FN Thomson Reuters Web of Science™ VR 1.0 PT J AU RICHARD, BL NOMIZU, M YAMADA, Y KLEINMAN, HK AF RICHARD, BL NOMIZU, M YAMADA, Y KLEINMAN, HK TI IDENTIFICATION OF SEQUENCES FROM LAMININ-1 AND LAMININ-2 (MEROSIN) ALPHA-CHAINS ACTIVE FOR NEURITE OUTGROWTH SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1627 EP 1627 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301625 ER PT J AU MAGNER, WJ CHANG, AC OWENS, J HONG, MJP BROOKS, A COLIGAN, JE AF MAGNER, WJ CHANG, AC OWENS, J HONG, MJP BROOKS, A COLIGAN, JE TI ABERRANT DIFFERENTIATION OF THYMOCYTES IN MICE LACKING LAMININ-2 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,MOLEC STRUCT LAB,BETHESDA,MD 20892. NIH,NCRR,SCI SECT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1630 EP 1630 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301629 ER PT J AU RIVAS, RJ KOLLINS, K POWELL, SK AF RIVAS, RJ KOLLINS, K POWELL, SK TI EXOGENOUS EXPRESSION OF GPI-ANCHORED ALKALINE-PHOSPHATASE IN PRIMARY NEURONS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV MARYLAND,DEPT ZOOL,COLLEGE PK,MD 20742. NIH,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1666 EP 1666 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301665 ER PT J AU CHUNG, KN KIM, CH ROBERTS, S KIRASSOVA, M CHO, D ELWOOD, PC AF CHUNG, KN KIM, CH ROBERTS, S KIRASSOVA, M CHO, D ELWOOD, PC TI SORTING AND FUNCTION OF THE HUMAN FOLATE RECEPTOR IS INDEPENDENT OF CAVEOLIN EXPRESSION IN FISCHER RAT-THYROID EPITHELIAL-CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,DCT,COP,MED BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1669 EP 1669 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301669 ER PT J AU RALSTON, E PLOUG, T AF RALSTON, E PLOUG, T TI GLUT4 IS STORED IN A SPECIFIC COMPARTMENT IN C2 MYOTUBES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NINCDS,NEUROBIOL LAB,BETHESDA,MD 20892. NIDDK,DIABET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1694 EP 1694 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301693 ER PT J AU LEE, Y KIM, Y AF LEE, Y KIM, Y TI IDENTIFICATION OF REGULATORY DOMAINS OF THE NK-4 HOMEODOMAIN TRANSCRIPTION FACTOR SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1769 EP 1769 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301769 ER PT J AU LIU, C LIU, Z SHEN, K NOGUCHI, CT AF LIU, C LIU, Z SHEN, K NOGUCHI, CT TI SPECIFICITY OF THE ERYTHROPOIETIN RECEPTOR GENE PROMOTER SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDKD,CHEM BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1772 EP 1772 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301771 ER PT J AU FRANK, DW HANOVER, JA AF FRANK, DW HANOVER, JA TI CHARACTERIZATION OF A NUCLEAR LUCIFERASE REPORTER ENZYME SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,DEPT BIOCHEM & BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1817 EP 1817 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301816 ER PT J AU MALECKI, M SKOWRON, P AF MALECKI, M SKOWRON, P TI NUCLEAR-LOCALIZATION SIGNAL FACILITATES INTRANUCLEAR ENTRY OF PLASMID DNA - POLYCATION COMPLEX SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,MOLEC BIOL LAB,IMR,MADISON,WI 53706. UNIV WISCONSIN,MCAARDLE LAB,MADISON,WI 53706. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1823 EP 1823 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301822 ER PT J AU SZEBENI, A WINGFIELD, PT OLSON, MOJ AF SZEBENI, A WINGFIELD, PT OLSON, MOJ TI NUCLEOLAR PROTEIN B23 STIMULATES THE NUCLEAR IMPORT OF NLS-CONTAINING PROTEINS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV MISSISSIPPI,MED CTR,DEPT BIOCHEM,JACKSON,MS 39216. NIH,PROT EXPRESS LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1825 EP 1825 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301826 ER PT J AU DIX, DJ BOBSEINE, KL ALLEN, JW COLLINS, BW MORI, C NAKAMURA, N POORMANALLEN, P GOULDING, EH EDDY, EM AF DIX, DJ BOBSEINE, KL ALLEN, JW COLLINS, BW MORI, C NAKAMURA, N POORMANALLEN, P GOULDING, EH EDDY, EM TI TARGETED DISRUPTION OF HSP70-2 LEADS TO FAILED MEIOSIS, GERM-CELL APOPTOSIS, AND MALE-INFERTILITY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 US EPA,NHEERL,RES TRIANGLE PK,NC 27711. KYOTO UNIV,KYOTO 60601,JAPAN. NIEHS,RES TRIANGLE PK,NC 27709. WELLCOME RES LABS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1829 EP 1829 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301828 ER PT J AU PUZIANOWSKAKUZNICKI, M SHI, YB AF PUZIANOWSKAKUZNICKI, M SHI, YB TI NUCLEAR FACTOR-I AS A POTENTIAL REGULATOR DURING ORGAN DEVELOPMENT SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1882 EP 1882 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301881 ER PT J AU LEE, SK HOFFMAN, MP KLEINMAN, HK YAMADA, Y AF LEE, SK HOFFMAN, MP KLEINMAN, HK YAMADA, Y TI STAGE-SPECIFIC MESSENGER-RNA EXPRESSION FOR GROWTH-FACTORS AND EXTRACELLULAR-MATRIX PROTEINS IN THE DEVELOPING MOUSE SALIVARY-GLAND SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1886 EP 1886 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301885 ER PT J AU ADLER, R BELECKYADAMS, T TOMAREV, S PLODER, L MCINNES, RR SUNDIN, O AF ADLER, R BELECKYADAMS, T TOMAREV, S PLODER, L MCINNES, RR SUNDIN, O TI PROX-1, PAX-6 AND CHX10 HOMEOBOX GENE-EXPRESSION CORRELATE WITH PHENOTYPIC FATE OF RETINAL PRECURSOR CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,WILMER EYE INST,DEPT OPHTHALMOL,BALTIMORE,MD. NEI,LMDB,BETHESDA,MD 20892. HOSP SICK CHILDREN,DEPT GENET,TORONTO,ON M5G 1X8,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1895 EP 1895 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301895 ER PT J AU TUMMINIA, SJ JONAK, GJ RUSSELL, P AF TUMMINIA, SJ JONAK, GJ RUSSELL, P TI CATARACTOGENESIS IN TRANSGENIC MICE CONTAINING THE HIV-1 PROTEASE LINKED TO THE LENS ALPHA-A-CRYSTALLIN PROMOTER SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,MECHANISMS OCULAR DIS LAB,BETHESDA,MD 20892. DUPONT MERCK PHARMACEUT CO,WILMINGTON,DE 19880. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1897 EP 1897 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301896 ER PT J AU NEALE, EA BOWERS, LM DUNLAP, V WILLIAMSON, LC AF NEALE, EA BOWERS, LM DUNLAP, V WILLIAMSON, LC TI BOTULINUM-NEUROTOXIN-A BLOCKS SYNAPTIC VESICLE EXOCYTOSIS BUT NOT MEMBRANE RETRIEVAL BY ENDOCYTOSIS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 4 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1899 EP 1899 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301900 ER PT J AU COLE, N ELLENBERG, J SONG, J LIPPINCOTTSCHWARTZ, J AF COLE, N ELLENBERG, J SONG, J LIPPINCOTTSCHWARTZ, J TI EVIDENCE FOR RECYCLING OF GOLGI RESIDENT PROTEINS THROUGH THE ER SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1913 EP 1913 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301913 ER PT J AU COLE, N SCIAKY, N MAROTTA, A SONG, J LIPPINCOTTSCHWARTZ, J AF COLE, N SCIAKY, N MAROTTA, A SONG, J LIPPINCOTTSCHWARTZ, J TI FRAGMENTATION OF THE GOLGI-COMPLEX DURING MICROTUBULE DISRUPTION - REGENERATION OF GOLGI MEMBRANES AT ER EXIT SITES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1914 EP 1914 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301911 ER PT J AU WILLIAMS, AO KNAPTON, AD LETTERIO, JJ GEISER, AD ROBERTS, AB AF WILLIAMS, AO KNAPTON, AD LETTERIO, JJ GEISER, AD ROBERTS, AB TI TRANSFORMING GROWTH-FACTOR-BETA AND HEPATIC MITOCHONDRIA SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,EXPTL PATHOL LAB,BETHESDA,MD 20892. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1925 EP 1925 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301925 ER PT J AU COOL, DR ZHANG, CF ZHANG, Y LOH, YP AF COOL, DR ZHANG, CF ZHANG, Y LOH, YP TI IDENTIFICATION OF A SPECIFIC BINDING-PROTEIN FOR THE REGULATED SECRETORY PATHWAY SORTING SIGNAL OF PROOPIOMELANOCORTIN IN GOLGI AND SECRETORY GRANULE MEMBRANES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,DEV NEUROBIOL LAB,CELLULAR NEUROBIOL SECT,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1930 EP 1930 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301928 ER PT J AU WEBSTER, EL CASTRO, M CHROUSOS, GP AF WEBSTER, EL CASTRO, M CHROUSOS, GP TI DEVELOPMENT OF AN ANTIBODY TO THE CORTICOTROPIN-RELEASING HORMONE (CRH) RECEPTOR SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,DEB,PEDIAT ENDOCRINOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1935 EP 1935 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301934 ER PT J AU COSO, OA CHIARIELLO, M YU, JC TERAMOTO, H CRESPO, P XU, NZ MIKI, T GUTKIND, JS AF COSO, OA CHIARIELLO, M YU, JC TERAMOTO, H CRESPO, P XU, NZ MIKI, T GUTKIND, JS TI THE SMALL GTP-BINDING PROTEINS RAC AND CDC42 REGULATE THE ACTIVITY OF THE JNK/SAPK SIGNALING PATHWAY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,LCDO,MSU,BETHESDA,MD 20892. NCI,LCMB,BETHESDA,MD 20892. RI Gutkind, J. Silvio/A-1053-2009; Crespo, Piero/M-3273-2014 OI Crespo, Piero/0000-0003-2825-7783 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1976 EP 1976 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301972 ER PT J AU RAMPALLI, AM ZELENKA, PS AF RAMPALLI, AM ZELENKA, PS TI CHANGES IN E2F BINDING ASSOCIATED WITH LENS FIBER CELL-DIFFERENTIATION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2014 EP 2014 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302012 ER PT J AU SANTONIRUGIU, E AUDOLFSSON, T JENSEN, MR KISS, A THORGEIRSSON, SS AF SANTONIRUGIU, E AUDOLFSSON, T JENSEN, MR KISS, A THORGEIRSSON, SS TI TRANSFORMING GROWTH-FACTOR-ALPHA (TGF-ALPHA) AND HEPATOCYTE GROWTH-FACTOR (HGF) HAVE OPPOSITE EFFECTS ON HEPATOCARCINOGENESIS IN C-MYC TRANSGENIC MICE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. RI Jensen, Michael/E-9677-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2016 EP 2016 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302013 ER PT J AU STRATAKIS, CA PRAS, E FARMAKIDIS, C CARNEY, JA KLEE, CB CHROUSOS, GP AF STRATAKIS, CA PRAS, E FARMAKIDIS, C CARNEY, JA KLEE, CB CHROUSOS, GP TI CARNEY COMPLEX, A NOVEL MULTIPLE ENDOCRINE NEOPLASIA AND CALCINEURIN-B (CALNB1) MAP TO CHROMOSOME 2P16 - IS CALNB1 THE RESPONSIBLE GENE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD 20892. NIAMS,ARB,BETHESDA,MD 20892. NCI,LB,BETHESDA,MD 20892. GEORGETOWN UNIV,CHILDRENS MED CTR,WASHINGTON,DC 20007. MAYO CLIN,ROCHESTER,MN 55905. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2033 EP 2033 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302033 ER PT J AU JONES, TLZ GUTKIND, JS AF JONES, TLZ GUTKIND, JS TI ACTIVATED G-ALPHA-12 REQUIRES ACYLATION FOR ITS TRANSFORMING ACTIVITY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,METAB DIS BRANCH,BETHESDA,MD 20892. NIDR,CELLULAR DEV & ONCOL LAB,BETHESDA,MD 20892. RI Gutkind, J. Silvio/A-1053-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2047 EP 2047 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302043 ER PT J AU FRAUNDORFER, P KASSESSINOFF, T BEAVEN, MA AF FRAUNDORFER, P KASSESSINOFF, T BEAVEN, MA TI G-PROTEIN-FACILITATED CALCIUM-INFLUX IN A RAT MAST-CELL LINE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,MOLEC IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2049 EP 2049 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302047 ER PT J AU LOWY, RJ DIMITROV, DS AF LOWY, RJ DIMITROV, DS TI INDUCTION OF APOPTOSIS IN J774.1 MACROPHAGES BY INFLUENZA-VIRUS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 ARMED FORCES RADIOBIOL RES INST,DEPT RPT,BETHESDA,MD. NCI,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892. NR 0 TC 2 Z9 3 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2063 EP 2063 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302060 ER PT J AU GENTLEMAN, S AF GENTLEMAN, S TI COPURIFICATION OF VISUAL ARRESTIN WITH TUBULIN ACETYLATION ACTIVITY IN BOVINE RETINA SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,RETINAL CELL & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2084 EP 2084 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302082 ER PT J AU KOWALSKI, RJ TERHAAR, E LONGLEY, RE GUNASEKERA, SP LIN, CM DAY, BV HAMEL, E AF KOWALSKI, RJ TERHAAR, E LONGLEY, RE GUNASEKERA, SP LIN, CM DAY, BV HAMEL, E TI COMPARISON OF NOVEL MICROTUBULE POLYMERIZING AGENTS, DLSCODERMOLIDE AND EPOTHILONE A/B, WITH TAXOL SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT ENVIRONM & OCCUPAT HLTH,PITTSBURGH,PA 15238. HARBOR BRANCH OCEANOG INST INC,FT PIERCE,FL 34946. NR 1 TC 12 Z9 12 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2137 EP 2137 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302137 ER PT J AU BERNIER, SM YAMADA, Y AF BERNIER, SM YAMADA, Y TI MODULATION OF ANNEXIN-V DURING CHONDROCYTIC DIFFERENTIATION IN-VITRO SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2274 EP 2274 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302273 ER PT J AU SRINIVASAN, S NUSSBAUM, RL AF SRINIVASAN, S NUSSBAUM, RL TI PUTATIVE ROLE OF A PIP2 PHOSPHATASE IN GOLGI VESICULAR TRAFFICKING SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV PENN,DEPT HUMAN GENET,PHILADELPHIA,PA 19104. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2308 EP 2308 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302305 ER PT J AU DOYLE, DD RANSCHT, B PAGE, E PALFREY, HC AF DOYLE, DD RANSCHT, B PAGE, E PALFREY, HC TI T-CADHERIN IS A MAJOR PHOSPHORYLATED AND ADP-RIBOSYLATED COMPONENT OF CARDIAC CAVEOLAE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV CHICAGO,DEPT PHARMACOL & PHYSIOL SCI,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. NCI,LA JOLLA CANC RES FDN,LA JOLLA,CA 92037. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2345 EP 2345 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302343 ER PT J AU KING, C EISENBERG, E GREENE, L AF KING, C EISENBERG, E GREENE, L TI EFFECT OF YEAST DNAJ ON CLATHRIN UNCOATING SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2389 EP 2389 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302387 ER PT J AU WU, C EISENBERG, E GREENE, L AF WU, C EISENBERG, E GREENE, L TI CHARACTERIZATION OF D10 MUTANT OF HSP70 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2391 EP 2391 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302388 ER PT J AU GAO, B PRASAD, K GREENE, L EISENBERG, E AF GAO, B PRASAD, K GREENE, L EISENBERG, E TI UNCOATING OF CLATHRIN BASKETS BY HSP70 - CAUSE OF THE INHIBITION FOLLOWING ONE ROUND OF UNCOATING SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2392 EP 2392 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302390 ER PT J AU SAKAI, C OLLMANN, M KOBAYASHI, T VIEIRA, WD MULLER, J BARSH, GS HEARING, VJ AF SAKAI, C OLLMANN, M KOBAYASHI, T VIEIRA, WD MULLER, J BARSH, GS HEARING, VJ TI MODULATION OF EXPRESSION AND ACTIVITY OF MELANOSOMAL PROTEINS IN MURINE MELANOCYTES TREATED WITH ALPHA-MSH OR AGOUTI SIGNAL PROTEIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,CELL BIOL LAB,BETHESDA,MD 20892. STANFORD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT PEDIAT,STANFORD,CA 94305. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2401 EP 2401 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302400 ER PT J AU TIFFANY, HL ROSENBERG, HF AF TIFFANY, HL ROSENBERG, HF TI PROMOTER AND INTRONIC ENHANCER SILENCER REGIONS OF THE EOSINOPHIL-DERIVED NEUROTOXIN GENE COOPERATE IN REGULATING ITS EXPRESSION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2405 EP 2405 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302405 ER PT J AU HAYES, WP KLEIN, DC BALER, R AF HAYES, WP KLEIN, DC BALER, R TI CELL-SPECIFIC EXPRESSION OF FRA-2 MESSENGER-RNA IN PINEALOCYTES AND HIPPOCAMPAL-NEURONS - IN-SITU EVIDENCE LINKING FRA-2 TO THE DIURNAL RHYTHM OF MELATONIN SYNTHESIS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 CATHOLIC UNIV AMER,DEPT BIOL,WASHINGTON,DC 20064. NICHHD,LDN,NEUROENDOCRINOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2408 EP 2408 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302404 ER PT J AU CHAUTHAIWALE, V WARWAR, R RAMPALLI, A WISTOW, G ZELENKA, P AF CHAUTHAIWALE, V WARWAR, R RAMPALLI, A WISTOW, G ZELENKA, P TI REGULATION OF DUCK ALPHA-ENOLASE PROMOTER BY C-MYC SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2409 EP 2409 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302407 ER PT J AU AGBOTTAH, E KUMAR, A BRADY, J KASHANCHI, F AF AGBOTTAH, E KUMAR, A BRADY, J KASHANCHI, F TI CELL-CYCLE REGULATION OF HIV-1 TAT FUNCTION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,DEPT BIOCHEM & MOLEC BIOL,WASHINGTON,DC 20052. NCI,MOLEC VIROL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2417 EP 2417 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302417 ER PT J AU NICHOLS, RC RABEN, N EXELBERT, R ZARETSKY, J ADAMS, E PLOTZ, PH AF NICHOLS, RC RABEN, N EXELBERT, R ZARETSKY, J ADAMS, E PLOTZ, PH TI TRANSCRIPTIONAL REGULATION OF THE ACID MALTASE GENE - RELEVANCE TO GLYCOGENOSIS TYPE-II SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAMS,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2423 EP 2423 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302423 ER PT J AU BALLOU, B FISHER, GW DENG, JS FARKAS, DL HAKALA, TR SRIVASTAVA, M AF BALLOU, B FISHER, GW DENG, JS FARKAS, DL HAKALA, TR SRIVASTAVA, M TI CELL-SURFACE EXPRESSION OF XENOGENEIC NUCLEOLIN IN TRANSFECTANTS AND HETEROKARYONS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV PITTSBURGH,SCH MED,DEPT SURG,DIV UROL SURG,PITTSBURGH,PA 15213. CARNEGIE MELLON UNIV,CTR LIGHT MISCOSCOPE IMAGING & BIOTECHNOL,PITTSBURGH,PA 15213. NIDDK,BETHESDA,MD 20892. NR 4 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2451 EP 2451 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302449 ER PT J AU MORI, C NAKAMURA, N WELCH, JE SHIOTA, K EDDY, EM AF MORI, C NAKAMURA, N WELCH, JE SHIOTA, K EDDY, EM TI EXPRESSION OF MESSENGER-RNA IN THE HUMAN TESTIS FOR UNIQUE TYPE-1 HEXOKINASES LACKING THE PORIN-BINDING DOMAIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 KYOTO UNIV,FAC MED,DEPT ANAT,KYOTO 606,JAPAN. NIEHS,LRDT,RES TRIANGLE PK,NC 27709. US EPA,NHEERL,DTD,RES TRIANGLE PK,NC 27711. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2495 EP 2495 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302495 ER PT J AU SCHWARTZ, GN SZABO, JM HALVORSEN, D GRESS, RE AF SCHWARTZ, GN SZABO, JM HALVORSEN, D GRESS, RE TI STIMULATORY EFFECTS IF IGF-II ON THE MAINTENANCE AND DIFFERENTIATION OF COMMITTED AND PRIMITIVE HEMATOPOIETIC PROGENITORS FROM CD34+ BONE-MARROW CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2516 EP 2516 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302514 ER PT J AU EMMERTBUCK, LT MAURIZI, MR GOTTESMAN, S GOTTESMAN, MM AF EMMERTBUCK, LT MAURIZI, MR GOTTESMAN, S GOTTESMAN, MM TI THE FUNCTIONAL-CHARACTERIZATION OF THE HUMAN MITOCHONDRIAL PROTEASE LON SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2526 EP 2526 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302522 ER PT J AU LOHRET, TA MURPHY, RC DRGON, T KINNALLY, KW AF LOHRET, TA MURPHY, RC DRGON, T KINNALLY, KW TI EVIDENCE THAT THE MITOCHONDRIAL MULTIPLE CONDUCTANCE CHANNEL, MCC, IS NOT RELATED TO THE ADENINE-NUCLEOTIDE TRANSLOCATOR SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,DIV MOLEC MED,ALBANY,NY 12201. SUNY ALBANY,DEPT BIOMED SCI,ALBANY,NY. SUNY ALBANY,DEPT BIOL SCI,ALBANY,NY 12222. RENSSELAER POLYTECH INST,DEPT BIOL,TROY,NY 12180. NIDDK,LBM,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2528 EP 2528 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302526 ER PT J AU BARBER, T DWYER, NK LEVIN, D LONDOS, C BLANCHETTEMACKIE, EJ AF BARBER, T DWYER, NK LEVIN, D LONDOS, C BLANCHETTEMACKIE, EJ TI ISOPROTERENOL-STIMULATED INTRACELLULAR TRANSLOCATION OF HORMONE-SENSITIVE LIPASE AND PERILIPIN IN 3T3-L1 ADIPOCYTES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,LIPID CELL BIOL & MEMBRANE REGULAT SECT,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2544 EP 2544 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302540 ER PT J AU JAMUR, MC MORENO, AN GRODZKI, ACG SIRAGANIAN, RP OLIVER, C AF JAMUR, MC MORENO, AN GRODZKI, ACG SIRAGANIAN, RP OLIVER, C TI IMMUNOMAGNETIC SEPARATION OF RAT PERITONEAL AND BONE-MARROW-DERIVED MAST-CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 FED UNIV PARANA,DEPT BIOL CELULAR,CURITIBA,PARANA,BRAZIL. NIDR,IMMUNOL LAB,BETHESDA,MD 20892. OFF NAVAL RES,ARLINGTON,VA 22217. RI Jamur, Maria Celia/L-5520-2016 OI Jamur, Maria Celia/0000-0001-7065-8543 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2600 EP 2600 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302597 ER PT J AU UNTERWALD, EM RUBENFELD, JM IMAI, Y WANG, JB UHL, GR KREEK, MJ AF UNTERWALD, EM RUBENFELD, JM IMAI, Y WANG, JB UHL, GR KREEK, MJ TI CHRONIC OPIOID ANTAGONIST ADMINISTRATION UP-REGULATES MU-OPIOID RECEPTOR-BINDING WITHOUT ALTERING MU-OPIOID RECEPTOR MESSENGER-RNA LEVELS SO MOLECULAR BRAIN RESEARCH LA English DT Note DE RECEPTOR REGULATION; MN OPIOID RECEPTOR MESSENGER-RNA; NALTREXONE; MU OPIOID RECEPTOR; RAT BRAIN; SOLUTION HYBRIDIZATION PROTECTION ASSAY; OPIOID RECEPTOR ANTAGONIST ID CHRONIC NALTREXONE TREATMENT; OPIATE RECEPTOR; UP-REGULATION; MESSENGER-RNA; BRAIN; RAT; EXPRESSION; MORPHINE; CLONING; SITES AB Chronic administration of opioid antagonists has been shown to increase radioligand binding to brain opioid receptors. The present study was conducted to determine whether chronic exposure to the opioid antagonist naltrexone would similarly increase mu opioid receptor gene expression as measured by mRNA levels. Male Sprague-Dawley rats were administered naltrexone, 7-8 mg/kg/day, or saline by osmotic minipumps for 7 days. As expected, the density of mu opioid receptor binding sites was significantly higher in the brains of animals treated chronically with naltrexone as compared with saline-treated control animals. However, mu opioid receptor mRNA content determined by a solution hybridization RNase protection assay was not significantly altered in any brain region investigated. These results indicate that the upregulation of mu opioid receptors as measured by radioligand binding is not accompanied by increased levels of mu receptor mRNA. C1 NIDA,INTRAMURAL RES PROGRAM,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21224. RP UNTERWALD, EM (reprint author), ROCKEFELLER UNIV,BIOL ADDICT DIS LAB,1230 YORK AVE,NEW YORK,NY 10021, USA. FU NIDA NIH HHS [DA00049, DA08267]; PHS HHS [P50-05130] NR 27 TC 67 Z9 68 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD NOV PY 1995 VL 33 IS 2 BP 351 EP 355 DI 10.1016/0169-328X(95)00143-G PG 5 WC Neurosciences SC Neurosciences & Neurology GA TA393 UT WOS:A1995TA39300022 PM 8750897 ER PT J AU PACKENHAM, JP TAYLOR, JA ANNA, CH WHITE, CM DEVEREUX, TR AF PACKENHAM, JP TAYLOR, JA ANNA, CH WHITE, CM DEVEREUX, TR TI HOMOZYGOUS DELETIONS BUT NO SEQUENCE MUTATIONS IN CODING REGIONS OF P15 OR P16 IN HUMAN PRIMARY BLADDER-TUMORS SO MOLECULAR CARCINOGENESIS LA English DT Note DE BLADDER CANCER; TUMOR SUPPRESSOR GENES; CHROMOSOME 9P21 ID CHROMOSOME-9; CANCER; DNA AB Chromosome 9p21 appears to harbor a tumor suppressor gene, as evidenced by deletions in this region in a variety of human primary tumors and cell lines. To map the deletion at 9p21 in bladder tumors, we analyzed DNA from 28 tumor and normal pairs at five microsatellite markers that flank the region occupied by the putative tumor suppressor genes p16 and p15. Loss of heterozygosity (LOH) at the markers human interferon (HIFN) alpha and D9S171, which are adjacent to the p15 and p16 loci, was detected in 41% and 33%, respectively, of informative cases of bladder tumors. No sequence mutations were detected in exons 1 or 2 of either p15 or p16 in any of the bladder tumors. Three sequence-tagged site markers in the region bordered by HIFN alpha and D9S171 were used to further map the deleted region by multiplex polymerase chain reaction with the HIFN gamma marker (on chromosome 12) as a control for amplification. Six of 11 tumors with LOH at surrounding markers had homozygous deletions of the marker c5.1, which is located within the p16 gene; and two tumors appeared to have homozygous deletions within p15 (RN1.1) but not p16 (c5.1). A recently identified microsatellite marker, p16-CA-1, located 16 kb distal to p16, proved valuable in defining the minimal deletion involved in these bladder tumors. Five tumors exhibited homozygous deletions of this marker but not HIFN alpha and two tumors showed LOH at this marker and homozygous deletion of p16. Although these data could not be used to identify p16 or p15 as the definitive tumor suppressor gene in this region that is involved in bladder carcinogenesis, they suggest that homozygous deletion is a common mechanism of loss of tumor suppressor gene function in this region. (C) 1995 Wiley-Liss, Inc. C1 NIEHS,EPIDEMIOL BRANCH,RES TRIANGLE PK,NC 27709. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. OI taylor, jack/0000-0001-5303-6398 NR 19 TC 42 Z9 42 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD NOV PY 1995 VL 14 IS 3 BP 147 EP 151 DI 10.1002/mc.2940140303 PG 5 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA TF285 UT WOS:A1995TF28500002 PM 7576106 ER PT J AU ENDO, H SCHUT, HAJ SNYDERWINE, EG AF ENDO, H SCHUT, HAJ SNYDERWINE, EG TI DISTRIBUTION OF THE DNA-ADDUCTS OF 2-AMINO-3-METHYLIMIDAZO[4,5-F]QUINOLINE AND 2-AMINO-1-METHYL-6-PHENYLIMIDAZO[4,5-B]PYRIDINE IN THE SUPF GENE AS DETERMINED BY POLYMERASE ARREST ASSAY SO MOLECULAR CARCINOGENESIS LA English DT Article DE THERMAL-CYCLE SEQUENCING; MUTAGENESIS; HETEROCYCLIC AMINES; P-32 POSTLABELING; DNA POLYMERASE ID SHUTTLE VECTOR PLASMID; HETEROCYCLIC AMINES; COOKED FOOD; HUMAN-CELLS; XERODERMA-PIGMENTOSUM; SEQUENCE SPECIFICITY; CARCINOGEN; IDENTIFICATION; MUTATIONS; MUTAGENICITY AB The distribution of the adducts of the cooked meat-derived heterocyclic amines 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhlP) was examined in the supF gene of PSP189 by a polymerase-arrest assay using thermal-cycle sequencing. The reactive N-acetoxy metabolites of both compounds showed an overwhelming preference for reacting with guanine residues in the supF gene of the shuttle vector pSP189. The distribution of the IQ and PhlP guanine adducts was not random; instead, patterns of adduct hot-spots and cold-spots were observed. There was a striking similarity between both compounds in their preferred sites of adduct formation. The finding that IQ and PhlP adducted to guanine concurred with previous results showing that the target sites for IQ and PhlP mutations in supF were also at guanine. However, the adduct hot-spot sites were not predictive of the known sites of mutation hot-spots. In addition, despite the similarity in adduct hot-spots for IQ and PhlP, their reported mutation spectra in the supF gene were different. Factors in addition to adduct location therefore appear to play a role in the mutation spectra induced by the heterocyclic amines in the supF gene. (C) 1995 Wiley-Liss, Inc. C1 NCI,DIV CANC ETIOL,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892. MED COLL OHIO,DEPT PATHOL,TOLEDO,OH 43699. NR 36 TC 10 Z9 10 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD NOV PY 1995 VL 14 IS 3 BP 198 EP 204 DI 10.1002/mc.2940140309 PG 7 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA TF285 UT WOS:A1995TF28500008 PM 7576112 ER PT J AU COUSE, JF CURTIS, SW WASHBURN, TF LINDZEY, J GOLDING, TS LUBAHN, DB SMITHIES, O KORACH, KS AF COUSE, JF CURTIS, SW WASHBURN, TF LINDZEY, J GOLDING, TS LUBAHN, DB SMITHIES, O KORACH, KS TI ANALYSIS OF TRANSCRIPTION AND ESTROGEN INSENSITIVITY IN THE FEMALE MOUSE AFTER TARGETED DISRUPTION OF THE ESTROGEN-RECEPTOR GENE SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID HUMAN BREAST-CANCER; PROGESTERONE-RECEPTOR; MESSENGER-RNA; STEM-CELLS; UTERUS; EXPRESSION; LACTOTRANSFERRIN; ORGANIZATION; COMPLEXES; SEQUENCES AB We employed homologous recombination in mouse embryonic stem cells to disrupt the estrogen receptor (ER) gene. Subsequently generated mice that are homozygous for the gene disruption, termed ERKO, possess no demonstrable wild-type ER by Western blot analysis. However, the presence of residual high affinity binding, as detected by [H-3]estradiol binding assays and sucrose gradients in uterine extracts from ERKO females prompted further investigation of transcription and translation products from the disrupted ER gene. Analysis of ERKO uterine messenger RNA (mRNA) by reverse transcriptase-polymerase chain reaction demonstrated that although no full-length wild-type ER mRNA was present, two smaller transcripts, labeled E1 and E2, were identified and partially sequenced. Both ERKO transcripts are splicing variants that result in the disrupting NEO sequence being partially or completely removed from the mRNA. In the ERKO-ES variant, this results in a frame shift and the creation of at least two stop codons downstream. In the ERKO-E1 variant, the ER reading frame is preserved and encodes for a smaller mutant ER that could be the source of the residual estradiol binding. When this mutant form is overexpressed and characterized in vitro, it results in a smaller protein of the predicted size that possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER. Despite residual amounts of an impaired ER variant, estrogen insensitivity in the female ERKOs was confirmed by the failure of estrogen treatment to induce known uterine markers of estrogen action, such as increased DNA synthesis, and transcription of the progesterone receptor, lactoferrin, and glucose-6-phosphate dehydrogenase genes. Furthermore, serum levels of estradiol in the ERKO female are more than 10-fold higher than those in the wild type, consistent with a syndrome of hormone insensitivity. C1 NIEHS, REPROD & DEV TOXICOL LAB, RECEPTOR BIOL SECT, RES TRIANGLE PK, NC 27709 USA. UNIV MISSOURI, DEPT BIOCHEM, COLUMBIA, MO 65211 USA. UNIV MISSOURI, DEPT CHILD HLTH, COLUMBIA, MO 65211 USA. UNIV N CAROLINA, DEPT PATHOL, CHAPEL HILL, NC 27599 USA. OI Korach, Kenneth/0000-0002-7765-418X NR 59 TC 354 Z9 357 U1 1 U2 9 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD NOV PY 1995 VL 9 IS 11 BP 1441 EP 1454 DI 10.1210/me.9.11.1441 PG 14 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TD095 UT WOS:A1995TD09500002 PM 8584021 ER PT J AU Cerretti, DP Bos, TV Nelson, N Kozlosky, CJ Reddy, P Maraskovsky, E Park, LS Lyman, SD Copeland, NG Gilbert, DJ Jenkins, NA Fletcher, FA AF Cerretti, DP Bos, TV Nelson, N Kozlosky, CJ Reddy, P Maraskovsky, E Park, LS Lyman, SD Copeland, NG Gilbert, DJ Jenkins, NA Fletcher, FA TI Isolation of LERK-5: A ligand of the eph-related receptor tyrosine kinases SO MOLECULAR IMMUNOLOGY LA English DT Article DE ligand; receptor tyrosine kinase; eph-family ID DECAY-ACCELERATING FACTOR; GENETIC-LINKAGE MAP; HUMAN INTERLEUKIN-8; MOUSE; PROTEIN; EXPRESSION; CLONING; HINDBRAIN; SEQUENCE AB Hek and elk are members of the eph-related family of receptor tyrosine kinases. Recently we isolated four cDNAs encoding membrane-bound ligands to hek and elk [Beckmann et al. (1994) EMBO J. 13, 3757-3762; Kozlosky et al. (1995) Oncogene 10, 299-306]. Because of the promiscuous nature of their binding, we have termed these proteins ligands of the eph-related kinases or LERKs. A search of GenBank revealed an expressed sequence tag (EST) with homology to the LERKs. Using this EST as a probe, we have isolated human and murine cDNAs that encode a protein which we call LERK-5. The human and murine cDNAs encode proteins of 333 and 336 amino acids, respectively, with a 97% amino acid identity; LERK-5 has an amino acid identity of 27-59% with the other reported LERKs. LERK-5 is a ligand for both elk and hek and induces receptor phosphorylation. It is expressed in adult lung and kidney and the fetal tissues heart, lung, kidney, and brain. In addition, Southern blot analysis of DNA from interspecific backcross mice indicated that LERK-5 (Eplg5) maps to the proximal region of mouse chromosome 8. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP Cerretti, DP (reprint author), IMMUNEX RES & DEV CORP,51 UNIV ST,SEATTLE,WA 98101, USA. FU NCI NIH HHS [N01-CO-46000] NR 48 TC 49 Z9 51 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD NOV PY 1995 VL 32 IS 16 BP 1197 EP 1205 DI 10.1016/0161-5890(95)00108-5 PG 9 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA TP948 UT WOS:A1995TP94800003 PM 8559144 ER PT J AU Valdez, BC Henning, D Busch, RK Srivastava, M Busch, H AF Valdez, BC Henning, D Busch, RK Srivastava, M Busch, H TI Immunodominant RNA recognition motifs of human nucleolin/C23 SO MOLECULAR IMMUNOLOGY LA English DT Article DE nucleolin/C23; epitopes; RNA recognition motifs ID SYSTEMIC LUPUS-ERYTHEMATOSUS; MAJOR NUCLEOLAR PROTEINS; MONOCLONAL-ANTIBODIES; U1 RNA; AUTOANTIBODIES; DISEASES; EPITOPE; PHOSPHOPROTEIN; IDENTIFICATION; DETERMINANTS AB Nucleolin/C23 is a nucleolar phosphoprotein implicated in the synthesis, processing and transport of ribosomal RNA and gene transcription. Auto-antibodies to human nucleolin/C23 have been reported in patients with systemic lupus erythematosus and other systemic autoimmune disorders. To identify immunodominant regions in nucleolin/C23, deletion fragments of nucleolin/C23 were fused in frame with the glutathione S-transferase gene. Seven monoclonal anti-nucleolin/C23 antibodies were used to determine the immunoreactivity of the bacterially expressed fusion proteins. Two sets of immunogenic regions at amino acids 314-389 and 387-461 were identified; each contained overlapping discontinuous epitopes and a centrally located RNA recognition motif. An auto-immune serum from a patient with systemic lupus erythematosus patient was found to contain antibodies against human nucleolin/C23 which recognized amino acids 387-461 of nucleolin/C23. C1 NCI,NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892. NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892. RP Valdez, BC (reprint author), BAYLOR COLL MED,DEPT PHARMACOL,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. NR 25 TC 27 Z9 27 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD NOV PY 1995 VL 32 IS 16 BP 1207 EP 1213 DI 10.1016/0161-5890(95)00093-3 PG 7 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA TP948 UT WOS:A1995TP94800004 PM 8559145 ER PT J AU VallsSole, J Hallett, M AF VallsSole, J Hallett, M TI Modulation of electromyographic activity of wrist flexor and extensor muscles in patients with writer's cramp SO MOVEMENT DISORDERS LA English DT Article DE electromyographic modulation; voluntary activity; segmental afferents; sensorimotor integration; writer's cramp ID RECIPROCAL INHIBITION; CUTANEOUS REFLEXES; FOCAL DYSTONIA; HUMAN FOREARM; HAND CRAMPS; H-REFLEX; EXCITABILITY; STIMULATION AB Patients with writer's cramp have two well-recognized neurophysiological abnormalities: reduced reciprocal inhibition of the wrist flexor motoneurons at rest, and increased cocontraction of antagonist muscles of the forearm during voluntary activity. In this article we present evidence for an impaired integration of sensory inputs into the voluntary motor activity during performance of a force-related task in patients with writer's cramp. Normal (control) subjects and patients activated wrist flexor and extensor muscles to maintain a predetermined level of force. Electrical stimuli were applied to median and radial nerve afferents and the modulatory effects induced in the electromyographic (EMG) activity were measured. For each muscle studied and nerve stimulated, we defined a characteristic sequence of excitatory (E) and inhibitory (I) phases of modulation of the averaged rectified EMG activity in control subjects. E and I phases were thought to represent excitation and inhibition, respectively, of the corresponding motoneuronal pool to homonymous or reciprocal afferent inputs. There were no differences between control subjects and patients regarding the level of background EMG activity in the agonist muscles during wrist flexion or wrist extension. In the agonist wrist flexors, patients had reduced homonymous and reciprocal inhibition. In the agonist wrist extensors, patients had reduced reciprocal excitation and reciprocal inhibition. These results are compatible with an abnormal CNS processing of the inputs generated by external stimuli during voluntary contraction of wrist flexor and extensor muscles. Defective integration of inputs from peripheral nerve afferents into the command for voluntary movement may partly underlie the pathophysiology of the motor dysfunction in patients with writer's cramp. C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. RP VallsSole, J (reprint author), UNIV BARCELONA,DEPT MED,HOSP CLIN,SERV NEUROL,UNITAT EMG,VILLARROEL 170,BARCELONA,SPAIN. NR 20 TC 27 Z9 27 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PD NOV PY 1995 VL 10 IS 6 BP 741 EP 748 DI 10.1002/mds.870100607 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA TL356 UT WOS:A1995TL35600006 PM 8749993 ER PT J AU DESERRES, FJ MALLING, HV WEBBER, BB BROCKMAN, HE AF DESERRES, FJ MALLING, HV WEBBER, BB BROCKMAN, HE TI QUANTITATIVE AND QUALITATIVE ASPECTS OF SPONTANEOUS SPECIFIC-LOCUS MUTATION IN THE AD-3 REGION OF HETEROKARYON-12 OF NEUROSPORA-CRASSA 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; AD-3B/AD-3A RATIO; SPONTANEOUS; AD-3 FORWARD-MUTATION ASSAY; NEUROSPORA CRASSA ID UNEXPECTEDLY HIGH-FREQUENCY; 2-COMPONENT HETEROKARYONS; IRREPARABLE MUTANTS; MULTILOCUS DELETION; RISK ASSESSMENT; GENOTYPE AD-3A; TESTS; ASSAY AB The data from forward-mutation experiments to obtain specific-locus mutations at 2 closely linked loci in the adenine-3 (ad-3) region of heterokaryon 12 (H-12) of Neurospora crassa have been tabulated to determine the frequency of spontaneous ad-3 mutations and to determine the percentages resulting from each of the 2 major genotypic classes: gene/point mutations and multilocus deletion mutations. Gene/point mutations. at the ad-3B locus (ad-3B(R)) have been characterized to determine the percentage showing allelic complementation to obtain a presumptive identification of the genetic alteration in each mutation at the molecular level. Data from experiments performed at 2 different laboratories have been compared to assess the interlaboratory reproducibility of quantitative data on H-li. No difference was found between the frequencies of spontaneous specific-locus mutations in the ad-3 region. Genetic analysis of 172 ad-3 mutants demonstrated that specific-locus mutations in the ad-3 region result from both gene/point mutations (82.0% [141/172]), and multilocus deletion mutations (14.5% [25/172]). Heterokaryon tests for allelic complementation demonstrated that 52.5% (53/101) spontaneous ad-3B(R) mutants show allelic complementation, and result from single base-pair alterations. In addition, 100% (25/25) of the spontaneous multilocus deletion mutations result from the 3 smallest sized genotypic subclasses. The implications of the present experimental data for the validation of the ad-3 specific-locus assay system in Neurospora are discussed. C1 MED COLL GEORGIA,DEPT CELL & MOLEC BIOL,AUGUSTA,GA 30912. ILLINOIS STATE UNIV,DEPT BIOL SCI,NORMAL,IL 61790. RP DESERRES, FJ (reprint author), NIEHS,ENVIRONM TOXICOL PROGRAM,TOXICOL BRANCH,MD A0-01,BLDG 101,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 24 TC 4 Z9 4 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 NOV PY 1995 VL 332 IS 1-2 BP 45 EP 54 DI 10.1016/0027-5107(95)00151-5 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TK344 UT WOS:A1995TK34400008 PM 7500991 ER PT J AU FRIEND, S BORRESEN, AL BRODY, L CASEY, G DEVILEE, P GAYTHER, S GOLDGAR, D MURPHY, P WEBER, BI WISEMAN, R AF FRIEND, S BORRESEN, AL BRODY, L CASEY, G DEVILEE, P GAYTHER, S GOLDGAR, D MURPHY, P WEBER, BI WISEMAN, R TI BREAST-CANCER INFORMATION ON THE WEB SO NATURE GENETICS LA English DT Letter C1 RADIUM HOSP,OSLO,NORWAY. NIH,BETHESDA,MD 20892. CLEVELAND CLIN,CLEVELAND,OH 44106. UNIV UTRECHT,UTRECHT,NETHERLANDS. UNIV CAMBRIDGE,CAMBRIDGE,ENGLAND. UNIV UTAH,SALT LAKE CITY,UT. ONCORMED INC,GAITHERSBURG,MD. UNIV PENN,PHILADELPHIA,PA 19104. NIEHS,RES TRIANGLE PK,NC 27709. RP FRIEND, S (reprint author), FRED HUTCHINSON CANC RES CTR,MOLEC PHARMACOL PROGRAM,SEATTLE,WA 98104, USA. NR 0 TC 32 Z9 32 U1 0 U2 0 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 NOV PY 1995 VL 11 IS 3 BP 238 EP 239 DI 10.1038/ng1195-238 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA TC639 UT WOS:A1995TC63900010 PM 7581445 ER PT J AU HU, S PATTATUCCI, AML PATTERSON, C LI, L FULKER, DW CHERNY, SS KRUGLYAK, L HAMER, DH AF HU, S PATTATUCCI, AML PATTERSON, C LI, L FULKER, DW CHERNY, SS KRUGLYAK, L HAMER, DH TI LINKAGE BETWEEN SEXUAL ORIENTATION AND CHROMOSOME XQ28 IN MALES BUT NOT IN FEMALES SO NATURE GENETICS LA English DT Article ID MALE HOMOSEXUALITY AB We have extended our analysis of the role of the long arm of the X chromosome (Xq28) in sexual orientation by DNA linkage analyses of two newly ascertained series of families that contained either two gay brothers or two lesbian sisters as well as heterosexual siblings. Linkage between the Xq28 markers and sexual orientation was detected for the gay male families but not for the lesbian families or for families that failed to meet defined inclusion criteria for the study of sex-linked sexual orientation. Our results corroborate the previously reported linkage between Xq28 and male homosexuality in selected kinships and suggest that this region contains a locus that influences individual variations in sexual orientation in men but not in women. C1 NCI, BIOCHEM LAB, BETHESDA, MD 20892 USA. UNIV COLORADO, INST BEHAV GENET, BOULDER, CO 80309 USA. MIT, WHITEHEAD INST BIOMED RES, CAMBRIDGE, MA 02139 USA. RI Cherny, Stacey/B-3315-2008 OI Cherny, Stacey/0000-0002-0269-3352 FU NICHD NIH HHS [HD-11681, HD-27802]; NIMH NIH HHS [MH-43899] NR 32 TC 162 Z9 166 U1 3 U2 49 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 1061-4036 J9 NAT GENET JI Nature Genet. PD NOV PY 1995 VL 11 IS 3 BP 248 EP 256 DI 10.1038/ng1195-248 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA TC639 UT WOS:A1995TC63900012 PM 7581447 ER PT J AU GROSSMAN, M RADER, DJ MULLER, DWM KOLANSKY, DM KOZARSKY, K CLARK, BJ STEIN, EA LUPIEN, PJ BREWER, HB RAPER, SE WILSON, JM AF GROSSMAN, M RADER, DJ MULLER, DWM KOLANSKY, DM KOZARSKY, K CLARK, BJ STEIN, EA LUPIEN, PJ BREWER, HB RAPER, SE WILSON, JM TI A PILOT-STUDY OF EX-VIVO GENE-THERAPY FOR HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA SO NATURE MEDICINE LA English DT Article ID LIVER-TRANSPLANTATION; LIPOPROTEIN RECEPTORS; HUMAN HEPATOCYTES; CHOLESTEROL; LOVASTATIN AB The outcome of the first pilot study of liver-directed gene therapy is reported here. Five patients with homozygous familial hypercholesterolaemia (FH) ranging in age from 7 to 41 years were enrolled; each patient tolerated the procedure well without significant complications. Transgene expression was detected in a limited number of hepatocytes of liver tissue harvested four months after gene transfer from all five patients. Significant and prolonged reductions in low density lipoprotein (LDL) cholesterol were demonstrated in three of five patients; in vivo LDL catabolism was increased 53% following gene therapy in a receptor negative patient, who realized a reduction in serum LDL equal to similar to 150 mg dl(-1). This study demonstrates the feasibility of engrafting limited numbers of retrovirus-transduced hepatocytes without morbidity and achieving persistent gene expression lasting at least four months after gene therapy. The variable metabolic responses observed following low-level genetic reconstitution in the five patients studied precludes a broader application of liver-directed gene therapy without modifications that consistently effect substantially greater gene transfer. C1 UNIV PENN,MED CTR,INST HUMAN GENE THERAPY,PHILADELPHIA,PA 19104. UNIV PENN,MED CTR,DEPT MOLEC & CELLULAR ENGN,PHILADELPHIA,PA 19104. UNIV PENN,MED CTR,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,MED CTR,DEPT SURG,PHILADELPHIA,PA 19104. UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,ANN ARBOR,MI 48109. UNIV PENN,MED CTR,DEPT PEDIAT,DIV CARDIOL,PHILADELPHIA,PA 19104. CHILDRENS HOSP,PHILADELPHIA,PA 19104. CHRIST HOSP,CARDIOVASC RES CTR,DIV LIPID METAB & PREVENT ATHEROSCLEROSIS,CINCINNATI,OH 45219. CHRIST HOSP,CARDIOVASC RES CTR,MED RES LABS,CINCINNATI,OH 45219. LAVAL UNIV HOSP,MED RES CTR,LIPID RES CTR,QUEBEC CITY,PQ G1V 4G2,CANADA. NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. RI Wilson, James/F-9220-2011 OI Wilson, James/0000-0002-9630-3131 NR 25 TC 359 Z9 371 U1 0 U2 5 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 NOV PY 1995 VL 1 IS 11 BP 1148 EP 1154 DI 10.1038/nm1195-1148 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TC537 UT WOS:A1995TC53700038 PM 7584986 ER PT J AU MAFFEI, M HALAAS, J RAVUSSIN, E PRATLEY, RE LEE, GH ZHANG, Y FEI, H KIM, S LALLONE, R RANGANATHAN, S KERN, PA FRIEDMAN, JM AF MAFFEI, M HALAAS, J RAVUSSIN, E PRATLEY, RE LEE, GH ZHANG, Y FEI, H KIM, S LALLONE, R RANGANATHAN, S KERN, PA FRIEDMAN, JM TI LEPTIN LEVELS IN HUMAN AND RODENT - MEASUREMENT OF PLASMA LEPTIN AND OB RNA IN OBESE AND WEIGHT-REDUCED SUBJECTS SO NATURE MEDICINE LA English DT Article ID LIPOPROTEIN-LIPASE; ADIPOSE-TISSUE; PIMA-INDIANS; MOUSE; MUTATION; MICE; RAT AB Leptin, the gene product of the obese gene, may play an important role in regulating body weight by signalling the size of the adipose tissue mass. Plasma leptin was found to be highly correlated with body mass index (BMI) in rodents and in 87 lean and obese humans. In humans, there was variability in plasma leptin at each BMI suggesting that there are differences in its secretion rate from fat. Weight loss due to food restriction was associated with a decrease in plasma leptin in samples from mice and obese humans. C1 ROCKEFELLER UNIV,MOLEC GENET LAB,NEW YORK,NY 10021. NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. BROOKWOOD BIOMED ACC,BIRMINGHAM,AL 35209. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. ROCKEFELLER UNIV,HOWARD HUGHES MED INST,NEW YORK,NY 10021. RI sheng, jian/E-9474-2012 FU NCRR NIH HHS [RR00862]; NIDDK NIH HHS [DK39176, DK41096] NR 47 TC 2510 Z9 2551 U1 8 U2 99 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 NOV PY 1995 VL 1 IS 11 BP 1155 EP 1161 DI 10.1038/nm1195-1155 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TC537 UT WOS:A1995TC53700039 PM 7584987 ER PT J AU PHELPS, CH AF PHELPS, CH TI CLINICALLY MEANINGFUL INTERFERENCE IN AD PROGRESSION SO NEUROBIOLOGY OF AGING LA English DT Article; Proceedings Paper CT Roundtable Discussion on Interfering with the Progress of Alzheimers Disease, at the 4th International Conference on Alzheimers Disease and Related Disorders CY NOV 02, 1994 CL MINNEAPOLIS, MN SP Janssen Pharm RP PHELPS, CH (reprint author), NIA,ALZHEIMERS DIS CTR PROGRAM,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD NOV-DEC PY 1995 VL 16 IS 6 BP 877 EP 878 DI 10.1016/0197-4580(96)81879-3 PG 2 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA TJ272 UT WOS:A1995TJ27200005 PM 8622777 ER PT J AU CIZZA, G BRADY, LS PACAK, K BLACKMAN, MR GOLD, PW CHROUSOS, GP AF CIZZA, G BRADY, LS PACAK, K BLACKMAN, MR GOLD, PW CHROUSOS, GP TI STRESS-INDUCED INHIBITION OF THE HYPOTHALAMIC-PITUITARY-THYROID AXIS IS ATTENUATED IN THE AGED FISCHER 344/N MALE-RAT SO NEUROENDOCRINOLOGY LA English DT Article DE STRESS; PROLACTIN; GROWTH HORMONE; THYROTROPIN; FISCHER RATS; AGING ID THYROTROPIN-RELEASING-HORMONE; TUBEROINFUNDIBULAR DOPAMINERGIC-NEURONS; MESSENGER-RIBONUCLEIC-ACID; PARAVENTRICULAR NUCLEUS; IMMOBILIZATION STRESS; PROLACTIN SECRETION; INVITRO; TRH; FEMALE; YOUNG AB Aging is associated with a progressive decrement in the basal activity of the hypothalamic-pituitary-thyroid axis in male Fischer 344/N rats. The aim of this study was to determine whether stress influences the activity of this axis in young and old rats. As prolactin and growth hormone share some regulatory mechanisms with thyrotropin-releasing and thyroid-stimulating hormones, which are influenced by stress, the plasma levels of these two hormones were also determined during immobilization (Immo). To accomplish this, young (3-month-old) and old (23-month-old) male 344/N Fischer rats were immobilized for 2 h; blood was collected by cannulation from the tail artery at different intervals during Immo (0, 5, 30, 60, and 120 min), and brains were removed at the end of Immo. The basal plasma levels of thyroid-stimulating hormone were similar in both groups, but were significantly and progressively inhibited by Immo in young, but not in old rats. The baseline plasma levels of total triiodothyronine were slightly lower in old than in young rats; Immo caused a significant decrease of total triiodothyronine levels only in the young animals. The baseline plasma levels of free triiodothyronine were similar and were not altered by Immo in either age group. The paraventricular nucleus thyrotropin-releasing hormone mRNA levels were lower in old than in young rats under basal conditions; under stress they were significantly inhibited in young, but remained unchanged in old rats, The basal thyroid-stimulating hormone beta mRNA levels in the anterior pituitary were significantly lower in old than in young rats, but were not affected by Immo in either age group. The plasma prolactin levels were similar at baseline and were significantly increased by Immo in both age groups, but significantly more in old than in young rats. The plasma growth hormone levels were also similar at baseline; they were significantly decreased by Immo to a similar extent in both age groups. In summary, these data indicate that the stress-induced decrease in plasma thyroid-stimulating hormone is in part mediated at the level of the hypothalamic thyrotropin-releasing hormone neuron and that this phenomenon is attenuated in the aged rat. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. NINCDS,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. RP CIZZA, G (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,ROOM 10N-262,10 CTR DR,BETHESDA,MD 20892, USA. NR 52 TC 24 Z9 25 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD NOV PY 1995 VL 62 IS 5 BP 506 EP 513 DI 10.1159/000127041 PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA TG096 UT WOS:A1995TG09600009 PM 8559282 ER PT J AU PAGE, WF MACK, TM KURTZKE, JF MURPHY, FM NORMAN, JE AF PAGE, WF MACK, TM KURTZKE, JF MURPHY, FM NORMAN, JE TI EPIDEMIOLOGY OF MULTIPLE-SCLEROSIS IN US VETERANS .6. POPULATION ANCESTRY AND SURNAME ETHNICITY AS RISK-FACTORS FOR MULTIPLE-SCLEROSIS SO NEUROEPIDEMIOLOGY LA English DT Article DE MULTIPLE SCLEROSIS; GEOGRAPHY; RISK; US VETERANS; ETHNICITY; POPULATION ANCESTRY ID UNITED-STATES VETERANS; MS AB Previously, we studied the effect of population ancestry on the risk of multiple sclerosis (MS) in US veterans of World War II, comparing by state 1980 US census ancestry data with MS case/control ratios. Here, the joint effects of population ancestry and surname-derived ethnicity on MS risk are examined in the same series. Census data are used again to characterize the population ancestry of the state from which each subject entered active duty (EAD) - that is, the proportions of the populace reporting various ancestries - and subjects were also individually categorized into a single ethnic group, without knowledge of case/control status, based on surname. In this study population, categorized ethnicity was strongly correlated with population ancestry, as expected. Although univariate analyses showed statistically significant associations between MS risk and several surname-derived ethnicities and ethnic groups, when residence at EAD was accounted for as well, there was almost no ethnic variation in MS risk. A logistic regression analysis further showed that variations in MS risk are associated most strongly with latitude and population ancestry group; in particular, subjects who entered military service from states with higher proportions of Swedish or French ancestry had higher risks of MS. After adjustment for characteristics of place, the only significant individual ethnicity factor found was Southern European ethnicity. In general, we conclude that an individual's ethnicity seems to be of less relative importance in determining MS risk than is the population ancestry of the state of EAD. These findings underscore the fact that MS is a disease of place, with 'place' including not only attributes of the locale (e.g., latitude), but also of its populace (e.g., ancestry). C1 UNIV SO CALIF,SCH MED,DEPT PREVENT MED,LOS ANGELES,CA 90033. VET AFFAIRS MED CTR,NEUROL SERV,WASHINGTON,DC 20422. NHLBI,BETHESDA,MD 20892. RP PAGE, WF (reprint author), NATL ACAD SCI,INST MED,MED FOLLOW UP AGCY,2101 CONSTITUT AVE NW,WASHINGTON,DC 20418, USA. NR 15 TC 11 Z9 11 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0251-5350 J9 NEUROEPIDEMIOLOGY JI Neuroepidemiology PD NOV-DEC PY 1995 VL 14 IS 6 BP 286 EP 296 DI 10.1159/000109804 PG 11 WC Public, Environmental & Occupational Health; Clinical Neurology SC Public, Environmental & Occupational Health; Neurosciences & Neurology GA TD601 UT WOS:A1995TD60100003 PM 8570000 ER PT J AU DECARLI, C MURPHY, DGM TRANH, M GRADY, CL HAXBY, JV GILLETTE, JA SALERNO, JA GONZALESAVILES, A HORWITZ, B RAPOPORT, SI SCHAPIRO, MB AF DECARLI, C MURPHY, DGM TRANH, M GRADY, CL HAXBY, JV GILLETTE, JA SALERNO, JA GONZALESAVILES, A HORWITZ, B RAPOPORT, SI SCHAPIRO, MB TI THE EFFECT OF WHITE-MATTER HYPERINTENSITY VOLUME ON BRAIN STRUCTURE, COGNITIVE PERFORMANCE, AND CEREBRAL METABOLISM OF GLUCOSE IN 51 HEALTHY-ADULTS SO NEUROLOGY LA English DT Article ID SPONTANEOUSLY HYPERTENSIVE RATS; COMPUTED TOMOGRAPHIC ANALYSIS; OXYGEN-METABOLISM; LEUKO-ARAIOSIS; RISK-FACTORS; BLOOD-FLOW; ELDERLY SUBJECTS; LEUKOARAIOSIS; DEMENTIA; LESIONS AB Objective: To assess the association of MRI white matter hyperintensities (WMHI) with cognitive performance, cerebral structure, and cerebral metabolism in 51 healthy individuals aged 19 to 91 years without cerebrovascular risk factors. Background: Abnormal white matter signals have been associated with brain atrophy, reduced cerebral blood flow, focal neurologic signs, gait disorder, and poorer neuropsychological test performance. Most studies of WMHI, however, include subjects with hypertension or other identifiable causes of cerebrovascular disease that may have an independent effect on brain structure and function. To assess brain changes associated with WMHI independent of cerebrovascular risk factors, we determined WMHI volume, brain volume, cerebral metabolism, and cognitive performance for a group of subjects free of medical illness. Regional cerebral metabolism and cognitive domain were also assessed to evaluate the possible role of frontal lobe dysfunction in subjects with WMHI. Design: Cross-sectional study of 51 very healthy subjects aged 19 to 91 years. Methods: WMHI, brain, and CSF volumes were determined by MRI segmentation. Neuropsychological tests were employed to assess multiple cognitive domains. Brain metabolism was determined from 18-fluoro-2-deoxy-n-glucose PET. Multivariate relations were tested with stepwise linear regression. Models included the potential confounders of age and education where appropriate. Results: The distribution of WMHI volume was bimodal, with five subjects having WMHI volumes beyond three SDs from the normally distributed population. A WMHI volume of greater than 0.5% of intracranial volume was considered abnormal. Within the multivariate models, WMHI volumes were significantly predictive of increased ventricular volume, reduced brain volume, and reduced cognitive scores. Subjects with greater than 0.5% WMHI volume also had significantly lower frontal lobe metabolism, significantly higher systolic blood pressure, significantly larger ventricular volume, and significantly lower scores on frontal lobe-mediated neuropsychological tests than age-matched controls. Conclusion: WMHI volume is associated with structural and functional brain changes even within a group of very healthy individuals. WMHI is associated with poorer frontal lobe cognitive function and, when severe, is accompanied by significantly reduced frontal lobe metabolism. Subjects with large WMHI volumes have significantly higher systolic blood pressure, brain atrophy, reduced cerebral metabolism, and lower scores on tests of frontal lobe function than age-matched controls. Large amounts of WMHI are, therefore, pathologic and may be related to elevated systolic blood pressure even when it is within the normal age-related range. C1 NINCDS,EPILEPSY RES BRANCH,BETHESDA,MD 20892. RP DECARLI, C (reprint author), NIA,NEUROSCI LAB,BRAIN AGING & DEMENTIA SECT,BLDG 10,ROOM 6C414,BETHESDA,MD 20892, USA. RI DeCarli, Charles/B-5541-2009 NR 50 TC 358 Z9 361 U1 2 U2 15 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV PY 1995 VL 45 IS 11 BP 2077 EP 2084 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA TG312 UT WOS:A1995TG31200024 PM 7501162 ER PT J AU RACE, RE PRIOLA, SA BESSEN, RA ERNST, D DOCKTER, J RALL, GF MUCKE, L CHESEBRO, B OLDSTONE, MBA AF RACE, RE PRIOLA, SA BESSEN, RA ERNST, D DOCKTER, J RALL, GF MUCKE, L CHESEBRO, B OLDSTONE, MBA TI NEURON-SPECIFIC EXPRESSION OF A HAMSTER PRION PROTEIN MINIGENE IN TRANSGENIC MICE INDUCES SUSCEPTIBILITY TO HAMSTER SCRAPIE AGENT SO NEURON LA English DT Article ID CREUTZFELDT-JAKOB-DISEASE; GERSTMANN-STRAUSSLER SYNDROME; INCUBATION PERIOD; ABNORMAL ISOFORM; CULTURED-CELLS; MESSENGER-RNA; PRP GENE; LINKAGE; INFECTIVITY; MUTATION AB To study the effect of cell type-restricted hamster PrP expression on susceptibility to the hamster scrapie agent, we generated transgenic mice using al kb hamster cDNA clone containing the 0.76 kb HPrP open reading frame under control of the neuron-specific enolase promoter. In these mice, expression of HPrP was detected only in brain tissue, with highest levels found in neurons of the cerebellum, hippocampus, thalamus, and cerebral cortex. These transgenic mice were susceptible to infection by the 263K strain of hamster scrapie with an average incubation period of 93 days, compared to 72 days in normal hamsters. In contrast, nontransgenic mice were not susceptible to this agent. These results indicate that neuron-specific expression of the 1 kb HPrP minigene including the HPrP open-reading frame is sufficient to mediate susceptibility to hamster scrapie, and that HPrP expression in nonneuronal brain cells is not necessary to overcome the TSE species barrier. C1 SCRIPPS RES INST, LA JOLLA, CA 92037 USA. RP RACE, RE (reprint author), NIAID, ROCKY MT LABS, PERSISTENT VIRAL DIS LAB, HAMILTON, MT 59840 USA. OI Rall, Glenn/0000-0003-2717-3238 NR 61 TC 116 Z9 117 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0896-6273 J9 NEURON JI Neuron PD NOV PY 1995 VL 15 IS 5 BP 1183 EP 1191 DI 10.1016/0896-6273(95)90105-1 PG 9 WC Neurosciences SC Neurosciences & Neurology GA TF887 UT WOS:A1995TF88700022 PM 7576660 ER PT J AU FREO, U PIETRINI, P PIZZOLATO, G FUREY, M MERICO, A RUGGERO, S DAM, M BATTISTIN, L AF FREO, U PIETRINI, P PIZZOLATO, G FUREY, M MERICO, A RUGGERO, S DAM, M BATTISTIN, L TI CEREBRAL METABOLIC RESPONSES TO CLOMIPRAMINE ARE GREATLY REDUCED FOLLOWING PRETREATMENT WITH THE SPECIFIC SEROTONIN NEUROTOXIN PARA-CHLOROAMPHETAMINE (PCA) - A 2-DEOXYGLUCOSE STUDY IN RATS SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE DEOXYGLUCOSE; CLOMIPRAMINE; SEROTONIN; ANTIDEPRESSANTS; AMPHETAMINE; RAT ID PLACEBO-CONTROLLED TRIAL; ANTI-DEPRESSANT DRUGS; GLUCOSE-UTILIZATION; PANIC DISORDER; RAPHE NUCLEI; AUTORADIOGRAPHIC LOCALIZATION; CONSCIOUS RAT; BRAIN; RECEPTORS; CHLOROPHENYLALANINE AB To determine if reported reductions of regional cerebral metabolic rates for glucose (rCMRglc) induced by the tryciclic antidepressant clomipramine (CMI) (10 mg/kg) are due to a presynaptic action on serotonin (5-HT) terminals, 3-month-old Fischer-344 vats were given parachloroamphetamine (PCA), a serotonin neurotoxin. rCMRglc was measured 3 weeks later in 55 brain regions after the administration of saline or CMI using the quantitative autoradiographic [C-14]2-deoxyglucose procedure. PCA alone increased rCMRglc in the visual cortex. CMI alone reduced rCMRglc in 18 (33%) of the studied regions, including telencephalic, diencephalic, limbic, and brain stem areas. In PCA-lesioned rats, metabolic responses to CMI (10 mg/kg) were greatly reduced, and significant rCMRglc decreases were observed only in 4 (7%) of the brain areas, including the hippocampus and raphe nuclei. Abolition by PCA of the metabolic responses to CMI confirms that CMI, at the dose studied, reduces rCMRglc via a presynaptic mechanism, likely the 5-HT reuptake sites. C1 CLIN MALATTIE NERVOSE & MENTALI,I-35100 PADUA,ITALY. CLIN PSICHIATR,I-56100 PISA,ITALY. RP FREO, U (reprint author), NIA,NEUROSCI LAB,BLDG 10,ROOM 6C414,BETHESDA,MD 20892, USA. RI Furey, Maura/H-5273-2013 NR 57 TC 5 Z9 5 U1 0 U2 1 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 NOV PY 1995 VL 13 IS 3 BP 215 EP 222 DI 10.1016/0893-133X(95)00053-G PG 8 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA TG529 UT WOS:A1995TG52900002 PM 8602894 ER PT J AU Basser, PJ AF Basser, PJ TI Inferring microstructural features and the physiological state of tissues from diffusion-weighted images SO NMR IN BIOMEDICINE LA English DT Article ID CEREBRAL-ISCHEMIA; T2-WEIGHTED MRI; SELF-DIFFUSION; WHITE MATTER; WATER; INVIVO; MUSCLE; STROKE; CATS AB We review several methods that have been developed to infer microstructural and physiological information about isotropic and anisotropic tissues from diffusion weighted images (DWIs), These include Diffusion Imaging (DI), Diffusion Tensor Imaging (DTI), isotropically weighted imaging, and q-space imaging. Just as DI provides useful information about molecular displacements in one dimension with which to characterize diffusion in isotropic tissues, DTI provides information about molecular displacements in three dimensions needed to characterize diffusion Is anisotropic tissues. DTI also furnishes scalar parameters that behave like quantitative histological or physiological 'stains' for different features of diffusion, These include Trace(D), which is related to the mean diffusivity, and a family of parameters derived from the diffusion tensor, D, which characterize different features of anisotropic diffusion, Simple thought experiments and geometrical constructs, such as the diffusion ellipsoid, can be used to understand water diffusion in isotropic add anisotropic media, and the NMR experiments used to characterize it. RP Basser, PJ (reprint author), NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,NIH,BLDG 13,ROOM 3N-17,13 SOUTH DR,BETHESDA,MD 20892, USA. RI Basser, Peter/H-5477-2011 NR 60 TC 864 Z9 873 U1 1 U2 35 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0952-3480 J9 NMR BIOMED JI NMR Biomed. PD NOV-DEC PY 1995 VL 8 IS 7-8 BP 333 EP 344 DI 10.1002/nbm.1940080707 PG 12 WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA UL587 UT WOS:A1995UL58700006 PM 8739270 ER PT J AU BECK, JC MCCLATCHEY, KD LESPERANCE, MM ESCLAMADO, RM CAREY, TE BRADFORD, CR AF BECK, JC MCCLATCHEY, KD LESPERANCE, MM ESCLAMADO, RM CAREY, TE BRADFORD, CR TI HUMAN PAPILLOMAVIRUS TYPES IMPORTANT IN PROGRESSION OF INVERTED PAPILLOMA SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Academy-of-Otolaryngology-Head-and-Neck-Surgery CY SEP 17-20, 1995 CL NEW ORLEANS, LA SP Amer Acad Otolaryngol Head & Neck Surg ID POLYMERASE CHAIN-REACTION; SQUAMOUS-CELL CARCINOMA; PARANASAL SINUSES; NASAL CAVITY; SCHNEIDERIAN PAPILLOMAS; INSITU HYBRIDIZATION; DNA; INFECTION; PRIMERS AB Recent evidence suggests that human papillomavirus may play a role in the pathogenesis of inverted papilloma, a benign but locally aggressive neoplasm with a high recurrence rate and an association with squamous cell carcinoma. Histologic features of inverted papilloma have not been useful in discriminating lesions at high risk for malignant transformation, We studied archival pathology specimens from 39 patients with inverted papilloma treated at the University of Michigan between 1980 and 1994 using polymerase chain reaction techniques and human papillomavirus L1 and E6 consensus primers, Previously we reported that 63% of these specimens tested positive for human papillomavirus sequences and that presence of human papillomavirus predicted recurrence of inverted papilloma. We used type-specific primer pairs and polymerase chain reaction techniques as well as hybridization with type-specific oligonucleotide probes to determine human papillomavirus type. A significant correlation was observed between the severity of the lesion (dysplasia or carcinoma) and high risk human papillomavirus type (p < 0.01). All 12 benign inverted papilloma specimens that contained human papillomavirus tested positive for human papillomavirus 6 or 11. Of seven inverted papilloma specimens that exhibited dysplasia, five were human papillomavirus positive, three contained human papillomavirus 6, one contained human papillomavirus 11, and one contained human papillomavirus 18, In each of the three specimens that contained inverted papilloma in association with squamous cell carcinoma, the inverted papilloma portion of the specimen tested positive for a single human papillomavirus type: human papillomavirus 6, 11, or 16, Of the four human papillomavirus-positive specimens with squamous cell carcinoma alone (patients who had an inverted papilloma previously resected at the same site), three tested positive for human papillomavirus 16, and 1 was untyped. C1 UNIV MICHIGAN,DEPT OTOLARYNGOL HEAD & NECK SURG,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109. DEPT VET AFFAIRS MED CTR,ANN ARBOR,MI. NIDOCD,GENET MOLEC LAB,BETHESDA,MD. NR 28 TC 46 Z9 47 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD NOV PY 1995 VL 113 IS 5 BP 558 EP 563 DI 10.1177/019459989511300506 PG 6 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA TE969 UT WOS:A1995TE96900005 PM 7478645 ER PT J AU PARK, KM MAX, MB ROBINOVITZ, E GRACELY, RH BENNETT, GJ AF PARK, KM MAX, MB ROBINOVITZ, E GRACELY, RH BENNETT, GJ TI EFFECTS OF INTRAVENOUS KETAMINE, ALFENTANIL, OR PLACEBO ON PAIN, PINPRICK HYPERALGESIA, AND ALLODYNIA PRODUCED BY INTRADERMAL CAPSAICIN IN HUMAN-SUBJECTS SO PAIN LA English DT Article DE N-METHYL-D-ASPARTATE; CENTRAL SENSITIZATION; KETAMINE; ALFENTANIL; CAPSAICIN ID REFLEX SYMPATHETIC DYSTROPHY; SPINOTHALAMIC TRACT NEURONS; AMINO-ACID ANTAGONISTS; DORSAL HORN NEURONS; RAT SPINAL-CORD; NEUROGENIC HYPERALGESIA; OPIOID INFUSIONS; NEUROPATHIC PAIN; WIND-UP; MORPHINE AB The importance of N-methyl-D-aspartate (NMDA) receptor-mediated sensitization of central nervous system (CNS) neurons is well established in animal models of acute and chronic pain. A human model of central sensitization would be useful in screening new NMDA antagonists and establishing dose regimens for clinical trials in patients with pain related to sensitization of CNS neurons. We used this model to examine the effects of intravenous infusions of two centrally acting analgesics, the NMDA receptor antagonist ketamine and the morphine-like opioid agonist alfentanil. Twelve normal subjects completed a 3-session, randomized, double-blind, crossover study. From 25 to 60 min after capsaicin injection, subjects were given intravenous infusions of ketamine (mean dose: 32 mg), alfentanil (mean dose: 3075 mu g), or saline placebo. Both drugs significantly reduced ongoing pain and pinprick-evoked hyperalgesia during the infusion. The reduction in allodynia evoked by light stroking was statistically significant only for alfentanil. Mean reduction +/-SEM relative to placebo were for ongoing pain: ketamine, 36+/-9%; alfentanil, 51+/-5%; area of pinprick hyperalgesia: ketamine, 34+/-7%; alfentanil, 35+/-7%; and area of mechanical allodynia: ketamine, 52+/-20%; alfentanil, 70+/-12%. Because the drugs were given systemically and produced side effects in all subjects, we cannot specify the site or sites of action nor conclusively rule out a non-specific 'active placebo' response as the cause for reduction of symptoms. Arguing against an 'active placebo' response, however, was the lack of analgesic effect of intravenous midazolam (mean dose; 3.4 mg, titrated to produce side effects of similar magnitude to ketamine and alfentanil) given at 145 min after capsaicin in 9 subjects who had received saline from 25 to 60 min. The results of this study suggest that neural systems sensitive to NMDA receptor antagonists and opioids participate in capsaicin-evoked pain phenomena, and support the feasibility of pharmacological studies using the intradermal capsaicin model. C1 NIH,DEPT NURSING,CTR CLIN,BETHESDA,MD 20892. NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. NR 52 TC 135 Z9 137 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD NOV PY 1995 VL 63 IS 2 BP 163 EP 172 DI 10.1016/0304-3959(95)00029-R PG 10 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA TG134 UT WOS:A1995TG13400004 PM 8628581 ER PT J AU CORNAGLIAFERRARIS, P DEMARIA, A CIRILLO, C CARA, A ALESSANDRI, G AF CORNAGLIAFERRARIS, P DEMARIA, A CIRILLO, C CARA, A ALESSANDRI, G TI ADHESION OF HUMAN NEUROBLASTS TO HIV-1 TAT SO PEDIATRIC RESEARCH LA English DT Article ID CELL-ADHESION; N-MYC; VIRUS; EXPRESSION; INFECTION; CHILDREN; PROTEIN; DIFFERENTIATION; ORGANIZATION; INTERFERON AB Several neuropathologic findings in infants and children with human immunodeficiency virus type-1 (HIV-1) infection are different from those observed in adults, probably related to the fact that the retroviral infection occurs in the setting of neurodevelopment. This report describes the interaction and biologic activity of tat, the HIV-1 trans-activating protein on human neuroblasts. Two human neuroblastoma cell lines, LAN-5 and GI-CA-N, have been studied for their capability to adhere to tat (full recombinant protein) and to two different peptide residues of it. Both cells adhere to tat and tat(46-60) basic domain, although not to tat(65-80) residue, which contains the RGD (arginine glycine-aspartic acid) motif. Adhesion to collagen I was inhibited by preincubating GI-CA-N cells with tat,(46-60) although not with tat,(65-80) indicating the capability of the basic residue to interfere with collagen I-induced cellular adhesion. The expression of 200-kD neurofilaments induced by collagen I was not induced by tat(46-60) indicating that neural differentiation along the same pathway is not mimicked by this peptide. Neuroblast cell proliferation was not affected by adhesion to tat(46-60) nor to tat.(65-80) GI-CA-N cells are not permissive to HIV-1 infection. However, proviral DNA was documented in the cell lysate for 14 consecutive in vitro passages, whereas HIV-1 transcription was never detectable. This would exclude the possibility that tar would be transduced by these cells. GI-CA-N stained negative for CD4, although positive for Gal-C, which may explain HIV-1 entry. Results show that immature human neural cells interact with tar protein and/or its basic residue in vitro. A mechanism similar to that herein described would possibly be active in vivo, which may help in clarifying the pathogenic mechanisms of neurologic dysfunction and destruction of the CNS observed in infants infected with HIV-1. C1 G GASLINI CHILDRENS HOSP,DEPT PEDIAT HEMATOL ONCOL,GENOA,ITALY. UNIV GENOA,SCH MED,DEPT INFECT DIS,GENOA,ITALY. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI Cara, Andrea/M-4865-2015; de maria, andrea/F-7116-2016 OI Cara, Andrea/0000-0003-4967-1895; de maria, andrea/0000-0001-5782-333X NR 35 TC 5 Z9 5 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 NOV PY 1995 VL 38 IS 5 BP 792 EP 796 DI 10.1203/00006450-199511000-00025 PG 5 WC Pediatrics SC Pediatrics GA TA408 UT WOS:A1995TA40800025 PM 8552450 ER PT J AU OH, W BLACKMON, LR ESCOBEDO, M FANAROFF, AA FERNBACH, SA KIRKPATRICK, BV LIGHT, IJ PAPILE, LA SHOEMAKER, CT MENNUTI, MT DICKERSON, VM GILSTRAP, LC HALL, GP HEYL, PS HOSKINS, IA MARTIN, JN PHELAN, ST AF OH, W BLACKMON, LR ESCOBEDO, M FANAROFF, AA FERNBACH, SA KIRKPATRICK, BV LIGHT, IJ PAPILE, LA SHOEMAKER, CT MENNUTI, MT DICKERSON, VM GILSTRAP, LC HALL, GP HEYL, PS HOSKINS, IA MARTIN, JN PHELAN, ST TI PERINATAL-CARE AT THE THRESHOLD OF VIABILITY SO PEDIATRICS LA English DT Article ID BIRTH-WEIGHT INFANTS; CESAREAN-SECTION; DELIVERY; MORBIDITY; GESTATION; OUTCOMES; SURVIVAL C1 AMER NURSES ASSOC,WASHINGTON,DC 20024. ASSOC WOMENS HLTH OBSTET & NEONATAL NURSES,WASHINGTON,DC 20005. AMER COLL OBSTETRICIANS & GYNECOLOGISTS,COMM OBSTETR PRACTICE,WASHINGTON,DC 20024. CANADIAN PEDIAT SOC,OTTAWA,ON,CANADA. CTR DIS CONTROL & PREVENT,ATLANTA,GA 30333. NICHHD,BETHESDA,MD 20892. AMER ACAD PEDIAT,SURG SECT,ELK GROVE VILLAGE,IL 60007. AMER SOC ANESTHESIOLOGISTS,PARK RIDGE,IL 60068. RP OH, W (reprint author), AMER ACAD PEDIAT,COMM FETUS & NEWBORN,141 NW POINT BLVD,ELK GROVE VILLAGE,IL 60007, USA. NR 14 TC 64 Z9 64 U1 1 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 NOV PY 1995 VL 96 IS 5 BP 974 EP 976 PN 1 PG 3 WC Pediatrics SC Pediatrics GA TE078 UT WOS:A1995TE07800024 ER PT J AU Quakyi, IA Miller, LH Good, MF Ahlers, JD Isaacs, SN Nunberg, JH Houghten, RA Keister, DB Coligan, JE Moss, B Alling, D Berzofsky, JA Kaslow, DC AF Quakyi, IA Miller, LH Good, MF Ahlers, JD Isaacs, SN Nunberg, JH Houghten, RA Keister, DB Coligan, JE Moss, B Alling, D Berzofsky, JA Kaslow, DC TI Synthetic peptides from P-falciparum sexual stage 25-kDa protein induce antibodies that react with the native protein: The role of IL-2 and conformational structure on immunogenicity of Pfs25 SO PEPTIDE RESEARCH LA English DT Article ID TRANSMISSION-BLOCKING ANTIBODIES; HUMAN IMMUNODEFICIENCY VIRUS; PLASMODIUM-FALCIPARUM; VACCINE CANDIDATE; ELECTROPHORETIC TRANSFER; POLYACRYLAMIDE GELS; HUMAN MALARIA; ANTIGENS; EPITOPES; CARRIER AB To identify B-cell epitopes of the Plasmodium falciparum 25-kDa ookinete protein, Pfs25, 41 overlapping synthetic peptides spanning the entire length of the protein were used individually to immunize CAF(1) (F-1 hybrid of BALB/c female and A/J male) mice. Antipeptide sera were tested for reactivity to live intact zygote/early ookinete (post-fertilization stage) by immunofluorescence, and by Western blot analysis under nonreducing and reducing conditions, immunoprecipitation of S-35-cysteine-labeled antigen and ELISA using a vaccinia recombinant Pfs25 antigen. Fourteen B-cell epitopes were identified. These peptides were immunogenic only when administered with high-dose recombinant interleukin-2. Antibodies to 11 peptides recognized only the native conformational structure, one peptide induced antibodies that recognized both reduced and native protein and two other peptides, after primary immunization, made antibodies to denatured Pfs25, but after boosting the antibodies reacted to both denatured and native Pfs25. Anti-sera to peptides in the first (peptide 7) and fourth (peptide 34) epidermal growth factor-like domains of Pfs25 reacted most strongly with, zygotes/ookinetes by immunofluorescence assay. The antibodies elicited by immunization with peptide 34 suppressed infectivity of the parasite to mosquitoes. We further observed that the secondary structure of Pfs25 may be important for immunogenicity because monoclonal antibodies (MAbs) IC7 and 1D2, both transmission-blocking MAbs, protected enzyme cleavage sites in Pfs25 from proteolysis, suggesting that discontinuous segments of Pfs25 may come together to form immunogenic epitopic sites. Thus, definition of B- and T-cell epitopes may be required to construct a Pfs25 vaccine for optimum immunogenicity. C1 NIH,BETHESDA,MD 20892. QUEENSLAND INST MED RES,BRISBANE,QLD 4006,AUSTRALIA. UNIV MONTANA,MISSOULA,MT 59812. TORREY PINES INST MOLEC STUDIES,SAN DIEGO,CA. RP Quakyi, IA (reprint author), GEORGETOWN UNIV,DEPT BIOL,406 REISS SCI BLDG,37TH & 0 STS NW,WASHINGTON,DC 20057, USA. NR 41 TC 7 Z9 7 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 1040-5704 J9 PEPTIDE RES JI Peptide Res. PD NOV-DEC PY 1995 VL 8 IS 6 BP 335 EP 344 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TR839 UT WOS:A1995TR83900005 PM 8838417 ER PT J AU Jonas, WB AF Jonas, WB TI Evaluating complementary therapies SO PERFUSION LA English DT Article RP Jonas, WB (reprint author), NIH,OFF ALTERNAT MED,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU VERLAG PERFUSION GMBH PI NURNBERG PA REGENSBURGER STR 44-46, 90478 NURNBERG, GERMANY SN 0935-0020 J9 PERFUSION JI Perfusion PD NOV PY 1995 VL 8 IS 11 BP 372 EP 373 PG 2 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TW410 UT WOS:A1995TW41000005 ER PT J AU LONG, RM AF LONG, RM TI NEWS FROM THE NATIONAL-INSTITUTE-OF-GENERAL-MEDICAL-SCIENCES (NIGMS) SO PHARMACEUTICAL RESEARCH LA English DT Editorial Material RP LONG, RM (reprint author), NIGMS,DIV PHARMACOL PHYSIOL & BIOL CHEM,PHARMACOL & PHYSIOL SCI BRANCH,BETHESDA,MD, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0724-8741 J9 PHARMACEUT RES JI Pharm. Res. PD NOV PY 1995 VL 12 IS 11 BP 1560 EP 1560 PG 1 WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Chemistry; Pharmacology & Pharmacy GA TG802 UT WOS:A1995TG80200001 ER PT J AU LAYER, RT POPIK, P OLDS, T SKOLNICK, P AF LAYER, RT POPIK, P OLDS, T SKOLNICK, P TI ANTIDEPRESSANT-LIKE ACTIONS OF THE POLYAMINE SITE NMDA ANTAGONIST, ELIPRODIL (SL-82.0715) SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE ELIPRODIL; SL-82.0715; ANTIDEPRESSANTS; NMDA RECEPTORS; BETA-ADRENOCEPTORS; FORCED SWIM TEST ID D-ASPARTATE RECEPTOR; SIGMA-BINDING SITES; ANTI-ISCHEMIC AGENTS; FORCED-SWIMMING TEST; EXHIBIT ANTIDEPRESSANT; BEHAVIORAL DESPAIR; RAT-BRAIN; IFENPRODIL; MODELS; MICE AB Functional N-methyl-D-aspartate (NMDA) antagonists including competitive antagonists, glycine partial agonists, and use-dependent channel blockers exhibit antidepressant-like actions in preclinical models. The present study examined the effects of eliprodil (SL-82.0715), an NMDA antagonist acting at polyamine sites, in behavioral and neurochemical tests predictive of antidepressant activity. In mice, eliprodil produced a dose-dependent reduction in immobility in the forced swim test, but was inactive in the tail suspension test. Chronic treatment with eliprodil produced both a significant downregulation of beta-adrenoceptors and a reduction in the potency of glycine to inhibit [H-3]5,7-dichlorokynurenic acid binding to strychnine-insensitive glycine receptors in neocortical membranes. In toto, these data indicate that like other NMDA antagonists, eliprodil possesses antidepressant-like actions in preclinical tests predictive of clinical efficacy. RP LAYER, RT (reprint author), NIDDKD,NEUROSCI LAB,BLDG 8,ROOM 111,BETHESDA,MD 20892, USA. RI Popik, Piotr/R-5383-2016 OI Popik, Piotr/0000-0003-0722-1263 NR 52 TC 91 Z9 93 U1 2 U2 5 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 NOV PY 1995 VL 52 IS 3 BP 621 EP 627 DI 10.1016/0091-3057(95)00155-P PG 7 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA RW583 UT WOS:A1995RW58300026 PM 8545484 ER PT J AU DUDLEY, CN BURKA, LT GRIFFIN, RJ AF DUDLEY, CN BURKA, LT GRIFFIN, RJ TI ACTIVITY OF HEPATIC DRUG-METABOLIZING-ENZYMES FOLLOWING NALIDIXIC-ACID DOSED FEED TREATMENT IN F344 RATS AND B6C3F1 MICE SO PHARMACOLOGY & TOXICOLOGY LA English DT Note ID LIVER C1 NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. NR 16 TC 1 Z9 1 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0901-9928 J9 PHARMACOL TOXICOL JI Pharmacol. Toxicol. PD NOV PY 1995 VL 77 IS 5 BP 352 EP 354 PG 3 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA TG552 UT WOS:A1995TG55200010 PM 8778749 ER PT J AU PODGORNIK, R AF PODGORNIK, R TI ORIENTATIONAL ORDERING OF POLYMERS ON A FLUCTUATING FLEXIBLE SURFACE SO PHYSICAL REVIEW E LA English DT Article ID LIQUID-CRYSTALLINE POLYMERS; MEMBRANES; FORCES; MODEL AB Arguments are presented to the effect that embedding semiflexible (wormlike) ideal polymers into a fluctuating, flexible surface leads to an effective attractive orientational interaction between polymer segments that precipitates an orientational ordering transition of the polymer chains on the surface even in the case of otherwise ideal (noninteracting) chains. The orientational interaction is analogous to the (zero order) Casimir force and is due to the energy change in surface conformational fluctuations in the presence of embedded semiflexible chains. RP PODGORNIK, R (reprint author), NATL INST HLTH,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 22 TC 7 Z9 7 U1 0 U2 1 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 NOV PY 1995 VL 52 IS 5 BP 5170 EP 5177 DI 10.1103/PhysRevE.52.5170 PN B PG 8 WC Physics, Fluids & Plasmas; Physics, Mathematical SC Physics GA TG337 UT WOS:A1995TG33700016 ER PT J AU GITTERMAN, M WEISS, GH AF GITTERMAN, M WEISS, GH TI COHERENT STOCHASTIC RESONANCE IN THE PRESENCE OF A FIELD SO PHYSICAL REVIEW E LA English DT Letter AB A recent paper by Bulsara, Lowen, and Rees [Phys. Rev. E 49, 4989 (1994)] presents a perturbation analysis of coherent stochastic resonance in a half-space in the presence of a field. We believe that the analysis there was flawed due to an improper use of the method of images and that a correct version of a perturbation analysis can be given by using a transformation of the underlying equations. The result still exhibits stochastic resonance. C1 NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. RP GITTERMAN, M (reprint author), BAR ILAN UNIV,DEPT PHYS,IL-52100 RAMAT GAN,ISRAEL. NR 17 TC 7 Z9 7 U1 0 U2 1 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 NOV PY 1995 VL 52 IS 5 BP 5708 EP 5711 DI 10.1103/PhysRevE.52.5708 PN B PG 4 WC Physics, Fluids & Plasmas; Physics, Mathematical SC Physics GA TG337 UT WOS:A1995TG33700077 ER PT J AU SHIRLEY, BW KUBASEK, WL STORZ, G BRUGGEMANN, E KOORNNEEF, M AUSUBEL, FM GOODMAN, HM AF SHIRLEY, BW KUBASEK, WL STORZ, G BRUGGEMANN, E KOORNNEEF, M AUSUBEL, FM GOODMAN, HM TI ANALYSIS OF ARABIDOPSIS MUTANTS DEFICIENT IN FLAVONOID BIOSYNTHESIS SO PLANT JOURNAL LA English DT Article ID ANTHOCYANIN BIOSYNTHESIS; TRANSCRIPTIONAL ACTIVATORS; LINKAGE MAP; THALIANA; GENE; PLANT; HOMOLOGY; PETUNIA; MYB; CONSTRUCTION AB Eleven loci that play a role in the synthesis of flavonoids in Arabidopsis are described. Mutations at these loci, collectively named transparent testa (tt), disrupt the synthesis of brown pigments in the seed coat (testa). Several of these loci (tt3, tt4, tt5 and ttg) are also required for the accumulation of purple anthocyanins in leaves and stems and one locus (ttg) plays additional roles in trichome and root hair development. Specific functions were previously assigned to tt1-7 and ttg. Here, the results of additional genetic, biochemical and molecular analyses of these mutants are described. Genetic map positions were determined for tt8, tt9 and tt10. Thin layer chromatography identified tissue- and locus-specific differences in the flavonols and anthocyanidins synthesized by mutant and wild-type plants. It was found that UV light reveals distinct differences in the floral tissues of tt3, tt4, tt5, tt6 and ttg, even though these tissues are indistinguishable under visible light. Evidence was also uncovered that tt8 and ttg specifically affect dihydroflavonol reductase gene expression. A summary of these and previously published results are incorporated into an overview of the genetics of flavonoid biosynthesis in Arabidopsis. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. WAGENINGEN UNIV AGR,DEPT GENET,6703 HA WAGENINGEN,NETHERLANDS. RP SHIRLEY, BW (reprint author), VIRGINIA POLYTECH INST & STATE UNIV,DEPT BIOL,BLACKSBURG,VA 24061, USA. RI Winkel, Brenda/A-6602-2008; OI Winkel, Brenda/0000-0003-3481-024X; Storz, Gisela/0000-0001-6698-1241; Koornneef, Maarten/0000-0002-7759-4869 NR 53 TC 314 Z9 331 U1 7 U2 49 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0960-7412 J9 PLANT J JI Plant J. PD NOV PY 1995 VL 8 IS 5 BP 659 EP 671 DI 10.1046/j.1365-313X.1995.08050659.x PG 13 WC Plant Sciences SC Plant Sciences GA TF908 UT WOS:A1995TF90800004 PM 8528278 ER PT J AU LI, LP DARDEN, T FOLEY, C HISKEY, R PEDERSEN, L AF LI, LP DARDEN, T FOLEY, C HISKEY, R PEDERSEN, L TI HOMOLOGY MODELING AND MOLECULAR-DYNAMICS SIMULATION OF HUMAN PROTHROMBIN FRAGMENT-1 SO PROTEIN SCIENCE LA English DT Article DE GLA DOMAIN; KRINGLE DOMAIN; PHOSPHOLIPID BINDING; PROTHROMBIN; VITAMIN-K-DEPENDENT PROTEINS ID GAMMA-CARBOXYGLUTAMIC ACID; K-DEPENDENT PROTEINS; FACTOR-IX; BOVINE PROTHROMBIN; MEMBRANE-BINDING; METAL; RESIDUES; DOMAIN; IONS; ACTIVATION AB The crystallographic structure of bovine prothrombin fragment 1 bound with calcium ions was used to construct the corresponding human prothrombin structure (hf1/Ca). The model structure was refined by molecular dynamics to estimate the average solution structure. Accommodation of long-range ionic forces was essential to reach a stable solution structure. The gamma-carboxyglutamic acid (Gla) domain and the kringle domain of hf1/Ca independently equilibrated. Likewise, the hydrogen bond network and the calcium ion coordinations were well preserved. A discussion of the phospholipid binding of the vitamin K-dependent coagulation proteins in the context of the structure and mutational data of the Gla domain is presented. C1 NIEHS,RES TRIANGLE PK,NC 27709. CRAY RES INC,RES TRIANGLE PK,NC 27709. RP LI, LP (reprint author), UNIV N CAROLINA,DEPT CHEM,CB 3290,CHAPEL HILL,NC 27599, USA. OI Foley, Charles/0000-0001-6578-9629 FU NHLBI NIH HHS [HL-27995, HL-06350] NR 35 TC 14 Z9 14 U1 0 U2 1 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 NOV PY 1995 VL 4 IS 11 BP 2341 EP 2348 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TE287 UT WOS:A1995TE28700012 PM 8563631 ER PT J AU MADEJ, T GIBRAT, JF BRYANT, SH AF MADEJ, T GIBRAT, JF BRYANT, SH TI THREADING A DATABASE OF PROTEIN CORES SO PROTEINS-STRUCTURE FUNCTION AND GENETICS LA English DT Article DE STRUCTURE PREDICTION; FOLD RECOGNITION; PROTEIN THREADING ID CRYSTAL-STRUCTURE; RESOLUTION; SEQUENCE; IDENTIFICATION; PREDICTION; ALIGNMENT; ALGORITHM; BINDING; COMPLEX; FOLDS AB We present an analysis of 10 blind predictions prepared for a recent conference, ''Critical Assessment of Techniques for Protein Structure Prediction.''(1) The sequences of these proteins are not detectably similar to those of any protein in the structure database then available, but we attempted, by a threading method, to recognize similarity to known domain folds. Four of the 10 proteins, as we subsequently learned, do indeed show significant similarity to then-known structures. For 2 of these proteins the predictions were accurate, in the sense that a similar structure was at or near the top of the list of threading scores, and the threading alignment agreed well with the corresponding structural alignment. For the best predicted model mean alignment error relative to the optimal structural alignment was 2.7 residues, arising entirely from small ''register shifts'' of strands or helices. In the analysis we attempt to identify factors responsible for these successes and failures, Since our threading method does not use gap penalties, we may readily distinguish between errors arising from our prior definition of the ''cores'' of known structures and errors arising from inherent limitations in the threading potential, It would appear from the results that successful substructure recognition depends most critically on accurate definition of the ''fold'' of a database protein. This definition must correctly delineate substructures that are, and are not, likely to be conserved during protein evolution. (C) 1995 Wiley-Liss, Inc.* C1 NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,COMPUTAT BIOL BRANCH,BETHESDA,MD 20894. NR 42 TC 317 Z9 327 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 0887-3585 J9 PROTEINS JI Proteins PD NOV PY 1995 VL 23 IS 3 BP 356 EP 369 DI 10.1002/prot.340230309 PG 14 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TH809 UT WOS:A1995TH80900008 PM 8710828 ER PT J AU DAVIS, LM WELLS, KB ROGERS, WH BENJAMIN, B NORQUIST, G KAHN, K KOSECOFF, J BROOK, R AF DAVIS, LM WELLS, KB ROGERS, WH BENJAMIN, B NORQUIST, G KAHN, K KOSECOFF, J BROOK, R TI EFFECTS OF MEDICARE PROSPECTIVE PAYMENT SYSTEM ON SERVICE USE BY DEPRESSED ELDERLY INPATIENTS SO PSYCHIATRIC SERVICES LA English DT Article ID GENERAL HOSPITALS; CARE; QUALITY; PSYCHIATRY; IMPACT AB Objective: To determine the effects of Medicare's prospective payment system (PPS) on hospital care, changes in length of stay and intensity of clinical services received by 2,746 depressed elderly patients in 297 acute care general medical hospitals were studied. Methods: A pre-post design was used, and differences in sickness at admission were controlled for. Data on length of stay and use of specific clinical services were obtained from the medical record using a medical record abstraction form. Care provided on units exempt from PPS was compared with care provided in nonexempt units. Results: After implementation of PPS, the average length of stay fell by up to three days within the different types of acute care settings studied, but this decline was partially offset by proportionately more admissions to psychiatric units, which had longer lengths of stay. Intensity of clinical services increased after PPS implementation, especially in nonexempt psychiatric units. Conclusion: Despite financial incentives for hospitals to reduce clinical services under PPS, its implementation was not associated with a marked decline in length of stay, when averaged across all treatment settings, and was associated with an increase in the intensity of many clinical services used by depressed elderly patients in general hospital. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA 02111. NIMH,ROCKVILLE,MD 20857. UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT MED,LOS ANGELES,CA 90024. VALUE HLTH SCI,LOS ANGELES,CA. RP DAVIS, LM (reprint author), RAND CORP,1700 MAIN ST,POB 2138,SANTA MONICA,CA 90407, USA. NR 30 TC 9 Z9 9 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1075-2730 J9 PSYCHIATR SERV JI Psychiatr. Serv. PD NOV PY 1995 VL 46 IS 11 BP 1178 EP 1184 PG 7 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA TC918 UT WOS:A1995TC91800014 PM 8564509 ER PT J AU Swerdlow, NR Lipska, BK Weinberger, DR Braff, DL Jaskiw, GE Geyer, MA AF Swerdlow, NR Lipska, BK Weinberger, DR Braff, DL Jaskiw, GE Geyer, MA TI Increased sensitivity to the sensorimotor gating-disruptive effects of apomorphine after lesions of medial prefrontal cortex or ventral hippocampus in adult rats SO PSYCHOPHARMACOLOGY LA English DT Article DE apomorphine; dopamine; frontal cortex; hippocampus; schizophrenia; startle ID IBOTENIC ACID LESIONS; NUCLEUS-ACCUMBENS; ACOUSTIC STARTLE; SCHIZOPHRENIC-PATIENTS; DOPAMINE-RECEPTORS; MESOLIMBIC DOPAMINE; PREPULSE INHIBITION; INDUCED LOCOMOTION; MONOZYGOTIC TWINS; ANIMAL-MODEL AB Sensorimotor gating of the startle reflex is impaired in humans with schizophrenia and in rats after mesolimbic D-2 dopamine receptor activation. The loss of startle gating after D-2 activation in rats has been used as an animal model of impaired sensorimotor gating in schizophrenia, because the ability of antipsychotics to restore startle gating in D-2-activated rats correlates significantly with antipsychotic clinical potency. Substantial evidence indicates that the pathophysiology of schizophrenia includes structural and functional deficits in prefrontal and temporal regions, particularly the dorsolateral prefrontal cortex and the hippocampus and parahippocampal gyrus. The present : study assessed startle gating in adult rats after ibotenic acid lesions of the medial prefrontal cortex or ventral hippocampus. Medial prefrontal cortex lesioned rats exhibited normal startle amplitude and normal sensorimotor gating, as reflected by prepulse inhibition (PPI) of the startle reflex. Hippocampus lesioned rats exhibited elevated startle amplitude, and similar to rats with medial prefrontal cortex lesions, did not show significant changes in basal PPI. Low doses. of the mixed dopamine agonist apomorphine did not significantly reduce PPI in sham lesioned rats, but significantly disrupted PPI in both medial prefrontal cortex and ventral hippo-campus lesioned rats. These data are consistent with the hypothesis that cell damage in frontal and temporal cortex increases the sensitivity to the sensorimotor gating-disruptive effects of dopamine receptor activation. C1 NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. VET ADM MED CTR,PSYCHIAT SERV 116AB,BRECKSVILLE,OH 44124. RP Swerdlow, NR (reprint author), UNIV CALIF SAN DIEGO,SCH MED,DEPT PSYCHIAT,0667,9500 GILLMAN DR,LA JOLLA,CA 92093, USA. RI Lipska, Barbara/E-4569-2017 FU NIMH NIH HHS [MH 01223, MH 42228, MH 48381] NR 68 TC 149 Z9 155 U1 1 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD NOV PY 1995 VL 122 IS 1 BP 27 EP 34 DI 10.1007/BF02246438 PG 8 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA TN130 UT WOS:A1995TN13000003 PM 8711061 ER PT J AU Lipska, BK Swerdlow, NR Geyer, MA Jaskiw, GE Braff, DL Weinberger, DR AF Lipska, BK Swerdlow, NR Geyer, MA Jaskiw, GE Braff, DL Weinberger, DR TI Neonatal excitotoxic hippocampal damage in rats causes post pubertal changes in prepulse inhibition of startle and its disruption by apomorphine SO PSYCHOPHARMACOLOGY LA English DT Article DE prepulse inhibition of startle; sensorimotor gating; neonatal lesion; hippocampus; ibotenic acid; apomorphine; startle ID ACOUSTIC STARTLE; SCHIZOPHRENIC-PATIENTS; NUCLEUS-ACCUMBENS; DOPAMINE INFUSION; GATING DEFICITS; ANIMAL-MODEL; REFLEX; HABITUATION; HALOPERIDOL; PHENCYCLIDINE AB Neonatal excitotoxic hippocampal damage in the rat results in postpubertal onset of a variety of abnormal behaviors related to excessive dopaminergic transmission in the mesolimbic/nigrostriatal system; and thus may be considered an animal model of some aspects of schizophrenia. Because sensorimotor gating is impaired in adult patients with schizophrenia and in rats with experimentally induced mesolimbic dopamine hyperactivity, the present experiments investigated the effects of neonatal (postnatal day 7, PD7) ibotenic acid (3 mu g) lesions of the ventral hippocampus (VH) on the amplitude and prepulse inhibition (PPI) of acoustic startle in prepubertal (PD35) and postpubertal (PD56) rats. Startle was elicited using 105 and 118-dB pulses alone or preceded by 4, 8, or 16 dB above-background prepulses in rats treated with vehicle or apomorphine (APO; 0.025 or 0.1 mg/kg SC). At PD35, PPI in VH-lesioned rats did not differ significantly from these measures in sham operated rats. Apomorphine significantly increased startle amplitude and reduced PPI in both sham operated and VH-lesioned rats at PD35. At PD56, startle amplitude in VH-lesioned rats was not significantly different from controls, but PPI was reduced significantly compared to controls. Ventral hippocampus lesioned rats also exhibited an exaggerated reduction in PPI after treatment with APO. These findings provide further evidence of postpubertal impairments that may be related to increased mesolimbic dopamine transmission and receptor sensitivity in rats with neonatal hippocampal damage. and provide further support for the fidelity of this animal model of schizophrenia. C1 UNIV CALIF SAN DIEGO,SCH MED,DEPT PSYCHIAT,LA JOLLA,CA 92093. VET ADM MED CTR,PSYCHIAT SERV 116AB,BRECKSVILLE,OH 44124. RP Lipska, BK (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. RI Lipska, Barbara/E-4569-2017 FU NIMH NIH HHS [K05-MH 01223, MH 48381, R37-MH 42228] NR 47 TC 275 Z9 277 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD NOV PY 1995 VL 122 IS 1 BP 35 EP 43 DI 10.1007/BF02246439 PG 9 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA TN130 UT WOS:A1995TN13000004 PM 8711062 ER PT J AU CURRAN, HV BARROW, S WEINGARTNER, H LADER, M BERNIK, M AF CURRAN, HV BARROW, S WEINGARTNER, H LADER, M BERNIK, M TI ENCODING, REMEMBERING AND AWARENESS IN LORAZEPAM INDUCED AMNESIA SO PSYCHOPHARMACOLOGY LA English DT Article DE IMPLICIT MEMORY TASKS; EXPLICIT MEMORY TASKS; LORAZEPAM; LEVELS OF PROCESSING; AWARENESS ID IMPLICIT MEMORY; RECOLLECTIVE EXPERIENCE; RECOGNITION; DIAZEPAM; BENZODIAZEPINES; WORDS AB The effects of lorazepam (1,2 mg) and placebo on encoding, remembering and awareness were assessed in a study with 54 healthy volunteers. All subjects studied stimulus materials in a levels of processing (L-o-p) task. Half the subjects were assessed on an explicit memory task of word recognition and the other half were given an implicit memory task of word-stem completion. Following the implicit task, awareness of retrieval was further investigated by questions and by subjects' recollective experience in recognising the actual words they had completed from stems. L-o-p effects and marked lorazepam-induced impairments were found in the implicit task of word-stem completion although the interaction between L-o-p and drug effects emerged only as a trend in the data. Lorazepam-induced impairments on stem-completion may then be explained at least in part as being due to contamination by explicit retrieval processes, but we cannot rule out the possible role of drug effects on perceptual processes at encoding. results from responses to ''awareness'' questions and from analysis of subsequent recollective experience indicated that subjects were not aware of using explicit retrieval during the implicit task. Results also replicated previous findings showing that both lorazepam and L-o-p independently affect performance in an explicit memory task of word recognition. Thus drug-induced deficits at encoding persist regardless of the level at which information is initially processed. C1 INST PSYCHIAT, LONDON SE5 8AF, ENGLAND. NIAAA, BETHESDA, MD USA. RP CURRAN, HV (reprint author), UCL, GOWER ST, LONDON WC1 6BT, ENGLAND. NR 29 TC 17 Z9 17 U1 3 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD NOV PY 1995 VL 122 IS 2 BP 187 EP 193 DI 10.1007/BF02246094 PG 7 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA TH402 UT WOS:A1995TH40200013 PM 8848535 ER PT J AU RUBINOW, DR ROCA, CA AF RUBINOW, DR ROCA, CA TI INFERTILITY AND DEPRESSION SO PSYCHOSOMATIC MEDICINE LA English DT Editorial Material ID RAT-BRAIN; GLUCOCORTICOIDS; INHIBITION; SECRETION; SEROTONIN; RECEPTOR; REGIONS; STRESS RP RUBINOW, DR (reprint author), NIMH,BLDG 10,ROOM 3N238,10 CTR DR MSC 1276,BETHESDA,MD 20892, USA. NR 15 TC 9 Z9 9 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD NOV-DEC PY 1995 VL 57 IS 6 BP 514 EP 516 PG 3 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA TH677 UT WOS:A1995TH67700002 ER PT J AU PATTERSON, SM KRANTZ, DS GOTTDIENER, JS HECHT, G VARGOT, S GOLDSTEIN, DS AF PATTERSON, SM KRANTZ, DS GOTTDIENER, JS HECHT, G VARGOT, S GOLDSTEIN, DS TI PROTHROMBOTIC EFFECTS OF ENVIRONMENTAL-STRESS - CHANGES IN PLATELET-FUNCTION, HEMATOCRIT, AND TOTAL PLASMA-PROTEIN SO PSYCHOSOMATIC MEDICINE LA English DT Article DE HEMOSTASIS; MENTAL STRESS; THROMBOSIS ID CORONARY-ARTERY DISEASE; ACUTE MYOCARDIAL-INFARCTION; ISCHEMIC-HEART-DISEASE; ACUTE MENTAL STRESS; RED-CELL COUNTS; BLOOD-VISCOSITY; BETA-THROMBOGLOBULIN; CEREBRAL THROMBOSIS; UNSTABLE ANGINA; CARDIAC DEATH AB Mental stress can affect a range of variables relevant to hemostasis and thrombosis. However, research has not clarified whether these effects occur as part of a generalized sympathoadrenal response or whether stress-induced increases in catecholamines and blood pressure have selective and independent effects on hematologic variables. This study assessed the effects of mental and cold presser stress on platelet activation, hematocrit, and total plasma protein and the relationship of these changes to sympathoadrenal and hemodynamic mechanisms, Platelet factor 4, beta-thromboglobulin, total plasma protein, hematocrit values, and hemoglobin were measured in 22 healthy men (32 +/- 7 years) during rest, mental arithmetic, and cold presser task. A no-stress control group of five male subjects was used to rule out the possible effects of blood withdrawal in producing these changes. Significant increases to mental arithmetic and cold presser (p < .001) were observed in platelet factor 4 and beta-thromboglobulin. Increases (p < .002) in hematocrit values and total plasma protein also occurred with mental arithmetic and cold presser. Correlational analyses revealed that changes in hematocrit and total plasma protein concentrations were related to increased mean arterial pressure during stress, and platelet activation correlated positively with norepinephrine and negatively with epinephrine; The present results indicate that acute psychologic and cold stress cause concurrent changes in several hemostatic factors (increased platelet activation, hematocrit, and total plasma protein) that may play key roles in thrombosis and ischemia. The relationships of hematocrit and total plasma protein to blood pressure increases and the associations between platelet activation and catecholamines support the notion that stress-induced increases in catecholamines and blood pressure have selective effects on specific hemostatic variables. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT MED & CLIN PSYCHOL,BETHESDA,MD 20814. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NHLBI,BETHESDA,MD 20892. RI Krantz, David/L-5364-2015 OI Krantz, David/0000-0002-1671-1355 FU NHLBI NIH HHS [HL47337] NR 66 TC 53 Z9 53 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD NOV-DEC PY 1995 VL 57 IS 6 BP 592 EP 599 PG 8 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA TH677 UT WOS:A1995TH67700012 PM 8600486 ER PT J AU Hanson, J AF Hanson, J TI Birth defects surveillance and the future of public health SO PUBLIC HEALTH REPORTS LA English DT Article RP Hanson, J (reprint author), NICHHD,CTR RES MOTHERS & CHILDREN,EXECUT BLDG,RM 4B05G,6100 EXECUT BLVD,MSC 7510,BETHESDA,MD 20892, USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD NOV-DEC PY 1995 VL 110 IS 6 BP 698 EP 699 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TR305 UT WOS:A1995TR30500019 PM 8570820 ER PT J AU MacKinnon, DP WilliamsAvery, RM Pentz, MA AF MacKinnon, DP WilliamsAvery, RM Pentz, MA TI Youth beliefs and knowledge about the risks of drinking while pregnant SO PUBLIC HEALTH REPORTS LA English DT Article ID FETAL ALCOHOL SYNDROME; PREVENTING ALCOHOL; PROBLEM DRINKERS; HEAVY DRINKING; WARNING LABEL; DRUG-USE; ADOLESCENTS; PREVALENCE; PROGRAM; COUNTY AB BECAUSE NO PUBLISHED studies of young persons' knowledge and awareness of fetal alcohol syndrome are available, the awareness and beliefs about drinking while pregnant in several large samples of young persons ages 13-20 are examined. Approximately 81 percent of the entire sample that completed questionnaires in school surveys believe that drinking alcohol while pregnant can definitely harm the fetus, although males and younger persons are less likely to believe in this risk A substantial proportion of respondents believe that occasional heavy use is not harmful and suggest a safe level of drinking that is higher than the Surgeon General's abstinence recommendations. Only 72 percent have heard of fetal alcohol syndrome, and more than one-third incorrectly report that it describes a baby born addicted to alcohol, that the syndrome can be inherited, and that it can be cured. As in prior studies of adults, beliefs about drinking while pregnant are inconsistent with the Surgeon General's recommendations. Implications for increasing the awareness of the risk of drinking while pregnant are discussed. C1 ARIZONA STATE UNIV,NATL INST MENTAL HLTH PREVENT INTERVENT,RES CTR,TEMPE,AZ 85287. UNIV SO CALIF,DEPT PREVENT MED,LOS ANGELES,CA 90089. UNIV SO CALIF,INST DIS PREVENT & HLTH PROMOT,LOS ANGELES,CA 90089. RP MacKinnon, DP (reprint author), ARIZONA STATE UNIV,DEPT PSYCHOL,TEMPE,AZ 85287, USA. RI MacKinnon, David /D-8727-2013 FU NIAAA NIH HHS [AA06201, AA8547]; NIDA NIH HHS [DA0396] NR 28 TC 7 Z9 7 U1 0 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD NOV-DEC PY 1995 VL 110 IS 6 BP 754 EP 763 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TR305 UT WOS:A1995TR30500030 PM 8570831 ER PT J AU Sherman, SE AF Sherman, SE TI The False Claims Act SO PUBLIC HEALTH REPORTS LA English DT Article RP Sherman, SE (reprint author), US DEPT HHS,NIH,PUBL HLTH DIV,OFF GEN COUNSEL,ROOM 2B-50,BLDG 31,MSC 2111,31 CTR DR,BETHESDA,MD 20892, USA. NR 1 TC 5 Z9 5 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD NOV-DEC PY 1995 VL 110 IS 6 BP 784 EP 789 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TR305 UT WOS:A1995TR30500034 PM 8570835 ER PT J AU REMETA, DP MILES, EW GINSBURG, A AF REMETA, DP MILES, EW GINSBURG, A TI THERMALLY-INDUCED UNFOLDING OF THE TRYPTOPHAN SYNTHASE ALPHA(2)BETA-2 MULTIENZYME COMPLEX FROM SALMONELLA-TYPHIMURIUM SO PURE AND APPLIED CHEMISTRY LA English DT Article ID DODECAMERIC GLUTAMINE-SYNTHETASE; DIFFERENTIAL SCANNING CALORIMETRY; ESCHERICHIA-COLI; PYRIDOXAL 5'-PHOSPHATE; ALPHA-SUBUNITS; TRANSITIONS; BINDING; DOMAINS AB Tryptophan synthase (TS) from Salmonella typhimurium (144,000 M(r)) is a bifunctional enzyme composed of two heterodimers arranged in an extended alpha beta beta alpha geometry [Hyde et al., J. Biol. Chem. 263, 17857, 1988]. The thermal unfolding of TS alpha(2) beta(2) and isolated alpha and beta subunits has been studied by differential scanning calorimetry (DSC), circular dichroism, and UV spectroscopy. DSC profiles of the holo-alpha(2) beta(2) complex containing pyridoxal phosphate (PLP) bound to each beta chain are characterized by two well-resolved endotherms centered at approximate to 52 and approximate to 81 degrees C. Conformational transitions in beta chains (T-m approximate to 46 degrees C) as well as sequential unfolding reactions in a chains contribute to the low-temperature endotherm whereas major unfolding of the beta dimer occurs between 74 and 82 degrees C. The thermally induced unfolding disrupts approximate to 70% of the secondary structure with a total enthalpy change of 3600 +/- 100 kJ mol(-1) for holo-alpha(2) beta(2). Stabilizing interactions between alpha and beta chains are apparent. The cofactor PLP not only markedly stabilizes beta chains in beta(2) but also increases the cooperativity of unfolding beta chains. Calorimetric and spectral measurements suggest a sequential unfolding pathway for the tryptophan synthase alpha(2) beta(2) complex. Thermodynamic results are correlated with available structural information. C1 NIDDK, BIOCHEM PHARMACOL LAB, ENZYME STRUCT & FUNCT SECT, BETHESDA, MD 20892 USA. RP REMETA, DP (reprint author), NHLBI, BIOCHEM LAB, PROT CHEM SECT, BLDG 3, BETHESDA, MD 20892 USA. NR 34 TC 8 Z9 8 U1 0 U2 1 PU WALTER DE GRUYTER GMBH PI BERLIN PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY SN 0033-4545 EI 1365-3075 J9 PURE APPL CHEM JI Pure Appl. Chem. PD NOV PY 1995 VL 67 IS 11 BP 1859 EP 1866 DI 10.1351/pac199567111859 PG 8 WC Chemistry, Multidisciplinary SC Chemistry GA TJ450 UT WOS:A1995TJ45000012 ER PT J AU WHITEHEAD, AS GALLAGHER, P MILLS, JL KIRKE, PN BURKE, H MOLLOY, AM WEIR, DG SHIELDS, DC SCOTT, JM AF WHITEHEAD, AS GALLAGHER, P MILLS, JL KIRKE, PN BURKE, H MOLLOY, AM WEIR, DG SHIELDS, DC SCOTT, JM TI A GENETIC-DEFECT IN 5,10-METHYLENETETRAHYDROFOLATE REDUCTASE IN NEURAL-TUBE DEFECTS SO QJM-MONTHLY JOURNAL OF THE ASSOCIATION OF PHYSICIANS LA English DT Article ID VITAMIN-B12; FOLATE AB It is now well-established that folic acid, taken periconceptionally, can reduce the risk of neural tube defects (NTDs). Recent work has demonstrated that an abnormality of homocysteine metabolism is a critical factor. The gene for 5, 10 methylenetetrahydrofolate reductase, an enzyme important in homocysteine metabolism, was studied in relation to NTDs. To determine the frequency of the allele for the thermolabile form of the reductase, DNA samples were collected from people with NTDs, parents of people with NTDs, and normal controls. Of 82 people with NTDs, 15 (18.3%) were homozygous for the abnormal, thermolabile allele. This was significantly higher (p = 0.01) than the rate of 6.1% in the control population (odds ratio 3.47, 95% Cl 1.28-9.41). This is the first specific genetic abnormality to be identified in NTDs. It explains the association between some NTDs and elevated homocysteine, given that the reductase is important in homocysteine metabolism. It also explains how folic acid supplementation prevents some NTDs, by overcoming a partial block in the conversion of 5,10 methylenetetrahydrofolate to 5 methyltetrahydrofolate. Genetic screening could identify women who will require folic acid supplements to reduce their risk of having a child with an NTD. C1 TRINITY COLL DUBLIN,DEPT BIOCHEM,DUBLIN 2,IRELAND. TRINITY COLL DUBLIN,DEPT GENET,DUBLIN 2,IRELAND. TRINITY COLL DUBLIN,INST BIOTECHNOL,DUBLIN 2,IRELAND. TRINITY COLL DUBLIN,DEPT CLIN MED,DUBLIN 2,IRELAND. NICHHD,BETHESDA,MD 20892. HLTH RES BOARD,DUBLIN,IRELAND. NR 11 TC 267 Z9 272 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0033-5622 J9 QJM-MON J ASSOC PHYS JI QJM-Mon. J. Assoc. Physicians PD NOV PY 1995 VL 88 IS 11 BP 763 EP 766 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA TC699 UT WOS:A1995TC69900004 PM 8542260 ER PT J AU MILLER, RW AF MILLER, RW TI DELAYED-EFFECTS OF EXTERNAL RADIATION EXPOSURE - A BRIEF-HISTORY SO RADIATION RESEARCH LA English DT Article ID ATOMIC-BOMB SURVIVORS; GLYCOPHORIN-A LOCUS; CANCER; HIROSHIMA; CHILDREN; NAGASAKI; IRRADIATION; MUTATIONS; FREQUENCY; HUMANS AB Within months of Roentgen's discovery of X rays, severe adverse effects were reported, but not well publicized. As a result, over the next two decades, fluoroscope operators suffered lethal skin carcinomas. Later, case reports appeared concerning leukemia in radiation workers, and infants born with severe mental retardation after their mothers had been given pelvic radiotherapy early in pregnancy. Fluoroscopy and radiotherapy for benign disorders continued to be used with abandon until authoritative reports were published on the adverse effects of ionizing radiation by the U.S. NAS-NRC and the UK MRC in 1956. Meanwhile, exposure to the atomic bombs in Japan had occurred and epidemics of delayed effects began to be recognized among the survivors: cataracts (1949), leukemia (1952) and severe mental retardation among newborn infants after intrauterine exposure (1952). No statistically significant excess of germ-cell genetic effects was detected by six clinical measurements (1956), the F-1 mortality (1981), cytogenetic studies (1987) or biochemical genetic studies (1988). Somatic cell effects were revealed by long-lasting chromosomal aberrations in peripheral lymphocytes (1968), and somatic cell mutations were found at the glycophorin A locus in erythrocytes (1992). Molecular biology is a likely focus of new studies based on the function of the gene for ataxia telangiectasia (1995), a disorder in which children have severe, even lethal acute radiation reactions when given conventional doses of radiotherapy for lymphoma, to which they are prone. Also, obligate heterozygote female relatives can be studied for increased susceptibility to radiation-induced breast cancer, as suggested by clinical studies. The tumor registries in Hiroshima and Nagasaki now provide incidence data that show the extent of increases in eight common cancers and no increase in eight others (1994). The possibility of very late effects of A-bomb exposure is suggested by recent reports of increased frequencies of hyperparathyroidism, parathyroid cancers and certain causes of death other than cancer. (C) 1995 by Radiation Research Society RP MILLER, RW (reprint author), NCI,GENET EPIDEMIOL BRANCH,EPN-400,BETHESDA,MD 20892, USA. NR 87 TC 30 Z9 31 U1 1 U2 6 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD NOV PY 1995 VL 144 IS 2 BP 160 EP 169 DI 10.2307/3579255 PG 10 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA TD528 UT WOS:A1995TD52800006 PM 7480642 ER PT J AU HOEKSTRA, HJ SINDELAR, WF SZABO, BG KINSELLA, TJ AF HOEKSTRA, HJ SINDELAR, WF SZABO, BG KINSELLA, TJ TI HEMIPELVECTOMY AND INTRAOPERATIVE RADIOTHERAPY FOR BONE AND SOFT-TISSUE SARCOMAS OF THE PELVIC GIRDLE SO RADIOTHERAPY AND ONCOLOGY LA English DT Note DE SARCOMA; BONE; SOFT TISSUE; INTRAOPERATIVE; RADIATION ID RADIATION-THERAPY AB Current treatment of locally advanced bone and soft tissue sarcomas of the pelvic girdle are associated with a high local and distant failure rate, and local tumor control after hemipelvectomy can be a significant problem. IORT has been used in conjunction with hemipelvectomy, both conventional (seven patients) and limb-sparing internal hemipelvectomy (one patient), in seven males and one female, median age 27 (range 24-57) years with locally extensive high grade bone (seven patients) or soft tissue (one patient) sarcomas. IORT (15-30 Gy, 8-16 MeV) was delivered to sacral resection margins and surrounding soft tissues considered likely to harbor microscopically residual disease. Four patients received 46-54 Gy postoperative radiotherapy in addition to IORT. During a median follow-up of 33 months (range 6-131 months) two patients developed a local recurrence (25%), and five patients distant metastases (62%). Three patients with pelvic girdle sarcomas remained free of tumor (37%) with a mean follow-up of 100 (range 49-131) months. There was no treatment-related mortality. Two patients developed radiation-induced necrosis of the coccyx (25%). On the basis of this preliminary experience, it appears that IORT may substantially help to control local recurrence and survival in patients with marginally resectable sarcomas of the pelvic girdle after hemipelvectomy. Since the majority of the patients die from metastatic disease, there is a need for adjuvant systemic treatment. C1 NCI,BETHESDA,MD 20892. RP HOEKSTRA, HJ (reprint author), UNIV GRONINGEN HOSP,DEPT SURG,DIV SURG ONCOL,POB 30001,9700 RB GRONINGEN,NETHERLANDS. NR 15 TC 8 Z9 8 U1 1 U2 1 PU ELSEVIER SCI PUBL IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0167-8140 J9 RADIOTHER ONCOL JI Radiother. Oncol. PD NOV PY 1995 VL 37 IS 2 BP 160 EP 163 DI 10.1016/0167-8140(95)01642-T PG 4 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA TJ935 UT WOS:A1995TJ93500010 PM 8747941 ER PT J AU STREIT, WJ KINCAIDCOLTON, CA AF STREIT, WJ KINCAIDCOLTON, CA TI THE BRAINS IMMUNE-SYSTEM SO SCIENTIFIC AMERICAN LA English DT Article C1 GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20057. NIH,BIOPHYS LAB,BETHESDA,MD 20892. MAX PLANCK INST PSYCHIAT,W-8033 MARTINSRIED,GERMANY. RP STREIT, WJ (reprint author), UNIV FLORIDA,INST BRAIN,GAINESVILLE,FL 32611, USA. NR 3 TC 77 Z9 78 U1 0 U2 6 PU SCI AMERICAN INC PI NEW YORK PA 415 MADISON AVE, NEW YORK, NY 10017 SN 0036-8733 J9 SCI AM JI Sci.Am. PD NOV PY 1995 VL 273 IS 5 BP 54 EP & PG 0 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TD999 UT WOS:A1995TD99900029 PM 8966536 ER PT J AU Campain, JA Slovak, ML Schoenlein, PV Popescu, NC Gottesman, MM Pastan, I AF Campain, JA Slovak, ML Schoenlein, PV Popescu, NC Gottesman, MM Pastan, I TI Acquisition of multiple copies of a mutant topoisomerase II alpha allele by chromosome 17 aneuploidy is associated with etoposide resistance in human melanoma cell lines SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID POINT MUTATION; DNA TOPOISOMERASES; ANTICANCER DRUGS; GENE; EXPRESSION; AMSACRINE; YEAST; CDNA; IDENTIFICATION; AMPLIFICATION AB Mutants of the human melanoma cell line, FEM-X, selected in multiple steps with VP-16 (etoposide), are cross resistant to the epipodophyllotoxins and doxorubicin. Complementary DNA's for topoisomerase II alpha were cloned from both FEM-X and FVP3, the most resistant mutant. Deletion of nucleotides 1320-1322 (or Ala429 from the resulting topoisomerase II alpha protein) was unique to the cDNA from the drug resistant cell line. Expression of the mutant mRNA increases in parallel with VP-16 resistance in this series of cell lines. Restriction analysis and Southern analysis with allele-specific oligonucleotide probes were used to quantify, the ratio of wild-type to mutant topoisomerase II alpha alleles present in DNA amplified by PCR from both FEM-X and the drug resistant sublines. This analysis shows that in cell lines of increasing drug resistance, the number of mutant topoisomerase II alpha alleles increases incrementally along with a concomitant decrease in the number of wild-type alleles. By quantitative Southern analysis of genomic DNA the total number of topoisomerase II alpha alleles in FVP3 is approximately 2-fold that in the parental cells. Fluorescence in situ hybridization with a chromosome 17 paint reveals that amplification of the topoisomerase II alpha locus in FVP3 correlates with an increase in the number of chromosome 17's, specifically the long arm. Cytogenetic analysis demonstrates that FEM-X contains three copies of chromosome 17, two of which are morphologically normal. During drug selection, FVP3 has gained 2-3 additional copies of the long arm of chromosome 17, the chromosomal location of the topoisomerase II alpha locus. In this subline it is likely that three copies of the topoisomerase II alpha gene are found on normal chromosome 17's and two on an isochromosome of the long arm of 17. By pulsed field gel electrophoresis, we were able to detect changes in the restriction pattern of the region of the long arm of chromosome 17 around the topoisomerase II alpha locus that correlate with observed cytogenetic changes in FVP3. These results suggest that the acquisition of the mutant allele of topoisomerase II alpha confers a selective advantage to cells in the presence of VP-16. As the drug concentration increased during the selection process, surviving sublines show preferential expression of the mutant topoisomerase II alpha mRNA over that of the wild-type which is associated with a concomitant increase in the number of mutant topoisomerase II alpha alleles. C1 NCI,NIH,DCBDC,MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,NIH,DCBDC,CELL BIOL LAB,BETHESDA,MD 20892. NCI,NIH,DCE,BIOL LAB,BETHESDA,MD 20892. CITY HOPE NATL MED CTR,DEPT CYTOGENET,DUARTE,CA 91010. MED COLL GEORGIA,DEPT CELLULAR BIOL & ANAT,AUGUSTA,GA 30912. FU NCI NIH HHS [CA33572] NR 37 TC 16 Z9 16 U1 0 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD NOV PY 1995 VL 21 IS 6 BP 451 EP 471 DI 10.1007/BF02310211 PG 21 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA UB376 UT WOS:A1995UB37600007 PM 8600572 ER PT J AU Howard, DH KwonChung, KJ AF Howard, DH KwonChung, KJ TI Zoopathogenic heterobasidiomycetous yeasts SO STUDIES IN MYCOLOGY LA English DT Article; Proceedings Paper CT Symposium on Systematics of Heterobasidiomycetous Yeasts and Filamentous Fungi, at the 5th International Mycological Congress CY AUG 14-21, 1994 CL VANCOUVER, CANADA DE Cryptococcus; heterobasidiomycetous yeasts; Malassezia; mycoses; Rhodotorula; Sporobolomyces; taxonomy; Trichosporon ID NEOFORMANS VAR GATTII; CRYPTOCOCCUS-NEOFORMANS; MALASSEZIA-FURFUR; VIRULENCE; INFECTIONS; SEROTYPE AB Among the heterobasidiomycetous yeasts only a single species, Filobasidiella neoformans (anamorph Cryptococcus neoformans), is regularly encountered as a pathogen of humans and animals. A number of other yeasts with heterobasidiomycete affinities are known to be pathogens of humans and animals or are encountered in clinical specimens. These include Malassezia furfur, M. pachydermatis and M. sympodialis; Rhodotorula glutinis, R. minuta, and R. rubra; Sporobolomyces spp.; and Trichosporon beigelii (and the other Trichosporon spp. that have been suggested in a recent revision of T. beigelii). In its most commonly encountered clinical form cryptococcosis is a disease of the central nervous system. The etiologic agent, C. neoformans, occurs in two varieties: C. neoformans var. neoformans and C. neoformans var, gattii, each with a separate ecological niche and geographic distribution. Humans are generally quite resistant to overt disease and immunosuppression is often associated with clinical disease. Malassezia furfur is a commensal of the skin and produces characteristic lesions of the skin and hair follicles under poorly understood conditions. Invasive, systemic disease is rarely seen, but has been reported in immunocompromised individuals. Trichosporon beigelii is the cause of a well-known hair affliction, white piedra. Its exact location in nature, i.e., skin commensal or saprophyte is unknown. Trichosporon spp. are customarily found as saprophytes. T. beigelii may cause invasive systemic disease in immunocompromised individuals. This species has recently been extensively revised, and a summary of that revision is presented. Rhodotorula rubra, the only species of Rhodotorula encountered in human infections, is a common commensal of the gastrointestinal tract. Invasive systemic disease caused by R. rubra occurs rarely in immunocompromised patients. Sporobolomyces spp. are encountered in clinical specimens, but pathogenicity has not been proven. C1 NIAID,CLIN INVEST LAB,CLIN MYCOL SECT,BETHESDA,MD 20892. RP Howard, DH (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024, USA. NR 40 TC 0 Z9 0 U1 1 U2 1 PU CENTRAALBUREAU SCHIMMELCULTURE PI BAARN PA PO BOX 273, 3740 BAARN, NETHERLANDS SN 0166-0616 J9 STUD MYCOL JI Stud. Mycol. PD NOV PY 1995 IS 38 BP 59 EP 66 PG 8 WC Mycology SC Mycology GA TM393 UT WOS:A1995TM39300006 ER PT J AU KwonChung, KJ Chang, YC Bauer, R Swann, EC Taylor, JW Goel, R AF KwonChung, KJ Chang, YC Bauer, R Swann, EC Taylor, JW Goel, R TI The characteristics that differentiate Filobasidiella depauperata from Filobasidiella neoformans SO STUDIES IN MYCOLOGY LA English DT Article; Proceedings Paper CT Symposium on Systematics of Heterobasidiomycetous Yeasts and Filamentous Fungi, at the 5th International Mycological Congress CY AUG 14-21, 1994 CL VANCOUVER, CANADA DE Cryptococcus neoformans; Filobasidiella neoformans; Filobasidiella depauperata; morphology; phylogeny; ultrastructure ID CRYPTOCOCCUS-NEOFORMANS; ULTRASTRUCTURE; APPARATUS; SEQUENCES; GENUS; FUNGI AB The basidial morphology of the two species in the genus Filobasidiella, F. neoformans and F. depauperata is very similar when observed with light microscopy. The two species can be separated by the presence or absence of clamp-connections and the shape of their basidiospores. F. neoformans produces clamp-connections on the hyphae and its basidiospores are subglobose to barrel-shaped, while F. depauperata lacks clamp-connections and produces oblong to pentagonal basidiospores. Although the basidial morphology undoubtedly places the two species in the same genus, there are fundamental differences between them. Unlike F. neoformans, F. depauperata does not have a yeast stage and lacks dikaryotic hyphae. F. depauperata also lacks the biochemical markers of F. neoformans such as urease activity, myo-inositol assimilation and starch formation, as well as growth at 37 degrees C. Most importantly, F. neoformans is a human pathogen while F. depauperata is not. A phylogenetic tree constructed on the basis of 18S rDNA sequence indicates that F. depauperata is most closely related to F. neoformans, and that the two species are closer related to the Tremellaceae than to the Filobasidiaceae. Hyphal septa of F. depauperata have dolipores with parenthesomes consisting of cupulate vesicles typical of Tremella species and Filobasidium capsuligenum. The nucleus in the basidium undergoes meiosis prior to spore formation. The spindle pole bodies (SPBs) of F. depauperata are nearly identical to those reported for F. neoformans and Tremella globispora. Molecular studies indicate that F. depauperata lacks the CNLAC1 gene which encodes laccase in F. neoformans. The present study indicates that the genus Filobasidiella belongs to the Tremella-lineage and that differences between the two species with regard to the presence or absence of an ontogenetic yeast stage and certain biochemical characteristics are less important for defining the genus than are basidium morphology, the manner of basidiospore production, and rDNA nucleotide sequences. C1 UNIV TUBINGEN,LEHRSTUHL SPEZIELLE BOT,TUBINGEN,GERMANY. UNIV MINNESOTA,DEPT PLANT BIOL,ST PAUL,MN 55108. UNIV CALIF BERKELEY,DEPT PLANT PATHOL,BERKELEY,CA 94720. RP KwonChung, KJ (reprint author), NIAID,CLIN INVEST LAB,BETHESDA,MD 20892, USA. NR 30 TC 13 Z9 15 U1 2 U2 3 PU CENTRAALBUREAU SCHIMMELCULTURE PI BAARN PA PO BOX 273, 3740 BAARN, NETHERLANDS SN 0166-0616 J9 STUD MYCOL JI Stud. Mycol. PD NOV PY 1995 IS 38 BP 67 EP 79 PG 13 WC Mycology SC Mycology GA TM393 UT WOS:A1995TM39300007 ER PT J AU Zhang, J Wenthold, RJ Yu, ZX Herman, EH Ferrans, VJ AF Zhang, J Wenthold, RJ Yu, ZX Herman, EH Ferrans, VJ TI Characterization of the pulmonary lesions induced in rats by human recombinant interleukin-2 SO TOXICOLOGIC PATHOLOGY LA English DT Article DE lymphokine-activated killer cells; cytotoxic T lymphocytes; interstitial dendritic cells; endothelial cells; pulmonary pathology; type II alveolar epithelial cells; apoptosis ID TUMOR-NECROSIS-FACTOR; VASCULAR LEAK SYNDROME; DENDRITIC CELLS; ENDOTHELIAL-CELLS; LUNG INJURY; MONOCLONAL-ANTIBODIES; ACCESSORY CELLS; LYMPHOCYTE-T; TNF-ALPHA; EDEMA AB Histologic, electron microscopic, and immunohistochemical studies were made to analyze the structural features and the cellular composition of the pulmonary lesions produced in rats by the administration of interleukin-2 (IL-2). This agent induced pulmonary edema; thickening of alveolar septa; damage to endothelial cells in capillaries and venules, marked interstitial infiltration by cytotoxic T lymphocytes, lymphokine-activated killer (LAK) cells, macrophages, and dendritic cells (as demonstrated by cell counting in preparations stained immunohistochemically with peroxidase- and fluorochrome-labeled antibodies); and injury to bronchiolar and alveolar epithelial cells. Granular and agranular lymphocytes often were closely apposed to endothelial cells in capillaries and venules. Contacts between lymphocytes and type II alveolar epithelial cells also were observed. Damaged type II alveolar epithelial cells showed nuclear and cytoplasmic features that are considered indicative of apoptosis (confirmed by nick end labeling). Phagocytosis of apoptotic bodies by macrophages was occasionally found. These results support the concept that IL-2 induces cytotoxic vascular and parenchymal cell damage that is mediated by LAK cells and cytotoxic T lymphocytes, which make contacts with endothelial cells and type II alveolar epithelial cells. This damage appears to be exacerbated by the secondary release of a variety of vasoactive agents and inflammatory mediators. C1 NHLBI,PATHOL SECT,BETHESDA,MD 20892. NR 47 TC 11 Z9 11 U1 0 U2 0 PU SOC TOXICOLOGIC PATHOLOGISTS PI LAWRENCE PA 1041 NEW HAMPSHIRE ST PO BOX 368, LAWRENCE, KS 66044 SN 0192-6233 J9 TOXICOL PATHOL JI Toxicol. Pathol. PD NOV-DEC PY 1995 VL 23 IS 6 BP 653 EP 666 PG 14 WC Pathology; Toxicology SC Pathology; Toxicology GA TP712 UT WOS:A1995TP71200003 PM 8772251 ER PT J AU Zuck, TF Thomson, RA Schreiber, GB Gilcher, RO Kleinman, SH Murphy, EL Ownby, HE Williams, AE Busch, MP Smith, JW Nass, CC Hollingsworth, CG Nemo, GJ AF Zuck, TF Thomson, RA Schreiber, GB Gilcher, RO Kleinman, SH Murphy, EL Ownby, HE Williams, AE Busch, MP Smith, JW Nass, CC Hollingsworth, CG Nemo, GJ TI The retrovirus epidemiology donor study (REDS): Rationale and methods SO TRANSFUSION LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; T-CELL LEUKEMIA; BLOOD-DONORS; LYMPHOMA VIRUS; HTLV-II; TRANSFUSION; TRANSMISSION; INFECTION; ANTIBODIES; RECIPIENTS C1 WESTAT CORP,ROCKVILLE,MD 20850. AMER RED CROSS,JEROME H HOLLAND LAB,ROCKVILLE,MD. OKLAHOMA BLOOD INST,SYLVAN N GOLDMAN CTR,OKLAHOMA CITY,OK. UNIV CALIF LOS ANGELES,DEPT PATHOL & LAB MED,LOS ANGELES,CA 90024. AMER RED CROSS,BLOOD SERV,SO CALIF REG,LOS ANGELES,CA 90006. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA. IRWIN MEM BLOOD CTR,RES & SCI SERV,SAN FRANCISCO,CA. AMER RED CROSS,BLOOD SERV,SE MICHIGAN REG,DETROIT,MI. AMER RED CROSS,BLOOD SERV,GREATER CHESAPEAKE & POTOMAC REG,BALTIMORE,MD. NHLBI,TRANSFUS MED BRANCH,BETHESDA,MD 20892. RP Zuck, TF (reprint author), UNIV CINCINNATI,MED CTR,HOXWORTH BLOOD CTR,3130 HIGHLAND AVE,POB 670055,CINCINNATI,OH 45267, USA. FU NHLBI NIH HHS [HB-89-01, HB-89-02] NR 39 TC 71 Z9 71 U1 0 U2 1 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD NOV-DEC PY 1995 VL 35 IS 11 BP 944 EP 951 DI 10.1046/j.1537-2995.1995.351196110900.x PG 8 WC Hematology SC Hematology GA TK995 UT WOS:A1995TK99500011 PM 8604493 ER PT J AU HENGEN, PN AF HENGEN, PN TI METHODS AND REAGENTS - QUANTITATIVE PCR - AN ACCURATE MEASURE OF MESSENGER-RNA SO TRENDS IN BIOCHEMICAL SCIENCES LA English DT Editorial Material RP HENGEN, PN (reprint author), NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702, USA. NR 6 TC 24 Z9 25 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0968-0004 J9 TRENDS BIOCHEM SCI JI Trends Biochem.Sci. PD NOV PY 1995 VL 20 IS 11 BP 476 EP 477 DI 10.1016/S0968-0004(00)89104-5 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TF674 UT WOS:A1995TF67400008 PM 8578592 ER PT J AU TAIRA, M EVRARD, JL STEINMETZ, A DAWID, IB AF TAIRA, M EVRARD, JL STEINMETZ, A DAWID, IB TI CLASSIFICATION OF LIM PROTEINS SO TRENDS IN GENETICS LA English DT Letter ID INSULIN GENE; HOMEODOMAIN; ELEGANS; DOMAIN C1 CNRS,INST BIOL MOLEC PLANTES,F-67084 STRASBOURG,FRANCE. RP TAIRA, M (reprint author), NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892, USA. NR 16 TC 68 Z9 68 U1 1 U2 2 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0168-9525 J9 TRENDS GENET JI Trends Genet. PD NOV PY 1995 VL 11 IS 11 BP 431 EP 432 DI 10.1016/S0168-9525(00)89139-8 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA TB638 UT WOS:A1995TB63800004 PM 8578598 ER PT J AU ROTH, GS JOSEPH, JA MASON, RP AF ROTH, GS JOSEPH, JA MASON, RP TI MEMBRANE-ALTERATIONS IN ALZHEIMERS-DISEASE AND AGING - REPLY SO TRENDS IN NEUROSCIENCES LA English DT Letter ID LIPID FLUIDITY; BRAIN; BINDING C1 TUFTS UNIV,USDA ARS,HUMAN NUTR RES CTR AGING,BOSTON,MA 02111. MED COLL PENN,NEUROSCI RES CTR,PITTSBURGH,PA 15212. HAHNEMANN UNIV,PITTSBURGH,PA 15212. RP ROTH, GS (reprint author), NIA,GERONTOL RES CTR,JOHNS HOPKINS BAYVIEW CTR,MOLEC PHYSIOL & GENET SECT,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 15 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD NOV PY 1995 VL 18 IS 11 BP 484 EP 484 DI 10.1016/0166-2236(95)90046-2 PG 1 WC Neurosciences SC Neurosciences & Neurology GA TC638 UT WOS:A1995TC63800008 ER PT J AU GAYDOS, C QUINN, T AF GAYDOS, C QUINN, T TI DNA AMPLIFICATION ASSAYS - A NEW STANDARD FOR DIAGNOSIS OF CHLAMYDIA-TRACHOMATIS INFECTIONS SO VENEREOLOGY-THE INTERDISCIPLINARY INTERNATIONAL JOURNAL OF SEXUAL HEALTH LA English DT Article; Proceedings Paper CT 1995 IUVDT World STD/AIDS Congress CY 1995 CL SINGAPORE, SINGAPORE ID POLYMERASE CHAIN-REACTION; MEMBRANE PROTEIN GENE; PELVIC INFLAMMATORY DISEASE; ENZYME-IMMUNOASSAY; NONGONOCOCCAL URETHRITIS; ENDOCERVICAL SPECIMENS; CLINICAL-EVALUATION; GENITAL-INFECTION; SEQUENCE; URINE AB Chlamydia trachomatis infection is one of the most common causes of sexually transmitted infections in the world. Due to their significant morbidity, their economic impact, and the fact that they are often asymptomatic, recommendations have been made that widespread screening of those individuals at most risk be performed. However, screening for C. trachomatis infections has been hampered in the past by the lack of sensitive, specific, and simple laboratory procedures. Until recently in vitro culture was considered to be the 'gold standard' for detection of chlamydia, but it was expensive, technically complex, and was known to be only 50-85% sensitive compared to nucleic acid amplification assays. With the introduction of new DNA amplification techniques, such as polymerase chain reaction (PCR) and ligase chain reaction (LCR) assays, there are now commercial tests that have sensitivities of 90-96% and specificities of 98-100%. These assays are especially attractive since they can be used with either cervical and urethral specimens, or urine which offers a non-invasive approach for large scale screening programs. Although the commercial assays utilise a chlamydial plasmid gene for amplification, the gene encoding the major outer membrane (omp1), has been used to generate PCR products for both nucleic acid sequencing and restriction fragment length polymorphism (RFLP), in order to better define the molecular epidemiology of C. trachomatis, Other DNA amplification assays, such as Q-beta replicase and transcription-mediated amplification (TMA), are also currently being developed for detection of C, trachomatis infections. PCR and LCR are both useful for detection of C. trachomatis in other types of clinical specimens, such as ocular specimens, tissue from cases of reactive arthritis, salpingitis, and tubal factor infertility. DNA amplification assays offer a valuable method to supplement chlamydia control programs by increasing the sensitivity and specificity of detection and treatment. C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. RP GAYDOS, C (reprint author), JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21205, USA. RI Gaydos, Charlotte/E-9937-2010 NR 88 TC 0 Z9 0 U1 0 U2 0 PU VENEREOLOGY PUBLISHING INC PI CARLTON PA MELBOURNE SEXUAL HEALTH CENTRE CARLTON 3053, AUSTRALIA SN 1032-1012 J9 VENEREOLOGY JI Venereol.-Interdiscip. Int. J. Sex. Health PD NOV PY 1995 VL 8 IS 4 BP 234 EP 239 PG 6 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA TJ515 UT WOS:A1995TJ51500009 ER PT J AU ALEXANDER, KA KAT, PW HOUSE, J HOUSE, C OBRIEN, SJ LAURENSON, MK MCNUTT, JW OSBURN, BI AF ALEXANDER, KA KAT, PW HOUSE, J HOUSE, C OBRIEN, SJ LAURENSON, MK MCNUTT, JW OSBURN, BI TI AFRICAN HORSE SICKNESS AND AFRICAN CARNIVORES SO VETERINARY MICROBIOLOGY LA English DT Article DE AFRICAN HORSE SICKNESS; CARNIVORES; DOMESTIC DOGS; AFRICAN WILD DOGS; LIONS; SPOTTED HYENAS ID HORSESICKNESS VIRUS; ANTIBODIES; SPAIN AB African horse sickness (AHS) is a disease that affects equids, and is principally transmitted by Culicoides spp, that are biological vectors of AHS viruses (AHSV). The repeated spread of AHSV from sub-Saharan Africa to the Middle East, northern Africa and the Iberian peninsula indicate that a better understanding of AHS epizootiology is needed. African horse sickness has long been known to infect and cause mortality among domestic dogs that ingest virus contaminated meat, but it is uncertain what role carnivores play in transmission of the virus. We present evidence of widespread natural AHS infection among a diversity of African carnivore species. We hypothesize that such infection resulted from ingestion of meat and organs from AHS-infected prey species. The effect of AHS on the carnivores is unknown, as is their role in the maintenance cycle of the disease. C1 USDA,APHIS,ANIM DIS DIAGNOST LAB,GREENPORT,NY 11944. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. GAME CONSERVANCY,UPLAND RES GRP,NEWTONMORE PH20 1BE,INVERNESS,SCOTLAND. UNIV CALIF DAVIS,DIV ENVIRONM STUDIES,DAVIS,CA 95616. RP ALEXANDER, KA (reprint author), UNIV CALIF DAVIS,SCH VET MED,DEPT VET PATHOL MICROBIOL & IMMUNOL,DAVIS,CA 95616, USA. NR 29 TC 14 Z9 18 U1 1 U2 11 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1135 J9 VET MICROBIOL JI Vet. Microbiol. PD NOV PY 1995 VL 47 IS 1-2 BP 133 EP 140 DI 10.1016/0378-1135(95)00059-J PG 8 WC Microbiology; Veterinary Sciences SC Microbiology; Veterinary Sciences GA TF680 UT WOS:A1995TF68000013 PM 8604545 ER PT J AU CHAMBERS, TC GERMANN, UA GOTTESMAN, MM PASTAN, I KUO, JF AMBUDKAR, SV AF CHAMBERS, TC GERMANN, UA GOTTESMAN, MM PASTAN, I KUO, JF AMBUDKAR, SV TI BACTERIAL EXPRESSION OF THE LINKER REGION OF HUMAN MDR1 P-GLYCOPROTEIN AND MUTATIONAL ANALYSIS OF PHOSPHORYLATION SITES SO BIOCHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; MULTIDRUG-RESISTANT CELLS; GLUTATHIONE S-TRANSFERASE; DRUG ACCUMULATION; TRANSPORT; GENE; IDENTIFICATION; INHIBITOR; SUBSTRATE; STAUROSPORINE AB Phosphorylation may play a role in modulating multidrug resistance by P-glycoprotein (P-gp). The linker region between the two homologous halves of human P-gp harbors several serine residues which are phosphorylated by protein kinase C (PKC) in vitro. We used the glutathione S-transferase gene fusion system to express and purify a series of fusion proteins containing the relevant portion (residues 644-689) of the linker region of the human MDR1 gene product. The fusion proteins were subjected to in vitro phosphorylation and phosphopeptide mapping analysis to identify specific phosphorylation sites. On the basis of a mutational strategy in which individual serine residues were systematically replaced with nonphosphorylatable alanine residues, Ser-661 and Ser-667 were identified as major PKC sites and Ser-683 was identified as a minor PKC site. Ser-661 and Ser-667 were also found to be the primary sites of phosphorylation for a novel membrane-associated P-gp specific kinase isolated from the muItidrug-resistant KB-V1 cell line. Individual phosphorylation sites were recognized independently of each other. These data show that the linker region of P-gp represents a target for multisite phosphorylation not only for PKC but also for the P-gp specific V1 kinase. Specific serine phosphorylation sites are identified, and evidence is presented that the V1 kinase has a specificity which overlaps, but is more restricted than, that of PKC. In addition, these studies also suggest that the use of GST fusion peptides may be applicable for the analysis of multisite and ordered protein phosphorylation in other systems. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,CELL BIOL LAB,BETHESDA,MD 20892. EMORY UNIV,DEPT PHARMACOL,ATLANTA,GA 30322. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV NEPHROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL,BALTIMORE,MD 21205. RP CHAMBERS, TC (reprint author), UNIV ARKANSAS MED SCI HOSP,DEPT BIOCHEM & MOLEC BIOL,LITTLE ROCK,AR 72205, USA. RI Ambudkar, Suresh/B-5964-2008 NR 39 TC 17 Z9 17 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 31 PY 1995 VL 34 IS 43 BP 14156 EP 14162 DI 10.1021/bi00043a021 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TD756 UT WOS:A1995TD75600021 PM 7578013 ER PT J AU OMATSUKANBE, M CUSHMAN, SW MANGANIELLO, VC TAIRA, M AF OMATSUKANBE, M CUSHMAN, SW MANGANIELLO, VC TAIRA, M TI INSULIN STIMULATES HORMONE-SENSITIVE CYCLIC GMP-INHIBITED CYCLIC-NUCLEOTIDE PHOSPHODIESTERASE IN RAT BROWN ADIPOSE-CELLS SO FEBS LETTERS LA English DT Article DE CGMP-INHIBITED CYCLIC NUCLEOTIDE PHOSPHODIESTERASE; INSULIN; ISOPROTERENOL; BROWN ADIPOSE CELL (RAT) ID CAMP PHOSPHODIESTERASE; UNCOUPLING PROTEIN; FAT-CELLS; AMP PHOSPHODIESTERASE; MOLECULAR-CLONING; GLUCOSE-TRANSPORT; COLD-ACCLIMATION; ADIPOCYTES; TISSUE; MOUSE AB The presence and regulation of a hormone-sensitive cyclic GMP-inhibited cyclic nucleotide phosphodiesterase (cGI PDE) in rat brown adipose cells was investigated, cDNA clones for two cGI PDE isoforms, cGIP1 and cGIP2, have been isolated, Using a rat cGIP1 (RcGIP1) cDNA probe, RcGIP1 mRNA (similar to 5,3 kb) was detected in Northern blots of both brown and white adipose RNA, cGI PDE was detected in both microsomal and plasma membrane fractions of brown and white adipose cells by Western blotting using anti-RcGIP1 peptide antibody, When cells were incubated with insulin before membrane preparation, cGI PDE activity in the microsomal fraction was increased by 2- to 2.5-fold within 10 min, Isoproterenol also stimulated the activity of cGI PDE in the microsomal fraction by 1,5-fold, In cells incubated with both insulin and isoproterenol, microsomal cGI PDE activity,vas similar to that in microsomal fractions isolated from cells incubated with insulin alone. These results suggest that the hormonal regulation of cGI PDE, presumably a cGIP1 isoform, in rat brown adipose cells is similar to that in white adipose cells. C1 NIDDKD,DIABET BRANCH,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD 20892. NHLBI,PULM CRIT CARE MED BRANCH,BIOCHEM PHYSIOL SECT,BETHESDA,MD 20892. NR 34 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD OCT 30 PY 1995 VL 374 IS 2 BP 187 EP 191 DI 10.1016/0014-5793(95)01112-R PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA TD124 UT WOS:A1995TD12400010 PM 7589531 ER PT J AU STEMMER, PM WANG, XT KRINKS, MH KLEE, CB AF STEMMER, PM WANG, XT KRINKS, MH KLEE, CB TI FACTORS RESPONSIBLE FOR THE CA2(+)-DEPENDENT INACTIVATION OF CALCINEURIN IN BRAIN SO FEBS LETTERS LA English DT Article DE CALMODULIN; CALCINEURIN; PROTEIN PHOSPHATASE; CA2(+) ID PROTEIN PHOSPHATASES; CELLULAR-REGULATION; SKELETAL-MUSCLE; CYCLOSPORINE-A; CALMODULIN; COMPLEXES; KINASE AB The Ca2+-dependent protein phosphatase activity of crude rat brain extracts measured in the presence of okadaic acid, exhibits the characteristic properties of the calmodulin-stimulated protein phosphatase, calcineurin. It is stimulated more than 200-fold by Ca2+ and inhibited by the calmodulin-binding peptide, M13, and by the immunosuppressive drug, PK506. It is insensitive to rapamycin at concentrations up to 1 mu M. Its specific activity, based on calcineurin concentration determined by quantitative analysis of Western blots exposed to anti-bovine brain IgG, is ten to twenty times that of purified rat brain calcineurin assayed under similar conditions, Unlike the purified enzyme it is rapidly and irreversibly inactivated in a time-, temperature-, and Ca2+/calmodulin-dependent fashion without evidence of extensive proteolytic degradation, The enzyme is converted to a state which does not lose activity by removal of low molecular weight material by gel filtration, Reconstitution of a labile enzyme is achieved by the addition of the low molecular weight-containing fraction eluted from the gel filtration column. These observations indicate that calcineurin in crude brain extracts is under the control of Ca2+/calmodulin-dependent positive and negative regulatory mechanisms which involve unidentified endogenous factor(s). C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 16 TC 31 Z9 31 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD OCT 30 PY 1995 VL 374 IS 2 BP 237 EP 240 DI 10.1016/0014-5793(95)01095-V PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA TD124 UT WOS:A1995TD12400022 PM 7589543 ER PT J AU ERICKSON, KL BEUTLER, JA CARDELLINA, JH BOYD, MR AF ERICKSON, KL BEUTLER, JA CARDELLINA, JH BOYD, MR TI ROTTNESTOL, A NEW HEMIKETAL FROM THE SPONGE HALICLONA SP SO TETRAHEDRON LA English DT Article ID MARINE SPONGE AB Rottnestol, a new hemiketal, was isolated from an Australian collection of the marine sponge Haliclona sp. Its structure was deduced as 3 from H-1, C-13, COSY, HMQC, HMBC and nOe NMR studies. Hemiketal 3 was readily converted to its epimer, 4, and the methyl ketal of 4. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21702. RI Beutler, John/B-1141-2009 OI Beutler, John/0000-0002-4646-1924 NR 13 TC 9 Z9 10 U1 0 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4020 J9 TETRAHEDRON JI Tetrahedron PD OCT 30 PY 1995 VL 51 IS 44 BP 11953 EP 11958 DI 10.1016/0040-4020(95)00761-V PG 6 WC Chemistry, Organic SC Chemistry GA TA952 UT WOS:A1995TA95200004 ER PT J AU LEVY, D AF LEVY, D TI HAVE EXPERT PANEL GUIDELINES KEPT PACE WITH NEW CONCEPTS IN HYPERTENSION SO LANCET LA English DT Editorial Material ID RISK RP LEVY, D (reprint author), NHLBI,BLDG 10,BETHESDA,MD 20892, USA. NR 16 TC 9 Z9 9 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 OCT 28 PY 1995 VL 346 IS 8983 BP 1112 EP 1113 DI 10.1016/S0140-6736(95)91792-6 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA TB549 UT WOS:A1995TB54900002 PM 7475595 ER PT J AU FOULKES, MA RIDA, WN HOFF, R AF FOULKES, MA RIDA, WN HOFF, R TI IMPACT OF IMPROVED TREATMENT OF SEXUALLY-TRANSMITTED DISEASE ON HIV-INFECTION SO LANCET LA English DT Letter RP FOULKES, MA (reprint author), NIAID,DIV AIDS,BETHESDA,MD 20892, USA. NR 2 TC 0 Z9 0 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 OCT 28 PY 1995 VL 346 IS 8983 BP 1158 EP 1158 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA TB549 UT WOS:A1995TB54900040 PM 7475616 ER PT J AU GHOSH, I RAGHAVAN, N FITZGERALD, PC SCOTT, AL AF GHOSH, I RAGHAVAN, N FITZGERALD, PC SCOTT, AL TI NUCLEOSIDE DIPHOSPHATE KINASE FROM THE PARASITIC NEMATODE BRUGIA-MALAYI SO GENE LA English DT Article DE FILARIAL PARASITE; SPLICED LEADER; CDNA LIBRARY; MOLECULAR MODELING ID SURFACE-ASSOCIATED ANTIGENS; MESSENGER-RNAS; EXPRESSION; PROTEINS; LARVAE; LEADER; GENE AB Using a reverse transcription-polymerase chain reaction (RT-PCR) procedure that exploited the presence of a conserved 22-nucleotide spliced leader (SL) sequence that is trans-spliced to the 5' end of nematode transcripts, a novel Brugia malayi (Bm) infective-stage SL cDNA expression library was constructed and characterized. The library was immunoscreened with rabbit anti-infective-stage antibodies (Ab) and an immunodominant clone, BmG4-7, was identified and characterized. BmG4-7 contained a full-length cDNA that had significant sequence similarity to nucleoside diphosphate kinase (NDK)-encoding sequences reported from a number of species, including Drosophila melanogaster and humans, BmNDK was found to be constitutively transcribed during all stages of parasite development. An anti-BmNDK Ab was used to immunostain a Western blot of extracts from adult and larval parasites. The Ab specifically recognized a 17.5-kDa molecule in all of the parasite extracts. Molecular modeling of the BmNDK showed several regions surrounding the conserved catalytic site that may be important in the design of drugs specific for the disruption of NTP synthesis in filarial parasites. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MOLEC MICROBIOL & IMMUNOL,BALTIMORE,MD 21205. NIH,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. FU NIAID NIH HHS [T32 AI007417, AI-29411, AI 02642] NR 23 TC 12 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD OCT 27 PY 1995 VL 164 IS 2 BP 261 EP 266 DI 10.1016/0378-1119(95)00500-6 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA TF481 UT WOS:A1995TF48100010 PM 7590340 ER PT J AU FURANO, AV USDIN, K AF FURANO, AV USDIN, K TI DNA FOSSILS AND PHYLOGENETIC ANALYSIS - USING L1 (LINE-1, LONG INTERSPERSED REPEATED) DNA TO DETERMINE THE EVOLUTIONARY HISTORY OF MAMMALS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID REVERSE-TRANSCRIPTASE; MUS-DOMESTICUS; MAURICEVILLE PLASMID; CDNA SYNTHESIS; SEQUENCE; ELEMENTS; FAMILY; MOUSE; IDENTIFICATION; MICE RP FURANO, AV (reprint author), NIDDK,BIOCHEM PHARMACOL LAB,GENOM STRUCT & FUNCT SECT,BETHESDA,MD 20893, USA. NR 66 TC 33 Z9 33 U1 1 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 27 PY 1995 VL 270 IS 43 BP 25301 EP 25304 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600001 PM 7592685 ER PT J AU KAPAS, S CATT, KJ CLARK, AJL AF KAPAS, S CATT, KJ CLARK, AJL TI CLONING AND EXPRESSION OF CDNA-ENCODING A RAT ADRENOMEDULLIN RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID HYPOTENSIVE PEPTIDE; MOLECULAR-CLONING; PROTEIN; GLOMERULOSA; FAMILY; LUNG AB Adrenomedullin is a potent vasodilator peptide that exerts major effects on cardiovascular function. Its actions are mediated through an abundant class of specific binding sites that activate adenylyl cyclase through a G protein-coupled mechanism. We report here the identification of a cDNA clone for the adrenomedullin receptor that was originally isolated as an orphan receptor from rat lung. The cDNA encodes a polypeptide of 395 residues that contains seven transmembrane domains and has a general structural resemblance to other members of the G protein-linked receptor superfamily. When expressed in COS-7 cells, this receptor mediates a cAMP response to adrenomedullin with an EC(50) of 7 x 10(-9) M, and binds I-125-adrenomedullin with a K-D of 8.2 x 10(-9) M, properties that are consistent with those observed in cardiovascular and other target tissues. The receptor gene is expressed as several mRNA species of which the most prominent is a 1.8-kilobase transcript found in the Lung, adrenal, heart, spleen, cerebellum, and other sites. Identification of this receptor cDNA should facilitate further investigation of the cellular actions of adrenomedullin and its regulatory effects in normal and disordered states of cardiovascular function. C1 ST BARTHOLOMEWS HOSP,COLL MED,DEPT CHEM ENDOCRINOL,LONDON EC1A 7BE,ENGLAND. NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. NR 30 TC 242 Z9 249 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 27 PY 1995 VL 270 IS 43 BP 25344 EP 25347 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600012 PM 7592696 ER PT J AU DUGI, KA DICHEK, HL SANTAMARINAFOJO, S AF DUGI, KA DICHEK, HL SANTAMARINAFOJO, S TI HUMAN HEPATIC AND LIPOPROTEIN-LIPASE - THE LOOP COVERING THE CATALYTIC SITE MEDIATES LIPASE SUBSTRATE-SPECIFICITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HIGH-DENSITY-LIPOPROTEIN; RELEASABLE LIVER LIPASE; TRIGLYCERIDE LIPASE; DIRECTED MUTAGENESIS; HUMAN-PLASMA; TRIACYLGLYCEROL LIPASE; INTERFACIAL ACTIVATION; PANCREATIC LIPASE; APOLIPOPROTEIN-E; CHIMERIC LIPASE AB Hepatic lipase (HL) and Lipoprotein Lipase (LPL) are key enzymes that mediate the hydrolysis of triglycerides (TG) and phospholipids (PL) present in circulating plasma lipoproteins. Relative to triacylglycerol hydrolysis, HL displays higher phospholipase activity than LPL. The structural basis for this difference in substrate specificity has not been definitively established. We recently demonstrated that the 22-amino acid loops (''lids'') covering the catalytic sites of LPL and HL are critical for the interaction with lipid substrate (Dugi, K. A. Dichek, H. L., Talley, G. D., Brewer, H. B., Jr., and Santamarina-Fojo, S. (1992) J. Biol. Chem. 267, 25086-25091). To determine whether the Lipase lid plays a role in conferring the different substrate specificities of HL and LPL, we have generated four chimeric lipases. Characterization of these chimeric enzymes using TG (triolein and tributyrin) or PL (dioleoylphosphatidylcholine (DOPC) vesicles, DOPC proteoliposomes, and DOPC-mixed liposomes) substrates demonstrated marked differences between their relative PL/TG hydrolyzing activities. Chimeric LPL containing the lid of HL had reduced triolein hydrolyzing activity (49% of the wild type), but increased phospholipase activity in DOPC vesicle, DOPC proteoliposome, and DOPC-mixed liposome assay systems (443, 628, and 327% of wild-type LPL, respectively). In contrast, chimeric BL containing the LPL lid was more active against triolein (123% of the wild type) and less active against DOPC (23, 0, and 30%, respectively) than normal HL. Similar results were obtained when the lipase lids were exchanged in chimeric enzymes containing the NH2-terminal end of LPL and the COOH-terminal domain of HL. Exchange of the LPL and HL Lids resulted in a reversal of the phospholipase/neutral Lipase ratio, establishing the important role of this region in mediating substrate specificity. In summary, the Lid covering the catalytic domains in LPL and HL plays a crucial role in determining Lipase substrate specificity. The lid of LPL confers preferential triglyceride hydrolysis, whereas the Lid of HL augments phospholipase activity. This study provides new insight into the structural basis for the observed in vivo differences in LPL and HL function. C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 67 TC 87 Z9 89 U1 0 U2 5 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 27 PY 1995 VL 270 IS 43 BP 25396 EP 25401 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600022 PM 7592706 ER PT J AU VONKOCH, CS LAHIRI, DK MAMMEN, AL COPELAND, NG GILBERT, DJ JENKINS, NA SISODIA, SS AF VONKOCH, CS LAHIRI, DK MAMMEN, AL COPELAND, NG GILBERT, DJ JENKINS, NA SISODIA, SS TI THE MOUSE APLP2 GENE - CHROMOSOMAL LOCALIZATION AND PROMOTER CHARACTERIZATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BETA-PROTEIN PRECURSOR; ALZHEIMERS-DISEASE; REGULATORY ELEMENTS; MAMMALIAN-CELLS; MESSENGER-RNA; REGION; EXPRESSION; CDNA; DNA; IDENTIFICATION AB Senile plaques are primarily comprised of deposits of the beta-amyloid protein derived from larger amyloid precursor proteins (APPs). APP is a member of a gene family, including amyloid precursor-like proteins APLP1 and APLP2. Using interspecific mouse backcross mapping, we localized the mouse APLP2 gene to the proximal region of mouse chromosome 9, syntenic with a region of human 11q. We cloned an similar to 1.2-kilobase mouse genomic fragment containing the APLP2 gene promoter. The APLP2 promoter lacks a typical TATA box, is CC-rich, and contains several sequences for transcription factor binding. S1 nuclease protection analysis revealed the presence of multiple transcription start sites. The lack of a TATA box, the presence of a high GC content, and multiple transcription start sites place the APLP2 promoter in the class of promoters of ''housekeeping genes.'' Regulatory regions within the promoter were assayed by transfection of mouse N2a and Ltk(-) cells with constructs containing progressive 5'-deletions of the APLP2 promoter fused to the bacterial chloramphenicol acetyl transferase (CAT) reporter gene. A minimal region that includes sequences 99 bp upstream of the predominant transcription start site of the APLP2 promoter was sufficient to direct high levels of CAT expression. C1 JOHNS HOPKINS UNIV,SCH MED,NEUROPATHOL LAB,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. INDIANA UNIV,SCH MED,DEPT PSYCHIAT,INDIANAPOLIS,IN 46202. INDIANA UNIV,SCH MED,DEPT MED & MOLEC GENET,INDIANAPOLIS,IN 46202. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-46000]; NIA NIH HHS [AG 05146] NR 40 TC 17 Z9 19 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 27 PY 1995 VL 270 IS 43 BP 25475 EP 25480 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600032 PM 7592716 ER PT J AU WANG, YX SANTINI, F QIN, KF HUANG, CY AF WANG, YX SANTINI, F QIN, KF HUANG, CY TI MG2+-DEPENDENT, CA2+-INHIBITABLE SERINE/THREONINE PROTEIN PHOSPHATASE FROM BOVINE BRAINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PYRUVATE-DEHYDROGENASE PHOSPHATASE; GLYCOGEN-SYNTHASE PHOSPHATASE; RABBIT SKELETAL-MUSCLE; RAT-LIVER; PHOSPHOPROTEIN PHOSPHATASE; MOLECULAR-CLONING; OKADAIC ACID; PURIFICATION; KINASE; IDENTIFICATION AB The Mg2+-dependent serine/threonine protein phosphatases, also known as type 2C phosphatases (PP2C), belong to a gene family distinct from the other serine/ threonine phosphatases and tyrosine phosphatases. Here we report the purification to apparent homogeneity of a novel Mg2+-dependent, Ca2+-inhibitable serine/ threonine protein phosphatase from bovine brain. It is a type 2C enzyme in view of its Mg2+ requirement, resistance to okadaic acid and calyculin A, inability to use phosphorylase a as substrate, and a segment of amino acid sequence typical of all PP2C type phosphatases known to date. However, it differs from the other PP2C enzymes, particularly the mammalian PP2C alpha and -beta isoforms, in that its molecular weight, 76,000, is considerably larger and that it is inhibited by Ca2+, NaF, and polycations, but not by orthovanadate. The Ca2+ inhibition may not be related to its cellular regulation because of K-i values in the 20-90 mu M range, but this property permits distinction of this enzyme from the other phosphatases. Although the precise physiological role of this phosphatase is not yet known, its ability to dephosphorylate a wide variety of phosphoproteins and its broad distribution, as shown by a survey of mouse tissues for its activity, suggest that it may serve an important cellular function. C1 NHLBI, BIOCHEM LAB, BETHESDA, MD 20892 USA. NR 38 TC 33 Z9 33 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 27 PY 1995 VL 270 IS 43 BP 25607 EP 25612 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600051 PM 7592734 ER PT J AU VAMBUTAS, V KAPLAN, DR SELLS, MA CHERNOFF, J AF VAMBUTAS, V KAPLAN, DR SELLS, MA CHERNOFF, J TI NERVE GROWTH-FACTOR STIMULATES TYROSINE PHOSPHORYLATION AND ACTIVATION OF SRC HOMOLOGY-CONTAINING PROTEIN-TYROSINE-PHOSPHATASE-1 IN PC12 CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SH2-CONTAINING PHOSPHOTYROSINE PHOSPHATASE; PHEOCHROMOCYTOMA CELLS; RECEPTOR-BETA; MOTH-EATEN; KINASE; DIFFERENTIATION; IDENTIFICATION; ASSOCIATION; CORKSCREW; MUTATIONS AB Rat PC12 cells respond to extracellular peptide growth factors in at least two distinct ways, When treated with nerve growth factor (NGF) PC12 cells exit the cell cycle and differentiate to a neuronal phenotype, whereas when treated with epidermal growth factor, they proliferate, We examined the potential role of Src homology 2 (SH2)-containing protein tyrosine phosphatases (PTPs) in the differentiation process, PC12 cells express substantial amounts of both SH-PTP1 and 2. SH-PTP1, but not SH-PTP2, becomes tyrosine phosphorylated following NGF, but not epidermal growth factor treatment, The enzymatic activity of SH-PTP1 toward an exogenous substrate following NGF treatment is increased 2-fold. We found that SH-PTP1 binds to the NGF receptor TrkA in vitro and that anti-TrkA immunoprecipitates have PTP activity. These results show that SH-PTP1 is differentially phosphorylated and activated by NGF in PC12 cells and suggest that this activation may play a role in NGF-induced differentiation. C1 FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOLEC MECHANISMS CARCINOGENESIS LAB,FREDERICK,MD 21702. RI Chernoff, Jonathan/I-7631-2014 OI Chernoff, Jonathan/0000-0002-4803-7836 FU NCI NIH HHS [R01 CA58836] NR 40 TC 54 Z9 54 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 27 PY 1995 VL 270 IS 43 BP 25629 EP 25633 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600054 PM 7592737 ER PT J AU BECERRA, SP SAGASTI, A SPINELLA, P NOTARIO, V AF BECERRA, SP SAGASTI, A SPINELLA, P NOTARIO, V TI PIGMENT EPITHELIUM-DERIVED FACTOR BEHAVES LIKE A NONINHIBITORY SERPIN - NEUROTROPHIC ACTIVITY DOES NOT REQUIRE THE SERPIN REACTIVE LOOP SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HIV-1 REVERSE-TRANSCRIPTASE; CONFORMATIONAL CHANGE; ALPHA-1-PROTEINASE INHIBITOR; OVALBUMIN; BINDING; ALPHA-1-ANTITRYPSIN; ANGIOTENSINOGEN; ANTITHROMBIN; FAMILY; IDENTIFICATION AB Pigment epithelium-derived factor (PEDF), a neurite-promoting factor, has an amino acid primary structure that is related to members of the serine protease inhibitor (serpin) family. Controlled proteolysis of native PEDF (50 kDa) with either trypsin, chymotrypsin, elastase, or subtilisin yields in each case one major limited product of 46 kDa as analyzed by SDS-polyacrylamide gel electrophoresis. N-terminal sequence analysis of the isolated 46-kDa products indicates a favored cleavage region located toward the C-terminal end of PEDF. A proteolyzed PEDF protein reaction mixture reveals two overlapping sequences: that of the N terminus of intact PEDF and that of an internal region, consistent with cleavage of PEDF about position 382. These data indicate that PEDF protein has a globular conformation with one protease-sensitive exposed loop that contains the homologous serpin-reactive site. Cleavage within the reactive-site loop of PEDF does not cause a conformational change in the molecules (the stressed (S) --> relaxed (R) transition) and results in heat denaturation identical to its native counterpart. This lack of conformational change is also seen upon cleavage within the reactive-site loop of the noninhibitory serpin ovalbumin. Furthermore, the PEDF neurite-promoting function is not lost with cleavage of the exposed loop, Recombinant PEDF polypeptide fragments with larger truncations from the C-terminal end show neurotrophic activity. Our results clearly indicate that integrity of the PEDF homologous serpin reactive center is dispensable for neurotrophic activity. Thus, the PEDF induction of neurites must be mediated by a mechanism other than serine protease inhibition. Altogether our data indicate that PEDF belongs to the subgroup of noninhibitory serpins and that its N-terminal region confers a neurite-promoting activity to the protein. The neurotrophic active site of PEDF is separated from the serpin reactive-site loop, not only in the primary structure, but also in the folded protein structure. C1 NIH,OFF INTRAMURAL RES,PROT EXPRESS LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,DEPT RADIAT MED,WASHINGTON,DC 20007. RP BECERRA, SP (reprint author), NEI,RETINAL CELL & MOLEC BIOL LAB,6 CTR DR,MSC 2740,BLDG 6,RM 308,BETHESDA,MD 20892, USA. NR 32 TC 164 Z9 173 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 27 PY 1995 VL 270 IS 43 BP 25992 EP 25999 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600107 PM 7592790 ER PT J AU ZHOU, YN CHATTERJEE, S ROY, S ADHYA, S AF ZHOU, YN CHATTERJEE, S ROY, S ADHYA, S TI THE NONINDUCIBLE NATURE OF SUPER-REPRESSORS OF THE GAL OPERON IN ESCHERICHIA-COLI SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE GAL REPRESSOR; TRANSCRIPTION; SUGAR BINDING ID RNA-POLYMERASE; GALACTOSE OPERON; LAC; TRANSCRIPTION; CHROMATOGRAPHY; PURIFICATION; OPERATOR; PROMOTER; COMPLEX; PROTEIN AB We isolated and characterized mutant repressors (GalR) of the gal operon in Escherichia coli. These repressors (super-repressors), called GalR(s), have a non-inducible phenotype. Repression of the gal operon by super-repressors cannot be lifted by inducer. The mutant galR genes, galR(s), have been cloned and the mutational changes determined. Two of them, galR(uv7)(s) and galR(78)(s), were located in the proposed sugar binding domains of the repressor. The repressor from wild-type (galR(+)), as well as from mutant galR(uv7)(s), was purified and characterized biochemically. The results showed that, like wild-type GalR(+), GalR(uv7)(s) binds to DNA normally and represses transcription from the P1 promoter and stimulates that from the P2 promoter of the gal operon. Nevertheless, compared to GalR(+), GalR(uv7)(s) is much less sensitive to the presence of the inducer, D-galactose. The affinity of D-galactose to GalR(uv7)(s) is 10 to 30-fold lower, as measured by the effect of the inducer on GalR tryptophan fluorescence; GalR complexes with DNA and on GalR repression of transcription. Our results suggest that the super-repressor phenotype of GalR(uv7)(s) is because of a defect in D-galactose binding rather than a defect in the ligand-induced allosteric change or increased affinity for the operator. (C) 1995 Academic Press Limited C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. BOSE INST,DEPT BIOPHYS,CALCUTTA 700054,W BENGAL,INDIA. NR 41 TC 10 Z9 10 U1 0 U2 0 PU ACADEMIC PRESS (LONDON) LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD OCT 27 PY 1995 VL 253 IS 3 BP 414 EP 425 DI 10.1006/jmbi.1995.0563 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB794 UT WOS:A1995TB79400004 PM 7473724 ER PT J AU ROY, SK KORZEKWA, KR GONZALEZ, FJ MOSCHEL, RC DOLAN, ME AF ROY, SK KORZEKWA, KR GONZALEZ, FJ MOSCHEL, RC DOLAN, ME TI HUMAN LIVER OXIDATIVE-METABOLISM OF O-6-BENZYLGUANINE SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE O-6-BENZYLGUANINE; O-6-BENZYL-8-OXOGUANINE; CYTOCHROME P450; ALKYLTRANSFERASE; DRUG METABOLISM; ALDEHYDE OXIDASE ID TUMOR XENOGRAFTS; 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA BCNU; ALKYLATING-AGENTS; CIGARETTE-SMOKING; O6-BENZYLGUANINE; CYTOCHROME-P450; SENSITIVITY; IDENTIFICATION; FURAFYLLINE; OXIDASE AB The oxidation of O-6-benzylguanine, an inactivator of O-6-alkylguanine-DNA alkyltransferase, was examined using human liver cytosol, microsomes, and several P450 isoforms. Incubation of O-6-benzylguanine with human liver cytosol resulted in the formation of O-6-benzyl-8-oxoguanine, which was inhibited by menadione, a potent inhibitor of aldehyde oxidase. Inhibition by allopurinol, a xanthine oxidase inhibitor, was less dramatic. Oxidation of O-6-benzylguanine also occurred with pooled human liver microsomes and was inhibited by both furafylline and troleandomycin, selective inhibitors of CYP1A2 and CYP3A4, respectively. Human P450s CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2E1, and CYP3A4 expressed in Hep G2 hepatoma cells using vaccinia virus vectors were incubated with 10 or 200 mu M O-6-benzylguanine. At 10 mu M, O-6-benzylguanine was oxidized primarily by CYP1A2 and to a lesser extent by CYP3A4. However, an appreciable increase in CYP3A4 contribution was noted at 200 mu M. CYP1A2 exhibited a more than 200-fold higher relative catalytic activity (V-max/K-m) compared with CYP3A4. Therefore, at therapeutically relevant concentrations of O-6-benzylguanine, CYP1A2 could be primarily involved in its oxidation since it shows a much lower K-m value (1.3 mu M) than CYP3A4 (52.2 mu M) and cytosol (81.5 mu M). However, one would expect interindividual variation in the extent of oxidation of O-6-benzylguanine depending on the levels of aldehyde oxidase, CYP1A2, and CYP3A4. C1 UNIV CHICAGO,HEMATOL ONCOL SECT,CHICAGO,IL 60637. NIH,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [CA57725, N01-CO-46000] NR 25 TC 29 Z9 29 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD OCT 26 PY 1995 VL 50 IS 9 BP 1385 EP 1389 DI 10.1016/0006-2952(95)02019-5 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TG549 UT WOS:A1995TG54900010 PM 7503788 ER PT J AU GERMOLEC, DR ADAMS, NH LUSTER, MI AF GERMOLEC, DR ADAMS, NH LUSTER, MI TI COMPARATIVE-ASSESSMENT OF METABOLIC ENZYME LEVELS IN MACROPHAGE POPULATIONS OF THE F344 RAT SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE CYTOCHROME P450 1A1; MACROPHAGES; TCDD; ALDEHYDE DEHYDROGENASE; AH RECEPTOR; DRUG-METABOLIZING ENZYMES ID ALDEHYDE DEHYDROGENASE; DRUG-METABOLISM; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN TCDD; CYTOCHROME-P-450 CONTENT; PERITONEAL-MACROPHAGES; AH LOCUS; ACTIVATION; INVITRO; EXPRESSION; LIVER AB The immune system is a direct target for toxic insult by a number of drugs and other chemicals, many of which require activation to toxic metabolites by drug-metabolizing enzymes. We compared the induction of drug-metabolizing enzymes, including cytochrome P450 1A1 (CYP1A1) and aldehyde dehydrogenase (ALDH), which are differentially expressed in various macrophage populations following treatment of F344 rats with the inducer 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Kupffer cells, alveolar macrophages and splenic macrophages from TCDD-treated animals expressed elevated levels of inducible CYP1A1 as compared to other macrophage subpopulations or cells from control rats. TCDD treatment also resulted in increased ethoxyresorufin-O-deethylase (EROD) activity and total cytochrome P450 content in tissue-derived macrophages. Immuno-reactive protein and mRNA transcripts for CYP1A1 were not detectable in resident peritoneal macrophages or peripheral blood monocytes. Examination of aromatic hydrocarbon receptor (AhR) levels in macrophage populations suggests that the ability of TCDD to induce metabolic enzymes in specific cell types correlates well with AhR expression. In vivo activation of macrophages, using either Bacillus of Calmette and Guerin, Mycobacterium tuberculosis (BCG) or polyinosinicipolycytidylic acid (Poly I:C), caused no significant alteration in the levels of induction of CYP1A1. ALDH-3 induction was similar in all macrophage populations examined. These studies indicate that macrophages, particularly those from portals of entry, may be induced to produce increased levels of specific enzymes, and the induction is dependent upon their maturational stage rather than their activation state. The metabolism of xenobiotics to toxic intermediates by immune cells and its role in immunosuppression are discussed. C1 N CAROLINA STATE UNIV,DEPT TOXICOL,RALEIGH,NC 27695. RP GERMOLEC, DR (reprint author), NIEHS,ENVIRONM IMMUNOL & NEUROBIOL SECT,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 57 TC 24 Z9 24 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD OCT 26 PY 1995 VL 50 IS 9 BP 1495 EP 1504 DI 10.1016/0006-2952(95)02062-4 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TG549 UT WOS:A1995TG54900023 PM 7503801 ER PT J AU GROGAN, J SHOU, MG ANDRUSIAK, EA TAMURA, S BUTERS, JTM GONZALEZ, FJ KORZEKWA, KR AF GROGAN, J SHOU, MG ANDRUSIAK, EA TAMURA, S BUTERS, JTM GONZALEZ, FJ KORZEKWA, KR TI CYTOCHROME-P450 2A1, 2E1, AND 2C9 CDNA-EXPRESSION BY INSECT CELLS AND PARTIAL-PURIFICATION USING HYDROPHOBIC CHROMATOGRAPHY SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE CYTOCHROME P450; CDNA EXPRESSION; PROTEIN PURIFICATION; BACULOVIRUS; HYDROPHOBIC CHROMATOGRAPHY; INSECT CELLS ID BACULOVIRUS-MEDIATED EXPRESSION; TESTOSTERONE; SYSTEM; PROTEINS; ENZYMES; OXIDASE; YEAST; LINE AB High-level expression of three cloned cytochrome P450 enzymes was accomplished using the baculovirus-insect cell expression system. The amount of enzyme expression was enhanced by cell infections in the presence of medium-supplements containing hemin and by growth in suspension cultures. Human cytochromes P450 2E1 and 2C9 and rat cytochrome P450 2A1 were partially purified from cell extracts using hydrophobic interaction and hydroxyapatite chromatography. The resulting enzymes were of estimated molecular masses similar to those reported previously and analyzed by PAGE. Reconstitution of enzyme activity resulted when the enzymes were incubated together with NADPH-cytochrome P450 reductase, phospholipid, NADPH, and appropriate substrates. The cytochrome P450 activity of the partially purified enzymes was comparable to that of the corresponding enzymes expressed in the vaccinia virus-Hep G2 system. These results provide evidence for a general means of obtaining cytochrome P450 enzymes for mechanistic, immunochemical, and biophysical investigations. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RI Buters, Jeroen/G-5070-2011 NR 29 TC 20 Z9 22 U1 0 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD OCT 26 PY 1995 VL 50 IS 9 BP 1509 EP 1515 DI 10.1016/0006-2952(95)02065-9 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TG549 UT WOS:A1995TG54900025 PM 7503803 ER PT J AU BEI, R SCHLOM, J KASHMIRI, SVS AF BEI, R SCHLOM, J KASHMIRI, SVS TI BACULOVIRUS EXPRESSION OF A FUNCTIONAL SINGLE-CHAIN IMMUNOGLOBULIN AND ITS IL-2 FUSION PROTEIN SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE BACULOVIRUS RECOMBINANT; SINGLE-CHAIN ANTIBODY; GLYCOSYLATION; TUMOR-ASSOCIATED GLYCOPROTEIN-72; MUCIN ID MONOCLONAL-ANTIBODY B72.3; GENERATION; ANTIGEN; CELLS; GENE; INTERLEUKIN-2; BINDING; VECTORS AB The baculovirus expression system has been used for the production of a variety of proteins, including antibodies. Two single-gene constructs encoding single-chain immunoglobulins have recently been developed. The antibody employed was monoclonal antibody (MAb) CC49 which reacts with the pancarcinoma antigen, tumor associated glycoprotein, TAG-72. One, single-chain construct designated SCA Delta C(L)C(H)1 (SCIg), consists of the CC49 sFv covalently joined to the human Fc (gamma 1) through the hinge region. The other, SCA Delta C(L)C(H)1-IL-2 (SCIg-IL-2), has a human IL-2 molecule attached to the carboxyl end of the SCIg. These constructs have been used to test the feasibility of producing biologically active antibodies using the baculovirus expression system. Both constructs have been succesfully expressed in insect cells and purified. The baculovirus recombinant single-chain antibodies have been designated, bV-SCA Delta C(L)C(H)1 (bV-SCIg) and bV-SCA Delta C(L)C(H)1-IL-2 (bV-SCIg-IL-2) they have been shown to be secreted in the culture supernatant as dimeric molecules of approximately 115 kDa and 140 kDa, respectively. The specificity and antibody dependent cellular cytolytic activity of the baculovirus recombinant single-chain antibodies were shown to be similar to that of the myeloma derived molecules. Glycosylation analysis showed that baculovirus derived proteins were N-glycosylated, but carried few if any high mannose residues. The biological activity of the IL-2 moiety was retained in bV-SCIg-IL-2, as evidenced by its stimulatory effect on the proliferation of the IL-2 dependent cell line HT-2. The observation that a significantly shorter time is required to develop baculovirus recombinant molecules as compared to myeloma derived molecules and that insect cells express single chain MAbs at acceptable levels may have implications for the production of these molecules for clinical use. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NR 36 TC 27 Z9 29 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD OCT 26 PY 1995 VL 186 IS 2 BP 245 EP 255 DI 10.1016/0022-1759(95)00149-5 PG 11 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA TB771 UT WOS:A1995TB77100010 PM 7594624 ER PT J AU SCHRAGER, LK FAUCI, AS AF SCHRAGER, LK FAUCI, AS TI HUMAN-IMMUNODEFICIENCY-VIRUS - TRAPPED BUT STILL DANGEROUS SO NATURE LA English DT Editorial Material ID INFECTION; TISSUE; HIV RP SCHRAGER, LK (reprint author), NIAID,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 11 TC 14 Z9 14 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 26 PY 1995 VL 377 IS 6551 BP 680 EP 681 DI 10.1038/377680a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB469 UT WOS:A1995TB46900029 PM 7477256 ER PT J AU DEWEERD, P GATTASS, R DESIMONE, R UNGERLEIDER, LG AF DEWEERD, P GATTASS, R DESIMONE, R UNGERLEIDER, LG TI RESPONSES OF CELLS IN MONKEY VISUAL-CORTEX DURING PERCEPTUAL FILLING-IN OF AN ARTIFICIAL SCOTOMA SO NATURE LA English DT Article ID RECEPTIVE-FIELDS; MACAQUE MONKEY; STRIATE CORTEX; CONNECTIONS AB WHEN we view a scene through one eye, we typically do not see the scotomas created by the optic disc and the blood vessels overlying the retinal surface. Similarly, when a texture field containing a hole is steadily viewed in peripheral vision (artificial scotoma), the hole appears to fill in with the surrounding texture in a matter of seconds, demonstrating that the visual system fills in information across regions where no information is available(1-5). Here we show that, in monkeys viewing a similar texture field with a hole, the responses of extrastriate visual neurons with receptive fields covering the hole increase gradually to a level comparable to that elicited by the same texture without a hole. The time course of these dynamic changes in activity parallels the time course of perceived filling-in of the hole by human observers, suggesting that this process mediates perceptual filling-in. C1 NIMH,PSYCHOL & PSYCHOPATHOL LAB,BETHESDA,MD 20892. NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. UNIV FED RIO DE JANEIRO,BIOPHYS INST CARLOS CHAGAS,DEPT NEUROBIOL,BR-21941 RIO JANEIRO,BRAZIL. NR 22 TC 141 Z9 141 U1 1 U2 6 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 26 PY 1995 VL 377 IS 6551 BP 731 EP 734 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB469 UT WOS:A1995TB46900056 PM 7477262 ER PT J AU POMBO, CM KEHRL, JH SANCHEZ, I KATZ, P AVRUCH, J ZON, LI WOODGETT, JR FORCE, T KYRIAKIS, JM AF POMBO, CM KEHRL, JH SANCHEZ, I KATZ, P AVRUCH, J ZON, LI WOODGETT, JR FORCE, T KYRIAKIS, JM TI ACTIVATION OF THE SAPK PATHWAY BY THE HUMAN STE20 HOMOLOG GERMINAL CENTER KINASE SO NATURE LA English DT Article AB EUKARYOTIC cells respond to different extracellular stimuli by recruiting homologous signalling pathways that use members of the MEKK, MEK and ERK families of protein kinases. The MEKK-->MEK-->ERK core pathways of Saccharomyces cerevisiae may themselves be regulated by members of the STE20 family of protein kinases(1,2). Here we report specific activation of the mammalian stress-activated protein kinase (SAPK) pathway by germinal centre kinase (GCK; ref. 3), a human STE20 homologue(3,4). SAPKs, members of the ERK family, are activated in situ by inflammatory stimuli, including tumour-necrosis factor (TNF) and interleukin-1, and phosphorylate and probably stimulate the transactivation function of c-Jun(5-7). Although GCK is found in many tissues, its expression in lymphoid follicles is restricted to the cells of the germinal centre, where it may participate in B-cell differentiation(3). Activation of the SAPK pathway by GCK illustrates further the striking, conservation of eukaryotic signalling mechanisms and defines the first physiological function of a mammalian Ste20. C1 MASSACHUSETTS GEN HOSP E,DIABET RES LAB,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP E,CARDIOL UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02129. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,DEPT MED,WASHINGTON,DC 20007. CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. PRINCESS MARGARET HOSP,ONTARIO CANC INST,TORONTO,ON M4X 1K9,CANADA. RI Woodgett, Jim/F-1087-2010 OI Woodgett, Jim/0000-0003-3731-5797 NR 23 TC 198 Z9 200 U1 0 U2 5 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 26 PY 1995 VL 377 IS 6551 BP 750 EP 754 DI 10.1038/377750a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB469 UT WOS:A1995TB46900062 PM 7477268 ER PT J AU MCKENZIE, R FRIED, MW SALLIE, R CONJEEVARAM, H DIBISCEGLIE, AM PARK, Y SAVARESE, B KLEINER, D TSOKOS, M LUCIANO, C PRUETT, T STOTKA, JL STRAUS, SE HOOFNAGLE, JH AF MCKENZIE, R FRIED, MW SALLIE, R CONJEEVARAM, H DIBISCEGLIE, AM PARK, Y SAVARESE, B KLEINER, D TSOKOS, M LUCIANO, C PRUETT, T STOTKA, JL STRAUS, SE HOOFNAGLE, JH TI HEPATIC-FAILURE AND LACTIC-ACIDOSIS DUE TO FIALURIDINE (FIAU), AN INVESTIGATIONAL NUCLEOSIDE ANALOG FOR CHRONIC HEPATITIS-B SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PLACEBO-CONTROLLED TRIAL; MITOCHONDRIAL-DNA; ULTRASTRUCTURAL-CHANGES; ADENINE-ARABINOSIDE; ALPHA-INTERFERON; VIRUS-INFECTION; E-ANTIGEN; THERAPY; MYOPATHY AB Background. We describe severe and unexpected multisystem toxicity that occurred during a study of the antiviral nucleoside analogue fialuridine (1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl)-5-iodouracil, or FIAU) as therapy for chronic hepatitis B virus infection. Methods. Fifteen patients with chronic hepatitis B were randomly assigned to receive fialuridine at a dose of either 0.10 or 0.25 mg per kilogram of body weight per day for 24 weeks and were monitored every 1 to 2 weeks by means of a physical examination, blood tests, and testing for hepatitis B virus markers. Results. During the 13th week lactic acidosis and liver failure suddenly developed in one patient. The study was terminated on an emergency basis, and all treatment with fialuridine was discontinued. Seven patients were found to have severe hepatotoxicity, with progressive lactic acidosis, worsening jaundice, and deteriorating hepatic synthetic function despite the discontinuation of fialuridine. Three other patients had mild hepatotoxicity. Several patients also had pancreatitis, neuropathy, or myopathy. Of the seven patients with severe hepatotoxicity, five died and two survived after liver transplantation. Histologic analysis of liver tissue revealed marked accumulation of microvesicular and macrovesicular fat, with minimal necrosis of hepatocytes or architectural changes. Electron microscopy showed abnormal mitochondria and the accumulation of fat in hepatocytes. Conclusions. In patients with chronic hepatitis B, treatment with fialuridine induced a severe toxic reaction characterized by hepatic failure, lactic acidosis, pancreatitis, neuropathy, and myopathy This toxic reaction was probably caused by widespread mitochondrial damage and may occur infrequently with other nucleoside analogues. C1 NIDDKD,DIGEST DIS BRANCH,LIVER DIS SECT,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD. NCI,CTR CLIN,DEPT NURSING,BETHESDA,MD. NCI,DEPT PATHOL,BETHESDA,MD. NINCDS,ELECTROMYOG SECT,BETHESDA,MD 20892. UNIV VIRGINIA,MED CTR,DEPT SURG,CHARLOTTESVILLE,VA. LILLY RES LABS,INDIANAPOLIS,IN. NR 43 TC 356 Z9 362 U1 1 U2 10 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 26 PY 1995 VL 333 IS 17 BP 1099 EP 1105 DI 10.1056/NEJM199510263331702 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA TA372 UT WOS:A1995TA37200002 PM 7565947 ER PT J AU BHAUMIK, SR CHARY, KVR GOVIL, G LIU, KL MILES, HT AF BHAUMIK, SR CHARY, KVR GOVIL, G LIU, KL MILES, HT TI NMR CHARACTERIZATION OF A TRIPLE-STRANDED COMPLEX FORMED BY HOMO-PURINE AND HOMO-PYRIMIDINE DNA STRANDS AT 1/1 MOLAR RATIO AND ACIDIC PH SO NUCLEIC ACIDS RESEARCH LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; HELIX; MACROMOLECULES AB Homo-purine (d-TGAGGAAAGAAGGT) and homopyrimidine (d-CICCTTTCTTCC) oligomers have been designed such that they are complementary in parallel orientation. When mixed in a 1:1 molar ratio, the system adopts an antiparallel duplex at neutral pH with three mismatched base pairs, On lowering the pH below 5.5, a new complex is formed, The NMR results show the coexistence of a intermolecular pyrimidine.purine:pyrimidine DNA tripler and a single stranded oligopurine at this PH. The tripler is stabilized by five T.A:T, four C+.G:C and two mismatched triads, namely, C+.G-T and T.A-C. This tripler is further stabilized by a Hoogsteen C+.G base-pair on one end, Temperature dependence of the imino proton resonances reveals that the triplex dissociates directly into single strands around 55 degrees C, without duplex intermediates. parallel duplexes are not formed under any of the conditions employed in this study. C1 NIDDKD,BETHESDA,MD 20892. RP BHAUMIK, SR (reprint author), TATA INST FUNDAMENTAL RES,CHEM PHYS GRP,HOMI BHABHA RD,BOMBAY 400005,MAHARASHTRA,INDIA. NR 32 TC 20 Z9 22 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD OCT 25 PY 1995 VL 23 IS 20 BP 4116 EP 4121 DI 10.1093/nar/23.20.4116 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TD372 UT WOS:A1995TD37200017 PM 7479074 ER PT J AU SCHUTTE, M DACOSTA, LT MOSKALUK, CA ROZENBLUM, E GUAN, XP DEJONG, PJ BITTNER, M MELTZER, PS TRENT, JM KERN, SE AF SCHUTTE, M DACOSTA, LT MOSKALUK, CA ROZENBLUM, E GUAN, XP DEJONG, PJ BITTNER, M MELTZER, PS TRENT, JM KERN, SE TI ISOLATION OF YAC INSERT SEQUENCES BY REPRESENTATIONAL DIFFERENCE ANALYSIS SO NUCLEIC ACIDS RESEARCH LA English DT Article ID CLONING; GENE; DNA; DELETION; IDENTIFICATION; HYBRIDIZATION; PATIENT; GENOME; PCR AB We present a method for the isolation of YAC insert sequences by representational difference analysis (RDA). To achieve maximal representation of the sequences, the amplicons were generated from a Mbol digestion product. RDA was performed using a 970 kb insert YAC clone. After two rounds of re-association and selective amplification 92% of the difference product represented sequences derived from the YAC insert. Twenty insert-specific sequence-tagged sites were readily defined. The difference product was also successfully used to isolate microsatellite markers, to identify clones from a human PAC library and as a chromosome painting probe in fluorescence in situ hybridization. C1 JOHNS HOPKINS MED INST,DEPT PATHOL,BALTIMORE,MD 21205. JOHNS HOPKINS MED INST,DEPT ONCOL,BALTIMORE,MD 21205. ROSWELL PK CANC INST,DEPT HUMAN GENET,BUFFALO,NY 14263. NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,BETHESDA,MD 20892. FU CSR NIH HHS [1R01 RG01165-01]; NCI NIH HHS [CA62924, CA-16056] NR 22 TC 7 Z9 7 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD OCT 25 PY 1995 VL 23 IS 20 BP 4127 EP 4133 DI 10.1093/nar/23.20.4127 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TD372 UT WOS:A1995TD37200019 PM 7479076 ER PT J AU PATTERTON, HG SIMPSON, RT AF PATTERTON, HG SIMPSON, RT TI MODIFIED CURVED DNA THAT COULD ALLOW LOCAL DNA UNDERWINDING AT THE NUCLEOSOMAL PSEUDODYAD FAILS TO POSITION A NUCLEOSOME IN-VIVO SO NUCLEIC ACIDS RESEARCH LA English DT Article ID YEAST MINICHROMOSOMES; HISTONE OCTAMER; CORE HISTONES; CHROMATIN; SEQUENCE; TRANSCRIPTION; FRAGMENTS; PROMOTER; RECONSTITUTION; SUFFICIENT AB In competitive in vitro reconstitution experiments synthetic DNA composed of tandem repeats of the repetitive sequence (A/T)(3)NN(G/C)(3)NN, specifically the 20 bp 'TG sequence' (5'-TCGGTGTTAGAGCCTGTAAC-3'), was reported to associate with the histone octamer with an affinity higher than that of nucleosomally derived DNA. However,at least two groups have independently shown that tandem repeats of the TG sequence do not accommodate a stably positioned nucleosome in vivo. It was suggested that the anisotropic flexibility of the TG sequence, governed by a 10 bp sequence periodicity, is incompatible with the required underwinding of the DMA helix at the nucleosome pseudodyad while maintaining a bending preference that can be accommodated in the remainder of the nucleosome. Here we test this hypothesis directly by studying the in vivo nucleosomal structure of modified TG sequences designed to accommodate underwinding at the pseudodyad. We show that these modifications are not sufficient to allow stable incorporation of the TG sequence repeat into a nucleosome in vivo, but do note invasion from one end of the TG heptamer of a translationally random but rotationally constrained nucleosome. We discuss possible reasons for the absence of nucleosomes from the TG sequence in vivo. C1 NIDDK,LCDB,BETHESDA,MD 20892. OI Patterton, Hugh-George/0000-0003-2550-0493 NR 52 TC 9 Z9 9 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD OCT 25 PY 1995 VL 23 IS 20 BP 4170 EP 4179 DI 10.1093/nar/23.20.4170 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TD372 UT WOS:A1995TD37200024 PM 7479081 ER PT J AU USDIN, K WOODFORD, KJ AF USDIN, K WOODFORD, KJ TI CGG REPEATS ASSOCIATED WITH DNA INSTABILITY AND CHROMOSOME FRAGILITY FORM STRUCTURES THAT BLOCK DNA-SYNTHESIS IN-VITRO SO NUCLEIC ACIDS RESEARCH LA English DT Article ID SITE AB A large increase in the length of a CGG tandem array is associated with a number of triplet expansion diseases, including fragile X syndrome, the most common cause of heritable mental retardation in humans. Expansion results in the appearance of a fragile site on the X chromosome in the region of the CGG array. We show here that CGG repeats readily form a series of barriers to DNA synthesis in vitro, These barriers form only when the (CGG)(n) strand is used as the template, are K+-dependent, template concentration-independent, and involve hydrogen bonding between guanines. Chemical modification experiments suggest these blocks to DMA synthesis result from the formation of a series of intrastrand tetraplexes, A number of lines of evidence suggest that both triplet expansion and chromosome fragility are the result of replication defects. Our data are discussed in the light of such evidence, RP USDIN, K (reprint author), NIDDK,GENOM STRUCT & FUNCT SECT,BETHESDA,MD 20892, USA. NR 25 TC 174 Z9 176 U1 0 U2 4 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD OCT 25 PY 1995 VL 23 IS 20 BP 4202 EP 4209 DI 10.1093/nar/23.20.4202 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TD372 UT WOS:A1995TD37200028 PM 7479085 ER PT J AU GRACE, MB BAMBECK, GS BUZARD, GS WEINTRAUB, BD AF GRACE, MB BAMBECK, GS BUZARD, GS WEINTRAUB, BD TI TRANSVERSE TEMPERATURE-GRADIENT SINGLE-STRAND CONFORMATION POLYMORPHISM ANALYSIS FOR TEMPERATURE OPTIMIZATION OF COLD-SSCP MUTATION DETECTION SO NUCLEIC ACIDS RESEARCH LA English DT Article ID POINT MUTATIONS C1 GEORGE WASHINGTON UNIV,DEPT GENET,WASHINGTON,DC 20052. ZAXIS INC,HUDSON,OH. NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21701. RP GRACE, MB (reprint author), NIDDK,MCEB,BLDG 10,ROOM 8D14,10 CTR DR,MSC 1758,BETHESDA,MD 20892, USA. NR 9 TC 1 Z9 1 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD OCT 25 PY 1995 VL 23 IS 20 BP 4224 EP 4226 DI 10.1093/nar/23.20.4224-a PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TD372 UT WOS:A1995TD37200032 PM 7479089 ER PT J AU HARTMANN, T GRACE, MB BUZARD, GS RUOSS, SJ AF HARTMANN, T GRACE, MB BUZARD, GS RUOSS, SJ TI THROMBIN RECEPTOR POLYMORPHISM IN CHINESE-HAMSTER SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PROTEOLYTIC MECHANISM; MOLECULAR-CLONING; ACTIVATION; PEPTIDES AB We report the existence of a new Chinese hamster thrombin receptor allele, characterized by an in-frame insertion of three nucleotides at position 250 of the published sequence. As a consequence, an additional proline is inserted into a proline-rich region of the extracellular aminoterminal domain of the receptor. A corresponding proline at this position is also found in the rat thrombin receptor. A silent base-pair change is found in the cytoplasmic tail of the receptor gene. Single-strand conformation polymorphism and sequence analysis indicate this new receptor allele is present in several cell lines derived from different individual Chinese hamsters. Embryonic CHEF IIC9 cells and primary culture cells are homozygous for this new allele. In contrast, the CCL39 lung fibroblast cell Line is heterozygous for both the new and old alleles. Both alleles are transcribed into mRNA and code for functional receptors. Given the allelic distribution and sequence alignment with thrombin receptors from other species, we propose that the new sequence represents the actual predominant allele in Chinese hamster. (C) 1995 Academic Press, Inc. C1 STANFORD UNIV,SCH MED,DEPT MED,STANFORD,CA 94305. NIDDKD,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NR 15 TC 0 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 24 PY 1995 VL 215 IS 3 BP 974 EP 980 DI 10.1006/bbrc.1995.2559 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TA982 UT WOS:A1995TA98200027 PM 7488069 ER PT J AU ORLOW, SJ HEARING, VJ SAKAI, C URABE, K ZHOU, BK SILVERS, WK MINTZ, B AF ORLOW, SJ HEARING, VJ SAKAI, C URABE, K ZHOU, BK SILVERS, WK MINTZ, B TI CHANGES IN EXPRESSION OF PUTATIVE ANTIGENS ENCODED BY PIGMENT GENES IN MOUSE MELANOMAS AT DIFFERENT STAGES OF MALIGNANT PROGRESSION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ALBINO LOCUS; BROWN LOCUS; SLATY LOCUS; SILVER LOCUS ID TYROSINASE-RELATED PROTEIN-1; TRANSGENIC MICE; MELANIN BIOSYNTHESIS; SKIN MELANOMA; MELANOCYTES; DOPACHROME; SEQUENCE; LOCUS; TRP-2; CDNA AB Cutaneous melanomas of Tyr-SV40E transgenic mice (mice whose transgene consists of the tyrosinase promotor fused to the coding regions of simian virus 40 early genes) strikingly resemble human melanomas in their development and progression. Unlike human melanomas, the mouse tumors all arise in genetically identical individuals, thereby better enabling expression of specific genes to be characterized in relation to advancing malignancy. The products of pigment genes are of particular interest because peptides derived from these proteins have been reported to function as autoantigens with immunotherapeutic potential in some melanoma patients. However, the diminished pigmentation characteristic of many advanced melanomas raises the possibility that some of the relevant products may no longer be expressed in the most malignant cells. We have therefore investigated the contributions of several pigment genes in melanotic vs, relatively amelanotic components of primary and metastatic mouse melanomas. The analyses reveal marked differences within and among tumors in levels of mRNAs and proteins encoded by the wild-type alleles at the albino, brown, slaty, and silver loci. Tyrosinase (the protein encoded by the albino locus) was most often either absent or undetectable as melanization declined. The protein encoded by the slaty locus (tyrosinase-related protein 2) was the only one of those tested that was clearly present in all the tumor samples. These results suggest that sole reliance on targeting tyrosinase-based antigens might selectively favor survival of more malignant cells, whereas targeting the ensemble of the antigens tested might contribute toward a more inclusive and effective antimelanoma strategy. C1 FOX CHASE CANC CTR,INST CANC RES,PHILADELPHIA,PA 19111. NYU,SCH MED,RONALD O PERELMAN DEPT DERMATOL,NEW YORK,NY 10016. NYU,SCH MED,DEPT CELL BIOL,NEW YORK,NY 10016. NCI,CELL BIOL LAB,BETHESDA,MD 20892. FOX CHASE CANC CTR,INST CANC RES,PHILADELPHIA,PA 19111. FU NCI NIH HHS [CA-06927, CA-42560]; NCRR NIH HHS [RR-05539] NR 41 TC 35 Z9 36 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 24 PY 1995 VL 92 IS 22 BP 10152 EP 10156 DI 10.1073/pnas.92.22.10152 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB467 UT WOS:A1995TB46700045 PM 7479744 ER PT J AU COLLIN, C DEVANE, WA DAHL, D LEE, CJ AXELROD, J ALKON, DL AF COLLIN, C DEVANE, WA DAHL, D LEE, CJ AXELROD, J ALKON, DL TI LONG-TERM SYNAPTIC TRANSFORMATION OF HIPPOCAMPAL CA1 GAMMA-AMINOBUTYRIC-ACID SYNAPSES AND THE EFFECT OF ANANDAMIDE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE LONG-TERM POTENTIATION; CL- CHANNELS; CANNABINOID RECEPTORS ID RAT HIPPOCAMPUS; PYRAMIDAL CELLS; RESPONSES; RECEPTOR; CHANNELS; NEURONS AB Evidence is presented for a distinctive type of hippocampal synaptic modification [previously described for a molluscan gamma-aminobutyric acid (GABA) synapse after paired pre- and postsynaptic excitation]: transformation of GABA-mediated synaptic inhibition into synaptic excitation. This transformation persists with no further paired stimulation for 60 min or longer and is termed long-term transformation. Long-term transformation is shown to contribute to pairing-induced long-term potentiation but not to long-term potentiation induced by presynaptic stimulation alone. Further support for such mechanistic divergence is provided by pharmacologic effects on long-term transformation as well as these two forms of long-term potentiation by Cl- channel blockers, glutamate and GABA antagonists, as well as the endogenous cannabinoid ligand anandamide. C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. UNIV TEXAS,SCH HUMAN DEV,SYNAPT PLAST LAB,RICHARDSON,TX 75083. RP COLLIN, C (reprint author), NINCDS,ADAPT SYST LAB,BETHESDA,MD 20892, USA. NR 27 TC 38 Z9 38 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 24 PY 1995 VL 92 IS 22 BP 10167 EP 10171 DI 10.1073/pnas.92.22.10167 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB467 UT WOS:A1995TB46700048 PM 7479747 ER PT J AU TSAI, S WEAR, DJ SHIH, JWK LO, SC AF TSAI, S WEAR, DJ SHIH, JWK LO, SC TI MYCOPLASMAS AND ONCOGENESIS - PERSISTENT INFECTION AND MULTISTAGE MALIGNANT TRANSFORMATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE PROKARYOTES; PARASITISM; AIDS ID TUMOR SUPPRESSOR GENES; CELLS; FERMENTANS; PENETRANS; CANCER AB Oncogenic potential of human mycoplasmas was studied using cultured mouse embryo cells, C3H/10T1/2 (C3H). Mycoplasma fermentans and Mycoplasma penetrans, mycoplasmas found in unusually high frequencies among patients with AIDS, were examined. Instead of acute transformation, a multistage process in promotion and progression of malignant cell transformation with long latency was noted; after 6 passages (1 wk per passage) of persistent infection with M. fermentans, C3H cells exhibited phenotypic changes with malignant characteristics that became progressively more prominent with further prolonged infection, Up to at least the 11th passage, all malignant changes were reversible if mycoplasmas were eradicated by antibiotic treatment, Further persistent infection with the mycoplasmas until 18 passages resulted in an irreversible form of transformation that included the ability to form tumors in animals and high soft agar cloning efficiency, Whereas chromosomal loss and translocational changes in C3H cells infected by either mycoplasma during the reversible stage were not prominent, the onset of the irreversible phase of transformation coincided with such karyotypic alteration, Genetic instability-i.e., prominent chromosomal alteration of permanently transformed cells-was most likely caused by mutation of a gene(s) responsible for fidelity of DNA replication or repair, Once induced, chromosomal alterations continued to accumulate both in cultured cells and in animals without the continued presence of the transforming microbes, Mycoplasma-mediated multistage oncogenesis exhibited here shares many characteristics found in the development of human cancer. C1 ARMED FORCES INST PATHOL,DEPT INFECT & PARASIT DIS PATHOL,AMER REGISTRY PATHOL,WASHINGTON,DC 20306. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892. FU NIAID NIH HHS [R01 AI-31830] NR 33 TC 95 Z9 117 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 24 PY 1995 VL 92 IS 22 BP 10197 EP 10201 DI 10.1073/pnas.92.22.10197 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB467 UT WOS:A1995TB46700054 PM 7479753 ER PT J AU VASCONCELOS, O SIVAKUMAR, K DALAKAS, MC QUEZADO, M NAGLE, J LEONMONZON, M DUBNICK, M GAJDUSEK, DC GOLDFARB, LG AF VASCONCELOS, O SIVAKUMAR, K DALAKAS, MC QUEZADO, M NAGLE, J LEONMONZON, M DUBNICK, M GAJDUSEK, DC GOLDFARB, LG TI NONSENSE MUTATION IN THE PHOSPHOFRUCTOKINASE MUSCLE SUBUNIT GENE ASSOCIATED WITH RETENTION OF INTRON-10 IN ONE OF THE ISOLATED TRANSCRIPTS IN ASHKENAZI-JEWISH PATIENTS WITH TARUI DISEASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GLYCOGENOSIS TYPE VII; PHOSPHOFRUCTOKINASE DEFICIENCY; HUMAN PFKM GENE ID SOMATIC-CELL HYBRIDS; REGIONAL ASSIGNMENT; POINT MUTATION; MESSENGER-RNA; DEFICIENCY; ANTIBODY; ISOZYMES; DEFECT; SITE AB Mutations in the human phosphofructokinase muscle subunit gene (PFKM) are known to cause myopathy classified as glycogenosis type VII (Tarui disease). Previously described molecular defects include base substitutions altering encoded amino acids or resulting in abnormal splicing. We report a mutation resulting in phosphofructokinase deficiency in three patients from an Ashkenazi Jewish family, Using a reverse transcription PCR assay, PFKM subunit transcripts differing by length were detected in skeletal muscle tissue of all three affected subjects, In the longer transcript, an insertion of 252 nucleotides totally homologous to the structure of the 10th intron of the PFKM gene,vas found separating exon 10 from exon 11, In addition, two single base transitions were identified by direct sequencing: [exon 6; codon 95; (C) under bar GA (Arg) to (T) under bar GA (stop)] and [exon 7; codon 172; AC (C) under bar (Thr) to AC (T) under bar (Thr)] in either transcript, Single-stranded conformational polymorphism and restriction enzyme analyses confirmed the presence of these point substitutions in genomic DNA and strongly suggested homozygosity for the pathogenic allele. The nonsense mutation at codon 95 appeared solely responsible for the phenotype in these patients, further expanding genetic heterogeneity of Tarui disease. Transcripts with and without intron 10 arising from identical mutant alleles probably resulted from differential pre-mRNA processing and may represent a novel message from the PFKM gene. C1 NINCDS,MED NEUROL BRANCH,NEUROL DIS SECT,BETHESDA,MD 20892. NINCDS,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. RP VASCONCELOS, O (reprint author), NINCDS,CLIN NEUROGENET UNIT,BLDG 36,RM 4D04,BETHESDA,MD 20892, USA. NR 32 TC 13 Z9 13 U1 2 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 24 PY 1995 VL 92 IS 22 BP 10322 EP 10326 DI 10.1073/pnas.92.22.10322 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB467 UT WOS:A1995TB46700079 PM 7479776 ER PT J AU BRINKMANN, U BRINKMANN, E GALLO, M PASTAN, I AF BRINKMANN, U BRINKMANN, E GALLO, M PASTAN, I TI CLONING AND CHARACTERIZATION OF A CELLULAR APOPTOSIS SUSCEPTIBILITY GENE, THE HUMAN HOMOLOG TO THE YEAST CHROMOSOME SEGREGATION GENE CSE1 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE IMMUNOTOXIN; PSEUDOMONAS EXOTOXIN; TUMOR NECROSIS FACTOR; ONCOGENE ID ELONGATION FACTOR-II; DIPHTHERIA-TOXIN; DNA FRAGMENTATION; ADP-RIBOSYLATION; CYTOLYSIS; PROTEIN; CELLS; LYSIS AB We recently isolated human cDNA fragments that render MCF-7 breast cancer cells resistant to cell death caused by Pseudomonas exotoxin, Pseudomonas exotoxin-derived immunotoxins, diphtheria toxin, and tumor necrosis factor. We report here that one of these fragments is an antisense fragment of a gene homologous to the essential yeast chromosome segregation gene CSE1. Cloning and analysis of the full-length cDNA of the human CSE1 homologue, which we name CAS for cellular apoptosis susceptibility gene, reveals a protein coding region with similar length (971 amino acids for CAS, 960 amino acids for CSE1) and 59% overall protein homology to the yeast CSE1 protein. The conservation of this gene indicates it has an important function in human cells consistent with the essential role of CSE1 in yeast. CAS is highly expressed in human tumor cell fines and in human testis and fetal liver, tissues that contain actively dividing cells. Furthermore, CAS expression increases when resting human fibroblasts are induced to proliferate and decreases when they are growth-arrested. Thus, CAS appears to play an important role in both toxin and tumor necrosis factor-mediated cell death, as well as in cell proliferation. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 16 TC 149 Z9 154 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 24 PY 1995 VL 92 IS 22 BP 10427 EP 10431 DI 10.1073/pnas.92.22.10427 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB467 UT WOS:A1995TB46700101 PM 7479798 ER PT J AU BERNARD, M DONOHUE, SJ KLEIN, DC AF BERNARD, M DONOHUE, SJ KLEIN, DC TI HUMAN HYDROXYINDOLE-O-METHYLTRANSFERASE IN PINEAL-GLAND, RETINA AND Y79 RETINOBLASTOMA CELLS SO BRAIN RESEARCH LA English DT Article DE HYDROXYINDOLE-O-METHYLTRANSFERASE; MELATONIN; PINEAL; RETINA; Y79 RETINOBLASTOMA; TISSUE-SPECIFIC ID NUCLEOTIDE-SEQUENCE; MOLECULAR-CLONING; RAT PINEAL; MELATONIN PRODUCTION; N-ACETYLTRANSFERASE; PROTEIN; LOCALIZATION; PURIFICATION; METABOLISM; DOPAMINE AB Hydroxyindole-O-methyltransferase (HIOMT, EC 2.1.1.4) was studied in extracts of human pineal gland, retina and Y79 retinoblastoma cells. HIOMT enzyme activity and immunoreactive protein (similar to 42 kDa) were undetectable in the human retina; very low levels of HIOMT mRNA were detected using a highly sensitive RT-PCR/Southern blot method, as has been reported. Analysis of extracts of Y79 cells indicated that HIOMT enzyme activity, immunoreactivity(similar to 42 kDa) and mRNA(similar to 1.3 kb) were detectable at similar to 1/5-1/40 the levels found in the pineal gland. This unambiguously establishes that the HIOMT gene is expressed in Y79 cells. Kinetic analysis of Y79- and pineal-derived HIOMT indicates that the enzyme is generally similar in both tissues; one difference, however, is that substrate inhibition by N-acetylserotonin is greater with the Y79-derived enzyme. These studies show that Y79 cells represent a valid model to study the regulation of human HIOMT protein and mRNA; the differences detected may reflect the existence of tissue-specific regulatory mechanisms or differential patterns of expression of HIOMT isoforms. C1 NICHHD,DEV NEUROBIOL LAB,NEUROENDOCRINOL SECT,BETHESDA,MD 20892. NR 36 TC 49 Z9 53 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD OCT 23 PY 1995 VL 696 IS 1-2 BP 37 EP 48 DI 10.1016/0006-8993(95)00651-6 PG 12 WC Neurosciences SC Neurosciences & Neurology GA TB490 UT WOS:A1995TB49000006 PM 8574683 ER PT J AU GALKINA, SI SUDINA, GF DERGACHEVA, GB MARGOLIS, LB AF GALKINA, SI SUDINA, GF DERGACHEVA, GB MARGOLIS, LB TI REGULATION OF INTRACELLULAR PH BY CELL-CELL ADHESIVE INTERACTIONS SO FEBS LETTERS LA English DT Article DE INTRACELLULAR PH; CELL-CELL INTERACTION; PHOSPHOLIPASE A2; PROTEIN KINASE C; H+-ATPASE; NA+/H+ ANTIPORTER; H+-CONDUCTANCE ID PROTEIN-KINASE-C; MOUSE MACROPHAGES; HUMAN-NEUTROPHILS; PLASMA-MEMBRANE; PROTON PUMPS; H+; EXCHANGE; NEURONS AB As was shown in our previous work, the intracellular pH (pH(i)) of cultured human fibroblasts depends on cell density, The pH(i) is low in single cells, higher in cells, forming small groups and maximal in a sparse monolayer, On the other hand, the pH(i) is low in areas of confluent monolayers. In the present work, we show that the effects of inhibitors of various pH-controlling mechanisms as well as inhibitors of key enzymes in signal transduction pathways depend on the local cell density, We have found that N-ethylhnaleimide and 7-chloro-4-nitrobenz-2-oxa-1,3-diazole, known as inhibitors of V-type H+ ATPase, inhibit the elevation of pH(i) induced by cell-cell contact interactions; meanwhile Cd2+ ions, which inhibit H+ conductive pathway, cause an increase of pH(i) in a confluent monolayer, Our data revealed also that the Na+/H+ antiporter does not play an essential role in the pH(i) regulation by intercellular contacts. Inhibitors of phospholipase A(2) (4-bromophenacyl-bromide), phospholipase C (neomycin) and protein kinase C (H-7) dramatically change the way the pH(i) is modulated by local cell density, It is suggested that cell-cell interactions regulate cell activities via modulation of pH(i), which is under positive control from phospholipase A2 and under negative control from protein kinase C. C1 NICHHD, THEORET & PHYS BIOL LAB, BETHESDA, MD 20892 USA. RP GALKINA, SI (reprint author), MOSCOW MV LOMONOSOV STATE UNIV, AN BELOZERSKY INST PHYSICOCHEM BIOL, MOSCOW 119899, RUSSIA. RI Galkina, Svetlana/E-4025-2012; Sud'ina, Galina/E-1053-2012 OI Sud'ina, Galina/0000-0001-7711-3167 NR 20 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 EI 1873-3468 J9 FEBS LETT JI FEBS Lett. PD OCT 23 PY 1995 VL 374 IS 1 BP 17 EP 20 DI 10.1016/0014-5793(95)00969-G PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA TB831 UT WOS:A1995TB83100004 PM 7589503 ER PT J AU DONCARLOS, LL MALIK, K MORRELL, JI AF DONCARLOS, LL MALIK, K MORRELL, JI TI REGION-SPECIFIC EFFECTS OF OVARIAN HORMONES ON ESTROGEN-RECEPTOR IMMUNOREACTIVITY SO NEUROREPORT LA English DT Article DE ESTROGEN RECEPTOR; IMMUNOCYTOCHEMISTRY; GUINEA PIG; OVARIAN HORMONES; HYPOTHALAMUS; PREOPTIC AREA ID MESSENGER-RIBONUCLEIC-ACID; RAT-BRAIN; STEROID-HORMONES; PREOPTIC AREA; GUINEA-PIGS; CELLS; HYPOTHALAMUS; ESTRADIOL; RNA; FOREBRAIN AB THE cell groups in which nuclear estrogen receptor (ER) expressing neurons are found have unique, often coordinated, functions. Regulation of ER content may be one mechanism through which feedback responses can be adjusted to match the function of a specific brain region and physiological circumstance. In these immunocytochemical experiments, estrogen decreased staining intensity for ER in the ventrolateral hypothalamus and bed nucleus of the stria terminalis, but not in the periventricular preoptic area. ER staining intensity was further decreased by progesterone, following estrogen, but not in all brain regions. These results suggest that ER is regulated by estrogen in a region-specific manner. Furthermore, inhibition of responses to estrogen by progesterone may involve progesterone-induced downregulation of ERs. C1 RUTGERS STATE UNIV,CTR MOLEC & BEHAV NEUROSCI,NEWARK,NJ 07102. NIMH,BETHESDA,MD 20892. RP DONCARLOS, LL (reprint author), LOYOLA UNIV,STRITCH SCH MED,DEPT CELL BIOL NEUROBIOL & ANAT,MAYWOOD,IL 60153, USA. FU NICHD NIH HHS [HD22983]; NIMH NIH HHS [MH48794] NR 23 TC 21 Z9 21 U1 1 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD OCT 23 PY 1995 VL 6 IS 15 BP 2054 EP 2058 DI 10.1097/00001756-199510010-00024 PG 5 WC Neurosciences SC Neurosciences & Neurology GA TD510 UT WOS:A1995TD51000023 PM 8580439 ER PT J AU MOGENSEN, CE KEANE, WF BENNETT, PH JERUMS, G PARVING, HH PASSA, P STEFFES, MW STRIKER, GE VIBERTI, GC AF MOGENSEN, CE KEANE, WF BENNETT, PH JERUMS, G PARVING, HH PASSA, P STEFFES, MW STRIKER, GE VIBERTI, GC TI PREVENTION OF DIABETIC RENAL-DISEASE WITH SPECIAL REFERENCE TO MICROALBUMINURIA SO LANCET LA English DT Review ID URINARY ALBUMIN EXCRETION; CONVERTING ENZYME-INHIBITION; GLOMERULAR-FILTRATION RATE; NEPHROPATHY; PREDICTOR; HYPERTENSION; INTERVENTION; PROTEINURIA; CREATININE; MORTALITY C1 HENNEPIN CTY MED CTR,MINNEAPOLIS,MN. NIDDK,PHOENIX,AZ. NIDDK,BETHESDA,MD. AUSTIN HOSP,HEIDELBERG,VIC 3084,AUSTRALIA. STENO DIABET CTR,GENTOFTE,DENMARK. HOP ST LOUIS,PARIS,FRANCE. UNIV MINNESOTA,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. GUYS HOSP,LONDON SE1 9RT,ENGLAND. RP MOGENSEN, CE (reprint author), AARHUS KOMMUNE HOSP,DK-8000 AARHUS,DENMARK. NR 49 TC 412 Z9 432 U1 0 U2 4 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0099-5355 J9 LANCET JI Lancet PD OCT 21 PY 1995 VL 346 IS 8982 BP 1080 EP 1084 DI 10.1016/S0140-6736(95)91747-0 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA TA697 UT WOS:A1995TA69700016 PM 7564792 ER PT J AU LIU, KJ SHI, XL JIANG, JJ GODA, F DALAL, N SWARTZ, HM AF LIU, KJ SHI, XL JIANG, JJ GODA, F DALAL, N SWARTZ, HM TI CHROMATE-INDUCED CHROMIUM(V) FORMATION IN LIVE MICE AND ITS CONTROL BY CELLULAR ANTIOXIDANTS - AN L-BAND ELECTRON-PARAMAGNETIC-RESONANCE STUDY SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID CARCINOGEN CHROMATE; PRINCIPAL REDUCTANT; GLUTATHIONE; METABOLITES; MECHANISM; ASCORBATE; CR(V); HPLC; ESR AB A recent note from our laboratory reported that L-band (1.2 GHz) electron paramagnetic resonance spectroscopy can be utilized in detecting the formation of Cr(V) intermediates from chromate-treated whole mice. Since Cr(V) is thought to be one of the key species in the mechanism of chromate's toxicity, we carried out additional measurements with improved sensitivity. The new spectra show partially resolved hyperfine structure from protons that suggests that the Cr(V) ion is ligated to NAD(P)H moieties via oxygens. Using laboratory-synthesized Cr(V) (K3CrO8) as a standard, the yield of Cr(V) formation was estimated to be 153 +/- 12 nmol after intravenous injection of 100 mu l of 100 mM sodium dichromate into mice. Pretreatment of the mice with ascorbic acid and glutathione significantly reduced the Cr(V) formation yield in a dose-related manner, while pretreatment with NADH had the opposite effect. Injection of ascorbic acid also had the effect of enhancing the rate of Cr(V) disappearance in vivo. By comparing these results with in vitro results utilizing L-band as well as X-band (9.6 GHz) measurements, we conclude that L-band spectroscopy can indeed be effectively utilized for following the metabolism of Cr(V) in live mice and that Cr(V) formation can be controlled by utilizing cellular antioxidants in vivo. (C) 1995 Academic Press, Inc C1 DARTMOUTH COLL SCH MED,DEPT RADIOL,HANOVER,NH 03755. NCI,EXPTL PATHOL LAB,BETHESDA,MD 20892. W VIRGINIA UNIV,DEPT CHEM,MORGANTOWN,WV 26506. RI Shi, Xianglin/B-8588-2012 FU NCRR NIH HHS [RR-01811] NR 28 TC 29 Z9 29 U1 2 U2 2 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 OCT 20 PY 1995 VL 323 IS 1 BP 33 EP 39 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TA747 UT WOS:A1995TA74700006 PM 7487070 ER PT J AU ISHWAD, CS FERRELL, RE ROSSIE, KM APPEL, BN JOHNSON, JT MYERS, EN LAW, JC SRIVASTAVA, S GOLLIN, SM AF ISHWAD, CS FERRELL, RE ROSSIE, KM APPEL, BN JOHNSON, JT MYERS, EN LAW, JC SRIVASTAVA, S GOLLIN, SM TI MICROSATELLITE INSTABILITY IN ORAL-CANCER SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID COLORECTAL-CANCER; MUTATIONS; HISTORY; HOMOLOG; COLON AB Generalized genomic instability, detected as somatic changes in allele sizes at microsatellite loci in tumors compared to peripheral lymphocyte DNA, is a recently recognized mechanism of mutation in cancer. Such instability results from the somatic loss of DNA mismatch repair capability. Germ-line mutations at DNA mismatch repair loci confer susceptibility to colon cancer in hereditary non-polyposis colorectal cancer. Somatic loss of DNA mismatch repair has been reported in a large variety of other tumor types. Our goal was to determine the frequency of microsatellite instability in a large series of oral tumors. Out of 91 tumors analyzed for microsatellite instability, 6 (7%) showed microsatellite instability. Instability was observed at multiple loci with a range of 50-74% of loci affected. Alterations include both increase (74%) and decrease (26%) in allele sizes. The proportion of alleles affected ranged from 30-58% of all alleles. Our data suggest that somatic genomic instability plays a role in the pathogenesis of a small subset of oral tumors. (C) 1995 Wiley-Liss, Inc. C1 UNIV PITTSBURGH,GRAD SCH PUBL HLTH,DEPT HUMAN GENET,PITTSBURGH,PA 15261. UNIV PITTSBURGH,DEPT DIAGNOST DENT SCI,PITTSBURGH,PA 15261. UNIV PITTSBURGH,DEPT OTOLARYNGOL,PITTSBURGH,PA 15261. NIH,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. FU NCI NIH HHS [CN-24428-33]; NIDCR NIH HHS [DE10513] NR 23 TC 53 Z9 53 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 20 PY 1995 VL 64 IS 5 BP 332 EP 335 DI 10.1002/ijc.2910640509 PG 4 WC Oncology SC Oncology GA TB577 UT WOS:A1995TB57700008 PM 7591306 ER PT J AU SINGER, MF AF SINGER, MF TI UNUSUAL REVERSE TRANSCRIPTASES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID MITOCHONDRIAL PLASMIDS; MAURICEVILLE PLASMID; CDNA SYNTHESIS; DNA; DROSOPHILA; RNA; NEUROSPORA; EVOLUTION; ELEMENTS; RETROTRANSPOSON C1 CARNEGIE INST WASHINGTON,WASHINGTON,DC 20005. NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 58 TC 16 Z9 16 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 20 PY 1995 VL 270 IS 42 BP 24623 EP 24626 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB465 UT WOS:A1995TB46500001 PM 7559567 ER PT J AU LUCARELLI, E KAPLAN, DR THIELE, CJ AF LUCARELLI, E KAPLAN, DR THIELE, CJ TI SELECTIVE REGULATION OF TRKA AND TRKB RECEPTORS BY RETINOIC ACID AND INTERFERON-GAMMA IN HUMAN NEUROBLASTOMA CELL-LINES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN NEURO-BLASTOMA; NERVE GROWTH-FACTOR; TYROSINE PROTEIN-KINASE; NEUROTROPHIC FACTOR; MESSENGER-RNA; PROTOONCOGENE PRODUCT; EXPRESSION; DIFFERENTIATION; NGF; GENE AB Trk receptors are a family of genes implicated in the survival, differentiation, and growth of certain neurons and tumors of the nervous system. A better understanding of the regulation of Trk receptors is relevant for developmental and oncological studies. Human neuroblastoma (NB) cell lines constitutively express low levels of TrkA mRNA, while TrkB mRNA is not readily detectable. Differentiation of NB cells is accompanied by a differential modulation of Trk expression in human NE cells. Nanomolar concentrations of RA induce a stable increase of TrkB mRNk. A transient induction of TrkA mRNA levels requires micromolar concentrations of RA. Induction of both TrkA and TrkB mRNA does not require new protein synthesis. However, RA-induced TrkB mRNA expression is transcriptionally regulated, while the transient RA-induced increase of TrkA mRNA is a consequence of extended mRNA stability. Interferon gamma (IFN-gamma) selectively increases TrkA mRNA without affecting TrkB mRNA levels. Similar to RA, IFN-gamma does not modify the transcriptional rate of TrkA mRNA, but rather increases TrkA mRNA stability. Thus, RA and IFN-gamma differentially regulate TrkA or TrkB expression in the same cell type by predominantly transcriptional (TrkB) or post transcriptional (TrkA) mechanisms. Such experiments indicate the complexity of Trk mRNA regulation and also indicate compounds that may affect neurotrophin responsiveness in developing neural cells. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MOLEC MECHANISMS CARCINOGENESIS LAB,FREDERICK,MD 21702. RP LUCARELLI, E (reprint author), NCI,PEDIAT BRANCH,CELLULAR & MOLEC BIOL SECT,BLDG 10,ROOM 13C218,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Lucarelli, Enrico/G-3588-2015 OI Lucarelli, Enrico/0000-0002-6681-6374 NR 63 TC 51 Z9 54 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 20 PY 1995 VL 270 IS 42 BP 24725 EP 24731 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB465 UT WOS:A1995TB46500022 PM 7559588 ER PT J AU GERSTEN, KM NATSUKA, S TRINCHERA, M PETRYNIAK, B KELLY, RJ HIRAIWA, N JENKINS, NA GILBERT, DJ COPELAND, NG LOWE, JB AF GERSTEN, KM NATSUKA, S TRINCHERA, M PETRYNIAK, B KELLY, RJ HIRAIWA, N JENKINS, NA GILBERT, DJ COPELAND, NG LOWE, JB TI MOLECULAR-CLONING, EXPRESSION, CHROMOSOMAL ASSIGNMENT, AND TISSUE-SPECIFIC EXPRESSION OF A MURINE ALPHA-(1,3)-FUCOSYL-TRANSFERASE LOCUS CORRESPONDING TO THE HUMAN ELAM-1 LIGAND FUCOSYL-TRANSFERASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BETA-GALACTOSIDE ALPHA-2,6-SIALYLTRANSFERASE; HUMAN ALPHA(1,3)FUCOSYLTRANSFERASE GENE; ELAM-1-DEPENDENT CELL-ADHESION; EMBRYONIC ANTIGEN SSEA-1; FULL-LENGTH CDNA; LEWIS-X; MONOCLONAL-ANTIBODIES; DETERMINES EXPRESSION; LEUKEMIA-VIRUS; MOUSE EMBRYOS AB Terminal Fuc alpha 1-3GlcNAc moieties are displayed by mammalian cell surface glycoconjugates in a tissue-specific manner. These oligosaccharides participate in selectin-dependent leukocyte adhesion and have been implicated in adhesive events during murine embryogenesis. Other functions for these molecules remain to be defined, as do the tissue-specific expression patterns of the corresponding alpha-(1-3)-fucosyltransferase (alpha 1-3FT) genes. This report characterizes a murine alpha 1-3FT that shares 77% amino acid sequence identity with human ELAM ligand fucosyltransferase (ELFT, also termed Fuc-TIV). The corresponding gene maps to mouse chromosome 9 in a region of homology with the Fuc-TIV locus on human chromosome 11q. In vitro, the murine (alpha 1-3FT can efficiently fucosylate the trisaccharide Gal alpha 1-3Gal beta 1-4GlcNAc (apparent K-m of 0.71 mM) to form an unusual tetrasaccharide (Gal alpha 1-3Gal beta 1-4[Fuc alpha 1-3]GlcNAc) described in periimplantation mouse tissues. The enzyme can also form the Lewis x determinant from Gal beta 1-4GlcNAc (K-m = 2.05 mM), and the sialyl Lewis x determinant from NeuNAc alpha 2-3Gal beta 1-4GlcNAc (K-m = 1.78 mM). However, it does not yield sialyl Lewis x determinants when expressed in a mammalian cell line that maintains sialyl Lewis x precursors. Transcripts from this gene accumulate to low levels in hematopoietic organs, but are unexpectedly abundant in epithelia that line the stomach, small intestine, colon, and epididymus. Epithelial cell-specific expression of this gene suggests function(s) in addition to, and distinct from, its proposed role in selectin ligand synthesis. C1 UNIV MICHIGAN,SCH MED,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT PATHOL,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT CELL & MOLEC BIOL PROGRAM,ANN ARBOR,MI 48109. NCI,FREDERICK CANC RES & DEV CTR,ABL INC,BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101]; NCRR NIH HHS [M01RR00042]; NIGMS NIH HHS [1R01GM47455] NR 78 TC 82 Z9 83 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 20 PY 1995 VL 270 IS 42 BP 25047 EP 25056 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB465 UT WOS:A1995TB46500069 PM 7559635 ER PT J AU TANIMURA, A KURIHARA, K RESHKIN, SJ TURNER, RJ AF TANIMURA, A KURIHARA, K RESHKIN, SJ TURNER, RJ TI INVOLVEMENT OF DIRECT PHOSPHORYLATION IN THE REGULATION OF THE RAT PAROTID NA+-K+-2CL(-) COTRANSPORTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SHARK RECTAL GLAND; K-CL COTRANSPORT; FLUID SECRETION; ACINAR-CELLS; BUMETANIDE-BINDING; NA/K/CL COTRANSPORTER; PROTEIN; PURIFICATION; INHIBITORS AB We identify a 175-kDa membrane phosphoprotein (pp175) in rat parotid acini whose properties correlate well with the Na+-K+-2Cl(-) cotransporter previously characterized functionally and biochemically in this tissue. pp175 was the only phosphoprotein immunoprecipitated by an anti-Na+-K+-2Cl(-) cotransporter antibody and the only membrane protein whose phosphorylation state was conspicuously altered after a brief (45-s) exposure of acini to the beta-adrenergic agonist isoproterenol. Phosphopeptide mapping provided evidence for three phosphorylation sites on pp175, only one of which was labeled in response to isoproterenol treatment. The half-maximal effect of isoproterenol on phosphorylation of pp175 (approximate to 20 nM) was in excellent agreement with its previously demonstrated up regulatory effect on cotransport activity. Increased phosphorylation of pp175 was also seen following acinar treatment with a permeant cAMP analogue and with forskolin, conditions that have likewise been shown to up-regulate the cotransporter. Combined with earlier results from our laboratory, these data provide strong evidence that the up-regulation of the cotransporter by these agents is due to direct phosphorylation mediated by protein kinase A. ALF(4)(-) treatment, which results in an up regulation of cotransport activity comparable with that observed with isoproterenol (similar to 6-fold), caused a similar increase in phosphorylation of pp175. However, hypertonic shrinkage and treatment with the protein phosphatase inhibitor calyculin A, which also up-regulate the cotransporter (similar to 3-fold and similar to 6-fold, respectively) caused no change in the phosphorylation level. Furthermore, although acinar treatment with the muscarinic agonist carbachol results in a dramatic up-regulation of cotransport activity and a concomitant phosphorylation of pp175, no phosphorylation of pp175 was seen with the Ca2+-mobilizing agent thapsigargin, which is able to fully mimic the up-regulatory effect of carbachol on transport activity. Taken together, these results indicate that direct phosphorylation is only one of the mechanisms involved in secretagogue-induced regulation of the rat parotid Na+K+-2Cl(-) cotransporter. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. NR 23 TC 46 Z9 48 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 20 PY 1995 VL 270 IS 42 BP 25252 EP 25258 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB465 UT WOS:A1995TB46500098 PM 7559664 ER PT J AU CRESPO, P CACHERO, TG XU, NZ GUTKIND, JS AF CRESPO, P CACHERO, TG XU, NZ GUTKIND, JS TI DUAL EFFECT OF BETA-ADRENERGIC RECEPTORS ON MITOGEN-ACTIVATED PROTEIN-KINASE - EVIDENCE FOR A BETA-GAMMA-DEPENDENT ACTIVATION AND A G-ALPHA(S)-CAMP-MEDIATED INHIBITION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL-PROLIFERATION; ADENYLYL CYCLASE; SIGNAL TRANSDUCTION; COUPLED RECEPTORS; RAS; GENE; EXPRESSION; SUBUNITS; CAMP; PATHWAY AB The enzymatic activity of mitogen-activated protein kinases (MAP kinases) increases in response to agents acting on a variety of cell surface receptors, including receptors linked to heterotrimeric G proteins of the G(i) and G(q) family. Recently, it has been shown that stimulation of beta-adrenergic receptors, which are typical of those that act through G(s) to activate adenylyl cyclases, potently activates MAP kinases in the heart, resulting in the hypertrophy of the cardiac muscle (Lazou, A., Bogoyevitch, M. A., Clerk, A., Fuller, S. J., Marshall, C. J., and Sudgen, P. H. (1994) Circ, Res, 75, 938-941). We have observed that exposure of COS-7 cells to a beta-adrenergic agonist, isoproterenol, raises intracellular levels of cAMP and effectively activates protein kinase A (PKA) and an epitope-tagged MAP kinase. However, MAP kinase stimulation by isoproterenol was neither mimicked by expression of an activated mutant of G alpha(s), nor by treatment with PKA-stimulating agents. Moreover, pretreatment of COS-7 with a permeable cAMP analog, 8-Br-cAMP, markedly decreased MAP kinase activation by either isoproterenol or epidermal growth factor. Thus, in COS-7 cells cAMP and PKA do not appear to mediate MAP kinase activation by beta-adrenergic receptors. Signaling from beta-adrenergic receptors to MAP kinase was inhibited by transfection of a chimeric molecule consisting of the CD8 receptor and the carboxyl terminus of the beta-adrenergic receptor kinase, which includes the beta gamma-binding domain. MAP kinase activation by isoproterenol was not affected by depletion of protein kinase C, but it was completely abolished by expression of Ras-inhibiting molecules. We conclude that signaling from beta-adrenergic receptors to MAP kinase involves an activating signal mediated by beta gamma subunits acting on a Ras-dependent pathway and a G alpha(s)-induced inhibitory signal mediated by cAMP and PKA. The balance between these two opposing mechanisms of regulation would be expected to control the MAP kinase response to beta-adrenergic agonists as well as to other biologically active agents known to act on G(s) coupled receptors, including a number of hormones, neurotransmitters, and lipid mediators. C1 NIDR,MOLEC SIGNALING UNIT,BETHESDA,MD 20892. RI Gutkind, J. Silvio/A-1053-2009; Crespo, Piero/M-3273-2014 OI Crespo, Piero/0000-0003-2825-7783 NR 49 TC 192 Z9 193 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 20 PY 1995 VL 270 IS 42 BP 25259 EP 25265 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB465 UT WOS:A1995TB46500099 PM 7559665 ER PT J AU BUJACZ, G JASKOLSKI, M ALEXANDRATOS, J WLODAWER, A MERKEL, G KATZ, RA SKALKA, AM AF BUJACZ, G JASKOLSKI, M ALEXANDRATOS, J WLODAWER, A MERKEL, G KATZ, RA SKALKA, AM TI HIGH-RESOLUTION STRUCTURE OF THE CATALYTIC DOMAIN OF AVIAN-SARCOMA VIRUS INTEGRASE SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE INTEGRASE; AIDS; X-RAY STRUCTURE; MULTIWAVELENGTH ANOMALOUS DIFFRACTION; STRUCTURE COMPARISON ID MACROMOLECULAR STRUCTURES; ESCHERICHIA-COLI; RIBONUCLEASE-H; DNA-BINDING; VIRAL-DNA; 3-DIMENSIONAL STRUCTURE; RETROVIRAL INTEGRATION; ANOMALOUS DIFFRACTION; CRYSTAL-STRUCTURE; HIV-1 INTEGRASE AB Retroviral integrase (IN) functions to insert retroviral DNA into the host cell chromosome in a highly coordinated manner. IN catalyzes two biochemically separable reactions: processing of the viral DNA ends and joining of these ends to the host DNA. Previous studies suggested that these two reactions are chemically similar and are carried out by a single active site that is characterized by a highly conserved constellation of carboxylate residues, the D,D(35)E motif. We report here the crystal structure of the isolated catalytic domain of avian sarcoma virus (ASV) IN, solved using multiwavelength anomalous diffraction data for a selenomethionine derivative and refined at 1.7 Angstrom resolution. The protein is a crystallographic dimer with each monomer featuring a five-stranded mixed beta-sheet region surrounded by five alpha-helices. Based on the general fold and the arrangement of catalytic carboxylate residues, it is apparent that ASV IN is a member of a superfamily of proteins that also includes two types of nucleases, RuvC and RNase H. The general fold and the dimer interface are similar to those of the analogous domain of HIV-1 IN, whose crystal structure has been determined at 2.5 Angstrom resolution. However, the ASV IN structure is more complete in that all three critical carboxylic acids, Asp64, Asp121 and Glu157, are ordered. The ordered active site and the considerably higher resolution of the present structure are all important to an understanding of the mechanism of retroviral DNA integration, as well as for designing antiviral agents that may be effective against HIV. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MACROMOLEC STRUCT LAB, FREDERICK, MD 21702 USA. POLISH ACAD SCI, INST BIOORGAN CHEM, CTR BIOCRYSTALLOG RES, POZNAN, POLAND. FOX CHASE CANC CTR, INST CANC RES, PHILADELPHIA, PA 19110 USA. FU NCI NIH HHS [N01-CO-46000, CA47486, CA06927] NR 49 TC 179 Z9 181 U1 0 U2 2 PU ACADEMIC PRESS (LONDON) LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD OCT 20 PY 1995 VL 253 IS 2 BP 333 EP 346 DI 10.1006/jmbi.1995.0556 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TA708 UT WOS:A1995TA70800010 PM 7563093 ER PT J AU MCCARTHY, MM NIELSEN, DA GOLDMAN, D AF MCCARTHY, MM NIELSEN, DA GOLDMAN, D TI ANTISENSE OLIGONUCLEOTIDE INHIBITION OF TRYPTOPHAN-HYDROXYLASE ACTIVITY IN MOUSE-BRAIN SO REGULATORY PEPTIDES LA English DT Article DE TRYPTOPHAN HYDROXYLASE; ANTISENSE OLIGONUCLEOTIDE; MOUSE BRAIN; INHIBITION ID RAT; TURNOVER; NEURONS AB To examine in vivo effectiveness of antisense oligonucleotides against tryptophan hydroxylase (TPH) mRNA, adult male swiss-NIH mice were implanted with in-dwelling cannula into the 4th ventricle and after recovery infused with either antisense oligonucleotide to TPH, scrambled control oligo or saline vehicle for four consecutive days. An additional group of animals bearing cannula were injected a single time i.p, with the TPH inhibitor para-chlorophenylalanine (PCPA; 300 mg/kg). All animals were sacrificed on the afternoon of the 4th day of treatment. TPH activity was measured by enzymatic assay and HPLC quantification of end-product,synthesis. There was a significant decrease (> 50%) in TPH activity in both the PCPA-treated and antisense-oligo infused animals compared to either scrambled-oligo or saline-infused subjects (ANOVA; P < 0.05). There was no difference between saline and scrambled oligo-infusion. In a separate group of animals treated in the same way, behavioral tests were conducted on the afternoon of the 4th day. Two tests of anxiety, the hole-board apparatus and the elevated plus-maze, indicated some significant effects of PCPA treatment and/or antisense oligo-infusion but confounding effects due to alterations in locomotion could not be ruled out. However, tests on a rotorod apparatus indicated that antisense oligo-infused animals retained good balance and coordination in that their performance significantly improved on the second test, as did that of scrambled-oligo infused animals. In contrast, PCPA-treated animals did not improve, suggesting that locomotor performance had been impaired. These data support the notion that antisense oligo blockade may offer advantages over pharmacological manipulations of enzyme activity. C1 NIH,NIAAA,NEUROGENET LAB,ROCKVILLE,MD. RP MCCARTHY, MM (reprint author), UNIV MARYLAND,SCH MED,DEPT PHYSIOL,655 W BALTIMORE ST,BALTIMORE,MD 21201, USA. RI Nielsen, David/B-4655-2009; Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 18 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD OCT 20 PY 1995 VL 59 IS 2 BP 163 EP 170 DI 10.1016/0167-0115(95)00102-H PG 8 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA TB275 UT WOS:A1995TB27500005 PM 8584751 ER PT J AU CHA, XY XU, H NI, Q PARTILLA, JS RICE, KC MATECKA, D CALDERON, SN PORRECA, F LAI, J ROTHMAN, RB AF CHA, XY XU, H NI, Q PARTILLA, JS RICE, KC MATECKA, D CALDERON, SN PORRECA, F LAI, J ROTHMAN, RB TI OPIOID PEPTIDE RECEPTOR STUDIES .4. ANTISENSE OLIGODEOXYNUCLEOTIDE TO THE DELTA-OPIOID RECEPTOR DELINEATES OPIOID RECEPTOR SUBTYPES SO REGULATORY PEPTIDES LA English DT Article DE OPIOID RECEPTOR; ANTISENSE OLIGODEOXYNUCLEOTIDE; LIGAND BINDING; DELTA OPIOID RECEPTOR; KAPPA OPIOID RECEPTOR ID RAT-BRAIN MEMBRANES; MU-OPIATE RECEPTOR; NCX BINDING-SITES; GUINEA-PIG BRAIN; MOUSE-BRAIN; FUNCTIONAL EXPRESSION; HIGH-AFFINITY; DRUGS; PURIFICATION; CLONING AB Prior work in our laboratory has identified putative subtypes of delta (delta(cx-1), delta(cx-2), delta(ncx-1), delta(ncx-2)) and kappa(2) (kappa(2a) and kappa(2b)) receptors, Previous studies showed that chronic (three day) i.c.v. administration of antisense oligodeoxynucleotide to the cloned delta opioid receptor selectively decreased [H-3][D-Ala(2),D-Leu(5)]enkephalin binding to the delta(ncx) site, not the delta(cx-2) site. The present study extends this work by demonstrating that delta antisense DNA selectively affects the delta(ncx-2) site sparing the other putative delta receptor subtypes and kappa(2) receptor subtypes. This selectivity is not due to anatomically specific effects of delta antisense DNA since autoradiograms show that delta binding is reduced in all regions of the brain after chronic i.c.v. administration of delta antisense DNA. These data strongly suggest that the delta(cx-1), delta(cx-2), delta(ncx-1), kappa(2a), and kappa(2b) binding sites are different proteins than the delta(ncx-2) binding site, which, based on its sensitivity to delta antisense DNA, is synonymous to the cloned delta opioid receptor, Viewed collectively, these data suggest that administration of delta antisense DNA, and by extension other receptor-selective antisense DNA, is a powerful approach to distinguishing between postulated receptor subtypes. C1 NIH,NIDA,DIR,CLIN PSYCHOPHARMACOL UNIT,BALTIMORE,MD 21224. NIH,NIDDK,MED CHEM LAB,BETHESDA,MD 20892. UNIV ARIZONA,COLL MED,DEPT PHARMACOL,TUCSON,AZ 85724. NR 45 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD OCT 20 PY 1995 VL 59 IS 2 BP 247 EP 253 DI 10.1016/0167-0115(95)00095-S PG 7 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA TB275 UT WOS:A1995TB27500015 PM 8584761 ER PT J AU HUDSON, KL ROTHENBERG, KH ANDREWS, LB KAHN, MJE COLLINS, FS AF HUDSON, KL ROTHENBERG, KH ANDREWS, LB KAHN, MJE COLLINS, FS TI GENETIC DISCRIMINATION AND HEALTH-INSURANCE - AN URGENT NEED FOR REFORM SO SCIENCE LA English DT Editorial Material C1 UNIV MARYLAND, SCH LAW, LAW & HLTH CARE PROGRAM, BALTIMORE, MD 21201 USA. NIH US DOE, WORKING GRP ETH LEGAL & SOCIAL IMPLICAT, BETHESDA, MD USA. CHICAGO KENT COLL LAW, CHICAGO, IL USA. NATL ACT PLAN BREAST CANC, HEREDITARY SUSCEPTIBIL WORKING GRP, BETHESDA, MD USA. RP NIH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA. NR 8 TC 166 Z9 166 U1 3 U2 9 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 EI 1095-9203 J9 SCIENCE JI Science PD OCT 20 PY 1995 VL 270 IS 5235 BP 391 EP 393 DI 10.1126/science.270.5235.391 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TA374 UT WOS:A1995TA37400028 PM 7569991 ER PT J AU BLAESE, RM CULVER, KW MILLER, AD CARTER, CS FLEISHER, T CLERICI, M SHEARER, G CHANG, L CHIANG, YW TOLSTOSHEV, P GREENBLATT, JJ ROSENBERG, SA KLEIN, H BERGER, M MULLEN, CA RAMSEY, WJ MUUL, L MORGAN, RA ANDERSON, WF AF BLAESE, RM CULVER, KW MILLER, AD CARTER, CS FLEISHER, T CLERICI, M SHEARER, G CHANG, L CHIANG, YW TOLSTOSHEV, P GREENBLATT, JJ ROSENBERG, SA KLEIN, H BERGER, M MULLEN, CA RAMSEY, WJ MUUL, L MORGAN, RA ANDERSON, WF TI T-LYMPHOCYTE-DIRECTED GENE-THERAPY FOR ADA(-) SCID - INITIAL TRIAL RESULTS AFTER 4 YEARS SO SCIENCE LA English DT Article ID ADENOSINE-DEAMINASE DEFICIENCY; SEVERE COMBINED IMMUNODEFICIENCY; BONE-MARROW TRANSPLANTATION; ENZYME REPLACEMENT THERAPY; CELL-LINES; RETROVIRAL VECTORS; AVIAN RETROVIRUS; VIRUS; EXPRESSION; SEQUENCES AB In 1990, a clinical trial was started using retroviral-mediated transfer of the adenosine deaminase (ADA) gene into the T cells of two children with severe combined immunodeficiency (ADA(-) SCID). The number of blood T cells normalized as did many cellular and humoral immune responses. Gene treatment ended after 2 years, but integrated vector and ADA gene expression in T cells persisted. Although many components remain to be perfected, it is concluded here that gene therapy can be a safe and effective addition to treatment for some patients with this severe immunodeficiency disease. C1 NCI,BETHESDA,MD 20892. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. NIH,CTR CLIN,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. GENET THERAPY,GAITHERSBURG,MD 20878. CASE WESTERN RESERVE UNIV,SCH MED,DEPT PEDIAT,CLEVELAND,OH 44106. RP BLAESE, RM (reprint author), NIH,NATL CTR HUMAN GENOME RES,BLDG 49,ROOM 2A03,BETHESDA,MD 20892, USA. OI Miller, Dusty/0000-0002-3736-3660 NR 75 TC 754 Z9 785 U1 7 U2 82 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 20 PY 1995 VL 270 IS 5235 BP 475 EP 480 DI 10.1126/science.270.5235.475 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TA374 UT WOS:A1995TA37400043 PM 7570001 ER PT J AU TOOHEY, K WEHRLY, K NISHIO, J PERRYMAN, S CHESEBRO, B AF TOOHEY, K WEHRLY, K NISHIO, J PERRYMAN, S CHESEBRO, B TI HUMAN-IMMUNODEFICIENCY-VIRUS ENVELOPE V1 AND V2 REGIONS INFLUENCE REPLICATION EFFICIENCY IN MACROPHAGES BY AFFECTING VIRUS SPREAD SO VIROLOGY LA English DT Article ID NECROSIS-FACTOR-ALPHA; TYPE-1 GP120; MONONUCLEAR PHAGOCYTES; CELL TROPISM; MONOCLONAL-ANTIBODIES; BIOLOGICAL PHENOTYPE; SYNCYTIUM FORMATION; SEQUENCE VARIATION; PRIMARY INFECTION; VPR GENE AB The vs hypervariable region of the HIV-I envelope protein is a major determinant of viral tropism for macrophages. However, the replication of macrophage-tropic HIV-1 strains varies considerably in macrophages, and this variability has been linked to the V1 and V2 envelope regions. In the present study, recombinant HIV clones were generated by inserting V1 and V2 sequences from the Ba-L HIV isolate, which has a high macrophage replication level, into the genomic background of a macrophage-tropic clone with a low macrophage replication level. Infection of macrophages with varying multiplicities of infection and direct detection of the number of infected macrophages per culture showed that the Ba-L V1 and V2 envelope sequences enhanced the ability of virus to spread in the cultures. In contrast, macrophage-tropic clones with low replication efficiency infected macrophages initially but showed no evidence of spread to additional cells during the culture period. This effect on virus spread appeared to be macrophage-specific as it was not observed in cultures of T lymphocytes. Comparison of recombinant clones containing V1, V2, and vs envelope sequences from high-efficiency Ba-L and JR-FL strains indicated that markedly different V1 and V2 sequences could impart the same rapidly spreading phenotype in macrophages. (C) 1995 Academic Press, Inc. C1 NIAID,ROCKY MT LAB,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 57 TC 117 Z9 118 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 0042-6822 J9 VIROLOGY JI Virology PD OCT 20 PY 1995 VL 213 IS 1 BP 70 EP 79 DI 10.1006/viro.1995.1547 PG 10 WC Virology SC Virology GA TA440 UT WOS:A1995TA44000008 PM 7483281 ER PT J AU HAGGARDLJUNGQUIST, E JACOBSEN, E RISHOVD, S SIX, EW NILSSEN, O SUNSHINE, MG LINDQVIST, BH KIM, KJ BARREIRO, V KOONIN, EV CALENDAR, R AF HAGGARDLJUNGQUIST, E JACOBSEN, E RISHOVD, S SIX, EW NILSSEN, O SUNSHINE, MG LINDQVIST, BH KIM, KJ BARREIRO, V KOONIN, EV CALENDAR, R TI BACTERIOPHAGE-P2 - GENES INVOLVED IN BASEPLATE ASSEMBLY SO VIROLOGY LA English DT Article ID ESCHERICHIA-COLI; SATELLITE BACTERIOPHAGE; RNA-POLYMERASE; CLONED GENES; CAPSID SIZE; PROTEIN; SEQUENCES; HELPER; MORPHOGENESIS; CONSTRUCTION AB The sequences of two previously defined tail genes, V and J, of the temperate bacteriophage P2, and those of two new essential tail genes, W and I, were determined. Their order is the late gene promoter, VWJI, followed by the tail fiber genes H and G, and a transcription terminator. The V gene product is the small spike at the tip of the tail, and the J gene product lies at the edge of the baseplate. The W gene product may be homologous to the product of gene 25 of T4 phage, which is part of the T4 baseplate. A temperature-sensitive mutation in gene V affects satellite phage P4 production more than it affects the production of P2 helper phage. P4 mutations that partially compensate for this defect of gene V lie in the P4 capsid size determination gene, sid. (C) 1995 Academic Press, Inc. C1 UNIV CALIF BERKELEY, DEPT MOLEC & CELL BIOL, BERKELEY, CA 94720 USA. UNIV STOCKHOLM, DEPT GENET, S-10691 STOCKHOLM, SWEDEN. UNIV OSLO, CTR BIOTECHNOL, N-0317 OSLO, NORWAY. UNIV OSLO, INST BIOL, N-0317 OSLO, NORWAY. UNIV IOWA, SCH MED, DEPT MICROBIOL, IOWA CITY, IA 52242 USA. LAB MICROBIAL GENE TECHNOL, N-1432 AS, NORWAY. NIH, NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA. FU NIAID NIH HHS [AI-08722, AI-04043] NR 44 TC 24 Z9 24 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD OCT 20 PY 1995 VL 213 IS 1 BP 109 EP 121 DI 10.1006/viro.1995.1551 PG 13 WC Virology SC Virology GA TA440 UT WOS:A1995TA44000012 PM 7483254 ER PT J AU RYANGRAHAM, MA PEDEN, KWC AF RYANGRAHAM, MA PEDEN, KWC TI BOTH VIRUS AND HOST COMPONENTS ARE IMPORTANT FOR THE MANIFESTATION OF A NEF(-) PHENOTYPE IN HIV-1 AND HIV-2 SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; NUCLEOTIDE-SEQUENCE; MUTATIONAL ANALYSIS; HTLV-III; LTR TRANSCRIPTION; TRANSGENIC MICE; DOWN-REGULATION; CELL-LINES; AIDS VIRUS; T-CELLS AB While it has been demonstrated that the Nef protein of simian immunodeficiency virus is obligatory for the establishment of high viral loads and the development of simian AIDS in rhesus macaques, demonstrating a critical role for the human immunodeficiency virus (HIV) Nef protein in tissue culture has been elusive. Data have been contradictory as to whether Nef has a negative or positive influence on in vitro virus replication. In an attempt to define a role for Nef during virus propagation in tissue culture and to obtain virus-host systems that could distinguish between the Nef mutant and wildtype viruses, we have introduced mutations into the nef genes of infectious molecular clones of three HIV-I strains and two isolates of the HIV-2(ROD) strain and have investigated the capacity of viruses derived from them to infect a number of CD4-positive T-cell lines and peripheral blood mononuclear cells (PBMC). Mutating the nef gene of all viruses had a modest negative effect on virus production in activated PBMC. In some T-cell lines with some viruses, the effects were severe, and little or no Nef mutant virus could be detected. In other cell lines, the result of mutating the nef gene either had no effect or had a slight negative effect on the replication kinetics. Therefore, whether the consequences of loss of Nef activity can be demonstrated in vitro depends on both the particular virus and the host cell used, suggesting that Nef is exerting its activity on some cellular pathway. In addition, we describe the construction and properties of hitherto unreported infectious molecular clones of the ROD strain of HIV-2. (C) 1995 Academic Press, Inc C1 US FDA,CBER,RETROVIRUS RES LAB,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. FU NIMHD NIH HHS [MD800803] NR 55 TC 43 Z9 43 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 0042-6822 J9 VIROLOGY JI Virology PD OCT 20 PY 1995 VL 213 IS 1 BP 158 EP 168 DI 10.1006/viro.1995.1556 PG 11 WC Virology SC Virology GA TA440 UT WOS:A1995TA44000017 PM 7483259 ER PT J AU AVINO, A GARCIA, RG MARQUEZ, VE ERITJA, R AF AVINO, A GARCIA, RG MARQUEZ, VE ERITJA, R TI PREPARATION AND PROPERTIES OF OLIGODEOXYNUCLEOTIDES CONTAINING 4-O-BUTYLTHYMINE, 2-FLUOROHYPOXANTHINE AND 5-AZACYTOSINE SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID SOLID-PHASE SYNTHESIS; BASE-PROTECTING GROUP; OLIGONUCLEOTIDE SYNTHESIS; NUCLEOTIDE CHEMISTRY; BLOCKING GROUP; CROSS-LINKING; DNA; NUCLEOSIDES; PHOSPHATE; ADDUCTS AB Oligonucleotides carrying the ammonia sensitive bases 4-O-butylthymine, 2-fluorohypoxanthine and 5-azacytosine have been prepared for the first time using a special protocol that avoids the use of nucleophiles during the final deprotection. C1 CSIC,CID,DEPT MOLEC GENET,E-08034 BARCELONA,SPAIN. EUROPEAN MOLEC BIOL LAB,D-69117 HEIDELBERG,GERMANY. NCI,MED CHEM LAB,BETHESDA,MD 20892. RI eritja, ramon/B-5613-2008; Avino, Anna/N-5223-2015 OI eritja, ramon/0000-0001-5383-9334; Avino, Anna/0000-0003-3047-738X NR 45 TC 11 Z9 11 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD OCT 19 PY 1995 VL 5 IS 20 BP 2331 EP 2336 DI 10.1016/0960-894X(95)00409-M PG 6 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA TA592 UT WOS:A1995TA59200006 ER PT J AU TROLLFORS, B TARANGER, J LAGERGARD, T LIND, L SUNDH, V ZACKRISSON, G LOWE, CU BLACKWELDER, W ROBBINS, JB AF TROLLFORS, B TARANGER, J LAGERGARD, T LIND, L SUNDH, V ZACKRISSON, G LOWE, CU BLACKWELDER, W ROBBINS, JB TI A PLACEBO-CONTROLLED TRIAL OF A PERTUSSIS-TOXOID VACCINE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID BORDETELLA-PERTUSSIS; ANTIBODY-RESPONSE; FILAMENTOUS HEMAGGLUTININ AB Background. Although many whole-cell vaccines have been effective in preventing pertussis, these vaccines are difficult to standardize and can produce side effects. In Sweden, pertussis became endemic during the 1970s despite vaccination. Because of its limited efficacy, the Swedish-made whole-cell vaccine was withdrawn in 1979. Methods. To evaluate the efficacy of an acellular vaccine consisting of pertussis toxin inactivated by hydrogen peroxide (pertussis toroid), we conducted a randomized, double-blind, placebo-controlled trial in Sweden. Infants were vaccinated with either diphtheria and tetanus toxoids atone (DT toxoids, 1726 infants) or diphtheria, tetanus, and pertussis toxoids (DTP toxoids, 1724 infants) at 3, 5, and 12 months of age. Results. There were no serious reactions. With the pertussis vaccine there were slightly more local reactions than with the DT toxoids alone, but the rates of postvaccination fever were the same. The main period of surveillance, which began 30 days after the third vaccination, continued for a median of 17.5 months. There were 312 cases of pertussis (72 in the DTP-toxoids group and 240 in the DT-toxoids group) that met the clinical criterion (paroxysmal cough lasting greater than or equal to 21 days) and laboratory criteria for pertussis as defined by the World Health Organization. The efficacy of this acellular vaccine was 71 percent (95 percent confidence interval, 63 to 78 percent). The recipients of DTP toxoids who had pertussis had cough of shorter duration than the recipients of DT toxoids, and fewer had whooping and vomiting. The vaccine efficacy after two doses was 55 percent (95 percent confidence interval, 12 to 78 percent), on the basis of 14 cases in the DTP-toxoids group and 31 in the DT-toxoids group that met the definition of the World Health Organization. Conclusions. A pharmacologically inert, acellular pertussis-toxoid vaccine that is easily standardized is safe and confers substantial protection against pertussis. C1 GOTHENBURG UNIV,DEPT PEDIAT,S-41124 GOTHENBURG,SWEDEN. GOTHENBURG UNIV,DEPT MED MICROBIOL & IMMUNOL,GOTHENBURG,SWEDEN. GOTHENBURG UNIV,DEPT CLIN BACTERIOL,GOTHENBURG,SWEDEN. GOTHENBURG UNIV,DEPT GERIATR MED,GOTHENBURG,SWEDEN. NICHHD,BETHESDA,MD 20892. NIAID,BETHESDA,MD 20892. FU NICHD NIH HHS [N01-HD-9-2905] NR 28 TC 218 Z9 221 U1 0 U2 5 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 19 PY 1995 VL 333 IS 16 BP 1045 EP 1050 DI 10.1056/NEJM199510193331604 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA RZ340 UT WOS:A1995RZ34000004 PM 7675047 ER PT J AU FUKASAWA, K ZHOU, RP MATTEN, WT ARMSTRONG, AJ DAAR, I OSKARSSON, M SATHYANARAYANA, BK MACLVOR, L WOOD, TG VANDEWOUDE, GF AF FUKASAWA, K ZHOU, RP MATTEN, WT ARMSTRONG, AJ DAAR, I OSKARSSON, M SATHYANARAYANA, BK MACLVOR, L WOOD, TG VANDEWOUDE, GF TI MUTAGENIC ANALYSIS OF FUNCTIONAL DOMAINS OF THE MOS PROTOONCOGENE AND IDENTIFICATION OF THE SITES IMPORTANT FOR MAPK ACTIVATION AND DNA-BINDING SO ONCOGENE LA English DT Article DE MOS; MAP KINASE; TRANSFORMATION; OOCYTE MATURATION ID XENOPUS-OOCYTES; V-MOS; PROTOONCOGENE PRODUCT; MEIOTIC MATURATION; KINASE-ACTIVITY; MEIOSIS-II; TUBULIN; INVITRO; CELLS; TRANSFORMATION AB We constructed in-frame deletion/replacement mutations in the Xenopus mos proto-oncogene that lie within conserved Mos-specific codons, but outside of the regions that are conserved among the src kinase family of genes, All gene products were assayed in vine for kinase activity and in vivo for their ability to induce oocyte maturation, embryonic cleavage arrest and cellular transformation, Most mutations in Mos eliminated both kinase and biological activity, However, a mutation in Mos that removed two basic amino acid residues (R94 and K97) downstream from the lysine at the ATP binding site (K90) markedly enhanced autophosphorylation activity, Moreover, this mutant displayed markedly reduced biological activity, lacked transforming activity, and failed to activate mitogen activated protein kinase (MAPK), A second mutant Mos product, lacking amino acids R45-A54, displayed a five-fold increase in cellular transforming activity, This Mos mutant specifically localized to the cytoplasm; in contrast to wild-type (wt) Mos that localized to both the nucleus and the cytoplasm, These data indicate that Mos transforming activity is mediated via signalling exerted in the cytoplasm, presumably through MAPK, and that nuclear localization of the oncogene product interferes with transforming activity, We also show that amino acids R45-A54 are important for Mos DNA binding activity. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. UNIV TEXAS,MED BRANCH,SEALY CTR MOLEC SCI,RECOMBINANT DNA LAB,GALVESTON,TX 77555. RI Wood, Thomas/B-6172-2012; OI Daar, Ira/0000-0003-2657-526X NR 52 TC 6 Z9 6 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 19 PY 1995 VL 11 IS 8 BP 1447 EP 1457 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA TC535 UT WOS:A1995TC53500003 PM 7478569 ER PT J AU SNELLER, MC AF SNELLER, MC TI OCULAR MANIFESTATIONS OF WEGENERS GRANULOMATOSIS - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter ID EXPERIENCE RP SNELLER, MC (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 18 PY 1995 VL 274 IS 15 BP 1200 EP 1200 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA RZ120 UT WOS:A1995RZ12000023 ER PT J AU VANLEEUWEN, FE KLOKMAN, WJ STOVALL, M HAGENBEEK, A VANDENBELTDUSEBOUT, AW NOYON, R BOICE, JD BURGERS, JMV SOMERS, R AF VANLEEUWEN, FE KLOKMAN, WJ STOVALL, M HAGENBEEK, A VANDENBELTDUSEBOUT, AW NOYON, R BOICE, JD BURGERS, JMV SOMERS, R TI ROLES OF RADIOTHERAPY AND SMOKING IN LUNG-CANCER FOLLOWING HODGKINS-DISEASE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID 2ND MALIGNANCIES; COLORADO PLATEAU; URANIUM MINERS; MORTALITY; RISK; RADIATION; EXPOSURE; LYMPHOMA; AGE AB Background: Several studies have shown that survivors of Hodgkin's disease have increased risk of lung cancer, but the factors responsible for this excess risk are not well known. Purpose: This study was undertaken to investigate the effects of radiation dose, chemotherapy, and smoking on the risk of lung cancer following treatment of Hodgkin's disease. Methods: We conducted a case-control study in a cohort of 1939 patients treated for Hodgkin's disease from 1966 through 1986 in The Netherlands. Detailed treatment information was collected from the medical records for 30 case patients with lung cancer following Hodgkin's disease and 82 matched control subjects who had not developed lung cancer. Multiple sources were used to obtain as complete smoking histories of the study participants as possible. For each case-control set, the radiation dose received by the area of the lung where the case patient developed the tumor was estimated on the basis of radiotherapy charts and experimental simulations of treatments. The estimates of relative risk (RR) for lung cancer associated with specific exposures were obtained from logistic regression methods, and all tests of statistical significance were two-sided. Results: A statistically significant increase in risk of lung cancer was observed with increasing radiation dose (P for trend = .01) with an RR of 9.6 (95% confidence interval [CI] = 0.93-98) for patients who received 9 Gy or more compared with those who received less than 1 Gy. Patients who smoked more than 10 pack-years after the diagnosis of Hodgkin's disease had a sixfold increase in the risk of lung cancer compared with patients who smoked less than 1 pack-year (P = .03). Positive interaction on a multiplicative scale was observed between the carcinogenic effects of smoking and radiation. The increase in risk of lung cancer with increasing radiation dose was much greater among the patients who smoked after diagnosis of Hodgkin's disease than among those who refrained from smoking (P = .04). There was no increase in lung cancer risk in relation to the number of cycles of chemotherapy or the cumulative doses of the drugs mechlorethamine and procarbazine. Conclusions: The excess risk of lung cancer in Hodgkin's disease patients treated with radiotherapy is related to the radiation dose received by the affected area of the lung. Smokers experience a significantly greater risk attributable to radiotherapy than nonsmokers. Implications: Physicians in charge of patient treatment should make a special effort to dissuade Hodgkin's disease patients from smoking after receiving radiotherapy. C1 NETHERLANDS CANC INST,DEPT RADIOTHERAPY,1066 CX AMSTERDAM,NETHERLANDS. NETHERLANDS CANC INST,DEPT MED ONCOL,1066 CX AMSTERDAM,NETHERLANDS. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT RADIAT PHYS,HOUSTON,TX 77030. DR DANIEL DEN HOED CANC CTR,DEPT HEMATOL,3008 AE ROTTERDAM,NETHERLANDS. NCI,DIV CANC ETIOL,RADIAT EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP VANLEEUWEN, FE (reprint author), NETHERLANDS CANC INST,DEPT EPIDEMIOL,PLESMANLAAN 121,1066 CX AMSTERDAM,NETHERLANDS. NR 31 TC 155 Z9 156 U1 0 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD OCT 18 PY 1995 VL 87 IS 20 BP 1530 EP 1537 DI 10.1093/jnci/87.20.1530 PG 8 WC Oncology SC Oncology GA RZ070 UT WOS:A1995RZ07000011 PM 7563187 ER PT J AU BAKER, SG FREEDMAN, LS AF BAKER, SG FREEDMAN, LS TI POTENTIAL IMPACT OF GENETIC TESTING ON CANCER PREVENTION TRIALS, USING BREAST-CANCER AS AN EXAMPLE - REPLY SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter C1 NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,BETHESDA,MD 20852. NR 1 TC 0 Z9 0 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD OCT 18 PY 1995 VL 87 IS 20 BP 1558 EP 1558 DI 10.1093/jnci/87.20.1558 PG 1 WC Oncology SC Oncology GA RZ070 UT WOS:A1995RZ07000017 ER PT J AU JOHNSTON, PG BEHAN, KA ALLEGRA, CJ DRAKE, JC AF JOHNSTON, PG BEHAN, KA ALLEGRA, CJ DRAKE, JC TI FLUOROURACIL - ACTIVE IN ZD1694 (TOMUDEX)-RESISTANT CELL-LINES WITH MARKEDLY ELEVATED THYMIDYLATE SYNTHASE LEVELS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter RP JOHNSTON, PG (reprint author), USN HOSP,NCI,NAVY MED ONCOL BRANCH,8901 WISCONSIN AVE,BLDG 8,RM 5101,BETHESDA,MD 20889, USA. NR 10 TC 14 Z9 14 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD OCT 18 PY 1995 VL 87 IS 20 BP 1558 EP 1559 DI 10.1093/jnci/87.20.1558-a PG 2 WC Oncology SC Oncology GA RZ070 UT WOS:A1995RZ07000018 PM 7563193 ER PT J AU GHIRLANDO, R KEOWN, MB MACKAY, GA LEWIS, MS UNKELESS, JC GOULD, HJ AF GHIRLANDO, R KEOWN, MB MACKAY, GA LEWIS, MS UNKELESS, JC GOULD, HJ TI STOICHIOMETRY AND THERMODYNAMICS OF THE INTERACTION BETWEEN THE FC FRAGMENT OF HUMAN IGG(1) AND ITS LOW-AFFINITY RECEPTOR FC-GAMMA-RIII SO BIOCHEMISTRY LA English DT Article ID IMMUNOGLOBULIN-E; 3-DIMENSIONAL STRUCTURE; SEGMENTAL FLEXIBILITY; CHIMERIC HUMAN; BINDING-SITE; LOCALIZATION; ANTIBODIES; OLIGOSACCHARIDES; GLYCOSYLATION; SEQUENCE AB IgG-Fc receptors, cell surface glycoproteins binding the Fc region of antibodies, play a crucial role in the immune system. To better understand the nature of the recognition process, we have examined the interaction between huIgG(1)-Fc and a soluble fragment of huFc gamma RIII (sCD16). Analytical ultracentrifugation experiments clearly demonstrate that IgG(1)-Fc and sCD 16 interact weakly to form a 1:1 complex with an association constant of 1.7 x 10(5) M(-1) in PBS at 22.0 degrees C. The thermodynamic parameters, obtained from the temperature dependence of the equilibrium binding constants, exhibit an enthalpy-entropy compensation with a favorable enthalpy at physiological temperatures. The Value of -360 cal mol(-1) K-1 for Delta C-p degrees possibly identifies the process as one in which local folding/rearrangement is coupled to complex formation. The 1:1 stoichiometry and thermodynamic parameters provide a basis for understanding the nature of the Fc gamma R-IgG interactions. C1 UNIV LONDON KINGS COLL, RANDALL INST, LONDON WC2B 5RL, ENGLAND. NIH, NATL CTR RES RESOURCES, BIOMED ENGN & INSTRUMENTAT PROGRAM, BETHESDA, MD 20892 USA. CUNY MT SINAI SCH MED, DEPT BIOCHEM, NEW YORK, NY 10029 USA. RP NIDDKD, MOLEC BIOL LAB, BETHESDA, MD 20892 USA. RI Ghirlando, Rodolfo/A-8880-2009; OI Mackay, Graham/0000-0002-9083-1304 FU NIAID NIH HHS [AI-24322] NR 54 TC 48 Z9 48 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 17 PY 1995 VL 34 IS 41 BP 13320 EP 13327 DI 10.1021/bi00041a007 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB584 UT WOS:A1995TB58400007 PM 7577916 ER PT J AU YEH, HJC SAYER, JM LIU, XH ALTIERI, AS BYRD, RA LAKSHMAN, MK YAGI, H SCHURTER, EJ GORENSTEIN, DG JERINA, DM AF YEH, HJC SAYER, JM LIU, XH ALTIERI, AS BYRD, RA LAKSHMAN, MK YAGI, H SCHURTER, EJ GORENSTEIN, DG JERINA, DM TI NMR SOLUTION STRUCTURE OF A NONANUCLEOTIDE DUPLEX WITH A DG MISMATCH OPPOSITE A 10S ADDUCT DERIVED FROM TRANS ADDITION OF A DEOXYADENOSINE N-6-AMINO GROUP TO (+)-(7R,8S,9S,10R)-7,8-DIHYDROXY-9,10-EPOXY-7,8,9,10-TETRAHYDROBENZO[A]P YRENE - AN UNUSUAL SYN GLYCOSIDIC TORSION ANGLE AT THE MODIFIED DA SO BIOCHEMISTRY LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; RELAXATION MATRIX APPROACH; DOSE-DEPENDENT DIFFERENCES; SOLUTION CONFORMATION; DIOL EPOXIDE; DNA DUPLEX; COUPLING-CONSTANTS; PROTON RESONANCES; BASE-STACKING; 2D NMR AB A nonanucleotide, d(G(1)G(2)T(3)C(4)[BaP]A(5)C(6)G(7)A(8)G(9)), in which (+)-(7R,8S,9S,10R)-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (7-hydroxyl group and epoxide oxygen are trans) is covalently bonded to the exocyclic N-6-amino group of deoxyadenosine (dA(5)) through trans addition at C10 of the epoxide (to give a 10S adduct) has been synthesized. The solution structure of the duplex, d(G(1)G(2)T(3)C(4)[BaP]A(5)C(6)G(7)A(8)G(9)). d(C(10)T(11)C(12)G(13)G(14)G(15)A(16)C(17)C(18)), containing a dG mismatch opposite the modified dA (designated 10S-[BaP]dA . dG 9-mer duplex) has been investigated using a combination of 1D and 2D (including COSY, PECOSY, TOCSY, NOESY, and indirect detection of H-1-P-31 HETCOR) NMR spectroscopies. The NMR results together with restrained molecular dynamics/energy minimization calculations show that the modified dA(5) adopts a syn glycosidic torsion angle whereas all other nucleotide residues adopt anti glycosidic torsion angles. The sugar ring of dA(5) is in the C3'-endo conformation, and the sugar rings of the other residues are in the C2'-endo conformation. The hydrocarbon attached at dA(5) orients toward the 3' end of the modified strand (i.e., dC(6) direction) and intercalates between and parallel to bases of dG(13) and dG(14) Of the complementary strand directly opposite dC(6) and dA(5), respectively. The edge of the hydrocarbon bearing H11 and H12 is positioned between the imino protons of dG(13) and dG(14) in the interior of the duplex, whereas H4 and H5 at the opposite edge are positioned near the sugar H1' and H2 '' protons of dG(13) and facing the exterior of the duplex. The mismatched AG base pair is stabilized by dA(sym)-dG(anti) base pairing in which the imino proton and the O-6 Of dG(14) are hydrogen bonded to N7- and the single N-6-amino proton, respectively, of the modified dA(5). The modified DNA duplex remains in a right-handed helix, which bends at the site of intercalation about 20 to 30 degrees away from the helical axis and toward the direction of the modified strand. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD 21702. PURDUE UNIV,DEPT CHEM,W LAFAYETTE,IN 47907. RP YEH, HJC (reprint author), NIDDK,BETHESDA,MD 20892, USA. RI Byrd, R. Andrew/F-8042-2015 OI Byrd, R. Andrew/0000-0003-3625-4232 FU NCI NIH HHS [N01-CO-46000] NR 55 TC 69 Z9 69 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 17 PY 1995 VL 34 IS 41 BP 13570 EP 13581 DI 10.1021/bi00041a037 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB584 UT WOS:A1995TB58400037 PM 7577946 ER PT J AU NOMOTO, M GONZALEZ, FJ MITA, T INOUE, N KAWAMURA, M AF NOMOTO, M GONZALEZ, FJ MITA, T INOUE, N KAWAMURA, M TI ANALYSIS OF CIS-ACTING REGIONS UPSTREAM OF THE RAT NA+/K+-ATPASE ALPHA-1 SUBUNIT GENE BY IN-VIVO FOOTPRINTING SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE ATPASE, NA+/K+-; PROMOTER; IN VIVO FOOTPRINTING ID LIGATION-MEDIATED PCR; TRANSCRIPTION FACTOR; ELEMENTS; INVIVO; DNA; PROMOTERS; CONTACTS; ISOFORMS; BINDING; COMMON AB By means of in vivo footprinting, we examined the putative cis-acting DNA elements located between -50 and -122 of rat Na+/K+-ATPase alpha 1 subunit gene ATP1A1. Proximal and distal GC box sequences and a consensus sequence for the active transcription factor (ATF) were protected for all the tissues examined (kidney, brain and liver). Putative cooperation between two binding factors on the ATF site and the proximal GC box was observed. The overall in vivo footprinting profiles of the three tissues did not exhibit any marked differences that could account for the variation in the extent of tissue-specific transcription. The alpha 1 regulatory element (ARE) found by Suzuki-Yagawa et al. does not appear to be an element responsible for tissue-specific regulation of the gene. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. YOKOHAMA CITY UNIV,SCH MED,DEPT BIOCHEM,YOKOHAMA,KANAGAWA 236,JAPAN. UNIV OCCUPAT & ENVIRONM HLTH,SCH MED,DEPT BIOL,KITAKYUSHU,FUKUOKA 807,JAPAN. RP NOMOTO, M (reprint author), UNIV OCCUPAT & ENVIRONM HLTH,SCH MED,DEPT BIOL MOLEC,YAHATA NISHI KU,KITAKYUSHU,FUKUOKA 807,JAPAN. NR 20 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD OCT 17 PY 1995 VL 1264 IS 1 BP 35 EP 39 DI 10.1016/0167-4781(95)00158-D PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TB191 UT WOS:A1995TB19100009 PM 7578254 ER PT J AU YOSHIKAWA, T XING, GQ DETERAWADLEIGH, SD AF YOSHIKAWA, T XING, GQ DETERAWADLEIGH, SD TI DETECTION, SIMULTANEOUS DISPLAY AND DIRECT SEQUENCING OF MULTIPLE NUCLEAR HORMONE-RECEPTOR GENES USING BILATERALLY TARGETED RNA FINGERPRINTING SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE PCR; RAT COUP-TFI; DNA BINDING DOMAIN; TI DOMAIN; (RAT BRAIN) ID COUP TRANSCRIPTION FACTOR; MESSENGER-RNA; DNA-POLYMERASE; SUPERFAMILY; FAMILY; EXPRESSION; CLONING; MEMBER; CELLS AB We have developed a PCR-based method to detect, display and directly sequence multiple members of the nuclear hormone receptor (NHR) gene family. Our approach employs the basic concepts of RNA fingerprinting (Welsh et al. (1992) Nucleic Acids Res. 20, 4965-4970; Stone, B. and Wharton, W. (1994) Nucleic Acids Res. 22, 2612-2618) and differential display PCR (Liang, P. and Pardee, A.B. (1992) Science 257, 967-971), with modifications. In contrast to the previous methods, two conserved regions within the gene family were targeted to derive primers for PCR amplification. One of the conserved sites was used to deduce primers for cDNA synthesis. We believe that this strategy led to increased specificity. The use of degenerate primers with low redundancy in both reverse transcription and PCR steps also contributed to enhanced signal-to-noise ratio. The ability to directly sequence the amplified fragments constitutes a vast improvement over the previous methods. This method permitted the successful identification and simultaneous display of six different NHR genes, which included the previously unreported rat homolog of COUP-TFI and a recently described orphan receptor. We believe that this approach provides a convenient and rapid screening method for detecting and characterizing members of a gene family. RP YOSHIKAWA, T (reprint author), NIMH,CLIN NEUROGENET BRANCH,GENE MAPPING & EXPRESS UNIT,BLDG 10,RM 3N218,BETHESDA,MD 20892, USA. NR 26 TC 8 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD OCT 17 PY 1995 VL 1264 IS 1 BP 63 EP 71 DI 10.1016/0167-4781(95)90106-F PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TB191 UT WOS:A1995TB19100013 PM 7578258 ER PT J AU VOORHEES, P DEIGNAN, E VANDONSELAAR, E HUMPHREY, J MARKS, MS PETERS, PJ BONIFACINO, JS AF VOORHEES, P DEIGNAN, E VANDONSELAAR, E HUMPHREY, J MARKS, MS PETERS, PJ BONIFACINO, JS TI AN ACIDIC SEQUENCE WITHIN THE CYTOPLASMIC DOMAIN OF FURIN FUNCTIONS AS A DETERMINANT OF TRANS-GOLGI NETWORK LOCALIZATION AND INTERNALIZATION FROM THE CELL-SURFACE SO EMBO JOURNAL LA English DT Article DE CYTOPLASMIC DOMAINS; FURIN; TRANS-GOLGI NETWORK; LOCALIZATION ID MANNOSE 6-PHOSPHATE RECEPTOR; FACTOR-II RECEPTOR; CASEIN KINASE-II; PROPROTEIN PROCESSING ENZYME; DENSITY-LIPOPROTEIN RECEPTOR; KEX1 GENE ENCODES; MEMBRANE-PROTEIN; YEAST KEX2; INTERLEUKIN-2 RECEPTOR; CARBOXYL-TERMINUS AB The mammalian endopeptidase, furin, is predominantly localized to the trans-Golgi network (TGN) at steady state. The localization of furin to this compartment seems to be the result of a dynamic process in which the protein undergoes cycling between the TGN and the plasma membrane. Both TGN localization and internalization from the plasma membrane are mediated by targeting information contained within the cytoplasmic domain of furin. Here, we report the results of a mutagenesis analysis aimed at identifying the source(s) of targeting information within the furin cytoplasmic domain. Our studies show that there are at least two cytoplasmic determinants that contribute to the steady-state localization and trafficking of furin. The first determinant corresponds to a canonical tyrosine-based motif, YKGL (residues 758-761), that functions mainly as an internalization signal. The second determinant consists of a strongly hydrophilic sequence (residues 766-783) that contains a large cluster of acidic residues (E and D) and is devoid of any tyrosine-based or di-leucine-based motifs. This second determinant is capable of conferring localization to the TGN as well as mediating internalization from the plasma membrane3. Thus, these observations establish the existence of a novel, autonomous determinant distinct from sorting signals described previously. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. UNIV UTRECHT,SCH MED,DEPT CELL BIOL,3584 CX UTRECHT,NETHERLANDS. UNIV UTRECHT,SCH MED,BIOMEMBRANE INST,3584 CX UTRECHT,NETHERLANDS. OI Marks, Michael/0000-0001-7435-7262 NR 80 TC 185 Z9 186 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD OCT 16 PY 1995 VL 14 IS 20 BP 4961 EP 4975 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TC470 UT WOS:A1995TC47000007 PM 7588625 ER PT J AU ZUBER, M HOOVER, TA DERTZBAUGH, MT COURT, DL AF ZUBER, M HOOVER, TA DERTZBAUGH, MT COURT, DL TI ANALYSIS OF THE DNAK MOLECULAR CHAPERONE SYSTEM OF FRANCISELLA-TULARENSIS SO GENE LA English DT Article DE TULAREMIA; CAPSULE; VIRULENCE; DNAJ; GRPE; HEAT-SHOCK PROTEIN ID LIVE VACCINE STRAIN; HEAT-SHOCK GENE; POLYMORPHONUCLEAR LEUKOCYTES; MACROPHAGES; SEQUENCE; IMMUNITY AB We have cloned the Francisella tularensis (Ft) grpE-dnaK-dnaJ heat-shock genes which are organized in that order. These genes allow heterologous genetic complementation of each respective mutant strain of Escherichia coli (Ec) for bacteriophage lambda growth. The nucleotide sequences of the Ft grpE-dnaK-dnaJ genes and the deduced amino-acid sequences share significant homologies with their respective Ec counterparts. The Ft DnaK and DnaJ proteins crossreact with polyclonal antibodies raised against the respective Ec proteins, The grpE-dnaK-dnaJ genes of Ft are organized in a fashion that is more characteristic of Gram(+) bacteria. C1 USA, MED RES INST INFECT DIS, DIV BACTERIOL, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, DIV TOXICOL, FREDERICK, MD 21702 USA. RP NCI, FREDERICK CANC RES & DEV CTR, CHROMOSOME BIOL LAB, MOLEC CONTROL & GENET SECT, FREDERICK, MD 21702 USA. NR 20 TC 21 Z9 24 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 EI 1879-0038 J9 GENE JI Gene PD OCT 16 PY 1995 VL 164 IS 1 BP 149 EP 152 DI 10.1016/0378-1119(95)00489-S PG 4 WC Genetics & Heredity SC Genetics & Heredity GA TC459 UT WOS:A1995TC45900027 PM 7590305 ER PT J AU MCCUTCHEN, CW AF MCCUTCHEN, CW TI STUDY SECTIONS - NIHS KANGAROO POLITBUROS SO SCIENTIST LA English DT Editorial Material AB NIH study sections are not unlike the former Soviet Union's Politburo, wlth a clique of influential scientists holding power over the granting process, charges Charles W. McCutchen, a physicist with the National Institute of Diabetes and Digestive and Kidney Diseases. RP MCCUTCHEN, CW (reprint author), NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SCIENTIST INC PI PHILADELPHIA PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104 SN 0890-3670 J9 SCIENTIST JI Scientist PD OCT 16 PY 1995 VL 9 IS 20 BP 13 EP 13 PG 1 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA TA174 UT WOS:A1995TA17400009 ER PT J AU CAPLAN, LS HELZLSOUER, KJ SHAPIRO, S FREEDMAN, LS COATES, RJ EDWARDS, BK AF CAPLAN, LS HELZLSOUER, KJ SHAPIRO, S FREEDMAN, LS COATES, RJ EDWARDS, BK TI SYSTEM DELAY IN BREAST-CANCER IN WHITES AND BLACKS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE BREAST NEOPLASMS; DELIVERY OF HEALTH CARE; DIAGNOSIS; ETHNIC GROUPS; PRIMARY HEALTH CARE; RACIAL STOCKS; SURVIVAL; TIME FACTORS ID WOMEN AB Survival differences have been noted between black women and white women with breast cancer. It is hypothesized that a prolonged interval between initial medical consultation and establishment of a diagnosis (system delay), resulting in a more advanced stage of disease at diagnosis, might explain part of this survival difference. This study was performed to determine whether system delay differs between black and white breast cancer patients, and to examine predictors of delay in blacks and whites. The study population consisted of 996 female breast cancer patients from the National Cancer Institute's Black/White Cancer Survival Study, a cohort study carried out in 1985-1986 in the metropolitan areas of Atlanta, Georgia, New Orleans, Louisiana, and San Francisco/Oakland, California. The median system delay was slightly longer for blacks than for whites-2.7 weeks versus 2.1 weeks-but this difference was not statistically significant. Having a palpable lump at diagnosis was associated with reduced system delay in both races, while use of a public clinic increased system delay for blacks. Older women were less likely to be subject to longer system delay than younger women, and this effect was somewhat more pronounced in whites. Survival differences between blacks and whites are probably not due to differences in system delay. However, many women had delays of at least 3 months. Given that younger age and the absence of a palpable lump were the factors most predictive of significant system delay, interventions should be targeted specifically toward reducing system delay in younger women who present without the classical painless lump. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DIV HLTH SERV RES,DEPT HLTH POLICY & MANAGEMENT,BALTIMORE,MD. NCI,DIV BIOMETRY,HLTH SURVEILLANCE RES BRANCH,BETHESDA,MD. EMORY UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,ATLANTA,GA. NCI,DIV CANC PREVENT & CONTROL,OFF ASSOCIATE DIRECTOR,BETHESDA,MD 20892. SUNY STONY BROOK,SCH MED,DEPT PREVENT MED,DIV EPIDEMIOL,STONY BROOK,NY 11794. NR 15 TC 50 Z9 50 U1 2 U2 4 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 OCT 15 PY 1995 VL 142 IS 8 BP 804 EP 812 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA TA756 UT WOS:A1995TA75600004 PM 7572956 ER PT J AU BRUCKERDAVIS, F SKARULIS, MC GRACE, MB BENICHOU, J HAUSER, P WIGGS, E WEINTRAUB, BD AF BRUCKERDAVIS, F SKARULIS, MC GRACE, MB BENICHOU, J HAUSER, P WIGGS, E WEINTRAUB, BD TI GENETIC AND CLINICAL-FEATURES OF 42 KINDREDS WITH RESISTANCE TO THYROID-HORMONE - THE NATIONAL-INSTITUTES-OF-HEALTH PROSPECTIVE-STUDY SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE THYROID HORMONES; THYROID HORMONE RESISTANCE SYNDROME; HEREDITARY DISEASES; PHENOTYPE; RECEPTORS, THYROID HORMONE ID RECEPTOR-BETA GENE; GENERALIZED RESISTANCE; CONGENITAL HYPOTHYROIDISM; INAPPROPRIATE SECRETION; BINDING GLOBULIN; LIGAND-BINDING; TRIIODOTHYRONINE; HYPERTHYROIDISM; MUTATIONS; THYROXINE AB Objective: To determine the genetic and clinical features of resistance to thyroid hormone in a study from a single institution. Design: Prospective, controlled study. Setting: National Institutes of Health. Patients: 104 patients with resistance to thyroid hormone from 42 kindreds and 114 unaffected relatives sharing the patients' environmental and genetic backgrounds. Measurements: Thyroid, cardiovascular, psychometric, hearing, speech, and growth testing; thyroid tests done at baseline and after TSH-releasing hormone stimulation; and DNA analysis for detection of mutations in the thyroid hormone receptor beta (TR beta) gene (exons 9 and 10). Assessment of tissue-specific compensation for resistance. Results: Inheritance was autosomal dominant in 22 families, sporadic in 14 families, and unknown in 6 families. We found mutations in 25 kindreds (64 patients); 16 mutations were in exon 9 and 9 were in exon 10 of the TR beta gene. In persons with resistance to thyroid hormone, we measured the increased incidence of goiter (65%), attention-deficit hyperactivity disorder (60%), IQ less than 85 (38%), speech impediment (35%), and short stature (18%). We also described new clinical features, such as frequent ear, nose, and throat infections (56%); low weight-for-height in children (32%); hearing loss (21%); and cardiac abnormalities (18%). Genotype, age, whether the mother had resistance to thyroid hormone, and sex influenced the phenotype. Tissue resistance varied from kindred to kindred and involved, in decreasing order, the pituitary gland, the brain, the bone, the liver, and the heart. Conclusions: This study underscores the incidence of classic features of resistance to thyroid hormone, describes new clinical characteristics of this condition for the first time, and stresses the heterogeneity of the phenotype. C1 NIDDK,MOLEC & CELLULAR ENDOCRINE BRANCH,BETHESDA,MD 20892. NCI,BETHESDA,MD 20892. NR 90 TC 149 Z9 156 U1 0 U2 3 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 OCT 15 PY 1995 VL 123 IS 8 BP 572 EP 583 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA RY828 UT WOS:A1995RY82800002 PM 7677297 ER PT J AU GILON, P OBIE, JF BIAN, XP BIRD, GS PUTNEY, JW AF GILON, P OBIE, JF BIAN, XP BIRD, GS PUTNEY, JW TI ROLE OF CYCLIC-GMP IN THE CONTROL OF CAPACITATIVE CA2+ ENTRY IN RAT PANCREATIC ACINAR-CELLS SO BIOCHEMICAL JOURNAL LA English DT Article ID INOSITOL TRISPHOSPHATE; INTRACELLULAR CALCIUM; PLASMA-MEMBRANE; NITRIC-OXIDE; STORES; DEPLETION; MECHANISM; ACTIVATION; MESSENGER; RELEASE AB We have investigated the possible roles of cyclic GMP (cGMP) in initiating or regulating capacitative Ca2+ entry in rat pancreatic acinar cells. In medium containing 1.8 mM external Ca2+, thapsigargin activated Ca2+ entry and slightly but significantly increased intracellular cGMP concentration. This rise in ccMP levels was prevented by pretreating the cells with the guanylate cyclase inhibitor, LY-83583, or by omitting Ca2+ during stimulation by thapsigargin or methacholine. LY-83583 and N-G-nitro-L-arginine (L-NA, an inhibitor of NO synthase) both had a small inhibitory effect on Ca2+ entry when they were added after thapsigargin in Ca2+-containing medium, and they reduced by 32 and 48% respectively the thapsigargin-induced capacitative Ca2+ entry when added to the cells during a 20 min preincubation period. However, neither dibutyryl cGMP (Bt(2)cGMP) nor sodium nitroprusside, an NO mimic, affected either basal intracellular Ca2+ concentration [Ca2+](i) or thapsigargin-induced capacitative Ca2+ entry. Further, the inhibitory effects observed after preincubation with LY-83583 or L-NA could not be prevented by preincubation with Bt(2)cGMP, nor could they be reversed by adding Bt(2)cGMP, 8-bromo-cGMP or sodium nitroprusside acutely after activation of capacitative Ca2+ entry by thapsigargin. Finally, pretreatment of cells with LY-83583 or L-NA did not affect Ca2+ signalling in response to I mu M methacholine, including the pattern of [Ca2+](i) oscillations. In conclusion, in pancreatic, acinar cells, the rise in cellular cGMP levels appears to depend on, rather than cause, the increase in [Ca2+](i) with agonist stimulation. C1 NIEHS,CELLULAR & MOLEC PHARMACOL LAB,CALCIUM REGULAT SECT,RES TRIANGLE PK,NC 27709. NR 34 TC 38 Z9 38 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD OCT 15 PY 1995 VL 311 BP 649 EP 656 PN 2 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TA258 UT WOS:A1995TA25800042 PM 7487909 ER PT J AU OSHAUGHNESSY, JA VENZON, DJ GOSSARD, M NOONE, MH DENICOFF, A TOLCHER, A DANFORTH, D JACOBSON, J KEEGAN, P MILLER, L CHOW, C GOLDSPIEL, B COWAN, KH AF OSHAUGHNESSY, JA VENZON, DJ GOSSARD, M NOONE, MH DENICOFF, A TOLCHER, A DANFORTH, D JACOBSON, J KEEGAN, P MILLER, L CHOW, C GOLDSPIEL, B COWAN, KH TI A PHASE-I STUDY OF SEQUENTIAL VERSUS CONCURRENT INTERLEUKIN-3 AND GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR IN ADVANCED BREAST-CANCER PATIENTS TREATED WITH FLAC (5-FLUOROURACIL, LEUCOVORIN, DOXORUBICIN, CYCLOPHOSPHAMIDE) CHEMOTHERAPY SO BLOOD LA English DT Article ID RECOMBINANT HUMAN INTERLEUKIN-3; TUMOR-NECROSIS-FACTOR; HEMATOPOIETIC GROWTH-FACTORS; HIGH-DOSE CHEMOTHERAPY; PROGENITOR CELLS; OVARIAN-CANCER; FACTOR-ALPHA; PRIMATES; THERAPY; INVIVO AB Cumulative thrombocytopenia is a dose-limiting toxicity of dose-intensive chemotherapy for advanced breast cancer. In this phase I study, we have studied the hematologic toxicity associated with sequential interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF; molgramostim) administration after multiple cycles of FLAC (5-fluorouracil, leucovorin, doxorubicin, cyclophosphamide) chemotherapy compared with that after concurrent cytokine administration or to each cytokine administered alone. Ninety-three patients with advanced breast cancer were treated with five cycles of FLAC chemotherapy and either IL-3 alone, GM-CSF alone, sequential IL-3 and GM-CSF administered by schedule A (5 days of IL-3 followed by 10 days of GM-CSF) or schedule B (9 days of IL-3 followed by 6 days of GM-CSF), or concurrent administration of IL-3 and GMCSF for 15 days. Cohorts of patients were treated with one of four dose levels of IL-3 (1, 2.5, 5, and 10 mu g/kg) administered subcutaneously for each schedule of cytokine administration. The GM-CSF dose in all schedules was 5 mu g/kg/day. Sequential IL-3 and GM-CSF (schedule B) was associated with higher platelet nadirs, shorter durations of platelet counts less than 50,000/mu L, and the need for fewer platelet transfusions over five cycles of FLAC chemotherapy compared with concurrent cytokines, sequential IL-3 and GM-CSF schedule A, and GM-CSF alone. Concurrent IL-3 and GM-CSF was associated with unexpected platelet toxicity. The duration of granulocytopenia after FLAC chemotherapy was significantly worse with IL-3 alone compared with each of the GM-CSF-containing cytokine regimens. Although no cycle 1 maximum tolerated dose for IL-3 was defined in this study, 5 mu g/kg was well tolerated over multiple cycles of therapy and is recommended for future studies. The data from this phase I study suggest that sequential IL-3 and GMCSF with IL-3 administered for 9 days before beginning GM-CSF may be superior to shorter durations of IL-3 administered sequentially with GM-CSF, to concurrent IL-3 and GM-CSF, and to either colony-stimulating factor alone in ameliorating the cumulative hematologic toxicity associated with multiple cycles of FLAC chemotherapy. Additional studies of sequential IL-3 and GM-CSF are warranted. This is a US government work. There are no restrictions on its use. C1 NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NCI,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892. NCI,DEPT RADIOL,BETHESDA,MD 20892. NCI,DEPT PHARM,BETHESDA,MD 20892. RP OSHAUGHNESSY, JA (reprint author), NCI,MED BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM 12N226,BETHESDA,MD 20892, USA. RI Venzon, David/B-3078-2008 NR 45 TC 16 Z9 16 U1 0 U2 1 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 OCT 15 PY 1995 VL 86 IS 8 BP 2913 EP 2921 PG 9 WC Hematology SC Hematology GA RZ071 UT WOS:A1995RZ07100006 PM 7579383 ER PT J AU SINHA, R ROTHMAN, N BROWN, ED SALMON, CP KNIZE, MG SWANSON, CA ROSSI, SC MARK, SD LEVANDER, OA FELTON, JS AF SINHA, R ROTHMAN, N BROWN, ED SALMON, CP KNIZE, MG SWANSON, CA ROSSI, SC MARK, SD LEVANDER, OA FELTON, JS TI HIGH-CONCENTRATIONS OF THE CARCINOGEN 2-AMINO-1-METHYL-6-PHENYLIMIDAZO-[4,5-B]PYRIDINE (PHIP) OCCUR IN CHICKEN BUT ARE DEPENDENT ON THE COOKING METHOD SO CANCER RESEARCH LA English DT Note ID COLON CANCER; FOOD; AMINES; RISK; MEAT AB Heterocyclic aromatic amines (HAAs) are mutagenic and carcinogenic compounds found in meats cooked at high temperatures. Although chicken is consumed in large quantities in the United States, there is little information on its HAA content. The objective of this study was to measure the five predominant HAAs (IQ, MeIQ, MeIQx, DiMeIQx, and PhIP) in chicken cooked by various methods to different degrees of doneness. Chicken breasts were panfried, oven-broiled, or grilled/barbecued. Whole thickens were roasted or stewed. Skinless, boneless chicken breasts were cooked to three degrees of doneness: just until done, well done, or very well done. High levels of PNP (ranging from 12 to 480 ng/g cooked meat) were found in chicken breasts when panfried, oven-broiled, and grilled/barbecued but not in whole roasted or stewed thicken. PhIP concentration increased in skinless, boneless chicken breast with longer cooking time, higher internal temperature, and greater degree of surface browning. PhIP concentration was also high in chicken breasts cooked with Skin and bones. MeIQx and DiMeIQx levels increased with the degree of doneness, whereas IQ and MeIQ were not detectable in any of these chicken samples. Certain cooking methods produce PhIP, a known colon and breast carcinogen in rodents and possibly a human carcinogen, at substantially higher levels in chicken than has been reported previously in red meat. C1 USDA,BELTSVILLE HUMAN NUTR RES CTR,NUTR REQUIREMENTS & FUNCT LAB,BELTSVILLE,MD 20705. LAWRENCE LIVERMORE NATL LAB,BIOL & BIOTECHNOL RES PROGRAM,LIVERMORE,CA 94550. NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,ROCKVILLE,MD 20892. RP SINHA, R (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,EXECUT PLAZA N,ROOM 443,6130 EXECUT BLVD,ROCKVILLE,MD 20892, USA. RI Sinha, Rashmi/G-7446-2015 OI Sinha, Rashmi/0000-0002-2466-7462 FU NCI NIH HHS [CA55861] NR 25 TC 219 Z9 222 U1 0 U2 1 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 OCT 15 PY 1995 VL 55 IS 20 BP 4516 EP 4519 PG 4 WC Oncology SC Oncology GA RZ069 UT WOS:A1995RZ06900005 PM 7553619 ER PT J AU KISHIDA, T STACKHOUSE, TM CHEN, F LERMAN, MI ZBAR, B AF KISHIDA, T STACKHOUSE, TM CHEN, F LERMAN, MI ZBAR, B TI CELLULAR PROTEINS THAT BIND THE VON HIPPEL-LINDAU DISEASE GENE-PRODUCT - MAPPING OF BINDING DOMAINS AND THE EFFECT OF MISSENSE MUTATIONS SO CANCER RESEARCH LA English DT Note AB The von Hippel-Lindau disease (VHL) gene is a novel tumor suppressor gene that plays a role in the pathogenesis of renal cell carcinomas and hemangioblastomas of the central nervous system, To begin an evaluation of the biological functions of the VHL gene product (pVHL), we prepared bacterial fusion protein between glutathione S-transferase and wild-type or mutant pVHLs, The fusion proteins were used to identify cellular proteins that bind to pVHL in vitro, Monkey kidney cells transfected with wild-type or mutant VHL cDNAs were used to identify cellular proteins that bind to pVHL in vivo. Wild-type pVHL consistently bound two cellular proteins with apparent molecular masses of 10 and 14 kilodaltons that were designated p10 and p14, respectively, Mapping studies with a panel of VHL deletion mutant proteins demonstrated that p10 and p14 bound to a 32-amino acid peptide located in the carboxy terminal portion of pVHL. Missense mutations located within this 32-amino acid peptide abrogated the ability of the VHL protein to bind p10 and p14. Of 67 VHL families with identified germline mutations, 42 families had mutations predicted to affect the p10/p14-binding region, Maintenance of the integrity of the p10/p14-binding region appears to be essential for cellular growth regulation by pVHL. C1 NCI,FREDERICK CANC RES FACIL & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES FACIL & DEV CTR,SCI APPLICAT INT CORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NR 20 TC 123 Z9 123 U1 0 U2 4 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 OCT 15 PY 1995 VL 55 IS 20 BP 4544 EP 4548 PG 5 WC Oncology SC Oncology GA RZ069 UT WOS:A1995RZ06900011 PM 7553625 ER PT J AU GUDAS, JM NGUYEN, H LI, T COWAN, KH AF GUDAS, JM NGUYEN, H LI, T COWAN, KH TI HORMONE-DEPENDENT REGULATION OF BRCA1 IN HUMAN BREAST-CANCER CELLS SO CANCER RESEARCH LA English DT Note ID GROWTH-FACTORS; MCF-7; CDNA; LINE AB BRCA1 mRNA and protein levels are regulated by the steroid hormones estrogen and progesterone in human breast cancer cells, BRCA1 mRNA and protein levels were significantly decreased in estrogen-depleted MCF-7 and BT20T cells and increased again after stimulation with beta-estradiol, The increase in BRCA1 expression upon stimulation with estrogen was not coordinated with the early induction of the estrogen-dependent pS2 gene but closely paralleled the delayed increase in the S-phase dependent marker cyclin A. T47-D cells deprived of steroid hormones and subsequently stimulated with progesterone also showed a delayed increase in BRCA1 mRNA expression, However, no change in BRCA1 protein was detected in these cells, When considered together, the data suggest that steroid hormones may affect BRCA1 expression indirectly by altering the proliferative status of the cells rather than acting directly on DNA sequences in the BRCA1 gene itself. RP GUDAS, JM (reprint author), NCI,DIV CANC TREATMENT,MED BRANCH,MED BREAST CANC SECT,BLDG 10,ROOM12N226,BETHESDA,MD 20892, USA. NR 17 TC 167 Z9 168 U1 0 U2 1 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 OCT 15 PY 1995 VL 55 IS 20 BP 4561 EP 4565 PG 5 WC Oncology SC Oncology GA RZ069 UT WOS:A1995RZ06900015 PM 7553629 ER PT J AU BERG, SL GERSON, SL GODWIN, K COLE, DE LIU, L BALIS, FM AF BERG, SL GERSON, SL GODWIN, K COLE, DE LIU, L BALIS, FM TI PLASMA AND CEREBROSPINAL-FLUID PHARMACOKINETICS OF O-6-BENZYLGUANINE AND TIME-COURSE OF PERIPHERAL-BLOOD MONONUCLEAR CELL O-6-METHYLGUANINE-DNA METHYLTRANSFERASE INHIBITION IN THE NONHUMAN PRIMATE SO CANCER RESEARCH LA English DT Article ID IN-VITRO; DNA; 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA; ALKYLTRANSFERASE; O6-BENZYLGUANINE; SENSITIVITY AB O-6-Benzylguanine (O(6)BG) enhances the cytotoxicity of the nitrosoureas by irreversibly binding and inhibiting the DNA repair enzyme O-6-methylguanine-DNA methyltransferase (MGMT). The plasma and cerebrospinal fluid (CSF) pharmacokinetics of O(6)BG and its active metabolite, O-6-benzyl-8-oxoguanine, were studied in a nonhuman primate model after 200 mg/m(2) had been injected i.v. The parent drug and the metabolite were measured with a reverse-phase HPLC assay, A pharmacokinetic model incorporating separate compartments for O(6)BG and the O-6-benzyl-8-oxoguanine metabolite, first-order conversion of O(6)BG to the metabolite, and additional first-order elimination rate constants for each compound, was simultaneously fitted to the parent drug and metabolite plasma concentration time data. Elimination of O(6)BG from plasma was rapid; it had a half-life of 1.6 h and a clearance of 68 ml/min/m(2). On the basis of the pharmacokinetic model, essentially all of the O(6)BG was converted to O-6-benzyl-8-osoguanine. The plasma pharmacokinetic profile of the metabolite differed considerably from that the parent drug. The half-life (14 h) was 10-fold longer and the area under the curve (2420 mu M/h) was 11-fold higher than that of O(6)BG (212 mu M/h). The clearance rate of O-6-benzyl-8-oxoguanine was 6.4 ml/min/m(2). The CSF:plasma ratio was 4.3% for O(6)BG and 36% for O-6-benzyl-8-oxoguanine, and the metabolite area under the curve was 90-fold higher than that of O(6)BG in CSF. The excellent CSF penetration of the active metabolite provides a rationale for the use of O(6)BG as a chemosensitizing agent for brain tumors, We also studied the duration of MGMT inhibition in peripheral blood mononuclear cells. By 2 h after a 200 mg/m(2) dose of O(6)BG, >98% of MGMT activity was suppressed, and >95% suppression of enzyme activity persisted at 18 and 48 h after the dose. By 2 weeks after the treatment, MGMT levels had returned to baseline, Persistent high concentrations of the active metabolite appear to provide a pharmacological explanation for the prolonged suppression of MGMT activity. C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. CASE WESTERN RESERVE UNIV,SCH MED,CANC RES CTR,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,SCH MED,DEPT MED,CLEVELAND,OH 44106. FU NCI NIH HHS [UOI CA57725, R0I CA63193, P0I CA 51183] NR 20 TC 24 Z9 24 U1 0 U2 1 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 OCT 15 PY 1995 VL 55 IS 20 BP 4606 EP 4610 PG 5 WC Oncology SC Oncology GA RZ069 UT WOS:A1995RZ06900023 PM 7553637 ER PT J AU BLAGOSKLONNY, MV SCHULTE, TW NGUYEN, P MIMNAUGH, EG TREPEL, J NECKERS, L AF BLAGOSKLONNY, MV SCHULTE, TW NGUYEN, P MIMNAUGH, EG TREPEL, J NECKERS, L TI TAXOL INDUCTION OF P21(WAF1) AND P53 REQUIRES C-RAF-1 SO CANCER RESEARCH LA English DT Article ID TYROSINE PHOSPHORYLATION; LEUKEMIA-CELLS; PROTEIN-KINASE; TUBULIN; LIPOPOLYSACCHARIDE; MECHANISM; LINES AB Taxol stabilizes microtubules, prevents tubulin depolymerization, and promotes tubulin bundling and is one of the most effective drugs for the treatment of metastatic breast and ovarian cancer. Although its interaction with tubulin has been well characterized, the mechanism by which taxol induces growth arrest and cytoxicity is not well understood. Herein, me show that taxol induced dose- and time-dependent accumulation of the cyclin inhibitor p21(WAF1) in both p53 wild-type and p53-null cells, although the degree of induction was greater in cells expressing wild-type p53. In MCM cells, wild-type p53 protein was also induced after taxol treatment, and this induction was mediated primarily by increased protein stability. Taxol induced both p21(WAF1) and wild-type p53 optimally in MCF7 cells after 20-24-h exposure with an EC(50)(3) of 5 nM. In p53-null PC3M cells, p21(WAF1) was similarly induced after 24-h exposure to taxol. Coincident with these biochemical effects, taxol altered the electrophoretic mobility of c-raf-1 and stimulated mitogen activated protein kinase. Previous depletion of c-raf-1 inhibited both the p21(WAF1)- and p53-inducing properties of taxol, as well as the activation of MAP kinase. These data suggest that induction of p21(WAF1) by taxol requires c-raf-1 activity, but that it is not strictly dependent on wild-type p53. Furthermore, the ability of taxol to bath induce wild-type p53 in MCF7 cells and activate MAP kinase is also dependent on c-raf-1 expression. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. NR 47 TC 214 Z9 220 U1 1 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 OCT 15 PY 1995 VL 55 IS 20 BP 4623 EP 4626 PG 4 WC Oncology SC Oncology GA RZ069 UT WOS:A1995RZ06900025 PM 7553639 ER PT J AU ZHANG, J CUI, P GLATFELTER, AA CUMMINGS, LM MELTZER, PS TRENT, JM AF ZHANG, J CUI, P GLATFELTER, AA CUMMINGS, LM MELTZER, PS TRENT, JM TI MICRODISSECTION BASED CLONING OF A TRANSLOCATION BREAKPOINT IN A HUMAN-MALIGNANT MELANOMA SO CANCER RESEARCH LA English DT Article ID TUMOR-SUPPRESSOR GENES; CHROMOSOME MICRODISSECTION; DNA; PROBES; IDENTIFICATION; AMPLIFICATION; LEUKEMIA; REGION; FUSION; CELLS AB Chromosome translocations in human malignancies have identified the genomic location of several important growth-regulatory sequences (e.g., cellular oncogenes and suppressor genes). Melanomas are characterized by recurring chromosome alterations, including deletion or translocations of the long arm of chromosome 6 (6q). This report details our efforts to clone the t(1;6)(q21;q14) breakpoint in a malignant melanoma to further our understanding of the biology of these tumors. The strategy utilized combined microdissection of the translocation chromosome, development and characterization of a DNA microclone library, isolation of cosmids and YACs from the breakpoint region, ordering of clones by two-color metaphase/interphase fluorescence in situ hybridization, and finally, identification of a YAC spanning the translocation breakpoint. By analogy to other tumor systems, molecular examination of the chromosome 6 breakpoint may provide insight into the pathobiology of this important neoplasm. C1 NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,BETHESDA,MD 20892. NR 36 TC 16 Z9 16 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 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1995 VL 55 IS 20 BP 4640 EP 4645 PG 6 WC Oncology SC Oncology GA RZ069 UT WOS:A1995RZ06900028 PM 7553642 ER PT J AU ARAI, AE KASSERRA, CE BALABAN, RS AF ARAI, AE KASSERRA, CE BALABAN, RS TI NONDESTRUCTIVE EVALUATION OF CARDIAC METABOLISM IN-VIVO USING OPTICAL AND NMR-SPECTROSCOPY SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,CARDIAC ENERGET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 309 EP 309 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000306 ER PT J AU SHAMBUREK, RD ZECH, LA TALLEY, G RONAN, R HEDRICK, C CASTELLANI, L BREWER, HB AF SHAMBUREK, RD ZECH, LA TALLEY, G RONAN, R HEDRICK, C CASTELLANI, L BREWER, HB TI APOE AND APOA-II METABOLISM IN TRANSGENIC MICE OVEREXPRESSING APOA-II SO CIRCULATION LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA. NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 491 EP 491 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000492 ER PT J AU FREAY, AD KORACH, KS LUBAHN, D RUBANYI, GM AF FREAY, AD KORACH, KS LUBAHN, D RUBANYI, GM TI DECREASED ENDOTHELIAL NITRIC-OXIDE PRODUCTION AND INCREASED SMOOTH-MUSCLE REACTIVITY TO KCL IN AORTAE OF ESTROGEN-RECEPTOR KNOCKOUT MICE SO CIRCULATION LA English DT Meeting Abstract C1 BERLEX BIOSCI,DEPT CARDIOVASC,RICHMOND,CA. NIEHS,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709. UNIV MISSOURI,DEPT BIOCHEM,COLUMBIA,MO. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 500 EP 500 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000496 ER PT J AU PAULY, R BILATO, C MONTICONE, R CURTO, K GLOE, T CAPOGROSSI, M CROW, M AF PAULY, R BILATO, C MONTICONE, R CURTO, K GLOE, T CAPOGROSSI, M CROW, M TI THE INHIBITION OF SMOOTH-MUSCLE CELL-MIGRATION BY A PEPTIDE ANTAGONIST OF THE VITRONECTIN RECEPTOR IS REVERSED BY EXPRESSION OF ACTIVATED CALCIUM CALMODULIN-DEPENDENT PROTEIN-KINASE-II SO CIRCULATION LA English DT Meeting Abstract C1 NIA,LCS,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 520 EP 520 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000516 ER PT J AU GLOE, TR PASSANITI, A CRYSTAL, RG CAPOGROSSI, MC AF GLOE, TR PASSANITI, A CRYSTAL, RG CAPOGROSSI, MC TI ADENOVIRUS-MEDIATED BASIC FIBROBLAST GROWTH-FACTOR EXPRESSION INDUCES ENDOTHELIAL-CELL DIFFERENTIATION BUT NOT PROLIFERATION SO CIRCULATION LA English DT Meeting Abstract C1 CORNELL UNIV,MED CTR,NEW YORK HOSP,NEW YORK,NY 10021. NIA,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 529 EP 529 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000525 ER PT J AU TZOUNOPOULOS, T DURREL, S GUY, R ADELMAN, JP MAYLIE, J AF TZOUNOPOULOS, T DURREL, S GUY, R ADELMAN, JP MAYLIE, J TI MIN K CHANNELS ARE FORMED BY THE COASSEMBLY OF AT LEAST 12 MIN K MONOMERS SO CIRCULATION LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 538 EP 538 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000533 ER PT J AU LAI, WW LIPSHULTZ, S EASLEY, K BRICKER, JT STARC, T COLAN, S MOODIE, D KAPLAN, S AF LAI, WW LIPSHULTZ, S EASLEY, K BRICKER, JT STARC, T COLAN, S MOODIE, D KAPLAN, S TI PREVALENCE OF CONGENITAL CARDIOVASCULAR MALFORMATION (CCM) IN CHILDREN OF HIV-INFECTED MOTHERS - THE PROSPECTIVE P2C2 STUDY SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 591 EP 591 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000586 ER PT J AU FANANAPAZIR, L MCAREAVEY, D AF FANANAPAZIR, L MCAREAVEY, D TI LONG-TERM RESULTS OF DUAL-CHAMBER (DDD) PACING IN PEDIATRIC-PATIENTS WITH OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY SO CIRCULATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 592 EP 592 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000593 ER PT J AU BENJAMIN, EJ LEVY, D DAGOSTINO, RB BELANGER, AJ WOLF, PA AF BENJAMIN, EJ LEVY, D DAGOSTINO, RB BELANGER, AJ WOLF, PA TI PREDICTORS OF MORTALITY FOLLOWING THE ONSET OF ATRIAL-FIBRILLATION SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. FRAMINGHAM STUDY,FRAMINGHAM,MA. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 663 EP 663 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000658 ER PT J AU CORTI, MC GURALNIK, JM SALIVE, ME FERRUCCI, L PAHOR, M WALLACE, RB HENNEKENS, CH AF CORTI, MC GURALNIK, JM SALIVE, ME FERRUCCI, L PAHOR, M WALLACE, RB HENNEKENS, CH TI SERUM IRON AND CORONARY HEART-DISEASE (CHD) MORTALITY IN OLDER PERSONS SO CIRCULATION LA English DT Meeting Abstract C1 NIA,EDB PROGRAM,BETHESDA,MD 20892. UNIV IOWA,IOWA CITY,IA. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 721 EP 721 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000715 ER PT J AU GUETTA, E GUETTA, V EPSTEIN, SE AF GUETTA, E GUETTA, V EPSTEIN, SE TI CYTOMEGALOVIRUS INTERACTION WITH MONOCYTES, ENDOTHELIAL-CELLS, AND OXIDIZED LOW-DENSITY-LIPOPROTEIN - A POSSIBLE MODEL FOR VIRAL REACTIVATION AND ATHEROSCLEROSIS DEVELOPMENT SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 768 EP 768 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000762 ER PT J AU ZHOU, YF GUERRA, E YU, ZX FINKEL, T EPSTEIN, SE AF ZHOU, YF GUERRA, E YU, ZX FINKEL, T EPSTEIN, SE TI HUMAN CYTOMEGALOVIRUS, THROUGH ITS IMMEDIATE-EARLY GENE-PRODUCT IE72, DIRECTLY ACTIVATES TRANSCRIPTION OF THE SCAVENGER RECEPTOR GENE IN HUMAN AORTIC SMOOTH-MUSCLE CELLS SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 769 EP 769 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000769 ER PT J AU GUETTA, V CANNON, RO AF GUETTA, V CANNON, RO TI THE EFFECT OF THE ANTIESTROGEN TAMOXIFEN ON LOW-DENSITY-LIPOPROTEIN OXIDATION IN POSTMENOPAUSAL WOMEN - A POTENTIAL MECHANISM FOR CARDIOVASCULAR BENEFIT SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 780 EP 780 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000779 ER PT J AU CURIEL, RV CANNON, RO LAURIENZO, JM UNGER, EF QUYYUMI, AA PANZA, JA AF CURIEL, RV CANNON, RO LAURIENZO, JM UNGER, EF QUYYUMI, AA PANZA, JA TI INVESTIGATION OF MYOCARDIAL-ISCHEMIA AS THE MECHANISM OF CHEST PAIN IN PATIENTS WITH NORMAL CORONARY-ARTERIES USING TRANSESOPHAGEAL DOBUTAMINE STRESS ECHOCARDIOGRAPHY SO CIRCULATION LA English DT Meeting Abstract C1 NIH,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 951 EP 951 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000948 ER PT J AU NASSBACHER, A GLOTH, ST FLEG, JL OCONNOR, F TOWNSEND, SN ALDAVE, J GERSTENBLITH, G SCHULMAN, SP AF NASSBACHER, A GLOTH, ST FLEG, JL OCONNOR, F TOWNSEND, SN ALDAVE, J GERSTENBLITH, G SCHULMAN, SP TI INCREASING ARTERIAL COMPLIANCE IMPROVES EJECTION FRACTION DURING MAXIMAL EXERCISE IN OLDER INDIVIDUALS SO CIRCULATION LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1009 EP 1009 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001003 ER PT J AU CHEN, L CHEN, MH LARSON, MG EVANS, JC BENJAMIN, EJ LEVY, D AF CHEN, L CHEN, MH LARSON, MG EVANS, JC BENJAMIN, EJ LEVY, D TI RISK-FACTORS FOR SYNCOPE IN A COMMUNITY-BASED SAMPLE - THE FRAMINGHAM HEART-STUDY SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1044 EP 1044 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001038 ER PT J AU SPEIR, E SHIBUTANI, T YU, ZX EPSTEIN, SE AF SPEIR, E SHIBUTANI, T YU, ZX EPSTEIN, SE TI ASPIRIN, BY INHIBITING FREE-RADICAL GENERATION INDUCED BY CYTOMEGALOVIRUS-INFECTION OF HUMAN SMOOTH-MUSCLE CELLS, INHIBITS CYTOMEGALOVIRUS GENE-EXPRESSION AND CYTOMEGALOVIRUS REPLICATION SO CIRCULATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 1092 EP 1092 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001086 ER PT J AU SPEIR, E SHIBUTANI, T YU, ZX EPSTEIN, SE AF SPEIR, E SHIBUTANI, T YU, ZX EPSTEIN, SE TI CYTOMEGALOVIRUS-INFECTION OF HUMAN SMOOTH-MUSCLE CELLS CAUSES A PROOXIDANT STATE THAT IS MEDIATED IN PART BY NADPH-OXIDASE SO CIRCULATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 1097 EP 1097 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001091 ER PT J AU SPEIR, E SHIBUTANI, T YU, ZX EPSTEIN, SE AF SPEIR, E SHIBUTANI, T YU, ZX EPSTEIN, SE TI THE ANTIOXIDANT N-ACETYLCYSTEINE INHIBITS, IN VASCULAR SMOOTH-MUSCLE CELLS, CYTOMEGALOVIRUS REPLICATION, CYTOPATHIC EFFECTS, AND ACTIVATION OF THE CYTOMEGALOVIRUS PROMOTER BY IE72 SO CIRCULATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 1099 EP 1099 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001093 ER PT J AU PEPE, S XIAO, RP HOHL, C ALTSCHULD, R LAKATTA, E AF PEPE, S XIAO, RP HOHL, C ALTSCHULD, R LAKATTA, E TI CARDIAC ADENYLYL-CYCLASE REGULATION BY OPIOID AND ADRENERGIC SIGNAL INTERACTIONS SO CIRCULATION LA English DT Meeting Abstract C1 NIA,LCS,BALTIMORE,MD 21224. OHIO STATE UNIV,COLUMBUS,OH 43210. NR 0 TC 0 Z9 0 U1 2 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 1127 EP 1127 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001121 ER PT J AU PANZA, JA CURIEL, RV LAURIENZO, JM UNGER, EF CANNON, RO AF PANZA, JA CURIEL, RV LAURIENZO, JM UNGER, EF CANNON, RO TI REDUCED INOTROPIC RESERVE IN ASYMPTOMATIC PATIENTS WITH CHRONIC SEVERE AORTIC REGURGITATION AND NORMAL RESTING LEFT-VENTRICULAR SYSTOLIC FUNCTION SO CIRCULATION LA English DT Meeting Abstract C1 NIH,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1303 EP 1303 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001296 ER PT J AU TAKEDA, K YU, ZX NISHIKAWA, T TANAKA, M ANDO, A FERRANS, VJ KASAJIMA, T AF TAKEDA, K YU, ZX NISHIKAWA, T TANAKA, M ANDO, A FERRANS, VJ KASAJIMA, T TI IMMUNOHISTOCHEMICAL STUDY OF APOPTOSIS IN THE BULBUS CORDIS OF THE DEVELOPING RAT-HEART SO CIRCULATION LA English DT Meeting Abstract C1 TOKYO WOMENS MED COLL,TOKYO 162,JAPAN. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1454 EP 1454 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001443 ER PT J AU BERARD, A BROUSSEAU, M HOEG, JM VAISMAN, B SAKAI, N WOOD, D HOYT, R MARCOVINA, S BREWER, HB SANTAMARINAFOJO, S AF BERARD, A BROUSSEAU, M HOEG, JM VAISMAN, B SAKAI, N WOOD, D HOYT, R MARCOVINA, S BREWER, HB SANTAMARINAFOJO, S TI LCAT MODULATES DIETARY-LIPID RESPONSE IN HLCAT TRANSGENIC RABBITS SO CIRCULATION LA English DT Meeting Abstract C1 NIH,MDB,BETHESDA,MD 20892. UNIV WASHINGTON,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1674 EP 1674 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001663 ER PT J AU GE, SP YAMADA, I ZHOU, XD HEINRICH, RS YOGANATHAN, AP AF GE, SP YAMADA, I ZHOU, XD HEINRICH, RS YOGANATHAN, AP TI CARDIAC WORK IN AORTIC REGURGITATION SO CIRCULATION LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NIH,LAMS,BETHESDA,MD 20892. GEORGIA INST TECHNOL,ATLANTA,GA 30332. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1695 EP 1695 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001684 ER PT J AU HOEG, JM SANTAMARINAFOJO, S VAISMAN, B HOYT, RF FELDMAN, S CORNHILL, F HERDERICK, E TALLEY, G WOOD, D MARCOVINA, S BREWER, HB AF HOEG, JM SANTAMARINAFOJO, S VAISMAN, B HOYT, RF FELDMAN, S CORNHILL, F HERDERICK, E TALLEY, G WOOD, D MARCOVINA, S BREWER, HB TI LECITHIN-CHOLESTEROL ACYL TRANSFERASE TRANSGENIC RABBITS - HYPERALPHALIPOPROTEINEMIA AND DIET-INDUCED ATHEROSCLEROSIS SO CIRCULATION LA English DT Meeting Abstract C1 CHICO STATE UNIV,CHICO,CA. UNIV WASHINGTON,SEATTLE,WA 98195. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1707 EP 1707 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001696 ER PT J AU BOLUYT, MO ZHENG, JS YOUNES, A ONEILL, L CROW, MT AF BOLUYT, MO ZHENG, JS YOUNES, A ONEILL, L CROW, MT TI P70/85 S6 KINASE ACTIVATION IS REQUIRED FOR ALPHA(1)-ADRENERGIC RECEPTOR-STIMULATED HYPERTROPHY IN NEONATAL RAT CARDIAC MYOCYTES SO CIRCULATION LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 1832 EP 1832 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001820 ER PT J AU KATUSIC, ZS MILSTIEN, S STELTER, A AF KATUSIC, ZS MILSTIEN, S STELTER, A TI ENDOTHELIUM AND TETRAHYDROBIOPTERIN LEVELS IN ISOLATED ARTERIES AND VEINS SO CIRCULATION LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. MAYO CLIN,ROCHESTER,MN. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1865 EP 1865 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001853 ER PT J AU TSANG, TSM SHOLINSKY, PD GARDIN, JM SMITH, VE GOTTDIENER, JS MANOLIO, TA AF TSANG, TSM SHOLINSKY, PD GARDIN, JM SMITH, VE GOTTDIENER, JS MANOLIO, TA TI DISTRIBUTION AND CORRELATES OF LEFT ATRIAL DIMENSION IN THE ELDERLY SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2001 EP 2001 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001988 ER PT J AU CLAYTON, DA WILLIAMS, RS LIANG, IY AF CLAYTON, DA WILLIAMS, RS LIANG, IY TI MEETING HIGHLIGHTS SO CIRCULATION LA English DT Editorial Material RP CLAYTON, DA (reprint author), NHLBI,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 8 Z9 8 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 OCT 15 PY 1995 VL 92 IS 8 BP 2022 EP 2023 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TA125 UT WOS:A1995TA12500002 ER PT J AU LENFANT, C AF LENFANT, C TI NHLBI COST-MANAGEMENT STRATEGIES - A SUCCESS STORY SO CIRCULATION LA English DT Editorial Material RP LENFANT, C (reprint author), NHLBI,BLDG 10,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 BP 2024 EP 2025 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TA125 UT WOS:A1995TA12500003 PM 7554174 ER PT J AU LI, ZH CHENG, L STETLERSTEVENSON, WG LAKATTA, EG FROEHLICH, J AF LI, ZH CHENG, L STETLERSTEVENSON, WG LAKATTA, EG FROEHLICH, J TI MATRIX METALLOPROTEINASE-2 (MMP-2) EXPRESSION IN THE THICKENED INTIMA OF AGING RAT AORTA SO CIRCULATION LA English DT Meeting Abstract C1 NIA,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. NCI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 2030 EP 2030 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002016 ER PT J AU DUGI, KA VAISMAN, BL KOBAYASHI, J BROWN, DR APPLEBAUMBOWDEN, D MEYN, SM BREWER, HB SANTAMARINAFOJO, S AF DUGI, KA VAISMAN, BL KOBAYASHI, J BROWN, DR APPLEBAUMBOWDEN, D MEYN, SM BREWER, HB SANTAMARINAFOJO, S TI ADENOVIRUS-MEDIATED TRANSFER OF HEPATIC LIPASE IN LCAT TRANSGENIC MICE PROVIDES NEW INSIGHTS INTO THE ROLE OF HEPATIC LIPASE IN HDL METABOLISM SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2031 EP 2031 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002017 ER PT J AU XIAO, RP LAKATTA, EG AF XIAO, RP LAKATTA, EG TI DIFFERENT MECHANISMS MEDIATE ACTIONS OF BETA(1)-ADRENERGIC AND BETA(2)-ADRENERGIC RECEPTOR STIMULATION ON CANINE CARDIAC L-TYPE CA(2+) CURRENT SO CIRCULATION LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 2 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 2063 EP 2063 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002048 ER PT J AU PANZA, JA CURIEL, RV LAURIENZO, JM QUYYUMI, AA DILSIZIAN, V AF PANZA, JA CURIEL, RV LAURIENZO, JM QUYYUMI, AA DILSIZIAN, V TI RELATION BETWEEN ISCHEMIC THRESHOLD MEASURED DURING DOBUTAMINE STRESS ECHOCARDIOGRAPHY AND KNOWN INDEXES OF POOR-PROGNOSIS IN PATIENTS WITH CORONARY-ARTERY DISEASE SO CIRCULATION LA English DT Article DE CORONARY DISEASE; ECHOCARDIOGRAPHY; ISCHEMIA; ANGIOGRAPHY ID LEFT-VENTRICULAR FUNCTION; TRANSESOPHAGEAL 2-DIMENSIONAL ECHOCARDIOGRAPHY; EXERCISE RADIONUCLIDE ANGIOGRAPHY; MILDLY SYMPTOMATIC PATIENTS; MEDICALLY TREATED PATIENTS; MYOCARDIAL-ISCHEMIA; ANATOMIC CORRELATIONS; CLINICAL-APPLICATIONS; IMAGE ORIENTATION; SINGLE AB Background Stress echocardiography has become an accepted methodology for the evaluation of coronary artery disease. One potential advantage of dobutamine over other stressors used with echocardiography is the possibility of assessing the ischemic threshold. However, whether this measurement correlates with indices associated with adverse outcome has not been established. Methods and Results One hundred four patients (91 men and 13 women; age, 61+/-9 years) with coronary artery disease were studied with transesophageal echocardiography during infusion of dobutamine 2.5 to 40 mu g/kg per minute. When regional dyssynergy developed, the dobutamine ischemic threshold (the dose of dobutamine at which induced regional wall motion abnormalities were first detected) was identified. The dobutamine stress echocardiogram was abnormal in 90 patients (sensitivity, 87%). The dobutamine ischemic threshold was 25.4+/-11.2 mu g/kg per minute in patients with single-vessel disease, 14.4+/-7.9 in patients with two-vessel disease, and 9.1+/-7.9 in patients with three-vessel disease (P<.0001). The dobutamine ischemic threshold correlated with the ejection fraction response to exercise measured by radionuclide angiography: Patients with low ischemic threshold had a mean fall in ejection fraction, and patients with high ischemic threshold or normal tests had a mean increase in ejection fraction. Conclusions In patients with coronary artery disease: the ischemic threshold measured during dobutamine stress echocardiography correlates with both the number of stenosed vessels and the left ventricular ejection fraction response to exercise. Because these variables are associated with poor prognosis, these findings provide further support regarding the utility of dobutamine stress echocardiography in the clinical evaluation of patients with chronic coronary artery disease. RP PANZA, JA (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 33 TC 27 Z9 28 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 OCT 15 PY 1995 VL 92 IS 8 BP 2095 EP 2101 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TA125 UT WOS:A1995TA12500016 PM 7554187 ER PT J AU KRITCHEVSKY, SB SHIMAKAWA, T TELL, GS DENNIS, B CARPENTER, M ECKFELDT, JH PEACHERRYAN, H HEISS, G AF KRITCHEVSKY, SB SHIMAKAWA, T TELL, GS DENNIS, B CARPENTER, M ECKFELDT, JH PEACHERRYAN, H HEISS, G TI DIETARY ANTIOXIDANTS AND CAROTID-ARTERY WALL THICKNESS - THE ARIC STUDY SO CIRCULATION LA English DT Article DE ANTIOXIDANTS; DIET; CAROTID ARTERIES; ATHEROSCLEROSIS ID LOW-DENSITY-LIPOPROTEIN; FOOD FREQUENCY QUESTIONNAIRE; NUTRITION INTERVENTION TRIALS; DISEASE-SPECIFIC MORTALITY; CORONARY HEART-DISEASE; VITAMIN-E CONSUMPTION; D-ALPHA-TOCOPHEROL; B-MODE ULTRASOUND; OXIDATIVE MODIFICATION; CARDIOVASCULAR-DISEASE AB Background Evidence that dietary antioxidants may prevent atherosclerotic disease is growing. The relationship between the intake of dietary and supplemental vitamin C, alpha-tocopherol, and provitamin A carotenoids and average carotid artery wall thickness was studied in 6318 female and 4989 male participants 45 to 64 years old in the Atherosclerosis Risk in Communities Study. Methods and Results Intake was assessed by use of a 66-item semiquantitative food-frequency questionnaire. Carotid artery intima-media wall thickness was measured as an indicator of atherosclerosis at multiple sites with B-mode ultrasound. Among men and women >55 years old who had not recently begun a special diet, there was a significant inverse relationship between vitamin C intake and average artery wall thickness adjusted for age, body mass index, fasting serum glucose, systolic and diastolic blood pressures, HDL and LDL cholesterol, total caloric intake, cigarette use, race, and education (test for linear trend across quintiles of intake, P=.019 for women and P=.035 for men). An inverse relationship was also seen between wall thickness and alpha-tocopherol intake but was significant only in women (test for linear trend, P=.033 for women and P=.13 for men). There was a significant inverse association between carotene intake and wall thickness in older men (test for linear trend, P=.015), but the association weakened after adjustment for potential confounders. No significant relationships were seen in participants <55 years old. Conclusions These data provide limited support for the hypothesis that dietary vitamin C and alpha-tocopherol may protect against atherosclerotic disease, especially in individuals >55 years old. C1 NHLBI, DIV EPIDEMIOL & CLIN APPLICAT, BETHESDA, MD 20892 USA. UNIV N CAROLINA, SCH PUBL HLTH, CTR COLLABORAT STUDIES COORDINATING, DEPT BIOSTAT, CHAPEL HILL, NC USA. UNIV N CAROLINA, SCH PUBL HLTH, DEPT EPIDEMIOL, CHAPEL HILL, NC USA. DEPT LAB MED & PATHOL, MINNEAPOLIS, MN USA. WAKE FOREST UNIV, BOWMAN GRAY SCH MED, DEPT PUBL HLTH SCI, WINSTON SALEM, NC 27103 USA. RP KRITCHEVSKY, SB (reprint author), UNIV TENNESSEE, DEPT PREVENT MED, DIV BIOSTAT & EPIDEMIOL, 877 MADISON AVE, MEMPHIS, TN 38163 USA. RI Tell, Grethe/G-5639-2015 OI Tell, Grethe/0000-0003-1386-1638 FU NHLBI NIH HHS [N01-HC-55016, HL-47408, N01-HC-55015] NR 53 TC 117 Z9 118 U1 1 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 BP 2142 EP 2150 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TA125 UT WOS:A1995TA12500023 PM 7554194 ER PT J AU CHEN, MH CHEN, LW LARSON, MG EVANS, JC BENJAMIN, EJ WOLF, PA LEVY, D AF CHEN, MH CHEN, LW LARSON, MG EVANS, JC BENJAMIN, EJ WOLF, PA LEVY, D TI SYNCOPE IS ASSOCIATED WITH ADVERSE OUTCOMES IN THE COMMUNITY-BASED FRAMINGHAM HEART-STUDY SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2308 EP 2308 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002291 ER PT J AU KOBAYASHI, J APPLEBAUMBODEN, D DUGI, K KASHYAP, V PARROTT, C MAEDA, N BREWER, HB SANTAMARINAFOJO, S AF KOBAYASHI, J APPLEBAUMBODEN, D DUGI, K KASHYAP, V PARROTT, C MAEDA, N BREWER, HB SANTAMARINAFOJO, S TI IN-VIVO ANALYSIS OF LPL AND HL STRUCTURE-FUNCTION - ADENOVIRUS-MEDIATED TRANSFER OF LIPASE LID MUTANT-GENES IN HEPATIC LIPASE DEFICIENT MICE SO CIRCULATION LA English DT Meeting Abstract C1 NIH,MDB,BETHESDA,MD 20892. UNIV N CAROLINA,CHAPEL HILL,NC 27515. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2363 EP 2363 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002346 ER PT J AU SAKAI, N VAISMAN, BL DUGI, KA BERARD, A BROWN, DR PARROTT, CL TALLEY, GD SANTAMARINAFOJO, S BREWER, HB AF SAKAI, N VAISMAN, BL DUGI, KA BERARD, A BROWN, DR PARROTT, CL TALLEY, GD SANTAMARINAFOJO, S BREWER, HB TI ANALYSIS OF LCAT AND CETP GENE-GENE INTERACTION USING ADENOVIRUS-MEDIATED GENE-TRANSFER OF CETP IN CONTROL AND LCAT TRANSGENIC MICE SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2365 EP 2365 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002348 ER PT J AU BROUSSEAU, ME ZECH, LA BERARD, A VAISMAN, BL MEYN, SM POWELL, D SANTAMARINAFOJO, S BREWER, HB HOEG, JM AF BROUSSEAU, ME ZECH, LA BERARD, A VAISMAN, BL MEYN, SM POWELL, D SANTAMARINAFOJO, S BREWER, HB HOEG, JM TI LCAT OVEREXPRESSION IN TRANSGENIC RABBITS DELAYS APOA-I CATABOLISM IN A GENE DOSE-DEPENDENT MANNER AND ENHANCES LDL REMODELING SO CIRCULATION LA English DT Meeting Abstract C1 NIH,MDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2366 EP 2366 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002349 ER PT J AU RADE, JJ SCHULICK, AH DICHEK, DA AF RADE, JJ SCHULICK, AH DICHEK, DA TI ADENOVIRUS-MEDIATED DELIVERY OF HIRUDIN TO INJURED RAT ARTERIES REDUCES NEOINTIMA FORMATION SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2394 EP 2394 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002376 ER PT J AU SCHULICK, AH DUNN, PF DONG, G RADE, JJ DICHEK, DA AF SCHULICK, AH DUNN, PF DONG, G RADE, JJ DICHEK, DA TI ADENOVIRAL ARTERIAL GENE-TRANSFER IS CRITICALLY DEPENDENT ON HOST IMMUNE STATUS SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2400 EP 2400 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002382 ER PT J AU SOLLOTT, SJ ZIMAN, B LAKATTA, EG AF SOLLOTT, SJ ZIMAN, B LAKATTA, EG TI NITRIC-OXIDE (NO) MODULATION OF CARDIAC MYOCYTE SIGNALING AND CONTRACTION SO CIRCULATION LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. NR 1 TC 1 Z9 1 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 2414 EP 2414 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002396 ER PT J AU MOSTERD, A DAGOSTINO, RB BELANGER, AJ SYTKOWSKI, PA KANNEL, WB GROBBEE, DE LEVY, D AF MOSTERD, A DAGOSTINO, RB BELANGER, AJ SYTKOWSKI, PA KANNEL, WB GROBBEE, DE LEVY, D TI SECULAR TRENDS IN HYPERTENSION TREATMENT AND IMPACT ON PREVALENCE OF HIGH BLOOD-PRESSURE AND LEFT-VENTRICULAR HYPERTROPHY - THE FRAMINGHAM HEART-STUDY SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. ERASMUS UNIV ROTTERDAM,ROTTERDAM,NETHERLANDS. RI Grobbee, Diederick/C-7651-2014 OI Grobbee, Diederick/0000-0003-4472-4468 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 2475 EP 2475 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002457 ER PT J AU CHEN, L LARSON, MG EVANS, JC LEVY, D AF CHEN, L LARSON, MG EVANS, JC LEVY, D TI ANTECEDENT HYPERTENSION CONFERS INCREASED RISK FOR ADVERSE OUTCOMES FOLLOWING INITIAL MYOCARDIAL-INFARCTION SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2476 EP 2476 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002458 ER PT J AU WILSON, PWF HOEG, JM BELANGER, A DAGOSTINO, R POEHLMAN, H OLEARY, D WOLF, P AF WILSON, PWF HOEG, JM BELANGER, A DAGOSTINO, R POEHLMAN, H OLEARY, D WOLF, P TI CHOLESTEROL-YEARS, BLOOD PRESSURE-YEARS, PACK-YEARS AND CAROTID STENOSIS SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2478 EP 2478 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002460 ER PT J AU LI, ZH LAKATTA, EG ROBINSON, KG BING, OHL AF LI, ZH LAKATTA, EG ROBINSON, KG BING, OHL TI DETECTION OF APOPTOSIS IN THE FAILING HEART OF SPONTANEOUSLY HYPERTENSIVE RATS SO CIRCULATION LA English DT Meeting Abstract C1 NIA,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. DEPT VET AFFAIRS MED CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 2509 EP 2509 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002491 ER PT J AU CURIEL, RV LAURIENZO, JM UNGER, EF PANZA, JA AF CURIEL, RV LAURIENZO, JM UNGER, EF PANZA, JA TI LACK OF RELATION BETWEEN MYOCARDIAL-CONTRACTION AT REST AND INOTROPIC RESERVE IN PATIENTS WITH CHRONIC CORONARY-ARTERY DISEASE AND LEFT-VENTRICULAR DYSFUNCTION SO CIRCULATION LA English DT Meeting Abstract C1 NIH,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2624 EP 2624 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002606 ER PT J AU REMALEY, AT STONIK, JA SCHUMACHER, UK HOEG, JM BREWER, B AF REMALEY, AT STONIK, JA SCHUMACHER, UK HOEG, JM BREWER, B TI DEFECTIVE PHOSPHOLIPID EFFLUX FROM TANGIER DISEASE FIBROBLASTS SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2656 EP 2656 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002638 ER PT J AU ZHENG, JS ONEILL, L LONG, XL BOLUYT, MO AF ZHENG, JS ONEILL, L LONG, XL BOLUYT, MO TI EXTRACELLULAR ATP INDUCES C-FOS MESSENGER-RNA AND ACTIVATES MULTIPLE 2ND-MESSENGER PATHWAYS VIA P2-PURINERGIC RECEPTORS IN CARDIAC FIBROBLASTS SO CIRCULATION LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2742 EP 2742 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002723 ER PT J AU LIPSHULTZ, SE EASLEY, K KAPLAN, S BRICKER, JT STARC, T LAI, W MOODIE, D COLAN, S AF LIPSHULTZ, SE EASLEY, K KAPLAN, S BRICKER, JT STARC, T LAI, W MOODIE, D COLAN, S TI ABNORMAL LEFT-VENTRICULAR STRUCTURE AND FUNCTION SHORTLY AFTER BIRTH IN INFANTS OF HIV-INFECTED MOTHERS - THE PROSPECTIVE NHLBI P2C2 STUDY SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,P2C2 STUDY GRP,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2780 EP 2780 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002761 ER PT J AU SHANDAS, R GHARIB, M JONES, M AF SHANDAS, R GHARIB, M JONES, M TI DIGITAL PARTICLE IMAGE VELOCIMETRY MEASUREMENTS OF VELOCITY PROFILES THROUGH BILEAFLET MECHANICAL VALVES - AN IN-VITRO STUDY SO CIRCULATION LA English DT Meeting Abstract C1 CALTECH,PASADENA,CA 91125. CHILDRENS HOSP,DENVER,CO 80218. NHLBI,LAMS,BETHESDA,MD 20892. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 2851 EP 2851 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002832 ER PT J AU ANDREWS, NP QUYYUMI, AA AF ANDREWS, NP QUYYUMI, AA TI THE EFFECT OF SYSTEMIC ALPHA(2) ADRENERGIC-BLOCKADE ON THE INCREASE IN PLATELET-AGGREGATION UPON ARISING AND WITH EXERCISE SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2856 EP 2856 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002837 ER PT J AU SIMONSMORTON, DG HUNSBERGER, SA VANHORN, L BARTON, BA ROBSON, A MUHONEN, L MCMAHON, RP LASSER, NL KWITEROVICH, PO KIMM, SYS GREENLICK, MR AF SIMONSMORTON, DG HUNSBERGER, SA VANHORN, L BARTON, BA ROBSON, A MUHONEN, L MCMAHON, RP LASSER, NL KWITEROVICH, PO KIMM, SYS GREENLICK, MR TI 3-YEAR LONGITUDINAL RELATIONSHIPS BETWEEN DIETARY NUTRIENTS AND BLOOD-PRESSURE IN CHILDREN IN THE DISC COHORT SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. RI McMahon, Robert/C-5462-2009 NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2962 EP 2962 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002942 ER PT J AU KEON, CA ANDERSON, YS KING, MT VEECH, RL RADDA, GK CLARKE, K AF KEON, CA ANDERSON, YS KING, MT VEECH, RL RADDA, GK CLARKE, K TI CHANGES IN MYOCARDIAL ENERGY TRANSDUCTION WITH THYROID STATUS - EVIDENCE FOR THE MITOCHONDRIAL PROTON LEAK SO CIRCULATION LA English DT Meeting Abstract C1 UNIV OXFORD,DEPT BIOCHEM,OXFORD OX1 3QU,ENGLAND. NIAAA,METAB LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3032 EP 3032 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003012 ER PT J AU MULCAHY, D HUSAIN, S ANDREWS, NP GUETTA, V MINCEMOYER, R JOHNSON, G PANZA, JA CANNON, RO QUYYUMI, AA AF MULCAHY, D HUSAIN, S ANDREWS, NP GUETTA, V MINCEMOYER, R JOHNSON, G PANZA, JA CANNON, RO QUYYUMI, AA TI IN-VIVO NITRIC-OXIDE ACTIVITY IN HUMAN SAPHENOUS-VEIN GRAFTS SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3081 EP 3081 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003060 ER PT J AU LONG, XL BOLUYT, MO LI, ZH CROW, MT LAKATTA, EG AF LONG, XL BOLUYT, MO LI, ZH CROW, MT LAKATTA, EG TI HYPOXIA-INDUCED EXPRESSION OF HEME OXYGENASE GENE-EXPRESSION IN CULTURED NEONATAL RAT CARDIAC MYOCYTES SO CIRCULATION LA English DT Meeting Abstract C1 NIA,CTR GERONTOL RES,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 3138 EP 3138 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003116 ER PT J AU LANKFORD, EB EPSTEIN, ND FANANAPAZIR, L SWEENEY, HL AF LANKFORD, EB EPSTEIN, ND FANANAPAZIR, L SWEENEY, HL TI ALTERED OSCILLATORY POWER OUTPUT IN FIBERS WITH MUTATED MYOSIN FROM PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY SO CIRCULATION LA English DT Meeting Abstract C1 UNIV PENN,PHILADELPHIA,PA 19104. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 3158 EP 3158 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003136 ER PT J AU VASAN, RS BENJAMIN, EJ EVANS, JC LARSON, MG REISS, CK LEVY, D AF VASAN, RS BENJAMIN, EJ EVANS, JC LARSON, MG REISS, CK LEVY, D TI PROGNOSIS OF DIASTOLIC HEART-FAILURE - FRAMINGHAM HEART-STUDY SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3193 EP 3193 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003171 ER PT J AU VASAN, RS BENJAMIN, EJ EVANS, JC LARSON, MG REISS, CK LEVY, D AF VASAN, RS BENJAMIN, EJ EVANS, JC LARSON, MG REISS, CK LEVY, D TI PREVALENCE AND CLINICAL CORRELATES OF DIASTOLIC HEART-FAILURE - FRAMINGHAM HEART-STUDY SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3195 EP 3195 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003173 ER PT J AU KRUTH, HS ZHANG, WY GAYNOR, PM AF KRUTH, HS ZHANG, WY GAYNOR, PM TI APO-E PRODUCED BY HUMAN MONOCYTE-DERIVED MACROPHAGES MEDIATES CHOLESTEROL EFFLUX FROM THESE CELLS SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3311 EP 3311 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003289 ER PT J AU CHEN, W STEENBERGEN, C LEVY, LA LONDON, RE MURPHY, E AF CHEN, W STEENBERGEN, C LEVY, LA LONDON, RE MURPHY, E TI SARCOPLASMIC-RETICULUM [CA2+] MEASURED IN RABBIT HEART USING TF-BAPTA SO CIRCULATION LA English DT Meeting Abstract C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. DUKE UNIV,DEPT PATHOL,DURHAM,NC 27706. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 3355 EP 3355 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003333 ER PT J AU VAZIRI, SM LARSON, MG BENJAMIN, EJ LEVY, D AF VAZIRI, SM LARSON, MG BENJAMIN, EJ LEVY, D TI SECULAR TRENDS IN ATRIAL-FIBRILLATION INCIDENCE ACID IMPACT OF RISK-FACTORS SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 3404 EP 3404 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003382 ER PT J AU ISHII, M JONES, M HEINRICH, RS AF ISHII, M JONES, M HEINRICH, RS TI TEMPORAL VARIABILITY OF COLOR DOPPLER IMAGED VENA CONTRACTA AND JET AREAS IN AORTIC REGURGITATION - A CHRONIC ANIMAL-MODEL STUDY SO CIRCULATION LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. GEORGIA INST TECHNOL,ATLANTA,GA 30332. NHLBI,LAMS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3465 EP 3465 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003443 ER PT J AU ISHII, M YAMADA, I HEINRICH, RS YOGANATHAN, AP AF ISHII, M YAMADA, I HEINRICH, RS YOGANATHAN, AP TI EVALUATION OF AORTIC REGURGITATION USING COLOR DOPPLER - A COMPARATIVE-STUDY USING FLOW CONVERGENCE, VENA CONTRACTA IMAGING OR JET AREA MEASUREMENT SO CIRCULATION LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NIH,LAMS,BETHESDA,MD 20892. GEORGIA INST TECHNOL,ATLANTA,GA 30332. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3466 EP 3466 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003444 ER PT J AU GE, SP JONES, M SHIOTA, T HEINRICH, RS AF GE, SP JONES, M SHIOTA, T HEINRICH, RS TI VALIDITY OF FLOW CONVERGENCE METHODS FOR ASSESSMENT OF AORTIC REGURGITATION IN A CHRONIC ANIMAL-MODEL WITH QUANTIFIABLE REGURGITATION SO CIRCULATION LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NHLBI,LAMS,BETHESDA,MD 20892. GEORGIA INST TECHNOL,ATLANTA,GA 30332. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3467 EP 3467 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003445 ER PT J AU QUYYUMI, AA HUSAIN, S MULCAHY, D ANDREWS, NP MINCEMOYER, R PANZA, JA CANNON, RO AF QUYYUMI, AA HUSAIN, S MULCAHY, D ANDREWS, NP MINCEMOYER, R PANZA, JA CANNON, RO TI NITRIC-OXIDE ACTIVITY IN THE HUMAN CORONARY AND PERIPHERAL-CIRCULATION SO CIRCULATION LA English DT Meeting Abstract C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3698 EP 3698 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003674 ER PT J AU LONG, X BOLUYT, MO CIRIELLI, C CAPOGROSSI, MC LAKATTA, EG CROW, MT AF LONG, X BOLUYT, MO CIRIELLI, C CAPOGROSSI, MC LAKATTA, EG CROW, MT TI ENHANCED EXPRESSION OF P53 IN HYPOXIA-INDUCED APOPTOSIS OF CULTURED NEONATAL RAT CARDIOMYOCYTES SO CIRCULATION LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 3714 EP 3714 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003690 ER PT J AU SHIOTA, T JONES, M DELABAYS, A DERMAN, R YAMADA, I SAHN, DJ PANDIAN, NG AF SHIOTA, T JONES, M DELABAYS, A DERMAN, R YAMADA, I SAHN, DJ PANDIAN, NG TI 3D RECONSTRUCTION OF FLOW CONVERGENCE AND JETS IN AORTIC REGURGITATION - A CHRONIC ANIMAL-MODEL STUDY SO CIRCULATION LA English DT Meeting Abstract C1 OREGON HLTH SCI UNIV,PORTLAND,OR 97201. TUFTS NEW ENGLAND MED CTR,BOSTON,MA. NIH,LAMS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3834 EP 3834 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003810 ER PT J AU WILSON, PWF GARRISON, RJ SAWIN, CT AF WILSON, PWF GARRISON, RJ SAWIN, CT TI HIGH SERUM THYROTROPIN (TSH) LEVELS AND DYSLIPIDEMIA IN WOMEN - THE FRAMINGHAM OFFSPRING STUDY SO CIRCULATION LA English DT Meeting Abstract C1 FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3845 EP 3845 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003821 ER PT J AU VAITKEVICIUS, PV NUSSBACHER, A SHAPIRO, EP OCONNOR, FC FLEG, JL AF VAITKEVICIUS, PV NUSSBACHER, A SHAPIRO, EP OCONNOR, FC FLEG, JL TI INDEPENDENT EFFECT OF ARTERIAL STIFFNESS ON LEFT-VENTRICULAR MASS IN HEALTHY-VOLUNTEERS SO CIRCULATION LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. JOHNS HOPKINS BAYVIEW MED CTR,BALTIMORE,MD. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3855 EP 3855 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003831 ER PT J AU GARDNER, RV VOLOSHIN, ON CAMERINIOTERO, RD AF GARDNER, RV VOLOSHIN, ON CAMERINIOTERO, RD TI THE IDENTIFICATION OF THE SINGLE-STRANDED DNA-BINDING DOMAIN OF THE ESCHERICHIA-COLI RECA PROTEIN SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article DE RECA PROTEIN; HOMOLOGOUS RECOMBINATION; SINGLE-STRANDED DNA BINDING; SYNTHETIC PEPTIDES; FILTER BINDING ID SITE-DIRECTED MUTAGENESIS; GEL-ELECTROPHORESIS; RECOMBINATION; PURIFICATION; ENDONUCLEASE; FILAMENTS; COMPLEXES; EXCHANGE; CLEAVAGE; PEPTIDES AB To identify the ssDNA-binding domain of Escherichia coli RecA protein, we examined the ssDNA-binding capabilities of synthetic peptides, the sequences of which were derived from the C- and N-termini and from sequences within loops L1 and L2 of the RecA molecule identified from the crystal structure. Synthetic peptides derived from amino acid residues 185-219 of several bacterial RecA proteins, which include loop L2 of RecA, bound to ssDNA in filter-binding assays, whereas three separate synthetic le point mutants of E. coli RecA in this region did not. The binding of RecA to ssDNA examined using a gel-shift assay was inhibited by a synthetic peptide derived from this ssDNA-binding region, but not by synthetic peptides derived from amino acid residues 301-329 of the C-ter minus or from N-terminal residues 6-39, A peptide corresponding to amino acid positions 152-169 of the RecA molecule and spanning loop L1 and its flanking regions did not bind ssDNA at peptide concentrations up to 250 mu M. We have also defined a synthetic 20-amino-acid peptide that comprises amino acid residues 193-212 and includes loop L2 of RecA as the minimum unit that can bind to ssDNA from this region of RecA. Finally, two maltose-binding protein-RecA fusion proteins were made, one containing amino acid residues 185-224 of RecA and the other the last 51 C-terminal residues of RecA (amino acid residues 303-353). In contrast to the C-terminus-derived fusion protein, the fusion protein containing the putative DNA-binding site demonstrated significant binding to single-stranded oligonucleotides in both filter-binding and gel-shift assays. These findings suggest that a portion of the region extending from amino acid residues 193-212 is either parr of or the whole ssDNA-binding domain of the RecA protein. C1 NIDDK,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 41 TC 24 Z9 25 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD OCT 15 PY 1995 VL 233 IS 2 BP 419 EP 425 DI 10.1111/j.1432-1033.1995.419_2.x PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB207 UT WOS:A1995TB20700004 PM 7588783 ER PT J AU MOVSAS, B MOVSAS, TZ STEINBERG, SM OKUNIEFF, P AF MOVSAS, B MOVSAS, TZ STEINBERG, SM OKUNIEFF, P TI LONG-TERM VISUAL CHANGES FOLLOWING PITUITARY IRRADIATION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE PITUITARY TUMOR; RADIATION THERAPY; VISION; NEUROVASCULAR; HEADACHES ID EMPTY SELLA SYNDROME; ADENOMAS; COMPLICATIONS AB Purpose: To analyze possible long-term effects of pituitary irradiation on visual fields and acuity. Methods and Materials: Eighty-six patients were treated with radiotherapy for pituitary tumors at the National Cancer Institute between 1980 and 1991. Twenty-one patients had baseline preradiation and longterm follow-up visual fields, Eyes were followed with serial Goldmann or Humphrey visual field testing. Neuroradiologic correlation was made with the available brain scans. There were 12 females and 9 males with an median age of 44. Eighteen patients had hormone-secreting tumors and three had chromophobe adenomas. All but one patient with an inoperable invasive macroadenoma were irradiated after one or more transphenoidal resections or a craniotomy. The indications for radiation in the operable patients were: nine patients, partial tumor resection; nine patients, tumor recurrence; and two patients, persistent hormonal elevation after surgery. The median dose delivered was 50 Gy (45-59.4 Gy). The average field size was 6 x 6 cm (5 x 5 cm to 10 x 12.5 cm). Results: With a median follow-up of 48 months (14-128) after radiotherapy, 1 out of 21 patients has recurred (at 8 months) and all patients are alive. Of the 38 sighted eyes, 27 had normal visual fields before and after radiation, 7 eyes showed improvement, and 4 eyes had a stable defect, mostly in the superior temporal region. There were no cases of radiation-induced visual field or acuity deterioration. Six out of 21 patients (29%) had neurologic symptoms in follow-up, most of which appeared vascular in nature. Four patients complained of atypical migranous-like headaches that first began 1.5-3 years following treatment. One patient complained of recurrent vertical diplopia and one patient had a cerebral vascular accident 7 years following therapy. A dose-related association with these neurovascular symptoms approached statistical significance. Only 1 out of 11 (9%) patients who received doses less than or equal to 50 Gy developed these symptoms, whereas 5 out of 10 (50%) patients who received doses greater than 50 Gy developed symptoms (p(2) = 0.064). Conclusion: Postoperative radiation for partially resected or recurrent pituitary adenomas using megavoltage radiation, as well as modern field arrangements and fractionation, is extremely effective and safe. Ninety-five percent of patients are free of recurrence with no deterioration in the visual fields or acuities. Some patients experienced neurovascular symptoms (mostly vascular headaches) following surgery and radiation, There is a trend (p(2) = 0.064) toward increased symptoms following higher radiation doses. C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. WASHINGTON HOSP CTR,WASHINGTON,DC 20010. NCI,CLIN ONCOL PROGRAM,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. NR 15 TC 18 Z9 18 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 15 PY 1995 VL 33 IS 3 BP 599 EP 605 DI 10.1016/0360-3016(95)00221-J PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA TA483 UT WOS:A1995TA48300007 PM 7558949 ER PT J AU SARIN, A CONANCIBOTTI, M HENKART, PA AF SARIN, A CONANCIBOTTI, M HENKART, PA TI CYTOTOXIC EFFECT OF TNF AND LYMPHOTOXIN ON T-LYMPHOBLASTS SO JOURNAL OF IMMUNOLOGY LA English DT Note ID TUMOR-NECROSIS-FACTOR; FACTOR-ALPHA; RECEPTOR; PROLIFERATION; RESPONSES; ENHANCEMENT; THYMOCYTES; INDUCTION; CELLS AB Recombinant TNF and lymphotoxin trigger the apoptotic death of normal mouse and human T lymphocyte blasts in vitro, This cytotoxic effect does not involve the Fas death pathway and differs from the TNF-triggered death of tumor cells in several respects: 1) It is a slower process, requiring 2 to 3 days; 2) it is blocked, rather than enhanced, by cycloheximide; and 3) based on the agonistic effect of anti-TNF receptor Abs, it involves a synergistic effect of both the 55-kDa TNFR1 and the 75-kDa TNFR2, as opposed to the dominance of TNFR1 for tumor cytotoxicity, The TNF-induced death of blasts is potently inhibited by IL-2, as well as by IL-1, IL-4, IFN-gamma, and IL-12, Because activated T cells secrete both TNF and LT, these findings reveal a new pathway for Ag-induced down-modulation of T cell responses. C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 23 TC 111 Z9 112 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 15 PY 1995 VL 155 IS 8 BP 3716 EP 3718 PG 3 WC Immunology SC Immunology GA RY581 UT WOS:A1995RY58100003 PM 7561073 ER PT J AU HAYES, BK ESQUIVEL, F BENNINK, JR YEWDELL, JW VARKI, A AF HAYES, BK ESQUIVEL, F BENNINK, JR YEWDELL, JW VARKI, A TI STRUCTURE OF THE N-LINKED OLIGOSACCHARIDES OF MHC CLASS-I MOLECULES FROM CELLS DEFICIENT IN THE ANTIGENIC PEPTIDE TRANSPORTER - IMPLICATIONS FOR THE SITE OF PEPTIDE ASSOCIATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HIGH MANNOSE OLIGOSACCHARIDES; CYTOTOXIC LYMPHOCYTES-T; ENDOPLASMIC-RETICULUM; RAT-LIVER; RMA-S; GLYCOPROTEIN GLUCOSYLTRANSFERASE; HISTOCOMPATIBILITY ANTIGENS; INTRACELLULAR-TRANSPORT; TRANSIENT GLUCOSYLATION; COMPLEX AB Class I molecules are N-linked glycoproteins encoded by the MHC, They carry cytosolic protein-derived peptides to the cell surface, displaying them to enable immune surveillance of cellular processes, Peptides are delivered to class I molecules by the transporter associated with Ag processing (TAP), Peptide association is known to occur before exposure of class I molecules to the medial Golgi-processing enzyme alpha-mannosidase II, but there is limited information regarding the location or timing of peptide binding within the earlier regions of the endoplasmic reticulum (ER)-Golgi pathway, A reported association of newly synthesized class I molecules with the ER chaperonin calnexin raises the possibility of persistence of the monoglycosylated N-linked oligosaccharide (NLO) Glc(1)Man(8)GlcNAc(2), known to be recognized by this lectin, To explore these matters, we determined the structure of the NLOs on the subset of newly synthesized class I molecules awaiting the loading of peptide, We pulse-labeled murine MHC H-2D(b) class I molecules in RMA/S cells, which lack one of the TAP subunits, causing the great majority of the molecules to be retained for prolonged periods in an early secretory compartment, awaiting peptide binding, MHC molecules pulse-labeled with [H-3]glucosamine were isolated, the NLOs specifically released and structurally analyzed by a variety of techniques. Within the chosen window of biosynthetic time, most D-b molecules from parental RMA cells carried mature NLOs of the biantennary complex-type, with one to two sialic acid residues, In RMA/S cells, such chains were in the minority, the majority consisting of the precursor forms Man(8)GlcNAc(2) and Man(9)GlcNAc(2). No glucosylated forms were detected, nor were the later processing intermediates Man(5-7)GlcNAc(2) or GlcNAc(1)Man(4-5)GlcNAc(2). Thus, most D-b molecules in TAP-deficient cells are retained in an early compartment of the secretory pathway, before the point of first access to the Golgi alpha-mannosidase I, which trims alpha 1-2 linked mannose residues, but beyond the point where the alpha 1-3-linked glucose residue is finally removed by the ER glucosidase II, Thus, structural analysis of NLOs on class I molecules within a defined biosynthetic window has established a biochemical measure of the timing of peptide association. C1 UNIV CALIF SAN DIEGO,CTR CANC,SCH MED,GLYCOBIOL PROGRAM,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RI yewdell, jyewdell@nih.gov/A-1702-2012 FU NCI NIH HHS [CA38701, P01CA58689] NR 66 TC 7 Z9 7 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 OCT 15 PY 1995 VL 155 IS 8 BP 3780 EP 3787 PG 8 WC Immunology SC Immunology GA RY581 UT WOS:A1995RY58100012 PM 7561082 ER PT J AU TAUB, DD SAYERS, TJ CARTER, CRD ORTALDO, JR AF TAUB, DD SAYERS, TJ CARTER, CRD ORTALDO, JR TI ALPHA-CHEMOKINE AND BETA-CHEMOKINE INDUCE NK CELL-MIGRATION AND ENHANCE NK-MEDIATED CYTOLYSIS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NATURAL-KILLER-CELLS; LARGE GRANULAR LYMPHOCYTES; CHEMOTACTIC CYTOKINES; ENDOTHELIAL-CELLS; ADHESION; BIOLOGY; BINDING; FIBRONECTIN; INVOLVEMENT; MIP-1-BETA AB Chemokines have been shown to play an important role in both the adhesion and migration of numerous leukocytic cell types, including granulocytes, monocytes, mast cells, and T lymphocytes. However, the biologic effects of chemokines on NK cells remain to be defined. Chemotaxis studies using purified human NK cells and a panel of human recombinant chemokines revealed that macrophage inflammatory protein (MIP)-1 alpha and IFN-inducible protein-10 (IP-10) are potent NK cell chemoattractants in vitro. Modest but significant chemotactic (not chemokinetic) responses were also observed in response to RANTES, MCP-1, MCP-2, MCP-3, and MIP-1 beta. Chemokine receptor expression on human NK cells was determined through displacement and Scatchard analyses, using a panel of radiolabeled chemokines, and revealed the presence of both distinct and shared chemokine receptors with affinities similar to those previously described for other cell types. Functional studies have also revealed that the beta chemokines and IP-10 are capable of augmenting NK- but not LAK- or ADCC-specific cytolytic responses in both a dose- and donor-dependent fashion. Neutralization analysis using Abs specific for various adhesion molecules revealed that NK:tumor cell conjugate formation is required for chemokine-induced NK killing. In addition; NK cells incubated in the presence of beta chemokines and IP-10 for 4 h induced the release of granule-derived serine esterases, suggesting a possible mechanism for chemokine-mediated NK killing. These results suggest that chemokines not only play an important role in the recruitment of NK cells, but also may be important mediators of NK cell degranulation augmenting local tumor cell destruction. C1 NCI, FREDERICK CANC RES & DEV CTR, SAIC FREDERICK, BIOL CARCINOGENESIS & DEV PROGRAM, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, DIV CANC TREATMENT, BIOL RESPONSE MODIFIERS PROGRAM, FREDERICK, MD 21702 USA. RP TAUB, DD (reprint author), NCI, FREDERICK CANC RES & DEV CTR,SAIC FREDERICK, CLIN SUPPORT LAB,CLIN SERV PROGRAM, BLDG 560, FREDERICK, MD 21702 USA. RI Sayers, Thomas/G-4859-2015 NR 39 TC 350 Z9 357 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD OCT 15 PY 1995 VL 155 IS 8 BP 3877 EP 3888 PG 12 WC Immunology SC Immunology GA RY581 UT WOS:A1995RY58100024 PM 7561094 ER PT J AU BADOLATO, R JOHNSTON, JA WANG, JM MCVICAR, D XU, LL OPPENHEIM, JJ KELVIN, DJ AF BADOLATO, R JOHNSTON, JA WANG, JM MCVICAR, D XU, LL OPPENHEIM, JJ KELVIN, DJ TI SERUM AMYLOID-A INDUCES CALCIUM MOBILIZATION AND CHEMOTAXIS OF HUMAN MONOCYTES BY ACTIVATING A PERTUSSIS-TOXIN-SENSITIVE SIGNALING PATHWAY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NUCLEOTIDE REGULATORY PROTEIN; CYTOKINES; RECEPTORS; MIGRATION; CHEMOATTRACTANTS; NEUTROPHILS AB We have previously reported that serum amyloid A (SAA) induces adhesion and chemotaxis of human monocytes and polymorphonuclear neutrophils, in vitro as well as in vivo. Since the mechanism of SAA signaling is unknown, we have investigated the possibility that SAA, like other chemoattractants such as the chemotactic peptide FMLP and chemokines, might induce migration of monocytes by G protein activation. We report here that preincubation of monocytes with pertussis toxin (PTx) inhibited SAA chemotaxis, while incubation with cholera toxin (CTx) did not, Staurosporine and H-7, both inhibitors of protein kinase C (PKC), significantly decreased rSAA-induced chemotaxis of monocytes, suggesting that PKC may be involved in the rSAA signaling pathway. Moreover, rSAA, at concentrations that were effective in chemoattracting monocytes, resulted in transient elevation of cytoplasmic calcium concentration ([Ca2+](i)), and incubation of cells with PTx markedly inhibited the mobilization of Ca2+ in response to rSAA. This suggests that both chemotaxis and the rise in [Ca2+](i), are mediated by G proteins of the Gi class. The increase in [Ca2+](i), induced in monocytes by rSAA, was comparable to that elicited by FMLP, and was severalfold greater than that induced by optimal concentrations of chemokine beta-family members such as RANTES, MCAF/MCP-1, and MIP-1 alpha. The chemoattractants FMLP, RANTES, MIP-1 alpha, and MCAF/MCP-1, all failed to desensitize rSAA-induced Ca2+ influx and chemotaxis in monocytes. This suggests that SAA uses a distinct receptor that is coupled to PTx-sensitive G proteins. C1 NCI,FREDERICK CANC RES & DEV CTR,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. 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,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. ROBARTS RES INST,AUTOIMMUN GRP,LONDON,ON N6A 5C1,CANADA. UNIV WESTERN ONTARIO,DEPT MICROBIOL & IMMUNOL,LONDON,ON,CANADA. RI Badolato, Raffaele/A-8081-2010 OI Badolato, Raffaele/0000-0001-7375-5410 NR 27 TC 110 Z9 110 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 OCT 15 PY 1995 VL 155 IS 8 BP 4004 EP 4010 PG 7 WC Immunology SC Immunology GA RY581 UT WOS:A1995RY58100039 PM 7561109 ER PT J AU WEISSMAN, D LI, YX ORENSTEIN, JM FAUCI, AS AF WEISSMAN, D LI, YX ORENSTEIN, JM FAUCI, AS TI BOTH A PRECURSOR AND A MATURE POPULATION OF DENDRITIC CELLS CAN BIND HIV - HOWEVER, ONLY THE MATURE POPULATION THAT EXPRESSES CD80 CAN PASS INFECTION TO UNSTIMULATED CD4(+) T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; LANGERHANS CELLS; PROVIDES ONE; MIGRATION; ANTIGEN; ALPHA; LYMPHOCYTES; ACTIVATION; MOLECULE; SIGNALS AB Dendritic cells (DC) are the principle APC involved in primary immune responses; their major functions to obtain Ag in tissues, migrate to lymphoid organs, and activate T cells. DC are also the first immune cells to arrive at sites of inflammation on mucous membranes, the major site of sexual transmission of HIV. We have demonstrated previously that three populations of cells that can develop a dendritic morphology are present in peripheral blood. Two of these populations can express CD83, a marker of DC, and appear to be at different stages of maturation: 1) a precursor population and 2) a mature immunostimulatory DC. Precursor-derived DC express high levels of CD86 (B7-2) and HLA-DR but no CD80 (B7-1), whereas mature DC have high levels of expression of all three markers. Mature DC in peripheral blood bind HIV to their surface and induce infection when added to autologous CD4(+) T cells in the absence of added stimuli, such as mitogens. These mature DC, when isolated directly from peripheral blood, appear to be conjugated to T cells, and these conjugates are infected easily and productively with HIV. These findings suggest a role for DC in early HIV infection in which they bind virus and interact with T cells locally or after migrating to a lymphoid organ, thus establishing a productive infection. Furthermore, they likely play a role in the propagation of HIV infection by activating T cells in the presence of HIV, which leads to viral replication and immune cell destruction. C1 GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20057. RP WEISSMAN, D (reprint author), NIAID,IMMUNOREGULAT LAB,10 CTR DR,MSC 1576,BETHESDA,MD 20892, USA. NR 32 TC 102 Z9 104 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 OCT 15 PY 1995 VL 155 IS 8 BP 4111 EP 4117 PG 7 WC Immunology SC Immunology GA RY581 UT WOS:A1995RY58100054 PM 7561124 ER PT J AU KIBBEY, MC JOHNSON, B PETRYSHYN, R JUCKER, M KLEINMAN, HK AF KIBBEY, MC JOHNSON, B PETRYSHYN, R JUCKER, M KLEINMAN, HK TI A 110-KD NUCLEAR SHUTTLING PROTEIN, NUCLEOLIN, BINDS TO THE NEURITE-PROMOTING IKVAV SITE OF LAMININ-1 SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE NUCLEOLIN; LAMININ PEPTIDE; LAMININ BINDING PROTEIN; APP ID SELF-CLEAVING ACTIVITY; A-CHAIN; SYNTHETIC PEPTIDE; HIGH-AFFINITY; BASEMENT-MEMBRANE; CELLS; IDENTIFICATION; RECEPTORS; OUTGROWTH; SEQUENCE AB The basement membrane protein laminin and the IKVAV-containing sequence from the laminin al chain have been found to promote the differentiation of primary neurons and a variety of neural cell lines, We previously reported that a 110-kd IKVAV-binding protein (LBP110) isolated from brain appears to be a member of the beta-amyloid precursor protein (APP) family by immunologic and functional studies, which showed that LBP110/APP is also important in neurite outgrowth (Kibbey et al.: Proc Natl Acad Sci USA 90:10150-10153, 1993), In the preparation of this binding protein, a contaminating IKVAV-binding protein of identical molecular weight, nucleolin, was also identified, Here we have studied the relationship between these binding proteins, We find that nucleolin binds specifically to the IKVAV sequence independently of LBP110/APP, We have also demonstrated significant levels of nucleolin in mature brain and in differentiating neural cells, suggesting that nucleolin functions not only in cell proliferation and in ribosome biogenesis as was previously reported, but also in the differentiation and maintenance of neural tissue, Our identification of cytoplasmic and cell-surface nucleolin, an IKVAV-binding protein, suggests that this protein may function in signalling by extracellular matrix. (C) 1995 Wiley-Liss, Inc. C1 NATL INST DENTAL RES,DEV BIOL LAB,BETHESDA,MD 20892. NIA,GERONTOL RES CTR,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,CTR CANC & TRANSPLANTAT BIOL,WASHINGTON,DC. GEORGE WASHINGTON UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20052. GEORGE WASHINGTON UNIV,SCH MED,DEPT BIOCHEM & MOLEC BIOL,WASHINGTON,DC 20052. FU NCI NIH HHS [CA421717] NR 38 TC 55 Z9 57 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD OCT 15 PY 1995 VL 42 IS 3 BP 314 EP 322 DI 10.1002/jnr.490420305 PG 9 WC Neurosciences SC Neurosciences & Neurology GA TC366 UT WOS:A1995TC36600004 PM 8583499 ER PT J AU DELEON, M NAHIN, RL MOLINA, CA DELEON, DD RUDA, MA AF DELEON, M NAHIN, RL MOLINA, CA DELEON, DD RUDA, MA TI COMPARISON OF C-JUN, JUNB, AND JUND MESSENGER-RNA EXPRESSION AND PROTEIN IN THE RAT DORSAL-ROOT GANGLIA FOLLOWING SCIATIC-NERVE TRANSECTION SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE TRANSCRIPTION FACTORS; NERVE REGENERATION; SENSORY NEURONS; AP-1 DNA BINDING SITE; C-FOS ID NITRIC-OXIDE SYNTHASE; MESSENGER-RNA; DNA-BINDING; TRANSCRIPTION FACTORS; DIFFERENTIAL EXPRESSION; AXONAL-TRANSPORT; SENSORY NEURONS; FOS; AP-1; ONCOGENE AB The present study was designed to compare the expression of the Jun family of protooncogenes following nerve injury. Adult rats were anesthetized and the sciatic nerve transected. Dorsal root ganglia (DRG) at 1, 2, 3, and 7 days after nerve transection were collected, their total RNA extracted, and Northern blots performed using P-32-labeled oligonucleotide probes. The constitutive expression of c-jun mRNA was very low in DRG. Induction of c-jun mRNA was observed by day 1 after nerve transection, with a sixfold peak at 3 days and a twofold induction still present by day 7. The constitutive expression of junB mRNA was also low in the DRG, and sciatic nerve transection produced only a modest induction (1.7-fold by day 3) in the DRG ipsilateral to the nerve cut. junD mRNA was constitutively expressed at high levels in the DRG, and its level of expression did not change after sciatic nerve transection. Immunocytochemistry studies demonstrated a pattern of c-Jun, JunB, and JunD immunoreactivity (IR) associated with the cell nuclei of DRG neurons. c-Jun IR was found at very low levels in the undamaged contralaterai DRG neurons, but sciatic nerve transection dramatically increased the number of c-Jun-immunoreactive neurons. Dot blot immunoblotting assay confirmed that the DRG ipsilateral to the sciatic nerve cut contained a higher level of c-Jun protein than the contralateral control DRG. Similar to c-Jun LR, JunB IR was minimal in the undamaged contralateral DRG. However, the DRG ipsilateral to the nerve transection did not show an increase in the number of immunoreactive neurons. JunD protein was expressed at high levels in the contralateral DRG, and this level of expression persisted after sciatic nerve transection in the ipsilateral DRG. DNA gel retardation assay experiments with an AP-1 consensus sequence showed a single DNA-protein complex. This complex was increased in ipsilateral as compared with contralateral DRG extracts. The amount of DNA-protein complex was reduced by c-Jun protein antiserum but was not altered when treated with a Fos antibody. We conclude that c-jun, junB and junD mRNAs and proteins are differentially regulated in the DRG after sciatic nerve transection. (C) 1995 Wiley-Liss, Inc. C1 NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BETHESDA,MD 20892. RP DELEON, M (reprint author), LOMA LINDA UNIV,DEPT PHYSIOL & PHARMACOL,LOMA LINDA,CA 92350, USA. RI De Leon, Marino/A-6922-2009 OI De Leon, Marino/0000-0001-6576-785X NR 51 TC 28 Z9 28 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD OCT 15 PY 1995 VL 42 IS 3 BP 391 EP 401 DI 10.1002/jnr.490420314 PG 11 WC Neurosciences SC Neurosciences & Neurology GA TC366 UT WOS:A1995TC36600013 PM 8583508 ER PT J AU STRZELECKA, TE CLORE, GM GRONENBORN, AM AF STRZELECKA, TE CLORE, GM GRONENBORN, AM TI THE SOLUTION STRUCTURE OF THE MU-NER PROTEIN REVEALS A HELIX-TURN-HELIX DNA RECOGNITION MOTIF SO STRUCTURE LA English DT Article DE DNA RECOGNITION; HELIX-TURN-HELIX; MU NER; NMR; SOLUTION STRUCTURE ID HETERONUCLEAR NMR-SPECTROSCOPY; NUCLEAR-MAGNETIC-RESONANCE; RESTRAINED MOLECULAR-DYNAMICS; REPRESSOR OPERATOR COMPLEX; BACTERIOPHAGE-MU; DISTANCE GEOMETRY; BINDING DOMAIN; PHOSPHOTRANSFERASE SYSTEM; 3-DIMENSIONAL STRUCTURE; SECONDARY STRUCTURE AB Background: The Mu Ner protein is a small (74 amino acids), basic, DNA-binding protein found in phage Mu. It belongs to a class of proteins, the cro and repressor proteins, that regulate the switch from the lysogenic to the lytic state of the phage life cycle. There is no significant sequence identity between Mu Ner and the cro proteins of other phages, despite their functional similarity. In addition, there is no significant sequence identity with any other DNA-binding proteins, with the exception of Ner from the related phage D108 and the Nlp protein of Escherichia coli. As the tertiary structures of Mu Ner and these two related proteins are unknown, it is clear that a three-dimensional (3D) structure of Mu Ner is essential in order to gain insight into its mode of DNA binding. Results: The 3D solution structure of Mu Ner has been solved by 3D and 4D heteronuclear magnetic resonance spectroscopy. The structure consists of five a helices, two of which comprise a helix-turn-helix (HTH) motif. Analysis of line broadening and disappearance of cross-peaks in a H-1-N-15 correlation spectrum of the Mu Ner-DNA complex suggests that residues in these two helices are most likely to be in contact with the DNA. Conclusions: Like the functionally analogous cro proteins from phages lambda and 434, the Mu Ner protein possesses a HTH DNA recognition motif. The Ner protein from phage D108 and the Nlp protein from E. coli are likely to have very similar tertiary structures due to high amino-acid-sequence identity with Mu Ner. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 69 TC 9 Z9 10 U1 0 U2 3 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0969-2126 J9 STRUCTURE JI Structure PD OCT 15 PY 1995 VL 3 IS 10 BP 1087 EP 1095 DI 10.1016/S0969-2126(01)00244-1 PG 9 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA TB710 UT WOS:A1995TB71000013 PM 8590003 ER PT J AU AHUJA, SS SHRIVASTAV, S DANIELPOUR, D BALOW, JE BOUMPAS, DT AF AHUJA, SS SHRIVASTAV, S DANIELPOUR, D BALOW, JE BOUMPAS, DT TI REGULATION OF TRANSFORMING GROWTH FACTOR-BETA(1) AND ITS RECEPTOR BY CYCLOSPORINE IN HUMAN T-LYMPHOCYTES SO TRANSPLANTATION LA English DT Article ID FACTOR-BETA; TGF-BETA; II RECEPTOR; 2 FORMS; CELLS; NEPHROTOXICITY; NEPHROPATHY; FIBRONECTIN; TGF-BETA-1; COLLAGEN AB Scarring, fibrosis, and immunosuppression occurs with chronic cyclosporine (CsA) administration. We postulated that CsA may induce transforming growth factor (TGF)-beta(1) secretion from human T lymphocytes, a cytokine with immunoregulatory effects that has beep implicated in the pathogenesis of wound healing ang scarring. TGF-beta(1) was measured in serum-free supernatants harvested from T lymphocytes stimulated in the presence of CsA by a specific sandwich ELISA. CsA (10-1000 ng/ml) enhanced TGF-beta(1) secretion by approximately 40-80% in a dose-dependent manner. Increased TGF-beta(1) secretion in the presence of CsA was accompanied by a 2- to 4-fold increase in TGF-beta(1) mRNA levels due to both enhancement of its nuclear transcription as well as prolongation of TGF-B-1 mRNA half-life, To determine whether the increase in TGF-beta(1) secretion was also accompanied by a concomitant change in its receptor, TGF-beta receptor expression was analyzed by cross-linking of radioiodinated TGF-beta(1). Unactivated T lymphocytes expressed both a 105-kDa and a 65-kDa TGF-beta receptor. Upon stimulation, a transient increase in receptor density was seen gt 12 hr, followed by a decline at later time points. Cells treated with CsA exhibited at least 2-fold higher levels of TGF-beta receptors in a dose-dependent manner, Thus, CsA enhances the production of TGF-beta(1) protein as well gs the expression of its receptor in activated T lymphocytes. Enhanced TGF-beta(1) production and binding may contribute to the immunosuppressive and fibrosis-promoting effects of CsA therapy. C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP AHUJA, SS (reprint author), NIDDKD,KIDNEY DIS SECT,BLDG 10,ROOM 32112,BETHESDA,MD 20892, USA. NR 31 TC 72 Z9 74 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD OCT 15 PY 1995 VL 60 IS 7 BP 718 EP 723 DI 10.1097/00007890-199510150-00018 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA RZ968 UT WOS:A1995RZ96800018 PM 7570983 ER PT J AU KATAYOSE, D WERSTO, R COWAN, K SETH, P AF KATAYOSE, D WERSTO, R COWAN, K SETH, P TI CONSEQUENCES OF P53 GENE-EXPRESSION BY ADENOVIRUS VECTOR ON CELL-CYCLE ARREST AND APOPTOSIS IN HUMAN AORTIC VASCULAR SMOOTH-MUSCLE CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID RAT; DEATH AB p53 shows its tumor suppresser activity by inducing cell cycle arrest and/or apoptosis of tumor cells and these activities are in part mediated by p21 cyclin-dependent kinase inhibitor (also called as WAF1, Cip1 and SDI1). Using human aortic vascular smooth muscle cells, here we demonstrate that adenovirus vector expressing p53-induced p21, cell cycle arrest at G1 and G2/M boundary, and accumulation of cells in G1 subgroup. However, adenovirus vector expressing p21 induced only G1 cell cycle arrest. The adenovirus vector expressing p53 was 200 times more cytotoxic to human aortic vascular smooth muscle cells than adenovirus vector expressing p21. These results suggest that adenovirus expressing p53 induces cytotoxicity in human vascular smooth muscle cells by apoptosis and this cytotoxicity can not be fully accounted by p21 induction. (C) 1995 Academic Press, Inc. C1 NCI,PATHOL BRANCH,BETHESDA,MD 20892. RP KATAYOSE, D (reprint author), NCI,MED BRANCH,MED BREAST CANC SECT,BLDG 10,ROOM 12C210,BETHESDA,MD 20892, USA. NR 22 TC 37 Z9 38 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 13 PY 1995 VL 215 IS 2 BP 446 EP 451 DI 10.1006/bbrc.1995.2485 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RZ365 UT WOS:A1995RZ36500003 PM 7487976 ER PT J AU MCMILLIAN, M KONG, LY SAWIN, SM WILSON, B DAS, K HUDSON, P HONG, JS BING, GY AF MCMILLIAN, M KONG, LY SAWIN, SM WILSON, B DAS, K HUDSON, P HONG, JS BING, GY TI SELECTIVE KILLING OF CHOLINERGIC NEURONS BY MICROGLIAL ACTIVATION IN BASAL FOREBRAIN MIXED NEURONAL/GLIAL CULTURES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID MACROPHAGES AB Microglia activation by lipopolysaccharides (LPS) significantly decreased choline acetyltransferase-immunopositive (ChAT+) neuron number and ChAT activity in rat primary basal forebrain mixed neuronal/glial cultures. The number of non-cholinergic (ChAT(-)) neurons was unaffected. LPS induced nitric oxide synthase (NOS) in microglia, increased the media level of the NO metabolite nitrite, and the NOS inhibitor N-G-nitro-L-arginine methylester (NAME) protected the ChAT+ neurons from LPS. The combination of beta-amyloid peptide (1-42) and interferon-gamma (INF-gamma) also increased the media nitrite level and decreased ChAT+ neuron number. Cholinergic neurons are lost early in the course of Alzheimer's disease, and the enhanced sensitivity of these neurons to microglial activation in mixed neuronal/glial culture may be useful for modeling Alzheimer's disease and developing therapeutic strategies to combat this disease. RP MCMILLIAN, M (reprint author), NIEHS,ENVIRONM NEUROSCI LAB,RES TRIANGLE PK,NC 27709, USA. OI Bing, Guoying/0000-0003-0609-8152 NR 17 TC 76 Z9 77 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 13 PY 1995 VL 215 IS 2 BP 572 EP 577 DI 10.1006/bbrc.1995.2503 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RZ365 UT WOS:A1995RZ36500021 PM 7487994 ER PT J AU WEEKS, BS NOMIZU, M OTAKA, A WESTON, CA OKUSU, A TAMAMURA, H YAMAMOTO, N FUJII, N AF WEEKS, BS NOMIZU, M OTAKA, A WESTON, CA OKUSU, A TAMAMURA, H YAMAMOTO, N FUJII, N TI THE SYNTHETIC [TYR(5,12),LYS(7)]-POLYPHEMUSIN-II PEPTIDE (T22) BINDS TO THE CD4 CELL-SURFACE MOLECULE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID HORSESHOE-CRAB HEMOCYTES; TACHYPLESIN-I; GALACTOSYL CERAMIDE; POLYPHEMUSIN-I; HIV-1 AB The [Tyr(5,12), Lys(7)]-polyphemusin II peptide (T22) inhibits HIV-1 replication in lymphocytes. The mechanism of T22 inhibition of HIV-1 replication may involve T22 competition with HIV-1 for attachment sites on the plasma membrane of targeted cells. Here we find that the T22 peptide binds to the CD4 molecule in affinity columns. We also find that antiserum to CD4 inhibits cell attachment to T22. Further CD4+ transfected cells attach to T22 while their parental cells which do not express CD4 do not attach to T22. These data demonstrate that T22 binds to the CD4 molecule and supports the hypothesis that T22 inhibits HIV-1 replication by binding to the cell surface CD4 molecule and inhibiting uptake of the virus. (C) 1995 Academic Press, Inc. C1 NIDR,DEV BIOL LAB,BETHESDA,MD 20892. KYOTO UNIV,FAC PHARMACEUT SCI,SAKYO KU,KYOTO 606,JAPAN. HAMILTON COLL,DEPT BIOL,CLINTON,NY 13323. TOKYO MED & DENT UNIV,SCH MED,DEPT MICROBIOL,BUNKYO KU,TOKYO 113,JAPAN. RP WEEKS, BS (reprint author), UNIV PENN,DEPT MED,DIV INFECT DIS,536 JOHNSON PAVIL,PHILADELPHIA,PA 19104, USA. NR 17 TC 11 Z9 12 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 13 PY 1995 VL 215 IS 2 BP 626 EP 631 DI 10.1006/bbrc.1995.2510 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RZ365 UT WOS:A1995RZ36500028 PM 7488001 ER PT J AU TASAKI, I AF TASAKI, I TI MECHANICAL AND THERMAL-CHANGES IN THE TORPEDO ELECTRIC ORGAN ASSOCIATED WITH ITS POSTSYNAPTIC POTENTIALS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID NERVE AB Rapid mechanical and thermal changes in slices of the Torpedo electric organ evoked by electric stimulation were investigated. The organ was found to swell simultaneously with the postsynaptic potential. This swelling was followed by prolonged shrinkage of the organ. These findings may be explained from the proven facts that the acetylcholine(ACh)-receptor proteins have a large binding capacity for Ca-ions and that addition of ACh to the medium can cause release of Ca-ions from the receptor proteins. (C) 1995 Academic Press, Inc. RP TASAKI, I (reprint author), NIMH,CELL BIOL LAB,BLDG 36,BETHESDA,MD 20892, USA. NR 16 TC 8 Z9 8 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 13 PY 1995 VL 215 IS 2 BP 654 EP 658 DI 10.1006/bbrc.1995.2514 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RZ365 UT WOS:A1995RZ36500032 PM 7488005 ER PT J AU CHARIOT, A MOREAU, L SENTERRE, G SOBEL, ME CASTRONOVO, V AF CHARIOT, A MOREAU, L SENTERRE, G SOBEL, ME CASTRONOVO, V TI RETINOIC ACID INDUCES 3 NEWLY CLONED HOXA1 TRANSCRIPTS IN MCF7 BREAST-CANCER CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID GENE-EXPRESSION; HOMEOTIC GENES; HOMEOBOX GENES; DROSOPHILA; SEQUENCES; PROTEIN AB Coordinated expression of genes involved in development, differentiation and malignant transformation is regulated by transcription factors including homeodomain-containing proteins. However, most of their cDNA sequences are still unknown. We report here the molecular characterization of three newly cloned HOXA1 transcripts from human breast cancer cells. In addition, we provide evidence that these alternatively spliced transcripts encode one homeodomain-containing protein and two products lacking the conserved DNA-binding domain. Moreover, we demonstrate that all three HOXA1 transcripts are induced by retinoic acid in MCF7 cells. Taken together, our results suggest that HOXA1 gene may be a key element in the establishment of the breast cancer cell phenotype. (C) 1995 Academic Press, Inc. C1 UNIV LIEGE,METASTASIS RES LAB,B-4000 LIEGE,BELGIUM. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 24 TC 32 Z9 33 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 13 PY 1995 VL 215 IS 2 BP 713 EP 720 DI 10.1006/bbrc.1995.2522 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RZ365 UT WOS:A1995RZ36500040 PM 7488013 ER PT J AU FREED, EO MARTIN, MA AF FREED, EO MARTIN, MA TI THE ROLE OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEINS IN VIRUS-INFECTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID PRINCIPAL NEUTRALIZING DETERMINANT; RECOMBINANT SOLUBLE CD4; HTLV-III/LAV ENVELOPE; AMINO-ACID CHANGES; CYTOPLASMIC DOMAIN; SYNCYTIUM FORMATION; TRANSMEMBRANE PROTEIN; MEMBRANE-FUSION; RECEPTOR-BINDING; LEUCINE ZIPPER C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NR 150 TC 195 Z9 201 U1 1 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 13 PY 1995 VL 270 IS 41 BP 23883 EP 23886 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TA217 UT WOS:A1995TA21700001 PM 7592573 ER PT J AU ROBEY, FA KELSONHARRIS, T ROLLER, PP ROBERTGUROFF, M AF ROBEY, FA KELSONHARRIS, T ROLLER, PP ROBERTGUROFF, M TI A HELICAL EPITOPE IN THE C4 DOMAIN OF HIV GLYCOPROTEIN-120 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID IMMUNODEFICIENCY-VIRUS TYPE-1; SYNTHETIC PEPTIDE POLYMERS; AUTOMATED SYNTHESIS; T4 MOLECULE; PROTEIN; RECEPTOR; GP120; CD4; RETROVIRUS; AFFINITY AB The fourth conserved domain of the human immunodeficiency virus type 1 (HIV-1) envelope, the C4 region of glycoprotein 120 (gp120), is an amphipathic stretch of amino acids that, based on mutational analyses, constitutes a major component of the CD4 binding region in gp120. In the absence of crystallographic and NMR data on C4 in intact gp120, we sought to gain insight into C4's conformation and accessibility in gp120 by taking an immunochemical approach. In this study, a peptomer composed of a repeat peptide of C4 amino acids 419-436 from gp120 of HIV-1(MN) was synthesized for use as a conformationally constrained immunogen. Circular dichroism studies disclosed that the polymerized peptide, peptomer-(419-436), in 0.01 M Na2HPO4 buffer, pH 7.4, at 25 degrees C contained a dominant alpha-helical structure (53 +/- 1%) compared with 2 +/- 4% alpha-helical content for the monomeric peptide-(419-436). The peptomer in Ribi's adjuvant induced the production of rabbit antibodies that recognized recombinant and native gp120 but, consistent with the literature, the C4 peptide having no conformational constraints did not. The experimental results show that only those antibodies formed against a helical immunogen from C4 will recognize recombinant and native gp120, and, therefore, the results support the notion that C4 is an alpha-helix in gp120. C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,MED CHEM LAB,BETHESDA,MD 20892. RP ROBEY, FA (reprint author), NIDR,CELLULAR DEV & ONCOL LAB,PEPTIDE & IMMUNOCHEM UNIT,BLDG 30,RM 211,BETHESDA,MD 20892, USA. NR 19 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 13 PY 1995 VL 270 IS 41 BP 23918 EP 23921 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TA217 UT WOS:A1995TA21700010 PM 7592582 ER PT J AU FORMISANO, P NAJJAR, SM GROSS, CN PHILIPPE, N ORIENTE, F KERNBUELL, CL ACCILI, D GORDEN, P AF FORMISANO, P NAJJAR, SM GROSS, CN PHILIPPE, N ORIENTE, F KERNBUELL, CL ACCILI, D GORDEN, P TI RECEPTOR-MEDIATED INTERNALIZATION OF INSULIN - POTENTIAL ROLE OF PP120/HA4, A SUBSTRATE OF THE INSULIN-RECEPTOR KINASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYROSINE KINASE; ENDOGENOUS SUBSTRATE; ECTO-ATPASE; BETA-SUBUNIT; ENDOCYTOSIS; GLYCOPROTEIN; DOMAIN; IDENTIFICATION; LOCALIZATION; PROTEIN AB pp120/HA4 is a hepatocyte membrane glycoprotein phosphorylated by the insulin receptor tyrosine kinase, In this study, we have investigated the role of pp120/HA4 in insulin action, Transfection of antisense pp120/HA4 cDNA in H35 hepatoma cells resulted in inhibition of pp120/HA4 expression and was associated with a 2-3-fold decrease in the rate of insulin internalization. Furthermore, insulin internalization in NIH 3T3 fibroblasts co-transfected with insulin receptors and pp120/HA4 was increased 2-fold compared with cells expressing insulin receptors alone. In contrast, no effect on internalization was observed in cells overexpressing a naturally occurring splice variant of pp120/HA4 that lacks the phosphorylation sites in the intracellular domain. Insulin lin internalization was also unaffected in cells expressing three site-directed mutants of pp120/HA4 in which the sites of phosphorylation by the insulin receptor kinase had been removed (Y488F, Y488F/Y513F, and S503A). Our data suggest that pp120/HA4 is part of a complex of proteins required for receptor-mediated internalization of insulin. It is possible that this function is regulated by insulin-induced phosphorylation of the intracellular domain of pp120/HA4. C1 NIDDK,DIABET BRANCH,BETHESDA,MD 20892. MED COLL OHIO,DEPT PHARMACOL,TOLEDO,OH 43699. OI Formisano, Pietro/0000-0001-7020-6870 NR 35 TC 53 Z9 53 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 13 PY 1995 VL 270 IS 41 BP 24073 EP 24077 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TA217 UT WOS:A1995TA21700035 PM 7592607 ER PT J AU SCHULTE, TW BLAGOSKLONNY, MV INGUI, C NECKERS, L AF SCHULTE, TW BLAGOSKLONNY, MV INGUI, C NECKERS, L TI DISRUPTION OF THE RAF-1-HSP90 MOLECULAR-COMPLEX RESULTS IN DESTABILIZATION OF RAF-1 AND LOSS OF RAF-1-RAS ASSOCIATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEAT-SHOCK PROTEIN; GLUCOCORTICOID RECEPTOR; SIGNAL TRANSDUCTION; KINASE-ACTIVITY; HSP90; INHIBITION; BINDS AB Cytosolic Raf-1 exists in a high molecular weight complex with the heat shock protein Hsp90, the purpose of which is unknown. The benzoquinone ansamycin, geld-anamycin, specifically binds to Hsp90 and disrupts certain multimolecular complexes containing this protein, Using this drug, we are able to demonstrate rapid dissociation of both Raf-1-Hsp90 and Raf-1-Ras multimolecular complexes, concomitant with a markedly decreased half-life of the Raf-1 protein. Continued disruption of the Raf-1-Hsp90 complex results in apparent loss of Raf-1 protein from the cell, although Raf-1 synthesis is actually increased. Prevention of Raf-1-Hsp90 complex formation interferes with trafficking of newly synthesized Raf-1 from cytosol to plasma membrane. These data indicate that association with Hsp90 is essential for both Raf-1 protein stability and its proper localization in the cell. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. NR 24 TC 376 Z9 379 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 13 PY 1995 VL 270 IS 41 BP 24585 EP 24588 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TA217 UT WOS:A1995TA21700106 PM 7592678 ER PT J AU BURKE, TR FESEN, MR MAZUMDER, A WANG, J CAROTHERS, AM GRUNBERGER, D DRISCOLL, J KOHN, K POMMIER, Y AF BURKE, TR FESEN, MR MAZUMDER, A WANG, J CAROTHERS, AM GRUNBERGER, D DRISCOLL, J KOHN, K POMMIER, Y TI HYDROXYLATED AROMATIC INHIBITORS OF HIV-1 INTEGRASE SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYROSINE KINASE INHIBITORS; CAFFEIC ACID-ESTERS; DNA INTEGRATION; PROTEIN; INVITRO; ISOQUINOLINES; INFECTION; FUTURE; COLON AB Efficient replication of HIV-1 requires integration of a DNA copy of the viral genome into a chromosome of the host cell. Integration is catalyzed by the viral integrase, and we have previously reported that phenolic moieties in compounds such as flavones, caffeic acid phenethyl ester (CAFE, 2), and curcumin confer inhibitory activity against HIV-1 integrase. We now extend these findings by performing a comprehensive structure-activity relationship using CAPE analogues. Approximately 30 compounds have been prepared as HIV integrase inhibitors based on the structural lead provided by CAPE, which has previously been shown to exhibit an IC50 value of 7 mu M in our integration assay. These analogues were designed to examine specific features of the parent CAFE structure which may be important for activity. Among the features examined for their effects on inhibitory potency were ring substitution, side chain length and composition, and phenyl ring conformational orientation. In an assay which measured the combined effect of two sequential steps, dinucleotide cleavage and strand transfer, several analogues have IC50 values for 3'-processing and strand transfer lower than those of CAFE. Inhibition of strand transfer was assayed using both blunt-ended and ''precleaved'' DNA substrates. Disintegration using an integrase mutant lacking the N-terminal zinc finger and C-terminal DNA-binding domains was also inhibited by these analogues, suggesting that the binding site for these compounds resides in the central catalytic core. Several CAFE analogues were also tested for selective activity against transformed cells. Taken together, these results suggest that the development of novel antiviral agents for the treatment of acquired immune deficiency syndrome can be based upon inhibition of HIV-1 integrase. C1 NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. COLUMBIA UNIV COLL PHYS & SURG,INST CANC RES,NEW YORK,NY 10032. RP BURKE, TR (reprint author), NCI,DIV CANC TREATMENT,MED CHEM LAB,DEV THERAPEUT PROGRAM,BLDG 37,RM 5C06,BETHESDA,MD 20892, USA. RI Burke, Terrence/N-2601-2014 NR 33 TC 158 Z9 163 U1 1 U2 10 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD OCT 13 PY 1995 VL 38 IS 21 BP 4171 EP 4178 DI 10.1021/jm00021a006 PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA TA407 UT WOS:A1995TA40700006 PM 7473544 ER PT J AU YE, B AKAMATSU, M SHOELSON, SE WOLF, G GIORGETTIPERALDI, S YAN, XJ ROLLER, PP BURKE, TR AF YE, B AKAMATSU, M SHOELSON, SE WOLF, G GIORGETTIPERALDI, S YAN, XJ ROLLER, PP BURKE, TR TI L-O-(2-MALONYL)TYROSINE - A NEW PHOSPHOTYROSYL MIMETIC FOR THE PREPARATION OF SRC-HOMOLOGY-2 DOMAIN INHIBITORY PEPTIDES SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID TYROSINE-PHOSPHORYLATED PEPTIDES; SOLID-PHASE SYNTHESIS; SH2 DOMAIN; BIOREVERSIBLE PROTECTION; BINDING; METHYLPHOSPHONATE; BIOACTIVATION; RECOGNITION; STABILITY; P56(LCK) AB Inhibition of Src homology 2 (SH2) domain-binding interactions affords one potential means of modulating protein-tyrosine kinase-dependent signaling. Small phosphotyrosyl (pTyr)-containing peptides are able to bind to SH2 domains and compete with larger pTyr peptides or native pTyr-containing protein ligands. Such pTyr-containing peptides are limited in their utility as SH2 domain inhibitors in vivo due to their hydrolytic lability to protein-tyrosine phosphatases (PTPs) and the poor cellular penetration of the ionized phosphate moiety. An important aspect of SH2 domain inhibitor design is the creation of pTyr mimetics which are stable to PTPs and have reasonable bioavailability. To date, most PTP-resistant pTyr mimetics which bind to SH2 domains are phosphonates such as (phosphonomethyl)phenylalanine (Pmp, 2), [(monofluorophosphono)methyl]phenylalanine (FPmp, 3) or [(difluorophosphono)-methyl]-phenylalanine (F(2)Pmp, 4). Herein we report the incorporation of a new non-phosphorus-containing pTyr mimetic, L-O-(2-malonyl)tyrosine (L-OMT, 5), into SH2 domain inhibitory peptides using the protected analogue L-N-alpha-Fmoc-O'-(O '', O ''-di-tert-butyl-2-malonyl)tyrosine (6) and solid-phase peptide synthesis techniques. Five OMT-containing peptides were prepared against the following SH2 domains: the PI-3 kinase C-terminal p85 SH2 domain (Ac-D-(L-OMT)-V-P-M-L-amide, 10, IC50 = 14.2 mu M), the Src SH2 domain (Ac-Q-(L-OMT)-E-E-I-P-amide, 11, IC50 = 25 mu M, and Ac-Q-(L-OMT)-(L-OMT)-E-I-P-amide, 14, IC50 = 23 mu M), the Grb2 SH2 domain (Ac-N-(L-OMT)-V-N-I-E-amide, 12, IC50 = 120 mu M), and the N-terminal SH-PTP2 SH2 domain (Ac-L-N-(L-OMT)-I-D-L-D-L-V-amide, 13, IC50 = 22.0 mu M). These results show that peptides 10, 11, 13, and 14 have reasonable affinity for their respective SH2 domains, with the IC50 value for the SH-PTPB SH2 domain-directed peptide 13 being equivalent to that previously observed for the corresponding F(2)Pmp-containing peptide. OMT may afford a new structural starting point for the development of novel and useful SH2 domain inhibitors. C1 NCI,DIV CANC TREATMENT,MED CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. RI Burke, Terrence/N-2601-2014 NR 45 TC 73 Z9 75 U1 0 U2 9 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD OCT 13 PY 1995 VL 38 IS 21 BP 4270 EP 4275 DI 10.1021/jm00021a016 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA TA407 UT WOS:A1995TA40700016 PM 7473554 ER PT J AU SHAH, JH IZENWASSER, S GETERDOUGLASS, B WITKIN, JM NEWMAN, AH AF SHAH, JH IZENWASSER, S GETERDOUGLASS, B WITKIN, JM NEWMAN, AH TI (+/-)-(N-ALKYLAMINO)BENZAZEPINE ANALOGS - NOVEL DOPAMINE D-1 RECEPTOR ANTAGONISTS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ADENYLYL-CYCLASE; MOLECULAR-BIOLOGY; CEREBRAL-CORTEX; BINDING-SITES; D1 RECEPTOR; SCH-23390; COCAINE; LIGAND; RAT; NEOSTRIATUM AB (+/-)-(N-Alkylamino)benzazepine analogs were prepared as novel dopamine D-1 receptor antagonists to further elucidate the role of these receptor subtypes in the pharmacology and toxicology of cocaine. In the first series of compounds, (+/-)-7-chloro-8-hydroxy-3-[6-(N,N-dimethylamino)-hexyl]-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (15) showed the highest affinity (K-i = 49.3 nM) and subtype-selectivity for dopamine D-1 over dopamine D-2 5-HT2a, and 5-HT2c receptors. Compounds 7a {(+/-)-7-Chloro-8-hydroxy-3-[4-(N,N-dimethylamino)butyl]-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine}, 11 {(+/-)-7-chloro-8-hydroxy-3-[6-[(N,N-dimethylamino)hexyl]-1-phenyl-2,3,4, 5-tetrahydro-1H-3-benzazepine-cyanoborane}, and 15 were moderately potent dopamine D-1 receptor antagonists as evidenced by their ability to block dopamine-stimulated adenylyl cyclase activity in rat caudate (predicted K-i values = 60, 34, and 21 nM, respectively). Compound 7a appears to be unique in that, despite its relatively potent inhibition of dopamine stimulated adenylyl cyclase, it demonstrated relatively weak binding affinity at the dopamine D-1 receptors (K-i = 811 nM). Unlike previously reported N-alkylbenzazepines, where a significant loss in dopamine D-1 receptor binding affinity was observed when successive increases in the alkyl side chain size at the benzazepine nitrogen were made, several of these novel N-alkylamino analogs demonstrated high-affinity binding with an optimal chain length of six carbons. This initial series of compounds appears to be identifying another binding domain on the dopamine D-1 receptor protein that has not previously been characterized and that accepts an amino function. Further, these compounds may serve as templates for the design of peripherally active dopamine D-1 receptor antagonists. C1 NIDA,DIV INTRAMURAL RES,PSYCHOL SECT,BALTIMORE,MD 21224. RI Izenwasser, Sari/G-9193-2012 NR 53 TC 21 Z9 21 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD OCT 13 PY 1995 VL 38 IS 21 BP 4284 EP 4293 DI 10.1021/jm00021a018 PG 10 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA TA407 UT WOS:A1995TA40700018 PM 7473556 ER PT J AU CONWAY, JF DUDA, RL CHENG, N HENDRIX, RW STEVEN, AC AF CONWAY, JF DUDA, RL CHENG, N HENDRIX, RW STEVEN, AC TI PROTEOLYTIC AND CONFORMATIONAL CONTROL OF VIRUS CAPSID MATURATION - THE BACTERIOPHAGE-HK97 SYSTEM SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE CAPSID ASSEMBLY; PROTEOLYSIS; BACTERIOPHAGE-HK97; VIRUS; STRUCTURE; CRYOELECTRON MICROSCOPY ID HERPES-SIMPLEX VIRUS; CRYO-ELECTRON-MICROSCOPY; RAMAN-SPECTROSCOPY; SIMIAN VIRUS-40; PROTEIN; RECONSTRUCTION; DNA; MICROGRAPHS; PARTICLES; SUBUNITS AB Bacteriophage capsid assembly pathways provide excellent model systems to study large-scale conformational changes and other mechanisms that regulate the formation of macromolecular complexes. These capsids are formed from proheads: relatively fragile precursor particles which mature by undergoing extensive remodeling. Phage HK97 employs novel features in its strategy for building capsids, including assembly without a scaffolding protein, and the formation of a network of covalent cross-links between neighboring subunits in the mature virion. In addition, proteolytic cleavage of the capsid protein from 42 kDa to 31 kDa is essential for maturation. To investigate the structural bases for proteolysis and cross-linking, we have used cryo-electron micrographs to reconstruct the three-dimensional structures of purified particles from four discrete stages in the assembly pathway: Prohead I, Prohead II, Head I and Head II. Prohead I has icosahedral T = 7 packing of blister-shaped pentamers and hexamers. The pentamers are 5-fold symmetric, but the hexamers exhibit an unusual departure from 6-fold symmetry, as if two trimers had undergone a shear dislocation of about 25 Angstrom. Proteolytic conversion to Prohead II leaves the outer surface largely unchanged, but a major loss of density from the inner surface is observed, which we infer to represent the excision of the amino-terminal domains of the capsid protein. Upon expansion to the Head I state, the capsid becomes markedly larger, thinner walled, and more polyhedral: moreover, the capsomer shapes change radically; especially notable is the disappearance of the large hexon dislocation. No differences between Head I and the covalently cross-linked Head II could be observed at the current resolution of about 25 Angstrom, from which we infer that it is the conformational rearrangements effected by expansion that create the micro-environments needed for the autocatalytic formation of the isodipeptide bonds found in the mature virions (''pseudo-active sites''). (C) 1995 Academic Press Limited C1 NIAMSD,STRUCT BIOL LAB,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT BIOL SCI,PITTSBURGH,PA 15260. RI Conway, James/A-2296-2010 OI Conway, James/0000-0002-6581-4748 FU NIGMS NIH HHS [GM47795] NR 61 TC 141 Z9 141 U1 0 U2 7 PU ACADEMIC PRESS (LONDON) LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD OCT 13 PY 1995 VL 253 IS 1 BP 86 EP 99 DI 10.1006/jmbi.1995.0538 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RZ240 UT WOS:A1995RZ24000009 PM 7473720 ER PT J AU NOHR, D EIDEN, LE WEIHE, E AF NOHR, D EIDEN, LE WEIHE, E TI COEXPRESSION OF VASOACTIVE-INTESTINAL-PEPTIDE, CALCITONIN-GENE-RELATED PEPTIDE AND SUBSTANCE-P IMMUNOREACTIVITY IN PARASYMPATHETIC NEURONS OF THE RHESUS-MONKEY LUNG SO NEUROSCIENCE LETTERS LA English DT Article DE SUBSTANCE P; CALCITONIN GENE-RELATED PEPTIDE; VASOACTIVE INTESTINAL PEPTIDE; LUNG; MONKEY; PARASYMPATHETIC INNERVATION ID LOWER RESPIRATORY-TRACT; GUINEA-PIG; REGULATORY PEPTIDES; SENSORY NERVES; COEXISTENCE; CAPSAICIN; MAMMALS; LOCALIZATION; POLYPEPTIDE; INNERVATION AB By the use of light microscopic immunohistochemistry, the present study investigates whether substance P (SP) and calcitonin gene-related peptide (CGRP), which are well documented neurotransmitter candidates in primary sensory fibers, are also expressed in parasympathetic neurons of the rhesus monkey lung. A combination of double fluorescence immunohistochemistry and staining of adjacent sections revealed triple coexistence of SP, CGRP and the cholinergic co-transmitter vasoactive intestinal peptide (VIP) in a large number of neuronal cell bodies in intrinsic peribronchial ganglia. In addition, there was co-localization of SP and CGRP in choline acetyltransferase (ChAT)-positive neurons. These data suggest that SP and CGRP, in addition to their sensory role, are cholinergic cotransmitter candidates in the postganglionic parasympathetic innervation of primate lung. Go-release and co-function of SP and CGRP with VIP and acetylcholine may be important in the regulation of pulmonary physiology and in pulmonary pathophysiology. C1 UNIV MAINZ,DEPT ANAT,D-55099 MAINZ,GERMANY. NIMH,BETHESDA,MD. UNIV MARBURG,DEPT ANAT & CELL BIOL,D-35033 MARBURG,GERMANY. OI Eiden, Lee/0000-0001-7524-944X NR 32 TC 14 Z9 14 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 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD OCT 13 PY 1995 VL 199 IS 1 BP 25 EP 28 DI 10.1016/0304-3940(95)12001-K PG 4 WC Neurosciences SC Neurosciences & Neurology GA TC534 UT WOS:A1995TC53400007 PM 8584218 ER PT J AU SUNDARESAN, M YU, ZX FERRANS, VJ IRANI, K FINKEL, T AF SUNDARESAN, M YU, ZX FERRANS, VJ IRANI, K FINKEL, T TI REQUIREMENT FOR GENERATION OF H2O2 FOR PLATELET-DERIVED GROWTH-FACTOR SIGNAL-TRANSDUCTION SO SCIENCE LA English DT Article ID VITAMIN-E CONSUMPTION; CELLS; PROTEIN; DISEASE; PHOSPHORYLATION; INHIBITION; EXPRESSION; APOPTOSIS; RECEPTOR; RISK AB Stimulation of rat vascular smooth muscle cells (VSMCs) by platelet-derived growth factor (PDGF) transiently increased the intracellular concentration of hydrogen peroxide (H2O2). This increase could be blunted by increasing the intracellular concentration of the scavenging enzyme catalase or by the chemical antioxidant N-acetylcysteine. The response of VSMCs to PDGF, which includes tyrosine phosphorylation, mitogen-activated protein kinase stimulation, DNA synthesis, and chemotaxis, was inhibited when the growth factor-stimulated rise in H2O2 concentration was blocked. These results suggest that H2O2 may act as a signal-transducing molecule, and they suggest a potential mechanism for the cardioprotective effects of antioxidants. C1 NHLBI, CARDIOL BRANCH, BETHESDA, MD 20892 USA. NHLBI, PATHOL SECT, BETHESDA, MD 20892 USA. NR 31 TC 1923 Z9 1969 U1 20 U2 90 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 EI 1095-9203 J9 SCIENCE JI Science PD OCT 13 PY 1995 VL 270 IS 5234 BP 296 EP 299 DI 10.1126/science.270.5234.296 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ342 UT WOS:A1995RZ34200038 PM 7569979 ER PT J AU PEGG, AE SWENN, K CHAE, MY DOLAN, ME MOSCHEL, RC AF PEGG, AE SWENN, K CHAE, MY DOLAN, ME MOSCHEL, RC TI INCREASED KILLING OF PROSTATE, BREAST, COLON, AND LUNG-TUMOR CELLS BY THE COMBINATION OF INACTIVATORS OF O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE AND N,N'-BIS(2-CHLOROETHYL)-N-NITROSOUREA SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; O-6-BENZYLGUANINE; 2,4-DIAMINO-6-BENZYLOXY-5-NITROSOPYRIMIDINE; 2,4-DIAMINO-6-BENZYLOXY-5-NITROPYRIMIDIN N,N'-BIS(2-CHLOROETHYL)-N-NITROSOUREA; CANCER CHEMOTHERAPY ID HUMAN O6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; ALKYLATING-AGENTS; CROSS-LINK; SENSITIVITY; DNA; O6-BENZYLGUANINE; 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA; DEPLETION; METHYLTRANSFERASE; O-6-BENZYLGUANINE AB The ability of a number of compounds that act as inactivators of O-6-alkylguanine-DNA alkyltransferase (AGT) to sensitize human tumor cell lines to the effects of N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU) were examined. The AGT inactivators tested included O-6-benzylguanine (BG) and its 8-aza-, 8-bromo-, 8-methyl-, 8-oxo, and 8-amino-derivatives and O-6-[p-(hydroxymethyl)benzyl]guanine. All of these compounds except the 8-amino-derivative were active in greatly increasing the killing of HT29 colon, Du145 prostate, MCF-7 breast and A549 lung tumor cells by BCNU. Their activities were comparable to those of BG. Two pyrimidines, 2,4-diamino-6-benzyloxy-5-nitrosopyrimidine and 2,4-diamino-6-benzyloxy-5-nitropyrimidine, were found to be considerably more potent than BG in enhancing BCNU-induced cell killing. The addition of a steroid group to the 9-position of BG forming either O-6-benzyl-9-[3-oxo-4-androsten-17 beta-yloxycarbonyl)methyl]guanine O-6-benzyl-9-[3-oxo-5 alpha-androstan-17 beta-yloxycarbonyl)methyl]guanine also produced compounds effective in enhancing the cytotoxicity of BCNU when added at 10 mu M. These results indicate that a range of potent compounds with potentially different pharmacokinetics is available to test the hypothesis that inactivation of AGT overcomes the resistance of many tumor cells to nitrosoureas. C1 PENN STATE UNIV,COLL MED,MILTON S HERSHEY MED CTR,DEPT PHARMACOL,HERSHEY,PA 17033. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702. UNIV CHICAGO,HEMATOL ONCOL SECT,CHICAGO,IL 60637. RP PEGG, AE (reprint author), PENN STATE UNIV,COLL MED,MILTON S HERSHEY MED CTR,DEPT CELLULAR & MOLEC PHYSIOL,POB 850,HERSHEY,PA 17033, USA. FU NCI NIH HHS [CA-57725, CA-18137] NR 32 TC 44 Z9 45 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD OCT 12 PY 1995 VL 50 IS 8 BP 1141 EP 1148 DI 10.1016/0006-2952(95)00249-Y PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TC823 UT WOS:A1995TC82300004 PM 7488227 ER PT J AU DALY, JW LUEDERS, J PADGETT, WL SHIN, Y GUSOVSKY, F AF DALY, JW LUEDERS, J PADGETT, WL SHIN, Y GUSOVSKY, F TI MAITOTOXIN-ELICITED CALCIUM INFLUX IN CULTURED-CELLS EFFECT OF CALCIUM-CHANNEL - EFFECT OF CALCIUM-CHANNEL BLOCKERS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE MAITOTOXIN; CALCIUM CHANNELS ID INTRACELLULAR CA2+ STORES; PHOSPHOINOSITIDE BREAKDOWN; CYTOCHROME-P-450; INHIBITION; ENTRY; RAT; MECHANISMS; MESSENGER; DEPLETION AB Maitotoxin elicited a marked influx of Ca-45(2+) into NIH 3T3 fibroblast cells. The influx was blocked by imidazoles (econazole, miconazole, SKF 96365, clotrimazole, calmidazolium) with IC50 values from 0.56 to 3 mu M. Phenylalkylamines (verapamil, methoxyverapamil) and nitrendipine were less potent, and diltiazem was very weak. Among other calcium blockers, the diphenylbutylpiperidines fluspirilene and penfluridol, the diphenylpropylpiperidine loperamide, and the local anesthetic proadifen were quite active with IC50 values of 2-4 mu M. The pattern of inhibition of maitotoxin-elicited calcium influx did not correspond to the ability of the agents to block elevation of calcium that ensues through calcium-release activated calcium (CRAC) channels after activation of phosphoinositide breakdown by ATP in HL-60 cells. The imidazoles did block CRAC channels, but fluspirilene, penfluridol, loperamide and proadifen were ineffective. Loperamide actually appeared to enhance influx of calcium via the activated CRAC channels. The imidazoles, in particular calmidazolium, caused an apparent influx of calcium and caused a stimulation of phosphoinositide breakdown in HL-60 cells. RP DALY, JW (reprint author), NIH,BLDG 8,RM 1A17,BETHESDA,MD 20892, USA. NR 34 TC 42 Z9 43 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD OCT 12 PY 1995 VL 50 IS 8 BP 1187 EP 1197 DI 10.1016/0006-2952(95)00257-Z PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TC823 UT WOS:A1995TC82300010 PM 7488233 ER PT J AU HUDGINS, WR SHACK, S MYERS, CE SAMID, D AF HUDGINS, WR SHACK, S MYERS, CE SAMID, D TI CYTOSTATIC ACTIVITY OF PHENYLACETATE AND DERIVATIVES AGAINST TUMOR-CELLS - CORRELATION WITH LIPOPHILICITY AND INHIBITION OF PROTEIN PRENYLATION SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE AROMATIC FATTY ACIDS; LIPOPHILICITY; CYTOSTASIS; PHENOTYPIC REVERSION; PROSTATE CANCER; GLIOBLASTOMA; MELANOMA; PLANTS ID FETAL HEMOGLOBIN PRODUCTION; ACID; 4-PHENYLBUTYRATE; DIFFERENTIATION; METABOLISM; PHENYL AB The aromatic fatty acid phenylacetate, a common metabolite of phenylalanine, shows promise as a relatively non-toxic drug for cancer treatment. This slowly metabolized fatty acid alters tumor cell lipid metabolism causing, among other effects, inhibition of protein prenylation critical to malignant growth. In pursuit of more potent analogues, we have examined the activity of related compounds against tumor cell lines established from patients with advanced prostatic carcinoma, glioblastomas, and malignant melanoma. Like phenylacetate, derivatives containing alpha-carbon or ring substitutions induced cytostasis and phenotypic reversion at non-toxic concentrations. Potency was correlated with the degree of calculated lipophilicity of the aromatic fatty acid, and the extent of inhibition of protein prenylation. Remarkably, a parallel cytostatic activity was reported in embryonic plant cells, which respond to phenylacetate and its analogues in the same concentration range and the same rank order of lipophilicity. These data suggest that phenylacetate and its analogues may act through common mechanisms to inhibit the growth of vastly divergent, undifferentiated cell types, and provide a basis for the development of new agents for the treatment of human malignancies. C1 NCI,DIV CANC TREATMENT,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. UNIV VIRGINIA,CTR CANC,CHARLOTTESVILLE,VA 22908. NR 31 TC 38 Z9 38 U1 2 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD OCT 12 PY 1995 VL 50 IS 8 BP 1273 EP 1279 DI 10.1016/0006-2952(95)02013-3 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TC823 UT WOS:A1995TC82300021 PM 7488244 ER PT J AU HUGIN, AW RUDIKOFF, E MORSE, HC AF HUGIN, AW RUDIKOFF, E MORSE, HC TI VARIABILITY IN THE GROWTH SUSTAINING CAPACITY OF MEDIUM BATCHES SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Note DE MEDIUM; PROLIFERATION; VARIABILITY; IN VITRO; QUALITY CONTROL AB Medium batches, analysed in various spontaneous and mitogen induced proliferation assays, revealed heterogeneity in their growth promoting activity. This can critically affect test results and suggests that culture media can be a source of variability and problems in cell culture work. The manufacturers of media should broaden their quality control of medium batches. C1 NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. OI Morse, Herbert/0000-0002-9331-3705 NR 3 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD OCT 12 PY 1995 VL 186 IS 1 BP 151 EP 154 DI 10.1016/0022-1759(95)00142-W PG 4 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA TA532 UT WOS:A1995TA53200015 PM 7561143 ER PT J AU GOLDSTEIN, AM FRASER, MC STRUEWING, JP HUSSUSSIAN, CJ RANADE, K ZAMETKIN, DP FONTAINE, LS ORGANIC, SM DRACOPOLI, NC CLARK, WH TUCKER, MA AF GOLDSTEIN, AM FRASER, MC STRUEWING, JP HUSSUSSIAN, CJ RANADE, K ZAMETKIN, DP FONTAINE, LS ORGANIC, SM DRACOPOLI, NC CLARK, WH TUCKER, MA TI INCREASED RISK OF PANCREATIC-CANCER IN MELANOMA-PRONE KINDREDS WITH P16(INK4) MUTATIONS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID MALIGNANT-MELANOMA; FAMMM SYNDROME; FAMILIAL MELANOMA; DYSPLASTIC NEVUS; PROGRESSION; LINKAGE; LOCUS AB Background. A gene on chromosome 9p, p16(INK4), has been implicated in the pathogenesis of cutaneous malignant melanoma in 19 melanoma-prone families. In 10 of these kindreds mutations that impaired the function of the p16(INK4) protein (p16M alleles) cosegregated with the disease. By contrast, in the other nine kindreds the mutation did not alter the function of p16(INK4) (p16W alleles). We looked for differences in clinical and genetic epidemiologic features in these two groups of families. Methods. We compared the median ages at diagnosis of melanoma, number of melanomas, thickness of the tumors, and number of nevi in the kindreds. We estimated prospectively the risks of melanoma or other cancers in families followed for 6 to 18 years and the risks of other cancers since 1925 (the entire period) by comparing the number of cancer cases observed with the number expected. Results. The risk of invasive melanoma was increased by a factor of 75 in kindreds with p16W alleles and a factor of 38 in kindreds with p16W alleles. Although this difference was not significant (P=0.14), there was a striking difference in the risk of other tumors. In kindreds with p16M alleles, the risk of pancreatic cancer was increased by a factor of 13 in the prospective period (2 cases observed, 0.15 expected; standardized incidence ratio, 13.1; 95 percent confidence interval, 1.5 to 47.4) and by a factor of 22 in the entire period (7 cases observed, 0.32 expected; standardized incidence ratio, 21.8; 95 percent confidence interval, 8.7 to 44.8). In contrast, we found no cases of pancreatic cancer in kindreds with p16W alleles. Conclusions. The development of pancreatic cancer in kindreds prone to melanoma may require a p16M mutation. Genetic factors, such as the kind of mutation found in p16(INK4), may explain the inconsistent occurrence of other cancers in these kindreds. C1 NIH, WARREN G MAGNUSON CLIN CTR, DEPT NURSING, BETHESDA, MD 20892 USA. NIH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA. WESTAT CORP, ROCKVILLE, MD USA. WASHINGTON UNIV, SCH MED, DEPT SURG, ST LOUIS, MO 63110 USA. BATTELLE SRA, ROCKVILLE, MD USA. SEQUANA THERAPEUT INC, LA JOLLA, CA USA. UNIV PENN, SCH MED, PIGMENTED LES STUDY GRP, PHILADELPHIA, PA 19104 USA. UNIV PENN, SCH MED, DEPT DERMATOL, PHILADELPHIA, PA 19104 USA. HARVARD UNIV, BETH ISRAEL HOSP, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. RP GOLDSTEIN, AM (reprint author), NCI, GENET EPIDEMIL BRANCH,EXECUT PLAZA N,RM 439, 6130 EXECUT BLVD, MSC 7372, BETHESDA, MD 20892 USA. RI Struewing, Jeffery/C-3221-2008; Tucker, Margaret/B-4297-2015; Struewing, Jeffery/I-7502-2013 OI Struewing, Jeffery/0000-0002-4848-3334 NR 32 TC 409 Z9 418 U1 1 U2 4 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 12 PY 1995 VL 333 IS 15 BP 970 EP 974 DI 10.1056/NEJM199510123331504 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA RY586 UT WOS:A1995RY58600004 PM 7666916 ER PT J AU FIGG, WD MIDDLEMAN, M SARTOR, O AF FIGG, WD MIDDLEMAN, M SARTOR, O TI MUTATED ANDROGEN RECEPTORS OF PROSTATE-CANCER CELLS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 LOUISIANA STATE UNIV,SHREVEPORT,LA 71130. RP FIGG, WD (reprint author), NCI,BETHESDA,MD 20892, USA. RI Figg Sr, William/M-2411-2016 NR 5 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 12 PY 1995 VL 333 IS 15 BP 1010 EP 1010 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA RY586 UT WOS:A1995RY58600023 PM 7666906 ER PT J AU MINKOFF, H WILLOUGHBY, A AF MINKOFF, H WILLOUGHBY, A TI PEDIATRIC HIV DISEASE, ZIDOVUDINE IN PREGNANCY, AND UNBLINDING HEELSTICK SURVEYS - REFRAMING THE DEBATE ON PRENATAL HIV TESTING SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID HUMAN-IMMUNODEFICIENCY-VIRUS; INFECTION; WOMEN; POPULATION C1 NICHHD,CTR RES MOTHERS & CHILDREN,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,ROCKVILLE,MD. RP MINKOFF, H (reprint author), SUNY HLTH SCI CTR,DEPT OBSTET & GYNECOL,450 CLARKSON AVE,BOX 24,BROOKLYN,NY 11203, USA. NR 14 TC 32 Z9 32 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 11 PY 1995 VL 274 IS 14 BP 1165 EP 1168 DI 10.1001/jama.274.14.1165 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA RY056 UT WOS:A1995RY05600033 PM 7563489 ER PT J AU GRANT, CM MILLER, PF HINNEBUSCH, AG AF GRANT, CM MILLER, PF HINNEBUSCH, AG TI SEQUENCES-5' OF THE FIRST UPSTREAM OPEN READING FRAME IN GCN4 MESSENGER-RNA ARE REQUIRED FOR EFFICIENT TRANSLATIONAL REINITIATION SO NUCLEIC ACIDS RESEARCH LA English DT Article ID MESSENGER-RNA; SACCHAROMYCES-CEREVISIAE; PROTEIN-SYNTHESIS; YEAST; MECHANISMS; INITIATION; ACTIVATOR; CODONS AB Translation of yeast GCN4 mRNA occurs by a reinitiation mechanism that is modulated by amino acid levels in the cell, Ribosomes which translate the first of four upstream open reading frames (uORFs) in the mRNA leader resume scanning and can reinitiate downstream, Under non-starvation conditions reinitiation occurs at one of the remaining three uORFs and GCN4 is repressed. Under starvation conditions, in contrast, ribosomes bypass the uORFs and reinitiate at GCN4 instead, The high frequency of reinitiation following uORF1 translation depends on an adequate distance to the next start codon and particular sequences surrounding the uORF1 stop codon, We present evidence that sequences 5' to uORF1 also strongly enhance reinitiation, First, reinitiation was severely inhibited when uORF1 was transplanted into the position of uORF4, even though the native sequence environment of the uORF1 stop codon was maintained, and this effect could not be accounted for by the decreased uORF1-GCN4 spacing, Second, insertions and deletions in the leader preceding uORF1 greatly reduced reinitiation at GCN4, Sequences 5' to uORF1 may influence the probability of ribosome release following peptide termination at uORF1. Alternatively, they may facilitate rebinding of an initiation factor required for reinitiation prior to resumption of the scanning process. C1 NICHHD,MOLEC GENET LAB,MOLEC GENET LOWER EUKARYOTES SECT,BETHESDA,MD 20892. NR 21 TC 29 Z9 30 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD OCT 11 PY 1995 VL 23 IS 19 BP 3980 EP 3988 DI 10.1093/nar/23.19.3980 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TC240 UT WOS:A1995TC24000027 PM 7479046 ER PT J AU BEIGELMAN, L MATULICADAMIC, J HAEBERLI, P USMAN, N DONG, BH SILVERMAN, RH KHAMNEI, S TORRENCE, PF AF BEIGELMAN, L MATULICADAMIC, J HAEBERLI, P USMAN, N DONG, BH SILVERMAN, RH KHAMNEI, S TORRENCE, PF TI SYNTHESIS AND BIOLOGICAL-ACTIVITIES OF A PHOSPHORODITHIOATE ANALOG OF 2',5'-OLIGOADENYLATE SO NUCLEIC ACIDS RESEARCH LA English DT Article ID CHEMICAL SYNTHESIS; INTERFERON-SYSTEM; PROTEIN-SYNTHESIS; 2-5A; BINDING; RNA; 5'-O-TRIPHOSPHOADENYLYL(2'->5')ADENYLYL(2'->5')ADENOSINE; OLIGORIBONUCLEOTIDES; OLIGONUCLEOTIDES; ACTIVATION AB To enhance the resistance of 2-5A (pppA2'p5'A2'p5'A) to degradation by exo- and endonucleases, a phosphorodithioate analog was synthesized using a solid-phase phosphite triester approach with N-6-benzoyl-5'-O-dimethoxytrityl-3'-O-t-butyldimethylsilyladenosine 2'- S-(beta-thiobenzoylethyl)-pyrrolidinophosphorothioamidite . 5'-Monophosphorylation was accomplished with 2- 2-(4,4'-dimethoxytrityloxy)-ethylsulfonly ethyl-(2-cyanoethyl)-(N,N-diisopropyl)-phosphoramidite. The resulting product, p5'A2'(s2p)- 5'A2'(s2p)5'A, was approximately 10-fold less effective as an activator of purified human recombinant 2-5A-dependent RNase than was 2-5A itself. This loss of activation ability was related directly to the loss of binding ability of the phosphorodithioate analog. As predicted, p5'A2'(s2p)5'A2'(s2p)5'A was stable to snake venom phosphodiesterase and the nucleolytic activities of both human lymphoblastoid CEM cell extracts and human serum, under conditions that led to facile degradation of parent 2-5A. This nuclease stability permitted the observation of the CEM cell extracts and human serum phosphatase activity which led to 5'-dephosphorylation of p5'A2'(s2p)5'A2'(s2p)5'A. C1 NIDDKD,MED CHEM LAB,BIOMED CHEM SECT,BETHESDA,MD 20892. RIBOZYME PHARMACEUT INC,DEPT CHEM & BIOCHEM,BOULDER,CO 80301. CLEVELAND CLIN FDN,RES INST,DEPT CANC BIOL,CLEVELAND,OH 44195. FU NCI NIH HHS [5RO1 CA44059] NR 44 TC 19 Z9 19 U1 1 U2 9 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD OCT 11 PY 1995 VL 23 IS 19 BP 3989 EP 3994 DI 10.1093/nar/23.19.3989 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TC240 UT WOS:A1995TC24000028 PM 7479047 ER PT J AU NAGY, B COSTELLO, R CSAKO, G AF NAGY, B COSTELLO, R CSAKO, G TI DOWNWARD BLOTTING OF PROTEINS IN A MODEL-BASED ON APOLIPOPROTEIN(A) PHENOTYPING SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID DIAZOBENZYLOXYMETHYL-PAPER; ELECTROPHORETIC TRANSFER; GEL-ELECTROPHORESIS; POLYACRYLAMIDE GELS; DNA; NITROCELLULOSE; POLYMORPHISM; ISOFORMS; ANTIBODY; RNA AB Standard immunoblotting (''Western blot'') involves electrotransfer of proteins from a separation gel (usually acrylamide) onto a membrane. Recently, a downward capillary method with increased hybridization efficiency was developed for DNA and RNA. The present work assessed the applicability of this method to proteins in a model based on human apolipoprotein(a) [apo(a)] isoforms which consist of a single, >200-kDa polypeptide chain varying in size with a repeat sequence. After reduction treatment and sodium dodecyl sulfate-agarose gel electrophoresis, serum proteins were transferred from the gel by upward or downward (Turboblotter) capillary action onto nitrocellulose membranes in Tris-buffered saline, pH 7.5, at room temperature. Increased detectability of apo(a) isoforms was achieved by substituting comparatively high molar concentrations of protein A for true second antibody. With downward capillary transfer and short 37 degrees C incubations, the apo(a) phenotyping could be completed in about 26 h and required less than 8 h effective processing time. The downward transfer was about twice as fast (complete within 1 h) as the upward version and with this speed it offers a good alternative to electroblotting as well. (C) 1995 Academic Press, Inc. C1 NIH, WARREN G MAGNUSON CLIN CTR, DEPT CLIN PATHOL, BETHESDA, MD 20892 USA. RI Nagy, Balint/F-6943-2012 NR 17 TC 3 Z9 3 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 0003-2697 EI 1096-0309 J9 ANAL BIOCHEM JI Anal. Biochem. PD OCT 10 PY 1995 VL 231 IS 1 BP 40 EP 45 DI 10.1006/abio.1995.1500 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA RZ602 UT WOS:A1995RZ60200006 PM 8678318 ER PT J AU BENNETT, LM HAUGENSTRANO, A COCHRAN, C BROWNLEE, HA FIEDOREK, FT WISEMAN, RW AF BENNETT, LM HAUGENSTRANO, A COCHRAN, C BROWNLEE, HA FIEDOREK, FT WISEMAN, RW TI ISOLATION OF THE MOUSE HOMOLOG OF BRCA1 AND GENETIC-MAPPING TO MOUSE CHROMOSOME-11 SO GENOMICS LA English DT Article ID PROTEIN; LINKAGE AB The BRCA1 gene is in large part responsible for hereditary human breast and ovarian cancer. Here we report the isolation of the murine Brca1 homologue cDNA clones. In addition, we identified genomic P1 clones that contain most, if not all, of the mouse Brca1 locus. DNA sequence analysis revealed that the mouse and human coding regions are 75% identical at the nucleotide level while the predicted amino acid identity is only 58%. A DNA sequence variant in the Brca1 locus was identified and used to map this gene on a (Mus m. musculus Czech II x C57BL/KsJ)F1 x C57BL/KsJ intersubspecific backcross to distal mouse chromosome 11. The mapping of this gene to a region highly syntenic with human chromosome 17, coupled with Southern and Northern analyses, confirms that we isolated the murine Brca1 homologue rather than a related RING finger gene. The isolation of the mouse Brca1 homologue will facilitate the creation of mouse models for germline BRCA1 defects. (C) 1995 Academic Press, Inc. C1 UNIV N CAROLINA,DEPT MED,CHAPEL HILL,NC 27599. RP BENNETT, LM (reprint author), NIEHS,MOLEC CARCINOGENESIS LAB,MD C4-06,111 ALEXANDER DR,RES TRIANGLE PK,NC 27709, USA. FU NIDDK NIH HHS [DK44074] NR 17 TC 41 Z9 42 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD OCT 10 PY 1995 VL 29 IS 3 BP 576 EP 581 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA TA966 UT WOS:A1995TA96600004 PM 8575748 ER PT J AU HULSEBOS, TJM GILBERT, DJ DELATTRE, O SMINK, LJ DUNHAM, I WESTERVELD, A THOMAS, G JENKINS, NA COPELAND, NG AF HULSEBOS, TJM GILBERT, DJ DELATTRE, O SMINK, LJ DUNHAM, I WESTERVELD, A THOMAS, G JENKINS, NA COPELAND, NG TI ASSIGNMENT OF THE BETA-B1 CRYSTALLIN GENE (CRYBB1) TO HUMAN-CHROMOSOME-22 AND MOUSE CHROMOSOME-5 SO GENOMICS LA English DT Article ID LENS CRYSTALLINS; EYE LENS; SEQUENCE; LINKAGE; RAT; POLYMORPHISM; POLYPEPTIDE; EVOLUTION; MUTATION; PROTEINS AB By using primers complementary to the rat beta B1 crystallin gene sequence, we amplified exons 5 and 6 of the orthologous human gene (CRYBB1). The amplified human segments displayed greater than 88% sequence homology to the corresponding rat and bovine sequences. CRYBB1 was assigned to the group 5 region in 22q11.2-q12.1 by hybridizing the exon 6 PCR product to somatic cell hybrids containing defined portions of human chromosome 22. The exon 5 and exon 6 PCR products of CRYBB1 were used to localize, by interspecific backcross mapping, the mouse gene (Crybb1) to the central portion of chromosome 5. Three other beta crystallin genes (beta B2(-1), beta B3, and beta A4) have previously been mapped to the same regions in human and mouse. We demonstrate that the beta B1 and beta A4 crystallin genes are very closely linked in the two species. These assignments complete the mapping and identification of the human and mouse homologues of the major beta crystallins genes that are expressed in the bovine lens. (C) 1995 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. INST CURIE,GENET TUMEURS LAB,PARIS,FRANCE. SANGER CTR,CAMBRIDGE CB10 1RQ,ENGLAND. RP HULSEBOS, TJM (reprint author), UNIV AMSTERDAM,FAC MED,ACAD MED CTR,INST HUMAN GENET,MEIBERGDREEF 15,1105 AZ AMSTERDAM,NETHERLANDS. FU PHS HHS [N01-C0-46000] NR 39 TC 11 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 0888-7543 J9 GENOMICS JI Genomics PD OCT 10 PY 1995 VL 29 IS 3 BP 712 EP 718 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA TA966 UT WOS:A1995TA96600020 PM 8575764 ER PT J AU BROOKER, DR KOZAK, CA KLEYMAN, TR AF BROOKER, DR KOZAK, CA KLEYMAN, TR TI EPITHELIAL SODIUM-CHANNEL GENES SCNN1B AND SCNN1G ARE CLOSELY LINKED ON DISTAL MOUSE CHROMOSOME-7 SO GENOMICS LA English DT Note ID SKELETAL-MUSCLE; ALPHA-SUBUNIT; ISOFORMS; BRAIN AB The chromosomal localizations of Scnn1b and Scnn1g, genes corresponding to the beta- and gamma-subunits, respectively, of an epithelial non-voltage-gated amiloride-sensitive sodium channel, were determined by analyses of two sets of multilocus crosses using probes generated by polymerase chain reaction and a mouse kidney cortical collecting tubule cell line (M1). Scnn1b and Scnn1g were determined to be closely linked on distal mouse chromosome 7, showing no recombination with Zp2, whereas the gene for the alpha-subunit, Scnn1a, was confirmed to map to distal mouse chromosome 6. (C) 1995 Academic Press, Inc. C1 UNIV PENN,DEPT MED,DIV RENAL,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NIAID,BETHESDA,MD 20892. FU NIDDK NIH HHS [DK07006] NR 26 TC 7 Z9 7 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 0888-7543 J9 GENOMICS JI Genomics PD OCT 10 PY 1995 VL 29 IS 3 BP 784 EP 786 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA TA966 UT WOS:A1995TA96600033 PM 8575777 ER PT J AU COSENTINO, GP VENKATESAN, S SERLUCA, FC GREEN, SR MATHEWS, MB SONENBERG, N AF COSENTINO, GP VENKATESAN, S SERLUCA, FC GREEN, SR MATHEWS, MB SONENBERG, N TI DOUBLE-STRANDED-RNA-DEPENDENT PROTEIN-KINASE AND TAR RNA-BINDING PROTEIN FORM HOMODIMERS AND HETERODIMERS IN-VIVO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE EIF-2-ALPHA KINASE; PROTEIN DIMERIZATION; YEAST 2-HYBRID ASSAY ID MOUSE FIBROBLASTS; INTERFERON ACTION; 2-HYBRID SYSTEM; P68 KINASE; MECHANISM; YEAST; DAI; PHOSPHORYLATION; TRANSFORMATION; ACTIVATION AB The yeast two-hybrid system and far-Western protein blot analysis were used to demonstrate dimerization of human double-stranded RNA (dsRNA)-dependent protein kinase (PKR) in vivo and in vitro. A catalytically inactive mutant of PKR with a single amino acid substitution (K296R) was found to dimerize in vive, and a mutant with a deletion of the catalytic domain of PKR retained the ability to dimerize. In contrast, deletion of the two dsRNA-binding motifs in the N-terminal regulatory domain of PKR abolished dimerization. In vitro dimerization of the dsRNA-binding domain required the presence of dsRNA. These results suggest that the binding of dsRNA by PKR is necessary for dimerization. The mammalian dsRNA-binding protein TRBP, originally identified on the basis of its ability to bind the transactivation region (TAR) of human immunodeficiency virus RNA, also dimerized with itself and with PKR in the yeast assay. Taken together, these results suggest that complexes consisting of different combinations of dsRNA-binding proteins may exist in vivo. Such complexes could mediate differential effects on gene expression and control of cell growth. C1 MCGILL UNIV,MCGILL CANC CTR,MONTREAL,PQ H3G 1Y6,CANADA. BIOMEGA BOEHRINGER INGELHEIM RES INC,LAVAL,PQ H7S 2G5,CANADA. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. COLD SPRING HARBOR LAB,COLD SPRING HARBOR,NY 11724. RP COSENTINO, GP (reprint author), MCGILL UNIV,DEPT BIOCHEM,3655 DRUMMOND ST,MONTREAL,PQ H3G 1Y6,CANADA. FU NIAID NIH HHS [AI34552] NR 54 TC 143 Z9 144 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9445 EP 9449 DI 10.1073/pnas.92.21.9445 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200004 PM 7568151 ER PT J AU WONG, WT SCHUMACHER, C SALCINI, AE ROMANO, A CASTAGNINO, P PELICCI, PG DIFIORE, PP AF WONG, WT SCHUMACHER, C SALCINI, AE ROMANO, A CASTAGNINO, P PELICCI, PG DIFIORE, PP TI A PROTEIN-BINDING DOMAIN, EH, IDENTIFIED IN THE RECEPTOR TYROSINE KINASE SUBSTRATE EPS15 AND CONSERVED IN EVOLUTION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DROSOPHILA-TRITHORAX; ACUTE LEUKEMIAS; SEQUENCE; TRANSLOCATIONS; ALIGNMENT; SITES AB In this report we structurally and functionally define a binding domain that is involved in protein association and that we have designated EH (for Eps15 homology domain). This domain was identified in the tyrosine kinase substrate Eps15 on the basis of regional conservation with several heterogeneous proteins of yeast and nematode. The EH domain spans about 70 amino acids and shows approximate to 60% overall amino acid conservation, We demonstrated the ability of the EH domain to specifically bind cytosolic proteins in normal and malignant cells of mesenchymal, epithelial, and hematopoietic origin. These observations prompted our search for additional EH-containing proteins in mammalian cells. Using an EH domain-specific probe derived from the eps15 cDNA, we cloned and characterized a cDNA encoding an EH-containing protein with overall similarity to Eps15; we designated this protein Eps15r (for Eps15-related), Structural comparison of Eps15 and Eps15r defines a family of signal transducers possessing extensive networking abilities including EH-mediated binding and association with Src homology 3-containing proteins. C1 NCI, CELLULAR & MOLEC BIOL LAB, BETHESDA, MD 20892 USA. NCI, EXPTL CARCINOGENESIS LAB, BETHESDA, MD 20892 USA. ROCKEFELLER UNIV, NEW YORK, NY 10021 USA. IEO, I-20141 MILAN, ITALY. RI Di Fiore, Pier Paolo/K-2130-2012 OI Di Fiore, Pier Paolo/0000-0002-2252-0950 NR 24 TC 124 Z9 127 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9530 EP 9534 DI 10.1073/pnas.92.21.9530 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200021 PM 7568168 ER PT J AU TZOUNOPOULOS, T GUY, HR DURELL, S ADELMAN, JP MAYLIE, J AF TZOUNOPOULOS, T GUY, HR DURELL, S ADELMAN, JP MAYLIE, J TI MIN-K CHANNELS FORM BY ASSEMBLY OF AT LEAST 14 SUBUNITS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID GATED POTASSIUM CHANNELS; MEMBRANE-PROTEIN; RAT UTERUS; EXPRESSION; ISK; STOICHIOMETRY; DROSOPHILA; CLONING; BRAIN AB Injection of min K mRNA into Xenopus oocytes results in expression of slowly activating voltage-dependent potassium channels, distinct from those induced by expression of other cloned potassium channels, The min K protein also differs in structure, containing only a single predicted transmembrane domain. While it has been demonstrated that all other cloned potassium channels form by association of four independent subunits, the number of min K monomers which constitute a functional channel is unknown. In rat min K, replacement of Ser-69 by Ala (S69A) causes a shift in the current-voltage (I-V) relationship to more depolarized potentials; currents are not observed at potentials negative to 0 mV. To determine the subunit stoichiometry of min K channels, wild-type and S69A subunits were coexpressed, Injections of a constant amount of wild-type mRNA with increasing amounts of S69A mRNA led to potassium currents of decreasing amplitude upon voltage commands to -20 mV. Applying a binomial distribution to the reduction of current amplitudes as a function of the different coinjection mixtures yielded a subunit stoichiometry of at least 14 monomers for each functional min K channel, A model is presented for how min K subunits may form a channel. C1 OREGON HLTH SCI UNIV,VOLLUM INST,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MOLEC & MED GENET,PORTLAND,OR 97201. NIH,MATH BIOL LAB,BETHESDA,MD 20892. RP TZOUNOPOULOS, T (reprint author), OREGON HLTH SCI UNIV,DEPT OBSTET & GYNECOL,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. NR 24 TC 29 Z9 30 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9593 EP 9597 DI 10.1073/pnas.92.21.9593 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200034 PM 7568179 ER PT J AU THIERRY, AR LUNARDIISKANDAR, Y BRYANT, JL RABINOVICH, P GALLO, RC MAHAN, LC AF THIERRY, AR LUNARDIISKANDAR, Y BRYANT, JL RABINOVICH, P GALLO, RC MAHAN, LC TI SYSTEMIC GENE-THERAPY - BIODISTRIBUTION AND LONG-TERM EXPRESSION OF A TRANSGENE IN MICE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GENE TRANSFER; LUCIFERASE; LIPOSOMES; EPISOMAL DNA VECTOR ID FIREFLY LUCIFERASE GENE; DNA LIPOSOME COMPLEXES; PLASMID DNA; DELIVERY; CELLS; INVIVO; ANTISENSE; TOXICITY; MOUSE AB We have investigated the in vivo efficacy of a systemic gene transfer method, which combines a liposomal delivery system (DLS liposomes) with episomally replicative DNA plasmids to effect long-term expression of a transgene in cells, A single i,v, injection of a plasmid DNA vector containing the luciferase gene as a marker was administered with the DLS liposomes in BALB/c mice. The luciferase gene and its product were found in all mouse tissues tested as determined by PCR analysis and immunohistochemistry. Luciferase activity was also detected in all tissues tested and was present in lung, liver, spleen, and heart up to 3 months postinjection, In contrast to the nonepisomal vectors tested (pRSV-luc and pCMVintlux), human papovavirus (BKV)-derived episomal vectors showed long-term transgene expression, We found that these episomal vectors replicated extrachromosomally in lung 2 weeks postinjection, Results indicated that transgene expression in specific tissues depended on the promoter element used, DNA/liposome formulation, dose of DNA per injection, and route of administration. C1 NINCDS,NEUROCHEM LAB,BETHESDA,MD 20892. NIDR,ANIM CARE UNIT,BETHESDA,MD 20892. RP THIERRY, AR (reprint author), NCI,TUMOR CELL BIOL LAB,BLDG 37,ROOM 6A09,37 CONVENT DR,BETHESDA,MD 20892, USA. RI thierry, alain/F-9492-2014 NR 21 TC 223 Z9 225 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9742 EP 9746 DI 10.1073/pnas.92.21.9742 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200064 PM 7568209 ER PT J AU ZWANZIG, R AF ZWANZIG, R TI SIMPLE-MODEL OF PROTEIN-FOLDING KINETICS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID GLOBULAR-PROTEINS; FOLDED STATES AB A simple model of the kinetics of protein folding is presented. The reaction coordinate is the ''correctness'' of a configuration compared with the native state. The model has a gap in the energy spectrum, a large configurational entropy, a free energy barrier between folded and partially folded states, and a good thermodynamic folding transition. Folding kinetics is described by a master equation. The folding time is estimated by means of a local thermodynamic equilibrium assumption and then is calculated both numerically and analytically by solving the master equation. The folding time has a maximum near the folding transition temperature and can have a minimum at a lower temperature. RP ZWANZIG, R (reprint author), NIH,PHYS CHEM LAB,BLDG 5,ROOM 116,BETHESDA,MD 20892, USA. NR 16 TC 156 Z9 157 U1 3 U2 21 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9801 EP 9804 DI 10.1073/pnas.92.21.9801 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200076 PM 7568221 ER PT J AU ENOCH, MA ROHRBAUGH, JW DAVIS, EZ HARRIS, CR ELLINGSON, RJ ANDREASON, P MOORE, V VARNER, JL BROWN, GL ECKARDT, MJ GOLDMAN, D AF ENOCH, MA ROHRBAUGH, JW DAVIS, EZ HARRIS, CR ELLINGSON, RJ ANDREASON, P MOORE, V VARNER, JL BROWN, GL ECKARDT, MJ GOLDMAN, D TI RELATIONSHIP OF GENETICALLY TRANSMITTED ALPHA-EEG TRAITS TO ANXIETY DISORDERS AND ALCOHOLISM SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE EEG; ANXIETY DISORDERS; ALCOHOLISM ID PANIC DISORDER; ELECTROENCEPHALOGRAM EEG; FREQUENCY ACTIVITY; DEPRESSION; VARIANTS; FAMILY; RISK; SONS; MEN AB We tested the hypothesis that a heritable EEG trait, the low voltage alpha (LV), is associated with psychiatric disorders, Modest to moderate evidence for genetic linkage of both panic disorder and the low voltage alpha trait to the same region of chromosome 20q has recently been reported, raising the issue of whether there is a phenotypic correlation between these traits, A total of 124 subjects including 50 unrelated index subjects and 74 relatives were studied, Alpha EEG power was measured and EEG phenotypes were impressionistically classified, Subjects were psychiatrically interviewed using the SADS-L and blind-rated by RDC criteria, Alcoholics were four times more likely to be LV (including so-called borderline low voltage alpha) than were nonalcoholic, nonanxious subjects. Alcoholics with anxiety disorder are 10 times more likely to be LV, However, alcoholics without anxiety disorder were similar to nonalcoholics in alpha power, An anxiety disorder (panic disorder, phobia, or generalized anxiety) was found in 14/17 LV subjects as compared to 34/101 of the rest of the sample (P < 0.01). Support for these observations was found in the unrelated index subjects in whom no traits would be shared by familial clustering. Lower alpha power in anxiety disorders was not state-dependent, as indicated by the Spielberger Anxiety Scale, Familial covariance of alpha power was 0.25 (P < 0.01), These findings indicate there may be a shared factor underlying the transmissible low voltage alpha EEG variant and vulnerability to anxiety disorders with associated alcoholism. This factor is apparently not rare, because LV was found in approximately 10% of unrelated index subjects and 5% of subjects free of alcoholism and anxiety disorders. (C) 1995 Wiley-Liss, Inc. C1 NIAAA,NEUROGENET LAB,BETHESDA,MD 20892. NIAAA,CLIN STUDIES LAB,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,DEPT PSYCHIAT,ST LOUIS,MO 63110. UNIV NEBRASKA,COLL MED,OMAHA,NE 68182. UNIV NEBRASKA,DEPT ELECT ENGN,LINCOLN,NE 68588. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 43 TC 38 Z9 41 U1 3 U2 6 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD OCT 9 PY 1995 VL 60 IS 5 BP 400 EP 408 DI 10.1002/ajmg.1320600510 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA RZ638 UT WOS:A1995RZ63800009 PM 8546153 ER PT J AU MCLAUGHLIN, JK CHOW, WH MANDEL, JS MELLEMGAARD, A MCCREDIE, M LINDBLAD, P SCHLEHOFER, B POMMER, W NIWA, S ADAMI, HO AF MCLAUGHLIN, JK CHOW, WH MANDEL, JS MELLEMGAARD, A MCCREDIE, M LINDBLAD, P SCHLEHOFER, B POMMER, W NIWA, S ADAMI, HO TI INTERNATIONAL RENAL-CELL CANCER STUDY .8. ROLE OF DIURETICS, OTHER ANTIHYPERTENSIVE MEDICATIONS AND HYPERTENSION SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID RISK-FACTORS; BLOOD-PRESSURE; CARCINOMA; MORTALITY AB Risk of renal-cell cancer in relation to use of diuretics, other anti-hypertensive medications and hypertension was assessed in a multi-center, population-based, case-control study conducted in Australia, Denmark, Germany, Sweden and the United States, using a shared protocol and questionnaire. A total of 1,732 histologically confirmed cases and 2,309 controls, frequency-matched to cases by age and sex, were interviewed. The association between renal-cell cancer and the drugs was estimated by relative risks (RRs) and 95% confidence intervals (Cls). Risks were increased among users of diuretics and other anti-hypertensive medications. After adjustment for hypertension, risk for diuretics was reduced to unity, except among long-term (15+ years) users. Risk for use of non-diuretic anti-hypertensive drugs remained significantly elevated and increased further with duration of use. Overall risk was not enhanced when both classes of medications were used. Excess risk was not restricted to any specific type of diuretic or anti-hypertensive drug and no trend was observed with estimated lifetime consumption of any particular type of product. The RR for hypertension after adjustment for diuretics and other anti-hypertensive medications was 1.4 (95% CI = 1.2-1.7), although among non-users of any anti-hypertensive medications, there was little excess risk associated with a history of hypertension. Exclusion of drug use that first occurred within 5 years of cancer diagnosis or interview did not alter the associations. Our findings suggest small effects on renal-cell cancer risk associated with hypertension and use of diuretics and other anti-hypertensive medications. However, because of potential misclassifications of these highly correlated variables, it is difficult to distinguish the effect of treatment from its indication, hypertension. (C) 1995 Wiley-Liss, Inc.* C1 NCI,BETHESDA,MD 20892. UNIV MINNESOTA,SCH PUBL HLTH,DIV ENVIRONM HLTH,MINNEAPOLIS,MN 55455. DANISH CANC SOC,DANISH CANC REGISTRY,COPENHAGEN,DENMARK. NEW S WALES CANC COUNCIL,CANC EPIDEMIOL RES UNIT,KINGS CROSS,AUSTRALIA. UNIV UPPSALA HOSP,DEPT CANC EPIDEMIOL,UPPSALA,SWEDEN. GERMAN CANC RES CTR,DIV CANC EPIDEMIOL,W-6900 HEIDELBERG,GERMANY. HUMBOLDT HOSP,BERLIN,GERMANY. WESTAT CORP,ROCKVILLE,MD. NR 21 TC 99 Z9 99 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 9 PY 1995 VL 63 IS 2 BP 216 EP 221 DI 10.1002/ijc.2910630212 PG 6 WC Oncology SC Oncology GA TB407 UT WOS:A1995TB40700011 PM 7591207 ER PT J AU KELLEY, MJ OTTERSON, GA KAYE, FJ POPESCU, NC JOHNSON, BE DIPAOLO, JA AF KELLEY, MJ OTTERSON, GA KAYE, FJ POPESCU, NC JOHNSON, BE DIPAOLO, JA TI CDKN2 IN HPV-POSITIVE AND HPV-NEGATIVE CERVICAL-CARCINOMA CELL-LINES SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID HUMAN PAPILLOMAVIRUS; RETINOBLASTOMA GENES; INTEGRATION; CANCER; P53; DNA AB Human cervical cancers frequently contain retinoblastoma protein (Rb) that is inactivated by binding with human papilloma virus (HPV) E7 protein or through mutation. The CDKN2 gene encodes p16(INKA) which inhibits cdk4-cyclin D phosphorylation of Rb, preventing the G(1)-S transition. To determine whether abnormalities of CDKN2 occur in cervical-cancer cells, II cervical cell lines, including 8 HPV-positive cell lines, 2 HPV-negative cell lines containing mutant Rb, and one tumorigenic cell line derived from normal cervical cells following transfection with HPV-16 and v-H-ros (CX16-2HR), were analyzed. No cell line had a homozygous deletion of exon I or 2 of CDKN2, and only one cell line, CX16-2HR, had an altered DNA sequence, which represents a common polymorphism at codon 148. To exclude the possibility of other subtle inactivating mutations, immunoblot analysis of protein lysates was performed using a polyclonal anti-p16(INKA) rabbit anti-serum. Abundant levels of normal-sized p16(INKA) were observed in all cell samples. Thus, no alterations of CDKN2 were detected in these cervical cell lines. These results confirm that mutational inactivation of p16(INKA) is a rare event in tumor samples with compromised Rb activity. (C) 1995 Wiley-Liss, Inc.* C1 NCI,BIOL LAB,BETHESDA,MD 20889. RP KELLEY, MJ (reprint author), NCI,NAVY MED ONCOL BRANCH,BLDG 8,ROOM 5101,BETHESDA,MD 20889, USA. RI kaye, frederic/E-2437-2011; OI Kelley, Michael/0000-0001-9523-6080 NR 34 TC 39 Z9 40 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 9 PY 1995 VL 63 IS 2 BP 226 EP 230 DI 10.1002/ijc.2910630214 PG 5 WC Oncology SC Oncology GA TB407 UT WOS:A1995TB40700013 PM 7591209 ER PT J AU HODGE, JW SCHLOM, J DONOHUE, SJ TOMASZEWSKI, JE WHEELER, CW LEVINE, BS GRITZ, L PANICALI, D KANTOR, JA AF HODGE, JW SCHLOM, J DONOHUE, SJ TOMASZEWSKI, JE WHEELER, CW LEVINE, BS GRITZ, L PANICALI, D KANTOR, JA TI A RECOMBINANT VACCINIA VIRUS EXPRESSING HUMAN PROSTATE-SPECIFIC ANTIGEN (PSA) - SAFETY AND IMMUNOGENICITY IN A NONHUMAN PRIMATE SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID PROTEINS; VECTORS; CDNA; GENE AB Prostate-specific antigen (PSA) is a serine protease secreted by prostatic epithelial cells acid is widely used as a marker for prostate cancer. The tissue specificity of PSA makes it a potential target for active specific immunotherapy, especially in prostate cancer patients who have undergone prostatectomy and in whom the only PSA-expressing tissue in the body resides in metastatic deposits. We report here the cloning, construction and immunological consequences of immunization of rhesus monkeys with a recombinant vaccinia virus expressing human BSA (designated rV-PSA). The prostate gland of the rhesus is structurally and functionally similar to the human prostate. While rodent and other mammalian species do not share homology with human PSA, there is 94% homology between the amino acid sequences of rhesus and human PSA. Immunization of rhesus monkeys with wild-type vaccinia virus or rV-PSA elicited the usual low-grade constitutional symptoms of vaccinia virus infection. There was no evidence of any adverse effects in any immunized monkeys. A short-lived PSA-specific IGM antibody response was noted in all rV-PSA immunized monkeys regardless of dose level. All monkeys receiving the 10(8)pfu dose of rV-PSA demonstrated PSA-specific T-cell responses that were maintained up to 270 days. No differences in anti-PSA immune responses or toxicity were observed in animals that received prostatectomy prior to immunization. Our results thus demonstrate the safety and immunogenicity of rV-PSA in a non-human primate and have implications for potential specific immunotherapy protocols using PSA as a target. (C) 1995 Wiley-Liss, Inc.* C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NCI,TOXICOL & PHARMACOL BRANCH,BETHESDA,MD 20892. UNIV ILLINOIS,DEPT PHARMACOL,TOXICOL RES LAB,CHICAGO,IL 60612. THER BIOL CORP,CAMBRIDGE,MA 02142. RI Hodge, James/D-5518-2015 OI Hodge, James/0000-0001-5282-3154 NR 30 TC 92 Z9 92 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 9 PY 1995 VL 63 IS 2 BP 231 EP 237 DI 10.1002/ijc.2910630215 PG 7 WC Oncology SC Oncology GA TB407 UT WOS:A1995TB40700014 PM 7591210 ER PT J AU BLOCK, MI FRAKER, DL STRASSMANN, G BILLINGSLEY, KG ARNOLD, WS PERLIS, C ALEXANDER, HR AF BLOCK, MI FRAKER, DL STRASSMANN, G BILLINGSLEY, KG ARNOLD, WS PERLIS, C ALEXANDER, HR TI ENDOGENOUS D-FACTOR ACTIVITY PARTIALLY MEDIATES THE TOXIC BUT NOT THE THERAPEUTIC EFFECTS OF TUMOR-NECROSIS-FACTOR SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID LEUKEMIA-INHIBITORY FACTOR; FACTOR-ALPHA; CELLS; DIFFERENTIATION; RECEPTOR; MELANOMA; SERUM; MICE AB We have earlier shown that passive immunization against differentiation-inducing factor/leukemia-inhibitory factor (D factor) activity improves the survival of endotoxemic mice, suggesting that D factor may contribute to the systemic toxicity associated with tumor necrosis factor (TNF). In the current experiments, TNF induced D-factor gene expression in various tissues of non-tumor-bearing female C57B1/6 mice. passive immunization against D-factor significantly improved survival after a lethal TNF challenge in both non-tumor-bearing (p(2) < 0.02) and tumor-bearing mice (p(2) < 0.01). In mice bearing 10-day s.c. MCA 105 sarcomas, D-factor antibody alone had no effect on tumor growth as compared with control IgG. Tumor regression and regrowth in mice treated i.v. with TNF was not affected by pre-treatment with D-factor antibody, as compared with pre-treatment with IgG. However, TNF-treatment-related mortality was abrogated by pre-treatment with D-factor antibody (0% vs. 36% for IgG-pre-treated controls). These results indicate that endogenous D-factor activity contributes to the toxicity but not to the anti-tumor effects of TNF therapy. With renewed interest in the use of TNF for the treatment of patients with cancer, improved understanding of the role of D factor in mediating the effects of TNF may have important clinical benefits. (C) 1995 Wiley-Liss, Inc. C1 NCI,SURG BRANCH,SURG METAB SECT,BETHESDA,MD 20892. OTSUKA AMER PHARMACEUT INC,MARYLAND RES LABS,DEPT IMMUNOL,ROCKVILLE,MD. NR 26 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 9 PY 1995 VL 63 IS 2 BP 245 EP 249 DI 10.1002/ijc.2910630217 PG 5 WC Oncology SC Oncology GA TB407 UT WOS:A1995TB40700016 PM 7591212 ER PT J AU EYMIN, B SOLARY, E CHEVILLARD, S DUBREZ, L GOLDWASSER, F DUCHAMP, O GENNE, P LETEURTRE, F POMMIER, Y AF EYMIN, B SOLARY, E CHEVILLARD, S DUBREZ, L GOLDWASSER, F DUCHAMP, O GENNE, P LETEURTRE, F POMMIER, Y TI CELLULAR PHARMACOLOGY OF AZATOXINS (TOPOISOMERASE-II AND TUBULIN INHIBITORS) IN P-GLYCOPROTEIN-POSITIVE AND P-GLYCOPROTEIN-NEGATIVE CELL-LINES SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID MULTIDRUG-RESISTANCE; ADRIAMYCIN; CANCER; DNA AB Azatoxin (NSC 640737), a synthetic molecule, was rationally designed as a topoisomerase-II inhibitor and was shown to be a potent cytotoxic: agent that inhibits both tubulin and topoisomerase II. A structure-activity relationship study allowed to select 3 derivatives that inhibit either tubulin (methylalatoxin) only or topoisomerase II (fluoroanilinoazatoxin and nitroanilino-azatoxin) in MTT assays performed on K562 and K562/ADM cells; the latter, expressing P-glycoprotein, indicated cross-resistance of K562/ADM cells to all 4 compounds. DNA double-strand breaks induced by the 3 azatoxins that inhibit topoisomerase II in vitro were decreased in K562/ADM as compared with K562 cells. Nitroanilino-azatoxin was the only compound for which resistance and reduced DNA damage observed in K562/ADM cells was partially reversed by verapamil, suggesting that nitroanilinoazatoxin was a substrate for P-glycoprotein, These results were confirmed by testing the cytotoxic activity of azatoxins on P-glycoprotein-expressing rat colon-carcinoma DHDK12/TRb cells in the absence and the presence of verapamil. Cell-cycle and mitotic-index studies indicated that azatoxin- and methylazatoxin-induced M-phase arrest was less in K562/ADM than in K562 cells. The G2 block induced by fluoro- and nitroanilinoazatoxins was delayed in K562/ADM cells, Verapamil increased cell-cycle inhibition induced by nitroanilinoalatoxin in K562/ADM cells without modifying cell-cycle effects of fluoroanilinoazatoxin, These results (i) are consistent with the specific inhibition of topoisomerase II or tubulin by azatoxin derivatives in cells; (ii) indicate that the nitro group of nitroanilinoazatoxin allows recognition and efflux by the P-glycoprotein; and (iii) suggest that cross-resistance of K562/ADM cells to other azatoxin derivatives is not mediated by P-glycoprotein. (C) 1995 Wiley-Liss, Inc. C1 FAC MED DIJON,ONCOHEMATOL & PHARMACOL LAB,F-21033 DIJON,FRANCE. INST CURIE,MOLEC BIOL LAB,PARIS,FRANCE. NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RI Eymin, Beatrice/M-1962-2013; Dubrez, Laurence/I-4971-2016 OI Dubrez, Laurence/0000-0002-7030-2181 NR 21 TC 14 Z9 14 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD OCT 9 PY 1995 VL 63 IS 2 BP 268 EP 275 DI 10.1002/ijc.2910630221 PG 8 WC Oncology SC Oncology GA TB407 UT WOS:A1995TB40700020 PM 7591216 ER PT J AU KLEINER, DE EMMERTBUCK, MR LIOTTA, LA AF KLEINER, DE EMMERTBUCK, MR LIOTTA, LA TI NECROPSY AS A RESEARCH METHOD IN THE AGE OF MOLECULAR PATHOLOGY SO LANCET LA English DT Review ID IMMUNE-DEFICIENCY SYNDROME; PARAFFIN-EMBEDDED TISSUES; POLYMERASE CHAIN-REACTION; AUTOPSY; DNA; LIVER; POSTMORTEM; AUDIT; RNA RP KLEINER, DE (reprint author), NCI,PATHOL LAB,BETHESDA,MD 20892, USA. OI Kleiner, David/0000-0003-3442-4453 NR 31 TC 28 Z9 29 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 OCT 7 PY 1995 VL 346 IS 8980 BP 945 EP 948 DI 10.1016/S0140-6736(95)91561-3 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA RY808 UT WOS:A1995RY80800013 PM 7564732 ER PT J AU STUDITSKY, VM CLARK, DJ FELSENFELD, G AF STUDITSKY, VM CLARK, DJ FELSENFELD, G TI OVERCOMING A NUCLEOSOMAL BARRIER TO TRANSCRIPTION SO CELL LA English DT Article ID RNA-POLYMERASE-II; ELONGATION COMPLEXES; HISTONE ACETYLATION; CHROMATIN STRUCTURE; BACTERIOPHAGE-T7; INITIATION; INVITRO; DNA; INHIBIT; GENES AB We have studied the kinetics of transcription through a nucleosome core. RNA polymerase transcribes the first similar to 25 bp of nucleosomal DNA rapidly, but then hits a barrier and continues slowly to the nucleosomal dyad region. Here, the barrier disappears and the transcript is completed at a rapid rate, as if on free DNA, indicating that histone octamer transfer is completed as polymerase reaches the dyad, If DNA behind the polymerase is removed during transcription, the barrier does not appear until the polymerase has penetrated up to 15 bp farther into the nucleosome. On a longer template, the barrier is almost eliminated. We have shown previously that the octamer is transferred around the transcribing polymerase via an intermediate containing an intranucleosomal DNA loop, Our results exclude the possibility that polymerase has difficulty breaking histone-DNA contacts and suggest instead that polymerase pauses because it has difficulty transcribing DNA in the loop. C1 NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. RI Studitsky, Vasily/A-9382-2014 NR 43 TC 122 Z9 127 U1 0 U2 4 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD OCT 6 PY 1995 VL 83 IS 1 BP 19 EP 27 DI 10.1016/0092-8674(95)90230-9 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RY583 UT WOS:A1995RY58300006 PM 7553869 ER PT J AU MARTINEZBALBAS, MA DEY, A RABINDRAN, SK OZATO, K WU, C AF MARTINEZBALBAS, MA DEY, A RABINDRAN, SK OZATO, K WU, C TI DISPLACEMENT OF SEQUENCE-SPECIFIC TRANSCRIPTION FACTORS FROM MITOTIC CHROMATIN SO CELL LA English DT Article ID LIGATION-MEDIATED PCR; HEAT-SHOCK FACTOR; CELL-CYCLE; DNASE-I; HISTONE MODIFICATIONS; NUCLEAR-PROTEIN; EXPRESSION; ACETYLATION; BINDING; GENE AB The general inhibition in transcriptional activity during mitosis abolishes the stress-inducible expression of the human hsp70 gene. Among the four transcription factors that bind to the human hsp70 promoter, the DNA-binding activities of three (C/EBP, GBF, and HSF1) were normal, while Sp1 showed reduced binding activity in mitotic cell extracts. In vivo footprinting and immunocytochemical analyses revealed that all of the sequence-specific transcription factors were displaced from promoter sequences as well as from bulk chromatin during mitosis. The correlation of transcription factor displacement with chromatin condensation suggests an involvement of chromatin structure in mitotic repression. However, retention of DNase I hypersensitivity suggests that the hsp70 promoter was not organized in a canonical nucleosome structure in mitotic chromatin. Displacement of transcription factors from mitotic chromosomes could present another window in the cell cycle for resetting transcriptional programs. C1 NICHHD,MOLEC GROWTH REGULAT LAB,BETHESDA,MD 20892. RP MARTINEZBALBAS, MA (reprint author), NCI,BIOCHEM LAB,BETHESDA,MD 20892, USA. OI Martinez-Balbas, Marian/0000-0003-0173-0964 NR 68 TC 283 Z9 284 U1 1 U2 8 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD OCT 6 PY 1995 VL 83 IS 1 BP 29 EP 38 DI 10.1016/0092-8674(95)90231-7 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA RY583 UT WOS:A1995RY58300007 PM 7553870 ER PT J AU BENHAR, I PASTAN, I AF BENHAR, I PASTAN, I TI IDENTIFICATION OF RESIDUES THAT STABILIZE THE SINGLE-CHAIN FV OF MONOCLONAL-ANTIBODIES B3 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACIDS; POLYMERASE; GENES; IMMUNOTOXIN; EXPRESSION; CLONING; PRIMERS AB B3(Fv)-PE38 is a recombinant single-chain immunotoxin in which the Fv portion of the B3 antibody in a single-chain form, which serves as the targeting moiety, is fused to PE38, a truncated form of Pseudomonas exotoxin A, which serves as the cytotoxic moiety, B3(FV)-PE38 is specifically cytotoxic to many human cancer cell lines and is currently evaluated in a clinical trial. Monoclonal antibodies B3 (IgG1k) and B5 (IgMk) recognize related carbohydrate epitopes on human carcinoma cells. The Fv regions of these antibodies were previously cloned and expressed as the single chain Fv-immunotoxins B3(Fv) PE38 and B5(Fv)-PE38, respectively. The B3(Fv)-PE38 immunotoxin binds to antigen positive cancer cells with a higher affinity than B5(Fv)-PE38 and is a more potent cytotoxic agent than B5(Fv)-PE38. However, it is less stable and rapidly aggregates upon incubation at 37 degrees C. The V-L domains of the two Fvs are very similar, differing by only three residues, the fourth and seventh Fr1 residues and the fifth CDR1 residue. The V-H domains of the two Fvs vary considerably. To investigate whether any of the different V-L residues may influence the stability of the B3(Fv), we constructed a chimeric immunotoxin containing the B3V(H) and the B5V(L). This chimera had an improved stability and a higher apparent antigen binding affinity and cytotoxic activity when compared with B3(Fv)-PE38. Site-specific mutagenesis was used to show that the V-L M4L mutation has an important role in stabilizing B3(Fv), although residues V-L Ser-7 and V-L Ile-28 also play a role in the increased stability. When tested in an in vivo model system, the chimera containing the B3V(H) and the B5V(L) had an improved antitumor activity in a human xenograft mouse model. These studies indicate that the common use of degenerate (''family-specific'') primers to clone Fv fragments may introduce destabilizing mutations. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 22 TC 32 Z9 33 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 6 PY 1995 VL 270 IS 40 BP 23373 EP 23380 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RY909 UT WOS:A1995RY90900024 PM 7559495 ER PT J AU UENO, T SHIRASAKA, T MITSUYA, H AF UENO, T SHIRASAKA, T MITSUYA, H TI ENZYMATIC CHARACTERIZATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 REVERSE-TRANSCRIPTASE RESISTANT TO MULTIPLE 2,3-DIDEOXYNUCLEOSIDE 5-TRIPHOSPHATES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; HIGH-LEVEL RESISTANCE; RIBONUCLEASE-H; HTLV-III; HIV-1; ZIDOVUDINE; SENSITIVITY; INHIBITOR; FIDELITY; INVITRO AB A set of five mutations (A62V, V75I, F77L, F116Y, and Q151M) in the polymerase domain of reverse transcriptase (RT) of human immunodeficiency virus type 1 (HIV-1), which confers on the virus a reduced sensitivity to multiple therapeutic dideoxynucleosides (ddNs), has been identified, In this study, we defined the biochemical properties of RT with such mutations by using site-directed mutagenesis, overproduction of recombinant RTs, and steady-state kinetic analyses, A single mutation, Q151M, which developed first among the five mutations in patients receiving therapy, most profoundly reduced the sensitivity of RT to multiple ddN 5'-triphosphates (ddNTPs). Addition of other mutations to Q151M further reduced the sensitivity of RT to ddNTPs. RT with the five mutations proved to be resistant by 65-fold to 3'-azido-2',3'-dideoxythymidine 5'-triphosphate (AZTTP), 12-fold to ddCTP, 8.8-fold to ddATP, and 3.3-fold to 2',3'-dideoxyguanosine 5'-triphosphate (ddGTP), compared with wild-type RT (RT(wt)). Steady-state kinetic studies revealed comparable catalytic efficiency (k(cat)/K-m) of RTs carrying combined mutations as compared with that of RT(wt) (<3-fold), although a marked difference was noted in inhibition constants (K-i) (e.g. K-i of a mutant RT carrying the five mutations was 62-fold higher for AZTTP than that of RT(wt)). Thus, we conclude that the alteration of RT's substrate recognition, caused by these mutations, accounts for the observed multi-ddN resistance of HIV-1. The features of multi-ddNTP-resistant RTs should provide insights into the molecular mechanism of RT discriminating ddNTPs from natural substrates. C1 NCI,DIV CANC TREATMENT,MED BRANCH,EXPTL RETROVIROL SECT,BETHESDA,MD 20892. RI Ueno, Takamasa/F-5788-2013 OI Ueno, Takamasa/0000-0003-4852-4236 NR 47 TC 97 Z9 98 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 6 PY 1995 VL 270 IS 40 BP 23605 EP 23611 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RY909 UT WOS:A1995RY90900055 PM 7559526 ER PT J AU HERNANDEZ, VJ CASHEL, M AF HERNANDEZ, VJ CASHEL, M TI CHANGES IN CONSERVED REGION-3 OF ESCHERICHIA-COLI SIGMA(70) MEDIATE PPGPP-DEPENDENT FUNCTIONS IN-VIVO SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE RPOD; PPGPP; RRNB P1; RPOS; GROWTH RATE CONTROL ID CORE RNA-POLYMERASE; GROWTH-RATE CONTROL; RIBOSOMAL-RNA; GUANOSINE TETRAPHOSPHATE; TRANSCRIPTION; STRINGENT; PROMOTER; RESISTANCE; MUTATIONS; PROTEINS AB In Escherichia coli, deletion of relA and spoT results in an inability to synthesize ppGpp, guanosine-3',5'-bis(pyrophosphate), and a loss in the ability to grow on amino acid-free minimal media. Two spontaneous missense suppressor alleles, rpoD(P504L) and rpoD(S506F), able to confer complete prototrophy without the reappearance of ppGpp, were localized to that portion of rpoD coding for conserved region 3.1 of sigma(70). Characterization of these mutants revealed distinct physiological effects. Both mutations cause growth rate defects exacerbated in the presence of ppGpp. and paralleled by reductions in rrnB P1-lacZ reporter gene expression, as if growth of these mutants is limited by um P1 promoter activity levels of ppGpp, as a function of growth rate, are lowered by a constant fraction (75%) in the rpoD(P504L) strain and by a decreasing fraction at lower growth rates in the rpoD(S506F) strain. Comparisons of rrnB P1-lacZ expression at different ppGpp levels is interpreted for the rpoD(P504L) mutant as resulting from a hypersensitivity to ppGpp. For the rpoD(S506F) mutant there is a normal sensitivity to ppGpp but the action of ppGpp is functionally mimicked; that is, a low intrinsic rrnB P1 promoter activity is manifested even in the absence of ppGpp. In addition to effects on rrnB P1 promoters, the accumulation of the stationary phase-specific sigma factor (sigma(s)), which is normally ppGpp-dependent, was assayed in the rpoD mutants and in one, rpoD(S505F), found to be restored in the absence of ppGpp. The behavior of these mutants thus seems consistent with a unitary effect of ppGpp on transcription resulting in both negative and positive regulation of gene expression. In addition, the cellular fraction of sigma(70) associated with holoenzyme appears reduced by both rpoD mutations as judged by comparison with wild-type and ppGpp-deficient strains. Interestingly, the amount of holoenzyme-associated sigma(70) was higher in the ppGpp-deficient than in the wild-type strain, possibly indicating that sigma(70)-core RNA polymerase interactions are decreased by ppGpp. (C) 1995 Academic Press Limited RP HERNANDEZ, VJ (reprint author), NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892, USA. NR 48 TC 83 Z9 83 U1 1 U2 2 PU ACADEMIC PRESS (LONDON) LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD OCT 6 PY 1995 VL 252 IS 5 BP 536 EP 549 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RY584 UT WOS:A1995RY58400004 PM 7563072 ER PT J AU ERZOUKI, HK ALLEN, AC NEWMAN, AH GOLDBERG, SR SCHINDLER, CW AF ERZOUKI, HK ALLEN, AC NEWMAN, AH GOLDBERG, SR SCHINDLER, CW TI EFFECTS OF COCAINE, COCAINE METABOLITES AND COCAINE PYROLYSIS PRODUCTS ON THE HINDBRAIN CARDIAC AND RESPIRATORY CENTERS OF THE RABBIT SO LIFE SCIENCES LA English DT Article DE COCAINE; COCAINE METABOLITES; COCAINE PYROLYSIS PRODUCTS; HINDBRAIN; CARDIAC CENTER; RESPIRATORY CENTER ID ANHYDROECGONINE METHYL-ESTER; CONSCIOUS RATS; NOREPINEPHRINE; COCAETHYLENE; DOPAMINE; SMOKERS AB Hemodynamic and respiratory effects of vertebral artery or i.v. administration of cocaine, cocaine metabolites and cocaine pyrolysis products were measured in anesthetized rabbits. Vertebral artery administration of 1 mg of cocaine produced decreases in blood pressure and heart rate and respiratory arrest. Cocaethylene (1 mg), a cocaine metabolite produced following co-administration of cocaine and ethanol, had comparable effects except that the respiratory arrest following cocaethylene had a longer duration of action than did cocaine. A decrease in blood pressure was also observed following 1 mg of norcocaine; however, unlike cocaine, norcocaine did not affect respiration. Acute tolerance was not observed to any of the effects of 1 mg of cocaine, cocaethylene or norcocaine following vertebral artery administration. None of these compounds had significant effects following i.v. administration of the same dose. The cocaine metabolites benzoylecgonine and ecgonine methyl ester were without effect by either route in doses up to 3 mg. In contrast to cocaine, the cocaine pyrolysis products anhydroecgonine methyl ester (3 mg) and noranhydroecgonine methyl ester (3 mg) produced similar effects via both routes of administration. Both compounds produced decreases in blood pressure and heart rate and an increase in respiratory rate. Anhydroecgonine ethyl ester (3 mg), a metabolite hypothetically formed from the cocaine pyrolysis product in individuals co-administering ethanol, had effects similar to the other pyrolysis products, although its effects were not as prominent via the i.v. route of administration. Acute tolerance was observed upon administration of the cocaine pyrolysis products. These results indicate that the cocaine pyrolysis products do not share a common mechanism of action with either cocaine or the cocaine metabolites. RP ERZOUKI, HK (reprint author), NIDA,ADDICT RES CTR,DIV INTRAMURAL RES,PRECLIN PHARMACOL LAB,POB 5180,BALTIMORE,MD 21224, USA. NR 28 TC 22 Z9 22 U1 1 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PD OCT 6 PY 1995 VL 57 IS 20 BP 1861 EP 1868 DI 10.1016/0024-3205(95)02166-G PG 8 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA RZ045 UT WOS:A1995RZ04500005 PM 7475933 ER PT J AU SIKORSKI, RS AF SIKORSKI, RS TI PAVING THE INFO SUPERHIGHWAY SO SCIENCE LA English DT Letter C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SIKORSKI, RS (reprint author), NCI,DIV BASIC SCI,BETHESDA,MD 20892, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 6 PY 1995 VL 270 IS 5233 BP 16 EP 17 DI 10.1126/science.270.5233.16 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RY302 UT WOS:A1995RY30200010 PM 7569943 ER PT J AU MASISON, DC WICKNER, RB AF MASISON, DC WICKNER, RB TI PRION-INDUCING DOMAIN OF YEAST URE2P AND PROTEASE RESISTANCE OF URE2P PRION-CONTAINING CELLS SO SCIENCE LA English DT Article ID SACCHAROMYCES-CEREVISIAE; PSI AB The genetic properties of the [URE3] non-Mendelian element of Saccharomyces cerevisiae suggest that it is a prion (infectious protein) form of Ure2p, a regulator of nitrogen catabolism. In extracts from [URE3] strains, Ure2p was partially resistant to proteinase K compared with Ure2p from wild-type extracts. Overexpression of Ure2p in wild-type strains induced a 20- to 200-fold increase in the frequency with which [URE3] arose, Overexpression of just the amino-terminal 65 residues of Ure2p increased the frequency of [URE3] induction 6000-fold. Without this ''prion-inducing domain'' the carboxyl-terminal domain performed the nitrogen regulation function of Ure2p, but could not be changed to the [URE3] prion state. Thus, this domain induced the prion state in trans, whereas in cis it conferred susceptibility of the adjoining nitrogen regulatory domain to prion infections. C1 NIDDKD,BIOCHEM PHARMACOL LAB,GENET SIMPLE EUKARYOTES SECT,BETHESDA,MD 20892. NR 26 TC 269 Z9 273 U1 0 U2 2 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 6 PY 1995 VL 270 IS 5233 BP 93 EP 95 DI 10.1126/science.270.5233.93 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RY302 UT WOS:A1995RY30200040 PM 7569955 ER PT J AU MARTIN, A HAXBY, JV LALONDE, FM WIGGS, CL UNGERLEIDER, LG AF MARTIN, A HAXBY, JV LALONDE, FM WIGGS, CL UNGERLEIDER, LG TI DISCRETE CORTICAL REGIONS ASSOCIATED WITH KNOWLEDGE OF COLOR AND KNOWLEDGE OF ACTION SO SCIENCE LA English DT Article ID VISUAL-CORTEX; PET IMAGES; VERBS; RETRIEVAL; SYSTEMS; NOUNS; BRAIN; COMPREHENSION; ACHROMATOPSIA; ORGANIZATION AB The areas of the brain that mediate knowledge about objects were investigated by measuring changes in regional cerebral blood flow (rCBF) using positron emission tomography (PET). Subjects generated words denoting colors and actions associated with static, achromatic line drawings of objects in one experiment, and with the written names of objects in a second experiment. In both studies, generation of color words selectively activated a region in the ventral temporal lobe just anterior to the area involved in the perception of color, whereas generation of action words activated a region in the middle temporal gyrus just anterior to the area involved in the perception of motion. These data suggest that object knowledge is organized as a distributed system in which the attributes of an object are stored close to the regions of the cortex that mediate perception of those attributes. RP MARTIN, A (reprint author), NIMH,PSYCHOL & PSYCHOPATHOL LAB,BLDG 10,ROOM 4C110,10 CTR DR,MSC 1366,BETHESDA,MD 20892, USA. RI martin, alex/B-6176-2009 NR 45 TC 723 Z9 737 U1 1 U2 22 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD OCT 6 PY 1995 VL 270 IS 5233 BP 102 EP 105 DI 10.1126/science.270.5233.102 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RY302 UT WOS:A1995RY30200043 PM 7569934 ER PT J AU OGAWA, Y LEI, PS KOVAC, P AF OGAWA, Y LEI, PS KOVAC, P TI SYNTHESIS OF LIGANDS RELATED TO THE VIBRIO-CHOLERAE O-SPECIFIC ANTIGEN .9. A FUNCTIONALIZED HEXASACCHARIDE PRECURSOR OF A GLYCOCONJUGATE VACCINE AGAINST CHOLERA SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID BRUCELLA-A-ANTIGEN; 2-(TRIMETHYLSILYL)ETHYL GLYCOSIDES; BLOCK SYNTHESIS; DETERMINANTS; PENTASACCHARIDE; TRANSFORMATION; THIOGLYCOSIDE; DERIVATIVES; SUGARS; PROBES AB A hexasaccharide fragment of the O-polysaccharide of Vibrio cholerae O:1, serotype Inaba was constructed from mono and disaccharides carrying azido groups. After the azido-->amino group conversion, the requisite N-acylation was achieved using as the reagent 4-O-benzyI-L-glycero-tetronic acid, prepared from the corresponding derivative of L-homoserine by deamination. C1 NIDDK,BETHESDA,MD 20892. NR 25 TC 8 Z9 8 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD OCT 5 PY 1995 VL 5 IS 19 BP 2283 EP 2286 DI 10.1016/0960-894X(95)00397-C PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA RY472 UT WOS:A1995RY47200020 ER PT J AU HUANG, Y SAEZ, R CHAO, L SANTOS, E AARONSON, SA CHAN, AML AF HUANG, Y SAEZ, R CHAO, L SANTOS, E AARONSON, SA CHAN, AML TI A NOVEL INSERTIONAL MUTATION IN THE TC21 GENE ACTIVATES ITS TRANSFORMING ACTIVITY IN A HUMAN LEIOMYOSARCOMA CELL-LINE SO ONCOGENE LA English DT Article DE RAS; TC21; ONCOGENE; SSCP; MUTATION; LEIOMYOSARCOMA ID RAS-RELATED GENE; MOLECULAR SWITCH; DIRECT REPEATS; DELETIONS; ONCOGENES; PROTEIN AB TC21 is the fourth member of the pas gene family to exhibit oncogenic activation in human tumor cells. To assess the prevalence of activated TC21 oncogenes in human tumors, we have developed sensitive single-strand conformational polymorphism (SSCP) conditions and immunological reagents for the detection of both single base alterations and/or overt overexpression in a wide spectrum of human tumor cell lines and surgical samples. In an initial examination of 33 human tumor specimens, we observed a novel nine basepair three amino acids insertion at TC21 codon 24 in one human uterine leiomyosarcoma cell line, SK-UT-1. This mutant allele when transfected into NIH3T3 cells, displayed high transforming activity comparable to that of the Leu72 oncogenic mutant identified by expression cDNA cloning from a human ovarian carcinoma cell line. Comparing the level of GTP-binding by the mutant and normal TC21 products revealed that this novel lesion increases the GTP-bound form of the TC21 molecule. These findings imply that the mechanism by which mutations activate the oncogenic properties of this ras-related molecule is analogous to that of previously known ras family members. C1 MT SINAI MED CTR,DERALD H RUTTENBERG CANC CTR,NEW YORK,NY 10029. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 26 TC 41 Z9 42 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 5 PY 1995 VL 11 IS 7 BP 1255 EP 1260 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA RY967 UT WOS:A1995RY96700005 PM 7478545 ER PT J AU LI, CCH DAI, RM LONGO, DL AF LI, CCH DAI, RM LONGO, DL TI INACTIVATION OF NF-KAPPA-B INHIBITOR I-KAPPA-B-ALPHA - UBIQUITIN-DEPENDENT PROTEOLYSIS AND ITS DEGRADATION PRODUCT SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID ACTIVATION; PROTEIN; PATHWAY; P105; GENE AB In most cells, the inactive dimeric NF-kappa B complexes an retained in the cytoplasm by binding to a group of inhibitory proteins, I kappa B. In response to extracellular stimuli, I kappa B is rapidly phosphorylated and degraded, thus, liberating the active NF-kappa B. To investigate the mechanisms involved, we have developed a cell-free system to study the degradation of the prototype I kappa B protein, I kappa B alpha. In this in vitro assay, ubiquitin, proteasome-containing S100 fraction and ATP are required for the proteolysis of I kappa B alpha. Both bound and free forms of I kappa B alpha isolated from intact cells can be degraded through this pathway. We also identified polyubiquitinated I kappa B alpha molecules and N-terminal truncated I kappa B alpha degradation product(s) both in vivo and in vitro. We conclude that the inactivation of I kappa B alpha occurs through a series of processes including phosphorylation, ATP-dependent ubiquitin conjugation and proteasome-mediated proteolysis. (C) 1995 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP LI, CCH (reprint author), SAIC FREDERICK,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. NR 34 TC 53 Z9 53 U1 1 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 4 PY 1995 VL 215 IS 1 BP 292 EP 301 DI 10.1006/bbrc.1995.2465 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RY308 UT WOS:A1995RY30800040 PM 7575604 ER PT J AU KUTTY, RK KUTTY, G HOOKS, JJ WIGGERT, B NAGINENI, CN AF KUTTY, RK KUTTY, G HOOKS, JJ WIGGERT, B NAGINENI, CN TI TRANSFORMING GROWTH-FACTOR-BETA INHIBITS THE CYTOKINE-MEDIATED EXPRESSION OF THE INDUCIBLE NITRIC-OXIDE SYNTHASE MESSENGER-RNA IN HUMAN RETINAL-PIGMENT EPITHELIAL-CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID MACROPHAGES; INDUCTION; CLONING; NITRATE; DNA AB Human retinal pigment epithelial (RPE) cells in culture respond to a mixture of cytokines (IFN-gamma, IL-1 beta, TNF-alpha) by producing large amounts of nitric oxide. Transforming growth factor-beta, unlike other growth factors, was found to inhibit this response by more than 75%. The expression of mRNA for the inducible form of nitric oxide synthase in RPE cells treated with cytokines was demonstrated by reverse transcription-polymerase chain reaction, sequencing of the PCR product and northern blotting. Transforming growth factor-beta was highly effective in inhibiting (by 75%) the cytokine-induced nitric oxide synthase mRNA expression. This response by RPE may play an important role in the etiology of infectious and inflammatory diseases affecting retina. (C) 1995 Academic Press, Inc. C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. RP KUTTY, RK (reprint author), NEI,RETINAL CELL & MOLEC BIOL LAB,MSC 2740,6 CTR DR,BLDG 6,ROOM 338,BETHESDA,MD 20892, USA. NR 22 TC 34 Z9 36 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 4 PY 1995 VL 215 IS 1 BP 386 EP 393 DI 10.1006/bbrc.1995.2477 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RY308 UT WOS:A1995RY30800052 PM 7575617 ER PT J AU GHOSH, P KOMSCHLIES, KL CIPPITELLI, M LONGO, DL SUBLESKI, J YE, JP SICA, A YOUNG, HA WILTROUT, RH OCHOA, AC AF GHOSH, P KOMSCHLIES, KL CIPPITELLI, M LONGO, DL SUBLESKI, J YE, JP SICA, A YOUNG, HA WILTROUT, RH OCHOA, AC TI GRADUAL LOSS OF T-HELPER-1 POPULATIONS IN SPLEEN OF MICE DURING PROGRESSIVE TUMOR-GROWTH SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID NF-KAPPA-B; RENAL-CELL CARCINOMA; EXPRESSION; ACTIVATION; CYTOKINES; IMMUNITY; PROFILES; PRODUCT; CLONES; GENE AB Background: The carefully orchestrated events that result in a protective immune response are coordinated to a large extent by cytokines produced by T helper 1 (Th1) and T helper 2 (Th2) T-cell subsets, which are two arms of the immune system, Th1 cells preferentially produce interleukin 2 (IL-2), interferon gamma (IFN gamma), and tumor necrosis factor (TNF), resulting in a cellular response that helps to eliminate infected cells, In contrast, Th2 cells produce IL-4, IL-5, IL-6, and IL-10 and stimulate an antibody response that helps to prevent the cells from becoming infected, The clinical progression of several infectious diseases, including human immunodeficiency virus, some types of parasitoses, and tuberculosis, is thought to be associated with the predominance of a Th2-type T-cell response, Recent reports have demonstrated the presence of T cells producing Th2 lymphokines (IL-4, IL-6, and IL-10) in tumor-infiltrating lymphocytes of renal cell carcinoma, Purpose: The purpose of this study was to investigate at the molecular level whether there was any change in the splenic T cells of mice with progressively growing tumors from a Th1 to a Th2 DNA-binding pattern or phenotype, Methods: Splenic T cells from mice bearing renal cell carcinoma or MCA-38 colon carcinoma were tested for cytokine production after in vitro activation, Nuclear extracts of splenic T cells were used for the DNA-binding assay using IFN-gamma core promoter region, the kappa B (kappa B) Site from immunoglobulin gene, and the nuclear factor of activated T-cell (NFAT) site from IL-2 gene, Results: Splenic T cells from mice bearing renal cell carcinoma or MCA-38 colon carcinoma preferentially produced Th2 cytokines (i.e., IL-4) upon activation and showed a marked decrease in Th1 cytokine (particularly IFN gamma) production compared with the production observed in normal splenic T cells, The DNA-binding assay with the IFN-gamma core promoter region confirmed the gradual decline in the nuclear transcription factors associated with the Th1 phenotype during tumor progression in both tumor models, Renal cell carcinoma-bearing mice, successfully treated with flavone-8-acetic acid and recombinant human IL-2, showed a reversion to a Th1-like pattern, In addition, nuclear extracts of T cells from tumor-bearing animals showed a Th2-type kappa B-binding pattern, Moreover, the NFAT complex present in the normal splenic T cells was lost at the later stages of tumor progression; instead, a new complex was present in mice bearing long-term tumors, Conclusion: T cells from tumor-bearing mice lose the Th1 phenotype with progressive tumor growth. C1 NCI,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21701. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,CLIN SERV IMMUNOL PROGRAM,FREDERICK,MD 21702. RP GHOSH, P (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,EXPTL IMMUNOL LAB,BLDG 560,RM 31-93,FREDERICK,MD 21701, USA. OI CIPPITELLI, Marco/0000-0002-9620-538X NR 31 TC 103 Z9 105 U1 1 U2 3 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD OCT 4 PY 1995 VL 87 IS 19 BP 1478 EP 1483 DI 10.1093/jnci/87.19.1478 PG 6 WC Oncology SC Oncology GA RW694 UT WOS:A1995RW69400012 PM 7674335 ER PT J AU BANIK, U ZHU, DM CHOCK, PB MILES, EW AF BANIK, U ZHU, DM CHOCK, PB MILES, EW TI THE TRYPTOPHAN SYNTHASE ALPHA-2-BETA-2 COMPLEX - KINETIC-STUDIES WITH A MUTANT ENZYME (BETA-K87T) TO PROVIDE EVIDENCE FOR ALLOSTERIC ACTIVATION BY AN AMINOACRYLATE INTERMEDIATE SO BIOCHEMISTRY LA English DT Article ID ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; BIENZYME COMPLEX; REACTION-MECHANISM; ALPHA-SUBUNIT; L-SERINE; IDENTIFICATION; LYSINE-87; CATALYSIS; INDOLE AB TO investigate the mechanism by which the tryptophan synthase beta subunit accelerates the cleavage of the indole-3-glycerol phosphate catalyzed by the alpha subunit (alpha reaction), kinetic experiments were carried out with wild-type and mutant forms of the alpha(2) beta(2) complex. Previous studies indicate that this activation can be attributed to the conformational changes associated with the formation of a Schiff base between aminoacrylate and pyridoxal phosphate at the beta site. To test this hypothesis, we investigated a mutant form of the alpha(2) beta(2) complex having the lysine-87 of its beta subunits replaced by threonine. The mutant alpha(2) beta(2) complex (K87T) exhibits normal activity for the a reaction but fails to catalyze formation of L-tryptophan from L-serine and indole (beta reaction). However, the mutant enzyme can form a Schiff base intermediate with L-serine at the beta site. Using a ''chemical rescue'' method, we converted K87T L-serine intermediate to an aminoacrylate intermediate. Steady-state kinetic studies reveal that the aminoacrylate derivative exhibits a 7-fold enhancement in k(cat)/K-m for the alpha reaction relative to that of the L-serine derivative of the mutant or the wild-type enzyme in the absence of L-serine. Rapid kinetic data show that the aminoacrylate derivative of the mutant enzyme exhibits a 6-fold increase in the rate constant for the indole-3-glycerol phosphate cleavage reaction. In addition, rate constants for the reverse reaction and product release steps are also altered. Together, these changes lead to a decrease in K-m and an increase in k(cat). The magnitude of this enhancement is lower than that observed with the wild-type enzyme with saturating L-serine; nevertheless, the results directly demonstrate the postulated allosteric activation in the absence of L-tryptophan formation at the beta site. C1 NIDDK, BIOCHEM PHARMACOL LAB, BETHESDA, MD 20892 USA. NHLBI, BIOCHEM LAB, BETHESDA, MD 20892 USA. NR 30 TC 22 Z9 22 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD OCT 3 PY 1995 VL 34 IS 39 BP 12704 EP 12711 DI 10.1021/bi00039a029 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RY460 UT WOS:A1995RY46000029 PM 7548023 ER PT J AU HIROSE, T OBRIEN, DA JETTEN, AM AF HIROSE, T OBRIEN, DA JETTEN, AM TI CLONING OF THE GENE ENCODING THE MURINE ORPHAN RECEPTOR TAK1 AND CELL-TYPE-SPECIFIC EXPRESSION IN TESTIS SO GENE LA English DT Article DE RECOMBINANT DNA; NUCLEAR RECEPTOR; CHROMOSOME; SPERMATOCYTE ID ISOLATED SPERMATOGENIC CELLS; SUPERFAMILY; MOUSE AB We have cloned the gene encoding the mouse homologue of the orphan receptor, TAK1, a member of the nuclear receptor superfamily, from a mouse testis cDNA library. The amino acid sequence of mouse TAK1 (mTAK1) is highly homologous to that of human TAK1, with an overall identity of 98%. Northern blot analysis using RNA from different testicular cell types showed that the mTAK1 transcript is predominantly expressed in pachytene spermatocytes at a low level in round spermatids, but not in germ cells at earlier phases of spermatogenesis or in Sertoli cells. Southern analysis using genomic DNA prepared from a panel of hamster/human and mouse/human hybrid cell lines indicated that the TAK1 gene is located on human chromosome 3. C1 NIEHS,CELL BIOL SECT,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,REPROD BIOL LABS,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27599. RI Hirose, Takahisa /E-6117-2011; OI Jetten, Anton/0000-0003-0954-4445 FU NCI NIH HHS [CA16086]; NICHD NIH HHS [HD26485, P30-HD18968, R01 HD026485] NR 11 TC 15 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD OCT 3 PY 1995 VL 163 IS 2 BP 239 EP 242 DI 10.1016/0378-1119(95)00414-2 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA RZ406 UT WOS:A1995RZ40600012 PM 7590273 ER PT J AU VOS, MD JONES, JE TRESTON, AM AF VOS, MD JONES, JE TRESTON, AM TI HUMAN PEPTIDYLGLYCINE ALPHA-AMIDATING MONOOXYGENASE TRANSCRIPTS DERIVED BY ALTERNATIVE MESSENGER-RNA SPLICING OF AN UNREPORTED EXON SO GENE LA English DT Article DE RECOMBINANT DNA; PCR; ALTERNATIVE SPLICING; PAM; PAL; PHM; LYASE ID LUNG-CANCER; BIOSYNTHESIS AB We are characterizing the alternatively spliced human peptidylglycine alpha-amidating monooxygenase (hPAM)-encoding mRNA transcripts expressed by human cells. Reverse transcription coupled to the polymerase chain reaction (RT-PCR) has been used to identify four alternatively spliced variants that differ in the region joining the two catalytic domains. Two of the transcripts represent previously reported splice variants differentiated by the presence (hPAM-A) or absence (hPAM-B) of a 321-nucleotide (nt) linker (optional exon A) which in the rat produce functionally distinct enzymes, Different mRNAs represent two splice variants, hPAM-C and hPAM-D, that show the presence of an exon unreported for PAM in any other species. This new exon, designated exon C, is 54 nt in length, encodes an 18-amino-acid (aa) peptide containing a conserved dibasic aa endoproteolytic processing motif, and is located 3' of exon A in human genomic DNA, We propose that cell-specific regulation of mRNA splicing would provide a mechanism for control of prohormone activation by these Variants of the PAM enzyme. C1 NCI,DCPC,BPRB,INTERVENT SECT,ROCKVILLE,MD 20850. NR 9 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD OCT 3 PY 1995 VL 163 IS 2 BP 307 EP 311 DI 10.1016/0378-1119(95)00364-C PG 5 WC Genetics & Heredity SC Genetics & Heredity GA RZ406 UT WOS:A1995RZ40600025 PM 7590286 ER PT J AU STEFFAN, W KOVAC, P ALBERSHEIM, P DARVILL, AG HAHN, MG AF STEFFAN, W KOVAC, P ALBERSHEIM, P DARVILL, AG HAHN, MG TI CHARACTERIZATION OF A MONOCLONAL-ANTIBODY THAT RECOGNIZES AN ARABINOSYLATED (1-]6)-BETA-D-GALACTAN EPITOPE IN PLANT-COMPLEX CARBOHYDRATES SO CARBOHYDRATE RESEARCH LA English DT Article DE (1-]6)-BETA-D-GALACTAN; ARABINOGALACTAN; ANTIBODY; MONOCLONAL; EPITOPE ID ARABINOGALACTAN-PROTEIN EPITOPE; METHYL BETA-GLYCOSIDES; DAUCUS-CAROTA L; RHAMNOGALACTURONAN-I; ACACIA-SENEGAL; CELL-SURFACE; SOMATIC EMBRYOGENESIS; BLOCKWISE APPROACH; POLYSACCHARIDE; GLYCOPROTEINS AB Monoclonal antibody CCRC-M7 is a representative of a group of antibodies with similar binding specificity that were generated using the plant cell-wall pectic polysaccharide, rhamnogalacturonan I, as immunogen. The epitope recognized by CCRC-M7 is present in several plant polysaccharides and membrane glycoproteins. Selective enzymatic or chemical removal of arabinosyl residues from rhamnogalacturonan I reduced, but did not abolish, the ability of CCRC-M7 to bind to the polysaccharide. In contrast, enzymatic removal of both arabinosyl and galactosyl residues from rhamnogalacturonan I completely abolished binding of CCRC-M7 to the resulting polysaccharide. Competitive ELISAs using chemically defined oligosaccharides to compete for the CCRC-M7 binding site showed that oligosaccharides containing (1 --> 6)-linked beta-D-galactosyl residues were the best competitors among those tested, with the tri-, penta-, and hexa-saccharides being equally effective. The combined results from indirect and competitive ELISAs suggest that the minimal epitope recognized by CCRC-M7 encompasses a (1 --> 6)-linked beta-galactan containing at least three galactosyl residues with at least one arabinosyl residue attached. C1 UNIV GEORGIA,COMPLEX CARBOHYDRATE RES CTR,ATHENS,GA 30602. NIDDK,BETHESDA,MD 20892. UNIV GEORGIA,DEPT BIOCHEM & MOLEC BIOL,ATHENS,GA 30602. UNIV GEORGIA,DEPT BOT,ATHENS,GA 30602. NR 36 TC 54 Z9 54 U1 0 U2 5 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD OCT 2 PY 1995 VL 275 IS 2 BP 295 EP 307 DI 10.1016/0008-6215(95)00174-R PG 13 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA TA515 UT WOS:A1995TA51500007 PM 8529225 ER PT J AU SGOURAS, DN ATHANASIOU, MA BEAL, GJ FISHER, RJ BLAIR, DG MAVROTHALASSITIS, GJ AF SGOURAS, DN ATHANASIOU, MA BEAL, GJ FISHER, RJ BLAIR, DG MAVROTHALASSITIS, GJ TI ERF - AN ETS DOMAIN PROTEIN WITH STRONG TRANSCRIPTIONAL REPRESSOR ACTIVITY, CAN SUPPRESS ETS-ASSOCIATED TUMORIGENESIS AND IS REGULATED BY PHOSPHORYLATION DURING CELL-CYCLE AND MITOGENIC STIMULATION SO EMBO JOURNAL LA English DT Article DE CDC2; ETS; MAP KINASE; REPRESSOR; SUPPRESSOR ID LONG TERMINAL REPEAT; DNA-BINDING; LEUKEMIA-VIRUS; SARCOMA-VIRUS; ONCOGENIC ACTIVITY; MAMMALIAN-CELLS; C-FOS; GENE; PROMOTER; EXPRESSION AB ERF (ETS2 Repressor Factor) is a novel member of the ets family of genes, which was isolated by virtue of its interaction with the ets binding site (EBS) within the ETS2 promoter. The 2.7 kb ubiquitously expressed ERF mRNA encodes a 548 amino acid phosphoprotein that exhibits strong transcriptional repressor activity on promoters that contain an EBS. The localization of the DNA-binding domain of the protein at the N-terminus and the repression domain at the C-terminus is reminiscent of the organization of ELK1-like members of the ets family; however, there is no significant homology between ERF and ELK1 or any other ets member outside the DNA-binding domain. The repressor activity of ERF can antagonize the activity of other ets genes that are known transcriptional activators. Furthermore, ERF can suppress the ets-dependent transforming activity of the gag-myb-ets fusion oncogene of ME26 virus. Although ERF protein levels remain constant throughout the cell cycle, the phosphorylation level of the protein is altered as a function of the cell cycle and after mitogenic stimulation. The ERF protein is also hyperphosphorylated in cells transformed by the activated Ha-ras and v-src genes and the transcription repressor activity of ERF is decreased after co-transfection with activated Ha-ras or the kinase domain of the c-Raf-1 gene, indicating that ERF activity is probably regulated by the ras/MAPK pathway. Consistent with the in who phosphorylation and inactivation by ras, ERP is efficiently phosphorylated in vitro by Erk2 and cdc2/cyclin B kinases, at sites similar to those detected in vivo. Furthermore, a single mutation at position 526 results in the loss of a specific phosphopeptide both in in vivo and in vitro (by Erk2) labeling. Substitution of Thr526 for glutamic acid also decreases the repression ability of ERF. Our data suggest a model in which modulation of ERF activity is involved in the transcriptional regulation of genes activated during entry into G(1) phase. Obstruction of the ERF repressor function by the transactivating members of the ets family of genes (i.e. gag-myb-ets) may be essential for the control of genes involved in cell proliferation and may also underlie their tumorigenic effects. C1 FREDERICK CANC RES & DEV CTR,SAIC,FREDERICK,MD 21702. RP SGOURAS, DN (reprint author), NCI,MOLEC ONCOL LAB,POB B,FREDERICK,MD 21702, USA. RI Fisher, Robert/B-1431-2009; Sgouras, Dionyssios Nicholas/D-9943-2012 OI Sgouras, Dionyssios Nicholas/0000-0003-0975-2607 NR 79 TC 122 Z9 124 U1 0 U2 8 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD OCT 2 PY 1995 VL 14 IS 19 BP 4781 EP 4793 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TA216 UT WOS:A1995TA21600015 PM 7588608 ER PT J AU SAVILAHTI, H RICE, PA MIZUUCHI, K AF SAVILAHTI, H RICE, PA MIZUUCHI, K TI THE PHAGE-MU TRANSPOSOSOME CORE - DNA REQUIREMENTS FOR ASSEMBLY AND FUNCTION SO EMBO JOURNAL LA English DT Article DE DNA TRANSPOSITION; PROTEIN-DNA COMPLEX; SITE-SPECIFIC RECOMBINATION ID STRAND-TRANSFER-REACTION; TRANSPOSITION INVITRO PROCEEDS; INTEGRATION HOST FACTOR; BACTERIOPHAGE-MU; RETROVIRAL DNA; B-PROTEIN; TARGET IMMUNITY; MECHANISM; SITE; INTERMEDIATE AB The two chemical steps of phage Mu transpositional recombination, donor DNA cleavage and strand transfer, take place within higher order protein-DNA complexes called transpososomes. At the core of these complexes is a tetramer of MuA (the transposase), bound to the two ends of the Mu genome. While transpososome assembly normally requires a number of cofactors, under certain conditions only MuA and a short DNA fragment are required, DNA requirements for this process, as well as the stability and activity of the ensuing complexes, were established. The divalent cation normally required for assembly of the stable complex could be omitted if the substrate was pre-nicked, if the flanking DNA was very short or if the two flanking strands were non-complementary. The presence of a single nucleotide beyond the Mu genome end on the non-cut strand was critical for transpososome stability, Donor cleavage additionally required at least two flanking nucleotides on the strand to be cleaved. The flanking DNA double helix was destabilized, implying distortion of the DNA near the active site. Although donor cleavage required Mg2+, strand transfer took place in the presence of Ca2+ as well, suggesting a conformational difference in the active site for the two chemical steps. C1 NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 51 TC 124 Z9 127 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD OCT 2 PY 1995 VL 14 IS 19 BP 4893 EP 4903 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TA216 UT WOS:A1995TA21600025 PM 7588618 ER PT J AU MADEJ, T BOGUSKI, MS BRYANT, SH AF MADEJ, T BOGUSKI, MS BRYANT, SH TI THREADING ANALYSIS SUGGESTS THAT THE OBESE GENE-PRODUCT MAY BE A HELICAL CYTOKINE SO FEBS LETTERS LA English DT Article DE OB GENE; LEPTIN; PROTEIN THREADING; STRUCTURE PREDICTION ID COLONY-STIMULATING FACTOR; 3-DIMENSIONAL STRUCTURE; STRUCTURE PREDICTION; PROTEIN-STRUCTURE; CRYSTAL-STRUCTURE; GROWTH-HORMONE; RECEPTOR; FOLD; SEQUENCE AB The ob gene encodes a protein that, in mutant form, is associated with obesity and type II diabetes in mice, Sequence analysis has revealed no similarities to other proteins, however, and no clues as to possible functions, The possibility nonetheless remains that ob is functionally or ancestrally related to other proteins, whose sequences are divergent to the point that only a comparison of three-dimensional structures might detect relationship, To explore this possibility, we conduct a 'threading' search of a 3-dimensional structure database, to determine whether the ob protein might adopt a fold similar to any known structure, This search reveals that the ob sequence is compatible, at a significance level of P < 0.05, with structures from the family of helical cytokines that includes interleukin-2 and growth hormone, A structural model of ob based upon these results is physically and biologically plausible and leads to testable predictions, including the prediction that ob may activate the JAK-STAT pathway, via binding to a receptor resembling those of the cytokine family. C1 NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,COMPUTAT BIOL BRANCH,BETHESDA,MD 20894. NR 39 TC 199 Z9 207 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD OCT 2 PY 1995 VL 373 IS 1 BP 13 EP 18 DI 10.1016/0014-5793(95)00977-H PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA RY517 UT WOS:A1995RY51700004 PM 7589424 ER PT J AU GEORGE, MS WASSERMANN, EM WILLIAMS, WA CALLAHAN, A KETTER, TA BASSER, P HALLETT, M POST, RM AF GEORGE, MS WASSERMANN, EM WILLIAMS, WA CALLAHAN, A KETTER, TA BASSER, P HALLETT, M POST, RM TI DAILY REPETITIVE TRANSCRANIAL MAGNETIC STIMULATION (RTMS) IMPROVES MOOD IN DEPRESSION SO NEUROREPORT LA English DT Article DE DEPRESSION; TRANSCRANIAL MAGNETIC STIMULATION; PREFRONTAL CORTEX; TREATMENTS; AFFECTIVE DISORDERS AB CONVERGING evidence points to hypofunction of the left prefrontal cortex in depression. Repetitive transcranial magnetic stimulation (rTMS) activates neurons near the surface of the brain. We questioned whether daily left prefrontal rTMS might improve mood in depressed subjects and report a pilot study of such treatment in six highly medication-resistant depressed inpatients. Depression scores significantly improved for the group as a whole (Hamilton Depression Scores decreased from 23.8 +/- 4.2 (s.d.) at baseline to 17.5 +/- 8.4 after treatment; t = 3.03, 5DF, p = 0.02, two-tailed paired t-test). Two subjects showed robust mood improvement which occurred progressively over the course of several weeks. In one subject, depression symptoms completely remitted for the first time in 3 years. Daily left prefrontal rTMS appears to be safe, well tolerated and may alleviate depression. C1 MED UNIV S CAROLINA,DEPT PSYCHIAT RADIOL & NEUROL,CHARLESTON,SC 29425. NIND,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20897. NIH,NCRR,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20897. NIAA,BETHESDA,MD 20897. RP GEORGE, MS (reprint author), NIMH,BIOL PSYCHIAT BRANCH,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. RI Basser, Peter/H-5477-2011 NR 10 TC 499 Z9 506 U1 5 U2 25 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD OCT 2 PY 1995 VL 6 IS 14 BP 1853 EP 1856 DI 10.1097/00001756-199510020-00008 PG 4 WC Neurosciences SC Neurosciences & Neurology GA RX808 UT WOS:A1995RX80800008 PM 8547583 ER PT J AU PARASURAMAN, R GREENWOOD, PM ALEXANDER, GE AF PARASURAMAN, R GREENWOOD, PM ALEXANDER, GE TI SELECTIVE IMPAIRMENT OF SPATIAL ATTENTION DURING VISUAL-SEARCH IN ALZHEIMERS-DISEASE SO NEUROREPORT LA English DT Article DE ATTENTION; ALZHEIMERS DISEASE; AGING; PARIETAL LOBES; VISUAL SEARCH ID FEATURE-INTEGRATION; DEMENTIA AB SPATIAL attention during visual search was examined in 14 persons with mild Alzheimer's disease (AD) and 28 healthy older subjects, 14 aged 65-74 (young-old), and 14 aged 75-85 (old-old). Subjects searched for single feature (color) or conjunction (color + letter) targets in displays of 10 or 15 letters. Precues of differing sizes were used to provide localizing information of varying precision. Effects of display size and cue size on reaction time (RT) for color search were similar in AD subjects and controls. For color + letter search, however, AD patients showed minimal effects of cue size, pointing to an impairment in AD in the spatial focusing of attention during visual search. Pathology affecting the association parietal and extrastriate areas may mediate impairment of spatial attention and visual search in AD. C1 NIA,NEUROSCI LAB,WASHINGTON,DC 20064. RP PARASURAMAN, R (reprint author), CATHOLIC UNIV AMER,COGNIT SCI LAB,WASHINGTON,DC 20064, USA. FU NIA NIH HHS [AG07569] NR 25 TC 34 Z9 35 U1 1 U2 3 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD OCT 2 PY 1995 VL 6 IS 14 BP 1861 EP 1864 DI 10.1097/00001756-199510020-00010 PG 4 WC Neurosciences SC Neurosciences & Neurology GA RX808 UT WOS:A1995RX80800010 PM 8547585 ER PT J AU BULTE, JWM DOUGLAS, T MANN, S VYMAZAL, J LAUGHLIN, PG FRANK, JA AF BULTE, JWM DOUGLAS, T MANN, S VYMAZAL, J LAUGHLIN, PG FRANK, JA TI INITIAL ASSESSMENT OF MAGNETOFERRITIN BIOKINETICS AND PROTON RELAXATION ENHANCEMENT IN RATS SO ACADEMIC RADIOLOGY LA English DT Article DE CONTRAST AGENT; SUPERPARAMAGNETIC IRON OXIDE; FERRITIN; LIVER; RELAXOMETRY; MAGNETIC RESONANCE IMAGING ID FERRITIN-BINDING PROTEIN; ALPHA-2-MACROGLOBULIN RECEPTOR; LIVER FERRITIN; SERUM; TURNOVER; PLASMA; KINETICS; ANTIGEN; CELLS AB Rationale and Objectives. We evaluated the biokinetics and proton relaxation enhancement of magnetoferritin, a recently developed class of superparamagnetic iron oxides, in rats. Methods. ''Equine'' magnetoferritin was administered intravenously at 5 mg protein and 1.4 mg Fe/kg in nude rats carrying subcutaneous xenografted human small-cell lung carcinoma with and without preinjection of 100 mg/kg equine apoferritin. Blood clearance, in vivo biodistribution, and proton relaxation enhancement were assessed by variable field relaxometry, immunohistochemistry, and magnetic resonance (MR) imaging at 1.5 T. Results. Magnetoferritin clearance from blood followed biexponential kinetics, with a short initial half-life of 1.4-1.7 min. A second, longer component lasted for several hours, Histochemical staining, MR imaging, and ex vivo relaxometry revealed rapid uptake of magnetoferritin in the liver, spleen, and lymph nodes. There was no difference in biodistribution after apoferritin preinjection. Conclusion. In the rat, equine magnetoferritin is rapidly sequestered by cells of the reticuloendothelial system, with no direct involvement of ferritin receptors, These properties may allow the use of magnetoferritin as an MR contrast agent for the liver and spleen. C1 UNIV BATH,SCH CHEM,BATH BA2 7AY,AVON,ENGLAND. PROT MAGNET,SAN LUIS OBISPO,CA. NIH,NEUROIMAGING BRANCH,BETHESDA,MD 20892. RP BULTE, JWM (reprint author), NIH,DIAGNOST RADIOL RES LAB,BLDG 10,ROOM B1N256,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Bulte, Jeff/A-3240-2008; Mann, Stephen/D-1332-2012; Douglas, Trevor/F-2748-2011 OI Bulte, Jeff/0000-0003-1202-1610; Mann, Stephen/0000-0003-3012-8964; NR 33 TC 27 Z9 27 U1 0 U2 3 PU ASSOC UNIV RADIOLOGISTS PI RESTON PA 1891 PRESTON WHITE DR, RESTON, VA 22091 SN 1076-6332 J9 ACAD RADIOL JI Acad. Radiol. PD OCT PY 1995 VL 2 IS 10 BP 871 EP 878 DI 10.1016/S1076-6332(05)80064-9 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA RW601 UT WOS:A1995RW60100007 PM 9419653 ER PT J AU Luyten, FP AF Luyten, FP TI Cartilage-derived morphogenetic proteins - Key regulators in chondrocyte differentiation? SO ACTA ORTHOPAEDICA SCANDINAVICA LA English DT Article ID TGF-BETA SUPERFAMILY; BONE DIFFERENTIATION; OSTEOGENIN; MEMBER; EXPRESSION; SEQUENCE; DEFECTS RP Luyten, FP (reprint author), NIDR,BONE RES BRANCH,DEV BIOL PROGRAM,BLDG 10,RM 1N108,BETHESDA,MD 20892, USA. NR 22 TC 3 Z9 3 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6470 J9 ACTA ORTHOP SCAND JI Acta Orthop. Scand. PD OCT PY 1995 VL 66 SU 266 BP 51 EP 54 PG 4 WC Orthopedics SC Orthopedics GA TQ513 UT WOS:A1995TQ51300012 ER PT J AU Fisher, LW Stubbs, JT Young, MF AF Fisher, LW Stubbs, JT Young, MF TI Antisera and cDNA probes to human and certain animal model bone matrix noncollagenous proteins SO ACTA ORTHOPAEDICA SCANDINAVICA LA English DT Article ID SMALL PROTEOGLYCAN-I; MESSENGER-RNA; BASEMENT-MEMBRANE; SIALOPROTEIN BSP; OSTEONECTIN; TISSUES; LOCALIZATION; SEQUENCE; HETEROGENEITY; OSTEOPONTIN RP Fisher, LW (reprint author), NIDR,BONE RES BRANCH,BLDG 30,ROOM 106,BETHESDA,MD 20892, USA. NR 23 TC 110 Z9 111 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6470 J9 ACTA ORTHOP SCAND JI Acta Orthop. Scand. PD OCT PY 1995 VL 66 SU 266 BP 61 EP 65 PG 5 WC Orthopedics SC Orthopedics GA TQ513 UT WOS:A1995TQ51300014 ER PT J AU MARMOR, M WINCHESTER, R ZELENIUCHJACQUOTTE, A WEISS, SH KRASINSKI, K SAXINGER, WC FRIEDMANKIEN, A WILLIAMS, DC DEMOPOULOS, R AF MARMOR, M WINCHESTER, R ZELENIUCHJACQUOTTE, A WEISS, SH KRASINSKI, K SAXINGER, WC FRIEDMANKIEN, A WILLIAMS, DC DEMOPOULOS, R TI EVIDENCE FOR AN EFFECT OF HUMAN-LEUKOCYTE ANTIGENS ON SUSCEPTIBILITY TO KAPOSIS-SARCOMA RELATED TO CHARGE AND PEPTIDE-BINDING PROPERTIES OF CLASS-I MOLECULES SO AIDS LA English DT Letter ID HLA C1 NYU,SCH MED,CTR AIDS RES,DEPT MED,NEW YORK,NY. NYU,SCH MED,KAPLAN COMPREHENS CANC CTR,NEW YORK,NY. NYU,SCH MED,DEPT PEDIAT,NEW YORK,NY. NYU,SCH MED,DEPT DERMATOL,NEW YORK,NY. NYU,SCH MED,DEPT MICROBIOL,NEW YORK,NY 10016. NYU,SCH MED,DEPT PATHOL,NEW YORK,NY. BELLEVUE HOSP CTR,NEW YORK,NY 10016. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT PREVENT MED,DIV INFECT DIS EPIDEMIOL,NEWARK,NJ 07103. NCI,BETHESDA,MD 20892. RP MARMOR, M (reprint author), NYU,SCH MED,DEPT ENVIRONM MED,NEW YORK,NY 10016, USA. OI Marmor, Michael/0000-0001-6605-2661 FU NCI NIH HHS [CA16087, CA33205]; PHS HHS [1P30A127742] NR 11 TC 3 Z9 3 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 OCT PY 1995 VL 9 IS 10 BP 1194 EP 1195 DI 10.1097/00002030-199510000-00013 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA RW132 UT WOS:A1995RW13200013 PM 8519458 ER PT J AU WIENER, L RIEKERT, KA THEUT, S STEINBERG, SM PIZZO, PA AF WIENER, L RIEKERT, KA THEUT, S STEINBERG, SM PIZZO, PA TI PARENTAL PSYCHOLOGICAL ADAPTATION AND CHILDREN WITH HIV - A FOLLOW-UP-STUDY SO AIDS PATIENT CARE LA English DT Article C1 NCI,PEDIAT BRANCH,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,SCH MED,CHILDRENS NATL MED CTR,WASHINGTON,DC. NCI,BIOSTAT & DATA MANAGEMENT SECT,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NCI,INFECT DIS SECT,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. RP WIENER, L (reprint author), NCI,PEDIAT BRANCH,PEDIAT HIV PSYCHOSOCIAL SUPPORT PROGRAM,BLDG 10,BETHESDA,MD 20892, USA. NR 9 TC 5 Z9 5 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0893-5068 J9 AIDS PATIENT CARE JI Aids Patient Care PD OCT PY 1995 VL 9 IS 5 BP 233 EP 239 DI 10.1089/apc.1995.9.233 PG 7 WC Public, Environmental & Occupational Health; Nursing SC Public, Environmental & Occupational Health; Nursing GA TG261 UT WOS:A1995TG26100004 PM 11361403 ER PT J AU LORI, F GALLO, RC AF LORI, F GALLO, RC TI HYDROXYUREA AND AIDS - AN OLD DRUG FINDS A NEW APPLICATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID REPLICATION; CELLS; LYMPHOCYTES; INTEGRATION C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 26 TC 22 Z9 22 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1149 EP 1151 DI 10.1089/aid.1995.11.1149 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800002 PM 8573369 ER PT J AU LAWRENCE, DN SCHULTZ, AM AF LAWRENCE, DN SCHULTZ, AM TI INTRODUCTION TO THE 1994 AIDS-VACCINE-CONFERENCE SUMMARIES AND A RETROSPECTIVE OVERVIEW OF THE 1988-1994 CONFERENCES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material RP LAWRENCE, DN (reprint author), NIAID,DIV AIDS,SOLAR BLDG,ROOM 2A11,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1275 EP 1276 DI 10.1089/aid.1995.11.1275 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800020 ER PT J AU VOGEL, FR ALVING, CR AF VOGEL, FR ALVING, CR TI ADJUVANTS AND NOVEL VACCINES - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 WALTER REED ARMY INST RES,DEPT MEMBRANE BIOCHEM,WASHINGTON,DC 20307. RP VOGEL, FR (reprint author), NIAID,DIV AIDS,VACCINE & PREVENT RES PROGRAM,SOLAR BLDG,ROM 2A28A,6003 EXECUT BLVD,ROCKVILLE,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1277 EP 1278 DI 10.1089/aid.1995.11.1277 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800021 ER PT J AU WALKER, MC FAST, PE GRAHAM, BS BELSHE, R DOLIN, R AF WALKER, MC FAST, PE GRAHAM, BS BELSHE, R DOLIN, R TI PHASE-I PHASE-II PREVENTIVE VACCINE TRIALS - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material ID LYMPHOCYTE PROLIFERATIVE RESPONSES; EXPRESSING HIV ENVELOPE; GP160 SUBUNIT VACCINE; RECOMBINANT GP160; CD4+; ANTIBODY; SAFETY; IMMUNOGENICITY; GLYCOPROTEIN; IMMUNIZATION C1 NIAID,DIV AIDS,CLIN DEV BRANCH,BETHESDA,MD 20892. VANDERBILT UNIV,SCH MED,DEPT MED,NASHVILLE,TN 37232. VANDERBILT UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,NASHVILLE,TN 37232. ST LOUIS UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. UNIV ROCHESTER,MED CTR,DEPT MED,ROCHESTER,NY 14642. NR 29 TC 9 Z9 9 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1279 EP 1285 DI 10.1089/aid.1995.11.1279 PG 7 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800022 ER PT J AU HOFF, R AF HOFF, R TI PROGRESS TOWARD READINESS FOR EFFICACY TRIALS IN THE UNITED-STATES - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material RP HOFF, R (reprint author), NIAID,DIV AIDS,6003 EXECUT BLVD,SOLAR BLDG,ROOM 2A12,BETHESDA,MD 20892, USA. NR 21 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1287 EP 1290 DI 10.1089/aid.1995.11.1287 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800023 ER PT J AU LAWRENCE, DN HOFF, R AF LAWRENCE, DN HOFF, R TI PROGRESS TOWARD READINESS FOR INTERNATIONAL TRIALS - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material RP LAWRENCE, DN (reprint author), NIAID,DIV AIDS,SOLAR BLDG,ROOM 2A11,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 27 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1291 EP 1295 DI 10.1089/aid.1995.11.1291 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800024 ER PT J AU BARKER, LF JAFFE, HW ROSENBERG, ZF AF BARKER, LF JAFFE, HW ROSENBERG, ZF TI PREVENTION RESEARCH AND VACCINE PREPAREDNESS - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material ID RISK REDUCTION; AIDS; INTERVENTIONS; BEHAVIOR; TRIAL C1 CTR DIS CONTROL & PREVENT,DIV HIV AIDS,ATLANTA,GA 30341. RP BARKER, LF (reprint author), NIAID,6003 EXECUT BLVD,ROCKVILLE,MD 20892, USA. NR 12 TC 0 Z9 0 U1 1 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1297 EP 1299 DI 10.1089/aid.1995.11.1297 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800025 ER PT J AU ROBB, M BRIDGES, S MMIRO, F FOWLER, MG FAST, P MCNAMARA, J AF ROBB, M BRIDGES, S MMIRO, F FOWLER, MG FAST, P MCNAMARA, J TI REPORT OF THE PREVENTION OF PERINATAL HIV TYPE-1 TRANSMISSION WORKSHOP - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 NIAID,DIV AIDS,BETHESDA,MD 20892. MAKERERE UNIV,DEPT OBSTET & GYNECOL,KAMPALA,UGANDA. RP ROBB, M (reprint author), WALTER REED ARMY INST RES,DIV RETROVIROL,13 TAFT COURT,SUITE 200,ROCKVILLE,MD 20850, USA. NR 9 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1301 EP 1303 DI 10.1089/aid.1995.11.1301 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800026 ER PT J AU GRAHAM, BS SAWYER, LA WALKER, MC FAST, PE HU, SL AF GRAHAM, BS SAWYER, LA WALKER, MC FAST, PE HU, SL TI INTERFACE BETWEEN ANIMAL-MODELS AND CLINICAL-PHASE-I TRIALS WORKSHOP - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 NIAID,DIV AIDS,VACCINE & PREVENT RES PROGRAM,PRECLIN RES BRANCH,BETHESDA,MD 20892. VANDERBILT UNIV,SCH MED,DEPT MED,NASHVILLE,TN 37232. VANDERBILT UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,NASHVILLE,TN 37232. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1305 EP 1306 DI 10.1089/aid.1995.11.1305 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800027 ER PT J AU WESCOTT, S SAVARESE, B SMITH, C AF WESCOTT, S SAVARESE, B SMITH, C TI PARTICIPATION OF MINORITY POPULATIONS IN PHASE-I PHASE-II CLINICAL-TRIALS OF CANDIDATE AIDS VACCINES - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 EMMES CORP,POTOMAC,MD 20854. RP WESCOTT, S (reprint author), NIAID,DIV AIDS,CLIN DEV BRANCH,SOLAR BLDG,ROOM 2A31,6003 EXECUT BLVD,ROCKVILLE,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1307 EP 1307 DI 10.1089/aid.1995.11.1307 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800028 ER PT J AU SHEON, AR AF SHEON, AR TI PREVENTING DISCRIMINATION AGAINST VOLUNTEERS IN PREVENTIVE HIV VACCINE EFFICACY TRIALS - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material AB A Workshop was held November 8, 1994 to discuss actual and theoretical risks for discrimination against volunteers in future HIV preventive vaccine efficacy trials. A small proportion of volunteers in ongoing Phase I/II vaccine trials have had positive HIV antibody tests due to vaccine-induced HIV antibody responses. Some volunteers had difficulty obtaining health and life insurance, employment with the U.S. military, and with foreign travel. Study staff were able to resolve almost all such problems. Gay men enrolled in prospective seroincidence studies experienced a 1.6% chance per year of undergoing required HIV antibody tests. Among subjects enrolled in future vaccine trials, the likelihood of such tests resulting in discrimination will depend on the type of vaccine and antibody tests used. The Americans with Disabilities Act may be used to prevent illegal discrimination against those actually, or erroneously thought to be HIV infected. A study is underway to estimate the frequency with which volunteers in a study of gp120 preventive vaccines have actually experienced legal and illegal discrimination as a result of trial participation. Data and Safety Monitoring Boards can evaluate such data and should recommend modification of trial procedures or termination of trials if volunteers experience severe social harm due to their participation in trials. RP SHEON, AR (reprint author), NIAID,DIV AIDS,6003 EXECUT BLVD,ROOM 2A10,BETHESDA,MD 20892, USA. NR 4 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1309 EP 1312 DI 10.1089/aid.1995.11.1309 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800029 ER PT J AU FOULKES, MA CONNELL, CA FISCHER, R AF FOULKES, MA CONNELL, CA FISCHER, R TI ETHICAL AND MONITORING ISSUES IN INTERNATIONAL TRIALS - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 FAMILY HLTH INT,DURHAM,NC 27713. RP FOULKES, MA (reprint author), NIAID,DIV AIDS,SOLAR BLDG,ROOM 2A01,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1313 EP 1314 DI 10.1089/aid.1995.11.1313 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800030 ER PT J AU RIDA, W FLEMING, T STEVENS, C AF RIDA, W FLEMING, T STEVENS, C TI ALTERNATIVE TRIAL DESIGNS - CONFERENCE SUMMARY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 UNIV WASHINGTON,DEPT BIOSTAT,SEATTLE,WA 98195. NEW YORK BLOOD CTR,NEW YORK,NY 10021. RP RIDA, W (reprint author), NIAID,DIV AIDS,BIOSTAT RES BRANCH,SOLAR BLDG,2A02,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD OCT PY 1995 VL 11 IS 10 BP 1317 EP 1319 DI 10.1089/aid.1995.11.1317 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA TD258 UT WOS:A1995TD25800032 ER PT J AU NOVORADOVSKY, A TSAI, SJL GOLDFARB, L PETERSON, R LONG, JC GOLDMAN, D AF NOVORADOVSKY, A TSAI, SJL GOLDFARB, L PETERSON, R LONG, JC GOLDMAN, D TI MITOCHONDRIAL ALDEHYDE DEHYDROGENASE POLYMORPHISM IN ASIAN AND AMERICAN-INDIAN POPULATIONS - DETECTION OF NEW ALDH2 ALLELES SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE ALDEHYDE DEHYDROGENASE; HUMAN POPULATIONS; GENETIC POLYMORPHISM; NEW ALLELES ID POLYMERASE CHAIN-REACTION; ALCOHOL SENSITIVITY; GENOTYPES; GENE; MUTANT AB Genetic deficiency of the mitochondrial aldehyde dehydrogenase (ALDH2) is frequent in Asian peoples where it is an important factor negatively regulating drinking behavior. To obtain additional information on gene geography of known ALDH2 alleles, and look for new variants, ALDH2 genes were evaluated in a Chinese population from Taiwan, a Yakut population of Siberia, and in five North American Indian populations. A novel approach based on a single-strand conformation polymorphism assay, and polymerase chain reaction-directed mutagenesis was developed for genotyping. In the Taiwan Chinese population, the ALDH2(2) allele frequency was 0.319 +/- 0.025, and this allele was not detected in the Yakut population nor in the five North American Indian populations. However, a new allele, ALDH2(3), was detected in Pima Indians at a frequency of 0.044 +/- 0.022, and this allele was also observed in 1 of 49 Pueblo samples. ALDH2(3) is a silent transition 1464 G --> A, and it possibly has a wide distribution among North American Indians. A new subtype of the ALDH2(2) allele, designated as ALDH2(2Taiwan), was found in 1 of 174 Chinese from Taiwan. ALDH2(2Taiwan) is characterized by two G --> A transitions at bases 1486 and 1510, resulting in Glu --> Lys substitutions at both the 479 and 487 positions. Thus, this second nonconservative ALDH2 substitution occurs within the sequence of the already inactive ALDH2(2) allele. C1 NINCDS,CLIN NEUROGENET UNIT,BETHESDA,MD. RP NOVORADOVSKY, A (reprint author), NHLBI,PULM CRIT CARE MED BRANCH,NEUROGENET LAB,10 CTR DR,RM 6D20,BETHESDA,MD 20892, USA. RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 30 TC 39 Z9 42 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD OCT PY 1995 VL 19 IS 5 BP 1105 EP 1110 DI 10.1111/j.1530-0277.1995.tb01587.x PG 6 WC Substance Abuse SC Substance Abuse GA TA738 UT WOS:A1995TA73800003 PM 8561277 ER PT J AU TATARANNI, PA RAVUSSIN, E AF TATARANNI, PA RAVUSSIN, E TI USE OF DUAL-ENERGY X-RAY ABSORPTIOMETRY IN OBESE INDIVIDUALS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE DUAL-ENERGY X-RAY ABSORPTIOMETRY; OBESITY; BODY COMPOSITION; HYDRODENSITOMETRY ID BODY-COMPOSITION; FAT; BONE AB Dual-energy X-ray absorptiometry (DXA) provides precise measurements of body composition in humans. Because its use in obese subjects is limited by the size of the scanning area, we explored the possibility of estimating whole-body composition from DXA half-body scans. Body composition of 183 subjects with a wide range of body sizes [body mass index (BMI; in kg/m(2)) of 17.7-52.8] was assessed by DXA and hydrodensitometry. Subjects fitting in the DXA scanning area (group A, n = 156) were scanned once whereas subjects exceeding it (group B, n = 27) were scanned twice, once for each side of the body. When body-composition results for the light and left sides were compared, only minimal differences between the two sides of the body were found in both groups. Least-squares-regression analysis of whole-body composition by hydrodensitometry on DXA gave the following results: percent body fat, r(2) = 0.89 (SEE = 4.1%); fat-free mass; r(2) = 0.89 (SEE = 3.72 kg); and fat mass, r(2) = 0.95 (SEE = 3.57 kg). Similar r(2) values and SEEs were obtained for percent body fat when only results from DXA half-body scans of all subjects were considered: right side, r(2) = 0.90 (SEE = 4.1%); and left side, r(2) = 0.89 (SEE = 4.2%). The error in predicting body composition by hydrodensitometry from DXA whole- or half-body scans was not affected by the subject's body size and/or scanning technique. Ln conclusion, our results indicate that half-body scan values by DXA accurately predict whole-body composition. C1 NIDDK, NUTR SECT, PHOENIX, AZ 85016 USA. RP TATARANNI, PA (reprint author), NIDDKD, DEPT CLIN DIABET, 4212 N 16TH ST, ROOM 541, PHOENIX, AZ 85016 USA. NR 17 TC 158 Z9 158 U1 2 U2 3 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998 USA SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD OCT PY 1995 VL 62 IS 4 BP 730 EP 734 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA RY074 UT WOS:A1995RY07400005 PM 7572700 ER PT J AU LARSON, DE FERRARO, RT ROBERTSON, DS RAVUSSIN, E AF LARSON, DE FERRARO, RT ROBERTSON, DS RAVUSSIN, E TI ENERGY-METABOLISM IN WEIGHT-STABLE POSTOBESE INDIVIDUALS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE RESPIRATORY CHAMBER; ENERGY EXPENDITURE; FAT OXIDATION; BODY COMPOSITION ID OBESE WOMEN; FAT OXIDATION; PIMA-INDIANS; BODY-WEIGHT; DIETARY-FAT; POST-OBESE; EXPENDITURE; GAIN; EXERCISE; RATIO AB A low metabolic rate for a given body size and body composition and a low ratio of fat to carbohydrate oxidation predict body weight gain. Such metabolic traits could also explain, in part, the propensity of previously obese (postobese) individuals to regain weight after dieting. We studied 11 postobese volunteers (4 males, 7 females; aged 43 +/- 13 y, weighing 80.6 +/- 10.2 kg, with 30 +/- 7% body fat; (x) over bar +/- SD) who lost 57 +/- 38 kg (23-139 kg) over 14 +/- 12 mo (6-48 mo) on various diet programs and had maintained this weight loss for greater than or equal to 2 mo (2-72 mo; 21 +/- 27 mo). After greater than or equal to 2 d of a weight-maintenance diet on a metabolic ward, 24-h energy expenditure and ratio of fat to carbohydrate oxidation were measured in a respiratory chamber. Compared with a central group (n = 110) with similar physical characteristics (aged 43 +/- 14 y, weighing 79.5 +/- 11.4 kg, with 30 +/- 12% body fat), postobese individuals had similar energy expenditures adjusted for fat-free mass, fat mass, age, and sex, but significantly higher respiratory quotients over 24 h (0.883 +/- 0.026 compared with 0.863 +/- 0.024, P < 0.01) and during sleep, 10 h after the last meal (0.894 +/- 0.063 compared with 0.845 +/- 0.055). These results suggest that postobese individuals have low rates of fat oxidation that may explain their propensity to regain weight. Therefore, obesity treatment and/or prevention should be aimed at reducing dietary fat and increasing fat oxidation (possibly by exercise) to prevent increases in body fat stores. C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. NR 34 TC 91 Z9 91 U1 2 U2 3 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 OCT PY 1995 VL 62 IS 4 BP 735 EP 739 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA RY074 UT WOS:A1995RY07400006 PM 7572701 ER PT J AU BHATHENA, SJ BERLIN, E JUDD, JT CLEVIDENCE, BA TAYLOR, PR CAMPBELL, WS NAIR, PP AF BHATHENA, SJ BERLIN, E JUDD, JT CLEVIDENCE, BA TAYLOR, PR CAMPBELL, WS NAIR, PP TI SELECTIVE RESPONSES OF HORMONES INVOLVED IN CARBOHYDRATE AND LIPID-METABOLISM AND PROPERTIES OF ERYTHROCYTE-MEMBRANES DURING THE MENSTRUAL-CYCLE IN PREMENOPAUSAL WOMEN CONSUMING MODERATE AMOUNTS OF ALCOHOL SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE PREMENOPAUSAL WOMEN; ALCOHOL; HORMONES; INSULIN RECEPTORS; MEMBRANE FLUIDITY ID FOOD-INTAKE; POSTMENOPAUSAL WOMEN; INSULIN-RECEPTORS; SEX-HORMONES; DIETARY-FAT; RAT; FLUIDITY; ETHANOL; BINDING; PLASMA AB The effects of chronic consumption of moderate amounts of alcohol on hormones associated with lipid and carbohydrate metabolism, plasma concentrations of triacylglycerol and cholesterol, insulin receptors on erythrocyte membranes, and erythrocyte membrane fluidity were studied during three phases of the menstrual cycle in 37 premenopausal women. Subjects were given either 30 g ethanol or an equienergetic fruit juice for three menstrual cycles in a crossover design. Blood samples were analyzed during the luteal, midcycle, and follicular phases. Administration of alcohol induced a significant rise in plasma glucagon and cortisol uniformly across the entire menstrual cycle. A similar rise in plasma growth hormone was observed at midcycle during the period when subjects consumed alcohol. A marginal effect was observed on cholesterol and somatomedin C concentrations. Insulin binding to erythrocyte ghosts was not affected by either alcohol or menstrual-cycle phase. Erythrocyte membranes were more fluid during the follicular phase than during the luteal phase of the menstrual cycle when the women were consuming the alcohol. There were no perceptible interactions between alcohol and phases of the menstrual cycle for the indexes studied, except membrane fluidity. C1 USDA ARS,BELTSVILLE HUMAN NUTR RES CTR,DIET & HUMAN PERFORMANCE LAB,BELTSVILLE,MD 20705. USDA ARS,BELTSVILLE HUMAN NUTR RES CTR,NUTRIENT REQUIREMENT & FUNCT LAB,BELTSVILLE,MD 20705. NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD. RP BHATHENA, SJ (reprint author), USDA ARS,BELTSVILLE HUMAN NUTR RES CTR,BLDG 307-E,ROOM 324,BELTSVILLE,MD 20705, USA. NR 63 TC 2 Z9 2 U1 0 U2 1 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 OCT PY 1995 VL 62 IS 4 BP 751 EP 756 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA RY074 UT WOS:A1995RY07400009 PM 7572704 ER PT J AU BROOKMEYER, R QUINN, T SHEPHARD, M MEHENDALE, S RODRIGUES, J BOLLINGER, R AF BROOKMEYER, R QUINN, T SHEPHARD, M MEHENDALE, S RODRIGUES, J BOLLINGER, R TI THE AIDS EPIDEMIC IN INDIA - A NEW METHOD FOR ESTIMATING CURRENT HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) INCIDENCE RATES SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Note DE ACQUIRED IMMUNODEFICIENCY SYNDROME; BIAS (EPIDEMIOLOGY); CROSS-SECTIONAL STUDIES; EPIDEMIOLOGIC METHODS; HIV; STATISTICS ID INFECTION AB Human immunodeficiency virus (HIV) incidence rates in India were estimated using a new method that accounts for follow-up bias. Follow-up bias arises in epidemiologic cohort studies when the incidence rate among individuals who do and do not return for follow-up are different, The new method combines data on the prevalence of p24 antigenemia among all those initially screened together with the longitudinal follow-up data on the subset of patients who returned for follow-up, Using these methods, the current HIV incidence rate among patients attending sexually transmitted disease clinics in Pune, India, was 18.6% per year, It was found that follow-up bias can cause significant underestimation in HIV incidence rates, perhaps by as much as 60%. These incidence estimates, together with other HIV seroprevalence studies, suggest the HIV epidemic in India is growing rapidly. C1 JOHNS HOPKINS UNIV,SCH MED,DIV INFECT DIS,BALTIMORE,MD 21205. NIAID,BETHESDA,MD 20892. NATL AIDS RES INST,POONA,MAHARASHTRA,INDIA. RP BROOKMEYER, R (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT BIOSTAT,615 N WOLFE ST,BALTIMORE,MD 21205, USA. FU NCRR NIH HHS [3M01RR00722]; NIAID NIH HHS [AI 33879-02]; OID CDC HHS [CH 48723] NR 16 TC 55 Z9 58 U1 0 U2 1 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD OCT 1 PY 1995 VL 142 IS 7 BP 709 EP 713 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA RW932 UT WOS:A1995RW93200005 PM 7572940 ER PT J AU ANDERSON, RL HAMMAN, RF SAVAGE, PJ SAAD, MF LAWS, A KADES, WW SANDS, RE CEFALU, W AF ANDERSON, RL HAMMAN, RF SAVAGE, PJ SAAD, MF LAWS, A KADES, WW SANDS, RE CEFALU, W TI EXPLORATION OF SIMPLE INSULIN SENSITIVITY MEASURES DERIVED FROM FREQUENTLY SAMPLED INTRAVENOUS GLUCOSE-TOLERANCE (FSIGT) TESTS - THE INSULIN-RESISTANCE ATHEROSCLEROSIS STUDY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE GLUCOSE CLAMP TECHNIQUE; GLUCOSE TOLERANCE TEST; INSULIN; INSULIN RESISTANCE ID MINIMAL MODEL; CLAMP; INDEX AB Both abnormal insulin levels and low insulin sensitivity have been implicated as risk factors for Type II diabetes mellitus and cardiovascular disease. While insulin level is relatively simple to assess, direct measurement of insulin sensitivity is much more invasive, costly, and time-consuming, The authors considered eight previously described measures or indices of insulin sensitivity derived from the frequently sampled intravenous glucose tolerance test (FSIGT). Each one was evaluated by strength and consistency of association with insulin sensitivity computed from glucose clamp (S-l(clamp), across three glucose tolerance groups, including participants with normal glucose tolerance (n = 11), impaired glucose tolerance (n = 20), and non-insulin-dependent diabetes mellitus (n = 24). Minimal model analysis (MINMOD S-l(22), based on the 22-sample FSIGT, performed best based on statistical criteria of strong and consistent association with S-l(clamp) . An insulin sensitivity measure similar to that of Galvin et al. (Diabetic Medicine 1990;9:921-8), defined as glucose disappearance (10-50 minutes) divided by insulin area under the curve above baseline from 0-50 minutes, performed best based on statistical criteria and time-savings. Galvin insulin sensitivity is simple to calculate, requires only a 50-minute FSIGT, and is significantly (p < 0.001) and not inconsistently (p = 0.12 for inconsistent association) associated with S-l(clamp) over a wide range of glucose tolerance. C1 WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,WINSTON SALEM,NC 27103. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT INTERNAL MED,WINSTON SALEM,NC 27103. UNIV COLORADO,HLTH SCI CTR,DEPT PREVENT MED & BIOMETR,DENVER,CO 80262. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. UNIV SO CALIF,SCH MED,DEPT MED,LOS ANGELES,CA 90033. STANFORD UNIV,SCH MED,DEPT MED,PALO ALTO,CA 94304. FU NHLBI NIH HHS [HL-47889, HL-47887, HL-47902] NR 22 TC 112 Z9 112 U1 1 U2 1 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD OCT 1 PY 1995 VL 142 IS 7 BP 724 EP 732 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA RW932 UT WOS:A1995RW93200008 PM 7572943 ER PT J AU CLEMENS, J RAO, M SACK, D AHMED, F KHAN, MR CHAKRABORTY, J KAY, B HUDA, S YUNUS, M VANLOON, F SVENNERHOLM, AM HOLMGREN, J AF CLEMENS, J RAO, M SACK, D AHMED, F KHAN, MR CHAKRABORTY, J KAY, B HUDA, S YUNUS, M VANLOON, F SVENNERHOLM, AM HOLMGREN, J TI IMPAIRED IMMUNE-RESPONSE TO NATURAL INFECTION AS A CORRELATE OF VACCINE FAILURE IN A FIELD TRIAL OF KILLED ORAL CHOLERA VACCINES SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE CHOLERA; CHOLERA VACCINE; SEROEPIDEMIOLOGIC METHODS ID BANGLADESH; RISK; TOXIN AB In a field trial carried out in 1985 in Matlab, Bangladesh, the authors evaluated whether subjects who developed Vibrio cholerae 01 infections during the first year after earlier receipt of B subunit-killed whole cell (BS-WC) or killed whole cell-only (WC) oral cholera vaccines exhibited deficient serum vibriocidal immune responses to these infections. After severe V. cholerae 01 infections (n = 70) in subjects > 5 years of age, the age group in which both vaccines were efficacious, a 6.5 geometric mean-fold rise of serum vibriocidal antibodies was observed among vaccinees, compared with an 18.6 geometric mean-fold rise in placebo-recipients (p < 0.01). Depressions of serum vibriocidal responses among vaccinees were even more marked after asymptomatic infections (n = 30): a 1.1 geometric mean-fold rise in vaccinees versus a 5.9 geometric mean-fold rise in placebo-recipients (p < 0.01). The authors conclude that subjects who failed to be protected by BS-WC and WC, despite being in the age group for which these vaccines were protective, exhibited poor immune responses even to the vigorous stimulus of natural infection. These findings raise the possibility that immune hyporesponsiveness may limit the potential efficacy attainable by cholera vaccines in populations with endemic cholera. C1 INT CTR DIARRHOEAL DIS RES,DHAKA 1000,BANGLADESH. CTR DIS CONTROL & PREVENT,ATLANTA,GA 30341. GOTHENBURG UNIV,GOTHENBURG,SWEDEN. JOHNS HOPKINS UNIV,SCH PUBL HLTH,BALTIMORE,MD. RP CLEMENS, J (reprint author), NICHHD,6100 EXECUT BLVD,ROOM 7B03,BETHESDA,MD 20892, USA. NR 18 TC 5 Z9 5 U1 2 U2 2 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 OCT 1 PY 1995 VL 142 IS 7 BP 759 EP 764 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA RW932 UT WOS:A1995RW93200012 PM 7572947 ER PT J AU WEINBERG, CR UMBACH, DM GREENLAND, S AF WEINBERG, CR UMBACH, DM GREENLAND, S TI WHEN WILL NONDIFFERENTIAL MISCLASSIFICATION OF AN EXPOSURE PRESERVE THE DIRECTION OF A TREND - REPLY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter C1 UNIV CALIF LOS ANGELES,SCH PUBL HLTH,DEPT EPIDEMIOL,LOS ANGELES,CA 90095. RP WEINBERG, CR (reprint author), NIEHS,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709, USA. NR 8 TC 10 Z9 10 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 OCT 1 PY 1995 VL 142 IS 7 BP 784 EP 784 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA RW932 UT WOS:A1995RW93200020 ER PT J AU HASEGAWA, S HIRUMA, H UYESAKA, N NOGUCHI, CT SCHECHTER, AN RODGERS, GP AF HASEGAWA, S HIRUMA, H UYESAKA, N NOGUCHI, CT SCHECHTER, AN RODGERS, GP TI FILTERABILITY OF MIXTURES OF SICKLE AND NORMAL ERYTHROCYTES SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE BLOOD TRANSFUSION; DEFORMABILITY; RETICULOCYTES; EXCHANGE TRANSFUSION; DENSE CELLS ID CELL DISEASE; TRANSFUSION THERAPY; RED-CELLS; HEMOGLOBIN; HETEROGENEITY; POLYMERIZATION; DEFORMABILITY; DENSITY; ANEMIA; BLOOD AB We investigated the deformability of sickle (SS) cells from 25 patients and mixtures of these SS cells with blood type-compatible normal (AA) cells, using a nickel mesh filtration system, with the aim of determining optimal goals for exchange therapy, We found that for air-equilibrated SS/AA cell mixtures the fraction of dense cells (MCHC > 37 g/dl) is the determinant factor in filterability and that the dense cells contribute in a linear fashion to the loss of filtration up to 15% dense cells (y = -4.41x + 98.23, r = 0.945, P < 0.0001), The slope of this effect is approximately 25 times steeper than that of the relationship between filtration and percent nondense (MCHC < 37/g/dl) SS cells (y = -0.17x + 106.53, r = 0.772, P < 0.0001). A comparison of the proportion of high fluorescence reticulocytes to total reticulocytes (HFR ratio), indicating an elevation of immature reticulocytes, between six nontransfused patients and six exchange-transfused patients showed significant higher values in the nontransfused individuals (D.154 +/- 0.051 versus 0.070 +/- 0.054, P < 0.003). These results may have implications regarding targets for exchange transfusion therapy. Further studies of the effect on transfusion, both simple and exchange, on the numbers of dense cells and the proportions and populations of reticulocytes and the theological characteristics of the erythrocyte subpopulations seems warranted. (C) 1995 Wiley-Liss, Inc. C1 NIDDKD,BIOL CHEM LAB,BETHESDA,MD 20892. NIPPON MED COLL,DEPT PHYSIOL,TOKYO,JAPAN. OI Schechter, Alan N/0000-0002-5235-9408 NR 36 TC 6 Z9 6 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 OCT PY 1995 VL 50 IS 2 BP 91 EP 97 DI 10.1002/ajh.2830500204 PG 7 WC Hematology SC Hematology GA RX490 UT WOS:A1995RX49000003 PM 7573006 ER PT J AU SHILOH, Y SAVITSKY, K BARSHIRA, A GILAD, S ZIV, Y TAGLE, DA SFEZ, S UZIEL, T PECKER, I VANAGAITE, L SMITH, S HARNIK, R COLLINS, FS ROTMAN, G AF SHILOH, Y SAVITSKY, K BARSHIRA, A GILAD, S ZIV, Y TAGLE, DA SFEZ, S UZIEL, T PECKER, I VANAGAITE, L SMITH, S HARNIK, R COLLINS, FS ROTMAN, G TI ATAXIA-TELANGIECTASIA - FROM PHENOTYPE TO GENE, ON TO BIOLOGY AND BACK TO THE PATIENT SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 TEL AVIV UNIV,DEPT HUMAN GENET,IL-69978 TEL AVIV,ISRAEL. NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 6 EP 6 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700006 ER PT J AU FUTRCAL, PA GUMBS, C BERCHUCK, A WISEMAN, RW AF FUTRCAL, PA GUMBS, C BERCHUCK, A WISEMAN, RW TI FREQUENT ALLELIC DELETION OF CHROMOSOME 1P IN PRIMARY OVARIAN-CANCER - MAPPING OF 2 TUMOR SUPRESSOR GENE REGIONS AND PRELIMINARY-ANALYSIS OF CANDIDATE GENES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DURHAM,NC. NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 11 EP 11 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700011 ER PT J AU RIZZO, WB ROGERS, GR MAREKOV, LN STEINERT, PM COMPTON, JG MARKOVA, N DELAURENZI, V AF RIZZO, WB ROGERS, GR MAREKOV, LN STEINERT, PM COMPTON, JG MARKOVA, N DELAURENZI, V TI SJOGREN-LARSSON SYNDROME (SLS) IS CAUSED BY MUTATIONS IN THE FATTY ALDEHYDE DEHYDROGENASE GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT HUMAN GENET,RICHMOND,VA 23298. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT PEDIAT,RICHMOND,VA 23298. NIAMS,SKIN BIOL LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 24 EP 24 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700026 ER PT J AU STICK, MJ HOFFMAN, HJ HERMAN, AA BAKEWELL, JM SCHRAMM, WF STOCKBAUER, JW ISHII, EK AF STICK, MJ HOFFMAN, HJ HERMAN, AA BAKEWELL, JM SCHRAMM, WF STOCKBAUER, JW ISHII, EK TI THE ROLE OF ENVIRONMENTAL AND GENETIC-FACTORS IN THE RECURRENCE RISK OF BIRTH-DEFECTS - A POPULATION-BASED STUDY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIDCD,BETHESDA,MD. NICHHD,BETHESDA,MD. MISSOURI DEPT HLTH,JEFFERSON CITY,MO. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 45 EP 45 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700045 ER PT J AU JANNE, PA BERNARD, D CANNA, C WYNSHAWBORIS, A GRIMES, P MCDONALD, M CRAWLEY, J OLIVOSGLANDER, IM SUCHY, SF NUSSBAUM, RL AF JANNE, PA BERNARD, D CANNA, C WYNSHAWBORIS, A GRIMES, P MCDONALD, M CRAWLEY, J OLIVOSGLANDER, IM SUCHY, SF NUSSBAUM, RL TI PRODUCTION OF MICE DEFICIENT IN THE LOWE SYNDROME GENE (OCRL-1) AND ITS HIGHLY RELATED HOMOLOG, INOSITOL POLYPHOSPHATE 5-PHOSPHATASE (INPP5B) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PENN,SCH MED,DEPT GENET,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT OPHTHALMOL,PHILADELPHIA,PA 19104. NATL CTR HUMAN GENOME RES,BETHESDA,MD. NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 57 EP 57 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700059 ER PT J AU NING, Y ROSENBERG, M BIESECKER, L SMITH, ACM RIETHMAN, H LEDBETTER, DH AF NING, Y ROSENBERG, M BIESECKER, L SMITH, ACM RIETHMAN, H LEDBETTER, DH TI ISOLATION OF CHROMOSOME-SPECIFIC TELOMERIC PROBES AND THEIR CLINICAL-APPLICATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 78 EP 78 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700078 ER PT J AU BIESECKER, LG ROSENBERG, M DZIADZIO, L STONE, D LEDBETTER, D NING, Y ROSENBAUM, K ROBINSON, H AF BIESECKER, LG ROSENBERG, M DZIADZIO, L STONE, D LEDBETTER, D NING, Y ROSENBAUM, K ROBINSON, H TI DETECTION OF SUBTLE TRANSLOCATIONS BY MICROSATELLITE ANALYSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NCHGR,GENET DIS RES LAB,BETHESDA,MD 20892. NIH,NCHGR,DIAG DEV BRANCH,BETHESDA,MD 20892. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC. TOLEDO HOSP,TOLEDO,OH. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 80 EP 80 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700079 ER PT J AU AVRAHAM, KB HASSON, T STEEL, KP KINGSLEY, DM RUSSELL, LB MOOSEKER, MS COPELAND, NG JENKINS, NA AF AVRAHAM, KB HASSON, T STEEL, KP KINGSLEY, DM RUSSELL, LB MOOSEKER, MS COPELAND, NG JENKINS, NA TI POSITIONAL CLONING OF THE SNELLS WALTZER GENE - A MOUSE MODEL FOR HUMAN AUTOSOMAL RECESSIVE DEAFNESS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,ABL,FREDERICK,MD 21702. YALE UNIV,DEPT BIOL,NEW HAVEN,CT. UNIV NOTTINGHAM,MRC,INST HEARING RES,NOTTINGHAM,ENGLAND. STANFORD UNIV,SCH MED,DEPT DEV BIOL,STANFORD,CA. OAK RIDGE NATL LAB,DIV BIOL,OAK RIDGE,TN 37831. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 141 EP 141 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700139 ER PT J AU HUGHES, MR HADDAD, BR SUBRAMANIAN, S NASONKIN, I COTA, J CHONG, SS AF HUGHES, MR HADDAD, BR SUBRAMANIAN, S NASONKIN, I COTA, J CHONG, SS TI SINGLE-CELL DETECTION OF THE FMR1, HD, AND SCA1 TRINUCLEOTIDE REPEATS - APPLICATION TO PREIMPLANTATION DIAGNOSIS AND INSTABILITY ANALYSIS OF FRAGILE-X SYNDROME, HUNTINGTON DISEASE, AND SPINO-CEREBELLAR ATAXIA TYPE-1 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. GEORGETOWN UNIV,WASHINGTON,DC. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 152 EP 152 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700151 ER PT J AU HADDAD, BR CHONG, SS SUBRAMANIAN, S COTA, J HUGHES, MR AF HADDAD, BR CHONG, SS SUBRAMANIAN, S COTA, J HUGHES, MR TI GENETIC TYPING OF SINGLE CELLS USING MULTIPLE TETRAMERIC TANDEM REPEATS AFTER WHOLE GENOME AMPLIFICATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. GEORGETOWN UNIV,WASHINGTON,DC. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 156 EP 156 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700155 ER PT J AU KUBOTA, T SUTCLIFFE, JS KAYAWESTERLOH, S BEAUDET, AL HORSTHEMKE, B LEDBETTER, DH AF KUBOTA, T SUTCLIFFE, JS KAYAWESTERLOH, S BEAUDET, AL HORSTHEMKE, B LEDBETTER, DH TI MOLECULAR DIAGNOSIS FOR PRADER-WILLI-SYNDROME USING PARENT-OF-ORIGIN SPECIFIC DNA METHYLATION IN THE CPG ISLAND AT THE 5' END OF THE SNRPN GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. BAYLOR COLL MED,HOWARD HUGHES MED INST,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT MOLEC & HUMAN GENET,HOUSTON,TX 77030. UNIV ESSEN GESAMTHSCH KLINIKUM,INST HUMANGENET,ESSEN,GERMANY. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 166 EP 166 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700168 ER PT J AU CHRISTIAN, SL SMITH, ACM BLACK, S ELDER, FFB JOHNSON, JMP RESTA, RG ROCKLIN, ML SURTI, U SUSLAK, L VERP, MS WILKINS, I LEDBETTER, DH AF CHRISTIAN, SL SMITH, ACM BLACK, S ELDER, FFB JOHNSON, JMP RESTA, RG ROCKLIN, ML SURTI, U SUSLAK, L VERP, MS WILKINS, I LEDBETTER, DH TI MOLECULAR INVESTIGATION OF MOSAIC TRISOMY-15 DEMONSTRATES MATERNAL MI NONDISJUNCTION AND HIGH-RISK FOR UNIPARENTAL DISOMY-15 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. GENET & IVF INST,FAIRFAX,VA 22039. UNIV TEXAS,SCH MED,HOUSTON,TX. WAYNE STATE UNIV,DETROIT,MI. SWEDISH MED CTR,SEATTLE,WA. MAGEE WOMENS HOSP,PITTSBURGH,PA. UNIV MED & DENT NEW JERSEY,NEWARK,NJ. UNIV CHICAGO,CHICAGO,IL 60637. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 167 EP 167 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700166 ER PT J AU CHONG, SS PACK, S TANIGAMI, A CARROZZO, R DOBYNS, WB LEDBETTER, DH AF CHONG, SS PACK, S TANIGAMI, A CARROZZO, R DOBYNS, WB LEDBETTER, DH TI SYSTEMATIC DELETION ANALYSIS OF MDS AND ILS PATIENTS EXCLUDES A CANDIDATE GENE AND DELINEATES THE LISSENCEPHALY GENE LOCUS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. UNIV MILAN,OSPED SAN RAFFAELE,I-20127 MILAN,ITALY. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. RI Pack, Svetlana/C-2020-2014 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 170 EP 170 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700170 ER PT J AU ROA, BB GREENBERG, F GUNARATNE, P SAUER, CM LUBINSKY, MS KOZMA, C MECK, JM MAGENIS, RE SHAFFER, LG LUPSKI, JR AF ROA, BB GREENBERG, F GUNARATNE, P SAUER, CM LUBINSKY, MS KOZMA, C MECK, JM MAGENIS, RE SHAFFER, LG LUPSKI, JR TI DUPLICATION OF THE PMP22 GENE IN 17P PARTIAL TRISOMY PATIENTS WITH CHARCOT-MARIE-TOOTH TYPE 1A NEUROPATHY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOUSTON,TX 77030. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. CHILDRENS HOSP WISCONSIN,MILWAUKEE,WI 53201. MED COLL WISCONSIN,MILWAUKEE,WI 53226. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 171 EP 171 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700171 ER PT J AU SHANNON, WD GOLDIN, LR CHASE, GA WEEKS, DE AF SHANNON, WD GOLDIN, LR CHASE, GA WEEKS, DE TI DISTINGUISHING TRUE AND FALSE-POSITIVE PEAKS IN ALLELE-SHARING STATISTICS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 WASHINGTON UNIV,SCH MED,ST LOUIS,MO. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. UNIV PITTSBURGH,PITTSBURGH,PA. WELLCOME TRUST CTR HUMAN GENET,OXFORD,ENGLAND. RI Weeks, Daniel/B-2995-2012 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 175 EP 175 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700175 ER PT J AU WANG, S DETERAWADLEIGH, S COON, H SUN, C GOLDIN, LR BYERLEY, WF GERSHON, ES DIEHL, SR AF WANG, S DETERAWADLEIGH, S COON, H SUN, C GOLDIN, LR BYERLEY, WF GERSHON, ES DIEHL, SR TI FURTHER EVIDENCE FOR A SUSCEPTIBILITY LOCUS FOR SCHIZOPHRENIA ON CHROMOSOME 6P23 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NIMH,BETHESDA,MD 20892. UNIV UTAH,SALT LAKE CITY,UT. NR 1 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 177 EP 177 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700179 ER PT J AU SPRITZ, RA HO, L FURUMURA, M HEARING, VJ AF SPRITZ, RA HO, L FURUMURA, M HEARING, VJ TI MUTATIONAL ANALYSIS OF COPPER-BINDING BY HUMAN TYROSINASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 185 EP 185 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700184 ER PT J AU SUCHY, SF OLIVOSGLANDER, IM NUSSBAUM, RL AF SUCHY, SF OLIVOSGLANDER, IM NUSSBAUM, RL TI LOWE SYNDROME GENE ENCODES A PHOSPHATIDYLINOSITOL 4,5-BISPHOSPHATE 5-PHOSPHATASE EXPRESSED IN THE GOLGI-APPARATUS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,GENET DIS RES LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 187 EP 187 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700187 ER PT J AU CAO, O CEDRONE, E KENG, P BARRETT, C WANG, N AF CAO, O CEDRONE, E KENG, P BARRETT, C WANG, N TI STUDY OF TUMOR SUPPRESSION IN HUMAN OVARIAN-CARCINOMA CELLS SKOY-3 BY MICROCELL-MEDIATED CHROMOSOME TRANSFER SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV ROCHESTER,DEPT PATHOL,ROCHESTER,NY 14627. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 233 EP 233 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700235 ER PT J AU BELLUS, GA SZABO, JK MCINTOSH, I KAITILA, I AYLSWORTH, AS HECHT, JT FRANCOMANO, CA AF BELLUS, GA SZABO, JK MCINTOSH, I KAITILA, I AYLSWORTH, AS HECHT, JT FRANCOMANO, CA TI HYPOCHONDROPLASIA - A 2ND RECURRENT MUTATION OF FIBROBLAST GROWTH-FACTOR RECEPTOR-3 (EGFR3) AT NUCLEOTIDE 1620 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,MED GENET BRANCH,BETHESDA,MD. JOHNS HOPKINS UNIV,SCH MED,CTR MED GENET,BALTIMORE,MD 21205. HELSINKI UNIV HOSP,DEPT CLIN GENET,HELSINKI,FINLAND. UNIV N CAROLINA,DEPT PEDIAT,CHAPEL HILL,NC. UNIV N CAROLINA,BRAIN DEV RES CTR,CHAPEL HILL,NC. UNIV TEXAS,SCH MED,DEPT PEDIAT,HOUSTON,TX. NR 1 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 240 EP 240 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700241 ER PT J AU HECHT, JT NELSON, LD CROWDER, E WANG, Y ELDER, FFB HARRISON, WR FRANCOMONO, CA PRANGE, CK LENNON, GG DEERE, M LAWLER, J AF HECHT, JT NELSON, LD CROWDER, E WANG, Y ELDER, FFB HARRISON, WR FRANCOMONO, CA PRANGE, CK LENNON, GG DEERE, M LAWLER, J TI MUTATIONS IN CARTILAGE OLIGOMERIC MATRIX PROTEIN (COMP) CAUSE PSEUDOACHONDROPLASIA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. LAWRENCE LIVERMORE NATL LAB,CTR HUMAN GENOME,LIVERMORE,CA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 242 EP 242 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700242 ER PT J AU MCCASKILL, C SUBRAMANIAN, S HUGHES, M SHAFFER, LG AF MCCASKILL, C SUBRAMANIAN, S HUGHES, M SHAFFER, LG TI SINGLE-CELL ANALYSIS OF MOSAIC TRISOMY-21 - ORIGIN AND MECHANISMS OF MOSAICISM SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BAYLOR COLL MED,DEPT MOLEC & HUMAN GENET,HOUSTON,TX. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 254 EP 254 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700254 ER PT J AU PEPPER, AE MIDDLETON, LA ISAKOV, J PUCK, JM AF PEPPER, AE MIDDLETON, LA ISAKOV, J PUCK, JM TI IMPLEMENTATION OF MOLECULAR PRENATAL AND CARRIER DIAGNOSIS FOR X-LINKED SEVERE COMBINED IMMUNODEFICIENCY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NATL CTR HUMAN GENOME RES,GENE TRANSFER LAB,BETHESDA,MD 20892. NIH,NATL CTR HUMAN GENOME RES,MED GENET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 255 EP 255 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700255 ER PT J AU PROIA, RL SANGO, K YAMANAKA, S OKUDA, Y GRINBERG, A WESTPHAL, H MCDONALD, M CRAWLEY, JN SUZUKI, K AF PROIA, RL SANGO, K YAMANAKA, S OKUDA, Y GRINBERG, A WESTPHAL, H MCDONALD, M CRAWLEY, JN SUZUKI, K TI MOUSE MODELS OF TAY-SACHS AND SANDHOFF DISEASES DISPLAY VASTLY DIFFERENT PHENOTYPES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIDDK,GBB,BETHESDA,MD 20892. NICHHD,LMGD,BETHESDA,MD 20892. NIMH,ETB,BETHESDA,MD 20892. UNIV N CAROLINA,DEPT PATHOL,CHAPEL HILL,NC. RI Proia, Richard/A-7908-2012 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 268 EP 268 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700270 ER PT J AU KIMONIS, VE GOLDSTEIN, AM PASTAKIA, B YANG, ML DIGIOVANNA, JJ BALE, AE BALE, SJ AF KIMONIS, VE GOLDSTEIN, AM PASTAKIA, B YANG, ML DIGIOVANNA, JJ BALE, AE BALE, SJ TI CLINICAL-FEATURES IN 101 PERSONS WITH NEVOID BASAL-CELL CARCINOMA (NBCC) SYNDROME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAMS,IRP,BETHESDA,MD. NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD. NIH,CTR CLIN,WASHINGTON,DC. VET ADM MED CTR,WASHINGTON,DC. YALE UNIV,SCH MED,NEW HAVEN,CT. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 281 EP 281 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700280 ER PT J AU STRATAKIS, CA PRAS, E LIN, JP KASTNER, DL CARNEY, JA CHROUSOS, GP AF STRATAKIS, CA PRAS, E LIN, JP KASTNER, DL CARNEY, JA CHROUSOS, GP TI CARNEY COMPLEX, A MULTIPLE ENDOCRINE NEOPLASIA AND FAMILIAL LENTIGINOSIS SYNDROME - CLINICAL ANALYSIS AND LINKAGE TO THE D2S123 LOCUS (CHROMOSOME 2P16) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD. NIAMS,ARTHRIT RHEUMATISM BRANCH,BETHESDA,MD. NIAMS,GENET STUDIES S LAB SKIN BIOL,BETHESDA,MD. MAYO CLIN & MAYO FDN,DEPT LAB MED & PATHOL,ROCHESTER,MN 55905. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 282 EP 282 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700283 ER PT J AU STRUEWING, JP BRODY, LC KASE, RG GIAMBARRESI, TA ERDOS, MR COLLINS, FS TUCKER, MA AF STRUEWING, JP BRODY, LC KASE, RG GIAMBARRESI, TA ERDOS, MR COLLINS, FS TUCKER, MA TI EPIDEMIOLOGIC AND GENETIC-CHARACTERISTICS OF 10 FAMILIES WITH BRCA1 MUTATIONS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI,BETHESDA,MD. NATL CTR HUMAN GENOME RES,BETHESDA,MD. WESTAT RES INC,ROCKVILLE,MD. RI Tucker, Margaret/B-4297-2015 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 284 EP 284 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700284 ER PT J AU DEBAUN, MR BROWN, M KESSLER, L AF DEBAUN, MR BROWN, M KESSLER, L TI SCREENING FOR CANCER IN CHILDREN WITH BECKWITH-WIEDEMANN SYNDROME (BWS) - A COST-EFFECTIVE ANALYSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD. NCI,APPL RES BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 301 EP 301 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700299 ER PT J AU CHENEVIXTRENCH, G GUSTAFSON, CE ANNAB, L BARRETT, C AF CHENEVIXTRENCH, G GUSTAFSON, CE ANNAB, L BARRETT, C TI FUNCTIONAL EVIDENCE FOR A TUMOR-SUPPRESSOR GENE ON CHROMOSOME-8 BY MONOCHROMOSOME TRANSFER INTO COLORECTAL-CANCER CELL-LINES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 QUEENSLAND INST MED RES,BRISBANE,QLD 4006,AUSTRALIA. NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 324 EP 324 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700326 ER PT J AU CHIDAMBARAM, A GERRARD, B BALE, A GOLDSTEIN, AM STEWART, C DEAN, M AF CHIDAMBARAM, A GERRARD, B BALE, A GOLDSTEIN, AM STEWART, C DEAN, M TI IDENTIFICATION AND CHARACTERIZATION OF A NOVEL KRUPPEL TYPE ZINC-FINGER LOCUS ON HUMAN-CHROMOSOME 9Q22-31 IN THE NEVOID BASAL-CELL CARCINOMA SYNDROME (NBCCS) REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BCDP,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,LVC,FREDERICK,MD. YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510. NCI,GENET EPIDEMIOL SECT,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 2 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 OCT PY 1995 VL 57 IS 4 SU S BP 325 EP 325 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700324 ER PT J AU DUMANOIR, S KNUTZEN, R STEINBECK, R SCHROCK, E AUER, G RIED, T AF DUMANOIR, S KNUTZEN, R STEINBECK, R SCHROCK, E AUER, G RIED, T TI CHROMOSOMAL GAINS AND LOSSES, DNA-PLOIDY AND P53- EXPRESSION DURING THE GENESIS OF COLORECTAL TUMORS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892. KAROLINSKA INST,STOCKHOLM,SWEDEN. INST PATHOL,FLENSBURG,GERMANY. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 330 EP 330 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700332 ER PT J AU GRACIA, E ELKAHLOUN, A TRENT, JM MELTER, PS AF GRACIA, E ELKAHLOUN, A TRENT, JM MELTER, PS TI MICRODISSECTION-MEDIATED CDNA CAPTURE - A STRATEGY FOR THE RAPID ISOLATION OF CDNAS AMPLIFIED CANCER SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 345 EP 345 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700343 ER PT J AU ISHWAD, CS FERRELL, RE ROSSIE, KM APPEL, BN JOHNSON, JT MYERS, EN LAW, JC SRIVASTAVA, S GOLLIN, SM AF ISHWAD, CS FERRELL, RE ROSSIE, KM APPEL, BN JOHNSON, JT MYERS, EN LAW, JC SRIVASTAVA, S GOLLIN, SM TI LOSS OF HETEROZYGOSITY ON THE SHORT ARM OF CHROMOSOME-3 AND CHROMOSOME-9 IN ORAL-CANCER SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA. UNIV PITTSBURGH,DEPT ORAL MED & PATHOL,PITTSBURGH,PA. UNIV PITTSBURGH,DEPT OTOLARYNGOL,PITTSBURGH,PA. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 355 EP 355 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700354 ER PT J AU KORCZAK, JF DIGIOVANNA, JJ BRAHIM, J KASE, RG GOLDSTEIN, AM AF KORCZAK, JF DIGIOVANNA, JJ BRAHIM, J KASE, RG GOLDSTEIN, AM TI GENE-ENVIRONMENT INTERACTION IN AN AFRICAN-AMERICAN CHILD WITH NEVOID BASAL-CELL CARCINOMA SYNDROME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIDR,BETHESDA,MD 20892. WESTAT CORP,ROCKVILLE,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 366 EP 366 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700368 ER PT J AU LIN, T GUAN, XY ANZICK, SL XU, J POLYMEROPOULOS, MH TRENT, JM MELTZER, PS AF LIN, T GUAN, XY ANZICK, SL XU, J POLYMEROPOULOS, MH TRENT, JM MELTZER, PS TI IDENTIFICATION OF A NOVEL AMPLIFIED GENE IN HUMAN BREAST-CANCER CONTAINING A POLYMORPHIC TRINUCLEOTIDE REPEAT SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 376 EP 376 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700376 ER PT J AU PRESSMAN, CL GAILANIL, MR LEFFELL, DJ YAVARI, R DEAN, M WAINWRIGHT, B BALEL, AE AF PRESSMAN, CL GAILANIL, MR LEFFELL, DJ YAVARI, R DEAN, M WAINWRIGHT, B BALEL, AE TI ISOLATION OF CANDIDATE SEQUENCES FROM THE GORLIN SYNDROME REGION UNDER-EXPRESSED IN RELATED NEOPLASMS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,NEW HAVEN,CT. NCI,FREDERICK,MD 21701. UNIV QUEENSLAND,CTR MOLEC & CELL BIOL,BRISBANE,QLD,AUSTRALIA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 404 EP 404 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700405 ER PT J AU SCHROCK, E HESELMEYER, K DUMANOIR, S SHAH, K STEINBECK, R AUER, G RIED, T AF SCHROCK, E HESELMEYER, K DUMANOIR, S SHAH, K STEINBECK, R AUER, G RIED, T TI SEQUENCE OF GENETIC EVENTS IN THE CARCINOGENESIS OF TUMORS OF THE UTERINE CERVIX SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892. KAROLINSKA HOSP & INST,STOCKHOLM,SWEDEN. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21218. TUMORARCHIV FLENSBURG,FLENSBURG,GERMANY. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 414 EP 414 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700416 ER PT J AU COHEN, MS SAMANGOSPROUSE, CA STERN, HJ ROSENBAUM, KN TIFFT, CJ AF COHEN, MS SAMANGOSPROUSE, CA STERN, HJ ROSENBAUM, KN TIFFT, CJ TI MACROCEPHALY IN NEUROFIBROMATOSIS TYPE-1 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 CHILDRENS NATL MED CTR,DEPT LAB MED,WASHINGTON,DC 20010. CHILDRENS NATL MED CTR,DEPT MED GENET,WASHINGTON,DC 20010. ALBERT EINSTEIN COLL MED,BRONX,NY 10467. NIDDK,GBB,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 465 EP 465 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700465 ER PT J AU BEHRENS, F CLAUSSEN, U GREEN, ED COUTELLE, C WILLIAMSON, R HUXLEY, C AF BEHRENS, F CLAUSSEN, U GREEN, ED COUTELLE, C WILLIAMSON, R HUXLEY, C TI ANALYSIS OF THE CENTROMERE REGION OF HUMAN-CHROMOSOME-7 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ST MARYS HOSP,SCH MED,DEPT BIOCHEM & MOLEC GENET,LONDON W2 1PG,ENGLAND. KLINIKUM FRIEDRICH SCHILLER UNIV,INST HUMANGENET,D-07743 JENA,GERMANY. NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 598 EP 598 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700598 ER PT J AU DUTRA, AS MIGNOT, E PUCK, JM AF DUTRA, AS MIGNOT, E PUCK, JM TI ESTABLISHING FISH METHODOLOGY TO STUDY SYNTENIC REGIONS BETWEEN CANINE AND HUMAN-CHROMOSOMES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,IMMUNOL DIS SECT,GENE TRANSFER LAB,BETHESDA,MD 20892. STANFORD UNIV,MED CTR,STANFORD CTR NARCOLEPSY RES,SLEEP RES CTR,PALO ALTO,CA 94304. NR 1 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 626 EP 626 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700624 ER PT J AU GOODMAN, BK GREEN, ED LEWANDA, AF ROSENGREN, S JABS, EW AF GOODMAN, BK GREEN, ED LEWANDA, AF ROSENGREN, S JABS, EW TI MOLECULAR CYTOGENETIC ANALYSIS OF CHROMOSOME 7P ANOMALIES AND CLINICAL CORRELATION WITH SAETHRE-CHOTZEN SYNDROME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD. NIH,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,WASHINGTON,DC 20010. UNIV CONNECTICUT,FARMINGTON,CT. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 636 EP 636 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700635 ER PT J AU HUANG, B CROLLA, JA PAPENHAUSEN, PR LEDBETTER, DH AF HUANG, B CROLLA, JA PAPENHAUSEN, PR LEDBETTER, DH TI IDENTIFICATION OF 2 CLASSES OF BREAKPOINTS IN SMALL INV DUP(15) CHROMOSOMES BY CYTOGENETIC AND MOLECULAR STUDIES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. WESSEX REG GENET LAB,SALISBURY,WILTS,ENGLAND. ROCHE BIOMED LABS INC,RES TRIANGLE PK,NC. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 651 EP 651 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700651 ER PT J AU JALAL, S GREENBERG, F MORRIS, C FLOM, K DEWALD, G KARNES, P AF JALAL, S GREENBERG, F MORRIS, C FLOM, K DEWALD, G KARNES, P TI UTILITY OF ELASTIN GENE FLUORESCENT-PROBE FOR DIAGNOSIS OF WILLIAMS-SYNDROME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MAYO CLIN & MAYO FDN,CYTOGENET LAB,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,DIV MED GENET,ROCHESTER,MN 55905. NIH,BETHESDA,MD 20892. UNIV NEVADA,SCH MED,LAS VEGAS,NV 89102. ONCOR INC,GAITHERSBURG,MD 20877. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 654 EP 654 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700653 ER PT J AU MECK, JM CHRISTIAN, SL PAULYSON, KJ SIQUES, MJ LEWIS, K GARNICA, A SEYDEL, FD LEDBETTER, DH AF MECK, JM CHRISTIAN, SL PAULYSON, KJ SIQUES, MJ LEWIS, K GARNICA, A SEYDEL, FD LEDBETTER, DH TI AN UNUSUAL CASE OF TRISOMY-16 MOSAICISM DUE TO PATERNAL NONDISJUNCTION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 674 EP 674 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700672 ER PT J AU POTOCKI, L GREENBERG, F SHAFFER, LG AF POTOCKI, L GREENBERG, F SHAFFER, LG TI INTERSTITIAL DELETION OF 11(P11.12P12) - A RARE CHROMOSOMAL SYNDROME WITH MENTAL-RETARDATION, PARIETAL FORAMINA, AND MULTIPLE EXOSTOSES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOUSTON,TX 77030. NIH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 688 EP 688 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700688 ER PT J AU STONE, D GUAN, XY NING, Y BIESECKER, L WYNSHAWBORIS, A AF STONE, D GUAN, XY NING, Y BIESECKER, L WYNSHAWBORIS, A TI CLARIFICATION OF A CHROMOSOMAL TRANSLOCATION USING A MICRODISSECTED FISH PROBE AND MICROSATELLITE MARKERS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,GENET DIS RES LAB,BETHESDA,MD. NIH,CANC GENET LAB,BETHESDA,MD. NIH,NCHGR,DIAGNOST DEV BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 718 EP 718 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700718 ER PT J AU ZHENG, CJ AF ZHENG, CJ TI GERMLINE MOSAICISM AND THE RECURRENCE OF DOWN-SYNDROME IN SIBLINGS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NIDCD,EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 740 EP 740 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700738 ER PT J AU LEI, KJ CHEN, YT CHEN, HW WONG, LJC LIU, JL MCCONKIEROSELL, A VANHOVE, JLK OU, HCY YEH, NJ PAN, LY CHOU, JY AF LEI, KJ CHEN, YT CHEN, HW WONG, LJC LIU, JL MCCONKIEROSELL, A VANHOVE, JLK OU, HCY YEH, NJ PAN, LY CHOU, JY TI GENETIC-BASIS OF GLYCOGEN-STORAGE-DISEASE TYPE 1A - PREVALENT MUTATIONS AT THE GLUCOSE-6-PHOSPHATASE LOCUS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID POLYMORPHISM ANALYSIS; METHYLATION; DNA AB Diagnosis of glycogen storage disease (GSD) type 1a currently is established by demonstrating the lack of glucose-6-phosphatase (G6Pase) activity in the patient's biopsied liver specimen. Recent cloning of the G6Pase gene and identification of mutations within the gene that causes GSD type 1a allow for the development of a DNA-based diagnostic method. Using SSCP analysis and DNA sequencing, we characterized the G6Pase gene of 70 unrelated patients with enzymatically confirmed diagnosis of GSD type 1a and detected mutations in all except 17 alleles (88%). Sixteen mutations were uncovered that were shown by expression to abolish or greatly reduce G6Pase activity and that therefore are responsible for the GSD type 1a disorder. R83C and Q347X are the most prevalent mutations found in Caucasians, 130X and R83C are most prevalent in Hispanics, and R83H is most prevalent in Chinese. The Q347X mutation has thus far been identified only in Caucasian patients, and the 130X mutation has been identified only in Hispanic patients. Our results demonstrate that the DNA-based analysis can accurately, rapidly, and noninvasively detect the majority of mutations in GSD type 1a. This DNA-based diagnosis now permits prenatal diagnosis among at-risk patients and serves as a database in screening and counseling patients clinically suspected of having this disease. C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT PEDIAT,DURHAM,NC 27710. BAYLOR COLL MED,DEPT MOLEC & HUMAN GENET,HOUSTON,TX 77030. FU NCRR NIH HHS [MO1-RR30] NR 22 TC 79 Z9 86 U1 0 U2 3 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 OCT PY 1995 VL 57 IS 4 BP 766 EP 771 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA RV793 UT WOS:A1995RV79300004 PM 7573034 ER PT J AU AI, Y JENKINS, NA COPELAND, NG GILBERT, DJ BERGSMA, DJ STAMBOLIAN, D AF AI, Y JENKINS, NA COPELAND, NG GILBERT, DJ BERGSMA, DJ STAMBOLIAN, D TI CLONING AND CHARACTERIZATION OF CDNA FOR MOUSE GALACTOKINASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PENN,SCH MED,DEPT OPHTHALMOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT GENET,PHILADELPHIA,PA 19104. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD. SMITHKLINE BEECHAM PHARMACEUT,DEPT MOLEC GENET,KING OF PRUSSIA,PA. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 787 EP 787 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700786 ER PT J AU ALLIKMETS, R LATIF, F BERNAL, R DUH, FM SMOLA, U ZABAROVSKY, ER DEAN, M MINNA, JD RAPP, UR SITHANANDAM, G AF ALLIKMETS, R LATIF, F BERNAL, R DUH, FM SMOLA, U ZABAROVSKY, ER DEAN, M MINNA, JD RAPP, UR SITHANANDAM, G TI 3PK, A NEW MAP KINASE ACTIVATED PROTEIN-KINASE, LOCATED IN THE SMALL-CELL LUNG-CANCER TUMOR-SUPPRESSOR GENE REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BCDP,SAIC FREDERICK,FREDERICK,MD. KAROLINSKA INST,MTC,STOCKHOLM,SWEDEN. UNIV TEXAS,HC SIMMONS COMPREHENS CANC CTR,DALLAS,TX. RI Zabarovsky, Eugene/A-6645-2010 NR 0 TC 0 Z9 0 U1 0 U2 3 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 OCT PY 1995 VL 57 IS 4 SU S BP 789 EP 789 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700789 ER PT J AU BERNSTEIN, SL BORST, DE WONG, PW AF BERNSTEIN, SL BORST, DE WONG, PW TI CHARACTERIZATION OF A HUMAN FOVEAL PRIMARY CDNA LIBRARY AND ISOLATION OF CANDIDATE GENES FOR MACULAR DYSTROPHIES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 793 EP 793 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700791 ER PT J AU OLIVOSGLANDER, IM JANNE, PA NUSSBAUM, RL AF OLIVOSGLANDER, IM JANNE, PA NUSSBAUM, RL TI THE OCULOCEREBRORENAL SYNDROME GENE-PRODUCT IS A 105-KD PROTEIN LOCALIZED TO THE GOLGI-COMPLEX SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID ADP-RIBOSYLATION FACTOR; GTP-BINDING-PROTEIN; BETA-COP; INOSITOL POLYPHOSPHATE-5-PHOSPHATASE; PHOSPHOLIPASE-D; MEMBRANES; LOWE; ARF AB The oculocerebrorenal syndrome of Lowe (OCRL) is a multisystem disorder affecting the lens, kidney, and CNS. The predicted amino acid sequence of the OCRL gene, OCRL-1, was used to develop antibodies against the OCRL-1 protein. Western blot analysis using affinity-purified serum against the amino terminus of the OCRL-1 gene product (ocrl-1) demonstrates a single protein of 105 kD in fibroblasts of a normal individual that is absent in fibroblasts of an OCRL patient who lacks OCRL-1 transcript. A single protein with the same electrophoretic mobility is found by western analysis in various human cultured cell lines, and approximately the same size protein is also found in all mouse tissues tested. Northern analysis of various human and mouse tissues demonstrate that OCRL-1 transcript is expressed in nearly all tissues examined. By immunofluorescence, the ocrl-1 antibody stains a juxtanuclear region in normal fibroblast cells, while no specific staining is evident in the OCRL patient who produces no transcript. Colocalization of the ocrl-1 protein to the Golgi complex was demonstrated using a known monoclonal antibody against a Golgi-specific coat protein, beta-COP (beta coatomer protein). C1 NIH,NCHGR,LGDR,BETHESDA,MD 20892. UNIV PENN,DEPT GENET,PHILADELPHIA,PA 19104. FU NICHD NIH HHS [R01HD23245]; NIGMS NIH HHS [T32GM07170] NR 23 TC 100 Z9 103 U1 0 U2 3 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 OCT PY 1995 VL 57 IS 4 BP 817 EP 823 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA RV793 UT WOS:A1995RV79300011 PM 7573041 ER PT J AU PADMA, T AYYAGARI, R MURTY, JS BASTI, S FLETCHER, T RAO, GN KAISERKUPFER, M HEJTMANCIK, JF AF PADMA, T AYYAGARI, R MURTY, JS BASTI, S FLETCHER, T RAO, GN KAISERKUPFER, M HEJTMANCIK, JF TI AUTOSOMAL-DOMINANT ZONULAR CATARACT WITH SUTURAL OPACITIES LOCALIZED TO CHROMOSOME 17Q11-12 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID CRYSTALLIN GENE; BETA-CRYSTALLIN; LENS; LINKAGE; MUTATION AB Congenital cataracts constitute a morphologically and genetically heterogeneous group of diseases that are a major cause of childhood blindness. Different loci for hereditary congenital cataracts have been mapped to chromosomes 1, 2, 16, and 17q24. We report linkage of a gene causing a unique form of autosomal dominant zonular cataracts with Y-sutural opacities to chromosome 17q11-12 in a three-generation family exhibiting a maximum lod score of 3.9 at D17S805. Multipoint analysis gave a l-lod confidence interval of 17 cM. This interval is bounded by the markers D17S799 and D17S798, a region that would encompass a number of candidate genes including that coding for beta A3/A1-crystallin. C1 NEI,LMOD,BETHESDA,MD 20892. LV PRASAD EYE INST,HYDERABAD,ANDHRA PRADESH,INDIA. OSMANIA UNIV,DEPT GENET,HYDERABAD 500007,ANDHRA PRADESH,INDIA. NR 30 TC 47 Z9 48 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 BP 840 EP 845 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA RV793 UT WOS:A1995RV79300014 PM 7573044 ER PT J AU OKABE, I NUSSBAUM, RL AF OKABE, I NUSSBAUM, RL TI IDENTIFICATION AND CHROMOSOMAL MAPPING OF THE MOUSE INOSITOL POLYPHOSPHATE 1-PHOSPHATASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,GENET DIS RES LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 845 EP 845 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700844 ER PT J AU OLIVOSGLANDER, IM JANNE, PA NUSSBAUM, RL AF OLIVOSGLANDER, IM JANNE, PA NUSSBAUM, RL TI THE LOWE SYNDROME GENE-PRODUCT HAS A DISTINCT DISSOCIATION PATTERN FROM GOLGI IN RESPONSE TO BREFELDIN-A SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PENN,DEPT MOLEC BIOL,PHILADELPHIA,PA. NIH,NATL CTR RES RESOURCES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 846 EP 846 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700847 ER PT J AU PHILIBERT, RA ROBB, AS BRENNAN, MB LONG, RT DAMSCHRODERWILLIAMS, P STUBBLEFIELD, B MARTIN, B GINNS, EI AF PHILIBERT, RA ROBB, AS BRENNAN, MB LONG, RT DAMSCHRODERWILLIAMS, P STUBBLEFIELD, B MARTIN, B GINNS, EI TI SYSTEMATIC CHARACTERIZATION OF LARGE GENOMIC CTG-CONTAINING TRINUCLEOTIDE REPEATS FROM THE HUMAN GENOME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 853 EP 853 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700851 ER PT J AU WONG, P ULYANOVA, T DARROW, R VANVEEN, T TENNISWOOD, M ORGANISCIAK, D CHADER, G AF WONG, P ULYANOVA, T DARROW, R VANVEEN, T TENNISWOOD, M ORGANISCIAK, D CHADER, G TI CORRELATION OF INCREASED CLUSTERIN/TRPM-2 LEVELS WITH NEURODEGENERATION IN MODELS OF RETINAL DEGENERATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. UNIV GOTHENBURG,DEPT ZOOL,GOTHENBURG,SWEDEN. WRIGHT STATE UNIV,W ALTON JONES CELL SCI CTR,DEPT BIOCHEM & MOLEC BIOL,DAYTON,OH. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 870 EP 870 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700871 ER PT J AU YOSHIKAWA, T LEACH, R DETERAWADLEIGH, SD AF YOSHIKAWA, T LEACH, R DETERAWADLEIGH, SD TI A NEW ISOFORM OF THE HUMAN NUCLEAR HORMONE-RECEPTOR, TR4 - THE GENOMIC STRUCTURE OF THE A/B DOMAIN AND CHROMOSOMAL LOCALIZATION OF THE GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH, BETHESDA, MD 20892 USA. UNIV TEXAS SAN ANTONIO, SAN ANTONIO, TX 78285 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 EI 1537-6605 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 877 EP 877 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700875 ER PT J AU MUDD, SH LEVY, HL TANGERMAN, A BOUJET, C BUIST, N DAVIDSONMUNDT, A HUDGINS, L OYANAGI, K NAGAO, M WILSON, WG AF MUDD, SH LEVY, HL TANGERMAN, A BOUJET, C BUIST, N DAVIDSONMUNDT, A HUDGINS, L OYANAGI, K NAGAO, M WILSON, WG TI ISOLATED PERSISTENT HYPERMETHIONINEMIA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID METHIONINE ADENOSYLTRANSFERASE DEFICIENCY; TRANSAMINATION; BALANCES; PATHWAY; HUMANS; DEFECT AB New information has been obtained on 30 patients with isolated persistent hypermethioninemia, most of them previously unreported. Biopsies to confirm the presumptive diagnosis of partially deficient activity of ATP: L-methionine S-adenosyltransferase (MAT; E.C.2.5.1.6) in liver were not performed on most of these patients. However, none showed the clinical findings or the extreme elevations of serum folate previously described in other patients with isolated hypermethioninemia considered not to have hepatic MAT deficiency. Patients ascertained on biochemical grounds had no neurological abnormalities, and 27/30 had IQs or Bayley development-index scores within normal limits or were judged to have normal mental development. Methionine transamination metabolites accumulated abnormally only when plasma methionine concentrations exceeded 300-350 mu M and did so more markedly after 0.9 years of age. Data were obtained on urinary organic acids as well as plasma creatinine concentrations. Patterns of inheritance of isolated hypermethioninemia were variable. Considerations as to the optimal management of this group of patients are discussed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. UNIV NIJMEGEN HOSP,DIV GASTROINTESTINAL & LIVER DIS,6500 HB NIJMEGEN,NETHERLANDS. CHU GRENOBLE,BIOCHIM METAB & EXPLORAT NUTR LAB,F-38043 GRENOBLE,FRANCE. OREGON HLTH SCI UNIV,CTR CHILD DEV & REHABIL,PORTLAND,OR 97201. UNIV COLORADO,CHILDRENS HOSP,HLTH SCI CTR,DENVER,CO 80218. UNIV ARIZONA,HLTH SCI CTR,MARICOPA MED CTR,PHOENIX,AZ. ODORI CHILDRENS CLIN,SAPPORO,HOKKAIDO,JAPAN. NATL OTARU HOSP,OTARU,HOKKAIDO,JAPAN. UNIV VIRGINIA,CHILDRENS MED CTR,CHARLOTTESVILLE,VA 22903. RP MUDD, SH (reprint author), NIMH,DIRP,LGCB,BLDG 36,ROOM 3D-06,36 CONVENT DR,MSC 4094,BETHESDA,MD 20892, USA. NR 42 TC 56 Z9 56 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 BP 882 EP 892 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA RV793 UT WOS:A1995RV79300020 PM 7573050 ER PT J AU LIN, JP AMOS, CI KANIK, K DOYLE, SZ PEDEN, S WILDER, RL BALE, SJ AF LIN, JP AMOS, CI KANIK, K DOYLE, SZ PEDEN, S WILDER, RL BALE, SJ TI RHEUMATOID-ARTHRITIS AND OTHER AUTOIMMUNE-DISEASES - FAMILIAL AGGREGATION AND COMPLEX SEGREGATION ANALYSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MD ANDERSON CANC CTR,HOUSTON,TX. LSB,GENET STUDIES SECT,BETHESDA,MD. NIAMS,ARTHRITIS RES BRANCH,BETHESDA,MD. NR 1 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 950 EP 950 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700950 ER PT J AU LYONS, LA OBRIEN, SJ AF LYONS, LA OBRIEN, SJ TI COMPARATIVE GENETICS - ITS ROLE IN HUMAN HEREDITARY-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,DIV CANC ETIOL,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 952 EP 952 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700951 ER PT J AU NOVORADOVSKY, A GOLDMAN, D AF NOVORADOVSKY, A GOLDMAN, D TI POPULATION-GENETICS OF MITOCHONDRIAL ALDEHYDE DEHYDROGENASE (ALDH2) IN AMERICAN-INDIAN AND ASIAN POPULATIONS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAAA,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 966 EP 966 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700964 ER PT J AU ROMERO, FC URBANEK, M GOLDMAN, D LONG, JC AF ROMERO, FC URBANEK, M GOLDMAN, D LONG, JC TI POPULATION-GENETICS OF ATHABASCAN-SPEAKING POPULATIONS IN INTERIOR ALASKA AND THE AMERICAN SOUTHWEST SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAAA,NEUROGENET LAB,BETHESDA,MD 20892. UNIV NEW MEXICO,DEPT ANTHROPOL,ALBUQUERQUE,NM 87131. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 975 EP 975 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700977 ER PT J AU STIVERS, DN CHAKRABORTY, R AF STIVERS, DN CHAKRABORTY, R TI SIMILARITY INDEX FROM DNA PROFILES AT HYPERVARIABLE LOCI REVISITED SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 986 EP 986 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700991 ER PT J AU WANG, YF CHEN, CJ HARRIS, EL KING, TM HSU, MM DIEHL, SR BEATY, TH AF WANG, YF CHEN, CJ HARRIS, EL KING, TM HSU, MM DIEHL, SR BEATY, TH TI COMPLEX SEGREGATION ANALYSIS OF NASOPHARYNGEAL CARCINOMA (NPC) IN TAIWAN SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,BALTIMORE,MD. NIDR,BETHESDA,MD 20892. NATL TAIWAN UNIV,TAIPEI 10764,TAIWAN. KAISER PERMANENTE CTR HLTH RES,PORTLAND,OR. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 995 EP 995 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700996 ER PT J AU ANDERSSON, HC VONFIGURA, K HILLEREHFELD, A KOHN, A GAHL, WA KOHN, LD AF ANDERSSON, HC VONFIGURA, K HILLEREHFELD, A KOHN, A GAHL, WA KOHN, LD TI 2 APPROACHES TO PURIFICATION OF NOVEL LYSOSOMAL MEMBRANE-PROTEINS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV GOTTINGEN,W-3400 GOTTINGEN,GERMANY. TULANE UNIV,HAYWARD GENET CTR,NEW ORLEANS,LA 70118. NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. NIDDK,BIOCHEM & METAB LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1000 EP 1000 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700999 ER PT J AU GAHL, W GUO, J KRASNEWICH, D BERNARDINI, I HOLT, G AF GAHL, W GUO, J KRASNEWICH, D BERNARDINI, I HOLT, G TI C-85 DOLICHOLS IN SLOUGHED RENAL-CELLS OF PATIENTS WITH HERMANSKY-PUDLAK SYNDROME (HPS) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,HUMAN BIOCHEM GENET SECT,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1022 EP 1022 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701022 ER PT J AU HOLT, G MCDOWELL, G BLITZER, M GAHL, W AF HOLT, G MCDOWELL, G BLITZER, M GAHL, W TI DEVELOPING SIMPLE HPLC SCREENING TECHNIQUES FOR CARBOHYDRATE STORAGE DISEASES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. UNIV MARYLAND,SCH MED,DIV HUMAN GENET,BALTIMORE,MD 21201. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1029 EP 1029 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701031 ER PT J AU MCKINNEY, CE LAMARCA, ME KONDO, R GINNS, EI AF MCKINNEY, CE LAMARCA, ME KONDO, R GINNS, EI TI MURINE MODELS OF GAUCHER DISEASE - INTRODUCTION OF THE N370S POINT MUTANT BY TAG AND EXCHANGE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1039 EP 1039 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701039 ER PT J AU RHEAD, WJ GRINDLE, K GAHL, W BUIST, N WILEY, B AF RHEAD, WJ GRINDLE, K GAHL, W BUIST, N WILEY, B TI GLUTATHIONE SYNTHETASE DEFICIENCY (5-OXOPROLINURIA) - TREATMENT WITH GLUTATHIONE MONOETHYL ESTER (GSH-EE) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV IOWA,IOWA CITY,IA. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NICHHD,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1046 EP 1046 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701046 ER PT J AU VASCONCELOS, O SIVAKUMAR, K OUEZADO, M NAGLE, J MONZON, M DUBNICK, M DALAKAS, MC GAJDUSEK, DC GOLDFARB, LG AF VASCONCELOS, O SIVAKUMAR, K OUEZADO, M NAGLE, J MONZON, M DUBNICK, M DALAKAS, MC GAJDUSEK, DC GOLDFARB, LG TI A NONSENSE MUTATION IN THE HUMAN PHOSPHOFRUCTOKINASE MUSCLE-SUBUNIT GENE ASSOCIATES WITH EXPRESSION OF MESSENGER-RNA SPECIES RETAINING INTRON-10 IN 3 ASHKENAZI JEWISH PATIENTS WITH GLYCOGENOSIS TYPE-VII SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NINCDS,NEUROGENT UNIT,BETHESDA,MD 20892. NINCDS,NEUROMUSCULAR DIS SECT,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1053 EP 1053 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701055 ER PT J AU BADNER, JA FERRARO, TN BERRETTINI, WH DETERAWADLEIGH, SD NURNBERGER, JI GOLDIN, LR GERSHON, ES AF BADNER, JA FERRARO, TN BERRETTINI, WH DETERAWADLEIGH, SD NURNBERGER, JI GOLDIN, LR GERSHON, ES TI TRANSMISSION DISEQUILIBRIUM ANALYSIS OF BIPOLAR DISORDER AND CHROMOSOME-18 LOCI SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD. THOMAS JEFFERSON UNIV,PHILADELPHIA,PA. INDIANA UNIV,INDIANAPOLIS,IN. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1065 EP 1065 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701067 ER PT J AU BERGER, R MEZEY, E CLANCY, K HARTA, G BROWN, RH BROWNSTEIN, M PATTERSON, D AF BERGER, R MEZEY, E CLANCY, K HARTA, G BROWN, RH BROWNSTEIN, M PATTERSON, D TI ALDEHYDE OXIDASE AND XANTHINE DEHYDROGENASE AS CANDIDATE GENES FOR ALS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ELEANOR ROOSEVELT INST,DENVER,CO. NIH,BETHESDA,MD. MASSACHUSETTS GEN HOSP,BOSTON,MA. UNIV COLORADO,HLTH SCI CTR,DENVER,CO. RI Brownstein, Michael/B-8609-2009 NR 1 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1072 EP 1072 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701071 ER PT J AU BLOUIN, JL CHRISTIE, DH CHAKRAVARTI, A LEDBETTER, D MORRIS, MA GOS, A ANTONARAKIS, SE AF BLOUIN, JL CHRISTIE, DH CHAKRAVARTI, A LEDBETTER, D MORRIS, MA GOS, A ANTONARAKIS, SE TI A NEW DINUCLEOTIDE REPEAT POLYMORPHISM AT THE TELOMERE OF CHROMOSOME 21Q REVEALS SIGNIFICANT DIFFERENCE BETWEEN MALE AND FEMALE RATES OF RECOMBINATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV GENEVA,SCH MED,CH-1211 GENEVA,SWITZERLAND. HOP CANTONAL GENEVA,GENEVA,SWITZERLAND. CASE WESTERN RESERVE UNIV,CLEVELAND,OH. NATL CTR HUMAN GENOME RES,BETHESDA,MD. RI Antonarakis, Stylianos/N-8866-2014 OI Antonarakis, Stylianos/0000-0001-8907-5823 NR 1 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1073 EP 1073 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701074 ER PT J AU COOK, EH VANDENBERGH, DJ STEIN, MA COX, NJ YAN, S KRASOWSKI, MD UHL, GR LEVENTHAL, BL AF COOK, EH VANDENBERGH, DJ STEIN, MA COX, NJ YAN, S KRASOWSKI, MD UHL, GR LEVENTHAL, BL TI MOLECULAR-GENETIC ANALYSIS OF THE DOPAMINE TRANSPORTER IN ATTENTION-DEFICIT/HYPERACTIVITY DISORDER (ADHD) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV CHICAGO,CHICAGO,IL. NIDA,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 1085 EP 1085 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701086 ER PT J AU CRAVCHIK, A BURGUESS, L SIBLEY, DR GEJMAN, PV AF CRAVCHIK, A BURGUESS, L SIBLEY, DR GEJMAN, PV TI FUNCTIONAL-ANALYSIS OF THE HUMAN DOPAMINE D2 RECEPTOR VARIANTS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD. NINCDS,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 1087 EP 1087 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701087 ER PT J AU DAVIS, S SCHROEDER, M GOLDIN, LR WEEKS, DE AF DAVIS, S SCHROEDER, M GOLDIN, LR WEEKS, DE TI NONPARAMETRIC SIMULATION-BASED STATISTICS FOR DETECTING LINKAGE IN GENERAL PEDIGREES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA. UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD. WELLCOME TRUST CTR HUMAN GENET,OXFORD,ENGLAND. RI Weeks, Daniel/B-2995-2012 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1091 EP 1091 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701092 ER PT J AU FRANCOMANO, CA DELUNA, RIO IDE, SE PYERITZ, RE WRIGHT, M POLYMEROPOULOS, MH AF FRANCOMANO, CA DELUNA, RIO IDE, SE PYERITZ, RE WRIGHT, M POLYMEROPOULOS, MH TI THE GENE FOR THE ELLIS VAN CREVELD SYNDROME MAPS TO CHROMOSOME 4P16 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NATL CTR HUMAN GENOME RES,MGB,BETHESDA,MD. NATL CTR HUMAN GENOME RES,LGDR,BETHESDA,MD. HOSP INFANTIL MEXICO DR FEDERICO GOMEZ,MEXICO CITY,DF,MEXICO. ALLEGHENY SINGER RES INST,PITTSBURGH,PA. UNIV NEWCASTLE UPON TYNE,NEWCASTLE TYNE,TYNE & WEAR,ENGLAND. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1098 EP 1098 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701096 ER PT J AU FREASLUTZ, DL WANG, S GILLANDERS, EM SUN, C ZHANG, YJ CHOPRA, N DIEHL, SR AF FREASLUTZ, DL WANG, S GILLANDERS, EM SUN, C ZHANG, YJ CHOPRA, N DIEHL, SR TI IMPROVED METHODS FOR LARGE-SCALE GENE-MAPPING PROJECTS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIDR,MEDIB,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1099 EP 1099 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701099 ER PT J AU GOLDSTEIN, AM GOLDIN, LR DRACOPOLI, NC TUCKER, MA AF GOLDSTEIN, AM GOLDIN, LR DRACOPOLI, NC TUCKER, MA TI 2-LOCUS LINKAGE ANALYSIS OF CUTANEOUS MALIGNANT-MELANOMA DYSPLASTIC NEVI (CMM/DN) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD. NCI,BETHESDA,MD. SEQUANA THERAPEUT INC,LA JOLLA,CA. RI Tucker, Margaret/B-4297-2015 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1101 EP 1101 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701103 ER PT J AU JAIN, PK DESHMUKH, D THOMAS, E KUMAR, S LALWANI, AK PLOPLIS, B SKARKA, H VERMAN, IC WILCOX, ER AF JAIN, PK DESHMUKH, D THOMAS, E KUMAR, S LALWANI, AK PLOPLIS, B SKARKA, H VERMAN, IC WILCOX, ER TI MAPPING A GENE FOR RECESSIVE NONSYNDROMIC HEARING IMPAIRMENT TO CHROMOSOME 9P21-Q21 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ALL INDIA INST MED SCI,NEW DELHI,INDIA. NIDCD,LMG,ROCKVILLE,MD. DEAF MUTE SCH,ICHALKARANJI,MAHARASHTRA,INDIA. INST SPEECH & HEARING,ICHALKARANJI,MAHARASHTRA,INDIA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 1112 EP 1112 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701112 ER PT J AU JOHNSON, EW GREEN, ED RICH, SS ORR, HT GILNAGEL, A KURTH, JH ZABRAMSKI, JM GLUSKER, P SPIEGEL, R MARCHUK, DA OTERO, E WEBER, JL AF JOHNSON, EW GREEN, ED RICH, SS ORR, HT GILNAGEL, A KURTH, JH ZABRAMSKI, JM GLUSKER, P SPIEGEL, R MARCHUK, DA OTERO, E WEBER, JL TI A GENE FOR FAMILIAL CEREBRAL CAVERNOUS MALFORMATION MAPS TO A 4-CM REGION OF CHROMOSOME 7Q IN SEVERAL FAMILIES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MARSHFIELD MED RES FDN,CTR MED GENET,MARSHFIELD,WI 54449. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI & NEUROL,WINSTON SALEM,NC. UNIV MINNESOTA,MINCEP,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,INST HUMAN GENET,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT NEUROL,MINNEAPOLIS,MN 55455. BARROW NEUROL INST,PHOENIX,AZ 85013. INST MED GENET,ZURICH,SWITZERLAND. DUKE UNIV,MED CTR,DEPT GENET,DURHAM,NC. NATL INST NEUROL & NEUROSURG,TLALPAN,DF,MEXICO. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1117 EP 1117 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701117 ER PT J AU LESPERANCE, MM HALL, JW LI, X BESS, FH JAIN, PK PLOPLIS, B SANAUGUSTIN, TB SKARKA, H SMITH, RJH WILLS, M WILCOX, ER AF LESPERANCE, MM HALL, JW LI, X BESS, FH JAIN, PK PLOPLIS, B SANAUGUSTIN, TB SKARKA, H SMITH, RJH WILLS, M WILCOX, ER TI A GENE FOR NONSYNDROMIC HEREDITARY HEARING IMPAIRMENT MAPS TO 4P16.3 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIDOCD,MOLEC GENET LAB,ROCKVILLE,MD. VANDERBILT UNIV,DEPT OTOLARYNGOL,DIV HEARING & SPEECH SCI,NASHVILLE,TN. NATL INST DISABIL & REHABIL RES,WASHINGTON,DC. UNIV IOWA,DEPT OTOLARYNGOL,MOLEC OTOLARYNGOL RES LABS,IOWA CITY,IA. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 1129 EP 1129 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701128 ER PT J AU MCINTOSH, I CLOUGH, MV PETERS, K GREENSPAN, D KWIATKOWSKI, DJ MCCORMICK, MK FRANCOMANO, CA AF MCINTOSH, I CLOUGH, MV PETERS, K GREENSPAN, D KWIATKOWSKI, DJ MCCORMICK, MK FRANCOMANO, CA TI NAIL-PATELLA SYNDROME - REFINED LINKAGE TO MARKERS ON 9Q34 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,CTR GENET MED,BALTIMORE,MD. NIH,NATL CTR HUMAN GENOME RES,MED GENET BRANCH,BETHESDA,MD 20892. KAISER PERMANENTE,SACRAMENTO,CA. UNIV WISCONSIN,SCH MED,MADISON,WI. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 2 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 OCT PY 1995 VL 57 IS 4 SU S BP 1135 EP 1135 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701134 ER PT J AU NORMAN, RA CHUNG, WK POWERKEHOE, L CHUA, SC LEIGEL, RL DEVOTO, M FANN, C OTT, J BOGARDUS, C RAVUSSIN, E AF NORMAN, RA CHUNG, WK POWERKEHOE, L CHUA, SC LEIGEL, RL DEVOTO, M FANN, C OTT, J BOGARDUS, C RAVUSSIN, E TI GENETIC-LINKAGE STUDIES OF HOMOLOGS TO RODENT OBESITY GENES IN PIMA-INDIANS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIDDK,CDNS,PHOENIX,AZ. ROCKEFELLER UNIV,HUMAN BEHAV & METAB LAB,NEW YORK,NY 10021. COLUMBIA UNIV,DEPT PSYCHIAT,NEW YORK,NY. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK STATE PSYCHIAT INST,NEW YORK,NY 10032. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1145 EP 1145 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701145 ER PT J AU POLYMEROPOULOS, MH DELUNA, RIO IDE, SE FRANCOMANO, CA AF POLYMEROPOULOS, MH DELUNA, RIO IDE, SE FRANCOMANO, CA TI MAPPING OF THE POLYSYNDACTYLY PHENOTYPE TO THE LONG ARM OF HUMAN-CHROMOSOME-2 IN A MEXICAN KINDRED SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NATL CTR HUMAN GENOME RES,LGDR,BETHESDA,MD. NATL CTR HUMAN GENOME RES,MGB,BETHESDA,MD. HOSP INFANTIL MEXICO DR FEDERICO GOMEZ,MEXICO CITY,DF,MEXICO. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1152 EP 1152 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701149 ER PT J AU ROGERS, GR RIZZO, WB ZLOTOGORSKI, A HASHEM, N LEE, M BALE, SJ COMPTON, JG AF ROGERS, GR RIZZO, WB ZLOTOGORSKI, A HASHEM, N LEE, M BALE, SJ COMPTON, JG TI SJOGREN-LARSSON SYNDROME (SLS) AND FATTY ALDEHYDE DEHYDROGENASE (FALDH) GENES MAP TO CHROMOSOME 17P SO AMERICAN JOURNAL OF HUMAN GENETICS 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 23298. HEBREW UNIV JERUSALEM,HADASSAH MED CTR,DEPT DERMATOL,JERUSALEM,ISRAEL. AIN SHAMS MED GENET CLIN,CAIRO,EGYPT. RI Lee, Minjoo/A-9720-2008 OI Lee, Minjoo/0000-0002-3151-3808 NR 2 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1160 EP 1160 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701159 ER PT J AU ROSENBERG, M DZIADZIO, L STONE, D BIESECKER, L AF ROSENBERG, M DZIADZIO, L STONE, D BIESECKER, L TI ISOLATION OF SUBTELOMERIC MICROSATELLITE MARKERS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCHGR,GENET DIS RES LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1162 EP 1162 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701160 ER PT J AU CERVENAKOVA, L GOLDFARB, LG BROWN, P KENNEY, K COCHRAN, EJ BENNETT, DA ROOS, R GAJDUSEK, DC AF CERVENAKOVA, L GOLDFARB, LG BROWN, P KENNEY, K COCHRAN, EJ BENNETT, DA ROOS, R GAJDUSEK, DC TI 3 NEW PRNP GENOTYPES ASSOCIATED WITH FAMILIAL CREUTZFELDT-JAKOB-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. UNIV CHICAGO,MED CTR,CHICAGO,IL 60637. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1207 EP 1207 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701206 ER PT J AU LAUE, L WU, SM KUDO, M HSUEH, AJW CUTLER, GB CHAN, WY AF LAUE, L WU, SM KUDO, M HSUEH, AJW CUTLER, GB CHAN, WY TI MISSENSE MUTATIONS IN EXON-10 AND EXON-11 OF THE HUMAN LUTEINIZING-HORMONE RECEPTOR GENE ARE ASSOCIATED WITH LEYDIG-CELL HYPOPLASIA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 GEORGETOWN UNIV,DEPT PEDIAT CELL BIOL & BIOCHEM,WASHINGTON,DC. STANFORD UNIV,DEPT OBSTET & GYNECOL,STANFORD,CA 94305. NICHHD,DEB,BETHESDA,MD. NR 0 TC 1 Z9 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 1252 EP 1252 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701250 ER PT J AU LINDER, CY BADER, PI GUAN, XY BRAYWARD, P BITTNER, M DUTRA, AS ZHANG, H MELTZER, PS TRENT, JM AF LINDER, CY BADER, PI GUAN, XY BRAYWARD, P BITTNER, M DUTRA, AS ZHANG, H MELTZER, PS TRENT, JM TI ISOLATION OF AN INVERSION BREAKPOINT REGION, INV(6)(P11.2-Q23.3), IMPLICATED IN CAUDAL DYSGENESIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. PARKVIEW MEM HOSP,FT WAYNE,IN. YALE UNIV,SCH MED,NEW HAVEN,CT. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1262 EP 1262 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701261 ER PT J AU NICHOLS, RC ZARETSKY, J RUDOLPHI, O EXELBERT, R PLOTZ, PH RABEN, N AF NICHOLS, RC ZARETSKY, J RUDOLPHI, O EXELBERT, R PLOTZ, PH RABEN, N TI MUSCLE PHOSPHOFRUCTOKINASE GENE (PFK-M) - MULTIPLE INTRON RETENTIONS RESULTING IN GLYCOGENOSIS TYPE-VII (TARUI DISEASE) IN A SWEDISH FAMILY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAMS,ARTHRITIS & RHEUMATISM BRANCH,BETHESDA,MD. UMEA UNIV HOSP,S-90185 UMEA,SWEDEN. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1283 EP 1283 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701283 ER PT J AU RICHARD, G WHYTE, YM ITIN, P HOHL, D GIROUX, JM CHARNAS, L COMPTON, JG BALE, SJ AF RICHARD, G WHYTE, YM ITIN, P HOHL, D GIROUX, JM CHARNAS, L COMPTON, JG BALE, SJ TI ERYTHROKERATODERMIA VARIABILIS (EKV) AND ERYTHROKERATODERMIA ASSOCIATED WITH ATAXIA BOTH MAP TO THE SAME REGION ON CHROMOSOME 1P32-31 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAMS,SKIN BIOL LAB,GENET STUDIES SECT,BETHESDA,MD. KANTONSSPITAL,DERMATOL KLIN & POLIKLIN,CH-4031 BASEL,SWITZERLAND. BEAUMONT HOSP,DEPT DERMATOL,LAUSANNE,SWITZERLAND. HOP HOTEL DIEU,DEPT MED,DERMATOL SECT,MONTREAL,PQ,CANADA. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1306 EP 1306 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701304 ER PT J AU RUSSELL, LJ WHYTE, YM DIGIOVANNA, JJ HASHEM, N BALE, SJ COMPTON, JG AF RUSSELL, LJ WHYTE, YM DIGIOVANNA, JJ HASHEM, N BALE, SJ COMPTON, JG TI THE MOLECULAR-BASIS OF AUTOSOMAL RECESSIVE ICHTHYOSES - MUTATIONS IN THE TRANSGLUTAMINASE-1 GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAMS,DERMATOL CLIN RES UNIV,BETHESDA,MD. NIAMS,LSB,GENET STUDIES SECT,BETHESDA,MD. AIN SHAMS MED GENET CLIN,CAIRO,EGYPT. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1308 EP 1308 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701305 ER PT J AU SMITH, ACM DAYSALVATORE, DL NING, Y MACHA, ME CHRISTIAN, SL TURNER, TH SCIORRA, LJ DOBYNS, WB LEDBETTER, DH AF SMITH, ACM DAYSALVATORE, DL NING, Y MACHA, ME CHRISTIAN, SL TURNER, TH SCIORRA, LJ DOBYNS, WB LEDBETTER, DH TI LOCALIZATION OF THE 3C SYNDROME OR A PHENOCOPY TO CHROMOSOME 1Q44-QTER SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. RUTGERS STATE UNIV,ROBERT WOOD JOHNSON MED SCH,PISCATAWAY,NJ 08854. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1320 EP 1320 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701317 ER PT J AU TAYEBI, N HERMAN, J STUBBLEFIELD, BK DAMSCHRODERWILLIAMS, P WINFIELD, S GINNS, EI SIDRANSKY, E AF TAYEBI, N HERMAN, J STUBBLEFIELD, BK DAMSCHRODERWILLIAMS, P WINFIELD, S GINNS, EI SIDRANSKY, E TI DIFFERENT RECOMBINATIONAL EVENTS BETWEEN THE GLUCOCEREBROSIDASE GENE AND PSEUDOGENE IN PATIENTS WITH TYPE-1, TYPE-2 AND TYPE-3 GAUCHER-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1329 EP 1329 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701330 ER PT J AU FRANGISKAKIS, JM EWART, AK MORRIS, CA ENSING, G MERVIS, CB BERTRAND, J GREEN, ED KEATING, MT AF FRANGISKAKIS, JM EWART, AK MORRIS, CA ENSING, G MERVIS, CB BERTRAND, J GREEN, ED KEATING, MT TI WS2 HEMIZYGOSITY MAY CONTRIBUTE TO THE WILLIAMS-SYNDROME COGNITIVE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV UTAH,DEPT HUMAN GENET,SALT LAKE CITY,UT. UNIV UTAH,HOWARD HUGHES MED INST,SALT LAKE CITY,UT. UNIV NEVADA,DEPT PEDIAT,LAS VEGAS,NV 89154. INDIANA UNIV,DEPT PEDIAT CARDIOL,INDIANAPOLIS,IN 46204. EMORY UNIV,DEPT PSYCHOL,ATLANTA,GA 30322. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. RI Toland, Amanda/E-4202-2011 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1383 EP 1383 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701381 ER PT J AU JALANKO, A ENOMAA, N ISONIEMI, A PELTOLA, M RIIKONEN, A TENHUNEN, K TIKKANEN, R GINNS, E PELTONEN, L AF JALANKO, A ENOMAA, N ISONIEMI, A PELTOLA, M RIIKONEN, A TENHUNEN, K TIKKANEN, R GINNS, E PELTONEN, L TI MOLECULAR PATHOGENESIS AND IN-VITRO CORRECTION OF ASPARTYLGLUCOSAMINURIA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NATL PUBL HLTH INST,DEPT HUMAN MOLEC GENET,HELSINKI,FINLAND. NIMH,MOLEC NEUROGENET SECT,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1405 EP 1405 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701404 ER PT J AU KLEIMAN, SE ISAKOV, J SEIDEL, N BODINE, D PASTAN, I GOTTESMAN, MM PUCK, JM AF KLEIMAN, SE ISAKOV, J SEIDEL, N BODINE, D PASTAN, I GOTTESMAN, MM PUCK, JM TI RETROVIRAL VECTOR SYSTEMS FOR THE CORRECTION OF X-LINKED SEVERE COMBINED IMMUNODEFICIENCY (XSCID) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NATL CTR HUMAN GENOME RES,GENE TRANSFER LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1413 EP 1413 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701411 ER PT J AU RABEN, N ZARETSKY, J NICHOLS, RC PAI, SI PLOTZ, PH AF RABEN, N ZARETSKY, J NICHOLS, RC PAI, SI PLOTZ, PH TI A MODEL OF THE MESSENGER-RNA SPLICING DEFECT IN ADULT LYSOSOMAL STORAGE DISEASE (GLYCOGENOSIS TYPE-II) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAMS,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1444 EP 1444 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701444 ER PT J AU SIDRANSKY, E TAYEBI, N HERMAN, J STUBBLEFIELD, BK DYMARSKAIA, I KLINEBURGESS, A GINNS, EI AF SIDRANSKY, E TAYEBI, N HERMAN, J STUBBLEFIELD, BK DYMARSKAIA, I KLINEBURGESS, A GINNS, EI TI GENOTYPIC AND PHENOTYPIC HETEROGENEITY IN TYPE-2 GAUCHER DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1453 EP 1453 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701452 ER PT J AU WANG, Q MARINI, JC AF WANG, Q MARINI, JC TI SELECTIVE IN-VITRO RIBOZYME CLEAVAGE OF MUTANT AND NORMAL TYPE-I COLLAGEN RNA FROM A CASE OF TYPE-III OSTEOGENESIS IMPERFECTS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. NR 1 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1470 EP 1470 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701469 ER PT J AU ZARETSKY, JZ CANDOTTI, F BOERKOEL, N RABEN, N NICHOLS, RC BLAESE, RM PLOTZ, PH AF ZARETSKY, JZ CANDOTTI, F BOERKOEL, N RABEN, N NICHOLS, RC BLAESE, RM PLOTZ, PH TI ACID ALPHA-MALTASE DEFICIENCY - APPROACH TO GENE-THERAPY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAMS,ARTHRIT & RHEUMATISM BRANCH,BETHESDA,MD. NIH,NCHGR,CLIN GENE THERAPY BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1475 EP 1475 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701472 ER PT J AU AKSENTIJEVICH, I ALTHERR, M APOSTOLOU, S BALOW, JE BLAKE, T CALLEN, DF CENTOLA, M CHEN, X CHEN, X COLLINS, FS DOGGETT, NA FISCHELGHODSIAN, N GARDNER, D GUMUCIO, D KRIZMAN, DB LEVY, E LIU, P MARRONE, BL PRAS, E PRAS, M RICHARDS, RI ROTTER, JI SHELTON, D SHOHAT, M SOOD, R WOOD, G KASTNER, DL AF AKSENTIJEVICH, I ALTHERR, M APOSTOLOU, S BALOW, JE BLAKE, T CALLEN, DF CENTOLA, M CHEN, X CHEN, X COLLINS, FS DOGGETT, NA FISCHELGHODSIAN, N GARDNER, D GUMUCIO, D KRIZMAN, DB LEVY, E LIU, P MARRONE, BL PRAS, E PRAS, M RICHARDS, RI ROTTER, JI SHELTON, D SHOHAT, M SOOD, R WOOD, G KASTNER, DL TI PHYSICAL AND TRANSCRIPTIONAL MAP OF THE FMF CANDIDATE REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIAMS,ARB,BETHESDA,MD. LOS ALAMOS NATL LAB,LOS ALAMOS,NM. WOMENS & CHILDRENS HOSP,ADELAIDE,SA,AUSTRALIA. NIH,NCHGR,LGT,BETHESDA,MD. CEDARS SINAI MED CTR,LOS ANGELES,CA. UNIV MICHIGAN,ANN ARBOR,MI. HELLER INST MED RES,TEL HASHOMER,ISRAEL. BEILINSON MED CTR,PETAH TIQWA,ISRAEL. RI Liu, Paul/A-7976-2012; Callen, David/G-1975-2012 OI Liu, Paul/0000-0002-6779-025X; NR 0 TC 0 Z9 0 U1 0 U2 2 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 OCT PY 1995 VL 57 IS 4 SU S BP 1479 EP 1479 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701479 ER PT J AU AYYAGARI, R NESTOROWICZ, A LI, Y SMITH, RJH KAISERKUPFER, M PERMUTT, MA HEJTMANCIK, JF AF AYYAGARI, R NESTOROWICZ, A LI, Y SMITH, RJH KAISERKUPFER, M PERMUTT, MA HEJTMANCIK, JF TI A CHROMOSOME 11P14-15.1 YAC CONTIG THAT ENCOMPASSES THE USHER SYNDROME TYPE 1C LOCUS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NEI,BETHESDA,MD. WASHINGTON UNIV,SCH MED,DIV METAB,ST LOUIS,MO 63110. UNIV IOWA,DEPT OPHTHALMOL,IOWA CITY,IA 52242. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 1484 EP 1484 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701482 ER PT J AU HENTHORN, KS KEEN, TJ INGLEHEARN, CF BHATTACHARYA, SS GREEN, ED AF HENTHORN, KS KEEN, TJ INGLEHEARN, CF BHATTACHARYA, SS GREEN, ED TI HIGH-RESOLUTION PHYSICAL MAPPING OF THE CANDIDATE REGION FOR AN AUTOSOMAL-DOMINANT FORM OF RETINITIS-PIGMENTOSA (RP9) ON CHROMOSOME 7P14-15 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. INST OPHTHALMOL,DEPT MOLEC GENET,LONDON,ENGLAND. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1511 EP 1511 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701510 ER PT J AU HIGGINS, MJ SMILINICH, NJ NI, L NOWAK, NJ QIN, S CHENG, YJ SAIT, SN DEJONG, PJ HEJTMANCIK, JF SMITH, RJH SHOWS, TB AF HIGGINS, MJ SMILINICH, NJ NI, L NOWAK, NJ QIN, S CHENG, YJ SAIT, SN DEJONG, PJ HEJTMANCIK, JF SMITH, RJH SHOWS, TB TI ISOLATION OF YAC CONTIGS IN THE USHER SYNDROME 1C LOCUS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ROSWELL PK CANC INST,BUFFALO,NY 14263. UNIV IOWA,IOWA CITY,IA. NEI,WASHINGTON,DC. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1512 EP 1512 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701511 ER PT J AU KEEN, TJ PATEL, RJ GREEN, ED PEACOCK, RE BHATTACHARYA, SS INGLEHEARN, CF AF KEEN, TJ PATEL, RJ GREEN, ED PEACOCK, RE BHATTACHARYA, SS INGLEHEARN, CF TI PROGRESS TOWARDS THE IDENTIFICATION OF THE RP9 AUTOSOMAL-DOMINANT RETINITIS-PIGMENTOSA GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 INST OPHTHALMOL,DEPT MOLEC GENET,LONDON EC1V 9EL,ENGLAND. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1516 EP 1516 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701513 ER PT J AU MCCORMICK, MK MCINTOSH, I RUTTER, M FRANCOMANO, C CUTONE, S AF MCCORMICK, MK MCINTOSH, I RUTTER, M FRANCOMANO, C CUTONE, S TI POSITIONAL CLONING OF THE NAIL-PATELLA SYNDROME GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. JOHNS HOPKINS UNIV,SCH MED,CTR MED GENET,BALTIMORE,MD 21205. NIH,NATL CTR HUMAN GENOME RES,MED GENET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1530 EP 1530 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701529 ER PT J AU MCDOWELL, G TOWN, M ISOGAI, T YE, P MATHEW, C VANTHOFF, W FARRALL, M WEISSENBACH, J TANIGAMI, A LEDBETTER, D POLYMEROPOULOS, M GAHL, W AF MCDOWELL, G TOWN, M ISOGAI, T YE, P MATHEW, C VANTHOFF, W FARRALL, M WEISSENBACH, J TANIGAMI, A LEDBETTER, D POLYMEROPOULOS, M GAHL, W TI GENETIC AND PHYSICAL MAPPING OF THE REGION OF THE CYSTINOSIS GENE ON 17P SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. UNITED MED & DENT SCH,GUYS HOSP,DIV MED & MOLEC GENET,LONDON SE1 9RT,ENGLAND. INST CHILD HLTH,LONDON,ENGLAND. NUFFIELD ORTHOPAED CTR,OXFORD OX3 7LD,ENGLAND. GENETHON,HUMAN GENOME RES CTR,EVRY,FRANCE. NIH,NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892. NIH,NATL CTR HUMAN GENOME RES,GENET DIS RES LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1533 EP 1533 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701533 ER PT J AU MCGUIRE, RE JORDAN, SA HUMPHRIES, P GREEN, ED DAIGER, SP AF MCGUIRE, RE JORDAN, SA HUMPHRIES, P GREEN, ED DAIGER, SP TI GENETIC AND PHYSICAL MAPPING OF THE RP10 REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV TEXAS,SCH PUBL HLTH,HOUSTON,TX. UNIV TEXAS,DEPT OPHTHALMOL,HOUSTON,TX. WESTERN GEN HOSP,MRC,HUMAN GENET UNIT,EDINBURGH EH4 2XU,MIDLOTHIAN,SCOTLAND. TRINITY COLL DUBLIN,WELLCOME OCULAR GENET UNIT,DUBLIN,IRELAND. NIH,DIAGNOST DEV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1534 EP 1534 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701531 ER PT J AU PRUESSNER, J RANADE, K DRACOPOLI, N SCHUTTE, BC AF PRUESSNER, J RANADE, K DRACOPOLI, N SCHUTTE, BC TI HIGH-EFFICIENCY CLONING OF PCR PRODUCTS INTO THE XCMI T-VECTOR PKRX SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV IOWA,IOWA CITY,IA. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. SEQUANA THERAPEUT INC,LA JOLLA,CA. NR 0 TC 2 Z9 2 U1 0 U2 2 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 OCT PY 1995 VL 57 IS 4 SU S BP 1556 EP 1556 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701554 ER PT J AU RUSSELL, MW DUMANOIR, S MUNROE, D COLLINS, FS BRODY, LC AF RUSSELL, MW DUMANOIR, S MUNROE, D COLLINS, FS BRODY, LC TI CHROMOSOMAL LOCALIZATION OF 15 ION CHANNELS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV MICHIGAN,ANN ARBOR,MI 48109. NCHGR,BETHESDA,MD. MIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 2 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 OCT PY 1995 VL 57 IS 4 SU S BP 1562 EP 1562 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701560 ER PT J AU TANIGAMI, A ROSCHKE, A NING, Y HUANG, B CHONG, S CARROZZO, R CHANDRASEKHARAPPA, S CHINAULT, AC NAKAMURA, Y LEDBETTER, DH AF TANIGAMI, A ROSCHKE, A NING, Y HUANG, B CHONG, S CARROZZO, R CHANDRASEKHARAPPA, S CHINAULT, AC NAKAMURA, Y LEDBETTER, DH TI PHYSICAL MAPPING OF 100 STSS AND 31 YACS AND ISOLATION OF 3 NEW SIMPLE-SEQUENCE REPEAT POLYMORPHIC MARKERS IN CHROMOSOME BAND 17P13 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. HOSP SAN RAFFAELE,I-20132 MILAN,ITALY. BAYLOR COLL MED,DEPT MOLEC & HUMAN GENET,HOUSTON,TX 77030. UNIV TOKYO,INST MED SCI,TOKYO 108,JAPAN. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1577 EP 1577 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701576 ER PT J AU THOMPSON, DB OSSOWSKI, VM SUTHERLAND, J APEL, W JANSSEN, RC AF THOMPSON, DB OSSOWSKI, VM SUTHERLAND, J APEL, W JANSSEN, RC TI PHYSICAL CHARACTERIZATION OF THE REGION AROUND D1S198 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,CLIN DIABET & NUTR SECT,PHOENIX,AZ. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1578 EP 1578 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701577 ER PT J AU TOJI, LH LEONARD, JC DRWINGA, L KIM, CH BECK, JC MULIVOR, RA AF TOJI, LH LEONARD, JC DRWINGA, L KIM, CH BECK, JC MULIVOR, RA TI REGIONAL MAPPING PANEL CELL-CULTURES AND DNA FOR HUMAN-CHROMOSOME-3 AND HUMAN-CHROMOSOME-X SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 CORIELL INST MED RES,CORIELL CELL REPOSITORIES,NIGMS HUMAN GENET MUTANT CELL REPOSITORY,CAMDEN,NJ 08103. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1579 EP 1579 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701580 ER PT J AU VERP, MS LINDGREN, V KNUTEL, T CHRISTIAN, S LEDBETTER, DH AF VERP, MS LINDGREN, V KNUTEL, T CHRISTIAN, S LEDBETTER, DH TI PROSPECTIVE PRENATAL DETECTION OF UNIPARENTAL DISOMY-15 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV CHICAGO,DEPT OBSTET & GYNECOL,CHICAGO,IL 60637. NIH,NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1687 EP 1687 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701685 ER PT J AU NACHEVA, E BITTNER, M LEDBETTER, D JENKINS, R SEELIG, S GRACE, C AF NACHEVA, E BITTNER, M LEDBETTER, D JENKINS, R SEELIG, S GRACE, C TI COMPARATIVE GENOMIC HYBRIDIZATION IN RELATION TO MOLECULAR AND CYTOGENETIC ANALYSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ADDENBROOKES NHS TRUST HOSP,DEPT HAEMATOL,CAMBRIDGE,ENGLAND. NIH,NATL CTR HUMAN GENOME RES,WASHINGTON,DC. MAYO CLIN,ROCHESTER,MN. VYSIS INC,NAPERVILLE,IL. DIGITAL SCI LTD,CAMBRIDGE,ENGLAND. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1756 EP 1756 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701757 ER PT J AU DEERE, M JOHNSON, J GARZA, S YAMADA, Y HOOK, M HECHT, JT AF DEERE, M JOHNSON, J GARZA, S YAMADA, Y HOOK, M HECHT, JT TI EPIPHYCAN (PG-LB), A SMALL DERMATAN SULFATE PROTEOGLYCAN EXPRESSED IN EMBRYONIC CARTILAGE, IS CONSERVED BETWEEN SPECIES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX. TEXAS A&M UNIV,INST BIOSCI & TECHNOL,HOUSTON,TX. NIDR,BETHESDA,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1816 EP 1816 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701817 ER PT J AU HANSON, RL KOBES, S THOMPSON, DB JANSSEN, RC PROCHAZKA, M KNOWLER, WC AF HANSON, RL KOBES, S THOMPSON, DB JANSSEN, RC PROCHAZKA, M KNOWLER, WC TI PARAMETRIC LINKAGE ANALYSES OF DIABETES-MELLITUS IN PIMA-INDIANS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIDDK,PHOENIX,AZ. NR 0 TC 0 Z9 0 U1 0 U2 1 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 OCT PY 1995 VL 57 IS 4 SU S BP 1877 EP 1877 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701876 ER PT J AU KANG, S GRAHAM, JM ABBOTT, M BIESECKER, LG AF KANG, S GRAHAM, JM ABBOTT, M BIESECKER, LG TI LINKAGE ANALYSIS OF PALLISTER-HALL SYNDROME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NCHGR,GENET DIS RES LAB,BETHESDA,MD. CEDARS SINAI MED CTR,DIV GENET,LOS ANGELES,CA. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1880 EP 1880 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701878 ER PT J AU KOBAYASHI, H BAUMBACH, L MATISE, TC SCHIAVI, A GREENBERG, F HOFFMAN, EP AF KOBAYASHI, H BAUMBACH, L MATISE, TC SCHIAVI, A GREENBERG, F HOFFMAN, EP TI A GENE FOR X-LINKED INFANTILE SPINAL MUSCULAR-ATROPHY (A SEVERE LETHAL FORM OF X-LINKED ARTHROGRYPOSIS) MAPS TO XP11.3-Q11.2 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA. UNIV MIAMI,SCH MED,MIAMI,FL. COLUMBIA UNIV,NEW YORK,NY. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1881 EP 1881 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701881 ER PT J AU TASSARA, C ROSENBERG, FJ PUCK, JM AF TASSARA, C ROSENBERG, FJ PUCK, JM TI SSCP POLYMORPHISMS IN THE HUMAN TUMOR-NECROSIS-FACTOR RECEPTOR-TYPE-I GENE (TNFR1) ON CHROMOSOME 12P13 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,GENE TRANSFER LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1896 EP 1896 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701895 ER PT J AU ZULLO, S CHIPPERFIELD, MA LEMKIN, P MERRIL, CR AF ZULLO, S CHIPPERFIELD, MA LEMKIN, P MERRIL, CR TI MITODAT - A MITOCHONDRIAL PROTEIN INFORMATION RESOURCE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,BIOCHEM GENET LAB,WASHINGTON,DC 20032. JOHNS HOPKINS UNIV,BALTIMORE,MD. NCI,FREDERICK CANC RES & DEV CTR,MATH BIOL LAB,IMAGE PROC SECT,FREDERICK,MD. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1906 EP 1906 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701903 ER PT J AU HEJTMANCIK, JF ALBERTI, G OGUNI, M PODGOR, M SPERDUTO, RD TOMAREV, S GRASSI, C WILLIAMS, S KAISERKUPFER, M MARAINI, G AF HEJTMANCIK, JF ALBERTI, G OGUNI, M PODGOR, M SPERDUTO, RD TOMAREV, S GRASSI, C WILLIAMS, S KAISERKUPFER, M MARAINI, G TI GLUTATHIONE-S-TRANSFERASE M1 GENOTYPE AND AGE-RELATED CATARACTS - LACK OF ASSOCIATION IN AN ITALIAN POPULATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PARMA,INST OPHTHALMOL,I-43100 PARMA,ITALY. NEI,OGCSB,BETHESDA,MD 20892. NEI,DBE,BETHESDA,MD 20892. NEI,LMDB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1917 EP 1917 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701914 ER PT J AU CERVENAKOVA, L SIVAKUMAR, K NAGLE, J ISAACSON, S DALAKAS, MC GOLDFARB, LG AF CERVENAKOVA, L SIVAKUMAR, K NAGLE, J ISAACSON, S DALAKAS, MC GOLDFARB, LG TI SEQUENCE-ANALYSIS OF THE PRNP GENE IN HEREDITARY INCLUSION-BODY MYOPATHY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1939 EP 1939 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701937 ER PT J AU SALAFIA, CM MINIOR, VK PEZZULLO, JC POPEK, EJ ROSENKRANTZ, TS VINTZILEOS, AM AF SALAFIA, CM MINIOR, VK PEZZULLO, JC POPEK, EJ ROSENKRANTZ, TS VINTZILEOS, AM TI INTRAUTERINE GROWTH RESTRICTION IN INFANTS OF LESS-THAN 32 WEEKS GESTATION - ASSOCIATED PLACENTAL PATHOLOGICAL FEATURES SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 15th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 23-28, 1995 CL ATLANTA, GA SP Soc Perinatal Obstetricians DE INTRAUTERINE GROWTH RESTRICTION; PLACENTAL PATHOLOGY; PREMATURITY; PREECLAMPSIA ID LOW-BIRTH-WEIGHT; PRETERM DELIVERY; FETAL GROWTH; RETARDATION; VILLITIS; LESIONS; TERM AB OBJECTIVE: Our purpose was to describe placental lesions associated with normal and abnormal fetal growth in infants delivered for obstetric indications at < 32 weeks' gestation. STUDY DESIGN: Maternal and neonatal charts and placental tissues from 420 consecutive nonanomalous live-born singleton infants delivered at < 32 weeks' gestation with accurate gestational dates were retrospectively studied. Excluded were cases with maternal diabetes, chronic hypertension, hydrops fetalis, diagnosed congenital viral infection, and placenta previa, leaving four primary indications for delivery: preeclampsia, preterm labor, premature rupture of membranes, and nonhypertensive abruptio placentae. The presence and severity of placental lesions was scored by a pathologist blinded to clinical data. Birth weight and length percentiles were calculated from published nomograms. Asymmetric intrauterine growth retardation (n = 32) was defined as birth weight < 10th percentile with length > 10th percentile and symmetric intrauterine growth retardation (n = 48) as both weight and length < 10th percentile for gestational age, A ''growth restriction index'' was developed to express a continuum of growth in both length and weight. Contingency tables, analyses of variance, and multiple regression analysis defined significance as p < 0.05 (with corrections for multiple comparisons). RESULTS: A greater proportion of cases with intrauterine growth retardation had lesions of uteroplacental insufficiency (p < 0.001) or chronic villitis (p < 0.02) than dib appropriately grown preterm infants. Cases with asymmetric intrauterine growth retardation tended to have more lesions than did cases with appropriate-for-gestational-age infants. Four multiple regression analyses used the growth restriction index as outcome and the histologic lesions that had significant relationships to fetal growth as independent predictors in univariate analyses. Overall, uteroplacental fibrinoid necrosis, circulating nucleated erythrocytes, avascular terminal villi, and villous infarct were significant independent predictors of fetal growth (adjusted R(2) = 0.312). With addition of preeclampsia as a variable, villous fibrosis, avascular villi, infarct, and preeclampsia were independent predictors of fetal growth (adjusted R(2) = 0.341). In the 65 preeclampsia cases no histologic lesion was an independent predictor of fetal growth, whereas in the nonpreeclampsia cases, villous fibrosis and avascular villi were independent predictors of fetal growth (adjusted R(2) = 0.075). CONCLUSIONS: In nonanomalous preterm infants intrauterine growth retardation is most commonly symmetric and is primarily related to the cumulative number and severity of lesions reflecting abnormal uteroplacental or fetoplacental blood flow. The growth restriction index may contribute to the study of the biologic range of fetal growth. The statistical relationship of most placental lesions to intrauterine growth retardation depends on the presence or absence of preeclampsia. C1 UNIV CONNECTICUT,CTR HLTH,DIV NEONATOL,FARMINGTON,CT. TEXAS CHILDRENS HOSP,DEPT PATHOL,HOUSTON,TX 77030. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,ST PETERS MED CTR,DIV MATERNAL FETAL MED,NEW BRUNSWICK,NJ 08903. GEORGETOWN UNIV,MED CTR,DEPT OBSTET & GYNECOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20007. NICHHD,PERNATAL PATHOL SECT,PERINATOL RES FACIL,WASHINGTON,DC. NICHHD,INFORMAT SECT,WASHINGTON,DC. RP SALAFIA, CM (reprint author), UNIV CONNECTICUT,CTR HLTH,DIV ANAT PATHOL,FARMINGTON,CT 06032, USA. FU NICHD NIH HHS [N01-HD 33198] NR 34 TC 176 Z9 179 U1 2 U2 4 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 OCT PY 1995 VL 173 IS 4 BP 1049 EP 1057 DI 10.1016/0002-9378(95)91325-4 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TC502 UT WOS:A1995TC50200008 PM 7485292 ER PT J AU SALAFIA, CM MINIOR, VK LOPEZZENO, JA WHITTINGTON, SS PEZZULLO, JC VINTZILEOS, AM AF SALAFIA, CM MINIOR, VK LOPEZZENO, JA WHITTINGTON, SS PEZZULLO, JC VINTZILEOS, AM TI RELATIONSHIP BETWEEN PLACENTAL HISTOLOGIC FEATURES AND UMBILICAL-CORD BLOOD-GASES IN PRETERM GESTATIONS SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 15th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 23-28, 1995 CL ATLANTA, GA SP Soc Perinatal Obstetricians DE UMBILICAL CORD BLOOD GASES; PREMATURITY; PLACENTAL PATHOLOGY; UTEROPLACENTAL VESSELS ID BED; PREGNANCY AB OBJECTIVE: Our purpose was to test the hypothesis that placental histologic lesions reflect abnormal placental respiratory function in preterm gestations. STUDY DESIGN: A retrospective study of preterm deliveries from 22 to 32 weeks revealed 431 patients with umbilical venous or arterial blood gas values. Excluded were stillbirth, multiple gestations, placenta previa, maternal medical diseases, and fetal anomalies. Charts were reviewed for principal indication of delivery, diagnosis of labor, and mode of delivery. Blood gases were studied within 10 minutes of delivery on a model 178 automatic pH analyzer (Coming Med, Boston). Placental data included uteroplacental vascular lesions and related villous lesions, lesions of acute inflammation, chronic inflammation, and coagulation. Contingency tables and analysis of variance considered p < 0.05 as significant. RESULTS: Mean +/- SD umbilical vein pH was 7.36 +/- 0.07 (range 6.94 to 7.56) and umbilical artery pH was 7.30 +/- 0.08 (range 6.83 to 7.55). Increasing severity of uteroplacental thrombosis, villous lesions reflective of uteroplacental vascular pathologic mechanisms, avascular villi, histologic evidence of abruptio placentae, chronic villitis, and increased circulating erythrocytes were associated with decrease in umbilical vein and artery pH, increase in umbilical vein and artery Pco(2), and decrease in umbilical vein and artery Po-2. Histologic evidence of acute infection and villous edema were associated with a higher pH and Po-2 and a lower Pco(2) in both umbilical vein and artery. Umbilical vein or artery base excess was not related to placental lesions. Labor was not related to blood gas values in this data set, although a subset of cases of extremely preterm premature rupture of membranes and preterm labor who labored and were delivered by cesarean section had significantly poorer umbilical Venous and fetal arterial blood gas values (all p < 0.005). lesions related to poorer blood gas values were significantly more frequent in preterm preeclampsia and nonhypertensive abruptio placentae than in premature rupture of membranes or preterm labor. CONCLUSIONS: Changes in umbilical vein and artery pH, Po-2 and Pco(2) are significantly related to lesions of uteroplacental vascular pathologic mechanisms and intraplacental thrombosis. Placental lesions may be associated with chronic fetal distress by altering fetal oxygen availability and acid-base status. Placental immaturity resulting from prematurity may be associated with inefficient placental respiratory function and an increased likelihood of cesarean delivery in cases of premature rupture of membranes or preterm labor. Altered fetal acid-base balance plus excess numbers of circulating nucleated erythrocytes suggests that placental respiratory function is functionally abnormal when these lesions are present and leads to fetal tissue hypoxia. C1 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,ST PETERS MED CTR,DIV MATERNAL FETAL MED,NEW BRUNSWICK,NJ 08903. NIDDKD,PERINATAL PATHOL SECT,PERINATOL RES FACIL,WASHINGTON,DC. NIDDKD,INFORMAT SECT,PERINATOL RES FACIL,WASHINGTON,DC. GEORGETOWN UNIV,MED CTR,DEPT OBSTET & GYNECOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20007. PONCE SCH MED,DEPT OBSTET & GYNECOL,PONCE,PR. RP SALAFIA, CM (reprint author), UNIV CONNECTICUT,CTR HLTH,DIV ANAT PATHOL,FARMINGTON,CT 06032, USA. FU NICHD NIH HHS [N01-HD 3-3198] NR 23 TC 33 Z9 35 U1 0 U2 2 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 OCT PY 1995 VL 173 IS 4 BP 1058 EP 1064 DI 10.1016/0002-9378(95)91326-2 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TC502 UT WOS:A1995TC50200009 PM 7485293 ER PT J AU SALAFIA, CM LOPEZZENO, JA SHERER, DM WHITTINGTON, SS MINIOR, VK VINTZILEOS, AM AF SALAFIA, CM LOPEZZENO, JA SHERER, DM WHITTINGTON, SS MINIOR, VK VINTZILEOS, AM TI HISTOLOGIC EVIDENCE OF OLD INTRAUTERINE BLEEDING IS MORE FREQUENT IN PREMATURITY SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 15th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 23-28, 1995 CL ATLANTA, GA SP Soc Perinatal Obstetricians DE PLACENTA ACCRETA; PREMATURITY; PREECLAMPSIA; UTEROPLACENTAL VASCULAR PATHOLOGICAL FEATURES; HEMOSIDERIN ID PRETERM DELIVERY; EARLY-PREGNANCY; PLACENTAL BED; FETAL GROWTH; VILLITIS; INFANTS; LESIONS; BIRTH AB OBJECTIVE: Our purpose was to study the incidence and location of histologic evidence of intrauterine bleeding in preterm and term placentas. STUDY DESIGN: A total of 462 consecutive placentas delivered at < 32 weeks' gestation, from which cases of placenta previa, stillbirth, and multiple gestation were excluded, were compared with 108 consecutive term placentas (with similar exclusion criteria) in regard to the presence of hemosiderin in decidua of basal plate or placental membranes. Of the 462 preterm cases, 448 charts made specific reference to the presence or absence of vaginal bleeding. Bloody show alone was not considered bleeding. The blinded scoring of lesions (including acute ascending infection, uteroplacental vascular pathologic processes and related ischemic damage, chronic inflammation, and coagulation related lesions) was analyzed by contingency tables (p < 0.05 significant). RESULTS: A total of 196 of 462 (43%) preterm placentas had any decidual hemosiderin compared with one of 108 (0.8%) at term (p < 0.00001). Among the preterm cases, hemosiderin was significantly more common in preeclampsia (45/76, 60%) and in cases clinically diagnosed as nonhypertensive abruptio placentae (21/33, 64%) than in premature membrane rupture (72/192, 37.5%) and preterm labor (58/161, 36%, p < 0.003). The incidence of placental lesions in preterm cases with extraplacental membrane hemosiderin was not different than it was in cases without hemosiderin. Placental lesions related to basal-plate decidual hemosiderin in the preterm cases were villous infarct (p < 0.0001), uteroplacental vessels with absence of physiologic change (p < 0.003) and increased numbers of circulating nucleated erythrocytes (p < 0.0007), uteroplacental thrombosis (p < 0.0001), and villous fibrosis (p < 0.0001) and hypovascularity (p < 0.0001). Among the preterm cases, 23 of 48 (48%) with first-trimester bleeding, 33 of 66 (50%) with second-trimester bleeding, and 31 of 64 (48%) with multiple episodes of bleeding had decidual hemosiderin (p < 0.0001). A clinical history of gestational bleeding was significantly less common in cases of preterm preeclampsia with histologic evidence of bleeding (four of 73, 5.5%) than in nonhypertensive abruptio placentae (18/31, 58%), premature rupture of membranes (52/183, 28%), or preterm labor (31/161, 19%, p < 0.0001). Hemosiderin was not related to clinical bleeding < 72 hours of delivery (p > 0.20). CONCLUSIONS: Decidual bleeding is common in all clinical types of preterm birth and is most common in preterm preeclampsia and nonhypertensive abruptio placentae. A clinical history of bleeding is not correlated with the presence of decidual hemosiderin. Bleeding in the basal plate is related to histologic evidence of chronic uteroplacental vascular pathologic processes, which in cases of spontaneous prematurity (premature rupture of membranes, preterm labor, nonhypertensive abruptio placentae) may be associated with decidual bleeding which occasionally may be clinically manifested as gestational bleeding. C1 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,ST PETERS MED CTR,DIV MATERNAL FETAL MED,NEW BRUNSWICK,NJ 08903. NIDDKD,PERINATAL RES FACIL,WASHINGTON,DC. GEORGETOWN UNIV,MED CTR,DEPT OBSTET & GYNECOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20007. PONCE SCH MED,DEPT OBSTET & GYNECOL,PONCE,PR. RP SALAFIA, CM (reprint author), UNIV CONNECTICUT,CTR HLTH,DIV ANAT PATHOL,FARMINGTON,CT 06032, USA. FU NICHD NIH HHS [N01-HD 3-3198] NR 24 TC 83 Z9 87 U1 1 U2 2 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 OCT PY 1995 VL 173 IS 4 BP 1065 EP 1070 DI 10.1016/0002-9378(95)91327-0 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TC502 UT WOS:A1995TC50200010 PM 7485294 ER PT J AU SALAFIA, CM PEZZULLO, JC LOPEZZENO, JA SIMMENS, S MINIOR, VK VINTZILEOS, AM AF SALAFIA, CM PEZZULLO, JC LOPEZZENO, JA SIMMENS, S MINIOR, VK VINTZILEOS, AM TI PLACENTAL PATHOLOGICAL FEATURES OF PRETERM PREECLAMPSIA SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 15th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 23-28, 1995 CL ATLANTA, GA SP Soc Perinatal Obstetricians DE PREECLAMPSIA; PREMATURITY; PLACENTAL PATHOLOGY ID SYSTEMIC LUPUS-ERYTHEMATOSUS; ANTIPHOSPHOLIPID ANTIBODIES; PRE-ECLAMPSIA; PREGNANCY; BED; INFANTS; WOMEN AB OBJECTIVE: Our purpose was to compare the incidence and interrelationships of uteroplacental vasculopathy and chronic inflammatory and placental vasoocclusive lesions in preeclampsia and spontaneous delivery before 32 weeks' gestation. STUDY DESIGN: Review of singleton live-born nonanomalous infants born at 22 to 32 weeks' gestation identified 76 cases of preeclamspia and 353 cases of spontaneous prematurity (spontaneous premature membrane rupture [n = 192], preterm labor, intact membranes [n = 161]). Histologic lesions were considered as belonging to one of five major pathophysiologic groups: (1) uteroplacental vascular lesions and related villous lesions, (2) chronic inflammatory lesions, (3) coagulation-related lesions, (4) acute inflammatory lesions, and (5) unclassified lesions. Contingency table analyses considered p < 0.05 significant. Factor analysis extracted combinations of related variables. RESULTS: More frequent in preeclampsia versus spontaneous prematurity were chronic uteroplacental vasculitis (29% vs 20%, p < 0.05), chronic villitis (20% vs 3%, p < 0.001), avascular villi (39% vs 16%, p < 0.001), and ''hemorrhagic endovasculitis'' (9% vs 2.5%, p < 0.03). In the preeclampsia cases factor analysis extracted 13 categories of related lesions. Four categories contained uteroplacental vascular lesions. Five categories included lesions related to chronic inflammation, and eight included lesions related to coagulation. Four categories loaded lesions from one major pathophysiologic group only. Three categories loaded lesions from all three pathophysiologic groups. Unclassified lesions loaded into two factor categories that were unrelated to the other lesions. CONCLUSIONS: Chronic inflammatory and placental vasoocclusive lesions are more common in preterm preeclampsia than in spontaneous prematurity. Immunopathologic processes and coagulation may be involved in the pathophysiologic mechanisms of preterm preeclampsia independent of uteroplacental vascular pathologic features. C1 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,ST PETERS MED CTR,DIV MATERNAL FETAL MED,NEW BRUNSWICK,NJ 08903. GEORGE WASHINGTON UNIV,DEPT HLTH CARE SCI,WASHINGTON,DC 20037. NIDDKD,PERINATAL PATHOL SECT,PERINATOL RES FACIL,WASHINGTON,DC. NIDDKD,INFORMAT SECT,PERINATOL RES FACIL,WASHINGTON,DC. GEORGETOWN UNIV,MED CTR,DEPT OBSTET & GYNECOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20007. PONCE SCH MED,DEPT OBSTET & GYNECOL,PONCE,PR. RP SALAFIA, CM (reprint author), UNIV CONNECTICUT,CTR HLTH,DIV ANAT PATHOL,FARMINGTON,CT 06032, USA. FU NICHD NIH HHS [N01-HD 3-3198] NR 36 TC 148 Z9 156 U1 1 U2 5 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 OCT PY 1995 VL 173 IS 4 BP 1097 EP 1105 DI 10.1016/0002-9378(95)91333-5 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TC502 UT WOS:A1995TC50200016 PM 7485300 ER PT J AU MEIS, PJ GOLDENBERG, RL MERCER, B MOAWAD, A DAS, A MCNELLIS, D JOHNSON, F IAMS, JD THOM, E ANDREWS, WW ROBERTS, JM HAUTH, JC COPPER, R MUELLERHEUBACH, E SWAIN, M FRYE, A MOAWAD, AH LINDHEIMER, M JONES, P MIODOVNIK, M SIDDIQI, TA ELDER, N LEUCHTENBURY, L FISCHER, M PAUL, RH KOVACS, B RABELLO, Y CARITIS, SN HARGER, JH COTRONEO, M STALLINGS, C YAFFE, SJ GATZ, C KLEBANOFF, M LANDON, MB THURNAU, GR CAREY, JC MEIER, A VANDORSTEN, JP NEWMAN, RB COLLINS, BA LEBOEUF, F SIBAI, B RAMSEY, R BOTTOMS, SF DOMBROWSKI, MP NORMAN, GS AF MEIS, PJ GOLDENBERG, RL MERCER, B MOAWAD, A DAS, A MCNELLIS, D JOHNSON, F IAMS, JD THOM, E ANDREWS, WW ROBERTS, JM HAUTH, JC COPPER, R MUELLERHEUBACH, E SWAIN, M FRYE, A MOAWAD, AH LINDHEIMER, M JONES, P MIODOVNIK, M SIDDIQI, TA ELDER, N LEUCHTENBURY, L FISCHER, M PAUL, RH KOVACS, B RABELLO, Y CARITIS, SN HARGER, JH COTRONEO, M STALLINGS, C YAFFE, SJ GATZ, C KLEBANOFF, M LANDON, MB THURNAU, GR CAREY, JC MEIER, A VANDORSTEN, JP NEWMAN, RB COLLINS, BA LEBOEUF, F SIBAI, B RAMSEY, R BOTTOMS, SF DOMBROWSKI, MP NORMAN, GS TI THE PRETERM PREDICTION STUDY - SIGNIFICANCE OF VAGINAL INFECTIONS SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 15th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 23-28, 1995 CL ATLANTA, GA SP Soc Perinatal Obstetricians DE BACTERIAL VAGINOSIS; SPONTANEOUS PRETERM BIRTH; BLACK RACE ID LOW BIRTH-WEIGHT; BACTERIAL VAGINOSIS; RISK-FACTORS; CHLAMYDIA-TRACHOMATIS; PREGNANCY; PREMATURITY AB OBJECTIVE: Our purpose was to evaluate the association oi bacterial vaginosis, trichomonas vaginitis, and monilial vaginitis with spontaneous preterm birth at < 35 weeks 0 days. STUDY DESIGN: A total of 2929 women at in centers were studied at 24 and 28 weeks' gestation by Gram stain of vaginal smear, wet mount, and 10% potassium hydroxide preparations to detect vaginal infections. RESULTS: The rates of detected infection at 24 and 28 weeks, respectively, were bacterial vaginosis 23.4% and 19.4%, trichomonas 3.3% and 2.7%, and monilia 21.1% and 19.5%. The occurrence of bacterial vaginosis at 28 weeks was associated with an increased risk of spontaneous preterm birth, odds ratio 1.84 (95% confidence interval 1.15 to 2.95, p < 0.01). Detection of Trichomonas vaginalis (by wet mount) or monilia (by potassium hydroxide preparation) had no significant associations with preterm birth. CONCLUSION: The presence of bacterial vaginosis at 28 weeks' gestation is associated with an increased risk of spontaneous preterm birth. C1 MAGEE WOMENS HOSP,PITTSBURGH,PA. UNIV ALABAMA,BIRMINGHAM,AL. UNIV CHICAGO,CHICAGO,IL 60637. UNIV CINCINNATI,CINCINNATI,OH 45221. GEORGE WASHINGTON UNIV,CTR BIOSTAT,WASHINGTON,DC 20052. UNIV SO CALIF,LOS ANGELES CTY MED CTR,LOS ANGELES,CA 90089. NICHHD,MATERNAL FETAL MED UNITS NETWORK,BETHESDA,MD. OHIO STATE UNIV,COLUMBUS,OH. UNIV OKLAHOMA,OKLAHOMA CITY,OK. MED UNIV S CAROLINA,CHARLESTON,SC. UNIV TENNESSEE,KNOXVILLE,TN 37996. WAYNE STATE UNIV,DETROIT,MI 48202. RP MEIS, PJ (reprint author), WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT OBSTET & GYNECOL,MED CTR BLVD,WINSTON SALEM,NC 27157, USA. NR 14 TC 246 Z9 251 U1 0 U2 8 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 OCT PY 1995 VL 173 IS 4 BP 1231 EP 1235 DI 10.1016/0002-9378(95)91360-2 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TC502 UT WOS:A1995TC50200043 PM 7485327 ER PT J AU GUINN, DA GOLDENBERG, RL HAUTH, JC ANDREWS, WW THOM, E ROMERO, R AF GUINN, DA GOLDENBERG, RL HAUTH, JC ANDREWS, WW THOM, E ROMERO, R TI RISK-FACTORS FOR THE DEVELOPMENT OF PRETERM PREMATURE RUPTURE OF THE MEMBRANES AFTER ARREST OF PRETERM LABOR SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 15th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 23-28, 1995 CL ATLANTA, GA SP Soc Perinatal Obstetricians DE PRETERM RUPTURE OF THE MEMBRANES; INFECTION; PREMATURITY ID FETAL MEMBRANES; AMNIOTIC-FLUID; INFECTION; BIRTH AB OBJECTIVE: Our purpose was to determine risk factors predictive of preterm premature rupture of the membranes in women treated for preterm labor with intact membranes. STUDY DESIGN: Women with intact membranes participating in a National Institute of Child Health and Human Development multicenter randomized trial of adjunctive antibiotic therapy for preterm labor (24 to 34 weeks) were studied (n = 275). After rendomization, 22 women continued to have contractions and were delivered of their infants. The remaining 253 women whose contractions had ceased composed our study population. Preterm premature rupture of the membranes was diagnosed if ruptured membranes occurred greater than or equal to 1 hour before the onset of recurrent preterm labor. As part of the study protocol, most women underwent amniocentesis on admission. RESULTS: Preterm premature rupture of the membranes developed in 44% women (17.4%), Women who had preterm premature rupture of the membranes were more likely to be black (p = 0.004), to be multiparous (p = 0.014), to have a history of abortion(s) (p = 0.001), to have had a preterm birth(s) (p = 0.036), to have early onset preterm labor (p = 0.04), to have more advanced cervical dilatation (p = 0.0001), to have one or more amniotic fluid markers suggestive of infection (p = 0.01, odds ratio 4.2), and to have positive amniotic fluid cultures (p = 0.0007, odds ratio 27). Assignment to antibiotic therapy did not prevent preterm premature rupture of the membranes in the 253 women randomized or in the 16 women with a positive amniotic fluid marker(s) of infection. CONCLUSION: Black race, multiparity, a history of abortion or preterm birth, advanced dilatation, and a positive amniotic fluid marker(s) are associated with preterm premature rupture of the membranes in women with preterm labor. Antibiotic treatment did not prevent preterm premature rupture of the membranes. C1 GEORGE WASHINGTON UNIV,CTR BIOSTAT,ROCKVILLE,MD. NICHHD,MATERNAL FETAL MED UNITS NETWORK,BETHESDA,MD 20892. RP GUINN, DA (reprint author), UNIV ALABAMA,DEPT OBSTET & GYNECOL,618 S 20TH ST,BIRMINGHAM,AL 35233, USA. NR 20 TC 32 Z9 33 U1 0 U2 1 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 OCT PY 1995 VL 173 IS 4 BP 1310 EP 1315 DI 10.1016/0002-9378(95)91377-7 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TC502 UT WOS:A1995TC50200060 PM 7485344 ER PT J AU BERRY, SM ROMERO, R GOMEZ, R PUDER, KS GHEZZI, F COTTON, DB BIANCHI, DW AF BERRY, SM ROMERO, R GOMEZ, R PUDER, KS GHEZZI, F COTTON, DB BIANCHI, DW TI PREMATURE PARTURITION IS CHARACTERIZED BY IN-UTERO ACTIVATION OF THE FETAL IMMUNE-SYSTEM SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 15th Annual Meeting of the Society-of-Perinatal-Obstetricians CY JAN 23-28, 1995 CL ATLANTA, GA SP Soc Perinatal Obstetricians DE PREMATURE LABOR; CORDOCENTESIS; FETAL MONOCYTE-NEUTROPHIL ACTIVATION ID EXPRESSION; CD14; NEUTROPHIL; CELLS; LEUKOCYTE; ANTIGENS; ALPHA; CD66 AB OBJECTIVE: At birth the fetus emerges from a sterile environment into a nonsterile one. This process is associated with activation of the fetal immune system which protects the fetus against infection in the newborn period. We conducted this study to determine whether activation of the monocyte-neutrophil system occurs in fetuses before premature birth. STUDY DESIGN: Forty patients in premature labor with intact membranes underwent cordocentesis for research purposes. Fetal blood was analyzed with the use of flow cytometry to measure the cell surface markers CD11c, CD13, CD15, and CD67, which are associated with monocyte and neutrophil activation, and CD14 and CD63, which were used as controls. RESULTS: Twenty-eight percent (11/40) of the infants were delivered prematurely within 72 hours of entering the study while the remainder were delivered at term. Our data clearly indicate that premature infants delivered within 72 hours had a higher percentage of CD11c, CD13, CD15, and CD67 than those delivered at term. In contrast, there were no significant differences in the percentages of CD14 acid CD63. CONCLUSION: Activation of the monocyte-neutrophil system exists in fetuses destined for premature delivery. These findings indicate that premature parturition is associated with in utero immune system activation. C1 NICHHD,PERINATOL RES BRANCH,WASHINGTON,DC. TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,BOSTON,MA 02111. RP BERRY, SM (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,DEPT OBSTET & GYNECOL,DIV MATERNAL FETAL MED,4707 ST ANTOINE BLVD,DETROIT,MI 48201, USA. OI Ghezzi, Fabio/0000-0003-3949-5410 NR 16 TC 52 Z9 53 U1 0 U2 1 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 OCT PY 1995 VL 173 IS 4 BP 1315 EP 1320 DI 10.1016/0002-9378(95)91378-5 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TC502 UT WOS:A1995TC50200061 PM 7485345 ER PT J AU SMITH, GH SHARP, R KORDON, EC JHAPPAN, C MERLINO, G AF SMITH, GH SHARP, R KORDON, EC JHAPPAN, C MERLINO, G TI TRANSFORMING GROWTH-FACTOR-ALPHA PROMOTES MAMMARY TUMORIGENESIS THROUGH SELECTIVE SURVIVAL AND GROWTH OF SECRETORY EPITHELIAL-CELLS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID HUMAN-BREAST CANCER; TRANSGENIC MICE; FACTOR RECEPTOR; TGF-ALPHA; EXPRESSION; GLAND; HYPERPLASIA; CARCINOMAS; TISSUE; DEATH AB Transforming growth factor (TGF)-alpha stimulates the growth and development of mammary epithelial cells and is implicated in the pathogenesis of human breast cancer. In this report we evaluate the consequences of overexpressing TGF-alpha in the mammary gland of transgenic mice and examine associated cellular mechanisms. When operating on a FVB/N genetic background (line MT100), TGF-alpha induced the stochastic development of mammary adenomas and adenocarcinomas of secretory epithelial origin in 64% of multiparous females. In contrast, tumors were exceedingly rare in virgin MT100 females, MT100 males, and multiparous FVB/N females. In MT100 females multiple foci of hyperplastic secretory lesions preceded the development of frank tumors; these initial lesions appeared during the involution period after the first lactation. Serial transplantation of these hyperplasias indicated nit absence of proliferative immortality. Nevertheless, they gave rise to tumors at a low frequency and after a prolonged latency in virgin hosts; in multiparous rous hosts, tumors developed earlier and at a high incidence. The TGF-alpha transgene was highly expressed in hyperplasias and tumors but not in virgin and nonlesion-bearing tissue, suggesting that TGF-alpha overexpression provides a selective growth advantage, TGF-alpha also induced at lactation a 6.4-fold increase in DNA synthesis in MT100 epithelial cells, many of which were binucleated MT100 mammary tissue experienced an obvious delay ill involution, resulting in the postlactational survival of a significant population of unregressed secretory epithelial cells. C1 NCI,MOLEC GENET SECT,MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NR 50 TC 55 Z9 56 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD OCT PY 1995 VL 147 IS 4 BP 1081 EP 1096 PG 16 WC Pathology SC Pathology GA RZ182 UT WOS:A1995RZ18200021 PM 7573353 ER PT J AU MUNDY, LM AUWAERTER, PG OLDACH, D WARNER, ML BURTON, A VANCE, E GAYDOS, CA JOSEPH, JM GOPALAN, R MOORE, RD QUINN, TC CHARACHE, P BARTLETT, JG AF MUNDY, LM AUWAERTER, PG OLDACH, D WARNER, ML BURTON, A VANCE, E GAYDOS, CA JOSEPH, JM GOPALAN, R MOORE, RD QUINN, TC CHARACHE, P BARTLETT, JG TI COMMUNITY-ACQUIRED PNEUMONIA - IMPACT OF IMMUNE STATUS SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID CHLAMYDIA-PNEUMONIAE; LEGIONNAIRES-DISEASE; ETIOLOGY AB This cross-sectional and prospective one year study evaluated adults admitted to an inner city hospital with community-acquired pneumonia. The study used extensive diagnostic methods to evaluate the etiologies of community-acquired pneumonia in hospitalized patients with differing immunologic status. Of 385 study patients, concurrent problems associated with immunosuppression were noted in 221 (57%) patients, 180 of whom were human immunodeficiency virus (HIV)-infected. The five most common causes of community-acquired pneumonia were: Streptococcus pneumoniae, Pneumocystis carinii, aspiration, Hemophilus influenzae, and gram-negative bacilli. Only 8.3% of patients had either Legionella, Chlamydia pneumoniae or Mycoplasma pneumoniae. Despite use of state-of-the-art diagnostic techniques, no diagnosis was made in 46 of 180 (25.6%) HIV-infected patients, 56 of 164 (34.1%) immunocompetent patients, and 20 of 41 (48.8%) non-HIV-infected immunosuppressed patients. The diagnostic yield of pre-antibiotic sputum culture for conventional bacteria was 99/155 (63.9%) compared to 52 of 169 patients (32.7%) with adequate post-antibiotic sputum culture (p < 0.0001). Although S. pneumonia continues to be the most commonly identified etiologic agent of commmunity-acquired pneumonia, it is surpassed by P. carinii in the HIV-infected patient population. The apparent decline in the frequency of S. pneumoniae in our series presumably reflects administration of antibiotics prior to procurement of sputum culture. The paucity of atypical agents in this study support the current American Thoracic Society guidelines for selective use of macrolide therapy in immunocompetent adults hospitalized with community-acquired pneumonia. The causes of community-acquired pneumonia in hospitalized adults in the 1990s reflects a changing patient population, in whom a majority may be immunosuppressed by HIV infection, transplantation, malignancy, or immunosuppressive drug regimens. C1 JOHNS HOPKINS MED INST,DEPT MED,BALTIMORE,MD 21205. UNIV MARYLAND,DIV INFECT DIS,BALTIMORE,MD 21201. MARYLAND DEPT HLTH & MENTAL HYG,ADM LABS,BALTIMORE,MD. GREATER BALTIMORE MED CTR,DEPT MED,BALTIMORE,MD 21204. NIAID,BETHESDA,MD 20892. UNIV COLORADO,HLTH SCI CTR,DIV PULM SCI & CRIT CARE MED,DENVER,CO. RI Gaydos, Charlotte/E-9937-2010; Quinn, Thomas/A-2494-2010 NR 34 TC 145 Z9 152 U1 2 U2 2 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD OCT PY 1995 VL 152 IS 4 BP 1309 EP 1315 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA RX731 UT WOS:A1995RX73100026 PM 7551387 ER PT J AU LINDROOS, PM COIN, PG OSORNIOVARGAS, AR BONNER, JC AF LINDROOS, PM COIN, PG OSORNIOVARGAS, AR BONNER, JC TI INTERLEUKIN-1-BETA (IL-1-BETA) AND THE IL-1-BETA-ALPHA(2)-MACROGLOBULIN COMPLEX UP-REGULATE THE PLATELET-DERIVED GROWTH-FACTOR ALPHA-RECEPTOR ON RAT PULMONARY FIBROBLASTS SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID SMOOTH-MUSCLE CELLS; OSTEOBLAST-ENRICHED CULTURES; FACTOR-BB ISOFORMS; ALVEOLAR MACROPHAGES; FACTOR PDGF; ALPHA-2-MACROGLOBULIN RECEPTOR; LUNG FIBROBLASTS; HIGH-AFFINITY; UP-REGULATION; RECOGNIZED ALPHA-2-MACROGLOBULIN AB Fibroblasts are the primary proliferating cell type in pulmonary fibrosis. We previously showed that inorganic, fibrogenic particles alter the platelet-derived growth factor (PDGF) receptor system on rat lung fibroblasts (Bonner, J. C., et al, 1993, J. Clin. Invest 92:425-430). In lung fibroblasts, PDGF is the most potent proliferative cytokine, and the responses to PDGF isoforms depend on the relative amounts of two PDGF receptors (PDGF-R alpha and PDGF-R beta). Interleukin 1 beta (IL-1 beta) production by lung macrophages is increased following exposure to fibrogenic particles. We have examined the role of IL-1 beta in regulating the lung fibroblast PDGF receptor system. IL-1 beta induced a 10-fold increase in the number of binding sites for [I-125]PDGF-AA, caused a 2-fold increase in affinity of [I-125]PDGF-AB, but it had no effect on [I-125]PDGF-BB binding. PDGF-R alpha gene expression was increased 5-fold after 4 h of IL-1 beta treatment. IL-1 beta increased the proliferative and chemotactic response to PDGF isoforms in the following order of potency: AA > AB > BB. IL-1 beta was tested for its ability to cause increased [I-125]PDGF-AA binding when complexed to its binding protein, alpha(2)-macroglobulin (alpha(2)M). IL-1 beta bound covalently to fast methylamine-activated alpha(2)M (alpha(2)M-MA). IL-1 beta-alpha(2)M-MA or alpha(2)M-MA alone possessed minimal activity for inducing an increase in [I-125]PDGF-AA binding. However, treatment of the IL-1 beta-alpha(2)M-MA complex with thioredoxin, which released bioactive IL-1 beta that was covalently bound to alpha(2)M, maximally increased [I-125]PDGF-AA binding to the same extent as free IL-1 beta. These results indicate that the fibroblast response to PDGF isoforms is modulated by a complex interaction involving IL-1 beta, alpha(2)M, and thioredoxin, all of which are produced in vivo by activated macrophages. C1 NIEHS, PULM PATHOBIOL LAB, RES TRIANGLE PK, NC 27709 USA. DEPT VET AFFAIRS MED CTR, DURHAM, NC USA. INST CANCEROL, DIV INVEST BASICA, MEXICO CITY, DF, MEXICO. RI Osornio Vargas, Alvaro/D-4012-2009; Osornio Vargas, Alvaro/B-4645-2010 OI Osornio Vargas, Alvaro/0000-0001-8287-7102 NR 64 TC 49 Z9 50 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 OCT PY 1995 VL 13 IS 4 BP 455 EP 465 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA RY419 UT WOS:A1995RY41900010 PM 7546776 ER PT J AU BONNER, JC BADGETT, A LINDROOS, PM OSORNIOVARGAS, AR AF BONNER, JC BADGETT, A LINDROOS, PM OSORNIOVARGAS, AR TI TRANSFORMING GROWTH-FACTOR-BETA-1 DOWN-REGULATES THE PLATELET-DERIVED GROWTH-FACTOR ALPHA-RECEPTOR SUBTYPE ON HUMAN LUNG FIBROBLASTS IN-VITRO SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID IDIOPATHIC PULMONARY FIBROSIS; SMOOTH-MUSCLE CELLS; CONNECTIVE-TISSUE CELLS; FACTOR PDGF; UP-REGULATION; ALVEOLAR MACROPHAGES; GENE-EXPRESSION; MESSENGER-RNA; TGF-BETA; IMMUNOHISTOCHEMICAL LOCALIZATION AB Fibroblasts are the central target cell in pulmonary fibrotic diseases, and their proliferation is mediated largely by platelet-derived growth factor (PDGF) isoforms secreted by activated lung macrophages. Several other macrophage-derived cytokines that are increased during fibrogenesis, including interleukin-1 beta and transforming growth factor-beta 1 (TGF-beta 1), could potentially modulate the mitogenic and chemotactic activity of PDGF by altering the expression of cell-surface PDGF receptors on fibroblasts, The PDGF receptor system on fibroblasts from a variety of tissues shows heterogeneous responses to TGF-beta 1. Lung fibroblasts have not been investigated in this regard. TGF-beta 1 downregulated the gene expression of the 6.5 kb PDGF-alpha receptor (PDGF-R alpha) transcript in normal human lung fibroblasts in a concentration dependent fashion that was maximal at 3 ng/ml TGF-beta 1; this corresponded with a decrease in cell-surface PDGF-R alpha as measured by radioligand binding assays using [I-125]PDGF-AA. The TGF-beta 1-induced downregulation of the PDGF-R alpha gene was rapid (maximal suppression by 2 h post-treatment) and preceded the decrease in cell-surface alpha-receptor (maximal reduction by 6 h post-treatment). TGF-beta 1 treatment did not alter the rate of PDGF-R alpha mRNA degradation following the inhibition of transcription using actinomycin D, indicating that TGF-beta 1 increases PDGF-R alpha transcription. Scatchard analysis of saturation binding data showed that TGF-beta 1 decreased the number of [I-125]PDGF-AA binding sites 5-fold without affecting receptor affinity. [I-125]PDGF-AB binding sites were downregulated approximately 25%, and the number of [I-125]PDGF-BB binding sites was not changed by TGF-beta 1 treatment, indicating that the PDGF-beta receptor was not affected, TGF-beta 1 reduced the mitogenic and chemotactic response to PDGF-AA by > 90%, whereas these biologic response to PDGF-AB and PDGF-BB were inhibited 50% to 80%. The proliferative and chemotactic responses of fibroblasts during tissue remodeling or during lung fibrosis are likely controlled by a complex network involving PDGF isoforms and cytokines that modify the PDGF receptor system. C1 NATL CANC INST,DIV CLIN INVEST,MEXICO CITY,DF,MEXICO. RP BONNER, JC (reprint author), NIEHS,PULM PATHOBIOL LAB,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Osornio Vargas, Alvaro/D-4012-2009; Osornio Vargas, Alvaro/B-4645-2010 OI Osornio Vargas, Alvaro/0000-0001-8287-7102 NR 59 TC 48 Z9 50 U1 0 U2 3 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 OCT PY 1995 VL 13 IS 4 BP 496 EP 505 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA RY419 UT WOS:A1995RY41900014 PM 7546780 ER PT J AU LEWIS, EN TREADO, PJ REEDER, RC STORY, GM DOWREY, AE MARCOTT, C LEVIN, IW AF LEWIS, EN TREADO, PJ REEDER, RC STORY, GM DOWREY, AE MARCOTT, C LEVIN, IW TI FOURIER-TRANSFORM SPECTROSCOPIC IMAGING USING AN INFRARED FOCAL-PLANE ARRAY DETECTOR SO ANALYTICAL CHEMISTRY LA English DT Article ID RAMAN; MICROSCOPE AB A powerful new mid-infrared spectroscopic chemical imaging technique combining step-scan Fourier transform Michelson interferometry with indium antimonide focal-plane array (FPA) image detection is described. The coupling of an infrared focal-plane array detector to an interferometer provides an instrumental multiplex/multichannel advantage. Specifically, the multiple detector elements enable spectra at all pixels to be collected simultaneously, while the interferometer portion of the system allows all the spectral frequencies to be measured concurrently. With this method of mid-infrared spectroscopic imaging, the fidelity of the generated spectral images is limited only by the number of pixels on the FPA detector, and only several seconds of staring time is required for spectral image acquisition. This novel, high-definition technique represents the future of infrared chemical imaging analysis, a new discipline within the chemical and material sciences, which combines the capability of spectroscopy for molecular analysis with the power of visualization. In particular, chemical imaging is broadly applicable for noninvasive, molecular characterization of heterogeneous materials, since all solid-state materials exhibit chemical nonuniformity that exists either by design or by development during the course of material preparation or fabrication. Imaging, employing Raman and infrared spectroscopy, allows the precise characterization of the chemical composition, domain structure, and chemical architecture of a variety of substances. This information is often crucial to a wide range of activities, extending from the fabrication of new materials to a basic understanding of biological samples. In this study, step-scan imaging principles, instrument design details, and infrared chemical imaging results are presented. Since the prospect of performing high-resolution and high-definition mid-infrared chemical imaging very rapidly has been achieved with the step-scan approach, the implications for the chemical analysis of materials are many and varied. C1 UNIV PITTSBURGH,DEPT CHEM,PITTSBURGH,PA 15260. PROCTER & GAMBLE CO,MIAMI VALLEY LABS,CINCINNATI,OH 45253. RP LEWIS, EN (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 32 TC 309 Z9 310 U1 6 U2 35 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0003-2700 J9 ANAL CHEM JI Anal. Chem. PD OCT 1 PY 1995 VL 67 IS 19 BP 3377 EP 3381 DI 10.1021/ac00115a003 PG 5 WC Chemistry, Analytical SC Chemistry GA RX222 UT WOS:A1995RX22200007 PM 8686889 ER PT J AU Pettit, GR Srirangam, JK Barkoczy, J Williams, MD Durkin, KPM Boyd, MR Bai, RL Hamel, E Schmidt, JM Chapuis, JC AF Pettit, GR Srirangam, JK Barkoczy, J Williams, MD Durkin, KPM Boyd, MR Bai, RL Hamel, E Schmidt, JM Chapuis, JC TI Antineoplastic agents .337. Synthesis of dolastatin 10 structural modifications SO ANTI-CANCER DRUG DESIGN LA English DT Article DE antineoplastic agents; dolastatin 10; structural modifications ID LEUKEMIA-CELL LINES AB New structural modifications of the marine shell-less mollusk peptide constituent dolastatin 10 (1) have been synthesized, and evaluated against a variety of cancer cell lines and for their ability to inhibit tubulin polymerization. A number of useful structure-activity relationships were uncovered. The most important observation was that the dolaphenine unit of dolastatin 10 could be satisfactorily replaced with a phenethylamine. Peptide 11C, designated auristatin PE, was found to exhibit inhibition of cancer cell growth and tubulin assembly comparable to that of dolastatin 10. C1 ARIZONA STATE UNIV, DEPT CHEM, TEMPE, AZ 85287 USA. NCI, FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT, DTP,LAB DRUG DISCOVERY RES & DEV, FREDERICK, MD 21702 USA. NCI, DIV CANC TREATMENT, DEV THERAPEUT PROGRAM, MOLEC PHARMACOL LAB, BETHESDA, MD 20892 USA. RP Pettit, GR (reprint author), ARIZONA STATE UNIV, CANC RES INST, BOX 871604, TEMPE, AZ 85287 USA. FU NCI NIH HHS [CA44344-01-07] NR 34 TC 59 Z9 62 U1 1 U2 17 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0266-9536 J9 ANTI-CANCER DRUG DES JI Anti-Cancer Drug Des. PD OCT PY 1995 VL 10 IS 7 BP 529 EP 544 PG 16 WC Biochemistry & Molecular Biology; Oncology; Chemistry, Medicinal; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy GA TL722 UT WOS:A1995TL72200002 PM 7495477 ER PT J AU CHOKEKIJCHAI, S KOJIMA, E ANDERSON, S NOMIZU, M TANAKA, M MACHIDA, M DATE, T TOYOTA, K ISHIDA, S WATANABE, K YOSHIOKA, H ROLLER, PP MURAKAMI, K MITSUYA, H AF CHOKEKIJCHAI, S KOJIMA, E ANDERSON, S NOMIZU, M TANAKA, M MACHIDA, M DATE, T TOYOTA, K ISHIDA, S WATANABE, K YOSHIOKA, H ROLLER, PP MURAKAMI, K MITSUYA, H TI NP-06 - A NOVEL ANTI-HUMAN-IMMUNODEFICIENCY-VIRUS POLYPEPTIDE PRODUCED BY A STREPTOMYCES SPECIES SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID HIV SYNTHETIC PEPTIDE AB From an extract of a Streptomyces culture, we identified and purified a novel compound, NP-06, which is active against human immunodeficiency virus (HIV) in vitro. Analyses indicate that NP-06 is a hydrophobic 21-mer oligopeptide, N terminally cyclized through the side chain of Asp-9, containing two intramolecular cystine linkages with a molecular weight of 2,163.4. The 50% inhibitory concentrations were 2.8 and 1.3 mu M when NP-06 was tested for in vitro anti-HIV-1 activity in ATH8 cells and phytohemagglutinin activated peripheral blood mononuclear cells, respectively. NP-06 appears to block the early stage of HIV-1 infection, most likely at the stage of virus-cell fusion. C1 NCI,DIV CANC TREATMENT,MED BRANCH,EXPTL RETROVIRUS SECT,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,MED CHEM LAB,BETHESDA,MD 20892. NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NIPPON PAPER IND CO LTD,BIOSCI RES LAB,IWAKUNI,JAPAN. NR 12 TC 23 Z9 23 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 OCT PY 1995 VL 39 IS 10 BP 2345 EP 2347 PG 3 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA RX469 UT WOS:A1995RX46900034 PM 8619594 ER PT J AU KAVLICK, MF SHIRASAKA, T KOJIMA, E PLUDA, JM HUI, F YARCHOAN, R MITSUYA, H AF KAVLICK, MF SHIRASAKA, T KOJIMA, E PLUDA, JM HUI, F YARCHOAN, R MITSUYA, H TI GENOTYPIC AND PHENOTYPIC CHARACTERIZATION OF HIV-1 ISOLATED FROM PATIENTS RECEIVING (-)-2',3'-DIDEOXY-3'-THIACYTIDINE SO ANTIVIRAL RESEARCH LA English DT Article DE HUMAN IMMUNODEFICIENCY VIRUS TYPE 1 (HIV-1); (-)-2',3'-DIDEOXY-3'-THIACYTIDINE (3TC); DRUG RESISTANCE ID IMMUNODEFICIENCY-VIRUS TYPE-1; HIGH-LEVEL RESISTANCE; REVERSE-TRANSCRIPTASE; 2'-DEOXY-3'-THIACYTIDINE BCH-189; REPLICATION INVITRO; ZIDOVUDINE AZT; 2',3'-DIDEOXY-3'-THIACYTIDINE; SENSITIVITY; MUTATION; 2',3'-DIDEOXYCYTIDINE AB We attempted to determine whether HIV-1 developed resistance to (-)-2',3'-dideoxy-3'-thiacytidine ((-)-3TC or 3TC, lamivudine) in patients with advanced human immunodeficiency virus type 1 (HIV-1) infection during therapy with 3TC. Genotypic analysis of HIV-1 strains isolated from 6 patients receiving 3TC revealed that as early as 2 months of therapy, HIV-1 developed a Met to Val amino acid substitution at codon 184 (Met(184) --> Val) in the reverse transcriptase-coding region of the pol gene. A detailed study of a series of HIV-1 strains isolated from a patient demonstrated that Met at codon 184 was first substituted with lle by 2 weeks of 3TC therapy, followed by the substitution with Val by 8 weeks. All HIV-1 strains with the Met(184) --> Val substitution were profoundly less susceptible to 3TC (1800- to 5500-fold decreased sensitivity) as compared to pretherapy virus strains, These strains were also moderately less sensitive to 2',3'-dideoxycytidine (4.5- to 9-fold), but more sensitive to 3'-azido-2',3'-dideoxythymidine (2- to 14-fold). A decrease in viremia levels and an increase in CD4 counts were observed early in therapy; however, these changes were only transient. Our data suggest that reversal of such beneficial changes is associated with the Met(184) --> Val substitution of the pol gene of HIV-1. The data also suggest that 3TC, as a single agent, may induce virologic and immunologic improvement in patients with advanced HIV-1 infection, but only transiently. C1 NCI,MED BRANCH,EXPTL RETROVIROL SECT,BETHESDA,MD 20892. NCI,MED BRANCH,RETROVIRAL DIS SECT,BETHESDA,MD 20892. NR 37 TC 67 Z9 71 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 OCT PY 1995 VL 28 IS 2 BP 133 EP 146 DI 10.1016/0166-3542(95)00044-M PG 14 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA TB328 UT WOS:A1995TB32800004 PM 8585767 ER PT J AU YU, H SIPES, JM CASHEL, J BAKOS, MA GOLDBLUM, RM ROBERTS, DD AF YU, H SIPES, JM CASHEL, J BAKOS, MA GOLDBLUM, RM ROBERTS, DD TI RECOGNITION OF TYPE-1 CHAIN OLIGOSACCHARIDES AND LACTO-SERIES GLYCOLIPIDS BY AN ANTIBODY TO HUMAN SECRETORY COMPONENT SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID MONOCLONAL-ANTIBODY; HUMAN MECONIUM; HUMAN-MILK; ANTIGEN; CANCER; SERUM AB Binding of the mouse IgM antibody 6C4 is lost after treatment of human free secretory component with peptide N-glycosidase F (Bakos et al. (1991) J. Immunol. 146, 162-168) or periodate, suggesting that asparagine-linked oligosaccharides contain the epitope recognized by this antibody, Inhibition of antibody binding to free secretory component by milk oligosaccharides established that lacto-N-tetraose is the minimum structure recognized by the antibody, but larger oligosaccharides with terminal Gal beta 1-3GlcNAc sequences bind with much higher affinity, Antibody binding is enhanced by substitution with the Lewis Fuc alpha 1-4 and is inhibited by Fuc alpha 1-2Gal substitution, Free secretory component, however, does not bind other antibodies that recognize Le(a) or Le(b) oligosaccharides, and binding is lost after digestion with a beta-galactosidase that cleaves Gal beta 1-3 linkages but not after digestion with alpha-L-fucosidase. Therefore, the major epitope recognized by 6C4 on free secretory component is probably not an asparagine-linked Le(a) oligosaccharide, The antibody also binds to human milk lactoferrin, some human mucins, and lacto-series glycolipids including III4 alpha Fuc-lactotetraosyl ceramide and lactotetraosyl ceramide, Based on affinity chromatography of oligosaccharides released from free secretory component, the epitope recognized by antibody 6C4 is present on approximately 3.5% of the asparagine-linked oligosaccharides. (C) 1995 Academic Press, Inc. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. UNIV TEXAS,MED BRANCH,DEPT PEDIAT,GALVESTON,TX 77550. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 21 TC 1 Z9 1 U1 0 U2 1 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 OCT 1 PY 1995 VL 322 IS 2 BP 299 EP 305 DI 10.1006/abbi.1995.1467 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RY950 UT WOS:A1995RY95000001 PM 7574700 ER PT J AU SAWAKI, K BAUM, BJ ROTH, GS AMBUDKAR, IS AF SAWAKI, K BAUM, BJ ROTH, GS AMBUDKAR, IS TI DECREASED M(3)-MUSCARINIC AND ALPHA(1)-ADRENERGIC RECEPTOR STIMULATION OF PIP2 HYDROLYSIS IN PAROTID-GLAND MEMBRANES FROM AGED RATS - DEFECT IN ACTIVATION OF G(ALPHA-Q/11) SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE MUSCARINIC RECEPTOR; ALPHA(1)-ADRENERGIC RECEPTOR; PHOSPHOLIPASE C; G(ALPHA-Q/11); RAT PAROTID GLANDS; AGING ID PHOSPHOLIPASE-C; ACINAR-CELLS; PROTEINS; RESPONSIVENESS; SECRETION AB m(3)-Muscarinic cholinergic receptor (m(3)-AChR) and alpha(1)-adrenergic receptor (alpha(1)-AR) stimulation of phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis (by a PIP2-specific phospholipase C, PLC) in rat parotid gland membranes is mediated via activation of alpha subunits of the G(q/11) family of G-proteins, This study examines m(3)-AChR and alpha(1)-AR stimulation of PIP2 hydrolysis in membranes isolated from parotid glands of old (24 months) and young (3 months) rats (old and young rat membranes), Old rat membranes exhibited reduced stimulation of PIP2 hydrolysis in response to the addition of guanosine-5'-O-(3-thiotrisphosphate) (GTP gamma S) alone or GTP gamma S plus either carbachol (m(3)-AChR agonist) or epinephrine (alpha(1)-AR agonist), This reduction in receptor-stimulated PIP2 hydrolysis was not due to a decrease in PLC activity per se since cholate-solubilized PLC activity was similar in old and young rat membranes, Additionally, these membranes exhibited comparable, immunologically detectable, levels of PLC beta(3), G alpha(q/11), and G(beta). In the presence of 10 mu M AlCl3 and 10 mM NaF, stimulation of PIP2 hydrolysis in both old and young rat membranes was similar, Preincubation of membranes from old rats with GTP gamma S induced a time-dependent increase in the rate of PIP2 hydrolysis and, with 20 min preincubation, the rates of hydrolysis in old and young rat membranes were not statistically different, In aggregate, these data indicate that there is a defect in the activation of G(alpha q/11) in parotid gland membranes from old rats. (C) 1995 Academic Press, Inc. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,SECRETARY PHYSIOL SECT,BETHESDA,MD 20892. NIA,GERONTOL RES CTR,MOLEC PHYSIOL & GENET SECT,BALTIMORE,MD 21224. NR 27 TC 10 Z9 10 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 OCT 1 PY 1995 VL 322 IS 2 BP 319 EP 326 DI 10.1006/abbi.1995.1470 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RY950 UT WOS:A1995RY95000004 PM 7574703 ER PT J AU HAMEL, E VAUGHNS, J GETAHUN, Z JOHNSON, R LIN, CM AF HAMEL, E VAUGHNS, J GETAHUN, Z JOHNSON, R LIN, CM TI INTERACTIONS OF TUBULIN WITH GUANINE-NUCLEOTIDES THAT HAVE PACLITAXEL-LIKE EFFECTS ON TUBULIN ASSEMBLY - 2',3'-DIDEOXYGUANOSINE 5'-[ALPHA,BETA-METHYLENE]TRIPHOSPHATE GUANOINE 5'-[ALPHA,BETA-METHYLENE]TRIPHOSPHATE, AND 2',3'-DIDEOXYGUANOSINE 5'-TRIPHOSPHATE SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID MICROTUBULE-ASSOCIATED PROTEINS; GUANOSINE 5'-TRIPHOSPHATE; GTP HYDROLYSIS; 5'-GUANYLYL IMIDODIPHOSPHATE; POLYMERIZATION; MECHANISM; INVITRO; TAXOL; SITE; BINDING AB Despite reduced affinity for the exchangeable nucleotide binding site of tubulin relative to GTP, 2',3'-dideoxyguanosine 5'-triphosphate (ddGTP) and guanosine 5'-[alpha,beta-methylene]triphosphate [pp(CH2)pG] are highly active in promoting tubulin assembly. Like the antimitotic drug paclitaxel, which interacts with the same part of the beta-tubulin molecule as exchangeable-site GTP, both analogs enhance nucleation reactions and promote formation of hyperstable polymers. These observations led us to synthesize the doubly modified analog 2',3'-dideoxyguanosine 5'-[alpha,beta-methylene]triphosphate [pp(CH2)pddG], We compared the effects of pp(CH2)pddG to those of ddGTP, pp(CH,)pG, and the three-cognate diphosphates in their interactions with tubulin. We found that pp(CH2)pddG was as active as ddGTP and pp(CH2)pG in supporting formation of polymer of increased stability, but that its affinity for the exchangeable site was lower than that of both singly modified analogs [relative affinities for the exchangeable site for pp(CH2)pddG:ddGTP:pp(CH2)pG:GTP were 1:2.8:10:273]. There were significant differences in interactions of each of the three analogs with tubulin, and the behavior of pp(CH2)pddG was intermediate between that of ddGTP and that of pp(CH2)pG. Most importantly, under the reaction conditions studied, with heat-treated microtubule-associated proteins (MAPs) ddGTP-induced polymer consisted of short microtubules, while polymer formed with both pp(CH2)pddG and pp(CH2)pG consisted of short sheets. On the other hand, assembly without MAPs had a fivefold lower critical concentration for tubulin with ddGTP and pp(CH2)pddG (0.5 mg/ml) than with pp(CH2)pG (2.5 mg/ml). De novo assembly, which occurs readily with 2',3'-dideoxyguanosine 5'-diphosphate, was not observed with either alpha,beta-methylenediphosphate GDP analog. (C) 1995 Academic Press, Inc. RP HAMEL, E (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BLDG 37,ROOM 5C25,BETHESDA,MD 20892, USA. NR 53 TC 3 Z9 3 U1 0 U2 3 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 OCT 1 PY 1995 VL 322 IS 2 BP 486 EP 499 DI 10.1006/abbi.1995.1492 PG 14 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA RY950 UT WOS:A1995RY95000026 PM 7574725 ER PT J AU ISHIDAYAMAMOTO, A IIZUKA, H MANABE, M OGUIN, WM HOHL, D KARTASOVA, T KUROKI, T ROOP, DR EADY, RAJ AF ISHIDAYAMAMOTO, A IIZUKA, H MANABE, M OGUIN, WM HOHL, D KARTASOVA, T KUROKI, T ROOP, DR EADY, RAJ TI ALTERED DISTRIBUTION OF KERATINIZATION MARKERS IN EPIDERMOLYTIC HYPERKERATOSIS SO ARCHIVES OF DERMATOLOGICAL RESEARCH LA English DT Article DE BULLOUS CONGENITAL ICHTHYOSIFORM ERYTHRODERMA; INVOLUCRIN; SPRR1; LORICRIN; TRICHOHYALIN ID CORNIFIED CELL-ENVELOPE; CROSS-LINKED ENVELOPE; EXPRESSION; INVOLUCRIN; TRICHOHYALIN; PROTEINS; LORICRIN; SKIN; KERATINOCYTES; LOCALIZATION AB Epidermolytic hyperkeratosis (EH) is a genetic disorder of keratins associated with epidermal differentiation. Affected individuals carry gene mutations for conserved sequences of keratins K1 or K10. The structural alterations of tonofilaments in EH seem to be a direct consequence of the keratin gene mutations, EH epidermis, however, shows many other unexplained abnormalities including acanthosis, hypergranulosis, and hyperkeratosis. To further elucidate the pathogenetic mechanism of EH, we studied distribution patterns of other keratinization-associated molecules including involucrin, small proline-rich protein (SPRR) 1, loricrin and trichohyalin in the skin of four patients by light and electron microscopic immunohistochemistry in conjunction with conventional transmission electron microscopy. The middle to upper epidermal cells showed moderate to strong immunoreactivities to involucrin, SPRR1 and loricrin antibodies. Both intracellular staining and cell peripheral staining was seen for involucrin and SPRR1 antibodies. Loricrin labelling was prematurely associated with the plasma membrane of granular cells, possibly relating to abnormal keratin filament aggregation and cellular vacuolization. Some loricrin labelling was localized on the keratin aggregates, suggesting intermolecular associations between keratin and loricrin. Trichohyalin, hardly detectable in normal epidermis, was present in some granular and cornified cells in EH in association with keratin filaments, suggesting that it may function as an intermediate filament-associated protein. While cornified cell envelopes were intensely labelled only with loricrin antibodies in normal skin, they were immunoreactive to involucrin, SPRR1 and loricrin antibodies in EH. Sequential change in electron density of the cornified cell envelopes, a constant feature in normal skin, was often absent in EH. These results suggest an altered assembly process of cornified cell envelopes in EH. C1 ST THOMAS HOSP,ST JOHNS INST DERMATOL,DEPT CELL PATHOL,LONDON,ENGLAND. JUNTENDO UNIV,SCH MED,DEPT DERMATOL,TOKYO 113,JAPAN. NYU,SCH MED,DEPT DERMATOL,EPITHELIAL BIOL UNIT,NEW YORK,NY. UNIV LAUSANNE HOSP,DEPT DERMATOL,LAUSANNE,SWITZERLAND. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. UNIV TOKYO,INST MED SCI,DEPT CANC CELL RES,TOKYO,JAPAN. BAYLOR COLL MED,DEPT CELL BIOL & DERMATOL,HOUSTON,TX. RP ISHIDAYAMAMOTO, A (reprint author), ASAHIKAWA MED COLL,DEPT DERMATOL,NISHIKAGURA 4-5-3-11,ASAHIKAWA,HOKKAIDO 078,JAPAN. RI Kuroki, Toshio/A-9500-2011 OI Kuroki, Toshio/0000-0001-6369-4351 NR 37 TC 18 Z9 18 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-3696 J9 ARCH DERMATOL RES JI Arch. Dermatol. Res. PD OCT PY 1995 VL 287 IS 8 BP 705 EP 711 DI 10.1007/BF01105793 PG 7 WC Dermatology SC Dermatology GA RZ165 UT WOS:A1995RZ16500002 PM 8554380 ER PT J AU TSAI, GC PASSANI, LA SLUSHER, BS CARTER, R BAER, L KLEINMAN, JE COYLE, JT AF TSAI, GC PASSANI, LA SLUSHER, BS CARTER, R BAER, L KLEINMAN, JE COYLE, JT TI ABNORMAL EXCITATORY NEUROTRANSMITTER METABOLISM IN SCHIZOPHRENIC BRAINS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PIG CEREBELLAR SLICES; N-ACETYLASPARTYLGLUTAMATE; AMINO-ACIDS; MK-801 BINDING; HUNTINGTONS-DISEASE; PURKINJE-CELLS; KAINIC ACID; RAT-BRAIN; GLUTAMATE; RECEPTOR AB Background: Schizophrenia has been hypothesized to be caused by a hypofunction of glutamatergic neurons. Findings of reduced concentrations of glutamate in the cerebrospinal fluid of patients with schizophrenia and the ability of glutamate-receptor antagonists to cause psychotic symptoms lend support to this hypothesis. N-acetylaspartylglutamate (NAAG), a neuropeptide that is highly concentrated in glutamatergic neurons, antagonizes the effects of glutamate at N-methyl-D-aspartate receptors. Moreover, NAAG is cleaved to glutamate and N-acetylaspartate by a specific peptidase, N-acetyl-alpha-linked acidic dipeptidase (NAALADase). To test the glutamatergic hypothesis of schizophrenia, we studied the NAAG-related glutamatergic variables in postmortem brains from patients with schizophrenia, neuroleptic-treated controls, and normal individuals, with particular emphasis on the prefrontal cortex and hippocampus. Method: Different regions of frozen brain tissue from three different groups (patients with schizophrenia, neuroleptic-treated controls, and normal controls) were assayed to determine levels of NAAG, N-acetylaspartate, NAALADase, and several amino acids, including aspartate and glutamate. Results: Our study demonstrates alterations in brain levels of aspartate, glutamate, and NAAG and in NAALADase activity. Levels of NAAG were increased and NAALADase activity and glutamate levels were decreased in the schizophrenic brains. Notably, the changes in NAAG level and NAALADase activity in schizophrenic brains were more selective than those for aspartate and glutamate. In neuroleptic-treated control brains, levels of aspartate, glutamate, and glycine were found to be increased. Conclusions: The changes in levels of aspartate, glutamate, NAAG, and NAALADase are prominent in the prefrontal and hippocampal regions, where previous neuropathological studies of schizophrenic brains demonstrate consistent changes. These findings support the hypothesis that schizophrenia results from a hypofunction of certain glutamatergic neuronal systems. They also suggest that the therapeutic efficacy of neuroleptics may be related to increased glutamatergic activity. C1 HARVARD UNIV,SCH MED,MOLEC & DEV NEUROSCI LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. FU NIMH NIH HHS [R01 MH51290-01] NR 46 TC 323 Z9 329 U1 5 U2 15 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD OCT PY 1995 VL 52 IS 10 BP 829 EP 836 PG 8 WC Psychiatry SC Psychiatry GA RY979 UT WOS:A1995RY97900005 PM 7575102 ER EF