FN Thomson Reuters Web of Science™ VR 1.0 PT J AU WERNER, MH HUTH, J CLORE, GM GRONENBORN, A AF WERNER, MH HUTH, J CLORE, GM GRONENBORN, A TI STRUCTURAL STUDIES OF PROTEIN/NUCLEIC ACID COMPLEXES BY ISOTOPE-SELECTED MULTIDIMENSIONAL NMR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,CHEM PHYS LAB,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 66 EP 66 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500225 ER PT J AU ERNST, JA CLUBB, RT ZHOU, HX GRONENBOM, AM CLORE, GM AF ERNST, JA CLUBB, RT ZHOU, HX GRONENBOM, AM CLORE, GM TI DEMONSTRATION OF POSITIONALLY DISORDERED WATER WITHIN A PROTEIN HYDROPHOBIC CAVITY BY NMR SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 71 EP 71 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500242 ER PT J AU GARRETT, DS GRONENBORN, AM CLORE, GM AF GARRETT, DS GRONENBORN, AM CLORE, GM TI AUTOMATED AND INTERACTIVE TOOLS FOR ASSIGNING 3D AND 4D NMR-SPECTRA OF PROTEINS - CAPP, STAPP AND PIPP SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 0 TC 1 Z9 1 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 71 EP 71 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500243 ER PT J AU ALTIERI, AS HINTON, DP BYRD, RA AF ALTIERI, AS HINTON, DP BYRD, RA TI ASSOCIATION OF BIOMOLECULAR SYSTEMS VIA PFG-NMR DIFFUSION MEASUREMENTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,MACROMOLEC NMR SECT,FREDERICK,MD 21701. UNIV VIRGINIA,DEPT CHEM,CHARLOTTESVILLE,VA 22903. NR 4 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 78 EP 78 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500271 ER PT J AU BALDISSERI, DM ALTIERI, AS TSANG, M WEATHERBEE, J ZHOU, L CHEN, H HINTON, DP PANNELL, L BYRD, RA AF BALDISSERI, DM ALTIERI, AS TSANG, M WEATHERBEE, J ZHOU, L CHEN, H HINTON, DP PANNELL, L BYRD, RA TI EFFECT OF CYTOKINE DIMERIZATION ON RECEPTOR-BINDING SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,MACROMOLEC NMR SECT,FREDERICK,MD 21701. UNIV VIRGINIA,DEPT CHEM,CHARLOTTESVILLE,VA 22903. R&D SYST,MINNEAPOLIS,MN 55413. NIDDKD,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 78 EP 78 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500273 ER PT J AU SALEHI, A VERHAAGEN, J KAPLAN, D SWAAB, DF AF SALEHI, A VERHAAGEN, J KAPLAN, D SWAAB, DF TI EXPRESSION OF HIGH-AFFINITY NEUROTROPHIN RECEPTORS (TRK-A, TRK-B AND TRK-C) IN THE NUCLEUS BASALIS OF MEYNERT OF HUMAN BRAIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NETHERLANDS INST BRAIN RES,GRAD SCH NEURO SCI AMSTERDAM,1105 AZ AMSTERDAM,NETHERLANDS. FREDERICK CANC RES & DEV CTR,EUKAROT SIGNAL TRANSDUCT,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 95 EP 95 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500317 ER PT J AU ZHAO, B SISODIA, SS KUSIAK, JW AF ZHAO, B SISODIA, SS KUSIAK, JW TI NEURONAL CELL-DEATH INDUCED BY MUTANT AMYLOID PRECURSOR PROTEIN VIA APOPTOSIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,MOLEC NEUROBIOL UNIT,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,DEPT PATHOL,BALTIMORE,MD 21205. NR 1 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 96 EP 96 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500322 ER PT J AU KIRSCHNER, MA COPELAND, NG GILBERT, DJ JENKINS, NA AMARA, SG AF KIRSCHNER, MA COPELAND, NG GILBERT, DJ JENKINS, NA AMARA, SG TI ISOLATION, CHARACTERIZATION, AND MAPPING OF MOUSE EXCITATORY AMINO-ACID TRANSPORTERS (EAATS) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,VOLLUM INST ADV BIOMED RES,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 98 EP 98 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500331 ER PT J AU BESSEN, RA KOCISKO, DA RAYMOND, GJ MARSH, RF LANSBURY, PT CAUGHEY, B AF BESSEN, RA KOCISKO, DA RAYMOND, GJ MARSH, RF LANSBURY, PT CAUGHEY, B TI STRAIN-SPECIFIC CELL-FREE FORMATION OF THE PRION PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,PERSISTANT VIRAL DIS LAB,HAMILTON,MT 59840. MIT,DEPT CHEM,CAMBRIDGE,MA 02139. UNIV WISCONSIN,DEPT ANIM HLTH & BIOMED SCI,MADISON,WI 53706. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 101 EP 101 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500341 ER PT J AU FLANDERS, KC LIPPA, CF POLLEN, DA SPORN, MB AF FLANDERS, KC LIPPA, CF POLLEN, DA SPORN, MB TI ALTERED EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA IN ALZHEIMERS-DISEASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV MASSACHUSETTS,MED CTR,DEPT NEUROL,WORCESTER,MA 01655. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. UNIV MASSACHUSETTS,MED CTR,DEPT PATHOL,WORCESTER,MA 01655. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 103 EP 103 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500347 ER PT J AU CREMER, C EILS, R RINKE, B SARACOGLU, K DIETZEL, S SCHROCK, E RIED, T BRADL, J LINDEK, S HAUSMANN, M STELZER, EKH HELL, SW CREMER, T AF CREMER, C EILS, R RINKE, B SARACOGLU, K DIETZEL, S SCHROCK, E RIED, T BRADL, J LINDEK, S HAUSMANN, M STELZER, EKH HELL, SW CREMER, T TI 3-DIMENSIONAL MICROSCOPY AND IMAGING APPROACHES FOR STUDIES OF CHROMOSOME TERRITORIES AND SUBREGIONAL CHROMOSOMAL TARGETS IN HUMAN CELL-NUCLEI SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV HEIDELBERG,GRAD COLL MODELLING & SCI COMP MATH & SCI,W-6900 HEIDELBERG,GERMANY. EUROPEAN MOLEC BIOL LAB,W-6900 HEIDELBERG,GERMANY. UNIV TURKU,DEPT MED PHYS,SF-20500 TURKU 50,FINLAND. UNIV HEIDELBERG,INST APPL PHYS,W-6900 HEIDELBERG,GERMANY. UNIV HEIDELBERG,INTERDISCIPLINARY CTR SCI COMP,W-6900 HEIDELBERG,GERMANY. UNIV HEIDELBERG,INST HUMAN GENET & ANTHROPOL,W-6900 HEIDELBERG,GERMANY. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. RI Stelzer, Ernst/A-7648-2011 OI Stelzer, Ernst/0000-0003-1545-0736 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 119 EP 119 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500397 ER PT J AU VANAGOSTON, D DOBI, AL AF VANAGOSTON, D DOBI, AL TI CALCIUM INDUCES DNA SLIDING IN THE DINUCLEOTIDE REPEAT (TG/AC)(N) SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,LDN,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 128 EP 128 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500420 ER PT J AU SIMPSON, RT ROTH, SY COOPER, JP PATTERTON, HG TSUKAGOSHI, Y AF SIMPSON, RT ROTH, SY COOPER, JP PATTERTON, HG TSUKAGOSHI, Y TI A REPRESSIVE CHROMATIN DOMAIN CLOTHES THE STE6 GENE IN ALPHA-CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,CELLULAR & DEV BIOL LAB,BETHESDA,MD 20892. PENN STATE UNIV,DEPT BIOCHEM & MOLEC BIOL,ALTHOUSE LAB 308,UNIVERSITY PK,PA 16802. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 151 EP 151 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500500 ER PT J AU URA, K WOLFFE, A AF URA, K WOLFFE, A TI STRUCTURAL CHARACTERIZATION AND TRANSCRIPTION OF A MODEL DINUCLEOSOME TEMPLATE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 160 EP 160 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500526 ER PT J AU MINUCCI, S SYLVESTER, I ZAND, D DEY, A SCHOLER, H KEIKOOZATO AF MINUCCI, S SYLVESTER, I ZAND, D DEY, A SCHOLER, H KEIKOOZATO TI IN-VIVO FOOTPRINTING OF THE MURINE OCT3/4 GENE IN EC CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. EMBL,GENE EXPRESS PROGRAMME,D-69012 HEIDELBERG,GERMANY. RI Minucci, Saverio/J-9669-2012 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 161 EP 161 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500530 ER PT J AU NIGHTINGALE, K REEVES, R WOLFFE, AP AF NIGHTINGALE, K REEVES, R WOLFFE, AP TI SPECIFIC BINDING OF B4 AND OR HMB-1 TO THE NUCLEOSOME SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. WASHINGTON STATE UNIV,DEPT BIOCHEM & BIOPHYS,PULLMAN,WA 99164. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 161 EP 161 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500531 ER PT J AU FREEMAN, LA WOLFFE, AP AF FREEMAN, LA WOLFFE, AP TI HISTONE DOMAINS REQUIRED FOR CHROMATIN ASSEMBLY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 165 EP 165 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500547 ER PT J AU LI, J SCHECHTER, AN NOGUCHI, CT AF LI, J SCHECHTER, AN NOGUCHI, CT TI MULTIPLE CONTROL ELEMENTS ARE FOUND IN DISTAL 5' FLANKING SEQUENCES OF THE HUMAN EMBRYONIC (EPSILON) GLOBIN GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDDK,CHEM BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 170 EP 170 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500565 ER PT J AU WONG, JM WOLFFE, A SHI, YB AF WONG, JM WOLFFE, A SHI, YB TI TRANSCRIPTION REGULATION OF XENOPUS TR-BETA-A GENE BY THYROID-HORMONE RECEPTOR AND EFFECT OF CHROMATIN ASSEMBLY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,MOLEC EMBRYOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 177 EP 177 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500593 ER PT J AU FAUCI, AS AF FAUCI, AS TI HOST FACTORS IN THE IMMUNOPATHOGENESIS OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) DISEASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 180 EP 180 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500596 ER PT J AU ARTHUR, LO BESS, JW HENDERSON, JE URBAN, R MANN, D BENVENISTE, RE AF ARTHUR, LO BESS, JW HENDERSON, JE URBAN, R MANN, D BENVENISTE, RE TI HLA-DR-IMMUNIZATION PROTECTS MACAQUES FROM CHALLENGE WITH SIV PROPAGATED IN HUMAN-CELLS BUT NOT MACAQUE CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 RRI DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NCI,FCRDC,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. HARVARD UNIV,DEPT BIOCHEM MOL BIOL,CAMBRIDGE,MA 02138. RI Bess, Jr., Julian/B-5343-2012 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 182 EP 182 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500602 ER PT J AU CLERICI, M PINTO, LA BERZOFSKY, JA SHEARER, GM AF CLERICI, M PINTO, LA BERZOFSKY, JA SHEARER, GM TI PROTECTION FROM HIV AND SIV INFECTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV MILAN,I-20122 MILAN,ITALY. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 182 EP 182 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500601 ER PT J AU TUDORWILLIAMS, G BANDA, NK COTTON, MF BABA, TW RUPRECHT, R DUPFER, A AF TUDORWILLIAMS, G BANDA, NK COTTON, MF BABA, TW RUPRECHT, R DUPFER, A TI APOPTOSIS OCCURS PREDOMINANTLY IN BYSTANDER CELLS AND NOT IN PRODUCTIVELY INFECTED-CELLS OF HIV-INFECTED AND SIV-INFECTED LYMPH-NODES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NATL JEWISH CTR IMMUNOL & RESP MED,DENVER,CO. NCI,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 182 EP 182 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500600 ER PT J AU ARUNAGIRI, C SANKOVICH, S PEDEN, K MCPHEE, D MACREADIE, I AZAD, A AF ARUNAGIRI, C SANKOVICH, S PEDEN, K MCPHEE, D MACREADIE, I AZAD, A TI NEF AND VPR PROTEINS OF HIV-1 ARE POSITIVE REGULATORS OF VIRUS-REPLICATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 BIOMOLEC RES INST,PARKVILLE 3052,AUSTRALIA. MACFARLANE BURNET CTR,FAIRFIELD 3078,AUSTRALIA. NIH,BETHESDA,MD 20892. RI Macreadie, Ian/F-5997-2010 OI Macreadie, Ian/0000-0001-5335-7220 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 185 EP 185 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500610 ER PT J AU BOUR, S SCHUBERT, U STREBEL, K AF BOUR, S SCHUBERT, U STREBEL, K TI THE HIV-1 VPU PROTEIN SPECIFICALLY BINDS TO THE CD4 CYTOPLASMIC DOMAIN - IMPLICATIONS FOR THE MECHANISMS OF CD4 DEGRADATION AND VIRAL PARTICLE RELEASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 187 EP 187 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500616 ER PT J AU CONANT, K MONACO, MCG ATWOOD, W DAYTON, A MAJOR, EO AF CONANT, K MONACO, MCG ATWOOD, W DAYTON, A MAJOR, EO TI THE ROLE OF NF-KB IN MAINTAINING HIV-1 LATENCY IN ASTROCYTES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 188 EP 188 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500620 ER PT J AU GLUSHAKOVA, S MARGOLIS, L BAIBAKOV, B ZIMMERBERG, J AF GLUSHAKOVA, S MARGOLIS, L BAIBAKOV, B ZIMMERBERG, J TI EVALUATION OF HIV GP120/41-INDUCED CELL-FUSION INSIDE HUMAN LYMPHOID-TISSUE IN-VITRO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,LTPB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 189 EP 189 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500627 ER PT J AU GORELICK, RJ CHABOT, DJ OTT, DE REIN, A HENDERSON, LE ARTHUR, LO AF GORELICK, RJ CHABOT, DJ OTT, DE REIN, A HENDERSON, LE ARTHUR, LO TI RETROVIRAL NUCLEOCAPSID PROTEINS WITH CCCC OR CCHH TYPE ZN++-FINGERS FUNCTION IN RNA PACKAGING BUT RENDER VIRUS-PARTICLES NONINFECTIOUS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD 21701. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 190 EP 190 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500630 ER PT J AU HENDERSON, LE SOWDER, RC OTT, DE REIN, AR ARTHUR, LO RICE, WG AF HENDERSON, LE SOWDER, RC OTT, DE REIN, AR ARTHUR, LO RICE, WG TI A NEW CLASS OF ANTIVIRAL DRUGS ATTACK HIGHLY CONSERVED ZINC FINGERS IN RETROVIRAL NUCLEOCAPSID PROTEINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21701. NCI,FCRDC,ABL,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 191 EP 191 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500635 ER PT J AU KERKAU, T SCHUBERT, U HUNIG, T SCHIMPL, A AF KERKAU, T SCHUBERT, U HUNIG, T SCHIMPL, A TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 VPU PROTEIN CONTRIBUTES TO THE DOWN-REGULATION OF MHC CLASS-I MOLECULES ON HIV-1-INFECTED CELLS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,DEPT MOLEC MICROBIOL,BETHESDA,MD 20892. UNIV WURZBURG,INST VIROL & IMMUNOBIOL,D-97079 WURZBURG,GERMANY. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 192 EP 192 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500639 ER PT J AU LORI, F CARA, A MALYKH, AG SUN, D LISZIEWICZ, J WEINSTEIN, J GALLO, RC AF LORI, F CARA, A MALYKH, AG SUN, D LISZIEWICZ, J WEINSTEIN, J GALLO, RC TI INTERFERING WITH HIV-1 REPLICATION BY AFFECTING CELLULAR FACTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Cara, Andrea/M-4865-2015 OI Cara, Andrea/0000-0003-4967-1895 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 193 EP 193 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500643 ER PT J AU OTTEKEN, A EARL, PL BRODER, CC MOSS, B AF OTTEKEN, A EARL, PL BRODER, CC MOSS, B TI FOLDING, ASSEMBLY AND INTRACELLULAR-TRANSPORT OF THE HIV-1 ENVELOPE PROTEIN ANALYZED WITH MONOCLONAL-ANTIBODIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 195 EP 195 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500649 ER PT J AU SCHNEIDER, R SONG, S NASIOULAS, G ZOLOTUKHIN, A FELBER, BK TRAUGER, R COX, J MANTHORPE, M PAVLAKIS, GN AF SCHNEIDER, R SONG, S NASIOULAS, G ZOLOTUKHIN, A FELBER, BK TRAUGER, R COX, J MANTHORPE, M PAVLAKIS, GN TI USE OF SIMPLE REV-INDEPENDENT HIV-1 GAG EXPRESSION VECTORS IN GENE-THERAPY AND GENE VACCINE APPLICATIONS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,HUMAN RETROVIRUS SECT,FREDERICK,MD 21701. NCI,FCRDC,ABL BASIC RES PROGRAM HUMAN RETROVIRUS PATHOGENESIS GRP,FREDERICK,MD 21701. IMMUNE RESPONSE CORP,CARLSBAD,CA 90028. VICAL INC,SAN DIEGO,CA. NR 2 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 197 EP 197 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500659 ER PT J AU SHIRASAKA, T CHOKEKIJCHAI, S GOSSELIN, G IMBACH, JL MITSUYA, H AF SHIRASAKA, T CHOKEKIJCHAI, S GOSSELIN, G IMBACH, JL MITSUYA, H TI DIVERGENT ANTI-HIV ACTIVITY OF DIDEOXY-NUCLEOSIDES IN RESTING AND ACTIVATED SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV MONTPELLIER 2,CHIM BIOORGAN LAB,F-34060 MONTPELLIER,FRANCE. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 198 EP 198 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500662 ER PT J AU BUTINI, L REGNERY, CM CAPORALETTI, T MALTONI, A PANTALEO, G FAUCI, AS MONTRONI, M AF BUTINI, L REGNERY, CM CAPORALETTI, T MALTONI, A PANTALEO, G FAUCI, AS MONTRONI, M TI HIV-SPECIFIC CTL ACTIVITY IN LYMPHOID ORGANS - RELATIONSHIP WITH DISEASE PROGRESSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 SERV IMMUNOL CLIN,ANCONA,ITALY. NIAID,BETHESDA,MD 20892. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 202 EP 202 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500676 ER PT J AU CLERICI, M MERONI, L BALOTTA, C FERRARIO, E RIVA, C TRABATTONI, D RIDOLFO, AL VILLA, ML SHEARER, GM MORONI, M GALLI, M AF CLERICI, M MERONI, L BALOTTA, C FERRARIO, E RIVA, C TRABATTONI, D RIDOLFO, AL VILLA, ML SHEARER, GM MORONI, M GALLI, M TI IMMUNOLOGICAL ANALYSES OF HIV-INFECTED PROGRESSORS AND NONPROGRESSORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV MILAN,CATIEDRA IMMUNOL,I-20122 MILAN,ITALY. UNIV MILAN,MALATTIE INFETT CLIN,I-20122 MILAN,ITALY. NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RI Trabattoni, Daria/G-7424-2012 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 203 EP 203 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500682 ER PT J AU COOMBS, RW REICHELDERFER, PS AF COOMBS, RW REICHELDERFER, PS TI VIRAL BURDEN, VIRULENCE AND VIRAL THRESHOLD IN HIV-1 DISEASE - IMPLICATIONS FOR CLINICAL-TRIAL DESIGN AND STUDIES ON PATHOGENESIS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV WASHINGTON,DEPT LAB MED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. NIH,DIV AIDS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 204 EP 204 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500684 ER PT J AU LANDAY, A CLERICI, M HASHEMI, F SHA, B KESSLER, H BERZOFSKY, J SHEARER, GM AF LANDAY, A CLERICI, M HASHEMI, F SHA, B KESSLER, H BERZOFSKY, J SHEARER, GM TI IN-VITRO EFFECT OF IL-12 AND ANTI-IL-10 IN RESTORING CELL-MEDIATED-IMMUNITY IN HIV-INFECTED INDIVIDUALS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 208 EP 208 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500702 ER PT J AU LUCEY, DR PINTO, LA BETHKE, FR RUSNAK, J MELCHER, GP HASHEMI, F LANDAY, A KESSLER, H PAXTON, RJ GRABSTEIN, K SHEARER, GM AF LUCEY, DR PINTO, LA BETHKE, FR RUSNAK, J MELCHER, GP HASHEMI, F LANDAY, A KESSLER, H PAXTON, RJ GRABSTEIN, K SHEARER, GM TI IL-15 INDUCTION OF LYMPHOKINE-ACTIVATED KILLER-CELLS AND IFN-GAMMA BUT NOT IL-2 FROM PBMCS OF HIV-POSITIVE PERSONS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,EIB,BETHESDA,MD 20892. WILFORD HALL USAF MED CTR,LACKLAND AFB,TX 78236. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. IMMUNEX CORP,SEATTLE,WA. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 209 EP 209 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500706 ER PT J AU NIGIDA, SM SMITH, CH SHOEMAKER, MR ARTHUR, LO AF NIGIDA, SM SMITH, CH SHOEMAKER, MR ARTHUR, LO TI SECRETION OF PREFORMED, MEMBRANE-BOUND ANTIBODIES TO HIV-1 BY CHIMPANZEE PERIPHERAL-BLOOD MONONUCLEAR-CELLS IN-VITRO SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,AIDS VACCINE DEV PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 211 EP 211 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500712 ER PT J AU BERGER, EA KENNEDY, PE BRODER, CC AF BERGER, EA KENNEDY, PE BRODER, CC TI FUSION INHIBITORY ACTIVITIES OF ANTI-ENV ANTIBODIES ASSAYED BY A VACCINIA-BASED QUANTITATIVE REPORTER GENE ACTIVATION ASSAY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 215 EP 215 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500729 ER PT J AU BINLEY, JM DITZEL, HJ PARREN, PHW HENDRY, RM SAWYER, LSW DUNLOP, N NARA, PL BARBAS, CF BURTON, DR AF BINLEY, JM DITZEL, HJ PARREN, PHW HENDRY, RM SAWYER, LSW DUNLOP, N NARA, PL BARBAS, CF BURTON, DR TI CLONING AND CHARACTERIZATION OF A LARGE PANEL OF ANTIBODIES TO GP41 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 SCRIPPS RES INST, LA JOLLA, CA USA. CALIF INST PUBL HLTH, BERKELEY, CA USA. NCI, TUMOR CELL BIOL LAB, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 216 EP 216 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500730 ER PT J AU DOMS, RW EARL, PL MASCOLA, JR HOXIE, JA BRODER, CC ABEDON, ST AF DOMS, RW EARL, PL MASCOLA, JR HOXIE, JA BRODER, CC ABEDON, ST TI THE HUMORAL RESPONSE TO OLIGIOMERIC HIV-1 ENV PROTEIN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 UNIV PENN,PHILADELPHIA,PA 19104. NIH,BETHESDA,MD 20892. WALTER REED ARMY INST RES,WASHINGTON,DC 20307. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 219 EP 219 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500742 ER PT J AU EARL, PL BRODER, CC ABEDON, ST DOMS, RW MOSS, B AF EARL, PL BRODER, CC ABEDON, ST DOMS, RW MOSS, B TI OLIGOMERIC HIV-1 ENVELOPE ELICITS A SPECTRUM OF CONFORMATION-DEPENDENT, CROSS-REACTIVE ANTIBODIES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. UNIV PENN,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 219 EP 219 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500743 ER PT J AU HENRARD, D PHILLIPS, JF PHELPS, B GOEDERT, JJ AF HENRARD, D PHILLIPS, JF PHELPS, B GOEDERT, JJ TI CHANGES IN CLONAL PATTERNS OF ANTI-P24 AND ANTI-GP41 ANTIBODY REFLECT RATE OF PROGRESSION TO AIDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 ABBOT LABS,N CHICAGO,IL. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 220 EP 220 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500749 ER PT J AU MCNEELY, TB DRIPPS, DJ EISENBERG, SP WAHL, SM AF MCNEELY, TB DRIPPS, DJ EISENBERG, SP WAHL, SM TI SECRETORY LEUKOCYTE PROTEASE INHIBITOR - A HUMAN SALIVA PROTEIN EXHIBITING ANTI-HIV ACTIVITY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. SYNERGEN INC,BOULDER,CO. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 222 EP 222 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500755 ER PT J AU MONTEFIORI, DC VASUDEVAN, B MARTIN, LN PANTALEO, G FAUCI, AS ZHOU, J AF MONTEFIORI, DC VASUDEVAN, B MARTIN, LN PANTALEO, G FAUCI, AS ZHOU, J TI ANTIBODIES THAT FORM IMMUNE-COMPLEXES CAPABLE OF BINDING COMPLEMENT RECEPTOR TYPE-1 (CR1/CD35) AS A CORRELATE OF IMMUNITY IN HIV-1 AND SIV INFECTION AND VACCINATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,NIH,AIDS VACCINE EVALUAT NETWORK,DURHAM,NC 27710. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. TULANE REG PRIMATE RES CTR,COVINGTON,LA 70433. RI Pantaleo, Giuseppe/K-6163-2016 NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 223 EP 223 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500759 ER PT J AU ROSSIO, JL WILTROUT, TA HENDERSON, LE ARTHUR, LO AF ROSSIO, JL WILTROUT, TA HENDERSON, LE ARTHUR, LO TI ANERGY INDUCTION TO COMMON ANTIGENS DUE TO PRESENTATION BY MHC CLASS-II ON HIV-1 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI,FCRDC,AIDS VACCINE PROGRAM,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 225 EP 225 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500769 ER PT J AU VALENTIN, A ZOLOTUKHIN, AS PAVLAKIS, GN FELBER, BK AF VALENTIN, A ZOLOTUKHIN, AS PAVLAKIS, GN FELBER, BK TI CONTINUOUS PROPAGATION OF REV-INDEPENDENT AND RRE-INDEPENDENT HIV-1 MOLECULAR CLONES IN PRIMATE CELLS - POTENTIAL CANDIDATES FOR ATTENUATED HIV-1 STRAINS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NCI, FREDERICK CANC RES & DEV CTR, FREDERICK, MD 21701 USA. NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, FREDERICK, MD 21701 USA. NR 3 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 228 EP 228 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500779 ER PT J AU BRODER, CC NUSSBAUM, O FENG, Y BERGER, EA AF BRODER, CC NUSSBAUM, O FENG, Y BERGER, EA TI CELLULAR FACTORS ASSOCIATED WITH THE SPECIFICITY OF HIV-1 FUSION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 232 EP 232 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500794 ER PT J AU MOFENSON, L LAMBERT, J FLETCHER, C STIEHM, ER MOYE, J MEYER, W NEMO, G MATHIESON, B HIRSCH, G AF MOFENSON, L LAMBERT, J FLETCHER, C STIEHM, ER MOYE, J MEYER, W NEMO, G MATHIESON, B HIRSCH, G TI PHARMACOKINETICS OF P24 ANTIBODY (AB) IN HIV-CIRCLE-PLUS PREGNANT FEMALE AND NEWBORNS RECEIVING HYPERIMMUNE HIV IMMUNOGLOBULIN (HIVIG) IN ACTG PROTOCOL 185 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. BAYLOR ACTG,HOUSTON,TX. WESTAT CORP,ROCKVILLE,MD. MARYLAND MED METPATH,BALTIMORE,MD. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 240 EP 240 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500826 ER PT J AU MORRISON, RP FEILZER, K TUMAS, DB AF MORRISON, RP FEILZER, K TUMAS, DB TI CHLAMYDIA-TRACHOMATIS GENITAL-TRACT INFECTION IN GENE KNOCKOUT MICE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NIAID,ROCKY MT LABS,INTERCELLULAR PARASITES LAB,HAMILTON,MT 59840. UNIV ALABAMA,SCH MED,DEPT MED,BIRMINGHAM,AL 35233. UNIV ALABAMA,SCH MED,DEPT MICROBIOL,BIRMINGHAM,AL 35233. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 254 EP 254 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500867 ER PT J AU ALEXANDER, NJ AF ALEXANDER, NJ TI BARRIER METHODS - THE PREVENTION OF STDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,CTR POPULAT RES,CONTRACEPT DEV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 255 EP 255 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500870 ER PT J AU MILLER, HG ZENILMAN, J TURNER, CF AF MILLER, HG ZENILMAN, J TURNER, CF TI BEHAVIORAL-CHANGE AND STDS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,STD BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. RES TRIANGLE INST,ROCKVILLE,MD. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 255 EP 255 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500872 ER PT J AU STRAUS, SE AF STRAUS, SE TI DEVELOPMENT AND TESTING OF PROPHYLACTIC AND THERAPEUTIC VACCINES FOR GENITAL HERPES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR 2 PY 1995 SU 21B BP 256 EP 256 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT865 UT WOS:A1995QT86500873 ER PT J AU TANIIKE, M YAMANAKA, S PROIA, RL LANGAMAN, C BONETURRENTINE, T SUZUKI, K AF TANIIKE, M YAMANAKA, S PROIA, RL LANGAMAN, C BONETURRENTINE, T SUZUKI, K TI NEUROPATHOLOGY OF MICE WITH TARGETED DISRUPTION OF HEXA GENE, A MODEL OF TAY-SACHS-DISEASE SO ACTA NEUROPATHOLOGICA LA English DT Article DE GM(2) GANGLIOSIDOSIS; GM(2) GANGLIOSIDE; BETA HEXOSAMINIDASE A; GENE TARGETING; MEMBRANOUS CYTOPLASMIC BODIES ID STORAGE DISEASE; GANGLIOSIDOSES AB A murine model of Tay-Sachs disease, the prototype of the GM(2) gangliosidoses, was produced through the targeted disruption of the Hexa gene encoding the subunit of alpha-hexosaminidase A. The mice were completely devoid of beta-hexosaminidase A activity and accumulated GM(2) ganglioside in the CNS in an age-dependent manner. Neurons with membranous cytoplasmic bodies (MCBs), identical to those described in Tay-Sachs disease, were identified in the brain of these mice. The neurons with MCBs were periodic acid-Schiff-positive on frozen sections and immunostained with anti-GM(2) ganglioside antibody. However, unlike Tay-Sachs disease in which neurons throughout the brain are affected, the localization of storage neurons in these mice appeared ts be limited to certain regions, i.e., cerebral cortex, the hippocampus, amygdala, hypothalamus, mammillary nucleus, etc. Storage neurons were absent in the olfactory bulb, cerebellar cortex and spinal anterior hems. The difference in the distribution of storage neurons suggests a difference of ganglioside metabolism between humans and mice. This model is useful for the study of the pathogenic mechanisms of neuronal storage in Tay-Sachs disease and for the evaluation of therapeutic strategies. C1 UNIV N CAROLINA,DEPT PATHOL,CHAPEL HILL,NC 27599. UNIV N CAROLINA,BRAIN & DEV RES CTR,CHAPEL HILL,NC 27599. NIDDKD,BIOCHEM GENET SECT,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. RI Proia, Richard/A-7908-2012 FU NICHD NIH HHS [HD03110]; NINDS NIH HHS [NS24453] NR 16 TC 55 Z9 56 U1 1 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0001-6322 J9 ACTA NEUROPATHOL JI Acta Neuropathol. PD APR PY 1995 VL 89 IS 4 BP 296 EP 304 PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA QM220 UT WOS:A1995QM22000002 PM 7610760 ER PT J AU KLOTMAN, PE RAPPAPORT, J RAY, P KOPP, JB FRANKS, R BRUGGEMAN, LA NOTKINS, AL AF KLOTMAN, PE RAPPAPORT, J RAY, P KOPP, JB FRANKS, R BRUGGEMAN, LA NOTKINS, AL TI TRANSGENIC MODELS OF HIV-1 SO AIDS LA English DT Review DE HIV-1; TRANSGENIC MICE; PATHOGENESIS; ANIMAL MODELS ID IMMUNODEFICIENCY-VIRUS TYPE-1; LONG TERMINAL REPEAT; CENTRAL-NERVOUS-SYSTEM; KAPOSIS SARCOMA; TAT GENE; NEF GENE; INVIVO ACTIVATION; HUMAN-CELLS; DNA DAMAGE; MICE C1 NIDR,VIRAL PATHOGENESIS UNIT,BETHESDA,MD 20892. NIDR,ORAL MED LAB,BETHESDA,MD 20892. OI Kopp, Jeffrey/0000-0001-9052-186X NR 62 TC 29 Z9 29 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD APR PY 1995 VL 9 IS 4 BP 313 EP 324 PG 12 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA QP022 UT WOS:A1995QP02200001 PM 7794536 ER PT J AU CLEGHORN, FR JACK, N MURPHY, JR EDWARDS, J MAHABIR, B PAUL, R WHITE, F BARTHOLOMEW, C BLATTNER, WA AF CLEGHORN, FR JACK, N MURPHY, JR EDWARDS, J MAHABIR, B PAUL, R WHITE, F BARTHOLOMEW, C BLATTNER, WA TI HIV-1 PREVALENCE AND RISK-FACTORS AMONG SEXUALLY-TRANSMITTED DISEASE CLINIC ATTENDERS IN TRINIDAD SO AIDS LA English DT Article DE HIV-1; TRINIDAD; PREVALENCE; RISK FACTORS; HETEROSEXUAL; CRACK COCAINE; SEXUALLY TRANSMITTED DISEASES; GENITAL ULCER DISEASE; EPIDEMIOLOGY ID IMMUNODEFICIENCY-VIRUS-INFECTION; HTLV-I; TRANSMISSION; MEN; PROSTITUTES; SPREAD; AFRICA; AIDS AB Objectives: To study trends in prevalence and to ascertain risk factors for HIV-1 among sexually transmitted disease (STD) clinic attenders in Trinidad. Design and methods: Serial cross-sectional studies were conducted in 1987-1988 and 1990-1991 at a centralized STD clinic in Port of Spain. A case-control study was carried out to examine in greater detail the demographic and behavioral risk factors for HIV-1 among self-declared heterosexuals in this population. Results: HIV-1 prevalence increased from 3.0% [95% confidence interval (CI), 2.3-3.9] in 1987-1988 to 13.6% (95% CI, 11.8-15.6) in 1990-1991. Age greater than or equal to 40 years [odds ratio (OR), 2.0; 95% CI, 1.4-2.8], urban residence (OR, 2.2; 95% CI, 1.6-3.0), and human T-lymphotropic virus-I seropositivity (OR, 3.1;95% CI, 1.6-6.0) were significant risk factors for HIV-1 in 1990-1991. In the case-control analysis, significant independent risk factors for men included current genital ulcer disease (OR, 5.2; 95% CI, 2.2-12.5), current genital warts (OR, 3.9; 95% CI, 1.2-12.0), having ever had syphilis (OR, 3.2; 95% Cl, 1.6-6.1), and use of crack cocaine in the preceding 6 months (OR, 6.2; 95% CI, 2.7-14.2). Corresponding risk factors for women were commercial sex work (OR, 5.7; 95% CI, 1.3-25.7), initiation of sexual activity before age 14 years (OR, 4.8; 95% CI, 1.5-16.0), and past non-gonococcal cervicitis (OR, 4.1; 95% CI, 1.3-13.1). Conclusions: HIV-1 in this setting is primarily heterosexually transmitted in a milieu of unprotected sexual activity fuelled by a crack cocaine epidemic. Targeted interventions to prevent, detect and treat STD and crack cocaine addiction, as well as disrupt their adverse synergism, may substantially reduce HIV-1 transmission in this population. C1 NCI,DIV CANC ETIOL,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. RES TRIANGLE INST,CTR EPIDEMIOL & MED STUDIES,WASHINGTON,DC. CARIBBEAN EPIDEMIOL CTR,PORT OF SPAIN,TRINID & TOBAGO. GOVT TRINIDAD & TOBAGO,MINIST HLTH,BARATARIA,TRINID & TOBAGO. UNIV W INDIES,DEPT MED,PORT OF SPAIN,TRINID & TOBAGO. FU NCI NIH HHS [NCI-CP-61022-21] NR 27 TC 24 Z9 27 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD APR PY 1995 VL 9 IS 4 BP 389 EP 394 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA QP022 UT WOS:A1995QP02200011 PM 7794544 ER PT J AU COTE, TR BIGGAR, RJ AF COTE, TR BIGGAR, RJ TI DOES ZIDOVUDINE CAUSE NON-HODGKINS-LYMPHOMA SO AIDS LA English DT Letter ID ANTIRETROVIRAL THERAPY; INFECTION RP COTE, TR (reprint author), NCI,VIRAL EPIDEMIOL BRANCH,AIDS CANC STUDY GRP,EPN-434,6130 EXECUT BLVD,ROCKVILLE,MD 20852, USA. NR 6 TC 4 Z9 4 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD APR PY 1995 VL 9 IS 4 BP 404 EP 405 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA QP022 UT WOS:A1995QP02200019 PM 7794552 ER PT J AU ELMER, GI GEORGE, FR AF ELMER, GI GEORGE, FR TI ANTAGONISM OF ETHANOL BY PRETREATMENT OR POSTTREATMENT WITH RO-15-4513 AND INDOMETHACIN ALONE OR IN COMBINATION SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE INDOMETHACIN; PROSTAGLANDINS; RO 15-4513; BENZODIAZEPINES; GABA ID SYNTHETASE INHIBITORS ANTAGONIZE; ARACHIDONIC-ACID METABOLITES; INDUCED MOTOR IMPAIRMENT; CENTRAL-NERVOUS-SYSTEM; PROSTAGLANDIN SYNTHETASE; INBRED MICE; TIME COURSE; MODULATION; RECEPTOR; RAT AB RO 15-4513, an inverse agonist at the GABA/benzodiazepine receptor Cl- channel complex, antagonizes multiple effects of ethanol. Prostaglandin synthesis inhibitors, such as indomethacin, also antagonize several effects of alcohols, However, prostaglandin synthesis inhibitors and RO 15-4513 each provide only partial antagonism of ethanol, typically seen as a dose-related effect with a maximum efficacy of similar to 50%. The purpose of this study was to: (i) compare the relative efficacy of these compounds for antagonizing ethanol; (2) compare the effectiveness of preethanol treatment versus postethanol treatment with each drug; and (3) compare the effect of RO 15-4513 and indomethacin in combination with the effects of each drug alone. The results show that indomethacin significantly decreased duration of loss of the righting reflex when administered either pre- or postethanol. Conversely, RO 15-4513 decreased duration of loss of the righting reflex only when given preethanol. When coadministered, RO 15-4513 and indomethacin did not show additive or synergistic effects, Compounds from these two drugs classes should continue to prove useful in elucidating ethanol's mechanisms of action. C1 SW INST DRUG & ALCOHOL STUDIES, ALBUQUERQUE, NM 87190 USA. NIDA, ADDICT RES CTR, PRECLIN PHARMACOL BRANCH, BALTIMORE, MD 21224 USA. FU NIAAA NIH HHS [AA-07754, AA-09549] NR 36 TC 2 Z9 4 U1 1 U2 2 PU WILEY PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0145-6008 EI 1530-0277 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD APR PY 1995 VL 19 IS 2 BP 490 EP 495 DI 10.1111/j.1530-0277.1995.tb01536.x PG 6 WC Substance Abuse SC Substance Abuse GA QT750 UT WOS:A1995QT75000035 PM 7625587 ER PT J AU CONWAY, JM YANOVSKI, SZ AVILA, NA HUBBARD, VS AF CONWAY, JM YANOVSKI, SZ AVILA, NA HUBBARD, VS TI VISCERAL ADIPOSE-TISSUE DIFFERENCES IN BLACK-AND-WHITE WOMEN SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE OBESITY; BODY COMPOSITION; REGIONAL ADIPOSITY; COMPUTED TOMOGRAPHY; ETHNICITY ID BODY-MASS INDEX; FAT DISTRIBUTION; BIOELECTRICAL IMPEDANCE; HEALTH RISKS; SERUM-LIPIDS; MEN BORN; OBESITY; ANTHROPOMETRY; POPULATION; MORTALITY AB Fat distribution and metabolic variables were studied in 8 black and 10 white age- and weight-matched obese women undergoing a 6-mo weight-reducing regimen. Fat patterning was determined by using anthropometry and computed tomography to quantitate total, subcutaneous, and visceral adipose tissue (VAT) areas at the L2-L3 and L4-L5 levels of the lumbar spine, before, during, and after a modified fast. Black women had smaller depots of VAT than white women at both the L2-L3 (P = 0.004) and L4-L5 (P = 0.054) sites. Differences persisted after an average 17.2-kg weight loss. Although waist-hip ratio was similar in both groups, black women had 23% less VAT than white women (P = 0.007). Black women had significantly lower plasma glucose (P = 0.031) and triglycerides (P = 0.006) with significantly higher plasma high-density-lipoprotein concentrations (P < 0.001). Data from this study suggest that racial differences exist in VAT and metabolic risk factors for obesity-related illness. C1 NIDDKD,NIMH,DEPT CLIN RADIOL,BETHESDA,MD 20892. RP CONWAY, JM (reprint author), USDA ARS,BELTSVILLE AGR RES CTR,BELTSVILLE HUMAN NUTR RES CTR,DHPL,BLDG 308,ROOM 101,BELTSVILLE,MD 20705, USA. NR 38 TC 198 Z9 201 U1 0 U2 5 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1995 VL 61 IS 4 BP 765 EP 771 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QQ342 UT WOS:A1995QQ34200004 PM 7702017 ER PT J AU FORMAN, MR MUESING, R BEECHER, GR LANZA, E GRAUBARD, BI SCHULMAN, J AF FORMAN, MR MUESING, R BEECHER, GR LANZA, E GRAUBARD, BI SCHULMAN, J TI A CONTROLLED DIET STUDY OF PLASMA CAROTENOIDS, LIPIDS, AND HORMONES DURING THE MENSTRUAL-CYCLE SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,WASHINGTON,DC. USDA,BELTSVILLE,MD 20705. GENET & IVF INST,FAIRFAX,VA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1995 VL 61 IS 4 BP 903 EP 903 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QQ342 UT WOS:A1995QQ34200094 ER PT J AU SNITKER, S LARSON, DE RAVUSSIN, E AF SNITKER, S LARSON, DE RAVUSSIN, E TI EFFECT OF GLYCOGEN DEPLETION ON FOOD-INTAKE IN HUMANS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1995 VL 61 IS 4 BP 903 EP 903 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QQ342 UT WOS:A1995QQ34200093 ER PT J AU SICHIERI, R EVERHART, JE AF SICHIERI, R EVERHART, JE TI GENDER DIFFERENCE IN THE ASSOCIATION OF REPORTED ENERGY-CONSUMPTION WITH ENERGY REQUIREMENT IN A SAMPLE OF BRAZILIAN WORKERS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract C1 UERJ,IMS,RIO JANEIRO,BRAZIL. NIDDK,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1995 VL 61 IS 4 BP 904 EP 904 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QQ342 UT WOS:A1995QQ34200097 ER PT J AU HENKIN, RI MARTIN, BM AGARWAL, RP AF HENKIN, RI MARTIN, BM AGARWAL, RP TI CARBONIC-ANHYDRASE V1 DEFICIENCY - A VIRAL INDUCED ENZYME DISORDER AMENABLE TO TREATMENT WITH EXOGENOUS ZINC SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract C1 TASTE & SMELL CLIN,WASHINGTON,DC. NIMH,NSB,BETHESDA,MD. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1995 VL 61 IS 4 BP 911 EP 911 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QQ342 UT WOS:A1995QQ34200143 ER PT J AU TATARANNI, PA CHRISTIN, L RAVUSSIN, E AF TATARANNI, PA CHRISTIN, L RAVUSSIN, E TI METABOLIC ADAPTATION TO SHORT-TERM STARVATION END OVERFEEDING IN LEAN OBESE PIMA-INDIANS AND CAUCASIANS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Meeting Abstract C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1995 VL 61 IS 4 BP 912 EP 912 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QQ342 UT WOS:A1995QQ34200145 ER PT J AU STRYDOM, C RETIEF, DH RUSSELL, CM DENYS, FR AF STRYDOM, C RETIEF, DH RUSSELL, CM DENYS, FR TI LABORATORY EVALUATION OF THE GLUMA 3-STEP BONDING SYSTEM SO AMERICAN JOURNAL OF DENTISTRY LA English DT Article ID POLYMERIZATION; PRETREATMENT AB Purpose: To determine in vitro (1) the shear bond strengths (SBS) of the modified Gluma system to enamel and dentin; (2) the qualitative and the quantitative microleakage (ML) of Class V preparations on the cemento-enamel junction (CEJ) and in dentin, respectively, restored with the Gluma system; and (3) the effect of the system's components on enamel and dentin by scanning electron microscopy. Materials and Methods: Seventy-five extracted human maxillary permanent central incisors and 75 permanent first and second molars were embedded in brass tooth cups with cold-cure acrylic resin. The facial surfaces of the anterior and the occlusal surfaces of the molar teeth were ground wet on 180- followed by 600-grit silicon carbide paper. Demarcated sites on the surfaces were treated according to the manufacturer's instructions and Pekafill composite was bonded to the treated surfaces. Fifteen specimens prepared on enamel were removed 1 minute after cure (A) and the SBS determined. The remaining specimens were removed 15 minutes after final cure, stored in saline at 37 degrees C for 24 hours (B), for 1 week without (C) and with temperature cycling (D), and for 4 weeks (E). Similar regimens were used for dentin, groups F, G, H, I and J. The SBS were determined and expressed in MPa. The data were analyzed by ANOVA, Student-Newman-Keuls and t-tests. For the qualitative ML evaluation, Class V cavities were prepared on the CEJ of 30 human premolars and restored with Gluma/Pekafill. After thermocycling in 0.5% basic fuchsin, the teeth were sectioned and ranked according to the degree of microleakage. Class V cavities were prepared on the facial root surfaces of 15 human premolars and restored. The ML was determined quantitatively by a spectrophotometric dye-recovery method and expressed as mu g dye/restoration. Results: The mean +/- SD of the SBS in MPa were: A: 14.6 +/- 2.2; B: 21.2 +/- 1.6; C: 20.5 +/- 1.4; D: 24.2 +/- 2.0; E: 22.8 +/- 3.7; F: 7.0 +/- 2.0 G: 16.1 +/- 4.0; H: 15.6 +/- 3.7; I: 10.9 +/- 3.3; J: 14.4 +/- 3.3. The quantitative ML was 1.00 +/- 0.39 mu g dye/restoration. The lowest SBS were obtained on specimens tested after 1 minute. Temperature cycling had a significantly adverse effect on the SBS to dentin (P=0.0003). Etch patterns conducive to bonding were produced on the enamel. The resin system penetrated into the dentin tubules. C1 UNIV ALABAMA,SCH DENT,DEPT BIOMAT,BIRMINGHAM,AL 35294. UNIV ALABAMA,SCH DENT,NIDR,POSTDOCTORAL TRAINING PROGRAM CARIES RES,BIRMINGHAM,AL 35294. MED COLL GEORGIA,SCH DENT,AUGUSTA,GA 30912. RP STRYDOM, C (reprint author), UNIV STELLENBOSCH,FAC DENT,DEPT RESTORAT DENT,PRIVATE BAG X1,TYGERBERG 7505,SOUTH AFRICA. NR 24 TC 5 Z9 5 U1 0 U2 0 PU MOSHER & LINDER, INC PI SAN ANTONIO PA 9859 IH-10 WEST, SUITE 107/489, SAN ANTONIO, TX 78230-2236 SN 0894-8275 J9 AM J DENT JI Am. J. Dent. PD APR PY 1995 VL 8 IS 2 BP 93 EP 98 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QT152 UT WOS:A1995QT15200006 PM 7546486 ER PT J AU LUNDGREN, JD MELBYE, M PEDERSEN, C ROSENBERG, PS GERSTOFT, J AF LUNDGREN, JD MELBYE, M PEDERSEN, C ROSENBERG, PS GERSTOFT, J TI CHANGING PATTERNS OF KAPOSIS-SARCOMA IN DANISH ACQUIRED-IMMUNODEFICIENCY-SYNDROME PATIENTS WITH COMPLETE FOLLOW-UP SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; CELL COUNT; HIV; IMMUNOSUPPRESSION; SARCOMA; KAPOSIS; T-LYMPHOCYTES ID HOMOSEXUAL MEN; AIDS; COHORT; EPIDEMIOLOGY; RISK AB The objective was to study changes in the occurrence of human immunodeficiency virus type 1-related Kaposi's sarcoma and the association with degree of immunodeficiency over time. Danish patients with acquired immunodeficiency syndrome (AIDS) diagnosed between 1979 and 1990 (n = 687) were followed clinically and with consecutive CD4 cell count measurement from time of AIDS-defining illness to date of death or censoring date, whichever came first. The proportion of home-/bisexual men (n = 520) with Kaposi's sarcoma (n = 100) at AIDS diagnosis declined from 31% before 1985 to 13% in 1990, whereas the proportion of patients who died with Kaposi's sarcoma remained constant over time. Furthermore, the CD4 cell count at time of AIDS for patients diagnosed with Kaposi's sarcoma has declined in recent years. A CD4 cell count <200 X 106/liter at the time of AIDS diagnosis predicted an increased risk of developing Kaposi's sarcoma after the AIDS diagnosis. Age, antiretroviral therapy, and primary Pneumocystis carinii pneumonia prophylaxis failed to influence the development of Kaposi's sarcoma. Thus, the occurrence of Kaposi's sarcoma remained constant over time but developed later in the course of AIDS and was associated with more severe immunosuppression in recent years. C1 STATE SERUM INST,DANISH EPIDEMIOL SCI CTR,EPIDEMIOL RES UNIT,COPENHAGEN,DENMARK. RIGSHOSP,DEPT INFECT DIS,COPENHAGEN,DENMARK. NCI,BETHESDA,MD. FREDERIKSBERG UNIV HOSP,DEPT MED,FREDERIKSBERG,DENMARK. RP LUNDGREN, JD (reprint author), UNIV COPENHAGEN,HVIDOVRE HOSP,DEPT INFECT DIS,UNIT 144,DK-2650 HVIDOVRE,DENMARK. OI Lundgren, Jens/0000-0001-8901-7850 NR 23 TC 39 Z9 39 U1 0 U2 0 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 1 PY 1995 VL 141 IS 7 BP 652 EP 658 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QP479 UT WOS:A1995QP47900006 PM 7702040 ER PT J AU HUMPHREY, JS CONLEY, CL AF HUMPHREY, JS CONLEY, CL TI DURABLE COMPLETE REMISSION OF MACROGLOBULINEMIA AFTER SPLENECTOMY - A REPORT OF 2 CASES AND REVIEW OF THE LITERATURE SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE SPLENECTOMY; WALDENSTROMS MACROGLOBULINEMIA; LEUKEMIA, LYMPHOCYTIC; IMMUNOGLOBULINS ID CELL LEUKEMIA BCL1; WALDENSTROMS MACROGLOBULINEMIA; MALIGNANT-LYMPHOMA; SPLEEN; IGM; ANTIBODY; KINETICS; GROWTH; MICE AB Two patients with macroglobulinemia (monoclonal IgM in the serum) and massive splenomegaly were incapacitated by progressive disease refractory to standard chemotherapy, In each case, palliative splenectomy was followed by a prompt, complete, and unexpected clinical remission with disappearance from the serum of the monoclonal IgM component, One patient remains free of disease 12 years after splenectomy, The other patient remained free of detectable macroglobulinemia for 13 years after splenectomy, A review of the literature revealed other cases of remission of macroglobulinemia attributable to splenectomy alone. Data in humans and animals suggest that the spleen may facilitate IgM secretion by normal and malignant B lymphocytes, Splenectomy should be considered a possible treatment option for patients with massive splenomegaly and macroglobulinemia who progress on chemotherapy. (C) 1995 Wiley-Liss, Inc. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV HEMATOL,BALTIMORE,MD 21205. RP HUMPHREY, JS (reprint author), NCI,MED BRANCH,BLDG 18T,ROOM 101,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 40 TC 18 Z9 18 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 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD APR PY 1995 VL 48 IS 4 BP 262 EP 266 DI 10.1002/ajh.2830480411 PG 5 WC Hematology SC Hematology GA QQ956 UT WOS:A1995QQ95600010 PM 7717376 ER PT J AU BOERKOEL, CF EXELBERT, R NICASTRI, C NICHOLS, RC MILLER, FW PLOTZ, PH RABEN, N AF BOERKOEL, CF EXELBERT, R NICASTRI, C NICHOLS, RC MILLER, FW PLOTZ, PH RABEN, N TI LEAKY SPLICING MUTATION IN THE ACID MALTASE GENE IS ASSOCIATED WITH DELAYED-ONSET OF GLYCOGENOSIS TYPE-II SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID LYSOSOMAL ALPHA-GLUCOSIDASE; PROTEIN MESSENGER-RNAS; DISEASE TYPE-II; MISSENSE MUTATION; DNA FRAGMENTS; POMPE DISEASE; ONE ALLELE; GC-CLAMP; DEFICIENCY; EXPRESSION AB An autosomal recessive deficiency of acid alpha-gIucosidase (GAA), type II glycogenosis, is genetically and clinically heterogeneous. The discovery of an enzyme-inactivating genomic deletion of exon 18 in three unrelated genetic compound patients-two infants and an adult-provided a rare opportunity to analyze the effect of the second mutation in patients who displayed dramatically different phenotypes. A deletion of Lys-903 in one patient and a substitution of Arg for Leu-299 in another resulted in the fatal infantile form. In the adult, a T-to-G base change at position -13 of intron 1 resulted in alternatively spliced transcripts with deletion of exon 2, the location of the start codon. The low level of active enzyme (12% of normal) generated from the leakage of normally spliced mRNA sustained the patient to adult life. C1 NIAMSD,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD 20892. US FDA,ROCKVILLE,MD 20857. OI Miller, Frederick/0000-0003-2831-9593 NR 61 TC 72 Z9 76 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD APR PY 1995 VL 56 IS 4 BP 887 EP 897 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA QP663 UT WOS:A1995QP66300010 PM 7717400 ER PT J AU HNIZDO, E AF HNIZDO, E TI RISK OF SILICOSIS - COMPARISON OF SOUTH-AFRICAN AND CANADIAN MINERS SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Letter DE SILICA EXPOSURE; SILICOSIS; GOLD MINERS; RISK ASSESSMENT ID EXPOSURE RP HNIZDO, E (reprint author), NIEHS,EPIDEMIOL BRANCH,MAIL DROP A3-05,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 10 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD APR PY 1995 VL 27 IS 4 BP 619 EP 622 DI 10.1002/ajim.4700270419 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QQ138 UT WOS:A1995QQ13800018 ER PT J AU STRIKER, GE AF STRIKER, GE TI SMALL BUSINESS PROGRAM PROMOTES TECHNOLOGICAL ADVANCES IN BIOMEDICAL-RESEARCH SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Note RP STRIKER, GE (reprint author), NIDDKD,DIV KIDNEY UROL & HEMATOL DIS,BETHESDA,MD, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD APR PY 1995 VL 25 IS 4 BP 660 EP 660 DI 10.1016/0272-6386(95)90141-8 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA QQ636 UT WOS:A1995QQ63600023 ER PT J AU WHEAT, J HAFNER, R KORZUN, AH LIMJOCO, MT SPENCER, P LARSEN, RA SIMPSON, M SKAHAN, KJ KEEFER, MC CLARK, R LAI, KK JACOBSON, JM SQUIRES, K BARTLETT, JA AF WHEAT, J HAFNER, R KORZUN, AH LIMJOCO, MT SPENCER, P LARSEN, RA SIMPSON, M SKAHAN, KJ KEEFER, MC CLARK, R LAI, KK JACOBSON, JM SQUIRES, K BARTLETT, JA TI ITRACONAZOLE TREATMENT OF DISSEMINATED HISTOPLASMOSIS IN PATIENTS WITH THE ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID AMPHOTERICIN-B; AIDS; DIAGNOSIS; THERAPY; ANTIGEN AB PURPOSE: Amphotericin B has been the treatment of choice for disseminated histoplasmosis in patients with acquired immunodeficiency syndrome (AIDS). Oral antifungal agents would be welcome alternatives to standard treatment of disseminated histoplasmosis in less severe cases. The purpose of this study was to assess the efficacy and safety of itraconazole therapy in patients with AIDS and disseminated histoplasmosis. PATIENTS AND METHODS: This was a multicenter, open-label, nonrandomized prospective trial conducted in university hospitals of the AIDS Clinical Trial Group. All patients had AIDS and first episodes of disseminated histoplasmosis. Patients with central nervous system involvement or with severe clinical manifestations were excluded. Patients were treated with itraconazole BID by mouth 300 mg for 3 days and then 200 mg BID for 12 weeks. Resolution of clinical findings, clearance of positive cultures, and drug tolerance were the main outcome measurements. A secondary objective was effect of therapy on Histoplasma capsulatum var capsulatum antigen levels. RESULTS: Of 59 evaluable patients, 50 (85%) responded to therapy. Five patients withdrew because of progressive infection, 1 died of a presumed pulmonary embolus within the first week of therapy without improvement, 2 withdrew because of toxicity, and 1 was lost to follow-up after week 2 of therapy. Patients with moderately severe clinical (fever >39.5 degrees C or Karnofsky score <60) or laboratory abnormalities (alkaline phosphatase >5 times normal or albumin <3 g/dL) at baseline tended to respond more poorly than did other patients. Resolution of complaints of fever and improvement in fatigue occurred after a median of 3 and 6 weeks, respectively, and weight gain after 2 weeks. Fungemia cleared after a median of 1 week. H capsulatum var capsulatum antigen cleared from the urine and serum at rates of 0.2 and 0.3 units per week, respectively. CONCLUSIONS: Itraconazole is safe and effective induction therapy for mild disseminated histoplasmosis in patients with AIDS, offering an alternative to amphotericin B in such cases. Patients with moderately severe or severe histoplasmosis should first be treated with amphotericin B and then may be switched to itraconazole after achieving clinical improvement. C1 INDIANA UNIV,DEPT MED,INDIANAPOLIS,IN. RICHARD L ROUDEBUSH VET AFFAIRS MED CTR,DEPT MED,INDIANAPOLIS,IN. ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY. NIAID,DIV AIDS,ROCKVILLE,MD. SDAC,AIDS CLIN TRIALS GRP,BOSTON,MA. UNIV SO CALIF,DEPT INFECT DIS,LOS ANGELES,CA. WASHINGTON UNIV,DEPT INFECT DIS,ST LOUIS,MO. UNIV MINNESOTA,DEPT MED,MINNEAPOLIS,MN. UNIV CINCINNATI,DEPT INFECT DIS INTERNAL MED,CINCINNATI,OH. UNIV ROCHESTER,DEPT INFECT DIS MED,ROCHESTER,NY. TULANE UNIV,DEPT MED,DIV INFECT DIS,NEW ORLEANS,LA. UNIV MASSACHUSETTS,MED CTR,DEPT MED,DIV INFECT DIS & IMMUNOL,WORCESTER,MA. CORNELL UNIV,DEPT INFECT DIS INTERNAL MED,NEW YORK,NY. DUKE UNIV,DEPT MED,DURHAM,ENGLAND. NR 14 TC 125 Z9 130 U1 0 U2 2 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1995 VL 98 IS 4 BP 336 EP 342 DI 10.1016/S0002-9343(99)80311-8 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA QQ863 UT WOS:A1995QQ86300004 PM 7709945 ER PT J AU FIGG, WD SARTOR, O COOPER, MR THIBAULT, A BERGAN, RC DAWSON, N REED, E MYERS, CE AF FIGG, WD SARTOR, O COOPER, MR THIBAULT, A BERGAN, RC DAWSON, N REED, E MYERS, CE TI PROSTATE-SPECIFIC ANTIGEN DECLINE FOLLOWING THE DISCONTINUATION OF FLUTAMIDE IN PATIENTS WITH STAGE D2 PROSTATE-CANCER SO AMERICAN JOURNAL OF MEDICINE LA English DT Note ID STEROID BINDING CHARACTERISTICS; COMBINATION THERAPY; WITHDRAWAL SYNDROME; ANDROGEN RECEPTOR; ANTIANDROGENS; TRIAL; CELLS; ORCHIECTOMY; MUTATION; DOMAIN RP FIGG, WD (reprint author), NCI,PHARMACOL BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD, USA. RI Figg Sr, William/M-2411-2016 NR 17 TC 70 Z9 73 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1995 VL 98 IS 4 BP 412 EP 414 DI 10.1016/S0002-9343(99)80323-4 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA QQ863 UT WOS:A1995QQ86300016 PM 7535978 ER PT J AU MCNELLIS, D CARITIS, SN AF MCNELLIS, D CARITIS, SN TI ON PROLONGED PREGNANCY - REPLY SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Letter C1 UNIV PITTSBURGH,MAGEE WOMENS HOSP,SCH MED,DEPT OBSTET & GYNECOL,PITTSBURGH,PA 15213. RP MCNELLIS, D (reprint author), NICHHD,BLDG 6100,ROOM 4B03,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD APR PY 1995 VL 172 IS 4 BP 1321 EP 1322 DI 10.1016/0002-9378(95)91505-2 PN 1 PG 2 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QU858 UT WOS:A1995QU85800040 ER PT J AU IGLESIAS, M PLOWMAN, GD WOODWORTH, CD AF IGLESIAS, M PLOWMAN, GD WOODWORTH, CD TI INTERLEUKIN-6 AND INTERLEUKIN-6 SOLUBLE RECEPTOR REGULATE PROLIFERATION OF NORMAL, HUMAN PAPILLOMAVIRUS-IMMORTALIZED, AND CARCINOMA-DERIVED CERVICAL CELLS IN-VITRO SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; FACTOR-ALPHA; HUMAN KERATINOCYTES; HUMAN-FIBROBLASTS; IL-6 FUNCTIONS; EXPRESSION; INVITRO; AMPHIREGULIN; TYPE-16; LINES AB A variety of sexually transmitted diseases frequently accompany infection with human papilomavirus and stimulate inflammation of the cervical mucosa. Inflammation and cell injury cause release of proinflammatory cytokines, which in turn might regulate growth of human papillomavirus-infected cells. This study compared the interaction of the proinflammatory cytokine, interleukin-6 (IL-6), and its soluble receptor with normal ecto- and endocervical cells, human papillomavirus-immortalized ectocervical cells, and squamous carcinoma-dervied cell lines. Proliferation of normal cervical cells was enhanced by IL-6 but inhibited by its soluble receptor. However, both IL-6 and its soluble receptor significantly stimulated growth of the three immortal and four cervical carcinoma-derived cell lines analyzed. Stimulation by IL-6 was dose dependent and was blocked by an antibody that neutralized IL-6 activity. IL-6-mediated proliferation was accompanied by increased expression of RNAs encoding transforming growth factor-alpha and amphiregulin, two epidermal growth factor receptor ligands. Furthermore, growth stimulation by IL-6 was significantly inhibited by antibodies that either blocked signal transduction by the epidermal growth factor receptor or that neutralized transforming growth factor-alpha or amphiregulin activity. Thus, IL-6 stimulates proliferation of human papillomavirus-immortalized cervical cells via an epidermal growth factor receptor-dependent pathway involving autocrine stimulation by transforming growth factor factor-alpha and amphiregulin. C1 SUGEN INC,REDWOOD CITY,CA. RP IGLESIAS, M (reprint author), NCI,BIOL LAB,BLDG 37,ROOM 2A05,BETHESDA,MD 20892, USA. RI PLOWMAN, Greg/E-2012-2011 NR 43 TC 62 Z9 64 U1 0 U2 2 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD APR PY 1995 VL 146 IS 4 BP 944 EP 952 PG 9 WC Pathology SC Pathology GA QR984 UT WOS:A1995QR98400015 PM 7717461 ER PT J AU SMITH, CB SUN, Y AF SMITH, CB SUN, Y TI INFLUENCE OF VALINE FLOODING ON CHANNELING OF VALINE INTO TISSUE POOLS AND ON PROTEIN-SYNTHESIS SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE AMINO ACID RECYCLING; AMINOACYL-TRANSFER-RNA; ADRENAL GLANDS; BRAIN; HEART; LIVER; SLOW-TWITCH MUSCLE; FAST-TWITCH MUSCLE; ALPHA-KETOISOVALERIC ACID; AMINO ACID FLOODING ID PERFUSED RAT-LIVER; LEUCYL-TRANSFER RNA; MYOSIN HEAVY-CHAIN; AMINO-ACIDS; SYNTHESIS INVIVO; CARDIAC-MUSCLE; PRECURSOR POOL; ADULT RATS; TURNOVER; BRAIN AB Rates of valine incorporation into protein were measured under control and valine-''flooding'' conditions and included correction for the degree of recycling of unlabeled valine derived from the steady-state breakdown of tissue protein into the precursor pool (tRNA bound). The correction factor lambda, which is the ratio of the steady-state specific activity of valine in the tissue tRNA-bound pool to that in the arterial plasma, was determined for each of the tissues. In controls, values of lambda ranged from 0.31 in adrenals to 0.54 in heart; in flooded animals, values were higher, but only in liver was the value of lambda close to 1.0. In control and flooded rats, rates of protein synthesis were highest in liver and adrenals and lowest in skeletal muscle, with intermediate values in brain and heart. Flooding resulted in increased rates of protein synthesis in liver and decreased rates in adrenals. Rates of protein synthesis in brain, heart, and skeletal muscle were not statistically significantly affected by flooding. RP NIMH, CEREBRAL METAB LAB, BLDG 36, RM 1A05, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 34 TC 21 Z9 21 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 EI 1522-1555 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD APR PY 1995 VL 268 IS 4 BP E735 EP E744 PG 10 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA QR801 UT WOS:A1995QR80100026 PM 7733274 ER PT J AU PRADHAN, TK QIAN, JM SUTLIFF, VE MANTEY, SA JENSEN, RT AF PRADHAN, TK QIAN, JM SUTLIFF, VE MANTEY, SA JENSEN, RT TI IDENTIFICATION OF CCK-A RECEPTORS ON CHIEF CELLS WITH USE OF A NOVEL, HIGHLY SELECTIVE LIGAND SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY LA English DT Article DE CHOLECYSTOKININ; GASTRIN; PEPSINOGEN RELEASE; GASTRIC MUCOSAL CELLS ID GUINEA-PIG STOMACH; STIMULATED PEPSINOGEN SECRETION; RAT PANCREATIC ACINI; CHOLECYSTOKININ RECEPTORS; DISTINCT RECEPTORS; GASTRIC GLANDS; RELEASE; BINDING; ANTAGONISTS; CA-2+ AB Functional studies suggest that guinea pig chief cells have both cholecystokinin-A (CCK-A) and CCK-B receptors (CCK-A-R and CCK-B-R, respectively). However, all efforts to directly characterize the specific CCK-A-R using binding have been unsuccessful. Recent studies describe specific CCK-A-R agonists such as A-71378 {[desamino-Nle(28,31)-(N-methyl)Asp(32)]CCK heptapeptide}. In the present study, [D-Tyr-Gly]A-71378 was synthesized, which has > 300-fold selectivity for CCK-A-R and can be iodinated. [D-Tyr-Gly]A-71378 was equipotent to A-71378 in stimulating pepsinogen release from purified guinea pig chief cells. Binding of I-125-labeled [D-Tyr-Gly]A-71378 was saturable and specific, Potencies for inhibiting binding were as follows: [D-Tyr-Gly]A-71378 = A-71378 = 4 x CCK octapeptide (CCK-8) > 1,000 x des(SO4)CCK-8, gastrin. In contrast, for I-125-gastrin binding they were CCK-8 > gastrin-17-I > des(SO4)-CCK-8 >> A-71378 or [n-Tyr-Gly]A-71378. Binding of [D-Tyr-Gly]A-71378 was best fitted by a two-site model. In contrast, I-125-gastrin binding was fitted with a single-site model. For inhibiting binding of I-125-[D-TyrGly]A-71378, the CCK antagonists had relative affinities of L-364,718 >> L-365,260, and the reverse was true with I-125-gastrin. Correlation of binding with changes in biological activity suggested low-affinity CCK-A-R were mediating these changes. These results demonstrate directly for the first time that guinea pig chief cells possess CCK-A-R and CCK-B-R. The pharmacology of these CCK-A-R resembles those on other tissues. This novel, highly selective CCK-A ligand should be useful because it will identify CCK-A-R when they make up as little as 0.2% of the total CCK receptor number. C1 NIDDKD, DIGEST DIS BRANCH, BETHESDA, MD 20892 USA. NR 40 TC 13 Z9 13 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1857 J9 AM J PHYSIOL-GASTR L JI Am. J. Physiol.-Gastroint. Liver Physiol. PD APR PY 1995 VL 268 IS 4 BP G605 EP G612 PG 8 WC Gastroenterology & Hepatology; Physiology SC Gastroenterology & Hepatology; Physiology GA QR813 UT WOS:A1995QR81300008 PM 7733286 ER PT J AU COBB, JP NATANSON, C QUEZADO, ZMN HOFFMAN, WD KOEV, CA BANKS, S CORREA, R LEVI, R ELIN, RJ HOSSEINI, JM DANNER, RL AF COBB, JP NATANSON, C QUEZADO, ZMN HOFFMAN, WD KOEV, CA BANKS, S CORREA, R LEVI, R ELIN, RJ HOSSEINI, JM DANNER, RL TI DIFFERENTIAL HEMODYNAMIC-EFFECTS OF L-NMMA IN ENDOTOXEMIC AND NORMAL DOGS SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE SEPTIC SHOCK; ENDOTOXIN; TOXICITY; MORTALITY ID NITRIC-OXIDE SYNTHESIS; TUMOR-NECROSIS-FACTOR; MONOMETHYL-L-ARGININE; HUMAN SEPTIC SHOCK; METHYL-L-ARGININE; ENDOTHELIAL-CELLS; BLOOD-PRESSURE; CANINE MODEL; INHIBITION; SYNTHASE AB We studied the differential hemodynamic effects of N-omega-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthesis, in normal and endotoxemic dogs and examined its activity across the venous, pulmonary, and systemic circulations. Survival was used to determine therapeutic efficacy. In both normal and endotoxemic animals, L-NMMA similarly increased systemic (P = 0.01) and pulmonary (P = 0.047) vascular resistance, marginally increased mean arterial pressure (P = 0.07), and decreased oxygen delivery (P = 0.01) compared with normal saline. In contrast, the effect of L-NMMA on mean pulmonary arterial pressure, central venous pressure, and pulmonary capillary wedge pressure was different in endotoxemic than in normal animals (P < 0.05), but this differential effect occurred >6 h after endotoxin challenge. L-NMMA (1-10 mg . kg(-1). h(-1)) did not significantly increase survival rates or times in endotoxemic animals, but the highest dose decreased survival times (P < 0.05). Thus the effect of L-NMMA was similar on the systemic arterial circulation in endotoxemic dogs compared with normal dogs but was increased in the venous and pulmonary vascular beds after endotoxin, suggesting that the induction of NO production was greater in low-resistance vessels. We were unable to show that nonselective inhibition of NO production was beneficial in endotoxemic dogs. C1 NIH, WARREN GRANT MAGNUSON CLIN CTR, DEPT CLIN PATHOL, BETHESDA, MD 20892 USA. ARMED FORCES INST PATHOL, DEPT CARDIOVASC PATHOL, WASHINGTON, DC 20306 USA. CORNELL UNIV, COLL MED, DEPT PHARMACOL, NEW YORK, NY 10021 USA. RP COBB, JP (reprint author), NIH, WARREN GRANT MAGNUSON CLIN CTR, DEPT CRIT CARE MED, BLDG 10, RM 7D-43, BETHESDA, MD 20892 USA. RI Quezado, Zenaide/O-4860-2016 OI Quezado, Zenaide/0000-0001-9793-4368 NR 37 TC 64 Z9 65 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD APR PY 1995 VL 268 IS 4 BP H1634 EP H1642 PG 9 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA QR787 UT WOS:A1995QR78700032 ER PT J AU HAY, JG DANEL, C CHU, CS CRYSTAL, RG AF HAY, JG DANEL, C CHU, CS CRYSTAL, RG TI HUMAN CC10 GENE-EXPRESSION IN AIRWAY EPITHELIUM AND SUBCHROMOSOMAL LOCUS SUGGEST LINKAGE TO AIRWAY DISEASE SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY LA English DT Article DE ALU FAMILY; ASTHMA; LINKAGE; POLYMORPHISM ID CELL 10-KDA PROTEIN; RABBIT UTEROGLOBIN; BRONCHOALVEOLAR LAVAGE; HORMONAL-REGULATION; REGION; DNA; CHROMOSOME-11Q; LOCALIZATION; SEQUENCES; REPEATS AB The CC10 gene encodes the Clara cell 10-kDa protein, which is expressed in airway epithelial cells. Quantification of CC10 gene expression in freshly isolated human proximal airway epithelial cells demonstrated very high mRNA levels, approximately fivefold greater than gamma-actin mRNA, and in situ hybridization localized CC10 mRNA to nonciliated airway epithelial cells. Sequence analysis demonstrated that the human CC10 gene is comprised of three short exons separated by a long first and short second intron, and with a 5' flanking region typical of a regulated gene. Three Alu repeats were observed in intron 1 and one in intron 2. Two polymorphic regions within the introns were identified. First, a microsatellite was localized 5' to the third Alu repeat in intron 1 with a variable number of 4- and 5-base pair (bp) repeats and a heterozygosity of 0.71. Second, in 3% of the 168 chromosomes examined, there was the insertion of a human-specific Alu repeat in intron 2, 45 bp 3' to the exon 2-intron junction. In three Centre d'Etude du Polymorphisme Humain families, meiotic breakpoint analysis using these two polymerphic loci localized the CC10 gene to 11 p12-q13 between markers D11S16 and D11S97, a region recently linked to atopy and to the beta-subunit of the high-affinity immunoglobulin E receptor. The observations in the present study of high-level expression of the CC10 gene in the epithelium of conducting airways and a subchromosomal localization of the gene to a region potentially linked to inflammatory airway disease, together with the reported anti-inflammatory and immune-modulating properties of the protein, suggest the CC10 gene product may be important in modulating inflammation within the airways. If so, the highly heterozygous microsatellite described in the present study should facilitate analysis of a possible linkage of the CC10 gene with an inherited susceptibility to asthma. C1 NHLBI, PULM BRANCH, BETHESDA, MD 20892 USA. CORNELL UNIV, COLL MED, DIV PULM & CRIT CARE MED, NEW YORK, NY 10021 USA. NR 37 TC 24 Z9 28 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1040-0605 J9 AM J PHYSIOL-LUNG C JI Am. J. Physiol.-Lung Cell. Mol. Physiol. PD APR PY 1995 VL 268 IS 4 BP L565 EP L575 PG 11 WC Physiology; Respiratory System SC Physiology; Respiratory System GA QT313 UT WOS:A1995QT31300005 PM 7733299 ER PT J AU GLADEN, BC ROGAN, WJ AF GLADEN, BC ROGAN, WJ TI DDE AND SHORTENED DURATION OF LACTATION IN A NORTHERN MEXICAN TOWN SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID POLYCHLORINATED-BIPHENYLS; DEVELOPING-COUNTRIES; PASSIVE SMOKING; INFANTS URINE; MILK; BEHAVIOR; HEALTH AB Objectives. Worldwide declines in the duration of lactation are cause for public health concern. Higher levels of dichlorodiphenyl dichloroethene (DDE) have been associated with shorter durations of lactation in the United States. This study examined whether this relationship would hold in an agricultural town in northern Mexico. Methods. Two hundred twenty-nine women were followed every 2 months from childbirth until weaning or until the child reached 18 months of age. DDE was measured in breast milk samples taken at birth, and women were followed to see how long they lactated. Results. Median duration was 7.5 months in the lowest DDE group and 3 months in the highest. The effect was confined to those who had lactated previously, and it persisted after statistical adjustment for other factors. These results are not due to overtly sick children being weaned earlier. Previous lactation lowers DDE levels, which produces an artifactual association, but simulations using best estimates show that an effect as large as that found here would arise through this mechanism only 6% of the time. Conclusions. DDE may affect women's ability to lactate. This exposure map be contributing to lactation failure throughout the world. C1 NIEHS,OFF SCI DIRECTOR,RES TRIANGLE PK,NC 27709. RP GLADEN, BC (reprint author), NIEHS,STAT & BIOMATH BRANCH,MAIL DROP A3-03,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Rogan, Walter/I-6034-2012 OI Rogan, Walter/0000-0002-9302-0160 NR 32 TC 90 Z9 94 U1 0 U2 2 PU AMER PUBLIC HEALTH ASSN INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD APR PY 1995 VL 85 IS 4 BP 504 EP 508 DI 10.2105/AJPH.85.4.504 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QR244 UT WOS:A1995QR24400008 PM 7702113 ER PT J AU SIEGFRIED, W ROSENFELD, M STIER, L STRATFORDPERRICAUDET, L PERRICAUDET, M PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF SIEGFRIED, W ROSENFELD, M STIER, L STRATFORDPERRICAUDET, L PERRICAUDET, M PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI POLARITY OF SECRETION OF ALPHA-1-ANTITRYPSIN BY HUMAN RESPIRATORY EPITHELIAL-CELLS AFTER ADENOVIRAL TRANSFER OF A HUMAN ALPHA-1-ANTITRYPSIN CDNA SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID DEFICIENCY; EXPRESSION; EMPHYSEMA; GENE; DNA; TRANSFORMATION; TRANSPORT; ELASTASE; THERAPY; PROTEIN AB alpha 1-Antitrypsin (alpha AT) deficiency, a hereditary cause of progressive emphysema, can potentially be treated by transfer of a functional human alpha 1AT gene to the respiratory epithelium. For such an approach to be successful, alpha 1AT must be provided to both the interstitium and the epithelial surface-that is, the alpha 1AT directed by the transferred gene must be secreted to both the apical and basolateral surfaces of the epithelial cells. To evaluate this concept, a recombinant, replication-deficient adenoviral vector (Ad-alpha 1AT) containing a human alpha 1AT cDNA driven by an adenovirus major late promoter was used to infect Bet-1A human respiratory epithelial cells. The infected cells expressed Ad-alpha 1AT-directed mRNA transcripts and synthesized and secreted functional human alpha 1AT as shown by [S-35]methionine labeling and immunoprecipitation of a 52-kD glycosylated human alpha 1AT molecule capable of interacting with neutrophil elastase, its natural substrate. Bet-1A cells grown on microporous polycarbonate membranes formed tight junctions (resistance > 150 Ohm x cm(2)). After infection with Ad-alpha 1AT, [S-35]methionine labeling and enzyme-linked immunoassay demonstrated that alpha 1AT was secreted into both the apical and basolateral compartments, with an average apical to basolateral ratio of 1.9 +/- 0.2. Thus, human respiratory epithelial cells infected with a recombinant adenoviral vector containing a human alpha 1AT cDNA secrete alpha 1AT across both the apical and basolateral cell membranes, suggesting that the respiratory epithelium could serve as a target for in vivo gene therapy of alpha 1AT deficiency. C1 CORNELL UNIV,MED CTR,NEW YORK HOSP,DIV PULM & CRIT CARE MED,NEW YORK,NY 10021. NHLBI,PULM BRANCH,BETHESDA,MD 20892. CNRS,U1301,INST GUSTAVE ROUSSY,VILLEJUIF,FRANCE. TRANSGENE SA,DEPT MOLEC & CELLULAR BIOL,STRASBOURG,FRANCE. NR 35 TC 12 Z9 12 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD APR PY 1995 VL 12 IS 4 BP 379 EP 384 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA QR240 UT WOS:A1995QR24000003 PM 7695917 ER PT J AU DOHERTY, MM LIU, JY RANDELL, SH CARTER, CA DAVIS, CW NETTESHEIM, P FERRIOLA, PC AF DOHERTY, MM LIU, JY RANDELL, SH CARTER, CA DAVIS, CW NETTESHEIM, P FERRIOLA, PC TI PHENOTYPE AND DIFFERENTIATION POTENTIAL OF A NOVEL RAT TRACHEAL EPITHELIAL-CELL LINE SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID GROWTH-FACTOR DEPENDENCE; NEOPLASTIC PROGRESSION; RTE CELLS; EXPRESSION; CULTURES; ACID; CARCINOGEN; MARKERS AB In this report we described the establishment and characterization of a continuous rat tracheal epithelial (RTE) cell line spontaneously derived from secondary RTE cell cultures. Designated SPOC1, this cell line is nontumorigenic and maintains a diploid karyotype with specific, nonrandom chromosomal alterations involving chromosomes 1, 3, and 6. SPOC1 cells demonstrate decreased requirements for peptide growth factors, compared with primary RTE cells. Upon inoculation into denuded rat tracheas, which are then implanted into syngeneic hosts, SPOC1 cells initially form a stratified squamous epithelium, which becomes less stratified with time and forms glandlike invaginations into the surrounding lamina propria. No evidence of ciliated cell differentiation is detected. The epithelium formed by SPOC1 cells in tracheal grafts reacts with antibodies specific for keratin 14, 13, and 19 (but not keratin 18) at both early and late time points, although the localization of antibody staining changes as the epithelium becomes less stratified with time. The suprabasal epithelial cells become positive for alcian blue-periodic acid-Schiff staining at later time points. The near-normal karyotype and differentiation potential of SPOC1 cells make this cell line a unique window into early changes occurring during immortalization of airway epithelial cells and will allow studies of relationships between differentiation state and neoplastic transformation. C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC. UNIV N CAROLINA,DEPT PATHOL,CHAPEL HILL,NC. UNIV N CAROLINA,DEPT PULM MED,CHAPEL HILL,NC. NR 41 TC 16 Z9 17 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD APR PY 1995 VL 12 IS 4 BP 385 EP 395 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA QR240 UT WOS:A1995QR24000004 PM 7535063 ER PT J AU LAWRENCE, JB LEIFER, DW MOURA, GL SOUTHERN, P EMERY, JD BODENHEIMER, SL KRAMER, WS AF LAWRENCE, JB LEIFER, DW MOURA, GL SOUTHERN, P EMERY, JD BODENHEIMER, SL KRAMER, WS TI SEX-DIFFERENCES IN PLATELET ADHERENCE TO SUBENDOTHELIUM - RELATIONSHIP TO PLATELET-FUNCTION TESTS AND HEMATOLOGIC VARIABLES SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Article DE PLATELET ADHERENCE; SUBENDOTHELIUM; BLEEDING TIME; PLATELET AGGREGATION; FIBRINOGEN ID ADHESIVE PROTEIN-BINDING; CORONARY HEART-DISEASE; BLEEDING-TIME; WHOLE-BLOOD; ARTERIAL SUBENDOTHELIUM; AGGREGATION; ASPIRIN; SECRETION; AGGREGOMETER; FIBRINOGEN AB Men have significantly more atherosclerotic disease than women. Platelet-mediated thrombosis plays a role in the initiation of myocardial infarction and stroke. Citrated whole blood from male and female donors was perfused through an annular system over everted human umbilical artery segments. Comparisons were made between platelet adherence and thrombus formation on subendothelium, platelet aggregation in citrated whole blood, hematologic variables, and the bleeding time. Platelet spreading and adherence were approximately 22% greater with male blood (P < 0.001), whereas thrombus formation on subendothelium and collagen- and arachidonic acid-induced platelet aggregation did not show sex-related differences. Platelet aggregation with adenosine diphosphate was greater in women, related to their lower hematocrit values. By contrast, in women hematocrit values showed a slight but significant positive correlation with platelet adherence on subendothelium. Fibrinogen was significantly correlated with collagen- and adenosine-diphosphate-induced platelet aggregation and with platelet adherence, spreading, and thrombus formation on subendothelium. The mean bleeding time was slightly longer in women than in men (P = 0.118). Platelet aggregation was not associated with the bleeding time except for collagen-induced platelet aggregation in males; the latter was significantly correlated with platelet adherence and spreading in both sexes, while arachidonic acid-induced platelet aggregation predicted platelet adherence and spreading in males. Male blood shows enhanced primary hemostatic activity; this may predispose men to atherosclerosis. C1 CASE WESTERN RESERVE UNIV,INST PATHOL,CLEVELAND,OH 44106. UNIV CLEVELAND HOSP,DEPT PATHOL,CLEVELAND,OH 44106. VIRGINIA COMMONWEALTH UNIV MED COLL VIRGINIA,DEPT PATHOL,RICHMOND,VA. NIH,CTR CLIN,DEPT CLIN PATHOL,SERV HEMATOL,BETHESDA,MD 20892. NR 30 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0002-9629 J9 AM J MED SCI JI Am. J. Med. Sci. PD APR PY 1995 VL 309 IS 4 BP 201 EP 207 DI 10.1097/00000441-199504000-00003 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA QP460 UT WOS:A1995QP46000003 PM 7900741 ER PT J AU CAMPBELL, PT LI, JS WALL, TC OCONNOR, CM VANTRIGT, P KENNEY, RT MELHUS, O COREY, GR AF CAMPBELL, PT LI, JS WALL, TC OCONNOR, CM VANTRIGT, P KENNEY, RT MELHUS, O COREY, GR TI CYTOMEGALOVIRUS PERICARDITIS - A CASE SERIES AND REVIEW OF THE LITERATURE SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Review DE CYTOMEGALOVIRUS; PERICARDITIS; CULTURE-PROVEN SUBXIPHOID PERICARDIOTOMY ID TRANSPLANT RECIPIENTS; INSITU HYBRIDIZATION; VIRUS INFECTION; DIAGNOSIS; PNEUMONIA; MONONUCLEOSIS; MYOCARDITIS; ETIOLOGY AB Cytomegalovirus (CMV) commonly infects both normal and immunocompromised hosts. Although it usually produces an asymptomatic infection to mild illness, CMV has the potential to significantly injure many different organs. Reports of CMV causing pericardial disease, however, are limited and documentation of infection by growth of the virus from tissue or fluid is rare. As part of a prospective trial of subxiphoid pericardial biopsy in 57 adult patients with large pericardial effusions, three culture-proven cases and one serologically confirmed case of CMV pericardial disease were discovered. Subsequently, CMV was grown from the pericardium of an infant with congenital heart disease. A review of the documented cases of CMV pericarditis is provided along with a discussion of the pathogenesis and significance of this perhaps not so uncommon disease. C1 DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. NIAID,BETHESDA,MD 20892. NR 30 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0002-9629 J9 AM J MED SCI JI Am. J. Med. Sci. PD APR PY 1995 VL 309 IS 4 BP 229 EP 234 DI 10.1097/00000441-199504000-00009 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA QP460 UT WOS:A1995QP46000009 PM 7900747 ER PT J AU ROMAN, GC AF ROMAN, GC TI ON POLITICS AND HEALTH - AN EPIDEMIC OF NEUROLOGIC DISEASE IN CUBA SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material AB Political decisions may cause disease. During 1992 and 1993, an epidemic of neuropathy in Cuba-largely overlooked by U.S. physicians-affected more than 50 000 persons and caused optic neuropathy, deafness, myelopathy, and sensory neuropathy. Patients with the neurologic disease responded to B group vitamins, and oral vitamin supplementation of the population curbed the epidemic. Dietary restrictions and excessive carbohydrate intake were the immediate cause of the epidemic; however, the primary cause might have been political. Political changes in eastern Europe had major repercussions on Cuba's economy and food supply. In turn, these changes compounded the effects of internal political decisions in the island, leading toward isolationism and economic dependence on the former Soviet Union. Also, for more than 30 years, the United States has maintained an economic embargo against Cuba. In 1992, the U.S. embargo was tightened by the Torricelli amendment (or the Cuba Democracy Act), which prohibited third-country subsidiaries of U.S. companies from trading with Cuba and prevented food and medicines from reaching the island; this amendment produced a virtual economic blockade. Penuries resulting from all these political events resulted in the largest epidemic of neurologic disease in this century. Physicians may need to use their influence to modify political decisions when these decisions result in adverse health consequences. The American Academy of Neurology has issued a plea to encourage physicians and other health personnel to support efforts leading to lifting of the U.S. embargo against Cuba for humanitarian reasons. C1 NIH,BETHESDA,MD 20892. NR 22 TC 34 Z9 35 U1 1 U2 5 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 1 PY 1995 VL 122 IS 7 BP 530 EP 533 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA QP008 UT WOS:A1995QP00800009 PM 7872589 ER PT J AU STEIN, C SCHAFER, M HASSAN, AHS AF STEIN, C SCHAFER, M HASSAN, AHS TI PERIPHERAL OPIOID RECEPTORS SO ANNALS OF MEDICINE LA English DT Article DE ANALGESIA; INFLAMMATION; NOCICEPTION; OPIOID RECEPTORS; OPIOID PEPTIDES; PAIN ID ARTHROSCOPIC KNEE SURGERY; SUBSTANCE-P RELEASE; CRUCIATE LIGAMENT REPAIR; INTRAARTICULAR MORPHINE; INFLAMED TISSUE; IMMUNE CELLS; PAIN RELIEF; INFLAMMATION; BUPIVACAINE; ANALGESIA AB Recent experimental and clinical research has demonstrated that opioids can produce potent and receptor-specific analgesic effects outside the central nervous system. Opioid receptors are localized on peripheral terminals of sensory nerves and their endogenous ligands, opioid peptides, have been discovered in immune cells within inflamed tissue. Many controlled clinical studies confirm the experimental data. These findings open up the exciting perspective of the development of an entirely novel generation of peripherally active opioid analgesics devoid of centrally mediated side effects. C1 NIDA,INTRAMURAL RES PROGRAM,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205. FU NINDS NIH HHS [R01 NS32466] NR 44 TC 60 Z9 62 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0785-3890 J9 ANN MED JI Ann. Med. PD APR PY 1995 VL 27 IS 2 BP 219 EP 221 DI 10.3109/07853899509031962 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA QY908 UT WOS:A1995QY90800013 PM 7632417 ER PT J AU PASS, HI STEVENS, EJ OIE, H TSOKOS, MG ABATI, AD FETSCH, PA MEW, DJY POGREBNIAK, HW MATTHEWS, WJ AF PASS, HI STEVENS, EJ OIE, H TSOKOS, MG ABATI, AD FETSCH, PA MEW, DJY POGREBNIAK, HW MATTHEWS, WJ TI CHARACTERISTICS OF 9 NEWLY DERIVED MESOTHELIOMA CELL-LINES SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT 41st Annual Meeting of the Southern-Thoracic-Surgical-Association CY NOV 10-12, 1994 CL MARCO ISL, FL SP SO THORAC SURG ASSOC ID HUMAN-MALIGNANT MESOTHELIOMA; PLEURAL MESOTHELIOMA; GROWTH; ESTABLISHMENT; INTERLEUKIN-6; BETA AB This report characterizes nine new cell lines derived from patients with malignant pleural mesothelioma. The lines were initiated between July 1990 and July 1992 from solid tumors (5 lines) or effusions (4 lines) and had proliferated for a period of at least 2 months without senescence. They were characterized by cell size, doubling time, immunohistochemical analyses, electron microscopy, and chromosomal karyotyping. Growth factor/cytokine elaboration was determined using enzyme-linked immunoassays. The established lines were similar in morphology to their parent tumor (ie, epithelial or sarcomatoid). Cell sizes ranged from 59 to 81 mu m, and the doubling times varied from 31 to 65 hours. The lines stained with cytokeratin and showed expected negative staining for adenomarkers including B72.3 and carcinoembryonic antigen. All cell lines exhibited aneuploidy, with modal chromosome numbers between 40 and 81 and had multiple chromosomal aberrations. Significant production of granulocyte-monocyte colony-stimulating factor, leukemia inhibitory factor, platelet-derived growth factor, and interleukin-6 was seen. These new cell lines derived from human mesotheliomas can now be used to aid in the design of innovative treatment strategies. C1 NCI,NAVAL MED ONCOL BRANCH,BETHESDA,MD 20892. NCI,PEDIAT TUMOR BIOL ULTRASTRUCT PATHOL SECT,BETHESDA,MD 20892. NCI,CYTOPATHOL SECT,BETHESDA,MD 20892. RP PASS, HI (reprint author), NCI,SURG BRANCH,THORAC ONCOL SECT,BLDG 10,RM 2B07,BETHESDA,MD 20892, USA. NR 17 TC 100 Z9 100 U1 0 U2 2 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD APR PY 1995 VL 59 IS 4 BP 835 EP 844 DI 10.1016/0003-4975(95)00045-M PG 10 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA QP487 UT WOS:A1995QP48700007 PM 7695406 ER PT J AU PETTIT, GR FREEMAN, S SIMPSON, MJ THOMPSON, MA BOYD, MR WILLIAMS, MD PETTIT, GR DOUBEK, DL AF PETTIT, GR FREEMAN, S SIMPSON, MJ THOMPSON, MA BOYD, MR WILLIAMS, MD PETTIT, GR DOUBEK, DL TI ANTINEOPLASTIC AGENTS .320. SYNTHESIS OF A PRACTICAL PANCRATISTATIN PRODRUG SO ANTI-CANCER DRUG DESIGN LA English DT Article DE CANCER; PANCRATISTATIN; PHOSPHATE; PRODRUG ID PHOSPHITYLATING AGENT; EFFICIENT PHOSPHORYLATION; DIBENZYL PHOSPHORAMIDITE; (+)-LYCORICIDINE; PHOSPHATES; ALKALOIDS; ALCOHOLS; REAGENT AB Owing to its sparingly soluble properties, the potential anticancer drug pancratistatin (1) resisted conventional drug formulation procedures and the synthesis of a water-soluble prodrug became necessary. That important objective for further pre-clinical development was met by devising a route to a disodium phosphate derivative (5). The key step in the synthesis of the phenolic phosphate was phosphorylation of 1,2,3,4-tetraacetoxy-pancratistatin (2) with dibenzyloxy(N,N-diisopropylamido)phosphine. Subsequent oxidation with m-chloroperbenzoic acid afforded phosphate 4a. Hydrogenolysis of the benzyl esters followed by base-catalysed hydrolysis of the acetate groups led to the water-soluble prodrug 5 in high yield. C1 ARIZONA STATE UNIV,DEPT CHEM,TEMPE,AZ 85287. UNIV ASTON,DEPT PHARMACEUT & BIOL SCI,BIRMINGHAM B4 7ET,W MIDLANDS,ENGLAND. NCI,FREDERICK CANC RES & DEV CTR,DCT,DTP,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. RP PETTIT, GR (reprint author), ARIZONA STATE UNIV,CANC RES INST,BOX 871604,TEMPE,AZ 85287, USA. FU NCI NIH HHS [CA-44344-01A1-04-06, CA-16049-05-12] NR 31 TC 37 Z9 37 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0266-9536 J9 ANTI-CANCER DRUG DES JI Anti-Cancer Drug Des. PD APR PY 1995 VL 10 IS 3 BP 243 EP 250 PG 8 WC Biochemistry & Molecular Biology; Oncology; Chemistry, Medicinal; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy GA QZ734 UT WOS:A1995QZ73400005 PM 7748458 ER PT J AU POLIS, MA SPOONER, KM BAIRD, BF MANISCHEWITZ, JF JAFFE, HS FISHER, PE FALLOON, J DAVEY, RT KOVACS, JA WALKER, RE WHITCUP, SM NUSSENBLATT, RB LANE, HC MASUR, H AF POLIS, MA SPOONER, KM BAIRD, BF MANISCHEWITZ, JF JAFFE, HS FISHER, PE FALLOON, J DAVEY, RT KOVACS, JA WALKER, RE WHITCUP, SM NUSSENBLATT, RB LANE, HC MASUR, H TI ANTICYTOMEGALOVIRAL ACTIVITY AND SAFETY OF CIDOFOVIR IN PATIENTS WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION AND CYTOMEGALOVIRUS VIRURIA SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID ANTIVIRAL ACTIVITY; (S)-1-(3-HYDROXY-2-PHOSPHONYLMETHOXYPROPYL)CYTOSINE; AIDS; (S)-1-<3-HYDROXY-2-(PHOSPHONYLMETHOXY)PROPYL>CYTOSINE; 9-(1,3-DIHYDROXY-2-PROPOXYMETHYL)GUANINE; INVITRO; HPMPC AB Cidofovir {HPMPC; (S)-1-[3-hydroxy-2-(phosphonylmethoxy)propyl]cytosine} is a nucleotide analog with activity against human (CMV). A phase I/II dose escalation trial was conducted with asymptomatic human immunodeficiency virus (HIV)-infected patients with CMV viruria to determine its pharmacokinetics, maximally tolerated dose, and preliminary antiviral activity against CMV. Qualitative CMV blood and urine cultures were monitored weekly to assess anti-CMV activity. Twenty-one HIV-infected persons with CD4 counts from 0 to 389 cells per mu l (median, 39) were enrolled in six dose-ranging groups. The first five groups enrolled four patients each to receive cidofovir infusions either weekly or biweekly for 4 weeks or every 3 weeks for 12 weeks. The sixth group enrolled one patient who received infusions of 5 mg/kg of body weight every other week. Patients receiving 0.5 or 1.5 mg/kg twice weekly experienced no serious toxicity. The first two patients who received 5 mg/kg twice weekly developed glycosuria and 2+ proteinuria. Subsequent patients received concomitant probenecid to attempt to ameliorate renal toxicity. Seventeen patients experienced proteinuria on one or more occasions; 6 of them experienced at least 2+ proteinuria. Four patients did not complete the study as planned because of renal toxicity. Positive CMV urine cultures reverted to negative in 2 of 8 patients receiving doses of less than or equal to 1.5 mg/kg twice weekly and 11 of 13 patients receiving higher doses. Cidofovir has in vivo anti-CMV activity demonstrated by prolonged clearing of CMV viruria, although this observation is tempered by the fact that clearance of viremia could not be demonstrated. The dose-limiting toxicity is renal; however, concurrent administration of probenecid may be protective. The maximally tolerated weekly intravenous dose with probenecid is approximately 5 mg/kg. Efficacy trials with CMV disease will define the therapeutic utility and optimal dosing interval for cidofovir. C1 NEI,DEPT CRIT CARE MED,BETHESDA,MD 20892. NIH,WARREN G MAGNUSON CLIN CTR,BETHESDA,MD 20892. US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD 20014. GILEAD SCI INC,FOSTER CITY,CA. RP POLIS, MA (reprint author), NIAID,LIR,BLDG 10,ROOM 11C103,BETHESDA,MD 20892, USA. OI Polis, Michael/0000-0002-9151-2268 NR 20 TC 99 Z9 103 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD APR PY 1995 VL 39 IS 4 BP 882 EP 886 PG 5 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA QQ123 UT WOS:A1995QQ12300016 PM 7785989 ER PT J AU KIMBERLIN, DW COEN, DM BIRON, KK COHEN, JI LAMB, RA MCKINLAY, M EMINI, EA WHITLEY, RJ AF KIMBERLIN, DW COEN, DM BIRON, KK COHEN, JI LAMB, RA MCKINLAY, M EMINI, EA WHITLEY, RJ TI MOLECULAR MECHANISMS OF ANTIVIRAL RESISTANCE SO ANTIVIRAL RESEARCH LA English DT Article; Proceedings Paper CT State-of-the-Art Symposium on Antiviral Resistance CY DEC 08-10, 1994 CL NEW YORK, NY SP MACRE GRP, INT SOC ANTIVIRAL RES, NIAID ID HUMAN-IMMUNODEFICIENCY-VIRUS; HERPES-SIMPLEX VIRUS; VARICELLA-ZOSTER VIRUS; REVERSE-TRANSCRIPTASE INHIBITORS; HIGH-LEVEL RESISTANCE; DNA-POLYMERASE GENE; KINASE-DEFICIENT MUTANTS; ION-CHANNEL ACTIVITY; HUMAN RHINOVIRUS 14; THYMIDINE KINASE C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA. BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC 27709. NIH,BETHESDA,MD 20892. HOWARD HUGHES MED INST,EVANSTON,IL. NORTHWESTERN UNIV,EVANSTON,IL. VIROPHARMA,COLLEGEVILLE,PA. MERCK RES LABS,W POINT,PA. RP KIMBERLIN, DW (reprint author), UNIV ALABAMA,DEPT PEDIAT,1600 7TH AVE S,SUITE 616,BIRMINGHAM,AL 35233, USA. NR 129 TC 52 Z9 53 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD APR PY 1995 VL 26 IS 4 BP 369 EP 401 DI 10.1016/0166-3542(95)00027-J PG 33 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA QZ059 UT WOS:A1995QZ05900002 PM 7574541 ER PT J AU KIMBERLIN, DW CRUMPACKER, CS STRAUS, SE BIRON, KK DREW, WL HAYDEN, FG MCKINLAY, M RICHMAN, DD WHITLEY, RJ AF KIMBERLIN, DW CRUMPACKER, CS STRAUS, SE BIRON, KK DREW, WL HAYDEN, FG MCKINLAY, M RICHMAN, DD WHITLEY, RJ TI ANTIVIRAL RESISTANCE IN CLINICAL-PRACTICE SO ANTIVIRAL RESEARCH LA English DT Article; Proceedings Paper CT State-of-the-Art Symposium on Antiviral Resistance CY DEC 08-10, 1994 CL NEW YORK, NY SP MACRE GRP, INT SOC ANTIVIRAL RES, NIAID ID HERPES-SIMPLEX VIRUS; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; VARICELLA-ZOSTER VIRUS; INFLUENZA-A VIRUS; HIV-1 REVERSE-TRANSCRIPTASE; ACYCLOVIR THERAPY; FOSCARNET THERAPY; INFECTION; PATIENT; TYPE-1 C1 BETH ISRAEL HOSP,BOSTON,MA 02215. NIH,BETHESDA,MD 20892. BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC. UNIV CALIF SAN FRANCISCO,MT ZION MED CTR,SAN FRANCISCO,CA. UNIV VIRGINIA,CHARLOTTESVILLE,VA. VIROPHARMA,COLLEGEVILLE,PA. UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. RP KIMBERLIN, DW (reprint author), UNIV ALABAMA,DEPT PEDIAT,1600 7TH AVE S,SUITE 616,BIRMINGHAM,AL 35233, USA. NR 63 TC 18 Z9 18 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD APR PY 1995 VL 26 IS 4 BP 423 EP 438 DI 10.1016/0166-3542(95)00031-G PG 16 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA QZ059 UT WOS:A1995QZ05900005 PM 7574544 ER PT J AU KIMBERLIN, DW COUCH, RB GALASSO, GJ RICHMAN, DD WHITLEY, RJ AF KIMBERLIN, DW COUCH, RB GALASSO, GJ RICHMAN, DD WHITLEY, RJ TI RESEARCH INITIATIVES IN STUDIES OF ANTIVIRAL RESISTANCE AND CONSENSUS POINTS AND RECOMMENDATIONS SO ANTIVIRAL RESEARCH LA English DT Article; Proceedings Paper CT State-of-the-Art Symposium on Antiviral Resistance CY DEC 08-10, 1994 CL NEW YORK, NY SP MACRE GRP, INT SOC ANTIVIRAL RES, NIAID C1 BAYLOR COLL MED,DEPT MICROBIOL & IMMUNOL,HOUSTON,TX 77030. NIH,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DEPT PATHOL,LA JOLLA,CA. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA. RP KIMBERLIN, DW (reprint author), UNIV ALABAMA,DEPT PEDIAT,BIRMINGHAM,AL 35294, USA. NR 0 TC 0 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD APR PY 1995 VL 26 IS 4 BP 439 EP 452 DI 10.1016/0166-3542(95)00029-L PG 14 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA QZ059 UT WOS:A1995QZ05900006 PM 7574545 ER PT J AU FASS, R BAHAR, S KAUFMAN, J SHILOACH, J AF FASS, R BAHAR, S KAUFMAN, J SHILOACH, J TI HIGH-YIELD PRODUCTION OF DIPHTHERIA-TOXIN MUTANTS BY HIGH-DENSITY CULTURE OF C7(BETA)(TOX+) STRAINS GROWN IN A NON-DEFERRATED MEDIUM SO APPLIED MICROBIOLOGY AND BIOTECHNOLOGY LA English DT Article ID CORYNEBACTERIUM-DIPHTHERIAE; BETA; MUTATIONS AB A high-density growth approach was utilized to produce mutated diphtheria toxin from two strains of Corynebacterium diphtheria: C7 (beta)((tox-201, tox-9)) and C7 (beta)((tox-107)). The cross-reacting mutants (CRM) of the diphtheria toxin are CRM9 and CRM107; both of them carry the mutation in their binding site and, as a result, have 1/300 of the systemic toxicity of the wild-type diptheria toxin. Since iron inhibits diphtheria toxin production, the traditional approach has been to grow the bacteria in a very low iron concentration. The procedure described here involved the use of a modified, non-deferrated, growth medium that provided fast and high-density growth of the bacteria, and which, when associated with simultaneous depletion of glucose and iron, enhanced the toxin production. Oxygen-enriched air was supplied to enable the bacteria to grow to a cell density giving an absorbance of 70 at 600 nm (15-20 g/l dry weight). The maximum toxin concentration in the culture supernatant was 150 mg/l. The CRM products, which remained stable following microfiltration and ultrafiltration, could be easily purified using a two-step chromatography procedure. C1 ISRAEL INST BIOL RES,DEPT BIOTECHNOL,IL-70450 NESS ZIONA,ISRAEL. UNIV SIMON BOLIVAR,CARACAS 1086A,VENEZUELA. RP FASS, R (reprint author), NIDDK,LCDB,BIOTECHNOL UNIT,BLDG 6,ROOM B1-33,BETHESDA,MD 20892, USA. NR 18 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0175-7598 J9 APPL MICROBIOL BIOT JI Appl. Microbiol. Biotechnol. PD APR PY 1995 VL 43 IS 1 BP 83 EP 88 PG 6 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA QT451 UT WOS:A1995QT45100015 PM 7766139 ER PT J AU EISENBERG, H AF EISENBERG, H TI LIFE IN UNUSUAL ENVIRONMENTS - PROGRESS IN UNDERSTANDING THE STRUCTURE AND FUNCTION OF ENZYMES FROM EXTREME HALOPHILIC BACTERIA SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID MALATE-DEHYDROGENASE; ESCHERICHIA-COLI; HALOBACTERIUM-MARISMORTUI; HALOARCULA-MARISMORTUI; SUBUNIT STRUCTURE; GENE; DENATURATION; EXPRESSION; SCATTERING AB Extreme halophilic archaea are saturated with salt and the intracellular electrolyte concentration exceeds that of the extracellular environment. Enzymes and other proteins from extreme halophilic archaea have been purified for many years and studied by biochemical and biophysical solution methodologies. They are active and stable at multimolar salt concentrations and denature below 2 to 3 M NaCl or KCl, Adaptation to these high concentrations of salt, genetic and evolutionary aspects, and the possibility of biotechnological applications are problems of considerable interest, Since the status of this fascinating field of research was reviewed in 1992, malate dehydrogenase from Haloarcula marismortui, now known to be a tetramer, was sequenced, its gene was cloned and expressed in active form, and its physical properties were redefined, A single mutation of Arg(100) (in the enzyme active site) to Gin switched the enzyme specificity from malate to lactate dehydrogenase, Recent determination of its molecular structure by X-ray crystallography (O, Dym ct al., in press) provides an exciting basis for the understanding of the structure and function of extreme halophilic enzymes, A major problem which so far has not been tackled in the study of extreme halophilic archaea is the understanding of protein nucleic acid interactions which are essential for the performance of biological function, Whereas the stability and activity of enzymes and other proteins can be modified to perform at high salt concentrations by use of currently known structural concepts, the existence of meaningful protein nucleic acid interactions in physiological concentrations of 4 to 5 M KCI constitutes an unsolved enigma worth intensive investigation. (C) 1995 Academic Press, Inc. C1 WEIZMANN INST SCI,DEPT BIOL STRUCT,IL-76100 REHOVOT,ISRAEL. RP EISENBERG, H (reprint author), NIDDK,MOLEC BIOL LAB,BLDG 5,ROOM 208,BETHESDA,MD 20892, USA. NR 28 TC 43 Z9 44 U1 0 U2 8 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR 1 PY 1995 VL 318 IS 1 BP 1 EP 5 DI 10.1006/abbi.1995.1196 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QU077 UT WOS:A1995QU07700001 PM 7726549 ER PT J AU ZOLKIEWSKI, M REDOWICZ, MJ KORN, ED GINSBURG, A AF ZOLKIEWSKI, M REDOWICZ, MJ KORN, ED GINSBURG, A TI THERMALLY-INDUCED UNFOLDING OF ACANTHAMOEBA MYOSIN-II AND SKELETAL-MUSCLE MYOSIN - NUCLEOTIDE EFFECTS SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE DIFFERENTIAL SCANNING CALORIMETRY; PROTEIN FOLDING; ATP BINDING; CIRCULAR DICHROISM; MYOSIN ID DIFFERENTIAL SCANNING CALORIMETRY; DODECAMERIC GLUTAMINE-SYNTHETASE; 3 PHOSPHORYLATION SITES; AMINO-ACID-SEQUENCE; HEAVY-CHAIN; ESCHERICHIA-COLI; ACTIN; PROTEINS; SUBFRAGMENT-1; TRANSITIONS AB The thermal unfolding of monomeric Acanthamoeba myosin II and rabbit skeletal muscle myosin at pH 7.5 in 0.6 M KCl has been studied by differential scanning calorimetry (DSC) and circular dichroism, A single endotherm (at similar to 40 to 45 degrees C) with a maximum at 41.7 +/- 0.1 degrees C and Delta H approximate to 1080 +/- 180 kcal/mol is observed for both dephospho- and phospho-myosin II, Skeletal muscle myosin unfolds with less cooperativity over a wider temperature range (similar to 40 to 60 degrees C) with Delta H approximate to 2500 kcal/mol, The thermal unfolding of either myosin results in a loss of similar to 70% of a-helical structures, Saturation of dephospho- or phospho-myosin II with 5'-adenylylimidodiphosphate (AMPPNP) in the presence of Mg2+ produces a second endotherm with a maximum at similar to 49 degrees C, The latter observation is attributed to a stabilization of head regions by nucleotide binding, Indeed, a purified N-terminal myosin II head fragment has been found to unfold with T-max similar to 41 and similar to 48 degrees C in the absence and presence of AMPPNP, respectively, The stabilization of the head regions is less with ADP + P-i and still smaller with ADP alone, In summary, thermally induced unfolding of myosin II is affected by nucleotide binding to heads, but not by phosphorylation or even removal of a 66-amino-acid tailpiece containing phosphorylation sites, The observed differences in the cooperativity of unfolding myosin II and skeletal muscle myosin relate to differences between rod structures and possibly also head-rod interactions. C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. RI Korn, Edward/F-9929-2012; Redowicz, Maria Jolanta/R-4083-2016 NR 39 TC 19 Z9 19 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR 1 PY 1995 VL 318 IS 1 BP 207 EP 214 DI 10.1006/abbi.1995.1222 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QU077 UT WOS:A1995QU07700027 PM 7726563 ER PT J AU GAGLIARDINO, JJ BORELLI, MI BOSCHERO, AC ROJAS, E ATWATER, I AF GAGLIARDINO, JJ BORELLI, MI BOSCHERO, AC ROJAS, E ATWATER, I TI MODULATORY MECHANISM OF ACTH ON INSULIN-SECRETION - EFFECT ON CYTOSOLIC CA2+, MEMBRANE-POTENTIAL AND CA2+-ATPASE ACTIVITY SO ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY LA English DT Article DE INSULIN SECRETION; PANCREATIC BETA-CELLS; PROOPIOMELANOCORTIN; CYTOSOLIC [CA2+]; MEMBRANE POTENTIAL ID PANCREATIC-ISLET CELLS; PROOPIOMELANOCORTIN GENE; GROWTH-HORMONE; B-CELL; RELEASE; LANGERHANS; PEPTIDE; TROPIN; PLASMA AB The aim of this work was to get some insight into the mechanism by which ACTH produces its enhancing effect on glucose-induced insulin secretion. For this purpose, we have determined: a) the release of insulin by isolated rat islets incubated with 3.3 or 16.6 mM glucose with or without the addition of 500 pg/ml ACTH, together with the changes induced by ACTH on b) cytosolic [Ca2+] of isolated B cells, c) islet plasma membrane Ca2+-ATPase activity and d) changes in membrane potential of single mouse islets. ACTH significantly enhanced the release of insulin elicited by either 3.3 or 16.6 mM glucose. This hormone concentratian also induced a significant increase in the cytosolic [Ca2+] in isolated B cells. ACTH did riot produce B cell membrane depolarization. Conversely, ACTH produced a significant decrease in islet plasma membrane Ca2+-ATPase activity. These results suggest that ACTH in concentrations similar to those attained by the endogenous peptide at the islet interstitium exerts its positive modulation on glucose-induced secretion of insulin, at least partly through its increasing effect oil cytosolic [Ca2+] of B cells. The latter might be the consequence of the decreasing effect of ACTH on Ca2+ -ATPase activity rather than to stimulation of voltage-dependent Ca2+-channels. C1 NIDDK,CELL BIOL & GENET LAB,BETHESDA,MD 20892. RP GAGLIARDINO, JJ (reprint author), UNLP,CONICET,CENEXA,CTR ENDOCRINOL EXPTL & APLICADA,CALLES 60 & 120,RA-1900 LA PLATA,ARGENTINA. RI Boschero, Antonio/O-7525-2014 OI Boschero, Antonio/0000-0003-3829-8570 NR 36 TC 6 Z9 6 U1 0 U2 0 PU SWETS ZEITLINGER BV PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1381-3455 J9 ARCH PHYSIOL BIOCHEM JI Arch. Physiol. Biochem. PD APR PY 1995 VL 103 IS 1 BP 73 EP 78 DI 10.3109/13813459509007567 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Endocrinology & Metabolism; Physiology SC Biochemistry & Molecular Biology; Biophysics; Endocrinology & Metabolism; Physiology GA RP695 UT WOS:A1995RP69500013 PM 8574781 ER PT J AU TSIGOS, C PAPANICOLAOU, DA CHROUSOS, GP AF TSIGOS, C PAPANICOLAOU, DA CHROUSOS, GP TI ADVANCES IN THE DIAGNOSIS AND TREATMENT OF CUSHINGS-SYNDROME SO BAILLIERES CLINICAL ENDOCRINOLOGY AND METABOLISM LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; BRONCHIAL CARCINOID-TUMORS; DIFFERENTIAL-DIAGNOSIS; ADRENOCORTICAL DISEASE; STIMULATION TEST; ADRENAL-TUMORS; ACTH; HYPERCORTISOLISM; DEXAMETHASONE; CT C1 NIH,PEDIAT ENDOCRINOL TRAINING PROGRAM,BETHESDA,MD 20892. RP TSIGOS, C (reprint author), NIH,DEV ENDOCRINOL BRANCH,PEDIAT ENDOCRINOL SECT,BLDG 10,ROOM 10N262,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 72 TC 19 Z9 19 U1 0 U2 0 PU BAILLIERE TINDALL PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0950-351X J9 BAILLIERE CLIN ENDOC JI Baillieres Clin. Endocrinol. Metab. PD APR PY 1995 VL 9 IS 2 BP 315 EP 336 DI 10.1016/S0950-351X(95)80354-8 PG 22 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QX905 UT WOS:A1995QX90500006 PM 7625987 ER PT J AU HAMBRECHT, FT AF HAMBRECHT, FT TI VISUAL PROSTHESES BASED ON DIRECT INTERFACES WITH THE VISUAL-SYSTEM SO BAILLIERES CLINICAL NEUROLOGY LA English DT Article ID HUMAN OCCIPITAL CORTEX; ELECTRICAL-STIMULATION; BLIND; MICROSTIMULATION; MICROELECTRODE RP HAMBRECHT, FT (reprint author), NIH,CTR CLIN,FED BLDG,ROOM 916,BETHESDA,MD 20892, USA. NR 24 TC 26 Z9 26 U1 0 U2 2 PU BAILLIERE TINDALL PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0961-0421 J9 BAILLIERE CLIN NEUR JI Baillieres Clin. Neurol. PD APR PY 1995 VL 4 IS 1 BP 147 EP 165 PG 19 WC Clinical Neurology SC Neurosciences & Neurology GA QY225 UT WOS:A1995QY22500011 PM 7633780 ER PT J AU MALKOVA, L MISHKIN, M BACHEVALIER, J AF MALKOVA, L MISHKIN, M BACHEVALIER, J TI LONG-TERM EFFECTS OF SELECTIVE NEONATAL TEMPORAL-LOBE LESIONS ON LEARNING AND MEMORY IN MONKEYS SO BEHAVIORAL NEUROSCIENCE LA English DT Article ID INTERTRIAL INTERVALS; HIPPOCAMPUS; AMYGDALA; REMOVAL; INFANT AB Rhesus monkeys with neonatal damage to either the medial temporal lobe or the inferior temporal cortical area TE, and their normal controls, were reassessed in visual habit formation (24-hour intertrial interval task) and visual recognition (delayed nonmatching to sample; DNMS) at 4-5 years of age and then tested on tactile and spatial DNMS. Results on the two visual tasks were the same as those obtained when the monkeys were under 1 year of age. Specifically, early medial temporal lesions, like late lesions, left habit formation intact but severely impaired recognition memory. Furthermore, the memory deficit extended to the tactile and spatial modalities. By contrast, early damage to TE, unlike late damage to it, yielded only mild deficits on both visual tasks and had no effect on tactile or spatial DNMS. Compensatory mechanisms that promote substantial and permanent recovery thus appear to be available after neonatal TE lesions but not after neonatal medial temporal lesions. RP MALKOVA, L (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 9,BETHESDA,MD 20892, USA. FU NIMH NIH HHS [MH49728] NR 27 TC 41 Z9 41 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0735-7044 J9 BEHAV NEUROSCI JI Behav. Neurosci. PD APR PY 1995 VL 109 IS 2 BP 212 EP 226 DI 10.1037/0735-7044.109.2.212 PG 15 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA QU667 UT WOS:A1995QU66700004 PM 7619312 ER PT J AU AMBROSIO, E GOLDBERG, SR ELMER, GI AF AMBROSIO, E GOLDBERG, SR ELMER, GI TI BEHAVIOR GENETIC INVESTIGATION OF THE RELATIONSHIP BETWEEN SPONTANEOUS LOCOMOTOR-ACTIVITY AND THE ACQUISITION OF MORPHINE SELF-ADMINISTRATION BEHAVIOR SO BEHAVIOURAL PHARMACOLOGY LA English DT Article DE ACI; BEHAVIOR GENETICS; F344; LEWIS; LOCOMOTOR ACTIVITY; MORPHINE; NBR; RAT; SELF-ADMINISTRATION ID INBRED RAT STRAINS; FISCHER; LEWIS; VULNERABILITY; ADDICTION; STRESS AB There is a significant degree of individual variability in response to drugs of abuse. A goal of behavior genetic studies has been to determine the extent to which observed heterogeneity in drug use can be attributed to genetic and environmental factors and to identify the neurobiological factors involved in vulnerability. Recent hypotheses regarding the predictive value of spontaneous locomotor activity in the acquisition of drug-reinforced behavior are amenable to testing using a behavior genetics approach. Genetic differences in locomotor response to a novel environment were determined in naive and catheterized Lewis, F344, NBR and ACI rats. Operant drug-reinforced behavior was examined in a 23 h access paradigm in which each lever press by a rat produced a 1 mg/kg injection of morphine with a 30 s timeout period (FR 1:TO 30''). Acquisition (7 days), extinction (6 days) and reacquisition (7 days) of morphine self-administration behavior was investigated in all four inbred strains. Large genetic differences in the rate of acquisition and extinction of morphine self-administration were found. Lewis rats responded at high rates beginning in the first two days, whereas F344 rats initially responded at low rates and responding increased gradually over seven days. NBR and ACI rats responded at intermediate levels. When vehicle was substituted for drug there was a significant effect of genotype on the rate of extinction; F344 and ACI increased responding to greater than 175% of drug-response levels, whereas the Lewis response rate decreased gradually and NBR response rate decreased immediately during the first several days. When drug was available again, rates of reacquisition did not differ from original acquisition rates. Drug maintained significantly greater amounts of behavior than vehicle in the Lewis, F344 and NBR rats and was thus shown to serve as a positive reinforcer in these three strains under these conditions. There was a significant genetic correlation among strains between drug intake during the first five days of acquisition and spontaneous locomotor response to a novel environment in catheterized rats. Only the ACI rats showed a significant within-strain correlation. The positive relationship between rate of acquisition of self-administration behavior and locomotor activity suggests that these two traits are influenced by common or closely linked genes. To this end, the neurobiological substrates that mediate spontaneous locomotor behavior under these environmental conditions may act, in part, as a template for determining the neurobiological substrates that mediate the relative rate of acquisition of morphine-taking behavior under these conditions. C1 NIDA,ADDICT RES CTR,DIV INTRAMURAL RES,PRECLIN PHARMACOL LAB,BEHAV PHARMACOL & GENET SECT,BALTIMORE,MD 21224. UNIV NACL EDUC DISTANCIA,DEPT PSICOBIOL,E-28040 MADRID,SPAIN. NR 26 TC 106 Z9 109 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8810 J9 BEHAV PHARMACOL JI Behav. Pharmacol. PD APR PY 1995 VL 6 IS 3 BP 229 EP 237 PG 9 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA QU950 UT WOS:A1995QU95000003 ER PT J AU WITKIN, JM ACRI, JB AF WITKIN, JM ACRI, JB TI EFFECTS OF IFENPRODIL ON STIMULATORY, DISCRIMINATIVE STIMULUS, AND CONVULSANT EFFECTS OF COCAINE SO BEHAVIOURAL PHARMACOLOGY LA English DT Article DE COCAINE; CONVULSIONS; DISCRIMINATIVE STIMULUS EFFECTS; DOPAMINE UPTAKE INHIBITORS; FIXED-INTERVAL RESPONDING; IFENPRODIL; LOCOMOTOR ACTIVITY; MICE; RATS ID SCHEDULE-CONTROLLED BEHAVIOR; SIGMA-BINDING SITES; DOPAMINE UPTAKE; RAT-BRAIN; NMDA RECEPTOR; ANTAGONISTS; SL-82.0715; INHIBITORS; COMPLEX; MK-801 AB Ifenprodil, like cocaine, binds to the dopamine transporter and blocks uptake of dopamine. In this study, the ability of ifenprodil to mimic, enhance or block behavioral and toxic effects of cocaine was evaluated. Fixed-interval responding maintained by food presentation In rats was increased by cocaine but decreased by ifenprodil. Low rates of responding during timeout periods were also increased by cocaine but not ifenprodil. Ifenprodil neither increased locomotor activity nor augmented the stimulatory effect of cocaine; however, ifenprodil attenuated the stimulant effects of cocaine at doses 0.5 log unit lower than those required to reduce spontaneous activity when given alone. Ifenprodil neither substituted for nor augmented the discriminative stimulus effects of cocaine in rats discriminating 10 mg/kg cocaine from saline. In contrast to cocaine, ifenprodil did not produce convulsions or signs of proconvulsant activity, and ifenprodil reduced the percentage of mice convulsing in the presence of cocaine. These results suggest that pharmacological actions in addition to blockade of dopamine uptake or novel interactions with the dopamine transporter may contribute to the non-stimulant behavioral profile and cocaine-blocking actions of ifenprodil. RP WITKIN, JM (reprint author), NIDA,ADDICT RES CTR,PSYCHOBIOL SECT,DRUG DEV GRP,POB 5180,BALTIMORE,MD 21224, USA. NR 61 TC 11 Z9 12 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8810 J9 BEHAV PHARMACOL JI Behav. Pharmacol. PD APR PY 1995 VL 6 IS 3 BP 245 EP 253 PG 9 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA QU950 UT WOS:A1995QU95000005 ER PT J AU HAHN, SH TANNER, MS DANKE, DM GAHL, WA AF HAHN, SH TANNER, MS DANKE, DM GAHL, WA TI NORMAL METALLOTHIONEIN SYNTHESIS IN FIBROBLASTS OBTAINED FROM CHILDREN WITH INDIAN CHILDHOOD CIRRHOSIS OR COPPER-ASSOCIATED CHILDHOOD CIRRHOSIS SO BIOCHEMICAL AND MOLECULAR MEDICINE LA English DT Note ID WILSONS-DISEASE; GENE; LIVER AB We previously demonstrated decreased metallothionein (MT) synthesis in cultured fibroblasts obtained from an American boy with findings typical of Indian Childhood Cirrhosis (ICC). We now report normal basal, copper-induced, and zinc-induced MT synthesis in the fibroblasts of two Indian boys and one Irish boy with typical ICC and one Indian boy with copper-associated childhood cirrhosis. This suggests that etiologies other than impaired MT production should be sought as the primary defect in these disorders. (C) 1995 Academic Press, Inc. C1 UNIV SHEFFIELD,SHEFFIELD CHILDRENS HOSP,DEPT PAEDIAT,SHEFFIELD S10 2TH,S YORKSHIRE,ENGLAND. ROYAL CHILDRENS HOSP,MURDOCH INST,MELBOURNE,VIC 3052,AUSTRALIA. RP HAHN, SH (reprint author), NICHHD,HUMAN GENET BRANCH,HUMAN BIOCHEM GENET SECT,BETHESDA,MD 20892, USA. NR 23 TC 61 Z9 63 U1 1 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 1077-3150 J9 BIOCHEM MOL MED JI Biochem. Mol. Med. PD APR PY 1995 VL 54 IS 2 BP 142 EP 145 DI 10.1006/bmme.1995.1021 PG 4 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA RD089 UT WOS:A1995RD08900011 PM 8581360 ER PT J AU KREITMAN, RJ PASTAN, I AF KREITMAN, RJ PASTAN, I TI IMPORTANCE OF THE GLUTAMATE RESIDUE OF KDEL IN INCREASING THE CYTOTOXICITY OF PSEUDOMONAS EXOTOXIN DERIVATIVES AND FOR INCREASED BINDING TO THE KDEL RECEPTOR SO BIOCHEMICAL JOURNAL LA English DT Article ID LUMINAL ER PROTEINS; ENDOPLASMIC-RETICULUM PROTEINS; RAT-LIVER; ANTI-TAC; DISULFIDE ISOMERASE; RETENTION SIGNAL; CHIMERIC TOXIN; SEQUENCE; GENE; IMMUNOTOXIN AB It was previously shown that amino acids 609-613 (REDLK) at the C-terminus of Pseudomonas exotoxin (PE) are necessary for cytotoxicity, presumably by directing the toxin to the endoplasmic reticulum (ER) [Chaudhary, Jinno, FitzGerald and Pastan (1990) Proc. Natl. Acad. Sci. U.S.A. 87, 308-312]. Using the anti-[interleukin 2 receptor (IL2R)] immunotoxin anti-Tac(Fv)PE38 (AT-PE38REDLK), it was found that removing the terminal lysine did not alter the activity, but replacing REDL with KDEL, the most common ER retention sequence, increased activity. To determine which amino acid in KDEL was responsible for the increase in activity, we tested eight C-terminal mutants of AT-PE38REDLK. Using IL2R-bearing MT-1 cells, we found that the glutamate residue of KDEL was required for high activity, as the cytotoxicity of AT-PE38 ending in KDEL, RDEL, KEEL or REEL was much greater than that of AT-PE38 ending in REDL, KEDL, RDDL or KDDL. Using freshly isolated lymphocytic leukaemia cells, AT-PE38 ending in KDEL, REEL or RDEL was more than 100-fold more cytotoxic than AT-PE38 ending in KEDL, REDL, RDDL or the native sequence REDLK. The RDEL sequence also improved the cytotoxic activity of an interleukin 4-PE38 toxin fusion protein. Improved cytotoxic activity correlated with improved binding of the C-termini to the KDEL receptor on rat Golgi membranes. These data indicate that the glutamate residue of KDEL improves the cytotoxicity of PE by increasing binding to a sorting receptor which transports the toxin from the transrecticular Golgi apparatus to the ER, where it is translocated to the cytosol and inhibits protein synthesis. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 40 TC 100 Z9 105 U1 1 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD APR 1 PY 1995 VL 307 BP 29 EP 37 PN 1 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QR101 UT WOS:A1995QR10100006 PM 7717988 ER PT J AU HASAN, CM HOSSAIN, MA RASHID, MA AF HASAN, CM HOSSAIN, MA RASHID, MA TI CLERODANE DITERPENOIDS FROM POLYALTHIA-LONGIFOLIA VAR PENDULLA SO BIOCHEMICAL SYSTEMATICS AND ECOLOGY LA English DT Note DE POLYALTHIA LONGIFOLIA; PENDULLA; ANNONACEAE; CLERODANE DITERPENOIDS; CHEMOTAXONOMY ID OCCURRING TERPENE DERIVATIVES; KOLAVANE; VIRIDIS C1 UNIV DHAKA,DEPT PHARM,DHAKA 1000,BANGLADESH. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. RP HASAN, CM (reprint author), DRUGS ADM,105-106 MOTJHEEL COMMERCIAL AREA,DHAKA 1000,BANGLADESH. NR 13 TC 2 Z9 3 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0305-1978 J9 BIOCHEM SYST ECOL JI Biochem. Syst. Ecol. PD APR PY 1995 VL 23 IS 3 BP 331 EP 332 DI 10.1016/0305-1978(95)00002-C PG 2 WC Biochemistry & Molecular Biology; Ecology; Evolutionary Biology SC Biochemistry & Molecular Biology; Environmental Sciences & Ecology; Evolutionary Biology GA RE639 UT WOS:A1995RE63900015 ER PT J AU MALINOWSKI, NM CYSYK, RL AUGUST, EM AF MALINOWSKI, NM CYSYK, RL AUGUST, EM TI A FILTER-PAPER ASSAY FOR HYALURONIC-ACID SYNTHETASE - APPLICATION TO THE ENZYME FROM SWISS-3T3-FIBROBLASTS SO BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL LA English DT Article ID DIFFERENTIATED TERATOCARCINOMA CELLS; OLIGODENDROGLIOMA CELLS; GROWTH-PHASE; SYNTHASE; STIMULATION; MECHANISM AB An improved assay for hyaluronic acid (HA) synthetase is described that is suitable for rapid processing of large numbers of samples. High background levels of unincorporated radioactivity are removed by passage of the reaction through a Sephadex G-50 spin column. The labeled HA product is then precipitated onto glass fiber filters with cetylpyridinium chloride. Apparent Km values for HA synthetase from Swiss 3T3 fibroblasts are 10.8 and 58.4 mu M for UDP-glucuronic acid and UDP-N-acetylglucosamine, respectively. HA synthetase activity of quiescent cells is 4.5% of that found in actively growing cells and is stimulated in response to 10% calf serum. There is a greater than 10-fold increase in HA synthetase activity when cells are harvested with hyaluronidase as compared with trypsin. RP MALINOWSKI, NM (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892, USA. NR 23 TC 3 Z9 3 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 1039-9712 J9 BIOCHEM MOL BIOL INT JI Biochem. Mol. Biol. Int. PD APR PY 1995 VL 35 IS 5 BP 1123 EP 1132 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB590 UT WOS:A1995TB59000023 PM 7549931 ER PT J AU NICKLAUS, MC WANG, SM DRISCOLL, JS MILNE, GWA AF NICKLAUS, MC WANG, SM DRISCOLL, JS MILNE, GWA TI CONFORMATIONAL-CHANGES OF SMALL MOLECULES BINDING TO PROTEINS SO BIOORGANIC & MEDICINAL CHEMISTRY LA English DT Article ID CRYSTALLOGRAPHIC DATA; CHEMICAL STRUCTURES; LIGAND-BINDING; DATA-BANK; CAMBRIDGE; SEARCH; CONCORD; DISPLAY; PROGRAM; MODEL AB Flexible molecules change their conformation upon binding to a protein. This was shown by the analysis of small molecules whose structures have been determined by X-ray crystallography of both the pure compound and the compound bound to a protein. Thirty-three compounds present both in the Cambridge Structural Database and the Brookhaven Protein Data Bank were analyzed, and both were compared with the global energy minimum conformation calculated by the molecular mechanics program CHARMm. It was found that the conformation bound to the protein differs from that in the crystal structure and also from that of the global energy minimum, and the degree of deformation depends upon the number of freely rotatable bonds in the molecule. Analysis of the conformational energies of the flexible molecules showed that, for most of those compounds, both the crystal and the protein-bound conformations are energetically well above the global minimum, and, in many cases, not even in any local energy minimum. Semi-empirical calculations performed for a select number of structures, using both the AM1 and PM3 hamiltonians, confirmed these results. These findings are discussed as to their impact upon contemporary methods of drug design. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MED CHEM LAB,BETHESDA,MD 20892. RI Nicklaus, Marc/N-4183-2014 NR 45 TC 167 Z9 171 U1 5 U2 17 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0968-0896 J9 BIOORGAN MED CHEM JI Bioorg. Med. Chem. PD APR PY 1995 VL 3 IS 4 BP 411 EP 428 DI 10.1016/0968-0896(95)00031-B PG 18 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry, Organic SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA RB118 UT WOS:A1995RB11800009 PM 8581425 ER PT J AU MINTON, AP AF MINTON, AP TI CONFINEMENT AS A DETERMINANT OF MACROMOLECULAR STRUCTURE AND REACTIVITY .2. EFFECTS OF WEAKLY ATTRACTIVE INTERACTIONS BETWEEN CONFINED MACROSOLUTES AND CONFINING STRUCTURES SO BIOPHYSICAL JOURNAL LA English DT Article AB The effect of weak, nonspecific interaction between molecules confined within restricted elements of volume (''pores'') and the boundary surfaces of the pore, upon the reactivity and physical state of the confined molecules, is explored by means of simple models. A confined molecule is represented by a rectangular parallelopiped having one of six orientations aligned with the cartesian coordinate axes, and the confining volume element is represented by a pair of parallel surfaces (planar pore), a tube of square cross section (square pore), or a cubical box (cubical pore). Weak interactions are modeled by square-well potentials having a defined range and well depth. Partition coefficients for distribution of molecules between the bulk and confined phase are calculated using an extension of the statistical-thermodynamic theory of Giddings et al. (1968). It is calculated that surface attraction with a potential of only a few kcal/mol monomer may result in large increases in the extent of self- or heteroassociation of confined molecules (as much as several orders of magnitude in favorable cases) linked to adsorption of the oligomeric species onto boundary surfaces. Calculations are also presented suggesting that surface attraction can lead to deformation of the native structure of adsorbed macromolecules. It is suggested that these findings are relevant to an understanding of the structure of eukaryotic cytoplasm. RP MINTON, AP (reprint author), NIDDKD,BIOCHEM PHARMACOL LAB,PHYS BIOL SECT,BLDG 8,ROOM 226,BETHESDA,MD 20892, USA. NR 12 TC 51 Z9 53 U1 1 U2 5 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1995 VL 68 IS 4 BP 1311 EP 1322 PG 12 WC Biophysics SC Biophysics GA RD163 UT WOS:A1995RD16300009 PM 7787020 ER PT J AU MAZUR, J JERNIGAN, RL AF MAZUR, J JERNIGAN, RL TI COMPARISON OF ROTATION MODELS FOR DESCRIBING DNA CONFORMATIONS - APPLICATION TO STATIC AND POLYMORPHIC FORMS SO BIOPHYSICAL JOURNAL LA English DT Article ID IRREGULAR NUCLEIC-ACIDS; DOUBLE-HELICAL DNA; SEQUENCE DEPENDENCE; BASE SEQUENCE; CURVED DNA; FLEXIBILITY; DODECAMER; CURVATURE AB A new method, based on a space-fixed rotation axis, or local helix axis, is proposed for the calculation of the relative orientation variables for a sequence of base pairs. With this method, orientation variables are determined through the rotation of a base pair about this axis. These variables uniquely determine a set of helical variables, similar to the roll, tilt, and twist, commonly used for a description of spatial orientations of internally rigid base pairs. The proposed identification of roll and tilt with the direction cosines of the space-fixed rotation axis agrees well with their customary definitions as the openings of the angles between adjoining base pairs toward the minor groove and toward the ascending (5' to 3') backbone strand, respectively. These new variables permit a more direct physical comprehension of DNA conformations and also the behavior of self-complementary sequences. These direction cosines, together with the rotation angle about the space-fixed axis, form a set of three independent orientation variables of the bases that afford some advantages over the variously defined twist, roll, and tilt angles, either for static or average forms. An example for the static form of these variables is shown through their use to interpret crystal coordinates. An example for the average of orientation variables is based on statistical calculations. In this example, the orientation variables, together with the translational variables that describe the relative displacements of a pair of adjacent base pairs, form a canonically distributed ensemble in phase space spanned by these variables. Two sets of conformational variables are generated by using two different methods for performing rotation operations on the sequences of base pairs. The first method is based on the new single rotation about a space-fixed axis of rotation. This space-fixed axis of rotation is, in fact, the local helicai axis as constructed previously by others. The second method is based on three consecutive rotations by Euler angles. Because of large flexibilities and anisotropies along various conformational variables of DNA base pairs, the two sets of generated conformational variables, based on these two different methods of performing rotation operations, lead to slightly different sets of structurally different, but energetically equivalent, spatial arrangements of the base pairs. C1 NCI,DIV CANC BIOL DIAG & CTR,MATH BIOL LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES FDN,PROGRAM RESOURCES INC DYNCORP,FREDERICK BIOMED SUPER COMP LAB,BETHESDA,MD 20892. RI Jernigan, Robert/A-5421-2012 FU NCI NIH HHS [N01-CO-74102] NR 35 TC 8 Z9 8 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1995 VL 68 IS 4 BP 1472 EP 1489 PG 18 WC Biophysics SC Biophysics GA RD163 UT WOS:A1995RD16300025 PM 7787033 ER PT J AU FACEMYER, KC SELLERS, JR CREMO, CR AF FACEMYER, KC SELLERS, JR CREMO, CR TI 2 HEADS ARE REQUIRED FOR PHOSPHORYLATION-DEPENDENT REGULATION OF SMOOTH-MUSCLE MYOSIN SO BIOPHYSICAL JOURNAL LA English DT Article; Proceedings Paper CT 7th Biophysical Discussions on Molecular Motors - Structure, Mechanics and Energy Transduction CY OCT 21-23, 1994 CL AIRLIE, VA SP US PHS, Natl Sci Fdn C1 NHLBI,BETHESDA,MD 20892. MOLEC CARDIOL LAB,BETHESDA,MD 20892. RP FACEMYER, KC (reprint author), WASHINGTON STATE UNIV,DEPT BIOCHEM & BIOPHYS,PULLMAN,WA 99164, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1995 VL 68 IS 4 SU S BP S228 EP S228 PG 1 WC Biophysics SC Biophysics GA RK090 UT WOS:A1995RK09000053 PM 7787082 ER PT J AU ITOH, K ADELSTEIN, RS AF ITOH, K ADELSTEIN, RS TI NEURONAL CELL EXPRESSION OF VERTEBRATE NONMUSCLE MYOSIN HEAVY-CHAIN II-B SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1995 VL 68 IS 4 SU S BP S334 EP S334 PG 1 WC Biophysics SC Biophysics GA RK090 UT WOS:A1995RK09000080 ER PT J AU IWASA, KH LI, M JIA, M AF IWASA, KH LI, M JIA, M TI CAN MEMBRANE-PROTEINS DRIVE A CELL SO BIOPHYSICAL JOURNAL LA English DT Article; Proceedings Paper CT 7th Biophysical Discussions on Molecular Motors - Structure, Mechanics and Energy Transduction CY OCT 21-23, 1994 CL AIRLIE, VA SP US PHS, Natl Sci Fdn ID OUTER HAIR CELL; CAPACITANCE C1 NINCDS,BIOPHYS SECT,BETHESDA,MD 20892. RP IWASA, KH (reprint author), NIDCD,BIOPHYS SECT,BETHESDA,MD 20892, USA. NR 8 TC 4 Z9 4 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1995 VL 68 IS 4 SU S BP S214 EP S214 PG 1 WC Biophysics SC Biophysics GA RK090 UT WOS:A1995RK09000041 PM 7787070 ER PT J AU KELLEY, CA ADELSTEIN, RS AF KELLEY, CA ADELSTEIN, RS TI CHARACTERIZATION OF MYOSIN-II ISOFORMS CONTAINING INSERTIONS OF AMINO-ACIDS IN THE FLEXIBLE LOOP NEAR THE ATP-BINDING POCKET SO BIOPHYSICAL JOURNAL LA English DT Article; Proceedings Paper CT 7th Biophysical Discussions on Molecular Motors - Structure, Mechanics and Energy Transduction CY OCT 21-23, 1994 CL AIRLIE, VA SP US PHS, Natl Sci Fdn ID CHAIN MESSENGER-RNAS; HEAVY-CHAIN; NONMUSCLE MYOSIN; B ISOFORM; CHICKEN; REGION; CDNA; IDENTIFICATION; CLONING; GENE RP KELLEY, CA (reprint author), NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892, USA. NR 10 TC 4 Z9 4 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1995 VL 68 IS 4 SU S BP S225 EP S225 PG 1 WC Biophysics SC Biophysics GA RK090 UT WOS:A1995RK09000050 PM 7787079 ER PT J AU SIDOROVA, NY RAU, DC AF SIDOROVA, NY RAU, DC TI THE OSMOTIC SENSITIVITY OF NETROPSIN ANALOG BINDING TO DNA SO BIOPOLYMERS LA English DT Article ID HYDRATION FORCES; PROTEIN SOLVATION; DOUBLE HELICES; WATER; SPECIFICITY; CYTOPLASM; CHANNEL; DRUG AB The binding of a netropsin analogue to random sequence DNA monitored by CD, is seen dependent on the concentration of neutral solutes. The binding free energy decreases linearly with solute osmolal concentration and the magnitude of the effect is insensitive to the chemical identity of the solute for betaine, sorbitol, and triethylene glycol. These solutes appear to modulate binding through their effect on water activity and changes in the hydration of the drug and DNA in the complex reaction, not through a direct interaction with the reactants or the product. The dependence of binding constant on solute concentration can be interpreted as an additional binding of some 50-60 extra solute excluding water molecules by the complex. A water sensitivity of drug binding is further seen from the dependence of binding constants on the type of anion in solution. Anions in the Hofmeister series strongly affect bulk water free energies and entropies. The differences in netropsin analogue binding to DNA with Cl-, F-, and ClO4- are consistent with the effect observed with neutral solutes. The ability to measure changes in water binding associated with a specific DNA interaction is a first step toward correlating changes in hydration with the strength and specificity of binding. (C) 1995 John Wiley & Sons, Inc. C1 NIDDK,BETHESDA,MD 20892. RP SIDOROVA, NY (reprint author), NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892, USA. NR 34 TC 42 Z9 43 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PD APR PY 1995 VL 35 IS 4 BP 377 EP 384 DI 10.1002/bip.360350405 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QM332 UT WOS:A1995QM33200004 PM 7711278 ER PT J AU VANEK, PG FABIAN, SJ FISHER, CL CHIRIKJIAN, JG COLLIER, GB AF VANEK, PG FABIAN, SJ FISHER, CL CHIRIKJIAN, JG COLLIER, GB TI ALTERNATIVE TO POLYACRYLAMIDE GELS IMPROVES THE ELECTROPHORETIC MOBILITY SHIFT ASSAY SO BIOTECHNIQUES LA English DT Note AB In this paper we outline a simplified protocol for the electrophoretic mobility shift assay utilizing TreviGelTM 500, a nontoxic alternative to polyacrylamide. The TreviGel 500 matrix combines the strength and resolution of polyacrylamide with the simplicity and flexibility of agarose in the casting of gels. Therefore, this method provides a simple, rapid and nontoxic alternative to current protocols for the investigation of protein:DNA interactions. C1 NCI,FREDERICK,MD 21701. TREVIGEN INC,GAITHERSBURG,MD. RP VANEK, PG (reprint author), GEORGETOWN UNIV,MED CTR,DEPT BIOCHEM,WASHINGTON,DC 20007, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD APR PY 1995 VL 18 IS 4 BP 704 EP 706 PG 3 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QR215 UT WOS:A1995QR21500035 PM 7598903 ER PT J AU ALTER, HJ AF ALTER, HJ TI TO C OR NOT TO C - THESE ARE THE QUESTIONS SO BLOOD LA English DT Review ID NON-B-HEPATITIS; TO-INFANT TRANSMISSION; POLYMERASE CHAIN-REACTION; PORPHYRIA-CUTANEA-TARDA; CHRONIC LIVER-DISEASE; NON-A-HEPATITIS; VIRUS-INFECTION; POSTTRANSFUSION HEPATITIS; HEPATOCELLULAR-CARCINOMA; CONTROLLED TRIAL RP ALTER, HJ (reprint author), NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,INFECT DIS SECT,BETHESDA,MD 20892, USA. NR 88 TC 256 Z9 261 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1995 VL 85 IS 7 BP 1681 EP 1695 PG 15 WC Hematology SC Hematology GA QP613 UT WOS:A1995QP61300001 PM 7535582 ER PT J AU WESSEL, K ZEFFIRO, T LEU, JS TORO, C HALLETT, M AF WESSEL, K ZEFFIRO, T LEU, JS TORO, C HALLETT, M TI REGIONAL CEREBRAL BLOOD-FLOW DURING A SELF-PACED SEQUENTIAL FINGER OPPOSITION TASK IN PATIENTS WITH CEREBELLAR DEGENERATION SO BRAIN LA English DT Article DE REGIONAL CEREBRAL BLOOD FLOW; CEREBELLAR DEGENERATION; MOTOR CORTEX; VOLUNTARY MOVEMENT; SUPPLEMENTARY MOTOR AREA ID POSITRON EMISSION TOMOGRAPHY; SUPPLEMENTARY MOTOR AREA; VOLUNTARY MOVEMENTS; BASAL GANGLIA; CORTICOSPINAL PROJECTIONS; CORTICAL AREAS; CEREBELLOCEREBRAL DIASCHISIS; INTRAVENOUS (H2O)-O-15; ARCUATE PREMOTOR; RHESUS-MONKEY AB The brain regions controlling self-paced sequential finger movements in patients with cerebellar degeneration were studied by measuring changes in regional cerebral blood flow (rCBF) in eight patients using bolus injections of (H2O)-O-15 and PET The results were compared with those obtained in eight normal age-matched control subjects. Patients and control subjects performed a self-paced sequential finger opposition task with the right hand, completing a sequence of movements every 4-6 s. Both groups had strong increases in the adjusted rCBF contralaterally in the primary motor cortex (M1) and ventral premotor area (PMv), in the caudal supplementary motor area (SMA) and cingulate motor area (CMA), and bilaterally in the prefrontal cortex (PFC), the lobus parietalis inferior (LPI), putamen and cerebellum. The cerebellum, PMv, rostral CMA, PFC and LPI were move active in the control subjects than in the patients, and the M1, SMA, caudal CMA and putamen were more active in the patients than in the control subjects. The reduced activity of the cerebellar neurons in the patients produced a complex pattern of rCBF increases and decreases in other brain regions. Our results suggest that for the preparation and execution of sequential finger movements, patients with cerebellar degeneration use a medial premotor system, including the SMA and caudal CMA, as well as the MI and putamen, rather than the PMv, PFC, LPI and rostral CMA. RP WESSEL, K (reprint author), NINCDS, MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT, BLDG 36,ROOM 5N226, 10 CTR DR MSC 1428, BETHESDA, MD 20892 USA. NR 81 TC 43 Z9 43 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD APR PY 1995 VL 118 BP 379 EP 393 DI 10.1093/brain/118.2.379 PN 2 PG 15 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA QX852 UT WOS:A1995QX85200005 PM 7735880 ER PT J AU NEUMANN, HPH LIPS, CJM HSIA, YE ZBAR, B AF NEUMANN, HPH LIPS, CJM HSIA, YE ZBAR, B TI VON HIPPEL-LINDAU SYNDROME SO BRAIN PATHOLOGY LA English DT Article ID RENAL-CELL CARCINOMA; POSTERIOR-FOSSA HEMANGIOBLASTOMAS; BILATERAL PAPILLARY CYSTADENOMA; BILE-DUCT OBSTRUCTION; CEREBELLAR HEMANGIOBLASTOMA; VONHIPPELLINDAU DISEASE; PANCREATIC INVOLVEMENT; VHL DISEASE; DIAGNOSIS; TUMORS AB After a decade of intensive clinical and molecular genetic efforts the von Hippel-Lindau (VHL) gene was cloned in 1993. The open reading frame encodes the putative protein of 284 amino acids. A large number of different mutations have been identified so far, including single base mutations, deletions, rearrangements and more complex mutations. So far, in about 75% of the VHL families germline mutations were detected. Geno-phenotypic comparision has revealed specific mutations with distinct manifestation patterns. Not all of the 6 classical lesions (hemangioblastoma of the CNS, retinal angiomatosis, pancreatic cysts, renal cysts and carcinoma, pheochromocytoma and epididymal cystadenoma) are present in VHL families. Pedigrees with pheochromocytoma but without renal cancer in general have point mutations. These recent results provide insight in the pathogenesis of a multiorgan cancer susceptibility tumor suppressor gene and allow determination of carrier status. C1 UNIV UTRECHT HOSP,DEPT INTERNAL MED,3508 UTRECHT,NETHERLANDS. UNIV HAWAII MANOA,JOHN A BURNS SCH MED,HONOLULU,HI 96813. NCI,IMMUNOBIOL LAB,FREDERICK,MD 20892. RP NEUMANN, HPH (reprint author), UNIV FREIBURG,DEPT MED,DIV NEPHROL & HYPERTENS,D-79106 FREIBURG,GERMANY. NR 92 TC 91 Z9 94 U1 0 U2 1 PU INT SOC NEUROPATHOLOGY PI ZURICH PA ISN JOURNAL PO BOX, CH-8033 ZURICH, SWITZERLAND SN 1015-6305 J9 BRAIN PATHOL JI Brain Pathol. PD APR PY 1995 VL 5 IS 2 BP 181 EP 193 DI 10.1111/j.1750-3639.1995.tb00592.x PG 13 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA RC531 UT WOS:A1995RC53100007 PM 7670659 ER PT J AU SHEN, DW AKIYAMA, S SCHOENLEIN, P PASTAN, I GOTTESMAN, MM AF SHEN, DW AKIYAMA, S SCHOENLEIN, P PASTAN, I GOTTESMAN, MM TI CHARACTERIZATION OF HIGH-LEVEL CISPLATIN-RESISTANT CELL-LINES ESTABLISHED FROM A HUMAN HEPATOMA-CELL LINE AND HUMAN KB ADENOCARCINOMA CELLS - CROSS-RESISTANCE AND PROTEIN-CHANGES SO BRITISH JOURNAL OF CANCER LA English DT Article DE HEPATOMA CELLS; ADENOCARCINOMA CELLS; 2-DIMENSIONAL GEL ELECTROPHORESIS; CISPLATIN; CROSS-RESISTANCE ID MULTIDRUG-RESISTANCE; ACQUIRED-RESISTANCE; ALKYLATING-AGENTS; MDR1 GENE; CIS-DIAMMINEDICHLOROPLATINUM(II); DNA; EXPRESSION; INVITRO; REPAIR; SENSITIVITY AB Human liver carcinoma cells (BEL-7404) and human KB adenocarcinoma cells were selected by stepwise increases in cisplatin. Drug sensitivity assays indicated that the IC50 value for 7404-CP7.5 cells was 49 mu g ml(-1) cisplatin, 111-fold higher than for the parental hepatoma cells. The IC50 value for KB-CP10 cells was 38 pg ml(-1) cisplatin, which is 1152-fold higher than for the parental KB cells. The 7404-CP7.5 cells were cross-resistant to methotrexate (39 x), 5-fluorouracil (23 x) and 6-mercaptopurine (13 x), but were sensitive to drugs which are known substrates for the multidrug transporter (P-glycoprotein), including colchicine, vinblastine and actinomycin D. Similar cross-resistance patterns were observed for KB-CP10 cells. No evidence of DNA amplification or expression of the MDR1 gene was found. One-dimensional sodium dodecyl sulphate-polyacrylamide gel electrophoresis showed increases in 52 kDa protein(s) in both the soluble cytosolic and crude membrane fractions in 7404-CPr cells and in KB-CPr cells. The amount of 52 kDa protein was proportional to the degree of resistance of the 7404-CPr cells to cisplatin. Two-dimensional gel analysis demonstrated that two polypeptides of molecular mass 52 and 50 kDa were overexpressed in the membrane fractions in both 7404-CP20 and KB-CP20 cells. Using amino acid microsequencing and Western blotting, the major 52 kDa protein was identified as the mitochondrial heat shock protein hsp60. Two-dimensional gels of [S-35]methionine-labelled polypeptides showed many other changes, including reduction in soluble proteins of approximately 57 kDa molecular weight in KB-CP20 cells, and of 35 kDa in both 7404-CP20 and KB-CP20 cells. These results suggest that alterations of certain proteins occur commonly in cisplatin-resistant cells, particularly proteins of molecular weight 52 and 50 kDa. C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. KAGOSHIMA UNIV,FAC MED,INST CANC RES,DEPT CANC CHEMOTHERAPY,KAGOSHIMA 890,JAPAN. MED COLL GEORGIA,DEPT ANAT & CELLULAR BIOL,AUGUSTA,GA 30912. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 35 TC 68 Z9 71 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD APR PY 1995 VL 71 IS 4 BP 676 EP 683 DI 10.1038/bjc.1995.134 PG 8 WC Oncology SC Oncology GA QQ312 UT WOS:A1995QQ31200005 PM 7710928 ER PT J AU SCHNEIDER, E YAMAZAKI, H SINHA, BK COWAN, KH AF SCHNEIDER, E YAMAZAKI, H SINHA, BK COWAN, KH TI BUTHIONINE SULFOXIMINE-MEDIATED SENSITIZATION OF ETOPOSIDE-RESISTANT HUMAN BREAST-CANCER MCF7 CELLS OVEREXPRESSING THE MULTIDRUG RESISTANCE-ASSOCIATED PROTEIN INVOLVES INCREASED DRUG ACCUMULATION SO BRITISH JOURNAL OF CANCER LA English DT Article DE MRP; CHEMOSENSITISATION; DRUG ACCUMULATION; MULTIDRUG RESISTANCE ID CYTO-TOXICITY; GLUTATHIONE DEPLETION; P-GLYCOPROTEIN; HL60/AR CELLS; BINDING; LINES; POTENTIATION; SULFOXIMINE; METABOLISM; MECHANISMS AB Preincubation of etoposide-resistant human MCF7 breast cancer cells (MCF7/VP) with buthionine sulphoximine (BSO) resulted in their sensitisation to etoposide and vincristine. Chemosensitisation was accompanied by elevated intracellular drug levels. In contrast, simultaneous exposure to BSO did not result in increased drug accumulation. Similar, but quantitatively smaller, effects were also observed when sensitive wild-type MCF7/WT cells were treated with BSO. In agreement with its effect on drug accumulation, BSO pretreatment also increased VP-16-stimulated cleavable complex formation between DNA topoisomerase II and cellular DNA. BSO treatment also led to a significant increase in acid-precipitable VP-16 levels in MCF7/VP, but not MCF7/WT cells. In contrast, no clear effects of BSO on drug efflux were observed and drug retention was only minimally increased after BSO treatment of both MCF7/WT and MCF7/VP cells and no difference between the two cell lines was detected. Thus, chemosensitisation by BSO appeared to be mediated through increased intracellular drug concentrations and/or protein binding. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. RP SCHNEIDER, E (reprint author), NCI,MED BRANCH,BLDG 10,BETHESDA,MD 20892, USA. NR 23 TC 80 Z9 86 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD APR PY 1995 VL 71 IS 4 BP 738 EP 743 DI 10.1038/bjc.1995.144 PG 6 WC Oncology SC Oncology GA QQ312 UT WOS:A1995QQ31200015 PM 7710938 ER PT J AU KANNEL, WB THOM, TJ DAGOSTINO, RB AF KANNEL, WB THOM, TJ DAGOSTINO, RB TI CONTROLLING CARDIOVASCULAR-DISEASE - A CHALLENGE FOR THE 21ST-CENTURY SO BRITISH JOURNAL OF CLINICAL PRACTICE LA English DT Article ID CORONARY HEART-DISEASE; MYOCARDIAL-INFARCTION; SECONDARY PREVENTION; CONTROLLED TRIAL; BLOOD-PRESSURE; FINAL REPORT; HYPERTENSION; CHOLESTEROL; FRAMINGHAM; THERAPY AB Prospects for the prevention of cardiovascular disease are excellent now that modifiable predisposing lifestyles and personal attributes have been identified. Multivariate risk profiles facilitate the efficient selection by physicians of high-risk candidates for preventive measures. This paper reviews the public health measures that can improve the average level of major risk factors in the general population and educate the public to make healthier choices in their living habits. The potential for secondary prevention continues to improve, with thrombolytic therapy, beta-blockers, ACE inhibitors, anticoagulants, platelet inhibitors, myocardial revascularisation and aggressive risk factor management in persons who have survived clinical events. The need for trials - to determine the efficacy of correcting dyslipidaemia in the elderly, in women and in blacks, and to examine the benefit of antihypertensive therapy in preventing coronary disease using agents that do not adversely affect lipids or glucose tolerance - is stressed, as is the need to make a serious effort to prevent hypertension. C1 BOSTON UNIV,SCH MED,EVANS MEM RES FDN,DEPT MED,BOSTON,MA 02118. BOSTON UNIV,SCH MED,EVANS MEM RES FDN,PREVENT MED & EPIDEMIOL SECT,BOSTON,MA 02118. NHLBI,BETHESDA,MD 20892. BOSTON UNIV,COLL LIBERAL ARTS,DEPT MATH,BOSTON,MA 02118. NR 34 TC 0 Z9 0 U1 0 U2 0 PU MEDICOM INTERNATIONAL PI KINGSTON-UPON-THAMES PA QUADRANT, 118 LONDON RD, KINGSTON-UPON-THAMES, ENGLAND KT2 6QJ SN 0007-0947 J9 BRIT J CLIN PRACT JI Br. J. Clin. Pract. PD APR PY 1995 SU 78 BP 1 EP 15 PG 15 WC Medicine, General & Internal SC General & Internal Medicine GA QX286 UT WOS:A1995QX28600001 ER PT J AU RUPP, A AF RUPP, A TI THE ECONOMIC CONSEQUENCES OF NOT TREATING DEPRESSION SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT Workshop on Economic Aspects of Psychiatric Treatment Programmes CY OCT, 1992 CL VENICE, ITALY ID MENTAL-HEALTH TREATMENT; VALIDITY; PROGRAM AB Background. A conceptual framework is described for a broad cost-benefit evaluation of improved financial access to treatment of untreated affective disorders. Method. The analysis provides an estimate of the value of resources needed to provide improved access to treatment, and it compares these resources to the value of resources the improved access to treatment might save. Results. The cost-benefit analyses based on recent cost of mental illness studies provide some evidence that appropriately treating people with untreated affective disorders is cost-beneficial. Conclusion. Patients, providers and buyers of health care should be further encouraged to pay more attention and to commit more financial resources to the treatment of affective disorders. RP RUPP, A (reprint author), NIMH,MENTAL HLTH ECON RES PROGRAM,5600 FISHERS LANE,RM 10C-06,ROCKVILLE,MD 20857, USA. NR 27 TC 38 Z9 39 U1 2 U2 2 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD APR PY 1995 VL 166 SU 27 BP 29 EP 33 PG 5 WC Psychiatry SC Psychiatry GA QW136 UT WOS:A1995QW13600006 ER PT J AU FEIDT, WB ROOS, C AF FEIDT, WB ROOS, C TI ENVIRONMENTAL INFORMATION RESOURCES ON THE INTERNET SO BULLETIN OF THE AMERICAN SOCIETY FOR INFORMATION SCIENCE LA English DT Article C1 NATL LIB MED,BETHESDA,MD 20894. DC ONLINE USERS GRP,WASHINGTON,DC. RP FEIDT, WB (reprint author), NATL AGR LIB,BELTSVILLE,MD 20705, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC INFORM SCI MEMBER #110113 PI SILVER SPRING PA 8720 GEORGIA AVE SUITE 501, SILVER SPRING, MD 20910 SN 0095-4403 J9 B AM SOC INFORM INF JI Bull. Amer. Soc. Inf. Sci. PD APR-MAY PY 1995 VL 21 IS 4 BP 22 EP 23 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA RZ964 UT WOS:A1995RZ96400006 ER PT J AU HARBOURT, AM KNECHT, LS HUMPHREYS, BL AF HARBOURT, AM KNECHT, LS HUMPHREYS, BL TI STRUCTURED ABSTRACTS IN MEDLINE(R), 1989-1991 SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article; Proceedings Paper CT 93rd Annual Meeting of the Medical-Library-Association CY MAY 14-20, 1993 CL CHICAGO, IL SP MED LIB ASSOC ID INFORMATIVE ABSTRACTS; ARTICLES AB OBJECTIVE: To characterize the structured abstracts in biomedical journals indexed in MEDLINE(R) over a three-year period as an initial step in exploring their utility in enhancing bibliographic retrieval. DESIGN: The study examined the occurrence of structured abstracts in MEDLINE from March 1989 to December 1991, characteristics of MEDLINE records for articles with structured abstracts, editorial policies of six selected MEDLINE journals on structured abstracts, and a sample of twenty-five structured abstracts from the six journals. RESULTS: The study revealed that the number of structured abstracts in MEDLINE and the number of MEDLINE journals publishing structured abstracts increased substantially between 1989 and 1998. On average, articles with structured abstracts had more access points (Medical Subject Heading [MeSH(R)] terms and text words) than MEDLINE articles as a whole. The average length of the structured abstract was greater than the average length of all abstracts in MEDLINE. CONCLUSIONS: The presence of structured abstracts may be associated with other article characteristics that lead to the assignment of a higher average number of MeSH headings or may itself contribute to the assignment of more headings. The variations in the structured-abstract formats prescribed by different journals may complicate the exploitation of these abstracts in bibliographic retrieval systems. More research is needed on a number of questions related to the quality and utility of structured abstracts. C1 NATL LIB MED,DIV BIBLIOG SERV,BETHESDA,MD 20894. RP HARBOURT, AM (reprint author), NATL LIB MED,LISTER HILL NATL CTR BIOMED COMMUN,COMP SCI BRANCH,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 12 TC 26 Z9 27 U1 0 U2 1 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD APR PY 1995 VL 83 IS 2 BP 190 EP 195 PG 6 WC Information Science & Library Science SC Information Science & Library Science GA QU673 UT WOS:A1995QU67300004 PM 7599584 ER PT J AU DUTCHER, GA ARNESEN, SJ AF DUTCHER, GA ARNESEN, SJ TI DEVELOPING A SUBJECT SPECIFIC GOPHER AT THE NATIONAL-LIBRARY-OF-MEDICINE SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article; Proceedings Paper CT Symposium on Acquiring and Organizing Materials Available on the Internet, at the 94th Annual Meeting of the Medical-Library-Association CY MAY 16, 1994 CL SAN ANTONIO, TX SP MED LIB ASSOC, TECH SERV SECT, MED LIB ASSOC, COLLECT DEV SECT AB Development of subject-specific Gophers is one method to make valuable health information more accessible to those who need it. The National Library of Medicine has developed a Gopher that provides access to information produced by many areas of the library. Recommendations from subject experts in two areas-AIDS, and toxicology and environmental health-led to the development of two subject-specific Gophers. These two Gopher services provide organized access to resources outside of the library as well as to information produced internally. A number of important issues need to be addressed when selecting and organizing outside resources for inclusion in such a service. RP DUTCHER, GA (reprint author), NATL LIB MED,SPECIALIZED INFORMAT SERV,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 2 TC 2 Z9 2 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD APR PY 1995 VL 83 IS 2 BP 228 EP 233 PG 6 WC Information Science & Library Science SC Information Science & Library Science GA QU673 UT WOS:A1995QU67300011 PM 7599590 ER PT J AU WHITE, JD ZAKNOEN, SL KASTENSPORTES, C TOP, LE NAVARROROMAN, L NELSON, DL WALDMANN, TA AF WHITE, JD ZAKNOEN, SL KASTENSPORTES, C TOP, LE NAVARROROMAN, L NELSON, DL WALDMANN, TA TI INFECTIOUS COMPLICATIONS AND IMMUNODEFICIENCY IN PATIENTS WITH HUMAN T-CELL LYMPHOTROPIC VIRUS I-ASSOCIATED ADULT T-CELL LEUKEMIA/LYMPHOMA SO CANCER LA English DT Article DE LEUKEMIA; T CELL; IMMUNOCOMPROMISED HOST; HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE I (HTLV-I) INFECTIONS; ANTIBODIES; MONOCLONAL; RECEPTORS; INTERLEUKIN-2 ID LEUKEMIA LYMPHOMA VIRUS; HODGKINS-DISEASE; STRONGYLOIDES-STERCORALIS; MONOCLONAL-ANTIBODY; PATHOGENESIS; JAPAN; TRIAL; TAC; ATL AB Background. Adult T-cell leukemia/lymphoma (ATL) is a malignancy of mature T-cells occurring in patients infected with the human T-cell lymphotropic virus-I. These patients frequently develop a variety of infections throughout their disease course. Methods. Charts and autopsy reports were reviewed for 41 patients with ATL with follow-up varying from 2 to 120 months. Infectious episodes were identified and documented. Analyses of humoral and cell-mediated immunity were performed. Cell-mediated immunity was assessed in vivo with the Merieux multitest skin test panel. Humoral immunity was assessed by quantitative immunoglobulin levels, by determining human antimouse antibody after murine monoclonal antibody infusion acid by an in vitro immunoglobulin biosynthesis coculture system. Results. A total of 112 infectious episodes were documented. Fifty-seven serious infections were identified. The incidence of total infections was 1.40/patient-year and for serious infections was 0.71/patient-year. The mean serum IgG and IgA levels were within normal range, the mean IgM level was at the lower limit of normal. Peripheral blood mononuclear cells from all patients studied failed to make meaningful amounts of IgG, M, or A when activated. Peripheral blood mononuclear cells of all of the 13 patients studied suppressed production of immunoglobulin by cocultured normal PBMC. Twenty-three of the 27 patients tested were anergic. Conclusions. ATL is a profoundly immunosuppressing malignancy. This is manifested by an extremely high incidence of infectious episodes/patient-year. The incidence of infection appears to be greater than for mycosis fungoides, Hodgkin's lymphoma and non-Hodgkin's lymphoma. C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892. RP WHITE, JD (reprint author), NCI,METAB BRANCH,BLDG 10,ROOM 4N115,BETHESDA,MD 20892, USA. NR 36 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 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1995 VL 75 IS 7 BP 1598 EP 1607 DI 10.1002/1097-0142(19950401)75:7<1598::AID-CNCR2820750708>3.0.CO;2-7 PG 10 WC Oncology SC Oncology GA QN813 UT WOS:A1995QN81300007 PM 8826916 ER PT J AU GOHAGAN, JK PROROK, PC KRAMER, BS HAYES, RB CORNETT, JE AF GOHAGAN, JK PROROK, PC KRAMER, BS HAYES, RB CORNETT, JE TI THE PROSTATE, LUNG, COLORECTAL, AND OVARIAN-CANCER SCREENING TRIAL OF THE NATIONAL-CANCER-INSTITUTE SO CANCER LA English DT Article; Proceedings Paper CT National Conference on Prostate Cancer CY SEP 29-OCT 01, 1994 CL PHILADELPHIA, PA DE PROSTATE; SCREENING; DETECTION; CLINICAL TRIALS ID DIGITAL RECTAL EXAMINATION; RADICAL PROSTATECTOMY; ANTIGEN; ULTRASONOGRAPHY; SERUM; ADENOCARCINOMA; POPULATION; CARCINOMA; DISEASE AB The two-year pilot phase of the Prostate, Lung, Colorectal, and Ovarian (PLCO) trial concluded September 29, 1994. The goals, organization, operation, and recruitment status of the trial are discussed. The PLCO trial is a 16-year randomized controlled screening trial involving 148,000 male and female participants. Screening for prostate cancer is by prostate specific antigen and digital rectal examination. A coordinating center and 10 screening centers located across the United States, a laboratory for prostate specific antigen and CA125 assays, and a biorepository are the primary components of the trial. Scientific direction is provided by National Cancer Institute scientific staff, a steering committee of study investigators, external expert consultants, and a data monitoring panel. Evaluation of the pilot phase is focused on recruitment; screening operations, including quality assurance; compliance; data management; and blood processing. Pilot phase results are anticipated in 1995. C1 NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT & COMMUNITY ONCOL PROGRAM,BETHESDA,MD 20891. NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,BETHESDA,MD 20891. NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20891. RP GOHAGAN, JK (reprint author), NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,EXECUT PLAZA N,ROOM 305,6130 EXECUT BLVD,BETHESDA,MD 20891, USA. NR 38 TC 58 Z9 58 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 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1995 VL 75 IS 7 SU S BP 1869 EP 1873 DI 10.1002/1097-0142(19950401)75:7+<1869::AID-CNCR2820751617>3.0.CO;2-7 PG 5 WC Oncology SC Oncology GA QP393 UT WOS:A1995QP39300015 ER PT J AU WILT, TJ BRAWER, MK AF WILT, TJ BRAWER, MK TI THE PROSTATE-CANCER INTERVENTION VERSUS OBSERVATION TRIAL (PIVOT) - A RANDOMIZED TRIAL COMPARING RADICAL PROSTATECTOMY VERSUS EXPECTANT MANAGEMENT FOR THE TREATMENT OF CLINICALLY LOCALIZED PROSTATE-CANCER SO CANCER LA English DT Article; Proceedings Paper CT National Conference on Prostate Cancer CY SEP 29-OCT 01, 1994 CL PHILADELPHIA, PA DE PROSTATE CANCER; RANDOMIZED TRIALS; RADICAL PROSTATECTOMY; EXPECTANT MANAGEMENT ID DECISION-ANALYSIS AB The Prostate cancer Intervention Versus Observation Trial (PIVOT) is a randomized trial designed to determine whether early intervention with radical prostatectomy or expectant management should be the preferred treatment for men with clinically localized prostate cancer. This trial will enroll 2000 participants younger than 75 years of age from 75 Department of Veterans Affairs and National Cancer Institute medical centers. Men will be excluded if they are judged not to be candidates for radical prostatectomy. Eligible participants will be randomized over a 3-year period and followed for a minimum of 12 years. Follow-up data will include urologic symptoms, disease- and treatment-related morbidity, and disease-specific and overall quality of life. Evidence of disease persistence, recurrence, or progression will be measured by questionnaire, physical examination, prostate specific antigen measure, and bone scan. The primary study end point will be all-cause mortality. Secondary outcomes will include prostate cancer and treatment-specific morbidity and mortality, health status, predictors of disease-specific outcomes, and cost-effectiveness. C1 DEPT VET AFFAIRS,WASHINGTON,DC 20420. NCI,COOPERAT STUDY 407,BETHESDA,MD 20892. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. VET AFFAIRS MED CTR,SEATTLE,WA 98108. UNIV WASHINGTON,SEATTLE,WA 98195. RP WILT, TJ (reprint author), VET AFFAIRS MED CTR,DEPT MED,GEN INTERNAL MED SECT,1 VET DR 111-0,MINNEAPOLIS,MN 55417, USA. NR 14 TC 22 Z9 22 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1995 VL 75 IS 7 SU S BP 1963 EP 1968 DI 10.1002/1097-0142(19950401)75:7+<1963::AID-CNCR2820751634>3.0.CO;2-T PG 6 WC Oncology SC Oncology GA QP393 UT WOS:A1995QP39300032 ER PT J AU BATES, SE MEADOWS, B GOLDSPIEL, BR DENICOFF, A LE, TB TUCKER, E STEINBERG, SM ELWOOD, LJ AF BATES, SE MEADOWS, B GOLDSPIEL, BR DENICOFF, A LE, TB TUCKER, E STEINBERG, SM ELWOOD, LJ TI A PILOT-STUDY OF AMIODARONE WITH INFUSIONAL DOXORUBICIN OR VINBLASTINE IN REFRACTORY BREAST-CANCER SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE AMIODARONE; P-GLYCOPROTEIN; BREAST CANCER ID P-GLYCOPROTEIN EXPRESSION; PHASE-I TRIAL; CONTINUOUS INTRAVENOUS-INFUSION; MULTIDRUG-RESISTANCE GENE; INVIVO MODULATION; DRUG-RESISTANCE; CELL-LINES; CHEMOTHERAPY; CYCLOSPORINE; ETOPOSIDE AB Increasing evidence suggests that P-glycoprotein (Pgp) expression can mediate drug resistance in refractory breast cancer. We studied 33 patients with refractory breast cancer enrolled in a pilot study of oral amiodarone as a Pgp antagonist given in combination with infusional doxorubicin or vinblastine. Whenever possible, tumors were biopsied and Pgp expression was assayed, Patients received either 60 mg/m(2) doxorubicin over 96 h or 8.5 mg/m(2) vinblastine over 120 h by continuous intravenous infusion. Beginning with the second cycle of chemotherapy, 600-800 mg amiodarone was given orally each day. Patients who experienced toxicity due to amiodarone but were responding to chemotherapy were placed on quinidine, Partial responses were observed in 9 of 33 patients on study and were sometimes observed after the first cycle of chemotherapy, before amiodarone was given, suggesting that some patients may have responded to treatment because of the infusional schedule. Toxicities were primarily the known side effects of the antineoplastic agents and of amiodarone, The major amiodarone toxicity was gastrointestinal, with nausea, vomiting, anorexia, or diarrhea being noted in 21 patients. Biopsy samples were obtained from 29 patients acid in 21 cases, viable tumor tissue was present and the results were interpretable. Of the 21 samples, 9 had Pgp expression as determined by immunohistochemical staining; 12 were considered negative. The presence of Pgp expression was associated with an acceleration of the time to treatment failure. Whereas normal-tissue toxicities related to the combination of a Pgp antagonist with chemotherapy were not observed, amiodarone was associated with too many untoward effects to be utilized as a drug resistance-reversing agent. C1 NCI,MED BRANCH,BETHESDA,MD 20892. WARREN G MAGNUSON CLIN CTR,DEPT PHARM,BETHESDA,MD 20892. NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20814. RP BATES, SE (reprint author), NIH,BLDG 10,ROOM 12N226,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 39 TC 23 Z9 23 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD APR PY 1995 VL 35 IS 6 BP 457 EP 463 DI 10.1007/BF00686829 PG 7 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA QK194 UT WOS:A1995QK19400002 PM 7882454 ER PT J AU SUN, Y HILDESHEIM, A LI, H LI, Y CHEN, JY CHENG, YJ HAYES, RB ROTHMAN, N BI, WF CAO, Y YAO, KT LANIER, AP HEGAMYER, G ELDEIRY, WS XIONG, Y COLBURN, NH AF SUN, Y HILDESHEIM, A LI, H LI, Y CHEN, JY CHENG, YJ HAYES, RB ROTHMAN, N BI, WF CAO, Y YAO, KT LANIER, AP HEGAMYER, G ELDEIRY, WS XIONG, Y COLBURN, NH TI NO POINT MUTATION BUT A CODON 31(SER-]ARG) POLYMORPHISM OF THE WAF-1/CIP-1/P21 TUMOR-SUPPRESSOR GENE IN NASOPHARYNGEAL CARCINOMA (NPC) - THE POLYMORPHISM DISTINGUISHES CAUCASIANS FROM CHINESE SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID CYCLIN-DEPENDENT KINASES; P53; DNA; PROGRESSION; PHENOTYPE; INHIBITOR; LINKAGE; CANCER; REGION; P21 AB Mutational inactivation of the p53 tumor suppressor gene is an infrequent event in human nasopharyngeal carcinoma (NPC), a malignancy showing a high incidence in southern China and southeast Asia. To examine the possible involvement of an inactivated p53 pathway in nasopharynx carcinogenesis, we have screened primary NPC biopsies for possible point mutations in WAF-1/CIP-1/p21, an effector gene transcriptionally regulated by and functioning as a mediator of the p53 tumor suppressor gene. Mutations in WAF-1/CIP-1/p21 might mimic p53 mutations in tumors having wild-type p53 such as most NPCs. The mutational analysis of WAF/CIP/p21 by PCR-single strand conformational polymorphism-direct sequencing revealed no point mutation in 41 primary NPC biopsies. A codon 31(ser-->arg) polymorphism was, however, detected. A striking difference in the distribution of the serine (WAF-ser) and arginine (WAF-arg) forms of WAF-1/CIP-1/p21 was observed when normal healthy Caucasians and Chinese were compared (P < 0.0001). The majority of Caucasians examined were found to be homozygous for WAF-ser (89%, n = 65), while Chinese living in areas of high NPC incidence show a greater than 86% homozygous or heterozygous WAF-arg (Taiwan, n = 66; Hunan, n = 32). The two forms of WAF-1/CIP-1/p21 were examined for potential functional differences in their ability to inhibit cyclin-dependent kinases and turner cell growth. No significant differences were detected. Furthermore, no association between WAF-1/CIP-1/p21 genotype and NPC risk was observed in a case-control study of 76 NPC cases and 66 normal controls conducted in Taiwan. We conclude from this study that: (a) mutational inactivation of WAF-1/CIP-1/p21 is not involved in the genesis of NPC; (b) there is race-dependent WAF-1 polymorphism; and (c) the lack of functional differences between the two forms of WAF-1, and the lack of an association between WAF-1 genotype and disease, argue against a causal role of this gene in the genesis of NPC. C1 NCI,VIRAL CARCINOGENESIS LAB,CELL BIOL SECT,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,CTR BIOL CARCINOGENESIS & DEV,FREDERICK,MD 21701. NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. UNIV N CAROLINA,LINEBERGER COMPREHENS CANC CTR,DEPT BIOCHEM & BIOPHYS,CHAPEL HILL,NC 27599. UNIV N CAROLINA,CURRICULUM GENET & MOLCE BIOL,CHAPEL HILL,NC 27599. NATL TAIWAN UNIV,COLL MED,INST MICROBIOL,TAIPEI 10764,TAIWAN. NATL TAIWAN UNIV,INST PUBL HLTH,TAIPEI 10764,TAIWAN. CHINESE ACAD PREVENT MED,BEIJING,PEOPLES R CHINA. HUNAN MED UNIV,HUNAN CANC INST,HUNAN,PEOPLES R CHINA. PUBL HLTH SERV,INDIAN HLTH SERV,AK AREA NAT HLTH SERV,ANCHORAGE,AK. JOHNS HOPKINS UNIV,SCH MED,CTR ONCOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,PROGRAM HUMAN GENET & MOLEC BIOL,BALTIMORE,MD 21205. NR 32 TC 55 Z9 62 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD APR-MAY PY 1995 VL 4 IS 3 BP 261 EP 267 PG 7 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA QT145 UT WOS:A1995QT14500011 PM 7606201 ER PT J AU STRICKLER, HD ESCOFFERY, C RATTRAY, C FUCHS, D WACHTER, H MANNS, A SCHIFFMAN, MH CRANSTON, B HANCHARD, B BLATTNER, WA AF STRICKLER, HD ESCOFFERY, C RATTRAY, C FUCHS, D WACHTER, H MANNS, A SCHIFFMAN, MH CRANSTON, B HANCHARD, B BLATTNER, WA TI CERVICAL INTRAEPITHELIAL NEOPLASIA IS NOT ASSOCIATED WITH ELEVATED SERUM NEOPTERIN LEVELS SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Note ID INFECTION AB Neopterin, a marker of cellular immune activation, was elevated in patients who had cervical cancer in previous studies. To examine neopterin in the presence of precursors to cervical cancer (i.e., cervical intraepithelial neoplasia) we measured serum levels in 185 colposcopy patients in Jamaica, a country with high cervical cancer incidence, and in 72 age-matched Jamaican women selected from a large population-based sample. We also measured serum levels of beta-2-microglobulin, another commonly used marker of immune activation. Neopterin and beta-2-microglobuIin levels were not elevated in colposcopy patients; neither were they related to severity of cervical neoplasia. In multivariable analysis, neither adjustments for detection of cervical human papillomavirus DNA by PCR nor detection of antibodies to human T-cell lymphotropic virus type I (a retrovirus endemic to Jamaica) altered our findings. The absence of a serologically detectable increase in cellular immune activation linked to cervical intraepithelial neoplasia suggests that the immunological response to cervical intraepithelial neoplasia does not involve substantial systemic cellular immune activation. C1 NCI, ENVIRONM EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. NCI, VIRAL EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. UNIV HOSP W INDIES, DEPT PATHOL, KINGSTON 7, JAMAICA. UNIV HOSP W INDIES, DEPT OBSTET GYNECOL, KINGSTON 7, JAMAICA. UNIV INNSBRUCK, INST MED CHEM & BIOCHEM, A-6020 INNSBRUCK, AUSTRIA. NR 11 TC 5 Z9 5 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD APR-MAY PY 1995 VL 4 IS 3 BP 295 EP 298 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA QT145 UT WOS:A1995QT14500016 PM 7606206 ER PT J AU ZIMONJIC, DB REZANKA, L DIPAOLO, JA POPESCU, NC AF ZIMONJIC, DB REZANKA, L DIPAOLO, JA POPESCU, NC TI REFINED LOCALIZATION OF THE ERBB-3 PROTOONCOGENE BY DIRECT VISUALIZATION OF FISH SIGNALS ON LUT-INVERTED AND CONTRAST-ENHANCED DIGITAL IMAGES OF DAPI-BANDED CHROMOSOMES SO CANCER GENETICS AND CYTOGENETICS LA English DT Article ID NONISOTOPIC INSITU HYBRIDIZATION; SINGLE-COPY GENES; TUMORS; LIPOSARCOMA; LIPOMAS; BENIGN AB Contrast-enhanced, look-up-table (LUT)-inverted digital images of DAPI-banded chromosomes after fluorescence in situ hybridization (FISH) permit direct regional chromosomal localization of the fluorescent signals of single-copy gene probes. Improved quality and resolution of chromosome banding allowed a refined localization of the erbB-3 protooncogene from chromosome band 12q13 to subbands 12q13.2-13.3. This procedure can be used for direct and precise mapping of single-copy genes on both normal and cancer-cell-rearranged chromosomes. C1 NCI,DEPT HLTH EDUC & WELF,BIOL LAB,BETHESDA,MD 20892. NR 21 TC 66 Z9 66 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0165-4608 J9 CANCER GENET CYTOGEN JI Cancer Genet. Cytogenet. PD APR PY 1995 VL 80 IS 2 BP 100 EP 102 DI 10.1016/0165-4608(94)00161-4 PG 3 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA QX054 UT WOS:A1995QX05400003 PM 7736422 ER PT J AU JOHNSTON, PG LENZ, HJ LEICHMAN, CG DANENBERG, KD ALLEGRA, CJ DANENBERG, PV LEICHMAN, L AF JOHNSTON, PG LENZ, HJ LEICHMAN, CG DANENBERG, KD ALLEGRA, CJ DANENBERG, PV LEICHMAN, L TI THYMIDYLATE SYNTHASE GENE AND PROTEIN EXPRESSION CORRELATE AND ARE ASSOCIATED WITH RESPONSE TO 5-FLUOROURACIL IN HUMAN COLORECTAL AND GASTRIC TUMORS SO CANCER RESEARCH LA English DT Note ID SYNTHETASE; CANCER; CELLS; CHEMOTHERAPY; QUANTITATION AB Thymidylate synthase (TS) is the target enzyme for 5-fluorouracil (5-FU). We have correlated TS protein and gene expression with the response in patients with colorectal (n = 9) and gastric cancer (n = 12) treated with infusional 5-FU plus leucovorin (LV) or infusional 5-FU/LV and cisplatin, respectively. TS protein expression was analyzed by Western blot using TS106 monoclonal antibody and densitometry scanning. TS gene expression was measured by PCR analysis using beta-actin as an internal standard and expressed as a TS:beta-actin mRNA ratio. A close linear relationship was noted between TS protein expression and TS gene expression (r(2) = 0.60) for the 21 tumor samples analyzed. TS immunohistochemical staining on 15 of the 21 samples revealed that the TS staining intensity correlated closely with TS protein and mRNA expression. In two biopsy samples, TS protein levels and TS gene expression did not correlate; however, one of these exhibited a focal TS staining pattern. Both the TS protein level and TS gene expression were significantly associated with response to 5-FU-hased therapy. Patients with responsive disease had a mean TS protein level of 0.17 +/- 0.03 arbitrary units (range, 0.05 to 0.38), whereas in patients whose tumors did not respond, the mean TS protein level was significantly higher 0,60 +/- 0.09 (range, 0.06 to 1.01; P < 0.01). A similar pattern was noted with TS gene expression. In patients with responsive disease, the mean TS:beta-actin gene ratio was 1.36 +/- 0.3 (range, 0.5-3.3 x 10(-3)). In contrast, biopsies from patients with unresponsive disease had a mean TS:beta-actin gene ratio of 15.4 +/- 2.6 x 10(-3) (range, 2.7-35.9; P < 0.01). TS protein and TS mRNA expression are highly correlated, and each predict for response to 5-FU/LV-based chemotherapy in patients with colorectal and gastric cancer. C1 UNIV SO CALIF, SCH MED, KENNETH NORRIS JR COMPREHENS CANC CTR, LOS ANGELES, CA 90033 USA. RP NCI, NATL NAVAL MED CTR,NCI NAVY MED ONCOL BRANCH, 8901 WISCONSIN AVE,BLDG 8, ROOM 5101, BETHESDA, MD 20889 USA. FU NCI NIH HHS [5 R01 CA56119, 5 U01 CA60108] NR 23 TC 573 Z9 586 U1 1 U2 11 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 EI 1538-7445 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1995 VL 55 IS 7 BP 1407 EP 1412 PG 6 WC Oncology SC Oncology GA QP009 UT WOS:A1995QP00900003 PM 7882343 ER PT J AU BHATIA, K FAN, SJ SPANGLER, G WEINTRAUB, M OCONNOR, PM JUDDE, JG MAGRATH, I AF BHATIA, K FAN, SJ SPANGLER, G WEINTRAUB, M OCONNOR, PM JUDDE, JG MAGRATH, I TI A MUTANT P21 CYCLIN-DEPENDENT KINASE INHIBITOR ISOLATED FROM A BURKITTS-LYMPHOMA SO CANCER RESEARCH LA English DT Note ID P53 MUTATIONS; ASSOCIATION; TUMORS; GENE AB The growth arrest mediated by p53 is caused at least in part by the p53 mediated expression of p21 (p21(waf1/Cip1)). Since only one-third of primary Burkitt's lymphomas (BL) demonstrate mutations in the p53 gene, we examined the structural integrity of the p21 coding region by single-strand conformational polymorphism and DNA sequence analysis to determine the extent to which this gene is mutated in BL. Of 34 BLs analyzed, a frequent change (38%) at codon 31 that replaced Ser with Arg was found in 13 samples, 10 of which were from Africa. This change at codon 31 is also detected in peripheral blood DNA from normal subjects and may thus represent a polymorphism. One BL cell line, DH978, carried a change at codon 63: Phe to Leu. This mutation was heterozygous, and both the wild-type and the mutated p21 mRNA were expressed in the tumor cell Line. By transfection experiments, the mutant p21 was less efficient in suppressing clonogenicity than wild-type p21. To our knowledge, this is the only mutation described in p21. The availability of this mutant p21 should further help in functional studies of p21. C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RP BHATIA, K (reprint author), NCI,LYMPHOMA BIOL SECT,BLDG 10-13C205,BETHESDA,MD 20892, USA. NR 17 TC 77 Z9 78 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1995 VL 55 IS 7 BP 1431 EP 1435 PG 5 WC Oncology SC Oncology GA QP009 UT WOS:A1995QP00900008 PM 7882347 ER PT J AU OTSUKI, T CLARK, HM WELLMANN, A JAFFE, ES RAFFELD, M AF OTSUKI, T CLARK, HM WELLMANN, A JAFFE, ES RAFFELD, M TI INVOLVEMENT OF CDKN2 (P16(INK4A)/MTS1) AND P15(INK4B)/MTS2 IN HUMAN LEUKEMIAS AND LYMPHOMAS SO CANCER RESEARCH LA English DT Note ID ACUTE LYMPHOBLASTIC-LEUKEMIA; SHORT ARM; CELL; ABNORMALITIES; FEATURES; GENES; CHROMOSOME-9; PROGRESSION; ASSOCIATION; INTERFERON AB CDKN2 (p(16INK4A)/MTS1) and p(15INK4B)/MTS2 have been shown recently to be potent inhibitors of the cyclin D/cyclin-dependent kinase 4 compler. Both genes are candidates for the putative tumor suppressor gene located at chromosome 9p21. We examined a series of 14 hematopoietic cell lines and 117 primary lymphoid tumors for deletion and mutation of these genes. The primary tumors included 65 T-cell malignancies and 52 B-cell malignancies. The cell line study revealed 4 of 4 T-ALL lines to have homozygous deletions of CDKN2. Two of the 4 lines also show ed homozygous deletions of MTS2, while the remaining 2 lines retained both MTS2 alleles. In the primary tumors, homozygous deletions of both CDKN2 and MTS2 were found in 35% of the T-ALL/lymphoblastic lymphoma (8 of 23), Homozygous deletions of both genes also occurred in 1 of 3 precursor B-ALLs. PCR-single strand conformational polymorphism analysis of CDKN2 exons 2 and 3 and MTS2 exon 2 failed to demonstrate mutations in either CDKN2 or MTS2 in any of the T- or B-cell malignancies, with two possible exceptions. These results are consistent with a role for CDKN2 and/or MTS2 in the pathogenesis of some IS mphoid leukemia/lymphomas, particularly in T-ALL/lymphoblastic lymphoma. C1 NCI,HEMATOPATHOL SECT,PATHOL LAB,BETHESDA,MD 20892. NR 31 TC 136 Z9 139 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1995 VL 55 IS 7 BP 1436 EP 1440 PG 5 WC Oncology SC Oncology GA QP009 UT WOS:A1995QP00900009 PM 7882348 ER PT J AU OKAMOTO, A HUSSAIN, SP HAGIWARA, K SPILLARE, EA RUSIN, MR DEMETRICK, DJ SERRANO, M HANNON, GJ SHISEKI, M ZARIWALA, M XIONG, Y BEACH, DH YOKOTA, J HARRIS, CC AF OKAMOTO, A HUSSAIN, SP HAGIWARA, K SPILLARE, EA RUSIN, MR DEMETRICK, DJ SERRANO, M HANNON, GJ SHISEKI, M ZARIWALA, M XIONG, Y BEACH, DH YOKOTA, J HARRIS, CC TI MUTATIONS IN THE P16(INK4)/MTS1/CDKN2, P15(INK4B)/MTS2, AND P18 GENES IN PRIMARY AND METASTATIC LUNG-CANCER SO CANCER RESEARCH LA English DT Note AB We examined the genomic status of cyclin-dependent kinase- 4 and -6 inhibitors, p16(INK4), p15(INK4B), and p18, in 40 primary lung cancers and 31 metastatic lung cancers. Alterations of the p16(INK4) gene were detected in 6 (2 insertions and 4 homozygous deletions) of 22 metastatic non-small cell lung cancers (NSCLCs; 27%), but none were detected in 25 primary NSCLCs, 15 primary small cell lung cancers (SCLCs), or 9 metastatic SCLCs, indicating that mutation in the p16(INK4) gene is a late event in NSCLC carcinogenesis. Although three intragenic mutations of the p15(INK4B) gene were detected in 25 primary NSCLCs (12%) and five homozygous deletions of the p15(INK4B) gene were detected in 22 NSCLCs (23%), no genetic alterations of the p15(INK4B) gene were found in primary and metastatic SCLCs. The p18 gene was wild type in these 71 lung cancers, except 1 metastatic NSCLC which showed loss of heterozygosity. We also examined alterations of these three genes and expression of p16(INK4) in 21 human lung cancer cell lines. Alterations of the p16(INK4) and p15(INK4B) genes were detected in 71% of the NSCLC tell lines (n = 14) and 50% of the NSCLC cell lines (n = 14), respectively, but there were none In the 7 SCLC cell lines studied. No p18 mutations were detected in these 21 cell lines. These results indicate that both p16(INK4) and P14(INK4B) gene mutations are associated with tumor progression of a subset of NSCLC, but not of SCLC, and that p15(INK4B) mutations might also be an early event in the molecular pathogenesis of a subset of NSCLC. C1 NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. COLD SPRING HARBOR LAB,COLD SPRING HARBOR,NY 11724. NATL CANC CTR,RES INST,CHUO KU,TOKYO 104,JAPAN. UNIV N CAROLINA,CHAPEL HILL,NC 27599. RI Serrano, Manuel/H-2634-2015 OI Serrano, Manuel/0000-0001-7177-9312 NR 27 TC 276 Z9 291 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1995 VL 55 IS 7 BP 1448 EP 1451 PG 4 WC Oncology SC Oncology GA QP009 UT WOS:A1995QP00900012 PM 7882351 ER PT J AU RAO, CV RIVENSON, A SIMI, B ZANG, E KELLOFF, G STEELE, V REDDY, BS AF RAO, CV RIVENSON, A SIMI, B ZANG, E KELLOFF, G STEELE, V REDDY, BS TI CHEMOPREVENTION OF COLON CARCINOGENESIS BY SULINDAC, A NONSTEROIDAL ANTIINFLAMMATORY AGENT SO CANCER RESEARCH LA English DT Article ID FAMILIAL ADENOMATOUS POLYPOSIS; MALE F344 RATS; PROSTAGLANDIN SYNTHESIS INHIBITORS; SIGNAL TRANSDUCTION; RECTAL ADENOMAS; PHOSPHOLIPASE-C; 2ND MESSENGERS; PROTEIN-KINASE; DESMOID TUMOR; DRUG-THERAPY AB Epidemiological and laboratory animal model studies have suggested that nonsteroidal anti-inflammatory drugs reduce the risk of development of colon cancer. The present study was designed to investigate the chemopreventive action of 160 and 320 ppm (equivalent to 40 and 80% maximum tolerated doses) sulindac, a nonsteroidal anti-inflammatory drug, fed during initiation and postinitiation stages and 320 ppm sulindac fed during promotion/progression stages of azoxymethane-induced colon carcinogenesis in male F344 rats. Also investigated was the modulating effect of this agent on the colonic mucosal and tumor phospholipase A(2), phosphatidylinositol-specific phospholipase C, lipoxygenase, and cyclooxygenase activities. At 5 weeks of age, groups of male F334 rats were fed control diet or diets containing 160 and 320 ppm of sulindac. At 7 weeks of age, all animals except those in the vehicle-treated groups were given two weekly s.c. injections of azoxymethane at a dose rate of 15 mg/kg body weight/week. Animals intended for tumor promotion/progression study were administered 320 ppm of sulindac in diet starting at 14 weeks after a second azoxymethane treatment. All animals continued on their respective dietary regimen until the termination of the experiment at 52 weeks after the carcinogen treatment. Colonic tumors were evaluated histopathologically. Colonic mucosa and tumors were analyzed for phospholipase A(2), phosphatidylinositol-specific phospholipase C, prostaglandin E2, cyclooxygenase, and lipoxygenase acti,ities. The levels of sulindac and its metabolites in stomach, cecal, and fecal contents and in serum were analyzed, The results indicate that dietary sulindac at 160 and 320 ppm levels inhibited the incidence of invasive and noninvasive adenocarcinomas of the colon (P < 0.01-0.001) as well as their multiplicity (P < 0.01-0.0001) in a dose-dependent manner. Also, feeding sulindac during promotion/progression stages significantly suppressed the incidence (P < 0.0001) and multiplicity (P < 0.0001) of colonic adenocarcinomas. Dietary sulindac also suppressed the colon tumor volume by >52-62% compared to the control diet. Dietary sulindac significantly decreased the activities of phosphatidy linositol-specific phospholipase C (32-51%) and levels of prostaglandin E(2) (>40% in the colonic mucosa and tumors, but it had no significant (P > 0.05) effect on phospholipase A(2) activity, The formation of cyclooxygenase metabolites, particularly prostaglandin E(2), prostaglandin F-2 alpha, prostaglandin D-2, 6-ketoprostaglandin F-1 alpha, and thromboxane B-2, and lipoxygenase metabolites such as 8(S)- and 12(S)-hydroxyeicosatetraenoic acids were significantly reduced in colonic mucosa and tumors of animals fed 320 ppm sulindac. Also, animals fed 320 ppm sulindac showed increased levels of microbial metabolites of sulindac in cecal and fecal contents and in serum as compared to those fed 160 ppm sulindac, Although the exact mechanism by which sulindac inhibits colon tumorigenesis remains to be elucidated, it is likely that its chemopreventive action, at least in part, mag be related to the modulation of arachidonic acid metabolism. C1 AMER HLTH FDN, DIV NUTR CARCINOGENESIS, VALHALLA, NY 10595 USA. AMER HLTH FDN, DIV PATHOL & TOXICOL, VALHALLA, NY 10595 USA. AMER HLTH FDN, DIV EPIDEMIOL, VALHALLA, NY 10595 USA. NCI, DIV CANC PREVENT & CONTROL, CHEMOPREVENT BRANCH, BETHESDA, MD 20892 USA. RI Chinthalapally, Rao/B-3633-2010 FU NCI NIH HHS [CA17613, CN85095-05] NR 64 TC 380 Z9 391 U1 0 U2 5 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 EI 1538-7445 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1995 VL 55 IS 7 BP 1464 EP 1472 PG 9 WC Oncology SC Oncology GA QP009 UT WOS:A1995QP00900015 PM 7882354 ER PT J AU DONG, ZG LAVROSKY, V COLBURN, NH AF DONG, ZG LAVROSKY, V COLBURN, NH TI TRANSFORMATION REVERSION INDUCED IN JB6 RT101 CELLS BY AP-1 INHIBITORS SO CARCINOGENESIS LA English DT Article ID RETINOIC ACID; C-JUN; GENE-EXPRESSION; FOS; STROMELYSIN; RAS; ONCOPROTEIN; PROGRESSION; ACTIVATION; INDUCTION AB The present study was directed to characterizing the reversion of neoplastic epidermal JB6 RT101 cells by AP-1 inhibiting drugs, Treatment of tumorigenic JB6 RT101 cells with retinoic acid (RA), fluocinolone acetonide (FA) or forskolin (FN) induced drug dependent (reversible) reversion of transformation. A synergistic effect on reversion was found with the three drugs in combination. Cells reverted by these three drugs also showed reduced levels of AP-1 transcription factor activity. After long term exposure of RT101 cells to FA, enrichment of hat revertants occurred in the population while a few unreverted cells formed foci. These unreverted cells appeared to be FA-resistant. Cloning of cells following RA treatment revealed stable reversion at least 2 months after drug withdrawal, Stable revertants showed lower basal AP-1 activity than RT101 cells (P < 0.01) and unstable revertants returned to transformed phenotype and elevated AP-1 activity within days following drug withdrawal. To our knowledge this is the first demonstration that drug induced reversion co-selects for reduced AP-1 activity, These data suggest that the JB6 RT101 cell line is a useful cell model for studying reversion of transformation and that inhibition of AP-1 activity may be one molecular mechanism of reversion, Considering the development of resistance with FA alone and the relative inefficiency of RA or FN alone, combinations of the three AP-1 activity inhibitors RA, FA and FN may be useful for further animal and clinical studies. C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,CELL BIOL SECT,FREDERICK,MD 21702. RP DONG, ZG (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. NR 39 TC 73 Z9 74 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1995 VL 16 IS 4 BP 749 EP 756 DI 10.1093/carcin/16.4.749 PG 8 WC Oncology SC Oncology GA QV719 UT WOS:A1995QV71900012 PM 7728951 ER PT J AU FAN, LJ SCHUT, HAJ SNYDERWINE, EG AF FAN, LJ SCHUT, HAJ SNYDERWINE, EG TI CYTOTOXICITY, DNA ADDUCT FORMATION AND DNA-REPAIR INDUCED BY 2-HYDROXYAMINO-3-METHYLIMIDAZO[4,5-F]QUINOLINE AND 2-HYDROXYAMINO-1-METHYL-6-PHENYLIMIDAZO[4,5-B]PYRIDINE IN CULTURED HUMAN MAMMARY EPITHELIAL-CELLS SO CARCINOGENESIS LA English DT Article ID HETEROCYCLIC AMINES; METABOLIC-ACTIVATION; COOKED FOOD; MUTAGENIC ACTIVATION; CYNOMOLGUS MONKEYS; PHIP; CARCINOGEN; BINDING; IQ; 2-AMINO-3-METHYLIMIDAZO<4,5-F>QUINOLINE AB 2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) are heterocyclic amines (HAs) found in cooked meats, Both compounds are mammary gland carcinogens in rats, The initiation of carcinogenesis by the HAs is believed to be associated with their DNA adduct formation that occurs after metabolic activation of the parent amines via cytochrome P-450-mediated N-hydroxylation and esterification, To assess the capacity of the human mammary epithelium to metabolically activate the HAs, we used the P-32-postlabeling method to measure the levels of DNA adducts in a culture of human mammary epithelial cells exposed to IQ, PhIP or their N-hydroxylamine metabolites. Whereas 50 mu M parent amines did not form detectable levels of DNA adducts ill cultured human mammary epithelial cells after 24 h incubations, concentrations as low as 1 mu M N-hydroxylamines produced detectable levels of adducts after 2 h incubations, N-Hydroxy-PhIP formed higher adduct levels than N-hydroxy-IQ at all concentrations tested, For example, following a 2 h incubation at 50 mu M, adduct levels (per 10(7) nucleotides) were 674 and 16 for N-hydroxy-PhIP and N-hydroxy-IQ, respectively, At similar initial adduct levels (10-11/10(7) nucleotides), 60-80% of IQ- and PhIP-DNA adducts were removed after 24 h, indicating that the mammary epithelial cell culture showed efficient repair of HA adducts, Whereas neither IQ nor PhIP was cytotoxic, both N-hydroxy-IQ and N-hydroxy-PhIP were cytotoxic as assessed by a dose-dependent inhibition of colony formation, After exposure to 0.1, 1, 10 or 50 mu M N-hydroxy-PhIP (or N-hydroxy-IQ), colony formation was 103 (94), 84 (74), 37 (29) and 3 (2)% of the control values, respectively, Only N-hydroxy-PhIP (at 10 and 50 mu M), however, was cytotoxic as assessed by the MTT cell survival assay (which measures the capacity of mitochondria to metabolize a tetrazolium salt), The ability of the N-hydroxylamines to form DNA adducts and to be cytotoxic in a culture of human mammary epithelial cells may implicate these metabolites as proximate carcinogenic forms of IQ and PhIP in the human mammary gland, However, whether there are inter-individual differences in N-hydroxylamine metabolism, adduct formation and repair in human mammary epithelial cells requires further study. The results from this study support the usefulness of cultured human mammary epithelial cells for studies on the genotoxicity and metabolism of the N-hydroxylamines of HA food mutagens. C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. MED COLL OHIO,DEPT PATHOL,TOLEDO,OH 43614. NR 35 TC 35 Z9 35 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1995 VL 16 IS 4 BP 775 EP 779 DI 10.1093/carcin/16.4.775 PG 5 WC Oncology SC Oncology GA QV719 UT WOS:A1995QV71900015 PM 7728954 ER PT J AU JAKOWLEW, SB MATHIAS, A CHUNG, P MOODY, TW AF JAKOWLEW, SB MATHIAS, A CHUNG, P MOODY, TW TI EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA LIGAND AND RECEPTOR MESSENGER-RNAS IN LUNG-CANCER CELL-LINES SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID II RECEPTOR; MEMBRANE-RECEPTOR; COMPLEMENTARY-DNA; FACTOR GENES; CLONING; BINDING; IDENTIFICATION; FACTOR-BETA-2; INHIBITION; TGF-BETA-1 AB Specific cDNA probes for transforming growth factor beta s (TGF-beta s) 1, 2, and 3 and TGF-beta types I, II, and III receptors were used to study expression of the mRNAs of the different TGF-beta ligand and TGF-beta receptor isoforms in cultured non-small cell lung cancer (NSCLC) cells and small cell lung cancer (SCLC) cells. Expression of TGF-beta 1 mRNA was detected in both cell types using Northern blot hybridization, with the level of expression of this mRNA being higher in several NSCLC cell lines. In addition, expression of TGF-beta 2 and TGF-beta 3 mRNAs was also detected in NSCLC and SCLC cells but at levels that were lower than that of TGF-beta 1 mRNA. Besides expression of a 3.4-kilobase (kb) TGF-beta 3 transcript, a smaller 2.8-kb TGF-beta 3 transcript was detected in some NSCLC and SCLC cells. TGF-beta 1 and TGF-beta 2 proteins were detected in the conditioned media of NSCLC and SCLC cells, with the levels being higher in several NSCLC cells than in SCLC cells. Expression of TGF-beta types I and II receptor mRNAs was also detected in most NSCLC and SCLC cells, with expression of a 5.5-kb type I receptor mRNA being higher than that of a 5.5-kb type II receptor mRNA in both cell types. In contrast, a 6-kb TGF-beta type III receptor mRNA was detected in only some NSCLC cells and could not be detected in the SCLC cells examined. Also, there was an inverse relationship between the level of expression of the 5.5-kb TGF-beta type I receptor mRNA and that of the 6-kb TGF-beta type III receptor mRNA. Addition of TGF-beta 1 and TGF-beta 2 proteins resulted in an increase in the mRNAs for TGF-beta s 1 and 2 and an increase in the amount of TGF-beta 1 protein in some NSCLC cells, indicating that these cells are responsive to TGF-beta and its effects. At the same time, a differential change in expression of the 2.8- and 3.4-kb TGF-beta 3 transcripts was detected in some lung cancer cells following the addition of TGF-beta 1 and TGF-beta 2. Also, addition of TGF-beta 1 to NSCLC cells inhibited colony formation of some of these cells in soft agarose in a dose-dependent manner. These results show that some lung cancer cells are responsive to the effects of TGF-beta and suggest that TGF-beta may have a role in controlling the proliferation of these cells. RP JAKOWLEW, SB (reprint author), NCI,BIOMARKERS & PREVENT RES BRANCH,9610 MED CTR DR,SUITE C300,ROCKVILLE,MD 20850, USA. NR 53 TC 52 Z9 53 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD APR PY 1995 VL 6 IS 4 BP 465 EP 476 PG 12 WC Cell Biology SC Cell Biology GA QR290 UT WOS:A1995QR29000012 PM 7794814 ER PT J AU LEBRETON, PR HUANG, CR FERNANDO, H ZAJC, B LAKSHMAN, MK SAYER, JM JERINA, DM AF LEBRETON, PR HUANG, CR FERNANDO, H ZAJC, B LAKSHMAN, MK SAYER, JM JERINA, DM TI MULTIPLE FLUORESCENCE LIFETIMES FOR OLIGONUCLEOTIDES CONTAINING SINGLE, SITE-SPECIFIC MODIFICATIONS AT GUANINE AND ADENINE CORRESPONDING TO TRANS ADDITION OF EXOCYCLIC AMINO-GROUPS TO (+)-(7R,8S,9S,10R)-7,8-DIHYDROXY-9,10-EPOXY-7,8,9,10-TETRAHYDROBENZO[A] PYRENE AND (-)-(7S,8R,9R,10S)-7,8-DIHYDROXY-9,10-EPOXY-7,8,9,10-TETRAHYDROBENZO[A] PYRENE SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID (+)-ANTI-BENZOPYRENE DIOL EPOXIDE; METABOLITE MODEL COMPOUNDS; DNA-ADDUCTS; COVALENT ADDUCTS; INTERCALATIVE BINDING; PHOTOEMISSION PROBES; BENZOPYRENE; COMPLEXES; 7,12-DIMETHYLBENZANTHRACENE; OLIGODEOXYNUCLEOTIDES AB Fluorescence decay profiles of four oligonucleotide duplexes, [GRAPHICS] ((+)- and (-)- trans-1) and [GRAPHICS] ((+)- and (-)-trans-2), in which an exocyclic amino group of deoxyadenosine (A*) or deoxyguanosine (G*) has been alkylated by trans opening at C-10 of the epoxide group of either the (+)-(R,S,S,R)- or (-)-(S,R,R,S)-enantiomer of (+)-7 beta,8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE in which the benzylic 7-hydroxy group and the epoxide oxygen are trans), exhibit more than one fluorescence lifetime. Decay profiles of the oligomers, measured at 15 degrees C with excitation and emission wavelengths of 335 and 400 nm, respectively, have been analyzed using a triple-exponential decay law. Results for (+)- and (-)-trans-1 and -2 have been compared with results for the modified, single-stranded oligonucleotides ((+)- and (-)-trans-SS-1, and (+)- and (-)-trans-SS-2) and for the cis and trans opened products formed on alkylation at the g-amino group of 2'-deoxyadenosine 5'-phosphate by (+)-(R,S,S,R)-BPDE ((+)-trans- and(+)-cis-A). The profiles of(+)-trans- and (+)-cis-A are well represented by single-exponential decay laws with lifetimes of 86 and 110 +/- 3 ns, respectively. For the single- and double-stranded oligomer adducts, which exhibit at least three fluorescence lifetimes, two of the lifetimes are short (0.5-14 +/- 1 ns) and one is long (35-59 +/- 3 ns). The fluorescence lifetimes and the amplitudes of the long-lived components in the decay profiles of the double-stranded oligomer adducts are generally smaller than those for the corresponding single-stranded adducts. The data provide evidence that the double-stranded oligomer adducts exist as multiple conformations. Previously reported NMR results suggest that the short-lifetime fluorescence components are due to major adduct conformations in which the pyrenyl group is intercalated ((+)- and (-)-trans-1) or lies in the minor groove ((+)- and (-)-trans-2). The observation of long lifetime fluorescence species for the double-stranded oligomers is consistent with the presence of minor conformations (similar to 1-5%) in which the double-stranded oligomer either is locally denatured or is a mixture of locally denatured double-stranded conformations and equilibrium concentrations of single-stranded oligomers. C1 NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RP LEBRETON, PR (reprint author), UNIV ILLINOIS,DEPT CHEM,CHICAGO,IL 60607, USA. NR 41 TC 16 Z9 16 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD APR-MAY PY 1995 VL 8 IS 3 BP 338 EP 348 DI 10.1021/tx00045a004 PG 11 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA QU473 UT WOS:A1995QU47300004 PM 7578919 ER PT J AU QIAN, CY DIPPLE, A AF QIAN, CY DIPPLE, A TI DIFFERENT MECHANISMS OF ARALKYLATION OF ADENOSINE AT THE 1-POSITION AND N-6-POSITION SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID STYRENE OXIDE; REACTION-PRODUCTS; DNA ADDUCTS; GUANOSINE; ADENINE; CARCINOGENESIS; REARRANGEMENT; DERIVATIVES; NUCLEOSIDES; BINDING AB The eight products resulting from opening of either enantiomer of styrene oxide at the alpha- or beta-carbon by the 1- or N-6-positions of adenosine were prepared and their configurations assigned. These markers allowed the mechanism of aralkylation of adenosine by styrene oxide to be investigated. It was found that formation of alpha-substituted products at the 1-position of adenosine involved total inversion of stereochemistry, whereas at the N-6-position inversion: retention was similar to 6:1. These differences in stereochemistry suggest that a more ionic form of styrene oxide is involved in N-6-aralkylation than in 1-aralkylation of adenosine. In the course of these studies, it was found that 1-substituted adenosines at the alpha- and beta-carbon of styrene oxide undergo Dimroth rearrangement at neutral pH and 37 degrees C and that the former compound also deaminates fairly readily under these conditions. RP QIAN, CY (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-46000] NR 26 TC 44 Z9 45 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD APR-MAY PY 1995 VL 8 IS 3 BP 389 EP 395 DI 10.1021/tx00045a010 PG 7 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA QU473 UT WOS:A1995QU47300010 PM 7578925 ER PT J AU LARYEA, A COSMAN, M LIN, JM LIU, TM AGARWAL, R SMIRNOV, S AMIN, S HARVEY, RG DIPPLE, A GEACINTOV, NE AF LARYEA, A COSMAN, M LIN, JM LIU, TM AGARWAL, R SMIRNOV, S AMIN, S HARVEY, RG DIPPLE, A GEACINTOV, NE TI DIRECT SYNTHESIS AND CHARACTERIZATION OF SITE-SPECIFIC ADENOSYL ADDUCTS DERIVED FROM THE BINDING OF A 3,4-DIHYDROXY-1,2-EPOXYBENZO[C]PHENANTHRENE STEREOISOMER TO AN 11-MER OLIGODEOXYRIBONUCLEOTIDE SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID BENZOPYRENE DIOL EPOXIDE; BENZOPHENANTHRENE DIHYDRODIOL EPOXIDES; POLYCYCLIC AROMATIC-HYDROCARBONS; SNAKE-VENOM PHOSPHODIESTERASE; DNA-ADDUCTS; DEOXYADENOSINE ADDUCTS; SOLUTION CONFORMATION; MODIFIED OLIGODEOXYNUCLEOTIDES; ABSOLUTE-CONFIGURATION; LIVER MICROSOMES AB Site-specifically modified oligonucleotides were obtained in milligram quantities by reacting racemic 3t,4r-dihydroxy-1,2t-epoxy-1,2,3,4-tetrahydrobenzo[c]phenanthrene (B[c]PhDE-2, or anti-B[c]PhDE) with the single deoxyadenosine (dA) residue in the oligodeoxynucleotide d(CTCTCACTTCC). Enzyme digestion of the covalently modified oligonucleotides with the exonuclease spleen phosphodiesterase yielded covalently linked B[c]PhDE-N-6-deoxyadenosyl monophosphate (dAMP) adducts. Comparisons of the reverse phase HPLC retention times and CD spectra of these B[c]PhDE-3'-dAMP mononucleotide adducts, with those of standards derived from the reaction of the enantiomers (+)- and (-)-anti-B[c]PhDE with 3'-dAMP, show that two major oligonucleotide adducts (I and II) were obtained upon reacting racemic anti-B[c]PhDE with d(CTCTCACTTCC). In oligonucleotide adduct I, the lesion is a (+)-trans-anti-B [c]PhDE-N-6-dA residue, and in oligonucleotide adduct II it is a (-)-trans-anti-B[c]PhDE-N-6-dA residue. These assignments were further confirmed using a standard P-32 postlabeling assay of B[c]PhDE-3'-dAMP mononucleotide adducts obtained from the digestion of oligonucleotides I and II by spleen phosphodiesterase. The melting points (T-m) of duplexes of modified oligonucleotides I and II and their natural complementary strands are not affected significantly by the presence of the covalently bound benzo[c]phenanthrenyl residues. Opposite stereoselective resistance to enzyme digestion by the exonucleases snake venom phosphodiesterase and spleen phosphodiesterase is exhibited by the stereoisomeric (+)-trans- and (-)-trans-anti-B[c]PhDE-modified oligonucleotide adducts I and II; these results are consistent with the intercalative insertion of the benzo[c]phenanthrenyl residues on the 5'-side of the modified dA residue in adduct I, and its insertion on the 3'-side of the dA residue in adduct II, as observed in the duplexes by high resolution NMR techniques [Cosman et al. (1993) Biochemistry 32, 12488-12497, and Cosman et al., Biochemistry, in press]. C1 NYU,DEPT CHEM,NEW YORK,NY 10003. MEM SLOAN KETTERING CANC CTR,CELLULAR BIOCHEM & BIOPHYS PROGRAM,NEW YORK,NY 10021. AMER HLTH FDN,VALHALLA,NY 10595. UNIV CHICAGO,BEN MAY INST,CHICAGO,IL 60637. NCI,FREDERICK CANC RES & DEV CTR,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-4600] NR 58 TC 34 Z9 34 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD APR-MAY PY 1995 VL 8 IS 3 BP 444 EP 454 DI 10.1021/tx00045a017 PG 11 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA QU473 UT WOS:A1995QU47300017 PM 7578932 ER PT J AU LEE, J BARCHI, JJ MARQUEZ, VE AF LEE, J BARCHI, JJ MARQUEZ, VE TI SYNTHESIS OF A RIGID DIACYLGLYCEROL ANALOG HAVING A BIS-GAMMA-BUTYROLACTONE SKELETON SEPARATED BY A CYCLOPENTANE RING SO CHEMISTRY LETTERS LA English DT Article ID FORMAL SYNTHESIS; ESTERS AB A very efficient method for the construction of a new bis-gamma-lactone system constructed on a cyclopenta[1,2-c:3,4-c']perhydrodifuran scaffold was developed from cyclopentadiene and methyl (S)-(Z)-4,5-O-isopropylidenepent-2-enoate. C1 NCI, DIV CANC TREATMENT, MED CHEM LAB, DEV THERAPEUT PROGRAM, BETHESDA, MD 20892 USA. RI Barchi Jr., Joseph/N-3784-2014 NR 9 TC 6 Z9 6 U1 0 U2 2 PU CHEMICAL SOC JAPAN PI TOKYO PA 1-5 KANDA-SURUGADAI CHIYODA-KU, TOKYO, 101-8307, JAPAN SN 0366-7022 EI 1348-0715 J9 CHEM LETT JI Chem. Lett. PD APR PY 1995 IS 4 BP 299 EP 300 DI 10.1246/cl.1995.299 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA QW531 UT WOS:A1995QW53100027 ER PT J AU JEONG, LS MARQUEZ, VE AF JEONG, LS MARQUEZ, VE TI THE STEREOCHEMICAL OUTCOME OF THE DAST FLUORINATION OF 4'-THIOPYRIMIDINE NUCLEOSIDES WITH UP HYDROXYL-GROUPS IS CONTROLLED BY THE OXIDATION-STATE OF THE SULFUR ATOM SO CHEMISTRY LETTERS LA English DT Article AB DAST fluorination of 1-(S-O-trityl-3-deoxy-4-thio-beta-D-threo-pentofuranosyl)uracil proceeds with retention of configuration, while the corresponding sulfoxide gives mainly the inverted product. The sulfone proceeds with elimination. C1 NCI, DIV CANC TREATMENT, MED CHEM LAB, DEV THERAPEUT PROGRAM, BETHESDA, MD 20892 USA. NR 5 TC 4 Z9 4 U1 0 U2 4 PU CHEMICAL SOC JAPAN PI TOKYO PA 1-5 KANDA-SURUGADAI CHIYODA-KU, TOKYO, 101-8307, JAPAN SN 0366-7022 EI 1348-0715 J9 CHEM LETT JI Chem. Lett. PD APR PY 1995 IS 4 BP 301 EP 302 DI 10.1246/cl.1995.301 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA QW531 UT WOS:A1995QW53100028 ER PT J AU LENFANT, C AF LENFANT, C TI INTEGRATIVE PHYSIOLOGY - REMEMBER THE BIG PICTURE SO CIRCULATION LA English DT Editorial Material RP LENFANT, C (reprint author), NHLBI,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR 1 PY 1995 VL 91 IS 7 BP 1901 EP 1901 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QP542 UT WOS:A1995QP54200001 ER PT J AU LUDDEN, LK STRONG, JM KOHN, EC COLLINS, JM AF LUDDEN, LK STRONG, JM KOHN, EC COLLINS, JM TI SIMILARITY OF METABOLISM FOR CAI (NSC-609974) IN HUMAN LIVER-TISSUE IN-VITRO AND IN HUMANS IN-VIVO SO CLINICAL CANCER RESEARCH LA English DT Article ID CYTOCHROMES-P450; L651582; CALCIUM; AGENT AB Metabolism of a new antitumor agent, CAI (NSC 609974), was investigated in human liver tissue in vitro and in plasma and urine of patients receiving CAI. Metabolites identified by HPLC following C-14-labeled CAI incubation with human liver microsomes and reported as percentage of total metabolites formed were M1 (0-3.4%), M2 (4.5-33%), M3 (60-79%), and M4 (7.2-19%). Ketoconazole, an inhibitor of cytochrome P450 3A4, prevented formation of M1, M3, and M4 (concentration of drug that inhibited metabolite formation by 50% when compared to maximum uninhibited activity, 3.0 mu M), but only weakly inhibited formation of M2 (concentration of drug that inhibited metabolite formation by 50% when compared to maximum uninhibited activity, > 50 mu M). CAI incubated with recombinant human P450 3A4 microsomes produced metabolites M3 and M4. Conjugation of M3, most likely a glucuronide, was observed after incubation of C-14-labeled CAI and UDP-glucuronic acid with human liver 13,000 x g supernatant. Plasma samples from patients receiving CAI contained CAI (3.1-5.0 mu g/ml), M1 (0.9-2.6 mu g/ml), and M2 (1.0-2.2 mu g/ml). CAI and M3 but not M4 were observed in the urine samples, After incubation of the urine samples with beta-glucuronidase, CAI concentrations increased 67%, M3 increased up to 9-fold, and M4 was detected. CAI is metabolized in vitro and in vivo by both Phase I and Phase II enzymes and is metabolized to M3 and M4 by P450 3A4. These studies suggest that elevated levels of CAI may result from P450 3A4 inhibition by ketoconazole if these two drugs are coadministered. Correlation between CAI metabolism in vitro and results obtained in patients demonstrates the usefulness of liver metabolism studies in vitro in the early stages of drug development. C1 NCI,PATHOL LAB,SIGNAL TRANSDUCT & PREVENT UNIT,BETHESDA,MD 20892. RP LUDDEN, LK (reprint author), US FDA,CTR DRUG EVALUAT & RES,DIV CLIN PHARMACOL,OFF RES RESOURCES,4 RES COURT,ROOM 314,ROCKVILLE,MD 20850, USA. NR 15 TC 14 Z9 14 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD APR PY 1995 VL 1 IS 4 BP 399 EP 405 PG 7 WC Oncology SC Oncology GA RJ530 UT WOS:A1995RJ53000005 ER PT J AU SUGIMOTO, Y HRYCYNA, CA AKSENTIJEVICH, I PASTAN, I GOTTESMAN, MM AF SUGIMOTO, Y HRYCYNA, CA AKSENTIJEVICH, I PASTAN, I GOTTESMAN, MM TI COEXPRESSION OF A MULTIDRUG-RESISTANCE GENE (MDR1) AND HERPES-SIMPLEX VIRUS THYMIDINE KINASE GENE AS PART OF A BICISTRONIC MESSENGER-RNA IN A RETROVIRUS VECTOR ALLOWS SELECTIVE KILLING OF MDR1-TRANSDUCED CELLS SO CLINICAL CANCER RESEARCH LA English DT Article ID P-GLYCOPROTEIN GENE; BONE-MARROW; TRANSGENIC MICE; MAMMALIAN-CELLS; BRAIN-TUMORS; EXPRESSION; CDNA; DNA; VINBLASTINE; COLCHICINE AB A new retroviral vector, pSXLC/pHa, was constructed to coexpress drug-selectable markers with a second gene of interest as a part of a bicistronic mRNA in a retroviral vector using an internal ribosome entry site (IRES) from encephalomyocarditis virus. This system was used to develop a new retroviral vector pHa-MDR-IRES-TK which expresses a single mRNA from which translation of the MDR1 gene is cap dependent and translation of the herpes simplex virus thymidine kinase gene is IRES dependent. The pHa-MDR-IRES-TK transfectants showed high levels of P-glycoprotein expression and multidrug resistance. More than 95% of the vincristine-resistant cells transfected or transduced with pHa-MDR-IRES-TK showed hypersensitivity to ganciclovir, which selects against cells expressing herpes simplex virus thymidine kinase. An amphotropic retrovirus titer of 7.8 x 10(4)/ml was obtained with this vector. This safety-modified vector should be useful for introducing the MDR1 gene into bone marrow cells to protect normal cells from the toxic effects of cancer chemotherapy because this vector allows the elimination of cancer cells that have been unintentionally transduced with the MDR1 vector. C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 32 TC 32 Z9 32 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD APR PY 1995 VL 1 IS 4 BP 447 EP 457 PG 11 WC Oncology SC Oncology GA RJ530 UT WOS:A1995RJ53000011 ER PT J AU CRITCHFIELD, JM LENARDO, MJ AF CRITCHFIELD, JM LENARDO, MJ TI ANTIGEN-INDUCED PROGRAMMED T-CELL DEATH AS A NEW APPROACH TO IMMUNE THERAPY SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Review ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MYELIN BASIC-PROTEIN; LYMPHOCYTES-T; PROLIFERATIVE RESPONSE; APOPTOSIS; RECEPTOR; INTERLEUKIN-2; ACTIVATION; INVITRO; CLONES AB We describe recent advances in understanding a mechanism of peripheral tolerance that operates through antigen-induced programmed cell death of mature T lymphocytes. A three-phase model of this process, termed propriocidal regulation, involves: (i) activation of T cells to express growth lymphokines and their receptors, (ii) lymphokine-stimulated cell-cycle progression, and (iii) T cell receptor reengagement leading to programmed cell death. Based on this model, antigen was used to treat experimental allergic encephalomyelitis and caused profound deletion of autoreactive, encephalitogenic T cells as well as dramatic clinical and pathological improvement of the disease. The potential strengths and weaknesses of this approach to the clinical treatment of T-cell-mediated diseases are discussed. (C) 1995 Academic Press, Inc. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 40 TC 30 Z9 31 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1995 VL 75 IS 1 BP 13 EP 19 DI 10.1006/clin.1995.1046 PG 7 WC Immunology; Pathology SC Immunology; Pathology GA QM343 UT WOS:A1995QM34300002 PM 7882590 ER PT J AU STIEHM, ER MOFENSON, L ZOLLAPAZNER, S JACKSON, B MARTIN, NL AMMANN, AJ AMMANN, A ANDRUS, L BURTON, D COOMBS, RW CUMMINS, L DULIEGE, AM FAST, P FOWLER, MG GOLDENTHAL, K KOENIG, S KOUP, R MADDON, P MARTIN, N MATHIESON, B MEYER, WA NEMO, G POTTS, B ROSSI, P PRINCE, A STEIMER, KS AF STIEHM, ER MOFENSON, L ZOLLAPAZNER, S JACKSON, B MARTIN, NL AMMANN, AJ AMMANN, A ANDRUS, L BURTON, D COOMBS, RW CUMMINS, L DULIEGE, AM FAST, P FOWLER, MG GOLDENTHAL, K KOENIG, S KOUP, R MADDON, P MARTIN, N MATHIESON, B MEYER, WA NEMO, G POTTS, B ROSSI, P PRINCE, A STEIMER, KS TI SUMMARY OF THE WORKSHOP ON PASSIVE IMMUNOTHERAPY IN THE PREVENTION AND TREATMENT OF HIV-INFECTION SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Editorial Material ID HUMAN-IMMUNODEFICIENCY-VIRUS; HUMAN MONOCLONAL-ANTIBODY; CD4 BINDING; GP120; TYPE-1; AIDS; IMMUNOGLOBULIN; NEUTRALIZATION; IMMUNIZATION; EPITOPE C1 PEDIATR AIDS FDN, NOVATO, CA USA. NEW YORK BLOOD CTR, NEW YORK, NY 10021 USA. SCRIPPS RES INST, LA JOLLA, CA USA. PACIFIC MED CTR, SEATTLE, WA USA. NABI, MIAMI, FL USA. NIAID, DIV AIDS, ROCKVILLE, MD USA. CASE WESTERN RESERVE UNIV, CLEVELAND, OH 44106 USA. MED IMMUNE CO, GAITHERSBURG, MD USA. AARON DIAMOND AIDS RES INST, NEW YORK, NY USA. PROGENICS, TARRYTOWN, NY USA. MARYLAND MED LAB INC, BALTIMORE, MD USA. NIAID, PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH, ROCKVILLE, MD USA. NHLBI, TRANSFUS MED BRANCH, BETHESDA, MD USA. UBI, HUAPPAUGE, NY USA. UNIV ROMA TOR VERGATA, I-00173 ROME, ITALY. UNIV CALIF LOS ANGELES, DEPT PEDIAT, LOS ANGELES, CA 90024 USA. NYU, SCH MED, NEW YORK, NY USA. RP STIEHM, ER (reprint author), CHIRON CORP, EMERYVILLE, CA USA. RI rossi, paolo/D-6504-2012; OI Mofenson, Lynne/0000-0002-2818-9808 NR 30 TC 13 Z9 13 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1995 VL 75 IS 1 BP 84 EP 93 DI 10.1006/clin.1995.1056 PG 10 WC Immunology; Pathology SC Immunology; Pathology GA QM343 UT WOS:A1995QM34300012 PM 7882595 ER PT J AU ZURLO, JJ WOOD, L GAGLIONE, MM POLIS, MA AF ZURLO, JJ WOOD, L GAGLIONE, MM POLIS, MA TI EFFECT OF SPLENECTOMY ON T-LYMPHOCYTE SUBSETS IN PATIENTS INFECTED WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID IMMUNE-DEFICIENCY; PERIPHERAL-BLOOD; HOMOSEXUAL MEN; COUNT; SUBPOPULATIONS; PERCENTAGE; TYPE-1; NUMBER; AIDS AB A case-control study was conducted at two institutions to determine whether the absolute CD4 lymphocyte count or the percentage of lymphocytes bearing the CD4 marker (i.e., the CD4 percentage) is a more accurate indicator of underlying immune status in splenectomized patients infected with human immunodeficiency virus (HIV). Each of nine splenectomized HIV-infected cases was matched with six nonsplenectomized HIV-infected controls-three matched for CD4 lymphocyte count and three for CD4 percentage. In analyses including the eight cases with an initial CD4 lymphocyte count of >200/mm(3), controlling for the CD4 count revealed differences between cases and controls in terms of CD4 percentage (range, 10%-41% and 17%-54%, respectively; P<.01) and Centers for Disease Control and Prevention (CDC) clinical stage (P =.06). Controlling for the CD4 percentage revealed a significant difference between cases and controls in terms of CD4 count (range, 396-1,040 and 55-784 cells/mm(3), respectively; P <.01) but not CDC clinical stage (P >.7). These data suggest that the numerical relationship between the CD4 lymphocyte count and the CD4 percentage among splenectomized HIV-infected patients with more than 200 CD4 cells/mm(3) differs from that among nonsplenectomized patients. The CD4 percentage appears to be a more accurate indicator of the underlying level of immune function in the former group of patients. C1 NIAID,BETHESDA,MD. RP ZURLO, JJ (reprint author), MILTON S HERSHEY MED CTR,DIV INFECT DIS,POB 850,HERSHEY,PA 17033, USA. OI Polis, Michael/0000-0002-9151-2268 NR 15 TC 16 Z9 17 U1 0 U2 0 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 1995 VL 20 IS 4 BP 768 EP 771 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QP662 UT WOS:A1995QP66200005 PM 7795071 ER PT J AU WALSH, TJ GONZALEZ, C ROILIDES, E MUELLER, BU AIL, N LEWIS, LL WHITCOMB, TO MARSHALL, DJ PIZZO, PA AF WALSH, TJ GONZALEZ, C ROILIDES, E MUELLER, BU AIL, N LEWIS, LL WHITCOMB, TO MARSHALL, DJ PIZZO, PA TI FUNGEMIA IN CHILDREN INFECTED WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS - NEW EPIDEMIOLOGIC PATTERNS, EMERGING PATHOGENS, AND IMPROVED OUTCOME WITH ANTIFUNGAL THERAPY SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID DISSEMINATED FUNGAL-INFECTIONS; CENTRAL VENOUS CATHETERS; FLUCONAZOLE PHARMACOKINETICS; DISSEMINATED HISTOPLASMOSIS; LYMPHOCYTE SUBSETS; CANDIDA-TROPICALIS; CANCER-PATIENTS; AIDS AB We characterized 27 episodes of fungemia in 22 children infected with the human immunodeficiency virus (HIV). Fungemia in these patients presented as a community-acquired infection in the setting of outpatient total parenteral nutrition or intravenous antibiotic therapy through a chronically indwelling central venous catheter (CVC). Fungemia developed only in patients with CVCs (P <. 001). Non-albicans Candida species, Torulopsis glabrata, Rhodotorula rubra, and Bipolaris spicifera constituted 52% of all causes. Fungemia was detected early, within a median of 2.4 days after the onset of new fever, which permitted prompt administration of amphotericin B (mean dosage, 0.7 mg/[kg . day]; median duration, 19 days), CVCs were removed in 23 (85%) of the episodes. We conclude that fungemia in HIV-infected children often presents as a community-acquired infection, is frequently due to newly emerging opportunistic fungi, and can be managed, with a high level of success (95% survival with no posttherapeutic sequelae), by early diagnosis, prompt initiation of amphotericin B therapy, and removal of the CVC. RP WALSH, TJ (reprint author), NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,ROOM 13N-240,BETHESDA,MD 20892, USA. NR 40 TC 60 Z9 64 U1 0 U2 0 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 1995 VL 20 IS 4 BP 900 EP 906 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QP662 UT WOS:A1995QP66200027 PM 7795092 ER PT J AU MUELLER, BU MACKAY, K CHESHIRE, LB CHOYKE, PL KITCHEN, B WIDEMANN, B PIZZO, PA AF MUELLER, BU MACKAY, K CHESHIRE, LB CHOYKE, PL KITCHEN, B WIDEMANN, B PIZZO, PA TI CYTOMEGALOVIRUS URETERITIS AS A CAUSE OF RENAL-FAILURE IN A CHILD INFECTED WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS SO CLINICAL INFECTIOUS DISEASES LA English DT Note ID BONE-MARROW TRANSPLANTATION; NEPHROPATHY; CYSTITIS; NEPHRITIS AB Cytomegalovirus (CMV) infection is common in patients infected with human immunodeficiency virus. Hemorrhagic cystitis and tubulointerstitial nephritis have been recognized as complications of CMV infection, and these complications lead to hematuria and compromised renal function. We describe a case of CMV infection of the ureters in a child with vertically acquired human immunodeficiency virus infection; the child presented with severe suprapubic pain, and prolonged macroscopic hematuria and intermittent acute renal failure developed subsequently. C1 NIDDKD,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT PATHOL,BETHESDA,MD 20892. RP MUELLER, BU (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA. NR 13 TC 12 Z9 14 U1 0 U2 0 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 1995 VL 20 IS 4 BP 1040 EP 1043 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QP662 UT WOS:A1995QP66200043 PM 7795047 ER PT J AU ALIM, TN ROSSE, RB VOCCI, FJ LINDQUIST, T DEUTSCH, SI AF ALIM, TN ROSSE, RB VOCCI, FJ LINDQUIST, T DEUTSCH, SI TI DIETHYLPROPION PHARMACOTHERAPEUTIC ADJUVANT THERAPY FOR INPATIENT TREATMENT OF COCAINE DEPENDENCE - A TEST OF THE COCAINE-AGONIST HYPOTHESIS SO CLINICAL NEUROPHARMACOLOGY LA English DT Review DE COCAINE; DIETHYLPROPION; DOPAMINE; CRAVING; ABSTINENCE ID ATTENTION DEFICIT DISORDER; METHYLPHENIDATE TREATMENT; ABUSE; BROMOCRIPTINE; AMANTADINE; INFUSIONS AB Fifty cocaine-dependent patients completed a 2-week double-blind, double-dummy, parallel-group comparison of four dosage levels of diethylpropion and placebo. This clinical trial was designed to evaluate both diethylpropion's ability to attenuate cocaine cue-induced craving and its potential for development as a medication with cocaine-agonist properties. The results indicated that diethylpropion was not superior to placebo and confirmed earlier reports that craving for cocaine diminishes over the course of an inpatient hospitalization. Moreover, the results showed that the cocaine cue-induced craving paradigm employed is effective in stimulating craving for cocaine. Medications that are effective in attenuating this type of ''conditioned'' craving may have relevance to the breaking of the cycle of relapse and the long-term treatment of cocaine dependence. Diethylpropion may not be an appropriate candidate for future medication development because of its lack of obvious therapeutic efficacy and the emergence of a significant number of side effects. However, a cocaine-agonist medication strategy may be appropriate for a subgroup of cocaine-dependent patients with coexisting attention deficit-hyperactivity disorder. C1 VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,WASHINGTON,DC 20422. VET AFFAIRS MED CTR,NIDA,VA,RES UNIT,WASHINGTON,DC 20422. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC. NIDA,DIV MEDICAT DEV,ROCKVILLE,MD. FU ONDIEH CDC HHS [RA-ND-90-10] NR 37 TC 21 Z9 21 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-5664 J9 CLIN NEUROPHARMACOL JI Clin. Neuropharmacol. PD APR PY 1995 VL 18 IS 2 BP 183 EP 195 DI 10.1097/00002826-199504000-00009 PG 13 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA QP331 UT WOS:A1995QP33100009 PM 8635177 ER PT J AU CHAO, KM ZHANG, JH OSTELL, J MILLER, W AF CHAO, KM ZHANG, JH OSTELL, J MILLER, W TI A LOCAL ALIGNMENT TOOL FOR VERY LONG DNA-SEQUENCES SO COMPUTER APPLICATIONS IN THE BIOSCIENCES LA English DT Article ID ESCHERICHIA-COLI GENOME; ALGORITHM; MINUTES; REGION; SUBSEQUENCES AB This paper presents a practical program, called sim2, for building local alignments of two sequences, each of which may be hundreds of kilobases long. sim2 first constructs n best non-intersecting chains of 'fragments', such as all occurrences of identical 5-tuples in each of two DNA sequences,for any specified n greater than or equal to 1. Each chain is then refined by delivering an optimal alignment in a region delimited by the chain. sim2 requires only space proportional to the size of the input sequences and the output alignments, and the same source code runs on Unix machines, on Macintoshes, on PCs, and on DEC Alpha PCs. We also describe an application of sim2 for aligning long DNA sequences from Escherichia coli. sim2 facilitates contig-building by providing a complete view of the related sequences, so differences can be analyzed and inconsistencies resolved Examples are shown using the alignment display and editing functions from the software tool ChromoScope. C1 NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA. RP PENN STATE UNIV, DEPT COMP SCI & ENGN, UNIVERSITY PK, PA 16802 USA. OI CHAO, KUN-MA0/0000-0003-2837-1279 FU NLM NIH HHS [R01 LM05110] NR 20 TC 31 Z9 31 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 1995 VL 11 IS 2 BP 147 EP 153 PG 7 WC Computer Science, Interdisciplinary Applications SC Computer Science GA QX809 UT WOS:A1995QX80900005 PM 7620986 ER PT J AU ZUCKER, DM LAKATOS, E WEBBER, LS MURRAY, DM MCKINLAY, SM FELDMAN, HA KELDER, SH NADER, PR AF ZUCKER, DM LAKATOS, E WEBBER, LS MURRAY, DM MCKINLAY, SM FELDMAN, HA KELDER, SH NADER, PR TI STATISTICAL DESIGN OF THE CHILD AND ADOLESCENT TRIAL FOR CARDIOVASCULAR HEALTH (CATCH) - IMPLICATIONS OF CLUSTER RANDOMIZATION SO CONTROLLED CLINICAL TRIALS LA English DT Article DE CLUSTER RANDOMIZATION; GROUP RANDOMIZATION; COMMUNITY STUDIES; MULTILEVEL MODELING; INTENTION-TO-TREAT PRINCIPLE ID GENERALIZED LINEAR-MODELS; COMMUNITY INTERVENTION; LONGITUDINAL DATA; PROMOTION; PREVENTION; REGRESSION; INFERENCE; DISEASE; ISSUES AB This paper describes some statistical considerations for the Child and Adolescent Trial for Cardiovascular Health (CATCH), a large-scale community health trial sponsored by the National Heart, Lung, and Blood Institute. The trial involves randomization of entire schools rather than individual students to the experimental arms. The paper discussed the implications of this form of randomization for the design and analysis of the trial. The power calculations and analysis plan for the trial are presented in detail. The handling of outmigrating and inmigrating students is also discussed. C1 NEW ENGLAND RES INST,WATERTOWN,MA 02172. NHLBI,BIOSTAT RES BRANCH,BETHESDA,MD. HEBREW UNIV JERUSALEM,DEPT STAT,IL-91905 JERUSALEM,ISRAEL. SEARLE PHARMACEUT,SKOKIE,IL. TULANE UNIV,SCH PUBL HLTH & TROP MED,DEPT BIOSTAT & EPIDEMIOL,NEW ORLEANS,LA. UNIV MINNESOTA,SCH PUBL HLTH,DIV EPIDEMIOL,MINNEAPOLIS,MN. UNIV TEXAS,HLTH SCI CTR,CTR HLTH PROMOT RES & DEV,HOUSTON,TX. UNIV CALIF SAN DIEGO,SCH MED,DEPT PEDIAT,SAN DIEGO,CA. FU NHLBI NIH HHS [U01 HL 39927, U01 HL 39825, U01 HL 39870] NR 40 TC 55 Z9 56 U1 1 U2 4 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD APR PY 1995 VL 16 IS 2 BP 96 EP 118 DI 10.1016/0197-2456(94)00026-Y PG 23 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA QR630 UT WOS:A1995QR63000002 PM 7789139 ER PT J AU VIKICTOPIC, D BECKER, ED HODOSCEK, M GRAOVAC, A AF VIKICTOPIC, D BECKER, ED HODOSCEK, M GRAOVAC, A TI LOWDIN ATOMIC CHARGES FOR MODELING LONG-RANGE DEUTERIUM-ISOTOPE SHIFTS IN C-13 NMR-SPECTRA OF BINUCLEAR AROMATIC-COMPOUNDS SO CROATICA CHEMICA ACTA LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; MOLECULAR-PROPERTIES; SUBSTITUENT; CONSTANTS AB An approach for modeling long range deuterium isotope effects on C-13 chemical shifts, based on ab initio calculations of the differences of atomic charges between parent and deuterated molecules, is proposed. The total atomic charges were calculated for a series of molecules consisting of two benzene rings linked directly or via different groups, the so called binuclear aromatic molecules: biphenyl, trans-stilbene, cis-stilbene, diphenylacetylene, diphenylbutadiene and their I-deuterated derivatives. The basis sets used were: STO-3G, 6-31G, 6-31G** and MIDI. The deuteration site, i.e. C-D bond was simulated by the shortening of the corresponding C-H bond length by 0.012 Angstrom or by the reduction of CCH in-plane or out-of-plane bending angle by 1.3 degrees and 2 degrees, respectively. Calculations were performed both for the X-ray geometries and 6-31G fully optimized geometries. The charge differences from Lowdin but not from Mulliken population analysis, calculated with 6-31G, 6-31G** and MIDI basis sets, showed good correlation with the measured longrange deuterium isotope effects on C-13 chemical shifts of C-atoms, five, six, seven, eight, ten and twelve bonds away from the site of deuteration. This correlation holds only for bond shortening but not for bending angle changes, which corresponds to the predominance of stretching over bending mode contributions to isotope effects. The vibrational analysis (6-31G) revealed no coupling of C-D stretching with the vibrations of remote C-atoms. Therefore, we assume that the symmetry breaking due to unsymmetrical deuterium substitution produces a small electric dipole moment by an unbalance in the normal vibrations which in turn polarizes pi-electrons, giving rise to charge changes throughout the molecule. Calculated charge redistribution due to deuterium, experimentally also observed by microwave spectroscopy, might induce long-range deuterium isotope effects on C-13 chemical shifts in agreement with the postulated C-C pi-bond polarization contribution to C-13 chemical shifts. C1 NIH,DCRT,MOLEC GRAPH & SIMULAT LAB,BETHESDA,MD 20892. RUDJER BOSKOVIC INST,ZAGREB 41001,CROATIA. INST CHEM,LJUBLJANA 61000,SLOVENIA. RP VIKICTOPIC, D (reprint author), NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 31 TC 7 Z9 7 U1 0 U2 4 PU CROATIAN CHEMICAL SOC PI ZAGREB PA MARULICEV TRG 19/II, 41001 ZAGREB, CROATIA SN 0011-1643 J9 CROAT CHEM ACTA JI Croat. Chem. Acta PD APR PY 1995 VL 68 IS 1 BP 193 EP 203 PG 11 WC Chemistry, Multidisciplinary SC Chemistry GA QW722 UT WOS:A1995QW72200016 ER PT J AU VANDERGEER, P WILEY, S LAI, VKM OLIVIER, JP GISH, GD STEPHENS, R KAPLAN, D SHOELSON, S PAWSON, T AF VANDERGEER, P WILEY, S LAI, VKM OLIVIER, JP GISH, GD STEPHENS, R KAPLAN, D SHOELSON, S PAWSON, T TI A CONSERVED AMINO-TERMINAL SHC DOMAIN BINDS TO PHOSPHOTYROSINE MOTIFS IN ACTIVATED RECEPTORS AND PHOSPHOPEPTIDES SO CURRENT BIOLOGY LA English DT Article ID PROTEIN-TYROSINE KINASES; GUANINE-NUCLEOTIDE EXCHANGE; GROWTH-FACTOR RECEPTORS; SIGNAL TRANSDUCTION; V-SRC; TRANSFORMING PROTEIN; ADAPTER PROTEIN; HIGH-AFFINITY; EGF RECEPTOR; GRB2 AB Background: Signal transduction by growth factor receptor protein-tyrosine kinases is generally initiated by autophosphorylation on tyrosine residues following ligand binding. Phosphotyrosines within activated receptors form binding sites for the Src homology 2 (SH2) domains of cytoplasmic signalling proteins. One such protein, Shc, is tyrosine phosphorylated in response to a large number of growth factors and cytokines. Phosphorylation of Shc on tyrosine residue Y317 allows binding to the SH2 domain of Grb2, and hence stimulation of the Ras pathway. Shc is therefore implicated as an adaptor protein able to couple normal and oncogenic protein-tyrosine kinases to Ras activation. Shc itself contains an SH2 domain at its carboxyl terminus, but the function of the amino-terminal half of the protein is unknown. Results: We have found that the Shc amino-terminal region binds to a number of tyrosine-phosphorylated proteins in v-src-transformed cells. This domain also bound directly to the activated epidermal growth factor (EGF) receptor. A phosphotyrosine (pY)-containing peptide modeled after the Shc-binding site in polyoma middle T antigen (LLSNPTpYSVMRSK) was able to compete efficiently with the activated EGF receptor for binding to the Shc amino terminus. This competition was dependent on phosphorylation of the tyrosine residue within the peptide, and was abrogated by deletion of the leucine residue at position -5. The Shc amino-terminal domain also bound to the autophosphorylated nerve growth factor receptor (Trk), but bound significantly less well to a mutant receptor in which tyrosine Y490 in the receptor's Shc-binding site had been substituted by phenylalanine. Conclusion: These data implicate the amino-terminal region of Shc in binding to activated receptors and other tyrosine-phosphorylated proteins. Binding appears to be specific for phosphorylated tyrosine residues within the sequence NPXpY, which is conserved in many Shc-binding sites. The Shc amino-terminal region bears only very limited sequence identity to known SH2 domains, suggesting that it represents a new class of phosphotyrosine-binding modules. Consistent with this view, the amino-terminal Shc domain is highly conserved in a Drosophila Shc homologue. Binding of Shc to activated receptors through its amino terminus could leave the carboxy-terminal SH2 domain free for other interactions. In this way, Shc may Function as an adaptor protein to bring two tyrosine-phosphorylated proteins together. C1 MT SINAI HOSP,SAMUEL LUNENFELD RES INST,PROGRAM MOLEC BIOL & CANC,TORONTO,ON M5G 1X5,CANADA. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Pawson, Tony/E-4578-2013; Gish, Gerald/C-7228-2017 NR 52 TC 159 Z9 160 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD APR 1 PY 1995 VL 5 IS 4 BP 404 EP 412 DI 10.1016/S0960-9822(95)00081-9 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT007 UT WOS:A1995QT00700018 PM 7542991 ER PT J AU RAO, CM QIN, CA ROBISON, WG ZIGLER, JS AF RAO, CM QIN, CA ROBISON, WG ZIGLER, JS TI EFFECT OF SMOKE CONDENSATE ON THE PHYSIOLOGICAL INTEGRITY AND MORPHOLOGY OF ORGAN-CULTURED RAT LENSES SO CURRENT EYE RESEARCH LA English DT Article DE LENS ORGAN CULTURE; SMOKE CONDENSATE; LENS EPITHELIUM; LENS MEMBRANES; RAT; [RB-86]-UPTAKE; [RB-86]-EFFLUX; CATARACT ID CIGARETTE-SMOKING; MOUSE SKIN; DNA DAMAGE; CATARACTS; PRODUCTS; INDIA; LUNG AB Smoke, either from cigarette smoking or from burning of organic fuels, has been proposed to be a major environmental risk factor for a variety of human diseases. Recently, smoke was implicated in cataract, an eye lens opacification which is a major cause of blindness. We have undertaken a study to investigate the effect of wood smoke condensate on the physiological integrity and morphology of organ cultured lenses. Lenses in organ culture are metabolically active and have functional defense systems, thus they provide an appropriate model for studying effects of smoke condensate. Our present study indicates that metabolites of wood smoke condensate accumulate in the lens. The ability of the lenses to accumulate rubidium-86 (mimic of potassium) and choline from the medium is compromised by exposure to smoke condensate. Rubidium efflux studies suggest that the damage is primarily at the uptake level and does not involve an overall increase in membrane permeability. Protein leakage experiments corroborate this suggestion. Histological data show distinct morphological changes such as hyperplasia, hypertrophy and multilayering of epithelial cells. C1 NEI,MECHANISM OCULAR DIS LAB,BETHESDA,MD 20892. RP RAO, CM (reprint author), CTR CELLULAR & MOLEC BIOL,HYDERABAD 500007,ANDHRA PRADESH,INDIA. NR 22 TC 21 Z9 22 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 1995 VL 14 IS 4 BP 295 EP 301 DI 10.3109/02713689509033529 PG 7 WC Ophthalmology SC Ophthalmology GA QU541 UT WOS:A1995QU54100008 PM 7606915 ER PT J AU NEUENSCHWANDER, H JULIA, C WYMAN, M KADOR, PF AF NEUENSCHWANDER, H JULIA, C WYMAN, M KADOR, PF TI ENDOTHELIAL CHANGES IN GALACTOSE-FED DOGS SO CURRENT EYE RESEARCH LA English DT Article DE ALDOSE REDUCTASE; CORNEAL ENDOTHELIUM; DIABETES MELLITUS; DOG; GALACTOSEMIA ID ALDOSE REDUCTASE INHIBITOR; CORNEAL ENDOTHELIUM; DIABETES-MELLITUS; RATS AB Specular microscopic studies indicate that the size (polymegathism) and shape (pleomorphism) of the hexagonal corneal endothelial cells change in diabetics. Similar morphometric changes of the corneal endothelium have also been experimentally observed in diabetic rats as well as in diabetic and galactose-fed dogs and concomitant administration of aldose reductase inhibitors reduced these morphological changes. The purpose of this study was to examine whether corneal endothelial changes in galactose-fed dogs are reversible by the marked reduction of galactitol production after stopping prolonged galactose feeding. Ten control dogs were fed a normal diet, while 48 dogs were fed a diet containing 30% galactose. The galactose diet was removed from 15 dogs after 24 months at which time pericyte ghosts in the retina had developed and another 15 dogs were removed from the galactose diet after 31 months when retinal microaneurysms had developed. Eighteen dogs remained on galactose diet throughout the study (38 months). Specular microscopy was conducted on members of all groups after 38 months of study and the photographs were analyzed in masked fashion on the Bambi image analysis system. The evaluation of the corneal endothelial cells revealed significant differences in the cell size and density between galactose-fed dogs in the three groups and normal, age-matched control dogs. Corneal endothelial changes were not significantly reduced in dogs fed galactose for either 24 months or 31 months and then fed a normal diet for 14 and 7 months, respectively, indicating that amelioration of endothelial cell changes requires therapy prior to the advent of endothelial morphologic changes. C1 NEI,OCULAR THERAPEUT LAB,BETHESDA,MD 20892. NR 25 TC 5 Z9 7 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 1995 VL 14 IS 4 BP 319 EP 322 DI 10.3109/02713689509033532 PG 4 WC Ophthalmology SC Ophthalmology GA QU541 UT WOS:A1995QU54100011 PM 7606918 ER PT J AU LEE, SB RHEE, SG AF LEE, SB RHEE, SG TI SIGNIFICANCE OF PIP2 HYDROLYSIS AND REGULATION OF PHOSPHOLIPASE-C ISOZYMES SO CURRENT OPINION IN CELL BIOLOGY LA English DT Article ID BETA-GAMMA-SUBUNITS; GROWTH-FACTOR RECEPTOR; PHOSPHATIDYLINOSITOL 4,5-BISPHOSPHATE; TYROSINE PHOSPHORYLATION; SIGNALING PROTEINS; POINT MUTATION; ALPHA-SUBUNITS; SH3 DOMAINS; ACTIVATION; GQ AB Phosphatidylinositol 4,5-bisphosphate (PIP2) is an important component of several intracellular signaling pathways. It serves as a substrate for phospholipase C, which produces the second messengers inositol 1,4,5-trisphosphate and diacylglycerol. It is also a substrate for a phosphatidylinositol 3-kinase, and regulates the function of a number of actin-binding proteins. PIP2 has been shown recently to serve as a cofactor for a phosphatidylcholine-specific phospholipase D and as a membrane-attachment site for many signaling proteins containing pleckstrin homology domains. The need to stringently regulate the cellular concentration of PIP2 is reflected in part by the fact that there are at least ten distinct mammalian phospholipase C isozymes and multiple mechanisms linking these isozymes to various receptors. RP LEE, SB (reprint author), NHLBI,CELL SIGNALING LAB,BETHESDA,MD 20892, USA. NR 57 TC 275 Z9 277 U1 0 U2 5 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0955-0674 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD APR PY 1995 VL 7 IS 2 BP 183 EP 189 DI 10.1016/0955-0674(95)80026-3 PG 7 WC Cell Biology SC Cell Biology GA QP349 UT WOS:A1995QP34900006 PM 7612269 ER PT J AU FOWLKES, BJ SCHWEIGHOFFER, E AF FOWLKES, BJ SCHWEIGHOFFER, E TI POSITIVE SELECTION OF T-CELLS SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID MICE AB In the past year, significant technical developments have provided the opportunity to investigate the more mechanistic features of positive selection. Major progress has been made in determining the structure and function of the early pre-T cell receptor, in defining cell types that mediate positive selection, and in analyzing the contribution of MHC and co-receptors to CD4/CD8 lineage commitment. The most revealing studies have been those addressing the role of peptides in thymic selection. RP FOWLKES, BJ (reprint author), NIAID,CELLULAR & MOLEC IMMUNOL LAB,BLDG 4,ROOM 111,BETHESDA,MD 20892, USA. NR 54 TC 74 Z9 74 U1 0 U2 4 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD APR PY 1995 VL 7 IS 2 BP 188 EP 195 DI 10.1016/0952-7915(95)80003-4 PG 8 WC Immunology SC Immunology GA QX634 UT WOS:A1995QX63400003 PM 7546378 ER PT J AU MORRIS, RGM AMARAL, DG MISHKIN, M AF MORRIS, RGM AMARAL, DG MISHKIN, M TI COGNITIVE NEUROSCIENCE - EDITORIAL OVERVIEW SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Editorial Material ID LONG-TERM POTENTIATION; MUTANT MICE; HIPPOCAMPAL C1 SUNY STONY BROOK,CTR BEHAV NEUROSCI,STONY BROOK,NY 11794. NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. RP MORRIS, RGM (reprint author), UNIV EDINBURGH,CTR NEUROSCI,SCH MED,CRICHTON ST,EDINBURGH EH8 9LE,MIDLOTHIAN,SCOTLAND. RI Morris, Richard/C-9982-2013 NR 11 TC 1 Z9 1 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-4388 J9 CURR OPIN NEUROBIOL JI Curr. Opin. Neurobiol. PD APR PY 1995 VL 5 IS 2 BP 137 EP 140 DI 10.1016/0959-4388(95)80018-2 PG 4 WC Neurosciences SC Neurosciences & Neurology GA QW012 UT WOS:A1995QW01200001 ER PT J AU GOLD, JM WEINBERGER, DR AF GOLD, JM WEINBERGER, DR TI COGNITIVE DEFICITS AND THE NEUROBIOLOGY OF SCHIZOPHRENIA SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Article ID CEREBRAL BLOOD-FLOW; MONOZYGOTIC TWINS DISCORDANT; NEUROPSYCHOLOGICAL FUNCTION; PSYCHIATRIC-SYMPTOMS; MEMORY; ABNORMALITIES; 1ST-EPISODE; DYSFUNCTION; IMPAIRMENT; CLOZAPINE AB Recent research in schizophrenia has demonstrated widespread abnormalities in patients' brain structure, cognitive function, and physiology. These abnormalities are most probably developmental in origin and involve a network of connected frontal-temporal-limbic structures. RP GOLD, JM (reprint author), NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. NR 60 TC 59 Z9 61 U1 5 U2 6 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-4388 J9 CURR OPIN NEUROBIOL JI Curr. Opin. Neurobiol. PD APR PY 1995 VL 5 IS 2 BP 225 EP 230 DI 10.1016/0959-4388(95)80030-1 PG 6 WC Neurosciences SC Neurosciences & Neurology GA QW012 UT WOS:A1995QW01200013 PM 7620311 ER PT J AU BRYANT, SH ALTSCHUL, SF AF BRYANT, SH ALTSCHUL, SF TI STATISTICS OF SEQUENCE-STRUCTURE THREADING SO CURRENT OPINION IN STRUCTURAL BIOLOGY LA English DT Article ID TERTIARY STRUCTURE PREDICTION; PROTEIN FOLD RECOGNITION; STRONG LIMIT-THEOREMS; 3-DIMENSIONAL STRUCTURES; DNA-SEQUENCES; PARTIAL-SUMS; SIMILARITIES; IDENTIFICATION; SEARCH; MODELS AB The past two years have seen the rapid development of new recognition methods for protein structure prediction. These algorithms 'thread' the sequence of one protein through the known structure of another, looking for an alignment that corresponds to an energetically favorable model structure. Because they are based on energy calculation, rather than evolutionary distance, these methods extend the possibility of structure prediction by comparative modeling to a larger class of new sequences, where similarity to known structures is recognizable by no other means. The strength of the evidence they offer should be judged by objective statistical tests, however, so as to rule out the possibility that favorable scores arise from chance factors such as similarity of length, composition, or the consideration of a large number of alternative alignments. Calculation of objective p-values by analytical means is not yet possible, but it would appear that approximate values may be obtained by simulation, as they are in gapped, global sequence alignment. We propose that the results of threading experiments should include Z-scores relative to the composition-corrected score distribution obtained for shuffled and optimally aligned sequences. RP BRYANT, SH (reprint author), NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,COMPUTAT BIOL BRANCH,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 73 TC 105 Z9 112 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-440X J9 CURR OPIN STRUC BIOL JI Curr. Opin. Struct. Biol. PD APR PY 1995 VL 5 IS 2 BP 236 EP 244 DI 10.1016/0959-440X(95)80082-4 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RA494 UT WOS:A1995RA49400014 PM 7648327 ER PT J AU CSERJESI, P BROWN, D LIGON, KL LYONS, GE COPELAND, NG GILBERT, DJ JENKINS, NA OLSON, EN AF CSERJESI, P BROWN, D LIGON, KL LYONS, GE COPELAND, NG GILBERT, DJ JENKINS, NA OLSON, EN TI SCLERAXIS - A BASIC HELIX-LOOP-HELIX PROTEIN THAT PREFIGURES SKELETAL FORMATION DURING MOUSE EMBRYOGENESIS SO DEVELOPMENT LA English DT Article DE BHLH PROTEIN; SCLEROTOME; SOMITES; CHONDROGENESIS; MOUSE; SCLERAXIS; SKELETAL FORMATION ID T-CELL LEUKEMIA; DNA-BINDING; NEURAL CREST; E2A PRODUCTS; HLH PROTEINS; LINKAGE MAP; GENE; EXPRESSION; SEQUENCE; SYSTEM AB Members of the basic helix-loop-helix (bHLH) family of transcription factors have been shown to regulate growth and differentiation of numerous cell types. Cell-type-specific bHLH proteins typically form heterodimers with ubiquitous bHLH proteins, such as E12, and bind a DNA consensus sequence known as an E-box, We used the yeast two-hybrid system to screen mouse embryo cDNA libraries for cDNAs encoding novel cell-type-specific bHLH proteins that dimerize with E12. One of the cDNAs isolated encoded a novel bHLH protein, called scleraxis. During mouse embryogenesis, scleraxis transcripts were first detected between day 9.5 and 10.5 post coitum (p.c.) in the sclerotome of the somites and in mesenchymal cells in the body wall and limb buds, Subsequently, scleraxis was expressed at high levels within mesenchymal precursors of the axial and appendicular skeleton and in cranial mesenchyme in advance of chondrogenesis; its expression pattern in these cell types foreshadowed the developing skeleton, Prior to formation of the embryonic cartilaginous skeleton, scleraxis expression declined to low levels, As development proceeded, high levels of scleraxis expression became restricted to regions where cartilage and connective tissue formation take place, Scleraxis bound the E-box consensus sequence as a heterodimer with E12 and activated transcription of a reporter gene linked to its DNA-binding site. The expression pattern, DNA-binding properties and transcriptional activity of scleraxis suggest that it is a regulator of gene expression within mesenchymal cell lineages that give rise to cartilage and connective tissue. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT BIOCHEM & MOLEC BIOL,HOUSTON,TX 77030. UNIV WISCONSIN,SCH MED,DEPT ANAT,MADISON,WI 53706. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 49 TC 245 Z9 253 U1 0 U2 5 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 1995 VL 121 IS 4 BP 1099 EP 1110 PG 12 WC Developmental Biology SC Developmental Biology GA QT121 UT WOS:A1995QT12100016 PM 7743923 ER PT J AU MURTOMAKI, S TRENKNER, E WRIGHT, JM SAKSELA, O LIESI, P AF MURTOMAKI, S TRENKNER, E WRIGHT, JM SAKSELA, O LIESI, P TI INCREASED PROTEOLYTIC ACTIVITY OF THE GRANULE NEURONS MAY CONTRIBUTE TO NEURONAL DEATH IN THE WEAVER MOUSE CEREBELLUM SO DEVELOPMENTAL BIOLOGY LA English DT Article ID OUTGROWTH-PROMOTING DOMAIN; CENTRAL-NERVOUS-SYSTEM; MUTANT MICE; PLASMINOGEN-ACTIVATOR; NEURITE OUTGROWTH; CELL-MIGRATION; LAMININ IMMUNOHISTOCHEMISTRY; EXTRACELLULAR-MATRIX; ADHESION MOLECULES; BERGMANN GLIA AB The weaver mouse mutation is a genetic defect of unknown origin that leads to impairment of cerebellar granule neuronal migration and to neuronal cell death, We investigated laminin expression and proteolytic enzyme activity in this migration-deficient mouse mutant in vivo and in vitro to search for a molecular basis for the weaver defect, The weaver cerebellum showed a general increase in immunoreactivity for laminin, for a neurite outgrowth domain of the B2 chain of laminin, and for tissue plasminogen activator compared to the normal animals, Zymographic assays and immunocytochemistry confirmed that tissue plasminogen activator was the proteolytic enzyme synthesized in excess in the weaver mouse cerebellum in vivo. When placed in culture, the weaver granule neurons survived poorly on a laminin substratum, and failed to extend long neurites, unlike the normal cerebellar granule neurons, The cultured weaver granule neurons were proteolytically overactive and secreted excessive amounts of tissue plasminogen activator, which was likely to interfere with their neurite outgrowth potential on a laminin substratum. Indeed, the weaver granule neurons but not the normal neurons degraded laminin from their culture substratum and deposited a neurite outgrowth domain of the B2 chain of laminin onto their surfaces, Electrophysiology showed that the weaver granule neurons had poor resting membrane potentials (-38 V), whereas the normal neurons had normal resting membrane potentials of (-61 V). The resting membrane potentials of the weaver granule neurons were restored to near normal (-59 V) by a protease inhibitor, aprotinin, Aprotinin also rescued the weaver granule neurons from death on a laminin substratum and promoted their neurite outgrowth to the level of the normal animals, These results indicate that increased proteolytic activity accompanied with increased synthesis of laminin, and its B2 chain, distinguish the weaver mutation from the normal animals. These molecular changes may contribute to the impairment of granule neuronal migration and to the neuronal death, characteristic of the weaver mutation. (C) 1995 Academic Press, Inc. C1 UNIV HELSINKI, DEPT ANAT, SF-00170 HELSINKI, FINLAND. INST BASIC RES DEV DISABIL, STATEN ISL, NY 10314 USA. NIAAA, MOLEC & CELLULAR NEUROBIOL LAB, ROCKVILLE, MD 20852 USA. HELSINKI UNIV, DEPT VIROL, SF-00270 HELSINKI, FINLAND. NR 82 TC 60 Z9 62 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD APR PY 1995 VL 168 IS 2 BP 635 EP 648 DI 10.1006/dbio.1995.1108 PG 14 WC Developmental Biology SC Developmental Biology GA QT125 UT WOS:A1995QT12500034 PM 7729594 ER PT J AU BELLAIRS, R LEAR, P YAMADA, KM RUTISHAUSER, U LASH, JW AF BELLAIRS, R LEAR, P YAMADA, KM RUTISHAUSER, U LASH, JW TI POSTERIOR EXTENSION OF THE CHICK NEPHRIC (WOLFFIAN) DUCT - THE ROLE OF FIBRONECTIN AND NCAM POLYSIALIC ACID SO DEVELOPMENTAL DYNAMICS LA English DT Article DE NEPHRIC DUCT; FIBRONECTIN; POLYSIALIC ACID-NCAM ID CELL-MIGRATION; SYNTHETIC PEPTIDES; PRONEPHRIC DUCT; ADHESION; SOMITOGENESIS; EMBRYO; INHIBITORS; SUBSTRATE; MEMBRANE; GUIDANCE AB The nephric duct of the chick embryo starts to form at about stage 10 of Hamburger and Hamilton ([1951] J. Morphol. 88:49-92) and extends posteriorly, fusing with the cloaca at about the end of the third day of incubation (HH stage 17), Evidence from the literature suggests that the extension involves active migration of the posterior tip, This investigation concerned some molecules that might control this migration: fibronectin, vitronectin, the pl integrin receptor, and NCAM polysialic acid, The concentration of fibronectin in the extracellular matrix was found by immunocytochemistry to be negligible at the posterior end of the duct; treatment of the living embryo with GRGDS failed to halt further extension of the duct; SEM examination of embryos treated with the synthetic peptides of fibronectin GRGDS, GRDGS, SDGR, and GRGES, or with vitronectin, revealed negligible morphological effects on the duct. It is concluded that there is yet no evidence that fibronectin is an important factor in duct migration, NCAM polysialic acid had a similar distribution to fibronectin, but treatment of the living embryo with Endo-N caused cessation of extension of the duct. Endo-N is an enzyme that specifically degrades PSA without affecting the NCAM polypeptide itself, It is suggested therefore that PSA may play an important role in duct extension. The synthetic peptides of fibronectin each produced distinctive patterns of blebbing on the surfaces of cells in trunk mesoderm, but the duct cells were unaffected. GRGES and SDGR caused blebbing on cells in the somites and the anterior segmental plate, though not on cells in the posterior segmental plate, This suggests that integrin receptors change in the anterior segmental plate as the mesoderm forms somites from somitomeres. (C) 1995 Wiley-Liss, Inc. C1 UNIV PENN,SCH MED,DEPT CELL & DEV BIOL,PHILADELPHIA,PA 19104. UNIV LONDON UNIV COLL,DEPT ANAT & DEV BIOL,LONDON WC1E 6BT,ENGLAND. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. CASE WESTERN RESERVE UNIV,DEPT GENET,CLEVELAND,OH 44106. OI Yamada, Kenneth/0000-0003-1512-6805 FU NICHD NIH HHS [HD18369, HD-21048]; Wellcome Trust NR 50 TC 16 Z9 16 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 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD APR PY 1995 VL 202 IS 4 BP 333 EP 342 PG 10 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA QU448 UT WOS:A1995QU44800002 PM 7542937 ER PT J AU ZHADANOV, AB BERTUZZI, S TAIRA, M DAWID, IB WESTPHAL, H AF ZHADANOV, AB BERTUZZI, S TAIRA, M DAWID, IB WESTPHAL, H TI EXPRESSION PATTERN OF THE MURINE LIM CLASS HOMEOBOX GENE LHX3 IN SUBSETS OF NEURAL AND NEUROENDOCRINE TISSUES SO DEVELOPMENTAL DYNAMICS LA English DT Article DE LHX3; LIM; HOMEODOMAIN; PITUITARY; CNS; DEVELOPMENT ID TOUCH RECEPTOR NEURONS; TRANSCRIPTION FACTORS; CELL PHENOTYPES; PROTEIN ISL-1; INSULIN GENE; FLOOR PLATE; BOX GENE; HOMEODOMAIN; ELEGANS; DOMAIN AB Murine Lhx3 cDNA isolated from the mouse pituitary cDNA Library encodes a LIM-type homeodomain protein that contains two tandemly repeated LIM domains and the homeodomain, The identities of predicted amino acid sequences between the mouse Lhx3 and Xenopus Xlim-3 genes are 80, 95, and 97% in the LIM domains 1 and 2, and the homeodomain, respectively, and 84% in the entire protein, 5'-RACE procedures and genomic cloning revealed that two distinct N-terminal sequences arise from. two different exons la and Ib, Exon 1a encodes a sequence similar to that of Xlim-3, whereas exon 1b encodes a different N-terminus. It is likely that there are two transcription initiation sites in the Lhx3 gene. The Lhx3 transcripts were detected by whole mount in situ hybridization as early as day E9.5 post coitum in Rathke's pouch and the dosing neural tube. During subsequent development, Lhx3 expression was observed in the anterior and intermediate but not in the posterior lobes of the pituitary, and in the ventral hindbrain and spinal cord. Northern blot analysis of adult tissues showed that Lhx3 mRNA persists in the pituitary. The expression pattern of Lhx3 is well conserved between Xenopus and mouse, underscoring the functional importance of this gene as a regulator of development. A number of established cell lines of pituitary origin express Lhx3 and therefore constitute a useful tool for further study of Lhx3 gene function. (C) 1995 Wiley-Liss, Inc. C1 NICHHD,GENET MOLEC LAB,BETHESDA,MD 20892. RP ZHADANOV, AB (reprint author), NICHHD,MAMMALIAN GENES & DEV LAB,BLDG 6B,ROOM 413,BETHESDA,MD 20892, USA. NR 42 TC 125 Z9 127 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 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD APR PY 1995 VL 202 IS 4 BP 354 EP 364 PG 11 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA QU448 UT WOS:A1995QU44800004 PM 7626792 ER PT J AU HANSON, RL PETTITT, DJ BENNETT, PH NARAYAN, KMV FERNANDES, R DECOURTEN, M KNOWLER, WC AF HANSON, RL PETTITT, DJ BENNETT, PH NARAYAN, KMV FERNANDES, R DECOURTEN, M KNOWLER, WC TI FAMILIAL RELATIONSHIPS BETWEEN OBESITY AND NIDDM SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; PIMA-INDIANS; GLUCOSE; TWINS AB Obesity and family history of diabetes are both risk factors for non-insulin-dependent diabetes mellitus (NIDDM), but it has been proposed that lean individuals with NIDDM have a greater load of diabetes susceptibility genes. If this is the case, one might expect a high prevalence of NIDDM in relatives of diabetic individuals with a low body mass index (BMI). Among Pima Indians participating in an epidemiological study, prevalence of NIDDM was evaluated in relation to BMI of a diabetic parent or to the average parental BMI when both parents had diabetes in 1,535 offspring from 547 families. Prevalence of NIDDM was also evaluated in relation to BMI of a randomly selected index diabetic sibling in 1,722 siblings from 721 families. NIDDM was diagnosed by an oral glucose tolerance test. Compared with offspring of diabetic parent(s) at the 25th percentile of BMI, the odds ratio (OR) for diabetes in offspring of diabetic parents at the 75th percentile was 0.6 (95% confidence interval [CI] 0.5-0.7), adjusted for age, sex, BMI in offspring, number of diabetic parents, and age at onset of diabetes and sex of the diabetic parent(s). In the analysis according to BMI in a diabetic sibling, the corresponding OR was 0.8 (95% CI 0.6-0.9), Risk ratios were only modestly higher when the analysis was restricted to relatives of subjects whose BMI had been determined before the onset of diabetes. NIDDM in the presence of a low BMI is more strongly familial than that at a higher BMI. This may indicate that a greater load of familial determinants of diabetes is present in leaner diabetic people, and it suggests that these determinants are largely separate from those that result in familial aggregation of obesity. RP HANSON, RL (reprint author), NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,DIABET & ARTHRITIS EPIDEMIOL SECT,PHOENIX,AZ 85014, USA. RI Narayan, K.M. Venkat /J-9819-2012; Hanson, Robert/O-3238-2015 OI Narayan, K.M. Venkat /0000-0001-8621-5405; Hanson, Robert/0000-0002-4252-7068 NR 30 TC 21 Z9 21 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 1995 VL 44 IS 4 BP 418 EP 422 DI 10.2337/diabetes.44.4.418 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QZ335 UT WOS:A1995QZ33500009 PM 7698510 ER PT J AU THOMPSON, DB JANSSEN, RC OSSOWSKI, VM PROCHAZKA, M KNOWLER, WC BOGARDUS, C AF THOMPSON, DB JANSSEN, RC OSSOWSKI, VM PROCHAZKA, M KNOWLER, WC BOGARDUS, C TI EVIDENCE FOR LINKAGE BETWEEN A REGION ON CHROMOSOME 1P AND THE ACUTE INSULIN-RESPONSE IN PIMA-INDIANS SO DIABETES LA English DT Note ID DEPENDENT DIABETES-MELLITUS; FAMILIAL NIDDM; RECEPTOR GENE; GLUCOSE; PATHOGENESIS; GLUCOKINASE; MUTATIONS AB A low acute insulin response (AIR) is a predictor of non-insulin-dependent diabetes mellitus (NIDDM) in insulin-resistant Pima Indians. We have initiated a search for regions of the genome linked with the AIR using sib-pair linkage analysis as a first step in identifying genes that are determinants of this phenotype. Eighteen short tandem-repeat polymorphisms from chromosome 1 were genotyped in over 900 Pima Indians and tested for linkage with NIDDM and in a subset of Pima Indians for linkage with ATR. The anonymous DNA marker D1S198 on chromosome 1p was linked with AIR (P = 0.000056) in 175 sib pairs from 60 families, all with normal glucose tolerance, but no linkage was observed between D1S198 and NIDDM (P = 0.44, 996 sib pairs). Additional markers genotyped on chromosome 1 did not show linkage with AIR or NIDDM. This study indicates that a locus on chromosome 1p may be a determinant of the phenotypic variation seen in the ATR. RP THOMPSON, DB (reprint author), NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,4212 N 16TH ST,ROOM 541,PHOENIX,AZ 85016, USA. FU NCRR NIH HHS [1-P41-RR-03655] NR 29 TC 51 Z9 51 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 1995 VL 44 IS 4 BP 478 EP 481 DI 10.2337/diabetes.44.4.478 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QZ335 UT WOS:A1995QZ33500019 PM 7698519 ER PT J AU WARNE, DK CHARLES, MA HANSON, RL JACOBSSON, LTH MCCANCE, DR KNOWLER, WC PETTITT, DJ AF WARNE, DK CHARLES, MA HANSON, RL JACOBSSON, LTH MCCANCE, DR KNOWLER, WC PETTITT, DJ TI COMPARISON OF BODY-SIZE MEASUREMENTS AS PREDICTORS OF NIDDM IN PIMA-INDIANS SO DIABETES CARE LA English DT Article ID DEPENDENT DIABETES-MELLITUS; FAT DISTRIBUTION; GLUCOSE-INTOLERANCE; INSULIN-RESISTANCE; MEXICAN-AMERICANS; OBESITY; ADIPOSITY; MEN; HYPERINSULINEMIA; WOMEN AB OBJECTIVE-To determine and compare the abilities of various anthropometric measurements to predict the development of non-insulin-dependent diabetes mellitus (NIDDM) in Pima Indian men and women. RESEARCH DESIGN AND METHODS-A total of 290 male and 443 female Pima Indians were followed for up to 6 years for the development of NIDDM. A proportional hazards analysis was used to assess the ability of anthropometric measurements evaluated at baseline to predict NIDDM. Receiver operating characteristic (ROC) curves were used to compare individual variables in predicting NIDDM. RESULTS-In separate models controlled for age and sex, body mass index (BMI), waist circumference, thigh circumference, waist-to-thigh ratio (WTR), weight, and percentage body fat (PBF) estimated by bioelectric resistance each predicted NIDDM, which developed in 30 men and 52 women. The highest incidence rate ratios (IRRs; for 1 SD of a variable) were for WTR in men and for PBF in women, although the confidence interval (CI) for PBF was wide. In stepwise analyses, WTR was the most significant predictor in men (IRR for 1 SD = 1.58, 95% CI = 1.20-2.07), and BMI was the most significant predictor in women (IRR for 1 SD = 1.65, 95% CI. = 1.29-2.11). However, by ROC analyses, thigh circumference was the only variable significantly worse than WTR in men or BMI in women at predicting NIDDM. CONCLUSIONS-Measurements such as waist circumference, WTR, weight, and BMI may be as useful as more complicated measurements, such as PBF by bioelectric resistance, for identifying groups of individuals whose body habitus places them at high risk of developing NIDDM. C1 NIDDKD,DIABET & ARTHRIT EPIDEMIOL SECT,PHOENIX,AZ 85014. RI Hanson, Robert/O-3238-2015 OI Hanson, Robert/0000-0002-4252-7068 NR 25 TC 40 Z9 40 U1 0 U2 2 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD APR PY 1995 VL 18 IS 4 BP 435 EP 439 DI 10.2337/diacare.18.4.435 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QQ216 UT WOS:A1995QQ21600001 PM 7497850 ER PT J AU ACCILI, D AF ACCILI, D TI MOLECULAR DEFECTS OF THE INSULIN-RECEPTOR GENE SO DIABETES-METABOLISM REVIEWS LA English DT Review RP ACCILI, D (reprint author), NIDDK,DIABET BRANCH,BLDG 10,ROOM 8N 244,BETHESDA,MD 20892, USA. NR 0 TC 29 Z9 29 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0742-4221 J9 DIABETES METAB REV JI Diabetes-Metab. Rev. PD APR PY 1995 VL 11 IS 1 BP 47 EP 62 PG 16 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QR199 UT WOS:A1995QR19900004 PM 7600907 ER PT J AU PROCHAZKA, M MOCHIZUKI, H BAIER, LJ COHEN, PTW BOGARDUS, C AF PROCHAZKA, M MOCHIZUKI, H BAIER, LJ COHEN, PTW BOGARDUS, C TI MOLECULAR AND LINKAGE ANALYSIS OF TYPE-1 PROTEIN PHOSPHATASE CATALYTIC BETA-SUBUNIT GENE - LACK OF EVIDENCE FOR ITS MAJOR ROLE IN INSULIN-RESISTANCE IN PIMA-INDIANS SO DIABETOLOGIA LA English DT Article DE INSULIN RESISTANCE; TYPE-1 PROTEIN PHOSPHATASE; PP1-BETA CATALYTIC SUBUNIT GENE; PIMA INDIANS ID ISOFORMS; MUSCLE; NIDDM AB Insulin resistance is believed to be a prediabetic condition that results from reduced rates of insulin-mediated glycogen synthesis in skeletal muscle. A decrease in activities of skeletal muscle glycogen synthase and of its regulatory enzyme type-1 protein phosphatase (PP 1) have been previously identified in insulin-resistant Pima Indians. Because the PP1 catalytic beta-subunit is presumed to be the major isoform in the glycogen-bound PP1 complex, we have selected the structural gene for this subunit (PPP1CB) as a candidate for a detailed genetic analysis. We have determined the exon-intron structure of PPP1CB, and have identified a polymorphic (CA)-repeat marker (D2S1237) at this gene. No sequence abnormalities were detected in PPP1CB by Southern blot analysis or by single-stranded conformational polymorphism analysis of all eight coding exons. Using sib-pair linkage analyses, no evidence for linkage was found between the D2S1237 marker at this locus and fasting insulin, insulin-stimulated glucose uptake in vivo, obesity, or non-insulin-dependent diabetes mellitus. Similarly, we have found no evidence for association of D2S1237 with any of these phenotypes. Based on our data we conclude that the structural gene for the PP1 catalytic beta-subunit does not appear to be a major genetic determinant responsible for the PP1 abnormalities characteristic of insulin resistance in Pima Indians. C1 UNIV DUNDEE,DEPT BIOCHEM,MRC,PROT PHOSPHORYLAT UNIT,DUNDEE DD1 4HN,SCOTLAND. RP PROCHAZKA, M (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,PHOENIX,AZ 85016, USA. FU NCRR NIH HHS [1P41RR03655] NR 22 TC 24 Z9 25 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD APR PY 1995 VL 38 IS 4 BP 461 EP 466 DI 10.1007/BF00410284 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QN462 UT WOS:A1995QN46200011 PM 7796987 ER PT J AU LIU, SY GONZALEZ, FJ AF LIU, SY GONZALEZ, FJ TI ROLE OF THE LIVER-ENRICHED TRANSCRIPTION FACTOR HNF-1-ALPHA IN EXPRESSION OF THE CYP2E1 GENE SO DNA AND CELL BIOLOGY LA English DT Article ID RAT ALBUMIN PROMOTER; MAMMALIAN-CELLS; PROTEINS; ELEMENTS; UPSTREAM; BINDING; HNF-1; DNA; DIMERIZATION; HETERODIMERS AB The role of the trans-acting factor HNF-1 alpha in activating CYP2E1 gene expression was confirmed by transient co-transfection of an HNF-1 alpha expression plasmid and the CYP2E1 promoter fused to the chloramphenicol acetyl transferase (CAT) reporter gene, Only HNF-1 alpha, and not HNF-1 beta, HNF-4, C/EBP alpha, C/EBP beta, or DBP, was able to activate the CYP2E1 promoter, The extent of activation was proportional to the number of copies of the HNF-1 binding sequence upstream of the promoter, Removal or mutation of the HNF-1 binding sequence led to inactivation of the promoter in response to HNF-1 alpha. Gel-shift Western blot analysis using a synthetic HNF-1 binding sequence derived from CYP2E1 and rat liver nuclear extract revealed that the protein-DNA complex obtained with adult rat liver nuclear extract consisted of both HNF-1 alpha and HNF-1 beta proteins, The shifted bands produced by nuclear extracts from adult, where the endogenous CYP2E1 gene is active, and fetal rat liver, where the gene is inactive, were found to migrate differently, suggesting that the population of factors, possibly including different ratios of HNF-1 alpha and HNF-1 beta proteins, map change during development, However, the co-transfection study did not show cooperativity between the two factors, Elements upstream of the HNF-1 binding site were found to affect the activity of the promoter negatively in the transfection assay, DNase I hypersensitive site mapping revealed a hypersensitive site in this inhibiting element in the adult rat liver sample but not in liver from newborn animals. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 38 TC 58 Z9 59 U1 0 U2 1 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 1995 VL 14 IS 4 BP 285 EP 293 DI 10.1089/dna.1995.14.285 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA QT799 UT WOS:A1995QT79900002 PM 7710685 ER PT J AU OTTERNESS, DM HER, C AKSOY, S KIMURA, S WIEBEN, ED WEINSHILBOUM, RM AF OTTERNESS, DM HER, C AKSOY, S KIMURA, S WIEBEN, ED WEINSHILBOUM, RM TI HUMAN DEHYDROEPIANDROSTERONE SULFOTRANSFERASE GENE - MOLECULAR-CLONING AND STRUCTURAL CHARACTERIZATION SO DNA AND CELL BIOLOGY LA English DT Article ID THERMOSTABLE PHENOL SULFOTRANSFERASE; HUMAN-LIVER; RAT-LIVER; ESTROGEN SULFOTRANSFERASE; SEQUENCE-ANALYSIS; MESSENGER-RNA; HYDROXYSTEROID SULFOTRANSFERASE; PST ACTIVITY; MOUSE-LIVER; CDNA AB Dehydroepiandrosterone sulfotransferase (DHEA ST) catalyzes the sulfate conjugation of DHEA and other steroids, From 20 to 25% of subjects are included in a subgroup with high levels of hepatic DHEA ST activity, raising the possibility that this enzyme activity might be controlled by a genetic polymorphism, To understand the molecular mechanisms involved in regulating levels of DHEA ST activity in human tissue, we cloned the human DHEA ST gene, STD, STD spans at least 17 kb and is composed of 6 exons and 5 introns, The locations of the splice junctions for several of the introns are identical to those present in the rat phenol or aryl ST gene, the only other cytosolic ST gene for which the entire exon/intron structure has been reported, as well as those present in two partially characterized genes for the rat senescence marker protein, genes that are also thought to encode ST enzymes, The 5'-flanking region of the human STD gene does not contain canonical TATA or CCAAT elements, but this region is capable of promoting transcription of a reporter gene in Hep G2 cells. Molecular cloning and structural characterization of the human STD gene will make it possible to study genetic mechanisms involved in the regulation of DHEA ST activity in human tissue. C1 MAYO CLIN & MAYO FDN,SCH MED,DEPT PHARMACOL,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,SCH MED,DEPT BIOCHEM & MOLEC BIOL,ROCHESTER,MN 55905. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM 35720, GM 28157] NR 55 TC 43 Z9 44 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 1995 VL 14 IS 4 BP 331 EP 341 DI 10.1089/dna.1995.14.331 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA QT799 UT WOS:A1995QT79900007 PM 7710689 ER PT J AU GRANT, BF AF GRANT, BF TI THE DSM-IV FIELD TRIAL FOR SUBSTANCE USE DISORDERS - MAJOR RESULTS SO DRUG AND ALCOHOL DEPENDENCE LA English DT Note RP GRANT, BF (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,SUITE 514,6000 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCI PUBL 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 1995 VL 38 IS 1 BP 71 EP 75 DI 10.1016/0376-8716(94)01093-Z PG 5 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA QZ667 UT WOS:A1995QZ66700010 ER PT J AU ISSAQ, HJ CHAN, KC AF ISSAQ, HJ CHAN, KC TI SEPARATION AND DETECTION OF AMINO-ACIDS AND THEIR ENANTIOMERS BY CAPILLARY ELECTROPHORESIS - A REVIEW SO ELECTROPHORESIS LA English DT Article DE CAPILLARY ELECTROPHORESIS; AMINO ACIDS; ENANTIOMERS; FLUOROGENIC REAGENTS; LASER INDUCED FLUORESCENCE DETECTION ID LASER-INDUCED FLUORESCENCE; MICELLAR ELECTROKINETIC CHROMATOGRAPHY; PERFORMANCE LIQUID-CHROMATOGRAPHY; HOST-GUEST COMPLEXATION; ZONE ELECTROPHORESIS; OPTICAL ISOMERS; RESOLUTION; OPTIMIZATION; DERIVATIVES; SENSITIVITY AB Since its introduction as an analytical technique capillary electrophoresis has been used for the separation of amino acids and their enantiomers; over 150 studies have been published to date. This review deals with their separation and detection. Amino acids have been resolved using both capillary zone electrophoresis and micellar electrokinetic chromatography. Pre-column derivatization schemes which are employed for the sensitive detection of amino acids are discussed. Criteria for the selection of the pre- or post-column derivatizing agent, chromophore or fluorophore, are presented. Detection systems, direct and indirect, that have been used are given with emphasis on fluorogenic reagents and laser induced fluorescence detection. Also, procedures for the separation of amino acid enantiomers are discussed and illustrated. RP ISSAQ, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,POB B,FREDERICK,MD 21702, USA. NR 78 TC 72 Z9 75 U1 2 U2 18 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD APR PY 1995 VL 16 IS 4 BP 467 EP 480 DI 10.1002/elps.1150160178 PG 14 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QZ376 UT WOS:A1995QZ37600002 PM 7588513 ER PT J AU CHAN, KC MUSCHIK, GM ISSAQ, HJ AF CHAN, KC MUSCHIK, GM ISSAQ, HJ TI ENANTIOMERIC SEPARATION OF AMINO-ACIDS USING MICELLAR ELECTROKINETIC CHROMATOGRAPHY AFTER PRECOLUMN DERIVATIZATION WITH THE CHIRAL REAGENT 1-(9-FLUORENYL)ETHYL CHLOROFORMATE SO ELECTROPHORESIS LA English DT Article DE MICELLAR ELECTROKINETIC CHROMATOGRAPHY; ENANTIOMERS; CYCLODEXTRIN; AMINO ACIDS ID CAPILLARY ZONE ELECTROPHORESIS; PRECOLUMN DERIVATIZATION; LIQUID-CHROMATOGRAPHY; COMPLEXATION; SURFACTANTS; RESOLUTION; PROTEINS; PEPTIDES AB Direct enantiomeric separations of some racemic amino acids derivatized with 9-fluorenylmethyl chloroformate were obtained using cyclodextrin-modified micellar electrokinetic chromatography (CD/MEKC) with a buffer made up of 5 mM sodium berate (pH 9.2), 150 mM sodium dodecyl sulfate (SDS) and 40 mM gamma-CD. Alternatively, enantiomeric separations were also achieved indirectly using MEKC after pre-column derivatization with (+)-1-(9-fluorenyl) ethyl chloroformate (FLEC). Using either a 10 mM sodium phosphate (pH 6.8) or a 5 mM sodium berate buffer (pH 9.2), each of which contained 25 mM SDS and 10-15% of acetonitrile, FLEC-derivatized serine, alanine, valine. methionine, leucine, phenylalanine, tryptophan, and their diastereomeric pairs were all separated: the L-isomers migrated faster than the corresponding D-isomers. However, when (-)-FLEC was used for derivatization, the D-isomers migrated faster than the corresponding L-isomers. Also, the diastereomers of aspartic acid, glutamic acid, and proline were resolved using a 10 mM sodium citrate buffer (pH 4.4). Using KrF (248 nm) laser-induced fluorescence, the detection limit of (+)-FLEC derivatized DL-amino acids was obtained at the nM level, which was about 100 X more sensitive than UV absorption at 200 nm. Analyte concentrations as low as 3 X 10(-8) M (DL-Val) could be derivatized with (+)-FLEC. RP CHAN, KC (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,POB B,FREDERICK,MD 21702, USA. NR 23 TC 30 Z9 32 U1 1 U2 6 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD APR PY 1995 VL 16 IS 4 BP 504 EP 509 DI 10.1002/elps.1150160183 PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA QZ376 UT WOS:A1995QZ37600007 PM 7588518 ER PT J AU AKSOY, S ARITURK, S ARMSTRONG, MYK CHANG, KP DORTBUDAK, Z GOTTLIEB, M OZCEL, MA RICHARDS, FF WESTERN, K AF AKSOY, S ARITURK, S ARMSTRONG, MYK CHANG, KP DORTBUDAK, Z GOTTLIEB, M OZCEL, MA RICHARDS, FF WESTERN, K TI THE GAP PROJECT IN SOUTHEASTERN TURKEY - THE POTENTIAL FOR EMERGENCE OF DISEASES SO EMERGING INFECTIOUS DISEASES LA English DT Letter C1 DICLE UNIV,DIYARBAKIR,TURKEY. CHICAGO MED SCH,CHICAGO,IL. NIAID,BETHESDA,MD. EGE UNIV,FAC MED,IZMIR,TURKEY. RP AKSOY, S (reprint author), YALE UNIV,SCH MED,NEW HAVEN,CT 06510, USA. OI Aksoy, Serap/0000-0001-9941-143X NR 14 TC 16 Z9 19 U1 0 U2 1 PU CENTER DISEASE CONTROL PI ATLANTA PA ATLANTA, GA 30333 J9 EMERG INFECT DIS JI Emerg. Infect. Dis PD APR-JUN PY 1995 VL 1 IS 2 BP 62 EP 63 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA TD318 UT WOS:A1995TD31800007 PM 8903163 ER PT J AU CETRON, MS JERNIGAN, DB BREIMAN, RF BIRKHEAD, G BUTLER, JC CARTTER, ML CHESNEY, JP CRAIG, W GAYNES, RP GILCHRIST, MJR HOFFMAN, RE JORGENSEN, J KLEIN, D OBRIEN, T SCHWARTZ, B SHELDON, A SPITALNY, KC TENOVER, FC TIMPERI, RJ AF CETRON, MS JERNIGAN, DB BREIMAN, RF BIRKHEAD, G BUTLER, JC CARTTER, ML CHESNEY, JP CRAIG, W GAYNES, RP GILCHRIST, MJR HOFFMAN, RE JORGENSEN, J KLEIN, D OBRIEN, T SCHWARTZ, B SHELDON, A SPITALNY, KC TENOVER, FC TIMPERI, RJ TI ACTION PLAN FOR DRUG-RESISTANT STREPTOCOCCUS-PNEUMONIAE SO EMERGING INFECTIOUS DISEASES LA English DT Note C1 NEW YORK STATE DEPT HLTH,ALBANY,NY 12237. COUNCIL STATE & TERR EPIDEMIOLOGISTS,AUSTIN,TX. CONNECTICUT DEPT PUBL HLTH & ADDICT SERV,HARTFORD,CT 06106. AMER ACAD PEDIAT,ELK GROVE VILLAGE,IL 60007. COLORADO DEPT PUBL HLTH & ENVIRONM,DENVER,CO 80222. NATL COMM CLIN LAB STAND,VILLANOVA,PA 19085. NIAID,BETHESDA,MD 20892. WHO,COLLABORATING CTR ANTIBIOT RESISTANCE,BOSTON,MA. US FDA,ROCKVILLE,MD 20857. NEW JERSEY STATE DEPT HLTH,TRENTON,NJ 08625. ASSOC STATE & TERR PUBL HLTH LAB DIRECTORS,WASHINGTON,DC. RP CETRON, MS (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,1600 CLIFTON RD,MAILSTOP C-12,ATLANTA,GA 30333, USA. NR 9 TC 12 Z9 12 U1 0 U2 0 PU CENTER DISEASE CONTROL PI ATLANTA PA ATLANTA, GA 30333 J9 EMERG INFECT DIS JI Emerg. Infect. Dis PD APR-JUN PY 1995 VL 1 IS 2 BP 64 EP 65 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA TD318 UT WOS:A1995TD31800008 PM 8903164 ER PT J AU LEROITH, D WERNER, H BEITNERJOHNSON, D ROBERTS, CT AF LEROITH, D WERNER, H BEITNERJOHNSON, D ROBERTS, CT TI MOLECULAR AND CELLULAR ASPECTS OF THE INSULIN-LIKE GROWTH-FACTOR-I RECEPTOR SO ENDOCRINE REVIEWS LA English DT Review ID HUMAN-BREAST-CANCER; NEURO-BLASTOMA CELLS; WILMS-TUMOR GENE; SH2-CONTAINING PHOSPHOTYROSINE PHOSPHATASE; GUANINE-NUCLEOTIDE EXCHANGE; MESSENGER-RIBONUCLEIC-ACID; DEPENDENT PROTEIN-KINASE; CENTRAL-NERVOUS-SYSTEM; HUMAN THYROID-TISSUE; IGF BINDING-PROTEIN RP LEROITH, D (reprint author), NIDDKD, DIABET BRANCH,MOLEC & CELLULAR PHYSIOL SECT, BLDG 10,ROOM 8S239, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. OI Roberts, Charles/0000-0003-1756-5772 NR 291 TC 399 Z9 419 U1 0 U2 8 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0163-769X EI 1945-7189 J9 ENDOCR REV JI Endocr. Rev. PD APR PY 1995 VL 16 IS 2 BP 143 EP 163 DI 10.1210/er.16.2.143 PG 21 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QT902 UT WOS:A1995QT90200002 ER PT J AU EVERSON, CA REED, HL AF EVERSON, CA REED, HL TI PITUITARY AND PERIPHERAL THYROID-HORMONE RESPONSES TO THYROTROPIN-RELEASING-HORMONE DURING SUSTAINED SLEEP-DEPRIVATION IN FREELY MOVING RATS SO ENDOCRINOLOGY LA English DT Article ID BROWN ADIPOSE-TISSUE; HYPOTHALAMIC RELEASE; TRIIODOTHYRONINE; HYPOTHYROIDISM; THYROXINE; SECRETION; COLD; 5'-DEIODINASE; 3,5,3'-TRIIODOTHYRONINE; THERMOGENESIS AB Sleep deprivation is associated with poor cognitive ability and impaired physical health, but the ways in which the brain and body become compromised are not understood. In sleep-deprived rats, plasma total T-4 and T-3 concentrations decline progressively to 78% and 47% below baseline values, respectively, brown adipose tissue 5'-deiodinase type II activity increases 100-fold, and serum TSH values are unknown. The progressive decline in plasma thyroid hormones is associated with a deep negative energy balance despite normal or increased food intake and malnutrition-like symptoms that eventuate in hypothermia and lethal systemic infections. The purpose of the present experiment was to evaluate the probable causes of the low plasma total T-4 during sleep deprivation by measuring the free hormone concentration to minimize binding irregularities and by challenging the pituitary-thyroid axis with iv TRH to determine both 1) the pituitary release of TSH and 2) the thyroidal response of free T-4 (FT4) and free T-3 (FT3) release to the TSH increment. Sleep-deprived rats were awake 91% of the total time compared with 63% of the total time in yoked control rats and 50% of the total time during the baseline period. Cage control comparison rats were permitted to sleep normally. Sustained sleep deprivation resulted in a decline from baseline in plasma FT4 of 73 +/- 6% and FT3 of 45 +/- 12%, which were similar to the declines in total hormone concentrations observed previously; nonstimulated TSH was unchanged. In the yoked and cage control groups, FT4 also declined, but much less than that of the sleep-deprived group. The relative changes in free compared with total hormone concentrations over the study were also less parallel than those in the sleep-deprived group. The plasma TSH response to TRH was similar in all groups across experimental days. The plasma FT4 and FT3 concentrations in sleep-deprived rats increased after TRH-stimulated TSH release to an extent comparable to control values. Taken together, low basal FT4 and FT3 hormone concentrations and unchanged TSH and thyroidal responses to TRH suggest a pituitary or hypothalamic contribution to the hypothyroxinemia during sleep deprivation. C1 WALTER REED ARMY MED CTR, ENDOCRINE SERV, WASHINGTON, DC 20307 USA. RP EVERSON, CA (reprint author), NIMH, CLIN PSYCHOBIOL BRANCH, BLDG 10, ROOM 4S-239, 10 CTR DR MSC 1390, BETHESDA, MD 20892 USA. NR 51 TC 22 Z9 22 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 1995 VL 136 IS 4 BP 1426 EP 1434 DI 10.1210/en.136.4.1426 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QP117 UT WOS:A1995QP11700015 PM 7895653 ER PT J AU TAKAHASHI, S REDDY, SV DALLAS, M DEVLIN, R CHOU, JY ROODMAN, GD AF TAKAHASHI, S REDDY, SV DALLAS, M DEVLIN, R CHOU, JY ROODMAN, GD TI DEVELOPMENT AND CHARACTERIZATION OF A HUMAN MARROW STROMAL CELL-LINE THAT ENHANCES OSTEOCLAST-LIKE CELL-FORMATION SO ENDOCRINOLOGY LA English DT Article ID HUMAN-BONE-MARROW; COLONY-STIMULATING FACTOR; MULTINUCLEATED CELLS; GROWTH-FACTOR; OSTEOPETROTIC MICE; OSTEOBLASTIC CELLS; MOLECULAR-CLONING; SIMIAN VIRUS-40; GENE-EXPRESSION; SPLEEN-CELLS AB We established a human bone marrow stromal cell line (Saka) by infecting marrow adherent cells from semisolid marrow cultures with a recombinant simian virus-40 (SV40) virus. The cells expressed SV40 large tumor antigen, had a fibroblast-like shape, and expressed fibronectin and vimentin. They did not contain detectable alkaline phosphatase activity; express myeloid, lymphoid, or factor VIII-associated antigens; or develop adipocyte-like characteristics with dexamethasone treatment. Polymerase chain reaction analysis of Saka cell RNA detected expression of messenger RNAs for interleukin-6 (IL-6), IL-1 beta, granulocyte-macrophage colony-stimulating factor, macrophage colony-stimulating factor, stem cell factor, and the 1,25-dihydroxyvitamin D-3 receptor. Coculture of Saka cells with human marrow mononuclear cells enhanced formation of osteoclast-like multinucleated cells (MNC) in long term human bone marrow cultures. These MNC expressed calcitonin receptors and formed resorption lacunae on dentine. In contrast, coculture of marrow mononuclear cells with other SV40-transformed human marrow stromal cell lines did not increase MNC formation. Conditioned medium from Saka cells or coculture of bone marrow and Saka cells separated by a Millipore membrane did not enhance MNC formation. Addition of a neutralizing antibody to IL-6 or IL-1 beta blocked the effects of Saka cells on MNC formation. These results suggest that marrow stromal cells enhance osteoclast formation in part through direct cell to cell contact and production of IL-6 and/or IL-1 beta. C1 AUDIE L MURPHY MEM VET ADM MED CTR, RES SERV 151, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. NIH, BETHESDA, MD 20892 USA. FU NCI NIH HHS [CA-40035]; NIADDK NIH HHS [AM-35188]; NIAMS NIH HHS [AR-39539] NR 44 TC 33 Z9 34 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 1995 VL 136 IS 4 BP 1441 EP 1449 DI 10.1210/en.136.4.1441 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QP117 UT WOS:A1995QP11700017 PM 7534699 ER PT J AU OSTROWSKI, NL YOUNG, WS LOLAIT, SJ AF OSTROWSKI, NL YOUNG, WS LOLAIT, SJ TI ESTROGEN INCREASES RENAL OXYTOCIN RECEPTOR GENE-EXPRESSION SO ENDOCRINOLOGY LA English DT Note ID MENSTRUAL-CYCLE; RAT-KIDNEY; VASOPRESSIN; OSMOREGULATION; STEROIDS; HORMONES; BINDING; LIVER AB Estrogens have been implicated in the sodium and fluid imbalances associated with the menstrual cycle and late pregnancy. An estrogen-dependent role for renal oxytocin receptors in fluid homeostasis is suggested by the present findings which demonstrate that estradiol benzoate treatment increases the expression of the oxytocin receptor messenger ribonucleic acid and I-125-OTA binding to oxytocin receptors in the renal cortex and medullary collecting ducts of ovariectomized female rats. Moreover, estradiol induced high levels of oxytocin receptor expression in outer stripe proximal tubules of ovariectomized female and adrenalectomized male rats. Proximal tubule induction was inhibited in a dose-dependent manner by the antiestrogen tamoxifen, but cortical expression of oxytocin receptors in macula densa cells was unaffected by tamoxifen. These data demonstrate cell-specific regulation of oxytocin receptor expression in macula densa and proximal tubule cells, and suggest a important role for these receptors in mediating estrogen-induced alterations in renal fluid dynamics by possibly affecting glomerular filtration and water and solute reabsorption during high estrogen states. RP OSTROWSKI, NL (reprint author), NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA. RI Young, W Scott/A-9333-2009 OI Young, W Scott/0000-0001-6614-5112 NR 24 TC 37 Z9 37 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 1995 VL 136 IS 4 BP 1801 EP 1804 DI 10.1210/en.136.4.1801 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QP117 UT WOS:A1995QP11700065 PM 7895693 ER PT J AU RODBELL, M AF RODBELL, M TI SIGNAL-TRANSDUCTION - EVOLUTION OF AN IDEA SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID ADENYLATE-CYCLASE SYSTEM; GTP-BINDING PROTEINS; GUANINE-NUCLEOTIDES; REGULATORY PROTEINS; PLASMA-MEMBRANES; GUANYL NUCLEOTIDES; ALPHA-SUBUNIT; RAT LIVER; GLUCAGON; DISAGGREGATION RP RODBELL, M (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 64 TC 1 Z9 1 U1 0 U2 0 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1995 VL 103 IS 4 BP 338 EP 345 DI 10.2307/3432286 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA RF452 UT WOS:A1995RF45200006 PM 7607133 ER PT J AU OIKARI, AOJ WALDEN, R PRITCHARD, JB AF OIKARI, AOJ WALDEN, R PRITCHARD, JB TI INHIBITION OF RENAL XENOBIOTIC EXCRETION BY TETRACHLOROGUAIACOL - MECHANISM AND POSSIBLE CONSEQUENCES SO ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY LA English DT Article DE ACTIVE TRANSPORT; KIDNEY MEMBRANES; P-AMINOHIPPURATE; PULP MILL EFFLUENT; CHLOROPHENOLICS ID BASOLATERAL MEMBRANE-VESICLES; MILL EFFLUENTS; RAT-KIDNEY; TRANSPORT; PULP; FISH; WATER; BIOACCUMULATION; AMINOHIPPURATE; TOXICITY AB The weak acid tetrachloroguaiacol (teCG; pK(a) 6.0) is the major chlorinated phenol produced during chlorine bleaching of wood pulp. Upon its release into the environment, it is persistent and markedly bioaccumulated (100- to 1,000-fold). Within the organism (pH similar to 7.4), it should be >95% ionized, making it a likely inhibitor of renal organic anion transport. Its effects on both passive membrane permeability and mediated transport processes were determined in basolateral (BLM) and luminal membrane (BBM) vesicles isolated from the rat kidney cortex. Vesicular solute uptake was measured by the rapid filtration technique at pH 7.5. Passive membrane permeability (assessed by mannitol uptake) was altered only at very high concentrations of teCG (greater than or equal to 1,000 mu M). In contrast, transport of the model organic anion p-aminohippurate (PAH) by BLM vesicles was significantly inhibited by as little as 5 mu M (1.3 mg/L) teCG and totally abolished by 200 mu M. Inhibition was competitive (K-i = 31.3 mu M). Decreasing assay pH diminished inhibition of the PAH uptake, reflecting the reduced concentration of ionized teCG. Other membrane effects were seen at higher teCG concentrations (>100 mu M). The BLM sodium/glutarate cotransport was modestly, but significantly, stimulated by 100 to 500 mu M teCG, whereas BBM sodium/glucose cotransport was inhibited by similar teCG concentrations. Thus, teCG has multiple effects on renal membrane function. However, al environmental levels (0.1 to 30 mu M in plasma), its principal membrane effects would be related to changes in organic anion secretion. C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,RES TRIANGLE PK,NC 27709. HELSINKI UNIV TECHNOL,ENVIRONM PROTECT LAB,SF-02150 ESPOO,FINLAND. NR 29 TC 5 Z9 5 U1 1 U2 2 PU SETAC PRESS PI PENSACOLA PA 1010 NORTH 12TH AVE, PENSACOLA, FL 32501-3370 SN 0730-7268 J9 ENVIRON TOXICOL CHEM JI Environ. Toxicol. Chem. PD APR PY 1995 VL 14 IS 4 BP 669 EP 677 DI 10.1897/1552-8618(1995)14[669:IORXEB]2.0.CO;2 PG 9 WC Environmental Sciences; Toxicology SC Environmental Sciences & Ecology; Toxicology GA QN885 UT WOS:A1995QN88500015 ER PT J AU MALOZOWSKI, S PARMER, TG TROJAN, S MERRIAM, GR GIBORI, G ROBERTS, CT LEROITH, D WERNER, H ZILBERSTEIN, M AF MALOZOWSKI, S PARMER, TG TROJAN, S MERRIAM, GR GIBORI, G ROBERTS, CT LEROITH, D WERNER, H ZILBERSTEIN, M TI GROWTH-HORMONE (GH) MODULATES INSULIN-LIKE GROWTH-FACTOR-I (IGF-I) AND TYPE-I IGF RECEPTOR MESSENGER-RNA LEVELS IN THE OVARY OF PREPUBERTAL GH-DEFICIENT RATS SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Article ID MESSENGER RIBONUCLEIC-ACID; MONOSODIUM GLUTAMATE; GENE-EXPRESSION; SOMATOMEDIN-C; GONADOTROPIN TREATMENT; OVULATION INDUCTION; GRANULOSA-CELLS; FOLLICLE; DIFFERENTIATION; SECRETION AB In order to explore the potential role of growth hormone (GH) in modulating insulin-like growth factor I (IGF-I) gene expression in the prepubertal rat ovary, female rats were rendered GH deficient by neonatal administration of monosodium glutamate (MSG). One group of rats received vehicle and served as the control. At 21 days of age, MSG-treated rats received either GH or vehicle for 2 weeks. On days 21, 24, 28 and 31 animals were weighed and subsets were sacrificed for liver RNA extraction. The remaining animals were sacrificed at day 35 when livers and ovaries were collected, and serum was obtained for GH determinations. The IGF-I mRNA levels were estimated by Northern blots and corroborated further by slot-blot analysis. The MSG-treated rats had lower body weights (p < 0.01) and GH levels (p < 0.05) than controls. Growth hormone replacement significantly accelerated the weight gain of MSG-treated rats. At day 24 and thereafter, three RNA IGF-I species (7.5, 1.8 and 0.8-1.2 kB) were seen in the liver. in the ovary, at age 35 days, two major IGF-I mRNA species (7.5 and 0.8-1.2 kb) were seen. The MSG treatment consistently reduced the levels of both IGF-I mRNA species in the ovary. Growth hormone administration partially restored their expression, both in the liver and in the ovary. In addition, ovarian type I IGF receptor mRNA levels were increased in the MSG-treated rats when compared to controls. This trend was reversed by GH replacement. In summary, we have found that in prepubertal female rats rendered GH deficient with MSG, ovarian IGF-I gene expression is reduced while type I IGF receptor mRNA levels are increased. These findings are reversed with GH replacement. These results suggest a physiological role for GH in modulating IGF-I and type I IGF receptor genes in the ovary. C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. US FDA,DIV METAB & ENDOCRINE DRUG PROD,ROCKVILLE,MD 20857. UNIV ILLINOIS,DEPT PHYSIOL & BIOPHYS,CHICAGO,IL 60612. AMER LAKE VET AFFAIRS MED CTR,SEATTLE,WA 98195. UNIV WASHINGTON,DIV ENDOCRINOL,SEATTLE,WA 98195. NIDDK,DIABET BRANCH,BETHESDA,MD 20892. FU NICHD NIH HHS [HD 11119] NR 35 TC 5 Z9 5 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0804-4643 J9 EUR J ENDOCRINOL JI Eur. J. Endocrinol. PD APR PY 1995 VL 132 IS 4 BP 497 EP 501 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QQ673 UT WOS:A1995QQ67300019 PM 7711889 ER PT J AU BIRKELAND, ML COPELAND, NG GILBERT, DJ JENKINS, NA BARCLAY, AN AF BIRKELAND, ML COPELAND, NG GILBERT, DJ JENKINS, NA BARCLAY, AN TI GENE STRUCTURE AND CHROMOSOMAL LOCALIZATION OF THE MOUSE HOMOLOG OF RAT OX40 PROTEIN SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE OX40; GENE; MOUSE; CHROMOSOME 4 ID TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR RECEPTOR; GENOMIC ORGANIZATION; LINKAGE MAP; FAS ANTIGEN; ACTIVATION; EXPRESSION; ASSIGNMENT; IDENTIFICATION; LYMPHOCYTES AB The OX40 protein is expressed only on activated rat CD4(+) T blasts and is a member of a superfamily of cell surface molecules which includes CD40, CD30, CD95 (Fas), CD27, 4-1BB antigens and the receptors for tumor necrosis factor (TNF) and nerve growth factor (NGF). The proteins of this group are related to each other by having three to six repeats of a cysteine-rich sequence in their extracellular domains. Members of this family of receptors have also been shown to bind to ligands which are structurally related to TNF. The mouse homologue of the rat OX40 protein was cloned at the cDNA and genomic levels. The gene structure shows that there are several intron/exon borders shared between OX40 and CD27, CD40,TNF receptor type I, CD95 and 4-1BB genes. This group of genes is less closely related structurally to the gene structure of the NGF receptor. The gene encoding murine OX40 has been placed on mouse chromosome 4, in an area which contains the genes for TNF receptor type II and 4-1BB, and is syntenic with a region of human chromosome 1 which contains human TNF receptor type II, OX40, and CD30 genes. C1 UNIV OXFORD,SIR WILLIAM DUNN SCH PATHOL,MRC,CELLULAR IMMUNOL UNIV,OXFORD OX1 3RE,ENGLAND. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD. FU NCI NIH HHS [N01-CO-74101] NR 32 TC 24 Z9 26 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD APR PY 1995 VL 25 IS 4 BP 926 EP 930 DI 10.1002/eji.1830250410 PG 5 WC Immunology SC Immunology GA QY508 UT WOS:A1995QY50800008 PM 7737295 ER PT J AU MUSTELIN, T WILLIAMS, S TAILOR, P COUTURE, C ZENNER, G BURN, P ASHWELL, JD ALTMAN, A AF MUSTELIN, T WILLIAMS, S TAILOR, P COUTURE, C ZENNER, G BURN, P ASHWELL, JD ALTMAN, A TI REGULATION OF THE P70(ZAP) TYROSINE PROTEIN-KINASE IN T-CELLS BY THE CD45 PHOSPHOTYROSINE PHOSPHATASE SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE TYROSINE PHOSPHORYLATION; PHOSPHATASE; PROTEIN TYROSINE KINASE; CD45; T CELL ANTIGEN RECEPTOR-ZETA ID LEUKOCYTE-COMMON ANTIGEN; SIGNAL TRANSDUCTION; ACTIVATION; RECEPTOR; PHOSPHORYLATION; LYMPHOCYTES; EXPRESSION; FAMILY; LCK; TRANSMEMBRANE AB Two classes of protein tyrosine kinases (PTK) are utilized by the T cell antigen receptor (TcR)/CD3 complex for initiation of the signaling cascade, the Src-family PTK p56(lck) and p59(fyn), and the Syk-family PTK p70(zap) and p72(syk). In addition, the CD45 phosphotyrosine phosphatase (PTPase) is required for the induction of tyrosine phosphorylation by the TcR/CD3, presumably by positively regulating Src-family PTK. Here we report that CD45 also regulates the Syk-family PTK p70(zap) (or ZAP-70). In CD45-negative T cells, p70(zap) was constitutively phosphorylated on tyrosine and co-immunoprecipitated with the TcR-zeta chain. In resting wild-type CD45-positive cells, p70(zap) was mainly unphosphorylated, but it was rapidly phosphorylated on tyrosine upon treatment of the cells with anti-CD3 or PTPase inhibitors. Finally, p70(zap) co-distributed with CD45 in intact T cells, and tyrosine phosphorylated p70(zap) was dephosphorylated by CD45 in vitro. These findings suggest that CD45 plays an important role, direct or indirect, in the regulation of p70(zap) and its function in TcR/CD3 signaling. C1 F HOFFMANN LA ROCHE & CO LTD,DEPT METAB DIS,NUTLEY,NJ. NIH,BIOL RESPONSE MODIFIERS PROGRAM,IMMUNE CELL BIOL LAB,BETHESDA,MD 20892. RP MUSTELIN, T (reprint author), LA JOLLA INST ALLERGY & IMMUNOL,DIV CELL BIOL,11149 N TORREY PINES RD,LA JOLLA,CA 92037, USA. FU NCI NIH HHS [CA35299]; NIAID NIH HHS [AI35603]; NIGMS NIH HHS [GM48960] NR 42 TC 58 Z9 61 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD APR PY 1995 VL 25 IS 4 BP 942 EP 946 DI 10.1002/eji.1830250413 PG 5 WC Immunology SC Immunology GA QY508 UT WOS:A1995QY50800011 PM 7737297 ER PT J AU LORENZO, NY BROMFIELD, EB THEODORE, WH AF LORENZO, NY BROMFIELD, EB THEODORE, WH TI CARBAMAZEPINE AND PHENYTOIN - COMBINATION VERSUS SINGLE DRUG-THERAPY SO EUROPEAN JOURNAL OF NEUROLOGY LA English DT Article DE CARBAMAZEPINE; COMBINATION THERAPY; COMPLEX PARTIAL SEIZURES; MONOTHERAPY; PHENYTOIN ID EPILEPTIC PATIENTS; MONOTHERAPY; REDUCTION; SEIZURES; EPOXIDE AB The records of 18 patients with intractable partial seizures who were observed on an in-patient epilepsy unit during single drug treatment with carbamezepine (CBZ) or phenytoin (PHT) and during combination therapy with both drugs were evaluated retrospectively. Seizure frequency was significantly lower during combination therapy (p < 0.01) and toxicity, as measured by an eight point objective scale, did not increase significantly (p > 0.10). In addition subjective signs of clinical toxicity (e.g. nausea, ataxia, etc.) increased only slightly during combination versus monotherapy. These findings were consistently seen whether the data were evaluated in total (i.e. treatment periods at least 7 weeks) or evaluated by using standardized 35 day treatment periods. In the absence of a blinded clinical trial evaluating PHT/CBZ combination, these findings support consideration of this combination in intractable patients who have failed rigorously administered monotherapy trials, recognizing however that only a small, percentage of patients will improve on combination therapy. C1 MAYO CLIN & MAYO FDN,DEPT NEUROL,ROCHESTER,MN 55905. TUFTS UNIV NEW ENGLAND MED CTR,DEPT NEUROL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,BOSTON,MA 02111. NINCDS,MED NEUROL BRANCH,CLIN EPILEPSY SECT,BETHESDA,MD 20892. NR 20 TC 1 Z9 1 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 1351-5101 J9 EUR J NEUROL JI Eur. J. Neurol. PD APR PY 1995 VL 2 IS 2 BP 101 EP 105 DI 10.1111/j.1468-1331.1995.tb00100.x PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA RN925 UT WOS:A1995RN92500004 PM 24283608 ER PT J AU KASHIMA, N UEOHZONO, T FORNACE, AJ IDE, T AF KASHIMA, N UEOHZONO, T FORNACE, AJ IDE, T TI INDUCTION OF GADD153 GENE IN G(0)-SPECIFIC TS MUTANT-CELLS AT NONPERMISSIVE TEMPERATURE SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID GROWTH ARREST; MAMMALIAN-CELLS; DNA; TSJT60; ACTIVATION; PROTEIN; AGENTS; CYCLE; LINE; TRANSFORMATION AB tsJT60 is a temperature-sensitive (ts) mutant of the cell cycle isolated from a rat cell line, It does not enter the cell cycle from the G(0) phase at a nonpermissive temperature (40 degrees C) but proliferates normally in log phase at both permissive (34 degrees C) and nonpermissive temperatures (G(0)-specific ts mutant), Here we examined whether tsJT60 fails to downregulate growth arrest-specific genes after growth stimulation from G(0) phase at 40 degrees C, Among growth arrest-specific genes examined, an expression of gadd153, which decreased after serum stimulation at 34 degrees C as expected, increased markedly at 40 degrees C. It is plausible to assume that induction of gadd153 at 40 degrees C is correlated with inability of tsJT60 to enter S phase from G(0) phase at 40 degrees C, because it also occurred in tsJT366 (another ts mutant clone in the same complementation group) but did not occur in parental 3Y1 and in other ts mutant lines of different complementation groups, However, gadd153 was also induced after the temperature upshift in tsJT60 cells growing in log phase or progressing S phase. (C) 1995 Academic Press, Inc. C1 HIROSHIMA UNIV,SCH MED,DEPT CELLULAR & MOLEC BIOL,HIROSHIMA 734,JAPAN. NCI,DCT,DTP,MOLEC PHARMACOL LAB,BETHESDA,MD 20205. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 26 TC 5 Z9 5 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD APR PY 1995 VL 217 IS 2 BP 324 EP 328 DI 10.1006/excr.1995.1093 PG 5 WC Oncology; Cell Biology SC Oncology; Cell Biology GA QP701 UT WOS:A1995QP70100016 PM 7698232 ER PT J AU BAE, I SMITH, ML FORNACE, AJ AF BAE, I SMITH, ML FORNACE, AJ TI INDUCTION OF P53-LIKE, MDM2-LIKE, AND WAF1/CIP1-LIKE MOLECULES IN INSECT CELLS BY DNA-DAMAGING AGENTS SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID FILTER HYBRIDIZATION; PROTEIN; GENE; MUTATIONS; PRODUCT; COMPLEX; GROWTH; FORMS AB Cellular responses following DNA damage are ubiquitous in the biological world. In response to DNA damage, cell cycle checkpoints are activated, which delay cell cycle progression and most likely serve to allow time for repair. One important checkpoint in mammalian cells, activated in the G(1) phase of the cell cycle, is dependent on the p53 tumor suppressor gene product. While p53 is responsible for inducing G(1) arrest, the product of the MDM2 gene is believed to alleviate the arrest, allowing continuation of the cell cycle after a transient delay. Inasmuch as MDM2 and WAF1/CTP1 are transactivated by p53, while MDM2 binds to and modulates the activity of p53, a ''feedback loop'' is thus created. This pathway has been highly conserved in mammalian cells, but its presence outside of vertebrates is unknown. By using human MDM2 and WAF1/CIP1 cDNA probes, and monoclonal antibodies to p53 and Mdm2, we demonstrate in insect cell lines evidence for the existence of p53-, MDM2-, and WAF1/CIP1-like molecules and a p53-regulated pathway following treatment by DNA-damaging agents. (C) 1995 Academic Press, Inc. C1 NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 28 TC 24 Z9 24 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD APR PY 1995 VL 217 IS 2 BP 541 EP 545 DI 10.1006/excr.1995.1120 PG 5 WC Oncology; Cell Biology SC Oncology; Cell Biology GA QP701 UT WOS:A1995QP70100043 PM 7698255 ER PT J AU BODINE, D AF BODINE, D TI MOBILIZATION OF PERIPHERAL-BLOOD STEM-CELLS - WHERE THERE IS SMOKE, IS THERE FIRE SO EXPERIMENTAL HEMATOLOGY LA English DT Editorial Material ID COLONY-STIMULATING FACTOR; MEDIATED GENE-TRANSFER; BONE-MARROW CELLS; PROGENITOR CELLS; AUTOLOGOUS TRANSPLANTATION; IN-VIVO; HEMATOPOIETIC RECONSTITUTION; ADENOSINE-DEAMINASE; GRANULOCYTE; MICE RP BODINE, D (reprint author), NIH,CLIN HEMATOL BRANCH,9000 ROCKVILLE PIKE,BLDG 49,ROOM 3A11,BETHESDA,MD 20892, USA. NR 40 TC 8 Z9 8 U1 0 U2 0 PU CARDEN JENNINGS PUBL COLTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD APR PY 1995 VL 23 IS 4 BP 293 EP 295 PG 3 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA QP510 UT WOS:A1995QP51000001 PM 7895778 ER PT J AU COTTLERFOX, M CIPOLONE, K YU, M BERENSON, R OSHAUGHNESSY, J DUNBAR, C AF COTTLERFOX, M CIPOLONE, K YU, M BERENSON, R OSHAUGHNESSY, J DUNBAR, C TI POSITIVE SELECTION OF CD34(+) HEMATOPOIETIC-CELLS USING AN IMMUNOAFFINITY COLUMN RESULTS IN T CELL-DEPLETION EQUIVALENT TO ELUTRIATION SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE T CELL-DEPLETION; CD34(+) CELL SELECTION; ACUTE GVHD; MARROW TRANSPLANTATION; PBSC TRANSPLANTATION ID BONE-MARROW TRANSPLANTATION; LYMPHOCYTES-T; GRAFT; LEUKEMIA; DONORS; PHASE AB Acute graft-vs.-host disease (GVHD) continues to present a barrier to successful allogeneic marrow transplantation. T cell-depletion may prevent severe GVHD but carries an increased risk of graft rejection and relapse posttransplant. Clinical trials have defined the number of lymphocytes associated with sustained engraftment but low risk of significant GVHD (greater than grade I or II skin only) as less than or equal to 10(5)/kg. We examined T cell-depletion resulting from positive selection of CD34(+) hematopoietic cells with a biotinylated monoclonal anti-CD34 antibody and an immunoaffinity column. Eleven patients (six myeloma and five breast cancer) underwent both peripheral blood stem cell (PBSC) collection and marrow harvest prior to autologous transplantation. One PBSC collection and one-third of each marrow underwent column separation. PBSCs were enriched for CD34(+) cells from an initial mean of 1.5 to 53.3%, while marrow went from an initial mean of 2.8 to 65.4%. PBSC were depleted of CD3(+) cells from an initial mean of 9.6 x 10(9) to 8.6 x 10(6). Marrow CD3(+) lymphocyte content was reduced from an initial mean of 5.6 x 10(9) to 8 x 10(5). Since the column permits quantification and salvage of depleted T cells, its use should allow re-addition of T cell-aliquots associated with minimal risk for GVHD and rejection. In addition, since PBSCs were as readily depleted as marrow, allogeneic PBSC transplant may be feasible using this method. C1 NHLBI,BETHESDA,MD 20892. CELLPRO INC,BOTHELL,WA. NCI,BETHESDA,MD 20892. RP COTTLERFOX, M (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BLDG 10-1C711,BETHESDA,MD 20892, USA. NR 18 TC 41 Z9 41 U1 0 U2 0 PU CARDEN JENNINGS PUBL COLTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD APR PY 1995 VL 23 IS 4 BP 320 EP 322 PG 3 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA QP510 UT WOS:A1995QP51000005 PM 7534711 ER PT J AU HINTZ, NJ ENNIS, DG LIU, WF LARSEN, SH AF HINTZ, NJ ENNIS, DG LIU, WF LARSEN, SH TI THE RECA GENE OF CHLAMYDIA-TRACHOMATIS - CLONING, SEQUENCE, AND CHARACTERIZATION IN ESCHERICHIA-COLI SO FEMS MICROBIOLOGY LETTERS LA English DT Article DE CHLAMYDIA TRACHOMATIS; RECA; COMPLEMENTATION; RECOMBINATION; REPAIR ID SOS MUTAGENESIS; CLEAVAGE; PROTEIN AB The recA gene of Chlanlydia trachomatis was isolated by complementation of an Escherichia coli recA mutant. The cloned gene restored resistance to methyl methanesulfonate in E. coli recA mutants. The DNA sequence of the chlamydial gene was determined and the deduced protein sequence compared with other RecA proteins. Ln E. coli recA deletion mutants, the cloned gene conferred moderate recombinational activity as assayed by Hfr matings. The chlamydial recA gene was efficient in repairing alkylated DNA but less so in repairing of UV damage when compared with the E. coli homologue. As detected by an SOS gene fusion, a small but measurable amount of LexA co-cleavage was indicated. C1 INDIANA UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,INDIANAPOLIS,IN 46202. NICHHD,DNA REPLICAT REPAIR & MUTAGENESIS SECT,BETHESDA,MD 20892. NR 15 TC 12 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1097 J9 FEMS MICROBIOL LETT JI FEMS Microbiol. Lett. PD APR 1 PY 1995 VL 127 IS 3 BP 175 EP 179 DI 10.1016/0378-1097(95)00058-D PG 5 WC Microbiology SC Microbiology GA QQ061 UT WOS:A1995QQ06100004 PM 7758931 ER PT J AU SHACTER, E WILLIAMS, JA LEVINE, RL AF SHACTER, E WILLIAMS, JA LEVINE, RL TI OXIDATIVE MODIFICATION OF FIBRINOGEN INHIBITS THROMBIN-CATALYZED CLOT FORMATION SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Note DE PROTEIN OXIDATION; FIBRINOGEN; CLOTTING; DYSFIBRINOGENEMIA; FREE RADICALS ID RADICAL-DAMAGED PROTEINS; OXYGEN RADICALS; GLUTAMINE-SYNTHETASE; REPERFUSION INJURY; LIVER-DISEASE; INACTIVATION; DEGRADATION; RESIDUES; DYSFIBRINOGENEMIA; ISCHEMIA AB Plasma fibrinogen plays a central role in controlling hemostasis. In an earlier report, we found that fibrinogen is oxidized when whole plasma is treated with a metal-catalyzed oxidation system. These studies show that oxidative modification of purified human fibrinogen leads to an exposure-dependent loss of thrombin-induced clot formation. Inhibition of clotting occurred when either metal-catalyzed oxidation or gamma-irradiation was employed to generate oxidizing radicals. Both systems caused covalent modification of fibrinogen, assessed by measuring incorporation of protein carbonyls. Thrombin-catalyzed fibrinopeptide release was normal in irradiated fibrinogen and was only slightly diminished in protein exposed to metal-catalyzed oxidation, indicating that the inhibition of clotting activity was due to impaired fibrin monomer polymerization. Thus, oxidative modification of normal fibrinogen causes dysfibrinogenemia and constitutes a novel mechanism for inhibition of thrombosis. C1 NCI,GENET LAB,BETHESDA,MD 20892. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RI Levine, Rodney/D-9885-2011 NR 52 TC 88 Z9 97 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD APR PY 1995 VL 18 IS 4 BP 815 EP 821 DI 10.1016/0891-5849(95)93872-4 PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA QH098 UT WOS:A1995QH09800019 PM 7750804 ER PT J AU PACAK, K PALKOVITS, M KOPIN, IJ GOLDSTEIN, DS AF PACAK, K PALKOVITS, M KOPIN, IJ GOLDSTEIN, DS TI STRESS-INDUCED NOREPINEPHRINE RELEASE IN THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND PITUITARY-ADRENOCORTICAL AND SYMPATHOADRENAL ACTIVITY - IN-VIVO MICRODIALYSIS STUDIES SO FRONTIERS IN NEUROENDOCRINOLOGY LA English DT Review ID CENTRAL AMYGDALOID NUCLEUS; TYROSINE-HYDROXYLASE ACTIVITY; VENTRAL NORADRENERGIC BUNDLE; HYPOPHYSEAL PORTAL BLOOD; FREELY MOVING RATS; PARVOCELLULAR NEUROSECRETORY NEURONS; IMMUNO-CYTOCHEMICAL LOCALIZATION; SPONTANEOUSLY HYPERTENSIVE RATS; FACTOR-LIKE IMMUNOREACTIVITY; MESSENGER-RNA RESPONSES AB The hypothalamic-pituitary-adrenocortical (HPA) axis and the autonomic nervous system are major effector systems that serve to maintain homeostasis during exposure to stressors. In the past decade, interest in neurochemical regulation and in pathways controlling activation of the HPA axis has focused on catecholamines, which are present in high concentrations in specific brain areas-especially in the hypothalamus. The work described in this review has concentrated on the application of in vivo microdialysis in rat brain regions such as the paraventricular nucleus (PVN) of the hypothalamus, the central nucleus of the amygdala (ACE), the bed nucleus of the stria terminalis (BNST), and the posterolateral hypothalamus in order to examine aspects of catecholaminergic function and relationships between altered catecholaminergic function and the HPA axis and sympathoadrenal system activation in stress. Exposure of animals to immobilization (IMMO) markedly and rapidly increases rates of synthesis, release, and metabolism of norepinephrine (NE) in all the brain areas mentioned above and supports previous suggestions that in the PVN NE stimulates release of corticotropin-releasing hormone (CRH). The role of NE in the ACE and the BNST and most other areas possessing noradrenergic innervation remains unclear. Studies involving lower brainstem hemisections show that noradrenergic terminals in the PVN are derived mainly from medullary catecholaminergic groups rather than from the locus ceruleus, which is the main source of NE in the brain. Moreover, the medullary catecholaminergic groups contribute substantially to IMMO-induced noradrenergic activation in the PVN. Data obtained from adrenalectomized rats, with or without glucocorticoid replacement, and from hypercortisolemic rats suggest that glucocorticoids feedback to inhibit CRH release in the PVN, via attenuation of noradrenergic activation. Results from rats exposed to different stressors have indicated substantial differences among stressors in eliciting PVN noradrenergic responses as well as of responses of the HPA, sympathoneural, and adrenomedullary systems. Finally, involvement of other areas that participate in the regulation of the HPA axis such as the ACE, the BNST, and the hippocampus and the importance of stress-induced changes in expression of immediate early genes such as c-fos are discussed. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP PACAK, K (reprint author), NINCDS,CLIN NEUROSCI BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM 5N214,BETHESDA,MD 20892, USA. RI Palkovits, Miklos/F-2707-2013; OI Palkovits, Miklos/0000-0003-0578-0387 NR 340 TC 272 Z9 279 U1 0 U2 12 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-3022 J9 FRONT NEUROENDOCRIN JI Front. Neuroendocrinol. PD APR PY 1995 VL 16 IS 2 BP 89 EP 150 DI 10.1006/frne.1995.1004 PG 62 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA QV931 UT WOS:A1995QV93100001 PM 7621982 ER PT J AU HEINDEL, JJ CHAPIN, RE GEORGE, J GULATI, DK FAIL, PA BARNES, LH YANG, RSH AF HEINDEL, JJ CHAPIN, RE GEORGE, J GULATI, DK FAIL, PA BARNES, LH YANG, RSH TI ASSESSMENT OF THE REPRODUCTIVE TOXICITY OF A COMPLEX MIXTURE OF 25 GROUNDWATER CONTAMINANTS IN MICE AND RATS SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID CHEMICAL-MIXTURE; MATERNAL EXPOSURE; FEED RESTRICTION; B6C3F1 MICE; TOXICOLOGY; CADMIUM; CHLORIDE; INVIVO AB The potential reproductive toxicity of a mixture of 25 chemicals (MIX) formulated to simulate contaminated groundwater supplies near hazardous waste dumps was evaluated in CD-1 Swiss mice and Sprague-Dawley rats using the reproductive assessment by continuous breeding protocol. Male and female mice and rats were exposed to MIX in the drinking water at concentrations of 1, 5, and 10% of a technically achievable stock solution. For mice, body weight and feed consumption were not affected by MIX but water consumption was decreased for both the 5 and 10% MIX groups in both F-0 and F-1 animals. For F-0 mice, the number of live pups/litter was decreased at 10% MIX and the number of females/litter was decreased 10 and 17% at the mid and high MIX dose, respectively. Vaginal cytology was normal, as were testis weight and testicular spermatid head count. For F-1 mice, fertility was unaffected, but there was a decreased number of female pups/litter (19%) and a decreased adjusted live pup weight at 10% MIX. At necropsy, cauda epididymal sperm concentration and spermatid head count were reduced (20%) in the presence of normal testis, epididymis, prostate, seminal vesicle, liver, and kidney/adrenal weight. Female estrous cyclicity was altered at 5 and 10% MIX with normal kidney/adrenal, uterus, and ovary/oviduct weight. For rats, F-0 body weight and feed consumption were not affected by MIX but water consumption was decreased 10, 30, and 40% in the low-, medium-, and high-dose MIX groups, respectively, and 39% in the high-dose MIX F-1 animals. Rat fertility was normal but there was a decreased number of male pups/litter (11%) and a decreased live pup weight (6%) at 10% MIX. Male and female (F-1) pup weights were decreased on Postnatal Days 0, 4, 7, 14, and 21 (10% MIX) and remained lower through necropsy on Day 120 +/- 10. F-1 fertility was normal but F-2 pup weights were decreased (10% MIX). At necropsy, F-1 (10% MIX) male body weight was decreased 16% and relative kidney, testis, epididymis, and prostate weights were increased in the presence of normal sperm concentration percentage motile sperm and percentage abnormal sperm. Estrous cyclicity was normal as were kidney/adrenal and ovary weight while female liver weight was reduced 14%. In summary, a ''cocktail'' of 25 chemicals commonly found in contaminated groundwater at or near hazardous waste sites was administered in drinking water at doses which resulted in severely decreased water consumption in both mice and rats. Despite the presence, albeit at relatively low concentrations, of many known reproductive toxicants including cadmium, mercury, lead, chloroform, di(2-ethylhexyl)phthalate, and methylene chloride, only minimal reproductive effects were observed in F-0 and F-1 mice and rats. (C) 1995 society of Toxicology. C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. ENVIRONM HLTH RES & TESTING INC,LEXINGTON,KY 40503. RP HEINDEL, JJ (reprint author), NIEHS,NATL TOXICOL PROGRAM,POB 12233,MD 3-03,RES TRIANGLE PK,NC 27709, USA. OI Chapin, Robert/0000-0002-5997-1261 FU NIEHS NIH HHS [N01-ES-65141, N01-ES-65142] NR 43 TC 33 Z9 33 U1 0 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1995 VL 25 IS 1 BP 9 EP 19 DI 10.1006/faat.1995.1035 PG 11 WC Toxicology SC Toxicology GA QQ799 UT WOS:A1995QQ79900002 PM 7601330 ER PT J AU OLYNYK, JK REDDY, KR DIBISCEGLIE, AM JEFFERS, LJ PARKER, TI RADICK, JL SCHIFF, ER BACON, BR AF OLYNYK, JK REDDY, KR DIBISCEGLIE, AM JEFFERS, LJ PARKER, TI RADICK, JL SCHIFF, ER BACON, BR TI HEPATIC IRON CONCENTRATION AS A PREDICTOR OF RESPONSE TO INTERFERON-ALFA THERAPY IN CHRONIC HEPATITIS-C SO GASTROENTEROLOGY LA English DT Article ID NON-B-HEPATITIS; CHRONIC NON-A; PLACEBO-CONTROLLED TRIAL; SERUM FERRITIN; DOUBLE-BLIND; HEMOCHROMATOSIS; VIRUS; INFECTION; ALPHA AB Background/Aims: It has been reported that hepatic iron concentration (HIC) may influence response to therapy in chronic viral hepatitis, The aim of this study was to determine the relationship between HIC and response to interferon alfa therapy in patients with chronic hepatitis C. Methods: HIC was measured in liver biopsy specimens from 58 patients with chronic hepatitis C treated at three centers. Three patients had mild chronic hepatitis C, 35 had moderate to severe chronic hepatitis C, and 20 had active cirrhosis. Serum ferritin levels were measured in 51 of these 58 patients. Response to therapy was defined as normalization of alanine aminotransferase levels at the end of treatment. Results:Twenty-four patients (41%) responded to therapy. HICs were generally within the normal range (<1500 mu g/g). The mean HIC in nonresponders (860 +/- 100 mu g/g; range, 116-2296 mu g/g) was significantly higher than in responders (548 +/- 85 mu g/ g; range, 29-1870 mu g/g) (P < 0.05). Eighty-eight percent of patients with an HIC of >1100 mu g/g and 87% of patients with an elevated serum ferritin concentration did not respond to interferon alfa therapy. Conclusions: HIC seems to influence response to interferon alfa therapy among patients with chronic hepatitis C. A subgroup of patients with chronic hepatitis C has been identified for which an HIC of >1100 mu g/g predicted nonresponse in 88% of patients. C1 ST LOUIS UNIV,HLTH SCI CTR,DIV GASTROENTEROL & HEPATOL,ST LOUIS,MO 63110. UNIV MIAMI,CTR LIVER DIS,MIAMI,FL. NIH,LIVER DIS SECT,BETHESDA,MD. OI Olynyk, John/0000-0003-0417-3411 FU NIDDK NIH HHS [R01-DK 41816] NR 28 TC 244 Z9 249 U1 0 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 1995 VL 108 IS 4 BP 1104 EP 1109 DI 10.1016/0016-5085(95)90209-0 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QP792 UT WOS:A1995QP79200020 PM 7698578 ER PT J AU BENYA, RV MROZINSKI, J KUSUI, T BATTEY, JF JENSEN, RT AF BENYA, RV MROZINSKI, J KUSUI, T BATTEY, JF JENSEN, RT TI THE ROLE OF PROTEIN-KINASE-C (PKC) IN REGULATING ACUTE AND CHRONIC DESENSITIZATION OF THE GASTRIN-RELEASING PEPTIDE RECEPTOR (GRPR) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 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 1995 VL 108 IS 4 SU S BP A343 EP A343 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86301362 ER PT J AU BENYA, RV MROZINSKI, J JENSEN, RT AF BENYA, RV MROZINSKI, J JENSEN, RT TI IDENTIFICATION OF A CRITICAL REGION WITHIN THE GASTRIN-RELEASING PEPTIDE RECEPTOR (GRP-R) 3RD INTRACELLULAR LOOP MEDIATING G-PROTEIN-COUPLING SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A951 EP A951 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303788 ER PT J AU BOCKMAN, DE MERLINO, G AF BOCKMAN, DE MERLINO, G TI REACTIVE CELLULARITY AND BACTERIAL INVASION IN THE STOMACH OF TRANSGENIC MICE OVEREXPRESSING TGF-ALPHA SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MED COLL GEORGIA,DEPT CELLULAR BIOL & ANAT,AUGUSTA,GA 30912. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A717 EP A717 DI 10.1016/0016-5085(95)27179-1 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86302857 ER PT J AU BOIRIVANT, M DEMARIA, R PICA, R TESTI, R PALLONE, F STROBER, W AF BOIRIVANT, M DEMARIA, R PICA, R TESTI, R PALLONE, F STROBER, W TI LAMINA PROPRIA MONONUCLEAR-CELLS (LPMC) APOPTOSIS IN RELATION TO DIFFERENT ACTIVATION PATHWAYS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV ROMA LA SAPIENZA,DIPARTIMENTO MED SPERIMENTALE,I-00185 ROME,ITALY. UNIV CALABRIA,DIPARTIMENTO MED SPERIMENTALE,I-87036 RENDE,ITALY. NIH,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. RI BOIRIVANT, MONICA/B-9977-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A785 EP A785 DI 10.1016/0016-5085(95)27451-0 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303129 ER PT J AU BUSCAIL, L ESTEVE, JP SAINTLAURENT, N BERTRAND, V CHASTRE, E VAILLANT, JC GESPACH, C REISINE, T OCARROLL, AM KALTHOF, H BELL, GI SCHALLY, AV VAYSSE, N SUSINI, C AF BUSCAIL, L ESTEVE, JP SAINTLAURENT, N BERTRAND, V CHASTRE, E VAILLANT, JC GESPACH, C REISINE, T OCARROLL, AM KALTHOF, H BELL, GI SCHALLY, AV VAYSSE, N SUSINI, C TI THE SOMATOSTATIN RECEPTOR SUBTYPE-SSTR2 AND SUBTYPE-SSTR5 MEDIATE THE INHIBITION OF CELL-PROLIFERATION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 CHU RANGUEIL,INSERM,U151,F-31054 TOULOUSE,FRANCE. INSERM,U55,F-75005 PARIS,FRANCE. PHILADELPHIA SCH MED,PHILADELPHIA,PA. NIMH,BETHESDA,MD 20892. CHRISTIAN ALBRECHTS UNIV KIEL,W-2300 KIEL 1,GERMANY. HHMI,CHICAGO,IL. TULANE UNIV,NEW ORLEANS,LA 70118. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A955 EP A955 DI 10.1016/0016-5085(95)28124-X PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303802 ER PT J AU CORLETO, VD COY, DH JENSEN, RT AF CORLETO, VD COY, DH JENSEN, RT TI SOMATOSTATIN HAS A DIFFERENT CELLULAR BASIS OF ACTION ON COLONIC SMOOTH-MUSCLE CELLS THAN GASTRIC SMOOTH-MUSCLE CELLS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. TULANE UNIV,NEW ORLEANS,LA 70118. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A958 EP A958 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303815 ER PT J AU ECKMANN, L SHEARS, SB SCHULTZ, C FIERER, J KAGNOFF, MF TRAYNORKAPLAN, A AF ECKMANN, L SHEARS, SB SCHULTZ, C FIERER, J KAGNOFF, MF TRAYNORKAPLAN, A TI D-MYO-INOSITOL 1,4,5,6-TETRAKISPHOSPHATE IS INCREASED IN EPITHELIAL-CELLS IN RESPONSE TO SALMONELLA-DUBLIN ENTRY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. NIEHS,RES TRIANGLE PK,NC 27709. UNIV BREMEN,DEPT CHEM,W-2800 BREMEN 33,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A282 EP A282 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86301118 ER PT J AU GABRIL, F REYNOLDS, JC DOPPMAN, JL CHEN, CC TERMANINI, B STEWART, CA JENSEN, RT AF GABRIL, F REYNOLDS, JC DOPPMAN, JL CHEN, CC TERMANINI, B STEWART, CA JENSEN, RT TI DOES THE USE OF OCTREOSCANNING ALTER MANAGEMENT IN PATIENTS WITH ZOLLINGER-ELLISON SYNDROME - A PROSPECTIVE-STUDY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A356 EP A356 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86301414 ER PT J AU GIBRIL, F DOPPMAN, JL TERMANINI, B STEWART, CA WEBER, HC JENSEN, RT AF GIBRIL, F DOPPMAN, JL TERMANINI, B STEWART, CA WEBER, HC JENSEN, RT TI IS SELECTIVE INTRAHEPATIC ARTERIAL SECRETIN STIMULATION USEFUL IN DETECTING METASTATIC HEPATIC GASTRINOMA - A PROSPECTIVE-STUDY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A357 EP A357 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86301415 ER PT J AU HAWN, MT CARETHERS, JM MARRA, G UMAR, A KUNKEL, TA KOI, M BOLAND, CR AF HAWN, MT CARETHERS, JM MARRA, G UMAR, A KUNKEL, TA KOI, M BOLAND, CR TI THE MISMATCH REPAIR GENE HMLH1 FUNCTIONS LIKE A TUMOR-SUPPRESSOR GENE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48109. NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A479 EP A479 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86301906 ER PT J AU HAYASHI, PH BEAMES, MP KUHNS, MC HOOFNAGLE, JH DIBISCEGLIE, AM AF HAYASHI, PH BEAMES, MP KUHNS, MC HOOFNAGLE, JH DIBISCEGLIE, AM TI SERUM LEVELS OF HEPATITIS-B E-ANTIGEN (HBEAG) IN PATIENTS WITH CHRONIC HEPATITIS-B - CHANGES WITH THERAPY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. ABBOTT LABS,ABBOTT PK,IL. ST LOUIS UNIV,ST LOUIS,MO 63103. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A1081 EP A1081 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86304305 ER PT J AU HONG, MK MONTGOMERY, EA LEWIS, JH SOBIN, LH ALLEGRA, CJ JOHNSTON, PG AF HONG, MK MONTGOMERY, EA LEWIS, JH SOBIN, LH ALLEGRA, CJ JOHNSTON, PG TI CORRELATION OF KI-67 STAINING PATTERN AND FLOW-CYTOMETRY WITH ROUTINE HISTOLOGIC ASSESSMENT FOR DYSPLASIA IN BARRETTS-ESOPHAGUS (BE) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GEORGETOWN UNIV HOSP,DEPT MED,WASHINGTON,DC 20007. GEORGETOWN UNIV HOSP,DEPT PATHOL,WASHINGTON,DC 20007. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NCI,NMOB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A481 EP A481 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86301914 ER PT J AU HUANG, SC FORTUNE, KP WANK, SA KOPIN, AS GARDNER, JD AF HUANG, SC FORTUNE, KP WANK, SA KOPIN, AS GARDNER, JD TI VARIOUS CHOLECYSTOKININ (CCK) RECEPTORS SHOW INTERACTIONS BETWEEN DIFFERENT AFFINITY STATES OF THE RECEPTOR SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. ST LOUIS UNIV,ST LOUIS,MO 63104. TUFTS UNIV,BOSTON,MA 02111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A978 EP A978 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303893 ER PT J AU HUANG, SC JOSHI, SN FORTUNE, KP WANK, SA POIROT, SS GARDNER, JD AF HUANG, SC JOSHI, SN FORTUNE, KP WANK, SA POIROT, SS GARDNER, JD TI IMPORTANCE OF THE C-TERMINAL DOMAIN OF THE PANCREATIC CHOLECYSTOKININ (CCK) RECEPTOR SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST LOUIS UNIV,ST LOUIS,MO 63104. NIH,BETHESDA,MD 20892. RI Poirot, Sandrine/D-5448-2017 NR 0 TC 0 Z9 0 U1 2 U2 2 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 1995 VL 108 IS 4 SU S BP A977 EP A977 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303892 ER PT J AU HUANG, SC FORTUNE, KP JOSHI, SN WANK, SA GARDNER, JD AF HUANG, SC FORTUNE, KP JOSHI, SN WANK, SA GARDNER, JD TI ACTIVATION OF HETEROTRIMERIC-G PROTEINS CONVERTS UNOCCUPIED CHOLECYSTOKININ (CCK) RECEPTORS IN THE HIGH AND LOW-AFFINITY STATES TO THE VERY-LOW AFFINITY STATE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST LOUIS UNIV,ST LOUIS,MO 63104. NIH,BETHESDA,MD 20892. RI Poirot, Sandrine/D-5448-2017 NR 0 TC 0 Z9 0 U1 2 U2 2 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 1995 VL 108 IS 4 SU S BP A977 EP A977 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303890 ER PT J AU JOSHI, SN HUANG, SC FORTUNE, KP WANK, SA GARDNER, JD AF JOSHI, SN HUANG, SC FORTUNE, KP WANK, SA GARDNER, JD TI DIFFERENT AFFINITY STATES OF CHOLECYSTOKININ(CCK) RECEPTORS ACCOUNT FOR THEIR ABILITIES TO ACTIVATE MULTIPLE SIGNAL-TRANSDUCTION MECHANISMS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. ST LOUIS UNIV,ST LOUIS,MO 63104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A979 EP A979 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303897 ER PT J AU JOSHI, SN HUANG, SC TALKAD, VD FORTUNE, KP WANK, SA GARDNER, JD AF JOSHI, SN HUANG, SC TALKAD, VD FORTUNE, KP WANK, SA GARDNER, JD TI CHARACTERISTICS OF DIFFERENT AFFINITY STATES OF THE PANCREATIC CHOLECYSTOKININ (CCK) RECEPTOR DEPEND ON THE RECEPTOR EXPRESSION SYSTEM SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST LOUIS UNIV,ST LOUIS,MO 63104. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A978 EP A978 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303896 ER PT J AU KUSUI, T TSUDA, T BENYA, RV JENSEN, RT AF KUSUI, T TSUDA, T BENYA, RV JENSEN, RT TI ACTIVATION OF NEUROMEDIN-B RECEPTORS INCREASES TYROSINE PHOSPHORYLATION OF FOCAL ADHESION KINASE (P125FAK) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A984 EP A984 DI 10.1016/0016-5085(95)28240-8 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303919 ER PT J AU KUSUI, T JENSEN, RT BENYA, RV AF KUSUI, T JENSEN, RT BENYA, RV TI GASTRIN-RELEASING PEPTIDE RECEPTOR MODULATION (INTERNALIZATION, DOWN-REGULATION, DESENSITIZATION) - EFFECTS OF MUTATIONS OF PROPOSED INTERNALIZATION MOTIFS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A984 EP A984 DI 10.1016/0016-5085(95)28240-8 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303918 ER PT J AU LYNN, RB COOPERMAN, RR MISELIS, RR HYDE, TM AF LYNN, RB COOPERMAN, RR MISELIS, RR HYDE, TM TI DISTRIBUTION OF BOMBESIN-LIKE IMMUNOREACTIVE (LI) NEURONS IN THE NUCLEUS OF THE SOLITARY TRACT (NTS) IN HUMANS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,DEPT MED,PHILADELPHIA,PA 19107. UNIV PENN,DEPT ANIM BIOL,PHILADELPHIA,PA 19104. NIMH,IRP,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A987 EP A987 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303931 ER PT J AU MATSUMOTO, T SAITOH, S SHIMODA, R TAKEHARA, K NAGAMINE, T MORI, M TAKEUCHI, T MERLINO, G TAKAGI, H AF MATSUMOTO, T SAITOH, S SHIMODA, R TAKEHARA, K NAGAMINE, T MORI, M TAKEUCHI, T MERLINO, G TAKAGI, H TI ANDROGEN REPLACEMENT FOR CASTRATED TGF-ALPHA TRANSGENIC MALE-MICE RECOVERED HEPATIC TUMORIGENESIS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GUNMA UNIV,SCH MED,DEPT INTERNAL MED 1,MAEBASHI,GUNMA 371,JAPAN. GUNMA UNIV,SCH MED,DEPT MOLEC ENDOCRINOL,MAEBASHI,GUNMA 371,JAPAN. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A990 EP A990 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303943 ER PT J AU NALIBOFF, B MUNAKATA, J GRACELY, R FULLERTON, S KODNER, A MAYER, EA AF NALIBOFF, B MUNAKATA, J GRACELY, R FULLERTON, S KODNER, A MAYER, EA TI IBS PATIENTS WITH LOW RECTAL DISCOMFORT THRESHOLDS SHOW NORMAL STIMULUS-RESPONSE FUNCTIONS FOR RECTAL SENSATIONS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT PHYSIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,CURE VA UCLA GASTROENTER BIOL CTR NEUROENTER BIOL GRP,LOS ANGELES,CA 90024. NR 1 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A656 EP A656 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86302611 ER PT J AU POIROT, SS WANK, SA AF POIROT, SS WANK, SA TI IDENTIFICATION OF THE AMINO-ACIDS RESPONSIBLE FOR CHOLECYSTOKININ RECEPTOR SUBTYPE SELECTIVITY FOR GASTRIN SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. RI Poirot, Sandrine/D-5448-2017 NR 0 TC 0 Z9 0 U1 2 U2 2 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 1995 VL 108 IS 4 SU S BP A895 EP A895 DI 10.1016/0016-5085(95)27886-9 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86303564 ER PT J AU RUBIN, SA NGUYEN, TT DYER, DL COWAN, KH SAID, HM AF RUBIN, SA NGUYEN, TT DYER, DL COWAN, KH SAID, HM TI INTESTINAL TRANSPORT OF FOLATE - IDENTIFICATION OF A MOUSE INTESTINAL CDNA AND LOCALIZATION OF ITS MESSENGER-RNA SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 VET ADM MED CTR,LONG BEACH,CA 90822. UNIV CALIF IRVINE,DEPT MED,IRVINE,CA 92717. UNIV CALIF IRVINE,DEPT PHYSIOL BIOPHYS,IRVINE,CA 92717. NCI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A320 EP A320 DI 10.1016/0016-5085(95)23940-5 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86301269 ER PT J AU SMOOF, DT RESAU, JH ELLIGET, KA EARLINGTON, MH WOOD, AW ASSEFFA, A AF SMOOF, DT RESAU, JH ELLIGET, KA EARLINGTON, MH WOOD, AW ASSEFFA, A TI HELICOBACTER-PYLORI BROTH CULTURE SUPERNATANTS ACTIVATE PROTEIN-KINASE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HOWARD UNIV,COLL MED,DEPT MED,WASHINGTON,DC 20001. HOWARD UNIV,COLL MED,DEPT BIOCHEM,WASHINGTON,DC 20001. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. NCI,FCRDC,ABL BRP,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A222 EP A222 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86300881 ER PT J AU SONNENBERG, A EVERHART, JE AF SONNENBERG, A EVERHART, JE TI CURRENT PREVALENCE RATES AND RISK-FACTORS OF PEPTIC-ULCER IN THE UNITED-STATES SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MED COLL WISCONSIN,MILWAUKEE,WI 53226. NIDDKD,BETHESDA,MD. NR 0 TC 3 Z9 3 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 1995 VL 108 IS 4 SU S BP A223 EP A223 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86300883 ER PT J AU STETTLER, C SCHMASSMANN, A TARASOVA, NI VARGA, L HALTER, F AF STETTLER, C SCHMASSMANN, A TARASOVA, NI VARGA, L HALTER, F TI IMMUNOHISTOLOGICAL LOCALIZATION OF GASTRIN RECEPTORS IN ANTRAL GASTRIC-MUCOSA IN MAN SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV HOSP BERN,INSELSPITAL,GASTROINTESTINAL UNIT,BERN,SWITZERLAND. NCI,FCRDC,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 2 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A1008 EP A1008 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86304016 ER PT J AU STEWART, CA TERMANINI, B GIBRIL, F WEBER, HC JENSEN, RT AF STEWART, CA TERMANINI, B GIBRIL, F WEBER, HC JENSEN, RT TI PROSPECTIVE-STUDY OF THE EFFECT OF LONG-TERM GASTRIC-ACID ANTISECRETORY TREATMENT ON SERUM VITAMIN-B12 LEVELS IN PATIENTS WITH ZOLLINGER-ELLISON SYNDROME SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD. 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A226 EP A226 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86300896 ER PT J AU TARASOVA, N WANK, SA HUDSON, E CZERWINSKI, G ROMANOV, VI RESAU, J MICHEJDA, CJ AF TARASOVA, N WANK, SA HUDSON, E CZERWINSKI, G ROMANOV, VI RESAU, J MICHEJDA, CJ TI ENDOCYTOSIS OF GASTRIN IN GASTRIN RECEPTOR-EXPRESSING CELLS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A1011 EP A1011 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86304027 ER PT J AU TERMANINI, B GIBRIL, F STEWART, CA WEBER, HC JENSEN, RT AF TERMANINI, B GIBRIL, F STEWART, CA WEBER, HC JENSEN, RT TI ZOLLINGER-ELLISON SYNDROME - A PROSPECTIVE-STUDY TO DETERMINE THE OPTIMAL STARTING DOSE OF OMEPRAZOLE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A238 EP A238 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86300945 ER PT J AU TSENG, CC BOYLAN, MO JARBOE, LA USDIN, TB WOLFE, MM AF TSENG, CC BOYLAN, MO JARBOE, LA USDIN, TB WOLFE, MM TI EXPRESSION OF THE GLUCOSE-DEPENDENT INSULINOTROPIC PEPTIDE (GIP) GENE AND CHRONIC HOMOLOGOUS DESENSITIZATION OF ITS RECEPTOR IN DIABETIC RATS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,DIV GASTROENTEROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A1013 EP A1013 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86304033 ER PT J AU WARGOVICH, MJ JIMENEZ, A STEELE, VE VELASCO, M KELLOFF, GJ AF WARGOVICH, MJ JIMENEZ, A STEELE, VE VELASCO, M KELLOFF, GJ TI EFFICACY OF POTENTIAL CHEMOPREVENTIVE AGENTS ON RAT COLON ABERRANT CRYPT FORMATION AND PROGRESSION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MD ANDERSON CANC CTR,DEPT GASTROINTESTINAL MED ONCOL,HOUSTON,TX. NCI,CHEMOPREVENT BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A551 EP A551 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86302192 ER PT J AU WEBER, HC MROZINSKI, JE JENSEN, RT BATTEY, JF AF WEBER, HC MROZINSKI, JE JENSEN, RT BATTEY, JF TI MOLECULAR-STRUCTURE AND REGULATION OF THE EXPRESSION BY DEXAMETHASONE AND CAMP OF THE GASTRIN-RELEASING PEPTIDE RECEPTOR GENE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 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 1995 VL 108 IS 4 SU S BP A1015 EP A1015 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86304044 ER PT J AU WILLIAMS, AO KNAPTON, AD KAIGHN, ME AF WILLIAMS, AO KNAPTON, AD KAIGHN, ME TI CRYSTALLINE SILICA-INDUCED CIRRHOSIS AND EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA-1 AND FACTOR-BETA-2 MESSENGER-RNAS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NCI,EXPTL PATHOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A1198 EP A1198 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86304771 ER PT J AU WILLIAMS, AO KNAPTON, AD GEISER, AG LETTERIO, JJ ROBERTS, AB AF WILLIAMS, AO KNAPTON, AD GEISER, AG LETTERIO, JJ ROBERTS, AB TI THE LIVER IN TRANSFORMING GROWTH-FACTOR-BETA-1 (TGF-BETA-1) NULI MICE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NCI,EXPTL PATHOL LAB,BETHESDA,MD 20892. NCI,DIV CANC ETIOL,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A1016 EP A1016 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86304045 ER PT J AU YUKI, M YOKOTA, K OKUYAMA, S OHTA, T IZUMI, S SHUDO, R UEHARA, A KITAMORI, S KOHGO, Y NAKAMURA, T AF YUKI, M YOKOTA, K OKUYAMA, S OHTA, T IZUMI, S SHUDO, R UEHARA, A KITAMORI, S KOHGO, Y NAKAMURA, T TI DISCRIMINATION BETWEEN LEIOMYOMA AND LEIOMYOSARCOMA OF THE STOMACH - ENDOSCOPIC ULTRASONOGRAPHY OR PROLIFERATION MARKER SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ASAHIKAWA MED COLL,DEPT INTERNAL MED 3,ASAHIKAWA 07811,JAPAN. FREDERICK CANC RES & DEV CTR,ABL BASC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1995 VL 108 IS 4 SU S BP A558 EP A558 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT863 UT WOS:A1995QT86302221 ER PT J AU DAWSEY, SM WANG, GQ KIDWELL, JA ZHOU, B FLEISCHER, DE AF DAWSEY, SM WANG, GQ KIDWELL, JA ZHOU, B FLEISCHER, DE TI ESOPHAGEAL STAINING WITH LUGOLS IODINE IDENTIFIES ADDITIONAL LESIONS IN HIGH-RISK CHINESE PATIENTS SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. GEORGETOWN UNIV,WASHINGTON,DC. CAMS,INST CANC,BEIJING,PEOPLES R CHINA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1995 VL 41 IS 4 BP 347 EP 347 DI 10.1016/S0016-5107(05)80241-X PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT419 UT WOS:A1995QT41900205 ER PT J AU KIDWELL, JA FLEISCHER, DE WANG, GQ ANDERSON, RM ZHOU, B DAWSEY, SM AF KIDWELL, JA FLEISCHER, DE WANG, GQ ANDERSON, RM ZHOU, B DAWSEY, SM TI MUCOSAL STAINING OF THE ESOPHAGUS WITH LUGOLS IODINE SOLUTION - TECHNICAL ASPECTS SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,WASHINGTON,DC 20007. CAMS,INST CANC,BEIJING,PEOPLES R CHINA. NCI,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1995 VL 41 IS 4 BP 352 EP 352 DI 10.1016/S0016-5107(05)80263-9 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QT419 UT WOS:A1995QT41900227 ER PT J AU GUNARATNE, PH NAKAO, M LEDBETTER, DH SUTCLIFFE, JS CHINAULT, AC AF GUNARATNE, PH NAKAO, M LEDBETTER, DH SUTCLIFFE, JS CHINAULT, AC TI TISSUE-SPECIFIC AND ALLELE-SPECIFIC REPLICATION TIMING CONTROL IN THE IMPRINTED HUMAN PRADER-WILLI-SYNDROME REGION SO GENES & DEVELOPMENT LA English DT Article DE REPLICATION TIMING; GENETIC IMPRINTING; PRADER-WILLI SYNDROME; SNRPN GENE ID BETA-GLOBIN GENE; INSITU HYBRIDIZATION; MOLECULAR DIAGNOSIS; ANGELMAN SYNDROMES; DNA METHYLATION; CHROMOSOME; SNRPN; TIME; EXPRESSION; ACTIVATION AB To examine the relationship between replication timing and differential gene transcription in tissue-specific and imprinted settings we have studied the replication timing properties of the human Prader-Willi syndrome (PWS) region on human chromosome 15q11-13. Interphase fluorescence in situ hybridization with an overlapping series of cosmid clones was used to map a PWS replication timing domain to a 500- to 650-kb region that includes the SNRPN gene. This PWS domain replicates late in lymphocytes but predominantly early in neuroblasts, with replication asynchrony observed in both tissues, and appears to colocalize with a genetically imprinted transcription domain showing prominent expression in the brain. A 5- to 30-kb deletion in the 5' region of SNRPN results in the loss of late replication control of this domain in lymphocytes when the deleted chromosome is inherited paternally. This potential allele-specific replication timing control region also appears to colocalize with a putative imprinting control region that has been shown previously to abolish the expression of three imprinted transcripts in this same region. C1 BAYLOR COLL MED,DEPT BIOCHEM,HOUSTON,TX 77030. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. RP GUNARATNE, PH (reprint author), BAYLOR COLL MED,DEPT MOLEC & HUMAN GENET,HOUSTON,TX 77030, USA. RI Sutcliffe, James/C-1348-2012 OI Sutcliffe, James/0000-0001-5200-6007 FU PHS HHS [8D20619] NR 43 TC 65 Z9 65 U1 0 U2 0 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 1 PY 1995 VL 9 IS 7 BP 808 EP 820 DI 10.1101/gad.9.7.808 PG 13 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA QT898 UT WOS:A1995QT89800004 PM 7705658 ER PT J AU DONEHOWER, LA GODLEY, LA ALDAZ, CM PYLE, R SHI, YP PINKEL, D GRAY, T BRADLEY, A MEDINA, D VARMUS, HE AF DONEHOWER, LA GODLEY, LA ALDAZ, CM PYLE, R SHI, YP PINKEL, D GRAY, T BRADLEY, A MEDINA, D VARMUS, HE TI DEFICIENCY OF P53 ACCELERATES MAMMARY TUMORIGENESIS IN WNT-1 TRANSGENIC MICE AND PROMOTES CHROMOSOMAL INSTABILITY SO GENES & DEVELOPMENT LA English DT Article DE P53; WNT-1; MAMMARY TUMORS; GENOMIC INSTABILITY; MOUSE; TUMOR MODEL ID WILD-TYPE P53; P53-DEFICIENT MICE; BREAST-CANCER; GENE AMPLIFICATION; NEU ONCOGENE; TUMOR VIRUS; INT-2 GENE; FGF GENE; C-MYC; MOUSE AB By crossing mice that carry a null allele of p53 with transgenic mice that develop mammary adenocarcinomas under the influence of a Wnt-1 transgene, we have studied the consequences of p53 deficiency in mammary gland neoplasia. In Wnt-1 transgenic mice homozygous for the p53 null allele, tumors appear at an earlier age than in animals heterozygous or wild-type at the p53 locus. About half of the tumors arising in p53 heterozygotes exhibit loss of the normal p53 allele, implying selection for p53-deficient cells. Mammary tumors lacking p53 display less fibrotic histopathology and increased genomic instability with aneuploidy, amplifications, and deletions, as detected by karyotype analysis and comparative genomic hybridization. In one tumor, the amplified region of chromosome 7 had an ectopically expressed int-2/FGF3 proto-oncogene, a gene known to cooperate with Wnt-1 in the production of mammary tumors. These findings favor a model in which p53 deficiency relaxes normal restraints on chromosomal number and organization during tumorigenesis. C1 NCI,VARMUS LAB,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM & BIOPHYS,SAN FRANCISCO,CA 94143. UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT CARCINOGENESIS,SMITHVILLE,TX 78957. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,DIV MOLEC CYTOMETRY,SAN FRANCISCO,CA 94143. BAYLOR COLL MED,HOWARD HUGHES MED INST,HOUSTON,TX 77030. BAYLOR COLL MED,INST MOLEC GENET,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT CELL BIOL,HOUSTON,TX 77030. NIH,OFF DIRECTOR,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT MICROBIOL & IMMUNOL,SAN FRANCISCO,CA 94143. RP DONEHOWER, LA (reprint author), BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030, USA. FU NCI NIH HHS [CA25215, CA54897, CA59967] NR 59 TC 237 Z9 238 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 1 PY 1995 VL 9 IS 7 BP 882 EP 895 DI 10.1101/gad.9.7.882 PG 14 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA QT898 UT WOS:A1995QT89800010 PM 7705663 ER PT J AU KOVAC, P RICE, KC AF KOVAC, P RICE, KC TI SYNTHESIS AND CHARACTERIZATION OF 6-O-ALPHA-D-GLUCOPYRANOSYLMORPHINE AND 6-O-BETA-D-GLUCOPYRANOSYLMORPHINE AND 6-O-BETA-D-GLUCOPYRANOSYL-CODEINE SO HETEROCYCLES LA English DT Article ID RESONANCE AB 6-O-alpha- and beta-D-glucopyranosylmorphine and 6-O-beta-D-glucopyranosylcodeine have been prepared by condensations of 2,3,4,6-tetra-O-acyl-alpha-D-glucopyranosyl bromides with 3-O-acetylmorphine and codeine, respectively, followed by deprotection. Depending upon the method of condensation, variable amounts of orthoesters were found among the final products of condensation together with the desired glycosides. Highest yields of glycosides were obtained when 2,3,4,6-tetra-O-benzoyl-alpha-D-glucopyranosyl bromide was the glycosyl donor, and when the condensation was promoted with silver triflate in the presence of a less than stoichiometric amount of 2,4,6-trimethylpyridine as the acid scavenger. RP KOVAC, P (reprint author), NIDDK,MED CHEM LAB,BLDG 8,RM B1-23,BETHESDA,MD 20892, USA. NR 14 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0385-5414 J9 HETEROCYCLES JI Heterocycles PD APR 1 PY 1995 VL 41 IS 4 BP 697 EP 707 PG 11 WC Chemistry, Organic SC Chemistry GA QT094 UT WOS:A1995QT09400009 ER PT J AU LEITOLF, H SZKUDLINSKI, MW HOANGVU, C THOTAKURA, NR VONZURMUHLEN, A BRABANT, G WEINTRAUB, BD AF LEITOLF, H SZKUDLINSKI, MW HOANGVU, C THOTAKURA, NR VONZURMUHLEN, A BRABANT, G WEINTRAUB, BD TI EFFECTS OF CONTINUOUS AND PULSATILE ADMINISTRATION OF PITUITARY RAT THYROTROPIN AND RECOMBINANT HUMAN THYROTROPIN IN A CHRONICALLY CANNULATED RAT SO HORMONE AND METABOLIC RESEARCH LA English DT Article DE THYROTROPIN; RECOMBINANT HUMAN THYROTROPIN; PULSATILITY; CHRONIC INFUSION MODEL ID HORMONE-SECRETION; SERUM THYROTROPIN; TSH; RECEPTOR; REFRACTORINESS; STIMULATION; SULFATION; HYPOTHYROIDISM; SIALYLATION; INDUCTION AB Pulsatile secretion of thyrotropin (TSH) is a well characterized phenomenon in the human, yet only limited data are available from animal studies. We propose a combined model of chronic catheterization and suppression of endogenous TSH release in the rat allowing us to apply quantified pulses of different preparations of thyrotropin intravenously with minimal interference with endogenously produced hormone. Sprague-Dawley rats treated with drinking water containing 3,5,3'-triiodothyronine (T3) showed a significant 6-fold decrease of the rat TSH (rTSH) level after four days. Free thyroxine (FT4) levels were 9-fold below unsuppressed levels; FT4 response to exogenous TSH application above this suppressed baseline level was selected as an endpoint. Infusion studies compared pulsatile with continuous TSH administration. A low and a high dose of rTSH and recombinant human TSH (rec-hTSH) were administered. Levels of FT4 were compared after two and four days and responsiveness to a standard high bolus of rTSH 6 h after end of infusion was assessed. With regard to its potency for FT4 release, differences indicating a general trend as to superior efficiency of pulsatile TSH stimulation of the thyroid gland in comparison to continuous stimulation could be observed in all four experiments. More pronounced effects were seen after 2 and 4 days of high rTSH infusion and after 4 days of low rec-hTSH infusion. Comparison of FT4 responses to rTSH boli showed a 2- and 6-fold higher response in the pulsatile group compared to the continuous group after low and high rTSH infusion, respectively. This was not observed in the animals receiving low rec-hTSH infusion. However, after high rec-hTSH infusion, a bolus following pulsatile infusion resulted in a lesser decrease in FT4 levels in comparison to that after continuous application. Our data suggest that pulsatile application of TSH might be of superior efficiency with regard to in vivo stimulation of thyroid hormone secretion, hence suggesting an underlying physiological significance of this release pattern. C1 NIDDK,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD 20892. HANNOVER MED SCH,ZENTRUM INNERE MED & DERMATOL,KLIN ENDOKRINOL ABT,HANNOVER,GERMANY. NR 31 TC 12 Z9 12 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0018-5043 J9 HORM METAB RES JI Horm. Metab. Res. PD APR PY 1995 VL 27 IS 4 BP 173 EP 178 DI 10.1055/s-2007-979933 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QV933 UT WOS:A1995QV93300003 PM 7750899 ER PT J AU STERNBERG, EM AF STERNBERG, EM TI NEUROENDOCRINE FACTORS IN SUSCEPTIBILITY TO INFLAMMATORY DISEASE - FOCUS ON THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS SO HORMONE RESEARCH LA English DT Article; Proceedings Paper CT XIIIth Annual Lilly International Symposium on Endocrinology and Development CY OCT 27-29, 1994 CL ROME, ITALY SP ELI LILLY DE INFLAMMATION; STRESS RESPONSE; CYTOKINES; HYPOTHALAMIC-PITUITARY-ADRENAL AXIS ID CORTICOTROPIN-RELEASING HORMONE; LEWIS RATS; ARTHRITIS; STRESS; ACTIVATION; BINDING AB Communication between the central components of the stress response and the immune system plays an important role in susceptibility to inflammatory disease. This communication occurs through hormonal and neuronal mechanisms. Hormonal mechanisms involve activation of the hypothalamic-pituitary-adrenal (HPA) axis by immune system products, e.g. cytokines. The stimulated HPA axis regulates immune responses through the immunosuppressive effects of glucocorticoids. Neuronal mechanisms include direct innervation of immune organs. Cytokine activation of the HPA axis and the resultant glucocorticoid-induced suppression of immune and inflammatory responses represent an important mechanism whereby the central stress response modulates peripheral inflammation. Interruption of this communication is associated with exacerbation of inflammatory disease. Conversely, intracerebroventricular transplantation of hypothalamic tissue from inflammatory resistant rats into susceptible rats reduces peripheral inflammation by more than 85%. RP STERNBERG, EM (reprint author), NIMH,BLDG 10,ROOM 3S-231,10 CTR DR,MSC 1284,BETHESDA,MD 20892, USA. NR 11 TC 31 Z9 32 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PD APR PY 1995 VL 43 IS 4 BP 159 EP 161 DI 10.1159/000184268 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QJ803 UT WOS:A1995QJ80300017 PM 7750921 ER PT J AU STRATAKIS, CA GOLD, PW CHROUSOS, GP AF STRATAKIS, CA GOLD, PW CHROUSOS, GP TI NEUROENDOCRINOLOGY OF STRESS - IMPLICATIONS FOR GROWTH AND DEVELOPMENT SO HORMONE RESEARCH LA English DT Article; Proceedings Paper CT XIIIth Annual Lilly International Symposium on Endocrinology and Development CY OCT 27-29, 1994 CL ROME, ITALY SP ELI LILLY DE NEUROENDOCRINOLOGY; STRESS; GROWTH; DEVELOPMENT; CORTICOTROPIN-RELEASING HORMONE; NEUROIMMUNOLOGY; PSYCHOSOCIAL SHORT STATURE; PUBERTY; ADOLESCENCE ID CORTICOTROPIN-RELEASING HORMONE; PITUITARY-ADRENAL AXIS; BODY-FAT DISTRIBUTION; SYSTEM DISORDERS; DISEASE AB A stressor above a threshold magnitude, or multiple stressors applied simultaneously, cause an organism to alter its behaviour and physiology, with the aim of maintaining homeostasis. The adaptive changes that occur are coordinated and mediated by the stress system in the central nervous system (which includes corticotrophin-releasing hormone and noradrenergic neurons in the hypothalamus and brainstem, respectively), and its peripheral limbs, the hypothalamic-pituitary-adrenal axis and the autonomic (sympathetic) system. Controlled or self-driven challenges to homeostasis and a normally functioning stress system are crucial for normal development and preservation of self and species. In childhood and adolescence, appropriately functioning neuroendocrine responses to stressors are necessary to allow growth and psychosexual maturation to progress normally. Maladaptive neuroendocrine responses, i.e. dysregulation of the stress system, may lead to disturbances in growth and development and cause psychiatric, endocrine/metabolic and/or autoimmune diseases or vulnerability to such diseases, not only during childhood and adolescence, but also in adulthood. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,CHILDRENS MED CTR,DEPT PAEDIAT,DIV GENET,WASHINGTON,DC 20007. RP STRATAKIS, CA (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10 N 262,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 22 TC 30 Z9 31 U1 0 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PD APR PY 1995 VL 43 IS 4 BP 162 EP 167 DI 10.1159/000184269 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QJ803 UT WOS:A1995QJ80300018 PM 7750922 ER PT J AU LESOONWOOD, LA KIM, WH KLEINMAN, HK WEINTRAUB, BD MIXSON, AJ AF LESOONWOOD, LA KIM, WH KLEINMAN, HK WEINTRAUB, BD MIXSON, AJ TI SYSTEMIC GENE-THERAPY WITH P53 REDUCES GROWTH AND METASTASES OF A MALIGNANT HUMAN BREAST-CANCER IN NUDE-MICE SO HUMAN GENE THERAPY LA English DT Article ID WILD-TYPE P53; DNA LIPOSOME COMPLEXES; TUMOR SUPPRESSION; CARCINOMA-CELLS; TRANSFER INVIVO; EXPRESSION; APOPTOSIS; INHIBITOR; PROTEIN; MUTANT AB We report on an in vivo delivery system that attenuates the growth, in nude mice, of a malignant human breast cancer cell line containing a p53 mutation. Nude mice, inoculated with breast carcinoma cells, were injected every 10-12 days with a liposome-p53 complex via the tail vein. A significant reduction of greater than 60% in primary tumor volume was observed as compared to the control groups. Furthermore, when individual growth patterns of the tumors were assessed, we found that primary tumor size regressed in the majority of p53-treated animals (8/15), whereas only one tumor in the control groups (1/22) regressed. The eight tumors that regressed with the liposome-p53 complex showed no evidence of relapse for 1 month after the cessation of treatment. We also determined that the administration of the liposome-p53 complex reduced the incidence of metastases. The MDA-MB-435 tumor cells, transduced with the lacZ gene, facilitated quantitation of beta-galactosidase activity and tumor burden in the lungs. The number of metastatic cells in the lung was significantly lower in the p53-treated group (0.53 +/- 0.43 x 10(6), p < 0.01) than in either the vector-treated (8.1 +/- 3.7 x 10(6)) or untreated control groups (15.8 +/- 5.9 x 10(6)). Thus, systemic administration of the liposome-p53 complex reduced not only the size of the primary tumors but, more importantly, prevented the relapse and metastases of these tumors. C1 NIDDKD,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD 20892. NIDR,DEV BIOL LAB,CELL BIOL SECT,BETHESDA,MD 20892. RI Kim, Wooho/G-3703-2011 NR 47 TC 134 Z9 136 U1 0 U2 1 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 1995 VL 6 IS 4 BP 395 EP 405 DI 10.1089/hum.1995.6.4-395 PG 11 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA QU204 UT WOS:A1995QU20400001 PM 7612697 ER PT J AU VANAGAITE, L JAMES, MR ROTMAN, G SAVITSKY, K BARSHIRA, A GILAD, S ZIV, Y UCHENIK, V SARTIEL, A COLLINS, FS SHEFFIELD, VC RICHARD, CW WEISSENBACH, J SHILOH, Y AF VANAGAITE, L JAMES, MR ROTMAN, G SAVITSKY, K BARSHIRA, A GILAD, S ZIV, Y UCHENIK, V SARTIEL, A COLLINS, FS SHEFFIELD, VC RICHARD, CW WEISSENBACH, J SHILOH, Y TI A HIGH-DENSITY MICROSATELLITE MAP OF THE ATAXIA-TELANGIECTASIA LOCUS SO HUMAN GENETICS LA English DT Note ID LOCALIZATION AB The locus of the autosomal recessive disorder ataxia-telangiectasia (A-T) has been assigned by linkage analysis with biallelic markers to a 4-Mb interval on chromosome 11q22-23, between GRIA4 and D11S1897. We have undertaken to saturate the A-T region with highly polymorphic microsatellite markers. To this end, we have identified seven new polymorphic CA-repeats in this region, and have mapped to it five new markers generated by Genethon and the Cooperative Human Linkage Center. These markers are in addition to 12 others that we have previously mapped or generated at the A-T locus. All 24 markers have been integrated into a high-density microsatellite map spanning some 6 Mb DNA. This map, which contains the A-T locus and flanking sequences, allows the construction of extensive, highly informative haplotypes. C1 TEL AVIV UNIV,SACKLER SCH MED,DEPT HUMAN GENET,IL-69978 RAMAT AVIV,ISRAEL. WELLCOME TRUST CTR HUMAN GENET,OXFORD OX3 7BN,ENGLAND. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. UNIV IOWA,CTR COOPERAT HUMAN LINKAGE,IOWA CITY,IA 52242. UNIV PITTSBURGH,WESTERN PSYCHIAT INST & CLIN,PITTSBURGH,PA 15231. GENETHON,F-91002 EVRY,FRANCE. FU NINDS NIH HHS [R01NS31763]; Wellcome Trust NR 16 TC 42 Z9 42 U1 0 U2 1 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 1995 VL 95 IS 4 BP 451 EP 454 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA QN565 UT WOS:A1995QN56500019 PM 7705845 ER PT J AU BECKER, KG NAGLE, JW CANNING, RD BIDDISON, WE OZATO, K DREW, PD AF BECKER, KG NAGLE, JW CANNING, RD BIDDISON, WE OZATO, K DREW, PD TI RAPID ISOLATION AND CHARACTERIZATION OF 118 NOVEL C2H2-TYPE ZINC-FINGER CDNAS EXPRESSED IN HUMAN BRAIN SO HUMAN MOLECULAR GENETICS LA English DT Article ID TRANSCRIPTION FACTOR; SEQUENCE TAGS; PROTEINS; GENE; DROSOPHILA; KRUPPEL; REGION; DOMAINS; LIBRARY; FAMILY AB C2H2-type zinc finger genes comprise one of the largest gene families in the human genome, These proteins are involved in genetic regulation and development and are quite conserved throughout evolution. The finger domains commonly contain the small linker peptide TGEKP between same finger units, Here, we report the isolation of 133 human zinc finger cDNAs, of which 118 are novel, These clones were isolated from human brain cDNA libraries using oligonucleotide hybridization followed by expressed sequence tag (EST) analysis, sequencing from the conserved linker region using degenerate oligonucleotide primers, This directed partial sequencing approach to cDNA isolation and characterization, signature sequencing, combines the speed of EST automatic sequencing with the focus of specific cDNA family analysis, Signature sequencing minimizes the generation of less informative random EST sequences and provides a unique relative position for sequence comparison. We also show that there is an even distribution of these RNAs from this brain cDNA library, and that these cDNAs contain N-terminal domains found in other zinc finger genes. This rapid focused sequencing approach should be applicable to any family of cDNAs containing short conserved signature peptide sequences. C1 NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. NINCDS,NEUROGENET SECT,BETHESDA,MD 20892. NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. OI Becker, Kevin/0000-0002-6794-6656 NR 41 TC 27 Z9 30 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1995 VL 4 IS 4 BP 685 EP 691 DI 10.1093/hmg/4.4.685 PG 7 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA QV814 UT WOS:A1995QV81400028 PM 7633419 ER PT J AU FURTH, PA SHAMAY, A HENNIGHAUSEN, L AF FURTH, PA SHAMAY, A HENNIGHAUSEN, L TI GENE-TRANSFER INTO MAMMALIAN-CELLS BY JET INJECTION SO HYBRIDOMA LA English DT Article; Proceedings Paper CT 2nd International Meeting on Idiotypic Network and Tumor Therapy - Immunological Approaches to Tumor Therapy CY FEB 03-05, 1994 CL BONN, GERMANY ID COTTONTAIL RABBIT PAPILLOMAVIRUS; DNA; IMMUNOTHERAPY; IMMUNIZATION; PROTEIN; TUMORS AB Jet injection of DNA in solution is a technique that can be used to transfer DNA into tissues of living animals, where the introduced genes are expressed.((1-5)) The muscle, fat, skin, and mammary tissue of mice, and the fat, skin, and mammary tissue of sheep can be transfected with DNA.((1)) A jet injector, such as the Ped-o-jet (Stirn Industries, Dayton, NJ), is used to form a jet from 100 to 300 mu l of a DNA solution, This jet has sufficient force to travel into and through tissues of adult and juvenile animals, The introduced DNA is found in cells surrounding the path of the jet, When jet injection is performed through the surface of intact skin, underlying muscle, mammary, and fat, cells up to 2 cm distant from the point of injection are transfected with DNA, In this study, we demonstrate that the efficiency of DNA transfer is dependent upon the force of injection, Jet injection is an alternative to needle injection, lipofection, and particle bombardment for the introduction of ''naked'' DNA into the tissues of animals, This technique has potential for the introduction of genes into living organisms for genetic vaccination and gene therapy. C1 MAX PLANCK INST BIOPHYS CHEM,DEPT MOLEC CELLULAR BIOL,W-3400 GOTTINGEN,GERMANY. TEL AVIV UNIV,SACKLER SCH MED,IL-69978 TEL AVIV,ISRAEL. NIDDK,BIOCHEM & METAB LAB,BETHESDA,MD 20892. RP FURTH, PA (reprint author), UNIV MARYLAND,VET ADM MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,10 N GREENE ST,ROOM 5D-136,BALTIMORE,MD 21201, USA. NR 18 TC 47 Z9 48 U1 0 U2 3 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0272-457X J9 HYBRIDOMA JI Hybridoma PD APR PY 1995 VL 14 IS 2 BP 149 EP 152 DI 10.1089/hyb.1995.14.149 PG 4 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Immunology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Immunology GA QZ646 UT WOS:A1995QZ64600010 PM 7590772 ER PT J AU LIN, JX MIGONE, TS TSANG, M FRIEDMANN, M WEATHERBEE, JA ZHOU, L YAMAUCHI, A BLOOM, ET MIETZ, J JOHN, S LEONARD, WJ AF LIN, JX MIGONE, TS TSANG, M FRIEDMANN, M WEATHERBEE, JA ZHOU, L YAMAUCHI, A BLOOM, ET MIETZ, J JOHN, S LEONARD, WJ TI THE ROLE OF SHARED RECEPTOR MOTIFS AND COMMON STAT PROTEINS IN THE GENERATION OF CYTOKINE PLEIOTROPY AND REDUNDANCY BY IL-2, IL-4, IL-7, IL-13, AND IL-15 SO IMMUNITY LA English DT Article ID BETA-CHAIN GENE; INTERLEUKIN-2 RECEPTOR; GAMMA-CHAIN; FUNCTIONAL COMPONENT; SIGNAL-TRANSDUCTION; ACTIVATION; PROLIFERATION; LYMPHOCYTES; REQUIREMENT; EXPRESSION AB To understand the molecular bases for cytokine redundancy and pleiotropy, we have compared the Stat proteins activated In peripheral blood lymphocytes (PBLs) by cytokines with shared and distinct actions. Interleukin-2 (IL-2) rapidly activated Stat5 in fresh PBL, and Stat3 and Stat5 in preactivated PBL. IL-7 and IL-15 induced the same complexes as IL-2, a feature explained by the existence of similar tyrosine-phosphorylated motifs in the cytoplasmic domains of IL-PRP and IL-7R that can serve as docking sites for Stat proteins. IL-13 induced the same complexes as IL-4, a finding explained by our studies implicating IL-4R as a shared component of the receptors. These studies demonstrate that a single cytokine can activate different combinations of Stat proteins under different physiological conditions, and also indicate two mechanisms by which distinct cytokines can activate the same Stat protein. C1 R & D SYST,MINNEAPOLIS,MN 55413. US FDA,CTR BIOL EVALUAT & RES,DIV CELL & GENE THERAPY,BETHESDA,MD 20892. RP LIN, JX (reprint author), NHLBI,MOLEC IMMUNOL LAB,BLDG 10,BETHESDA,MD 20892, USA. NR 53 TC 591 Z9 593 U1 1 U2 9 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD APR PY 1995 VL 2 IS 4 BP 331 EP 339 DI 10.1016/1074-7613(95)90141-8 PG 9 WC Immunology SC Immunology GA QU616 UT WOS:A1995QU61600003 PM 7719938 ER PT J AU KEARSE, KP ROBERTS, JL SINGER, A AF KEARSE, KP ROBERTS, JL SINGER, A TI TCR-ALPHA-CD3-DELTA-EPSILON ASSOCIATION IS THE INITIAL STEP IN ALPHA-BETA DIMER FORMATION IN MURINE T-CELLS AND IS LIMITING IN IMMATURE CD4(+)CD8(+) THYMOCYTES SO IMMUNITY LA English DT Article ID ANTIGEN RECEPTOR; MONOCLONAL-ANTIBODY; ENDOPLASMIC-RETICULUM; CD3 COMPLEX; DELTA-CHAIN; DEGRADATION; PROTEIN; IDENTIFICATION; BIOSYNTHESIS; EXPRESSION AB The present study has examined the molecular events leading to formation of up dimers in normal murine thymocytes and mature T cells. We demonstrate that TCR assembly proceeds by initial association of TCR alpha with CD3 delta epsilon proteins and by association of ICRP with CD3 gamma epsilon proteins to form alpha delta epsilon and beta gamma epsilon trimers; these trimers then associate to form alpha delta epsilon-beta gamma epsilon complexes, within which alpha-beta disulfide bond formation occurs. We also show that TCR-associated protein (TRAP) associates uniquely with CD3 gamma epsilon pairs and that formation of beta gamma epsilon trimers occurs subsequent to TRAP dissociation. Importantly, we document that the assembly step that is quantitatively limiting in CD4(+)CD8(+) thymocytes is the initial association of TCR alpha with CD3 delta epsilon chains, which appears necessary to protect nascent TCR alpha proteins from accelerated degradation within the ER of immature thymocytes. RP KEARSE, KP (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,BETHESDA,MD 20892, USA. NR 26 TC 65 Z9 65 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD APR PY 1995 VL 2 IS 4 BP 391 EP 399 PG 9 WC Immunology SC Immunology GA QU616 UT WOS:A1995QU61600009 PM 7719941 ER PT J AU SUZUKI, H PUNT, JA GRANGER, LG SINGER, A AF SUZUKI, H PUNT, JA GRANGER, LG SINGER, A TI ASYMMETRIC SIGNALING REQUIREMENTS FOR THYMOCYTE COMMITMENT TO THE CD4(+) VERSUS CD8(+) T-CELL LINEAGES - A NEW PERSPECTIVE ON THYMIC COMMITMENT AND SELECTION SO IMMUNITY LA English DT Article ID CLASS-II MOLECULES; DEFICIENT MICE; INSTRUCTIVE MODEL; DIFFERENTIATION; EXPRESSION; RECEPTOR; BETA-2-MICROGLOBULIN; ASSOCIATION; LYMPHOCYTES; INDUCTION AB Differentiation of immature CD4(+)CD8(+) thymocytes into mature CD4(+)CD8(-) and CD4(-)CD8(+) T cells requires that synthesis of one or the other coreceptor molecule be terminated, a process referred to as lineage commitment. The present study has utilized a novel coreceptor reexpression assay to identify lineage commitment in immature thymocytes and has found that the MHC recognition requirements for CD4 commitment and CD8 commitment fundamentally differ from one another. Remarkably, we found that thymocyte commitment to the CD8(+) lineage requires MHC class I-dependent instructional signals, whereas thymocyte commitment to the CD4(+) lineage is MHC independent and may occur by default. In addition, an unanticipated relationship between lineage commitment and surface phenotype has been identified. These results are incompatible with current concepts and require a new perspective on lineage commitment and positive selection, which we refer to as asymmetric commitment. RP SUZUKI, H (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,BETHESDA,MD 20892, USA. RI Suzuki, Harumi/L-1271-2013 OI Suzuki, Harumi/0000-0003-3616-9361 NR 43 TC 189 Z9 189 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD APR PY 1995 VL 2 IS 4 BP 413 EP 425 DI 10.1016/1074-7613(95)90149-3 PG 13 WC Immunology SC Immunology GA QU616 UT WOS:A1995QU61600011 PM 7719943 ER PT J AU BARRON, KS DEULOFEUT, H ROBINSON, MA AF BARRON, KS DEULOFEUT, H ROBINSON, MA TI TCRBV20S1 ALLELE FREQUENCIES VARY AMONG HUMAN-POPULATIONS SO IMMUNOGENETICS LA English DT Note ID V-BETA-GENE; RECEPTOR; DIVERSITY; CHAIN; DNA RP BARRON, KS (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK FACIL 2,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 12 TC 8 Z9 8 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 1995 VL 41 IS 6 BP 383 EP 385 DI 10.1007/BF00163997 PG 3 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA QW712 UT WOS:A1995QW71200008 PM 7759136 ER PT J AU HAYNIE, DL LAMB, ME AF HAYNIE, DL LAMB, ME TI POSITIVE AND NEGATIVE FACIAL EXPRESSIVENESS IN 7-MONTH-OLD, 10-MONTH-OLD, AND 13-MONTH-OLD INFANTS SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE FACIAL EXPRESSIVENESS; TEMPERAMENT; TEMPORAL STABILITY; RELIABILITY; HEDONIC TONE AB Episode-by-episode indices of the duration and latency of facial expressions, coded during emotion-eliciting stimuli using the AFFEX coding system, were combined to create highly reliable and temporally stable composite measures of positive and negative responding. These were unrelated to maternal perceptions of temperament. RP HAYNIE, DL (reprint author), NATL INST CHILD HLTH & DEV,BETHESDA,MD 20814, USA. OI Haynie, Denise/0000-0002-8270-6079 NR 4 TC 4 Z9 4 U1 0 U2 0 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 1995 VL 18 IS 2 BP 257 EP 259 DI 10.1016/0163-6383(95)90055-1 PG 3 WC Psychology, Developmental SC Psychology GA RM317 UT WOS:A1995RM31700014 ER PT J AU RUSSO, TA SHARMA, G BROWN, CR CAMPAGNARI, AA AF RUSSO, TA SHARMA, G BROWN, CR CAMPAGNARI, AA TI LOSS OF THE O4 ANTIGEN MOIETY FROM THE LIPOPOLYSACCHARIDE OF AN EXTRAINTESTINAL ISOLATE OF ESCHERICHIA-COLI HAS ONLY MINOR EFFECTS ON SERUM SENSITIVITY AND VIRULENCE IN-VIVO SO INFECTION AND IMMUNITY LA English DT Article ID PERMEABILITY-INCREASING PROTEIN; K54 CAPSULAR POLYSACCHARIDE; URINARY-TRACT INFECTION; GRAM-NEGATIVE BACTERIA; POLYACRYLAMIDE GELS; GENE-CLUSTER; RESISTANCE; TNPHOA; DISRUPTION; STRAINS AB The O-specific antigen in extraintestinal isolates of Escherichia coli is believed to be an important virulence factor. To assess its role in the pathogenic process, proven isogenic derivatives with either a complete (CP921) or nearly complete (CP920) deficiency of the O4 antigen were obtained by TnphoA'1-mediated transposon mutagenesis of an O4/K54/H5 blood isolate (CP9), By utilizing a previously reported isogenic K54 capsule-deficient derivative (CP9.137), additional isogenic derivatives deficient in both the K54 capsular antigen and either all (CP923) or nearly all (CP922) of the O4 antigen were also constructed, These strains and their wild-type parent were evaluated in vitro for serum sensitivity and in vivo by intraperitoneal challenge of outbred mice, The complete or nearly complete loss of the O4 antigen (CP920 and CP921) resulted in only a minor increase in serum sensitivity, In contrast, CP9.137 had a significant increase in serum sensitivity, and CP922 and CP923 were extremely serum sensitive. When tested in vivo, the complete or nearly complete loss of the O4 antigen resulted in a small but significant increase (P less than or equal to 0.05), not the expected decrease, in virulence compared with its wild-type parent. In contrast, CP9.137 and CP922 were significantly less virulent (P 0.05). These studies do not exclude a role for the O4 antigen moiety of lipopolysaccharide in the pathogenesis of extraintestinal E. coli infection; however, they demonstrate that the O4 antigen plays only a minor role in serum resistance in vitro and that its loss does not diminish and perhaps enhances the virulence of CP9 in vivo after intraperitoneal challenge. C1 SUNY BUFFALO,DEPT MICROBIOL,BUFFALO,NY 14215. NIAID,CLIN INVEST LAB,BACTERIAL PATHOGENESIS UNIT,BETHESDA,MD 20892. RP RUSSO, TA (reprint author), SUNY BUFFALO,CTR CLIN,DEPT MED,DIV INFECT DIS,ROOM BB132,462 GRIDER ST,BUFFALO,NY 14215, USA. NR 46 TC 34 Z9 34 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1995 VL 63 IS 4 BP 1263 EP 1269 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QP134 UT WOS:A1995QP13400020 PM 7890383 ER PT J AU FLAVIN, M SAINTJEANNET, JP DUPRAT, AM STRAUSS, F AF FLAVIN, M SAINTJEANNET, JP DUPRAT, AM STRAUSS, F TI 115-KDA PROTEIN FROM XENOPUS-LAEVIS EMBRYOS RECOGNIZED BY ANTIBODIES DIRECTED AGAINST THE XENOPUS HOMEOPROTEIN XIHBOX-1 SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY LA English DT Article DE XENOPUS EMBRYOGENESIS; HOMEODOMAIN PROTEIN; HOMEOBOX; IMMUNOBLOT IMMUNOHISTOCHEMISTRY ID HOMEOBOX GENE; MOUSE EMBRYOS; EXPRESSION; LOCALIZATION; EMBRYOGENESIS; HOMEODOMAIN AB Using antibodies against homeoprotein XlHbox 1 from Xenopus laevis, we have detected a new embryonic protein with a much larger molecular weight, 115 kDa. Antibodies fractionated according to their affinity for 3 different domains of the XlHbox 1 protein were used to show that this new protein is related to the C-terminal region of XlHbox 1 protein, downstream from the homeodomain. By immunohistochemistry, the protein was shown to be localized in nuclei of embryonic cells. On SDS-polyacrylamide gels, the 115 kDa protein appears as a set of closely spaced bands whose pattern varies with the stage of development and with the parental origin of the embryos. The protein could be extracted from embryos in a multiprotein complex of approximately 600 kDa. In contrast, the 18 and 27 kDa proteins predicted from the sequence of cloned cDNA to be transcribed and translated from the XlHbox 1 gene could not be detected, suggesting that they are rare or unstable in embryos. These data suggest that the new protein is involved in the development of Xenopus embryos, with a function possibly related to that of the homeoprotein XlHbox 1. C1 NIH,BETHESDA,MD 20892. UNIV TOULOUSE 3,CTR DEV BIOL,F-31062 TOULOUSE,FRANCE. RP FLAVIN, M (reprint author), INST JACQUES MONOD,2 PL JUSSIEU,F-75251 PARIS 05,FRANCE. NR 20 TC 0 Z9 0 U1 0 U2 0 PU UNIV BASQUE COUNTRY PRESS PI BILBAO PA POST BOX 1397, E-48080 BILBAO, SPAIN SN 0214-6282 J9 INT J DEV BIOL JI Int. J. Dev. Biol. PD APR PY 1995 VL 39 IS 2 BP 309 EP 315 PG 7 WC Developmental Biology SC Developmental Biology GA RB280 UT WOS:A1995RB28000002 PM 7669543 ER PT J AU BOLIS, CL ABRAHAM, G ARAKI, S BRAMBILLA, F BREWERTON, T CASPER, R HALMI, K HERHOLZ, K KAYE, W KUBOKI, T LICINIO, J MAGISTRETTI, P MULLER, E NEGRAO, A NDIAYE, P PIRKE, K SUEMATSU, H THOMAS, PK WAKELING, T ZHOU, DF AF BOLIS, CL ABRAHAM, G ARAKI, S BRAMBILLA, F BREWERTON, T CASPER, R HALMI, K HERHOLZ, K KAYE, W KUBOKI, T LICINIO, J MAGISTRETTI, P MULLER, E NEGRAO, A NDIAYE, P PIRKE, K SUEMATSU, H THOMAS, PK WAKELING, T ZHOU, DF TI ANOREXIA-NERVOSA - DIRECTIONS FOR FUTURE-RESEARCH SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Note ID SEROTONIN ACTIVITY; BULIMIA-NERVOSA AB On September 27-29, 1993, the Study Group on Anorexia Nervosa (AN): Basic Mechanisms, Clinical Approaches and Treatment met in Geneva, Switzerland to discuss recent progress in research on anorexia nervosa, and to identify directions for future studies. Anorexia nervosa is a disorder of unknown etiology, without a specific curative treatment, affecting mostly individuals in adolescence and early adulthood, with significant morbidity and mortality and having a major impact on psychosocial and vocational development. In anorexia nervosa there are severe disturbances in virtually every endocrine system, such as the hypothalamic-pituitary-adrenal (HPA) axis, the hypothalamic-pituitary-gondal (HPG) axis, the hypothalamic-pituitary-thyroid (HPT) axis, the growth hormone (GH)/somatomedin C (IGF-1) system, and the central and peripheral arginine vasopressin (AVP) systems. Furthermore, classical neurotransmitter systems, such as the cholinergic noradrenergic, and serotonergic systems, are abnormally regulated in anorexia nervosa. New research data is also emerging on the abnormal regulation of immune function in this disorder. The Study Group concluded that even though several biological systems are abnormally regulated in anorexia nervosa, there is no biological test which is specific enough to make the diagnosis of the disorder. New directions for research in anorexia nervosa are identified and discussed in this report. Finally, the Study Group proposed future meetings to bring together clinical and pre-clinical (pharmacological, biochemical, and molecular) scientists studying topics, such as neuroendocrine function, which are important in the biology of anorexia nervosa. (C) 1995 by John Wiley and Sons, Inc. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,CLIN RES UNIT,BETHESDA,MD 20892. RI Negrao, Andre Brooking/C-9526-2014; Licinio, Julio/L-4244-2013 OI Negrao, Andre Brooking/0000-0002-8133-6723; Licinio, Julio/0000-0001-6905-5884 NR 13 TC 11 Z9 11 U1 0 U2 7 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 1995 VL 17 IS 3 BP 235 EP 241 PG 7 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA QM866 UT WOS:A1995QM86600003 ER PT J AU BULBULYAN, MA FIGGS, LW ZAHM, SH SAVITSKAYA, T GOLDFARB, A ASTASHEVSKY, S ZARIDZE, D AF BULBULYAN, MA FIGGS, LW ZAHM, SH SAVITSKAYA, T GOLDFARB, A ASTASHEVSKY, S ZARIDZE, D TI CANCER INCIDENCE AND MORTALITY AMONG BETA-NAPHTHYLAMINE AND BENZIDINE DYE WORKERS IN MOSCOW SO INTERNATIONAL JOURNAL OF EPIDEMIOLOGY LA English DT Article ID BLADDER-CANCER; RISK-FACTORS; AROMATIC-AMINES; EXPOSED WORKERS; URINARY-BLADDER; EPIDEMIOLOGY; TUMORS; DRINKING; L5178Y; CELLS AB Background. Cancer incidence and mortality were evaluated among 4581 aniline dye production workers in Moscow. Methods. A historical cohort was assembled and followed-up from 1 January 1975 to 31 December 1989. Moscow district oncologic dispensary registries furnished case ascertainment and employer records provided job exposure data. Expected cancers and deaths were calculated based on gender-, age-, and calendar time-specific incidence and mortality rates for the Moscow general population applied to the cohort's person-years of follow-up. Disease-specific standardized mortality and incidence values were derived from ratios of observed to expected cancers. Results. Men experienced elevated total cancer mortality (standardized mortality ratio [SMR] = 125; 95% Cl : 110-142) and urinary bladder cancer mortality (SMR = 279; 95% Cl : 192-391), and increased all malignancy (standardized incidence ratio [SIR] = 142; 95% Cl : 125-160), oesophageal (SIR = 203; 95% Cl : 108-347), respiratory tract (SIR = 154; 95% Cl : 120-194) and bladder (SIR = 394; 95% Cl : 268-559) cancer incidence. Women had elevated oesophageal (SMR = 313; 95% Cl : 124-664) and bladder (SMR = 311; 95% Cl : 149-571) cancer mortality and elevated all malignancy (SIR = 124; 95% Cl : 106-144), oesophageal (SIR = 348; 95% Cl : 140-719), and bladder (SIR = 861; 95% Cl : 458-8002) cancer incidence. Bladder cancer rate increased with employment duration and younger age first hired. Rate estimates were highest among beta-naphthylamine exposed workers but was also increased among workers with other chemical exposures. A cancer prevention and control effort that limited benzidine exposure to less than or equal to 3 years was apparently unsuccessful as indicated by a significant excess of bladder cancer (SIR = 1773; 95% Cl : 356-5180) among these workers. Conclusion. Relative rates of oesophageal, lung, and stomach cancer were also elevated among all workers, but did not increase with total years worked, age first hired, or year first hired, suggesting a non-occupational aetiology. C1 NCI,EPIDEMIOL & BIOSTAT PROGRAM,ENVIRONM EPIDEMIOL BRANCH,OCCUPAT STUDIES SECT,ROCKVILLE,MD 20892. NN BLOKHIN CANC RES CTR,INST CARCINOGENESIS,DEPT CANC EPIDEMIOL & PREVENT,MOSCOW,RUSSIA. RI Zahm, Shelia/B-5025-2015 NR 42 TC 29 Z9 30 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 1995 VL 24 IS 2 BP 266 EP 275 DI 10.1093/ije/24.2.266 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA RA032 UT WOS:A1995RA03200002 PM 7635585 ER PT J AU RUTKA, JT MATSUZAWA, K HUBBARD, SL FUKUYAMA, K BECKER, LE STETLERSTEVENSON, W EDWARDS, DR DIRKS, PB AF RUTKA, JT MATSUZAWA, K HUBBARD, SL FUKUYAMA, K BECKER, LE STETLERSTEVENSON, W EDWARDS, DR DIRKS, PB TI EXPRESSION OF TIMP-1, TIMP-2, 72-KDA AND 92-KDA TYPE-IV COLLAGENASE TRANSCRIPTS IN HUMAN ASTROCYTOMA CELL-LINES - CORRELATION WITH ASTROCYTOMA CELL INVASIVENESS SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE TIMP-1; TIMP-2; TYPE IV COLLAGENASE; ASTROCYTOMA CELL LINES ID HUMAN-BRAIN-TUMORS; TISSUE INHIBITOR; GLIOMA-CELLS; METALLOPROTEINASE INHIBITORS; EXTRACELLULAR-MATRIX; ENDOTHELIAL-CELLS; 72-KDA GELATINASE; HUMAN PROSTATE; INVASION; PURIFICATION AB Malignant astrocytomas are highly invasive neoplasms which infiltrate diffusely into regions of normal brain. As evidence to support one mechanism by which tumor cells are known to invade, we have previously shown that astrocytoma cell lines secrete a variety of matrix metalloproteinases (MMPs) and metalloproteinase inhibitors (Apodaca et al: Cancer Res 50: 2322-2329, 1990). In the present study we determined the expression of tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, 72-kDa and 92-kDa type IV collagenase transcripts among human astrocytoma cell lines. In addition, we sought to correlate MMP and TIMP transcript levels with astrocytoma invasiveness. RNA from seven well characterized human astrocytoma cell lines was extracted before and after phorbol ester treatment and Northern blot analyses were performed using cDNA probes for the MMPs and TIMPs. All astrocytoma cell lines and normal human leptomeningeal cells were tested for their relative invasive potential using an in vitro invasion assay. There was variable expression of MMP and TIMP transcripts among astrocytoma cell lines. SF-188 was the only cell line to demonstrate a relative abundance of 72- and 92-kDa type IV collagenase transcripts over TIMP-1 and TIMP-2 transcript levels. Interestingly, this cell line was the most highly invasive in the in vitro invasion assay system. U 343 MG-A demonstrated relative abundance of TIMP-1 and -2 transcripts over 72- and 92-kDa type IV collagenase transcripts and was the least invasive cell line. Prior treatment of astrocytoma cell lines with phorbol ester upregulated TIMP-1 and 92-kDa type IV collagenase transcripts, but not TIMP-2 and 72-kDa type IV collagenase transcripts. We conclude that there is only partial correlation between MMP and TIMP transcript levels and in vitro cell invasiveness among the astrocytoma cell lines studied. Our analysis has led to the identification of an astrocytoma cell line, SF-188, which appears to overexpress the 72-kDa and 92-kDa type IV collagenase transcripts relative to low level TIMP-1 and TIMP-2 transcripts. This particular cell line will continue to be of considerable value in dissecting some of the molecular mechanisms involved in astrocytoma cell invasion. C1 UNIV TORONTO,HOSP SICK CHILDREN,BRAIN TUMOR RES LAB,TORONTO,ON M5G 1X8,CANADA. UNIV TORONTO,HOSP SICK CHILDREN,DIV NEUROPATHOL,TORONTO,ON M5G 1X8,CANADA. NCI,PATHOL LAB,BETHESDA,MD 20892. UNIV CALGARY,DEPT PHARMACOL & THERAPEUT,CALGARY,AB,CANADA. RP RUTKA, JT (reprint author), UNIV TORONTO,HOSP SICK CHILDREN,DIV NEUROSURG,SUITE 1502,555 UNIV AVE,TORONTO,ON M5G 1X8,CANADA. RI Edwards, Dylan/B-4734-2009; Stetler-Stevenson, William/H-6956-2012 OI Edwards, Dylan/0000-0002-3292-2064; Stetler-Stevenson, William/0000-0002-5500-5808 NR 51 TC 49 Z9 49 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD APR PY 1995 VL 6 IS 4 BP 877 EP 884 PG 8 WC Oncology SC Oncology GA QN715 UT WOS:A1995QN71500019 PM 21556615 ER PT J AU KONAI, M WHITCOMB, RF TULLY, JG ROSE, DL CARLE, P BOVE, JM HENEGAR, RB HACKETT, KJ CLARK, TB WILLIAMSON, DL AF KONAI, M WHITCOMB, RF TULLY, JG ROSE, DL CARLE, P BOVE, JM HENEGAR, RB HACKETT, KJ CLARK, TB WILLIAMSON, DL TI SPIROPLASMA VELOCICRESCENS SP-NOV, FROM THE VESPID WASP MONOBIA QUADRIDENS SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID CLASS MOLLICUTES; CLASSIFICATION AB Spiroplasma strain MQ-4(T) (T = type strain), which was isolated from the hemolymph of the vespid wasp Monobia quadridens, was serologically distinct from other spiroplasma species, groups, putative groups, and subgroups. Each strain MQ-4(T) cell was helical and motile and was surrounded by a single cytoplasmic membrane; there was no evidence of a cell wall. The strain grew well in 1% serum fraction medium, as well as in SM-1, M1D, and SP-4 liquid media, under both aerobic and anaerobic conditions. Strain MQ-4(T) grew at temperatures ranging from 10 to 41 degrees C hut did not grow at 43 degrees C. The strain grew optimally at 37 degrees C with a doubling time of 0.6 h, the shortest doubling time recorded fog any spiroplasma. Strain MQ-4(T) catabolized glucose and arginine but did not hydrolyze urea. The guanine-plus-cytosine content of the DNA was about 27.5 +/- 1 mol%. The genome size was 1,480 kbp (940 MDa). Strain MQ-4 (= ATCC 35262) designated the type strain of a new species, Spiroplasma velocicrescens. C1 USDA ARS,BELTSVILLE AGR RES CTR,INSECT BIOCONTROL LAB,BELTSVILLE,MD 20705. NCI,FREDERICK CANC RES FACIL,MOLEC MICROBIOL LAB,MYCOPLASMA SECT,FREDERICK,MD 21701. INRA,BIOL CELLULAIRE & MOLEC LAB,PONT DE LA MAYE,FRANCE. SUNY STONY BROOK,DEPT ANAT SCI,STONY BROOK,NY 11794. NR 32 TC 7 Z9 8 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1995 VL 45 IS 2 BP 203 EP 206 PG 4 WC Microbiology SC Microbiology GA QR834 UT WOS:A1995QR83400001 PM 7727271 ER PT J AU WHITEOLSON, A AF WHITEOLSON, A TI AIDS ADDENDUM SO INTERNET WORLD LA English DT Letter RP WHITEOLSON, A (reprint author), NATL LIB MED,BETHESDA,MD 20894, USA. NR 1 TC 2 Z9 2 U1 0 U2 0 PU MECKLERMEDIA CORP PI WESTPORT PA 20 KETCHUM ST, WESTPORT, CT 06880 SN 1064-3923 J9 INTERNET WORLD JI Internet World PD APR PY 1995 VL 6 IS 4 BP 8 EP 8 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA RP498 UT WOS:A1995RP49800005 ER PT J AU SILVER, PB RIZZO, LV CHAN, CC DONOSO, LA WIGGERT, B CASPI, RR AF SILVER, PB RIZZO, LV CHAN, CC DONOSO, LA WIGGERT, B CASPI, RR TI IDENTIFICATION OF A MAJOR PATHOGENIC EPITOPE IN THE HUMAN IRBP MOLECULE RECOGNIZED BY MICE OF THE H-2(R) HAPLOTYPE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE UVEITIS; EAU; MOUSE; AUTOIMMUNE DISEASE; PEPTIDES ID EXPERIMENTAL AUTOIMMUNE UVEORETINITIS; RETINOID-BINDING-PROTEIN; S-ANTIGEN; UVEITIS; PINEALITIS; RATS; MODEL; MOUSE; MHC AB Purpose. Mice of the H-2(b), H-2(k), and H-2(r) haplotypes develop experimental autoimmune uveoretinitis (EAU) after immunization with interphotoreceptor retinoid-binding protein (IRBP) of bovine or monkey origin. The purpose of this study was to identify putative pathogenic epitope(s) of IRBP and to establish their immunodominance within the IRBP molecule. Methods. Overlapping 20-amino acid peptides, spanning the entire human IRBP molecule, were synthesized and used to immunize C57BL/10 (H-2(b)), B10.BR (H-2(k)), and B10.RIII (H-2(r)) mice. Bovine IRBP was used as a positive control. Experimental autoimmune uveoretinitis was examined by histopathology 21 days after immunization. Immunologic responses were assessed by delayed-type hypersensitivity (DH) and lymphocyte proliferation assays. Results. Peptide 161-180, spanning the sequence SGIPYIISYLHPGNTILHVD, was found to be highly pathogenic for B10.RIII mice but not for the other strains. A dose-response curve showed that peptide 161-180 was maximally pathogenic at 50 mu g, but incidence and scores were reduced at 10 mu g. The truncated 13-mer 165-177 was also highly pathogenic (100 to 200 mu g), suggesting that it contained the pathogenic epitope. Mice immunized with the peptide, or with whole IRBP, had positive DH and lymphocyte responses to the immunizing as well as to the reciprocal antigen. A cell line derived to peptide 161-180 was also pathogenic for B10.RIII mice after adoptive transfer and responded (proliferation) to native IRBP. Conclusions. High incidence and high severity scores, as well as immunologic cross-recognition of peptide 161-180 and native IRBP in vivo and in vitro, suggest that this peptide contains a major epitope recognized as pathogenic by B10.RIII mice. C1 NEI,MOLEC CELL BIOL LAB,BETHESDA,MD 20892. WILLS EYE HOSP & RES INST,PHILADELPHIA,PA. RP SILVER, PB (reprint author), NEI,IMMUNOL LAB,BLDG 10,ROOM 10N218,BETHESDA,MD 20892, USA. RI Rizzo, Luiz Vicente/B-4458-2009 NR 22 TC 71 Z9 71 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD APR PY 1995 VL 36 IS 5 BP 946 EP 954 PG 9 WC Ophthalmology SC Ophthalmology GA QQ756 UT WOS:A1995QQ75600023 PM 7706044 ER PT J AU ZAPPALA, G MEASSO, G CAVARZERAN, F GRIGOLETTO, F LEBOWITZ, B PIROZZOLO, F AMADUCCI, L MASSARI, D CROOK, T AF ZAPPALA, G MEASSO, G CAVARZERAN, F GRIGOLETTO, F LEBOWITZ, B PIROZZOLO, F AMADUCCI, L MASSARI, D CROOK, T TI AGING AND MEMORY - CORRECTIONS FOR AGE, SEX AND EDUCATION FOR 3 WIDELY USED MEMORY TESTS SO ITALIAN JOURNAL OF NEUROLOGICAL SCIENCES LA English DT Article DE PROGETTO MEMORIA; MEMORY AND AGING; NORMATIVE VALUES; MEMORY TESTS AB The associate learning subtest from the Wechsler Memory Scale; Benton's Visual Retention test and a Controlled Word Association Task (FAS) were administered to a random sample of normal, healthy individuals whose age ranged from 20 to 79 years, recruited within the Italian peninsula. The neuropsychological examination took place on a mobile unit and the tests were given by the same team of neuropsychologists to reduce variability among examiners. The Research Project was known as Progetto Memoria. Corrections to the scores of these tests were calculated for age, sex, and education. These corrected values will allow clinicians to screen for memory impairment with greater precision among normally aging individuals, thus improving differential diagnosis between physiologic and pathologic deterioration of cognitive functions. C1 BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX. EXPHARMA SRL,MONTEGROTTO TERME,ITALY. MEMORY ASSESSMENT CLIN,BETHESDA,MD. FIDIA SPA,CTR RIC MEMORIA,ABANO TERME,ITALY. UNIV PADUA,IST IG,PADUA,ITALY. NIMH,BETHESDA,MD. UNIV FLORENCE,DIPARTIMENTO NEUROL & PSICHIAT,FLORENCE,ITALY. CNR,FLORENCE,ITALY. RP ZAPPALA, G (reprint author), USL 34 CATANIA,OSPED GARIBALDI,DIV NEUROL,PO GARIBALDI,VIA XX SETTEMBRE 199,I-95040 MOTTA S ANASTASIA,ITALY. NR 20 TC 12 Z9 12 U1 1 U2 2 PU MASSON DIVISIONE PERIODICI PI MILAN PA VIA STATUTO 2/4, 20121 MILAN, ITALY SN 0392-0461 J9 ITAL J NEUROL SCI JI Ital. J. Neurol. Sci. PD APR PY 1995 VL 16 IS 3 BP 177 EP 184 DI 10.1007/BF02282985 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA RD070 UT WOS:A1995RD07000006 PM 7558772 ER PT J AU PENNYPACKER, C PERELSON, AS NYS, N NELSON, G SESSLER, DI AF PENNYPACKER, C PERELSON, AS NYS, N NELSON, G SESSLER, DI TI LOCALIZED OR SYSTEMIC IN-VIVO HEAT INACTIVATION OF HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) - A MATHEMATICAL-ANALYSIS SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV; MATHEMATICAL MODEL; HEAT INACTIVATION ID WHOLE-BODY HYPERTHERMIA; REVERSE-TRANSCRIPTASE; PERIPHERAL-BLOOD; T-CELL; LYMPHOCYTES; INFECTION; SKIN; CD4; TEMPERATURE; INDIVIDUALS AB Temperatures greater than or equal to 42 degrees C, maintained for greater than or equal to 25 min, inactivate approximate to 25% of human immunodeficiency virus (HIV). HIV-infected T cells are more sensitive to heat than healthy lymphocytes, and susceptibility increases when the cells are presensitized by exposure to tumor necrosis factor. Thus, induction of a whole-body hyperthermia or hyperthermia specifically limited to tissues having a high viral load is a potential antiviral therapy for acquired immunodeficiency syndrome (AIDS). Accordingly, we incorporated therapeutic hyperthermia into an existing mathematical model that evaluates the interaction between HIV and CD4(+) T cells. Given the assumptions and limitations of this model, the results indicate that a daily therapy lowering the population of actively infected cells by 40% or infectious virus by 40% would effectively reverse the depletion of T cells. In contrast, a daily decline of 20% of either actively infected cells or infectious virus would have a marginal effect. However, daily reduction by 20% of both actively infected cells and infectious virus could restore T-cell numbers, assuming that permanent damage had not been inflicted on the thymus. Since daily treatments would probably be excessively stressful, whole-body hyperthermia seems unlikely to be clinically useful. In contrast, heating directed specifically to areas of viral concentration may be effective and have a suitable risk/benefit ratio. C1 UNIV CALIF BERKELEY,SPACE SCI LAB,BERKELEY,CA 94720. LOS ALAMOS NATL LAB,DIV THEORET,LOS ALAMOS,NM. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. UNIV CALIF SAN FRANCISCO,DEPT ANESTHESIA,SAN FRANCISCO,CA 94143. RP PENNYPACKER, C (reprint author), UNIV CALIF BERKELEY,LAWRENCE BERKELEY LAB,BERKELEY,CA 94720, USA. FU NIGMS NIH HHS [GM 39723, GM 49670] NR 45 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD APR 1 PY 1995 VL 8 IS 4 BP 321 EP 329 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QL406 UT WOS:A1995QL40600001 PM 7882096 ER PT J AU GAN, KD SANKARAN, K WILLIAMS, MG ALDEA, M RUDD, KE KUSHNER, SR WU, HC AF GAN, KD SANKARAN, K WILLIAMS, MG ALDEA, M RUDD, KE KUSHNER, SR WU, HC TI THE UMPA GENE OF ESCHERICHIA-COLI ENCODES PHOSPHATIDYLGLYCEROL-PROLIPOPROTEIN DIACYLGLYCERYL TRANSFERASE (LGT) AND REGULATES THYMIDYLATE SYNTHASE LEVELS THROUGH TRANSLATIONAL COUPLING SO JOURNAL OF BACTERIOLOGY LA English DT Note ID STRUCTURAL GENE; MUTANT; IDENTIFICATION; PROTEINS AB Using a combination of biochemical, physical, and genetic techniques, we have shown that the umpA gene of Escherichia coli is allelic with the lgt (phosphatidylglycerol:prolipoprotein diacylglyceryl transferase) of Salmonella typhimurium. These genes are essential for the viability of the respective organism and exhibit 92.8% sequence identity at the amino acid level. In E. coli, lgt and thyA (thymidylate synthase) form an operon. Thymidylate synthase levels are regulated by transcription from the lgt promoter and by translational coupling. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MICROBIOL & IMMUNOL,BETHESDA,MD 20814. UNIV GEORGIA,DEPT GENET,ATHENS,GA 30602. NIH,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. RI Aldea, Marti/K-3962-2014 OI Aldea, Marti/0000-0002-8710-5336 FU NIGMS NIH HHS [GM28811, GM27997] NR 14 TC 21 Z9 25 U1 0 U2 1 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 1995 VL 177 IS 7 BP 1879 EP 1882 PG 4 WC Microbiology SC Microbiology GA QP810 UT WOS:A1995QP81000032 PM 7896715 ER PT J AU MCCUTCHEN, CW AF MCCUTCHEN, CW TI COMMENT ON THE BIPHASIC POROVISCOELASTIC BEHAVIOR OF ARTICULAR-CARTILAGE - ROLE OF THE SURFACE ZONE IN GOVERNING THE COMPRESSIVE BEHAVIOR SO JOURNAL OF BIOMECHANICS LA English DT Letter RP MCCUTCHEN, CW (reprint author), NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9290 J9 J BIOMECH JI J. Biomech. PD APR PY 1995 VL 28 IS 4 BP 479 EP 479 DI 10.1016/0021-9290(94)00095-L PG 1 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA QM536 UT WOS:A1995QM53600014 PM 7738058 ER PT J AU MOORADIAN, DL HUTSELL, TC KEEFER, LK AF MOORADIAN, DL HUTSELL, TC KEEFER, LK TI NITRIC-OXIDE (NO) DONOR MOLECULES - EFFECT OF NO RELEASE RATE ON VASCULAR SMOOTH-MUSCLE CELL-PROLIFERATION IN-VITRO SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article DE ANGIOPLASTY; HYPERPLASIA; NITRIC OXIDE; PROLIFERATION; RESTENOSIS; VASCULAR SMOOTH MUSCLE ID CONTROLLED BIOLOGICAL RELEASE; RIBONUCLEOTIDE REDUCTASE; NUCLEOPHILE COMPLEXES; ORGANIC NITRATES; VASODILATORS; INHIBITION; MECHANISM; RELAXATION; CULTURE; PRODUCT AB Nitric oxide (NO) inhibits vascular smooth muscle cell (SMC) growth in vitro. To determine the effects of release rate and exposure time on SMC growth inhibition by NO, we compared the activities of five NO donors that generate NO with half-lives of 2 min (DEA/NO, Et(2)N[N2O2]Na), 15 min (PAPA/NO, CH3(CH2)(2)N[N2O2](-)(CH2)(3)NH3+), 39 min, (SPER/NO, H2N(CH2)(3)NH2+(CH2)(4)N[N2O2](-)(CH2)(3)NH2), 3 h (DPTA/NO, H2N(CH2)(3)N[N2O2](-)(CH2)(3)NH3+), and 20 h (DETA/NO, H2N(CH2)(2)N[N2O2](-)(CH2)(2)NH3+). After 22-h treatment, rat aorta SMC (RA-SMC) DNA synthesis was inhibited with IC,, values of 180, 60, and 40 mu M for SPER/NO, DPTA/NO, and DETA/NO, respectively. DEA/NO and PAPA/NO did not inhibit DNA synthesis significantly at any concentration tested (20-500 mu M). The inhibitory effect of NO on RA-SMC DNA synthesis was thus greatest when a given molar dose of NO was delivered slowly throughout the 22-h period. The antiproliferative effect of DETA/NO was confirmed by measurement of cell numbers for 7 days. When RA-SMC were treated with 500 mu M DETA/NO on days 1, 3, and 5, growth was completely suppressed. Cell viability was >95%, confirming that DETA/NO was not cytotoxic. The results suggest that NO donors may be useful inhibitors of intimal hyperplasia and restenosis after vascular injury such as balloon angioplasty. C1 COMEDICUS INC,COLUMBIA HTS,MN. NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,CHEM SECT,FREDERICK,MD 21702. RP MOORADIAN, DL (reprint author), UNIV MINNESOTA,CTR BIOMED ENGN,DEPT LAB MED & PATHOL,BOX 107 UMHC,420 DELAWARE ST SE,MINNEAPOLIS,MN 55455, USA. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 NR 21 TC 191 Z9 198 U1 1 U2 10 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0160-2446 J9 J CARDIOVASC PHARM JI J. Cardiovasc. Pharmacol. PD APR PY 1995 VL 25 IS 4 BP 674 EP 678 DI 10.1097/00005344-199504000-00023 PG 5 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA QP820 UT WOS:A1995QP82000023 PM 7596138 ER PT J AU KRUTH, HS SKARLATOS, SI LILLY, K CHANG, J IFRIM, I AF KRUTH, HS SKARLATOS, SI LILLY, K CHANG, J IFRIM, I TI SEQUESTRATION OF ACETYLATED LDL AND CHOLESTEROL CRYSTALS BY HUMAN MONOCYTE-DERIVED MACROPHAGES SO JOURNAL OF CELL BIOLOGY LA English DT Article ID LOW-DENSITY-LIPOPROTEIN; MOUSE PERITONEAL-MACROPHAGES; INTRACELLULAR LIPID-ACCUMULATION; ATHEROSCLEROTIC LESIONS; ELECTRON-MICROSCOPY; APOLIPOPROTEIN-E; BETA-VLDL; CELL; AGGREGATION; SURFACE AB Monocyte-derived macrophages accumulate and process cholesterol in atherosclerotic lesions. Because of the importance of this process, we examined the interaction of cholesterol crystals and acetylated low density lipoprotein (AcLDL) with human monocyte-macrophages in a combined chemical and morphological study. These two forms of cholesterol induced extensive compartmentalization of the macrophage cytoplasm, Unexpectedly, the compartments maintained a physical connection to the extracellular space as demonstrated with ruthenium red staining. The compartments formed through invagination of the top surface of the macrophage plasma membrane. Some cholesterol crystals and AcLDL were sequestered within these surface-connected compartments for up to five days in the case of the crystals and for one day in the case of AcLDL. Pulse-chase studies of fractionated macrophages indicated that [H-3]cholesterol redistributed from the surface-connected compartments into lysosomes (where the cholesterol remained unesterified) and into lipid droplets (where the cholesterol was stored as cholesteryl ester). Intracellular uptake and esterification of cholesterol was blocked by cytochalasin D. However, once cholesterol was sequestered in the surface-connected compartments, subsequent esterification of the cholesterol could not be inhibited by cytochalasin D. Apolipoprotein E was localized within the surface-connected compartments by immunogold labeling suggesting a possible function for this protein in the processing of lipid taken up through the sequestration pathway. Removal of microcrystalline cholesterol from the medium resulted in release of most of the accumulated cholesterol microcrystals from the macrophages, as well as disappearance of the surface-connected compartments. Thus, sequestration is a novel endocytic mechanism in which endocytic compartments remain connected to the extracellular space. This differs from phagocytosis where endocytic vacuoles rapidly pinch off from the plasma membrane. Sequestration provides a means for macrophages to remove substances from the extracellular space and later release them. RP KRUTH, HS (reprint author), NHLBI,EXPTL ATHEROSCLEROSIS SECT,BLDG 10,ROOM 5N-113,BETHESDA,MD 20892, USA. NR 41 TC 69 Z9 69 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1995 VL 129 IS 1 BP 133 EP 145 DI 10.1083/jcb.129.1.133 PG 13 WC Cell Biology SC Cell Biology GA QP894 UT WOS:A1995QP89400012 PM 7698980 ER PT J AU LAROCHELLE, WJ DIRSCH, OR FINCH, PW CHEON, HG MAY, M MARCHESE, C PIERCE, JH AARONSON, SA AF LAROCHELLE, WJ DIRSCH, OR FINCH, PW CHEON, HG MAY, M MARCHESE, C PIERCE, JH AARONSON, SA TI SPECIFIC RECEPTOR DETECTION BY A FUNCTIONAL KERATINOCYTE GROWTH FACTOR-IMMUNOGLOBULIN CHIMERA SO JOURNAL OF CELL BIOLOGY LA English DT Article ID IGG FUSION PROTEINS; MONOCLONAL-ANTIBODY; EXPRESSION; CELLS; LIGAND; KGF; DIFFERENTIATION; LOCALIZATION; INHIBITION; CLONING AB Fibroblast growth factor receptors (FGFRs) are encoded by at least four distinct highly conserved genes, and alternative splicing generates multiple gene products. The close relationship among different FGFRs has greatly increased the difficulty in generating specific immunochemical probes. As an alternative strategy, we constructed a fusion protein comprising keratinocyte growth factor (KGF) and an IgG(1) Fc domain (HFc). The chimeric molecule was efficiently secreted from transfectants as a disulfide-linked dimer that bound KGFRs with high affinity. Moreover, the KGFHFc, like native KGF, induced DNA synthesis by epithelial cells implying normal functional receptor activation, Because it retained the convenient detection properties of an immunoglobulin, it was possible to use the KGF-HFc in ligand-mediated histochemical analysis of KGFRs. Flow cytometry revealed KGE-HFc chimera detection of the KGFR, an alternative FGFR2 product, but not FGFR1 (flg) or FGFR2 (bek). Histochemical analysis of normal skin demonstrated the specific localization of KGFRs within the spinous layer, a zone of epithelial cell differentiation. KGFRs were also localized to epithelial cells within a specific region of the hair follicle, and they were not detectable in cells of the sweat gland. Tissue sections of soft palate and tonsil, two examples of nonkeratinizing epithelium, revealed staining of stratum spinosum and some staining of the basal cell layer as well. Neither salivary gland epithelium nor lymphoid cells were positive. The ciliated epithelium of the trachea exhibited KGFR expression in intermediate and basal cell layers. In striking contrast to the normal pattern of staining in the adjacent epithelium, a squamous cell carcinoma of skin lacked detectable KGFRs. Our present findings suggest that growth factor-Ig fusion proteins may be generally applicable in ligand-mediated histochemical detection and localization of growth factor receptors. C1 UNIV ROMA LA SAPIENZA,I-00161 ROME,ITALY. RP LAROCHELLE, WJ (reprint author), NCI,BLDG 37,ROOM 1E24,BETHESDA,MD 20892, USA. NR 36 TC 60 Z9 61 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1995 VL 129 IS 2 BP 357 EP 366 DI 10.1083/jcb.129.2.357 PG 10 WC Cell Biology SC Cell Biology GA QU091 UT WOS:A1995QU09100007 PM 7721940 ER PT J AU TOURNIER, S GERBAUD, P ANDERSON, WB LOHMANN, SM EVAINBRION, D RAYNAUD, F AF TOURNIER, S GERBAUD, P ANDERSON, WB LOHMANN, SM EVAINBRION, D RAYNAUD, F TI POSTTRANSLATIONAL ABNORMALITY OF THE TYPE-II CYCLIC-AMP-DEPENDENT PROTEIN-KINASE IN PSORIASIS - MODULATION BY RETINOIC ACID SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE CAMP-PKII; RETINOIC ACID; PSORIASIS; PHOSPHORYLATION; RII-ALPHA ID REGULATORY SUBUNIT; MOLECULAR-CLONING; CATALYTIC SUBUNIT; GOLGI-COMPLEX; RECEPTOR; FIBROBLASTS; BINDING; PHOSPHORYLATION; IDENTIFICATION; KERATINOCYTES AB Previously, we have reported a decrease in the binding of a cAMP analog to the regulatory subunits of cAMP-dependent protein kinase (cAMP-PK), as well as a decrease in cAMP-PK activities, in psoriatic cells. Retinoic acid (RA) treatment of these cells can induce an increase in cAMP-PK toward normal levels. To better define the effect of retinoic acid on the cAMP-PK system in psoriatic fibroblasts, Western blot analysis using an RII alpha specific antibody and in vivo phosphorylation experiments were carried out to determine possible changes in the RII regulatory subunit. Our results indicate a decrease in the binding of the cAMP analog 8-azido-[P-32]-cAMP with no change in the level of RII protein in psoriatic fibroblasts. In addition, by two-dimensional gel electrophoresis we observed the presence oi a phosphorylated Form of RII unique to psoriatic cells which is suppressed by RA treatment. This study suggests an altered posttranslational modification of the cAMP-PKII in psoriatic fibroblasts which can be reversed by exposure of these cells to RA. (C) 1995 Wiley-Liss, Inc. C1 ECOLE NORMALE SUPER,PHYSIOPATHOL DEV LAB,F-75230 PARIS 05,FRANCE. UNIV WURZBURG,MED KLIN,KLIN BIOCHEM LAB,W-8700 WURZBURG,GERMANY. NCI,CELLULAR ONCOL LAB,BETHESDA,MD 20892. NR 30 TC 13 Z9 13 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD APR PY 1995 VL 57 IS 4 BP 647 EP 654 DI 10.1002/jcb.240570409 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT272 UT WOS:A1995QT27200008 PM 7615649 ER PT J AU LI, LW TUCKER, RW HENNINGS, H YUSPA, SH AF LI, LW TUCKER, RW HENNINGS, H YUSPA, SH TI CHELATION OF INTRACELLULAR CA2+ INHIBITS MURINE KERATINOCYTE DIFFERENTIATION IN-VITRO SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID MOUSE EPIDERMAL-CELLS; CULTURED HUMAN KERATINOCYTES; TERMINAL DIFFERENTIATION; FREE CALCIUM; EXTRACELLULAR CALCIUM; E-CADHERIN; NEOPLASTIC KERATINOCYTES; EXPRESSION; GENE; INVITRO AB The role of intracellular Ca2+ in the regulation of Ca2+-induced terminal differentiation of mouse keratinocytes was investigated using the intracellular Ca2+ chelator 1,2-bis(o-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA). A cell permeable acetoxymethyl (AM) ester derivative BAPTA (BAPTA/AM) was loaded into primary mouse keratinocytes in 0.05 mM Ca2+ medium, and then the cells were induced to differentiate by medium containing 0.12 or 0.5 mM Ca2+ Intracellular BAPTA loaded by BAPTA/AM (15-30 mu M) inhibited the expression of epidermal differentiation-specific proteins keratin 1 (K1), keratin 10(K10), filaggrin and loricrin as detected by immunoblotting. The differentiation-associated redistribution of E-cadherin on the cell membrane was delayed but not inhibited as determined by immunofluorescence. BAPTA also inhibited the expression of K1, K10 and loricrin mRNA. Furthermore, BAPTA prevented the decrease in DNA synthesis induced by 0.12 and 0.5 mM Ca2+, indicating the drug was inhibiting differentiation but was not toxic to keratinocytes. To evaluate the influence of BAPTA on intracellular Ca2+, the concentration of intracellular free Ca2+ (Ca-i) in BAPTA-loaded keratinocytes was examined by digital image analysis using the Ca2+-sensitive fluorescent probe fura-2, and Ca2+ influx was measured by Ca-45(2+) uptake studies. Increase in extracellular Ca2+ (Ca-o) in the culture medium of keratinocytes caused a sustained increase in both Ca-i and Ca2+ localized to ionomycin-sensitive intracellular stores in keratinocytes. BAPTA lowered basal Ca-i concentration and prevented the Ca-i increase. After 12 hours of BAPTA treatment, the basal level of Ca-i returned to the control value, but the Ca2+ localized in intracellular stores was substantially decreased. Ca-45(2+) uptake was initially (within 30 min) increased in BAPTA-loaded cells. However, the total Ca-45(2+) accumulation over 24 hours in BAPTA-loaded cells remained unchanged from control values. These results indicate that keratinocytes can maintain Ca-i and total cellular Ca2+ content in the presence of increased amount of intracellular Ca2+ buffer (e.g., BAPTA) by depleting intracellular Ca2+ stores over a long period. The inhibition by BAPTA of keratinocyte differentiation marker expression may result from depletion of the Ca2+-stores since this is the major change in intracellular Ca2+ detected at the time keratinocytes express the differentiation markers. In contrast, the redistribution of E-cadherin on the cell membrane may be more directly associated with Ca-i change. (C) 1995 Wiley-Liss, Inc. C1 NCI, CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB, BETHESDA, MD 20892 USA. JOHNS HOPKINS UNIV, CTR ONCOL, BALTIMORE, MD 21205 USA. NR 49 TC 79 Z9 79 U1 0 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0021-9541 EI 1097-4652 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD APR PY 1995 VL 163 IS 1 BP 105 EP 114 DI 10.1002/jcp.1041630112 PG 10 WC Cell Biology; Physiology SC Cell Biology; Physiology GA QN686 UT WOS:A1995QN68600011 PM 7896886 ER PT J AU CHATTOPADHYAY, TK PALMER, RA MAHADEVAN, D AF CHATTOPADHYAY, TK PALMER, RA MAHADEVAN, D TI MOLECULAR AND ABSOLUTE CRYSTAL-STRUCTURE OF PINDOLOL-1-(1H-INDOL-4-YLOXY)-3-[(1-METHYLETHYL)AMINO]-2-PROPANOL - A SPECIFIC BETA-ADRENOCEPTOR ANTAGONIST WITH PARTIAL AGONIST ACTIVITY SO JOURNAL OF CHEMICAL CRYSTALLOGRAPHY LA English DT Article DE PINDOLOL; BETA BLOCKERS; AMIDE AB The crystal and molecular structure of pindolol, 1-(1H indol-4-yloxy)-3-[(1-methylethyl)amino]-2-propanol, has been determined by direct methods. Crystals are tetragonal, P (4) over bar 2(1)c, a = b = 15.809(4), c = 11.246(2) Angstrom, Z = 8, D-c = 1.174 mg m(-3). The final R-factor for 2271 reflections with I > 2 sigma(I) is 0.038. Refinement by full-matrix least-squares on F-2 also enabled the absolute configuration of the structure to be established. The molecule is essentially planar, including much of the side-chain which is stabilized by the existence of two intramolecular H-bonds, between the ethyl oxygen and OH group, and between the OH and side-chain amide groups, respectively. The crystal structure is formed by three intermolecular hydrogen bonds including two side-chain-sidechain interactions, between ethyl oxygen to amide and OH to amide, and an interaction between the side-chain OH to indole NH. C1 UNIV LONDON BIRKBECK COLL,DEPT CRYSTALLOG,LONDON WC1E 7HX,ENGLAND. NCI,BETHESDA,MD 20892. RI G, Neela/H-3016-2014 NR 6 TC 9 Z9 9 U1 1 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 1074-1542 J9 J CHEM CRYSTALLOGR JI J. Chem. Crystallogr. PD APR PY 1995 VL 25 IS 4 BP 195 EP 199 DI 10.1007/BF01666106 PG 5 WC Crystallography; Spectroscopy SC Crystallography; Spectroscopy GA RC454 UT WOS:A1995RC45400007 ER PT J AU WERBELOW, LG LONDON, RE AF WERBELOW, LG LONDON, RE TI DYNAMIC NUCLEAR-MAGNETIC-RESONANCE FREQUENCY-SHIFTS FOR SPIN-1/2 NUCLEI COUPLED TO EFFICIENTLY RELAXED SPIN-GREATER-THAN-1/2 NUCLEI SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID TRANSITION-STATE ANALOGS; HIGHER-RANK MULTIPOLES; PORPHOBILINOGEN SYNTHASE; 280000-DALTON PROTEIN; PHENYLBORONIC ACID; LINE-SHAPES; RELAXATION; NMR; QUADRUPOLAR; CHYMOTRYPSIN C1 NEW MEXICO INST MIN & TECHNOL,DEPT CHEM,SOCORRO,NM 87801. NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NR 72 TC 27 Z9 27 U1 0 U2 4 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0021-9606 J9 J CHEM PHYS JI J. Chem. Phys. PD APR 1 PY 1995 VL 102 IS 13 BP 5181 EP 5189 DI 10.1063/1.469243 PG 9 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA QP515 UT WOS:A1995QP51500008 ER PT J AU FRIEDMAN, TC YANOVSKI, JA JAYASVASTI, V YANOVSKI, SZ KOENIG, RJ WILK, S AF FRIEDMAN, TC YANOVSKI, JA JAYASVASTI, V YANOVSKI, SZ KOENIG, RJ WILK, S TI PYROGLUTAMYL PEPTIDASE-II (THYROLIBERINASE) ACTIVITY IN HUMAN SERUM - INFLUENCE OF WEIGHT AND THYROID STATUS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID THYROTROPIN-RELEASING-HORMONE; TRH-DEGRADING ENZYME; PROLYL ENDOPEPTIDASE; RAT SERUM; RABBIT BRAIN; DEGRADATION; AMINOPEPTIDASE; TSH; NEUROPEPTIDE; INHIBITORS AB The tripeptide hormone, TRH, is metabolized by three enzymes, the most specific of which is pyroglutamyl peptide hydrolase-II (also termed thyroliberinase), a metalloenzyme present in serum and brain. Because pyroglutamyl peptidase-II activity in rat serum is regulated by thyroid hormone levels, we tested the hypothesis that this activity is similarly altered in humans. We studied serum pyroglutamyl peptidase-II activity in 6 patients with hyperthyroidism, 18 patients with hypothyroidism, and 31 euthyroid, normal weight volunteers. Because TRH [or its metabolite cyclo(His-Pro)] is believed to be an important hormone regulating appetite and metabolism, we also evaluated pyroglutamyl peptidase-II activity in 27 euthyroid patients with obesity. Serum pyroglutamyl peptidase-II activity was elevated in patients with hypothyroidism (mean +/- SEM, 33.9 +/- 3.7 nmol/mL.h) compared to that in euthyroid, normal weight volunteers (24.5 +/- 2.8 nmol/mL.h; P < 0.05), but not that in patients with hyperthyroidism (28.3 +/- 4.1 nmol/mL.h; P = NS). Euthyroid obese patients had the highest pyroglutamyl peptidase-II activity (43.6 +/- 2.8 nmol/mL.h; P < 0.0001 vs. normal weight volunteers). Pyroglutamyl peptidase-II activity was positively correlated with body mass index (r(2) = 0.30; P < 0.0001). After correction for body mass index, there were no difference in pyroglutamyl peptidase-II activity in hypothyroid, hyperthyroid, and euthyroid individuals. We conclude that serum pyroglutamyl peptidase-II activity is regulated by, or regulates, body weight. C1 NICHHD, DEV NEUROBIOL LAB, BETHESDA, MD 20892 USA. NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. UNIV MICHIGAN, MED CTR, DIV ENDOCRINOL, ANN ARBOR, MI 48109 USA. CUNY MT SINAI SCH MED, DEPT PHARMACOL, NEW YORK, NY 10029 USA. NR 43 TC 10 Z9 10 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1995 VL 80 IS 4 BP 1086 EP 1089 DI 10.1210/jc.80.4.1086 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QR243 UT WOS:A1995QR24300011 PM 7714073 ER PT J AU YANO, K SAJI, M HIDAKA, A MORIYA, N OKUNO, A KOHN, LD CUTLER, GB AF YANO, K SAJI, M HIDAKA, A MORIYA, N OKUNO, A KOHN, LD CUTLER, GB TI A NEW CONSTITUTIVELY ACTIVATING POINT MUTATION IN THE LUTEINIZING-HORMONE CHORIOGONADOTROPIN RECEPTOR GENE IN CASES OF MALE-LIMITED PRECOCIOUS PUBERTY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID INOSITOL PHOSPHATE LEVELS; THYROTROPIN TSH RECEPTOR; 3RD CYTOPLASMIC LOOP; SEXUAL PRECOCITY; ALPHA-1B-ADRENERGIC RECEPTOR; DNA; PHOSPHOINOSITIDE; AUTOANTIBODIES; SUBSTITUTIONS; MUTAGENESIS AB A single point mutation that encodes an aspartic acid (Asp(578)) to glycine substitution in the LH/CG receptor (LH/CGR) gene, D578G, was recently found in American patients with familial male-limited precocious puberty and in a Japanese patient with a sporadic form of the disorder. Transfection of the mutant, compared to the wild-type, LH/CGR complementary DNA into COS-7 cells results in higher basal cAMP production, but a normal agonist-induced response; the mutation is, therefore, proposed to constitutively activate Leydig cells and elevate serum testosterone, despite low levels of gonadotropin. In the current study we examined two additional Japanese patients with male-limited precocious puberty without a family history of the disease. We describe a heterozygous cytosine (C) to thymine (T) transition at nucleotide 1715 in both; the mutation encodes an alanine to valine substitution in codon 572 of transmembrane helix 6, A572V. Transfected into COS-7 cells, the A572V mutant exhibited the same constitutively high basal cAMP levels and normal agonist-induced cAMP response as the D578G mutant. We conclude that the constitutively higher cAMP levels caused by the A572V mutation led to Leydig cell activation and male-limited precocious puberty, as in the previously described D578G mutation. As the mother of one of the two patients had the same heterozygous mutation, this patient represents the first recognized case of inherited male-limited precocious puberty in the Japanese population. The previously described D578G mutant did not increase basal or agonist-induced inositol phosphate production in transfected COS-7 cells, or the number of LH/CGRs or their affinity for LH/CG. In contrast, transfection of the A572V mutation in COS-7 cells exhibited significantly higher inositol phosphate levels basally and at 10(-11) mol/L hCG, but significantly lower inositol phosphate levels at 10(-7) mol/L hCG. These data suggest that the A572V mutation of the LH/CGR may have effects on the guanine nucleotide binding protein which activates phospholipase C (G(q)) coupling and phospholipase-C activation in addition to its effects on G(s) coupling and activation of adenylyl cyclase. A572V-transfected cells also exhibited a higher affinity, despite an apparent decrease in the number of binding sites, for [I-125]hCG, compared to transfectants with the wild-type LH/CGR. We hypothesize that these differences between the A572V and D578G mutations reflect a greater impact of the A572V mutation on receptor conformation. C1 NIDDKD, BIOCHEM & METAB LAB, CELL REGULAT SECT, BETHESDA, MD 20892 USA. YAMAGATA UNIV, SCH MED, DEPT PEDIAT, YAMAGATA 99023, JAPAN. ASAHIKAWA MED COLL, DEPT PEDIAT, ASAHIKAWA 078, HOKKAIDO, JAPAN. RP YANO, K (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N262, BETHESDA, MD 20892 USA. NR 28 TC 71 Z9 72 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1995 VL 80 IS 4 BP 1162 EP 1168 DI 10.1210/jc.80.4.1162 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QR243 UT WOS:A1995QR24300024 PM 7714085 ER PT J AU OLSON, BR CARTLEDGE, T SEBRING, N DEFENSOR, R NIEMAN, L AF OLSON, BR CARTLEDGE, T SEBRING, N DEFENSOR, R NIEMAN, L TI SHORT-TERM FASTING AFFECTS LUTEINIZING-HORMONE SECRETORY DYNAMICS BUT NOT REPRODUCTIVE FUNCTION IN NORMAL-WEIGHT SEDENTARY WOMEN SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID INVIVO BIOLOGICAL VALIDATION; ENDOCRINE PEAK DETECTION; MENSTRUAL-CYCLE; ANOREXIA-NERVOSA; POSITIVE ACCURACY; SERUM THYROTROPIN; MACACA-MULATTA; PULSE SIGNAL; PULSATILE; AMENORRHEA AB Acute food withdrawal reversibly inhibits the hypothalamic-pituitary-gonadal axis in men and in rhesus monkeys, and it produces defects in LH pulsatility in normal-weight women. However, the clinical effect of short-term nutritional deprivation on the reproductive axis of normally cycling women has not been evaluated. Thus we studied the effect of a 3-day fast during the midfollicular phase on menstrual cycle length, gonadotropin secretory patterns, follicular development, and ovulation. After a baseline ovulatory cycle, 12 women within 15% of ideal body weight were randomized to be fed (n = 7) or fasted (n = 10) on cycle days 7 to 9. Five of the women repeated the study and received the alternate diet. Endocrine and metabolic parameters of fasting and reproductive physiology were measured on cycle days 6 to 12. Fasted physiology was demonstrated by characteristic alterations in growth hormone, insulin-like growth factor I, TSH, and T-3 levels. During fed cycles, the number of LH pulses remained constant on cycle days 6, 9 and 11, whereas mean LH levels, LH area under the curve, and LH pulse amplitude increased significantly over this time (all P < 0.05). In contrast, fasted cycles were marked by a significant decrease in the number of LH pulses on the last day of the fast (cycle day 9, P < 0.05) and by a lack of increase over time of mean LH values, LH area under the curve, and LH pulse amplitude. Follicle development, as assessed by daily ultrasound examination and estradiol measurements, was similar in all cycles and was followed by ovulation in all women; follicular and luteal phase lengths of fasted and fed cycles were similar. We conclude that the alterations in LH secretory dynamics that occur during a S-day fast are not sufficient to perturb follicle development and cycle lengths in normal-weight sedentary women. The resilience of the reproductive axis in these healthy women contrasts with the sensitivity of the hypothalamic-pituitary-gonadal axis to acute nutritional withdrawal in men and in monkeys. We speculate that differences in the set point for sensing fuel availability or in the status of energy balance before the initiation of food deprivation may account for these species-specific and sex-specific variabilities. C1 NICHHD, DEV ENDOCRINOL BRANCH, WARREN G MAGNUSON CLIN CTR, DEPT NUTR, BETHESDA, MD 20892 USA. RP OLSON, BR (reprint author), NICHHD, DEV ENDOCRINOL BRANCH,WARREN G MAGNUSON CLIN CTR, DEPT NURSING,BLDG 10, 10N262, BETHESDA, MD 20892 USA. NR 39 TC 36 Z9 36 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1995 VL 80 IS 4 BP 1187 EP 1193 DI 10.1210/jc.80.4.1187 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QR243 UT WOS:A1995QR24300028 PM 7714088 ER PT J AU BOUILLON, R BEX, M VANHERCK, E LAUREYS, J DOOMS, L LESAFFRE, E RAVUSSIN, E AF BOUILLON, R BEX, M VANHERCK, E LAUREYS, J DOOMS, L LESAFFRE, E RAVUSSIN, E TI INFLUENCE OF AGE, SEX, AND INSULIN ON OSTEOBLAST FUNCTION - OSTEOBLAST DYSFUNCTION IN DIABETES-MELLITUS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GROWTH FACTOR-I; D-ENDOCRINE SYSTEM; METABOLIC BONE-DISEASE; ALKALINE-PHOSPHATASE; SOMATOMEDIN-C; BB-RATS; OSTEOCALCIN SYNTHESIS; PARATHYROID-HORMONE; MINERAL METABOLISM; BINDING-PROTEIN AB The osteoblast function was evaluated in normal and diabetic children and adults by measurements of the serum concentration of the carboxy-terminal extension peptide of procollagen (PICP), total and skeletal alkaline phosphatase (ALP), and osteocalcin. Moreover, the osteoblast-stimulating growth factor, insulin-like growth factor I (IGF-I), was measured in the same samples. In normal children (n = 420; age, 5-20 yr), a marked pubertal increase of serum IGF-I (peak values at age 14-16 yr in both sexes), osteocalcin, and total and skeletal ALP (peak values earlier in girls than in boys) and a small increase in PICP were observed. All osteoblast markers and IGF-I were markedly lower in normal adults (n = 229; age, 21-69 yr) than in children. All osteoblast parameters showed a high degree of correlation (P < 0.001) with each other. In adolescents (n = 104) treated for insulin-dependent diabetes mellitus (IDDM), serum IGF-I (-19%), osteocalcin (-28%), and skeletal ALP (-28%) were markedly decreased, whereas total ALP was significantly increased (29%), and serum PICP remained normal. In adult IDDM (n = 125), both serum IGF-I (-41%) and osteocalcin (-24%) were decreased, but skeletal ALP and PICP remained normal. A similar abnormality in serum IGF-I and osteocalcin was observed in white (n = 61) and Pima Indian (n = 16) non-IDDM patients. The concentration of skeletal ALP was highly significantly correlated (r greater than or equal to 0.9) with total ALP in both normal and diabetic subjects, but the slope of the regression was significantly different, indicating the presence of other, probably intestinal, ALP in all types of diabetes. In conclusion, the osteoblast function is significantly decreased in diabetic patients, which can best be characterized as a maturation defect, since the early osteoblast marker, PICP, remained normal in all types of diabetes, whereas a later marker, skeletal ALP, is frankly abnormal only in diabetic children. The most mature osteoblast marker, osteocalcin, is decreased in all types of diabetes irrespective of age. C1 CATHOLIC UNIV LEUVEN, HOSP GASTHUISBERG, EXPTL GENEESKUNDE & ENDOCRINOL, B-3000 LOUVAIN, BELGIUM. CATHOLIC UNIV LEUVEN, HOSP GASTHUISBERG, DEPT PEDIAT ENDOCRINOL, B-3000 LOUVAIN, BELGIUM. CATHOLIC UNIV LEUVEN, HOSP GASTHUISBERG, CTR BIOSTAT, B-3000 LOUVAIN, BELGIUM. NIH, DEPT HLTH & HUMAN SERV, PHOENIX, AZ USA. NR 52 TC 160 Z9 164 U1 0 U2 2 PU ENDOCRINE SOC PI WASHINGTON PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1995 VL 80 IS 4 BP 1194 EP 1202 DI 10.1210/jc.80.4.1194 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QR243 UT WOS:A1995QR24300029 PM 7714089 ER PT J AU SUZUKI, Y HATANAKA, Y TAIRA, M SHIMADA, F HASHIMOTO, N TAKAYANAGI, M TAYLOR, SI MAKINO, H YOSHIDA, S AF SUZUKI, Y HATANAKA, Y TAIRA, M SHIMADA, F HASHIMOTO, N TAKAYANAGI, M TAYLOR, SI MAKINO, H YOSHIDA, S TI INSULIN-RESISTANCE ASSOCIATED WITH DECREASED LEVELS OF INSULIN-RECEPTOR MESSENGER-RIBONUCLEIC-ACID - EVIDENCE OF A DE-NOVO MUTATION IN THE MATERNAL ALLELE SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID POLYMERASE CHAIN-REACTION; TYROSINE KINASE DOMAIN; NONSENSE MUTATION; VARIABLE NUMBER; MUTANT ALLELES; GENE; RNA; DNA; AMPLIFICATION; SEQUENCE AB Mutations in the insulin receptor gene may lead to insulin resistance and diabetes mellitus in some patients. We have studied an insulin-resistant patient with leprechaunism. Insulin binding to the patient's fibroblasts was markedly decreased. Determination of the nucleotide sequence of the patient's insulin receptor gene revealed heterozygosity for a 2-basepair deletion in exon 15. If the premessenger ribonucleic acid (pre-mRNA) is spliced normally, it causes a replacement of codon 970 in the beta-subunit with a premature chain termination codon, thereby deleting most of the intracellular domain of the receptor. The mRNA transcribed from the allele with a 2-basepair deletion is likely to be unstable because mRNA transcripts from this allele could not be detected by complementary DNA sequencing. Northern blot analysis showed that the patient's insulin receptor mRNA was decreased by 90% compared with that of a control subject, thus suggesting that the patient is a compound heterozygote for two mutations that decrease levels of insulin receptor mRNA. This deletion mutation in exon 15 seems to be a de novo mutation, because it was not detected in either parent. Investigation of the inheritance of a silent sequence polymorphism in exon 17 provided that the deletion occurred in the maternal allele. Furthermore, linkage analysis suggests that the second mutation is derived from the patient's father, although we could not directly identify it by sequencing the coding region of the insulin receptor gene. Therefore, it is possible that this mutation is present in a regulatory domain of the insulin receptor gene, acting in cis-dominant fashion to reduce the levels of insulin receptor mRNA. Analyses of the hypervariable region in the myoglobin and pMCT118 loci were consistent with the assumption that the father and mother studied here are indeed the biological parents of the diseased patient. We hereby conclude that the patient is a compound heterozygote for two mutant alleles, both of which are responsible for the reduced levels of insulin receptor mRNA and insulin binding. C1 CHIBA UNIV, SCH MED, DEPT INTERNAL MED 2, CHUO KU, CHIBA 260, JAPAN. CHIBA CHILDRENS HOSP, DEPT PEDIAT, CHIBA, JAPAN. NIDDKD, DIABET BRANCH, BETHESDA, MD 20892 USA. NR 30 TC 4 Z9 5 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1995 VL 80 IS 4 BP 1214 EP 1220 DI 10.1210/jc.80.4.1214 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QR243 UT WOS:A1995QR24300032 PM 7714091 ER PT J AU FEUILLAN, PP JONES, J ROSS, JL AF FEUILLAN, PP JONES, J ROSS, JL TI GROWTH-HORMONE HYPERSECRETION IN A GIRL WITH MCCUNE-ALBRIGHT SYNDROME - COMPARISON WITH CONTROLS AND RESPONSE TO A DOSE OF LONG-ACTING SOMATOSTATIN ANALOG SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID STIMULATORY G-PROTEIN; PRECOCIOUS PUBERTY; ACTIVATING MUTATIONS; IMPAIRED GROWTH; SHORT STATURE; CHILDREN; THERAPY; TESTOLACTONE; SECRETION; AXIS AB GH every 20 min for 24 h, insulin-like growth factor I (IGF-I), IGF-binding protein 3, and estradiol (E(2)) were measured in a 7.3-yr-old girl with precocious puberty due to McCune-Albright syndrome (MAS) who developed stigmata of early acromegaly and in 9 other MAS patients who had no signs of acromegaly. To determine whether the MAS patients had subtle abnormalities in GH secretion, a computerized pulse analysis program was used to compare the MAS data with those from 27 control girls with central precocious puberty who had a similar rate of bone age advance, E(2), and body mass index. We found no differences in mean GH, GH pulse frequency, pulse height, or pulse area between MAS patients and controls except in patient 1, who had an elevated mean +/- SD GH compared with controls (15.4 +/- 2 vs. 4.8 +/- 2.3 mu g/L; P < 0.01) and an elevated IGF-I (908 mu g/L) and IGF-binding protein 3 (5.6 mg/L). None of the GH parameters correlated with body mass index, age, bone age, or E(2) levels in either group. The serum GH in patient 1 fell to near-undetectable levels from 60-180 min after a 100-mu g sc dose of long-acting somatostatin, confirming that this farm of therapy can be effective in cases of GH hypersecretion due to MAS. C1 THOMAS JEFFERSON UNIV HOSP, DEPT PEDIAT, PHILADELPHIA, PA 19107 USA. RP FEUILLAN, PP (reprint author), NICHHD, DEV ENDOCRINOL BRANCH, BLDG 10, ROOM 10N 262, BETHESDA, MD 20892 USA. NR 29 TC 21 Z9 24 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1995 VL 80 IS 4 BP 1357 EP 1360 DI 10.1210/jc.80.4.1357 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QR243 UT WOS:A1995QR24300057 PM 7714111 ER PT J AU PAOLISSO, G RAVUSSIN, E AF PAOLISSO, G RAVUSSIN, E TI INTRACELLULAR MAGNESIUM AND INSULIN-RESISTANCE - RESULTS IN PIMA-INDIANS AND CAUCASIANS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HYPERTENSION AB Intracellular magnesium is a cofactor for numerous enzymes involved in carbohydrate metabolism. Magnesium accumulation is dependent upon insulin action and correlates with insulin-mediated glucose uptake. As Pima Indians are known to be insulin resistant, we investigated whether, in response to insulin infusion, they have lower erythrocyte magnesium accumulation than Caucasians. Insulin-mediated glucose uptake was determined by a euglycemic hyperinsulinemic glucose clamp in 29 obese nondiabetic volunteers: 15 Caucasians (8 males and 7 females) and 14 Pima Indians (8 males and 6 females). Pima Indians were younger than Caucasians (mean +/- SD, 28 +/- 7 vs. 39 +/- 8 yr; P < 0.01), but had similar body mass index and fasting/2-h plasma glucose concentrations. Despite higher steady state plasma insulin levels (692 +/- 260 us. 540 +/- 70 pmol/L; P < 0.03), Pima Indians had lower insulin-mediated glucose uptake than Caucasians (108 +/- 20 vs. 244 +/- 32 mg/m(2) . min; P < 0.0001). The mean fasting plasma magnesium concentration was lower in Pima Indians than in Caucasians (0.79 +/- 0.05 vs. 0.85 +/- 0.06 mmol/L; P < 0.01), whereas the mean fasting erythrocyte magnesium concentrations (1.98 +/- 0.10 vs. 2.03 +/- 0.14 mmol/L) were similar in the 2 groups. In response to insulin infusion, erythrocyte magnesium content increased less in Pima Indians than in Caucasians (0.15 +/- 0.07 vs. 0.28 +/- 0.21 mmol/L; P < 0.03). However, this increase was similar in the 2 groups when values were adjusted for insulin-mediated glucose uptake. In conclusion, nondiabetic Pima Indians have a lower erythrocyte magnesium accumulation in response to insulin infusion; this is probably due to their high degree of insulin resistance. The biochemical and physiological consequences of decreased intracellular magnesium uptake are discussed. C1 NIDDKD, CLIN DIABET & NUTR SECT, PHOENIX, AZ 85016 USA. OI Paolisso, Giuseppe/0000-0002-2137-455X NR 23 TC 45 Z9 46 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1995 VL 80 IS 4 BP 1382 EP 1385 DI 10.1210/jc.80.4.1382 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QR243 UT WOS:A1995QR24300061 PM 7714114 ER PT J AU BRINTON, LA TONIOLO, P PASTERNACK, BS AF BRINTON, LA TONIOLO, P PASTERNACK, BS TI EPIDEMIOLOGIC FOLLOW-UP-STUDIES OF BREAST AUGMENTATION PATIENTS SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE BREAST; IMPLANTATION; MAMMAPLASTY; SILICONE ID CANCER; CARCINOGENICITY; MAMMAPLASTY; CARCINOMA; 2,4-TOLUENEDIAMINE; MAMMOGRAPHY; SILICONE; IMPLANTS; WOMEN; RATS AB Although hundreds of thousands of women in this country have had augmentation mammaplasty, little is known about long-term effects. Clinical studies have documented a decreased ability to detect breast lesions in women with implants, leading to concerns regarding breast cancer risk. There is also anecdotal evidence that implants might have effects on a variety of immune conditions. More recently, concern over carcinogenic effects has heightened given findings that the polyurethane foam, used in a minority of implants to envelope silicone gel, contains chemicals linked to cancer in laboratory animals. Only a few epidemiologic studies on long-term effects have been published, and all have had methodologic limitations, including the possibility of inappropriate comparison rates, limited and/or incomplete follow-up, absence of information on patients characteristics, and lack of specific information on types of implanted material. Several case-control and cohort studies are currently underway which are attempting to overcome methodologic limitations of previous studies. Past descriptive and analytic studies are reviewed. In addition, ongoing follow-up efforts are discussed, with attention given to the methodologic adjuncts necessary for allowing valid assessments of long-term disease effects. C1 NYU,MED CTR,DEPT ENVIRONM MED,DIV EPIDEMIOL & BIOSTAT,NEW YORK,NY 10010. RP BRINTON, LA (reprint author), NCI,ENVIRONM EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 443,BETHESDA,MD 20892, USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 34 TC 21 Z9 21 U1 0 U2 0 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 1995 VL 48 IS 4 BP 557 EP 563 DI 10.1016/0895-4356(94)00213-A PG 7 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA QV706 UT WOS:A1995QV70600018 PM 7722612 ER PT J AU REINHARDT, RR CHIN, E ZHOU, J TAIRA, M MURATA, T MANGANIELLO, VC BONDY, CA AF REINHARDT, RR CHIN, E ZHOU, J TAIRA, M MURATA, T MANGANIELLO, VC BONDY, CA TI DISTINCTIVE ANATOMICAL PATTERNS OF GENE-EXPRESSION FOR CGMP-INHIBITED CYCLIC-NUCLEOTIDE PHOSPHODIESTERASES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CYCLIC NUCLEOTIDE PHOSPHODIESTERASE; PDE3; CGMP; CAMP; MESSENGER-RNA ID RAT ADIPOSE-TISSUE; GROWTH FACTOR-I; AMP PHOSPHODIESTERASE; CAMP-PHOSPHODIESTERASE; MOLECULAR-CLONING; SMOOTH-MUSCLE; STIMULATED PHOSPHODIESTERASE; DROSOPHILA-MELANOGASTER; VENTRICULAR MYOCARDIUM; INSULIN AB Type III cGMP-inhibited phosphodiesterases (PDE3s) play important roles in hormonal regulation of lipolysis, platelet aggregation, myocardial contractility, and smooth muscle relaxation. We have recently characterized two PDE3 subtypes (PDE3A and PDE3B) as products of distinct but related genes. To elucidate their biological roles, in this study we compare cellular patterns of gene expression for these two enzymes during rat embryonic and postnatal development using in situ hybridization. PDE3A mRNA is abundant in adipose tissue and is also expressed in hepatocytes throughout development. This mRNA is also highly abundant in embryonic neuroepithelium including the neural retina, but expression is greatly reduced in the mature nervous system. Finally, PDE3A mRNA is localized in spermatocytes and renal collecting duct epithelium in adult rats. PDE3B mRNA is highly expressed in the cardiovascular system, including myocardium and arterial and venous smooth muscle, throughout development. It is also abundant in bronchial, genitourinary and gastrointestinal smooth muscle and epithelium, megakaryocytes, and oocytes. PDE3B mRNA demonstrates a complex, developmentally regulated pattern of gene expression in the central nervous system. In summary, the two different PDE3s show distinctive tissue-specific patterns of gene expression suggesting that PDE3A is involved in hormonal regulation of lipolysis and glycogenolysis, while regulation of myocardial and smooth muscle contractility appears to be a function of PDE3B. In addition, the present findings suggest previously unsuspected roles for these enzymes in gametogenesis and neural development. C1 NHLBI,PULM CRIT CARE MED BRANCH,BETHESDA,MD 20892. RP REINHARDT, RR (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N-262,BETHESDA,MD 20892, USA. NR 50 TC 123 Z9 127 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1995 VL 95 IS 4 BP 1528 EP 1538 DI 10.1172/JCI117825 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QQ596 UT WOS:A1995QQ59600016 PM 7706458 ER PT J AU FIORELLI, V GENDELMAN, R SAMANIEGO, F MARKHAM, PD ENSOLI, B AF FIORELLI, V GENDELMAN, R SAMANIEGO, F MARKHAM, PD ENSOLI, B TI CYTOKINES FROM ACTIVATED T-CELLS INDUCE NORMAL ENDOTHELIAL-CELLS TO ACQUIRE THE PHENOTYPIC AND FUNCTIONAL FEATURES OF AIDS-KAPOSIS SARCOMA SPINDLE CELLS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE FVIII-RA; HIV-1; TAT PROTEIN; BFGF; ENDOTHELIAL CELL CYCLE; INFLAMMATORY CYTOKINES; AIDS ID TUMOR-NECROSIS-FACTOR; FIBROBLAST GROWTH-FACTOR; IMMUNODEFICIENCY-VIRUS TYPE-1; IMMUNE-DEFICIENCY SYNDROME; FACTOR GENE-EXPRESSION; YOUNG HOMOSEXUAL MEN; SMOOTH-MUSCLE CELLS; FACTOR-ALPHA; VONWILLEBRAND-FACTOR; SURFACE-ANTIGENS AB Kaposi's sarcoma (KS) is a proliferative disease of vascular origin particularly frequent in HIV-1-infected homosexual men (AIDS-KS) and characterized by proliferating spindle-shaped cells, angiogenesis, and inflammatory cell infiltration, Previous work has suggested that KS spindle cells are of endothelial cell origin and that chronic immune activation via the release of inflammatory cytokines may cooperate with basic fibroblast growth factor (bFGF) and the HIV-1 Tat protein in the induction and progression of AIDS-KS. Here we show that KS spindle cells have features of activated endothelial cells, and that conditioned media from activated T cells, rich in the same inflammatory cytokines increased in HIV-1-infected individuals, induce normal endothelial cells to acquire the phenotypic and functional features of KS cells, These include (a) acquisition of a similar pattern of cell surface antigen expression; (b) similar proliferative response to bFGF; (c) induction of the responsiveness to the mitogenic effect of extracellular HIV-1 Tat protein that is now able to promote the G1-S transition of endothelial cell cycle; and (d) induction in nude mice of vascular lesions closely resembling early KS as well as the lesions induced by inoculation of KS cells, These results suggest that chronic immune activation, via release of inflammatory cytokines, may play a role in the induction of KS. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD 20895. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 80 TC 136 Z9 137 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1995 VL 95 IS 4 BP 1723 EP 1734 DI 10.1172/JCI117849 PG 12 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QQ596 UT WOS:A1995QQ59600040 PM 7535796 ER PT J AU QUYYUMI, AA DAKAK, N ANDREWS, NP HUSAIN, S ARORA, S GILLIGAN, DM PANZA, JA CANNON, RO AF QUYYUMI, AA DAKAK, N ANDREWS, NP HUSAIN, S ARORA, S GILLIGAN, DM PANZA, JA CANNON, RO TI NITRIC-OXIDE ACTIVITY IN THE HUMAN CORONARY CIRCULATION - IMPACT OF RISK-FACTORS FOR CORONARY ATHEROSCLEROSIS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE NITRIC OXIDE; CORONARY CIRCULATION; ENDOTHELIUM-DEPENDENT VASODILATION; CORONARY RISK FACTORS ID ENDOTHELIUM-DEPENDENT VASODILATION; L-ARGININE; SMOOTH-MUSCLE; BLOOD-FLOW; VASOMOTOR RESPONSE; RELAXING FACTOR; VASCULAR RELAXATION; MEDIATED DILATION; CONSCIOUS DOGS; AWAKE DOGS AB The bioavailability of nitric oxide (NO) in the human coronary circulation at rest and after acetylcholine (ACH)-induced vasodilation was investigated in 32 patients with angiographically normal coronary arteries, The effects of intracoronary L-N-G monomethyl arginine (L-NMMA) were investigated at rest and after AGH, sodium nitroprusside, and adenosine, L-NMMA (64 mu mol/min) increased resting coronary vascular resistance by 22% (P<0.001), reduced distal epicardial coronary artery diameter by 12.6% (P<0.001), and inhibited AGH-induced coronary epicardial and microvascular vasodilation. These effects were reversed with intracoronary L-arginine. L-NMMA did not inhibit dilation in response to sodium nitroprusside and adenosine, 23 patients were exposed to one or more coronary risk factors, The vasoconstrictor effect of L-NMMA on the epicardial and microvessels was greater in patients free of risk factors: Coronary vascular resistance was 36% higher in patients without risks, compared to 17% higher in patients with risks (P<0.05), Both epicardial and microvascular dilator effects of ACH were greater in patients without risk factors, and the inhibition of these effects by L-NMMA was also greater in patients without risk factors, Thus: (a) NO contributes importantly to resting epicardial and coronary microvascular tone, (b) coronary vascular dilation in response to ACH is predominantly due to increased production of NO, and (c) despite the absence of angiographic evidence of atherosclerosis, exposure to coronary risk factors is associated with reduced resting and stimulated bioavailability of NO from the human coronary circulation. C1 UNIV W VIRGINIA HOSP,MORGANTOWN,WV 26506. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DIV CARDIOL,RICHMOND,VA 23298. RP QUYYUMI, AA (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 62 TC 343 Z9 349 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1995 VL 95 IS 4 BP 1747 EP 1755 DI 10.1172/JCI117852 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QQ596 UT WOS:A1995QQ59600043 PM 7706483 ER PT J AU SOLLOTT, SJ CHENG, L PAULY, RR JENKINS, GM MONTICONE, RE KUZUYA, M FROEHLICH, JP CROW, MT LAKATTA, EG ROWINSKY, EK KINSELLA, JL AF SOLLOTT, SJ CHENG, L PAULY, RR JENKINS, GM MONTICONE, RE KUZUYA, M FROEHLICH, JP CROW, MT LAKATTA, EG ROWINSKY, EK KINSELLA, JL TI TAXOL INHIBITS NEOINTIMAL SMOOTH-MUSCLE CELL ACCUMULATION AFTER ANGIOPLASTY IN THE RAT SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE RESTENOSIS; ATHEROSCLEROSIS; MICROTUBULES; TUBULIN; DEUTERIUM OXIDE ID MICROTUBULE-DISRUPTING AGENTS; FIBROBLAST GROWTH-FACTOR; DNA-SYNTHESIS; PHASE-II; BASEMENT-MEMBRANE; LESION FORMATION; PROLIFERATION; TUBULIN; INVITRO; INJURY AB Despite significant improvements in the primary success rate of the medical and surgical treatments for atherosclerotic disease, including angioplasty, bypass grafting, and endarterectomy, secondary failure due to late restenosis continues to occur in 30-50% of individuals. Restenosis and the later stages in atherosclerotic lesions are due to a complex series of fibroproliferative responses to vascular injury involving potent growth-regulatory molecules (such as platelet-derived growth factor and basic fibroblast growth factor) and resulting in vascular smooth muscle cell (VSMC) proliferation, migration, and neointimal accumulation, We show here, based on experiments with both taxol and deuterium oxide, that microtubules are necessary for VSMCs to undergo the multiple transformations contributing to the development of the neointimal fibroproliferative lesion. Taxol was found to interfere both with platelet-derived growth factor-stimulated VSMC migration and with VSMC migration and with VSMC proliferation, at nanomolar levels in vitro. In vivo, taxol prevented medial VSMC proliferation and the neointimal VSMC accumulation in the rat carotid artery after balloon dilatation and endothelial denudation injury, This effect occurred at plasma levels approximately two orders of magnitude lower than that used clinically to treat human malignancy (peak levels achieved in this model were similar to 50-60 nM), Taxol may therefore be of therapeutic value in preventing human restenosis with minimal toxicity. C1 NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. JOHNS HOPKINS MED INST,CTR ONCOL,DIV PHARMACOL & EXPTL THERAPEUT,BALTIMORE,MD 21205. RI Kuzuya, Masafumi/I-1583-2012 NR 64 TC 172 Z9 189 U1 0 U2 12 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1995 VL 95 IS 4 BP 1869 EP 1876 DI 10.1172/JCI117867 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QQ596 UT WOS:A1995QQ59600058 PM 7706494 ER PT J AU LU, W DUHAMEL, GE HOSHINO, Y BENFIELD, DA NELSON, EA HESSE, RA AF LU, W DUHAMEL, GE HOSHINO, Y BENFIELD, DA NELSON, EA HESSE, RA TI CHARACTERIZATION OF THE BOVINE GROUP-A ROTAVIRUS STRAIN NEONATAL CALF DIARRHEA VIRUS-CODY (NCDV-CODY) SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note ID PLAQUE-REDUCTION NEUTRALIZATION; REACTION-GENERATED PROBES; GNOTOBIOTIC CALVES; ESCHERICHIA-COLI; CDNA PROBES; GENE; SEROTYPES AB The neonatal calf diarrhea virus-Cody (NCDV-Cody) strain was found to contain a mixture of rotaviruses with G6 and G8 VP7 genes. Challenge exposure of calves with the mixed virus inoculum indicated that both viruses were maintained by passage in vivo. This is the first P1:G8 rotavirus to be characterized in cattle in the United States. C1 UNIV NEBRASKA,DEPT VET & BIOMED SCI,LINCOLN,NE 68583. NIH,INFECT DIS LAB,BETHESDA,MD 20892. S DAKOTA STATE UNIV,DEPT VET SCI,BROOKINGS,SD 57007. SCHERING PLOUGH ANIM HLTH,ELKHORN RES CTR,OMAHA,NE. OI Benfield, David/0000-0001-6492-3830 NR 34 TC 8 Z9 9 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 1995 VL 33 IS 4 BP 990 EP 994 PG 5 WC Microbiology SC Microbiology GA QM888 UT WOS:A1995QM88800043 PM 7790474 ER PT J AU GREVER, M KOPECKY, K FOUCAR, MK HEAD, D BENNETT, JM HUTCHISON, RE CORBETT, WEN CASSILETH, PA HABERMANN, T GOLOMB, H RAI, K EISENHAUER, E APPELBAUM, F CHESON, BD AF GREVER, M KOPECKY, K FOUCAR, MK HEAD, D BENNETT, JM HUTCHISON, RE CORBETT, WEN CASSILETH, PA HABERMANN, T GOLOMB, H RAI, K EISENHAUER, E APPELBAUM, F CHESON, BD TI RANDOMIZED COMPARISON OF PENTOSTATIN VERSUS INTERFERON ALFA-2A IN PREVIOUSLY UNTREATED PATIENTS WITH HAIRY-CELL LEUKEMIA - AN INTERGROUP STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ALPHA-2 INTERFERON; CLINICAL-TRIALS; DEOXYCOFORMYCIN; 2'-DEOXYCOFORMYCIN; 2-CHLORODEOXYADENOSINE; REMISSIONS; INFECTIONS; INDUCTION; RECOVERY AB Purpose: Therapy of hairy cell leukemia has markedly improved. Interferon alfa-2a and pentostatin are active agents. The National Cancer Institute organized an intergroup trial to compare these agents prospectively in untreated patients. Methods: Patients were randomized to receive either interferon alfa-2a (3 x 10(6) U subcutaneously three times per week) or pentostatin (4 mg/m(2) intravenously every 2 weeks). Patients who did not respond to initial treatment were crossed over. Results: Of 356 patients on study, 313 were eligible. Among interferon patients, 17 of 159 (11%) achieved a confirmed complete remission and 60 of 159 (38%) had a confirmed complete or partial remission. Among pentostatin patients, 117 of 154 (76%) achieved a confirmed complete remission and 121 of 154 (79%) had a confirmed complete or partial remission. Additional patients achieved criteria for complete remission, but lacked con firmatory follow-up evaluation. Response rates were significantly higher (P < .0001) and relapse-free survival was significantly longer with pentostatin than interferon (P < .0001). The median follow-up duration is 57 months (range, 19 to 82). Myelosuppression was more frequent with pentostatin (P = .013). A multivariate logistic regression analysis of the confirmed complete remissions on pentostatin showed the following factors to be im portant for achieving a complete remission: high hemoglobin level (two-tailed P = .024), young age (P = .0085), and no or little splenomegaly (P = .0029). Conclusion: Both agents were well tolerated. Pentostatin higher response rates, and the responses were durable. Patient age and clinical status had an impact on outcome with pentostatin. Pentostatin is effective therapy for hairy cell leukemia. J Clin Oncol 13:974-982. (C) 1995 by American Society of Clinical Oncology. C1 NCI, BETHESDA, MD USA. PUGET SOUND ONCOL CONSORTIUM, SEATTLE, WA USA. UNIV NEW MEXICO, ALBUQUERQUE, NM USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN USA. UNIV ROCHESTER, ROCHESTER, NY 14627 USA. SUNY HLTH SCI CTR, SYRACUSE, NY USA. LONG ISL JEWISH MED CTR, NEW HYDE PK, NY USA. KINGSTON GEN HOSP, KINGSTON, ON K7L 2V7, CANADA. NATL CANC INST CANADA, CLIN TRIALS GRP, KINGSTON, ON, CANADA. UNIV MIAMI HOSP & CLIN, MIAMI, FL USA. MAYO CLIN & MAYO FDN, ROCHESTER, MN USA. UNIV CHICAGO, CHICAGO, IL USA. RP GREVER, M (reprint author), SW ONCOL GRP, OPERAT OFF, CTR STAT, 8691, 14980 OMICRON DR, SAN ANTONIO, TX 78245 USA. FU NCI NIH HHS [CA-20319, CA-04920, CA-38926] NR 39 TC 166 Z9 171 U1 0 U2 2 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1995 VL 13 IS 4 BP 974 EP 982 PG 9 WC Oncology SC Oncology GA QQ608 UT WOS:A1995QQ60800025 PM 7707126 ER PT J AU PISCITELLI, SC THIBAULT, A FIGG, WD TOMPKINS, A HEADLEE, D LIEBERMANN, R SAMID, D MYERS, CE AF PISCITELLI, SC THIBAULT, A FIGG, WD TOMPKINS, A HEADLEE, D LIEBERMANN, R SAMID, D MYERS, CE TI DISPOSITION OF PHENYLBUTYRATE AND ITS METABOLITES, PHENYLACETATE AND PHENYLACETYLGLUTAMINE SO JOURNAL OF CLINICAL PHARMACOLOGY LA English DT Article ID WASTE NITROGEN-EXCRETION; DIFFERENTIATION; UREA; ACID AB Phenylacetate, an inducer of tumor cytostasis and differentiation, shows promise as a relatively nontoxic antineoplastic agent, Phenylacetate, however, has an unpleasant odor that might limit patient acceptability. Phenylbutyrate, an odorless compound that also has activity in tumor models, is known to undergo rapid conversion to phenylacetate by beta-oxidation in vivo. This phase I study examined the pharmacokinetics of phenylbutyrate and characterized the disposition of the two metabolites, phenylacetate and phenylacetylglutamine, Fourteen patients with cancer (aged 51.8 +/- 13.8 years) received a 30-minute infusion of phenylbutyrate at 3 dose levels (600, 1200, and 2000 mg/m(2)), Serial blood samples and 24-hour urine collections were obtained. Samples were assayed by high-performance liquid chromatography. A model to simultaneously describe the pharmacokinetics of all three compounds was developed using ADAPT II. Data were modeled as molar equivalents. The model Ft the data well os shown by mean (+/-SD) coefficients of determination (r(2)) for phenylbutyrate, phenylacetate, and phenylacetylglutamine, which were 0.96 +/- 0.07, 0.88 +/- 0.10, and 0.92 +/- 0.06, respectively. The intrapatient coefficient of variation percentage (CV%) around the parameter estimates were small (range 7.2-33.5%). Phenylbutyrate achieved peak concentrations in the range of in vitro tumor activity (500-2000 mu mol/L) and exhibited saturable elimination (K-m = 34.1 +/- 18.1 mu g/mL and V-max = 18.1 +/- 18 mg/h/kg). Metabolism was rapid; the rimes to maximum concentration for phenylacetate and phenylacetylglutamine were 1 and 2 hours, respectively. The conversion of phenylbutyrate to phenylacetate was extensive (80 +/- 12.6%), but serum concentrations of phenylacetate were low owing to rapid, subsequent conversion to phenylacetylglutamine. The ratio of phenylbutyrate AUC to phenylacetate AUC was 2.66. Thus, phenylbutyrate may not be a prodrug for phenylacetate and should be pursued as an independent antitumor agent. C1 NCI,CLIN PHARMACOL BRANCH,CLIN PHARMACOKINET SECT,BETHESDA,MD 20892. NIH,CTR CLIN,DEPT PHARM,CLIN PHARMACOKINET RES LAB,BETHESDA,MD 20892. US FDA,CTR DRUG EVALUAT & RES,ROCKVILLE,MD 20857. RI Figg Sr, William/M-2411-2016 NR 17 TC 58 Z9 61 U1 0 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0091-2700 J9 J CLIN PHARMACOL JI J. Clin. Pharmacol. PD APR PY 1995 VL 35 IS 4 BP 368 EP 373 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QT480 UT WOS:A1995QT48000006 PM 7650225 ER PT J AU MCCAULEY, E ROSS, JL KUSHNER, H CUTLER, G AF MCCAULEY, E ROSS, JL KUSHNER, H CUTLER, G TI SELF-ESTEEM AND BEHAVIOR IN GIRLS WITH TURNER SYNDROME SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE SELF-ESTEEM; BEHAVIOR; SEX CHROMOSOME ANOMALIES; SHORT STATURE AB Data on social competence, behavior, and self-esteem were gathered from a large sample of girls with Turner syndrome to determine whether psychological difficulties were associated with Turner syndrome. Subjects included 97 girls with Turner syndrome, 7 to 14 years of age, and 93 girls without Turner syndrome recruited from public schools. The two groups of girls were similar in age, verbal intelligence scores, and racial composition. The girls with Turner syndrome were found, based on both parental and self-report, to be more immature than the girls in the comparison group, with weaker social relationships, school performance, and self-esteem. A decline in self-esteem was also documented for the girls with Turner syndrome, but not the comparison group, as they moved into early adolescence. Although the findings support an increased risk for subtle behavioral problems among girls with Turner syndrome, in most cases the problems endorsed were not severe enough to suggest clinical impairment. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT PEDIAT,PHILADELPHIA,PA 19107. HAHNEMANN UNIV,DEPT BIOSTAT,PHILADELPHIA,PA 19102. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP MCCAULEY, E (reprint author), UNIV WASHINGTON,CHILDRENS HOSP & MED CTR,DEPT PSYCHIAT & BEHAV SCI,SEATTLE,WA 98105, USA. FU NINDS NIH HHS [R01 NS 29857] NR 13 TC 48 Z9 51 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 1995 VL 16 IS 2 BP 82 EP 88 PG 7 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA QT662 UT WOS:A1995QT66200003 PM 7790519 ER PT J AU TSIGOS, C GIBSON, S CROSBY, SR WHITE, A YOUNG, RJ AF TSIGOS, C GIBSON, S CROSBY, SR WHITE, A YOUNG, RJ TI CEREBROSPINAL-FLUID LEVELS OF BETA-ENDORPHIN IN PAINFUL AND PAINLESS DIABETIC POLYNEUROPATHY SO JOURNAL OF DIABETES AND ITS COMPLICATIONS LA English DT Article AB beta endorphin (beta-EP) is an important modulator of central pain pathways. To examine whether changes in central production of beta-EP contribute to the pathogenesis of diabetic neuropathic pain, we compared the cerebrospinal fluid (CSF) levels of beta-EP and its precursor proopiomelanocortin (POMC) between 15 diabetic patients with chronic painful diabetic polyneuropathy, eight patients with severe painless diabetic neuropathy, and ten nondiabetic controls. Both peptides were measured by specific monoclonal antibody-based two-site immunoradiometric assays (IRMAs). In the diabetic patients with painful neuropathy, mean +/- SD CSF beta-EP concentrations (5.7 +/- 2.2 pmol/L) were comparable to those of the diabetic patients with painless neuropathy (6.0 +/- 2.3 pmol/L) and did nor correlate with the severity of neuropathic pain. CSF beta-EP, but not POMC, concentrations were lower in the diabetic neuropathic patients overall (5.8 +/- 1.9 pmol/L compared to the control subjects (7.6 +/- 2.2 pmol/L) (P < 0.05). CSF POMC showed no intergroup differences. However, POMC levels were 80-fold higher than those of beta-EP and should always be considered when interpreting immunoreactive beta-EP or other derivative peptide levels in CSF. We conclude that CSF beta-EP levels appear to be reduced in diabetic polyneuropathy but they do not relate to the presence of neuropathic pain. This might explain why opioid analgesics are of little, if any, help in alleviating diabetic neuropathic pain. RP TSIGOS, C (reprint author), NIH,CTR CLIN,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N262,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI White, Anne/C-3753-2011 NR 0 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1056-8727 J9 J DIABETES COMPLICAT JI J. Diabetes Complications PD APR-JUN PY 1995 VL 9 IS 2 BP 92 EP 96 DI 10.1016/1056-8727(94)00024-I PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA RK850 UT WOS:A1995RK85000005 PM 7599354 ER PT J AU MORIOKA, H TACHIBANA, M AF MORIOKA, H TACHIBANA, M TI ULTRASTRUCTURAL-LOCALIZATION OF PENICILLIN-BINDING SITES IN STAPHYLOCOCCUS-AUREUS USING PENICILLIN G-BSA-GOLD SO JOURNAL OF ELECTRON MICROSCOPY LA English DT Article DE PENICILLIN-BINDING SITES; PENICILLIN-BINDING PROTEINS; PENICILLIN G-BSA-GOLD; ELECTRON MICROSCOPY; STAPHYLOCOCCUS AUREUS ID BETA-LACTAM ANTIBIOTICS; CELL-WALL; PROTEINS; PEPTIDOGLYCAN; MECHANISM; MUROSOMES; DIVISION; GROWTH; ENZYME AB Penicillin G (PcG) conjugated to bovine serum albumin (BSA) was found to retain antibacterial activity against Staphylococcus aureus as judged by growth inhibition and by ultrastructural analyses of the PcG-BSA-treated bacterium. Using the PcG-BSA conjugated to colloidal gold, binding sites of PcG were localized in S. aureus with electron microscopy using a postembedding labeling technique, To our surprise, labeling was observed both on the cell wall and in the cytoplasm of S. aureus. A part of the labeling observed may be attributed to penicillin-binding proteins (PBPs) or their precursors. Also there may be other molecules which bind with PcG in the cell wall and cytoplasm of S. aureus. C1 NATL INST DEAFNESS & OTHER COMMUN DISORDERS,GENET MOLEC LAB,BETHESDA,MD 20892. RP MORIOKA, H (reprint author), KYOTO PREFECTURAL UNIV MED,ELECTRON MICROSCOPY LAB,KAMIKYO KU,KYOTO 602,JAPAN. NR 26 TC 0 Z9 0 U1 0 U2 1 PU JAPANESE SOC ELECTRON MICRO BUS CENTER ACAD SOC JAPAN PI TOKYO PA 16-9 HONKOMAGOME, 5-CHOME BUNKYO-KU, TOKYO 113, JAPAN SN 0022-0744 J9 J ELECTRON MICROSC JI J. Electron Microsc. PD APR PY 1995 VL 44 IS 2 BP 66 EP 71 PG 6 WC Microscopy SC Microscopy GA RC028 UT WOS:A1995RC02800002 PM 7544391 ER PT J AU LUSSO, P GARZINODEMO, A CROWLEY, RW MALNATI, MS AF LUSSO, P GARZINODEMO, A CROWLEY, RW MALNATI, MS TI INFECTION OF GAMMA/DELTA T-LYMPHOCYTES BY HUMAN HERPESVIRUS-6 - TRANSCRIPTIONAL INDUCTION OF CD4 AND SUSCEPTIBILITY TO HIV-INFECTION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID NATURAL-KILLER-CELLS; SIMPLEX VIRUS; MARROW TRANSPLANTATION; RECEPTOR; AIDS; PNEUMONITIS; FIBROBLASTS; RETROVIRUS; INHIBITION; HHV-6 AB Human herpesvirus 6 (HHV-6), a T-lymphotropic human herpesvirus, is a potentially immunosuppressive agent that has been suggested to play a role as a cofactor in the natural history of human immunodeficiency virus (HIV) infection. We studied the interactions between HHV-6 and gamma/delta T lymphocytes, a subset of T cells involved in the protective immune response against specific microorganisms. Polyclonal gamma/delta T cell populations, purified from the peripheral blood of healthy adults and activated in vitro with phytohemagglutinin, were exposed to HHV-6, strain GS (subgroup A), at the approximate multiplicity of infection (MOI) of 1. Signs of virus replication were detected as early as 72 h after infection, as documented by immunofluorescence, electron microscopy, and transmission of extracellular virus. Progression of the infection was associated with the appearance of typical cytomorphological changes and, eventually, massive cell death. In contrast, no signs of infection or cytopathic effects were detected after exposure of gamma/delta T lymphocytes to HHV-7, a CD4(+) T-lymphotropic virus closely related to HHV-6. Polyclonal gamma/delta T cells displayed cytolytic activity against both autologous and heterologous target cells infected with HHV-6 and maintained this activity for at least 72 h after infection with HHV-6, despite the high MOI used. As previously documented in mature CD8(+) alpha/beta T cells and natural killer cells, HHV-6 infection induced gamma/delta T lymphocytes to express de novo CD4 messenger RNA and protein, as detected by reverse transcriptase-polymerase chain reaction and fluorocytometry, respectively. Whereas purified CD4(-) gamma/delta T cell populations were per se refractory to HIV infection, they became susceptible to productive infection by HIV-1, strain IIIB, after induction of CD4 expression by HHV-6. These results demonstrate that gamma/delta T cells can be directly targeted and killed by a herpesvirus and may have implications for the potential role of HHV-6 in AIDS. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 35 TC 76 Z9 77 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1995 VL 181 IS 4 BP 1303 EP 1310 DI 10.1084/jem.181.4.1303 PG 8 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QQ192 UT WOS:A1995QQ19200005 PM 7699322 ER PT J AU MUSSO, T JOHNSTON, JA LINNEKIN, D VARESIO, L ROWE, TK OSHEA, JJ MCVICAR, DW AF MUSSO, T JOHNSTON, JA LINNEKIN, D VARESIO, L ROWE, TK OSHEA, JJ MCVICAR, DW TI REGULATION OF JAK3 EXPRESSION IN HUMAN MONOCYTES - PHOSPHORYLATION IN RESPONSE TO INTERLEUKIN-2, INTERLEUKIN-4, AND INTERLEUKIN-7 SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID PERIPHERAL-BLOOD MONOCYTES; RECEPTOR GAMMA-CHAIN; CELL-LINE; FUNCTIONAL COMPONENT; SIGNAL-TRANSDUCTION; MACROPHAGES; IL-2 AB The Janus family of kinases (JAKs) has been shown to be involved in the signal transduction of a number of cytokine receptors. Recently, we have cloned a novel JAK family member, JAK3, that is expressed in natural killer and activated T cells and is coupled functionally and physically to the interleukin 2 (IL-2) receptor in these cells. Here we report that JAK3 was expressed at low but detectable levels in human monocytes. In contrast, JAK3 expression was strongly induced during activation by interferon gamma (IFN-gamma) or lipopolysaccharide. Moreover, JAK3 became tyrosine phosphorylated in response to IL-2, IL-4, and IL-7 but not response to IFN-gamma or granulocyte/macrophage colony-stimulating factor. Together, these findings suggest that JAK3 is functionally important in activated monocytes and cells of the myeloid lineage and is involved in signaling responses of cytokines that use the common gamma-chain of the IL-2 receptor. C1 NCI,FREDERICK CANC RES & DEV CTR,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,LEUKOCYTE BIOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP MUSSO, T (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702, USA. RI McVicar, Daniel/G-1970-2015; varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 35 TC 93 Z9 99 U1 1 U2 4 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1995 VL 181 IS 4 BP 1425 EP 1431 DI 10.1084/jem.181.4.1425 PG 7 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QQ192 UT WOS:A1995QQ19200017 PM 7535338 ER PT J AU LENO, M SIMPSON, RM BOWERS, FS KINDT, TJ AF LENO, M SIMPSON, RM BOWERS, FS KINDT, TJ TI HUMAN T-LYMPHOCYTE VIRUS-1 FROM A LEUKEMOGENIC CELL-LINE MEDIATES IN-VIVO AND IN-VITRO LYMPHOCYTE APOPTOSIS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID TROPICAL SPASTIC PARAPARESIS; HUMAN-IMMUNODEFICIENCY-VIRUS; LEUKEMIA-VIRUS; NUCLEOTIDE-SEQUENCE; ACTIVATION; INVIVO; DEATH; RABBITS; ANTIBODIES; THYMOCYTES AB HTLV-1 is implicated in the development of diverse diseases. However, most HTLV-1-infected individuals remain asymptomatic. How HTLV-1 infection leads to disparate consequences remains a mystery, despite extensive investigation of HTLV-1 isolates from infected individuals. As in human infection, experimental HTLV-1 infection in rabbits is generally benign, although HTLV-1-infected rabbit T cell lines that mediate lethal leukemia-like disease have been reported. We report here that thymuses from mature outbred rabbits inoculated with a lethal HTLV-1 T cell line (RH/K34) showed morphological and biochemical evidence of apoptosis, whereas thymuses from rabbits inoculated with nonlethal HTLV-1 T cell lines showed no signs of apoptosis. Exposure of rabbit or human lymphocytes to purified virus from RH/K34 caused rapid induction of apoptosis, providing an in vitro correlate to the pathogenic effects. By contrast, virus isolated from a nonlethal cell line mediated dose-dependent lymphocyte proliferation. These data implicate lymphocyte apoptosis as a potential mechanism by which the lethal HTLV-1 cell line causes fulminant disease and provide a means to identify factors contributing to HTLV-1 disease. Results from this HTLV-1 infection model can provide insight into variations in HTLV-1 pathogenicity in human infection. C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 33 TC 26 Z9 26 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1995 VL 181 IS 4 BP 1575 EP 1580 DI 10.1084/jem.181.4.1575 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QQ192 UT WOS:A1995QQ19200032 PM 7699338 ER PT J AU LITTLE, JT SATLIN, A SUNDERLAND, T VOLICER, L AF LITTLE, JT SATLIN, A SUNDERLAND, T VOLICER, L TI SUNDOWN SYNDROME IN SEVERELY DEMENTED PATIENTS WITH PROBABLE ALZHEIMERS-DISEASE SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID NURSING-HOME RESIDENTS; SLEEPING AIDS; BENZODIAZEPINES; EFFICACY; DECLINE AB A retrospective review of 71 patients with probable Alzheimer's disease was analyzed with respect to nursing evaluations of sundowning status (recurring confusion or agitation in the late afternoon or early evening). The prevalence of sundowning (including probable sundowners) was 24%. Sundowners and non-sundowners differed with regard to number of sedatives received daily, particularly chloral hydrate, and the number of days on the inpatient unit. There were no differences between sundowners and non-sundowners with respect to other types of medications, medical diagnoses, current age, age of onset of Alzheimer's disease, or Mini-Mental State Exam. Restlessness was the most common sundowning behavior, although multiple behavioral disturbances were seen. This survey suggests that the sundown syndrome is a common problem in severely demented Alzheimer's patients and requires further study. C1 E N ROGERS MEM VET HOSP,BEDFORD,MA. BOSTON UNIV,SCH MED,BOSTON,MA 02118. NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MCLEAN HOSP,MAILMAN RES CTR,BELMONT,MA 02178. NIMH,CLIN SCI LAB,GERIATR PSYCHIAT SECT,BETHESDA,MD 20892. NR 27 TC 30 Z9 31 U1 1 U2 5 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON ST, PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD APR PY 1995 VL 8 IS 2 BP 103 EP 106 PG 4 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA QR239 UT WOS:A1995QR23900005 PM 7794472 ER PT J AU ADAMCZEWSKI, M NUMEROF, RP KORETZKY, GA KINET, JP AF ADAMCZEWSKI, M NUMEROF, RP KORETZKY, GA KINET, JP TI REGULATION BY CD45 OF THE TYROSINE PHOSPHORYLATION OF HIGH-AFFINITY IGE RECEPTOR BETA-CHAINS AND GAMMA-CHAINS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL ANTIGEN RECEPTOR; LEUKOCYTE-COMMON ANTIGEN; T-CELL; SIGNAL-TRANSDUCTION; PHOSPHATASE CD45; FC-RECEPTORS; MONOCLONAL-ANTIBODIES; ETA-CHAIN; ACTIVATION; SUBUNIT AB Previous studies using tyrosine phosphatase inhibitors have implicated tyrosine phosphatases in the signal transduction pathway initiated by aggregation of Fc epsilon RI, the high affinity receptor for IgE. To define more precisely a role for the tyrosine phosphatase CD45 in Fc epsilon RI-mediated signaling, we have transfected the three subunits of Fc epsilon RI into wild-type jurkat and a CD45-deficient jurkat derivative. Here we demonstrate that CD45 is necessary for the initiation of calcium flux through the transfected Fc epsilon RI. In contrast to the effect of phosphatase inhibitors, the tyrosine phosphorylation levels of beta and gamma after aggregation of Fc epsilon RI are surprisingly reduced, relative to wild-type jurkat, in the CD45-deficient cells. After reconstitution of the CD45-deficient cells with a chimeric molecule containing the cytoplasmic phosphatase domains of CD45, both the base line and activation-induced tyrosine phosphorylation levels are increased. By examining Lck autophosphorylation, we find that Fc epsilon RI aggregation induces an increase in Lck enzymatic activity only in wild-type Jurkat and the CD45-deficient Jurkat reconstituted with chimeric CD45. This regulation of src-family tyrosine kinase activity may be the means by which CD45 controls aggregation-induced receptor phosphorylation. C1 NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. UNIV IOWA,COLL MED,DEPT INTERNAL MED,IOWA CITY,IA 52242. UNIV IOWA,DEPT PHYSIOL & BIOPHYS,IOWA CITY,IA 52242. FU NCI NIH HHS [CA56050, CA56843] NR 51 TC 27 Z9 27 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 1995 VL 154 IS 7 BP 3047 EP 3055 PG 9 WC Immunology SC Immunology GA QN459 UT WOS:A1995QN45900001 PM 7897197 ER PT J AU FISCHER, RT LONGO, DL KENNY, JJ AF FISCHER, RT LONGO, DL KENNY, JJ TI A NOVEL PHOSPHOCHOLINE ANTIGEN PROTECTS BOTH NORMAL AND X-LINKED IMMUNE-DEFICIENT MICE AGAINST STREPTOCOCCUS-PNEUMONIAE - COMPARISON OF THE 6-O-PHOSPHOCHOLINE HYDROXYHEXANOATE-CONJUGATE WITH OTHER PHOSPHOCHOLINE-CONTAINING VACCINES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ANTIBODY-RESPONSE; PNEUMOCOCCAL VACCINE; FATAL INFECTION; PHOSPHORYLCHOLINE ANTIBODIES; MONOCLONAL-ANTIBODIES; IMMUNOLOGICAL MEMORY; POLYSACCHARIDE; IMMUNOGENICITY; CHILDREN; IDIOTYPE AB A novel form of phosphocholine (PC), p-nitrophenyl-6-(O-phosphocholine)hydroxy (EPC) coupled to keyhole limpet hemocyanin (KLH) has been compared with unencapsulated, avirulent Streptococcus pneumoniae (R36a) and with the traditional thymus-dependent form of PC, diazophenylphosphocholine (DPPC)-conjugated KLH for its vaccine potential against virulent S. pneumoniae. Immunization with any of these three PC-containing Ags protects normal mice against a lethal challenge with 10(4) S. pneumoniae, whereas only EPC-KLH provides total protection to Xid mice. DPPC-KLH and unencapsulated S. pneumoniae confer less than 40% protection in Xid mice. Passive transfer of a PC-specific hybridoma Ab made from EPC-KLH-immunized Xid mice also provided protection against lethal challenge with S. pneumoniae, Protective anti-PC Ab were capable of binding to the surface of virulent bacteria, whereas anti-PC Ab incapable of binding to the bacterial surface failed to protect. Furthermore, serum Ab from EPC-KLH immunized and protected mice bound to S. pneumoniae, whereas secondary Abs from DPPC-KLH- or R36a-immunized mice failed to bind to the bacteria. EPC-KLH is potentially a vaccine candidate for pneumococcal prophylaxis in settings of immune compromise. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,LEUKOCYTE BIOL LAB,FREDERICK,MD 21702. NR 51 TC 19 Z9 19 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 1995 VL 154 IS 7 BP 3373 EP 3382 PG 10 WC Immunology SC Immunology GA QN459 UT WOS:A1995QN45900034 PM 7897220 ER PT J AU KAMBAYASHI, T ALEXANDER, HR FONG, M STRASSMANN, G AF KAMBAYASHI, T ALEXANDER, HR FONG, M STRASSMANN, G TI POTENTIAL INVOLVEMENT OF IL-10 IN SUPPRESSING TUMOR-ASSOCIATED MACROPHAGES - COLON-26-DERIVED PROSTAGLANDIN E(2) INHIBITS TNF-ALPHA RELEASE VIA A MECHANISM INVOLVING IL-10 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EXPERIMENTAL CANCER CACHEXIA; GENE-EXPRESSION; INTERLEUKIN-10; CARCINOMA; MICE; ENDOTOXEMIA; MONOCYTES; LETHALITY; MEDIATOR AB The administration of murine TNF-alpha to colon (C)-26 bearing mice, significantly protects the host against the catabolic effects of the tumor. This effect of exogenous TNF-alpha can be primarily attributed to tumor lysis rather than to a direct anticachectic action. Murine peritoneal macrophages cultured with the C-26 line or with C-26 culture supernatant do not release TNF-alpha in response to LPS stimulation. The reduction in TNF-alpha levels is associated with a significant increase in IL-10 levels. Single cell suspension of freshly disaggregated C-26 tumor (which contains host macrophages), do not produce TNF-alpha but contain significant levels of PGE(2) and IL-10. In contrast, PGE(2) but not TNF-alpha or IL-70 can be detected in the C-26.IVX cell line that is used to generate tumors in vivo. Neutralizing anti IL-10 Ab but not isotype-matched Ab, significantly reverses the inhibitory effect of the tumor cells and their culture supernatant on macrophage TNF-alpha release. Additional evidence is presented to indicate that the C-26-derived inhibitory activity is related to PGE(2). Taken together, these results support the hypothesis that tumor-derived PGE(2) prevents tumor-infiltrating macrophages from producing TNF-alpha, in part by augmenting macrophage IL-10 synthesis. C1 OTSUKA AMER PHARMACEUT INC,ROCKVILLE,MD 20850. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 35 TC 103 Z9 108 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1995 VL 154 IS 7 BP 3383 EP 3390 PG 8 WC Immunology SC Immunology GA QN459 UT WOS:A1995QN45900035 PM 7897221 ER PT J AU BLAUVELT, A CLERICI, M LUCEY, DR STEINBERG, SM YARCHOAN, R WALKER, R SHEARER, GM KATZ, SI AF BLAUVELT, A CLERICI, M LUCEY, DR STEINBERG, SM YARCHOAN, R WALKER, R SHEARER, GM KATZ, SI TI FUNCTIONAL-STUDIES OF EPIDERMAL LANGERHANS CELLS AND BLOOD MONOCYTES IN HIV-INFECTED PERSONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; IMMUNE-DEFICIENCY SYNDROME; POLYMERASE CHAIN-REACTION; TRANSGENIC MICE; VIRUS INFECTION; DENDRITIC CELLS; KAPOSIS-SARCOMA; SELECTIVE LOSS; SYNDROME AIDS; TAT GENE AB APC dysfunction may be important in immune dysregulation associated with HIV disease. Langerhans cells, epidermal APC, can be infected with HIV, although their function in HIV-infected persons has not been studied. Therefore, we studied the immunologic function of Langerhans cells, in parallel with blood APC (enriched for monocytes/macrophages (M phi)) function, in 21 HIV-seropositive (HIV+) and 21 HIV-seronegative volunteers, including three monozygotic twin pairs discordant for HIV serology. Langerhans cells from HIV+ patients were quantitatively normal and expressed normal levels of HLA-DR. However, Langerhans cells from AIDS patients and M phi from both AIDS and HIV+ non-AIDS patients stimulated allogeneic T cells less well compared with control APC. In addition, decreased recall Ag- and mitogen-induced T cell responsiveness was observed in HIV+ patients using either autologous Langerhans cells or autologous M phi as APC/accessory cells. Interestingly, Langerhans cells and M phi isolated from HIV+ twins (CD4(+) cell counts of 181, 271, and 562/mm(3)) were able to present recall Ag normally to HIV-uninfected syngeneic T cells. In summary, APC from HIV+ patients were impaired in their ability to generate a primary immune response (i.e., alloantigen-induced T cell stimulation), but they retained the ability to generate a secondary immune response (i.e., recall Ag-induced syngeneic T cell stimulation). Thus, these findings suggest that defects in secondary immune responses commonly observed in HIV disease are dependent on T cell dysfunction alone, whereas defective primary immune responses may be secondary to both T cell and APC dysfunction. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP BLAUVELT, A (reprint author), NCI,DERMATOL BRANCH,BLDG 10,ROOM 12N238,10 CTR DR MSC 1908,BETHESDA,MD 20892, USA. NR 56 TC 78 Z9 78 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 1995 VL 154 IS 7 BP 3506 EP 3515 PG 10 WC Immunology SC Immunology GA QN459 UT WOS:A1995QN45900049 PM 7897231 ER PT J AU SAMANIEGO, F MARKHAM, PD GALLO, RC ENSOLI, B AF SAMANIEGO, F MARKHAM, PD GALLO, RC ENSOLI, B TI INFLAMMATORY CYTOKINES INDUCE AIDS-KAPOSIS SARCOMA-DERIVED SPINDLE CELLS TO PRODUCE AND RELEASE BASIC FIBROBLAST GROWTH-FACTOR AND ENHANCE KAPOSIS SARCOMA-LIKE LESION FORMATION IN NUDE-MICE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; SUBENDOTHELIAL EXTRACELLULAR-MATRIX; ACQUIRED IMMUNODEFICIENCY SYNDROME; HEPARIN-LIKE MOLECULES; TYPE-1 TAT PROTEIN; ALPHA TNF-ALPHA; GENE-EXPRESSION; ENDOTHELIAL-CELLS; SIGNAL SEQUENCE; INTERLEUKIN-1 AB Homosexual males often present signs of immune activation and are likely to have increased levels of inflammatory cytokines such as IL-1 beta, TNF-alpha, and IFN-gamma. These individuals develop Kaposi's sarcoma (AIDS-KS) more frequently than other HIV-1-infected groups. Our previous work demonstrated that inflammatory cytokines stimulate the growth of spindle cells derived from AIDS-KS lesions (AIDS-KS cells) and that these cells produce high levels of bFGF that mediate autocrine and paracrine (endothelial) cell growth and angiogenesis. Here we show that AIDS-KS cells constitutively produce and release bioactive bFGF in the absence of cell death, and that extracellular bFGF exist in both a soluble and a bound form; the latter can be released by treatment with trypsin, heparin, or heparinase I. Inflammatory cytokines stimulate both the synthesis and release of biologically active bFGF from KS cells and enhance their ability to induce angiogenic KS-like lesions in nude mice. Because bFGF is highly expressed in primary KS lesions, and is a mediator of KS-like lesion formation, these results suggest that the export of bFGF induced by inflammatory cytokines may play a critical role in the induction and progression of KS in HIV-1-infected homosexual men. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD 20895. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 44 TC 102 Z9 105 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 1995 VL 154 IS 7 BP 3582 EP 3592 PG 11 WC Immunology SC Immunology GA QN459 UT WOS:A1995QN45900056 PM 7897237 ER PT J AU THOMAS, DL ZENILMAN, JM ALTER, HJ SHIH, JW GALAI, N CARELLA, AV QUINN, TC AF THOMAS, DL ZENILMAN, JM ALTER, HJ SHIH, JW GALAI, N CARELLA, AV QUINN, TC TI SEXUAL TRANSMISSION OF HEPATITIS-C VIRUS AMONG PATIENTS ATTENDING SEXUALLY-TRANSMITTED DISEASES CLINICS IN BALTIMORE - AN ANALYSIS OF 309 SEX PARTNERSHIPS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; NON-B-HEPATITIS; INTRAVENOUS-DRUG-USERS; RECOMBINANT IMMUNOBLOT ASSAY; POLYMERASE CHAIN-REACTION; HOMOSEXUAL MEN; NON-A; RISK-FACTORS; UNITED-STATES; INFECTION AB The prevalence of antibodies to hepatitis C virus (anti-HCV), the behavioral and laboratory-derived risk factors for anti-HCV, and the quantity and homology of HCV RNA were assessed among 1039 non-injection drug-using sexually transmitted disease (STD) patients representing 309 sex partnerships. Thirty-seven (7%) of 555 males and 19 (4%) of 484 females had anti-HCV. In logistic regression analyses, factors associated with anti-HCV included age (P < .001), greater numbers of lifetime sex partners (P = .023), human immunodeficiency virus infection (P < .001), Trichomonas infection (P < .001), cigarette smoking (P < .001), and male homosexual exposure (P = .012). Among couples, females whose sex partners were anti-HCV positive were 3.7 times more likely to have anti-HCV than females whose sex partners were anti-HCV negative (P = .039). The proportion of RNA homology between anti-HCV positive females and their male partners (94%) was higher than among randomly selected patients (82%). Sexual transmission of HCV may contribute to the high prevalence of anti-HCV reported in urban settings. C1 JOHNS HOPKINS UNIV, SCH PUBL HLTH, DEPT EPIDEMIOL, BALTIMORE, MD 21205 USA. BALTIMORE CITY DEPT HLTH, BALTIMORE, MD USA. NIAID, DEPT TRANSFUS MED, BETHESDA, MD 20892 USA. NIAID, IMMUNOREGULAT LAB, BETHESDA, MD 20892 USA. RP THOMAS, DL (reprint author), JOHNS HOPKINS UNIV, SCH MED, DIV INFECT DIS, 1155 ROSS BLDG, 720 RUTLAND AVE, BALTIMORE, MD 21205 USA. RI Quinn, Thomas/A-2494-2010 FU NIAID NIH HHS [AI-16959, AI-29508] NR 52 TC 200 Z9 205 U1 1 U2 5 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0022-1899 EI 1537-6613 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1995 VL 171 IS 4 BP 768 EP 775 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QP912 UT WOS:A1995QP91200002 PM 7535827 ER PT J AU APOLONIO, EG HOOVER, DR HE, YH SAAH, AJ LYTER, DW DETELS, R KASLOW, RA PHAIR, JP AF APOLONIO, EG HOOVER, DR HE, YH SAAH, AJ LYTER, DW DETELS, R KASLOW, RA PHAIR, JP TI PROGNOSTIC FACTORS IN HUMAN IMMUNODEFICIENCY VIRUS-POSITIVE PATIENTS WITH A CD4(+) LYMPHOCYTE COUNT LESS-THAN-50/MU-L SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID PNEUMOCYSTIS-CARINII PNEUMONIA; MULTICENTER AIDS COHORT; HIV-INFECTION; AFRICAN-AMERICANS; ZIDOVUDINE; THERAPY; RISK AB This analysis investigated variability of survival time in a cohort of 553 human immunodeficiency virus type 1 (HIV-1)-infected homosexual or bisexual men with <50 CD4(+) cells/mu L. Median survival after the first CD4(+) cell count <50/mu L was 1.34 years; 25% survived greater than or equal to 2 years. Multivariate analysis showed longer survival with concurrent acyclovir and zidovudine use, hemoglobin greater than or equal to 12 g/dL, and full-time employment (P < .0001). Other significant covariates associated with longer survival included African-American race, no prior AIDS illness, weight loss <4.5 kg, and zidovudine use (with or without concurrent acyclovir) after CD4(+) cells fell to <50/mu L. An easily derived score identified Multicenter AIDS Cohort Study subjects likely to survive >2 years after CD4(+) cell count was <50/mu L. Survival once CD4(+) cell count fell below 50/mu L may be longer for persons with a good performance status and specific clinical markers. Health care providers should consider these variables in decision-making strategies and design of clinical trials. C1 JOHNS HOPKINS UNIV,SCH PUBL HLTH,BALTIMORE,MD. NIAID,BETHESDA,MD 20892. UNIV PITTSBURGH,DIV MED ONCOL,PITTSBURGH,PA. UNIV PITTSBURGH,DEPT MED,DIV HEMATOL,PITTSBURGH,PA. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,LOS ANGELES,CA 90024. RP APOLONIO, EG (reprint author), NORTHWESTERN UNIV,SCH MED,PASSAVANT PAVIL,8TH FLOOR E,303 E SUPER ST,CHICAGO,IL 60611, USA. FU NIAID NIH HHS [AI-35041, AI-35040, AI-35039] NR 25 TC 43 Z9 44 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1995 VL 171 IS 4 BP 829 EP 836 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QP912 UT WOS:A1995QP91200010 PM 7706809 ER PT J AU VITEK, CR GRACIA, FI GIUSTI, R FUKUDA, K GREEN, DB CASTILLO, LC ARMIEN, B KHABBAZ, RF LEVINE, PH KAPLAN, JE BLATTNER, WA AF VITEK, CR GRACIA, FI GIUSTI, R FUKUDA, K GREEN, DB CASTILLO, LC ARMIEN, B KHABBAZ, RF LEVINE, PH KAPLAN, JE BLATTNER, WA TI EVIDENCE FOR SEXUAL AND MOTHER-TO-CHILD TRANSMISSION OF HUMAN T-LYMPHOTROPIC VIRUS TYPE-II AMONG GUAYMI INDIANS, PANAMA SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID LEUKEMIA LYMPHOMA VIRUS; HTLV-II; INFECTION AB Guaymi Indians, a non-intravenous drug-using population in which human T cell lymphotropic virus type II (HTLV-II) is endemic, were studied in Changuinola, Panama, to identify the prevalence and modes of transmission of HTLV-II, A population-based survey showed that 352 (9.5%) of the 3686 participants were seropositive for HTLV-II, Infection rates were the same for male and female subjects and increased significantly with age, beginning in young adulthood. HTLV-II infection status was highly concordant among spouses (P < .001) and between mother and child; of children aged 1-10 years, 36 of 219 born to seropositive mothers were seropositive compared with 3 of 997 born to seronegative mothers (P < .001), The strong associations of HTLV-II infection with age and with an infected spouse in adults and of infection in children with infection in their mothers strongly suggest sexual and mother-to-child transmission of HTLV-II in this population. C1 CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIAL DIS,RETROVIRUS DIS BRANCH,ATLANTA,GA 30341. CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIAL DIS,ATLANTA,GA 30341. GORGAS MEM LAB,PANAMA CITY,PANAMA. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 15 TC 29 Z9 31 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1995 VL 171 IS 4 BP 1022 EP 1026 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QP912 UT WOS:A1995QP91200040 PM 7706781 ER PT J AU FREIFELD, AG HILLIARD, J SOUTHERS, J MURRAY, M SAVARESE, B SCHMITT, JM STRAUS, SE AF FREIFELD, AG HILLIARD, J SOUTHERS, J MURRAY, M SAVARESE, B SCHMITT, JM STRAUS, SE TI A CONTROLLED SEROPREVALENCE SURVEY OF PRIMATE HANDLERS FOR EVIDENCE OF ASYMPTOMATIC HERPES B-VIRUS-INFECTION SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID ANTIBODIES AB Herpes B virus (BV) is a common cause of recurring mucocutaneous infections in monkeys of the genus Macaca, Like its human counterpart, herpes simplex virus (HSV), BV establishes lifelong latency and can be reactivated from infected monkeys symptomatically or asymptomatically, Incidental infection of humans handling BV-shedding monkeys can result in fatal meningoencephalitis, To determine whether humans exposed to infected monkeys can acquire asymptomatic BV infections, 480 subjects were evaluated in a controlled seroprevalence study, Sera from 321 primate handlers, including many with repeated injuries inflicted by Macaca monkeys, and 159 people never exposed to monkeys were tested in blinded fashion by both competition ELISA and Western blot to determine the prevalence of BV and HSV seropositivity, Although 293 persons proved positive for HSV antibodies, no primate handlers or control subjects showed BV-specific antibody responses, There is no serologic evidence that BV causes asymptomatic infections in humans. C1 NIAID,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,CLIN INVEST LAB,BETHESDA,MD 20892. NIH,DIV SAFETY,OCCUPAT MED SERV,BETHESDA,MD 20892. SW FDN BIOMED RES,SAN ANTONIO,TX 78284. NR 16 TC 38 Z9 40 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1995 VL 171 IS 4 BP 1031 EP 1034 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QP912 UT WOS:A1995QP91200042 PM 7706783 ER PT J AU SHATA, MT FALTYNEK, CR LEWIS, GK KAMINLEWIS, RM AF SHATA, MT FALTYNEK, CR LEWIS, GK KAMINLEWIS, RM TI ABSENCE OF HIGH-AFFINITY BINDING-SITES FOR INTERFERON-ALPHA/BETA IN VARIANT MURINE CD4(+) T-LYMPHOCYTES NOT EXPRESSING THE T-CELL ANTIGEN RECEPTOR SO JOURNAL OF INTERFERON AND CYTOKINE RESEARCH LA English DT Article ID MONOCLONAL-ANTIBODY; IFN-GAMMA; CLONES; RECOMBINANT; MOLECULE AB The T cell antigen receptor complex (CD3/Ti) plays a sole in specific antigen recognition as well as in signal transduction, with its surface expression required for the function of several other structurally distinct receptor systems, including CD2, Ly-6(TAP), and Thy-1. In this communication, evidence is presented suggesting an association between the surface expression of CD3/Ti and that of the type 1 interferon (IFN) receptor in a CD4(+) murine T cell clone, We tested the proliferative responses and their capacity to be inhibited by type 1 IFN with the wild-type, CD3/Ti-positive T cell clone and its CD3/Ti-negative variants, The CD3/Ti-negative variants did not respond to specific antigen or anti-CD3 antibody stimulation but they did respond to T cell growth factor (TCGF), stimulation as did the wild-type parental cells, Therefore, the type 1 IFN inhibition of TCGF-stimulated proliferative responses of wild-type and variant cells were compared, Both natural and recombinant type 1 IFNs inhibited TCGF-induced tritiated thymidine (H-3-TdR) incorporation in the wild-type T cell clone, with a ID50 of 60-80 U/ml. By contrast, the variants required much higher doses of type 1 IFN. The ID50 with natural murine IFN-beta was 10,000 U/ml, but this same dose of human IFN-alpha A/D gave only a marginal inhibitory effect, Accompanying the loss of IFN responsiveness, these variants also exhibited a loss of high-affinity type 1 IFN receptors, Taken together, these data suggest that the CD3/Ti complex plays a role in the surface expression of the type 1 IFN receptor in a CD4(+) T cell clone, Given the role of the CD3/Ti in several other receptor systems, the present observations further implicate the central position of the CD3/Ti complex in orchestrating ligand-receptor events on the T cell surface. C1 UNIV MARYLAND,SCH MED,DEPT MICROBIOL & IMMUNOL,BALTIMORE,MD 21201. NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21701. FU NINDS NIH HHS [NS-26665]; PHS HHS [AL-25862] NR 21 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1079-9907 J9 J INTERF CYTOK RES JI J. Interferon Cytokine Res. PD APR PY 1995 VL 15 IS 4 BP 291 EP 296 DI 10.1089/jir.1995.15.291 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA QU330 UT WOS:A1995QU33000003 PM 7627803 ER PT J AU KIM, IG PARK, IS STEINERT, PM AF KIM, IG PARK, IS STEINERT, PM TI EXPRESSION OF FILAGGRIN IN HUMAN EPIDERMAL-KERATINOCYTES - EFFECTS ON KERATIN INTERMEDIATE FILAMENT STRUCTURE AND CELL MORPHOLOGY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 SEOUL NATL UNIV,SCH MED,DEPT BIOCHEM,SEOUL,SOUTH KOREA. NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 555 EP 555 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200025 ER PT J AU BLAUVELT, A CHOUGNET, C SHEARER, GM KATZ, SI AF BLAUVELT, A CHOUGNET, C SHEARER, GM KATZ, SI TI ANTI-IL-10 ANTIBODIES AND RIL-12 ENHANCE RECALL ANTIGEN-INDUCED IL-2 PRODUCTION IN HIV DISEASE 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 SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 556 EP 556 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200030 ER PT J AU KOCH, PJ AMAGAI, M NISHIKAWA, T STANLEY, JR AF KOCH, PJ AMAGAI, M NISHIKAWA, T STANLEY, JR TI PEMPHIGUS-VULGARIS (PV) ANTIGEN (DSG3) IS LOCALIZED IN THE LOWER EPIDERMIS WHERE BV BLISTERS OCCUR SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 KEIO UNIV,SCH MED,TOKYO,JAPAN. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 557 EP 557 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200040 ER PT J AU MOTOKI, K ISHIKAWA, H SILOS, SA TAMAI, K COPELAND, NG GILBERT, DJ JENKINS, NA UITTO, J AF MOTOKI, K ISHIKAWA, H SILOS, SA TAMAI, K COPELAND, NG GILBERT, DJ JENKINS, NA UITTO, J TI CDNA CLONING AND CHROMOSOMAL ASSIGNMENT OF THE MOUSE GENE FOR DESMOGLEIN-3 (DSG3), THE PEMPHIGUS-VULGARIS ANTIGEN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT DERMATOL,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT BIOCHEM & MOLEC BIOL,PHILADELPHIA,PA 19107. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 557 EP 557 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200037 ER PT J AU CANDI, E MELINO, G MEI, G TARCSA, E MAREKOV, LN STEINERT, PM AF CANDI, E MELINO, G MEI, G TARCSA, E MAREKOV, LN STEINERT, PM TI THE PROPERTIES OF BACTERIALLY-EXPRESSED HUMAN LORICRIN - BIOCHEMICAL-CHARACTERIZATION OF THE MAJOR EPIDERMAL CORNIFIED CELL-ENVELOPE PROTEIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV ROMA TOR VERGATA,DEPT EXPTL MED,ROME,ITALY. NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. IST DERMOPAT IMMACOLATA,ROME,ITALY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 561 EP 561 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200063 ER PT J AU KIM, SY CHUNG, SI STEINERT, PM AF KIM, SY CHUNG, SI STEINERT, PM TI THE SOLUBLE TRANSGLUTAMINASE ACTIVITY OF KERATINOCYTES IS DUE TO HIGHLY-PROCESSED FORMS OF THE TRANSGLUTAMINASE-1 SYSTEMS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NIDR,LDCO,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 561 EP 561 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200064 ER PT J AU MAREKOV, LN STEINERT, PM AF MAREKOV, LN STEINERT, PM TI ELAFIN, FILAGGRIN, KERATIN INTERMEDIATE FILAMENTS, SPRS AND LORICRIN ARE ISODIPEPTIDE CROSS-LINKED COMPONENTS OF THE HUMAN EPIDERMAL CORNIFIED CELL-ENVELOPE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 562 EP 562 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200071 ER PT J AU MAURER, D EBNER, C REININGER, B FIEBIGER, E KRAFT, D KINET, JP STINGL, G AF MAURER, D EBNER, C REININGER, B FIEBIGER, E KRAFT, D KINET, JP STINGL, G TI FC-EPSILON-RI MEDIATES IGE-DEPENDENT ALLERGEN PRESENTATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV VIENNA,SCH MED,DEPT DERMATOL,DIAID,VIENNA,AUSTRIA. NIAID,MOLEC ALLERGY & IMMUNOL SECT,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 565 EP 565 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200088 ER PT J AU SCHWARZENBERGER, K UDEY, MC AF SCHWARZENBERGER, K UDEY, MC TI IN-VIVO MODULATION OF E-CADHERIN ON LANGERHANS CELLS BY CONTACT ALLERGENS AND PROINFLAMMATORY CYTOKINES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 567 EP 567 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200096 ER PT J AU BORKOWSKI, TA LETTERIO, J MACKALL, C FARR, A GEISER, D GRESS, R UDEY, MC AF BORKOWSKI, TA LETTERIO, J MACKALL, C FARR, A GEISER, D GRESS, R UDEY, MC TI THE SKIN OF TGF-BETA-1 NULL MICE IS DEVOID OF EPIDERMAL LANGERHANS CELLS (LC) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV WASHINGTON,SEATTLE,WA 98195. NR 0 TC 3 Z9 3 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 568 EP 568 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200107 ER PT J AU RUSSELL, LJ ROGERS, GR DIGIOVANNA, JJ HASHEM, N BALE, SJ COMPTON, JG AF RUSSELL, LJ ROGERS, GR DIGIOVANNA, JJ HASHEM, N BALE, SJ COMPTON, JG TI POINT MUTATIONS IN THE TRANSGLUTAMINASE-1 GENE ARE ASSOCIATED WITH SEVERE LAMELLAR ICHTHYOSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NIAMS,DERMATOL CLIN RES UNIT,BETHESDA,MD. AIN SHAMS UNIV,MED GENET CLIN,CAIRO,EGYPT. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 568 EP 568 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200103 ER PT J AU WIENECKE, R KONIG, A LOWY, DR DECLUE, JE AF WIENECKE, R KONIG, A LOWY, DR DECLUE, JE TI TUBERIN, THE PRODUCT OF THE TUBEROSCLEROSIS-2 GENE (TSC-2), IS A 180-KD PROTEIN THAT REGULATES THE RAS-RELATED PROTEIN RAPIA 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 SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 568 EP 568 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200105 ER PT J AU HERTL, M SUNDARAM, H STANLEY, J AMAGAI, M KATZ, SI AF HERTL, M SUNDARAM, H STANLEY, J AMAGAI, M KATZ, SI TI CHARACTERIZATION OF T-CELL EPITOPES OF THE PEMPHIGUS-VULGARIS ANTIGEN (PVA) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. KEIO UNIV,TOKYO,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 569 EP 569 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200110 ER PT J AU CAVANI, A KATZ, SI AF CAVANI, A KATZ, SI TI THE POSITION AND ORIENTATION OF HAPTENS ON MHC-ANCHORED PEPTIDES IS CRITICAL IN THE IN-VIVO ACTIVATION OF CD4+ T-CELLS AND IN THE INDUCTION OF CONTACT SENSITIVITY (CS) 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 SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 571 EP 571 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200123 ER PT J AU DLUGOSZ, AA CHENG, CC WILLIAMS, EK DARWICHE, N DEMPSEY, PJ MANN, B DUNN, AR COFFEY, RJ YUSPA, SH AF DLUGOSZ, AA CHENG, CC WILLIAMS, EK DARWICHE, N DEMPSEY, PJ MANN, B DUNN, AR COFFEY, RJ YUSPA, SH TI TGFA IS NOT REQUIRED FOR EPIDERMAL NEOPLASIA INDUCED BY THE V-RAS(HA) ONCOGENE - POTENTIAL ROLE OF ALTERNATE EGF RECEPTOR LIGANDS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. VANDERBILT UNIV,NASHVILLE,TN. LUDWIG INST CANC RES,MELBOURNE,VIC 3050,AUSTRALIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 575 EP 575 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200147 ER PT J AU LEE, SC MAREKOV, LN STEINERT, PM TARCSA, E AF LEE, SC MAREKOV, LN STEINERT, PM TARCSA, E TI HUMAN TRICHOHYALIN IS A COMPLETE TRANSGLUTAMINASE SUBSTRATE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 CHONNAM NATL UNIV,SCH MED,DEPT DERMATOL,KWANGJU 501190,SOUTH KOREA. NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 576 EP 576 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200153 ER PT J AU KOVACS, SO DUNSMORE, S RUBIN, JS PARKS, WC WELGUS, HG AF KOVACS, SO DUNSMORE, S RUBIN, JS PARKS, WC WELGUS, HG TI HGF/SF, A DERMALLY-DERIVED GROWTH-FACTOR, STIMULATES KERATINOCYTE METALLOPROTEINASE PRODUCTION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 WASHINGTON UNIV,JEWISH HOSP ST LOUIS,SCH MED,DIV DERMATOL,ST LOUIS,MO. NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 581 EP 581 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200185 ER PT J AU LAZAROVA, Z YEE, C DARLING, T BRIGGAMAN, RA YANCEY, KB AF LAZAROVA, Z YEE, C DARLING, T BRIGGAMAN, RA YANCEY, KB TI PASSIVE TRANSFER OF ANTI-LAMININ-5 ANTIBODIES TO NEONATAL MICE INDUCES SUBEPIDERMAL BLISTERS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,DERMATOL BRANCH,BETHESDA,MD. UNIV N CAROLINA,DEPT DERMATOL,CHAPEL HILL,NC 27514. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 582 EP 582 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200188 ER PT J AU ROH, JY STANLEY, JR AF ROH, JY STANLEY, JR TI PLAKOGLOBIN (PG) BINDING BY PEMPHIGUS-VULGARIS ANTIGEN (PVA) IN KERATINOCYTES REQUIRES ITS INTRACYTOPLASMIC CADHERIN-LIKE SUBDOMAIN (ICCS) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,DERMATOL BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 583 EP 583 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200192 ER PT J AU ENK, CD MAHANTY, S BLAUVELT, A KATZ, SI AF ENK, CD MAHANTY, S BLAUVELT, A KATZ, SI TI INDUCTION OF IL-12 GENE-EXPRESSION IN HUMAN KERATINOCYTES BY ULTRAVIOLET-B RADIATION IN-VIVO AND IN-VITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 587 EP 587 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200219 ER PT J AU DENNING, MF YUSPA, SH AF DENNING, MF YUSPA, SH TI CHOLESTEROL SULFATE INDUCES GRANULAR-CELL DIFFERENTIATION AND MODULATES CA2+ INDEPENDENT PROTEIN-KINASE-C ISOENZYMES IN CULTURED MURINE KERATINOCYTES 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 SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 591 EP 591 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200242 ER PT J AU STANWELL, C DENNING, MF CHENG, C YUSPA, SH DLUGOSZ, AD AF STANWELL, C DENNING, MF CHENG, C YUSPA, SH DLUGOSZ, AD TI STAUROSPORINE INDUCES DIFFERENTIATION IN NORMAL AND NEOPLASTIC MURINE KERATINOCYTES VIA A COORDINATED PROGRAM OF LATE DIFFERENTIATION MARKER GENE-EXPRESSION MODULATED BY PROTEIN-KINASE-C 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 SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 591 EP 591 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200243 ER PT J AU STEINERT, PM MAREKOV, LN CANDI, E AF STEINERT, PM MAREKOV, LN CANDI, E TI IDENTIFICATION OF AN ESSENTIAL FUNCTION FOR THE AMINO-TERMINAL DOMAIN OF TYPE-II KERATIN INTERMEDIATE FILAMENT CHAINS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 592 EP 592 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200249 ER PT J AU WALKER, PS HENGGE, UR VOGEL, JC AF WALKER, PS HENGGE, UR VOGEL, JC TI SIMULTANEOUS IN-VITRO TRANSDUCTION OF FIBROBLASTS AND KERATINOCYTES WITH 2 RETROVIRAL VECTORS 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 SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 596 EP 596 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200270 ER PT J AU BOISSY, RE ZHAO, H OETTING, WS KOBAYASHI, T AUSTIN, LM WILDENBERG, SC BOISSY, YL ZHAO, Y HEARING, VJ KING, RA NORDLUND, JJ AF BOISSY, RE ZHAO, H OETTING, WS KOBAYASHI, T AUSTIN, LM WILDENBERG, SC BOISSY, YL ZHAO, Y HEARING, VJ KING, RA NORDLUND, JJ TI MUTATION IN AND LACK OF EXPRESSION OF TYROSINASE-RELATED PROTEIN-1 (TRP-1) IN MELANOCYTES FROM AN INDIVIDUAL WITH TYROSINASE-POSITIVE OCULOCUTANEOUS ALBINISM - A NEW SUBTYPE OF ALBINISM CLASSIFIED AS OCA3 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV CINCINNATI,DEPT DERMATOL,CINCINNATI,OH. UNIV MINNESOTA,DEPT MED & PEDIAT,MINNEAPOLIS,MN. UNIV MINNESOTA,INST HUMAN GENET,MINNEAPOLIS,MN. NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 597 EP 597 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200275 ER PT J AU LEVY, DD SEIDMAN, MM AF LEVY, DD SEIDMAN, MM TI VARIATION OF DNA-SEQUENCE ALTERS MUTAGENIC PROCESSING OF PROXIMAL AND DISTAL UV LESIONS IN XERODERMA-PIGMENTOSUM CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. OTSUKA PHARMACEUT CO LTD,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 599 EP 599 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200292 ER PT J AU WEINBERG, WC AZZOLI, CG WU, AJ SAGAR, M MORGAN, DL YUSPA, SH AF WEINBERG, WC AZZOLI, CG WU, AJ SAGAR, M MORGAN, DL YUSPA, SH TI RECONSTITUTION OF P53-NULL KERATINOCYTE CELL-LINES WITH TEMPERATURE-SENSITIVE P53 - A MODEL FOR EXPLORING THE ROLE OF P53 IN EPIDERMAL BIOLOGY SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. RI Weinberg, Wendy/A-8920-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 599 EP 599 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200287 ER PT J AU KOWALCZYK, AP ANDERSON, JE BORGWARDT, JE HASHIMOTO, T STANLEY, JR GREEN, KJ AF KOWALCZYK, AP ANDERSON, JE BORGWARDT, JE HASHIMOTO, T STANLEY, JR GREEN, KJ TI PEMPHIGUS SERA RECOGNIZE CONFORMATIONALLY LABILE EPITOPES WITHIN THE AMINO-TERMINAL REGION OF DSG1 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 KEIO UNIV,SCH MED,DEPT DERMATOL,TOKYO 108,JAPAN. NORTHWESTERN UNIV,SCH MED,DEPT PATHOL,CHICAGO,IL 60611. NCI,DERMATOL BRANCH,CHICAGO,IL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 602 EP 602 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200308 ER PT J AU MORIWAKI, S STEFANINI, M LEHMANN, A HOEIJMAKERS, JHJ KRAEMER, KH AF MORIWAKI, S STEFANINI, M LEHMANN, A HOEIJMAKERS, JHJ KRAEMER, KH TI DNA-REPAIR AND ULTRAVIOLET MUTAGENESIS IN XERODERMA-PIGMENTOSUM GROUP-G COCKAYNE-SYNDROME CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 CNR,I-27100 PAVIA,ITALY. NCI,BETHESDA,MD 20892. UNIV SUSSEX,CELL MUTAT UNIT,BRIGHTON,E SUSSEX,ENGLAND. ERASMUS UNIV ROTTERDAM,ROTTERDAM,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 605 EP 605 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200328 ER PT J AU TARCSA, E LEE, SC STEINERT, PM MAREKOV, LN AF TARCSA, E LEE, SC STEINERT, PM MAREKOV, LN TI PEPTIDYLARGININE DEIMINASE MODIFICATION OF HUMAN TRICHOHYALIN AND OTHER SUBSTRATES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. CHONNAM NATL UNIV,SCH MED,DEPT DERMATOL,KWANGJU 501190,SOUTH KOREA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 606 EP 606 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200333 ER PT J AU KARTASOVA, T PARRY, DAD STEINERT, PM AF KARTASOVA, T PARRY, DAD STEINERT, PM TI MODELING OF SMALL PROLINE-RICH PROTEIN EVOLUTION AND STRUCTURE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. MASSEY UNIV,DEPT PHYS,PALMERSTON NORTH,NEW ZEALAND. NR 0 TC 4 Z9 4 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 611 EP 611 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200360 ER PT J AU LICHTI, U SCANDURRO, AB DENNING, M WIRTH, PJ YUSPA, SH KARTASOVA, T AF LICHTI, U SCANDURRO, AB DENNING, M WIRTH, PJ YUSPA, SH KARTASOVA, T TI GROWTH-FACTOR OVERPRODUCING FIBROBLAST CELL-LINE INDUCES WRINKLED SKIN FORMATION WHEN GRAFTED WITH KERATINOCYTES ON NUDE-MICE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 614 EP 614 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200379 ER PT J AU SUZUKI, I HEARING, V CONE, R NORDLUND, J ABDELMALEK, Z AF SUZUKI, I HEARING, V CONE, R NORDLUND, J ABDELMALEK, Z TI MELANOTROPIC HORMONES STIMULATE HUMAN MELANOCYTE PIGMENTATION AND PROLIFERATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIH,CELL BIOL LAB,BETHESDA,MD 20892. POLA LABS,YOKOHAMA,KANAGAWA,JAPAN. VOLLUM INST,PORTLAND,OR. UNIV CINCINNATI,DEPT DERMATOL,CINCINNATI,OH. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 617 EP 617 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200397 ER PT J AU CHIPEV, CC WOODWORTH, CD AF CHIPEV, CC WOODWORTH, CD TI AN ASSAY TO DISTINGUISH THE EXPRESSION OF THE NORMAL AND MUTANT ALLELE OF KERATIN-10 IN CELLS DERIVED FROM A PATIENT WITH EPIDERMOLYTIC HYPERKERATOSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NCI,LB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 626 EP 626 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200453 ER PT J AU JANG, SI STEINERT, PM MARKOVA, NG AF JANG, SI STEINERT, PM MARKOVA, NG TI CHARACTERIZATION OF A KERATINOCYTE-SPECIFIC SILENCER ELEMENT IN THE PROXIMAL PROMOTER REGION OF THE HUMAN PROFILAGGRIN GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 626 EP 626 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200450 ER PT J AU JANG, SI STEINERT, PM MARKOVA, NG AF JANG, SI STEINERT, PM MARKOVA, NG TI AP1 AND ETS-LIKE TRANSCRIPTION FACTORS ARE INVOLVED IN THE SPECIFICITY OF TRANSCRIPTION OF THE HUMAN PROFILAGGRIN GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 627 EP 627 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200460 ER PT J AU LEE, JH STEINERT, PM JANG, SI MARKOVA, NG YANG, JM AF LEE, JH STEINERT, PM JANG, SI MARKOVA, NG YANG, JM TI A POSITIVE ELEMENT THAT CONTROLS THE EXPRESSION OF THE HUMAN TRANSGLUTAMINASE-3 GENE IS LOCATED IN THE PROXIMAL PROMOTER REGION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 627 EP 627 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200457 ER PT J AU DELAURENZI, V MAREKOV, LN STEINERT, PM CANDI, E AF DELAURENZI, V MAREKOV, LN STEINERT, PM CANDI, E TI LORICRIN IS AN ABUNDANT SOLUBLE PHOSPHORYLATED PROTEIN IN MAMMALIAN EPIDERMIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL BRANCH,BETHESDA,MD. UNIV ROMA TOR VERGATA,DEPT EXPTL MED,ROME,ITALY. IST DERMOPATICO INMACOLATA,ROME,ITALY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 642 EP 642 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200547 ER PT J AU FUJIMOTO, W NAKANISHI, G ARATA, J JETTEN, AM AF FUJIMOTO, W NAKANISHI, G ARATA, J JETTEN, AM TI EXPRESSION OF CORNIFIN-ALPHA AND CORNIFIN-BETA IN NORMAL SKIN, ORAL EPITHELIA AND VARIOUS SKIN DISEASES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 OKAYAMA UNIV,SCH MED,DEPT DERMATOL,OKAYAMA,JAPAN. NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 643 EP 643 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200551 ER PT J AU HENGGE, UR FOSTER, RA WALKER, PS VOGEL, JC AF HENGGE, UR FOSTER, RA WALKER, PS VOGEL, JC TI CYTOKINE GENE-EXPRESSION IN EPIDERMIS WITH BIOLOGICAL EFFECTS FOLLOWING LOCAL INJECTION OF NAKED DNA 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 SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 675 EP 675 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200744 ER PT J AU RICHARD, G KORGE, BP WRIGHT, AR MAZZANTI, C COMPTON, JG BALE, SJ AF RICHARD, G KORGE, BP WRIGHT, AR MAZZANTI, C COMPTON, JG BALE, SJ TI REFINEMENT OF THE LOCATION OF HAILEY-HAILEY DISEASE ON CHROMOSOME SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. UNIV COLOGNE,DERMATOL KLIN & POLIKLIN,W-5000 COLOGNE,GERMANY. INST DERMOPAT IMMACOLATA,ROME,ITALY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 675 EP 675 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200743 ER PT J AU ROGERS, GR RIZZO, WB LEE, MJ COMPTON, JG BALE, SJ AF ROGERS, GR RIZZO, WB LEE, MJ COMPTON, JG BALE, SJ TI SJOGREN-LARSSON SYNDROME LINKED TO CHROMOSOME-17 SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,GENET STUDIES SECT,BETHESDA,MD. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT HUMAN GENET & PEDIAT,RICHMOND,VA. RI Lee, Minjoo/A-9720-2008 OI Lee, Minjoo/0000-0002-3151-3808 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 675 EP 675 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200746 ER PT J AU LAKKAKORPI, JT BERNSTEIN, EF FISHER, LW LI, KH LEBARON, RG TAN, EML UITTO, J AF LAKKAKORPI, JT BERNSTEIN, EF FISHER, LW LI, KH LEBARON, RG TAN, EML UITTO, J TI DIFFERENTIAL EXPRESSION OF THE VERSICAN AND DECORIN GENES IN PHOTOAGED AND SUN-PROTECTED SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV, JEFFERSON MED COLL, DEPT DERMATOL, PHILADELPHIA, PA 19107 USA. THOMAS JEFFERSON UNIV, JEFFERSON MED COLL, DEPT PATHOL, PHILADELPHIA, PA 19107 USA. NIDR, BONE RES BRANCH, BETHESDA, MD 20892 USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0022-202X EI 1523-1747 J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 676 EP 676 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200754 ER PT J AU MARKOVA, NG ANDREOLI, JM STEINERT, PM JANG, SI AF MARKOVA, NG ANDREOLI, JM STEINERT, PM JANG, SI TI CHARACTERIZATION OF A KERATINOCYTE-SPECIFIC POSITIVE ELEMENT IN THE PROXIMAL PROMOTER REGION OF THE HUMAN PROFILAGGRIN GENE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 676 EP 676 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200749 ER PT J AU SOLLITTO, RB REYNOLDS, JC STEINBERG, SM DIGIOVANNA, JJ AF SOLLITTO, RB REYNOLDS, JC STEINBERG, SM DIGIOVANNA, JJ TI ETRETINATE-INDUCED OSTEOPOROSIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NCI,COP,BETHESDA,MD 20892. NIAMS,DERMATOL CLIN RES UNIT,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 689 EP 689 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200830 ER PT J AU SOLLITTO, RB KRAEMER, KH DIGIOVANNA, JJ AF SOLLITTO, RB KRAEMER, KH DIGIOVANNA, JJ TI NORMAL VITAMIN-D LEVELS IN SUN-PROTECTED PATIENTS WITH XERODERMA-PIGMENTOSUM SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIAMS,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1995 VL 104 IS 4 BP 689 EP 689 PG 1 WC Dermatology SC Dermatology GA QR532 UT WOS:A1995QR53200827 ER PT J AU ROILIDES, E HOLMES, A BLAKE, C PIZZO, PA WALSH, TJ AF ROILIDES, E HOLMES, A BLAKE, C PIZZO, PA WALSH, TJ TI EFFECTS OF GRANULOCYTE-COLONY-STIMULATING FACTOR AND INTERFERON-GAMMA ON ANTIFUNGAL ACTIVITY OF HUMAN POLYMORPHONUCLEAR NEUTROPHILS AGAINST PSEUDOHYPHAE OF DIFFERENT MEDICALLY IMPORTANT CANDIDA SPECIES SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Article DE CANDIDIASIS; PHAGOCYTES; MYCOSES; FUNGI; CYTOKINES ID ASPERGILLUS-FUMIGATUS HYPHAE; TUMOR-NECROSIS-FACTOR; HUMAN-IMMUNODEFICIENCY-VIRUS; FUNGICIDAL ACTIVITY; RESPIRATORY BURST; FACTOR-ALPHA; ALBICANS; INVITRO; ACTIVATION; DAMAGE AB Polymorphonuclear neutrophils (PMNs) are the major host defense against pseudohyphae, the invasive form of Candida species. We studied the effects of granulocyte colony-stimulating factor (G-CSF) and interferon-gamma (IFN-gamma) on the PMN-induced damage of pseudohyphae of Candida albicans, Candida tropicalis, and Candida parapsilosis in vitro by using two antifungal assays: a modified limiting dilution assay and a colorimetric metabolic 3-(4,5-dimethylthiazlol-2-yl)-2,5-diphenyl- tetrazolium bromide assay. PMNs from healthy volunteers were incubated with either G-CSF (100-10,000 U/ml) or IFN-gamma (10-5000 U/ml) or buffer at 37 degrees C for 90 min and their capacity to damage nonopsonized pseudohyphae was then measured. C. tropicalis appeared to be the most susceptible species, whereas C. parapsilosis showed the highest rate of resistance to PMN damage. G-CSF (500-10,000 U/ml) and IFN-gamma (100-1000 U/ml) enhanced the antifungal activity of PMNs against C. albicans pseudohyphae (P < .01 and P < .05). Among the others, G-CSF enhanced PMN-induced damage of C. parapsilosis at concentrations 500-10,000 U/ml(P < .05), whereas it enhanced damage of C. tropicalis only at 10,000 U/ml (P < .01). IFN-gamma (100-1000 U/ml)-primed PMNs also caused augmented damage of C. parapsilosis (P < .05) but not of C. tropicalis at the same concentrations. Species-dependent differences exist in the responses of PMNs to Candida pseudohyphae and G-CSF as well as IFN-gamma are important immunomodulators of phagocytic host defenses against them. C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892. NR 38 TC 66 Z9 67 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PD APR PY 1995 VL 57 IS 4 BP 651 EP 656 PG 6 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA QU085 UT WOS:A1995QU08500020 PM 7536791 ER PT J AU VANGELDEREN, P DUYN, JH MOONEN, CTW AF VANGELDEREN, P DUYN, JH MOONEN, CTW TI ANALYTICAL SOLUTION FOR PHASE MODULATION IN BURST IMAGING WITH OPTIMUM SENSITIVITY SO JOURNAL OF MAGNETIC RESONANCE SERIES B LA English DT Article ID SEQUENCE AB In order to improve the efficiency of BURST imaging, a new phase-modulation scheme of the DANTE-type RF excitation is proposed. It is shown that analytical optimization of the phase-modulation scheme with optimal SNR can be found for an arbitrary number N of subpulses in the RF excitation. Both theory and experiment indicate a maximum attainable gain in efficiency of the square root of N, compared to nonmodulated (constant-phase) excitation schemes. (C) 1995 Academic Press, Inc. C1 NIH,OIR,DIAGNOST RADIOL RES LAB,BETHESDA,MD 20892. RP VANGELDEREN, P (reprint author), NIH,NCRR,BEIP,NMR RES CTR,BLDG 10,ROOM B1D-125,10 CTR DR MSC 1060,BETHESDA,MD 20892, USA. RI Duyn, Jozef/F-2483-2010; Moonen, Chrit/K-4434-2016 OI Moonen, Chrit/0000-0001-5593-3121 NR 8 TC 9 Z9 9 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 1064-1866 J9 J MAGN RESON SER B JI J. Magn. Reson. Ser. B PD APR PY 1995 VL 107 IS 1 BP 78 EP 82 DI 10.1006/jmrb.1995.1061 PG 5 WC Physics, Atomic, Molecular & Chemical SC Physics GA QR242 UT WOS:A1995QR24200011 PM 7743076 ER PT J AU SHI, Q CHEN, K LI, LP CHANG, JJ AUTRY, C KOZUKA, M KONOSHIMA, T ESTES, JR LIN, CM HAMEL, E MCPHAIL, AT MCPHAIL, DR LEE, KH AF SHI, Q CHEN, K LI, LP CHANG, JJ AUTRY, C KOZUKA, M KONOSHIMA, T ESTES, JR LIN, CM HAMEL, E MCPHAIL, AT MCPHAIL, DR LEE, KH TI ANTITUMOR AGENTS .154. CYTOTOXIC AND ANTIMITOTIC FLAVONOLS FROM POLANISIA-DODECANDRA SO JOURNAL OF NATURAL PRODUCTS-LLOYDIA LA English DT Article ID GUTIERREZIA-MICROCEPHALA; CELL LINES; ANALOGS; TUBULIN AB Three flavonols, 5,3'-dihydroxy-3,6,7,8,4'-pentamethoxyflavone [1],5,4'-dihydroxy-3,6,7,8,3'-pentamethoxyflavone [2], and quercetin 3-0-beta-D-glucopyranosyl-7-0-alpha-L-rhamnopyranoside [3], were isolated from Polanisia dodecandra. Compound 1 showed remarkable cytotoxicity in vitro against panels of central nervous system cancer (SF-268, SF-539, SNB-75, U-251), non-small cell lung cancer (HOP-62, NCI-H266, NCI-H460, NCI-H522), small cell lung cancer (DMS-114), ovarian cancer (OVCAR-3, SK-OV-3), colon cancer (HCT-116), renal cancer (UO-31), a melanoma cell line (SK-MEL-5), and two leukemia cell lines (HL-60 [TB], SR), with GI(50) values in the low micromolar to nanomolar concentration. range. This substance also inhibited tubulin polymerization (IC50=0.83 +/- 0.2 mu M) and the binding of radiolabeled colchicine to tubulin with 59% inhibition when present in equimolar concentrations with colchicine. Compound 2 also showed cytoxicity against medulloblastoma (TE-671) tumor cells with an ED(50) value of 0.98 mu g/ml. Compound 1 appears to be the first example of a flavonol to exhibit potent inhibition of tubulin polymerization and, therefore, warrants further investigation as an antimitotic agent. C1 DUKE UNIV,PAUL M GROSS CHEM LAB,DEPT CHEM,DURHAM,NC 27706. UNIV N CAROLINA,SCH MED,ANIM MED LAB,CHAPEL HILL,NC 27599. KYOTO PHARMACEUT UNIV,YAMASHIMA KU,KYOTO 607,JAPAN. UNIV OKLAHOMA,DEPT BOT,NORMAN,OK 73019. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. UNIV N CAROLINA,SCH PHARM,DIV MED CHEM & NAT PROD,NAT PROD LAB,CHAPEL HILL,NC 27599. FU NCI NIH HHS [CA-17625] NR 24 TC 61 Z9 66 U1 0 U2 4 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PRODUCTS JI J. Nat. Prod. PD APR PY 1995 VL 58 IS 4 BP 475 EP 482 DI 10.1021/np50118a001 PG 8 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA RC194 UT WOS:A1995RC19400001 PM 7623025 ER PT J AU RASHID, MA GUSTAFSON, KR CARDELLINA, JH BOYD, MR AF RASHID, MA GUSTAFSON, KR CARDELLINA, JH BOYD, MR TI PATELLAMIDE-F, A NEW CYTOTOXIC CYCLIC PEPTIDE FROM THE COLONIAL ASCIDIAN LISSOCLINUM-PATELLA SO JOURNAL OF NATURAL PRODUCTS-LLOYDIA LA English DT Note ID MARINE TUNICATE; SOLUTION-STATE; BISTRATUM; ULITHIACYCLAMIDE; MACROLIDE; VAREAU AB Cytocoxicity-directed fractionation of an organic extract of the tunicaee Lissoclinum patella afforded a new cyclic octapeptide, patellamide F [1]. The structure and absolute stereochemistry of 1 were established by a combination of spectroscopic and chemical methods. Three known cyclic peptides, patellamide B [2], ulithiacyclamide, and lissoclinamide 3, were also isolated and identified. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. NR 28 TC 24 Z9 26 U1 0 U2 4 PU AMER SOC PHARMACOGNOSY PI CINCINNATI PA LLOYD LIBRARY & MUSEUM 917 PLUM ST, CINCINNATI, OH 45202 SN 0163-3864 J9 J NAT PRODUCTS JI J. Nat. Prod. PD APR PY 1995 VL 58 IS 4 BP 594 EP 597 DI 10.1021/np50118a020 PG 4 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA RC194 UT WOS:A1995RC19400020 PM 7623037 ER PT J AU GEORGE, MS AF GEORGE, MS TI FEMINIST PERSPECTIVES ON EATING DISORDERS - FALLON,P, KATZMAN,MA, WOOLEY,SC SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Book Review RP GEORGE, MS (reprint author), NIMH,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 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 1995 VL 183 IS 4 BP 275 EP 276 PG 2 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QV309 UT WOS:A1995QV30900021 ER PT J AU IZENWASSER, S COTE, TE AF IZENWASSER, S COTE, TE TI INHIBITION OF ADENYLYL-CYCLASE ACTIVITY BY A HOMOGENEOUS POPULATION OF DOPAMINE-RECEPTORS - SELECTIVE BLOCKADE BY ANTISERA DIRECTED AGAINST G(I1) AND/OR G(I2) SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE DOPAMINE; COCAINE; D-2 DOPAMINE RECEPTOR ID GTP-BINDING PROTEIN; ALLELIC ASSOCIATION; OPIOID RECEPTORS; ASSAY METHOD; GENE; MEMBRANES; AGONISTS; BRAIN; 7315C; RAT AB The 7315c pituitary tumor cell expresses a homogeneous population of dopamine receptors that are functionally similar to brain dopamine D-2 receptors. [H-3]-Sulpiride binding to 7315c cell homogenates was specific and saturable, and K-I Values for compounds to compete for these sites were highly correlated with values for the same compounds at D-2 receptors in brain. Dopamine maximally inhibited similar to 65% of forskolin-stimulated cyclase activity in cell membranes. Some D-2 agonists had lower efficacies, suggesting that some compounds are partial agonists at this receptor. Removal of GTP from the assay buffer or pretreatment of the tissue with pertussis toxin abolished the Inhibition of adenylyl cyclase by dopamine. Immunodetection of most of the known G alpha subunits revealed that G(i1), G(i2), G(i3), G(o) G(q) and G(s) are present in the 7315c membrane. Pretreatment with the AS antibody (which recognizes the C-terminal regions of G alpha(i1) and G alpha(I2)) significantly attenuated the inhibition of adenylyl cyclase activity by dopamine, whereas antibodies to C-terminal regions of the other G alpha subunits had no effect. These findings suggest that the dopamine D-2 receptor regulates cyclase inhibition predominantly via G(i1) and/or G(i2) and that the 7315c tumor cells provide a useful model for studying naturally expressed dopamine D-2 receptors in the absence of other dopamine receptor subtypes. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PHARMACOL,BETHESDA,MD 20814. RP IZENWASSER, S (reprint author), NIDA,DIV INTRAMURAL RES,PSYCHOBIOL SECT,POB 5180,BALTIMORE,MD 21224, USA. RI Izenwasser, Sari/G-9193-2012 NR 29 TC 11 Z9 11 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD APR PY 1995 VL 64 IS 4 BP 1614 EP 1621 PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA QN150 UT WOS:A1995QN15000023 PM 7891089 ER PT J AU HA, JH SEI, Y BASILE, AS AF HA, JH SEI, Y BASILE, AS TI STRIATAL MET-ENKEPHALIN AND SUBSTANCE-P LEVELS ARE DECREASED IN MICE INFECTED WITH THE LP-BM5 MURINE LEUKEMIA-VIRUS SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE AIDS DEMENTIA MODEL; LP-BM5 MURINE LEUKEMIA VIRUS; STRIATUM; MET-ENKEPHALIN; SUBSTANCE P ID INDUCED IMMUNODEFICIENCY SYNDROME; CENTRAL-NERVOUS-SYSTEM; QUINOLINIC ACID; HUNTINGTONS-DISEASE; CEREBROSPINAL-FLUID; NEURONS AB Mice infected with the LP-BM5 murine leukemia virus mixture develop severe immunosuppression and an encephalopathy characterized by spatial learning deficits. Twelve weeks after infection of C57BL/6J mice with LP-BM5, significant (50-60%) reductions in Met-enkephalin and substance P levels were observed in the striatum, whereas somatostatin levels were unchanged. In addition, a 39% decrease in hypothalamic substance P concentrations was observed, with no alteration in Metenkephalin levels. The apparent selectivity of the decrease in neuropeptide concentrations indicates that a functional alteration of the primary striatal efferent neurons occurs in this infection, which may contribute to the impairment of spatial learning observed in these mice. Moreover, this decrease in striatal neuropeptide levels is similar to the neuropathological changes in basal ganglia observed in HIV-infected individuals and is consistent with previous studies suggesting that the LP-BM5-infected mouse mat serve as a useful model of AIDS dementia. C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. NR 22 TC 18 Z9 18 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 1995 VL 64 IS 4 BP 1896 EP 1898 PG 3 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA QN150 UT WOS:A1995QN15000059 PM 7534338 ER PT J AU HITRI, A KAROUM, F WYATT, RJ AF HITRI, A KAROUM, F WYATT, RJ TI QUESTIONS ABOUT THE DOPAMINE TERMINALS IN HUMAN FRONTAL-CORTEX SO JOURNAL OF NEUROCHEMISTRY LA English DT Letter C1 GEORGETOWN UNIV,SCH MED,WASHINGTON,DC. NIMH,NEUROPSYCHIAT BRANCH,WASHINGTON,DC. RP HITRI, A (reprint author), DVAMC,WASHINGTON,DC, USA. NR 14 TC 1 Z9 1 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 1995 VL 64 IS 4 BP 1901 EP 1902 PG 2 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA QN150 UT WOS:A1995QN15000062 PM 7891122 ER PT J AU KUSTOV, AA ROBINSON, DL AF KUSTOV, AA ROBINSON, DL TI MODIFIED SACCADES EVOKED BY STIMULATION OF THE MACAQUE SUPERIOR COLLICULUS ACCOUNT FOR PROPERTIES OF THE RESETTABLE INTEGRATOR SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Note ID LOCAL FEEDBACK; EYE-MOVEMENTS; MONKEY; LOCALIZATION; GENERATOR; POSITION AB 1. Models of the saccadic system propose that there is an integration of the pulse signal, and there is good evidence that the integrator is reset gradually (Nichols and Sparks 1994, 1995). Other studies of the superior collicular contribution to the saccadic system have proposed a sensory, not motor, nature for its signal. 2. To test experimentally the resetting of the integrator and the nature of the collicular signal, we electrically stimulated the superior colliculus during periods of fixation and during the course of visually guided saccades. Trains of stimuli which were presented during periods of fixation evoked saccades with fixed vectors. Identical stimulation at the beginning of a visually guided saccade evoked saccades whose direction was rotated and amplitude extended from the fixed vector. The direction of the rotation was opposite that of the visually guided saccade, and the magnitude of this rotation could be as large as 80 degrees. 3. Stimulation which was applied at progressively later times during the visually guided saccade, evoked saccades with progressively smaller rotations and progressively less elongations. The time period during which saccades were modified persisted beyond the end of the visually guided saccade, when the eyes were stationary. Thus, we confirm the previous findings (Nichols and Sparks 1994, 1995; Robinson, 1972), that the end of the saccade is not a period of quiescence within the oculomotor pathways. 4. Our results confirm that the resetting of the integration of the saccade signal is gradual rather than abrupt. Furthermore, these data suggest that the superior colliculus signals a motor error. C1 NCI,SENSORIMOTOR RES LAB,VISUAL BEHAV SECT,BETHESDA,MD 20892. NR 18 TC 42 Z9 42 U1 0 U2 0 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 1995 VL 73 IS 4 BP 1724 EP 1728 PG 5 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA QT906 UT WOS:A1995QT90600034 PM 7643180 ER PT J AU SOMOGYI, R WEN, XL MA, W BARKER, JL AF SOMOGYI, R WEN, XL MA, W BARKER, JL TI DEVELOPMENTAL KINETICS OF GAD FAMILY MESSENGER-RNAS PARALLEL NEUROGENESIS IN THE RAT SPINAL-CORD SO JOURNAL OF NEUROSCIENCE LA English DT Article DE GAD; ONTOGENY; NEUROGENESIS; ALTERNATIVE SPLICING; RAT; SPINAL CORD; QUANTITATIVE PCR; MATHEMATICAL MODEL ID GLUTAMIC-ACID DECARBOXYLASE; MESSENGER-RNA LEVELS; REVERSE TRANSCRIPTION; NEUROFILAMENT PROTEIN; CEREBRAL-CORTEX; GABA; EXPRESSION; NEURONS; CELLS; CLONING AB GABA (gamma-amino butyric acid), a fast-acting synaptic transmitter in the mature CNS, is synthesized from glutamate by GAD (glutamic acid decarboxylase). We have developed an ultrasensitive PCR technique to quantify the expression of GAD-related mRNAs during the development of the rat cervical spinal cord and have localized them using in situ hybridization. GAD65, GAD67, and an alternatively spliced variant of GAD67, EP10, were quantified each day from embryonic (E) day 11 through E21, and at postnatal days 0, 7, 14, and adult, GAD65 and GAD67 mRNAs were detected at E11 and increased exponentially over three orders of magnitude during embryonic development, then declined approximately threefold in the first 2 postnatal weeks, While the exponential growth phase coincided with the progressive appearance of GAD67 in situ signals in both the ventral and dorsal cord, the postnatal decline coincided with the virtual disappearance of expression in the ventral region, EP10 expression was prominent in the embryo, then declined markedly together with the mRNA encoding the neuroepithelial stem cell marker, nestin. The concerted appearance of GAD-related mRNAs paralleled transcripts encoding neuronal markers (light and heavy neurofilaments) and also closely correlated with the expression of GABA, mRNAs encoding GABA(A) receptor subunits, and depolarizing responses to GABA, We have used the results on GAD-related mRNA expressions to formulate a simple, minimal mathematical model that accounts for their kinetics in terms of positive and negative feedback loops. RP SOMOGYI, R (reprint author), NINCDS,NEUROPHYSIOL LAB,BLDG 36-2C02,BETHESDA,MD 20892, USA. NR 47 TC 89 Z9 90 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1995 VL 15 IS 4 BP 2575 EP 2591 PG 17 WC Neurosciences SC Neurosciences & Neurology GA QT913 UT WOS:A1995QT91300001 PM 7722616 ER PT J AU LI, YW HOLTZMAN, DM KROMER, LF KAPLAN, DR CHUACOUZENS, J CLARY, DO KNUSEL, B MOBLEY, WC AF LI, YW HOLTZMAN, DM KROMER, LF KAPLAN, DR CHUACOUZENS, J CLARY, DO KNUSEL, B MOBLEY, WC TI REGULATION OF TRKA AND CHAT EXPRESSION IN DEVELOPING RAT BASAL FOREBRAIN - EVIDENCE THAT BOTH EXOGENOUS AND ENDOGENOUS NGF REGULATE DIFFERENTIATION OF CHOLINERGIC NEURONS SO JOURNAL OF NEUROSCIENCE LA English DT Article DE NGF; NGF RECEPTOR; TRKA; CHAT; BASAL FOREBRAIN CHOLINERGIC NEURONS (BFCNS); DEVELOPMENT; NGF ANTISERUM ID NERVE GROWTH-FACTOR; PC12 PHEOCHROMOCYTOMA CELLS; TYROSINE KINASE-ACTIVITY; HIGH-AFFINITY RECEPTORS; FACTOR MESSENGER-RNA; PROTOONCOGENE PRODUCT; GENE-EXPRESSION; ADULT-RAT; PHOSPHATIDYLINOSITOL 3-KINASE; NEUROTROPHIN RECEPTORS AB TrkA is a receptor tyrosine kinase whose activation transduces NGF signaling. TrkA expression has been demonstrated in NGF-responsive adult basal forebrain cholinergic neurons (BFCNs). Several lines of evidence have suggested that endogenous NGF plays a role in the development and differentiation of these neurons. We examined TrkA expression during development. TrkA mRNA and protein were present in basal forebrain neurons during the entire postnatal period; the distribution of neurons bearing these markers was identical to that for those containing choline acetyltransferase (ChAT) mRNA, suggesting that, as in the adult, TrkA gene expression is localized to BFCNs. The expression of TrkA and ChAT followed a very similar temporal pattern, suggesting regulation by the same factor(s). We discovered that NGF administration in vivo activated TrkA receptors, and increased both TrkA and ChAT mRNA; conversely, anti-NGF infusions suppressed expression of both genes. These results suggest that endogenous NGF regulates expression of TrkA and ChAT. Finally, while NGF infusion increased the size of developing BFCNs, NGF antibodies inhibited the normal developmental increase. The results are evidence that endogenous NGF acts on developing BFCNs to enhance gene expression and cellular differentiation. C1 UNIV CALIF SAN FRANCISCO,DEPT NEUROL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,PROGRAM NEUROSCI,SAN FRANCISCO,CA 94143. GEORGETOWN UNIV,MED CTR,DEPT CELL BIOL,WASHINGTON,DC 20007. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,EUKARYOL SIGNAL TRANSDUCT GRP,FREDERICK,MD 21702. UNIV SO CALIF,ANDRUS GERONTOL CTR,DIV NEUROGERONTOL,LOS ANGELES,CA 90089. UNIV SO CALIF,DEPT SCI BIOL,LOS ANGELES,CA 90089. FU NINDS NIH HHS [NS 24054, NS 31445] NR 83 TC 179 Z9 184 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR PY 1995 VL 15 IS 4 BP 2888 EP 2905 PG 18 WC Neurosciences SC Neurosciences & Neurology GA QT913 UT WOS:A1995QT91300027 PM 7536822 ER PT J AU YAO, DL WEST, NR BONDY, CA BRENNER, M HUDSON, LD ZHOU, J COLLINS, GH WEBSTER, HD AF YAO, DL WEST, NR BONDY, CA BRENNER, M HUDSON, LD ZHOU, J COLLINS, GH WEBSTER, HD TI CRYOGENIC SPINAL-CORD INJURY INDUCES ASTROCYTIC GENE-EXPRESSION OF INSULIN-LIKE GROWTH-FACTOR-I AND INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEIN-2 DURING MYELIN REGENERATION SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE IGF-I; IGF BINDING PROTEIN; ASTROCYTE; MYELIN REGENERATION ID FIBRILLARY ACIDIC PROTEIN; HYPOXIC-ISCHEMIC INJURY; CENTRAL-NERVOUS-SYSTEM; RAT-BRAIN; RECEPTOR GENE; OLIGODENDROCYTE DEVELOPMENT; INSITU HYBRIDIZATION; TRANSGENIC MICE; FREEZING-INJURY; MESSENGER-RNA AB To study injury-induced astrocytic responses associated with regrowth of axons and regeneration of myelin, the method of Collins and colleagues was used to make focal cryogenic lesions in spinal cords of adult rats (Collins et al.: J Neuropathol Exp Neurol 45: 742-757, 1986). The duration of cryogenic injury (CI), the size of the cryode, and its temperature were chosen to destroy all myelin sheaths and axons without producing cavities or hemorrhages, Messenger RNA and peptide distributions of insulin-like growth factor I (IGF-I), IGF-I receptor (IGFR-I), IGF binding protein 2 (IGFBP-2), glial fibrillary acidic protein (GFAP), and myelin basic protein (MBP) were studied 3-56 days after CI by in situ hybridization and immunocytochemistry, At 3 days, vimentin-positive, GFAP-negative astrocyte-like cells in the lesion expressed IGF-I mRNA and peptide and 7 days after CI, both were expressed by typical GFAP-positive, hypertrophic astrocytes, many of which also were vimentin-positive. Levels of IGF-I, IGFBP-2, and GFAP mRNA and peptide were higher in lesion astrocytes after 14 days, They attained maximum levels at 21-28 days before declining to near control levels at 56 days, Decreasing relative levels of oligodendroglial MBP mRNA were found in and around lesions 7-14 days after CI; subsequently, rising levels accompanied remyelination, At 28 and 56 days after CI, some transferrin-positive, oligodendroglia-like cells also were immunostained by anti-IGFR-I. Our findings suggest that early astrocytic production of IGF-I and IGFBP-2 may be involved in the myelin regeneration which occurs in this model of spinal cord injury. (c) 1995 Wiley-Liss, Inc.(*) C1 NINCDS, VIRAL & MOLEC PATHOGENESIS LAB, BETHESDA, MD 20892 USA. NICHHD, DEV ENDOCRINOL BRANCH, BETHESDA, MD 20892 USA. SUNY SYRACUSE, HLTH SCI CTR, DEPT PATHOL, SYRACUSE, NY 13210 USA. RP YAO, DL (reprint author), NINCDS, STROKE BRANCH, EXPTL NEUROPATHOL LAB, BLDG 36, RM 4A-29, BETHESDA, MD 20892 USA. NR 48 TC 82 Z9 82 U1 0 U2 3 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD APR 1 PY 1995 VL 40 IS 5 BP 647 EP 659 DI 10.1002/jnr.490400510 PG 13 WC Neurosciences SC Neurosciences & Neurology GA QQ442 UT WOS:A1995QQ44200009 PM 7541476 ER PT J AU DIVGI, CR SCOTT, AM DANTIS, L CAPITELLI, P SILER, K HILTON, S FINN, RD KEMENY, N KELSEN, D KOSTAKOGLU, L SCHLOM, J LARSON, SM AF DIVGI, CR SCOTT, AM DANTIS, L CAPITELLI, P SILER, K HILTON, S FINN, RD KEMENY, N KELSEN, D KOSTAKOGLU, L SCHLOM, J LARSON, SM TI PHASE-I RADIOIMMUNOTHERAPY TRIAL WITH IODINE-131-CC49 IN METASTATIC COLON-CARCINOMA SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE RADIOIMMUNOTHERAPY; IODINE-131-CC49; HEMATOPOIETIC TOXICITY; COLORECTAL CARCINOMA ID B-CELL LYMPHOMA; SINGLE-CHAIN FV; MONOCLONAL-ANTIBODIES; RADIOLABELED-ANTIBODY; IMMUNE-RESPONSE; CANCER-PATIENTS; THERAPY; I-131; BINDING; B72.3 AB CC49 is a murine monoclonal antibody (MAb) that reacts against the TAG-72 antigen. We carried out a Phase I study with escalating doses of I-131-CC49 in patients with advanced colorectal cancer expressing the TAG-72 antigen to determine the dose-limiting toxicity and therapeutic efficacy, if any, of the radioimmunoconjugate. Methods: Twenty-four patients with TAG-72- expressing colorectal cancer were treated with escalating doses of I-131-CC49 Starting at 15 mCi/m(2) and going up to 90 mCi/m(2) of I-131 labeled to 20 mg MAb CC49. Patients were selected if TAG-72 was expressed in greater than or equal to 50% of cells in previously resected tumor and at least one metastasis was demonstrable on standard imaging such as CT. All patients had failed conventional chemotherapy and had not received prior radiotherapy or murine MAb. Patients were under radiation isolation precautions until whole-body radioactivity decreased to less than or equal to 5 mR/hr at 1 m. Whole-body scintigrams were obtained prior to discharge and 1 and 2 wk after infusion in all patients. SPECT imaging was carried out at least once in all patients. Results: All patients had excellent targeting of radioactivity to known tumor sites. There was no nonhematologic toxicity. Hematologic toxicity was more pronounced in those patients who had received extensive prior chemotherapy. There were no major responses. All patients developed an immune response (HAMA) within 4 wk of therapy. Conclusion: Radioimmunotherapy with I-131-CC49 is safe and there is significant therapeutic efficacy in this Phase I trial at the doses studied. There is excellent targeting of radioactivity to antigen-positive tumors. Dose-limiting toxicity is hematopoietic, with the maximum tolerated dose in this group of heavily pretreated patients being 75 mCi/m(2). C1 NCI,BETHESDA,MD 20892. RP DIVGI, CR (reprint author), MEM SLOAN KETTERING CANC CTR,DEPT RADIOL,NUCL MED SERV,1275 YORK AVE,NEW YORK,NY 10021, USA. FU NCI NIH HHS [N01-CA-97609] NR 28 TC 85 Z9 87 U1 0 U2 2 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD APR PY 1995 VL 36 IS 4 BP 586 EP 592 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QQ908 UT WOS:A1995QQ90800019 PM 7699446 ER PT J AU ZIMRAN, A ELSTEIN, D SCHIFFMANN, R ABRAHAMOV, A GOLDBERG, M BARMAOR, JA BRADY, RO GUZZETTA, PC BARTON, NW AF ZIMRAN, A ELSTEIN, D SCHIFFMANN, R ABRAHAMOV, A GOLDBERG, M BARMAOR, JA BRADY, RO GUZZETTA, PC BARTON, NW TI OUTCOME OF PARTIAL SPLENECTOMY FOR TYPE-I GAUCHER DISEASE SO JOURNAL OF PEDIATRICS LA English DT Note AB Partial splenectomy was introduced to achieve the benefits of splenectomy and to avoid the risk of overwhelming infection in patients with symptomatic Gaucher disease. We observed regrowth of the splenic remnant, reemergence of preoperative symptoms, and new bone involvement among most of our patients who had undergone partial splenectomy. Enzyme replacement therapy has markedly limited indications for splenectomy, partial or total, for Gaucher disease. C1 SHAARE ZEDEK MED CTR, DEPT SURG A, IL-91031 JERUSALEM, ISRAEL. RAMBAM MED CTR, DEPT PEDIAT SURG, HAIFA, ISRAEL. NATL INST HLTH, DEV & METAB NEUROL BRANCH, BETHESDA, MD USA. UNIV TEXAS, SW MED CTR, DIV PEDIAT SURG, DALLAS, TX 75235 USA. RP ZIMRAN, A (reprint author), SHAARE ZEDEK MED CTR, GAUCHER CLIN, POB 3235, IL-91031 JERUSALEM, ISRAEL. NR 8 TC 34 Z9 35 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 1995 VL 126 IS 4 BP 596 EP 597 DI 10.1016/S0022-3476(95)70358-6 PG 2 WC Pediatrics SC Pediatrics GA QR212 UT WOS:A1995QR21200016 PM 7699540 ER PT J AU DULIEGE, AM AMOS, CI FELTON, S BIGGAR, RJ ZIEGLER, J CRUIKSHANK, M LEVY, J MEATES, MA GIBB, D MAYAUX, MJ TEGLAS, JP LAURENT, C BLANCHE, S ROUZIOUX, C HELLINGGIESE, G MATTNER, U HOEGER, PH CONLON, T GRIFFIN, E DEMARIA, A BENEDETTO, A PRINCIPI, N GIAQUINTO, C GIANCOMELLI, A MOK, J CASABONA, J FORTUNY, C URIZ, S PEREZ, JM TUSETRUIZ, MC LEON, P ELORZA, JFY CANOSA, C BRANDLE, B SEGER, R NADAL, D IRION, O WYLER, CA DAVIS, P LALLEMANT, M LALLEMANTLECOEUR, S HITIMANA, DG LEPAGE, P VANDEPERRE, P DABIS, F MARUM, L NDUGWA, C TINDYEBWA, D ACENG, E MMIRO, F SUTONGAS, T OLNESS, K LAPOINTE, N RUBINSTEIN, A BURGE, D STECHENBERG, BW COOPER, E REGAN, AM SHIPKOWITZ, S WIZNIA, A BRUNELL, PA COURVILLE, T RUTSTEIN, R MCINTOSH, K PETRU, A OLEARY, M CHURCH, J TAYLOR, S SQUIRES, J MALLORY, M YOGEV, R KLAUKE, B RAKUSAN, T PLUMLEY, S SHELTON, MM WILFERT, C LANE, B ABRAMS, EJ RANA, S CHANDAVASU, O PUVABANDITSIN, S CHOW, JH SHAH, K NACHMAN, S ONEILL, R SELWYN, P SHOENBAUM, E BARZILAI, A WARFORD, R GUPTA, A AHERN, L PAHWA, S PNUGOTI, N GARCIATRIAS, DE BAKSHI, S LANDESMAN, S MENDEZ, H MOROSO, G MENDEZBAUTISTA, RD FIKRIG, S BELMAN, A KLINE, MW HANSON, C EDELSON, P HINDS, G VANDYKE, R CLARK, R WARA, DW MANIO, EB JOHNSON, G WELLS, L JOHNSON, JP ALGER, L LUZURIAGA, K MASTRUCCI, T SUNKUTU, MR RODRIGUEZ, Z DOYLE, M REUBEN, J BRYSON, Y DILLON, M SIMPSON, BJ ANDIMAN, W URIBE, P AF DULIEGE, AM AMOS, CI FELTON, S BIGGAR, RJ ZIEGLER, J CRUIKSHANK, M LEVY, J MEATES, MA GIBB, D MAYAUX, MJ TEGLAS, JP LAURENT, C BLANCHE, S ROUZIOUX, C HELLINGGIESE, G MATTNER, U HOEGER, PH CONLON, T GRIFFIN, E DEMARIA, A BENEDETTO, A PRINCIPI, N GIAQUINTO, C GIANCOMELLI, A MOK, J CASABONA, J FORTUNY, C URIZ, S PEREZ, JM TUSETRUIZ, MC LEON, P ELORZA, JFY CANOSA, C BRANDLE, B SEGER, R NADAL, D IRION, O WYLER, CA DAVIS, P LALLEMANT, M LALLEMANTLECOEUR, S HITIMANA, DG LEPAGE, P VANDEPERRE, P DABIS, F MARUM, L NDUGWA, C TINDYEBWA, D ACENG, E MMIRO, F SUTONGAS, T OLNESS, K LAPOINTE, N RUBINSTEIN, A BURGE, D STECHENBERG, BW COOPER, E REGAN, AM SHIPKOWITZ, S WIZNIA, A BRUNELL, PA COURVILLE, T RUTSTEIN, R MCINTOSH, K PETRU, A OLEARY, M CHURCH, J TAYLOR, S SQUIRES, J MALLORY, M YOGEV, R KLAUKE, B RAKUSAN, T PLUMLEY, S SHELTON, MM WILFERT, C LANE, B ABRAMS, EJ RANA, S CHANDAVASU, O PUVABANDITSIN, S CHOW, JH SHAH, K NACHMAN, S ONEILL, R SELWYN, P SHOENBAUM, E BARZILAI, A WARFORD, R GUPTA, A AHERN, L PAHWA, S PNUGOTI, N GARCIATRIAS, DE BAKSHI, S LANDESMAN, S MENDEZ, H MOROSO, G MENDEZBAUTISTA, RD FIKRIG, S BELMAN, A KLINE, MW HANSON, C EDELSON, P HINDS, G VANDYKE, R CLARK, R WARA, DW MANIO, EB JOHNSON, G WELLS, L JOHNSON, JP ALGER, L LUZURIAGA, K MASTRUCCI, T SUNKUTU, MR RODRIGUEZ, Z DOYLE, M REUBEN, J BRYSON, Y DILLON, M SIMPSON, BJ ANDIMAN, W URIBE, P TI BIRTH-ORDER, DELIVERY ROUTE, AND CONCORDANCE IN THE TRANSMISSION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 FROM MOTHERS TO TWINS SO JOURNAL OF PEDIATRICS LA English DT Article ID POLYMERASE CHAIN-REACTION; HIV-1 INFECTION; WOMEN; RISK; CHILDREN; INFANTS; ANTIBODIES; SECRETIONS; DIAGNOSIS; LABOR AB Background: We evaluated data from prospectively identified twins to understand better the mechanisms and covariates of mother-to-infant transmission of human immunodeficiency virus (HIV). Methods: Using data obtained from an international collaboration and multivariate quasilikelihood modeling, we assessed concordance, birth order, route of delivery, and other factors for HIV infection in 115 prospectively studied twin pairs born to HIV-infected women. Actuarial methods were used to evaluate overall survival and survival free of acquired immunodeficiency syndrome for HIV-infected twins. Results: Infection with HIV occurred in 35% of vaginally delivered firstborn (A) twins, 16% of cesarean-delivered A twins, 15% of vaginally delivered second-born (B) twins, and 8% of cesarean-delivered B twins. In a multivariate model, the adjusted odds ratios for HIV infection were 11.8 (confidence interval: 3.1 to 45.3) for concordance of infection with the co-twin, 2.8 (confidence interval: 1.6 to 5.0) for A versus B twins, and 2.7 (confidence interval: 1.1 to 6.6) for vaginally delivered versus cesarean-delivered twins. Among A twins, 52% (lower confidence limit: 6%) of the transmission risk was related to vaginal delivery, Comparing vaginally delivered A twins (infants most exposed to vaginal mucus and blood) to cesarean-delivered B twins (infants least exposed), 76% (lower confidence limit: 48%) of the transmission risk was related to vaginal exposure. Infected B twins had slightly reduced Quetelet indexes and more rapid development of illnesses related to acquired immunodeficiency syndrome. Conclusions: These results indicate that HIV infection of B twins occurs predominantly in utero, whereas infection of A twins (and, by implication, singletons) occurs predominantly intrapartum, We propose that intrapartum transmission is responsible for the majority of pediatric HIV infections and that reducing exposure to HIV in the birth canal may reduce transmission of the virus from mother to infant. C1 BIOCINE CO, EMERYVILLE, CA USA. MD ANDERSON CANC CTR, DEPT EPIDEMIOL, HOUSTON, TX USA. RES TRIANGLE INST, WASHINGTON, DC USA. NCI, VIRAL EPIDEMIOL BRANCH, ROCKVILLE, MD USA. UNIV NEW S WALES, RANDWICK, NSW, AUSTRALIA. HOP ST PIERRE & ERASME, BRUSSELS, BELGIUM. ROYAL FREE HOSP, LONDON NW3 2QG, ENGLAND. GREAT ORMOND ST HOSP SICK CHILDREN, LONDON, ENGLAND. FRAUNKLIN FINKENAU, HAMBURG, GERMANY. COOMBE LYING IN HOSP, DUBLIN 8, IRELAND. UNIV GENOA, HOSP S MARTINO, I-16126 GENOA, ITALY. SAN CAMILLO HOSP, ROME, ITALY. UNIV MILAN, MILAN, ITALY. UNIV PADUA, PADUA, ITALY. CITY HOSP, EDINBURGH, MIDLOTHIAN, SCOTLAND. CATALAN REGISTRY SEROPOSIT CHILDREN, BARCELONA, SPAIN. GEN HOSP, VALENCIA, SPAIN. UNIV HOSP VALENCIA, VALENCIA, SPAIN. KINDERSPITAL ZURICH, CH-8032 ZURICH, SWITZERLAND. LA FE CHILDRENS HOSP, VALENCIA, SPAIN. UNIV HOSP GENEVA, GENEVA, SWITZERLAND. LLANDOUGH HOSP, CARDIFF, S GLAM, WALES. HARVARD UNIV, SCH PUBL HLTH, ORSTOM, CONGO FRANCE, BOSTON, MA 02115 USA. CTR HOSP KIGALI, KIGALI, RWANDA. UGANDA CASE WESTERN RESERVE UNIV COLLABORAT, KAMPALA, UGANDA. PROJET SIDA, KINSHASA, ZAIRE. CTR DIS CONTROL & PREVENT, ATLANTA, GA 30341 USA. ALBERT EINSTEIN COLL MED, BRONX, NY 10467 USA. HOP ST JUSTINE, MONTREAL, PQ H3T 1C5, CANADA. BAY STATE MED CTR, SPRINGFIELD, MA USA. BOSTON CITY HOSP, BOSTON, MA 02118 USA. BRIDGEPORT HOSP, BRIDGEPORT, CT USA. BRONX LEBANON HOSP CTR, DEPT MED, BRONX, NY 10457 USA. CEDARS SINAI LOS ANGELES, LOS ANGELES, CA USA. CHILDRENS HOSP PHILADELPHIA, PHILADELPHIA, PA 19104 USA. CHILDRENS HOSP, BOSTON, MA USA. CHILDRENS HOSP NO CALIF, OAKLAND, CA USA. CHILDRENS HOSP LOS ANGELES, LOS ANGELES, CA 90027 USA. CHILDRENS MED CTR, DALLAS, TX 75235 USA. CHILDRENS MEM HOSP, CHICAGO, IL 60614 USA. CHILDRENS NATL MED CTR, WASHINGTON, DC 20010 USA. COOK FT WORTH CHILDRENS MED CTR, FT WORTH, TX USA. DUKE UNIV, MED CTR, DURHAM, NC USA. HARLEM HOSP MED CTR, NEW YORK, NY USA. HOWARD UNIV HOSP, WASHINGTON, DC USA. JERSEY CITY MED CTR, JERSEY CITY, NJ USA. LINCOLN HOSP CTR, BRONX, NY USA. MONTEFIORE MED CTR, BRONX, NY 10467 USA. NEW YORK MED COLL, NEW YORK, NY USA. N SHORE UNIV HOSP, MANHASSET, NY USA. ARNAU UNIV HOSP, BAYAMON, PR USA. ST LUKES ROOSEVELT HOSP, BAYSIDE, NY USA. SUNY HLTH SCI CTR, BROOKLYN, NY 11203 USA. SUNY STONY BROOK, CHILDRENS MED CTR, STONY BROOK, NY 11794 USA. TEXAS CHILDRENS HOSP, BAYLOR COLL MED, HOUSTON, TX 77030 USA. CORNELL UNIV, MED CTR, NEW YORK HOSP, NEW YORK, NY 10021 USA. TULANE UNIV, SCH MED, NEW ORLEANS, LA 70112 USA. UNIV CALIF SAN FRANCISCO, SAN FRANCISCO, CA 94143 USA. UNIV CONNECTICUT, CTR HLTH, FARMINGTON, CT USA. UNIV ILLINOIS, CHICAGO, IL USA. UNIV MARYLAND, BALTIMORE, MD 21201 USA. UNIV MASSACHUSETTS, WORCESTER, MA 01605 USA. UNIV MIAMI, MIAMI, FL 33152 USA. UNIV TEXAS, SCH MED, HOUSTON, TX USA. UNIV CALIF LOS ANGELES, MED CTR, LOS ANGELES, CA 90024 USA. YALE NEW HAVEN MED CTR, NEW HAVEN, CT 06504 USA. UNIV CHILE, SANTIAGO, CHILE. RI Van de Perre, Philippe/B-9692-2008 OI Van de Perre, Philippe/0000-0002-3912-0427 FU NCI NIH HHS [N01-CP-95612] NR 31 TC 86 Z9 90 U1 2 U2 6 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 1995 VL 126 IS 4 BP 625 EP 632 DI 10.1016/S0022-3476(95)70365-9 PG 8 WC Pediatrics SC Pediatrics GA QR212 UT WOS:A1995QR21200022 PM 7699546 ER PT J AU MILLER, RW AF MILLER, RW TI PROFILES IN PEDIATRICS .2. WARKANY,JOSEF SO JOURNAL OF PEDIATRICS LA English DT Biographical-Item RP MILLER, RW (reprint author), NCI, EPN-400, BETHESDA, MD 20892 USA. NR 0 TC 1 Z9 1 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 1995 VL 126 IS 4 BP 669 EP 672 DI 10.1016/S0022-3476(95)70375-6 PG 4 WC Pediatrics SC Pediatrics GA QR212 UT WOS:A1995QR21200031 PM 7699554 ER PT J AU TIRELLI, E WITKIN, JM AF TIRELLI, E WITKIN, JM TI DIFFERENTIAL-EFFECTS OF DIRECT AND INDIRECT DOPAMINE AGONISTS ON THE INDUCTION OF GNAWING IN C57BL/6J MICE SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID DISCRIMINATIVE STIMULUS PROPERTIES; D-AMPHETAMINE; STEREOTYPED BEHAVIOR; APOMORPHINE; COCAINE; RATS; RECEPTORS; NEUROLEPTICS; PHENYLETHYLAMINE; PHARMACOLOGY AB The ability of indirect dopamine agonists to induce gnawing in male C57Bl/6J mice was compared to that of direct dopamine agonists acting at dopamine D-1 or D-2 receptor subtypes. Holes left by the mice on the corrugations of packing cardboard were used as an objective index of gnawing. Indirect dopamine agonists, including dopamine releasers such as fencamfamine, (+)-amphetamine and amfenolic acid and dopamine uptake inhibitors such as cocaine, GBR 12909 {1-[2-[bis(4-fluorophenyl)methoxy]ethyl]-4-[3-phenylpropyl]piperazine diHCl} and nomifensine produced dose-dependent increases in gnawing. None of the direct agonists (e.g., apomorphine, quinpirole or SKF 82958 [(+/-)-6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine]) increased gnawing. Although these compounds varied in potency and efficacy, 18 structurally diverse compounds induced gnawing in 100% of the mice tested. Four weak indirect agonists (3,4-methylenedioxymethamphetamine, amantadine, 2-phenylethylamine and benztropine) failed to induce gnawing. The lack of efficacy of postsynaptic dopamine agonists was not changed by various combinations of postsynaptic agonists (e.g., dopamine D-1 and D-2 agonists in combination). Nonetheless, the dopaminergic nature of the gnawing response was confirmed in experiments in which a host of compounds with primary actions at nondopaminergic sites did not induce gnawing; compounds included nicotine, caffeine, dizocilpine, lidocaine, fluoxetine and nisoxetine. In addition, both the dopamine D-1 antagonist SCH 23390 [R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine], the D-2 antagonist eticlopride and the dopamine D-1/D-2 antagonist flupenthixol produced dose-dependent blockade of gnawing induced by either cocaine or methylphenidate, All of the antagonists blocked gnawing at doses below those producing decreases in spontaneous locomotor activity, with eticlopride showing the greatest selectivity in blocking gnawing over locomotor suppression (7- to 14-fold). Given the general contrast between the effects of direct and indirect dopamine agonists, the present procedure could serve as a rapid in vivo method of distinguishing direct- from indirect-acting dopamine agonists. C1 NIDA,ADDICT RES CTR,PSYCHOBIOL LAB,DRUG DEV GRP,BALTIMORE,MD 21224. NR 72 TC 16 Z9 16 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 1995 VL 273 IS 1 BP 7 EP 15 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QT226 UT WOS:A1995QT22600002 PM 7714815 ER PT J AU PELLON, R FLORES, P ALLING, K WITKIN, JM KATZ, JL AF PELLON, R FLORES, P ALLING, K WITKIN, JM KATZ, JL TI PHARMACOLOGICAL ANALYSIS OF THE SCRATCHING PRODUCED BY DOPAMINE D-2 AGONISTS IN SQUIRREL-MONKEYS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID RECEPTOR AGONISTS; SELECTIVE D-1; ANTAGONISTS; MICE; D1; HYPERACTIVITY; APOMORPHINE; SDZ-208-911; STEREOTYPY; BEHAVIORS AB Several dopamine agonists, administered i.m., produced persistent, excessive and non-localized scratching in squirrel monkeys (Saimiri sciureus). Studies were conducted with a series of drugs to determine the pharmacological mechanisms responsible for this effect. All of the dopamine D-2 agonists studied produced dose-related increases in scratching, whereas several dopamine D-1 receptor agonists, indirect dopamine agonists and drugs acting on other receptors failed to produce dose-related increases in scratching. The scratching produced by D-2 agonists was stereospecific; (-)-NPA produced scratching whereas its (+)-enantiomer was inactive up to doses 300-fold higher. Scratching induced by quinpirole was attenuated by both D-2 and D-1 antagonists, and this antagonism was stereospecific, with the D-2 antagonist (-)-eticlopride, but not its enantiomer, active. Sensitivity developed to the effects of D-2 agonists with the quinpirole dose-effect curve shifting to the left by a factor of approximately 64. Two partial D-2 receptor agonists (SDZ 208-911 and SDZ 208-912) had limited efficacy in producing scratching, however, one partial D-2 receptor agonist (terguride) was fully efficacious, suggesting that there are spare receptors for this effect. The peripherally active dopamine antagonist domperidone and the histamine antagonist diphenhydramine also reduced the scratching induced by D-2 agonists, but not to the same extent as centrally acting D-2 antagonists. Scratching in squirrel monkeys is an effect that appears to be due to agonist actions at D-2 receptors, and may be mediated by a release of histamine. This behavioral activity may be useful as an in vivo indication of D-2 receptor activity in primates. C1 NIDA,INTRAMURAL RES PROGRAM,PRECLIN PHARMACOL LAB,PSYCHOL SECT,BALTIMORE,MD 21224. RI Flores, Pilar/B-9217-2008 OI Flores, Pilar/0000-0001-7950-2086 NR 38 TC 5 Z9 5 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 1995 VL 273 IS 1 BP 138 EP 145 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QT226 UT WOS:A1995QT22600018 PM 7714759 ER PT J AU GOZES, I LILLING, G GLAZER, R TICHER, A ASHKENAZI, IE DAVIDSON, A RUBINRAUT, S FRIDKIN, M BRENNEMAN, DE AF GOZES, I LILLING, G GLAZER, R TICHER, A ASHKENAZI, IE DAVIDSON, A RUBINRAUT, S FRIDKIN, M BRENNEMAN, DE TI SUPERACTIVE LIPOPHILIC PEPTIDES DISCRIMINATE MULTIPLE VASOACTIVE-INTESTINAL-PEPTIDE RECEPTORS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID RAT SUPRACHIASMATIC NUCLEUS; ISOLEUCINE-MESSENGER-RNA; FUNCTIONAL EXPRESSION; NEUROTROPHIC ACTION; NEURONAL SURVIVAL; CEREBRAL-CORTEX; VIP ANTAGONIST; CYCLIC-AMP; CELLS; LOCALIZATION AB To distinguish vasoactive intestinal peptide (VIP) receptors in the brain-mediating neurotransmission and neurotrophism, potent VIP analogues were designed. Using a single amino acid substitution and the addition of a fatty acyl moiety, an analogue was devised that exhibited both a 100-fold greater potency than VIP and specificity for a VIP receptor associated with neuronal survival. This VIP agonist increased neuronal survival via a cAMP-independent mechanism. Identical chemical modification of a prototype VIP antagonist (Met-Hybrid, Neurotensin(6-11)-VIP7-28) also resulted in a 100-fold greater potency in blocking VIP-mediated increases in neuronal survival. Blockade of circadian activity rhythms was limited to VIP antagonists that could inhibit VIP-mediated increases in cAMP. These lipophilic peptides provide novel tools in receptor discrimination and drug design. C1 TEL AVIV UNIV,SACKLER SCH MED,DEPT HUMAN GENET,IL-69978 TEL AVIV,ISRAEL. TEL AVIV UNIV,SACKLER SCH MED,DEPT HUMAN GENET,IL-69978 TEL AVIV,ISRAEL. WEIZMANN INST SCI,DEPT ORGAN CHEM,IL-76100 REHOVOT,ISRAEL. NICHHD,DEV NEUROBIOL LAB,DEV & MOLEC PHARMACOL SECT,BETHESDA,MD 20892. RP GOZES, I (reprint author), TEL AVIV UNIV,SACKLER SCH MED,DEPT CLIN BIOCHEM,IL-69978 TEL AVIV,ISRAEL. NR 40 TC 93 Z9 95 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 1995 VL 273 IS 1 BP 161 EP 167 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QT226 UT WOS:A1995QT22600021 PM 7714762 ER PT J AU YURDAYDIN, C LI, Y HA, JH JONES, EA ROTHMAN, R BASILE, AS AF YURDAYDIN, C LI, Y HA, JH JONES, EA ROTHMAN, R BASILE, AS TI BRAIN AND PLASMA-LEVELS OF OPIOID-PEPTIDES ARE ALTERED IN RATS WITH THIOACETAMIDE-INDUCED FULMINANT HEPATIC-FAILURE - IMPLICATIONS FOR THE TREATMENT OF HEPATIC-ENCEPHALOPATHY WITH OPIOID ANTAGONISTS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID BENZODIAZEPINE RECEPTOR LIGANDS; BETA-ENDORPHIN CONCENTRATIONS; MET-ENKEPHALIN; METHIONINE ENKEPHALIN; LEU-ENKEPHALIN; LIVER-DISEASE; ANIMAL-MODEL; STRESS; IMMUNOREACTIVITY; NALOXONE AB Although plasma levels of Met-enkephalin and beta-endorphin are elevated in patients suffering from liver failure, it is not known whether central nervous system (CNS) opioidergic neurotransmission is altered in these patients. Such changes may contribute to the motor dysfunction, psychiatric abnormalities and CNS depression observed in hepatic encephalopathy (HE). Therefore, Met- and Leu-enkephalin, dynorphin A and beta-endorphin levels were measured in discrete brain regions and plasma from thioacetamide-treated rats in Stages II to IV of HE. Pituitary and plasma beta-endorphin, Met- and Leu-enkephalin concentrations increased with the severity of HE by 50 to 290%. Pituitary and brainstem dynorphin A levels increased whereas plasma levels decreased in rats with thioacetamide-induced fulminant hepatic failure. Both striatal Met- and Leu-enkephalin levels increased and hypothalamic concentrations decreased in HE. Concurrent with the increase in striatal Met-enkephalin levels was a 26 to 48% decrease in the density of striatal and hypothalamic delta receptors. No change in either the density or affinity of radioligand binding to mu or delta receptors was observed in the CNS. Finally, administering (+/-)-naloxone (5 and 10 mg/kg) or (+/-)-naltrexone (5-15 mg/kg), but not (+)-naloxone (10 mg/kg), significantly increased the motor activity of rats with Stage III HE. Whereas elevated plasma levels of opioid peptides may play a role in the peripheral manifestations of hepatic failure (ascites and hypotension), increased CNS levels of these peptides may be involved in the neuropsychiatric abnormalities characteristic of HE. Thus, opioid antagonists may be effective in ameliorating some of the neurological manifestations of HE. C1 NIADDKD,LIVER DIS SECT,BETHESDA,MD 20892. NIH,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,BETHESDA,MD 20892. NIADDKD,NEUROSCI LAB,BETHESDA,MD. NR 41 TC 32 Z9 33 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 1995 VL 273 IS 1 BP 185 EP 192 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QT226 UT WOS:A1995QT22600024 PM 7714765 ER PT J AU SILVERTHORN, ML DERSCH, CM BAUMANN, MH CADET, JL PARTILLA, JS RICE, KC CARROLL, FI BECKETTS, KM BROCKINGTON, A ROTHMAN, RB AF SILVERTHORN, ML DERSCH, CM BAUMANN, MH CADET, JL PARTILLA, JS RICE, KC CARROLL, FI BECKETTS, KM BROCKINGTON, A ROTHMAN, RB TI STUDIES OF THE BIOGENIC-AMINE TRANSPORTERS .5. DEMONSTRATION OF 2 BINDING-SITES FOR THE COCAINE ANALOG [I-125] RTI-55 ASSOCIATED WITH THE 5-HT TRANSPORTER IN RAT-BRAIN MEMBRANES SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID NOREPINEPHRINE UPTAKE SITES; DOPAMINE UPTAKE COMPLEX; SEROTONIN UPTAKE SITES; HIGH-AFFINITY BINDING; GUINEA-PIG BRAIN; UPTAKE INHIBITOR; LIGAND-BINDING; STRIATAL MEMBRANES; NEURONAL DOPAMINE; H-3 NISOXETINE AB Earlier work characterized the binding of the high-affinity cocaine analog 3 beta-(4-(125)iodophenyl)-tropane-2-carboxylic acid methyl ester ([I-125]RTI-55) to membranes prepared from rat caudate. That investigation demonstrated that [I-125]RTI-55-labeled serotonin (5-HT) transporters in addition to dopamine (DA) transporters and resolved [I-125]RTI-55 binding to 5-HT transporters into two distinct components. In the present study, we characterized [I-125]RTI-55 binding to membranes prepared from whole rat brain minus caudate. The first series of experiments established that [I-125]RTI-55 labels both DA and 5-HT transporters and that 50 nM paroxetine and either 1000 nM 1-[2-(diphenyl methoxy)ethyl]-4-(3-phenylpropyl)homopiperazine (LR1111) or 500 nM (RTI-120) could be used to block [I-125]RTI-55 binding to the 5-HT and DA transporters, thereby generating selective assay conditions for the DA and 5-HT transporters, respectively. Selective lesioning of dopaminergic and serotonergic neurons with intracerebroventricular 6-hydroxydopamine and 5,7-dihydroxytryptamine selectively decreased [I-125]RTI-55 binding to DA and 5-HT transporters, respectively, thereby confirming the selectivity of the assay conditions. The ligand-selectivity pattern of the whole brain minus caudate 5-HT transporter correlated significantly with that of the caudate 5-HT transporter, although there were some striking differences for selected test agents. Additional experiments resolved [I-125]RTI-55 binding to the 5-HT transporter into two components. A ligand-selectivity analysis of the two components failed to identify a highly selective test agent. In summary, the major findings of the present study are that [I-125]RTI-55 labels both DA and 5-HT transporters in membranes prepared from whole brain minus caudate, that 50 nM paroxetine and either 1000 nM LR1111 or 500 nM RTI-120 can be used as a blocking agent to generate selective assay conditions for the DA and 5-HT transporters, respectively, and that [I-125]RTI-55 binding to the 5-HT transporter can be resolved into two similar components. C1 NIDA,ADDICT RES CTR,IRP,CLIN PSYCHOPHARMACOL SECT,BALTIMORE,MD 21224. NIDA,IRP,MOLEC NEUROPSYCHIAT SECT,BALTIMORE,MD 21224. NIDDK,MED CHEM LAB,BETHESDA,MD 20892. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. NR 61 TC 13 Z9 13 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 1995 VL 273 IS 1 BP 213 EP 222 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QT226 UT WOS:A1995QT22600028 PM 7714769 ER PT J AU BILSKY, EJ CALDERON, SN WANG, T BERNSTEIN, RN DAVIS, P HRUBY, VJ MCNUTT, RW ROTHMAN, RB RICE, KC PORRECA, F AF BILSKY, EJ CALDERON, SN WANG, T BERNSTEIN, RN DAVIS, P HRUBY, VJ MCNUTT, RW ROTHMAN, RB RICE, KC PORRECA, F TI SNC-80, A SELECTIVE, NONPEPTIDIC AND SYSTEMICALLY ACTIVE OPIOID-DELTA AGONIST SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID GASTROINTESTINAL TRANSIT; RECEPTOR SUBTYPES; BW373U86; MICE; MOUSE; ANTAGONIST; ANALGESIA; MORPHINE; POTENT; ENKEPHALIN AB The present study has investigated the pharmacology of SNC 80, a nonpeptidic ligand proposed to be a selective delta agonist in vitro and in vivo. SNC 80 was potent in producing inhibition of electrically induced contractions of mouse vas deferens, but not in inhibiting contractions of the guinea pig isolated ileum (IC50 values of 2.73 nM and 5457 nM, respectively). The delta selective antagonist ICI 174,864 (1 mu M) and the mu selective antagonist CTAP (1 mu M) produced 236- and 1.9-fold increases, respectively, in the SNC 80 IC50 value in the mouse vas deferens. SNC 80 preferentially competed against sites labeled by [H-3]naltrindole (delta receptors) rather than against those labeled by [H-3]DAMGO (mu receptors) or [H-3]U69, 593 kappa receptors) in mouse whole-brain assays. The ratios of the calculated K-i values for SNC 80 at mu/delta and kappa/delta sites were 495- and 248-fold, respectively, which indicates a significant degree of delta selectivity for this compound in radioligand binding assays. SNC 80 produced dose- and time-related antinociception in the mouse warm-water tail-flick test after i.c.v., i.th, and i.p. administration. The calculated A(50) values (and 95% C.I.) for SNC 80 administered i.c.v., i.th, and i.p. were 104.9 (63.7-172.7) nmol, 69 (51.8-92.1) nmol and 57 (44.5-73.1) mg/kg, respectively. The i.c.v, administration of SNC 80 also produced dose- and time-related antinociception in the hot-plate test, with a calculated A(50) value (and 95% C.I.) of 91.9 (60.3-140.0) nmol. Intraperitoneal SNC 80 antinociception was antagonized by pretreatment with i.c.v. naloxone (3 nmol), with i.c.v. or i.th. N,N-diallyl-Tyr-(Aib)(2)-Phe-Leu-OH(Aib = alpha-amino isobutyric acid) (4.4 nmol) or with i.p. naltrindole (20 mg/kg), but not i.c.v. or i.th. beta-FNA (18.8 nmol at -24 hr). Furthermore, the antinociceptive effects of i.c.v. SNC 80 were antagonized by i.c.v, pretreatment with either [D-Ala(2),Leu(5),Cys(6)]enkephalin (a putative delta(1) antagonist) or [D-Ala(2), Cys(4)]deltorphin (a putative delta(2) antagonist), but not by beta-funaltrexamine (a mu antagonist). This suggests that the antinociceptive actions of SNC 80 are produced via both opioid delta(1) and delta(2), but not mu, receptors. On the basis of its profile in vivo and in vitro, SNC 80 is perhaps the first highly selective, nonpeptidic and systemically active opioid delta agonist. SNC 80 promises to be a useful compound for the exploration of opioid delta-receptor pharmacology and provides a basis for the further identification of selective nonpeptidic delta ligands. C1 UNIV ARIZONA,HLTH SCI CTR,DEPT PHARMACOL,TUCSON,AZ 85724. UNIV ARIZONA,DEPT CHEM,TUCSON,AZ 85721. BURROUGHS WELLCOME CO,DIV ORGAN CHEM,RES TRIANGLE PK,NC 27709. NIDDK,MED CHEM LAB,BETHESDA,MD 20892. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. RI Polt, Robin/E-2339-2017 OI Polt, Robin/0000-0003-0756-3183 NR 34 TC 174 Z9 175 U1 0 U2 5 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 1995 VL 273 IS 1 BP 359 EP 366 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QT226 UT WOS:A1995QT22600048 PM 7714789 ER PT J AU JENSEN, PS AF JENSEN, PS TI SCALES VERSUS CATEGORIES - NEVER PLAY AGAINST A STACKED DECK SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Discussion RP JENSEN, PS (reprint author), NIMH,CHILD & ADOLESCENT DISORDERS RES BRANCH,ROOM 18C-17,PARKLAWN BLDG,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 5 TC 7 Z9 7 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD APR PY 1995 VL 34 IS 4 BP 485 EP 487 PG 3 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA QP335 UT WOS:A1995QP33500018 ER PT J AU BROWN, LJ CALDWELL, SB EKLUND, SA AF BROWN, LJ CALDWELL, SB EKLUND, SA TI HOW FEE AND INSURANCE CHANGES COULD AFFECT DENTISTRY - RESULTS FROM A MICROSIMULATION MODEL SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article AB Dentists have become concerned about the possible impact of reductions in dental insurance coverage. The authors used a microsimulation model of the dental sector to assess the potential impact of reductions in the percentage of Americans with dental insurance, in universal dental insurance coverage for children and in fees paid to dentists for their services. The model predicted that reductions in dental insurance coverage would reduce per capita dental expenditures, but that the impact would not be large. Fee reductions had the greatest impact on dental expenditures of any change simulated by the model. C1 NIDR,ORAL DIS PREVENT PROGRAM,BETHESDA,MD 20892. CORNELL UNIV,ITHACA,NY 14853. UNIV MICHIGAN,ANN ARBOR,MI 48109. RP BROWN, LJ (reprint author), NIDR,DIV EPIDEMIOL,45 CTR DR,MSC 6401,NATCHER BLDG,ROOM 4AS 13-E,BETHESDA,MD 20892, USA. NR 17 TC 3 Z9 3 U1 0 U2 3 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD APR PY 1995 VL 126 IS 4 BP 449 EP 459 PG 11 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QR225 UT WOS:A1995QR22500012 PM 7722105 ER PT J AU FLANDERS, RA BHAT, M AF FLANDERS, RA BHAT, M TI THE INCIDENCE OF OROFACIAL INJURIES IN SPORTS - A PILOT-STUDY IN ILLINOIS SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article ID PLAYERS; TRAUMA AB This pilot study of sports-related injuries in Illinois confirms that football players do not encounter orofacial injuries as often as other athletes. The authors attribute this to mandatory use of face-guards and mouth protectors in football and recommend that mouthguards be used by all players of contact sports. C1 NIDR,CRANIOFACIAL DEV & DISORDERS PROGRAM,EXTRAMURAL PROGRAM,BETHESDA,MD 20892. RP FLANDERS, RA (reprint author), ILLINOIS DEPT PUBL HLTH,DIV DENT HLTH,525-535 W JEFFERSON ST,SPRINGFIELD,IL 62761, USA. NR 18 TC 57 Z9 60 U1 0 U2 0 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD APR PY 1995 VL 126 IS 4 BP 491 EP 496 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QR225 UT WOS:A1995QR22500018 PM 7722111 ER PT J AU SALBE, AD AF SALBE, AD TI RD INTERVENTION IMPROVED NUTRITIONAL-STATUS - REPLY SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION LA English DT Letter RP SALBE, AD (reprint author), NATL INST DIABET & DIGEST & KIDNEY DIS,CLIN DIABET & NUTR SECT,PHOENIX,AZ, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER DIETETIC ASSN PI CHICAGO PA 216 W JACKSON BLVD #800, CHICAGO, IL 60606-6995 SN 0002-8223 J9 J AM DIET ASSOC JI J. Am. Diet. Assoc. PD APR PY 1995 VL 95 IS 4 BP 412 EP 412 DI 10.1016/S0002-8223(95)00106-9 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QT197 UT WOS:A1995QT19700003 ER PT J AU WETLE, T SCHERR, P BRANCH, LG RESNICK, NM HARRIS, T EVANS, D TAYLOR, JO AF WETLE, T SCHERR, P BRANCH, LG RESNICK, NM HARRIS, T EVANS, D TAYLOR, JO TI DIFFICULTY WITH HOLDING URINE AMONG OLDER PERSONS IN A GEOGRAPHICALLY DEFINED COMMUNITY - PREVALENCE AND CORRELATES SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID INCONTINENCE; QUESTIONNAIRE; POPULATION; SYMPTOMS; PATTERNS; SEVERITY; IMPACT; WOMEN; HOME AB OBJECTIVE: The goal of this study was to estimate the prevalence and correlates of difficulty holding urine among a population of community-dwelling older people. DESIGN: Population-based cross-sectional study. SUBJECTS: A population census identified all residents aged 65 years and older residing in East Boston, Massachusetts, in 1982. MEASURES: Data collected via in-home interviews were used to estimate the prevalence of difficulty holding urine and to provide information regarding potential, correlates of urinary difficulty. RESULTS: Of the 3809 study participants (85% response rate), 28% reported having ''difficulty holding urine until they can get to a toilet'' at least some of the time, and 8% reported difficulty ''most'' or ''all of the time.'' Difficulty was associated with age and sex; 44% of women and 34% of men reported some difficulty (P <.001), and 9% of women and 6% of men (P <.001) reported difficulty most or all of the time. For respondents aged 65 to 74 years, 40% reported some difficulty, compared with 47% of those aged 85 and older (P-trend <.001); difficulty most or all of the time was reported by 6% of those aged 65 to 74 and 12% of those aged 85 and older (P-trend <0.01) Difficulty holding urine was associated with important health and functional measures including depression, stroke, chronic cough, night awakening, fecal incontinence, problems with activities of daily living, decreased frequency and ease in getting out of the house, and poor self-perception of health. CONCLUSIONS: Difficulty holding urine is a prevalent condition among older people living in the community and is associated highly with a number of health conditions and functional problems. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH MED,DIV AGING,BOSTON,MA 02115. CTR DIS CONTROL & PREVENT,AGING STUDIES BRANCH,ATLANTA,GA 30341. BOSTON UNIV,SCH MED,BOSTON,MA 02118. ABT ASSOCIATES INC,BOSTON,MA. W ROXBURY DVAMC,GRECC,BROCKTON,MA. HEBREW REHABIL CTR AGED,DIV UROL,BOSTON,MA. UNIV CONNECTICUT,CTR HLTH,DEPT COMMUNITY MED & HLTH CARE,STORRS,CT 06269. NIA,BETHESDA,MD 20892. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. RP WETLE, T (reprint author), INST LIVING,400 WASHINGTON ST,HARTFORD,CT 06106, USA. FU NIA NIH HHS [N0 1-AG-0-2106] NR 42 TC 98 Z9 98 U1 2 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 1995 VL 43 IS 4 BP 349 EP 355 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA QR082 UT WOS:A1995QR08200004 PM 7706622 ER PT J AU DUBERSEIN, PR CONWELL, Y COX, C PODGORSKI, CA GLAZER, RS CAINE, ED AF DUBERSEIN, PR CONWELL, Y COX, C PODGORSKI, CA GLAZER, RS CAINE, ED TI ATTITUDES TOWARD SELF-DETERMINED DEATH - A SURVEY OF PRIMARY-CARE PHYSICIANS SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ASSISTED SUICIDE AB OBJECTIVE: To survey physicians to determine whether sociodemographic and practice-related variables are predictive of their attitudes toward suicide. DESIGN: Mailed questionnaire survey. SETTING: Monroe County, New York. PARTICIPANTS: A 50 percent random sample of practicing primary care physicians. Of 186 potential respondents, 114 (61.3%) physicians returned questionnaires. MEASUREMENT: In addition to age and gender, independent variables included medical specialty, practice composition defined in terms of patient age, and textbook knowledge of depression and suicide. The dependent variable, attitude toward suicide, was measured using four standard opinion survey questions and six items based on a case vignette. Dependent variables were rated on a Likert-type scale and subsequently dichotomized for use in logistic regression analysis. RESULTS: Approximately 61 percent of the respondents believe that suicide can be rational under certain circumstances, 51 percent believe that physicians should not assist suicides under any circumstances, and 31 percent support legalization of assisted suicide under certain circumstances. Regression analyses revealed that gender was a significant predictor for three of the ten attitude items. Medical specialty, clinical and epidemiological knowledge of depression and suicide, and physician age significantly predicted one attitude item. CONCLUSIONS: These results suggest that physicians' attitudes toward suicide are multidetermined. Although gender, age, medical specialty, and knowledge of depression and suicide predict certain attitudes, the logistic regression analyses were not highly successful in predicting respondents' attitudes. Given the power of physicians to command public attention and to influence public and legal opinion, it is vital that future research continue to explore the determinants of physicians' attitudes toward self-determined death. C1 UNIV ROCHESTER,SCH MED,DEPT PSYCHIAT,ROCHESTER,NY 14627. UNIV ROCHESTER,SCH MED,DEPT BIOSTAT,ROCHESTER,NY 14627. RP DUBERSEIN, PR (reprint author), UNIV ROCHESTER,MED CTR,NIMH,CLIN RES CTR STUDY PSYCHOPATHOL ELDERLY,300 CRITTENDEN BLVD,ROCHESTER,NY 14642, USA. FU PHS HHS [K07 00748, P30 40381] NR 28 TC 46 Z9 46 U1 0 U2 1 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 1995 VL 43 IS 4 BP 395 EP 400 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA QR082 UT WOS:A1995QR08200012 PM 7706630 ER PT J AU VEITH, FJ ABBOTT, WM YAO, JST GOLDSTONE, J WHITE, RA ABEL, D DAKE, MD ERNST, CB FOGARTY, TJ JOHNSTON, KW MOORE, WS VANBREDA, A SOPKO, G DIDISHEIM, P RUTHERFORD, RB KATZEN, BT MILLER, DC AF VEITH, FJ ABBOTT, WM YAO, JST GOLDSTONE, J WHITE, RA ABEL, D DAKE, MD ERNST, CB FOGARTY, TJ JOHNSTON, KW MOORE, WS VANBREDA, A SOPKO, G DIDISHEIM, P RUTHERFORD, RB KATZEN, BT MILLER, DC TI GUIDELINES FOR DEVELOPMENT AND USE OF TRANSLUMINALLY PLACED ENDOVASCULAR PROSTHETIC GRAFTS IN THE ARTERIAL SYSTEM SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID ABDOMINAL AORTIC-ANEURYSM; VASCULAR-SURGERY; ANGIOPLASTY; RECOMMENDATIONS; FEASIBILITY; STANDARDS; DISEASE C1 SOC VASC SURG,MANCHESTER,MA. INT SOC CARDIOVASC SURG,MANCHESTER,MA. US FDA,ROCKVILLE,MD 20857. NHLBI,BETHESDA,MD 20892. RP VEITH, FJ (reprint author), MONTEFIORE MED CTR,DEPT SURG,111 E 210TH ST,BRONX,NY 10467, USA. NR 37 TC 80 Z9 83 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD APR PY 1995 VL 21 IS 4 BP 670 EP 685 DI 10.1016/S0741-5214(95)70198-2 PG 16 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA QT922 UT WOS:A1995QT92200013 PM 7707571 ER PT J AU ZHAO, TM ROBINSON, MA BOWERS, FS KINDT, TJ AF ZHAO, TM ROBINSON, MA BOWERS, FS KINDT, TJ TI CHARACTERIZATION OF AN INFECTIOUS MOLECULAR CLONE OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE-I SO JOURNAL OF VIROLOGY LA English DT Article ID TROPICAL SPASTIC PARAPARESIS; COMPLETE NUCLEOTIDE-SEQUENCE; HTLV-I; GENE; PARTICLES; PROVIRUS; LYMPHOMA; DISEASE; RABBITS; RETROVIRUSES AB An infectious molecular clone of human T-cell leukemia virus type I (HTLV-I) was derived from an HTLV-I-transformed rabbit T-cell line, RH/K30, obtained by coculture of rabbit peripheral blood mononuclear cells (PBMC) with the human HTLV-I-transformed cell line MT-2. The RH/K30 cell line contained two integrated proviruses, an intact HTLV-I genome and an apparently defective provirus with an in-frame stop codon in the env gene. A genomic DNA fragment containing the intact HTLV-I provirus was cloned into bacteriophage lambda (K30 phi) and subcloned into a plasmid vector (K30p). HTLV-I p24(gag) protein was detected in culture supernatants of human and rabbit T-cell and fibroblast lines transfected with these clones, at levels comparable to those of the parental cell line RH/K30. Persistent expression of virus was observed in one of these lines, RL-5/K30p, for more than 24 months. Biologic characterization of this cell line revealed the presence of integrated HTLV-I provirus, spliced and unspliced mRNA transcripts, and typical extracellular type C retrovirus particles. As expected, these virus particles contained HTLV-I RNA and reverse transcriptase activity. The transfected cells also expressed surface major histocompatibility complex class II, whereas no expression of this molecule was detected in the parental RL-5 cell line. Virus was passaged by cocultivation of irradiated RL-5/K30p cells with either rabbit PBMC or human cord blood mononuclear cells, demonstrating in vitro infectivity. The virus produced in these cells was also infectious in vivo, since rabbits injected with RL-5/K30p cells became productively infected, as evidenced by seroconversion, amplification of HTLV-I-specific sequences by PCR from PBMC DNA, and virus isolation from PBMC. Availability of infectious molecular clones will facilitate functional studies of HTLV-I genes and gene products. C1 NIAID,TWINBROOK FACIL 2,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 47 TC 52 Z9 52 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 1995 VL 69 IS 4 BP 2024 EP 2030 PG 7 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300005 PM 7884847 ER PT J AU URCELAY, E WARD, P WIENER, SM SAFER, B KOTIN, RM AF URCELAY, E WARD, P WIENER, SM SAFER, B KOTIN, RM TI ASYMMETRIC REPLICATION IN-VITRO FROM A HUMAN SEQUENCE ELEMENT IS DEPENDENT ON ADENOASSOCIATED VIRUS REP PROTEIN SO JOURNAL OF VIROLOGY LA English DT Article ID ORIGIN-BINDING-PROTEIN; DNA POLYMERASE-ALPHA; ADENOASSOCIATED VIRUS; SV40 DNA; INVITRO REPLICATION; VIRAL REPLICATION; MAMMALIAN-CELLS; T-ANTIGEN; SITE; INTEGRATION AB The DNA of human parvovirus adeno-associated virus type 2 (AAV) integrates preferentially into a defined region of human chromosome 19. Southern blots of genomic DNA from latently infected cell lines revealed that the provirus was not simply inserted into the cellular DNA. Both, the proviral and adjoining cellular DNA organization indicated that integration occurred by a complex, coordinated process involving limited DNA replication and rearrangements. However, the mechanism for targeted integration has remained obscure. The two larger nonstructural proteins (Rep68 and Rep78) of AAV bind to a sequence element that is present in both the integration locus (P1) and the AAV inverted terminal repeat. This binding may be important for targeted integration. To investigate the mechanism of targeted integration, we tested the cloned integration site subfragment in a cell-free replication assay in the presence or absence of recombinant Rep proteins. Extensive, asymmetric replication of linear or open-circular template DNA was dependent on the presence of P1 sequence and Rep protein. The activities of Rep on the cloned P1 element are analogous to activities on the AAV inverted terminal repeat. Replication apparently initiates from a 3'-OH generated by the sequence specific nicking activity of Rep. This results in a covalent attachment between Rep and the 5'-thymidine of the nick The complexity of proviral structures can be explained by the participation of limited DNA replication facilitated by Rep during integration. C1 NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. CORNELL UNIV,COLL MED,DEPT MICROBIOL,NEW YORK,NY 10021. RI kotin, robert/B-8954-2008 FU ADAMHA HHS [CRADA 91-02] NR 44 TC 110 Z9 111 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 1995 VL 69 IS 4 BP 2038 EP 2046 PG 9 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300007 PM 7884849 ER PT J AU NEUMANN, M FELBER, BK KLEINSCHMIDT, A FROESE, B ERFLE, V PAVLAKIS, GN BRACKWERNER, R AF NEUMANN, M FELBER, BK KLEINSCHMIDT, A FROESE, B ERFLE, V PAVLAKIS, GN BRACKWERNER, R TI RESTRICTION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PRODUCTION IN A HUMAN ASTROCYTOMA CELL-LINE IS ASSOCIATED WITH A CELLULAR BLOCK IN REV FUNCTION SO JOURNAL OF VIROLOGY LA English DT Article ID NECROSIS-FACTOR-ALPHA; VIRAL MESSENGER-RNA; GLIAL-CELLS; TARGET SEQUENCE; GENE-EXPRESSION; TRANS-ACTIVATOR; HTLV-III; HIV-1; PROTEIN; INFECTION AB Chronically human immunodeficiency virus type 1 (HIV-1) strain IIIB-infected human TH4-7-5 astrocytoma cells show low-level virus production. Cocultivation of TH4-7-5 cells,vith myelomonocytic cells led to active virus production in these target cells after a lag period, indicating cell-determined restriction of virus replication in the glial cells. HIV-1 transcript patterns of TH4-7-5 cells contained only a small proportion of Rev-dependent mRNA species, mimicking a Rev-negative phenotype despite the presence of rev mRNAs and protein. Sequencing of the single provirus integrated in TH4-7-5 cells demonstrated that the rev gene and the Rev-responsive element are intact. These results suggested inhibited function of the Rev-regulatory unit in these astrocytoma cells. Transfection of TH4-7-5 cells with a Rev expression plasmid resulted in weak or no induction of proviral p24(gag) antigen levels compared with the dramatic increase observed in Rev-permissive HeLa cells. Immunofluorescence analysis of TH4-7-5 cells transfected with a rev-expressing plasmid revealed prominent cytoplasmic and nuclear-nucleolar localization of Rev, in contrast to the predominant nuclear-nucleolar localization pattern of Rev in HeLa cells. We conclude that restriction of virus production in TH4-7-5 cells is at least partially due to a block in Rev-dependent posttranscriptional regulation of HIV expression. C1 GSF, INST MOLEC VIROL, D-85758 OBERSCHLEISSHEIM, GERMANY. NCI, FREDERICK CANC RES FACIL, ALB BASIC RES PROGRAM, HUMAN RETROVIRUS PATHOGENESIS GRP, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES FACIL, ALB BASIC RES PROGRAM, HUMAN RETROVIRUS SECT, FREDERICK, MD 21702 USA. FU NCI NIH HHS [N0-CO-74101] NR 89 TC 104 Z9 105 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1995 VL 69 IS 4 BP 2159 EP 2167 PG 9 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300022 PM 7884864 ER PT J AU RODERIQUEZ, G ORAVECZ, T YANAGISHITA, M BOUHABIB, DC MOSTOWSKI, H NORCROSS, MA AF RODERIQUEZ, G ORAVECZ, T YANAGISHITA, M BOUHABIB, DC MOSTOWSKI, H NORCROSS, MA TI MEDIATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 BINDING BY INTERACTION OF CELL-SURFACE HEPARAN-SULFATE PROTEOGLYCANS WITH THE V3 REGION OF ENVELOPE GP120-GP41 SO JOURNAL OF VIROLOGY LA English DT Article ID NEUTRALIZING MONOCLONAL-ANTIBODIES; GLYCOPROTEIN GP120; SOLUBLE CD4; SYNCYTIUM FORMATION; HIV-1 VIRIONS; AIDS VIRUS; INFECTION; DOMAIN; RETROVIRUS; GENERATION AB The mechanism of heparan sulfate (HS)-mediated human immunodeficiency virus type 1 (HIV-1) binding to and infection of T cells was investigated with a clone (H9h) of the T-cell line H9 selected on the basis of its high level of cell surface CD4 expression. Semiquantitative PCR analysis revealed that enzymatic removal of cell surface HS by heparitinase resulted in a reduction of the amount of HIV-1 DNA present in H9h cells 4 h after exposure to virus. Assays of the binding of recombinant envelope proteins to H9h cells demonstrated a structural requirement for an oligomeric form of gp120/gp41 for HS-dependent binding to the cell surface, The ability of the HIV-1 envelope to bind simultaneously to HS and CD4 was shown by immunoprecipitation of HS with either antienvelope or anti-CD4 antibodies from (SO42-)-S-35-labeled H9h cells that had been incubated with soluble gp140. Soluble HS blocked the binding of monoclonal antibodies that recognize the V3 and C4 domains of the envelope protein to the surface of H9 cells chronically infected with HIV-1(IIIB). The V3 domain was shown to be the major site of envelope-HS interaction by examining the effects of both antienvelope monoclonal antibodies and heparitinase on the binding of soluble gp140 to H9h cells. C1 US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL PROD,BETHESDA,MD 20892. NIDR,BONE RES BRANCH,BETHESDA,MD 20892. NR 50 TC 185 Z9 186 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 1995 VL 69 IS 4 BP 2233 EP 2239 PG 7 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300030 PM 7884870 ER PT J AU OTT, DE NIGIDA, SM HENDERSON, LE ARTHUR, LO AF OTT, DE NIGIDA, SM HENDERSON, LE ARTHUR, LO TI THE MAJORITY OF CELLS ARE SUPERINFECTED IN A CLONED CELL-LINE THAT PRODUCES HIGH-LEVELS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 STRAIN MN SO JOURNAL OF VIROLOGY LA English DT Article ID HTLV-III; ENVELOPE GLYCOPROTEIN; SURFACE CD4; T-CELLS; NONCYTOPATHIC INFECTION; REVERSE-TRANSCRIPTASE; PRODUCTIVELY INFECT; MOLECULAR CLONE; DOWN-REGULATION; AIDS AB We have isolated seven single-cell clones from an H9 culture infected with human immunodeficiency virus type 1 strain MN so that a stable producer of virus could be obtained. DNAs from these clones were examined by Southern blot analysis and found to contain between one and four proviruses per clone. One of these cell lines, Clone 4, produced high levels of replication-competent virus and contained two proviruses. Southern blot analysis of DNAs from Clone 4 revealed that, after extended culture, some of the cells had acquired additional proviruses, presumably by superinfection. Analysis of Clone 4 single-cell subclones isolated from a late-passage culture found that 14 out of 20 (70%) subclones were reinfected and that 8 out of 20 (40%) were reinfected more than once. Fluorescence-activated cell sorter analysis showed that surface CD4 levels on Clone 4 cells were appropriately down-regulated. Our results indicate that while there is significant interference to superinfection in the Clone 4 culture, it is not absolute and that superinfected cells accumulate in the culture over time in the presence of high virus exposure and extensive cell-to-cell contact. Given our data, it seems likely that superinfection can occur in vivo within the lymphoid reservoirs that harbor human immunodeficiency virus type 1 during the clinically latent period and may contribute to disease progression. RP OTT, DE (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21702, USA. NR 66 TC 34 Z9 34 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 1995 VL 69 IS 4 BP 2443 EP 2450 PG 8 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300057 PM 7884892 ER PT J AU BATTEGAY, M FIKES, J DIBISCEGLIE, AM WENTWORTH, PA SETTE, A CELIS, E CHING, WM GRAKOUL, A RICE, CM KUROKOHCHI, K BERZOFSKY, JA HOOFNAGLE, JH FEINSTONE, SM AKATSUKA, T AF BATTEGAY, M FIKES, J DIBISCEGLIE, AM WENTWORTH, PA SETTE, A CELIS, E CHING, WM GRAKOUL, A RICE, CM KUROKOHCHI, K BERZOFSKY, JA HOOFNAGLE, JH FEINSTONE, SM AKATSUKA, T TI PATIENTS WITH CHRONIC HEPATITIS-C HAVE CIRCULATING CYTOTOXIC T-CELLS WHICH RECOGNIZE HEPATITIS-C VIRUS-ENCODED PEPTIDES BINDING TO HLA-A2.1 MOLECULES SO JOURNAL OF VIROLOGY LA English DT Article ID TERM FOLLOW-UP; LYMPHOCYTE-T; ANTIGENIC SITES; CTL RESPONSES; NON-A; GENOME; SEQUENCE; INTERFERON; INFECTION; INDUCTION AB Antiviral cytotoxic T lymphocytes (CTL) may play a role in clearance of hepatitis C virus (HCV)-infected cells and thereby cause hepatocellular injury during acute and chronic HCV infection. The aim of this study was to identify HLA-A2.1-restricted HCV T-cell epitopes and to evaluate whether anti-HCV-specific CTL are present during chronic hepatitis C. Peripheral blood mononuclear cells from four HLA-A2-positive patients with chronic hepatitis C and from two individuals after recovery from HCV infection were tested against a panel of HCV-encoded peptides derived from different regions of the genome, including some peptides containing HLA-A2.1 binding moths. HLA-A2-negative patients,vith chronic hepatitis C as well as healthy HLA-A2-positive (anti-HCV-negative) donors served as controls. Peripheral blood mononuclear cells stimulated repeatedly with several HCV-encoded peptides (three in core, one in NS4B, and one in NS5B) yielded cytolytic responses. All four HLA-A2-positive patients with active infection had CTL specific for at least one of the identified epitopes, whereas two patients who had recovered from HCV infection had almost no CTL responses. Monoclonal antibody blocking experiments performed for two epitopes demonstrated a class I- and HLA-A2-restricted CTL response. CTL epitopes could partially be predicted by HLA-AZ, binding motifs and more reliably by quantitative HLA-A2.1 molecule binding assays. Most of the identified epitopes could also be produced via the endogenous pathway. Specific CTL against multiple, mostly highly conserved epitopes of HCV were detected during chronic HCV infection. This finding may be important for further investigations of the immunopathogenesis of HCV, the development of potential therapies against HCV on the basis of induction or enhancement of cellular immunity, and the design of vaccines. C1 US FDA,CTR BIOL EVALUAT & RES,DIV VIROL,HEPATITIS RES LAB,BETHESDA,MD 20892. USN,MED RES INST,BETHESDA,MD. NIDDKD,LIVER DIS SECT,BETHESDA,MD. NCI,MOLEC IMMUNOGENET & VACCINE RES SECT,BETHESDA,MD. CYTEL CORP,SAN DIEGO,CA. WASHINGTON UNIV,SCH MED,DEPT MOLEC MICROBIOL,ST LOUIS,MO. RI Yang, Chen/G-1379-2010 FU NCI NIH HHS [CA57973] NR 68 TC 199 Z9 203 U1 0 U2 1 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 1995 VL 69 IS 4 BP 2462 EP 2470 PG 9 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300059 PM 7884894 ER PT J AU FENG, YX FU, W WINTER, AJ LEVIN, JG REIN, A AF FENG, YX FU, W WINTER, AJ LEVIN, JG REIN, A TI MULTIPLE REGIONS OF HARVEY SARCOMA-VIRUS RNA CAN DIMERIZE IN-VITRO SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; CIS ELEMENTS; GENOMIC RNA; INVITRO; SEQUENCES; HIV-1 AB Retroviruses contain a dimeric RNA consisting of two identical molecules of plus-strand genomic RNA. The structure of the linkage between the two monomers is not known, but they are believed to be joined near their 5' ends. Darlix and coworkers have reported that transcripts of retroviral RNA sequences can dimerize spontaneously in vitro (see, for example, E. Bieth, C. Gabus, and J. L. Darlix, Nucleic Acids Res. 18:119-127, 1990). As one approach to identification of sequences which might participate in the linkage, we have mapped sequences derived from the 5' 378 bases of Harvey sarcoma virus (HaSV) RNA which can dimerize in vitro. We found that at least three distinct regions, consisting of nucleotides 37 to 229, 205 to 272, and 271 to 378, can form these dimers. Two of these regions contain nucleotides 205 to 226; computer analysis suggests that this region can form a stem-loop with an inverted repeat in the loop. We propose that this hypothetical structure is involved in dimer formation by these two transcripts. We also compared the thermal stabilities of each of these dimers with that of HaSV viral RNA. Dimers of nucleotides 37 to 229 and 205 to 272 both exhibited melting temperatures near that of viral RNA, while dimers of nucleotides 271 to 378 are quite unstable. We also found that dimers of nucleotides 37 to 378 formed at 37 degrees C are less thermostable than dimers of the same RNA formed at 55 degrees C. It seems possible that bases from all of these regions participate in the dimer linkage present in viral RNA. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MOLEC VIROL & CARCINOGENESIS LAB, FREDERICK, MD 21702 USA. CNRS, INST BIOL MOLEC & CELLULAIRE, UPR 9002, F-67084 STRASBOURG, FRANCE. NICHHD, MOLEC GENET LAB, BETHESDA, MD 20892 USA. FU NCI NIH HHS [N01-CO-74101] NR 30 TC 37 Z9 38 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1995 VL 69 IS 4 BP 2486 EP 2490 PG 5 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300062 PM 7884897 ER PT J AU GOLETTI, D KINTER, AL BISWAS, P BENDE, SM POLI, G FAUCI, AS AF GOLETTI, D KINTER, AL BISWAS, P BENDE, SM POLI, G FAUCI, AS TI EFFECT OF CELLULAR-DIFFERENTIATION ON CYTOKINE-INDUCED EXPRESSION OF HUMAN-IMMUNODEFICIENCY-VIRUS IN CHRONICALLY INFECTED PROMONOCYTIC CELLS - DISSOCIATION OF CELLULAR-DIFFERENTIATION AND VIRAL EXPRESSION SO JOURNAL OF VIROLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; LONG TERMINAL REPEAT; NF-KAPPA-B; MONONUCLEAR PHAGOCYTES; FACTOR-ALPHA; HIV-1 INFECTION; BRAIN-TISSUE; BONE-MARROW; MONOCYTES; AIDS AB Cellular differentiation is thought to play an important role in the susceptibility of monocytic lineage cells to human immunodeficiency virus (HIV) infection as well as in their ability to support virus replication. In addition, virus replication in monocytes/macrophages has been demonstrated in vitro to be strongly modulated by several cytokines such as tumor necrosis factor alpha and granulocyte-macrophage colony-stimulating factor. The purpose of the present study was to investigate the interaction between cellular differentiation and cytokines in the regulation of HIV expression from chronically infected monocytic lineage cells. U1, a persistently HIV-infected promonocytic cell line, is characterized by low levels of virus expression which can be modulated by several cytokines. 1 alpha,-25-Dihydroxyvitamin D3 (Vit.D3), a well-known differentiating agent for myelomonocytic cells which has been previously reported to modulate HIV replication in other in vitro systems, induced maturation of U1 cells toward a macrophage-like phenotype, as demonstrated by the induction of the differentiation-associated cell surface markers CD14 and CD11b. Vit.D3-induced differentiation did not result in induction of HIV expression; however, when U1 cells were stimulated with tumor necrosis factor alpha in the presence of Vit.D3, a synergistic induction of cell differentiation and viral expression was demonstrated. In contrast, Vit.D3 suppressed the induction of HIV expression in U1 cells stimulated,vith gamma interferon, interleukin-6, and granulocyte-macrophage colony-stimulating factor, although synergy between Vit.D3 and these cytokines was observed in terms of cellular differentiation. These data suggest that differentiation of monocytic cells does not necessarily correlate with increased HIV expression. RP GOLETTI, D (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,ROOM 6A33,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. OI Goletti, Delia/0000-0001-8360-4376 NR 44 TC 28 Z9 29 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 1995 VL 69 IS 4 BP 2540 EP 2546 PG 7 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300069 PM 7884904 ER PT J AU HASENKRUG, KJ VALENZUELA, A LETTS, VA NISHIO, J CHESEBRO, B FRANKEL, WN AF HASENKRUG, KJ VALENZUELA, A LETTS, VA NISHIO, J CHESEBRO, B FRANKEL, WN TI CHROMOSOME MAPPING OF RFV3, A HOST-RESISTANCE GENE TO FRIEND MURINE RETROVIRUS SO JOURNAL OF VIROLOGY LA English DT Note ID VIRUS-INDUCED IMMUNOSUPPRESSION; RECOMBINANT-INBRED STRAINS; BETA-CHAIN GENE; LEUKEMIA-VIRUS; EXTENDED GLOBOGLYCOLIPIDS; MOLECULAR-BIOLOGY; MOUSE KIDNEY; RECEPTOR; MICE; INTERLEUKIN-2 AB Inoculation of adult mice with Friend virus complex usually induces rapid viremia and erythroleukemia, resulting in death in 1 to 3 months, In certain mouse strains, a single host gene, Rfv3, controls the ability to mount a virus-specific neutralizing antibody response which results in elimination of viremia. In this study, microsatellite markers were used to localize the Rfv3 gene to a 20-centimorgan region of mouse chromosome 15 unlinked to immunoglobulin loci, T-cell receptor loci, or the major histocompatibility complex. Potential candidate genes for Rfv3 are several genes expressed in cells of the immune system and previously mapped to the same region, including a T-cell antigen gene, Ly6, and three cytokine receptor genes, IL2rb, IL3rb1, and IL3rb2. C1 JACKSON LAB,BAR HARBOR,ME 04609. RP HASENKRUG, KJ (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,903 S 4TH ST,HAMILTON,MT 59840, USA. FU NICHD NIH HHS [HD28882]; NINDS NIH HHS [NS31348] NR 39 TC 28 Z9 29 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 1995 VL 69 IS 4 BP 2617 EP 2620 PG 4 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300079 PM 7884913 ER PT J AU FUENTESPANANA, EM LOPEZ, S GORZIGLIA, M ARIAS, CF AF FUENTESPANANA, EM LOPEZ, S GORZIGLIA, M ARIAS, CF TI MAPPING THE HEMAGGLUTINATION DOMAIN OF ROTAVIRUSES SO JOURNAL OF VIROLOGY LA English DT Note ID SIALIC-ACID; IDENTIFICATION; ANTIBODIES; BINDING; VP4-PROTEIN; CULTURE; INVITRO; INVIVO; VIRUS; CELLS AB Most strains of animal rotaviruses are able to agglutinate erythrocytes, and the surface protein VP4 is the virus hemagglutinin. To map the hemagglutination domain on VP4 while preserving the conformation of the protein, we constructed full-length chimeras between the VP4 genes of hemagglutinating (YM) and nonhemagglutinating (KU) rotavirus strains. The parental and chimeric genes were expressed in insect cells, and the recombinant VP4 proteins were evaluated for their capacity to agglutinate human type O erythrocytes. Three chimeric genes, encoding amino acids 1 to 208 (QKU), 93 to 208 (QC), and 93 to 776 (QYM) of the YM VP4 protein in a KU VP4 background, were constructed. YM VP4 and chimeras QKU and QC were shown to specifically hemagglutinate, indicating that the region between amino acids 93 and 208 of YM VP4 is sufficient to determine the hemagglutination activity of the protein. C1 UNIV NACL AUTONOMA MEXICO,INST BIOTECHNOL,DEPT GENET & FISIOL MOLEC,CUERNAVACA 62271,MORELOS,MEXICO. NIAID,INFECT DIS LAB,EPIDEMIOL SECT,BETHESDA,MD 20892. NR 24 TC 30 Z9 30 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 1995 VL 69 IS 4 BP 2629 EP 2632 PG 4 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300081 PM 7884915 ER PT J AU MORIUCHI, H MORIUCHI, M SMITH, HA STRAUS, SE COHEN, JI AF MORIUCHI, H MORIUCHI, M SMITH, HA STRAUS, SE COHEN, JI TI VARICELLA-ZOSTER VIRUS OPEN READING FRAME-61 PROTEIN IS FUNCTIONALLY HOMOLOGOUS TO HERPES-SIMPLEX VIRUS TYPE-1 ICP0 (VOL 66, PG 7303, 1992) SO JOURNAL OF VIROLOGY LA English DT Correction, Addition RP MORIUCHI, H (reprint author), NIAID,CLIN INVEST LAB,MED VIROL SECT,BETHESDA,MD 20892, USA. NR 1 TC 1 Z9 1 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 1995 VL 69 IS 4 BP 2723 EP 2723 PG 1 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300104 ER PT J AU NAGPAL, S OSTROVE, JM AF NAGPAL, S OSTROVE, JM TI CHARACTERIZATION OF A POTENT VARICELLA-ZOSTER VIRUS-ENCODED TRANS-REPRESSOR (VOL 65, PG 5289, 1991) SO JOURNAL OF VIROLOGY LA English DT Correction, Addition RP NAGPAL, S (reprint author), NIAID,CLIN INVEST LAB,MED VIROL SECT,BETHESDA,MD 20892, USA. NR 1 TC 0 Z9 0 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 1995 VL 69 IS 4 BP 2723 EP 2723 PG 1 WC Virology SC Virology GA QL683 UT WOS:A1995QL68300102 ER PT J AU SMALE, G BENDELE, A HORTON, WE AF SMALE, G BENDELE, A HORTON, WE TI COMPARISON OF AGE-ASSOCIATED DEGENERATION OF ARTICULAR-CARTILAGE IN WISTAR AND FISCHER-344 RATS SO LABORATORY ANIMAL SCIENCE LA English DT Article ID GUINEA-PIGS; OSTEOARTHRITIS AB We have carried out a comparison of cartilage degeneration that develops spontaneously with age in the Wistar and Fischer 344 rats, Young adult (6-month-old) Wistar rats were essentially free of any relevant lesion in the articular cartilage of the knee, Aged (24-month-old) Wistar rats had minimal to mild lesions found mainly in the medial tibial plateau, These lesions were indicated by a focal loss of toluidine blue staining and limited fibrillation. Approximately 68% of the old Wistar rats had some degree of pathologic change, In comparison, 100% of the Fischer 344 rats examined, both young and old, had cartilage degeneration, However, the severity of the lesions increased with age, These two rat strains have variable degrees of spontaneous age-associated cartilage degeneration and would be suitable for testing treatments to prevent or repair the cartilage damage. C1 SYNERGEN CORP,BOULDER,CO 80301. RP SMALE, G (reprint author), NIA,GERONTOL RES CTR,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 14 TC 16 Z9 17 U1 0 U2 1 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI CORDOVA PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018 SN 0023-6764 J9 LAB ANIM SCI JI Lab. Anim. Sci. PD APR PY 1995 VL 45 IS 2 BP 191 EP 194 PG 4 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA QU962 UT WOS:A1995QU96200013 PM 7603023 ER PT J AU YOU, WC ZHAO, L CHANG, YS BLOT, WJ FRAUMENI, JF AF YOU, WC ZHAO, L CHANG, YS BLOT, WJ FRAUMENI, JF TI PROGRESSION OF PRECANCEROUS GASTRIC-LESIONS SO LANCET LA English DT Letter ID CANCER C1 BEIJING INST CANC RES,BEIJING,PEOPLES R CHINA. INT EPIDEMIOL INST,ROCKVILLE,MD. RP YOU, WC (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,EPN ROOM 431,BETHESDA,MD 20892, USA. NR 2 TC 14 Z9 16 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0099-5355 J9 LANCET JI Lancet PD APR 1 PY 1995 VL 345 IS 8953 BP 866 EP 867 DI 10.1016/S0140-6736(95)93006-X PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA QQ195 UT WOS:A1995QQ19500056 PM 7898258 ER PT J AU LI, CCH OCONNELL, CD BECKWITH, M LONGO, DL AF LI, CCH OCONNELL, CD BECKWITH, M LONGO, DL TI DETECTION OF P53 MUTATIONS IN B-CELL NON-HODGKINS-LYMPHOMA CELL-LINES SO LEUKEMIA LA English DT Article DE P53 MUTATION; B CELL LINE; SSCP ID TUMOR-ANTIGEN; SV40-TRANSFORMED CELLS; ACTIVATING MUTATIONS; MALIGNANT-LYMPHOMAS; BURKITT-LYMPHOMA; T-ANTIGEN; WILD-TYPE; GENE; TRANSFORMATION; EXPRESSION AB The p53 tumor suppressor gene is frequently mutated within its evolutionarily conserved regions in a number of human cancers. Previous reports demonstrated mutations of this gene in both Burkitt's lymphoma and B cell chronic lymphocytic leukemia. However, dissimilar results were obtained in non-Hodgkin's lymphoma (NHL). In one study, no mutation was detected in 43 NHL tissues. A second study reported p53 mutations in eight (all with advanced stage disease) out of 48 tissues obtained from Japanese NHL patients. Using both immunoblotting and radio-immunoprecipitation, we detected mutant p53 proteins in nine out of 10 B cell lines established from NHL tissues. The mutations were confirmed by reverse transcription polymerase chain reaction-mediated single-strand conformational polymorphism (RT-PCR-SSCP) analysis in eight cell lines. The high frequency of p53 mutation in NHL B cell lines and the relatively low frequency of p53 mutations in fresh lymphoma tissue suggests that p53 gene alteration may play a role in lymphomagenesis and/or disease progression in a subset of B cell lymphomas and that the p53 mutation conveys a proliferative advantage on lymphoma cells that permits their in vitro growth. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP LI, CCH (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. NR 44 TC 14 Z9 15 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 1995 VL 9 IS 4 BP 650 EP 655 PG 6 WC Oncology; Hematology SC Oncology; Hematology GA QU877 UT WOS:A1995QU87700017 PM 7723400 ER PT J AU WILSON, WA MORGAN, OS BARTON, EN SMIKLE, M HANCHARD, B BLATTNER, WA DOGGETT, S GHARAVI, AE AF WILSON, WA MORGAN, OS BARTON, EN SMIKLE, M HANCHARD, B BLATTNER, WA DOGGETT, S GHARAVI, AE TI IGA ANTIPHOSPHOLIPID ANTIBODIES IN HTLV-1-ASSOCIATED TROPICAL SPASTIC PARAPARESIS SO LUPUS LA English DT Article DE PHOSPHOLIPID ANTIBODIES; TROPICAL SPASTIC PARAPARESIS ID ANTICARDIOLIPIN ANTIBODIES; INFECTION; SYPHILIS AB A retrovirus, human T cell lymphotropic virus type 1 (HTLV-1), is an essential but not a sufficient aetiologic factor for tropical spastic paraparesis (TSP). Because some TSP patients have biological false positive tests for treponemal infections (BFP-STS), we used ELISA to study BFP-STS and anticardiolipin antibodies in 42 Jamaican TSP patients. The data indicate that in TSP anticardiolipin antibodies occur in about 26% of patients, are associated with biological false positive treponemal serology, are relatively restricted to the IgA isotype and may be induced by HTLV-1 or other non-treponemal infections. C1 UNIV W INDIES,KINGSTON,JAMAICA. NIH,BETHESDA,MD. RP WILSON, WA (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT MED,1542 TULANE AVE,NEW ORLEANS,LA 70112, USA. NR 18 TC 18 Z9 18 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0961-2033 J9 LUPUS JI Lupus PD APR PY 1995 VL 4 IS 2 BP 138 EP 141 DI 10.1177/096120339500400210 PG 4 WC Rheumatology SC Rheumatology GA QW364 UT WOS:A1995QW36400010 PM 7795617 ER PT J AU DU, Y REMMERS, EF ZHA, H GOLDMUNTZ, EA SZPIRER, J SZPIRER, C WILDER, RL AF DU, Y REMMERS, EF ZHA, H GOLDMUNTZ, EA SZPIRER, J SZPIRER, C WILDER, RL TI A GENETIC-MAP OF MICROSATELLITE MARKERS ON RAT CHROMOSOME-7 SO MAMMALIAN GENOME LA English DT Article ID POLYMORPHIC MARKERS; LINKAGE MAP; SEQUENCES; NORVEGICUS; LOCI; DNA AB Nine microsatellite loci were mapped to rat Chromosome (Chr) 7 by genetic linkage and somatic cell hybrid analysis. These loci include the gene encoding a member of the IID subfamily of cytochrome P450 (Cyp2d), a gene with repetitive sequences expressed during myotube formation (D7Arble), four anonymous loci, D7Arb81, D7Arb208, D7Arb569, D7Arb609a, and three DNA loci defined by MapPair(TM) markers R245, R513, and R1071. The nine loci were all identified by PCR-based microsatellite polymorphism analysis and were characterized in 40 F-2 intercross progeny of Fischer (F344/N) and Lewis (LEW/N) rats for segregation analysis. These markers formed a single linkage group spanning 76.8 cM with the following order and distances: D7Arb569-11.4 cM-D7Arb81-9.7 cM-R513-2.6 cM-Cyp2d-0.0 cM-R245-1.3 cM-D7Arble-10.4 cM-R1071-15.9 cM-D7Arb609a-15.4 cM-D7Arb208. Physical mapping of Cyp2d by somatic cell hybrid analysis allowed us to assign this linkage group to rat Chr 7. For each marker, two to six alleles were detected in a panel of 16 inbred rat strains (ACI/N, BN/SsN, BUF/N, DA/Bkl, F344/N, LER/N, LEW/N, LOU/MN, MNR/N, MR/N, SHR/N, SR/Jr, SS/Jr, WBB1/N, WBB2/N, WKY/N). C1 FREE UNIV BRUSSELS,DEPT BIOL MOLEC,B-1640 RHODE ST GENESE,BELGIUM. RP DU, Y (reprint author), NIAMSD,ARTHRITIS & RHEUMATISM BRANCH,BLDG 10,ROOM 9N228,BETHESDA,MD 20892, USA. NR 19 TC 10 Z9 10 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD APR PY 1995 VL 6 IS 4 BP 295 EP 298 DI 10.1007/BF00352420 PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA QT164 UT WOS:A1995QT16400017 PM 7613038 ER PT J AU SCHERER, SW HENG, HHQ ROBINSON, GW MAHON, KA EVANS, JP TSUI, LC AF SCHERER, SW HENG, HHQ ROBINSON, GW MAHON, KA EVANS, JP TSUI, LC TI ASSIGNMENT OF THE HUMAN HOMOLOG OF MOUSE DLX3 TO CHROMOSOME 17Q21.3-Q22 BY ANALYSIS OF SOMATIC-CELL HYBRIDS AND FLUORESCENCE IN-SITU HYBRIDIZATION SO MAMMALIAN GENOME LA English DT Note ID REGIONS; FAMILY; GENES C1 UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO,ON M5G 1X8,CANADA. HOSP SICK CHILDREN,DEPT GENET,TORONTO,ON M5G 1X8,CANADA. NICHHD,MAMMALIAN GENES & DEV LAB,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT MED,CHAPEL HILL,NC. RI Tsui, Lap-chee/A-1081-2010; Robinson, Gertraud/I-2136-2012; Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013 OI Scherer, Stephen /0000-0002-8326-1999 NR 10 TC 19 Z9 19 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD APR PY 1995 VL 6 IS 4 BP 310 EP 311 DI 10.1007/BF00352432 PG 2 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA QT164 UT WOS:A1995QT16400029 PM 7613049 ER PT J AU WARBURG, A PIMENTA, PF AF WARBURG, A PIMENTA, PF TI A CYTOPLASMIC POLYHEDROSIS-VIRUS IN THE PHLEBOTOMINE SANDFLY LUTZOMYIA-LONGIPALPIS SO MEDICAL AND VETERINARY ENTOMOLOGY LA English DT Note DE LEISHMANIA DONOVANI CHAGASI; LUTZOMYIA LONGIPALPIS; PHLEBOTOMUS PAPATSI; PHLEBOTOMINAE; PSYCHODIDAE; CYTOPLASMIC POLYHEDROSIS VIRUS; VECTOR COMPETENCE; BRAZIL ID LEISHMANIASIS C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RP WARBURG, A (reprint author), HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PARASITOL,IL-91010 JERUSALEM,ISRAEL. NR 8 TC 4 Z9 4 U1 1 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-283X J9 MED VET ENTOMOL JI Med. Vet. Entomol. PD APR PY 1995 VL 9 IS 2 BP 211 EP 213 DI 10.1111/j.1365-2915.1995.tb00182.x PG 3 WC Entomology; Veterinary Sciences SC Entomology; Veterinary Sciences GA QQ941 UT WOS:A1995QQ94100018 PM 7787233 ER PT J AU LADANYI, A TIMAR, J BOCSI, J TOVARI, J LAPIS, K AF LADANYI, A TIMAR, J BOCSI, J TOVARI, J LAPIS, K TI SEX-DEPENDENT LIVER METASTASIS OF HUMAN-MELANOMA LINES IN SCID MICE SO MELANOMA RESEARCH LA English DT Article DE MELANOMA; METASTASIS; SCID MICE; SEX HORMONES AB The liver metastasis formation of two human melanoma cell lines were compared in male and female SCID mice. The intrasplenic injection of both tumour lines resulted in a significantly higher number of liver metastases in male than in female mice; the incidence and weight of spleen tumours, as well as the incidence of metastases were similar. Both melanoma cell lines bound fluorescent oestradiol, progesterone and testosterone conjugates, and proved to be positive for oestrogen receptor-related protein by immunocytochemistry, These observations support the view that endocrine factors influence the progression of human melanomas. This SCID mouse model could be useful in studying the effects of hormonal manipulations on human melanoma metastases. RP LADANYI, A (reprint author), NCI,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2B37,BETHESDA,MD 20892, USA. NR 0 TC 18 Z9 18 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0960-8931 J9 MELANOMA RES JI Melanoma Res. PD APR PY 1995 VL 5 IS 2 BP 83 EP 86 DI 10.1097/00008390-199504000-00002 PG 4 WC Oncology; Dermatology; Medicine, Research & Experimental SC Oncology; Dermatology; Research & Experimental Medicine GA QP161 UT WOS:A1995QP16100002 PM 7620343 ER PT J AU RUSSO, TA SHARMA, G WEISS, J BROWN, C AF RUSSO, TA SHARMA, G WEISS, J BROWN, C TI THE CONSTRUCTION AND CHARACTERIZATION OF COLANIC ACID-DEFICIENT MUTANTS IN AN EXTRAINTESTINAL ISOLATE OF ESCHERICHIA-COLI (O4/K54/H5) SO MICROBIAL PATHOGENESIS LA English DT Article DE ESCHERICHIA COLI; VIRULENCE; CAPSULAR POLYSACCHARIDE; COLANIC ACID; COMPLEMENT; BACTERICIDAL PERMEABILITY-INCREASING PROTEIN; ANIMAL MODEL ID CAPSULAR POLYSACCHARIDE SYNTHESIS; PERMEABILITY-INCREASING PROTEIN; ANTIGEN; LIPOPOLYSACCHARIDE; GENERATION; EXPRESSION; DISRUPTION; FRAGMENT; GENES; RCSA AB Extraintestinal strains of Escherichia coli possess a variety of virulence factors that enable them to cause disease. These strains express a group 2 capsular polysaccharide which is important in the pathogenic process. Extraintestinal strains evaluated to date are also capable of producing the group 1 capsular polysaccharide colanic acid. The blood isolate CP9 (O4/K54/H5) constitutively produces the group 2, K54 capsule but can be induced to produce colanic acid. In this report we assess whether colanic acid contributes to the pathogenesis of this extraintestinal pathogen. CP9 and its derivatives that are deficient in their ability to produce colanic acid (TR94), the K54 group 2 capsule +/- colanic acid (CP9.137, TR1374) and the O4 specific antigen +/- colanic acid (CP921,CP925) were used to test whether the group 1 capsule colanic acid conferred protection against the bactericidal effects of serum and recombinant bactericidal/permeability-increasing protein (rBPI-23) in vitro. Additionally, CP9, CP9.137 and TR94 were evaluated in the rat granuloma pouch, an in vivo model for localized infection, and. by intraperitoneal inoculation into mice, a systemic infection model. In summary, the inability of CP9 to produce colanic acid in the presence or absence of its K54 and O4 antigens had no effect on its ability to survive these host defenses in vitro and did not affect its virulence in these two in vivo models of infection. C1 NIAID, CLIN INVEST LAB, BACTERIAL PATHOGENESIS UNIT, BETHESDA, MD 20892 USA. NYU, SCH MED, DEPT MICROBIOL, NEW YORK, NY 10016 USA. NYU, SCH MED, DEPT MED, NEW YORK, NY 10016 USA. RP RUSSO, TA (reprint author), SUNY BUFFALO, CTR CLIN, DEPT MED, ROOM BB103, 462 GRIDER ST, BUFFALO, NY 14215 USA. NR 26 TC 18 Z9 18 U1 0 U2 1 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0882-4010 J9 MICROB PATHOGENESIS JI Microb. Pathog. PD APR PY 1995 VL 18 IS 4 BP 269 EP 278 DI 10.1016/S0882-4010(05)80003-8 PG 10 WC Immunology; Microbiology SC Immunology; Microbiology GA RL154 UT WOS:A1995RL15400003 PM 7476092 ER PT J AU MYERS, RB SCHLOM, J SRIVASTAVA, S GRIZZLE, WE AF MYERS, RB SCHLOM, J SRIVASTAVA, S GRIZZLE, WE TI EXPRESSION OF TUMOR-ASSOCIATED GLYCOPROTEIN-72 IN PROSTATIC INTRAEPITHELIAL NEOPLASIA AND PROSTATIC ADENOCARCINOMA SO MODERN PATHOLOGY LA English DT Article DE TUMOR-ASSOCIATED GLYCOPROTEIN 72; PROSTATIC ADENOCARCINOMAS; PROSTATIC INTRAEPITHELIAL NEOPLASIA ID MONOCLONAL-ANTIBODY B72.3; ANTIGEN; DYSPLASIA; REACTIVITY; CARCINOMA; CANCER AB Tumor-associated glycoprotein 72 is a high-molecular-weight sialomucin that is expressed selectively in various adenocarcinomas, including those of the prostate. We utilized the monoclonal antibodies B72.3 and CC49 to examine the expression of TAG-72 in high-grade prostatic intraepithelial neoplasia (PIN), localized adenocarcinomas (pathologic stages B and C), as well as matching primary and nodal lesions from patients with stage D adenocarcinomas. Immunoreactivity within PIN lesions was detected within 20 (87%) and 17 (74%) of 23 specimens immunostained with B72.3 and CC49, respectively. Benign epithelium and stromal tissue did not immunostain with either antibody at the concentrations tested. Immunostaining was detected within the malignant cells in 30 (77%) and 35 (90%) of 39 localized adenocarcinomas using B72.3 and CC49, respectively. Immunostaining was localized to the cytoplasm and cellular membranes of the malignant cells and within the lumen of malignant glands. Seven of 17 (41%) primary lesions from patients with stage D adenocarcinomas demonstrated immunoreactivity when stained with B72.3. Immunoreactivity was detected in 8 of 10 (80%) of these tissues immunostained with CC49. Within nodal lesions obtained from these patients, immunostaining was observed in 3 of 17 (18%) and 6 of 10 (60%) of the specimens immunostained with B72.3 and CC49, respectively. We used a semiquantitative technique to compare the extent of immunoreactivity among well-differentiated (Gleason score <6), moderately differentiated (Gleason 6-7), and poorly differentiated (Gleason score >7) tumors. We observed an inverse correlation of TAG-72 expression to Gleason scores. Furthermore, TAG-72 expression was reduced in the matching primary and metastatic lesions of stage D adenocarcinomas as compared to localized lesions. These findings demonstrate a phenotypic relationship of PIN to invasive adenocarcinomas and support the concept that PIN is a preinvasive neoplastic lesion. Furthermore, expression of TAG-72 may represent an early event in the neoplastic transformation of the prostatic epithelium. The data demonstrate a diminution in TAG-72 expression in poorly differentiated and advanced-stage prostatic adenocarcinomas. C1 UNIV ALABAMA,DEPT PATHOL,BIRMINGHAM,AL 35294. NATL CANC INST,BETHESDA,MD. NR 23 TC 18 Z9 18 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD APR PY 1995 VL 8 IS 3 BP 260 EP 265 PG 6 WC Pathology SC Pathology GA QV864 UT WOS:A1995QV86400011 PM 7617651 ER PT J AU SHERMAN, ME FRIEDMAN, HB BUSSENIERS, AE KELLY, WF CARNER, TC SAAH, AJ AF SHERMAN, ME FRIEDMAN, HB BUSSENIERS, AE KELLY, WF CARNER, TC SAAH, AJ TI METHODS IN PATHOLOGY - CYTOLOGIC DIAGNOSIS OF ANAL INTRAEPITHELIAL NEOPLASIA USING SMEARS AND CYTYC THIN-PREPS SO MODERN PATHOLOGY LA English DT Article DE ANAL INTRAEPITHELIAL NEOPLASIA; DYSPLASIA; SQUAMOUS INTRAEPITHELIAL LESIONS; CYTYC; THIN-PREP; CYTOLOGY; HUMAN IMMUNODEFICIENCY VIRUS; HUMAN PAPILLOMAVIRUS ID HUMAN PAPILLOMAVIRUS INFECTION; HUMAN IMMUNODEFICIENCY VIRUS; MULTICENTER AIDS COHORT; HOMOSEXUAL MEN; HIV-INFECTION; ASSOCIATION; DYSPLASIA; CANCER; WARTS AB To investigate the optimal cytologic method for detecting anal intraepithelial neoplasia, the quality and diagnostic findings in 117 conventionally prepared smears and 191 CYTYC Thin-Preps were compared, Samples were obtained with a dacron swab from subjects participating in a longitudinal study of gay or bisexual men known as the Study to Help the AIDS Research Effort (SHARE). The smear takers were general clinicians who had no experience in obtaining cytologic specimens from the anus. Smears were entirely satisfactory in 48 (41.0%) subjects, limited for interpretation in 41 (35.0%), and unsatisfactory in 28 (23.9%). CYTYC preparations were satisfactory in 158 (82.7%) cases and unsatisfactory in 33 (17.3%). Insufficient cellularity was the most frequent reason for both unsatisfactory smears and CYTYC preparations, but air drying artifact was present in nearly every smear. Squamous intraepithelial lesions (SILs) were detected in four (4.5%) smears compared to 53 (33.6%) CYTYC slides. The detection of SIL correlated with the presence of glandular and metaplastic cells in CYTYC preparations, but this association disappeared if only satisfactory specimens were considered, In conclusion, CYTYC Thin-Preps were satisfactory twice as often as conventional smears (P < 0.005) and detected nearly eight times as many SILs (P < 0.005). C1 JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NIH,BETHESDA,MD 20892. RP SHERMAN, ME (reprint author), GEORGE WASHINGTON UNIV,MED CTR,SCH MED,2300 EYE ST NW,WASHINGTON,DC 20037, USA. FU NCRR NIH HHS [MO1-RR-00722]; NIAID NIH HHS [UO1-AI-35042] NR 28 TC 23 Z9 23 U1 1 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD APR PY 1995 VL 8 IS 3 BP 270 EP 274 PG 5 WC Pathology SC Pathology GA QV864 UT WOS:A1995QV86400013 PM 7617653 ER PT J AU DEBRABANT, A GOTTLIEB, M DWYER, DM AF DEBRABANT, A GOTTLIEB, M DWYER, DM TI ISOLATION AND CHARACTERIZATION OF THE GENE ENCODING THE SURFACE-MEMBRANE 3'-NUCLEOTIDASE NUCLEASE OF LEISHMANIA-DONOVANI SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE HUMAN PARASITE; KALA AZAR; KINETOPLASTID; NUCLEOTIDE MONOPHOSPHOESTERASE; SINGLE-STRAND SPECIFIC NUCLEASE; TRYPANOSOMATID ID AMINO-ACID-SEQUENCE; PENICILLIUM-CITRINUM; POLYACRYLAMIDE GELS; CRITHIDIA-LUCILIAE; PROTEINS; PROMASTIGOTES; PURIFICATION; 5'-NUCLEOTIDASE; ELECTROPHORESIS; LOCALIZATION AB Leishmania donovani and related trypanosomatid protozoa possess an externally oriented surface membrane enzyme capable of hydrolyzing both 3'-nucleotides and nucleic acids. By virtue of these activities, this 3'-nucleotidase/nuclease (3'-NT/Nu), previously shown to be analogous to fungal and plant class-I single-strand-specific nucleases, is thought to play a critical role in the salvage of purines, essential for the survival of these organisms. The 43-kDa 3'-NT/Nu was purified from L. donovani promastigotes and trypsin treated. Four of the released tryptic peptide fragments yielded amino-acid sequence information (Pept-1 to Pept-4) which provided the basis for the preparation of oligonucleotide primers used for PCR amplification of an approx. 300-bp DNA fragment. This fragment was cloned, sequenced and used to probe a genomic L. donovani cosmid library. Nucleotide sequence analysis of a 4.5-kb SmaI fragment, isolated from a cosmid clone, revealed an open reading frame (ORF) of 1434 nt encoding a 477-amino-acid protein. Pept-1 to Pept-4 were mapped onto the ORF-deduced protein sequence. Peptides corresponding to Pept-1 to Pept-4 were synthesized and used to immunize rabbits. The resulting anti-peptide antibodies recognized the 43-kDa protein on Western blots and immunoprecipitated the native 3'-nucleotidase activity from L. donovani membrane extracts. Further, the ORF-deduced protein shared significant sequence identity with the S1 and P1 fungal nucleases of Aspergillus oryzae and Penicillium citrinum, respectively. Cumulatively, these results demonstrated that the ORF corresponded to a gene for the L, donovani 3'-nucleotidase/nuclease. In Northern blots a nucleotide probe specific for the 3'-NT/Nu gene hybridized to a single 2.5-kb messenger RNA. Results of Southern blot analyses were consistent with the 3'-NT/Nu being encoded by a single copy gene. These data constitute the first report of the gene for this unique trypanosomatid surface membrane enzyme. C1 NIAID,DIV INTRAMURAL RES,CELL BIOL SECT,PARASIT DIS LAB,BETHESDA,MD 20892. NIAID,DIV MICROBIOL & INFECT DIS,PARASITOL & TROP DIS BRANCH,BETHESDA,MD 20892. NR 44 TC 51 Z9 51 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 1995 VL 71 IS 1 BP 51 EP 63 DI 10.1016/0166-6851(95)00035-Y PG 13 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA QZ099 UT WOS:A1995QZ09900005 PM 7630383 ER PT J AU HAAS, NB CANTWELL, CA JOHNSON, PF BURCH, JBE AF HAAS, NB CANTWELL, CA JOHNSON, PF BURCH, JBE TI DNA-BINDING SPECIFICITY OF THE PAR BASIC LEUCINE-ZIPPER PROTEIN VBP PARTIALLY OVERLAPS THOSE OF THE C/EBP AND CREB/ATF FAMILIES AND IS INFLUENCED BY DOMAINS THAT FLANK THE CORE BASIC REGION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DIMERIZATION SPECIFICITY; TRANSCRIPTION FACTOR; SEQUENCE RECOGNITION; BZIP PROTEINS; HALF-SITE; GCN4; FOS; JUN; IDENTIFICATION; EXPRESSION AB The PAR subfamily of basic leucine zipper (bZIP) factors comprises three proteins (VBP/TEF, DBP, and HLF) that have conserved basic regions flanked by proline- and acidic-amino-acid-rich (PAR) domains acid functionally compatible leucine zipper dimerization domains. We show that VBP preferentially binds to sequences that consist of abutted GTAAY half-sites (which we refer to as PAR sites) as well as to sequences that contain either a C/EBP half-site (GCAAT) or a CREB/ATF half-site (GTCAT) in place of one of the PAR half-sites. Since the sequences that we describe as PAR sites and PAR-CREB/ATF chimeric sites, respectively, were both previously described as high-affinity binding sites for the E4BP4 transcriptional repressor, we infer that these sequences may be targets for positive and negative regulation. Similarly, since the sequences that we describe as PAR-C/EBP and PAR-CREB/ATF chimeric sites are known to be high-affinity binding sites for C/EBP acid CREB/ATF factors, respectively, we infer that these sites may each be targets for multiple subfamilies of bZIP factors. To gain insights regarding the molecular basis for the binding-site specificity of PAR factors, we also carried out an extensive mutational analysis of VBP. By substituting five amino acid residues that differ between the Drosophila giant bZIP factor and the vertebrate PAR bZIP factors, we show that the fork region, which bridges the basic and leucine zipper domains, contributes to half site sequence specificity. In addition, we report that at least two domains amino terminal to the core basic region are required for VBP to bind to the Full spectrum of PAR target sites. Thus, whereas direct base contacts may be restricted to basic-region residues (as indicated by GCN4-DNA crystal structures), several other domains also influence the DNA-binding specificity of PAR bZIP proteins. C1 FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. RI Johnson, Peter/A-1940-2012 OI Johnson, Peter/0000-0002-4145-4725 FU NCI NIH HHS [CA-06927, T32 CA-09035-19]; PHS HHS [35535] NR 36 TC 57 Z9 58 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 1995 VL 15 IS 4 BP 1923 EP 1932 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QM492 UT WOS:A1995QM49200010 PM 7891686 ER PT J AU CHANG, DY SASAKITOZAWA, N GREEN, LK MARAIA, RJ AF CHANG, DY SASAKITOZAWA, N GREEN, LK MARAIA, RJ TI A TRINUCLEOTIDE REPEAT-ASSOCIATED INCREASE IN THE LEVEL OF ALU RNA-BINDING PROTEIN OCCURRED DURING THE SAME PERIOD AS THE MAJOR ALU AMPLIFICATION THAT ACCOMPANIED ANTHROPOID EVOLUTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SIGNAL RECOGNITION PARTICLE; 7SL RNA; POLYMERASE-III; HUMAN GENOME; TRANSCRIPTIONAL REPRESSION; REPETITIVE SEQUENCES; POSSIBLE MECHANISM; CYTOPLASMIC RNAS; SRP-RNA; DNA AB Nearly 1 million Alu elements in human DNA were inserted by an RNA-mediated retroposition-amplification process that clearly decelerated about 30 million years ago. Since then, Alu sequences have proliferated at a lower rate, including within the human genome, in which Alu mobility continues to generate genetic variability. Initially derived from 7SL RNA of the signal recognition particle (SRP), Alu became a dominant retroposon while retaining secondary structures found in 7SL RNA. We previously identified a human Alu RNA-binding protein as a homolog of the 14-kDa Alu-specific protein of SRP and have shown that its expression is associated with accumulation of 3'-processed Alu RNA. Here, we show that in early anthropoids, the gene encoding SRP14 Alu RNA-binding protein was duplicated and that SRP14-homologous sequences currently reside on different human chromosomes. In anthropoids, the active SRP14 gene acquired a GCA trinucleotide repeat in its 3'-coding region that produces SRP14 polypeptides with extended C-terminal tails. A C --> G substitution in this region converted the mouse sequence CCA GCA to GCA GCA in prosimians, which presumably predisposed this locus to GCA expansion in anthropoids and provides a model for other triplet expansions. Moreover, the presence of the trinucleotide repeat in SRP14 DNA and the corresponding C-terminal tail in SRP14 are associated with a significant increase in SRP14 polypeptide and Alu RNA-binding activity. These genetic events occurred during the period in which an acceleration in Alu retroposition was followed by a sharp deceleration, suggesting that Alu repeats coevolved with C-terminal variants of SRP14 in higher primates. C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. NR 79 TC 22 Z9 22 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 1995 VL 15 IS 4 BP 2109 EP 2116 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QM492 UT WOS:A1995QM49200030 PM 7534378 ER PT J AU PENNIE, WD HAGER, GL SMITH, CL AF PENNIE, WD HAGER, GL SMITH, CL TI NUCLEOPROTEIN STRUCTURE INFLUENCES THE RESPONSE OF THE MOUSE MAMMARY-TUMOR VIRUS PROMOTER TO ACTIVATION OF THE CYCLIC-AMP SIGNALING PATHWAY SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID LONG TERMINAL REPEAT; PHOSPHOENOLPYRUVATE CARBOXYKINASE GENE; HUMAN PROGESTERONE RECEPTORS; SILENT MATING LOCI; PROTEIN KINASE-A; GLUCOCORTICOID RECEPTOR; MMTV PROMOTER; NEGATIVE REGULATION; DNA-BINDING; SACCHAROMYCES-CEREVISIAE AB Recent studies have provided evidence of crosstalk between steroid receptors and cyclic AMP (cAMP) signalling pathways in the regulation of gene expression. A synergism between intracellular phosphorylation inducers and either glucocorticoids or progestins has been shown to occur during activation of the mouse mammary tumor virus (MMTV) promoter. We have investigated the effect of 8-Br-cAMP and okadaic acid, modulators of cellular kinases and phosphatases, on the hormone-induced activation of the MMTV promoter in two forms: a transiently transfected template with a disorganized, accessible nucleoprotein structure and a stably replicating template with an ordered, inaccessible nucleoprotein structure. Both okadaic acid and 8-Br-cAMP synergize significantly with either glucocorticoids or progestins in activating the transiently transfected MMTV template. In contrast, 8-Br-cAMP, but not okadaic acid, is antagonistic to hormone-induced activation of the stably replicating MMTV template. Nuclear run-on experiments demonstrate that this inhibition is a transcriptional effect on both hormone-induced transcription and basal transcription. Surprisingly, 8-Br-cAMP does not inhibit glucocorticoid-induced changes in restriction enzyme access and nuclear factor 1 binding. However, association of a complex with the TATA hox region is inhibited in the presence of 8-Br-cAMP. Thus, cAMP treatment interferes with the initiation process but does not inhibit interaction of the receptor with the template. Since the replicated, ordered MMTV templates and the transfected, disorganized templates show opposite responses to 8-Br-cAMP treatment, we conclude that chromatin structure can influence the response of a promoter to activation of the cAMP signalling pathway. C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. NR 68 TC 44 Z9 44 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 1995 VL 15 IS 4 BP 2125 EP 2134 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QM492 UT WOS:A1995QM49200032 PM 7891707 ER PT J AU DATTA, K FRANKE, TF CHAN, TO MAKRIS, A YANG, SI KAPLAN, DR MORRISON, DK GOLEMIS, EA TSICHLIS, PN AF DATTA, K FRANKE, TF CHAN, TO MAKRIS, A YANG, SI KAPLAN, DR MORRISON, DK GOLEMIS, EA TSICHLIS, PN TI AH/PH DOMAIN-MEDIATED INTERACTION BETWEEN AKT MOLECULES AND ITS POTENTIAL ROLE IN AKT REGULATION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SIGNALING PROTEINS; TYROSINE KINASES; C-AKT; V-AKT; ONCOGENE; GENE; EXPRESSION; SUBFAMILY; CLONING; REGION AB The cytoplasmic serine-threonine protein kinase coded for by the e-akr proto-oncogene features a protein kinase C-like catalytic domain and a unique NH2-terminal domain (AH domain). The AH domain is a member of a domain superfamily whose prototype was observed in pleckstrin (pleckstrin homology, or PH, domain). In this communication, we present evidence that the AH/PH domain is a domain of protein-protein interaction which mediates the formation of Akt protein complexes. The interaction between c-akt AH/PH domains is highly specific, as determined by the failure of this domain to bind AKT2. The AH/PH domain-mediated interactions depend on the integrity of the entire domain. Akt molecules with deletions of the NH2-terminal portion (amino acids 11 to 60) and AH/PH constructs with deletions of the C-terminal portion of this domain (amino acids 107 to 147) fail to interact with c-akt. To determine the significance of these findings, we carried out in vitro kinase assays using Akt immunoprecipitates from serum-starved and serum-starved, platelet-derived growth factor-stimulated NIH 3T3 cells. Addition of maltose-binding protein-AH/PH fusion recombinant protein, which is expected to bind Akt, to the immunoprecipitates from serum-starved cells induced the activation of the Akt kinase. C1 FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. OI Chan , Tung/0000-0001-6574-9555 FU NCI NIH HHS [CA06927, R01 CA38047] NR 30 TC 147 Z9 148 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 1995 VL 15 IS 4 BP 2304 EP 2310 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QM492 UT WOS:A1995QM49200050 PM 7891724 ER PT J AU ROTMAN, G VANAGAITE, L COLLINS, FS SHILOH, Y AF ROTMAN, G VANAGAITE, L COLLINS, FS SHILOH, Y TI RAPID IDENTIFICATION OF POLYMORPHIC CA-REPEATS IN YAC CLONES SO MOLECULAR BIOTECHNOLOGY LA English DT Article DE POLYMORPHIC MARKERS; YAC CLONES; CA-REPEATS ID YEAST ARTIFICIAL CHROMOSOMES; SEQUENCES; GENE; CONSTRUCTION; MARKERS; LOCI AB Positional cloning of rare disease genes depends on the availability of highly polymorphic markers near the disease loci. The most abundant class of polymorphic markers in the human genome is CA-repeats. We have developed a strategy for the rapid isolation of highly polymorphic CA-repeats from YAC clones. Total DNA of yeast clones containing partly overlapping YACs is digested with frequent cutter restriction enzymes, blotted and hybridized with a poly(CA/GT) probe under high stringency conditions that enable preferential detection of long CA-repeats. The repeats detected in this way are isolated by PCR using vectorette linkers, sequenced, and appropriate flanking markers are constructed for genotyping, All of the CA-repeats identified using this approach were highly polymorphic. This simple and rapid approach should allow the development of highly polymorphic markers at any genomic region cloned in YACs. C1 TEL AVIV UNIV,SACKLER SCH MED,DEPT HUMAN GENET,IL-69978 RAMAT AVIV,ISRAEL. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 20 TC 2 Z9 2 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07012 SN 1073-6085 J9 MOL BIOTECHNOL JI Mol. Biotechnol. PD APR PY 1995 VL 3 IS 2 BP 85 EP 92 DI 10.1007/BF02789104 PG 8 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA QW398 UT WOS:A1995QW39800002 PM 7620980 ER PT J AU PALKOVITS, M AF PALKOVITS, M TI NEUROPEPTIDE MESSENGER PLASTICITY IN THE CNS NEURONS FOLLOWING AXOTOMY SO MOLECULAR NEUROBIOLOGY LA English DT Article; Proceedings Paper CT Satellite of the 14th ISN Meeting/1st International Workshop on Neuronal Phenotype - Molecular Biology, Cell Specification, and Therapeutic Frontiers CY AUG 19-20, 1993 CL LOZARI, FRANCE SP Int Soc Neurochemist, NICHD, NIH DE NEUROPEPTIDES; NEUROPEPTIDE MESSENGER-RNA; AXOTOMY; CENTRAL NERVOUS SYSTEM; NEURONAL PLASTICITY ID PEPTIDE (CGRP)-LIKE IMMUNOREACTIVITY; INSITU HYBRIDIZATION HISTOCHEMISTRY; CORTICOTROPIN-RELEASING FACTOR; PERIPHERAL-NERVE SECTION; SPINAL-CORD TRANSECTION; RAT FACIAL MOTONEURONS; IMMEDIATE EARLY GENES; DORSAL-ROOT GANGLION; OLIVOCEREBELLAR TRACT; LUMBAR MOTONEURONS AB Neuronal peptides exert neurohormonal and neurotransmitter (neuromodulator) functions in the central nervous system (CNS). Besides these functions, a group of neuropeptides may have a capacity to create cell proliferation, growth, and survival. Axotomy induces transient (1-21 d) - upregulation of synthesis and gene expression of neuropeptides, such as galanin, corticotropin releasing factor, dynorphin, calcitonin gene-related peptide, vasoactive intestinal polypeptide, cholecystokinin, angiotensin II, and neuropeptide Y. These neuropeptides are colocalized with ''classic'' neurotransmitters (acetylcholine, aspartate, glutamate) or neurohormones (vasopressin, oxytocin) that are downregulated by axotomy in the same neuronal cells. It is more likely that neuronal cells, in response to axotomy, increase expression of neuropeptides that promote their survival and regeneration, and may downregulate substances related to their transmitter or secretory activities. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP PALKOVITS, M (reprint author), SEMMELWEIS UNIV MED,NEUROMORPHOL LAB,H-1085 BUDAPEST,HUNGARY. RI Palkovits, Miklos/F-2707-2013; OI Palkovits, Miklos/0000-0003-0578-0387 NR 48 TC 35 Z9 35 U1 0 U2 2 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07012 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD APR-JUN PY 1995 VL 10 IS 2-3 BP 91 EP 103 DI 10.1007/BF02740669 PG 13 WC Neurosciences SC Neurosciences & Neurology GA RH683 UT WOS:A1995RH68300004 PM 7576312 ER PT J AU DOBI, AL PALKOVITS, M PALKOVITS, CG SANTHA, E VONAGOSTON, D AF DOBI, AL PALKOVITS, M PALKOVITS, CG SANTHA, E VONAGOSTON, D TI PROTEIN-DNA INTERACTIONS DURING PHENOTYPIC DIFFERENTIATION SO MOLECULAR NEUROBIOLOGY LA English DT Article; Proceedings Paper CT Satellite of the 14th ISN Meeting/1st International Workshop on Neuronal Phenotype - Molecular Biology, Cell Specification, and Therapeutic Frontiers CY AUG 19-20, 1993 CL LOZARI, FRANCE SP Int Soc Neurochemist, NICHD, NIH DE PROTEIN-DNA INTERACTIONS; PHENOTYPIC DIFFERENTIATION; RENK GENE ID HUMAN PROENKEPHALIN GENE; MESSENGER-RNA; SPINAL-CORD; POSTNATAL-DEVELOPMENT; DEPENDENT REGULATION; SIGNAL-TRANSDUCTION; INDUCIBLE ENHANCER; TRANSGENIC MICE; NERVOUS-SYSTEM; RAT STRIATUM AB We have been studying the molecular mechanism of neuronal differentiation through which the multipotent precursor becomes limited to the final transmitter phenotype. Here we focused on the role of the 5' proximal regulatory cassette (-190; +53 bp) of the rat enkephalin (rENK) gene in the developmental regulation of the enkephalin phenotype. Several well characterized cis-elements, including AP2, CREB, NF1, and NFkB, reside on this region of the rENK gene. These motifs were sufficient to confer activity-dependent expression of the gene during neuro-differentiation when it was tested using transient transfection assays of primary developing spinal cord neurons treated with tetrodotoxin (TTX). This region was then used as a DNA probe in mobility shift assays, with nuclear proteins derived from phenotypically and ontogenetically distinct brain regions. Only a few low abundance protein-DNA complexes were detected and only with nuclear proteins derived from developing but not from adult brain. The spatiotemporal pattern of these complexes did not show correlation with enkephalin expression which was assessed by RT-PCR. We employed synthetic probes corresponding to consensus as well as ENK-specific sequences of the individual motifs to identify the nature of the observed bands. Although both consensus NF1 and enkCRE1(NF1) formed complexes with nuclear proteins derived from the striatum and cortex at various ages, the appearance of the bands was not correlated with ENK expression. Surprisingly, no complexes were detected if other ENK-specific motifs were used as probes. We also tested nuclear extracts derived from forskolin-induced and control C6 glioma cells, again using the whole proximal regulatory cassette as well as individual motifs. These experiments showed the formation of elaborate protein-DNA bands. There was no direct correlation between the appearance of bands and forskolin-induced ENK expression. Unexpectedly, all ENK-specific motifs formed specific and highly abundant protein-DNA complexes when nuclear extracts from the human tumor cell line (HeLa), which does not express ENK, were used. Based on these observations, we concluded that: 1. Interactions between the proximal regulatory cassette and additional probably far distant regions of the rENK gene and their binding proteins may be necessary to confer developmentally regulated, cell-specific expression of the ENK gene; and 2. Inducibility of the gene by common cis-elements can be governed by this region; however, the cell-specificity of the induction remains elusive. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP DOBI, AL (reprint author), NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892, USA. RI Palkovits, Miklos/F-2707-2013; OI Palkovits, Miklos/0000-0003-0578-0387 NR 48 TC 9 Z9 9 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07012 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD APR-JUN PY 1995 VL 10 IS 2-3 BP 185 EP 203 DI 10.1007/BF02740675 PG 19 WC Neurosciences SC Neurosciences & Neurology GA RH683 UT WOS:A1995RH68300010 PM 7576307 ER PT J AU WASCHEK, JA VONAGOSTON, D AF WASCHEK, JA VONAGOSTON, D TI PROCEEDINGS OF THE SATELLITE OF THE 14TH ISN MEETING AND THE FIRST INTERNATIONAL WORKSHOP - THE NEURONAL PHENOTYPE - MOLECULAR-BIOLOGY, CELL SPECIFICATION, AND THERAPEUTIC FRONTIERS - LOZARI, CORSICA, FRANCE, AUGUST 19-20 1993 - INTRODUCTION SO MOLECULAR NEUROBIOLOGY LA English DT Editorial Material C1 NIH,BETHESDA,MD 20892. RP WASCHEK, JA (reprint author), UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07012 SN 0893-7648 J9 MOL NEUROBIOL JI Mol. Neurobiol. PD APR-JUN PY 1995 VL 10 IS 2-3 BP R9 EP R10 DI 10.1007/BF02740667 PG 2 WC Neurosciences SC Neurosciences & Neurology GA RH683 UT WOS:A1995RH68300002 ER PT J AU BOJA, JW CADET, JL KOPAJTIC, TA LEVER, J SELTZMAN, HH WYRICK, CD LEWIN, AH ABRAHAM, P CARROLL, FI AF BOJA, JW CADET, JL KOPAJTIC, TA LEVER, J SELTZMAN, HH WYRICK, CD LEWIN, AH ABRAHAM, P CARROLL, FI TI SELECTIVE LABELING OF THE DOPAMINE TRANSPORTER BY THE HIGH-AFFINITY LIGAND 3-BETA-(4-[I-125]IODOPHENYL)TROPANE-2-BETA-CARBOXYLIC ACID ISOPROPYL ESTER SO MOLECULAR PHARMACOLOGY LA English DT Article ID COCAINE BINDING-SITES; H-3 COCAINE; I-125 RTI-55; STRIATAL MEMBRANES; NONHUMAN-PRIMATES; RAT; BRAIN; RECEPTORS; GBR-12935; ANALOGS AB The iodine-125 analog of the dopaminergically selective cocaine analog 3 beta-(4-iodophenyl)tropane-2 beta-carboxylic acid isopropyl ester (RTI-121) was evaluated as a probe for the dopamine transporter in rat striatum. Saturation and kinetic studies indicated that [I-125]RTI-121 binds to both high and low affinity components. The K-d of the high affinity component was 0.14 +/- 0.01 nM (mean +/- standard error), whereas the low affinity component demonstrated an affinity of 1.59 +/- 0.09 nM. The corresponding numbers of striatal binding sites labeled by [I-125]RT1-121 were 295 +/- 6 and 472 +/- 59 pmol/g of tissue (original wet weight), respectively. Intrastriatal injections of 6-hydroxydopamine eliminated >90% of specific [I-125]RTI-121 binding in the striatum. The pharmacological profile of specific [I-125]RTI-121 binding in the rat striatum was consistent with that of the dopamine transporter. There was a strong (r = 0.98, p < 0.0001) correlation between the potencies of drugs that displaced specific [I-125]RTI-121 binding and the potencies of these drugs to inhibit the uptake of [H-3]dopamine. In contrast, no correlation was found for the potencies of drugs to inhibit the uptake of either [H-3]norepinephrine or [H-3]serotonin. Autoradiographs produced using [I-125]RT1-121 demonstrated a distribution of label consistent with the distribution of dopaminergic neurons in rat brain. Because of its high affinity and high selectivity for the dopamine transporter, [I-125]RTI-121 may be an extremely useful ligand for the dopamine transporter. C1 NIDA,INTRAMURAL RES PROGRAM,MOLEC PHARMACOL SECT,BALTIMORE,MD 21224. NIDA,INTRAMURAL RES PROGRAM,MOLEC NEUROPSYCHIAT,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,BALTIMORE,MD 21224. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. FU NIDA NIH HHS [DA05477] NR 46 TC 69 Z9 69 U1 2 U2 2 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 1995 VL 47 IS 4 BP 779 EP 786 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QT945 UT WOS:A1995QT94500016 PM 7723739 ER PT J AU SNYDER, BW VITALE, J MILOS, P GOSSELIN, J GILLESPIE, F EBERT, K HAGUE, BF KINDT, TJ WADSWORTH, S LEIBOWITZ, P AF SNYDER, BW VITALE, J MILOS, P GOSSELIN, J GILLESPIE, F EBERT, K HAGUE, BF KINDT, TJ WADSWORTH, S LEIBOWITZ, P TI DEVELOPMENTAL AND TISSUE-SPECIFIC EXPRESSION OF HUMAN CD4 IN TRANSGENIC RABBITS SO MOLECULAR REPRODUCTION AND DEVELOPMENT LA English DT Article DE CD4; CD8; AIDS; MODEL; HIV ID HUMAN-IMMUNODEFICIENCY-VIRUS; SMALL ANIMAL-MODEL; T-CELL; HIV-INFECTION; MICE; CHIMPANZEES; RECEPTOR; TYPE-1; AIDS; IDENTIFICATION AB A major obstacle to understanding AIDS is the lack of a suitable small animal model for studying HIV-1 infection and the subsequent development of AIDS, and for testing diagnostic, therapeutic, and preventive modalities. Our goal is to produce a rabbit model for the study of AIDS. Here we report on the generation of transgenic rabbits that express the human CD4 (hCD4) gene. The transgene, which contains the coding region for hCD4 and approximately 23 kb of sequence upstream of the translation start site, was used previously to direct hCD4 expression on the surface of CD4(+) T cells of transgenic mice (Gillespie et al., 1993: Mol Cell Biol 13:2952-2958). The hCD4 transgene was detected in five males and two females derived from the microinjection of 271 rabbit embryos. Both hCD4 RNA and protein were expressed in peripheral blood lymphocytes (PBLs) from all five males but neither of the females. Human CD4 was expressed on PBLs from F-1 offspring of all-founder males. T-cell subset analysis revealed that hCD4 expression was restricted to rabbit CD4 (rCD4) expressing lymphocytes; mature rCD4(-)rCD8(+) lymphocytes did not express hCD4. In preliminary studies, PBLs from hCD4 transgenic rabbits produced greater amounts of HIV-1 p24 core protein following HIV-I infection in vitro than HIV-1 p24 antigen in nontransgenic rabbit infected cultures. These results extend to rabbits our previous observation that this transgene contains the sequence elements required for high-level expression in the appropriate cells of transgenic mice. Furthermore, these and previous studies demonstrating that expression of hCD4 protein enhances HIV-I infection of rabbit T cells in vitro, coupled with reports that normal, nontransgenic rabbits are susceptible to HIV-1 infection, suggests that the hCD4 transgenic rabbits described herein will have an increased susceptibility to HIV-1 infection. In vivo HIV-1 infection studies with these rabbits are under way. (C) 1995 Wiley-Liss, Inc. C1 EXEMPLAR CORP,WALTHAM,MA. TUFTS UNIV,SCH VET MED,N GRAFTON,MA 01536. NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. FU NCRR NIH HHS [1 R43RR06155-01] NR 32 TC 26 Z9 27 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 1040-452X J9 MOL REPROD DEV JI Mol. Reprod. Dev. PD APR PY 1995 VL 40 IS 4 BP 419 EP 428 DI 10.1002/mrd.1080400405 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology GA QQ271 UT WOS:A1995QQ27100004 PM 7598907 ER PT J AU CALABRESI, PA SILVESTRI, G DIMAURO, S GRIGGS, RC AF CALABRESI, PA SILVESTRI, G DIMAURO, S GRIGGS, RC TI EKBOMS SYNDROME - (A REPLY) SO MUSCLE & NERVE LA English DT Letter C1 COLUMBIA UNIV,DEPT NEUROL,NEW YORK,NY 10032. UNIV ROCHESTER,MED CTR,ROCHESTER,NY 14620. RP CALABRESI, PA (reprint author), NIH,NEUROIMMUNOL BRANCH,BLDG 10,ROOM 5B-16,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PD APR PY 1995 VL 18 IS 4 BP 478 EP 478 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA QN272 UT WOS:A1995QN27200023 ER PT J AU DESERRES, FJ BROCKMAN, HE AF DESERRES, FJ BROCKMAN, HE TI ETHYLENE-OXIDE - INDUCTION OF SPECIFIC-LOCUS MUTATIONS IN THE AD-3 REGION OF HETEROKARYON-12 OF NEUROSPORA-CRASSA AND IMPLICATIONS FOR GENETIC RISK ASSESSMENT OF HUMAN EXPOSURE IN THE WORKPLACE SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article DE HETEROKARYON 12; GENE/POINT MUTATION; MULTIPLE-LOCUS MUTATION; MULTILOCUS DELETION MUTATION; AD-3 REGION; AD-3A LOCUS; AD-3B LOCUS; RECESSIVE LETHAL MUTATION; ETHYLENE OXIDE; CHEMICAL CARCINOGEN; MUTATIONAL SPECTRUM ID EXCISION-REPAIR-PROFICIENT; 2-COMPONENT HETEROKARYONS; HERITABLE TRANSLOCATIONS; ENVIRONMENTAL CHEMICALS; MUTAGENIC ACTIVITY; POINT MUTATIONS; DROSOPHILA; INHALATION; SPECTRA; MUTANTS AB Ethylene oxide (ETO) is an important industrial intermediate used extensively in the production of ethylene glycol, as a fumigant, and as a sterilant of choice for various medical devices. The mutagenicity of ETO was studied for the induction of specific-locus mutations in the adenine-3 (ad-3) region of a two-component heterokaryon (H-12) of Neurospora crassa. The objectives of these studies with ETO were to rank its mutagenic potency and to compare its mutational spectrum for induced specific-locus mutations with other chemical mutagens in this lower eukaryotic organism. Specific-locus mutations in the ad-3 region of heterokaryon H-12 result from gene/point mutations at the closely linked ad-M and ad-3B loci, multilocus deletion mutations and multiple-locus mutations. These major genotypic classes are similar to the types of specific-locus mutations that can be detected in higher organisms. Conidial suspensions of H-12 were treated with five different concentrations of ETO (0.1-0.35%) for 3 h at 25 degrees C. Control and ETO-treated conidial suspensions were used to obtain dose-response curves for inactivation as well as the overall induction of ad-3 forward mutations using a non-selective method based on pigment accumulation rather than a requirement for adenine. The results from these experiments are: (1) the slope of the dose-response curve for ETC-induced specific-locus mutations in the ad-3 region is 1.49+/-0.07, and (2) the maximum forward-mutation frequency fell between 10 and 100 ad-3 mutations per 10(6) survivors; therefore, ETO is a moderate mutagen. Classical genetic tests were used to characterize the ETO-induced ad-3 mutations from each of two treatments (0.25 and 0.35%). The overall data base demonstrates that ETC-induced ad-3 mutations result from a high percentage (96.9%) of gene/point mutations at the ad-3A and ad-3B loci, as well as from a low percentage (3.1%) of multilocus deletion mutations. The mutagenic activity of ETO is compared with the mutagenic specificity of other chemical mutagens and carcinogens in the ad-3 forward-mutation assay in Neurospora. The utilization of the Neurospora specific-locus data on ETO and those from experiments in the mouse and Drosophila, by others, is discussed far genetic risk assessment of germ-cell effects resulting from human exposure to ETO in the workplace. C1 ILLINOIS STATE UNIV,DEPT BIOL SCI,NORMAL,IL 61790. RP DESERRES, FJ (reprint author), NIEHS,DIV INTRAMURAL RES,ENVIRONM TOXICOL PROGRAM,TOXICOL BRANCH,MD 19-02,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 42 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD APR PY 1995 VL 328 IS 1 BP 31 EP 47 DI 10.1016/0027-5107(94)00194-A PG 17 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA QP322 UT WOS:A1995QP32200004 PM 7898502 ER PT J AU OLIVERO, OA SEMINO, C KASSIM, A LOPEZLARRAZA, DM POIRIER, MC AF OLIVERO, OA SEMINO, C KASSIM, A LOPEZLARRAZA, DM POIRIER, MC TI PREFERENTIAL BINDING OF CISPLATIN TO MITOCHONDRIAL-DNA OF CHINESE-HAMSTER OVARY SO MUTATION RESEARCH LETTERS LA English DT Article DE CISPLATIN; DNA ADDUCT; MITOCHONDRIAL DNA; ELECTRON MICROSCOPY ID ANTICANCER DRUG CISPLATIN; CARCINOMA CELLS; COLLOIDAL GOLD; DAMAGED DNA; ADDUCTS; REPAIR; CIS-DIAMMINEDICHLOROPLATINUM(II); PROTEINS; INVIVO; BENZOPYRENE AB Some chemical carcinogens localize preferentially in mitochondrial DNA (mtDNA) when compared with genomic DNA (gDNA). Here we compare the ability of cisplatin (cis-diamminedichloroplatinum[II]) to induce DNA adducts in both genomic and mtDNA of Chinese hamster ovary (CHO) cells in culture. Cytotoxicity was examined by cell survival 4, 8 and 24 h after exposure to 50 mu M cisplatin. Cisplatin-DNA adducts were measured in DNA from nuclear and mitochondrial fractions by dissociation-enhanced lanthanide fluoroimmunoassay (DELFIA), a sensitive competitive microtiter-based immunoassay utilizing antiserum elicited against cisplatin-modified DNA. An additional comparison of cisplatin-DNA binding in both compartments was performed by immunoelectron microscopy using the cisplatin-DNA antiserum and colloidal gold. DELFIA analysis of cisplatin-DNA adducts in gDNA and mtDNA showed a six-fold higher incorporation of drug into mtDNA as compared to gDNA. Morphometric studies of colloidal gold distribution in photomicrographs of CHO cells showed mtDNA to contain a four-fold higher concentration of cisplatin as compared to nuclear DNA. Therefore, both methods demonstrated a preferential binding of cisplatin to mtDNA versus gDNA. C1 NIDCD,MOLEC OTOL LAB,BETHESDA,MD. RP OLIVERO, OA (reprint author), NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BLDG 37,RM 3B12,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 46 TC 52 Z9 53 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-7992 J9 MUTAT RES LETT JI Mutat. Res. Lett. PD APR PY 1995 VL 346 IS 4 BP 221 EP 230 DI 10.1016/0165-7992(95)90039-X PG 10 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA QX647 UT WOS:A1995QX64700006 PM 7753115 ER PT J AU COLLINS, FS AF COLLINS, FS TI POSITIONAL CLONING MOVES FROM PERDITIONAL TO TRADITIONAL SO NATURE GENETICS LA English DT Article ID MUTATIONS; GENE; LOCATION; DISEASE; CANCER AB The technique of positional cloning has become a familiar component of modern human genetics research. After a halting start in the mid-1980s, the number of disease genes succumbing to cloning efforts based solely on pinpointing their position in the genome is growing exponentially. More than 40 genes have been identified so far. But the positional candidate approach, which combines knowledge of map position with the increasingly dense human transcript map, greatly expedites the search process and will soon become the predominant method of disease gene discovery. The challenge ahead is to apply such methods to identifying genes involved in complex polygenic disorders. RP COLLINS, FS (reprint author), NIH,NATL CTR HUMAN GENOME RES,BLDG 31,ROOM 4B09,BETHESDA,MD 20892, USA. NR 24 TC 469 Z9 480 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD APR PY 1995 VL 9 IS 4 BP 347 EP 350 DI 10.1038/ng0495-347 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA QQ753 UT WOS:A1995QQ75300010 PM 7795639 ER PT J AU VISAKORPI, T HYYTINEN, E KOIVISTO, P TANNER, M KEINANEN, R PALMBERG, C PALOTIE, A TAMMELA, T ISOLA, J KALLIONIEMI, OP AF VISAKORPI, T HYYTINEN, E KOIVISTO, P TANNER, M KEINANEN, R PALMBERG, C PALOTIE, A TAMMELA, T ISOLA, J KALLIONIEMI, OP TI IN-VIVO AMPLIFICATION OF THE ANDROGEN RECEPTOR GENE AND PROGRESSION OF HUMAN PROSTATE-CANCER SO NATURE GENETICS LA English DT Article ID CARCINOMA AB Overexpression of amplified genes is often associated with the acquisition of resistance to cancer therapeutic agents in vitro. We have identified a similar molecular mechanism in vivo for endocrine treatment failure in human prostate cancer which involves amplification of the androgen receptor (AR) gene. Comparative genomic hybridization shows that amplification of the Xq11-q13 region (the location), is common in tumours recurring during androgen deprivation therapy. We found high-level AR amplification in seven of 23 (30%) recurrent tumours, but in none of the specimens taken from the same patients prior to therapy. Our results suggest that AR amplification emerges during androgen deprivation therapy by facilitating tumour cell growth in low androgen concentrations. C1 INST MED TECHNOL,SF-33521 TAMPERE,FINLAND. NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,BETHESDA,MD 20892. TAMPERE UNIV HOSP,DEPT SURG,DIV UROL,SF-33521 TAMPERE,FINLAND. TAMPERE UNIV,DEPT CLIN SCI,SF-33521 TAMPERE,FINLAND. UNIV HELSINKI,CENT HOSP,DEPT CLIN CHEM,SF-00290 HELSINKI,FINLAND. RP VISAKORPI, T (reprint author), TAMPERE UNIV HOSP,CANC GENET LAB,POB 2000,SF-33521 TAMPERE,FINLAND. RI Kallioniemi, Olli/H-5111-2011; Kallioniemi, Olli/H-4738-2012 OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332 NR 30 TC 922 Z9 940 U1 3 U2 37 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD APR PY 1995 VL 9 IS 4 BP 401 EP 406 DI 10.1038/ng0495-401 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA QQ753 UT WOS:A1995QQ75300018 PM 7795646 ER PT J AU MERAJVER, SD PHAM, TM CADUFF, RF CHEN, M POY, EL COONEY, KA WEBER, BL COLLINS, FS JOHNSTON, C FRANK, TS AF MERAJVER, SD PHAM, TM CADUFF, RF CHEN, M POY, EL COONEY, KA WEBER, BL COLLINS, FS JOHNSTON, C FRANK, TS TI SOMATIC MUTATIONS IN THE BRCA1 GENE IN SPORADIC OVARIAN-TUMORS SO NATURE GENETICS LA English DT Article ID FAMILIAL BREAST; ALLELE LOSSES; CANCER; CHROMOSOME-17; LINKAGE; REGION; TUMORS AB The BRCA1 gene on chromosome 17q21 is responsible for an autosomal dominant syndrome of increased susceptibility to breast and ovarian cancer but no somatic mutations in tumours have yet been described. To study the potential role of BRCA1 in sporadic carcinogenesis, we analysed the genomic DNA of tumour and normal fractions of 47 ovarian cancers for mutations in BRCA1 using the single-strand conformation polymorphism technique. We now describe somatic mutations in the DNA of four tumours which also had loss of heterozygosity (LOH) at a BRCA1 intragenic marker. Our data support a tumour suppressor mechanism for BRCA1; somatic mutations and LOH may result in inactivation of BRCA1 in at least a small number of ovarian cancers. C1 UNIV MICHIGAN,SCH MED,DEPT PATHOL,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT OBSTET & GYNECOL,ANN ARBOR,MI 48109. UNIV PENN,SCH MED,DEPT GENET,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT INTERNAL MED,PHILADELPHIA,PA 19104. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. RP MERAJVER, SD (reprint author), UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,ANN ARBOR,MI 48109, USA. FU NCRR NIH HHS [3M01RR00042-34S1] NR 22 TC 355 Z9 358 U1 0 U2 7 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD APR PY 1995 VL 9 IS 4 BP 439 EP 443 DI 10.1038/ng0495-439 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA QQ753 UT WOS:A1995QQ75300024 PM 7795652 ER PT J AU MATHIESON, BJ AF MATHIESON, BJ TI CTL TO HIV-1 - SURROGATES OR SIRENS SO NATURE MEDICINE LA English DT Editorial Material ID CYTOTOXIC LYMPHOCYTES-T; IMMUNODEFICIENCY-VIRUS TYPE-1; RHESUS-MONKEYS; SEROPOSITIVE INDIVIDUALS; IMMUNE-RESPONSES; EPITOPES; VACCINES RP MATHIESON, BJ (reprint author), NIAID,DIV AIDS,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 24 TC 5 Z9 5 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD APR PY 1995 VL 1 IS 4 BP 304 EP 305 DI 10.1038/nm0495-304 PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA RN098 UT WOS:A1995RN09800023 PM 7585057 ER PT J AU KARP, JE BRODER, S AF KARP, JE BRODER, S TI MOLECULAR FOUNDATIONS OF CANCER - NEW TARGETS FOR INTERVENTION SO NATURE MEDICINE LA English DT Review ID FIBROBLAST GROWTH-FACTOR; NONPOLYPOSIS COLORECTAL-CANCER; NUCLEAR ANTIGEN EXPRESSION; TUMOR-SUPPRESSOR GENE; BREAST-CANCER; CELL-CYCLE; RETINOBLASTOMA PROTEIN; ATAXIA-TELANGIECTASIA; EXTRACELLULAR-MATRIX; PROSTATE-CANCER RP KARP, JE (reprint author), NCI,BETHESDA,MD 20892, USA. NR 133 TC 99 Z9 99 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD APR PY 1995 VL 1 IS 4 BP 309 EP 320 DI 10.1038/nm0495-309 PG 12 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA RN098 UT WOS:A1995RN09800026 PM 7585060 ER PT J AU ABIMIKU, AG FRANCHINI, G TARTAGLIA, J ALDRICH, K MYAGKIKH, M MARKHAM, PD CHONG, PL KLEIN, M KIENY, MP PAOLETTI, E GALLO, RC ROBERTGUROFF, M AF ABIMIKU, AG FRANCHINI, G TARTAGLIA, J ALDRICH, K MYAGKIKH, M MARKHAM, PD CHONG, PL KLEIN, M KIENY, MP PAOLETTI, E GALLO, RC ROBERTGUROFF, M TI HIV-1 RECOMBINANT POXVIRUS VACCINE INDUCES CROSS-PROTECTION AGAINST HIV-2 CHALLENGE IN RHESUS MACAQUES SO NATURE MEDICINE LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; TOXIC LYMPHOCYTES-T; ENVELOPE GLYCOPROTEIN; SYNTHETIC PEPTIDES; INFECTION; TYPE-1; NEUTRALIZATION; ANTIBODIES; EXPRESSION; EPITOPE AB Rhesus macaques were immunized with attenuated vaccinia or canarypox human immunodeficiency virus type 1 (HIV-1) recombinants and boosted with HIV-1 protein subunits formulated in alum. Following challenge with HIV-2(SBL6669), three out of eight immunized macaques resisted infection for six months and another exhibited significantly delayed infection, whereas all three naive controls became infected. Immunizations elicited both humoral and cellular immune responses; however, no clear correlates of protection were discerned. Although more extensive studies are now called for, this first demonstration of cross-protection between HIV-1 and -2 suggests that viral variability may not be an insurmountable problem in the design of a global AIDS vaccine. C1 VIROGENET CORP,TROY,NY 12180. ADV BIOSCI LABS INC,KENSINGTON,MD 20895. CONNAUGHT LABS,N YORK,ON M2R 3T4,CANADA. TRANSGENE SA,F-67082 STRASBOURG,FRANCE. RP ABIMIKU, AG (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,ROOM 6A09,37 CONVENT DR MSC 4255,BETHESDA,MD 20892, USA. RI Chong, Pele/E-3855-2010 NR 50 TC 59 Z9 60 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD APR PY 1995 VL 1 IS 4 BP 321 EP 329 DI 10.1038/nm0495-321 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA RN098 UT WOS:A1995RN09800027 PM 7585061 ER PT J AU KOENIG, S CONLEY, AJ BREWAH, YA JONES, GM LEATH, S BOOTS, LJ DAVEY, V PANTALEO, G DEMAREST, JF CARTER, C WANNEBO, C YANNELLI, JR ROSENBERG, SA LANE, HC AF KOENIG, S CONLEY, AJ BREWAH, YA JONES, GM LEATH, S BOOTS, LJ DAVEY, V PANTALEO, G DEMAREST, JF CARTER, C WANNEBO, C YANNELLI, JR ROSENBERG, SA LANE, HC TI TRANSFER OF HIV-1-SPECIFIC CYTOTOXIC T-LYMPHOCYTES TO AN AIDS PATIENT LEADS TO SELECTION FOR MUTANT HIV VARIANTS AND SUBSEQUENT DISEASE PROGRESSION SO NATURE MEDICINE LA English DT Article ID INFECTED RHESUS-MONKEYS; CYTO-TOXIC RESPONSES; ADOPTIVE TRANSFER; NEF PROTEIN; VIRUS; CD8+; CELLS; PROTECTION; VACCINE; INVIVO AB An HIV-1-seropositive volunteer was infused with an expanded autologous cytotoxic T lymphocyte (CTL) clone directed against the HIV-1 nef protein. This clone was adoptively transferred to determine whether supplementing CTL activity could reduce viral load or improve clinical course. Unexpectedly, infusion was followed by a decline in circulating CD4(-) T cells and a rise in viral load. Some of the HIV isolates obtained from the plasma or CD4(-) cells of the patient were lacking the nef epitope. These results suggest that active CTL selection of viral variants could contribute to the pathogenesis of AIDS and that clinical progression can occur despite high levels of circulating HIV-1-specific CTLs. C1 MERCK RES LABS,W POINT,PA 19486. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NCI,CTR CLIN,TRANSFUS MED BRANCH,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. RP KOENIG, S (reprint author), MEDIMMUNE INC,35 W WATKINS MILL RD,GAITHERSBURG,MD 20878, USA. RI Pantaleo, Giuseppe/K-6163-2016 NR 40 TC 287 Z9 288 U1 1 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD APR PY 1995 VL 1 IS 4 BP 330 EP 336 DI 10.1038/nm0495-330 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA RN098 UT WOS:A1995RN09800028 PM 7585062 ER PT J AU NICHOLSON, LK YAMAZAKI, T TORCHIA, DA GRZESIEK, S BAX, A STAHL, SJ KAUFMAN, JD WINGFIELD, PT LAM, PYS JADHAV, PK HODGE, CN DOMAILLE, PJ CHANG, CH AF NICHOLSON, LK YAMAZAKI, T TORCHIA, DA GRZESIEK, S BAX, A STAHL, SJ KAUFMAN, JD WINGFIELD, PT LAM, PYS JADHAV, PK HODGE, CN DOMAILLE, PJ CHANG, CH TI FLEXIBILITY AND FUNCTION IN HIV-1 PROTEASE SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID HETERONUCLEAR NMR-SPECTROSCOPY; MODEL-FREE APPROACH; MAGNETIC-RESONANCE RELAXATION; BACKBONE DYNAMICS; CROSS-CORRELATION; STAPHYLOCOCCAL NUCLEASE; METHYL-GROUPS; N-15; PROTEINS; MACROMOLECULES AB HIV protease is a homodimeric protein whose activity is essential to viral function. We have investigated the molecular dynamics of the HIV protease, thought to be important for proteinase function, bound to high affinity inhibitors using NMR techniques. Analysis of N-15 spin refaxation parameters, of all but 13 backbone amide sites, reveals the presence of significant internal motions of the protein backbone. In particular, the flaps that cover the proteins active site of the protein have terminal loops that undergo large aCnpIitude motions on the ps to ns time scale, while the tips of the flaps undergo a conformational exchange on the mu s time scale. This enforces the idea that the flaps of the proteinase are flexible structures that facilitate function by permitting substrate access to and product release from the active site of the enzyme. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NIH,OFF DIRECTOR,PROT EXPRESS LAB,BETHESDA,MD 20892. DUPONT MERCK PHARMACEUT CO,DEPT CHEM & PHYS SCI,WILMINGTON,DE 19880. RP NICHOLSON, LK (reprint author), NIDR,STRUCT MOLEC BIOL UNIT,BETHESDA,MD 20892, USA. NR 42 TC 212 Z9 214 U1 3 U2 11 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD APR PY 1995 VL 2 IS 4 BP 274 EP 280 DI 10.1038/nsb0495-274 PG 7 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA RH379 UT WOS:A1995RH37900007 PM 7796263 ER PT J AU CLORE, GM ERNST, J CLUBB, R OMICHINSKI, JG KENNEDY, WMP SAKAGUCHI, K APPELLA, E GRONENBORN, AM AF CLORE, GM ERNST, J CLUBB, R OMICHINSKI, JG KENNEDY, WMP SAKAGUCHI, K APPELLA, E GRONENBORN, AM TI REFINED SOLUTION STRUCTURE OF THE OLIGOMERIZATION DOMAIN OF THE TUMOR-SUPPRESSOR P53 SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; DNA-BINDING; MUTANT P53; PROTEIN; MUTATIONS; CANCER; ENERGY; SPECTROSCOPY; DYNAMICS AB The NMR solution structure of the oligomerization domain of the tumour suppressor p53 (residues 319-360) has been refined. The structure comprises a dimer of dimers, oriented in an approximately orthogonal manner. The present structure determination is based on 4,472 experimental NMR restraints which represents a three and half fold increase over our previous work in the number of NOE restraints at the tetramerization interface. A comparison with the recently solved 1.7 Angstrom resolution X-ray structure shows that the structures are very similar and that the average angular root-mean-square difference in the interhelical angles is about 1 degrees. The results of recent extensive mutagenesis data and the possible effects of mutations which have been identified in human cancers are discussed in the light of the present structure. C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. RP CLORE, GM (reprint author), NIDDKD,CHEM PHYS LAB,BLDG 5,BETHESDA,MD 20892, USA. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 58 TC 164 Z9 165 U1 0 U2 8 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD APR PY 1995 VL 2 IS 4 BP 321 EP 333 DI 10.1038/nsb0495-321 PG 13 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA RH379 UT WOS:A1995RH37900013 PM 7796267 ER PT J AU COLLINS, JR BURT, SK ERICKSON, JW AF COLLINS, JR BURT, SK ERICKSON, JW TI FLAP OPENING IN HIV-1 PROTEASE SIMULATED BY ACTIVATED MOLECULAR-DYNAMICS SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID INHIBITOR; COMPLEX AB We have used an 'activated' molecular dynamics approach to simulate flap opening in HIV-1 protease. An initial impulse for flap opening was provided by applying harmonic constraints to non-flap residues. After an initial 'melting' phase, the two beta-hairpin structures that constitute the flaps opened to a 25 Angstrom gap within 200 ps of simulation. Analysis of backbone torsion angles suggests that flap opening is related to conformational changes at Lys 45, Met 46, Gly 52 and Phe 53. In contrast, similar molecular dynamics simulations on the M46l mutant, which is associated with drug resistance, indicates that this mutation stabilizes the flaps in a dosed conformation. C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK BIOMED SUPERCOMP CTR,FREDERICK,MD 21702. NR 10 TC 123 Z9 125 U1 1 U2 8 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD APR PY 1995 VL 2 IS 4 BP 334 EP 338 DI 10.1038/nsb0495-334 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA RH379 UT WOS:A1995RH37900014 PM 7796268 ER PT J AU AGUILERA, G YOUNG, WS KISS, A BATHIA, A AF AGUILERA, G YOUNG, WS KISS, A BATHIA, A TI DIRECT REGULATION OF HYPOTHALAMIC CORTICOTROPIN-RELEASING-HORMONE NEURONS BY ANGIOTENSIN-II SO NEUROENDOCRINOLOGY LA English DT Article DE CORTICOTROPIN RELEASING HORMONE; PARAVENTRICULAR NUCLEUS; ANGIOTENSIN; ANGIOTENSIN RECEPTOR; ANGIOTENSIN MESSENGER-RNA; IN SITU HYBRIDIZATION; VASOPRESSIN; OXYTOCIN ID ANTERIOR-PITUITARY HORMONES; RAT-BRAIN; PARAVENTRICULAR NUCLEUS; MESSENGER-RNA; ADRENOCORTICOTROPIN SECRETION; SUPRAOPTIC NUCLEI; ACTH-SECRETION; CONSCIOUS RATS; ADULT-RAT; RECEPTOR AB The possible role of angiotensin II (AII) in the control of the hypothalamic-pituitary-adrenal (HPA) axis was studied in the rat by examining the regulation and cellular localization of AII receptors in the paraventricular nucleus (PVN) of the hypothalamus and the effect of AII on corticotropin-releasing hormone (CRH) and vasopressin (VP) mRNA levels. In situ hybridization studies using cRNA S-35-labelled probes showed that while type 1 AII receptor (AT(1)) mRNA levels were high in the periventricular and parvicellular pars of the PVN, only very low levels were present in the magnocellular pars. A similar distribution of AT(1) receptor binding in the periventricular, parvicellular and magnocellular divisions of the PVN was observed in autoradiographic studies in hypothalamic sections labelled with I-125[Sar(1),Ile(8)]AII. In addition, AII receptor binding was clearly evident in nerve fibers adjacent to the PVN. Double-labelling hybridization using digoxigenin-labelled CRH, VP and oxytocin probes and S-35-labelled AT(1) receptor cRNA probes showed AT(1) receptor mRNA in cells stained for CRH mRNA, but not in VP or oxytocin cells. Four hours after a single intracerebroventricular (i.c.v.) injection of 50 ng AII in conscious rats, CRH mRNA levels in the PVN were increased by 43%, similar to the increases observed following acute stress by intraperitoneal (i.p.) injection of 1.5 M NaCl (76%). On the other hand, while i.p. hypertonic saline injection increased VP mRNA levels by 29% in the PVN and by 32% in the supraoptic nucleus, i.c.v. AII injection had no significant effect. The data strongly suggest that AII modulates CRH neurons directly through receptors in PVN perikarya, whereas regulation of magnocellular function is at least partly indirect via receptors associated with afferent innervation to the PVN. The data support a direct role for AII in the regulation of PVN function. C1 NICHHD,DEV ENDOCRINOL BRANCH,ENDOCRINE PHYSIOL SECT,BETHESDA,MD 20892. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RI Young, W Scott/A-9333-2009 OI Young, W Scott/0000-0001-6614-5112 NR 43 TC 102 Z9 103 U1 0 U2 3 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD APR PY 1995 VL 61 IS 4 BP 437 EP 444 DI 10.1159/000126866 PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA QQ838 UT WOS:A1995QQ83800011 PM 7783857 ER PT J AU SLOAN, MA PRICE, TR PETITO, CK RANDALL, AMY SOLOMON, RE TERRIN, ML GORE, J COLLEN, D KLEIMAN, N FEIT, F BABB, J HERMAN, M ROBERTS, WC SOPKO, G BOVILL, E FORMAN, S KNATTERUD, GL AF SLOAN, MA PRICE, TR PETITO, CK RANDALL, AMY SOLOMON, RE TERRIN, ML GORE, J COLLEN, D KLEIMAN, N FEIT, F BABB, J HERMAN, M ROBERTS, WC SOPKO, G BOVILL, E FORMAN, S KNATTERUD, GL TI CLINICAL-FEATURES AND PATHOGENESIS OF INTRACEREBRAL HEMORRHAGE AFTER RT-PA AND HEPARIN-THERAPY FOR ACUTE MYOCARDIAL-INFARCTION - THE THROMBOLYSIS IN MYOCARDIAL-INFARCTION (TIMI)-II PILOT AND RANDOMIZED CLINICAL-TRIAL COMBINED EXPERIENCE SO NEUROLOGY LA English DT Article ID TISSUE PLASMINOGEN-ACTIVATOR; CEREBRAL AMYLOID ANGIOPATHY; INTRACRANIAL HEMORRHAGE; CORONARY THROMBOLYSIS; INTRAVENOUS STREPTOKINASE; ALZHEIMERS-DISEASE; PHASE-II; RISK; COMPLICATIONS; STROKE AB Parenchymatous intracerebral hemorrhage (ICH) is a serious, infrequent complication of thrombolytic therapy for acute myocardial, infarction. We studied the clinical and radiologic features, manner of presentation, associated factors, and temporal course in 23 patients with ICH associated with 150 mg or 100 mg recombinant tissue-type plasminogen activator (rt-PA) and heparin therapy for acute myocardial infarction in the Thrombolysis in Myocardial Infarction (TIMI) II Pilot and Randomized Clinical Trial. In TIMI II, 13 of the 23 ICH patients developed or maintained systolic blood pressure greater than or equal to 160 mm Hg or diastolic blood pressure greater than or equal to 90 mm Hg during the rt-PA infusion and before the onset of neurologic symptoms. Six patients (26%) had life-threatening ventricular arrhythmias, five before onset of neurologic symptoms. A decreased level of consciousness was the earliest neurologic abnormality in 15 (65%) and the most common initial physical finding (in 19, or 82%). Onset was usually gradual (70%), but time to maximal deficit was frequently (61%) within 6 hours of onset. The locations of the primary ICH sites were lobar in 16 (70%), thalamic in four (17%), and brainstem-cerebellum in three (13%), but the putamen was never the primary site. Multiple lobar hemorrhages occurred in six cases (26%). The timing and size of ICH was similar among patients treated with 150 mg rt-PA and 100 mg rt-PA. Brain CT demonstrated an arteriovenous malformation in one case. Four patients had hypofibrinogenemia, which was profound in three patients. Pathologic findings were available for five patients. Of these, three patients had cerebral amyloid angiopathy, and one had hemorrhagic transformation of an ischemic cerebral infarction found at autopsy. We conclude that ICH following rt-PA and heparin therapy for acute myocardial infarction presents as a distinctive clinical syndrome. Intracerebral bleeding after combined thrombolytic and antithrombotic therapy may be associated with cerebral amyloid angiopathy and other vascular lesions. Acute or persistent hypertension before or during rt-PA infusion, life-threatening ventricular arrhythmias, and hypofibrinogenemia, either alone or in combination, may play roles in some cases. Care should be exercised when considering thrombolytic therapy for patients with risk factors for ICH. C1 MARYLAND MED RES INST,BALTIMORE,MD. UNIV MARYLAND,SCH MED,DEPT NEUROL,BALTIMORE,MD 21201. UNIV MIAMI,SCH MED,DEPT PATHOL,MIAMI,FL 33152. NHLBI,OFF PROGRAM PLANNING & EVALUAT,BETHESDA,MD 20892. UNIV MASSACHUSETTS,SCH MED,DEPT MED,WORCESTER,MA 01605. UNIV VERMONT,COLL MED,DEPT BIOCHEM,BURLINGTON,VT 05405. BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. NYU,SCH MED,DEPT MED,NEW YORK,NY 10016. BRIDGEPORT HOSP,CARDIOL SECT,BRIDGEPORT,CT. NEW YORK MED COLL,DEPT MED,VALHALLA,NY 10595. BAYLOR UNIV,MED CTR,BAYLOR CARDIOVASC INST,DALLAS,TX 75246. NHLBI,DIV HEART & VASC DIS,BETHESDA,MD 20892. UNIV VERMONT,SCH MED,DEPT PATHOL,BURLINGTON,VT 05405. NR 78 TC 85 Z9 87 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1995 VL 45 IS 4 BP 649 EP 658 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA QT454 UT WOS:A1995QT45400010 PM 7723950 ER PT J AU DELLAROCCHETTA, AI GADIAN, DG CONNELLY, A POLKEY, CE JACKSON, GD WATKINS, KE JOHNSON, CL MISHKIN, M VARGHAKHADEM, F AF DELLAROCCHETTA, AI GADIAN, DG CONNELLY, A POLKEY, CE JACKSON, GD WATKINS, KE JOHNSON, CL MISHKIN, M VARGHAKHADEM, F TI VERBAL MEMORY IMPAIRMENT AFTER RIGHT TEMPORAL-LOBE SURGERY - ROLE OF CONTRALATERAL DAMAGE AS REVEALED BY H-1 MAGNETIC-RESONANCE SPECTROSCOPY AND T-2 RELAXOMETRY SO NEUROLOGY LA English DT Article AB We assessed performance on selected tests of verbal memory in 48 patients who had undergone either anterior temporal lobectomy or selective amygdalo-hippocampectomy for the relief of pharmacologically intractable epilepsy. We related performance both to the side of surgical excision and to the presence or absence df abnormalities in the contralateral, unoperated, temporal lobe, as revealed by proton magnetic resonance spectroscopy (H-1 MRS) or T-2 relaxometry. There were abnormalities on the unoperated side detected by 1H MRS in 50% of the 34 patients who successfully underwent spectroscopy, and by T-2 relaxometry in 33% of the complete series of 48 patients. There was no systematic relationship between seizure outcome and the presence or absence of abnormalities on the unoperated side. Verbal memory deficits were present in patients with left-sided excision, regardless of whether there were abnormalities on the unoperated side. The patients with right-sided excision also had verbal memory deficits, but only in the group with magnetic resonance abnormalities on the contralateral (ie, left) side and only on delayed recall. The study extends previous findings on the role of the temporal lobes in memory and highlights the role of these new magnetic resonance techniques in relating cognitive processes to brain structures. C1 INST CHILD HLTH,RADIOL & PHYS UNIT,LONDON,ENGLAND. NIH,BETHESDA,MD 20892. MAUDSLEY HOSP & INST PSYCHIAT,LONDON,ENGLAND. GREAT ORMOND ST HOSP CHILDRENS NHS TRUST,DEPT RADIOL,LONDON,ENGLAND. GREAT ORMOND ST HOSP CHILDRENS NHS TRUST,DEPT PSYCHOL MED,LONDON,ENGLAND. RP DELLAROCCHETTA, AI (reprint author), INST CHILD HLTH,WOLFSON CTR,NEUROSCI UNIT,MECKLENBURGH SQ,LONDON WC1N 2AP,ENGLAND. RI Gadian, David/C-4961-2008; Watkins, Kate/A-6559-2012; Connelly, Alan/A-9065-2013; Jackson, Graeme/A-9064-2013 OI Jackson, Graeme/0000-0002-7917-5326 NR 12 TC 73 Z9 73 U1 0 U2 4 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1995 VL 45 IS 4 BP 797 EP 802 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA QT454 UT WOS:A1995QT45400033 ER PT J AU CRAPANZANO, KA CASANOVA, MF MANNHEIM, G AF CRAPANZANO, KA CASANOVA, MF MANNHEIM, G TI ASSOCIATION BETWEEN LITHIUM, GENDER, ABNORMAL EEGS, DEMENTIA, AND INCREASED CSF PROTEIN SO NEUROLOGY PSYCHIATRY AND BRAIN RESEARCH LA English DT Article DE LITHIUM; GENDER; DEMENTIA; BIPOLAR; DISORDER; ELECTROENCEPHALOGRAM; CEREBROSPINAL FLUID PROTEIN ID NEUROTOXICITY; DISORDER; LEVEL AB This retrospective chart review identifies a series of females who were all being treated with lithium and who developed dementia, increased CSF protein, and abnormal electroencephalograms. Previous reports have linked increased CSF protein primarily to males with an affective disorder. Treatment implications for the use of lithium in elderly females are discussed. C1 MED COLL GEORGIA,GEORGIA REG HOSP,AUGUSTA,GA 30907. NIMH,ST ELIZABETHS HOSP,WASHINGTON,DC. NR 14 TC 0 Z9 0 U1 0 U2 0 PU UNIVERSITATSVERLAG ULM GMBH PI ULM PA BENZSTRASSE 12, 89079 ULM, GERMANY SN 0941-9500 J9 NEUROL PSYCHIAT BR JI Neurol. Psychiatr. Brain Res. PD APR PY 1995 VL 3 IS 1 BP 17 EP 20 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA TC708 UT WOS:A1995TC70800003 ER PT J AU PARTIN, KM BOWIE, D MAYER, ML AF PARTIN, KM BOWIE, D MAYER, ML TI STRUCTURAL DETERMINANTS OF ALLOSTERIC REGULATION IN ALTERNATIVELY SPLICED AMPA RECEPTORS SO NEURON LA English DT Article ID D-ASPARTATE RECEPTOR; GLUTAMATE RECEPTORS; HIPPOCAMPAL-NEURONS; MOLECULAR-CLONING; PREGNENOLONE SULFATE; SYNAPTIC CURRENTS; DESENSITIZATION; MODULATION; CHANNELS; KAINATE AB The flip and flop splice variants of AMPA receptors show strikingly different sensitivity to allosteric regulation by cyclothiazide; heteromers assembled from GluR-A and GluR-B also exhibit splice variant-dependent differences in efficacy for activation by glutamate and kainate. The sensitivity for attenuation of desensitization by cyclothiazide for homomeric GluR-A was solely dependent upon exchange of Ser-750 (flip) and Asn-750 (flop), and was unaffected by mutagenesis of other divergent residues. In contrast, substantial alteration of the relative efficacy of glutamate versus kainate required mutation of multiple residues in the flip/flop region. Modulation by cyclothiazide was abolished by mutation of Ser-750 to Gln, the residue found at the homologous site in kainate-preferring subunits, whereas introduction of Ser at this site in GluR6 imparted sensitivity to cyclothiazide. RP PARTIN, KM (reprint author), NICHHD,CELLULAR & MOLEC NEUROPHYSIOL LAB,BETHESDA,MD 20892, USA. RI Mayer, Mark/H-5500-2013; Partin, Kathryn/A-8706-2015 OI Partin, Kathryn/0000-0003-3801-3299 NR 44 TC 130 Z9 133 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD APR PY 1995 VL 14 IS 4 BP 833 EP 843 DI 10.1016/0896-6273(95)90227-9 PG 11 WC Neurosciences SC Neurosciences & Neurology GA QU826 UT WOS:A1995QU82600017 PM 7718245 ER PT J AU COWLEY, DS ROYBYRNE, PP RADANT, A RITCHIE, JC GREENBLATT, DJ NEMEROFF, CB HOMMER, DW AF COWLEY, DS ROYBYRNE, PP RADANT, A RITCHIE, JC GREENBLATT, DJ NEMEROFF, CB HOMMER, DW TI BENZODIAZEPINE SENSITIVITY IN PANIC DISORDER - EFFECTS OF CHRONIC ALPRAZOLAM TREATMENT SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE PANIC DISORDER; BENZODIAZEPINES; ALPRAZOLAM; EYE MOVEMENTS; SACCADES ID RECEPTOR DOWN-REGULATION; SACCADIC EYE-MOVEMENTS; DIAZEPAM; TOLERANCE; PSYCHOMOTOR; PERFORMANCE; WITHDRAWAL; BINDING; PLACEBO; CLONAZEPAM AB The aim of the current study was to determine the degree to which patients with panic disorder develop tolerance to subjective and physiological effects of benzodiazepine after chronic treatment with alprazolam. Response to acute administration of diazepam was assessed in 19 panic disorder patients receiving chronic treatment with alprazolam and 23 untreated panic disorder patients. At baseline in the laboratory, the two groups did not differ in peak saccadic eye movement velocity, saccade latency, short-term memory, plasma cortisol and growth hormone concentrations, heart rate, and self-rated levels of sedation and anxiety. Compared with untreated patients, alprazolam-treated patients displayed significantly less diazepam-induced change in peak saccadic velocity, saccade latency, growth hormone secretion, memory, and self-rated levels of sedation. There was no difference between groups in diazepam effects on plasma cortisol concentrations or self-rated anxiety. Within alprazolam-treated patients, diazepam-induced slowing of peak saccade velocity was significantly inversely correlated with illness severity, as measured by reported panic attacks per week and severity of phobic avoidance, but not with alprazolam dose, blood level, or duration of treatment. Because the alprazolam-treated group reported more panic attacks per week than the untreated panic patients, treated patients were divided into those who were asymptomatic versus those with continuing panic attacks. The subgroup of nine alprazolam-treated subjects who were asymptomatic also showed significantly less diazepam effects than the group of untreated panic disorder patients, suggesting that overall group differences were at least partially attributable to the development of tolerance to selected benzodiazepine effects with chronic alprazolam treatment. C1 VET AFFAIRS MED CTR,DEPT PSYCHIAT & BEHAV SCI,SEATTLE,WA 98108. DUKE UNIV,MED CTR,DEPT PHARMACOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT PSYCHIAT,DURHAM,NC 27710. NIAAA,DURHAM,NC. TUFTS UNIV,NEW ENGLAND MED CTR,DIV CLIN PHARMACOL,BOSTON,MA 02111. EMORY UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,ATLANTA,GA. RP COWLEY, DS (reprint author), UNIV WASHINGTON,HARBORVIEW MED CTR,DEPT PSYCHIAT & BEHAV SCI ZA99,325 9TH AVE,SEATTLE,WA 98104, USA. FU NIAAA NIH HHS [AA08161]; NIMH NIH HHS [MH43449, MH49413] NR 54 TC 28 Z9 29 U1 0 U2 2 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD APR PY 1995 VL 12 IS 2 BP 147 EP 157 DI 10.1016/0893-133X(94)00074-A PG 11 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA QQ364 UT WOS:A1995QQ36400006 PM 7779243 ER PT J AU NIKULA, TK CURCIO, MJ BRECHBIEL, MW GANSOW, OA FINN, RD SCHEINBERG, DA AF NIKULA, TK CURCIO, MJ BRECHBIEL, MW GANSOW, OA FINN, RD SCHEINBERG, DA TI A RAPID, SINGLE-VESSEL METHOD FOR PREPARATION OF CLINICAL GRADE LIGAND CONJUGATED MONOCLONAL-ANTIBODIES SO NUCLEAR MEDICINE AND BIOLOGY LA English DT Note ID M195; ANTIGEN; DTPA AB A rapid, single Vessel method for the preparation of clinical grade chelate conjugated monoclonal antibodies has been developed. By use of an Amicon concentrator with reservoir, each of the steps necessary for the preparation of the conjugated drug may be performed in a single vessel. Advantages include reduced risk of metal, pyrogen and bacterial contamination; buffer exchanges are achieved rapidly and efficiently using a continuous dilution method. The radiolabeling efficiency, the radiochemical purity, the total immunoreactivity and the affinity of the final product have been evaluated in the production of CHXA-DTPA-chelate conjugated HuM195. The characteristics compare favorably to those achieved using our conventional synthetic methods. C1 MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. NCI,BETHESDA,MD 20892. MAP MED TECHNOL INC,SF-41160 TIKKAKOSKI,FINLAND. FU PHS HHS [RDI 33549, UO158260] NR 14 TC 56 Z9 56 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0883-2897 J9 NUCL MED BIOL JI Nucl. Med. Biol. PD APR PY 1995 VL 22 IS 3 BP 387 EP 390 DI 10.1016/0969-8051(94)00126-5 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QW845 UT WOS:A1995QW84500015 PM 7627155 ER PT J AU CLIVER, SP GOLDENBERG, RL CUTTER, GR HOFFMAN, HJ DAVIS, RO NELSON, KG AF CLIVER, SP GOLDENBERG, RL CUTTER, GR HOFFMAN, HJ DAVIS, RO NELSON, KG TI THE EFFECT OF CIGARETTE-SMOKING ON NEONATAL ANTHROPOMETRIC MEASUREMENTS SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID MATERNAL SMOKING; BIRTH-WEIGHT; FETAL GROWTH; RISK-FACTORS; PREGNANCY AB Objective: To estimate the effect of maternal cigarette smoking on birth weight, crown-heel length, and ten other neonatal anthropometric measurements. Methods: Data are from a cohort study on risk factors for fetal growth retardation (FGR) in multiparous women conducted from December 1985 through October 1988. Information on smoking status was collected four times during pregnancy. Data analysis included 1205 singleton infants of women delivering at term. Neonatal anthropometric measurements were obtained within 48 hours of birth, including birth weight, crown-heel length, ponderal index, head and abdominal circumferences, arm length and circumference, femur length and thigh circumference, and triceps, thigh, and subscapular skinfold measurements. Analysis of covariance models were used to assess the independent effect of smoking on each neonatal measurement. Results: Neonates born to women who reported smoking during the first trimester had a 0.6-1.9% reduction in most neonatal anthropometric measurements, resulting in an overall reduction of birth weight of 130 g (4%). Neonates born to women who continued to smoke throughout pregnancy had an average adjusted reduction in birth weight of 189 g (5.9%), compared with a 55 g (1.7%) reduction for neonates born to women who stopped smoking after the first trimester. For women who continued to smoke throughout pregnancy, an increased number of cigarettes smoked was associated with increased reductions in birth weight and neonatal chest and abdominal circumferences. For women who stopped smoking after the first trimester, stopping was a better predictor of neonatal anthropometric measurements than the number of cigarettes smoked early in pregnancy. Conclusions: Except for the ponderal index, all neonatal anthropometric measurements studied showed some negative effect of maternal cigarette smoking. Head circumference is the measurement least reduced. Smoking cessation is a better predictor of infant size than the number of cigarettes smoked in the first trimester. C1 NIDOCD,DIV EPIDEMIOL,STAT & DATA SYST BRANCH,BETHESDA,MD. CHILDRENS HOSP,DEPT PEDIAT,BIRMINGHAM,AL. AMC,CANC RES CTR,DENVER,CO. RP CLIVER, SP (reprint author), UNIV ALABAMA,DEPT OBSTET & GYNECOL,CTR OBSTET RES,DIV MATERNAL FETAL MED,620 S 20TH ST,ROOM 454,BIRMINGHAM,AL 35233, USA. FU BHP HRSA HHS [DHHS 282-92-0055]; NICHD NIH HHS [N01-HD-4-2811] NR 15 TC 101 Z9 102 U1 0 U2 1 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD APR PY 1995 VL 85 IS 4 BP 625 EP 630 DI 10.1016/0029-7844(94)00437-I PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA QN352 UT WOS:A1995QN35200026 PM 7898845 ER PT J AU KLEBANOFF, MA SHIONO, PH AF KLEBANOFF, MA SHIONO, PH TI TOP-DOWN, BOTTOM UP AND INSIDE-OUT - REFLECTIONS ON PRETERM BIRTH SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY LA English DT Discussion ID SERUM ALPHA-FETOPROTEIN; GROWTH-RETARDATION; DELIVERY; PREGNANCY; MEMBRANES; INFECTION C1 DAVID & LUCILE PACKARD FDN,CTR FUTURE CHILDREN,LOS ALTOS,CA. RP KLEBANOFF, MA (reprint author), NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,6100 BLDG,ROOM 7B03,BETHESDA,MD 20892, USA. NR 16 TC 54 Z9 54 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0269-5022 J9 PAEDIATR PERINAT EP JI Paediatr. Perinat. Epidemiol. PD APR PY 1995 VL 9 IS 2 BP 125 EP 129 DI 10.1111/j.1365-3016.1995.tb00126.x PG 5 WC Public, Environmental & Occupational Health; Obstetrics & Gynecology; Pediatrics SC Public, Environmental & Occupational Health; Obstetrics & Gynecology; Pediatrics GA QR951 UT WOS:A1995QR95100001 PM 7596888 ER PT J AU POGUE, GP KOUL, S LEE, NS DWYER, DM NAKHASI, HL AF POGUE, GP KOUL, S LEE, NS DWYER, DM NAKHASI, HL TI IDENTIFICATION OF INTRASPECIFIC AND INTERSPECIFIC LEISHMANIA GENETIC - POLYMORPHISMS BY ARBITRARY PRIMED POLYMERASE CHAIN-REACTIONS AND USE OF POLYMORPHIC DNA TO IDENTIFY DIFFERENTIALLY REGULATED GENES SO PARASITOLOGY RESEARCH LA English DT Article ID INFANTUM NICOLLE; KINETOPLAST DNA; DONOVANI; AMPLIFICATION; EVOLUTION; PROTOZOA; MARKERS; STRAINS; STOCKS; TOOL AB Arbitrary primed polymerase chain reactions (AP-PCR) were used to amplify different polymorphic genomic DNA fragments from various Old World Leishmania species. Using four 10-mer AP primers, geographic isolates of L. donovani and various Old World species of Leishmania could be readily distinguished from one another by the pattern of amplified DNA products. Our studies confirmed two important characteristics of AP-PCR: its abilities to amplify a consistent pattern of DNA fragments from the genomes of different isolates of a single species and to identify genetic polymorphisms between the species isolates. We selected three polymerphic DNA fragments that differentiate L. donovani geographic isolates for further analysis. Sequence analysis of the clones derived from these three polymorphic fragments revealed eight unique sequences. Six of eight unique clones hybridized to distinct RNAs upon Northern-blot analysis. Three of these six clones hybridized to RNAs expressed differentially in in vitro grown L. donovani pro- and ''amastigotes.'' One of the differentially expressed clones, LdE-6-1, exhibited restriction length polymorphisms that distinguished L. donovani from L. tropica and L. major. Comparative Northern blotting revealed that LdE-6-1 was differentially expressed in some members of the L. donovani species complex but not in L. major or L. tropica. These results demonstrate that AP-PCR can be used to generate products reflecting particular genes in organisms with low-complexity genomes. C1 US FDA,CTR BIOL EVALUAT & RES,DIV HEMATOL PROD,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 28 TC 20 Z9 20 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0044-3255 J9 PARASITOL RES JI Parasitol. Res. PD APR PY 1995 VL 81 IS 4 BP 282 EP 290 DI 10.1007/BF00931531 PG 9 WC Parasitology SC Parasitology GA QT555 UT WOS:A1995QT55500003 PM 7624284 ER PT J AU MCCUTCHAN, TF LI, J MCCONKEY, GA ROGERS, MJ WATERS, AP AF MCCUTCHAN, TF LI, J MCCONKEY, GA ROGERS, MJ WATERS, AP TI THE CYTOPLASMIC RIBOSOMAL-RNAS OF PLASMODIUM SPP SO PARASITOLOGY TODAY LA English DT Review ID GENES; FALCIPARUM; MALARIA; BERGHEI; IDENTIFICATION; SEQUENCE; EXPRESSION; CLONING; NUMBER AB Plasmodium spp maintain several structurally distinct sets of ribosomal RNA genes whose expression is developmentally regulated. This feature sets them apart from all other eukaryotes studied to date. In this review, Thomas McCutchan, Jun Li, Glenn McConkey, John Rogers and Andy Waters give an account of the progress in our understanding of this unusual phenomenon as it relates to the biology of the parasite. They also outline an interesting turnabout in scientific direction involving the use of the parasite as an important new model for the study of the eukaryotic ribosome. C1 LEIDEN UNIV,PARASITOL LAB,2300 RC LEIDEN,NETHERLANDS. RP MCCUTCHAN, TF (reprint author), NIAID,PARASIT DIS LAB,GROWTH & DEV SECT,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Waters, Andy/C-9377-2009 OI Waters, Andy/0000-0001-8900-2982 NR 32 TC 70 Z9 72 U1 0 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0169-4758 J9 PARASITOL TODAY JI Parasitol. Today PD APR PY 1995 VL 11 IS 4 BP 134 EP 138 DI 10.1016/0169-4758(95)80132-4 PG 5 WC Parasitology SC Parasitology GA QN612 UT WOS:A1995QN61200003 PM 15275356 ER PT J AU LANZARO, GC WARBURG, A AF LANZARO, GC WARBURG, A TI GENETIC-VARIABILITY IN PHLEBOTOMINE SANDFLIES - POSSIBLE IMPLICATIONS FOR LEISHMANIASIS EPIDEMIOLOGY SO PARASITOLOGY TODAY LA English DT Article ID FLY LUTZOMYIA-LONGIPALPIS; SAND FLIES DIPTERA; PSYCHODOPYGUS-COMPLEXUS DIPTERA; BRAIN-CELL KARYOTYPES; CUTANEOUS LEISHMANIASIS; PAPATASI DIPTERA; MAJOR INFECTION; CAUSATIVE AGENT; NORTH TUNISIA; PSYCHODIDAE AB The vast majority of genetic studies of phlebotomine sandflies have had as their goal the resolution of taxonomic problems. In this paper, Gregory Lanzaro and Alon Warburg summarize the literature describing levels of genetic polymorphism, both within and between sandfly species, and speculate on the significance of variability in the vector to the complex epidemiology of leishmoniasis. C1 HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT PARASITOL,IL-91010 JERUSALEM,ISRAEL. RP LANZARO, GC (reprint author), NIAID,MALARIA RES LAB,9000 ROCKVILLE PIKE,BLDG 4,ROOM 126,BETHESDA,MD 20892, USA. NR 42 TC 41 Z9 41 U1 0 U2 5 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0169-4758 J9 PARASITOL TODAY JI Parasitol. Today PD APR PY 1995 VL 11 IS 4 BP 151 EP 154 DI 10.1016/0169-4758(95)80137-5 PG 4 WC Parasitology SC Parasitology GA QN612 UT WOS:A1995QN61200008 ER PT J AU EPPS, RP MANLEY, MW GLYNN, TJ AF EPPS, RP MANLEY, MW GLYNN, TJ TI TOBACCO USE AMONG ADOLESCENTS - STRATEGIES FOR PREVENTION SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID SMOKELESS TOBACCO; SMOKING CESSATION; TRAINING PHYSICIANS; CIGARETTE-SMOKING; CHILDREN; CALIFORNIA; PROGRAM; TRIAL; YOUTH; RISK AB Tobacco use is a major public health issue that has its onset primarily during the pediatric years. Preventing the onset of tobacco use by children and adolescents should be a priority. A comprehensive strategy includes interventions by pediatricians and other health professionals, policy changes, advertising restrictions, comprehensive school health education programs, and community advocacy. Because the physician-parent-chiId relationship is unique, physicians have many opportunities to help prevent tobacco use, both in their offices and in their communities. C1 HOWARD UNIV,COLL MED,DEPT PEDIAT & CHILD HLTH,WASHINGTON,DC. RP EPPS, RP (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC CONTROL SCI PROGRAM,PUBL HLTH APPLICAT RES BRANCH,EPN 241,BETHESDA,MD 20892, USA. NR 68 TC 21 Z9 22 U1 2 U2 6 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0031-3955 J9 PEDIATR CLIN N AM JI Pediatr. Clin. N. Am. PD APR PY 1995 VL 42 IS 2 BP 389 EP 402 PG 14 WC Pediatrics SC Pediatrics GA QT960 UT WOS:A1995QT96000012 PM 7724265 ER PT J AU FRATES, RC SCOTT, S HAMMOND, KB BROOKS, JO RICHARDSON, CJ ROBERTS, DD AF FRATES, RC SCOTT, S HAMMOND, KB BROOKS, JO RICHARDSON, CJ ROBERTS, DD TI INFANTS AND YOUNG-CHILDREN WITH CYSTIC-FIBROSIS HAVE HIGH-LEVELS OF SERUM SIALYL LEWIS(A) ANTIGEN SO PEDIATRIC RESEARCH LA English DT Article ID MONOCLONAL-ANTIBODY 19-9; MUCIN-ASSOCIATED ANTIGEN; GASTROINTESTINAL CANCER; BLOOD-GROUP; CA-19-9; ASSAY; EXPRESSION; MARKER; GENE AB Previous studies suggest that serum levels of the mucin-associated sialyl Lewis(a) (Le(a)) antigen (NeuAC alpha 2-3 Gal beta 1-3 [Fuc alpha 1-4]GlcNAc beta 1...) correlate with the pulmonary status of cystic fibrosis (CF) patients who have Le(a) or Lewis(b) blood types and can form the antigen. However, there is little information on serum sialyl Le(a) antigen levels in CF patients or normal children younger than 9 y. We measured serum antigen levels using the MAb 19-9 in normal term neonates, CF infants and young children, and infants and children who had bronchopulmonary dysplasia or asthma. The mean serum sialyl Le(a) antigen level of the CF patients was 46.7 U/mL, significantly above (p < 0.01) the mean levels of the three other groups. The mean serum sialyl Le(a) levels of the three non-CF groups were not significantly different from one another or from published normal values. We conclude that serum sialyl Le(a) antigen levels are elevated early in CF, but are normal in asthma and bronchopulmonary dysplasia patients. C1 CHILDRENS HOSP,PEDIAT CRC CORE LAB,DENVER,CO 80262. STANFORD UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,STANFORD,CA 94305. UNIV TEXAS,MED BRANCH,DEPT PEDIAT,GALVESTON,TX 77550. NCI,PATHOL LAB,BETHESDA,MD 20892. RP FRATES, RC (reprint author), UNIV TEXAS,SCH MED,DEPT PEDIAT,MSB 3228,6431 FANNIN ST,HOUSTON,TX 77030, USA. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 FU NCRR NIH HHS [M01-RR00069] NR 31 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP 460 EP 464 DI 10.1203/00006450-199504000-00013 PN 1 PG 5 WC Pediatrics SC Pediatrics GA QP080 UT WOS:A1995QP08000013 PM 7596685 ER PT J AU ABRAMS, SA RITCHIE, LD OBRIEN, KO WOODHOUSE, LR YERGEY, AL VIEIRA, NE FUNG, EB KING, JC AF ABRAMS, SA RITCHIE, LD OBRIEN, KO WOODHOUSE, LR YERGEY, AL VIEIRA, NE FUNG, EB KING, JC TI PREGNANCY AND LACTATION ARE ASSOCIATED WITH CHANGES IN MATERNAL CALCIUM KINETICS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 BAYLOR COLL MED, USDA ARS, CHILDRENS NUTR RES CTR, HOUSTON, TX 77030 USA. NICHHD, BETHESDA, MD 20892 USA. UNIV CALIF BERKELEY, BERKELEY, CA 94720 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A301 EP A301 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201787 ER PT J AU BARON, J WINER, KK YANOVSKI, JA CUNNINGHAM, AW LAUE, L ZIMMERMAN, D CUTLER, GB AF BARON, J WINER, KK YANOVSKI, JA CUNNINGHAM, AW LAUE, L ZIMMERMAN, D CUTLER, GB TI GAIN-OF-FUNCTION MUTATIONS OF THE CA2+-SENSING RECEPTOR CAUSE AUTOSOMAL-DOMINANT HYPOPARATHYROIDISM SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, DEV ENDOCRINOL, BETHESDA, MD USA. MAYO CLIN & MAYO FDN, DEPT PEDIAT, ROCHESTER, MN 55905 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A84 EP A84 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200492 ER PT J AU BOYCE, WT HIGLEY, JD JEMERIN, JJ CHAMPOUX, M SUOMI, SJ AF BOYCE, WT HIGLEY, JD JEMERIN, JJ CHAMPOUX, M SUOMI, SJ TI TYMPANIC TEMPERATURE ASYMMETRY AND STRESS BEHAVIOR IN RHESUS MACAQUES AND CHILDREN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UCSF, DEPT PEDIAT, SAN FRANCISCO, CA USA. NICHHD, COMPARAT ETHOL LAB, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A13 EP A13 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200065 ER PT J AU CORWIN, M COTTON, T NEUMAN, M BAIRD, T BROOKS, L CROWELL, D TINSLEY, L HOPPENBROUWERS, T KEENS, T DAVIDSONWARD, S RAMANATHAN, R HUNT, C HUFFORD, D LISTER, G WEESEMAYER, D SILVESTRI, J WILLINGER, M AF CORWIN, M COTTON, T NEUMAN, M BAIRD, T BROOKS, L CROWELL, D TINSLEY, L HOPPENBROUWERS, T KEENS, T DAVIDSONWARD, S RAMANATHAN, R HUNT, C HUFFORD, D LISTER, G WEESEMAYER, D SILVESTRI, J WILLINGER, M TI THE CHIME PILOT-STUDY SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, ROCKVILLE, MD USA. BOSTON UNIV, DEPT PEDIAT, BOSTON, MA 02215 USA. CASE WESTERN RESERVE UNIV, DEPT PEDIAT, CLEVELAND, OH 44106 USA. UNIV HAWAII, DEPT PEDIAT, HONOLULU, HI 96822 USA. UNIV SO CALIF, LOS ANGELES, CA 90089 USA. MED COLL OHIO, TOLEDO, OH 43699 USA. YALE UNIV, NEW HAVEN, CT 06520 USA. RUSH UNIV, CHICAGO, IL 60612 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A389 EP A389 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08202318 ER PT J AU CROWE, JE BUI, PT KARRON, RA CLEMENTS, ML WRIGHT, PF CHANOCK, RM MURPHY, BR AF CROWE, JE BUI, PT KARRON, RA CLEMENTS, ML WRIGHT, PF CHANOCK, RM MURPHY, BR TI LIVE ATTENUATED MUTANTS OF RESPIRATORY SYNCYTIAL VIRUS (RSV) - IN-VITRO MARKERS AND REPLICATION IN MICE OR CHIMPANZEES CORRELATE WITH LEVEL OF ATTENUATION FOR SERONEGATIVE HUMAN INFANTS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIH, INFECT DIS LAB, BETHESDA, MD 20892 USA. VANDERBILT UNIV, CTR VACCINE EVALUAT, NASHVILLE, TN 37240 USA. JOHNS HOPKINS UNIV, CTR IMMUNIZ RES, BALTIMORE, MD 21218 USA. RI Crowe, James/B-5549-2009 OI Crowe, James/0000-0002-0049-1079 NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A172 EP A172 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201018 ER PT J AU DONOVAN, EF EHRENKRANZ, RA TYSON, JE VERTER, JI WRIGHT, LL AF DONOVAN, EF EHRENKRANZ, RA TYSON, JE VERTER, JI WRIGHT, LL TI GESTATIONAL-AGE BY NEW BALLARD SCORE (NBS) IS GREATER-THAN THE BEST OBSTETRICAL ESTIMATE OF GESTATIONAL-AGE IN 24-TO-27-WEEK INFANTS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL RES NETWORK, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A203 EP A203 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201202 ER PT J AU EHRENKRANZ, RA YOUNES, N FANAROFF, AA WRIGHT, LL STEVENSON, DK SHANKARAN, S DONOVAN, EF PAPILE, L AF EHRENKRANZ, RA YOUNES, N FANAROFF, AA WRIGHT, LL STEVENSON, DK SHANKARAN, S DONOVAN, EF PAPILE, L TI PREDICTING BPD AND OXYGEN DEPENDENCE AT 36 WEEKS POST-CONCEPTUAL AGE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL RES NETWORK, BETHESDA, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 W CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A330 EP A330 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201965 ER PT J AU EHRENKRANZ, RA VERTER, J FANAROFF, AA WRIGHT, LL STEVENSON, DK SHANKARAN, S PAPILE, L DONOVAN, EF AF EHRENKRANZ, RA VERTER, J FANAROFF, AA WRIGHT, LL STEVENSON, DK SHANKARAN, S PAPILE, L DONOVAN, EF TI BPD - WHATS IN A DEFINITION SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL RES NETWORK, BETHESDA, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 W CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A330 EP A330 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201964 ER PT J AU GRAHAM, JM BIESECKER, LG AF GRAHAM, JM BIESECKER, LG TI THE GENETICS OF PALLISTER-HALL SYNDROME SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, CEDARS SINAI MED CTR, CTR MED GENET BIRTH DEFECTS, LOS ANGELES, CA 90024 USA. NIH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A82 EP A82 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200480 ER PT J AU HAYEK, A BEATTIE, GM MALLY, MI LOPEZ, AD RUBIN, J OTONKOSKI, T QUARANTA, V AF HAYEK, A BEATTIE, GM MALLY, MI LOPEZ, AD RUBIN, J OTONKOSKI, T QUARANTA, V TI EPITHELIAL CELL-CELL CONTACT MEDIATED MECHANISMS REGULATE INSULIN GENE-TRANSCRIPTION IN HUMAN FETAL PANCREATIC-CELLS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO, SCH MED, DEPT PEDIAT, WHITTIER INST, LA JOLLA, CA 92093 USA. SCRIPPS RES INST, LA JOLLA, CA USA. NCI, BETHESDA, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A62 EP A62 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200359 ER PT J AU HU, N MACLENNAN, MJ YOSHIGI, M KELLER, BB AF HU, N MACLENNAN, MJ YOSHIGI, M KELLER, BB TI ATRIAL EJECTION VOLUME MATCHES VENTRICULAR ACTIVE FILLING VOLUME IN THE STAGE 16 TO 27 CHICK-EMBRYO SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV ROCHESTER, NIH, SCOR PEDIATR CARDIOVASC DIS, ROCHESTER, NY 14627 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A27 EP A27 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200148 ER PT J AU HU, N MACLENNAN, MJ TINNEY, JP KELLER, BB AF HU, N MACLENNAN, MJ TINNEY, JP KELLER, BB TI ATRIAL PRESSURE-VOLUME LOOP CHARACTERISTICS IN THE STAGE 16 TO 27 CHICK-EMBRYO SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV ROCHESTER, STRONG CHILDRENS RES CTR, NIH, SCOR PEDIATR CARDIOVASC DIS, ROCHESTER, NY 14627 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A27 EP A27 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200147 ER PT J AU JOHNSON, YR HERMAN, AA YU, KF HOFFMAN, HJ AF JOHNSON, YR HERMAN, AA YU, KF HOFFMAN, HJ TI TIME TO SUBSEQUENT PREGNANCY AS A FUNCTION OF AGE AT 1ST PREGNANCY AND PERINATAL OUTCOME OF THE PREVIOUS PREGNANCY IN A COHORT OF ADOLESCENT WOMEN - A SURVIVAL ANALYSIS OF MISSOURI VITAL BIRTH AND DEATH RECORDS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A6 EP A6 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200024 ER PT J AU KALER, SG GAHL, WA AF KALER, SG GAHL, WA TI MOLECULAR INFLUENCE ON RESPONSIVENESS TO VERY EARLY COPPER REPLACEMENT IN CLASSICAL MENKES DISEASE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, HGB, HUMAN BIOCHEM GENET SECT, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A149 EP A149 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200879 ER PT J AU KENNEY, LB MILLER, BA RIES, LAG NICHOLSON, HS BYRNE, J REAMAN, GH AF KENNEY, LB MILLER, BA RIES, LAG NICHOLSON, HS BYRNE, J REAMAN, GH TI INCREASED INCIDENCE OF CANCER IN UNITED-STATES INFANTS, 1980 TO 1990 SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV, CHILDRENS NATL MED CTR, DEPT HEMATOL ONCOL, WASHINGTON, DC 20052 USA. NCI, DIV CANC PREVENT & CONTROL, BETHESDA, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A159 EP A159 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200941 ER PT J AU KLEBANOFF, M CLEMENS, J AF KLEBANOFF, M CLEMENS, J TI MATERNAL SMOKING DURING PREGNANCY AND CHILDHOOD-CANCER SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A108 EP A108 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200635 ER PT J AU KOHN, DB WEINBERG, KI LENARSKY, C CROOKS, G HEISS, LN NOLTA, JA WARA, D ELDER, M WILLIAMSHERMAN, D BOWEN, T MOEN, RC BLAESE, RM AF KOHN, DB WEINBERG, KI LENARSKY, C CROOKS, G HEISS, LN NOLTA, JA WARA, D ELDER, M WILLIAMSHERMAN, D BOWEN, T MOEN, RC BLAESE, RM TI GENE-THERAPY FOR NEONATES WITH ADA DEFICIENCY BY TRANSFER OF THE HUMAN ADA CDNA INTO UMBILICAL-CORD CD34+ CELLS 2-YEAR FOLLOW-UP SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP, LOS ANGELES, CA 90027 USA. DUKE UNIV, DURHAM, NC 27706 USA. NIH, BETHESDA, MD 20892 USA. CALGARY CHILDRENS HOSP, CALGARY, AB, CANADA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A9 EP A9 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200038 ER PT J AU LEE, HN BROUWERS, P DECARLI, C CIVITELLO, LA GANZEVOORT, JW PIZZO, PA AF LEE, HN BROUWERS, P DECARLI, C CIVITELLO, LA GANZEVOORT, JW PIZZO, PA TI CEREBRAL CALCIFICATIONS ON COMPUTED-TOMOGRAPHY BRAIN-SCANS ARE A VALID MEASURE OF UNDERLYING NEUROPATHOLOGY IN CHILDREN WITH AIDS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA. RI DeCarli, Charles/B-5541-2009 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A382 EP A382 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08202274 ER PT J AU LEONG, GM MERCADOASIS, LB REYNOLDS, JC PARISI, R NIEMAN, LK CUTLER, GB CHROUSOS, GP AF LEONG, GM MERCADOASIS, LB REYNOLDS, JC PARISI, R NIEMAN, LK CUTLER, GB CHROUSOS, GP TI THE LONG-TERM EFFECTS OF PEDIATRIC CUSHING SYNDROME ON BONE-MINERAL DENSITY AND IMPLICATIONS FOR PEAK BONE MASS ACCRUAL SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, DEB, DEPTS NUCL MED, BETHESDA, MD USA. NIH, CC, DEPT CLIN NUTR, BETHESDA, MD 20892 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A93 EP A93 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200542 ER PT J AU MARINI, JC WANG, Q AF MARINI, JC WANG, Q TI ANTISENSE OLIGONUCLEOTIDES SELECTIVELY SUPPRESS PRODUCTION OF MUTANT ALPHA-2(I) COLLAGEN IN OSTEOGENESIS IMPERFECTA TYPE-IV FIBROBLASTS - AN APPROACH TO GENE-THERAPY FOR A DOMINANT DISORDER OF MATRIX STRUCTURAL PROTEIN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, HUMAN GENET BRANCH, BETHESDA, MD USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A150 EP A150 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200885 ER PT J AU MAURAS, N VIEIRA, N YERGEY, AL AF MAURAS, N VIEIRA, N YERGEY, AL TI ESTROGEN THERAPY ENHANCES CALCIUM-ABSORPTION AND DIMINISHES BONE TURNOVER IN YOUNG HYPOGONADAL GIRLS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, BETHESDA, MD USA. NEMOURS CHILDRENS CLIN, DIV ENDO, JAX, FL USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A94 EP A94 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200550 ER PT J AU MCCUNE, SK BRENNEMAN, DE HILL, JM AF MCCUNE, SK BRENNEMAN, DE HILL, JM TI THE ACUTE EFFECT OF DEXAMETHASONE ADMINISTRATION OF VIP MESSENGER-RNA EXPRESSION IN THE RAT CNS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV, DEPT PEDIAT, DIV NEONATOL, BALTIMORE, MD 21218 USA. NICHHD, DEV NEUROBIOL LAB, DEV & MOLEC PHARMACOL SECT, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A383 EP A383 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08202278 ER PT J AU MILLS, JL RAYMOND, E FEARS, T ROBISON, L NICHOLSON, S SKLAR, C BYRNE, J AF MILLS, JL RAYMOND, E FEARS, T ROBISON, L NICHOLSON, S SKLAR, C BYRNE, J TI MENARCHE IN LONG-TERM SURVIVORS OF ACUTE LYMPHOCYTIC-LEUKEMIA (ALL) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, ARCADIA, CA USA. NCI, ARCADIA, CA USA. CHILDRENS CANC GRP, ARCADIA, CA USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A162 EP A162 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200959 ER PT J AU MOHAN, P KALER, SG ARTHURSMITH, A KERZNER, B ROSE, MC AF MOHAN, P KALER, SG ARTHURSMITH, A KERZNER, B ROSE, MC TI DETECTION OF COPPER-BINDING LIGANDS IN RAT BILE BY A NEW TECHNIQUE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV, CHILDRENS RES INST, DEPT PEDIAT, DIV GASTROENTEROL, WASHINGTON, DC 20052 USA. NICHHD, HUMAN GENET BRANCH, BETHESDA, MD 20892 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A129 EP A129 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200760 ER PT J AU MUELLER, BU TANNENBAUM, S PIZZO, PA AF MUELLER, BU TANNENBAUM, S PIZZO, PA TI BONE-MARROW FINDINGS IN CHILDREN WITH HUMAN IMMUNODEFICIENCY (HIV) INFECTION SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA. WARREN GRANT MAGNUSON CLIN CTR, DEPT CLIN PATHOL, HEMATOL SERV, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A163 EP A163 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200962 ER PT J AU NUNEZ, SB MEDIN, JA SEGARS, JH AF NUNEZ, SB MEDIN, JA SEGARS, JH TI PATTERN OF RXR-BETA PPAR-ALPHA HETERODIMERIZATION BINDING TO THE ERE COMPARED TO THE ESTROGEN-RECEPTOR BINDING SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, DEB, LMMB, BETHESDA, MD 20892 USA. NINCDS, DMNB, MMGS, BETHESDA, MD 20892 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A95 EP A95 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200556 ER PT J AU RAY, PE BRYANT, JL KLOTMAN, PE AF RAY, PE BRYANT, JL KLOTMAN, PE TI INCREASED BFGF BINDING TO HEPARAN-SULFATE PROTEOGLYCANS IN HIV-ASSOCIATED NEPHROPATHY IN TRANSGENIC MICE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS NATL MED CTR, CTR I CRI, WASHINGTON, DC USA. NIDR, LDB, BETHESDA, MD 20892 USA. NIDR, LOM, BETHESDA, MD 20892 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A368 EP A368 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08202189 ER PT J AU SARAFOVA, AP MARINI, JC AF SARAFOVA, AP MARINI, JC TI CULTURED OSTEOBLASTS FROM OSTEOGENESIS IMPERFECTA PATIENTS SYNTHESIZE COLLAGEN WHICH IS ELECTROPHORETICALLY DISTINCT FROM PATIENTS FIBROBLAST COLLAGEN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, HUMAN GENET BRANCH, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A152 EP A152 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200896 ER PT J AU SARNAIK, SA SIMPSON, P KAPLAN, J SCHIFFMAN, G SCHNEERSON, R AF SARNAIK, SA SIMPSON, P KAPLAN, J SCHIFFMAN, G SCHNEERSON, R TI RESPONSE TO CONJUGATE PNEUMOCOCCAL VACCINE TYPE 6B-TT IN INFANTS WITH SICKLE-CELL DISEASES SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP MICHIGAN, CTR SICKLE CELL, DETROIT, MI 48201 USA. NICHHD, BETHESDA, MD 20892 USA. SUNY HLTH SCI CTR, BROOKLINE, NY USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A187 EP A187 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201109 ER PT J AU SHANDAS, R SOLOWIEJCYK, D JONES, M VALDESCRUZ, L AF SHANDAS, R SOLOWIEJCYK, D JONES, M VALDESCRUZ, L TI A NEW METHOD FOR CALCULATING FLOW-THROUGH BILEAFLET MECHANICAL VALVES BASED ON THE PROXIMAL FLOW CONVERGENCE TECHNIQUE - STUDIES IN A CHRONIC ANIMAL-MODEL SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NHLBI, LAMS, BETHESDA, MD 20892 USA. CHILDRENS HOSP, DENVER, CO 80218 USA. COLUMBIA UNIV, NEW YORK, NY 10027 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A35 EP A35 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200193 ER PT J AU SHANDAS, R JONES, M VALDESCRUZ, L AF SHANDAS, R JONES, M VALDESCRUZ, L TI DIGITAL PARTICLE IMAGE VELOCIMETRY MEASUREMENTS OF VELOCITY PROFILES PROXIMAL AND DISTAL TO BILEAFLET MECHANICAL VALVES - AN IN-VITRO STUDY SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP, DENVER, CO 80218 USA. NHLBI, LAMS, BETHESDA, MD 20892 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A34 EP A34 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200192 ER PT J AU SHANKARAN, S FANAROFF, AA WRIGHT, LL VERTER, J STEVENSON, D EHRENKRANZ, R DONOVAN, E AF SHANKARAN, S FANAROFF, AA WRIGHT, LL VERTER, J STEVENSON, D EHRENKRANZ, R DONOVAN, E TI CHARACTERISTICS OF EARLY (LESS-THAN-OR-EQUAL-TO-12 HR) DEATH AMONG VLBW NEONATES SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL RES NETWORK, BETHESDA, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A236 EP A236 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201402 ER PT J AU SIDRANSKY, E FARTASCH, M ELIAS, PM GINNS, EI HOLLERAN, WM AF SIDRANSKY, E FARTASCH, M ELIAS, PM GINNS, EI HOLLERAN, WM TI UNIQUE EPIDERMAL ABNORMALITIES RESULTING FROM SEVERE GLUCOCEREBROSIDASE DEFICIENCY MAY DISTINGUISH TYPE-2 FROM OTHER TYPES OF GAUCHER DISEASE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR, SAN FRANCISCO, CA USA. NIMH, CLIN NEUROSCI BRANCH, BETHESDA, MD 20892 USA. UNIV CALIF SAN FRANCISCO, SCH MED, DEPT DERMATOL, SAN FRANCISCO, CA 94143 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A152 EP A152 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200900 ER PT J AU STAAT, MA DELORIA, MA SHADLE, C BOHIDAR, N MENDELMAN, PM SANTOSHAM, M HIGHAM, S GUPTA, RK KASLOW, RA SIBER, GR AF STAAT, MA DELORIA, MA SHADLE, C BOHIDAR, N MENDELMAN, PM SANTOSHAM, M HIGHAM, S GUPTA, RK KASLOW, RA SIBER, GR TI SIMULTANEOUS ADMINISTRATION OF HAEMOPHILUS-INFLUENZAE TYPE-B CONJUGATE VACCINE (PRP-OMP) AND DIPHTHERIA-TETANUS-PERTUSSIS VACCINE (DTP) - THE EFFECT OF PRP-OMP ON THE DTP IMMUNE-RESPONSE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS PUBL HLTH BIOL LABS, BOSTON, MA USA. MERCK RES LAB, W POINT, PA USA. JOHNS HOPKINS UNIV, BALTIMORE, MD 21218 USA. NIAID, BETHESDA, MD 20892 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A115 EP A115 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200678 ER PT J AU STARC, TJ LIPSHULTZ, S EASLEY, K KAPLAN, S BRICKER, T LAI, W COLAN, S SCHLUCHTER, M AF STARC, TJ LIPSHULTZ, S EASLEY, K KAPLAN, S BRICKER, T LAI, W COLAN, S SCHLUCHTER, M TI CARDIAC COMPLICATIONS IN HIV-INFECTED CHILDREN - THE NHLBI P2C2 STUDY SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NHLBI, BETHESDA, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A189 EP A189 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201116 ER PT J AU STEVENSON, DK FANAROFF, AA DONOVAN, EF EHRENKRANZ, RA SHANKARAN, S VERTER, J WRIGHT, LL AF STEVENSON, DK FANAROFF, AA DONOVAN, EF EHRENKRANZ, RA SHANKARAN, S VERTER, J WRIGHT, LL TI WHY IS MALE GENDER A RISK FACTOR FOR VERY-LOW-BIRTH-WEIGHT (501-1500G) MORBIDITIES SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL RES NETWORK, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A238 EP A238 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201415 ER PT J AU STRATAKIS, CA GIRALDEZ, RA HARRIS, CP GERNICA, A FEUILLAN, P RENNERT, OM CHROUSOS, GP AF STRATAKIS, CA GIRALDEZ, RA HARRIS, CP GERNICA, A FEUILLAN, P RENNERT, OM CHROUSOS, GP TI RAPID-DETERMINATION OF CHROMOSOME X MONOSOMY AND OR MOSAICISM IN BUCCAL SMEARS OF PATIENTS WITH TURNER SYNDROME BY FLUORESCENT IN-SITU HYBRIDIZATION (FISH) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, DEB, BETHESDA, MD USA. ONCOR INC, GAITHERSBURG, MD USA. UNIV WISCONSIN, STATE LAB HYG, MADISON, WI 53706 USA. GEORGETOWN UNIV, CHILDRENS MED CTR, WASHINGTON, DC 20007 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A153 EP A153 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200903 ER PT J AU STRATAKIS, CA PRAS, E TSIGOS, C KARL, M PAPANICOLAOU, DA KASTNER, DL CARNEY, JA CHROUSOS, GP AF STRATAKIS, CA PRAS, E TSIGOS, C KARL, M PAPANICOLAOU, DA KASTNER, DL CARNEY, JA CHROUSOS, GP TI GENETICS OF CARNEY COMPLEX - PARENT-OF-ORIGIN EFFECTS AND PUTATIVE NON-MENDELIAN FEATURES IN AN AUTOSOMAL-DOMINANT DISORDER - ABSENCE OF COMMON DEFECTS OF THE ACTH RECEPTOR AND RET GENES SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, DEB, BETHESDA, MD USA. NIAM, ARB, BETHESDA, MD USA. GEORGETOWN UNIV, CHILDRENS MED CTR, WASHINGTON, DC 20007 USA. MAYO CLIN & MAYO FDN, ROCHESTER, MN 55905 USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A99 EP A99 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200580 ER PT J AU TAYEBI, N STUBBLEFIELD, B ELIASON, W KLINEBURGESS, A GINNS, EI SIDRANSKY, E AF TAYEBI, N STUBBLEFIELD, B ELIASON, W KLINEBURGESS, A GINNS, EI SIDRANSKY, E TI MOLECULAR ANALYSIS OF SEVERE TYPE-2 GAUCHER DISEASE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NIMH, CLIN NEUROSCI BRANCH, BETHESDA, MD 20892 USA. NR 0 TC 1 Z9 1 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A153 EP A153 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200904 ER PT J AU VREMAN, HJ STEVENSON, DK OH, W LEMONS, JA VERTER, J FANAROFF, AA WRIGHT, LL AF VREMAN, HJ STEVENSON, DK OH, W LEMONS, JA VERTER, J FANAROFF, AA WRIGHT, LL TI VARIABILITY OF INTERLABORATORY BILIRUBIN MEASUREMENTS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL RES NETWORK, BETHESDA, MD USA. STANFORD UNIV, MED CTR, SCH MED, DEPT PEDIAT, STANFORD, CA 94305 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A243 EP A243 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201443 ER PT J AU WALSHSUKYS, M FANAROFF, A WRIGHT, L VERTER, J BAUER, C KORONES, S STEVENSON, D TYSON, I AF WALSHSUKYS, M FANAROFF, A WRIGHT, L VERTER, J BAUER, C KORONES, S STEVENSON, D TYSON, I TI PERSISTENT PULMONARY-HYPERTENSION OF THE NEWBORN (PPHN) - PROSPECTIVE MULTICENTER STUDY OF TREATMENTS AND OUTCOMES SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL NETWORK, BETHESDA, MD USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A244 EP A244 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201446 ER PT J AU WALSHSUKYS, M FANAROFF, A WRIGHT, L VERTER, J BAUER, C KOROPES, S STEVENSON, D TYSON, I AF WALSHSUKYS, M FANAROFF, A WRIGHT, L VERTER, J BAUER, C KOROPES, S STEVENSON, D TYSON, I TI PERSISTENT PULMONARY-HYPERTENSION OF THE NEW (PPHN) - PRACTICE VARIATION AMONG ACADEMIC NICUS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL RES NETWORK, BETHESDA, MD USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A244 EP A244 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201447 ER PT J AU WALSHSUKYS, M TYSON, J FANAROFF, A WRIGHT, L VERTER, J BAUER, C KORONES, S STEVENSON, D AF WALSHSUKYS, M TYSON, J FANAROFF, A WRIGHT, L VERTER, J BAUER, C KORONES, S STEVENSON, D TI USE OF UNPROVED THERAPIES IN CRITICALLY ILL NEONATES SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, NEONATAL NETWORK, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A40 EP A40 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200227 ER PT J AU WANG, Q LEWIS, MB MARINI, JC AF WANG, Q LEWIS, MB MARINI, JC TI A NOVEL DELETION INSERTION MUTATION IN THE MESSENGER-RNA TRANSCRIBED FROM ONE ALPHA-1(I) COLLAGEN ALLELE IN FAMILY WITH DOMINANT TYPE-III OI AND GERMLINE MOSAICISM SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NICHHD, HUMAN GENET BRANCH, BETHESDA, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A155 EP A155 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200913 ER PT J AU WOODS, J WARD, G SALEM, N AF WOODS, J WARD, G SALEM, N TI LINOLENIC ACID (LNA) IN FORMULA MAY SUPPORT PROPER DOCOSAHEXAENOIC ACID (DHA) ACCRETION IN THE BRAIN BUT NOT IN THE RETINA SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 NATL INST ALCOHOLISM & ALCOHOL ABUSE, MEMBRANE BIOCHEM & BIOPHYS LAB, ROCKVILLE, MD USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A323 EP A323 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08201920 ER PT J AU YOSHIGI, M HU, N TINNEY, JP KELLER, BB AF YOSHIGI, M HU, N TINNEY, JP KELLER, BB TI FLOW DEPENDENCE OF ARTERIAL IMPEDANCE IN STAGE 24 CHICK-EMBRYOS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV ROCHESTER, NIH, SCOR PEDIAT CARDIOVASC DIS, ROCHESTER, NY 14627 USA. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A38 EP A38 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08200212 ER PT J AU MAYES, LC BORNSTEIN, MH CHAWARSKA, K GRANGER, RH AF MAYES, LC BORNSTEIN, MH CHAWARSKA, K GRANGER, RH TI INFORMATION-PROCESSING AND DEVELOPMENTAL ASSESSMENTS IN 3-MONTH-OLD INFANTS EXPOSED PRENATALLY TO COCAINE SO PEDIATRICS LA English DT Article DE COCAINE CRACK; HABITUATION; BAYLEY; RECOGNITION MEMORY; NOVEL REACTIVITY; ATTENTION; SUBJECT LOSS ID RECOGNITION MEMORY; SUBJECT LOSS; HABITUATION; PREGNANCY; PERFORMANCE; TEMPERAMENT; CONTINUITY; ABILITIES; GROWTH AB Objective. To determine the effect of prenatal cocaine exposure on 3-month infant information processing and developmental assessments. Methods. One hundred and eight infants, 61 cocaine-exposed and 47 controls, participated at 3 months of age in an infant-control habituation and novelty responsiveness procedure and in a developmental assessment using the Bayley Scales of Infant Development both administered by experimenters blind to the drug exposure status of the infant. Results. Compared to the non-drug-exposed group, infants exposed prenatally to cocaine were significantly more likely to fail to start the habituation procedure and, for those who did, significantly more likely to react with irritability early in the procedure. The majority of infants in both groups reached the habituation criterion, and among those who did there were no significant differences between cocaine and non-cocaine-exposed infants in habituation or in recovery to a novel stimulus. Infants who were cocaine-exposed showed comparatively depressed performance on the motor (Psychomotor Developmental Index) but not the mental (Mental Developmental Index (MDI)) scales of the Bayley. These results obtained for habituation and Bayley MDI controlling for both perinatal and sociodemographic factors. Conclusions. Differences in reactivity to novelty but not in information processing between cocaine-exposed and non-cocaine-exposed infants suggest that the effects of prenatal cocaine exposure may be on arousal and attention regulation rather than early cognitive processes. C1 NICHHD,NEW HAVEN,CT 06510. RP MAYES, LC (reprint author), YALE UNIV,CTR CHILD STUDY,230 S FRONTAGE RD,NEW HAVEN,CT 06510, USA. NR 55 TC 99 Z9 102 U1 1 U2 2 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 1995 VL 95 IS 4 BP 539 EP 545 PG 7 WC Pediatrics SC Pediatrics GA QR321 UT WOS:A1995QR32100015 PM 7700755 ER PT J AU DOWNING, GJ KILBRIDE, HW AF DOWNING, GJ KILBRIDE, HW TI EVALUATION OF AIRWAY COMPLICATIONS IN HIGH-RISK PRETERM INFANTS - APPLICATION OF FLEXIBLE FIBEROPTIC AIRWAY ENDOSCOPY SO PEDIATRICS LA English DT Article DE BRONCHOSCOPY; SUBGLOTTIC STENOSIS; TRACHEOMALACIA; MECHANICAL VENTILATION; BRONCHOPULMONARY; DYSPLASIA ID BIRTH-WEIGHT INFANT; SUBGLOTTIC STENOSIS; BRONCHOPULMONARY DYSPLASIA; ENDOTRACHEAL INTUBATION; CHILDREN; COLLAPSE AB Objectives. We sought to determine factors that would predict the development of subglottic stenosis (SGS) and tracheomalacia (TM) in preterm infants. The utility of a semiquantitative measurement of airway dimensions was assessed in relation to signs of airway complications. We also sought to determine from a high-risk population of infants those likely to have abnormal findings identified by bronchoscopic examination. Methods. Prospective airway endoscopy was performed for preterm infants who were intubated for 7 days or more or who demonstrated chronic oxygen needs beyond 28 days after birth and 36 weeks postconceptional age. Subjects were 117 preterm (less than 36 weeks' gestation) infants from two level III intensive care nurseries. Endoscopy was used to classify the type and degree of airway injury. Subglottic stenosis was defined subjectively and compared with an objective measurement using subglottic spatial relations described as a trans-subglottic/vocal cord ratio (TSG/VC). Clinical signs and symptoms and other risk factors were evaluated as significant predictors of SGS and TM, identified by bronchoscopy. Results. Moderate or severe airway abnormalities were identified in 32 patients (27.3%); 13 with SGS, 17 with TM, and 2 with both. All but one infant with TSG/VC less than 0.83 had signs and symptoms of airway dysfunction. Variables more commonly found in patients with SGS included greater number of intubations, use of inappropriately large endotracheal tubes, and longer duration of intubation. Higher averaged mean airway pressure during the first week after birth and lower gestational age were clinical features associated with TM. Conclusions. Flexible bronchoscopic evaluation of a high-risk population demonstrated a higher incidence of moderate or severe SGS or TM than previously sub suspected, Subglottic stenosis and TM appear to have different etiologies based on different factors associated with their development. The TSG/VC ratio correlated well with obstructive symptoms and may represent a means to quantitate clinically subglottic narrowing. Infants with chronic lung disease who have persistently elevated partial pressure of carbon dioxide, apnea, or phonation abnormalities are most likely to have airway abnormalities identifiable by bronchoscopy. C1 CHILDRENS MERCY HOSP,DEPT NEONATOL,KANSAS CITY,MO 64108. NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD. UNIV MISSOURI,KANSAS CITY,MO 64110. NR 27 TC 34 Z9 34 U1 0 U2 1 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 1995 VL 95 IS 4 BP 567 EP 572 PG 6 WC Pediatrics SC Pediatrics GA QR321 UT WOS:A1995QR32100021 PM 7700760 ER PT J AU ETCHES, PC FINER, NN EHRENKRANZ, RA WRIGHT, LL AF ETCHES, PC FINER, NN EHRENKRANZ, RA WRIGHT, LL TI CLINICAL MONITORING OF INHALED NITRIC-OXIDE SO PEDIATRICS LA English DT Letter C1 YALE UNIV,SCH MED,DEPT PEDIAT,NEW HAVEN,CT. NICHHD,CTR RES MOTHERS & CHILDRENS,BETHESDA,MD. RP ETCHES, PC (reprint author), UNIV ALBERTA,DEPT PEDIAT,DEPT NEWBORN MED,EDMONTON,AB,CANADA. NR 14 TC 5 Z9 5 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 1995 VL 95 IS 4 BP 620 EP 621 PG 2 WC Pediatrics SC Pediatrics GA QR321 UT WOS:A1995QR32100044 PM 7700777 ER PT J AU CAPORASO, N GOLDSTEIN, A AF CAPORASO, N GOLDSTEIN, A TI CANCER GENES - SINGLE AND SUSCEPTIBILITY - EXPOSING THE DIFFERENCE SO PHARMACOGENETICS LA English DT Editorial Material DE CANCER GENES; SINGLE GENES; SUSCEPTIBILITY GENES; EPIDEMIOLOGY ID BLADDER-CANCER; LUNG-CANCER; RISK; EXPOSURE; LINKAGE AB 'Single' genes, necessary and sufficient to cause cancer, are contrasted with 'susceptibility' genes that are neither, but may act in the presence of specific environmental exposures to alter the chances of cancer in the host. The former are rare, are of high absolute and relative risks, have minimal dependence on exposures and therefore have low population attributable risks. A small number of such genes are well established in the literature and typically exhibit familial aggregations of disease that serve as a starting point for genetic studies. 'Susceptibility' genes, as typified by the pharmacogenetic model, are common, have low relative and absolute risk, are strongly dependent upon exposure, and may have potentially high population attributable risks. Methanistic and epidemiologic data are suggestive but currently fall short of confirmation for these associations. Familial aggregation is not a prominent feature and epidemiological study designs with careful exposure assessment is the investigative method of choice. Both approaches require interdisciplinary expertise and benefit from advances in molecular biology. RP CAPORASO, N (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,GENET EPIDEMIOL BRANCH,EXECUT PLAZA N 439,6130 EXECUT BLVD,ROCKVILLE,MD 20892, USA. NR 27 TC 59 Z9 60 U1 0 U2 2 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD APR PY 1995 VL 5 IS 2 BP 59 EP 63 DI 10.1097/00008571-199504000-00001 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA RC328 UT WOS:A1995RC32800001 PM 7663529 ER PT J AU ONO, S TSUTSUI, M GONZALEZ, FJ SATOH, T MASUBUCHI, Y HORIE, T SUZUKI, T NARIMATSU, S AF ONO, S TSUTSUI, M GONZALEZ, FJ SATOH, T MASUBUCHI, Y HORIE, T SUZUKI, T NARIMATSU, S TI OXIDATIVE-METABOLISM OF BUNITROLOL BY COMPLEMENTARY DNA-EXPRESSED HUMAN CYTOCHROME-P450 ISOZYMES IN A HUMAN HEPATOMA-CELL LINE (HEP G2) USING RECOMBINANT VACCINIA VIRUS SO PHARMACOGENETICS LA English DT Article DE BUNITROLOL; OXIDATIVE METABOLISM; HUMAN CYTOCHROMES P450; VACCINIA VIRUS ID HUMAN-LIVER; MEPHENYTOIN HYDROXYLATION; ENZYME-ACTIVITIES; CYP2C SUBFAMILY; MICROSOMES; 4-HYDROXYLASE; POLYMORPHISM; INHIBITION; P-450; CDNA AB We examined the oxidative metabolism of a beta-blocker bunitrolol (ETL) by 10 human cytochromes P450 (CYP) (1A2, 2A6, 2B6, 2C8, 2C9, 2D6, 2E1, 3A3, 3A4 or 3A5), which were individually expressed in Hep G2 cells with a vaccinia virus complementary DNA expression system, Among the 10 isozymes, only CYP2D6 and 1A2 at a substrate concentration of 5 mu m, and CYP2C8 and 2C9 in addition to the two isozymes at a BTL concentration of 1 mM, exhibited detectable BTL 4-hydroxylase activities, The activities at 1 mM ETL were on the order of CYP2D6 (100% as relative activity) > CYP1A2 (86%) >> CYP2C8 and 2C9 (7-8%). Enzyme kinetic parameters of CYP2D6 were calculated to be 4.41 mu m as a K-m value and 0.442 nmol min(-1) per nmol CYP as a V-max value, Kinetic parameters of CYP1A2 were calculated as 295 mu m and 0.411 nmol min(-1) per nmol CYP for K-m and V-m values, respectively. These results suggest that both CYP2D6 and 1A2 primarily catalyse BTL 4-hydroxylation, but that the former is a predominant isozyme responsible for the reaction at a low substrate concentration range of BTL in human liver. C1 CHIBA UNIV,FAC PHARMACEUT SCI,BIOPHARMACEUT LAB,INAGE KU,CHIBA 263,JAPAN. CENT LAB,CHIBA 27014,JAPAN. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. CHIBA UNIV,FAC PHARMACEUT SCI,BIOCHEM PHARMACOL & TOXICOL LAB,INAGE KU,CHIBA 263,JAPAN. NR 30 TC 16 Z9 16 U1 0 U2 2 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0960-314X J9 PHARMACOGENETICS JI Pharmacogenetics PD APR PY 1995 VL 5 IS 2 BP 97 EP 102 DI 10.1097/00008571-199504000-00006 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy SC Biotechnology & Applied Microbiology; Genetics & Heredity; Pharmacology & Pharmacy GA RC328 UT WOS:A1995RC32800006 PM 7663534 ER PT J AU HOLMES, PV BLANCHARD, DC BLANCHARD, RJ BRADY, LS CRAWLEY, JN AF HOLMES, PV BLANCHARD, DC BLANCHARD, RJ BRADY, LS CRAWLEY, JN TI CHRONIC SOCIAL STRESS INCREASES LEVELS OF PREPROGALANIN MESSENGER-RNA IN THE RAT LOCUS-COERULEUS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Note DE GALANIN; IN SITU HYBRIDIZATION; VISIBLE BURROW SYSTEM; DOMINANT; SUBORDINATE ID GALANIN GENE-EXPRESSION; CENTRAL NERVOUS-SYSTEM; CERULEUS NEURONS; TYROSINE-HYDROXYLASE; NEUROPEPTIDE-Y; PARAVENTRICULAR NUCLEUS; INSITU HYBRIDIZATION; MESSENGER-RNA; BRAIN; IMMUNOREACTIVITY AB Galanin is a 29 amino acid neuropeptide that coexists with norepinephrine in approximately 80% of locus coeruleus (LC) neurons in the rat. The effects of chronic, naturalistic stress on preprogalanin mRNA in the LC was studied. The visible burrow system (VBS) served as the stress paradigm. Long-Evans rats (three males and two females) were housed together in the VBS for 13 days. The males established dominance hierarchies during this period. On day 14, preprogalanin mRNA in the LC was significantly elevated in subordinate rats compared to dominant and control rats, as measured by quantitative in situ hybridization. Levels of mRNA were positively correlated with the number of wounds by day 7 and day 14 and negatively correlated with body weight gain by day 14. These results suggest that the neuropeptide galanin may be overexpressed during chronic stress in rats. C1 NIMH,FUNCT NEUROANAT SECT,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. UNIV HAWAII,JOHN A BURNS SCH MED,DEPT ANAT & REPROD BIOL,HONOLULU,HI 96822. UNIV HAWAII,PACIFIC BIOMED RES CTR,HONOLULU,HI 96822. UNIV HAWAII,DEPT PSYCHOL,HONOLULU,HI 96822. RP HOLMES, PV (reprint author), NIMH,BEHAV NEUROPHARMACOL SECT,EXPTL THERAPEUT BRANCH,BLDG 10,ROOM 4N214,BETHESDA,MD 20892, USA. NR 30 TC 63 Z9 67 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD APR PY 1995 VL 50 IS 4 BP 655 EP 660 DI 10.1016/0091-3057(94)00334-3 PG 6 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA QN046 UT WOS:A1995QN04600026 PM 7542391 ER PT J AU PODGORNIK, R AF PODGORNIK, R TI SURFACE POLYMER NETWORK MODEL AND EFFECTIVE MEMBRANE CURVATURE ELASTICITY SO PHYSICAL REVIEW E LA English DT Article ID MECHANOCHEMICAL PROPERTIES; BOUNDARY SURFACE; ROUGH SURFACES; IONIC GEL; SHAPES; ADSORPTION; SKELETON RP PODGORNIK, R (reprint author), NIH,DIV COMP RES & TECHNOL,STRUCT BIOL LAB,BETHESDA,MD 20892, USA. RI Podgornik, Rudolf/C-6209-2008 OI Podgornik, Rudolf/0000-0002-3855-4637 NR 23 TC 9 Z9 9 U1 0 U2 3 PU AMERICAN PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 1063-651X J9 PHYS REV E JI Phys. Rev. E PD APR PY 1995 VL 51 IS 4 BP 3368 EP 3375 DI 10.1103/PhysRevE.51.3368 PN A PG 8 WC Physics, Fluids & Plasmas; Physics, Mathematical SC Physics GA QV540 UT WOS:A1995QV54000089 ER PT J AU INSEL, TR PRESTON, S WINSLOW, JT AF INSEL, TR PRESTON, S WINSLOW, JT TI MATING IN THE MONOGAMOUS MALE - BEHAVIORAL CONSEQUENCES SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE VOLE; PAIR BONDING; PLUS MAZE; PREFERENCE; AGGRESSION; REPRODUCTIVE BEHAVIOR ID VOLES MICROTUS-OCHROGASTER; ELEVATED PLUS-MAZE; PRAIRIE VOLES; AFFILIATIVE BEHAVIOR; ANXIETY; MONTANUS; RAT AB In monogamous mammals, males typically show selective affiliation with a single mate, high levels of paternal care, and aggression towards conspecifics to protect mate and offspring. We have previously described how selective aggression and affiliation increase after mating in the male prairie vole, Microtus ochrogaster. The current studies further explored the behavioral changes that follow mating in the male of this species. The first set of experiments tested males on several behavioral measures after 24 h of either mating, social (but not sexual) exposure, or no social contact. After 24 h of mating, but not after the other two conditions, aggression and affiliation (partner preference) increased as previously reported. In addition, mated animals showed increased exploration of the open arms of a plus maze, consistent with decreased fearfulness. There were no group differences in paternal behavior (which was high in all three conditions) or analgesia (assessed by tail flick latency). To determine the minimum amount of mating necessary for the induction of aggression, males were tested in a resident-intruder paradigm after 1,6, or 24 h of mating. Although 1 h of mating was associated with a transient increase in the frequency of threats and attacks, the full spectrum of enduring aggression was observed only in the males given 24 h of mating. In a final experiment, the behavioral consequences of mating were studied in males of the closely related montane vole (Microtus montanus) which does not pair bond. Males of this nonmonogamous vole species did not show increased aggression, partner preference, or alterations in plus maze exploration following 24 h of mating. These results demonstrate the importance of prolonged mating for the induction of pair bonding in the monogamous male and they suggest that increases in aggression and affiliation are associated with decreased fearfulness in pair bonded males. C1 NIMH,NEUROPHYSIOL LAB,POOLESVILLE,MD 20837. NR 31 TC 132 Z9 136 U1 0 U2 13 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 1995 VL 57 IS 4 BP 615 EP 627 DI 10.1016/0031-9384(94)00362-9 PG 13 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA QL348 UT WOS:A1995QL34800001 PM 7777594 ER PT J AU KAMEYAMA, K SAKAI, C KUGE, S NISHIYAMA, S TOMITA, Y ITO, S WAKAMATSU, K HEARING, VJ AF KAMEYAMA, K SAKAI, C KUGE, S NISHIYAMA, S TOMITA, Y ITO, S WAKAMATSU, K HEARING, VJ TI THE EXPRESSION OF TYROSINASE, TYROSINASE-RELATED PROTEIN-1 AND PROTEIN-2 (TRP1 AND TRP2), THE SILVER PROTEIN, AND A MELANOGENIC INHIBITOR IN HUMAN-MELANOMA CELLS OF DIFFERING MELANOGENIC ACTIVITIES SO PIGMENT CELL RESEARCH LA English DT Article DE MELANIN; MELANOGENESIS; FLOW CYTOMETRY ID VENTRALLY LOCALIZED INHIBITOR; DOPACHROME TAUTOMERASE; MAMMALIAN TYROSINASE; 5,6-DIHYDROXYINDOLE-2-CARBOXYLIC ACID; PIGMENTATION GENES; B-LOCUS; MOUSE; MURINE; MAPS; PURIFICATION AB The expression of various melanogenic proteins, including tyrosinase, the tyrosinase-related proteins 1 (TRP1) and 2 (TRP2/DOPAchrome tautomerase), and the silver protein in human melanocytes was studied in six different human melanoma cell lines and compared to a mouse derived melanoma cell line. Analysis of the expression of tyrosinase, TRP1, TRP2, and the silver protein using flow cytometry revealed that in general there was a positive correlation between melanin formation and the expression of those melanogenic enzymes. Although several of the melanoma cell lines possessed significant activities of TRP2, the levels of DOPAchrome tautomerase in extracts of human cells were relatively low compared to those in murine melanocytes. Melanins derived from melanotic murine JB/MS cells, from melanotic human Ihara cells and HM-IY cells, from sepia melanin, and from C57BL/6 mouse hair were chemically analyzed. JB/MS cells, as well as Ihara cells and HM-TY cells, possessed significant amounts of 5,6-dihydroxyindole-2-carboxylic acid (DHICA) derived melanins, this being dependent on the activity of TRP2. Kinetic HPLC assays showed that 5,6-dihydroxyindole (DHI) produced during melanogenesis was metabolized quickly to melanin in pigmented KHm-1/4 cells, whereas DHI was stable in amelanotic human SK-MEL-24 cells. A melanogenic inhibitor that has been purified from SK-MEL-24 cells that suppressed oxidation of DHI in the presence or absence of tyrosinase, but had no effect on DHICA oxidation. The sum of these results suggest that the expression of melanogenic enzymes as well as the activity of a melanogenic inhibitor are critical to the production of melanin synthesis in humans. C1 MED CTR HOSP,KITASATO INST,DEPT DERMATOL,SAITAMA,JAPAN. MED CTR HOSP,KITASATO INST,DIV BIOMED RES,SAITAMA,JAPAN. KITASATO UNIV,SCH MED,DEPT DERMATOL,KANAGAWA,JAPAN. AKITA UNIV,SCH MED,DEPT DERMATOL,AKITA 010,JAPAN. FUJITA HLTH UNIV,SCH HLTH SCI,AICHI,JAPAN. NIH,CELL BIOL LAB,BETHESDA,MD 20892. NR 52 TC 35 Z9 37 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0893-5785 J9 PIGM CELL RES JI Pigm. Cell. Res. PD APR PY 1995 VL 8 IS 2 BP 97 EP 104 DI 10.1111/j.1600-0749.1995.tb00648.x PG 8 WC Cell Biology; Dermatology SC Cell Biology; Dermatology GA RC327 UT WOS:A1995RC32700006 PM 7659683 ER PT J AU FANCI, AS AF FANCI, AS TI AIDS - NEWER CONCEPTS IN THE IMMUNOPATHOGENIC MECHANISMS OF HUMAN-IMMUNODEFICIENCY-VIRUS DISEASE SO PROCEEDINGS OF THE ASSOCIATION OF AMERICAN PHYSICIANS LA English DT Article ID IMMUNE-DEFICIENCY SYNDROME; HUMAN-BONE-MARROW; HIV-INFECTION; THYMUS; TYPE-1; CELLS; INVOLUTION RP FANCI, AS (reprint author), NIAID,IMMUNOREGULAT LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 25 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 1081-650X J9 P ASSOC AM PHYSICIAN JI Proc. Assoc. Am. Phys. PD APR PY 1995 VL 107 IS 1 BP 1 EP 7 PG 7 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA TF497 UT WOS:A1995TF49700001 ER PT J AU ENSOLI, B GALLO, RC AF ENSOLI, B GALLO, RC TI AIDS-ASSOCIATED KAPOSIS-SARCOMA - A NEW PERSPECTIVE OF ITS PATHOGENESIS AND TREATMENT SO PROCEEDINGS OF THE ASSOCIATION OF AMERICAN PHYSICIANS LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; FIBROBLAST GROWTH-FACTOR; TUMOR-NECROSIS-FACTOR; FACTOR GENE-EXPRESSION; YOUNG HOMOSEXUAL MEN; TRANS-ACTIVATOR GENE; SMOOTH-MUSCLE CELLS; LONG-TERM CULTURE; TAT PROTEIN; INTERFERON-GAMMA RP ENSOLI, B (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,RM 6A09,37 CONVENT DR MSC 4255,BETHESDA,MD 20892, USA. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 90 TC 18 Z9 18 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 1081-650X J9 P ASSOC AM PHYSICIAN JI Proc. Assoc. Am. Phys. PD APR PY 1995 VL 107 IS 1 BP 8 EP 18 PG 11 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA TF497 UT WOS:A1995TF49700002 PM 8630748 ER PT J AU MOMOEDA, M KAWASE, M YOUNG, NS KAJIGAYA, S AF MOMOEDA, M KAWASE, M YOUNG, NS KAJIGAYA, S TI PURIFICATION OF FUNCTIONAL RECOMBINANT YY1 EXPRESSED IN SF9 INSECT CELLS SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article ID SERUM RESPONSE FACTOR; TRANSCRIPTION FACTOR; NF-E1 YY-1; C-MYC; BINDS; PROMOTER; DELTA; SP1; IDENTIFICATION; YIN-YANG-1 AB We expressed a gene for YY1, the multifunctional mammalian transcription factor, with a recombinant baculovirus in insect cells and obtained high levels of protein in cell. lysates. A simple and efficient purification method was developed. In the final step, we used DNA affinity chromatography with concatermerized sequence derived from the upstream region of the B19 parvovirus P6 promoter, which has strong affinity for YY1, Approximately 1.8 mg of highly purified YY1 was obtained from 10(9) Sf9 cells. Highly purified YY1 behaved as authentic YY1 on electrophoretic mobility shift assays and in enhancing transcription from the P6 promoter. YY1 produced in a baculovirus system should prove useful for in vitro transcription assays of YY1 and related regulatory proteins. (C) 1995 Academic Press, Inc. C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. NR 22 TC 1 Z9 1 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 1046-5928 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD APR PY 1995 VL 6 IS 2 BP 169 EP 175 DI 10.1006/prep.1995.1021 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA QP770 UT WOS:A1995QP77000008 PM 7606165 ER PT J AU ZHU, PP LECCHI, P PANNELL, L JAFFE, H PETERKOFSKY, A AF ZHU, PP LECCHI, P PANNELL, L JAFFE, H PETERKOFSKY, A TI OVERPRODUCTION AND PURIFICATION OF THE MYCOPLASMA CAPRICOLUM PHOSPHOCARRIER PROTEIN, HPR, OF THE PHOSPHOENOLPYRUVATE - SUGAR PHOSPHOTRANSFERASE SYSTEM SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article ID ESCHERICHIA-COLI; BACILLUS-SUBTILIS; NUCLEOTIDE-SEQUENCE; AMINO-ACID; PTSH; OPERON; GENE; SPECTROSCOPY; RESOLUTION; BACTERIA AB The gene (ptsH) for the phosphocarrier protein, HPr, of the phosphoenolpyruvate:sugar phosphotransferase system from Mycoplasma capricolum was previously cloned and sequenced. We present here the results of experiments in which the ptsH gene was cloned into a vector for high level expression in Escherichia coli of the phosphocarrier protein, Conditions were developed for overproduction and purification of HPr by a two-column procedure. The purified protein, analyzed by Edman degradation and mass spectrometry, was found to have been processed by removal of the N-terminal methionine residue. Examination of the purified protein by gel electrophoresis under isoelectric focusing conditions revealed that it has an unusually high isoelectric point. (C) Academic Press, Inc. RP ZHU, PP (reprint author), NIH,BETHESDA,MD 20852, USA. NR 32 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 1046-5928 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD APR PY 1995 VL 6 IS 2 BP 189 EP 195 DI 10.1006/prep.1995.1024 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA QP770 UT WOS:A1995QP77000011 PM 7606168 ER PT J AU LOWTHER, WT MAJER, P DUNN, BM AF LOWTHER, WT MAJER, P DUNN, BM TI ENGINEERING THE SUBSTRATE-SPECIFICITY OF RHIZOPUSPEPSIN - THE ROLE OF ASP-77 OF FUNGAL ASPARTIC PROTEINASES IN FACILITATING THE CLEAVAGE OF OLIGOPEPTIDE SUBSTRATES WITH LYSINE IN P-1 SO PROTEIN SCIENCE LA English DT Article DE ASPARTIC PROTEINASE; CHROMOGENIC SUBSTRATE; ELECTROSTATIC INTERACTIONS; HYDROGEN BONDING; INHIBITORS; RHIZOPUSPEPSIN; SUBSTRATE SPECIFICITY ID OPIOMELANOCORTIN-CONVERTING ENZYME; YEAST CANDIDA-TROPICALIS; HUMAN CATHEPSIN-D; ACTIVE-SITE; SEQUENCE-ANALYSIS; RENIN INHIBITORS; CRYSTALLOGRAPHIC ANALYSIS; ACID PROTEINASES; X-RAY; BINDING AB Rhizopuspepsin and other fungal aspartic proteinases are distinct from the mammalian enzymes in that they are able to cleave substrates with lysine in the P-1, position. Sequence and structural comparisons suggest that two aspartic acid residues, Asp 30 and Asp 77 (pig pepsin numbering), may be responsible for generating this unique specificity. Asp 30 and Asp 77 were changed to the corresponding residues in porcine pepsin, Ile 30 and Thr 77, to create single and double mutants. The zymogen forms of the wild-type and mutant enzymes were overexpressed in Escherichia coli as inclusion bodies. Following solubilization, denaturation, refolding, activation, and purification to homogeneity, structural and kinetic comparisons were made. The mutant enzymes exhibited a high degree of structural similarity to the wild-type recombinant protein and a native isozyme. The catalytic activities of the recombinant proteins were analyzed with chromogenic substrates containing lysine in the P-1, P-2, or P-3 positions. Mutation of Asp 77 resulted in a loss of 7 kcal mol(-1) of transition-state stabilization energy in the hydrolysis of the substrate containing lysine in P-1. An inhibitor containing the positively charged P-1-lysine side chain inhibited only the enzymes containing Asp 77. Inhibition of the Asp 77 mutants of rhizopuspepsin and several mammalian enzymes was restored upon acetylation of the lysine side chain. These results suggest that an exploitation of the specific electrostatic interaction of Asp 77 in the active site of fungal enzymes may lead to the design of compounds that preferentially inhibit a variety of related Candida proteinases in immunocompromised patients. C1 UNIV FLORIDA,COLL MED,DEPT BIOCHEM & MOLEC BIOL,GAINESVILLE,FL 32610. NCI,PRI DYNCORP,STRUCT BIOCHEM PROGRAM,FREDERICK,MD 21702. FU NIDDK NIH HHS [DK18865] NR 63 TC 34 Z9 34 U1 2 U2 3 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0961-8368 J9 PROTEIN SCI JI Protein Sci. PD APR PY 1995 VL 4 IS 4 BP 689 EP 702 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QU440 UT WOS:A1995QU44000009 PM 7613467 ER EF