FN Thomson Reuters Web of Science™ VR 1.0 PT J AU LEE, YB WOLFF, EC PARK, MH FOLK, JE AF LEE, YB WOLFF, EC PARK, MH FOLK, JE TI DEVELOPMENT OF INHIBITORS OF DEOXYHYPUSINE SYNTHASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1347 EP A1347 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600727 ER PT J AU LEE, YH ALBERTA, IA GONZALEZ, FI WAXMAN, DI AF LEE, YH ALBERTA, IA GONZALEZ, FI WAXMAN, DI TI MULTIPLE, FUNCTIONAL DBP SITES ON THE PROMOTER OF THE CHOLESTEROL 7-ALPHA-HYDROXYLASE-P450 GENE PROMOTER SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1252 EP A1252 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600183 ER PT J AU LETEURTRE, F GUPTA, M KOHLHAGEN, G POMMIER, Y AF LETEURTRE, F GUPTA, M KOHLHAGEN, G POMMIER, Y TI MAPPING OF TOPOISOMERASE CLEAVAGE SITES IN THE HUMAN C-MYC PROTOONCOGENE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,DCT,DTP,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1272 EP A1272 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600291 ER PT J AU LEVY, DD PARRIS, CN JESSE, J SEIDMAN, MM AF LEVY, DD PARRIS, CN JESSE, J SEIDMAN, MM TI EFFECT OF SEQUENCE CONTEXT ON THE INTENSITY OF UV-INDUCED MUTATION HOTSPOTS IN SHUTTLE VECTOR PLASMIDS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. LIFE TECHNOL INC,GAITHERSBURG,MD. OTSUKA PHARMACEUT CO LTD,ROCKVILLE,MD 20850. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1332 EP A1332 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600638 ER PT J AU LIU, K MILES, HT FRAZIER, J SASISEKHARAN, V AF LIU, K MILES, HT FRAZIER, J SASISEKHARAN, V TI CC+ CONSTRAINED PARALLEL DOUBLE HELICES WITH DONOHUE (REVERSE WATSON-CRICK) BASE-PAIRING SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDKD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1266 EP A1266 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600259 ER PT J AU LUBAS, WA HANOVER, J AF LUBAS, WA HANOVER, J TI GLYCOSYLATION OF THE NUCLEAR-PORE PROTEIN-P62 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1425 EP A1425 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601183 ER PT J AU LUBET, RA SINCLAIR, PR SINCLAIR, JF NIMS, RW AF LUBET, RA SINCLAIR, PR SINCLAIR, JF NIMS, RW TI DOSE-RESPONSES FOR CYP2B INDUCTION IN RAT-LIVER AND RAT HEPATOCYTE CULTURES - SIMILARITIES AND IMPLICATIONS FOR MECHANISTIC STUDIES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FCRDC,LCC,FREDERICK,MD 21702. VA,WHITE RIVER JCT,VT 05009. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,HANOVER,NH 03756. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1250 EP A1250 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600171 ER PT J AU MALINOWSKI, N CYSYK, RL AUGUST, EM AF MALINOWSKI, N CYSYK, RL AUGUST, EM TI A RAPID AND SENSITIVE PRECIPITATION ASSAY FOR HYALURONIC-ACID SYNTHETASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1291 EP A1291 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600405 ER PT J AU MASON, MM LEE, E WESTPHAL, H REITMAN, M AF MASON, MM LEE, E WESTPHAL, H REITMAN, M TI DEVELOPMENTAL REGULATION OF THE COMPLETE CHICKEN BETA-GLOBIN CLUSTER IN TRANSGENIC MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,DIABET BRANCH,BETHESDA,MD 20892. NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1335 EP A1335 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600657 ER PT J AU MAZUMDER, A COONEY, D AGBARIA, R GUPTA, M POMMIER, Y AF MAZUMDER, A COONEY, D AGBARIA, R GUPTA, M POMMIER, Y TI INHIBITION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INTEGRASE BY 3'-AZIDO-2',3'-DIDEOXYTHYMIDYLATE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,DCT,DTP,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NCI,DCT,DTP,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1468 EP A1468 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601431 ER PT J AU MERTA, A AKSAMIT, R CANTONI, GL AF MERTA, A AKSAMIT, R CANTONI, GL TI RAT S-ADENOSYLHOMOCYSTEINE GENE STRUCTURE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1441 EP A1441 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601276 ER PT J AU MOODY, TW CHUNG, P PARK, M JAKOWLEW, S BIRRER, M DRAOUI, M AF MOODY, TW CHUNG, P PARK, M JAKOWLEW, S BIRRER, M DRAOUI, M TI BOMBESIN STIMULATES C-FOS AND C-JUN GENE-EXPRESSION IN SMALL-CELL LUNG-CANCER CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,DEPT GENET,WASHINGTON,DC 20037. GEORGE WASHINGTON UNIV,MED CTR,DEPT BIOCHEM & MOLEC BIOL,WASHINGTON,DC 20037. NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD 20850. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1459 EP A1459 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601379 ER PT J AU MOUSSAVI, RS ITOH, K ADELSTEIN, RS AF MOUSSAVI, RS ITOH, K ADELSTEIN, RS TI BOVINE BRAIN MYOSIN HEAVY-CHAINS CAN BE PHOSPHORYLATED AT 2 DIFFERENT SITES BY PROTEIN-KINASE-C SO FASEB JOURNAL LA English DT Meeting Abstract ID ISOFORM C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1302 EP A1302 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600468 ER PT J AU MURATA, J ARESTAD, A LIOTTA, LA STRACKE, ML AF MURATA, J ARESTAD, A LIOTTA, LA STRACKE, ML TI PARTIAL CDNA CLONING OF THE AUTOCRINE CELL MOTILITY FACTOR, AUTOTAXIN (ATX) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1445 EP A1445 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601299 ER PT J AU NEGISHI, M DARDEN, TA IWASAKI, M SUEYOSHI, T DAVIS, DG PEDERSEN, LG AF NEGISHI, M DARDEN, TA IWASAKI, M SUEYOSHI, T DAVIS, DG PEDERSEN, LG TI GEOMETRICAL-FLEXIBILE BINDING POCKET AND INHERENT VERSATILITY OF P450 ACTIVITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1243 EP A1243 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600126 ER PT J AU NERURKAR, PV SCHUT, HAJ ANDERSON, LM SNYDERWINE, EG THORGEIRSSON, SS WEBER, WW RICE, JM LEVY, GN AF NERURKAR, PV SCHUT, HAJ ANDERSON, LM SNYDERWINE, EG THORGEIRSSON, SS WEBER, WW RICE, JM LEVY, GN TI INFLUENCE OF THE AH LOCUS ON MOUSE-LIVER IQ-DNA ADDUCTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21702. NCI,BETHESDA,MD 20892. MED COLL OHIO,TOLEDO,OH 43699. UNIV MICHIGAN,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1383 EP A1383 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600936 ER PT J AU NESTEROVA, M BUDILLON, A PEPE, S CERESETO, A CHOCHUNG, YS AF NESTEROVA, M BUDILLON, A PEPE, S CERESETO, A CHOCHUNG, YS TI INTRODUCING AN AUTOPHOSPHORYLATION SITE MUTATION IN THE RII-BETA-REGULATORY SUBUNIT OF CAMP-DEPENDENT PROTEIN-KINASE ABOLISHES THE RII-BETA-MEDIATED REGULATORY FUNCTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1328 EP A1328 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600617 ER PT J AU NETTO, LES CHAE, HZ RHEE, SG STADTMAN, ER AF NETTO, LES CHAE, HZ RHEE, SG STADTMAN, ER TI STUDIES ON THE ANTIOXIDANT MECHANISM OF TSA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1412 EP A1412 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601109 ER PT J AU NIEBYLSKI, CD HINES, KG SALEM, N AF NIEBYLSKI, CD HINES, KG SALEM, N TI THE EFFECT OF SN-2 ACYL-CHAIN LENGTH AND DEGREE OF UNSATURATION ON PHOSPHOLIPID-BILAYER STRUCTURE - A FLUORESCENCE ANISOTROPY AND DIFFERENTIAL SCANNING CALORIMETRY STUDY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,DICBR,MEMBRANE BIOCHEM & BIOPHYS LAB,FLUORESCENCE STUDIES SECT,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1450 EP A1450 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601329 ER PT J AU NIMS, RW BEEBE, LE MELLINI, DW UTERMAHLEN, WE THOMAS, PE LUBET, RA AF NIMS, RW BEEBE, LE MELLINI, DW UTERMAHLEN, WE THOMAS, PE LUBET, RA TI COMPARATIVE PHARMACODYNAMICS OF HEPATIC CYP2B INDUCTION IN MALE B6C3F1 MICE AND F344/NCR RATS EXPOSED TO PHENOBARBITAL OR TCPOBOP SO FASEB JOURNAL LA English DT Meeting Abstract C1 PRI DYNCORP,FCRDC,CSAL,FREDERICK,MD 21702. RUTGERS STATE UNIV,PISCATAWAY,NJ 08855. NCI,LCC,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1246 EP A1246 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600145 ER PT J AU NOH, DY BAE, YS LEE, KH HWANG, SC RHEE, SG AF NOH, DY BAE, YS LEE, KH HWANG, SC RHEE, SG TI DISTRIBUTION OF PHOSPHOLIPASE ISOZYMES IN RAT SKELETAL, SMOOTH, AND CARDIAC MUSCLES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1438 EP A1438 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601256 ER PT J AU NORFLUS, F YAMANAKA, S PROIA, RL AF NORFLUS, F YAMANAKA, S PROIA, RL TI CHARACTERIZATION OF THE PROMOTERS FOR THE BETA-HEXOSAMINIDASE GENES, HEXA AND HEXB SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. RI Proia, Richard/A-7908-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1276 EP A1276 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600316 ER PT J AU PANYUTIN, IG HSIEH, P AF PANYUTIN, IG HSIEH, P TI THE KINETICS OF SPONTANEOUS DNA BRANCH MIGRATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1395 EP A1395 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601010 ER PT J AU PARK, DJ KANG, SC LEE, HH YOO, OJ RHEE, SG AF PARK, DJ KANG, SC LEE, HH YOO, OJ RHEE, SG TI CLONING AND EXPRESSION OF A FULL CDNA FOR PHOSPHOLIPASE-C (PLC)-BETA-3 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1438 EP A1438 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601257 ER PT J AU PARK, MH WOLFF, EC LEE, YB FOLK, JE AF PARK, MH WOLFF, EC LEE, YB FOLK, JE TI INHIBITION OF THE GROWTH OF CHINESE-HAMSTER OVARY CELLS BY GUANYL DIAMINES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1310 EP A1310 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600519 ER PT J AU PAWLOSKY, R SALEM, N AF PAWLOSKY, R SALEM, N TI CHRONIC ALCOHOL EXPOSURE LEADS TO REMODELING OF CNS LIPIDS IN FELINES - LONG-CHAIN N-6 POLYUNSATURATES REPLACE DOCOSAHEXAENOIC ACID-22-6N3, IN THE BRAIN AND RETINA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1471 EP A1471 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601449 ER PT J AU PENNYBACKER, M PROIA, RL AF PENNYBACKER, M PROIA, RL TI LOCALIZATION OF SUBSTRATE-SPECIFICITY DOMAINS OF BETA-HEXOSAMINIDASE USING CHIMERIC ENZYME CONSTRUCTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. RI Proia, Richard/A-7908-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1347 EP A1347 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600730 ER PT J AU POSTNIKOV, Y LEHN, D ROBINSON, R FRIEDMAN, F SHILOACH, J BUSTIN, M AF POSTNIKOV, Y LEHN, D ROBINSON, R FRIEDMAN, F SHILOACH, J BUSTIN, M TI MUTATIONS IN THE DNA-BINDING DOMAIN OF CHROMOSOMAL PROTEIN HMG-14 ABOLISH THE COOPERATIVE BINDING TO NUCLEOSOMES SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1271 EP A1271 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600286 ER PT J AU PREUSCH, PC AF PREUSCH, PC TI REPORT OF THE NIGMS WORKSHOP ON THE STRUCTURAL BIOLOGY OF MEMBRANE-PROTEINS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIGMS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1450 EP A1450 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601328 ER PT J AU RANDAZZO, PA KAHN, RA AF RANDAZZO, PA KAHN, RA TI GTP HYDROLYSIS BY ADP-RIBOSYLATION FACTOR (ARF) IS DEPENDENT ON BOTH AN ARF GAP AND ACID PHOSPHOLIPIDS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1402 EP A1402 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601045 ER PT J AU RAO, PV HORWITZ, J ZIGLER, JS AF RAO, PV HORWITZ, J ZIGLER, JS TI STUDIES ON ALPHA-CRYSTALLIN CHAPERONE-LIKE ACTIVITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI, MECH OCULAR DIS LAB, BETHESDA, MD 20892 USA. UNIV CALIF LOS ANGELES, SCH MED, JULES STEIN EYE INST, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1354 EP A1354 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600768 ER PT J AU REMALEY, AT SCHUMACHER, UK BREWER, HB HOEG, JM AF REMALEY, AT SCHUMACHER, UK BREWER, HB HOEG, JM TI IDENTIFICATION OF NOVEL HEPATIC GENES REGULATED BY DIETARY-CHOLESTEROL BY A NONTARGETED GENE APPROACH SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1343 EP A1343 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600706 ER PT J AU RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B AF RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B TI BINDING OF HSP-70 AND ACTIN FROM EBV-TRANSFORMED HUMAN-B CELLS TO A UVEITOPATHOGENIC PEPTIDE OF BOVINE IRBP SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1353 EP A1353 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600764 ER PT J AU REX, J FURTH, P CHOE, WT BYRNE, J BAKER, C AF REX, J FURTH, P CHOE, WT BYRNE, J BAKER, C TI SEQUENCES HOMOLOGOUS TO 5' SPLICE SITES ARE REQUIRED FOR THE INHIBITORY ACTIVITY OF PAPILLOMAVIRUS LATE 3' UNTRANSLATED REGIONS SO FASEB JOURNAL LA English DT Meeting Abstract ID ELEMENT C1 NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1270 EP A1270 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600283 ER PT J AU ROBERTS, BJ SHOAF, SE AF ROBERTS, BJ SHOAF, SE TI THE EFFECTS OF ETHANOL WITHDRAWAL ON MIXED-FUNCTION MONOOXYGENASE ACTIVITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,METAB LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1252 EP A1252 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600182 ER PT J AU ROLLER, PP NOMIZU, M OTAKA, A SMYTH, MS WOLF, G CASE, R SHOELSON, SE BURKE, TR AF ROLLER, PP NOMIZU, M OTAKA, A SMYTH, MS WOLF, G CASE, R SHOELSON, SE BURKE, TR TI STRUCTURE-ACTIVITY STUDIES OF SH2 DOMAIN BINDING PEPTIDES CONTAINING O-PHOSPHOTYROSINE ANALOGS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,DTP,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1391 EP A1391 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600984 ER PT J AU ROSE, MC MEERZAMAN, D CHARLES, P DASKAL, E MARTIN, BM AF ROSE, MC MEERZAMAN, D CHARLES, P DASKAL, E MARTIN, BM TI A 3.6 KB CDNA CLONE IS A CANDIDATE FOR THE MUC5 GENE AND ENCODES HUMAN TRACHEOBRONCHIAL MUCIN, A MAJOR AIRWAY GLYCOPROTEIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 CHILDRENS NATL MED CTR,WASHINGTON,DC 20010. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. NIMH,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1424 EP A1424 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601175 ER PT J AU ROSENTHAL, D SHIMA, T SCHLEGEL, R CELLI, G DE LUCA, LM SMULSON, M AF ROSENTHAL, D SHIMA, T SCHLEGEL, R CELLI, G DE LUCA, LM SMULSON, M TI AN ENGINEERED HUMAN SKIN MODEL USING POLY(ADP-RIBOSE) POLYMERASE ANTISENSE EXPRESSION SHOWS A REDUCED RESPONSE TO DNA-DAMAGE SO FASEB JOURNAL LA English DT Meeting Abstract C1 GEORGETOWN UNIV, SCH MED, DEPT BIOCHEM & MOLEC BIOL, WASHINGTON, DC 20007 USA. NCI, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1408 EP A1408 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601085 ER PT J AU SACKETT, DL WOLFF, J AF SACKETT, DL WOLFF, J TI MULTIPLE STEPS IN THE UNFOLDING OF TUBULIN BY UREA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,BIOCHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1388 EP A1388 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600967 ER PT J AU SALOMON, D BRANDT, R NORMANNO, N CIARDIELLO, F GULLICK, WJ SCHNEIDER, D HARKINS, R ALESSANDRE, F PERSICO, MG AF SALOMON, D BRANDT, R NORMANNO, N CIARDIELLO, F GULLICK, WJ SCHNEIDER, D HARKINS, R ALESSANDRE, F PERSICO, MG TI PHYSIOCHEMICAL AND BIOLOGICAL PROPERTIES OF A NOVEL EPIDERMAL GROWTH FACTOR-RELATED PROTEIN - CRIPTO-1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 CNR,INT INST GENET & BIOPHYS,I-80125 NAPLES,ITALY. NCI,LTIB,TUMOR GROWTH FACTOR SECT,BETHESDA,MD 20892. UNIV NAPLES,CATTEDRA ONCOL MED,I-80134 NAPLES,ITALY. HAMMERSMITH HOSP,ICRF,MOLEC ONCOL LAB,LONDON W12 0HS,ENGLAND. BERLEX BIOSCI INC,DEPT PROT CHEM,RICHMOND,CA 94804. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1460 EP A1460 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601386 ER PT J AU SELLERS, JR PATO, MD PRESTON, YA HARVEY, EV ADELSTEIN, RS AF SELLERS, JR PATO, MD PRESTON, YA HARVEY, EV ADELSTEIN, RS TI EXPRESSION OF ACTIVE HEAVY MEROMYOSIN-LIKE ISOFORMS OF CHICKEN BRAIN MYOSIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1304 EP A1304 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600480 ER PT J AU SENTERRE, G CHARIOT, A GILLET, C CASTRONOVO, V SOBEL, ME AF SENTERRE, G CHARIOT, A GILLET, C CASTRONOVO, V SOBEL, ME TI IDENTIFICATION OF AN NHEI RESTRICTION SITE IN THE 3' UNTRANSLATED REGION OF HOXA4 MESSENGER-RNA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1333 EP A1333 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600647 ER PT J AU SHIN, SH LEE, KH HWANG, SC LEE, SB RHEE, SG AF SHIN, SH LEE, KH HWANG, SC LEE, SB RHEE, SG TI THE DIFFERENTIAL EXPRESSION OF THE PHOSPHOLIPASE-C ISOZYMES IN THE RAT DIGESTIVE ORGANS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1438 EP A1438 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601259 ER PT J AU SINGH, SK MAURIZI, MR AF SINGH, SK MAURIZI, MR TI MUTATIONAL ANALYSIS OF THE 2 ATP-BINDING SITES OF CLP-A, THE REGULATORY SUBUNIT OF ESCHERICHIA-COLI CLP PROTEASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1374 EP A1374 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600886 ER PT J AU SMITH, CB DEIBLER, GE SUN, Y AF SMITH, CB DEIBLER, GE SUN, Y TI IN-VIVO RATES OF PROTEIN-SYNTHESIS UNDER FLOODING CONDITIONS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1312 EP A1312 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600529 ER PT J AU SMITH, PB TIANO, HF PHILPOT, RM NESNOW, S LANGENBACH, RJ AF SMITH, PB TIANO, HF PHILPOT, RM NESNOW, S LANGENBACH, RJ TI CYTOTOXICITY OF 4-IPOMEANOL (4-IPO) IN C3H/10T1/2 CELLS EXPRESSING PULMONARY CYTOCHROME-P-450 4B1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 WAKE FOREST UNIV,MED CTR,DEPT BIOCHEM,WINSTON SALEM,NC 27157. NIEHS,RES TRIANGLE PK,NC 27709. US EPA,RES TRIANGLE PK,NC 27711. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1249 EP A1249 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600161 ER PT J AU STRACKE, ML LEVINE, M ARESTAD, A LIOTTA, LA AF STRACKE, ML LEVINE, M ARESTAD, A LIOTTA, LA TI GLYCOSYLATION OF THE TUMOR-CELL MOTILITY FACTOR, AUTOTAXIN, IS NOT REQUIRED FOR ACTIVITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1424 EP A1424 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601180 ER PT J AU SURMACZ, E SELL, C KATO, H ROBERTS, CT LEROITH, D BASERGA, R AF SURMACZ, E SELL, C KATO, H ROBERTS, CT LEROITH, D BASERGA, R TI DISSOCIATION BETWEEN MITOGENESIS AND TRANSFORMING ACTIVITY IN THE TYPE-1 IGF RECEPTOR WITH A C-TERMINAL TRUNCATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,PHILADELPHIA,PA 19107. NIDDK,DIABET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1320 EP A1320 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600574 ER PT J AU SWEITZER, TD HANOVER, J AF SWEITZER, TD HANOVER, J TI RECONSTITUTION OF NUCLEOLAR TRANSPORT IN A PERMEABILIZED-CELL SYSTEM SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1459 EP A1459 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601377 ER PT J AU TAKADA, T IIDA, K MOSS, J AF TAKADA, T IIDA, K MOSS, J TI EXPRESSION OF NAD GLYCOHYDROLASE ACTIVITY BY RAT MAMMARY ADRENOCARCINOMA CELLS TRANSFORMED WITH RAT T-CELL ALLOANTIGEN RT6.2 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1407 EP A1407 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601079 ER PT J AU TAOUIS, M LEVYTOLEDANO, R ROACH, P TAYLOR, SI GORDEN, P AF TAOUIS, M LEVYTOLEDANO, R ROACH, P TAYLOR, SI GORDEN, P TI INSULIN BINDING TO A HYBRID INSULIN-RECEPTOR COMPOSED OF NON-BINDING AND NORMAL HALF RECEPTORS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,DIABET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1319 EP A1319 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600572 ER PT J AU TEKLE, E ASTUMIAN, RD CHOCK, PB AF TEKLE, E ASTUMIAN, RD CHOCK, PB TI SELECTIVE AND ASYMMETRIC MOLECULAR-TRANSPORT ACROSS ELECTROPORATED CELL-MEMBRANES SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CHICAGO,SBRI,DEPT SURG,CHICAGO,IL 60637. NHLBI,LB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1428 EP A1428 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601200 ER PT J AU THIES, F KIM, HY AF THIES, F KIM, HY TI INCORPORATION OF DOCOSAHEXAENOIC ACID (22-6N3) AND ARACHIDONIC-ACID INTO BRAIN SUBCELLULAR-FRACTIONS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,DICBR,LMBB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1338 EP A1338 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600674 ER PT J AU THOMPSON, MW MAURIZI, MR AF THOMPSON, MW MAURIZI, MR TI ANALYSIS OF AN ALLOSTERIC BINDING-SITE FOR PEPTIDES ON THE REGULATORY SUBUNIT OF THE ATP-DEPENDENT CLP PROTEASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1374 EP A1374 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600883 ER PT J AU TRIESCHMANN, L CRIPPA, MP ALFONSO, PJ WOLFFE, AP BUSTIN, M AF TRIESCHMANN, L CRIPPA, MP ALFONSO, PJ WOLFFE, AP BUSTIN, M TI HIGH-MOBILITY GROUP PROTEINS HMG-14/17 ENHANCE TRANSCRIPTION OF CHROMATIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. RI Bustin, Michael/G-6155-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1271 EP A1271 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600285 ER PT J AU TSAI, L FRIGUET, B SZWEDA, LI AF TSAI, L FRIGUET, B SZWEDA, LI TI FORMATION OF PROTEIN CROSS-LINK AND FLUORESCENCE - REACTION OF 4-HYDROXY-2-NONENAL WITH LYSINE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1357 EP A1357 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600786 ER PT J AU TSUCHIYA, N SATO, K KASHIWAYA, Y KEON, C CLARKE, K VEECH, RL AF TSUCHIYA, N SATO, K KASHIWAYA, Y KEON, C CLARKE, K VEECH, RL TI ESTIMATION OF PROTON-PI GRADIENTS BETWEEN MITOCHONDRIA AND CYTOPLASM USING P-31 NMR AND FREEZE-CLAMP ENZYMATIC ANALYSIS IN WORKING RAT HEARTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,METAB LAB,ROCKVILLE,MD 20852. DEPT BIOCHEM,OXFORD,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1299 EP A1299 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600451 ER PT J AU TSYRLOV, IB GELBOIN, HV AF TSYRLOV, IB GELBOIN, HV TI A COEXPRESSION OF MAMMALIAN P450S AND NADPH-OXIDOREDUCTASE IN HUMAN-CELLS - ENZYME-KINETIC AND IMMUNOCHEMICAL STUDY SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1256 EP A1256 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600202 ER PT J AU TUMMINIA, SJ RUSSELL, P AF TUMMINIA, SJ RUSSELL, P TI ALPHA-B-CRYSTALLIN EXPRESSION AND INDUCTION IN HUMAN ASTROGLIOMA CELL-LINE U373 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI,MECH OCULAR DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1354 EP A1354 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600771 ER PT J AU VARMA, J SACKETT, DL AF VARMA, J SACKETT, DL TI COLCHICINE SITE AND VINBLASTINE SITE LIGANDS CAUSE DIFFERENT STRUCTURAL-CHANGES IN TUBULIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDKD,BIOCHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1469 EP A1469 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601439 ER PT J AU WANG, J JEONG, KS SADDIG, MC CRUTCHFIELD, C ZHANG, H SONG, BJ VEECH, RL AF WANG, J JEONG, KS SADDIG, MC CRUTCHFIELD, C ZHANG, H SONG, BJ VEECH, RL TI MEASUREMENT OF CYTOCHROME-P450 2E1 IN ETHANOL-TREATED RATS BY QUANTITATIVE COMPETITIVE POLYMERASE CHAIN-REACTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,MED CHEM LAB,BETHESDA,MD 20892. NIAAA,METAB LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1252 EP A1252 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600180 ER PT J AU WANGE, RL ISAKOV, N WATTS, JD AEBERSOLD, R SAMELSON, LE AF WANGE, RL ISAKOV, N WATTS, JD AEBERSOLD, R SAMELSON, LE TI LOCALIZATION OF ZAP-70 TO THE TCR IS MEDIATED BY BINDING OF TYROSINE-PHOSPHORYLATED TAMS TO THE TANDEM SH2 DOMAINS OF ZAP-70 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,CBMB,BETHESDA,MD 20892. BEN GURION UNIV NEGEV,IL-84105 BEER SHEVA,ISRAEL. UNIV BRITISH COLUMBIA,DEPT BIOCHEM & BIOMED RES,VANCOUVER V6I 1Z3,BC,CANADA. RI ISAKOV, NOAH/F-1659-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1228 EP A1228 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600044 ER PT J AU WARD, G PAWLOSKY, R SALEM, N AF WARD, G PAWLOSKY, R SALEM, N TI ETHANOL-CONSUMPTION ALTERS POLYUNSATURATED FATTY-ACID TURNOVER AND PEROXIDATION IN C57BL/6J MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,LMBB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1471 EP A1471 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601452 ER PT J AU WELCH, RW CROSSMAN, A KIRK, K MATECKA, D RICE, KC LEVINE, M AF WELCH, RW CROSSMAN, A KIRK, K MATECKA, D RICE, KC LEVINE, M TI INHIBITION OF ASCORBIC-ACID TRANSPORT IN HUMAN FIBROBLASTS WITH ASCORBIC-ACID ANALOGS AT CARBONS 2-6 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDKD,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1457 EP A1457 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601369 ER PT J AU YAMAZAKI, H MIMURA, M SHIMADA, T FUNAE, Y GONZALEZ, FJ GUO, Z GUENGERICH, FP AF YAMAZAKI, H MIMURA, M SHIMADA, T FUNAE, Y GONZALEZ, FJ GUO, Z GUENGERICH, FP TI OXIDATION OF BUFURALOL BY RAT AND HUMAN CYTOCHROME-P450 ENZYMES SO FASEB JOURNAL LA English DT Meeting Abstract C1 VANDERBILT UNIV,MED CTR,SCH MED,NASHVILLE,TN 37232. OSAKA PREFECTURAL INST PUBL HLTH,OSAKA 537,JAPAN. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1248 EP A1248 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600156 ER PT J AU YANCEYWRONA, JE CAMERINIOTERO, RD AF YANCEYWRONA, JE CAMERINIOTERO, RD TI A KINETIC SCHEME FOR THE HOMOLOGY SEARCH CARRIED OUT BY RECA PROTEIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,GENET & BIOCHEM BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1331 EP A1331 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600633 ER PT J AU YIM, HS KANG, SO YIM, MB AF YIM, HS KANG, SO YIM, MB TI STRUCTURAL IDENTIFICATION OF FREE-RADICALS FORMED IN THE REACTION BETWEEN METHYLGLYOXAL AND AMINO-ACIDS - A MODEL FOR GLYCATION REACTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 SEOUL NATL UNIV,DEPT MICROBIOL,SEOUL 151,SOUTH KOREA. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1358 EP A1358 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600790 ER PT J AU YIM, MB CHAE, HZ KWAK, HS RHEE, SG CHOCK, PB STADTMAN, ER AF YIM, MB CHAE, HZ KWAK, HS RHEE, SG CHOCK, PB STADTMAN, ER TI THIYL RADICALS, DAMAGING SPECIES, AND THE THIOL-SPECIFIC ANTIOXIDANT ENZYME SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1357 EP A1357 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600789 ER PT J AU ZHANG, C ROSENWALD, AG WILLINGHAM, MC SKUNTZ, S CLARK, J KAHN, RA AF ZHANG, C ROSENWALD, AG WILLINGHAM, MC SKUNTZ, S CLARK, J KAHN, RA TI EXPRESSION OF A DOMINANT ALLELE OF HUMAN ADP-RIBOSYLATION FACTOR-I (ARF1) INHIBITS MEMBRANE TRAFFIC IN-VIVO SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1314 EP A1314 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600540 ER PT J AU ZHOU, D CAM, LL LAUGHTON, CA KORZEKWA, KR CHEN, S AF ZHOU, D CAM, LL LAUGHTON, CA KORZEKWA, KR CHEN, S TI A MUTAGENESIS STUDY AT ISOLEUCINE-474 OF AROMATASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 CITY HOPE NATL MED CTR,BECKMAN RES INT,DUARTE,CA 91010. INST CANC RES,SUTTON SM2 5PX,SURREY,ENGLAND. NIH,BETHESDA,MD 20892. RI Laughton, Charles/E-5667-2010 OI Laughton, Charles/0000-0003-4090-3960 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1382 EP A1382 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600930 ER PT J AU ZHU, DM TEKLE, E CHOCK, PB HUANG, CY AF ZHU, DM TEKLE, E CHOCK, PB HUANG, CY TI VITAL REVERSIBLE PHOSPHORYLATION STEPS IN HELA-CELL CA2+ OSCILLATIONS INVOLVING CALMODULIN-DEPENDENT KINASE-II AND A CALYCULIN A-INHIBITABLE PHOSPHATASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1434 EP A1434 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51601234 ER PT J AU ZIMMERMAN, SB MURPHY, LD AF ZIMMERMAN, SB MURPHY, LD TI MACROMOLECULAR CROWDING EFFECTS ON THE INTERACTION OF DNA WITH ESCHERICHIA-COLI DNA-BINDING PROTEINS - A MODEL FOR BACTERIAL NUCLEOID STABILIZATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 19 PY 1994 VL 8 IS 7 BP A1330 EP A1330 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH516 UT WOS:A1994NH51600630 ER PT J AU RIUS, RA MOLLNER, S PFEUFFER, T LOH, YP AF RIUS, RA MOLLNER, S PFEUFFER, T LOH, YP TI DEVELOPMENTAL-CHANGES IN GS AND G(OLF) PROTEINS AND ADENYLYL CYCLASES IN MOUSE-BRAIN MEMBRANES SO BRAIN RESEARCH LA English DT Article DE CENTRAL NERVOUS SYSTEM; DEVELOPMENT; G PROTEIN; ADENYLYL CYCLASE ID BINDING REGULATORY PROTEINS; SIGNAL TRANSDUCTION PROTEIN; BETA-ADRENERGIC RECEPTORS; RAT-BRAIN; 2 FORMS; MONOCLONAL-ANTIBODIES; ESCHERICHIA-COLI; ALPHA-SUBUNITS; LYMPHOMA-CELLS; CHOLERA TOXIN AB Guanine nucleotide-binding (G) proteins, Gs and G(olf) mediate the increase in cAMP formation through the activation of adenylyl cyclases. The developmental profiles of Gs, G(olf) and adenylyl cyclases were determined in mouse striatum and whole brain using immunobloting with specific antisera. Gs and the 115 kDa and 150 kDa adenylyl cyclases were present at the earliest age tested, embryonic day (E) 14.5. G(olf) and the 160 kDa adenylyl cyclase emerged in parallel, postnatally; during this period the increase in the relative abundance of the 150 kDa was observed. Gpp[NH]p activated Gs/G(olf) in a dose dependent manner, with a smaller response observed in embryos compared to adults. Mn2+ and forskolin activated the adenylyl cyclases and this activation increased during development. At E 14.5, maximal activation with Mn2+ and forskolin elicited a similar increase in cAMP levels, but from postnatal day 1, a nearly two fold higher response was obtained with forskolin compared to Mn2+; at the same time the 160 kDa adenylyl cyclase was detected. These data suggest that the appearance of certain forms of stimulatory G proteins was developmentally correlated with the expression of specific adenylyl cyclases. C1 UNIV DUSSELDORF,DEPT PHYSIOL CHEM 2,D-40001 DUSSELDORF,GERMANY. RP RIUS, RA (reprint author), NICHHD,DEV NEUROBIOL LAB,CELLULAR NEUROBIOL SECT,BLDG 49 5A 38,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 62 TC 23 Z9 23 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 18 PY 1994 VL 643 IS 1-2 BP 50 EP 58 DI 10.1016/0006-8993(94)90007-8 PG 9 WC Neurosciences SC Neurosciences & Neurology GA NG736 UT WOS:A1994NG73600006 PM 8032932 ER PT J AU YAMANAKA, K OGURA, T KOONIN, EV NIKI, H HIRAGA, S AF YAMANAKA, K OGURA, T KOONIN, EV NIKI, H HIRAGA, S TI MULTICOPY SUPPRESSORS, MSSA AND MSSB, OF AN SMBA MUTATION OF ESCHERICHIA-COLI SO MOLECULAR AND GENERAL GENETICS LA English DT Article DE SMBA; ASPARTOKINASE; GENE EXPRESSION; NMP KINASE; RNA HELICASE ID NUCLEOTIDE-SEQUENCE; ADENYLATE KINASE; DNA CLONING; THRA GENE; PROTEIN; CHROMOSOME; VECTORS; CONSTRUCTION; OPERON; FAMILY AB We have isolated and characterized two multicopy suppressors, mssA and mssB, which suppress the cold-sensitive growth phenotype of the smbA2 mutant of Escherichia coli. The mssA gene is located immediately upstream of the rpsA gene (20.5 min). MssA protein was found to be related to nucleoside monophosphate kinases. The mssB gene was found to be identical to the deaD gene (69 min), which encodes a putative RNA helicase. The SmbA protein belongs to the aspartokinase family and probably represents a new, fourth aspartokinase species in E. coli. Expression of the smbA gene is essential for cell growth. The smbA2 mutant shows a pleiotropic phenotype characterized by cold-sensitive growth, hypersensitivity to the detergent sodium dodecyl sulfate, and formation of a translucent segment at midcell or at a pole of the cell when grown at 22 degrees C. In addition, some cellular proteins were either increased or decreased in amount in the smbA2 mutant. SmbA may be a regulatory factor in the expression of a battery of genes. MssA and MssB might also relate to the expression of some of these genes. Multiple copies mssA and mssB suppressed the various phenotypic features of the smbA2 mutant to various extents, suppressing the cold-sensitive growth completely. C1 NIH, NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, BETHESDA, MD 20894 USA. RP KUMAMOTO UNIV, SCH MED, INST MOLEC EMBRYOL & GENET, DEPT MOLEC CELL BIOL, KUMAMOTO 862, JAPAN. NR 30 TC 27 Z9 31 U1 0 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD APR 18 PY 1994 VL 243 IS 1 BP 9 EP 16 DI 10.1007/BF00283870 PG 8 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA NH704 UT WOS:A1994NH70400002 PM 8190075 ER PT J AU COX, DA ROGERS, WJ AGUIRRE, FV FORMAN, S SOLOMON, R ZARET, BL AF COX, DA ROGERS, WJ AGUIRRE, FV FORMAN, S SOLOMON, R ZARET, BL TI EFFECT ON OUTCOME OF THE PRESENCE OR ABSENCE OF CHEST PAIN AT INITIATION OF RECOMBINANT TISSUE-PLASMINOGEN ACTIVATOR THERAPY IN ACUTE MYOCARDIAL-INFARCTION SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID PHASE-II TRIAL; THROMBOLYTIC THERAPY; CREATINE-KINASE; TIMI; REPERFUSION; LESSONS AB To ascertain whether the outcome of patients with suspected myocardial infarction differs when chest pain is still present at initiation of thrombolytic therapy, participants in the Thrombolysis in Myocardial Infarction Phase II study, all of whom presented within 4 hours of symptoms onset, were retrospectively divided into 2 groups: (1) those with chest pain present at onset of intravenous thrombolysis, n = 3,000; and (2) those who were free of chest pain on beginnings intravenous thrombolytic therapy, n = 337. Patients free of chest pain were older (58 vs 57 years, p = 0.01), more often women (23 vs 17%, p = 0.01), had fewer electrocardiographic leads with ST elevation (3.8 vs 4.1, p <0.001), and the presenting event was confirmed less often as myocardial infarction than as chest pain without infarction (88 vs 96%, p <0.001). There were no significant differences between the 2 groups for in-hospital death, reinfarction, recurrent ischemic events, stroke, overall hemorrhagic complications, coronary angioplasty or bypass surgery. At 6-weeks follow-up, more pain-free patients had resting ejection fraction >0.55 (35 vs 31%, p = 0.001) and fewer developed congestive heart failure (12 vs 20%). At 1-year follow-up, fewer pain-free patients developed congestive heart failure (15 vs 21%, p = 0.009), but no differences existed between the 2 groups in frequency of death, reinfarction, coronary angioplasty, bypass surgery or anginal class. Thus, there are several observations in patients who were free of chest pain at onset of lytic therapy. (1) The majority developed enzymatic or electrocardiographic evidence of acute myocardial infarction. (2) Lytic therapy was safe and without excessive complications. (3) Higher ejection fraction was noted at 6 weeks, and at 1-year follow-up there was a lower incidence of congestive heart failure than among patients having pain at onset of lytic therapy. These observational data suggest that, for patients presenting within 4 hours of onset of clinical and electrocardiographic evidence of myocardial infarction, it is reasonable to administer thrombolytic therapy, even if symptoms have subsided. C1 UNIV ALABAMA,MED CTR,BIRMINGHAM,AL 35294. ST LOUIS UNIV,MED CTR,ST LOUIS,MO. MARYLAND MED RES INST,BALTIMORE,MD. NHLBI,BETHESDA,MD. YALE UNIV,MED CTR,NEW HAVEN,CT. NR 21 TC 9 Z9 9 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD APR 15 PY 1994 VL 73 IS 11 BP 729 EP 736 DI 10.1016/0002-9149(94)90872-9 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NG546 UT WOS:A1994NG54600001 PM 8160607 ER PT J AU MELBYE, M RABKIN, C FRISCH, M BIGGAR, RJ AF MELBYE, M RABKIN, C FRISCH, M BIGGAR, RJ TI CHANGING PATTERNS OF ANAL CANCER INCIDENCE IN THE UNITED-STATES, 1940-1989 SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ACQUIRED IMMUNODEFICIENCY SYNDROME; ANUS NEOPLASMS; HIV; HOMOSEXUALITY; INCIDENCE; NEOPLASMS; RISK FACTORS ID INTRAEPITHELIAL NEOPLASIA; CERVICAL-CANCER; MARITAL-STATUS; CARCINOMA; RISK; EPIDEMIOLOGY; ASSOCIATION; BEHAVIOR; SMOKING; WOMEN AB Anal cancer has been hypothesized to be associated with a sexual ly transmitted agent and, more recently, with the epidemic of human immunodeficiency virus (HIV). The authors used a descriptive incidence study to evaluate these hypotheses based on US data from the Surveillance, Epidemiology, and End Results (SEER) program for 1973-1989 and from the Connecticut Tumor Registry for 1940-1988. Since 1960, anal cancer incidence in Connecticut increased 1.9-fold among men and 2.3-fold among women. Based on information from SEER, the incidence was lowest among white men (1973-1989 average: 0.41/100,000) and highest among black women (1973-1989 average: 0.74/100,000). Residents of the metropolitan areas had a twofold risk of anal cancer compared with populations in less densely populated areas, The most dramatic change in incidence was observed for white men in the San Francisco Bay area, among whom the incidence increased from 0.5/100,000 in 1973-1975 to 1.2/100,000 in 1988-1989 (p trend < 0.001). The relative risks (95% confidence intervals) of anal cancer among never married men compared with ever married men in the urban areas rose from 5.8 (0.9-8.7) in 1973-1978 to 6.7 (4.7-9.5) in 1979-1984 and 10.3 (7.5-14.1) in 1985-1989 (p trend = 0.02). No significant difference was observed among women. In conclusion, anal cancer incidence in the United States has increased significantly during the past 30 years and is now higher in women than men, in blacks than whites, and in residents of metropolitan rather than rural areas. Some of this changing pattern clearly relates to the period prior to the acquired immunodeficiency syndrome (AIDS) epidemic and argues that behavioral changes are important in anal cancer development. However, the recent remarkable change in rates among never married men and men living in the San Francisco Bay area suggests that homosexual men are at special and increasing risk. The authors speculate whether part of this recent increase could be attributed to the AIDS epidemic. C1 NCI,VIRAL STUDIES BRANCH,BETHESDA,MD 20892. RP MELBYE, M (reprint author), STATENS SERUM INST,DANISH EPIDEMIOL SCI CTR,EPIDEMIOL RES UNIT,ARTILLERIVEJ 5,DK-2300 COPENHAGEN,DENMARK. RI Frisch, Morten/E-9206-2016 OI Frisch, Morten/0000-0002-3864-8860 NR 30 TC 108 Z9 111 U1 1 U2 3 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 15 PY 1994 VL 139 IS 8 BP 772 EP 780 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NJ044 UT WOS:A1994NJ04400005 PM 8178790 ER PT J AU WEINBERG, CR AF WEINBERG, CR TI TOWARD A CLEARER DEFINITION OF CONFOUNDING - REPLY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter RP WEINBERG, CR (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 15 PY 1994 VL 139 IS 8 BP 855 EP 855 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NJ044 UT WOS:A1994NJ04400016 ER PT J AU KOVELESKY, RA MINOR, JR AF KOVELESKY, RA MINOR, JR TI OCTREOTIDE FOR HIV-RELATED DIARRHEA SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Letter ID ANALOG OCTREOTIDE; AIDS; SOMATOSTATIN; INFECTIONS; THERAPY RP KOVELESKY, RA (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT PHARM,BETHESDA,MD 20892, USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD APR 15 PY 1994 VL 51 IS 8 BP 996 EP 1001 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NG900 UT WOS:A1994NG90000009 PM 8037226 ER PT J AU GOLDSTEIN, AM PASTAKIA, B DIGIOVANNA, JJ POLIAK, S SANTUCCI, S KASE, R BALE, AE BALE, SJ AF GOLDSTEIN, AM PASTAKIA, B DIGIOVANNA, JJ POLIAK, S SANTUCCI, S KASE, R BALE, AE BALE, SJ TI CLINICAL FINDINGS IN 2 AFRICAN-AMERICAN FAMILIES WITH THE NEVOID BASAL-CELL CARCINOMA SYNDROME (NBCC) SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE NEVOID BASAL CELL CARCINOMA SYNDROME (NBCC); AFRICAN-AMERICANS; CLINICAL FINDINGS ID GORLIN SYNDROME; GENE AB The nevoid basal cell carcinoma syndrome (NBCC) is an autosomal dominant multi-system disorder with variable expressivity. We present the clinical findings on 11 African-American NBCC cases from 2 families and a review of the literature of NBCC in African-Americans. The 2 new families, as well as those previously reported, suggest minimal expression of the basal cell carcinomas and full expression of the other components of the syndrome. The 3 most common findings in the 11 cases were jaw cysts, palmar and/or plantar pits, and calcification of the falx cerebri. Only 44% (4/11) of these cases had one or more confirmed basal cell carcinomas. This frequency is substantially less than that observed in whites (90% with basal cell carcinomas). The relative lack of these skin tumors in African-Americans partly reflects ultraviolet radiation protection resulting from increased skin pigmentation. Future research should help identify the specific mutation(s) in blacks as well as other modifying genes and environmental exposures that may contribute to the varied manifestations of the syndrome. (C) 1994 Wiley-Liss, Inc. C1 NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NCI,CLIN EPIDEMIOL BRANCH,BETHESDA,MD 20892. NIH,CLIN CTR,DEPT RADIOL 2,BETHESDA,MD 20892. WESTAT CORP,ROCKVILLE,MD. YALE UNIV,SCH MED,DEPT GENET,NEW HAVEN,CT 06510. NIAMSD,SKIN BIOL LAB,GENET STUDIES SECT,BETHESDA,MD. RP GOLDSTEIN, AM (reprint author), NCI,GENET EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 439,BETHESDA,MD 20892, USA. NR 31 TC 38 Z9 39 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD APR 15 PY 1994 VL 50 IS 3 BP 272 EP 281 DI 10.1002/ajmg.1320500311 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA NE022 UT WOS:A1994NE02200010 PM 8042672 ER PT J AU BECKER, RC TERRIN, M ROSS, R KNATTERUD, GL DESVIGNENICKENS, P GORE, JM BRAUNWALD, E AF BECKER, RC TERRIN, M ROSS, R KNATTERUD, GL DESVIGNENICKENS, P GORE, JM BRAUNWALD, E TI COMPARISON OF CLINICAL OUTCOMES FOR WOMEN AND MEN AFTER ACUTE MYOCARDIAL-INFARCTION SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE MYOCARDIAL INFARCTION; THROMBOLYTIC THERAPY; SEX FACTORS; AGE FACTORS; DIABETES MELLITUS ID CORONARY HEART-DISEASE; LONG-TERM SURVIVAL; THROMBOLYTIC THERAPY; DIABETES-MELLITUS; SEX-DIFFERENCES; BYPASS-SURGERY; ARTERY DISEASE; GENDER BIAS; PHASE-II; MORTALITY AB Objectives: To assess differences in morbidity and mortality between men and women with acute myocardial infarction treated with thrombolytic therapy and the relation of differences to baseline patient characteristics and clinical features. Design: Secondary analysis of observational findings among women and men enrolled in a clinical trial. Setting: Hospitals participating in the Thrombolysis in Myocardial Infarction Phase II trial. Measurements: Recurrent infarctions and deaths were assessed. Main Results: The 6-week mortality rate was greater for women than for men (9% compared with 4%; adjusted relative risk, 1.54; P = 0.01). Death or reinfarction occurred in 15.9% of women and 9.5% of men (adjusted relative risk, 1.33; P = 0.02). Among patients enrolled for treatment with 100 mg of recombinant tissue plasminogen activator and assigned to a conservative strategy of watchful waiting with appropriate backup, the 6-week incidence of death was 7.5% for women and 3.8% for men (P = 0.01). The 6-week incidences of death or reinfarction were 14.2% and 8.9% (P = 0.01) among women and men, respectively. Conclusions: Among patients in the Thrombolysis in Myocardial Infarction Phase II Trial, who all were diagnosed with myocardial infarction and were eligible to receive thrombolytic therapy, women had higher rates of mortality and morbidity than did men. Older age at the time of myocardial infarction and a history of diabetes accounted for much but probably not all of this difference. C1 MARYLAND MED RES INST,BALTIMORE,MD 21210. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA 19104. NHLBI,DHDV,CARDIAC DIS BRANCH,BETHESDA,MD 20892. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. RP BECKER, RC (reprint author), UNIV MASSACHUSETTS,THROMBOSIS RES CTR,SCH MED,55 LAKE AVE N,WORCESTER,MA 01655, USA. FU NHLBI NIH HHS [HL38460, HL35058] NR 49 TC 166 Z9 169 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 15 PY 1994 VL 120 IS 8 BP 638 EP 645 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA NE850 UT WOS:A1994NE85000003 PM 8135447 ER PT J AU ROSENSTEIN, DL ELIN, RJ HOSSEINI, JM GROVER, G RUBINOW, DR AF ROSENSTEIN, DL ELIN, RJ HOSSEINI, JM GROVER, G RUBINOW, DR TI MAGNESIUM MEASURES ACROSS THE MENSTRUAL-CYCLE IN PREMENSTRUAL-SYNDROME SO BIOLOGICAL PSYCHIATRY LA English DT Article DE PMS; MAGNESIUM; MENSTRUAL CYCLE; MOOD; BLOOD; RED BLOOD CELL (RBC) ID SYMPTOMS; TENSION AB The purpose of this study was to evaluate blood magnesium (Mg) measures across the menstrual cycle in women with premenstrual syndrome (PMS) and control women. Longitudinal determinations of plasma, red blood cell (RBC) and mononuclear blood cell (MBC) Mg were made in 26 women with prospectively confirmed PMS and in a control group of 19 Women. Data were analyzed using analysis of variance with repeated measures and Spearman rank correlations. Significant diagnostic group effects were observed for RBC and MBC Mg concentrations (p < 0.05). These effects reflected lower Mg concentrations in PMS patients at each sampling time. No significant effects were observed for either plasma Mg or MBC Mg content, nor were there significant time by diagnosis effects for any of the measures. Consistent with earlier studies, we found decreased RBC Mg concentrations and additionally observed decreased MBC Mg concentrations in women. with PMS. However, neither of these relative deficits were confined to the luteal phase. C1 NIH,CTR CLIN,DEPT CLIN PATHOL,BETHESDA,MD 20892. NIH,CTR CLIN,MENTAL HLTH ALCOHOL NEUROL & AGING NURSING SERV,BETHESDA,MD 20892. RP ROSENSTEIN, DL (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BEHAV ENDOCRINOL SECT,BLDG 10,ROOM 3N238,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 28 TC 23 Z9 25 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 1994 VL 35 IS 8 BP 557 EP 561 DI 10.1016/0006-3223(94)90103-1 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA NJ347 UT WOS:A1994NJ34700007 PM 8038300 ER PT J AU SZNOL, M PARKINSON, DR AF SZNOL, M PARKINSON, DR TI INTERLEUKIN-2 IN THERAPY OF HEMATOLOGIC MALIGNANCIES SO BLOOD LA English DT Editorial Material ID LYMPHOMA C1 NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,INVEST DRUG BRANCH,EPN 715,ROCKVILLE,MD 20852. NR 14 TC 22 Z9 22 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1994 VL 83 IS 8 BP 2020 EP 2022 PG 3 WC Hematology SC Hematology GA NF967 UT WOS:A1994NF96700002 PM 8161773 ER PT J AU DAWSEY, SM LEWIN, KJ LIU, FS WANG, GQ SHEN, Q AF DAWSEY, SM LEWIN, KJ LIU, FS WANG, GQ SHEN, Q TI ESOPHAGEAL MORPHOLOGY FROM LINXIAN, CHINA - SQUAMOUS HISTOLOGIC-FINDINGS IN 754 PATIENTS SO CANCER LA English DT Article DE ENDOSCOPY; PATHOLOGY; ESOPHAGUS; NORMAL HISTOLOGY; ESOPHAGITIS; SQUAMOUS DYSPLASIA; PRECANCEROUS CONDITIONS ID HIGH-RISK; LANGERHANS CELLS; LESIONS; CANCER; POPULATIONS; MUCOSA; IRAN AB Background. Linxian, China, has one of the highest rates of esophageal cancer in the world. Other authors have described high prevalences of histologic esophagitis, atrophy, and dysplasia in Linxian and have suggested that these findings may represent precancerous lesions in this population. In 1987, a new endoscopic survey allowed the authors to make an independent study of esophageal histology in Linxian. Methods. There were 1567 satisfactory squamous esophageal biopsies available from 754 patients. These biopsies were classified as normal, atrophy, acanthosis, esophagitis, squamous dysplasia, or squamous cancer. Results. Classified by their worst diagnosis, 56.5% of the 754 patients had normal mucosa, 0.0% atrophy, 11.5% acanthosis, 4.6% esophagitis, 22.7% squamous dysplasia, and 4.6% squamous cancer. Conclusions. The results show a different distribution of esophageal squamous diagnoses than has been reported previously from this population. The authors believe that the major reason for this discrepancy was differences in histologic criteria. In this survey, seemingly small differences in criteria could cause large differences in apparent disease prevalence; this was especially true for esophagitis. By the criteria used in this study, histologic esophagitis and atrophy are uncommon findings in Linxian, raising questions about their significance as precursor lesions of esophageal cancer in this population. C1 UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT PATHOL,LOS ANGELES,CA 90024. CHINESE ACAD MED SCI,CANC INST & HOSP,DEPT PATHOL,BEIJING 100037,PEOPLES R CHINA. CHINESE ACAD MED SCI,CANC INST & HOSP,DEPT CHEST SURG,BEIJING 100037,PEOPLES R CHINA. HENAN MED UNIV,DEPT PRECANCEROUS STUDIES,ZHENGZHOU,PEOPLES R CHINA. RP DAWSEY, SM (reprint author), NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,EXECUT PLAZA N,ROOM 211,BETHESDA,MD 20892, USA. FU NCI NIH HHS [N01-CP-05634, N01-CP-95616] NR 22 TC 74 Z9 80 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 15 PY 1994 VL 73 IS 8 BP 2027 EP 2037 DI 10.1002/1097-0142(19940415)73:8<2027::AID-CNCR2820730803>3.0.CO;2-3 PG 11 WC Oncology SC Oncology GA NF160 UT WOS:A1994NF16000002 PM 8156507 ER PT J AU RAM, Z WALBRIDGE, S OSHIRO, EM VIOLA, JJ CHIANG, YW MUELLER, SN BLAESE, RM OLDFIELD, EH AF RAM, Z WALBRIDGE, S OSHIRO, EM VIOLA, JJ CHIANG, YW MUELLER, SN BLAESE, RM OLDFIELD, EH TI INTRATHECAL GENE-THERAPY FOR MALIGNANT LEPTOMENINGEAL NEOPLASIA SO CANCER RESEARCH LA English DT Article ID MENINGEAL CARCINOMATOSIS; GLIOMA-CELLS; KINASE GENE; BRAIN; RAT; BEARING; TUMORS; LINE AB In meningeal carcinomatosis, retroviral vector-producer cells can be introduced into the thecal sac and circulate in the cerebrospinal fluid to reach malignant tumor cells in the leptomeninges, release vector particles, and selectively infect and transfer a gene of interest to these cells. Gene transfer experiments with the lacZ gene and in vitro retroviral titer measurements showed that retroviral vectors can survive in the cerebrospinal fluid, retain their infectivity, and successfully transduce tumor cells. To examine the potential of intrathecal gene therapy, we evaluated the antitumor efficacy of in situ transduction with the herpes simplex-thymidine kinase gene followed by ganciclovir therapy in a rat model of leptomeningeal neoplasia. Fischer rats were inoculated via a subarachnoid catheter implanted at the upper thoracic level, and thymidine kinase vector-producer cells were injected into the subarachnoid space the day of tumor inoculation. Seven days later, rats received ganciclovir for 14 days by daily i.p. injections (30 mg/kg/ml) or intrathecal injections (25 mu g/kg or 600 mu g/kg) for 14 days. To evaluate possible enhancement of tumor eradication by the ability of helper virus to package the vector in the cells and further extend gene transfer, additional rats received thymidine kinase vector-producer cells that had been previously coinfected with a replication-competent retrovirus (4070A). In all groups, control rats received i.p. or intrathecal saline injections. Ganciclovir administration i.p. resulted in significant prolongation of survival in rats given injections of thymidine kinase vector-producer cells. Injection of producer cells coinfected with the 4070A retrovirus did not improve antitumor efficacy. Intrathecal administration of ganciclovir (low and high doses) did not extend survival; histological examination of the spinal cords showed elimination of the infiltrative tumor in the leptomeninges, but residual tumor mass was present at the inoculation site, consistent with limited penetration of topical ganciclovir into the tumor. These results support the potential application of gene therapy using the thymidine kinase/ganciclovir approach for treatment of meningeal carcinomatosis. C1 NCI,METAB BRANCH,BETHESDA,MD 20892. GENET THERAPY INC,GAITHERSBURG,MD 20878. RP RAM, Z (reprint author), NINCDS,SURG NEUROL BRANCH,BLDG 10,ROOM 5D-37,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 15 TC 54 Z9 54 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1994 VL 54 IS 8 BP 2141 EP 2145 PG 5 WC Oncology SC Oncology GA NE849 UT WOS:A1994NE84900020 PM 8174120 ER PT J AU SAGA, T WEINSTEIN, JN JEONG, JM HEYA, T LEE, JT LE, N PAIK, CH SUNG, C NEUMANN, RD AF SAGA, T WEINSTEIN, JN JEONG, JM HEYA, T LEE, JT LE, N PAIK, CH SUNG, C NEUMANN, RD TI 2-STEP TARGETING OF EXPERIMENTAL LUNG METASTASES WITH BIOTINYLATED ANTIBODY AND RADIOLABELED STREPTAVIDIN SO CANCER RESEARCH LA English DT Article ID BINDING-SITE BARRIER; HEPATO-CARCINOMA MODEL; MONOCLONAL-ANTIBODY; SOLID TUMORS; INTERSTITIAL PRESSURE; BLOOD-FLOW; MACROMOLECULES; LOCALIZATION; XENOGRAFTS; TRANSPORT AB Two-step monoclonal antibody tumor targeting using an avidin-biotin system has unique characteristics because of the high-affinity binding (10(15) M(-1)) and the lower molecular weight ligands (avidin, streptavidin, or biotin) used as carriers of radioisotopes, toxins, or drugs. The distribution of radiolabeled streptavidin in a two-step targeting strategy was investigated in lung metastases of line 10 carcinoma in guinea pigs. The microdistribution of administered D3 monoclonal antibody and I-125-labeled streptavidin in metastatic nodules was examined by immunohistochemistry and autoradiography, and the uptake was quantitated. With monoclonal antibody pretargeting, streptavidin was found mainly at the periphery of metastatic nodules 1.5 h after injection; it had penetrated deeper at 4 h and was approaching homogeneity in many of the tumor nodules at 24 h. These results indicate that streptavidin can penetrate into metastatic nodules more rapidly than can the antibody. The concentration of streptavidin in metastatic nodules 4 h after injection was 5.6 times higher for the pretargeted group than for the nonpretargeted group, and the pretargeting index was 4.7. Although the absolute uptake of streptavidin had decreased between 4 and 24 h, the metastasis:blood ratio had increased from 1.2 to 2.4. When compared with the animals injected with I-125-labeled D3 antibody alone, the pretargeted group achieved higher tumor:blood and tumor:lung ratios and a higher localization index at early times after injection of the radiolabeled species. C1 NCI,CTR CLIN,DEPT NUCL MED,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RI Jeong, Jae Min/E-2102-2012 OI Jeong, Jae Min/0000-0003-2611-6020 NR 52 TC 69 Z9 70 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1994 VL 54 IS 8 BP 2160 EP 2165 PG 6 WC Oncology SC Oncology GA NE849 UT WOS:A1994NE84900023 PM 8174123 ER PT J AU SUNG, C VANOSDOL, WW SAGA, T NEUMANN, RD DEDRICK, RL WEINSTEIN, JN AF SUNG, C VANOSDOL, WW SAGA, T NEUMANN, RD DEDRICK, RL WEINSTEIN, JN TI STREPTAVIDIN DISTRIBUTION IN METASTATIC TUMORS PRETARGETED WITH A BIOTINYLATED MONOCLONAL-ANTIBODY - THEORETICAL AND EXPERIMENTAL PHARMACOKINETICS SO CANCER RESEARCH LA English DT Article ID BINDING-SITE BARRIER; SOLID TUMORS; AVIDIN; HAPTENS; PHARMACOLOGY; CARCINOMA; TRANSPORT; EQUATIONS; AFFINITY; TISSUES AB We have developed a pharmacokinetic model for the analysis of a protocol that involves injection of a biotinylated monoclonal antibody followed at a later time by radiolabeled streptavidin. Three distinct phys iological spaces are described: an avascular tumor nodule, the normal tissue surrounding the tumor, and the plasma. The model incorporates processes such as plasma kinetics, transcapillary transport, interstitial diffusion, binding reactions, and lymphatic clearances. We have modeled cases in which antigen turnover does not occur, in which antigen turnover does occur (24-h time constant), and in which circulating antibody is cleared from the plasma immediately prior to injection of streptavidin. We have calculated the spatial and temporal distributions of a tumor-specific antibody and of streptavidin in the tumor nodule using parameter values that simulate conditions of recent experiments on metastatic nodules in the guinea pig lung. The theoretical distribution of streptavidin in the tumor nodule shows an initial localization at the periphery that progresses to a fairly uniform distribution throughout the nodule, a temporal sequence that is very similar to experimental observation. This finding indicates that, in a tumor pretargeted with biotinylated antibody, streptavidin can encounter significant retardation in its penetration as a consequence of the high affinity interaction between these two species. Tumor:blood and tumor:lung ratios were calculated and compared to experimental results. In addition, the calculated tumor:blood ratios, tumor:lung ratios, and relative exposures were compared to values obtained from a model of one-step antibody delivery. The two-step protocol yielded an approximately 2- to 3-fold enhancement in these pharmacokinetic indices compared with the one-step method. C1 NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. NIH,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,BETHESDA,MD 20892. RP SUNG, C (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BLDG 13,ROOM 3N17,BETHESDA,MD 20892, USA. NR 36 TC 46 Z9 48 U1 1 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 APR 15 PY 1994 VL 54 IS 8 BP 2166 EP 2175 PG 10 WC Oncology SC Oncology GA NE849 UT WOS:A1994NE84900024 PM 8174124 ER PT J AU HUGIN, AW CERNY, A MORSE, HC AF HUGIN, AW CERNY, A MORSE, HC TI MICE WITH AN ACQUIRED IMMUNODEFICIENCY (MAIDS) DEVELOP A PERSISTENT INFECTION AFTER INJECTION WITH LISTERIA-MONOCYTOGENES SO CELLULAR IMMUNOLOGY LA English DT Note ID RETROVIRUS-INDUCED IMMUNODEFICIENCY; MURINE LEUKEMIA VIRUSES; TUMOR NECROSIS FACTOR; T-CELLS; CYTOKINE GENES; C57BL/6 MICE; NUDE MICE; RESISTANCE; MOUSE; AIDS AB Mice with a retrovirus-induced immunodeficiency were challenged with Listeria monocytogenes and resistance to this facultative intracellular bacterium was analyzed. Early innate immunity was unaltered or enhanced. Although immunodeficient mice had reduced bacterial titers after these reached their peak on Day 3, infection with L. monocytogenes generally resulted in a low-grade persistent infection and occasionally there was a delayed resolution of bacterial infection. Endogenous cytokines are important in the containment of bacteria as mice often developed a high load of bacteria or succumbed to infection in the absence of cytokine action. There was a substantial heterogeneity in disease after bacterial challenge which probably reflects the variability found in retrovirus-infected mice during the later stages of this immunodeficiency syndrome. (C) 1994 Academic Press, Inc. C1 NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. OI Morse, Herbert/0000-0002-9331-3705 NR 43 TC 7 Z9 7 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD APR 15 PY 1994 VL 155 IS 1 BP 246 EP 252 DI 10.1006/cimm.1994.1117 PG 7 WC Cell Biology; Immunology SC Cell Biology; Immunology GA NH461 UT WOS:A1994NH46100021 PM 8168147 ER PT J AU LIPSKA, BK WEINBERGER, DR AF LIPSKA, BK WEINBERGER, DR TI GONADECTOMY DOES NOT PREVENT NOVELTY OR DRUG-INDUCED MOTOR HYPERRESPONSIVENESS IN RATS WITH NEONATAL HIPPOCAMPAL DAMAGE SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE GONADAL HORMONE; CASTRATION; NEONATAL LESION; HIPPOCAMPUS; IBOTENIC ACID; AMPHETAMINE; STEREOTYPY; APOMORPHINE; DOPAMINE ID APOMORPHINE; CASTRATION; DOPAMINE; NEURONS; BRAIN; REPLACEMENT; AMPHETAMINE; METABOLISM; BEHAVIOR; HORMONES AB To explore the possibility that gonadal hormones are required for triggering the postpubertal emergence of enhanced dopamine-related behaviors in rats with neonatal excitotoxic lesions of the ventral hippocampus (VH), we assessed behavioral changes in castrated VH lesioned rats. The VH of rat pups was lesioned with ibotenic acid on day 7 after birth (PD7). Rats were castrated on PD21. Novelty- and amphetamine-induced locomotor activity were tested on PD56, and apomorphine-induced stereotypic behaviors and locomotion were evaluated on PD98. As demonstrated previously, the VH lesioned rats expressed enhanced novelty-, amphetamine- and apomorphine-induced hyperlocomotion (PD56) as well as potentiated apomorphine-induced stereotypic behaviors (PD98) in young adulthood as compared with sham-lesioned counterparts. Castration had no significant effect on novelty-induced locomotion or apomorphine-induced stereotypies but potentiated amphetamine- and apomorphine-induced hyperactivity in lesioned rats. These results indicate that the absence of gonadal hormones not only does not prevent the appearance in adulthood of behavioral disturbances linked to increased DA transmission in rats with neonatal lesions of the VH but even exaggerates those linked primarily to the mesolimbic DA system. RP LIPSKA, BK (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. NR 23 TC 31 Z9 31 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD APR 15 PY 1994 VL 78 IS 2 BP 253 EP 258 DI 10.1016/0165-3806(94)90033-7 PG 6 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA NH414 UT WOS:A1994NH41400013 ER PT J AU BINDER, R HOROWITZ, JA BASILION, JP KOELLER, DM KLAUSNER, RD HARFORD, JB AF BINDER, R HOROWITZ, JA BASILION, JP KOELLER, DM KLAUSNER, RD HARFORD, JB TI EVIDENCE THAT THE PATHWAY OF TRANSFERRIN RECEPTOR MESSENGER-RNA DEGRADATION INVOLVES AN ENDONUCLEOLYTIC CLEAVAGE WITHIN THE 3' UTR AND DOES NOT INVOLVE POLY(A) TAIL SHORTENING SO EMBO JOURNAL LA English DT Article DE ENDONUCLEASE; MESSENGER-RNA STABILITY; POLY(A) TAIL; RIBONUCLEASE; TRANSFERRIN RECEPTOR MESSENGER-RNA ID MESSENGER-RNA DEGRADATION; IRON-DEPENDENT REGULATION; ELEMENT BINDING-PROTEIN; UNTRANSLATED REGION; TRANSLATION INITIATION; RESPONSIVE ELEMENTS; CODING REGION; GM-CSF; C-FOS; STABILITY AB The stability of transferrin receptor (TfR) mRNA is regulated by iron availability. When a human plasma-cytoma cell line (ARH-77) is treated with an iron source (hemin), the TfR mRNA is destabilized and a shorter TfR RNA appears. A similar phenomenon is also observed in mouse fibroblasts expressing a previously characterized iron-regulated human TfR mRNA (TRS-1). In contrast, mouse cells expressing a constitutively unstable human TfR mRNA (TRS-4) display the shorter RNA irrespective of iron treatment. These shorter RNAs found in both the hemin-treated ARH-77 cells and in the mouse fibroblasts are shown to be the result of a truncation within the 3' untranslated regions of the mRNAs. The truncated RNA is generated by an endonuclease, as most clearly evidenced by the detection of the matching 3' endonuclease product. The cleavage site of the human TfR mRNA in the mouse fibroblasts has been mapped to single nucleotide resolution to a single-stranded region near one of the iron-responsive elements contained in the 3' UTR. Site-directed mutagenesis demonstrates that the sequence surrounding the mapped endonuclease cleavage site is required for both iron-regulated mRNA turnover and generation of the truncated degradation intermediate. The TfR mRNA does not undergo poly(A) tail shortening prior to rapid degradation since the length of the poly(A) tail does not decrease during iron-induced destabilization. Moreover, the 3' endonuclease cleavage product is apparently polyadenylated to the same extent as the full-length mRNA. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NR 57 TC 225 Z9 226 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 APR 15 PY 1994 VL 13 IS 8 BP 1969 EP 1980 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NH082 UT WOS:A1994NH08200023 PM 7909515 ER PT J AU MARK, SD LIU, SF LI, JY GAIL, MH SHEN, Q DAWSEY, SM LIU, FS TAYLOR, PR LI, B BLOT, WJ AF MARK, SD LIU, SF LI, JY GAIL, MH SHEN, Q DAWSEY, SM LIU, FS TAYLOR, PR LI, B BLOT, WJ TI THE EFFECT OF VITAMIN AND MINERAL SUPPLEMENTATION ON ESOPHAGEAL CYTOLOGY - RESULTS FROM THE LINXIAN DYSPLASIA TRIAL SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID CHINA; CANCER AB The population of Linxian in China has one of the world's highest rates for esophageal/gastric cardia cancer, as well as documented nutritional deficiencies. To determine whether dietary supplementation with a multi-vitamin multi-mineral preparation could reduce the risk of esophageal cancer and favorably influence precursor lesions, 3,318 individuals age 40-69 with cytologically determined grade 1 or grade 2 esophageal dysplasia were randomly assigned to receive either an active multi-vitamin multi-mineral supplement or a placebo. Pills were distributed at monthly visits and incident cancers or deaths were recorded. At 30 and 72 months subsequent to randomization all living participants without a known incident cancer were asked to undergo repeat cytological examination of their esophagus. Based on these procedures participants were classified as having no dysplasia, dysplasia grade 1, dysplasia grade 2 or near cancer dysplasia. Diagnoses of cancer were based on the cytology findings plus available histologic, radiologic and clinical materials. At the end of the study there was little overall difference in cumulative risk of esophageal cancer between those receiving vitamin/mineral supplementation and those receiving placebo. There was, however, a significant increase in reversion to non-dysplastic cytology among the group receiving the active treatment. The odds of not having any dysplasia at the two post-randomization screens was 1.23 times higher in the active treatment group than in the placebo group. Within each treatment group higher categories of dysplasia were associated with higher rates of cancer. (C) 1994 Wiley-Liss, Inc. C1 CHINESE ACAD MED SCI,INST CANC,BEIJING 100021,PEOPLES R CHINA. HUNAN MED UNIV,ZHENGZHOU,PEOPLES R CHINA. RP MARK, SD (reprint author), NCI,BETHESDA,MD 20892, USA. NR 11 TC 33 Z9 33 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 15 PY 1994 VL 57 IS 2 BP 162 EP 166 DI 10.1002/ijc.2910570205 PG 5 WC Oncology SC Oncology GA NG294 UT WOS:A1994NG29400004 PM 8157352 ER PT J AU SPRENGER, H LLOYD, AR LAUTENS, LL BONNER, TI KELVIN, DJ AF SPRENGER, H LLOYD, AR LAUTENS, LL BONNER, TI KELVIN, DJ TI STRUCTURE, GENOMIC ORGANIZATION, AND EXPRESSION OF THE HUMAN INTERLEUKIN-8 RECEPTOR-B GENE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MESSENGER-RNA; BETA-2-ADRENERGIC RECEPTOR; FUNCTIONAL EXPRESSION; MOLECULAR-CLONING; PROMOTER REGION; BINDING-PROTEIN; TATA-BOX; SEQUENCE; TRANSCRIPTION; FAMILY AB Two distinct receptors for the chemoattractant interleukin-8 (designated IL-8RA and -B) have been cloned recently. The receptors are expressed almost exclusively on neutrophils and myelomonocytic cell lines. In an attempt to understand the tissue-specific expression and to identify transcriptional regulatory elements we have cloned, sequenced, and characterized the human IL-8RB gene. The gene consists of 3 exons, interrupted by two introns of 3 and 5.4 kilobases (kb). A 1065-base pair open reading frame is encoded entirely in the third exon. A 1.4-kb 3'-untranslated region contains clustered AU-rich elements, similar to those described for genes regulated by altering mRNA stability. The start site of transcription was mapped by a modified rapid amplification of cDNA ends technique and revealed an unexpectedly long 5'-untranslated region of 423 base pairs. A TATA box equivalent was found in the 5'-flanking region 20 nucleotides upstream of the start of the first exon. The promoter was separated from the ATG-initiation codon by 8.75 kb. Comparison of the IL-8RB promoter with the promoter region of the receptor for another chemoattractant ligand, the bacterial peptide f-Met-Leu-Phe, revealed 3 novel but conserved motifs occupying similar positions. The immediate 5'-flanking region was GC-rich with 3 SP-1-like and 2 AP-2 sites identified in close proximity to the transcription start site. This essential promoter region was found to be responsible for constitutive expression, inducible by granulocyte colony-stimulating factor and controlled by silencer elements located further upstream between positions -779 and -118. C1 NCI, FREDERICK CANC RES & DEV CTR, DIV CANC TREATMENT, BIOL RESPONSE MODIFIERS PROGRAM, FREDERICK, MD 21702 USA. NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA. NR 44 TC 48 Z9 49 U1 0 U2 2 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 APR 15 PY 1994 VL 269 IS 15 BP 11065 EP 11072 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF966 UT WOS:A1994NF96600018 PM 7512557 ER PT J AU KOZYAVKIN, SA KRAH, R GELLERT, M STETTER, KO LAKE, JA SLESAREV, AI AF KOZYAVKIN, SA KRAH, R GELLERT, M STETTER, KO LAKE, JA SLESAREV, AI TI A REVERSE GYRASE WITH AN UNUSUAL STRUCTURE - A TYPE-I DNA TOPOISOMERASE FROM THE HYPERTHERMOPHILE METHANOPYRUS-KANDLERI IS A 2-SUBUNIT PROTEIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GTP-BINDING PROTEIN; ESCHERICHIA-COLI; DESULFUROCOCCUS-AMYLOLYTICUS; SUPERHELICAL TURNS; CLEAVAGE REACTION; SUPERCOILED DNA; ATPASE ACTIVITY; NALIDIXIC-ACID; GENE-PRODUCT; DUPLEX DNA AB Reverse gyrase, an ATP-dependent topoisomerase that positively supercoils DNA, has been purified to near-homogeneity from the hyperthermophile Methanopyrus kandleri. It migrates on SDS-polyacrylamide gel electrophoresis as two principal bands with apparent molecular masses of 150 and 50 kDa. Both proteins remain associated throughout all chromatographic steps. Transfer of a radioactive phosphate from DNA to the 50-kDa protein and gel retardation experiments indicate that this protein forms the covalent complex with DNA. A blot overlay assay identifies the 150-kDa protein as the potential ATPase. This is the first evidence that a reverse gyrase can be a topoisomerase consisting of two protomers. In analogy with the DNA gyrase A subunit (DNA breakage and reunion activity) and the B subunit (ATPase), the 50- and 150-kDa components of Mka reverse gyrase have been designated the A and B subunits, respectively. Methanopyrus reverse gyrase changes DNA linking number in steps of one and its A subunit covalently binds to the 5'-DNA phosphoryl group. It nicks DNA at sites that predominantly have a cytosine at the -4-position. The same rule was derived previously for monomeric reverse gyrase from sulfur-metabolizing hyperthermophiles and for topoisomerase I from mesophilic bacteria. Based on these results, Mka reverse gyrase is classified as belonging to group A of type I topoisomerases. The structural diversity of type I group A topoisomerases parallels the diversity of type II enzymes and suggests the evolution of an essential function by gene fusion. C1 UNIV REGENSBURG,W-8400 REGENSBURG,GERMANY. UNIV CALIF LOS ANGELES,INST MICROBIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT BIOL,LOS ANGELES,CA 90024. RP KOZYAVKIN, SA (reprint author), NIDDKD,MOLEC BIOL LAB,BLDG 5,RM 238,BETHESDA,MD 20892, USA. NR 90 TC 29 Z9 29 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1994 VL 269 IS 15 BP 11081 EP 11089 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF966 UT WOS:A1994NF96600020 PM 8157633 ER PT J AU CAMERON, CE RIDKY, TW SHULENIN, S LEIS, J WEBER, IT COPELAND, T WLODAWER, A BURSTEIN, H BIZUBBENDER, D SKALKA, AM AF CAMERON, CE RIDKY, TW SHULENIN, S LEIS, J WEBER, IT COPELAND, T WLODAWER, A BURSTEIN, H BIZUBBENDER, D SKALKA, AM TI MUTATIONAL ANALYSIS OF THE SUBSTRATE-BINDING POCKETS OF THE ROUS-SARCOMA VIRUS AND HUMAN IMMUNODEFICIENCY VIRUS-1 PROTEASES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AVIAN RETROVIRAL PROTEASE; HIV-1 PROTEASE; POL POLYPROTEINS; TYPE-1 PROTEASE; RESOLUTION; INHIBITOR; COMPLEX; GAG; CLEAVAGE; PROTEINS AB Mutations, designed by analysis of the crystal structures of Rous sarcoma virus (RSV) and human immunodeficiency virus type 1 (HIV-1) protease (PR), were introduced into the substrate binding pocket of RSV PR. The mutations substituted nonconserved residues of RSV PR, located within 10 angstrom of the substrate, for those in structurally equivalent positions of HIV-1 PR. Changes in the activity of purified mutants were detected in vitro by following cleavage of synthetic peptides representing wild-type and modified RSV and HIV-1 gag and pol polyprotein cleavage sites. Substituting threonine for valine 104 (V104T), S107N, I44V, Q63M or deletion of residues 61-63 produced enzymes that were 2.5-7-fold more active than the wild type RSV PR. Substituting I42D, M73V, and A100L produced enzymes with lower activity, whereas a mutant that included both M73V and A100L was as active as wild type. Several substitutions altered the specificity for substrate. These include I42D and I44V, which contribute to the S2 and S2' subsites. These proteins exhibited HIV-1 PR specificity for P2- or P2'-modified peptide substrates but unchanged specificity with P4-, P3-, P1-, P1'-, and P3'-modified substrates. Changes in specificity in the S4 subsite were detected by deletion of residues 61-63. These results confirm the hypothesis that the subsites of the substrate binding pocket of the retroviral protease are capable of acting independently in the selection of substrate amino acids. C1 CASE WESTERN RESERVE UNIV,SCH MED,CLEVELAND,OH 44106. THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,PHILADELPHIA,PA 19107. NCI,FREDERICK CANC RES & DEV CTR,ADV BIOSCI LAB,BASIC RES PROGRAM,FREDERICK,MD 21702. FOX CHASE CANC CTR,INST CANC,PHILADELPHIA,PA 19111. FU NCI NIH HHS [CA06937, CA47486, CA52047, R01 CA052047, R01 CA052047-09] NR 25 TC 27 Z9 27 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1994 VL 269 IS 15 BP 11170 EP 11177 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF966 UT WOS:A1994NF96600032 PM 8157644 ER PT J AU EGERTON, M SAMELSON, LE AF EGERTON, M SAMELSON, LE TI BIOCHEMICAL-CHARACTERIZATION OF VALOSIN-CONTAINING PROTEIN, A PROTEIN-TYROSINE KINASE SUBSTRATE IN HEMATOPOIETIC-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECEPTOR ZETA-CHAIN; ANTIGEN RECEPTOR; T-CELLS; PHOSPHOLIPASE C-GAMMA-1; SIGNAL TRANSDUCTION; ACTIVATION; PHOSPHORYLATION; YEAST; GENE; CD4 AB Engagement of the T cell antigen receptor (TCR) leads to activation of multiple tyrosine kinases and rapid tyrosine phosphorylation of intracellular protein substrates. A number of these substrates have been identified and they include TCR subunits, phospholipase C-gamma1, p95vav, and ezrin. In a recent study we have demonstrated that VCP (valosin-containing protein) becomes tyrosine phosphorylated upon TCR cross-linking. Analysis of the predicted amino acid sequence of this protein indicates that it is a member of a family of oligomeric proteins containing duplicated domains with predicted ATPase activity. In the current study we determine the site of tyrosine phosphorylation in VCP, demonstrate that murine VCP indeed is an oligomeric ATPase, and show that the tyrosine phosphorylation of the protein has no effect on VCP ATPase activity. Recent evidence suggests that VCP associates with clathrin. A possible role of tyrosine phosphorylation in regulating this protein-protein interaction is discussed. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NR 46 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 APR 15 PY 1994 VL 269 IS 15 BP 11435 EP 11441 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF966 UT WOS:A1994NF96600068 PM 8157674 ER PT J AU BLUML, K MUTSCHLER, E WESS, J AF BLUML, K MUTSCHLER, E WESS, J TI FUNCTIONAL-ROLE OF A CYTOPLASMIC AROMATIC AMINO-ACID IN MUSCARINIC RECEPTOR-MEDIATED ACTIVATION OF PHOSPHOLIPASE-C SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BETA-ADRENERGIC-RECEPTOR; ACETYLCHOLINE-RECEPTOR; LIGAND-BINDING; PHOSPHATIDYLINOSITOL HYDROLYSIS; INTRACELLULAR LOOP; DOMAINS; GS; SUBTYPES; SELECTIVITY; IDENTIFICATION AB The N-terminal portion of the third intracellular loop (i3) of muscarinic acetylcholine and other G protein-coupled receptors has been shown to largely determine the G protein coupling profile of a given receptor subtype. Using the rat m3 muscarinic receptor as a model system, we have recently demonstrated that a tyrosine residue (Tyr-254), located at the beginning of the i3 domain, is critically involved in muscarinic receptor-mediated stimulation of phosphatidylinositol (PI) hydrolysis (Bluml, K., Mutschler, E., and Wess, J. (1994) J. Biol. Chem. 269, 402-405). This study was designed to investigate the functional role of this amino acid in further molecular detail. Replacement of Tyr-254 (rat m3 receptor) with alanine or exchange of its position with Ile-253 virtually abolished receptor-mediated stimulation of PI hydrolysis studied in transfected COS-7 cells. In contrast, substitution of Tyr-254 by other aromatic residues such as phenylalanine or tryptophan resulted in mutant receptors that behaved functionally similar to the wild type m3 receptor. Introduction of Tyr-254 into the corresponding position (Ser-210) of the m2 muscarinic receptor (which is only poorly coupled to PI turnover) did not result in an enhanced PI response. However, ''reinsertion'' of Tyr-254 into a functionally inactive chimeric m3/m2 muscarinic receptor (containing m2 receptor sequence at the N terminus of the i3 loop) yielded a mutant receptor that was able to stimulate PI hydrolysis to a similar maximum extent as the wild type m3 receptor. Taken together, our data provide strong evidence that muscarinic receptor-mediated stimulation of PI metabolism is critically dependent on the presence and proper positioning of an aromatic residue at the beginning of the i3 loop. C1 NIDDKD,BIOORGAN CHEM LAB,BLDG 8A,RM B1A-09,BETHESDA,MD 20892. UNIV FRANKFURT,DEPT PHARMACOL,D-60053 FRANKFURT,GERMANY. NR 36 TC 39 Z9 40 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1994 VL 269 IS 15 BP 11537 EP 11541 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF966 UT WOS:A1994NF96600083 PM 8157684 ER PT J AU KAZANIETZ, MG BUSTELO, XR BARBACID, M KOLCH, W MISCHAK, H WONG, G PETTIT, GR BRUNS, JD BLUMBERG, PM AF KAZANIETZ, MG BUSTELO, XR BARBACID, M KOLCH, W MISCHAK, H WONG, G PETTIT, GR BRUNS, JD BLUMBERG, PM TI ZINC-FINGER DOMAINS AND PHORBOL ESTER PHARMACOPHORE - ANALYSIS OF BINDING TO MUTATED FORM OF PROTEIN KINASE-C-TAU AND THE VAV AND C-RAF PROTOONCOGENE PRODUCTS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID REGULATORY DOMAIN; MOUSE-BRAIN; ACTIVATION; DIACYLGLYCEROL; RECEPTOR; GENE; ZETA; PHOSPHORYLATION; PHOSPHOLIPIDS; INHIBITORS AB The phorbol ester binding domain consists of a cysteine-rich region with a postulated consensus sequence for binding that includes 15 amino acids (Ahmed, S., Kozma, R., Lee, J., Monfries, C., Harden, N., and Lim, L. (1991) Biochem. J. 280,233-241). In PKC zeta, the only PKC isoform lacking phorbol ester binding, this region differs in a single residue from the consensus (proline in position 11 of the motif). Restoration of this proline by site-directed mutagenesis of PKC zeta does not restore binding of either [H-3]phorbol 12,13-dibutyrate or of the ultrapotent ligand [H-3]bryostatin 1, suggesting that even a low affinity ligand interaction is absent. In addition, the vav and c-raf proto-oncogene products, proteins that possess cysteine-rich regions with high homology to PKC isozymes and other phorbol ester receptors, are unable to bind any of these ligands. Instead, all of these cysteine-rich regions bind zinc. Our results suggest that other amino acids besides those postulated for the consensus must be necessary for ligand binding and argue against direct modulation of PKC zeta, Vav, and c-Raf by phorbol esters. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT,BETHESDA,MD 20892. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,DEPT MOLEC BIOL,PRINCETON,NJ 08543. GSF MUNICH,INST CLIN MOLEC BIOL & TUMOR GENET,HAEMATOLOGIKUM,W-8000 MUNICH 70,GERMANY. NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892. ARIZONA STATE UNIV,CANC RES INST,TEMPE,AZ 85287. RI Mischak, Harald/E-8685-2011 NR 33 TC 107 Z9 107 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1994 VL 269 IS 15 BP 11590 EP 11594 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF966 UT WOS:A1994NF96600091 PM 8157692 ER PT J AU SWENDEMAN, SL SPIELHOLZ, C JENKINS, NA GILBERT, DJ COPELAND, NG SHEFFERY, M AF SWENDEMAN, SL SPIELHOLZ, C JENKINS, NA GILBERT, DJ COPELAND, NG SHEFFERY, M TI CHARACTERIZATION OF THE GENOMIC STRUCTURE, CHROMOSOMAL LOCATION, PROMOTER, AND DEVELOPMENTAL EXPRESSION OF THE GAMMA-GLOBIN TRANSCRIPTION FACTOR CP2 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ERYTHROID CELL-PROTEINS; FIREFLY LUCIFERASE GENE; BINDING PROTEINS; MAMMALIAN-CELLS; LINKAGE MAP; DROSOPHILA; HYBRIDIZATION; MOUSE; RNA; ORGANIZATION AB We recently cloned murine and human cDNAs that encode CP2, a cellular transcription factor that interacts with the alpha-globin promoter as well as with additional cellular and viral promoter elements. We have now characterized the genomic structure, chromosome location, promoter, and expression pattern of the factor. Genes for the murine and human mRNAs contained 16 and 15 exons, respectively. Both genes spanned approximately 30 kilobases of chromosomal DNA, and among coding exons, all exon/intron boundaries were conserved. The human gene for CP2 was found to reside on chromosome 12 while the murine gene mapped to the distal end of chromosome 15, near Gdc-1, Wnt-1, and Rarg, a region syntenic with human chromosome 12. The murine and human promoters initiated mRNAs at multiple start sites in a conserved region that spanned more than 450 nucleotides. Lastly, a study of the pattern of CP2 gene expression showed that the factor was expressed in all adult and fetal murine tissues examined from at least day 9.5 of development. C1 CORNELL UNIV,MEM SLOAN KETTERING CANC CTR,GRAD SCH MED SCI,NEW YORK,NY 10021. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP SHEFFERY, M (reprint author), CORNELL UNIV,MOLEC BIOL PROGRAM,NEW YORK,NY 10021, USA. FU NCI NIH HHS [N01-CO-74101, P30-CA-08748]; NIDDK NIH HHS [DK-37513] NR 39 TC 38 Z9 39 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1994 VL 269 IS 15 BP 11663 EP 11671 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF966 UT WOS:A1994NF96600102 PM 8157699 ER PT J AU SPENCER, RGS FISHBEIN, KW LEVITT, MH GRIFFIN, RG AF SPENCER, RGS FISHBEIN, KW LEVITT, MH GRIFFIN, RG TI ROTATIONAL RESONANCE WITH MULTIPLE-PULSE SCALING IN SOLID-STATE NUCLEAR-MAGNETIC-RESONANCE SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID CORRELATION SPECTROSCOPY; FLOQUET THEORY; SPIN SYSTEMS; NMR; BACTERIORHODOPSIN; CONFORMATION; SPECTRA; PAIRS AB Multiple-pulse techniques are applied to rotational resonance experiments in solid-state nuclear magnetic resonance. The usual rotational resonance condition is satisfied when an integral multiple of the magic-angle spinning speed equals the difference in isotropic chemical shifts of the two members of a homonuclear spin-1/2 pair. We show that sequences of rapid periodic radio-frequency pulses scale and rotate both the Zeeman and dipole-dipole Hamiltonians, leading to a modification of the resonance condition and to the introduction of new, single- and double-quantum, rotational resonances. Experimental results are presented which demonstrate these effects in the spectra of doubly C-13-labeled solids. C1 NIA,CELLULAR & MOLEC BIOL LAB,BALTIMORE,MD 21224. MIT,DEPT CHEM,CAMBRIDGE,MA 02139. UNIV STOCKHOLM,FYS KEMI,S-10691 STOCKHOLM,SWEDEN. RP SPENCER, RGS (reprint author), MIT,FRANCIS BITTER NATL MAGNET LAB,CAMBRIDGE,MA 02139, USA. RI Levitt, Malcolm/B-3746-2010; OI Levitt, Malcolm/0000-0001-9878-1180; Fishbein, Kenneth/0000-0002-6353-4603 NR 35 TC 12 Z9 12 U1 1 U2 3 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0021-9606 J9 J CHEM PHYS JI J. Chem. Phys. PD APR 15 PY 1994 VL 100 IS 8 BP 5533 EP 5545 DI 10.1063/1.467171 PG 13 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA NF081 UT WOS:A1994NF08100015 ER PT J AU BRYNGELSON, JD AF BRYNGELSON, JD TI WHEN IS A POTENTIAL ACCURATE ENOUGH FOR STRUCTURE PREDICTION - THEORY AND APPLICATION TO A RANDOM HETEROPOLYMER MODEL OF PROTEIN-FOLDING SO JOURNAL OF CHEMICAL PHYSICS LA English DT Article ID GLOBULAR-PROTEINS; FOLDED STATES; CHAINS AB Attempts to predict molecular structure often try to minimize some potential function over a set of structures. Much effort has gone into creating potential functions and into creating algorithms for minimizing these potential functions. This paper develops a formalism that addresses a complementary question: What are the accuracy requirements for a potential function that predicts molecular structure? The formalism is applied to a simple model of a protein structure potential. The results of this calculation suggest that high accuracy predictions (approximately 1 angstrom rms deviation in alpha-carbon positions) of protein structures require monomer-monomer interaction energies accurate to within 5% to 15%. The paper closes with a discussion of the implications of these results for practical structure prediction. RP BRYNGELSON, JD (reprint author), NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892, USA. NR 18 TC 41 Z9 41 U1 1 U2 3 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0021-9606 J9 J CHEM PHYS JI J. Chem. Phys. PD APR 15 PY 1994 VL 100 IS 8 BP 6038 EP 6045 DI 10.1063/1.467114 PG 8 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA NF081 UT WOS:A1994NF08100065 ER PT J AU BEIER, DC COX, JH VINING, DR CRESSWELL, P ENGELHARD, VH AF BEIER, DC COX, JH VINING, DR CRESSWELL, P ENGELHARD, VH TI ASSOCIATION OF HUMAN CLASS-I MHC ALLELES WITH THE ADENOVIRUS E3/19K PROTEIN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL-SURFACE EXPRESSION; TRANSPLANTATION ANTIGENS; ENDOPLASMIC-RETICULUM; MONOCLONAL-ANTIBODIES; INTRACELLULAR-TRANSPORT; LYMPHOCYTES-T; HEAVY-CHAINS; REGION E3; GLYCOPROTEIN; HLA AB A panel of HLA-A and -B locus products was analyzed for their ability to associate with the adenovirus E3/19K (E19) protein in a co-immunoprecipitation assay. Three general categories of binding were identified. HLA-A2.1 and -B7 bind very well to E19. Compared with A2.1, 6- to 30-fold less E19 was associated with HLA-A3, -A1, and -Aw69; 50- to 150-fold less E19 was associated with HLA-Aw68, -B27, and -Bw58. Digestion with endoglycosidase H indicated that all levels of association resulted in inhibition of intracellular transport and processing, however, a fraction of Aw68, B27, and Bw58 escaped from intracellular retention. In contrast to the human class I molecules analyzed, transport of the murine H-2D(d) molecule was not inhibited in the presence of E19. Hybrid class I molecules, in which exons encoding domains of A2.1 and H-2D(d) had been exchanged, were used to define the regions of A2.1 required for E19 association. The alpha 1 and alpha 2 domains of A2.1 contain the minimum residues necessary for both stable association with E19 and subsequent inhibition of transport. A hybrid construct containing only the alpha 2 domain of A2.1 associated weakly with E19, but its post-translational processing was completely inhibited. In contrast, although a construct containing only the alpha 1 domain of A2.1 also associated weakly with E19, its intracellular transport was slowed rather than completely inhibited. Taken together, these results indicate that residues in both the alpha 1 and alpha 2 domains of A2.1 and D-d can influence stable binding of E19, with the phenotypic changes dominated by the origin of the alpha 2 domain. C1 UNIV VIRGINIA,DEPT MICROBIOL,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,BEIRNE CARTER CTR IMMUNOL RES,CHARLOTTESVILLE,VA 22908. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. YALE UNIV,SCH MED,HOWARD HUGHES MED INST,IMMUNOBIOL SECT,NEW HAVEN,CT 06517. FU NIAID NIH HHS [AI20963] NR 53 TC 91 Z9 92 U1 0 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1994 VL 152 IS 8 BP 3862 EP 3872 PG 11 WC Immunology SC Immunology GA NF018 UT WOS:A1994NF01800018 PM 8144956 ER PT J AU KUBO, RT SETTE, A GREY, HM APPELLA, E SAKAGUCHI, K ZHU, NZ ARNOTT, D SHERMAN, N SHABANOWITZ, J MICHEL, H BODNAR, WM DAVIS, TA HUNT, DF AF KUBO, RT SETTE, A GREY, HM APPELLA, E SAKAGUCHI, K ZHU, NZ ARNOTT, D SHERMAN, N SHABANOWITZ, J MICHEL, H BODNAR, WM DAVIS, TA HUNT, DF TI DEFINITION OF SPECIFIC PEPTIDE MOTIFS FOR 4 MAJOR HLA-A ALLELES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CLASS-I MOLECULES; HISTOCOMPATIBILITY COMPLEX MHC; NUCLEOTIDE-SEQUENCE; ANTIGEN PRESENTATION; MONOCLONAL-ANTIBODY; T-CELLS; CDNA; GENE; BINDING; PROTEIN AB Allele-specific motifs for the human MHC class I molecules, HLA-A1, A3, A11, and A24 were characterized by three complementary approaches. First, amino acid sequence analysis of acid eluted peptide pools from affinity purified class I molecules defined putative motifs 9 or 10 amino acids in length and bearing critical anchor residues at position 2 and at the COOH-terminal. These motifs were distinct, with the exception of the HLA-A3 and A11 motifs that were very similar to each other. Second, the correctness of these putative motifs was verified by analyzing the binding capacity of polyalanine peptide analogues to purified HLA-A molecules. Several alternative anchor residues that were not obvious from the pooled peptide sequencing analysis were identified. Third, sequences of individual peptides eluted from HLA-A1, A11, and A24 were determined by tandem mass spectrometry. Nonamers were the predominant species, although peptides of 8, 10, 11, and 12 amino acids in length were also identified. These peptides displayed anchor residues predicted by the specific motifs at position 2 and at the COOH-terminal, regardless of peptide length. Synthetic versions of the naturally processed peptides were shown to bind to the appropriate HLA-A alleles with IC50 values in the 0.3- to 200-nM range. A rational approach to search Ags with known amino acid sequences for epitopes restricted by some of the most common HLA-A types and of potential clinical importance is now feasible. C1 NCI,BETHESDA,MD 20892. UNIV VIRGINIA,DEPT CHEM,CHARLOTTESVILLE,VA 22901. RP KUBO, RT (reprint author), CYTEL CORP,DEPT IMMUNOL,3525 JOHN HOPKINS COURT,SAN DIEGO,CA 92121, USA. RI Hunt, Donald/I-6936-2012 OI Hunt, Donald/0000-0003-2815-6368 FU NIAID NIH HHS [AI-18634]; NIGMS NIH HHS [GM3 7537] NR 67 TC 267 Z9 268 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1994 VL 152 IS 8 BP 3913 EP 3924 PG 12 WC Immunology SC Immunology GA NF018 UT WOS:A1994NF01800023 PM 8144960 ER PT J AU VANDERVORT, AL YAN, L MADARA, PJ COBB, JP WESLEY, RA CORRIVEAU, CC TROPEA, MM DANNER, RL AF VANDERVORT, AL YAN, L MADARA, PJ COBB, JP WESLEY, RA CORRIVEAU, CC TROPEA, MM DANNER, RL TI NITRIC-OXIDE REGULATES ENDOTOXIN-INDUCED TNF-ALPHA PRODUCTION BY HUMAN NEUTROPHILS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; FACTOR GENE-EXPRESSION; VASCULAR ENDOTHELIAL-CELLS; PURIFIED GUANYLATE-CYCLASE; SMOOTH-MUSCLE CELLS; PLATELET-AGGREGATION; CYCLIC-GMP; MONONUCLEAR-CELLS; L-ARGININE; RELEASE AB We studied the effect of nitric oxide on LPS-induced TNF-cr production by human neutrophils. Human neutrophils exposed to LPS and IFN-gamma did not show measurable increases in intracellular cyclic GMP (cGMP). However, cGMP increased upto 30-fold (p < 0.01) in neutrophils incubated with both sodium nitroprusside (SNP), an exogenous source of nitric oxide, and N-acetylcysteine (NAC), which increases the bioavailability oi nitric oxide; this increase indicates that neutrophils contain a nitric oxide-sensitive guanylate cyclase. SNP, with or without NAC, did not increase TNF-alpha production in human neutrophils cultured in medium alone. However, LPS-dependent TNF-alpha production was increased by exposure to SNP (p < 0.05); this effect was further increased by the addition of NAC (p < 0.02). IFN-gamma greatly increased LPS-mediated TNF-alpha production by human neutrophils (p < 0.01), and SNP plus NAC was found to further augment this production (p < 0.01). The up-regulation of TNF-alpha production by nitric oxide was not associated with increased amounts of LPS-induced TNF-alpha mRNA, and was not reproduced by exposing neutrophils to cGMP analogues. These data suggest that nitric oxide released by endothelial and vascular smooth muscle cells may exert a paracrine effect on human neutrophils and augment the inflammatory response in sepsis by increasing the production of cytokines. Although the mechanism of this effect remains unknown, it does not seem to be dependent on cGMP or increased levels of TNF-alpha mRNA. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,WASHINGTON,DC 20010. NR 60 TC 118 Z9 119 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1994 VL 152 IS 8 BP 4102 EP 4109 PG 8 WC Immunology SC Immunology GA NF018 UT WOS:A1994NF01800043 PM 8144975 ER PT J AU MAKINO, M TANG, Y MURPHY, DB FREDRICKSON, TN OKADA, Y FUJIWARA, M CHATTOPADHYAY, SK MIZUOCHI, T KOMURO, K MORSE, HC HARTLEY, JW AF MAKINO, M TANG, Y MURPHY, DB FREDRICKSON, TN OKADA, Y FUJIWARA, M CHATTOPADHYAY, SK MIZUOCHI, T KOMURO, K MORSE, HC HARTLEY, JW TI INFLUENCE OF H-2 CLASS-II ANTIGENS ON THE DEVELOPMENT OF MURINE AIDS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID RETROVIRUS-INDUCED IMMUNODEFICIENCY; T-CELL; TRANSGENIC MICE; LEUKEMIA-VIRUS; STAPHYLOCOCCAL ENTEROTOXINS; FUNCTIONAL EXPRESSION; LYMPHOCYTES-T; MOUSE; GENE; MHC AB Inbred strains of mice differ markedly in their relative susceptibility to the development of lymphoproliferation and immunodeficiency, a syndrome termed mouse AIDS (MAIDS), after infection with the LP-BM5 mixture of murine leukemia viruses (MuLV). The etiologic virus in this mixture is replication defective (BM5def) and encodes only a variant gag protein. Genetic determinants of resistance and susceptibility to induction of MAIDS reside both within and outside the MHC. In strains with C57BL background genes, the MHC haplotypes associated with resistance to disease include d and a, whereas haplotypes b, s, and q are associated with sensitivity. Previous studies showed that MHC class I genes (H-2D(d), H-2L(d)) mapping in the D end of H-2 and other genes mapping proximal to the D end determine resistance to MAIDS. This paper examines the nature of these non-D end MHC genes using assays of MHC recombinant and transgenic mice. We demonstrate that expression of E alpha(d) confers significant resistance to MAIDS, even in mice that do not express H-2D(d)/H-2L(d). Unexpectedly, we found that E alpha polymorphisms can significantly influence resistance, with H-2(b) mice bearing E alpha(d) as a transgene having greater resistance to MAIDS than mice bearing an E alpha(k) transgene. E alpha(d)-mediated resistance to MAIDS was associated with decreased levels oi the BM5def genome in splenic DNA, suggesting that E alpha genes exert their effect by enhancing antiviral activity. C1 NIAID,IMMUNOPATHOL LAB,BETHESDA,MD 20892. NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,IMMUNOL LAB,ALBANY,NY 12201. NCI,REGISTRY EXPTL CANC,BETHESDA,MD 20892. UNIV TOKYO,SCH MED,CTR ANIM CARE,TOKYO 113,JAPAN. RP MAKINO, M (reprint author), NATL INST HLTH & NUTR,DEPT BACTERIAL & BLOOD PROD,SHINJU KU,1-23-1-TOYAMA,TOKYO 162,JAPAN. OI Morse, Herbert/0000-0002-9331-3705 FU NIAID NIH HHS [AI-14349-14, N0-AI-72622] NR 52 TC 11 Z9 11 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1994 VL 152 IS 8 BP 4157 EP 4164 PG 8 WC Immunology SC Immunology GA NF018 UT WOS:A1994NF01800049 PM 8144977 ER PT J AU QIAN, JH BOURS, V MANISCHEWITZ, J BLACKBURN, R SIEBENLIST, U GOLDING, H AF QIAN, JH BOURS, V MANISCHEWITZ, J BLACKBURN, R SIEBENLIST, U GOLDING, H TI CHEMICALLY SELECTED SUBCLONES OF THE CEM CELL-LINE DEMONSTRATE RESISTANCE TO HIV-1 INFECTION RESULTING FROM A SELECTIVE LOSS OF NF-KAPPA-B DNA-BINDING PROTEINS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR-NECROSIS-FACTOR; LONG TERMINAL REPEAT; HUMAN T-CELLS; FACTOR-ALPHA; KINASE-C; GENE-EXPRESSION; ACTIVATION; TYPE-1; TRANSCRIPTION AB To delineate cellular genes that are required for optimal HIV-1 infection, CEM cells were subjected to treatment with the chemical mutagen ethylmethanesulfonate (EMS) and subclones were selected based on their increased resistance to HIV-1 infection and reduced syncytium formation, despite relatively normal CD4 expression (20,000 to 25,000 receptors/cell). Two subclones with this phenotype demonstrated a diminished capacity of HIV-1 long terminal repeat-chloramphenicol acetyl transferase expression either after treatment with the protein kinase C activator PMA, or through Tat-mediated transactivation. In this study, we show that the cellular levels of the NF-kappa B DNA binding proteins (but not AP1 or SP1) are markedly reduced in these cell mutants both at the mRNA and protein levels, resulting in reduced nuclear localization of p50/p65 after PMA induction or treatment with the lymphokine TNF-alpha. Transient reconstitution with a plasmid expressing p50 resulted in partial recovery of PMA-inducible LTR-chloramphenicol acetyl transferase expression. These data suggest that, at least in the CEM T cell line, a selective reduction in the NF-kappa B DNA binding proteins is sufficient to curtail HIV-1 infection. C1 US FDA,CTR BIOL EVALUAT & RES,DIV VIRAL PROD,RETROVIRUS RES LAB,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 40 TC 28 Z9 28 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1994 VL 152 IS 8 BP 4183 EP 4191 PG 9 WC Immunology SC Immunology GA NF018 UT WOS:A1994NF01800052 PM 8144979 ER PT J AU GREER, J ERICKSON, JW BALDWIN, JJ VARNEY, MD AF GREER, J ERICKSON, JW BALDWIN, JJ VARNEY, MD TI APPLICATION OF THE 3-DIMENSIONAL STRUCTURES OF PROTEIN TARGET MOLECULES IN STRUCTURE-BASED DRUG DESIGN SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Review ID CARBONIC ANHYDRASE-II; MAMMALIAN SERINE PROTEASES; C2 SYMMETRICAL INHIBITORS; SYNTHETIC HIV-1 PROTEASE; MULTIPLE-MINIMA PROBLEM; CRYSTAL-STRUCTURE; 3-DIMENSIONAL STRUCTURE; RETROVIRAL PROTEASES; HYDROPHOBIC POCKET; RENIN INHIBITORS C1 NCI, FREDERICK CANC RES & DEV CTR, PRI DYNCORP, STRUCT BIOCHEM PROGRAM, FREDERICK, MD 21702 USA. MERCK SHARP & DOHME LTD, MERCK SHARP & DOHME RES LABS, DEPT MED CHEM, W POINT, PA 19486 USA. AGOURON PHARMACEUT, DEPT MED CHEM, SAN DIEGO, CA 92121 USA. RP GREER, J (reprint author), ABBOTT LABS, DEPT BIOL STRUCT, DIV PHARMACEUT PROD, ABBOTT PK, IL 60064 USA. NR 117 TC 190 Z9 194 U1 4 U2 15 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 EI 1520-4804 J9 J MED CHEM JI J. Med. Chem. PD APR 15 PY 1994 VL 37 IS 8 BP 1035 EP 1054 DI 10.1021/jm00034a001 PG 20 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA NG936 UT WOS:A1994NG93600001 PM 8164249 ER PT J AU LI, L WANG, HK KUO, SC WU, TS LEDNICER, D LIN, CM HAMEL, E LEE, KH AF LI, L WANG, HK KUO, SC WU, TS LEDNICER, D LIN, CM HAMEL, E LEE, KH TI ANTITUMOR AGENTS .150. 2',3',4',5',5,6,7-SUBSTITUTED 2-PHENYL-4-QUINOLONES AND RELATED-COMPOUNDS - THEIR SYNTHESIS, CYTOTOXICITY, AND INHIBITION OF TUBULIN POLYMERIZATION SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID ANTIMITOTIC AGENTS; ANTICANCER AGENTS; COLCHICINE; DERIVATIVES; ANALOGS; PODOPHYLLOTOXIN; SEPARATION; TAXOL AB As part of our continuing search for potential anticancer drug candidates in the 2-phenyl-4-quinolone series, we have synthesized a series of 6,7-methylenedioxy-substituted and unsubstituted 2-phenyl-4-quinolones, as well as related compounds. Their in vitro inhibition of human tumor cell lines and tubulin polymerization is reported. In general, a good correlation was found between cytotoxicity and inhibition of tubulin polymerization. Compounds 7, 9, 13, 16, 22, 23, 36, and 37 showed potent inhibitory effects in both assays. AH rigid analogs (47-49) and trimethoxy-substituted compounds showed little or no activity. Substitution at the 4'-position also resulted in compounds with little or no activity, except for hydroxyl or methyl groups at this position. Further investigation is underway to determine if substitution at the 3'-position will result in compounds with increased activity. C1 UNIV N CAROLINA,SCH PHARM,DIV MED CHEM & NAT PROD,NAT PROD LAB,CHAPEL HILL,NC 27599. CHINA MED COLL,GRAD INST PHARMACEUT CHEM,TAICHUNG 400,TAIWAN. NATL CHENG KUNG UNIV,DEPT CHEM,TAINAN 70101,TAIWAN. NCI,DRUG SYNTH & CHEM BRANCH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA 17625] NR 40 TC 117 Z9 118 U1 1 U2 8 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 15 PY 1994 VL 37 IS 8 BP 1126 EP 1135 DI 10.1021/jm00034a010 PG 10 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA NG936 UT WOS:A1994NG93600010 PM 8164254 ER PT J AU BOJA, JW KUHAR, MJ KOPAJTIC, T YANG, E ABRAHAM, P LEWIN, AH CARROLL, FI AF BOJA, JW KUHAR, MJ KOPAJTIC, T YANG, E ABRAHAM, P LEWIN, AH CARROLL, FI TI SECONDARY AMINE ANALOGS OF 3-BETA-(4'-SUBSTITUTED PHENYL)TROPANE-2-BETA-CARBOXYLIC ACID-ESTERS AND N-NORCOCAINE EXHIBIT ENHANCED AFFINITY FOR SEROTONIN AND NOREPINEPHRINE TRANSPORTERS SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Note ID DOPAMINE TRANSPORTER; COCAINE RECEPTOR; LIGAND-BINDING; INHIBITION; DERIVATIVES AB N-Norcocaine (2) and six N-nor-3 beta-(4'-substituted phenyl)tropane-2 beta-carboxylic acid esters (4a-f) were synthesized by N-demethylation of cocaine (1) and the appropriate 3 beta-(substituted phenyl)tropane analogues (3a-f) with alpha-chloroethyl chloroformate. Radioligand binding affinities of 2 and 4a-f at the DA, 5-HT, and NE transporter were measured and compared to those of 1 and 3a-f. N-Demethylation produced relatively small effects at the DA transporter. In contrast, 4-19-fold and 2-44-fold enhanced affinity at the serotonin and norepinephrine transporter resulted from demethylation. N-Nor-3 beta-(4'-iodophenyl)tropane-2 beta-carboxylic acid methyl ester (4d) with an IC50 = 0.36 nM showed the greatest affinity for the serotonin transporter. However, N-nor-3 beta-(4'-ethylphenyl)tropane-2 beta-carboxylic acid methyl ester (4e) showed the greatest selectivity for the serotonin transporter. C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. NIDA,ADDICT RES CTR,BALTIMORE,MD 21224. FU NIDA NIH HHS [DA05477] NR 25 TC 96 Z9 96 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 15 PY 1994 VL 37 IS 8 BP 1220 EP 1223 DI 10.1021/jm00034a021 PG 4 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA NG936 UT WOS:A1994NG93600021 PM 8164265 ER PT J AU GOLOMB, D RINZEL, J AF GOLOMB, D RINZEL, J TI CLUSTERING IN GLOBALLY COUPLED INHIBITORY NEURONS SO PHYSICA D LA English DT Article ID ELECTROPHYSIOLOGICAL PROPERTIES; RELAY NEURONS; MODEL; NUCLEUS AB A model of a large Population of identical excitable neurons with a global slowly decaying inhibitory coupling is studied and its patterns of synchrony are examined. In addition to converging to a homogeneous fixed point and a homogeneous limit cycle, the system exhibits cluster states, in which it breaks spontaneously into a few macroscopically big clusters, each of which is fully synchronized. A method for calculating the stability of cluster states is described and used for investigating the dynamical behavior of the network versus the parameters that describe the neurons and synapses. Effects of stochastic noise on the network dynamics are discussed. At large enough noise the system goes to a globally stationary state. Low levels of noise preserve the cluster-like neuron trajectories. In the regime where a noiseless system converges to a fully synchronized periodic state, relatively low noise levels cause neurons to burst only every two or more consecutive time periods. RP GOLOMB, D (reprint author), NIDDK, MATH RES BRANCH, BLDG 31, RM 4B-54, BETHESDA, MD 20892 USA. NR 33 TC 122 Z9 122 U1 0 U2 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-2789 J9 PHYSICA D JI Physica D PD APR 15 PY 1994 VL 72 IS 3 BP 259 EP 282 DI 10.1016/0167-2789(94)90214-3 PG 24 WC Mathematics, Applied; Physics, Multidisciplinary; Physics, Mathematical SC Mathematics; Physics GA NH331 UT WOS:A1994NH33100007 ER PT J AU GEORGOPAPADAKOU, NH WALSH, TJ AF GEORGOPAPADAKOU, NH WALSH, TJ TI HUMAN MYCOSES - DRUGS AND TARGETS FOR EMERGING PATHOGENS SO SCIENCE LA English DT Editorial Material ID PNEUMOCYSTIS-CARINII PNEUMONIA; ELONGATION FACTOR-III; AMPHOTERICIN-B; CANDIDA-ALBICANS; IMMUNOCOMPROMISED PATIENTS; SACCHAROMYCES-CEREVISIAE; FUNGAL-INFECTIONS; THERAPY; DNA; TOPOISOMERASES C1 NCI,INFECT DIS SECT,BETHESDA,MD 20892. RP GEORGOPAPADAKOU, NH (reprint author), ROCHE RES CTR,DEPT ONCOL,NUTLEY,NJ 07110, USA. NR 45 TC 167 Z9 174 U1 0 U2 7 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 15 PY 1994 VL 264 IS 5157 BP 371 EP 373 DI 10.1126/science.8153622 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NG194 UT WOS:A1994NG19400025 PM 8153622 ER PT J AU KAMB, A GRUIS, NA WEAVERFELDHAUS, J LIU, QY HARSHMAN, K TAVTIGIAN, SV STOCKERT, E DAY, RS JOHNSON, BE SKOLNICK, MH AF KAMB, A GRUIS, NA WEAVERFELDHAUS, J LIU, QY HARSHMAN, K TAVTIGIAN, SV STOCKERT, E DAY, RS JOHNSON, BE SKOLNICK, MH TI A CELL-CYCLE REGULATOR POTENTIALLY INVOLVED IN GENESIS OF MANY TUMOR TYPES SO SCIENCE LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ALPHA-INTERFERON; DELETIONS; ONCOGENE; CARCINOMAS; BCL-1 AB A putative tumor suppressor locus on the short arm of human chromosome 9 has been localized to a region of less than 40 kilobases by means of homozygous deletions in melanoma cell lines. This region contained a gene, Multiple Tumor Suppressor 1 (MTS1), that encodes a previously identified inhibitor (pl 6) of cyclin-dependent kinase 4. MTS1 was homozygously deleted at high frequency in cell lines derived from tumors of lung, breast, brain, bone, skin, bladder, kidney, ovary, and lymphocyte. Melanoma cell lines that carried at least one copy of MTS1 frequently carried nonsense, missense, or frameshift mutations in the gene. These findings suggest that MTS1 mutations are involved in tumor formation in a wide range of tissues. C1 NCI,LUNG CANC BIOL SECT,BETHESDA,MD 20889. MYRIAD GENET INC,SALT LAKE CITY,UT 84108. MEM SLOAN KETTERING CANC CTR,LUDWIG INST CANC RES,NEW YORK,NY 10021. CROSS CANC INST,DEPT MED,EDMONTON T6G 1Z2,ALBERTA,CANADA. UNIV UTAH,MED CTR,DEPT MED INFORMAT,SALT LAKE CITY,UT 84112. RP KAMB, A (reprint author), MYRIAD GENET INC,SALT LAKE CITY,UT 84108, USA. RI Yang, Chen/G-1379-2010; OI Gruis, Nelleke/0000-0002-5210-9150 FU NCI NIH HHS [CA-48711] NR 28 TC 2467 Z9 2665 U1 13 U2 59 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 15 PY 1994 VL 264 IS 5157 BP 436 EP 440 DI 10.1126/science.8153634 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NG194 UT WOS:A1994NG19400044 PM 8153634 ER PT J AU STORM, EE HUYNH, TV COPELAND, NG JENKINS, NA KINGSLEY, DM LEE, SJ AF STORM, EE HUYNH, TV COPELAND, NG JENKINS, NA KINGSLEY, DM LEE, SJ TI LIMB ALTERATIONS IN BRACHYPODISM MICE DUE TO MUTATIONS IN A NEW MEMBER OF THE TGF-BETA-SUPERFAMILY SO NATURE LA English DT Article ID MOUSE; BONE; MORPHOGENESIS; PROTEIN; LINKAGE; FAMILY; LOCUS AB THE mutation brachypodism (bp) alters the length and number of bones in the limbs of mice but spares the axial skeleton1,2. It illustrates the importance of specific genes in controlling the morphogenesis of individual skeletal elements in the tetrapod limb3,4. We now report the isolation of three new members of the transforming growth factor-beta (TGF-beta) superfamily5 (growth/differentiation factors (GDF) 5, 6 and 7) and show by mapping, expression patterns and sequencing that mutations in Gdf5 are responsible for skeletal alterations in bp mice. GDF5 and the closely related GDF6 and GDF7 define a new subgroup of factors related to known bone- and cartilage-inducing molecules, the bone morphogenetic proteins (BMPs)6. Studies of Bmp5 mutations in short ear mice have shown that at least one other BMP gene is also required for normal skeletal development7. The highly specific skeletal alterations in bp and short ear mice suggest that different members of the BMP family control the formation of different morphological features in the mammalian skeleton. C1 STANFORD UNIV,MED CTR,SCH MED,DEPT DEV BIOL,BECKMAN CTR B300,STANFORD,CA 94305. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. NR 26 TC 649 Z9 674 U1 0 U2 11 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD APR 14 PY 1994 VL 368 IS 6472 BP 639 EP 643 DI 10.1038/368639a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF392 UT WOS:A1994NF39200062 PM 8145850 ER PT J AU HEINONEN, OP HUTTUNEN, JK ALBANES, D HAAPAKOSKI, J PALMGREN, J PIETINEN, P PIKKARAINEN, J RAUTALAHTI, M VIRTAMO, J EDWARDS, BK GREENWALD, P HARTMAN, AM TAYLOR, PR HAUKKA, J JARVINEN, P MALILA, N RAPOLA, S JOKINEN, P KARJALAINEN, J LAURONEN, J MUTIKAINEN, J SARJAKOSKI, M SUORSA, A TIAINEN, M VERKASALO, M BARRETT, M ALFTHAN, G EHNHOLM, C GREF, CG SUNDVALL, J HAAPA, E OVASKAINEN, ML PALVAALHOLA, M ROOS, E PUKKALA, E TEPPO, L FRICK, H PASTERNACK, A BROWN, BW DEMETS, DL KOKKOLA, K TALA, E AALTO, E MAENPAA, V TIENHAARA, L JARVINEN, M KUULIALA, I LINKO, L MIKKOLA, E NYRHINEN, J RONKANEN, A VUORELA, A KOSKINEN, S LOHELA, P VILJANEN, T GODENHJELM, K KALLIO, T KASKINEN, M HAVU, M KIRVES, P TAUBERT, K ALKIO, H KOSKINEN, R LAINE, K MAKITALO, K RASTAS, S TANI, P NIEMISTO, M SELLERGREN, TL AIKAS, C PEKKANEN, PS TARVALA, R ALANKO, K MAKIPAJA, K VAARA, S SIUKO, H TUOMINEN, V ALAKETOLA, L HAAPANEN, A HAVERI, M KESKINISULA, L KOKKO, E KOSKENKARI, M LINDEN, P NURMENNIEMI, A RANINEN, R RAUDASKOSKI, T TOIVAKKA, SK VIEROLA, H KYRONPALOKAUPPINEN, S SCHOULTZ, E JAAKKOLA, M LEHTINEN, E RAUTASEPPA, K SAARIKOSKI, M LIIPPO, K REUNANEN, K SALOMAA, ER ETTINGER, D HIETANEN, P MAENPAA, H TEERENHOVI, L PROUT, G TASKINEN, E ASKIN, F EROZAN, Y NORDLING, S VIROLAINEN, M KOSS, L SIPPONEN, P LEWIN, K FRANSSILA, K KARKKAINEN, P HEINONEN, M HYVONEN, L KOIVISTOINEN, P OLLILAINEN, V PIIRONEN, V VARO, P BILHUBER, W SALKELD, R SCHALCH, W SPEISER, R AF HEINONEN, OP HUTTUNEN, JK ALBANES, D HAAPAKOSKI, J PALMGREN, J PIETINEN, P PIKKARAINEN, J RAUTALAHTI, M VIRTAMO, J EDWARDS, BK GREENWALD, P HARTMAN, AM TAYLOR, PR HAUKKA, J JARVINEN, P MALILA, N RAPOLA, S JOKINEN, P KARJALAINEN, J LAURONEN, J MUTIKAINEN, J SARJAKOSKI, M SUORSA, A TIAINEN, M VERKASALO, M BARRETT, M ALFTHAN, G EHNHOLM, C GREF, CG SUNDVALL, J HAAPA, E OVASKAINEN, ML PALVAALHOLA, M ROOS, E PUKKALA, E TEPPO, L FRICK, H PASTERNACK, A BROWN, BW DEMETS, DL KOKKOLA, K TALA, E AALTO, E MAENPAA, V TIENHAARA, L JARVINEN, M KUULIALA, I LINKO, L MIKKOLA, E NYRHINEN, J RONKANEN, A VUORELA, A KOSKINEN, S LOHELA, P VILJANEN, T GODENHJELM, K KALLIO, T KASKINEN, M HAVU, M KIRVES, P TAUBERT, K ALKIO, H KOSKINEN, R LAINE, K MAKITALO, K RASTAS, S TANI, P NIEMISTO, M SELLERGREN, TL AIKAS, C PEKKANEN, PS TARVALA, R ALANKO, K MAKIPAJA, K VAARA, S SIUKO, H TUOMINEN, V ALAKETOLA, L HAAPANEN, A HAVERI, M KESKINISULA, L KOKKO, E KOSKENKARI, M LINDEN, P NURMENNIEMI, A RANINEN, R RAUDASKOSKI, T TOIVAKKA, SK VIEROLA, H KYRONPALOKAUPPINEN, S SCHOULTZ, E JAAKKOLA, M LEHTINEN, E RAUTASEPPA, K SAARIKOSKI, M LIIPPO, K REUNANEN, K SALOMAA, ER ETTINGER, D HIETANEN, P MAENPAA, H TEERENHOVI, L PROUT, G TASKINEN, E ASKIN, F EROZAN, Y NORDLING, S VIROLAINEN, M KOSS, L SIPPONEN, P LEWIN, K FRANSSILA, K KARKKAINEN, P HEINONEN, M HYVONEN, L KOIVISTOINEN, P OLLILAINEN, V PIIRONEN, V VARO, P BILHUBER, W SALKELD, R SCHALCH, W SPEISER, R TI EFFECT OF VITAMIN-E AND BETA-CAROTENE ON THE INCIDENCE OF LUNG-CANCER AND OTHER CANCERS IN MALE SMOKERS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID PLATELET-FUNCTION; ALPHA-TOCOPHEROL; RISK; SELENIUM; RETINOL; REDUCE AB Background. Epidemiologic evidence indicates that diets high in carotenoid-rich fruits and vegetables, as well as high serum levels of vitamin E (alphatocopherol) and beta carotene, are associated with a reduced risk of lung cancer. Methods. We performed a randomized, double-blind, placebo-controlled primary-prevention trial to determine whether daily supplementation with alpha-tocopherol, beta carotene, or both would reduce the incidence of lung cancer and other cancers. A total of 29,133 male smokers 50 to 69 years of age from southwestern Finland were randomly assigned to one of four regimens: alpha-tocopherol (50 mg per day) alone, beta carotene (20 mg per day) alone, both alpha-tocopherol and beta carotene, or placebo. Follow-up continued for five to eight years. Results. Among the 876 new cases of lung cancer diagnosed during the trial, no reduction in incidence was observed among the men who received alpha-tocopherol (change in incidence as compared with those who did not, -2 percent; 95 percent confidence interval, -14 to 12 percent). Unexpectedly, we observed a higher incidence of lung cancer among the men who received beta carotene than among those who did not (change in incidence, 18 percent; 95 percent confidence interval, 3 to 36 percent). We found no evidence of an interaction between alpha-tocopherol and beta carotene with respect to the incidence of lung cancer. Fewer cases of prostate cancer were diagnosed among those who received alpha-tocopherol than among those who did not. Beta carotene had little or no effect on the incidence of cancer other than lung cancer. Alpha-tocopherol had no apparent effect on total mortality, although more deaths from hemorrhagic stroke were observed among the men who received this supplement than among those who did not. Total mortality was 8 percent higher (95 percent confidence interval, 1 to 16 percent) among the participants who received beta carotene than among those who did not, primarily because there were more deaths from lung cancer and ischemic heart disease. C1 NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. FINNISH CANC REGISTRY,HELSINKI,FINLAND. UNIV HELSINKI,HELSINKI,FINLAND. UNIV TAMPERE,SF-33101 TAMPERE,FINLAND. STANFORD UNIV,PALO ALTO,CA 94304. UNIV WISCONSIN,MADISON,WI. UNIV TURKU,CENT HOSP,SF-20520 TURKU,FINLAND. HARMA HOSP,ALAHARMA,FINLAND. KANTA HAME CENT HOSP,HAMEENLINNA,FINLAND. KESKI SUOMI CENT HOSP,JYVASKYLA,FINLAND. KILJAVA HOSP,NURMIJARVI,FINLAND. KOTKA HLTH CTR HOSP,KOTKA,FINLAND. KYMENLAAKSO CENT HOSP,KOTKA,FINLAND. LAAKSO AURORA HOSP,HELSINKI,FINLAND. MELTOLA HOSP,KARJAA,FINLAND. PORVOO REG HOSP,PORVOO,FINLAND. PAIJAT HAME CENT HOSP,LAHTI,FINLAND. PAIJAT HAME CENT HOSP,LAHTI,FINLAND. SEINAJIKI CENT HOSP,SEINAJOKI,FINLAND. TAMPERE HLTH CTR HOSP,TAMPERE,FINLAND. TAMPERE UNIV HOSP,TAMPERE,FINLAND. UNIV TURKU,CENT HOSP,SF-20520 TURKU,FINLAND. JOHNS HOPKINS UNIV,BALTIMORE,MD. UNIV HELSINKI,CENT HOSP,HELSINKI,FINLAND. HARVARD UNIV,SCH MED,BOSTON,MA. MONTEFIORE MED CTR,BRONX,NY 10467. JORVI HOSP,SF-02740 ESPOO,FINLAND. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. HOFFMANN LA ROCHE AG,BASEL,SWITZERLAND. RP HEINONEN, OP (reprint author), NATL PUBL HLTH INST,MANNERHEIMINTIE 166,SF-00300 HELSINKI,FINLAND. RI Albanes, Demetrius/B-9749-2015; Haukka, Jari/G-1484-2014 OI Haukka, Jari/0000-0003-1450-6208 NR 29 TC 2554 Z9 2594 U1 9 U2 108 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 14 PY 1994 VL 330 IS 15 BP 1029 EP 1035 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA NF022 UT WOS:A1994NF02200001 ER PT J AU DEGERMAN, E MOOS, M RASCON, A VASTA, V MEACCI, E SMITH, CJ LINDGREN, S ANDERSSON, KE BELFRAGE, P MANGANIELLO, V AF DEGERMAN, E MOOS, M RASCON, A VASTA, V MEACCI, E SMITH, CJ LINDGREN, S ANDERSSON, KE BELFRAGE, P MANGANIELLO, V TI SINGLE-STEP AFFINITY PURIFICATION, PARTIAL STRUCTURE AND PROPERTIES OF HUMAN PLATELET CGMP INHIBITED CAMP-PHOSPHODIESTERASE SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEIN STRUCTURE AND MOLECULAR ENZYMOLOGY LA English DT Article DE PHOSPHODIESTERASE; PLATELET; PROTEIN PURIFICATION; PROTEIN STRUCTURE; (HUMAN) ID CYCLIC-NUCLEOTIDE PHOSPHODIESTERASE; AMP PHOSPHODIESTERASE; SELECTIVE INHIBITORS; ADIPOSE-TISSUE; SMOOTH-MUSCLE; RAT-LIVER; FAT-CELLS; PHOSPHORYLATION; INSULIN; ACTIVATION AB The human platelet cilostamide-and cGMP-inhibited cAMP phosphodiesterase (cGI-PDE) was rapidly purified approximate to 19000-fold to apparent homogeneity using single step affinity chromatography on the isothiocyanate derivative of cilostamide coupled to aminoethyl agarose. Within 24 h, 30 mu g of enzyme protein was obtained from 20 ml of packed platelets. V-max for cAMP and cGMP was 6.1 and 0.9 mu mol/min per mg protein, respectively. Several polypeptides (110/105, 79, 62, 55/53 kDa) were identified after SDS-PAGE, all of which were immunologically related to cGI-PDE and represented approx. 5, 20, 50 and 20% of the total protein, respectively. Limited proteolysis of the cGI-PDE with chymotrypsin produced a major fragment of approximate to 47 kDa (and at least two smaller peptides) with catalytic activity and sensitivity to cGMP and OPC 3911 similar to controls. Phosphorylation of the cGI-PDE by cAMP-dependent protein kinase (A-kinase) resulted in maximal incorporation of 0.6-1.8 mol of P-32/mol 110/105 and 79 kDa polypeptides; much lower and variable amounts of phosphate were incorporated into the 62 and 55/53 kDa polypeptides. After digestion of cGI-PDE with several proteinases a number of peptides were isolated and sequenced. Most of the peptide sequences obtained could be aligned within the carboxy terminal domain of the deduced sequence of the human cardiac cGI-PDE. These and other results suggest that the subunit size of the intact platelet cGI-PDE is 110 kDa and that proteolytic fragments of 79, 62 and 55/53 kDa are produced during purification. The smaller fragments (62 and 55/53 kDa) contain the catalytic domain; the larger fragments (110 and 79 kDa) also contain the regulatory domain with phosphorylation sites for A-kinase C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. LUND UNIV,DEPT CLIN PHARMACOL,LUND,SWEDEN. RP DEGERMAN, E (reprint author), LUND UNIV,DEPT MED & PHYSIOL CHEM,POB 94,S-22100 LUND,SWEDEN. NR 39 TC 33 Z9 35 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4838 J9 BBA-PROTEIN STRUCT M JI Biochim. Biophys. Acta-Protein Struct. Molec. Enzym. PD APR 13 PY 1994 VL 1205 IS 2 BP 189 EP 198 DI 10.1016/0167-4838(94)90233-X PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NH277 UT WOS:A1994NH27700006 PM 8155697 ER PT J AU TSYRLOV, IB MIKHAILENKO, VM GELBOIN, HV AF TSYRLOV, IB MIKHAILENKO, VM GELBOIN, HV TI ISOZYME-SPECIFIC AND SPECIES-SPECIFIC SUSCEPTIBILITY OF CDNA-EXPRESSED CYP1A P-450S TO DIFFERENT FLAVONOIDS SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEIN STRUCTURE AND MOLECULAR ENZYMOLOGY LA English DT Article DE CDNA-EXPRESSED CYTOCHROME; HEPATIC CYTOCHROME; FLAVONOID; INHIBITION; ACTIVATION (MOUSE); (HUMAN) ID HUMAN-LIVER MICROSOMES; RAT-LIVER; CYTOCHROME-P-450 ENZYMES; METABOLISM; ACTIVATION; BENZO(A)PYRENE; INHIBITION; 7,8-BENZOFLAVONE; 2-ACETYLAMINOFLUORENE; CYTOCHROMES-P-450 AB The inhibitory and stimulatory effects of six flavonoids with distinct hydroxylation patterns on the recombinant and hepatic mouse and human CYP1A P-450s were studied. cDNA-expressed mouse CYP1A1 and CYP1A2 differed in their sensitivity to both hydroxylated and nonhydroxylated flavonoids, respectively. A comparison between the mouse and human CYP1A2 revealed that cu-naphthoflavone and flavone did not change the benzo[cy]pyrene 3-hydroxylation activity of human CYP1A2 but inhibited its 7-ethoxyresorufin and 7-methoxyresorufin O-dealkylation activities. In contrast, hydroxylated flavonoids increased the 7-methoxyresorufin O-demethylation and acetanilide 4-hydroxylation activities of cDNA-expressed human CYP1A2 and in human liver microsomes. These compounds inhibited the benzo[a]pyrene 3-hydroxylase activity of cDNA-expressed CYP1A1 and CYP1A2s as well as in mouse and human liver microsomes. Hydroxylated flavonoids did not inhibit NADPH-cytochrome P-450 oxidoreductase activity but inhibited NADPH-2,6-dichlorophenolindophenol oxidoreductase activity in liver microsomes and in microsomes from recombinant Hep G2 cells. Structure-activity relationships indicated the importance of hydroxyl groups in the 5- and 7-positions on the A ring of the flavane nucleus. These hydroxyl groups accounted for the inhibitory potency of chrysin on each of the activities of the expressed P-450s, while presence of a hydroxyl group at the 4'-position on the B ring decreased the inhibitory potency of naringenin compared to that of chrysin. The ortho-orientation of a hydroxyl group on the B ring was of importance, inasmuch as quercetin was more potent than morin as an inhibitor of cDNA-expressed and hepatic microsomal monooxygenases. RP TSYRLOV, IB (reprint author), NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 42 TC 89 Z9 94 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4838 J9 BBA-PROTEIN STRUCT M JI Biochim. Biophys. Acta-Protein Struct. Molec. Enzym. PD APR 13 PY 1994 VL 1205 IS 2 BP 325 EP 335 DI 10.1016/0167-4838(94)90252-6 PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NH277 UT WOS:A1994NH27700025 PM 8155716 ER PT J AU LAUNER, LJ HARRIS, T RUMPEL, C MADANS, J AF LAUNER, LJ HARRIS, T RUMPEL, C MADANS, J TI BODY-MASS INDEX, WEIGHT CHANGE, AND RISK OF MOBILITY DISABILITY IN MIDDLE-AGED AND OLDER WOMEN - THE EPIDEMIOLOGIC FOLLOW-UP-STUDY OF NHANES-I SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID CARDIOVASCULAR-DISEASE; MUSCLE LOSS; OVERWEIGHT; POPULATION; STRATEGIES; ARTHRITIS; MORTALITY; STRENGTH; OBESITY; ADULTS AB Objective.-As disability is highly prevalent among older women, is costly, and affects the quality of life, preventable causes of disability must be identified. In this study, we investigated the relationship between the body mass index (BMI), weight change, and the onset of disability in older women. Design.-Prospective cohort study. Setting.-The nationally representative US epidemiologic follow-up study of the National Health and Nutrition Examination Survey (NHANES) I (1971 through 1987). Patients.-White women classified as young-old (mean age 60 years at baseline, mean age 65 years at follow-up) and old-old (mean age 76 years at baseline, mean age 80 years at follow-up). Main Outcome Measures.-The relative odds for the onset of mobility disability associated with tertiles of past BMI (measured 8 to 16 years prior to disability ascertainment) and current BMI (measured 2 to 5 years prior to disability ascertainment) and with weight change between the two weight measurements. Results.-In both cohorts, women in the high past BMI group (>27 in the young-old and >28.1 in the old-old cohort) had a twofold increase in the risk for disability compared with women in the low past BMI group. High current BMI was as strongly related as past-BMI to risk of disability in the young-old women; it was not as strong a predictor in old-old women. In the old-old group only, women who experienced a weight loss of more than 5% had a twofold increase in risk of disability compared with weight-stable women. These results were adjusted for age, smoking, education, and study time and were not importantly modified with the addition into the models of single or multiple health conditions. Conclusions.-These prospective data suggest that high BMI is a strong predictor of long-term risk for mobility disability in older women and that this risk persists even to very old age. However, the paradoxical increase in risk associated with weight loss in the old-old women requires further study. Programs to prevent over weight may have potential for decreasing disability in women. C1 ERASMUS UNIV ROTTERDAM,SCH MED,DEPT EPIDEMIOL & BIOSTAT,3000 DR ROTTERDAM,NETHERLANDS. NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892. NATL CTR HLTH STAT,HYATTSVILLE,MD 20782. RP LAUNER, LJ (reprint author), FREE UNIV AMSTERDAM,DEPT PSYCHIAT,1007 MC AMSTERDAM,NETHERLANDS. NR 33 TC 319 Z9 325 U1 0 U2 10 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 13 PY 1994 VL 271 IS 14 BP 1093 EP 1098 DI 10.1001/jama.271.14.1093 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA NE228 UT WOS:A1994NE22800031 PM 8151851 ER PT J AU CHENG, SY RANSOM, SC MCPHIE, P BHAT, MK MIXSON, AJ WEINTRAUB, BD AF CHENG, SY RANSOM, SC MCPHIE, P BHAT, MK MIXSON, AJ WEINTRAUB, BD TI ANALYSIS OF THE BINDING OF 3,3',5-TRIIODO-L-THYRONINE AND ITS ANALOGS TO MUTANT HUMAN BETA-1 THYROID-HORMONE RECEPTORS - A MODEL OF THE HORMONE-BINDING SITE SO BIOCHEMISTRY LA English DT Article ID C-ERBA; GENERALIZED RESISTANCE; LIGAND-BINDING; DNA-BINDING; AUXILIARY PROTEIN; BARREL ENZYMES; RETINOIC ACID; KINDREDS; HETERODIMERIZATION; SUPERFAMILY AB To understand the nature of the thyroid hormone binding site, we characterized the binding of 3,3',5-triiodo-L-thyronine (T3) and its analogues to eight naturally occurring mutated human beta1 thyroid hormone receptors (h-TRbeta1). The mutant receptors were derived from patients with the syndrome of generalized thyroid hormone resistance, and each has a point mutation in the hormone binding domain (KT, R338W; TP, L450H; IR, D322H; NN, G347E; AH, P453H; OK, M442V; RL, F459C; and ED, A317T). Compared to the wild-type h-TRbeta1, binding of T3 was reduced by as much as 97% for the mutants. The order of binding affinity of wild-type h-TRbeta1 to the analogues is T3 > D-T3 > L-thyroxine > 3,5-diiodo-L-thyronine > 3,3',5'-triiodo-L-thyronine. The mutant receptors showed essentially the same order of reduced affinities for the analogues, but the amounts of the reductions varied in each case. These results suggest specific local interactions (interplay) of analogues with the mutated residues in the receptors. On the basis of these data and a putative structure of the hormone binding domain as an eight-stranded alpha/beta barrel, we propose the location of the hormone in the binding site of h-TRbeta1. Ionic bonds anchor the hormone's alanine side chain to loop 4 of the 8-fold alpha/beta barrel. The phenyl ring lies across the amino-terminal face of the domain with the phenoxy ring pointing downward into the barrel interacting with beta-strand 8 on the opposite side. Loops 1 and 7, which are located on the same face as the DNA binding domain, fold over the top of the barrel toward the bound hormone. The T3-induced conformational changes observed by us and others may be partly mediated by loops 1 and 7. The present model should provide a basis for further studies to understand the T3-dependent transcriptional activity of h-TRbeta1. C1 NIDDKD,BIOCHEM PHARMACOL LAB,BETHESDA,MD 20892. NIDDKD,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD 20892. RP CHENG, SY (reprint author), NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 38 TC 25 Z9 25 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 12 PY 1994 VL 33 IS 14 BP 4319 EP 4326 DI 10.1021/bi00180a028 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF701 UT WOS:A1994NF70100028 PM 8155649 ER PT J AU BERNIER, M LIOTTA, AS KOLE, HK SHOCK, DD ROTH, J AF BERNIER, M LIOTTA, AS KOLE, HK SHOCK, DD ROTH, J TI DYNAMIC REGULATION OF INTACT AND C-TERMINAL TRUNCATED INSULIN-RECEPTOR PHOSPHORYLATION IN PERMEABILIZED CELLS SO BIOCHEMISTRY LA English DT Article ID PHOSPHOTYROSYL-PROTEIN PHOSPHATASES; GROWTH-FACTOR RECEPTORS; ALPHA-1-INHIBITOR-III MESSENGER-RNA; TYROSINE KINASE-ACTIVITY; PHOSPHATIDYLINOSITOL 3-KINASE; STIMULATED PHOSPHORYLATION; AUTOPHOSPHORYLATION SITES; ENDOGENOUS SUBSTRATE; HUMAN-PLACENTA; DIABETIC RATS AB Using digitonin-permeabilized Chinese hamster ovary (CHO) cells that were transfected with intact human insulin receptors (CHO/HlRc cells), we examined insulin receptor phosphorylation and dephosphorylation using pulse-chase techniques. Insulin activated receptor autophosphorylation on tyrosyl residues to a level severalfold over basal, reaching maximal levels after 2, 5, and 10 min of stimulation at 34, 18, and 6-degrees-C, respectively. Phosphopeptide analysis revealed that the triply phosphorylated form of the 1146-kinase domain of the insulin receptor was the major species, which is characteristic of the fully active tyrosine kinase function. The dephosphorylation reaction was time- and temperature-dependent with t1/2 values of 0.67 and 2 min at 18 and 6-degrees-C, respectively. Vanadate completely inhibited dephosphorylation. Under similar permeabilization conditions when compared with CHO/HIRc cells, CHO/DELTACT cells (CHO cells overexpressing a mutated form of the receptor with a 43 amino acid deletion at the C-terminus) stimulated with insulin exhibited larger increases in receptor autophosphorylation levels and in tyrosine kinase activity toward a synthetic peptide substrate; the rate of CHO/DELTACT receptor dephosphorylation was not reduced. There was near-complete absence of insulin receptor substrate 1 (IRS-1) in the cell ghosts after permeabilization. We therefore examined the pattern of tyrosine phosphorylation and dephosphorylation of residual cellular proteins in permeabilized CHO/HlRc cells by Western blot analysis. In addition to the 95-kDa receptor beta-subunit, we detected the phosphorylation of two glycoproteins which included the commonly found 120-kDa protein and a novel 195-kDa protein whose dephosphorylation rate is slower than that of receptor beta-subunit. We conclude that there is an intimate association between insulin receptor and the protein(s) involved in the dephosphorylation cascade which is maintained in these permeabilized cells, even in the absence of IRS-1. This cell system allows new insights into insulin action (independent of IRS-1) by studying the effect of biological substances on the dynamic regulation of receptor phosphorylation and dephosphorylation as well as tyrosine kinase activity of the receptor beta-subunit. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV GERIATR MED & GERONTOL,BALTIMORE,MD 21224. RP BERNIER, M (reprint author), NIA,GERONTOL RES CTR,CLIN PHYSIOL LAB,DIABET UNIT,ROOM 2B-01,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. OI Bernier, Michel/0000-0002-5948-368X NR 58 TC 25 Z9 25 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 12 PY 1994 VL 33 IS 14 BP 4343 EP 4351 DI 10.1021/bi00180a031 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF701 UT WOS:A1994NF70100031 PM 8155652 ER PT J AU SHI, XL DONG, ZG DALAL, NS GANNETT, PM AF SHI, XL DONG, ZG DALAL, NS GANNETT, PM TI CHROMATE-MEDIATED FREE-RADICAL GENERATION FROM CYSTEINE, PENICILLAMINE, HYDROGEN-PEROXIDE, AND LIPID HYDROPEROXIDES SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE LA English DT Article DE HYDROXYL RADICAL; THIYL RADICAL; CHROMIUM(V); SPIN TRAPPING; HYDROGEN PEROXIDE; LIPID HYDROPEROXIDE ID CHROMIUM(VI)-INDUCED DNA DAMAGE; CARCINOGEN CHROMATE; GLUTATHIONE; REDUCTION; CHROMIUM; MECHANISM; THIOLS; INVITRO; ACIDS; CR(V) AB The Cr(VI)-mediated free radical generation from cysteine, penicillamine, hydrogen peroxide, and model lipid hydroperoxides was investigated utilizing the electron spin resonance (ESR) spin trapping technique. Incubation of Cr(VI) with cysteine (Cys) generated cysteinyl radical. Radical yield depended on the relative concentrations of Cr(VI) and Cys. The radical generation became detectable at a cysteine:Cr(VI) ratio of about 5, reached its highest level at a ratio of 30, and declined thereafter. Cr(VI) or Cys alone did not generate a detectable amount of free radicals. Similar results were obtained with penicillamine. Incubation of Cr(VI), Cys or penicillamine and H2O2 led to hydroxyl(.OH) radical generation, which was verified by quantitative competition experiments utilizing ethanol. The mechanism for .OH radical generation is considered to be a Cr(VI)-mediated Fenton-like reaction. When model lipid hydroperoxides such as t-butyl hydroperoxide and cumene hydroperoxide were used in place of H2O2, hydroperoxide-derived free radicals were produced. Since thiols, such as Cys, exist in cellular systems at relatively high concentrations, Cr(VI)-mediated free radical generation in the presence of thiols may participate in the mechanisms of Cr(VI)-induced toxicity and carcinogenesis. C1 NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. W VIRGINIA UNIV,DEPT CHEM,MORGANTOWN,WV 26506. W VIRGINIA UNIV,DEPT BASIC PHARMACEUT SCI,MORGANTOWN,WV 26506. RP SHI, XL (reprint author), NCI,EXPTL PATHOL LAB,BLDG 41,ROOM C301,BETHESDA,MD 20892, USA. RI Shi, Xianglin/B-8588-2012; Gannett, Peter/J-3347-2015 OI Gannett, Peter/0000-0002-7859-5468 NR 56 TC 56 Z9 57 U1 0 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4439 J9 BBA-MOL BASIS DIS JI Biochim. Biophys. Acta-Mol. Basis Dis. PD APR 12 PY 1994 VL 1226 IS 1 BP 65 EP 72 DI 10.1016/0925-4439(94)90060-4 PG 8 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA NG545 UT WOS:A1994NG54500010 PM 8155741 ER PT J AU YAMAZAKI, H SCHNEIDER, E MYERS, CE SINHA, BK AF YAMAZAKI, H SCHNEIDER, E MYERS, CE SINHA, BK TI ONCOGENE OVEREXPRESSION AND DE-NOVO DRUG-RESISTANCE IN HUMAN PROSTATE-CANCER CELLS SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE LA English DT Article DE ONCOGENE; CISPLATIN; ETOPOSIDE; DRUG RESISTANCE; HUMAN PROSTATE TUMOR CELL ID TUMOR-CELLS; FOS-PROTEIN; C-FOS; EXPRESSION; LINES; MECHANISM; AGENTS; GROWTH; MYC AB We have isolated a variant [PC3(R)] of the human prostate PC3 tumor cell line which showed resistance to several anticancer drugs. Studies to evaluate the mechanisms of resistance to anticancer drugs in the PC3(R) cell line indicated that mdr1 was not overexpressed. Studies also indicated that activities of topo I and topo II were not different in these cell lines, nor was there any difference in the formation of drug-induced KCI-SDS precipitable complexes, indicating that topoisomerases were not involved in the development of resistance in PC3(R) cells. While the activity of glutathione S-transferase and total glutathione levels were also similar in these cell lines, the glutathione peroxidase activity in PC3(R) cells was 5-fold lower than in PC3 cells. Furthermore, proto-oncogene expression for c-jun, c-myc, and H-ras was Significantly higher in resistant cells than in sensitive cells, indicating that the amplification of early response genes may play a role in the emergence of de novo resistance in PC3(R) cells. C1 NCI,CLIN PHARMACOL BRANCH,BIOCHEM & MOLEC PHARMACOL SECT,BETHESDA,MD 20892. NCI,MED BRANCH,BETHESDA,MD 20892. NR 31 TC 23 Z9 23 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4439 J9 BBA-MOL BASIS DIS JI Biochim. Biophys. Acta-Mol. Basis Dis. PD APR 12 PY 1994 VL 1226 IS 1 BP 89 EP 96 DI 10.1016/0925-4439(94)90063-9 PG 8 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA NG545 UT WOS:A1994NG54500013 PM 8155744 ER PT J AU LAW, LW VIEIRA, WD HEARING, VJ GERSTEN, DM AF LAW, LW VIEIRA, WD HEARING, VJ GERSTEN, DM TI FURTHER-STUDIES OF THE THERAPEUTIC EFFECTS OF MURINE MELANOMA-SPECIFIC MONOCLONAL-ANTIBODIES SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE LA English DT Article DE MELANOMA-SPECIFIC MONOCLONAL ANTIBODY; METASTASIS; B700 ANTIGEN; ANTIMETASTATIC; ABROGATION ID TUMOR REJECTION; NATURAL-KILLER; ANTIGEN; CELLS; METASTASES; B700; MICE; EXPRESSION; LIVER; LUNG AB The results presented here further characterize four murine monoclonal antibodies (mAb) that recognize melanoma-specific antigens (9B6, T97, 2-3-1 and 2-3-3). These melanoma-specific mAbs are of the IgG(2b) isotype and are significantly therapeutic when administered systemically against established pulmonary melanoma metastases. Here we show a consistent and significant inhibition of the growth of melanoma lung metastases by all four mAbs and the existence of a time 'window' at days 5-8 after tumor inoculation for optimal therapy. Since these mAbs were found not to be cytotoxic or cytolytic in vitro, we looked for host immune response regulation as being responsible for the therapeutic effects. Natural killer (NK) cells were implicated as one arm of the host immune system involved in this response since depletion of NK cells in vivo by alpha asialoGM1 or alpha NK1.1 antibodies partially abrogated the inhibitory effect of the mAbs. The observed antimetastatic effects could also be partially abrogated using antibodies directed against the T-cell subset surface markers, CD4(+) and CD8(+). Intramuscular melanoma tumor growth was also found to be suppressed by mAb 2-3-1, but only if administered in the area of tumor growth and only if multiple inoculations are administered over a 13-day period. The beneficial effect of mAb antimetastatic therapy was found to be useful against several syngeneic melanomas, including JB/MS, B16 and several sublines of the B16 F10 melanoma. C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. RP LAW, LW (reprint author), NCI,GENET LAB,BLDG 37,BETHESDA,MD 20892, USA. NR 25 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4439 J9 BBA-MOL BASIS DIS JI Biochim. Biophys. Acta-Mol. Basis Dis. PD APR 12 PY 1994 VL 1226 IS 1 BP 105 EP 109 DI 10.1016/0925-4439(94)90065-5 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA NG545 UT WOS:A1994NG54500015 PM 7908833 ER PT J AU SAINTJEANNET, JP DAWID, IB AF SAINTJEANNET, JP DAWID, IB TI VERTICAL VERSUS PLANAR NEURAL INDUCTION IN RANA-PIPIENS EMBRYOS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GASTRULATION; NEURAL INDUCTION; AMPHIBIAN ID MONOCLONAL-ANTIBODY EPITOPES; XENOPUS-LAEVIS; FUNCTIONAL DETERMINANTS; AMPHIBIAN EMBRYOS; NERVOUS-SYSTEM; CELL-MIGRATION; FROG EMBRYOS; GASTRULATION; FIBRONECTIN; EXTENSION AB The neural plate in the amphibian embryo is induced in the ectoderm by signals from the dorsal mesoderm. In the extensively studied species Xenopus laevis, such signals are believed to proceed along two alternate pathways, defined as vertical and planar induction. We have studied the relative importance of these pathways in Rana pipiens. In the embryo of this frog, dorsal mesoderm involution can be diverted from its normal course by injection of peptides that inhibit interaction of fibronectin with its receptor. In such embryos, dorsal mesoderm failed to migrate across the blastocoel roof but moved bilaterally along the equator, leading to the formation of two notochords. Neural tissue differentiation occurred in close association with each notochord, but no neural tissue formed along the dorsal midline as might have been predicted by a predominantly planar induction model. While in X. laevis planar induction has been reported to be a major pathway in neuralizing the ectoderm, the results presented here indicate that vertical induction predominates in initiating neural development in R. pipiens embryos. C1 NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. NR 49 TC 21 Z9 21 U1 0 U2 1 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 APR 12 PY 1994 VL 91 IS 8 BP 3049 EP 3053 DI 10.1073/pnas.91.8.3049 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800039 PM 8159704 ER PT J AU TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M AF TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M TI IDENTIFICATION OF A BREFELDIN-A-INSENSITIVE GUANINE NUCLEOTIDE-EXCHANGE PROTEIN FOR ADP-RIBOSYLATION FACTOR IN BOVINE BRAIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CHOLERA TOXIN; GOLGI APPARATUS ID GOLGI MEMBRANES; CHOLERA-TOXIN; BETA-COP; BINDING; ARF; GTP AB ADP-ribosylation factors (ARFs) are almost-equal-to 20-kDa guanine nucleotide-binding proteins that participate in vesicular transport in the Golgi and other intracellular compartments and stimulate cholera toxin ADP-ribosyltransferase activity. ARFs are active in the GTP-bound form; hydrolysis of bound GTP to GDP, possibly with the assistance of a GTP hydrolysis (GTPase)-activating protein results in inactivation. Exchange of GDP for GTP and reactivation were shown by other workers to be enhanced by Golgi membranes in a brefeldin A-sensitive reaction, leading to the proposal that the guanine nucleotide-exchange protein (GEP) was a target of brefeldin A. In the studies reported here, a soluble GEP was partially purified from bovine brain. Exchange of nucleotide on ARFs 1 and 3, based on increased ARF activity in a toxin assay and stimulation of binding of guanosine 5'-[gamma-[S-35]thio]triphosphate, was dependent on phospholipids, with phosphatidylserine being more effective than cardiolipin. GEP appeared to increase the rate of nucleotide exchange but did not affect the affinity of ARF for GTP. Whereas the crude GEP had a size of almost-equal-to 700 kDa, the partially purified GEP behaved on Ultrogel AcA 54 as a protein of 60 kDa. With purification, the GEP activity became insensitive to brefeldin A, consistent with the conclusion that, in contrast to earlier inferences, the exchange protein is not itself the target of brefeldin A. RP TSAI, SC (reprint author), NHLBI,CELLULAR METAB LAB,BLDG 10,ROOM 5N-307,BETHESDA,MD 20892, USA. NR 19 TC 49 Z9 49 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 APR 12 PY 1994 VL 91 IS 8 BP 3063 EP 3066 DI 10.1073/pnas.91.8.3063 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800042 PM 8159707 ER PT J AU KENT, UM MAO, SY WOFSY, C GOLDSTEIN, B ROSS, S METZGER, H AF KENT, UM MAO, SY WOFSY, C GOLDSTEIN, B ROSS, S METZGER, H TI DYNAMICS OF SIGNAL-TRANSDUCTION AFTER AGGREGATION OF CELL-SURFACE RECEPTORS - STUDIES ON THE TYPE-I RECEPTOR FOR IGE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE FC RECEPTOR; MAST CELL; PHOSPHOTYROSINE ID BASOPHILIC LEUKEMIA-CELLS; PROTEIN-TYROSINE PHOSPHORYLATION; FC-EPSILON-RI; HISTAMINE-RELEASE; IMMUNOGLOBULIN-E; MAST-CELLS; RAT; COMPONENT; COMPLEXES; PATHWAYS AB Many ligands stimulate cellular responses by aggregating the cell-surface receptors to which they are bound. We investigated several mechanistic questions related to aggregation of receptors by using the high-affinity receptor for IgE (Fc(epsilon)RI) on mast cells as a model system. We briefly exposed cells to covalently cross-linked oligomers of IgE and then added excess monomeric IgE to prevent further aggregation. Early events were examined by monitoring the phosphorylation of protein tyrosines; later events were examined by monitoring secretion. We found that aggregated receptors continue to signal both late and early events in the absence of formation of new aggregates. Additional experiments suggested that the clustered receptors undergo a dynamic process of phosphorylation and dephosphorylation. Our findings suggest that for these and related receptors that function by aggregation, the persistence of signal transduction is directly related to the intrinsic affinity of the ligand for the individual receptor. C1 UNIV NEW MEXICO,DEPT MATH & STAT,ALBUQUERQUE,NM 87131. LOS ALAMOS NATL LAB,LOS ALAMOS,NM 87545. RP KENT, UM (reprint author), NIAMSD,BETHESDA,MD 20892, USA. FU NIGMS NIH HHS [GM35556] NR 36 TC 42 Z9 42 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 APR 12 PY 1994 VL 91 IS 8 BP 3087 EP 3091 DI 10.1073/pnas.91.8.3087 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800047 PM 7512721 ER PT J AU KANTOROW, M PIATIGORSKY, J AF KANTOROW, M PIATIGORSKY, J TI ALPHA-CRYSTALLIN SMALL HEAT-SHOCK PROTEIN HAS AUTOKINASE ACTIVITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE LENS; PHOSPHORYLATION ID CREUTZFELDT-JAKOB DISEASE; B-CRYSTALLIN; ESCHERICHIA-COLI; LENS CRYSTALLINS; SKELETAL-MUSCLE; PHOSPHORYLATION; EXPRESSION; GENE; TISSUES; KINASE AB The alpha-crystallins (alphaA and alphaB) are major water-soluble proteins of the transparent eye lens that are expressed in a variety of tissues and can function as molecular chaperones. AlphaB-crystallin is also a small heat shock protein associated with numerous degenerative diseases and abnormal growth patterns. Previous experiments have shown that alphaA- and alphaB-crystallin are phosphorylated on specific serine residues by a cAMP-dependent pathway. Here we provide evidence that either total bovine alpha-crystallin or its isolated polypeptides can autophosphorylate serine by a cAMP-independent mechanism in the presence of Mg2+ and [gamma-P-32]ATP; the autophosphorylated products isoelectrically focus with the authentic phosphorylated forms of the alpha-crystallin polypeptides. Thus, the alphaA- and alphaB-crystallin/small heat shock protein polypeptides are enzyme-crystallins which may be involved in metabolic pathways important for the development, maintenance, or pathology of the lens and other tissues. RP NEI, MOLEC & DEV BIOL LAB, BETHESDA, MD 20892 USA. NR 74 TC 117 Z9 119 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 12 PY 1994 VL 91 IS 8 BP 3112 EP 3116 DI 10.1073/pnas.91.8.3112 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800052 PM 8159713 ER PT J AU ARAN, JM GOTTESMAN, MM PASTAN, I AF ARAN, JM GOTTESMAN, MM PASTAN, I TI DRUG-SELECTED COEXPRESSION OF HUMAN GLUCOCEREBROSIDASE AND P-GLYCOPROTEIN USING A BICISTRONIC VECTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MULTIDRUG RESISTANCE; RETROVIRUS; GENE THERAPY; LYSOSOMES; GAUCHER DISEASE ID MULTIDRUG-RESISTANCE GENE; HEMATOPOIETIC STEM-CELLS; BONE-MARROW CELLS; GAUCHER DISEASE; ADENOSINE-DEAMINASE; TRANSGENIC MICE; FOREIGN GENES; EXPRESSION; THERAPY; MDR1 AB Bicistronic cassettes under control of a single promoter have recently been suggested as useful tools for coordinate expression of two different foreign proteins in mammalian cells. Using the long 5' untranslated region of encephalomyocarditis virus as translational enhancer of the second gene, a bicistronic unit composed of cDNA for human P-glycoprotein [the product of the multidrug resistance gene, MDR1 (also called PGY1)] as selectable marker and cDNA for human glucocerebrosidase (GC; EC 3.2.1.45) (a membrane-associated lysosomal hydrolase) was constructed. NIH 3T3 cells transfected with a Harvey murine sarcoma virus retroviral vector carrying this bicistronic cassette (pHaMCG) express active P-glycoprotein and GC and expression of both proteins augments coordinately with selection for increased colchicine resistance. Percoll gradient analysis of homogenates showed that GC was targeted to the lysosomal fraction. The ability to select for expression of GC with natural product drugs after introduction of the pHaMCG retroviral vector may be useful in gene therapy strategies for Gaucher disease. C1 NCI,DIV CANC BIOL DIAGNOSIS & CTR,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NCI,DIV CANC BIOL DIAGNOSIS & CTR,CELL BIOL LAB,BETHESDA,MD 20892. NR 34 TC 89 Z9 89 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 APR 12 PY 1994 VL 91 IS 8 BP 3176 EP 3180 DI 10.1073/pnas.91.8.3176 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800065 PM 7909160 ER PT J AU PENDE, M HOLTZCLAW, LA CURTIS, JL RUSSELL, JT GALLO, V AF PENDE, M HOLTZCLAW, LA CURTIS, JL RUSSELL, JT GALLO, V TI GLUTAMATE REGULATES INTRACELLULAR CALCIUM AND GENE-EXPRESSION IN OLIGODENDROCYTE PROGENITORS THROUGH THE ACTIVATION OF DL-ALPHA-AMINO-3-HYDROXY-5-METHYL-4-ISOXAZOLEPROPIONIC ACID RECEPTORS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE IMMEDIATE EARLY GENES; NGFI-A; O-2A PROGENITORS; KAINATE RECEPTORS ID RAT OPTIC-NERVE; CHANNEL EXPRESSION; TYPE-2 ASTROCYTES; C-FOS; CELL; DIFFERENTIATION; PROLIFERATION; PERMEABILITY; CULTURES; INVITRO AB Oligodendrocytes and their progenitors (O-2A) express functional kainate- and DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-preferring glutamate receptors. The physiological consequences of activation of these receptors were studied in purified rat cortical O-2A progenitors and in the primary oligodendrocyte cell line CG-4. Changes in the mRNA levels of a set of immediate early genes were studied and were correlated to intracellular Ca2+ concentration, as measured by fura-2 Ca2+ imaging. Both in CG-4 and in cortical O-2A progenitors, basal mRNA levels of NGFI-A were much higher than c-fos, c-jun, or jun-b. Glutamate, kainate, and AMPA greatly increased NGFI-A mRNA and protein by activation of membrane receptors in a Ca2+-dependent fashion. Agonists at non-N-methyl-D-aspartate receptors promoted transmembrane Ca2+ influx through voltage-dependent channels as well as kainate and/or AMPA channels. The influx of Ca2+ ions occurring through glutamate-gated channels was sufficient by itself to increase the expression of NGFI-A mRNA. AMPA receptors were found to be directly involved in intracellular Ca2+ and NGFI-A mRNA regulation, because the effects of kainate were greatly enhanced by cyclothiazide, an allosteric modulator that selectively suppresses desensitization of AMPA but not kainate receptors. Our results indicate that glutamate acting at AMPA receptors regulates immediate early gene expression in cells of the oligodendrocyte lineage by increasing intracellular calcium. Consequently, modulation of these receptor channels may have immediate effects at the genomic level and regulate oligodendrocyte development at critical stages. C1 NICHHD,CELLULAR & MOLEC NEUROPHYSIOL LAB,BLDG 49,ROOM 5A-78,BETHESDA,MD 20892. NR 37 TC 89 Z9 89 U1 0 U2 1 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 APR 12 PY 1994 VL 91 IS 8 BP 3215 EP 3219 DI 10.1073/pnas.91.8.3215 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800073 PM 8159727 ER PT J AU AVERBUCHHELLER, L PRUGININ, M KAHANE, N TSOULFAS, P PARADA, L ROSENTHAL, A KALCHEIM, C AF AVERBUCHHELLER, L PRUGININ, M KAHANE, N TSOULFAS, P PARADA, L ROSENTHAL, A KALCHEIM, C TI NEUROTROPHIN-3 STIMULATES THE DIFFERENTIATION OF MOTONEURONS FROM AVIAN NEURAL-TUBE PROGENITOR CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AVIAN EMBRYO; SURVIVAL; TROPHIC FACTORS; TYROSINE KINASE RECEPTOR ID FIBROBLAST GROWTH-FACTOR; NERVOUS-SYSTEM; EMBRYONIC MOTONEURONS; MESSENGER-RNA; SPINAL-CORD; CREST CELLS; EXPRESSION; PROLIFERATION; DEATH; SURVIVAL AB Neurotrophin 3 (NT-3) promotes differentiation of neural tube progenitors into motoneurons expressing the BEN/SC1 and islet-1 epitopes. A 1.75- to 6.7-fold increase in BEN-positive motoneurons was obtained when quail neural tube cells were cultured with NT-3 at 0.1-10 ng/ml, respectively. In contrast, the overall number of cells, as well as the proportion of motoneurons that developed from cycling precursors, did not change. Addition of NT-3 at 1 ng/ml to cells obtained from ventral half-neural tubes promoted a 2.5-fold stimulation in motoneuron number, confirming the specificity of the effect. Moreover, NT-3 had no significant effect on survival of differentiated avian motoneurons. The distribution of trkC mRNA, which encodes the high-affinity receptor for NT-3, is consistent with these findings. trkC expression is homogeneous in the embryonic day 2 (E2) neural tube, becomes restricted to the mantle layer on E3, where differentiation occurs, and disappears from the ventral third of the E4-E5 spinal cord right before the onset of normal motoneuron death. These results suggest that NT-3 and trkC regulate early neurogenesis in the avian central nervous system. C1 HEBREW UNIV JERUSALEM,HADASSAH MED SCH,DEPT ANAT & EMBRYOL,POB 1172,IL-91120 JERUSALEM,ISRAEL. GENENTECH INC,DEPT NEUROSCI,S SAN FRANCISCO,CA 94080. NCI,FREDERICK CANC RES & DEV CTR,MOLEC EMBRYOL SECT,FREDERICK,MD 21702. OI Tsoulfas, Pantelis/0000-0003-1974-6366 NR 34 TC 48 Z9 50 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 APR 12 PY 1994 VL 91 IS 8 BP 3247 EP 3251 DI 10.1073/pnas.91.8.3247 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800080 PM 8159733 ER PT J AU ROESSLER, E GRANT, A JU, G TSUDO, M SUGAMURA, K WALDMANN, TA AF ROESSLER, E GRANT, A JU, G TSUDO, M SUGAMURA, K WALDMANN, TA TI COOPERATIVE INTERACTIONS BETWEEN THE INTERLEUKIN-2 RECEPTOR-ALPHA AND BETA-CHAINS ALTER THE INTERLEUKIN-2-BINDING AFFINITY OF THE RECEPTOR SUBUNITS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AFFINITY CONVERSION ID HUMAN IL-2 RECEPTOR; CELL GROWTH-FACTOR; MONOCLONAL-ANTIBODY; LIGAND-BINDING; SIGNAL TRANSDUCTION; GAMMA-CHAIN; COMPLEX; TAC; IDENTIFICATION; DISTINCT AB The interleukin 2 (IL-2) receptor (IL-2R) is a multisubunit receptor that includes three major IL-2 binding subunits, the IL-2R alpha, beta, and gamma chains. We have detected and analyzed cooperative interactions between the IL-2R alpha and beta chains (IL-2Ralpha and IL2Rbeta, respectively) in COS cells transfected with cDNAs encoding the IL-2Ralpha, the IL-2Rbeta, or both cDNAs. We demonstrated that IL-2 F42A, an analog that fails to bind to the isolated IL-2Ralpha subunit and would be predicted by the hierarchical affinity-conversion model to have impaired binding to cells expressing both chains, instead readily binds to the IL-2Ralpha/beta heterodimer in COS cells. Furthermore, this binding is abolished by the antibody HIEI that separates the two IL-2R subunits. The monoclonal antibodies anti-Tac and Mik-beta1 directed at the IL-2-binding sites on IL-2Ralpha and IL-2Rbeta, respectively; block ligand binding to the heterodimer. This binding pattern is inconsistent with the strict hierarchical affinity-conversion model that mandates an initial binding of IL-2 to IL-2Ralpha followed by binding of the IL-2/IL-2Ralpha complex to IL-2Rbeta. Instead, our results support an alternative model of preformed complexes of IL-2Rbeta with other IL-2R subunits. In this alternative model, IL-2Ralpha and -beta exist in part as preformed complexes in which the affinity of IL-2Rbeta for IL-2 is altered by the proximity of IL-2Ralpha, through mechanisms that do not require the prior binding of IL-2 to IL-2Ralpha. C1 KYOTO KATSURA HOSP,KYOTO 615,JAPAN. TOHOKU UNIV,SCH MED,SENDAI,MIYAGI 980,JAPAN. HOFFMANN LA ROCHE INC,ROCHE RES CTR,DEPT INFLAMMAT AUTOIMMUNE DIS,NUTLEY,NJ 07110. RP ROESSLER, E (reprint author), NCI,METAB BRANCH,BETHESDA,MD 20892, USA. NR 39 TC 30 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 APR 12 PY 1994 VL 91 IS 8 BP 3344 EP 3347 DI 10.1073/pnas.91.8.3344 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800100 PM 8159750 ER PT J AU ARANKALLE, VA CHADHA, MS TSAREV, SA EMERSON, SU RISBUD, AR BANERJEE, K PURCELL, RH AF ARANKALLE, VA CHADHA, MS TSAREV, SA EMERSON, SU RISBUD, AR BANERJEE, K PURCELL, RH TI SEROEPIDEMIOLOGY OF WATER-BORNE HEPATITIS IN INDIA AND EVIDENCE FOR A 3RD ENTERICALLY-TRANSMITTED HEPATITIS AGENT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID NON-B HEPATITIS; NON-A; E VIRUS; EPIDEMIC; CITY AB Many epidemics of water-borne hepatitis have occurred throughout India. These were thought to be epidemics of hepatitis A until 1980, when evidence for an enterically transmitted non-A, non-B hepatitis was first reported. Subsequently, hepatitis E virus was discovered and most recent epidemics of enterically transmitted non-A, non-B hepatitis have been attributed to hepatitis E virus infection. However, only a limited number of cases have been confirmed by immuno electron microscopy, polymerase chain reaction, or seroconversion. In the present study we have performed a retrospective seroepidemiologic study of 17 epidemics of water-borne hepatitis in India. We have confirmed that 16 of the 17 epidemics were caused at least in part by serologically closely related hepatitis E viruses. However, one epidemic, in the Andaman Islands, and possibly a significant minority of cases in other epidemics, appears to have been caused by a previously unrecognized hepatitis agent. C1 NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,BETHESDA,MD 20892. RP ARANKALLE, VA (reprint author), INDIAN COUNCIL MED RES,NATL INST VIROL,20-A DR AMBEDKAR RD,POONA 411001,MAHARASHTRA,INDIA. NR 20 TC 122 Z9 128 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 APR 12 PY 1994 VL 91 IS 8 BP 3428 EP 3432 DI 10.1073/pnas.91.8.3428 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NF968 UT WOS:A1994NF96800117 PM 8159764 ER PT J AU GOPALSRIVASTAVA, R PIATIGORSKY, J AF GOPALSRIVASTAVA, R PIATIGORSKY, J TI IDENTIFICATION OF A LENS-SPECIFIC REGULATORY REGION (LSR) OF THE MURINE ALPHA-B-CRYSTALLIN GENE SO NUCLEIC ACIDS RESEARCH LA English DT Article ID NONLENTICULAR TISSUES; A-CRYSTALLIN; HA-RAS; V-MOS; EXPRESSION; PROTEINS; ASSIGNMENT; EVOLUTION; DISEASE AB Previous studies have shown that the - 661/+ 44 sequence of the murine alpha B-crystallin gene contains a muscle-preferred enhancer (- 426/- 257) and can drive the bacterial chloramphenicol acetyltransferase (CAT) gene in the lens, skeletal muscle and heart of transgenic mice. Here we show that transgenic mice carrying a truncated - 164/ + 44 fragment of the alpha B-crystallin gene fused to the CAT gene expressed exclusively in the lens; by contrast mice carrying a - 426/+ 44 fragment of the alpha B gene fused to CAT expressed highly in the lens, skeletal muscle and heart, and slightly in the lung, brain, kidney, spleen and liver. DNase I protection experiments indicated that the - 147/- 118 sequence is protected by nuclear proteins from alpha TN4-1 lens cell line, but not by nuclear proteins from myotubes of the C2C12 cell line. Site directed mutagenesis of this sequence decreased promoter activity in transiently-transfected lens cells, consistent with this sequence being a lens-specific regulatory region (LSR). We conclude that the - 426/- 257 enhancer is required for expression in skeletal muscle, heart and possibly other tissues, and that the - 164/+ 44 sequence of the alpha B-crystallin gene is sufficient for expression in the lens of transgenic mice. RP NEI, MOLEC & DEV BIOL LAB, BETHESDA, MD 20892 USA. NR 37 TC 33 Z9 33 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 EI 1362-4962 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 11 PY 1994 VL 22 IS 7 BP 1281 EP 1286 DI 10.1093/nar/22.7.1281 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NH132 UT WOS:A1994NH13200024 PM 8165144 ER PT J AU HOELZEL, AR AF HOELZEL, AR TI IMPROVED RESOLUTION OF (CAC)(N) DNA FINGERPRINTS SO NUCLEIC ACIDS RESEARCH LA English DT Note RP HOELZEL, AR (reprint author), NCI,LVC,BLDG 560,,FREDERICK,MD 21701, USA. NR 5 TC 3 Z9 3 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 11 PY 1994 VL 22 IS 7 BP 1315 EP 1315 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NH132 UT WOS:A1994NH13200029 PM 8165148 ER PT J AU BILSKI, P DABESTANI, R CHIGNELL, CF AF BILSKI, P DABESTANI, R CHIGNELL, CF TI PHOTOPROCESSES OF EOSIN AND ROSE-BENGAL ION-PAIRS WITH CATIONIC SURFACTANT IN NONPOLAR-SOLVENTS - APPLICATION IN PHOTOSENSITIZATION STUDIES SO JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY A-CHEMISTRY LA English DT Article ID POLYMER-BASED SENSITIZERS; SINGLET MOLECULAR-OXYGEN; ELECTRON-TRANSFER; AQUEOUS-SOLUTION; QUANTUM YIELD; XANTHENE DYES; DERIVATIVES; AGGREGATION; EXTRACTION; COMPLEXES AB The anionic dyes (D) eosine (Eo) and rose bengal (RB) form hydrophobic neutral ion pairs (DS2) with cationic surfactants (S) which are soluble in non-polar solvents (Bilski et al. J. Phys. Chem., 95 (1991) 5784). The solubility of DS2 in non-polar solvents increases with increasing size of the surfactant cation. We have studied the photoproperties of ion pairs formed between RB or Eo and the dimethyldioctadecylammonium cation (RBS2 and EoS2) in isooctane, CCl4, toluene and CH2Cl2. No significant concentration-dependent aggregation occurred in the dye solutions at room temperature. However, some features of initially formed ''loose'' aggregates developed in isooctane, CCl4 and toluene, while in CH2Cl2 all DS2 spectra were characteristic of the monomeric dyes. DS2 showed a red shift in absorption/fluorescence and low-temperature phosphorescence which is characteristic of xanthene chromophores placed in an aprotic environment. The fluorescence intensity was also high in CH2Cl2 owing to its aproticity and the lack of aggregation. By contrast, aggregation lowered the fluorescence of the dyes in isooctane. Transient absorption measurements in degassed toluene indicated the formation of a triplet state (lambda(max)=630 nm for RB and 600 nm for Eo) which was self-quenched giving rise to transient absorbances at 380 and 460 nm, probably due to the formation of the dye radical anion and cation respectively. We found no evidence for photoredox reactions between the ion pair constituents, S+ and D2-. In aerated solutions, strong O-1(2) phosphorescence at 1268 nm was detected; we have compared the efficiency of O-1(2) phosphorescence emission by the DS2 ion pair with that of tetraphenylporphine zinc complex. The quantum yield of photodepletion of 1,3-diphenylisobenzofuran (DPBF) sensitized by RBS2 (7 muM) in toluene was 0.89. The quantum yield of oxygen consumption during this reaction was 0.75; Eo was about three times less efficient as a sensitizer. The photostability of hydrophobic EoS2 and RBS2 ion pairs, as well as the photosensitization in non-polar solvents, are similar to those in H2O for both dyes. DS2 may be the photosensitizer of choice in some non-polar solvents. RP BILSKI, P (reprint author), NIEHS, MOLEC BIOPHYS LAB, RES TRIANGLE PK, NC 27709 USA. NR 55 TC 22 Z9 22 U1 3 U2 20 PU ELSEVIER SCIENCE SA PI LAUSANNE PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND SN 1010-6030 J9 J PHOTOCH PHOTOBIO A JI J. Photochem. Photobiol. A-Chem. PD APR 10 PY 1994 VL 79 IS 1-2 BP 121 EP 130 DI 10.1016/1010-6030(93)02777-7 PG 10 WC Chemistry, Physical SC Chemistry GA NG405 UT WOS:A1994NG40500018 ER PT J AU MCCANCE, DR PETTITT, DJ HANSON, RL JACOBSSON, LTH KNOWLER, WC BENNETT, PH AF MCCANCE, DR PETTITT, DJ HANSON, RL JACOBSSON, LTH KNOWLER, WC BENNETT, PH TI BIRTH-WEIGHT AND NON-INSULIN-DEPENDENT DIABETES - THRIFTY GENOTYPE, THRIFTY PHENOTYPE, OR SURVIVING SMALL BABY GENOTYPE SO BRITISH MEDICAL JOURNAL LA English DT Article ID IMPAIRED GLUCOSE-TOLERANCE; PIMA INDIAN WOMEN; MELLITUS; PREGNANCY; GROWTH; FETAL AB Objective-To determine the prevalence of diabetes in relation to birth weight in Pima Indians. Design-Follow up study of infants born during 1940-72 who had undergone a glucose tolerance test at ages 20-39 years. Setting-Gila River Indian community, Arizona. Subjects-1179 American Indians. Main outcome measure-Prevalence of non-insulin dependent diabetes mellitus (plasma glucose concentration greater-than-or-equal-to 11.1 mmol/l two hours after ingestion of carbohydrate). Results-The prevalence was greatest in those with the lowest and highest birth weights. The age adjusted prevalences for birth weights <2500 g, 2500-4499 g, and greater-than-or-equal-to 4500 g were 30%, 17%, and 32%, respectively. When age, sex, body mass index, maternal diabetes during pregnancy, and birth year were controlled for, subjects with birth weights < 2500 g had a higher rate than those with weights 2500-4499 g (odds ratio 3.81; 95% confidence interval 1.70 to 8.52). The risk for subsequent diabetes among higher birthweight infants (greater-than-or-equal-to 4500 g) was associated with maternal diabetes during pregnancy. Most diabetes, however, occurred in subjects with intermediate birth weights (2500-4500 g). Conclusions-The relation of the prevalence of diabetes to birth weight in the Pima Indians is U shaped and is related to parental diabetes. Low birth weight is associated with non-insulin dependent diabetes. Given the high mortality of low birthweight infants selective survival in infancy of those genetically predisposed to insulin resistance and diabetes provides an explanation for the observed relation between low birth weight and diabetes and the high prevalence of diabetes in many populations. C1 NIDDKD,PHOENIX EPIDEMIOL & CLIN RES BRANCH,DIABET & ARTHRIT EPIDEMIOL SECT,PHOENIX,AZ 85014. RI Hanson, Robert/O-3238-2015 OI Hanson, Robert/0000-0002-4252-7068 NR 28 TC 461 Z9 469 U1 0 U2 16 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0959-8138 J9 BRIT MED J JI Br. Med. J. PD APR 9 PY 1994 VL 308 IS 6934 BP 942 EP 945 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA NF485 UT WOS:A1994NF48500015 PM 8173400 ER PT J AU STEEL, C GUINEA, A MCCARTHY, JS OTTESEN, EA AF STEEL, C GUINEA, A MCCARTHY, JS OTTESEN, EA TI LONG-TERM EFFECT OF PRENATAL EXPOSURE TO MATERNAL MICROFILAREMIA ON IMMUNE RESPONSIVENESS TO FILARIAL PARASITE ANTIGENS SO LANCET LA English DT Article ID LYMPHATIC FILARIASIS; ONCHOCERCA-VOLVULUS; ENDEMIC FILARIASIS; BRUGIA-PAHANGI; PACIFIC ISLAND; INFECTION; UNRESPONSIVENESS; SENSITIZATION; RESPONSES; TOLERANCE AB To identify long-term effects of prenatal exposure to maternal filarial-parasite infection, we assessed lymphocyte responses in 21 Polynesian children born 17-19 years previously to mothers diagnosed as being microfilaraemic or infection-free. All children lived on an island endemic for bancroftian filariasis but were free from infection at the ti me of study. While children (n = 10) of infection-free mothers responded vigorously to microfilarial antigen with lymphocyte proliferation, production of interleukin 2 (IL-2), IL-5, IL-10, granulocyte macrophage colony-stimulating factor (GM-CSF), and interferon gamma (IFN-gamma), cellular hyporesponsiveness was seen in children (n = 11) born to microfilaraemic mothers. The hyporesponsiveness appeared restricted to microfilarial antigens and did not extend to non-parasite antigens. These findings suggest that hyporesponsiveness resulted from in-utero acquisition of tolerance to microfilarial antigens in chronically-infected mothers. C1 HLTH DEPT,MAUKE,COOK ISLANDS. RP STEEL, C (reprint author), NIH,PARASIT DIS LAB,BLDG 4 ROOM 126,BETHESDA,MD 20892, USA. RI McCarthy, James/C-1681-2009 NR 30 TC 124 Z9 124 U1 0 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 9 PY 1994 VL 343 IS 8902 BP 890 EP 893 DI 10.1016/S0140-6736(94)90009-4 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA NF213 UT WOS:A1994NF21300009 PM 7908359 ER PT J AU BROWN, KE GREEN, SW DEMAYOLO, JA BELLANTI, JA SMITH, SD SMITH, TJ YOUNG, NS AF BROWN, KE GREEN, SW DEMAYOLO, JA BELLANTI, JA SMITH, SD SMITH, TJ YOUNG, NS TI CONGENITAL ANEMIA AFTER TRANSPLACENTAL B19 PARVOVIRUS INFECTION SO LANCET LA English DT Note AB We report three children with congenital anaemia after intrauterine infection with B19 parvovirus. All the fetuses developed hydrops fetails that was treated by blood transfusion. After delivery the infants had hypo-gammaglobulinaemia. In three, sera lacked B19 but viral DNA was found in bone marrow. All were treated with immunoglobulin. One child died and B19 was found in various tissues. In the other two cases, virus could no longer be detected after therapy but the patients remain persistently anaemic. Persistent B19 infection should be suspected in infants with congenital red-cell aplasia. C1 GEORGETOWN UNIV,SCH MED,INT CTR INTERDISCIPLINARY STUDIES IMMUNOL,WASHINGTON,DC. UNIV CHICAGO,MED CTR,PEDIAT HEMATOL ONCOL SECT,CHICAGO,IL 60637. CLIN HEMATOL ONCOL ASSOCIATES,DENVER,CO. PRESBYTERIAN ST LUKES HOSP,ROCKY MT CHILDRENS CANC CTR,DENVER,CO. RP BROWN, KE (reprint author), NHLBI,HEMATOL BRANCH,10-7C218,BETHESDA,MD 20892, USA. NR 9 TC 94 Z9 97 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 9 PY 1994 VL 343 IS 8902 BP 895 EP 896 DI 10.1016/S0140-6736(94)90011-6 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA NF213 UT WOS:A1994NF21300011 PM 7908361 ER PT J AU ALPEROVITCH, A BROWN, P WEBER, T POCCHIARI, M HOFMAN, A WILL, R AF ALPEROVITCH, A BROWN, P WEBER, T POCCHIARI, M HOFMAN, A WILL, R TI INCIDENCE OF CREUTZFELDT-JAKOB-DISEASE IN EUROPE IN 1993 SO LANCET LA English DT Letter ID EPIDEMIOLOGY C1 NIH,CNS STUDIES LAB,BETHESDA,MD 20892. UNIV GOTTINGEN,NEUROL KLIN & POLIKLIN,W-3400 GOTTINGEN,GERMANY. IST SUPER SANITA,REGISTRO NAZL MALATTIA CREUTZFELDT JAKOB,I-00161 ROME,ITALY. ERASMUS UNIV ROTTERDAM,SCH MED,DEPT EPIDEMIOL & BIOSTAT,3000 DR ROTTERDAM,NETHERLANDS. WESTERN GEN HOSP,NATL CREUTZFELDT JAKOB DIS SURVEILLANCE UNIT,EDINBURGH EH4 2XU,MIDLOTHIAN,SCOTLAND. RP ALPEROVITCH, A (reprint author), INSERM,U360,VILLEJUIF,FRANCE. NR 3 TC 22 Z9 22 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 9 PY 1994 VL 343 IS 8902 BP 918 EP 918 DI 10.1016/S0140-6736(94)90037-X PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA NF213 UT WOS:A1994NF21300040 PM 7908378 ER PT J AU WOLFFE, AP AF WOLFFE, AP TI TRANSCRIPTION - IN TUNE WITH THE HISTONES SO CELL LA English DT Review ID CHROMATIN STRUCTURE; TERMINAL MUTATIONS; YEAST; NUCLEOSOME; REPRESSION; PROMOTER; COMPLEX; SWI1 RP WOLFFE, AP (reprint author), NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892, USA. NR 26 TC 232 Z9 232 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD APR 8 PY 1994 VL 77 IS 1 BP 13 EP 16 DI 10.1016/0092-8674(94)90229-1 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NF211 UT WOS:A1994NF21100004 PM 8156588 ER PT J AU VERES, Z KIM, IY SCHOLZ, TD STADTMAN, TC AF VERES, Z KIM, IY SCHOLZ, TD STADTMAN, TC TI SELENOPHOSPHATE SYNTHETASE - ENZYME PROPERTIES AND CATALYTIC REACTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PYRUVATE PHOSPHATE DIKINASE; SELD GENE-PRODUCT; ESCHERICHIA-COLI; SELENIUM METABOLISM; TRANSFER-RNAS; NUCLEOSIDE; MUTANT; 5-METHYLAMINOMETHYL-2-SELENOURIDINE; INTERMEDIATE; GENISTEIN AB Selenophosphate synthetase, the product of the selD gene, produces the biologically active selenium donor compound, monoselenophosphate, from ATP and selenide. Isolation of the enzyme and characterization of some of its physical and catalytic properties are described. Magnesium ion and a monovalent cation, K+, NH4+ , or Rb+, are required for catalytic activity. Polyphosphates and other common nucleotide triphosphates do not replace ATP as substrate. The stoichiometry of the catalytic reaction (Reaction 1) was established using P-31 NMR, anaerobic molecular sieve chromatography, and radiochemical labeling procedures. ATP + selenide + H2O --> selenophosphate + P-i + AMP In the absence of selenide, ATP is converted completely to AMP and orthophosphate upon prolonged incubation with elevated levels of enzyme. AMP is a competitive inhibitor of ATP, K-i = 170 mu m, whereas selenophosphate and orthophosphate are weak inhibitors indicating a multistep reaction. Attempts to obtain direct evidence for a postulated enzyme-pyrophosphate intermediate using several experimental approaches are described. No exchange of [C-14]AMP with ATP could be detected after the enzyme was freed of traces of contaminating adenylate kinase by chromatography on phenyl-Sepharose. C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. HUNGARIAN ACAD SCI,CENT RES INST CHEM,H-1025 BUDAPEST,HUNGARY. UNIV IOWA,DEPT PEDIAT,IOWA CITY,IA 52242. NR 32 TC 99 Z9 103 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 8 PY 1994 VL 269 IS 14 BP 10597 EP 10603 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF017 UT WOS:A1994NF01700062 PM 8144648 ER PT J AU YU, JC MAHADEVAN, D LAROCHELLE, WJ PIERCE, JH HEIDARAN, MA AF YU, JC MAHADEVAN, D LAROCHELLE, WJ PIERCE, JH HEIDARAN, MA TI STRUCTURAL COINCIDENCE OF ALPHA-PDGFR EPITOPES BINDING TO PLATELET-DERIVED GROWTH FACTOR-AA AND A POTENT NEUTRALIZING MONOCLONAL-ANTIBODY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FACTOR RECEPTORS; SIGNAL TRANSDUCTION; CELLS; DIMERIZATION; LOCALIZATION; EXPRESSION; ACTIVATION; PATHWAYS; CLONING; PROTEIN AB We have generated two groups of deletion mutants of the alpha PDGFR and one group of chimeras between alpha PDGFR and beta PDGFR to further investigate the structural requirements of the alpha PDGFR for binding to platelet-derived growth factor (PDGF)-AA and to a monoclonal antibody against alpha PDGFR (designated as mAb-alpha R1). The mAb-alpha R1 has recently been reported to block high affinity binding of PDGF-AA to alpha PDGFR The first group of mutants were carboxyl-terminal deletion mutants encoding the first two immunoglobulin (Ig)-like domains (alpha R1-216), the first four Ig-Like domains (alpha R1-415), or all five Ig-like domains (alpha R1-530) of the alpha PDGFR Since these mutants lacked transmembrane domains, their expression in NIH/3T3 cells resulted in secretion of the truncated alpha PDGFRs. Using conditioned medium from NIH/3T3 transfectants, we showed that mAb-alpha R1 was able to immunoprecipitate each of these secreted form of alpha PDGFRs, suggesting that the epitope recognized by mAb-alpha R1 is located within Ig-like domains 1 and 2 of the alpha PDGFR. Furthermore, PDGF-AA exhibited detectable binding to alpha R1-415 or alpha 1-530 but failed to interact with alpha R1-216, suggesting that the first two Ig-like domains of the alpha PDGFR are not sufficient for PDGF-AA binding. The second group of alpha PDGFR mutants were internal deletion mutants lacking Ig-like loop 1 (alpha R(Delta 49-100)), Ig-like loop 2 (alpha R(Delta 150-189)), Ig-like loop 3 (alpha R(Delta 235-290)), or part of Ig-like loops 4 and 5 (alpha R(Delta 375-450)). The internal deletion mutants were transfected into 32D cells which lack both alpha PDGFR and beta PDGFR PDGF-AA bound with high affinity to 32D cells expressing alpha R(Delta 375-450) but not to 32D cells expressing the other three internal deletion mutants, suggesting that the region required for PDGF-AA binding should be within the first three Ig-like domains of the alpha PDGFR. In addition, mAb-alpha R1 bound to 32D cells expressing alpha R(Delta 235-290) but failed to bind 32D cells transfected with alpha R(Delta 49-100) or alpha R(Delta 150-189). Since this antibody could immunoprecipitate alpha R(Delta 49-100), but not alpha R(Delta 150-189) in cell lysates of the 32D transfectants, these results suggest that Ig-like loop 1 is dispensible for mAb-alpha R1 recognition and deletion of Ig-like loop 1 of alpha PDGFR significantly inhibits cell surface expression. The two alpha/beta PDGFR chimeras generated were an alpha PDGFR containing the first Ig-like domain of beta PDGFR (beta(126)alpha(127)R) and a beta PDGFR possessing the first Ig-Like domain of alpha PDGFR (alpha(119)beta(119)R). PDGF-AA-bound to 32D cells expressing beta(126)alpha(127)R, but not to those expressing alpha(119)beta(119)R, suggesting that Ig-like domain 1 is not required for conferring PDGF-AA binding specificity. Taken together, we conclude that major high affinity sites for PDGF-AA binding are located within Ig-like domains 2 and 3 and that the epitope recognized by mAb-alpha R1 is located within Ig-like domain 2 of the alpha PDGFR. C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 32 TC 23 Z9 23 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 8 PY 1994 VL 269 IS 14 BP 10668 EP 10674 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF017 UT WOS:A1994NF01700072 PM 7511602 ER PT J AU MORROW, CS NAKAGAWA, M GOLDSMITH, ME MADDEN, MJ COWAN, KH AF MORROW, CS NAKAGAWA, M GOLDSMITH, ME MADDEN, MJ COWAN, KH TI REVERSIBLE TRANSCRIPTIONAL ACTIVATION OF MDR1 BY SODIUM-BUTYRATE TREATMENT OF HUMAN COLON-CANCER CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MULTIDRUG-RESISTANCE GENE; TUMOR VIRUS PROMOTER; S-TRANSFERASE-PI; HISTONE ACETYLATION; MAMMALIAN-CELLS; HEAT-SHOCK; DRUG-RESISTANCE; MESSENGER-RNA; RAT-LIVER; EXPRESSION AB We investigated the mechanism of sodium butyrate (NaB)-mediated induction of mdr1 mRNA in parental (wild type) and multidrug-resistant (Ad1000) SW620 colon cancer cell lines. NaB treatment resulted in reversible, time-dependent increases in nuclear run-on transcription of endogenous mdr1 in these cell lines that paralleled the reversible increases of mdr1 mRNA in both timing and magnitude. In contrast, NaB treatment had no effect on mdr1 mRNA stability. Thus, the effects of NaB on mdr1 mRNA levels are fully attributable to altered mdr1 transcription. Furthermore, NaB induces the expression of transiently transfected chloramphenicol acetyltransferase reporter plasmids that are under the transcriptional control of the mdr1 promoter (mdrCAT vectors). Transfections using mdrCAT vectors modified by deletion and site-directed mutagenesis of the mdr1 promoter indicate that NaB-mediated induction of these vectors is at least partially dependent upon sequences present in the basal mdr1 promoter between -89 and +11 relative to the start site of transcription. The Y-box moth located between -82 and -73 contributes to NaB inducibility of mdrCAT vector expression in Ad1000 SW620 cells. C1 NCI,MED BRANCH,BETHESDA,MD 20892. RP MORROW, CS (reprint author), WAKE FOREST UNIV,MED CTR,DEPT BIOCHEM,MED CTR BLVD,WINSTON SALEM,NC 27157, USA. FU NCI NIH HHS [CA-12197] NR 53 TC 47 Z9 48 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 8 PY 1994 VL 269 IS 14 BP 10739 EP 10746 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF017 UT WOS:A1994NF01700082 PM 7908296 ER PT J AU CHEDID, M RUBIN, JS CSAKY, KG AARONSON, SA AF CHEDID, M RUBIN, JS CSAKY, KG AARONSON, SA TI REGULATION OF KERATINOCYTE GROWTH-FACTOR GENE-EXPRESSION BY INTERLEUKIN-1 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELLS; MORPHOGENESIS; KGF; DIFFERENTIATION; INDUCTION; INVITRO; FAMILY AB Keratinocyte growth factor (KGF) is a stromally derived member of the fibroblast growth factor family (FGF7) with potent mitogenic activity on a variety of epithelial cells. To identify molecules that regulate the expression of this paracrine mediator of epithelial proliferation, we investigated the effects of various cytokines and growth factors on KGF production by fibroblasts. The proinflammatory cytokine interleukin 1 (IL1) strongly induced the expression of KGF RNA in fibroblasts from multiple sources. Platelet-derived growth factor BB, IL6, and transforming growth factor a caused a moderate elevation, while tumor necrosis factor a and basic FGF did not alter the level of KGF RNA expression. The induction by IL1 of KGF transcript levels was time and dose dependent and specifically blocked by anti-IL1 antibodies. Nuclear run on experiments indicated that IL1 stimulated KGF gene transcription. Western blot analysis and keratinocyte proliferation assays demonstrated a corresponding increase in mitogenically active KGF protein in conditioned medium obtained from IL1-treated fibroblasts. The stimulation of KGF expression by IL1 and other cytokines such as IL6, transforming growth factor alpha, and platelet-derived growth factor may provide a mechanism for KGF induction during inflammation that would support its proposed role as mediator of reepithelialization and wound healing. RP CHEDID, M (reprint author), NCI,CELLULAR & MOLEC BIOL LAB,BLDG 37,BETHESDA,MD 20892, USA. NR 36 TC 172 Z9 174 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 8 PY 1994 VL 269 IS 14 BP 10753 EP 10757 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF017 UT WOS:A1994NF01700084 PM 7511604 ER PT J AU RANDAZZO, PA KAHN, RA AF RANDAZZO, PA KAHN, RA TI GTP HYDROLYSIS BY ADP-RIBOSYLATION FACTOR IS DEPENDENT ON BOTH AN ADP-RIBOSYLATION FACTOR GTPASE-ACTIVATING PROTEIN AND ACID PHOSPHOLIPIDS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SACCHAROMYCES-CEREVISIAE; RAS GTPASE; BINDING-PROTEIN; ENDOSOME FUSION; CHOLERA-TOXIN; GENE; COFACTOR; ENCODES; DOMAIN; TRANSPORT AB ADP-ribosylation factor (ARF) is a 21-kDa GTP binding protein that regulates eukaryotic membrane traffic. Both the binding and hydrolysis of GTP by ARF have been shown to be necessary for this function. However, purified mammalian ARF lacks intrinsic GTPase activity (<0.0015 min(-1)). We document the presence, in bovine brain extracts, of a protein with the predicted properties for an ARF GTPase activating protein (ARF GAP). This activity was highly dependent on phospholipids. An acid phospholipid fraction from bovine brain (containing primarily phosphatidylinositol 4,5-bisphosphate (PIP2), phosphatidylinositol 4-phosphate, phosphatidylinositol, and phosphatidylserine) had no effect on intrinsic GTPase activity of purified ARF but increased the ARF GAP activity of bovine brain homogenates about 8-fold. This dependence on acid phospholipids was retained after >100-fold purification of ARF GAP, making it, likely, an inherent property of this reaction. PIP2 alone stimulated ARF GAP activity up to 30-fold with a half-maxmal effect at 100-300 mu M but had no effect on the GTPase rate of ARF alone. Phosphatidylinositol 4-phosphate was also active but had only 50% of the maximal effect and twice the EC(50) of PIP2. Phosphatidylserine, phosphatidylethanolamine, phosphatidylcholine, phosphatidylinositol, and diacylglycerol either alone or in the presence of ARF GAP do not stimulate ARF GTPase activity. ARF proteins have been identified recently as regulators of phospholipase D. The product of the phospholipase D reaction, phosphatidic acid, stimulated ARF GAP approximately 5-fold and reduced the PIP2 concentration needed for GAP stimulation about 6-fold. The substrate of phospholipase D, phosphatidylcholine, inhibited ARF GAP activity, but this inhibition seen with phosphatidylcholine was partially reversed by phosphatidic acid. A feedback loop for the coordinate regulation of phospholipase D and ARF activities is proposed. RP RANDAZZO, PA (reprint author), NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BIOL CHEM LAB,BETHESDA,MD 20892, USA. NR 45 TC 174 Z9 176 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 8 PY 1994 VL 269 IS 14 BP 10758 EP 10763 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF017 UT WOS:A1994NF01700085 PM 8144664 ER PT J AU CLARK, DP DURELL, S MALOY, WL ZASLOFF, M AF CLARK, DP DURELL, S MALOY, WL ZASLOFF, M TI RANALEXIN - A NOVEL ANTIMICROBIAL PEPTIDE FROM BULLFROG (RANA-CATESBEIANA) SKIN, STRUCTURALLY RELATED TO THE BACTERIAL ANTIBIOTIC, POLYMYXIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AMINO-ACID-SEQUENCE; ANTIBACTERIAL PEPTIDES; FROG-SKIN; BOVINE NEUTROPHILS; AMPHIBIAN SKIN; PIG INTESTINE; IMMUNITY; CDNA; DERMORPHIN; PRECURSOR AB Antimicrobial peptides comprise a diverse class of molecules used in host defense by plants, insects, and animals. In this study we have isolated a novel antimicrobial peptide from the skin of the bullfrog, Rana catesbeiana. This 20 amino acid peptide, which we have termed Ranalexin, has the amino acid sequence: NH2-Phe-Leu-Gly-Gly-Leu-Ile-Lys-Ile-Val-Pro-Ala-Met-Ile- Cys-Ala-Val-Thr-Lys-Lys-Cys-COOH, and it contains a single intramolecular disulfide bond which forms a heptapeptide ring within the molecule. Structurally, Ranalexin resembles the bacterial antibiotic, polymyxin, which contains a similar heptapeptide ring. We have also cloned the cDNA for Ranalexin from a metamorphic R. catesbeiana tadpole cDNA library. Based on the cDNA sequence, it appears that Ranalexin is initially synthesized as a propeptide with a putative signal sequence and an acidic amino acid-rich region at its amino-terminal end. Interestingly, the putative signal sequence of the Ranalexin cDNA is strikingly similar to the signal sequence of opioid peptide precursors isolated from the skin of the South American frogs Phyllomedusa sauvagei and Phyllomedusa bicolor. Northern blot analysis and in situ hybridization experiments demonstrated that Ranalexin mRNA is first expressed in R. catesbeiana skin at metamorphosis and continues to be expressed into adulthood. C1 MAGAININ PHARMACEUT INC,MAGAININ RES INST,PLYMOUTH MEETING,PA 19462. HOSP UNIV PENN,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. CHILDRENS HOSP,DIV HUMAN GENET & MOLEC BIOL,PHILADELPHIA,PA 19104. NCI,MATH BIOL LAB,BETHESDA,MD 20892. NR 52 TC 167 Z9 176 U1 0 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 APR 8 PY 1994 VL 269 IS 14 BP 10849 EP 10855 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF017 UT WOS:A1994NF01700097 PM 8144672 ER PT J AU BOWDITCH, RD HARIHARAN, M TOMINNA, EF SMITH, JW YAMADA, KM GETZOFF, ED GINSBERG, MH AF BOWDITCH, RD HARIHARAN, M TOMINNA, EF SMITH, JW YAMADA, KM GETZOFF, ED GINSBERG, MH TI IDENTIFICATION OF A NOVEL INTEGRIN BINDING-SITE IN FIBRONECTIN - DIFFERENTIAL UTILIZATION BY BETA-3 INTEGRINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IIB-IIIA COMPLEX; IMMUNOGLOBULIN-LIKE DOMAINS; CELL-ADHESION; DIRECTED MUTAGENESIS; VITRONECTIN RECEPTOR; SECONDARY STRUCTURE; SYNTHETIC PEPTIDES; PLASMA FIBRONECTIN; RIBBON MODELS; HUMAN CD4 AB Fibronectin (Fn) binding to the integrins alpha IIb beta 3 and alpha v beta 3 involves the Arg-Gly-Asp sequence. The identification of other regions of Fn that interact with alpha IIb beta 3 suggests a potential mechanism for differential ligand recognition by integrins. We report here the identification of an 11-residue peptide sequence from the 9th type III repeat of Fn (3Fn9), which inhibits ligand binding to alpha IIb beta 3 by interacting directly with this receptor. Mutational analysis demonstrated that this same region was involved in the formation of epitopes for two anti-Fn mAbs that inhibit Fn binding to alpha IIb beta 3, thus emphasizing the role of this site in the macromolecule. Molecular modeling of the 3Fn9-10 modules suggested that Fn residues Asp(1373)-Th-1383 are at least 25 Angstrom distant from the Arg-Gly-Asp site and therefore does not directly interact with it. The 3Fn9 site was differentially recognized by the beta 3 integrin family. The Asp(1373)-Thr(1383) peptide failed to inhibit ligand binding to alpha v beta 3, a recombinant Fn Ala(1235)-Ser(1436) fragment was not recognized by alpha v beta 3, and addition of the 3Fn9 module to the amino terminus of the 3Fn10 did not affect the potency of inhibiton of Fn binding to alpha v beta 3. Thus, a novel integrin recognition site in the 3Fn9 module of Fn that is differentially recognized by the beta 3 integrins has been localized within the residues Asp(1373)-Thr(1383). C1 SCRIPPS RES INST, DEPT MOLEC BIOL, LA JOLLA, CA 92037 USA. NIDR, DEV BIOL LAB, BETHESDA, MD 20892 USA. RP BOWDITCH, RD (reprint author), SCRIPPS RES INST, DEPT VASC BIOL, COMM VASC BIOL, 10666 N TORREY PINES RD, LA JOLLA, CA 92037 USA. FU NHLBI NIH HHS [HL16411, HL28235, HL31950] NR 60 TC 170 Z9 171 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 8 PY 1994 VL 269 IS 14 BP 10856 EP 10863 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF017 UT WOS:A1994NF01700098 PM 7511609 ER PT J AU HILL, JM AGOSTON, DV GRESSENS, P MCCUNE, SK AF HILL, JM AGOSTON, DV GRESSENS, P MCCUNE, SK TI DISTRIBUTION OF VIP MESSENGER-RNA AND 2 DISTINCT VIP BINDING-SITES IN THE DEVELOPING RAT-BRAIN - RELATION TO ONTOGENIC EVENTS SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE GLIOGENESIS; IN VITRO AUTORADIOGRAPHY; IN SITU HYBRIDIZATION; NEUROPEPTIDES; CNS DEVELOPMENT ID VASOACTIVE-INTESTINAL-PEPTIDE; SUPERIOR CERVICAL-GANGLION; MAJOR CEREBRAL-ARTERIES; ADENYLATE-CYCLASE; MESSENGER-RNA; SPINAL-CORD; SUPRACHIASMATIC NUCLEUS; NEUROTROPHIC ACTION; HIPPOCAMPAL REGION; NERVOUS-SYSTEM AB The peptide neurotransmitter vasoactive intestinal peptide (VIP) has neurotrophic properties and influences neurobehavioral development. To assess the role of VIP during neural ontogeny, the present work traces the development of VIP mRNA with in situ hybridization and VIP receptors with in vitro autoradiography in rat central nervous system (CNS) from embryonic day 14 (E14) to the adult. VIP mRNA was not evident in the CNS until birth. Postnatally, it was expressed in several distinct brain regions, but its distribution bore little relation to that of VIP receptors. VIP receptors were present and expressed changing patterns of distribution throughout CNS development. The changing patterns were the result of 1) the transient appearance of GTP-insensitive VIP receptors in several regions undergoing mitosis or glial fasciculation and 2) the transient appearance of GTP-sensitive VIP receptors homogeneously distributed throughout the CNS during the first 2 postnatal weeks, the period of the brain growth spurt. At E14-16 VIP binding was dense throughout the brainstem and spinal cord, but limited in the rest of the brain. From E19 to postnatal day 14 (P14), while VIP binding was higher in germinal zones, it tended to be uniformly dense throughout the remainder of the brain. By P21 the adult pattern began to emerge; VIP binding was unevenly distributed and was related to specific cytoarchitectural sites. Since the expression of VIP in the CNS is Limited to postnatal development but VIP receptors are abundant prenatally, we suggest that extraembryonic VIP may act upon prenatal VIP receptors to regulate ontogenic events in the brain. (C) 1994 Wiley-Liss, Inc.* C1 NICHHD,DEV NEUROBIOL LAB,MOLEC CONTROL NEURODIFFERENTIAT UNIT,BETHESDA,MD 20892. NINCDS,EXPTL NEUROPATHOL LAB,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,DEPT NEONATOL,WASHINGTON,DC 20010. RP HILL, JM (reprint author), NICHHD,DEV NEUROBIOL LAB,DEV & MOLEC PHARMACOL SECT,BLDG 49,ROOM 5A38,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 79 TC 73 Z9 73 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD APR 8 PY 1994 VL 342 IS 2 BP 186 EP 205 DI 10.1002/cne.903420204 PG 20 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA NA983 UT WOS:A1994NA98300003 PM 8201031 ER PT J AU YENIDUNYA, A DAVEY, C CLARK, D FELSENFELD, G ALLAN, J AF YENIDUNYA, A DAVEY, C CLARK, D FELSENFELD, G ALLAN, J TI NUCLEOSOME POSITIONING ON CHICKEN AND HUMAN GLOBIN GENE PROMOTERS IN-VITRO NOVEL MAPPING TECHNIQUES SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE CHROMATIN; NUCLEOSOME POSITIONING; CORE HISTONES; GLOBIN GENES ID RICH HISTONE KERNEL; SACCHAROMYCES-CEREVISIAE; CHROMATIN STRUCTURE; PROTEIN-BINDING; PHO5 PROMOTER; DNA-SEQUENCE; YEAST; CORE; TRANSCRIPTION; PLACEMENT C1 UNIV LONDON KINGS COLL,RANDALL INST,LONDON WC2B 5RL,ENGLAND. NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. FU Wellcome Trust NR 58 TC 29 Z9 29 U1 0 U2 2 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD APR 8 PY 1994 VL 237 IS 4 BP 401 EP 414 DI 10.1006/jmbi.1994.1243 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NF554 UT WOS:A1994NF55400005 PM 8151701 ER PT J AU LAKSHMAN, MK XIAO, W SAYER, JM CHEH, AM JERINA, DM AF LAKSHMAN, MK XIAO, W SAYER, JM CHEH, AM JERINA, DM TI SYNTHESIS AND ASSIGNMENT OF ABSOLUTE-CONFIGURATION TO THE N(6)-DEOXYADENOSINE ADDUCTS RESULTING FROM CIS AND TRANS RING-OPENING OF PHENANTHRENE 9,10-OXIDE SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Article ID FACILE SYNTHESIS; DIOL EPOXIDES; ARENE OXIDES; CHRYSENE; TUMORIGENICITY; MUTAGENICITY; DERIVATIVES AB Reaction of calf thymus DNA with phenanthrene 9,10-oxide in vitro results in alkylation of the exocyclic amino groups of the purine bases. Adducts result from both cis and trans opening of the epoxide. In the present study, structures of the N-6-deoxyadenosine adducts have been unequivocally assigned by synthesis from optically pure cis- and trans-9-amino-10-hydroxy-9,10-dihydrophethrene. Resolution of trans-9-azido-10-hydroxy-9,10-dihydrophenanthrene as its acetate was achieved on a chiral. HPLC column. The early-eluting (-)-enantiomer was assigned (9R,10R)-absolute configuration based on a characteristic negative CD band at 232 nm due to the helicity of its biphenyl chromophore, in combination with a H-1 NMR coupling constant that indicated pseudodiaxial orientation of the substituents at C-9 and C-10. Aminolysis of the ester followed by reduction of the azido group provided the desired, optically active trans (9R,10R) amino alcohol. As a starting material for synthesis of the cis amino alcohol, trans-9-bromo-10-acetoxy-9,10-dihydrophe was resolved by chiral HPLC. As above, the early-eluting (-)-enantiomer was assigned (9R,10R)absolute configuration based on a characteristic negative CD band at 234 nm. Displacement of bromine with inversion of configuration by azide, aminolysis of the ester, and reduction provided optically pure cis-(9S,10R)-9-amino-10-hydroxy-9,10-dihydrophenanthrene. Coupling of the optically active amino alcohols with 6-fluoro-9-(2-deoxy-beta-D-erythro-pentofuranosyl) purine (the 6-fluoro analog of dA) yielded the corresponding N-6-deoxyadenosine adducts. Comparison of CD spectra and HPLC retention times of the synthetic adducts with those of the adducts obtained from calf thymus DNA make it possible to assign unambiguously the structures of the DNA adducts. C1 NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD 20892. AMERICAN UNIV,DEPT CHEM,WASHINGTON,DC 20016. NR 22 TC 10 Z9 10 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD APR 8 PY 1994 VL 59 IS 7 BP 1755 EP 1760 DI 10.1021/jo00086a027 PG 6 WC Chemistry, Organic SC Chemistry GA NF807 UT WOS:A1994NF80700027 ER PT J AU MAJER, P RANDAD, RS AF MAJER, P RANDAD, RS TI A SAFE AND EFFICIENT METHOD FOR PREPARATION OF N,N'-UNSYMMETRICALLY DISUBSTITUTED UREAS UTILIZING TRIPHOSGENE SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Note C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,STRUCT BIOCH PROGRAM,FREDERICK,MD 21702. NR 14 TC 162 Z9 165 U1 2 U2 17 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD APR 8 PY 1994 VL 59 IS 7 BP 1937 EP 1938 DI 10.1021/jo00086a061 PG 2 WC Chemistry, Organic SC Chemistry GA NF807 UT WOS:A1994NF80700061 ER PT J AU ADMAN, E GELLERT, M COHEN, M ALLEWELL, NM BAKER, BS VILLAFRANCA, J AF ADMAN, E GELLERT, M COHEN, M ALLEWELL, NM BAKER, BS VILLAFRANCA, J TI NATIONAL PROTEIN AND NUCLEIC-ACID DATABASES SO SCIENCE LA English DT Letter C1 NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DIV HUMAN GENET,BALTIMORE,MD 21201. UNIV MINNESOTA,DEPT BIOCHEM,ST PAUL,MN 55108. STANFORD UNIV,DEPT BIOL SCI,STANFORD,CA 94305. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,PRINCETON,NJ 08543. RP ADMAN, E (reprint author), UNIV WASHINGTON,SCH MED,DEPT BIOL STRUCT,SEATTLE,WA 98195, USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 8 PY 1994 VL 264 IS 5156 BP 187 EP 187 DI 10.1126/science.7511836 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NE410 UT WOS:A1994NE41000007 PM 7511836 ER PT J AU GU, W BHATIA, K MAGRATH, IT DANG, CV DALLAFAVERA, R AF GU, W BHATIA, K MAGRATH, IT DANG, CV DALLAFAVERA, R TI BINDING AND SUPPRESSION OF THE MYC TRANSCRIPTIONAL ACTIVATION DOMAIN BY P107 SO SCIENCE LA English DT Article ID RETINOBLASTOMA GENE-PRODUCT; HELIX ZIPPER PROTEIN; LARGE T-ANTIGEN; C-MYC; CYCLIN-A; MAX; E2F; EXPRESSION; IDENTIFICATION; SEQUENCE AB An amino-terminal transactivation domain is required for Myc to function as a transcription factor controlling cell proliferation, differentiation, and apoptosis. A complementary DNA expression library was screened with a Myc fusion protein to identify proteins interacting with this domain, and a clone encoding the Rb-related p107 protein was isolated. The p107 protein was shown to associate with Myc in vivo and to suppress the activity of the Myc transactivation domain. However, mutant forms of Myc from Burkitt lymphoma cells, which contain sequence alterations in the transactivation domain, were resistant to p107-mediated suppression. Thus, disruption of a regulatory interaction between Myc and p107 may be important in tumorigenesis. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT PATHOL,DIV ONCOL,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT GENET & DEV,NEW YORK,NY 10032. NCI,PEDIAT ONCOL BRANCH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT CELL BIOL & ANAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD 21205. FU NCI NIH HHS [CA 37165, CA 51497] NR 41 TC 206 Z9 209 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 8 PY 1994 VL 264 IS 5156 BP 251 EP 254 DI 10.1126/science.8146655 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NE410 UT WOS:A1994NE41000034 PM 8146655 ER PT J AU SUZUKI, CK SUDA, K WANG, N SCHATZ, G AF SUZUKI, CK SUDA, K WANG, N SCHATZ, G TI REQUIREMENT FOR THE YEAST GENE LON IN INTRAMITOCHONDRIAL PROTEOLYSIS AND MAINTENANCE OF RESPIRATION SO SCIENCE LA English DT Article ID ATP-DEPENDENT PROTEASE; ESCHERICHIA-COLI; INTERMEMBRANE SPACE; LIVER-MITOCHONDRIA; PROTEINS; MECHANISM; IMPORT; CELLS; ION AB The role of protein degradation in mitochondrial homeostasis was explored by cloning of a gene from Saccharomyces cerevisiae that encodes a protein resembling the adenosine triphosphate (ATP)-dependent bacterial protease Lon. The predicted yeast protein has a typical mitochondrial matrix-targeting sequence at its amino terminus. Yeast cells lacking a functional LON gene contained a nonfunctional mitochondrial genome, were respiratory-deficient, and lacked an ATP-dependent proteolytic activity present in the mitochondria of Lon+ cells. Lon- cells were also impaired in their ability to catalyze the energy-dependent degradation of several mitochondrial matrix proteins and they accumulated electron-dense inclusions in their mitochondrial matrix. C1 NCI,CELL BIOL LAB,BETHESDA,MD 20892. RP SUZUKI, CK (reprint author), UNIV BASEL,BIOCTR,CH-4056 BASEL,SWITZERLAND. NR 22 TC 183 Z9 186 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 8 PY 1994 VL 264 IS 5156 BP 273 EP 276 DI 10.1126/science.8146662 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA NE410 UT WOS:A1994NE41000041 PM 8146662 ER PT J AU YAGEN, B PU, YM YEH, HJC ZIFFER, H AF YAGEN, B PU, YM YEH, HJC ZIFFER, H TI TANDEM SILICA GEL-CATALYZED REARRANGEMENTS AND SUBSEQUENT BAEYER-VILLIGER REACTIONS OF ARTEMISININ DERIVATIVES SO JOURNAL OF THE CHEMICAL SOCIETY-PERKIN TRANSACTIONS 1 LA English DT Article ID ANTIMALARIAL DRUG; QINGHAOSU ARTEMISININ AB Novel silica gel-catalysed reactions of dihydroartemisinin 1b to deoxyartemisinin 11 and 11 beta-hydroxy-11-epidihydroartemisinin 8 to compound 9 under mild conditions are described. The structures of the products were determined by mass spectrometry and 1D- and 2D-NMR spectroscopy. A mechanism for their formation is proposed. C1 NIDDKD,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,SCH PHARM,DEPT NAT PROD,IL-91120 JERUSALEM,ISRAEL. NR 15 TC 17 Z9 17 U1 1 U2 1 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK MILTON ROAD, CAMBRIDGE, CAMBS, ENGLAND CB4 4WF SN 0300-922X J9 J CHEM SOC PERK T 1 JI J. Chem. Soc.-Perkin Trans. 1 PD APR 7 PY 1994 IS 7 BP 843 EP 846 DI 10.1039/p19940000843 PG 4 WC Chemistry, Organic SC Chemistry GA NF450 UT WOS:A1994NF45000015 ER PT J AU FITZHUGH, AL AKEE, RK RUEI, FC WU, J KLOSE, JR CHABNER, BA AF FITZHUGH, AL AKEE, RK RUEI, FC WU, J KLOSE, JR CHABNER, BA TI FIRST COMPLETELY CHEMICAL SYNTHESIS OF [(6S)-N-5-FORMYLTETRAHYDROPTEROYL]POLY-GAMMA-L-GLUTAMIC ACID-DERIVATIVE SO JOURNAL OF THE CHEMICAL SOCIETY-PERKIN TRANSACTIONS 1 LA English DT Article ID METHOTREXATE AB The synthesis of (6S)-N-5-formyl-5,6,7,8-tetrahydropteroyl-di-, tri-,-tetra- and -penta-gamma-L-glutamic acid derivatives 9a-d has been achieved for the first time through a three-step sequence of chemical reactions. The process involves converting [(6S)-N-5-formyl-5,6,7,8-tetrahydropteroyl] mono-L-glutamic acid 6 into the alpha-benzyl monoester 7, which is then coupled in four separate reactions to performed polybenzyl esters of mono-, di-, tri-, and tetra-gamma-L-glutamate. The resulting (GS)-N-5-formyl-5,6,7,8-tetrahydropteroyl-di-, -tri-, -tetra- and -penta-gamma-L-glutamate polybenzyl ester derivatives 8a-d are then subjected to hydrogenolysis, giving polyacids 9a-d. The overall yields for the individual sequences range from 37 to 49%. Importantly, enzymic and chiral chromatographic analyses of compounds 9a-d indicate that their stereochemical purity exceeds 99%. C1 NCI,DIV CANC TREATMENT,BETHESDA,MD 20892. RP FITZHUGH, AL (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,CHEM SYNTHESIS & ANAL LAB,MED CHEM SECT,POB B,FREDERICK,MD 21702, USA. NR 33 TC 1 Z9 1 U1 1 U2 2 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK MILTON ROAD, CAMBRIDGE, CAMBS, ENGLAND CB4 4WF SN 0300-922X J9 J CHEM SOC PERK T 1 JI J. Chem. Soc.-Perkin Trans. 1 PD APR 7 PY 1994 IS 7 BP 897 EP 902 DI 10.1039/p19940000897 PG 6 WC Chemistry, Organic SC Chemistry GA NF450 UT WOS:A1994NF45000024 ER PT J AU SCHAEFER, EJ LAMONFAVA, S JENNER, JL MCNAMARA, JR ORDOVAS, JM DAVIS, CE ABOLAFIA, JM LIPPEL, K LEVY, RI AF SCHAEFER, EJ LAMONFAVA, S JENNER, JL MCNAMARA, JR ORDOVAS, JM DAVIS, CE ABOLAFIA, JM LIPPEL, K LEVY, RI TI LIPOPROTEIN(A) LEVELS AND RISK OF CORONARY HEART-DISEASE IN MEN - THE LIPID RESEARCH CLINICS CORONARY PRIMARY PREVENTION TRIAL SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID LOW-DENSITY-LIPOPROTEIN; FAMILIAL HYPERCHOLESTEROLEMIA; ARTERY DISEASE; MYOCARDIAL-INFARCTION; SERUM LIPOPROTEIN(A); LP(A) LIPOPROTEIN; PLASMA-LEVELS; APOLIPOPROTEIN(A); PLASMINOGEN; ATHEROSCLEROSIS AB Objective.-To examine the relationship between elevated levels of lipoprotein(a) [Lp(a)] and coronary heart disease (CHD) risk in a prospective study. Design.-Nested case-control study. The cohort consisted of participants in the Lipid Research Clinics Coronary Primary Prevention Trial. Setting.-Lipid research clinics. Participants.-The Lipid Research Clinics Coronary Primary Prevention Trial participants (n=3806) were men, aged 35 to 59 years, with plasma cholesterol levels of 6.85 mmol/L (265 mg/dL) or greater, low-density lipoprotein cholesterol levels of 4.91 mmol/L (190 mg/dL) or greater, and triglyceride levels less than 3.39 mmol/L. Subjects were randomly assigned to either cholestyramine or placebo treatment. The Lp(a) levels were measured in plasma samples obtained prior to randomization in 233 cases (participants who developed CHD in the course of the study) and 390 matched CHD-free controls. A total of 96.95% of the subjects were white, 2.25% were black, and 0.80% were of other race. Main Outcome Measure.-Coronary heart disease (either fatal or nonfatal) events during a follow-up of 7 to 10 years. Results.-The Lp(a) levels were significantly higher (21%) in cases than in controls (23.7 mg/dL [0.59 mmol/L] and 19.5 mg/dL [0.49 mmol/L], respectively; P<.02). This difference was still statistically significant (P<.01) after controlling for age, body mass index, cigarette smoking, blood pressure, low-density lipoprotein cholesterol level, and high-density lipoprotein cholesterol level. When subjects were divided by treatment, both cholestyramine-treated and placebo-treated CHD subjects had Lp(a) levels 200/. to 220/o greater than their matched controls. However, possibly because of smaller sample sizes, these differences were no longer statistically significant. Conclusions.-Our data are consistent with the concept that an elevated Lp(a) level is an independent risk factor for CHD in hypercholesterolemic white men. C1 UNIV N CAROLINA,DEPT BIOSTAT,CHAPEL HILL,NC 27514. NHLBI,DIV HEART & VASC DIS,BETHESDA,MD 20892. RP SCHAEFER, EJ (reprint author), TUFTS UNIV,USDA,HUMAN NUTR RES CTR AGING,LIPID METAB LAB,711 WASHINGTON ST,BOSTON,MA 02111, USA. OI Ordovas, Jose/0000-0002-7581-5680 FU NHLBI NIH HHS [HV83-03] NR 44 TC 409 Z9 413 U1 0 U2 6 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 6 PY 1994 VL 271 IS 13 BP 999 EP 1003 DI 10.1001/jama.271.13.999 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA ND949 UT WOS:A1994ND94900029 PM 8139085 ER PT J AU SPORN, MB ROBERTS, AB AF SPORN, MB ROBERTS, AB TI CERVICAL DYSPLASIA REGRESSION INDUCED BY ALL-TRANS-RETINOIC ACID SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID CANCER; CELLS; GENE RP SPORN, MB (reprint author), NCI,DIV CANC ETIOL,CHEMOPREVENT LAB,BLDG 41,RM 3915,BETHESDA,MD 20892, USA. NR 11 TC 21 Z9 21 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 6 PY 1994 VL 86 IS 7 BP 476 EP 477 PG 2 WC Oncology SC Oncology GA ND811 UT WOS:A1994ND81100002 PM 8133526 ER PT J AU FRIEDMAN, MA TRIMBLE, EL ABRAMS, JS AF FRIEDMAN, MA TRIMBLE, EL ABRAMS, JS TI TAMOXIFEN - TRIALS, TRIBULATIONS, AND TRADE-OFFS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID ENDOMETRIAL CARCINOMA; POSTMENOPAUSAL WOMEN; CANCER RP FRIEDMAN, MA (reprint author), NCI,DIV CANC TREATMENT,CANC THERAPY EVALUAT PROGRAM,EPN,RM 742,BETHESDA,MD 20892, USA. NR 15 TC 18 Z9 18 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 6 PY 1994 VL 86 IS 7 BP 478 EP 479 DI 10.1093/jnci/86.7.478 PG 2 WC Oncology SC Oncology GA ND811 UT WOS:A1994ND81100003 PM 8133527 ER PT J AU KIRNBAUER, R HUBBERT, NL WHEELER, CM BECKER, TM LOWY, DR SCHILLER, JT AF KIRNBAUER, R HUBBERT, NL WHEELER, CM BECKER, TM LOWY, DR SCHILLER, JT TI A VIRUS-LIKE PARTICLE ENZYME-LINKED-IMMUNOSORBENT-ASSAY DETECTS SERUM ANTIBODIES IN A MAJORITY OF WOMEN INFECTED WITH HUMAN PAPILLOMAVIRUS TYPE-16 SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID CERVICAL INTRAEPITHELIAL NEOPLASIA; CANCER; PREVALENCE; VIRIONS; RISK AB Background: Previous studies have demonstrated that genital infection with high-risk types of human papillomavirus (HPV), most often HPV16, is the most significant risk factor for the development of cervical cancer. However, serologic assays that have been developed to identify high-risk HPV infection have either failed to associate serum reactivity with other indicators of HPV infection or have identified only a minority of HPV-infected individuals. Purpose: Our purpose was to determine whether a specifically developed enzyme-linked immunosorbent assay (ELISA) could detect IgG anti-HPV16 virion antibodies in the sera of women who had tested positive for genital HPV16 infection by DNA-based methods. Methods: An ELISA was developed using newly developed HPV16 virus-like particles as antigens to detect anti-HPV16 virion IgG antibodies. These particles are comprised of HPV16 structural proteins that are self-assembled in insect cells after expression by recombinant baculoviruses. The sera of 122 women, whose HPV status had been previously evaluated by nucleic acid-based methods, were tested by this ELISA. Results: The sera of 59% of women (32 of 54) positive for genital HPV16 DNA by polymerase chain reaction (PCR) were positive in the ELISA assay compared with sera from women who had tested negative for HPV DNA (P<.0005). In contrast. 6% of HPV DNA-negative women (two of 31) and 9% of women positive for low-risk HPV6/11 DNA (one of 11) were ELISA positive by this criterion. The sera of women who were DNA positive for two additional high-risk HPV types were evaluated; the sera of 31% of HPV18-positive (four of 13) and 38% of HPV31-positive women (five of 13) were positive in the HPV16 particle ELISA. The sera of 75% of HPV16 DNA-positive women with severe dysplasias (12 of 16) gave positive ELISA results. The sera of 67% of women (28 of 42) who tested positive for HPV16 DNA by both PCR and the less sensitive ViraType assay tested positive in the ELISA compared with 33% of women (four of 12) who were positive by PCR but negative by ViraType (P<.05). Conclusion: The majority of women with cervical HPV16 infection generate an IgG antibody response to conformationally dependent epitopes of HPV6/11 that can be detected by ELISA. Implication: This particular ELISA, or a similar one incorporating virus-like particles of additional HPV types, may be useful in determining the natural history of high-risk HPV infection and perhaps help to identify women at risk for developing cervical cancer. C1 NCI,CELLULAR ONCOL LAB,BLDG 36,RM 1D19,BETHESDA,MD 20892. NEW MEXICO CANC CTR,DEPT CELL BIOL,ALBUQUERQUE,NM. NEW MEXICO TUMOR REGISTRY,ALBUQUERQUE,NM. UNIV NEW MEXICO,DEPT MED,ALBUQUERQUE,NM 87131. UNIV NEW MEXICO,DEPT FAMILY & COMMUNITY MED,ALBUQUERQUE,NM 87131. FU Austrian Science Fund FWF [P 18990]; NCI NIH HHS [CA48003]; PHS HHS [R0132917-03] NR 23 TC 274 Z9 280 U1 0 U2 10 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 6 PY 1994 VL 86 IS 7 BP 494 EP 499 DI 10.1093/jnci/86.7.494 PG 6 WC Oncology SC Oncology GA ND811 UT WOS:A1994ND81100011 PM 8133532 ER PT J AU SONDIK, EJ AF SONDIK, EJ TI SCREENING FOR BREAST-CANCER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter RP SONDIK, EJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892, USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 6 PY 1994 VL 86 IS 7 BP 560 EP 561 DI 10.1093/jnci/86.7.560 PG 2 WC Oncology SC Oncology GA ND811 UT WOS:A1994ND81100023 ER PT J AU RAYNAL, P POLLARD, HB AF RAYNAL, P POLLARD, HB TI ANNEXINS - THE PROBLEM OF ASSESSING THE BIOLOGICAL ROLE FOR A GENE FAMILY OF MULTIFUNCTIONAL CALCIUM-BINDING AND PHOSPHOLIPID-BINDING PROTEINS SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON BIOMEMBRANES LA English DT Review ID PLACENTAL ANTICOAGULANT PROTEIN; ROUS-SARCOMA VIRUS; PLATELET-ACTIVATING-FACTOR; ADRENAL CHROMAFFIN CELLS; AMINO-ACID-SEQUENCE; HUMAN LIPOCORTIN-I; ANTIINFLAMMATORY PEPTIDES ANTIFLAMMINS; FACTOR-DEPENDENT PHOSPHORYLATION; HUMAN RECOMBINANT LIPOCORTIN-1; TYROSINE KINASE SUBSTRATE-P36 C1 NIDDK,CELL BIOL & GENET LAB,BETHESDA,MD 20892. NR 353 TC 926 Z9 954 U1 3 U2 22 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-4157 J9 BBA-REV BIOMEMBRANES JI Biochim. Biophys. Acta-Rev. Biomembr. PD APR 5 PY 1994 VL 1197 IS 1 BP 63 EP 93 DI 10.1016/0304-4157(94)90019-1 PG 31 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA NG548 UT WOS:A1994NG54800004 PM 8155692 ER PT J AU JUNG, G HAMMER, JA AF JUNG, G HAMMER, JA TI THE ACTIN-BINDING SITE IN THE TAIL DOMAIN OF DICTYOSTELIUM MYOSIN-IC (MYOC) RESIDES WITHIN THE GLYCINE-RICH AND PROLINE-RICH SEQUENCE (TAIL HOMOLOGY REGION-2) SO FEBS LETTERS LA English DT Article DE MYOSIN I; ACTIN BINDING; SH3 DOMAIN; DICTYOSTELIUM ID HEAVY-CHAIN; PROTEIN; SH3; AMEBAS; GENE; RHO; IB AB The majority of protozoan myosins I possess tail domains composed of three distinct and conserved regions of sequence, referred to as tail homology regions 1, 2 and 3 (TH.1, TH.2 and TH.3). While the N-terminal similar to half of the tail (corresponding to TH.1) has been implicated in membrane binding, all or some portion of the C-terminal similar to half of the tail (corresponding to TH.2 plus TH.3) has been implicated in binding to F-actin in a nucleotide-insensitive fashion. Here we show, using fusion proteins containing portions of the Dictyostelium myosin IC (myoC) tail domain and F-actin sedimentation assays, that the ability of the myoC tail to bind to actin resides entirely within the glycine- and proline-rich TH.2 domain. The src-like TH.3 domain does not bind to actin, nor does it augment the binding properties of the TH.2 domain. In addition to defining more precisely the location of the actin binding site in the tail domain of a protozoan myosin I, these results have implications for the function of the src-like TH.3 domain in myosins I and other proteins. C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NR 32 TC 62 Z9 62 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD APR 4 PY 1994 VL 342 IS 2 BP 197 EP 202 DI 10.1016/0014-5793(94)80500-8 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA NE895 UT WOS:A1994NE89500020 PM 8143877 ER PT J AU PU, YM YAGEN, B ZIFFER, H AF PU, YM YAGEN, B ZIFFER, H TI STEREOSELECTIVE OXIDATIONS OF A BETA-METHYLGLYCAL, ANHYDRODIHYDROARTEMISININ SO TETRAHEDRON LETTERS LA English DT Article ID ANTIMALARIAL DRUG; REARRANGEMENT; ARTEMISININ; ARTEETHER AB Anhydrodihydroartemisinin (1) was epoxidized with MCPBA-2KF and the resulting 11 beta,12 beta-epoxide (2) treated with acidic aqueous acetone to yield 11 beta-hydroxydihydroepiartemisinin (5). The major product of the reaction of 1 with catalytic quantities of osmium tetroxide using NMO as a co-oxidant was 11 alpha-hydroxydihydroartemisinin (4). Both 4 and 5 were oxidized to the corresponding 11-hydroxyartemisinins. C1 NIH,BETHESDA,MD 20892. NR 13 TC 10 Z9 10 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4039 J9 TETRAHEDRON LETT JI Tetrahedron Lett. PD APR 4 PY 1994 VL 35 IS 14 BP 2129 EP 2132 DI 10.1016/S0040-4039(00)76777-3 PG 4 WC Chemistry, Organic SC Chemistry GA NE621 UT WOS:A1994NE62100005 ER PT J AU ADAMS, DH SHAW, S AF ADAMS, DH SHAW, S TI LEUKOCYTE-ENDOTHELIAL INTERACTIONS AND REGULATION OF LEUKOCYTE MIGRATION SO LANCET LA English DT Review ID LEUKOCYTE ADHESION DEFICIENCY; MOLECULE-1; CELLS; INFLAMMATION; EXPRESSION; TISSUES; SELECTINS; INTEGRIN; BINDING; ELAM-1 C1 NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. RP ADAMS, DH (reprint author), QUEEN ELIZABETH HOSP,LIVER RES LABS,BIRMINGHAM B15 2TH,W MIDLANDS,ENGLAND. RI Adams, David/C-9092-2009 NR 44 TC 516 Z9 526 U1 2 U2 9 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 2 PY 1994 VL 343 IS 8901 BP 831 EP 836 DI 10.1016/S0140-6736(94)92029-X PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA ND792 UT WOS:A1994ND79200012 PM 7908081 ER PT J AU TAYLOR, SI ACCILI, D HAFT, CR HONE, J IMAI, Y LEVYTOLEDANO, R QUON, MJ SUZUKI, Y WERTHEIMER, E AF TAYLOR, SI ACCILI, D HAFT, CR HONE, J IMAI, Y LEVYTOLEDANO, R QUON, MJ SUZUKI, Y WERTHEIMER, E TI MECHANISMS OF HORMONE RESISTANCE - LESSONS FROM INSULIN-RESISTANT PATIENTS SO ACTA PAEDIATRICA LA English DT Article; Proceedings Paper CT 2nd International Workshop on Growth Hormone Insensitivity CY OCT 17-18, 1993 CL ESTORIL, PORTUGAL ID TYROSINE KINASE DOMAIN; DEPENDENT PROTEIN-KINASE; RECEPTOR MESSENGER-RNA; 2 MUTANT ALLELES; BETA-SUBUNIT; NONSENSE MUTATION; ALPHA-SUBUNIT; ACANTHOSIS NIGRICANS; EXTRACELLULAR DOMAIN; IMPAIRS TRANSPORT RP TAYLOR, SI (reprint author), NIDDKD,DIABET BRANCH,BLDG 10,ROOM 8S-239,BETHESDA,MD 20892, USA. RI Quon, Michael/B-1970-2008; OI Quon, Michael/0000-0002-9601-9915; Quon , Michael /0000-0002-5289-3707 NR 73 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0803-5253 J9 ACTA PAEDIATR JI Acta Paediatr. PD APR PY 1994 VL 83 SU 399 BP 95 EP 104 DI 10.1111/j.1651-2227.1994.tb13300.x PG 10 WC Pediatrics SC Pediatrics GA PC976 UT WOS:A1994PC97600017 ER PT J AU MIDANIK, LT HARFORD, TC AF MIDANIK, LT HARFORD, TC TI ALCOHOL-CONSUMPTION MEASUREMENT - INTRODUCTION TO THE WORKSHOP SO ADDICTION LA English DT Editorial Material C1 UNIV CALIF BERKELEY,SCH SOCIAL WELF,BERKELEY,CA 94720. NIAAA,DIV BIOMETRY & EPIDEMIOL,ROCKVILLE,MD 20857. RP MIDANIK, LT (reprint author), CALIF PACIFIC MED RES INST,ALCOHOL RES GRP,2000 HEARST AVE,BERKELEY,CA 94709, USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0965-2140 J9 ADDICTION JI Addiction PD APR PY 1994 VL 89 IS 4 BP 393 EP 394 DI 10.1111/j.1360-0443.1994.tb00911.x PG 2 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA NF947 UT WOS:A1994NF94700003 ER PT J AU HARFORD, TC AF HARFORD, TC TI THE EFFECTS OF ORDER OF QUESTIONS ON REPORTED ALCOHOL-CONSUMPTION SO ADDICTION LA English DT Article; Proceedings Paper CT Workshop on Measurement Issues in Alcohol Consumption, at 18th Annual Alcohol Epidemiology Symposium of Kettil-Brunn-Soc-of-Social-and-Epidemiological-Research-on-Alcohol CY MAY 30-JUN 05, 1992 CL TORONTO, CANADA SP KETTIL BRUNN SOC SOCIAL & EPIDEMIOL RES ALCOHOL AB This research note draws upon the US National Longitudinal Survey (NLS) of Labor Market Experience among youths aged 17-24 to report the effects of variation in the ordering of alcohol questions upon the prevalence of heavier drinking. A secondary analysis of the NLS indicated a substantial decrease in the prevalence of heavier drinking between 1984 and 1985 which is attributed to the order of presentation of two differently styled questions regarding heavier drinking. RP HARFORD, TC (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,5600 FISHERS LANE,ROOM 14C-26,ROCKVILLE,MD 20857, USA. NR 6 TC 17 Z9 18 U1 0 U2 0 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0965-2140 J9 ADDICTION JI Addiction PD APR PY 1994 VL 89 IS 4 BP 421 EP 424 DI 10.1111/j.1360-0443.1994.tb00916.x PG 4 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA NF947 UT WOS:A1994NF94700008 PM 8025495 ER PT J AU HENNINGFIELD, JE AF HENNINGFIELD, JE TI DO NICOTINE REPLACEMENT MEDICATIONS WORK - A UNIQUE STANDARD FOR NICOTINE SO ADDICTION LA English DT Note RP HENNINGFIELD, JE (reprint author), NIDA,ADDICT RES CTR,CLIN PHARMACOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA. NR 6 TC 2 Z9 2 U1 0 U2 0 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0965-2140 J9 ADDICTION JI Addiction PD APR PY 1994 VL 89 IS 4 BP 434 EP 436 DI 10.1111/j.1360-0443.1994.tb00921.x PG 3 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA NF947 UT WOS:A1994NF94700013 PM 8025500 ER PT J AU ROTH, GS AF ROTH, GS TI ENTROPY THEORIES OF AGING REVISITED SO AGING-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Letter RP ROTH, GS (reprint author), NIA,FRANCIS SCOTT KEY MED CTR,GERONTOL RES CTR,BALTIMORE,MD 21224, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-9532 J9 AGING-CLIN EXP RES JI Aging-Clin. Exp. Res. PD APR PY 1994 VL 6 IS 2 BP 139 EP 140 PG 2 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA NJ446 UT WOS:A1994NJ44600010 PM 7918731 ER PT J AU JACOBSON, MA WULFSOHN, M FEINBERG, JE DAVIS, R POWER, M OWENS, S CAUSEY, D HEATHCHIOZZI, ME MURPHY, RL CHEUNG, TW DIETERICH, DT SPECTOR, SA MCKINLEY, GF PARENTI, DM CRUMPACKER, C NISHIMOTO, B LEEDOM, JM KRAMER, F COHEN, C LOFTUS, J KESSLER, HA POTTAGE, JC BENSON, CA PHAIR, JP GERITS, P CHUSID, E SACKS, HS FRIEDBERG, D CURRANKRIKORIAN, K VALENTINE, FT MENG, TC FREEMAN, WR MEIXNER, L RICHMAN, D ODONNELL, JJ KIMBRELL, C BOGGIO, K LARSON, J WHITMORE, PV SIMON, GL LELACHEUR, S FIFE, K ZWICKL, B RELUE, J STEIGBIGEL, RT FUHRER, J DONLON, W BURK, RA PORTMORE, AC WEISSBACH, NE HOOTON, TM HOLZWORTH, P DAVISON, S COLLIER, AC POWDERLY, WG KLEBERT, M ROYAL, M SEYFRIED, W SQUIRES, KC WEISS, W BARBACCI, M BECKER, RL JABS, D BARTLETT, JG PARA, MF JONES, M NEIDIG, JL FASS, RJ VANDERHORST, C KYLSTRA, J RAASCH, R BLOODGOOD, K WOLITZ, R KIRK, S ROLFE, L PATRONEREESE, J BARTLETT, JA WASKIN, HA WILLIAMS, DK SHIP, KW KAHL, P ASSAYKEEN, T KAROL, C MARTINMUNLEY, S SUMNER, P AF JACOBSON, MA WULFSOHN, M FEINBERG, JE DAVIS, R POWER, M OWENS, S CAUSEY, D HEATHCHIOZZI, ME MURPHY, RL CHEUNG, TW DIETERICH, DT SPECTOR, SA MCKINLEY, GF PARENTI, DM CRUMPACKER, C NISHIMOTO, B LEEDOM, JM KRAMER, F COHEN, C LOFTUS, J KESSLER, HA POTTAGE, JC BENSON, CA PHAIR, JP GERITS, P CHUSID, E SACKS, HS FRIEDBERG, D CURRANKRIKORIAN, K VALENTINE, FT MENG, TC FREEMAN, WR MEIXNER, L RICHMAN, D ODONNELL, JJ KIMBRELL, C BOGGIO, K LARSON, J WHITMORE, PV SIMON, GL LELACHEUR, S FIFE, K ZWICKL, B RELUE, J STEIGBIGEL, RT FUHRER, J DONLON, W BURK, RA PORTMORE, AC WEISSBACH, NE HOOTON, TM HOLZWORTH, P DAVISON, S COLLIER, AC POWDERLY, WG KLEBERT, M ROYAL, M SEYFRIED, W SQUIRES, KC WEISS, W BARBACCI, M BECKER, RL JABS, D BARTLETT, JG PARA, MF JONES, M NEIDIG, JL FASS, RJ VANDERHORST, C KYLSTRA, J RAASCH, R BLOODGOOD, K WOLITZ, R KIRK, S ROLFE, L PATRONEREESE, J BARTLETT, JA WASKIN, HA WILLIAMS, DK SHIP, KW KAHL, P ASSAYKEEN, T KAROL, C MARTINMUNLEY, S SUMNER, P TI PHASE-II DOSE-RANGING TRIAL OF FOSCARNET SALVAGE THERAPY FOR CYTOMEGALOVIRUS RETINITIS IN AIDS PATIENTS INTOLERANT OF OR RESISTANT TO GANCICLOVIR (ACTG PROTOCOL 093) SO AIDS LA English DT Article DE CYTOMEGALOVIRUS RETINITIS; FOSCARNET; AIDS ID ACQUIRED IMMUNODEFICIENCY SYNDROME; VIRUS RETINITIS; DISEASE; PREVALENCE AB Objective: To document response to foscarnet salvage therapy in patients with cytomegalovirus (CMV) retinitis who are intolerant of or resistant to ganciclovir. Methods: Patients with AIDS and CMV retinitis who had documented hematologic intolerance or resistance to ganciclovir therapy received an induction course of foscarnet, 60 mg/kg every 8h for 14 days, and subsequent chronic maintenance foscarnet therapy at a daily dose of 60, 90 or 120 mg/kg/day. The first 87 patients were randomly assigned to receive maintenance foscarnet at a dose of 60 or 90 mg/kg/day; all subsequent patients were assigned a maintenance dose of 120 mg/kg/day. Results: A total of 156 evaluable patients were enrolled. Median time to retinitis progression and survival did not differ significantly among groups assigned to different maintenance foscarnet doses. Among patients with retinitis progression documented ophthalmologically occuring at less-than-or-equal-to 2 week intervals, despite optimal doses of ganciclovir, time to progression on foscarnet therapy was a median 8 weeks at all doses studied. By dose assignment, there were no significant differences in serious drug-associated toxicity, although trends toward increased renal and hypocalcemic adverse events were observed at higher maintenance doses. Conclusion: in patients intolerant of ganciclovir, salvage foscarnet therapy resulted in a longer time to retinitis progression than reported previously in historic controls who terminated ganciclovir therapy. In patients who exhibited clinical resistance to ganciclovir, foscarnet appeared to have efficacy in controlling retinitis. No significant differences in either efficacy or toxicity were observed in the range of foscarnet maintenance doses studied. C1 UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT OPHTHALMOL,SAN FRANCISCO,CA 94143. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. NIAID,DIV AIDS,AIDS CLIN TRIALS GRP,BETHESDA,MD 20892. UNIV SO CALIF,LOS ANGELES CTY MED CTR,DEPT MED,LOS ANGELES,CA 90033. UNIV SO CALIF,LOS ANGELES CTY MED CTR,DEPT OPHTHALMOL,LOS ANGELES,CA 90033. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. NYU,SCH MED,NEW YORK,NY 10003. UNIV CALIF SAN DIEGO,DEPT PEDIAT,SAN DIEGO,CA 92103. UNIV CALIF SAN DIEGO,CTR MOLEC GENET,SAN DIEGO,CA 92103. ST LUKES ROOSEVELT HOSP,NEW YORK,NY. GEORGE WASHINGTON UNIV,SCH MED,WASHINGTON,DC 20052. MT SINAI HOSP,MINNEAPOLIS,MN 55404. INDIANA UNIV,BLOOMINGTON,IN 47401. SUNY STONY BROOK,STONY BROOK,NY 11794. UNIV ROCHESTER,ROCHESTER,NY 14627. UNIV WASHINGTON,SEATTLE,WA 98195. WASHINGTON UNIV,ST LOUIS,MO 63130. CORNELL UNIV,ITHACA,NY 14853. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. OHIO STATE UNIV,COLUMBUS,OH 43210. UNIV N CAROLINA,CHAPEL HILL,NC 27514. STANFORD UNIV,STANFORD,CA 94305. MIAMI UNIV,OXFORD,OH 45056. DUKE UNIV,DURHAM,NC 27706. ALBERT EINSTEIN MONTEFIORE MED CTR,NEW YORK,NY. ASTRA PHARMACEUT,SYDNEY,AUSTRALIA. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. RP JACOBSON, MA (reprint author), SAN FRANCISCO GEN HOSP,MED & OPHTHALMOL SERV,WARD 84,BLDG 80,995 POTRERO,SAN FRANCISCO,CA 94110, USA. OI Murphy, Robert/0000-0003-3936-2052 NR 28 TC 22 Z9 23 U1 1 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD APR PY 1994 VL 8 IS 4 BP 451 EP 459 DI 10.1097/00002030-199404000-00006 PG 9 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NC298 UT WOS:A1994NC29800006 PM 8011248 ER PT J AU GOEDERT, JJ GARVEY, L HILGARTNER, MW BLATT, PM ALEDORT, LM COHEN, AR KESSLER, CM WHITE, GC MANDALAKI, T COOK, RA MANCOJOHNSON, MJ SCHRAMM, W LEISSINGER, CA RAGNI, MV EICHINGER, S LEDERMAN, MM BRAY, GL BOSSER, C WILSON, SE EYSTER, ME AF GOEDERT, JJ GARVEY, L HILGARTNER, MW BLATT, PM ALEDORT, LM COHEN, AR KESSLER, CM WHITE, GC MANDALAKI, T COOK, RA MANCOJOHNSON, MJ SCHRAMM, W LEISSINGER, CA RAGNI, MV EICHINGER, S LEDERMAN, MM BRAY, GL BOSSER, C WILSON, SE EYSTER, ME TI RISK OF HIV-INFECTION AND AIDS IN WOMEN AND GIRLS WITH COAGULATION DISORDERS SO AIDS LA English DT Letter ID BLOOD-TRANSFUSION; PERIOD C1 RES TRIANGLE INST,ROCKVILLE,MD 20852. CORNELL UNIV,MED CTR,NEW YORK,NY 10021. CHRISTIANA HOSP,NEWARK,DE 19713. MT SINAI MED CTR,NEW YORK,NY 10029. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA 19104. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. UNIV N CAROLINA,CHAPEL HILL,NC 27514. UNIV ATHENS,LAIKON GEN HOSP,SCH MED,GR-11527 ATHENS,GREECE. CARDELA FDN,CTR HEMOPHILIA,PHILADELPHIA,PA 19107. UNIV MUNICH,W-8000 MUNICH 2,GERMANY. TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. UNIV PITTSBURGH,PITTSBURGH,PA 15219. UNIV VIENNA,A-1090 VIENNA,AUSTRIA. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. PENN STATE UNIV,MILTON S HERSHEY MED CTR,SCH MED,HERSHEY,PA 17033. CROIX ROUGE FRANCAISE,HEMOPHILIA TREATMENT SERV,F-73230 ST ALBAN LEYSSE,FRANCE. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010. ATLANTIC RES CORP,ROCKVILLE,MD. RP GOEDERT, JJ (reprint author), NCI,VIRAL EPIDEMIOL BRANCH,AIDS & CANC SECT,BETHESDA,MD 20892, USA. FU NCI NIH HHS [N01-CP-85649] NR 5 TC 2 Z9 2 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD APR PY 1994 VL 8 IS 4 BP 564 EP 565 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NC298 UT WOS:A1994NC29800029 PM 8011269 ER PT J AU ABACIOGLU, YH FOUTS, TR LAMAN, JD CLAASSEN, E PINCUS, SH MOORE, JP ROBY, CA KAMINLEWIS, R LEWIS, GK AF ABACIOGLU, YH FOUTS, TR LAMAN, JD CLAASSEN, E PINCUS, SH MOORE, JP ROBY, CA KAMINLEWIS, R LEWIS, GK TI EPITOPE MAPPING AND TOPOLOGY OF BACULOVIRUS-EXPRESSED HIV-1 GP160 DETERMINED WITH A PANEL OF MURINE MONOCLONAL-ANTIBODIES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HTLV-III; CONFERS PROTECTION; VARIABLE REGIONS; GP120; INFECTION; VACCINE; AIDS; CHIMPANZEES; MACAQUES AB To define protein folding-patterns of HIV-1 Env subunit vaccines, we have isolated a set of 30 monoclonal antibodies (MAbs) from BALB/c mice immunized with a recombinant gp160 vaccine (rgp160) expressed in a baculovirus system. This article describes epitope mapping for the MAb panel and topology of the epitopes for rgp160 and a recombinant gp120 (rgp120) also expressed in a baculovirus system. The following results are reported: (1) rgp160 harbors a minimum of 4 antigenic domains, 3 mapping to the C1, C2, and C3/V4 regions of gp120 and 1 mapping to the cytoplasmic tail of gp41; (2) there are at least 3 adjacent or overlapping epitopes in each antigenic domain; (3) a minimum of 14 independent epitopes were mapped, ah of which are continuous sites; (4) each of the epitopes is exposed on rgp160 without prior manipulation of the protein; and (5) by contrast, 6 of the 8 epitopes mapping to the C1, C2, and C3/V4 regions arenot exposed on rgp120, but become exposed when the protein is denatured. Taken together, these results show that rgp160 and rgp120 are folded differently, illustrating the use of this MAb panel to compare epitope topographies of recombination HIV-I Env proteins. This MAb panel may aid in the refinement of HIV-1 Env subunit vaccines. C1 UNIV MARYLAND,SCH MED,DEPT MICROBIOL & IMMUNOL,BALTIMORE,MD 21201. TNO,DEPT IMMUNOL & MED MICROBIOL,MED BIOL LAB,2280 HV RIJSWIJK,NETHERLANDS. NIAID,ROCKY MT LAB,MICROBIAL STRUCT & FUNCT LAB,HAMILTON,MT 59840. NYU,SCH MED,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10016. OI Fouts, Timothy/0000-0002-2429-2859 FU NIAID NIH HHS [AI-33230, AI-25863]; NINDS NIH HHS [NS-26665] NR 36 TC 149 Z9 151 U1 0 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 371 EP 381 DI 10.1089/aid.1994.10.371 PG 11 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000009 PM 8068416 ER PT J AU MILMAN, G DSOUZA, MP AF MILMAN, G DSOUZA, MP TI HIV-MEDIATED DEFECTS IN IMMUNE REGULATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID RETROVIRUS-INDUCED IMMUNODEFICIENCY; COAT PROTEIN; T-CELLS; ACTIVATION; INFECTION; VIRUS; AIDS; INVITRO; MICE AB The Division of AIDS (DAIDS), National Institute of Allergy and Infectious Diseases (NIAID), sponsored a Workshop on HIV-Mediated Defects in Immune Regulation on September 29-30, 1993. Workshop participants included investigators in basic research of immune regulation, animal models of HIV disease, HIV epidemiology, and HIV clinical research and treatment. The purpose of the workshop was to describe and evaluate biological mechanisms of HIV-mediated immune deficiency other than direct killing of infected CD4(+) cells. The workshop focused on HIV-mediated dysfunction in signal transduction and in T cell development and maturation. Mechanisms by which HIV has been proposed to influence signal transduction include gp120 ligation to CD4, HIV superantigen(s), and HIV-mediated perturbations in signal pathway components (e.g., receptors, kinases, phosphatases, cytokines, and cyclins). As a result of signal dysfunction, cells may fail to respond to foreign antigens (anergy) or become predisposed to enter suicide pathways, otherwise known as programmed cell death or apoptosis. programmed cell death is a normal immune regulatory mechanism that is activated to prevent anti-self responses and also to delete expanded but no longer needed cell populations. In the immune system, new cells are constantly produced from stem cells to replace those that die from age, pathological response, or programmed cell death. Dysfunction in these new cells may occur if HIV causes changes in the structural environment of the thymus and lymph nodes, or in cytokine signals. RP MILMAN, G (reprint author), NIAID,DIV AIDS,6003 EXECUT BLVD,SOLAR BLDG,ROOM 2B33,BETHESDA,MD 20892, USA. NR 45 TC 9 Z9 10 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 421 EP 430 DI 10.1089/aid.1994.10.421 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000015 PM 8068418 ER PT J AU MULLOY, JC BOERI, E GALLO, RC LEONARD, WJ FRANCHINI, G AF MULLOY, JC BOERI, E GALLO, RC LEONARD, WJ FRANCHINI, G TI THE HTLV-I-P12 PROTEIN BINDS TO THE IMMATURE FORMS OF THE IL-2 RECEPTOR BETA-CHAIN AND GAMMA-CHAIN - POSSIBLE IMPLICATION IN IL-2R SIGNALING SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 443 EP 443 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000018 ER PT J AU WEISS, SH CLERICI, M MAYUR, RK DENNY, TN QUIRINALE, JE BERZOFSKY, JA SHEARER, GM AF WEISS, SH CLERICI, M MAYUR, RK DENNY, TN QUIRINALE, JE BERZOFSKY, JA SHEARER, GM TI IMPACT OF HTLV-II INFECTION UPON CELLULAR IMMUNOLOGICAL RESPONSE TO HIV EXPOSURE IN HIV SERONEGATIVE DRUG-USERS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UMDNJ,SCH MED,NEWARK,NJ. NCI,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 444 EP 444 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000022 ER PT J AU LEHKY, TJ FOX, CH KOENIG, S IZUMO, S SATO, E RAINE, CS OSAME, M JACOBSON, S AF LEHKY, TJ FOX, CH KOENIG, S IZUMO, S SATO, E RAINE, CS OSAME, M JACOBSON, S TI DETECTION OF HTLV-I TAX IN THE CNS FROM HAM/TSP PATIENTS BY IN-SITU HYBRIDIZATION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 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 APR PY 1994 VL 10 IS 4 BP 445 EP 445 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000029 ER PT J AU MANNS, A MANN, D WILKS, R HANCHARD, B BLATTNER, W AF MANNS, A MANN, D WILKS, R HANCHARD, B BLATTNER, W TI RELATIONSHIP OF HLA TO HTLV-I SEROCONVERSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV W INDIES,KINGSTON 7,JAMAICA. 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 APR PY 1994 VL 10 IS 4 BP 445 EP 445 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000026 ER PT J AU REID, R MIRESKANDARI, A BRADY, JN AF REID, R MIRESKANDARI, A BRADY, JN TI INTERACTION OF HTLV-I TAX(1) WITH CELLULAR PROTEINS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,MOLEC VIROL LAB,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 446 EP 446 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000030 ER PT J AU GIUSTI, RM GRACIA, F STEPHENS, K FUKUDA, K VITEK, C HARTGE, P LEVIN, A BLATTNER, W LEVINE, P KAPLAN, J AF GIUSTI, RM GRACIA, F STEPHENS, K FUKUDA, K VITEK, C HARTGE, P LEVIN, A BLATTNER, W LEVINE, P KAPLAN, J TI A SEARCH FOR DISEASES ASSOCIATED WITH HTLV-II AMONG GUAYMI PATIENTS, PANAMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. GORGAS MEM LAB,PANAMA CITY,FL. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. CDC,RETROVIRUS DIS BRANCH,ATLANTA,GA. 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 APR PY 1994 VL 10 IS 4 BP 447 EP 447 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000037 ER PT J AU SUITE, M JACK, N BASDEOMAHARAJ, K EDWARDS, J WHITE, F BLATTNER, W BARTHOLOMEW, C AF SUITE, M JACK, N BASDEOMAHARAJ, K EDWARDS, J WHITE, F BLATTNER, W BARTHOLOMEW, C TI INFECTIVE DERMATITIS IN TRINIDAD-AND-TOBAGO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UWI,GEN HOSP,CAREC,PORT OF SPAIN,TRINID & TOBAGO. NCI,DCE,BETHESDA,MD 20892. NR 0 TC 14 Z9 15 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 447 EP 447 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000036 ER PT J AU WEISS, SH MAYUR, RK QUIRINALE, JE FRENCH, J GOODE, R BLATTNER, WA AF WEISS, SH MAYUR, RK QUIRINALE, JE FRENCH, J GOODE, R BLATTNER, WA TI EXCESS MORTALITY AMONG PERSONS INFECTED WITH HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-II (HTLV-II) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UMDNJ,NEW JERSEY MED SCH,NEWARK,NJ. NJ DEPT HLTH,TRENTON,NJ. NCI,BETHESDA,MD 20892. NR 0 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 APR PY 1994 VL 10 IS 4 BP 447 EP 447 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000035 ER PT J AU FRANCHINI, G MARKHAM, P GIRI, A DIGILIO, L HURTEAU, G GALLO, RC AF FRANCHINI, G MARKHAM, P GIRI, A DIGILIO, L HURTEAU, G GALLO, RC TI ISOLATION OF A NOVEL SIMIAN T-CELL LYMPHOTROPIC VIRUS FROM PAN-PANISCUS, STLV(PAN-P), RELATED TO THE HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I AND TYPE-II SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. ADV BIOSCI LABS INC,KENSINGTON,MD. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 450 EP 450 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000046 ER PT J AU VITEK, CR GRACIA, F FUKUDA, K GREEN, D GIUSTI, R KHABBAZ, R LEVINE, P KAPLAN, J BLATTNER, W AF VITEK, CR GRACIA, F FUKUDA, K GREEN, D GIUSTI, R KHABBAZ, R LEVINE, P KAPLAN, J BLATTNER, W TI EVIDENCE FOR SEXUAL AND MOTHER-TO-CHILD TRANSMISSION OF HTLV-II AMONG GUAYMI INDIANS, PANAMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CDC,RETROVIRUS DIS BRANCH,ATLANTA,GA. NCI,VIRAL EPIDEMIOL SECT,BETHESDA,MD 20892. GORGAS MEM LAB,PANAMA CITY,PANAMA. 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 APR PY 1994 VL 10 IS 4 BP 451 EP 451 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000050 ER PT J AU CERESETO, A BERNEMAN, Z KORALNIK, I FRANCHINI, G GALLO, RC KLOTMAN, ME AF CERESETO, A BERNEMAN, Z KORALNIK, I FRANCHINI, G GALLO, RC KLOTMAN, ME TI DETECTION AND QUANTITATION OF ALTERNATIVELY SPLICED PX MESSENGER-RNAS IN ADULT T-CELL LEUKEMIA (ATL) AND TROPICAL SPASTIC PARAPARESIS (TSP/HAM) SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RI klotman, mary/A-1921-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 452 EP 452 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000057 ER PT J AU DERSE, D MIKOVITS, J POLIANOVA, M RUSCETTI, F AF DERSE, D MIKOVITS, J POLIANOVA, M RUSCETTI, F TI BIOLOGICAL CHARACTERIZATION OF A CLONED HTLV-I PROVIRUS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21701. NCI,LEUKOCYTE BIOL LAB,FREDERICK,MD 21701. NCI,FREDERICK CANC RES & DEV CTR,PRI,DYNCORP,BCDP,FREDERICK,MD 21701. NR 0 TC 1 Z9 1 U1 0 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 APR PY 1994 VL 10 IS 4 BP 453 EP 453 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000061 ER PT J AU LUNARDIISKANDAR, Y BRYANT, JL LAM, VH ZEMAN, RA GESSAIN, A GILL, P VARRICCHIO, F GALLO, RC AF LUNARDIISKANDAR, Y BRYANT, JL LAM, VH ZEMAN, RA GESSAIN, A GILL, P VARRICCHIO, F GALLO, RC TI A MODEL OF SEVERAL ASPECTS OF TROPICAL SPASTIC PARAPARESIS HTLV-I-ASSOCIATED MYELOPATHY (TSP/HAM) DISEASE IN IMMUNODEFICIENT MICE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NIDR,ANIM CARE UNIT,BETHESDA,MD 20892. US FDA,NIH,CBER,BETHESDA,MD 20892. INST PASTEUR,PARIS,FRANCE. UNIV SO CALIF,SCH MED,LOS ANGELES,CA. 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 APR PY 1994 VL 10 IS 4 BP 455 EP 455 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000066 ER PT J AU JONES, KS ROBBINS, DS DERSE, DD MORTON, SE MIKOVITS, JA RUSCETTI, FW HOFFMAN, PM AF JONES, KS ROBBINS, DS DERSE, DD MORTON, SE MIKOVITS, JA RUSCETTI, FW HOFFMAN, PM TI EVIDENCE FOR INFECTION IN RATS FOLLOWING EXPOSURE TO A MOLECULAR CLONE OF HTLV-I SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 VET ADM MED CTR,BALTIMORE,MD 21218. UNIV MARYLAND,BALTIMORE,MD 21201. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. NR 0 TC 1 Z9 1 U1 0 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 APR PY 1994 VL 10 IS 4 BP 457 EP 457 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000072 ER PT J AU LENO, M SIMPSON, RM BOWERS, FS KINDT, TJ AF LENO, M SIMPSON, RM BOWERS, FS KINDT, TJ TI LYMPHOCYTE APOPTOSIS TRIGGERED BY A LETHAL LEUKEMOGENIC HTLV-I INFECTED CELL-LINE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. 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 APR PY 1994 VL 10 IS 4 BP 457 EP 457 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000073 ER PT J AU SIMPSON, RM CHOUCHANE, L BOWERS, FS SAWASDIKOSOL, S KINDT, TJ AF SIMPSON, RM CHOUCHANE, L BOWERS, FS SAWASDIKOSOL, S KINDT, TJ TI ANTI-HEAT SHOCK PROTEIN ANTIBODIES IN HTLV-I INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIAID,ROCKVILLE,MD. NR 0 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 APR PY 1994 VL 10 IS 4 BP 458 EP 458 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000075 ER PT J AU CIMINALE, V DAGOSTINO, DM FRANCHINI, G FELBER, BK CHIECOBIANCHI, L AF CIMINALE, V DAGOSTINO, DM FRANCHINI, G FELBER, BK CHIECOBIANCHI, L TI EXPRESSION AND CHARACTERIZATION OF PROTEINS ENCODED IN THE PROXIMAL X-REGION OF HTLV-II SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV PADUA,INST ONCOL,PADUA,ITALY. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD. 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 APR PY 1994 VL 10 IS 4 BP 461 EP 461 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000084 ER PT J AU WATERS, D BLATTNER, W BRINING, S BENVENISTE, R ARTHUR, L AF WATERS, D BLATTNER, W BRINING, S BENVENISTE, R ARTHUR, L TI CELL-FREE TRANSMISSION TO AND TITRATION OF HTLV-1 VIRUS ON RHESUS LUNG-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,FREDERICK,MD 21702. NCI,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 464 EP 464 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000094 ER PT J AU LEHKY, TJ JACOBSON, S AF LEHKY, TJ JACOBSON, S TI INFECTION OF NEURONAL CELLS WITH HTLV-I SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD. 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 APR PY 1994 VL 10 IS 4 BP 466 EP 466 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000101 ER PT J AU LEVIN, M WALTER, M LEHKY, T FOX, CH JACOBSON, S AF LEVIN, M WALTER, M LEHKY, T FOX, CH JACOBSON, S TI DETECTION OF HTLV-I SEQUENCES BY PCR/IN-SITU HYBRIDIZATION (PCR/ISH) IN TARGET TISSUES OF HAM/TSP PATIENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 466 EP 466 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000102 ER PT J AU STRICKLER, HD RATTRAY, C ESCOFFERY, C MANNS, A SCHIFFMAN, MH HANCHARD, B PALEFSKY, J BLATTNER, W AF STRICKLER, HD RATTRAY, C ESCOFFERY, C MANNS, A SCHIFFMAN, MH HANCHARD, B PALEFSKY, J BLATTNER, W TI HTLV-I IS ASSOCIATED WITH CERVICAL-CARCINOMA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV W INDIES,KINGSTON 7,JAMAICA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. 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 APR PY 1994 VL 10 IS 4 BP 468 EP 468 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000110 ER PT J AU BARTHOLOMEW, C EDWARDS, J JACK, N CLEGHORN, F POONKING, P WHITE, F BLATTNER, W AF BARTHOLOMEW, C EDWARDS, J JACK, N CLEGHORN, F POONKING, P WHITE, F BLATTNER, W TI HTLV-1 ASSOCIATED FACIAL-NERVE PALSY IN TRINIDAD-AND-TOBAGO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 GEN HOSP,CAREC,UWI,PORT OF SPAIN,TRINID & TOBAGO. NCI,DIV CANC ETIOL,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 469 EP 469 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000113 ER PT J AU HOFFMAN, PM MIKOVITS, JA BOUDREAU, KA RUSCETTI, FW DHIBJALBUT, S AF HOFFMAN, PM MIKOVITS, JA BOUDREAU, KA RUSCETTI, FW DHIBJALBUT, S TI HTLV-1 INTERACTION WITH GLIAL-CELLS - IMPLICATIONS FOR HAM/TSP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 VET ADM MED CTR,BALTIMORE,MD 21218. UNIV MARYLAND,BALTIMORE,MD 21201. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 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 APR PY 1994 VL 10 IS 4 BP 469 EP 469 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000114 ER PT J AU BARTHOLOMEW, C EDWARDS, J JACK, N CORBIN, D MURPHY, J CLEGHORN, F WHITE, F BLATTNER, W AF BARTHOLOMEW, C EDWARDS, J JACK, N CORBIN, D MURPHY, J CLEGHORN, F WHITE, F BLATTNER, W TI STUDIES ON MATERNAL TRANSMISSION OF HTLV-1 PATIENTS WITH ADULT T-CELL LEUKEMIA (ATL) IN TRINIDAD-AND-TOBAGO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 QUEEN ELIZABETH HOSP,BRIDGETOWN,BARBADOS. NCI,DIV CANC ETIOL,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 470 EP 470 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000119 ER PT J AU WILKS, R MANNS, A MURPHY, EL HANCHARD, B CRANSTON, B HAYNES, G BRAHAM, J BLATTNER, W AF WILKS, R MANNS, A MURPHY, EL HANCHARD, B CRANSTON, B HAYNES, G BRAHAM, J BLATTNER, W TI CLINICAL AND LABORATORY OUTCOMES FOLLOWING TRANSFUSION ACQUIRED HTLV-I INFECTION IN JAMAICA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV W INDIES,TROP METAB RES UNIT,KINGSTON 7,JAMAICA. UNIV W INDIES,DEPT PATHOL,KINGSTON 7,JAMAICA. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. UNIV CALIF BERKELEY,BERKELEY,CA 94720. 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 APR PY 1994 VL 10 IS 4 BP 470 EP 470 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000118 ER PT J AU LOUGHRAN, TP RUSCETTI, FW MONTAGNA, RA STARKEBAUM, G POIESZ, BJ AF LOUGHRAN, TP RUSCETTI, FW MONTAGNA, RA STARKEBAUM, G POIESZ, BJ TI SEROREACTIVITY TO HTLV-I/II IN LGL LEUKEMIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 SYRACUSE UNIV,SYRACUSE,NY 13210. FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. VET ADM MED CTR,SYRACUSE,NY 13210. VET ADM MED CTR,SEATTLE,WA 98108. NR 0 TC 1 Z9 1 U1 0 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 APR PY 1994 VL 10 IS 4 BP 471 EP 471 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000120 ER PT J AU LEONMONZON, M DALAKAS, M AF LEONMONZON, M DALAKAS, M TI THE ROLE OF VIRUS IN HTLV-1-ASSOCIATED POLYMYOSITIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NINCDS,MED NEUROL BRANCH,NEUROMUSCULAR DIS SECT,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 472 EP 472 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000126 ER PT J AU MORGAN, O GILBERT, D RODGERSJOHNSON, P CHAR, G HANCHARD, B BLATTNER, W AF MORGAN, O GILBERT, D RODGERSJOHNSON, P CHAR, G HANCHARD, B BLATTNER, W TI POLYMYOSITIS IN HTLV-I SEROPOSITIVE AND SERONEGATIVE JAMAICANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV W INDIES,KINGSTON 7,JAMAICA. NCI,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 472 EP 472 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000124 ER PT J AU MURPHY, EL MILLER, K SACHER, R FRIDEY, J SMITH, J KLEINMAN, S MATIJAS, L KAPLAN, J KHABBAZ, R NEMO, G AF MURPHY, EL MILLER, K SACHER, R FRIDEY, J SMITH, J KLEINMAN, S MATIJAS, L KAPLAN, J KHABBAZ, R NEMO, G TI UNEXPECTED HEALTH-EFFECTS OF INFECTION WITH HTLV-I AND HTLV-II - THE REDS COHORT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,REDS,ROCKVILLE,MD. NR 0 TC 1 Z9 1 U1 0 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 APR PY 1994 VL 10 IS 4 BP 472 EP 472 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000127 ER PT J AU LEHKY, TJ KATZ, D NISHIMURA, M ROBINSON, S MCFARLIN, DE HEISS, J DJIBJALBUT, S JACOBSON, S AF LEHKY, TJ KATZ, D NISHIMURA, M ROBINSON, S MCFARLIN, DE HEISS, J DJIBJALBUT, S JACOBSON, S TI ISOLATION OF HTLV-II FROM A PATIENT WITH A CHRONIC PROGRESSIVE NEUROLOGIC DISEASE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 473 EP 473 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000131 ER PT J AU MURPHY, EL FRIDEY, J SMITH, JW ARMSTRONG, K STEVENS, J SACHER, RA MILLER, K ENGSTROM, JW KAPLAN, J KHABBAZ, R KLEINMAN, S HANSMA, D THOMSON, R NEMO, G AF MURPHY, EL FRIDEY, J SMITH, JW ARMSTRONG, K STEVENS, J SACHER, RA MILLER, K ENGSTROM, JW KAPLAN, J KHABBAZ, R KLEINMAN, S HANSMA, D THOMSON, R NEMO, G TI PREVALENCE OF HTLV-II AND HTLV-I-ASSOCIATED MYELOPATHY (HAM) IN A COHORT OF SEROPOSITIVE BLOOD-DONORS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,REDS,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 473 EP 473 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000128 ER PT J AU CLEGHORN, F MANNS, A FALK, R HARTGE, P JAFFE, E HANCHARD, B BARTHOLOMEW, C BLATTNER, W AF CLEGHORN, F MANNS, A FALK, R HARTGE, P JAFFE, E HANCHARD, B BARTHOLOMEW, C BLATTNER, W TI INCIDENCE OF NON-HODGKINSS LYMPHOMA AND RELATIONSHIP TO HTLV-I EXPOSURE IN JAMAICA AND TRINIDAD SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,DIV CANC ETIOL,BETHESDA,MD 20892. UNIV W INDIES,KINGSTON 7,JAMAICA. UNIV W INDIES,ST AUGUSTINE,TRINID & TOBAGO. 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 APR PY 1994 VL 10 IS 4 BP 475 EP 475 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000138 ER PT J AU RABKIN, CS CORBIN, D FELTON, S BARKER, H DAVISON, D DEARDEN, C EVANS, AS AF RABKIN, CS CORBIN, D FELTON, S BARKER, H DAVISON, D DEARDEN, C EVANS, AS TI HTLV-I INFECTION IN BARBADOS - RESULTS OF A 20-YEAR FOLLOW-UP-STUDY SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. QUEEN ELIZABETH HOSP,BRIDGETOWN,BARBADOS. RTI,WASHINGTON,DC. YALE UNIV,NEW HAVEN,CT. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD APR PY 1994 VL 10 IS 4 BP 475 EP 475 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000137 ER PT J AU HANCHARD, B WILLIAMS, E WILLIAMS, NP GREEN, M WILKS, R CRANSTON, B CHOY, L MANNS, A BLATTNER, W AF HANCHARD, B WILLIAMS, E WILLIAMS, NP GREEN, M WILKS, R CRANSTON, B CHOY, L MANNS, A BLATTNER, W TI GEOGRAPHIC DIVERSITY IN ATL - COMPARISON OF JAMAICAN AND JAPANESE CASES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV W INDIES,LYMPHOMA STUDY GRP,KINGSTON 7,JAMAICA. UNIV W INDIES,DEPT PATHOL,KINGSTON 7,JAMAICA. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 476 EP 476 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000143 ER PT J AU HARRINGTON, W CABRAL, L POIESZ, BJ AF HARRINGTON, W CABRAL, L POIESZ, BJ TI HTLV-I RELATED DISEASES IN MIAMI SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV MIAMI,SCH MED,MIAMI,FL. SYRACUSE UNIV,SYRACUSE,NY 13210. FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. CELLULAR PROD,BUFFALO,NY. VET ADM MED CTR,SYRACUSE,NY 13210. VET ADM MED CTR,SEATTLE,WA 98108. 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 APR PY 1994 VL 10 IS 4 BP 476 EP 476 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000141 ER PT J AU DOSIK, H WELLES, SL JOSEPH, EM GOBERDHAM, LJ LEE, SL MIOTTI, A CERVANTES, J BERTONI, M ROTHENBERG, S LEVINE, PH AF DOSIK, H WELLES, SL JOSEPH, EM GOBERDHAM, LJ LEE, SL MIOTTI, A CERVANTES, J BERTONI, M ROTHENBERG, S LEVINE, PH TI CLINICAL-FEATURES OF ADULT T-CELL LEUKEMIA/LYMPHOMA IN BROOKLYN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 SUNY HLTH SCI CTR,INTERFAITH MED CTR,BROOKLYN,NY 11203. BROOKDALE HOSP,BROOKLYN,NY. BROOKLYN HOSP,BROOKLYN,NY. ST MARYS HOSP,BROOKLYN,NY. WYCKOFF HTS HOSP,BROOKLYN,NY. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 477 EP 477 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000145 ER PT J AU RODGERSJOHNSON, P SERJEANT, GR JOHNSON, B STONE, G GIBBS, CJ AF RODGERSJOHNSON, P SERJEANT, GR JOHNSON, B STONE, G GIBBS, CJ TI PATTERN OF RETROVIRAL INFECTION IN PATIENTS WITH HOMOZYGOUS SICKLE-CELL DISEASE IN JAMAICA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV W INDIES,DEPT MED,KINGSTON 7,JAMAICA. UNIV W INDIES,MRC LABS JAMAICA,KINGSTON 7,JAMAICA. NIH,LCNSS,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 478 EP 478 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000151 ER PT J AU RODGERSJOHNSON, P HICKLING, F JOHNSON, B STONE, G GIBBS, CJ AF RODGERSJOHNSON, P HICKLING, F JOHNSON, B STONE, G GIBBS, CJ TI RETROVIRUSES IN JAMAICANS SCHIZOPHRENIC-PATIENTS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV W INDIES,KINGSTON 7,JAMAICA. NIH,LCNSS,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 478 EP 478 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000149 ER PT J AU LAGRENADE, L MORGAN, OS CARBERRY, C HANCHARD, B FLETCHER, V GRAY, R CRANSTON, B ROGERSJOHNSON MANNS, A AF LAGRENADE, L MORGAN, OS CARBERRY, C HANCHARD, B FLETCHER, V GRAY, R CRANSTON, B ROGERSJOHNSON MANNS, A TI TROPICAL SPASTIC PARAPARESIS OCCURRING IN HTLV-1 ASSOCIATED INFECTIVE DERMATITIS - A REPORT OF 2 CASES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV W INDIES,DEPT MED,MONA,JAMAICA. UNIV W INDIES,DEPT PATHOL,MONA,JAMAICA. UNIV W INDIES,DEPT CHILD HLTH,MONA,JAMAICA. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 0 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 APR PY 1994 VL 10 IS 4 BP 479 EP 479 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000152 ER PT J AU KHABBAZ, RF KAPLAN, JE MATIJAS, L WRIGHT, D LAL, R RUDOLPH, D MURPHY, E KLEINMAN, S SCHREIBER, G AF KHABBAZ, RF KAPLAN, JE MATIJAS, L WRIGHT, D LAL, R RUDOLPH, D MURPHY, E KLEINMAN, S SCHREIBER, G TI RISK-FACTORS FOR HTLV-I AND HTLV-II SEXUAL TRANSMISSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NHLBI,REDS,BALTIMORE,MD. NHLBI,REDS,WASHINGTON,DC. NHLBI,REDS,DETROIT,MI. NHLBI,REDS,LOS ANGELES,CA. NHLBI,REDS,OKLAHOMA CITY,OK. NHLBI,REDS,SAN FRANCISCO,CA. CDC,ATLANTA,GA. NHLBI,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 481 EP 481 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000159 ER PT J AU NEEL, J BIGGAR, RJ SUKARNIK, R AF NEEL, J BIGGAR, RJ SUKARNIK, R TI GENETIC AND VIROLOGICAL CORRELATES WITH THE ORIGIN OF AMERINDIANS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV MICHIGAN,ANN ARBOR,MI 48109. NCI,BETHESDA,MD 20892. RUSSIAN ACAD SCI,NOVOSIBIRSK,RUSSIA. 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 APR PY 1994 VL 10 IS 4 BP 481 EP 481 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000158 ER PT J AU COTE, T MANNS, A HANCHARD, B WILKS, R CRANSTON, B SMITH, L BLATTNER, W AF COTE, T MANNS, A HANCHARD, B WILKS, R CRANSTON, B SMITH, L BLATTNER, W TI HTLV-1 SERO-INCIDENCE AMONG JAMAICAN FOOD HANDLERS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV W INDIES,KINGSTON 7,JAMAICA. 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 APR PY 1994 VL 10 IS 4 BP 484 EP 484 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000168 ER PT J AU LAL, RB MANNS, A MINGLE, J LEVINE, PH AF LAL, RB MANNS, A MINGLE, J LEVINE, PH TI PRESENCE OF HUMAN T-LYMPHOTROPIC VIRUS TYPE-II IN GHANA, WEST-AFRICA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CDC,RETROVIRUS DIS BRANCH,ATLANTA,GA. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. BURKITT TUMOR PROJECT,ACCRA,GHANA. 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 APR PY 1994 VL 10 IS 4 BP 485 EP 485 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000174 ER PT J AU WELLES, SL DOSIK, H JOSEPH, EM GOBERDHAM, LJ BERTONI, M CERVANTES, J LEE, S MIOTTI, A JAFFE, E LEVINE, PH AF WELLES, SL DOSIK, H JOSEPH, EM GOBERDHAM, LJ BERTONI, M CERVANTES, J LEE, S MIOTTI, A JAFFE, E LEVINE, PH TI ADULT T-CELL LEUKEMIA/LYMPHOMA IN BROOKLYN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. INTERFAITH MED CTR,BROOKLYN,NY. WYCKOFF HOSP,BROOKLYN,NY. ST MARYS HOSP,BROOKLYN,NY. BROOKDALE HOSP,BROOKLYN,NY. BROOKLYN HOSP,BROOKLYN,NY. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. RI Jaffe, Elaine/G-8984-2014 OI Jaffe, Elaine/0000-0003-4632-0301 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 APR PY 1994 VL 10 IS 4 BP 486 EP 486 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000179 ER PT J AU CLEGHORN, F JACK, N EDWARDS, J MURPHY, J MAHABIR, B PAUL, R WHITE, F BARTHOLOMEW, C BLATTNER, W AF CLEGHORN, F JACK, N EDWARDS, J MURPHY, J MAHABIR, B PAUL, R WHITE, F BARTHOLOMEW, C BLATTNER, W TI HTLV-I INFECTION IN AN STD CLINIC IN TRINIDAD SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NCI,DIV CANC ETIOL,BETHESDA,MD 20892. MINIST HLTH,CAREC,ST JOSEPH,TRINID & TOBAGO. 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 APR PY 1994 VL 10 IS 4 BP 488 EP 488 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000187 ER PT J AU SNG, I CHAN, R WATERS, D LAL, R ALEXANDER, S SNG, E LEVIN, A BLATTNER, W AF SNG, I CHAN, R WATERS, D LAL, R ALEXANDER, S SNG, E LEVIN, A BLATTNER, W TI HTLV INFECTION IN PROSTITUTES AND LYMPHOMA PATIENTS IN SINGAPORE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 SINGAPORE GEN HOSP,SINGAPORE 0316,SINGAPORE. NATL SKIN CTR,SINGAPORE 1130,SINGAPORE. PRI LABS,FREDERICK,MD. CDC,ATLANTA,GA. CBC,ROCKVILLE,MD. ST BARTHOLOMEWS HOSP,RTI UNIT,LONDON,ENGLAND. NCI,ROCKVILLE,MD. 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 APR PY 1994 VL 10 IS 4 BP 489 EP 489 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000188 ER PT J AU JACK, N CLEGHORN, F MURPHY, J WHITE, F BARTHOLOMEW, C BLATTNER, W AF JACK, N CLEGHORN, F MURPHY, J WHITE, F BARTHOLOMEW, C BLATTNER, W TI THE SEROPREVALENCE OF HTLV-I IN THE ISLAND OF TOBAGO SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV W INDIES,ST AUGUSTINE,TRINID & TOBAGO. NCI,DIV CANC ETIOL,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 491 EP 491 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000199 ER PT J AU LEVIN, A BRUBAKER, G WATERS, D ALEXANDER, S SHAO, J BLATTNER, W AF LEVIN, A BRUBAKER, G WATERS, D ALEXANDER, S SHAO, J BLATTNER, W TI EVIDENCE FOR HTLV INFECTION IN NORTHWEST TANZANIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 ST BARTHOLOMEWS HOSP,DEPT VIROL,RTI UNIT,LONDON,ENGLAND. SHIRATI HOSP,SHIRATI,TANZANIA. PRI DYNCORP,FREDERICK,MD 21701. CAMBRIDGE BIOTECH CORP,CAMBRIDGE,MD. MUHIMBILI MED CTR,DAR ES SALAAM,TANZANIA. NCI,ROCKVILLE,MD. 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 APR PY 1994 VL 10 IS 4 BP 491 EP 491 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000196 ER PT J AU NERURKAR, VR JOHNSON, BK VONBRIESEN, H RUBSAMENWAIGMANN, H MANIAR, JK MAHAMBRE, G YANAGIHARA, R AF NERURKAR, VR JOHNSON, BK VONBRIESEN, H RUBSAMENWAIGMANN, H MANIAR, JK MAHAMBRE, G YANAGIHARA, R TI SEROPREVALENCE OF HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I INFECTION IN WESTERN INDIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. CHEMOTHERAPEUT FORSCHUNGSINST,FRANKFURT,GERMANY. STD CLIN,BOMBAY,MAHARASHTRA,INDIA. DIRECTORATE HLTH SERV,PANAJI,GOA,INDIA. 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 APR PY 1994 VL 10 IS 4 BP 492 EP 492 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000201 ER PT J AU ALEXANDER, S GALLO, D YAMAGUCHI, K LAL, R WATERS, D YOSHIHARA, N SNG, I BRUBAKER, G LAVANGE, L LEVINE, P TAKATSUKI, K LEVIN, A BLATTNER, W AF ALEXANDER, S GALLO, D YAMAGUCHI, K LAL, R WATERS, D YOSHIHARA, N SNG, I BRUBAKER, G LAVANGE, L LEVINE, P TAKATSUKI, K LEVIN, A BLATTNER, W TI SENSITIVITY AND SPECIFICITY ANALYSIS OF THE MULTICENTER SERUM TESTING BY THE KUMAMOTO-WORKSHOP-GROUP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CAMBRIDGE BIOTECH CORP,ROCKVILLE,MD. CA DEPT HLTH SERV,BERKELEY,CA. KUMAMOTO UNIV,SCH MED,KUMAMOTO 860,JAPAN. CDC,ATLANTA,GA. PRI DYNCORP,FREDERICK,MD 21701. NATL INST MED RES,TOKYO,JAPAN. SINGAPORE GEN HOSP,SINGAPORE 0316,SINGAPORE. SHIRATI HOSP,SHIRATI,TANZANIA. NCI,BETHESDA,MD 20892. ST BARTHOLOMEWS HOSP,RTI,LONDON,ENGLAND. 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 APR PY 1994 VL 10 IS 4 BP 495 EP 495 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000213 ER PT J AU ROBERTSON, E STEPHENS, J CHAN, E MOTLEY, C BUYTENDORP, M PRILLAMAN, J COLEMAN, C GARRETT, P WEIBLAN, B CONTOREGGI, C HOFFMAN, W PHELPS, B AF ROBERTSON, E STEPHENS, J CHAN, E MOTLEY, C BUYTENDORP, M PRILLAMAN, J COLEMAN, C GARRETT, P WEIBLAN, B CONTOREGGI, C HOFFMAN, W PHELPS, B TI EVALUATION OF AN HTLV-II RISK POPULATION WITH AN HTLVI/HTLV-II COMBINATION IMMUNOASSAY AND AN HTLV-I/II WESTERN IMMUNOBLOT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 BBI,BOSTON,MA. NIDA,BALTIMORE,MD. ABBOTT LABS,N CHICAGO,IL 60064. 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 APR PY 1994 VL 10 IS 4 BP 497 EP 497 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000218 ER PT J AU PARDI, D RUDOLPH, DL COLIGAN, JE LAL, RB AF PARDI, D RUDOLPH, DL COLIGAN, JE LAL, RB TI IMMUNODOMINANT EPITOPES OF THE REGULATORY PROTEINS, TAX AND REX, IN HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-II SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CDC,RETROVIRUS DIS BRANCH,ATLANTA,GA. NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 498 EP 498 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000221 ER PT J AU RUDOLPH, DL COLIGAN, JE LAL, RB AF RUDOLPH, DL COLIGAN, JE LAL, RB TI SYNTHETIC PEPTIDE-BASED IMMUNOASSAY FOR THE DETECTION OF ANTIBODIES TO HTLV-I TAX SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 CDC,RETROVIRUS DIS BRANCH,ATLANTA,GA. NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 499 EP 499 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000225 ER PT J AU YANAGIHARA, R SAITOU, N NERURKAR, VR SONG, KJ BASTIAN, I FRANCHINI, G GAJDUSEK, DC AF YANAGIHARA, R SAITOU, N NERURKAR, VR SONG, KJ BASTIAN, I FRANCHINI, G GAJDUSEK, DC TI MOLECULAR PHYLOGENY AND GLOBAL DISSEMINATION OF HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I VIEWED WITHIN THE CONTEXT OF PRIMATE EVOLUTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NATL INST GENET,MISHIMA,SHIZUOKA 411,JAPAN. MENZIES SCH HLTH RES,DARWIN,AUSTRALIA. 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 APR PY 1994 VL 10 IS 4 BP 501 EP 501 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000233 ER PT J AU NERURKAR, VR ACHIRON, A SONG, KJ MELLAND, RR YANAGIHARA, R AF NERURKAR, VR ACHIRON, A SONG, KJ MELLAND, RR YANAGIHARA, R TI HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-I FROM IRANIAN-BORN MASHHADI JEWS - PHYLOGENETIC LINK WITH VIRUS-STRAINS FROM SOUTHERN INDIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. BEILINSON MED CTR,DEPT NEUROL,IL-49100 PETAH TIQWA,ISRAEL. 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 APR PY 1994 VL 10 IS 4 BP 504 EP 504 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000245 ER PT J AU NERURKAR, VR DUENASBARAJAS, E NAGLE, JW BERNAL, JE DUENAS, DR GAJDUSEK, DC YANAGIHARA, R AF NERURKAR, VR DUENASBARAJAS, E NAGLE, JW BERNAL, JE DUENAS, DR GAJDUSEK, DC YANAGIHARA, R TI VIROLOGICAL EVIDENCE FOR HUMAN T-CELL LYMPHOTROPIC VIRUS TYPE-II INFECTION AMONG THE WAYUU INDIANS OF COLOMBIA SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. PONTIFICIA UNIV JAVERIANA,INST GENET,SANTA FE BOGATA,COLOMBIA. NR 0 TC 1 Z9 1 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 APR PY 1994 VL 10 IS 4 BP 505 EP 505 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000250 ER PT J AU MALONEY, E MANN, D WIKTOR, S PATE, E GRAY, B MANNS, A BLATTNER, W AF MALONEY, E MANN, D WIKTOR, S PATE, E GRAY, B MANNS, A BLATTNER, W TI THE EFFECT OF HTLV-I INFECTION ON T-CELL SUBSETS IN JAMAICAN CHILDREN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 UNIV W INDIES,KINGSTON 7,JAMAICA. NCI,BETHESDA,MD 20892. 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 APR PY 1994 VL 10 IS 4 BP 507 EP 507 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA NK470 UT WOS:A1994NK47000257 ER PT J AU HARFORD, TC PARKER, DA AF HARFORD, TC PARKER, DA TI ANTISOCIAL-BEHAVIOR, FAMILY HISTORY, AND ALCOHOL DEPENDENCE SYMPTOMS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE ANTISOCIAL BEHAVIOR; FAMILY HISTORY; ALCOHOLISM; ALCOHOL DEPENDENCE ID YOUNG ADULTHOOD; FOLLOW-UP; PERSONALITY; ADOLESCENCE; DRINKING AB Drawing on data from the National Longitudinal Survey of young adults, this study examines the effects of antisocial behavior on alcohol dependence among young men and women in the United States. An analysis of the data from the study indicates that there are effects of antisocial behavior and that these effects cannot be attributed to a lower social class family of origin or to a positive family history of alcoholism. The analysis also indicates that the strongest effects are found among young adults with both antisocial behavior and a positive family history. RP HARFORD, TC (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,ROOM 14C26,PARLAWN BLDG,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 23 TC 17 Z9 17 U1 2 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 APR PY 1994 VL 18 IS 2 BP 265 EP 268 DI 10.1111/j.1530-0277.1994.tb00012.x PG 4 WC Substance Abuse SC Substance Abuse GA NK244 UT WOS:A1994NK24400011 PM 8048725 ER PT J AU HASIN, DS GRANT, B AF HASIN, DS GRANT, B TI NOSOLOGICAL COMPARISONS OF DSM-III-R AND DSM-IV ALCOHOL-ABUSE AND DEPENDENCE IN A CLINICAL FACILITY - COMPARISON WITH THE 1988 NATIONAL-HEALTH INTERVIEW SURVEY RESULTS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE ALCOHOL ABUSE; ALCOHOL DEPENDENCE; DSM-III-R; DSM-IV; NOSOLOGICAL COMPARISON ID DISORDERS; VALIDITY AB The purpose of this study was to compare DSM-III-R and proposed formulations of DSM-IV diagnoses of alcohol use disorders in a clinical sample with the same assessment methods used in a large national survey previously reported. Issues included the number of symptoms required for abuse and dependence diagnoses, the effects of requiring evidence of physiological dependence to make the dependence diagnosis (Option 1 vs. Option 2), whether to require a duration criterion, and the concept of alcohol abuse. The diagnostic criteria proposed in the 1991 DSM-IV options book were the criteria investigated in this study. Concordance between DSM-III-R and DSM-IV was closest when the form of DSM-IV used was most similar to DSM-IIII-R. The duration criterion had much less effect on a dependence diagnosis in this clinical sample than in the general population. DSM-IV Option 2 for alcohol dependence excluded a number of cases from the dependence diagnosis who received such a diagnosis under DSM-III R and DSM-IV Option 1. Abuse continued to function as a residual category, especially noticeable under increasingly restrictive definitions of dependence, and was rare in both the clinical and general population sample. Implications of the findings for research and other purposes are discussed. C1 NIAAA,DIV BIOMETRY & EPIDEMIOL,ROCKVILLE,MD 20852. RP HASIN, DS (reprint author), COLUMBIA UNIV,DEPT PSYCHIAT,BOX 123,722 W 168TH ST,NEW YORK,NY 10032, USA. FU NIAAA NIH HHS [AA-08159]; NIMH NIH HHS [MH-30906] NR 14 TC 33 Z9 33 U1 1 U2 1 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 APR PY 1994 VL 18 IS 2 BP 272 EP 279 DI 10.1111/j.1530-0277.1994.tb00014.x PG 8 WC Substance Abuse SC Substance Abuse GA NK244 UT WOS:A1994NK24400013 PM 8048727 ER PT J AU HIGUCHI, S PARRISH, KM DUFOUR, MC TOWLE, LH HARFORD, TC AF HIGUCHI, S PARRISH, KM DUFOUR, MC TOWLE, LH HARFORD, TC TI RELATIONSHIP BETWEEN AGE AND DRINKING PATTERNS AND DRINKING PROBLEMS AMONG JAPANESE, JAPANESE-AMERICANS, AND CAUCASIANS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE ETHNIC DIVERSITY; AGE; DRINKING PATTERNS; ALCOHOL-RELATED PROBLEMS ID BEHAVIOR AB Comparing alcohol consumption patterns by age and gender among Japanese in Japan and Japanese-Americans and Caucasians in the United States, this study examined the associations between age and both heavy drinking and social problems using logistic regression for each ethnic group of male current drinkers. As reported in previous studies of Caucasians, men drink more alcohol than women, older respondents are more likely than younger ones to be abstainers, and the percentages of heavier drinkers and problem drinkers are higher among the young than among older people. Although Japanese-Americans reported consuming less alcohol than Caucasians, their drinking patterns by age were similar: among both United States populations, younger respondents are at higher risk for drinking problems than older respondents, even when alcohol consumption and sociodemographic variables are controlled by logistic regression. However, this association of age and drinking patterns and drinking problems is not universal. Japanese men consumed more alcohol and had a higher proportion of heavier drinkers in the middle age groups; the association between age and drinking problems also varied in this group. In addition to aging, sociocultural factors such as drinking norms probably account for the differences in drinking behavior among different age groups. This study may stimulate further cross-cultural comparison of drinking patterns and problems. C1 NIAAA,DIV BIOMETRY & EPIDEMIOL,ROCKVILLE,MD 20852. NIAAA,OFF INT & INTERGOVT AFFAIRS,ROCKVILLE,MD 20852. UNIV WASHINGTON,DEPT HLTH SERV,SEATTLE,WA 98195. OI Makimoto, Kiyoko/0000-0003-0242-1290 NR 26 TC 25 Z9 25 U1 1 U2 3 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 APR PY 1994 VL 18 IS 2 BP 305 EP 310 DI 10.1111/j.1530-0277.1994.tb00018.x PG 6 WC Substance Abuse SC Substance Abuse GA NK244 UT WOS:A1994NK24400017 PM 8048731 ER PT J AU COWLEY, DS ROYBYRNE, PP RADANT, A HOMMER, DW GREENBLATT, DJ VITALIANO, PP GODON, C AF COWLEY, DS ROYBYRNE, PP RADANT, A HOMMER, DW GREENBLATT, DJ VITALIANO, PP GODON, C TI EYE-MOVEMENT EFFECTS OF DIAZEPAM IN SONS OF ALCOHOLIC FATHERS AND MALE CONTROL SUBJECTS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE SACCADE VELOCITY; SMOOTH PURSUIT; CHILDREN OF ALCOHOLICS; DIAZEPAM ID CENTRAL-NERVOUS-SYSTEM; BENZODIAZEPINE SENSITIVITY; RAT-BRAIN; ETHANOL; DRINKING; RESPONSES; EXPECTANCIES; MEN; INTOXICATION; INHERITANCE AB Both animal and human studies suggest that the GABA-benzodiazepine receptor complex may be involved in the acute effects of ethanol, as well as the development of tolerance and dependence with chronic ethanol use. The current study was performed to assess sensitivity to benzodiazepines, and thus the functional sensitivity of the GABA-benzodiazepine receptor system, in subjects at high risk for alcoholism. Sons of alcoholic fathers (SOAs; n = 27) were compared with male controls without a family history of alcoholism (n = 23) in response to diazepam versus placebo. SOAs and controls received four logarithmically increasing doses of intravenous diazepam or placebo in randomized order on 2 days at least 1 week apart. Effects of diazepam were assessed using two eye movement tasks, peak saccadic eye movement velocity, and average smooth pursuit eye movement gain, which provide reliable, quantitative measures of benrodiazepine effects. In addition, memory, self-rated sedation, and pleasurable drug effects were measured. In comparison with control subjects, SOAs displayed significantly less diazepam effects on peak saccade velocity, average smooth pursuit gain, memory, and self-rated sedation, but significantly greater pleasurable drug effects. Differences in response to diazepam between SOAs and male controls may reflect altered functional sensitivity of the central GABA-benzodiazepine receptor system or a more general difference between groups in the effects of CNS active or sedating drugs. C1 UNIV WASHINGTON,VET AFFAIRS MED CTR,DEPT PSYCHIAT & BEHAV SCI,SEATTLE,WA. UNIV WASHINGTON,MED CTR,DEPT PSYCHIAT & BEHAV SCI,SEATTLE,WA 98195. UNIV WASHINGTON,HARBORVIEW MED CTR,DEPT PSYCHIAT & BEHAV SCI,SEATTLE,WA 98104. NIAAA,BETHESDA,MD. TUFTS UNIV,NEW ENGLAND MED CTR,DIV CLIN PHARMACOL,BOSTON,MA 02111. FU NIAAA NIH HHS [R29 AA08161]; NIMH NIH HHS [R01 MH49413] NR 58 TC 38 Z9 38 U1 1 U2 4 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 APR PY 1994 VL 18 IS 2 BP 324 EP 332 DI 10.1111/j.1530-0277.1994.tb00021.x PG 9 WC Substance Abuse SC Substance Abuse GA NK244 UT WOS:A1994NK24400020 PM 8048734 ER PT J AU GRANT, KA HELLEVUO, K TABAKOFF, B AF GRANT, KA HELLEVUO, K TABAKOFF, B TI THE 5-HT3 ANTAGONIST MDL-72222 EXACERBATES ETHANOL WITHDRAWAL SEIZURES IN MICE SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Note DE SEROTONIN; ALCOHOL DEPENDENCE; 5-HT3 ANTAGONISTS; DRUG WITHDRAWAL SEIZURES ID RECEPTOR ANTAGONISTS; CONSUMPTION; DOPAMINE; RATS AB Ethanol-dependent mice were treated with the 5-HT3 antagonist MDL 72222 after withdrawal from ethanol. Treatment with unit doses (0, 5.6, 10, and 17.0 mg/kg) of MDL 72222 at 0, 4, and 7 hr after withdrawal dose dependently exacerbated the severity of ethanol withdrawal seizures. Treatment with a single dose (17 mg/kg) of MDL 72222 at 5 hr after withdrawal also exacerbated the severity of ethanol withdrawal seizures. Ethanol naive mice treated with MDL 72222 (56 mg/kg) did not display any seizures. Treatment with another 5-HT3 antagonist, ICS 205-930 (23 and 46 mg/kg), or the 5-HT2 receptor antagonist ketanserin, did not affect ethanol withdrawal seizures. The findings suggest MDL 72222 selectively enhances sensitivity to withdrawal seizures following chronic ethanol exposure. C1 NIAAA,DIV CLIN & BIOL RES,ROCKVILLE,MD. UNIV COLORADO,HLTH SCI CTR,DEPT PHARMACOL,DENVER,CO 80262. RP GRANT, KA (reprint author), BOWMAN GRAY SCH MED,DEPT PHYSIOL & PHARMACOL,MED CTR BLVD,WINSTON SALEM,NC 27157, USA. FU NIAAA NIH HHS [AA-09014, AA-09346] NR 21 TC 23 Z9 23 U1 0 U2 0 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 APR PY 1994 VL 18 IS 2 BP 410 EP 414 DI 10.1111/j.1530-0277.1994.tb00034.x PG 5 WC Substance Abuse SC Substance Abuse GA NK244 UT WOS:A1994NK24400033 PM 8048747 ER PT J AU HOCHMAN, JS BROOKS, AMM MORRIS, BM AHMAD, T ROGERS, WJ EPSTEIN, AE ARCINIEGAS, JG CROSSLEY, GH DAILEY, SM KAY, GN LITTLE, RE MACLEAN, WAH PAPAPIETRO, SE PLUMB, VJ SILBER, S BAKER, AR CARLISLE, K COHEN, N COX, M THOMAS, C LEVSON, L VONHAGEL, D WALTON, AE PRATT, CM MAHMARIAN, J MORRIS, G CAPONE, RJ BERGER, EE CHMIELEWSKI, C GORKIN, L KHAN, AH KORR, K HANDSHAW, K CONNOLLY, E FITZPATRICK, D CAMERON, T WYSE, DG DUFF, HJ MITCHELL, LB GILLIS, AM WARNICA, JW SHELDON, RS LESOWAY, NR KELLEN, J HALE, C INKSTER, M BRODSKY, M WOLFF, L ALLEN, B ZELMAN, R THOMAS, G CAUDILLO, G TAKEDA, D SHERWOOD, C RANAZZI, R RAPAPORT, E DOHRMANN, ML RASKIN, S DREW, DW SOMELOFSKI, CA DANFORTH, JW KUI, PY JOHNSON, MR LABARCA, JR WALDO, AL CARLSON, MD ADLER, DS HOLLAND, JB BUCHTER, CM BAHLER, RC PAMELIA, FX JOSEPHSON, RA HENTHORN, RW ZUELGARAY, JG WOOD, K REDMON, P VARGAS, MA VARGO, L SCHALLER, SE KOBUS, CE CHOBAN, NL BIGGER, NYJ GREENBERG, HM GREGORY, JJ RADOSLOVICH, G STEINBERG, JS ROTHBART, ST CASE, R DWYER, EM SQUATRITO, A KELLY, M CAMPION, JM TORMEY, D ANTHONY, R CALLAGHAN, E CHAPNICK, M RIPLEY, B FONTANA, C SCHLANT, RC ARENSBERG, D CORSO, JA HURST, JW MORRIS, DC SHERMAN, SW SILVERMAN, BD SILVERMAN, ME ROBERTS, JS BALLOU, SK JEFFRIES, VD BRACKNEY, BA SEALS, AA HARTLEY, J BAKER, RM GILMOUR, KE BAKER, SB HOWARD, J KATZ, RJ BESCH, GA BRILL, D DIBIANCO, R DONOHUE, D FISHER, G FRANCIS, C FRIEDMAN, D GOLDBERG, D GOLDBERG, S KOSS, G LARCA, L LEONARD, R LINDGREN, K RONAN, J ROSENBLATT, A ROSING, D ROSS, A ROTSZTAIN, A SHAWL, F SINDERSON, T STEVENSON, R TINKER, B VARGHESE, J YACKEE, J BIGHAM, H FRANKLIN, W GOLD, R GRAHAM, G GROSSBERG, D HOARE, R LEVY, W MAHMOOD, T TANNENBAUM, E TULLNER, W EISENHOWER, E GERACI, T WILHELMSEN, L BERGSTRAND, R FREDLUND, BO SIGURDSSON, A SIVERTSSON, R SWEDBERG, K HOULTZ, B WIKLUND, I SCHLYTER, G HEDELIN, G LEIJON, M MORGANROTH, J CARVER, J HOROWITZ, L KUTALEK, S PAPA, L SANDBERG, J VICTOR, M CESARE, S VRABEL, C TALARICO, K LUHMANN, S PALAZZO, D GOLDSTEIN, S GOLDBERG, AD FRUMIN, H WESTVEER, D DEBUTLIER, M SCHAIRER, J STOMEL, R FRANK, DM JARANDILLA, R DAVEY, D HASSE, C SHINNEY, S MORLEDGE, JH FARNHAM, DJ HINDERACKER, PH MUSSER, WE DEVRIES, K KUSHNER, JA RAO, R PETERSON, DT MCCAULEY, CS BERGEN, TS BOWMAN, KO GILLMAN, A FULLER, L OBRIEN, J MORLEDGE, J DEMARIA, AN KUO, CS KAMMERLING, JM CORUM, J THIEMANN, M SCHRODT, R PETERS, R SUTTON, F GOTTLIEB, S PAPUCHIS, G MATTIONI, T TODD, L CUSACK, C SCHECK, J HUANG, SKS ALPERT, JS GORE, JM RYAN, M COLLETTWILLEY, P CHAHINE, RA SEQUEIRA, RF LOWERY, MH DELGADO, LM CORREA, JL LASO, LJ HODGES, M SALERNO, D ANDERSON, B COLLINS, R DENES, P DUNBAR, D GRANRUD, G HAUGLAND, J HESSION, W MCBRIDE, J GORNICK, C SIMONSON, J TOLINS, M ETTINGER, A PETERSON, S SLIVKEN, R GRIMALDI, L ROY, D THEROUX, P LEMERY, R MORISSETTE, D BEAUDOIN, D GIRARD, L LAVALLEE, E MCANULTY, JH REINHART, SE MAURICE, G MURPHY, ES KRON, J MARCHANT, C BOXER, J PRINCEHOUSE, L SINNER, K BEANLANDS, D DAVIES, R GREEN, M WILLIAMS, W BAIRD, MJ GARRARD, L HEAL, S HASPECT, A BORTHWICK, J MAROIS, L WOODEND, K AKIYAMA, T HOOD, WB EASLEY, R RYAN, G KENIEN, G PATT, M KAZIERAD, D GOLDFARB, A BUTLER, LL KELLER, ML STANLEY, P PEEBLES, J SYROCKI, D LAVIN, D SCHOENBERGER, JA LIEBSON, PR STAMATO, NJ PETROPULOS, PR BUCKINGHAM, TA REMIJAS, T KOCOUREK, J JANKO, K BARKER, AH ANDERSON, JL FOWLES, RE KEITH, TB WILLIAMS, CB MORENO, FL DORAN, EN FOWLER, B SUMMERS, K WHITE, C OHARA, G ROULEAU, JL PLANTE, S VINCENT, C BOUCHARD, D ZOBLE, RG OTERO, JE BUGNI, WJ SCHWARTZ, KM SHETTIGAR, UR BREWINGTON, JA UMBERGER, J COHEN, JD BJERREGAARD, P HAMILTON, WP GARNER, M ANDERSON, S ELSHERIF, N URSELL, SN GABOR, GE IBRAHIM, B ASSADI, M BREZSNYAK, ML PORTER, AV STANIORSKI, A WOOSLEY, RL RODEN, DM CAMPBELL, WB ECHT, DS LEE, JT MURRAY, KT SPELL, JD BONHOTAL, ST JARED, LL THOMAS, TI GOLDNER, F RICHARDSON, DW ROMHILT, DW ELLENBOGEN, KA BANE, BB FIELDS, J SHRADER, S POWELL, E CHAFFIN, CF WELLS, A CONWAY, KT PLATIA, EV ODONOGHUE, S TRACY, CM ALI, N BOWEN, P BROOKS, KM OETGEN, W WESTON, LT CARSON, P OBIASMANNO, D HARRISON, J SAYLOR, A POWELL, S HAAKENSON, CM SATHER, MR MALONE, LA HALLSTROM, AP MCBRIDE, R GREENE, HL BROOKS, MM LEDINGHAM, R REYNOLDSHAERTLE, R HUTHER, M SCHOLZ, M MORRIS, M FRIEDMAN, LM SCHRON, E VERTER, J JENNINGS, C PROSCHAN, M BRISTOW, JD DEMETS, DL FISCH, C NIES, AS RUSKIN, J STRAUSS, H WALTERS, L AF HOCHMAN, JS BROOKS, AMM MORRIS, BM AHMAD, T ROGERS, WJ EPSTEIN, AE ARCINIEGAS, JG CROSSLEY, GH DAILEY, SM KAY, GN LITTLE, RE MACLEAN, WAH PAPAPIETRO, SE PLUMB, VJ SILBER, S BAKER, AR CARLISLE, K COHEN, N COX, M THOMAS, C LEVSON, L VONHAGEL, D WALTON, AE PRATT, CM MAHMARIAN, J MORRIS, G CAPONE, RJ BERGER, EE CHMIELEWSKI, C GORKIN, L KHAN, AH KORR, K HANDSHAW, K CONNOLLY, E FITZPATRICK, D CAMERON, T WYSE, DG DUFF, HJ MITCHELL, LB GILLIS, AM WARNICA, JW SHELDON, RS LESOWAY, NR KELLEN, J HALE, C INKSTER, M BRODSKY, M WOLFF, L ALLEN, B ZELMAN, R THOMAS, G CAUDILLO, G TAKEDA, D SHERWOOD, C RANAZZI, R RAPAPORT, E DOHRMANN, ML RASKIN, S DREW, DW SOMELOFSKI, CA DANFORTH, JW KUI, PY JOHNSON, MR LABARCA, JR WALDO, AL CARLSON, MD ADLER, DS HOLLAND, JB BUCHTER, CM BAHLER, RC PAMELIA, FX JOSEPHSON, RA HENTHORN, RW ZUELGARAY, JG WOOD, K REDMON, P VARGAS, MA VARGO, L SCHALLER, SE KOBUS, CE CHOBAN, NL BIGGER, NYJ GREENBERG, HM GREGORY, JJ RADOSLOVICH, G STEINBERG, JS ROTHBART, ST CASE, R DWYER, EM SQUATRITO, A KELLY, M CAMPION, JM TORMEY, D ANTHONY, R CALLAGHAN, E CHAPNICK, M RIPLEY, B FONTANA, C SCHLANT, RC ARENSBERG, D CORSO, JA HURST, JW MORRIS, DC SHERMAN, SW SILVERMAN, BD SILVERMAN, ME ROBERTS, JS BALLOU, SK JEFFRIES, VD BRACKNEY, BA SEALS, AA HARTLEY, J BAKER, RM GILMOUR, KE BAKER, SB HOWARD, J KATZ, RJ BESCH, GA BRILL, D DIBIANCO, R DONOHUE, D FISHER, G FRANCIS, C FRIEDMAN, D GOLDBERG, D GOLDBERG, S KOSS, G LARCA, L LEONARD, R LINDGREN, K RONAN, J ROSENBLATT, A ROSING, D ROSS, A ROTSZTAIN, A SHAWL, F SINDERSON, T STEVENSON, R TINKER, B VARGHESE, J YACKEE, J BIGHAM, H FRANKLIN, W GOLD, R GRAHAM, G GROSSBERG, D HOARE, R LEVY, W MAHMOOD, T TANNENBAUM, E TULLNER, W EISENHOWER, E GERACI, T WILHELMSEN, L BERGSTRAND, R FREDLUND, BO SIGURDSSON, A SIVERTSSON, R SWEDBERG, K HOULTZ, B WIKLUND, I SCHLYTER, G HEDELIN, G LEIJON, M MORGANROTH, J CARVER, J HOROWITZ, L KUTALEK, S PAPA, L SANDBERG, J VICTOR, M CESARE, S VRABEL, C TALARICO, K LUHMANN, S PALAZZO, D GOLDSTEIN, S GOLDBERG, AD FRUMIN, H WESTVEER, D DEBUTLIER, M SCHAIRER, J STOMEL, R FRANK, DM JARANDILLA, R DAVEY, D HASSE, C SHINNEY, S MORLEDGE, JH FARNHAM, DJ HINDERACKER, PH MUSSER, WE DEVRIES, K KUSHNER, JA RAO, R PETERSON, DT MCCAULEY, CS BERGEN, TS BOWMAN, KO GILLMAN, A FULLER, L OBRIEN, J MORLEDGE, J DEMARIA, AN KUO, CS KAMMERLING, JM CORUM, J THIEMANN, M SCHRODT, R PETERS, R SUTTON, F GOTTLIEB, S PAPUCHIS, G MATTIONI, T TODD, L CUSACK, C SCHECK, J HUANG, SKS ALPERT, JS GORE, JM RYAN, M COLLETTWILLEY, P CHAHINE, RA SEQUEIRA, RF LOWERY, MH DELGADO, LM CORREA, JL LASO, LJ HODGES, M SALERNO, D ANDERSON, B COLLINS, R DENES, P DUNBAR, D GRANRUD, G HAUGLAND, J HESSION, W MCBRIDE, J GORNICK, C SIMONSON, J TOLINS, M ETTINGER, A PETERSON, S SLIVKEN, R GRIMALDI, L ROY, D THEROUX, P LEMERY, R MORISSETTE, D BEAUDOIN, D GIRARD, L LAVALLEE, E MCANULTY, JH REINHART, SE MAURICE, G MURPHY, ES KRON, J MARCHANT, C BOXER, J PRINCEHOUSE, L SINNER, K BEANLANDS, D DAVIES, R GREEN, M WILLIAMS, W BAIRD, MJ GARRARD, L HEAL, S HASPECT, A BORTHWICK, J MAROIS, L WOODEND, K AKIYAMA, T HOOD, WB EASLEY, R RYAN, G KENIEN, G PATT, M KAZIERAD, D GOLDFARB, A BUTLER, LL KELLER, ML STANLEY, P PEEBLES, J SYROCKI, D LAVIN, D SCHOENBERGER, JA LIEBSON, PR STAMATO, NJ PETROPULOS, PR BUCKINGHAM, TA REMIJAS, T KOCOUREK, J JANKO, K BARKER, AH ANDERSON, JL FOWLES, RE KEITH, TB WILLIAMS, CB MORENO, FL DORAN, EN FOWLER, B SUMMERS, K WHITE, C OHARA, G ROULEAU, JL PLANTE, S VINCENT, C BOUCHARD, D ZOBLE, RG OTERO, JE BUGNI, WJ SCHWARTZ, KM SHETTIGAR, UR BREWINGTON, JA UMBERGER, J COHEN, JD BJERREGAARD, P HAMILTON, WP GARNER, M ANDERSON, S ELSHERIF, N URSELL, SN GABOR, GE IBRAHIM, B ASSADI, M BREZSNYAK, ML PORTER, AV STANIORSKI, A WOOSLEY, RL RODEN, DM CAMPBELL, WB ECHT, DS LEE, JT MURRAY, KT SPELL, JD BONHOTAL, ST JARED, LL THOMAS, TI GOLDNER, F RICHARDSON, DW ROMHILT, DW ELLENBOGEN, KA BANE, BB FIELDS, J SHRADER, S POWELL, E CHAFFIN, CF WELLS, A CONWAY, KT PLATIA, EV ODONOGHUE, S TRACY, CM ALI, N BOWEN, P BROOKS, KM OETGEN, W WESTON, LT CARSON, P OBIASMANNO, D HARRISON, J SAYLOR, A POWELL, S HAAKENSON, CM SATHER, MR MALONE, LA HALLSTROM, AP MCBRIDE, R GREENE, HL BROOKS, MM LEDINGHAM, R REYNOLDSHAERTLE, R HUTHER, M SCHOLZ, M MORRIS, M FRIEDMAN, LM SCHRON, E VERTER, J JENNINGS, C PROSCHAN, M BRISTOW, JD DEMETS, DL FISCH, C NIES, AS RUSKIN, J STRAUSS, H WALTERS, L TI PROGNOSTIC-SIGNIFICANCE OF LEFT-VENTRICULAR ANEURYSM IN THE CARDIAC-ARRHYTHMIA-SUPPRESSION-TRIAL (CAST) POPULATION SO AMERICAN HEART JOURNAL LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; EXPANSION AB Left ventricular aneurysm has been associated with increased mortality rates. The Cardiac Arrhythmia Suppression Trial (CAST) database was used prospectively to assess (1) the prognostic significance of left ventricular (LV) aneurysm after myocardial infarction on mortality rates and (2) the relation of LV aneurysm to ventricular arrhythmias and their suppressibility. All patients in the CAST study were enrolled after myocardial infarction. They had greater than or equal to 6 ventricular premature depolarizations (VPDs) per hour and ejection fraction less than or equal to 55%; they were enrolled in the study an average of 96 days after the index myocardial infarction. Of 2494 patients with wall motion data, 164 had LV aneurysm, 600 had only dyskinesis, 913 had only akinesis, and 817 had none of these. Radionuclide scan was used in 39%, two-dimensional echocardiography in 30%, and LV angiogram in 31%. Baseline VPDs and nonsustained ventricular tachycardia were similar in all groups. LV aneurysm patients were more frequently eliminated during open-label titration. The incidence of sustained VT during follow-up was only 2.8% for aneurysm patients, a rate that was similar to the other groups. Patients with LV aneurysm had significantly lower survival rates (82% vs 91%) at 16 months after study entry than those without these wall motion abnormalities (p < 0.005). When survival rates were adjusted for ejection fraction there was still a moderately large hazard ratio (1.34) of LV aneurysm that was not statistically significant (p = 0.18). We conclude that (1) the presence of LV aneurysm does not independently worsen prognosis, and (2) older concepts of LV aneurysm and ventricular arrhythmias must be reevaluated. C1 COLUMBIA UNIV, COLL PHYS & SURG, NEW YORK, NY USA. UNIV WASHINGTON, DEPT BIOSTAT, SEATTLE, WA USA. UNIV ALABAMA, BIRMINGHAM, AL USA. BAYLOR COLL MED, HOUSTON, TX USA. BROWN UNIV, AFFILIATED HOSP CTR, PROVIDENCE, RI USA. UNIV CALGARY & COOPERATING HOSP, CALGARY, AB, CANADA. UNIV CALIF IRVINE, IRVINE MED CTR, ORANGE, CA 92668 USA. UNIV CALIF SAN FRANCISCO, SAN FRANCISCO AFFILIATED HOSP, SAN FRANCISCO, CA USA. CASE WESTERN RESERVE UNIV, CLEVELAND, OH USA. COLUMBIA UNIV AFFILIATED HOSP, NEW YORK, NY USA. EMORY UNIV, SCH MED, ATLANTA, GA USA. UNIV FLORIDA, JACKSONVILLE, FL USA. GEORGE WASHINGTON UNIV, MED CTR, WASHINGTON, DC 20037 USA. GOTHENBURG UNIV, GOTHENBURG, SWEDEN. HAHNEMANN UNIV, PHILADELPHIA, PA USA. HENRY FORD HOSP, DETROIT, MI USA. JACKSON FDN MED EDUC & RES, MADISON, WI USA. UNIV KENTUCKY, LEXINGTON, KY USA. UNIV MARYLAND, BALTIMORE, MD USA. UNIV MASSACHUSETTS, WORCESTER, MA USA. UNIV MIAMI, MIAMI, FL USA. UNIV MINNESOTA, MINNEAPOLIS, MN USA. MONTREAL HEART INST, MONTREAL, PQ, CANADA. OREGON HLTH SCI UNIV, PORTLAND, OR USA. UNIV OTTAWA, INST HEART, OTTAWA, ON, CANADA. UNIV ROCHESTER, ROCHESTER, NY USA. RUSH PRESBYTERIAN ST LUKES MED CTR, CHICAGO, IL USA. SALT LAKE CLIN, RES FDN, SALT LAKE CITY, UT USA. UNIV SHERBROOKE, CHUS, SHERBROOKE, PQ, CANADA. UNIV S FLORIDA, TAMPA, FL USA. ST LOUIS UNIV, MED CTR, ST LOUIS, MO USA. SUNY HLTH SCI CTR, BROOKLYN, NY USA. VANDERBILT UNIV, NASHVILLE, TN USA. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, RICHMOND, VA 23298 USA. WASHINGTON HOSP CTR, WASHINGTON, DC USA. DRUG DISTRIBUT CTR, VET ADM COOPERAT STUDIES PROGRAM, CTR CLIN RES PHARM COORDINAT, ALBUQUERQUE, NM USA. UNIV WASHINGTON, CTR COORDINAT, SEATTLE, WA USA. NHLBI, DIV EPIDEMIOL & CLIN APPLICAT, CLIN TRIALS BRANCH, PROGRAM OFF, BETHESDA, MD 20892 USA. UNIV WISCONSIN, MADISON, WI USA. INDIANA UNIV, SCH MED, KRANNERT INST CARDIOL, INDIANAPOLIS, IN 46202 USA. UNIV COLORADO, SCH MED, DENVER, CO USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. DUKE UNIV, MED CTR, DURHAM, NC USA. GEORGETOWN UNIV, KENNEDY INST ETH, WASHINGTON, DC 20057 USA. RP HOCHMAN, JS (reprint author), ST LUKES ROOSEVELT HOSP, DIV CARDIOL, AMSTERDAM AVE & 114TH ST, FLOOR S&R3, ROOM 8-325, NEW YORK, NY 10025 USA. OI Brooks, Maria/0000-0002-2030-7873 NR 12 TC 8 Z9 8 U1 2 U2 5 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-8703 EI 1097-5330 J9 AM HEART J JI Am. Heart J. PD APR PY 1994 VL 127 IS 4 BP 824 EP 832 DI 10.1016/0002-8703(94)90549-5 PN 1 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA NF398 UT WOS:A1994NF39800012 PM 8154420 ER PT J AU CASSEDY, JH AF CASSEDY, JH TI FARMCARTS TO FORDS - A HISTORY OF THE MILITARY AMBULANCE, 1790-1925 - HALLER,JS SO AMERICAN HISTORICAL REVIEW LA English DT Book Review RP CASSEDY, JH (reprint author), NATL LIB MED,BETHESDA,MD 20209, USA. NR 1 TC 0 Z9 0 U1 0 U2 2 PU AMER HISTORICAL REVIEW PI WASHINGTON PA 400 A ST SE, WASHINGTON, DC 20003 SN 0002-8762 J9 AM HIST REV JI Am. Hist. Rev. PD APR PY 1994 VL 99 IS 2 BP 525 EP 525 DI 10.2307/2167304 PG 1 WC History SC History GA NJ047 UT WOS:A1994NJ04700041 ER PT J AU RISING, R HARPER, IT FONTVIELLE, AM FERRARO, RT SPRAUL, M RAVUSSIN, E AF RISING, R HARPER, IT FONTVIELLE, AM FERRARO, RT SPRAUL, M RAVUSSIN, E TI DETERMINANTS OF TOTAL DAILY ENERGY-EXPENDITURE - VARIABILITY IN PHYSICAL-ACTIVITY SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE OBESITY; INDIRECT CALORIMETRY; DOUBLY LABELED WATER ID DOUBLY LABELED WATER; OBESE SUBJECTS; PIMA-INDIANS; EXERCISE; WOMEN; RISK; MEN; REQUIREMENTS; VALIDATION; WEIGHT AB Excessive energy intake and/or reduced total daily energy expenditure (TEE) causes obesity. To determine the relationship between obesity and TEE in an obesity-prone population, we measured TEE. 24-h sedentary energy expenditure (SEDEE), and basal metabolic rate (BMR) in 30 Pima Indian men (83.6 +/- 20.0 kg and 31 +/- 9% fat) by the doubly labeled water method and a respiratory chamber. The energy expenditure for physical activity (EEACT) was calculated as TEE - (BMR + 0.1 TEE), where 10% of TEE is an estimate of the thermic effect of food. Fat-free mass was the best single determinant (P < 0.01) of TEE, explaining 48% of its variance. TEE, SEDEE, BMR, and EEACT were 12 010 +/- 2292, 9945 +/- 1559, 7677 +/- 1901, and 3297 +/- 1732 kJ/d, respectively. Because EEACT is dependent on body weight, EEACT/kg body wt (41.7 - 23.2 kJ . d-1 . kg-1) and TEE/(BMR + 0.1 TEE) (1.39 +/- 0.22) were used as indexes of the level of physical activity. Both indexes correlated negatively with percent body fat (r = -0.56, P < 0.01 and r = -0.42, P < 0.03, respectively). These results suggest that obesity is associated with lower levels of physical activity. C1 NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,ROOM 541-A,PHOENIX,AZ 85016. NR 37 TC 117 Z9 119 U1 4 U2 8 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1994 VL 59 IS 4 BP 800 EP 804 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA ND885 UT WOS:A1994ND88500002 PM 8147322 ER PT J AU KHOROSHKOV, VS ONOSOVSKY, KK KLENOV, GI ZINK, S AF KHOROSHKOV, VS ONOSOVSKY, KK KLENOV, GI ZINK, S TI MOSCOW HOSPITAL-BASED PROTON THERAPY FACILITY DESIGN SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS LA English DT Article DE PROTON; FACILITY; ACCELERATOR; SYNCHROTRON; GANTRY AB An innovative design for a hospital-based proton therapy facility is described here in two versions: a single level (3600 m2) and a three-level plan (700-720 m2). The facility is designed to have 5 to 6 treatment rooms working simultaneously and independently of each other. The accelerator is a 250 MeV H-synchrotron, which produces a small external beam capable of pencil-beam scanning treatments. The small emittance of the beam yields cost savings in the size and weight of the magnets and the amount of concrete shielding. The beam delivery systems, including an isocentric gantry, are designed to use elements that are well known and thoroughly tested. Initial cost of a facility using this new design is estimated to be only 25-30% higher than construction of a facility delivering conventional photon treatments. C1 MOSCOW THEORET & EXPTL PHYS INST,MOSCOW,RUSSIA. MOSCOW RADIOTECH INST,MOSCOW,RUSSIA. NCI,BETHESDA,MD 20892. NR 14 TC 3 Z9 3 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3732 J9 AM J CLIN ONCOL-CANC JI Am. J. Clin. Oncol.-Cancer Clin. Trials PD APR PY 1994 VL 17 IS 2 BP 109 EP 114 DI 10.1097/00000421-199404000-00004 PG 6 WC Oncology SC Oncology GA ND170 UT WOS:A1994ND17000004 PM 8141102 ER PT J AU KEEHN, R AUERBACH, O NAMBU, S CARTER, D SHIMOSATO, Y GREENBERG, SD TATEISHI, R SACCOMANNO, G TOKUOKA, S LAND, C AF KEEHN, R AUERBACH, O NAMBU, S CARTER, D SHIMOSATO, Y GREENBERG, SD TATEISHI, R SACCOMANNO, G TOKUOKA, S LAND, C TI REPRODUCIBILITY OF MAJOR DIAGNOSES IN A BINATIONAL STUDY OF LUNG-CANCER IN URANIUM MINERS AND ATOMIC-BOMB SURVIVORS SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE INTERNATIONAL VARIABILITY OF DIAGNOSES; LUNG CARCINOMA; REPRODUCIBILITY OF DIAGNOSES; WHO CRITERIA FOR LUNG TUMORS ID TUMORS AB A binational panel of four Japanese and four American pathologists examined 208 pulmonary neoplasms, according to the World Health Organization (WHO) recommendations, second edition, for the histologic typing of lung tumors. The study design included independent evaluations by pathologists working alone, followed by group reviews. The individual evaluations, and their implications for reproducibility of the WHO recommendations, are reported. Consensus (agreement by six or more pathologists) with respect to major (ie, first digit) diagnosis was obtained for 76.4% of the cases. Consensus was obtained for 72.5% of the cases with any major diagnosis of small cell cancer; the comparable figures for adenocarcinoma and squamous cell carcinoma were 56% and 48%, respectively. American pathologists were twice as likely as Japanese pathologists to diagnose large-cell national difference. Consensus was far less frequent with the minor tie, second digit) diagnosis categories. This study shows that lung cancers continue to be difficult to classify reproducibly. C1 NATL RES COUNCIL,BOARD RADIAT EFFECTS RES,WASHINGTON,DC 20418. VET ADM MED CTR,E ORANGE,NJ. RED CROSS HOSP,HIROSHIMA,JAPAN. YALE UNIV,SCH MED,NEW HAVEN,CT. NATL CANC CTR,TOKYO 104,JAPAN. BAYLOR UNIV,SCH MED,HOUSTON,TX 77030. CTR ADULT DIS,OSAKA 537,JAPAN. ST MARYS HOSP,GRAND JCT,CO. HIROSHIMA UNIV,SCH MED,HIROSHIMA,JAPAN. RADIAT EFFECTS RES FDN,HIROSHIMA,JAPAN. NCI,BETHESDA,MD 20892. NR 7 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD APR PY 1994 VL 101 IS 4 BP 478 EP 482 PG 5 WC Pathology SC Pathology GA NE911 UT WOS:A1994NE91100016 PM 8160641 ER PT J AU DORGAN, JF BROWN, C BARRETT, M SPLANSKY, GL KREGER, BE DAGOSTINO, RB ALBANES, D SCHATZKIN, A AF DORGAN, JF BROWN, C BARRETT, M SPLANSKY, GL KREGER, BE DAGOSTINO, RB ALBANES, D SCHATZKIN, A TI PHYSICAL-ACTIVITY AND RISK OF BREAST-CANCER IN THE FRAMINGHAM HEART-STUDY SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE BREAST NEOPLASMS; EXERCISE; PROSPECTIVE STUDIES ID DIETARY-FAT; NONDIFFERENTIAL MISCLASSIFICATION; MAMMARY CARCINOGENESIS; REPRODUCTIVE-SYSTEM; CALORIC RESTRICTION; PROLONGED EXERCISE; LOWER PREVALENCE; UNTRAINED WOMEN; RESPONSES; EXPOSURE AB The authors analyzed data from the Framingham Heart Study to evaluate the association between physical activity and breast cancer risk. Physical activity was ascertained by a physician-administered questionnaire from 2,321 women at the fourth biennial examination conducted in 1954-1956. Breast cancers were identified by self-report, surveillance of admissions to Framingham Union Hospital, and review of death records; all but one were histologically confirmed. During 28 years of follow-up, 117 breast cancer cases were diagnosed among the 2,307 women with data on physical activity and reproductive history (a potential confounder). Analysis was performed using Cox proportional hazards models with age as the underlying time variable. Models were adjusted for age at physical activity assessment, menopausal status, age at first pregnancy, parity, education, occupation, and alcohol ingestion. We observed a gradient of increasing risk of breast cancer with increasing physical activity (trend p = 0.06). The relative risk for women in the highest versus lowest activity quartile was 1.6 (95% confidence interval 0.9-3.0; p = 0.13). Although both moderate-to-heavy leisure and occupational activities were associated with an increased risk, the association was marginally significant only for leisure activity (p = 0.06). Our findings do not support a protective effect of physical activity during adulthood for breast cancer, but suggest an increased risk among more active women. C1 INFORMAT MANAGEMENT SERV INC,SILVER SPRING,MD. BOSTON UNIV,SCH MED,BOSTON,MA 02118. BOSTON UNIV,DEPT MATH,BOSTON,MA 02215. RP DORGAN, JF (reprint author), NATL CANC INST,EPN,DIV CANC PREVENT & CONTROL,ROOM 211,6130 EXECUT BLVD,ROCKVILLE,MD 20852, USA. RI Albanes, Demetrius/B-9749-2015 NR 50 TC 99 Z9 99 U1 1 U2 9 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 1 PY 1994 VL 139 IS 7 BP 662 EP 669 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NG906 UT WOS:A1994NG90600003 PM 8166127 ER PT J AU SILVA, AE HOSEIN, B BOYLE, RW FANG, CT SHINDO, M WAGGONER, JG HOOFNAGLE, JH DIBISCEGLIE, AM AF SILVA, AE HOSEIN, B BOYLE, RW FANG, CT SHINDO, M WAGGONER, JG HOOFNAGLE, JH DIBISCEGLIE, AM TI DIAGNOSIS OF CHRONIC HEPATITIS-C - COMPARISON OF IMMUNOASSAYS AND THE POLYMERASE CHAIN-REACTION SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID BLOOD-DONORS; NON-A; VIRUS; ANTIBODIES; INTERFERON; INFECTION; VIREMIA; ASSAYS AB We evaluated a series of first- and second-generation enzyme-linked immunoassays for anti-HCV and compared the findings to those with two confirmatory assays, the recombinant immunoblot assay and serum HCV RNA, in patients with chronic hepatitis C, primary biliary cirrhosis, and chronic hepatitis B. All second-generation immunoassays had good sensitivities (98-100%). Interestingly, detection of HCV RNA had a sensitivity of only 93%, although it was 100% specific. The recombinant immunoblot assay and a peptide-based immunoassay also had good specificity (97% and 100%, respectively), whereas the second-generation immunoassay based on recombinant proteins had a high rate of false positivity, particularly among patients with primary biliary cirrhosis and hyperglobulinemia (specificity 68%). Thus, the diagnosis of HCV infection appears to require the use of more than one test. Whereas a second-generation enzyme-linked immunoassay can be used as an initial test, a confirmatory test (such as recombinant immunoblot assay or determination of hepatitis C viral RNA) may be required if the diagnosis remains uncertain. C1 NIDDKD,LIVER DIS SECT,BLDG 10,ROOM 9C 103B,BETHESDA,MD 20892. UNITED BIOMED INC,LAKE SUCCESS,NY. AMER RED CROSS,BLOOD SERV,NATL REFERENCE LAB INFECT DIS,ROCKVILLE,MD. NR 12 TC 22 Z9 22 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD APR PY 1994 VL 89 IS 4 BP 493 EP 496 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NE375 UT WOS:A1994NE37500005 PM 8147348 ER PT J AU GERSHON, ES GOLDIN, LR AF GERSHON, ES GOLDIN, LR TI REPLICATION OF GENETIC-LINKAGE BY FOLLOW-UP OF PREVIOUSLY STUDIED PEDIGREES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID LOD SCORES AB Independent replication of linkage in previously studied pedigrees is desirable when genetic heterogeneity is suspected or when the illness is very rare. When the likelihood of the new data in this type of replication study is computed as conditional on the previously reported linkage results, it can be considered independent. We describe a simulation method using the SLINK program in which the initial data are fixed and newly genotyped individuals are simulated under theta = .01 and theta = .50. These give appropriate lod score criteria for rejection and acceptance of linkage in the follow-up study, which take into account the original marker genotypes in the data. An estimate of the power to detect linkage in the follow-up data is also generated. RP GERSHON, ES (reprint author), NIMH,CLIN NEUROGENET BRANCH,10-3N218,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 13 TC 3 Z9 3 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD APR PY 1994 VL 54 IS 4 BP 715 EP 718 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA NC836 UT WOS:A1994NC83600017 PM 8128970 ER PT J AU MILLER, BA BLAIR, A REED, EJ AF MILLER, BA BLAIR, A REED, EJ TI EXTENDED MORTALITY FOLLOW-UP AMONG MEN AND WOMEN IN A US-FURNITURE-WORKERS-UNION SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE NEOPLASMS; COHORT STUDY; FURNITURE INDUSTRY; TEXTILES; WOOD DUSTS; METAL DUSTS; MINORITY RACES; PLURAL MESOTHELIOMA; FEMALE MORTALITY ID COLORECTAL-CANCER; MANUFACTURING-INDUSTRY; OCCUPATIONAL EXPOSURE; UNITED-STATES; LUNG-CANCER; MAKERS; PATTERNS; RISKS AB The addition of 5 years of follow-up and over 411,000 person-years of observation to a cohort of 34,081 men and women employed in U.S. furniture and other related industries allowed the investigation of mortality patterns among women and minority races in addition to white men. A significant excess of pleural mesotheliomas occurred among white men (standardized mortality ratio [SMR] = 3.7, 95% confidence interval [CI] = 1.2-8.7) but could not be linked to a particular type of furniture manufacturing. SMRs for myeloid leukemia and chronic nephritis were elevated among white men employed in the wood furniture industry but were not statistically significant. Males in the black/other race categories in wood furniture plants showed nonsignificant mortality excesses for infectious diseases and cancers of the prostate and colon and rectum. Among white women employed in wood furniture plants, mortality was elevated for cancers of the pancreas and lung during die most recent follow-up period. In metal furniture plants, mortality was raised among men in both race groups for kidney cancer (black/other SMR = 8.0, 95% CI = 1.6-23.2; white SMR = 2.1, 95% CI = 0.4-6.2) and diabetes mellitus (black/other SMR = 2.2, 95% CI = 0.6-5.6; white SMR = 1.8, 95% CI = 0.7-3.9). Stomach cancer mortality was significantly elevated (SMR = 3.3, 95% CI = 1.3-6.8) among white men in metal furniture plants and was of the same magnitude over both the previous and the most recent follow-up periods. Among those working with textiles, SMRs were significantly elevated for leukemia (SMR = 6.1, 95% CI = 1.2-7.8) and cancers of the colon and rectum (SMR = 3.2, 95% CI = 1.3-4.5) for white women. Lung cancer mortality was increased for white men and women in textile operations, but SMRs were not statistically significant. SMRs for a number of other causes of death that were elevated at the end of the earlier follow-up period were not increased during the new follow-up period. (C) 1994 Wiley-Liss, Inc.* C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. RP MILLER, BA (reprint author), NCI,DIV CANC PREVENT & CONTROL,SURVEILLANCE PROGRAM,EPN ROOM 343J,BETHESDA,MD 20892, USA. NR 38 TC 26 Z9 26 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD APR PY 1994 VL 25 IS 4 BP 537 EP 549 DI 10.1002/ajim.4700250408 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NA133 UT WOS:A1994NA13300007 PM 8010296 ER PT J AU BLAIR, A STEWART, PA AF BLAIR, A STEWART, PA TI COMMENTS ON THE STERLING AND WEINKAM ANALYSIS OF DATA FROM THE NATIONAL-CANCER-INSTITUTE FORMALDEHYDE STUDY SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Note DE LUNG CANCER; MORTALITY; FORMALDEHYDE SMRS; DRRS ID LUNG-CANCER; MORTALITY; EXPOSURE; REANALYSIS; INDUSTRY; COHORT RP BLAIR, A (reprint author), NCI,OCCUPAT STUDIES SECT,BETHESDA,MD 20892, USA. NR 21 TC 6 Z9 6 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD APR PY 1994 VL 25 IS 4 BP 603 EP 606 DI 10.1002/ajim.4700250414 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NA133 UT WOS:A1994NA13300013 ER PT J AU LAIDLAW, SA BERG, RL KOPPLE, JD NAITO, H WALKER, WG WALSER, M AF LAIDLAW, SA BERG, RL KOPPLE, JD NAITO, H WALKER, WG WALSER, M TI PATTERNS OF FASTING PLASMA AMINO-ACID LEVELS IN CHRONIC RENAL-INSUFFICIENCY - RESULTS FROM THE FEASIBILITY PHASE OF THE MODIFICATION OF DIET IN RENAL-DISEASE STUDY SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE CHRONIC RENAL FAILURE; PLASMA AMINO ACIDS; GLOMERULAR FILTRATION RATE ID MAINTENANCE HEMODIALYSIS; METABOLISM; FAILURE; PROTEIN; UREMIA C1 NIDDKD,BETHESDA,MD. NR 28 TC 39 Z9 39 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD APR PY 1994 VL 23 IS 4 BP 504 EP 513 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA NF034 UT WOS:A1994NF03400003 PM 8154485 ER PT J AU DOPPMAN, JL AF DOPPMAN, JL TI SOMATOSTATIN RECEPTOR SCINTIGRAPHY AND THE ECTOPIC ACTH SYNDROME - THE SOLUTION OR JUST ANOTHER TEST SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material ID ADRENOCORTICAL DISEASE; HORMONE; TUMORS; CT RP DOPPMAN, JL (reprint author), NIH,DEPT DIAGNOST RADIOL,NIH BLDG 10,ROOM 1C-660,BETHESDA,MD 20892, USA. NR 9 TC 8 Z9 8 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1994 VL 96 IS 4 BP 303 EP 304 DI 10.1016/0002-9343(94)90058-2 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA NG901 UT WOS:A1994NG90100002 PM 8166147 ER PT J AU SARTOR, O COOPER, MR KHLEIF, SN MYERS, CE AF SARTOR, O COOPER, MR KHLEIF, SN MYERS, CE TI SURAMIN DECREASES CIRCULATING LEVELS OF INSULIN-LIKE GROWTH-FACTOR-I SO AMERICAN JOURNAL OF MEDICINE LA English DT Note ID PROSTATE-SPECIFIC ANTIGEN; CANCER RP SARTOR, O (reprint author), NCI,CLIN PHARMACOL BRANCH,CLIN ONCOL PROGRAM,BETHESDA,MD 20892, USA. NR 15 TC 6 Z9 6 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1994 VL 96 IS 4 BP 390 EP 390 DI 10.1016/0002-9343(94)90073-6 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA NG901 UT WOS:A1994NG90100016 PM 8166161 ER PT J AU DECARLI, C MURPHY, DGM GILLETTE, JA HAXBY, JV TEICHBERG, D SCHAPIRO, MB HORWITZ, B AF DECARLI, C MURPHY, DGM GILLETTE, JA HAXBY, JV TEICHBERG, D SCHAPIRO, MB HORWITZ, B TI LACK OF AGE-RELATED DIFFERENCES IN TEMPORAL-LOBE VOLUME OF VERY HEALTHY-ADULTS SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE BRAIN, MAGNETIC RESONANCE; BRAIN, MEASUREMENTS; BRAIN, TEMPORAL LOBE; BRAIN, VOLUME; AGE AND AGING ID CEREBROSPINAL-FLUID; GRAY-MATTER; WHITE MATTER; MR IMAGES; BRAIN; ATROPHY; QUANTIFICATION; HYPERTENSION; TOMOGRAPHY; VALIDATION AB PURPOSE: To evaluate age-related differences in temporal and supratemporal brain regions in carefully selected, very healthy men 19 to 92 years of age. METHODS: MR quantification of brain regions used image segmentation into cerebrospinal fluid and brain matter based on nonlinear modeling of pixel intensity distributions. RESULTS: There was a significant age-related decrease (approximately 1% per decade) of posterior frontal lobe volume, but not of temporal lobe volume. The mean volume of the right temporal lobe was significantly greater than the left, and this relation did not change with age. CONCLUSION: In very healthy aging, the Volume of the temporal lobes remains constant over the age range of human life. RP DECARLI, C (reprint author), NIA,NEUROSCI LAB,BLDG 10,ROOM 6 C414,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI DeCarli, Charles/B-5541-2009 NR 25 TC 86 Z9 87 U1 0 U2 1 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD APR PY 1994 VL 15 IS 4 BP 689 EP 696 PG 8 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA NG864 UT WOS:A1994NG86400013 PM 8010271 ER PT J AU CHIN, E BONDY, CA AF CHIN, E BONDY, CA TI DIETARY PROTEIN-INDUCED RENAL GROWTH - CORRELATION BETWEEN RENAL IGF-I SYNTHESIS AND HYPERPLASIA SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE THICK ASCENDING LIMB; MESSENGER RIBONUCLEIC ACID; HYPERTROPHY; HYPERPLASIA; INSULIN-LIKE GROWTH FACTOR BINDING PROTEIN 1; DEOXYRIBONUCLEIC ACID SYNTHESIS; OSMOTIC LOAD; NEPHRON ID RECEPTOR GENE-EXPRESSION; HORMONE-RELEASING-FACTOR; THICK ASCENDING LIMB; UNILATERAL NEPHRECTOMY; BINDING PROTEIN-1; MESSENGER-RNA; RATS; KIDNEY; HYPERTROPHY; SERUM AB Insulin-like growth factor I (IGF-I) and IGF binding protein 1 (IGFBP-1) mRNAs are colocalized in the medullary thick ascending limb (MTAL) of the rat nephron, a segment that undergoes selective growth in response to elevated dietary protein. In the present study, rats were fed isocaloric diets containing variable protein content (6-40%) for 1-7 days, and changes in fractional renal weight, MTAL length, and regional DNA synthesis were assayed and compared with local changes in IGF-I/IGFBP-1 mRNAs, as determined by quantitative in situ hybridization. Rats switched to high-protein diets demonstrated increased IGF-I and decreased IGFBP-1 mRNA levels in MTALs, whereas those switched to low protein showed inverse changes. The increase in renal IGF-I mRNA was maximal at 2 days and was closely paralleled by significant increases in fractional renal weight, DNA synthesis, and MTAL length. Similar changes were seen in vasopressin-deficient Brattleboro and growth hormone (GH)deficient dwarf rats in response to high-protein diets, suggesting that the effects of dietary protein in this model are not mediated by vasopressin or GH. The close spatial and temporal correlation between changes in renal IGF-I expression and changes in regional growth parameters strongly supports a role for locally produced IGF-I in the induction of protein-induced renal growth. RP CHIN, E (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,BLDG 10,RM 10N262,BETHESDA,MD 20892, USA. NR 43 TC 32 Z9 32 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP C1037 EP C1045 PN 1 PG 9 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400018 ER PT J AU GARNER, MM BURG, MB AF GARNER, MM BURG, MB TI MACROMOLECULAR CROWDING AND CONFINEMENT IN CELLS EXPOSED TO HYPERTONICITY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Review DE EXCLUDED VOLUME; MACROMOLECULES; OSMOTIC REGULATION; CELL VOLUME; WATER; DIFFUSION; VISCOSITY; POTASSIUM; BETAINE; ORGANIC OSMOLYTES ID PROTEIN-DNA INTERACTIONS; RENAL MEDULLARY CELLS; PERMEABILIZED L-929 CELLS; PRIMARY VOLUME SIGNAL; RED-BLOOD-CELLS; ESCHERICHIA-COLI; THERMODYNAMIC ACTIVITY; INTERACTIONS INVIVO; VILLUS ENTEROCYTES; PROXIMAL TUBULES AB The nonideal properties of solutions containing high concentrations of macromolecules can result in enormous increases in the activity of the individual macromolecules. It has been proposed that molecular crowding and confinement occur in cells and are major determinants of the activity of the proteins and other intracellular macromolecules. This concept has important implications for cell volume regulation because, under crowded conditions, relatively small changes in concentration, consequent to alterations of water content, lead to large changes in macromolecular activity. This review considers several aspects of macromolecular crowding and confinement, including: 1) the physical chemical principles involved; 2) in vitro demonstrations of the effects; 3) relation to water activity; 4) estimates of the actual intracellular activity of water and macromolecules; 5) relation to osmotic regulation in various types of cells, including bacteria, red blood cells, and complex nucleated cells; and 6) the relation to inorganic ions and organic osmolytes in cells stressed by hypertonicity. We conclude that, while there is compelling evidence for important effects of molecular crowding in vitro and in red blood cells, the role of macromolecular crowding and confinement in osmotic regulation of more complex cells is an open question that deserves the extensive attention it is currently receiving. C1 NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. NR 136 TC 63 Z9 63 U1 1 U2 10 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP C877 EP C892 PN 1 PG 16 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400001 PM 8178962 ER PT J AU MORI, H STONE, K MOTT, DM AF MORI, H STONE, K MOTT, DM TI TRYPSIN-MN2+-RESISTANT FORM OF TYPE-1 PROTEIN PHOSPHATASE IN HUMAN MUSCLE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INSULIN RESISTANCE; DIABETES; GLYCOGEN SYNTHASE; DISULFIDES; MICROSOMES ID RABBIT SKELETAL-MUSCLE; PHOSPHORYLASE-PHOSPHATASE; GLYCOGEN-SYNTHASE; CELLULAR-REGULATION; MAMMALIAN-TISSUES; CATALYTIC SUBUNIT; INSULIN; ACTIVATION; RAT; IDENTIFICATION AB Reduced type 1 protein phosphatase (PP-1) activity in human muscle extracts may contribute to the reduced insulin-stimulated glycogen synthase activity associated with insulin resistance for glucose disposal in humans. Because inactive forms of PP-1 can be activated with trypsin plus Mn2+, these reagents were used to compare the PP-1 activities in skeletal muscle extracts before and after separation into cytosolic and glycogen microsomal (GM) fractions. PP-1 activities were reduced in the GM fraction from insulin-resistant subjects (54 +/- 2 vs. 61 +/- 1, P < 0.01) but, in contrast to our previously published results, were elevated in the extract (33 +/- 6 vs. 18 +/- 3, P < 0.05). Recombination of the cytosol and GM fractions (reconstituted extract) demonstrated that the low extract PP-1 activities could only be regenerated when the GM fraction from insulin-sensitive subjects was recombined with cytosol from either group. The results indicate that the elevated PP-1 activity observed in extracts of insulin-resistant compared with insulin-sensitive subjects is caused by an inhibitor of extract PP-1 activity that sediments with the GM pellet and is more active in the insulin-sensitive subjects. C1 NIDDKD,CLIN DIABET & NUTR SECT,PHOENIX,AZ 85016. NR 34 TC 3 Z9 3 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP E574 EP E582 PN 1 PG 9 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400036 PM 8178978 ER PT J AU OPARA, EC GARFINKEL, M HUBBARD, VS BURCH, WM AKWARI, OE AF OPARA, EC GARFINKEL, M HUBBARD, VS BURCH, WM AKWARI, OE TI EFFECT OF FATTY-ACIDS ON INSULIN RELEASE - ROLE OF CHAIN-LENGTH AND DEGREE OF UNSATURATION SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MICRODISSECTION; ISLETS; PERIFUSION; SECRETION; STIMULATION; SUPPRESSION ID RAT PANCREAS; SECRETION; OXIDATION; PALMITATE; POTENCY; CELLS AB The purpose of the present study was to examine the role played by structural differences among fatty acids in their effect on insulin secretion by isolated perifused murine islets. Insulin secretion measured by radioimmunoassay was assessed either as total insulin output (ng.6 islets(-1) 20 min(-1)) or as percent of basal insulin secretion. Raising the glucose concentration from a basal 5.5 to 27.7 mM caused an increase of insulin output from 6.69 +/- 1.59 to 19.92 +/- 4.99 ng 6.islets(-1).20 min(-1) (P < 0.05) in control (untreated) islets. However, after 20-min exposure of islets to 5 mM 16:0 or 18:2, the effect of 27.7 mM glucose was enhanced or diminished, respectively. Basal insulin output (100% basal) changed to 44 +/- 10% basal (P < 0.005) with the addition of 5 mM 4:0 but was not altered when 4:0 was replaced by 6:0. Insulin output increased modestly with 5 mM 8:0 but significantly (P < 0.05) with 10:0 until a maximal of 280 +/- 24% basal with 12:0 (P < 0.01), then fell to 110 +/- 18 and 93 +/- 15% basal(P < 0.05) with 14:0 and 16:0, respectively. The addition of 5 mM 18:0 inhibited insulin secretion to 30 +/- 10% of basal (P < 0.003), and this effect was not caused by fatty acid interference with insulin assay. In the presence of 2 mM of each fatty acid, insulin secretion was unaffected by 18:0 but increased to 137 +/- 29, 156 +/- 12 (P < 0.05), and 206 +/- 16% (P < 0.01) basal, with 18:1, 18:2, and 18:3, respectively. The 18:3 and 20:4 (2 mM each) were equipotent. In conclusion, the effect of fatty acids on insulin release is dependent both on their chain length and degree of unsaturation. C1 DUKE UNIV,MED CTR,DEPT MED,DURHAM,NC 27710. NIDDKD,NUTR SCI BRANCH,BETHESDA,MD 20892. RP OPARA, EC (reprint author), DUKE UNIV,MED CTR,DEPT SURG,POB 3076,DURHAM,NC 27710, USA. NR 32 TC 70 Z9 70 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP E635 EP E639 PN 1 PG 5 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400044 PM 8178984 ER PT J AU TAYLOR, GT SCHERRER, J WEISS, J PITHA, J AF TAYLOR, GT SCHERRER, J WEISS, J PITHA, J TI ENDOCRINE INTERACTIONS - ADRENAL-STEROIDS AND PRECURSORS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE DEHYDROEPIANDROSTERONE; ANDROSTENEDIONE; METABOLIC PATHWAYS; BETA-CYCLODEXTRIN; COPULATION; SEXUAL MOTIVATION; AGGRESSION; PROSTATE GLAND; SEMINAL VESICLES; BULBOSPONGIOSUS MUSCLES ID MALE-RATS; MALE-MICE; DEHYDROEPIANDROSTERONE; ANDROSTENEDIONE; TESTOSTERONE; FEMALES; PREGNENOLONE; METABOLISM; CONVERSION; BEHAVIOR AB Adult male rats (n = 48) were castrated and treated daily for 4 wk with adrenal steroids in the presence or absence of adjuvant testosterone. Dehydroepiandrosterone (DHEA), DHEA sulfate, and androstenedione (2 mg/kg body wt) were administered as cyclodextrin complexes to mimic the pharmacodynamics of the endogenous products. Although they are the substrates for testosterone synthesis in target tissues, supplements of adrenal steroids alone were unable to maintain integrity of sociosexual responses and androgen target tissues after castration. More surprising, groups administered adrenal precursor plus testosterone showed substantial suppression of the typical restoration of reproductive systems in castrates receiving androgen therapy. The adrenal steroids, however, were not functionally identical. Each steroid interacted with testosterone to leave its own distinctive ''footprint'' on androgen-sensitive systems. The conclusion is that the endogenous adrenal products are not simply passive precursors of testosterone. Adrenal steroids may serve as endocrine regulators of androgen bioavailability and bioactivity. C1 UNIV HEIDELBERG,DEPT MOLEC BIOL,W-6900 HEIDELBERG,GERMANY. NIA,DEPT CHEM,BALTIMORE,MD 21224. RP TAYLOR, GT (reprint author), UNIV MISSOURI,PSYCHOBIOL LAB,8001 NAT BRIDGE RD,ST LOUIS,MO 63121, USA. NR 31 TC 8 Z9 9 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP E676 EP E681 PN 1 PG 6 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400050 PM 8178990 ER PT J AU KITSUKAWA, Y FELLEY, C METZ, DC JENSEN, RT AF KITSUKAWA, Y FELLEY, C METZ, DC JENSEN, RT TI THAPSIGARGIN DEFINES ROLES OF CA2+ IN INITIAL, SUSTAINED, AND POTENTIATED STIMULATION OF PEPSINOGEN SECRETION SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CYTOPLASMIC CALCIUM; CHOLECYSTOKININ; SECRETIN; GASTRIC SECRETION ID DISPERSED CHIEF CELLS; GUINEA-PIG STOMACH; PAROTID ACINAR-CELLS; TUMOR PROMOTER; INTRACELLULAR CA-2+; AMYLASE RELEASE; INOSITOL TRISPHOSPHATE; SARCOPLASMIC-RETICULUM; CELLULAR CALCIUM; PANCREATIC ACINI AB The roles of Ca2+ in agonist-induced pepsinogen secretion from guinea pig chief cells remain unclear. We used cholecystokinin octapeptide (CCK-8) or secretin alone or with thapsigargin (TG) to clarify these roles. TG releases Ca2+ from intracellular stores by inhibiting microsomal Ca2+-adenosinetriphosphatase (ATPase), thereby depleting intracellular Ca2+ (Ca-i(2+)) stores. In most cells TG also causes Ca2+ influx. In the present study, with an extracellular Ca2+ concentration ([Ca2+](o)) of 1.5 mM, CCK-8 (0.1 mu M) caused a rapid increase in pepsinogen secretion; however, the rate decreased with time. With [Ca2+](o) = 0, the initial increase was similar but later secretion was abolished, suggesting that Ca2+ influx was important for sustained secretion. With [Ca2+](o) = 1.5 mM, TG (0.1 mu M) caused a 2.7-fold sustained increase in in Ca-i(2+) concentration ([Ca2+](i)) and a ninefold sustained increase in pepsinogen secretion. With [Ca2+](o) = 0, TG caused a transient 66% increase in [Ca2+](i) and a 50% increase in pepsinogen secretion. The time course of TG-induced pepsinogen secretion correlated with the time course of TG-induced increases in [Ca2+](i). These data demonstrated that Ca2+ influx itself was a potent stimulant of pepsinogen secretion. We further focused on the roles of increasing [Ca2+](i) from Ca-i(2+) stores. With or without extracellular Ca2+ (Ca-o(2+)) present, addition of CCK-8 (0.1 mu M) 10 min after TG caused no further increase in [Ca2+](i), demonstrating depletion of the inositol 1,4,5-trisphosphate-sensitive pool. The Ca2+-mobilizing agent CCK-8 caused no pepsinogen secretion 10 min after TG preincubation, demonstrating that mobilization of Ca2+ from intracellular stores was important in the rapid initial phase stimulation of pepsinogen secretion caused by CCK-8. In contrast, preincubation with TG had no effect on pepsinogen secretion by secretin, an agent that increases adenosine 3',5'-cyclic monophosphate. A 6-min preincubation with TG potentiated the subsequent stimulation of pepsinogen secretion caused by secretin in the presence of Ca2+ where [Ca2+](i) remained elevated. However, TG-induced potentiation of secretin-stimulated pepsinogen secretion was abolished once [Ca2+](i) had returned to the basal level in the absence of Ca2+. These results suggest that 1) increases in [Ca2+](i) due to Ca2+ influx caused by TG or CCK-8 can result in pepsinogen secretion, 2) mobilization of Ca2+ from intracellular stores is important in the rapid initial phase stimulation of pepsinogen secretion caused by CCK-8, and 3) the increase in [Ca2+](i) per se, whether caused by mobilization from Ca-i(2+) stores or Ca2+ influx, is responsible for CCK-8 or TG potentiating secretin-stimulated pepsinogen secretion. C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 42 TC 9 Z9 9 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP G613 EP G623 PN 1 PG 11 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400060 PM 8179000 ER PT J AU KITSUKAWA, Y GU, ZF HILDEBRAND, P JENSEN, RT AF KITSUKAWA, Y GU, ZF HILDEBRAND, P JENSEN, RT TI GASTRIC SMOOTH-MUSCLE CELLS POSSESS 2 CLASSES OF ENDOTHELIN RECEPTORS BUT ONLY ONE ALTERS CONTRACTION SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MOTILITY; MUSCLE CONTRACTION; GASTROINTESTINAL SMOOTH MUSCLE ID PANCREATIC ACINAR-CELLS; VASOCONSTRICTOR PEPTIDE; FUNCTIONAL EXPRESSION; RAT ENDOTHELIN; LIGAND-BINDING; CLONING; CDNA; IMMUNOREACTIVITY; LOCALIZATION; SUBTYPES AB Endothelin (ET)-like immunoreactivity and ET binding sites are widely distributed in the gastrointestinal tract, and ET causes contraction of stomach muscle strips. To determine whether ETs could interact with gastric smooth muscle cells directly and alter function, we measured binding of I-125-ET-1, I-125-ET-2, and I-125-ET-3 to dispersed gastric smooth muscle cells from guinea pig and their abilities to alter cell length. Each ligand bound in a time- and temperature-dependent manner, which was specific and saturable. Analysis of the dose-inhibition curves of both ET-I and ET-3 for binding of each ligand indicated the presence of two classes of receptors, one class (ETA receptor) with a high affinity for ET-1 and ET-2 but a low affinity for ET-3, and the other (ET(B) receptor) with a high affinity for ET-1, ET-2, and ET-3. The ligands were rapidly internalized by both receptors; however, it was greater with ET(A) receptors. ET-1 stimulated muscle contraction (50% effective concentration similar to 2 nM), whereas ET-3 did not stimulate contraction or cause relaxation. These results demonstrate that gastric smooth muscle cells possess two classes of ET receptors. One type (ETA) has a high affinity for ET-1 and ET-2 and a low affinity for ET-3, and receptor occupation results in rapid ligand internalization and muscle contraction; the other type (ET(A)) has a high affinity for ET-1, ET-2, and ET-3, and receptor occupation results in a lesser degree of ligand internalization than the ETA receptor and does not alter contractile behavior. C1 NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 40 TC 22 Z9 22 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP G713 EP G721 PN 1 PG 9 WC Physiology SC Physiology GA NJ994 UT WOS:A1994NJ99400070 PM 8179006 ER PT J AU UNGER, EF BANAI, S SHOU, MT LAZAROUS, DF JAKLITSCH, MT SCHEINOWITZ, M CORREA, R KLINGBEIL, C EPSTEIN, SE AF UNGER, EF BANAI, S SHOU, MT LAZAROUS, DF JAKLITSCH, MT SCHEINOWITZ, M CORREA, R KLINGBEIL, C EPSTEIN, SE TI BASIC FIBROBLAST GROWTH-FACTOR ENHANCES MYOCARDIAL COLLATERAL FLOW IN A CANINE MODEL SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE NEOVASCULARIZATION; COLLATERAL CIRCULATION; BROMODEOXYURIDINE; DEOXYRIBONUCLEIC ACID REPLICATION ID BLOOD-FLOW; INFARCTED MYOCARDIUM; CORONARY ANASTOMOSES; CELL-PROLIFERATION; MICROSPHERES; ANGIOGENESIS; CAPILLARIES; CIRCULATION; MUSCLE; HEART AB Basic fibroblast growth factor (FGF) is a multifunctional peptide that may play an integral role in angiogenesis associated with coronary collateral formation and myocardial infarct healing. We sought to determine the effects of exogenously administered basic FGF on collateral blood flow to ischemic myocardium. Ameroid constrictors were used to cause gradual occlusion of the left circumflex coronary artery in dogs. Basic FGF (110 mu g, n = 9) or saline (n = 12) was given as a daily bolus injection directly into the collateral-dependent zone, beginning 10 days after placement of the Ameroid and continuing for 28 days. Collateral flow was assessed weekly as the ratio of collateral to normal zone (CZ/NZ) blood flow during maximal pharmacologically induced coronary vasodilation. The CZ/NZ increased in both treated and control dogs as a function of time; however, transmural collateral flow in basic FGF-treated dogs significantly exceeded that of control dogs by the second week of treatment. Final CZ/NZ blood flow ratios were 0.49 +/- 0.05 and 0.35 +/- 0.02 in the treated and control groups, respectively (means +/- SE, P = 0.0002). Treatment with basic FGF was also associated with significant increases in the numerical density of distribution vessels and endothelial cell DNA synthesis within the CZ. We also found that basic FGF had acute effects as a coronary vasodilator. Thus exogenous administration of basic FGF enhances maximal collateral blood flow in dogs with myocardial ischemia secondary to single-vessel coronary occlusion, an effect that is likely mediated through the direct angiogenic effects of the peptide, although its acute vasodilatory effects may also play a role. C1 NHLBI,PATHOL BRANCH,BETHESDA,MD 20892. SCIOS NOVA INC,MT VIEW,CA 94043. RP UNGER, EF (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,RM 7B15,BETHESDA,MD 20892, USA. NR 32 TC 264 Z9 268 U1 2 U2 6 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1994 VL 266 IS 4 BP H1588 EP H1595 PN 2 PG 8 WC Physiology SC Physiology GA NJ996 UT WOS:A1994NJ99600041 ER PT J AU BAUER, MS CALABRESE, J DUNNER, DL POST, R WHYBROW, PC GYULAI, L TAY, LK YOUNKIN, SR BYNUM, D LAVORI, P PRICE, RA AF BAUER, MS CALABRESE, J DUNNER, DL POST, R WHYBROW, PC GYULAI, L TAY, LK YOUNKIN, SR BYNUM, D LAVORI, P PRICE, RA TI MULTISITE DATA REANALYSIS OF THE VALIDITY OF RAPID-CYCLING AS A COURSE MODIFIER FOR BIPOLAR DISORDER IN DSM-IV SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID ANTI-DEPRESSANTS; ILLNESS; PROPHYLAXIS; FAMILY AB Objective: The validity of rapid cycling as a distinct course modifier for bipolar disorder was assessed by comparing patients with and without a history of rapid cycling (4 or more affective episodes in 12 months) on demographic, clinical, family history, and outcome variables. These data were also used to formulate operational criteria for the modifier. Method: Data on subjects with rapid-cycling (N=120) and nonrapid-cycling (N=119) bipolar disorder from four sites were pooled and analyzed by using case-control and historical cohort methods. Results: The rapid-cycling group contained more women and more subjects from higher social classes than the nonrapid-cycling group. Family history did not differ between the groups. The diagnosis had predictive validity in that the rapid-cycling patients bad more episodes than the nonrapid-cycling patients during prospective follow-up. The relationship between gender and episode frequency supported the validity of the cutoff point of 4-8 episodes per year. The data regarding whether patients with rapid cycling based on truncated episodes more closely resembled rapid-cycling or nonrapid-cycling patients were equivocal. Patients whose only rapid cycling was associated with antidepressants resembled spontaneously rapid-cycling patients, while the majority of spontaneously rapid-cycling patients also bad periods of antidepressant-associated rapid cycling. Conclusion: The validity of rapid cycling as a distinct course modifier for bipolar disorder is supported by differences in gender, prospectively assessed outcome, and perhaps social class between rapid-cycling and nonrapid-cycling patients. The relationship of gender to episode frequency supports the cutoff of 4 or more episodes per year. C1 BROWN UNIV,PROGRAM MED,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. CASE WESTERN RESERVE UNIV,SCH MED,DEPT PSYCHIAT,CLEVELAND,OH 44106. UNIV WASHINGTON,SCH MED,DEPT PSYCHIAT,SEATTLE,WA 98195. NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. STANFORD UNIV,SCH MED,DEPT HLTH RES & POLICY,DIV BIOSTAT,PALO ALTO,CA 94304. NR 24 TC 130 Z9 131 U1 1 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1994 VL 151 IS 4 BP 506 EP 515 PG 10 WC Psychiatry SC Psychiatry GA ND883 UT WOS:A1994ND88300007 PM 8147448 ER PT J AU OREN, DA MOUL, DE SCHWARTZ, PJ BROWN, C YAMADA, EM ROSENTHAL, NE AF OREN, DA MOUL, DE SCHWARTZ, PJ BROWN, C YAMADA, EM ROSENTHAL, NE TI EXPOSURE TO AMBIENT LIGHT IN PATIENTS WITH WINTER SEASONAL AFFECTIVE-DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Note AB In a study of the quantitative relationship between ambient light and depression in winter seasonal affective disorder, 13 outpatients and 13 normal comparison subjects each wore a light monitor for 1 week. The patients and normal subjects showed similar light exposure profiles; among the patients, severity of depression was inversely related to photoperiod, and there was a trend toward a correlation between greater severity of depression and later time of onset of morning light exposure. These findings suggest that vulnerability to short photoperiods may be related to depression in winter seasonal affective disorder. C1 NIMH,DIV EPIDEMIOL & SERV RES,BETHESDA,MD 20892. RP OREN, DA (reprint author), NIMH,CLIN PSYCHOBIOL BRANCH,ENVIRONM PSYCHIAT SECT,BLDG 10,RM 4S-239,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 10 TC 20 Z9 20 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1994 VL 151 IS 4 BP 591 EP 593 PG 3 WC Psychiatry SC Psychiatry GA ND883 UT WOS:A1994ND88300020 PM 8147459 ER PT J AU ROY, A WOLKOWITZ, OM BISSETTE, G NEMEROFF, CB AF ROY, A WOLKOWITZ, OM BISSETTE, G NEMEROFF, CB TI DIFFERENCES IN CSF CONCENTRATIONS OF THYROTROPIN-RELEASING-HORMONE IN DEPRESSED-PATIENTS AND NORMAL SUBJECTS - NEGATIVE FINDINGS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Note ID CEREBROSPINAL-FLUID; ELECTROCHEMICAL DETECTION; TRH AB Since there have been reports of elevated CSF concentrations of thyrotropin-releasing hormone (TRH) in depression, the authors compared the TRH levels of 17 depressed patients and 19 normal subjects. All subjects underwent lumbar punctures after fasting overnight, and CSF concentrations of TRH were determined by radioimmunoassay. CSF concentrations of norepinephrine and monoamine metabolites were also measured. There was no significant difference between the two groups on any measure, and in the depressed patients there was no significant relation between CSF concentrations of TRH and thyrotropin-stimulating hormone responses to TRH infusion. C1 NIMH,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT PSYCHIAT,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT PHARMACOL,DURHAM,NC 27710. FU NIMH NIH HHS [NIMH MH-45975] NR 10 TC 16 Z9 17 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1994 VL 151 IS 4 BP 600 EP 602 PG 3 WC Psychiatry SC Psychiatry GA ND883 UT WOS:A1994ND88300023 PM 7511876 ER PT J AU HAREL, Y OVERPECK, MD JONES, DH SCHEIDT, PC BIJUR, PE TRUMBLE, AC ANDERSON, J AF HAREL, Y OVERPECK, MD JONES, DH SCHEIDT, PC BIJUR, PE TRUMBLE, AC ANDERSON, J TI THE EFFECTS OF RECALL ON ESTIMATING ANNUAL NONFATAL INJURY RATES FOR CHILDREN AND ADOLESCENTS SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID EVENTS AB Objectives. This study used a recent national population survey on childhood and adolescent nonfatal injuries to investigate the effects of recall bias on estimating annual injury rates. Strategies to adjust for recall bias are recommended. Methods. The 1988 Child Health Supplement to the National Health Interview Survey collected 12-month recall information on injuries that occurred to a national sample of 17 110 children aged 0 through 17 years. Using information on timing of interviews and reported injuries, estimated annual injury rates were calculated for 12 accumulative recall periods (from 1 to 12 months). Results. The data show significantly declining rates, from 24.4 per 100 for a 1-month recall period to 14.7 per 100 for a 12-month recall period. The largest declines were found for the 0- through 4-year-old age group and for minor injuries. Rates of injuries that caused a school loss day, a bed day, surgery, or hospitalization showed higher stability throughout recall periods. Conclusions. Varying recall periods have profound effects on the patterns of childhood injury epidemiology that emerge from the data. Recall periods of between 1 and 3 months are recommended for use in similar survey settings. C1 NICHHD,BETHESDA,MD. CTR DIS CONTROL & PREVENT,ATLANTA,GA 30341. ALBERT EINSTEIN COLL MED,BRONX,NY 10467. NR 17 TC 166 Z9 169 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD APR PY 1994 VL 84 IS 4 BP 599 EP 605 DI 10.2105/AJPH.84.4.599 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA NM620 UT WOS:A1994NM62000015 PM 8154563 ER PT J AU SETOGUCHI, Y JAFFE, HA CHU, CS CRYSTAL, RG AF SETOGUCHI, Y JAFFE, HA CHU, CS CRYSTAL, RG TI INTRAPERITONEAL IN-VIVO GENE-THERAPY TO DELIVER ALPHA-1-ANTITRYPSIN TO THE SYSTEMIC CIRCULATION SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; DRUG-THERAPY; DEFICIENCY; ADENOVIRUS; DNA; EMPHYSEMA; DISEASE; INVIVO; TRANSPLANTATION; EXPRESSION AB The utility of replication-deficient recombinant adenovirus vector-mediated transfer and expression of the alpha-antitrypsin (alpha 1AT) cDNA to peritoneal mesothelial tissues was evaluated as a means of delivering alpha 1AT to the systemic circulation. Preliminary studies with Ad. RSV beta gal, an adenovirus vector expressing the Escherichia coli lacZ gene (beta-galactosidase), showed that intraperitoneal injection of 10(9) plaque-forming units (pfu) to cotton rats resulted in beta-galactosidase activity in mesothelial cells lining the peritoneal cavity. After intraperitoneal administration of 10(9) pfu of Ad alpha 1AT (an adenovirus vector containing the human alpha 1AT cDNA), human alpha 1AT was detectable in serum for up to 24 days, with a maximal level of 3.4 mu g/ml at 4 days. Expression of the exogenous gene was localized to the peritoneal mesothelium as PCR analyses detected no evidence of expression of the exogenous gene in any other tissues evaluated. Anti-adenovirus vector antibodies were detectable in serum after intraperitoneal administration of the recombinant vectors, including antibodies with neutralizing activity. Repeat administrations of adenovirus vectors to the peritoneal cavity at 1 wk and 1 mo after the initial dose failed to show gene expression, but repeat administration 3 mo after demonstrated measurable gene transfer and expression. Together these observations suggest replication-deficient adenovirus-mediated gene transfer to the peritoneal mesothelium offers a promising means to transfer alpha 1AT to the systemic circulation, although immunity induced against the adenovirus may limit frequent repetitive dosing. C1 NHLBI,PULM BRANCH,BETHESDA,MD 20892. CORNELL UNIV,COLL MED,DIV PULM & CRIT CARE MED,NEW YORK,NY. NR 49 TC 94 Z9 94 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD APR PY 1994 VL 10 IS 4 BP 369 EP 377 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA NE367 UT WOS:A1994NE36700004 PM 8136153 ER PT J AU NAVARROROMAN, L MEDEIROS, LJ KINGMA, DW ZARATEOSORNO, A NGUYEN, V SAMOSZUK, M JAFFE, ES AF NAVARROROMAN, L MEDEIROS, LJ KINGMA, DW ZARATEOSORNO, A NGUYEN, V SAMOSZUK, M JAFFE, ES TI MALIGNANT-LYMPHOMAS OF B-CELL LINEAGE WITH MARKED TISSUE EOSINOPHILIA - A REPORT OF 5 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE EOSINOPHILIA; MALIGNANT LYMPHOMA; B-CELL IMMUNOPHENOTYPE; EPSTEIN-BARR VIRUS; INTERLEUKIN-5 ID INTERLEUKIN-5 MESSENGER-RNA; NON-HODGKINS LYMPHOMA; EPSTEIN-BARR-VIRUS; PRODUCE INTERLEUKIN-5; T-CELLS; DISEASE; GENE; EXPRESSION; LEUKEMIA; MUCOSA AB Tissue eosinophilia is commonly seen in Hodgkin's disease and non-Hodgkin's lymphomas of T-cell lineage. In contrast, eosinophilia is infrequent in non-Hodgkin's lymphomas of B-cell origin. We describe five-B-cell lymphomas with exuberant tissue eosinophils. According to the Working Formulation, three were classified as large-cell immunoblastic, one as small lymphocytic lymphoma/chronic lymphocytic leukemia, and one as low-grade, not further subclassified, with features of monocytoid B-cell lymphoma. Immunophenotypic studies in each case revealed B-cell lineage; neoplastic cells expressed monotypic immunoglobulin light chain (four of five cases) or pan-B-cell antigens (five of five cases) and were negative for T-cell antigens. Southern blot hybridization in one case revealed immunoglobulin gene rearrangements, further confirming B-cell lineage. Eosinophilopoiesis is stimulated by interleukin 5 (IL-5), and Epstein-Barr virus (EBV) has been shown to upregulate IL-5 production. Therefore, both EBV infection and IL-5 expression were investigated as possibly pathogenetic mechanisms for the eosinophilia. However, both in situ hybridization studies for EBV mRNA and IL-5 mRNA were negative in the neoplastic cells. In one tumor, IL-5 was abundant in the cytoplasm of the eosinophils, a pattern similar to that seen in five cases of Hodgkin's disease studied with the same technique. Although rare, marked tissue eosinophilia may be associated with B-cell non-Hodgkin's lymphomas. Immunophenotypic or molecular genetic analyses are needed to make the correct diagnosis. C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,ROOM 2N202,BETHESDA,MD 20892. RHODE ISL HOSP,DEPT PATHOL,PROVIDENCE,RI 02902. UNIV CALIF IRVINE,DEPT PATHOL,IRVINE,CA 92717. NR 30 TC 23 Z9 23 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD APR PY 1994 VL 18 IS 4 BP 347 EP 356 DI 10.1097/00000478-199404000-00003 PG 10 WC Pathology; Surgery SC Pathology; Surgery GA ND581 UT WOS:A1994ND58100003 PM 8141429 ER PT J AU ECKELS, KH DUBOIS, DR SUMMERS, PL SCHLESINGER, JJ SHELLY, M COHEN, S ZHANG, YM LAI, CJ KURANE, I ROTHMAN, A HASTY, S HOWARD, B AF ECKELS, KH DUBOIS, DR SUMMERS, PL SCHLESINGER, JJ SHELLY, M COHEN, S ZHANG, YM LAI, CJ KURANE, I ROTHMAN, A HASTY, S HOWARD, B TI IMMUNIZATION OF MONKEYS WITH BACULOVIRUS-DENGUE TYPE-4 RECOMBINANTS CONTAINING ENVELOPE AND NONSTRUCTURAL PROTEINS - EVIDENCE OF PRIMING AND PARTIAL PROTECTION SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID MONOCLONAL-ANTIBODIES; RHESUS-MONKEYS; YELLOW-FEVER; VIRUS; MICE; ENCEPHALITIS; VIRULENCE; VACCINE; NS1 AB Groups of rhesus monkeys were immunized with baculovirus-dengue type-4 (DEN-4) recombinant-infected cell extracts. One recombinant contained all of the DEN-4 structural proteins and two nonstructural (NS) proteins (C-M-E-NS1-NS2a), while the other was a fusion protein containing a portion of the respiratory syncytial virus G glycoprotein and DEN-4 envelope glycoprotein (RSVG-E). Both preparations were immunogenic; all monkeys receiving either immunogen responded with the production of antivirion antibodies in enzyme immunoassays. All except one monkey receiving the recombinant b(C-M-E-NS1-NS2a) made antibodies to NS1. One monkey that received b(RSVG-E) showed the production of low levels of neutralizing antibodies. Following challenge with unmodified DEN-4 virus, seven of nine monkeys in the immunized group became infected and were viremic for a mean of 4.1 days. The control, sham-inoculated monkeys were also viremic; the mean number of days of viremia in this group was 4.7 days. The remaining monkeys in the immunized group (n = 7), although not protected, had evidence of priming. Hemagglutination inhibition antibody responses following challenge indicated an anamnestic response in this group of animals. Based on these results, it was concluded that future immunization schedules should be altered to optimize immune responses and that immunization with more potent and purified immunogens would probably result in higher seroconversion rates and antibody levels in monkeys. C1 UNIV ROCHESTER,SCH MED,ROCHESTER,NY 14621. INST BIOL RES,REHOVOT,ISRAEL. NIAID,BETHESDA,MD 20892. UNIV MASSACHUSETTS,SCH MED,DEPT MED,WORCESTER,MA 01655. USA,INFECT DIS RES INST,FREDERICK,MD. RP ECKELS, KH (reprint author), WALTER REED ARMY INST RES,DEPT BIOL RES,WASHINGTON,DC 20307, USA. NR 16 TC 33 Z9 36 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD APR PY 1994 VL 50 IS 4 BP 472 EP 478 PG 7 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA NK485 UT WOS:A1994NK48500012 PM 8166355 ER PT J AU DUNN, MA CHEEVER, AW PAGLIA, LM KELLY, EP DUVALL, RH ANDRADE, ZA GOLDNER, FH AF DUNN, MA CHEEVER, AW PAGLIA, LM KELLY, EP DUVALL, RH ANDRADE, ZA GOLDNER, FH TI REVERSAL OF ADVANCED LIVER FIBROSIS IN RABBITS WITH SCHISTOSOMIASIS-JAPONICA SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID MURINE SCHISTOSOMIASIS; HEPATIC-FIBROSIS; COLLAGEN-SYNTHESIS; PRAZIQUANTEL; MANSONI AB Advanced liver fibrosis is generally considered to be irreversible. We studied the reversibility of marked liver fibrosis in rabbits infected with Schistosoma japonicum. We determined liver collagen content, collagen biosynthesis, and collagenase activity using serial biopsy specimens obtained 20, 40, and 60 weeks after infection. Reversibility of this process was investigated in rabbits cured of infection at 21 weeks; control rabbits not cured of infection were also studied. At 20 weeks, liver collagen content was 16-fold greater than normal, with accumulation of collagen types I, III, and V. Synthesis of collagen within fibrotic liver slices was 10-fold greater than normal. Liver collagenolytic activity for a type I substrate was 19-fold greater than normal. After parasitologic cure, a striking morphologic reversal of fibrosis occurred during the subsequent 40 weeks, with the return of liver collagen content to three-fold greater than normal and a 75% decrease in synthetic rates compared with those at 20 weeks (P < 0.01). Collagenolytic activity remained elevated to the same degree noted at 20 weeks. A similar but lesser resolution of fibrosis also occurred in untreated control rabbits, coincident with a spontaneous decrease in new egg deposition known to occur in this model system. We conclude that advanced liver fibrosis in S. japonicum-infected rabbits is slowly reversible after cure or senescence of the infection. A possible mechanism for this reversal is persistently increased collagenolysis as collagen synthesis diminishes. C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. BAYNE JONES ARMY COMMUNITY HOSP,FT POLK,LA 71459. WALTER REED ARMY INST RES,DEPT GASTROENTEROL,DIV MED,WASHINGTON,DC 20307. ALBERT EINSTEIN COLL MED,DEPT BIOCHEM,BRONX,NY 10461. UNIFORMED SERV UNIV HLTH SCI,DEPT MED,DIV DIGEST DIS,BETHESDA,MD 20852. GONCALO MONIZ RES CTR,DEPT PATHOL,BR-41945 SALVADOR,BA,BRAZIL. NR 26 TC 14 Z9 15 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD APR PY 1994 VL 50 IS 4 BP 499 EP 505 PG 7 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA NK485 UT WOS:A1994NK48500015 PM 8166357 ER PT J AU VIEIRA, NE YERGEY, AL ABRAMS, SA AF VIEIRA, NE YERGEY, AL ABRAMS, SA TI EXTRACTION OF MAGNESIUM FROM BIOLOGICAL-FLUIDS USING 8-HYDROXYQUINOLINE AND CATION-EXCHANGE CHROMATOGRAPHY FOR ISOTOPIC ENRICHMENT ANALYSIS USING THERMAL IONIZATION MASS-SPECTROMETRY SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID LEAFY VEGETABLES; STABLE MG-26; ABSORPTION; INFANTS AB The use of 8-hydroxyquinoline to precipitate magnesium was evaluated as a method for preparing biological samples for isotopic enrichment analysis using thermal ionization mass spectrometry (TIMS). Standard curves in matrices of water, serum, and urine were prepared using varying amounts of Mg-25. The Mg-25/Mg-24 isotope ratio was measured by TIMS using a silica gel/phosphoric acid technique. Although the total Mg recovered by precipitation from the matrices varied considerably and was dependent on matrix, recovery was sufficient for isotopic enrichment analysis. Urine samples required cation-exchange chromatography (Bio-Rex AG 50W-X8 filter membrane, Bio-Rad Laboratories) prior to precipitation to remove contaminants which interfered with the thermal ionization process. The observed versus expected Mg-25/Mg-24 enrichments were evaluated using linear regression analysis: water, y = 0.016 + 1.022x; serum, y = 0.5 + 1.097x; urine, y = -0.004 + 0.943x. This method has proven useful for the isolation of magnesium from the biofluids tested. C1 BAYLOR COLL MED,DEPT PEDIAT,USDA ARS,CHILDRENS NUTR RES CTR,HOUSTON,TX 77096. RP VIEIRA, NE (reprint author), NICHHD,THEORET & PHYS BIOL LAB,METAB ANAL & MASS SPECTR SECT,BETHESDA,MD 20892, USA. OI Abrams, Steven/0000-0003-4972-9233 NR 12 TC 15 Z9 15 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD APR PY 1994 VL 218 IS 1 BP 92 EP 97 DI 10.1006/abio.1994.1145 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA ND426 UT WOS:A1994ND42600012 PM 8053573 ER PT J AU WERTHEIMER, BM FRAKER, DL AF WERTHEIMER, BM FRAKER, DL TI CAUSE OF HYPOTENSION AFTER ISOLATED LIMB PERFUSION WITH TUMOR-NECROSIS-FACTOR SO ANESTHESIOLOGY LA English DT Letter C1 NCI,SURG BRANCH,BETHESDA,MD 20892. RP WERTHEIMER, BM (reprint author), GEORGETOWN UNIV,MED CTR,CTR CLIN,ANESTHESIA SECT,WASHINGTON,DC 20057, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD APR PY 1994 VL 80 IS 4 BP 961 EP 961 DI 10.1097/00000542-199404000-00039 PG 1 WC Anesthesiology SC Anesthesiology GA NG521 UT WOS:A1994NG52100040 PM 7517650 ER PT J AU BONDY, CA UNDERWOOD, LE CLEMMONS, DR GULER, HP BACH, MA SKARULIS, M AF BONDY, CA UNDERWOOD, LE CLEMMONS, DR GULER, HP BACH, MA SKARULIS, M TI CLINICAL USES OF INSULIN-LIKE GROWTH-FACTOR-I SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID STRUCTURAL DETERMINANTS; LINEAR GROWTH; LARON-TYPE; IGF-I; HORMONE; RECEPTOR; DWARFISM; INFUSION; BINDING; SERUM AB Insulin-like growth factor I (IGF-I) has acute insulinlike metabolic effects and long-term anabolic actions. The therapeutic potential of recombinant human IGF-I treatment is being investigated in various growth hormone-resistant and insulin-resistant disorders. Recent studies have shown that IGF-I may substitute for growth hormone in promoting linear growth in children with growth hormone insensitivity. The anabolic, protein-sparing action of IGF-I is being evaluated as a potential therapy for adults with catabolic diseases. Patients with insulin-dependent diabetes mellitus have reduced endogenous IGF-I production, and studies are in progress to determine whether treatment with IGF-I in addition to insulin may improve their metabolic/ anabolic status. Insulin-like growth factor I treatment may reduce glucose and triglyceride levels in adults with non-insulin-dependent diabetes mellitus and in some patients with extreme insulin resistance. Further studies are needed to evaluate the efficacy and safety of IGF-I treatment in these and other conditions and to provide a better understanding of this hormone's normal physiologic role(s) and complex relations with growth hormone and insulin. RP BONDY, CA (reprint author), NIH,BLDG 10,ROOM 10N 262, 9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 50 TC 110 Z9 114 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 1 PY 1994 VL 120 IS 7 BP 593 EP 601 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA NC764 UT WOS:A1994NC76400011 PM 8116999 ER PT J AU CZAJA, R MCFALL, SL WARNECKE, RB FORD, L KALUZNY, AD AF CZAJA, R MCFALL, SL WARNECKE, RB FORD, L KALUZNY, AD TI PREFERENCES OF COMMUNITY PHYSICIANS FOR CANCER SCREENING GUIDELINES SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID FAMILY PHYSICIANS; PRIMARY CARE; PATTERNS; MAMMOGRAPHY; PREVENTION; MEDICINE AB Objective: To assess factors related to consensus among community physicians regarding appropriate screening intervals for eight cancer screening procedures for which guidelines have been published. Design: Interviews were conducted with a national random sample of 3436 physicians in family practice, internal medicine, general surgery, and gynecology by mail or telephone or both. The overall response rate was 67%. Measurements: Consensus by specialization and by physician and practice characteristics on the appropriate screening intervals for early detection of cancers of the breast, cervix, colon and rectum, and lung for asymptomatic adults at normal risk. ii Results: More than 60% of the physicians surveyed agreed on the length of the screening intervals for six of eight procedures. Consensus most closely followed American Cancer Society- and National Cancer Institute-recommended screening intervals for all procedures except chest roentgenogram Acceptance of screening intervals was not related to the extent of agreement among published guidelines. Surgeons tended to favor more aggressive screening than family physicians and internists; gynecologists most consistently favored aggressive screening for cancers occurring in women. Older physicians and those in solo practice tended to favor outmoded procedures such as routine chest roentgenograms and to be more conservative about screening intervals. Conclusions: Physicians stated that they follow the American Cancer Society and National Cancer Institute guidelines for cancer screening more than the guidelines published by their own specialty societies, but they also reported procedures not recommended in any guidelines. These findings suggest that changing physician screening practices will be difficult. C1 UNIV ILLINOIS,SURVEY RES LAB,CHICAGO,IL. UNIV OKLAHOMA,HLTH SCI CTR,DEPT HLTH PROMOT SCI,OKLAHOMA CITY,OK 73190. NCI,BETHESDA,MD 20892. UNIV N CAROLINA,CECIL G SHEPS HLTH SERV RES CTR,CHAPEL HILL,NC 27599. UNIV N CAROLINA,SCH PUBL HLTH,CHAPEL HILL,NC 27599. N CAROLINA STATE UNIV,RALEIGH,NC. FU NCI NIH HHS [N01CN75435] NR 36 TC 69 Z9 69 U1 1 U2 2 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 1 PY 1994 VL 120 IS 7 BP 602 EP 608 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA NC764 UT WOS:A1994NC76400012 PM 8117000 ER PT J AU DALAKAS, MC LEONMONZON, ME BERNARDINI, I GAHL, WA JAY, CA AF DALAKAS, MC LEONMONZON, ME BERNARDINI, I GAHL, WA JAY, CA TI ZIDOVUDINE-INDUCED MITOCHONDRIAL MYOPATHY IS ASSOCIATED WITH MUSCLE CARNITINE DEFICIENCY AND LIPID STORAGE SO ANNALS OF NEUROLOGY LA English DT Note ID HUMAN-IMMUNODEFICIENCY-VIRUS; DNA; DYSFUNCTION AB The use of zidovudine (AZT) for the treatment of acquired immunodeficiency syndrome (AIDS) induces a DNA-depleting mitochondrial myopathy, which is histologically characterized by the presence of muscle fibers with ''ragged-red''-like features, red-rimmed or empty cracks, granular degeneration, and rods (AZT fibers). Because dysfunctioning muscle mitochondria may lead to defects of beta-oxidation of fatty acids, we examined the degree of neutral fat accumulation and muscle carnitine levels in the muscle biopsy specimens from 21 patients with AZT-induced myopathic symptoms of varying severity. Six patients with no AZT fibers had normal endomyofibrillar lipid deposits and muscle carnitine levels; 7 patients with fewer than 5 AZT fibers per field had a mild (+) to moderate (++) increase in lipid droplets, and reduced muscle carnitine levels (3 patients); and 8 patients with more than 5 AZT fibers had severe muscle changes, a ++ to marked (+++) increase in lipid droplets, and reduced muscle carnitine levels (6 patients). Serial sections showed lipid globules often within ''cracks'' or vacuoles of the abnormal muscle fibers. We conclude that the muscle mitochondrial impairment caused by AZT results in (1) accumulation of lipid within the muscle fibers owing to poor utilization of long-chain fatty acids, (2) reduction of muscle carnitine levels probably due to decreased carnitine uptake by the muscle, and (3) depletion of energy scores within the muscle fibers. The findings may have potential therapeutic implications in the treatment of AZT-induced myopathic symptoms using oral carnitine supplementation. C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. RP DALAKAS, MC (reprint author), NINCDS,NEUROMUSCULAR DIS SECT,BLDG 10,RM 4N248,BETHESDA,MD 20892, USA. NR 18 TC 93 Z9 95 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1994 VL 35 IS 4 BP 482 EP 487 DI 10.1002/ana.410350418 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NF250 UT WOS:A1994NF25000017 PM 8154877 ER PT J AU UHL, GR WALTHER, D MASH, D FAUCHEUX, B JAVOYAGID, F AF UHL, GR WALTHER, D MASH, D FAUCHEUX, B JAVOYAGID, F TI DOPAMINE TRANSPORTER MESSENGER-RNA IN PARKINSONS-DISEASE AND CONTROL SUBSTANTIA-NIGRA NEURONS SO ANNALS OF NEUROLOGY LA English DT Note ID EXPRESSION; CLONING; COCAINE; RECEPTORS; BRAIN; CDNA; RAT AB Dopamine transporter messenger RNA (mRNA) expression was assessed by in situ hybridization over individual pigmented neurons from the substantia nigra pars compacta in midbrain sections from 7 parkinsonian and 7 age-matched, neurologically normal patients. In the normal control brains, high levels of expression of dopamine transporter mRNA were noted over pigmented neurons in the substantia nigra pars compacta; neurons in the adjacent nucleus paranigralis of the ventral tegmental area displayed less hybridization. Nigra compacta neurons surviving in brains of patients with Parkinson's disease displayed only 57% of the dopamine transporter mRNA hybridization intensity displayed by nigral neurons in normal control brains. The disease-related decrease in the apparent level of dopamine transporter mRNA expression in remaining neurons could reflect neuronal dysfunction. Conceivably, it might also reflect differential vulnerability of those neurons that initially expressed higher levels of this transporter to the insult of parkinsonism. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. UNIV MIAMI,SCH MED,DEPT NEUROL,MIAMI,FL. UNIV MIAMI,SCH MED,DEPT MOLEC & CELLULAR PHARMACOL,MIAMI,FL 33101. HOP LA PITIE SALPETRIERE,EXPTL MED LAB,INSERM,U289,PARIS 13,FRANCE. RP UHL, GR (reprint author), NIDA,ADDICT RES CTR,POB 5180,BALTIMORE,MD 21224, USA. NR 34 TC 113 Z9 114 U1 2 U2 6 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1994 VL 35 IS 4 BP 494 EP 498 DI 10.1002/ana.410350421 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NF250 UT WOS:A1994NF25000020 PM 8154880 ER PT J AU MENDELOFF, EN LIANG, IYS SWAIN, JA CLARK, RE AF MENDELOFF, EN LIANG, IYS SWAIN, JA CLARK, RE TI THROMBOXANE A(2) RECEPTOR-SPECIFIC ANTAGONISM IN HYPOTHERMIC CARDIOPULMONARY BYPASS SO ANNALS OF THORACIC SURGERY LA English DT Article ID COMPLEMENT ACTIVATION; PULMONARY-HYPERTENSION; PROTAMINE REVERSAL; HEPARIN; THROMBOLYSIS; REPERFUSION; RELEASE; SHEEP; C5A AB Using a thromboxane A, receptor-specific antagonist, SQ 30,741, this study was undertaken to define the role of thromboxane A, in postischemic myocardial reperfusion injury and in the heparin-protamine reaction. Eighteen heparinized (300 units/kg) sheep were placed on cardiopulmonary bypass (CPB) after complete instrumentation, cooled to 28 degrees C, and had their aortas crossclamped for 1 hour. They were then rewarmed to 36 degrees C and weaned from CPB without inotropic support. Control sheep (n = 6) received a saline infusion throughout the procedure. Bolus animals (n = 6) received 5 mg/kg of SQ 30,741 at 5 minutes after discontinuation of CPB and before protamine sulfate administration. Infusion animals (n = 6) received an SQ 30,741 bolus of 5 mg/kg followed by a continuous infusion of 5 mg.kg(-1) hr(-1) of SQ 30,741 initiated before CPB. All animals received 5 mg/kg of protamine sulfate over a 15-second period 15 minutes after being weaned from CPB. Control animals exhibited significantly decreased global myocardial function after the 1-hour ischemic interval. Further significant functional decline and increase in pulmonary pressure occurred after protamine sulfate administration. Bolus animals experienced a similar postischemic injury, but had no further decrease in function following protamine infusion. Infusion animals had significantly improved global myocardial function after bypass compared with both other groups and were also protected from the deleterious effects of protamine sulfate administration. We conclude that (1) thromboxazne A(2) receptor-specific blockade prevents the marked increase in pulmonary vascular resistance index resulting from protamine sulfate administration and (2) a major component of the ischemic-reperfusion injury associated with CPB is mediated by thromboxane A, receptors. Blockade of these receptors markedly preserved ventricular function in a severe injury model. C1 NHLBI,SURG BRANCH,BETHESDA,MD 20892. NR 14 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD APR PY 1994 VL 57 IS 4 BP 999 EP 1006 PG 8 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA NF982 UT WOS:A1994NF98200044 PM 8166557 ER PT J AU TEMECK, BK PASS, HI AF TEMECK, BK PASS, HI TI A METHOD TO FACILITATE SUBXIPHOID PERICARDIOTOMY SO ANNALS OF THORACIC SURGERY LA English DT Note ID MALIGNANCY; EFFUSIONS; WINDOW AB Pericardial effusion can be treated effectively by the technique of subxiphoid pericardial window. We present a case in which the Cooper retractor designed for transcervical thymectomy facilitated this operation. When available, the Cooper retractor can be useful in selected patients. C1 NCI,SURG BRANCH,THORAC ONCOL SECT,BETHESDA,MD 20892. NR 8 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD APR PY 1994 VL 57 IS 4 BP 1015 EP 1017 PG 3 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA NF982 UT WOS:A1994NF98200048 PM 8166498 ER PT J AU BROWN, TD OROURKE, TJ KUHN, JG CRAIG, JB HAVLIN, K BURRIS, HA CAGNOLA, J HAMILTON, JM GRINDEY, GB SATTERLEE, WG VONHOFF, DD AF BROWN, TD OROURKE, TJ KUHN, JG CRAIG, JB HAVLIN, K BURRIS, HA CAGNOLA, J HAMILTON, JM GRINDEY, GB SATTERLEE, WG VONHOFF, DD TI PHASE-I TRIAL OF SULOFENUR (LY186641) GIVEN ORALLY ON A DAILY X 21 SCHEDULE SO ANTI-CANCER DRUGS LA English DT Article DE SULOFENUR; PHASE I; SULFONYLUREA; METHEMOGLOBINEMIA; HEMOLYSIS; PHARMACOLOGY ID DIARYLSULFONYLUREAS; AGENT AB Sulofenur (LY186641), a diarylsulfonylurea, was evaluated clinically utilizing either a daily x 21 schedule or a daily x 5 (with 2 days off) for 3 weeks schedule. Eighteen patients with refractory solid tumors received 47 evaluable courses of sulofenur given p.o. daily x 21 every 28 days at five dose levels while 14 received 29 courses of sulofenur given daily x 5 for 3 weeks every 28 days at three dose levels. Toxicities included anemia, methemoglobinemia and hemolysis. One patient experienced a fatal subendocardial infarction on the daily x 21 schedule. One partial response was observed in a patient with a sertoli cell tumor on the daily x 5 for 3 weeks schedule. Daily x 5 for 3 weeks is the schedule recommended for phase II trials. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. DUKE UNIV,MED CTR,DURHAM,NC 27710. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. CANC THERAPY & RES CTR S TEXAS,SAN ANTONIO,TX 78229. NCI,BETHESDA,MD 20889. ELI LILLY & CO,INDIANAPOLIS,IN 46285. FU NCRR NIH HHS [RR01346] NR 9 TC 11 Z9 11 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4973 J9 ANTI-CANCER DRUG JI Anti-Cancer Drugs PD APR PY 1994 VL 5 IS 2 BP 151 EP 159 DI 10.1097/00001813-199404000-00005 PG 9 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA NH844 UT WOS:A1994NH84400005 PM 8049498 ER PT J AU KAUR, G GAZIT, A LEVITZKI, A STOWE, E COONEY, DA SAUSVILLE, EA AF KAUR, G GAZIT, A LEVITZKI, A STOWE, E COONEY, DA SAUSVILLE, EA TI TYRPHOSTIN INDUCED GROWTH-INHIBITION - CORRELATION WITH EFFECT ON P210(BCR-ABL) AUTOKINASE ACTIVITY IN K562 CHRONIC MYELOGENOUS LEUKEMIA SO ANTI-CANCER DRUGS LA English DT Article DE BCR-ABL; CHRONIC MYELOGENOUS LEUKEMIA; TYROSINE KINASE ID C-ABL-ONCOGENE; TYROSINE KINASE INHIBITOR; CELLS; PROTEINS; BCR; TRANSLOCATION; TRANSDUCTION AB We have examined a series of tyrosine kinase inhibitors structurally related to erbstatin (tyrphostins) for inhibition of p210(bcr-abl) autokinase activity in vitro and for growth inhibition of chronic myelogenous leukemia (CML) K562 cells. Of the tyrphostins with IC50 for growth <50 mu M, AG814, AG946, AG952, AG896, AG953, AG956 and AG957 (structurally related to lavendustin A and piceatannol) completely inhibited p210(bcr-abl) kinase activity in an immune complex kinase assay. Another group of tyrphostins (AG807, AG568, AG763, AG1076, AG490, AG1318, AG556, AG1319, AG555 and AG1111) inhibits growth of K562 cells but not p210(bcr-abl) tyrosine kinase activity. Of the compounds which inhibit growth and p210(bcr-abl) tyrosine kinase activity, AG957 inhibits DNA synthesis as early as 2 h (60% inhibition at 20 mu M of AG957), a time and concentration of drug where RNA and protein synthesis were not affected. AG957 inhibits p210(bcr-abl) tyrosine phosphorylation in living cells by 1 h without an inhibition of total protein phosphorylation. Growth inhibition by AG957 was reversible after 4 h of exposure, but irreversible after 24 h. AG957 can be considered as an important lead structure for the development of anti-bcr-abl tyrosine kinase antagonists. These data also raise the possibility that bcr-abl kinase activity is directly linked to maintenance of DNA synthesis in Philadelphia chromosome positive (Ph(+)) CML cells. C1 HEBREW UNIV JERUSALEM, DEPT BIOL CHEM, IL-91904 JERUSALEM, ISRAEL. HEBREW UNIV JERUSALEM, DEPT ORGAN CHEM, IL-91904 JERUSALEM, ISRAEL. NCI, MED CHEM LAB, BETHESDA, MD 20892 USA. RP NCI, BIOL CHEM LAB, BLDG 37, RM 5D02, 900 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 32 TC 75 Z9 79 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA SN 0959-4973 EI 1473-5741 J9 ANTI-CANCER DRUG JI Anti-Cancer Drugs PD APR PY 1994 VL 5 IS 2 BP 213 EP 222 DI 10.1097/00001813-199404000-00013 PG 10 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA NH844 UT WOS:A1994NH84400013 PM 8049505 ER PT J AU LEE, JW AMANTEA, MA FRANCIS, PA NAVARRO, EE BACHER, J PIZZO, PA WALSH, TJ AF LEE, JW AMANTEA, MA FRANCIS, PA NAVARRO, EE BACHER, J PIZZO, PA WALSH, TJ TI PHARMACOKINETICS AND SAFETY OF A UNILAMELLAR LIPOSOMAL FORMULATION OF AMPHOTERICIN-B (AMBISOME) IN RABBITS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID FUNGAL-INFECTIONS; PHARMACOLOGY AB A unilamellar liposomal formulation of amphotericin B (LAmB) known as AmBisome was safely administered intravenously to 20 rabbits at 0.5, 1.0, 2.5, 5, or 10 mg/kg of body weight, whereas of 12 rabbits given desoxycholate amphotericin B (DAmB) intravenously at 0.5, 1.0, or 1.5 mg/kg, 2 died of acute cardiac toxicity when DAmB was administered at the highest dose. Single-dose LAmB (1 mg/kg) achieved a maximum concentration in serum (C(max)) of 26 +/- 2.4 mug/ml and an area under the curve to infinity (AUC0-infinity) of 60 +/- 16 mug . h/ml, while single-dose DAmB (1.0 mg/kg), by comparison, achieved a lower C(max) (4.7 +/- 0.2 mug/ml; P = 0.001) and a lower AUC0-infinity (30.6 +/- 2.2 mug . h/ml; P = 0.07). Following administration of a single dose of LAmB (10 mg/kg), a disproportionately higher C(max) (287 +/- 14 mug/ml) and AUC0-infinity (2,223 +/- 246 mug . h/ml) occurred, indicating saturable elimination. After chronic dosing (n = 4) with LAmB at 5.0 mg/kg/day for 28 days or DAmB at 1.0 mg/kg/day for 28 days, LAmB achieved daily peak levels of 122.8 +/- 5.8 mug/ml and trough levels of 34.9 +/- 1.8 mug/ml, while DAmB reached a peak of only 1.76 +/- 0.11 mug/ml and a trough of 0.46 +/- 0.04 mug/ml (P less-than-or-equal-to 0.001). Significant accumulations of amphotericin B into reticuloendothelial organs were observed, with 239 +/- 39 mug/g found in the liver after chronic LAmB dosing (5 mg/kg/day), which was seven times higher than the 33 +/- 6 mug/g after DAmB dosing (1 mg/kg/day) (P = 0.002). Accumulation in kidneys, however, remained 14-fold lower (P = 0.04) following LAmB dosing (0.87 +/- 0.61 mug/g) than after DAmB dosing (12.7 +/- 4.6 mug/g). Nephrotoxicity occurred in only one of four LAmB-treated animals, while it occurred in all four chronically DAmB-treated animals; mild hepatotoxicity with transaminase elevations was seen in one LAmB-treated rabbit. We conclude that LAmB safely achieved higher C(max)s and AUC(0-infinity)s and demonstrated saturable, nonlinear elimination from plasma via reticuloendothelial organ uptake. The reduced nephrotoxicity of LAmB correlated with diminished levels of amphotericin B in the kidneys. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT PHARM,BETHESDA,MD 20892. NCRR,VET RESOURCES PROGRAM,SURG BRANCH,BETHESDA,MD 20892. RP WALSH, TJ (reprint author), NCI,PEDIAT BRANCH,INFECT DIS SECT,BLDG 10,RM 13N-240,BETHESDA,MD 20892, USA. NR 13 TC 85 Z9 89 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD APR PY 1994 VL 38 IS 4 BP 713 EP 718 PG 6 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA NE046 UT WOS:A1994NE04600014 PM 8031034 ER PT J AU CARRASCO, MA SIERRALTA, J DEMAZANCOURT, P AF CARRASCO, MA SIERRALTA, J DEMAZANCOURT, P TI CHARACTERIZATION AND SUBCELLULAR-DISTRIBUTION OF G-PROTEINS IN HIGHLY PURIFIED SKELETAL-MUSCLE FRACTIONS FROM RABBIT AND FROG SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID GTP-GAMMA-S; TRANSVERSE TUBULES; SARCOPLASMIC-RETICULUM; ADENYLYL CYCLASE; CA-2+-DEPENDENT ATPASE; SIGNAL TRANSDUCTION; GOLGI MEMBRANES; PLASMA-MEMBRANE; CA-2+ CHANNELS; ALPHA-SUBUNITS AB The presence of G-proteins in highly purified fractions from frog and rabbit skeletal muscles was analyzed by Bordetella pertussis toxin-catalyzed ADP-ribosylation and by immunoblots. Two B. pertussis toxin substrates were present in transverse tubules and sarcoplasmic reticulum from frog and rabbit skeletal muscle. Immunoblot analysis suggested that the two B. pertussis toxin substrates present in rabbit sarcoplasmic reticulum are possibly alphai2 and alphai3, but the corresponding substrates in sarcoplasmic reticulum from frog are still unidentified. Transverse tubules isolated from both rabbit and frog also contained alphai2 and alphai3; additionally, beta35, beta36, alphao (weak immunoreactivity), alphai1 (and/or alphai3 in frog), as (short form only in frog), and alphaq were found. Sarcoplasmic reticulum from rabbit also contained alphas (predominantly alphas short), beta36, and alphaq. The presence of alphaq in sarcoplasmic reticulum, in addition to transverse tubules, is potentially a very important finding since this G-protein has been described only in plasma membranes so far. Also, this study describes the candidate G-proteins for the control of excitation-contraction coupling in skeletal muscle. (C) 1994 Academic Press, Inc. C1 UNIV CHILE, FAC MED, DEPT FISIOL & BIOFIS, SANTIAGO, 20892, CHILE. CTR ESTUDIOS CIENT, SANTIAGO, CHILE. NIDDKD, MOLEC PATHOPHYSIOL BRANCH, BETHESDA, MD USA. RI Sierralta, Jimena/A-7591-2008 NR 46 TC 10 Z9 10 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR PY 1994 VL 310 IS 1 BP 76 EP 81 DI 10.1006/abbi.1994.1142 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA ND427 UT WOS:A1994ND42700011 PM 8161224 ER PT J AU BLAUVELT, A TURNER, ML AF BLAUVELT, A TURNER, ML TI GIANOTTI-CROSTI SYNDROME AND HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO ARCHIVES OF DERMATOLOGY LA English DT Article ID HEPATITIS-B AB Background: Patients with Gianotti-Crosti syndrome (GCS) present with a distinctive self-limiting acral papular or papulovesicular eruption associated with an underlying viral illness. Gianotti-Crosti syndrome in patients infected with human immunodeficiency virus has not been previously reported. Observations: We report on two children infected with human immunodeficiency virus who had GCS. Both patients had clinical and histopathologic findings characteristic of GCS. The first patient had evidence of prior infection with cytomegalovirus, without evidence of active viral illness. The second patient had evidence of subclinical infection with cytomegalovirus, positive hepatitis C antibody, and active infection with Mycobacterium avium-intracellulare at the time the skin eruption began. Conclusions: We call attention to a previously unreported skin eruption, GCS, in the setting of human immunodeficiency virus infection and emphasize that determining the etiologic factors for human immunodeficiency virus-associated GCS will be difficult; such patients will probably have a variety of clinical and subclinical infections that complicate this issue. RP BLAUVELT, A (reprint author), NATL CANC INST,DERMATOL BRANCH,BETHESDA,MD, USA. NR 13 TC 27 Z9 28 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD APR PY 1994 VL 130 IS 4 BP 481 EP 483 DI 10.1001/archderm.130.4.481 PG 3 WC Dermatology SC Dermatology GA NG493 UT WOS:A1994NG49300011 PM 7880219 ER PT J AU GOLD, JM HERMANN, BP RANDOLPH, C WYLER, AR GOLDBERG, TE WEINBERGER, DR AF GOLD, JM HERMANN, BP RANDOLPH, C WYLER, AR GOLDBERG, TE WEINBERGER, DR TI SCHIZOPHRENIA AND TEMPORAL-LOBE EPILEPSY - A NEUROPSYCHOLOGICAL ANALYSIS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID CARD SORTING TEST; MONOZYGOTIC TWINS DISCORDANT; TEST-PERFORMANCE; TARDIVE-DYSKINESIA; HEAD-INJURY; DYSFUNCTION; DISORDERS; DEFICITS; MEMORY; IMPAIRMENT AB Background: Recent neuroimaging studies have reported structural abnormalities of mesial temporal lobe structures in schizophrenia. This study compared the neuropsychological performance of patients with schizophrenia with patients with either left or right temporal lobe epilepsy to determine if lateralized, developmental temporal lobe dysfunction provides a model of the congnitive impairments observed in schizophrenia. Methods: A total 66 patients with schizophrenia and 101 patients with medically intractable focal temporal lobe epilepsy (48 left temporal, 53 right temporal) received a comprehensive neuropsychological battery. Results: The three groups did not differ on age, years of education, or Full-Scale IQ. However, clear differences were noted in performance profiles. Patients with schizophrenia scored significantly higher than either epilepsy group on a measure of word reading thought to reflect premorbid competence. Patients with schizophrenia demonstrated greater attentional impairment and motor slowing than either epilepsy group. The patients with schizophrenia had superior semantic knowledge and verbal memory compared with the left temporal lobe group. On the Wisconsin Card Sorting Test the patients' with schizophrenia obtained significantly fewer categories than either temporal lobe group, but were not significantly more perseverative. Conclusions: Data suggest lateralized temporal lobe dysfunction does not provide an adequate model of the cognitive impairments seen in schizophrenia. The disorders seem to follow different developmental paths: In early-onset epilepsy, the acquisition of cognitive skills and academic knowledge is compromised, while in schizophrenia congnitive functions are lost. Extratemporal pathologic features, most likely of the frontal lobe, are implicated in the cognitive dysfunction of schizophrenia. C1 NIMH,DIV INTRAMURAL RES PROGRAMS,CLIN & RES SERV BRANCH,WASHINGTON,DC. NIMH,DIV INTRAMURAL RES PROGRAMS,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC. UNIV TENNESSEE,BAPTIST MEM HOSP,DEPT PSYCHIAT,EPICARE CTR,MEMPHIS,TN. UNIV TENNESSEE,BAPTIST MEM HOSP,DEPT NEUROSURG,EPICARE CTR,MEMPHIS,TN. SEMMES MURPHEY CLIN,MEMPHIS,TN. NINCDS,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892. NR 73 TC 63 Z9 63 U1 6 U2 6 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD APR PY 1994 VL 51 IS 4 BP 265 EP 272 PG 8 WC Psychiatry SC Psychiatry GA NF265 UT WOS:A1994NF26500001 PM 8161286 ER PT J AU APPOLLONIO, I GRAFMAN, J CLARK, K NICHELLI, P ZEFFIRO, T HALLETT, M AF APPOLLONIO, I GRAFMAN, J CLARK, K NICHELLI, P ZEFFIRO, T HALLETT, M TI IMPLICIT AND EXPLICIT MEMORY IN PATIENTS WITH PARKINSONS-DISEASE WITH AND WITHOUT DEMENTIA SO ARCHIVES OF NEUROLOGY LA English DT Article ID ALZHEIMERS-DISEASE; MULTIPLE-SCLEROSIS; EMERGING CONCEPT; NORMAL PEOPLE; FREQUENCY; DYSFUNCTION; MOTOR; DEFICITS; AMNESIA; SKILL AB Objective: To study explicit and implicit memory processes in patients with Parkinson's disease. Design: Case-control design. All subjects were given a neuropsychological test battery, and the test scores were compared among the groups. Setting: Government-funded research facility. All subjects were examined as outpatients. Patients: We tested nondemented (n=13) and demented (n=5) patients with Parkinson's disease and normal controls (n=12) matched for age, gender, and educational level. Main Outcome Measures: Memory for verbal and pictorial stimuli under both explicit and implicit retrieval conditions. Results: Both nondemented and demented patients with Parkinson's disease exhibited impairment on tests of explicit memory. Their impairment could be graded based on the level of effort required by the task: impaired free recall in nondemented patients and impaired free recall, cued recall, and recognition in demented patients. By contrast, neither group showed evidence of impairment on automatic (modality monitoring and word frequency estimation) or implicit (word and picture fragment identification) memory tasks. Correlation analyses did not support any association between the effortful memory deficits and neurologic variables, mood, or performance on executive function tests. Conclusions: Memory deficits in patients with Parkinson's disease primarily involve the conscious, effortful strategic aspects of searching long-term memory. C1 NINCDS,COGNIT NEUROSCI SECT,BETHESDA,MD 20892. NINCDS,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. NINCDS,MED NEUROL BRANCH,BETHESDA,MD 20892. UNIV MILAN,SAN GERARDO HOSP,DEPT NEUROL,MONZA,ITALY. UNIV MODENA,DEPT NEUROL,I-41100 MODENA,ITALY. RI Nichelli, Paolo/F-7336-2015; OI Nichelli, Paolo/0000-0001-9756-6796; Grafman, Jordan H./0000-0001-8645-4457 NR 63 TC 47 Z9 48 U1 2 U2 7 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD APR PY 1994 VL 51 IS 4 BP 359 EP 367 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA NF056 UT WOS:A1994NF05600006 PM 8155013 ER PT J AU PARKS, DJ CHEUNG, MK CHAN, CC ROBERGE, FG AF PARKS, DJ CHEUNG, MK CHAN, CC ROBERGE, FG TI THE ROLE OF NITRIC-OXIDE IN UVEITIS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID NECROSIS-FACTOR-ALPHA; METHYL-L-ARGININE; SEPTIC SHOCK; HYPOTENSION; SYNTHASE; INVIVO; INHIBITORS; ENDOTOXIN; MECHANISM; CELLS AB Objective: To evaluate the possible role played by nitric oxide in the pathogenesis of uveitis. Methods: Uveitis was induced in rats with subcutaneous lipopolysaccharide. Lipopolysaccharide stimulates nitric oxide production from L-arginine. The animals were treated with N-G-nitro-L-arginine methyl ester, an L-arginine analogue acting as a specific inhibitor of nitric oxide synthesis. Ocular inflammation was evaluated by measuring protein concentration and leukocyte number in the aqueous humor of one eye, and by histopathologic examination of the contralateral eye. Results: Aqueous humor protein levels were reduced 73% to 82% and cellular infiltration was almost abrogated in N-G-nitro-L-arginine methyl ester-treated rats compared with controls. The histopathologic examination also showed a similar inhibition of uveal tissue inflammation in treated rats. Conclusion: By inhibiting nitric oxide synthesis, N-G-nitro-L-arginine methyl ester inhibits the induction of endotoxin-induced uveitis in the rat. This observation demonstrates that nitric oxide is an important mediator of anterior uveitis in this model system and suggests that nitric oxide may also be implicated in human uveitis. C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. NR 26 TC 73 Z9 76 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD APR PY 1994 VL 112 IS 4 BP 544 EP 546 PG 3 WC Ophthalmology SC Ophthalmology GA NF266 UT WOS:A1994NF26600024 PM 8155054 ER PT J AU COTTLERFOX, M KLEIN, HG AF COTTLERFOX, M KLEIN, HG TI TRANSFUSION SUPPORT OF HEMATOLOGY AND ONCOLOGY PATIENTS - THE ROLE OF RECOMBINANT HEMATOPOIETIC GROWTH-FACTORS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID COLONY-STIMULATING FACTOR; ADOPTIVE IMMUNOTHERAPY; APLASTIC-ANEMIA; CHRONIC DISEASE; STEM-CELLS; TRANSPLANTATION; THERAPY; BLOOD; ERYTHROPOIETIN; CANCER AB Recombinant DNA technology has made more than a dozen human cytokines available to treat patients with hematologic and oncologic disorders. These small glycoproteins mediate cell growth and differentiation and regulate complex cellular networks by autocrine, paracrine, and endocrine mechanisms. Direct infusions of hematopoietic cytokines can decrease the requirement for transfusion in many patients with hematologic disorders and malignancies and permit more aggressive myelosuppressive therapy. Stimulation of blood donors with cytokines may enhance collection of a variety of transfusion components from granulocytes to peripheral blood progenitor cells. Using combinations of recombinant growth factors can effect ex vivo cell expansion and differentiation. Such cellular components are currently being studied in immunotherapy of cancer, in molecular approaches to inherited and acquired genetic abnormalities, and in bone marrow transplantation. In the future, this technology may be applied to producing transfusion components. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892. NR 41 TC 3 Z9 3 U1 0 U2 0 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD APR PY 1994 VL 118 IS 4 BP 417 EP 420 PG 4 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA NF053 UT WOS:A1994NF05300013 PM 7909429 ER PT J AU HISNANICK, J CODDINGTON, DA GERGEN, PJ AF HISNANICK, J CODDINGTON, DA GERGEN, PJ TI TRENDS IN ASTHMA-RELATED ADMISSIONS AMONG AMERICAN-INDIAN AND ALASKAN NATIVE CHILDREN FROM 1979 TO 1989 - UNIVERSAL HEALTH-CARE IN THE FACE OF POVERTY SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID ACUTE CHILDHOOD ASTHMA; LOW-BIRTH-WEIGHT; CHANGING PATTERNS; HOSPITALIZATION; PREVALENCE; MORTALITY; SMOKING; SEVERITY; ILLNESS; SERVICE AB Objective: To describe changes in asthma-related hospitalizations in Indian Health Service facilities and compare with national trends. Design: Trend analysis. Patients and Setting: Hospital discharge records of patients aged 17 years and younger treated by the Indian Health Service between 1979 and 1989. Main Outcome Measures: Patients discharged with asthma as the first listed diagnosis. Results: The rates of asthma-related hospitalizations increased an average of 2.6% (95% confidence interval [CI], 0.1 to 5.2) per year between 1979 and 1989 among American Indian and Alaskan Native children aged 0 to 17 years. The increase was 3.7% among the 0- to 4-year age group (95% CI, 2.0 to 5.5) and 0.3% (95% CI, 0.26 to 0.3) among the 5- to 17-year age group. Boys tended to have a higher rate of increase (4.3% [95% CI, -0.1 to 8.7]) compared with girls (2.6% [95% CI, -0.2 to 5.4]). The rates for any hospitalization decreased during this period for 0- to di-year-olds (-7.5% [95% CI, -10.5 to -4.5]). Little change was noted in hospitalization rates for lower respiratory tract diseases. Diagnostic transfer from bronchitis/bronchiolitis to asthma could not explain the increase. Both first admission and readmission for treatment of asthma contributed to the increase. Compared with previously published data, 0- to 4-year-old American Indian and Alaskan Native children more closely approximate white children than black children in both rates of hospitalization (1979-1987) and annual percentage increase in hospitalization (1979-1989 for American Indian and Alaskan Native children and 1979-1987 for white and black children) for the treatment of asthma. Conclusions: American Indian and Alaskan Native children who are cared for by the Indian Health Service have asthma-related hospitalization patterns that are similar to those seen in white children despite having socioeconomic characteristics more similar to those of black children. C1 INDIAN HLTH SERV,OFF HLTH PROGRAM,TUCSON,AZ. CHILDRENS NATL MED CTR,DEPT GEN PEDIAT,WASHINGTON,DC 20010. NIAID,DIV ALLERGY IMMUNOL & TRANSPLANTAT,BETHESDA,MD 20892. RP HISNANICK, J (reprint author), US DEPT VET AFFAIRS,NVCAS 008C12,810 VERMONT AVE NW,WASHINGTON,DC 20420, USA. NR 44 TC 17 Z9 17 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD APR PY 1994 VL 148 IS 4 BP 357 EP 363 PG 7 WC Pediatrics SC Pediatrics GA NF055 UT WOS:A1994NF05500003 PM 8148934 ER PT J AU FISHER, WR ZECH, LA STACPOOLE, PW AF FISHER, WR ZECH, LA STACPOOLE, PW TI APO-B METABOLISM IN FAMILIAL HYPERCHOLESTEROLEMIA - INCONSISTENCIES WITH THE LDL RECEPTOR PARADIGM SO ARTERIOSCLEROSIS AND THROMBOSIS LA English DT Review DE APOLIPOPROTEIN-B; LDL; FAMILIAL HYPERCHOLESTEROLEMIA; COMPARTMENTAL MODELING; LDL RECEPTOR; CHOLESTEROL ESTERS ID LOW-DENSITY-LIPOPROTEIN; CHOLESTERYL ESTER TRANSFER; BILE-ACID SYNTHESIS; VERY-LOW-DENSITY; APOLIPOPROTEIN-B PRODUCTION; STEROL REGULATORY ELEMENT; COA REDUCTASE-ACTIVITY; COENZYME-A REDUCTASE; TRANSFER PROTEIN; HYPERTRIGLYCERIDEMIC SUBJECTS AB The biology of the low-density lipoprotein (LDL) receptor has been examined in detail, and a paradigm for LDL metabolism has evolved from comparative studies of cholesterol metabolism in a variety of cells cultured from normal individuals and subjects with familial hypercholesterolemia (FH). Cultured cells from patients with homozygous FH lack a functional LDL receptor and show diminished LDL clearance, induction of the enzyme hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase, increased cholesterol synthesis, decreased cholesterol ester production, and depleted cholesterol ester stores. The observed decrease in the fractional catabolic rate (FCR) of LDL is attributed to the mutated LDL receptor gene. However, in the experimental animal model of this disease, the Watanabe heritable hyperlipidemic (WHHL) rabbit, cholesterol ester stores are increased, while hepatic cholesterol synthesis is decreased. Furthermore, in humans HMG-CoA reductase is suppressed, and the LDL apolipoprotein (apo) B production rate is increased in patients with FH. These findings raise questions about the adequacy of the paradigm in understanding hepatic cholesterol metabolism in vivo. In humans, apoB metabolism is believed to be principally determined by the liver, where apoB is both synthesized and catabolized. Assuming the neutral lipid content of the liver is the major determinant of apoB metabolism, we postulated that the changes in apoB metabolism in FH are predictable when based on the assumption of an increase in hepatic cholesterol and cholesterol ester content, as observed both in the WHHL rabbit and in humans. We examined this hypothesis in vivo in patients with heterozygous FH by using tracer kinetic methodology and have used similar data from normal and hypertriglyceridemic (HTG) subjects as controls. Whereas normal and HTG subjects secrete apoB primarily as large, triglyceride-enriched very-low-density lipoprotein (VLDL), heterozygous FH patients have an absolute decrease in apoB production and secrete almost 40% of apoB as smaller intermediate-density lipoprotein (IDL)/LDL. In normal humans, about half of secreted apoB is catabolized rather than being converted to LDL. In HTG subjects two thirds of apoB follows this same route, by which VLDL remnants remaining after triglyceride hydrolysis are largely returned to the liver. In contrast, in FH subjects secreted apoB is fully converted to LDL. Thus, although total apoB secretion is reduced in FH subjects, total LDL production is greater than in either normal or HTG subjects. Under basal conditions the elevated LDL in heterozygous FH is due to both decreased LDL receptor-mediated catabolism and increased LDL production. However, the number of LDL receptors actually expressed is suppressed below the number of potentially functional receptors. Support for this conclusion is derived from the findings that when diets or drugs are administered that decrease the hepatic concentration of cholesterol esters, the FCR of LDL increases to normal values, reflecting an increase in expressed hepatic LDL receptors. Apparently in heterozygous patients these receptors are normally suppressed below the upper limit that can be expressed by a single functional gene. In summary, three major changes occur in apoB metabolism in heterozygous FH subjects: (1) a decrease in total and VLDL apoB secretion with a shift to the production of smaller IDL/LDL species; (2) the loss of the catabolic pathway for VLDL apoB remnants; and (3) a reversible decrease in the FCR of LDL apoB, which is normalized by dietary or drug perturbations that reduce hepatic cholesterol. All these findings are explainable as an adaptation to an increase in hepatic cholesterol ester content but not by the classic LDL receptor paradigm. How this pathophysiology arises from the mutation of the LDL receptor gene is unknown. C1 UNIV FLORIDA,J HILLIS MILLER HLTH CTR,COLL MED,DEPT BIOCHEM & MOLEC BIOL,GAINESVILLE,FL 32610. NIH,MATH BIOL LAB,BETHESDA,MD 20892. RP FISHER, WR (reprint author), UNIV FLORIDA,J HILLIS MILLER HLTH CTR,COLL MED,DEPT MED,BOX 100226,GAINESVILLE,FL 32610, USA. FU NHLBI NIH HHS [HL-29394]; NIDDK NIH HHS [DK-40439] NR 101 TC 27 Z9 27 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 1049-8834 J9 ARTERIOSCLER THROMB JI Arterioscler. Thromb. PD APR PY 1994 VL 14 IS 4 BP 501 EP 510 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NE051 UT WOS:A1994NE05100001 PM 8148348 ER PT J AU HOFFMAN, GS LEAVITT, RY KERR, GS ROTTEM, M SNELLER, MC FAUCI, AS AF HOFFMAN, GS LEAVITT, RY KERR, GS ROTTEM, M SNELLER, MC FAUCI, AS TI TREATMENT OF GLUCOCORTICOID-RESISTANT OR RELAPSING TAKAYASU ARTERITIS WITH METHOTREXATE SO ARTHRITIS AND RHEUMATISM LA English DT Article ID RHEUMATOID-ARTHRITIS; WEGENERS GRANULOMATOSIS; THERAPY; DISEASE AB Objective. To identify the role of methotrexate (MTX) in the treatment of persistent or recurrent Takayasu arteritis that is refractory to treatment with glucocorticoids (GC) alone. Methods. An open-label pilot study of weekly low-dose MTX + GC treatment was performed. Outcome was evaluated according to clinical characteristics, laboratory abnormalities, findings on routinely performed angiographic studies, and ability to withdraw GC and MTX therapy. Eighteen patients entered the study; 2 dropped out, and 16 were followed up for a mean period of 2.8 years (range 1.3-4.8 years). Results. Weekly administration of MTX (mean stable dose of 17.1 mg) and GC resulted in remissions in 13 of 16 patients (81%). However, 7 patients (44%) had relapses as GC was tapered to or near discontinuation. Retreatment again led to remission, and 3 of 7 patients in this group have successfully stopped GC therapy. Of those patients who achieved remission, 8 (50%) have sustained remissions of 4-34 months (mean 18 months), and 4 of this group have not required GC or MTX therapy for 7-18 months (mean 11.3 months). Three patients experienced disease progression in spite of treatment. Conclusion. About half of all Takayasu arteritis patients have chronic active disease for which GC therapy alone does not provide sustained remissions that allow withdrawal of treatment. Weekly low-dose MTX is an effective means of inducing remission and minimizing GC therapy and toxicity in most of these patients. Further long-term studies will be required to assess the durability of remission and the need for maintenance MTX therapy in this subset of Takayasu arteritis patients. C1 NIAID,BETHESDA,MD 20892. NR 18 TC 189 Z9 192 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD APR PY 1994 VL 37 IS 4 BP 578 EP 582 DI 10.1002/art.1780370420 PG 5 WC Rheumatology SC Rheumatology GA NF044 UT WOS:A1994NF04400019 PM 7908520 ER PT J AU KERR, G HOFFMAN, GS AF KERR, G HOFFMAN, GS TI RELATIONSHIP BETWEEN ANTINEUTROPHIL CYTOPLASMIC ANTIBODY-LEVELS AND DISEASE-ACTIVITY IN WEGENERS GRANULOMATOSIS - REPLY SO ARTHRITIS AND RHEUMATISM LA English DT Letter C1 CLEVELAND CLIN FDN,CLEVELAND,OH 44195. RP KERR, G (reprint author), NIH,BETHESDA,MD 20892, USA. NR 5 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD APR PY 1994 VL 37 IS 4 BP 596 EP 597 DI 10.1002/art.1780370425 PG 2 WC Rheumatology SC Rheumatology GA NF044 UT WOS:A1994NF04400024 ER PT J AU ARAI, K CHROUSOS, GP AF ARAI, K CHROUSOS, GP TI GLUCOCORTICOID RESISTANCE SO BAILLIERES CLINICAL ENDOCRINOLOGY AND METABOLISM LA English DT Article ID PRIMARY CORTISOL RESISTANCE; HORMONE-BINDING DOMAIN; MINERALOCORTICOID RECEPTOR; RHEUMATOID-ARTHRITIS; BRONCHIAL-ASTHMA; ACTH-SECRETION; LOCALIZATION; PROTEIN; COMPLEX; DNA RP ARAI, K (reprint author), NICHHD,DEV ENDOCRINOL BRANCH,PEDIAT ENDOCRINOL SECT,BETHESDA,MD 20892, USA. NR 60 TC 16 Z9 17 U1 0 U2 0 PU BAILLIERE TINDALL PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0950-351X J9 BAILLIERE CLIN ENDOC JI Baillieres Clin. Endocrinol. Metab. PD APR PY 1994 VL 8 IS 2 BP 317 EP 331 DI 10.1016/S0950-351X(05)80255-1 PG 15 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NR779 UT WOS:A1994NR77900006 PM 7980839 ER PT J AU TAKASUNA, M NEGUS, SS DECOSTA, BR WOODS, JH AF TAKASUNA, M NEGUS, SS DECOSTA, BR WOODS, JH TI OPIOID PHARMACOLOGY OF THE ANTINOCICEPTIVE EFFECTS OF LOPERAMIDE IN MICE SO BEHAVIOURAL PHARMACOLOGY LA English DT Article DE ANTINOCICEPTION; LOPERAMIDE; MICE; OPIOIDS; PERIPHERAL OPIOID RECEPTORS ID ANTAGONISTS; RECEPTOR; MORPHINE; BINDING; INVITRO; INVIVO; POTENT; DRUGS AB Loperamide (0.1-3.2 mg/kg i.p.) produced dose-dependent and complete suppression of writhing in the acetic acid-induced writhing assay in mice. Naltrexone (NTX; 0.1-10.0 mg/kg s.c.) and its N-methylated derivative quaternary naltrexone (QNTX; 1.0 and 10.0 mg/kg s.c.) were roughly equipotent in antagonizing the antinociceptive effects of loperamide. In contrast, NTX was approximately 100-fold more potent than QNTX in antagonizing the antinociceptive effects of the classical mu agonist morphine. Furthermore, the antinociceptive effects of loperamide were not antagonized by central administration of the selective mu antagonist D-Phe Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP; 300 ng i.c.v.), or by systemic administration of either the kappa selective antagonist nor-binaltorphimine (nor-BNI; 32.0 mg/kg s.c.), or the delta antagonist naltrindole (NTI; 10.0 mg/kg s.c.). These doses of CTAP, nor-BNI and NTI were effective antagonists of morphine, the kappa agonist U69,593 and the delta agonist BW 373U86 [(+/-)-4-((R*)-a-((2S*5R*)-4-allyl-2,5-dimethyl-1-piperazinal)-3-hydroxybenzyl)-N,N-diethylbenzamide dihydrochloride], respectively. These results indicate that the antinociceptive effects of loperamide in mice are mediated, at least in part, by opioid receptors; however, these receptors are distinct from the opioid receptors mediating the effects of morphine, U69,593 and BW 373U86. These results are consistent with the hypothesis that loperamide produces its antinociceptive effects by acting, at least in part, at peripheral opioid receptors. C1 UNIV MICHIGAN,DEPT PHARMACOL,ANN ARBOR,MI 48109. NIDDK,BETHESDA,MD 20892. NR 40 TC 20 Z9 21 U1 1 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0955-8810 J9 BEHAV PHARMACOL JI Behav. Pharmacol. PD APR PY 1994 VL 5 IS 2 BP 189 EP 195 PG 7 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA NH764 UT WOS:A1994NH76400010 ER PT J AU WOLFFE, AP AF WOLFFE, AP TI STRUCTURAL AND FUNCTIONAL-PROPERTIES OF THE EVOLUTIONARILY ANCIENT Y-BOX FAMILY OF NUCLEIC-ACID BINDING-PROTEINS SO BIOESSAYS LA English DT Review ID OOCYTE-SPECIFIC PROTEINS; XENOPUS-LAEVIS OOCYTES; YEAST NSR1 PROTEIN; DNA-BINDING; MESSENGER-RNA; COLD SHOCK; ESCHERICHIA-COLI; TRANSCRIPTION FACTOR; MOLECULAR-CLONING; RIBOSOMAL-RNA AB The Y-box proteins are the most evolutionarily conserved nucleic acid binding proteins yet defined in bacteria, plants and animals. The central nucleic acid binding domain of the vertebrate proteins is 43% identical to a 70-amino-acid-long protein (CS7.4) from E. coli. The structure of this domain consists of an antiparallel five-stranded beta-barrel that recognizes both DNA and RNA. The diverse biological roles of these Y-box proteins range from the control of the E. coli cold-shock stress response to the translational masking of messenger RNA in vertebrate gametes. This review discusses the organization of the prokaryotic and eukaryotic Y-box proteins, how they interact with nucleic acids, and their biological roles, both proven and potential. RP WOLFFE, AP (reprint author), NICHHD,MOLEC EMBRYOL LAB,BLDG 6,ROOM B1A-13,BETHESDA,MD 20892, USA. NR 66 TC 298 Z9 301 U1 0 U2 5 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD APR PY 1994 VL 16 IS 4 BP 245 EP 251 DI 10.1002/bies.950160407 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA NH290 UT WOS:A1994NH29000006 PM 8031301 ER PT J AU PODGORNIK, R RAU, DC PARSEGIAN, VA AF PODGORNIK, R RAU, DC PARSEGIAN, VA TI PARAMETRIZATION OF DIRECT AND SOFT STERIC-UNDULATORY FORCES BETWEEN DNA DOUBLE-HELICAL POLYELECTROLYTES IN SOLUTIONS OF SEVERAL DIFFERENT ANIONS AND CATIONS SO BIOPHYSICAL JOURNAL LA English DT Article ID HYDRATION FORCES; INTERMOLECULAR FORCES; DOUBLE-LAYER; ORGANIZATION; FLUCTUATIONS; MEMBRANES; MOLECULES; POLYIONS; ENTROPY; PHASES AB Directly measured forces between DNA helices in ordered arrays have been reduced to simple force coefficients and mathematical expressions for the interactions between pairs of molecules. The tabulated force parameters and mathematical expressions can be applied to parallel molecules or, by transformation, to skewed molecules of variable separation and mutual angle. This ''toolbox'' of intermolecular forces is intended for use in modelling molecular interactions, assembly, and conformation. The coefficients characterizing both the exponential hydration and the electrostatic interactions depend strongly on the univalent counterion species in solution, but are only weakly sensitive to anion type and temperature (from 5 to 50 degrees C). Interaction coefficients for the exponentially varying hydration force seen at spacings less than 10 to 15 Angstrom between surfaces are extracted directly from pressure versus interaxial distance curves. Electrostatic interactions are only observed at larger spacings and are always coupled with configurational fluctuation forces that result in observed exponential decay lengths that are twice the expected Debye-Huckel length. The extraction of electrostatic force parameters relies on a theoretical expression describing steric forces of molecules ''colliding'' through soft exponentially varying direct interactions. C1 NIH,DCRT,STRUCT BIOL LAB,BETHESDA,MD 20892. NIDDK,BETHESDA,MD 20892. RI Podgornik, Rudolf/C-6209-2008 OI Podgornik, Rudolf/0000-0002-3855-4637 NR 28 TC 128 Z9 129 U1 0 U2 9 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1994 VL 66 IS 4 BP 962 EP 971 PG 10 WC Biophysics SC Biophysics GA ND194 UT WOS:A1994ND19400004 PM 8038400 ER PT J AU BURBELO, PD IADAROLA, MJ AF BURBELO, PD IADAROLA, MJ TI RAPID PLASMID DNA-SEQUENCING WITH MULTIPLE OCTAMER PRIMERS SO BIOTECHNIQUES LA English DT Note ID CAENORHABDITIS-ELEGANS; HUMAN GENOME; LIBRARY; TAGS AB Oligonucleotide walking is an important technique for generating new DNA sequence information. We have developed an efficient sequencing method based on the use of octamer primers, which can potentially simplify and reduce the cost of sequencing. In this procedure the plasmid DNA is thoroughly denatured in the presence of heat and NaOH. Following cooling, the mixture is aliquoted into tubes containing the different octamer primers and neutralized by the addition of HCI. The mixture is then sequenced by a modified Sequenase (R) protocol that involves performing the initial labeling reactions at low temperature (on ice) and the termination reactions at high temperatures (43 degrees C). Analysis of sequencing gels revealed octamer sequencing to be as effective as sequencing with 17-mer primers. RP BURBELO, PD (reprint author), NIDR,BLDG 30,ROOM 410,BETHESDA,MD 20892, USA. RI Burbelo, Peter/B-1027-2009 NR 9 TC 3 Z9 3 U1 0 U2 1 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD APR PY 1994 VL 16 IS 4 BP 645 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NE764 UT WOS:A1994NE76400020 PM 8024784 ER PT J AU CLAXTON, DF LIU, P HSU, HB MARLTON, P HESTER, J COLLINS, F DEISSEROTH, AB ROWLEY, JD SICILIANO, MJ AF CLAXTON, DF LIU, P HSU, HB MARLTON, P HESTER, J COLLINS, F DEISSEROTH, AB ROWLEY, JD SICILIANO, MJ TI DETECTION OF FUSION TRANSCRIPTS GENERATED BY THE INVERSION 16-CHROMOSOME IN ACUTE MYELOGENOUS LEUKEMIA SO BLOOD LA English DT Note ID MESSENGER-RNA; CHROMOSOME-16; ABNORMALITIES; POLYOMAVIRUS; LYMPHOMA C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT MOLEC GENET,HOUSTON,TX 77025. UNIV MICHIGAN,HOWARD HUGHES INST,ANN ARBOR,MI 48109. NIH,CTR HUMAN GENOME RES,BETHESDA,MD 20892. UNIV CHICAGO,PRITZKER SCH MED,CHICAGO,IL 60637. RP CLAXTON, DF (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,DEPT HEMATOL,BOX 24,1515 HOLCOMBE BLVD,HOUSTON,TX 77025, USA. RI Marlton, Paula/F-3026-2011; Liu, Paul/A-7976-2012 OI Liu, Paul/0000-0002-6779-025X FU NCI NIH HHS [CA167721, CA42557, CA55164] NR 24 TC 147 Z9 148 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 APR 1 PY 1994 VL 83 IS 7 BP 1750 EP 1756 PG 7 WC Hematology SC Hematology GA NE411 UT WOS:A1994NE41100006 PM 8142642 ER PT J AU RUCHKIN, DS GRAFMAN, J KRAUSS, GL JOHNSON, R CANOUNE, H RITTER, W AF RUCHKIN, DS GRAFMAN, J KRAUSS, GL JOHNSON, R CANOUNE, H RITTER, W TI EVENT-RELATED BRAIN POTENTIAL EVIDENCE FOR A VERBAL WORKING-MEMORY DEFICIT IN MULTIPLE-SCLEROSIS SO BRAIN LA English DT Article DE MULTIPLE SCLEROSIS; WORKING MEMORY; PHONOLOGICAL LOOP; EVENT-RELATED POTENTIALS; LEFT ANTERIOR NEGATIVITY ID SHORT-TERM-MEMORY; COMPONENT; FREQUENCY; SPEECH; MODELS AB Memory deficits are frequently identified in patients with multiple sclerosis. Both working (short-term) and long-term memory appear affected, particularly on free-recall tasks. The focus of our study was to examine neurophysiological correlates of working memory processes and to identify the specific components responsible for the working memory deficits reported in multiple sclerosis. Event-related brain potentials (ERPs) were recorded from the scalp of mildly afflicted multiple sclerosis patients and their matched normal controls during the performance of phonological and visuo-spatial working memory tasks. Neuropsychological test, behavioural performance and ERP data all indicated that verbal working memory is especially susceptible to impairment by multiple sclerosis, while visuospatial working memory is less susceptible. The pattern of results further indicated that the verbal working memory dysfunction in multiple sclerosis is at least partially due to impairment in the phonological loop, a rehearsal mechanism for retaining verbal information in working memory. C1 JOHNS HOPKINS UNIV HOSP,DEPT NEUROL,BALTIMORE,MD. NINCDS,MED NEUROL BRANCH,COGNIT NEUROSCI SECT,BETHESDA,MD 20892. CUNY QUEENS COLL,DEPT PSYCHOL,FLUSHING,NY 11367. CUNY,LEHMAN COLL,DEPT PSYCHOL,NEW YORK,NY 10021. ALBERT EINSTEIN COLL MED,DEPT NEUROSCI,NEW YORK,NY. RP RUCHKIN, DS (reprint author), UNIV MARYLAND,SCH MED,DEPT PHYSIOL,BALTIMORE,MD 21201, USA. OI Grafman, Jordan H./0000-0001-8645-4457 FU NINDS NIH HHS [NINDS NS11199, NINDS NS30029] NR 48 TC 76 Z9 77 U1 2 U2 8 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0006-8950 J9 BRAIN JI Brain PD APR PY 1994 VL 117 BP 289 EP 305 DI 10.1093/brain/117.2.289 PN 2 PG 17 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA NN887 UT WOS:A1994NN88700007 PM 8186956 ER PT J AU DONOSO, AO SELTZER, AM NAVARRO, CE CABRERA, RJ LOPEZ, FJ NEGROVILAR, A AF DONOSO, AO SELTZER, AM NAVARRO, CE CABRERA, RJ LOPEZ, FJ NEGROVILAR, A TI REGULATION OF LUTEINIZING-HORMONE-RELEASING HORMONE AND LUTEINIZING HORMONES SECRETION BY HYPOTHALAMIC AMINO-ACIDS SO BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH LA English DT Article; Proceedings Paper CT Miguel R Covian Symposium CY AUG 22-24, 1993 CL RIBEIRO PRETO, BRAZIL DE LUTEINIZING HORMONE-RELEASING HORMONE; LUTEINIZING HORMONE; GLUTAMATE; GABA; NORADRENALINE ID N-METHYL-D; D-ASPARTIC ACID; INDUCED LH SURGE; GABA-B RECEPTOR; OVARIECTOMIZED RATS; FEMALE RATS; NEUROENDOCRINE REGULATION; SEXUAL-MATURATION; PREOPTIC AREA; NEURONS AB 1. The present review discusses the proposed roles of the amino acids glutamate and GABA in the central regulation of luteinizing hormone-releasing hormone (LHRH)and in luteinizing hormone (LH) secretion. 2. Descriptions of the mechanisms of action of these neurotransmitters have focused on two diencephalic areas, namely, the preoptic-anterior hypothalamic area where the cell bodies of LHRH neurons are located, and the medial basal hypothalamus which contains the nerve endings of the LHRH system. Increasing endogenous GABA concentration by drugs, GABA agonists, or blockade of glutamatergic neurotransmission by selective antagonists in rats and non-human primates prevents ovulation and pulsatile LH release, and blunts the LH surges induced by estrogen or an estrogen-progesterone combination. In contrast, glutamate and different glutamate agonists such as NMDA, AMPA and kainate, can increase LHRH/LH secretion. 3. The simultaneous enhancement of glutamatergic activity and a decrease of GABAergic tone may positively influence the maturation of the pituitary-gonadal system in rats and non-human primates. Administration of glutamate receptor agonists has been shown to significantly advance the onset of puberty. Conversely, glutamate antagonists or increased endogenous GABA levels may delay the onset of puberty. The physiological regulation of LHRH/LH secretion may thus involve a GABA-glutamate interaction and a cooperative action of the various types of ionotropic glutamate receptors. 4. The inhibitory actions of GABA on LH release and ovulation may be exerted at the level of afferent nerve terminals that regulate LHRH secretion. A likely candidate is noradrenaline, as suggested by the synaptic connections between noradrenergic nerve terminals and GABAergic interneurons in the preoptic area. Recent experiments have provided complementary evidence for the physiological balance between inhibitory and excitatory transmission resulting in modulation of the action of noradrenaline to evoke LHRH release. C1 NIEHS,LMIN,REPROD NEUROENDOCRINOL SECT,RES TRIANGLE PK,NC 27709. RP DONOSO, AO (reprint author), UNC,FAC CIENCIAS MED,CONICET,LINCE,INVEST CEREBRALES LAB,CASILLA CORREO 425,RA-5500 MENDOZA,ARGENTINA. NR 56 TC 31 Z9 31 U1 0 U2 0 PU ASSOC BRAS DIVULG CIENTIFICA PI SAO PAULO PA FACULDADE MEDICINA, SALA 21, 14049 RIBEIRAO PRETO, SAO PAULO, BRAZIL SN 0100-879X J9 BRAZ J MED BIOL RES JI Brazilian J. Med. Biol. Res. PD APR PY 1994 VL 27 IS 4 BP 921 EP 932 PG 12 WC Biology; Medicine, Research & Experimental SC Life Sciences & Biomedicine - Other Topics; Research & Experimental Medicine GA NE415 UT WOS:A1994NE41500009 PM 8087094 ER PT J AU BRADBURY, AW CARTER, DC MILLER, WR CHOCHUNG, YS CLAIR, T AF BRADBURY, AW CARTER, DC MILLER, WR CHOCHUNG, YS CLAIR, T TI PROTEIN KINASE-A (PK-A) REGULATORY SUBUNIT EXPRESSION IN COLORECTAL-CANCER AND RELATED MUCOSA SO BRITISH JOURNAL OF CANCER LA English DT Article ID MOLECULAR-CLONING; BINDING-PROTEINS; HUMAN TESTIS; RI SUBUNIT; CELLS; CDNA; ADENOSINE-3',5'-MONOPHOSPHATE; ACCUMULATION; SEQUENCE; GROWTH AB Photaffinity labelling (PAL) with [P-32]8-azido-cAMP and polyacrylamide gel electrophoresis (PAGE) has been used to identify three specific cAMP-binding proteins (cAMP-BPs) within cytosols derived from the centre and periphery of 32 human colorectal cancers and from related adjacent (less than 5 cm from the tumour) and distant (more than 5 cm from the tumour) microscopically benign mucosa. By immunoprecipitation with specific anti-RI and anti-RII antibodies these proteins have subsequently been characterised as a single form of RI (48 kDa) and two forms of RII (50 and 52 kDa). The relative expression of isoforms in each specimen has been quantified by laser densitometry. There was significantly more RI expressed in both tumour centre and periphery than in either adjacent or distant mucosa (P<0.008 by Wilcoxon signed-rank test). There was no significant difference in relative RI expression between tumour centre and periphery, or between adjacent and distant mucosa. There was no association between relative RI expression and Dukes' stage. Poorly differentiated tumours expressed significantly more RI than those that were either moderately or well differentiated (P = 0.016 by Mann-Whitney U-test). This study is the first to have characterised cAMP-BPs within human colorectal tissues and has demonstrated that colorectal cancers, and in particular those of poor histological grade, relatively overexpress RI when compared with related benign mucosa. C1 NCI,TUMOR IMMUNOL & BIOL LAB,CELLULAR BIOCHEM SECT,BETHESDA,MD 20892. RP BRADBURY, AW (reprint author), UNIV EDINBURGH,ROYAL INFIRM,DEPT SURG,EDINBURGH EH3 9YW,MIDLOTHIAN,SCOTLAND. NR 32 TC 72 Z9 75 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD APR PY 1994 VL 69 IS 4 BP 738 EP 742 DI 10.1038/bjc.1994.139 PG 5 WC Oncology SC Oncology GA NC610 UT WOS:A1994NC61000017 PM 8142263 ER PT J AU RAYMOND, EG CNATTINGIUS, S KIELY, JL AF RAYMOND, EG CNATTINGIUS, S KIELY, JL TI EFFECTS OF MATERNAL AGE, PARITY, AND SMOKING ON THE RISK OF STILLBIRTH SO BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY LA English DT Article ID PERINATAL-MORTALITY; DELAYED CHILDBEARING; INFANT-MORTALITY; NEONATAL DEATH; PREGNANCY; FETAL; COMPLICATIONS; POPULATION; GROWTH; SWEDEN AB Objective To examine the effects of advanced maternal age, nulliparity, and smoking on risk of stillbirth as gestation advances, and to explore possible clinical mediators of these effects. Design A population based cohort study. Setting Sweden, 1983 to 1989. Subjects All singleton pregnancies of 28 weeks gestation or greater in Nordic citizens at least 20 years old (n = 638242). Main outcome measures Crude and adjusted risks of stillbirth; gestational age specific risks of stillbirth Results Older women (35 years or older), smokers, and nulliparas had elevated risks of stillbirth. The elevated stillbirth risk in smokers was eliminated when women with intrauterine growth retardation, placental abruption, and placenta previa were excluded from the analysis. However, the higher risks in older women and nulliparas persisted even when the analysis excluded women with hypertension, diabetes, placental complications, or growth retardation. Over the course of the third trimester, the age related risk of stillbirth increased, the smoking related risk decreased, and the higher risk in nulliparas showed no clear trend with gestational age. Conclusions The association between smoking and stillbirth is explained entirely by the higher incidence of growth retardation and placental complications in smokers. The clinical mediators of the associations of maternal age and parity with stillbirth remain unexplained. Gestational age is an important modifier of the effects of advanced maternal age and smoking on stillbirth risk. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,ROCKVILLE,MD. UPPSALA UNIV,DEPT SOCIAL MED,UPPSALA,SWEDEN. CTR DIS CONTROL & PREVENT,NATL CTR HLTH STAT,DIV ANAL,HYATTSVILLE,MD 20782. NR 25 TC 128 Z9 130 U1 0 U2 4 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0306-5456 J9 BRIT J OBSTET GYNAEC JI Br. J. Obstet. Gynaecol. PD APR PY 1994 VL 101 IS 4 BP 301 EP 306 DI 10.1111/j.1471-0528.1994.tb13614.x PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA NF505 UT WOS:A1994NF50500006 PM 8199075 ER PT J AU HYDE, TM NAWROZ, S GOLDBERG, TE BIGELOW, LB STRONG, D OSTREM, JL WEINBERGER, DR KLEINMAN, JE AF HYDE, TM NAWROZ, S GOLDBERG, TE BIGELOW, LB STRONG, D OSTREM, JL WEINBERGER, DR KLEINMAN, JE TI IS THERE COGNITIVE DECLINE IN SCHIZOPHRENIA - A CROSS-SECTIONAL STUDY SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID MINI-MENTAL STATE; ANATOMICAL ABNORMALITIES; ALZHEIMERS-DISEASE; VENTRICULAR SIZE; BRAIN; PATHOLOGY; PSYCHOSIS; DEFICITS; DEMENTIA; GLIOSIS AB The issue of progressive cognitive decline in patients with schizophrenia has been debated. We performed a cross-sectional study of patients with chronic schizophrenia, aged from 18 to 69 years, in order to address this issue. The patients included in this study passed a rigorous screen for any comorbid condition with an adverse impact on central nervous system function. We assessed intellectual deterioration with a battery of neuropsychological tests known to be sensitive to cognitive impairment in progressive dementia. No evidence of accelerated intellectual decline was found. No significant differences were found between the five age-derived cohorts (18-29, 30-39, 40-49, 50-59, and 60-69 years of age) on the Mini-Mental State Examination, Dementia Rating Scale, or other tests sensitive to dementia. While performance on the Boston Naming Test significantly declined with age, this was mainly due to age rather than duration of illness. However, it is important to note that mean performances on the majority of the tests were abnormal across all cohorts studied. These results suggest that intellectual function does not markedly decline during the adulthood of patients with schizophrenia. The course of schizophrenia is more consistent with a static encephalopathy than a dementing disorder. RP HYDE, TM (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,CLIN BRAIN DISORDERS BRANCH,INTRAMURAL RES PROGRAM,WASHINGTON,DC 20032, USA. NR 54 TC 118 Z9 122 U1 7 U2 10 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD APR PY 1994 VL 164 BP 494 EP 500 DI 10.1192/bjp.164.4.494 PG 7 WC Psychiatry SC Psychiatry GA NF414 UT WOS:A1994NF41400012 PM 8038938 ER PT J AU SHAHABUDDIN, M KASLOW, DC AF SHAHABUDDIN, M KASLOW, DC TI BIOLOGY OF THE DEVELOPMENT OF PLASMODIUM IN THE MOSQUITO MIDGUT - A MOLECULAR AND CELLULAR VIEW SO BULLETIN DE L INSTITUT PASTEUR LA English DT Article DE MALARIA; PLASMODIUM; MOSQUITO; MIDGUT; MOLECULAR AND CELLULAR VIEW; DEVELOPMENT; REVIEW ID SUSCEPTIBLE AEDES-AEGYPTI; PERITROPHIC MEMBRANES; PARASITE CHITINASE; SURFACE RECEPTORS; MALARIA PARASITES; ANOPHELES-GAMBIAE; BLOOD MEAL; GALLINACEUM; FALCIPARUM; INVITRO RP SHAHABUDDIN, M (reprint author), NIAID,MALARIA RES LAB,MOLEC VACCINE SECT,BETHESDA,MD 20892, USA. NR 64 TC 21 Z9 21 U1 0 U2 1 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0020-2452 J9 B I PASTEUR JI Bull. Inst. Pasteur PD APR-JUN PY 1994 VL 92 IS 2 BP 119 EP 132 PG 14 WC Immunology; Microbiology; Virology SC Immunology; Microbiology; Virology GA PB804 UT WOS:A1994PB80400005 ER PT J AU LACROIX, EM AF LACROIX, EM TI SAIL - AUTOMATING INTERLIBRARY LOAN SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Article; Proceedings Paper CT 93rd Annual Meeting of the Medical-Library-Association CY MAY 14-20, 1993 CL CHICAGO, IL SP MED LIB ASSOC AB The National Library of Medicine (NLM) initiated the System for Automated Interlibrary Loan (SAIL) pilot project to study the feasibility of using imaging technology linked to the DOCLINE(R) system to deliver copies of journal articles. During the project, NLM converted a small number of print journal issues to electronic form, linking the captured articles to the MEDLINE citation unique identifier. DOCLINE requests for these journals that could not be filled by network libraries were routed to SAIL. Nearly 23,000 articles from sixty-four journals recently selected for indexing in Index Medicus were scanned to convert them to electronic images. During fiscal year 1992, 4,586 scanned articles were used to fill 10,444 interlibrary loan (ILL) requests, and more than half of these were used only once. Eighty percent of all the articles were not requested at all. The total cost per article delivered was $10.76, substantially more than it costs to process a photocopy request, Because conversion costs were the major component of the total SAIL cost, and most of the articles captured for the project were not requested, this model was not cost-effective. Data on SAIL journal article use was compared with all ILL requests filled by NLM for the same period. Eighty-eight percent of all articles requested from NLM were requested only once. The results of the SAIL project demonstrated that converting journal articles to electronic images and storing them in anticipation of repeated requests would not meet NLM's objective to improve interlibrary loan. RP LACROIX, EM (reprint author), NATL LIB MED,DIV PUBL SERV,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD APR PY 1994 VL 82 IS 2 BP 171 EP 175 PG 5 WC Information Science & Library Science SC Information Science & Library Science GA NF278 UT WOS:A1994NF27800009 PM 8004020 ER PT J AU MARX, SJ BARSONY, J AF MARX, SJ BARSONY, J TI RECEPTORS FOR STEROID-RELATED AGONISTS MEDIATE RAPID, NONGENOMIC EFFECTS SO CALCIFIED TISSUE INTERNATIONAL LA English DT Meeting Abstract C1 NCI,METAB DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD APR PY 1994 VL 54 IS 4 BP 334 EP 334 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NB462 UT WOS:A1994NB46200028 ER PT J AU SPORN, MB ROBERTS, AB WAKEFIELD, LM AF SPORN, MB ROBERTS, AB WAKEFIELD, LM TI INTERACTIONS OF TRANSFORMING GROWTH-FACTOR-BETA AND LIGANDS OF THE STEROID RETINOID RECEPTOR SUPERFAMILY SO CALCIFIED TISSUE INTERNATIONAL LA English DT Meeting Abstract C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD APR PY 1994 VL 54 IS 4 BP 335 EP 335 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NB462 UT WOS:A1994NB46200031 ER PT J AU MIGLIACCIO, S NEWBOLD, RR LUBAHN, DB KORACH, KS AF MIGLIACCIO, S NEWBOLD, RR LUBAHN, DB KORACH, KS TI CHANGES OF ESTROGEN-LEVELS AND ESTROGEN RESPONSIVENESS DURING DEVELOPMENT AFFECT THE FEMALE MICE SKELETON SO CALCIFIED TISSUE INTERNATIONAL LA English DT Meeting Abstract C1 NIEHS,LRDT,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,DEPT REPROD BIOL,CHAPEL HILL,NC 27514. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD APR PY 1994 VL 54 IS 4 BP 341 EP 341 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NB462 UT WOS:A1994NB46200054 ER PT J AU LEONG, GM MERCADOASIS, LB CHROUSOS, GP AF LEONG, GM MERCADOASIS, LB CHROUSOS, GP TI THE EFFECTS OF PEDIATRIC CUSHING SYNDROME ON BONE-MINERAL DENSITY AND BONE METABOLISM SO CALCIFIED TISSUE INTERNATIONAL LA English DT Meeting Abstract C1 NICHHD,DEB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD APR PY 1994 VL 54 IS 4 BP 352 EP 352 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NB462 UT WOS:A1994NB46200090 ER PT J AU RON, E TARONE, RE MODAN, B CHAKI, R ALFANDARY, E PARRY, DM MAKAR, M SETLOW, N MULVIHILL, JJ MILLER, RW SETLOW, RB AF RON, E TARONE, RE MODAN, B CHAKI, R ALFANDARY, E PARRY, DM MAKAR, M SETLOW, N MULVIHILL, JJ MILLER, RW SETLOW, RB TI IN-VITRO RADIOSENSITIVITY OF FIBROBLASTS FROM THYROID AND SKIN-CANCER PATIENTS TREATED WITH X-RAYS FOR TINEA-CAPITIS SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID ATAXIA TELANGIECTASIA HETEROZYGOTES; RADIATION; IDENTIFICATION; HEAD; NECK AB To investigate the hypothesis that persons who developed thyroid or skin cancer subsequent to scalp irradiation for tinea capitis are particularly sensitive to radiation, possibly because of a high frequency of ataxia-telagiectasia, we used an in vitro cell survival assay to evaluate radiosensitivity of their fibroblast cell strains. Study subjects were selected from a cohort of 10,834 Israelis irradiated during childhood for tinea capitis. Skin fibroblasts were obtained from thyroid and skin cancer patients (cases) as well as a sample of subjects who did not have cancer (controls). Fibroblasts were cultured and then loss of colony-forming ability as a result of acute X-irradiation was evaluated. Comparison of survival curve parameters (mean inverse of the slope and the dose needed to reduce colony survival to 10%) between 12 thyroid cancer and 12 control strains showed no differences (P > 0.5). A slightly increased radiation sensitivity of the skin cancer cases compared with their controls was observed. Although based on few subjects (14 cases and 11 controls), the findings were similar whether the mean inverse of the slope (P = 0.06) or the dose needed to reduce colony survival to 10% (P = 0.05) was evaluated. However, because of the small size of the study and potential errors inherent in survival assays, our finding that cell strains derived from patients who developed skin cancer exhibit enhanced radiosensitivity should be viewed as preliminary and interpreted cautiously. C1 NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. CHAIM SHEBA MED CTR,DEPT CLIN EPIDEMIOL,IL-52621 TEL HASHOMER,ISRAEL. CHAIM SHEBA MED CTR,DEPT GENET,IL-52621 TEL HASHOMER,ISRAEL. BROOKHAVEN NATL LAB,DEPT MED,UPTON,NY 11973. BROOKHAVEN NATL LAB,DEPT BIOL,UPTON,NY 11973. UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA 15260. RP RON, E (reprint author), NCI,DIV CANC ETIOL,6130 EXECUT BLVD,EPN 408,ROCKVILLE,MD 20852, USA. FU NCI NIH HHS [N01-CP-01042] NR 20 TC 5 Z9 5 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD APR-MAY PY 1994 VL 3 IS 3 BP 229 EP 232 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA NE773 UT WOS:A1994NE77300008 PM 8019372 ER PT J AU REYNOLDS, P BOYD, PT BLACKLOW, RS JACKSON, JS GREENBERG, RS AUSTIN, DF CHEN, VW EDWARDS, BK AF REYNOLDS, P BOYD, PT BLACKLOW, RS JACKSON, JS GREENBERG, RS AUSTIN, DF CHEN, VW EDWARDS, BK TI THE RELATIONSHIP BETWEEN SOCIAL TIES AND SURVIVAL AMONG BLACK-AND-WHITE BREAST-CANCER PATIENTS SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID ALAMEDA COUNTY; FOLLOW-UP; HEART-DISEASE; LIFE STRESS; MEN BORN; MORTALITY; NETWORKS; SUPPORT; HEALTH; PREDICTORS AB The relationship between social ties, stage of disease, and survival was analyzed in a population-based sample of 525 black and 486 white women with newly diagnosed breast cancer. There were significant differences between the two race groups in reported social ties. Using logistic regression to adjust for the effects of age, race, study area, education, and the presence of symptoms, there was little or no evidence for an association between individual network measures of social ties and stage of disease. However, a summary measure of social networks was found to be associated modestly with late stage disease, attributable in part to significantly more advanced disease among black, but not white, women reporting few friends and relatives [relative risk (RR) = 1.8; 95% confidence interval (CI) = 1.1-3.0]. With adjustments for differences in stage of disease and other covariates, and with the use of Cox proportional hazards modeling to estimate hazard ratios, the absence of close ties and perceived sources of emotional support were associated significantly with an increased breast cancer death rate. White women in the lowest quartile of reported close friends and relatives had twice the breast cancer death rate of white women in the highest quartile (RR = 2.1; 95% CI = 1.1-4.4). Notably, both black and white women reporting few sources of emotional support had a higher death rate from their disease during the 5-year period of follow-up (RR = 1.8; 95% CI = 1.3-2.5). This association was stronger for black women (RR = 1.9; 95% CI = 1.3-3.0) and for women presenting with late stage disease (RR = 1.9; 95% CI = 1.3-2.7). Although the absence of close ties was associated with late diagnosis among black women, and was associated with poorer survival among white women, the absence of sources of emotional support had a consistent effect on both groups of women. These data suggest that functional (''perceived emotional support'') rather than structural (''social network'') measures of social relationships may be important in influencing disease prognosis. C1 CALIF PUBL HLTH FDN,BERKELEY,CA 94704. NE OHIO UNIV,COLL MED,ROOTSTOWN,OH 44272. UNIV MICHIGAN,HORACE H RACKHAM GRAD SCH,ANN ARBOR,MI 48109. EMORY UNIV,SCH PUBL HLTGH,ATLANTA,GA 30329. CTR DIS PREVENT & CONTROL,PORTLAND,OR 97232. LOUISIANA STATE UNIV,MED CTR,DEPT PATHOL,NEW ORLEANS,LA 70112. NCI,ROCKVILLE,MD 20852. RP REYNOLDS, P (reprint author), CALIF DEPT HLTH SERV,ENVIRONM EPIDEMIOL SECT,5900 HOLLIS ST,SUITE E,EMERYVILLE,CA 94608, USA. FU NCI NIH HHS [N01-CN-25501, N01-CN-45174, N01-CN-35043] NR 31 TC 80 Z9 81 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 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD APR-MAY PY 1994 VL 3 IS 3 BP 253 EP 259 PG 7 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA NE773 UT WOS:A1994NE77300012 PM 8019376 ER PT J AU KALUZNY, AD LACEY, LM WARNECKE, R MORRISSEY, JP SONDIK, E FORD, L AF KALUZNY, AD LACEY, LM WARNECKE, R MORRISSEY, JP SONDIK, E FORD, L TI USING A COMMUNITY CANCER-TREATMENT TRIALS NETWORK FOR CANCER PREVENTION AND CONTROL RESEARCH - CHALLENGES AND OPPORTUNITIES SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID CLINICAL ONCOLOGY PROGRAM; PERFORMANCE; ADOPTION; SIZE AB Using data collected as part of a larger evaluation of the National Cancer Institute-funded Community Clinical Oncology Program (CCOP), this paper examines the degree to which selected community, interorganizational, and structural characteristics associated with accural to cancer treatment protocols share equal importance in accruing patients to cancer prevention and control research protocols. Analysis reveals that there are similarities in the factors that prove to be effective for accrual to both types of protocols; however, the two are not isomorphic. CCOP structure was an important predictor of treatment accrual but was not significant for cancer control accrual. Variables measuring the community health resources available to the CCOP were not significant for either treatment or cancer prevention and control research accrual when CCOP structure and interaction with participating research bases were considered. Only CCOP interaction with participating research bases was a significant predictor of both treatment and cancer prevention and control research accrual. The policy implications of these findings are discussed. C1 UNIV ILLINOIS,SURVEY RES LAB,CHICAGO,IL 60680. NCI,COMMUNITY ONCOL & REHABIL BRANCH,BETHESDA,MD 20892. NCI,DIV CANC PREVENT & CONTROL,BETHESDA,MD 20892. RP KALUZNY, AD (reprint author), UNIV N CAROLINA,CECIL G SHEPS CTR HLTH SERV RES,CAMPUS BOX 7590,725 AIRPORT RD BLDG,CHAPEL HILL,NC 27599, USA. NR 23 TC 8 Z9 8 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD APR-MAY PY 1994 VL 3 IS 3 BP 261 EP 269 PG 9 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA NE773 UT WOS:A1994NE77300013 PM 8019377 ER PT J AU RAO, M LIU, FS DAWSEY, SM YANG, K LIPKIN, M LI, JY TAYLOR, PR LI, B BLOT, WJ WANG, GQ LEWIN, KJ YU, Y YANG, CS AF RAO, M LIU, FS DAWSEY, SM YANG, K LIPKIN, M LI, JY TAYLOR, PR LI, B BLOT, WJ WANG, GQ LEWIN, KJ YU, Y YANG, CS TI EFFECTS OF VITAMIN MINERAL SUPPLEMENTATION ON THE PROLIFERATION OF ESOPHAGEAL SQUAMOUS EPITHELIUM IN LINXIAN, CHINA SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Note ID HIGH-RISK POPULATION; CANCER INCIDENCE; INTERVENTION AB Abnormalities of epithelial proliferation have been proposed as an early step in gastrointestinal carcinogenesis. To determine whether micronutrient supplementation may reduce squamous epithelial proliferation in the esophagus, we evaluated proliferation in subjects participating in a randomized nutrition intervention trial in Linxian, China, where esophageal cancer rates are among the highest in the world. After 30 months of intervention involving daily supplementation with multiple vitamins and minerals, an endoscopic survey was performed and squamous biopsies from 512 subjects were labeled with tritiated thymidine and autoradiographed. Analysis showed no treatment effect on the overall amount of squamous epithelial proliferation measured by the total labeling index. However, a measure of the vertical distribution of labeled cells showed lower values with supplementation: a 14% reduction in all subjects (P = 0.29), and a 29% reduction in nonsmokers (P = 0.03). These results suggest a potential modest benefit for short-term intervention with multiple vitamins and minerals on squamous epithelial cell proliferation of the esophagus in this high-risk population. C1 NCI,DIV CANC PREVENT & CONTROL,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. CHINESE ACAD MED SCI,INST CANC,BEIJING,PEOPLES R CHINA. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. RUTGERS STATE UNIV,PISCATAWAY,NJ 08854. FU NCI NIH HHS [N01-CP-41019]; PHS HHS [N01-263-88-C-0138] NR 13 TC 20 Z9 20 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD APR-MAY PY 1994 VL 3 IS 3 BP 277 EP 279 PG 3 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA NE773 UT WOS:A1994NE77300015 PM 8019379 ER PT J AU CHEN, LC KIRCHHOFF, S DE LUCA, LM AF CHEN, LC KIRCHHOFF, S DE LUCA, LM TI EFFECT OF EXCESS DIETARY RETINOIC ACID ON SKIN PAPILLOMA AND CARCINOMA FORMATION INDUCED BY A COMPLETE CARCINOGENESIS PROTOCOL IN FEMALE SENCAR MICE SO CANCER LETTERS LA English DT Article DE RETINOIC ACID; SKIN CARCINOGENESIS; COMPLETE CARCINOGENESIS; MALIGNANT CONVERSION ID TUMOR PROMOTION; INHIBITION; TUMORIGENESIS; CONVERSION AB Previously, we have shown that dietary retinoic acid (RA) at pharmacological doses (30 mu g/g of diet) inhibited the malignant conversion of skin papillomas to carcinomas induced by a two-stage carcinogenesis protocol with 7,12-dimethylbenz[a]anthracene (DMBA) as initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as promoter (De Luca et al., Carcinogenesis, 14 (1993) 539-542). The purpose of this study was to determine the effect of dietary RA on skin papilloma and carcinoma formation induced by a complete carcinogenesis protocol with repeated DMBA treatment in female Sencar mice. Mice at 3 weeks of age were weaned onto a diet containing either 3 (control) or 30 (excess) mu g of RA/g of diet and treated topically with DMBA (25.5 mu g) once per week for 20 weeks. Mice fed excess dietary RA did not significantly differ from control mice in the following parameters: body weight, survival rate, papilloma incidence, cumulative carcinoma incidence (19.4% versus 23.7%), carcinoma yield (0.19 versus 0.26 per mouse), carcinoma conversion efficiency (5.2% versus 3.9%), and average age of carcinoma development (22.7 +/- 4.7 versus 23.3 +/- 2.8 weeks). However, papilloma yield was decreased by about 50% (i.e. 3.7 versus 7.0 at week 20, P <0.01) between weeks 17 and 22 of age by excess dietary RA treatment. Contrary to other routes of administration (i.e. topical and systemic) of RA (Verma et al., Cancer Res., 42 (1982) 3519-3525), excess dietary RA did not enhance skin tumor formation. In addition, excess dietary RA failed to inhibit malignant conversion of papillomas to carcinomas in the complete carcinogenesis protocol. Thus, the modulation of RA on skin papilloma and carcinoma formation is dependent on carcinogenesis protocol and route of RA administration. C1 NCI, DIFFERENTIAT CONTROL SECT, CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB, BETHESDA, MD 20892 USA. BIOCON INC, ROCKVILLE, MD USA. NR 20 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD APR 1 PY 1994 VL 78 IS 1-3 BP 63 EP 67 DI 10.1016/0304-3835(94)90032-9 PG 5 WC Oncology SC Oncology GA NJ747 UT WOS:A1994NJ74700010 PM 8180970 ER PT J AU KRUH, GD CHAN, A MYERS, K GAUGHAN, K MIKI, T AARONSON, SA AF KRUH, GD CHAN, A MYERS, K GAUGHAN, K MIKI, T AARONSON, SA TI EXPRESSION COMPLEMENTARY-DNA LIBRARY TRANSFER ESTABLISHES MRP AS A MULTIDRUG-RESISTANCE GENE SO CANCER RESEARCH LA English DT Note ID P-GLYCOPROTEIN; CELL-LINES; ADRIAMYCIN RESISTANCE; CLONING SYSTEM; CDNA CLONING; HL60 CELLS; LEUKEMIA; MDR1; TRANSPORTER; MECHANISMS AB The emergence of drug-resistant cancer cells is a major obstacle to cancer treatment. Resistant cells often display a multidrug-resistant phenotype that reduces the promise of combination chemotherapy, the classic approach to the prevention of drug resistance. mdr1, a member of the ABC cassette superfamily of transporters which encodes an energy-dependent drug efflux pump, is the only gene known to confer the multidrug-resistant phenotype. Other multidrug resistance mechanisms must exist, since cell lines which have this phenotype in the absence of mdr1 overexpression have been described. We report here the application of a novel approach involving expression complementary DNA library transfer to the identification of drug-resistant genes. Using this approach we establish that mrp, a member of the ABC cassette superfamily of transporters, is capable of conferring a multidrug-resistant phenotype. This approach should be useful in the identification of other novel resistance genes. C1 NCI,CELLULAR & MOLEC BIOL LAB,BALTIMORE,MD 21211. DERALD R RUTTENBERG CANC CTR,NEW YORK,NY 10029. RP KRUH, GD (reprint author), FOX CHASE CANC CTR,DEPT MED ONCOL,ROOM W304,PHILADELPHIA,PA 19111, USA. NR 28 TC 135 Z9 138 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 BP 1649 EP 1652 PG 4 WC Oncology SC Oncology GA ND238 UT WOS:A1994ND23800010 PM 8137275 ER PT J AU ANZANO, MA SMITH, JM USKOKOVIC, MR PEER, CW MULLEN, LT LETTERIO, JJ WELSH, MC SHRADER, MW LOGSDON, DL DRIVER, CL BROWN, CC ROBERTS, AB SPORN, MB AF ANZANO, MA SMITH, JM USKOKOVIC, MR PEER, CW MULLEN, LT LETTERIO, JJ WELSH, MC SHRADER, MW LOGSDON, DL DRIVER, CL BROWN, CC ROBERTS, AB SPORN, MB TI 1-ALPHA,25-DIHYDROXY-16-ENE-23-YNE-26,27-HEXAFLUOROCHOLECALCIFEROL (RO24-5531), A NEW DELTANOID (VITAMIN-D ANALOG) FOR PREVENTION OF BREAST-CANCER IN THE RAT SO CANCER RESEARCH LA English DT Note ID TAMOXIFEN; DIFFERENTIATION; CALCIUM; 1-ALPHA,25-DIHYDROXYVITAMIN-D3; CARCINOGENESIS; DISEASE; GROWTH; CELLS AB We have used the vitamin D analogue, 1alpha,25-dihydroxy-16-ene-23-yne-26,27-hexafluorocholecalciferol (Ro24-5531), for inhibition or mammary carcinogenesis induced by N-nitroso-N-methylurea (NMU) in Sprague-Dawley rats. Rats were first treated with a single dose of either 15 or 50 mg/kg body weight NMU and then fed Ro24-5531 (2.5 or 1.25 nmol/kg of diet) for 5-7 months. Ro24-5531 significantly extended tumor latency and lessened tumor incidence as well as tumor number in rats treated with the lower dose of NMU. In rats treated with the higher dose of NMU, Ro24-5531 was fed in combination with tamoxifen; in these experiments, Ro24-5531 significantly enhanced the ability of tamoxifen to reduce total tumor burden, as well as to increase the probability that an animal would be tumor free at the end of the experiment. In vitro, Ro24-5531 was 10-100 times more potent than 1,25-dihydroxyvitamin D3, for inhibition of proliferation of human breast cancer cell lines as well as primary cultures of cells from 2 patients with acute myelogenous leukemia. When fed chronically, Ro24-5531 did not elevate serum calcium in the present studies. We propose the new term, ''deltanoids,'' for the set of molecules composed of vitamin D and its synthetic analogues. in a manner similar to the naming of ''retinoids'' for the corresponding set of molecules related to vitamin A. C1 HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. NCI,FREDERICK CANC RES & DEV CTR,PRI DYN CORP,INVIVO CARCINOGENESIS PROGRAM,FREDERICK,MD 21702. NCI,BIOMETRY BRANCH,BETHESDA,MD 20892. RP ANZANO, MA (reprint author), NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892, USA. NR 25 TC 128 Z9 129 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 BP 1653 EP 1656 PG 4 WC Oncology SC Oncology GA ND238 UT WOS:A1994ND23800011 PM 8137276 ER PT J AU THIBAULT, A COOPER, MR FIGG, WD VENZON, DJ SARTOR, AO TOMPKINS, AC WEINBERGER, MS HEADLEE, DJ MCCALL, NA SAMID, D MYERS, CE AF THIBAULT, A COOPER, MR FIGG, WD VENZON, DJ SARTOR, AO TOMPKINS, AC WEINBERGER, MS HEADLEE, DJ MCCALL, NA SAMID, D MYERS, CE TI A PHASE-I AND PHARMACOKINETIC STUDY OF INTRAVENOUS PHENYLACETATE IN PATIENTS WITH CANCER SO CANCER RESEARCH LA English DT Article ID FETAL HEMOGLOBIN; DIFFERENTIATION; HYPERAMMONEMIA; ACID AB Phenylacetate has recently been shown to suppress tumor growth and promote differentiation in experimental models. A phase I trial of phenylacetate was conducted in 17 patients with advanced solid tumors. Each patient received a single i.v. bolus dose followed by a 14-day continuous i.v. infusion of the drug. Twenty-one cycles of therapy were administered at four dose levels, achieved by increasing the rate of the continuous i.v. infusion. Phenylacetate displayed nonlinear pharmacokinetics [K(m) = 105.1 +/- 44.5 (SD) mug/ml, V(max) = 24.1 +/- 5.2 mg/kg/h and V(d) = 19.2 +/- 3.3 L]. There was also evidence for induction of drug clearance. Ninety-nine % of phenylacetate elimination was accounted for by conversion to phenylacetylglutamine, which was excreted in the urine. Continuous i.v. infusion rates resulting in serum phenylacetate concentrations exceeding K(m) often resulted in rapid drug accumulation and dose-limiting toxicity, which consisted of reversible central nervous system depression, preceded by emesis. Three of nine patients with metastatic, hormone-refractory prostate cancer maintained stable prostatic specific antigen levels for more than 2 months; another had less bone pain. One of six patients with glioblastoma multiforme, whose steroid dosage has remained unchanged for the duration of therapy, has sustained functional improvement for more than 9 months. The use of adaptive control with feedback for the dosing of each patient enabled us to safely maintain stable phenylacetate concentrations up to the range of 200-300 mug/ml, which resulted in clinical improvement in some patients with advanced disease. C1 NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. RP THIBAULT, A (reprint author), NCI,CLIN PHARMACOL BRANCH,BLDG 10,ROOM 12C103,BETHESDA,MD 20892, USA. RI Venzon, David/B-3078-2008; Figg Sr, William/M-2411-2016 NR 16 TC 135 Z9 136 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 BP 1690 EP 1694 PG 5 WC Oncology SC Oncology GA ND238 UT WOS:A1994ND23800018 PM 8137283 ER PT J AU WEBER, J SALGALLER, M SAMID, D JOHNSON, B HERLYN, M LASSAM, N TREISMAN, J ROSENBERG, SA AF WEBER, J SALGALLER, M SAMID, D JOHNSON, B HERLYN, M LASSAM, N TREISMAN, J ROSENBERG, SA TI EXPRESSION OF THE MAGE-1 TUMOR-ANTIGEN IS UP-REGULATED BY THE DEMETHYLATING AGENT 5-AZA-2'-DEOXYCYTIDINE SO CANCER RESEARCH LA English DT Article ID TOXIC LYMPHOCYTES-T; HUMAN GENE MAGE-1; INFILTRATING LYMPHOCYTES; HUMAN-MELANOMA; DNA METHYLATION; CELL CLONES; RECOMBINANT INTERLEUKIN-2; ADOPTIVE IMMUNOTHERAPY; PROLIFERATE INVIVO; REJECTION ANTIGEN AB MAGE-1 is a gene that encodes an antigen on a melanoma cell line that is recognized by cytolytic T-cells. We have used a reverse transcription-polymerase chain reaction assay to analyze expression of the MAGE-1 gene by cell lines from different types of tumors, melanomas from different stages of disease progression, normal diploid cell lines, and melanocyte and nevus tissue from which malignant melanomas are derived. MAGE-1 is expressed by melanoma tissue from all stages of disease, but not melanocytes, nevus tissue, or any normal diploid cell line tested. A fraction of tumor lines derived from various epithelial and neuroectodermal malignancies expressed MAGE-1 but not peripheral blood cells from patients with melanoma. 5-Aza-2'-deoxycytidine (DAC), a demethylating agent, was capable of inducing MAGE-1 expression by a MAGE-1-negative melanoma cell line 888-mel as well as by a number of other melanoma cell lines. At an optimum concentration of 1 muM DAC, MAGE-1 expression was detectable by 24 h, plateaued by 72 h, but remained high for two weeks after removal of DAC from treated 888-mel cells, consistent with induction by demethylation. With the exception of tumor-infiltrating leukocytes, no normal diploid cell line could be induced with DAC to up-regulate MAGE-1 expression. DAC-treated 888-mel cells were lysed by a MAGE-1-specific major histocompatibility complex restricted cytolytic T-cell clone, whereas control untreated cells were not, suggesting that production of the antigen encoded by the MAGE-1 gene was induced by DAC and that it was presented in association with major histocompatibility complex class I molecules at the cell surface for T-cell recognition. C1 NCI,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. NCI,USN MED ONCOL BRANCH,BETHESDA,MD 20892. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. TORONTO BAYVIEW HOSP,TORONTO,ON,CANADA. RP WEBER, J (reprint author), NCI,SURG BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2B42,BETHESDA,MD 20892, USA. NR 48 TC 205 Z9 210 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 APR 1 PY 1994 VL 54 IS 7 BP 1766 EP 1771 PG 6 WC Oncology SC Oncology GA ND238 UT WOS:A1994ND23800030 PM 7511051 ER PT J AU FUTREAL, PA COCHRAN, C MARKS, JR IGLEHART, JD ZIMMERMAN, W BARRETT, JC WISEMAN, RW AF FUTREAL, PA COCHRAN, C MARKS, JR IGLEHART, JD ZIMMERMAN, W BARRETT, JC WISEMAN, RW TI MUTATION ANALYSIS OF THE THRA1 GENE IN BREAST-CANCER - DELETION FUSION OF THE GENE TO A NOVEL SEQUENCE ON 17Q IN THE BT474 CELL-LINE SO CANCER RESEARCH LA English DT Article ID FAMILIAL BREAST; P53 AB We have previously described a common region of deletion and allele loss on chromosome 17q in sporadic breast cancers that is likely to contain a tumor suppressor gene. The region, mapped to 17q12-q21, was bordered by D17S250 and D17S579 on the centromeric and telomeric sides, respectively. This deletion region overlaps the BRCA1 locus, which predisposes to familial breast and ovarian cancer. The most frequent loss of heterozygosity was observed at the thyroid hormone receptor alpha (THRA1) locus. Southern analysis revealed a rearrangement of THRA1 in the BT474 breast cancer cell line. This rearrangement represented a deletion of exons 8-10 of one THRA1 allele that was also coamplified with ERBB2. Northern blots showed two mutant transcripts in BT474 cells. Analysis of the mutant transcripts revealed fusion of the THRA1 exon 7 by splicing to a novel sequence designated BTR for ''BT474 transcribed rearrangement.'' BTR was found to be highly conserved and mapped to 17q. The deletion in BT474 cells spans the entire BRCAI region. To search for additional mutations in the THRA1 gene, all nine protein-encoding exons of THRA1 were examined for point mutations via single strand conformation analysis in a series of primary breast tumors, breast cancer cell lines, and lymphoblastoid cell lines derived from the youngest affected members of several German breast cancer families. No point mutations were detected, including the unrearranged THRA1 allele in BT474. We have thus excluded THRA1 as a commonly mutated sporadic breast cancer tumor suppressor gene and as the BRCA1 gene. C1 NIEHS,MOLEC CARCINOGENESIS LAB,MAIL DROP C4-06,BLDG 10,111 ALEXANDER DR,RES TRIANGLE PK,NC 27709. DUKE UNIV,DEPT SURG,DURHAM,NC 27706. FREE UNIV BERLIN,ROBERT KOCH INST,INST VIROL,W-1115 BERLIN,GERMANY. UNIV N CAROLINA,DEPT PATHOL,CHAPEL HILL,NC 27599. NR 21 TC 17 Z9 17 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 BP 1791 EP 1794 PG 4 WC Oncology SC Oncology GA ND238 UT WOS:A1994ND23800035 PM 7511052 ER PT J AU HAHN, SM KRISHNA, CM SAMUNI, A DEGRAFF, W CUSCELA, DO JOHNSTONE, P MITCHELL, JB AF HAHN, SM KRISHNA, CM SAMUNI, A DEGRAFF, W CUSCELA, DO JOHNSTONE, P MITCHELL, JB TI POTENTIAL USE OF NITROXIDES IN RADIATION ONCOLOGY SO CANCER RESEARCH LA English DT Article; Proceedings Paper CT 4th International Conference on Anticarcinogenesis and Radiation Protection: Mechanisms, Biomarkers, Molecular Diagnostics and Preventive Strategies CY APR 18-23, 1993 CL BALTIMORE, MD SP COCA COLA CO, HENKEL CORP, MARION MERRILL DOW INC, CANC RES FDN AMER, US DOE, NCI, NIEHS, JOHNS HOPKINS ENVIRONM HLTH SCI CTR ID SUPEROXIDE; DAMAGE; MICE; RADIOPROTECTOR; PROTECTION; INHIBITION; RADICALS; WR-2721; TISSUES; OXYGEN AB The identification of radioprotectors is an important goal for those involved in radiation oncology and for those interested in the investigation of the mechanisms of radiation cytotoxicity. Recently, a new class of in vitro and in vivo radioprotectors, the nitroxides, has been discovered. The nitroxides are low-molecular-weight stable free radicals which are freely membrane permeable and which have been shown to act as superoxide dismutase mimics. Further investigation of these compounds has shown that a water-soluble nitroxide, Tempol, protects cultured Chinese hamster V79 cells from the cytotoxicity caused by superoxide, hydrogen peroxide, and t-butyl hydroperoxide. Tempol and five other water-soluble nitroxides have also been shown to protect V79 cells against radiation-induced cytotoxicity. Potential mechanisms of protection by the nitroxides include oxidation of reduced transition metals, superoxide dismutase-like activity, and scavenging of oxy- and carbon-based free radicals. In vivo studies reveal that Tempol protects C3H mice from the lethal effects of radiation with a dose causing 50% lethality within 30 days of 9.97 Gy and 7.84 Gy in Tempol-treated and saline-treated mice, respectively, and a dose modification factor of 1.3. The nitroxides represent a new class of non-thiol radioprotectors which may also have application as general antioxidants. Additional work is necessary to screen other nitroxides for in vivo radio-protection and toxicity as well as to fully evaluate the extent to which these compounds protect tumors. C1 NCI,RADIAT BIOL SECT,BETHESDA,MD 20892. HEBREW UNIV JERUSALEM,SCH MED,IL-91010 JERUSALEM,ISRAEL. RP HAHN, SM (reprint author), NCI,RADIAT ONCOL BRANCH,9000 ROCKVILLE PIKE,BLDG 10,ROOM B3B69,BETHESDA,MD 20892, USA. NR 43 TC 65 Z9 68 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 APR 1 PY 1994 VL 54 IS 7 SU S BP S2006 EP S2010 PG 5 WC Oncology SC Oncology GA NE168 UT WOS:A1994NE16800030 ER PT J AU HELZLSOUER, KJ BLOCK, G BLUMBERG, J DIPLOCK, AT LEVINE, M MARNETT, LJ SCHULPLEIN, RJ SPENCE, JT SIMIC, MG AF HELZLSOUER, KJ BLOCK, G BLUMBERG, J DIPLOCK, AT LEVINE, M MARNETT, LJ SCHULPLEIN, RJ SPENCE, JT SIMIC, MG TI SUMMARY OF THE ROUND-TABLE DISCUSSION ON STRATEGIES FOR CANCER PREVENTION - DIET, FOOD, ADDITIVES, SUPPLEMENTS, AND DRUGS SO CANCER RESEARCH LA English DT Article ID LARGE-BOWEL CANCER; BETA-CAROTENE; ASCORBIC-ACID; COLON CANCER; ASPIRIN USE; VITAMIN-E; RISK; SAFETY; FOLATE AB A Round Table Discussion was held at the Fourth International Conference on Anticarcinogenesis and Radiation Protection. Scientists from government and academia were brought together to discuss the evidence for the preventive effect of foods, specific nutrients and drugs against cancer, and the most appropriate methods of initiating nutritional cancer prevention activities to improve the health of the public. The panel reviewed the epidemiological evidence of the role of diet and specific micronutrients for the prevention of cancer, the doses of specific micronutrients required for preventive effects and their safety, the evidence for aspirin as a chemopreventive agent, the issue of foods versus specific micronutrients in the prevention of cancer, food safety, and approaches to prevention such as food fortification or dietary supplements. The remarks of the panel members are summarized. C1 UNIV LONDON, GUYS HOSP, DIV BIOCHEM & MOLEC BIOL, FREE RAD RES GRP, LONDON SE1 9RJ, ENGLAND. NIDDKD, CELL BIOL & GENET, BETHESDA, MD USA. VANDERBILT UNIV, MED CTR,SCH MED,DEPT BIOCHEM, AB HANCOCK JR MEM LAB CANC RES, NASHVILLE, TN 37232 USA. US FDA, CTR FOOD SAFETY & APPL NUTR, WASHINGTON, DC 20204 USA. USDA, BELTSVILLE HUMAN NUTR RES CTR, BELTSVILLE, MD 20705 USA. UNIV PENN, DEPT RADIAT ONCOL, PHILADELPHIA, PA 19104 USA. UNIV CALIF BERKELEY, SCH PUBL HLTH, DEPT SOCIAL & ADM HLTH SCI, BERKELEY, CA 94720 USA. TUFTS UNIV, USDA, HUMAN NUTR RES CTR AGING, BOSTON, MA 02111 USA. RP HELZLSOUER, KJ (reprint author), JOHNS HOPKINS UNIV, SCH HYG & PUBL HLTH, DEPT EPIDEMIOL, 615 N WOLFE ST, BALTIMORE, MD 21205 USA. RI Block, Gladys/E-3304-2010 NR 38 TC 21 Z9 21 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 EI 1538-7445 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 SU S BP S2044 EP S2051 PG 8 WC Oncology SC Oncology GA NE168 UT WOS:A1994NE16800037 ER PT J AU KELLOFF, GJ BOONE, CW STEELE, VE CROWELL, JA LUBET, R SIGMAN, CC AF KELLOFF, GJ BOONE, CW STEELE, VE CROWELL, JA LUBET, R SIGMAN, CC TI PROGRESS IN CANCER CHEMOPREVENTION - PERSPECTIVES ON AGENT SELECTION AND SHORT-TERM CLINICAL INTERVENTION TRIALS SO CANCER RESEARCH LA English DT Article; Proceedings Paper CT 4th International Conference on Anticarcinogenesis and Radiation Protection: Mechanisms, Biomarkers, Molecular Diagnostics and Preventive Strategies CY APR 18-23, 1993 CL BALTIMORE, MD SP COCA COLA CO, HENKEL CORP, MARION MERRILL DOW INC, CANC RES FDN AMER, US DOE, NCI, NIEHS, JOHNS HOPKINS ENVIRONM HLTH SCI CTR ID EPITHELIAL-CELL PROLIFERATION; INDUCED MAMMARY-TUMORS; D-LIMONENE; ORAL LEUKOPLAKIA; CERVICAL-CANCER; COLON CANCER; HIGH-RISK; BLADDER-CANCER; BETA-CAROTENE; BREAST-CANCER AB The basic cancer-related chemical and biological sciences, pathology, and epidemiology have contributed to the understanding that anti-mutagenesis and antiproliferation are the important general mechanisms of chemoprevention and to the development of antimutagenic and anti-proliferative agents as potential chemopreventive drugs. These disciplines have also provided the biochemical and histopathological bases for identifying intermediate biomarkers that can be used as surrogate end points for cancer incidence in clinical chemoprevention trials and for selecting cohorts for these trials. Particularly important as histological biomarkers of cancer are the cytonuclear morphological and densitometric changes that define intraepithelial neoplasia (IEN). IEN changes are on the causal pathway to cancer. They may serve as target lesions in Phase II chemoprevention trials and as standards against which other earlier cellular and molecular biomarkers can be evaluated. Strategies for the clinical evaluation of chemopreventive agents have been defined for seven targets-colorectal, prostate, lung, breast, bladder, oral, and cervical cancers. Cohorts have been identified for short-term Phase II trials that investigate the effects of chemopreventive agents on IEN and on earlier biomarkers. Patients with adenomas serve as a cohort for trials in colon. One cohort for Phase II trials in prostate is patients with early stage cancers scheduled for prostatectomy; another is patients with prostatic intraepithelial neoplasia (without prostatic carcinoma). Patients treated for lung cancer are at high risk for bronchial dysplasia and second cancers; such patients are a cohort for Phase II trials in lung cancer. Presurgical breast cancer patients and patients with ductal or lobular carcinoma in situ are cohorts for studies in breast. Patients with superficial bladder cancers (T(a)/T1 with or without carcinoma in situ) are cohorts for studies of chemoprevention in bladder, and patients with dysplastic oral leukoplakia are evaluated for chemoprevention of oral cancers. Cervical intraepithelial neoplasia is a prototype IEN, and patients with cervical intraepithelial neoplasia are a cohort for studies of cervical cancer. C1 CCS ASSOCIATES,PALO ALTO,CA 94300. RP KELLOFF, GJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT INVEST DRUG UNIT,BETHESDA,MD 20892, USA. NR 104 TC 133 Z9 132 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 SU S BP S2015 EP S2024 PG 10 WC Oncology SC Oncology GA NE168 UT WOS:A1994NE16800032 ER PT J AU LUETHY, JD HOLBROOK, NJ AF LUETHY, JD HOLBROOK, NJ TI THE PATHWAY REGULATING GADD153 INDUCTION IN RESPONSE TO DNA-DAMAGE IS INDEPENDENT OF PROTEIN-KINASE-C AND TYROSINE KINASES SO CANCER RESEARCH LA English DT Article; Proceedings Paper CT 4th International Conference on Anticarcinogenesis and Radiation Protection: Mechanisms, Biomarkers, Molecular Diagnostics and Preventive Strategies CY APR 18-23, 1993 CL BALTIMORE, MD SP COCA COLA CO, HENKEL CORP, MARION MERRILL DOW INC, CANC RES FDN AMER, US DOE, NCI, NIEHS, JOHNS HOPKINS ENVIRONM HLTH SCI CTR ID PROMOTER OKADAIC ACID; GENE-EXPRESSION; IONIZING-RADIATION; ACTIVATION; FOS; INHIBITION; AGENTS; CELLS; JUN; UV AB Treatment of cells with agents that damage DNA leads to the induction of numerous genes. Recent studies aimed at understanding the events preceding the transcriptional activation of some of these DNA damage-inducible genes in mammalian cells have demonstrated that various extranuclear protein kinases are involved in the signaling cascades. The mammalian GADD153 gene, a member of the CCAAT enhancer-binding protein family of transcription factors, is highly induced by a variety of DNA-damaging agents as well as by certain growth arrest conditions and oxidative stresses. We have examined the effects of numerous protein kinase and phosphatase inhibitors on the DNA damage-induced expression of GADD153, to identify the signal transduction components involved in its transcriptional regulation. In contrast to the transcriptional activation of c-jun and collagenase in response to DNA damage, GADD153 induction involves neither protein kinase C nor tyrosine kinases but does appear to require an unidentified serine-threonine kinase. Elevation of intracellular glutathione levels by treatment with N-acetylcysteine did not affect the methyl methanesulfonate-induced expression of the GADD153 gene, although it did diminish cadmium chloride-induced expression. These findings suggest that oxidative stress and DNA damage regulate GADD153 transcription through different pathways. Based on our findings and those of others with respect to other DNA damage-inducible genes, we propose a model depicting the complex pathways which appear to be involved in the regulation of mammalian genes in response to genotoxic stress and in which the DNA damage-induced expression of GADD153 represents a unique pathway independent of either protein kinase C or tyrosine kinase. C1 NIA,MOLEC GENET LAB,4940 EASTERN AVE,BALTIMORE,MD 21224. NR 35 TC 31 Z9 31 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 SU S BP S1902 EP S1906 PG 5 WC Oncology SC Oncology GA NE168 UT WOS:A1994NE16800008 ER PT J AU SCHIFFMAN, MH SCHATZKIN, A AF SCHIFFMAN, MH SCHATZKIN, A TI TEST RELIABILITY IS CRITICALLY IMPORTANT TO MOLECULAR EPIDEMIOLOGY - AN EXAMPLE FROM STUDIES OF HUMAN PAPILLOMAVIRUS INFECTION AND CERVICAL NEOPLASIA SO CANCER RESEARCH LA English DT Article; Proceedings Paper CT 4th International Conference on Anticarcinogenesis and Radiation Protection: Mechanisms, Biomarkers, Molecular Diagnostics and Preventive Strategies CY APR 18-23, 1993 CL BALTIMORE, MD SP COCA COLA CO, HENKEL CORP, MARION MERRILL DOW INC, CANC RES FDN AMER, US DOE, NCI, NIEHS, JOHNS HOPKINS ENVIRONM HLTH SCI CTR ID RISK-FACTORS; CANCER AB To demonstrate that it is critically important to achieve excellent test reliability before conducting full-scale molecular epidemiological studies, data were compared from two consecutive case-control studies of human papillomavirus (HPV) infection and cervical intraepithelial neoplasia. The major methodological difference between the two studies was the much greater reliability of the HPV test used in the second study. Although the first study used an assay considered state-of-the-art at that time, mediocre test reliability led to (a) a weakened association between HPV and risk of cervical intraepithelial neoplasia, (b) a weakened association between known risk factors for cervical intraepithelial neoplasia and HPV prevalence, (c) failure to demonstrate that HPV infection explains the known risk factors for cervical intraepithelial neoplasia, and (d) a marked reduction in the estimated proportion of cervical intraepithelial neoplasia attributable to HPV infection. With an improved assay, the second study strongly supported the idea that HPV infection is an intermediate end point explaining the known epidemiology of cervical intraepithelial neoplasia. Based on this experience and supportive theoretical considerations, we recommend that researchers optimize the reliability of innovative assays before application to full-scale molecular epidemiological projects. C1 NCI,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. RP SCHIFFMAN, MH (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892, USA. NR 23 TC 49 Z9 51 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 SU S BP S1944 EP S1947 PG 4 WC Oncology SC Oncology GA NE168 UT WOS:A1994NE16800017 PM 7794294 ER PT J AU TAYLOR, PR LI, B DAWSEY, SM LI, JY YANG, CS GUO, WD BLOT, WJ LI, JY WENG, W LIU, BQ ZHENG, SF YANG, Q YU, Y SUN, Y LI, GY LIU, SF ZHOU, XN WU, YP WANG, Z LU, SX ZHANG, YH YANG, K YANG, G CHEN, Z WANG, ZY ZHENG, DH LIAN, GT TANGREA, JA ERSHOW, AG MARK, SD GAIL, M STONE, BJ FRAUMENI, JF GREENWALD, P YANG, CS LEWIN, K NIEBERG, R WEINER, M WEINSTEIN, W ENGSTROM, P CORREA, P LAGAKOS, S AF TAYLOR, PR LI, B DAWSEY, SM LI, JY YANG, CS GUO, WD BLOT, WJ LI, JY WENG, W LIU, BQ ZHENG, SF YANG, Q YU, Y SUN, Y LI, GY LIU, SF ZHOU, XN WU, YP WANG, Z LU, SX ZHANG, YH YANG, K YANG, G CHEN, Z WANG, ZY ZHENG, DH LIAN, GT TANGREA, JA ERSHOW, AG MARK, SD GAIL, M STONE, BJ FRAUMENI, JF GREENWALD, P YANG, CS LEWIN, K NIEBERG, R WEINER, M WEINSTEIN, W ENGSTROM, P CORREA, P LAGAKOS, S TI PREVENTION OF ESOPHAGEAL CANCER - THE NUTRITION INTERVENTION TRIALS IN LINXIAN, CHINA SO CANCER RESEARCH LA English DT Article AB In Linxian China, the esophageal/gastric cardia cancer mortality rates are among the highest in the world. There is suspicion that the population's chronic deficiencies of multiple micronutrients are etiologically involved. We conducted two randomized, placebo-controlled nutrition intervention trials to test the effects of vitamin and mineral supplements in lowering the rates of esophageal/gastric cancer. In the first trial, the dysplasia trial, 3318 adults with a cytological diagnosis of esophageal dysplasia received daily supplementation with 26 vitamins and minerals in doses typically 2-3 times the United States Recommended Daily Allowances, or placebos, for 6 years. The second trial, the general population trial, involved 29,584 adults and used a one-half replicate of a 2(4) factorial experimental design which tested the effects of four combinations of nutrients: A, retinol and zinc; B, riboflavin and niacin; C, vitamin C and molybdenum; and D, beta-carotene, vitamin E, and selenium. Doses for these daily supplements ranged from 1 to 2 times the United States Recommended Daily Allowances, and the different vitamin/mineral combinations or placebos were taken for a period of 5.25 years. As part of the general population trial, and end-of-intervention endoscopy survey was carried out in a small (1.3%) sample of subjects to see if supplementation affected the prevalence of dysplasia and early cancer. Herein we review the methods of these trials and the results of the endoscopic survey. Fifteen esophageal and 16 gastric cancers were identified in endoscopic biopsies from the 391 subjects evaluated from two villages, and nearly all were asymptomatic. No significant reductions in the prevalence of esophageal or gastric dysplasia or cancer were seen with any of the four supplement groups. However, the prevalence of gastric cancer among participants receiving retinol and zinc was 62% lower than those not receiving those supplements (P = 0.09), while participants receiving beta-carotene, vitamin E, and selenium had a 42% reduction in esophageal cancer prevalence (0.34). We have reported separately that cancer mortality over the entire 5.25-year period was significantly reduced among those receiving beta-carotene, vitamin E, and selenium. The findings from the overall trial and the endoscopic sample offer a hopeful sign and should encourage additional studies with these agents in larger numbers of subjects. C1 RUTGERS STATE UNIV, PISCATAWAY, NJ 08854 USA. LINXIAN BUR PUB HLTH, LINXIAN, PEOPLES R CHINA. ESOPHAGEAL CANC INST, LINXIAN, PEOPLES R CHINA. UNIV CALIF LOS ANGELES, LOS ANGELES, CA USA. FOX CHASE CANC CTR, PHILADELPHIA, PA 19111 USA. LOUISIANA STATE UNIV, MED CTR, BATON ROUGE, LA 70803 USA. HARVARD UNIV, SCH PUBL HLTH, BOSTON, MA 02115 USA. CHINESE ACAD MED SCI, INST CANC, BEIJING, PEOPLES R CHINA. HENAN MED UNIV, ZHENGZHOU, PEOPLES R CHINA. RP TAYLOR, PR (reprint author), NCI, EPN ROOM 211, BETHESDA, MD 20892 USA. NR 14 TC 97 Z9 97 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1994 VL 54 IS 7 SU S BP S2029 EP S2031 PG 3 WC Oncology SC Oncology GA NE168 UT WOS:A1994NE16800034 ER PT J AU WESTON, A LINGCAWLEY, HM CAPORASO, NE BOWMAN, ED HOOVER, RN TRUMP, BF HARRIS, CC AF WESTON, A LINGCAWLEY, HM CAPORASO, NE BOWMAN, ED HOOVER, RN TRUMP, BF HARRIS, CC TI DETERMINATION OF THE ALLELIC FREQUENCIES OF AN L-MYC AND A P53 POLYMORPHISM IN HUMAN LUNG-CANCER SO CARCINOGENESIS LA English DT Article ID FRAGMENT-LENGTH-POLYMORPHISM; GENETIC-LINKAGE MAP; RARE ALLELES; LOCUS; METASTASIS AB The L-myc and p53 genes have been implicated in lung cancer. Both of these genes have restriction fragment length polymorphisms (RFLPs) that could account for differential expression or activity of variant forms. An EcoRI restriction site in the L-myc gene was previously reported to be a predictor of poor prognosis in Japanese lung cancer patients. There are several RFLPs in the p53 gene. In exon 4 there is a polymorphism that codes for either an arginine or proline residue at codon 72. We previously reported the frequency of DNA-RFLPs at these gene loci revealed by EcoRI and AccII respectively. Here we report results from a study comparing lung cancer cases (n = 31) with chronic obstructive pulmonary disease controls (n = 49). No association was found between these RFLPs and disease status. Previous observations that the frequencies of these RFLPs varied by race were confirmed. The p53 arginine allele was found to be more common in Caucasians (0.71) than African-Americans (0.50). The EcoRI restriction site present allele in L-myc was more frequent in African-Americans (0.71) than Caucasians (0.49). Thus, the allelic frequency for L-myc was similar in African-Americans to that reported for Japanese, and the allelic frequency for p53 was similar in Caucasians to that reported for Japanese. C1 NCI, HUMAN CARCINOGENESIS LAB, BETHESDA, MD 20892 USA. NCI, GENET EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. NCI, ENVIRONM EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. UNIV MARYLAND, SCH MED, DEPT PATHOL, BALTIMORE, MD 21201 USA. NR 41 TC 89 Z9 91 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 EI 1460-2180 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1994 VL 15 IS 4 BP 583 EP 587 DI 10.1093/carcin/15.4.583 PG 5 WC Oncology SC Oncology GA NE665 UT WOS:A1994NE66500004 PM 7908608 ER PT J AU SONE, T ZUKOWSKI, K LAND, SJ KING, CM MARTIN, BM POHL, LR WANG, CY AF SONE, T ZUKOWSKI, K LAND, SJ KING, CM MARTIN, BM POHL, LR WANG, CY TI CHARACTERISTICS OF A PURIFIED DOG HEPATIC-MICROSOMAL N,O-ACYLTRANSFERASE SO CARCINOGENESIS LA English DT Article ID URINARY-BLADDER; CARCINOGENIC ARYLAMINES; GLYCOPROTEIN ESTERASE; UROTHELIAL CELLS; REPAIR SYNTHESIS; RAT-LIVER; DNA; PURIFICATION; DERIVATIVES; ACETYLATION AB Dog liver microsomes have at least three different enzymes that are capable of the deacylation of amides, N-arylhydroxamic acids and carboxylesters, the acyltransfer of N-arylhydroxamic acids and the N-acetylation of arylamines. As judged by SDS - PAGE stained with silver nitrate, one of these enzymes was purified to homogeneity by sequential treatment with Triton X-100, ion-exchange column chromatography, gel filtration and chromatofocusing. The protein was a glycoprotein trimer with a subunit weight of similar to 60 kDa. It showed microheterogeneity on analytical isoelectric focusing (IEF) in polyacrylamide with pls of 5.4-5.6. Following digestion with endoglycosidase H, its subunit weight was reduced to similar to 58 kDa, and it appeared to be homogeneous on IEF with a pi of similar to 5.6. A monoclonal antibody prepared against this enzyme also reacted with the pi 6.0 carboxylesterase of rat liver microsomes, but did not react with the other two dog hepatic acyltransferases. Conversely, a polyclonal antibody raised against the rat esterase reacted with the dog enzyme. The N-terminal sequence of the enzyme was Y-P-S-GP-P-V-V-D-T-V-Q-G-K-V-, which was homologous to the form 1 carboxylesterase of rabbit liver and the pl 6.0 carboxylesterase of rat liver. Immunohistochemical analyses showed the presence of this enzyme in the epithelium of dog liver and urinary bladder, human liver and rat liver, esophagus, forestomach, glandular stomach, small and large intestines, renal tubules, trachea and prostate and alveolar cells of lung. Since this enzyme is present in the urothelium, it may be important for the activation of urinary metabolites of carcinogenic arylamines for the initiation of bladder carcinogenesis in the dog. C1 MICHIGAN CANC FDN,DEPT CHEM CARCINOGENESIS,DETROIT,MI 48201. NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA 23800, CA 23386] NR 34 TC 6 Z9 6 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1994 VL 15 IS 4 BP 595 EP 599 DI 10.1093/carcin/15.4.595 PG 5 WC Oncology SC Oncology GA NE665 UT WOS:A1994NE66500006 PM 8149467 ER PT J AU DAVIS, CD SCHUT, HAJ SNYDERWINE, EG AF DAVIS, CD SCHUT, HAJ SNYDERWINE, EG TI ADDUCTION OF THE HETEROCYCLIC AMINE FOOD MUTAGENS IQ AND PHIP TO MITOCHONDRIAL AND NUCLEAR-DNA IN THE LIVER OF FISCHER-344 RATS SO CARCINOGENESIS LA English DT Article ID COOKED FOOD; CARCINOGEN; REPAIR; CELLS; BINDING; 2-AMINO-1-METHYL-6-PHENYLIMIDAZO<4,5-B>PYRIDINE; 2-AMINO-3-METHYLIMIDAZO<4,5-F>QUINOLINE; IDENTIFICATION; AFLATOXIN-B1; MUTATIONS AB The heterocyclic amines 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) are carcinogens that form DNA adducts. In the present study, we used the P-32-postlabeling method to measure the levels of IQ and PhIP adducts in hepatic nuclear and mitochondrial DNA of Fischer-344 rats given a single dose (100 mg/kg, p.o.) or 10 doses of either carcinogen. After a single dose of IQ, adduct levels were > 2-fold higher in hepatic nuclear than in mitochondrial DNA; however, after repeated IQ exposure, the levels of adducts in nuclear and mitochondrial DNA were not significantly different. In contrast, after a single dose of PhIP, there were no significant differences in adduct levels in nuclear and mitochondrial DNA; however, after multiple doses of PhIP, adduct levels were significantly higher in mitochondrial DNA than in nuclear DNA. The percentages of individual IQ or PhIP adducts were different between nuclear DNA and mitochondrial DNA, particularly after 10 doses. With IQ, the C8-guanine adduct accounted for 72% of the total IQ adduct levels in nuclear DNA but only 40% of total adduct levels in mitochondrial DNA. After 10 doses of PhIP, the C8-guanine adduct accounted for 48% and 15% of total adduct levels in nuclear DNA and mitochondrial DNA respectively. In addition, the percentage of an uncharacterized PhIP adduct was 14% in nuclear DNA but <1% in mitochondrial DNA. The percentages of individual adducts were approximately the same 3, 24, 120 and 240 h after a single dose of either compound, though total IQ and PhIP adduct levels appeared to decline over time in both organelles. The significance of IQ and PhIP mitochondrial DNA adduction and the influence of distinct heterocyclic amine adducts on carcinogenesis merit further investigation. C1 MED COLL OHIO,DEPT PATHOL,TOLEDO,OH 43614. RP DAVIS, CD (reprint author), NCI,EXPTL CARCINOGENESIS LAB,BETHESDA,MD 20892, USA. NR 39 TC 21 Z9 21 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1994 VL 15 IS 4 BP 641 EP 645 DI 10.1093/carcin/15.4.641 PG 5 WC Oncology SC Oncology GA NE665 UT WOS:A1994NE66500013 PM 8149474 ER PT J AU KANEDA, K PILARO, AM SAYERS, TJ NAGASHIMA, K GONDA, MA ORTALDO, JR WILTROUT, RH AF KANEDA, K PILARO, AM SAYERS, TJ NAGASHIMA, K GONDA, MA ORTALDO, JR WILTROUT, RH TI QUANTITATIVE-ANALYSIS OF ROD-CORED VESICLES AND DENSE GRANULES OF LARGE GRANULAR LYMPHOCYTES IN THE LIVER, SPLEEN, AND PERIPHERAL-BLOOD OF RATS SO CELL AND TISSUE RESEARCH LA English DT Article DE ROD-CORED VESICLES; GRANULES; LYMPHOCYTES; LIVER; ELECTRON MICROSCOPY; RAT (FISCHER F344/NCR) ID NATURAL-KILLER ACTIVITY; BIOLOGICAL RESPONSE MODIFIERS; PIT CELLS; TISSUE LOCALIZATION; AUGMENTATION; PROLIFERATION; SINUSOIDS; MICE AB Large granular lymphocytes (LGL) comprise a natural defense system in the liver and exert an inhibitory effect on tumor cell metastasis. In order to demonstrate the maturation of LGL in the liver from the morphological aspect, we evaluated electron-microscopically the frequency of 0.2 mu m vesicles (rod-cored and ''empty'' vesicles) and dense granules in LGL from the liver, spleen, and peripheral blood of the rat. Both of these cell organelles are characteristic to LGL and may relate to natural killer-mediated cytolysis. On the average, there were 12.7 of the 0.2 mu m vesicles and 4.3 rod-cored vesicles (RCV) per cell section in the liver, 6.6 0.2 mu m vesicles and 1.6 RCV in the spleen, and 8.6 0.2 mu m vesicles and 0.9 RCV in the peripheral blood. The number of 0.2 mu m vesicles per cell section ranged from 0 to 19 with the exception of a few higher instances. Therefore, LGL were divided into vesicle-rich (>9 0.2 mu m vesicles per cell section) and vesicle-poor (<8 per cell section) populations. Hepatic LGL consisted mainly of a vesicle-rich population while splenic LGL consisted mainly of a vesicle-poor population, and peripheral blood contained equal proportions of both populations. In addition to diversity with regard to the number of 0.2 mu m vesicles, LGL obtained from various organs also displayed heterogeneity in the number and size of dense granules. Since the number of dense granules per cell section usually ranged from 1, to 13, LGL were divided into 2 populations, i.e., LGL with many (>7 per cell section) granules and those with a few (<6 per cell section) granules. Specifically, splenic LGL had a few small (average diameter, less than 400 nm) dense granules, while sections of LGL from the granules and a few large (>400 nm) ones, respectively, in addition to the populations seen in the spleen. Thus, the present study has demonstrated a difference in the distribution of 0.2 mu m vesicles in LGL based on the tissue of origin. The present study has revealed the difference in the distribution of 0.2 mu m vesicles of LGL by tissue and indicated that immature LGL are predominant in the spleen, while hepatic LGL are generally more mature as defined by the number of vesicles. These data suggest that the microenvironment of the liver may contribute to the increased expression of these vesicles in LGL. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DYNCORP INC,PROGRAM RESOURCES INC,CELL & MOLEC STRUCT LAB,FREDERICK,MD. RI Sayers, Thomas/G-4859-2015 NR 18 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0302-766X J9 CELL TISSUE RES JI Cell Tissue Res. PD APR PY 1994 VL 276 IS 1 BP 187 EP 195 DI 10.1007/BF00354799 PG 9 WC Cell Biology SC Cell Biology GA MZ694 UT WOS:A1994MZ69400023 PM 8187160 ER PT J AU STEEL, JH MARTINEZ, A SPRINGALL, DR TRESTON, AM CUTTITTA, F POLAK, JM AF STEEL, JH MARTINEZ, A SPRINGALL, DR TRESTON, AM CUTTITTA, F POLAK, JM TI PEPTIDYLGLYCINE ALPHA-AMIDATING MONOOXYGENASE (PAM) IMMUNOREACTIVITY AND MESSENGER-RNA IN HUMAN PITUITARY AND INCREASED EXPRESSION IN PITUITARY-TUMORS SO CELL AND TISSUE RESEARCH LA English DT Article DE PITUITARY; TUMORS; PEPTIDYLGLYCINE ALPHA-AMIDATING MONOOXYGENASE; IMMUNOCYTOCHEMISTRY; IN SITU HYBRIDIZATION; HUMAN ID VASOACTIVE INTESTINAL POLYPEPTIDE; RAT ANTERIOR-PITUITARY; NEUROMEDIN-B; SUBSTANCE-P; PEPTIDE; HORMONE; CELLS; SECRETION; MANIPULATIONS; LOCALIZATION AB Bioactivity of many peptides depends upon post-translational alpha-amidation of inactive precursors by two enzyme activities known collectively as peptidylglycine alpha-amidating monooxygenase (PAM). PAM enzymes are particularly abundant in the pituitary. The distribution of PAM immunoreactivity and messenger ribonucleic acid (mRNA) in the adult human pituitary and in pituitary tumours was investigated by use of immunocytochemistry and in situ hybridisation. Immunoreactivity was present in numerous cells of the anterior lobe: staining was intense in a proportion of gonadotrophs and folliculo-stellate cells, but weaker in the majority of somatotrophs and lactotrophs, a few corticotrophs and occasional thyrotrophs. PAM staining was also present in nerves, pituicytes and some endocrine cells within the posterior lobe (the human intermediate zone). Forty pituitary tumours of various types were immunoreactive for PAM; more intensely and uniformly stained than normal anterior lobe. In situ hybridisation with digoxigenin-labelled probes demonstrated intense labelling for PAM mRNA in numerous cells in normal anterior pituitary and in tumours. Many regulatory peptides that require amidation for activity, potential targets for PAM, are present in the pituitary. Many tumour growth factors also require amidation and PAM may regulate these mitogenic peptides in tumours. C1 UNIV NAVARRA,DEPT HISTOL & PATHOL ANAT,PAMPLONA,SPAIN. NCI,DIV CANC PREVENT & CONTROL,ROCKVILLE,MD 20850. RP STEEL, JH (reprint author), ROYAL POSTGRAD MED SCH,DEPT HISTOCHEM,DU CANE RD,LONDON W12 0NN,ENGLAND. RI Martinez, Alfredo/A-3077-2013; Steel, Jennifer/B-4737-2013 OI Martinez, Alfredo/0000-0003-4882-4044; Steel, Jennifer/0000-0003-4439-0090 NR 36 TC 22 Z9 22 U1 1 U2 5 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0302-766X J9 CELL TISSUE RES JI Cell Tissue Res. PD APR PY 1994 VL 276 IS 1 BP 197 EP 207 DI 10.1007/BF00354800 PG 11 WC Cell Biology SC Cell Biology GA MZ694 UT WOS:A1994MZ69400024 PM 8187161 ER PT J AU JHAPPAN, C TAKAYAMA, H DICKSON, RB MERLINO, G AF JHAPPAN, C TAKAYAMA, H DICKSON, RB MERLINO, G TI TRANSGENIC MICE PROVIDE GENETIC-EVIDENCE THAT TRANSFORMING GROWTH-FACTOR-ALPHA PROMOTES SKIN TUMORIGENESIS VIA H-RAS-DEPENDENT AND H-RAS-INDEPENDENT PATHWAYS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID MOUSE SKIN; TGF-ALPHA; HUMAN KERATINOCYTES; SIGNAL TRANSDUCTION; PAPILLOMA FORMATION; MENETRIERS DISEASE; TUMOR PROGRESSION; PHORBOL ESTERS; MAMMARY-GLAND; LIVER-TUMORS AB The epidermal growth factor receptor (EGFR), which mediates the mitogenic activity of transforming growth factor alpha (TGF-alpha), has been shown to activate Ras in cultured cells through well-defined intermediary proteins. To examine the in vivo relationship between EGFR and Ras, chemical carcinogenesis of TGF-alpha transgenic mouse skin was chosen as an experimental model. Transgenic mice overexpressing TCF-alpha in a wide variety of epithelial tissues by virtue of a metallothionein promoter demonstrate a multitude of premalignant and neoplastic lesions but not spontaneous skin tumors. Transgenic skin was initiated with a single dose of 7,12-dimethylbenz[a]anthracene (DMBA), shown previously to induce, in concert with a tumor promoter, murine papillomas that consistently contain specific H-ras mutations. Virtually all DMBA-treated TGF-alpha transgenic mice, but not treated control animals, developed hyperplasias, papillomas, sebaceous adenomas, and more infrequently, sebaceous and squamous cell carcinomas. Therefore, TGF-alpha functions as an autonomous tumor promoter in DMBA-initiated transgenic skin. Skin tumors could be separated into two mutually exclusive genetic classes. In tumors harboring mutant H-ras, TGF-alpha transgene expression was relatively low and essentially unchanged relative to untreated skin; however, only 42% of skin tumors contained mutations in H-ras. Conversely, in most tumors with wild-type H-ras, transgenic TGF-alpha transcripts were enhanced 10- to 20-fold. These results suggest that strong constitutive EGFR stimulation, through TGF-alpha transgene overexpression, can substitute functionally for mutational activation of H-ras in skin tumorigenesis. Moreover, because H-ras mutational activation could not induce skin tumors without TGF-alpha transgene activity, simultaneous stimulation of an EGFR-mediated H-Ras-independent pathway appears to be required for tumor development as well. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,DEPT ANAT & CELL BIOL,WASHINGTON,DC 20007. NR 68 TC 46 Z9 46 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 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD APR PY 1994 VL 5 IS 4 BP 385 EP 394 PG 10 WC Cell Biology SC Cell Biology GA NF150 UT WOS:A1994NF15000005 PM 8043512 ER PT J AU GIVOL, I TSARFATY, I RESAU, J SHEN, RL DASILVA, PP NASIOULAS, G DUHADAWAY, J HUGHES, SH EWERT, DL AF GIVOL, I TSARFATY, I RESAU, J SHEN, RL DASILVA, PP NASIOULAS, G DUHADAWAY, J HUGHES, SH EWERT, DL TI BCL-2 EXPRESSED USING A RETROVIRAL VECTOR IS LOCALIZED PRIMARILY IN THE NUCLEAR-MEMBRANE AND THE ENDOPLASMIC-RETICULUM OF CHICKEN-EMBRYO FIBROBLASTS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID PROGRAMMED CELL-DEATH; HUMAN FOLLICULAR LYMPHOMA; PRE-B-CELLS; C-MYC; TRANSGENIC MICE; CHROMOSOMAL BREAKPOINT; DEREGULATED BCL2; PROTEIN; GENE; SURVIVAL AB A complementary DNA for human bcl-2 was cloned into the replication competent avian retrovirus vector RCASBP, and the resulting virus was used to express human Bcl-2 protein at high levels in chicken embryo fibroblasts. The expression of Bcl-2 did not transform or significantly alter the longevity of the chicken embryo fibroblasts in the presence of normal amounts of serum. However, the expression of Bcl-2 blocked c-Myc-induced apoptosis in these cells. Fractionation of the infected chicken embryo fibroblasts indicated that the protein was distributed equally between nuclear and high density cytoplasmic membranes. Immunofluorescence analysis by confocal microscopy and immunoelectron microscopy showed that the Bcl-2 protein was primarily associated with the nuclear membrane and with the endoplasmic reticulum. Reduced amounts of the protein were associated with other membranes in the cytoplasm. These data show that, in this system, the Bcl-2 protein associates with the nuclear membrane and intracytoplasmic membranes but is not preferentially associated with mitochondria. C1 NCI,FREDERICK CANC RES & DEV CTR,ALB BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,STRUCT BIOL SECT,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MATH BIOL LAB,FREDERICK,MD 21702. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. RI Shen, Rulong/E-4079-2011 FU NCI NIH HHS [CA57516, CA 50551, N01-CO-74101] NR 47 TC 36 Z9 37 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD APR PY 1994 VL 5 IS 4 BP 419 EP 429 PG 11 WC Cell Biology SC Cell Biology GA NF150 UT WOS:A1994NF15000009 PM 8043516 ER PT J AU SZABO, E PREIS, LH BIRRER, MJ AF SZABO, E PREIS, LH BIRRER, MJ TI CONSTITUTIVE C-JUN EXPRESSION INDUCES PARTIAL MACROPHAGE DIFFERENTIATION IN U-937 CELLS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID C-JUN EXPRESSION; PROMYELOCYTIC LEUKEMIA-CELLS; EMBRYONAL CARCINOMA-CELLS; COLONY-STIMULATING FACTOR; TRANSCRIPTION FACTOR AP-1; PROTO-ONCOGENE; GENE-EXPRESSION; MONOCYTIC DIFFERENTIATION; TERMINAL DIFFERENTIATION; ENHANCER ACTIVITY AB Previous studies have shown that phorbol ester induced macrophage differentiation in the leukemic cell line U-937 is tightly linked to the expression of the c-jun protooncogene and the generation of AP-1 transcriptional activity. We expressed the c-jun protooncogene in U-937 cells to examine the role of c-jun in the differentiation of these cells. AP-1 DNA binding activity and the expression of AP-1 controlled downstream genes were increased in all clones expressing exogenous cJun. More importantly, these transfectants showed evidence of differentiation as measured by the acquisition of phagocytic capacity, although they did not develop morphological changes associated with differentiation such as adherence. Furthermore, they became committed to terminal differentiation after significantly shorter exposures to phorbol esters than did control cell lines. These data show that cJun expression induces partial differentiation along the macrophage pathway in U-937 cells. C1 NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD 20850. NR 44 TC 57 Z9 58 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD APR PY 1994 VL 5 IS 4 BP 439 EP 446 PG 8 WC Cell Biology SC Cell Biology GA NF150 UT WOS:A1994NF15000011 PM 8043518 ER PT J AU SHIN, YM MONI, RW LUEDERS, JE DALY, JW AF SHIN, YM MONI, RW LUEDERS, JE DALY, JW TI EFFECTS OF THE AMPHIPHILIC PEPTIDES MASTOPARAN AND ADENOREGULIN ON RECEPTOR-BINDING, G-PROTEINS, PHOSPHOINOSITIDE BREAKDOWN, CYCLIC-AMP GENERATION, AND CALCIUM INFLUX SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article ID SWISS 3T3 CELLS; HIGH-AFFINITY RECEPTORS; PERITONEAL MAST-CELLS; WASP VENOM; PANCREATIC-ISLETS; ALPHA-SUBUNIT; SUBSTANCE-P; PC12 CELLS; RELEASE; TOXIN AB 11. The amphiphilic peptide mastoparan is known to affect phosphoinositide breakdown, calcium influx, and exocytosis of hormones and neurotransmitters and to stimulate the GTPase activity of guanine nucleotide-binding regulatory proteins. Another amphiphilic peptide, adenoregulin was recently identified based on stimulation of agonist binding to A(1)-adenosine receptors. 2. A comparison of the effects of mastoparan and adenoregulin reveals that these peptides share many properties. Both stimulate binding of agonists to receptors and binding of GTP gamma S to G proteins in brain membranes. The enhanced guanyl nucleotide exchange may be responsible for the complete conversion of receptors to a high-affinity state, complexed with guanyl nucleotide-free G proteins. 3. Both peptides increase phosphoinositide breakdown in NIH 3T3 fibroblasts. Pertussis toxin partially inhibits the phosphoinositide breakdown elicited by mastoparan but has no effect on the response to adenoregulin. N-Ethylmaleimide inhibits the response to both peptides. 4. In permeabilized 3T3 cells, both adenoregulin and mastoparan inhibit GTP gamma S-stimulated phosphoinositide breakdown. Mastoparan slightly increases basal cyclic AMP levels in cultured cells, followed at higher concentrations by an inhibition, while adenoregulin has minimal effects. 5. Both peptides increase calcium influx in cultured cells and release of norepinephrine in pheochromocytoma PC12 cells. The calcium influx elicited by the peptides in 3T3 cells is not markedly altered by N-ethylmaleimide. 6. Multiple sites of action appear likely to underlie the effects of on receptors, G proteins, phospholipase C, and calcium. C1 NIDDKD,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 39 TC 15 Z9 16 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD APR PY 1994 VL 14 IS 2 BP 133 EP 157 DI 10.1007/BF02090781 PG 25 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA PL747 UT WOS:A1994PL74700003 PM 7842473 ER PT J AU PURI, RK DEBINSKI, W OBIRI, N KREITMAN, R PASTAN, I AF PURI, RK DEBINSKI, W OBIRI, N KREITMAN, R PASTAN, I TI HUMAN RENAL CELL-CARCINOMA CELLS ARE SENSITIVE TO THE CYTOTOXIC EFFECT OF A CHIMERIC PROTEIN COMPOSED OF HUMAN INTERLEUKIN-4 AND PSEUDOMONAS EXOTOXIN SO CELLULAR IMMUNOLOGY LA English DT Article ID FACTOR-I RECEPTOR; HIGH-AFFINITY; FUSION PROTEIN; UP-REGULATION; EXPRESSION; ALPHA AB We have previously demonstrated that functional high-affinity interleukin-4 receptors (IL-4R) are expressed on human renal cell carcinoma (RCC) cells (N. I. Obiri et al., J. Clin. Invest. 91, 88, 1993). In the present study, we examined the cytotoxic effect (determined by inhibition of protein synthesis) of a chimeric protein composed of human IL-4 and Pseudomonas exotoxin (PE) on human RCC tumor samples obtained from patients undergoing nephrectomy. The chimeric gene encoding hIL4-PE4E was constructed by fusing a cDNA clone for human IL-4 to the 5' end of a mutated cDNA encoding a full-length PE molecule. This gene was expressed in Escherichia coli, and large quantities of this recombinant protein were isolated to more than 95% purity. This chimeric protein, hIL4-PE4E, was highly cytotoxic to all six RCC cell lines examined. The concentration of hIL4-PE4E at which 50% inhibition of protein synthesis was obtained ranged from <1 ng/ml (12 pM) to 10 ng/ml (120 pM) in five of the six isolates of RCC and 40-70 ng/ml in one other. A mutant chimeric protein which can bind to IL-4R but lacks the ADP ribosylation activity of PE was not cytotoxic to the RCC cells. The cytotoxic effect of hIL4-PE4E was IL-4R mediated because a fourfold molar excess of IL-4 abrogated the cytotoxic effect of hIL4-PE4E. A neutralizing monoclonal antibody to IL-4 also abrogated the cytotoxic effect of hIL4-PE4E. hIL4-PE4E showed very little cytotoxic activity to a normal human umbilical vein endothelial cell line (ID50 = 1000 ng/ml) and a human fibroblast cell line (ID50 similar to 400 ng/ml). Nonactivated human peripheral blood lymphocytes (PBL) were also insensitive to hlL4-PE4E (ID50 similar to 500 ng/ml), whereas phytohemagglutinin-activated PBL were highly susceptible to the cytotoxic effect of hIL4-PE4E (ID50 similar to 4 ng/ml). These data indicate that hIL4-PE4E may be a useful agent for the treatment of human RCC without affecting normal and resting immune cells. (C) 1994 Academic Press, Inc. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. RP PURI, RK (reprint author), US FDA,CTR BIOL EVALUAT & RES,DIV CELLULAR & GENE THERAPIES,MOLEC TUMOR BIOL LAB,NIH BLDG 29A,BETHESDA,MD 20892, USA. NR 22 TC 22 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD APR 1 PY 1994 VL 154 IS 2 BP 369 EP 379 DI 10.1006/cimm.1994.1084 PG 11 WC Cell Biology; Immunology SC Cell Biology; Immunology GA NB455 UT WOS:A1994NB45500010 PM 8131209 ER PT J AU BIESSMANN, H KASRAVI, B BUI, T FUJIWARA, G CHAMPION, LE MASON, JM AF BIESSMANN, H KASRAVI, B BUI, T FUJIWARA, G CHAMPION, LE MASON, JM TI COMPARISON OF 2 ACTIVE HET-A RETROPOSONS OF DROSOPHILA-MELANOGASTER SO CHROMOSOMA LA English DT Article ID BROKEN CHROMOSOME ENDS; R HYBRID DYSGENESIS; 5' END; TRANSPOSABLE ELEMENTS; DNA-SEQUENCES; I-FACTOR; MAMMALIAN LINES; IDENTIFICATION; FAMILY; GENE AB HeT-A elements are Drosophila melanogaster LINE-like retroposons that transpose to broken chromosome ends by attaching themselves with an oligo(A) tail. Since this family of elements is believed to be involved in the vital function of telomere elongation in Drosophila, it is important to understand their transposition mechanism and the molecular aspects of activity. By comparison of several elements we have defined here the unit length of HeT-A elements to be approximately 6 kb. Also, we studied an active HeT-A element that had transposed very recently to the end of a terminally deleted X chromosome. The 12 kb of newly transposed DNA consisted of a tandem array of three different HeT-A elements joined by oligo(A) tails to each other and to the chromosome end broken in the yellow gene. Such an array may have transposed as a single unit or resulted from rapid successive transpositions of individual HeT-A elements. By sequence comparison with another recently transposed HeT-A element, conserved domains in the single open reading frame (ORF), encoding a gag-like polypeptide, of these elements were defined. We conclude that for transposition an intact ORF is required in cis, while the reverse transcriptase is not encoded on the HeT-A element but is provided in tl ans. This would make HeT-A elements dependent on an external reverse transcriptase for transposition and establish control of the genome over the activity of HeT-A elements. This distinguishes the Drosophila HeT-A element, which has been implicated in Drosophila telomere elongation, from the other, 'selfish' LINE-like elements. C1 NIEHS, GENET GRP, RES TRIANGLE PK, NC 27709 USA. RP UNIV CALIF IRVINE, CTR DEV BIOL, IRVINE, CA 92717 USA. FU NIGMS NIH HHS [GM46211] NR 49 TC 45 Z9 45 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0009-5915 EI 1432-0886 J9 CHROMOSOMA JI Chromosoma PD APR PY 1994 VL 103 IS 2 BP 90 EP 98 DI 10.1007/s004120050011 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA NJ739 UT WOS:A1994NJ73900003 PM 8055715 ER PT J AU LENFANT, C AF LENFANT, C TI PREVENTION AND TRANSLATION ACTIVITIES - DELIVERING THE GOODS SO CIRCULATION LA English DT Editorial Material RP LENFANT, C (reprint author), NHLBI,BLDG 10,BETHESDA,MD 20892, USA. 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 APR PY 1994 VL 89 IS 4 BP 1497 EP 1498 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NG469 UT WOS:A1994NG46900002 PM 8149513 ER PT J AU BRAUNWALD, E MCCABE, CH CANNON, CP MULLER, JE KNATTERUD, G THOMPSON, B PRIOR, MJ KUFERA, J WILKINS, P GIRO, R RANDALL, A FREDERICK, M CANNER, M DEPKIN, J MONROE, L BELL, P DESVIGNENICKENS, P LETENDRE, C MANN, KG BOVILL, E COLLEN, D TRACY, RP CORNELL, E COLLING, CL PETERSON, J CHAITMAN, B SHAW, L STOCKE, K STONE, PH RUTHERFORD, JD MACCALLUM, G WILLIAMS, DO SHARAF, BL MCKENDALL, GR RILEY, RS THOMAS, ES FERREIRA, P MIELE, NJ ZARET, BL WACKERS, FJ JAIN, D MCMAHON, M THEROUX, P DEGUISE, P JUNEAU, M SEGUIN, MA NASMITH, JB PALISAITIS, D GAUDETTE, G DIVER, DJ BREALL, J BERGER, C BAIM, DS DUNN, S KIRSHENBAUM, J CANNON, C BATESRIORDAN, D HERSON, S DAUM, R CAREY, G MUELLER, HS GOLDBERGER, M GREENBERG, MA MENEGUS, MA VENTURA, B HEMINGWAY, K STEINGART, R GAMBINO, A COGLIANESE, ME BILODEAU, S ROBERTS, R KLEIMAN, NS HABIB, G PULEO, P TRAINOR, K ROSE, D DANGOISSE, V COTE, M DUMAIS, B HARVEY, R GERVAIS, A PROULX, G MIGNAULT, JD ROULEAU, JL PLANTE, S OHARA, G LEPAGE, S DANGOISSE, J LETOURNEAU, C HOCHMAN, J PEPE, AJ WONG, SC BROGUS, D MCANULTY, M THOMPSON, CR WEBB, JG PRIMEAU, A BULLER, C SAUNDERS, L LEYA, F MCKIERNAN, T GRASSMAN, E GALBRAITH, E PICCHI, R WILLERSON, JT ANDERSON, HV WEIGELT, LA SANFORD, CF MURPHY, G SCHWIEGER, MJ PORWAY, MN JOELSON, J PETERMAN, M MARANTZ, T WARWICK, D GIBSON, RS POWERS, ER FAUBER, NM SAYRE, SL BELENKIE, I WARNICA, JW HALL, C CHURCHILLSMITH, T SHOOK, TL MATTHEWS, RV GRAY, C MAHRER, PR JORGENSEN, MB NOCEDA, J MAGORIEN, R EATON, G SHARPWILMER, J BECKER, RC GORE, JM WEINER, BH CORRAO, JM COHEN, LS REMETZ, M MIRTO, G ALEXANDER, J GEGNY, A HAMILTON, W THORNTON, T MAJOR, M BIERMAN, K STONNER, T KRONENBERG, MW CONTI, VR DAVIS, MJ FARRELL, RW NUSYNOWITZ, ML SCHMEDTJE, JF ZWISCHENBERGER, JB IBRAHIM, A PALMERI, ST MOREVRA, AE HOSLER, M CASAZZA, L KELLS, CM ONEILL, BJ FOSTER, CJ FAWCETT, T NEDULCU, V WILLIAMS, M JACKSON, M FELDMAN, T SORRENTINO, M PASTORET, A MCCABE, C BROWN, BG CANNON, CD COHEN, LE RAPAPORT, E CRAWFORD, M GERSTENBLITH, G HARKER, LA SMITH, H TILLEY, B ANDERSON, J TERRIN, ML TOFLER, G SCHERLIS, L BAKER, WP COWLEY, M GUERCI, AD HIRSHFELD, JW AF BRAUNWALD, E MCCABE, CH CANNON, CP MULLER, JE KNATTERUD, G THOMPSON, B PRIOR, MJ KUFERA, J WILKINS, P GIRO, R RANDALL, A FREDERICK, M CANNER, M DEPKIN, J MONROE, L BELL, P DESVIGNENICKENS, P LETENDRE, C MANN, KG BOVILL, E COLLEN, D TRACY, RP CORNELL, E COLLING, CL PETERSON, J CHAITMAN, B SHAW, L STOCKE, K STONE, PH RUTHERFORD, JD MACCALLUM, G WILLIAMS, DO SHARAF, BL MCKENDALL, GR RILEY, RS THOMAS, ES FERREIRA, P MIELE, NJ ZARET, BL WACKERS, FJ JAIN, D MCMAHON, M THEROUX, P DEGUISE, P JUNEAU, M SEGUIN, MA NASMITH, JB PALISAITIS, D GAUDETTE, G DIVER, DJ BREALL, J BERGER, C BAIM, DS DUNN, S KIRSHENBAUM, J CANNON, C BATESRIORDAN, D HERSON, S DAUM, R CAREY, G MUELLER, HS GOLDBERGER, M GREENBERG, MA MENEGUS, MA VENTURA, B HEMINGWAY, K STEINGART, R GAMBINO, A COGLIANESE, ME BILODEAU, S ROBERTS, R KLEIMAN, NS HABIB, G PULEO, P TRAINOR, K ROSE, D DANGOISSE, V COTE, M DUMAIS, B HARVEY, R GERVAIS, A PROULX, G MIGNAULT, JD ROULEAU, JL PLANTE, S OHARA, G LEPAGE, S DANGOISSE, J LETOURNEAU, C HOCHMAN, J PEPE, AJ WONG, SC BROGUS, D MCANULTY, M THOMPSON, CR WEBB, JG PRIMEAU, A BULLER, C SAUNDERS, L LEYA, F MCKIERNAN, T GRASSMAN, E GALBRAITH, E PICCHI, R WILLERSON, JT ANDERSON, HV WEIGELT, LA SANFORD, CF MURPHY, G SCHWIEGER, MJ PORWAY, MN JOELSON, J PETERMAN, M MARANTZ, T WARWICK, D GIBSON, RS POWERS, ER FAUBER, NM SAYRE, SL BELENKIE, I WARNICA, JW HALL, C CHURCHILLSMITH, T SHOOK, TL MATTHEWS, RV GRAY, C MAHRER, PR JORGENSEN, MB NOCEDA, J MAGORIEN, R EATON, G SHARPWILMER, J BECKER, RC GORE, JM WEINER, BH CORRAO, JM COHEN, LS REMETZ, M MIRTO, G ALEXANDER, J GEGNY, A HAMILTON, W THORNTON, T MAJOR, M BIERMAN, K STONNER, T KRONENBERG, MW CONTI, VR DAVIS, MJ FARRELL, RW NUSYNOWITZ, ML SCHMEDTJE, JF ZWISCHENBERGER, JB IBRAHIM, A PALMERI, ST MOREVRA, AE HOSLER, M CASAZZA, L KELLS, CM ONEILL, BJ FOSTER, CJ FAWCETT, T NEDULCU, V WILLIAMS, M JACKSON, M FELDMAN, T SORRENTINO, M PASTORET, A MCCABE, C BROWN, BG CANNON, CD COHEN, LE RAPAPORT, E CRAWFORD, M GERSTENBLITH, G HARKER, LA SMITH, H TILLEY, B ANDERSON, J TERRIN, ML TOFLER, G SCHERLIS, L BAKER, WP COWLEY, M GUERCI, AD HIRSHFELD, JW TI EFFECTS OF TISSUE-PLASMINOGEN ACTIVATOR AND A COMPARISON OF EARLY INVASIVE AND CONSERVATIVE STRATEGIES IN UNSTABLE ANGINA AND NON-Q-WAVE MYOCARDIAL-INFARCTION - RESULTS OF THE TIMI IIIB TRIAL SO CIRCULATION LA English DT Article DE MYOCARDIAL INFARCTION; ANGINA ID ACUTE CORONARY SYNDROMES; PLACEBO-CONTROLLED TRIAL; THROMBOLYTIC THERAPY; ARTERY DISEASE; DOUBLE-BLIND; INTRAVENOUS STREPTOKINASE; PLATELET ACTIVATION; THROMBIN ACTIVITY; RANDOMIZED TRIAL; ERYTHROCYTE-RICH AB Background Although coronary thrombosis plays a critical role in the pathogenesis of unstable angina and non-Q-wave myocardial infarction (NQMI), the effects of thrombolytic therapy in these disorders is not clear. Also, the role of routine early coronary arteriography followed by revascularization has not been established. Methods and Results Patients (n=1473) seen within 24 hours of ischemic chest discomfort at rest, considered to represent unstable angina or NQMI, were randomized using a 2x2 factorial design to compare (1) TPA versus placebo as initial therapy and (2) an early invasive strategy (early coronary arteriography followed by revascularization when the anatomy was suitable) versus an early conservative strategy (coronary arteriography followed by revascularization if initial medical therapy failed). All patients were treated with bed rest, anti-ischemic medications, aspirin, and heparin. The primary end point for the TPA-placebo comparison (death, myocardial infarction, or failure of initial therapy at 6 weeks) occurred in 54.2% of the TPA-treated patients and 55.5% of the placebo-treated patients (P=NS). Fatal and nonfatal myocardial infarction after randomization (reinfarction in NQMI patients) occurred more frequently in TPA-treated patients (7.4%) than in placebo-treated patients (4.9%, P=.04, Kaplan-Meier estimate). Four intracranial hemorrhages occurred in the TPA-treated group versus none in the placebo-treated group (P=.06). The end point for the comparison of the two strategies (death, myocardial infarction, or an unsatisfactory symptom-limited exercise stress test at 6 weeks) occurred in 18.1% of patients assigned to the early conservative strategy and 16.2% of patients assigned to the early invasive strategy (P=NS). In the latter, the average length of initial hospitalization, incidence of rehospitalization within 6 weeks, and days of rehospitalization all were significantly lower. Conclusions In the overall trial, patients with unstable angina and NQMI were managed with low rates of mortality (2.4%) and myocardial infarction or reinfarction (6.3%) at the time of the 6-week visit. These results can be achieved using either an early conservative or early invasive strategy, the latter resulting in a reduced incidence of days of hospitalization and of rehospitalization and in the use of antianginal drugs. The addition of a thrombolytic agent is not beneficial and may be harmful. C1 HARVARD UNIV,SCH MED,BOSTON,MA. MARYLAND MED RES INST,BALTIMORE,MD. NIH,NATL HEART LUNG & BLOOD INST PROGRAM OFF,BETHESDA,MD. UNIV VERMONT,COLCHESTER,VT. VET ADM MED RES SERV,ALBUQUERQUE,NM. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. RHODE ISL HOSP,PROVIDENCE,RI 02902. YALE UNIV,SCH MED,NEW HAVEN,CT. UNIV MONTREAL,MONTREAL HEART INST,MONTREAL,PQ,CANADA. HOP SACRE COEUR,MONTREAL H4J 1C5,PQ,CANADA. ALBERT EINSTEIN COLL MED,MONTEFIORE MED CTR,BRONX,NY 10467. WINTHROP UNIV HOSP,MINEOLA,NY 11501. BAYLOR COLL MED,HOUSTON,TX 77030. CHU SHERBROOKE,SHERBROOKE,PQ,CANADA. COLUMBIA UNIV,ST LUKES ROOSEVELT HOSP CTR,NEW YORK,NY. UNIV BRITISH COLUMBIA,ST PAULS HOSP,VANCOUVER,BC,CANADA. VANCOUVER GEN HOSP,VANCOUVER,BC,CANADA. LOYOLA UNIV,FOSTER MCGAW HOSP,MED CTR,MAYWOOD,IL 60153. UNIV TEXAS,SCH MED,HOUSTON,TX. BAYSTATE MED CTR,SPRINGFIELD,MA 01107. UNIV VIRGINIA,HLTH SCI CTR,CHARLOTTESVILLE,VA. UNIV CALGARY,FOOTHILLS PROV GEN HOSP,CALGARY,AB,CANADA. HOSP GOOD SAMARITAN,LOS ANGELES,CA 90017. KAISER PERMANENTE MED CTR,LOS ANGELES,CA. OHIO STATE UNIV,COLUMBUS,OH 43210. UNIV MASSACHUSETTS,SCH MED,WORCESTER,MA. YALE UNIV,NEW HAVEN HOSP,SCH MED,NEW HAVEN,CT. DANBURY HOSP,DANBURY,CT. ST LOUIS UNIV,MED CTR,ST LOUIS,MO. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. UNIV MED & DENT NEW JERSEY,NEW BRUNSWICK,NJ. VICTORIA GEN HOSP,HALIFAX B3H 2Y9,NS,CANADA. UNIV N CAROLINA,CHAPEL HILL,NC. UNIV CHICAGO HOSP & CLIN,CHICAGO,IL. RP BRAUNWALD, E (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 64 TC 595 Z9 612 U1 3 U2 8 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR PY 1994 VL 89 IS 4 BP 1545 EP 1556 PG 12 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NG469 UT WOS:A1994NG46900010 ER PT J AU FERRANS, VJ MCALLISTER, HA AF FERRANS, VJ MCALLISTER, HA TI LYMPHOCYTIC MYOCARDITIS SO CIRCULATION LA English DT Note C1 NHLBI,PATHOL 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 APR PY 1994 VL 89 IS 4 BP 1890 EP 1891 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA NG469 UT WOS:A1994NG46900049 PM 8149554 ER PT J AU SUN, Y OBERLEY, LW AF SUN, Y OBERLEY, LW TI SUITABILITY OF COPPER CHLORIDE AS A REACTION TERMINATOR FOR SUPEROXIDE-DISMUTASE ACTIVITY ASSAY SO CLINICA CHIMICA ACTA LA English DT Letter ID ISCHEMIA-REPERFUSION; TRANSPLANTATION; INJURY; SOD C1 UNIV IOWA,RADIAT RES LAB,MED LABS 14,IOWA CITY,IA 52242. RP SUN, Y (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,CELL BIOL SECT,BLDG 560,RM 21-89,FREDERICK,MD 21702, USA. NR 14 TC 18 Z9 18 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-8981 J9 CLIN CHIM ACTA JI Clin. Chim. Acta PD APR PY 1994 VL 226 IS 1 BP 101 EP 103 DI 10.1016/0009-8981(94)90108-2 PG 3 WC Medical Laboratory Technology SC Medical Laboratory Technology GA NM436 UT WOS:A1994NM43600012 PM 8070127 ER PT J AU AVANZINI, MA BJORKANDER, J SODERSTROM, R SODERSTROM, T SCHNEERSON, R ROBBINS, JB HANSON, LA AF AVANZINI, MA BJORKANDER, J SODERSTROM, R SODERSTROM, T SCHNEERSON, R ROBBINS, JB HANSON, LA TI QUALITATIVE AND QUANTITATIVE-ANALYSES OF THE ANTIBODY-RESPONSE ELICITED BY HAEMOPHILUS-INFLUENZAE TYPE-B CAPSULAR POLYSACCHARIDE TETANUS TOXOID CONJUGATES IN ADULTS WITH IGG SUBCLASS DEFICIENCIES AND FREQUENT INFECTIONS SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE IGG SUBCLASSES; CAPSULAR POLYSACCHARIDE; ANTIBODY RESPONSE ID RESPIRATORY-TRACT INFECTION; CHILDREN; IMMUNOGENICITY; INFANTS AB Twenty-one IgG subclass-deficient adult patients with repeated infections of the respiratory tract, were immunized with Haemophilus influenzae type b capsular polysaccharide (HibCP) covalently bound to tetanus toxoid (TT). Specific immunoglobulin and IgG subclasses to HibCP and TT were quantified; the biological activities of HibCP antibodies were also investigated. Most patients showed an antibody response similar to that observed in healthy adults, and the bactericidal activity related to the post-immunization levels of HibCP antibodies. No relation was found between immunoglobulin isotype deficiency, the clinical symptoms and the IgG subclass responsiveness, and no relation was observed between HibCP and TT antibody responses. Our data indicate that some, but not all, patients with recurrent infections and IgG subclass deficiency have an abnormal serum antibody response to polysaccharide and protein epitopes of Hib-TT conjugate vaccine. Analysis of the antibody response after vaccination with HibCP-TT conjugate vaccine did not seem to predict the clinical course of such patients. C1 UNIV PAVIA,DEPT PAEDIAT,I-27100 PAVIA,ITALY. GOTHENBURG UNIV,DEPT CLIN IMMUNOL,S-41124 GOTHENBURG,SWEDEN. GOTHENBURG UNIV,ASTHMA & ALLERGY RES CTR,S-41124 GOTHENBURG,SWEDEN. NICHHD,DEV & MOLEC IMMUN LAB,BETHESDA,MD 20892. NR 19 TC 7 Z9 8 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD APR PY 1994 VL 96 IS 1 BP 54 EP 58 PG 5 WC Immunology SC Immunology GA ND728 UT WOS:A1994ND72800010 PM 8149666 ER PT J AU MAEKAWA, M SUDO, K KOBAYASHI, A SUGIYAMA, E LI, SSL KANNO, T AF MAEKAWA, M SUDO, K KOBAYASHI, A SUGIYAMA, E LI, SSL KANNO, T TI FAST-TYPE ELECTROPHORETIC VARIANT OF LACTATE-DEHYDROGENASE M(A) AND COMPARISON WITH OTHER MISSENSE MUTATIONS IN LACTATE-DEHYDROGENASE M(A) AND H(B) GENES SO CLINICAL CHEMISTRY LA English DT Note DE ISOENZYMES; GENETIC VARIATION; SINGLE-STRAND CONFORMATION POLYMORPHISM ID A MUSCLE; B HEART; MOLECULAR CHARACTERIZATION; C TESTIS; DNA; DEFICIENCY; MOUSE; AMPLIFICATION; ORGANIZATION; EVOLUTION AB An electrophoretic variant of lactate dehydrogenase (LD) M(A) subunit was discovered in a female patient with chest pain. Her LD activity in serum was within the normal reference interval, and analysis of her LD isoenzyme pattern showed an abnormal migration indicating a fast-type LD-M(A) subunit variant. DNA analysis of the mutant LD-M gene detected a single base substitution, an A to G transition at codon 220 (AAA-->GAA). This mutation resulted in the replacement of a lysine by a glutamic acid (mutation K220E) and produced a subunit variant (electrophoretic fast type). This missense mutation was also observed in the patient's son, and genotypes of mother and son were consistent with their biochemical phenotypes, as evaluated by LD isoenzyme analysis. C1 JIKEI UNIV, DAISAN HOSP, SCH MED, DEPT LAB MED, KOMAE, TOKYO 201, JAPAN. MED CO LTD, CLIN LABS, SHIGA 52023, JAPAN. NIEHS, GENET LAB, RES TRIANGLE PK, NC 27709 USA. RP MAEKAWA, M (reprint author), HAMAMATSU UNIV SCH MED, DEPT LAB MED, HANDA CHO, HAMAMATSU, SHIZUOKA 43131, JAPAN. NR 31 TC 8 Z9 9 U1 0 U2 1 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD APR PY 1994 VL 40 IS 4 BP 665 EP 668 PG 4 WC Medical Laboratory Technology SC Medical Laboratory Technology GA NE582 UT WOS:A1994NE58200029 PM 7908613 ER PT J AU FOWLER, MG MOFENSON, L ROGERS, M AF FOWLER, MG MOFENSON, L ROGERS, M TI SYMPOSIUM-IN-WRITING - INTRODUCTION SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Editorial Material C1 CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,DIV HIV AIDS,EPIDEMIOL BRANCH,ATLANTA,GA. NICHHD,CTR RES MOTHERS & CHILDREN,ADOLESCENT & MATERNAL AIDS BRANCH,BETHESDA,MD. RP FOWLER, MG (reprint author), NIAID,DIV AIDS,VACCINE TRIALS & EPIDEMIOL BRANCH,PERINATAL TRANSMISS & PEDIAT SECT,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1994 VL 71 IS 1 BP 1 EP 1 DI 10.1006/clin.1994.1042 PG 1 WC Immunology; Pathology SC Immunology; Pathology GA NE054 UT WOS:A1994NE05400001 ER PT J AU FRANCO, A APPELLA, E KAGNOFF, MF CHOWERS, Y SAKAGUCHI, K GREY, HM SETTE, A AF FRANCO, A APPELLA, E KAGNOFF, MF CHOWERS, Y SAKAGUCHI, K GREY, HM SETTE, A TI PERIPHERAL T-CELL RESPONSE TO A-GLIADIN IN CELIAC-DISEASE - DIFFERENTIAL PROCESSING AND PRESENTATION CAPACITIES OF EPSTEIN-BARR-TRANSFORMED B-CELLS AND FIBROBLASTS SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID HLA-DQ; GRAVES-DISEASE; HETERODIMER; LYMPHOCYTES; PEPTIDES; ASSOCIATION; COMPONENTS; MOLECULES AB Celiac disease (CD) is a small intestinal disorder characterized by the malabsorption of most nutrients. Disease pathogenesis appears to be associated with immune-mediated pathology. Susceptibility is associated with genes coding for DQw2 class II molecules. In the present report we investigated T cell responses to A-gliadin (AGL), a major alpha-gliadin component known to activate disease. Gliadin-specific lines were generated from a CD patient and a normal donor. Three major points were revealed by the analysis of these T cells: (1) On the basis of mapping experiments using Epstein-Barr virus (EBV) lines and DR-transfected fibroblasts and DR-, DP-, and DQ-specific monoclonal antibodies (mAb), all responses appeared to be DR-restricted. Thus, in contrast to the strong association of disease susceptibility with DQ molecules, no DO-restricted, gliadin-specific response was detectable. (2) Fine specificity analysis, using a panel of synthetic peptides spanning the entire a-gliadin component molecule, revealed that the clones derived from the normal donor were DR53-restricted and AGL 21-40-specific, while clones derived from the CD patient were DR7-restricted and peptide 1-20-specific. (3) Both whole AGL and AGL 1-20 were presented to the patient-derived clones with much higher efficiency by DDR-transfected fibroblasts than by EBV lines. These data suggested that fibroblasts processed this determinant efficiently, while EBV lines were unable to do so. Indeed, analysis of a panel of truncated AGL 1-20 analogs revealed that peptide AGL 1-8, which contained the minimal T cell epitope, was presented with equal efficiency by fixed or irradiated EBV and irradiated DR7-transfected fibroblasts. (C) 1994 Academic Press, Inc. C1 NCI,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. RP FRANCO, A (reprint author), CYTEL CORP,3525 JOHN HOPKINS COURT,SAN DIEGO,CA 92121, USA. FU NIAID NIH HHS [AI18634]; NIDDK NIH HHS [DK35108] NR 22 TC 19 Z9 19 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1994 VL 71 IS 1 BP 75 EP 81 DI 10.1006/clin.1994.1054 PG 7 WC Immunology; Pathology SC Immunology; Pathology GA NE054 UT WOS:A1994NE05400013 PM 7511085 ER PT J AU MOFENSON, LM AF MOFENSON, LM TI PREVENTION OF INFECTIONS IN CHILDREN WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION - PRACTICAL RECOMMENDATIONS SO CLINICAL IMMUNOTHERAPEUTICS LA English DT Article ID PNEUMOCYSTIS-CARINII PNEUMONIA; ACQUIRED HIV-INFECTION; LYMPHOCYTE SUBSETS; HEALTHY-CHILDREN; PROPHYLAXIS; POPULATION; RISK; PENTAMIDINE; DIAGNOSIS; NEWBORNS AB Infection with HIV in children is superimposed on the immunological naivety inherent to infancy and on an immature immune system undergoing developmental maturation. Therefore, in addition to the opportunistic infections characteristic of HIV infection in adults, severe infections with common bacterial and viral organisms are frequent early manifestations of HIV infection in children. Recurrent serious bacterial infections are the second most frequent AIDS-defining infection in children, with only Pneumocystis carinii pneumonia (PCP) more common. Mycobacterium avium complex infection is also assuming increasing importance as a pathogen in HIV-infected children. Two randomized placebo-controlled clinical trials of intravenous immunoglobulin (IVIG) prophylaxis of bacterial infections in paediatric HIV infection have recently been completed. The data indicate that IVIG reduces the rate of serious and minor bacterial infections and decreases hospitalizations in HIV-infected children with both mild and advanced HIV disease. In children receiving zidovudine, this effect is independent of CD4+ count at initiation of therapy. In children receiving zidovudine who also receive concomitant prophylaxis with cotrimoxazole (trimethoprim-sulfamethoxazole) for PCP, IVIG may not provide additional benefit for reduction of bacterial infections, although definitive recommendations must await the results of further studies. Recommendations for prophylaxis of PCP in pediatric HIV infection are complicated by normal age-related changes in CD4+ lymphocyte count. Recent guidelines from the US Public Health Service are reviewed. Finally, the incidence of Mycobacterium avium complex disease in paediatric HIV infection is examined, and potential prophylactic regimens discussed. RP MOFENSON, LM (reprint author), NICHHD,CTR RES MOTHERS & CHILDREN,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,6100 EXECUT BLVD,ROCKVILLE,MD 20852, USA. NR 47 TC 0 Z9 0 U1 0 U2 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1172-7039 J9 CLIN IMMUNOTHER JI Clin. Immunother. PD APR PY 1994 VL 1 IS 4 BP 258 EP 270 PG 13 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA NM975 UT WOS:A1994NM97500003 ER PT J AU BEEKMANN, SE VLAHOV, D KOZIOL, DE MCSHALLEY, ED SCHMITT, JM HENDERSON, DK AF BEEKMANN, SE VLAHOV, D KOZIOL, DE MCSHALLEY, ED SCHMITT, JM HENDERSON, DK TI TEMPORAL ASSOCIATION BETWEEN IMPLEMENTATION OF UNIVERSAL PRECAUTIONS AND A SUSTAINED, PROGRESSIVE DECREASE IN PERCUTANEOUS EXPOSURES TO BLOOD SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID HEALTH-CARE WORKERS; IMMUNODEFICIENCY-VIRUS TYPE-1; NEEDLESTICK INJURIES; OCCUPATIONAL EXPOSURES; EDUCATIONAL-PROGRAM; SHARPS CONTAINERS; HEPATITIS-B; FREQUENCY; INFECTION; EPIDEMIOLOGY AB To evaluate whether implementation of universal precautions was temporally associated with a decrease in reported parenteral exposures to blood, we analyzed data on self-reported parenteral injuries that were prospectively collected at the Clinical Center, National Institutes of Health (Bethesda, MD), from 1985 through 1991. We also assessed whether implementation of universal precautions, in concert with initiation of a program of postexposure chemoprophylaxis with zidovudine, was associated with decreased time to reporting of occupational exposures. Our data, possibly confounded by the occurrence of an occupational infection due to human immunodeficiency virus infection in 1988, nonetheless demonstrate a temporal association between a progressive, significant decrease in percutaneous injuries and the implementation of universal precautions that has been sustained through subsequent years. The analysis remains significant, regardless of the surrogate denominator chosen for analysis. No trend toward more rapid reporting of exposures was identified. Implementation of universal precautions appears to have contributed to decreased parenteral injuries in our hospital but did not affect reporting efficiency. C1 NIH,DIV SAFETY,OCCUPAT MED SERV,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD 21218. NIH,CTR CLIN,OFF DIRECTOR,HOSP EPIDEMIOL SERV,BETHESDA,MD 20892. NR 31 TC 62 Z9 64 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD APR PY 1994 VL 18 IS 4 BP 562 EP 569 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NE074 UT WOS:A1994NE07400009 PM 8038311 ER PT J AU GORDIN, F MASUR, H AF GORDIN, F MASUR, H TI PROPHYLAXIS OF MYCOBACTERIUM-AVIUM COMPLEX BACTEREMIA IN PATIENTS WITH AIDS SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT Official Satellite Symposium on Management of Mycobacterium Avium Complex in Patients with HIV Infection, to the IX International Conference on AIDS CY JUN 08, 1993 CL BERLIN, GERMANY ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; INFECTION; INTRACELLULARE; RIFABUTIN; ANSAMYCIN; EPIDEMIOLOGY; CLOFAZIMINE; INVITRO; THERAPY AB Prevention of opportunistic infections is an integral part of caring for patients infected with human immunodeficiency virus. Mycobacterium avium complex (MAC) bacteremia can cause severe morbidity and excess mortality among these patients. Controlled trials of rifabutin for the prophylaxis of MAC bacteremia have been completed. Rifabutin reduced the incidence of MAC bacteremia by approximately one-half and, when disseminated disease due to MAC (DMAC) did develop, reduced the frequency of associated clinical symptoms. Moreover, prophylaxis with rifabutin was well tolerated. Prophylaxis of MAC bacteremia with macrolide antibiotics is currently being investigated, but no data from large-scale prospective trials are yet available. On the basis of trials completed thus far, the U.S. Public Health Service has recently recommended the use of rifabutin (300 mg/d) as prophylaxis for MAC bacteremia in patients with fewer than 100 CD4(+) lymphocytes/mm(3). The widespread use of this prophylactic regimen could reduce the rates of morbidity and mortality caused by DMAC. However, rifabutin must be administered only after careful consideration of the circumstances of individual patients. Potential drug interactions, cost, and compliance are important factors in the decision about which patients should receive prophylaxis. C1 NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892. RP GORDIN, F (reprint author), VET ADM MED CTR,DIV INFECT DIS,50 IRVING ST NW,WASHINGTON,DC 20422, USA. NR 28 TC 19 Z9 19 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD APR PY 1994 VL 18 SU 3 BP S223 EP S226 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NF364 UT WOS:A1994NF36400003 PM 8204774 ER PT J AU MASUR, H AF MASUR, H TI MANAGEMENT OF MYCOBACTERIUM-AVIUM COMPLEX IN PATIENTS WITH HIV-INFECTION SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material RP MASUR, H (reprint author), NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892, USA. 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 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD APR PY 1994 VL 18 SU 3 BP S217 EP S217 PG 1 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NF364 UT WOS:A1994NF36400001 ER PT J AU MASUR, H PINCHING, AJ AF MASUR, H PINCHING, AJ TI MANAGEMENT OF MYCOBACTERIUM-AVIUM COMPLEX IN PATIENTS WITH HIV-INFECTION - CONCLUSION SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material C1 ST BARTHOLOMEWS HOSP,COLL MED,LONDON,ENGLAND. RP MASUR, H (reprint author), NIH,DEPT CRIT CARE MED,BETHESDA,MD 20892, USA. 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 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD APR PY 1994 VL 18 SU 3 BP S243 EP S243 PG 1 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA NF364 UT WOS:A1994NF36400007 ER PT J AU ALIM, TN ROSSE, RB VOCCI, FJ DEUTSCH, SI AF ALIM, TN ROSSE, RB VOCCI, FJ DEUTSCH, SI TI OPEN-LABEL, DOSE RUN-UP STUDY OF DIETHYLPROPION IN INITIAL COCAINE ABSTINENCE SO CLINICAL NEUROPHARMACOLOGY LA English DT Review DE COCAINE; DOPAMINE; DIETHYLPROPION; DEPENDENCE; ABSTINENCE; CRAVING ID ABUSE; BROMOCRIPTINE; PERFORMANCE; AMANTADINE; DEPENDENCE; INFUSIONS; EXPOSURE; USERS AB An open-label, dose run-up clinical trial of diethylpropion, a mild psychostimulant medication with an approved indication for the short-term treatment of exogenous obesity, was conducted in 10 cocaine dependent patients. A ''cocaine agonist'' strategy has been proposed as a potential pharmacotherapy to assist in the initiation of cocaine abstinence in severely dependent patients. Diethylpropion exhibits many of the desirable properties of a medication with cocaine agonist properties. The current trial was conducted to obtain preliminary data on the safety, tolerability and efficacy of diethylpropion in cocaine dependent patients. Moreover, the study was conducted to obtain guidelines for dosing in future clinical trials. The results of this preliminary study suggest possible anti-craving efficacy and mood elevating properties for diethylpropion in this population. However, side effects were noted. Although most were not of a serious nature, one involved the precipitation of a manic episode. Nevertheless, because of diethylpropion's potential clinical efficacy in this population, further cautious investigation of the efficacy of this medication for the treatment of cocaine dependence is indicated. C1 DEPT VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,WASHINGTON,DC 20422. DEPT VET AFFAIRS MED CTR,NIDA,VA,RES UNIT,WASHINGTON,DC 20422. GEORGETOWN UNIV,SCH MED,DEPT PSYCHIAT,WASHINGTON,DC. NIDA,DIV MEDICAT DEV,ROCKVILLE,MD. NR 35 TC 12 Z9 12 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-5664 J9 CLIN NEUROPHARMACOL JI Clin. Neuropharmacol. PD APR PY 1994 VL 17 IS 2 BP 175 EP 187 DI 10.1097/00002826-199404000-00007 PG 13 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA NE939 UT WOS:A1994NE93900007 ER PT J AU WILSON, JT KEARNS, GL MURPHY, D YAFFE, SJ AF WILSON, JT KEARNS, GL MURPHY, D YAFFE, SJ TI PEDIATRIC LABELING REQUIREMENTS - IMPLICATIONS FOR PHARMACOKINETIC STUDIES SO CLINICAL PHARMACOKINETICS LA English DT Review ID EXTENDED LEAST-SQUARES; PEDIATRIC CLINICAL-PHARMACOLOGY; HEPATIC DRUG CLEARANCE; FEBRILE CHILDREN; PHARMACODYNAMIC INTERFACE; POPULATION ANALYSIS; VIRUS-INFECTION; INFANTS; ACETAMINOPHEN; DISPOSITION AB The US Food and Drug Administration (FDA) has proposed new labelling regulations that describe alternative approaches for providing additional information to support labelling a drug, already approved for use in adults, for use in children. Therefore, the study of drugs in paediatric populations may now be encouraged. Paediatric pharmacokinetic studies are an important part of these trials. This action by the FDA may help resolve the ethical and technological concerns about the performance of clinical trials in children, and may render paediatric clinical trials more feasible. Most investigations in children are opportunistic in nature and their design is often constrained by a requisite noninvasive approach. Appropriately applied population-based techniques for both pharmacokinetic and pharmacodynamic data analysis may represent the most robust approach for generating a sufficiently large and accurate database for the use of new or old drugs in paediatric patients. Accordingly, this information, which is crucial for paediatric labelling of any drug product, must be obtained in infants and children if we are to truly individualise therapy for paediatric patients. The funding of 6 Pediatric Pharmacology Research Units by the US National Institutes of Health, and guidelines for application of pharmacokinetic methods to children may further contribute to the performance of paediatric clinical trials. C1 LOUISIANA STATE UNIV,MED CTR,DEPT PEDIAT,SHREVEPORT,LA 71105. UNIV ARKANSAS MED SCI HOSP,DEPT PEDIAT,LITTLE ROCK,AR. US FDA,DIV ANTIVIRAL DRUG PROD,ROCKVILLE,MD. NIH,CTR RES MOTHERS & CHILDREN,BETHESDA,MD 20892. RP WILSON, JT (reprint author), LOUISIANA STATE UNIV,MED CTR,DEPT PHARMACOL,CLIN PHARMACOL SECT,1501 KINGS HIGHWAY,SHREVEPORT,LA 71130, USA. NR 112 TC 30 Z9 30 U1 0 U2 2 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 0312-5963 J9 CLIN PHARMACOKINET JI Clin. Pharmacokinet. PD APR PY 1994 VL 26 IS 4 BP 308 EP 325 PG 18 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA NF533 UT WOS:A1994NF53300006 PM 8013163 ER PT J AU AGRAWAL, S TANG, J SUN, D GALLO, RC LISZIEWICZ, J AF AGRAWAL, S TANG, J SUN, D GALLO, RC LISZIEWICZ, J TI GEM 91 - AN ANTISENSE OLIGONUCLEOTIDE AS THERAPEUTIC AGENT FOR AIDS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A282 EP A282 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000971 ER PT J AU ANDERSON, BD KAGEYAMA, S UENO, T MITSUYA, H AF ANDERSON, BD KAGEYAMA, S UENO, T MITSUYA, H TI IN-VITRO INDUCTION AND CHARACTERIZATION OF HIV-1 WITH REDUCED SENSITIVITY TO HIV PROTEASE INHIBITORS, KNI-227 AND KNI-272 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A281 EP A281 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000963 ER PT J AU BAGDADE, I RITTER, M NAGI, D KNOWLER, W AF BAGDADE, I RITTER, M NAGI, D KNOWLER, W TI DOES ABERRANT PLASMA TRAFFICKING OF CHOLESTERYL ESTER IN PIMA-INDIANS CONVEY IMMUNITY TO CORONARY HEART-DISEASE (CHD) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 RUSH MED COLL,CHICAGO,IL 60612. NIH,PHOENIX,AZ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A159 EP A159 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000275 ER PT J AU BIRX, DL MICHAEL, N REDFIELD, R REITZ, M BURKE, D BLATTNER, W AF BIRX, DL MICHAEL, N REDFIELD, R REITZ, M BURKE, D BLATTNER, W TI HIV-1-INFECTED LABORATORY WORKERS - PROFILE OF CELLULAR-RESPONSES TO HIV-1 ANTIGENS AND ALTERATION WITH ACTIVE IMMUNIZATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 WALTER REED ARMY INST RES,DEPT RETROVIRAL RES,WASHINGTON,DC 20307. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A156 EP A156 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000258 ER PT J AU BURTON, JD BAMFORD, RN PETERS, C GRANT, AJ KURYS, G GOLDMAN, CK BRENNAN, J ROESSLER, E WALDMANN, TA AF BURTON, JD BAMFORD, RN PETERS, C GRANT, AJ KURYS, G GOLDMAN, CK BRENNAN, J ROESSLER, E WALDMANN, TA TI A NOVEL CYTOKINE PROVISIONALLY TERMED IL-T THAT STIMULATES T-CELL AND LAK ACTIVITY REQUIRES IL-2R-BETA FOR ITS ACTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A305 EP A305 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02001100 ER PT J AU BUSBYWHITEHEAD, J TSIAO, C VITTONE, J ROTH, J HARMAN, SM BLACKMAN, MR SPENCER, R AF BUSBYWHITEHEAD, J TSIAO, C VITTONE, J ROTH, J HARMAN, SM BLACKMAN, MR SPENCER, R TI THE EFFECTS OF GHRH ON SKELETAL-MUSCLE BIOENERGETICS IN HEALTHY OLD MEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A216 EP A216 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000598 ER PT J AU CHOI, BG KATSIYIANNIS, PT DILSIZIAN, V PANZA, JA YAMINE, A JOHNSON, G NEBLETT, J CHOI, BW AF CHOI, BG KATSIYIANNIS, PT DILSIZIAN, V PANZA, JA YAMINE, A JOHNSON, G NEBLETT, J CHOI, BW TI FUNCTIONAL DIFFERENCE BETWEEN ISOTONIC AND ISOMETRIC-EXERCISE IN ROWERS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A322 EP A322 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02001199 ER PT J AU CHOU, CL LUTHER, A KNEPPER, MA AF CHOU, CL LUTHER, A KNEPPER, MA TI OXYTOCIN IS AN ANTIDIURETIC-HORMONE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A265 EP A265 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000872 ER PT J AU CID, MC ESPARZA, J GRANT, DG MORALES, D KELLY URBANOMARQUEZ, A SCHNAPER, WH KLEINMAN, HK AF CID, MC ESPARZA, J GRANT, DG MORALES, D KELLY URBANOMARQUEZ, A SCHNAPER, WH KLEINMAN, HK TI ESTRADIOL INCREASES ENDOTHELIAL-CELL ATTACHMENT TO EXTRACELLULAR-MATRIX PROTEINS THROUGH AN INCREASE IN INTEGRIN EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HOSP CLIN BARCELONA,DEPT INTERNAL MED,BARCELONA 36,SPAIN. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 2 TC 3 Z9 3 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A131 EP A131 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000113 ER PT J AU DEBINSKI, W LIND, P PASTAN, I AF DEBINSKI, W LIND, P PASTAN, I TI MONOVALENT RECOMBINANT IMMUNOTOXINS COMPOSED OF A C242 MONOCLONAL-ANTIBODY AND PSEUDOMONAS EXOTOXIN-A SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UM,HDM,MOLEC TARGETING LAB,MONTREAL,PQ,CANADA. KABI PHARM BIOSCI CTR,STOCKHOLM,SWEDEN. NCI,DCBDC,LMB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A251 EP A251 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000794 ER PT J AU EGAN, J MONTROSERAFIZADEH, C BERNIER, M ROTH, J AF EGAN, J MONTROSERAFIZADEH, C BERNIER, M ROTH, J TI GLUCAGON-LIKE PEPTIDE-1 ENHANCES INSULIN-STIMULATED GLUCOSE-METABOLISM IN 3T3-L1 ADIPOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,BALTIMORE,MD 21224. JHU,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A211 EP A211 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000566 ER PT J AU EHMANN, WC RABKIN, CS EYSTER, ME AF EHMANN, WC RABKIN, CS EYSTER, ME TI THROMBOCYTOPENIA IN HIV-INFECTED HEMOPHILIACS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 PENN STATE UNIV,COLL MED,DEPT MED,UNIV PK,PA 16802. NCI,VIRAL EPIDEMIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A279 EP A279 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000952 ER PT J AU FIGG, WD PLUDA, JM WYVILL, K SAVILLE, W THIBAULT, A MCCALL, NA SOGOCIO, T REED, E BRODER, S YARCHOAN, R AF FIGG, WD PLUDA, JM WYVILL, K SAVILLE, W THIBAULT, A MCCALL, NA SOGOCIO, T REED, E BRODER, S YARCHOAN, R TI THE PHARMACOKINETICS OF TNP-470, A NEW ANGIOGENESIS INHIBITOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. RI Figg Sr, William/M-2411-2016 NR 2 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A253 EP A253 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000805 ER PT J AU FRANZOSO, G BISWAS, P POLI, G BROWN, K CARLSON, L FAUCI, AS SIEBENLIST, U AF FRANZOSO, G BISWAS, P POLI, G BROWN, K CARLSON, L FAUCI, AS SIEBENLIST, U TI A NOVEL NF-KAPPA-B COMPLEX IS GENERATED BY UNIQUE GRANULAR SERINE PROTEASES DURING EXTRACTION OF MYELO-MONOCYTIC CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A155 EP A155 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000250 ER PT J AU GAO, WY JOHNS, DG MITSUYA, H AF GAO, WY JOHNS, DG MITSUYA, H TI ANTI-HIV-1 ACTIVITY OF HYDROXYUREA IN COMBINATION WITH 2',3'-DIDEOXYNUCLEOSIDES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,MED BRANCH,EXPTL PETROVIROL SECT,BETHESDA,MD 20892. NCI,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A280 EP A280 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000961 ER PT J AU HAHN, SH KRASNEWICH, DM GAHL, WA AF HAHN, SH KRASNEWICH, DM GAHL, WA TI MUTATION ANALYSIS OF THE FUMARYLACETOACETATE HYDROLASE GENE IN AN AMERICAN BOY WITH TYROSINEMIA TYPE-I SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A200 EP A200 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000507 ER PT J AU HANSS, BG RAPPAPORT, J BRUGGEMAN, LA COFFMAN, TM KLOTMAN, PE AF HANSS, BG RAPPAPORT, J BRUGGEMAN, LA COFFMAN, TM KLOTMAN, PE TI KIDNEY SERVES AS A CRITICAL ORGAN FOR THE HANDLING OF SYSTEMIC ANTISENSE FOR GENE-THERAPY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,LOM,BETHESDA,MD 20892. DUKE UNIV,DEPT MED,DURHAM,NC 27706. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A221 EP A221 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000623 ER PT J AU HARRIS, T ROUBENOFF, R WILSON, P CANNON, J ABAD, J ABAD, L DINARELLO, CA AF HARRIS, T ROUBENOFF, R WILSON, P CANNON, J ABAD, J ABAD, L DINARELLO, CA TI INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR IN OLD-AGE - THE FRAMINGHAM HEART-STUDY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A218 EP A218 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000606 ER PT J AU HARRISON, K DRUEY, K DEGUCHI, Y KEHRL, JH AF HARRISON, K DRUEY, K DEGUCHI, Y KEHRL, JH TI A HUMAN HOMEOBOX GENE-RELATED TO PROBOSCIPEDIA IS EXPRESSED IN LYMPHOID-TISSUES AND PANCREAS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A123 EP A123 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000066 ER PT J AU HOLLAND, SM FRUCHT, DM GALLIN, JI AF HOLLAND, SM FRUCHT, DM GALLIN, JI TI TREATMENT OF PULMONARY MYCOBACTERIUM-AVIUM COMPLEX INFECTIONS WITH INTERFERON-GAMMA - A PRELIMINARY-REPORT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEFENSES LAB,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A302 EP A302 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02001083 ER PT J AU JACKSON, SH TOMS, A MARROQUIN, P KUHNS, DB ROTROSEN, D GALLIN, JI HOLLAND, SM AF JACKSON, SH TOMS, A MARROQUIN, P KUHNS, DB ROTROSEN, D GALLIN, JI HOLLAND, SM TI GRANULOMATOUS COLITIS AS THE SOLE MANIFESTATION OF CHRONIC GRANULOMATOUS-DISEASE IN AN X-LINKED KINDRED - CLINICAL AND MOLECULAR CHARACTERIZATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEFENSES LAB,BETHESDA,MD 20892. PRI DYNCORP,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A242 EP A242 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000744 ER PT J AU JUSTICE, JM STEVENS, LA BLIZIOTES, MM MOSS, J VAUGHAN, M AF JUSTICE, JM STEVENS, LA BLIZIOTES, MM MOSS, J VAUGHAN, M TI CHIMERIC ALPHA-SUBUNITS OF THE HETEROTRIMERIC GUANINE-NUCLEOTIDE-BINDING PROTEINS REVEAL AMINO-TERMINAL SPECIFICITY OF MONOCLONAL-ANTIBODIES LAS-1 AND LAS-2 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A332 EP A332 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02001256 ER PT J AU KANG, V HONG, JX KEHRI, JH AF KANG, V HONG, JX KEHRI, JH TI BL34 IS DISTANTLY RELATED TO HELIX-LOOP-HELIX PROTEINS AND LOCALIZED IN GERMINAL CENTER B-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A205 EP A205 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000531 ER PT J AU KAVLICK, MF KOJIMA, E SHIRASAKA, T PLUDA, J YARCHOAN, R MITSUYA, H AF KAVLICK, MF KOJIMA, E SHIRASAKA, T PLUDA, J YARCHOAN, R MITSUYA, H TI DEVELOPMENT OF 3TC-RESISTANT HIV-1 IN PATIENTS RECEIVING 3TC SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,EXP RETROVIRAL SECT,BETHESDA,MD 20892. NCI,MED BRANCH,RETROVIRAL DIS SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A280 EP A280 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000962 ER PT J AU KELSALL, BL EISENSTEIN, EM STROBER, W AF KELSALL, BL EISENSTEIN, EM STROBER, W TI MESSENGER-RNA FOR INTERLEUKIN-12 IS PRODUCED BY DENDRITIC CELLS FROM THE SPLEEN AND PEYERS PATCH OF MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A308 EP A308 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02001116 ER PT J AU KLEIN, RC GUDAS, JM COWAN, KH AF KLEIN, RC GUDAS, JM COWAN, KH TI ROLE OF C-MYB PROTOONCOGENE IN BREAST-CANCER SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,MED BRANCH,MED BREAST CANC SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A122 EP A122 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000062 ER PT J AU KOPP, JB NAGY, P SANDERSON, N WAKEFIELD, L ROBERTS, AB SPORN, MB THORGEIRSSON, SS KLOTMAN, PE AF KOPP, JB NAGY, P SANDERSON, N WAKEFIELD, L ROBERTS, AB SPORN, MB THORGEIRSSON, SS KLOTMAN, PE TI CIRCULATING TGF-BETA-1 AND RENAL-DISEASE IN TRANSGENIC MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,LOM,BETHESDA,MD 20892. NCI,LCP,BETHESDA,MD 20892. NCI,LEC,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A144 EP A144 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000189 ER PT J AU KRASNEWICH, DM BRANTLY, M SKOVBY, F REDWINE, J GAHL, W HOLT, G AF KRASNEWICH, DM BRANTLY, M SKOVBY, F REDWINE, J GAHL, W HOLT, G TI EVIDENCE FOR ABNORMAL SYNTHESIS OF DOLICHOL-LINKED OLIGOSACCHARIDES IN CARBOHYDRATE-DEFICIENT GLYCOPROTEIN SYNDROME SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,HUMAN GENET BRANCH,BETHESDA,MD 20892. RIGSHOSP,DEPT PEDIAT,DIV CLIN GENET,DK-2100 COPENHAGEN,DENMARK. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A201 EP A201 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000510 ER PT J AU LETHBRIDGECEIKU, M HOCHBERG, MC SCOTT, WW REICHLE, R ZONDERMAN, A AF LETHBRIDGECEIKU, M HOCHBERG, MC SCOTT, WW REICHLE, R ZONDERMAN, A TI ASSOCIATION OF KNEE PAIN WITH RADIOGRAPHIC FEATURES OF OSTEOARTHRITIS IN PERSONS AGED 60 AND ABOVE - DATA FROM THE BALTIMORE LONGITUDINAL-STUDY OF AGING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MARYLAND,SCH MED,BALTIMORE,MD 21201. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A218 EP A218 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000607 ER PT J AU LIAO, F FARBER, JM AF LIAO, F FARBER, JM TI CHARACTERIZATION OF MIG, A NOVEL CHEMOKINE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A306 EP A306 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02001106 ER PT J AU MARSHALL, MA ACTOR, JK SHER, A BERZOFSKY, JA AF MARSHALL, MA ACTOR, JK SHER, A BERZOFSKY, JA TI SUPPRESSION OF HIV-SPECIFIC CTL RESPONSE BY LYMPHOCYTES FROM HELMINTH-INFECTED MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,METAB BRANCH,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A273 EP A273 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000917 ER PT J AU MAWHORTER, SD STEPHANY, DA NUTMAN, TB OTTESEN, EA AF MAWHORTER, SD STEPHANY, DA NUTMAN, TB OTTESEN, EA TI FLOW CYTOMETRIC ANALYSIS OF EOSINOPHIL SURFACE MOLECULES IN WHOLE-BLOOD SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A277 EP A277 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000945 ER PT J AU MCVICAR, DW KAWAMURA, M LAL, BK CHEN, YQ ZHANG, X LLOYD, A STAPLES, JE ORTALDO, JR OSHEA, JJ AF MCVICAR, DW KAWAMURA, M LAL, BK CHEN, YQ ZHANG, X LLOYD, A STAPLES, JE ORTALDO, JR OSHEA, JJ TI NOVEL PROTEIN-TYROSINE KINASES (PTK) IN NATURAL-KILLER (NK) CELLS AND ACTIVATED T-LYMPHOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,FCRDC,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. NCI,FCRDC,PRI DYNCORP,BCDP,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A206 EP A206 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000538 ER PT J AU MERTINS, SD KIND, PD TRUNK, SL CHANOCK, SJ AF MERTINS, SD KIND, PD TRUNK, SL CHANOCK, SJ TI EFFECTS OF HIV ENVELOPE PROTEINS, GP120 AND GP160, ON THE PRODUCTION OF SUPEROXIDE (O2-) IN NEUTROPHILS (PMN) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A156 EP A156 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000253 ER PT J AU MONTROSERAFIZADEH, C EGAN, J ROTH, J AF MONTROSERAFIZADEH, C EGAN, J ROTH, J TI INCRETIN HORMONES REGULATE GLUCOSE-DEPENDENT INSULIN-SECRETION IN THE RIN 1046-38 CELLS - MECHANISMS OF ACTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIA,BALTIMORE,MD 21224. JHU,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A213 EP A213 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000581 ER PT J AU MURPHY, WJ FUNAKOSHI, S BECKWITH, M ARMITAGE, RJ LONGO, DL AF MURPHY, WJ FUNAKOSHI, S BECKWITH, M ARMITAGE, RJ LONGO, DL TI ANTIBODIES TO CD40 PROMOTE NORMAL HUMAN B-CELL ENGRAFTMENT AND INHIBIT B-CELL LYMPHOMAGENESIS IN-VIVO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,FCRDC,PRI DYNCORP,FREDERICK,MD 21701. NCI,FCRDC,DCT,BRMP,LLB,FREDERICK,MD 21701. IMMUNEX CORP,SEATTLE,WA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A310 EP A310 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02001129 ER PT J AU NEWMAN, T FRIEDMAN, TC MASTORAKOS, G BOUZAS, EA MULLEN, NM HORTON, E CHROUSOS, GP AF NEWMAN, T FRIEDMAN, TC MASTORAKOS, G BOUZAS, EA MULLEN, NM HORTON, E CHROUSOS, GP TI CARBOHYDRATE-METABOLISM, BONE-DENSITY AND OPHTHALMOLOGIC FINDINGS IN ENDOGENOUS HYPERCORTISOLISM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD. NICHHD,DEB,BETHESDA,MD. NEI,OPHTHALM GENET & CLIN SERV BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A270 EP A270 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000899 ER PT J AU OLSON, BR RUBINO, DM GUMOWSKY, J OLDFIELD, EH AF OLSON, BR RUBINO, DM GUMOWSKY, J OLDFIELD, EH TI HYPONATREMIA FOLLOWING TRANSSPHENOIDAL SURGERY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD. NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A223 EP A223 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000633 ER PT J AU PETERS, B FIBACH, E DINH, K SCHECHTER, AN NOGUCHI, CT AF PETERS, B FIBACH, E DINH, K SCHECHTER, AN NOGUCHI, CT TI AN ERYTHROID-SPECIFIC FACTOR MAY REPRESS SIGMA-GLOBIN GENE-EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDDK,CHEM BIOL LAB,BETHESDA,MD. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A237 EP A237 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000715 ER PT J AU PILLEMER, SR CROFFORD, LJ CASH, JM WILDER, RL DALE, JK BENSONGRIGG, E STRAUS, S AF PILLEMER, SR CROFFORD, LJ CASH, JM WILDER, RL DALE, JK BENSONGRIGG, E STRAUS, S TI DIFFERENCES BETWEEN CHRONIC FATIGUE SYNDROME AND FIBROMYALGIA PATIENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Crofford, Leslie/J-8010-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A142 EP A142 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000174 ER PT J AU PLOWE, CV BOARE, M DJIMDE, A DOUMBO, O WELLEMS, TE AF PLOWE, CV BOARE, M DJIMDE, A DOUMBO, O WELLEMS, TE TI MOLECULAR EPIDEMIOLOGY OF PYRIMETHAMINE AND PROGUANIL RESISTANT MALARIA IN MALI SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NATL SCH MED & PHARM,BAMAKO,MALI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A283 EP A283 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000976 ER PT J AU PRAS, E ARBER, N AKSENTIJEVICH, I WEISSENBACH, J PRAS, M KASTNER, DL AF PRAS, E ARBER, N AKSENTIJEVICH, I WEISSENBACH, J PRAS, M KASTNER, DL TI LINKAGE OF CYSTINURIA TO CHROMOSOME-2P SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,BETHESDA,MD. BEILINSON MED CTR,IL-49100 PETAH TIQWA,ISRAEL. INST PASTEUR,F-75724 PARIS 15,FRANCE. CHAIM SHEBA MED CTR,IL-52621 TEL HASHOMER,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A202 EP A202 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000516 ER PT J AU PUCK, JM LIU, X HENTHORN, PS AF PUCK, JM LIU, X HENTHORN, PS TI MUTATIONS CAUSING X-LINKED SEVERE COMBINED IMMUNODEFICIENCY IN THE GENE ENCODING THE GAMMA-CHAIN OF THE INTERLEUKIN-2 RECEPTOR COMPLEX SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. UNIV PENN,SCH VET MED,PHILADELPHIA,PA 19104. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A201 EP A201 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000512 ER PT J AU QAZILBASH, M WALSH, C YOUNG, N LIU, J AF QAZILBASH, M WALSH, C YOUNG, N LIU, J TI PROGRESS TOWARDS GENE-THERAPY OF X-LINKED SCID SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NHLBI,HEMATOL BRANCH,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A202 EP A202 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000514 ER PT J AU RAPPAPORT, J ARYA, SK NOTKINS, AL RICHARDSON, MW KLOTMAN, PE AF RAPPAPORT, J ARYA, SK NOTKINS, AL RICHARDSON, MW KLOTMAN, PE TI MOLECULAR INHIBITION OF HIV-1 REPLICATION BY A NONCYTOPATHIC HIV-2 PROVIRUS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIDR,ORAL MED LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A154 EP A154 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000245 ER PT J AU RIVA, A WILSON, GL KEHRL, JH AF RIVA, A WILSON, GL KEHRL, JH TI MOLECULAR MECHANISMS REGULATING CD19 GENE-TRANSCRIPTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A123 EP A123 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000064 ER PT J AU ROSENBERG, HF MORRISON, RP LI, F AF ROSENBERG, HF MORRISON, RP LI, F TI CMP40 - A NOVEL PROTEIN EXPRESSED IN EARLY HEMATOPOIETIC PROGENITOR CELLS WITH HOMOLOGY TO THE HSP60 MOLECULAR CHAPERONES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,HOST DEFENSES LAB,BETHESDA,MD 20892. NIAID,INTRACELLULAR PARASITES LAB,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A234 EP A234 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000696 ER PT J AU STANLEY, SK SULLIVAN, M JUSTEMENT, JS FAUCI, AS AF STANLEY, SK SULLIVAN, M JUSTEMENT, JS FAUCI, AS TI EFFECTS OF IMMUNOMODULATORY DRUGS ON HIV-INFECTION IN THE SCID-HU THYMUS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A156 EP A156 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000257 ER PT J AU TALAL, N DANG, H GEISER, A LETTERIO, J SPORN, M AF TALAL, N DANG, H GEISER, A LETTERIO, J SPORN, M TI GENERALIZED AUTOIMMUNITY AND LYMPHOPROLIFERATION IN TGF-BETA-1 KNOCK-OUT MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A304 EP A304 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02001096 ER PT J AU THEVENIN, C WILSON, GL KEHRL, JH AF THEVENIN, C WILSON, GL KEHRL, JH TI THE CD20 GENE IS AN EXCELLENT PROTOTYPE FOR THE STUDY OF B-LINEAGE SPECIFIC GENE-EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A123 EP A123 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000065 ER PT J AU TUSCANO, JM KEHRL, JH AF TUSCANO, JM KEHRL, JH TI THE ARH1 MOTIF OF CD22 BINDS LYN, SYK, AND PI-3 KINASES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,LIR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A205 EP A205 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000533 ER PT J AU VITTONE, J HARMAN, SM ROGERS, M TOBIN, J BELLANTONI, M BUSBYWHITEHEAD, J STEVENS, T BAROFSKY, I STEWART, K DOI, S BAUMANN, G BLACKMAN, MR AF VITTONE, J HARMAN, SM ROGERS, M TOBIN, J BELLANTONI, M BUSBYWHITEHEAD, J STEVENS, T BAROFSKY, I STEWART, K DOI, S BAUMANN, G BLACKMAN, MR TI EFFECTS OF GROWTH-HORMONE RELEASING HORMONE (GHRH) IN HEALTHY ELDERLY MEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 FRANCIS SCOTT KEY MED CTR,DEPT MED,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NIA,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A216 EP A216 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000597 ER PT J AU WASHBURN, RG JULIAN, NC CHANG, YC KWONCHUNG, KJ AF WASHBURN, RG JULIAN, NC CHANG, YC KWONCHUNG, KJ TI PIGMENT PRODUCTION BY ASPERGILLUS-FUMIGATUS CONIDIA INFLUENCES ALTERNATIVE COMPLEMENT PATHWAY-MEDIATED OPSONIZATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 WAKE FOREST UNIV,MED CTR,DEPT MED,WINSTON SALEM,NC 27109. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A153 EP A153 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000240 ER PT J AU WELLEMS, TE SU, X VAIDYA, AB KASLOW, DC SCHERF, A AF WELLEMS, TE SU, X VAIDYA, AB KASLOW, DC SCHERF, A TI MALARIA GENETICS - MAPPING DETERMINANTS OF DRUG-RESISTANCE AND INFECTIVITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. HAHNEMANN UNIV,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19102. INST PASTEUR,UNITE PARASITOL,F-75724 PARIS 15,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A283 EP A283 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000975 ER PT J AU XU, LC DONAHUE, RC KLUEPFELSTAHL, S BYRNE, E AGRICOLA, B KESSLER, S DUNBAR, C CLINE, A BRADY, RO NIENHUIS, AW KARLSSON, S AF XU, LC DONAHUE, RC KLUEPFELSTAHL, S BYRNE, E AGRICOLA, B KESSLER, S DUNBAR, C CLINE, A BRADY, RO NIENHUIS, AW KARLSSON, S TI RETROVIRAL SUPERNATANT TRANSDUCTION RESULTS IN LONG-TERM LEUKOCYTE MARKING OF RHESUS-MONKEYS WITH THE HUMAN GLUCOCEREBROSIDASE GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NINCDS,BETHESDA,MD 20892. NHLBI,SURG ONCOL BRANCH,BETHESDA,MD 20892. USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A237 EP A237 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000713 ER PT J AU YANO, T LEWIS, B HOANG, A BARRETT, J RAFFELD, M DANG, CV AF YANO, T LEWIS, B HOANG, A BARRETT, J RAFFELD, M DANG, CV TI LYMPHOMA-DERIVED C-MYC MUTANTS RESIST SUPPRESSION BY RETINOBLASTOMA-RELATED PROTEIN P107 SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV HEMATOL,BALTIMORE,MD 21205. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A125 EP A125 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000080 ER PT J AU ZHOU, J JENSEN, SM AVIS, I TRESTON, A SCOTT, F CUTTITTA, F MULSHINE, J LINNOILA, R AF ZHOU, J JENSEN, SM AVIS, I TRESTON, A SCOTT, F CUTTITTA, F MULSHINE, J LINNOILA, R TI EXPRESSION OF EARLY LUNG-CANCER DETECTION MARKER (P-31) IN NEOPLASTIC AND NONNEOPLASTIC RESPIRATORY EPITHELIUM SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 NCI,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1994 VL 42 IS 2 BP A127 EP A127 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA NF020 UT WOS:A1994NF02000090 ER PT J AU HELOE, LA GRYTTEN, J WARREN, GB BROWN, LJ AF HELOE, LA GRYTTEN, J WARREN, GB BROWN, LJ TI A COMPARATIVE-STUDY OF COSTS FOR DENTAL SERVICES AND DENTISTS INCOMES IN THE UNITED-STATES AND NORWAY SO COMMUNITY DENTISTRY AND ORAL EPIDEMIOLOGY LA English DT Article DE DENTAL SERVICES, COSTS; DENTIST INCOME; US; NORWAY AB The United States and Norway have approximately the same per capita Gross Domestic Product (GDP) and average personal income, but their per capita health spending patterns are quite different. In 1982, the US spent 6.5% of its total health expenditures on dental services while Norway spent 5.4%. A higher percentage of Norwegian adults see a dentist annually as compared to US adults. In 1984, the mean net income of dentists in private practice was $66940 in the US and $27 125 in Norway; this is respectively 5 and 1 3/4 times the average per capita income in those countries. The American publicly-employed dentist earned approximately two-thirds of what the American private practitioner made, while still earning approximately 50% more than his Norwegian counterpart. Some basic information concerning the ratios of dentists, specialists, and dental hygienists to the population is given. The relative proportion of women dentists in the two countries is contrasted. Finally, data on graduates from the dental schools, enrollment cuts, and estimated dentist to population ratios by the year 2000 are described to compare future man-power that will be available to the two countries. Several dissimilarities in the political and social systems are described and discussed. It is emphasized that caution should be used when interpreting and comparing data about countries with different dental delivery, political, and social systems. C1 NIDR,BETHESDA,MD 20892. RP HELOE, LA (reprint author), UNIV OSLO,INST COMMUNITY DENT,POB 1052,N-0316 OSLO,NORWAY. NR 30 TC 3 Z9 3 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0301-5661 J9 COMMUNITY DENT ORAL JI Community Dentist. Oral Epidemiol. PD APR PY 1994 VL 22 IS 2 BP 65 EP 70 DI 10.1111/j.1600-0528.1994.tb01574.x PG 6 WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational Health GA NH439 UT WOS:A1994NH43900001 PM 8205781 ER PT J AU KEENAN, TW ZIERDT, CH AF KEENAN, TW ZIERDT, CH TI LIPID BIOSYNTHESIS BY AXENIC STRAINS OF BLASTOCYSTIS-HOMINIS SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY LA English DT Article DE LIPID BIOSYNTHESIS; AXENIC STRAINS; BLASTOCYSTIS HOMINIS ID PROTOZOAN AB Axenic strains of Blastocystis hominis incorporated (32)p, added to the medium as orthophosphate, into a number of phospholipids, including sphingomyelin, cardiolipin, phosphatidic acid, the phosphoglycerides of choline, ethanolamine, serine, and inositol and some other minor phospholipids. Radioactive palmitate and glycerol provided in the growth medium introduced radiolabel into diacylglycerols, triacylglycerols, and all major phosphoglycerides found in the organism. Palmitate is a major fatty acid of cholesterol esters in B. hominis, but radioactive palmitate did not enter the cholesterol ester pool. Radioactive acetate was not incorporated into any lipids. Cholesterol and cholesterol esters of the organism were not labeled when cells were grown in the presence of radioactive glucose, mevalonic acid, or mevalonolactone. Radioactive cholesterol added to the medium became stably associated with B. hominis cells, but none of the radioactive cholesterol entered the cholesterol ester pool. Cholesterol-[H-3]-palmitate added to the medium became stably associated with the organism, and most of the radioactivity associated with the cells remained in the cholesterol ester fraction on extended incubation. These results show that this parasitic protozoan has the capacity to synthesize most cellular lipids de novo, but suggest that it acquires free cholesterol and intact cholesterol esters directly from growth medium. C1 VIRGINIA POLYTECH INST & STATE UNIV,DEPT BIOCHEM & ANAEROB MICROBIOL,BLACKSBURG,VA 24061. NIH,DEPT CLIN PATHOL,MICROBIOL SERV,BETHESDA,MD 20205. FU NIGMS NIH HHS [GM31244] NR 14 TC 3 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0305-0491 J9 COMP BIOCHEM PHYS B JI Comp. Biochem. Physiol. B-Biochem. Mol. Biol. PD APR PY 1994 VL 107 IS 4 BP 525 EP 531 DI 10.1016/0305-0491(94)90180-5 PG 7 WC Biochemistry & Molecular Biology; Zoology SC Biochemistry & Molecular Biology; Zoology GA NF560 UT WOS:A1994NF56000005 PM 8205379 ER PT J AU CONNOR, RJ ENG, D PROROK, PC AF CONNOR, RJ ENG, D PROROK, PC TI ISSUES IN THE MORTALITY ANALYSIS OF RANDOMIZED CONTROLLED TRIALS OF CANCER SCREENING SO CONTROLLED CLINICAL TRIALS LA English DT Article ID HEALTH-INSURANCE PLAN; BREAST-CANCER; AGE AB This paper is concerned with the analysis and interpretation of randomized controlled trials (RCTs) of periodic screening programs for the early detection of cancer in which there is a lengthy follow-up period without screening being offered. That is, screening is offered for a limited time with a subsequent follow-up period during which the cancer mortality is observed. The paper focuses on tests for a mortality reduction due to screening. Two approaches are presented, one based on the experience of all those randomized to the test and control groups, and the other based on the experience of selected groups of cancer cases found during the trial. In the latter approach it is necessary that the two groups selected for analysis be comparable groups of cancers. The concept of comparability is discussed with emphasis on factors that determine comparability and on ways to assess it. Examples from completed cancer screening RCTs are used to illustrate the ideas and methods presented. RP CONNOR, RJ (reprint author), NCI,DIV CANC PREVENT & CONTROL,BIOMETRY BRANCH,9000 ROCKVILLE PIKE,EPN 344,BETHESDA,MD 20892, USA. NR 16 TC 20 Z9 20 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD APR PY 1994 VL 15 IS 2 BP 81 EP 99 DI 10.1016/0197-2456(94)90014-0 PG 19 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA NM878 UT WOS:A1994NM87800001 PM 8205806 ER PT J AU CHEN, TT SIMON, RM AF CHEN, TT SIMON, RM TI EXTENSION OF ONE-SIDED TEST TO MULTIPLE TREATMENT TRIALS SO CONTROLLED CLINICAL TRIALS LA English DT Article DE MULTIPLE STEP; BUBBLE SORTING; SELECTION; MULTIPLE COMPARISON; SAMPLE SIZE AB In a two-treatment clinical trial, a one-sided test is sometimes used in reaching a decision. Usually we are interested in doing a one-sided test because of the existence of an unequal preference between the two treatments. When a standard control is just as good or better than the new experimental treatment (which has more toxicity or cost), we will stay with the standard control. In this paper, we extend the concept of a one-sided test to the multiple treatment trial where three or more treatments are involved. We assume that there is an order of strictly decreasing preference among the treatments. We propose two multiple-step decision procedures that are similar to the bubble sorting algorithm and will guarantee a high probability of finally selecting the correct treatment. We also provide methods to calculate the sample size required to detect a specific difference. The derivation is based on normal data, and the extension to binomial or exponential data with random censoring is through large sample approximation. RP CHEN, TT (reprint author), NCI,BIOMETRIC RES BRANCH,EPN-739,BETHESDA,MD 20892, USA. NR 10 TC 5 Z9 5 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0197-2456 J9 CONTROL CLIN TRIALS JI Controlled Clin. Trials PD APR PY 1994 VL 15 IS 2 BP 124 EP 134 PG 11 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA NM878 UT WOS:A1994NM87800003 PM 8205803 ER PT J AU VANDERVORT, AL DANNER, RL AF VANDERVORT, AL DANNER, RL TI ANTIENDOTOXIN APPROACHES TO SEPTIC SHOCK THERAPY SO CRITICAL CARE MEDICINE LA English DT Editorial Material DE SHOCK, SEPTIC; MONOCLONAL ANTIBODIES; ENDOTOXIN; GRAM-NEGATIVE BACTERIA; CRITICAL ILLNESS ID TUMOR-NECROSIS-FACTOR; GRAM-NEGATIVE BACTEREMIA; POLYMYXIN-B SULFATE; CANINE MODEL; LIPOPOLYSACCHARIDE LPS; MONOCLONAL-ANTIBODIES; BINDING-PROTEIN; ENDOTOXIN; DYSFUNCTION; INTERLEUKIN-6 C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT CRIT CARE MED,BETHESDA,MD 20892. NR 36 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD APR PY 1994 VL 22 IS 4 BP 539 EP 541 PG 3 WC Critical Care Medicine SC General & Internal Medicine GA NF153 UT WOS:A1994NF15300001 PM 8143457 ER PT J AU KEHRL, JH AF KEHRL, JH TI HOMEOBOX GENES IN HEMATOPOIESIS SO CRITICAL REVIEWS IN ONCOLOGY/HEMATOLOGY LA English DT Review ID DROSOPHILA HOMEODOMAIN PROTEINS; DNA-BINDING DOMAIN; T-CELL LEUKEMIA; TRANSCRIPTION FACTOR; PRE-B; MYELOID-LEUKEMIA; RESTRICTED EXPRESSION; TRANSLOCATION PROTEIN; MOLECULAR CONTROL; HOMEOTIC GENES RP KEHRL, JH (reprint author), NIAID,IMMUNOREGULAT LAB,CELL MOLEC BIOL SECT B,BLDG 10,RM 11B-13,BETHESDA,MD 20892, USA. OI Kehrl, John/0000-0002-6526-159X NR 109 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1040-8428 J9 CRIT REV ONCOL HEMAT JI Crit. Rev. Oncol./Hematol. PD APR PY 1994 VL 16 IS 2 BP 145 EP 156 DI 10.1016/1040-8428(94)90046-9 PG 12 WC Oncology; Hematology SC Oncology; Hematology GA NT972 UT WOS:A1994NT97200004 PM 7915117 ER PT J AU DRESSLER, GR AF DRESSLER, GR TI THE PROS AND CONS OF C-RET SO CURRENT BIOLOGY LA English DT Note ID RECEPTOR; EXPRESSION RP DRESSLER, GR (reprint author), NICHHD,BETHESDA,MD 20892, USA. NR 15 TC 3 Z9 3 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD APR 1 PY 1994 VL 4 IS 4 BP 354 EP 356 DI 10.1016/S0960-9822(00)00078-6 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NF783 UT WOS:A1994NF78300011 PM 7922346 ER PT J AU METZGER, H AF METZGER, H TI INSIDE JOB SO CURRENT BIOLOGY LA English DT Note RP METZGER, H (reprint author), NIAMS,BETHESDA,MD 20892, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD APR 1 PY 1994 VL 4 IS 4 BP 377 EP 379 DI 10.1016/S0960-9822(00)00085-3 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NF783 UT WOS:A1994NF78300018 PM 7922351 ER PT J AU SCHULKIN, J AF SCHULKIN, J TI MELANCHOLIC DEPRESSION AND THE HORMONES OF ADVERSITY - A ROLE FOR THE AMYGDALA SO CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE LA English DT Article ID BIOCHEMICAL MANIFESTATIONS; STRESS; NEUROBIOLOGY RP SCHULKIN, J (reprint author), NIMH,NEUROENDOCRINOL BRANCH,BEHAV NEUROSCI UNIT,BLDG 10,ROOM 35231,BETHESDA,MD 20892, USA. NR 24 TC 7 Z9 8 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0963-7214 J9 CURR DIR PSYCHOL SCI JI Curr. Dir. Psychol. PD APR PY 1994 VL 3 IS 2 BP 41 EP 44 DI 10.1111/1467-8721.ep10769930 PG 4 WC Psychology, Multidisciplinary SC Psychology GA NM279 UT WOS:A1994NM27900003 ER PT J AU RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B AF RENGARAJAN, K DESMET, MD CHADER, GJ WIGGERT, B TI IDENTIFICATION OF HEAT-SHOCK PROTEINS BINDING TO AN IMMUNODOMINANT UVEITOPATHOGENIC PEPTIDE OF IRBP SO CURRENT EYE RESEARCH LA English DT Article DE CHAPERONE; UVEITIS; B CELL; PEPTIDES; INTERPHOTORECEPTOR RETINOID-BINDING PROTEIN (IRBP); BEHCETS DISEASE; HUMAN; HEAT SHOCK PROTEINS ID EXPERIMENTAL AUTOIMMUNE UVEORETINITIS; T-CELL LINES; MAJOR HISTOCOMPATIBILITY COMPLEX; LYMPHOCYTES-B; IMMUNE RESPONSIVENESS; S-ANTIGEN; UVEITIS; DETERMINANT; PINEALITIS; INDUCTION AB Intracellular binding proteins have been identified and isolated from B cells by their ability to bind to the synthetic peptide (1169-1191), the major immunodominant epitope of bovine interphotoreceptor retinoid-binding protein (IRBP) coupled to cyanogen bromide activated Sepharose 4B. After SDS-PAGE, two discrete protein bands of approximate to 72 and 74 kDa, were found to be present in B cells of naive Lewis rats as well as in EBV transformed B cells from a human patient with ocular Behcet's disease. Enhanced expression of these peptide-binding proteins was achieved by incubating the cells with Lipopolysaccharide (LPS) from S. thyphimurium. The approximate to 72 and 74 kDa peptide-binding proteins reacted in western blot with monoclonal antibodies specific for both constitutively expressed and inducible 72/74 kDa hsp 70 proteins. The demonstration that these proteins bind to the immunodominant epitope of IRBP indicates that they may play a role in the processing and presentation of antigens by antigen-presenting cell (APC). C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. RP RENGARAJAN, K (reprint author), NEI,RETINAL CELL & MOLEC BIOL LAB,BLDG 6,ROOM 338,BETHESDA,MD 20892, USA. OI de Smet, Marc/0000-0002-9217-5603 NR 39 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 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD APR PY 1994 VL 13 IS 4 BP 289 EP 296 DI 10.3109/02713689408995790 PG 8 WC Ophthalmology SC Ophthalmology GA NF934 UT WOS:A1994NF93400007 PM 8033590 ER PT J AU MISHKIN, M MURRAY, EA AF MISHKIN, M MURRAY, EA TI STIMULUS-RECOGNITION SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Article ID INFERIOR TEMPORAL CORTEX; SHORT-TERM-MEMORY; MATCH-TO-SAMPLE; HIPPOCAMPAL-FORMATION; OBJECT-RECOGNITION; PARAHIPPOCAMPAL GYRUS; VISUAL RECOGNITION; BASAL FOREBRAIN; MONKEYS; LESIONS AB This review covers recent research on the neural process through which a novel stimulus becomes familiar. Lesion and recording studies have provided data sufficient to outline a tentative stimulus-recognition circuit and to suggest how the circuit might operate to form the new and relatively lasting stimulus traces that must underlie delayed stimulus recognition. The research has reached a stage where further progress could well be hastened by interaction between experiment and the formal, neurobiologically constrained models that are beginning to appear. RP MISHKIN, M (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 49,ROOM 1B80,BETHESDA,MD 20892, USA. OI Murray, Elisabeth/0000-0003-1450-1642 NR 65 TC 103 Z9 103 U1 0 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-4388 J9 CURR OPIN NEUROBIOL JI Curr. Opin. Neurobiol. PD APR PY 1994 VL 4 IS 2 BP 200 EP 206 DI 10.1016/0959-4388(94)90073-6 PG 7 WC Neurosciences SC Neurosciences & Neurology GA NJ148 UT WOS:A1994NJ14800010 PM 8038577 ER PT J AU PARASURAMAN, R MARTIN, A AF PARASURAMAN, R MARTIN, A TI COGNITION IN ALZHEIMERS-DISEASE - DISORDERS OD ATTENTION AND SEMANTIC KNOWLEDGE SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Article ID SELECTIVE ATTENTION; DEMENTIA; MEMORY; IMPAIRMENT; CORTEX; NETWORKS; OBJECT; BRAIN AB Alzheimer's disease leads to a selective decline of cognitive skills, particularly semantic knowledge and visuospatial attention. Recent advances suggest that, although the two systems responsible for these skills can interact, the semantic memory deficit seen in Alzheimer's disease cannot be solely attributed to attention or retrieval deficiencies. This is consistent with a modular view of cognition, which postulates that disruption to these systems is selective in Alzheimer's disease. Cortico-cortical disconnection of association areas may disrupt widespread networks mediating attention and semantic knowledge in Alzheimer's disease. C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP PARASURAMAN, R (reprint author), CATHOLIC UNIV AMER,COGNIT SCI LAB,WASHINGTON,DC 20064, USA. RI martin, alex/B-6176-2009 FU NIA NIH HHS [NIA AG07569] NR 70 TC 38 Z9 38 U1 1 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-4388 J9 CURR OPIN NEUROBIOL JI Curr. Opin. Neurobiol. PD APR PY 1994 VL 4 IS 2 BP 237 EP 244 DI 10.1016/0959-4388(94)90079-5 PG 8 WC Neurosciences SC Neurosciences & Neurology GA NJ148 UT WOS:A1994NJ14800016 PM 8038583 ER PT J AU SINGER, HS CHIU, AY MEIRI, KF MORELL, P NELSON, PG TENNEKOON, G AF SINGER, HS CHIU, AY MEIRI, KF MORELL, P NELSON, PG TENNEKOON, G TI ADVANCES IN UNDERSTANDING THE DEVELOPMENT OF THE NERVOUS-SYSTEM SO CURRENT OPINION IN NEUROLOGY LA English DT Editorial Material ID CILIARY NEUROTROPHIC FACTOR; VASOACTIVE-INTESTINAL-PEPTIDE; FLOOR PLATE; FACTOR CNTF; REGIONAL DISTRIBUTION; NEURONAL MIGRATION; TYPE-2 ASTROCYTES; FACTOR PREVENTS; MOTOR NEURONS; RAT-BRAIN AB Over the past several years remarkable progress has been made towards unraveling the complex mechanisms that regulate neuronal development. Because the end results of abnormalities in brain development are often developmental disabilities, it is timely to review several recent advances in the field of neurobiology. This review, with contributions from several co-authors, provides a synopsis of breakthroughs from the fields of embryology, cell biology, and molecular genetics that hold promise for exciting clinical application. This article is arranged to reflect the stages of normal development. Understanding the mechanisms underlying neuronal induction, regional specification, neuronal specification, migration, axonal growth, neurotrophic factors, and myelination should clarify the pathophysiology of numerous neurological disorders, and provide new insights into their treatment. C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD. BECKMAN RES INST CITY HOPE,DUARTE,CA. SUNY HLTH SCI CTR,SYRACUSE,NY 13210. UNIV N CAROLINA,CHAPEL HILL,NC. NICHHD,BETHESDA,MD 20892. UNIV MICHIGAN,ANN ARBOR,MI 48109. NR 67 TC 12 Z9 12 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 1350-7540 J9 CURR OPIN NEUROL JI Curr. Opin. Neurol. PD APR PY 1994 VL 7 IS 2 BP 153 EP 159 DI 10.1097/00019052-199404000-00012 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA ND724 UT WOS:A1994ND72400010 PM 8019661 ER PT J AU JERNIGAN, R RAGHUNATHAN, G BAHAR, I AF JERNIGAN, R RAGHUNATHAN, G BAHAR, I TI CHARACTERIZATION OF INTERACTIONS AND METAL-ION BINDING-SITES IN PROTEINS SO CURRENT OPINION IN STRUCTURAL BIOLOGY LA English DT Article ID BACKBONE DYNAMICS; NMR-SPECTROSCOPY; CALMODULIN; THERMODYNAMICS; RECOGNITION; PEPTIDE AB Recent investigations show that as a class of interactions for designing proteins, hydrophobic interactions are not specific enough, hydrophilic interactions are typically too weak, and water interactions are always on the exterior. In terms of overall protein stability, there is a substantial advantage to a nucleus with strong, directional interactions. Metal ion sites in proteins exhibit strong directional preferences for their coordinate ligands, and the specificities manifested by ions have been demonstrated to be useful in reducing molecular fluctuations. The engineered introduction of zinc binding sites has been shown to improve the stabilities of designed proteins. Metal binding sites can therefore provide important structural building blocks for protein design. C1 BOGAZICI UNIV, POLYMER RES CTR, DEPT CHEM ENGN, BEBEK 80815, TURKEY. TUBITAK, ADV POLYMER MAT RES CTR, BEBEK 80815, TURKEY. RP JERNIGAN, R (reprint author), NCI, DCBDC, MATH BIOL LAB, BETHESDA, MD 20892 USA. RI Jernigan, Robert/A-5421-2012 NR 51 TC 60 Z9 60 U1 1 U2 8 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0959-440X J9 CURR OPIN STRUC BIOL JI Curr. Opin. Struct. Biol. PD APR PY 1994 VL 4 IS 2 BP 256 EP 263 DI 10.1016/S0959-440X(94)90317-4 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NG689 UT WOS:A1994NG68900014 ER PT J AU SOBEL, DO EWEL, CH ZELIGS, B ABBASSI, V ROSSIO, J BELLANTI, JA AF SOBEL, DO EWEL, CH ZELIGS, B ABBASSI, V ROSSIO, J BELLANTI, JA TI POLY I-C INDUCTION OF ALPHA-INTERFERON IN THE DIABETES-PRONE BB AND NORMAL WISTAR RATS - DOSE-RESPONSE RELATIONSHIPS SO DIABETES LA English DT Article ID BETA-CELL DESTRUCTION; INSULIN; MELLITUS; SERUM; INTERLEUKIN-2; STIMULATION; EXPRESSION; DISEASE; GAMMA AB Although the administration of a fixed dose of the alpha-interferon (alpha-IFN) inducer, polyinosinic polycytidilic acid (poly I:C), accelerates the development of diabetes in DP-BB rats, no reports have characterized the dose-response relationship of poly I:C with serum alpha-IFN levels and the development of diabetes. This study examines the dose-response relationships of poly I:C with the induction of serum alpha-IFN and the development of diabetes in DP-BB and normal Wistar rats. Also tested in this study is the hypothesis that the lack of development of diabetes in poly I:C-treated normal Wistar rats is attributable to a deficient alpha-IFN response. Using poly I:C doses of 0.5, 1.5, 5, and 10 mug/g body weight, a direct dose-response relationship was observed in DP-BB rats with the serum alpha-IFN response. Moreover, all doses of poly I:C accelerated the onset of diabetes in BB rats. Serum alpha-IFN levels inversely correlated with time of onset of diabetes (P < 0.01). Also, BB rats with higher levels of serum alpha-IFN were associated with earlier onset of diabetes (P < 0.001). Poly I:C-induced serum alpha-IFN levels were significantly lower in diabetic than in nondiabetic BB rats. In normal Wistar rats, although all doses of poly I:C significantly increased serum alpha-IFN levels, diabetes was not induced. The results of this study indicate that poly I:C administration elevates serum alpha-IFN and accelerates the development of diabetes in BB rats at even very low doses. This finding in conjunction with the correlation of serum alpha-IFN with the onset of diabetes is consistent with a pathogenetic role of alpha-IFN. The absence of a diabetogenic effect of poly I:C in Wistar rats suggests that alpha-IFN alone cannot induce diabetes in this animal. C1 NCI,FCRDC,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21701. GEORGETOWN UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20057. GEORGETOWN UNIV,SCH MED,INT CTR INTERDISCIPLINARY STUDIES IMMUNOL,WASHINGTON,DC 20057. GEORGETOWN UNIV,SCH MED,DEPT MICROBIOL,WASHINGTON,DC 20057. OI Bellanti, Joseph/0000-0002-5038-7202 NR 28 TC 26 Z9 28 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD APR PY 1994 VL 43 IS 4 BP 518 EP 522 DI 10.2337/diabetes.43.4.518 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NC859 UT WOS:A1994NC85900002 PM 8138055 ER PT J AU JANSSEN, RC BOGARDUS, C TAKEDA, J KNOWLER, WC THOMPSON, DB AF JANSSEN, RC BOGARDUS, C TAKEDA, J KNOWLER, WC THOMPSON, DB TI LINKAGE ANALYSIS OF ACUTE INSULIN-SECRETION WITH GLUT2 AND GLUCOKINASE IN PIMA-INDIANS AND THE IDENTIFICATION OF A MISSENSE MUTATION IN GLUT2 SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; GLUCOSE TRANSPORTER; LIVER; GENE; POLYMORPHISMS; NIDDM; EXPRESSION; TWINS; LOCUS AB The acute insulin response (AIR), a measure of pancreatic beat-cell function, aggregates in families and is a predictor for the development of non-insulin-dependent diabetes mellitus (NIDDM) in insulin-resistant Pima Indians. To assess the genetic components of AIR and NIDDM, polymorphic dinucleotide repeat regions in two candidate genes, the liver/islet glucose transporter gene (GLUT2) and the glucokinase gene, were evaluated. Sib-pair linkage analyses were performed to determine if linkage exists between these marker loci and measurements of AIR and NIDDM. No linkage was found between glucokinase and either AIR or NIDDM. Robust sib-pair linkage analyses suggest linkage between GLUT2 and acute insulin response (P = 0.04), but no linkage was observed with NIDDM. The coding region of the GLUT2 gene was screened for mutations using polymerase chain reaction-single-strand conformation polymorphism analysis. A single base change was identified in exon 3 in -5% of the study population, and it constitutes the first reported mutation in the human GLUT2 gene. This base change resulted in an amino acid substitution (Thr110 --> Ile110) in the second membrane-spanning region of the GLUT2 protein. No significant association was noted between AIR and the presence or absence of the mutation. Thus, this mutation in GLUT2 is unlikely the cause of a low AIR in Pima Indians. C1 NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,PHOENIX,AZ 85016. ARIZONA STATE UNIV,DEPT ZOOL,TEMPE,AZ 85287. NIDDKD,DIABET & ARTHRIT EPIDEMIOL SECT,PHOENIX,AZ 85016. UNIV CHICAGO,DEPT BIOCHEM & MOLEC BIOL,CHICAGO,IL 60637. UNIV CHICAGO,HOWARD HUGHES MED INST,CHICAGO,IL 60637. FU NCRR NIH HHS [1P41-RR-03655] NR 43 TC 35 Z9 35 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD APR PY 1994 VL 43 IS 4 BP 558 EP 563 DI 10.2337/diabetes.43.4.558 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NC859 UT WOS:A1994NC85900009 PM 8138061 ER PT J AU KIDD, GL REDDAN, JR RUSSELL, P AF KIDD, GL REDDAN, JR RUSSELL, P TI DIFFERENTIATION AND ANGIOGENIC GROWTH-FACTOR MESSAGE IN 2 MAMMALIAN LENS EPITHELIAL-CELL LINES SO DIFFERENTIATION LA English DT Article ID CRYSTALLIN GENE-EXPRESSION; ALPHA-A; CHICK LENS; INSITU HYBRIDIZATION; MESSENGER-RNA; MOUSE LENS; CULTURE; LOCALIZATION; FIBRONECTIN; LAMININ AB Lens epithelial cells in culture can sometimes be induced to form spheroid aggregates termed lentoid bodies, composed of cells exhibiting various characteristics of the more highly differentiated lens fiber cells. However, lentoid bodies are often slow to form, and the ability to produce them declines with serial subculture. It was therefore of interest to establish and/or characterize lens epithelial cell lines capable of forming lentoid bodies. The differentiation state was assessed in lentoid bodies formed by each of two lens epithelial cell lines, the transformed alphaTN4 cell line from mouse and the nontransformed N/N1135A cell line from rabbit. Lentoid and monolayer cultures of each cell line were examined for transcripts of the lens-specific alphaA-crystallin (''alphaA''), gammaD-crystallin (''gammaD''; formerly gamma1-crystallin) and MP26 genes. alphaTN4 lentoid bodies contained 2.5 times the alphaA RNA found in monolayer cells, but lacked detectable gammaD and MP26 RNA. None of the three markers were detected in either lentoid or monolayer N/N1135A cultures grown under the conditions described. Lentoid body formation alone, therefore, does not indicate the extent of differentiation occurring. At least some of the changes in cell adhesion occurring during lentoid body formation involve laminin-like and fibronectin-like interactions, and are reminiscent of those observed during embryonic lens formation. Finally, vascular endothelial growth factor mRNA was absent from the lens but present in alphaTN4 cells, suggestin a mechanism whereby the lens tumors of the founder mouse became vascularized. C1 OAKLAND UNIV,ROCHESTER,MI 48309. RP KIDD, GL (reprint author), NEI,MECH OCULAR DIS LAB,BETHESDA,MD 20892, USA. FU NEI NIH HHS [EY00362] NR 39 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD APR PY 1994 VL 56 IS 1-2 BP 67 EP 74 PG 8 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA ND485 UT WOS:A1994ND48500008 PM 8026648 ER PT J AU LAZOWSKI, KW MERTZ, PM REDMAN, RS KOUSVELARI, E AF LAZOWSKI, KW MERTZ, PM REDMAN, RS KOUSVELARI, E TI TEMPORAL AND SPATIAL EXPRESSION OF LAMININ, COLLAGEN TYPE-IV AND TYPE-I AND ALPHA-6/BETA-1 INTEGRIN RECEPTOR IN THE DEVELOPING RAT PAROTID-GLAND SO DIFFERENTIATION LA English DT Article ID FIBRONECTIN RECEPTOR; BRANCHING MORPHOGENESIS; SALIVARY-GLAND; SEQUENCES; PEPTIDES; PROTEINS; HOMOLOGY; FAMILY; CELLS; GENES AB We have examined the temporal expression and cellular localization of the genes and proteins for the extracellular matrix (ECM) proteins laminin (B1, B2 and A chain), collagen types alpha1 (IV) and alpha1 (1) and the integrin receptor complex alpha6/beta, during parotid gland postnatal development. Laminin B1 and B2 isoforms and collagens alpha1 (IV) and alpha (I) mRNA steady-state levels were highest at ages 0, 7 and 14 days after birth and declined to the adult (90 days) level at 21 days and older. Laminin A chain transcripts were not detected at any age. Collagen alpha1 (IV) and laminin were localized in the basal membrane of the developing acinar and ductal cells, while collagen alpha1 (1) was localized in the stroma surrounding the cells. The amounts of these ECM components were high at the early stages of development and lower at later times. The pattern of expression of the alpha6/beta1 integrin genes during development was similar to those of laminin and collagens alpha1 (IV) and alpha1 (I). Accumulations of mRNA were high at 0, 7 and 14 days after birth and lower at 21 days and older. High levels of beta1 integrin were localized in the developing acinar and ductal cell membranes at early ages (7 days); lower amounts were present in the same distribution pattern at later stages of gland development. These data suggest that laminin B1 and B2 and collagen type alpha1 (IV) and alpha1 (I) are consistently coexpressed with the alpha6/beta1 integrin receptor complex in the developing acinar and ductal cells during parotid gland postnatal development. Their expression is concomitant with the morphologic and proliferative changes occurring in these cells during this period. C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. DEPT VET AFFAIRS MED CTR,ORAL PATHOL RES LAB,WASHINGTON,DC 20422. NR 31 TC 13 Z9 13 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD APR PY 1994 VL 56 IS 1-2 BP 75 EP 82 DI 10.1046/j.1432-0436.1994.56120075.x PG 8 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA ND485 UT WOS:A1994ND48500009 PM 8026649 ER PT J AU PRESTON, KL SULLIVAN, JT TESTA, M JASINSKI, DR AF PRESTON, KL SULLIVAN, JT TESTA, M JASINSKI, DR TI PSYCHOPHARMACOLOGY AND ABUSE POTENTIAL OF TRANSNASAL BUTORPHANOL SO DRUG AND ALCOHOL DEPENDENCE LA English DT Article DE BUTORPHANOL; ABUSE LIABILITY; TRANSNASAL; HUMAN SUBJECTS; SUBJECTIVE EFFECTS ID AGONIST-ANTAGONIST OPIOIDS; STADOL DEPENDENCE; DISCRIMINATION; HUMANS; PAIN AB The effects of butorphanol administered by a nasal spray (transnasal, TN) and by intramuscular (IM) injection were compared to determine the onset of action, relative potency, profile of effects, and relative abuse liability of TN butorphanol. TN/IM placebo and TN and IM butorphanol (1, 2, and 4 mg) were tested in seven male opioid abusers not currently physically dependent on opioids using a double-blind, double-dummy, Latin square design. Measures of subjective, behavioral and physiological response were assessed. The onset and duration of action of butorphanol administered by the IM and TN routes were similar at low doses, but onset of TN butorphanol 4 mg was slower than that of 4 mg IM. IM butorphanol produced miosis, some opiate-like behavioral and subjective effects, and increasing dysphoric sedation and perceptual effects with increasing dose. TN and IM butorphanol 1 and 2 mg produced effects that were qualitatively and quantitatively similar; however, TN butorphanol 4 mg was less potent than 4 mg IM. Pharmacodynamic evidence suggests that the abuse potential of TN butorphanol is not different from that of IM butorphanol. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21224. RP PRESTON, KL (reprint author), NIDA,ADDICT RES CTR,CLIN TRIALS SECT,POB 5180,BALTIMORE,MD 21224, USA. RI Preston, Kenzie/J-5830-2013 OI Preston, Kenzie/0000-0003-0603-2479 NR 21 TC 9 Z9 9 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0376-8716 J9 DRUG ALCOHOL DEPEN JI Drug Alcohol Depend. PD APR PY 1994 VL 35 IS 2 BP 159 EP 167 DI 10.1016/0376-8716(94)90123-6 PG 9 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA NM360 UT WOS:A1994NM36000010 PM 8055737 ER PT J AU PANIZZA, M NILSSON, J ROTH, BJ ROTHWELL, J HALLETT, M AF PANIZZA, M NILSSON, J ROTH, BJ ROTHWELL, J HALLETT, M TI THE TIME CONSTANTS OF MOTOR AND SENSORY PERIPHERAL-NERVE FIBERS MEASURED WITH THE METHOD OF LATENT ADDITION SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE NERVE FIBER; TIME CONSTANT; MOTOR NERVE FIBER; SENSORY NERVE FIBER; ULNAR NERVE; MEDIAN NERVE; TIBIAL NERVE; LATENT ADDITION ID STIMULUS-DURATION; STIMULATION AB The time constants of motor and sensory fibers in the human ulnar, median and tibial nerves were determined using the method of latent addition. Two square-wave stimuli were applied: the first one was subthreshold and the second, at various delays relative to the first, was adjusted to achieve threshold activation. Strength-delay curves were obtained, from which the time constant was determined using a mathematical model. Sensory fibers had time constants that were about 3 times the time constant for motor fibers. The strength-delay curves gave similar time constants as those obtained from strength-duration curves. C1 NINCDS,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. IRCCS,FDN CLIN LAVORO,CLIN NEUROPHYSIOL LAB,CASTEL GOFFREDO,ITALY. INST NEUROL,MRC,HUMAN MOVEMENT & BALANCE UNIT,LONDON WC1N 3BG,ENGLAND. NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. RI Roth, Bradley/A-4920-2008; OI Rothwell, John/0000-0003-1367-6467 NR 16 TC 51 Z9 51 U1 0 U2 3 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD APR PY 1994 VL 93 IS 2 BP 147 EP 154 DI 10.1016/0168-5597(94)90078-7 PG 8 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA NH901 UT WOS:A1994NH90100009 PM 7512921 ER PT J AU BARBATO, G BARKER, C BENDER, C GIESEN, HA WEHR, TA AF BARBATO, G BARKER, C BENDER, C GIESEN, HA WEHR, TA TI EXTENDED SLEEP IN HUMANS IN 14 HOUR NIGHTS (LD-10/14) - RELATIONSHIP BETWEEN REM DENSITY AND SPONTANEOUS AWAKENING SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE AROUSAL; AWAKENING; HUMAN SLEEP; NREM-REM CYCLE; PHOTOPERIOD; REM DENSITY ID EYE-MOVEMENT DENSITY; EEG POWER-DENSITY; YOUNG-ADULTS; TIME COURSE; VARIABLES AB The sleep patterns of 8 normal subjects living in a winter-type photoperiod (10 h light and 14 h darkness; LD 10:14) for 4 weeks were characterized by the presence of periods of spontaneous wakefulness alternating with periods of spontaneous sleep. Transitions from sleep to wakefulness occurred much more frequently out of REM sleep than out of NREM sleep (P < 0.002). REM periods that terminated in wakefulness showed shorter REM durations (P < 0.0005) and higher REM densities (P < 0.0005) than REM periods that did not terminate in wakefulness. The authors discuss these results in terms of a possible relationship between REM density and arousal level. The higher REM density preceding wakefulness and the increased number of REM periods terminating in spontaneous awakenings could reflect an enhanced level of a brain arousing process, resulting from reduced sleep pressure in the extended nights. C1 NIMH,CLIN PSYCHOBIOL BRANCH,BETHESDA,MD 20892. RP BARBATO, G (reprint author), UNIV NAPLES,FAC MED 2,PSICHIAT CLIN,VIA PANSINI 5,I-80131 NAPLES,ITALY. OI Barbato, Giuseppe/0000-0001-6523-5327 NR 45 TC 37 Z9 37 U1 0 U2 7 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD APR PY 1994 VL 90 IS 4 BP 291 EP 297 DI 10.1016/0013-4694(94)90147-3 PG 7 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA NG235 UT WOS:A1994NG23500005 PM 7512910 ER PT J AU ALESSI, DR SAITO, Y CAMPBELL, DG COHEN, P SITHANANDAM, G RAPP, U ASHWORTH, A MARSHALL, CJ COWLEY, S AF ALESSI, DR SAITO, Y CAMPBELL, DG COHEN, P SITHANANDAM, G RAPP, U ASHWORTH, A MARSHALL, CJ COWLEY, S TI IDENTIFICATION OF THE SITES IN MAP KINASE KINASE-1 PHOSPHORYLATED BY P74(RAF-1) SO EMBO JOURNAL LA English DT Article DE MAP KINASE; MAP KINASE KINASE; ONCOGENE; PHOSPHOPEPTIDE; RAF; SITE-DIRECTED MUTAGENESIS ID NERVE GROWTH-FACTOR; ACTIVATED PROTEIN-KINASE; RABBIT SKELETAL-MUSCLE; NUCLEOTIDE-SEQUENCE; FISSION YEAST; GENE; CELLS; RAF; CASCADE AB Many growth factors whose receptors are protein tyrosine kinases stimulate the MAP kinase pathway by activating first the GTP-binding protein Ras and then the protein kinase p74(raf-1). p74(raf-1) phosphorylates and activates MAP kinase kinase (MAPKK). To understand the mechanism of activation of MAPKK, we have identified Ser217 and Ser221 of MAPKK1 as the sites phosphorylated by p74(raf-1). This represents the first characterization of sites phosphorylated by this proto-oncogene product. Ser217 and Ser221 lie in a region of the catalytic domain where the activating phosphorylation sites of several other protein kinases are located. Among MAPKK family members, this region is the most conserved, suggesting that all members of the family are activated by the phosphorylation of these sites. A 'kinase-dead' MAPKK1 mutant was phosphorylated at the same residues as the wild-type enzyme, establishing that both sites are phosphorylated directly by p74(raf-1), and not by autophosphorylation. Only the diphosphorylated form of MAPKK1 (phosphorylated at both Ser217 and Ser221) was detected, even when the stoichiometry of phosphorylation of one of these sites is rate limiting, phosphorylation of the second then occurring extremely rapidly. Ser217 and Ser221 were both phosphorylated in vivo within minutes when PC12 cells were stimulated with nerve growth factor. Analysis of MAPKK1 mutants in which either Ser217 or Ser221 were changed to glutamic acid, and the finding that inactivation of maximally activated MAPKK1 required the dephosphorylation of both serines, shows that phosphorylation of either residue is sufficient for maximal activation. C1 INST CANC RES,CHESTER BEATTY LABS,LONDON SW3 6JB,ENGLAND. UNIV DUNDEE,DEPT BIOCHEM,MRC,PROT PHOSPHORYLAT UNIT,DUNDEE DD1 4HN,SCOTLAND. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RI Campbell, David/K-1874-2015; OI Campbell, David/0000-0003-2278-2149; Cowley, Sally/0000-0003-0297-6675 NR 55 TC 456 Z9 464 U1 0 U2 9 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR 1 PY 1994 VL 13 IS 7 BP 1610 EP 1619 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA NF928 UT WOS:A1994NF92800015 PM 8157000 ER PT J AU CIZZA, G CALOGERO, AE BRADY, LS BAGDY, G BERGAMINI, E BLACKMAN, MR CHROUSOS, GP GOLD, PW AF CIZZA, G CALOGERO, AE BRADY, LS BAGDY, G BERGAMINI, E BLACKMAN, MR CHROUSOS, GP GOLD, PW TI MALE FISCHER-344/N-RATS SHOW A PROGRESSIVE CENTRAL IMPAIRMENT OF THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS WITH ADVANCING AGE SO ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; RECEPTOR MESSENGER-RNA; DIMINISHED DIURNAL SECRETION; OLD MALE-RATS; CORTICOSTERONE RESPONSES; PARAVENTRICULAR NUCLEUS; VASOPRESSIN; BRAIN; ACTH; INVITRO AB We investigated the effects of aging on the regulation of hypothalamic-pituitary-adrenal function and hippocampal steroid receptors in a series of in vivo and in vitro studies conducted in healthy intact 2-, 8-, 18-, and 24-month-old male Fischer 344/N rats. Basal plasma ACTH levels were similar among age groups, and basal plasma corticosterone levels showed a significant aging-associated decline. Two iv doses (2 and 20 mug/kg BW) of rat CRF elicited significantly greater and delayed ACTH and greater corticosterone responses in older rats, consistent with the pattern encountered in hypothalamic CRF deficiency. In contrast, the iv injection of a muscarinic agonist, arecoline, elicited similar ACTH and corticosterone responses in all age groups. An iv injection of ACTH-(1-24) evoked lower corticosterone responses in the older (18- and 24-month-old) than in the younger (2- and 8-month-old) groups of rats, consistent with an impairment of hypothalamic-pituitary-adrenal axis function in older animals. Steady state mRNA levels of mineralocorticoid and glucocorticoid receptors were significantly decreased in the hippocampus of the 8-, 18-, and 24-month-old rats, compatible with maturational, rather than senescent, changes. CRF mRNA levels in the paraventricular nucleus of the hypothalamus, CRF content, and in vitro secretion by whole explanted hypothalami were progressively and significantly reduced with age, whereas the steady state levels of arginine vasopressin mRNA were significantly increased with age. Steady state levels of POMC mRNA were decreased, and ACTH content and in vitro secretion by corticotrophs were increased with age in the anterior pituitary. We conclude that male Fischer 344/N rats show a progressive hypothalamic CRH deficiency with advancing age, which appears to be associated with elevated production of arginine vasopressin in the hypothalamus. C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. FRANCIS SCOTT KEY MED CTR,DEPT MED,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21224. UNIV PISA,IST PATOL GEN,I-56100 PISA,ITALY. RP CIZZA, G (reprint author), NIMH,CLIN NEUROENDOCRINOL BRANCH,BLDG 10,ROOM 35-229,BETHESDA,MD 20892, USA. OI Bagdy, Gyorgy/0000-0001-8141-3410 NR 53 TC 65 Z9 66 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1994 VL 134 IS 4 BP 1611 EP 1620 DI 10.1210/en.134.4.1611 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NC427 UT WOS:A1994NC42700003 PM 8137722 ER PT J AU ROJAS, E CARROLL, PB RICORDI, C BOSCHERO, AC STOJILKOVIC, SS ATWATER, I AF ROJAS, E CARROLL, PB RICORDI, C BOSCHERO, AC STOJILKOVIC, SS ATWATER, I TI CONTROL OF CYTOSOLIC-FREE CALCIUM IN CULTURED HUMAN PANCREATIC BETA-CELLS OCCURS BY EXTERNAL CALCIUM-DEPENDENT AND INDEPENDENT MECHANISMS SO ENDOCRINOLOGY LA English DT Article ID STIMULATED INSULIN RELEASE; B-CELLS; PITUITARY GONADOTROPHS; ELECTRICAL-ACTIVITY; HUMAN ISLETS; GLUCOSE; MOUSE; CURRENTS; CHANNELS; CARBAMYLCHOLINE AB Changes in cytosolic intracellular free Ca2+ ([Ca2+]i) in response to glucose, glyburide, cholinergic agonists, and elevated [K+]o (external potassium concentration) were measured in cultured human islet beta-cells. In the absence of glucose, the mean resting [Ca2+]i in single beta-cells was 84.5 +/- 4.7 nM (n = 86) and remained unchanged in low external [Ca2+]o (Ca2+ concentration) (<0.2 muM) at 23-25 C. Glucose (5.6-33 mM) induced a slow dose-related [Ca2+]i rise up to 300.0 +/- 50.6 nm (n = 19). This [Ca2+]i rise always occurred with a delay that varied from cell to cell (approximately 10-120 sec), and the steady state [Ca2+]i exhibited a sigmoidal dependence on glucose concentration (midpoint at 14.9 mM). The glucose-induced rise in [Ca2+]i was attenuated by about 62% in low external [Ca2+]o and was not affected by dantrolene, a drug that inhibits Ca2+ release from the endoplasmic reticulum. In the absence or presence of glucose, cholinergic receptor agonists evoked a biphasic increase in [Ca2+]i up to 350 nM; the delayed component of the [Ca2+]i rise was blocked by dantrolene. A rapid elevation of [K+]o to 40 mM also elicited a biphasic rise in [Ca2+]i, which peaked at about 250 nm and was inhibited by the Ca2+ channel antagonist nifedipine. Glyburide (4 muM) in the absence of glucose also induced a [Ca2+]o-dependent rise in [Ca2+]i. Increasing the concentration of glucose from 4 to 16.7 mm evoked a biphasic pattern of insulin secretion from perifused isolated islets at 37 C. Finally, in the presence of 4 mm glucose, a cholinergic muscarinic receptor agonist stimulated insulin secretion. A glucose-stimulated [Ca2+]i rise was also studied at 24 and 37 C in cultured rat islet cells. Our results suggest that the Ca2+ required for glucose-induced and muscarinic agonist-potentiated insulin release enters the cytosol from both extracellular and intracellular Ca2+ stores. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT MED,PITTSBURGH,PA 15213. UNIV PITTSBURGH,DEPT SURG,PITTSBURGH,PA 15213. RP ROJAS, E (reprint author), NIDDKD,CELL BIOL & GENET LAB,BLDG 8,ROOM 326,BETHESDA,MD 20892, USA. RI Boschero, Antonio/O-7525-2014; OI Boschero, Antonio/0000-0003-3829-8570; Ricordi, Camillo/0000-0001-8092-7153 NR 36 TC 64 Z9 64 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1994 VL 134 IS 4 BP 1771 EP 1781 DI 10.1210/en.134.4.1771 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NC427 UT WOS:A1994NC42700025 PM 8137742 ER PT J AU HAYES, WP WRAY, S BATTEY, JF AF HAYES, WP WRAY, S BATTEY, JF TI THE FROG GONADOTROPIN-RELEASING HORMONE-I (GNRH-I) GENE HAS A MAMMALIAN-LIKE EXPRESSION PATTERN AND CONSERVED DOMAINS IN GNRH-ASSOCIATED PEPTIDE, BUT BRAIN ONSET IS DELAYED UNTIL METAMORPHOSIS SO ENDOCRINOLOGY LA English DT Article ID OLFACTORY PLACODE ABLATION; XENOPUS-LAEVIS; MOLECULAR-FORMS; NERVOUS-SYSTEM; LHRH NEURONS; IMMUNOHISTOCHEMICAL LOCALIZATION; AMPHIBIAN METAMORPHOSIS; SYMPATHETIC NEURONS; MULTIPLE FORMS; MESSENGER-RNA AB Recent evidence indicates a localized origin in the olfactory placode for the mammalian forebrain neurons that express GnRH. To identify the cellular and molecular signals that induce the GnRH phenotype, we cloned and characterized a cDNA encoding the GnRH prohormone, the precursor for both GnRH-I and GnRH-associated peptide in the frog, Xenopus laevis, an embryonic model accessible to experimental manipulation. The 396-base cDNA represented a single mRNA species encoding an 89-amino acid prepro-GnRH that, unlike a recently cloned fish GnRH gene, was identical to both the mammalian GnRH decapeptide as well as multiple domains within GnRH-associated peptide. Serial section in situ hybridization histochemistry and immunocytochemistry in adult frog localized a forebrain system comprising 250-350 cell bodies whose overall neuroanatomy, including fiber projections, was very similar to that described for mammals. However, neither Northern nor in situ hybridization detected GnRH expression in mid-brain, arguing that another frog gene encodes the midbrain GnRH-II expression pattern described by many others using antisera directed against the fish GnRH-I or chicken GnRH-II decapeptides. In contrast to mammals and birds, in which GnRH-expressing cells migrate into embryonic forebrain, frog GnRH cells were first detected after they reached their final position in the preoptic area during the late larval period. Thus, although previous studies proposed a complex organization for the GnRH system in the frog, our findings show that similar to mammals, there is a single gene that can account for the continuum of GnRH-I cells spanning frog forebrain. However, unlike mammals, in frogs, for unknown reasons, GnRH-I gene expression is suppressed until metamorphic climax. C1 NINCDS, NEUROCHEM LAB, BETHESDA, MD 20892 USA. RP NICHHD, DEV NEUROBIOL LAB, CELLULAR NEUROBIOL SECT, BLDG 49, ROOM 5A38, BETHESDA, MD 20892 USA. OI wray, susan/0000-0001-7670-3915 NR 74 TC 55 Z9 56 U1 0 U2 3 PU ENDOCRINE SOC PI WASHINGTON PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1994 VL 134 IS 4 BP 1835 EP 1845 DI 10.1210/en.134.4.1835 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NC427 UT WOS:A1994NC42700034 PM 8137750 ER PT J AU DELEON, DD TERRY, C NISSLEY, SP AF DELEON, DD TERRY, C NISSLEY, SP TI DIRECT-DETECTION OF INSULIN-LIKE GROWTH FACTOR-II (IGF-II) BY CHEMILUMINESCENCE WITHOUT INTERFERENCE BY IGF BINDING-PROTEINS SO ENDOCRINOLOGY LA English DT Note ID RAT-LIVER CELLS; RADIOIMMUNOASSAY; SERUM; RADIOLIGAND; EXPRESSION AB A dot blot method for the detection of picogram quantities of human and rat insulin-like growth factor II (IGF-II) in serum-free conditioned media is described. The crossreactivity of human recombinant IGF-I in the assay was <10%. None of the IGF binding proteins (IGFBP 1-6) diminished the IGF-II signal. In contrast, significant interference by the IGFBPs was observed when the same concentrations of IGFBPs and I-125-IGF-II were used in a radioimmunoassay which utilized the same antibody. Why IGF-II is detected in the dot blot assay without IGFBP interference is not understood. We speculate that the conformation of the IGF-II/binding protein complex may be altered by binding to the nitrocellulose, exposing the IGF-II epitope that is recognized by the antibody. IGF-II was detected in 1 mul of serum-free conditioned media from BRL 3A cells (which secrete IGF-II) while no signal was generated by 50 mul of BRL 3A2 conditioned media (which do not secrete IGF-II) . In summary, this method is ideal for screening cells in serum free-culture for production of IGF-II without the need for separation of IGF-II from cell derived IGFBPs. RP DELEON, DD (reprint author), NCI,METAB BRANCH,BETHESDA,MD 20892, USA. OI De Leon, Daisy D./0000-0002-2693-0957 NR 21 TC 17 Z9 17 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1994 VL 134 IS 4 BP 1960 EP 1963 DI 10.1210/en.134.4.1960 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA NC427 UT WOS:A1994NC42700051 PM 7511096 ER PT J AU GOYER, RA EPSTEIN, S BHATTACHARYYA, M KORACH, KS POUNDS, J AF GOYER, RA EPSTEIN, S BHATTACHARYYA, M KORACH, KS POUNDS, J TI ENVIRONMENTAL RISK-FACTORS FOR OSTEOPOROSIS SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material C1 ALBERT EINSTEIN MED CTR,DIV ENDOCRINOL & METAB,PHILADELPHIA,PA 19141. ARGONNE NATL LAB,ARGONNE,IL 60439. WAYNE STATE UNIV,INST CHEM TOXICOL,DETROIT,MI 48201. RP GOYER, RA (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. OI Pounds, Joel/0000-0002-6616-1566; Korach, Kenneth/0000-0002-7765-418X NR 0 TC 30 Z9 33 U1 1 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1994 VL 102 IS 4 BP 390 EP 394 DI 10.2307/3431628 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA NP808 UT WOS:A1994NP80800009 PM 7925179 ER PT J AU DING, L SHEVACH, EM AF DING, L SHEVACH, EM TI ACTIVATION OF CD4(+) T-CELLS BY DELIVERY OF THE B7 COSTIMULATORY SIGNAL ON BYSTANDER ANTIGEN-PRESENTING CELLS (TRANS-COSTIMULATION) SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE B7; COSTIMULATION; NAIVE; MEMORY CD4 T CELLS; ANERGY ID INTERCELLULAR-ADHESION MOLECULE-1; HEAT-STABLE ANTIGEN; LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; DIFFERENTIATION ANTIGENS; EXPRESSION; INDUCTION; RECEPTOR; ICAM-1; CLONES AB Increasing evidence in both murine and human systems suggests that the interaction of the T cell surface antigens CD28/CTLA4 with their ligand B7 on the antigen-presenting cells (APC) is the critical costimulatory pathway involved in the induction of maximal T cell activation and the prevention of induction of anergy. It has also been demonstrated that efficient induction of clonal expansion of normal CD4(+) T cells requires the delivery of the T cell receptor (TCR) ligand and costimulation by the same APC. We demonstrate here that normal murine CD4(+) T cells can be efficiently activated by soluble anti-CD3 cross-linked by fixed macrophages and by a costimulatory signal delivered by a bystander APC, B7-transfected L cells. The major factor which determined the ability of an APC to provide costimulation in ''trans'' was the level of cell surface B7 expression. The requirement for B7 costimulation appears to be at initial stage of TCR engagement since optimal T cell activation was only observed when TCR triggering and B7 costimulatory activity were delivered at same time by different APC. Induction of maximal proliferation of both naive CD45RB(hi) and memory CD45RB(lo) CD4(+) T cells was B7 dependent and both populations of cells responded equally well to the B7 costimulation delivered in ''trans''. Furthermore, trans-costimulation provided by B7 transfected L cells efficiently prevented the induction of anergy in normal murine CD4(+) T cells induced by anti-CD3 cross-linked by fixed-resting macrophages. Addition of exogenous interleukin-2 (IL-2) and IL-7 to the primary culture in the absence of B7-transfected L cells or addition of IL-2 to the culture containing the B7 transfectant and CTLA4Ig completely prevented the induction of hyporesponsiveness. These findings raise the possibility that in certain pathological states, CD4(+) T cells in vivo may be activated by costimulation delivered by bystander APC. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NR 54 TC 82 Z9 84 U1 0 U2 2 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD APR PY 1994 VL 24 IS 4 BP 859 EP 866 DI 10.1002/eji.1830240413 PG 8 WC Immunology SC Immunology GA NG465 UT WOS:A1994NG46500012 PM 7512033 ER PT J AU JARAQUEMADA, D MARTI, M MARTIN, R WAGNER, A MACFARLAND, HF ROSENBRONSON, S AF JARAQUEMADA, D MARTI, M MARTIN, R WAGNER, A MACFARLAND, HF ROSENBRONSON, S TI DIFFERENT REQUIREMENTS OF ICAM-1/LFA-1 ADHESION IN ALLORECOGNITION AND SELF-RESTRICTED ANTIGEN RECOGNITION BY CLASS II-SPECIFIC T-CELL CLONES SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE ADHESION MOLECULES; ANTIGEN RECOGNITION; ALLOREACTIVITY; T CELL CLONES ID MYELIN BASIC-PROTEIN; HLA-DR; INVARIANT CHAIN; EXPRESSION; PEPTIDE; INDIVIDUALS; HLA-DR2A; MOLECULE; PATHWAY; GAMMA AB We have analyzed the influence of non-antigen-specific interactions between ICAM-1 and LFA-1 in target recognition by allospecific and antigen-specific T cells at the clonal level, using human and mouse fibroblasts transfected with HLA-DR1 or DR2 with or without co-expression of ICAM-1, as antigen-presenting cells. The results show a great heterogeneity in the requirements for ICAM-1/LFA-1 interactions for antigen-specific and alloreactive T cell responses and this requirement may depend on the avidity of any particular interaction. The data also show that for most alloreactive clones, ICAM-1/LFA-1 adhesion is not sufficient to facilitate efficient T cell recognition of its target molecule. HLA class II recognition by a large proportion of the DR1- and DR2-specific alloreactive clones studied was different for class II molecules expressed on murine or human fibroblasts compared to human lymphoid cells, and was independent of ICAM-1 expression on the stimulator cells. The inability of some T cell clones to recognize HLA-class II expressed on non-lymphoid cells suggests the absence of specific epitopes and could be due to the lack of the relevant peptides, either because they are derived from species-specific proteins or to differences in processing of endogenous antigen in the transfected stimulator cells. C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. UNIV TUBINGEN,DEPT NEUROL,W-7400 TUBINGEN,GERMANY. NINCDS,NEUROIMMUNOL BRANCH,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC. RP JARAQUEMADA, D (reprint author), UNIV AUTONOMA BARCELONA,HOSP GERMANS TRIAS & PUJOL,IMMUNOL UNIT,POB 72,E-08916 BADALONA,SPAIN. NR 26 TC 5 Z9 5 U1 0 U2 1 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD APR PY 1994 VL 24 IS 4 BP 947 EP 951 DI 10.1002/eji.1830240425 PG 5 WC Immunology SC Immunology GA NG465 UT WOS:A1994NG46500024 PM 7908635 ER PT J AU BERTRAND, R SOLARY, E OCONNOR, P KOHN, KW POMMIER, Y AF BERTRAND, R SOLARY, E OCONNOR, P KOHN, KW POMMIER, Y TI INDUCTION OF A COMMON PATHWAY OF APOPTOSIS BY STAUROSPORINE SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID PROTEIN-KINASE-C; PROGRAMMED CELL-DEATH; DNA FRAGMENTATION; IONIZING-RADIATION; POTENT INHIBITOR; MAMMALIAN-CELLS; GENE-EXPRESSION; BCL-2; GROWTH; THYMOCYTES AB The present observations show that staurosporine can rapidly trigger both the morphological changes and intranucleosomal DNA fragmentation typical of apoptosis. This occurred in a number of cell lines from various origins regardless of the state of differentiation and cell cycle phase, suggesting the presence of a common inducible suicide pathway. The broad apoptotic activity of staurosporine appears to be unique among other protein kinase or phosphatase inhibitors we tested. Results obtained in a cell-free assay suggest that cytoplasmic proteins directly modulated by staurosporine may be involved in a ubiquitous signal for the induction of DNA fragmentation and apoptosis. (C) 1994 Academic Press, Inc. C1 CHU BOCAGE,DEPT HEMATOL,F-21000 DIJON,FRANCE. NCI,DCT,DTP,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. RP BERTRAND, R (reprint author), INST CANC MONTREAL,CTR RECH LOUIS CHARLES SIMARD,1560 SHERBROOKE EST,MONTREAL H2L 4M1,PQ,CANADA. NR 43 TC 420 Z9 421 U1 3 U2 14 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD APR PY 1994 VL 211 IS 2 BP 314 EP 321 DI 10.1006/excr.1994.1093 PG 8 WC Oncology; Cell Biology SC Oncology; Cell Biology GA NE897 UT WOS:A1994NE89700019 PM 8143779 ER PT J AU RUBINI, M WERNER, H GANDINI, E ROBERTS, CT LEROITH, D BASERGA, R AF RUBINI, M WERNER, H GANDINI, E ROBERTS, CT LEROITH, D BASERGA, R TI PLATELET-DERIVED GROWTH-FACTOR INCREASES THE ACTIVITY OF THE PROMOTER OF THE INSULIN-LIKE GROWTH-FACTOR-I (IGF-1) RECEPTOR GENE SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID FACTOR-I RECEPTOR; CULTURED HUMAN-FIBROBLASTS; HEMATOPOIETIC-CELLS; 3T3 CELLS; EXPRESSION; BINDING; PROTEIN; HAMSTER; SINGLE AB Stimulation by platelet-derived growth factor (PDGF) is known to increase the number of IGF-I binding sites in cells in culture. We show here that PDGF also increases the levels of IGF-1 receptor mRNA. Using cell lines stably transfected with an expression plasmid in which the reporter luciferase gene is under the control of the rat IGF-1 receptor gene promoter, we find that PDGF increases the activity of this promoter. A short IGF-1 receptor gene promoter, comprising about 100 base pairs of the sequence immediately upstream of the initiation of transcription site, is sufficient for a response to the stimulatory action of PDGF. These results suggest that an increase in RNA levels and in promoter activity may play an important role in the increase in IGF-1 receptor levels that occurs after stimulation by PDGF. (C) 1994 Academic Press, Inc. C1 THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,PHILADELPHIA,PA 19107. NIDDKD,DIABET BRANCH,BETHESDA,MD 20892. UNIV FERRARA,IST GENET MED,I-44100 FERRARA,ITALY. OI Rubini, Michele/0000-0003-1448-9516 FU NCI NIH HHS [CA 53484, CA 56309] NR 44 TC 85 Z9 92 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD APR PY 1994 VL 211 IS 2 BP 374 EP 379 DI 10.1006/excr.1994.1101 PG 6 WC Oncology; Cell Biology SC Oncology; Cell Biology GA NE897 UT WOS:A1994NE89700027 PM 8143786 ER PT J AU DASH, A CHUNG, S ZELENKA, PS AF DASH, A CHUNG, S ZELENKA, PS TI EXPRESSION OF HSP70 MESSENGER-RNA IN THE EMBRYONIC CHICKEN LENS - ASSOCIATION WITH DIFFERENTIATION SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE HEAT SHOCK PROTEINS; MESSENGER-RNA; PCR; DIFFERENTIATION ID HEAT-SHOCK PROTEINS; DELTA-CRYSTALLIN SYNTHESIS; MESSENGER-RNA; CELL-CYCLE; C-MYC; COATED VESICLES; CHAIN-REACTION; GENE; TRANSCRIPTION; POLYMERASE C1 NEI,MOLEC & DEV BIOL LAB,CELLULAR DIFFERENTIAT SECT,BETHESDA,MD 20892. NR 42 TC 27 Z9 27 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD APR PY 1994 VL 58 IS 4 BP 381 EP 387 DI 10.1006/exer.1994.1030 PG 7 WC Ophthalmology SC Ophthalmology GA NK169 UT WOS:A1994NK16900001 PM 7925675 ER PT J AU NEBEN, S DONALDSON, D SIEFF, C MAUCH, P BODINE, D FERRARA, J YETZALDAPE, J TURNER, K AF NEBEN, S DONALDSON, D SIEFF, C MAUCH, P BODINE, D FERRARA, J YETZALDAPE, J TURNER, K TI SYNERGISTIC EFFECTS OF INTERLEUKIN-11 WITH OTHER GROWTH-FACTORS ON THE EXPANSION OF MURINE HEMATOPOIETIC PROGENITORS AND MAINTENANCE OF STEM-CELLS IN LIQUID CULTURE SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE INTERLEUKIN-11; STEM CELLS; STEEL FACTOR; HEMATOPOIESIS ID MEDIATED GENE-TRANSFER; C-KIT; INVITRO; PROLIFERATION; LIGAND; MICE; IDENTIFICATION; SURVIVAL; CYTOKINE; NUMBER AB The effect of interleukin-11 (IL-11), alone and in combination with other hematopoietic growth factors, was studied in liquid suspension cultures of murine bone marrow. Stem and progenitor cell contents of input bone marrow 2 days after 5-fluorouracil (5-FU) treatment (FU(2d)BM) and lineage-depleted, Sca-1-positive FU(2d)BM (Lid(-)Sca(+)FU(2d)BM) were compared with output values obtained after 6 days in different growth factor combinations. Stem and progenitor cell recoveries were measured by long-term in vivo competitive repopulation, spleen colony-forming unit (CFU-S), and in vitro limiting dilution long-term bone marrow culture (cobblestone area-forming cell [CAFC]) assays. IL-11, IL-3, IL-6, and Steel factor (SF) were tested separately and in combinations of two, three, and four factors. IL-11 was incapable of maintaining the survival of stem or progenitor cells as a single agent but synergized with either IL-3 or SF to expand progenitor cell output in cultures of FU(2d)BM. IL-11 greatly enhanced progenitor cell expansion from FU(2d)BM when added to two- and three-factor combinations of SF, IL-3, and IL6, The recovery of long-term repopulating ability was enhanced four-fold by incubation in SF plus IL-11 compared to SF alone. IL-11 in combination with SF, IL-3, and IL-6 stimulated a 24,000-fold expansion of progenitor cells from stem cell-enriched Lin(-)Sca(+)FU(2d)BM, Overall, the results indicate that IL-11 is a potent synergistic factor for stem cell proliferation and expansion of progenitors in liquid culture. C1 DANA FARBER CANC INST,DIV PEDIAT HEMATOL & ONCOL,BOSTON,MA. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. RP NEBEN, S (reprint author), GENET INST INC,87 CAMBRIDGEPK DR,CAMBRIDGE,MA 02140, USA. NR 43 TC 50 Z9 52 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD APR PY 1994 VL 22 IS 4 BP 353 EP 359 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA NE560 UT WOS:A1994NE56000003 PM 8150033 ER PT J AU BILLINGSLEY, ML ELLIS, C KINCAID, RL MARTIN, J SCHMIDT, ML LEE, VMY TROJANOWSKI, JQ AF BILLINGSLEY, ML ELLIS, C KINCAID, RL MARTIN, J SCHMIDT, ML LEE, VMY TROJANOWSKI, JQ TI CALCINEURIN IMMUNOREACTIVITY IN ALZHEIMERS-DISEASE SO EXPERIMENTAL NEUROLOGY LA English DT Article ID CYCLIC-NUCLEOTIDE PHOSPHODIESTERASE; PAIRED HELICAL FILAMENTS; SENILE PLAQUE NEURITES; NEUROFIBRILLARY TANGLES; PROTEIN PHOSPHATASE-2A; TAU-FACTOR; RAT-BRAIN; EXPRESSION; SUBUNIT; DEPHOSPHORYLATION AB Aberrant phosphorylation of tau is linked to formation of the paired helical filaments (PHF) seen in Alzheimer's disease. Protein kinases such as mitogen-activated protein kinase, and calcium-regulated protein kinases may, in part, be responsible for addition of phosphate groups to serine residues of PHFtau; however, less is known concerning the phosphatases which regulate tau. In this report, we used several well-characterized antibodies to document calcineurin immunoreactivity in brain tissue from patients with Alzheimer's disease. We now report that levels of immunoreactive calcineurin are not significantly altered in neocortex and cerebellum of Alzheimer's patients relative to similar regions of age-matched controls. Immunocytochemical studies indicated that calcineurin immunoreactivity was present in dendrites and perikarya of many different neuronal populations in both control and Alzheimer brain. When specific antibodies against PHFtau were used in double-labeling experiments with anti-calcineurin antibodies, calcineurin immunoreactivity was seen in association with neurofibrillary tangles. However, calcineurin was not seen in all tangle bearing neurons. These data suggest that calcineurin levels per se are not significantly altered in Alzheimer's disease, but that calcineurin is distributed around some neurofibrillary tangles and may play a role in regulation of tau phosphorylation. (C) 1994 Academic Press, Inc. C1 NIAAA,ROCKVILLE,MD 20892. UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,DIV ANAT PATHOL,PHILADELPHIA,PA 19104. RP BILLINGSLEY, ML (reprint author), PENN STATE UNIV,COLL MED,DEPT PHARMACOL,HERSHEY,PA 17033, USA. FU NIA NIH HHS [AG-09215] NR 28 TC 28 Z9 28 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD APR PY 1994 VL 126 IS 2 BP 178 EP 184 DI 10.1006/exnr.1994.1056 PG 7 WC Neurosciences SC Neurosciences & Neurology GA NM716 UT WOS:A1994NM71600004 PM 7925818 ER PT J AU AGOSTON, DV KOMOLY, S PALKOVITS, M AF AGOSTON, DV KOMOLY, S PALKOVITS, M TI SELECTIVE UP-REGULATION OF NEUROPEPTIDE SYNTHESIS BY BLOCKING THE NEURONAL-ACTIVITY - GALANIN EXPRESSION IN SEPTOHIPPOCAMPAL NEURONS SO EXPERIMENTAL NEUROLOGY LA English DT Article ID NERVE GROWTH-FACTOR; SEPTAL CHOLINERGIC NEURONS; VASOACTIVE-INTESTINAL-PEPTIDE; GENE-EXPRESSION; MESSENGER-RNA; HIPPOCAMPAL-NEURONS; NEUROTROPHIC FACTOR; CLASSICAL NEUROTRANSMITTERS; INSITU HYBRIDIZATION; DEPENDENT REGULATION AB Neuronal activity regulates expression of phenotype-specific genes, including galanin, which coexists with choline acetyltransferase in septal and basal forebrain neurons. Transections of the fornix and the diagonal band alter galanin expression in septohippocampal neurons attributed to a deficit in target-derived trophic factors. The present study demonstrates that tetrodotoxin-induced blockade of neuronal activity fully mimicked the effect of axotomy (transection of the septohippocampal fibers) in the neurons of the nucleus of the diagonal band, and caused a dramatic, although temporary, up-regulation of galanin immunoreactivity and galanin mRNA without significant alteration in choline acetyltransferase expression. This finding suggests that in the septohippocampal cholinergic system perturbance of electrical activity alone can lead to temporary up-regulation of galanin expression, previously attributed exclusively to a ''lesion effect.'' (C) 1994 Academic Press, Inc. C1 NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA. NINCDS, EXPTL NEUROPATHOL LAB, BETHESDA, MD USA. RP NICHHD, MCN, LDN, BLDG 49, ROOM 5A38, BETHESDA, MD 20892 USA. RI Palkovits, Miklos/F-2707-2013; OI Palkovits, Miklos/0000-0003-0578-0387 NR 58 TC 34 Z9 34 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 0014-4886 EI 1090-2430 J9 EXP NEUROL JI Exp. Neurol. PD APR PY 1994 VL 126 IS 2 BP 247 EP 255 DI 10.1006/exnr.1994.1062 PG 9 WC Neurosciences SC Neurosciences & Neurology GA NM716 UT WOS:A1994NM71600010 PM 7523176 ER PT J AU WEINSTATSASLOW, D STEEG, PS AF WEINSTATSASLOW, D STEEG, PS TI ANGIOGENESIS AND COLONIZATION IN THE TUMOR METASTATIC PROCESS - BASIC AND APPLIED ADVANCES SO FASEB JOURNAL LA English DT Review DE METASTASIS; ANGIOGENESIS; COLONIZATION; TGF-BETA; NM23 ID FIBROBLAST GROWTH-FACTOR; ENDOTHELIAL-CELL ADHESION; INVASIVE BREAST-CARCINOMA; PLATELET FACTOR-IV; NM23 GENE; PENTOSAN POLYSULFATE; FACTOR-BETA; INHIBITION; CANCER; EXPRESSION AB Tumor metastasis is a major cause of death for cancer patients. This review proposes that the final steps in the development of a distant metastasis may be the most productive targets for clinical development. It cannot be guaranteed that, in ''metastasis-free'' patients, tumor cells have not invaded out of the primary lesion, intravasated and extravasated from the circulatory system, and are sitting at distant sites as occult micrometastases. The remaining processes involved in outgrowth at metastatic sites, colonization and angiogenesis, are reviewed. Colonization is thought to be accomplished by clonally dominant cell populations through progressive independence from exogenous growth factors, production of growth factors, and stimulatory proliferative responses to traditionally inhibitory cytokines. Therapeutic efforts aimed at interrupting the switch in tumor cell responsiveness to cytokines, rather than to any one specific cytokine, may be most successful at inhibiting metastatic colonization. Angiogenesis has been demonstrated to be directly or indirectly induced by a plethora of cytokines. Partial suppression of neovascularization can be achieved in tissue culture and animal models using various natural and pharmaceutical angiostatic agents. However, as with clonal dominance, such agents must be able to suppress the redundant effects of angiogenesis-promoting factors. This review discusses the current literature on colonization and angiogenesis, emphasizing its underlying mechanisms and potential therapeutic applications. RP WEINSTATSASLOW, D (reprint author), NCI, PATHOL LAB, WOMEN CANC SECT, BLDG 10, RM 2A33, BETHESDA, MD 20892 USA. NR 76 TC 160 Z9 161 U1 2 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 1 PY 1994 VL 8 IS 6 BP 401 EP 407 PG 7 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA NH250 UT WOS:A1994NH25000006 PM 7513289 ER PT J AU BATISTA, MC CARTLEDGE, TP NIEMAN, LK BRAVO, N LORIAUX, DL MERRIAM, GR AF BATISTA, MC CARTLEDGE, TP NIEMAN, LK BRAVO, N LORIAUX, DL MERRIAM, GR TI CHARACTERIZATION OF THE NORMAL PROGESTERONE AND PLACENTAL PROTEIN-14 RESPONSES TO HUMAN CHORIONIC-GONADOTROPIN STIMULATION IN THE LUTEAL-PHASE SO FERTILITY AND STERILITY LA English DT Article DE HUMAN CHORIONIC GONADOTROPIN; PROGESTERONE; PLACENTAL PROTEIN 14; LUTEAL PHASE ID CORPUS-LUTEUM; SECRETORY ENDOMETRIAL; MENSTRUAL-CYCLE; SERUM; RADIOIMMUNOASSAY; RECEPTORS; PP14 AB Objective: To examine whether midluteal phase administration of the luteotrophic hormone hCG can result in higher and more stable serum levels than random sampling of P and placental protein 14 (PP14). C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT NURSING,BETHESDA,MD 20892. NR 25 TC 6 Z9 7 U1 0 U2 0 PU AMER SOC REPRODUCTIVE MEDICINE PI BIRMINGHAM PA 1209 MONTGOMERY HIGHWAY, BIRMINGHAM, AL 35216-2809 SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD APR PY 1994 VL 61 IS 4 BP 637 EP 644 PG 8 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA NE515 UT WOS:A1994NE51500011 PM 8150104 ER PT J AU GONDA, MA FONG, SE TOBIN, GJ AF GONDA, MA FONG, SE TOBIN, GJ TI BOVINE IMMUNODEFICIENCY VIRUS - EMERGING BIOLOGY OF A NONACUTE PATHOGENIC LENTIVIRUS OF CATTLE SO FOOD MICROBIOLOGY LA English DT Article ID BIOLOGICALLY-ACTIVE PROVIRUSES; LONG TERMINAL REPEAT; WESTERN-BLOT ASSAY; RECOMBINANT BACULOVIRUS; NUCLEOTIDE-SEQUENCE; MOLECULAR-CLONING; VISNA VIRUS; GAG GENE; INFECTIONS; RETROVIRUS RP GONDA, MA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,CELL & MOLEC STRUCT LAB,POB B,FREDERICK,MD 21702, USA. NR 55 TC 1 Z9 1 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0740-0020 J9 FOOD MICROBIOL JI Food Microbiol. PD APR PY 1994 VL 11 IS 2 BP 149 EP 160 DI 10.1006/fmic.1994.1018 PG 12 WC Biotechnology & Applied Microbiology; Food Science & Technology; Microbiology SC Biotechnology & Applied Microbiology; Food Science & Technology; Microbiology GA NL287 UT WOS:A1994NL28700007 ER PT J AU CROWELL, JA GOLDENTHAL, EI KELLOFF, GJ MALONE, WF BOONE, CW AF CROWELL, JA GOLDENTHAL, EI KELLOFF, GJ MALONE, WF BOONE, CW TI CHRONIC TOXICITY STUDIES OF THE POTENTIAL CANCER PREVENTIVE 2-(DIFLUOROMETHYL)-DL-ORNITHINE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID SKIN TUMOR PROMOTION; ALPHA-DIFLUOROMETHYLORNITHINE; ORNITHINE DECARBOXYLASE; MOUSE SKIN; POLYAMINE BIOSYNTHESIS; IRREVERSIBLE INHIBITOR; MAMMARY CARCINOGENESIS; CHEMOPREVENTION; PIROXICAM; ACID AB The synthetic compound 2-(difluoromethyl)-dl-ornithine irreversibly inhibits ornithine decarboxylase and reduces the intracellular levels of the polyamine cell cycle factors putrescine and spermidine. The drug has shown chemopreventive efficacy in numerous laboratory epithelial cancer models and is a prototype for antiproliferative agents. Chronic toxicity studies in rats and dogs were performed to characterize the toxicities of the compound at high dosages and to support its further development in clinical trials as a potential chemopreventive agent. Chronic administration (52 weeks) by gavage to Charles River CD rats at dosages of 400, 800, and 1600 mg/kg produced weight loss, increased platelets, alopecia and skin abrasions, dermatitis, liver necrosis, and gastric inflammation. The no-effect dose in this study was considered 400 mg/kg. Chronic administration by capsule to dogs at dosages of 50, 100, and 200 mg/kg produced conjunctivitis, hyperkeratosis and alopecia, and cystic intestinal crypts. A no-effect dose was not determined in this study. The toxicities demonstrated in these studies may be minimized at lower dosages and support the further development of this compound in chemopreventive clinical investigations. (C) 1994 Society of Toxicology. C1 INT RES & DEV CORP,MATTAWAN,MI 49071. RP CROWELL, JA (reprint author), NCI,DIV CANC PREVENT & CONTROL,CHEMOPREVENT BRANCH,BLDG EPN,SUITE 201,BETHESDA,MD 20892, USA. FU NCI NIH HHS [NCI N01-CN-55507-09] NR 37 TC 17 Z9 17 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1994 VL 22 IS 3 BP 341 EP 354 DI 10.1006/faat.1994.1040 PG 14 WC Toxicology SC Toxicology GA NG988 UT WOS:A1994NG98800003 PM 8050630 ER PT J AU HASEMAN, JK LOCKHART, A AF HASEMAN, JK LOCKHART, A TI THE RELATIONSHIP BETWEEN USE OF THE MAXIMUM TOLERATED DOSE AND STUDY SENSITIVITY FOR DETECTING RODENT CARCINOGENICITY SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID ANIMAL CARCINOGENICITY; CHEMICAL CARCINOGENESIS; STATISTICAL ISSUES; LONG-TERM; SELECTION; TOXICITY; DESIGN; RISK AB The relationship between maximum tolerated dose (MTD) and study sensitivity for detecting rodent carcinogenicity was evaluated for 216 chemicals found to be carcinogens in laboratory animal studies conducted by the National Cancer Institute (NCI) and the National Toxicology Program (NTP). Approximately two-thirds of these rodent carcinogens would have been detected even without the top dose (estimated MTD), but in many of these studies, some site-specific carcinogenic effects would have been missed. Among the remaining one-third of the rodent carcinogens that required the top dose for statistical significance, approximately 80% had numerically elevated rates of the same site-specific tumors at lower doses as well. Only 13 of the NCI/NTP rodent carcinogens had increased tumor rates limited to the top dose for all sites of carcinogenicity. Alternatively, of the 838 site-specific carcinogenic effects observed in the NCI/ NTP studies, 447 (53%) would have been detected even without the top dose. Of the remaining effects, 75% (294/391) showed numerically elevated site-specific tumor rates at lower doses. Our evaluation indicates that most carcinogenic effects observed at the top dose in rodent studies are also present (with reduced incidence that might or might not be statistically significant) at the lower doses typically employed (1/2MTD, 1/4MTD). (C) 1993 Society of Toxicology. C1 COMP SCI CORP,RES TRIANGLE PK,NC 27709. RP HASEMAN, JK (reprint author), NIEHS,DIV INTRAMURAL RES,STAT & BIOMATH BRANCH,RES TRIANGLE PK,NC 27709, USA. NR 35 TC 32 Z9 32 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1994 VL 22 IS 3 BP 382 EP 391 DI 10.1006/faat.1994.1043 PG 10 WC Toxicology SC Toxicology GA NG988 UT WOS:A1994NG98800006 PM 8050633 ER PT J AU DUNNICK, JK ELWELL, MR BUCHER, JR AF DUNNICK, JK ELWELL, MR BUCHER, JR TI COMPARATIVE TOXICITIES OF O-NITROTOLUENE, M-NITROTOLUENE, AND P-NITROTOLUENE IN 13-WEEK FEED STUDIES IN F344 RATS AND B6C3F(1) MICE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID ZERO DOSE CONTROL; LONG-TERM; FISCHER-344 RATS; CARCINOGENESIS; MONONITROTOLUENES; PROLIFERATION; RESTRICTION; METABOLISM; WEIGHT; CELLS AB Nitrotoluenes are high-production-volume chemicals used in the synthesis of agricultural chemicals and in various dyes. Because of differences in the metabolism of the three isomers and their capabilities to bind to DNA, comparative toxicity studies of o-, m-, and p-nitrotoluene were conducted in F344 rats and B6C3F(1) mice. o-, m-, or p-Nitrotoluene was administered in the feed to male and female rats and mice at doses ranging from 625 to 10,000 ppm for 13 weeks. These doses delivered approximately 40 to 700 mg/kg body wt/day for rats and 100 to 1700 mg/kg/day for mice. There were no treatment-related effects on survival in any of the studies. Decreased body weights relative to controls occurred in dosed rats and mice in all studies at the higher dose levels and were most pronounced in rats receiving o-nitrotoluene. Mesotheliomas of the tunica vaginalis were observed in 3 of 10 male rats receiving o-nitrotoluene at 5000 ppm, and mesothelial cell hyperplasia was observed in 2 of 10 male rats receiving o-nitrotoluene at 10,000 ppm. Kidney toxicity was observed in male rats receiving o-, m-, or p-nitrotoluene and included hyaline droplet nephropathy and an associated increase in the renal concentration of alpha(2U)-globulin. Evidence of liver toxicity in the male rats receiving o-nitrotoluene included hepatocyte vacuolization, oval cell hyperplasia, and increased serum bile acids, sorbitol dehydrogenase, and alanine aminotransferase. Although there was no histopathologic evidence of hepatic toxicity in male or female rats given the m- or p-isomers or in female rats given the o-isomer, treatment-related hepatic effects were detected in these groups, as measured by an increase in the relative liver weights and by elevations in serum bile acids and liver-specific enzymes. The spleens of treated male and female rats had a mild increase in hematopoiesis, hemosiderin deposition, and/or congestion. These splenic changes were slightly more prominent in rats administered the o- and p-isomers. Administration of o-, m-, or p-nitrotoluene impaired testicular function in the rat, as shown by testicular degeneration and reduction in the density, motility, and number of sperm cells. Administration of each isomer to rats caused increases in the length of the estrus cycle. The only histopathologic evidence for treatment-related toxicity in mice in the 13-week studies occurred in animals receiving the o-nitrotoluene isomer where the chemical caused degeneration and metaplasia of the olfactory epithelium. These comparative toxicity studies of o-, m-, or p-nitrotoluene showed that all three chemicals caused toxicity in the kidney, spleen, liver, and/or reproductive system in rats. In general, toxicity was most severe with the ortho-isomer. In mice, olfactory epithelium degeneration was the only treatment-related lesion induced by o-nitrotoluene. Elevations in liver weights were observed at the higher dose levels in rats and mice treated with any of the three isomers. o-Nitrotoluene was carcinogenic in male rats, as indicated by the occurrence of mesotheliomas at 5000 ppm and mesothelial cell hyperplasia at 10,000 ppm. (C) 1994 Society of Toxicology. RP DUNNICK, JK (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 32 TC 17 Z9 18 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1994 VL 22 IS 3 BP 411 EP 421 DI 10.1006/faat.1994.1047 PG 11 WC Toxicology SC Toxicology GA NG988 UT WOS:A1994NG98800010 PM 7519572 ER PT J AU KAWAHITO, Y SANO, H KAWATA, M YURI, K MUKAI, S YAMAMURA, Y KATO, H CHROUSOS, GP WILDER, RL KONDO, M AF KAWAHITO, Y SANO, H KAWATA, M YURI, K MUKAI, S YAMAMURA, Y KATO, H CHROUSOS, GP WILDER, RL KONDO, M TI LOCAL SECRETION OF CORTICOTROPIN-RELEASING HORMONE BY ENTEROCHROMAFFIN CELLS IN HUMAN COLON SO GASTROENTEROLOGY LA English DT Article ID HUMAN GASTROINTESTINAL-TRACT; RHEUMATOID-ARTHRITIS; SYNOVIAL TISSUES; NERVOUS-SYSTEM; WALL ARTHRITIS; SUBSTANCE-P; LEWIS RATS; PEPTIDES; IMMUNOREACTIVITY; NEUROHORMONE AB Background/Aims: Corticotropin-releasing hormone (CRH) is a regulator of the hypothalamic-pituitary-adrenal axis and a coordinator of the gastrointestinal response to stress. In addition to its central effects, CRH has peripheral effects on the immune system. CRH is present in several human tissues, such as the brain, spinal cord, adrenal medulla, lung, liver, peripheral blood leukocytes, as well as the gastrointestinal tract. The current study examined the local production of CRH in the normal human colon. Methods: Normal human colonic tissues obtained by endoscopic biopsy were immunostained with anti-CRH and anti-5-hydroxytryptamine antibody and analyzed for CRH messenger (m)RNA by a reverse-transcribed polymerase chain reaction method and by in situ hybridization. Results: Immunoreactive CRH and CRH mRNA were detected in the colonic mucosal cells in the neighborhood of the base of the crypts. The mucosal cells that expressed CRH mRNA also immunostained with anti-5-hydroxytryptamine antibody. Conclusions: Normal human colonic mucosal enterochromaffin cells produce CRH. CRH in the colonic mucosa may play a role in the modulation of the intestinal immune system and/or other gastrointestinal functions basally during stressful conditions. C1 KYOTO PREFECTURAL UNIV MED,DEPT INTERNAL MED 1,465 KAJII CHO,KAMIGYO KU,KYOTO 602,JAPAN. KYOTO PREFECTURAL UNIV MED,DEPT ANAT,KYOTO 602,JAPAN. MEIJI COLL ORIENTAL MED,KYOTO,JAPAN. NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD. NIAMSD,ARTHRIT & RHEUMAT BRANCH,BETHESDA,MD. NR 44 TC 94 Z9 94 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 BP 859 EP 865 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NE093 UT WOS:A1994NE09300004 PM 7511553 ER PT J AU BANKS, AT NGUYEN, CC AF BANKS, AT NGUYEN, CC TI GASTROINTESTINAL MANIFESTATIONS OF METASTATIC MELANOMA SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,GEORGETOWN GASTROENTEROL SERV,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A368 EP A368 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901462 ER PT J AU BENYA, RV MROZINSKI, JE BATTEY, JF JENSEN, RT AF BENYA, RV MROZINSKI, JE BATTEY, JF JENSEN, RT TI SPECIFIC STRUCTURAL ELEMENTS IN THE NEUROMEDIN-B RECEPTOR (NMBR) CARBOXYL-TERMINUS MEDIATE INTERNALIZATION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 DDB,BETHESDA,MD. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A799 EP A799 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903180 ER PT J AU BENYA, RV AKESON, M BATTEY, JF JENSEN, RT AF BENYA, RV AKESON, M BATTEY, JF JENSEN, RT TI INTERNALIZATION OF THE GASTRIN-RELEASING PEPTIDE RECEPTOR (GRP-R) IS NOT TOTALLY DEPENDENT ON PHOSPHOLIPASE-C ACTIVATION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 DDB,BETHESDA,MD. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A799 EP A799 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903178 ER PT J AU BENYA, RV BATTEY, JF JENSEN, RT AF BENYA, RV BATTEY, JF JENSEN, RT TI SERINES AND THREONINES IN THE GASTRIN-RELEASING PEPTIDE RECEPTOR (GRP-R) CARBOXYL-TERMINUS ARE NECESSARY FOR INTERNALIZATION AND DESENSITIZATION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. DDB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A285 EP A285 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901129 ER PT J AU BOLD, RJ LOWRY, PS BATTEY, JF ISHIZUKA, J TOWNSEND, CM THOMPSON, JC AF BOLD, RJ LOWRY, PS BATTEY, JF ISHIZUKA, J TOWNSEND, CM THOMPSON, JC TI RECEPTOR-SPECIFIC GROWTH-REGULATORY MECHANISMS OF BOMBESIN (BBS) IN HUMAN STOMACH-CANCER SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV TEXAS,MED BRANCH,DEPT SURG,GALVESTON,TX 77550. NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A800 EP A800 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903182 ER PT J AU CHUNG, YH DIBISCEGLIE, AM AF CHUNG, YH DIBISCEGLIE, AM TI EXPRESSION OF TRANSFORMING GROWTH-FACTOR-ALPHA (TGF-ALPHA) IN LIVER OF PATIENTS WITH CHRONIC VIRAL-HEPATITIS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,LIVER DIS SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A877 EP A877 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903487 ER PT J AU EVANS, DC JACOBS, J JOHNSON, BG CANTRELL, BE ROTHMAN, RB SCHOEPP, DD ZIMMERMAN, DM LEANDER, JD GIDDA, JS AF EVANS, DC JACOBS, J JOHNSON, BG CANTRELL, BE ROTHMAN, RB SCHOEPP, DD ZIMMERMAN, DM LEANDER, JD GIDDA, JS TI LY246736 - A SELECTIVE ANTAGONIST FOR PERIPHERAL MU-OPIOID RECEPTORS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ELI LILLY & CO,LILLY RES LAB,CNS GI GU DIV,LILLY CORP CTR,INDIANAPOLIS,IN 46285. NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL LAB,BALTIMORE,MD. NR 0 TC 2 Z9 2 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A495 EP A495 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901969 ER PT J AU EYSTER, ME SANDERS, JC DIBISCEGLIE, AM AF EYSTER, ME SANDERS, JC DIBISCEGLIE, AM TI INTERACTION BETWEEN HBV, HDV, AND HCV IN HEMOPHILIACS WITH HIV-INFECTION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 PENN STATE UNIV,COLL MED,UNIV PK,PA 16802. NIH,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A889 EP A889 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903538 ER PT J AU FELLEY, CF SUTLIFF, VE MANTEY, SA JENSEN, RT AF FELLEY, CF SUTLIFF, VE MANTEY, SA JENSEN, RT TI BINDING TO RECEPTORS FOR INSULIN, ENDOTHELIN AND SOMATOSTATIN ON CHIEF CELLS IS MODULATED BY SECRETAGOGUES SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DDB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A76 EP A76 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90900299 ER PT J AU GIBRIL, F MROZINSKI, JE GRIFFIN, T COY, DH BENYA, RV BATTEY, JF JENSEN, RT AF GIBRIL, F MROZINSKI, JE GRIFFIN, T COY, DH BENYA, RV BATTEY, JF JENSEN, RT TI IDENTIFICATION OF SELECTIVE AGONISTS AND ANTAGONISTS FOR HUMAN BOMBESIN RECEPTORS USING STABLY TRANSFECTED CELL-LINES SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. TULANE UNIV,NEW ORLEANS,LA 70118. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A809 EP A809 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903220 ER PT J AU HAMILTONAUGUSTUS, Y HARRIS, CC SMOOT, DT AF HAMILTONAUGUSTUS, Y HARRIS, CC SMOOT, DT TI INTERLEUKIN-6 STIMULATES GROWTH AND INHIBITS AFLATOXIN INDUCED CYTOTOXICITY OF SV40 T-ANTIGEN TRANSFORMED HUMAN LIVER EPITHELIAL-CELLS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HOWARD UNIV,DEPT MED,WASHINGTON,DC 20059. NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A904 EP A904 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903596 ER PT J AU HAYASHI, PH BEAMES, MP HOOFNAGLE, JH DIBISCEGLIE, AM AF HAYASHI, PH BEAMES, MP HOOFNAGLE, JH DIBISCEGLIE, AM TI SERUM LEVELS OF IGM ANTI-HBC IN PATIENTS WITH CHRONIC HEPATITIS-B - CHANGES WITH THERAPY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,LIVER DIS SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A905 EP A905 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903600 ER PT J AU HONG, MK LASKIN, WB HERMAN, BE STEINBERG, SM ALLEGRA, CJ JOHNSTON, PG AF HONG, MK LASKIN, WB HERMAN, BE STEINBERG, SM ALLEGRA, CJ JOHNSTON, PG TI EXPANSION OF THE KI-67 PROLIFERATIVE COMPARTMENT CORRELATES WITH THE DEGREE OF DYSPLASIA IN BARRETTS-ESOPHAGUS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NCI,NAVAL MED CTR,DEPT ONCOL,BETHESDA,MD 20892. NCI,NAVAL MED CTR,DEPT GASTROENTEROL,BETHESDA,MD 20892. NCI,NAVAL MED CTR,DEPT PATHOL,BETHESDA,MD 20892. NCI,NAVAL MED CTR,DEPT BIOSTAT & DATA MANAGEMENT,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A393 EP A393 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901562 ER PT J AU HUANG, SC FORTUNE, KP WANK, SA KOPIN, AS GARDNER, JD AF HUANG, SC FORTUNE, KP WANK, SA KOPIN, AS GARDNER, JD TI CHARACTERISTICS OF DIFFERENT CHOLECYSTOKININ (CCK) RECEPTORS IN TERMS OF INDIVIDUAL AFFINITY STATES SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST LOUIS UNIV,ST LOUIS,MO 63104. TUFTS UNIV,BOSTON,MA 02111. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A816 EP A816 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903247 ER PT J AU HUANG, SC TALKAD, VD FORTUNE, KP WANK, SA GARDNER, JD AF HUANG, SC TALKAD, VD FORTUNE, KP WANK, SA GARDNER, JD TI MULTIPLE AFFINITY STATES OF THE PANCREATIC CCK RECEPTOR ARE INTRINSIC-PROPERTIES OF THE RECEPTOR MOLECULE ITSELF SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. ST LOUIS UNIV,ST LOUIS,MO 63104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A816 EP A816 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903246 ER PT J AU HUANG, SC FORTUNE, KP WANK, SA GARDNER, JD AF HUANG, SC FORTUNE, KP WANK, SA GARDNER, JD TI DEMONSTRATION OF MULTIPLE AFFINITY STATES OF CHOLECYSTOKININ(B) (CCK(B)) RECEPTORS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST LOUIS UNIV,DEPT INTERNAL MED,ST LOUIS,MO 63104. NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A815 EP A815 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903244 ER PT J AU KUSUI, T BENYA, RV BATTEY, JF JENSEN, RT AF KUSUI, T BENYA, RV BATTEY, JF JENSEN, RT TI CHARACTERIZATION OF THE OLIGOSACCHARIDE CHAIN ON BOMBESIN (BN) RECEPTORS AND ITS IMPORTANCE IN RECEPTOR-LIGAND INTERACTION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A821 EP A821 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903267 ER PT J AU KUSUI, T WANG, LH BATTEY, JF BENYA, RV JENSEN, RT AF KUSUI, T WANG, LH BATTEY, JF BENYA, RV JENSEN, RT TI CHARACTERIZATION OF THE GASTRIN-RELEASING PEPTIDE RECEPTOR (GRP-R) EXPRESSED IN SF9 INSECT CELLS USING BACULOVIRUS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A301 EP A301 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901193 ER PT J AU MAHANEY, K TEDESCHI, V DIBISCEGLIE, AM MAERTENS, G SALLIE, R AF MAHANEY, K TEDESCHI, V DIBISCEGLIE, AM MAERTENS, G SALLIE, R TI A NOVEL AND RAPID METHOD OF GENOTYPING HEPATITIS-C VIRUS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,LIVER DIS SECT,BETHESDA,MD 20892. CBER,HEPATITIS RES LAB,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A936 EP A936 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903724 ER PT J AU MANTEY, SA PISEGNA, JR WANK, SA JENSEN, RT AF MANTEY, SA PISEGNA, JR WANK, SA JENSEN, RT TI COMPARATIVE ABILITY OF AGONISTS AND ANTAGONISTS TO DISCRIMINATE HUMAN CCK(A) (HCCK(A)-R) AND CCK(B) (HCCK(B)-R) RECEPTORS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A305 EP A305 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901211 ER PT J AU METZ, DC WEBER, C ORBUCH, M STRADER, DB GIBRIL, F JENSEN, RT AF METZ, DC WEBER, C ORBUCH, M STRADER, DB GIBRIL, F JENSEN, RT TI HELICOBACTER-PYLORI (HP) INFECTION AND ACID OUTPUT IN ZOLLINGER-ELLISON SYNDROME (ZES) - A PROSPECTIVE-STUDY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV PENN,DIV GI,PHILADELPHIA,PA 19104. NIDDK,DDB,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A138 EP A138 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90900545 ER PT J AU ORBUCH, M LUBENSKY, IA WEBER, HC STRADER, DB GIBRIL, F JENSEN, RT AF ORBUCH, M LUBENSKY, IA WEBER, HC STRADER, DB GIBRIL, F JENSEN, RT TI PROLONGED, MARKED HYPERGASTRINEMIA DOES NOT INCREASE THE RATE OF COLONIC NEOPLASIA SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A152 EP A152 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90900601 ER PT J AU PHAM, DQ NGUYEN, CC METCALFE, DD AF PHAM, DQ NGUYEN, CC METCALFE, DD TI ENDOSCOPIC AND HISTOLOGIC-FINDINGS IN SYSTEMIC MASTOCYTOSIS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,DIV GASTROENTEROL,WASHINGTON,DC 20057. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A21 EP A21 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90900080 ER PT J AU PISEGNA, JR POPE, SH WANK, SA AF PISEGNA, JR POPE, SH WANK, SA TI MOLECULAR-CLONING AND FUNCTIONAL EXPRESSION OF 2 SPLICE VARIANTS OF THE HUMAN PITUITARY ADENYLATE-CYCLASE ACTIVATING POLYPEPTIDE RECEPTOR (PACAP-R) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A832 EP A832 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903310 ER PT J AU PRADHAN, TK SUTLIFF, VE QIAN, JM JENSEN, RT AF PRADHAN, TK SUTLIFF, VE QIAN, JM JENSEN, RT TI IDENTIFICATION OF CCKA RECEPTORS ON CHIEF CELLS USING A NOVEL, HIGHLY SELECTIVE LIGAND SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A161 EP A161 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90900637 ER PT J AU ROFAIL, M GUPTA, PK MAHER, KA CANNON, RO LEWIS, JH BENJAMIN, SB AF ROFAIL, M GUPTA, PK MAHER, KA CANNON, RO LEWIS, JH BENJAMIN, SB TI A PROSPECTIVE, BLINDED EVALUATION OF AFFERENT BLOCKADE WITH ONDANSETRON (OND) AND INTRAESOPHAGEAL BALLOON DISTENSION (IEBD) IN PATIENTS WITH CHEST PAIN OF UNDETERMINED ETIOLOGY (CPUE) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,DIV GASTROENTEROL,WASHINGTON,DC 20007. NHLBI,CARDIOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A166 EP A166 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90900659 ER PT J AU ROSSOWSKI, WJ GU, ZF AKARCA, US JENSEN, RT COY, DH AF ROSSOWSKI, WJ GU, ZF AKARCA, US JENSEN, RT COY, DH TI GASTROINTESTINAL EFFECTS OF A PANEL OF SOMATOSTATIN ANALOGS SELECTIVE FOR 3 RECEPTOR SUBTYPES SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD 20892. TULANE UNIV,SCH MED,DEPT MED,PEPTIDE RES LABS,NEW ORLEANS,LA 70112. TULANE UNIV,SCH MED,DEPT MED,GASTROENTEROL SECT,NEW ORLEANS,LA 70112. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A837 EP A837 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903329 ER PT J AU SAITOH, S MATSUMOTO, T MORIGUCHI, M TAKEHARA, K NAGAMINE, T YANAGITA, M TAKEUCHI, T MERLINO, G TAKAGI, H AF SAITOH, S MATSUMOTO, T MORIGUCHI, M TAKEHARA, K NAGAMINE, T YANAGITA, M TAKEUCHI, T MERLINO, G TAKAGI, H TI HEPATIC REGENERATION IN TGF-ALPHA TRANSGENIC MOUSE SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GUNMA UNIV,SCH MED,DEPT INTERNAL MED 1,MAEBASHI,GUNMA 371,JAPAN. GUNMA UNIV,INST ENDOCRINOL,DIV MOLEC ENDOCRINOL,MAEBASHI,GUNMA 371,JAPAN. NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 2 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A972 EP A972 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903869 ER PT J AU SCHMIDT, HHJ REMALEY, AT STONIK, JA RONAN, R WELLMANN, A FAIRWELL, T ZECH, LA BREWER, HB HOEG, JM AF SCHMIDT, HHJ REMALEY, AT STONIK, JA RONAN, R WELLMANN, A FAIRWELL, T ZECH, LA BREWER, HB HOEG, JM TI THE CARBOXY-TERMINAL DOMAIN IS CRITICAL TO THE METABOLISM OF APOLIPOPROTEIN-A-I SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A978 EP A978 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903890 ER PT J AU SHAKIL, AO CONRYCANTILENA, C MELPOLDER, J ALTER, HJ HOOFNAGLE, JH KRAWCZYNSKI, K TADESCHI, V DIBISCEGLIE, AM AF SHAKIL, AO CONRYCANTILENA, C MELPOLDER, J ALTER, HJ HOOFNAGLE, JH KRAWCZYNSKI, K TADESCHI, V DIBISCEGLIE, AM TI LIVER HISTOPATHOLOGY IN BLOOD-DONORS WITH HEPATITIS-C AND NORMAL SERUM ALT LEVELS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. US FDA,BETHESDA,MD 20014. CTR DIS CONTROL,ATLANTA,GA 30333. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A981 EP A981 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903901 ER PT J AU STRADER, DB BENJAMIN, SB METZ, DC JENSEN, RT AF STRADER, DB BENJAMIN, SB METZ, DC JENSEN, RT TI DO HIGH-CONCENTRATIONS OF GASTRIN ALTER ESOPHAGEAL MOTILITY OR LOWER ESOPHAGEAL SPHINCTER (LES) FUNCTION SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A185 EP A185 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90900735 ER PT J AU TARASOVA, NI ROMANOV, VA HERNANDEZ, L MICHEJDA, CJ AF TARASOVA, NI ROMANOV, VA HERNANDEZ, L MICHEJDA, CJ TI GASTRIN RECEPTOR LOCALIZATION IN STOMACH SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NCI,FCRDC,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A845 EP A845 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903364 ER PT J AU WANK, SA PISEGNA, JR POIROT, SS AF WANK, SA PISEGNA, JR POIROT, SS TI FUNCTIONAL-SIGNIFICANCE OF POTENTIAL SPLICE VARIANTS OF THE HUMAN CHOLECYSTOKININ (CCK) B-RECEPTOR SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK,DIGEST DIS BRANCH,BETHESDA,MD. RI Poirot, Sandrine/D-5448-2017 NR 0 TC 11 Z9 11 U1 2 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A850 EP A850 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90903383 ER PT J AU WEBER, HC VENZON, DJ FISHBEIN, VA ORBUCH, M STRADER, DB GIBRIL, F JENSEN, RT AF WEBER, HC VENZON, DJ FISHBEIN, VA ORBUCH, M STRADER, DB GIBRIL, F JENSEN, RT TI DETERMINANTS OF METASTATIC RATE AND SURVIVAL IN PATIENTS WITH ZOLLINGER-ELLISON SYNDROME (ZES) - RESULTS OF A PROSPECTIVE LONG-TERM STUDY SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDKD,BETHESDA,MD. NCI,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A330 EP A330 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90901308 ER PT J AU WHITEHEAD, WE LI, Z DROSSMAN, D COSTA, P TAUB, E COOK, E AF WHITEHEAD, WE LI, Z DROSSMAN, D COSTA, P TAUB, E COOK, E TI FACTOR-ANALYSIS OF GI SYMPTOMS SUPPORTS ROME CRITERIA FOR FUNCTIONAL GI DISORDERS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV N CAROLINA,CHAPEL HILL,NC 27514. NIA,BALTIMORE,MD 21224. UNIV ALABAMA,BIRMINGHAM,AL 35294. NR 2 TC 4 Z9 4 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A589 EP A589 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90902341 ER PT J AU YUAN, DS DANCIS, A KLAUSNER, RD AF YUAN, DS DANCIS, A KLAUSNER, RD TI VACUOLAR FUNCTION IS REQUIRED FOR COPPER-METABOLISM IN YEAST SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A1012 EP A1012 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90904027 ER PT J AU YURDAYDIN, C SWAIN, M VERGALLA, J KLEINER, D PAUL, S JONES, EA AF YURDAYDIN, C SWAIN, M VERGALLA, J KLEINER, D PAUL, S JONES, EA TI ORNITHINE DECARBOXYLASE INHIBITION IS ASSOCIATED WITH INCREASED SURVIVAL IN THIOACETAMIDE-INDUCED HEPATITIS SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1994 VL 106 IS 4 SU S BP A1012 EP A1012 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA NH909 UT WOS:A1994NH90904028 ER PT J AU CURCIO, MJ GARFINKEL, DJ AF CURCIO, MJ GARFINKEL, DJ TI HETEROGENEOUS FUNCTIONAL TY1 ELEMENTS ARE ABUNDANT IN THE SACCHAROMYCES-CEREVISIAE GENOME SO GENETICS LA English DT Article ID VIRUS-LIKE PARTICLES; RETROTRANSPOSON TY; GENE-EXPRESSION; NUCLEOTIDE-SEQUENCE; RIBOSOMAL DNA; S-CEREVISIAE; SPT3 GENE; YEAST; TRANSPOSITION; RECOMBINATION AB Despite the abundance of Ty1 RNA in Saccharomyces cerevisiae, Ty1 retrotransposition is a rare event. To determine whether transpositional dormancy is the result of defective Ty1 elements, functional and defective alleles of the retrotransposon in the yeast genome were quantitated. Genomic Ty1 elements were isolated by gap repair-mediated recombination of pGTY 1-H3 (Delta 475-3944) H1S3, a multicopy plasmid containing a GAL1/Ty1-HS fusion element lacking most of the gag domain (TYA) and the protease (PR) and integrase (IN) domains. Of 39 independent gap repaired pGTyHIS3 elements isolated, 29 (74%) transposed at high levels following galactose induction. The presence of restriction site polymorphisms within the gap repaired region of the 29 functional pGTyHIS3 elements indicated that they were derived from at least eight different genomic Ty1 elements and one Ty2 element. Of the 10 defective pGTyHIS3 elements, one was a partial gap repair event while the other nine were derived from at least six different genomic Ty1 elements. These results suggest that most genomic Ty1 elements encode functional TYA, PR and IN proteins. To understand how functional Ty1 elements are regulated, we tested the hypothesis that a TYB protein associates preferentially in cis with the RNA template that encodes it, thereby promoting transposition of its own element. A genomic Ty1 mhis3AI element containing either an in-frame insertion in PR or a deletion in TYB transposed at the same rate as a wild-type Ty1mhis3AI allele, indicating that TYB proteins act efficiently in trans. This result suggests in principle that defective genomic Ty1 elements could encode transacting repressors of transposition; however, expression of only one of the nine defective pGTy1 isolates had a negative effect on genomic Ty1 mhis3AI element transposition in trans, and this effect was modest. Therefore, the few defective Ty1 elements in the genome are not responsible for transpositional dormancy. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL,EUCARYOT GENE EXPRESS LAB,BASIC RES PROGRAM,FREDERICK,MD 21702. RP CURCIO, MJ (reprint author), NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,MOLEC GENET PROGRAM,ALBANY,NY 12201, USA. OI Curcio, M. Joan/0000-0001-5361-3909 FU NCI NIH HHS [N01-CO-74101] NR 55 TC 49 Z9 49 U1 0 U2 0 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD APR PY 1994 VL 136 IS 4 BP 1245 EP 1259 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA NB821 UT WOS:A1994NB82100003 PM 8013902 ER PT J AU LOCK, LF GILBERT, DJ STREET, VA MIGEON, MB JENKINS, NA COPELAND, NG TEMPEL, BL AF LOCK, LF GILBERT, DJ STREET, VA MIGEON, MB JENKINS, NA COPELAND, NG TEMPEL, BL TI VOLTAGE-GATED POTASSIUM CHANNEL GENES ARE CLUSTERED IN PARALOGOUS REGIONS OF THE MOUSE GENOME SO GENOMICS LA English DT Article ID INTERSPECIFIC BACKCROSS ANALYSIS; LINKAGE MAP; CHROMOSOMAL LOCATION; COMPLEMENTARY-DNA; ALPHA-SUBUNIT; SHAKER LOCUS; DROSOPHILA; MURINE; EXPRESSION; CLONING AB Cloning of the Drosophila Shaker gene established that a neurological phenotype including locomotor dysfunction can be caused by a mutation in a voltage-gated potassium (K) channel gene. Shaker sequences have been used to isolate a large family of related K channel genes from both flies and mammals. Toward elucidating the evolutionary relationship between loci and the potential causal connection that K channels may have to mammalian genetic disorders, we report here the genetic mapping of 12-16 different murine, voltage-gated K channel genes. We find that multiple genes, in some cases from distantly related K channel subfamilies, occur in clusters in the mouse genome. These mapping results suggest that the K channel gene subfamilies arose through ancient localized gene duplication events, followed by chromosomal duplications and rearrangements as well as further gene duplication. We also note that several neurologic disorders of both mouse and human are associated with the chromosomal regions containing K channel genes. (C) 1994 Academic Press, Inc. C1 VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN 182B,SEATTLE,WA 98108. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. UNIV WASHINGTON,SCH MED,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,DEPT PHARMACOL,SEATTLE,WA 98195. FU NINDS NIH HHS [NS-27206]; PHS HHS [N01-C0-74101] NR 77 TC 38 Z9 38 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1994 VL 20 IS 3 BP 354 EP 362 DI 10.1006/geno.1994.1188 PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NF578 UT WOS:A1994NF57800003 PM 8034307 ER PT J AU BROWN, A COPELAND, NG GILBERT, DJ JENKINS, NA ROSSANT, J KOTHARY, R AF BROWN, A COPELAND, NG GILBERT, DJ JENKINS, NA ROSSANT, J KOTHARY, R TI THE GENOMIC STRUCTURE OF AN INSERTIONAL MUTATION IN THE DYSTONIA-MUSCULORUM LOCUS SO GENOMICS LA English DT Article ID TRANSGENIC MICE; DEVELOPMENTAL ARREST; DNA REARRANGEMENTS; MOUSE; GENE; MUTAGENESIS; H-BETA-58; EMBRYO; LINE AB We have previously identified a line of transgenic mice, Tg4, in which an hsp68-lacZ hybrid gene has inserted into the dystonia musculorum (dt) locus on chromosome 1. We have confirmed the localization of the Tg4 integration site to the proximal region of mouse chromosome 1 by interspecific backcross analysis. One end of the integration complex has been cloned and we have used single-copy probes from the flanking region to screen a mouse genomic library. Several overlapping lambda phage clones have been isolated and arranged into a contig spanning 75 kb of genomic DNA. Probes from the genomic contig have enabled us to characterize the wildtype and Tg4 loci. We report that the integration of the transgene was accompanied by a deletion of 45 kb of host genomic sequences with no other detectable rearrangement in the Tg4 genome. (C) 1994 Academic Press,Inc. C1 MT SINAI HOSP,SAMUEL LUNENFELD RES INST,DIV MOLEC & DEV BIOL,TORONTO M5G 1X5,ON,CANADA. UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO,ON,CANADA. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. UNIV MONTREAL,DEPT MED,MONTREAL,PQ,CANADA. RP BROWN, A (reprint author), CTR RECH LC SIMARD,INST CANC MONTREAL,MONTREAL H2L 4M1,PQ,CANADA. RI Brown, Arthur/K-8328-2013; OI Kothary, Rashmi/0000-0002-9239-7310 FU NCI NIH HHS [N01-CO-74101] NR 31 TC 29 Z9 30 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1994 VL 20 IS 3 BP 371 EP 376 DI 10.1006/geno.1994.1190 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NF578 UT WOS:A1994NF57800005 PM 8034309 ER PT J AU KOU, K JENKINS, NA GILBERT, DJ COPELAND, NG ROTWEIN, P AF KOU, K JENKINS, NA GILBERT, DJ COPELAND, NG ROTWEIN, P TI ORGANIZATION, EXPRESSION, AND CHROMOSOMAL LOCATION OF THE MOUSE INSULIN-LIKE GROWTH-FACTOR BINDING-PROTEIN-5 GENE SO GENOMICS LA English DT Article ID IGF; DNA; LOCALIZATION; DIFFERENTIATION; IDENTIFICATION; FIBROBLASTS; FRAGMENTS; SEQUENCES; RECEPTOR; CLONING AB Insulin-like growth factor binding proteins (IGFBPs) constitute a family of at least six secreted proteins that bind insulin-like growth factors I and II (IGF-I and -II) and are capable of modifying IGF actions on target cells. We previously have purified an similar to 29-kDa IGFBP that is secreted by myoblasts during their terminal differentiation, have identified the protein as mouse IGFBP-5, and have cloned its cDNA (James ct al., 1993). In this study, we have characterized the mouse IGFBP-5 gene, established its pattern of expression in the adult mouse, and defined its chromosomal location. The 17-kb gene was isolated on overlapping cosmid and lambda clones, and the four exons encoding the 5914-bp mRNA were sequenced. The 5' end of the gene was mapped by solution-hybridization ribonuclease protection assay to two discrete sites in exon 1 that were separated by 21 bp. The relative use of each transcription start site was found to vary among different mouse tissues. By interspecies backcross mapping using progeny derived from matings of [(C57BL/6J X Mus spretus)F-1 X C57BL/6J] mice, the IGFBP-5 gene was localized to the proximal region of chromosome 1 in tight linkage with fibronectin 1 (0 recombinants in 168 mice analyzed). Since this part of chromosome 1 shares homology with human chromosome 2q, and since fibronectin has been mapped to 2q34-q36, it is likely that human IGFBP-5 will reside on 2q as well. Characterization of the mouse IGFBP-5 gene now provides a starting point for studying the roles and regulation of this protein in development. (C) 1994 Academic Press, Inc. C1 WASHINGTON UNIV,SCH MED,DEPT BIOCHEM & MOLEC BIOPHYS,ST LOUIS,MO 63110. ST LOUIS UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101]; NIDDK NIH HHS [R01 DK042748, DK42748] NR 43 TC 25 Z9 26 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1994 VL 20 IS 3 BP 412 EP 418 DI 10.1006/geno.1994.1195 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NF578 UT WOS:A1994NF57800010 PM 7518410 ER PT J AU COOKSON, BT ENGELHARDT, S SMITH, C BAMFORD, HA PROCHAZKA, M TAIT, JF AF COOKSON, BT ENGELHARDT, S SMITH, C BAMFORD, HA PROCHAZKA, M TAIT, JF TI ORGANIZATION OF THE HUMAN ANNEXIN-V (ANX5) GENE SO GENOMICS LA English DT Article ID PLACENTAL ANTICOAGULANT PROTEIN; PHOSPHOLIPID-BINDING-PROTEINS; HUMAN ENDONEXIN-II; LIPOCORTIN-I; CALCIUM; FAMILY; EXPRESSION; SEQUENCES; PURIFICATION; LOCALIZATION AB We characterized the region of human chromosome 4q26-q28 that contains the gene encoding annexin V (placental anticoagulant protein I), a member of a family of calcium-dependent phospholipid binding proteins. A total of 14.5 kb, containing 9 introns, could be directly amplified from genomic DNA; the remainder was characterized from genomic clones a phage lambda and a yeast artificial chromosome. The gene was mapped with restriction enzymes BamHI, EcoRI, HindIII, SacI, StuI, and XbaI: the transcribed region spans 28 kb and contains 13 exons (44 to 530 bp in size) and 12 introns (0.23 to 8.8 kb in size). Several putative transcription factor binding sites are present in the 5'-region, but the promoter has no recognizable TATA box. this study will facilitate further analysis of the functions of annexin V and its role in disease. (C) 1994 Academic Press, Inc. C1 UNIV WASHINGTON,DEPT LAB MED,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT PATHOL,SEATTLE,WA 98195. NIDDKD,PHOENIX,AZ 85016. FU NHLBI NIH HHS [HL-40801, HL-47151] NR 33 TC 23 Z9 31 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1994 VL 20 IS 3 BP 463 EP 467 DI 10.1006/geno.1994.1201 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NF578 UT WOS:A1994NF57800016 PM 8034319 ER PT J AU HAKE, LE KUEMMERLE, N HECHT, NB KOZAK, CA AF HAKE, LE KUEMMERLE, N HECHT, NB KOZAK, CA TI THE GENES ENCODING THE SOMATIC AND TESTIS-SPECIFIC ISOTYPES OF THE MOUSE CYTOCHROME-C GENES MAP TO PARALOGOUS REGIONS OF CHROMOSOME-6 AND CHROMOSOME-2 SO GENOMICS LA English DT Note AB Using mouse probes specific to cytochrome c, and to cytochrome c(T), the single-copy genes encoding these two proteins have been mapped to paralogous chromosomal regions by analysis of restriction fragment length variants in interspecific crosses. The gene for cytochrome c(S), Cycs, maps to a position between Tcrb and Cbl-1 on proximal mouse Chromosome 6, and the gene for cytochrome c(T), Cyct, maps between Gad-1 and Sfpi-1 on mouse Chromosome 2. (C) 1994 Academic Press, Inc. C1 TUFTS UNIV,DEPT BIOL,MEDFORD,MA 02155. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. FU NICHD NIH HHS [HD 11878] NR 18 TC 17 Z9 19 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1994 VL 20 IS 3 BP 503 EP 505 DI 10.1006/geno.1994.1210 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NF578 UT WOS:A1994NF57800025 PM 8034327 ER PT J AU HAMEL, CP JENKINS, NA GILBERT, DJ COPELAND, NG REDMOND, TM AF HAMEL, CP JENKINS, NA GILBERT, DJ COPELAND, NG REDMOND, TM TI THE GENE FOR THE RETINAL-PIGMENT EPITHELIUM-SPECIFIC PROTEIN RPE65 IS LOCALIZED TO HUMAN 1P31 AND MOUSE-3 SO GENOMICS LA English DT Note AB The human and murine chromosomal localization for the gene for the retinal pigment epithelium-specific protein RPE65 was determined. Using interspecific backcross analysis, we mapped Rpe65 to the distal end of mouse chromosome 3. In the human, using a human-hamster hybrid panel, RPE65 was mapped to chromosome 1. By the use of fluorescence in situ hybridization, this localization was refined to 1p31. The mouse and human loci for this potential candidate gene for hereditary retinal disease do not match those of any known disease in mouse or man. (C) 1994 Academic Press, Inc. C1 NEI,LRCMB,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. OI Redmond, T. Michael/0000-0002-1813-5291 FU NCI NIH HHS [N01-CO-74101] NR 10 TC 51 Z9 51 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1994 VL 20 IS 3 BP 509 EP 512 DI 10.1006/geno.1994.1212 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NF578 UT WOS:A1994NF57800027 PM 8034329 ER PT J AU KUTTY, RK KUTTY, G RODRIGUEZ, IR CHADER, GJ WIGGERT, B AF KUTTY, RK KUTTY, G RODRIGUEZ, IR CHADER, GJ WIGGERT, B TI CHROMOSOMAL LOCALIZATION OF THE HUMAN HEME OXYGENASE GENES - HEME OXYGENASE-1 (HMOX1) MAPS TO CHROMOSOME 22Q12 AND HEME OXYGENASE-2 (HMOX2) MAPS TO CHROMOSOME 16P13.3 SO GENOMICS LA English DT Note ID BILIVERDIN REDUCTASE; MESSENGER-RNA; RAT-LIVER; PURIFICATION; INDUCTION; CDNA AB Heme oxygenase catalyzes the oxidation of heme to biliverdin, the precursor of the bile pigment bilirubin, and carbon monoxide, a putative neurotransmitter. We have employed polymerase chain reaction and fluorescence in situ hybridization to determine the chromosome localization of the genes coding for the two known heme oxygenase isozymes. Heme oxygenase-1 (HMOX1), the inducible form, was localized to human chromosome 22q12, while heme oxygenase-2 (HMOX2), the constitutive form, was localized to chromosome 16p13.3. (C) 1994 Academic Press,Inc. RP KUTTY, RK (reprint author), NEI,LRCMB,BLDG 6,ROOM 338,BETHESDA,MD 20892, USA. NR 14 TC 80 Z9 82 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1994 VL 20 IS 3 BP 513 EP 516 DI 10.1006/geno.1994.1213 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA NF578 UT WOS:A1994NF57800028 PM 8034330 ER PT J AU REDDY, GP ABEYGUNAWARDANA, C BUSH, CA CISAR, JO AF REDDY, GP ABEYGUNAWARDANA, C BUSH, CA CISAR, JO TI THE CELL-WALL POLYSACCHARIDE OF STREPTOCOCCUS-GORDONII-38 - STRUCTURE AND IMMUNOCHEMICAL COMPARISON WITH THE RECEPTOR POLYSACCHARIDES OF STREPTOCOCCUS-ORALIS-34 AND STREPTOCOCCUS-MITIS J22 SO GLYCOBIOLOGY LA English DT Article DE CELL WALL POLYSACCHARIDE; COMPARISON; IMMUNOCHEMISTRY; STREPTOCOCCUS GORDONII; STRUCTURE ID ACTINOMYCES-VISCOSUS T14V; MULTIPLE QUANTUM NMR; COAGGREGATION; SPECTROSCOPY; SURFACE; NAESLUNDII; RESOLUTION; H-1 AB As part of our ongoing investigations involving lectin-mediated adhesion among oral bacteria, the receptor polysaccharide from Streptococcus gordonii 38 was isolated and characterized. Carbohydrate analysis of the hydrolysed; S. gordonii 38 polysaccharide by high-performance anion-exchange chromatography with pulsed amperometric detection (HPAEC-PAD) showed galactose (Gal) (2 mel), N-acetylgalactosamine (GalNAc) (1 mel), rhamnose (Rha) (2 mel), glucose (Glc) (1 mel) and galactosamine-6-phosphate (1 mol). Mild acid hydrolysis of the polysaccharide yielded a heptasaccharide repeating unit, The structure of the heptasaccharide repeating unit was determined by high-resolution NMR spectroscopy which includes various homonuclear (DQF-COSY, TQF-COSY, NOESY and HOHAHA) and heteronuclear experiments (HMQC), including linkage assignments by H-1-C-13 long-range correlation (HMBC). Complete H-1 and C-13 NMR assignments for the intact polysaccharide yielded the covalent structure of a heptasaccharide repeating unit: [-->6)Gal(p)NAc alpha(1-->3)-Rha(p) beta-(1-->4)-Glc(p) beta-(1-->6)-Gal(f) beta-(1-->6)- Rha(p) alpha-(1-->2)-NE arrow Gal(p)NAc beta-(1-->3)-Gal(p) alpha-(1-->PO4--](n) The structure of the strain 38 polysaccharide is closely related to those of Streptococcus mitis J22 and Streptococcus oralis 34. Thus, the difference between the strain 38 and J22 heptasaccharides was at their reducing ends, with GalNAc beta-(1-->3)-Gal in the former and Gal beta-(1-->3)-GalNAc in the latter, while the difference between the 38 heptasaccharide and 34 hexasaccharide was at the non-reducing ends, where a rhamnose branch occurred in the former but not the latter structure. When compared by their quantitative precipitin curves with rabbit antibodies against each streptococcal strain, the strain 38 polysaccharide reacted more like the polysaccharide of strain J22 than that of strain 34. In contrast, each strain was recognized by the Gal- and GalNAc-reactive lectins of Actinomyces spp., but only strains 38 and 34 were recognized by GalNAc-sensitive lectins of other streptococci. These findings strongly support the hypothesis that the immunogenic features of these polysaccharides are distinct from those detected by lectin binding. C1 UNIV MARYLAND,DEPT CHEM & BIOCHEM,BALTIMORE,MD 21228. NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. FU NIDCR NIH HHS [DE-09445] NR 31 TC 18 Z9 18 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0959-6658 J9 GLYCOBIOLOGY JI Glycobiology PD APR PY 1994 VL 4 IS 2 BP 183 EP 192 DI 10.1093/glycob/4.2.183 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA NM089 UT WOS:A1994NM08900011 PM 8054717 ER PT J AU TERAN, JC MULLEN, KD HOOFNAGLE, JH MCCULLOUGH, AJ AF TERAN, JC MULLEN, KD HOOFNAGLE, JH MCCULLOUGH, AJ TI DECREASE IN SERUM LEVELS OF MARKERS OF HEPATIC CONNECTIVE-TISSUE TURNOVER DURING AND AFTER TREATMENT OF CHRONIC HEPATITIS-B WITH INTERFERON-ALPHA SO HEPATOLOGY LA English DT Article ID ALCOHOLIC LIVER-DISEASE; III PROCOLLAGEN PEPTIDE; PRIMARY BILIARY-CIRRHOSIS; CHRONIC ACTIVE HEPATITIS; N-TERMINAL PROPEPTIDE; COLLAGEN TYPE-III; BASEMENT-MEMBRANE; AMINOTERMINAL PROPEPTIDE; FIBROBLAST COLLAGEN; CONTROLLED TRIAL AB Interferon-alpha induces remission in 30% to 40% of patients with chronic hepatitis B, but its effect on hepatic connective tissue turnover has not been well documented. We studied the changes in serum procollagen III propeptide and laminin-PI peptide (Lam-P1) in 33 patients with chronic hepatitis B (11 nontreated controls and 22 treated patients) during a 4-mo randomized trial of interferon-alpha. Liver biopsy specimens were obtained at the start of treatment and 12 mo later. Liver biochemical tests, procollagen III propeptide, laminin-P1 peptide and hepatitis B virus DNA polymerase were determined before treatment with interferon was begun (mo -3), at the initiation (0 time) and completion of treatment (mo 4) and also at 8, 12 and 18 mo. Treated patients were classified as ''responders'' and ''nonresponders'' on the basis of clearance of HBV e antigen from serum. There were no significant changes in the control group, whereas the responders had persistent decreases in ALT, AST, hepatitis B virus dna polymerase, procollagen I propeptide and laminin-P1 peptide. The nonresponders had transient ALT, AST and hepatitis B virus dna polymerase reductions that returned toward baseline levels during follow-up, but procollagen III propeptide and laminin-P1 peptide persisted below the baseline at mo 18. Significant correlations between procollagen III propeptide and laminin-P1 peptide with ALT, AST and liver histologic specimens were noted at baseline but not after 12 mo. Changes in procollagen III propeptide levels also correlated with changes in AST, ALT and liver histologic specimens. On the basis of logistic regression, neither markers of connective tissue turnover nor histology improved the accuracy of AST, ALT and hepatitis B virus dna polymerase for predicting response to interferon. We conclude that interferon treatment induces a persistent suppression in serum markers of hepatic connective tissue turnover in chronic hepatitis B patients independent of its effect on viral replication and hepatic necroinflammation. C1 CASE WESTERN RESERVE UNIV,METROHLTH MED CTR,DIV GASTROENTEROL,2500 METROHLTH DR,CLEVELAND,OH 44109. NIDDKD,DIGEST DIS BRANCH,LIVER DIS SECT,BETHESDA,MD 20892. NR 51 TC 21 Z9 21 U1 0 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1994 VL 19 IS 4 BP 849 EP 856 DI 10.1016/0270-9139(94)90282-8 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ND702 UT WOS:A1994ND70200007 PM 8138256 ER PT J AU MUNOZ, LE SANDOVAL, CA CALDERON, IE TORRES, E NACCHA, LR MONTOYA, R CHENG, CS HANSEN, C BENNETT, WP HARRIS, CC AF MUNOZ, LE SANDOVAL, CA CALDERON, IE TORRES, E NACCHA, LR MONTOYA, R CHENG, CS HANSEN, C BENNETT, WP HARRIS, CC TI CLINICAL-STUDIES AND P53 MUTATIONS IN HEPATOCELLULAR-CARCINOMA FROM MONTERREY, MEXICO SO HEPATOLOGY LA English DT Meeting Abstract C1 AUTONOMOUS UNIV NUEVO LEON,DR JOSE E GONZALEZ UNIV HOSP,MONTERREY,NUEVO LEON,MEXICO. NCI,HUMAN CARTINOGENESIS LAB,BETHESDA,MD 20892. AUTONOMOUS UNIV NUEVO LEON,SCH MED,DEPT GASTROENTEROL,LIVER UNIT,MONTERREY,NUEVO LEON,MEXICO. AUTONOMOUS UNIV NUEVO LEON,SCH MED,DEPT ANALYT CHEM,MONTERREY,NUEVO LEON,MEXICO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1994 VL 19 IS 4 BP I106 EP I106 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA ND702 UT WOS:A1994ND70200309 ER PT J AU PRICE, RA CHARLES, MA PETTITT, DJ KNOWLER, WC AF PRICE, RA CHARLES, MA PETTITT, DJ KNOWLER, WC TI OBESITY IN PIMA-INDIANS - GENETIC SEGREGATION ANALYSES OF BODY-MASS INDEX COMPLICATED BY TEMPORAL INCREASES IN OBESITY SO HUMAN BIOLOGY LA English DT Article DE OBESITY; OVERWEIGHT; BODY MASS INDEX; MAJOR GENE INHERITANCE; SECULAR TRENDS; TEMPORAL TRENDS; GENETIC INTERACTION ID DANISH YOUNG MEN; SECULAR TRENDS; EXTREME OVERWEIGHT; SKINFOLD THICKNESS; DIABETES INCIDENCE; UNIFIED MODEL; DISTRIBUTIONS; WEIGHT; WOMEN; SCHOOLCHILDREN AB During the past half-century the prevalence-of obesity in developed countries has increased greatly. Such short-term changes in prevalence must be environmentally determined, but:genes can mediate response to environmental change, for example, through variable gene penetrance and expression. Obesity differences between birth cohorts complicate the interpretation of phenotypic comparisons between generations that span periods of change. Genetic segregation analyses of the body mass index in 618 Pima Indian nuclear families (2 generations) identified recessive major gene inheritance, which is the same pattern of transmission that has been found in several other populations. However, within-birth-cohort analyses of siblings (one generation) uniformly supported codominant major gene inheritance with no polygenic heritability. For untransformed data transmission probabilities were Mendelian in the later-born cohort and in the combined sample of siblings. After transformation to remove skewness, transmission probabilities were Mendelian only in the earlier-born cohort (i.e., those siblings born before a period of marked temporal increase following World War II). A higher penetrance of codominant obesity susceptibility genes in the younger generation would result in some genetically obese individuals who have no affected parents, thus simulating recessive inheritance. Taken together, the results of these analyses suggest that the recessive pattern we identified in the Pima Indian nuclear families could be accounted for by temporal changes in penetrance of codominant obesity-predisposing genes. By implication, more modest temporal increases in white and black populations could in part account for the recessive pattern of inheritance described by several investigators. C1 NIDDKD,PHOENIX,AZ. RP PRICE, RA (reprint author), UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104, USA. FU NIDDK NIH HHS [R01-DK44073] NR 38 TC 14 Z9 14 U1 0 U2 0 PU WAYNE STATE UNIV PRESS PI DETROIT PA 4809 WOODWARD AVE, DETROIT, MI 48201-1309 SN 0018-7143 J9 HUM BIOL JI Hum. Biol. PD APR PY 1994 VL 66 IS 2 BP 251 EP 274 PG 24 WC Biology; Genetics & Heredity SC Life Sciences & Biomedicine - Other Topics; Genetics & Heredity GA MZ587 UT WOS:A1994MZ58700004 PM 8194846 ER PT J AU BRODY, SL JAFFE, HA HAN, SK WERSTO, RP CRYSTAL, RG AF BRODY, SL JAFFE, HA HAN, SK WERSTO, RP CRYSTAL, RG TI DIRECT IN-VIVO GENE-TRANSFER AND EXPRESSION IN MALIGNANT-CELLS USING ADENOVIRUS VECTORS SO HUMAN GENE THERAPY LA English DT Article ID MEDIATED TRANSFER; ARTERIAL-WALL; INVIVO; THERAPY; CANCER; INTERLEUKIN-4; EPITHELIUM; POTENT; HEART; ALPHA AB To evaluate the ability of replication-deficient, recombinant adenovirus vectors' to transfer genes to human tumor cells in vivo, adenovirus vectors containing the Escherichia coli lacZ (Ad.RSV beta gal) gene (coding for beta-galactosidase; used as a cell marker for gene transfer) or the human alpha 1-antitrypsin (Ad-alpha 1AT) cDNA (used as an example of a secreted protein) were administered intraperitoneally to nude mice with human malignant mesothelioma cell (H-MESO-1) malignant ascites. Preliminary in vitro studies showed that both vectors effectively transferred genes to H-MESO-1 cells. Tumor cells recovered from ascites of animals intraperitoneally administered a control adenovirus revealed no evidence of beta-galactosidase (beta-gal) activity 3 or 14 days later. In contrast, beta-gal activity was detected at the same time points in tumor cells from animals receiving intraperitoneal Ad.RSV beta gal. Flow cytometric quantification of beta-gal activity in recovered cells showed <3% beta-gal-positive cells in animals administered control virus, but in animals administered intraperitoneal Ad.RSV beta gal there was a mean of 71 +/- 18% positive cells at 3 days and 56 +/- 27% at 14 days. Human alpha 1AT was not detected by enzyme-linked immunosorbent assay (ELISA) in ascites of animals receiving a control virus; however, in ascites of animals administered Ad-alpha 1AT, 21,000 +/- 3,800 ng/ml of human alpha 1AT was detected at 3 days and 4,900 +/- 1,700 ng/ml at 14 days. These data demonstrate that replication-deficient recombinant adenovirus vectors can be used to transfer genes to malignant cells in vivo and suggest a new strategy for genetic modification for antitumor therapy. C1 NHLBI, PULM BRANCH, BETHESDA, MD 20892 USA. NR 46 TC 62 Z9 64 U1 0 U2 1 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1043-0342 EI 1557-7422 J9 HUM GENE THER JI Hum. Gene Ther. PD APR PY 1994 VL 5 IS 4 BP 437 EP 447 DI 10.1089/hum.1994.5.4-437 PG 11 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA NJ877 UT WOS:A1994NJ87700003 PM 7519451 ER PT J AU DEAN, M SANTIS, G AF DEAN, M SANTIS, G TI HETEROGENEITY IN THE SEVERITY OF CYSTIC-FIBROSIS AND THE ROLE OF CFTR GENE-MUTATIONS SO HUMAN GENETICS LA English DT Review ID TRANSMEMBRANE CONDUCTANCE REGULATOR; DEPENDENT DIABETES-MELLITUS; EXOCRINE PANCREATIC FUNCTION; MILD PULMONARY-DISEASE; DELTA-F508 MUTATION; VAS-DEFERENS; NONSENSE MUTATIONS; CHLORIDE CHANNELS; COMMON MUTATION; MOLECULAR-BASIS AB Cystic fibrosis is a common, fatal disorder caused by abnormalities in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. CFTR encodes a chloride channel that regulates secretion in many exocrine tissues. The presentation of cystic fibrosis is highly variable as measured by the age of onset of disease, the presence of pancreatic insufficiency, or the progression of lung disease. Over 400 mutations in the CFTR gene have been described in cystic fibrosis patients and considerable effort has focused on the correlation between specific mutations and genotypes and clinical characteristics. Individual tissues display variation in their sensitivity to CFTR mutations. The vas deferens is functionally disrupted in nearly all males, whereas mild and severe pancreatic involvement is determined by the patient's genotype. The severity of pulmonary disease is poorly correlated with genotype, suggesting that there are other important genetic and/or environmental factors that contribute to lung infections and the subsequent disruption of lung function. C1 ROYAL BROMPTON NATL HEART & LUNG HOSP,LONDON,ENGLAND. RP DEAN, M (reprint author), NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,BLDG 560,FREDERICK,MD 21702, USA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 NR 46 TC 74 Z9 77 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD APR PY 1994 VL 93 IS 4 BP 364 EP 368 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA ND553 UT WOS:A1994ND55300001 PM 7513291 ER PT J AU TACHIBANA, M PEREZJURADO, LA NAKAYAMA, A HODGKINSON, CA LI, X SCHNEIDER, M MIKI, T FEX, J FRANCKE, U ARNHEITER, H AF TACHIBANA, M PEREZJURADO, LA NAKAYAMA, A HODGKINSON, CA LI, X SCHNEIDER, M MIKI, T FEX, J FRANCKE, U ARNHEITER, H TI CLONING OF MITF, THE HUMAN HOMOLOG OF THE MOUSE MICROPHTHALMIA GENE AND ASSIGNMENT TO CHROMOSOME 3P14.1 - P12.3 SO HUMAN MOLECULAR GENETICS LA English DT Article ID WAARDENBURG SYNDROME; PROTO-ONCOGENE; MUTATION; PROTOONCOGENE; EXPRESSION; RECEPTOR; VITILIGO; LOCUS AB The mouse microphthalmia (mi) gene encodes a basic - helix - loop - helix - zipper protein whose mutations may lead to loss of pigmentation in the eye, inner ear and skin, and to reduced eye size and early onset deafness. Mice with mutations at mi serve as models for human pigment disturbances in skin and eye that may be combined with sensorineural deafness. We have now obtained cDNA and genomic clones of the human homolog of mouse mi, identified a restriction fragment length polymorphism in the gene, and mapped the gene by somatic cell hybrid and fluorescence in situ hybridization techniques to a region of human chromosome 3 that shows a disrupted syntenic conservation with the region on mouse chromosome 6 to which mi maps. These studies will help to verify if any of the hereditary pigment disturbances in humans are due to mutations in this gene. C1 NINCDS,VIRAL & MOLEC PATHOGENESIS LAB,BETHESDA,MD 20892. NATL INST DEAFNESS & OTHER COMMUN DISORDERS,MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. STANFORD UNIV,MED CTR,DEPT GENET,STANFORD,CA 94305. STANFORD UNIV,MED CTR,DEPT PEDIAT,STANFORD,CA 94305. STANFORD UNIV,MED CTR,HOWARD HUGHES MED INST,STANFORD,CA 94305. RI Perez Jurado, Luis Alberto/M-7706-2015 NR 36 TC 149 Z9 154 U1 2 U2 5 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1994 VL 3 IS 4 BP 553 EP 557 DI 10.1093/hmg/3.4.553 PG 5 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA NH456 UT WOS:A1994NH45600004 PM 8069297 ER PT J AU RICHARDS, FM CROSSEY, PA PHIPPS, ME FOSTER, K LATIF, F EVANS, G SAMPSON, J LERMAN, MI ZBAR, B AFFARA, NA FERGUSONSMITH, MA MAHER, ER AF RICHARDS, FM CROSSEY, PA PHIPPS, ME FOSTER, K LATIF, F EVANS, G SAMPSON, J LERMAN, MI ZBAR, B AFFARA, NA FERGUSONSMITH, MA MAHER, ER TI DETAILED MAPPING OF GERMLINE DELETIONS OF THE VON HIPPEL-LINDAU DISEASE TUMOR-SUPPRESSOR GENE SO HUMAN MOLECULAR GENETICS LA English DT Article ID SMALL REGION; LOCUS; CHROMOSOME-3; MECHANISMS; FEATURES AB Von Hippel-Lindau disease is a dominantly inherited familial cancer syndrome characterised by the development of retinal angiomatosis, cerebellar and spinal hemangioblastoma, renal cell carcinoma, phaeochromocytoma and pancreatic tumours. A cDNA (g7) which detects frequent genomic rearrangements in VHL disease patients on Southern analysis, and contains the partial coding sequence of the VHL gene has been isolated recently. To characterise the nature of the genomic rearrangements in VHL disease we initially screened 116 patients with VHL disease and identified 22 patients (19%) with abnormal fragments in EcoR1 digested DNA probed with g7. We then established that the coding sequence contained within g7 is represented in 3 exons, and designed exon specific probes to investigate the 22 patients with genomic rearrangements. All 22 patients were demonstrated to have germline deletions, but the deletions were heterogeneous with 7 patients having deletions confined to the 5' exon 1, and 8 with nonoverlapping deletions of exon 3. In 7 unrelated patients, including 2 new mutations, the germline deletions were similar in size and position. There was no relationship between the clinical phenotype and the deletion of individual exons. Although phaeochromocytoma was less frequent in kindreds with germline deletions than those without detectable deletions, the difference was not statistically significant (1/19 versus 16/72 respectively, chi(2) = 1.84 p > 0.1). C1 UNIV CAMBRIDGE,DEPT PATHOL,CAMBRIDGE CB2 1QP,ENGLAND. NCI,FREDERICK CANC RES & DEV CTR,IMMUNOL LAB,FREDERICK,MD 21702. ST MARYS HOSP,DEPT MED GENET,MANCHESTER M13,LANCS,ENGLAND. UNIV WALES HOSP,INST MED GENET,CARDIFF,WALES. RI MAHER, EAMONN/A-9507-2008 OI MAHER, EAMONN/0000-0002-6226-6918 NR 28 TC 71 Z9 71 U1 0 U2 10 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1994 VL 3 IS 4 BP 595 EP 598 DI 10.1093/hmg/3.4.595 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA NH456 UT WOS:A1994NH45600012 PM 8069305 ER PT J AU SCHMIDT, L POZZATTI, R LI, H WEI, MH VOCKE, C LINEHAN, WM TORY, K AF SCHMIDT, L POZZATTI, R LI, H WEI, MH VOCKE, C LINEHAN, WM TORY, K TI A MICROSATELLITE, D8S602, ADJACENT TO THE MSR GENE SO HUMAN MOLECULAR GENETICS LA English DT Article ID HUMAN GENOME; LINKAGE MAP C1 NCI,SURG BRANCH,BETHESDA,MD 20892. RP SCHMIDT, L (reprint author), NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21702, USA. NR 3 TC 2 Z9 2 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD APR PY 1994 VL 3 IS 4 BP 679 EP 679 DI 10.1093/hmg/3.4.679 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA NH456 UT WOS:A1994NH45600036 PM 8069323 ER PT J AU MIYAZAWA, M MORI, S SPANGRUDE, GJ WOLFINBARGER, JB BLOOM, ME AF MIYAZAWA, M MORI, S SPANGRUDE, GJ WOLFINBARGER, JB BLOOM, ME TI PRODUCTION AND CHARACTERIZATION OF NEW MONOCLONAL-ANTIBODIES THAT DISTINGUISH SUBSETS OF MINK LYMPHOID-CELLS SO HYBRIDOMA LA English DT Article ID DISEASE PARVOVIRUS; ALEUTIAN DISEASE; T-CELL; GENETIC-CONTROL; COMPLEX; ANTIGENS; IDENTIFICATION; REPLICATION; ARTHRITIS AB Several hybridoma clones that produce monoclonal antibodies (MAbs) reacting with subpopulations of mink lymphoid cells were established. Two of the MAbs, MTS-4.3 and MTS-9.3, reacted with relatively small populations of surface immunoglobulin (Ig)-negative (Ig(-)) lymphocytes. MTS-4.3(+) and MTS-9.3(+) cells were distributed in the thymic cortex and medulla, paracortical areas of lymph nodes, and periarterial lymphoid sheaths of the spleen, indicating that these MAbs identify T lymphocytes. Another MAb, MTB-5.6, reacted with a large proportion of surface Ig(+) lymph node cells, but not with surface Ig(-) cells. In immunohistochemistry this MAb stained dendritic epithelial cells of thymic cortex, large polygonal cells of thymic medulla, a large proportion of lymphocytes in the mantle zone of lymphoid follicles, dendritic-shaped cells of paracortical area, and some lymphocytes and macrophage-like cells of medullary cords and sinuses of lymph nodes. The expression of the cell-surface antigen reacting with MTB-5.6 on Ig(+) lymph node cells was increased after concanavalin A stimulation. These new reagents may be useful to analyze cellular basis of the abnormal immune responses observed in Aleutian mink disease, a classical model of human autoimmune diseases. C1 NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840. NR 27 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0272-457X J9 HYBRIDOMA JI Hybridoma PD APR PY 1994 VL 13 IS 2 BP 107 EP 114 PG 8 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Immunology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Immunology GA NK048 UT WOS:A1994NK04800003 PM 8050775 ER PT J AU LEONARD, WJ NOGUCHI, M RUSSELL, SM MCBRIDE, OW AF LEONARD, WJ NOGUCHI, M RUSSELL, SM MCBRIDE, OW TI THE MOLECULAR-BASIS OF X-LINKED SEVERE COMBINED IMMUNODEFICIENCY - THE ROLE OF THE INTERLEUKIN-2 RECEPTOR-GAMMA CHAIN AS A COMMON GAMMA-CHAIN, GAMMA(C) SO IMMUNOLOGICAL REVIEWS LA English DT Review ID CELL GROWTH-FACTOR; POLYMORPHIC DNA MARKERS; HUMAN IL-2 RECEPTOR; BETA-CHAIN; FETAL THYMOCYTES; T-CELLS; CHROMOSOME INACTIVATION; IMMATURE THYMOCYTES; SIGNAL TRANSDUCER; ALPHA-CHAIN C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. RP LEONARD, WJ (reprint author), NHLBI,PULM & MOLEC IMMUNOL SECT,BLDG 10,RM 7N244,BETHESDA,MD 20892, USA. RI Russell, Sarah/B-9341-2009 OI Russell, Sarah/0000-0001-5826-9641 NR 124 TC 134 Z9 138 U1 0 U2 16 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0105-2896 J9 IMMUNOL REV JI Immunol. Rev. PD APR PY 1994 VL 138 BP 61 EP 86 DI 10.1111/j.1600-065X.1994.tb00847.x PG 26 WC Immunology SC Immunology GA NK307 UT WOS:A1994NK30700004 PM 8070818 ER PT J AU RITTER, M HUBER, C AUBOCK, J POHLMARKL, H TROPPMAIR, J HEROLD, M GACHTER, A NUSSBAUMER, W BOCK, G NACHBAUR, D WESTHOFF, U EIBL, B SCHWAIGHOFER, H THALER, J GROSSEWILDE, H NIEDERWIESER, D AF RITTER, M HUBER, C AUBOCK, J POHLMARKL, H TROPPMAIR, J HEROLD, M GACHTER, A NUSSBAUMER, W BOCK, G NACHBAUR, D WESTHOFF, U EIBL, B SCHWAIGHOFER, H THALER, J GROSSEWILDE, H NIEDERWIESER, D TI LYTIC SUSCEPTIBILITY OF TARGET-CELLS TO CYTOTOXIC T-CELLS IS DETERMINED BY THEIR CONSTITUTIVE MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I ANTIGEN EXPRESSION AND CYTOKINE-INDUCED ACTIVATION STATUS SO IMMUNOLOGY LA English DT Article ID ADHESION MOLECULE-1 ICAM-1; LINKED-IMMUNOSORBENT-ASSAY; INTERFERON-GAMMA; TRANSPLANTATION ANTIGENS; LYMPHOCYTES-T; BINDING SITE; HLA-DR; LFA-1; KERATINOCYTES; INDUCTION AB Cytotoxic T-cell lines (TCL) were raised in vitro using stimulator cells with a defined major histocompatibility complex (MHC) mismatch and tested in a cytotoxic chromium-release assay against haemopoietic and non-haemopoietic target cells from the original stimulator. Monoclonal antibody (mAb)-blocking experiments and simultaneous determination of MHC class I, class II, lymphocyte function-associated antigen-1 (LFA-1) and intracellular adhesion molecule-1 (ICAM-1) density by quantitative radioimmunometric methods and flow cytometry on target cells demonstrated that lysis was restricted by MHC class I and dependent upon the constitutive MHC class I antigen expression. Measurements showed a high constitutive expression of class I MHC antigens on peripheral blood mononuclear cells (PBMC), but a low one on keratinocytes (K). Also, PBMC were more susceptible to lysis by TCL than K. Interferon-gamma (IFN-gamma) treatment of K resulted in increased MHC class I antigen expression and enhanced lytic susceptibility to TCL. IFN-alpha and tumour necrosis factor-alpha (TNF-alpha) treatment, which did not modulate MHC class I antigen expression on K, did not influence the amount of K lysis either. None of the cytokines tested in this analysis, however, increased the expression of MHC class I, class II, ICAM-1 and LFA-1 on PBMC. Only IFN-gamma pretreatment showed a minimal, statistically significant increase in MHC class I antigen expression. In spite of the minimal effect of IFN-gamma and no effect of IFN-alpha on class I MHC expression, pretreatment of target cells with both cytokines considerably increased their lytic susceptibility. The mechanism of cytokine-induced enhanced lytic susceptibility to TCL was not explained by increased MHC class I, LFA-1 or ICAM-1 expression, since no correlation was found between surface expression of these molecules and lytic susceptibility to TCL. These data demonstrate that: (1) the constitutive density of MHC class I antigens determines the extent of TCL lysis; (2) IFN-gamma, and not IFN-alpha or TNF-alpha, controls the amount of K target cell lysis by increasing their MHC class I antigen expression; and (3) IFN-gamma and IFN-alpha control the amount of PBMC target cell lysis by a mechanism independent of MHC class I, ICAM-1 or LFA-1 expression. C1 UNIV INNSBRUCK, DEPT INTERNAL MED, DIV CLIN IMMUNOBIOL, A-6020 INNSBRUCK, AUSTRIA. UNIV INNSBRUCK, DEPT DERMATOL, A-6020 INNSBRUCK, AUSTRIA. UNIV INNSBRUCK, INST BLOOD TRANSFUS, A-6020 INNSBRUCK, AUSTRIA. UNIV INNSBRUCK, DEPT GEN & EXPTL PATHOL, A-6020 INNSBRUCK, AUSTRIA. UNIV MAINZ, DEPT HEMATOL, W-6500 MAINZ, GERMANY. UNIV ESSEN GESAMTHSCH HOSP, DEPT IMMUNOL, ESSEN, GERMANY. NCI, VIRAL PATHOL SECT, FREDERICK, MD 21701 USA. NR 44 TC 11 Z9 11 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD APR PY 1994 VL 81 IS 4 BP 569 EP 577 PG 9 WC Immunology SC Immunology GA ND746 UT WOS:A1994ND74600013 PM 7913694 ER PT J AU DESANCTIS, JB VARESIO, L RADZIOCH, D AF DESANCTIS, JB VARESIO, L RADZIOCH, D TI PROSTAGLANDINS INHIBIT LIPOPROTEIN-LIPASE GENE-EXPRESSION IN MACROPHAGES SO IMMUNOLOGY LA English DT Article ID TUMOR NECROSIS FACTOR; MOUSE PERITONEAL-MACROPHAGES; CYCLIC-NUCLEOTIDES; INTERFERON-GAMMA; HUMAN-MONOCYTES; CELL-LINES; INTERLEUKIN-1; SUPPRESSES; SEQUENCE; CULTURE AB In the present investigation of the effects of prostaglandin E(2) (PGE(2)) on lipoprotein lipase (LPL) gene expression in macrophages, we observed that treatment of macrophages with PGE(2) increased the levels of adenosine 3',5'-cyclic monophosphate (cAMP), while the addition of exogenous 5-bromo-cAMP to macrophage cultures resulted in down-regulation of LPL expression. Using indomethacin (INDO), an inhibitor of cyclo-oxygenase and prostaglandins production, we determined that PGE(2) acts as a feedback inhibitor of LPL expression. We found that inhibited secretion of LPL protein in lipopolysaccharide (LPS)-treated macrophages could be restored to control levels by the addition of INDO to the medium. In contrast, INDO did not reverse the inhibition of LPL mRNA induced by LPS. Overall, our results have demonstrated that PGE(2) is a potent inhibitor of LPL gene expression and indicated that its action may play an important physiological role in the regulation of LPL gene expression during bacterial infections. C1 MCGILL UNIV,MONTREAL GEN HOSP,MCGILL CTR STUDY HOST RESISTANCE,MONTREAL H3G 1A4,PQ,CANADA. CENT UNIV VENEZUELA,INST IMMUNOL,CARACAS,VENEZUELA. NCI,FREDERICK CANC RES FACIL,FREDERICK,MD. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 30 TC 17 Z9 17 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD APR PY 1994 VL 81 IS 4 BP 605 EP 610 PG 6 WC Immunology SC Immunology GA ND746 UT WOS:A1994ND74600018 PM 8039811 ER EF