction. However, supplementation of the deficient enzyme preparation with the purified selD gene product (SELD protein) restored synthesis of seleno-tRNAs. In the absence of the complementary enzyme(s), the SELD protein catalyzes the synthesis of a labile selenium donor compound from selenide and ATP. P-31 NMR studies show that among the products of this reaction are AMP and a compound containing selenium bonded to phosphorus. The reaction is completely dependent on the addition of both selenide and magnesium. The dependence of reaction velocity on ATP concentration shows sigmoidal kinetics, whereas dependence on selenide concentration obeys Michaelis-Menten kinetics indicating a K(m) value of 46-mu-M for selenide. C1 NHLBI,BIOCHEM LAB,BLDG 3,ROOM 108,BETHESDA,MD 20892. NHLBI,CARDIAC ENERGET LAB,BETHESDA,MD 20892. HUNGARIAN ACAD SCI,CENT RES INST CHEM,H-1025 BUDAPEST,HUNGARY. RI Balaban, Robert/A-7459-2009 OI Balaban, Robert/0000-0003-4086-0948 NR 17 TC 100 Z9 101 U1 1 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2975 EP 2979 DI 10.1073/pnas.89.7.2975 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600096 PM 1557403 ER PT J AU BERNEMAN, ZN GARTENHAUS, RB REITZ, MS BLATTNER, WA MANNS, A HANCHARD, B IKEHARA, O GALLO, RC KLOTMAN, ME AF BERNEMAN, ZN GARTENHAUS, RB REITZ, MS BLATTNER, WA MANNS, A HANCHARD, B IKEHARA, O GALLO, RC KLOTMAN, ME TI EXPRESSION OF ALTERNATIVELY SPLICED HUMAN T-LYMPHOTROPIC VIRUS TYPE-I PX MESSENGER-RNA IN INFECTED CELL-LINES AND IN PRIMARY UNCULTURED CELLS FROM PATIENTS WITH ADULT T-CELL LEUKEMIA LYMPHOMA AND HEALTHY CARRIERS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ADULT T-CELL LEUKEMIA; ALTERNATIVE SPLICING; GENE EXPRESSION; HUMAN RETROVIRUS; REGULATORY GENES ID HTLV-I; GENE; TRANSFORMATION; INVITRO; FRESH; ACID; DNA; LYMPHOCYTES; METHYLATION; TRANSCRIPTS AB Although human T-cell lymphotropic virus type I (HTLV-I) is the etiologic agent of adult T-cell leukemia/lyumphoma (ATL), the role of viral gene expression in the progression to and maintenance of the leukemic state in vivo is unclear because of the inability of most previous studies to readily detect HTLV-I RNA in infected individuals. By using the reverse transcriptase-polymerase chain reaction, we detected spliced messages for the HTLV-I pX regulatory genes in primary uncultured cells from ATL patients and healthy asymptomatic carriers. In addition to the expected doubly spliced pX message, three alternatively spliced mRNAs were demonstrated (pX-DELTA-17, pX-p21rex, and pX-orfII mRNAs, where orf = open reading frame). The same splice sites were shown in the messages from uncultured ATL cells and from the HTLV-I-producing C10/MJ cell line. Alternatively spliced pX mRNAs have the potential to code for known and putative pX gene products. Among the transcripts is a monocistronic mRNA likely to code for p21rex (pX-p21rex mRNA). Since alternative splicing of HTLV-I pX mRNA can be found in primary uncultured cells, it is likely to have a functional significance in vivo. This suggests possible roles for HTLV-I gene expression in the progression to and maintenance of ATL, as well as in the phase preceding it. C1 NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. OKINAWA CHUBU HOSP,DEPT INTERNAL MED,OKINAWA,JAPAN. UNIV W INDIES,KINGSTON 7,JAMAICA. RP BERNEMAN, ZN (reprint author), NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892, USA. RI klotman, mary/A-1921-2016 NR 39 TC 137 Z9 137 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 3005 EP 3009 DI 10.1073/pnas.89.7.3005 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600102 PM 1348363 ER PT J AU GUO, NH KRUTZSCH, HC NEGRE, E VOGEL, T BLAKE, DA ROBERTS, DD AF GUO, NH KRUTZSCH, HC NEGRE, E VOGEL, T BLAKE, DA ROBERTS, DD TI HEPARIN-BINDING AND SULFATIDE-BINDING PEPTIDES FROM THE TYPE-I REPEATS OF HUMAN THROMBOSPONDIN PROMOTE MELANOMA CELL-ADHESION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE TRYPTOPHAN; LAMININ; PROPERDIN REPEATS ID PLATELET THROMBOSPONDIN; CIRCUMSPOROZOITE PROTEIN; SEQUENCE; DOMAIN; GLYCOPROTEIN; GLYCOLIPIDS; EXPRESSION; ACID AB Peptides from the three type I repeats of human endothelial cell thrombospondin, containing the consensus sequence-Trp-Ser-Xaa-Trp-, bind to sulfated glycoconjugates including heparin and sulfatide. The peptides are potent inhibitors for the binding of thrombospondin, laminin, or apolipoprotein E to these ligands. The thrombospondin peptides that inhibit heparin binding, but not adjacent peptides from the thrombospondin sequence containing the previously identified adhesive motif Val-Thr-Cys-Gly, promote melanoma cell adhesion when immobilized on plastic. Melanoma cell adhesion to the immobilized peptides is inhibited by soluble recombinant heparin-binding fragment of thrombospondin. The peptides also inhibit heparin-dependent binding of thrombospondin or laminin to human melanoma cells. The active peptides lack any previously identified heparin-binding consensus sequences and most do not contain any basic amino acids. Studies with homologous peptides showed that the tryptophan residues are required for binding. Adjacent basic residues in the second type I repeat enhance binding to heparin but not to sulfatide. Thus the type I peptides of thrombospondin define a distinct class of heparin-binding peptides. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. MEHARRY MED COLL,DEPT BIOCHEM,NASHVILLE,TN 37208. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 FU NEI NIH HHS [R01 EY09092] NR 30 TC 143 Z9 144 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 3040 EP 3044 DI 10.1073/pnas.89.7.3040 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600109 PM 1557410 ER PT J AU BRINKMANN, U PAI, LH FITZGERALD, DJ PASTAN, I AF BRINKMANN, U PAI, LH FITZGERALD, DJ PASTAN, I TI ALTERATION OF A PROTEASE-SENSITIVE REGION OF PSEUDOMONAS EXOTOXIN PROLONGS ITS SURVIVAL IN THE CIRCULATION OF MICE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE IMMUNOTOXIN; CANCER; PROTEIN ENGINEERING; TRYPSIN; PLASMIN ID ESCHERICHIA-COLI; ANIMAL TOXICITY; TOXIN; AERUGINOSA; PLASMINOGEN; EXPRESSION; CLONING; GENE AB Pseudomonas exotoxin A (PE) is a single-chain 66-kDa polypeptide that kills eukaryotic cells by ADP-ribosylation of translational elongation factor 2. PE is composed of three major structural domains whose functions are binding of cells (I), translocation (II), and ADP-ribosylation (III). Here we describe a protease cleavage target that is located near arginine-490 on the surface of domain III. We made several different types of mutations near arginine-490. Deletion of arginine-490 or replacement of arginine-490 and -492 with serine and lysine or with two lysines resulted in protease-resistant molecules that were fully cytotoxic and had normal ADP-ribosylation activity. However, the half-life in mouse blood of the PE-DELTA-490 mutant was 24 min whereas that of PE was 13 min. Furthermore, two PE mutants that were protease-hypersensitive, PEGlu246,247,249 and PEGlu57,246,247,249 (in which glutamate residues replace basic residues at the indicated positions), had very short half-lives. These data indicate that protease sensitivity is an important determinant in the half-life of PE in the circulation and suggest that the half-life of other proteins may be prolonged by removal of protease sites. Deletion of arginine-492 or the replacement of amino acids 486-491 with three glycines markedly diminished ADP-ribosylation activity and cytotoxicity, indicating that this region of domain III is also important for catalytic activity. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 22 TC 20 Z9 20 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 3065 EP 3069 DI 10.1073/pnas.89.7.3065 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600114 PM 1557414 ER PT J AU BRINKMANN, U BUCHNER, J PASTAN, I AF BRINKMANN, U BUCHNER, J PASTAN, I TI INDEPENDENT DOMAIN FOLDING OF PSEUDOMONAS EXOTOXIN AND SINGLE-CHAIN IMMUNOTOXINS - INFLUENCE OF INTERDOMAIN CONNECTIONS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE B3(FV)-PE38KDEL; RENATURATION; PROTEIN ENGINEERING ID ASPARTOKINASE-HOMOSERINE DEHYDROGENASE; ESCHERICHIA-COLI; SUBUNIT INTERACTIONS; OLIGOMERIC PROTEINS; ANIMAL TOXICITY; AERUGINOSA; TOXIN; EXPRESSION; POLYMERASE; SEQUENCE AB We have studied the refolding of completely unfolded and reduced Pseudomonas exotoxin (PE) and of recombinant single-chain immunotoxins made with monoclonal antibody B3 that are composed of a heavy-chain variable region connected by a flexible linker to the corresponding light-chain variable region (Fv), which is in turn fused to a truncated form of PE. We have found by direct activity assays that different functional domains of these multifunctional proteins fold independently with different kinetics. The ADP-ribosylation domain of PE and of the recombinant immunotoxin fold rapidly, whereas the assembly of the binding and/or translocation domains is regained more slowly. The complete refolding of native PE occurs more rapidly than the refolding of the recombinant immunotoxins. To determine the influence of the connector region between the B3(Fv) moiety and the toxin on the folding process of the recombinant immunotoxin B3(Fv)-PE38KDEL, we have made two different mutations in the peptide that connects the single-chain Fv domain to domain II of PE. These molecules show different folding kinetics, differences in their propensity to aggregate, and different yields of correctly folded molecules. A mutation that decreases aggregation increases the rate of formation and the yield of active immunotoxin molecules. RP BRINKMANN, U (reprint author), NCI,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,37-4E16,BETHESDA,MD 20892, USA. RI Buchner, Johannes/A-2651-2010 NR 33 TC 92 Z9 96 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 3075 EP 3079 DI 10.1073/pnas.89.7.3075 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600116 PM 1557415 ER PT J AU WANK, SA HARKINS, R JENSEN, RT SHAPIRA, H DEWEERTH, A SLATTERY, T AF WANK, SA HARKINS, R JENSEN, RT SHAPIRA, H DEWEERTH, A SLATTERY, T TI PURIFICATION, MOLECULAR-CLONING, AND FUNCTIONAL EXPRESSION OF THE CHOLECYSTOKININ RECEPTOR FROM RAT PANCREAS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GASTROINTESTINAL PEPTIDE RECEPTOR; NEUROPEPTIDE RECEPTOR; G-PROTEIN-COUPLED RECEPTOR; GASTRIN RECEPTOR ID XENOPUS-OOCYTES; PHOSPHOLIPASE-C; CDNA CLONING; PROTEIN; ANTAGONIST; SEQUENCE; BINDING; POTENT; PROBES; GENE AB The cholecystokinin (CCK) family of peptides and their receptors are widely distributed throughout the gastrointestinal and central nervous systems where they regulate secretion, motility, growth, anxiety, and satiety. The CCK receptors can be subdivided into at least two subtypes, CCK(A) and CCK(B) on the basis of pharmacological studies. We report here the purification of the CCK(A) receptor to homogeneity from rat pancreas by using ion-exchange and multiple affinity chromatographic separations. This allowed partial peptide sequencing after chemical/enzymatic cleavage and synthesis of degenerate oligonucleotide primers. These primers were used for initial cloning of the cDNA from rat pancreas by PCR. The predicted protein sequence of the cDNA clone contained the five partial peptide sequences obtained from the purified protein. Seven putative transmembrane domains suggest its membership in the guanine nucleotide-binding regulatory protein-coupled receptor superfamily. In vitro transcripts of the cDNA clone were functionally expressed in Xenopus oocytes and displayed the expected agonist and antagonist specificity. C1 BERLEX BIOSCI,ALAMEDA,CA 94501. NINCDS,NEUROCHEM LAB,BETHESDA,MD 20892. RP WANK, SA (reprint author), NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892, USA. NR 36 TC 405 Z9 409 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 3125 EP 3129 DI 10.1073/pnas.89.7.3125 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600127 PM 1313582 ER PT J AU ROMANCZUK, H HOWLEY, PM AF ROMANCZUK, H HOWLEY, PM TI DISRUPTION OF EITHER THE E1-REGULATORY OR THE E2-REGULATORY GENE OF HUMAN PAPILLOMAVIRUS TYPE-16 INCREASES VIRAL IMMORTALIZATION CAPACITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HUMAN EPITHELIAL CELLS; IMMORTALIZATION ID CARCINOMA CELL-LINES; PRIMARY HUMAN KERATINOCYTES; HPV18 REGULATORY REGION; CERVICAL-CARCINOMA; TRANSCRIPTIONAL REGULATION; GENITAL TUMORS; DNA; IDENTIFICATION; PROTEIN; SEQUENCES AB The "high-risk" human papillomavirus types 16 (HPV-16) and 18 (HPV-18) have been etiologically implicated in the majority of human cervical carcinomas. In these cancers, the viral DNAs are often integrated into the host genome so that expression of the E1 and the E2 genes is lost, suggesting that disruption of these regulatory genes plays an important role in carcinogenic progression. Previous studies defining the viral genes affecting HPV-16 transformation functions have used the "prototype" viral genome, which was cloned from a human cervical carcinoma and later discovered to harbor a mutation in the E1 gene. In this study, we have corrected this mutation and have evaluated the effect of mutations of either the E1 or the E2 gene on the efficiency of HPV-16 immortalization of human keratinocytes. Mutation of either the E1 gene or the E2 gene in the background of a "wild-type" HPV-16 genome markedly increased immortalization capacity. Mutations were also generated in the E2-binding sites located upstream of the P97 promoter, which directs synthesis of the viral E6 and E7 transforming genes. E2 negatively regulates the P97 promoter through binding at adjacent sites. Surprisingly, the mutation of these sites only partially relieved the negative effect of E2 on viral immortalization, implicating additional mechanisms in the E2 repression of viral immortalization functions. Our results provide genetic evidence that the E1 and E2 gene products each can repress HPV-16 immortalization and support the hypothesis that a selective growth advantage is provided by integration of the viral genome in a manner that causes the loss of expression of either E1 or E2. RP ROMANCZUK, H (reprint author), NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892, USA. NR 41 TC 204 Z9 210 U1 1 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 3159 EP 3163 DI 10.1073/pnas.89.7.3159 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600134 PM 1313584 ER PT J AU MAJEWSKA, MD AF MAJEWSKA, MD TI NEUROSTEROIDS - ENDOGENOUS BIMODAL MODULATORS OF THE GABA-A RECEPTOR - MECHANISM OF ACTION AND PHYSIOLOGICAL SIGNIFICANCE SO PROGRESS IN NEUROBIOLOGY LA English DT Review ID CENTRAL NERVOUS-SYSTEM; RAT-BRAIN; PREGNENOLONE-SULFATE; DEHYDROEPIANDROSTERONE SULFATE; 3-ALPHA-HYDROXYSTEROID OXIDOREDUCTASE; PROGESTERONE 5-ALPHA-REDUCTASE; STEROID ANESTHETICS; A RECEPTORS; GUINEA-PIG; POTENTIATION C1 NIDA, ADDICT RES CTR, NEUROPHARMACOL LAB, BALTIMORE, MD USA. NR 127 TC 988 Z9 1004 U1 2 U2 26 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0301-0082 J9 PROG NEUROBIOL JI Prog. Neurobiol. PD APR PY 1992 VL 38 IS 4 BP 379 EP 395 DI 10.1016/0301-0082(92)90025-A PG 17 WC Neurosciences SC Neurosciences & Neurology GA HL070 UT WOS:A1992HL07000002 PM 1349441 ER PT J AU CITRON, BA DAVIS, MD KAUFMAN, S AF CITRON, BA DAVIS, MD KAUFMAN, S TI PURIFICATION AND BIOCHEMICAL-CHARACTERIZATION OF RECOMBINANT RAT-LIVER PHENYLALANINE-HYDROXYLASE PRODUCED IN ESCHERICHIA-COLI SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article ID AMINO-ACIDS; ACTIVATION; IRON; 4-MONOOXYGENASE; PHOSPHORYLATION; LYSOLECITHIN; STIMULATION; PHOSPHATE; SEQUENCE; PROTEINS RP CITRON, BA (reprint author), NIMH,NEUROCHEM LAB,ROOM 3D30,BLDG 36,BETHESDA,MD 20892, USA. NR 44 TC 21 Z9 21 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 1046-5928 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD APR PY 1992 VL 3 IS 2 BP 93 EP 100 DI 10.1016/S1046-5928(05)80024-5 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA HR334 UT WOS:A1992HR33400002 PM 1422220 ER PT J AU HONG, W CHAN, L ZHENG, DC WANG, C AF HONG, W CHAN, L ZHENG, DC WANG, C TI NEURASTHENIA IN CHINESE STUDENTS AT UCLA SO PSYCHIATRIC ANNALS LA English DT Article ID DEPRESSION; PREVALENCE RP HONG, W (reprint author), NIMH,BLDG 10,ROOM 4N-214,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 8 TC 3 Z9 3 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD APR PY 1992 VL 22 IS 4 BP 199 EP 201 PG 3 WC Psychiatry SC Psychiatry GA HN245 UT WOS:A1992HN24500008 ER PT J AU MERTZ, PM FOX, PC PLUTA, A BAUM, BJ KOUSVELARI, EE AF MERTZ, PM FOX, PC PLUTA, A BAUM, BJ KOUSVELARI, EE TI EFFECTS OF IONIZING-RADIATION AND BETA-ADRENERGIC STIMULATION ON THE EXPRESSION OF EARLY RESPONSE GENES IN RAT PAROTID-GLANDS SO RADIATION RESEARCH LA English DT Article ID GROWTH-FACTORS; JUN PROTEINS; C-JUN; FOS; CELLS; MOUSE; IRRADIATION; INVITRO; INDUCTION; SECRETION C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. NR 39 TC 17 Z9 17 U1 0 U2 1 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD APR PY 1992 VL 130 IS 1 BP 104 EP 112 DI 10.2307/3578486 PG 9 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA HM582 UT WOS:A1992HM58200015 PM 1561308 ER PT J AU CHOYKE, PL MILLER, DL LOTZE, MT WHITEIS, JM EBBITT, B ROSENBERG, SA AF CHOYKE, PL MILLER, DL LOTZE, MT WHITEIS, JM EBBITT, B ROSENBERG, SA TI DELAYED-REACTIONS TO CONTRAST-MEDIA AFTER INTERLEUKIN-2 IMMUNOTHERAPY SO RADIOLOGY LA English DT Article DE COMPUTED TOMOGRAPHY (CT), CONTRAST MEDIA; CONTRAST MEDIA, TOXICITY; DIATRIZOATE; IOPAMIDOL; LYMPHOKINES ID ACTIVATED KILLER CELLS; HYPERSENSITIVITY; CORTICOSTEROIDS; TOXICITY AB A prospective study was conducted by means of a questionnaire to determine the prevalence of delayed reactions to contrast media administered intravenously (iopamidol) and orally (diatrizoate sodium) in 170 patients who had received interleukin-2 (IL-2) and in 631 patients who did not. Another control group of 100 non-IL-2 patients received only oral contrast medium. Delayed reactions (eg, fever, rash, flulike symptoms, joint pain, flushing, pruritis, and dizziness) were reported in 3.9% (25 of 631) of non-IL-2 patients and in 11.8% (20 of 170) of IL-2 patients. Reactions were mild in the non-IL-2 patients but were more severe in the IL-2 patients. Two IL-2 patients required hospitalization. Only rash, flulike symptoms, and pruritis were statistically more common in IL-2 patients than in non-IL-2 patients. The prevalence of delayed reactions to nonionic contrast medium is higher in patients who have received IL-2 than in the general population. Most delayed reactions do not require therapy, but, when necessary, therapy is usually limited to relief of symptoms. C1 UNIV PITTSBURGH,PITTSBURGH CANC INST,DEPT SURG,DIV SURG ONCOL,PITTSBURGH,PA 15260. NCI,SURG BRANCH,BETHESDA,MD 20892. RP CHOYKE, PL (reprint author), NCI,DEPT DIAGNOST RADIOL,BLDG 10,RM IC660,BETHESDA,MD 20892, USA. NR 18 TC 44 Z9 45 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 1992 VL 183 IS 1 BP 111 EP 114 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HJ874 UT WOS:A1992HJ87400020 PM 1549655 ER PT J AU STACEYCLEAR, A MCCARTHY, KA HALL, DA PILESPELLMAN, ER MROSE, HE WHITE, G CARDENOSA, G SAWICKA, J MAHONEY, E KOPANS, DB AF STACEYCLEAR, A MCCARTHY, KA HALL, DA PILESPELLMAN, ER MROSE, HE WHITE, G CARDENOSA, G SAWICKA, J MAHONEY, E KOPANS, DB TI CALCIFIED SUTURE MATERIAL IN THE BREAST AFTER RADIATION-THERAPY SO RADIOLOGY LA English DT Article DE BREAST, CALCIFICATION; BREAST NEOPLASMS, DIAGNOSIS; BREAST NEOPLASMS, POSTOPERATIVE; BREAST NEOPLASMS, THERAPY ID IRRADIATED BREAST; CALCIFICATIONS; CANCER; RECURRENCE; EXCISION AB Of 335 women who underwent lumpectomy and radiation therapy for breast cancer, 42 subsequently developed calcifications. Particles typical of calcified suture material were identified in 21 of the 42 women (50%). No obvious calcified suture material was found in approximately 1,140 women of 38,000 (3%) who had undergone mammography after they had previously undergone breast biopsy for a benign lesion and thus had not undergone radiation therapy. Calcified suture material rarely develops in the nonirradiated breast, but it is common after radiation therapy and should not be confused with recurrent breast cancer. These calcifications are likely the result of delayed resorption of catgut sutures, which provide a matrix on which calcium can precipitate in a suitable local environment. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. NIH,DEPT RADIOL,BETHESDA,MD 20892. ILLINOIS MASONIC MED CTR,DEPT RADIAT MED,CHICAGO,IL 60657. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. SUSAN KOMEN BREAST CTR,PEORIA,IL. NR 13 TC 6 Z9 6 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 1992 VL 183 IS 1 BP 207 EP 208 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HJ874 UT WOS:A1992HJ87400038 PM 1549672 ER PT J AU GREM, JL CHU, E BOARMAN, D BALIS, FM MURPHY, RF MCATEE, N ALLEGRA, CJ AF GREM, JL CHU, E BOARMAN, D BALIS, FM MURPHY, RF MCATEE, N ALLEGRA, CJ TI BIOCHEMICAL MODULATION OF FLUOROURACIL WITH LEUCOVORIN AND INTERFERON - PRECLINICAL AND CLINICAL INVESTIGATIONS SO SEMINARS IN ONCOLOGY LA English DT Article ID METASTATIC COLORECTAL-CARCINOMA; INTRACELLULAR FOLATE POOLS; THYMIDYLATE SYNTHETASE; CELL-LINES; RANDOMIZED TRIAL; BREAST-CANCER; FOLINIC ACID; METHOTREXATE; 5-FLUOROURACIL; INHIBITION RP GREM, JL (reprint author), NCI,MED BRANCH,BLDG 10,RM 12N226,BETHESDA,MD 20892, USA. NR 29 TC 42 Z9 42 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 1992 VL 19 IS 2 SU 3 BP 36 EP 44 PG 9 WC Oncology SC Oncology GA HN629 UT WOS:A1992HN62900006 PM 1557656 ER PT J AU GREM, JL AF GREM, JL TI BIOCHEMICAL MODULATION OF FLUOROURACIL BY DIPYRIDAMOLE - PRECLINICAL AND CLINICAL-EXPERIENCE SO SEMINARS IN ONCOLOGY LA English DT Article ID COLON CANCER-CELLS; PHASE-I TRIAL; CYTO-TOXICITY; NUCLEOSIDE SALVAGE; INHIBITION; 5-FLUOROURACIL; AUGMENTATION; ACIVICIN; METHOTREXATE; ENHANCEMENT RP GREM, JL (reprint author), NCI,MED BRANCH,DIV CANC TREATMENT,CLIN ONCOL PROGRAM,BLDG 10,RM 12N-226,BETHESDA,MD 20892, USA. NR 20 TC 25 Z9 25 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 1992 VL 19 IS 2 SU 3 BP 56 EP 65 PG 10 WC Oncology SC Oncology GA HN629 UT WOS:A1992HN62900009 PM 1557658 ER PT J AU KORN, EL DOREY, FJ AF KORN, EL DOREY, FJ TI APPLICATIONS OF CRUDE INCIDENCE CURVES SO STATISTICS IN MEDICINE LA English DT Article ID COMPETING-RISKS; PROSTATE-CANCER; SAMPLE; PROBABILITIES; SURVIVAL AB Crude incidence curves display the cumulative number of failures of interest as a function of time. With competing causes of failure, they are distinct from cause-specific incidence curves that treat secondary types of failures as censored observations. After briefly reviewing their definition and estimation, we present five applications of crude incidence curves to show their utility in a broad range of studies. In some of these applications it is helpful to model survival-time distributions with use of two different time metameters, for example, time from diagnosis and age of the patient. We describe how one can incorporate published vital statistics into the models when secondary types of failure correspond to common causes of death. C1 UNIV CALIF LOS ANGELES,DIV ORTHOPAED SURG,LOS ANGELES,CA 90024. RP KORN, EL (reprint author), NCI,BIOMETR RES BRANCH,EPN ROOM 739,BETHESDA,MD 20892, USA. NR 17 TC 91 Z9 92 U1 0 U2 4 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR PY 1992 VL 11 IS 6 BP 813 EP 829 DI 10.1002/sim.4780110611 PG 17 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA HU098 UT WOS:A1992HU09800009 PM 1594819 ER PT J AU TIZABI, Y CALOGERO, AE AF TIZABI, Y CALOGERO, AE TI EFFECT OF VARIOUS NEUROTRANSMITTERS AND NEUROPEPTIDES ON THE RELEASE OF CORTICOTROPIN-RELEASING HORMONE FROM THE RAT CORTEX INVITRO SO SYNAPSE LA English DT Article DE HYPOTHALAMUS; ACETYLCHOLINE; GLUTAMATE; SEROTONIN; SOMATOSTATIN; NEUROPEPTIDE-Y ID SOMATOSTATIN-LIKE IMMUNOREACTIVITY; CENTRAL NERVOUS-SYSTEM; HYPOPHYSEAL PORTAL BLOOD; ALZHEIMERS-DISEASE; CEREBRAL-CORTEX; GROWTH-HORMONE; HYPOTHALAMUS INVITRO; FACTOR RECEPTORS; MEDIAN-EMINENCE; SECRETION INVITRO AB Corticotropin-releasing hormone (CRH), in addition to its neuroendocrine role, may act as a central neurotransmitter. Cerebral cortical CRH may have an important role in behavioral and neurodegenerative disorders. To gain an understanding of factors that may influence cortical CRH, we investigated the effect of several neurotransmitters and neuropeptides on the release of immunoreactive CRH (iCRH) from various cerebral cortical regions [frontal (FC), parietal (PC), temporal (TC), and occipital (OC)] in vitro. The hypothalamic release of iCRH was also evaluated under the same experimental conditions. Basal release of iCRH was approximately 2-fold, and KCl-stimulated iCRH release was approximately 4-fold higher in the hypothalamus than in any of the cortical regions. Cortical iCRH release was stimulated by 10 nM somatostatin (SRIF) in PC and 1 nM neuropeptide Y (NPY) in TC. Cortical iCRH release was inhibited by 1 and 10 nM acetylcholine (ACh), 0.1-mu-M glutamate, and 10 nM NPY. These effects were confined to the FC and/or PC. Hypothalamic iCRH release was stimulated by 1 and 10 nM ACh, 10-mu-M GABA, and 1 and 10 nM serotonin but was inhibited by 10 nM SRIF and 1-mu-M GABA. Growth hormone-releasing hormone did not affect cortical or hypothalamic iCRH release. These results demonstrate that CRH release from the cerebral cortex and the hypothalamus are under different regulatory mechanism(s). Furthermore, they indicate that the release of CRH in various cortical regions may be regulated differentially by the same neurotransmitter. C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP TIZABI, Y (reprint author), HOWARD UNIV,COLL MED,DEPT PHARMACOL,WASHINGTON,DC 20059, USA. NR 77 TC 18 Z9 19 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 0887-4476 J9 SYNAPSE JI Synapse PD APR PY 1992 VL 10 IS 4 BP 341 EP 348 DI 10.1002/syn.890100409 PG 8 WC Neurosciences SC Neurosciences & Neurology GA HJ964 UT WOS:A1992HJ96400008 PM 1350113 ER PT J AU SCHWETZ, BA AF SCHWETZ, BA TI CRITERIA FOR JUDGING THE RELATIVE TOXICITY OF CHEMICALS FROM DEVELOPMENTAL TOXICITY DATA - A WORKSHOP SUMMARY SO TERATOLOGY LA English DT Article RP SCHWETZ, BA (reprint author), NIEHS,DIV TOXICOL RES & TESTING,SYST TOXIC BRANCH,RES TRIANGLE PK,NC 27709, USA. NR 3 TC 9 Z9 9 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 0040-3709 J9 TERATOLOGY JI Teratology PD APR PY 1992 VL 45 IS 4 BP 337 EP 339 DI 10.1002/tera.1420450403 PG 3 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA HK973 UT WOS:A1992HK97300002 PM 1350114 ER PT J AU COOGAN, TP BARE, RM WAALKES, MP AF COOGAN, TP BARE, RM WAALKES, MP TI CADMIUM-INDUCED DNA STRAND DAMAGE IN CULTURED LIVER-CELLS - REDUCTION IN CADMIUM GENOTOXICITY FOLLOWING ZINC PRETREATMENT SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID ISOLATED RAT HEPATOCYTES; WISTAR CRL-(WI)BR RATS; DOSE-RESPONSE ANALYSIS; CHINESE-HAMSTER CELLS; MAMMALIAN-CELLS; TUMOR-INDUCTION; INJECTION SITE; CYTO-TOXICITY; METALLOTHIONEIN; CHLORIDE RP COOGAN, TP (reprint author), NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,INORGAN CARCINOGENESIS SECT,FREDERICK,MD 21702, USA. NR 45 TC 103 Z9 112 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD APR PY 1992 VL 113 IS 2 BP 227 EP 233 DI 10.1016/0041-008X(92)90118-C PG 7 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA HP304 UT WOS:A1992HP30400007 PM 1561631 ER PT J AU BERLIN, PJ BACHER, JD SHARROW, SO GONZALEZ, C GRESS, RE AF BERLIN, PJ BACHER, JD SHARROW, SO GONZALEZ, C GRESS, RE TI MONOCLONAL-ANTIBODIES AGAINST HUMAN T-CELL ADHESION MOLECULES - MODULATION OF IMMUNE FUNCTION IN NONHUMAN-PRIMATES SO TRANSPLANTATION LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; BONE-MARROW TRANSPLANTATION; ALLOGRAFT-REJECTION; GRAFT-REJECTION; ORGAN-TRANSPLANTATION; INTERLEUKIN-2; PREVENTION; OKT3; IMMUNOSUPPRESSION; THERAPY AB The cytotoxic T cell is thought to be a primary effector of allograft rejection. In vitro studies have demonstrated that the interaction between cytotoxic T cells and target cells involves cell surface adhesion molecules that result in conjugate formation, with subsequent antigen recognition, T cell activation, and target cell lysis. Experiments have also demonstrated the ability of monoclonal antibodies with specificity for two human T cell adhesion molecules, lymphocyte function associated (LFA) antigen-1 (LFA-1, CD11a, alpha-chain/CD18, beta-chain) and LFA-2 (CD2), to inhibit conjugate formation in vitro. Studies in a nonhuman primate model were undertaken to determine whether the in vivo administration of monoclonal antibodies with specificity for the alpha chain of LFA-1 (CD11a) or with specificity for CD2 could modulate in vivo T cell function. Cynomolgus monkeys (Macaca fascicularis) received 10 daily intravenous infusions of either anti-CD11a, anti-CD2 or both anti-CD11a and anti-CD2 monoclonal antibodies. Antibody administration was well tolerated and resulted in high levels of circulating murine monoclonal antibody in the peripheral circulation. Nearly all the animals generated antimurine antibodies that were specific for both idiotypic and nonidiotypic determinants of the infused mouse protein. Circulating lymphocytes and T cells were not depleted by treatment with anti-CD11a or anti-CD2 mAbs; in fact, treatment with the combination of anti-CD11a plus anti-CD2 or anti-CD11a alone led to increased numbers of circulating lymphocytes and T cells. Modulation of the LFA-1 molecule on circulating T cells occurred as a result of treatment with anti-CD11a (or the combination of anti-CD11a plus anti-CD2), whereas treatment with anti-CD2 (or anti-CD11a plus anti-CD2) did not result in modulation of the CD2 antigen despite detectable levels of circulating anti-CD2 mAb. In vivo T cell function was assessed by placement of skin allografts. As compared with treatment with saline or a control mAb, allograft survival was significantly prolonged in animals treated with anti-CD11a or combination treatment but not in animals receiving anti-CD2 alone. We conclude that the in vivo administration of anti-LFA-1 mAb may be useful for the blockade of effector T cell activity during allograft rejection, that saturation of antigen and antigen modulation may be important for efficacy of such antibody effects in vivo, and that monoclonal antibodies with specificity for functionally important T cell surface molecules may alter T cell function in vivo without lymphocyte depletion. C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B17,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NIH,DIV RES SERV,VET RESOURCES BRANCH,BETHESDA,MD 20892. NR 40 TC 40 Z9 41 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD APR PY 1992 VL 53 IS 4 BP 840 EP 849 DI 10.1097/00007890-199204000-00026 PG 10 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HP306 UT WOS:A1992HP30600026 PM 1348883 ER PT J AU EMERY, DW SHAFER, GE KARSON, EM SACHS, DH LEGUERN, C AF EMERY, DW SHAFER, GE KARSON, EM SACHS, DH LEGUERN, C TI EXPRESSION OF ALLOGENEIC CLASS-II CDNA IN SWINE BONE-MARROW CELLS TRANSDUCED WITH A RECOMBINANT RETROVIRUS SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 1ST INTERNATIONAL CONGRESS ON XENOTRANSPLANTATION CY AUG 25-28, 1991 CL MINNEAPOLIS, MN SP UNIV MINNESOTA, DEPT SURG C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH-E,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. NR 7 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1992 VL 24 IS 2 BP 468 EP 469 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HN857 UT WOS:A1992HN85700018 PM 1566392 ER PT J AU SYKES, M SACHS, DH AKSENTIJEVICH, I AF SYKES, M SACHS, DH AKSENTIJEVICH, I TI EFFECT OF NATURAL ANTIBODY ON XENOGENEIC BONE-MARROW ENGRAFTMENT SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 1ST INTERNATIONAL CONGRESS ON XENOTRANSPLANTATION CY AUG 25-28, 1991 CL MINNEAPOLIS, MN SP UNIV MINNESOTA, DEPT SURG ID MOUSE C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. RP SYKES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,TRANSPLANTAT BIOL RES CTR,MGH-E,BLDG 149,BOSTON,MA 02129, USA. NR 8 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1992 VL 24 IS 2 BP 497 EP 498 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HN857 UT WOS:A1992HN85700032 PM 1566403 ER PT J AU JUSTICE, MJ JENKINS, NA COPELAND, NG AF JUSTICE, MJ JENKINS, NA COPELAND, NG TI RECOMBINANT INBRED MOUSE STRAINS - MODELS FOR DISEASE STUDY SO TRENDS IN BIOTECHNOLOGY LA English DT Review ID DETERMINING ATHEROSCLEROSIS SUSCEPTIBILITY; DENSITY LIPOPROTEIN LEVELS; GENE; MICE; POLYMORPHISM; LINKAGE; LUPUS; LINES; TOOL AB Recombinant inbred (RI) strains of mice and the closely related recombinant congenic strains offer considerable promise for identifying and characterizing genes causally associated with many different diseases. Loci associated with diseases such as heart disease, autoimmune disease and leukemia have already been identified through the use of these unique strains. RP JUSTICE, MJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [5F32CA08853-02, N01-CO-74101] NR 43 TC 15 Z9 15 U1 2 U2 4 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-7799 J9 TRENDS BIOTECHNOL JI Trends Biotechnol. PD APR PY 1992 VL 10 IS 4 BP 120 EP 126 DI 10.1016/0167-7799(92)90193-Y PG 7 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA HQ057 UT WOS:A1992HQ05700006 PM 1368097 ER PT J AU ROBINSON, DL PETERSEN, SE AF ROBINSON, DL PETERSEN, SE TI THE PULVINAR AND VISUAL SALIENCE SO TRENDS IN NEUROSCIENCES LA English DT Review ID BEHAVING RHESUS-MONKEY; INDUCED STIMULUS MOVEMENT; SUPERIOR COLLICULUS; SPATIAL ATTENTION; RECEPTIVE-FIELDS; MACACA-MULATTA; CEBUS MONKEY; RESPONSES; PROJECTIONS; NEURONS AB One of the major problems of living in a rich visual environment is deciding which particular object or location should be chosen for complete processing or attention; that is, deciding which object is most salient at any particular time. The pulvinar has enlarged substantially during evolution, although little has previously been known about its function. Recent studies suggest that the pulvinar contains neurons that generate signals related to the salience of visual objects. This evidence includes: (1) anatomical and physiological observations of visual function; (2) augmented responses in the pulvinarfor visual stimuli presented in important contexts; (3) suppression of activity for stimuli presented in irrelevant conditions; (4) thalamic modulation producing behavioral changes in cued attention paradigms; and (5) similar changes with visual distracter tasks. C1 WASHINGTON UNIV,SCH MED,MCDONNELL CTR STUDIES HIGHER BRAIN FUNCT,DEPT NEUROL & NEUROL,ST LOUIS,MO 63110. RP ROBINSON, DL (reprint author), NEI,SENSORIMOTOR RES LAB,BETHESDA,MD 20892, USA. FU NEI NIH HHS [EY 08775]; NINDS NIH HHS [NS 06833] NR 47 TC 289 Z9 290 U1 1 U2 10 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD APR PY 1992 VL 15 IS 4 BP 127 EP 132 DI 10.1016/0166-2236(92)90354-B PG 6 WC Neurosciences SC Neurosciences & Neurology GA HL264 UT WOS:A1992HL26400005 PM 1374970 ER PT J AU GERFEN, CR AF GERFEN, CR TI THE NEOSTRIATAL MOSAIC - MULTIPLE LEVELS OF COMPARTMENTAL ORGANIZATION SO TRENDS IN NEUROSCIENCES LA English DT Review ID NIGRA PARS RETICULATA; CALCIUM-BINDING PROTEIN; D1 DOPAMINE RECEPTOR; SUBSTANTIA-NIGRA; OCULOMOTOR FUNCTIONS; BASAL GANGLIA; INTRACELLULAR INJECTION; CAUDATE-NUCLEUS; GLOBUS PALLIDUS; HORSERADISH-PEROXIDASE AB The striatum, which is the major component of the basal ganglta, displays a complex mosaic organization of neurochemical systems that are related to its neuroanatomical connections. This mosaic organization reflects multiple levels of functional compartments. The first level is determined by the segregation of two major striatal output systems, one to the globus pallidus (external segment) and the other to the entopeduncular nucleus and substantia nigra. The second level segregates the cortical outputs of sublaminae of layer V between the patch and matrix compartments of the striatum, which project to the dopaminergic and GABAergic neurons in the substantia nigra, respectively. The third level is related to the topography of cortical inputs by which regions of the striatum may be functionally defined on the basis of the cortical areas with which they are connected Neurochemical markers display complex mosaic patterns in the striatum that, when examined in the context of the multi-level compartmental organization of the striatum, reveal the highly organized manner by which the striatum processes cortical information. RP GERFEN, CR (reprint author), NIMH,CELL BIOL LAB,BLDG 36,ROOM 2D-10,BETHESDA,MD 20892, USA. NR 69 TC 865 Z9 873 U1 1 U2 15 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD APR PY 1992 VL 15 IS 4 BP 133 EP 139 DI 10.1016/0166-2236(92)90355-C PG 7 WC Neurosciences SC Neurosciences & Neurology GA HL264 UT WOS:A1992HL26400006 PM 1374971 ER PT J AU DIMITROV, DS WILLEY, RL MARTIN, MA BLUMENTHAL, R AF DIMITROV, DS WILLEY, RL MARTIN, MA BLUMENTHAL, R TI KINETICS OF HIV-1 INTERACTIONS WITH SCD4 AND CD4+ CELLS - IMPLICATIONS FOR INHIBITION OF VIRUS-INFECTION AND INITIAL STEPS OF VIRUS ENTRY INTO CELLS SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; RECOMBINANT SOLUBLE CD4; AIDS-RELATED COMPLEX; T-CELLS; HUMAN RETROVIRUS; FUSION; RECEPTOR; INVITRO; MEMBRANE; PROTEIN C1 NCI,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 42 TC 37 Z9 37 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1992 VL 187 IS 2 BP 398 EP 406 DI 10.1016/0042-6822(92)90441-Q PG 9 WC Virology SC Virology GA HH591 UT WOS:A1992HH59100002 PM 1347667 ER PT J AU CHEN, W DRILLIEN, R SPEHNER, D BULLER, RML AF CHEN, W DRILLIEN, R SPEHNER, D BULLER, RML TI RESTRICTED REPLICATION OF ECTROMELIA VIRUS IN CELL-CULTURE CORRELATES WITH MUTATIONS IN VIRUS-ENCODED HOST RANGE GENE SO VIROLOGY LA English DT Article ID HAMSTER OVARY CELLS; VACCINIA VIRUS; COWPOX VIRUS; MOUSEPOX VIRUS; SEQUENCE; DNA; PROTEIN; RESISTANCE; MULTIPLICATION; MUTANT C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. FAC MED STRASBOURG,INST VIROL,INSERM,U74,F-67000 STRASBOURG,FRANCE. FAC MED STRASBOURG,INST VIROL,LAB COMMUN UNIV LOUIS PASTEUR SYNTHELABO,F-67000 STRASBOURG,FRANCE. NR 37 TC 77 Z9 78 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 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1992 VL 187 IS 2 BP 433 EP 442 DI 10.1016/0042-6822(92)90445-U PG 10 WC Virology SC Virology GA HH591 UT WOS:A1992HH59100006 PM 1546448 ER PT J AU MENDELSON, E GROSSMAN, Z MILEGUIR, F RECHAVI, G CARTER, BJ AF MENDELSON, E GROSSMAN, Z MILEGUIR, F RECHAVI, G CARTER, BJ TI REPLICATION OF ADENOASSOCIATED VIRUS TYPE-2 IN HUMAN LYMPHOCYTIC CELLS AND INTERACTION WITH HIV-1 SO VIROLOGY LA English DT Article ID HERPES-SIMPLEX VIRUS; INHIBITS CELLULAR-TRANSFORMATION; VIRAL REP GENE; DNA AMPLIFICATION; ADENOASSOCIATED VIRUS; BOVINE PAPILLOMAVIRUS; PRODUCTIVE INFECTION; HUMAN PARVOVIRUS; MAMMALIAN-CELLS; CAPSID PROTEIN C1 CHAIM SHEBA MED CTR,DEPT HEMATOL,IL-52621 TEL HASHOMER,ISRAEL. NIDDKD,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. RP MENDELSON, E (reprint author), CHAIM SHEBA MED CTR,CENT VIROL LAB,IL-52621 TEL HASHOMER,ISRAEL. NR 60 TC 18 Z9 18 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 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1992 VL 187 IS 2 BP 453 EP 463 DI 10.1016/0042-6822(92)90447-W PG 11 WC Virology SC Virology GA HH591 UT WOS:A1992HH59100008 PM 1372138 ER PT J AU SADAIE, MR KALYANARAMAN, VS MUKOPADHAYAYA, R TSCHACHLER, E GALLO, RC WONGSTAAL, F AF SADAIE, MR KALYANARAMAN, VS MUKOPADHAYAYA, R TSCHACHLER, E GALLO, RC WONGSTAAL, F TI BIOLOGICAL CHARACTERIZATION OF NONINFECTIOUS HIV-1 PARTICLES LACKING THE ENVELOPE PROTEIN SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; SITE-DIRECTED MUTAGENESIS; VIRAL GENE-EXPRESSION; TRANS-ACTIVATOR GENE; HTLV-III; CELL-LINE; CD4-INDEPENDENT INFECTION; GAG PRECURSOR; T4 MOLECULE; TAT-III C1 ADV BIOSCI LABS INC,DEPT CELL BIOL,KENSINGTON,MD 20850. UNIV CALIF SAN DIEGO,SCH MED,LA JOLLA,CA 92093. RP SADAIE, MR (reprint author), NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 45 TC 16 Z9 16 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 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1992 VL 187 IS 2 BP 604 EP 611 PG 8 WC Virology SC Virology GA HH591 UT WOS:A1992HH59100023 PM 1546456 ER PT J AU ZHANG, YF MOSS, B AF ZHANG, YF MOSS, B TI IMMATURE VIRAL ENVELOPE FORMATION IS INTERRUPTED AT THE SAME STAGE BY LAC OPERATOR-MEDIATED REPRESSION OF THE VACCINIA VIRUS D13L GENE AND BY THE DRUG RIFAMPICIN SO VIROLOGY LA English DT Article ID POLYPEPTIDE; MUTANT; MORPHOGENESIS; RESISTANCE; EXPRESSION; PRECURSORS; BIOGENESIS; SEPARATION; SEQUENCE; CLUSTER C1 NIAID,VIRAL DIS LAB,BLDG 4,ROOM 229,BETHESDA,MD 20892. NR 31 TC 72 Z9 73 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 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1992 VL 187 IS 2 BP 643 EP 653 DI 10.1016/0042-6822(92)90467-4 PG 11 WC Virology SC Virology GA HH591 UT WOS:A1992HH59100028 PM 1546459 ER PT J AU FREDRICKSON, TN SECHLER, JMG PALUMBO, GJ ALBERT, J KHAIRALLAH, LH BULLER, RML AF FREDRICKSON, TN SECHLER, JMG PALUMBO, GJ ALBERT, J KHAIRALLAH, LH BULLER, RML TI ACUTE INFLAMMATORY RESPONSE TO COWPOX VIRUS-INFECTION OF THE CHORIOALLANTOIC MEMBRANE OF THE CHICK-EMBRYO SO VIROLOGY LA English DT Article ID GENERALIZED VIRAL-INFECTION; MEDIATED CYTO-TOXICITY; INFLUENZA-VIRUS; CELLS; MECHANISMS; RECOVERY; MOUSEPOX; PROTEIN; CYTOTOXICITY; NEUTROPHILS C1 NIAID,VIRAL DIS LAB,BLDG 4,ROOM 238,BETHESDA,MD 20892. UNIV CONNECTICUT,DEPT PHYSIOL & NEUROBIOL,STORRS,CT 06268. UNIV CONNECTICUT,DEPT PATHOBIOL,STORRS,CT 06268. GEORGETOWN UNIV,MED CTR,DIV MOLEC VIROL & IMMUNOL,ROCKVILLE,MD 20852. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NR 58 TC 24 Z9 24 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 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1992 VL 187 IS 2 BP 693 EP 704 DI 10.1016/0042-6822(92)90472-2 PG 12 WC Virology SC Virology GA HH591 UT WOS:A1992HH59100033 PM 1312273 ER PT J AU SHEIKH, MS SHAO, ZM CLEMMONS, DR LEROITH, D ROBERTS, CT FONTANA, JA AF SHEIKH, MS SHAO, ZM CLEMMONS, DR LEROITH, D ROBERTS, CT FONTANA, JA TI IDENTIFICATION OF THE INSULIN-LIKE GROWTH-FACTOR BINDING PROTEIN-5 AND PROTEIN-6 (IGFBP-5 AND IGFBP-6) IN HUMAN BREAST-CANCER CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID IGF-II RECEPTORS; DEOXYRIBONUCLEIC-ACID; RIBONUCLEIC-ACID; CLONING; SECRETION; LINES C1 UNIV MARYLAND,DEPT MED,BALTIMORE,MD 21201. VET ADM MED CTR,BALTIMORE,MD 21202. UNIV N CAROLINA,SCH MED,DEPT MED,CHAPEL HILL,NC 27514. NIH,DIABET BRANCH,BETHESDA,MD 20892. UNIV MARYLAND,CTR CANC,BALTIMORE,MD 21201. NR 24 TC 69 Z9 69 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 MAR 31 PY 1992 VL 183 IS 3 BP 1003 EP 1010 DI 10.1016/S0006-291X(05)80290-6 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HM246 UT WOS:A1992HM24600013 PM 1373605 ER PT J AU LANGFORD, K FRENZEL, K MARTIN, BM BERNSTEIN, KE AF LANGFORD, K FRENZEL, K MARTIN, BM BERNSTEIN, KE TI THE GENOMIC ORGANIZATION OF THE RAT AT1 ANGIOTENSIN RECEPTOR SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article C1 NIMH,ADM ALCOHOL ABUSE & MENTAL HLTH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP LANGFORD, K (reprint author), EMORY UNIV,DEPT PATHOL,ATLANTA,GA 30322, USA. FU NIDDK NIH HHS [DK39777, DK44280] NR 13 TC 49 Z9 50 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 MAR 31 PY 1992 VL 183 IS 3 BP 1025 EP 1032 DI 10.1016/S0006-291X(05)80293-1 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HM246 UT WOS:A1992HM24600016 PM 1533121 ER PT J AU VASTA, V SMITH, CJ CALVO, J BELFRAGE, P MANGANIELLO, VC AF VASTA, V SMITH, CJ CALVO, J BELFRAGE, P MANGANIELLO, VC TI INSULIN AND ISOPROTERENOL INDUCE PHOSPHORYLATION OF THE PARTICULATE CYCLIC GMP-INHIBITED, LOW KM CYCLIC-AMP PHOSPHODIESTERASE (CGI PDE) IN 3T3-L1 ADIPOCYTES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID KM CAMP PHOSPHODIESTERASE C1 NHLBI,CELLULAR METAB LAB,BLDG 10,ROOM SN-307,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NICHHD,THEORET BIOL LAB,BETHESDA,MD 20892. UNIV LUND,DEPT PHYSIOL CHEM,S-22101 LUND,SWEDEN. NIH,BETHESDA,MD 20892. NR 8 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 MAR 31 PY 1992 VL 183 IS 3 BP 1070 EP 1075 DI 10.1016/S0006-291X(05)80299-2 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HM246 UT WOS:A1992HM24600022 PM 1314573 ER PT J AU WATANABE, T WADA, N CHOU, JY AF WATANABE, T WADA, N CHOU, JY TI STRUCTURAL AND FUNCTIONAL-ANALYSIS OF HUMAN GERM-CELL ALKALINE-PHOSPHATASE BY SITE-SPECIFIC MUTAGENESIS SO BIOCHEMISTRY LA English DT Article ID ASPARAGINE-LINKED OLIGOSACCHARIDES; PHOSPHATIDYLINOSITOL-GLYCAN; CHORIONIC-GONADOTROPIN; CHORIOCARCINOMA CELLS; GENE; EXPRESSION; BIOSYNTHESIS; SECRETION; GLYCOSYLATION; EVOLUTION AB Human germ cell alkaline phosphatase (GCAP), which shares 98% amino acid sequence identity with the placental AP (PLAP), is expressed by malignant trophoblasts. Protein sequence analysis suggests that the Ser residue at position 92 is the putative active site of GCAP which contains two recognition sequences (Asn122-Thr-Thr124 and Asn249-Arg-Thr251) for asparagine-linked glycosylation. To examine the roles of the Ser residue and glycan moieties on GCAP activity and processing, we altered the GCAP cDNA by site-directed mutagenesis and expressed the GCAP mutants in COS-1 cells. Substitution of Ser-92 with either a Thr (S92T) or an Ala (S92A) residue yielded a GCAP devoid of catalytic activity, suggesting that the Ser codon 92 is the active site of GCAP. Six GCAP mutants that lack one or both glycosylation sites were constructed by substituting either Asn-122 or Asn-249 with an Asp residue or either Thr-124 or Thr-251 with an Ala residue. The mature GCAP migrated as a 65-kDa product, but GCAP mutants lacking one or both glycosylation sites migrated as 62- or 58-kDa polypeptides, respectively, indicating that both sites were glycosylated. All six glycosylated mutants were active enzymatically and, in addition, were equally sensitive to heat, L-leucine, and EDTA inhibition as the parental enzyme. GCAP as well as its two active-site and six glycosylation mutants could be released from the plasma membrane of transfected COS-1 cells by the proteinase bromelain. This indicates that GCAP is a membrane-bound enzyme located on the outer surface of the plasma membrane and substitution of Ser-92 or removal of oligosaccharide side chains did not prevent membrane anchoring of GCAP. The half-life values of GCAP, S92T, S92A, and the two double-glycosylation mutants were similar (45-46 h). However, the rate of AP synthesis and the total phosphatase activity in cells transfected with a double-glycosylation mutant were reduced when compared with cells transfected with a wild-type or a single-glycosylation mutant. Thus, removing both sugar side chains interferes with enzyme synthesis, but the glycan moieties are not essential for activity, stability, and membrane anchoring of GCAP. C1 NICHHD,HUMAN GENET BRANCH,BLDG 10,ROOM 95242,BETHESDA,MD 20892. NR 42 TC 8 Z9 8 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 MAR 31 PY 1992 VL 31 IS 12 BP 3051 EP 3058 DI 10.1021/bi00127a004 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HL679 UT WOS:A1992HL67900004 PM 1554693 ER PT J AU KOVACIK, V KOVAC, P GRUTZMACHER, HF AF KOVACIK, V KOVAC, P GRUTZMACHER, HF TI POSITIONAL IDENTIFICATION OF FLUORINE IN METHYL PER-O-ACETYL-X-DEOXY-X-FLUORO-ALPHA-D-HEXOPYRANOSIDES BY ELECTRON-IMPACT AND CHEMICAL IONIZATION MASS-SPECTROMETRY SO CARBOHYDRATE RESEARCH LA English DT Article ID IONIZATION; SPECTRA AB Fully acetylated methyl x-deoxy-x-fluoro-alpha-D-glucopyranosides have been studied using electron impact and ammonia chemical ionisation mass spectrometry. Mass analysed metastable ion kinetic energy spectroscopy (MIKE), collisional activation (CID), and accelerated voltage scanning have been used to evaluate complete fragmentation schemes. Characteristic differences in the fragmentation of positional isomers were noted on analysis of the spectra, and these make it possible to determine the location of fluorine in the molecules studied. Collisionally activated fragmentation of [M - OCH3]+ ions, produced by electron impact, provides an alternative method for localisation of the fluorine atoms. To the contrary, MIKE and CID spectra of [M + NH4]+ cluster ions produced by chemical ionisation did not afford such structural information. C1 NIDDK,BETHESDA,MD 20892. UNIV BIELEFELD,FAC CHEM,W-4800 BIELEFELD,GERMANY. RP KOVACIK, V (reprint author), SLOVAK ACAD SCI,INST CHEM,CS-84238 BRATISLAVA,CZECHOSLOVAKIA. NR 11 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD MAR 30 PY 1992 VL 226 IS 2 BP 189 EP 196 DI 10.1016/0008-6215(92)84066-2 PG 8 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA HN058 UT WOS:A1992HN05800001 PM 1617684 ER PT J AU HUNT, D VARIGOS, J DIENSTL, F LECHLEITNER, P DEBACKER, G KORNITZER, M CAIRNS, J TURPIE, A FRITZHANSEN, P SKAGEN, K KALA, R HEIKKILA, J BOISSEL, JP LEIZOROVICZ, A SCHRODER, R KOTHE, K KARATZAS, N HORGAN, J OCALLAGHAN, D TOGNONI, G FRANZOSI, MG MAGGIONI, A COHEN, A KOSTER, R WHITE, H MACMAHON, S KJEKSHUS, J REIKVAM, A CEREMUZYNSKI, L PAOLASSO, E DIAZ, R VALENTIN, V WILHELMSEN, L LUNDKVIST, L MOCCETTI, T MALACRIDA, R GENONI, M COLLINS, R SLEIGHT, P PETO, R PARISH, S DOLL, R ARMITAGE, P CEDERHOLMWILLIAMS, S CONWAY, M DOVE, P FLATHER, M MARSHALL, J YOUNGMAN, L JULIAN, D CHAMBERLAIN, D WARLOW, C SANDERCOCK, P FOX, K HENNEKENS, C GOLDHABER, S TIMMIS, G YUSUF, S MEIER, P AF HUNT, D VARIGOS, J DIENSTL, F LECHLEITNER, P DEBACKER, G KORNITZER, M CAIRNS, J TURPIE, A FRITZHANSEN, P SKAGEN, K KALA, R HEIKKILA, J BOISSEL, JP LEIZOROVICZ, A SCHRODER, R KOTHE, K KARATZAS, N HORGAN, J OCALLAGHAN, D TOGNONI, G FRANZOSI, MG MAGGIONI, A COHEN, A KOSTER, R WHITE, H MACMAHON, S KJEKSHUS, J REIKVAM, A CEREMUZYNSKI, L PAOLASSO, E DIAZ, R VALENTIN, V WILHELMSEN, L LUNDKVIST, L MOCCETTI, T MALACRIDA, R GENONI, M COLLINS, R SLEIGHT, P PETO, R PARISH, S DOLL, R ARMITAGE, P CEDERHOLMWILLIAMS, S CONWAY, M DOVE, P FLATHER, M MARSHALL, J YOUNGMAN, L JULIAN, D CHAMBERLAIN, D WARLOW, C SANDERCOCK, P FOX, K HENNEKENS, C GOLDHABER, S TIMMIS, G YUSUF, S MEIER, P TI ISIS-3 - A RANDOMIZED COMPARISON OF STREPTOKINASE VS TISSUE PLASMINOGEN-ACTIVATOR VS ANISTREPLASE AND OF ASPIRIN PLUS HEPARIN VS ASPIRIN ALONE AMONG 41,299 CASES OF SUSPECTED ACUTE MYOCARDIAL-INFARCTION SO LANCET LA English DT Article ID CONTINUOUS INTRAVENOUS HEPARIN; CLINICAL-TRIAL METHODOLOGY; LOW-DOSE ASPIRIN; CORONARY THROMBOLYSIS; SUBCUTANEOUS HEPARIN; RT-PA; VENTRICULAR-FUNCTION; VEIN THROMBOSIS; TIMI TRIAL; PHASE-I AB 41 299 patients entering 914 hospitals up to 24 h (median 4 h) after the onset of suspected acute myocardial infarction were randomised between streptokinase (SK: 1.5 MU infused over about 1 h), tissue plasminogen activator (tPA, duteplase: 0.60 MU/kg infused over about 4 h), or anisoylated plasminogen-streptokinase activator complex (APSAC, anistreplase: 30 U over about 3 min). All patients were to receive aspirin (162 mg/day enteric-coated), with the first tablet chewed for rapid and full antiplatelet effect. Half of all patients were randomly allocated subcutaneous calcium heparin (12 500 IU starting at 4 h and given twice daily for 7 days or until prior discharge) in addition to aspirin, and the other half were to receive aspirin alone. Aspirin plus heparin versus aspirin alone-The addition of heparin to aspirin was associated with an excess of transfused or other major non-cerebral bleeds (1.0% aspirin plus heparin vs 0.8% aspirin alone; 2p < 0.01) and of definite or probable cerebral haemorrhage (0.56% vs 0.40%; 2p < 0.05), but with no significant differences in total stroke (1.28% vs 1.18%). Reinfarctions were slightly less common among those allocated aspirin plus heparin (3.16% vs 3.47%; 2p = 0.09). There was no significant difference in the pre-specified endpoint of 35-day mortality (2132 [10.3%] aspirin plus heparin vs 2189 [10.6%] aspirin alone). During the scheduled heparin treatment period there were slightly fewer deaths in the aspirin plus heparin group (days 0.7 in hospital: 1534 [7.4%] vs 1633 [7.9%]; 2p = 0.06), with a slight convergence by day 35 (598 further deaths [3.1% of survivors] vs 556 [2.9%]). The pattern was similar to that observed in the GISSI-2 trial, so that in both trials combined there was a significant reduction in mortality during the scheduled treatment period (2071 [6.8% vs 2239 [7.3%]; 2p < 0.01). This indicates avoidance of 5 deaths (SD 2) per 1000 patients allocated this high-dose subcutaneous heparin regimen in addition to aspirin, but some of any early benefit may be lost after heparin ceases, with no significant mortality advantage in days 0.35 (both trials: 3100 [10.0%] vs 3172 (10.2%]) or during follow-up to 6 months. SK versus APSAC-APSAC was associated with significantly more reports of allergy causing persistent symptoms and of non-cerebral bleeds, but not of transfused bleeds or of reinfarctions. There was a slight excess of strokes with APSAC (1.04% SK vs 1.26% APSAC; 2p = 0.08), much of it appearing soon after treatment started (strokes during days 0-1: 0.50% SK vs 0.73% APSAC; 2p < 0.02) and being attributed to cerebral haemorrhage (0.24% SK vs 0.55% APSAC; 2p < 0.0001). No significant difference was observed in reinfarction (3.47% SK vs 3.55% APSAC). There was no significant mortality difference during days 0.35, either among all randomised patients (1455 [10.6%] SK vs 1448 [10.5%] APSAC) or among the pre-specified subset presenting within 0.6 h of pain onset and with ST elevation on the electrocardiogram in whom fibrinolytic treatment may have most to offer (861 [10.0%] SK vs 855 [9.9%] APSAC). No significant difference in 6-month survival was apparent overall or in the subset. SK versus tPA-tPA was associated with significantly fewer reports of allergy causing persistent symptoms and of hypotension requiring drug treatment, and with significantly more reports of non-cerebral bleeds, but not of transfused bleeds. There was a significant excess of strokes with tPA (1.04% SK vs 1.39% tPA; 2p < 0.01 ), much of it appearing soon after treatment started (strokes during days 0-1: 0.50% SK vs 0.92% tPA; 2p <0.0001) and being attributed to cerebral haemorrhage (0.24% SK vs 0.66% tPA; 2p < 0.00001). Fewer reinfarctions were observed with tPA (3.47% SK vs 2.93% tPA; 2p < 0.02).There was no significant mortality difference during days 0-35, either among all randomised patients (1455 [10.6%] SK vs 1418 [10.3%] tPA) or among the 0-6 h ST elevation subset (861 [10.0%] SK vs 822 [9.6%] tPA), and no difference in 6-month survival was apparent. These findings reinforce those from the similar GISSI-2 trial with, in both trials combined, zero difference in 35-day mortality (2413/24 176 [10.0%] SK vs 2411/24 118 [10.0%] tPA) and no significant difference in 6-month survival. There were 5 per 1000 fewer reinfarctions with tPA (783 [3.26%] SK vs 671 [2.80%] tPA; 2p < 0.005), and 4 per 1000 more strokes with tPA (239 [1.00%] SK vs 324 [1.35%] tPA; 2p < 0.001), with half of this excess being of fatal stroke and half of non-fatal stroke. C1 ROYAL MELBOURNE HOSP,PARKVILLE,VIC 3050,AUSTRALIA. UNIV KLIN INNSBRUCK,INNSBRUCK,AUSTRIA. UNIV ZIEKENHUIS GENT,GHENT,BELGIUM. ERASME UNIV HOSP,BRUSSELS,BELGIUM. HAMILTON GEN HOSP,HAMILTON L8L 2X2,ONTARIO,CANADA. MARIA HOSP,HELSINKI,FINLAND. UNIV HELSINKI,CENT HOSP,SF-00290 HELSINKI 29,FINLAND. HOP CARDIOL,LYONS,FRANCE. KLINIKUM STEGLITZ,BERLIN,GERMANY. CTR HUMAN DRUG RES,LEIDEN,NETHERLANDS. GREEN LANE HOSP,AUCKLAND 3,NEW ZEALAND. BAERUM HOSP,BAERUM,NORWAY. GROCHOWSKI HOSP,WARSAW,POLAND. CHARITE HOSP,BERLIN,GERMANY. HYGEIA HOSP,ATHENS,GREECE. BEAUMONT HOSP,DUBLIN,IRELAND. MARIO NEGRI HOSP,MILAN,ITALY. DR PESET ALEXANDRE HOSP,VALENCIA,SPAIN. OSTRA HOSP,S-41685 GOTHENBURG,SWEDEN. HUDIKSVALL HOSP,HUDIKSVALL,SWEDEN. CIVICO HOSP,LUGANO,SWITZERLAND. SAN GIOVANNI HOSP,BELLINZONA,SWITZERLAND. UNIV OXFORD,RADCLIFFE INFIRM,OXFORD OX2 6HE,ENGLAND. UNIV OXFORD,JOHN RADCLIFFE HOSP,OXFORD OX3 9DU,ENGLAND. BRITISH HEART FDN,LONDON,ENGLAND. ROYAL SUSSEX CTY HOSP,BRIGHTON BN2 5BE,E SUSSEX,ENGLAND. WESTERN GEN HOSP,EDINBURGH EH4 2XU,MIDLOTHIAN,SCOTLAND. NATL HEART HOSP,LONDON W1M 8BA,ENGLAND. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. WILLIAM BEAUMONT HOSP,ROYAL OAK,MI 48072. NHLBI,CLIN TRIALS BRANCH,BETHESDA,MD 20892. UNIV CHICAGO,CHICAGO,IL 60637. RADCLIFFE INFIRM,INT STUDY INFARCT SURVIVAL,DEPT CARDIOVASC MED,OXFORD OX2 6HE,ENGLAND. RP HUNT, D (reprint author), RADCLIFFE INFIRM,INT STUDY INFARCT SURVIVAL,CLIN TRIAL SERV UNIT,OXFORD OX2 6HE,ENGLAND. NR 61 TC 480 Z9 495 U1 1 U2 7 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAR 28 PY 1992 VL 339 IS 8796 BP 753 EP 770 PG 18 WC Medicine, General & Internal SC General & Internal Medicine GA HL501 UT WOS:A1992HL50100001 ER PT J AU EWING, SE WEBER, RJ ZAUNER, A PLUNKETT, RJ AF EWING, SE WEBER, RJ ZAUNER, A PLUNKETT, RJ TI RECOVERY IN HEMIPARKINSONIAN RATS FOLLOWING INTRASTRIATAL IMPLANTATION OF ACTIVATED LEUKOCYTES SO BRAIN RESEARCH LA English DT Article DE 6-HYDROXYDOPAMINE; HEMIPARKINSONIAN RAT; ACTIVATED LEUKOCYTE; CENTRAL NERVOUS SYSTEM IMPLANTATION; FLUORESCENT ACTIVATED CELL SORTING ID NERVE GROWTH-FACTOR; ADULT MAMMALIAN BRAIN; PARKINSONS-DISEASE; CELLS; INJURY; PROLIFERATION; INTERLEUKIN-2; STIMULATION; INVITRO; GRAFTS AB Behavioral improvement has been seen in hemiparkinsonian animals after surgical lesions of the denervated caudate nucleus. This study was designed to investigate the role of inflammatory cells in injury-induced recovery. A hemiparkinsonian syndrome was induced in rats by unilateral injections of 6-hydroxydopamine into the pars compacta of the substantia nigra. Phytohemagglutinin-stimulated rat peritoneal cells, predominantly T cells and macrophages, were stereotactically implanted in the lesioned caudate-putamen, and amphetamine-induced turning was used to assess recovery. Animals receiving implants of activated peritoneal cells showed a 47% decrease in amphetamine-induced turning 8 weeks after implantation, which was not seen in control or sham-operated animals. Immunocytochemistry revealed increased tyrosine hydroxylase reactive fibers in the leukocyte-implanted striatum. We conclude that implantation of activated leukocytes promotes functional recovery in hemiparkinsonian rats. C1 NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. NIDDKD,MED CHEM LAB,NEUROIMMUNOL UNIT,BETHESDA,MD 20892. NR 40 TC 30 Z9 30 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 MAR 27 PY 1992 VL 576 IS 1 BP 42 EP 48 DI 10.1016/0006-8993(92)90607-B PG 7 WC Neurosciences SC Neurosciences & Neurology GA HN917 UT WOS:A1992HN91700004 PM 1515912 ER PT J AU PATEL, A BOJA, JW LEVER, J LEW, R SIMANTOV, R CARROLL, FI LEWIN, AH PHILIP, A GAO, YG KUHAR, MJ AF PATEL, A BOJA, JW LEVER, J LEW, R SIMANTOV, R CARROLL, FI LEWIN, AH PHILIP, A GAO, YG KUHAR, MJ TI A COCAINE ANALOG AND A GBR ANALOG LABEL THE SAME PROTEIN IN RAT STRIATAL MEMBRANES SO BRAIN RESEARCH LA English DT Note DE COCAINE; DOPAMINE UPTAKE; DOPAMINE TRANSPORTER; PHOTOAFFINITY LABELING; DEEP ID TRANSPORTER AB Because some evidence suggests that cocaine and GBR12935 bind to different sites, we utilized photoaffinity probes from both classes of compounds to see if they label the same protein. [I-125]RTI-82 a cocaine analog, and [I-125]DEEP, a GBR analog, labeled protein(s) showing the same molecular weight, a similar pharmacological profile and a similar sensitivity to neuraminidase. C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,POB 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,BALTIMORE,MD 21205. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. NR 12 TC 20 Z9 20 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 MAR 27 PY 1992 VL 576 IS 1 BP 173 EP 174 DI 10.1016/0006-8993(92)90627-L PG 2 WC Neurosciences SC Neurosciences & Neurology GA HN917 UT WOS:A1992HN91700024 PM 1515909 ER PT J AU CHOLERTON, S IDLE, ME VAS, A GONZALEZ, FJ IDLE, JR AF CHOLERTON, S IDLE, ME VAS, A GONZALEZ, FJ IDLE, JR TI COMPARISON OF A NOVEL THIN-LAYER CHROMATOGRAPHIC-FLUORESCENCE DETECTION METHOD WITH A SPECTROFLUOROMETRIC METHOD FOR THE DETERMINATION OF 7-HYDROXYCOUMARIN IN HUMAN URINE SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Note ID COUMARIN AB A novel method for the determination of 7-hydroxycoumarin in human urine which combines thin-layer chromatography (TLC) with fluorescence detection (FD) has been devised. The limit of detection (I ng/ml) enables determination of 7-hydroxycoumarin after both administration of coumarin and environmental exposure to this fragrance material. When compared to a spectrofluorometric method of analysis, the TLC-FD method proved to be more selective for the analysis of 7-hydroxycoumarin in human urine. C1 NIH,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP CHOLERTON, S (reprint author), UNIV NEWCASTLE UPON TYNE,DEPT PHARMACOL SCI,PHARMACOGENET RES UNIT,NEWCASTLE TYNE NE2 4HH,ENGLAND. OI Idle, Jeff/0000-0002-6143-1520 FU Wellcome Trust NR 10 TC 70 Z9 72 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR-BIOMED JI J. Chromatogr.-Biomed. Appl. PD MAR 27 PY 1992 VL 575 IS 2 BP 325 EP 330 DI 10.1016/0378-4347(92)80166-N PG 6 WC Chemistry, Analytical SC Chemistry GA HM931 UT WOS:A1992HM93100022 PM 1629314 ER PT J AU BODENTEICH, M MARQUEZ, VE HALLOWS, WH GOLDSTEIN, BM AF BODENTEICH, M MARQUEZ, VE HALLOWS, WH GOLDSTEIN, BM TI SYNTHESIS AND STRUCTURAL DETERMINATION OF (+/-)-NEPLANOCIN-F SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Article ID S-ADENOSYLHOMOCYSTEINE HYDROLASE; NEPLANOCIN-A; ANTIVIRAL ACTIVITIES; 3-DEAZANEPLANOCIN-A; (-)-NEPLANOCIN-A; NUCLEOSIDES; INHIBITOR; POTENT AB Neplanocin F (2), a minor constituent of the family of neplanocin antibiotics, was synthesized as a racemate in 12 steps from cyclopentenone 3/4, which in turn was available from D-ribonolactone. The carbocyclic ring of neplanocin F corresponds to the allylic rearranged isomer of the biologically active agent neplanocin A. Regiospecific reduction of the racemic cyclopentenone 3/4 and protection of the resulting alpha-alcohol as a benzyl ether 6 produced, after removal of the isopropylidene moiety, a compound (7) having allylic and homoallylic secondary alcohol functionalities. Differences in the reactivity of these two secondary alcohols were successfully manipulated to prepare the homoallylic substituted azide 14, which was then reduced and converted to the desired adenine ring by conventional methods. The spectral properties of the synthesized material [(+/-)-neplanocin F] were identical to those of the natural product, except for its lack of optical rotation. X-ray crystallographic analysis helped corroborate the structure. In contrast to its bioactive isomer, neoplanocin A, neplanocin F was devoid of cytotoxicity and in vitro antiviral activity. C1 NCI,DCT,DTP,MED CHEM LAB,BETHESDA,MD 20892. UNIV ROCHESTER,MED CTR,DEPT BIOCHEM,ROCHESTER,NY 14642. UNIV ROCHESTER,MED CTR,DEPT BIOPHYS,ROCHESTER,NY 14642. NR 22 TC 13 Z9 13 U1 0 U2 2 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 MAR 27 PY 1992 VL 57 IS 7 BP 2071 EP 2076 DI 10.1021/jo00033a031 PG 6 WC Chemistry, Organic SC Chemistry GA HL660 UT WOS:A1992HL66000031 ER PT J AU WATANABEFUKUNAGA, R BRANNAN, CI COPELAND, NG JENKINS, NA NAGATA, S AF WATANABEFUKUNAGA, R BRANNAN, CI COPELAND, NG JENKINS, NA NAGATA, S TI LYMPHOPROLIFERATION DISORDER IN MICE EXPLAINED BY DEFECTS IN FAS ANTIGEN THAT MEDIATES APOPTOSIS SO NATURE LA English DT Article ID TUMOR-NECROSIS-FACTOR; LPR LPR MICE; GENE; RECEPTOR; GLD; LYMPHADENOPATHY; TOLERANCE; INDUCTION; LYMPHOCYTES; ENVIRONMENT AB Fas antigen is a cell-surface protein that mediates apoptosis. It is expressed in various tissues including the thymus and has structural homology with a number of cell-surface receptors, including tumour necrosis factor receptor and nerve growth factor receptor. Mice carrying the lymphoproliferation (lpr) mutation have defects in the Fas antigen gene. The lpr mice develop lymphadenopathy and suffer from a systemic lupus erythematosus-like autoimmune disease, indicating an important role for Fas antigen in the negative selection of autoreactive T cells in the thymus. C1 OSAKA BIOSCI INST,6-2-4 FURUEDAI,SUITA,OSAKA 565,JAPAN. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 34 TC 2342 Z9 2357 U1 0 U2 28 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 26 PY 1992 VL 356 IS 6367 BP 314 EP 317 DI 10.1038/356314a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HK794 UT WOS:A1992HK79400054 PM 1372394 ER PT J AU SPERLING, RS STRATTON, P OSULLIVAN, MJ BOYER, P WATTS, DH LAMBERT, JS HAMMILL, H LIVINGSTON, EG GLOEB, DJ MINKOFF, H FOX, HE AF SPERLING, RS STRATTON, P OSULLIVAN, MJ BOYER, P WATTS, DH LAMBERT, JS HAMMILL, H LIVINGSTON, EG GLOEB, DJ MINKOFF, H FOX, HE TI A SURVEY OF ZIDOVUDINE USE IN PREGNANT-WOMEN WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CONTROLLED TRIAL; AZT AB Background and Methods. The expanding indications for zidovudine treatment make it important to elucidate the safety and toxicity of this drug for pregnant women and their fetuses. We asked pediatricians and obstetricians at the AIDS (acquired immunodeficiency syndrome) Clinical Trials Units to report information about pregnant women infected with the human immunodeficiency virus who were continuing their pregnancies and had received, or were receiving, zidovudine during gestation. Results. Reports of 43 women were received from 17 institutions. Doses of zidovudine ranged from 300 to 1200 mg per day, and 24 women took the drug for at least two trimesters. There were two reported instances of maternal toxicity (one gastrointestinal and one hematologic). No teratogenic abnormalities occurred in the 12 infants with first-trimester exposure to zidovudine. All the infants, including two sets of twins, were born alive. The 38 singleton infants born at term for whom birth weights were reported had a mean birth weight of 3287 +/- 670 g; two cases of intrauterine growth retardation were reported among the infants delivered at term. Hemoglobin values, which were available for 31 newborns, ranged from 7.0 to 12.4 mmol per liter (11.2 to 20 g per deciliter); 3 of the 7 newborns with hemoglobin values of less than 8.4 mmol per liter (13.5 g per deciliter) were born prematurely. Conclusions. Zidovudine was well tolerated by the pregnant women and was apparently not associated with malformations in the newborns, premature birth, or fetal distress. No pattern of hematologic toxicity was observed in the newborns, but the anemia and growth retardation seen in a minority of the infants could, in part, have resulted from their mothers' treatment with zidovudine. C1 NICHHD,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,BETHESDA,MD 20892. UNIV MIAMI,SCH MED,DEPT OBSTET & GYNECOL,MIAMI,FL 33152. UNIV CALIF LOS ANGELES,SCH MED,DEPT OBSTET & GYNECOL,LOS ANGELES,CA 90024. UNIV WASHINGTON,DEPT OBSTET & GYNECOL,SEATTLE,WA 98195. UNIV ROCHESTER,MED CTR,DEPT MED,ROCHESTER,NY 14642. BAYLOR COLL MED,DEPT OBSTET & GYNECOL,HOUSTON,TX 77030. DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DURHAM,NC 27710. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT OBSTET & GYNECOL,BRONX,NY 10461. SUNY HLTH SCI CTR,DEPT OBSTET & GYNECOL,BROOKLYN,NY. COLUMBIA PRESBYTERIAN MED CTR,DEPT OBSTET & GYNECOL,NEW YORK,NY 10032. RP SPERLING, RS (reprint author), MT SINAI MED CTR,DEPT OBSTET GYNECOL & REPROD SCI,BOX 1173,1 GUSTAVE LEVY PL,NEW YORK,NY 10029, USA. FU NIAID NIH HHS [U01-AI-27667] NR 18 TC 90 Z9 90 U1 0 U2 1 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 MAR 26 PY 1992 VL 326 IS 13 BP 857 EP 861 DI 10.1056/NEJM199203263261303 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HK523 UT WOS:A1992HK52300003 PM 1542322 ER PT J AU WEISS, KB GERGEN, PJ HODGSON, TA AF WEISS, KB GERGEN, PJ HODGSON, TA TI AN ECONOMIC-EVALUATION OF ASTHMA IN THE UNITED-STATES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CHANGING PATTERNS; CHILDHOOD ASTHMA; HOSPITALIZATION; CHILDREN; MORTALITY; COST AB Background. Asthma is a common chronic illness. Recently, increases in morbidity and mortality due to this disease have been reported. We studied the distribution of health care resources used for asthma in order to lay the groundwork for further policy decisions aimed at reducing the economic burden of this disorder. Methods. Estimates of direct medical expenditures and indirect costs (in 1985 dollars) were derived from data available from the National Center for Health Statistics. These cost estimates were projected to 1990 dollars. Results. The cost of illness related to asthma in 1990 was estimated to be $6.2 billion. Inpatient hospital services represented the largest single direct medical expenditure for this chronic condition, approaching $1.6 billion. The value of reduced productivity due to loss of school days represented the largest single indirect cost, approaching $1 billion in 1990. Although asthma is often considered to be a mild chronic illness treatable with ambulatory care, we found that 43 percent of its economic impact was associated with emergency room use, hospitalization, and death. Nearly two thirds of the visits for ambulatory care were to physicians in three primary care specialties - pediatrics, family medicine or general practice, and internal medicine. Conclusions. Potential reductions in the costs related to asthma in the United States may be identified through a closer examination of the effectiveness of care associated with each category of cost. Future health policy efforts to improve the effectiveness of primary care interventions for asthma in the ambulatory setting may reduce the costs of this common illness. C1 GEORGE WASHINGTON UNIV,MED CTR,DEPT MED,WASHINGTON,DC 20037. GEORGE WASHINGTON UNIV,CTR HLTH POLICY RES,WASHINGTON,DC 20052. NIAID,DIV ALLERGY IMMUNOL & TRANSPLANTAT,BETHESDA,MD 20892. CTR DIS CONTROL,NATL CTR HLTH STAT,OFF ANAL & EPIDEMIOL,HYATTSVILLE,MD. RP WEISS, KB (reprint author), GEORGE WASHINGTON UNIV,MED CTR,DEPT HLTH CARE SCI,RM 2B-401,2150 PENN AVE NW,WASHINGTON,DC 20037, USA. NR 41 TC 762 Z9 770 U1 4 U2 45 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 MAR 26 PY 1992 VL 326 IS 13 BP 862 EP 866 DI 10.1056/NEJM199203263261304 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HK523 UT WOS:A1992HK52300004 PM 1542323 ER PT J AU WINGARD, JR MERZ, WG RINALDI, MG KARP, JE SARAL, R AF WINGARD, JR MERZ, WG RINALDI, MG KARP, JE SARAL, R TI PROPHYLACTIC FLUCONAZOLE AND CANDIDA-KRUSEI INFECTIONS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 JOHNS HOPKINS UNIV,BALTIMORE,MD 20205. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NCI,BETHESDA,MD 20892. RP WINGARD, JR (reprint author), EMORY UNIV,SCH MED,ATLANTA,GA 30322, USA. NR 6 TC 3 Z9 3 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 MAR 26 PY 1992 VL 326 IS 13 BP 892 EP 893 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HK523 UT WOS:A1992HK52300018 ER PT J AU KISS, Z CRILLY, KS ROSSI, MA ANDERSON, WB AF KISS, Z CRILLY, KS ROSSI, MA ANDERSON, WB TI SELECTIVE-INHIBITION BY 4-HYDROXYNONENAL OF SPHINGOSINE-STIMULATED PHOSPHOLIPASE-D IN NIH-3T3 CELLS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Note DE SPHINGOSINE; 4-HYDROXYNONENAL; PHOSPHOLIPASE-D; PHOSPHOLIPID HYDROLYSIS ID PROTEIN-KINASE-C; SWISS 3T3 CELLS; PHOSPHATIDIC-ACID; PRODUCTS; PHOSPHATIDYLETHANOLAMINE; SPHINGOLIPIDS; PROLIFERATION; HYDROLYSIS; BREAKDOWN AB In fibroblasts, the mitogenic effects of sphingosine involves a rapid rise in the cellular content of phosphatidic acid (PtdOH) which may be due to the stimulation of phospholipase D, or inhibition of PtdOH phosphohydrolase, or both. Here, we demonstrate that in fibroblasts, 4-hydroxynonenal is a selective inhibitor of sphingosine-stimulated phospholipid hydrolysis, and it also inhibits sphingosine-induced formation of PtdOH. C1 UNIV TURIN,GEN PATHOL SECT,DEPT EXPTL MED & ONCOL,I-10124 TURIN,ITALY. NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. RP KISS, Z (reprint author), UNIV MINNESOTA,HORMEL INST,801 16TH AVE NE,AUSTIN,MN 55912, USA. NR 20 TC 8 Z9 8 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 MAR 25 PY 1992 VL 1124 IS 3 BP 300 EP 302 DI 10.1016/0005-2760(92)90143-J PG 3 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HN137 UT WOS:A1992HN13700012 PM 1576170 ER PT J AU LIN, AY IHDE, DC AF LIN, AY IHDE, DC TI RECENT DEVELOPMENTS IN THE TREATMENT OF LUNG-CANCER SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID THERAPY ONCOLOGY GROUP; LYMPH-NODE METASTASES; SMALL-CELL CARCINOMA; RADIATION-THERAPY; RANDOMIZED TRIAL; STAGE-II; CHEMOTHERAPY; RADIOTHERAPY; IRRADIATION; SURVIVAL C1 NCI,OSN,MED ONCOL BRANCH,BLDG 31,ROOM 11A48,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NR 32 TC 14 Z9 15 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 MAR 25 PY 1992 VL 267 IS 12 BP 1661 EP 1664 DI 10.1001/jama.267.12.1661 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HJ597 UT WOS:A1992HJ59700035 PM 1311778 ER PT J AU LEE, CS OKA, T AF LEE, CS OKA, T TI A PREGNANCY-SPECIFIC MAMMARY NUCLEAR FACTOR INVOLVED IN THE REPRESSION OF THE MOUSE BETA-CASEIN GENE-TRANSCRIPTION BY PROGESTERONE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MULTIGENE FAMILY; TRANSGENIC MICE; FINE-STRUCTURE; MESSENGER-RNA; PLASMID DNA; EXPRESSION; GLAND; PROTEIN; QUANTITATION; PROLACTIN AB The sequence-specific binding pattern of mammary nuclear proteins to the 545-base pair (bp) 5'-flanking region of the mouse beta-casein gene was compared between pregnant and lactating mice by a gel mobility shift assay. By using appropriate probes, two complexes were detected only during pregnancy, whereas an additional four complexes were detected during both pregnancy and lactation. The two pregnancy-specific complexes showed identical electrophoretic mobility and were cross-competed with two unlabeled DNA fragments used to generate the probes. Methylation interference experiments indicated that the two binding regions involved guanosine residues at nucleotides -350 and -8, and the sequences around each guanosine residue have a common palindromic sequence, 5'-TGAT/ATCA-3'. This binding factor is termed pregnancy-specific mammary nuclear factor. In gene transfection experiments, expression of the chimeric beta-casein-CAT gene linked to the 545 bp of mouse beta-casein gene promoter region was maximally induced when transfected mammary epithelial cells were cultured with the lactogenic hormones prolactin, hydrocortisone, and insulin, whereas it was very low when insulin alone was added. The addition of progesterone together with the lactogenic hormones inhibited the hormonal induction of the chimeric gene, whereas co-transfection with an oligonucleotide containing the pregnancy-specific mammary nuclear factor binding site substantially overcame the progesterone-mediated repression of transcription. Furthermore, mutation of the pregnancy-specific mammary nuclear factor binding sites of the chimeric beta-casein-CAT gene resulted in attenuation of the inhibitory effect of progesterone without blocking the stimulatory effect of the lactogenic hormones. These results indicate the presence of a pregnancy-specific mammary nuclear factor(s) that bind to two separate sites of the beta-casein gene promoter and suggest that it may serve as a repressor that mediates the inhibitory action of progesterone on beta-casein gene transcription. RP LEE, CS (reprint author), NIDDKD,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892, USA. NR 31 TC 46 Z9 47 U1 1 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 MAR 25 PY 1992 VL 267 IS 9 BP 5797 EP 5801 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800015 PM 1556095 ER PT J AU THOMPSON, DB SOMMERCORN, J AF THOMPSON, DB SOMMERCORN, J TI USE OF A MULTIPLE S1 NUCLEASE PROTECTION ASSAY TO MONITOR CHANGES IN RNA LEVELS FOR TYPE-1 PHOSPHATASE AND SEVERAL PROTOONCOGENES IN RESPONSE TO INSULIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN SKELETAL-MUSCLE; GENE-EXPRESSION; MESSENGER-RNA; OLIGONUCLEOTIDE PROBES; NUCLEOTIDE-SEQUENCE; HEPATOMA-CELLS; FOS-PROTEIN; TRANSCRIPTION; LOCALIZATION; CLONING AB Changes in insulin-regulated gene expression occur in a time- and tissue-dependent fashion. To monitor these changes we have adapted the S1 nuclease protection assay to allow simultaneous estimation of multiple RNA species in a single sample by using synthetic oligonucleotides of various lengths as probes for specific RNA species, which can then be resolved by electrophoresis. The multiple S1 nuclease protection assay was used to assess the influence of insulin on the RNA concentrations of 12 different genes in human skeletal muscle. Estimates obtained by this assay were comparable with those obtained by Northern analysis. RNA levels for proto-oncogene c-src displayed a transient 4-fold increase, whereas RNA levels for type 1 protein phosphatase were suppressed by 50% during the same time period. RNAs corresponding to known insulin-responsive genes such as c-fos, c-myc, c-Ha-ras, and c-src displayed rapid and transient 2-4-fold increases between 30 and 60 min as detected by either Northern analysis or the multiple S1 nuclease protection assay. In addition, RNA levels for the insulin receptor, Glut-4, Glut-3, and c-jun were apparently unaffected by exposure of the cells to insulin. RP THOMPSON, DB (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016, USA. NR 53 TC 4 Z9 4 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 MAR 25 PY 1992 VL 267 IS 9 BP 5921 EP 5926 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800034 PM 1372896 ER PT J AU MOSCOW, JA MORROW, CS HE, R MULLENBACH, GT COWAN, KH AF MOSCOW, JA MORROW, CS HE, R MULLENBACH, GT COWAN, KH TI STRUCTURE AND FUNCTION OF THE 5'-FLANKING SEQUENCE OF THE HUMAN CYTOSOLIC SELENIUM-DEPENDENT GLUTATHIONE-PEROXIDASE GENE (HGPX1) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN CDNA SEQUENCE; S-TRANSFERASE-PI; MESSENGER-RNA; BREAST-CANCER; BUTHIONINE SULFOXIMINE; NUCLEOTIDE-SEQUENCE; RAT-LIVER; TRANSCRIPTIONAL REGULATION; MULTIDRUG RESISTANCE; CELL-LINE AB Human selenium-dependent glutathione peroxidase (hGPx1) (EC 1.11.1.9) is thought to be involved in many critical cellular functions as a result of its role in glutathione-mediated reduction of toxic peroxides, and it is implicated as a mechanism of resistance against oxygen free radicals. Previous studies have demonstrated that the gene encoding hGPx1 (hgpx1) is more highly expressed in multidrug-resistant AdrR MCF-7 human breast cancer cells than in the parental WT MCF-7 cell line. In order to further study the transcriptional regulation of hgpx1, we have cloned the genomic hgpx1 gene and determined its nucleotide sequence. The 2550-base pair (bp) 5'-flanking sequence of hgpx1 contained the terminal 511 bp of the 3' end of a previously reported rhoH12 cDNA (Yeramian, P., Chardin, P., Madaule, P., and Tavitian, A. (1987) Nucleic Acids Res. 15, 1989), a ras-related oncogene. Further downstream from rhoH12, but before the start of transcription of hgpx1, RNase protection analysis revealed a transcribed sequence of at least 270 bp which we have called mid. RNA transcripts homologous to both rhoH12 (1.8 and 1.5 kilobase pairs (kb)) and mid (1.8 kb) are also more highly expressed in AdrR MCF-7 cells than in WT MCF-7 cells. We screened an AdrR MCF-7 cDNA library with the mid sequence and isolated a partial cDNA clone which contains both mid and rhoH12 sequences and is colinear with the genomic sequence which extends from 10 bp 3' to the rhoH12 stop codon to 810 bp 5' to the start of transcription of hgpx1. The start of transcription of hgpx1 in AdrR MCF-7 cells was determined by primer extension analysis. The promoter and 2 kb of the 5'-flanking sequence of hgpx1 was fused to the bacterial chloramphenicol acetyltransferase gene (hGPx1-CAT1). Analysis of deletion constructs of hGPx1-CAT1 revealed three possible cis-acting regulatory regions. The transcriptional regulation of hgpx1 was examined using the hGPx1-CAT hybrid genes and nuclear run-on studies. We found no evidence that increased mRNA transcript formation could account for different levels of hgpx1 RNA either in different breast cancer cell lines or in response to selenium. C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. RP MOSCOW, JA (reprint author), NCI,MED BRANCH,BLDG 10,RM 12N226,BETHESDA,MD 20892, USA. NR 52 TC 60 Z9 62 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 MAR 25 PY 1992 VL 267 IS 9 BP 5949 EP 5958 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800039 PM 1556108 ER PT J AU TAUB, R HSU, JC GARSKY, VM HILL, BL ERLANGER, BF KOHN, LD AF TAUB, R HSU, JC GARSKY, VM HILL, BL ERLANGER, BF KOHN, LD TI PEPTIDE SEQUENCES FROM THE HYPERVARIABLE REGIONS OF 2 MONOCLONAL ANTIIDIOTYPIC ANTIBODIES AGAINST THE THYROTROPIN (TSH) RECEPTOR ARE SIMILAR TO TSH AND INHIBIT TSH-INCREASED CAMP PRODUCTION IN FRTL-5 THYROID-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ALPHA-SUBUNIT PEPTIDES; MOLECULAR-CLONING; PLASMA-MEMBRANES; BINDING; AUTOANTIBODIES; EXPRESSION; DIGESTION; STRATEGY; DOMAIN; SITES AB Monoclonal antibodies, D2 and 4G11, selected by the autoantiidiotypic approach following injection of thyrotropin (TSH) into mice, mimic TSH in binding to receptors on thyroid membranes. Based on TSH receptor transfection studies, D2 and 4G11 show unequivocal specificity for the TSH receptor. To see if the complementary determining regions (CDRs) of these antibodies share any primary sequence similarities to regions of TSH critical for receptor binding, we deduced the primary structure of the variable regions of D2 and 4G11 by sequencing the immunoglobulin mRNA. We found that CDR1 of 4G11K and CDR2 of D2-mu show sequence similarity to regions of TSH-alpha and TSH-beta that had been previously implicated in the interaction of the hormone with its receptor. We tested the inhibitory effects of synthetic peptides from D2-mu-CDR2 and 4G11K-CDR1 on the binding of the corresponding antibodies to rat thyroid FRTL-5 cells and found an EC50 of 0.1 and 1-mu-M, respectively. TSH-derived peptides with similarity to D2-mu-CDR2 and 4G11K-CDR1 showed a significant but lesser effect on the binding of 4G11 or D2 to thyroid cells. Additionally, we tested the effects of the CDR peptides and TSH-derived peptides on TSH-stimulated cAMP production in FRTL-5 cells and found that D2-mu-CDR2 and 4G11K-CDR1 inhibited this activity, D2-mu-CDR2 most strongly (EC50 10-mu-M). Thus, linear sequences from the CDRs of these autoantiidiotypic antibodies with similarity to sequences from both subunits of TSH appear to interact with the TSH receptor. These data support previous studies indicating the complexity of the interaction between TSH and its receptor and advance earlier findings that such immunologic approaches are useful in dissecting receptor-ligand interactions. C1 UNIV PENN,SCH MED,HOWARD HUGHES MED INST,PHILADELPHIA,PA 19104. MERCK SHARP & DOHME LTD,DEPT MED CHEM,W POINT,PA 19486. COLUMBIA UNIV,DEPT MICROBIOL,NEW YORK,NY 10032. NIDDKD,BIOCHEM & METAB LAB,CELL REGULAT SECT,BETHESDA,MD 20892. RP TAUB, R (reprint author), UNIV PENN,SCH MED,DEPT HUMAN GENET,PHILADELPHIA,PA 19104, USA. FU NINDS NIH HHS [NS15581] NR 53 TC 32 Z9 32 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 MAR 25 PY 1992 VL 267 IS 9 BP 5977 EP 5984 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800043 PM 1313425 ER PT J AU WOLFF, EC KINZY, TG MERRICK, WC PARK, MH AF WOLFF, EC KINZY, TG MERRICK, WC PARK, MH TI 2 ISOFORMS OF EIF-5A IN CHICK-EMBRYO - ISOLATION, ACTIVITY, AND COMPARISON OF SEQUENCES OF THE HYPUSINE-CONTAINING PROTEINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID EUKARYOTIC INITIATION FACTOR-4D; HAMSTER OVARY CELLS; SACCHAROMYCES-CEREVISIAE; RABBIT RETICULOCYTES; AMINO-ACID; FACTOR 4D; IDENTIFICATION; PURIFICATION; PRECURSOR; SPERMIDINE AB Eukaryotic translation initiation factor 5A (eIF-5A) (older terminology, eIF-4D) is unique in that it contains the unusual amino acid hypusine (N(epsilon)-(4-amino-2-hydroxybutyl)lysine). Hypusine is formed by a posttranslational event in which a specific lysine residue is modified by a structural contribution from spermidine. Metabolic labeling of chick embryo fibroblasts with [H-3]spermidine or [H-3]lysine gives rise to two distinct proteins, designated I (approximately 20 kDa and pI 5.6) and II (approximately 18 kDa and pI 5.35), that contain [H-3]hypusine. Upon incubation with [H-3]lysine the labeling of the two proteins followed a similar time course and showed approximately the same ratio over the 6-h incubation period. [H-3]Hypusine-containing proteins from cells which had been cultured with [H-3]spermidine were employed as tracers for isolation of hypusine-containing proteins from whole chick embryos. Four such proteins were obtained. Two of these proteins, I and II, correspond to the two native proteins synthesized in chick embryo fibroblasts; the other two forms, Ia and IIa, displayed properties suggesting that they were derived from the native proteins, I and II, respectively, during purification. The amino acid compositions and the tryptic peptide maps of the 20-kDa protein (I) and the 18-kDa protein (II) suggest that they are closely related but distinct proteins. In fact, amino acid sequence analysis of the two major proteins revealed differences in the polypeptide backbone of the two proteins. In spite of structural differences, the two native forms (I and II), as well as the two altered forms (Ia and IIa), were effective in stimulating methionyl-puromycin synthesis, providing evidence that they are indeed functional isoforms of eIF-5A. C1 CASE WESTERN RESERVE UNIV,SCH MED,DEPT BIOCHEM,CLEVELAND,OH 44106. RP WOLFF, EC (reprint author), NIDR,CELLULAR DEV & ONCOL LAB,BLDG 30,RM 211,BETHESDA,MD 20892, USA. FU NIADDK NIH HHS [AM-07319]; NIGMS NIH HHS [GM-26796] NR 40 TC 13 Z9 15 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 MAR 25 PY 1992 VL 267 IS 9 BP 6107 EP 6113 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800060 PM 1556119 ER PT J AU KWON, HM YAMAUCHI, A UCHIDA, S PRESTON, AS GARCIAPEREZ, A BURG, MB HANDLER, JS AF KWON, HM YAMAUCHI, A UCHIDA, S PRESTON, AS GARCIAPEREZ, A BURG, MB HANDLER, JS TI CLONING OF THE CDNA FOR A NA+/MYO-INOSITOL COTRANSPORTER, A HYPERTONICITY STRESS PROTEIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MYOINOSITOL TRANSPORT; NUCLEOTIDE-SEQUENCE; SYMPORT CARRIER; NA+/GLUCOSE; GLUCOSE; CELLS; GENE AB Kidney medullary cells in situ, as well as kidney-derived Madin-Darby canine kidney (MDCK) cells accumulate nonperturbing, small organic solutes (osmolytes), including myo-inositol, when bathed in hypertonic media. Accumulation of osmolytes balances the osmolality of extracellular fluid without raising intracellular salts that would perturb cellular functions. In hypertonic media, increased myo-inositol accumulation is the result of increased activity of a Na+/myo-inositol cotransporter. We have isolated a cDNA encoding a Na+/myo-inositol cotransporter from MDCK cells using expression in Xenopus oocytes. The cDNA sequence predicts a protein of 718 amino acids with a significant amino acid sequence similarity to the Na+/D-glucose cotransporters of absorbing epithelia. Transporter mRNA is present in kidney and brain and is markedly induced in MDCK cells by medium hypertonicity, demonstrating that adaptation to hypertonic stress involves up-regulation of transporter mRNA accumulation. C1 JOHNS HOPKINS UNIV,SCH MED,DIV NEPHROL,ROSS BLDG,9TH FLOOR S,720 RUTLAND AVE,BALTIMORE,MD 21205. NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. RI Lee-Kwon, Whaseon/D-6021-2011; Uchida, Shinichi/D-1111-2013 FU NIDDK NIH HHS [DK42479] NR 27 TC 296 Z9 297 U1 0 U2 3 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 MAR 25 PY 1992 VL 267 IS 9 BP 6297 EP 6301 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800087 PM 1372904 ER PT J AU IKURA, M BAX, A AF IKURA, M BAX, A TI ISOTOPE-FILTERED 2D NMR OF A PROTEIN PEPTIDE COMPLEX - STUDY OF A SKELETAL-MUSCLE MYOSIN LIGHT CHAIN KINASE FRAGMENT BOUND TO CALMODULIN SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; BINDING DOMAIN; SPECTRA; IDENTIFICATION; SPECTROSCOPY; MELITTIN AB An NMR approach is demonstrated for elucidating the conformation of a peptide when tightly bound to a protein. A 26-residue peptide derived from rabbit skeletal muscle myosin light chain kinase, comprising the binding site for calmodulin, was complexed with uniformly (> 95%) N-15- and C-13-enriched calmodulin. Improved isotope-filtered two-dimensional NMR techniques were developed for suppressing NMR calmodulin signals. NOE patterns indicate that residues Arg-3 through Ser-21 of the bound peptide form an alpha-helix. NOE interactions between the peptide and the protein indicate that the N-terminal half of the peptide interacts with the C-terminal domain of calmodulin, and the C-terminal half interacts with the N-terminal calmodulin domain. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NR 35 TC 254 Z9 257 U1 1 U2 11 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 MAR 25 PY 1992 VL 114 IS 7 BP 2433 EP 2440 DI 10.1021/ja00033a019 PG 8 WC Chemistry, Multidisciplinary SC Chemistry GA HK671 UT WOS:A1992HK67100019 ER PT J AU FRAZIER, JS NAKATA, H JACOBOWITZ, DM AF FRAZIER, JS NAKATA, H JACOBOWITZ, DM TI CHYMOTRYPSIN-REACTIVE ANTIBODIES IN INSULIN-DEPENDENT DIABETES-MELLITUS SO MOLECULAR AND CELLULAR BIOCHEMISTRY LA English DT Article DE DIABETES-MELLITUS; ANTIBODIES; CHYMOTRYPSIN ID PANCREATIC ACINAR-CELLS; PROTEINS; RATS AB In a previous study (Frazier et al., 1990), it was demonstrated that two patients with type 1 (insulin-dependent) diabetes mellitus had antibodies in their serum which reacted with four 29 kDa pancreas-specific proteins on two-dimensional immunoblots. This paper reports on the purification and identification of these pancreatic proteins. The protein with the pI closest to pH7 was purified through the use of ammonium sulfate fractionation and ion-exchange chromatography. Gel filtration chromatography established that the protein's molecular weight was closer to 25 kDa. Amino acid composition and sequence analyses demonstrated homology between the protein and chymotrypsin. It is suggested that an abnormal regulation of chymotrypsin activity might be related to antibodies formed in some diabetic patients. C1 NIMH,CLIN SCI LAB,BLDG 10,RM 3D-48,BETHESDA,MD 20892. NR 18 TC 1 Z9 1 U1 0 U2 0 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 MAR 25 PY 1992 VL 110 IS 2 BP 175 EP 180 DI 10.1007/BF02454196 PG 6 WC Cell Biology SC Cell Biology GA HN700 UT WOS:A1992HN70000010 PM 1584208 ER PT J AU MORGAN, RA COUTURE, L ELROYSTEIN, O RAGHEB, J MOSS, B ANDERSON, WF AF MORGAN, RA COUTURE, L ELROYSTEIN, O RAGHEB, J MOSS, B ANDERSON, WF TI RETROVIRAL VECTORS CONTAINING PUTATIVE INTERNAL RIBOSOME ENTRY SITES - DEVELOPMENT OF A POLYCISTRONIC GENE-TRANSFER SYSTEM AND APPLICATIONS TO HUMAN GENE-THERAPY SO NUCLEIC ACIDS RESEARCH LA English DT Article ID ENCEPHALOMYOCARDITIS VIRUS-RNA; CAP-INDEPENDENT TRANSLATION; HUMAN ADENOSINE-DEAMINASE; 5' NONTRANSLATED REGION; POLIOVIRUS RNA; MESSENGER-RNA; HEMATOPOIETIC-CELLS; EXPRESSION SYSTEM; MAMMALIAN-CELLS; LINES AB Recombinant retroviral vectors producing multicistronic mRNAs were constructed. Picornavirus putative internal ribosome entry sites (IRES) were used to confer cap-independent translation of an internal cistron. Internal cistrons were engineered by ligation of various lengths of the IRES of encephalomyocarditis (EMC) virus or polio virus to the E. coli chloramphenicol acetyltransferase (CAT) gene. The IRES/CAT fusions were introduced into retroviral vectors 3' to the translation stop codon of the neomycin phosphotransferase (NEO) gene, and the molecular constructs transfected into retroviral vector packaging lines. Retroviral vector producer cells efficiently express the internal CAT gene product only when the full length IRES is used. Both the EMC/CAT and polio/CAT retroviral vectors produced high titer vector supernatant capable of productive transduction of target cells. To test the generality of this gene transfer system, a retroviral vector containing an IRES fusion to the human adenosine deaminase (ADA) gene was constructed. Producer cell supernatant was used to transduce NIH/3T3 cells, and transduced cells were shown to express NEO, and ADA. Novel three-gene-containing retroviral vectors were constructed by introducing the EMC/ADA fusion into either an existing internal-promoter-containing vector, or a polio/CAT bicistronic vector. Producer cell clones of the three-gene vectors synthesize all three gene products, were of high titer, and could productively transduce NIH/3T3 cells. By utilizing cap-independent translation units, IRES vectors can produce polycistronic mRNAs which enhance the ability of retroviral-mediated gene transfer to engineer cells to produce multiple foreign proteins. C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RP MORGAN, RA (reprint author), NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892, USA. NR 34 TC 209 Z9 218 U1 0 U2 5 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 MAR 25 PY 1992 VL 20 IS 6 BP 1293 EP 1299 DI 10.1093/nar/20.6.1293 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HM420 UT WOS:A1992HM42000017 PM 1313966 ER PT J AU POLYMEROPOULOS, MH RATH, DS XIAO, H MERRIL, CR AF POLYMEROPOULOS, MH RATH, DS XIAO, H MERRIL, CR TI TETRANUCLEOTIDE REPEAT POLYMORPHISM AT THE HUMAN BETA-ACTIN RELATED PSEUDOGENE H-BETA-AC-PSI-2 (ACTBP2) SO NUCLEIC ACIDS RESEARCH LA English DT Note RP POLYMEROPOULOS, MH (reprint author), ST ELIZABETH HOSP,NATL INST MENTAL HLTH,CTR NEUROSCI,ROOM 131,WASHINGTON,DC 20032, USA. NR 3 TC 132 Z9 136 U1 0 U2 1 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 MAR 25 PY 1992 VL 20 IS 6 BP 1432 EP 1432 DI 10.1093/nar/20.6.1432 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HM420 UT WOS:A1992HM42000054 PM 1561114 ER PT J AU GAWRISCH, K PARSEGIAN, VA HAJDUK, DA TATE, MW GRUNER, SM FULLER, NL RAND, RP AF GAWRISCH, K PARSEGIAN, VA HAJDUK, DA TATE, MW GRUNER, SM FULLER, NL RAND, RP TI ENERGETICS OF A HEXAGONAL LAMELLAR HEXAGONAL-PHASE TRANSITION SEQUENCE IN DIOLEOYLPHOSPHATIDYLETHANOLAMINE MEMBRANES SO BIOCHEMISTRY LA English DT Article ID HII PHASE; L-ALPHA; INTRINSIC CURVATURE; LIPIDS; PHOSPHATIDYLETHANOLAMINES; SPECTROSCOPY; TEMPERATURE; HYDRATION; BEHAVIOR; CHAINS AB The phase diagram of DOPE/water dispersions was investigated by NMR and X-ray diffraction in the water concentration range from 2 to 20 water molecules per lipid and in the temperature range from -5 to +50-degrees-C. At temperatures above 22-degrees-C, the dispersions form an inverse (H(II)) phase at all water concentrations. Below 25-degrees-C, an H(II) phase occurs at high water concentrations, an L(alpha) phase is formed at intermediate water concentrations, and finally the system switches back to an H(II) phase at low water concentrations. The enthalpy of the L(alpha)-H(II)-phase transition is +0.3 kcal/mol as measured by differential scanning calorimetry. Using P-31 and H-2 NMR and X-ray diffraction, we measured the trapped water volumes in H(II) and L(alpha) phases as a function of osmotic pressure. The change of the H(II)-phase free energy as a function of hydration was calculated by integrating the osmotic pressure vs trapped water volume curve. The phase diagram calculated on the basis of the known enthalpy of transition and the osmotic pressure vs water volume curves is in good agreement with the measured one. The H(II)-L(alpha)-H(II) double-phase transition at temperatures below 22-degrees-C can be shown to be a consequence of (i) the greater degree of hydration of the H(II) phase in excess water and (ii) the relative sensitivities with which the lamellar and hexagonal phases dehydrate with increasing osmotic pressure. These results demonstrate the usefulness of osmotic stress measurements to understand lipid-phase diagrams. C1 PRINCETON UNIV,DEPT PHYS,PRINCETON,NJ 08544. BROCK UNIV,ST CATHARINES L2S 3A1,ONTARIO,CANADA. RP GAWRISCH, K (reprint author), NIH,DCRT,BETHESDA,MD 20892, USA. RI Gruner, Sol/G-2924-2010 OI Gruner, Sol/0000-0002-1171-4426 FU NIGMS NIH HHS [GM32614] NR 35 TC 119 Z9 123 U1 3 U2 12 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 24 PY 1992 VL 31 IS 11 BP 2856 EP 2864 DI 10.1021/bi00126a003 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK524 UT WOS:A1992HK52400003 PM 1550812 ER PT J AU MURAKAMI, T SIMONDS, WF SPIEGEL, AM AF MURAKAMI, T SIMONDS, WF SPIEGEL, AM TI SITE-SPECIFIC ANTIBODIES DIRECTED AGAINST G-PROTEIN BETA-SUBUNIT AND GAMMA-SUBUNIT - EFFECTS ON ALPHA-SUBUNIT AND BETA-GAMMA-SUBUNIT INTERACTION SO BIOCHEMISTRY LA English DT Article ID ROD OUTER SEGMENTS; CARBOXYL-TERMINAL DECAPEPTIDE; NUCLEOTIDE-BINDING PROTEINS; GTP-BINDING; ADENYLATE-CYCLASE; LIMITED PROTEOLYSIS; MONOCLONAL-ANTIBODY; ADP-RIBOSYLATION; PERTUSSIS TOXIN; TRANSDUCIN AB Little is known about the specific domains of G protein beta and gamma-subunits which interact with each other and with the a subunit. We used site-specific anti-peptide antibodies directed against beta and gamma-subunits to investigate domains on beta and gamma-subunits involved in alpha-subunit interaction. Antibodies included four against the transducin (G) beta-subunit (residues 1-10 = MS, 127-136 = KT, 256-265 = RA, and 330-340 = SW) and two against the gamma-subunit (residues 2-12 = PV and 58-68 = PE). All antisera, when affinity-purified on peptide columns, yielded antibodies capable of recognizing the denatured cognate subunit on immunoblots, but only RA, SW, PV, and PE recognized native beta-gamma(t) subunits. Affinity purification of MS and KT antisera on columns of immobilized native G(t) yielded antibodies capable of recognizing native beta-gamma(t), subunits. The functional effects of each antibody preparation on alpha(t)-beta-gamma(t) interaction were assessed by assaying the ability of the preparations to immunoprecipitate beta-gamma(t) subunits in the presence of excess alpha-subunits and by testing the inhibition of beta-gamma(t)-dependent ADP-ribosylation of alpha(t)-subunits catalyzed by pertussis toxin. On the basis of the results, we conclude that the domains on beta-gamma(t) which may be directly involved in alpha(t)-beta-gamma(t) interaction include the extreme amino terminus, residues 127-136 and 256-265 of beta(t), and the carboxyl terminus of gamma(t). The carboxyl-terminal region of beta(t) and the amino terminus of gamma(t) are less likely to be directly involved in alpha(t)-beta-gamma(t) interaction. RP MURAKAMI, T (reprint author), NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BLDG 10,ROOM 8D-17,BETHESDA,MD 20892, USA. NR 48 TC 37 Z9 37 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 MAR 24 PY 1992 VL 31 IS 11 BP 2905 EP 2911 DI 10.1021/bi00126a009 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK524 UT WOS:A1992HK52400009 PM 1550816 ER PT J AU BUTZOW, JJ STANKIS, RG AF BUTZOW, JJ STANKIS, RG TI IDENTIFICATION OF A COMPONENT SEPARATED ON MONO-Q PURIFICATION OF ESCHERICHIA-COLI RNA-POLYMERASE AS AN NTPASE SO FEBS LETTERS LA English DT Article DE RNA POLYMERASE; NTPASE (NUCLEOSIDE 5' TRIPHOSPHATASE) ID DNA; CHROMATOGRAPHY; MECHANISM AB Standard preparations of Escherichia coli RNA polymerase (RNAP) contain NTPase activity. High-performance anion-exchange chromatography on Mono Q has recently been used by Hager et al. [1990, Biochemistry 29, 7890-7894] to fractionate RNAP into holoenzyme (alpha-2-beta-beta'-sigma) and core alpha-2-beta-beta') forms, plus other protein components. We found that one of these components, of protomer size slightly larger than the sigma-70 subunits, has NTPase activity; it is efficiently separated on Mono Q, leaving transcriptionally active holoenzyme and core apparently free of NTPase activity. Because of the similarity in size with sigma-70, the NTPase component may escape detection by routine gel electrophoresis. RP BUTZOW, JJ (reprint author), NIA,GERONTOL RES CTR,BALTIMORE,MD 21224, USA. NR 10 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAR 23 PY 1992 VL 300 IS 1 BP 71 EP 72 DI 10.1016/0014-5793(92)80166-E PG 2 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA HK982 UT WOS:A1992HK98200016 PM 1312487 ER PT J AU NUSSINOV, R AF NUSSINOV, R TI THE EUKARYOTIC CCAAT AND TATA BOXES, DNA SPACER FLEXIBILITY AND LOOPING SO JOURNAL OF THEORETICAL BIOLOGY LA English DT Article ID ESCHERICHIA-COLI; TRANSCRIPTIONAL ACTIVATION; SEQUENCE DEPENDENCE; BASE COMPOSITION; BINDING-PROTEIN; DA-DT; PROMOTER; REPRESSOR; SITES; INITIATION C1 TEL AVIV UNIV,SACKLER FAC MED,SACKLER INST MOLEC MED,IL-69978 TEL AVIV,ISRAEL. RP NUSSINOV, R (reprint author), FREDERICK CANC RES & DEV CTR,PRI DYN CORP NATL CANC INST,MATH BIOL LAB,BLDG 469,ROOM 151,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [1-CO-74102] NR 45 TC 3 Z9 3 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-5193 J9 J THEOR BIOL JI J. Theor. Biol. PD MAR 21 PY 1992 VL 155 IS 2 BP 243 EP 270 DI 10.1016/S0022-5193(05)80597-1 PG 28 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA HK798 UT WOS:A1992HK79800005 PM 1453699 ER PT J AU IKEDA, H MARKEY, CJ MARKEY, SP AF IKEDA, H MARKEY, CJ MARKEY, SP TI SEARCH FOR NEUROTOXINS STRUCTURALLY RELATED TO 1-METHYL-4-PHENYLPYRIDINE (MPP+) IN THE PATHOGENESIS OF PARKINSONS-DISEASE SO BRAIN RESEARCH LA English DT Article DE PARKINSONS DISEASE; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; MPTP; 1-METHYL-4-PHENYLPYRIDINE; MPP+; PATHOGENESIS; IMMUNOASSAY ID 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE MPTP; MONOAMINE-OXIDASE; SUBSTANTIA NIGRA; PRIMATE MODEL; MACAQUE MONKEY; BRAIN; METABOLISM; INHIBITION; TOXICITY; N-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE AB Immunoassays sensitive to a broad range of compounds structurally related to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridine (MPP+) have been developed and used to test for the presence of possible chemically related neurotoxins in the brains of Parkinson's disease patients. The sensitivity and chemical reactivity of the polyclonal antibodies used in these assays have been characterized with a range of endogenous and chemically related materials. Two methods were developed and tested for extraction followed by chromatographic separation which would be applicable to stored or accumulated substances. The immunoassays were tested and applied to the assay of tissue extracts from MPTP or MPTP-analogue exposed animals, and indicated detectability of MPP+-immunoreactivity > 8 weeks after exposure to MPTP in monkey brain. No difference in immunoactivity was measured in extracts from human brains of Parkinson's disease patients or controls, and particularly low levels of immunoactivity were found in the striatum relative to the levels measured in several cortical regions. From these studies, there is no evidence for the role of an environmental neurotoxin chemically related to MPTP in the pathogenesis of Parkinson's disease. C1 NIMH,CLIN SCI LAB,ANALYT BIOCHEM SECT,BLDG 10,RM 3D40,BETHESDA,MD 20892. FU NIMH NIH HHS [MH/NS 31862] NR 70 TC 28 Z9 28 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 MAR 20 PY 1992 VL 575 IS 2 BP 285 EP 298 DI 10.1016/0006-8993(92)90092-N PG 14 WC Neurosciences SC Neurosciences & Neurology GA HM252 UT WOS:A1992HM25200015 PM 1571786 ER PT J AU SHERMAN, CA HIGGINS, GA AF SHERMAN, CA HIGGINS, GA TI REGULATED SPLICING OF THE AMYLOID PRECURSOR PROTEIN GENE DURING POSTNATAL-DEVELOPMENT OF THE RAT BASAL FOREBRAIN SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE RNA PROCESSING; NEUROTROPHIN; CHOLINERGIC NEURON; NERVE GROWTH FACTOR RECEPTOR ID MESSENGER-RNA; ALZHEIMERS-DISEASE; KUNITZ DOMAIN; MOUSE HOMOLOG; HUMAN-BRAIN; NEXIN-II; EXPRESSION; RECEPTOR; TRANSCRIPTS; CORTEX AB The expression of the amyloid precursor protein (APP) gene has been examined in the basal forebrain of rats from birth to adulthood. Levels of total APP mRNA are highest at birth and at postnatal day 15 (P15). The most abundant transcript in rat brain is APP-695, whose expression has previously been found to be largely restricted to the central nervous system. Comparison of the developmental profiles of APP-695 mRNA with that of Kunitz-protease inhibitor (KPI)-containing APP mRNA shows that the greatest difference in expression occurs at P15, when APP-695 message levels are over 6-fold higher than KPI-containing APP mRNA (APP-751, APP-770). This is the largest difference in the APP-695/KPI-APP ratio observed during postnatal development and coincides with the period of maximal neurotrophic responsiveness in the basal forebrain. These results suggest that the APP gene is alteratively spliced during postnatal development and that regulated expression of APP-695 may be influenced by neurotrophic factors in vivo. C1 NIA,GERONTOL RES CTR,MOLEC NEUROBIOL SECT,BIOL CHEM LAB,4940 EASTERN AVE,BALTIMORE,MD 21224. NR 39 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD MAR 20 PY 1992 VL 66 IS 1 BP 63 EP 69 DI 10.1016/0165-3806(92)90141-I PG 7 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA HL970 UT WOS:A1992HL97000008 ER PT J AU BARG, J RIUS, RA BEM, WT BELCHEVA, MM LOH, YP COSCIA, CJ AF BARG, J RIUS, RA BEM, WT BELCHEVA, MM LOH, YP COSCIA, CJ TI DIFFERENTIAL DEVELOPMENT OF BETA-ENDORPHIN AND MU-OPIOID BINDING-SITES IN MOUSE-BRAIN SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE ONTOGENY; OPIOID PEPTIDE; OPIOID RECEPTOR; PHENOTYPIC EXPRESSION; MOUSE CENTRAL NERVOUS SYSTEM ID DEVELOPING RAT-BRAIN; GUINEA-PIG BRAIN; POSTNATAL-DEVELOPMENT; CELL-PROLIFERATION; RECEPTORS; OPIATE; KAPPA; EXPRESSION; DELTA; MEMBRANES AB Mouse brains of various ages from embryonal day 14 (E14) to adult were analyzed for opioid receptor binding using the enkephalin analog Tyr-D-Ala-Gly-NMe-Phe-Gly-ol (DAMGE) and the opiate alkaloid dihydromorphine (DHM) as mu-selective radioligands. Binding parameters were estimated from homologous and heterologous competition binding curves. During the postnatal period, K(d) values for [H-3]DAMGE did not change but B(max) values (fmol/mg protein) increased 2.7 fold from postnatal day 3 (P3) to P7. Miner receptor density fluctuations were evident from P7 to adult. Similar results were obtained with [H-3]DHM. In contrast, estimation of total mu-binding sites (fmol/brain) revealed a continuous rise from P3 to the adult. The postnatal developmental profile of total mu-binding sites was comparable to the weight gain of mouse brain and the increase in protein content. In contrast, during the same period beta-endorphin immunoreactivity (IR) levels undergo an increase that is inversely proportional to mu-opioid receptor B(max) values. [H-3]DAMGE binding to E14 membrane preparations was inhibited to a greater extent by Gpp(NH)p than that to P1 or adult. Additional characterization of mu-receptors was accomplished by heterologous competition binding assays. IC50 values for beta-endorphin in competition with [H-3]DHM and [H-3]DAMGE were age dependent and differed for the two radiohgands. These results suggest that mu-receptor selectivity for mu-specific peptide and alkaloid ligands changes as a function of age. C1 ST LOUIS UNIV,SCH MED,DEPT BIOCHEM & MOLEC BIOL,1402 S GRAND BLVD,ST LOUIS,MO 63104. NICHHD,CELLULAR NEUROBIOL SECT,DEV NEUROBIOL LAB,BETHESDA,MD 20891. NR 38 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD MAR 20 PY 1992 VL 66 IS 1 BP 71 EP 76 DI 10.1016/0165-3806(92)90142-J PG 6 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA HL970 UT WOS:A1992HL97000009 ER PT J AU EPLER, KS SANDER, LC ZIEGLER, RG WISE, SA CRAFT, NE AF EPLER, KS SANDER, LC ZIEGLER, RG WISE, SA CRAFT, NE TI EVALUATION OF REVERSED-PHASE LIQUID-CHROMATOGRAPHIC COLUMNS FOR RECOVERY AND SELECTIVITY OF SELECTED CAROTENOIDS SO JOURNAL OF CHROMATOGRAPHY LA English DT Article ID GRADIENT ELUTION TECHNIQUE; FATTY-ACID ESTERS; BETA-CAROTENE; ALPHA-TOCOPHEROL; HPLC DETERMINATION; SERUM RETINOL; HUMAN-PLASMA; VITAMIN-A; INTERNAL STANDARD; PAPRIKA PIGMENTS AB Sixty commercially available and five experimental liquid chromatography columns were evaluated for the separation and recovery of seven carotenoid compounds. Methanol- and acetonitrile-based solvents (either straight or modified with ethyl acetate or tetrahydrofuran) were compared to determine which solvent systems and which columns provided better selectivity and recovery. Methanol-based solvents typically provided higher recoveries than did acetonitrile-based solvents. Polymeric C-18 phases generally provided better selectivity for the difficult separation of lutein and zeaxanthin than did monomeric C-18 phases. C1 NATL INST STAND & TECHNOL,DIV ORGAN ANALYT RES,CHEM SCI & TECHNOL LAB,GAITHERSBURG,MD 20899. NCI,ENVIRONM EPIDEMIOL BRANCH,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. FU NCI NIH HHS [Y01-CP9-0513] NR 58 TC 102 Z9 106 U1 1 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 J9 J CHROMATOGR PD MAR 20 PY 1992 VL 595 IS 1-2 BP 89 EP 101 DI 10.1016/0021-9673(92)85149-N PG 13 WC Chemistry, Analytical SC Chemistry GA HM930 UT WOS:A1992HM93000006 PM 1577914 ER PT J AU CARROLL, FI LEWIN, AH BOJA, JW KUHAR, MJ AF CARROLL, FI LEWIN, AH BOJA, JW KUHAR, MJ TI COCAINE RECEPTOR - BIOCHEMICAL-CHARACTERIZATION AND STRUCTURE-ACTIVITY-RELATIONSHIPS OF COCAINE ANALOGS AT THE DOPAMINE TRANSPORTER SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID MEDIAL PREFRONTAL CORTEX; VENTRAL TEGMENTAL AREA; NUCLEUS ACCUMBENS; UPTAKE SITES; 6-HYDROXYDOPAMINE LESIONS; NONHUMAN-PRIMATES; UPTAKE COMPLEX; BINDING-SITES; H-3 COCAINE; THREO-(+/-)-METHYLPHENIDATE BINDING C1 NATL INST DRUG ABUSE,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224. RP CARROLL, FI (reprint author), RES TRIANGLE INST,POB 12194,RES TRIANGLE PK,NC 27709, USA. NR 98 TC 292 Z9 294 U1 2 U2 6 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 MAR 20 PY 1992 VL 35 IS 6 BP 969 EP 981 DI 10.1021/jm00084a001 PG 13 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA HK860 UT WOS:A1992HK86000001 PM 1552510 ER PT J AU GETAHUN, Z JURD, L CHU, PS LIN, CM HAMEL, E AF GETAHUN, Z JURD, L CHU, PS LIN, CM HAMEL, E TI SYNTHESIS OF ALKOXY-SUBSTITUTED DIARYL COMPOUNDS AND CORRELATION OF RING SEPARATION WITH INHIBITION OF TUBULIN POLYMERIZATION - DIFFERENTIAL ENHANCEMENT OF INHIBITORY EFFECTS UNDER SUBOPTIMAL POLYMERIZATION REACTION CONDITIONS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID METHYL-ETHER; B-RING; ANTINEOPLASTIC AGENTS; ANTIMITOTIC AGENT; BINDING-SITE; COLCHICINE; DERIVATIVES; COMBRETASTATIN; ANALOGS; PODOPHYLLOTOXIN AB A number of cytostatic compounds (2-4, 7, and 8), which can be described as ''diaryl'', inhibit tubulin polymerization, cause cells to accumulate in mitotic arrest, and competitively inhibit the binding of colchicine to tubulin. They differ, however, in the separation of the two aryl moieties. To attempt to understand this variability we prepared a series of analogues modeled on 3 and 4 (''benzodioxole series'') and on 7 and 8 (''combretastatin series'') which differed only in the number of methylene units (ranging from none to four) separating the aryl moieties. These compounds were evaluated for their effects on tubulin polymerization, colchicine binding, and the growth of L1210 murine leukemia cells. In terms of inhibitory effects on tubulin polymerization, for the combretastatin series there was an optimal separation of the two phenyl rings by a two-carbon bridge (compound 24), with progressively decreasing inhibitory activity when the separation was by one carbon (20), three carbons (25), or four carbons (28) (the biphenyl analogue 16 was inactive). The benzodioxole series, however, did not permit us to generalize this finding, because the least active agents prepared (39 and 40) had a two-carbon bridge, while those with one- (5 and 6) and three-carbon (46 and 47) bridges were nearly equivalent in potency. Submicromolar IC50 values for inhibition of L1210 cell growth were only obtained for compounds 20 (IC50, 0.2-mu-M), 24 (0.07-mu-M), and 25 (0.4-mu-M). While evaluating the effects of these agents on tubulin polymerization, we noted with the combretastatin series and with several standard agents that apparent potency (in terms of IC50 values) was always lower if the reaction was performed at 30-degrees-C, with 0.25 mM MgCl2, than at 37-degrees-C, with 1.0 mM MgCl2. This enhancement of IC50 values in the former system as compared with the latter was particularly dramatic for the less active agents (e.g., 28) as compared with the more active (e.g. 24). C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BLDG 37,ROOM 5C25,BETHESDA,MD 20892. USDA ARS,WESTERN REG RES CTR,WESTERN REG RES CTR,BERKELEY,CA 94710. NR 46 TC 73 Z9 74 U1 0 U2 6 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 MAR 20 PY 1992 VL 35 IS 6 BP 1058 EP 1067 DI 10.1021/jm00084a011 PG 10 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA HK860 UT WOS:A1992HK86000011 PM 1552500 ER PT J AU SMAR, MW ARES, JJ NAKAYAMA, T ITABE, H KADOR, PF MILLER, DD AF SMAR, MW ARES, JJ NAKAYAMA, T ITABE, H KADOR, PF MILLER, DD TI SELECTIVE IRREVERSIBLE INHIBITORS OF ALDOSE REDUCTASE SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID HUMAN PSOAS MUSCLE; DIABETIC COMPLICATIONS; ALDEHYDE REDUCTASE; SITE AB A series of 5-substituted-1,3-dioxo-1H-benz[de]isoquinoline-2(3H)-acetic acid analogues have been examined as irreversible inhibitors of aldose reductase. The 5-alpha-bromoacetamide and 5-alpha-iodoacetamide analogues 5 and 6 gave irreversible inhibition of aldose reductase while the 5-alpha-chloroacetamide analogue 3 did not show this type of inhibition. Protection studies indicate that irreversible inhibitions are occurring at the inhibitor binding site. Comparative irreversible inhibition studies with rat lens aldose reductase (RLAR) and rat kidney aldehyde reductase (RKALR) indicate that 5-alpha-haloacetamide analogues 5 and 6 are much more effective inhibitors of RLAR. C1 OHIO STATE UNIV,COLL PHARM,DIV MED CHEM & PHARMACOGNOSY,COLUMBUS,OH 43210. NEI,BETHESDA,MD 20892. S DAKOTA STATE UNIV,COLL PHARM,BROOKINGS,SD 57007. NR 21 TC 19 Z9 19 U1 1 U2 2 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 MAR 20 PY 1992 VL 35 IS 6 BP 1117 EP 1120 DI 10.1021/jm00084a017 PG 4 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA HK860 UT WOS:A1992HK86000017 PM 1552504 ER PT J AU ARCHER, TK LEFEBVRE, P WOLFORD, RG HAGER, GL AF ARCHER, TK LEFEBVRE, P WOLFORD, RG HAGER, GL TI TRANSCRIPTION FACTOR LOADING ON THE MMTV PROMOTER - A BIMODAL MECHANISM FOR PROMOTER ACTIVATION SO SCIENCE LA English DT Article ID NUCLEAR FACTOR-I; MAMMALIAN-CELLS; BINDING-SITE; DNA-BINDING; PROTEINS; EXTRACTS; ELEMENT; INVIVO; CRUDE; SP1 AB The mouse mammary tumor virus (MMTV) promoter attains a phased array of six nucleosomes when introduced into rodent cells. This architecture excludes nuclear factor 1/CCAAT transcription factor (NF1/CTF) from the promoter before glucocorticoid treatment and hormone-dependent access of nucleolytic agents to promoter DNA. In contrast, when the promoter was transiently introduced into cells, NF1/CTF was bound constitutively and nucleolytic attack was hormone-independent. Thus, induction at this promoter was a bimodal process involving receptor-dependent remodeling of chromatin that allows NF1/CTF loading and direct receptor-mediated recruitment of additional transcription factors. C1 NCI,MOLEC VIROL LAB,HORMONE ACT & ONCOGENESIS SECT,BETHESDA,MD 20892. RI Lefebvre, Philippe/F-2685-2010 OI Lefebvre, Philippe/0000-0002-9366-5129 NR 26 TC 361 Z9 362 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 MAR 20 PY 1992 VL 255 IS 5051 BP 1573 EP 1576 DI 10.1126/science.1347958 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ809 UT WOS:A1992HJ80900041 PM 1347958 ER PT J AU SABLJIC, A MCDIARMID, R GEDANKEN, A AF SABLJIC, A MCDIARMID, R GEDANKEN, A TI A 2-PHOTON RESONANT MULTIPHOTON IONIZATION STUDY OF THE 3P-RYDBERG[-X TRANSITIONS OF CYCLOPENTADIENE SO JOURNAL OF PHYSICAL CHEMISTRY LA English DT Article ID SPECTRUM; VALENCE; ACETONE; BENZENE AB The polarization-selected two-photon resonant multiphoton ionization spectra of cyclopentadiene and cyclopentadiene-d6 have been measured in the 3p-Rydberg <-- X approximately region of the spectrum. The spectra were analyzed to provide experimental assignments for all three 3p-Rydberg origins and three a1, three b1, and one a2 fundamental vibrational frequencies in the 3p-Rydberg states. The allowed origins of the B1 and A1 3p-Rydberg <-- X approximately transitions were not observed; Herzberg-Teller induced false origins were observed from the ground to these states in their stead. The false origins were deduced to arise from coupling of the intermediate state of the two-photon transition to a state of A1 symmetry, probably the 3A1 valence state. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. BAR ILAN UNIV,DEPT CHEM,IL-52100 RAMAT GAN,ISRAEL. RI Sabljic, Aleksandar/D-4146-2011 NR 22 TC 17 Z9 17 U1 0 U2 1 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 MAR 19 PY 1992 VL 96 IS 6 BP 2442 EP 2448 DI 10.1021/j100185a011 PG 7 WC Chemistry, Physical SC Chemistry GA HK717 UT WOS:A1992HK71700011 ER PT J AU BOICE, JD HARVEY, EB BLETTNER, M STOVALL, M FLANNERY, JT AF BOICE, JD HARVEY, EB BLETTNER, M STOVALL, M FLANNERY, JT TI CANCER IN THE CONTRALATERAL BREAST AFTER RADIOTHERAPY FOR BREAST-CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID RADIATION-THERAPY; IRRADIATION; RISK; SURGERY; CERVIX; WOMEN AB Background. Patients with breast cancer have a threefold increase in the risk that a second breast cancer will develop. Radiation treatment for the initial cancer can result in moderately high doses to the contralateral breast, possibly contributing to this heightened risk. Methods. We conducted a case-control study in a cohort of 41,109 women diagnosed with breast cancer between 1935 and 1982 in Connecticut. We reviewed the medical records of 655 women in whom a second breast cancer developed five or more years after the initial tumor and compared their radiation exposure with that of 1189 matched controls from the cohort who did not have a second cancer. The dose of radiation to the contralateral breast was estimated from the original radiotherapy records. Among the exposed women, the average radiation dose to the contralateral breast was 2.82 Gy (maximum, 7.10). Results. Overall, 23 percent of the women who had a second breast cancer and 20 percent of the controls had received radiotherapy (relative risk of a second breast cancer associated with radiotherapy, 1.19). Among women who survived for at least 10 years, radiation treatment was associated with a small but marginally significant elevation in the risk of a second breast cancer (relative risk, 1.33); the risk increased significantly with the dose of radiation. An increase in risk in association with radiotherapy was evident only among women who were under 45 years of age when they were treated (relative risk, 1.59) and not among older women (relative risk, 1.01). Conclusions. Radiotherapy for breast cancer contributes little to the already high risk of a second cancer in the opposite breast. Fewer than 3 percent of all second breast cancers in this study could be attributed to previous radiation treatment; the risk, however, was significantly increased among women who underwent irradiation at a relatively young age (< 45 years). Radiation exposure after the age of 45 entails little, if any, risk of radiation-induced breast cancer. C1 CONNECTICUT TUMOR REGISTRY,HARTFORD,CT. UNIV TEXAS,CTR CANC,HOUSTON,TX 77025. RP BOICE, JD (reprint author), NCI,RADIAT EPIDEMIOL BRANCH,EXECUT PLAZA N,RM 408,6130 EXECUT BLVD,ROCKVILLE,MD 20852, USA. FU NCI NIH HHS [N01-CP0-5609, N01-CP8-5604, N01-CP9-5614] NR 29 TC 270 Z9 273 U1 0 U2 4 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 MAR 19 PY 1992 VL 326 IS 12 BP 781 EP 785 DI 10.1056/NEJM199203193261201 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HJ592 UT WOS:A1992HJ59200001 PM 1538720 ER PT J AU POWDERLY, WG SAAG, MS CLOUD, GA ROBINSON, P MEYER, RD JACOBSON, JM GRAYBILL, JR SUGAR, AM MCAULIFFE, VJ FOLLANSBEE, SE TUAZON, CU STERN, JJ FEINBERG, J HAFNER, R DISMUKES, WE AF POWDERLY, WG SAAG, MS CLOUD, GA ROBINSON, P MEYER, RD JACOBSON, JM GRAYBILL, JR SUGAR, AM MCAULIFFE, VJ FOLLANSBEE, SE TUAZON, CU STERN, JJ FEINBERG, J HAFNER, R DISMUKES, WE TI A CONTROLLED TRIAL OF FLUCONAZOLE OR AMPHOTERICIN-B TO PREVENT RELAPSE OF CRYPTOCOCCAL MENINGITIS IN PATIENTS WITH THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID ORAL FLUCONAZOLE; CLINICAL-TRIALS; NEOFORMANS; AIDS; INFECTION; THERAPY AB Background. After primary treatment for cryptococcal meningitis, patients with the acquired immunodeficiency syndrome (AIDS) require some form of continued suppressive therapy to prevent relapse. Methods. We conducted a multicenter, randomized trial that compared fluconazole (200 mg per day given orally) with amphotericin B (1 mg per kilogram of body weight per week given intravenously) in patients with AIDS who had completed primary therapy for cryptococcal meningitis with amphotericin B (greater-than-or-equal-to 15 mg per kilogram). To be eligible, patients had to have at least two negative cultures of cerebrospinal fluid immediately before randomization. The primary end point was relapse of cryptococcal disease as confirmed by biopsy or culture. Results. Of 218 patients initially enrolled, 119 were assigned to fluconazole and 99 to amphotericin B. Twenty-three patients were found not to have met the entry criteria; six other patients assigned to amphotericin B did not receive it and were lost to follow-up. of the remaining 189 patients, after a median follow-up of 286 days 14 of 78 receiving amphotericin B (18 percent) and 2 of 111 assigned to fluconazole (2 percent) had relapses of symptomatic cryptococcal disease (P < 0.001 by Fisher's exact test). There was a difference of 19 percent in the estimated probability of remaining relapse-free at one year between the fluconazole group (97 percent) and the amphotericin B group (78 percent) (95 percent confidence interval, 7 percent to 31 percent; P < 0.001). Serious drug-related toxicity was more frequent in the amphotericin B group (P = 0.02), as were bacterial infections (P = 0.004) and bacteremia (P = 0.002). Conclusions. Fluconazole taken by mouth is superior to weekly intravenous therapy with amphotericin B to prevent relapse in patients with AIDS-associated cryptococcal meningitis after primary treatment with amphotericin B. C1 GEORGE WASHINGTON UNIV,DIV INFECT DIS,WASHINGTON,DC 20052. ST LOUIS VET AFFAIRS MED CTR,ST LOUIS,MO. VET AFFAIRS MED CTR,BRONX,NY. AUDIE MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX. DAVIES MED CTR,SAN FRANCISCO,CA. BOSTON CITY HOSP,DEPT MED,BOSTON,MA 02118. CEDARS SINAI MED CTR,DEPT MED,DIV INFECT DIS,LOS ANGELES,CA 90048. UNIV ALABAMA,SCH MED,DEPT MED,DIV INFECT DIS,BIRMINGHAM,AL 35233. UNIV ALABAMA,SCH MED,CTR COMPREHENS CANC,DIV BIOSTAT,BIRMINGHAM,AL 35233. NIAID,DIV AIDS,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. VET AFFAIRS MED CTR,BIRMINGHAM,AL. NYU MED CTR,NEW YORK,NY 10016. PENN HOSP,PHILADELPHIA,PA 19107. PFIZER INC,CENT RES,GROTON,CT 06340. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. MT SINAI MED CTR,DEPT MED,DIV INFECT DIS,NEW YORK,NY 10029. BOSTON UNIV HOSP,BOSTON,MA 02218. RP POWDERLY, WG (reprint author), WASHINGTON UNIV,SCH MED,DIV INFECT DIS,BOX 8011,660 S EUCLID,ST LOUIS,MO 63110, USA. FU NCI NIH HHS [CA 13148]; NIAID NIH HHS [N01 AI52562] NR 17 TC 258 Z9 264 U1 1 U2 2 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 MAR 19 PY 1992 VL 326 IS 12 BP 793 EP 798 DI 10.1056/NEJM199203193261203 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HJ592 UT WOS:A1992HJ59200003 PM 1538722 ER PT J AU HUBBARD, RC MCELVANEY, NG BIRRER, P SHAK, S ROBINSON, WW JOLLEY, C WU, M CHERNICK, MS CRYSTAL, RG AF HUBBARD, RC MCELVANEY, NG BIRRER, P SHAK, S ROBINSON, WW JOLLEY, C WU, M CHERNICK, MS CRYSTAL, RG TI A PRELIMINARY-STUDY OF AEROSOLIZED RECOMBINANT HUMAN DEOXYRIBONUCLEASE-I IN THE TREATMENT OF CYSTIC-FIBROSIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note ID SPUTUM; IDENTIFICATION; VISCOSITY; GENE C1 NHLBI,PULM BRANCH,BLDG 10,RM 6D03,BETHESDA,MD 20892. GENENTECH INC,DEPT IMMUNOBIOL,S SAN FRANCISCO,CA. NIDDKD,PEDIAT METAB BRANCH,BETHESDA,MD. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BIOSTAT RES BRANCH,BETHESDA,MD 20892. RI McElvaney, Noel/A-6809-2010 NR 17 TC 157 Z9 156 U1 0 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 MAR 19 PY 1992 VL 326 IS 12 BP 812 EP 815 DI 10.1056/NEJM199203193261207 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HJ592 UT WOS:A1992HJ59200007 PM 1538726 ER PT J AU LONGNECKER, MP MARTINMORENO, JM KNEKT, P NOMURA, AMY SCHOBER, SE STAHELIN, HB WALD, NJ GEY, KF WILLETT, WC AF LONGNECKER, MP MARTINMORENO, JM KNEKT, P NOMURA, AMY SCHOBER, SE STAHELIN, HB WALD, NJ GEY, KF WILLETT, WC TI SERUM ALPHA-TOCOPHEROL CONCENTRATION IN RELATION TO SUBSEQUENT COLORECTAL-CANCER - POOLED DATA FROM 5 COHORTS SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID VITAMIN-E; PLASMA-LEVELS; COLON CANCER; RISK; CHOLESTEROL; PREVENTION; SELENIUM; DISEASE; DIETARY; POLYPS AB Background: Vitamin E is an antioxidant that inhibits mutagenesis and cell transformation. Previous findings in five prospective epidemiologic studies suggested that the level of serum alpha-tocopherol, the predominant form of vitamin E in the blood, was lower in subjects who subsequently developed colorectal cancer than in control subjects. However, the difference was neither obvious nor statistically significant in any one of these five studies. Purpose: To evaluate in greater detail the association between serum alpha-tocopherol concentration and risk of colorectal cancer, we pooled and analyzed the original data from the five studies. Our analyses were designed to (a) test the hypothesis with greater statistical power, (b) examine the association after adjustment for serum cholesterol levels, and (c) evaluate the association after uniform exclusion of cases diagnosed shortly after blood specimens were drawn. Methods: Data for individual subjects were analyzed. To make the design of the component investigations uniformly nested case-control studies with individual matching, we matched controls to cases in two of the cohorts. Subjects were categorized according to study-specific quartile of serum alpha-tocopherol level within the study. The pooled analysis included 289 cases of colorectal cancer and 1267 matched controls. Results: For cancers of the colon and rectum combined, the matched odds ratio (OR) for the highest quartile of serum alpha-tocopherol concentration compared with the lowest was 0.6 (95% confidence interval [CI] = 0.4-1.0). Adjustment for serum cholesterol level attenuated the OR to 0.7 (95% CI = 0.4-1.1). Conclusion: The results suggest that serum alpha-tocopherol concentration may be inversely related to risk of colorectal cancer. It is unclear whether an association exists, however, because the association between serum alpha-tocopherol level and decreased risk of colorectal cancer was modest, the CIs were wide, and, overall, the tests for trend in effect were not significant. Implications: Larger observational studies with concurrent dietary data are needed to determine whether vitamin E has a modest but potentially important protective effect against colorectal cancer. C1 ESCUELA NACL SANIDAD, MADRID, SPAIN. SOCIAL INSURANCE INST, SOCIAL SECUR RES INST, HELSINKI, FINLAND. KUAKINI MED CTR, JAPAN HAWAII CANC STUDY, HONOLULU, HI USA. NIDA, DIV EPIDEMIOL & PREVENT RES, ROCKVILLE, MD USA. KANTONSSPITAL, MED GERIATR KLIN, CH-4004 BASEL, SWITZERLAND. MED COLL ST BARTHOLOMEW, DEPT ENVIRONM & PREVENT MED, LONDON, ENGLAND. UNIV BERN, INST BIOCHEM & MOLEC BIOL, VITAMIN UNIT, CH-3000 BERN, SWITZERLAND. HARVARD UNIV, SCH PUBL HLTH, DEPT EPIDEMIOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH PUBL HLTH, DEPT NUTR, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MED, CHANNING LAB, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. RP UNIV CALIF LOS ANGELES, SCH PUBL HLTH, DEPT EPIDEMIOL, 10833 LE CONTE AVE, LOS ANGELES, CA 90024 USA. RI Martin-Moreno, Jose M./S-7733-2016; OI Martin-Moreno, Jose M./0000-0002-8648-5541; Longnecker, Matthew/0000-0001-6073-5322 NR 27 TC 83 Z9 84 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 EI 1460-2105 J9 JNCI-J NATL CANCER I JI JNCI-J. Natl. Cancer Inst. PD MAR 18 PY 1992 VL 84 IS 6 BP 430 EP 435 DI 10.1093/jnci/84.6.430 PG 6 WC Oncology SC Oncology GA HU833 UT WOS:A1992HU83300016 PM 1531683 ER PT J AU SCHIFFMAN, MH AF SCHIFFMAN, MH TI RECENT PROGRESS IN DEFINING THE EPIDEMIOLOGY OF HUMAN PAPILLOMAVIRUS INFECTION AND CERVICAL NEOPLASIA SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID GENITAL HUMAN PAPILLOMAVIRUS; HERPES-SIMPLEX VIRUS; RISK-FACTORS; CANCER; DNA; PREVALENCE; TYPE-16; ASSOCIATION; WOMEN; CARCINOMA RP SCHIFFMAN, MH (reprint author), NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,EXECUT PLAZA N,RM 443,BETHESDA,MD 20892, USA. NR 52 TC 283 Z9 287 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 MAR 18 PY 1992 VL 84 IS 6 BP 394 EP 398 DI 10.1093/jnci/84.6.394 PG 5 WC Oncology SC Oncology GA HU833 UT WOS:A1992HU83300011 PM 1311392 ER PT J AU TORRI, V SIMON, R RUSSEKCOHEN, E MIDTHUNE, D FRIEDMAN, M AF TORRI, V SIMON, R RUSSEKCOHEN, E MIDTHUNE, D FRIEDMAN, M TI STATISTICAL-MODEL TO DETERMINE THE RELATIONSHIP OF RESPONSE AND SURVIVAL IN PATIENTS WITH ADVANCED OVARIAN-CANCER TREATED WITH CHEMOTHERAPY SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID RANDOMIZED CLINICAL-TRIAL; COMBINATION CHEMOTHERAPY; PLUS CYCLOPHOSPHAMIDE; STAGE-III; 2ND-LOOK LAPAROTOMY; COMPARING CISPLATIN; META-ANALYSIS; SINGLE AGENT; CIS-PLATINUM; HEXA-CAF AB Background: A statistically appropriate analysis of the association between survival and response measures in patients with ovarian cancer could help to define the role of response rate in planning, monitoring, and interpreting the results of clinical trials. Purpose: This study was designed to investigate the relationship between antitumor response determined by clinical or pathological means and survival in patients with advanced ovarian cancer with no previous treatment. We focused on avoiding the limitations of the usual approach of comparing durations of survival for patients responding to therapy with those for nonresponders. Methods: A new meta-analytic statistical model we developed was used to analyze data from 26 randomized clinical trials published between 1975 and 1989. Our model incorporates intra-study and inter-study sources of variability in the estimates of response and survival. The study also addresses the methodological problems of evaluating response as a surrogate end point and the relevance of this association to clinical decision making and the design of clinical trials. Results: For 13 studies in which response was pathologically assessed, an improvement in surgically documented complete response rate was associated with an increase in median survival. A similar but apparently smaller effect was found for the association between objective clinical response and median survival in the 25 studies reporting these data. Conclusions: These results suggest that therapeutic measures must produce large improvements in clinical response rates to achieve meaningful effects on median survival. Improvement in surgically documented complete response rate appears to be more strongly associated with increased median survival and, hence, might be used for interim monitoring in clinical trials, but the role of second-look procedures in clinical management is controversial. C1 NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,BIOMETR RES BRANCH,EXECUT PLAZA N,BETHESDA,MD 20892. INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. NR 43 TC 42 Z9 44 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 MAR 18 PY 1992 VL 84 IS 6 BP 407 EP 414 DI 10.1093/jnci/84.6.407 PG 8 WC Oncology SC Oncology GA HU833 UT WOS:A1992HU83300013 PM 1531682 ER PT J AU KLEINBERG, ME MITAL, D ROTROSEN, D MALECH, HL AF KLEINBERG, ME MITAL, D ROTROSEN, D MALECH, HL TI CHARACTERIZATION OF A PHAGOCYTE CYTOCHROME-B558 91-KILODALTON SUBUNIT FUNCTIONAL DOMAIN - IDENTIFICATION OF PEPTIDE SEQUENCE AND AMINO-ACIDS ESSENTIAL FOR ACTIVITY SO BIOCHEMISTRY LA English DT Article ID CHRONIC GRANULOMATOUS-DISEASE; RESPIRATORY BURST OXIDASE; PLASMA-MEMBRANE; NADPH OXIDASE; ACTIVATION; CLONING; CHAIN; EXPRESSION; PROTEIN; CELLS AB The phagocyte NADPH oxidase is a multicomponent membrane-bound electron transport chain that catalyzes the reduction of O2 to superoxide. Cytochrome b558, the terminal electron donor to O2, is an integral membrane heterodimer containing 91- and 22-kDa subunits (gp91-phox and p22-phox, respectively). Synthetic peptides, whose amino acid sequences correspond to a gp91-phox carboxyl-terminal domain, inhibit superoxide production by blocking assembly of the oxidase from membrane and cytosol components. In this study, we examined the amino acid sequence requirements of a series of synthetic truncated gp91-phox peptides for inhibition of human neutrophil NADPH oxidase activation. RGVHFIF, corresponding to gp91-phox residues 559-565, was the minimum sequence capable of inhibiting superoxide generation. Contributions of individual amino acids to overall RGVHFIF inhibitory activity were determined by comparing the abilities of alanine-substituted RGVHFIF peptides to inhibit superoxide production. Substitution of alanine for arginine, valine, isoleucine, or either of the phenylalanines (but not glycine or histidine) within RGVHFIF resulted in loss of inhibitory activity. Synthetic gp91-phox carboxyl-terminal peptides are likely to be competitive inhibitors of the corresponding carboxyl-terminal domain of native gp91-phox by virtue of amino acid identity. We conclude that properties of arginine valine, isoleucine, and phenylalanine side chains within an RGVHFIF-containing domain of gp91-phox contribute significantly to cytochrome b558-mediated activation of the oxidase. C1 DEPT VET AFFAIRS MED CTR,BALTIMORE,MD 21201. NIAID,HOST DEF LAB,BETHESDA,MD 20892. RP KLEINBERG, ME (reprint author), UNIV MARYLAND,SCH MED,DEPT MED,ROOM 900 MSTF,10 S PINE ST,BALTIMORE,MD 21201, USA. NR 20 TC 41 Z9 41 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 MAR 17 PY 1992 VL 31 IS 10 BP 2686 EP 2690 DI 10.1021/bi00125a008 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HJ429 UT WOS:A1992HJ42900008 PM 1312344 ER PT J AU ASHIZAWA, K FUKUDA, T CHENG, SY AF ASHIZAWA, K FUKUDA, T CHENG, SY TI TRANSCRIPTIONAL STIMULATION BY THYROID-HORMONE OF A CYTOSOLIC THYROID-HORMONE BINDING-PROTEIN WHICH IS HOMOLOGOUS TO A SUBUNIT OF PYRUVATE KINASE-M1 SO BIOCHEMISTRY LA English DT Article ID RAT-KIDNEY; MONOCLONAL-ANTIBODIES; NUCLEOTIDE-SEQUENCE; GENE-EXPRESSION; TRIIODOTHYRONINE; ISOZYMES; LIVER; INDUCTION; GROWTH; CELLS AB We have recently shown that the monomer of rat pituitary pyruvate kinase subtype M1 (p58-M1) is a cytosolic binding protein for 3,3',5-triiodo-L-thyronine (T3). To understand the role p58-M1 plays in thyroid hormone action, we examined the regulation of p58-M1 by T3 in GH3 cells. Expression of p58-M1 was evaluated by metabolically labeling GH3 cells cultured in regular medium, thyroid hormone depleted medium (T(d) medium), or T(d) medium supplemented with T3 (T(d) + T3 medium) followed by immunoprecipitation. T3 stimulates the expression of p58-M1 by 2-fold. Analysis by pulse-chase experiments indicates that the increased expression is not due to the increase of stability of p58-M1. Northern analysis of mRNA prepared from cells cultured in regular, T(d), or T(d) + T3 medium demonstrates that T3 increases the accumulation of cytoplasmic mRNA by 2-fold. Nuclei from cells cultured in the three conditions were prepared, and the rates of synthesis of nascent nuclear RNA were compared by an in vitro transcription assay. Addition of T3 stimulates the rate of transcription by 2-fold. The parallel and identical magnitude in the increase of transcription rate and the accumulation of mRNA indicates that T3 stimulates the synthesis of p58-M1 by increasing the transcriptional activity of its gene. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BLDG 37,ROOM 4B09,BETHESDA,MD 20892. NR 30 TC 9 Z9 9 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 MAR 17 PY 1992 VL 31 IS 10 BP 2774 EP 2778 DI 10.1021/bi00125a018 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HJ429 UT WOS:A1992HJ42900018 PM 1547217 ER PT J AU CHRISTOU, M MITCHELL, MJ AOYAMA, T GELBOIN, HV GONZALEZ, FJ JEFCOATE, CR AF CHRISTOU, M MITCHELL, MJ AOYAMA, T GELBOIN, HV GONZALEZ, FJ JEFCOATE, CR TI SELECTIVE SUPPRESSION OF THE CATALYTIC ACTIVITY OF CDNA-EXPRESSED CYTOCHROME-P4502B1 TOWARD POLYCYCLIC-HYDROCARBONS IN THE MICROSOMAL MEMBRANE - MODIFICATION OF THIS EFFECT BY SPECIFIC AMINO-ACID SUBSTITUTIONS SO BIOCHEMISTRY LA English DT Article ID RAT-LIVER CYTOCHROME-P-450; CRYSTAL-STRUCTURE; METABOLISM; ISOZYMES; 7,12-DIMETHYLBENZANTHRACENE; CYTOCHROMES-P-450; REGIOSELECTIVITY; PURIFICATION; FORMS; STEREOSPECIFICITY AB Human hepatoma HEPG2 cells were infected with recombinant vaccinia virus vectors containing cDNAs encoding both known and variant rat cytochromes P450 (CYP). CYP2B1 and CYP2B2 were equally well expressed (110-140 pmol/mg of microsomal protein) and catalyzed metabolism of 7,12-dimethylbenz[a]anthracene (DMBA). Their regioselectivity for DMBA metabolism paralleled that of the respective purified rat liver enzymes and reproduced previously reported regioselective differences between CYP2B1 and CYP2B2 [Wilson et al. (1984) Carcinogenesis 5, 1475-1483]. CYP2A1 and Cyp2A2 expressed in HEPG2 microsomes exhibited nearly equal DMBA-metabolizing activities that closely matched that of purified CYP2A1. Although purified rat liver CYP2B1 was 3 times more active, than purified rat liver CYP2B2, the expressed recombinant microsomal CYP2B1 (rCYP2B1) was 20 times less active than rCYP2B2, where activity matched that of the purified cytochrome. Microsomal suppression of rCYP2B1 catalytic activity was also observed for benzo[a]pyrene. Specific ami no acid substitution at equivalent positions of the completely homologous NH2-terminal halves of rCYP2B1 and rCYP2B2 changed this suppression effect. Thus, a L58 --> F, I114 --> F double mutant exhibited 3 times the normal activity for rCYP2B1 while remaining inhibitory for rCYP2B2. The single substitutions produced very different effects. The L58 --> F substitution prevented expression of rCYP2B1, while the I114 --> F substitution was inhibitory for both rCYP2B1 and rCYP2B2 (40 and 70%). A single E282 --> V mutation produced a stimulation of rCYP2B1 activity comparable to that of the L58 --> F, I114 --> F double substitution. Since this double mutation decreases testosterone metabolism by rCYP2B1 [Aoyama et al. (1989) J. Biol. Chem. 264, 21327-21333], the selective effects on DMBA metabolism by rCYP2B1 mutants may result from relief of the membrane restriction that affects this bulky lipophilic substrate. C1 UNIV WISCONSIN,SCH MED,DEPT PHARMACOL,1300 UNIV AVE,MADISON,WI 53706. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA16265] NR 40 TC 27 Z9 27 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 MAR 17 PY 1992 VL 31 IS 10 BP 2835 EP 2841 DI 10.1021/bi00125a027 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HJ429 UT WOS:A1992HJ42900027 PM 1547225 ER PT J AU SCHINDLER, CW TELLA, SR KATZ, JL GOLDBERG, SR AF SCHINDLER, CW TELLA, SR KATZ, JL GOLDBERG, SR TI EFFECTS OF COCAINE AND ITS QUATERNARY DERIVATIVE COCAINE METHIODIDE ON CARDIOVASCULAR FUNCTION IN SQUIRREL-MONKEYS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE COCAINE; COCAINE METHIODIDE; BLOOD PRESSURE; HEART RATE; NOREPINEPHRINE; (SQUIRREL MONKEY) ID NOREPINEPHRINE; MECHANISMS; RELEASE; SYSTEM; RATS AB The effects of cocaine and its quarternary derivative cocaine methiodide, which does not cross the blood-brain barrier, were studied on cardiovascular function in squirrel monkeys. In conscious monkeys, cocaine produced clear dose-dependent increases in blood pressure and heart rate, while cocaine methiodide did not. Both cocaine and cocaine methiodide enhanced the effects of norepinephrine in anesthetized animals, suggesting that both inhibit neuronal uptake of norepinephrine; cocaine was approximately 30 times more potent than cocaine methiodide. In anesthetized monkeys both cocaine and cocaine methiodide produced small, short duration pressor effects, although cocaine was at least 10 times more potent than cocaine methiodide. Cocaine's effects in anesthetized animals were clearly blunted in comparison to its effects in conscious animals. These effects of cocaine on blood pressure occurred at doses lower than those required to enhance norepinephrine's effects, indicating that the norepinephrine uptake blocking effects of the drugs cannot fully account for their cardiovascular effects. The greatly enhanced effect of cocaine in conscious animals and the finding that cocaine methiodide had little effect in conscious animals indicates that central mechanisms are involved in the effects of cocaine on cardiovascular function in conscious animals. C1 UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21201. GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20007. RP SCHINDLER, CW (reprint author), NIDA,ADDICT RES CTR,PRECLIN PHARMACOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA. OI Katz, Jonathan/0000-0002-1068-1159 NR 21 TC 26 Z9 26 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD MAR 17 PY 1992 VL 213 IS 1 BP 99 EP 105 DI 10.1016/0014-2999(92)90238-Y PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HP231 UT WOS:A1992HP23100014 PM 1499661 ER PT J AU LEE, JW TENG, K MARQUEZ, VE AF LEE, JW TENG, K MARQUEZ, VE TI SYNTHESIS OF 2 RIGID DIACYLGLYCEROL ANALOGS HAVING A BIS-BUTYROLACTONE SKELETON SO TETRAHEDRON LETTERS LA English DT Article ID PROTEIN KINASE-C; DESIGN AB The stereoselective synthesis of two rigid diacylglycerol analogues starting from protected D-apio-L-furanose (apiose) is described. The construction of the desired bis-butyrolactone bicyclic structure was accomplished via an intramolecular radical cyclization. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. NR 11 TC 12 Z9 12 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD MAR 17 PY 1992 VL 33 IS 12 BP 1539 EP 1542 DI 10.1016/S0040-4039(00)91668-X PG 4 WC Chemistry, Organic SC Chemistry GA HJ784 UT WOS:A1992HJ78400003 ER PT J AU RUGGIERO, M CASAMASSIMA, F MAGNELLI, L PACINI, S PIERCE, JH GREENBERGER, JS CHIARUGI, VP AF RUGGIERO, M CASAMASSIMA, F MAGNELLI, L PACINI, S PIERCE, JH GREENBERGER, JS CHIARUGI, VP TI MITOGENIC SIGNAL TRANSDUCTION - A COMMON TARGET FOR ONCOGENES THAT INDUCE RESISTANCE TO IONIZING-RADIATIONS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PROTEIN-KINASE-C; RAS ONCOGENE; TRANSFORMED-CELLS; DIACYLGLYCEROL; EXPRESSION; ACTIVATION; RECEPTORS; TURNOVER; DENOVO C1 NCI,LCMB,BETHESDA,MD 20892. UNIV FLORENCE,DEPT CLIN PHYSIOPATHOL,I-50121 FLORENCE,ITALY. UNIV MASSACHUSETTS,DEPT RADIAT ONCOL,WORCESTER,MA 01605. RP RUGGIERO, M (reprint author), LAB MOLEC BIOL,VIALE MORGAGNI 50,I-50134 FLORENCE,ITALY. NR 19 TC 15 Z9 15 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 MAR 16 PY 1992 VL 183 IS 2 BP 652 EP 658 DI 10.1016/0006-291X(92)90532-P PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HJ115 UT WOS:A1992HJ11500045 PM 1550572 ER PT J AU ALEMANY, J KLEMENT, JF BORRAS, T DEPABLO, F AF ALEMANY, J KLEMENT, JF BORRAS, T DEPABLO, F TI DNA-BINDING FACTORS WHICH INTERACT WITH THE SP1 SITE OF THE CHICKEN-DELTA-1-CRYSTALLIN PROMOTER ARE DEVELOPMENTALLY REGULATED SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID DELTA-CRYSTALLIN GENE; CHICKEN DELTA-1-CRYSTALLIN GENE; POLYMERASE CHAIN-REACTION; GROWTH FACTOR-I; MESSENGER-RNA; LENS; PROTEIN; EXPRESSION; ACTIVATION; ELEMENTS C1 CSIC,CTR INVEST BIOL,VELAZQUEZ 144,E-28006 MADRID,SPAIN. NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. PHARMAGEN,E-28760 MADRID,SPAIN. NR 22 TC 17 Z9 17 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 MAR 16 PY 1992 VL 183 IS 2 BP 659 EP 665 DI 10.1016/0006-291X(92)90533-Q PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HJ115 UT WOS:A1992HJ11500046 PM 1550573 ER PT J AU RASCON, A LINDGREN, S STAVENOW, L BELFRAGE, P ANDERSSON, KE MANGANIELLO, VC DEGERMAN, E AF RASCON, A LINDGREN, S STAVENOW, L BELFRAGE, P ANDERSSON, KE MANGANIELLO, VC DEGERMAN, E TI PURIFICATION AND PROPERTIES OF THE CGMP-INHIBITED CAMP PHOSPHODIESTERASE FROM BOVINE AORTIC SMOOTH-MUSCLE SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE CGMP-INHIBITED CYCLIC NUCLEOTIDE PHOSPHODIESTERASE; SMOOTH MUSCLE; PHOSPHODIESTERASE INHIBITOR; (BOVINE AORTA) ID CYCLIC-AMP PHOSPHODIESTERASE; HUMAN MESENTERIC VESSELS; NUCLEOTIDE PHOSPHODIESTERASE; CONTRACTILE RESPONSES; ADIPOSE-TISSUE; CARDIAC-MUSCLE; RAT-LIVER; MILRINONE; PHOSPHORYLATION; SENSITIVITY AB Pure cGMP-inhibited cAMP phosphodiesterase (cGI-PDE) in mu-g quantities was isolated from bovine aortic smooth muscle after more than 500-fold purification using DEAE ion-exchange and affinity chromatography with a derivative of the specific cGI-PDE inhibitor cilostamide conjugated as a ligand to aminoethyl agarose (CIT-agarose). The cGI-PDE, which constituted about half of the high affinity cAMP-PDE activity of a tissue homogenate, was identified with a 105-kDa protein on SDS-PAGE through use of antibodies towards the human platelet, bovine cardiac and bovine adipose tissue cGI-PDE in Western blot and immunoprecipitation/immunoinactivation analysis. As observed during purification of the enzyme from other tissues the enzyme protein was exquisitely sensitive to proteolytic nicking during purification, resulting in several 30-77-kDa polypeptide fragments. Rapid immunoprecipitation from fresh tissue extracts was the only way found to partially prevent the proteolysis. The native enzyme had apparent molecular sizes of approx. 100 000 or, mainly approx. 220 000 by gel chromatography, presumably indicating the presence of monomeric and dimeric forms. The enzyme hydrolyzed cAMP and cGMP with normal Michaelis-Menten kinetics with K(m) of 0.16 and 0.09-mu-M, respectively, with V(max) for hydrolysis of cGMP of 0.3 compared to 3.1-mu-mol/min per mg protein for cAMP. The enzyme was potently and selectively inhibited by cGMP (IC50 almost-equal-to 0.25-mu-M) and the cardiotonic/vasodilatory drugs OPC-3911 (a cilostamide derivative), milrinone and CI-930 (IC50 almost-equal-to 0.05, 0.40 and 0.25-mu-M, respectively). The cGI-PDE was phosphorylated by cAMP-dependent protein kinase as has been reported for the analogous enzymes in heart, adipose tissue and platelets. The identification of a cGI-PDE in the aortic smooth muscle and its inhibitor specificity is consistent with the hypothesis that inhibition of this enzyme is important in the mechanism through which these drugs produce vasorelaxation. C1 UNIV LUND,DEPT CLIN PHARMACOL,S-22100 LUND,SWEDEN. UNIV LUND,MALMO GEN HOSP,DEPT INTERNAL MED,S-21401 MALMO,SWEDEN. NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. RP RASCON, A (reprint author), UNIV LUND,DEPT MED & PHYSIOL CHEM,POB 94,S-22100 LUND,SWEDEN. NR 33 TC 40 Z9 41 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 MAR 16 PY 1992 VL 1134 IS 2 BP 149 EP 156 DI 10.1016/0167-4889(92)90038-D PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HM554 UT WOS:A1992HM55400008 PM 1313303 ER PT J AU GOSTI, F LI, SSL MAUNOURY, R BORNENS, M AF GOSTI, F LI, SSL MAUNOURY, R BORNENS, M TI HUMAN CENTROSOMAL EPITOPE IS SHARED SPECIFICALLY WITH HUMAN LACTATE DEHYDROGENASE-B ISOZYME SO FEBS LETTERS LA English DT Article DE LDH-B; CENTROSOME; HUMAN HEPATIC CELL ID HUMAN CELL-LINES; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; ELECTROPHORETIC TRANSFER; POLYACRYLAMIDE GELS; PROTEINS; GENE; IDENTIFICATION; NITROCELLULOSE; MICROTUBULES; SEQUENCES AB A rabbit serum (0013) used to identify pericentriolar proteins from isolated centrosomes (Gosti-Testu, F., Marty, M.C., Berges, J., Maunoury, R. and Bornens, M. (1986) EMBO J. 5, 2545 2550) was shown also to react through the same epitope with several non-centrosomal proteins including a major 36 kDa cytosolic antigen. This protein was identified to be human lactate dehydrogenase and the co-distribution of 0013 epitope on the centrosomal protein and on lactate dehydrogenase (LDH) was shown to be specific for human cells (Gosti, F., Marty, M.C., Courvalin, J.C., Maunoury, R. and Bornens, M. (1987) Proc. Natl. Acad. Sci. USA 84, 1000-1004). Human hepatic cells constitute, so far, the only exception to this co-distribution rule. By using this cell type which expresses only the LDH-A4 isozyme, we demonstrate that 0013 epitope is specific for the human LDH-B subunit, making serum 0013 the strongest anti-LDH-B available so far. The evolutionary and physiological significance of this situation is discussed. C1 CTR HOSP ST ANNE,ANAT PATHOL LAB,F-75674 PARIS,FRANCE. NIEHS,GENET LAB,RES TRIANGLE PK,NC 27709. RP GOSTI, F (reprint author), CNRS,CTR GENET MOLEC,2 AV TERRASSE,F-91190 GIF SUR YVETTE,FRANCE. NR 27 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAR 16 PY 1992 VL 299 IS 3 BP 231 EP 234 DI 10.1016/0014-5793(92)80121-V PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA HJ961 UT WOS:A1992HJ96100007 PM 1371976 ER PT J AU SHETTY, KT VEERANNA GURU, SC AF SHETTY, KT VEERANNA GURU, SC TI PHOSPHATASE-ACTIVITY AGAINST NEUROFILAMENT PROTEINS FROM BOVINE SPINAL-CORD - EFFECT OF ALUMINUM AND NEUROPSYCHOACTIVE DRUGS SO NEUROSCIENCE LETTERS LA English DT Article DE NEUROFILAMENT; PROTEIN PHOSPHATASE; ALUMINUM; NEUROPSYCHOACTIVE DRUG ID AXONAL-TRANSPORT; MOTOR NEURONS; PHOSPHORYLATION AB Protein phosphatase activity associated with neurofilament (NF) rich (Triton X-100 insoluble) fraction was extracted and partially characterised by using known inhibitors of protein phosphatases such as vanadate and fluoride. Protein phosphatase activity was demonstrated with reference to the dephosphorylation of endogenous substrate, NF protein and exogenous protein substrates, casein and phosvitin. Phosphoamino acids and beta-glycerophosphate were found to be poor substrates. Further, new observations have been made regarding the in vitro inhibitory effect of aluminium and the differential effects of some of the neuropsychoactive drugs. The findings could possibly lead to studies explaining the biochemical basis of aluminium induced neurotoxicity as well as the side effects associated with the long term medication of neuropsychoactive drugs. C1 NEURO SCI,BANGALORE,INDIA. RP SHETTY, KT (reprint author), NIMH,DEPT NEUROCHEM,BLDG 36,NINDS ROOM 4D20,BETHESDA,MD 20892, USA. NR 22 TC 17 Z9 17 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 MAR 16 PY 1992 VL 137 IS 1 BP 83 EP 86 PG 4 WC Neurosciences SC Neurosciences & Neurology GA HL202 UT WOS:A1992HL20200021 PM 1320755 ER PT J AU KIDD, GL AF KIDD, GL TI UNITED-STATES RESEARCH UNIVERSITIES NOW CONFRONT FATEFUL CHOICES - COMMENT SO SCIENTIST LA English DT Letter RP KIDD, GL (reprint author), NEI,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SCIENTIST INC PI PHILADELPHIA PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104 SN 0890-3670 J9 SCIENTIST JI Scientist PD MAR 16 PY 1992 VL 6 IS 6 BP 13 EP 13 PG 1 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA HH446 UT WOS:A1992HH44600015 ER PT J AU SWINNE, CJ SHAPIRO, EP LIMA, SD FLEG, JL AF SWINNE, CJ SHAPIRO, EP LIMA, SD FLEG, JL TI AGE-ASSOCIATED CHANGES IN LEFT-VENTRICULAR DIASTOLIC PERFORMANCE DURING ISOMETRIC-EXERCISE IN NORMAL SUBJECTS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Note ID DOPPLER ECHOCARDIOGRAPHY; HEART-RATE; MEN; RESPONSES C1 FRANCIS SCOTT KEY MED CTR,DIV CARDIOL,BALTIMORE,MD. RP SWINNE, CJ (reprint author), NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BETHESDA,MD 20892, USA. NR 18 TC 44 Z9 44 U1 1 U2 1 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 MAR 15 PY 1992 VL 69 IS 8 BP 823 EP 826 DI 10.1016/0002-9149(92)90518-4 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HJ098 UT WOS:A1992HJ09800027 PM 1546666 ER PT J AU MELBYE, M BIGGAR, RJ AF MELBYE, M BIGGAR, RJ TI INTERACTIONS BETWEEN PERSONS AT RISK FOR AIDS AND THE GENERAL-POPULATION IN DENMARK SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; BLOOD DONORS; HIV; HOMOSEXUALITY; POPULATION SURVEILLANCE; RISK FACTORS; SEX BEHAVIOR; SUBSTANCE ABUSE; INTRAVENOUS ID HUMAN-IMMUNODEFICIENCY-VIRUS; SEXUAL-BEHAVIOR; HOMOSEXUAL MEN; UNITED-STATES; HIV-INFECTION; HTLV-III; PREVALENCE; TRANSMISSION; KNOWLEDGE; ANTIBODY AB A nationwide study of sexual behavior was undertaken among 4,680 randomly selected Danes aged 18-59 years. The median number of sexual partners (lifetime) was highest for men aged 30-34 years (eight partners) and for women aged 25-29 years (seven partners). After adjustment for age and sex, having had greater-than-or-equal-to 5 sexual partners in the past year was strongly associated with living in larger cities, intravenous drug use, and having sex with a prostitute, a bisexual man, an intravenous drug user, or a resident of sub-Saharan Africa. The frequency of ever having had anal intercourse was highest among women aged 20-34 years (range, 27%-36%) and was independently associated only with increasing number of sexual partners (lifetime). Overall, 2.7% of men reported any homosexual experience, among whom most (88%) had also had heterosexual intercourse. Prostitute contact (ever) was reported by 13% of all men and was associated with a high educational level, a history of travel, a greater number of sexual partners, and intravenous drug use. Overall, sexual contact with someone considered at high risk of human immunodeficiency virus (HIV) infection (a homosexual/bisexual man, intravenous drug user, prostitute, or sub-Saharan African resident) was reported by 15.9% of men and 4.8% of women. Among active blood donors (past year), 12.5% of men and 4.0% of women had engaged in potentially risky behavior. HIV testing was deliberately sought more often by respondents exposed to someone at increased risk of HIV infection (10.6%) than by those unexposed (6.5%, p < 0.01). Exposure to persons at risk of HIV infection is considerable in Denmark. The majority of persons who have had potential exposure to HIV have not yet been tested for HIV. C1 NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP MELBYE, M (reprint author), STATE SERUM INST,DEPT EPIDEMIOL,ARTILLERIVEJ 5,DK-2300 COPENHAGEN,DENMARK. NR 26 TC 66 Z9 66 U1 1 U2 3 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 15 PY 1992 VL 135 IS 6 BP 593 EP 602 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HR866 UT WOS:A1992HR86600001 PM 1580235 ER PT J AU SANDLER, RS SANDLER, DP MCDONNELL, CW WURZELMANN, JI AF SANDLER, RS SANDLER, DP MCDONNELL, CW WURZELMANN, JI TI CHILDHOOD EXPOSURE TO ENVIRONMENTAL TOBACCO-SMOKE AND THE RISK OF ULCERATIVE-COLITIS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Note DE COLITIS, ULCERATIVE; INFLAMMATORY BOWEL DISEASES; TOBACCO SMOKE POLLUTION ID INFLAMMATORY BOWEL-DISEASE; CIGARETTE-SMOKING; CROHNS-DISEASE; EPIDEMIOLOGY; SELECTION; CANCER; BIAS AB Previous reports have suggested that there may be a protective effect of active cigarette smoking on the risk of ulcerative colitis. Because passive smoking may also have other health consequences, the authors examined the effect of exposure to environmental tobacco smoke during childhood on adult risk of ulcerative colitis in a case-control study of 172 cases drawn in 1986-1987 from the rosters of North Carolina chapters of the Crohn's & Colitis Foundation of America and 131 peer-nominated neighborhood controls. Active smokers were less likely to develop ulcerative colitis than were nonexposed nonsmokers (odds ratio = 0.53, 95% confidence interval 0.24-1.14). The risk was also decreased in passive smokers, i.e., those whose parents had smoked (odds ratio = 0.50, 95% confidence interval 0.25-1.00). Risk estimates were not related to sex, education, age at onset of symptoms, or year of onset of symptoms. Both active smoking in adulthood and passive childhood exposure to environmental tobacco smoke appear to decrease the risk of ulcerative colitis. The results indicate that childhood passive smoke exposures can influence adult susceptibility to ulcerative colitis. C1 UNIV N CAROLINA,CTR GASTROINTESTINAL BIOL & DIS,CHAPEL HILL,NC 27599. NIEHS,DIV BIOMETRY & RISK ASSESSMENT,RES TRIANGLE PK,NC 27709. RP SANDLER, RS (reprint author), UNIV N CAROLINA,DIV DIGEST DIS & NUTR,CB 7080,423A BURNETT WOMACK BLDG,CHAPEL HILL,NC 27599, USA. OI Sandler, Dale/0000-0002-6776-0018 FU NCRR NIH HHS [M01 RR 00046]; NIDDK NIH HHS [T32 DK 7634, P30 DK 34987] NR 29 TC 41 Z9 41 U1 0 U2 2 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 15 PY 1992 VL 135 IS 6 BP 603 EP 608 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HR866 UT WOS:A1992HR86600002 PM 1580236 ER PT J AU ORDEN, SR DYER, AR LIU, K PERKINS, L RUTH, KJ BURKE, G MANOLIO, TA AF ORDEN, SR DYER, AR LIU, K PERKINS, L RUTH, KJ BURKE, G MANOLIO, TA TI RANDOM DIGIT DIALING IN CHICAGO CARDIA - COMPARISON OF INDIVIDUALS WITH UNLISTED AND LISTED TELEPHONE NUMBERS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE EPIDEMIOLOGIC METHODS; RESEARCH DESIGN; SAMPLING STUDIES ID DESIGN; CANCER AB Young adult blacks and whites aged 18-30 years of both low and high educational levels were recruited through random digit dialing to participate in the Chicago, Illinois, portion of a longitudinal study, Coronary Artery Risk Development in Young Adults (CARDIA). Overall, 31% of randomly selected persons eligible to participate had unlisted telephone numbers-about 50% of black men and women and 11% and 17% of white men and women, respectively. There was no difference in proportions of numbers unlisted by educational level, except for white men, who were more likely to have unlisted numbers at a low educational level than at a high educational level. There was no consistent pattern of differences in rates of participation across race, sex, or education subgroups for unlisted and listed numbers, and there were no significant differences for selected health measures, except smoking. The findings suggest that in Chicago, there is a potential bias in estimates of sociodemographic characteristics from the exclusion of unlisted numbers, but it is likely to be insignificant if recruitment is stratified according to race, sex, and education. Within strata, there was little bias with respect to the attributes measured. Ideally, to guard against possible bias, random digit dialing is recommended as the preferred way to select a representative population-based sample. C1 UNIV ALABAMA,CTR CARDIA COORDINATING,BIRMINGHAM,AL 35294. UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN 55455. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. RP ORDEN, SR (reprint author), NORTHWESTERN UNIV,SCH MED,DEPT COMMUNITY HLTH & PREVENT MED,680 N LAKE SHORE DR,SUITE 1102,CHICAGO,IL 60611, USA. FU NHLBI NIH HHS [N01-HC-48048, N01-HC-048049, N01-HC-4807] NR 31 TC 23 Z9 23 U1 1 U2 1 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 15 PY 1992 VL 135 IS 6 BP 697 EP 709 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HR866 UT WOS:A1992HR86600012 PM 1580246 ER PT J AU JOHN, EM SAVITZ, DA SANDLER, DP AF JOHN, EM SAVITZ, DA SANDLER, DP TI PRENATAL EXPOSURE TO PARENTS SMOKING AND CHILDHOOD-CANCER - REPLY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter C1 UNIV N CAROLINA,DEPT EPIDEMIOL,CHAPEL HILL,NC 27599. NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709. RP JOHN, EM (reprint author), STANFORD UNIV,MED CTR,SCH MED,DEPT HLTH RES & POLICY,STANFORD,CA 94305, USA. NR 8 TC 2 Z9 2 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAR 15 PY 1992 VL 135 IS 6 BP 714 EP 715 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HR866 UT WOS:A1992HR86600018 ER PT J AU LOPEZ, JS DESMET, MD MASUR, H MUELLER, BU PIZZO, PA NUSSENBLATT, RB AF LOPEZ, JS DESMET, MD MASUR, H MUELLER, BU PIZZO, PA NUSSENBLATT, RB TI ORALLY-ADMINISTERED 566C80 FOR TREATMENT OF OCULAR TOXOPLASMOSIS IN A PATIENT WITH THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Letter C1 NCI,DEPT CRIT CARE MED,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. RP LOPEZ, JS (reprint author), NEI,BLDG 10,RM 10N226,BETHESDA,MD 20892, USA. NR 5 TC 15 Z9 15 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 MAR 15 PY 1992 VL 113 IS 3 BP 331 EP 333 PG 3 WC Ophthalmology SC Ophthalmology GA HG922 UT WOS:A1992HG92200016 PM 1543229 ER PT J AU HOFFMAN, GS KERR, GS LEAVITT, RY HALLAHAN, CW LEBOVICS, RS TRAVIS, WD ROTTEM, M FAUCI, AS AF HOFFMAN, GS KERR, GS LEAVITT, RY HALLAHAN, CW LEBOVICS, RS TRAVIS, WD ROTTEM, M FAUCI, AS TI WEGENER GRANULOMATOSIS - AN ANALYSIS OF 158 PATIENTS SO ANNALS OF INTERNAL MEDICINE LA English DT Review DE WEGENERS GRANULOMATOSIS; CYCLOPHOSPHAMIDE; GLUCOCORTICOIDS; GLOMERULONEPHRITIS; DRUG TOXICITY ID CONTROLLED CLINICAL-TRIAL; RHEUMATOID-ARTHRITIS; TRIMETHOPRIM-SULFAMETHOXAZOLE; LUPUS NEPHRITIS; ANTICYTOPLASMIC AUTOANTIBODIES; INTRAVENOUS CYCLOPHOSPHAMIDE; IMMUNODIAGNOSTIC VALUE; PULSE METHOTREXATE; THERAPY; DIAGNOSIS AB Objective: To prospectively study the clinical features, pathophysiology, treatment, and prognosis of Wegener granulomatosis. Design: Of the 180 patients with Wegener granulomatosis referred to the National Institute of Allergy and Infectious Diseases during the past 24 years, 158 have been followed for 6 months to 24 years (a total of 1229 patient-years). Measurements: Characteristics of clinical presentation, surgical pathology, course of illness, laboratory and radiographic findings, and the results of medical and surgical treatment have been recorded in a computer-based information retrieval system. Setting: The Warren Magnuson Clinical Center of the National Institutes of Health. Main Results: Men and women were equally represented; 97% of patients were white, and 85% were more than 19 years of age. The mean period of follow-up was 8 years. One hundred and thirty-three patients (84%) received "standard" therapy with daily low-dose cyclophosphamide and glucocorticoids. Eight (5.0%) received only low-dose cyclophosphamide. Six (4.0%) never received cyclophosphamide and were treated with other cytotoxic agents and glucocorticoids. Ten patients (6.0%) were treated with only glucocorticoids. Ninety-one percent of patients experienced marked improvement, and 75% achieved complete remission. Fifty percent of remissions were associated with one or more relapses. Of 99 patients followed for > 5 years, 44% had remissions of > 5 years duration. Thirteen percent of patients died of Wegener granulomatosis, treatment-related causes, or both. Almost all patients had serious morbidity from irreversible features of their disease (86%) or side effects of treatment (42%). Conclusions: The course of Wegener granulomatosis has been dramatically improved by daily treatment with cyclophosphamide and glucocorticoids. Nonetheless, disease- and treatment-related morbidity is often profound. Alternative forms of therapy have not yet achieved the high rates of remission induction and successful maintenance that have been reported with daily cyclophosphamide treatment. Despite continued therapeutic success with cyclophosphamide, our long-term follow-up of patients with Wegener granulomatosis has led to increasing concerns about toxicity resulting from prolonged cyclophosphamide therapy and has encouraged investigation of other therapeutic regimens. RP HOFFMAN, GS (reprint author), NIH,BLDG 10,ROOM 11B12,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 45 TC 1754 Z9 1811 U1 0 U2 15 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 MAR 15 PY 1992 VL 116 IS 6 BP 488 EP 498 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA HJ598 UT WOS:A1992HJ59800010 PM 1739240 ER PT J AU IHDE, DC AF IHDE, DC TI DOES RADIATION INCREASE SURVIVAL IN NONRESECTABLE LUNG-CANCER - REPLY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP IHDE, DC (reprint author), NIH,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 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 MAR 15 PY 1992 VL 116 IS 6 BP 525 EP 525 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HJ598 UT WOS:A1992HJ59800031 ER PT J AU REX, J AF REX, J TI ITRACONAZOLE-DIGOXIN INTERACTION SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP REX, J (reprint author), NIH,BETHESDA,MD 20892, USA. NR 5 TC 35 Z9 35 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 MAR 15 PY 1992 VL 116 IS 6 BP 525 EP 525 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HJ598 UT WOS:A1992HJ59800032 PM 1310840 ER PT J AU EVANS, GA WAHL, LM FARRAR, WL AF EVANS, GA WAHL, LM FARRAR, WL TI INTERLEUKIN-2-DEPENDENT PHOSPHORYLATION OF THE RETINOBLASTOMA-SUSCEPTIBILITY-GENE PRODUCT P110-115RB IN HUMAN T-CELLS SO BIOCHEMICAL JOURNAL LA English DT Article ID PROTEIN KINASE-C; SV40 LARGE-T; E1A PROTEINS; CDC2 PROTEIN; CYCLE; ACTIVATION; RECEPTOR; TRANSCRIPTION; BINDING; MITOSIS AB The state of phosphorylation of the retinoblastoma-susceptibility gene product, p110-115RB, is thought to have fundamental importance in controlling the progression of the cell through the cell cycle. We have studied RB phosphorylation in human T-cells in the context of T-cell activation, stimulated by phytohaemagglutinin (PHA) and interleukin-2 (IL-2). We show that, of the signals associated with T-cell activation, only signals that directly lead to movement into S phase of the cell cycle are capable of stimulating RB phosphorylation. Cyclosporin A (CsA), a potent inhibitor of IL-2 synthesis and cellular proliferation, blocked RB phosphorylation, and this was recovered with exogenous IL-2, indicating a direct involvement of IL-2 in controlling RB phosphorylation. We found that PHA did not stimulate RB phosphorylation within 10 h of treatment, but IL-2 could effectively stimulate RB phosphorylation within 2 h. and this approached a maximum within 8-10 h of IL-2 treatment. Further, by using actinomycin D to inhibit new gene transcription following IL-2 stimulation, we found that early-cell-cycle phosphorylation of RB required IL-2-stimulated gene transcription. From these data we conclude that, in human T-cells, RB phosphorylation is not directly associated with T-cell receptor-mediated events, but requires the interaction of IL-2 and new gene transcription following IL-2 stimulation. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS DEV PROGRAM,FREDERICK,MD 21702. NIH,IMMUNOL LAB,CELLULAR IMMUNOL SECT,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74102] NR 28 TC 12 Z9 12 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAR 15 PY 1992 VL 282 BP 759 EP 764 PN 3 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK342 UT WOS:A1992HK34200023 PM 1554358 ER PT J AU NAGARAJAN, S CHEN, HC LI, SC LI, YT LOCKYER, JM AF NAGARAJAN, S CHEN, HC LI, SC LI, YT LOCKYER, JM TI EVIDENCE FOR 2 CDNA CLONES ENCODING HUMAN GM2-ACTIVATOR PROTEIN SO BIOCHEMICAL JOURNAL LA English DT Article ID AMINO-ACID-SEQUENCE; ACTIVATOR PROTEIN; HEXOSAMINIDASE-A; ENZYMATIC-HYDROLYSIS; ENZYMIC-HYDROLYSIS; GM2 GANGLIOSIDOSIS; BETA-GLUCOSIDASE; SULFATIDE ACTIVATOR; GAUCHER SPLEEN; HUMAN LIVER AB Two cDNAs encoding GM2 activator, pGM2A (648 bp) and GAP (1093 bp), were isolated from human placenta lambda-gt11 libraries. The DNA sequence of pGM2A from 1 to 302 was almost identical with GAP, but diverged from 303-648. PCR was used to demonstrate the presence of both species of GM2 activator in placental RNA. Both cDNAs hybridized to mRNAs of approximately 2.3 kb and to identical single bands on genomic Southern blots. C1 TULANE UNIV,SCH MED,DEPT BIOCHEM,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,HUMAN GENET PROGRAM,NEW ORLEANS,LA 70112. NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. FU NINDS NIH HHS [NS09626] NR 43 TC 21 Z9 22 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAR 15 PY 1992 VL 282 BP 807 EP 813 PN 3 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK342 UT WOS:A1992HK34200029 PM 1554364 ER PT J AU LEVIN, FR LEVIN, HR NAGOSHI, C AF LEVIN, FR LEVIN, HR NAGOSHI, C TI AUTONOMIC FUNCTIONING AND CIGARETTE-SMOKING - HEART-RATE SPECTRAL-ANALYSIS SO BIOLOGICAL PSYCHIATRY LA English DT Note ID RATE-VARIABILITY; STIMULATION; AGE C1 NIDA,ADDICT RES CTR,TREATMENT BRANCH,BALTIMORE,MD. NR 17 TC 26 Z9 27 U1 0 U2 1 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 MAR 15 PY 1992 VL 31 IS 6 BP 639 EP 643 DI 10.1016/0006-3223(92)90254-W PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA HQ245 UT WOS:A1992HQ24500015 PM 1581447 ER PT J AU YOUNG, NS AF YOUNG, NS TI THE PROBLEM OF CLONALITY IN APLASTIC-ANEMIA - DR DAMESHEK RIDDLE, RESTATED SO BLOOD LA English DT Editorial Material ID PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; BONE-MARROW TRANSPLANTATION; HEMATOPOIETIC STEM-CELLS; ACUTE MYELOID-LEUKEMIA; DNA FRAGMENTATION; MYELODYSPLASTIC SYNDROME; ANTITHYMOCYTE GLOBULIN; PROLIFERATIVE CAPACITY; PROGENITOR CELLS; SELF-RENEWAL RP YOUNG, NS (reprint author), NHLBI,CLIN HEMATOL BRANCH,CELL BIOL SECT,BLDG 10,RM 7C103,BETHESDA,MD 20892, USA. NR 96 TC 208 Z9 211 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 MAR 15 PY 1992 VL 79 IS 6 BP 1385 EP 1392 PG 8 WC Hematology SC Hematology GA HH745 UT WOS:A1992HH74500001 PM 1547338 ER PT J AU WHITE, MV IGARASHI, Y EMERY, BE LOTZE, MT KALINER, MA AF WHITE, MV IGARASHI, Y EMERY, BE LOTZE, MT KALINER, MA TI EFFECTS OF INVIVO ADMINISTRATION OF INTERLEUKIN-2 (IL-2) AND IL-4, ALONE AND IN COMBINATION, ON EXVIVO HUMAN BASOPHIL HISTAMINE-RELEASE SO BLOOD LA English DT Article ID HEMATOPOIETIC GROWTH-FACTORS; COLONY-STIMULATING FACTOR; HUMAN-BLOOD BASOPHILS; HUMAN B-CELLS; MAST-CELLS; BINDING-SITES; IFN-GAMMA; IGE; DIFFERENTIATION; ACTIVATION C1 NCI,SURG BRANCH,BETHESDA,MD 20892. LOUISIANA STATE UNIV,DEPT OTOLARYNGOL HEAD & NECK SURG,SHREVEPORT,LA 71105. RP WHITE, MV (reprint author), NIAID,CLIN IMMUNOL LAB,ALLERG DIS SECT,BLDG 10,RM 11C207,BETHESDA,MD 20892, USA. NR 32 TC 13 Z9 13 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 MAR 15 PY 1992 VL 79 IS 6 BP 1491 EP 1495 PG 5 WC Hematology SC Hematology GA HH745 UT WOS:A1992HH74500015 PM 1372188 ER PT J AU STEWART, WW AF STEWART, WW TI DIATRIBE CLOAKED IN SCIENTIFIC LANGUAGE SO CANADIAN MEDICAL ASSOCIATION JOURNAL LA English DT Letter RP STEWART, WW (reprint author), NIH,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CANADIAN MEDICAL ASSOCIATION PI OTTAWA PA 1867 ALTA VISTA DR, OTTAWA ON K1G 3Y6, CANADA SN 0820-3946 J9 CAN MED ASSOC J JI Can. Med. Assoc. J. PD MAR 15 PY 1992 VL 146 IS 6 BP 818 EP & PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA HJ881 UT WOS:A1992HJ88100013 PM 1544070 ER PT J AU DESMEULES, M BERKEL, H DAVIS, DL GOLD, E HILL, G HOWE, G LINDSAY, J MAO, Y MIKKELSEN, T MORRISON, H PRESTONMARTIN, S RAPOPORT, S SEMENCIW, R SMITH, M SQUIRES, BP WIGLE, D AF DESMEULES, M BERKEL, H DAVIS, DL GOLD, E HILL, G HOWE, G LINDSAY, J MAO, Y MIKKELSEN, T MORRISON, H PRESTONMARTIN, S RAPOPORT, S SEMENCIW, R SMITH, M SQUIRES, BP WIGLE, D TI INCREASING INCIDENCE OF BRAIN CANCER SO CANADIAN MEDICAL ASSOCIATION JOURNAL LA English DT Editorial Material ID TUMORS C1 ALBERTA CANC BOARD,EDMONTON,ALBERTA,CANADA. NATL RES COUNCIL,WASHINGTON,DC 20418. UNIV CALIF DAVIS,INST ENVIRONM HLTH RES,DAVIS,CA 95616. NATL CANC INST CANADA,TORONTO M5S 2V7,ONTARIO,CANADA. LUDWIG INST CANC RES,SAN DIEGO,CA. UNIV SO CALIF,DEPT PREVENT MED,LOS ANGELES,CA 90089. NIA,BETHESDA,MD 20892. HLTH & WELF CANADA,NATL HLTH RES & DEV PROGRAM,OTTAWA K1A 0L2,ONTARIO,CANADA. RP DESMEULES, M (reprint author), LAB CTR DIS CONTROL,BUR CHRON DIS EPIDEMIOL,TUNNEYS PASTURE,OTTAWA K1A 0L2,ONTARIO,CANADA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU CANADIAN MEDICAL ASSOCIATION PI OTTAWA PA 1867 ALTA VISTA DR, OTTAWA ON K1G 3Y6, CANADA SN 0820-3946 J9 CAN MED ASSOC J JI Can. Med. Assoc. J. PD MAR 15 PY 1992 VL 146 IS 6 BP 847 EP 848 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HJ881 UT WOS:A1992HJ88100020 ER PT J AU HENSON, DE AF HENSON, DE TI AMERICAN-CANCER-SOCIETY AND AMERICAN-JOINT-COMMITTEE-ON-CANCER WORKSHOP ON MOLECULAR MARKERS IN THE CLASSIFICATION AND STAGING OF CANCER - THE RITZ-CARLTON, BUCKHEAD - ATLANTA, GEORGIA - DECEMBER 13-14, 1990 - INTRODUCTION SO CANCER LA English DT Editorial Material RP HENSON, DE (reprint author), NCI,AMER JOINT COMM CANC,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 1 U2 1 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 MAR 15 PY 1992 VL 69 IS 6 SU S BP 1519 EP 1519 DI 10.1002/1097-0142(19920315)69:6+<1519::AID-CNCR2820691302>3.0.CO;2-O PG 1 WC Oncology SC Oncology GA HJ806 UT WOS:A1992HJ80600001 ER EF