FN Thomson Reuters Web of Science™ VR 1.0 PT J AU GUZMAN, K HART, DW HOOK, GER AF GUZMAN, K HART, DW HOOK, GER TI THE EFFECT OF SERUM-FREE MEDIUM ON SURFACTANT PROTEIN GENE-EXPRESSION IN PRIMARY TYPE-II CELL-CULTURES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A205 EP A205 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501187 ER PT J AU HAUN, RS TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M AF HAUN, RS TSAI, SC ADAMIK, R MOSS, J VAUGHAN, M TI MYRISTOYLATION OF AN ADP-RIBOSYLATION FACTOR, A SIMILAR-TO-20-KDA GUANINE NUCLEOTIDE-BINDING PROTEIN, IS ESSENTIAL FOR ITS BINDING TO GOLGI SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A220 EP A220 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501278 ER PT J AU HUMPHREY, IS PETERS, PJ YUAN, LC BONIFACINO, JS AF HUMPHREY, IS PETERS, PJ YUAN, LC BONIFACINO, JS TI A TYROSINE-CONTAINING SEQUENCE WITHIN THE CYTOPLASMIC DOMAIN OF TGN38 CONFERS LOCALIZATION TO THE TRANS-GOLGI NETWORK SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A54 EP A54 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500309 ER PT J AU JAEGER, M DODANE, V KACHAR, B AF JAEGER, M DODANE, V KACHAR, B TI A SOLUBLE, THERMOLABILE FACTOR SECRETED INTO THE APICAL MEDIUM OF EPITHELIAL-CELLS MONOLAYERS PROMOTES INCREASE OF TRANSEPITHELIAL ELECTRICAL-RESISTANCE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDCD,CELLULAR BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A218 EP A218 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501266 ER PT J AU JAFFE, LA TERASAKI, M AF JAFFE, LA TERASAKI, M TI CONTINUITY OF THE ENDOPLASMIC-RETICULUM IN SEA-URCHIN EGGS AND ITS STRUCTURAL-CHANGES DURING FERTILIZATION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV CONNECTICUT,CTR HLTH,DEPT PHYSIOL,FARMINGTON,CT 06032. NIH,NEUROBIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A33 EP A33 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500189 ER PT J AU JUNG, G HAMMER, JA AF JUNG, G HAMMER, JA TI MYOSIN-I ISOFORM SUBFAMILIES AND MUTANTS IN DICTYOSTELIUM SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A44 EP A44 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500251 ER PT J AU KALINEC, F URRUTIA, RA JAEGER, RG KACHAR, B AF KALINEC, F URRUTIA, RA JAEGER, RG KACHAR, B TI IDENTIFICATION OF PROTEINS OF THE MIP AND AE FAMILIES IN THE ORGAN OF CORTI USING ANTIBODIES AGAINST SYNTHETIC PEPTIDES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDCD,CELLULAR BIOL LAB,BETHESDA,MD 20892. RI Jaeger, Ruy/G-8230-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A302 EP A302 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501754 ER PT J AU KELLEY, CA TAKAHASHI, M YU, JH ADELSTEIN, RS AF KELLEY, CA TAKAHASHI, M YU, JH ADELSTEIN, RS TI FUNCTIONAL-SIGNIFICANCE OF SMOOTH-MUSCLE MYOSIN HEAVY-CHAIN ISOFORMS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. RI Takahashi, Masayuki/D-8079-2012 NR 3 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A159 EP A159 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500923 ER PT J AU KELLY, D OREILLY, MA RIZZINO, A AF KELLY, D OREILLY, MA RIZZINO, A TI DIFFERENTIAL REGULATION OF THE TRANSFORMING GROWTH-FACTOR TYPE-BETA-2 (TGF-BETA-2) GENE PROMOTER IN EMBRYONIC-CELL LINES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV NEBRASKA,MED CTR,EPPLEY INST RES CANC,OMAHA,NE 68198. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A330 EP A330 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501916 ER PT J AU KOJI, T CHEDID, M RUBIN, JS SLAYDEN, OD KAYNARD, AH AARONSON, SA BRENNER, RM AF KOJI, T CHEDID, M RUBIN, JS SLAYDEN, OD KAYNARD, AH AARONSON, SA BRENNER, RM TI KERATINOCYTE GROWTH-FACTOR (KGF) MESSENGER-RNA EXPRESSION IN THE RHESUS-MONKEY UTERUS ASSESSED BY NORTHERN BLOT ANALYSIS AND INSITU HYBRIDIZATION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 OREGON REG PRIMATE RES CTR,DIV REPROD SCI,BEAVERTON,OR 97006. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A144 EP A144 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500836 ER PT J AU KULESZALIPKA, D BRZESKA, H BAINES, I KORN, ED AF KULESZALIPKA, D BRZESKA, H BAINES, I KORN, ED TI INTERACTIONS OF ACANTHAMOEBA MYOSIN-I HEAVY-CHAIN KINASE, MYOSIN-I AND MEMBRANES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A43 EP A43 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500244 ER PT J AU LAPHAM, C YEWDELL, J BENNINK, J AF LAPHAM, C YEWDELL, J BENNINK, J TI THE USE OF BREFELDIN-A TO LOCALIZE THE INTRACELLULAR ASSOCIATION OF CLASS-I MHC WITH NATURALLY PROCESSED PEPTIDE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,VIS,LVD,BETHESDA,MD 20892. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A112 EP A112 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500650 ER PT J AU LIPPINCOTTSCHWARTZ, J BLOOM, G AF LIPPINCOTTSCHWARTZ, J BLOOM, G TI MICROTUBULES AND ER GOLGI TRAFFICKING - LOCALIZATION OF MEMBRANE-BOUND KINESIN ON ER TO GOLGI TRANSPORT INTERMEDIATES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,BETHESDA,MD 20892. UNIV TEXAS,SW MED CTR,DEPT CELL BIOL,DALLAS,TX 75235. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A220 EP A220 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501276 ER PT J AU LIU, YH TENG, CT AF LIU, YH TENG, CT TI COUP-TF MODULATES ESTROGEN-STIMULATED RESPONSE OF MOUSE LACTOFERRIN GENE BY DIRECT COMPETITION FOR THE OVERLAPPING BINDING-SITE OF THE ER SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIEHS,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A81 EP A81 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500469 ER PT J AU LYSZ, T LIN, C ZELENKA, P AF LYSZ, T LIN, C ZELENKA, P TI 12-HETE REGULATES DNA-SYNTHESIS AND C-MYC EXPRESSION IN NEONATAL RAT LENS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT ANAT,NEWARK,NJ 07103. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT CELL BIOL,NEWARK,NJ 07103. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT INJURY SCI,NEWARK,NJ 07103. NEI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A277 EP A277 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501610 ER PT J AU MORCOS, P CLEMENS, K CANNON, J AF MORCOS, P CLEMENS, K CANNON, J TI ROLE OF TYPE-1 PROTEIN PHOSPHATASE IN THE SACCHAROMYCES-CEREVISIAE CELL-DIVISION CYCLE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. UNIV MISSOURI,DEPT MOLEC MICROBIOL & IMMUNOL,COLUMBIA,MO 65201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A152 EP A152 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500883 ER PT J AU MOUSSAVI, RS MCPHIE, P BEKELMAN, JE LI, D CHANTLER, PD OZAWA, K BEAVEN, MA ADELSTEIN, RS AF MOUSSAVI, RS MCPHIE, P BEKELMAN, JE LI, D CHANTLER, PD OZAWA, K BEAVEN, MA ADELSTEIN, RS TI PHOSPHORYLATION OF BOVINE BRAIN MYOSIN HEAVY CHAIN-II BY PROTEIN-KINASE-C SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. NIADDKD,BETHESDA,MD 20892. MED COLL PENN,DEPT ANAT & NEUROBIOL,PHILADELPHIA,PA 19129. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A157 EP A157 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500911 ER PT J AU MUCCI, DM FORRISTAL, JJ MORRIS, RE THOMPSON, M FITZGERALD, D STRICKLAND, DK SAELINGER, CB AF MUCCI, DM FORRISTAL, JJ MORRIS, RE THOMPSON, M FITZGERALD, D STRICKLAND, DK SAELINGER, CB TI THE ALPHA-2MACROGLOBULIN RECEPTOR LDL RECEPTOR RELATED PROTEIN BINDS AND INTERNALIZES PSEUDOMONAS EXOTOXIN-A SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,AMER RED CROSS,CINCINNATI,OH. UNIV CINCINNATI,CINCINNATI,OH 45267. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A298 EP A298 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501733 ER PT J AU NEGRE, E VOGEL, T WERBER, MM WALSH, TJ ROBERTS, DD AF NEGRE, E VOGEL, T WERBER, MM WALSH, TJ ROBERTS, DD TI BINDING OF FIBRONECTIN TO CANDIDA-ALBICANS IS MEDIATED BY THE GELATIN-BINDING, CELL-BINDING AND FIBRIN I DOMAINS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,BETHESDA,MD 20892. BIOTECHNOL GEN LTD,REHOVOT,ISRAEL. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 NR 0 TC 1 Z9 1 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A69 EP A69 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500400 ER PT J AU OBRIEN, DA WELCH, JE GOULDING, EH TAYLOR, AA BABA, T HECHT, NB EDDY, EM AF OBRIEN, DA WELCH, JE GOULDING, EH TAYLOR, AA BABA, T HECHT, NB EDDY, EM TI EXPRESSION OF BOAR PROACROSIN IN TRANSGENIC MICE DISRUPTS SPERMATOGENESIS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 TUFTS UNIV,DEPT BIOL,MEDFORD,MA 02155. UNIV TSUKUBA,INST APPL BIOCHEM,TSUKUBA,JAPAN. UNIV N CAROLINA,REPROD BIOL LABS,CHAPEL HILL,NC 27514. NIEHS,GAMETE BIOL SECT,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A100 EP A100 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500580 ER PT J AU OSTROWSKI, LE GRAY, TE RANDELL, SH NETTESHEIM, P AF OSTROWSKI, LE GRAY, TE RANDELL, SH NETTESHEIM, P TI EXPRESSION OF A NOVEL TGF-BETA-1 TRANSCRIPT IN RAT TRACHEAL EPITHELIAL-CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIEHS,PULM PATHOBIOL LAB,RES TRIANGLE PK,NC 27709. NR 1 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A28 EP A28 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500157 ER PT J AU PAOLINI, R NUMEROF, R KINET, JP AF PAOLINI, R NUMEROF, R KINET, JP TI PHOSPHORYLATION/DEPHOSPHORYLATION OF HIGH-AFFINITY IGE RECEPTORS - A MECHANISM FOR COUPLING UNCOUPLING A LARGE SIGNALING COMPLEX SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A149 EP A149 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500863 ER PT J AU PIMENTA, PFP HOU, WY DASILVA, PP KEREN, Z DIAMOND, LS MIRELMAN, D AF PIMENTA, PFP HOU, WY DASILVA, PP KEREN, Z DIAMOND, LS MIRELMAN, D TI DISTINCTIVE ULTRASTRUCTURAL ASPECTS OF THE CELL-SURFACE CHARACTERIZE NONPATHOGENIC AND PATHOGENIC ENTAMOEBA-HISTOLYTICA STRAINS - FREEZE-FRACTURE AND FRACTURE-FLIP SURVEY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NCI,STRUCT BIOL SECT,BETHESDA,MD 20892. WEIZMANN INST SCI,IL-76100 REHOVOT,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A63 EP A63 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500363 ER PT J AU PRASAD, K BAROUCH, W GREENE, L EISENBERG, E AF PRASAD, K BAROUCH, W GREENE, L EISENBERG, E TI REQUIREMENT OF A FACTOR FOR UNCOATING OF CLATHRIN BASKETS BY UNCOATING ATPASE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A112 EP A112 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500645 ER PT J AU PURI, A KRUMBIEGEL, M DIMITROV, D PREVEC, L BLUMENTHAL, R AF PURI, A KRUMBIEGEL, M DIMITROV, D PREVEC, L BLUMENTHAL, R TI FLUORESCENCE DEQUENCHING OF OCTADECYLRHODAMINE LABELED PLASMA-MEMBRANE VESICLES FUSING WITH CELLS EXPRESSING VESICULAR STOMATITIS-VIRUS GLYCOPROTEIN - A NEW APPROACH TO MEASURE FUSION ACTIVITY OF CLONED VIRAL ENVELOPE PROTEINS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,MEMBRANE STRUCT & FUNCT SECT,BETHESDA,MD 20892. MCMASTER UNIV,HAMILTON L8S 4L8,ONTARIO,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A212 EP A212 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501227 ER PT J AU RAU, D GANGULY, C KORN, ED AF RAU, D GANGULY, C KORN, ED TI STRUCTURAL DIFFERENCE BETWEEN FILAMENTS OF ACANTHAMOEBA PHOSPHORYLATED AND DEPHOSPHORYLATED MYOSIN-II REVEALED BY ELECTRIC BIREFRINGENCE STUDIES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,CELL BIOL LAB,BETHESDA,MD 20892. NHLBI,BIOCHEM & METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A43 EP A43 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500245 ER PT J AU REDOWICZ, MJ ZOLKIEWSKI, M GANGULY, C KORN, ED GINSBURG, A AF REDOWICZ, MJ ZOLKIEWSKI, M GANGULY, C KORN, ED GINSBURG, A TI THERMALLY INDUCED UNFOLDING OF MYOSIN-II FROM ACANTHAMOEBA-CASTELLANII SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NHLBI,BETHESDA,MD 20892. RI Redowicz, Maria Jolanta/R-4083-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A43 EP A43 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500247 ER PT J AU RICHARDSON, LL KLEINMAN, HK DYM, M AF RICHARDSON, LL KLEINMAN, HK DYM, M TI BASEMENT-MEMBRANE GENE-EXPRESSION IN RAT SERTOLI AND PERITUBULAR MYOID CELLS-INVITRO SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 GEORGETOWN UNIV,MED CTR,DEPT ANAT & CELL BIOL,WASHINGTON,DC 20007. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A227 EP A227 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501316 ER PT J AU RISCO, C ROMERO, C BOSCH, MA DASILVA, PP AF RISCO, C ROMERO, C BOSCH, MA DASILVA, PP TI ULTRASTRUCTURAL-STUDY OF ISOLATED RAT TYPE-II PNEUMOCYTES BY FREEZE-FRACTURE AND FRACTURE-FLIP SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,STRUCT BIOL SECT,MATH BIOL LAB,FREDERICK,MD 21702. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A62 EP A62 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500358 ER PT J AU RIVOLTA, MN FEX, J SLEPECKY, N WILCOX, E AF RIVOLTA, MN FEX, J SLEPECKY, N WILCOX, E TI A NOVEL ZINC FINGER ENCODING GENE IS EXPRESSED IN THE ORGAN OF CORTI SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDCD,MOLEC BIOL LAB,BETHESDA,MD 20892. SYRACUSE UNIV,INST SENSORY RES,SYRACUSE,NY 13244. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A202 EP A202 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501172 ER PT J AU ROCHLIN, MW PHILLIPS, CL YAMAKAWA, K ADELSTEIN, RS BRIDGMAN, PC AF ROCHLIN, MW PHILLIPS, CL YAMAKAWA, K ADELSTEIN, RS BRIDGMAN, PC TI THE DISTRIBUTION OF MYOSIN-II A-AND-B ISOFORMS IN GROWTH CONES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 WASHINGTON UNIV,DEPT ANAT & NEUROBIOL,ST LOUIS,MO 63110. NIH,MOLEC CARDIOL LAB,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A160 EP A160 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500930 ER PT J AU RONDINONE, CM GREENBERG, AS LONDOS, C AF RONDINONE, CM GREENBERG, AS LONDOS, C TI COMPARISON OF IL-6 AND TNF STIMULATED PROTEIN-PHOSPHORYLATION IN 3T3-L1 ADIPOCYTES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDDK,LCDB,MEMBRANE REGULAT SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A150 EP A150 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500871 ER PT J AU RULONG, S TSARFATY, I WRESCHNER, DH KEYDAR, I DASILVA, PP AF RULONG, S TSARFATY, I WRESCHNER, DH KEYDAR, I DASILVA, PP TI SUBCELLULAR-LOCALIZATION OF HUMAN BREAST CANCER-ASSOCIATED ANTIGEN-H23AG AS REVEALED BY THIN-SECTION, LABEL-FRACTURE AND FRACTURE-FLIP IMMUNOELECTRON MICROSCOPY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,MEMBRANE BIOL SECT,FREDERICK,MD 21702. NCI,FREDERICK CANC RES FACIL,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. DEPT CELL RES & IMMUNOL,TEL AVIV,ISRAEL. RI Shen, Rulong/E-4079-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A292 EP A292 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501695 ER PT J AU SHAILUBHAI, K SHARP, C NEVILLE, DM AF SHAILUBHAI, K SHARP, C NEVILLE, DM TI APICAL AND BASOLATERAL DISTRIBUTION OF HB-EGF-LIKE GROWTH-FACTOR DT-RECEPTOR IN POLARIZED MDCK, BEWO AND CACO CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIMH,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A113 EP A113 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500656 ER PT J AU SHI, YB BROWN, DD AF SHI, YB BROWN, DD TI THE REGULATION OF GASTROINTESTINAL METAMORPHOSIS IN XENOPUS-LAEVIS BY THYROID-HORMONE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 CARNEGIE INST WASHINGTON,BALTIMORE,MD 21210. NICHHD,MOLEC EMBRYOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A107 EP A107 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500615 ER PT J AU SMITH, GH JHAPPAN, C GALLAHAN, D MERLINO, G CALLAHAN, R AF SMITH, GH JHAPPAN, C GALLAHAN, D MERLINO, G CALLAHAN, R TI CONSTITUTIVE INT-3 GENE-EXPRESSION UNCOUPLES EPITHELIAL DIFFERENTIATIVE PROCESSES IN DEVELOPING MOUSE MAMMARY-GLANDS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NCI,DCBDC,TUMOR IMMUNOL & BIOL & MOLEC BIOL LABS,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A22 EP A22 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500123 ER PT J AU SWAIM, WD OLIVER, C SIRAGANIAN, RP AF SWAIM, WD OLIVER, C SIRAGANIAN, RP TI THE ANTIGANGLIOSIDE MAB AA4 INDUCES PROTEIN TYROSINE PHOSPHORYLATION IN RBL-2H3 CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDR,LICIS,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A150 EP A150 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500870 ER PT J AU TORRE, E URRUTIA, R KACHAR, B MCNIVEN, MA AF TORRE, E URRUTIA, R KACHAR, B MCNIVEN, MA TI EFFECT OF DYNAMIN ANTISENSE OLIGONUCLEOTIDES ON HIPPOCAMPAL-NEURONS DEVELOPING IN CULTURE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV VIRGINIA,HLTH SCI CTR,DEPT NEUROSCI,CHARLOTTESVILLE,VA 22908. NIDCD,CELLULAR BIOL LAB,BETHESDA,MD 20892. MAYO CLIN & MAYO FDN,CTR BASIC RES DIGEST DIS,ROCHESTER,MN 55905. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A283 EP A283 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501640 ER PT J AU URRUTIA, R MURPHY, DB KACHAR, B MCNIVEN, MA AF URRUTIA, R MURPHY, DB KACHAR, B MCNIVEN, MA TI KINESIN-MEDIATED MICROTUBULE DYNAMICS INVITRO SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIDCD,DEPT CELL BIOL,MOLEC OTOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. MAYO CLIN & MAYO FDN,CTR BASIC RES DIGEST DIS,ROCHESTER,MN 55905. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A279 EP A279 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501618 ER PT J AU VOGEL, SS CHERNOMORDIK, LV ZIMMERBERG, I AF VOGEL, SS CHERNOMORDIK, LV ZIMMERBERG, I TI ISOLATED SEA-URCHIN CORTICAL GRANULES CAN FUSE WITH LIPOSOMES IN RESPONSE TO A CALCIUM TRIGGER SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. RI Vogel, Steven/A-3585-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A212 EP A212 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501229 ER PT J AU WANG, XM YEW, N VANDEWOUDE, GF BORISY, GG AF WANG, XM YEW, N VANDEWOUDE, GF BORISY, GG TI MICROINJECTION OF C-MOS PROTEIN BLOCKS MITOTIC PROGRESSION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV WISCONSIN,MOLEC BIOL LAB,MADISON,WI 53706. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A25 EP A25 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500138 ER PT J AU WARD, GE MILLER, LH DVORAK, JA AF WARD, GE MILLER, LH DVORAK, JA TI THE ORIGIN OF PARASITOPHOROUS VACUOLE MEMBRANE-LIPIDS IN MALARIA-INFECTED ERYTHROCYTES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,MALARIA RES LAB,BETHESDA,MD 20892. NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A60 EP A60 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500346 ER PT J AU WATSON, G ROBERTS, J PARAKKAL, M KACHAR, B AF WATSON, G ROBERTS, J PARAKKAL, M KACHAR, B TI CHEMORECEPTOR-MEDIATED MOBILIZATION OF ACTIN INTO AND OUT OF ANEMONE HAIR BUNDLES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV SW LOUISIANA,DEPT BIOL,LAFAYETTE,LA 70504. NIDCD,BETHESDA,MD 20892. NR 0 TC 6 Z9 6 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A39 EP A39 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500223 ER PT J AU WIEST, DL SAMELSON, LE SINGER, A AF WIEST, DL SAMELSON, LE SINGER, A TI THE REGULATION OF T-CELL RECEPTOR EXPRESSION BY CD4 IN CD4+CD8+ THYMOCYTES REQUIRES TYROSINE KINASE-ACTIVITY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A148 EP A148 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500858 ER PT J AU WILDMAN, DE TAMIR, H LEBERER, E NORTHUP, JK DENNIS, M AF WILDMAN, DE TAMIR, H LEBERER, E NORTHUP, JK DENNIS, M TI PRENYL MODIFICATION OF G-PROTEIN (2) SUBUNIT NOT REQUIRED FOR INTERACTIONS WITH GT OR RHODOPSIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06540. NIMH,LCB,BETHESDA,MD 20892. BIOTECHNOL RES INST,MONTREAL,QUEBEC,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A243 EP A243 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25501409 ER PT J AU WILSON, BS HERMOUET, S DEMAZANCOURT, P SPIEGEL, A FARQUHAR, MG AF WILSON, BS HERMOUET, S DEMAZANCOURT, P SPIEGEL, A FARQUHAR, MG TI LOCALIZATION OF GI3 ALPHA-SUBUNIT IS DEPENDENT ON CELL TYPE AND LEVEL OF EXPRESSION - IMPLICATIONS FOR GOLGI FUNCTION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO,DIV CELLULAR & MOLEC MED,LA JOLLA,CA 92093. NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A34 EP A34 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500196 ER PT J AU YABKOWITZ, R DIXIT, VM ROBERTS, DD SHIMIZU, Y AF YABKOWITZ, R DIXIT, VM ROBERTS, DD SHIMIZU, Y TI INVOLVEMENT OF BETA-1-INTEGRINS IN CD4+ T-CELL ADHESION TO THROMBOSPONDIN SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH MED,DEPT PATHOL,ANN ARBOR,MI 48104. UNIV MICHIGAN,SCH MED,DEPT MICROBIOL & IMMUNOL,ANN ARBOR,MI 48104. NCI,PATHOL LAB,BETHESDA,MD 20892. RI Roberts, David/A-9699-2008; dixit, vishva/A-4496-2012 OI Roberts, David/0000-0002-2481-2981; dixit, vishva/0000-0001-6983-0326 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A68 EP A68 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500391 ER PT J AU YANG, N TENG, CT AF YANG, N TENG, CT TI IDENTIFICATION OF REGULATORY SEQUENCES AND PROTEIN-BINDING SITES OF THE HUMAN LACTOFERRIN GENE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 NIEHS,REPROD & DEV TOXICOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOLOGY PI BETHESDA PA PUBL OFFICE, 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD SEP PY 1992 VL 3 SU S BP A81 EP A81 PG 1 WC Cell Biology SC Cell Biology GA JR255 UT WOS:A1992JR25500471 ER PT J AU JOY, JE JOHNSON, GS LAZAR, T RALPH, MR HOCHSTRASSER, AC MENAKER, M MERRIL, CR AF JOY, JE JOHNSON, GS LAZAR, T RALPH, MR HOCHSTRASSER, AC MENAKER, M MERRIL, CR TI PROTEIN DIFFERENCES IN TAU-MUTANT HAMSTERS - CANDIDATE CLOCK PROTEINS SO MOLECULAR BRAIN RESEARCH LA English DT Article DE TAU-MUTANT HAMSTER; CIRCADIAN PACEMAKER; PROTEIN; 2-DIMENSIONAL ELECTROPHORESIS ID PERIOD GENE-PRODUCT; SUPRACHIASMATIC NUCLEUS; CIRCADIAN-RHYTHMS; DROSOPHILA CLOCK; BIOLOGICAL RHYTHMS; MESSENGER-RNA; RAT-BRAIN; EXPRESSION; SYSTEM; ELECTROPHORESIS AB In the tau mutant hamster, the period of the circadian rhythm is shortened from about 24 h to about 22 h in heterozygotes and to about 20 h in homozygotes. Understanding the biochemical basis of the period changes in the tau mutant may elucidate the regulation of the vertebrate pacemaker. Using two-dimensional gel electrophoresis, we have found two sets of proteins that differ between the different genotypes. P33tau (about 33 kDa; pI 6.5) was found in all gels from wild type and heterozygous animals, but was absent in gels from all except one of the homozygous mutant animals. P32tau (about 32 kDa; pI 4.8) was a chain of spots, which showed a striking difference in pattern between gels from wild type animals and from mutant animals. P33tau was greatly enriched in soluble cellular fractions. whereas P32tau was found only in insoluble fractions, These differences between P33tau and P32tau were apparent in gels from both SCN and cortical tissue, suggesting that both proteins are distributed throughout the brain. These proteins should be useful as new tools to explore the biochemistry of circadian pacemakers. C1 UNIV VIRGINIA,DEPT BIOL,CHARLOTTESVILLE,VA 22901. RP JOY, JE (reprint author), ST ELIZABETH HOSP,CTR NEUROSCI,NIMH,BIOCHEM GENET LAB,WASHINGTON,DC 20032, USA. NR 42 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD SEP PY 1992 VL 15 IS 1-2 BP 8 EP 14 DI 10.1016/0169-328X(92)90144-Z PG 7 WC Neurosciences SC Neurosciences & Neurology GA JN171 UT WOS:A1992JN17100002 ER PT J AU PENNYPACKER, KR ZHANG, WQ YE, H HONG, JS AF PENNYPACKER, KR ZHANG, WQ YE, H HONG, JS TI APOMORPHINE INDUCTION OF AP-1 DNA-BINDING IN THE RAT STRIATUM AFTER DOPAMINE DEPLETION SO MOLECULAR BRAIN RESEARCH LA English DT Note DE TRANSCRIPTION FACTOR; STRIATUM; 6-HYDROXYDOPAMINE; JUN PROTEIN, FOS-RELATED ANTIGEN; C-FOS PROTEIN; AP-1 DNA BINDING ID C-FOS; SUBSTANTIA-NIGRA; STRIATONIGRAL PATHWAY; EXPRESSION; GENE; DYNORPHIN; SYSTEM; ENKEPHALIN; METABOLISM; NEURONS AB The expression of AP-1 transcription factors was assessed in the dopamine-depleted rat striatum over a 1 week period of repeated apomorphine injections. A single injection of apomorphine increased the expression of a 35 kDa Fos-related antigen and Jun proteins and their expression continued to increase until day 3 of repeated apomorphine treatment in dopamine-depleted striata. Apomorphine induces AP-1 transcription factors which may be involved in modulating gene expression in the striatum. RP PENNYPACKER, KR (reprint author), NIEHS,NEUROPHARMACOL SECT,MOLEC & INTEGRAT NEUROSCI LAB,MD 14-06,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Pennypacker, Keith/I-5092-2012 NR 25 TC 37 Z9 37 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD SEP PY 1992 VL 15 IS 1-2 BP 151 EP 155 DI 10.1016/0169-328X(92)90163-6 PG 5 WC Neurosciences SC Neurosciences & Neurology GA JN171 UT WOS:A1992JN17100021 ER PT J AU VANDENBERGH, DJ PERSICO, AM UHL, GR AF VANDENBERGH, DJ PERSICO, AM UHL, GR TI A HUMAN DOPAMINE TRANSPORTER CDNA PREDICTS REDUCED GLYCOSYLATION, DISPLAYS A NOVEL REPETITIVE ELEMENT AND PROVIDES RACIALLY-DIMORPHIC TAQI RFLPS SO MOLECULAR BRAIN RESEARCH LA English DT Note DE COCAINE; DRUG RECEPTOR; PARKINSONISM; TANDEM REPEAT; TOURETTES SYNDROME ID PARKINSONS-DISEASE; CLONING; COCAINE; EXPRESSION; INHERITANCE; ALCOHOLISM; RECEPTORS AB We describe a cDNA for the human dopamine transporter, which has been implicated in several human disorders linked to dopaminergic function. The cDNA predicts reduced glycosylation of the protein with respect to the rat transporter, as well as a novel repetitive element in the 3' untranslated region of the cDNA. A TaqI RFLP is also reported that shows a race-specific difference in allelic frequencies. C1 NIDA,ADDICT RES CTR,MOLEC NEUROBIOL LAB,POB 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21224. NR 23 TC 159 Z9 161 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD SEP PY 1992 VL 15 IS 1-2 BP 161 EP 166 DI 10.1016/0169-328X(92)90165-8 PG 6 WC Neurosciences SC Neurosciences & Neurology GA JN171 UT WOS:A1992JN17100023 ER PT J AU BERRODIN, TJ MARKS, MS OZATO, K LINNEY, E LAZAR, MA AF BERRODIN, TJ MARKS, MS OZATO, K LINNEY, E LAZAR, MA TI HETERODIMERIZATION AMONG THYROID-HORMONE RECEPTOR, RETINOIC ACID RECEPTOR, RETINOID-X RECEPTOR, CHICKEN OVALBUMIN UPSTREAM PROMOTER TRANSCRIPTION FACTOR, AND AN ENDOGENOUS LIVER PROTEIN SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID VITAMIN-D RECEPTOR; RESPONSE ELEMENT; DNA-BINDING; NUCLEAR-PROTEIN; GENE-TRANSCRIPTION; LEUCINE-ZIPPER; RAR-ALPHA; EXPRESSION; IDENTIFICATION; SUPERFAMILY AB Thyroid hormone receptor (TR) binds to DNA as a monomer, homodimer, and heterodimer with nuclear proteins. We have confirmed that the TR can heterodimerize with retinoid X receptors (RXRs)-alpha and -beta, and have found that another member of the nuclear receptor superfamily, chicken ovalbumin upstream promoter transcription factor (COUP-TF), also formed heterodimers with the TR in the context of binding to a palindromic thyroid hormone-responsive element (TREp). The interaction between COUP-TF and the TR was confirmed using specific antibodies which supershifted the COUP-TF/TR DNA complexes. The complex between the TR and the major TR heterodimerization partner in liver was unaffected by antibodies to COUP-TF and RXRbeta, but was supershifted by an anti-RXRalpha antibody, indicating that the liver protein is highly related to RXRalpha. Indeed, the TR/RXR and TR/liver protein heterodimers contact the same guanidine residues in TREp. The retinoic acid receptor (RAR) also heterodimerized with COUP-TF as well as with RXRalpha, RXRbeta, and the TR heterodimerization partner in liver. In contrast to its ability to heterodimerize with the TR and RAR, we did not detect heterodimers between COUP-TF and either RXRalpha, RXRbeta, or the liver nuclear protein in the context of binding to the TREp. These results show that the major TR heterodimerization partner in liver is highly related to RXRalpha, but that other nuclear receptors such as COUP-TF can heterodimerize with the TR and RAR, suggesting that selective protein-protein interactions may be involved in the tissue and target gene specificities of hormone action. C1 UNIV PENN, SCH MED, DEPT MED, 611 CRB, 422 CURIE BLVD, PHILADELPHIA, PA 19104 USA. UNIV PENN, SCH MED, DEPT HUMAN GENET, PHILADELPHIA, PA 19104 USA. NICHHD, MOLEC GROWTH REGULAT LAB, BETHESDA, MD 20892 USA. DUKE UNIV, MED CTR, DEPT MICROBIOL & IMMUNOL, DURHAM, NC 27710 USA. OI Marks, Michael/0000-0001-7435-7262 FU NIDDK NIH HHS [1RO1-DK-43806-01] NR 61 TC 128 Z9 129 U1 0 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD SEP PY 1992 VL 6 IS 9 BP 1468 EP 1478 DI 10.1210/me.6.9.1468 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JR184 UT WOS:A1992JR18400014 PM 1331778 ER PT J AU ANDERSON, RW BENNINK, JR YEWDELL, JW MALOY, WL COLIGAN, JE AF ANDERSON, RW BENNINK, JR YEWDELL, JW MALOY, WL COLIGAN, JE TI INFLUENZA BASIC POLYMERASE-2 PEPTIDES ARE RECOGNIZED BY INFLUENZA NUCLEOPROTEIN-SPECIFIC CYTOTOXIC LYMPHOCYTES-T SO MOLECULAR IMMUNOLOGY LA English DT Article ID CLASS-I; SYNTHETIC PEPTIDES; ANTIGEN PRESENTATION; CELLS RECOGNIZE; GENE-PRODUCTS; VIRUS; EPITOPES; PROTEIN; H-2KB; HEMAGGLUTININ AB Cytotoxic T lymphocytes (CTL) play an important role in limiting viral infections and in eradicating virus from host tissues. Recent progress in understanding the processing and presentation of viral antigens to CTL indicates that the CTL antigen receptor recognizes peptides derived from viral proteins that are bound to an antigen binding groove present in class I major histocompatibility complex (MHC) molecules. In understanding CTL anti-viral responses and in creating vaccines designed to elicit CTL responses, it is critical to identify the portions of viral proteins that bind class I molecules and are recognized by T cell receptors. Previous findings have indicated that a significant portion of the CTL response of H-2d Mice to influenza virus is specific for one of the viral polymerases (PB2). To identify the region of PB2 naturally processed and presented by influenza virus-infected mouse cells to CTL, 31 PB2 peptides of 9-16 residues in length were chosen and chemically synthesized. Two peptides, PB2, residues 146-159 and 187-195, were found to sensitize histocompatible target cells for recognition by influenza virus-specific CTL. When CTL were generated to individual viral proteins using influenza-vaccinia recombinant viruses, we found, to our surprise, that PB2-specific CTL failed to recognize cells sensitized with PB2 peptides 146-159 and 187-195. Further analysis showed that these PB2 peptides were, in fact, recognized by nucleoprotein (NP)-specific CTL generated by NP-vac virus priming and influenza A virus stimulation, or NP peptide stimulation in vitro of NP-vac or influenza A-primed CTL. These results demonstrate that while screening peptide libraries one cannot assume that positive peptides necessarily identify the viral protein to which the CTL response is directed. C1 NIAID,BIOL RESOURCES BRANCH,BLDG 4,ROOM 413,BETHESDA,MD 20892. NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RI yewdell, jyewdell@nih.gov/A-1702-2012 NR 41 TC 29 Z9 29 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD SEP PY 1992 VL 29 IS 9 BP 1089 EP 1096 DI 10.1016/0161-5890(92)90041-U PG 8 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA JH971 UT WOS:A1992JH97100008 PM 1495499 ER PT J AU CARRENO, BM KOENIG, S COLIGAN, JE BIDDISON, WE AF CARRENO, BM KOENIG, S COLIGAN, JE BIDDISON, WE TI THE PEPTIDE BINDING-SPECIFICITY OF HLA CLASS-I MOLECULES IS LARGELY ALLELE-SPECIFIC AND NONOVERLAPPING SO MOLECULAR IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; TOXIC LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; CELL RECOGNITION; SELF-PEPTIDES; SIDE-CHAINS; ANTIGENS; HLA-B27; PROTEIN; VIRUS AB To understand better the specificity of peptide binding by MHC class I molecules, we have evaluated the capacity of a panel of unrelated peptides to compete for the presentation of viral peptides presented by HLA-A3 and HLA-B27. The HIV-Nef7F peptide (74-82) was presented by HLA-A3 to Nef-specific HLA-A3-restricted CTL lines, and the influenza nucleoprotein peptide NP(380-393) was presented by HLA-B27 to NP(380-393)-specific HLA-B27-restricted CTL lines. In addition, we have extended studies from our group that have evaluated the capacity of a similar panel of peptides to inhibit presentation of an influenza nucleoprotein peptide NP (335-349) by HLA-B37 and a matrix peptide, M1 (57-68), by HLA-A2 to the appropriate peptide-specific CTL lines. Out of 41 peptides tested, only five bound to more than one of the MHC molecules analyzed. Pairwise comparisons of the peptide binding specificities among these four different class I molecules revealed no common competitor peptides in four of the six possible comparisons. Thus, each class I molecule appears to have a functionally distinct peptide binding site, as reflected by the ability to bind largely non-overlapping sets of peptides. C1 NINCDS,MOLEC IMMUNOL SECT,BETHESDA,MD 20892. MEDIMMUNE INC,GAITHERSBURG,MD 20879. NIAID,BIOL RESOURCES BRANCH,BETHESDA,MD 20892. NR 45 TC 21 Z9 21 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD SEP PY 1992 VL 29 IS 9 BP 1131 EP 1140 DI 10.1016/0161-5890(92)90046-Z PG 10 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA JH971 UT WOS:A1992JH97100013 PM 1379681 ER PT J AU WU, TT KABAT, EA AF WU, TT KABAT, EA TI POSSIBLE USE OF SIMILAR FRAMEWORK REGION AMINO-ACID-SEQUENCES BETWEEN HUMAN AND MOUSE IMMUNOGLOBULINS FOR HUMANIZING MOUSE ANTIBODIES SO MOLECULAR IMMUNOLOGY LA English DT Article ID RESHAPING HUMAN-ANTIBODIES; HUMAN MONOCLONAL-ANTIBODY; IMMUNOGENICITY; RESOURCE; THERAPY; PROPHET; DOMAINS; GENES AB We have previously noted that a specific amino acid sequence could form the second framework region of human, mouse and rabbit immunoglobulin light chains, suggesting that this sequence has been preserved for 80 million years. Through divergent evolution, each species has acquired a different set of framework region sequences; however, these sets still share a few similar or identical amino acid sequences. In the present study, we have identified such sequences for all four framework regions between human and mouse immunoglobulin light and heavy chains. They may be useful in humanizing or reshaping mouse or rat antibodies for therapeutic applications in human patients. C1 NORTHWESTERN UNIV,DEPT MOLEC BIOL & CELL BIOL,EVANSTON,IL 60208. NORTHWESTERN UNIV,DEPT BIOMED ENGN,EVANSTON,IL 60208. NORTHWESTERN UNIV,DEPT ENGN SCI & APPL MATH,EVANSTON,IL 60208. COLUMBIA UNIV COLL PHYS & SURG,DEPT MICROBIOL,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT GENET & DEV,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT NEUROL,NEW YORK,NY 10032. NIH,OFF DIRECTOR,BETHESDA,MD 20892. RP WU, TT (reprint author), NORTHWESTERN UNIV,DEPT BIOCHEM,EVANSTON,IL 60208, USA. RI Wu, Tai/B-7638-2009 FU NIAID NIH HHS [3RO1-AI-27508, 5RO1-AI-125616] NR 18 TC 14 Z9 16 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD SEP PY 1992 VL 29 IS 9 BP 1141 EP 1146 PG 6 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA JH971 UT WOS:A1992JH97100014 PM 1495500 ER PT J AU PALMER, TM JACOBSON, KA STILES, GL AF PALMER, TM JACOBSON, KA STILES, GL TI IMMUNOLOGICAL IDENTIFICATION OF A2 ADENOSINE RECEPTORS BY 2 ANTIPEPTIDE ANTIBODY PREPARATIONS SO MOLECULAR PHARMACOLOGY LA English DT Article ID BINDING SUBUNIT; RAT-BRAIN; PROTEINS; FAMILY; ERYTHROCYTE; EXPRESSION AB Two antipeptide antibody preparations were raised against deduced amino acid sequences within the presumed second extracellular loop (antibody TP/1) and the carboxyl-terminal domain (antibody TP/2) of the canine-derived A2 adenosine receptor (A2AR) cDNA species termed RDC8. Immunoblotting of canine liver plasma membranes with both TP/1 and TP/2 identified a single band of 52 kDa, which co-migrated with I-125-2-[4-[2-[2-[(4-azidophenyl) methylcarbonylamino]ethylaminocarbonyl]ethyl] phenyl]ethylamino-5'-N-ethylcarboxamidoadenosine-labeled receptor. However, in membranes prepared from canine striatum, photoaffinity labeling and immunoblotting with TP/2, but not TP/1, revealed a single band of 34 kDa; the identity of the band observed on the immunoblot as an A2AR was confirmed by the ability of TP/2 to specifically immunoprecipitate photoaffinity-labeled receptor from crude canine striatal membranes. The size difference between liver and striatal A2ARs was not due to tissue-specific proteolysis, because membranes from striatum were prepared with a protease inhibitor cocktail previously shown to be effective in inhibiting endogenous A2AR proteolysis during membrane preparation. Also, the protease-sensitive carboxyl-terminal region of the receptor had remained intact, because the peptide used to raise TP/2 antibodies resides in this domain of the molecule. The difference in size was also not due to a greater carbohydrate content of the liver receptor, because treatment of liver and striatal membranes with endoglycosidase F produced small mobility shifts for both receptors. Removal of N-linked carbohydrate chains also did not alter the inability of TP/1 to recognize the striatal A2AR. Hence, we conclude that the A2AR present in liver, which displays the predicted immunoreactivity of RDC8, is immunologically distinct from the A2AR expressed in striatum and that the latter may represent an additional A2AR subtype. C1 DUKE UNIV,MED CTR,DEPT MED,BOX 3444,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT PHARMACOL,DURHAM,NC 27710. NIDDKD,CHEM LABS,BETHESDA,MD 20892. RI Palmer, Timothy/C-4975-2009; Jacobson, Kenneth/A-1530-2009; Palmer, Timothy/E-7290-2013 OI Jacobson, Kenneth/0000-0001-8104-1493; Palmer, Timothy/0000-0002-9803-7164 FU Intramural NIH HHS [Z01 DK031117-20]; NHLBI NIH HHS [P50HL 17670, R01HL35134] NR 29 TC 27 Z9 27 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD SEP PY 1992 VL 42 IS 3 BP 391 EP 397 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JP050 UT WOS:A1992JP05000002 PM 1328841 ER PT J AU BELCHEVA, MM BARG, J GLOECKNER, C GAO, XM CHUANG, DM COSCIA, CJ AF BELCHEVA, MM BARG, J GLOECKNER, C GAO, XM CHUANG, DM COSCIA, CJ TI ANTAGONIST-INDUCED TRANSIENT DOWN-REGULATION OF DELTA-OPIOID RECEPTORS IN NG108-15 CELLS SO MOLECULAR PHARMACOLOGY LA English DT Article ID NEURO-BLASTOMA CELLS; HYBRID-CELLS; OPIATE RECEPTOR; TRITIATED ENKEPHALIN; ADRENERGIC-RECEPTORS; ATYPICAL AGONISTS; UP-REGULATION; BINDING; TOLERANCE; REDUCTION AB According to current concepts, agonists can effect the down-regulation of cell surface receptors, whereas antagonists can cause their up-regulation. We have discovered that the opioid antagonists naltrexone, naloxone, and ICI174864 induce a transient down-regulation of delta-opioid receptors before up-regulation, in NG108-15 cells. The possibility of an apparent loss of sites due to blockade by residual antagonist was ruled out by several lines of evidence. The reduction in delta-receptors was time, temperature, and antagonist concentration dependent. This down-regulation could not be induced by either the highly mu-selective opioid antagonist cyclic -D-Phe-Cys-Try-D-Trp-Arg-Thr-Pen-Thr-amide or the muscarinic antagonist atropine. In the same neurohybrid cells, the opioid agonist [D-Ala2,D-Leu5]enkephalin (0.1-mu-N, 60 min) effected a greater down-regulation of delta-opioid receptors. Similar qualitative changes in opioid binding of subcellular fractions were elicited with [D-Ala2,D-Leu5]enkephalin and naltrexone. However, the agonist was 2-fold more effective in reducing the heavy membrane population of receptors and 4-fold more potent in increasing the light membrane sites. Because heavy membranes are enriched in plasma membrane, whereas light membranes contain intracellular sites, these findings indicate that internalization occurs in both instances. Naltrexone and the delta-specific antagonists ICI174864 and naltrindole also diminished specific activities of two lysosomal enzymes, whereas opioid agonist-induced down-regulation was accompanied by an increase in their specific activities. Pretreatment of cell cultures with concanavalin A blocked both down-regulation and alterations in the lysosomal enzyme activities elicited by agonists and antagonists, suggesting that the latter is an opioid receptor-mediated process. The up-regulation of delta-opioid receptors by antagonists appears, then, to entail down-regulation that differs from that of agonists. C1 ST LOUIS UNIV,SCH MED,EA DOISY DEPT BIOCHEM & MOLEC BIOL,1402 S GRAND BLVD,ST LOUIS,MO 63104. NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. NR 26 TC 20 Z9 20 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD SEP PY 1992 VL 42 IS 3 BP 445 EP 452 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JP050 UT WOS:A1992JP05000010 PM 1328845 ER PT J AU BONDOC, LL AHLUWALIA, G COONEY, DA HARTMAN, NR JOHNS, DG FRIDLAND, A AF BONDOC, LL AHLUWALIA, G COONEY, DA HARTMAN, NR JOHNS, DG FRIDLAND, A TI METABOLIC PATHWAYS FOR THE ACTIVATION OF THE ANTIVIRAL AGENT 2',3'-DIDEOXYGUANOSINE IN HUMAN LYMPHOID-CELLS SO MOLECULAR PHARMACOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; IMP DEHYDROGENASE STIMULATE; HUMAN T-LYMPHOBLASTS; PYRIMIDINE 2',3'-DIDEOXYNUCLEOSIDES; PURINE 2',3'-DIDEOXYNUCLEOSIDES; CELLULAR PHARMACOLOGY; DEOXYCYTIDINE KINASE; ADENOSINE KINASE; HTLV-III/LAV; INVITRO AB 2',3'-Dideoxyguanosine (ddGuo) is a selective inhibitor of the replication of human immunodeficiency virus in vitro and the most active antihepadnavirus nucleoside analog known in vitro and in vivo, in a Peking duck model. However, the exact route by which this and related guanosine analogs are anabolized to their putative active metabolites in target cells is controversial. The anabolic pathway for the activation of ddGuo was investigated with the use of mutant human lymphoid CCRF-CEM and WI-L2 cell lines deficient in known nucleoside kinases. Uptake of ddGuo by human lymphoid cells and subsequent conversion to mono-, di-, and triphosphorylated metabolites is dose dependent and occurs proportionately to the exogenous concentration of drug. Studies with kinase-deficient CCRF-CEM and WI-L2 mutants revealed that at least two different routes of metabolism are operating in these cells to initiate the phosphorylation of ddGuo to its active dideoxynucleotides, one being deoxycytidine (dCyd) kinase and the other a cytosolic-5'-nucleotidase acting in the anabolic direction as a phosphotransferase. The evidence for this included 1) a lower but significant accumulation of drug anabolites in dCyd kinase-deficient mutants, 2) a lack of cross-resistance of the kinase-deficient mutants to growth inhibition by ddGuo, compared with that by the related analogs dideoxycytidine and arabinosylcytosine, known substrates for dCyd kinase, and 3) identification of different phosphorylation activities for ddGuo in extracts of wild-type cells and kinase-deficient mutants. Knowledge of the enzyme systems involved in anabolism of ddGuo analogs should be important for both new drug design and optimal therapeutic application. C1 ST JUDE CHILDREN RES HOSP,DEPT INFECT DIS,332 N LAUDERDALE,MEMPHIS,TN 38105. UNIV TENNESSEE,COLL MED,DEPT PHARMACOL,MEMPHIS,TN 38101. NCI,DIV CANC TREATMENT,MED CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. FU NCI NIH HHS [P0 30 CA 21765]; NIAID NIH HHS [AI 27652, AI 31145] NR 26 TC 10 Z9 10 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD SEP PY 1992 VL 42 IS 3 BP 525 EP 530 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JP050 UT WOS:A1992JP05000021 PM 1328848 ER PT J AU TOPKA, H HALLETT, M AF TOPKA, H HALLETT, M TI PERIORAL REFLEXES IN OROFACIAL DYSKINESIA AND SPASMODIC DYSPHONIA SO MUSCLE & NERVE LA English DT Article DE PERIORAL REFLEXES; TRIGEMINOFACIAL REFLEXES; SPASMODIC DYSPHONIA; OROFACIAL DYSKINESIA ID BLINK REFLEX; OROMANDIBULAR DYSTONIA; PARKINSONS-DISEASE; FACIAL NUCLEUS; BRAIN-STEM; BLEPHAROSPASM; CAT; EXCITABILITY; ORGANIZATION; INTERNEURONS AB In order to assess the clinical utility of trigemino-facial reflexes in lower facial muscles, we studied perioral reflexes to mechanical and electrical stimulation in 13 patients with spasmodic dysphonia and orofacial dyskinesia and in 7 healthy subjects. Mechanical stimulation of the upper lip of all patients and electrical stimulation of the infraorbital nerve of patients with oro-facial dyskinesia elicited larger perioral reflexes than in controls. In the majority of patients, hyperexcitable perioral reflexes were accompanied by increased gain of the blink reflex. In 4 patients, however, trigemino-facial reflexes were enhanced selectively in either the perioral muscles or orbicularis oculi. Our findings suggest that the quantitative assessment of perioral reflexes may provide information about the excitability of brainstem interneurons in cranial dystonia that is complementary to blink reflex studies. C1 NINCDS,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BLDG 10,ROOM 5N226,BETHESDA,MD 20892. NR 27 TC 13 Z9 13 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PD SEP PY 1992 VL 15 IS 9 BP 1016 EP 1022 DI 10.1002/mus.880150906 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA JJ690 UT WOS:A1992JJ69000005 PM 1518510 ER PT J AU WITT, KL GUDI, R BISHOP, JB AF WITT, KL GUDI, R BISHOP, JB TI INDUCTION OF KINETOCHORE POSITIVE AND NEGATIVE MICRONUCLEI IN MOUSE BONE-MARROW CELLS BY SALICYLAZOSULFAPYRIDINE AND SULFAPYRIDINE SO MUTATION RESEARCH LA English DT Article DE SALICYLAZOSULFAPYRIDINE; SULFAPYRIDINE; ANEUPLOIDY; KINETOCHORES; MICRONUCLEUS ID ANEUPLOIDY-INDUCING AGENTS; ANTIKINETOCHORE ANTIBODY; HUMAN-LYMPHOCYTES; ERYTHROCYTES; IDENTIFICATION; SULPHASALAZINE; INVIVO; ASSAY AB Salicylazosulfapyridine (SASP) and its major metabolite sulfapyridine (SP) have been shown to induce chromosomal damage in vivo. Both chemicals were tested in the micronucleus (MN)/kinetochore (KC) staining test to gain insight into the question of whether chromosomal breakage, aneuploidy-inducing events, or both were important to the observed production of MN in bone marrow cells of mice. In this test, both SASP and SP were shown to be strong inducers of kinetochore positive (KC+) MN. Although small increases in, kinetochore negative (KC -) MN were also observed in SP treated mice, as well as in mice receiving the highest dose of SASP tested, the results suggest that both chemicals induce predominantly aneuploidogenic type damage. C1 NIEHS,EXPTL CARCINOGENESIS & MUTAGENESIS BRANCH,POB 12233,MD E403,RES TRIANGLE PK,NC 27709. OAK RIDGE ASSOCIATED UNIV,OAK RIDGE,TN 37830. SITEK RES LAB,ROCKVILLE,MD. NR 21 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD SEP PY 1992 VL 283 IS 1 BP 53 EP 57 DI 10.1016/0165-7992(92)90121-W PG 5 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA JL410 UT WOS:A1992JL41000008 PM 1380663 ER PT J AU WITT, KL BISHOP, JB MCFEE, AF KUMAROO, V AF WITT, KL BISHOP, JB MCFEE, AF KUMAROO, V TI INDUCTION OF CHROMOSOMAL DAMAGE IN MAMMALIAN-CELLS INVITRO AND INVIVO BY SULFAPYRIDINE OR 5-AMINOSALICYLIC ACID SO MUTATION RESEARCH LA English DT Article DE SALICYLAZOSULFAPYRIDINE; SULFAPYRIDINE; 5-AMINOSALICYLIC ACID; MICRONUCLEUS; SISTER-CHROMATID EXCHANGES; CHROMOSOMAL ABERRATIONS ID MUTAGENICITY AB Sulfapyridine (SP) and 5-aminosalicylic acid (5-ASA) are the two primary metabolites of the anti-inflammatory drug salicylazosulfapyridine (SASP). These two metabolites were studied for induction of chromosomal damage in mammalian cells, in vitro and in vivo, in an attempt to understand better the genetic effects produced by SASP in humans and laboratory mice. To this end, SP and 5-ASA were tested for induction of sister-chromatid exchanges (SCE) and chromosomal aberrations (Abs) in Chinese hamster ovary (CHO) cells in vitro. In addition, they were tested in vivo for induction of micronuclei (MN) in mouse bone marrow polychromatic erythrocytes (PCE). SP gave positive results in the in vitro SCE test and the in vivo MN test, and negative results in the in vitro Abs test. 5-ASA was negative in all three tests. These results indicate that it is the SP metabolite of SASP that is necessary for the induction of chromosomal damage reported to occur in humans and mice after treatment with SASP. C1 NIEHS,EXPTL CARCINOGENESIS & MUTAGENESIS BRANCH,POB 12233,MDE403,RES TRIANGLE PK,NC 27709. OAK RIDGE ASSOCIATED UNIV,OAK RIDGE,TN 37830. SITEK RES LAB,ROCKVILLE,MD. NR 7 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD SEP PY 1992 VL 283 IS 1 BP 59 EP 64 DI 10.1016/0165-7992(92)90122-X PG 6 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA JL410 UT WOS:A1992JL41000009 PM 1380664 ER PT J AU LANGENBACH, R SMITH, PB CRESPI, C AF LANGENBACH, R SMITH, PB CRESPI, C TI RECOMBINANT-DNA APPROACHES FOR THE DEVELOPMENT OF METABOLIC SYSTEMS USED IN INVITRO TOXICOLOGY SO MUTATION RESEARCH LA English DT Review DE RECOMBINANT DNA APPROACHES; DRUG METABOLIZING ENZYMES; GENETIC INFORMATION TRANSFER; CYTOCHROME-P450 ENZYMES ID HUMAN CELL-LINE; CHINESE-HAMSTER-CELLS; SACCHAROMYCES-CEREVISIAE; MEDIATED MUTAGENESIS; STABLE EXPRESSION; MAMMALIAN-CELLS; COS-1 CELLS; MOUSE EMBRYO; LUNG-CANCER; HUMAN-LIVER AB In the past few years there has been considerable progress in the development of mammalian cell systems for use in genetic toxicology by the stable transfer of genes/cDNAs coding for drug metabolizing enzymes directly into the target cell. Alternative approaches have also been developed in which mammalian cells are transiently transfected with cDNAs coding for drug-metabolizing enzymes and S9 preparations expressing a single metabolizing enzyme isolated and used for metabolic activation. Progress in these areas is reviewed here and the relative merits of the different approaches are discussed. Work to date has focused primarily on the cytochrome P450 family of enzymes, although other enzyme systems involved in xenobiotic metabolism have been used. The central theme of this review is the transfer of genetic information to improve the metabolic capability of cell systems used in genetic toxicology. However, a basic philosophy of the review is that genetic manipulation of cultured mammalian cells has the potential for developing systems to be used to better understand chemically induced toxicological effects. C1 GENTEST CORP,WOBURN,MA 01801. RP LANGENBACH, R (reprint author), NIEHS,EXPTL CARCINOGENESIS & MUTAGENESIS BRANCH,E4-05,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 127 TC 48 Z9 48 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD SEP PY 1992 VL 277 IS 3 BP 251 EP 275 DI 10.1016/0165-1110(92)90047-D PG 25 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA JN077 UT WOS:A1992JN07700006 PM 1381053 ER PT J AU CZEIZEL, AE SZABADOS, A SUSANSZKY, E AF CZEIZEL, AE SZABADOS, A SUSANSZKY, E TI LOWER BIRTH-WEIGHT OF OFFSPRING BORN AFTER SELF-POISONING OF PARENT SO MUTATION RESEARCH LA English DT Article DE BIRTH WEIGHT; PARENTAL SELF-POISONING ID MICE; INDUCTION; ANOMALIES AB Birth weight was evaluated in 777 and 217 livebirths, respectively, of index females and female partners of index males born before and after severe self-poisoning with drugs. Birth weight was also evaluated in matched controls. Babies born to index females months or years after an attempted self-poisoning were found to have a lower birth weight than before this suicide attempt. The difference in the birth weight of subsequent pregnancies of index and control females was also highly significant. A similar trend was observed in livebirths of female partners of index males. However, the differences were not significant between previous and subsequent pregnancies and between index cases and matched controls. C1 NIH,WHO,COLLABORATING CTR COMMUNITY CONTROL HEREDITARY DIS,BETHESDA,MD 20892. NR 14 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0921-8262 J9 MUTAT RES PD SEP PY 1992 VL 269 IS 1 BP 35 EP 39 DI 10.1016/0027-5107(92)90158-X PG 5 WC Genetics & Heredity; Toxicology SC Genetics & Heredity; Toxicology GA JN076 UT WOS:A1992JN07600004 PM 1381469 ER PT J AU FROMTLING, RA DIXON, DM AF FROMTLING, RA DIXON, DM TI SHADOMY,SMITH 1931-1991 - OBITUARY SO MYCOPATHOLOGIA LA English DT Item About an Individual C1 NIH,BETHESDA,MD 20892. RP FROMTLING, RA (reprint author), MERCK & CO INC,SCI & TECHNOL POLICY,RAHWAY,NJ, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0301-486X J9 MYCOPATHOLOGIA JI Mycopathologia PD SEP PY 1992 VL 119 IS 3 BP 127 EP 128 DI 10.1007/BF00448807 PG 2 WC Mycology SC Mycology GA JV070 UT WOS:A1992JV07000001 ER PT J AU AHUJA, SK OZCELIK, T MILATOVITCH, A FRANCKE, U MURPHY, PM AF AHUJA, SK OZCELIK, T MILATOVITCH, A FRANCKE, U MURPHY, PM TI MOLECULAR EVOLUTION OF THE HUMAN INTERLEUKIN-8 RECEPTOR GENE-CLUSTER SO NATURE GENETICS LA English DT Article ID PLATELET FACTOR-4; HUMAN-NEUTROPHILS; IL-1 RECEPTOR; EXPRESSION; CLONING; FAMILY; SUPERFAMILY; NUCLEOTIDE; PROTEINS; CYTOKINE AB Interleukin-8 (IL-8) is the prototype for a family of at least eight neutrophil chemoattractants whose genes map to human chromosome 4q13-q21. Two human IL-8 receptors, IL8RA and IL8RB, are known from cDNA cloning; IL8RA is a promiscuous receptor for at least two other related ligands, GRO-alpha and NAP-2. We now report cloning of the genes for IL8RA, IL8RB and a recently inactivated pseudogene of receptor A (IL8RAP). These form a cluster of only three genes in the superfamily of G protein-coupled receptors (GPCRs) and map to 2q34-q35. The coevolutionary diversity displayed by the IL-8 ligand-receptor complex - ligand promiscuity for IL-8, receptor promiscuity for IL8RA, gene duplication for both ligands and receptors and gene extinction in the case of IL8RAP - is unprecedented for the GPCR superfamily. C1 NIAID,HOST DEF LAB,BETHESDA,MD 20892. STANFORD UNIV,MED CTR,HOWARD HUGHES MED INST,STANFORD,CA 94305. STANFORD UNIV,MED CTR,DEPT GENET,STANFORD,CA 94305. STANFORD UNIV,MED CTR,DEPT PEDIAT,STANFORD,CA 94305. NR 46 TC 99 Z9 105 U1 0 U2 3 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD SEP PY 1992 VL 2 IS 1 BP 31 EP 36 DI 10.1038/ng0992-31 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA JM646 UT WOS:A1992JM64600012 PM 1303245 ER PT J AU LIFTON, RP DLUHY, RG POWERS, M RICH, GM GUTKIN, M FALLO, F GILL, JR FELD, L GANGULY, A LAIDLAW, JC MURNAGHAN, DJ KAUFMAN, C STOCKIGT, JR ULICK, S LALOUEL, JM AF LIFTON, RP DLUHY, RG POWERS, M RICH, GM GUTKIN, M FALLO, F GILL, JR FELD, L GANGULY, A LAIDLAW, JC MURNAGHAN, DJ KAUFMAN, C STOCKIGT, JR ULICK, S LALOUEL, JM TI HEREDITARY HYPERTENSION CAUSED BY CHIMERIC GENE DUPLICATIONS AND ECTOPIC EXPRESSION OF ALDOSTERONE SYNTHASE SO NATURE GENETICS LA English DT Article ID POLYMERASE CHAIN-REACTION; GLUCOCORTICOID-SUPPRESSIBLE ALDOSTERONISM; HYPER-ALDOSTERONISM; DNA; CLONING; IDENTIFICATION; 18-OXOCORTISOL; POLYMORPHISMS; LOCALIZATION; FRAGMENTS AB Patients with glucocorticoid-remediable aldosteronism (GRA) from 12 kindreds possess chimaeric gene duplications arising from unequal crossing-over, fusing regulatory sequences of steroid 11-beta-hydroxylase to coding sequences of aldosterone synthase. These chimaeric genes are specific for GRA and explain the biochemistry, physiology and genetics of this form of hypertension. Sites of crossing over range from intron 2 to intron 4. Most mutations have arisen independently from either sister or non-sister chromatid exchange between these genes, which are only 45 kilobases apart. The possibility of a susceptibility allele for GRA of Irish origin is suggested. These findings indicate the utility of a direct genetic test for this disorder. C1 UNIV UTAH,DEPT HUMAN GENET,SALT LAKE CITY,UT 84112. BRIGHAM & WOMENS HOSP,DIV ENDOCRINE HYPERTENS,BOSTON,MA 02115. HYPERTENS RENAL GRP,LIVINGSTON,NJ 07039. UNIV PADUA,INST SEMEIOT MED,I-35100 PADUA,ITALY. NHLBI,BETHESDA,MD 20892. CHILDRENS HOSP,DIV NEPHROL,BUFFALO,NY 14222. UNIV S FLORIDA,COLL MED,DEPT MED,TAMPA,FL 33620. CANADIAN CANC SOC,TORONTO M4V 3B1,ONTARIO,CANADA. REG HOSP CORK,DEPT MED,CORK,IRELAND. UNIV OKLAHOMA,HLTH SCI CTR,NEPHROL SECT,OKLAHOMA CITY,OK 73112. ALFRED HOSP,EWEN DOWNIE METAB UNIT,MELBOURNE,VIC 3181,AUSTRALIA. VET AFFAIRS HOSP,BRONX,NY 10468. RP LIFTON, RP (reprint author), UNIV UTAH,HOWARD HUGHES MED INST,SALT LAKE CITY,UT 84112, USA. OI FALLO, FRANCESCO/0000-0002-7511-0226 NR 32 TC 242 Z9 251 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD SEP PY 1992 VL 2 IS 1 BP 66 EP 74 DI 10.1038/ng0992-66 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA JM646 UT WOS:A1992JM64600019 PM 1303253 ER PT J AU LIN, WW CHUANG, DM AF LIN, WW CHUANG, DM TI POTENTIATION BY CA-2+ IONOPHORES AND INHIBITION BY EXTRACELLULAR KCL OF ENDOTHELIN-INDUCED PHOSPHOINOSITIDE TURNOVER IN C-6 GLIOMA-CELLS SO NEUROCHEMISTRY INTERNATIONAL LA English DT Article ID INOSITOL PHOSPHOLIPID HYDROLYSIS; CORTICAL SLICES; SMOOTH-MUSCLE; GLIAL-CELLS; RAT-BRAIN; ASTROCYTES; RECEPTOR; DEPOLARIZATION; ACETYLCHOLINE; REQUIREMENT AB Interactions between endothelin-1 (ET)-induced phosphoinositide (PI) hydrolysis and agents that increase Ca2+ influx (i.e. A23187 and ionomycin) or induce depolarization (i.e. KCl) were investigated using C6 glioma. A23187 dose-dependently potentiated ET (30 nM)- and ATP (100-mu-M)-induced [H-3]inositol phosphate (IP) accumulation. This potentiation was associated with an increase in the maximal stimulation elicited by both ET and ATP but their EC50 values were unchanged. This effect of A23187 occurred at concentrations that did not affect basal PI turnover; i.e. 10 nM-3-mu-M. Ionomycin within the range of 1 nM-1-mu-M also significantly enhanced ET-induced PI breakdown and this effect was associated with an increase of [Ca2+]i. KCl in a concentration-dependent manner (14.7-54.7 mM) markedly inhibited PI breakdown elicited by ET and ATP, but had much less inhibition on basal activity and no effect on A23187- and ionomycin-induced responses. In parallel, KCl added before or after ET, sharply attenuated the increase of ET-induced [Ca2+]i but did not affect basal level or ionomycin-induced [Ca2+]i response. Neither the potentiation by A23187 nor the inhibition by KCl of ET-induced PI turnover was observed in cultured cerebellar astrocytes. Our results suggest that the cell type-specific regulation by Ca2+ ionophores and KCl on ET-induced PI metabolism is closely related to perturbation of [Ca2+]i. C1 NIMH,BIOL PSYCHIAT BRANCH,MOLEC NEUROBIOL SECT,BLDG 10,RM 3N 2-2,BETHESDA,MD 20892. NATL TAIWAN UNIV,COLL MED,DEPT PHARMACOL,TAIPEI,TAIWAN. OI Lin, Wan Wan/0000-0002-3207-734X NR 31 TC 6 Z9 6 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-0186 J9 NEUROCHEM INT JI Neurochem. Int. PD SEP PY 1992 VL 21 IS 2 BP 293 EP 301 DI 10.1016/0197-0186(92)90161-J PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA JG178 UT WOS:A1992JG17800021 PM 1338900 ER PT J AU CSIFFARY, A RUTTNER, Z TOTH, Z PALKOVITS, M AF CSIFFARY, A RUTTNER, Z TOTH, Z PALKOVITS, M TI OXYTOCIN NERVE-FIBERS INNERVATE BETA-ENDORPHIN NEURONS IN THE ARCUATE NUCLEUS OF THE RAT HYPOTHALAMUS SO NEUROENDOCRINOLOGY LA English DT Article DE OXYTOCIN; BETA-ENDORPHIN; ARCUATE NUCLEUS; DOUBLE IMMUNOSTAINING; ELECTRON-MICROSCOPIC IMMUNOHISTOCHEMISTRY; ANTEROGRADE TRACT TRACING ID VENTRAL BRAIN SURFACE; PARAVENTRICULAR NUCLEUS; MEDIAN-EMINENCE; SEROTONIN NEURONS; SUPRAOPTIC NUCLEI; OPIOID-PEPTIDES; LACTATING RATS; ORIGIN; LOCALIZATION; VASOPRESSIN AB Fine, varicose oxytocin-containing nerve fibers have been demonstrated in the hypothalamic arcuate nucleus in rats. Using Phaseolus vulgaris leukoagglutinin as an anterograde tracer, fine neuronal fibers of paraventricular nucleus origin could be seen throughout the arcuate nucleus. Using double immunostaining, oxytocin-immunoreactive varicose fibers were observed around or in the close vicinity of beta-endorphin-immunoreactive neurons. Silver-gold-labeled oxytocin-immunoreactive presynaptic boutons were shown to make synaptic contacts with diaminobenzidine-labeled beta-endorphin-immunoreactive neurons by electron microscopy. These findings provide morphological evidence for a possible influence of oxytocin on the activity of the brain beta-endorphin system at the hypothalamic level. C1 SEMMELWEIS UNIV MED,SCH MED,NEUROMORPHOL LAB,TUZOLTO U 58,H-1450 BUDAPEST,HUNGARY. NIAAA,METAB & MOLEC BIOL LAB,ROCKVILLE,MD 20852. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RI Palkovits, Miklos/F-2707-2013 NR 36 TC 20 Z9 20 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD SEP PY 1992 VL 56 IS 3 BP 429 EP 435 DI 10.1159/000126259 PG 7 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA JT849 UT WOS:A1992JT84900019 PM 1279446 ER PT J AU SCHEFFERS, MK JOHNSON, R GRAFMAN, J DALE, JK STRAUS, SE AF SCHEFFERS, MK JOHNSON, R GRAFMAN, J DALE, JK STRAUS, SE TI ATTENTION AND SHORT-TERM-MEMORY IN CHRONIC FATIGUE SYNDROME PATIENTS - AN EVENT-RELATED POTENTIAL ANALYSIS SO NEUROLOGY LA English DT Article ID BARR VIRUS-INFECTION; MYALGIC ENCEPHALOMYELITIS; SPATIAL ATTENTION; P300 LATENCY; DEPRESSION; DEMENTIA; SEARCH; TIME AB We recorded event-related brain potentials (ERPs) from 13 patients with chronic fatigue syndrome (CFS) and 13 matched normal controls. To assess attentional and memory deficits in CFS patients, we used a short-term memory task in which events occurred in different spatial locations and the patients made a rapid response (RT) when a letter in a relevant location matched a letter in the prememorized set (Attention paradigm). Time-on-task effects on the ERP and behavioral measures were assessed over the 2 1/4-hour duration of this task. Both groups also performed a visual Oddball paradigm, with an RT, before and after the Attention paradigm. The patients' RTs were much more variable and, in nine of 13 cases, slower than the mean RT of the controls in both paradigms. The patients' memory performance was not significantly different from that of the controls and there were no group differences in the overall amplitude, latency, or scalp distribution of the N1, P2, N2, or P300 components of the ERP in either paradigm. The ERP and performance data from both paradigms suggest that perceptual, attentional, and short-term memory processes were unaffected in CFS patients and that the differences were limited to response-related processes. C1 NINCDS,COGNIT NEUROPHYSIOL UNIT,BLDG 10,ROOM 5C422,BETHESDA,MD 20892. NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. OI Grafman, Jordan H./0000-0001-8645-4457 NR 31 TC 57 Z9 58 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD SEP PY 1992 VL 42 IS 9 BP 1667 EP 1675 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA JM884 UT WOS:A1992JM88400005 PM 1513453 ER PT J AU FILLINGKATZ, MR MILLER, SPF MERRICK, HF TRAVIS, WD GREGG, RE TSOKOS, M COMLY, M KANESKI, CR MACKIE, S LEBOVICS, RS BLANCHETTEMACKIE, EJ BRADY, RO PENTCHEV, PG AF FILLINGKATZ, MR MILLER, SPF MERRICK, HF TRAVIS, WD GREGG, RE TSOKOS, M COMLY, M KANESKI, CR MACKIE, S LEBOVICS, RS BLANCHETTEMACKIE, EJ BRADY, RO PENTCHEV, PG TI CLINICAL, PATHOLOGICAL, AND BIOCHEMICAL FEATURES OF A CHOLESTEROL LIPIDOSIS ACCOMPANIED BY HYPERLIPIDEMIA AND XANTHOMAS SO NEUROLOGY LA English DT Article ID NIEMANN-PICK DISEASE; LOW-DENSITY LIPOPROTEIN; ESTER STORAGE DISEASE; CULTURED FIBROBLASTS; METABOLISM; PATIENT; ACID AB We describe the unique clinical and histopathologic features of a child with biochemical and immunocytochemical features of Niemann-Pick disease type C (NPC). Clinically, she was found to have multiple xanthomas of the upper aerodigestive tract with dysphagia and expressive language delay, splenomegaly, bony infarcts, and type IIb hyperlipidemia. Neurologic examination was otherwise normal. Microscopy revealed foam cells in her bone marrow, liver, tongue, tonsils, glottis, and in normal-appearing peritonsillar mucosa. Lipid analysis of a liver biopsy specimen showed a small increase in phospholipids, a twofold increase in sphingomyelin, a fivefold increase in cholesterol, and a marked (25-fold) increase in bis(monoacylglycerol) phosphate. Lysosomal acid hydrolase activities in cultured skin fibroblasts were nondiagnostic. Biochemical and immunocytochemical studies of cultured fibroblasts demonstrated lysosomal accumulation of unesterified LDL-derived cholesterol as well as delayed induction of homeostatic responses to endogenous cholesterol consistent with a diagnosis of NPC. Based upon these observations, we speculate that this patient could have a new phenotypic expression of NPC or represents a new cholesterol lipidosis biochemically resembling NPC. The chance occurrence of two separate lipid disorders seems less likely. C1 NIAAA,CLIN STUDIES LAB,BLDG 10 ROOM 3D-11,BETHESDA,MD 20892. NINCDS,DEV & METAB NEUROL BRANCH,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. NIDCD,BETHESDA,MD 20892. NIDDKD,CELLULAR & DEV BIOL,BETHESDA,MD 20892. NR 23 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD SEP PY 1992 VL 42 IS 9 BP 1768 EP 1774 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA JM884 UT WOS:A1992JM88400023 PM 1513468 ER PT J AU HOLTZMAN, DM LI, YW PARADA, LF KINSMAN, S CHEN, CK VALLETTA, JS ZHOU, J LONG, JB MOBLEY, WC AF HOLTZMAN, DM LI, YW PARADA, LF KINSMAN, S CHEN, CK VALLETTA, JS ZHOU, J LONG, JB MOBLEY, WC TI P140TRK MESSENGER-RNA MARKS NGF-RESPONSIVE FOREBRAIN NEURONS - EVIDENCE THAT TRK GENE-EXPRESSION IS INDUCED BY NGF SO NEURON LA English DT Article ID NERVE GROWTH-FACTOR; TYROSINE PROTEIN-KINASE; HIGH-AFFINITY RECEPTORS; NEUROTROPHIC FACTOR; CHOLINERGIC NEURONS; BASAL FOREBRAIN; MOLECULAR-CLONING; FACTOR FAMILY; RAT-BRAIN; DEVELOPMENTAL EXPRESSION AB Nerve growth factor (NGF) appears to act as a neurotrophic factor for basal forebrain and caudate-putamen cholinergic neurons. The mechanism by which NGF transduces its signal in these neurons is yet to be defined. Recent data indicate that the product of the trk gene, p140trk, is a critical component of the NGF receptor. Herein, we show that p140trk mRNA is highly restricted in its distribution in the adult rat forebrain, that it is present in cholinergic neurons, and that most if not all cholinergic neurons contain p140trk mRNA. Furthermore, induction of trk expression by NGF suggests that neurotrophin-mediated up-regulation of their receptor tyrosine kinases is an important feature of their actions and that neurotrophins may regulate the activity of responsive neurons through increasing the level of their receptors. C1 UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,NEUROSCI PROGRAM,SAN FRANCISCO,CA 94143. NCI,FREDERICK CANC RES & DEV CTR,BASIC RES PROGRAM,ADV BIOSCI LAB,FREDERICK,MD 21701. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. KENNEDY KRIEGER INST,BALTIMORE,MD 21205. WALTER REED ARMY MED CTR,NEUROPHARMACOL BRANCH,DEPT MED NEUROSCI,WASHINGTON,DC 20307. RP HOLTZMAN, DM (reprint author), UNIV CALIF SAN FRANCISCO,DEPT NEUROL,SAN FRANCISCO,CA 94143, USA. RI Parada, luis/B-9400-2014 FU NIA NIH HHS [AG10672, AG00445-02]; NINDS NIH HHS [NS24054] NR 76 TC 354 Z9 358 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD SEP PY 1992 VL 9 IS 3 BP 465 EP 478 DI 10.1016/0896-6273(92)90184-F PG 14 WC Neurosciences SC Neurosciences & Neurology GA JM571 UT WOS:A1992JM57100008 PM 1524827 ER PT J AU GILAD, GM GILAD, VH WYATT, RJ AF GILAD, GM GILAD, VH WYATT, RJ TI POLYAMINES MODULATE THE BINDING OF GABA-A-BENZODIAZEPINE RECEPTOR LIGANDS IN MEMBRANES FROM THE RAT FOREBRAIN SO NEUROPHARMACOLOGY LA English DT Article DE POLYAMINES, DIAZEPAM; GABAA/BENZODIAZEPINE RECEPTOR; BRAIN; RAT ID NMDA RECEPTOR; BRAIN; SPERMINE; SITE AB The effects of spermine, spermidine and putrescine on the binding of the GABA(A)-benzodiazepine receptor complex were examined in the hippocampus and frontal cortex membranes of the rat. The results demonstrated modulatory effects of polyamines on the binding of diazepam and flunitrazepam but not on that of GABA, muscimol and Ro 15-1788. When membranes were prepared without detergent, the polyamines enhanced the binding of diazepam. However, while the binding capacity increased after homogenization in the presence of the non-ionic detergent Triton X-100, the polyamines did not enhance the binding but inhibited the binding of diazepam and flunitrazepam at greater concentrations. Considered together with other studies, the present findings indicate that polyamines can modulate the binding characteristics of several different neurotransmitter receptor-ionophore complexes. C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. NR 14 TC 23 Z9 24 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0028-3908 J9 NEUROPHARMACOLOGY JI Neuropharmacology PD SEP PY 1992 VL 31 IS 9 BP 895 EP 898 DI 10.1016/0028-3908(92)90127-B PG 4 WC Neurosciences; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA JL876 UT WOS:A1992JL87600010 PM 1331843 ER PT J AU LICINIO, J WONG, ML GOLD, PW AF LICINIO, J WONG, ML GOLD, PW TI NEUTROPHIL-ACTIVATING PEPTIDE-1 INTERLEUKIN-8 MESSENGER-RNA IS LOCALIZED IN RAT HYPOTHALAMUS AND HIPPOCAMPUS SO NEUROREPORT LA English DT Article DE INTERLEUKIN-8; PARAVENTRICULAR HYPOTHALAMIC NUCLEUS; HIPPOCAMPUS; MESSENGER RNA; NUCLEIC ACID HYBRIDIZATION; RAT ID TUMOR-NECROSIS-FACTOR; EXPRESSION; GENE; INHIBITION; INDUCTION; CYTOKINE; BRAIN AB NEUTROPHIL-ACTIVATING peptide-1/interleukin-8 (NAP-1/IL-8) is a cytokine synthesized by various cell types. In the immune system NAP-1/IL-8 is part of an immune cascade initiated by IL-1 production. NAP-1/IL-8 affects hypothalamic function and its production is suppressed by steroids. Therefore, it might be expected that NAP-1/IL-8 would be produced in brain areas involved in the control of the hypothalamic-pituitary-adrenocortical axis (HPA). NAP-1/IL-8 mRNA was localized by in situ hybridization in the paraventricular nucleus of the hypothalamus and hippocampus. Those areas also express the genes encoding interleukin-l-alpha (IL-1alpha), IL-1beta, IL-1 receptors, and IL-1 receptor antagonist (IL-1ra). This suggests that an immune cascade, which is well characterized in the immune system, may exist in brain, in areas of relevance to the regulation of stress-related neuroendocrine function. C1 NIMH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892. RP LICINIO, J (reprint author), YALE UNIV,W HAVEN VET AFFAIRS MED CTR,SCH MED,DEPT PSYCHIAT,116A,950 CAMPBELL AVE,W HAVEN,CT 06516, USA. RI Wong, Ma-Li/D-7903-2011; Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 25 TC 19 Z9 20 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD SEP PY 1992 VL 3 IS 9 BP 753 EP 756 DI 10.1097/00001756-199209000-00008 PG 4 WC Neurosciences SC Neurosciences & Neurology GA JY018 UT WOS:A1992JY01800008 PM 1421131 ER PT J AU HAMPSON, DR HUANG, XP OBERDORFER, MD GOH, JW AUYEUNG, A WENTHOLD, RJ AF HAMPSON, DR HUANG, XP OBERDORFER, MD GOH, JW AUYEUNG, A WENTHOLD, RJ TI LOCALIZATION OF AMPA RECEPTORS IN THE HIPPOCAMPUS AND CEREBELLUM OF THE RAT USING AN ANTIRECEPTOR MONOCLONAL-ANTIBODY SO NEUROSCIENCE LA English DT Article ID KAINIC ACID RECEPTOR; KAINATE-BINDING-PROTEIN; CENTRAL-NERVOUS-SYSTEM; GLUTAMATE RECEPTOR; FROG BRAIN; SUBCELLULAR-LOCALIZATION; FUNCTIONAL EXPRESSION; CLONING; SUBUNIT; SITES AB The primary amino acid sequences of the kainate binding proteins from the amphibian and avian central nervous systems are homologous with the functional alpha-amino-3-hydroxyl-5-methyl-isoxazole-4-propionate receptors that have been cloned from rat brain. In this study, we have analysed the anatomical and subcellular distribution of the alpha-amino-3-hydroxyl-5-methyl-isoxazole-4-propionate receptors in the rat hippocampus and cerebellum, using a monoclonal antibody that was raised against a kainate binding protein purified from frog brain. Immunoblots of rat hippocampus and cerebellum, and membranes from COS cells transfected with rat brain alpha-amino-3-hydroxyl-5-methyl-isoxazole-4-propionate receptor cDNAs (GluR1, GluR2, or GluR3) showed a major immunoreactive band migrating at a relative molecular weight of 107,000. In the cerebellum, an additional immunoreactive protein of approximately 128,000 mol. wt was also seen on immunoblots probed with the antibody. The distribution of this protein is apparently restricted to the cerebellum since the 128,000 mol. wt band was not present in other brain areas examined. The identity of the 128,000 mol. wt cerebellar protein is not known. Immunocytochemical analyses of the hippocampus demonstrated that alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate receptor subunits are present in the cell bodies and dendrites of pyramidal cells. The granule cells were also immunostained. All of the pyramidal cell subfields were heavily labeled. In the pyramidal cell bodies, a high level of immunoreactivity was observed throughout the cytoplasm. In the cerebellum, the Purkinje cell bodies and dendrites also displayed very high levels of immunoreactivity. In addition to the Purkinje neurons, the Bergmann glia and some Golgi neurons were clearly immunostained. Subcellular fractionation and lesioning experiments using the excitotoxin domoic acid indicated that the alpha-amino-3-hydroxyl-5-methyl-isoxazole-4-propionate receptor subunits were associated with postsynaptic membranes. Direct visualization of the immunoreactivity using electron microscopy confirmed the postsynaptic localization of the staining in the dendritic areas in both the hippocampus and the cerebellum. Thus, unlike the kainate binding proteins, which are found primarily extrasynaptically in the frog and on glial cells in the chicken cerebellum, the GluR1, GluR2, and GluR3 receptor subunits are localized to the postsynaptic membrane in the dendrites of neurons in the rat central nervous system. C1 NIDOCD,NEUROCHEM LAB,BETHESDA,MD 20892. QUEENS UNIV,DEPT PHARMACOL & TOXICOL,KINGSTON K7L 3N6,ONTARIO,CANADA. RP HAMPSON, DR (reprint author), UNIV TORONTO,FAC PHARM,19 RUSSELL ST,TORONTO M5S 2S2,ONTARIO,CANADA. NR 38 TC 76 Z9 76 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD SEP PY 1992 VL 50 IS 1 BP 11 EP 22 DI 10.1016/0306-4522(92)90378-F PG 12 WC Neurosciences SC Neurosciences & Neurology GA JM226 UT WOS:A1992JM22600003 PM 1328932 ER PT J AU WINSKY, L MONTPIED, P ARAI, R MARTIN, BM JACOBOWITZ, DM AF WINSKY, L MONTPIED, P ARAI, R MARTIN, BM JACOBOWITZ, DM TI CALRETININ DISTRIBUTION IN THE THALAMUS OF THE RAT - IMMUNOHISTOCHEMICAL AND INSITU HYBRIDIZATION HISTOCHEMICAL ANALYSES SO NEUROSCIENCE LA English DT Article ID CALCIUM-BINDING PROTEIN; CENTRAL NERVOUS-SYSTEM; CONTAINING NEURONS; RETICULAR NUCLEUS; MESSENGER-RNA; BRAIN; LOCALIZATION; IMMUNOREACTIVITY; ENKEPHALIN; EXPRESSION AB The distribution of calretinin-containing cells was examined by in situ hybridization histochemistry and compared with the immunohistochemical mapping of calretinin in the thalamus of the rat. Results revealed a close correspondence between the immunohistochemical localization of cell bodies and the messenger RNA label produced by the calretinin oligonucleotide probe. Calretinin cells were most prominent in the midline (paraventricular, reuniens, rhomboid) and intralaminar (central medial, paracentral) nuclei and in a group of cells along the rostral central gray which appeared continuous with the caudal extent of the midline nuclei. A subpopulation of calretinin cell bodies was also identified in the reticular nucleus. The mediorostral lateral posterior nucleus, subparafascicular, lateral geniculate and habenular nuclei also contained calretinin messenger RNA probe label. In contrast, no positive cells were found in the anterior, ventral or posterior thalamic nuclei. The distribution of calretinin cells did not correspond directly with that of other histochemical markers. Thus, the in situ hybridization histochemical and immunohistochemical results revealed calretinin as a unique identifying marker for distinct sets of thalamic neurons. C1 NIMH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. RP WINSKY, L (reprint author), NIMH,CLIN SCI LAB,BLDG 10,ROOM 3D-48,BETHESDA,MD 20892, USA. NR 43 TC 66 Z9 66 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD SEP PY 1992 VL 50 IS 1 BP 181 EP 196 DI 10.1016/0306-4522(92)90391-E PG 16 WC Neurosciences SC Neurosciences & Neurology GA JM226 UT WOS:A1992JM22600016 PM 1407555 ER PT J AU HEISHMAN, SJ HENNINGFIELD, JE AF HEISHMAN, SJ HENNINGFIELD, JE TI STIMULUS FUNCTIONS OF CAFFEINE IN HUMANS - RELATION TO DEPENDENCE POTENTIAL SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE CAFFEINE; DRUG DEPENDENCE; DEPENDENCE POTENTIAL; DRUG ABUSE; SUBJECTIVE EFFECTS; DISCRIMINATIVE FUNCTIONS; REINFORCING FUNCTIONS; DRUG SELF-ADMINISTRATION; DRUG LIKING; PHYSICAL DEPENDENCE; TOLERANCE; CLINICAL PHARMACOLOGY; BEHAVIORAL PHARMACOLOGY; STIMULUS CONTROL; D-AMPHETAMINE; HUMANS; ANIMALS ID HUMAN COFFEE-DRINKING; ABUSE LIABILITY; DISCRIMINATIVE STIMULUS; PHYSICAL-DEPENDENCE; D-AMPHETAMINE; PSYCHIATRIC-INPATIENTS; WITHDRAWAL HEADACHE; DRUG PREFERENCE; BLOOD-PRESSURE; CONSUMPTION AB The interoceptive stimulus functions common to drugs of dependence include positive subjective effects, discriminative functions, and reinforcing functions. Data from studies measuring these stimulus functions constitute the objective assessment of a drug's dependence potential. This paper reviews the subjective effects, discriminative stimulus, and reinforcing stimulus functions of caffeine in humans to assess the dependence potential of caffeine. The stimulus effects of caffeine are compared with those of d-amphetamine, a prototypic CNS stimulant that has been studied under similar conditions, to evaluate the relative dependence potential of caffeine. Finally, caffeine's effects are evaluated in terms of generally accepted criteria for defining drug dependence. It is concluded that caffeine partially meets the primary criteria of drug dependence: 1) the majority of caffeine use is highly controlled, but not compulsive; 2) caffeine is psychoactive; and 3) caffeine functions as a reinforcer under certain conditions in humans, but not in animals. Caffeine thus has limited dependence potential. Additionally, although caffeine shares stimulus functions with d-amphetamine, it does so under limited conditions and should be considered to have a relatively lower dependence potential. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,BALTIMORE,MD 21224. RP HEISHMAN, SJ (reprint author), NIDA,ADDICT RES CTR,CLIN PHARMACOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA. NR 179 TC 26 Z9 27 U1 2 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0149-7634 J9 NEUROSCI BIOBEHAV R JI Neurosci. Biobehav. Rev. PD FAL PY 1992 VL 16 IS 3 BP 273 EP 287 DI 10.1016/S0149-7634(05)80202-7 PG 15 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA JL650 UT WOS:A1992JL65000001 PM 1528521 ER PT J AU WEHR, TA AF WEHR, TA TI A BRAIN-WARMING FUNCTION FOR REM-SLEEP SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE REM SLEEP; THERMOGENESIS; THERMOREGULATION; HOMEOTHERMY; METABOLISM; CIRCADIAN RHYTHM; SLOW-WAVE SLEEP; HYPOTHALAMUS; RHOMBENCEPHALON ID BROWN ADIPOSE-TISSUE; EYE-MOVEMENT SLEEP; CEREBRAL BLOOD-FLOW; FREELY MOVING CATS; PARADOXICAL SLEEP; BODY-TEMPERATURE; LOCUS COERULEUS; ENVIRONMENTAL-TEMPERATURE; WAKEFULNESS CYCLE; AMBIENT-TEMPERATURES AB During REM sleep, arterial blood flow, neuronal firing rates, metabolism, and temperature increase in many parts of the CNS. Eye muscle tone also increases, and the eyes exhibit bursts of rapid movements. If one of the functions of sleep is to conserve energy, then it is curious that energy is so conspicuously expended in the vicinity of the CNS during REM sleep. The author hypothesizes that homeotherms use REM sleep to produce heat in order to maintain a high, stable temperature in a restricted CNS core during sleep. The fact that several of the active features of REM sleep heat the CNS, and the fact that REM sleep propensity increases when core temperature physiologically decreases, seem consistent with the hypothesis that REM sleep is a regulated mechanism for warming the CNS. RP WEHR, TA (reprint author), NIMH,INTRAMURAL RES PROGRAM,CLIN PSYCHOBIOL BRANCH,ROOM 4S-239,BLDG 10,BETHESDA,MD 20892, USA. RI Sanguansri, Luz/B-6630-2011 OI Sanguansri, Luz/0000-0003-1908-7604 NR 154 TC 57 Z9 58 U1 1 U2 5 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0149-7634 J9 NEUROSCI BIOBEHAV R JI Neurosci. Biobehav. Rev. PD FAL PY 1992 VL 16 IS 3 BP 379 EP 397 DI 10.1016/S0149-7634(05)80208-8 PG 19 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA JL650 UT WOS:A1992JL65000007 PM 1528526 ER PT J AU LEVIN, HS ALDRICH, EF SAYDJARI, C EISENBERG, HM FOULKES, MA BELLEFLEUR, M LUERSSEN, TG JANE, JA MARMAROU, A MARSHALL, LF YOUNG, HF SHAPIRO, K JOHNSON, DL AF LEVIN, HS ALDRICH, EF SAYDJARI, C EISENBERG, HM FOULKES, MA BELLEFLEUR, M LUERSSEN, TG JANE, JA MARMAROU, A MARSHALL, LF YOUNG, HF SHAPIRO, K JOHNSON, DL TI SEVERE HEAD-INJURY IN CHILDREN - EXPERIENCE OF THE TRAUMATIC COMA DATA-BANK SO NEUROSURGERY LA English DT Article DE CHILDREN; HEAD INJURY; PREDICTORS OF OUTCOME; COMPUTED TOMOGRAPHY ID ADOLESCENTS; AGE AB THE OUTCOME AT discharge, 6 months, and 1 year after they had sustained severe head injuries was investigated in children (0-15 yr old at injury) who were admitted to the neurosurgery service at one of four centers participating in the Traumatic Coma Data Bank. Of 103 eligible children, the quality of recovery was assessed by the Glasgow Outcome Scale (GOS) at 6 months after injury in 92 patients (86% of series) and at 1 year in 82 patients (73% of series). The lowest post-resuscitation Glasgow Coma Scale score and pupillary reactivity were predictive of the 6-month GOS as were their interaction. Analysis of the first computed tomographic scan disclosed that bilateral swelling with/without midline shift was related to a poor outcome as was the presence of mass lesions. Comparison of age-defined subgroups of patients revealed that outcome was poorest in the 0- to 4-year-old patients, as reflected by their mortality, which increased to 62% by 1 year. Distinctive features of the injuries in the 0- to 4-year-olds included evacuated subdural hematomas (20% of patients) and hypotension (32% of patients). The most favorable outcome was attained by 5- to 10-year-olds (2/3 had a good recovery by 1 yr), whereas the GOS distribution of adolescents was intermediate between the children and adults. In summary, the GOS data reflect heterogeneity in the quality of outcome after severe head injury depending on age, neurological indices, and computed tomographic scan diagnostic category. C1 NATL INST NEUROL DISORDERS & STROKE,BIOMETRY & FIELD STUDIES BRANCH,BETHESDA,MD. UNIV TEXAS,MED BRANCH,DEPT ANESTHESIOL,GALVESTON,TX 77555. JAMES WHITCOMB RILEY HOSP CHILDREN,INDIANAPOLIS,IN 46202. UNIV VIRGINIA,DEPT NEUROL SURG,CHARLOTTESVILLE,VA 22903. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DIV NEUROSURG,RICHMOND,VA 23298. UNIV CALIF SAN DIEGO,DIV NEUROSURG,LA JOLLA,CA 92093. RP LEVIN, HS (reprint author), UNIV TEXAS,MED BRANCH,DIV NEUROSURG D-73,GALVESTON,TX 77555, USA. FU NINDS NIH HHS [N01-NS-3-2339, N01-NS-3-2341, N01-NS-3-2340] NR 17 TC 165 Z9 165 U1 3 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD SEP PY 1992 VL 31 IS 3 BP 435 EP 444 PG 10 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA JN834 UT WOS:A1992JN83400008 PM 1407426 ER PT J AU SHTERN, F AF SHTERN, F TI CLINICAL EXPERIMENTATION IN MAGNETIC-RESONANCE SPECTROSCOPY - A PERSPECTIVE FROM THE NATIONAL-CANCER-INSTITUTE SO NMR IN BIOMEDICINE LA English DT Article; Proceedings Paper CT 17TH GRAY CONF ON TUMOUR ASSESSMENT AND RESPONSE TO THERAPY STUDIED BY MAGNETIC RESONANCE SPECTROSCOPY CY APR 13-16, 1992 CL UNIV KENT, CANTERBURY, ENGLAND SP L H GRAY MEM TRUST HO UNIV KENT ID MR SPECTROSCOPY; NMR-SPECTROSCOPY; TUMORS; TISSUE; DIAGNOSIS; INSITU AB This paper describes the National Cancer Institute activities in clinical MRS, including a recent international conference organized by the Diagnostic Imaging Research Branch, a research agenda developed by the conference faculty members and one of the research programs proposed by the author. RP SHTERN, F (reprint author), NCI,DIAGNOST IMAGING RES BRANCH,6130 EXECUT BLVD,ROOM 800,ROCKVILLE,MD 20852, USA. NR 17 TC 4 Z9 4 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0952-3480 J9 NMR BIOMED JI NMR Biomed. PD SEP-OCT PY 1992 VL 5 IS 5 BP 325 EP 328 DI 10.1002/nbm.1940050519 PG 4 WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA JV867 UT WOS:A1992JV86700018 PM 1449971 ER PT J AU COX, JT SCHIFFMAN, MH WINZELBERG, AJ PATTERSON, JM AF COX, JT SCHIFFMAN, MH WINZELBERG, AJ PATTERSON, JM TI AN EVALUATION OF HUMAN PAPILLOMAVIRUS TESTING AS PART OF REFERRAL TO COLPOSCOPY CLINICS SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID ATYPICAL SQUAMOUS CELLS; DEOXYRIBONUCLEIC-ACID; PAPANICOLAOU SMEARS; CERVICAL NEOPLASIA; INFECTION; ASSOCIATION; HYBRIDIZATION; POPULATION; WOMEN; YOUNG AB Objective: To determine the usefulness of human papillomavirus (HPV) testing as a triage method for predicting which women referred to a colposcopy clinic were most likely to have histologically confirmed cervical intraepithelial neoplasia (CIN). Methods. Papanicolaou tests, ViraPap tests for HPV infection, and colposcopically directed biopsies were performed concurrently on 482 women referred to a student health colposcopy clinic. Results: The results demonstrated that HPV positivity was associated with a greatly increased likelihood of histologic confirmation of CIN, especially among women with concurrent cytologic findings that were negative or showed only atypical squamous cells of undetermined significance. Conclusions: Testing for HPV appears to have a role in the triage of students now being referred to our colposcopy clinic. A combination of HPV testing and repeated cytologic screening would provide reasonably sensitive screening for cervical neoplasia while limiting the use of colposcopic services, which are currently overburdened. The eventual usefulness of HPV testing will depend on the cost and availability of colposcopy services, the cost of Papanicolaou tests, the cost and accuracy of HPV tests, and the predictive value of HPV detection in the population being screened. C1 NCI,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. BIOSITE DIAGNOST,SAN DIEGO,CA. RP COX, JT (reprint author), UNIV CALIF SANTA BARBARA,SANTA BARBARA STUDENT HLTH SERV,WOMENS CLIN,BLDG 588,SANTA BARBARA,CA 93106, USA. NR 17 TC 67 Z9 67 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD SEP PY 1992 VL 80 IS 3 BP 389 EP 395 PN 1 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA JJ702 UT WOS:A1992JJ70200015 PM 1323087 ER PT J AU RAYMOND, E CLEMENS, JD AF RAYMOND, E CLEMENS, JD TI PROSPECTIVE RISK OF STILLBIRTH SO OBSTETRICS AND GYNECOLOGY LA English DT Letter RP RAYMOND, E (reprint author), NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892, USA. NR 3 TC 1 Z9 1 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD SEP PY 1992 VL 80 IS 3 BP 473 EP 474 PN 1 PG 2 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA JJ702 UT WOS:A1992JJ70200034 PM 1495709 ER PT J AU LAUTENBERGER, JA BURDETT, LA GUNNELL, MA QI, SM WATSON, DK OBRIEN, SJ PAPAS, TS AF LAUTENBERGER, JA BURDETT, LA GUNNELL, MA QI, SM WATSON, DK OBRIEN, SJ PAPAS, TS TI GENOMIC DISPERSAL OF THE ETS GENE FAMILY DURING METAZOAN EVOLUTION SO ONCOGENE LA English DT Article ID PUTATIVE ONCOGENE SPI-1; PROTO-ONCOGENE; C-ETS; CHROMOSOMAL LOCALIZATION; TRANSCRIPTION FACTOR; DEVELOPMENTAL EXPRESSION; MOLECULAR-ORGANIZATION; C-ETS-1 PROTOONCOGENE; TRANSFORMING GENE; LEUKEMIA-VIRUS AB Evolutionary homologs of the ets proto-oncogene have been discovered in the genomes of widely divergent eucaryote species from Drosophila to sea urchin to vertebrates. The prototype mammalian ets-1 and ets-2 genes are divided into three coding domains that differ in their rate of accumulation of sequence divergence. An analysis of sequence divergence of ets gene homologs in various species has produced a phylogenetic history of the ets gene family in the context of metazoan evolutionary radiation. A minimum of five duplication events of ets primordial genes were evident, namely (1) a duplication that separates primitive ets genes (Drosophila precursor of 74E, mouse PU.1 and human ELK1) from the ets-1, ets-2, erg ancestor; (2) and (3) two duplications that established separate ets, erg and elg/GABP-alpha lineages which occurred prior to invertebrate-vertebrate divergence; (4) divergence of ets-1 and ets-2 gene family also associated with vertebrate-invertebrate divergence; (5) duplication of ets-1 and ets-2 in Xenopus laevis to produce two ets-1 genes and two ets-2 genes during genomic tetraploidation in the recent ancestry of this species. C1 FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD 21702. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RP LAUTENBERGER, JA (reprint author), NCI,MOLEC ONCOL LAB,FREDERICK,MD 21702, USA. NR 58 TC 58 Z9 58 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD SEP PY 1992 VL 7 IS 9 BP 1713 EP 1719 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA JJ376 UT WOS:A1992JJ37600006 PM 1501883 ER PT J AU MARRIOTT, SJ TRINH, D BRADY, JN AF MARRIOTT, SJ TRINH, D BRADY, JN TI ACTIVATION OF INTERLEUKIN-2 RECEPTOR-ALPHA EXPRESSION BY EXTRACELLULAR HTLV-I TAX1 PROTEIN - A POTENTIAL ROLE IN HTLV-I PATHOGENESIS SO ONCOGENE LA English DT Article ID T-CELL LEUKEMIA; VIRUS TYPE-I; TROPICAL SPASTIC PARAPARESIS; PERIPHERAL-BLOOD LYMPHOCYTES; GROWTH-FACTOR RECEPTOR; MONOCLONAL-ANTIBODIES; GENE-EXPRESSION; IL-2 RECEPTOR; TAT GENE; TRANSFORMATION AB The Tax1 protein of human T cell leukemia/lymphoma virus type I (HTLV-1) has been shown to stimulate the proliferation of human lymphocytes. Here we report that lymphocyte proliferation can be induced at extracellular Tax1 concentrations as low as 25 pM. The proliferative response induced by extracellular Tax1 is accompanied by an activation of endogenous interleukin-2 receptor alpha-chain (IL-2R-alpha) expression in human lymphocytes. Functional activation of IL-2R-alpha expression in peripheral blood lymphocytes treated with Tax1 was demonstrated using an [I-125]IL-2-binding assay. In addition, an enzyme-linked immunosorbent assay demonstrated that soluble IL-2R-alpha in the medium of IL-2- and Tax1-treated cells was over 13-fold greater than in the medium of control treated cells. Overexpression of IL-2R-alpha is a common clinical feature of some patients with adult T-cell leukemia (ATL) and tropical spastic paraparesis/HTLV-I-associated myopathy (TSP/HAM). The ability of extracellular Tax1 protein to activate expression of IL-2R-alpha in both infected and uninfected lymphocytes may contribute to the abnormal lymphocyte proliferation observed in both ATL and TSP/HAM. C1 NIH,MOLEC VIROL LAB,BETHESDA,MD 20892. RP MARRIOTT, SJ (reprint author), BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030, USA. NR 45 TC 45 Z9 46 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD SEP PY 1992 VL 7 IS 9 BP 1749 EP 1755 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA JJ376 UT WOS:A1992JJ37600011 PM 1501887 ER PT J AU TROPPMAIR, J BRUDER, JT APP, H HONG, C LIPTAK, L SZEBERENYI, J COOPER, GM RAPP, UR AF TROPPMAIR, J BRUDER, JT APP, H HONG, C LIPTAK, L SZEBERENYI, J COOPER, GM RAPP, UR TI RAS CONTROLS COUPLING OF GROWTH-FACTOR RECEPTORS AND PROTEIN-KINASE-C IN THE MEMBRANE TO RAF-1 AND B-RAF PROTEIN SERINE KINASES IN THE CYTOSOL SO ONCOGENE LA English DT Article ID STIMULATING FACTOR-I; SIGNAL TRANSDUCTION; PC12 CELLS; PHOSPHORYLATION; ONCOGENES; DIFFERENTIATION; ACTIVATION; INSULIN; TYROSINE; GENE AB A dominant negative mutant of Ras, M17 Ras, was used to study the role of Ras in receptor coupling of Raf-1 and B-Raf protein serine/threonine kinases (PSKs). We found that mutant Ras blocks serum- and 12-O-tetradecanoyl phorbol 13-acetate-induced activation of Raf-1 kinase in NIH3T3 cells and Raf-1 as well as B-Raf PSK stimulation by nerve growth factor (NGF) in PC12 pheochromocytoma cells. Mitogen stimulation of Raf kinase was measured by determination of Raf hyperphosphorylation and activity towards exogenous substrates and both of these events were inhibited in cells expressing M17 Ras. In contrast, tyrosine phosphorylation of a direct substrate of activated tyrosine kinase receptors, phospholipase C-gamma-1 (PLC-gamma-1), was unaffected. These data indicate that tyrosine phosphorylation of PLC-gamma-1 is not sufficient for growth induction in NIH3T3 cells and that Ras mediates signal transfer from activated membrane receptors to Raf kinases in the cytosol. As activated Raf induced differentiation in PC12 cells expressing M17 Ras we conclude that Raf kinase activation may be sufficient to account for this aspect of NGF function. C1 NCI,VIRAL CARCINOGENESIS LAB,VIRAL PATHOL SECT,FREDERICK,MD 21702. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 45 TC 116 Z9 116 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD SEP PY 1992 VL 7 IS 9 BP 1867 EP 1873 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA JJ376 UT WOS:A1992JJ37600024 PM 1386920 ER PT J AU FLYNN, HW CHEW, EY SIMONS, BD BARTON, FB REMALEY, NA FERRIS, FL AF FLYNN, HW CHEW, EY SIMONS, BD BARTON, FB REMALEY, NA FERRIS, FL TI PARS-PLANA VITRECTOMY IN THE EARLY TREATMENT DIABETIC-RETINOPATHY STUDY - ETDRS REPORT NUMBER 17 SO OPHTHALMOLOGY LA English DT Article ID TRACTION RETINAL-DETACHMENT; NEOVASCULAR GLAUCOMA; VITREOUS HEMORRHAGE; COMPLICATIONS; MACULA AB Background. The Early Treatment Diabetic Retinopathy Study (ETDRS) enrolled 3711 patients with mild-to-severe nonproliferative or early proliferative diabetic retinopathy in both eyes. Patients were randomly assigned to aspirin 650 mg/day or placebo. One eye of each patient was assigned randomly to early photocoagulation and the other to deferral of photocoagulation. Follow-up examinations were scheduled at least every 4 months, and photocoagulation was initiated in eyes assigned to deferral as soon as high-risk proliferative retinopathy was detected. Aspirin was not found to have an effect on retinopathy progression or rates of vitreous hemorrhage. The risk of a combined end point, severe visual loss or vitrectomy, was low in eyes assigned to deferral (6% at 5 years) and was reduced by early photocoagulation (4% at 5 years). Vitrectomy was carried out in 208 patients during the 9 years of the study. This report presents baseline and previtrectomy characteristics and visual outcome in these patients. Methods: Information collected at baseline and during follow-up as part of the ETDRS protocol was supplemented by review of clinic charts for visual acuity and ocular status immediately before vitrectomy. Results: Vitrectomy was performed in 208 (5.6%) of the 3711 patients (243 eyes) enrolled in the ETDRS. The 5-year vitrectomy rates for eyes. grouped by their initial photocoagulation assignment were as follows: 2.1% in the early full scatter photocoagulation group, 2.5% in the early mild scatter group, and 4.0% in the deferral group. The 5-year rates of vitrectomy (in one or both eyes) were 5.4% in patients assigned to aspirin and 5.2% in patients assigned to a placebo. The indications for vitrectomy were either vitreous hemorrhage (53.9%) or retinal detachment with or without vitreous hemorrhage (46.1%). Before vitrectomy, visual acuity was 5/200 or worse in 66.7% of eyes and better than 20/100 in 6.2%. One year after vitrectomy, the visual acuity was 20/100 or better in 47.6% of eyes, including 24.0% with visual acuity of 20/40 or better. Conclusions: With frequent follow-up examinations and timely scatter (panretinal) photocoagulation, the 5-year cumulative rate of pars plana vitrectomy in ETDRS patients was 5.3%. Aspirin use did not influence the rate of vitrectomy. C1 UNIV MIAMI, SCH MED, BASCOM PALMER EYE INST, DEPT OPHTHALMOL, MIAMI, FL 33152 USA. MARYLAND MED RES INST, BALTIMORE, MD USA. RP FLYNN, HW (reprint author), NEI, BIOMETRY & EPIDEMIOL PROGRAM, BLDG 31, ROOM 6A24, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. FU Intramural NIH HHS [Z99 EY999999] NR 22 TC 77 Z9 82 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0161-6420 EI 1549-4713 J9 OPHTHALMOLOGY JI Ophthalmology PD SEP PY 1992 VL 99 IS 9 BP 1351 EP 1357 PG 7 WC Ophthalmology SC Ophthalmology GA JM227 UT WOS:A1992JM22700010 PM 1407968 ER PT J AU MAX, MB AF MAX, MB TI WHAT SHOULD MEDICAL-STUDENTS LEARN ABOUT PAIN SO PAIN LA English DT Editorial Material ID PHYSICIAN EDUCATION INTERVENTION; IMPROVE PRIMARY CARE; LOW-BACK-PAIN; IMPACT; SKILLS RP MAX, MB (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,PAIN RES CLIN,BLDG 10,ROOM 3C-405,BETHESDA,MD 20892, USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD SEP PY 1992 VL 50 IS 3 BP 249 EP 250 DI 10.1016/0304-3959(92)90027-9 PG 2 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA JQ383 UT WOS:A1992JQ38300001 PM 1454381 ER PT J AU REN, K HYLDEN, JLK WILLIAMS, GM RUDA, MA DUBNER, R AF REN, K HYLDEN, JLK WILLIAMS, GM RUDA, MA DUBNER, R TI THE EFFECTS OF A NONCOMPETITIVE NMDA RECEPTOR ANTAGONIST, MK-801, ON BEHAVIORAL HYPERALGESIA AND DORSAL HORN NEURONAL-ACTIVITY IN RATS WITH UNILATERAL INFLAMMATION SO PAIN LA English DT Article DE SPINAL DORSAL HORN; RECEPTIVE FIELD; INFLAMMATION; HYPERALGESIA; MK-801; COMPLETE FREUND ADJUVANT ID CUTANEOUS MECHANORECEPTIVE FIELDS; N-METHYLASPARTATE RECEPTORS; CENTRAL NERVOUS-SYSTEM; AMINO-ACID RECEPTORS; LUMBAR SPINAL-CORD; D-ASPARTIC ACID; SUBSTANCE-P; ENDOGENOUS GLUTAMATE; CONVERGENT NEURONS; AFFERENT TERMINALS AB The involvement of NMDA receptors in rats with peripheral inflammation and hyperalgesia was evaluated by administration of the non-competitive NMDA receptor antagonist, MK-801. Inflammation and hyperalgesia was induced by intradermal injection of complete Freund's adjuvant (CFA) or carrageenan into the left hind paw. The latency of paw withdrawal from a thermal stimulus was used as a measure of hyperalgesia in awake rats. MK-801 (1.6 mg/kg, i.p., or 31.5 mug, intrathecal) significantly attenuated thermal hyperalgesia and reduced its duration in comparison to saline-injected rats (P < 0.05). The receptive field size of nociceptive-specific and wide-dynamic-range neurons in the superficial and deep spinal dorsal horn recorded 24 h after injection of CFA was significantly reduced to 73 +/- 6% (P < 0.05, n = 8) and 74 +/- 4% (P < 0.05, n = 8) of control values, respectively, by a cumulative dose of 3 mg/kg of MK-801 (iv.). MK-801 (2 mg/kg) prevented the expansion of the receptive fields of dorsal horn neurons recorded 5 +/- 0.4 h (n = 5) after intradermal injection of CFA as compared to saline-injected rats (P < 0.05). MK-801 had no significant effect on receptive field size of dorsal horn neurons in rats without CFA-induced inflammation but blocked a transient expansion of the receptive fields induced by 1 Hz, C-fiber intensity electrical stimulation of the sciatic nerve. The background activity and noxious heat-evoked response of dorsal horn neurons in rats with CFA-induced inflammation were primarily inhibited and noxious pinch-evoked activity was both facilitated and inhibited by the administration of MK-801. These results support the hypothesis that NMDA receptors are involved in the dorsal horn neuronal plasticity and behavioral hyperalgesia that follows peripheral tissue inflammation. RP REN, K (reprint author), NIDR, NEUROBIOL & ANESTHESIOL BRANCH, BLDG 30, ROOM B-20, BETHESDA, MD 20892 USA. NR 71 TC 349 Z9 351 U1 0 U2 6 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD SEP PY 1992 VL 50 IS 3 BP 331 EP 344 DI 10.1016/0304-3959(92)90039-E PG 14 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA JQ383 UT WOS:A1992JQ38300013 PM 1454389 ER PT J AU TEIGEN, PM AF TEIGEN, PM TI THE HASKELL-F-NORMAN-LIBRARY-OF-SCIENCE-AND-MEDICINE - HOOK,DH, NORMAN,JM SO PAPERS OF THE BIBLIOGRAPHICAL SOCIETY OF AMERICA LA English DT Book Review RP TEIGEN, PM (reprint author), NATL LIB MED,DIV HIST MED,BETHESDA,MD 20894, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BIBLIOGRAPHICAL SOC AMER PI NEW YORK PA BOX 397 GRAND CENTRAL STATION, NEW YORK, NY 10163 SN 0006-128X J9 PAP BIBLIOGR SOC AM JI Pap. Bibliogra. Soc. Am. PD SEP PY 1992 VL 86 IS 3 BP 341 EP 344 PG 4 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA LH312 UT WOS:A1992LH31200004 ER PT J AU LENSEN, AHW VANGEMERT, GJA BOLMER, MG MEIS, JFGM KASLOW, D MEUWISSEN, JHET PONNUDURAI, T AF LENSEN, AHW VANGEMERT, GJA BOLMER, MG MEIS, JFGM KASLOW, D MEUWISSEN, JHET PONNUDURAI, T TI TRANSMISSION BLOCKING ANTIBODY OF THE PLASMODIUM-FALCIPARUM ZYGOTE OOKINETE SURFACE PROTEIN PFS25 ALSO INFLUENCES SPOROZOITE DEVELOPMENT SO PARASITE IMMUNOLOGY LA English DT Article DE MALARIA; PLASMODIUM-FALCIPARUM; TRANSMISSION BLOCKADE; SPOROZOITES ID ANOPHELES-STEPHENSI; MOSQUITOS; INFECTIVITY; SPOROGONY AB The Plasmodium falciparum zygote/ookinete surface protein, Pfs25, persists in the oocyst wall throughout its development. Anti-25 kD transmission blocking antibody, given to infected Anopheles stephensi or A. gambiae mosquitoes in an additional bloodmeal, 3-6 days after being fed gametocyte infected blood, penetrated the oocyst and reacted with the 25 kD protein within it. This reaction caused a significant reduction in the number of developing sporozoites. Mouse serum containing antibodies raised by immunization with a recombinant 25 kD yeast product showed a similar effect. C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. RP LENSEN, AHW (reprint author), CATHOLIC UNIV NIJMEGEN,DEPT PARASITOL,INST MED MICROBIOL,GEERT GROOTEPLEIN ZUID 24,6500 HB NIJMEGEN,NETHERLANDS. RI Meis, Jacques/A-9241-2010 OI Meis, Jacques/0000-0003-3253-6080 NR 15 TC 29 Z9 30 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0141-9838 J9 PARASITE IMMUNOL JI Parasite Immunol. PD SEP PY 1992 VL 14 IS 5 BP 471 EP 479 DI 10.1111/j.1365-3024.1992.tb00021.x PG 9 WC Immunology; Parasitology SC Immunology; Parasitology GA JN750 UT WOS:A1992JN75000002 PM 1437237 ER PT J AU KOZAKEWICH, H FOX, K PLATO, CC CRONK, C MANDELL, F VAWTER, GF AF KOZAKEWICH, H FOX, K PLATO, CC CRONK, C MANDELL, F VAWTER, GF TI DERMATOGLYPHICS IN SUDDEN-INFANT-DEATH-SYNDROME SO PEDIATRIC PATHOLOGY LA English DT Article DE SUDDEN INFANT DEATH SYNDROME; DERMATOGLYPHICS ID FETAL AB An analysis of digital and palmar dermatoglyphic patterns was conducted in 173 victims of the sudden infant death syndrome (SIDS). The results expose four dermatoglyphic regions with pattern frequencies differing from those in a control population. These are an excess of Sydney creases, hypothenar patterns, open fields (with fewer vestiges) in interdigital region IV, and arches on all digits (females only). These findings indicate a genetic or early intrauterine environmental influence in SIDS infants. An increased incidence of dysmorphism and anomalies including recognition of specific syndromes support this contention. One could speculate that these dermatoglyphic deviations reflect specific genotypes and/or phenotypes particularly vulnerable to postnatal challenges. Differences in multiple dermatoglyphic categories support the concept of heterogeneity of the SIDS population and multicausality of SIDS. C1 UNIV MARYLAND,DEPT EPIDEMIOL & PREVENT MED,BALTIMORE,MD 21201. NIH,GERONTOL RES CTR,BALTIMORE,MD 21224. SO ILLINOIS UNIV,DEPT ANTHROPOL,CARBONDALE,IL 62901. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP KOZAKEWICH, H (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PATHOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 35 TC 1 Z9 3 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0277-0938 J9 PEDIATR PATHOL PD SEP-OCT PY 1992 VL 12 IS 5 BP 637 EP 651 PG 15 WC Pathology; Pediatrics SC Pathology; Pediatrics GA JP743 UT WOS:A1992JP74300002 PM 1437876 ER PT J AU CRYSTAL, RG AF CRYSTAL, RG TI INVIVO GENE-TRANSFER STRATEGIES FOR THE RESPIRATORY MANIFESTATIONS OF CYSTIC-FIBROSIS SO PEDIATRIC PULMONOLOGY LA English DT Article; Proceedings Paper CT 6TH ANNUAL NORTH AMERICAN CONF ON CYSTIC FIBROSIS CY OCT 15-18, 1992 CL WASHINGTON, DC SP CYSTIC FIBROSIS FDN, GLAXO, MCNEIL PHARM, SOLVAY PHARM, BAXTER HLTH, GENENTECH, DEVILBISS HLTH CARE, INTEGRATED GENET, MEDICANA, MENLO CARE RP CRYSTAL, RG (reprint author), NHLBI,PULM BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 8755-6863 J9 PEDIATR PULM JI Pediatr. Pulmonol. PD SEP PY 1992 SU 8 BP 67 EP 67 PG 1 WC Pediatrics; Respiratory System SC Pediatrics; Respiratory System GA JM110 UT WOS:A1992JM11000004 ER PT J AU AMOS, JA OATES, RD DEAN, M ANGUIANO, A BEJJANI, B GERRARD, B MAHER, TA MICKLE, JE STEWART, C MILUNSKY, A AF AMOS, JA OATES, RD DEAN, M ANGUIANO, A BEJJANI, B GERRARD, B MAHER, TA MICKLE, JE STEWART, C MILUNSKY, A TI CONGENITAL ABSENCE OF THE VAS-DEFERENS - A PRIMARILY GENITAL FORM OF CYSTIC-FIBROSIS SO PEDIATRIC PULMONOLOGY LA English DT Article; Proceedings Paper CT 6TH ANNUAL NORTH AMERICAN CONF ON CYSTIC FIBROSIS CY OCT 15-18, 1992 CL WASHINGTON, DC SP CYSTIC FIBROSIS FDN, GLAXO, MCNEIL PHARM, SOLVAY PHARM, BAXTER HLTH, GENENTECH, DEVILBISS HLTH CARE, INTEGRATED GENET, MEDICANA, MENLO CARE C1 BOSTON UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT UROL,BOSTON,MA 02118. NCI,VIRAL CARCINOGENESIS LAB,BETHESDA,MD 20892. RP AMOS, JA (reprint author), BOSTON UNIV,SCH MED,CTR HUMAN GENET,BOSTON,MA 02118, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 8755-6863 J9 PEDIATR PULM JI Pediatr. Pulmonol. PD SEP PY 1992 SU 8 BP 142 EP 143 PG 2 WC Pediatrics; Respiratory System SC Pediatrics; Respiratory System GA JM110 UT WOS:A1992JM11000043 ER PT J AU POLLARD, H AF POLLARD, H TI EXOCYTOSIS - CALCIUM, CAMP, ANNEXINS AND CFTR SO PEDIATRIC PULMONOLOGY LA English DT Article; Proceedings Paper CT 6TH ANNUAL NORTH AMERICAN CONF ON CYSTIC FIBROSIS CY OCT 15-18, 1992 CL WASHINGTON, DC SP CYSTIC FIBROSIS FDN, GLAXO, MCNEIL PHARM, SOLVAY PHARM, BAXTER HLTH, GENENTECH, DEVILBISS HLTH CARE, INTEGRATED GENET, MEDICANA, MENLO CARE RP POLLARD, H (reprint author), NIDDK,CELL BIOL & GENET,BETHESDA,MD 20892, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 8755-6863 J9 PEDIATR PULM JI Pediatr. Pulmonol. PD SEP PY 1992 SU 8 BP 202 EP 203 PG 2 WC Pediatrics; Respiratory System SC Pediatrics; Respiratory System GA JM110 UT WOS:A1992JM11000074 ER PT J AU AHMED, F CLEMENS, JD RAO, MR SACK, DA KHAN, MR HAQUE, E AF AHMED, F CLEMENS, JD RAO, MR SACK, DA KHAN, MR HAQUE, E TI COMMUNITY-BASED EVALUATION OF THE EFFECT OF BREAST-FEEDING ON THE RISK OF MICROBIOLOGICALLY CONFIRMED OR CLINICALLY PRESUMPTIVE SHIGELLOSIS IN BANGLADESHI CHILDREN SO PEDIATRICS LA English DT Article DE BREAST-FEEDING; DIARRHEA; DYSENTERY; SHIGELLA ID RURAL BANGLADESH; HUMAN-MILK; SALMONELLA; ANTIBODIES; DIARRHEA; FIELD AB To assess the association between breast-feeding and the risk of microbiologically confirmed or clinically presumptive shigellosis, the authors performed a case-control analysis of Bangladeshi children younger than 3 years of age who were followed up for 1 month after exposure to Shigella in their residential neighborhoods. Two hundred sixty-nine cases with culture-confirmed shigellosis (n = 119) or clinically presumptive shigellosis (culture-negative dysentery, n = 150) were compared with 819 controls without Shigella diarrhea or other invasive diarrheal illnesses. The odds ratio relating breast-feeding to confirmed or presumptive shigellosis, adjusted for potentially confounding variables, was 0.48 (95% confidence interval = 0.32 to 0.72; P < .001), suggesting a substantial protective effect. The protective association decreased with age but was still significant during the third year of life, appeared to be directly related to the degree of stunting; and was equivalent for confirmed and presumptive shigellosis. Notably, the protective association remained substantial against episodes due to Shigella which were resistant to at least one of the antibiotics customarily used for treatment of Shigella diarrhea (age-adjusted odds ratio = 0.40, 95% confidence interval = 0.22 to 0.74; P < .01). These data suggest that breast-feeding confers a high level of protection against shigellosis throughout the first 3 years of life, especially among nutritionally compromised children, and thereby underscore the importance of promotion of breast-feeding as a central component of Shigella control programs in less developed settings. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,6100 EXECUT PLAZA BLDG,BETHESDA,MD 20892. INT CTR DIARRHOEAL DIS RES,DHAKA,BANGLADESH. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT INT HLTH,BALTIMORE,MD 21218. NR 28 TC 39 Z9 39 U1 1 U2 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD SEP PY 1992 VL 90 IS 3 BP 406 EP 411 PG 6 WC Pediatrics SC Pediatrics GA JM412 UT WOS:A1992JM41200015 PM 1518697 ER PT J AU ANDRICH, MP MAJD, M AF ANDRICH, MP MAJD, M TI DIAGNOSTIC-IMAGING IN THE EVALUATION OF THE 1ST URINARY-TRACT INFECTION IN INFANTS AND YOUNG-CHILDREN SO PEDIATRICS LA English DT Article DE URINARY TRACT INFECTION; PYELONEPHRITIS; VESICOURETERAL REFLUX; CYSTOGRAPHY; RENAL CORTICAL SCINTIGRAPHY; OBSTRUCTIVE UROPATHY ID TC-99M DIMERCAPTOSUCCINIC ACID; VESICOURETERAL REFLUX; ACUTE PYELONEPHRITIS; RADIONUCLIDE CYSTOGRAPHY; ESCHERICHIA-COLI; RENAL SCARS; SCINTIGRAPHY; DMSA; NEPHROPATHY; PREVENTION AB The evaluation of infants and children after the first urinary tract infection has undergone change in recent years. Standard diagnostic imaging studies are being utilized on a more frequent basis, because these procedures can provide information which often has a direct impact on patient care. Selection of the proper tests requires an understanding of how they are performed and the basis for their choice. The rationale for the use of different imaging studies and their application to patient care are discussed. C1 CHILDRENS NATL MED CTR,DEPT DIAGNOST IMAGING & RADIOL,111 MICHIGAN AVE NW,WASHINGTON,DC 20010. NIH,WARREN G MAGNUSON CLIN CTR,DEPT NUCL MED,BETHESDA,MD 20892. NR 36 TC 45 Z9 45 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD SEP PY 1992 VL 90 IS 3 BP 436 EP 441 PG 6 WC Pediatrics SC Pediatrics GA JM412 UT WOS:A1992JM41200021 PM 1518703 ER PT J AU MUELLER, BU BUTLER, KM HIGHAM, MC HUSSON, RN MONTRELLA, KA PIZZO, PA FEUERSTEIN, IM MANJUNATH, K AF MUELLER, BU BUTLER, KM HIGHAM, MC HUSSON, RN MONTRELLA, KA PIZZO, PA FEUERSTEIN, IM MANJUNATH, K TI SMOOTH-MUSCLE TUMORS IN CHILDREN WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO PEDIATRICS LA English DT Article ID IMMUNE-DEFICIENCY-SYNDROME; CENTRAL-NERVOUS-SYSTEM; KAPOSIS-SARCOMA; PRIMARY LYMPHOMA; HIV INFECTION; AIDS; PATIENT; THERAPY; LEIOMYOSARCOMA; ZIDOVUDINE C1 NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N24O,BETHESDA,MD 20892. NIH,CTR DIAGNOST RADIOL CLIN,BETHESDA,MD 20892. GEORGETOWN UNIV HOSP,WASHINGTON,DC 20007. ALBANY MED CTR,DEPT PEDIAT,ALBANY,NY. NR 44 TC 56 Z9 57 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD SEP PY 1992 VL 90 IS 3 BP 460 EP 463 PG 4 WC Pediatrics SC Pediatrics GA JM412 UT WOS:A1992JM41200026 PM 1518708 ER PT J AU KLEINMAN, RE BAKER, SS BELL, EF HATCH, TF KLISH, WJ LEIBEL, RL UDALL, JN BENSON, JD LIEN, E THEUER, RC CHENEY, M CHOPRA, J DANIELS, PN HARRIS, SS HUBBARD, VS LEVIN, E PRENDERGAST, A STEMARIE, M SMITH, AE YIP, R LAUER, RM AF KLEINMAN, RE BAKER, SS BELL, EF HATCH, TF KLISH, WJ LEIBEL, RL UDALL, JN BENSON, JD LIEN, E THEUER, RC CHENEY, M CHOPRA, J DANIELS, PN HARRIS, SS HUBBARD, VS LEVIN, E PRENDERGAST, A STEMARIE, M SMITH, AE YIP, R LAUER, RM TI STATEMENT ON CHOLESTEROL SO PEDIATRICS LA English DT Article ID BOGALUSA HEART; CARDIOVASCULAR-DISEASE; PRIMARY PREVENTION; CHILDHOOD; HYPERCHOLESTEROLEMIA; ATHEROSCLEROSIS; LIPOPROTEIN; CHILDREN; DIETARY; HISTORY C1 BUR NUTR SCI,OTTAWA,ONTARIO,CANADA. US FDA,WASHINGTON,DC 20204. USDA,WASHINGTON,DC 20250. INT LIFE SCI INST,WASHINGTON,DC. NATL INST DIABETES DIGEST & KIDNEY DIS,BETHESDA,MD. NICHHD,BETHESDA,MD 20892. CTR DIS CONTROL,ATLANTA,GA 30333. CANADIAN PAEDIAT SOC,OTTAWA,ONTARIO,CANADA. AMER DIETET ASSOC,CHICAGO,IL. NR 32 TC 86 Z9 91 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD SEP PY 1992 VL 90 IS 3 BP 469 EP 473 PG 5 WC Pediatrics SC Pediatrics GA JM412 UT WOS:A1992JM41200030 ER PT J AU ROTHMAN, RB BYKOV, V XUE, BG XU, H DECOSTA, BR JACOBSON, AE RICE, KC KLEINMAN, JE BRADY, LS AF ROTHMAN, RB BYKOV, V XUE, BG XU, H DECOSTA, BR JACOBSON, AE RICE, KC KLEINMAN, JE BRADY, LS TI INTERACTION OF OPIOID-PEPTIDES AND OTHER DRUGS WITH MULTIPLE KAPPA-RECEPTORS IN RAT AND HUMAN BRAIN - EVIDENCE FOR SPECIES-DIFFERENCES SO PEPTIDES LA English DT Article DE OPIOID RECEPTORS; KAPPA RECEPTORS; U69,593; LIGAND BINDING STUDIES; AUTORADIOGRAPHY ID GUINEA-PIG BRAIN; OPIATE BINDING-SITES; BOVINE ADRENAL-MEDULLA; SPINAL-CORD; DELTA-OPIATE; AFFINITY STATES; LIGAND-BINDING; MU-OPIATE; AGONIST; MEMBRANES AB Previous experiments resolved four kappa binding sites in guinea pig brain terMed kappa1a, kappa1b, kappa2a, and kappa2b. The present study was undertaken to examine the occurrence of kappa receptor subtypes in rat and human brain. [H-3]U69,593 and [H-3]bremazocine were used to label kappa1 and kappa2 binding sites. respectively, present in brain membranes depleted of mu and delta binding sites by pretreatment with the irreversible ligands, BIT and FIT. Low levels of [H-3]U69,593 binding precluded a detailed quantitative study of kappa1 binding sites in these species. Quantitative examination of [H-3]bremazocine binding resolved two kappa2 binding sites in both rat and human brain whose ligand selectivity patterns differed from that of the guinea pig. These observations suggest that there may be considerable variation in the ligand recognition site Of kappa receptor subtypes among mammalian species. C1 NIDDK,MED CHEM,BETHESDA,MD 20892. ST ELIZABETH HOSP,NIMH,WILLIAM A WHITE CTR NEUROSCI,WASHINGTON,DC 20032. NIMH,FUNCT NEUROANAT SECT,BETHESDA,MD 20892. UNIV CALIF IRVINE,IRVINE,CA 92717. RP ROTHMAN, RB (reprint author), NIDA,ADDICT RES CTR,CLIN PSYCHOPHARMACOL SECT,POB 5180,BALTIMORE,MD 21224, USA. NR 47 TC 46 Z9 50 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0196-9781 J9 PEPTIDES JI Peptides PD SEP-OCT PY 1992 VL 13 IS 5 BP 977 EP 987 DI 10.1016/0196-9781(92)90059-C PG 11 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Pharmacology & Pharmacy GA JY481 UT WOS:A1992JY48100020 PM 1336192 ER PT J AU KENAKIN, TP BOND, RA BONNER, TI AF KENAKIN, TP BOND, RA BONNER, TI TI DEFINITION OF PHARMACOLOGICAL RECEPTORS SO PHARMACOLOGICAL REVIEWS LA English DT Review ID MUSCARINIC ACETYLCHOLINE-RECEPTOR; BETA-ADRENERGIC-RECEPTOR; OPIOID RECEPTORS; ALPHA-2-ADRENERGIC RECEPTOR; RESULTANT ANALYSIS; ADENYLATE-CYCLASE; BINDING PROTEINS; AGONIST AFFINITY; BRAIN; CLASSIFICATION C1 BAYLOR COLL MED,CTR EXPTL THERAPEUT,HOUSTON,TX 77030. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP KENAKIN, TP (reprint author), GLAXO RES INST,DIV PHARMACOL,RES TRIANGLE PK,NC 27709, USA. NR 61 TC 110 Z9 111 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-6997 J9 PHARMACOL REV JI Pharmacol. Rev. PD SEP PY 1992 VL 44 IS 3 BP 351 EP 362 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JQ156 UT WOS:A1992JQ15600002 PM 1438521 ER PT J AU UHDE, TW MALLOY, LC SLATE, SO AF UHDE, TW MALLOY, LC SLATE, SO TI FEARFUL BEHAVIOR, BODY SIZE, AND SERUM IGF-I LEVELS IN NERVOUS AND NORMAL POINTER DOGS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE ANIMAL BEHAVIOR; ANXIETY DISORDERS; BODY SIZE; BODY WEIGHT; DOGS; GENDER DIFFERENCES; GROWTH; INSULIN-LIKE GROWTH FACTOR-I SOMATOMEDIN-C ID GROWTH FACTOR-I; ADENOSINE RECEPTOR ALTERATIONS; THYROTROPIN-RELEASING-HORMONE; PANIC DISORDER; HYPOPHYSECTOMIZED RATS; SOMATOMEDIN ACTIVITY; DEPRESSION; CLONIDINE; RESPONSES; ANXIETY AB Panic disorder in adult humans is associated with disturbances in hypothalamic-growth hormone (GH) function and children with emotional deprivation or severe anxiety develop growth retardation. Nervous pointer dogs, a genetic animal model of panic disorder or severe anxiety, are characterized by extreme fearfulness and avoidance of novel stimuli. This experiment investigated indices of body stature, weight, and insulin-like growth factor I (IGF-I) levels in a colony of purebred nervous and purebred normal pointer dogs. The genetic line of nervous dogs had significantly greater scores of fearfulness, lower total body weights, lower weight/height ratio, and lower serum IGF-I levels than the normal line of pointer dogs. There was an inverse relationship between degree of fearfulness and total body weight in female, but not male, dogs. Stepwise logistic regression analysis indicated that the severity of fear behaviors, height, and weight were significantly associated with IGF-I levels. The best predictor of IGF-I levels in the dogs, however, was the severity of fearful behaviors elicited by exposure to novel stimuli and humans. These observations suggest that the neurobiological substrates of alarm, arousal, and fear influence hypothalamic-GH-somatomedin-mediated effects on weight and, to a lesser extent, height. Findings are discussed in terms of their relevance to future research in humans with anxiety disorders. RP UHDE, TW (reprint author), NIMH,BIOL PSYCHIAT BRANCH,INTRAMURAL RES PROGRAM,ANXIETY & AFFECT DISORDERS SECT,BETHESDA,MD 20892, USA. NR 45 TC 15 Z9 15 U1 7 U2 13 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD SEP PY 1992 VL 43 IS 1 BP 263 EP 269 DI 10.1016/0091-3057(92)90667-5 PG 7 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA JK367 UT WOS:A1992JK36700034 PM 1409812 ER PT J AU CROWELL, MD MUSIAL, F FRENCH, W KITTUR, D ANDERSON, D WHITEHEAD, WE AF CROWELL, MD MUSIAL, F FRENCH, W KITTUR, D ANDERSON, D WHITEHEAD, WE TI PROLONGED AMBULATORY MONITORING OF COLONIC MOTOR-ACTIVITY IN THE PIG SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE PIGS; AMBULATORY MONITORING; MOTILITY; PROLONGED RECORDING ID YUCATAN MINIATURE PIG; INTESTINE AB The aim of this study was to develop a chronic model suitable for repeated, long-term studies of the interaction of behavior and colonic function in unrestrained pigs. Cecostomies were created in three 20-30 kg micropigs under general anesthesia. Fistulas were created by suturing the bowel to the abdominal wall. Recordings were made by passing a small (8F) solid-state pressure transducer through the fistula into the proximal bowel and connecting it to a battery-operated data logger worn in a vest on the pig's back. Cecostomies have remained patent and trouble-free for over 18 months. No serious infections have occurred. Preliminary data from a total of thirteen 24-h recording sessions showed 54% of all contractile activity to be in the 2-4 cpm frequency range. Increased motility was seen following meals and upon morning awakening. Motility was minimal during the night. Infrequent (10.31 +/- 2.05/24 h; mean +/-SD) propagated contractions were also noted. These contractions were generally of low amplitude (33.24 +/- 3.81 mmHg). These techniques allow prolonged, intraluminal recordings to be made from the colon of the unrestrained pig. C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. OI Crowell, Michael/0000-0002-1162-3831 NR 11 TC 15 Z9 15 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD SEP PY 1992 VL 52 IS 3 BP 471 EP 474 DI 10.1016/0031-9384(92)90332-V PG 4 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA JL838 UT WOS:A1992JL83800008 PM 1409906 ER PT J AU SHRAYER, D GERSTEN, DM KONESS, J MAIZEL, A WANEBO, H HEARING, VJ AF SHRAYER, D GERSTEN, DM KONESS, J MAIZEL, A WANEBO, H HEARING, VJ TI B700 ANTIGEN AS A COMPONENT OF AN ANTIMELANOMA VACCINE - FORMALINIZED EXTRACELLULAR ANTIGENS SO PIGMENT CELL RESEARCH LA English DT Article DE MELANOMA; ANTIGENS; ANTIBODIES; VACCINATION ID ACTIVE-SPECIFIC IMMUNOTHERAPY; PURIFIED GM2 GANGLIOSIDE; MELANOMA PATIENTS; TUMOR REJECTION; ANTIBODIES AB Formalin fixation has enjoyed widespread use in the preparation of antibacterial and other vaccines, but rather less use in antitumor vaccines. Previous studies from our laboratories have demonstrated the efficacy of antimelanoma vaccines in mice, produced from formalinized antigens shed by cultured melanoma cells. In this study, we provide evidence that the immunodominant component of that vaccine is the well-characterized B700 melanoma antigen. C1 GEORGETOWN UNIV, MED CTR, DEPT PATHOL, WASHINGTON, DC 20007 USA. BROWN UNIV, ROGER WILLIAMS MED CTR, DEPT SURG, PROVIDENCE, RI 02912 USA. NCI, CELL BIOL LAB, BETHESDA, MD 20892 USA. RP SHRAYER, D (reprint author), BROWN UNIV, ROGER WILLIAMS MED CTR, DEPT EXPTL PATHOL, PROVIDENCE, RI 02908 USA. NR 20 TC 11 Z9 11 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0893-5785 J9 PIGM CELL RES JI Pigm. Cell. Res. PD SEP PY 1992 VL 5 IS 3 BP 107 EP 112 DI 10.1111/j.1600-0749.1992.tb00006.x PG 6 WC Cell Biology; Dermatology SC Cell Biology; Dermatology GA JK873 UT WOS:A1992JK87300002 PM 1409447 ER PT J AU RIPAMONTI, U MA, SS VANDENHEEVER, B REDDI, AH AF RIPAMONTI, U MA, SS VANDENHEEVER, B REDDI, AH TI OSTEOGENIN, A BONE MORPHOGENETIC PROTEIN, ADSORBED ON POROUS HYDROXYAPATITE SUBSTRATA, INDUCES RAPID BONE DIFFERENTIATION IN CALVARIAL DEFECTS OF ADULT PRIMATES SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article AB Osteogenin, a bone morphogenetic protein, in conjunction with insoluble collagenous bone matrix initiates local endochondral bone differentiation by induction in vivo. This study, by exploiting the affinity of native osteogenin for hydroxyapatite, was designed to construct a delivery system for the expression of the biologic activity of osteogenin in nonhealing calvarial defects of adult primates. After exposure of the calvaria, 64 cranial defects, 25 mm in diameter, were prepared in 16 adult male baboons (Papio ursinus). Defects were implanted with disks of porous nonresorbable and resorbable hydroxyapatite substrata obtained after hydrothermal conversion of calcium carbonate exoskeletons of corals. In each animal, one disk of each hydroxyapatite preparation was treated with osteogenin isolated and purified from baboon bone matrix after sequential chromatography on heparin-Sepharose, hydroxyapatite, and Sephacryl S-200 gel filtration columns. The remaining two defects were implanted with one disk of each hydroxyapatite preparation without osteogenin as control. Histomorphometry on decalcified sections prepared on days 30 and 90 showed superior osteogenesis in osteogenin-treated nonresorbable hydroxyapatite specimens as compared with controls. On day 90, substantial bone formation also had occurred in control nonresorbable hydroxyapatite specimens. On day 90, but not on day 30, significantly greater amounts of bone had formed in osteogenin-treated resorbable specimens as compared with resorbable controls. Overall, resorbable substrata performed poorly when compared with nonresorbable substrata, perhaps due to a premature dissolution of the implants. These results provide evidence that the biologic activity of osteogenin can be restored and delivered by a substratum other than the organic collagenous matrix, inducing rapid bone differentiation in calvarial defects of adult nonhuman primates. The adsorption strategy of osteogenin on porous inorganic nonimmunogenic substrata may help to design appropriate osteogenic delivery systems for craniofacial and orthopedic applications in humans. C1 NIDR,DENT RES INST,BONE CELL BIOL SECT,BETHESDA,MD 20892. RP RIPAMONTI, U (reprint author), UNIV WITWATERSRAND,MRC,DENT RES INST,JOHANNESBURG 2050,SOUTH AFRICA. NR 29 TC 131 Z9 132 U1 1 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD SEP PY 1992 VL 90 IS 3 BP 382 EP 393 PG 12 WC Surgery SC Surgery GA JL532 UT WOS:A1992JL53200004 PM 1325064 ER PT J AU LANGE, WR WHITE, N ROBINSON, N AF LANGE, WR WHITE, N ROBINSON, N TI MEDICAL COMPLICATIONS OF SUBSTANCE-ABUSE SO POSTGRADUATE MEDICINE LA English DT Article ID RISK FACTOR; DRUG-ABUSE; COCAINE; CARDIOMYOPATHY; MARIJUANA; ALCOHOL AB Substance abuse is involved in many instances of intentional and unintentional injury. It can also cause medical complications that affect various organ systems-among them, the cardiac, vascular, neurologic, pulmonary, gastrointestinal immunologic, and reproductive systems. Even though there is pressure to create a new medical specialty to specifically address substance-abuse issues, the truth is that any physician, regardless of specialty, may encounter patients with substance-abuse problems. Alcoholism and drug abuse, with their associated psychosocial and dinical ramifications and complications, cut across all specialty fields. Consequently, all physicians need to be familiar with the spectrum of clinical problems associated with substance abuse and comfortable with addressing these problems prudently and promptly, C1 JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. RP LANGE, WR (reprint author), JOHNS HOPKINS UNIV,NIDR,ADDICT RES CTR,BAYVIEW RES CAMPUS,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 37 TC 7 Z9 7 U1 1 U2 1 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 0032-5481 J9 POSTGRAD MED JI Postgrad. Med. PD SEP 1 PY 1992 VL 92 IS 3 BP 205 EP & PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA JM908 UT WOS:A1992JM90800017 PM 1518754 ER PT J AU GRALNICK, HR WILLIAMS, S MCKEOWN, L KRAMER, W KRUTZSCH, H GORECKI, M PINET, A GARFINKEL, LI AF GRALNICK, HR WILLIAMS, S MCKEOWN, L KRAMER, W KRUTZSCH, H GORECKI, M PINET, A GARFINKEL, LI TI A MONOMERIC VONWILLEBRAND-FACTOR FRAGMENT, LEU-504-SER-728, INHIBITS VONWILLEBRAND-FACTOR INTERACTION WITH GLYCOPROTEIN-IB-IX SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE GLYCOPROTEIN-IB; THROMBOSIS ID VON-WILLEBRAND FACTOR; MURINE MONOCLONAL-ANTIBODY; ESCHERICHIA-COLI; BINDING DOMAIN; PLATELET-AGGREGATION; VENOM COAGGLUTININ; CORONARY-ARTERIES; SHEAR-STRESS; DISEASE; COLLAGEN AB von Willebrand factor interaction with glycoprotein Ib(alpha) (GPIb(alpha)) plays a critical role in the initial phase of platelet adhesion at high shear rates, and it may also play a role in platelet thrombus formation in partially occluded arteries. Previous studies have indicated that two peptides, Cys-474-Pro-488 (peptide 153) and Ser-692-Pro-708 (peptide 154), inhibit von Willebrand factor-GPIb(alpha) interaction. We have expressed a recombinant fragment of von Willebrand factor, Leu-504-Ser-728, with a single intrachain disulfide bond linking residues Cys-509-Cys-695 and examined its ability to inhibit von Willebrand factor-GPIb(alpha) interactions and platelet adhesion at high shear forces. This recombinant fragment, named VCL, inhibits ristocetin-induced, botrocetin-induced, and asialo-von Willebrand factor-induced platelet aggregation and binding to platelets at an IC50 = 0.011-0.260-mu-M, significantly lower than the IC50 of peptide 153 or 154, IC50 = 86-700-mu-M. Peptides 153 and 154 did not result in any inhibition of platelet adhesion (IC50 > 500-mu-M). In contrast, VCL inhibited 50% of platelet adhesion at 0.94-mu-M and at 7.6-mu-M inhibited > 80% of platelet adhesion to human umbilical artery subendothelium at high shear forces. VCL inhibited the contact and spreading of platelets and also caused a marked decrease in thrombus formation. These studies indicate that VCL may be an effective antithrombotic agent in preventing arterial thrombus formation in areas of high shear force. C1 NCI,PATHOL LAB,BETHESDA,MD 20892. BIOTECHNOL GEN LTD,REHOVOT,ISRAEL. RP GRALNICK, HR (reprint author), NIH,HEMATOL SERV,BLDG 10,ROOM 2C390,BETHESDA,MD 20892, USA. NR 42 TC 57 Z9 57 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD SEP 1 PY 1992 VL 89 IS 17 BP 7880 EP 7884 DI 10.1073/pnas.89.17.7880 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL614 UT WOS:A1992JL61400007 PM 1518808 ER PT J AU HAGUE, BF SAWASDIKOSOL, S BROWN, TJ LEE, K RECKER, DP KINDT, TJ AF HAGUE, BF SAWASDIKOSOL, S BROWN, TJ LEE, K RECKER, DP KINDT, TJ TI CD4 AND ITS ROLE IN INFECTION OF RABBIT-CELL LINES BY HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID SOLUBLE CD4; T-CELL; HIV-1 INFECTION; SYNCYTIUM FORMATION; BINDING-SITE; ANTIGEN; PROTEIN; BRAIN; AIDS; RETROVIRUS AB Human CD4 (HuCD4) is the principal receptor for human immunodeficiency virus type 1 (HIV-1) in human cell infection. Susceptibility of rabbit cell lines to infection with HIV-1 raised questions concerning whether a CD4 homolog serves as HIV-1 receptor on rabbit cells. Sequence comparisons of rabbit CD4 (RbCD4) cloned from a rabbit thymus cDNA library showed that 6 of the 18 residues implicated in HIV-1 binding by CD4 differ between the human and rabbit proteins. No correlation between RbCD4 expression by rabbit cell lines and their ability to support HIV-1 infection was seen. Transfection of RbCD4-negative, HTLV-1-transformed cell lines with HuCD4 significantly enhanced HIV-1 infectivity, suggesting that these lines lack a receptor present on other RbCD4-negative lines that produce high levels of p24 in their native state. Inhibition of HIV-1 infection with soluble HuCD4 was demonstrated for all rabbit lines tested, but complete inhibition was obtained only with a rabbit T-cell line expressing RbCD4 and with HuCD4 transfectants. The results suggest that HIV-1 infection of the RbCD4-positive line proceeds through a receptor similar to HuCD4 but that an additional receptor or receptors may serve this purpose in RbCD4-negative lines. RP HAGUE, BF (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK 2 FACIL,12441 PARKLAWN DR,BETHESDA,MD 20892, USA. NR 48 TC 29 Z9 30 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD SEP 1 PY 1992 VL 89 IS 17 BP 7963 EP 7967 DI 10.1073/pnas.89.17.7963 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL614 UT WOS:A1992JL61400024 PM 1518821 ER PT J AU COHEN, JI AF COHEN, JI TI A REGION OF HERPES-SIMPLEX VIRUS VP16 CAN SUBSTITUTE FOR A TRANSFORMING DOMAIN OF EPSTEIN-BARR-VIRUS NUCLEAR PROTEIN-2 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HERPESVIRUS; TRANSCRIPTION; TRANSACTIVATION ID LARGE T-ANTIGEN; TRANSCRIPTIONAL ACTIVATOR; LYMPHOCYTES-B; EXPRESSION; CD23; DNA; SEQUENCE; EBNA-2; GENOME; LMP1 AB Epstein-Barr virus (EBV) nuclear protein 2 (EBNA-2) is essential for EBV-induced B-cell transformation in vitro. EBNA-2 contains a 14-amino acid domain that directly activates transcription and is required for transformation. To determine whether another transcriptional activator can substitute for this function, a chimeric virus was constructed that contained a portion of the transcriptional activation domain from the herpes simplex virus VP16 protein inserted in place of the 14-amino acid domain of EBNA-2. The chimeric virus was able to transform B cells efficiently and transactivate expression of EBV and B-cell genes. Randomization of the 14-amino acid sequence in the domain markedly reduced its transcriptional activating activity and the transforming efficiency of the recombinant EBV. Mutation of a tryptophan within the 14-amino acid domain of EBNA-2 completely abolished transcriptional activation and B-cell transformation. These experiments indicate that EBNA-2 and VP16 activate transcription by similar mechanisms and that transcriptional activation is required for EBV-induced B-cell transformation. RP COHEN, JI (reprint author), NIH,CLIN INVEST LAB,BETHESDA,MD 20892, USA. NR 24 TC 44 Z9 45 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD SEP 1 PY 1992 VL 89 IS 17 BP 8030 EP 8034 DI 10.1073/pnas.89.17.8030 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL614 UT WOS:A1992JL61400038 PM 1325641 ER PT J AU SIEGFRIED, JM KASPRZYK, PG TRESTON, AM MULSHINE, JL QUINN, KA CUTTITTA, F AF SIEGFRIED, JM KASPRZYK, PG TRESTON, AM MULSHINE, JL QUINN, KA CUTTITTA, F TI A MITOGENIC PEPTIDE AMIDE ENCODED WITHIN THE E-PEPTIDE DOMAIN OF THE INSULIN-LIKE GROWTH FACTOR-IB PROHORMONE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CELL LUNG-CANCER; FACTOR MESSENGER-RNA; SOMATOMEDIN-C; HUMAN-LIVER; GENE; PRECURSOR; RECEPTORS; BOMBESIN; BIOSYNTHESIS; ORGANIZATION AB We have identified an amino acid sequence within the E peptide of the insulin-like growth factor IB (IGF-IB) precursor that is biologically active and designated this peptide insulin-like growth factor IB-(103-124) E1 amide (IBE1). Its existence was predicted by a flanking Gly-Lys-Lys-Lys, a signal sequence for sequential proteolytic cleavage and peptidyl C-terminal amidation. A synthetic analog of the predicted IBE1 peptide, designated Y-23-R-NH2, was generated with tyrosine added at position 0. This peptide at 2-20 nM had growth-promoting effects on both normal and malignant human bronchial epithelial cells. Y-23-R-NH2 bound to specific high-affinity receptors (K(d) = 2.8 +/- 1.4 x 10(-11) M) present at 1-2 x 10(4) binding sites per cell. Ligand binding was not inhibited by recombinant insulin or recombinant IGF-I. Furthermore, a monoclonal antibody antagonist to the IGF-I receptor (alpha-IR3) did not suppress the proliferative response induced by Y-23-R-NH2. In addition, C-terminal amidation was shown to be important in receptor recognition since the free-acid analog of IBE1 (Y-23-R-OH) did not effectively compete for binding and was not a potent agonist of proliferation. Immunoblot analysis of human lung tumor cell line extracts using an antibody raised against Y-23-R-NH2 detected a low molecular mass band of almost-equal-to 5 kDa, implying that a protein product is produced that has immunological similarity to IBE1. Extracts of human, mammalian, and avian livers analyzed on an immunoblot with the anti-Y-23-R-NH2 antibody contained proteins of almost-equal-to 21 kDa that were specifically recognized by the antiserum and presumably represent an IGF-I precursor molecule. This implies that in species where an IGF-I mRNA with homology to the human IGF-IB E domain has not yet been described, an alternate mRNA must be produced that contains a sequence similar to that of the midportion of the human IGF-IB E domain. Our findings demonstrate that IBE1 is a growth factor that mediates its effect through a specific high-affinity receptor and is most likely conserved in many species. C1 MOLEC ONCOL INC,GAITHERSBURG,MD 20878. NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,KENSINGTON,MD 20895. RP SIEGFRIED, JM (reprint author), UNIV PITTSBURGH,DEPT PHARMACOL,PITTSBURGH,PA 15261, USA. FU NCI NIH HHS [CA50694] NR 42 TC 87 Z9 88 U1 0 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD SEP 1 PY 1992 VL 89 IS 17 BP 8107 EP 8111 DI 10.1073/pnas.89.17.8107 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL614 UT WOS:A1992JL61400054 PM 1325646 ER PT J AU TAKEDA, Y ROSS, PD MUDD, CP AF TAKEDA, Y ROSS, PD MUDD, CP TI THERMODYNAMICS OF CRO PROTEIN DNA INTERACTIONS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ENTHALPY; ENTROPY; HEAT CAPACITY CHANGE; CALORIMETRY; DNA SEQUENCE RECOGNITION ID LAC REPRESSOR; OPERATOR DNA; CRYSTAL-STRUCTURE; BINDING; RESOLUTION; ASSOCIATION; COMPLEX; LAMBDA; RECOGNITION; STABILITY AB Using a highly sensitive pulsed-flow microcalorimeter, we have measured the changes in enthalpy and determined the thermodynamic parameters DELTA-H, DELTA-S-degrees, DELTA-G-degrees, and DELTA-C(p) for Cro protein-DNA association reactions. The reactions studied include sequence-nonspecific DNA association and sequence-specific DNA associations involving single- and multiple-base alterations and/or single-amino acid alteration mutants. (i) The association of Cro protein with nonspecific DNA at 15-degrees-C is characterized by DELTA-H = +4.4 kcal.mol-1 (1 cal = 4.18J), DELTA-S-degrees = 49 cal.mol-1.K-1, DELTA-G-degrees = -9.7 kcal.mol-1, and DELTA-C(p) congruent-to 0; the association this specific high-affinity operator OR3 DNA is characterized by DELTA-H = +0.8 kcal.mol-1, DELTA-S-degrees 59 cal.mol-1.K-1, DELTA-G-degrees = -16.1 kcal.mol-1, and DELTA-C(p) = -360 cal.mol-1.K-1, respectively. Both nonspecific and specific Cro-DNA associations are entropy-driven. (ii) Plots of DELTA-H vs. DELTA-C(p) and DELTA-S-degrees vs. DELTA-C(p) for the 20 association reactions studied fall into two correlation groups with linear slopes of +9.4 K and -20.5 K and of -0.03 and -0.14, respectively. These regression lines have common intercepts, at the DELTA-H and DELTA-S-degrees values of nonspecific association (where DELTA-C(p) congruent-to 0). The results suggest that there are, at least, two distinct conformational subclasses in specific Cro-DNA complexes, stabilized by different combinations of enthalpic and entropic contributions. The DELTA-G-degrees and DELTA-C(p) values form an approximately single linear correlation group as a consequence of compensatory contributions from DELTA-H and DELTA-S-degrees to DELTA-G-degrees and to DELTA-C(p). Cro protein-DNA associations share some similar thermodynamic properties with protein folding, but their overall energetics are quite different. Although the nonspecific complex is stabilized predominantly by electrostatic forces, it appears that H bonds, van der Waals contacts, hydrophobic effects, and charge interactions all contribute to the stability (DELTA-G-degrees and DELTA-C(p)) of the specific complex. (iii) The variations in the values of the thermodynamic parameters are in general accord with our knowledge of the structure of the Cro-DNA complex. C1 NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. RP TAKEDA, Y (reprint author), NCI,FREDERICK CANC RES FACIL,PROGRAM RESOURCES INC,MOLEC BIOL LAB,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74102] NR 37 TC 111 Z9 112 U1 0 U2 7 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD SEP 1 PY 1992 VL 89 IS 17 BP 8180 EP 8184 DI 10.1073/pnas.89.17.8180 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL614 UT WOS:A1992JL61400070 PM 1518844 ER PT J AU LIPMAN, PD CAPLAN, LJ AF LIPMAN, PD CAPLAN, LJ TI ADULT AGE-DIFFERENCES IN MEMORY FOR ROUTES - EFFECTS OF INSTRUCTION AND SPATIAL DIAGRAM SO PSYCHOLOGY AND AGING LA English DT Article ID ELDERLY ADULTS; INFORMATION; YOUNG; ACQUISITION; EXPERIENCE; KNOWLEDGE; COGNITION; DISTANCE; BEHAVIOR AB Free-recall and multiple-choice measures of memory for landmarks. sequential order, turns, and route configurations were obtained from younger and older adults after they viewed slides of 2 overlapping routes. Instructions focused attention on either the contents of the slides or on the course of the path; a control condition provided no orientational instructions. Half the subjects viewed maplike diagrams of the joint spatial configuration. Age interacted with instruction only for multiple-choice tests of landmark memory. Age interacted with diagram for each of the other 3 route memory components, although the generality of this interaction across instruction condition depended on whether free-recall or multiple-choice tests were used. The results suggest that route memory may involve both scene and layout representation, which may be differentially sensitive to age and presentational variables. RP LIPMAN, PD (reprint author), NIMH,FED BLDG,ROOM BLA-14,7550 WISCONSIN AVE,BETHESDA,MD 20892, USA. NR 19 TC 32 Z9 34 U1 3 U2 6 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0882-7974 J9 PSYCHOL AGING JI Psychol. Aging PD SEP PY 1992 VL 7 IS 3 BP 435 EP 442 DI 10.1037//0882-7974.7.3.435 PG 8 WC Gerontology; Psychology, Developmental SC Geriatrics & Gerontology; Psychology GA JN086 UT WOS:A1992JN08600014 PM 1388865 ER PT J AU ANDERSON, DE COYLE, K HAYTHORNTHWAITE, JA AF ANDERSON, DE COYLE, K HAYTHORNTHWAITE, JA TI AMBULATORY MONITORING OF RESPIRATION - INHIBITORY BREATHING IN THE NATURAL-ENVIRONMENT SO PSYCHOPHYSIOLOGY LA English DT Article DE VENTILATION; BREATHING RATE; TIDAL VOLUME; AMBULATORY MONITORING; INDUCTIVE PLETHYSMOGRAPHY ID SLEEP-APNEA SYNDROME; INDUCTIVE PLETHYSMOGRAPH; ESSENTIAL-HYPERTENSION; VENTILATION; POPULATION AB Because previous work found that sustained inhibitory breathing (i.e., low frequency breathing without increased tidal volume) can occur in laboratory animals under conditions of behavioral stress, this study sought to determine whether a comparable respiratory pattern could be observed in ambulatory human subjects in their natural environments. Tidal volume, breathing frequency, and minute ventilation were monitored continuously during 24-hour sessions via inductive plethysmography and a portable microprocessor. Mean tidal volume and minute ventilation were significantly higher during the daytime than at night for all subjects. However, mean breathing frequency was not consistently higher during the daytime, because episodes of low frequency breathing offset episodes of high breathing frequency. Tidal volume during low frequency breathing was comparable to that observed during medium or high frequency breathing. Thus, low frequency breathing was indicative of low minute ventilation. The eliciting stimuli, physiological concomitants, and relevance to health of this energetically inefficient breathing pattern remain to be determined. C1 NATL INST AGING,BEHAV SCI LAB,BETHESDA,MD. NR 36 TC 21 Z9 21 U1 1 U2 1 PU SOC PSYCHOPHYSIOL RES PI WASHINGTON PA 1010 VERMONT AVE NW SUITE 1100, WASHINGTON, DC 20005 SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PD SEP PY 1992 VL 29 IS 5 BP 551 EP 557 DI 10.1111/j.1469-8986.1992.tb02029.x PG 7 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA JQ382 UT WOS:A1992JQ38200006 PM 1410184 ER PT J AU KUTNER, NG ORY, MG BAKER, DI SCHECHTMAN, KB HORNBROOK, MC MULROW, CD AF KUTNER, NG ORY, MG BAKER, DI SCHECHTMAN, KB HORNBROOK, MC MULROW, CD TI MEASURING THE QUALITY-OF-LIFE OF THE ELDERLY IN HEALTH PROMOTION INTERVENTION CLINICAL-TRIALS SO PUBLIC HEALTH REPORTS LA English DT Article ID OF-LIFE; PERFORMANCE; DISEASE; ISSUES; STATE AB The Multicenter Trials of Frailty and Injuries: Cooperative Studies of Intervention Techniques (FICSIT) is a series of clinical trials Of biomedical, behavioral, and environmental interventions to reduce the risks of frailty and injury among the elderly. Reliable assessment of the quality of life reported by the subjects is a central issue in evaluating the interventions. An intervention may have a significant impact on an elderly person's sense of well-being, even though significant improvement is not observed in selected physical outcome measures. Elderly persons' compliance with particular intervention regimens may be influenced by the quality of life effects that they perceive in relation to the intervention. The researchers review the definition and measurement of quality of life in the trials, with particular attention to issues in determining common measures used at all study locations. considerations in the selection and use of quality of life measures in both community and institutional populations are addressed. Topics discussed include the interrelation of aging, functional capacities, and quality of life, the multi-dimensionality of quality of life in relation to differential intervention effects; and age-related issues in the collection of quality of life data. Preliminary observations are reviewed, and potential contributions of FICSIT to intervention-sensitive quality of life assessments among the elderly are noted. C1 NIA,SOCIAL SCI RES AGING,BETHESDA,MD 20892. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. UNIV OREGON,EUGENE,OR 97403. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP KUTNER, NG (reprint author), EMORY UNIV,SCH MED,1441 CLIFTON RD NE,ATLANTA,GA 30322, USA. FU NIA NIH HHS [U01-AG09089] NR 39 TC 30 Z9 30 U1 5 U2 6 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0033-3549 J9 PUBLIC HEALTH REP JI Public Health Rep. PD SEP-OCT PY 1992 VL 107 IS 5 BP 530 EP 539 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JR213 UT WOS:A1992JR21300007 PM 1410233 ER PT J AU RIMOLDI, D FLESSATE, DM SAMID, D AF RIMOLDI, D FLESSATE, DM SAMID, D TI CHANGES IN GENE-EXPRESSION BY 193-NM AND 248-NM EXCIMER LASER-RADIATION IN CULTURED HUMAN FIBROBLASTS SO RADIATION RESEARCH LA English DT Article ID IMMUNODEFICIENCY VIRUS TYPE-1; HUMAN-SKIN FIBROBLASTS; MAMMALIAN-CELLS; DNA DAMAGE; C-FOS; PLASMINOGEN-ACTIVATOR; EXTRACELLULAR FACTOR; NONIRRADIATED CELLS; ULTRAVIOLET-LIGHT; CYTO-TOXICITY C1 UNIFORMED SERV UNIV HLTH SCI,DEPT PATHOL,BETHESDA,MD 20814. NCI,DIV CANC TREATMENT,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. FU NEI NIH HHS [R03-EY0822001] NR 38 TC 12 Z9 13 U1 0 U2 0 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD SEP PY 1992 VL 131 IS 3 BP 325 EP 331 DI 10.2307/3578423 PG 7 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA JN370 UT WOS:A1992JN37000013 PM 1332110 ER PT J AU DOPPMAN, JL GILL, JR MILLER, DL CHANG, R GUPTA, R FRIEDMAN, TC CHOYKE, PL FEUERSTEIN, IM DWYER, AJ JICHA, DL WALTHER, MM NORTON, JA LINEHAN, WM AF DOPPMAN, JL GILL, JR MILLER, DL CHANG, R GUPTA, R FRIEDMAN, TC CHOYKE, PL FEUERSTEIN, IM DWYER, AJ JICHA, DL WALTHER, MM NORTON, JA LINEHAN, WM TI DISTINCTION BETWEEN HYPERALDOSTERONISM - DUE TO BILATERAL HYPERPLASIA AND UNILATERAL ALDOSTERONOMA - RELIABILITY OF CT SO RADIOLOGY LA English DT Article DE ADRENAL GLAND, CT; ADRENAL GLAND, DISEASES; ADRENAL GLAND, NEOPLASMS; COMPUTED TOMOGRAPHY (CT), COMPARATIVE STUDIES; VEINS, BLOOD SAMPLING ID PRIMARY HYPER-ALDOSTERONISM; COMPUTED-TOMOGRAPHY; ADRENAL-TUMORS; LOCALIZATION; DIAGNOSIS AB Hyperaldosteronism due to a unilateral adenoma must be distinguished from hyperaldosteronism due to bilateral hyperplasia to enable the proper choice between surgical treatment (for adenoma) or medical treatment (for hyperplasia). To compare the efficacy of computed tomography (CT) and adrenal venous sampling, both examinations were performed in 24 patients with primary aldosteronism. All patients with a diagnosis of adenoma based on findings at venous sampling underwent adrenalectomy. The CT-based diagnosis was unilateral aldosteronoma in 17 patients and hyperplasia in seven patients. On the basis of venous sampling, unilateral adenoma was diagnosed in 22 patients; this diagnosis was confirmed by means of unilateral adrenalectomy in 21 patients. The most common error was diagnosis of hyperplasia based on the presence of bilateral nodules on CT scans: In six of seven patients with such a diagnosis, venous sampling and subsequent surgery revealed a unilateral adenoma. In hyperaldosteronism with multiple bilateral nodules, CT cannot reliably permit distinction between hyperplasia and adenoma. C1 NHLBI,DIV INTRAMURAL RES HYPERTENS ENDOCRINE BRANCH,BETHESDA,MD 20892. NICHHD,DEV NEUROBIOL LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,DEPT RADIOL,WASHINGTON,DC 20007. NCI,DIV CANC TREATMENT,SURG BRANCH,BETHESDA,MD 20892. RP DOPPMAN, JL (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT DIAGNOST RADIOL,BLDG 10,RM 1C660,BETHESDA,MD 20892, USA. NR 17 TC 109 Z9 117 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD SEP PY 1992 VL 184 IS 3 BP 677 EP 682 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JJ866 UT WOS:A1992JJ86600019 PM 1509049 ER PT J AU MULE, JJ MARCUS, SG YANG, JC WEBER, JS ROSENBERG, SA AF MULE, JJ MARCUS, SG YANG, JC WEBER, JS ROSENBERG, SA TI CLINICAL-APPLICATION OF IL6 IN CANCER-THERAPY SO RESEARCH IN IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; RECOMBINANT INTERLEUKIN-6; INDUCTION; IL-6; MICE RP MULE, JJ (reprint author), NCI,SURG BRANCH,BETHESDA,MD 20892, USA. NR 18 TC 20 Z9 20 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD SEP PY 1992 VL 143 IS 7 BP 777 EP 779 DI 10.1016/0923-2494(92)80023-E PG 3 WC Immunology SC Immunology GA JV754 UT WOS:A1992JV75400017 PM 1439156 ER PT J AU SEHGAL, PB AKIRA, S VANSNICK, J ISHIBACHI, T ASANO, S GAULDIE, J MARTINEZMAZA, O MULE, JJ AF SEHGAL, PB AKIRA, S VANSNICK, J ISHIBACHI, T ASANO, S GAULDIE, J MARTINEZMAZA, O MULE, JJ TI 46TH FORUM IN IMMUNOLOGY - DISCUSSION SO RESEARCH IN IMMUNOLOGY LA English DT Discussion DE INTERLEUKIN, INTERFERON, IMMUNOREGULATION, IL6; FORUM ID B-CELLS; DIFFERENTIATION C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. OSAKA UNIV,INST MOLEC & CELLULAR BIOL,SUITA,OSAKA 565,JAPAN. LUDWIG INST CANC RES,B-1200 BRUSSELS,BELGIUM. FUKUSHIMA MED SCH,DEPT INTERNAL MED 1,FUKUSHIMA 960,JAPAN. UNIV TOKYO,INST MED SCI,DEPT HEMATOL ONCOL,TOKYO 113,JAPAN. NCI,SURG BRANCH,BETHESDA,MD 20892. MCMASTER UNIV,DEPT PATHOL,HAMILTON L8N 3Z5,ONTARIO,CANADA. UNIV CALIF LOS ANGELES,SCH MED,DEPT OBSTET & GYNECOL,LOS ANGELES,CA 90024. RP SEHGAL, PB (reprint author), NEW YORK MED COLL,DEPT MICROBIOL & IMMUNOL,BASIC SCI BLDG,VALHALLA,NY 10595, USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD SEP PY 1992 VL 143 IS 7 BP 779 EP 783 PG 5 WC Immunology SC Immunology GA JV754 UT WOS:A1992JV75400018 ER PT J AU STGEORGIEV, V AF STGEORGIEV, V TI TREATMENT AND DEVELOPMENTAL THERAPEUTICS IN ASPERGILLOSIS .1. AMPHOTERICIN-B AND ITS DERIVATIVES SO RESPIRATION LA English DT Review DE ASPERGILLOSIS, TREATMENT OF; AMPHOTERICIN-B; ESTERS OF AMPHOTERICIN-B; POLYENE ANTIBIOTICS; BENZO[A]NAPHTHACENE ANTIBIOTICS; NIKKOMYCINS; CILOFUNGIN ID INVASIVE PULMONARY ASPERGILLOSIS; ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS; ANTIFUNGAL ANTIBIOTICS; INFECTIOUS COMPLICATIONS; PRADIMICIN-A; SUCCESSFUL MANAGEMENT; PERITONEAL-DIALYSIS; CANDIDA-ALBICANS; EARLY DIAGNOSIS; BENANOMICIN-A AB In recent years, the frequency of infections caused by Aspergillus sp. has been on the rise. Immunocompromised patients are especially vulnerable to such infections. The polyene antibiotic amphotericin B is currently considered to be therapeutically the most effective drug against Aspergillus-induced infections. In the present review, the clinical efficacy of amphotericin B, its toxicities and various routes of applications, are discussed. Different combinations of ampbotericin B with other drugs have also been reviewed, along with the anti-Aspergillus activity of various other antibiotics and some ester derivatives of amphotericin B. RP STGEORGIEV, V (reprint author), NIAID,SOLAR BLDG,ROOM 4C-39,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 137 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0025-7931 J9 RESPIRATION JI Respiration PD SEP-OCT PY 1992 VL 59 IS 5 BP 291 EP 302 PG 12 WC Respiratory System SC Respiratory System GA KD146 UT WOS:A1992KD14600008 ER PT J AU STGEORGIEV, V AF STGEORGIEV, V TI TREATMENT AND DEVELOPMENTAL THERAPEUTICS IN ASPERGILLOSIS .2. AZOLES AND OTHER ANTIFUNGAL DRUGS SO RESPIRATION LA English DT Review DE ASPERGILLOSIS, TREATMENT OF; ASPERGILLOMA, TREATMENT OF; AZOLE DERIVATIVES; ALLERGIC BRONCHOPULMONARY; ASPERGILLOSIS, THERAPY OF; ASPERGILLUS OTOMYCOSIS, THERAPY OF ID ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS; CHRONIC GRANULOMATOUS-DISEASE; SYSTEMIC FUNGAL-INFECTIONS; COLONY-STIMULATING FACTOR; PULMONARY ASPERGILLOSIS; INVASIVE ASPERGILLOSIS; TOPICAL KETOCONAZOLE; MURINE ASPERGILLOSIS; MYCOTIC KERATITIS; FOLLOW-UP AB The present article surveys the anti-Aspergillus activity of various azole derivatives as well as a number of miscellaneous other antifungal agents. The drawbacks of sodium (potassium) iodide therapy in the management of pulmonary aspergilloma are discussed along with current efforts at treatment of allergic bronchopulmonary aspergillosis and Aspergillus-induced otomycosis. RP STGEORGIEV, V (reprint author), NIAID,SOLAR BLDG,ROOM 4C-39,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 131 TC 5 Z9 5 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0025-7931 J9 RESPIRATION JI Respiration PD SEP-OCT PY 1992 VL 59 IS 5 BP 303 EP 313 PG 11 WC Respiratory System SC Respiratory System GA KD146 UT WOS:A1992KD14600009 ER PT J AU TUDORWILLIAMS, G EMERY, VC AF TUDORWILLIAMS, G EMERY, VC TI DEVELOPMENT OF INVITRO RESISTANCE TO ZIDOVUDINE IS LIKELY TO BE CLINICALLY SIGNIFICANT SO REVIEWS IN MEDICAL VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-1 REVERSE-TRANSCRIPTASE; POLYMERASE CHAIN-REACTION; PLAQUE REDUCTION ASSAY; HIGH-LEVEL RESISTANCE; REDUCED SENSITIVITY; MULTIPLE MUTATIONS; PROLONGED THERAPY; AZT; SUSCEPTIBILITIES C1 ROYAL FREE HOSP,DIV COMMUNICABLE DIS,LONDON NW3 2QG,ENGLAND. RP TUDORWILLIAMS, G (reprint author), NCI,PEDIAT BRANCH,BETHESDA,MD 20892, USA. NR 34 TC 6 Z9 6 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 1052-9276 J9 REV MED VIROL JI Rev. Med. Virol. PD SEP PY 1992 VL 2 IS 3 BP 123 EP 129 DI 10.1002/rmv.1980020302 PG 7 WC Virology SC Virology GA JT045 UT WOS:A1992JT04500001 ER PT J AU GOLD, JM RANDOLPH, C COPPOLA, R CARPENTER, CJ GOLDBERG, TE WEINBERGER, DR AF GOLD, JM RANDOLPH, C COPPOLA, R CARPENTER, CJ GOLDBERG, TE WEINBERGER, DR TI VISUAL ORIENTING IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Article DE VISUAL ORIENTING; ATTENTIONAL DEFICITS; (SCHIZOPHRENIA) ID SPATIAL ATTENTION; REACTION-TIME; DISENGAGEMENT; ASYMMETRIES; LESIONS AB Patients with schizophrenia demonstrate a variety of attentional impairments which have proven difficult to relate to specific neural systems. Posner et al. (1988) reported an asymmetric slowing of right visual field orienting in schizophrenia similar to that observed in patients with parietal lesions. We examined the visual orienting performance of 19 patients and controls using two different versions of the Posner paradigm. In overall ANOVAs we found main effects of group, cue condition, and delay interval. However, we did not observe any main effect of visual field or interactions involving visual field. There was some evidence of an asymmetric cost of invalid cues similar to those reported by Posner et al. The bulk of data suggests bilateral attentional deficits. RP GOLD, JM (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032, USA. NR 21 TC 34 Z9 34 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD SEP PY 1992 VL 7 IS 3 BP 203 EP 209 DI 10.1016/0920-9964(92)90013-U PG 7 WC Psychiatry SC Psychiatry GA JT252 UT WOS:A1992JT25200002 PM 1390400 ER PT J AU GOLDMANRAKIC, PS AF GOLDMANRAKIC, PS TI WORKING MEMORY AND THE MIND SO SCIENTIFIC AMERICAN LA English DT Article C1 YALE UNIV,SCH MED,NEW HAVEN,CT 06510. RP GOLDMANRAKIC, PS (reprint author), NIMH,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892, USA. NR 4 TC 84 Z9 86 U1 1 U2 4 PU SCI AMERICAN INC PI NEW YORK PA 415 MADISON AVE, NEW YORK, NY 10017 SN 0036-8733 J9 SCI AM JI Sci.Am. PD SEP PY 1992 VL 267 IS 3 BP 111 EP 117 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JK965 UT WOS:A1992JK96500012 ER PT J AU GERSHON, ES RIEDER, RO AF GERSHON, ES RIEDER, RO TI MAJOR DISORDERS OF MIND AND BRAIN SO SCIENTIFIC AMERICAN LA English DT Article ID SCHIZOPHRENIA RP GERSHON, ES (reprint author), NIMH,INTRAMURAL RES PROGRAM,BETHESDA,MD 20892, USA. NR 5 TC 4 Z9 4 U1 1 U2 1 PU SCI AMERICAN INC PI NEW YORK PA 415 MADISON AVE, NEW YORK, NY 10017 SN 0036-8733 J9 SCI AM JI Sci.Am. PD SEP PY 1992 VL 267 IS 3 BP 127 EP 133 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JK965 UT WOS:A1992JK96500014 ER PT J AU SCHOOLER, C AF SCHOOLER, C TI IN DEFENSE OF MODERNITY - ROLE COMPLEXITY AND INDIVIDUAL AUTONOMY - COSER,RL SO SOCIAL FORCES LA English DT Book Review RP SCHOOLER, C (reprint author), NIMH,SOCIO ENVIRONM STUDIES LAB,BETHESDA,MD 20205, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU UNIV NORTH CAROLINA PRESS PI CHAPEL HILL PA BOX 2288, CHAPEL HILL, NC 27515-2288 SN 0037-7732 J9 SOC FORCES JI Soc. Forces PD SEP PY 1992 VL 71 IS 1 BP 230 EP 232 PG 3 WC Sociology SC Sociology GA JR104 UT WOS:A1992JR10400016 ER PT J AU POLVINO, WJ DICHEK, DA MASON, J ANDERSON, WF AF POLVINO, WJ DICHEK, DA MASON, J ANDERSON, WF TI MOLECULAR-CLONING AND NUCLEOTIDE-SEQUENCE OF CDNA-ENCODING A FUNCTIONAL MURINE LOW-DENSITY-LIPOPROTEIN RECEPTOR SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID LDL RECEPTOR; FAMILIAL HYPERCHOLESTEROLEMIA; DEFICIENT RABBITS; MESSENGER-RNA; GENE-TRANSFER; T-CELLS; EXPRESSION; MICE; RECOMBINATION; PRECURSOR AB The low-density-lipoprotein (LDL) receptor is an important mediator of mammalian cholesterol metabolism; its congenital absence in humans is characterized by hypercholesterolemia, atherosclerosis, and coronary artery disease. We report here the identification and cloning of a cDNA encoding the murine LDL receptor. The cDNA insert is 4467 base pairs in length and the deduced amino acid sequence bears 78.2% homology with the reported human sequence. This murine cDNA was subcloned into a retroviral-based expression vector, LmLSN1, and transfected into 3T3 cells. The production of functional LDL receptor was confirmed by ligand binding of DiI-LDL cholesterol. C1 MERCK SHARP & DOHME LTD,RAHWAY,NJ 07065. RP POLVINO, WJ (reprint author), NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892, USA. NR 29 TC 12 Z9 13 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD SEP PY 1992 VL 18 IS 5 BP 443 EP 450 DI 10.1007/BF01233084 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA KH367 UT WOS:A1992KH36700007 PM 1475710 ER PT J AU WRIGHT, LL AF WRIGHT, LL TI STUDENTS - THE OVERLOOKED, UNTAPPED RESOURCE WITHIN NEARLY EVERY CHAPTER SO SPECIAL LIBRARIES LA English DT Article AB The Special Libraries Association (SLA) has experienced an unprecedented increase among student members. Nearly every Chapter has student members but little is known how these Chapters serve their student members to retain them as full members after they graduate. Data presented here offer a profile of activities SLA provides for students at the Chapter level. The data expose critical areas where Chapters are deficient in serving student members. Alternatively, this study reveals activities that are successful and may be emulated elsewhere to offset deficiencies. The study offers a standard by which Chapters can measure their progress with involving students in local SLA activities. RP WRIGHT, LL (reprint author), NIEHS,RES TRIANGLE PK,NC 27709, USA. NR 6 TC 0 Z9 0 U1 0 U2 1 PU SPECIAL LIBRARIES ASSN PI WASHINGTON PA 1700 EIGHTEENTH ST NW, WASHINGTON, DC 20009-2508 SN 0038-6723 J9 SPEC LIBR JI Spec. Libr. PD FAL PY 1992 VL 83 IS 4 BP 211 EP 218 PG 8 WC Information Science & Library Science SC Information Science & Library Science GA JR729 UT WOS:A1992JR72900003 ER PT J AU BARTH, RJ MERINO, MJ SOLOMON, D YANG, JC BAKER, AR AF BARTH, RJ MERINO, MJ SOLOMON, D YANG, JC BAKER, AR TI A PROSPECTIVE-STUDY OF THE VALUE OF CORE NEEDLE-BIOPSY AND FINE NEEDLE ASPIRATION IN THE DIAGNOSIS OF SOFT-TISSUE MASSES SO SURGERY LA English DT Article ID TRU-CUT; SARCOMAS; CYTOLOGY; TUMORS; LESIONS AB We prospectively sampled 38 large soft tissue masses in 3 7 patients with both core needle biopsy (CNBX) and fine-needle aspiration (FNA) to determine the diagnostic utility of these biopsy methods. In 27 cases the histologic diagnosis made from the resected specimen was compared with the diagnosis based on the biopsy. CNBX correctly identified 16 of 16 malignant sarcomas and 10 of 11 benign masses (one was indeterminate). The grade of the sarcoma was determined correctly in every case There were no false malignant or false benign CNBX diagnoses. FNA correctly classified 12 of 14 malignant sarcomas and four of 11 benign lesions. Diagnoses based on FNA were limited by a high proportion of samples, especially from benign lesions, that were inadequate for definitive diagnosis and by an inability to grade many malignant sarcomas. There were no significant complications resulting from the biopsies. We conclude that CNBX is a highly accurate, easily performed method for the diagnosis of large soft tissue masses that can be accomplished with minimal morbidity. C1 NCI,SURG BRANCH,PATHOL LAB,BETHESDA,MD 20892. NCI,CYTOPATHOL LAB,BETHESDA,MD 20892. NR 17 TC 73 Z9 75 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD SEP PY 1992 VL 112 IS 3 BP 536 EP 543 PG 8 WC Surgery SC Surgery GA JL180 UT WOS:A1992JL18000010 PM 1519170 ER PT J AU BOJA, JW MITCHELL, WM PATEL, A KOPAJTIC, TA CARROLL, FI LEWIN, AH ABRAHAM, P KUHAR, MJ AF BOJA, JW MITCHELL, WM PATEL, A KOPAJTIC, TA CARROLL, FI LEWIN, AH ABRAHAM, P KUHAR, MJ TI HIGH-AFFINITY BINDING OF [I-125] RTI-55 TO DOPAMINE AND SEROTONIN TRANSPORTERS IN RAT-BRAIN SO SYNAPSE LA English DT Article DE DOPAMINE UPTAKE; BINDING SITES; SEROTONIN UPTAKE; COCAINE ID CENTRAL NERVOUS-SYSTEM; UPTAKE SITES; COCAINE RECEPTORS; H-3 COCAINE; UPTAKE INHIBITOR; GBR-12935 BINDING; STRIATAL MEMBRANES; LIGAND; CITALOPRAM; COMPLEX AB RTI-55 (3-beta-(4-iodophenyl)tropan-2-beta-carboxylic acid methyl ester), one of the most potent inhibitors of dopamine uptake reported to date, was radioiodinated and tested as a probe for the cocaine receptor in Sprague-Dawley rat brain. Saturation and kinetic studies in the striatum revealed that [I-125]RTI-55 bound to both a high- and low-affinity site. The K(d) for the high-affinity site was 0.2 nM, while the K(d) for the low-affinity site was 5.8 nM. The corresponding number of binding sites in the striatum was 37 and 415 pmol/g protein. The pharmacological profile of speCifiC [I-125]RTI-55 binding in the striatum was consistent with that of the dopamine transporter. Additionally, [I-125]RTI-55 was found to bind with high affinity to the cerebral cortex. Scatchard analysis revealed a single high-affinity component of 0.2 nM with a density of 2.5 pmol/g protein. The pharmacological profile demonstrated by [I-125]RTI-55 in the cerebral cortex matched that of the serotonin transporter. Autoradiographic analysis of sagittal brain sections with [I-125]RTI-55 binding was consistent with these findings. Specific binding of [I-125]RTI-55 was blocked by dopamine uptake inhibitors in areas rich in dopaminergic nerve terminals. Conversely, serotonin uptake inhibitors blocked the binding of [I-125]RTI-55 in brain areas rich in serotonergic neurons. These results demonstrate that [I-125]RTI-55 may be a very useful ligand for the dopamine and serotonin transporters. C1 RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. RP BOJA, JW (reprint author), NIDA,ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224, USA. FU NIDA NIH HHS [DA05477] NR 32 TC 208 Z9 208 U1 1 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-4476 J9 SYNAPSE JI Synapse PD SEP PY 1992 VL 12 IS 1 BP 27 EP 36 DI 10.1002/syn.890120104 PG 10 WC Neurosciences SC Neurosciences & Neurology GA JM201 UT WOS:A1992JM20100003 PM 1411961 ER PT J AU CLINE, EJ SCHEFFEL, U BOJA, JW MITCHELL, WM CARROLL, FI ABRAHAM, P LEWIN, AH KUHAR, MJ AF CLINE, EJ SCHEFFEL, U BOJA, JW MITCHELL, WM CARROLL, FI ABRAHAM, P LEWIN, AH KUHAR, MJ TI INVIVO BINDING OF [I-125] RTI-55 TO DOPAMINE TRANSPORTERS - PHARMACOLOGY AND REGIONAL DISTRIBUTION WITH AUTORADIOGRAPHY SO SYNAPSE LA English DT Article DE WIN 35,065-2 ANALOGS; SEROTONIN TRANSPORTER; HALOPERIDOL ID COCAINE BINDING; UPTAKE SITES; NONHUMAN-PRIMATES; LIGAND-BINDING; H-3 COCAINE; GBR-12935 BINDING; STRIATAL MEMBRANES; RAT STRIATUM; RECEPTORS; BRAIN AB Previous studies have demonstrated that para-substituted WIN 35,065-2 analogs of cocaine show high binding affinity for dopamine uptake sites both in vitro and in vivo, and inhibit DA uptake in vitro. These analogs also produce potent cocaine-like behavioral effects in various procedures. The purpose of the present studies was to evaluate the iodinated WIN 35,065-2 analog [I-125]RTI-55 as an in vivo ligand for the DA transporter. Following intravenous injection in mice, [I-125]RTI-55 showed highest accumulation in areas with high densities of dopamine uptake sites. Light microscopic autoradiography was used to examine binding with higher resolution. Displacement studies demonstrated that [I-125]RTI-55 binding in dopamine containing regions, striatum and olfactory tubercles, was saturable and inhibited by other cocaine analogs. GBR 12909 and WIN 35,428 significantly inhibited [I-125]RTI-55 binding in striatum, while paroxetine significantly inhibited hypothalamic binding but had little effect in striatum. The latter finding suggests that [I-125]RTI-55 also binds to the serotonin transporter. Haloperidol had no effect on [I-125]RTI-55 binding in any brain region measured. In addition, treatment of animals with the dopamine neurotoxin MPTP caused significant reductions in striatal [I-125]RTI-55 binding. The results of these studies indicate that [I-125]RTI-55 binds primarily to the dopamine transporter in the mouse striatum in vivo. C1 NIDA,ADDICT RES CTR,NEUROSCI BRANCH,POB 5180,BALTIMORE,MD 21224. JOHNS HOPKINS MED INST,DEPT RADIOL,DIV NUCL MED,BALTIMORE,MD 21205. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. FU NCI NIH HHS [CA 32845]; NIDA NIH HHS [DA05477]; NINDS NIH HHS [NS 15080] NR 40 TC 66 Z9 66 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 0887-4476 J9 SYNAPSE JI Synapse PD SEP PY 1992 VL 12 IS 1 BP 37 EP 46 DI 10.1002/syn.890120105 PG 10 WC Neurosciences SC Neurosciences & Neurology GA JM201 UT WOS:A1992JM20100004 PM 1411962 ER PT J AU DECOSTA, BR RADESCA, L AF DECOSTA, BR RADESCA, L TI A PRACTICAL TRIPHENYLCARBENIUM TETRAFLUOROBORATE MEDIATED ONE-POT SYNTHESIS OF 1-SUBSTITUTED N-ALKYL-1,2,3,4-TETRAHYDROISOQUINOLINES SO SYNTHESIS-STUTTGART LA English DT Article ID ASYMMETRIC ALKYLATION; TERTIARY-AMINES; TETRAHYDROISOQUINOLINES AB Treatment of 2-methyl-1,2,3,4-tetrahydroisoquinoline (1) with 1 - 2 molar equivalents of triphenylcarbenium tetrafluoroborate at 20-degrees-C in either chloroform or acetonitrile resulted in the formation of 2-methyl-3,4-dihydroisoquinolinium tetrafluoroborate (2), whereas triethylamine and N-methylpiperidine were unaffected under these reaction conditions. This hydride abstraction was exploited in a one-pot preparation of 1-functionalized 2-alkyl-1,2,3,4-tetrahydro-isoquinolines. Thus, treatment of 2 with aqueous potassium hydroxide afforded 1-hydroxy-2-methyl-1,2,3,4-tetrahydroisoquinoline (9) (61 % from 1). Similarly, potassium cyanide in acetonitrile provided 1-cyano-2-methyl-1,2,3,4-tetrahydroisoquinoline (10, 77 %). Quenching of 2 with Grignard reagents in tetrahydrofuran afforded the corresponding 1-alkyl and 1-aryl substituted tetrahydroisoquinolines (31 to 78 %). Interestingly, nitrile 10 reacted very rapidly (< 2 min at O-degrees-C) with phenylmagnesium bromide to give 2-methyl-1-phenyl-1,2,3,4-tetrahydroisoquinoline (3, 100 %), but failed to react with excess phenyllithium even at 20-degrees-C. RP DECOSTA, BR (reprint author), NATL INST DIABET & DIGEST & KIDNEY DIS,MED CHEM LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 31 TC 9 Z9 9 U1 1 U2 1 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0039-7881 J9 SYNTHESIS-STUTTGART JI Synthesis PD SEP PY 1992 IS 9 BP 887 EP 890 PG 4 WC Chemistry, Organic SC Chemistry GA JN488 UT WOS:A1992JN48800024 ER PT J AU FUKUDA, Y HERMAN, EH FERRANS, VJ AF FUKUDA, Y HERMAN, EH FERRANS, VJ TI EFFECT OF ICRF-187 ON THE PULMONARY DAMAGE INDUCED BY HYPEROXIA IN THE RAT SO TOXICOLOGY LA English DT Article DE HISTOPATHOLOGY; ELECTRON MICROSCOPY; OXYGEN FREE RADICALS; IRON CHELATION ID CHRONIC DAUNORUBICIN CARDIOTOXICITY; CHRONIC DOXORUBICIN CARDIOTOXICITY; OXYGEN RADICAL PRODUCTION; LUNG INJURY; ANTIOXIDANT ENZYMES; N-ACETYLCYSTEINE; TOXICITY; PROTECTION; (+)-1,2-BIS(3,5-DIOXOPIPERAZINYL-1-YL)PROPANE; ADRIAMYCIN AB Histological and ultrastructural studies were made of the lungs of rats that were exposed to 100% oxygen for 60 h and were treated with either normal saline or with ICRF-187, a bis-diketopiperazine derivative of EDTA that has the capacity to chelate iron. This metal is thought to be needed to catalyze the formation of toxic oxygen free radicals. ICRF- 1 87 (20 mg/kg) was given intraperitoneally at approximately 12 h intervals (5 doses) during the 60 h exposure. Seven of the ten saline-treated rats exposed to oxygen died prior to the end of the study whereas only one of the 10 rats in the ICRF-187-treated group died. This difference in mortality is found to be statistically significant (P < 0.05). All saline-treated rats showed light and electron microscopic evidence of pulmonary damage. ICRF-187 attenuated the morphologic alterations observed by light microscopy (intra-alveolar edema, inflammatory exudates and bronchiolar epithelial cell swelling and hyperplasia; P < 0.05). In addition, electron microscopic evaluation revealed that capillary thrombi, endothelial cell alterations and alveolar epithelial cell damage also were less severe in ICRF-187-treated rats. It is concluded that ICRF-187 may provide a new and useful approach for the prevention of hyperoxia-induced pulmonary damage. C1 NHLBI,PATHOL BRANCH,ULTRASTRUCT SECT,9000 ROCKVILLE PIKE,BLDG 10,ROOM 7N236,BETHESDA,MD 20892. US FDA,DIV DRUG RES & TESTING,WASHINGTON,DC 20204. NIPPON MED COLL,DEPT PATHOL,TOKYO 113,JAPAN. NR 37 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0300-483X J9 TOXICOLOGY JI Toxicology PD SEP PY 1992 VL 74 IS 2-3 BP 185 EP 202 DI 10.1016/0300-483X(92)90138-5 PG 18 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA JL955 UT WOS:A1992JL95500007 PM 1519241 ER PT J AU MCCURDY, PR NEMO, GJ AF MCCURDY, PR NEMO, GJ TI WHITE CELL REDUCTION, ULTRAVIOLET-IRRADIATION, AND PLATELET REFRACTORINESS IN ACUTE MYELOID-LEUKEMIA - REPLY SO TRANSFUSION LA English DT Letter C1 NHLBI,TRANSFUS MED BRANCH,BETHESDA,MD 20892. RP MCCURDY, PR (reprint author), NHLBI,DIV BLOOD DIS & RESOURCES,BONE MARROW TRANSPLANTAT BRANCH,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD SEP PY 1992 VL 32 IS 7 BP 688 EP 689 PG 2 WC Hematology SC Hematology GA JM761 UT WOS:A1992JM76100020 ER PT J AU ROSENGARD, BR OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K BOORSTEIN, SM HILL, GS FISHBEIN, JM SACHS, DH AF ROSENGARD, BR OJIKUTU, CA GUZZETTA, PC SMITH, CV SUNDT, TM NAKAJIMA, K BOORSTEIN, SM HILL, GS FISHBEIN, JM SACHS, DH TI INDUCTION OF SPECIFIC TOLERANCE TO CLASS-I - DISPARATE RENAL-ALLOGRAFTS IN MINIATURE SWINE WITH CYCLOSPORINE SO TRANSPLANTATION LA English DT Article ID EXTRACTED HISTOCOMPATIBILITY ANTIGEN; LONG-TERM SURVIVAL; LUNG TRANSPLANTATION; SUPPRESSOR CELLS; HEART GRAFTS; A TREATMENT; LYMPHOCYTES; RATS; REJECTION; PROLONGATION AB Previous studies in miniature swine have suggested that the mechanism underlying the spontaneous development of tolerance in one third of one-haplotype class I disparate renal allografts (i.e., ag-->ad) involves a relative T cell help deficit at the time of first exposure to antigen. If this hypothesis were correct, then one might expect the administration of an immunosuppressive agent capable of inhibiting lymphokine production during this period to lead to the induction of tolerance to class I MHC antigens in two-haplotype class I mismatched renal allografts (i.e., gg-->dd), which are otherwise uniformly and acutely rejected. This hypothesis was tested in eight two-haplotype class I disparate, class II matched donor-recipient pairs, in which recipients were treated with cyclosporine 10 mg/kg, i.v. q.d. for 12 days. This protocol led to the induction of long-term (>100 days) specific tolerance in 100% of recipients, as compared with control animals that rejected grafts in 13.7 +/- 0.9 days (P<0.0001). The specificity of tolerance was assessed both in vivo with subsequent skin grafts and in vitro by mixed lymphocyte response (MLR) and cell-mediated lymphocytotoxicity (CML). Survival of donor-specific skin grafts was prolonged compared with skin grafts bearing third-party class I antigens (19.5+/-2.0 versus 11.5+/-2.0 days, n=4, P<0.05). Tolerant recipients had markedly diminished or absent anti-donor MLR and CML responses, but maintained normal reactivity to third party. Four of eight CsA-treated recipients showed detectable levels of anti-donor IgM, while none demonstrated the presence of anti-donor IgG, which was found in all rejecting controls. C1 NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. RP ROSENGARD, BR (reprint author), MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129, USA. FU NIAID NIH HHS [AI-31046] NR 44 TC 135 Z9 135 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD SEP PY 1992 VL 54 IS 3 BP 490 EP 497 DI 10.1097/00007890-199209000-00020 PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA JP018 UT WOS:A1992JP01800020 PM 1412729 ER PT J AU GONZALEZ, FJ AF GONZALEZ, FJ TI HUMAN CYTOCHROMES-P450 - PROBLEMS AND PROSPECTS SO TRENDS IN PHARMACOLOGICAL SCIENCES LA English DT Review ID CDNA-DIRECTED EXPRESSION; CATALYZES COUMARIN 7-HYDROXYLATION; HUMAN LIVER-MICROSOMES; AMINO-ACID SEQUENCE; SUBSTRATE-SPECIFICITY; MOLECULAR-GENETICS; CIGARETTE-SMOKING; MESSENGER-RNA; LUNG-CANCER; BREATH TEST AB Cytochromes P450 are a superfamily of haem-containing monooxygenases. In mammals, two general classes of P450s exist: six families involved in steroid and bile acid biosynthetic pathways of metabolism; four families containing numerous individual P450s, mainly responsible for metabolism of foreign compounds. Many of the latter P450s, particularly those in the CYP2 family, exhibit a large degree of inter- and intra-species variability in regulation and catalytic activities. From a practical standpoint, these variabilities suggest the need for careful characterization of P450 catalytic activities and determination of P450 expression levels in humans. Human P450-based in vitro systems are being developed to evaluate drug and carcinogen metabolism. RP GONZALEZ, FJ (reprint author), NCI,BETHESDA,MD 20892, USA. NR 59 TC 371 Z9 377 U1 1 U2 11 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0165-6147 J9 TRENDS PHARMACOL SCI JI Trends Pharmacol. Sci. PD SEP PY 1992 VL 13 IS 9 BP 346 EP 352 DI 10.1016/0165-6147(92)90107-H PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JK662 UT WOS:A1992JK66200004 PM 1529480 ER PT J AU SIMPSON, RM WATERS, DJ GEBHARD, DH CASEY, HW AF SIMPSON, RM WATERS, DJ GEBHARD, DH CASEY, HW TI MASSIVE THYMOMA WITH MEDULLARY DIFFERENTIATION IN A DOG SO VETERINARY PATHOLOGY LA English DT Article DE DOGS; FLOW CYTOMETRY; IMMUNOLOGY; THYMOMA; THYMUS; ULTRASTRUCTURE ID RATS RP SIMPSON, RM (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK 2 CAMPUS,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 10 TC 6 Z9 6 U1 0 U2 0 PU AMER COLL VET PATHOLOGIST PI LAWRENCE PA 810 EAST 10TH STREET, LAWRENCE, KS 66044 SN 0300-9858 J9 VET PATHOL JI Vet. Pathol. PD SEP PY 1992 VL 29 IS 5 BP 416 EP 419 PG 4 WC Pathology; Veterinary Sciences SC Pathology; Veterinary Sciences GA JL965 UT WOS:A1992JL96500007 PM 1413409 ER PT J AU FAN, LJ PEDEN, K AF FAN, LJ PEDEN, K TI CELL-FREE TRANSMISSION OF VIF MUTANTS OF HIV-1 SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; NUCLEOTIDE-SEQUENCE ANALYSIS; SOR GENE-PRODUCT; HTLV-III/LAV; GENOME ORGANIZATION; TYPE-1 VIF; INFECTION; PROTEIN; AIDS; SERA C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. FU NIMHD NIH HHS [MD800803] NR 37 TC 92 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 0042-6822 J9 VIROLOGY JI Virology PD SEP PY 1992 VL 190 IS 1 BP 19 EP 29 DI 10.1016/0042-6822(92)91188-Z PG 11 WC Virology SC Virology GA JL549 UT WOS:A1992JL54900003 PM 1529528 ER PT J AU NAKAGAWA, Y PETRICOIN, EF AKAI, H GRIMLEY, PM RUPP, B LARNER, AC AF NAKAGAWA, Y PETRICOIN, EF AKAI, H GRIMLEY, PM RUPP, B LARNER, AC TI INTERFERON-ALPHA-INDUCED GENE-EXPRESSION - EVIDENCE FOR A SELECTIVE EFFECT OF OUABAIN ON ACTIVATION OF THE ISGF3 TRANSCRIPTION COMPLEX SO VIROLOGY LA English DT Article ID SIGNAL TRANSDUCTION PATHWAYS; PROTEIN-KINASE-C; GUANYLATE-BINDING PROTEIN; GAMMA-INTERFERON; INDUCIBLE GENE; BETA-INTERFERON; NA+-K+; STIMULATED TRANSCRIPTION; METALLOTHIONEIN GENES; E1A ONCOGENE C1 NIH,CTR BIOL EVALUAT & RES,CYTOKINE RES LAB,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DEPT PATHOL,BETHESDA,MD 20892. NR 74 TC 16 Z9 16 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD SEP PY 1992 VL 190 IS 1 BP 210 EP 220 DI 10.1016/0042-6822(92)91207-B PG 11 WC Virology SC Virology GA JL549 UT WOS:A1992JL54900022 PM 1529530 ER PT J AU VASUDEVACHARI, MB BATTISTA, C LANE, HC PSALLIDOPOULOS, MC ZHAO, B COOK, J PALMER, JR ROMERO, DL TARPLEY, WG SALZMAN, NP AF VASUDEVACHARI, MB BATTISTA, C LANE, HC PSALLIDOPOULOS, MC ZHAO, B COOK, J PALMER, JR ROMERO, DL TARPLEY, WG SALZMAN, NP TI PREVENTION OF THE SPREAD OF HIV-1 INFECTION WITH NONNUCLEOSIDE REVERSE-TRANSCRIPTASE INHIBITORS SO VIROLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; PERIPHERAL-BLOOD; AZIDOTHYMIDINE AZT; ZIDOVUDINE AZT; HTLV-III/LAV; DOUBLE-BLIND; T-CELL; TYPE-1 C1 GEORGETOWN UNIV,MED CTR,DEPT MICROBIOL,MOLEC RETROVIROL LAB,WASHINGTON,DC 20007. NIAID,IMMUNOREGULAT LAB,CLIN & MOLEC RETROVIROL SECT,BETHESDA,MD 20892. UPJOHN CO,LABS,CANC & INFECT DIS RES,KALAMAZOO,MI 49001. UPJOHN CO,LABS,MED CHEM RES,KALAMAZOO,MI 49001. FU PHS HHS [N01-A1-05058] NR 42 TC 61 Z9 61 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD SEP PY 1992 VL 190 IS 1 BP 269 EP 277 DI 10.1016/0042-6822(92)91213-E PG 9 WC Virology SC Virology GA JL549 UT WOS:A1992JL54900028 PM 1382341 ER PT J AU CICALA, C POMPETTI, F NGUYEN, P DIXON, K LEVINE, AS CARBONE, M AF CICALA, C POMPETTI, F NGUYEN, P DIXON, K LEVINE, AS CARBONE, M TI SV40 SMALL T-DELETION MUTANTS PREFERENTIALLY TRANSFORM MONONUCLEAR PHAGOCYTES AND LYMPHOCYTES-B INVIVO SO VIROLOGY LA English DT Note ID SIMIAN VIRUS-40; PROTEIN PHOSPHATASE-2A; MONOCLONAL-ANTIBODIES; ANTIGEN; TUMORS; CELLS; GENOME; MICE C1 NICHHD,VIRUSES & CELLULAR BIOL SECT,BLDG 6A,ROOM 1A11,BETHESDA,MD 20892. NR 28 TC 28 Z9 29 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD SEP PY 1992 VL 190 IS 1 BP 475 EP 479 DI 10.1016/0042-6822(92)91237-O PG 5 WC Virology SC Virology GA JL549 UT WOS:A1992JL54900052 PM 1529547 ER PT J AU MERCHLINSKY, M MOSS, B AF MERCHLINSKY, M MOSS, B TI INTRODUCTION OF FOREIGN DNA INTO THE VACCINIA VIRUS GENOME BY INVITRO LIGATION - RECOMBINATION-INDEPENDENT SELECTABLE CLONING VECTORS SO VIROLOGY LA English DT Note ID TEMPERATURE-SENSITIVE MUTANTS; GENE-EXPRESSION; POLYMERASE; INSERTION; SELECTION; DELETION; MARKER C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 23 TC 48 Z9 53 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD SEP PY 1992 VL 190 IS 1 BP 522 EP 526 DI 10.1016/0042-6822(92)91246-Q PG 5 WC Virology SC Virology GA JL549 UT WOS:A1992JL54900061 PM 1529553 ER PT J AU JIANG, BM TSUNEMITSU, H GENTSCH, JR GLASS, RI GREEN, KY QIAN, Y SAIF, LJ AF JIANG, BM TSUNEMITSU, H GENTSCH, JR GLASS, RI GREEN, KY QIAN, Y SAIF, LJ TI NUCLEOTIDE-SEQUENCE OF GENE-5 ENCODING THE INNER CAPSID PROTEIN (VP6) OF BOVINE GROUP-C ROTAVIRUS - COMPARISON WITH CORRESPONDING GENES OF GROUP-C, GROUP-A, AND GROUP-B ROTAVIRUSES SO VIROLOGY LA English DT Note ID POLYPEPTIDES; DIARRHEA; OUTBREAK; CLONING C1 HOKKAIDO PREFECTURAL SHINTOKU ANIM HUSBANDRY EXPT STN,SHINTO KU,HOKKAIDO 081,JAPAN. OHIO STATE UNIV,OHIO AGR RES & DEV CTR,FOOD ANIM HLTH RES PROGRAM,WOOSTER,OH 44691. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. EMORY UNIV,SCH MED,DEPT PEDIAT,ATLANTA,GA 30322. RP JIANG, BM (reprint author), CTR DIS CONTROL,NATL CTR INFECT DIS,DIV VIRAL & RICKETTSIAL DIS,ATLANTA,GA 30333, USA. FU NIAID NIH HHS [YO2-AI-90002-02] NR 30 TC 16 Z9 17 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD SEP PY 1992 VL 190 IS 1 BP 542 EP 547 DI 10.1016/0042-6822(92)91250-X PG 6 WC Virology SC Virology GA JL549 UT WOS:A1992JL54900065 PM 1326819 ER PT J AU SUBBARAO, EK PERKINS, M TREANOR, JJ MURPHY, BR AF SUBBARAO, EK PERKINS, M TREANOR, JJ MURPHY, BR TI THE ATTENUATION PHENOTYPE CONFERRED BY THE M-GENE OF THE INFLUENZA A/ANN-ARBOR/6/60 COLD-ADAPTED VIRUS (H2N2) ON THE A/KOREA/82 (H3N2) REASSORTANT VIRUS RESULTS FROM A GENE CONSTELLATION EFFECT SO VIRUS RESEARCH LA English DT Article DE ATTENUATION PHENOTYPE; COLD-ADAPTED INFLUENZA-A VIRUS; M-GENE ID ADULT SERONEGATIVE VOLUNTEERS; A VIRUS; AVIAN-HUMAN; WILD-TYPE; RNA SEGMENT-7; INACTIVATED VACCINE; NUCLEOTIDE-SEQUENCE; YOUNG-CHILDREN; PROTEIN GENES; DONOR VIRUS AB A single gene reassortant (SGR) virus that derived its M gene from the attenuated influenza A/Ann Arbor/6/60 cold-adapted (CA) donor virus and the remaining genes from the A/Korea/82 (H3N2) wild type (WT) virus (designated A/Korea/82 CA M-SGR) was previously shown to be attenuated in mice, hamsters, ferrets, and humans. The attenuation (ATT) phenotype of this SGR virus could result directly from an altered function of the mutant M gene product of the A/Ann Arbor/6/60 CA virus, which differs from the M gene of the A/Ann Arbor/6/60 WT virus at only one amino acid or, indirectly from a gene constellation effect in which ATT results from an inefficient interaction between the products of the M gene of the A/Ann Arbor/6/60 virus and other genes of the A/Korea/82 virus. Several lines of evidence from the present study are consistent with our interpretation that the ATT phenotype of the A/Korea/82 CA M-SGR results from a gene constellation effect. First, the A/Korea/82 CA M-SGR and an A/Korea/82 SGR containing the A/Ann Arbor/6/60 WT M gene were each restricted in replication in the upper and lower respiratory tract of mice compared with the A/Korea/82 WT virus. Second, an A/Udorn/72 CA M-SGR containing the M gene from the A/Ann Arbor/6/60 CA donor virus in a background of other genes derived from the A/Udorn/72 (H3N2) WT virus was not attenuated in the respiratory tract of mice. These data suggest that the change in the amino acid sequence of the M gene product from the A/Ann Arbor/6/60 WT to CA virus is not responsible for the ATT phenotype of the A/Korea/82 CA M-SGR. In addition, evidence of the genetic instability of the A/Korea/82 CA M-SGR is presented, specifically, an extragenic mutation that results in loss of the ATT phenotype. The implications of these findings for the ATT phenotype of the live attenuated reassortant viruses derived from the A/Ann Arbor/6/60 CA donor virus are discussed. C1 UNIV ROCHESTER,SCH MED,DIV INFECT DIS,ROCHESTER,NY 14627. RP SUBBARAO, EK (reprint author), NIAID,INFECT DIS LAB,RESP VIRUSES SECT,BLDG 7,ROOM 106,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 40 TC 33 Z9 34 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-1702 J9 VIRUS RES JI Virus Res. PD SEP 1 PY 1992 VL 25 IS 1-2 BP 37 EP 50 DI 10.1016/0168-1702(92)90098-T PG 14 WC Virology SC Virology GA JN652 UT WOS:A1992JN65200004 PM 1413993 ER PT J AU ZIBERT, A SELINKA, HC ELROYSTEIN, O WIMMER, E AF ZIBERT, A SELINKA, HC ELROYSTEIN, O WIMMER, E TI THE SOLUBLE FORM OF 2 N-TERMINAL DOMAINS OF THE POLIOVIRUS RECEPTOR IS SUFFICIENT FOR BLOCKING VIRAL-INFECTION SO VIRUS RESEARCH LA English DT Article DE POLIOVIRUS RECEPTOR; GLYCOPROTEIN; INACTIVATION ID BACTERIOPHAGE-T7 RNA-POLYMERASE; IMMUNOGLOBULIN SUPERFAMILY; CELLULAR RECEPTOR; MAMMALIAN-CELLS; VACCINIA VIRUS; HELA-CELLS; SITE; EXPRESSION; NEUTRALIZATION; BINDING AB By means of deleting a C-terminal portion of the open reading frame of the poliovirus receptor cDNA, and by vaccinia virus-mediated overexpression we have produced a protein corresponding to the first two N-terminal Ig-like domains of the poliovirus receptor. This protein that lacked the third Ig-like domain, the transmembrane region and most of the intracellular C-terminal tail was detected in the medium of vaccinia virus infected cells. The properties of the truncated PVR cDNA were further characterized by in vitro translation and modification. The molecular weight of the unmodified protein was found to be 27 kDa; translation in the presence of dog pancreas microsomes led to an increase in molecular weights which we attribute to N-glycosylation. Upon incubation with poliovirus at 37-degrees-C, the vaccinia-virus generated protein specifically reduced infectivity of poliovirus. Sucrose gradients of poliovirus particles derived after incubation with the protein showed the induction of a slower sedimenting particle (135S). Our experiments suggest that the two N-terminal domains of the poliovirus receptor in soluble form are sufficient for the conversion of poliovirus into a non-infectious particle. C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. RP ZIBERT, A (reprint author), SUNY STONY BROOK,DEPT MICROBIOL,STONY BROOK,NY 11794, USA. FU NCI NIH HHS [CA-28146]; NIAID NIH HHS [AI-15122] NR 29 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-1702 J9 VIRUS RES JI Virus Res. PD SEP 1 PY 1992 VL 25 IS 1-2 BP 51 EP 61 DI 10.1016/0168-1702(92)90099-U PG 11 WC Virology SC Virology GA JN652 UT WOS:A1992JN65200005 PM 1329376 ER PT J AU STOKES, A TIERNEY, EL MURPHY, BR HALL, SL AF STOKES, A TIERNEY, EL MURPHY, BR HALL, SL TI THE COMPLETE NUCLEOTIDE-SEQUENCE OF THE JS STRAIN OF HUMAN PARAINFLUENZA VIRUS TYPE-3 - COMPARISON WITH THE WASH/47885/57 PROTOTYPE STRAIN SO VIRUS RESEARCH LA English DT Article DE HUMAN PARAINFLUENZA VIRUS; NUCLEOTIDE SEQUENCE ID AMINO-ACID-SEQUENCE; HEMAGGLUTININ-NEURAMINIDASE GLYCOPROTEIN; RECOMBINANT BACULOVIRUS; MOLECULAR-CLONING; SURFACE GLYCOPROTEINS; FUSION GLYCOPROTEIN; FLANKING REGIONS; INSECT CELLS; INFLUENZA; PROTEIN AB The nucleotide sequence of the JS strain of human parainfluenza virus type 3 (PIV3) was determined from a series of 14 overlapping cDNA clones and was compared to that of the previously sequenced prototype PIV3 strain, Wash/47885/57 (Galinski, 1991). Overall, there were 630 (4%) nucleotide differences between the two viruses. 15462 nucleotides comprised the JS genome in contrast to 15463 which constituted the genome of the prototype virus. This was accounted for by a single nucleotide deletion in the 5' non-coding region of the JS phosphoprotein gene. Four nucleotide substitutions were found in the leader region at the 3' end of the viral genome at positions 24, 28, 42 and 45, whereas no differences were found in the 44 base trailer region. All of the transcription start and stop signals and intergenic sequences were conserved between the two viruses with the exception of the transcription stop signal of the matrix (M) gene where there was a nucleotide transposition between bases 7 and 8. A comparison of all of the nucleotide differences in the 3' and 5' non-coding regions of each gene showed a variability of 9.8% and 10.5%, respectively. The 3' non-coding regions of the nucleocapsid (NP) and M genes were completely conserved in contrast to the polymerase (L) gene in which 25% of the nucleotides were different. Differences were observed in the 5' non-coding regions of each gene and ranged from 5.9% for the hemagglutinin neuraminidase (HN) gene to 14.6% for the M gene. An analysis of the amino acid differences in each open reading frame revealed that of all the genes, the coding region of the M gene was the most highly conserved (1.1% amino acid variability), while the phosphoprotein (P) gene was the most variable (5.8% amino acid variability). As these two viruses are wild type strains, these differences in nucleotide and amino acid sequence are compatible with efficient replication in vivo. RP STOKES, A (reprint author), NIAID,INFECT DIS LAB,BETHESDA,MD 20892, USA. NR 36 TC 23 Z9 24 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-1702 J9 VIRUS RES JI Virus Res. PD SEP 1 PY 1992 VL 25 IS 1-2 BP 91 EP 103 DI 10.1016/0168-1702(92)90102-F PG 13 WC Virology SC Virology GA JN652 UT WOS:A1992JN65200008 PM 1329377 ER PT J AU BOUSSAOUD, D DESIMONE, R UNGERLEIDER, LG AF BOUSSAOUD, D DESIMONE, R UNGERLEIDER, LG TI SUBCORTICAL CONNECTIONS OF VISUAL AREAS MST AND FST IN MACAQUES SO VISUAL NEUROSCIENCE LA English DT Article DE PULVINAR; CLAUSTRUM; STRIATUM; PONS; EXTRASTRIATE CORTEX ID PURSUIT EYE-MOVEMENTS; SUPERIOR TEMPORAL SULCUS; DORSOLATERAL PONTINE NUCLEUS; MONKEY AOTUS-TRIVIRGATUS; INFERIOR PARIETAL LOBULE; DORSAL TERMINAL NUCLEUS; ACCESSORY OPTIC TRACT; RHESUS-MONKEY; CORTICAL CONNECTIONS; HORSERADISH-PEROXIDASE AB To examine the subcortical connections of the medial superior temporal and fundus of the superior temporal visual areas (MST and FST, respectively), we injected anterograde and retrograde tracers into 16 physiologically identified sites within the two areas in seven macaque monkeys. The subcortical connections of MST and FST were found to be very similar. Both areas were found to be reciprocally connected with the pulvinar, mainly with its medial subdivision, and with the claustrum. Nonreciprocal projections from both MST and FST were consistently found in the striatum (caudate and putamen), reticular nucleus of the thalamus, and the pontine nuclei. The labeled terminals in the pons were in the dorsolateral, lateral, dorsal, and peduncular nuclei. Additional nonreciprocal projections were found in one MST and one FST case to the nucleus of the optic tract, and, in one FST case, to the lateral terminal nucleus. Finally, three cases showed a nonreciprocal projection to FST from the basal forebrain. The subcortical structures containing label following MST and FST injections were largely the same as those labeled after injections of the middle temporal visual area (MT), but the label within each structure after MST and FST injections was more widespread than that from MT, overlapping the distribution of label that has been reported after injections of parietal visual areas. This finding is consistent with the known contributions of MST and FST to the functions of parietal cortex, such as eye-movement control. C1 NIMH,NEUROPSYCHOL LAB,BLDG 9,ROOM 1E104,BETHESDA,MD 20892. RI Boussaoud, Driss/B-6932-2008 NR 71 TC 95 Z9 95 U1 0 U2 7 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0952-5238 J9 VISUAL NEUROSCI JI Visual Neurosci. PD SEP-OCT PY 1992 VL 9 IS 3-4 BP 291 EP 302 PG 12 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA JN067 UT WOS:A1992JN06700009 PM 1390388 ER PT J AU OSAWA, Y HIGHET, RJ POHL, LR AF OSAWA, Y HIGHET, RJ POHL, LR TI THE USE OF STABLE ISOTOPES TO IDENTIFY REACTIVE METABOLITES AND TARGET MACROMOLECULES ASSOCIATED WITH TOXICITIES OF HALOGENATED HYDROCARBON COMPOUNDS SO XENOBIOTICA LA English DT Article ID CARBON-TETRACHLORIDE; ELECTROPHILIC CHLORINE; HALOTHANE HEPATITIS; MOUSE KIDNEY; CHLOROFORM; HEME; NEOANTIGENS; PHOSGENE; BRCCL3; BIOTRANSFORMATION AB 1. Halogenated compounds, such as the inhalation anaesthetics, halothane and enflurane, and the chemicals chloroform, carbon tetrachloride, and bromotrichloromethane can cause hepatotoxicity, nephrotoxicity, and inactivation of cytochromes P-450. Each of these toxicities is mediated by reactive metabolites. 2. Stable isotopes of hydrogen, carbon, chlorine and oxygen have been used in conjunction with mass spectrometry and n.m.r. spectrometry to identify the structures of these metabolites, to elucidate the mechanisms of their formation, and to characterize the structures of their macromolecular adducts. 3. In a number of cases, oxidative pathways of metabolism to toxic metabolites have been defined by kinetic deuterium isotope effects. 4. Recently, we have found that the trichloromethyl radical metabolite of bromotrichloromethane can activate myoglobin by causing the covalent cross-linking of haem to protein. The structure of a haem-myoglobin adduct has been defined by the use of stable isotope studies. C1 NHLBI,CHEM LAB,BETHESDA,MD 20892. NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. NR 25 TC 3 Z9 3 U1 0 U2 1 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0049-8254 J9 XENOBIOTICA JI Xenobiotica PD SEP-OCT PY 1992 VL 22 IS 9-10 BP 1147 EP 1156 PG 10 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA JR412 UT WOS:A1992JR41200011 PM 1441605 ER PT J AU JENSEN, RT AF JENSEN, RT TI PANCREATIC PATHOLOGY SO YALE JOURNAL OF BIOLOGY AND MEDICINE LA English DT Editorial Material ID LUNG-CANCER CELLS; RAT PANCREAS; CCK RECEPTORS; CHOLECYSTOKININ RECEPTORS; ENZYME-SECRETION; GASTRIN; AFFINITY; PARIETAL; CERULEIN; DESENSITIZATION RP JENSEN, RT (reprint author), NIDDKD,DIGEST DIS BRANCH,BETHESDA,MD, USA. NR 27 TC 0 Z9 0 U1 1 U2 1 PU YALE J BIOL MED INC PI NEW HAVEN PA 333 CEDAR ST, NEW HAVEN, CT 06510 SN 0044-0086 J9 YALE J BIOL MED JI Yale J. Biol. Med. PD SEP-OCT PY 1992 VL 65 IS 5 BP 465 EP 469 PG 5 WC Biology; Medicine, General & Internal; Medicine, Research & Experimental SC Life Sciences & Biomedicine - Other Topics; General & Internal Medicine; Research & Experimental Medicine GA LR886 UT WOS:A1992LR88600010 ER PT J AU LEE, YJ WICKNER, RB AF LEE, YJ WICKNER, RB TI AFG1, A NEW MEMBER OF THE SEC18-NSF, PAS1, CDC48-VCP, TBP FAMILY OF ATPASES SO YEAST LA English DT Article DE SACCHAROMYCES-CEREVISIAE; ATPASE; CHROMOSOME-V ID SECRETORY PATHWAY; FUSION PROTEIN; YEAST; TRANSPORT; NSF AB We have sequenced a gene that encodes a 377 amino acid putative protein with an ATPase motif typical of the protein family including SEC18p (NSF = N-ethyl maleimide-sensitive fusion protein; vesicle-mediated endoplasmic reticulum to Golgi protein transfer), PAS1p (peroxisome assembly), CDC48p (VCP = valosin-containing protein; cell cycle) and TBP1 (Tat-binding protein). This gene, AFG1 for ATPase family gene, also has substantial homology to these proteins outside the ATPase domain. AFG1 is located on chromosome V immediately centromere-proximal to MAK10. RP LEE, YJ (reprint author), NIDDKD,BIOCHEM PHARMACOL LAB,GENET SIMPLE EUKARYOTES SECT,BLDG 8,ROOM 207,BETHESDA,MD 20892, USA. NR 16 TC 18 Z9 19 U1 1 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0749-503X J9 YEAST JI Yeast PD SEP PY 1992 VL 8 IS 9 BP 787 EP 790 DI 10.1002/yea.320080912 PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Microbiology; Mycology GA JP855 UT WOS:A1992JP85500011 PM 1441755 ER PT J AU BETTELHEIM, FA REID, MB MCPHIE, P GARLAND, D AF BETTELHEIM, FA REID, MB MCPHIE, P GARLAND, D TI ON THE STABILITY OF BOVINE GAMMA-II CRYSTALLIN SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PHASE-SEPARATION; COLD CATARACT; LENS; WATER; HYDRATION C1 NEI,BETHESDA,MD 20892. NIDDKD,BETHESDA,MD 20892. RP BETTELHEIM, FA (reprint author), ADELPHI UNIV,DEPT CHEM,GARDEN CITY,NY 11530, USA. FU NEI NIH HHS [EY-02751] NR 16 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD AUG 31 PY 1992 VL 187 IS 1 BP 39 EP 44 DI 10.1016/S0006-291X(05)81455-X PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JL671 UT WOS:A1992JL67100007 PM 1520325 ER PT J AU RIECKMANN, P THEVENIN, C KEHRL, JH AF RIECKMANN, P THEVENIN, C KEHRL, JH TI OKADAIC ACID IS A POTENT INDUCER OF AP-1, NF-KAPPA-B, AND TUMOR-NECROSIS-FACTOR-ALPHA IN HUMAN B LYMPHOCYTES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PROTEIN TYROSINE KINASE; CELL ANTIGEN RECEPTOR; T-CELLS; ACTIVATION; PHOSPHATASES; PHOSPHORYLATION; INTERLEUKIN-1; TRANSCRIPTION; INHIBITION; PROMOTER C1 NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 28 TC 47 Z9 47 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD AUG 31 PY 1992 VL 187 IS 1 BP 51 EP 57 DI 10.1016/S0006-291X(05)81457-3 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JL671 UT WOS:A1992JL67100009 PM 1520341 ER PT J AU DANISHEFSKY, AT BURTON, LE RUBIN, JR AF DANISHEFSKY, AT BURTON, LE RUBIN, JR TI CRYSTALLIZATION AND PRELIMINARY CHARACTERIZATION OF 3 CRYSTAL FORMS OF HUMAN RECOMBINANT TRANSFORMING GROWTH FACTOR-ALPHA SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID MAMMARY EPITHELIAL-CELLS; TRANSGENIC MICE; TGF-ALPHA; FACTOR RECEPTOR; EXPRESSION; INDUCTION; OVEREXPRESSION; LOCALIZATION; PURIFICATION; HYPERPLASIA C1 GENENTECH INC,DEPT PROC DEV,SAN FRANCISCO,CA 94010. RP DANISHEFSKY, AT (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,POB B,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 37 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD AUG 31 PY 1992 VL 187 IS 1 BP 146 EP 151 DI 10.1016/S0006-291X(05)81471-8 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JL671 UT WOS:A1992JL67100023 PM 1520295 ER PT J AU UEKI, K MURAMATSU, T KINCAID, RL AF UEKI, K MURAMATSU, T KINCAID, RL TI STRUCTURE AND EXPRESSION OF 2 ISOFORMS OF THE MURINE CALMODULIN-DEPENDENT PROTEIN PHOSPHATASE REGULATORY SUBUNIT (CALCINEURIN-B) SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID CATALYTIC SUBUNIT; CDNA CLONE; IDENTIFICATION; SEQUENCE; DOMAIN; BRAIN RP UEKI, K (reprint author), NIAAA,MOLEC & CELLULAR NEUROBIOL LAB,IMMUNOL SECT,ROCKVILLE,MD 20852, USA. NR 22 TC 54 Z9 56 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD AUG 31 PY 1992 VL 187 IS 1 BP 537 EP 543 DI 10.1016/S0006-291X(05)81527-X PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JL671 UT WOS:A1992JL67100079 PM 1325794 ER PT J AU WLODAVER, A PAVLOVSKY, A GUSTCHINA, A AF WLODAVER, A PAVLOVSKY, A GUSTCHINA, A TI CRYSTAL-STRUCTURE OF HUMAN RECOMBINANT INTERLEUKIN-4 AT 2.25-ANGSTROM RESOLUTION SO FEBS LETTERS LA English DT Article DE CYTOKINE; X-RAY CRYSTALLOGRAPHY; PROTEIN STRUCTURE; REFINEMENT ID 3-DIMENSIONAL STRUCTURE; CRYSTALLIZATION; CRYSTALLOGRAPHY; GROWTH AB The crystal structure of human recombinant interleukin-4 (IL-4) has been solved by multiple isomorphous replacement, and refined to an R factor of 0.218 at 2.25 angstrom resolution. The molecule is a left-handed four-helix bundle with a short stretch of beta-sheet. The structure bears close resemblance to other cytokines such as granulocyte-macrophage colony stimulating factor (GM-CSF). Although no sequence similarity of IL-4 to GM-CSF and other related cytokines has been previously postulated, structure-based alignment of IL-4 and GM-CSF revealed that the core of the molecules, including large parts of all four helices and extending over half of the molecule, has 30% sequence identity. This may have identified regions which are not only important to maintain structure, but could also play a role in receptor binding. RP WLODAVER, A (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 21 TC 129 Z9 130 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD AUG 31 PY 1992 VL 309 IS 1 BP 59 EP 64 DI 10.1016/0014-5793(92)80739-4 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA JL068 UT WOS:A1992JL06800014 PM 1511746 ER PT J AU COLAIANNI, LA AF COLAIANNI, LA TI RETRACTION, COMMENT, AND ERRATA POLICIES OF THE UNITED-STATES-NATIONAL-LIBRARY-OF-MEDICINE SO LANCET LA English DT Article RP COLAIANNI, LA (reprint author), NATL LIB MED,BETHESDA,MD 20894, USA. NR 0 TC 7 Z9 8 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 AUG 29 PY 1992 VL 340 IS 8818 BP 536 EP 537 DI 10.1016/0140-6736(92)91723-L PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JL234 UT WOS:A1992JL23400015 PM 1354288 ER PT J AU PACAK, K ARMANDO, I FUKUHARA, K KVETNANSKY, R PALKOVITS, M KOPIN, IJ GOLDSTEIN, DS AF PACAK, K ARMANDO, I FUKUHARA, K KVETNANSKY, R PALKOVITS, M KOPIN, IJ GOLDSTEIN, DS TI NORADRENERGIC ACTIVATION IN THE PARAVENTRICULAR NUCLEUS DURING ACUTE AND CHRONIC IMMOBILIZATION STRESS IN RATS - AN INVIVO MICRODIALYSIS STUDY SO BRAIN RESEARCH LA English DT Article DE NOREPINEPHRINE; DIHYDROXYPHENYLGLYCOL; DIHYDROXYPHENYLACETIC ACID ID INDIVIDUAL HYPOTHALAMIC NUCLEI; NORADRENALINE RELEASE; TYROSINE-HYDROXYLASE; HIPPOCAMPAL NOREPINEPHRINE; EXTRACELLULAR DOPAMINE; SUPRAOPTIC NUCLEI; NEURON SYSTEMS; BRAIN-STEM; CATECHOLAMINES; PLASMA AB In vivo microdialysis was used to study the effects of single (2 h) or repeated (2 h for 7 consecutive days) immobilization (IMMO) stress on extracellular fluid concentrations of norepinephrine (NE) and the deaminated metabolites of NE and dopamine, dihydroxyphenylglycol (DHPG) and dihydroxyphenylacetic acid (DOPAC) in the paraventricular nucleus of conscious rats. During IMMO, NE, DHPG, and DOPAC levels increased markedly, with similar peak values and time courses in the repeatedly stressed and previously unstressed groups. NE levels during a 2-h baseline period were lower in the repeatedly stressed group than in the unstressed group (99 +/- 9 pg/ml vs. 167 +/- 13 pg/ml, P < 0.05), whereas DHPG (1,697 +/- 263 pg/ml vs. 1,424 +/- 194 pg/ml) and DOPAC (5,989 +/- 863 pg/ml vs. 4,428 +/- 1150 pg/ml) levels tended to be higher, so that the NE/DHPG ratio at baseline was significantly lower in the repeatedly stressed group (P < 0.05). The results indicate that IMMO stress enhances NE release, reuptake, metabolism, and synthesis in the PVN. Repeated exposure to IMMO may decrease the microdialysate NE/DHPG ratio by inhibiting exocytotic release or enhancing neuronal reuptake of NE. In either case, the results suggest that repeated exposure to stress alters the release and disposition of NE in the PVN of conscious animals. C1 NINCDS,CLIN NEUROSCI BRANCH,BLDG 10,ROOM 5N214,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RI Palkovits, Miklos/F-2707-2013; OI Palkovits, Miklos/0000-0003-0578-0387 NR 44 TC 108 Z9 108 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD AUG 28 PY 1992 VL 589 IS 1 BP 91 EP 96 DI 10.1016/0006-8993(92)91165-B PG 6 WC Neurosciences SC Neurosciences & Neurology GA JL781 UT WOS:A1992JL78100011 PM 1422825 ER PT J AU STADTMAN, ER AF STADTMAN, ER TI PROTEIN OXIDATION AND AGING SO SCIENCE LA English DT Article ID MIXED-FUNCTION OXIDATION; METAL-CATALYZED OXIDATION; RED BLOOD-CELLS; GLUTAMINE-SYNTHETASE; OXYGEN RADICALS; NONENZYMATIC GLYCOSYLATION; CYSTEINE PROTEINASE; DENATURED PROTEINS; OXIDIZED PROTEINS; DEGRADATION AB A number of systems that generate oxygen free radicals catalyze the oxidative modification of proteins. Such modifications mark enzymes for degradation by cytosolic neutral alkaline proteases. Protein oxidation contributes to the pool of damaged enzymes, which increases in size during aging and in various pathological states. The age-related increase in amounts of oxidized protein may reflect the age-dependent accumulation of unrepaired DNA damage that, in a random manner, affects the concentrations or activities of numerous factors that govern the rates of protein oxidation and the degradation of oxidized protein. RP STADTMAN, ER (reprint author), NHLBI,BIOCHEM LAB,BETHESDA,MD 20892, USA. NR 58 TC 2046 Z9 2119 U1 24 U2 114 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD AUG 28 PY 1992 VL 257 IS 5074 BP 1220 EP 1224 DI 10.1126/science.1355616 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL050 UT WOS:A1992JL05000017 PM 1355616 ER PT J AU TSARFATY, I RESAU, JH SHEN, RL KEYDAR, I FALETTO, DL VANDEWOUDE, GF AF TSARFATY, I RESAU, JH SHEN, RL KEYDAR, I FALETTO, DL VANDEWOUDE, GF TI THE MET PROTOONCOGENE RECEPTOR AND LUMEN FORMATION SO SCIENCE LA English DT Article ID HEPATOCYTE GROWTH-FACTOR; C-MET; SCATTER FACTOR; MOLECULAR-CLONING; KINASE-ACTIVITY; CELL-LINE; EXPRESSION; PROTOONCOGENE; IDENTIFICATION; ACTIVATION AB The met proto-oncogene product (Met) and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), have been implicated in cell mitogenic response, cell motility, and the promotion of the ordered spatial arrangement of tissue. By means of confocal laser-scanning microscopy, it was shown that Met is expressed in cells bordering lumen-like structures that resemble ducts in the human mammary cell line T47D. In human breast tissue biopsies, Met staining was intense in normal cells bordering mammary ducts but was reduced in adjacent tumor tissue. Met staining in lumen-forming organs colocalizes with staining of antibody to phosphotyrosine, which suggests that the Met receptor and its substrates may be activated in lumen structures or ducts. HGF/SF treatment of human epithelial carcinoma cell lines resulted in the formation of lumen-like structures in vitro. Reduced expression of Met could be related to the extent ot tumor cell differentiation. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,DIV CANC ETIOL,MOLEC ONCOL LAB,BETHESDA,MD 20892. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. TEL AVIV UNIV,DEPT CELL RES & IMMUNOL,IL-69978 TEL AVIV,ISRAEL. RI Shen, Rulong/E-4079-2011 FU PHS HHS [N01-C0-74101] NR 35 TC 247 Z9 251 U1 1 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 AUG 28 PY 1992 VL 257 IS 5074 BP 1258 EP 1261 DI 10.1126/science.1387731 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JL050 UT WOS:A1992JL05000027 PM 1387731 ER PT J AU KAHN, JO LAGAKOS, SW RICHMAN, DD CROSS, A PETTINELLI, C LIOU, SH BROWN, M VOLBERDING, PA CRUMPACKER, CS BEALL, G SACKS, HS MERIGAN, TC BELTANGADY, M SMALDONE, L DOLIN, R AF KAHN, JO LAGAKOS, SW RICHMAN, DD CROSS, A PETTINELLI, C LIOU, SH BROWN, M VOLBERDING, PA CRUMPACKER, CS BEALL, G SACKS, HS MERIGAN, TC BELTANGADY, M SMALDONE, L DOLIN, R TI A CONTROLLED TRIAL COMPARING CONTINUED ZIDOVUDINE WITH DIDANOSINE IN HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; AZIDOTHYMIDINE AZT; TOXICITY; INVITRO; THERAPY; HIV; 2',3'-DIDEOXYINOSINE; INHIBITION AB Background, Although zidovudine is effective in patients with human immunodeficiency virus (HIV) infection, its efficacy may decline with prolonged use. Didanosine is another inhibitor of HIV reverse transcriptase. We evaluated the effectiveness of changing anti-HIV treatment from zidovudine to didanosine. Methods. This multicenter, double-blind study involved 913 patients who had tolerated zidovudine for at least 16 weeks. The patients had the acquired immunodeficiency syndrome (AIDS), AIDS-related complex with less-than-or-equal-to 300 CD4 cells per cubic millimeter, or asymptomatic HIV infection with less-than-or-equal-to 200 CD4 cells per cubic millimeter. They were randomly assigned to receive 600 mg per day of zidovudine, 750 mg per day of didanosine, or 500 mg per day of didanosine. Results. There were significantly fewer new AIDS-defining events and deaths among the 298 subjects assigned to 500 mg per day of didanosine than among the subjects who continued to receive zidovudine (relative risk, 1.39; 95 percent confidence interval, 1.06 to 1.82; P = 0.015). With 750 mg of didanosine, there was no clear benefit over zidovudine (relative risk, 1.10; 95 percent confidence interval, 0.86 to 1.42). The efficacy of didanosine was unrelated to the duration of previous zidovudine treatment. In the two didanosine groups, there were improvements in the number of CD4 cells (P<0.001 for both groups) and in p24 antigen levels (P = 0.03 in the 500-mg group; P = 0.005 in the 750-mg group), as compared with the zidovudine group. Conclusions. Changing treatment from zidovudine to 500 mg per day of didanosine appears to slow the progression of HIV disease. C1 UNIV ROCHESTER,ROCHESTER,NY 14627. VET AFFAIRS MED CTR,SAN DIEGO,CA. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,WALLINGFORD,CT. STANFORD UNIV,STANFORD,CA 94305. UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,TORRANCE,CA 90509. HARVARD UNIV,BOSTON,MA 02115. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. NIAID,DIV AIDS,BETHESDA,MD 20892. RP KAHN, JO (reprint author), SAN FRANCISCO GEN HOSP,AIDS PROGRAM,WARD 84,995 POTRERO AVE,SAN FRANCISCO,CA 94110, USA. NR 37 TC 354 Z9 357 U1 0 U2 2 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 27 PY 1992 VL 327 IS 9 BP 581 EP 587 DI 10.1056/NEJM199208273270901 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA JK204 UT WOS:A1992JK20400001 PM 1353607 ER PT J AU HEALY, B AF HEALY, B TI ON GENE PATENTING SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article RP HEALY, B (reprint author), NIH,BETHESDA,MD 20892, USA. NR 5 TC 27 Z9 27 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 27 PY 1992 VL 327 IS 9 BP 664 EP 668 DI 10.1056/NEJM199208273270930 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JK204 UT WOS:A1992JK20400034 PM 1640972 ER PT J AU AVIGAN, J MURTAGH, JJ STEVENS, LA ANGUS, CW MOSS, J VAUGHAN, M AF AVIGAN, J MURTAGH, JJ STEVENS, LA ANGUS, CW MOSS, J VAUGHAN, M TI PERTUSSIS TOXIN-CATALYZED ADP-RIBOSYLATION OF GO-ALPHA WITH MUTATIONS AT THE CARBOXYL TERMINUS SO BIOCHEMISTRY LA English DT Article ID NUCLEOTIDE-BINDING-PROTEINS; ESCHERICHIA-COLI; BETA-GAMMA; GI-ALPHA; SUBUNIT; EXPRESSION; TRANSDUCIN; CHAIN; DNA; MYRISTOYLATION AB The guanine nucleotide-binding protein G(o-alpha) has been implicated in the regulation of Ca2+ channels in neural tissues. Covalent modification of G(o-alpha) by pertussis toxin-catalyzed ADP-ribosylation of a cysteine (position 351) four amino acids from the carboxyl terminus decouples G(o-alpha) from receptor. To define the structural requirements for ADP-ribosylation, preparations of recombinant G(o-alpha) with mutations within the five amino acids at the carboxyl terminus were evaluated for their ability to serve as pertussis toxin substrates. As expected, the mutant in which cysteine 351 was replaced by glycine (C351G) was not a toxin substrate. Other inactive mutants were G352D and L353-DELTA/Y354-DELTA. Mutations that had no significant effect on toxin-catalyzed ADP-ribosylation included G350D, G350R, Y354-DELTA, and L353V/Y354-DELTA. Less active mutants were L353G/Y354-DELTA, L353-DELTA/Y354-DELTA, and L353G. ADP-ribosylation of the active mutants, like that of wild-type G(o-alpha), was enhanced by the beta-gamma subunits of bovine transducin. It appears that three of the four terminal amino acids critically influence pertussis toxin-catalyzed ADP-ribosylation of G(o-alpha). RP AVIGAN, J (reprint author), NHLBI,CELLULAR METAB LAB,BETHESDA,MD 20892, USA. NR 31 TC 18 Z9 18 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD AUG 25 PY 1992 VL 31 IS 33 BP 7736 EP 7740 DI 10.1021/bi00148a039 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JK533 UT WOS:A1992JK53300039 PM 1510959 ER PT J AU REN, K WILLIAMS, GM HYLDEN, JLK RUDA, MA DUBNER, R AF REN, K WILLIAMS, GM HYLDEN, JLK RUDA, MA DUBNER, R TI THE INTRATHECAL ADMINISTRATION OF EXCITATORY AMINO-ACID RECEPTOR ANTAGONISTS SELECTIVELY ATTENUATED CARRAGEENAN-INDUCED BEHAVIORAL HYPERALGESIA IN RATS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE SPINAL CORD; CARRAGEENAN; THERMAL HYPERALGESIA; ANTINOCICEPTION; NMDA (NORMAL-METHYL-D-ASPARTATE); OPIOIDS; (RAT); (INTRATHECAL) ID REDUCES SPINAL NOCICEPTION; DORSAL HORN NEURONS; NMDA RECEPTOR; OPIATE RECEPTORS; MK-801 BLOCKS; GLYCINE SITE; PAIN; CORD; INFLAMMATION; MODEL AB A single unilateral injection of carrageenan (4.5-6.0 mg in 0.15-0.20 ml saline) into the rat hindpaw induced behavioral hyperalgesia as evidenced by a significant reduction in hindpaw withdrawal latency to a noxious thermal stimulus. The involvement of N-methyl-D-aspartate (NMDA) receptors in this model of hyperalgesia was examined by intrathecal administration of the selective excitatory amino acid (EAA) receptor antagonists: (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), ketamine hydrochloride (ketamine), 7-chlorokynurenic acid (7-Cl kynurenic acid), and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The effects of dizocilpine maleate (MK-801) were studied under the same conditions and published previously (Ren et al., 1992) and the data are presented for comparison. While the withdrawal latencies of the non-injected paws and of the paws of naive rats were not significantly affected by application of the EAA receptor antagonists at doses tested, the paw withdrawal latencies of the carrageenan-injected paws were elevated dose dependently. The rank order of potency of these agents to reduce hyperalgesia was: MK-801 greater-than-or-equal-to AP-5 greater-than-or-equal-to CPP = 7-C] kynurenic acid = ketamine much greater than CNQX > 0. In contrast, intrathecal injection of the opioid receptor agonists, [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAMGO, mu-selective) and [D-Pen2,D-Pen5] enkephalin (DPDPE, delta-selective), produced antinociception in both injected and non-injected paws. DAMGO was much more potent, while DPDPE was less potent, than MK-801. It is concluded that NMDA receptors are involved in the development of carrageenan-induced thermal hyperalgesia. RP REN, K (reprint author), NIDR,NEUROBIOL & ANESTHESIOL BRANCH,BLDG 30,ROOM B-20,BETHESDA,MD 20892, USA. NR 43 TC 205 Z9 206 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD AUG 25 PY 1992 VL 219 IS 2 BP 235 EP 243 DI 10.1016/0014-2999(92)90301-J PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JL895 UT WOS:A1992JL89500008 PM 1358641 ER PT J AU HOLBROOK, PG PANNELL, LK MURATA, Y DALY, JW AF HOLBROOK, PG PANNELL, LK MURATA, Y DALY, JW TI MOLECULAR-SPECIES ANALYSIS OF A PRODUCT OF PHOSPHOLIPASE-D ACTIVATION - PHOSPHATIDYLETHANOL IS FORMED FROM PHOSPHATIDYLCHOLINE IN PHORBOL ESTER-STIMULATED AND BRADYKININ-STIMULATED PC12-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN-KINASE-C; TANDEM MASS-SPECTROMETRY; FATTY-ACID COMPOSITION; FAST ATOM BOMBARDMENT; GLIOMA HYBRID-CELLS; PHOSPHATIDIC-ACID; DIACYLGLYCEROL FORMATION; P2-PURINERGIC AGONISTS; SIGNAL TRANSDUCTION; HL-60 GRANULOCYTES AB Tumor-promoting phorbol esters or calcium-mobilizing receptor ligands stimulate phosphatidylcholine breakdown and in many cells this is accompanied by phospholipase D (PLD) activation. We tested whether or not a direct relationship exists between these two phenomena. Pheochromocytoma (PC12) cells were stimulated with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate or with the calcium-mobilizing receptor ligand bradykinin in media containing 1% ethanol. The fatty acid composition of the molecular species of phosphatidylethanol (PEt), a product of PLD activation, formed in stimulated cells was compared with the molecular species of endogenous phospholipids isolated from unstimulated PC12 cells. PEt was isolated and analyzed by fast atom bombardment-mass spectrometry (FAB-MS) in the negative ion mode. Fatty acid composition and headgroup structure of the major PEt molecular ions were confirmed by linked scan analysis. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol were isolated from unstimulated cells and converted into phosphatidic acids using PLD. Mass spectra of the respective phosphatidic acids were obtained by fast atom bombardment-mass spectrometry as described above. The molecular species of PEt formed in 12-O-tetradecanoylphorbol-13-acetate- and bradykinin-stimulated PC12 cell were identical to those of phosphatidylcholine isolated from untreated cells. RP HOLBROOK, PG (reprint author), NIDDKD,BIOORGAN CHEM LAB,BLDG 10,RM 5N307,BETHESDA,MD 20814, USA. NR 55 TC 44 Z9 44 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 25 PY 1992 VL 267 IS 24 BP 16834 EP 16840 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JL053 UT WOS:A1992JL05300019 PM 1512226 ER PT J AU THEUER, CP FITZGERALD, D PASTAN, I AF THEUER, CP FITZGERALD, D PASTAN, I TI A RECOMBINANT FORM OF PSEUDOMONAS EXOTOXIN DIRECTED AT THE EPIDERMAL GROWTH-FACTOR RECEPTOR THAT IS CYTOTOXIC WITHOUT REQUIRING PROTEOLYTIC PROCESSING SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DIPHTHERIA-TOXIN; DOMAIN-II; ESCHERICHIA-COLI; FUSION PROTEIN; LOW PH; TRANSLOCATION; SEQUENCE; TERMINUS; BINDING; GENE AB Pseudomonas exotoxin A is composed of three structural domains that mediate cell recognition (I), membrane translocation (II), and ADP-ribosylation (III). Within the cell, the toxin is cleaved within domain II to produce a 37-kDa carboxyl-terminal fragment, containing amino acids 280-613, which is translocated to the cytosol and causes cell death. In this study, we constructed a mutant protein (PE37), composed of amino acids 280-613 of Pseudomonas exotoxin A, which does not require proteolysis to translocate. PE37 was targeted specifically to cells with epidermal growth factor receptors by inserting transforming growth factor-alpha (TGF-alpha) after amino acid 607 near the carboxyl terminus of Pseudomonas exotoxin A. PE37/TGF-alpha was very cytotoxic to cells with epidermal growth factor receptors. It was severalfold more cytotoxic than a derivative of full-length Pseudomonas exotoxin A containing TGF-alpha in the same position, probably because the latter requires intracellular proteolytic processing to exhibit its cytotoxicity, and proteolytic processing is not 100% efficient. Deletion of 2, 4, or 7 amino acids from the amino terminus of PE37/TGF-alpha greatly diminished cytotoxic activity, indicating the need for a proper amino-terminal sequence. In addition, a mutant containing an internal deletion of amino acids 314-380 was minimally active, indicating that other regions of domain II are also required for the cytotoxic activity of Pseudomonas exotoxin A. C1 NCI,DIV CANC BIOL DIAGNOSIS & CTR,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 32 TC 36 Z9 36 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 AUG 25 PY 1992 VL 267 IS 24 BP 16872 EP 16877 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JL053 UT WOS:A1992JL05300025 PM 1512230 ER PT J AU LAROCHELLE, WJ PIERCE, JH MAYSIROFF, M GIESE, N AARONSON, SA AF LAROCHELLE, WJ PIERCE, JH MAYSIROFF, M GIESE, N AARONSON, SA TI 5 PDGF-B AMINO-ACID SUBSTITUTIONS CONVERT PDGF-A TO A PDGF B-LIKE TRANSFORMING MOLECULE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SIMIAN SARCOMA-VIRUS; GROWTH-HORMONE RECEPTOR; V-SIS; GENE; BINDING; CHAIN; MUTAGENESIS; IDENTIFICATION; DIMERIZATION; LOCALIZATION AB We used site-directed mutagenesis to determine the minimum number of PDGF B residues needed to convert PDGF A to a potently transforming PDGF B-like molecule. Substitution of two PDGF B subdomains, 106-115 and 135-144, were found to be critical. These substitutions were sufficient to broaden the ability of PDGF A to activate beta as well as alpha-platelet-derived growth factor (PDGF) receptors and increase its transforming efficiency to that of PDGF B. Within subdomain I, either PDGF B residues Arg- 109 and Asn-115 or Arg-109, Leu-110, and Arg-113, in combination with subdomain II PDGF B residues Asn-136, Arg-137, and Arg-142 were identified as being essential. Those mutants with transforming ability comparable with PDGF B showed significantly lower efficiencies of beta-receptor triggering. Thus, our studies identify a small number of PDGF B amino acids indispensable for beta-PDGF receptor interaction and suggest that a low level of beta-PDGF receptor activation is sufficient to dramatically increase PDGF transforming efficiency in NIH 3T3 cells. RP LAROCHELLE, WJ (reprint author), NIH,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892, USA. NR 28 TC 33 Z9 33 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 AUG 25 PY 1992 VL 267 IS 24 BP 17074 EP 17077 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JL053 UT WOS:A1992JL05300054 PM 1380958 ER PT J AU NOVAK, JM STEIN, MP LITTLE, SF LEPPLA, SH FRIEDLANDER, AM AF NOVAK, JM STEIN, MP LITTLE, SF LEPPLA, SH FRIEDLANDER, AM TI FUNCTIONAL-CHARACTERIZATION OF PROTEASE-TREATED BACILLUS-ANTHRACIS PROTECTIVE ANTIGEN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PSEUDOMONAS EXOTOXIN; ADENYLATE-CYCLASE; DIPHTHERIA-TOXIN; LETHAL TOXIN; EUKARYOTIC CELLS; RECEPTOR-BINDING; LOW PH; ENTRY; PURIFICATION; ENDOCYTOSIS AB Characterization of the functional domains of Bacillus anthracis protective antigen (PA, 83-kDa), the common cellular binding molecule for both anthrax edema toxin and anthrax lethal toxin, is important for understanding the mechanism of entry and action of the anthrax toxins. In this study, we generated both biologically active (facilitates killing of J774A.1 cells in combination with lethal factor, LF) and inactive preparations of PA by protease treatment. Limited proteolytic digestion of PA in vitro with trypsin generated a 20-kDa fragment and a biologically active 63-kDa fragment. In contrast, limited digestion of PA with chymotrypsin yielded a preparation containing 37- and 47-kDa fragments defective for biological activity. Treatment with both chymotrypsin and trypsin generated three major fragments, 20, "17," and 47 kDa as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. This PA preparation was also biologically inactive. To investigate the nature of the defect resulting from chymotrypsin treatment, we assayed PA preparations for the ability to bind to the cellular receptor and to bind and internalize I-125-LF. All radiolabeled PA preparations bound with specificity to J774A.1 cells and exhibited affinities similar to native 83-kDa PA. Once bound to the cell surface receptor, both trypsin-treated PA and chymotrypsin/trypsin-treated PA specifically bound I-125-LF with high affinity. Finally, these PA preparations delivered I-125-LF to a Pronase-resistant cellular compartment in a time- and temperature-dependent fashion. Thus, the biological defect exhibited by chymotrypsin-treated PA is not at the level of cell binding or internalization but at a step later, such as toxin routing or processing by J774A.1 cells. These protease-treated preparations of PA should prove useful in both elucidating the intracellular processing of anthrax lethal toxin and determining the structure-function relationship of PA and LF. C1 NIDR, MICROBIAL ECOL LAB, BETHESDA, MD 20892 USA. RP USA, MED RES INST INFECT DIS, DIV BACTERIOL, FT DETRICK, FREDERICK, MD 21702 USA. NR 40 TC 55 Z9 55 U1 0 U2 3 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 AUG 25 PY 1992 VL 267 IS 24 BP 17186 EP 17193 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JL053 UT WOS:A1992JL05300071 PM 1512256 ER PT J AU LIN, XL LIN, YZ KOELSCH, G GUSTCHINA, A WLODAWER, A TANG, J AF LIN, XL LIN, YZ KOELSCH, G GUSTCHINA, A WLODAWER, A TANG, J TI ENZYMATIC-ACTIVITIES OF 2-CHAIN PEPSINOGEN, 2-CHAIN PEPSIN, AND THE AMINO-TERMINAL LOBE OF PEPSINOGEN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IMMUNODEFICIENCY-VIRUS PROTEASE; ASPARTIC PROTEINASES; INTRAMOLECULAR ACTIVATION; PORCINE PEPSINOGEN; ACID PROTEASES; ACTIVE-SITE; RESOLUTION; PURIFICATION; MECHANISM; FORM AB In order to study the relationships of aspartic proteases, we have modified pepsin, a single-chain eukaryotic enzyme, to a two-chain heterodimer, which resembles aspartic proteases from retrovirus, including human immunodeficiency virus. Two fragments of pepsinogen, residues 1P-172 and 173-326, were expressed separately in Escherichia coli. Mixtures of chains were refolded from urea solutions to generate an active two-chain pepsinogen, which was converted to two-chain pepsin in acid solutions. The intramolecular and bimolecular activation constants (k1 and k2) of two-chain pepsinogen are about 1.5-fold and one-sixth, respectively, of those for pepsinogen. Structural evidence suggests that the faster k1 of two-chain pepsinogen is due to decreased interaction of the propeptide with the pepsin moiety, implying that the rate-limiting step in the intramolecular activation of pepsinogen is the "conformational dissociation" of its propeptide. Two-chain pepsin has the same K(m) but only one-sixth of the k(cat), of pepsin. Both pepsinogen chains are capable of independent refolding. The refolding of the NH2-terminal chain, which contains the propeptide and the NH2-terminal lobe, generated a small amount of proteolytic activity which is likely derived from the homodimer of the NH2-terminal lobe. It has been postulated that mammalian aspartic proteases, which contain two structurally homologous lobes, are derived in evolution from a homodimer enzyme by gene duplication and fusion (Tang, J., James, M. N. G., Hsu, I.-N., Jenkins, J. A., and Blundell, T. L. (1978) Nature 271, 618-621). The observation of the homodimer activity of the NH2-terminal lobe of pepsinogen suggests that the interface of the lobes is conservative in evolution. C1 OKLAHOMA MED RES FDN,PROT STUDIES PROGRAM,825 NE 13TH ST,OKLAHOMA CITY,OK 73104. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD 21702. UNIV OKLAHOMA,HLTH SCI CTR,DEPT BIOCHEM & MOLEC BIOL,OKLAHOMA CITY,OK 73104. FU NIAID NIH HHS [AI-26762]; NIDDK NIH HHS [DK-01107]; PHS HHS [N01-C0-74101] NR 33 TC 27 Z9 28 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 AUG 25 PY 1992 VL 267 IS 24 BP 17257 EP 17263 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JL053 UT WOS:A1992JL05300080 PM 1512263 ER PT J AU SOLTOFF, SP RABIN, SL CANTLEY, LC KAPLAN, DR AF SOLTOFF, SP RABIN, SL CANTLEY, LC KAPLAN, DR TI NERVE GROWTH-FACTOR PROMOTES THE ACTIVATION OF PHOSPHATIDYLINOSITOL 3-KINASE AND ITS ASSOCIATION WITH THE TRK TYROSINE KINASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CYTOPLASMIC SIGNALING PROTEINS; PC12 PHEOCHROMOCYTOMA CELLS; PHOSPHOLIPASE-C-GAMMA; PDGF BETA-RECEPTOR; PROTOONCOGENE PRODUCT; PROTO-ONCOGENE; NGF RECEPTOR; LOW-AFFINITY; PHOSPHORYLATION; BINDING AB We investigated the involvement of phosphatidylinositol 3-kinase (PtdIns 3-kinase) in the initiation of signal transduction by nerve growth factor (NGF) in the rat pheochromocytoma PC12 cell line. PtdIns 3-kinase catalyzes the formation of phosphoinositides with phosphate in the D-3 position of the inositol ring and previously has been found to associate with other activated protein tyrosine kinases, including growth factor receptor tyrosine kinases. Anti-phosphotyrosine immunoprecipitates had PtdIns 3-kinase activity that reached a maximum (9 times the basal activity) after a 5-min exposure of PC12 cells to NGF (100 ng/ml). Since NGF activates the tyrosine kinase activity of gp140trk, the protein product of the trk proto-oncogene, we also examined the association of PtdIns 3-kinase with gp140trk. Anti-gp140trk immunoprecipitates from NGF-stimulated PC12 cells had increased PtdIns 3-kinase activity compared to that of unstimulated cells, and larger increases were detected in cells overexpressing gp140trk, indicating that PtdIns 3-kinase associates with gp140trk. NGF produced large increases in [P-32]phosphatidylinositol 3,4-bisphosphate and [P-32]phosphatidylinositol 3,4,5-trisphosphate in PC12 cells labeled with [P-32]orthophosphate, indicating an increase in PtdIns 3-kinase activity in intact cells. Using an anti-85-kDa PtdIns 3-kinase subunit antibody, we found that NGF promoted the tyrosine phosphorylation of an 85-kDa protein and two proteins close to 110 kDa. These studies demonstrate that NGF activates PtdIns 3-kinase and promotes its association with gp140trk and also show that NGF promotes the tyrosine phosphorylation of the 85-kDa subunit of PtdIns 3-kinase. Thus, PtdIns 3-kinase activation appears to be involved in differentiation as well as mitogenic responses. C1 NCI,FREDERICK CANC RES & DEV CTR,BASIC RES PROGRAM,ADV BIOSCI LAB,FREDERICK,MD 21702. RP SOLTOFF, SP (reprint author), TUFTS UNIV,DEPT PHYSIOL,136 HARRISON AVE,BOSTON,MA 02111, USA. RI Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 FU NCI NIH HHS [N01-CO-74101]; NIGMS NIH HHS [GM-41890, R01 GM041890] NR 48 TC 212 Z9 213 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 AUG 25 PY 1992 VL 267 IS 24 BP 17472 EP 17477 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JL053 UT WOS:A1992JL05300110 PM 1380963 ER PT J AU BURKHART, JG BURKHART, BA SAMPSON, K MALLING, HV AF BURKHART, JG BURKHART, BA SAMPSON, K MALLING, HV TI EVIDENCE FOR A PREVIOUSLY UNDETECTED CPG METHYL-DIRECTED RESTRICTION SYSTEM IN ESCHERICHIA-COLI SO NUCLEIC ACIDS RESEARCH LA English DT Article ID ESCHERICHIA-COLI; DNA; STRAIN; RESCUE RP BURKHART, JG (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 6 TC 15 Z9 15 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 AUG 25 PY 1992 VL 20 IS 16 BP 4368 EP 4368 DI 10.1093/nar/20.16.4368 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JL464 UT WOS:A1992JL46400038 PM 1387206 ER PT J AU BENTON, D AF BENTON, D TI AN INFORMATION ENGINEERING OVERVIEW OF THE HUMAN GENOME PROJECT SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 1 EP CINF PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200985 ER PT J AU BRYANT, S AF BRYANT, S TI WINDOWS ON BIOLOGICAL FUNCTION - AN OVERVIEW OF STRUCTURED DATABASES, SOFTWARE TOOLKITS, AND INFORMATICS RESEARCH AT NCBI SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20209. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 2 EP CINF PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200986 ER PT J AU MESSINA, M AF MESSINA, M TI PROGRAM PERSPECTIVES - FOOD FOR CANCER PREVENTION SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 7 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200007 ER PT J AU GANSOW, OA AF GANSOW, OA TI MEDICAL APPLICATION OF GENERATOR PRODUCED RADIONUCLIDES - CURRENT CLINICAL-RESULTS WITH ANTIBODIES AND FUTURE-DIRECTIONS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,CHEM SECT,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 9 EP NUCL PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ313 UT WOS:A1992JJ31300009 ER PT J AU XIE, FM FORD, H HEGEDUS, L KELLEY, JA AF XIE, FM FORD, H HEGEDUS, L KELLEY, JA TI HPLC APPROACHES FOR THE SELECTIVE MEASUREMENT OF ENDOGENOUS PYRIMIDINE RIBONUCLEOSIDES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 10 EP ANYL PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200411 ER PT J AU HUTCHINSON, KD BUNCE, DM AF HUTCHINSON, KD BUNCE, DM TI EVALUATION OF TEACHING SKILLS OF PARTICIPANTS IN AN INSTITUTE FOR CHEMICAL EDUCATION (ICE) IN-SERVICE WORKSHOP SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDDK,LBC,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 12 EP CHED PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200843 ER PT J AU WU, CC MIRZADEH, S RAUBITSCHEK, A KUMAR, K PARKER, D GANSOW, OA AF WU, CC MIRZADEH, S RAUBITSCHEK, A KUMAR, K PARKER, D GANSOW, OA TI THE CHEMICAL FATE OF BI-212-CHELATES FORMED BY BETA-DECAY OF PB-212-CHELATES IN SOLUTION AND LOCALIZED IN CELLS BY LINKAGE TO INTERNALIZING MONOCLONAL-ANTIBODIES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,CHEM SECT,BETHESDA,MD 20892. UNIV DURHAM,DEPT CHEM,DURHAM DH1 3HP,ENGLAND. CITY HOPE NATL MED CTR,DUARTE,CA 91010. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 16 EP NUCL PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ313 UT WOS:A1992JJ31300016 ER PT J AU DATTA, AK KASPRZAK, KS AF DATTA, AK KASPRZAK, KS TI POSSIBLE INVOLVEMENT OF OXIDATIVE DNA DAMAGE IN THE MECHANISM(S) OF CARCINOGENESIS BY NICKEL, A HUMAN RESPIRATORY-TRACT CARINOGEN SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES FACIL,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 21 EP CHAS PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200803 ER PT J AU KEEFER, LK CHRISTODOULOU, D DUNAMS, TM HRABIE, JA MARAGOS, CM SAAVEDRA, JE WINK, DA AF KEEFER, LK CHRISTODOULOU, D DUNAMS, TM HRABIE, JA MARAGOS, CM SAAVEDRA, JE WINK, DA TI CHEMISTRY OF THE NONOATES, UNUSUAL N-NITROSO COMPOUNDS FORMED BY REACTING NITRIC-OXIDE WITH NUCLEOPHILES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. PRI DYN CORP,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 1 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 23 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200023 ER PT J AU SAAVEDRA, JE DUNAMS, TM FLIPPENANDERSON, JL KEEFER, LK AF SAAVEDRA, JE DUNAMS, TM FLIPPENANDERSON, JL KEEFER, LK TI ELECTROPHILIC ADDITION TO AMINONONOATE [R1R2NN(O)NO-] IONS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21702. USN,RES LAB,WASHINGTON,DC 20375. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 27 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200027 ER PT J AU FRALIX, TA MURPHY, E LONDON, RE AF FRALIX, TA MURPHY, E LONDON, RE TI GLYCOLYSIS IN THE HEART - BENEFICIAL OR DELETERIOUS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 46 EP CARB PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200613 ER PT J AU PIPPIN, CG AF PIPPIN, CG TI RADIOLABELED MONOCLONAL-ANTIBODIES - AN EXAMPLE OF APPLIED NUCLEAR-SCIENCE FOR HIGH-SCHOOL-STUDENTS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,CHEM SECT,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 54 EP NUCL PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ313 UT WOS:A1992JJ31300054 ER PT J AU BARRETT, JC AF BARRETT, JC TI MECHANISMS OF MULTISTEP CARCINOGENESIS AND CARCINOGEN RISK ASSESSMENT SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 58 EP AGRO PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200293 ER PT J AU MAILLARD, M BERKICH, D NIKODIJEVIC, O EVELETH, D JI, XD VANGALEN, PJM HIRAMATSU, K KASSELL, N LEE, KS BARTUS, RT DALY, J LANOUE, K JACOBSON, KA AF MAILLARD, M BERKICH, D NIKODIJEVIC, O EVELETH, D JI, XD VANGALEN, PJM HIRAMATSU, K KASSELL, N LEE, KS BARTUS, RT DALY, J LANOUE, K JACOBSON, KA TI SYNTHESIS AND BIOLOGICAL-ACTIVITY OF PERIPHERALLY SELECTIVE, WATER-SOLUBLE ADENOSINE AGONISTS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIDDK,BETHESDA,MD. UNIV PENN,MED CTR,HERSHEY,PA. UNIV VIRGINIA,DEPT NEUROSURG,CHARLOTTESVILLE,VA 22908. CORTEX PHARMACEUT INC,IRVINE,CA. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 60 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202418 ER PT J AU HECHT, SS CARMELLA, SG TRUSHIN, N YOUNGSCIAME, R WANG, MY CHUNG, FL ANDERSON, LM RICE, JM AF HECHT, SS CARMELLA, SG TRUSHIN, N YOUNGSCIAME, R WANG, MY CHUNG, FL ANDERSON, LM RICE, JM TI CYCLIC AND TOBACCO-SPECIFIC NITROSAMINES - METABOLISM AND MACROMOLECULAR ADDUCT FORMATION SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 AMER HLTH FDN,VALHALLA,NY 10595. NCI,FREDERICK,MD 21707. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 68 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200068 ER PT J AU ANANTHAN, S CLAYTON, SD WONG, G SKOLNICK, P AF ANANTHAN, S CLAYTON, SD WONG, G SKOLNICK, P TI SYNTHESIS AND STRUCTURE-ACTIVITY-RELATIONSHIPS OF IMIDAZO[1,5-A][1,4]-BENZODIAZEPIN-6-ONES AT DIAZEPAM-SENSITIVE AND DIAZEPAM-INSENSITIVE BENZODIAZEPINE RECEPTORS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 SO RES INST,BIRMINGHAM,AL 35255. NIDDKD,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 70 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202428 ER PT J AU MICHEJDA, CJ KOEPKE, SR KROEGERKOEPKE, M HERNANDEZ, L AF MICHEJDA, CJ KOEPKE, SR KROEGERKOEPKE, M HERNANDEZ, L TI ACTIVATION OF BETA-HYDROXYALKYLNITROSAMINES TO ALKYLATING-AGENTS - EVIDENCE FOR INVOLVEMENT OF SULFOTRANSFERASE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FREDRICK CANC RES & DEV CTR,ABL,BRP,MSL,MOLEC ASPECTS DRUG DESIGN SECT,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 70 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200070 ER PT J AU HUGHES, LJ CHMURNY, GN BAX, A HILTON, B ROWANGORDON, N AF HUGHES, LJ CHMURNY, GN BAX, A HILTON, B ROWANGORDON, N TI PROTON NMR-STUDIES OF RUTHENIUM BIPYRIDYL DIHYDROXYANTHRAQUINONE COMPLEXES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES CTR,LCP,BETHESDA,MD 20892. AMERICAN UNIV,WASHINGTON,DC 20016. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 79 EP INOR PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31201930 ER PT J AU GUSSIO, R POU, S KLINE, RH WRIGHT, J AF GUSSIO, R POU, S KLINE, RH WRIGHT, J TI PSEUDORECEPTOR MODELING OF COCAINE ANALOGS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 PRI DYNCORP,NCI,FREDERICK CANC RES CTR,CTR BIOMED SUPERCOMP,FREDERICK,MD 21702. UNIV MARYLAND,SCH PHARM,DEPT PHARMACOL & TOXICOL,BALTIMORE,MD 21201. UNIV MARYLAND,SCH PHARM,DEPT BIOMED CHEM,BALTIMORE,MD 21201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 91 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202449 ER PT J AU WINK, DA NIMS, RW SAAVEDRA, JE DESROSIERS, MF FORD, PC AF WINK, DA NIMS, RW SAAVEDRA, JE DESROSIERS, MF FORD, PC TI THE OXIDATION OF ALKYLNITROSAMINES VIA THE FENTON REAGENT - THE USE OF NITROSAMINES TO PROBE OXIDATIVE INTERMEDIATES IN THE FENTON REACTION SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21702. NATL INST STAND & TECHNOL,GAITHERSBURG,MD 20899. UNIV CALIF SANTA BARBARA,SANTA BARBARA,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 95 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200095 ER PT J AU CHRISTODOULOU, D WINK, DA GEORGE, C SAAVEDRA, JE KEEFER, LK AF CHRISTODOULOU, D WINK, DA GEORGE, C SAAVEDRA, JE KEEFER, LK TI NITRIC-OXIDE NUCLEOPHILE COMPLEXES AS LIGANDS - STRUCTURAL ASPECTS OF THE COORDINATED NONOATE FUNCTIONAL-GROUP IN NOVEL MIXED-LIGAND, NONNITROSYL METAL-COMPLEXES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21702. USN,RES LAB,WASHINGTON,DC 20375. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 97 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200097 ER PT J AU MIRVISH, SS HUANG, Q LAWSON, TA CHEN, SC STONER, G GELBOIN, HV PARK, SS AF MIRVISH, SS HUANG, Q LAWSON, TA CHEN, SC STONER, G GELBOIN, HV PARK, SS TI METHYLBUTYLNITROSAMINE (MBN) METABOLISM BY RAT-TISSUES AND METHYLAMYLNITROSAMINE (MNAN) METABOLISM BY HUMAN AND RAT ESOPHAGUS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 EPPLEY INST RES CANC,OMAHA,NE 68198. MED COLL OHIO,TOLEDO,OH 43699. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 101 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200101 ER PT J AU JAMESON, CW ELWELL, M EUSTIS, SL HONG, LH AF JAMESON, CW ELWELL, M EUSTIS, SL HONG, LH TI TOXICOLOGY AND CARCINOGENICITY STUDIES OF D-LIMONENE IN MALE AND FEMALE F344 RATS AND B6C3F1 MICE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 104 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200104 ER PT J AU WEBB, TE STROMBERG, PC ISSA, HA MOESCHBERGER, M PIERSON, H CURLEY, RW AF WEBB, TE STROMBERG, PC ISSA, HA MOESCHBERGER, M PIERSON, H CURLEY, RW TI IMPACT OF DIETARY SOYBEAN AND LICORICE ON PARAMETERS RELEVANT TO CANCER CHEMOPREVENTION IN THE RAT SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. OHIO STATE UNIV,COLL MED,COLUMBUS,OH 43210. OHIO STATE UNIV,COLL VET MED & PHARM,COLUMBUS,OH 43210. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 106 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200106 ER PT J AU LEE, J MARQUEZ, VE BLUMBERG, PM KAZANIETZ, MG AF LEE, J MARQUEZ, VE BLUMBERG, PM KAZANIETZ, MG TI 1,5-LACTONES VS 1,4-LACTONES AS RIGID DIACYLGLYCEROL (DAG) TEMPLATES AND THEIR INTERACTION WITH PROTEIN-KINASE-C (PK-C) SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,MED CHEM LAB,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DTP,BETHESDA,MD 20892. NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 110 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202468 ER PT J AU LIJINSKY, W AF LIJINSKY, W TI THE RELATION OF NITROSAMINE CARCINOGENESIS TO CHEMICAL-STRUCTURE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIEHS,DBRA,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 118 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200118 ER PT J AU XIAO, W LAKSHMAN, MK SAYER, JM CHEH, AM JERINA, DM AF XIAO, W LAKSHMAN, MK SAYER, JM CHEH, AM JERINA, DM TI STRUCTURES OF 2' - DEOXYADENOSINE ADDUCTS FORMED FROM THE REACTION OF PHENANTHRENE 9, 10-OXIDE WITH CALF THYMUS DNA SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 AMERICAN UNIV,DEPT CHEM,WASHINGTON,DC 20016. NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 118 EP ORGN PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ313 UT WOS:A1992JJ31300244 ER PT J AU BURKE, TR MARQUEZ, VE AF BURKE, TR MARQUEZ, VE TI 6,7 AND 7,8-DIHYDROXYISOQUINOLINE-3-CARBOXAMIDES - CONFORMATIONALLY CONSTRAINED PROTEIN-TYROSINE KINASE INHIBITORS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,DIV CANC TREATMENT,DTP,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 121 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202479 ER PT J AU SMYTH, MS NOMIZU, M ROLLER, PP RUSS, PL BURKE, TR AF SMYTH, MS NOMIZU, M ROLLER, PP RUSS, PL BURKE, TR TI MONO AND DIFLUORO PHOSPHONOMETHYL PHENYLALANINE - ANALOGS FOR STUDYING PHOSPHOTYROSINE-UTILIZING SIGNAL TRANSDUCTION PATHWAYS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,DIV CANC TREATMENT,DTP,MED CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 122 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202480 ER PT J AU PERLMAN, ME DAVIS, DG KOSZALKA, GW TUTTLE, JV KRENITSKY, TA LONDON, RE AF PERLMAN, ME DAVIS, DG KOSZALKA, GW TUTTLE, JV KRENITSKY, TA LONDON, RE TI DETERMINATION OF CONFORMATION OF AN INHIBITOR BOUND TO PURINE NUCLEOSIDE PHOSPHORYLASE USING THE TRANSFERRED NOE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. WELLCOME RES LABS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 128 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202486 ER PT J AU JOHN, CS SAGA, T KINUYA, S PAIK, CH REBA, RC VARMA, VM MCAFEE, JG AF JOHN, CS SAGA, T KINUYA, S PAIK, CH REBA, RC VARMA, VM MCAFEE, JG TI STRUCTURE ACTIVITY RELATIONSHIP OF [I-125] IODOBENZAMIDE ANALOGS AS POTENTIAL MALIGNANT-MELANOMA IMAGING AGENTS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,RADIOPHARM CHEM SECT,WASHINGTON,DC 20037. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 131 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202489 ER PT J AU SIDDIQUI, MA DRISCOLL, JS MARQUEZ, VE MITSUYA, H KELLEY, JA AF SIDDIQUI, MA DRISCOLL, JS MARQUEZ, VE MITSUYA, H KELLEY, JA TI ADENOSINE DEAMINASE-ACTIVATED PRODRUGS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,DTP,MED CHEM LAB,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,COP,MED BRANCH,EXPTL RETROVIRAL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 136 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202494 ER PT J AU POIRIER, MC AF POIRIER, MC TI DNA ADDUCT DETERMINATION BY IMMUNOASSAY AND IMMUNOHISTOCHEMISTRY SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 140 EP ANYL PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200539 ER PT J AU CLORE, GM GRONENBORN, AM BARCHI, JJ AF CLORE, GM GRONENBORN, AM BARCHI, JJ TI INVESTIGATIONS OF THE INTERNAL DYNAMICS OF THE IMMUNOGLOBULIN BINDING DOMAIN OF STREPTOCOCCAL PROTEIN-G BY 2-DIMENSIONAL INVERSE DETECTED N-15-H-1 NMR-SPECTROSCOPY SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,DIV CANC TREATMENT,DTP,MED CHEM LAB,BETHESDA,MD 20892. NIDDK,CHEM PHYS LAB,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008 OI Clore, G. Marius/0000-0003-3809-1027 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 151 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202509 ER PT J AU FENSELAU, C BRYANT, D FABRIS, D BOWERS, MA SOWDER, RC HENDERSON, LE AF FENSELAU, C BRYANT, D FABRIS, D BOWERS, MA SOWDER, RC HENDERSON, LE TI MASS-SPECTROMETRIC STUDIES OF GAG PROTEINS FROM HIGHLY REPLICATING HIV-1(MN) SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 UNIV MARYLAND,DEPT CHEM & BIOCHEM,CATONSVILLE,MD 21228. NCI,INC DYNCORP,AIDS VACCINE PROGRAM,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 168 EP ANYL PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200567 ER PT J AU KEEFER, LK AF KEEFER, LK TI COMPLEXES OF NITRIC-OXIDE WITH NUCLEOPHILES AS AGENTS FOR THE CONTROLLED BIOLOGICAL RELEASE OF NITRIC-OXIDE SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NCI,FCRDC,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 178 EP MEDI PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202536 ER PT J AU BEECHER, G KHACHIK, F HOLDEN, J MANGELS, AR CHUGAHUJA, J TONUCCI, LH FORMAN, M AF BEECHER, G KHACHIK, F HOLDEN, J MANGELS, AR CHUGAHUJA, J TONUCCI, LH FORMAN, M TI CAROTENOID CONTENT OF FOODS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 USDA ARS,BELTSVILLE AGR RES CTR,NUTR COMP LAB,BELTSVILLE,MD 20705. NCI,DCPC,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 226 EP AGFD PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31200226 ER PT J AU KONDO, T KIRSCHENBAUM, LJ KIM, H RIESZ, P AF KONDO, T KIRSCHENBAUM, LJ KIM, H RIESZ, P TI A SONOCHEMICAL STUDY OF DIMETHYLSULFOXIDE-WATER MIXTURES SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 FUKUI MED SCH,FUKUI 91011,JAPAN. UNIV RHODE ISL,DEPT CHEM,KINGSTON,RI 02881. NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 246 EP INOR PN 1 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ312 UT WOS:A1992JJ31202097 ER PT J AU CODE, JE SCHUMACHER, GE ANTONUCCI, JM AF CODE, JE SCHUMACHER, GE ANTONUCCI, JM TI ASCORBIC-ACID AS AN ETCHANT CONDITIONER FOR RESIN BONDING TO DENTIN SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIH,CODC,CTR CLIN,BETHESDA,MD 20892. NIST,DIV POLYMERS,GAITHERSBURG,MD 20899. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 278 EP POLY PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ313 UT WOS:A1992JJ31301474 ER PT J AU HUTCHINSON, KD DALY, JW GARRAFFO, HM SPANDE, TF AF HUTCHINSON, KD DALY, JW GARRAFFO, HM SPANDE, TF TI AN APPROACH TOWARDS THE SYNTHESIS OF PYRROLIZIDINE OXIMES - NOVEL ALKALOIDS ISOLATED FROM DENDROBATES-PUMILIO SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD AUG 23 PY 1992 VL 204 BP 324 EP ORGN PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA JJ313 UT WOS:A1992JJ31300450 ER PT J AU TANGREA, JA TAYLOR, PR HARTMAN, AM EDWARDS, BK KILCOYNE, RF HELSEL, WE ADRIANZA, ME PECK, GL AF TANGREA, JA TAYLOR, PR HARTMAN, AM EDWARDS, BK KILCOYNE, RF HELSEL, WE ADRIANZA, ME PECK, GL TI ISOTRETINOIN AND THE AXIAL SKELETON SO LANCET LA English DT Letter C1 UNIV COLORADO, DEPT RADIOL, BOULDER, CO 80309 USA. INFORMAT MANAGEMENT SERV INC, SILVER SPRING, MD USA. UNIV MARYLAND, DEPT DERMATOL, COLL PK, MD 20742 USA. RP TANGREA, JA (reprint author), NCI, DIV PREVENT & CONTROL, BETHESDA, MD 20892 USA. NR 5 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0140-6736 EI 1474-547X J9 LANCET JI Lancet PD AUG 22 PY 1992 VL 340 IS 8817 BP 495 EP 496 DI 10.1016/0140-6736(92)91825-S PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JJ877 UT WOS:A1992JJ87700057 PM 1354829 ER PT J AU LANKER, S BUSHMAN, JL HINNEBUSCH, AG TRACHSEL, H MUELLER, PP AF LANKER, S BUSHMAN, JL HINNEBUSCH, AG TRACHSEL, H MUELLER, PP TI AUTOREGULATION OF THE YEAST LYSYL-TRANSFER RNA-SYNTHETASE GENE GCD5/KRS1 BY TRANSLATIONAL AND TRANSCRIPTIONAL CONTROL MECHANISMS SO CELL LA English DT Article ID AMINO-ACID BIOSYNTHESIS; GCN4 MESSENGER-RNA; SACCHAROMYCES-CEREVISIAE; INITIATION-FACTOR; PROTEIN-SYNTHESIS; MUTATIONS; DNA; SPECIFICITY; EXPRESSION; REPRESSOR AB We cloned the GCD5 gene of S. cerevisiae and found it to be identical to KRS1, which encodes lysyl-tRNA synthetase (LysRS). The mutation gcd5-1 changes a conserved residue in the putative lysine-binding domain of LysRS. This leads to a defect in lysine binding and, consequently, to reduced charging of tRNA(Lys). Mutant gcd5-1 cells compensate for the defect in LysRS by increasing GCN4 expression at the translational level. GCN4 protein in turn stimulates transcription of GCD5, leading to increased LysRS activity. We propose an autoregulatory model in which uncharged tRNA(Lys) stimulates the protein kinase GCN2, a translational activator of GCN4, and thereby increases transcription of GCD5 and other genes regulated by GCN4. C1 NICHHD,MOLEC GENET LOWER EUKARYOTES SECT,BETHESDA,MD 20892. RP LANKER, S (reprint author), UNIV BERN,INST BIOCHEM & MOLEC BIOL,CH-3000 BERN 9,SWITZERLAND. NR 39 TC 45 Z9 46 U1 1 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD AUG 21 PY 1992 VL 70 IS 4 BP 647 EP 657 DI 10.1016/0092-8674(92)90433-D PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JJ886 UT WOS:A1992JJ88600013 PM 1505029 ER PT J AU WEISZ, A SCHER, AL ANDRZEJEWSKI, D SHIBUSAWA, Y ITO, Y AF WEISZ, A SCHER, AL ANDRZEJEWSKI, D SHIBUSAWA, Y ITO, Y TI COMPLEMENTARY USE OF COUNTERCURRENT CHROMATOGRAPHY AND PREPARATIVE REVERSED-PHASE HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY IN THE SEPARATION OF A SYNTHETIC MIXTURE OF BROMINATED TETRACHLOROFLUORESCEINS SO JOURNAL OF CHROMATOGRAPHY LA English DT Article ID COIL PLANET CENTRIFUGE; PURIFICATION AB A synthetically prepared mixture of brominated 4,5,6,7-tetrachlorofluoresceins was separated by a combination of preparative reversed-phase high-performance liquid chromatography and high-speed counter-current chromatography. Two new lower-brominated subsidiary colors of D&C Red Nos. 27 and 28 (phloxine B), 4',5'-dibromo-4,5,6,7-tetrachlorofluorescein and 2',4',5'-tribromo-4,5,6,7-tetrachlorofluorescein, were isolated and characterized by H-1 NMR and chemical ionization mass spectrometry. C1 US FDA,DIV CONTAMINANTS CHEM,WASHINGTON,DC 20204. NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. RP WEISZ, A (reprint author), US FDA,DIV COLORS & COSMET,CTR FOOD SAFETY & APPL NUTR,HFF-445,WASHINGTON,DC 20204, USA. NR 8 TC 13 Z9 13 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0021-9673 J9 J CHROMATOGR PD AUG 21 PY 1992 VL 607 IS 1 BP 47 EP 53 DI 10.1016/0021-9673(92)87053-B PG 7 WC Chemistry, Analytical SC Chemistry GA JL066 UT WOS:A1992JL06600007 PM 1332984 ER PT J AU GABRIELSEN, B PHELAN, MJ BARTHELROSA, L SEE, C HUGGINS, JW KEFAUVER, DF MONATH, TP USSERY, MA CHMURNY, GN SCHUBERT, EM UPADHYA, K KWONG, C CARTER, DA SECRIST, JA KIRSI, JJ SHANNON, WM SIDWELL, RW KINI, GD ROBINS, RK AF GABRIELSEN, B PHELAN, MJ BARTHELROSA, L SEE, C HUGGINS, JW KEFAUVER, DF MONATH, TP USSERY, MA CHMURNY, GN SCHUBERT, EM UPADHYA, K KWONG, C CARTER, DA SECRIST, JA KIRSI, JJ SHANNON, WM SIDWELL, RW KINI, GD ROBINS, RK TI SYNTHESIS AND ANTIVIRAL EVALUATION OF N-CARBOXAMIDINE-SUBSTITUTED ANALOGS OF 1-BETA-D-RIBOFURANOSYL-1,2,4-TRIAZOLE-3-CARBOXAMIDINE HYDROCHLORIDE SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID PARAINFLUENZA TYPE-3 VIRUSES; TISSUE-CULTURE; ANTITUMOR-ACTIVITY; COTTON RATS; RIBAVIRIN; DERIVATIVES; SELENAZOFURIN; NUCLEOSIDES; TIAZOFURIN; TOXICITY AB Ten, hitherto unreported, analogues of 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamidine hydrochloride (2a, ribamidine) and methyl carboximidate 5 have been synthesized. These include the N-cyano (2b), N-alkyl (2c-e), N-amino acid (2f-h), NN'-disubstituted (6, 7a,b), and the N-methylated carboxamide (1f) analogues of ribavirin. In addition, a new facile synthesis of carboxamidine 2a was also developed. All compounds were evaluated for biological activity against the following RNA viruses: Punta Toro (PT) and sandfly fever (SF) viruses (bunyaviruses); Japanese encephalitis (JE), yellow fever (YF), and dengue-4 viruses (flaviviruses); parainfluenza type 3 (PIV3), respiratory syncytial virus (RSV), and measles viruses (paramyxoviruses); influenza A and influenza B viruses (orthomyxoviruses); Venezuelan equine encephalomyelitis virus (VEE, alphavirus); human immunodeficiency virus type-1 (HIV-1, lentivirus); the DNA-containing vaccinia (VV) virus (poxvirus); and adeno type 5 (Ad5) viruses. All of the compounds except for 2b and 7a,b exhibited activity against the bunyaviruses such as that observed with 2a; however, higher IC50 values were generally observed. Glycine analogue 2f showed activity in PT-virus-infected mice in terms of increased survivors and decreased markers of viral pathogenicity. Carboxamidine 2a, carboximidate 5, and dimethyl amidine 6 exhibited activity against dengue type-4 virus. Monomethyl amidine 2c demonstrated activity against RSV, PIV3, and, to a lesser extent, influenza A and B. Activity of 2c generally required higher IC50 values than unsubstituted 2a. The latter exhibited hitherto unreported activity against RSV; therapeutic indices for 2a against RSV and PIV3 were >64 and >21. No substantial in vitro activity was observed for any of the compounds tested against Ad5, measles, JE, YF, VEE, or HIV-1. In addition, evidence is presented which argues in favor of a distinct antiviral mechanism of action for carboxamidines, e.g. 6, in contrast to a role as a carboxamide precursor. C1 USA,MED RES INST INFECT DIS,FREDERICK,MD 21701. US FDA,ROCKVILLE,MD 20855. UNIV NEVADA,DEPT CHEM,RENO,NV 89557. PHARM ECO LABS INC,SIMI VALLEY,CA 93065. SO RES INST,BIRMINGHAM,AL 35255. UTAH STATE UNIV,DEPT ANIM DAIRY & VET SCI,LOGAN,UT 84322. BAXTER DIAGNOST INC,DIV MICROSCAN,SACRAMENTO,CA 95691. UNIV CALIF SAN DIEGO,SCH MED,DEPT PHARMACOL,LA JOLLA,CA 92093. RP GABRIELSEN, B (reprint author), NCL,FREDERICK CANC RES FACIL,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,POB B,BLDG 427,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 32 TC 35 Z9 36 U1 10 U2 16 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 AUG 21 PY 1992 VL 35 IS 17 BP 3231 EP 3238 DI 10.1021/jm00095a020 PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA JK324 UT WOS:A1992JK32400020 PM 1507208 ER PT J AU KRAUSE, RM AF KRAUSE, RM TI THE ORIGIN OF PLAGUES - OLD AND NEW SO SCIENCE LA English DT Article ID SHOCK-LIKE SYNDROME; EMERGING VIRUSES; VIRAL DISEASES; LYME-DISEASE; AIDS; AGENT; HIV-1 AB Viruses and bacteria emerge in new and old forms to cause disease epidemics. Some microorganisms recur when changing life-styles (including increased international travel) offer new opportunities; others arise from new genetic variations. These various epidemics connect the future with the past, offering lessons for guarding the health of generations to come-lessons learned from diseases such as tuberculosis, toxic shock syndrome, Lyme disease, streptococcal infection, influenza, and acquired immunodeficiency syndrome (AIDS). The public must be vigilant to the possibility of new epidemics, learn more about the biology and epidemiology of microbes, and strengthen systems of surveillance and detection. RP KRAUSE, RM (reprint author), NIH,FOGARTY INT CTR ADV STUDY HLTH SCI,BETHESDA,MD 20892, USA. NR 41 TC 73 Z9 75 U1 1 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 AUG 21 PY 1992 VL 257 IS 5073 BP 1073 EP 1078 DI 10.1126/science.257.5073.1073 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ884 UT WOS:A1992JJ88400022 PM 1509258 ER PT J AU RADOVICK, S NATIONS, M DU, YF BERG, LA WEINTRAUB, BD WONDISFORD, FE AF RADOVICK, S NATIONS, M DU, YF BERG, LA WEINTRAUB, BD WONDISFORD, FE TI A MUTATION IN THE POU-HOMEODOMAIN OF PIT-1 RESPONSIBLE FOR COMBINED PITUITARY-HORMONE DEFICIENCY SO SCIENCE LA English DT Article ID THYROID-STIMULATING HORMONE; TRANSCRIPTION FACTOR PIT-1; RAT GROWTH-HORMONE; BETA-SUBUNIT GENE; PROLACTIN PROMOTER; INHIBITORY ELEMENT; DOMAIN PROTEIN; EXPRESSION; ACTIVATION; RESISTANCE AB Pit-1 is a pituitary-specific transcription factor responsible for pituitary development and hormone expression in mammals. Mutations in the gene encoding Pit-1 have been found in two dwarf mouse strains displaying hypoplasia of growth hormone, prolactin, and thyroid-stimulating, hormone-secreting cell types in the anterior pituitary. A point mutation in this gene was identified on one allele in a patient with combined pituitary hormone deficiency. Mutant Pit-1 binds DNA normally but acts as a dominant inhibitor of Pit-1 action in the pituitary. C1 RAINBOW BABIES & CHILDRENS HOSP,DEPT PEDIAT,DIV ENDOCRINOL,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,SCH MED,CLEVELAND,OH 44106. UNIV HOSP CLEVELAND,DEPT MED,DIV ENDOCRINOL & HYPERTENS,CLEVELAND,OH 44106. NIDDKD,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD 20892. NR 31 TC 332 Z9 338 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 AUG 21 PY 1992 VL 257 IS 5073 BP 1115 EP 1118 DI 10.1126/science.257.5073.1115 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ884 UT WOS:A1992JJ88400032 PM 1509262 ER PT J AU RAMSDELL, F FOWLKES, BJ AF RAMSDELL, F FOWLKES, BJ TI MAINTENANCE OF INVIVO TOLERANCE BY PERSISTENCE OF ANTIGEN SO SCIENCE LA English DT Article ID T-CELL-RECEPTOR; MAMMARY-TUMOR VIRUS; TRANSGENIC MICE; CLONAL ANERGY; TRANSPLANTATION TOLERANCE; NEGATIVE SELECTION; DELETION; INDUCTION; INACTIVATION; ELIMINATION AB T cells of the immune system respond only to foreign antigens because those cells with reactivity for self proteins are either deleted during their development or rendered nonresponsive (anergic). The maintenance of the nonresponsive state was found to require the continual exposure of the anergic T cells to antigen. When anergic T cells were removed from the self antigen by adoptive transfer to a mouse strain lacking the antigen or by in vitro culture, nonresponsiveness was reversed and the anergic cells returned to normal functional status. C1 NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892. NR 30 TC 205 Z9 209 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 AUG 21 PY 1992 VL 257 IS 5073 BP 1130 EP 1134 DI 10.1126/science.257.5073.1130 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ884 UT WOS:A1992JJ88400037 PM 1354889 ER PT J AU KANG, SM BEVERLY, B TRAN, AC BRORSON, K SCHWARTZ, RH LENARDO, MJ AF KANG, SM BEVERLY, B TRAN, AC BRORSON, K SCHWARTZ, RH LENARDO, MJ TI TRANSACTIVATION BY AP-1 IS A MOLECULAR TARGET OF T-CELL CLONAL ANERGY SO SCIENCE LA English DT Article ID LYMPHOCYTE-SPECIFIC FACTORS; HUMAN IL-2 GENE; INTERLEUKIN-2 GENE; CYCLOSPORINE-A; COSTIMULATORY SIGNAL; ANTIGEN RECEPTOR; SELF-TOLERANCE; ACTIVATION; EXPRESSION; ENHANCER AB Anergy is a mechanism of T lymphocyte tolerance induced by antigen receptor stimulation in the absence of co-stimulation. Anergic T cells were shown to have a defect in antigen-induced transcription of the interleukin-2 gene. Analysis of the promoter indicated that the transcription factor AP-1 and its corresponding cis element were specifically down-regulated. Exposure of anergic T cells to interleukin-2 restored both antigen responsiveness and activity of the AP-1 element. C1 NIAID,IMMUNOL LAB,BETHESDA,MD 20892. NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892. NR 79 TC 330 Z9 332 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 AUG 21 PY 1992 VL 257 IS 5073 BP 1134 EP 1138 DI 10.1126/science.257.5073.1134 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ884 UT WOS:A1992JJ88400038 PM 1509265 ER PT J AU CLERICI, M BERZOFSKY, JA SHEARER, GM GIORGI, JV TACKET, C AF CLERICI, M BERZOFSKY, JA SHEARER, GM GIORGI, JV TACKET, C TI HIV-1 FROM A SERONEGATIVE TRANSPLANT DONOR SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID HUMAN-IMMUNODEFICIENCY-VIRUS; INFECTION C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. UNIV MARYLAND,BALTIMORE,MD 21201. RP CLERICI, M (reprint author), NCI,BETHESDA,MD 20892, USA. NR 10 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 20 PY 1992 VL 327 IS 8 BP 564 EP 565 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JJ457 UT WOS:A1992JJ45700013 PM 1635574 ER PT J AU DOVER, GJ BRUSILOW, S SAMID, D AF DOVER, GJ BRUSILOW, S SAMID, D TI INCREASED FETAL HEMOGLOBIN IN PATIENTS RECEIVING SODIUM 4-PHENYLBUTYRATE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID SICKLE-CELL-ANEMIA C1 NCI,BETHESDA,MD 20892. RP DOVER, GJ (reprint author), JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205, USA. NR 6 TC 115 Z9 116 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 20 PY 1992 VL 327 IS 8 BP 569 EP 570 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JJ457 UT WOS:A1992JJ45700027 PM 1378939 ER PT J AU HUBBARD, RC SHAK, S CRYSTAL, RG AF HUBBARD, RC SHAK, S CRYSTAL, RG TI AEROSOLIZED RECOMBINANT HUMAN DEOXYRIBONUCLEASE-1 IN THE TREATMENT OF CYSTIC-FIBROSIS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 GENENTECH INC,SAN FRANCISCO,CA 94080. RP HUBBARD, RC (reprint author), NHLBI,BETHESDA,MD 20892, USA. NR 2 TC 3 Z9 3 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 20 PY 1992 VL 327 IS 8 BP 571 EP 571 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JJ457 UT WOS:A1992JJ45700030 ER PT J AU WEISS, KB GERGEN, PJ HODGSON, TA AF WEISS, KB GERGEN, PJ HODGSON, TA TI AN ECONOMIC-EVALUATION OF ASTHMA IN THE UNITED-STATES - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 NIAID,ROCKVILLE,MD 20892. NATL CTR HLTH STAT,HYATTSVILLE,MD 20782. RP WEISS, KB (reprint author), GEORGE WASHINGTON UNIV,WASHINGTON,DC 20037, USA. NR 1 TC 1 Z9 1 U1 1 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 20 PY 1992 VL 327 IS 8 BP 572 EP 572 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JJ457 UT WOS:A1992JJ45700032 ER PT J AU KASLOW, RA AF KASLOW, RA TI ERYTHEMA MIGRANS IN LYME-DISEASE - A CORRECTION - REPLY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP KASLOW, RA (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD AUG 19 PY 1992 VL 268 IS 7 BP 874 EP 874 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JH588 UT WOS:A1992JH58800034 ER PT J AU CNATTINGIUS, S FORMAN, MR BERENDES, HW ISOTALO, L AF CNATTINGIUS, S FORMAN, MR BERENDES, HW ISOTALO, L TI DELAYED CHILDBEARING AND RISK OF ADVERSE PERINATAL OUTCOME - A POPULATION-BASED STUDY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID LOW-BIRTH-WEIGHT; MATERNAL AGE; PREGNANCY; OLDER AB Objective.-To investigate the effect of advancing maternal age on pregnancy outcome among healthy nulliparous women, after adjustment for demographic characteristics, smoking, history of infertility, and other medical conditions. Design.-A population-based cohort study was conducted with prospectively collected data from the Swedish Medical Birth Register. Patients.-Nulliparous Nordic women (N=173715), aged 20 years and above, who delivered single births at Swedish hospitals from 1983 through 1987. Outcome Measures.-Late fetal and early neonatal death rates; rates of very low birth weight (VLBW, <1500 g), moderately low birth weight (MLBW, 1500 through 2499 g), very preterm delivery (less-than-or-equal-to 32 weeks), moderately preterm delivery (33 through 36 weeks), and small-for-gestational-age (SGA) infants (<-2 SDs). Results.-Compared with women aged 20 to 24 years, women aged 30 to 34 years had significantly higher adjusted odds ratios (ORs) of late fetal deaths (OR=1.4); VLBW (OR=1.2); MLBW (OR=1.4); very preterm birth (OR=1.2); and SGA infants (OR=1.4). Among women aged 35 to 39 years, the adjusted OR was significantly higher for VLBW (OR=1.9); MLBW (OR=1.7); very preterm birth (OR=1.7); moderately preterm birth (OR=1.2); and SGA infants (OR=1.7). Among women 40 years old and older, the adjusted OR was significantly higher for VLBW (OR=1.8); MLBW (OR=2.0); very preterm birth (OR=1.9); moderately preterm birth (OR=1.5); and SGA infants (OR=1.4). Conclusions.-Delayed childbearing is associated with an increased risk of poor pregnancy outcomes after adjustment for maternal complications and other risk factors. C1 NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. NCI,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. NR 29 TC 102 Z9 111 U1 3 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD AUG 19 PY 1992 VL 268 IS 7 BP 886 EP 890 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JH588 UT WOS:A1992JH58800039 PM 1640617 ER PT J AU RUMSEY, JM AF RUMSEY, JM TI THE BIOLOGY OF DEVELOPMENTAL DYSLEXIA SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID LEARNING-DISABILITIES; READING-DISABILITY; BRAIN MORPHOLOGY; PREVALENCE; DISORDERS; SKILLS RP RUMSEY, JM (reprint author), NIMH,CHILD PSYCHIAT BRANCH,BLDG 10,ROOM 6N240,BETHESDA,MD 20892, USA. NR 30 TC 20 Z9 20 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD AUG 19 PY 1992 VL 268 IS 7 BP 912 EP 915 DI 10.1001/jama.268.7.912 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA JH588 UT WOS:A1992JH58800045 PM 1640623 ER PT J AU STORM, HH ANDERSSON, M BOICE, JD BLETTNER, M STOVALL, M MOURIDSEN, HT DOMBERNOWSKY, P ROSE, C JACOBSEN, A PEDERSEN, M AF STORM, HH ANDERSSON, M BOICE, JD BLETTNER, M STOVALL, M MOURIDSEN, HT DOMBERNOWSKY, P ROSE, C JACOBSEN, A PEDERSEN, M TI ADJUVANT RADIOTHERAPY AND RISK OF CONTRALATERAL BREAST-CANCER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID TAMOXIFEN THERAPY; RANDOMIZED TRIAL; BOMB SURVIVORS; IRRADIATION; MASTECTOMY; TUBERCULOSIS; CHEMOTHERAPY; MORTALITY AB Background: The risk of contralateral breast cancer is increased twofold to fivefold for breast cancer patients. A registry-based cohort study in Denmark suggested that radiation treatment of the first breast cancer might increase the risk for contralateral breast cancer among 10-year survivors. Purpose: Our goal was to assess the role of radiation in the development of contralateral breast cancer. Methods: A nested case-control study was conducted in a cohort of 56 540 women in Denmark diagnosed with invasive breast cancer from 1943 through 1978. Case patients were 529 women who developed contralateral breast cancer 8 or more years after first diagnosis. Controls were women with breast cancer who did not develop contralateral breast cancer. One control was matched to each case patient on the basis of age, calendar year of initial breast cancer diagnosis, and survival time. Radiation dose to the contralateral breast was estimated for each patient on the basis of radiation measurements and abstracted treatment information. The anatomical position of each breast cancer was also abstracted from medical records. Results: Radiotherapy had been administered to 82.4% of case patients and controls, and the mean radiation dose to the contralateral breast was estimated to be 2.51 Gy. Radiotherapy did not increase the overall risk of contralateral breast cancer (relative risk = 1.04; 95% confidence interval = 0.74-1.46), and there was no evidence that risk varied with radiation dose, time since exposure, or age at exposure. The second tumors in case patients were evenly distributed in the medial, lateral, and central portions of the breast, a finding that argues against a causal role of radiotherapy in tumorigenesis. Conclusions: The majority of women in our series were perimenopausal or postmenopausal (53% total versus 38% premenopausal and 9% of unknown status) and received radiotherapy at an age when the breast tissue appears least susceptible to the carcinogenic effects of radiation. Based on a dose of 2.51 Gy and estimates of radiation risk from other studies, a relative risk of only 1.18 would have been expected for a population of women exposed at an average age of 51 years. Thus, our data provide additional evidence that there is little if any risk of radiation-induced breast cancer associated with exposure of breast tissue to low-dose radiation (e.g., from mammographic x rays or adjuvant radiotherapy) in later life. C1 UNIV COPENHAGEN HOSP,DEPT ONCOL,DK-2100 COPENHAGEN,DENMARK. NCI,DIV CANC ETIOL,RADIAT EPIDEMIOL BRANCH,BETHESDA,MD 20892. GERMAN CANC RES CTR,DIV EPIDEMIOL,W-6900 HEIDELBERG 1,GERMANY. UNIV TEXAS,CTR SYST CANC,HOUSTON,TX 77025. ODENSE UNIV HOSP,DEPT ONCOL,DK-5000 ODENSE,DENMARK. AARHUS KOMMUNE HOSP,RADIUMSTN,DK-8000 AARHUS,DENMARK. AALBORG HOSP,RADIUMSTN,DK-9000 AALBORG,DENMARK. RP STORM, HH (reprint author), DANISH CANC SOC,INST CANC EPIDEMIOL,DANISH CANC REGISTRY,ROSENVAENGETS HOVEDVEJ 35,BOX 839,DK-2100 COPENHAGEN,DENMARK. FU NCI NIH HHS [N01CP-51057] NR 36 TC 100 Z9 100 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 AUG 19 PY 1992 VL 84 IS 16 BP 1245 EP 1250 DI 10.1093/jnci/84.16.1245 PG 6 WC Oncology SC Oncology GA JJ414 UT WOS:A1992JJ41400010 PM 1640483 ER PT J AU KNELLER, RW YOU, WC CHANG, YS LIU, WD ZHANG, L ZHAO, L XU, GW FRAUMENI, JF BLOT, WJ AF KNELLER, RW YOU, WC CHANG, YS LIU, WD ZHANG, L ZHAO, L XU, GW FRAUMENI, JF BLOT, WJ TI CIGARETTE-SMOKING AND OTHER RISK-FACTORS FOR PROGRESSION OF PRECANCEROUS STOMACH LESIONS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Note ID GASTRIC-CANCER; ATROPHIC GASTRITIS; DIET; EPIDEMIOLOGY AB Background: Stomach cancer is generally thought to evolve through a series of gastric mucosal changes, but the determinants of the precancerous lesions are not well understood. Purpose: Our purpose was to assess risk factors for intestinal metaplasia and gastric dysplasia arising from chronic atrophic gastritis in a general population at high risk for stomach cancer. Methods: A population-based gastroscopic screening of more than 3000 residents was conducted in a county in China with one of the world's highest rates of stomach cancer. Information on the lifestyle and other characteristics of the participants was obtained by interview, and responses were compared between those in whom the most advanced gastric lesion was dysplasia or intestinal metaplasia versus those with chronic atrophic gastritis. Results: Cigarette smoking was found to nearly double the risk of transition to dysplasia and to be a mild risk factor for intestinal metaplasia. Smoking accounted almost entirely for the 55% higher prevalence of dysplasia among men than among women. Risk of transition to dysplasia had a weak association with several dietary factors and was increased among those participants with a family history of stomach cancer and with blood type A. Conclusions: The findings provide strong evidence for a role of tobacco consumption and offer clues to other environmental and genetic factors involved in the process of gastric carcinogenesis. C1 NCI,DIV CANC ETIOL,EXECUT PLAZA N,RM 431,BETHESDA,MD 20892. BEIJING INST CANC RES,BEIJING,PEOPLES R CHINA. WEIFANG MED INST,WEIFANG,PEOPLES R CHINA. LINQU PUBL HLTH BUR,LINQU,PEOPLES R CHINA. FU NCI NIH HHS [N01CP-05631, N01CP-15620, N01CP-95660] NR 34 TC 102 Z9 114 U1 1 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD AUG 19 PY 1992 VL 84 IS 16 BP 1261 EP 1266 DI 10.1093/jnci/84.16.1261 PG 6 WC Oncology SC Oncology GA JJ414 UT WOS:A1992JJ41400013 PM 1640486 ER PT J AU KENNA, JG MARTIN, JL POHL, LR AF KENNA, JG MARTIN, JL POHL, LR TI THE TOPOGRAPHY OF TRIFLUOROACETYLATED PROTEIN ANTIGENS IN LIVER MICROSOMAL FRACTIONS FROM HALOTHANE TREATED RATS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID HEPATITIS FOLLOWING HALOTHANE; ENDOPLASMIC-RETICULUM; INTRACELLULAR MEMBRANES; DISULFIDE-ISOMERASE; ANTIBODIES; CYTOCHROME-P-450; NEOANTIGENS; SERA; HEPATOTOXICITY; PURIFICATION AB Sera from patients with halothane hepatitis contain immunoglobulin G (IgG) antibodies to trifluoroacetylated liver microsomal proteins of 100, 76, 59, 57 and 54 kDa, which are produced as a consequence of metabolism of halothane to trifluoroacetyl halide by cytochrome(s) P450. In the present study, the membrane topographies of the various antigens in rat liver microsomal fractions were investigated. Liver microsomal fractions from rats treated with halothane in vivo, and rat liver microsomal fractions which had been incubated with halothane in vitro, were used as the source of trifluoroacetyl antigens. The antigens were detected by immunoblotting. Whereas the 100, 76, 59 and 57 kDa antigens were solubilized from the microsomal membrane by either 0.1 M sodium carbonate or 0.1% (w/v) sodium deoxycholate, the 54 kDa antigen was not solubilized by 0.1% (w/v) sodium deoxycholate. In intact microsomal fractions, the 100, 76, 59 and 57 kDa antigens were not degraded appreciably by trypsin unless detergent was added to permeabilize the microsomal membrane. These results indicate that the 54 kDa antigen is an integral membrane protein, whereas the 100, 76, 59 and 57 kDa antigens are peripheral membrane proteins situated within the lumen of microsomal vesicles, and hence presumably located within the lumen of the endoplasmic reticulum in vivo. C1 NHLBI,CHEM PHARMACOL LAB,BETHESDA,MD 20892. JOHNS HOPKINS MED INST,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205. RP KENNA, JG (reprint author), UNIV LONDON IMPERIAL COLL SCI & TECHNOL,ST MARYS HOSP,SCH MED,DEPT PHARMACOL & TOXICOL,LONDON W2 1PG,ENGLAND. FU Wellcome Trust NR 43 TC 28 Z9 28 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD AUG 18 PY 1992 VL 44 IS 4 BP 621 EP 629 DI 10.1016/0006-2952(92)90395-Y PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JL095 UT WOS:A1992JL09500003 PM 1510711 ER PT J AU MCTIGUE, MA DAVIES, JF KAUFMAN, BT KRAUT, J AF MCTIGUE, MA DAVIES, JF KAUFMAN, BT KRAUT, J TI CRYSTAL-STRUCTURE OF CHICKEN LIVER DIHYDROFOLATE-REDUCTASE COMPLEXED WITH NADP+ AND BIOPTERIN SO BIOCHEMISTRY LA English DT Article ID ESCHERICHIA-COLI; LACTOBACILLUS-CASEI; WILD-TYPE; HYDRIDE TRANSFER; FUNCTIONAL-ROLE; BINDING; SUBSTRATE; MECHANISM; FOLATE; TRIMETHOPRIM AB The 2.2-angstrom crystal structure of chicken liver dihydrofolate reductase (EC 1.5.1.3, DHFR) has been solved as a ternary complex with NADP+ and biopterin (a poor substrate). The space group and unit cell are isomorphous with the previously reported structure of chicken liver DHFR complexed with NADPH and phenyltriazine [Volz, K. W., Matthews, D. A., Alden, R. A., Freer, S. T., Hansch, C., Kaufman. B. T., & Kraut, J. (1982) J. Biol. Chem. 257, 2528-2536]. The structure contains an ordered water molecule hydrogen-bonded to both hydroxyls of the biopterin dihydroxypropyl group as well as to O4 and N5 of the biopterin pteridine ring. This water molecule, not observed in previously determined DHFR structures, is positioned to complete a proposed route for proton transfer from the side-chain carboxylate of E30 to N5 of the pteridine ring. Protonation of N5 is believed to occur during the reduction of dihydropteridine substrates. The positions of the NADP+ nicotinamide and biopterin pteridine rings are quite similar to the nicotinamide and pteridine ring positions in the Escherichia coli DHFR.NADP+.folate complex [Bystroff, C., Oatley, S. J., & Kraut, J. (1990) Biochemistry 29, 3263 3277], suggesting that the reduction of biopterin and the reduction of folate occur via similar mechanisms, that the binding geometry of the nicotinamide and pteridine rings is conserved between DHFR species, and that the p-aminobenzoylglutamate moiety of folate is not required for correct positioning of the pteridine ring in ground-state ternary complexes. Instead, binding of the p-aminobenzoylglutamate moiety of folate may induce the side chain of residue 31 (tyrosine or phenylalanine) in vertebrate DHFRs to adopt a conformation in which the opening to the pteridine binding site is too narrow to allow the substrate to diffuse away rapidly. A reverse conformational change of residue 31 is proposed to be required for tetrahydrofolate release. C1 UNIV CALIF SAN DIEGO,DEPT CHEM,LA JOLLA,CA 92093. NIDDK,BETHESDA,MD 20892. FU NCI NIH HHS [CA 17374]; NIGMS NIH HHS [GM07313] NR 53 TC 73 Z9 75 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD AUG 18 PY 1992 VL 31 IS 32 BP 7264 EP 7273 DI 10.1021/bi00147a009 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ578 UT WOS:A1992JJ57800009 PM 1510919 ER PT J AU MAUTNER, GC ROBERTS, WC AF MAUTNER, GC ROBERTS, WC TI REPORTED FREQUENCY OF CORONARY ARTERIAL NARROWING BY ANGIOGRAM IN PATIENTS WITH VALVULAR AORTIC-STENOSIS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Note ID ANGINA-PECTORIS; VALVE DISEASE; ARTERIOGRAPHY; ATHEROSCLEROSIS; REPLACEMENT AB During the past 25 years most patients aged >40 years of age having aortic valve replacement have had coronary angiography preoperatively. At least 33 studies have reported the frequency of significant (>50% diameter reduction) coronary arterial narrowing in patients with valvular aortic stenosis, and most of these reported studies included only patients who had the stenotic valve replaced with a prosthesis or bioprosthesis1-33 (Table I). Patients with mitral valve dysfunction usually were excluded. Analysis of the studies, which unfortunately also included a small percentage of patients <40 years of age, disclosed that 37% of the patients (1,302 of 3,509) had significant narrowing by angiogram of 1 or more major epicardial coronary arteries. RP MAUTNER, GC (reprint author), NHLBI,PATHOL BRANCH,BETHESDA,MD 20892, USA. NR 32 TC 21 Z9 21 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD AUG 15 PY 1992 VL 70 IS 4 BP 539 EP 540 DI 10.1016/0002-9149(92)91206-J PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JH364 UT WOS:A1992JH36400025 PM 1642197 ER PT J AU LIE, RT IRGENS, LM SKJAERVEN, R REITAN, JB STRAND, P STRAND, T AF LIE, RT IRGENS, LM SKJAERVEN, R REITAN, JB STRAND, P STRAND, T TI BIRTH-DEFECTS IN NORWAY BY LEVELS OF EXTERNAL AND FOOD-BASED EXPOSURE TO RADIATION FROM CHERNOBYL SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE ABNORMALITIES; RADIATION-INDUCED ID FALLOUT PATTERN; SOIL SAMPLES; ACCIDENT AB In Norway, external doses of radiation resulting from fallout from the Chernobyl nuclear accident were estimated from detailed measurements, including soil deposition patterns. Internal doses were estimated from measurements of radioactive cesium in meat and milk supplies. The doses were calculated as average monthly doses for each of 454 municipalities during 36 consecutive months after the accident in spring 1986. Prospectively collected data on all newborns listed in the Medical Birth Registry of Norway who were conceived in the period May 1983-April 1989 were used to assess possible dose-response relations between estimated external and food-based exposures and congenital malformations and some other conditions. A positive association was observed between total radiation dose (external plus food-based) and hydrocephaly, while a negative association was observed for Down's syndrome. However, an important conclusion of the study was that no associations were found for conditions previously reported to be associated with radiation, i.e., small head circumference, congenital cataracts, anencephaly, spina bifida, and low birth weight. Potential sources of bias, including exposure misclassification and incomplete ascertainment of cases, are discussed. C1 UNIV BERGEN, MED BIRTH REGISTRY NORWAY, N-5014 BERGEN, NORWAY. UNIV BERGEN, MED INFORMAT & STAT SECT, N-5014 BERGEN, NORWAY. NIEHS, RES TRIANGLE PK, NC 27709 USA. NR 26 TC 27 Z9 27 U1 1 U2 5 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 AUG 15 PY 1992 VL 136 IS 4 BP 377 EP 388 PG 12 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JR447 UT WOS:A1992JR44700001 PM 1415157 ER PT J AU GLASNER, PD SILVEIRA, C KRUSZONMORAN, D MARTINS, MC BURNIER, M SILVEIRA, S CAMARGO, ME NUSSENBLATT, RB KASLOW, RA BELFORT, R AF GLASNER, PD SILVEIRA, C KRUSZONMORAN, D MARTINS, MC BURNIER, M SILVEIRA, S CAMARGO, ME NUSSENBLATT, RB KASLOW, RA BELFORT, R TI AN UNUSUALLY HIGH PREVALENCE OF OCULAR TOXOPLASMOSIS IN SOUTHERN BRAZIL SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID CONGENITAL TOXOPLASMOSIS; PREGNANT-WOMEN; INFECTION AB Because of the frequency of ocular toxoplasmosis and its occurrence in multiple siblings in southern Brazil, a population-based household survey was performed to better understand the epidemiologic characteristics of the disease in this region. Of 1,042 individuals examined, 184 (17.7%) were deemed to have ocular toxoplasmosis on the basis of conservative assessment of ophthalmic findings. Of those with ocular toxoplasmosis, 183 (99.5%) had specific IgG antibodies, compared with only 140 of 181 age-matched control subjects (77.4%; P < .001). The prevalence of ocular toxoplasmosis was 0.9% in 1- to 8-year-olds, 4.3% in 9- to 12-year-olds, 14.3% in 13- to 16-year-olds, and 21.3% (95% confidence interval, 18.6% to 24.2%) in all individuals 13 years or older. The prevalence of ocular toxoplasmosis in this population was more than 30 times higher than previous estimates for the same condition elsewhere. The low prevalence in the young children we studied supplements previous data suggesting that, in this population, ocular toxoplasmosis is a sequela of postnatal rather than congenital infection. C1 CLIN SILVEIRA,ERECHIM,RS,BRAZIL. LAB FLEURY,DEPT IMMUNOL,SAO PAULO,BRAZIL. NEI,IMMUNOL LAB,BETHESDA,MD 20892. ESCOLA PAULISTA MED SCH,DEPT OFTALMOL,BR-04023 SAO PAULO,BRAZIL. RP GLASNER, PD (reprint author), NIAID,DIV MICROBIOL & INFECT DIS,EPIDEMIOL & BIOMETRY BRANCH,SOLAR BLDG,BETHESDA,MD 20892, USA. RI Belfort Jr, Rubens/E-2252-2012 OI Belfort Jr, Rubens/0000-0002-8422-3898 NR 22 TC 201 Z9 215 U1 1 U2 3 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD AUG 15 PY 1992 VL 114 IS 2 BP 136 EP 144 PG 9 WC Ophthalmology SC Ophthalmology GA JH622 UT WOS:A1992JH62200003 PM 1642287 ER PT J AU CASASFINET, JR WILSON, SH KARPEL, RL AF CASASFINET, JR WILSON, SH KARPEL, RL TI SELECTIVE PHOTOCHEMICAL MODIFICATION BY TRICHLOROETHANOL OF TRYPTOPHAN RESIDUES IN PROTEINS WITH A HIGH TYROSINE-TO-TRYPTOPHAN RATIO SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID HELIX-DESTABILIZING PROTEIN; SINGLE-STRANDED-DNA; AMINO-ACID SEQUENCE; GENE-32 PROTEIN; RADICAL-ANIONS; CALF THYMUS; FLUORESCENCE; PHAGE-T4; BINDING; BACTERIOPHAGE-T4 C1 UNIV MARYLAND,DEPT CHEM & BIOCHEM,CATONSVILLE,MD 21228. NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 38 TC 7 Z9 7 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD AUG 15 PY 1992 VL 205 IS 1 BP 27 EP 35 DI 10.1016/0003-2697(92)90574-Q PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA JH733 UT WOS:A1992JH73300005 PM 1332536 ER PT J AU SAROFF, HA AF SAROFF, HA TI ANALYSIS OF INDIVIDUAL-SITE BINDING DATA SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID IONIZATION RP SAROFF, HA (reprint author), NIDDKD,BIOCHEM PHARMACOL LAB,BLDG 8,ROOM 227,BETHESDA,MD 20892, USA. NR 12 TC 2 Z9 2 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 AUG 15 PY 1992 VL 205 IS 1 BP 143 EP 150 DI 10.1016/0003-2697(92)90591-T PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA JH733 UT WOS:A1992JH73300022 PM 1443553 ER PT J AU SCHLUEDERBERG, A STRAUS, SE PETERSON, P BLUMENTHAL, S KOMAROFF, AL SPRING, SB LANDAY, A BUCHWALD, D AF SCHLUEDERBERG, A STRAUS, SE PETERSON, P BLUMENTHAL, S KOMAROFF, AL SPRING, SB LANDAY, A BUCHWALD, D TI CHRONIC FATIGUE SYNDROME RESEARCH - DEFINITION AND MEDICAL OUTCOME ASSESSMENT SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE FATIGUE SYNDROME, CHRONIC; OUTCOME AND PROCESS ASSESSMENT (HEALTH CARE); PSYCHIATRIC STATUS RATING SCALES; DIAGNOSIS, DIFFERENTIAL; SLEEP DISORDERS ID BARR VIRUS-INFECTION; FIBROMYALGIA; POPULATION AB A workshop was held 18 to 19 March 1991 at the National Institutes of Health to address critical issues in research concerning the chronic fatigue syndrome (CFS). Case definition, confounding diagnoses, and medical outcome assessment by laboratory and other means were considered from the perspectives of key medical specialties involved in CFS research. It was recommended that published Centers for Disease Control (CDC) case-definition criteria be modified to exclude fewer patients from analysis because of a history of psychiatric disorder. Specific recommendations were made concerning the inclusion or exclusion of other major confounding diagnoses, and a standard panel of laboratory tests was specified for initial patient evaluation. The workshop emphasized the importance of recognizing other conditions that could explain the patient's symptoms and that may be treatable. It was viewed as essential for the investigator to screen for psychiatric disorder using a combination of self-report instruments followed by at least one structured interview to identity patients who should be excluded from studies or considered as a separate subgroup in data analysis. Because CFS is not a homogeneous abnormality and because there is no single pathogenic mechanism, research progress may depend upon delineation of these and other patient subgroups for separate data analysis. Despite preliminary data, no physical finding or laboratory test was deemed confirmatory of the diagnosis of CFS. For assessment of clinical status, investigators must rely on the use of standardized instruments for patient self-reporting of fatigue, mood disturbance, functional status, sleep disorder, global well-being, and pain. Further research is needed to develop better instruments for quantifying these domains in patients with CFS. C1 NIMH,BETHESDA,MD 20892. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. BRIGHAM & WOMENS HOSP,DIV GEN MED,BOSTON,MA 02115. RUSH UNIV,MED CTR,DEPT IMMUNOL MICROBIOL,CHICAGO,IL 60612. UNIV WASHINGTON,HARBORVIEW MED CTR,SEATTLE,WA 98104. RP SCHLUEDERBERG, A (reprint author), NIAID,DMID,VIROL BRANCH,ROOM 3A-16,SOLAR BLDG,BETHESDA,MD 20892, USA. NR 37 TC 247 Z9 248 U1 2 U2 4 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 AUG 15 PY 1992 VL 117 IS 4 BP 325 EP 331 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA JH464 UT WOS:A1992JH46400010 PM 1322076 ER PT J AU PARKINSON, DR SMITH, MA AF PARKINSON, DR SMITH, MA TI RETINOID THERAPY FOR ACUTE PROMYELOCYTIC LEUKEMIA - A COMING OF AGE FOR THE DIFFERENTIATION THERAPY OF MALIGNANCY SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material DE RETINOIDS; LEUKEMIA, PROMYELOCYTIC, ACUTE; CERVIX NEOPLASMS; SKIN NEOPLASMS; CARCINOMA, SQUAMOUS CELL ID RAR-ALPHA; ACID; TRANSLOCATION; T(15-17); PML AB Positive therapeutic results have recently been achieved with retinoids used either as single agents in the treatment of acute promyelocytic leukemia or used together with alpha-interferon in the treatment of squamous cell carcinomas arising in skin or cervix. These findings have led to enhanced interest in the induction of differentiation as an approach to the treatment of cancer. Complexities related to the clinical use of trans-retinoic acid that have emerged in these early trials include issues related to its pharmacology, the biology of acquired resistance to this agent, and the occasional development of a complicating cardiopulmonary syndrome unique to its administration in acute promyelocytic leukemia. RP PARKINSON, DR (reprint author), NCI,DCT,INVEST DRUG BRANCH,CANC THERAPY EVALUAT PROGRAM,ROOM 715,BETHESDA,MD 20892, USA. NR 21 TC 6 Z9 6 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD AUG 15 PY 1992 VL 117 IS 4 BP 338 EP 340 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA JH464 UT WOS:A1992JH46400013 PM 1637030 ER PT J AU KOMAROFF, AL HENRY, B ABLASHI, DV AF KOMAROFF, AL HENRY, B ABLASHI, DV TI CHRONIC FATIGUE SYNDROME CONTROVERSY - REPLY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 FORENS SCI DIV,RENO,NV 89512. NCI,BETHESDA,MD 20892. RP KOMAROFF, AL (reprint author), BRIGHAM & WOMENS HOSP,BOSTON,MA 02115, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD AUG 15 PY 1992 VL 117 IS 4 BP 344 EP 344 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JH464 UT WOS:A1992JH46400017 ER PT J AU SMITH, PD MASUR, H JANOFF, EN AF SMITH, PD MASUR, H JANOFF, EN TI DIAGNOSTIC WORK-UP OF AIDS-ASSOCIATED DIARRHEA - REPLY SO ANNALS OF INTERNAL MEDICINE LA English DT Letter C1 VET AFFAIRS MED CTR,MINNEAPOLIS,MN 55417. UNIV MINNESOTA,SCH MED,MINNEAPOLIS,MN 55417. RP SMITH, PD (reprint author), NIH,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD AUG 15 PY 1992 VL 117 IS 4 BP 346 EP 347 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JH464 UT WOS:A1992JH46400024 ER PT J AU CASTRONOVO, V LUYTEN, F VANDENBRULE, F SOBEL, ME AF CASTRONOVO, V LUYTEN, F VANDENBRULE, F SOBEL, ME TI IDENTIFICATION OF A 14-KDA LAMININ BINDING-PROTEIN (HLBP14) IN HUMAN-MELANOMA CELLS THAT IS IDENTICAL TO THE 14-KDA GALACTOSIDE BINDING LECTIN SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID EXTRACELLULAR-MATRIX; ELASTIN RECEPTOR; MESSENGER-RNA; ADHESION; CARBOHYDRATE; METASTASIS; FIBRONECTIN; SEQUENCE; DOMAINS; CHAINS C1 NIDR,BONE CELL BIOL SECT,BETHESDA,MD 20892. NCI,TUMOR INOAS & METASTASIS SECT,BETHESDA,MD 20892. NR 47 TC 48 Z9 49 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD AUG 15 PY 1992 VL 297 IS 1 BP 132 EP 138 DI 10.1016/0003-9861(92)90650-L PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JF099 UT WOS:A1992JF09900018 PM 1386213 ER PT J AU PERNO, CF COONEY, DA GAO, WY HAO, Z JOHNS, DG FOLI, A HARTMAN, NR CALIO, R BRODER, S YARCHOAN, R AF PERNO, CF COONEY, DA GAO, WY HAO, Z JOHNS, DG FOLI, A HARTMAN, NR CALIO, R BRODER, S YARCHOAN, R TI EFFECTS OF BONE-MARROW STIMULATORY CYTOKINES ON HUMAN-IMMUNODEFICIENCY-VIRUS REPLICATION AND THE ANTIVIRAL ACTIVITY OF DIDEOXYNUCLEOSIDES IN CULTURES OF MONOCYTE MACROPHAGES SO BLOOD LA English DT Article ID PERIPHERAL-BLOOD MONOCYTES; IMMUNE-DEFICIENCY SYNDROME; HTLV-III INFECTIVITY; AIDS-RELATED COMPLEX; CELLULAR PHARMACOLOGY; MONONUCLEAR PHAGOCYTES; HUMAN-ERYTHROPOIETIN; PROGENITOR CELLS; ZIDOVUDINE AZT; HIV C1 NCI,MED CHEM LAB,MED BRANCH,BLDG 10,RM 12N226,BETHESDA,MD 20892. NCI,OFF DIRECTOR,BETHESDA,MD 20892. UNIV ROME 2,DEPT EXPTL MED,ROME,ITALY. RI perno, carlo federico/O-1544-2016 NR 48 TC 80 Z9 80 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 AUG 15 PY 1992 VL 80 IS 4 BP 995 EP 1003 PG 9 WC Hematology SC Hematology GA JJ576 UT WOS:A1992JJ57600020 PM 1379854 ER PT J AU BURT, RK SHARFMAN, WH KARP, BI WILSON, WH AF BURT, RK SHARFMAN, WH KARP, BI WILSON, WH TI MENTAL NEUROPATHY (NUMB CHIN SYNDROME) - A HARBINGER OF TUMOR PROGRESSION OR RELAPSE SO CANCER LA English DT Article ID SYSTEMIC CANCER; LEUKEMIA; NERVE AB The authors report four patients whose initial symptom of tumor recurrence or progression was unilateral numbness of the chin. Two patients had Hodgkin lymphoma, one had malignant melanoma, and one had prostate cancer. Physical examination was notable only for unilateral anesthesia of the chin and lower lip. Diagnostic evaluation, including computed tomography (CT) scan and magnetic resonance imaging (MRI) of the brain, plain radiographs of the mandible, and cerebrospinal fluid analysis for protein, glucose, and cytology were normal. Bone scans revealed osseous lesions in the axial skeleton of all patients, whereas only two patients had abnormal uptake in the mandible. The authors conclude that in the setting of a negative evaluation for central nervous system (CNS) or local mandibular disease, mental neuropathy is associated with recurrent or progressive skeletal disease. In addition, to document relapsed or progressive cancer, the skeletal system may have to be examined at sites distant from the mandible. C1 NCI,DIV CANC TREATMENT,OFF DIRECTOR,BLDG 31,ROOM 3A44,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NINCDS,BIOL RESPONSE MODIFIERS PROGRAM,BETHESDA,MD 20892. NINCDS,CLIN ONCOL PROGRAM,BETHESDA,MD 20892. NR 18 TC 56 Z9 58 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD AUG 15 PY 1992 VL 70 IS 4 BP 877 EP 881 DI 10.1002/1097-0142(19920815)70:4<877::AID-CNCR2820700425>3.0.CO;2-G PG 5 WC Oncology SC Oncology GA JH654 UT WOS:A1992JH65400024 PM 1643620 ER PT J AU JOHNSTON, PG DRAKE, JC TREPEL, J ALLEGRA, CJ AF JOHNSTON, PG DRAKE, JC TREPEL, J ALLEGRA, CJ TI IMMUNOLOGICAL QUANTITATION OF THYMIDYLATE SYNTHASE USING THE MONOCLONAL-ANTIBODY TS 106 IN 5-FLUOROURACIL-SENSITIVE AND 5-FLUOROURACIL-RESISTANT HUMAN CANCER CELL-LINES SO CANCER RESEARCH LA English DT Article ID BREAST-CANCER; MOUSE FIBROBLASTS; SYNTHETASE; CARCINOMA; GENE; CHEMOTHERAPY; COMPLEX; 2'-DEOXYURIDYLATE; INHIBITION; RESISTANCE AB Thymidylate synthase (TS) (EC 2.1.1.45) is an important cellular target for the fluoropyrimidine cytotoxic drugs that are widely used in the treatment of solid tumors. Using the TS 106 monoclonal antibody to human TS, we have compared the immunological quantitation of TS by Western immunoblot and immunofluorescent techniques to the conventional biochemical 5-fluorodeoxyuridine monophosphate binding assay in a panel of 5-fluorouracil (5-FU)-sensitive and -resistant human cancer cell lines. Densitometric quantitation of TS 106-labeled Western immunoblot analysis of cell lysates from two 5-FU-resistant colon carcinoma cell lines, NCI H630R1 and NCI H630R10, revealed 12.8- and 16-fold increases in TS, respectively, compared to the parent 5-FU-sensitive NCI H630 colon cell line. By biochemical analysis, the TS level was 15- and 23-fold higher, respectively, in these resistant cell lines. Similarly, immunoblot analysis of cell lysates from two 5-FU-resistant breast cancer cell lines, MCF-Ad5 and MCF-Ad10, detected a 2.3- and 6.3-fold increase in TS, respectively, compared to the parent MCF-7 cell line. By biochemical assay the TS activity was 1.8- and 7.0-fold higher in these resistant breast cell lines. Western immunoblotting analysis revealed a 35-fold range of TS protein concentrations among the 10 cell lines examined, compared to a 38-fold range demonstrated by the biochemical assay. Direct comparison of Western blotting and the biochemical assay revealed a highly significant correlation (r2 = 0.93) between the two assays. Moreover, using the monoclonal antibody TS 106, the Western blotting technique was capable of detecting TS protein levels as low as 0.3 fmol in cellular lysates. Quantitation of TS in intact cells by immunofluorescent TS labeling and flow cytometric analysis was performed using three of the cell lines, NCI H630, NCI H630R10, and MCF-Ad10. This revealed a 26-fold increase in TS in the 5-FU-resistant NCI H630R10 line compared to the parent NCI H630 line and a 3.5-fold increase in TS compared to the 5-FU-resistant MCF-Ad10 breast cell line. The 5-FU-resistant MCF-Ad10 breast cell line, in turn, displayed a 7.7-fold increase in TS, compared to the 5-FU-sensitive NCI H630 cell lines. TS immunofluorescent analysis was capable of measuring TS within individual cells. The development of these immunological assays using an anti-TS monoclonal antibody will facilitate the quantitation of TS in cell lines and tissue samples. C1 NCI,DIV CANC TREATMENT,CLIN PHARMACOL BRANCH,BETHESDA,MD 20892. RP JOHNSTON, PG (reprint author), NCI,NAVY MED ONCOL BRANCH 8-5101,BETHESDA,MD 20892, USA. NR 37 TC 197 Z9 197 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 AUG 15 PY 1992 VL 52 IS 16 BP 4306 EP 4312 PG 7 WC Oncology SC Oncology GA JJ837 UT WOS:A1992JJ83700002 PM 1643628 ER PT J AU GAETANO, C MATSUMOTO, K THIELE, CJ AF GAETANO, C MATSUMOTO, K THIELE, CJ TI INVITRO ACTIVATION OF DISTINCT MOLECULAR AND CELLULAR PHENOTYPES AFTER INDUCTION OF DIFFERENTIATION IN A HUMAN NEUROBLASTOMA CELL-LINE SO CANCER RESEARCH LA English DT Article ID HUMAN NEURO-BLASTOMA; N-MYC; MESSENGER-RNA; EXPRESSION; CDNA; MODULATION; SEQUENCE; SIZE AB In this report we provide evidence for the activation of distinct differentiation pathways during treatment of the neuroblastoma cell line SMS-KCNR with 1 mM dibutyryl cyclic AMP (dbcAMP) and/or 5-mu-M retinoic acid (RA). Our results show that the adrenal gland specific gene pG2 is induced only during dbcAMP treatment, while RA induces a neuronal phenotype and expression of all neural related genes while decreasing the expression of many chromaffin related genes. Furthermore dbcAMP does not affect the DNA content distribution of SMS-KCNR cells [G1=61.8 +/- 4.1% (SD); S = 20.3 +/- 6.3%; G2-M = 18 +/-5.4%] despite morphological and molecular signs of cellular differentiation. Conversely, RA arrests cell growth causing a decrease in cells in the growth fraction (S + G2 + M = 15.6 +/- 6.1%) and an increase in cells in G1 (G1=84.3 +/- 5%). Using cyclic AMP and RA in combination, we found that RA inhibited expression of adrenal gland specific gene pG2 and induced a neuronal phenotype. Since dbcAMP does not cause a significant G1 block in SMS-KCNR cells we propose that this agent may be able to induce SMS-KCNR only to an intermediate stage of chromaffin differentiation in which cells retain their proliferative potential. C1 NCI,PEDIAT BRANCH,MOLEC GENET SECT,BETHESDA,MD 20892. OI Gaetano, Carlo/0000-0002-5238-1832 NR 35 TC 40 Z9 40 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 AUG 15 PY 1992 VL 52 IS 16 BP 4402 EP 4407 PG 6 WC Oncology SC Oncology GA JJ837 UT WOS:A1992JJ83700016 PM 1322787 ER PT J AU MICKISCH, GH PAI, LH GOTTESMAN, MM PASTAN, I AF MICKISCH, GH PAI, LH GOTTESMAN, MM PASTAN, I TI MONOCLONAL-ANTIBODY MRK16 REVERSES THE MULTIDRUG RESISTANCE OF MULTIDRUG-RESISTANT TRANSGENIC MICE SO CANCER RESEARCH LA English DT Article ID P-GLYCOPROTEIN; TUMOR-CELLS; DRUG-RESISTANCE; BONE-MARROW; PSEUDOMONAS EXOTOXIN; GENE; TRANSPORTER; EXPRESSION; CANCER; MDR1 AB Using multidrug-resistant (MDR)-transgenic mice, whose bone marrow cells express the human MDR1 gene at a level approximately equal to that found in many human cancers, we determined the efficacy of human-specific anti-P-glycoprotein monoclonal antibody MRK16 in overcoming multidrug resistance in an intact animal. MRK16 alone (2 mg) did not significantly affect the WBC counts of the MDR-transgenic mice, but MRK16, as well as the F(ab')2 fragments of MRK16, led to a dose-dependent circumvention of bone marrow resistance against daunomycin, doxorubicin, vincristine, vinblastine, etoposide, and taxol. This sensitizing effect could not be enhanced by combining MRK16 with low molecular weight chemosensitizing agents such as verapamil, quinine, quinidine, or cyclosporin A. We also investigated the concept of specifically targeting and killing multidrug-resistant cells by using MRK16 coupled to Pseudomonas exotoxin (PE). MRK16-PE resulted in a dose-dependent killing of bone marrow cells in MDR-transgenic mice, whereas no bone marrow toxicity was observed in normal control mice. Administration of excess MRK16 prior to injection of MRK16-PE successfully blocked the effect of MRK16-PE. MOPC-PE, a non-MDR-related control monoclonal antibody conjugate, did not target and kill multidrug-resistant bone marrow cells in MDR-transgenic mice. Thus, these immunological approaches to reversing multidrug resistance appear to be both specific and effective. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,BLDG 37,ROOM 4E16,BETHESDA,MD 20892. NCI,DIV CANC BIOL DIAG & CTR,CELL BIOL LAB,BETHESDA,MD 20892. NR 28 TC 57 Z9 58 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 AUG 15 PY 1992 VL 52 IS 16 BP 4427 EP 4432 PG 6 WC Oncology SC Oncology GA JJ837 UT WOS:A1992JJ83700020 PM 1353705 ER PT J AU LETEURTRE, F MADALENGOITIA, J ORR, A CUZI, TJ LEHNERT, E MACDONALD, T POMMIER, Y AF LETEURTRE, F MADALENGOITIA, J ORR, A CUZI, TJ LEHNERT, E MACDONALD, T POMMIER, Y TI RATIONAL DESIGN AND MOLECULAR EFFECTS OF A NEW TOPOISOMERASE-II INHIBITOR, AZATOXIN SO CANCER RESEARCH LA English DT Article ID MEDIATED DNA CLEAVAGE; TUBULIN POLYMERIZATION; ANTITUMOR DRUGS; STRAND CLEAVAGE; KB CELLS; ANALOGS; INDUCTION; IDENTIFICATION; INTERCALATORS; DERIVATIVES AB Azatoxin [NSC 640737-M; 5.R,11aS-1H,6H,3-one-5,4,11,11a-tetrahydro-5-(3,5-dimethoxy-4-hydroxyphenyl) oxazolo (3',4':1,6)pyrido-(3,4-b)indole] was rationally designed from a model for the pharmacophore of drugs with topoisomerase II inhibition activity. This pharmacophore has at least 2 domains: a quasiplanar polycyclic ring system proposed to bind between the DNA base pairs and a pendant substituent proposed to interact with the enzyme and/or to the DNA grooves. The present study shows that, in cell free systems, azatoxin induces a large number of double strand-breaks in linear Simian virus 40 and human c-myc DNA. These breaks yield cleavage patterns that are different from those of well established topoisomerase II inhibitors (epipodophyllotoxins, amsacrine, mitoxantrone). Azatoxin also inhibits the catalytic activity of purified topoisomerase II, and is a nonintercalator. The structure-activity relationship of 3 isomers and 6 derivatives of azatoxin shows a stringent stereochemical requirement for activity. The effects of azatoxin pendant ring substitution on topoisomerase II mediated DNA cleavage activity were similar to the relationship observed for etoposide. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,MOLEC PHARMACOL LAB,BLDG 37,ROOM 5C27,BETHESDA,MD 20892. UNIV VIRGINIA,DEPT CHEM,CHARLOTTESVILLE,VA 22901. FU NCI NIH HHS [CA54347] NR 31 TC 76 Z9 76 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD AUG 15 PY 1992 VL 52 IS 16 BP 4478 EP 4483 PG 6 WC Oncology SC Oncology GA JJ837 UT WOS:A1992JJ83700028 PM 1322792 ER PT J AU GARBISA, S SCAGLIOTTI, G MASIERO, L DIFRANCESCO, C CAENAZZO, C ONISTO, M MICELA, M STETLERSTEVENSON, WG LIOTTA, LA AF GARBISA, S SCAGLIOTTI, G MASIERO, L DIFRANCESCO, C CAENAZZO, C ONISTO, M MICELA, M STETLERSTEVENSON, WG LIOTTA, LA TI CORRELATION OF SERUM METALLOPROTEINASE LEVELS WITH LUNG-CANCER METASTASIS AND RESPONSE TO THERAPY SO CANCER RESEARCH LA English DT Note ID COLLAGEN AB Cancer cells elaborate metalloproteinases which may play a role in invasion and metastasis. The serum level of the M(r) 72,000 type IV collagenase (MMP-2) was measured in 87 lung cancer patients. Stage IV cancer levels were significantly elevated (P < 0.0001) compared to normal sera. A significant difference (P < 0.01) was found between enzyme levels in the presence versus the absence of distant metastasis. For 29 patients treated with combination chemotherapy, a positive relationship was noted between response failure and elevated enzyme levels. Serum metalloproteinase levels may provide information relevant to prognosis as well as treatment decisions. C1 UNIV PADUA,INST HISTOL,I-35100 PADUA,ITALY. UNIV TURIN,DEPT CLIN & BIOL SCI,I-10124 TURIN,ITALY. NCI,PATHOL LAB,BETHESDA,MD 20892. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 10 TC 139 Z9 141 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 AUG 15 PY 1992 VL 52 IS 16 BP 4548 EP 4549 PG 2 WC Oncology SC Oncology GA JJ837 UT WOS:A1992JJ83700040 PM 1322794 ER PT J AU FLEMING, TP SAXENA, A CLARK, WC ROBERTSON, JT OLDFIELD, EH AARONSON, SA ALI, IU AF FLEMING, TP SAXENA, A CLARK, WC ROBERTSON, JT OLDFIELD, EH AARONSON, SA ALI, IU TI AMPLIFICATION AND OR OVEREXPRESSION OF PLATELET-DERIVED GROWTH-FACTOR RECEPTORS AND EPIDERMAL GROWTH-FACTOR RECEPTOR IN HUMAN GLIAL TUMORS SO CANCER RESEARCH LA English DT Note ID MALIGNANT HUMAN GLIOMAS; GLIOBLASTOMA-MULTIFORME; FACTOR-ALPHA; GENE AMPLIFICATION; HUMAN ASTROCYTOMAS; MESSENGER-RNA; CELL-LINES; EXPRESSION; PDGF; CHROMOSOME-17 AB Analysis of genomic organization and expression of platelet-derived growth factor receptors (PDGFR) and epidermal growth factor receptor (EGFR) in human malignant gliomas showed amplification and overexpression of both receptors in distinct subsets of tumors. Amplification of the alpha-PDGFR was detected in 4 of 50 glioblastomas (8%). EGFR was amplified in 9 of the 50 tumors (18%). Western blot analysis showed elevated expression of alpha-PDGFR and EGFR proteins in 4 (24%) and 3 (18%), respectively, of 17 tumor specimens analyzed. Increased production of alpha-PDGFR as well as EGFR proteins was observed in the presence or absence of gene amplification. Three of the 4 tumors with elevated levels of alpha-PDGFR also overexpressed the beta-PDGFR, which was present as a single copy gene in all 50 tumors analyzed. Our findings suggest that the amplification and/or overexpression either of EGFR or of the alpha-PDGFR along with the coordinate overexpression of the beta-PDGFR can contribute to the malignant phenotype of distinct subsets of human glioblastoma. C1 NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. UNIV TENNESSEE,DEPT NEUROSURG,MEMPHIS,TN 38119. NR 36 TC 306 Z9 312 U1 1 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 AUG 15 PY 1992 VL 52 IS 16 BP 4550 EP 4553 PG 4 WC Oncology SC Oncology GA JJ837 UT WOS:A1992JJ83700041 PM 1322795 ER PT J AU MCDERMOTT, JB PETERSON, CA PIATIGORSKY, J AF MCDERMOTT, JB PETERSON, CA PIATIGORSKY, J TI STRUCTURE AND LENS EXPRESSION OF THE GENE ENCODING CHICKEN BETA-A3/A1-CRYSTALLIN SO GENE LA English DT Article DE GENOMIC SEQUENCE; MURINE; HUMAN; PROMOTER; TRANSCRIPTIONAL REGULATION; PRIMER EXTENSION ID ALPHA-B-CRYSTALLIN; EYE LENS; IMMUNOREACTIVE ALPHA; PROMOTER ELEMENTS; MESSENGER-RNAS; EVOLUTION; PROTEIN; TRANSCRIPTION; TISSUES; CDNA AB The beta-A1- and beta-A3-crystallins are major polypeptides in the lenses of vertebrates. We present evidence that a single beta-A3/A1 gene encodes these two proteins in the chicken. The beta-A3/A1 gene has been sequenced and its functional promoter identified in transfection experiments. The chicken beta-A3/A1 gene has the same structure as the human orthologue: six exons with standard splice sites and two alternative start codons from which the protein products are apparently translated. Northern analysis revealed an abundant 0.9-kb transcript in the lenses of 1-2-day-old chickens and no detectable transcripts in the rest of the eye, brain, heart, kidney, liver or skeletal muscle. The 5'-flanking sequence of the chicken beta-A3/A1 gene is very similar to that of the human and mouse genes, suggesting conservation of important putative regulatory sequences in addition to the TATA box. A thymidine-rich element (bp -218 to -163) and a potential AP-1-binding site (bp -264 to -258) are present within the chicken 5'-flanking region. A DNA fragment from -382 to +22 of the chicken beta-A3/A1 gene is sufficient to promote expression of the bacterial cat gene in transfected chicken primary lens epithelial cells, but not in transfected dermal fibroblasts. Moreover, the sequence from positions -382 to -143 of the chicken beta-A3/A1 promoter appears to be critical for proper transcription initiation and expression in the transfected lens cells. C1 NEI,MOLEC & DEV BIOL LAB,BLDG 6,RM 201,BETHESDA,MD 20892. NR 43 TC 15 Z9 16 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD AUG 15 PY 1992 VL 117 IS 2 BP 193 EP 200 DI 10.1016/0378-1119(92)90729-9 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA JH231 UT WOS:A1992JH23100005 PM 1353472 ER PT J AU LEE, CH PARK, D WU, DQ RHEE, SG SIMON, MI AF LEE, CH PARK, D WU, DQ RHEE, SG SIMON, MI TI MEMBERS OF THE GQ-ALPHA-SUBUNIT GENE FAMILY ACTIVATE PHOSPHOLIPASE-C BETA-ISOZYMES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID ADENYLYL CYCLASE; G-PROTEINS; IDENTIFICATION; PURIFICATION; HYDROLYSIS; DIVERSITY; CELLS AB The relative specificities of members of the G-alpha(q) family of GTP-binding proteins were tested for their ability to activate different phosphoinositide-specific phospholipase C (PI-PLC) beta-isozymes. Cos-7 cells were transfected with cDNA corresponding to G-alpha(q), G-alpha-11, G-alpha-14, and G-alpha-16. Most of the recombinant protein was bound to the cell membrane and these membranes were washed to elute endogenous PI-PLC activity. The membrane preparation was reconstituted with purified preparations of the PI-PLC beta-isozymes and guanosine 5'-O-thiotriphosphate (GTP-gamma-S)-stimulated enzyme activity was measured. All four proteins of the G-alpha(q) family were found to stimulate PI-PLC beta-1, with G-alpha(q) and G-alpha-11 being most efficient. On the other hand, G-alpha-16 was found to most effectively activate PI-PLC beta-2, while G-alpha(q), G-alpha-11, and G-alpha-14 showed less stimulation. Specific anti-G-alpha-16 antibody blocked the stimulation of both PI-PLC beta-1 and PI-PLC beta-2 in the enriched membrane fraction. We conclude that there is specificity in the interaction of different members of the G(q) family with different PI-PLC beta-effectors. This specificity may be important in generating tissue- or receptor-specific responses in vivo. C1 CALTECH,DIV BIOL,PASADENA,CA 91125. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM 34236] NR 24 TC 247 Z9 249 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 AUG 15 PY 1992 VL 267 IS 23 BP 16044 EP 16047 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ458 UT WOS:A1992JJ45800011 PM 1322889 ER PT J AU PARK, D JHON, DY KRIZ, R KNOPF, J RHEE, SG AF PARK, D JHON, DY KRIZ, R KNOPF, J RHEE, SG TI CLONING, SEQUENCING, EXPRESSION, AND GQ-INDEPENDENT ACTIVATION OF PHOSPHOLIPASE-C-BETA-2 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BOVINE BRAIN; ALPHA-SUBUNITS; G-PROTEINS; TYROSINE PHOSPHORYLATION; IMMUNOLOGICAL IDENTIFICATION; SIGNAL TRANSDUCTION; BETA-1 ISOZYME; C ISOZYMES; PURIFICATION; DIVERSITY AB cDNAs corresponding to a previously uncharacterized phospholipase C were isolated from an HL-60 cell cDNA library. The cDNAs encodes a putative polypeptide of 1181 amino acids with a calculated molecular mass of 133,700 daltons. Comparison of the amino acid sequence of the predicted protein with those of five mammalian phospholipase C isoforms (PLC-beta-1, PLC-gamma-1, PLC-gamma-2, PLC-delta-1, and PLC-delta-2) revealed that the new enzyme is most closely related to PLC-beta-1 with an overall amino acid sequence identity of 48%. Thus, the new phospholipase C was named PLC-beta-2. The least similarity between PLC-beta-1 and PLC-beta-2 is apparent in the carboxyl-terminal 450 amino acids. Both PLC-beta-1 and PLC-beta-2 were purified from extracts of HeLa cells that had been transfected with vaccinia virus containing the corresponding cDNAs. Like other mammalian PLC isoforms, including PLC-beta-1, the catalytic activity of PLC-beta-2 was entirely dependent on Ca2+, and PLC-beta-2 preferred phosphatidylinositol 4,5-bisphosphate to phosphatidylinositol as substrate. Recently, the alpha-subunit of the pertussis toxin-insensitive G-protein alpha(q) has been shown to activate PLC-beta-1 but not PLC-gamma-1 and PLC-delta-1. When alpha(q) purified from bovine brain was reconstituted with PLC-beta-1 or PLC-beta-2, no stimulation of PLC-beta-2 was observed in the presence of either AlF4- or guanosine 5-O-(3-thiotriphosphate) (GTP-gamma-S), whereas PLC-beta-1 activity was enhanced markedly in the presence of AlF4- and less markedly but significantly in the presence of GTP-gamma-S. These results suggest that the receptor-dependent stimulation of PLC-beta-1 and that of PLC-beta-2 may require different G-protein alpha-subunits. C1 NHLBI,BIOCHEM LAB,9000 ROCKVILLE PIKE,BLDG 3,RM 122,BETHESDA,MD 20892. GENET INST,CAMBRIDGE,MA 02140. NR 49 TC 141 Z9 142 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 AUG 15 PY 1992 VL 267 IS 23 BP 16048 EP 16055 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ458 UT WOS:A1992JJ45800012 PM 1644792 ER PT J AU BARGON, J TRAPNELL, BC YOSHIMURA, K DALEMANS, W PAVIRANI, A LECOCQ, JP CRYSTAL, RG AF BARGON, J TRAPNELL, BC YOSHIMURA, K DALEMANS, W PAVIRANI, A LECOCQ, JP CRYSTAL, RG TI EXPRESSION OF THE CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR GENE CAN BE REGULATED BY PROTEIN-KINASE-C SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CFTR CHLORIDE CHANNEL; EPITHELIAL-CELLS; MESSENGER-RNA; NONSENSE MUTATIONS; AIRWAY EPITHELIA; XENOPUS OOCYTES; PHORBOL ESTER; CAMP; IDENTIFICATION; CALCIUM AB Epithelial cells utilize at least two types of apical Cl- channels, the cAMP-activated cystic fibrosis transmembrane conductance regulator (CFTR) and the Ca2+/calmodulin-dependent Cl- channel. While phorbol ester (PMA) activates only CFTR-dependent Cl- secretion and the Ca2+ ionophore A23187 only the Ca2+/calmodulin-dependent Cl- secretion, PMA and A23187 share the ability to down-regulate expression of the CFTR gene at the transcriptional level. Since both PMA and A23187 can activate protein kinases, we hypothesized that protein kinase pathways may be involved in the regulation of CFTR gene expression. Exposure of HT-29 human colon carcinoma cells to the protein kinase C activator SC9 down-regulated CFTR mRNA levels in a dose-dependent fashion, similar to that seen with PMA. The reduction in CFTR transcript levels by SC9 and PMA was blocked by H7, an inhibitor of protein kinases. In a similar fashion, the down-regulation of CFTR transcript levels by A23187 was blocked by H7 as well as staurosporine, another protein kinase inhibitor. Interestingly, both H7 and staurosporine themselves increased CFTR mRNA levels. Quantification of CFTR gene transcription rate showed a reduction by SC9 (similar to that with PMA and A23187) that was prevented by H7 and that H7 by itself increased CFTR transcription. Together, these observations suggest that protein kinase pathways, likely including protein kinase C, are involved in the regulation of CFTR gene expression, with activation or inhibition of protein kinase activity down-regulating or up-regulating CFTR gene expression, respectively. C1 NHLBI,PULM BRANCH,BLDG 10,RM 6D03,BETHESDA,MD 20892. TRANSGENE SA,F-67082 STRASBOURG,FRANCE. NR 52 TC 34 Z9 34 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 AUG 15 PY 1992 VL 267 IS 23 BP 16056 EP 16060 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ458 UT WOS:A1992JJ45800013 PM 1379589 ER PT J AU LEI, KJ SARTWELL, AD PAN, CJ CHOU, JY AF LEI, KJ SARTWELL, AD PAN, CJ CHOU, JY TI CLONING AND EXPRESSION OF GENES ENCODING HUMAN PREGNANCY-SPECIFIC GLYCOPROTEINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN CARCINOEMBRYONIC ANTIGEN; SODIUM-BUTYRATE; BETA-1-GLYCOPROTEIN GENES; MOLECULAR-CLONING; MAMMALIAN-CELLS; CDNA SEQUENCE; MESSENGER-RNA; FAMILY MEMBER; RETINOIC ACID; FETAL LIVER AB The pregnancy-specific glycoproteins (PSGs) of the human placenta and the carcinoembryonic antigens comprise a subfamily within the immunoglobulin superfamily. There may be as many as 20 different PSG genes which are predominantly expressed in the placenta. As an initial step toward understanding the control of PSG expression, we isolated and characterized two nearly identical PSG genes, PSG1 and PSG1-I. PSG1, which lacks exon 1 (5'/L), but contains exons 2 (L/N), 3 (A1), 4 (A2), and 5 (B2-C), encodes five previously identified type I transcripts, PSG1a, 1b, 1c, 1d, and 1e in a L/N-A1-A2-B2-C domain arrangement. PSG1-I which contains a complete transcriptional unit consisting of exons 5'/L, L/N, A1, and B2-C, encodes type II PSG transcripts in a L/N-A1-B2-C domain arrangement. The predicted PSG1-I-encoded proteins share nearly complete sequence identity with the PSG1-encoded members, except the latter contain extra A domains. Amplification by polymerase chain reaction of placental or hydatidiform mole cDNA demonstrates that PSG1-I is a functional type II PSG gene. Using transient expression assays, we demonstrated that the -834/-34 region upstream of the translational start site of the PSG1-I gene contained the PSG promoter elements and the -834 to -456 region contained negative control elements. Sodium butyrate, an inducer of PSG synthesis, greatly stimulated expression of all PSG1-I-chloramphenicol acetyltransferase (CAT) fusion gene constructs. However, butyrate was at least 2-fold more effective in stimulating CAT activity of fusion genes containing upstream sequences (-834 to -576) than those containing proximal sequences (-456 to -172), suggesting two regions in the PSG1-I gene that mediate the butyrate response. C1 NICHHD,HUMAN GENET BRANCH,BLDG 10,RM 9S242,BETHESDA,MD 20892. NR 62 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 15 PY 1992 VL 267 IS 23 BP 16371 EP 16378 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ458 UT WOS:A1992JJ45800061 PM 1644821 ER PT J AU MOLLOY, SS BRESNAHAN, PA LEPPLA, SH KLIMPEL, KR THOMAS, G AF MOLLOY, SS BRESNAHAN, PA LEPPLA, SH KLIMPEL, KR THOMAS, G TI HUMAN FURIN IS A CALCIUM-DEPENDENT SERINE ENDOPROTEASE THAT RECOGNIZES THE SEQUENCE ARG-X-X-ARG AND EFFICIENTLY CLEAVES ANTHRAX TOXIN PROTECTIVE ANTIGEN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROPROTEIN PROCESSING ENZYME; GENE-EXPRESSION; MAMMALIAN-CELLS; BASIC RESIDUES; YEAST KEX2; PROTEASE; PROHORMONE; PRECURSOR; SITE; ENDOPEPTIDASE AB Previous work demonstrated that human furin is a predominantly Golgi membrane-localized endoprotease that can efficiently process precursor proteins at paired basic residues (-Lys-Arg- or -Arg-Arg-) in transfected cells. Anion-exchange chromatography of culture supernatant from cells expressing a soluble truncated form of human furin resulted in a greatly enriched preparation of the endoprotease (approximately 70% pure as determined by protein staining). Enzymatic studies show that furin is a calcium-dependent (K0.5 = 200-mu-M) serine endoprotease which has greater than 50% of maximal activity between pH 6.0 and 8.5. The inhibitor sensitivity of furin suggests that it is similar to, yet distinct from, other calcium-dependent proteases. Evidence that furin may require a P4 Arg in fluorogenic peptide substrates suggested that this enzyme might cleave the protective antigen (PA) component of anthrax toxin at the sequence -Arg-Lys-Lys-Arg-. Indeed, PA was cleaved by purified furin at the proposed consensus site (-Arg-X-Lys/Arg-Arg(down)-) at a rate (8-mu-mol/min/mg total protein) 400-fold higher than that observed with synthetic peptides. In addition, the processing of mutant PA molecules with altered cleavage sites suggests that furin-catalyzed endoproteolysis minimally requires an -Arg-X-X-Arg- recognition sequence for efficient cleavage. Together, these results support the hypothesis that furin processes protein precursors containing this cleavage site motif in the exocytic pathway and in addition, raises the possibility that the enzyme also cleaves extracellular substrates, including PA. C1 OREGON HLTH SCI UNIV,VOLLUM INST,PORTLAND,OR 97201. NIDR,MICROBIAL ECOL LAB,BETHESDA,MD 20892. FU NIDDK NIH HHS [DK08703, DK37274, DK44629] NR 45 TC 534 Z9 544 U1 0 U2 7 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 AUG 15 PY 1992 VL 267 IS 23 BP 16396 EP 16402 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ458 UT WOS:A1992JJ45800065 PM 1644824 ER PT J AU LEE, AW NIENHUIS, AW AF LEE, AW NIENHUIS, AW TI FUNCTIONAL DISSECTION OF STRUCTURAL DOMAINS IN THE RECEPTOR FOR COLONY-STIMULATING FACTOR-I SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; FACTOR-I RECEPTOR; PHOSPHATIDYLINOSITOL KINASE-ACTIVITY; DEPENDENT PROTEIN-KINASE; GLYCOPHORIN-A; SIGNAL TRANSDUCTION; MONOCLONAL-ANTIBODIES; INSULIN-RECEPTORS; TYROSINE KINASES; TRANSMEMBRANE DOMAIN AB Receptor tyrosine kinases (RTKs) transduce external signals to the interior of the cell via a cytoplasmic kinase domain. We demonstrated previously that ligand-induced kinase activation of the colony-stimulating factor-1 receptor (CSF-1R) occurs via receptor oligomerization without propagation of conformational changes through the transmembrane (TM) domain (Lee, A. W., and Nienhuis, A. W. (1990) Proc. Natl. Acad. Sci. U. S. A. 87, 7270-7274). We have now examined the role of the different subdomains in the metabolic and signaling properties of CSF-1R. Two types of chimeric receptors have been utilized, Glyfms A, with the extracellular and TM domains of glycophorin A (GpA) and the cytoplasmic domain of CSF-1R, and Glyfms B, where only the extracellular domain originates from GpA. Glyfms A was found to exhibit a higher basal level of in vitro kinase activity, an increased associated phosphatidylinositol (PtdIns) 3-kinase activity and to support enhanced cellular mitogenesis, compared with wild-type CSF-1R or to Glyfms B. The constitutive activation of Glyfms A is consistent with the hypothesis that the TM domain may play a role in receptor oligomerization. Cross-linking with anti-GpA antibodies activated the kinase function of Glyfms B leading to an increase in PtdIns 3-kinase association and to the transmission of a mitogenic signal. Our results indicate that an activated kinase domain contains the major determinant for coupling with PtdIns 3-kinase, independent of extracellular and TM sequences and of ligand binding. Both chimeric receptors underwent internalization in the presence of anti-GpA antibodies but were not degraded, including the tyrosine-phosphorylated and kinase-active population. These results suggest that structural determinants in the extracellular domain must be important for targeting internalized receptors for lysosomal degradation. RP LEE, AW (reprint author), NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892, USA. NR 71 TC 10 Z9 10 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 AUG 15 PY 1992 VL 267 IS 23 BP 16472 EP 16483 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JJ458 UT WOS:A1992JJ45800076 PM 1322904 ER PT J AU BARRETT, TA GAJEWSKI, TF DANIELPOUR, D CHANG, EB BEAGLEY, KW BLUESTONE, JA AF BARRETT, TA GAJEWSKI, TF DANIELPOUR, D CHANG, EB BEAGLEY, KW BLUESTONE, JA TI DIFFERENTIAL FUNCTION OF INTESTINAL INTRAEPITHELIAL LYMPHOCYTE SUBSETS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL RECEPTOR; MOUSE SMALL-INTESTINE; GROWTH FACTOR-BETA; EPITHELIAL-CELLS; ALPHA-BETA; MONOCLONAL-ANTIBODY; MURINE CD3+; IFN-GAMMA; EXPRESSION; DELTA AB It has been proposed that intestinal intraepithelial lymphocytes (I-IEL) perform immune surveillance of the epithelial layer (1) and regulate mucosal humoral responses to exogenous Ag (2). To better understand the functional potential of this unique population, purified murine I-IEL were analyzed phenotypically and functionally. Initial studies determined that I-IEL could be distinguished based on several phenotypic characteristics including: TCR (TCR-alpha-beta vs TCR-gamma-delta); Thy-1, CD45R/B220, CD5, and CD8 (CD8-alpha-alpha vs CD8-alpha-beta) expression. Using anti-TCR mAb, individual I-IEL subsets were activated and examined functionally. Both TCR-alpha-beta and TCR-gamma-delta I-IEL were found to synthesize an array of lymphokines that included IL-2, IL-3, and IL-6 but not IL-4 or IL-5. Additionally, a number of lymphokines were detected that directly influence epithelial function (IFN-gamma, TNF-alpha, and TGF-beta-1). However, the majority of the I-IEL function was localized within the Thy-1+, CD45R/B220- I-IEL subset. In addition those TCR-alpha-beta I-IEL expressing the CD8-alpha-beta heterodimer were more easily activated. Thus, a subset of I-IEL have the capacity to respond to TCR-mediated stimuli. The functional activities of these cells may influence both local immune cell populations as well as epithelial differentiation. C1 UNIV CHICAGO,BEN MAY INST,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MED,GASTROENTEROL SECT,CHICAGO,IL 60637. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. UNIV ALABAMA,DEPT MED,GASTROENTEROL SECT,BIRMINGHAM,AL 35294. RI Beagley, Kenneth/J-1129-2012 OI Beagley, Kenneth/0000-0003-3112-6557 FU NCI NIH HHS [CA 14599]; NIAID NIH HHS [R01 AI 26847] NR 45 TC 156 Z9 158 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 AUG 15 PY 1992 VL 149 IS 4 BP 1124 EP 1130 PG 7 WC Immunology SC Immunology GA JJ092 UT WOS:A1992JJ09200002 PM 1380032 ER PT J AU VOS, Q JONES, LA KRUISBEEK, AM AF VOS, Q JONES, LA KRUISBEEK, AM TI MICE DEPRIVED OF EXOGENOUS ANTIGENIC-STIMULATION DEVELOP A NORMAL REPERTOIRE OF FUNCTIONAL T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; MAMMARY-TUMOR VIRUS; RECEPTOR TRANSGENIC MICE; ANTIBODY-SECRETING CELLS; NEONATAL BALB/C MICE; MONOCLONAL-ANTIBODY; CLONAL DELETION; POSITIVE SELECTION; LYMPHOCYTES-T; GENE-PRODUCTS AB The development of T cells and the selection of the TCR repertoire in the absence of exogenous antigenic stimulation were investigated. For this purpose germfree BALB/c mice fed an ultrafiltered solution of chemically defined low m.w. nutrients (GF-CD) were used. Previous studies on B cell development and differentiation in GF-CD mice have demonstrated a high reduction in the number of cells secreting Ig of the non-IgM isotypes but an Ig-V(H) gene usage and a B cell specificity repertoire that is substantially different from that observed in conventional adult mice and more closely resembles that of neonatal conventional mice. In contrast, the present comparison of the various lymphocyte populations in the thymus, lymph nodes, and spleen from GF-CD and conventional mice using flow cytometry analysis revealed no significant differences. Analysis of the TCR-V-beta expression on both mature thymocytes and lymph node T cells showed a high degree of similarity between GF-CD and conventional mice. These findings indicate a marked difference in the influence of exogenous antigenic stimulation on the development of B and T cells. Additionally, development in an environment free of exogenous antigenic stimulation allows for full functional maturation of T cells to occur, because MLC showed that GF-CD splenic T cells could mount allogeneic responses in a way similar to T cells generated in a conventional environment. Most importantly, full Th cell function is generated, because activation of GF-CD spleen cells by cross-linking with mAb against CD3 resulted in the induction of cells secreting IFN-gamma and Ig of the non-IgM isotypes, which cannot be detected in GF-CD sera. These findings demonstrate that functional T and B cells develop in mice that have not been exposed to exogenous Ag, and that the TCR repertoire, in contrast to the B cell compartment, is predominantly shaped by endogenously expressed Ag. C1 ERASMUS UNIV,DEPT IMMUNOL,3000 DR ROTTERDAM,NETHERLANDS. NCI,BIOL RESPONSE MODIFIERS PROGRAM,BETHESDA,MD 20892. RP VOS, Q (reprint author), NCI,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B17,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 72 TC 26 Z9 26 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 AUG 15 PY 1992 VL 149 IS 4 BP 1204 EP 1210 PG 7 WC Immunology SC Immunology GA JJ092 UT WOS:A1992JJ09200014 PM 1386859 ER PT J AU CHOUCHANE, L KINDT, TJ AF CHOUCHANE, L KINDT, TJ TI MAPPING OF THE RABBIT MHC REVEALS THAT CLASS-I GENES ARE ADJACENT TO THE DR SUBREGION AND DEFINES AN INSERTION DELETION-RELATED POLYMORPHISM IN THE CLASS-II REGION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; FIELD GEL-ELECTROPHORESIS; STEROID 21-HYDROXYLASE GENES; BETA-GENE; FACTOR-B; EXPRESSION; HLA; COMPONENT; SEQUENCE; HOMOLOGY AB Molecular analyses of genes in the rabbit MHC (RLA) by pulsed field gel electrophoresis have shown that the relative order of class II genes (DP, DO, DQ, DR) is identical to that in humans and similar to that in the mouse. However, a major difference from either HLA or H-2 was observed at the DR end of the RLA class II complex: class I genes are located in close proximity to DR with no interposed class III sequences. A MluI fragment of 180 kb and a 210-kb SalI fragment both hybridized with the DR probe as well as with different class I probes including that for pR27, a class I gene with T cell-limited pattern of expression. Comparison of two different RLA haplotypes, A and B, indicated that the distance between the DQ and DR subregions differs by approximately 700 kb in the two haplotypes. Testing other unrelated rabbits suggested that this difference segregates within the rabbit population and presumably derives from an insertion/deletion event in different haplotypes. A further difference between the A and B haplotypes included variable distance between genes encoding DO-beta and DP; the DR end of the complex and the class I genes linkage was conserved in the two haplotypes. RP CHOUCHANE, L (reprint author), NIAID,IMMUNOGENET LAB,TWINBROOK II FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852, USA. NR 39 TC 16 Z9 16 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 AUG 15 PY 1992 VL 149 IS 4 BP 1216 EP 1222 PG 7 WC Immunology SC Immunology GA JJ092 UT WOS:A1992JJ09200016 PM 1500713 ER PT J AU SMITH, MR RAMSBURG, EA KUNG, HF DURUM, SK AF SMITH, MR RAMSBURG, EA KUNG, HF DURUM, SK TI COMPONENTS OF THE PROTEIN-KINASE-C PATHWAY INDUCE IA EXPRESSION AFTER INJECTION INTO MACROPHAGES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MURINE PERITONEAL-MACROPHAGES; PHOSPHOLIPASE-C; ANTIGEN EXPRESSION; IFN-GAMMA; SIGNAL TRANSDUCTION; INTRACELLULAR ROLE; RAS PROTEINS; BOVINE BRAIN; ACTIVATION; CELLS AB Macrophages are activated by a variety of microbial and cytokine stimuli. One feature of activation is the induction of class II Ag (Ia) on the cell surface. To understand the intracellular events that occur during activation, we investigated various agents with intracellular activities, and examined their effects on the induction of Ia. We first noted that several agents that activate protein kinase C (PKC) induced Ia, and that several inhibitors of PKC inhibited Ia induction by IFN-gamma. To directly test whether PKC induced Ia, we microinjected normal peritoneal macrophages with this enzyme and other intracellular mediators, then examined la expression. We observed that injection of PKC itself, or of other intracellular proteins thought to participate in the PKC pathway (Ras ot phospholipase C-gamma) strongly induced Ia expression. The Ia-inducing activity of transforming Ras protein was blocked by kinase inhibitor treatment of cells, suggesting that Ras signal transduction requires kinase activity. On the other hand, components of the protein kinase A pathway (phospholipase A2 and protein kinase A itself) did not induce Ia. Thus, the PKC pathway can control expression of macrophage surface Ia, possibly by regulating the genes of the MHC, and may play many other roles in the activation of macrophages. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21701. RP SMITH, MR (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PROGRAM RESOURCES INC,FREDERICK,MD 21701, USA. FU NCI NIH HHS [N01-CO-74102] NR 43 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 AUG 15 PY 1992 VL 149 IS 4 BP 1304 EP 1310 PG 7 WC Immunology SC Immunology GA JJ092 UT WOS:A1992JJ09200029 PM 1380038 ER PT J AU HOSMALIN, A KUMAR, S BARND, D HOUGHTEN, R SMITH, GE HUGHES, SH BERZOFSKY, JA AF HOSMALIN, A KUMAR, S BARND, D HOUGHTEN, R SMITH, GE HUGHES, SH BERZOFSKY, JA TI IMMUNIZATION WITH SOLUBLE PROTEIN-PULSED SPLEEN-CELLS INDUCES CLASS-I-RESTRICTED CYTOTOXIC LYMPHOCYTES-T THAT RECOGNIZE IMMUNODOMINANT EPITOPIC PEPTIDES FROM PLASMODIUM-FALCIPARUM AND HIV-1 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; FREE SYNTHETIC PEPTIDE; ANTIGEN PRESENTATION; VIRUS; INVIVO; RESPONSES; SEQUENCE; PATHWAY; INVITRO; MOUSE AB CTL lines specific for two different proteins derived from the human pathogens, Plasmodium falciparum (malaria) circumsporozoite protein and HIV-1 reverse transcriptase, were obtained by immunizing mice with protein-pulsed syngeneic spleen cells. The lysis of the target cells was dependent on a class I MHC molecule and the accessory molecule CD8. Immunodominant epitopic peptides were identified previously in the two proteins using murine CTL derived after immunization with recombinant virus or sporozoites, or using CTL from HIV-1-infected patients. These peptides were also recognized by the CTL lines obtained after protein-pulsed spleen-cell immunization. A new CTL antigenic determinant was localized in HIV-1 reverse transcriptase to residues 514 to 528, a sequence that, if folded as an alpha-helix, would be strongly amphipathic. The determinant was tentatively narrowed, using overlapping peptides, to a core of at least nine residues, 515 to 523. This site was also recognized by CTL obtained by the two different methods of immunization. Therefore, extracellular proteins incubated with spleen cells can be processed and presented in vivo in the same way as intracellular proteins, resulting in recognition of the same epitopes in association with the same class I MHC molecules. The potential implications for vaccine development and for the understanding of class I-restricted Ag presentation are discussed. C1 NCI,METAB BRANCH,MOLEC IMMUNOGENET & VACCINE RES SECT,BLDG 10,ROOM 6B-12,BETHESDA,MD 20892. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. TORREY PINES INST MOLEC STUDIES,SAN DIEGO,CA 92121. MICROGENESYS INC,W HAVEN,CT. NCI,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD 21701. FU NCI NIH HHS [N01-CO-74101] NR 47 TC 25 Z9 25 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD AUG 15 PY 1992 VL 149 IS 4 BP 1311 EP 1318 PG 8 WC Immunology SC Immunology GA JJ092 UT WOS:A1992JJ09200030 PM 1380039 ER PT J AU ANDERSON, GJ LESUISSE, E DANCIS, A ROMAN, DG LABBE, P KLAUSNER, RD AF ANDERSON, GJ LESUISSE, E DANCIS, A ROMAN, DG LABBE, P KLAUSNER, RD TI FERRIC IRON REDUCTION AND IRON ASSIMILATION IN SACCHAROMYCES-CEREVISIAE SO JOURNAL OF INORGANIC BIOCHEMISTRY LA English DT Article; Proceedings Paper CT 10TH INTERNATIONAL CONF ON IRON AND IRON PROTEINS CY JUL 27-31, 1991 CL KEBLE COLL, OXFORD UNIV, OXFORD, ENGLAND SP BLACKWELLS SCI PUBLICAT OXFORD, BLOOD RES FUND CARDIFF, BRIT SOC IMMUNOL, BRIT TECHNOL GRP, CIBA GEIGY, GLAXO, HAUSMANN, IMPERIAL CHEM IND, INORGAN BIOCHEM DISCUSS GRP, ROUSSEL HO KEBLE COLL, OXFORD UNIV ID PLASMA-MEMBRANE; MECHANISMS; TRANSPORT AB We have used the yeast Saccharomyces cerevisiae as a model organism to study the role of ferric iron reduction in eucaryotic iron uptake. S. cerevisiae is able to utilize ferric chelates as an iron source by reducing the ferric iron to the ferrous form, which is subsequently internalized by the cells. A gene (FRE1) was identified which encodes a protein required for both ferric iron reduction and efficient ferric iron assimilation, thus linking these two activities. The predicted FRE1 protein appears to be a membrane protein and shows homology to the beta-subunit of the human respiratory burst oxidase. These data suggest that FRE1 is a structural component of the ferric reductase. Subcellular fractionation studies showed that the ferric reductase activity of isolated plasma membranes did not reflect the activity of the intact cells, implying that cellular integrity was necessary for function of the major S. cerevisiae ferric reductase. An NADPH-dependent plasma membrane ferric reductase was partially purified from plasma membranes. Preliminary evidence suggests that the cell surface ferric reductase may, in addition to mediating cellular iron uptake, help modulate the intracellular redox potential of the yeast cell. C1 NICHHD,CBMB,BLDG 18T,ROOM 101,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. UNIV PARIS 07,INST JACQUES MONOD,BIOCHIM PORPHYRINES LAB,F-75251 PARIS 05,FRANCE. RI Anderson, Gregory/G-4148-2013 OI Anderson, Gregory/0000-0002-8814-5866 NR 17 TC 17 Z9 18 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0162-0134 J9 J INORG BIOCHEM JI J. Inorg. Biochem. PD AUG 15 PY 1992 VL 47 IS 3-4 BP 249 EP 255 DI 10.1016/0162-0134(92)84070-4 PG 7 WC Biochemistry & Molecular Biology; Chemistry, Inorganic & Nuclear SC Biochemistry & Molecular Biology; Chemistry GA JG962 UT WOS:A1992JG96200011 PM 1431884 ER PT J AU RAVUSSIN, E SWINBURN, BA AF RAVUSSIN, E SWINBURN, BA TI PATHOPHYSIOLOGY OF OBESITY SO LANCET LA English DT Article ID DOUBLY-LABELED WATER; ENERGY-EXPENDITURE; WEIGHT-GAIN; PHYSICAL-ACTIVITY; METABOLIC-RATE; PIMA-INDIANS; DIETARY-FAT; CARBOHYDRATE; OXIDATION; DETERMINANTS C1 UNIV AUCKLAND,SCH MED,DEPT COMMUNITY HLTH,AUCKLAND,NEW ZEALAND. RP RAVUSSIN, E (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,ROOM 541-A,PHOENIX,AZ 85016, USA. NR 37 TC 167 Z9 168 U1 2 U2 5 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD AUG 15 PY 1992 VL 340 IS 8816 BP 404 EP 408 DI 10.1016/0140-6736(92)91480-V PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JJ449 UT WOS:A1992JJ44900013 PM 1353565 ER PT J AU TAITELBAUM, H KOO, YEL HAVLIN, S KOPELMAN, R WEISS, GH AF TAITELBAUM, H KOO, YEL HAVLIN, S KOPELMAN, R WEISS, GH TI EXOTIC BEHAVIOR OF THE REACTION FRONT IN THE A+B-]C REACTION-DIFFUSION SYSTEM SO PHYSICAL REVIEW A LA English DT Note ID PRECIPITATION AB A dynamic reaction zone is produced in the A + B --> C reaction-diffusion system with initially separated components. Our perturbation analysis results predict a rich behavior for the kinetics of the reaction front in the short-time limit, with variety of universality classes. In particular, we show that the center of the front can change its direction of motion. Our experimental data support this prediction and demonstrate that this behavior is measurable over a time scale of hours in bimolecular reactions at room temperature. C1 UNIV MICHIGAN,DEPT CHEM,ANN ARBOR,MI 48109. BAR ILAN UNIV,DEPT PHYS,IL-52100 RAMAT GAN,ISRAEL. NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892. RP TAITELBAUM, H (reprint author), UNIV MARYLAND,INST PHYS SCI & TECHNOL,COLL PK,MD 20742, USA. NR 19 TC 88 Z9 88 U1 0 U2 2 PU AMERICAN PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 1050-2947 J9 PHYS REV A JI Phys. Rev. A PD AUG 15 PY 1992 VL 46 IS 4 BP 2151 EP 2154 DI 10.1103/PhysRevA.46.2151 PG 4 WC Optics; Physics, Atomic, Molecular & Chemical SC Optics; Physics GA JK630 UT WOS:A1992JK63000057 ER PT J AU HAVLIN, S LARRALDE, H TRUNFIO, P KIEFER, JE STANLEY, HE WEISS, GH AF HAVLIN, S LARRALDE, H TRUNFIO, P KIEFER, JE STANLEY, HE WEISS, GH TI NUMBER OF DISTINCT SITES VISITED BY N-PARTICLES DIFFUSING ON A FRACTAL SO PHYSICAL REVIEW A LA English DT Note ID LONG-TIME PROPERTIES; RANDOM-WALKS AB We study the mean number of distinct sites, S(N)(t), visited up to time t by N much greater than 1 noninteracting random walkers all starting from the same origin on a fractal substrate of dimension d(f). Using analytic arguments and numerical simulations, we find S(N)(t) approximately (lnN)(df/delta) t(ds/2) for fractals with spectral dimension d(s) = 2d(f)/d(w) < 2, where delta = d(w)/(d(w) - 1) and d(w) is the fractal dimension of a random walk. C1 BAR ILAN UNIV,DEPT PHYS,IL-52900 RAMAT GAN,ISRAEL. NIH,DIV COMP RES & TECHNOL,PHYS SCI LAB,BETHESDA,MD 20892. RP HAVLIN, S (reprint author), BOSTON UNIV,CTR POLYMER STUDIES,DEPT PHYS,BOSTON,MA 02215, USA. NR 16 TC 21 Z9 21 U1 1 U2 3 PU AMERICAN PHYSICAL SOC PI COLLEGE PK PA ONE PHYSICS ELLIPSE, COLLEGE PK, MD 20740-3844 USA SN 1050-2947 J9 PHYS REV A JI Phys. Rev. A PD AUG 15 PY 1992 VL 46 IS 4 BP R1717 EP R1719 PG 3 WC Optics; Physics, Atomic, Molecular & Chemical SC Optics; Physics GA JK630 UT WOS:A1992JK63000003 ER PT J AU APERIA, A IBARRA, F SVENSSON, LB KLEE, C GREENGARD, P AF APERIA, A IBARRA, F SVENSSON, LB KLEE, C GREENGARD, P TI CALCINEURIN MEDIATES ALPHA-ADRENERGIC STIMULATION OF NA+,K+-ATPASE ACTIVITY IN RENAL TUBULE CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID PROTEIN PHOSPHATASE; K+-ATPASE; DOPAMINE; PHOSPHOPROTEIN; RECEPTORS; DARPP-32; DEPHOSPHORYLATION; INHIBITION; ACTIVATION; TRANSPORT AB The alpha-adrenergic agonist oxymetazoline increased Na+,K+-ATPase activity of single proximal convoluted tubules dissected from rat kidney. Activation of the enzyme by oxymetazoline was prevented by either the alpha-1-adrenergic antagonist prazosin or the alpha-2-adrenergic antagonist yohimbine and was mimicked by the calcium ionophore A23187. The effect of oxymetazoline on Na+,K+-ATPase activity was prevented by a specific peptide inhibitor of calcineurin, as well as by FK 506, an immunosuppressant agent known to inhibit calcineurin; these results indicate that the action of oxymetazoline is mediated via activation of calcineurin (a calcium/calmodulin-dependent protein phosphatase). Activation of the Na+,K+-ATPase by either oxymetazoline or A23187 was associated with a > 2-fold increase in its affinity for Na+. The results provide a biochemical mechanism by which norepinephrine, released from renal nerve terminals, stimulates Na+ retention. C1 ROCKEFELLER UNIV,MOLEC & CELLULAR NEUROSCI LAB,NEW YORK,NY 10021. NCI,BETHESDA,MD 20892. RP APERIA, A (reprint author), KAROLINSKA INST,ST GORANS CHILDRENS HOSP,DEPT PEDIAT,S-11281 STOCKHOLM,SWEDEN. FU NIMH NIH HHS [MH40899] NR 24 TC 177 Z9 177 U1 1 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1992 VL 89 IS 16 BP 7394 EP 7397 DI 10.1073/pnas.89.16.7394 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100023 PM 1380157 ER PT J AU MCBRIDE, AA KLAUSNER, RD HOWLEY, PM AF MCBRIDE, AA KLAUSNER, RD HOWLEY, PM TI CONSERVED CYSTEINE RESIDUE IN THE DNA-BINDING DOMAIN OF THE BOVINE PAPILLOMAVIRUS TYPE-1 E2 PROTEIN CONFERS REDOX REGULATION OF THE DNA-BINDING ACTIVITY INVITRO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CARBOXY-TERMINAL DOMAIN; TRANSCRIPTIONAL REPRESSOR; DISULFIDE EXCHANGE; GENE-PRODUCT; OXIDATION; TRANSACTIVATION; ACTIVATION; ENHANCER; SEQUENCE; ENCODES AB The bovine papillomavirus type 1 E2 open reading frame encodes three proteins involved in viral DNA replication and transcriptional regulation. These polypeptides share a carboxyl-terminal domain with a specific DNA-binding activity; through this domain the E2 polypeptides form dimers. In this study, we demonstrate the inhibition of E2 DNA binding in vitro by reagents that oxidize or otherwise chemically modify the free sulfydryl groups of reactive cysteine residues. However, these reagents had no effect on DNA-binding activity when the E2 polypeptide was first bound to DNA, suggesting that the free sulfydryl group(s) may be protected by DNA binding. Sensitivity to sulfydryl modification was mapped to a cysteine residue at position 340 in the E2 DNA-binding domain, an amino acid that is highly conserved among the E2 proteins of different papillomaviruses. Replacement of this residue with other amino acids abrogated the sensitivity to oxidation-reduction changes but did not affect the DNA-binding property of the E2 protein. These results suggest that papillomavirus DNA replication and transcriptional regulation could be modulated through the E2 proteins by changes in the intracellular redox environment. Furthermore, a motif consisting of a reactive cysteine residue carboxyl-terminal to a lysine residue in a basic region of the DNA-binding domain is a feature common to a number of transcriptional regulatory proteins that, like E2, are subject to redox regulation. Thus, posttranslational regulation of the activity of these proteins by the intracellular redox environment may be a general phenomenon. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. RP MCBRIDE, AA (reprint author), NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892, USA. OI McBride, Alison/0000-0001-5607-5157 NR 31 TC 83 Z9 85 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1992 VL 89 IS 16 BP 7531 EP 7535 DI 10.1073/pnas.89.16.7531 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100051 PM 1323841 ER PT J AU HAILE, DJ ROUAULT, TA TANG, CK CHIN, J HARFORD, JB KLAUSNER, RD AF HAILE, DJ ROUAULT, TA TANG, CK CHIN, J HARFORD, JB KLAUSNER, RD TI RECIPROCAL CONTROL OF RNA-BINDING AND ACONITASE ACTIVITY IN THE REGULATION OF THE IRON-RESPONSIVE ELEMENT BINDING-PROTEIN - ROLE OF THE IRON-SULFUR CLUSTER SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID FERRITIN MESSENGER-RNA; TRANSFERRIN RECEPTOR; UNTRANSLATED REGION; IDENTIFICATION; TRANSLATION; EXPRESSION; MECHANISM; SYNTHASE; SEQUENCE; MURINE AB Several mechanisms of posttranscriptional gene regulation are involved in regulation of the expression of essential proteins of iron metabolism. Coordinate regulation of ferritin and transferrin receptor expression is produced by binding of a cytosolic protein, the iron-responsive element binding protein (IRE-BP) to specific stem-loop structures present in target RNAs. The affinity of this protein for its cognate RNA is regulated by the cell in response to changes in iron availability. The IRE-BP demonstrates a striking level of amino acid sequence identity to the iron-sulfur (Fe-S) protein mitochondrial aconitase. Moreover, the recombinant IRE-BP has aconitase function. The lability of the Fe-S cluster in mitochondrial aconitase has led us to propose that the mechanism by which iron levels are sensed by the IRE-BP involves changes in an Fe-S cluster in the IRE-BP. In this study, we demonstrate that procedures aimed at altering the IRE-BP Fe-S cluster in vitro reciprocally alter the RNA binding and aconitase activity of the IRE-BP. The changes in the RNA binding of the protein produced in vitro appear to match the previously described alterations of the protein in response to iron availability in the cell. Furthermore, iron manipulation of cells correlates with the activation or inactivation of the IRE-BP aconitase activity. The results are consistent with a model for the posttranslational regulation of the IRE-BP in which the Fe-S cluster is altered in response to the availability of intracellular iron and this, in turn, regulates the RNA-binding activity. C1 NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. NR 31 TC 208 Z9 207 U1 1 U2 4 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1992 VL 89 IS 16 BP 7536 EP 7540 DI 10.1073/pnas.89.16.7536 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100052 PM 1502165 ER PT J AU SPOUGE, JL AF SPOUGE, JL TI STATISTICAL-ANALYSIS OF SPARSE INFECTION DATA AND ITS IMPLICATIONS FOR RETROVIRAL TREATMENT TRIALS IN PRIMATES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANIMAL TRIAL; INFECTIVITY ASSAY; STATISTICS; COMPUTER PROGRAM ID HUMAN-IMMUNODEFICIENCY-VIRUS; GLYCOPROTEIN GP120; CONFERS PROTECTION; CHIMPANZEES; VACCINE; IMMUNIZATION; CHALLENGE; HIV-1; RECOMBINANT; PREVENTION AB Reports on retroviral primate trials rarely publish any statistical analysis. Present statistical methodology lacks appropriate tests for these trials and effectively discourages quantitative assessment. This paper describes the theory behind VACMAN, a user-friendly computer program that calculates statistics for in vitro and in vivo infectivity data. VACMAN's analysis applies to many retroviral trials using i.v. challenges and is valid whenever the viral dose-response curve has a particular shape. Statistics from actual i.v. retroviral trials illustrate some unappreciated principles of effective animal use: dilutions other than 1:10 can improve titration accuracy; infecting titration animals at the lowest doses possible can lower challenge doses; and finally, challenging test animals in small trials with more virus than controls safeguards against false successes, "reuses" animals, and strengthens experimental conclusions. The theory presented also explains the important concept of viral saturation, a phenomenon that may cause in vitro and in vivo titrations to agree for some retroviral strains and disagree for others. RP SPOUGE, JL (reprint author), NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894, USA. NR 34 TC 55 Z9 55 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1992 VL 89 IS 16 BP 7581 EP 7585 DI 10.1073/pnas.89.16.7581 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100061 PM 1323844 ER PT J AU LIN, KH ASHIZAWA, K CHENG, SY AF LIN, KH ASHIZAWA, K CHENG, SY TI PHOSPHORYLATION STIMULATES THE TRANSCRIPTIONAL ACTIVITY OF THE HUMAN BETA-1 THYROID-HORMONE NUCLEAR RECEPTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DNA-BINDING ACTIVITY; RESPONSE ELEMENTS; ACTIVATION; PROTEIN; DOMAIN; GROWTH; CELLS; PHOSPHOTYROSINE; MUTATIONS; PROMOTERS AB The role of phosphorylation on the gene activation activity of the human beta-1 thyroid hormone nuclear receptor (h-TR-beta-1) was examined. h-TR-beta-1 was found to be a phosphoprotein when expressed in COS-1 cells, with serine, threonine, and tyrosine (85:10:5) as the phosphorylation sites. Okadaic acid (a potent inhibitor of phosphatases 1 and 2A) at 0.1, 0.25, and 0.5-mu-M increased the phosphorylation of h-TR-beta-1 by 3-, 7-, and 11-fold, respectively. The increase in phosphorylation was accompanied by a concomitant increase in receptor-mediated transcription in transient transfection assays. h-TR-beta-1 purified from Escherichia coli was phosphorylated in vitro by the endogenous kinase from cellular extracts. Serine, threonine, and tyrosine were phosphorylated in a similar ratio to that found in COS-1 cells. The in vitro phosphorylation was stimulated by okadaic acid. Phosphorylation did not affect the binding of h-TR-beta-1 to 3,3',5-triiodo-L-thyronine. However, phosphorylation of h-TR-beta-1 resulted in an increase of its binding to DNA and conferred on it the ability to bind to nuclear accessory proteins. The results indicate that phosphorylation plays an important role in the transcriptional activity of h-TR-beta-1. C1 NCI,DIV CANC BIOL DIAG & CTR,MOLEC BIOL LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NR 33 TC 77 Z9 77 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1992 VL 89 IS 16 BP 7737 EP 7741 DI 10.1073/pnas.89.16.7737 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100093 PM 1502193 ER PT J AU NATUK, RJ CHANDA, PK LUBECK, MD DAVIS, AR WILHELM, J HJORTH, R WADE, MS BHAT, BM MIZUTANI, S LEE, S EICHBERG, J GALLO, RC HUNG, PP ROBERTGUROFF, M AF NATUK, RJ CHANDA, PK LUBECK, MD DAVIS, AR WILHELM, J HJORTH, R WADE, MS BHAT, BM MIZUTANI, S LEE, S EICHBERG, J GALLO, RC HUNG, PP ROBERTGUROFF, M TI ADENOVIRUS HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) ENVELOPE RECOMBINANT VACCINES ELICIT HIGH-TITERED HIV-NEUTRALIZING ANTIBODIES IN THE DOG-MODEL SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID GLYCOPROTEIN GP120; CHIMPANZEES; TYPE-1; EXPRESSION; INFECTION; DETERMINANT; AIDS AB Recombinant human adenoviruses (Ads) (types 4, 5, and 7) expressing the HIV-1 envelope membrane glycoprotein (gp160) were tested for immunogenicity in the dog. Administration of recombinant Ad7-env by intratracheal inoculation resulted in a low serum antibody response to gp160, which developed over several weeks. A strong neutralizing antibody response to the Ad7 vector developed within 1 week of infection. A subsequent booster inoculation 12 weeks later with the heterotypic Ad4-env recombinant virus resulted in significantly enhanced humoral responses directed at the envelope antigen, as measured by both ELISA and Western blot analysis as well as high-titer type-specific neutralizing antibodies, with some animals achieving neutralization titers approaching 1000. Recombinant HIV envelope glycoprotein derived from Ad-HIV-infected cell cultures was used as a subunit booster injection for dogs that had previously received sequential immunizations with heterotypic recombinant Ads. Significant immune responses against the envelope developed as measured by ELISA, Western blot analysis, and neutralization assays. These data indicate that live recombinant Ad-HIV vaccines are capable of inducing high-titer type-specific neutralizing antibodies to gp160 in vivo. Recombinant HIV envelope glycoprotein subunit vaccines, prepared from Ad-envinfected cells, are capable of boosting these responses. C1 WYETH AYERST,DEPT MICROBIOL,PHILADELPHIA,PA 19101. NCI,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. RP NATUK, RJ (reprint author), WYETH AYERST RES,DEPT BIOTECHNOL,DIV BIOTECHNOL & MICROBIOL,POB 8299,PHILADELPHIA,PA 19101, USA. NR 24 TC 46 Z9 46 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1992 VL 89 IS 16 BP 7777 EP 7781 DI 10.1073/pnas.89.16.7777 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100101 PM 1502197 ER PT J AU KITAYAMA, S SHIMADA, S XU, HX MARKHAM, L DONOVAN, DM UHL, GR AF KITAYAMA, S SHIMADA, S XU, HX MARKHAM, L DONOVAN, DM UHL, GR TI DOPAMINE TRANSPORTER SITE-DIRECTED MUTATIONS DIFFERENTIALLY ALTER SUBSTRATE TRANSPORT AND COCAINE BINDING SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE 1-METHYL-4-PHENYLPYRIDINUM; REUPTAKE; LIGAND RECOGNITION ID LIGAND-BINDING; SEROTONIN TRANSPORTER; RAT-BRAIN; EXPRESSION; CLONING; RECEPTOR; MUTAGENESIS; INHIBITION AB Polar amino acids lying within three hydrophobic regions of the dopamine transporter (DAT) are analogous to those important for ligand recognition by catecholamine receptors. Possible functional significance of these amino acids was examined by expressing DAT cDNAs mutated in these polar residues. Replacement of aspartate at position 79 with alanine, glycine, or glutamate dramatically reduced uptake of [H-3]dopamine and the tritium-labeled Parkinsonism-inducing neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and reduced the mutants' affinity for the tritium-labeled cocaine analog (-)-2-beta-carbomethoxy-3-beta-(4-fluorophenyl)tropane (CFT) without affecting B(max). Replacement of the serine residues at positions 356 and 359 in the seventh hydrophobic region by alanine or glycine caused reductions in [H-3]dopamine and [H-3]MPP+ uptake, whereas [H-3]CFT binding was less affected. Substitution of two serines in the eighth hydrophobic region yielded wild-type values for [H-3]dopamine and [H-3]MPP+ uptake and [H-3]CFT binding. These results demonstrate that aspartate and serine residues lying within the first and seventh hydrophobic putative transmembrane regions are crucial for DAT function and provide identification of residues differentially important for cocaine binding and for dopamine uptake. C1 NIDA,ADDICT RES CTR,MOLEC NEUROBIOL LAB,POB 5180,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. NR 24 TC 344 Z9 347 U1 1 U2 5 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 15 PY 1992 VL 89 IS 16 BP 7782 EP 7785 DI 10.1073/pnas.89.16.7782 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JJ321 UT WOS:A1992JJ32100102 PM 1502198 ER PT J AU JAYARAM, HN GHAREHBAGHI, K JAYARAM, NH RIESER, J KROHN, K PAULL, KD AF JAYARAM, HN GHAREHBAGHI, K JAYARAM, NH RIESER, J KROHN, K PAULL, KD TI CYTOTOXICITY OF A NEW IMP DEHYDROGENASE INHIBITOR, BENZAMIDE RIBOSIDE, TO HUMAN MYELOGENOUS LEUKEMIA K562 CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID MECHANISM; TIAZOFURIN; NUCLEOSIDE; LINES C1 UNIV GESAMTHSCH PADERBORN,DIV ORGAN CHEM,W-4790 PADERBORN,GERMANY. NCI,INFORMAT TECHNOL BRANCH,BETHESDA,MD 20892. RP JAYARAM, HN (reprint author), INDIANA UNIV,SCH MED,EXPTL ONCOL LAB,INDIANAPOLIS,IN 46202, USA. FU NCI NIH HHS [CA-51770] NR 12 TC 57 Z9 58 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD AUG 14 PY 1992 VL 186 IS 3 BP 1600 EP 1606 DI 10.1016/S0006-291X(05)81591-8 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JJ803 UT WOS:A1992JJ80300061 PM 1354960 ER PT J AU HILAKIVICLARKE, LA ARORA, PK SABOL, MB CLARKE, R DICKSON, RB LIPPMAN, ME AF HILAKIVICLARKE, LA ARORA, PK SABOL, MB CLARKE, R DICKSON, RB LIPPMAN, ME TI ALTERATIONS IN BEHAVIOR, STEROID-HORMONES AND NATURAL-KILLER-CELL ACTIVITY IN MALE TRANSGENIC TGF-ALPHA MICE SO BRAIN RESEARCH LA English DT Article DE TRANSFORMING GROWTH FACTOR-ALPHA; DEPRESSION; AGGRESSION; ESTROGEN; NATURAL KILLER CELL ACTIVITY; HEPATOCARCINOMA ID TRANSFORMING GROWTH-FACTOR; HEPATOCELLULAR-CARCINOMA; GENETIC-CONTROL; STRESS; RAT; EXPRESSION; INDUCTION; ESTRADIOL; CANCER; TUMORS AB The expression of transforming growth factor-alpha (TGF-alpha) is widely distributed throughout many normal and neoplastic tissues, but its physiological significance remains unclear. We have utilized male transgenic mice overexpressing the gene encoding human TGF-alpha in multiple tissues to further identify those functions which are influenced by this protein. Male TGF-alpha mice develop hepatocellular carcinoma at the age of 10-15 months. At the age of 2-3 months these mice, compared to age matched CD-1 controls, spent significantly longer times immobile in Porsolt's swim test, a model of stress and depressive behavior, and exhibiting aggressive behavior in the resident-intruder test. In contrast, the transgenic TGF-alpha mice did not differ from the controls in either the plusmaze test of anxiety, or in their voluntary alcohol intake. Significantly, the TGF-alpha mice exhibited a 25% lower Natural Killer (NK) cell activity and a four-fold increase in the plasma levels of 17-beta-estradiol (E2) than the controls. No significant changes in plasma testosterone or corticosterone levels were noted. The results indicate that transgenic male mice overexpressing TGF-alpha exhibit behaviors characteristic of both an impaired ability to cope with stress and an increased aggressivity. The TGF-alpha mice also show reduced NK cell activity and increased plasma estradiol concentrations. The present data suggest that TGF-alpha may be important in influencing behavioral, immunological and hormonal systems prior to the onset of tumors. It remains to be determined whether hepatocarcinoma is associated with the direct proliferative and transforming effects of TGF-alpha and/or indirect effects mediated through immune, hormonal and behavioral mechanisms. C1 NIDDK,NEUROSCI LAB,BETHESDA,MD 20892. RP HILAKIVICLARKE, LA (reprint author), GEORGETOWN UNIV,SCH MED,LOMBARDI CANC RES CTR,ROOM S128,3800 RESERVOIR RD,WASHINGTON,DC 20007, USA. RI Clarke, Robert/A-6485-2008 OI Clarke, Robert/0000-0002-9278-0854 NR 60 TC 36 Z9 36 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 AUG 14 PY 1992 VL 588 IS 1 BP 97 EP 103 DI 10.1016/0006-8993(92)91348-I PG 7 WC Neurosciences SC Neurosciences & Neurology GA JL387 UT WOS:A1992JL38700012 PM 1393573 ER PT J AU VONLUBITZ, DKJE LIN, RCS MCKENZIE, RJ DEVLIN, TM MCCABE, RT SKOLNICK, P AF VONLUBITZ, DKJE LIN, RCS MCKENZIE, RJ DEVLIN, TM MCCABE, RT SKOLNICK, P TI A NOVEL TREATMENT OF GLOBAL CEREBRAL-ISCHEMIA WITH A GLYCINE PARTIAL AGONIST SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE GLOBAL ISCHEMIA; 1-AMINOCYCLOPROPANECARBOXYLIC ACID; GLYCINE RECEPTORS; NMDA RECEPTORS; (GERBIL) ID NMDA RECEPTOR COMPLEX; FUNCTIONAL ANTAGONISTS; EXHIBIT ANTIDEPRESSANT; ISCHEMIA; PROTECT; 1-AMINOCYCLOPROPANECARBOXYLATES; CONVULSIONS; FOREBRAIN; GERBILS; DAMAGE AB Chronic treatment of gerbils with 1-aminocyclopropanecarboxylic acid (a high affinity, partial agonist at strychnine-insensitive glycine receptors) resulted in a 3-fold increase in survival, a significant improvement in neurological status, and an extensive protection of vulnerable brain regions following severe forebrain ischaemia. A bolus of 1-aminocyclopropanecarboxylic acid 30 min prior to ischaemia did not further improve outcome compared to gerbils receiving their last injection 24 h prior to ischaemia. These findings are consistent with the hypothesis that chronic treatment with a glycine partial agonist desensitizes the N-methyl-D-aspartate receptor complex. Pharmacological intervention at the strychnine-insensitive glycine receptor may be an effective means of ameliorating the consequences of neuronal degeneration caused by excitotoxic phenomena. C1 HAHNEMANN UNIV,DEPT BIOPHYS,PHILADELPHIA,PA 19102. HAHNEMANN UNIV,DEPT BIOCHEM & PHYSIOL,PHILADELPHIA,PA 19102. RP VONLUBITZ, DKJE (reprint author), NIDDK,NEUROSCI LAB,BLDG 8,ROOM 111,BETHESDA,MD 20892, USA. NR 28 TC 59 Z9 59 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD AUG 14 PY 1992 VL 219 IS 1 BP 153 EP 158 DI 10.1016/0014-2999(92)90594-T PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JJ611 UT WOS:A1992JJ61100023 PM 1327834 ER PT J AU RANDAZZO, PA KAHN, RA NORTHUP, JK AF RANDAZZO, PA KAHN, RA NORTHUP, JK TI NUCLEOSIDE DIPHOSPHATE KINASE - CONCLUSIONS WITHDRAWN SO SCIENCE LA English DT Letter C1 NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RP RANDAZZO, PA (reprint author), NCI,DIV CANC TREATMENT,BIOL CHEM LAB,BETHESDA,MD 20892, USA. NR 3 TC 8 Z9 8 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 AUG 14 PY 1992 VL 257 IS 5072 BP 862 EP 862 DI 10.1126/science.1323875 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JH827 UT WOS:A1992JH82700007 PM 1323875 ER PT J AU ADLER, RG AF ADLER, RG TI GENOME RESEARCH - FULFILLING THE PUBLICS EXPECTATIONS FOR KNOWLEDGE AND COMMERCIALIZATION SO SCIENCE LA English DT Article ID BIOTECHNOLOGY; PROJECT; PATENTS AB This article provides a historical perspective for the patenting of gene sequences and describes the fundamentals and evolution of patent law. It summarizes federal technology transfer law and policy and assesses the impacts of patenting on academic research. The patentability of gene sequences is then considered along with potential impacts that published sequence data may have on obtaining patent protection for downstream products. Industry's position on gene patenting is summarized and perspectives from the emerging public record on these issues are presented. The article discussing points at which the filing of patent applications and the licensing of patents may be appropriate. It concludes that technology transfer policies for genome research must be adopted carefully so that they remain viable in a time of rapid technological change. RP ADLER, RG (reprint author), NIH,OFF TECHNOL TRANSFER,BETHESDA,MD 20892, USA. NR 40 TC 31 Z9 31 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 AUG 14 PY 1992 VL 257 IS 5072 BP 908 EP 914 DI 10.1126/science.1502557 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JH827 UT WOS:A1992JH82700022 PM 1502557 ER PT J AU SHAANAN, B GRONENBORN, AM COHEN, GH GILLILAND, GL VEERAPANDIAN, B DAVIES, DR CLORE, GM AF SHAANAN, B GRONENBORN, AM COHEN, GH GILLILAND, GL VEERAPANDIAN, B DAVIES, DR CLORE, GM TI COMBINING EXPERIMENTAL INFORMATION FROM CRYSTAL AND SOLUTION STUDIES - JOINT X-RAY AND NMR REFINEMENT SO SCIENCE LA English DT Article ID NUCLEAR-MAGNETIC-RESONANCE; INTERPROTON DISTANCE RESTRAINTS; AMYLASE INHIBITOR TENDAMISTAT; MOLECULAR-DYNAMICS; SINGLE-CRYSTALS; R-FACTOR; PROTEINS; INTERLEUKIN-1-BETA; DIFFRACTION; RESOLUTION AB Joint refinement of macromolecules against crystallographic and nuclear magnetic resonance (NMR) observations is presented as a way of combining experimental information from the two methods. The model of interleukin-1-beta derived by the joint x-ray and NMR refinement is shown to be consistent with the experimental observations of both methods and to have crystallographic R value and geometrical parameters that are of the same quality as or better than those of models obtained by conventional crystallographic studies. The few NMR observations that are violated by the model serve as an indicator for genuine differences between the crystal and solution structures. The joint x-ray-NMR refinement can resolve structural ambiguities encountered in studies of multidomain proteins, in which low- to medium-resolution diffraction data can be complemented by higher resolution NMR data obtained for the individual domains. C1 NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892. NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NATL INST STAND & TECHNOL,ROCKVILLE,MD 20850. UNIV MARYLAND,MARYLAND BIOTECHNOL INST,CTR ADV RES BIOTECHNOL,SHADY GROVE,MD. RI Clore, G. Marius/A-3511-2008; Shaanan, Boaz/F-1202-2012 OI Clore, G. Marius/0000-0003-3809-1027; NR 25 TC 51 Z9 52 U1 1 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 AUG 14 PY 1992 VL 257 IS 5072 BP 961 EP 964 DI 10.1126/science.1502561 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JH827 UT WOS:A1992JH82700034 PM 1502561 ER PT J AU EGAN, M FLOTTE, T AFIONE, S SOLOW, R ZEITLIN, PL CARTER, BJ GUGGINO, WB AF EGAN, M FLOTTE, T AFIONE, S SOLOW, R ZEITLIN, PL CARTER, BJ GUGGINO, WB TI DEFECTIVE REGULATION OF OUTWARDLY RECTIFYING CL- CHANNELS BY PROTEIN KINASE-A CORRECTED BY INSERTION OF CFTR SO NATURE LA English DT Article ID CYSTIC-FIBROSIS GENE; CHLORIDE CHANNELS; EPITHELIAL-CELLS; EXPRESSION; CONDUCTANCE; ACTIVATION; DISEASE AB CYSTIC fibrosis (CF) is a lethal genetic disease resulting in a reduced Cl- permeability1, increased mucous sulphation2, increased Na+ absorption3 and defective acidification of lysosomal vesicles4. The CF gene encodes a protein (the cystic fibrosis transmembrane conductance regulator, CFTR5) that can function as a low-conductance Cl- channel with a linear current-voltage relationship whose regulation is defective in CF patients6-8. Larger conductance, outwardly rectifying Cl- channels are also defective in CF and fail to activate when exposed either to cyclic AMP-dependent protein kinase A or to protein kinase C9-13. The role of the outwardly rectifying Cl- channel in CF has been questioned14. We report here that expression of recombinant CF genes using adeno-associated virus vectors in CF bronchial epithelial cells corrects defective Cl- secretion, that it induces the appearance of small, linear conductance Cl- channels, and restores protein kinase A activation of outwardly rectifying Cl- channels. These results re-establish an involvement of outwardly rectifying Cl- channels in CF and suggest that CFTR regulates more than one conductance pathway in airway tissues. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,BALTIMORE,MD 21205. NIDDKD,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD. NR 25 TC 381 Z9 381 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD AUG 13 PY 1992 VL 358 IS 6387 BP 581 EP 584 DI 10.1038/358581a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JH829 UT WOS:A1992JH82900059 PM 1380129 ER PT J AU QUINN, TC AF QUINN, TC TI SCREENING FOR HIV-INFECTION - BENEFITS AND COSTS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID HUMAN-IMMUNODEFICIENCY-VIRUS; RISK RP QUINN, TC (reprint author), NIAID,BETHESDA,MD 20892, USA. NR 15 TC 16 Z9 16 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 13 PY 1992 VL 327 IS 7 BP 486 EP 488 DI 10.1056/NEJM199208133270708 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA JH340 UT WOS:A1992JH34000008 PM 1625739 ER PT J AU HERWALDT, BL NEVA, FA BERMAN, JD AF HERWALDT, BL NEVA, FA BERMAN, JD TI ALLOPURINOL IN THE TREATMENT OF AMERICAN CUTANEOUS LEISHMANIASIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID EFFICACY C1 NIH,BETHESDA,MD 20892. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. RP HERWALDT, BL (reprint author), CTR DIS CONTROL,ATLANTA,GA 30333, USA. NR 8 TC 10 Z9 10 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 13 PY 1992 VL 327 IS 7 BP 498 EP 498 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JH340 UT WOS:A1992JH34000021 PM 1625745 ER PT J AU URBA, WJ LONGO, DL AF URBA, WJ LONGO, DL TI HODGKINS-DISEASE - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID CHEMOTHERAPY C1 NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. RP URBA, WJ (reprint author), PROGRAM RESOURCES INC,DYN CORP,FREDERICK,MD 21702, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 13 PY 1992 VL 327 IS 7 BP 499 EP 500 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JH340 UT WOS:A1992JH34000026 ER PT J AU PIERCE, JP MILLS, SL SHOPLAND, DR MARCUS, SE AF PIERCE, JP MILLS, SL SHOPLAND, DR MARCUS, SE TI ACCESSIBILITY OF CIGARETTES TO YOUTHS AGED 12-17 (REPRINTED FROM MMWR, VOL 41, PG 485-488, 1992) SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Reprint ID MINORS; SALES C1 NCI,BETHESDA,MD 20892. NIDR,BETHESDA,MD 20892. CTR DIS CONTROL,NATL CTR CHRON DIS PREVENT & HLTH PROMOT,OFF SMOKING & HLTH,ATLANTA,GA 30333. CTR DIS CONTROL,DIV ANAL,OFF ANAL & EPIDEMIOL,ATLANTA,GA 30333. CTR DIS CONTROL,DIV HLTH INTERVIEW STAT,ATLANTA,GA 30333. CTR DIS CONTROL,OFF VITAL & HLTH STAT,ATLANTA,GA 30333. RP PIERCE, JP (reprint author), UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093, USA. NR 10 TC 2 Z9 2 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD AUG 12 PY 1992 VL 268 IS 6 BP 706 EP 707 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JG666 UT WOS:A1992JG66600006 ER PT J AU BRODER, S AF BRODER, S TI CIGARETTE ADVERTISING AND CORPORATE-RESPONSIBILITY SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material RP BRODER, S (reprint author), NCI,BLDG 31,ROOM 11A48,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 9 TC 0 Z9 0 U1 1 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD AUG 12 PY 1992 VL 268 IS 6 BP 782 EP 783 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JG666 UT WOS:A1992JG66600024 PM 1640582 ER PT J AU BAX, A MAX, D ZAX, D AF BAX, A MAX, D ZAX, D TI MEASUREMENT OF LONG-RANGE C-13-C-13 J COUPLINGS IN A 20-KDA PROTEIN-PEPTIDE COMPLEX SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Note ID ABUNDANCE C1 MAGNEX SCI LTD,ABINGDON OX14 1DY,ENGLAND. CORNELL UNIV,DEPT CHEM,BAKER LAB,ITHACA,NY 14853. RP BAX, A (reprint author), NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892, USA. NR 11 TC 109 Z9 109 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD AUG 12 PY 1992 VL 114 IS 17 BP 6923 EP 6925 DI 10.1021/ja00043a052 PG 3 WC Chemistry, Multidisciplinary SC Chemistry GA JH996 UT WOS:A1992JH99600052 ER PT J AU TSOKOS, DC OMATA, Y ROBINSON, RC KRUTZSCH, HC GELBOIN, HV FRIEDMAN, FK AF TSOKOS, DC OMATA, Y ROBINSON, RC KRUTZSCH, HC GELBOIN, HV FRIEDMAN, FK TI A PROTEOLYTICALLY SENSITIVE REGION COMMON TO SEVERAL RAT-LIVER CYTOCHROMES-P450 - EFFECT OF CLEAVAGE ON SUBSTRATE BINDING SO BIOCHEMISTRY LA English DT Article ID MEMBRANE-BOUND CYTOCHROMES-P450; MONOCLONAL-ANTIBODIES; CRYSTAL-STRUCTURE; SECONDARY STRUCTURE; SPIN EQUILIBRIUM; INDUCIBLE RAT; CYTOCHROME-P-450; SEQUENCE; IDENTIFICATION; PURIFICATION AB Limited proteolysis of rat liver microsomes was used to probe the topography and structure of cytochrome P450 bound to the endoplasmic reticulum. Three cytochromes P450 from two families were examined. Monoclonal antibodies to cytochrome P450 forms 1A1, 2B1, and 2E1 were used to immunopurify these proteolyzed cytochromes P450 from microsomes from rats treated with 3-methylcholanthrene, phenobarbital, and acetone, respectively. Electrophoretic and immunoblot analysis of tryptic fragments revealed a highly sensitive cleavage site in all three cytochromes P450. N-Terminal sequencing was performed on the fragments after transfer onto poly(vinylidene difluoride) membranes and showed that this preferential cleavage site is at amino acid position 298 of P450 1A1, position 277 of P450 2B1, and position 278 of P450 2E1. Multiple sequence alignment revealed that these positions are at the amino terminal of a highly conserved region of these cytochromes P450. The important functional role implied by primary sequence conservation along with the proteolytic sensitivity at its amino terminal suggests that this region is a protein domain. Comparison with the known structure of the bacterial cytochrome P450cam predicts that this proteolytically sensitive site is within an interhelical turn region connected to the distal helix that partially encompasses the heme-containing active site. Substrate binding to the cleaved cytochromes P450 was examined in order to determine whether the newly added conformational freedom near the cleavage site functionally altered these cytochromes P450. Cleavage of P450 2B1 abolished benzphetamine binding, which indicates that the cleavage site contains an important structural determinant for binding this substrate. However, cleavage did not affect benzo[a]pyrene binding to P450 1A1. C1 NCI,MOLEC CARCINOGENESIS LAB,BLDG 37,ROOM 3E-24,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. RI Friedman, Fred/D-4208-2016 NR 39 TC 11 Z9 11 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD AUG 11 PY 1992 VL 31 IS 31 BP 7155 EP 7159 DI 10.1021/bi00146a018 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JH598 UT WOS:A1992JH59800018 PM 1643049 ER PT J AU SMITH, RH PRUSKI, B DAY, CS PFALTZGRAFF, TD MICHEJDA, CJ AF SMITH, RH PRUSKI, B DAY, CS PFALTZGRAFF, TD MICHEJDA, CJ TI FORMATION OF ALIPHATIC AZIMINES IN AN UNEXPECTED REACTION SO TETRAHEDRON LETTERS LA English DT Article DE ALKYLAZIDES; GRIGNARD REAGENTS; TRIAZENES; CYCLIZATION; AZIMINES AB The reactions of 1-azido-3-chloropropane with various Grignard reagents, followed by the treatment of the reaction mixture with isopropylamine result in the formation, in high yields, of 1-[alkyl (or aryl) imino]-4,5-dihydro-3H-pyrazoles, a new class of azimines. C1 NCI,FREDERICK CANC RES DEV CTR,ABL BASIC RES PROGRAM,MOLEC ASPECTS DRUG DESIGN SECT,FREDERICK,MD 21702. RP SMITH, RH (reprint author), WESTERN MARYLAND COLL,DEPT CHEM,WESTMINSTER,MD 21157, USA. NR 5 TC 4 Z9 4 U1 1 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 AUG 11 PY 1992 VL 33 IS 33 BP 4683 EP 4686 DI 10.1016/S0040-4039(00)61258-3 PG 4 WC Chemistry, Organic SC Chemistry GA JH763 UT WOS:A1992JH76300003 ER PT J AU SORLIE, P ROGOT, E ANDERSON, R JOHNSON, NJ BACKLUND, E AF SORLIE, P ROGOT, E ANDERSON, R JOHNSON, NJ BACKLUND, E TI BLACK-WHITE MORTALITY DIFFERENCES BY FAMILY INCOME SO LANCET LA English DT Article ID NATIONAL-DEATH-INDEX; UNITED-STATES; EXCESS MORTALITY; RISK-FACTORS; DISEASE; HEALTH; RACE AB Death rates among US black men and women under 75 years of age are higher than for their white counterparts. The explanation for this excess risk, though attributed to socioeconomic factors, remains unclear. We calculated mortality rates by family income for blacks and whites in a respresentative sample of the US population (National Longitudinal Mortality Study). For persons aged less than 65 years of age, mortality rates are lower in those with higher family income for both blacks and whites, and both men and women. However, at each level of income, blacks have higher mortality than whites. Higher levels of family income are also associated with lower death rates from cardiovascular disease, cancer, and deaths from causes other than cardiovascular disease or cancer. After adjustment for income, blacks have higher death rates from each of these three general causes. For subjects below 65 years, the mortality gradient by income is larger than the gradient by race. The differences in mortality rates by race not accounted for by income may be due to other differences such as access to health care, type or quality of medical care, or behavioural risk factors that disadvantage black populations. C1 WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,EPIDEMIOL SECT,WINSTON SALEM,NC 27103. US BUR CENSUS,SUITLAND,MD. RP SORLIE, P (reprint author), NHLBI,FED BLDG,ROOM 3A10,BETHESDA,MD 20892, USA. NR 33 TC 108 Z9 109 U1 0 U2 2 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD AUG 8 PY 1992 VL 340 IS 8815 BP 346 EP 350 DI 10.1016/0140-6736(92)91413-3 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JH125 UT WOS:A1992JH12500012 PM 1353813 ER PT J AU KRAMER, A GOEDERT, JJ WACHTER, H FUCHS, D AF KRAMER, A GOEDERT, JJ WACHTER, H FUCHS, D TI PROGNOSTIC VALUE OF SERUM BETA-2-MICROGLOBULIN IN HIV-INFECTION SO LANCET LA English DT Letter ID IMMUNODEFICIENCY VIRUS TYPE-1; PREDICTIVE MARKER; NEOPTERIN C1 UNIV INNSBRUCK,INST MED CHEM & BIOCHEM,A-6020 INNSBRUCK,AUSTRIA. NCI,VIRAL EPIDEMIOL SECT,ROCKVILLE,MD. RP KRAMER, A (reprint author), UNIV TUBINGEN,INST MED BIOMETRY,W-7400 TUBINGEN 1,GERMANY. NR 7 TC 1 Z9 1 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 AUG 8 PY 1992 VL 340 IS 8815 BP 371 EP 371 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JH125 UT WOS:A1992JH12500030 PM 1379663 ER PT J AU LOGAN, A FRAUTSCHY, SA GONZALEZ, AM SPORN, MB BAIRD, A AF LOGAN, A FRAUTSCHY, SA GONZALEZ, AM SPORN, MB BAIRD, A TI ENHANCED EXPRESSION OF TRANSFORMING GROWTH-FACTOR BETA-1 IN THE RAT-BRAIN AFTER A LOCALIZED CEREBRAL INJURY SO BRAIN RESEARCH LA English DT Article DE TRANSFORMING GROWTH FACTOR BETA-1; MESSENGER-RNA; INJURY; CENTRAL NERVOUS SYSTEM; GLIAL SCAR; ASTROCYTE ID MESSENGER-RNA; CELLS; FIBROBLASTS; MACROPHAGE; COLLAGEN; NEURONS; INVITRO; NERVE; FACTOR-BETA-1; REGENERATION AB It is becoming clear that transforming growth factor-beta (TGf-beta) may be a key factor regulating inflammatory and tissue specific wound responses. Because the formation of a glial-collagen scar at CNS lesion sites is thought to contribute to the pathology associated with penetrating CNS injuries, and because in the periphery TGF-beta-1 stimulates fibroblast deposition of scar tissue, we used in situ hybridization and immunohistochemistry to investigate the effect of a defined cerebral lesion on the local expression of TGF-beta-1. Induction of TGF-beta-1 mRNA and protein is relatively diffuse in the neuropile around the margins of the lesion at 1, 2 and 3 days, but becomes localized to the region of the glial scar at 7 and 14 days. The signal intensity for TGF-beta-1 mRNA and protein is maximal between 2 and 3 days and decreases between 7 and 14 days after lesion. The predominant cell types in the neuropile localizing TGF-beta-1 mRNA and protein have the morphological characteristics of astrocytes, although macrophages are also detected. An induction of TGF-beta-1 mRNA was also observed in endothelial cells of the meninges, hippocampal fissure and choroid plexus, at 2 and 3 days. However, this is dramatically reduced by 7 days and has disappeared by 14 days. These results suggest a role for TGF-beta-1, not only in inflammation, but also in the tissue-specific glial scar formation that occurs in the CNS. Furthermore, they suggest a potential therapeutic use of TGF-beta-1 antagonists in the CNS to help limit the pathogenesis associated with matrix deposition in the wound. C1 WHITTIER INST DIABET & ENDOCRINOL,DEPT MOLEC & CELLULAR GROWTH BIOL,LA JOLLA,CA 92037. UNIV BIRMINGHAM,DEPT CLIN CHEM,BIRMINGHAM B15 2TT,W MIDLANDS,ENGLAND. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. FU NIA NIH HHS [R01 AG010685]; NIDDK NIH HHS [P01 DK018811]; NINDS NIH HHS [NS-28121, P01 NS028121]; Wellcome Trust NR 52 TC 194 Z9 199 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD AUG 7 PY 1992 VL 587 IS 2 BP 216 EP 225 DI 10.1016/0006-8993(92)91000-5 PG 10 WC Neurosciences SC Neurosciences & Neurology GA JK435 UT WOS:A1992JK43500006 PM 1525658 ER PT J AU BOJE, KM ARORA, PK AF BOJE, KM ARORA, PK TI MICROGLIAL-PRODUCED NITRIC-OXIDE AND REACTIVE NITROGEN-OXIDES MEDIATE NEURONAL CELL-DEATH SO BRAIN RESEARCH LA English DT Article DE GLIAL CELL; NITRIC OXIDE; REACTIVE NITROGEN OXIDE; CYTOKINE; MICROGLIA; NEUROTOXICITY; NITRIC OXIDE SYNTHASE; ENDOTOXIN ID TUMOR-NECROSIS-FACTOR; CENTRAL-NERVOUS-SYSTEM; L-ARGININE; MULTIPLE-SCLEROSIS; RELAXING FACTOR; CYTO-TOXICITY; MURINE MACROPHAGES; AMEBOID MICROGLIA; INTERFERON-GAMMA; FACTOR-ALPHA AB The role of inflammatory cytokines in the pathogenesis of neurological diseases is not well understood. The neurotoxic effects of cytokines could be mediated by immunostimulation of glial cells to produce toxic concentrations of nitric oxide (NO) and reactive nitrogen oxides. Cultured microglia and meningeal fibroblasts, but not Type 1 astrocytes, were induced by lipopolysaccharides and cytokines to synthesize NO and reactive nitrogen oxides from L-arginine. In co-cultures of immunostimulated microglia and cerebellar granule neurons, neurotoxicity was blocked by an inhibitor of NO synthase, N(G)-nitroarginine, and by oxyhemoglobin, which inactivates NO. Microglial-induced neurotoxicity was also partially attenuated by the N-methyl-D-aspartate (NMDA) receptor antagonists, MK-801 and 2-amino-5-phosphovalerate (APV). Superoxide dismutase, which stabilizes NO through inactivation of superoxide anion, augmented microglial-mediated neurotoxicity either alone or in combination with MK-801 or APV. Hence, immunostimulated microglia mediate neurotoxicity by NO, reactive nitrogen oxides, superoxide anion and NMDA-like substances. These findings suggest a novel role for microglial-produced NO and reactive nitrogen oxides as a neurotoxic agent in neurodegenerative disease states. RP BOJE, KM (reprint author), NIDDKD,NEUROSCI LAB,BLDG 8,RM 11,BETHESDA,MD 20892, USA. NR 54 TC 744 Z9 757 U1 0 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD AUG 7 PY 1992 VL 587 IS 2 BP 250 EP 256 DI 10.1016/0006-8993(92)91004-X PG 7 WC Neurosciences SC Neurosciences & Neurology GA JK435 UT WOS:A1992JK43500010 PM 1381982 ER PT J AU BERSTEIN, G BLANK, JL JHON, DY EXTON, JH RHEE, SG ROSS, EM AF BERSTEIN, G BLANK, JL JHON, DY EXTON, JH RHEE, SG ROSS, EM TI PHOSPHOLIPASE C-BETA-1 IS A GTPASE-ACTIVATING PROTEIN FOR GQ/11, ITS PHYSIOLOGICAL REGULATOR SO CELL LA English DT Article ID ROD OUTER SEGMENTS; ADENYLATE-CYCLASE; BOVINE BRAIN; COUPLED RECEPTORS; BINDING PROTEIN; ALPHA-SUBUNITS; K+ CHANNEL; RAS; MECHANISM; PURIFICATION AB Purified M1 muscarinic cholinergic receptor and G(q/11) were coreconstituted in lipid vesicles. Addition of purified phospholipase C-beta-1 (PLC-beta-1) further stimulated the receptor-promoted steady-state GTPase activity of G(q/11) up to 20-fold. Stimulation depended upon receptor-mediated GTP-GDP exchange. Addition of PLC-beta-1 caused a rapid burst of hydrolysis of G(q/11)-bound GTP that was at least 50-fold faster than in its absence. Thus, PLC-beta-1 stimulates hydrolysis of G(q/11)-bound GTP and acts as a GTPase-activating protein (GAP) for its physiologic regulator, G(q/11). GTPase-stimulating activity was specific both for PLC-beta-1 and G(g/11). Such GAP activity by an effector coupled to a trimeric G protein can reconcile slow GTP hydrolysis by pure G proteins in vitro with fast physiologic deactivation of G protein-mediated signaling. C1 VANDERBILT UNIV,MED CTR,SCH MED,HOWARD HUGHES MED INST,DEPT MOLEC PHYSIOL & BIOPHYS,NASHVILLE,TN 37232. NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. RP BERSTEIN, G (reprint author), UNIV TEXAS,SW MED CTR,DEPT PHARMACOL,DALLAS,TX 75235, USA. FU FIC NIH HHS [TW04475]; NIGMS NIH HHS [GM30355] NR 45 TC 335 Z9 338 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD AUG 7 PY 1992 VL 70 IS 3 BP 411 EP 418 DI 10.1016/0092-8674(92)90165-9 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JH124 UT WOS:A1992JH12400006 PM 1322796 ER PT J AU DEUTSCH, J HEGEDUS, L GREIG, NH RAPOPORT, SI SONCRANT, TT AF DEUTSCH, J HEGEDUS, L GREIG, NH RAPOPORT, SI SONCRANT, TT TI ELECTRON-IMPACT AND CHEMICAL IONIZATION DETECTION OF NICOTINE AND COTININE BY GAS-CHROMATOGRAPHY MASS-SPECTROMETRY IN RAT PLASMA AND BRAIN SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Article ID URINE AB Nicotine and its metabolite, cotinine, were measured in rat plasma and brain by gas chromatography mass spectrometry. Both agents were extracted from plasma and brain, separated on a capillary column, and quantified by single-ion monitoring. The major fragment ions of nicotine and cotinine at m/z 84 and m/z 98, respectively, were monitored by electron-impact ionization detection and the protonated molecular ions at m/z 163 and m/z 177, respectively, were monitored by chemical ionization detection. Both compounds were quantified using deuterium-labeled nicotine and cotinine, respectively, as internal standards. C1 NIA,NEUROSCI LAB,10-6C103,BETHESDA,MD 20892. NR 16 TC 25 Z9 27 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR-BIOMED JI J. Chromatogr.-Biomed. Appl. PD AUG 7 PY 1992 VL 579 IS 1 BP 93 EP 98 DI 10.1016/0378-4347(92)80366-X PG 6 WC Chemistry, Analytical SC Chemistry GA JK247 UT WOS:A1992JK24700010 PM 1447354 ER PT J AU DEMBY, KB WHITE, TC GHANAYEM, BI AF DEMBY, KB WHITE, TC GHANAYEM, BI TI DETERMINATION OF METHACRYLONITRILE IN SERUM USING GAS-CHROMATOGRAPHY AND FLAME IONIZATION DETECTION SO JOURNAL OF CHROMATOGRAPHY-BIOMEDICAL APPLICATIONS LA English DT Note ID ACRYLONITRILE AB A gas chromatographic method is described for the quantitation of methacrylonitrile in serum. Methacrylonitrile was extracted from rat serum with diethyl ether and then quantified using a gas chromatograph equipped with a flame ionization detector and a 60-m megabore column coated with polyethylene glycol polymer. The recoveries obtained following a one-step extraction with diethyl ether varied from 60% at 3.2-mu-g/ml to 70% at 80-mu-g/ml. The coefficient of variation for the analysis ranged from 2.5% at 400-mu-g/ml to 15.0% at 3.2-mu-g/ml. C1 N CAROLINA STATE UNIV,SCH VET MED,RALEIGH,NC 27606. RP DEMBY, KB (reprint author), NIEHS,POB 12233,MD C3-02,RES TRIANGLE PK,NC 27709, USA. NR 12 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-4347 J9 J CHROMATOGR-BIOMED JI J. Chromatogr.-Biomed. Appl. PD AUG 7 PY 1992 VL 579 IS 1 BP 153 EP 157 DI 10.1016/0378-4347(92)80373-X PG 5 WC Chemistry, Analytical SC Chemistry GA JK247 UT WOS:A1992JK24700017 PM 1447342 ER PT J AU FULLER, RW CARDELLINA, JH KATO, Y BRINEN, LS CLARDY, J SNADER, KM BOYD, MR AF FULLER, RW CARDELLINA, JH KATO, Y BRINEN, LS CLARDY, J SNADER, KM BOYD, MR TI A PENTAHALOGENATED MONOTERPENE FROM THE RED ALGA PORTIERIA-HORNEMANNII PRODUCES A NOVEL CYTOTOXICITY PROFILE AGAINST A DIVERSE PANEL OF HUMAN TUMOR-CELL LINES SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID TROPICAL MARINE-ALGAE; PLOCAMIUM-CARTILAGINEUM; NATURAL-PRODUCTS; SEA HARE AB A polyhalogenated acyclic monoterpene, 6(R)-bromo-3(S)-(bromomethyl)-7-methyl-2,3,7-trichloro-1-octene (1) was obtained as a major component of the organic extract of the red alga Portieria hornemannii. X-ray diffraction analysis provided the complete structure, including correct placement of the different halogen atoms and determination of the absolute stereochemistry. Detailed NMR analyses provided complete H-1 and C-13 assignments. Compound 1 exhibited highly differential cytotoxicity against the U.S. National Cancer Institute's new in vitro human tumor cell line screening panel; brain tumor, renal, and colon tumor cell lines were most sensitive to 1, while leukemia and melanoma lines were relatively less sensitive. A second collection of P. hornemanni yielded the novel, monocyclic 2, considerably less cytotoxic and devoid of differential activity. On the basis of its unprecedented cytotoxicity profile in the NCI primary screen, compound 1 has been selected by the NCI Decision Network Committee for preclinical drug development. C1 NCI,FREDERICK CANCER RES & DEV CTR,DEV THERAPEUT PROGRAM,NAT PROD BRANCH,FREDERICK,MD 21702. CORNELL UNIV,DEPT CHEM,BAKER LAB,ITHACA,NY 14853. RP FULLER, RW (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES & DEV LAB,BLDG 1052,FREDERICK,MD 21702, USA. FU NCI NIH HHS [CA 24487] NR 22 TC 90 Z9 93 U1 1 U2 12 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 AUG 7 PY 1992 VL 35 IS 16 BP 3007 EP 3011 DI 10.1021/jm00094a012 PG 5 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA JH469 UT WOS:A1992JH46900012 PM 1501227 ER PT J AU CENCIARELLI, C HOU, D HSU, KC RELLAHAN, BL WIEST, DL SMITH, HT FRIED, VA WEISSMAN, AM AF CENCIARELLI, C HOU, D HSU, KC RELLAHAN, BL WIEST, DL SMITH, HT FRIED, VA WEISSMAN, AM TI ACTIVATION-INDUCED UBIQUITINATION OF THE T-CELL ANTIGEN RECEPTOR SO SCIENCE LA English DT Article ID ZETA-CHAIN; COMPLEX; PHOSPHORYLATION; IDENTIFICATION; POLYPEPTIDE; DEGRADATION; COMPONENT; ANTIBODY; PROTEIN; SUBUNIT AB The zeta-subunit of the T cell antigen receptor (TCR) exists primarily as a disulfide-linked homodimer. This receptor subunit is important in TCR-mediated signal transduction and is a substrate for a TCR-activated protein tyrosine kinase. The zeta-chain was found to undergo ubiquitination in response to receptor engagement. This posttranslational modification occurred in normal T cells and tumor lines. Both nonphosphorylated and phosphorylated zeta-molecules were modified, and at least one other TCR subunit, CD3-delta, was also ubiquitinated after activation of the receptor. These findings suggest an expanded role for ubiquitination in transmembrane receptor function. C1 NCI,DIV CANC BIOL DIAG & CTR,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NEW YORK MED COLL,DEPT CELL BIOL & ANAT,VALHALLA,NY 10595. OI Wiest, David/0000-0002-0792-3188 NR 32 TC 189 Z9 190 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 AUG 7 PY 1992 VL 257 IS 5071 BP 795 EP 797 DI 10.1126/science.1323144 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JG851 UT WOS:A1992JG85100034 PM 1323144 ER PT J AU BENJAMIN, EJ PLEHN, JF DAGOSTINO, RB BELANGER, AJ COMAI, K FULLER, DL WOLF, PA LEVY, D AF BENJAMIN, EJ PLEHN, JF DAGOSTINO, RB BELANGER, AJ COMAI, K FULLER, DL WOLF, PA LEVY, D TI MITRAL ANNULAR CALCIFICATION AND THE RISK OF STROKE IN AN ELDERLY COHORT SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID MATCHED CONTROL SUBJECTS; ANULAR CALCIUM; CARDIAC ABNORMALITIES; ISCHEMIC ATTACKS; ECHOCARDIOGRAPHY; DISEASE; FIBROSUS; VALVE AB Background. Previous clinical studies have suggested that there is an association between mitral annular calcification and the risk of stroke, but it is unclear whether this association is independent of the traditional risk factors for stroke. We examined the relation between mitral annular calcification and the incidence of stroke in a population-based study. Methods. Subjects in the Framingham Study receiving a routine examination underwent M-mode echocardiography to determine the presence and severity (thickness in millimeters) of mitral annular calcification. The incidence of stroke during eight years of follow-up was analyzed with a proportional-hazards model adjusting for the calcification, age, sex, systolic blood pressure, diabetes mellitus, cigarette smoking, atrial fibrillation, and coronary heart disease or congestive heart failure. Results. Among 1159 subjects whose echocardiograms could be assessed for mitral annular calcification and who had no history or current evidence of stroke at the index examination (51 percent of all subjects), the prevalence of mitral annular calcification was 10.3 percent in the men and 15.8 percent in the women. Multivariate analysis demonstrated that the presence of mitral annular calcification was associated with a relative risk of stroke of 2.10 (95 percent confidence interval, 1.24 to 3.57; P = 0.006). There was a continuous relation between the incidence of stroke and the severity of mitral annular calcification; each millimeter of thickening as shown on the echocardiogram represented a relative risk of stroke of 1.24 (95 percent confidence interval, 1.1 2 to 1.37; P<0.001). Furthermore, even when subjects with coronary heart disease or congestive heart failure were excluded from the analysis, subjects with mitral annular calcification still had twice the risk of stroke. Conclusions. In an elderly, longitudinally followed population-based cohort, mitral annular calcification was associated with a doubled risk of stroke, independently of traditional risk factors for stroke. Whether such calcification contributes causally to the risk of stroke or is merely a marker of increased risk because of its association with other precursors of stroke remains unknown. C1 BOSTON CITY HOSP,DEPT CARDIOL,BOSTON,MA 02118. BOSTON UNIV,DEPT MATH,BOSTON,MA 02215. NHLBI,BETHESDA,MD 20892. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT PREVENT MED,BOSTON,MA 02118. BETH ISRAEL HOSP,DIV CARDIOL,BOSTON,MA 02215. BETH ISRAEL HOSP,DIV CLIN EPIDEMIOL,BOSTON,MA 02215. DARTMOUTH HITCHCOCK MED CTR,CARDIOL SECT,LEBANON,NH. RP BENJAMIN, EJ (reprint author), FRAMINGHAM HEART DIS EPIDEMIOL STUDY,5 THURBER ST,FRAMINGHAM,MA 01701, USA. FU NHLBI NIH HHS [N01-HC-38038]; NINDS NIH HHS [2-R01-NS-17950-09] NR 39 TC 219 Z9 223 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 6 PY 1992 VL 327 IS 6 BP 374 EP 379 DI 10.1056/NEJM199208063270602 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA JG356 UT WOS:A1992JG35600002 PM 1625711 ER PT J AU CHESON, BD AF CHESON, BD TI THE MATURATION OF DIFFERENTIATION THERAPY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID ACUTE PROMYELOCYTIC LEUKEMIA; TRANS-RETINOIC ACID; CELL DIFFERENTIATION RP CHESON, BD (reprint author), NCI,BETHESDA,MD 20852, USA. NR 15 TC 8 Z9 8 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 6 PY 1992 VL 327 IS 6 BP 422 EP 424 DI 10.1056/NEJM199208063270612 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA JG356 UT WOS:A1992JG35600012 PM 1625719 ER PT J AU DELANEY, TF PIERCE, LJ AF DELANEY, TF PIERCE, LJ TI CANCER IN THE CONTRALATERAL BREAST AFTER RADIOTHERAPY FOR BREAST-CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID RANDOMIZED TRIAL; IRRADIATION; MASTECTOMY RP DELANEY, TF (reprint author), NCI,BETHESDA,MD 20892, USA. NR 5 TC 1 Z9 1 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 6 PY 1992 VL 327 IS 6 BP 430 EP 430 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JG356 UT WOS:A1992JG35600014 PM 1625721 ER PT J AU BOICE, JD STOVALL, M BLETTNER, M AF BOICE, JD STOVALL, M BLETTNER, M TI CANCER IN THE CONTRALATERAL BREAST AFTER RADIOTHERAPY FOR BREAST-CANCER - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 UNIV TEXAS,CTR CANC,HOUSTON,TX 77030. GERMAN CANC RES CTR,W-6900 HEIDELBERG,GERMANY. RP BOICE, JD (reprint author), NCI,BETHESDA,MD 20892, USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 6 PY 1992 VL 327 IS 6 BP 431 EP 432 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JG356 UT WOS:A1992JG35600018 ER PT J AU TAKIMOTO, CH AF TAKIMOTO, CH TI CANCER IN THE CONTRALATERAL BREAST AFTER RADIOTHERAPY FOR BREAST-CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID TAMOXIFEN RP TAKIMOTO, CH (reprint author), NCI,BETHESDA,MD 20892, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD AUG 6 PY 1992 VL 327 IS 6 BP 431 EP 431 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA JG356 UT WOS:A1992JG35600016 PM 1625724 ER PT J AU SOLOMON, SD GERRITY, ET MUFF, AM AF SOLOMON, SD GERRITY, ET MUFF, AM TI EFFICACY OF TREATMENTS FOR POSTTRAUMATIC-STRESS-DISORDER - AN EMPIRICAL REVIEW SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Review ID COMBAT VETERANS; PTSD; TRIAL; PSYCHOTHERAPY; DEPRESSION; ALPRAZOLAM; PREVALENCE; PHENELZINE; IMIPRAMINE; SURVIVORS AB Objective.-The purpose of this article is to review the empirical evidence for the efficacy of a range of treatments for posttraumatic stress disorder (PTSD). Reviewed studies focused on rape victims, combat veterans, the tragically bereaved, torture victims, accident victims, victims of physical assault, and child abuse victims. Data Sources.-Peer-reviewed journals (Psych-Info, MEDLINE), book chapters (PILOTS database), active investigators, abstracts from the 1990 and 1991 International Society for Traumatic Stress Studies. Study Selection.-We identified 255 English-language reports of treatment for PTSD. We restricted our focus to randomized, clinical trials that included a systematic assessment of PTSD using DSM-III or DSM-III-R criteria (N=11). Data Extraction.-Studies were assessed according to methodological strength: random assignment to the treatment of interest, and either an alternative treatment or control group; sample selection; and inclusion of statistical tests of significance. Data Synthesis.-Drug studies show a modest but clinically meaningful effect on PTSD. Stronger effects were found for behavioral techniques involving direct therapeutic exposure, particularly in terms of reducing PTSD intrusive symptoms. However, severe complications have also been reported from the use of these techniques in patients suffering from other psychiatric disorders. Studies of cognitive therapy, psychodynamic therapy, and hypnosis suggest that these approaches may also hold promise. However, further research is needed before any of these approaches can be pronounced effective as lasting treatment of PTSD. Conclusions.-Further studies should specifically address combined treatment approaches, optimal treatment length and timing, effects of comorbidity, and unstudied traumatized populations. RP SOLOMON, SD (reprint author), NIMH,DIV APPL & SERV RES,VIOLENCE & TRAUMAT STRESS RES BRANCH,ROCKVILLE,MD 20857, USA. NR 59 TC 239 Z9 241 U1 9 U2 36 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 AUG 5 PY 1992 VL 268 IS 5 BP 633 EP 638 DI 10.1001/jama.268.5.633 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA JF473 UT WOS:A1992JF47300030 PM 1629993 ER PT J AU ULLRICH, SJ ANDERSON, CW MERCER, WE APPELLA, E AF ULLRICH, SJ ANDERSON, CW MERCER, WE APPELLA, E TI THE P53 TUMOR SUPPRESSOR PROTEIN, A MODULATOR OF CELL-PROLIFERATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID LARGE-T-ANTIGEN; WILD-TYPE P53; NUCLEAR-LOCALIZATION; MONOCLONAL-ANTIBODY; DNA-REPLICATION; CYCLE CONTROL; TRANSCRIPTIONAL ACTIVATION; SV40-TRANSFORMED CELLS; TRANSFORMED-CELLS; GROWTH-REGULATION C1 BROOKHAVEN NATL LAB,DEPT BIOL,UPTON,NY 11973. THOMAS JEFFERSON UNIV,JEFFERSON CANC INST,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19107. RP ULLRICH, SJ (reprint author), NCI,CELL BIOL LAB,BETHESDA,MD 20892, USA. FU NCI NIH HHS [CA 42866]; NCRR NIH HHS [S07 RR05417] NR 86 TC 223 Z9 225 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 5 PY 1992 VL 267 IS 22 BP 15259 EP 15262 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG113 UT WOS:A1992JG11300001 PM 1639769 ER PT J AU FRIDMAN, R FUERST, TR BIRD, RE HOYHTYA, M OELKUCT, M KRAUS, S KOMAREK, D LIOTTA, LA BERMAN, ML STETLERSTEVENSON, WG AF FRIDMAN, R FUERST, TR BIRD, RE HOYHTYA, M OELKUCT, M KRAUS, S KOMAREK, D LIOTTA, LA BERMAN, ML STETLERSTEVENSON, WG TI DOMAIN-STRUCTURE OF HUMAN 72-KDA GELATINASE TYPE-IV COLLAGENASE CHARACTERIZATION OF PROTEOLYTIC ACTIVITY AND IDENTIFICATION OF THE TISSUE INHIBITOR OF METALLOPROTEINASE-2 (TIMP-2) BINDING REGIONS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN FIBROBLAST COLLAGENASE; RHEUMATOID SYNOVIAL FIBROBLASTS; BRONCHIAL EPITHELIAL-CELLS; MATRIX METALLOPROTEINASES; INTERSTITIAL COLLAGENASE; EXPRESSION; PURIFICATION; ACTIVATION; STROMELYSIN; INVASION AB The 72-kDa gelatinase/type IV collagenase, a metalloproteinase thought to play a role in metastasis and in angiogenesis, forms a noncovalent stoichiometric complex with the tissue inhibitor of metalloproteinase-2 (TIMP-2), a potent inhibitor of enzyme activity. To define the regions of the 72-kDa gelatinase responsible for TIMP-2 binding, a series of NH2- and COOH-terminal deletions of the enzyme were constructed using the polymerase chain reaction technique. The full-length and the truncated enzymes were expressed in a recombinant vaccinia virus mammalian cell expression system (Vac/T7). Two truncated enzymes ending at residues 425 (DELTA-426-631) and 454 (DELTA-455-631) were purified. Like the full-length recombinant 72-kDa gelatinase, both COOH-terminally truncated enzymes were activated with organomercurial and digested gelatin and native collagen type IV. In contrast to the full-length enzyme, DELTA-426-631 and DELTA-455-631 enzymes were less sensitive to TIMP-2 inhibition requiring 10 mol of TIMP-2/mol of enzyme to achieve maximal inhibition of enzymatic activity. The activated but not the latent forms of the DELTA-426-631 and DELTA-455-631 proteins formed a complex with TIMP-2 only when excess molar concentrations of inhibitor were used. We also expressed the 205-amino acid COOH-terminal fragment, DELTA-1-426, and found that it binds TIMP-2. In addition, a truncated version of the 72-kDa gelatinase lacking the NH2-terminal 78 amino acids (DELTA-1-78) of the proenzyme retained the ability to bind TIMP-2. These studies demonstrate that 72-kDa gelatinases lacking the COOH-terminal domain retain full enzymatic activity but acquire a reduced sensitivity to TIMP-2 inhibition. These data suggest that both the active site and the COOH-terminal tail of the 72-kDa gelatinase independently and cooperatively participate in TIMP-2 binding. C1 MEDIMMUNE,GAITHERSBURG,MD 20878. NCI,PATHOL LAB,BETHESDA,MD 20892. RP FRIDMAN, R (reprint author), MOLEC ONCOL INC,19 FIRSTFIELD RD,GAITHERSBURG,MD 20878, USA. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 FU NCI NIH HHS [1R43CA56257-01] NR 40 TC 199 Z9 205 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 AUG 5 PY 1992 VL 267 IS 22 BP 15398 EP 15405 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG113 UT WOS:A1992JG11300024 PM 1322396 ER PT J AU ARORA, N KLIMPEL, KR SINGH, Y LEPPLA, SH AF ARORA, N KLIMPEL, KR SINGH, Y LEPPLA, SH TI FUSIONS OF ANTHRAX TOXIN LETHAL FACTOR TO THE ADP-RIBOSYLATION DOMAIN OF PSEUDOMONAS EXOTOXIN-A ARE POTENT CYTOTOXINS WHICH ARE TRANSLOCATED TO THE CYTOSOL OF MAMMALIAN-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ADENYLATE-CYCLASE TOXIN; BACILLUS-ANTHRACIS; PROTECTIVE ANTIGEN; DIPHTHERIA-TOXIN; ESCHERICHIA-COLI; BORDETELLA-PERTUSSIS; EUKARYOTIC CELLS; RECEPTOR-BINDING; TERMINAL END; LOW-PH AB The lethal factor (LF) and edema factor (EF) components of anthrax toxin are toxic to animal cells only if internalized by interaction with the protective antigen (PA) component. PA binds to a cell surface receptor and is proteolytically cleaved to expose a binding site for LF and EF. To study how LF and EF are internalized and trafficked within cells, LF was fused to the translocation and ADP-ribosylation domains (domains II and III, respectively) of Pseudomonas exotoxin A. LF fusion proteins containing Pseudomonas exotoxin A domains II and III were less toxic than those containing only domain III. Fusion proteins with a functional endoplasmic reticulum retention sequence, REDLK, at the carboxyl terminus of domain III were less toxic than those with a nonfunctional sequence, LDER. The most potent fusion protein, FP33, had an EC50 = 2 pM on Chinese hamster ovary cells, exceeding that of native Pseudomonas exotoxin A (EC50 = 420 pm). Toxicity of all the fusion proteins required the presence of PA and was blocked by monensin. These data suggest that LF and LF fusion proteins are efficiently translocated from acidified endosomes directly to the cytosol without trafficking through other organelles, as is required for Pseudomonas exotoxin A. This system provides a potential vehicle for importing diverse proteins into the cytosol of mammalian cells. C1 NIDR, MICROBIOL ECOL LAB, BLDG 30, RM 309, BETHESDA, MD 20892 USA. NR 52 TC 92 Z9 93 U1 0 U2 4 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 AUG 5 PY 1992 VL 267 IS 22 BP 15542 EP 15548 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG113 UT WOS:A1992JG11300046 PM 1639793 ER PT J AU FARSETTI, A DESVERGNE, B HALLENBECK, P ROBBINS, J NIKODEM, VM AF FARSETTI, A DESVERGNE, B HALLENBECK, P ROBBINS, J NIKODEM, VM TI CHARACTERIZATION OF MYELIN BASIC-PROTEIN THYROID-HORMONE RESPONSE ELEMENT AND ITS FUNCTION IN THE CONTEXT OF NATIVE AND HETEROLOGOUS PROMOTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MALIC ENZYME GENE; RETINOIC-ACID; NUCLEAR RECEPTORS; BINDING; TRANSCRIPTION; EXPRESSION; CELLS; BRAIN AB In this report we have characterized further the myelin basic protein (MBP) gene thyroid hormone response element (TRE) by functional and binding analysis. Mutation and deletion experiments revealed that this TRE, confined to the sequences -184 to -167 of the MBP promoter, is able to function as a classical regulatory element in the context of the native and a heterologous promoter. it is comprised of two regions, containing a motif that is highly conserved among other TREs: AGGACA, arranged as an inverted palindrome. Any mutation within the footprinted region impaired receptor binding and function. Moreover, the deletion of sequences outside of the receptor footprinted region (MBP-TRE-18) resulted in a higher triiodothyronine responsiveness and a concomitant increase in receptor-dependent, hormone-independent repression. Results of transfection assays showed that both receptors alpha and beta-elicit indistinguishable triiodothyronine responses when the MBP-TRE functions as a regulator of a heterologous promoter activity. However, a preferential beta-receptor transactivation was observed when the MBP-TRE was placed in the context of its native promoter. C1 NIDDKD,GENET & BIOCHEM BRANCH,BLDG 10,RM 8N317,BETHESDA,MD 20892. RI Desvergne, Beatrice/C-8892-2016 OI Desvergne, Beatrice/0000-0001-5483-288X NR 32 TC 135 Z9 135 U1 2 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD AUG 5 PY 1992 VL 267 IS 22 BP 15784 EP 15788 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG113 UT WOS:A1992JG11300080 PM 1379237 ER PT J AU LACEY, SF REARDON, JE FURFINE, ES KUNKEL, TA BEBENEK, K ECKERT, KA KEMP, SD LARDER, BA AF LACEY, SF REARDON, JE FURFINE, ES KUNKEL, TA BEBENEK, K ECKERT, KA KEMP, SD LARDER, BA TI BIOCHEMICAL-STUDIES ON THE REVERSE-TRANSCRIPTASE AND RNASE-H ACTIVITIES FROM HUMAN-IMMUNODEFICIENCY-VIRUS STRAINS RESISTANT TO 3'-AZIDO-3'-DEOXYTHYMIDINE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PLACEBO-CONTROLLED TRIAL; ZIDOVUDINE AZT; DNA-POLYMERASE; DOUBLE-BLIND; HIV; 5'-TRIPHOSPHATE; SENSITIVITY; SPECIFICITY; MUTATIONS; EFFICACY AB A series of biochemical investigations to compare the DNA polymerase and RNase H functions of the reverse transcriptases (RTs) corresponding to azidothymidine (AZT)-sensitive and -resistant human immunodeficiency virus (HIV) strains are described. Steady-state kinetic studies with purified recombinant enzymes utilizing several templates and three inhibitors, 3'azido-3'deoxythymidine triphosphate (AZTTP), 3-aminothymidine 5'-triphosphate, and 2',3'-didehydro-2',3'-dideoxythymidine 5'-triphosphate, found consistent 2-4-fold differences between the enzymes from the two strains over a wide pH range. A strong pH dependence for all three inhibitors was found at pH values below 7.4 and suggested an ionizable group on the enzyme with a pK of about 7. The sensitivities of the RNase H activities of the two enzymes to AZTTP and AZTMP were also compared and found to be similar. The nucleotide incorporation fidelities of recombinant RTs corresponding to AZT-sensitive and -resistant clinical isolates were compared and the error specificities determined. No significant differences were found. Both enzymes were equally able to incorporate AZTTP into an elongating M13 DNA strand with concomitant chain termination. Purified wild-type and mutant virions from cell-culture supernatants were compared in "endogenous" DNA synthesis reactions, and the sensitivities of this activity to AZTTP were found to be similar. The contrast between the small differences found in this study and the high level of viral resistance in tissue culture presumably reflects an incomplete understanding of AZT inhibition of HIV in the cell. C1 WELLCOME RES LABS,DEPT EXPTL THERAPY,RES TRIANGLE PK,NC 27709. NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709. RP LACEY, SF (reprint author), WELLCOME RES LABS,DEPT MOLEC SCI,BECKENHAM BR3 3BS,KENT,ENGLAND. NR 23 TC 126 Z9 128 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 AUG 5 PY 1992 VL 267 IS 22 BP 15789 EP 15794 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG113 UT WOS:A1992JG11300081 PM 1379238 ER PT J AU GORMAN, DM ITOH, N JENKINS, NA GILBERT, DJ COPELAND, NG MIYAJIMA, A AF GORMAN, DM ITOH, N JENKINS, NA GILBERT, DJ COPELAND, NG MIYAJIMA, A TI CHROMOSOMAL LOCALIZATION AND ORGANIZATION OF THE MURINE GENES ENCODING THE BETA-SUBUNITS (AIC2A AND AIC2B) OF THE INTERLEUKIN-3, GRANULOCYTE/MACROPHAGE COLONY-STIMULATING FACTOR, AND INTERLEUKIN-5 RECEPTORS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN ERYTHROPOIETIN RECEPTOR; GM-CSF RECEPTOR; BINDING PROTEIN; 2ND SUBUNIT; CELL-LINE; MACROPHAGE; CLONING; TRANSCRIPTION; RECONSTITUTION; IDENTIFICATION AB Chromosomal genes for two mouse homologous beta-subunits (AIC2A and AIC2B) of the interleukin-3, granulocyte/macrophage colony-stimulating factor, and interleukin-5 receptors were characterized. Both AIC2A and AIC2B genes were present on a 250-kilobase MluI restriction fragment and were mapped on murine chromosome 15 (these loci were provisionally designated as Il3rb-1 (AIC2A) and Il3rb-2 (AIC2B)), closely linked to the c-sis locus. Both genes consist of 14 exons and span about 28 kb each. The major transcription inititation sites of both genes were mapped at 194 bp from the initiation codon. These genes are 95% identical up to 700 bp from the transcription initiation sites. Potential recognition sequences for hemopoietic transcription factors including GATA-1 and PU.1 in addition to a TATA-like sequence are present in the 5'-flanking region. A stretch of 20 bp including the initiation site is homologous to the corresponding region of the erythropoietin receptor and the interleukin-7 receptor genes and to the initiator sequence of the adeno-associated virus P5 promoter, suggesting a possible role in transcription initiation. Comparison of the exon/intron boundaries of AIC2A and AIC2B genes with those of other members of the cytokine receptor superfamily reveals a conserved evolutionary structure. Isolation of various forms of AIC2 cDNAs reveals differential splicing of the transcripts. C1 DNAX RES INST MOLEC & CELLULAR BIOL INC,DEPT MOLEC BIOL,901 CALIF AVE,PALO ALTO,CA 94304. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ADV BIOSCI LAB,BASIC RES PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101] NR 46 TC 65 Z9 66 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 AUG 5 PY 1992 VL 267 IS 22 BP 15842 EP 15848 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG113 UT WOS:A1992JG11300089 PM 1386365 ER PT J AU WEICKERT, MJ ADHYA, S AF WEICKERT, MJ ADHYA, S TI A FAMILY OF BACTERIAL REGULATORS HOMOLOGOUS TO GAL AND LAC REPRESSORS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ALPHA-AMYLASE GENE; AMINO-ACID-SEQUENCE; ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; MOLECULAR-CLONING; LACTOSE REPRESSOR; CYTR REPRESSOR; TRANSCRIPTIONAL REGULATION; KLEBSIELLA-PNEUMONIAE; CATABOLITE REPRESSION AB We describe a family of proteins which regulate transcription of inducible genes in bacteria (GalR-LacI family). An alignment of the proteins in the GalR-LacI family is presented in which these proteins show a very high degree of similarity (60%) throughout the entire sequences. The homology is greatest among the amino-terminal DNA binding domains. Since a portion of the operator sequences occupied by these proteins is also conserved, a similar DNA structure may be required for specific recognition of DNA by members of the GalR-LacI family. Highly conserved motifs involved in effector binding and oligomerization are also identified. This compilation suggests a widespread conservation of these regulators among bacteria, and have strong implications for further study of peptide motifs in domain function, as well as pathways of protein evolution. C1 NCI,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 62 TC 308 Z9 309 U1 0 U2 8 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 AUG 5 PY 1992 VL 267 IS 22 BP 15869 EP 15874 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG113 UT WOS:A1992JG11300092 PM 1639817 ER PT J AU SHIRINSKY, VP BIRYUKOV, KG HETTASCH, JM SELLERS, JR AF SHIRINSKY, VP BIRYUKOV, KG HETTASCH, JM SELLERS, JR TI INHIBITION OF THE RELATIVE MOVEMENT OF ACTIN AND MYOSIN BY CALDESMON AND CALPONIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SMOOTH-MUSCLE MYOSIN; ATPASE ACTIVITY; LIGHT-CHAIN; CYTOPLASMIC MYOSINS; QUANTITATIVE ASSAY; INVITRO MOVEMENT; HEAVY-MEROMYOSIN; SKELETAL-MUSCLE; PHOSPHORYLATION; BINDING AB Contractile activity of myosin II in smooth muscle and non-muscle cells requires phosphorylation of myosin by myosin light chain kinase. in addition, these cells have the potential for regulation at the thin filament level by caldesmon and calponin, both of which bind calmodulin. We have investigated this regulation using in vitro motility assays. Caldesmon completely inhibited the movement of actin filaments by either phosphorylated smooth muscle myosin or rabbit skeletal muscle heavy meromyosin. The amount of caldesmon required for inhibition was decreased when tropomyosin is present. Similarly, calponin binding to actin resulted in inhibition of actin filament movement by both smooth muscle myosin and skeletal muscle heavy meromyosin. Tropomyosin had no effect on the amount of calponin needed for inhibition. High concentrations of calmodulin (10-mu-M) in the presence of calcium completely reversed the inhibition. The nature of the inhibition by the two proteins was markedly different. Increasing caldesmon concentrations resulted in graded inhibition of the movement of actin filaments until complete inhibition of movement was obtained. Calponin inhibited actin sliding in a more "all or none" fashion. As the calponin concentration was increased the number of actin filaments moving was markedly decreased, but the velocity of movement remained near control values. C1 NHLBI, MOLEC CARDIOL LAB, BLDG 10, RM 8N202, BETHESDA, MD 20892 USA. RUSSIAN ACAD MED SCI, NATL CARDIOL RES CTR, 121552 MOSCOW, USSR. NR 42 TC 164 Z9 168 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 AUG 5 PY 1992 VL 267 IS 22 BP 15886 EP 15892 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG113 UT WOS:A1992JG11300094 PM 1639818 ER PT J AU FORONI, L BOEHM, T WHITE, L FORSTER, A SHERRINGTON, P LIAO, XB BRANNAN, CI JENKINS, NA COPELAND, NG RABBITTS, TH AF FORONI, L BOEHM, T WHITE, L FORSTER, A SHERRINGTON, P LIAO, XB BRANNAN, CI JENKINS, NA COPELAND, NG RABBITTS, TH TI THE RHOMBOTIN GENE FAMILY ENCODE RELATED LIM-DOMAIN PROTEINS WHOSE DIFFERING EXPRESSION SUGGESTS MULTIPLE ROLES IN MOUSE DEVELOPMENT SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE RHOMBOTIN GENES; DEVELOPMENT; B-CELL; THYMUS; LEUKEMIA ID T-CELL ONCOGENE; ACUTE LYMPHOBLASTIC-LEUKEMIA; DNA-BINDING MOTIF; CHROMOSOMAL TRANSLOCATION; INSITU HYBRIDIZATION; LYMPHOID TUMORS; MESSENGER-RNAS; GAMMA-GENES; C-DELTA; SEQUENCES C1 PRINCE WALES CHILDRENS HOSP,DIV HAEMATOL ONCOL,RANDWICK,NSW 2031,AUSTRALIA. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP FORONI, L (reprint author), MRC,MOLEC BIOL LAB,HILLS RD,CAMBRIDGE CB2 2QH,ENGLAND. FU PHS HHS [N01-C0-74101] NR 55 TC 122 Z9 126 U1 1 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD AUG 5 PY 1992 VL 226 IS 3 BP 747 EP 761 DI 10.1016/0022-2836(92)90630-3 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JH989 UT WOS:A1992JH98900015 PM 1507224 ER PT J AU SMIGEL, K OLDEN, K AF SMIGEL, K OLDEN, K TI OLDEN,KEN HAS CLEAR VISION AS NIEHS DIRECTOR SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD AUG 5 PY 1992 VL 84 IS 15 BP 1140 EP 1142 DI 10.1093/jnci/84.15.1140 PG 3 WC Oncology SC Oncology GA JG357 UT WOS:A1992JG35700002 PM 1635077 ER PT J AU LI, FP GARBER, JE FRIEND, SH STRONG, LC PATENAUDE, AF JUENGST, ET REILLY, PR CORREA, P FRAUMENI, JF AF LI, FP GARBER, JE FRIEND, SH STRONG, LC PATENAUDE, AF JUENGST, ET REILLY, PR CORREA, P FRAUMENI, JF TI RECOMMENDATIONS ON PREDICTIVE TESTING FOR GERM LINE P53 MUTATIONS AMONG CANCER-PRONE INDIVIDUALS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID HUNTINGTON DISEASE; FRAUMENI SYNDROME; BREAST-CANCER; FAMILIES; GENETICS; POLICY; GENES C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,EXECUT PLAZA N,RM 543,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MD ANDERSON CANC CTR,HOUSTON,TX. NATL CTR HUMAN GENOME RES,BETHESDA,MD. SHRIVER CTR MENTAL RETARDAT,WALTHAM,MA. LOUISIANA STATE UNIV,MED CTR,NEW ORLEANS,LA 70112. OI Juengst, Eric/0000-0002-8374-5774 NR 29 TC 121 Z9 121 U1 1 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD AUG 5 PY 1992 VL 84 IS 15 BP 1156 EP 1160 DI 10.1093/jnci/84.15.1156 PG 5 WC Oncology SC Oncology GA JG357 UT WOS:A1992JG35700012 PM 1635084 ER PT J AU CASTRONOVO, V CAMPO, E VANDENBRULE, FA CLAYSMITH, AP CIOCE, V LIU, FT FERNANDEZ, PL SOBEL, ME AF CASTRONOVO, V CAMPO, E VANDENBRULE, FA CLAYSMITH, AP CIOCE, V LIU, FT FERNANDEZ, PL SOBEL, ME TI INVERSE MODULATION OF STEADY-STATE MESSENGER-RNA LEVELS OF 2 NONINTEGRIN LAMININ-BINDING PROTEINS IN HUMAN COLON-CARCINOMA SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID TUMOR-CELLS; EXTRACELLULAR-MATRIX; MOLECULAR-CLONING; RECEPTOR; EXPRESSION; LECTIN; METASTASIS; CANCER; GLYCOPROTEIN; PROGRESSION AB Background: Interactions between cells and the basement membrane glycoprotein laminin are altered during colon cancer progression. Colon carcinoma and normal mucosa cells express a variety of laminin-binding proteins, including the 67-kd laminin receptor (67 LR) and a 31-kd human laminin-binding protein (HLBP31) homologous to the 31-kd human IgE-binding protein/galactoside-binding lectin. Purpose: To investigate whether various laminin-binding proteins are differentially expressed in human colon carcinoma, we studied messenger RNA (mRNA) levels of the 67 LR and HLBP31 in matched tumor and adjacent normal mucosa samples from a series of 21 patients. Methods: Total cellular RNA from tumor and normal mucosa was isolated and analyzed by Northern and slot blot hybridization. In addition, HLBP31 protein levels were assessed by the immunoblot technique. Quantitative laminin affinity chromatography was also used to measure the synthesis of HLBP31 protein in five human cancer cell lines. Results: The steady-state mRNA level of HLBP31 was downregulated (i.e., decreased) in 18 of 21 human colon carcinomas compared with the level in their corresponding normal colonic mucosa. On average, the level of HLBP31 mRNA was decreased 50% +/- 30% (+/- SD) in the colon cancers. The mean ratio of colon cancer HLBP31 mRNA to adjacent normal mucosa HLBP31 mRNA was twofold lower in primary tumors of patients with metastases (0.3 +/- 0.2 SD) than in primary tumors of patients free of metastatic lesions (0.6 +/- 0.2 SD). The differences between the two groups of patients were statistically significant (P<.05, Wilcoxon-Mann-Whitney test). We have previously shown that the ratio of colon cancer 67 LR mRNA to corresponding normal mucosa 67 LR mRNA was increased in the same patient population. When the two ratios (ratio of cancer to normal HLBP31 mRNA and ratio of cancer to normal 67 LR mRNA) were compared, HLBP31 mRNA/67 LR mRNA was significantly lower (P<.05) in primary tumors with metastases (mean +/- SD, 0.3 +/- 0.2) than in primary cancers without metastases (mean +/- SD, 0.7 +/- 0.5). The steady-state level of HLBP31 mRNA was directly correlated with the amount of HLBP31 protein in both colon tissue samples and human cancer cell lines. Conclusion: HLBP31 mRNA expression in colon cancer tissues is modulated inversely to that of 67 LR mRNA expression. The downregulation of HLBP31 appears to be associated with the metastatic capabilities of colon cancer cells. Implications: Prospective studies on a large cohort should determine if the systematic detection of HLBP31 and 67 LR protein and/or mRNA can be a valuable adjunct in the prognostic evaluation of primary colon cancers. C1 SCRIPPS CLIN & RES FDN,LA JOLLA,CA 92037. RP CASTRONOVO, V (reprint author), NCI,DIV CANC BIOL DIAG & CTR,PATHOL LAB,BLDG 10,RM 2A33,BETHESDA,MD 20892, USA. NR 50 TC 102 Z9 102 U1 0 U2 1 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD AUG 5 PY 1992 VL 84 IS 15 BP 1161 EP 1169 DI 10.1093/jnci/84.15.1161 PG 9 WC Oncology SC Oncology GA JG357 UT WOS:A1992JG35700013 PM 1386115 ER PT J AU MURPHY, WJ LONGO, DL AF MURPHY, WJ LONGO, DL TI HEMATOPOIETIC GROWTH-PROMOTING EFFECTS OF NATURAL-KILLER-CELLS IN MICE IN RESPONSE TO INVIVO ADMINISTRATION OF HUMAN INTERLEUKIN-2 SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID BONE-MARROW TRANSPLANTATION; MACROPHAGE COLONY FORMATION; RECOMBINANT INTERLEUKIN-2; T-CELLS; REJECTION; IMMUNOTHERAPY; EXPRESSION; RECEPTOR; LEUKEMIA; BIOLOGY AB Background: Interleukin-2 (IL-2) is currently being evaluated as an anti-neoplastic agent because of its stimulatory effects on the immune system. However, little is known about the effects of systemic IL-2 administration on hematopoietic parameters. Purpose: Recombinant human IL-2 (rHuIL-2) was administered to mice to evaluate its in vivo hematopoietic effects. The mechanism underlying the effects of rHuIL-2 administration was also determined. Methods: Mice were given 5 x 10(4) IU of rHuIL-2 for 5 days, and their hematopoietic progenitor cell status was determined as measured by growth in soft agar. Antiserum to natural killer (NK) cell-specific markers was used to ascertain if NK cells were responsible for the hematopoietic effects of rHuIL-2. NK cells were purified and cultured in vitro with rHuIL-2 and then adoptively transferred into syngeneic mice to determine the effects on hematopoiesis. Results: Treatment of mice with rHuIL-2 resulted in a significant increase in bone marrow and splenic hematopoietic progenitor cell content. Mice with severe combined immune deficiency (SCID), which lack T cells and B cells vet have NK cells, also responded to the myelostimulatory effects of rHuIL-2. However, removal of NK cells from the SCID mice with antiserum to NK cell-specific markers abrogated the myelostimulatory properties of rHuIL-2. Adoptive transfer of NK cells that were propagated in vitro with rHuIL-2 into mice also resulted in an increase in splenic hematopoietic progenitor cells. Conclusions: rHuIL-2 exerts significant myelostimulatory effects after in vivo administration, and NK cells are responsible for at least some of these effects. Implications: These results suggest that NK cells and rHuIL-2 may be of use clinically to promote hematopoiesis after bone marrow transplantation or in the face of other myelotoxic therapy in the treatment of cancer. RP MURPHY, WJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,BLDG 567,FREDERICK,MD 21702, USA. NR 25 TC 7 Z9 7 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 AUG 5 PY 1992 VL 84 IS 15 BP 1195 EP 1200 DI 10.1093/jnci/84.15.1195 PG 6 WC Oncology SC Oncology GA JG357 UT WOS:A1992JG35700018 PM 1635088 ER PT J AU MEROPOL, NJ MILLER, LL KORN, EL BRAITMAN, LE MACDERMOTT, ML SCHUCHTER, LM AF MEROPOL, NJ MILLER, LL KORN, EL BRAITMAN, LE MACDERMOTT, ML SCHUCHTER, LM TI SEVERE MYELOSUPPRESSION RESULTING FROM CONCURRENT ADMINISTRATION OF GRANULOCYTE COLONY-STIMULATING FACTOR AND CYTOTOXIC CHEMOTHERAPY SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Note ID TRANSITIONAL-CELL-CARCINOMA; BONE-MARROW TRANSPLANTATION; INTENSIVE CHEMOTHERAPY; LUNG-CANCER; FLUOROURACIL; NEUTROPENIA; UROTHELIUM; RECOVERY C1 NCI,CANC THERAPY EVALUAT PROGRAM,BETHESDA,MD 20892. HOSP UNIV PENN,HEMATOL ONCOL SECT,PHILADELPHIA,PA 19104. FU NHLBI NIH HHS [HL-08268] NR 16 TC 83 Z9 83 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 AUG 5 PY 1992 VL 84 IS 15 BP 1201 EP 1202 DI 10.1093/jnci/84.15.1201 PG 2 WC Oncology SC Oncology GA JG357 UT WOS:A1992JG35700019 PM 1378905 ER PT J AU BUCHER, JR DUNNICK, JK AF BUCHER, JR DUNNICK, JK TI DIURETIC USE AND RISK-FACTORS FOR CANCER - RESULTS OF ANIMAL STUDIES SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter ID B6C3F1 MICE; F344 RATS; CARCINOGENICITY; TOXICOLOGY RP BUCHER, JR (reprint author), NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709, USA. NR 13 TC 3 Z9 3 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD AUG 5 PY 1992 VL 84 IS 15 BP 1209 EP 1210 DI 10.1093/jnci/84.15.1209 PG 2 WC Oncology SC Oncology GA JG357 UT WOS:A1992JG35700021 PM 1635090 ER PT J AU GILAD, GM GILAD, VH AF GILAD, GM GILAD, VH TI POLYAMINES IN NEUROTRAUMA - UBIQUITOUS MOLECULES IN SEARCH OF A FUNCTION SO BIOCHEMICAL PHARMACOLOGY LA English DT Note ID ORNITHINE DECARBOXYLASE ACTIVITY; METHYL-D-ASPARTATE; CENTRAL NERVOUS-SYSTEM; RAT-BRAIN; SYMPATHETIC NEURONS; AXONAL INJURY; ELECTRICAL-STIMULATION; NMDA RECEPTOR; GROWTH-FACTOR; MONKEY BRAIN C1 NIMH,NEUROSCI CTR ST ELIZABETHS,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. NR 87 TC 90 Z9 92 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD AUG 4 PY 1992 VL 44 IS 3 BP 401 EP 407 DI 10.1016/0006-2952(92)90428-L PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JJ523 UT WOS:A1992JJ52300001 PM 1510691 ER PT J AU GEGG, CV ROBERTS, DD SEGEL, IH ETZLER, ME AF GEGG, CV ROBERTS, DD SEGEL, IH ETZLER, ME TI CHARACTERIZATION OF THE ADENINE BINDING-SITES OF 2 DOLICHOS-BIFLORUS LECTINS SO BIOCHEMISTRY LA English DT Article ID BEANS PHASEOLUS-LUNATUS; SEED LECTIN; PLANT-LECTINS; LEAVES; STEMS; SPECIFICITY; SUBUNITS AB The seed lectin and a stem and leaf lectin (DB58) from Dolichos biflorus have high-affinity hydrophobic sites that bind to adenine. The present study employs a centrifugal filtration assay to characterize these sites. The seed lectin contains two identical sites with K(a)'s of 7.31 X 10(5) L/mol whereas DB58 has a single site with a K(a) of 1.07 x 10(6) L/mol. The relative affinities of these sites for a host of adenine analogs and derivatives were determined by competitive displacement assays. The most effective competitors for adenine were the cytokinins, a class of plant hormone, for which the lectins had apparent K(a)'s of 1.96 x 10(5)-4.90 X 10(4) L/mol. Direct binding of the cytokinin 6-(benzylamino)purine (BAP) to both lectins showed positive cooperativity for only the seed lectin, indicating the interaction of this ligand with more than one class of hydrophobic binding site. Fluorescence enhancement assays demonstrate cooperativity between hydrophobic sites of the seed lectin and also suggest that BAP binds to more than one class of site. C1 UNIV CALIF DAVIS,DEPT BIOCHEM & BIOPHYS,DAVIS,CA 95616. NCI,PATHOL LAB,BETHESDA,MD 20892. RI Roberts, David/A-9699-2008 OI Roberts, David/0000-0002-2481-2981 FU NIGMS NIH HHS [GM21882, GM29470] NR 29 TC 40 Z9 42 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD AUG 4 PY 1992 VL 31 IS 30 BP 6938 EP 6942 DI 10.1021/bi00145a011 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JG667 UT WOS:A1992JG66700011 PM 1637827 ER PT J AU CRUCIANI, RA BARKER, JL DURELL, SR RAGHUNATHAN, G GUY, HR ZASLOFF, M STANLEY, EF AF CRUCIANI, RA BARKER, JL DURELL, SR RAGHUNATHAN, G GUY, HR ZASLOFF, M STANLEY, EF TI MAGAININ-2, A NATURAL ANTIBIOTIC FROM FROG-SKIN, FORMS ION CHANNELS IN LIPID BILAYER-MEMBRANES SO EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION LA English DT Article DE ANTIBACTERIAL PEPTIDE; ARTIFICIAL BILAYER; ION CHANNEL RECONSTITUTION; PEPTIDE ION CHANNEL ID ANTIMICROBIAL ACTIVITY; PEPTIDE MAGAININ-2; ALAMETHICIN; ANALOGS; VESICLES; ENERGY AB We have examined the ion channel forming properties of magainin 2 by incorporating the peptide into artificial lipid bilayers held under voltage clamp. Magainin 2 increased lipid bilayer conductance in a concentration dependent manner with a Hill coefficient of 1.7. The magainin 2 conductance was selective for monovalent cations over anions with a ratio of 5:1 and had both voltage-sensitive and -insensitive components. Two structurally related but antibiotically less potent analogues, magainin 1 and Z-12, also increased lipid bilayer conductance with a similar ion selectivity but these peptides were less potent than magainin 2. We propose that the weak cation selectivity of the magainin channels can be accounted for by the inclusion of negatively charged lipids in the channel complex and suggest two possible structures for such a channel. The ionophoric properties of these peptides are likely to be proximal to their antibiotic activities. C1 NCID,MATH BIOL LAB,BETHESDA,MD. NICHHD,HUMAN GENET BRANCH,BETHESDA,MD. NINCDS,NEUROPHYSIOL LAB,BETHESDA,MD 20892. NINCDS,BIOPHYS LAB,BETHESDA,MD 20892. NR 32 TC 167 Z9 168 U1 0 U2 14 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0922-4106 J9 EUR J PHARM-MOLEC PH JI Eur. J. Pharmacol.-Molec. Pharmacol. Sect. PD AUG 3 PY 1992 VL 226 IS 4 BP 287 EP 296 DI 10.1016/0922-4106(92)90045-W PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JG592 UT WOS:A1992JG59200002 PM 1383011 ER PT J AU LITVAN, I BERRETTINI, WH ATACK, JR CHASE, TN AF LITVAN, I BERRETTINI, WH ATACK, JR CHASE, TN TI CSF GALANIN AND NEUROPEPTIDE-Y IMMUNOREACTIVITY IN PROGRESSIVE SUPRANUCLEAR PALSY SO ACTA NEUROLOGICA SCANDINAVICA LA English DT Article DE GALANIN; NEUROPEPTIDE-Y; CSF; PROGRESSIVE SUPRANUCLEAR PALSY ID CEREBROSPINAL-FLUID; ALZHEIMERS-DISEASE; VENTRAL HIPPOCAMPUS; PARKINSONS-DISEASE; DEMENTIA; ACETYLCHOLINE; NUCLEUS; RAT; PHYSOSTIGMINE; RECEPTORS AB Progressive supranuclear palsy (PSP) has been associated with degenerative changes in cholinergic and dopaminergic neurons in several brain regions. Since acetylcholine is colocalized with the neuropeptide galanin in certain neuronal populations, we measured the concentration of this neuropeptide and neuropeptide Y in cerebrospinal-fluid (CSF) of 11 patients with PSP and in 16 age-matched healthy controls. No significant alterations in the CSF levels of galanin or neuropeptide Y were found. C1 NINCDS,EXPTL THERAPEUT BRANCH,BLDG 10,RM 5C103,BETHESDA,MD 20892. NIMH,BETHESDA,MD 20892. NIA,BETHESDA,MD 20892. OI Litvan, Irene/0000-0002-3485-3445 NR 23 TC 4 Z9 4 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-6314 J9 ACTA NEUROL SCAND JI Acta Neurol. Scand. PD AUG PY 1992 VL 86 IS 2 BP 204 EP 206 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA JL205 UT WOS:A1992JL20500018 PM 1384261 ER PT J AU GONDA, MA AF GONDA, MA TI BOVINE IMMUNODEFICIENCY VIRUS SO AIDS LA English DT Review DE BOVINE IMMUNODEFICIENCY VIRUS; LENTIVIRUSES; AIDS; HIV; EVOLUTIONARY RELATIONSHIPS; MOLECULAR BIOLOGY; PATHOGENICITY; SEROEPIDEMIOLOGY; ANIMAL MODELS ID BIOLOGICALLY-ACTIVE PROVIRUSES; DEPENDENT DNA POLYMERASE; INFECTIOUS-ANEMIA VIRUS; LONG TERMINAL REPEAT; VISNA VIRUS; REVERSE-TRANSCRIPTASE; NUCLEOTIDE-SEQUENCE; GENOME ORGANIZATION; LYMPHOTROPIC VIRUS; HUMAN RETROVIRUSES 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. FU NCI NIH HHS [N01-CO-74102] NR 100 TC 48 Z9 48 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 AUG PY 1992 VL 6 IS 8 BP 759 EP 776 DI 10.1097/00002030-199208000-00001 PG 18 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JG079 UT WOS:A1992JG07900001 PM 1329846 ER PT J AU KOFF, WC GLASS, MJ AF KOFF, WC GLASS, MJ TI FUTURE-DIRECTIONS IN HIV VACCINE DEVELOPMENT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS RP KOFF, WC (reprint author), NIAID,DIV AIDS,BASIC RES & DEV PROGRAM,VACCINE RES & DEV BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD AUG PY 1992 VL 8 IS 8 BP 1313 EP 1315 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400002 PM 1466948 ER PT J AU ADA, G KOFF, W PETRICCIANI, J AF ADA, G KOFF, W PETRICCIANI, J TI THE NEXT STEPS IN HIV VACCINE DEVELOPMENT SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS C1 PHARMACEUT MANUFACTURERS ASSOC,WASHINGTON,DC. NIAID,DIV AIDS,WASHINGTON,DC. RP ADA, G (reprint author), AUSTRALIAN NATL UNIV,JOHN CURTIN SCH MED RES,CANBERRA,ACT 2601,AUSTRALIA. NR 17 TC 8 Z9 8 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 AUG PY 1992 VL 8 IS 8 BP 1317 EP 1319 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400003 PM 1466949 ER PT J AU ZUNICH, KM LANE, HC DAVEY, RT FALLOON, J POLIS, M KOVACS, JA MASUR, H AF ZUNICH, KM LANE, HC DAVEY, RT FALLOON, J POLIS, M KOVACS, JA MASUR, H TI PHASE-I/II STUDIES OF THE TOXICITY AND IMMUNOGENICITY OF RECOMBINANT GP160 AND P24 VACCINES IN HIV-INFECTED INDIVIDUALS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS RP ZUNICH, KM (reprint author), NIAID,IMMUNOREGULAT LAB,BLDG 10,RM 11B13,BETHESDA,MD 20892, USA. 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 AUG PY 1992 VL 8 IS 8 BP 1335 EP 1335 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400008 PM 1466952 ER PT J AU MANN, DL CARRINGTON, M ODONNELL, M MILLER, T GOEDERT, J AF MANN, DL CARRINGTON, M ODONNELL, M MILLER, T GOEDERT, J TI HLA PHENOTYPE IS A FACTOR IN DETERMINING RATE OF DISEASE PROGRESSION AND OUTCOME IN HIV-1-INFECTED INDIVIDUALS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS C1 NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP MANN, DL (reprint author), NCI,VIRAL CARCINOGENESIS LAB,IMMUNOGENET SECT,FREDERICK,MD 21702, USA. OI O'Donnell, Martin/0000-0002-7347-7761 FU NCI NIH HHS [N01-CO-74102] NR 0 TC 14 Z9 14 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 AUG PY 1992 VL 8 IS 8 BP 1345 EP 1346 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400011 PM 1361351 ER PT J AU PINCUS, SH MESSER, K AF PINCUS, SH MESSER, K TI HUMORAL IMMUNE-RESPONSES TO HOMOLOGOUS ENVELOPE PEPTIDES IN VACCINEES AND LAB WORKERS INFECTED WITH HIV SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS RP PINCUS, SH (reprint author), NIAID,ROCKY MT LABS,HAMILTON,MT 59840, USA. 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 AUG PY 1992 VL 8 IS 8 BP 1347 EP 1347 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400012 PM 1466954 ER PT J AU MOSIER, DE GULIZIA, RJ MACISAAC, P MATHIESON, BJ SMITH, G HU, SL COREY, L GREENBERG, P AF MOSIER, DE GULIZIA, RJ MACISAAC, P MATHIESON, BJ SMITH, G HU, SL COREY, L GREENBERG, P TI EVALUATION OF GP160 VACCINEES IN THE HU-PBL-SCID MOUSE MODEL SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS C1 MED BIOL INST,LA JOLLA,CA 92037. MICROGENE SYS,MERIDEN,CT 06450. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,SEATTLE,WA 98195. NIAID,DAIDS,BETHESDA,MD 20892. UNIV WASHINGTON,SCH MED,SEATTLE,WA 98195. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 NR 0 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD AUG PY 1992 VL 8 IS 8 BP 1387 EP 1387 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400025 PM 1466962 ER PT J AU BRADAC, J HO, D AF BRADAC, J HO, D TI SUMMARY OF THE ANTIGENIC VARIATION WORKING GROUP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 NYU,SCH MED,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10003. RP BRADAC, J (reprint author), NIAID,DIV AIDS,BRDP,VACCINE RES & DEV BRANCH,BETHESDA,MD 20892, USA. 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 AUG PY 1992 VL 8 IS 8 BP 1419 EP 1421 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400035 PM 1466971 ER PT J AU ALVING, CR GLASS, M DETRICK, B AF ALVING, CR GLASS, M DETRICK, B TI SUMMARY - ADJUVANTS CLINICAL-TRIALS WORKING GROUP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS C1 GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20037. NIAID,DIV AIDS,BETHESDA,MD 20892. RP ALVING, CR (reprint author), WALTER REED ARMY MED CTR,DEPT MEMBRANE BIOCHEM,WASHINGTON,DC 20307, USA. NR 0 TC 13 Z9 13 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 AUG PY 1992 VL 8 IS 8 BP 1427 EP 1430 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400037 PM 1466973 ER PT J AU MOFENSON, LM WRIGHT, PF FAST, PE AF MOFENSON, LM WRIGHT, PF FAST, PE TI SUMMARY OF THE WORKING GROUP ON PERINATAL INTERVENTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 NIAID,DIV AIDS,VACCINE RES & DEV BRANCH,BETHESDA,MD 20892. VANDERBILT UNIV,MED CTR,SCH MED,DEPT PEDIAT INFECT DIS,NASHVILLE,TN 37232. RP MOFENSON, LM (reprint author), NICHHD,PEDIAT ADOLESCENT & MATERNAL AIDS BRANCH,BETHESDA,MD 20892, USA. OI Mofenson, Lynne/0000-0002-2818-9808 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 AUG PY 1992 VL 8 IS 8 BP 1435 EP 1438 PG 4 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400040 PM 1466976 ER PT J AU SCHULTZ, AM AF SCHULTZ, AM TI SUMMARY OF THE SIV WORKING GROUP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material RP SCHULTZ, AM (reprint author), NIAID,DIV AIDS,BRDP,VACCINE RES & DEV BRANCH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD AUG PY 1992 VL 8 IS 8 BP 1439 EP 1440 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400041 PM 1466977 ER PT J AU ZOLLAPAZNER, S MATHIESON, BJ WALKER, MC WALKER, B AF ZOLLAPAZNER, S MATHIESON, BJ WALKER, MC WALKER, B TI SUMMARY - CLINICAL IMMUNOLOGY WORKING GROUP SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Editorial Material C1 VET AFFAIRS MED CTR,LAB SERV,NEW YORK,NY 10010. NIAID,DIV AIDS,BASIC RES & DEV PROGRAM,VACCINE RES & DEV BRANCH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ZOLLAPAZNER, S (reprint author), NYU MED CTR,DEPT PATHOL,NEW YORK,NY 10016, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD AUG PY 1992 VL 8 IS 8 BP 1441 EP 1443 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400042 PM 1361354 ER PT J AU SHAFFERMAN, A LEWIS, MG MCCUTCHAN, FE BENVENISTE, RE JAHRLING, PB HICKMAN, RL LAI, CY BURKE, DS EDDY, GA AF SHAFFERMAN, A LEWIS, MG MCCUTCHAN, FE BENVENISTE, RE JAHRLING, PB HICKMAN, RL LAI, CY BURKE, DS EDDY, GA TI VACCINATION OF MACAQUES WITH SIV CONSERVED ENVELOPE PEPTIDES SUPPRESSED INFECTION AND PREVENTED DISEASE PROGRESSION AND TRANSMISSION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS ID IMMUNODEFICIENCY VIRUS-INFECTION; RHESUS MACAQUES; CYNOMOLGUS MONKEYS; IMMUNE-RESPONSE; PROTECTION; SEQUENCES; ANTIBODY C1 HENRY M JACKSON FDN,RES LAB,ROCKVILLE,MD 20852. FREDERICK RES CTR,FREDERICK,MD 21701. NCI,VIRAL CARCINOGENESIS LAB,BETHESDA,MD 20892. USA,MED RES INST INFECT DIS,FREDERICK,MD 21701. WALTER REED ARMY MED CTR,DIV VIROL,WASHINGTON,DC 20307. RP SHAFFERMAN, A (reprint author), ISRAEL INST BIOL RES,DEPT BIOCHEM,IL-70450 NESS ZIONA,ISRAEL. OI /0000-0002-5704-8094 NR 17 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD AUG PY 1992 VL 8 IS 8 BP 1483 EP 1487 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400054 PM 1281660 ER PT J AU HU, SL TRAVIS, BM STALLARD, V ABRAMS, K MISHER, L MORAN, P ZARLING, JM LANGLOIS, AJ KULLER, L MORTON, WR BENVENISTE, RE AF HU, SL TRAVIS, BM STALLARD, V ABRAMS, K MISHER, L MORAN, P ZARLING, JM LANGLOIS, AJ KULLER, L MORTON, WR BENVENISTE, RE TI IMMUNE-RESPONSES TO SIV(MNE) ENVELOPE GLYCOPROTEINS PROTECT MACAQUES FROM HOMOLOGOUS SIV INFECTION SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS ID HUMAN-IMMUNODEFICIENCY-VIRUS; RECOMBINANT VACCINIA VIRUS; NEUTRALIZING ANTIBODIES; CONFERS PROTECTION; HIV-1; GP160; IMMUNIZATION; CHIMPANZEES; MONKEYS C1 UNIV WASHINGTON,SEATTLE,WA 98195. DUKE UNIV,MED CTR,DURHAM,NC 27710. NCI,FREDERICK,MD 21701. RP HU, SL (reprint author), BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,3005 1ST AVE,SEATTLE,WA 98121, USA. RI Hu, Shiu-Lok/A-3196-2008 OI Hu, Shiu-Lok/0000-0003-4336-7964 FU NCRR NIH HHS [RR00166]; NIAID NIH HHS [AI26503, R01AI28065] NR 26 TC 15 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 AUG PY 1992 VL 8 IS 8 BP 1489 EP 1494 PG 6 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400055 PM 1466988 ER PT J AU JOHNSON, PR MONTEFIORI, DC GOLDSTEIN, S HAMM, TE ZHOU, JY KITOV, S HAIGWOOD, NL MISHER, L LONDON, WT GERIN, JL ALLISON, A PURCELL, RH CHANOCK, RM HIRSCH, VM AF JOHNSON, PR MONTEFIORI, DC GOLDSTEIN, S HAMM, TE ZHOU, JY KITOV, S HAIGWOOD, NL MISHER, L LONDON, WT GERIN, JL ALLISON, A PURCELL, RH CHANOCK, RM HIRSCH, VM TI INACTIVATED WHOLE SIV VACCINE IN MACAQUES - EVALUATION OF PROTECTIVE EFFICACY AGAINST CHALLENGE WITH CELL-FREE VIRUS OR INFECTED-CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS ID SIMIAN IMMUNODEFICIENCY VIRUS; HIV-2 C1 GEORGETOWN UNIV,DEPT MICROBIOL,DIV MOLEC VIROL & IMMUNOL,ROCKVILLE,MD. CHIRON CORP,EMERYVILLE,CA. SYNTEX INC,PALO ALTO,CA. NIAID,INFECT DIS LAB,BETHESDA,MD 20892. VANDERBILT UNIV,DEPT PATHOL,NASHVILLE,TN 37240. RI Johnson, Philip/A-6892-2009 NR 11 TC 22 Z9 22 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 AUG PY 1992 VL 8 IS 8 BP 1501 EP 1505 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400058 PM 1466990 ER PT J AU PETRICCIANI, JC KOFF, WC ADA, GL AF PETRICCIANI, JC KOFF, WC ADA, GL TI EFFICACY TRIALS FOR HIV AIDS VACCINES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT INTERNATIONAL CONF ON ADVANCES IN AIDS VACCINE DEVELOPMENT / 4TH ANNUAL MEETING OF THE NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUP FOR AIDS CY OCT 15-19, 1991 CL MARCO ISLAND, FL SP NATL COOPERAT VACCINE DEV GRP AIDS C1 NIAID,DIV AIDS,VACCINE RES & DEV BRANCH,BETHESDA,MD 20892. AUSTRALIAN NATL UNIV,JOHN CURTIN SCH MED RES,DIV CELL BIOL,CANBERRA,ACT 2601,AUSTRALIA. RP PETRICCIANI, JC (reprint author), PHARMACEUT MANUFACTURERS ASSOC,1100 15TH ST NW,WASHINGTON,DC 20005, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD AUG PY 1992 VL 8 IS 8 BP 1527 EP 1529 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JR904 UT WOS:A1992JR90400065 PM 1466997 ER PT J AU KARP, RW AF KARP, RW TI D2 OR NOT D2 SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Editorial Material ID DOPAMINE-D2 RECEPTOR GENE; GROUP-SPECIFIC COMPONENT; ASSOCIATION; ALCOHOLISM; LINKAGE; LOCUS; DRD2 RP KARP, RW (reprint author), NATL INST ALCOHOL ABUSE & ALCOHOLISM,DIV BASIC RES,5600 FISHERS LANE,ROCKVILLE,MD 20857, USA. NR 16 TC 6 Z9 6 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 AUG PY 1992 VL 16 IS 4 BP 786 EP 787 DI 10.1111/j.1530-0277.1992.tb00679.x PG 2 WC Substance Abuse SC Substance Abuse GA JK612 UT WOS:A1992JK61200023 PM 1326905 ER PT J AU BERTONCINI, J DARAWSHE, S MINTON, A AF BERTONCINI, J DARAWSHE, S MINTON, A TI AUTOMATED MICROFRACTIONATION OF SMALL CENTRIFUGE TUBES - APPLICATIONS IN ANALYTICAL AND PREPARATIVE ULTRACENTRIFUGATION SO AMERICAN BIOTECHNOLOGY LABORATORY LA English DT Article ID SEDIMENTATION EQUILIBRIUM; ULTRA-CENTRIFUGE C1 NIDDKD,BIOCHEM PHARMACOL LAB,PHYS BIOCHEM SECT,BETHESDA,MD. RP BERTONCINI, J (reprint author), BIOMED RES & DEV LABS INC,GAITHERSBURG,MD, USA. NR 12 TC 0 Z9 0 U1 1 U2 1 PU INT SCIENTIFIC COMMUN INC PI SHELTON PA PO BOX 870, 30 CONTROLS DRIVE, SHELTON, CT 06484-0870 SN 0749-3223 J9 AM BIOTECHNOL LAB JI Am. Biotechnol. Lab. PD AUG PY 1992 VL 10 IS 8 BP 24 EP 25 PG 2 WC Biotechnology & Applied Microbiology; Medical Laboratory Technology SC Biotechnology & Applied Microbiology; Medical Laboratory Technology GA JJ812 UT WOS:A1992JJ81200003 PM 1368446 ER PT J AU BANGDIWALA, SI WEINER, DH BOURASSA, MG FRIESINGER, GC GHALI, JK YUSUF, S AF BANGDIWALA, SI WEINER, DH BOURASSA, MG FRIESINGER, GC GHALI, JK YUSUF, S TI STUDIES OF LEFT-VENTRICULAR DYSFUNCTION (SOLVD) REGISTRY - RATIONALE, DESIGN, METHODS AND DESCRIPTION OF BASE-LINE CHARACTERISTICS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID HEART-FAILURE AB The Studies of Left Ventricular Dysfunction (SOLVD) comprises 2 double-blind, randomized clinical trials to test improved survival by an angiotensin-converting enzyme inhibitor in patients with left ventricular dysfunction, with or without congestive heart failure. Patients entering the trials may be a highly selected subset of the population of such patients; those with the worst and best prognosis are likely to be excluded. To obtain the clinical history of a broader group, a registry of 6,273 patients included a relatively unselected cohort of patients with heart failure or left ventricular dysfunction, or both, from SOLVD hospitals. Registry data were obtained from hospital records. Because data collection from medical records may lead to incomplete data and more investigations in "sicker" patients, 898 randomly chosen subjects from different disease strata were seen in clinic where neurohumoral measures, echocardiograms, x-rays and electrocardiograms were obtained, and a 6-minute walking test was performed. The design and methodologic features, and the baseline characteristics of the participants in this 2-tiered registry are described, and its use in complementing the results and interpretation of the SOLVD trials is discussed. C1 MONTREAL CHILDRENS HOSP,RES CTR,MONTREAL H3H 1P3,QUEBEC,CANADA. LOUISIANA STATE UNIV,MED CTR,SHREVEPORT,LA 71105. NHLBI,CLIN TRIALS BRANCH,BETHESDA,MD 20892. RP BANGDIWALA, SI (reprint author), UNIV N CAROLINA,CTR COLLABORAT STUDIES COORDINATING,DEPT BIOSTAT,137 E FRANKLIN ST,CHAPEL HILL,NC 27514, USA. OI Bourassa, Martial G./0000-0002-4439-8650 NR 13 TC 38 Z9 41 U1 1 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD AUG 1 PY 1992 VL 70 IS 3 BP 347 EP 353 DI 10.1016/0002-9149(92)90617-8 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JE543 UT WOS:A1992JE54300015 PM 1632401 ER PT J AU TAMURA, T GOLDENBERG, RL FREEBERG, LE CLIVER, SP CUTTER, GR HOFFMAN, HJ AF TAMURA, T GOLDENBERG, RL FREEBERG, LE CLIVER, SP CUTTER, GR HOFFMAN, HJ TI MATERNAL SERUM FOLATE AND ZINC CONCENTRATIONS AND THEIR RELATIONSHIPS TO PREGNANCY OUTCOME SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE FOLATE; ZINC; BIRTH WEIGHT; APGAR SCORE; PREGNANCY OUTCOME ID FOLIC-ACID SUPPLEMENTATION; GROWTH-RETARDATION; IRON; ABSORPTION; NUTRITURE; HUMANS; WEIGHT AB To evaluate the relationship between folate and zinc, and its effect on pregnancy outcome, maternal serum folate and zinc concentrations were determined at 18 and 30 wk gestation in a defined population of 285 pregnant women as part of a large-scale study to identify risk factors for fetal growth retardation (FGR). These results were correlated with birth weight and Apgar scores of newborn infants and with maternal infections during the perinatal period. A weak linear relationship was observed between maternal serum folate and zinc concentrations at 30 wk gestation. Folic acid supplementation had favorable effects on birth weight and Apgar scores of newborns, and reduced prevalence of FGR and maternal infections. No significant correlation was found between serum zinc concentration and birth weight of infants. The concept that folic acid supplementation has an adverse effect on maternal zinc nutriture and pregnancy outcome was not supported. C1 UNIV ALABAMA,DEPT OBSTET & GYNECOL,BIRMINGHAM,AL 35294. NICHHD,DIV EPIDEMIOL STAT & PREVENT RES,BETHESDA,MD 20892. RP TAMURA, T (reprint author), UNIV ALABAMA,DEPT NUTR SCI,BIRMINGHAM,AL 35294, USA. FU NCI NIH HHS [5P01-CA-28103]; NICHD NIH HHS [N01-HD-4-2811] NR 32 TC 73 Z9 76 U1 1 U2 4 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 AUG PY 1992 VL 56 IS 2 BP 365 EP 370 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA JF490 UT WOS:A1992JF49000008 PM 1636615 ER PT J AU MAUTNER, SL SANCHEZ, JA RADER, DJ MAUTNER, GC FERRANS, VJ FREDRICKSON, DS BREWER, HB ROBERTS, WC AF MAUTNER, SL SANCHEZ, JA RADER, DJ MAUTNER, GC FERRANS, VJ FREDRICKSON, DS BREWER, HB ROBERTS, WC TI THE HEART IN TANGIER DISEASE - SEVERE CORONARY ATHEROSCLEROSIS WITH NEAR ABSENCE OF HIGH-DENSITY-LIPOPROTEIN CHOLESTEROL SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE TANGIER DISEASE; ATHEROSCLEROSIS; HIGH-DENSITY LIPOPROTEIN; LOW-DENSITY LIPOPROTEIN; CORONARY ARTERY DISEASE; CORONARY ARTERY BYPASS SURGERY ID APOLIPOPROTEIN-A-I; MORPHOMETRIC ANALYSIS; ARTERY DISEASE; C-III; DEFICIENCY; PLAQUES; METABOLISM; PATHOLOGY; FEATURES; AGE AB Cardiac necropsy findings are described in a 72-year-old man with Tangier disease whose plasma total cholesterol levels averaged 70 mg/dL, low-density lipoprotein cholesterol level was 45 mg/dL, and high-density lipoprotein cholesterol level was 1.4 mg/dL, and who had coronary artery bypass grafting for severe atherosclerotic coronary artery disease. At necropsy, 24 of the 72 (33%) 5-mm segments of the 4 major (right, left main, left anterior descending, and left circumflex) native coronary arteries and 4 of the 27 (15%) 5-mm segments of the saphenous vein aortocoronary bypass conduits were narrowed by more than 75% in cross-sectional area by atherosclerotic plaques. The plaques were composed primarily (91 % to 97%) of fibrous tissue. Oil red O staining, polarized light microscopy, and electron microscopy revealed cholesterol deposits in the plaques and in the walls of coronary arteries, saphenous vein grafts, and aorta. Such deposits also were found in foam cells of histiocytic origin, fibroblasts in all four cardiac valves and in Schwann cells of cardiac nerves. C1 NHLBI,MOLEC DIS BRANCH,BETHESDA,MD 20892. RP MAUTNER, SL (reprint author), NHLBI,PATHOL BRANCH,BLDG 10,ROOM 2N-258,BETHESDA,MD 20892, USA. NR 25 TC 13 Z9 13 U1 0 U2 1 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 AUG PY 1992 VL 98 IS 2 BP 191 EP 198 PG 8 WC Pathology SC Pathology GA JK803 UT WOS:A1992JK80300011 PM 1380771 ER PT J AU HAUPT, HM STERN, JB BERLIN, SJ AF HAUPT, HM STERN, JB BERLIN, SJ TI IMMUNOHISTOCHEMISTRY IN THE DIFFERENTIAL-DIAGNOSIS OF NODULAR HIDRADENOMA AND GLOMUS TUMOR SO AMERICAN JOURNAL OF DERMATOPATHOLOGY LA English DT Article DE HIDRADENOMA; GLOMUS TUMOR; IMMUNOHISTOCHEMISTRY; IMMUNOPEROXIDASE ID SWEAT GLAND TUMORS; CARCINOEMBRYONIC ANTIGEN; S100 PROTEIN; SKIN TUMORS; BENIGN; CELLS; EXPRESSION; MARKERS; TISSUES; ORIGIN AB The histologic distinction between nodular hidradenoma and glomus tumor is an occasional difficult diagnostic problem. Both tumors may show circumscribed aggregates of uniform epithelioid cells, a myxoid stroma, and variable numbers of blood vessels. Especially troublesome are solid cellular hidradenomas without duct-like structures and glomus tumors without a vascular pattern. To develop an immunohistochemical profile useful in this differential diagnosis, 25 selected skin tumors and four normal glomus bodies were studied with antibodies against low molecular-weight cytokeratin (CAM 5.2), epithelial membrane antigen (EMA), carcino-embryonic antigen (CEA), S-100, and vimentin (VIM). The tumors included eight unequivocal hidradenomas, seven unequivocal glomus tumors, and 10 histologically equivocal cases, originally diagnosed as glomus tumors. In all unequivocal glomus tumors and glomus bodies, only VIM was positive. Of the eight unequivocal hidradenomas, three were positive for CAM 5.2, EMA, CEA, S-100, and VIM; two for CAM 5.2 only; one for CAM 5.2, EMA, and S-100; one for CAM 5.2, EMA, and CEA; and one for CEA only. In the histologically equivocal cases, eight were positive for VIM only, characteristic of glomus tumor; and two were positive for CAM 5.2, EMA, CEA, S-100, and VIM, and were reclassified as hidradenomas. The study suggests that morphologic criteria may not always accurately differentiate between hidradenoma and glomus tumor and that in equivocal cases immunohistochemistry may be useful in the differential diagnosis. C1 NIH,BETHESDA,MD 20892. DERMATOPATHOL CONSULTAT SERV,DAMASCUS,SYRIA. PODIATR PATHOL LABS INC,BALTIMORE,MD. RP HAUPT, HM (reprint author), PENN HOSP,DEPT PATHOL,8TH & SPRUCE ST,PHILADELPHIA,PA 19107, USA. NR 34 TC 19 Z9 20 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0193-1091 J9 AM J DERMATOPATH JI Am. J. Dermatopathol. PD AUG PY 1992 VL 14 IS 4 BP 310 EP 314 DI 10.1097/00000372-199208000-00004 PG 5 WC Dermatology SC Dermatology GA JF688 UT WOS:A1992JF68800004 PM 1380207 ER PT J AU BUTLER, KM HUSSON, RN LEWIS, LL MUELLER, BU VENZON, D PIZZO, PA AF BUTLER, KM HUSSON, RN LEWIS, LL MUELLER, BU VENZON, D PIZZO, PA TI CD4 STATUS AND P24 ANTIGENEMIA - ARE THEY USEFUL PREDICTORS OF SURVIVAL IN HIV-INFECTED CHILDREN RECEIVING ANTIRETROVIRAL THERAPY SO AMERICAN JOURNAL OF DISEASES OF CHILDREN LA English DT Article ID PNEUMOCYSTIS-CARINII PNEUMONIA AB Objective.-To determine the relationship between CD4 status and the P24 antigen level and survival in children infected with the human immunodeficiency virus. Design.-Cohort, case-control. Setting.-Clinical Center at the National Institutes of Health, Bethesda, Md. Participants.-One hundred forty-seven children infected with the human immunodeficiency virus enrolled in antiretroviral therapy protocols at the National Cancer Institute were reviewed and the relationships between CD4 counts, P24 antigenemia, and death were analyzed. Interventions.-None. Measurements/Main Results.-The presence of a very low CD count, less than 21% of the lower limit of normal values for age (equivalent to 0.05X10(9)/L in an adult), was associated with a significantly increased risk of death within 2 years. Although the risk of death was highest for children with CD4 counts below this level and who had detectable P24 antigen levels, P24 antigenemia by itself contributed little to the prognostic value of the CD4 count alone. However, it was also notable that a group of children with low CD4 counts also experienced prolonged survival. Conclusions.-The association between low CD4 counts and death suggests that the age-adjusted CD4 count should be used as a marker to guide therapeutic intervention. At the same time, the presence of a very low CD4 count alone should not be considered a reason for therapeutic nihilism. C1 NCI,PEDIAT BRANCH,CLIN ONCOL SERV,BLDG 10,ROOM 13N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,BETHESDA,MD 20892. RI Venzon, David/B-3078-2008 NR 5 TC 24 Z9 24 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0002-922X J9 AM J DIS CHILD JI Am. J. Dis. Child. PD AUG PY 1992 VL 146 IS 8 BP 932 EP 936 PG 5 WC Pediatrics SC Pediatrics GA JG682 UT WOS:A1992JG68200025 PM 1353299 ER PT J AU KAPLAN, N WEIR, BS AF KAPLAN, N WEIR, BS TI EXPECTED BEHAVIOR OF CONDITIONAL LINKAGE DISEQUILIBRIUM SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID NON-RANDOM ASSOCIATION; GLOBIN GENE-CLUSTER; HUNTINGTONS-DISEASE; FINITE POPULATIONS; COALESCENT PROCESS; SELECTION; RECOMBINATION; MODELS AB The ubiquitousness of RFLPs in the human genome has greatly helped the mapping of human disease genes, and it has been suggested that population measures of association between disease and marker loci could help with this mapping. For rare diseases, random samples are taken from within disease genotypes in order to obtain reasonable sample sizes, but this sampling strategy requires a modification of the usual measures of association. We present theoretical predictions for the mean and variance of such a modified measure, under the assumption that the disease gene is maintained at a constant low frequency in the population. The coefficient of variation of this modified measure is large enough that caution is needed in using the measure to locate disease genes, and, furthermore, the coefficient of variation cannot be made arbitrarily small by increasing sample size. The modified association measure is calculated for recently published data on cystic fibrosis. C1 N CAROLINA STATE UNIV, DEPT STAT, PROGRAM STAT GENET, RALEIGH, NC 27695 USA. RP KAPLAN, N (reprint author), NIEHS, DIV BIOMETRY & RISK ASSESSMENT, POB 12233, RES TRIANGLE PK, NC 27709 USA. FU NIGMS NIH HHS [GM45344] NR 29 TC 28 Z9 31 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD AUG PY 1992 VL 51 IS 2 BP 333 EP 343 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA JF776 UT WOS:A1992JF77600013 PM 1353663 ER PT J AU LIN, HJ HAN, CY NIENHUIS, AW AF LIN, HJ HAN, CY NIENHUIS, AW TI FUNCTIONAL PROFILE OF THE HUMAN FETAL GAMMA-GLOBIN GENE UPSTREAM PROMOTER REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID GREEK HEREDITARY PERSISTENCE; TRANSGENIC MICE; MAMMALIAN-CELLS; BINDING-FACTOR; BRITISH FORM; CAP SITE; HEMOGLOBIN; EXPRESSION; MUTATION; HPFH AB We performed a systematic functional analysis of the human gamma-globin promoter to identify its activator domains. We used a panel of truncation and scanning mutants as well as transfection in human K562 fetal erythroid cells. The various mutations produced relatively small changes in promoter function in both transient and stable transfection assays. The CACCC region and the region containing the binding sites for protein GATA-1 behaved as activator domains. We also obtained evidence for a minor activator site in the -200 to -190 region. The results are consistent with the interpretation that gamma-globin gene regulation may occur in part through multiple small effects of promoter elements. C1 NHLBI,CLIN HEMATOL BRANCH,BETHESDA,MD 20892. RP LIN, HJ (reprint author), UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,DEPT PEDIAT,DIV MED GENET,BLDG E-4,TORRANCE,CA 90502, USA. NR 43 TC 8 Z9 8 U1 2 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD AUG PY 1992 VL 51 IS 2 BP 363 EP 370 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA JF776 UT WOS:A1992JF77600016 PM 1642236 ER PT J AU DRUCKER, L PROIA, RL NAVON, R AF DRUCKER, L PROIA, RL NAVON, R TI IDENTIFICATION AND RAPID DETECTION OF 3 TAY-SACHS MUTATIONS IN THE MOROCCAN JEWISH POPULATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID BETA-HEXOSAMINIDASE; ASHKENAZI JEWS; ALPHA-SUBUNIT; DISEASE; GENE; INSERTION; CARRIERS; DEFECT; CHAIN; DNA AB Infantile Tay-Sachs disease (TSD) is caused by mutations in the HEXA gene that result in the complete absence of beta-hexosaminidase A activity. It is well known that an elevated frequency of TSD mutations exists among Ashkenazi Jews. More recently it has become apparent that elevated carrier frequencies for TSD also occur in several other ethnic groups, including Moroccan Jews, a subgroup of Sephardic Jews. Elsewhere we reported an in-frame deletion of one of the two adjacent phenylalanine codons at position 304 or 305 (DELTA-F304/305) in one HEXA allele of a Moroccan Jewish TSD patient and in three obligate carriers from six unrelated Moroccan Jewish families. We have now identified two additional mutations within exon 5 of the HEXA gene that account for the remaining TSD alleles in the patient and carriers. One of the mutations is a novel C-to-G transversion, resulting in a replacement of Tyr180 by a stop codon. The other mutation is a G-to-A transition resulting in an Arg170-to-Gln substitution. This mutation is at a CpG site in a Japanese infant with Tay-Sachs disease and was described elsewhere. Analysis of nine obligate carriers from seven unrelated families showed that four harbor the DELTA-F304/305 mutation, two the Arg170-->Gln mutation, and one the Tyr180-->Stop mutation. We also have developed rapid, nonradioactive assays for the detection of each mutation, which should be helpful for carrier screening. C1 SAPIR MED CTR,MOLEC GENET UNIT,IL-44281 KEFAR SAVA,ISRAEL. TEL AVIV UNIV,SACKLER SCH MED,DEPT HUMAN GENET,TEL AVIV,ISRAEL. NIDDKD,GENET & BIOCHEM BRANCH,BETHESDA,MD. RI Proia, Richard/A-7908-2012 NR 33 TC 19 Z9 20 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 AUG PY 1992 VL 51 IS 2 BP 371 EP 377 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA JF776 UT WOS:A1992JF77600017 PM 1322637 ER PT J AU AMANDUS, HE CASTELLAN, RM SHY, C HEINEMAN, EF BLAIR, A AF AMANDUS, HE CASTELLAN, RM SHY, C HEINEMAN, EF BLAIR, A TI REEVALUATION OF SILICOSIS AND LUNG-CANCER IN NORTH-CAROLINA DUSTY TRADES WORKERS SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE CANCER; PMF; PNEUMOCONIOSIS; DUSTY TRADES; SILICA EXPOSURES ID SMOKING AB We previously reported on the lung cancer mortality through 1983 of 760 males who were diagnosed with silicosis during 1930-1983 by the State of North Carolina's medical examination program for dusty trades workers. The lung cancer SMR (95% confidence interval) was 2.6 (1.8-3.6) among 655 white members of this group. In this paper, we report the results of a reanalysis of mortality among a subgroup for whom chest radiographs were currently available for rereading. Technically acceptable radiographs were available for 306 white males and were independently reclassified for pneumoconiosis by 3 "B" readers using the 1980 ILO Classification. Lung cancer SMRs were 1.7 (0.8-3.1) for the entire group of 306 white males, 2.5 (1.1-4.9) for 143 subjects reclassified as simple silicosis, and 1.0 (0.1-3.5) for 96 subjects whose radiographs were reclassified as ILO category 0. There were no lung cancer deaths among 67 subjects whose radiographs were reclassified as progressive massive fibrosis. Corresponding lung cancer SMRs for subjects who had never been employed in a job with exposure to known occupational carcinogens were 1.2 (0.2-4.4) for those reclassified as category 0, and 2.4 (1.0-5.0) for those reclassified as having simple silicosis. The age-adjusted lung cancer rate ratio among subjects with simple silicosis compared to those with category 0 was 1.5 (0.4-5.8). Our findings from this reanalysis, which effectively controls for misclassification of silicosis due to errors in radiograph interpretation by North Carolina program readers, offer additional evidence consistent with the hypothesis of an association between silicosis and lung cancer in this study group. C1 NIOSH,DIV RESP DIS STUDIES,944 CHESTNUT RIDGE RD,MORGANTOWN,WV 26505. UNIV N CAROLINA,SCH PUBL HLTH,DEPT EPIDEMIOL,CHAPEL HILL,NC 27514. NCI,OCCUPAT STUDIES SECT,ROCKVILLE,MD. NR 11 TC 30 Z9 30 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD AUG PY 1992 VL 22 IS 2 BP 147 EP 153 DI 10.1002/ajim.4700220202 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JD718 UT WOS:A1992JD71800001 PM 1415283 ER PT J AU STRIKER, GE AF STRIKER, GE TI KUH ESTABLISHES ELECTRONIC BULLETIN BOARD SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Note RP STRIKER, GE (reprint author), NIDDKD,DIV KIDNEY UROL & HEMATOL DIS,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD AUG PY 1992 VL 20 IS 2 BP 195 EP 195 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA JH862 UT WOS:A1992JH86200015 ER PT J AU SMITH, RJH PELIAS, MZ DAIGER, SP KEATS, B KIMBERLING, W HEJTMANCIK, JF AF SMITH, RJH PELIAS, MZ DAIGER, SP KEATS, B KIMBERLING, W HEJTMANCIK, JF TI CLINICAL VARIABILITY AND GENETIC-HETEROGENEITY WITHIN THE ACADIAN USHER POPULATION SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE USHER SYNDROME TYPE-1(USH1); USHER SYNDROME TYPE-2 (USH2); USHER PHENOTYPE; USHER GENOTYPE ID SYNDROME TYPE-II; LINKAGE; CHROMOSOME-1Q AB A number of Usher syndrome (USH) families are found among the French-Acadians living in southwestern Louisiana. These families are descended from a few common ancestors, suggesting that USH may be homogeneous within this ethnic group. However, we report distinct phenotypic variability. Based on differences in psychomotor development and tests of auditory and vestibular function, Acadian individuals with both USH Type 1 and Type 2 can be identified. One additional family, with unusual findings, represents a third clinical phenotype. Linkage data strongly support these clinical observations. C1 UNIV IOWA HOSP & CLIN,IOWA CITY,IA 52242. LOUISIANA STATE UNIV,MED CTR,NEW ORLEANS,LA 70112. UNIV TEXAS,CTR SCI,HOUSTON,TX 77025. BOYS TOWN NATL RES HOSP,OMAHA,NE. NIH,BETHESDA,MD 20892. FU NCRR NIH HHS [RR-05425]; NEI NIH HHS [R01 EY007142, EYO7142] NR 15 TC 20 Z9 20 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 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 1 PY 1992 VL 43 IS 6 BP 964 EP 969 DI 10.1002/ajmg.1320430612 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA JH159 UT WOS:A1992JH15900011 PM 1415347 ER PT J AU KALER, SG GARRITY, AM STERN, HJ ROSENBAUM, KN ORRISON, BM MARINI, JC BERNARDINI, I SAAL, HM AF KALER, SG GARRITY, AM STERN, HJ ROSENBAUM, KN ORRISON, BM MARINI, JC BERNARDINI, I SAAL, HM TI NEW AUTOSOMAL RECESSIVE SYNDROME OF SPARSE HAIR, OSTEOPENIA, AND MENTAL-RETARDATION IN MENNONITE SISTERS SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE GENETIC ISOLATES; OSTEOGENESIS IMPERFECTA; DEFECTIVE COLLAGEN BIOSYNTHESIS ID LETHAL OSTEOGENESIS IMPERFECTA; I COLLAGEN AB We report on 2 Mennonite sisters with a syndrome of sparse hair, osteopenia, mental retardation, minor facial abnormalities, joint laxity, and hypotonia. Their asymptomatic consanguineous parents (inbreeding coefficient F = 1/64) have 6 other offspring, 3 of whom died in infancy of type II osteogenesis imperfecta (OI), and 3 of whom are normal. We analyzed collagens synthesized by cultured fibroblasts from these 2 sisters and their parents and detected no major abnormalities. Results of chromosomal and metabolic evaluations including amino acid analysis of plasma, urine, and hair were unremarkable. A literature search and survey of a computerized syndrome identification database did not disclose an identical phenotype. The sisters bear superficial resemblance to several known syndromes which we excluded on clinical and/or biochemical grounds. We conclude that they represent a new autosomal recessive syndrome, distinct from type II OI and perhaps unique to the Mennonite population or to this particular family. C1 GEORGE WASHINGTON UNIV,SCH MED,CHILDRENS NATL MED CTR,DEPT MED GENET,WASHINGTON,DC 20052. GEORGE WASHINGTON UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20052. RP KALER, SG (reprint author), NICHHD,HUMAN GENET BRANCH,BLDG 10,ROOM 95-242,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 16 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 1 PY 1992 VL 43 IS 6 BP 983 EP 988 DI 10.1002/ajmg.1320430615 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA JH159 UT WOS:A1992JH15900014 PM 1415349 ER PT J AU ZURLO, JJ FEUERSTEIN, IM LEBOVICS, R LANE, HC AF ZURLO, JJ FEUERSTEIN, IM LEBOVICS, R LANE, HC TI SINUSITIS IN HIV-1 INFECTION SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; IMMUNE-DEFICIENCY SYNDROME; SYNDROME AIDS; ABNORMALITIES AB PURPOSE: To determine the clinical and radio-graphic characteristics of sinusitis in patients with human immunodeficiency virus type 1 (HIV-1) infection. PATIENTS AND METHODS: A retrospective study was performed that identified all HIV-1-infected patients with sinus radiographs, sinus computed tomograms, or magnetic resonance imaging of the head between 1982 and 1989 (n = 145). Medical record review detailed the clinical course and laboratory parameters in all patients. RESULTS: Eighty-nine patients had radiographic evidence of sinusitis; 75 patients had adequate clinical data and comprise the study group. Acute sinusitis was seen in 10 patients (13%), while all 75 patients had mucosal thickening indicative of chronic sinusitis. Fifty patients (67%) were symptomatic with fever, nasal congestion or discharge, and headache being the most common symptoms; nineteen patients (25%) were asymptomatic when their radiographs showed active disease. The mean CD4 count for the group was 276 cells/mm3; 32 (43%) had CD4 counts less than or equal to 100 cells/mm3. Twenty-three patients (31%) received antibiotics orally, parenterally, or both. CONCLUSIONS: Sinusitis appears to occur frequently in HIV-infected patients, is often asymptomatic, may be recurrent or refractory, and may be associated with declining immunocompetence in HIV-infected patients. C1 NIAID,BETHESDA,MD 20892. NIH,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD 20892. GEORGETOWN UNIV HOSP,WASHINGTON,DC 20007. NR 17 TC 64 Z9 65 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 AUG PY 1992 VL 93 IS 2 BP 157 EP 162 DI 10.1016/0002-9343(92)90045-D PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA JH744 UT WOS:A1992JH74400007 PM 1353944 ER PT J AU BAUMRIND, S BENBASSAT, Y KORN, EL BRAVO, LA CURRY, S AF BAUMRIND, S BENBASSAT, Y KORN, EL BRAVO, LA CURRY, S TI MANDIBULAR REMODELING MEASURED ON CEPHALOGRAMS .1. OSSEOUS CHANGES RELATIVE TO SUPERIMPOSITION ON METALLIC IMPLANTS SO AMERICAN JOURNAL OF ORTHODONTICS AND DENTOFACIAL ORTHOPEDICS LA English DT Article ID ACTIVATOR TREATMENT; GROWTH AB We report the results of a study aimed at quantifying remodeling of mandibular surfaces in a sample of growing children who represent those usually treated by orthodontists in the mixed and early adult dentition. The sample, 31 patients with metallic implants of the Bjork-type, was monitored at annual intervals between 8 1/2 and 15 1/2 years of age. (Maxillary remodeling changes for the sample have been reported earlier.) The present article reports findings concerning changes at condyle, gonion, menton, pogonion, and point B as identified on lateral cephalograms. Data are reported in the Frankfort plane frame of reference with the cephalograms from different time points superimposed on the metallic implants. Mean displacement at condyle was larger than that at any other landmark and was similar in magnitude and direction to the observations of Bjork when the difference in orientation of the vertical axis in the two studies is taken into account. The mean displacement of gonion was in an upward and backward direction at an angle of approximately 45-degrees to the Frankfort plane. Mean displacements at menton and pogonion were in a downward and backward direction but were very small. Mean displacement at point B was somewhat greater than that of menton and gonion, oriented in an upward and backward direction. Individual variation for most of the parameters measured was sufficiently large to warrant the inference that caution should be used when mean values are applied to the analysis of individual cases. C1 HEBREW UNIV JERUSALEM,HADASSAH SCH DENT MED,DEPT ORTHODONT,JERUSALEM,ISRAEL. NCI,BIOMETR RES BRANCH,BETHESDA,MD 20892. TRIMBLE NAVIGAT LTD,SUNNYVALE,CA. UNIV MURCIA,FAC MED,SCH STOMATOL,MURCIA,SPAIN. RP BAUMRIND, S (reprint author), UNIV CALIF SAN FRANCISCO,SCH DENT,DEPT GROWTH & DEV,CRANIOFACIAL RES INSTRUMENTAT LAB,SAN FRANCISCO,CA 94143, USA. FU NIDCR NIH HHS [DE07332, DE03598] NR 20 TC 33 Z9 36 U1 1 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0889-5406 J9 AM J ORTHOD DENTOFAC JI Am. J. Orthod. Dentofac. Orthop. PD AUG PY 1992 VL 102 IS 2 BP 134 EP 142 DI 10.1016/0889-5406(92)70025-6 PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JH855 UT WOS:A1992JH85500006 PM 1636630 ER PT J AU POULSOM, R PIGNATELLI, M STETLERSTEVENSON, WG LIOTTA, LA WRIGHT, PA JEFFERY, RE LONGCROFT, JM ROGERS, L STAMP, GWH AF POULSOM, R PIGNATELLI, M STETLERSTEVENSON, WG LIOTTA, LA WRIGHT, PA JEFFERY, RE LONGCROFT, JM ROGERS, L STAMP, GWH TI STROMAL EXPRESSION OF 72 KDA TYPE-IV COLLAGENASE (MMP-2) AND TIMP-2 MESSENGER-RNAS IN COLORECTAL NEOPLASIA SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID BASEMENT-MEMBRANE COLLAGEN; NECROSIS FACTOR-ALPHA; TISSUE INHIBITOR; CELL-LINES; INTERSTITIAL COLLAGENASE; FIBROBLAST COLLAGENASE; HUMAN MACROPHAGES; METALLOPROTEINASES; CARCINOMA; BREAST AB We undertook an in situ hybridization study to localize the MRNAs for the 72 kda type IV collagenase (MMP-2) and its specific inhibitor (TIMP-2) in 12 colorectal carcinomas, 3 adenomas, and 4 uninvolved resection margins to see how their distributions correlated with that of the reported distribution of MMP-2 protein. Labeling for MMP-2 and TIMP-2 mRNAs was detectable in 10 of 12 carcinomas and in 2 of 3 adenomas. Unexpectedly, we found much stronger signals for MMP-2 and TIMP-2 mRNAs within the mesenchymal cells in the desmoplastic stroma, of endothelial and/or (myo)fibroblastic nature, rather than in tumor epithelial cells in which localization of MMP-2 was anticipated Our data indicate that stromal cells may have the ability to synthesize a metalloproteinase that degrades basement membrane, and may together with the neoplastic epithelial cells participate actively in the tissue remodeling and disruption of the basement membrane integrity which is characteristic of invasive tumors. C1 ROYAL POSTGRAD MED SCH,DEPT HISTOPATHOL,DU CANE RD,LONDON W12 0HS,ENGLAND. IMPERIAL CANC RES FUND,RCS,HISTOPATHOL UNIT,LONDON WC2A 3PX,ENGLAND. NCI,TUMOR INVAS & METASTASIS SECT,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. UNIV WALES COLL MED,CARDIFF CF4 4XN,S GLAM,WALES. RI Stetler-Stevenson, William/H-6956-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808 NR 46 TC 343 Z9 353 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD AUG PY 1992 VL 141 IS 2 BP 389 EP 396 PG 8 WC Pathology SC Pathology GA JH625 UT WOS:A1992JH62500014 PM 1323219 ER PT J AU JANSON, CH BOINSKI, S AF JANSON, CH BOINSKI, S TI MORPHOLOGICAL AND BEHAVIORAL ADAPTATIONS FOR FORAGING IN GENERALIST PRIMATES - THE CASE OF THE CEBINES SO AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY LA English DT Article; Proceedings Paper CT 58TH ANNUAL MEETING OF THE AMERICAN ASSOC OF PHYSICAL ANTHROPOLOGISTS CY APR 07, 1989 CL SAN DIEGO, CA SP AMER ASSOC PHYS ANTHROPOLOGISTS DE CEBINAE; SAIMIRI; CEBUS; OMNIVORY; FORAGING; BODY SIZE ID BROWN CAPUCHIN MONKEYS; INDIVIDUAL SPATIAL CHOICE; SQUIRREL-MONKEYS; CEBUS-APELLA; SAIMIRI-OERSTEDI; GENUS SAIMIRI; CAPUCINUS; DIMENSIONS; PREDATION; HABITAT AB In addition to being frugivorous, Cebus and Saimiri stand out among the New World primates of similar body size in being heavily dependent on animal matter for protein (faunivory). A detailed description of the morphology and behavior of the two genera is presented with the object of evaluating the interaction and respective contributions of morphological and behavioral adaptations to foraging patterns. Our conclusions include the following: First, body size is extremely important in explaining the observed variation in diet. Second, the emphasis on faunivory is facilitated more by behavioral than by morphological specialization. Third, whatever morphological specializations are present, particularly in Cebus, are probably favored by diet at the most food-depauperate time of year. Fourth, although morphology may well reveal what a primate may potentially eat, to map this potential onto actual diet requires a detailed knowledge of its natural ecosystem. Finally, we consider whether the behavioral data support the tenuous morphological evidence for grouping Cebus and Saimiri within the clade Cebinae. C1 NICHHD,CTR ANIM,COMPARAT ETHOL LAB,POOLESVILLE,MD 20837. RP JANSON, CH (reprint author), SUNY STONY BROOK,DEPT ECOL & EVOLUT,STONY BROOK,NY 11794, USA. NR 67 TC 127 Z9 132 U1 0 U2 19 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0002-9483 J9 AM J PHYS ANTHROPOL JI Am. J. Phys. Anthropol. PD AUG PY 1992 VL 88 IS 4 BP 483 EP 498 DI 10.1002/ajpa.1330880405 PG 16 WC Anthropology; Evolutionary Biology SC Anthropology; Evolutionary Biology GA JD592 UT WOS:A1992JD59200004 PM 1503120 ER PT J AU ZURLO, F FERRARO, RT FONTVIEILLE, AM RISING, R BOGARDUS, C RAVUSSIN, E AF ZURLO, F FERRARO, RT FONTVIEILLE, AM RISING, R BOGARDUS, C RAVUSSIN, E TI SPONTANEOUS PHYSICAL-ACTIVITY AND OBESITY - CROSS-SECTIONAL AND LONGITUDINAL-STUDIES IN PIMA-INDIANS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INDIRECT CALORIMETRY; RESPIRATORY CHAMBER; BODY WEIGHT; BODY COMPOSITION; FAMILIAL TRAIT; WEIGHT CHANGE ID RESTING METABOLIC-RATE; ENERGY-EXPENDITURE; WEIGHT-GAIN; CARBOHYDRATE; CHAMBER; RISK; FAT AB Healthy, nondiabetic Pima Indians [103 males, 77 females; 27 +/- 6 (SD) yr, 97 +/- 25 kg, 33 +/- 9% body fat] were studied in a respiratory chamber in which spontaneous physical activity (SPA) was measured by two microwave sensors. SPA, defined as the percentage of time the subjects were active, varied widely from 4.4 to 17.5%. It was higher in males (9.3 +/- 2.0%) than in females (8.6 +/- 2.3%; P < 0.05) and was not related to body fatness in either sex. However, SPA accounted for a significant portion of the daily energy expenditure (24-h EE) in males (1,389 +/- 423 kJ/day) and females (1,163 +/- 351 kJ/day) and correlated positively with 24-h EE adjusted for differences in fat-free mass, fat mass, age, and sex (r = 0.42, P < 0.0001). In 88 siblings, family membership accounted for 57% of the variance in SPA (r(i) = 0.57, P < 0.02). Body composition was reassessed in a subgroup of 123 subjects (65 males, 58 females) 33 +/- 14 mo later. In males only, SPA correlated inversely to the rate of subsequent body weight change (r = -0.25, P < 0.05) and the rate of fat-mass change (r = -0.35, P < 0.005). We conclude that spontaneous physical activity is a familial trait that may play a role in the pathogenesis of obesity. C1 NATL INST DIABET & DIGEST & KIDNEY DIS,CLIN DIABET & NUTR SECT,4212 N 16TH ST,RM 541,PHOENIX,AZ 85016. NR 31 TC 110 Z9 110 U1 0 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 AUG PY 1992 VL 263 IS 2 BP E296 EP E300 PN 1 PG 5 WC Physiology SC Physiology GA JJ958 UT WOS:A1992JJ95800055 PM 1514610 ER PT J AU MAEDA, Y TERADA, Y NONOGUCHI, H KNEPPER, MA AF MAEDA, Y TERADA, Y NONOGUCHI, H KNEPPER, MA TI HORMONE AND AUTACOID REGULATION OF CAMP PRODUCTION IN RAT IMCD SUBSEGMENTS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE COLLECTING DUCT; TRANSPORT REGULATION; ADENYLYL CYCLASE ID MEDULLARY COLLECTING DUCT; CYCLIC ADENOSINE-MONOPHOSPHATE; ADENYLATE-CYCLASE ACTIVITY; SINGLE NEPHRON SEGMENTS; TUBULE CELLS; RENAL ALPHA-2-ADRENOCEPTORS; RABBIT NEPHRON; 2ND MESSENGERS; VASOPRESSIN; KIDNEY AB The inner medullary collecting duct (IMCD) of the rat consists of two structurally and functionally distinct segments, i.e., the initial and the terminal IMCD. To identify factors that may regulate the transport function in the IMCD segments, we assessed whether catecholamines, carbachol, prostaglandin E2 (PGE2), bradykinin, glucagon, calcitonin, parathyroid hormone, or epidermal growth factor affects adenosine 3',5'-cyclic monophosphate (cAMP) production in microdissected tubules in the presence and absence of arginine vasopressin (AVP, 0.1 nM). All experiments were performed in the presence of 3-isobutyl-1-methylxanthine, and cAMP was measured by radioimmunoassay. Epinephrine (greater-than-or-equal-to 50 nM) and clonidine (greater-than-or-equal-to 1-mu-M) markedly decreased AVP-induced cAMP levels in both IMCD segments. However, phenylephrine did not show an effect. The inhibitory effect of epinephrine was blocked by yohimbine (50 nM) but not by prazosin (50 nM). In isolated perfused terminal IMCDs, epinephrine inhibited AVP-stimulated urea permeability. Isoproterenol (1-mu-M), in the absence of AVP, caused a significant increase in cAMP level only in the initial IMCD. Propranolol (1-mu-M) inhibited this isoproterenol effect, but atenolol did not. Dopamine (less-than-or-equal-to 1-mu-M) had no effect on cAMP levels in either IMCD segment. Carbachol, PGE2, and the various peptide hormones had no effect on cAMP levels (+/-AVP) in either IMCD segment. We conclude that an adrenergic beta-2-receptor is present only in the initial IMCD, where its occupation increases cAMP production. We conclude also that an adrenergic alpha-2-receptor is present in both IMCD segments, where its occupation inhibits AVP-induced cAMP production. The study also showed that carbachol, PGE2, and several peptide hormones had no effect on cAMP production in both IMCD segments. C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,BLDG 10,RM 6N307,BETHESDA,MD 20892. NR 40 TC 54 Z9 54 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 AUG PY 1992 VL 263 IS 2 BP F319 EP F327 PN 2 PG 9 WC Physiology SC Physiology GA JJ960 UT WOS:A1992JJ96000097 PM 1354941 ER PT J AU POST, RM AF POST, RM TI TRANSDUCTION OF PSYCHOSOCIAL STRESS INTO THE NEUROBIOLOGY OF RECURRENT AFFECTIVE-DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID FOS MESSENGER-RNA; INDUCED BEHAVIORAL SENSITIZATION; CORTICOTROPIN-RELEASING HORMONE; IMMEDIATE-EARLY GENES; NERVE GROWTH-FACTOR; C-FOS; LIFE EVENTS; RAT-BRAIN; MOUSE-BRAIN; GLUCOCORTICOID RECEPTOR AB Early clinical observations and recent systematic studies overwhelmingly document a greater role for psychosocial stressors in association with the first episode of major affective disorder than with subsequent episodes. The author postulates that both sensitization to stressors and episode sensitization occur and become encoded at the level of gene expression. In particular, stressors and the biochemical concomitants of the episodes themselves can induce the proto-oncogene c-fos and related transcription factors, which then affect the expression of transmitters, receptors, and neuropeptides that alter responsivity in a long-lasting fashion. Thus, both stressors and episodes may leave residual traces and vulnerabilities to further occurrences of affective illness. These data and concepts suggest that the biochemical and anatomical substrates underlying the affective disorders evolve over time as a function of recurrences, as does pharmacological responsivity. This formulation highlights the critical importance of early intervention in the illness in order to prevent malignant transformation to rapid cycling, spontaneous episodes, and refractoriness to drug treatment. RP POST, RM (reprint author), NIMH,BIOL PSYCHIAT BRANCH,BLDG 10,RM 3N212,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 125 TC 1156 Z9 1174 U1 3 U2 41 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 AUG PY 1992 VL 149 IS 8 BP 999 EP 1010 PG 12 WC Psychiatry SC Psychiatry GA JF708 UT WOS:A1992JF70800002 PM 1353322 ER PT J AU BONE, CR HIGGINS, MW HURD, SS REYNOLDS, HY AF BONE, CR HIGGINS, MW HURD, SS REYNOLDS, HY TI RESEARCH NEEDS AND OPPORTUNITIES RELATED TO RESPIRATORY HEALTH OF WOMEN SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Editorial Material ID PHARYNGEAL C1 NHLBI,DLD,WESTWOOD BLDG,ROOM 6A-15,BETHESDA,MD 20892. NR 21 TC 14 Z9 14 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD AUG PY 1992 VL 146 IS 2 BP 528 EP 535 PG 8 WC Respiratory System SC Respiratory System GA JP348 UT WOS:A1992JP34800047 PM 1489153 ER PT J AU CAHNMANN, HJ GONCALVES, E ITO, Y FALES, HM SOKOLOSKI, EA AF CAHNMANN, HJ GONCALVES, E ITO, Y FALES, HM SOKOLOSKI, EA TI SYNTHESIS AND PROPERTIES OF N-BROMOACETYL-L-THYROXINE SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID 3,3',5-TRIIODO-L-THYRONINE BINDING-PROTEIN; RAT-LIVER; THYROID-HORMONE; STRUCTURAL SIMILARITIES; CULTURED-CELLS; GLIAL-CELLS; GH3 CELLS; AFFINITY; IDENTIFICATION; N-BROMOACETYL-3,3',5-TRIIODO-L-THYRONINE C1 NHLBI,BIOPHYS CHEM LAB,BETHESDA,MD 20892. RP CAHNMANN, HJ (reprint author), NIDDK,GENET & BIOCHEM BRANCH,BLDG 10,ROOM 8N311,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 25 TC 3 Z9 3 U1 1 U2 5 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 AUG 1 PY 1992 VL 204 IS 2 BP 344 EP 350 DI 10.1016/0003-2697(92)90250-B PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA JF829 UT WOS:A1992JF82900020 PM 1443534 ER PT J AU HARFORD, JB AF HARFORD, JB TI A GENERAL-METHOD FOR THE DETECTION AND QUANTITATION OF ANTIGENS IN SOLUBILIZED CELLS USING RADIOLABELED FAB FRAGMENT SO ANALYTICAL BIOCHEMISTRY LA English DT Note ID HUMAN TRANSFERRIN RECEPTOR; GROWTH-FACTOR; BINDING RP HARFORD, JB (reprint author), NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892, USA. NR 12 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 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD AUG 1 PY 1992 VL 204 IS 2 BP 409 EP 411 DI 10.1016/0003-2697(92)90261-5 PG 3 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA JF829 UT WOS:A1992JF82900031 PM 1443545 ER PT J AU MAROTA, JJA CROSBY, G UHL, GR AF MAROTA, JJA CROSBY, G UHL, GR TI SELECTIVE EFFECTS OF PENTOBARBITAL AND HALOTHANE ON C-FOS AND JUN-B GENE-EXPRESSION IN RAT-BRAIN SO ANESTHESIOLOGY LA English DT Article DE ANESTHESIA, GENERAL; ANESTHETICS, INTRAVENOUS, PENTOBARBITAL; ANESTHETICS, VOLATILE, HALOTHANE; BRAIN, METABOLISM; CELLS, METABOLISM; GENETIC FACTORS, C-FOS; JUN-B; PROTOONCOGENES; METABOLISM, DEOXYRIBONUCLEIC ACID; RIBONUCLEIC ACID ID IMMEDIATE EARLY GENES; SPINAL-CORD; NOXIOUS-STIMULATION; NERVOUS-SYSTEM; MESSENGER-RNA; PROTEIN; NEURONS; INDUCTION; PAIN; IMMUNOREACTIVITY AB The effects of pentobarbital and halothane anesthesia on the expression in brain of the immediate-early genes c-fos and jun-B were investigated. Pentobarbital-anesthetized rats (n = 10) received a single intraperitoneal injection of pentobarbital 65 mg/kg in a vehicle of 40% propylene glycol and 10% ethanol and then were placed in a plexiglass box flushed continuously with 100% oxygen at 5 l/min. Halothane-anesthetized rats (n = 10) received an intraperitoneal injection of vehicle only and were transferred to a box flushed continuously with oxygen plus 1.5% halothane. Unanesthetized control rats (n = 10) received an intraperitoneal injection of vehicle and were placed in a box flushed continuously with 100% oxygen. Four additional rats received no intraperitoneal injection but were handled and otherwise treated identically to the control group, and six others had a femoral arterial catheter inserted for blood pressure and blood gas measurements. Five animals from the control and both anesthetized groups were killed at 30 and 120 min postinjection and their brains rapidly removed and frozen. The messenger ribonucleic acid transcription products of the genes c-fos, jun-B, and beta-actin from whole cerebral hemispheres were analyzed autoradiographically after Northern blot hybridization with P-32-labeled deoxyribonucleic acid probes. Relative levels of c-fos and jun-B messenger ribonucleic acid were determined from optical density measurements of the autoradiographic bands, with beta-actin measurements being used to correct for sample-to-sample variation. Rats became immobile within minutes of drug administration and remained anesthetized until they were killed. The anesthetics had little effect on mean arterial blood pressure, rectal temperature, and Pa(O2); however, pentobarbital-anesthetized rats were hypercarbic at both 30 and 120 min. Because halothane also produced hypercarbia at 120 min, there were no physiologic differences between anesthetics at this later point. Handling of rats did not change c-fos or jun-B expression. Intraperitoneal injection produced a 2- to 3-fold increase i n the whole brain levels of c-fos and jun-B messenger ribonucleic acid (P < 0.01 for all comparisons) at 30 min versus 120 min. Neither anesthetic modified this increase in c-fos and jun-B expression at 30 min postinjection. At 120 min postinjection, selective anesthetic effects were apparent. Jun-B expression was 25% greater than that of control in pentobarbital-anesthetized rats (P < 0.05) and 38% lower in halothane-anesthetized rats (P < 0.01), but neither anesthetic affected c-fos expression. Because immediate-early genes are thought to play a pivotal role in neural mechanisms of stress, memory, and pain/analgesia, anesthetic-induced changes in jun-B expression may pertain to modifications that occur in these biological processes during the anesthetic state. In a broader sense, these data indicate that general anesthetics selectively alter expression of genes in the central nervous system. C1 NIDA,ADDICT RES CTR,MOLEC NEUROBIOL LAB,BALTIMORE,MD. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ANESTHESIA SERV,BOSTON,MA 02114. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. FU NIGMS NIH HHS [R01-GM 42466] NR 37 TC 38 Z9 40 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD AUG PY 1992 VL 77 IS 2 BP 365 EP 371 DI 10.1097/00000542-199208000-00021 PG 7 WC Anesthesiology SC Anesthesiology GA JG533 UT WOS:A1992JG53300021 PM 1642355 ER PT J AU HOLLAND, FW BROWN, PS CLARK, RE AF HOLLAND, FW BROWN, PS CLARK, RE TI ACUTE SEVERE POSTISCHEMIC MYOCARDIAL DEPRESSION REVERSED BY TRIIODOTHYRONINE SO ANNALS OF THORACIC SURGERY LA English DT Article ID EUTHYROID SICK SYNDROME; CARDIOPULMONARY BYPASS; OXYGEN-CONSUMPTION; THYROID-FUNCTION; RAT-HEART; ISCHEMIA AB The purpose of this study was to determine the effects of triiodothyronine (T3) on postischemic left ventricular performance and high-energy phosphate content in a severe injury model. Isolated working rat hearts (n = 63) received 20 mL of hyperkalemic NIH No. 1 cardioplegia and were subjected to 20 minutes of ischemia at 37-degrees-C. Treated hearts were reperfused with T3-supplemented modified Krebs-Henseleit buffer. Control hearts did not receive T3 supplementation. All treated hearts (n = 44) performed work after ischemia, whereas 26% (5/19) of the control hearts were not able to perform any left ventricular work after ischemia. Comparisons with preischemic values demonstrated significant progressive hemodynamic recovery with increasing concentrations of T3 (0, 0.06, 0.15, and 0.60 ng/mL) with concomitant recovery of left ventricular stroke work index (63%, 72%, 89% [p < 0.05], and 99% [p < 0.05], respectively). There were corresponding increases in recovery of aortic flow, systolic pressure, cardiac index, and stroke volume index (p < 0.05). There were no significant changes in coronary sinus flow or heart rate in any group compared with preischemic values. Comparisons of postischemic high-energy phosphate concentrations also demonstrated no change between treated and untreated groups (p > 0.05). We conclude that administration of T3 in a severe left ventricular injury model significantly augments rapid ventricular recovery with no change in postischemic high-energy phosphate concentrations. C1 NHLBI,SURG BRANCH,BETHESDA,MD 20892. NR 23 TC 34 Z9 36 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 AUG PY 1992 VL 54 IS 2 BP 301 EP 305 PG 5 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA JF486 UT WOS:A1992JF48600021 PM 1637224 ER PT J AU TREADO, PJ LEVIN, IW LEWIS, EN AF TREADO, PJ LEVIN, IW LEWIS, EN TI HIGH-FIDELITY RAMAN IMAGING SPECTROMETRY - A RAPID METHOD USING AN ACOUSTOOPTIC TUNABLE FILTER SO APPLIED SPECTROSCOPY LA English DT Note DE IMAGING; MICROSCOPY; RAMAN SPECTROSCOPY; ACOUSTOOPTICS; CHARGE-COUPLED DEVICES; LASERS; HOLOGRAPHIC FILTERS; AMINO ACIDS; PHOSPHOLIPIDS ID SPECTROSCOPY; DETECTOR; MICROSCOPY; LASER AB In this communication, we describe a technique for obtaining high-fidelity Raman images and Raman spectra. The instrumentation provides the ability to rapidly collect large-format images with the number of image pixels limited only by the number of detector elements in the silicon charge-coupled device (CCD). Wavelength selection is achieved with an acousto-optic tunable filter (AOTF), which maintains image fidelity while providing spectral selectivity. Under computer control the AOTF is capable of mu-s tuning speeds within the operating range of the filter (400-1900 nm). The AOTF is integrated with the CCD and holographic Raman filters to comprise an entirely solid-state Raman imager containing no moving parts. In operation, the AOTF is placed in front of the CCD and tuned over the desired spectral interval. The two-dimensional CCD detector is employed as a true imaging camera, providing a full multichannel advantage over competitive Raman imaging techniques. Images and spectra are presented of a mixture of dipalmitoyl-phosphatidylcholine ( DPPC) and L-asparagine, which serves as a model system for the study of both lipid/peptide and lipid/protein interactions in intact biological materials. The Raman images are collected in only several seconds and indicate the efficacy of this rapid technique for discriminating between multiple components in complex matrices. Additionally, high-quality Raman spectra of the spatially resolved microscopic regions are easily obtained. C1 NATL INST DIABET DIGEST & KIDNEY DIS,CHEM PHYS LAB,BLDG 2,ROOM 114,BETHESDA,MD 20892. NR 17 TC 91 Z9 91 U1 1 U2 10 PU SOC APPLIED SPECTROSCOPY PI FREDERICK PA 201B BROADWAY ST, FREDERICK, MD 21701 SN 0003-7028 J9 APPL SPECTROSC JI Appl. Spectrosc. PD AUG PY 1992 VL 46 IS 8 BP 1211 EP 1216 DI 10.1366/0003702924123980 PG 6 WC Instruments & Instrumentation; Spectroscopy SC Instruments & Instrumentation; Spectroscopy GA JJ474 UT WOS:A1992JJ47400002 ER PT J AU HANNA, PM CHAMULITRAT, W MASON, RP AF HANNA, PM CHAMULITRAT, W MASON, RP TI WHEN ARE METAL ION-DEPENDENT HYDROXYL AND ALKOXYL RADICAL ADDUCTS OF 5,5-DIMETHYL-1-PYRROLINE N-OXIDE ARTIFACTS SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID SPIN; DMPO; HYDROPEROXIDE; SUPEROXIDE; OXIDATION RP HANNA, PM (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 13 TC 97 Z9 97 U1 2 U2 11 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 AUG 1 PY 1992 VL 296 IS 2 BP 640 EP 644 DI 10.1016/0003-9861(92)90620-C PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JD476 UT WOS:A1992JD47600036 PM 1321591 ER PT J AU CHAMULITRAT, W IWAHASHI, H KELMAN, DJ MASON, RP AF CHAMULITRAT, W IWAHASHI, H KELMAN, DJ MASON, RP TI EVIDENCE AGAINST THE 1-2-2-1 QUARTET DMPO SPECTRUM AS THE RADICAL ADDUCT OF THE LIPID ALKOXYL RADICAL SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID SPIN-RESONANCE SPECTROSCOPY; LIQUID-CHROMATOGRAPHY; HYDROPEROXIDES; HYDROXYL; PEROXYL; ION RP CHAMULITRAT, W (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 23 TC 17 Z9 17 U1 0 U2 4 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD AUG 1 PY 1992 VL 296 IS 2 BP 645 EP 649 DI 10.1016/0003-9861(92)90621-3 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JD476 UT WOS:A1992JD47600037 PM 1321592 ER PT J AU CERNY, A IZUI, S SAURAT, JH WALDVOGEL, FA MORSE, HC HAUSER, C AF CERNY, A IZUI, S SAURAT, JH WALDVOGEL, FA MORSE, HC HAUSER, C TI EPIDERMAL AND SPLENIC ANTIGEN-PRESENTING CELL-FUNCTION IN A RETROVIRALLY INDUCED MURINE IMMUNODEFICIENCY SYNDROME (MAIDS) SO ARCHIVES OF DERMATOLOGICAL RESEARCH LA English DT Article DE LANGERHANS CELLS; MURINE AIDS; ANTIGEN PRESENTING CELL ID POLYMERASE CHAIN-REACTION; LANGERHANS CELLS; B-CELLS; T-CELLS; VIRUS; INDUCTION; MICE; DISEASE; ABNORMALITIES; INFECTION AB Since alterations of epidermal Langerhans cells (LC) have been observed in humans infected with HIV, we investigated the morphology and function of these cells in murine acquired immunodeficiency syndrome (MAIDS), a murine model closely resembling human AIDS. The number as well as the shape of dendritic MHC class II+ cells from ear skin of C57BL/6 mice were similar in normal and infected animals. In mixed epidermal cell (EC) lymphocyte cultures, EC from infected mice and from normal mice stimulated allogeneic T cell proliferation to the same extent. In contrast to T cells from normal mice, however, T cells from infected mice did not respond to allogeneic spleen cells, confirming the presence of a T-cell defect in MAIDS. Subcutaneous injection of syngeneic mice with trinitrophenyl-modified MAIDS EC resulted in delayed ear swelling responses after challenge that were equivalent to those induced by hapten-modified EC from normal mice, suggesting that the contact sensitivity inducing potential of MAIDS LC was preserved. To investigate antigen presenting and processing function, EC and spleen cells were tested with the ovalbumin-specific IA(b)-restricted T cell hybridoma BO.17.10 and either ovalbumin 323-339 peptide or intact ovalbumin protein. MAIDS spleen cells had a reduced antigen presenting capacity compared with normal spleen cells, whereas EC from these mice showed the same processing and presenting capacity as normal controLs. In summary, our results demonstrate that the frequency, morphology, level of MHC class II antigen expression and ability to process and present antigen is normal for LC from mice with MAIDS whereas the function of splenic T cells and APC from infected mice is significantly impaired. C1 HOP CANTONAL UNIV,DEPT DERMATOL,24 RUE MICHELI DU CREST,CH-1211 GENEVA,SWITZERLAND. HOP CANTONAL UNIV,DEPT MED,CH-1211 GENEVA,SWITZERLAND. HOP CANTONAL UNIV,DEPT PATHOL,CH-1211 GENEVA,SWITZERLAND. NIAID,IMMUNOPATHOL LAB A,BETHESDA,MD 20892. OI Morse, Herbert/0000-0002-9331-3705 FU NIAID NIH HHS [N01-AI-72622] NR 22 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-3696 J9 ARCH DERMATOL RES JI Arch. Dermatol. Res. PD AUG PY 1992 VL 284 IS 4 BP 189 EP 192 DI 10.1007/BF00375791 PG 4 WC Dermatology SC Dermatology GA JM458 UT WOS:A1992JM45800001 PM 1329674 ER PT J AU SAFAVI, K AF SAFAVI, K TI SERUM VITAMIN-A LEVELS IN PSORIASIS - RESULTS FROM THE 1ST NATIONAL-HEALTH AND NUTRITION EXAMINATION SURVEY SO ARCHIVES OF DERMATOLOGY LA English DT Letter RP SAFAVI, K (reprint author), NIAMSD,OFF PREVENT EPIDEMIOL & CLIN APPLICAT,BLDG 31,ROOM 4C13,BETHESDA,MD 20892, USA. NR 5 TC 13 Z9 13 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 AUG PY 1992 VL 128 IS 8 BP 1130 EP 1131 DI 10.1001/archderm.128.8.1130 PG 2 WC Dermatology SC Dermatology GA JH724 UT WOS:A1992JH72400022 PM 1497375 ER PT J AU STRAUS, SE AF STRAUS, SE TI DEFINING THE CHRONIC FATIGUE SYNDROME SO ARCHIVES OF INTERNAL MEDICINE LA English DT Editorial Material RP STRAUS, SE (reprint author), NIH,CLIN INVEST LAB,BLDG 10,ROOM 11N228,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 12 TC 7 Z9 7 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD AUG PY 1992 VL 152 IS 8 BP 1569 EP 1570 DI 10.1001/archinte.152.8.1569 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA JH363 UT WOS:A1992JH36300001 PM 1323245 ER PT J AU LEVINE, PH JACOBSON, S POCINKI, AG CHENEY, P PETERSON, D CONNELLY, RR WEIL, R ROBINSON, SM ABLASHI, DV SALAHUDDIN, SZ PEARSON, GR HOOVER, R AF LEVINE, PH JACOBSON, S POCINKI, AG CHENEY, P PETERSON, D CONNELLY, RR WEIL, R ROBINSON, SM ABLASHI, DV SALAHUDDIN, SZ PEARSON, GR HOOVER, R TI CLINICAL, EPIDEMIOLOGIC, AND VIROLOGICAL STUDIES IN 4 CLUSTERS OF THE CHRONIC FATIGUE SYNDROME SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID EPSTEIN-BARR VIRUS; CELL LYMPHOTROPIC VIRUS; HTLV-I; INFECTION; PERSISTENT; REACTIVITY; ILLNESS; PANAMA; HBLV AB Background.-The purpose of this study is to provide a case definition of chronic fatigue syndrome in an outbreak occurring in the Nevada-California region to evaluate candidate etiologic agents and observe the natural history of the illness. Methods.-Patients diagnosed as having chronic fatigue syndrome were studied by repeated interviews, questionnaires, and blood collection over a 3-year period. Serum samples were tested for antibodies to Epstein-Barr virus, human herpesvirus-6, and human T-lymphotropic viruses I and II. Leukocytes from typical cases were also assayed for human T-lymphotropic viruses I and II. Results.-Cases were defined as persons who had: (1) severe persistent fatigue following an acute illness appearing in an individual with no previous physical or psychological symptoms; (2) presenting signs and symptoms of an acute infection; (3) severe and persistent headache and/or myalgias, and (4) abrupt change in cognitive function or the appearance of a new mood disorder. After 3 years of follow-up, almost all study subjects were able to return to pre-illness activity. None of the viruses evaluated-human T-lymphotropic viruses I and II, Epstein-Barr virus, or human herpesvirus-6-could be etiologically linked to these outbreaks. Conclusion.-Clinical features of outbreaks of chronic fatigue syndrome differ sufficiently to suggest different etiologic agents. Giardiasis appears to have precipitated one of the four clusters in this study but the cause(s) of the other three outbreaks is as yet uncertain. The overall prognosis of chronic fatigue syndrome is usually favorable. C1 CHENEY CLIN,CHARLOTTE,NC. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. RP LEVINE, PH (reprint author), NCI,DIV CANC ETIOL,ENVIRONM EPIDEMIOL BRANCH,EXECUT PLAZA N,ROOM 434,BETHESDA,MD 20892, USA. NR 45 TC 51 Z9 51 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD AUG PY 1992 VL 152 IS 8 BP 1611 EP 1616 DI 10.1001/archinte.152.8.1611 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA JH363 UT WOS:A1992JH36300008 PM 1323246 ER PT J AU MURPHY, DGM DECARLI, C SCHAPIRO, MB RAPOPORT, SI HORWITZ, B AF MURPHY, DGM DECARLI, C SCHAPIRO, MB RAPOPORT, SI HORWITZ, B TI AGE-RELATED DIFFERENCES IN VOLUMES OF SUBCORTICAL NUCLEI, BRAIN MATTER, AND CEREBROSPINAL-FLUID IN HEALTHY-MEN AS MEASURED WITH MAGNETIC-RESONANCE-IMAGING SO ARCHIVES OF NEUROLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; CEREBROVASCULAR RISK-FACTORS; CEREBRAL GLUCOSE-UTILIZATION; MR SIGNAL ABNORMALITIES; COMPUTED-TOMOGRAPHY; WHITE MATTER; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; ATROPHY; DEMENTIA AB Magnetic resonance imaging was used to determine the volumes of brain, subcortical gray matter nuclei, and the ventricular and sulcal cerebrospinal fluid in 27 healthy men. Subjects were divided into young (<35 years, n=10) and old (>60 years, n= 17) groups. Volumes were normalized as percent intracranial volume. Older subjects had significantly less brain mass and significantly larger ventricular and peripheral cerebrospinal fluid volumes than the younger men. The caudate and lenticular nuclei were significantly smaller in older than younger men. This significant difference remained when their volumes were expressed as a ratio of cerebral brain matter volume. This cross-sectional study demonstrates age-related atrophy and concurrent dilation of cerebrospinal fluid spaces in healthy subjects. Of brain regions affected, the caudate and lenticular nuclei are significantly more affected by healthy aging than is cerebral brain matter; this may account for some of the motor abnormalities in aging. RP MURPHY, DGM (reprint author), NIA,NEUROSCI LAB,BETHESDA,MD 20892, USA. RI DeCarli, Charles/B-5541-2009 NR 68 TC 174 Z9 176 U1 2 U2 6 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 AUG PY 1992 VL 49 IS 8 BP 839 EP 845 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA JH365 UT WOS:A1992JH36500009 PM 1343082 ER PT J AU WILSON, CA BERKOWITZ, BA MCCUEN, BW CHARLES, HC AF WILSON, CA BERKOWITZ, BA MCCUEN, BW CHARLES, HC TI MEASUREMENT OF PRERETINAL OXYGEN-TENSION IN THE VITRECTOMIZED HUMAN EYE USING F-19 MAGNETIC-RESONANCE SPECTROSCOPY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID F-19 NMR; VITREOUS REPLACEMENT; VEIN OCCLUSION; INVIVO; LIQUID; PERFLUOROTRIBUTYLAMINE; TOLERANCE; HYPOXIA AB We obtained oxygen measurements from a human eye that contained small preretinal droplets of perfluorotributylamine (FTBA) by using fluorine-19 magnetic resonance spectroscopy. These droplets were the remainder of a larger volume of FTBA that was used as an intraoperative retinal tamponade during retinal detachment repair. The spin-lattice relaxation rate ([T1]-1) of the FTBA fluorine nuclide was obtained that could then be related, by direct proportionality, to droplet Po2. With the patient in a supine position, the droplets could be positioned over the macula in the preretinal vitreous space, whereon the FTBA Po2 could be influenced by the preretinal oxygen concentration. Preretinal Po2 values, derived from magnetic resonance spectroscopy, were in the range of 6 to 9 mm Hg, although multiple components were identified that were suggestive of a heterogeneous distribution of Po2 values in the population of droplets. To our knowledge, this investigation is the first to demonstrate the feasibility of this approach to performing long-term, noninvasive preretinal oxygen measurements in the vitrectomized human eye by using small droplets of a liquid perfluorochemical. C1 DUKE UNIV,MED CTR,DEPT OPHTHALMOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT RADIOL,DURHAM,NC 27710. NIEHS,RES TRIANGLE PK,NC 27709. RI Charles, Hal/C-7772-2017 OI Charles, Hal/0000-0002-1414-2494 NR 24 TC 31 Z9 32 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 AUG PY 1992 VL 110 IS 8 BP 1098 EP 1100 PG 3 WC Ophthalmology SC Ophthalmology GA JH496 UT WOS:A1992JH49600022 PM 1497523 ER PT J AU WILSON, CA BERKOWITZ, BA SATO, Y ANDO, N HANDA, JT DEJUAN, E AF WILSON, CA BERKOWITZ, BA SATO, Y ANDO, N HANDA, JT DEJUAN, E TI TREATMENT WITH INTRAVITREAL STEROID REDUCES BLOOD-RETINAL BARRIER BREAKDOWN DUE TO RETINAL PHOTOCOAGULATION SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID PROLIFERATIVE VITREORETINOPATHY; GROWTH-FACTOR; DETACHMENT; INJECTION; CELLS; PROSTAGLANDIN-E2; DEXAMETHASONE; MACROPHAGES; GRANULOCYTE; INHIBITION AB The effect of corticosteroid treatment on blood-retinal barrier breakdown caused by argon-laser panretinal photocoagulation was evaluated in the rabbit eye. One day before photocoagulation, eyes were given either a sub-Tenon (20-mg) or intravitreal (2-mg) injection of triamcinolone acetonide. The severity of blood-retinal barrier breakdown was measured after photocoagulation using rapid sequential magnetic resonance imaging following intravenous administration of gadolinium diethylenetriaminepentaacetic acid. Leakage of gadolinium diethylenetriaminepentaacetic acid into the vitreous space was significantly lower in eyes that received intravitreal triamcinolone acetonide than in control eyes (P=.007); however, sub-Tenon triamcinolone acetonide produced no significant reduction in leakage (P=.65) compared with controls. Fluorescein angiography supported the magnetic resonance imaging findings. We conclude that retinal photocoagulation in the rabbit eye produces blood-retinal barrier breakdown that is partially amenable to corticosteroid treatment. C1 DUKE UNIV,MED CTR,DEPT OPHTHALMOL,BOX 3802,DURHAM,NC 27710. NIEHS,RES TRIANGLE PK,NC 27709. FU NEI NIH HHS [R01 EY07576] NR 37 TC 176 Z9 192 U1 0 U2 1 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 AUG PY 1992 VL 110 IS 8 BP 1155 EP 1159 PG 5 WC Ophthalmology SC Ophthalmology GA JH496 UT WOS:A1992JH49600035 PM 1497531 ER PT J AU TSOKOS, M WEBBER, BL PARHAM, DM WESLEY, RA MISER, A MISER, JS ETCUBANAS, E KINSELLA, T GRAYSON, J GLATSTEIN, E PIZZO, PA TRICHE, TJ AF TSOKOS, M WEBBER, BL PARHAM, DM WESLEY, RA MISER, A MISER, JS ETCUBANAS, E KINSELLA, T GRAYSON, J GLATSTEIN, E PIZZO, PA TRICHE, TJ TI RHABDOMYOSARCOMA - A NEW CLASSIFICATION SCHEME RELATED TO PROGNOSIS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID CHILDHOOD RHABDOMYOSARCOMA; INTERGROUP RHABDOMYOSARCOMA; CHILDREN; CHEMOTHERAPY; SURGERY; TUMORS; HEAD; NECK AB We classified 159 cases of rhabdomyosarcoma (RMS) according to the conventional scheme adopted by the World Health Organization and a modified conventional scheme established at the National Cancer Institute (NCI), Bethesda, Md. The major modification in the NCI scheme was the inclusion of compact round-cell RMS with scant myogenesis in the group of alveolar RMS despite lack of an alveolar architecture. These tumors were previously considered to be embryonal RMS, but their cytologic features are quite different from those seen in embryonal RMS and are indistinguishable from those encountered in alveolar RMS. These tumors are referred to as "solid alveolar RMS." Survival curves were constructed with the method of Kaplan-Meier and compared with the unstratified and stratified methods of Mantel-Haenszel (with stratification factors being stage, site, and age) and with the Cox regression analysis. Both histologic schemes showed a statistically significant prognostic value in unstratified analyses, but the NCI scheme demonstrated prognostic value even in stratified analyses and in the Cox regression analysis in our series of cases. The data indicate that the NCI scheme can serve as a highly predictive, independent prognostic factor in RMS and that the alveolar category should be expanded to include the solid round-cell RMS, even in the absence of a classic alveolar architecture. C1 NIH, PATHOL LAB, BETHESDA, MD 20892 USA. NIH, DEPT BIOSTAT, BETHESDA, MD 20892 USA. NIH, PEDIAT BRANCH, BETHESDA, MD 20892 USA. NIH, RADIAT ONCOL BRANCH, BETHESDA, MD 20892 USA. ST JUDE CHILDRENS RES HOSP, DIV LAB MED & PATHOL, MEMPHIS, TN 38101 USA. ST JUDE CHILDRENS RES HOSP, DIV HEMATOL ONCOL, MEMPHIS, TN 38101 USA. NR 38 TC 135 Z9 137 U1 0 U2 2 PU COLL AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD AUG PY 1992 VL 116 IS 8 BP 847 EP 855 PG 9 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA JG534 UT WOS:A1992JG53400016 PM 1497467 ER PT J AU ZARATEOSORNO, A JAFFE, ES MEDEIROS, J AF ZARATEOSORNO, A JAFFE, ES MEDEIROS, J TI METASTATIC NASOPHARYNGEAL CARCINOMA INITIALLY PRESENTING AS CERVICAL LYMPHADENOPATHY - A REPORT OF 2 CASES THAT RESEMBLED HODGKINS-DISEASE SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID IMMUNOHISTOCHEMISTRY; DIAGNOSIS; LYMPHOMA; TUMORS AB We describe two patients with nasopharyngeal carcinoma who initially presented with cervical lymphadenopathy. Lymph node biopsy specimens in each patient were initially diagnosed as Hodgkin's disease. In both cases, the neoplastic cells had large, vesicular nuclei with prominent eosinophilic nucleoli; some neoplastic cells were identified in lacunar spaces. In addition, numerous inflammatory cells were present, including eosinophils, lymphocytes, and plasma cells. At the time of referral, the correct diagnosis of metastatic carcinoma was made, and primary nasopharyngeal carcinomas were subsequently identified. The possibility of metastatic nasopharyngeal carcinoma should always be considered in adults with enlarged cervical lymph nodes that resemble Hodgkin's disease. The cytologic features of the malignant cells are the clue to the correct diagnosis. Immunophenotypic studies easily resolve this diagnostic dilemma if the possibility of metastatic nasopharyngeal carcinoma is considered. C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,ROOM 2N108,BETHESDA,MD 20892. NR 11 TC 13 Z9 13 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 AUG PY 1992 VL 116 IS 8 BP 862 EP 865 PG 4 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA JG534 UT WOS:A1992JG53400018 PM 1379793 ER PT J AU PURIFOY, FE GRODSKY, A GIAMBRA, LM AF PURIFOY, FE GRODSKY, A GIAMBRA, LM TI THE RELATIONSHIP OF SEXUAL DAYDREAMING TO SEXUAL-ACTIVITY, SEXUAL DRIVE, AND SEXUAL ATTITUDES FOR WOMEN ACROSS THE LIFE-SPAN SO ARCHIVES OF SEXUAL BEHAVIOR LA English DT Article DE FEMALE SEXUALITY; AGING; SEXUAL DAYDREAMS; SEX DRIVE; SEXUAL ATTITUDES ID FANTASIES AB The association among sexual daydreaming and sexual attitudes and activity was examined in a cross-sectional life-span sample of women (N = 117, 26 to 78 years). Sexual daydreaming was measured using the Imaginal Processes Inventory (IPI) while sexual history measures of sexual activity, sexual drive, and sexual attitudes were derived from a comprehensive personal interview. A factor analysis and varimax rotation of the sexual history variables, age, and the Sexual Daydream Scale of the IPI revealed three primary factors representing dimensions of sexual activity and drive, attitudes toward sexual activity, and sexual satisfaction. Age was associated with less sexual daydreaming, less sexual drive, less sexual activity, and more negative sexual attitudes. Sexual daydreaming varied directly with sexual drive and sexual activity and with a positive sexual attitude. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP PURIFOY, FE (reprint author), UNIV LOUISVILLE,DEPT ANTHROPOL,LOUISVILLE,KY 40292, USA. NR 32 TC 24 Z9 25 U1 1 U2 7 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0004-0002 J9 ARCH SEX BEHAV JI Arch. Sex. Behav. PD AUG PY 1992 VL 21 IS 4 BP 369 EP 385 DI 10.1007/BF01542026 PG 17 WC Psychology, Clinical; Social Sciences, Interdisciplinary SC Psychology; Social Sciences - Other Topics GA JD137 UT WOS:A1992JD13700004 PM 1497475 ER PT J AU BURNS, CM TSAI, V ZVAIFLER, NJ AF BURNS, CM TSAI, V ZVAIFLER, NJ TI HIGH PERCENTAGE OF CD8+, LEU-7+ CELLS IN RHEUMATOID-ARTHRITIS SYNOVIAL-FLUID SO ARTHRITIS AND RHEUMATISM LA English DT Article ID NATURAL-KILLER CELLS; BONE-MARROW TRANSPLANTATION; CYTOMEGALO-VIRUS INFECTION; DEFICIENCY SYNDROME AIDS; LYMPHOCYTE-T SUBSETS; HUMAN NK-CELLS; MONOCLONAL-ANTIBODIES; PERIPHERAL-BLOOD; HNK-1+ LEU-7; HELPER INDUCER AB Objective. While analyzing the phenotype of the synovial fluid mononuclear cells (SFMC) clustered about dendritic cells in rheumatoid arthritis (RA) joint effusions, it was noted that most of the clustering cells were CD8+ and coexpressed Leu-7. Therefore, the present study was conducted to investigate the frequency of CD8+, Leu 7+ cells in RA SF. Methods. SFMC from 13 patients with RA and from 12 patients with non-RA inflammatory arthritides were examined for CD8 and Leu-7 expression using 2-color immunofluorescence flow cytometry. Results. RA SFMC had statistically significantly greater percentages of total CD8+ cells, total Leu-7+ cells, and CD8+, Leu-7+ cells, compared with SFMC from the non-RA patients. These RA CD8+, Leu-7+ SFMC had a distinctive electron microscopic appearance compared with CD8+, Leu-7- SFMC. When peripheral blood mononuclear cells (PBMC) from 31 RA patients (including 7 from the SFMC group) were compared with PBMC from 15 normal controls, the percentage of CD8+, Leu-7+ cells was not significantly greater in the RA patients. However, the combination of a modest increase in CD8+, Leu-7+ cells and a decrease in total CD8 cells in RA PBMC altered the composition of the RA CD8 population compared with normal PBMC, such that over 40% of RA peripheral blood CD8 cells coexpressed Leu-7. Conclusion. The increased frequency of CD8+, Leu-7+ cells in RA SFMC may arise from the fact that a high percentage of the CD8+ PBMC in RA patients are also Leu-7+. This altered composition of CD8 cells in RA SF may have a role in the pathogenesis of the disease. C1 UNIV CALIF SAN DIEGO,DEPT MED,DIV RHEUMATOL,MED CTR 8417,225 DICKINSON ST,SAN DIEGO,CA 92103. NCI,BIOL RESPONSE MODIFIERS PROGRAM,BETHESDA,MD 20892. NR 43 TC 19 Z9 20 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 AUG PY 1992 VL 35 IS 8 BP 865 EP 873 DI 10.1002/art.1780350804 PG 9 WC Rheumatology SC Rheumatology GA JH178 UT WOS:A1992JH17800003 PM 1379428 ER PT J AU GLOWA, JR SULLIVAN, JV BACHER, JD AF GLOWA, JR SULLIVAN, JV BACHER, JD TI A SUBCUTANEOUS INTRACEREBRAL DRUG DELIVERY DEVICE FOR USE IN RHESUS-MONKEYS SO BEHAVIOR RESEARCH METHODS INSTRUMENTS & COMPUTERS LA English DT Article ID CORTICOTROPIN RELEASING HORMONE AB This large-animal intracerebral drug administration unit is designed to allow the delivery of drugs or other agents to discrete loci within the brains of animals while maintaining sterile conditions. It is an improvement over existing designs because it (1) maintains an absolute minimal dead space within the system, (2) is smaller in diameter (by approximately 80% than existing shunt catheters, minimizing tissue damage during placement, (3) is easily secured and requires minimal clearance over the cranium, and (4) maintains a sterile seal between the brain and periphery. Preliminary studies indicate that the device is well accepted by monkeys and is fully functional for periods up to a year. The device is intended for permanent implantation. C1 NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD. NATL CTR RES RESOURCES,VET RESOURCES PROGRAM,BETHESDA,MD. RP GLOWA, JR (reprint author), NIMH,CNE,BIOPSYCHOL UNIT,CLIN NEUROENDOCRINOL BRANCH,BLDG 14D,ROOM 311,BETHESDA,MD 20892, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU PSYCHONOMIC SOC INC PI AUSTIN PA 1710 FORTVIEW RD, AUSTIN, TX 78704 SN 0743-3808 J9 BEHAV RES METH INSTR JI Behav. Res. Methods Instr. Comput. PD AUG PY 1992 VL 24 IS 3 BP 402 EP 406 DI 10.3758/BF03203569 PG 5 WC Psychology, Mathematical; Psychology, Experimental SC Psychology GA JG543 UT WOS:A1992JG54300002 ER PT J AU WU, YN VU, ND WAGNER, PD AF WU, YN VU, ND WAGNER, PD TI ANTI-(14-3-3 PROTEIN) ANTIBODY INHIBITS STIMULATION OF NORADRENALINE (NOREPINEPHRINE) SECRETION BY CHROMAFFIN-CELL CYTOSOLIC PROTEINS SO BIOCHEMICAL JOURNAL LA English DT Note ID ACTIVATES TRYPTOPHAN 5-MONOOXYGENASE; BRAIN 14-3-3 PROTEIN; PHORBOL ESTER TPA; KINASE-C; CATECHOLAMINE SECRETION; TYROSINE 3-MONOOXYGENASE; EXOCYTOSIS; CALCIUM; PURIFICATION; CALPACTIN AB Incubation of digitonin-permeabilized bovine chromaffin cells in the absence of Ca2+ results in a loss of both cytosolic proteins and Ca2+-dependent secretion. Addition of these leaked proteins prevents this loss of secretory activity. We have purified a protein from an extract of bovine adrenal medulla which can partially prevent this loss of Ca2+-dependent secretion. Antibody against this protein inhibited the ability of leaked chromaffin-cell proteins to prevent the loss of Ca2+-dependent secretion. Sequence analysis showed it to have sequence identity with bovine brain 14-3-3 protein. These results demonstrate that 14-3-3 protein makes a significant contribution to the ability of leaked chromaffin-cell proteins to maintain secretory activity. C1 NCI,BIOCHEM LAB,BETHESDA,MD 20892. NR 26 TC 30 Z9 30 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD AUG 1 PY 1992 VL 285 BP 697 EP 700 PN 3 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JH247 UT WOS:A1992JH24700003 PM 1497607 ER PT J AU GARCIA, GG EVANS, GA MICHIEL, DF FARRAR, WL AF GARCIA, GG EVANS, GA MICHIEL, DF FARRAR, WL TI CHARACTERIZATION OF A TYROSINE KINASE-ACTIVITY ASSOCIATED WITH THE HIGH-AFFINITY INTERLEUKIN-2 RECEPTOR COMPLEX SO BIOCHEMICAL JOURNAL LA English DT Article ID P70-75 BETA-SUBUNIT; IL-2 RECEPTOR; SIGNAL TRANSDUCTION; SRC-FAMILY; CHAIN; ERYTHROPOIETIN; THREONINE; HOMOLOGY; BINDING; CLONING AB The IL-2 receptor complex is minimally composed of two genetically unrelated subunits of relative molecular masses 55 and 75 kDa respectively. Structural information deduced from the cDNA sequences of either subunit have not revealed significant information as to the basis of the mechanisms of IL-2 receptor signal transduction. Nevertheless, IL-2 stimulates the activation of one or more tyrosine kinases requiring the functional participation of the p75 member of the receptor complex. Here we have developed the methods to isolate the receptor complex with an associated tyrosine protein kinase. Extracts of membrane glycoproteins from activated normal human T lymphocytes and cell lines demonstrated catalytic activation of tyrosine kinase activity when stimulated with IL-2. Purification of the receptor complex with biotinylated IL-2 revealed the presence of two dominant phosphotyrosyl-proteins of approximate molecular masses 58 and 97 kDa. Denaturation gel electrophoresis followed by renaturation of proteins associated with the IL-2 receptor complex demonstrated that the 97 kDa protein had catalytic autophosphorylation activity. The results indicate that the 58 and 97 kDa phosphotyrosyl-proteins can be found to co-precipitate with the IL-2 receptor complex and that the 97 kDa protein was demonstrated to have protein kinase activity. The association of such kinases with receptors devoid of catalytic structure may represent a unique paradigm of growth-factor receptor mechanisms. C1 NCI,CYTOKINE MOLEC MECHANISMS SECT,MOLEC IMMUNOREGULAT LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD 21701. FU NCI NIH HHS [N01-CO-74102] NR 23 TC 14 Z9 14 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD AUG 1 PY 1992 VL 285 BP 851 EP 856 PN 3 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JH247 UT WOS:A1992JH24700028 PM 1497623 ER PT J AU KISO, Y MCBEY, BA MASON, L CROY, BA AF KISO, Y MCBEY, BA MASON, L CROY, BA TI HISTOLOGICAL ASSESSMENT OF THE MOUSE UTERUS FROM BIRTH TO PUBERTY FOR THE APPEARANCE OF LGL-1+ NATURAL-KILLER-CELLS SO BIOLOGY OF REPRODUCTION LA English DT Article ID METRIAL GLAND-CELLS; ADULT MICE; DIFFERENTIATION; TROPHOBLAST; ORIGIN AB The appearance of natural killer (NK) cells during growth and maturation of the murine uterus was studied by immunohistochemistry, using the monoclonal antibody LGL-1. To determine the contributions of microorganisms in the environment and of T-cell and B-cell regulation to die establishment of a uterine NK cell population, uteri from barrier-raised, flora-defined, random-bred CD-1 mice and from genetically T-cell- and B-cell-deficient SCID mice (genotype C.B-17 scid/scid) were compared to uteri from conventionally raised CD-1 mice. Uteri were studied from birth to the ages at which these mice are normally paired for mating (7-10 wk). Absolute uterine weight and the ratio of uterine weight to body weight increased remarkably between 3 and 5 wk of age in each group of animals. Growth continued beyond Week 5 of age, and in all groups the ratio of uterine weight to body weight was similar at puberty, although both the flora-defined CD-1 and SCID mice were significantly smaller than conventionally reared mice. LGL-1+ cells could not be detected in any of the neonatal uteri examined. LGL-1+ cells were first detected at 2 wk of age in uteri from the conventional and flora-defined CD-1 mice. A significant increase in the number of LGL-1+ NK cells occurred in the CD-1 uterus between Weeks 2 and 3 of age and again between Weeks 5 and 7 of age. Environmental conditions did not alter the frequency of LGL-1+ cells between the two groups of CD-1 mice at any age studied. In the SCID mice, LGL-1+ cells were first observed in the uterus at 5 wk of age, and the number of positive cells increased more slowly than in immunocompetent mice. These data establish that the appearance of NK cells expressing the LGL-1 phenotype in the uterus is a postnatal event not related to puberty, not influenced by microbial environment, and only slightly delayed in the absence of T cells and B cells. C1 NCI,FREDERICK CANC RES FACIL,EXPTL IMMUNOL LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. RP KISO, Y (reprint author), UNIV GUELPH,ONTARIO VET COLL,DEPT BIOMED SCI,GUELPH N1G 2W1,ONTARIO,CANADA. NR 38 TC 42 Z9 42 U1 0 U2 0 PU SOC STUDY REPRODUCTION PI MADISON PA 1603 MONROE ST, MADISON, WI 53711-2021 SN 0006-3363 J9 BIOL REPROD JI Biol. Reprod. PD AUG PY 1992 VL 47 IS 2 BP 227 EP 232 DI 10.1095/biolreprod47.2.227 PG 6 WC Reproductive Biology SC Reproductive Biology GA JE589 UT WOS:A1992JE58900010 PM 1391328 ER PT J AU JACOBSON, KA KARTON, Y BAUMGOLD, J AF JACOBSON, KA KARTON, Y BAUMGOLD, J TI MUSCARINIC RECEPTOR PROBES BASED ON AMINE CONGENERS OF PIRENZEPINE AND TELENZEPINE SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID SITE-DIRECTED MUTAGENESIS; ADENOSINE RECEPTOR; ANTAGONISTS; IDENTIFICATION; INHIBITION; AGONIST; BINDING AB The N-methyl groups of pirenzepine and telenzepine (M1-antagonists) were modified to produce chemically functionalized N-alkyl analogs using a "functionalized congener" approach. The derivatives were tested in binding assays vs. [H-3]N-methylscopolamine in rat forebrain and cardiac membranes. The potency/selectivity were highly dependent on substitutions of the N-methyl group. The affinity in a series of n-alkyl amino derivatives progressively increased with the number of methylene groups. The amines were acylated with various reporter groups resulting in molecular probes of nanomolar affinity. The effect of chain length on aryl isothiocyanate affinity labels is explored. C1 GEORGE WASHINGTON UNIV,DEPT RADIOL,WASHINGTON,DC 20037. RP JACOBSON, KA (reprint author), NIDDK,BIOORGAN CHEM LAB,BETHESDA,MD 20892, USA. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 NR 18 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD AUG PY 1992 VL 2 IS 8 BP 845 EP 850 DI 10.1016/S0960-894X(00)80542-9 PG 6 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA JK712 UT WOS:A1992JK71200013 ER PT J AU STERN, MD AF STERN, MD TI THEORY OF EXCITATION-CONTRACTION COUPLING IN CARDIAC-MUSCLE SO BIOPHYSICAL JOURNAL LA English DT Article ID SARCOPLASMIC-RETICULUM VESICLES; CALCIUM-INDUCED RELEASE; VENTRICULAR MYOCYTES; SKELETAL-MUSCLE; PURKINJE-CELL; INTRACELLULAR CALCIUM; INWARD CURRENT; RAT VENTRICLE; ACTIVATION; CHANNEL AB The consequences of cardiac excitation-contraction coupling by calcium-induced calcium release were studied theoretically, using a series of idealized models solved by analytic and numerical methods. "Common-pool" models, those in which the trigger calcium and released calcium pass through a common cytosolic pool, gave nearly all-or-none regenerative calcium releases (in disagreement with experiment), unless their loop gain was made sufficiently low that it provided little amplification of the calcium entering through the sarcolemma. In the linear (small trigger) limit, it was proven rigorously that no common-pool model can give graded high amplification unless it is operated on the verge of spontaneous oscillation. To circumvent this problem, we considered two types of "local-control" models. In the first type, the local calcium from a sarcolemmal L-type calcium channel directly stimulates a single, immediately opposed SR calcium release channel. This permits high amplification without regeneration, but requires high conductance of the SR channel. This problem is avoided in the second type of local control model, in which one L-type channel triggers a regenerative cluster of several SR channels. Statistical recruitment of clusters results in graded response with high amplification. In either type of local-control model, the voltage dependence of SR calcium release is not exactly the same as that of the macroscopic sarcolemmal calcium current, even though calcium is the only trigger for SR release. This results from the existence of correlations between the stochastic openings of individual sarcolemmal and SR channels. Propagation of regenerative calcium-release waves (under conditions of calcium overload) was analyzed using analytically soluble models in which SR calcium release was treated phenomenalogically. The range of wave velocities observed experimentally is easily explained; however, the observed degree of refractoriness to wave propagation requires either a strong dependence of SR calcium release on the rate of rise of cytosolic calcium or localization of SR release sites to one point in the sarcomere. We conclude that the macroscopic behavior of calcium-induced calcium release depends critically on the spatial relationships among sarcolemmal and SR calcium channels, as well as on their kinetics. C1 NIA,GERONTOL RES CTR,BALTIMORE,MD 21224. RP STERN, MD (reprint author), JOHNS HOPKINS MED INST,DIV CARDIOL,592 CARNEGIE BLDG,BALTIMORE,MD 21205, USA. NR 49 TC 510 Z9 517 U1 2 U2 26 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD AUG PY 1992 VL 63 IS 2 BP 497 EP 517 PG 21 WC Biophysics SC Biophysics GA JH782 UT WOS:A1992JH78200022 PM 1330031 ER PT J AU TASAKI, I BYRNE, PM AF TASAKI, I BYRNE, PM TI DISCONTINUOUS VOLUME TRANSITIONS IN IONIC GELS AND THEIR POSSIBLE INVOLVEMENT IN THE NERVE EXCITATION PROCESS SO BIOPOLYMERS LA English DT Article ID SQUID GIANT-AXON; ACTION-POTENTIALS AB Discontinuous volume changes in polymer gels carrying negatively ionized groups were studied by varying the molarities of univalent and bivalent cations in the bathing solution. These studies offer a sound basis for elucidating the origin of rapid swelling and heat production in nerve fibers associated with the process of excitation. RP TASAKI, I (reprint author), NIMH,CELL BIOL LAB,BETHESDA,MD 20892, USA. NR 20 TC 36 Z9 37 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PD AUG PY 1992 VL 32 IS 8 BP 1019 EP 1023 DI 10.1002/bip.360320812 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JD771 UT WOS:A1992JD77100011 PM 1420969 ER PT J AU PAINE, PL JOHNSON, ME LAU, YT TLUCZEK, LJM MILLER, DS AF PAINE, PL JOHNSON, ME LAU, YT TLUCZEK, LJM MILLER, DS TI THE OOCYTE NUCLEUS ISOLATED IN OIL RETAINS INVIVO STRUCTURE AND FUNCTIONS SO BIOTECHNIQUES LA English DT Article ID XENOPUS-LAEVIS OOCYTES; MATURATION; TRANSCRIPTION; EGGS; RNA; MICROINJECTION; TRIPHOSPHATE; INITIATION; PRINCIPLE; BREAKDOWN AB We describe a technique for isolating the nucleus of the giant amphibian oocyte under paraffin oil. The method precludes the losses of small solutes and proteins that accompany isolation of nuclei into aqueous media. An individual oocyte is blotted, placed under oil, punctured near the animal pole and then squeezed to gently extrude the nucleus into the oil, thereby avoiding exposure to any aqueous environment. Light and electron microscopy of the oil-isolated nucleus demonstrate that its in vivo morphology is preserved. We also describe techniques that facilitate the study of nuclear functions under oil. Oil-isolated oocyte nuclei retain many in vivo functions for several hours, including size-selective envelope permeability, RNA synthesis and the ability to break down in response to cdc2/cyclin meiotic maturation promoting factor. C1 MICHIGAN CANC FDN,DETROIT,MI 48201. NIEHS,RES TRIANGLE PK,NC 27709. RP PAINE, PL (reprint author), ST JOHNS UNIV,DEPT BIOL SCI,INTRACELLULAR BIOPHYS LAB,GRAND CENT & UTOPIA PKWY,JAMAICA,NY 11439, USA. FU NIGMS NIH HHS [GM44390] NR 43 TC 43 Z9 43 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD AUG PY 1992 VL 13 IS 2 BP 238 EP 246 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JH645 UT WOS:A1992JH64500019 PM 1382465 ER PT J AU DUBOIS, CM RUSCETTI, FW JACOBSEN, SEW OPPENHEIM, JJ KELLER, JR AF DUBOIS, CM RUSCETTI, FW JACOBSEN, SEW OPPENHEIM, JJ KELLER, JR TI HEMATOPOIETIC GROWTH-FACTORS UP-REGULATE THE P65 TYPE-II INTERLEUKIN-1 RECEPTOR ON BONE-MARROW PROGENITOR CELLS-INVITRO SO BLOOD LA English DT Article ID COLONY-STIMULATING FACTOR; IL-1 RECEPTOR; CYTOKINE RECEPTORS; INVIVO; MURINE; MICE; FIBROBLASTS; EXPRESSION; MODULATION; GRANULOPOIESIS C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP INC,PROGRAM RESOURCES,FREDERICK,MD 21702. NCI,BIOL RESPONSE MODIFIERS PROGRAM,IMMUNOREGULAT LAB,FREDERICK,MD 21701. FU NCI NIH HHS [N01-CO-74102] NR 48 TC 18 Z9 18 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 AUG 1 PY 1992 VL 80 IS 3 BP 600 EP 608 PG 9 WC Hematology SC Hematology GA JF855 UT WOS:A1992JF85500006 PM 1379082 ER PT J AU MURPHY, WJ KELLER, JR HARRISON, CL YOUNG, HA LONGO, DL AF MURPHY, WJ KELLER, JR HARRISON, CL YOUNG, HA LONGO, DL TI INTERLEUKIN-2-ACTIVATED NATURAL-KILLER-CELLS CAN SUPPORT HEMATOPOIESIS INVITRO AND PROMOTE MARROW ENGRAFTMENT INVIVO SO BLOOD LA English DT Article ID RECEPTOR GENES; REJECTION; MICE; TRANSPLANTATION; SUBSET C1 NCI,FREDERICK CANC RES & DEV CTR,DYNCORP INC,PROGRAM RESOURCES,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. RP MURPHY, WJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,BLDG 567,ROOM 141,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 24 TC 74 Z9 77 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 AUG 1 PY 1992 VL 80 IS 3 BP 670 EP 677 PG 8 WC Hematology SC Hematology GA JF855 UT WOS:A1992JF85500014 PM 1379086 ER PT J AU JACOBSEN, SEW RUSCETTI, FW DUBOIS, CM WINE, J KELLER, JR AF JACOBSEN, SEW RUSCETTI, FW DUBOIS, CM WINE, J KELLER, JR TI INDUCTION OF COLONY-STIMULATING FACTOR RECEPTOR EXPRESSION ON HEMATOPOIETIC PROGENITOR CELLS - PROPOSED MECHANISM FOR GROWTH-FACTOR SYNERGISM SO BLOOD LA English DT Article ID MURINE SARCOMA-CELLS; FACTOR-BETA; STEM-CELLS; BINDING; PROLIFERATION; DIFFERENTIATION; HEMOPOIETIN-1; INTERLEUKIN-6; SYSTEM; LINES C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DYNCORP INC,PROGRAM RESOURCES,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. FU NCI NIH HHS [N01-CO-74102] NR 39 TC 32 Z9 32 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 AUG 1 PY 1992 VL 80 IS 3 BP 678 EP 687 PG 10 WC Hematology SC Hematology GA JF855 UT WOS:A1992JF85500015 PM 1379087 ER PT J AU PANG, YB NORIHISA, Y BENJAMIN, D KANTOR, RRS YOUNG, HA AF PANG, YB NORIHISA, Y BENJAMIN, D KANTOR, RRS YOUNG, HA TI INTERFERON-GAMMA GENE-EXPRESSION IN HUMAN B-CELL LINES - INDUCTION BY INTERLEUKIN-2, PROTEIN-KINASE-C ACTIVATORS, AND POSSIBLE EFFECT OF HYPOMETHYLATION ON GENE-REGULATION SO BLOOD LA English DT Article ID LARGE GRANULAR LYMPHOCYTES; IMMUNE INTERFERON; DNA METHYLATION; HUMAN THYMOCYTES; GENOMIC DNA; IFN-GAMMA; LYMPHOMA; IMMUNOGLOBULIN; REARRANGEMENT; AUGMENTATION C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,BLDG 560,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. OHIO STATE UNIV,ARTHUR G JAMES CANC INST,DIV HEMATOL & ONCOL,COLUMBUS,OH 43210. FU NCI NIH HHS [N01-CO-74102]; NIAID NIH HHS [R01-AI-31262] NR 41 TC 65 Z9 66 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 AUG 1 PY 1992 VL 80 IS 3 BP 724 EP 732 PG 9 WC Hematology SC Hematology GA JF855 UT WOS:A1992JF85500020 PM 1322203 ER PT J AU YANO, T JAFFE, ES LONGO, DL RAFFELD, M AF YANO, T JAFFE, ES LONGO, DL RAFFELD, M TI MYC REARRANGEMENTS IN HISTOLOGICALLY PROGRESSED FOLLICULAR LYMPHOMAS SO BLOOD LA English DT Article ID NON-HODGKINS-LYMPHOMA; EPSTEIN-BARR-VIRUS; B-CELL LEUKEMIA; C-MYC; CHROMOSOME-TRANSLOCATION; GENOMIC REARRANGEMENT; IMMUNOGLOBULIN GENES; CYTOGENETIC ANALYSIS; MALIGNANT-LYMPHOMAS; MOLECULAR ANALYSIS C1 NCI,DIAG & CTR,DIV CANC BIOL,PATHOL LAB,HEMATOPATHOL SECT,BLDG 10,BETHESDA,MD 20892. NCI,FREDERICK CANC RES & DEV CTR,DIV CANC TREATMENT,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD. NR 66 TC 189 Z9 190 U1 1 U2 4 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 AUG 1 PY 1992 VL 80 IS 3 BP 758 EP 767 PG 10 WC Hematology SC Hematology GA JF855 UT WOS:A1992JF85500025 PM 1638027 ER PT J AU PASCUALLEONE, A VALLSSOLE, J WASSERMANN, EM BRASILNETO, J COHEN, LG HALLETT, M AF PASCUALLEONE, A VALLSSOLE, J WASSERMANN, EM BRASILNETO, J COHEN, LG HALLETT, M TI EFFECTS OF FOCAL TRANSCRANIAL MAGNETIC STIMULATION ON SIMPLE REACTION-TIME TO ACOUSTIC, VISUAL AND SOMATOSENSORY STIMULI SO BRAIN LA English DT Article ID VOLUNTARY MOVEMENT; PRECENTRAL CORTEX; NEURONAL-ACTIVITY; MOTOR AREAS; MONKEY; FACILITATION; ENHANCEMENT; POTENTIALS; PREMOTOR; HUMANS AB In a simple reaction time (RT) paradigm, magnetic stimulation of different intensities was delivered over different scalp positions and at variable delays before (negative) or after (positive) the go-signal. Magnetic stimulation shortened RT to different go-signals (auditory, visual and somatosensory stimuli) by approximately 30 ms when delivered over the motor cortex contralateral to the responding arm at intensities below motor threshold. This effect was maximal at a delay of approximately + 10 ms. A similar effect was found with suprathreshold stimulation to the ipsilateral motor cortex. Magnetic stimulation over other scalp areas did not affect RT regardless of the delay. No differences were found between the effects on elbow flexion and thumb abduction. The shortening of RT was not associated with changes in the timing development of premovement excitability increase in the motor cortex. We conclude that magnetic stimulation shortens RT by inducing an earlier initiation of this excitability increase. C1 NINCDS,MED NEUROL BRANCH,HUMAN CORT PHYSIOL UNIT,HUMAN MOTOR CONTROL SECT,BLDG 10,BETHESDA,MD 20892. RI Brasil-Neto, Joaquim/A-1171-2009 NR 37 TC 122 Z9 124 U1 1 U2 6 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 AUG PY 1992 VL 115 BP 1045 EP 1059 DI 10.1093/brain/115.4.1045 PN 4 PG 15 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA JR003 UT WOS:A1992JR00300006 PM 1393501 ER PT J AU CHOU, SP PICKERING, RP AF CHOU, SP PICKERING, RP TI EARLY ONSET OF DRINKING AS A RISK FACTOR FOR LIFETIME ALCOHOL-RELATED PROBLEMS SO BRITISH JOURNAL OF ADDICTION LA English DT Article ID AGE AB Heavy drinking among students has been a major public health concern over the past decade. A nationally representative 1988 survey on drinking practices and related problems examined the effect of age of onset of drinking on lifetime alcohol-related problems. Prevalence estimates were obtained for major demographic subgroups of the population. Results and implications are discussed in the context of minimum legal drinking age. RP CHOU, SP (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,5600 FISHERS LANE,ROOM 14C-26,ROCKVILLE,MD 20857, USA. NR 8 TC 117 Z9 119 U1 0 U2 6 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0952-0481 J9 BRIT J ADDICT PD AUG PY 1992 VL 87 IS 8 BP 1199 EP 1204 PG 6 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA JG538 UT WOS:A1992JG53800012 PM 1511233 ER PT J AU UHLEN, S XIA, Y CHHAJLANI, V FELDER, CC WIKBERG, JES AF UHLEN, S XIA, Y CHHAJLANI, V FELDER, CC WIKBERG, JES TI [H-3] MK-912 BINDING DELINEATES 2 ALPHA-2-ADRENOCEPTOR SUBTYPES IN RAT CNS ONE OF WHICH IS IDENTICAL WITH THE CLONED PA2D ALPHA-2-ADRENOCEPTOR SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE ALPHA-ADRENOCEPTOR SUBTYPES; CEREBRAL CORTEX; SPINAL CORD; ALPHA-2-ADRENOCEPTOR GENE EXPRESSION; RECEPTOR CLASSIFICATION; [H-3]-MK-912 LIGAND BINDING; COMPUTER MODELING ID ALPHA-2 ADRENERGIC-RECEPTORS; CEREBRAL-CORTEX; MOLECULAR CHARACTERIZATION; ANTAGONIST BINDING; HUMAN-PLATELETS; OPOSSUM KIDNEY; SPINAL-CORD; GUINEA-PIG; CELL-LINE; OK CELL AB 1 Simultaneous computer modelling of control and guanfacine-masked [H-3]-MK 912 saturation curves as well as guanfacine competition curves revealed that the drugs bound to two alpha-2-adrenoceptor subtypes in the rat cerebral cortex with very different selectivities. These alpha-2-adrenoceptor subtypes were designated alpha-2A and alpha-2C. The K(d) value of [H-3]-MK 912 for the alpha-2A-subtype was 1.77 nm and for the alpha-2C-subtype 0.075 nm; the receptor sites showing capacities 296 and 33 fmol mg-1 protein, respectively. The K(d)s of guanfacine were 19.9 and 344 nm, respectively. 2 Binding constants of 26 compounds for the two rat cerebral cortex alpha-2-adrenoceptor subtypes were determined by simultaneous computer modelling of control and guanfacine-masked drug competition curves as well as plain guanfacine competition curves using [H-3]-MK912 as labelled ligand (i.e. a '3-curve assay'). Of the tested drugs WB4101, corynanthine, rauwolscine, yohimbine, ARC 239 and prazosin were found to be clearly alpha-2C-selective with selectivities ranging from 16 to 30 fold whereas guanfacine, oxymetazoline, BRL 44408 and BRL 41992 were found to be alpha-2A-selective with selectivities ranging from 9 to 22 fold. 3 The K(d)s of compounds obtained for the cerebral cortex alpha-2C-adrenoceptors showed an almost 1:1 correlation with the corresponding K(d)s for alpha-2-adrenoceptors expressed by the pA2d-gene (the rat 'alpha-2-C4' adrenoceptor) in CHO-cells. The cerebral cortex alpha-2A-adrenoceptors did not correlate well with the pA2d alpha-2-adrenoceptor K(d)s. 4 In the rat spinal cord [H-3]-MK 912 bound to alpha-2A- and alpha-2C-adrenoceptor sites with similar affinities as in the cerebral cortex and with densities 172 a. id 7.4 fmol mg-1 protein, respectively. Drug affinities for some compounds showing major selectivity for alpha-2A- and alpha-2C-adrenoceptors were fully compatible with the notion that the spinal cord sites were alpha-2A- and alpha-2C-adrenoceptors. C1 NIMH,DEPT HLTH & HUMAN SERV,BETHESDA,MD 20892. RP UHLEN, S (reprint author), UMEA UNIV,DEPT PHARMACOL,S-90187 UMEA,SWEDEN. NR 38 TC 102 Z9 102 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD AUG PY 1992 VL 106 IS 4 BP 986 EP 995 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JG088 UT WOS:A1992JG08800040 PM 1356570 ER PT J AU CASH, JM WILDER, RL AF CASH, JM WILDER, RL TI NEUROBIOLOGY AND INFLAMMATORY ARTHRITIS SO BULLETIN ON THE RHEUMATIC DISEASES LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; LEWIS RATS; CORTICOSTEROIDS RP CASH, JM (reprint author), NIH,BETHESDA,MD 20892, USA. NR 11 TC 12 Z9 12 U1 0 U2 0 PU ARTHRITIS FOUNDATION PI ATLANTA PA 1314 SPRING STREET NW, ATLANTA, GA 30309 SN 0007-5248 J9 B RHEUM DIS JI Bull. Rheum. Dis. PD AUG PY 1992 VL 41 IS 5 BP 1 EP 3 PG 3 WC Rheumatology SC Rheumatology GA JJ605 UT WOS:A1992JJ60500001 PM 1291026 ER PT J AU JANOV, AJ ANDERSON, J CELLA, DF ZUCKERMAN, E KORNBLITH, AB HOLLAND, JC KANTOR, AF LI, FP AF JANOV, AJ ANDERSON, J CELLA, DF ZUCKERMAN, E KORNBLITH, AB HOLLAND, JC KANTOR, AF LI, FP TI PREGNANCY OUTCOME IN SURVIVORS OF ADVANCED HODGKIN DISEASE SO CANCER LA English DT Article DE HODGKIN DISEASE; PREGNANCY OUTCOME; SURVIVORS; LATE EFFECTS ID TERM FOLLOW-UP; OVARIAN-FUNCTION; WILMS TUMOR; COMBINATION CHEMOTHERAPY; GONADAL-FUNCTION; CANCER; WOMEN; CHILDHOOD; RADIATION; LEUKEMIA AB Background. Pregnancy outcome was reported by 139 survivors of advanced Hodgkin disease treated on nine protocols of Cancer and Leukemia Group B from 1966 to 1986. Methods. These patients provided data on 302 singleton pregnancies of a duration of at least 20 weeks that occurred before, during, or after treatment for Hodgkin disease (252, 26, and 24 pregnancies, respectively). Results. There were 4 perinatal deaths, as compared with 5.7 expected. Cancer subsequently developed in 2 offspring (expected, 1.2). However, 22 newborn infants had low a birth weight, exceeding the expected number of 13.7 (relative risk 1.6; 95% confidence interval, 1.0-2.4). The excess number of low weight births occurred primarily during the period of Hodgkin disease diagnosis and treatment but is based on small numbers. Conclusion. No increase in adverse outcome occurred in pregnancies that antedated the development of Hodgkin disease. C1 NCI,CLIN EPIDEMIOL BRANCH,CLIN STUDIES SECT,BETHESDA,MD 20892. UNIV NEBRASKA,MED CTR,CALGB BIOSTAT CTR,OMAHA,NE 68105. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. RP JANOV, AJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,ROOM M3A28,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA31946] NR 36 TC 8 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD AUG 1 PY 1992 VL 70 IS 3 BP 688 EP 692 DI 10.1002/1097-0142(19920801)70:3<688::AID-CNCR2820700325>3.0.CO;2-V PG 5 WC Oncology SC Oncology GA JF196 UT WOS:A1992JF19600022 PM 1623485 ER PT J AU WAUD, WR PLOWMAN, J HARRISON, SD DYKES, DJ ANDERSON, WK GRISWOLD, DP AF WAUD, WR PLOWMAN, J HARRISON, SD DYKES, DJ ANDERSON, WK GRISWOLD, DP TI ANTITUMOR-ACTIVITY AND CROSS-RESISTANCE OF CARMETHIZOLE HYDROCHLORIDE IN PRECLINICAL MODELS IN MICE SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE CARMETHIZOLE; ANTITUMOR ACTIVITY; CROSS-RESISTANCE ID CELL-LINES; AGENT CARMETHIZOLE; P388 LEUKEMIA; L1210 CELLS; ADRIAMYCIN; INVITRO; CANCER; INVIVO AB Carmethizole hydrochloride [1-methyl-2-methylthio-4,5-bis(hydroxymethyl)imidazole-4', 5'-bis(N-methylcarbamate)hydrochloride, NSC 602668; hereafter called carmethizole] is a new antitumor drug that has shown relatively broad activity in initial evaluations against several murine tumors and human tumor xenografts in vivo. The present studies were designed to address questions about carmethizole's activity against established disease, its activity on different treatment schedules, and the extent of its cross-resistance with established drugs. Human MX-1 mammary carcinoma, human NCI-H82 small-cell lung carcinoma, and human LOX amelanotic melanoma xenografts in athymic mice were used to determine the drug's activity against established disease; the NCI-H82 lung-tumor xenograft in athymic mice was used to explore its schedule dependence; and a series of drug-resistant murine leukemias provided an in vivo cross-resistance profile. When injected i.p., carmethizole exhibited antitumor activity against advanced-stage s.c. MX-1 mammary, s.c. NCI-H82 lung, and i.p. LOX melanoma xenografts and was as effective against established disease (MX-1 and LOX) as it was against early-stage disease (no data are available for early-stage NCI-H82). The therapeutic effect of carmethizole was not route-dependent, as was evidenced by the similar delays observed in tumor growth following i.p. and i.v. administration. The use of a splitdose schedule on a single day instead of one bolus injection yielded an increase in the total dose delivered, resulting in an increased delay in tumor growth. Murine leukemias resistant to vincristine (VCR), amsacrine (AMSA), or methotrexate (MTX) were not cross-resistant to carmethizole. However, murine leukemias resistant to doxorubicin (ADR), melphalan (L-PAM), cisplatin (DDPt), l-beta-D-arabinofuranosylcytosine (ara-C), and 5-fluorouracil (5-FU) were cross-resistant to carmethizole, suggesting that patients who have previously been treated with any of these agents might be less likely to respond to carmethizole than those who have had no opportunity to develop resistance to any of these compounds. We anticipate that the information derived from these studies may be useful in the design of clinical trails of carmethizole and may stimulate additional basic research on the mechanism of action of this new agent. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. SUNY BUFFALO,SCH PHARM,FACHBEREICH MED CHEM,BUFFALO,NY 14260. RP WAUD, WR (reprint author), SO RES INST,BIRMINGHAM,AL 35255, USA. FU NCI NIH HHS [N01-CM-07315] NR 20 TC 6 Z9 6 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD AUG PY 1992 VL 30 IS 4 BP 261 EP 266 DI 10.1007/BF00686292 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA JF451 UT WOS:A1992JF45100002 PM 1322803 ER PT J AU BAILEY, H WILDING, G TUTSCH, KD ARZOOMANIAN, RZ ALBERTI, D TOMBES, MB GREM, JL SPRIGGS, DR AF BAILEY, H WILDING, G TUTSCH, KD ARZOOMANIAN, RZ ALBERTI, D TOMBES, MB GREM, JL SPRIGGS, DR TI A PHASE-I TRIAL OF 5-FLUOROURACIL, LEUCOVORIN, AND DIPYRIDAMOLE GIVEN BY CONCURRENT 120-H CONTINUOUS INFUSIONS SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE 5-FLUOROURACIL; LEUCOVORIN; DIPYRIDAMOLE; CONTINUOUS INFUSION ID COLON CANCER-CELLS; THYMIDYLATE SYNTHETASE; NUCLEOSIDE SALVAGE; COLORECTAL-CANCER; CYTO-TOXICITY; FOLINIC ACID; CHEMOTHERAPY; FLUOROURACIL; INHIBITION; DERIVATIVES AB A phase I trial of 5-fluorouracil (FUra) and leucovorin (LV) given with and without dipyridamole (DP) by concurrent 120-h continuous infusion was performed in 27 patients with advanced solid malignancies, 8 of whom had previously received FUra. The LV and DP doses were fixed at 500 mg/m2 daily and 7.7 mg/kg daily, respectively, whereas the FUra dose was escalated. Level 3 (450 mg/m2 FUra daily) represented the maximum tolerated dose for both FUra/LV + DP and FUra/LV. Dose-limiting stomatitis (greater-than-or-equal-to grade 3 or grade 2 occurring during the infusion) was encountered in 75% of the first courses given at level 4 (600 mg/m2 daily). Stomatitis was observed in 44/78 (56%) courses. Diarrhea was infrequent and mild. DP infusions were complicated by mild to moderate headache, which was controlled with narcotic analgesics, and mild to moderate nausea/vomiting. FUra-related toxicity was not enhanced by DP administration. Limited pharmacokinetic sampling at levels 3 and 4 revealed mean steady-state FUra concentrations of around 1.0-mu-M with infusions of FUra/LV + DP. Among three paired courses given with and without DP, no statistically significant difference was found in the total body clearance of FUra (P = 0.44). One partial response was seen in a patient with metastatic gastric carcinoma. For phase II trials, we recommend that concurrent 120-h continuous infusions of FUra (450 mg/m2 daily) and LV (500 mg/m2 daily) be given with and without DP (7.7 mg/kg daily) every 21 days. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. NCI,BETHESDA,MD 20892. RP BAILEY, H (reprint author), UNIV WISCONSIN,CTR CLIN CANC,K4-666,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [N01-CM-07306, N01-CM-57735]; NCRR NIH HHS [MO1 RR03186] NR 27 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD AUG PY 1992 VL 30 IS 4 BP 297 EP 302 DI 10.1007/BF00686299 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA JF451 UT WOS:A1992JF45100009 PM 1643698 ER PT J AU DAMIA, G KOMSCHLIES, KL FUTAMI, H BACK, T GRUYS, ME LONGO, DL KELLER, JR RUSCETTI, FW WILTROUT, RH AF DAMIA, G KOMSCHLIES, KL FUTAMI, H BACK, T GRUYS, ME LONGO, DL KELLER, JR RUSCETTI, FW WILTROUT, RH TI PREVENTION OF ACUTE CHEMOTHERAPY-INDUCED DEATH IN MICE BY RECOMBINANT HUMAN INTERLEUKIN-1 - PROTECTION FROM HEMATOLOGICAL AND NONHEMATOLOGICAL TOXICITIES SO CANCER RESEARCH LA English DT Article ID TUMOR NECROSIS FACTOR; COLONY-STIMULATING FACTOR; HEMATOPOIETIC PROGENITOR CELLS; FACTOR-ALPHA; 5-FLUOROURACIL TREATMENT; INVIVO; RESISTANCE; INFECTIONS; INDUCTION; ENDOTOXIN AB Previous studies have demonstrated that interleukin 1 (IL-1) can protect most mice from the acute lethal toxicity mediated by high doses of radiation and/or some chemotherapeutic drugs. The results presented herein demonstrate that the pretreatment of mice with recombinant human interleukin 1-alpha (rhIL-1-alpha) protects mice from the lethal effects of several myelotoxic chemotherapeutic drugs, including 5-fluorouracil (5FUra), cyclophosphamide, cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II), and 1,3-bis-(2-chloroethyl)-1-nitrosourea. However, pretreatment with rhIL-1-alpha was not effective against the acute lethal toxicity generated by doxorubicin and cisplatin. The chemoprotective effects appear to be at least partially due to myeloprotection/restoration, since the recovery of myeloid colony-forming units and the total cellularity in the bone marrow and spleen were accelerated in the rhIL-1-alpha-pretreated mice. However, the chemoprotective effects of rhIL-1-alpha are apparently not limited to myeloprotection, since pretreatment with rhIL-1-alpha protects mice against the lethal toxicity of both 5FUra and cyclophosphamide, yet bone marrow transplants rescue mice treated with 5FUra but not those treated with cyclophosphamide. The chemoprotective effects of rhIL-1-alpha may be at least partially indirect, since the efficacy of chemoprotection by rhIL-1-alpha is reduced in athymic mice, and interleukin 6, but not tumor necrosis factor-alpha, can substitute for rhIL-1-alpha in chemoprotection from 5FUra. C1 NCI,FREDERICK CANC RES & DEV CTR,EXPTL IMMUNOL LAB,BLDG 560,ROOM 31-93,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,PRI DYNCORP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74102] NR 52 TC 25 Z9 25 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 AUG 1 PY 1992 VL 52 IS 15 BP 4082 EP 4089 PG 8 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600003 PM 1638519 ER PT J AU GREENBERG, AS NORDAN, RP MCINTOSH, J CALVO, JC SCOW, RO JABLONS, D AF GREENBERG, AS NORDAN, RP MCINTOSH, J CALVO, JC SCOW, RO JABLONS, D TI INTERLEUKIN 6 REDUCES LIPOPROTEIN-LIPASE ACTIVITY IN ADIPOSE-TISSUE OF MICE INVIVO AND IN 3T3-L1 ADIPOCYTES - A POSSIBLE ROLE FOR INTERLEUKIN-6 IN CANCER CACHEXIA SO CANCER RESEARCH LA English DT Article ID TUMOR NECROSIS FACTOR; HYBRIDOMA GROWTH-FACTOR; HEPATIC LIPASE; BEARING MICE; SERUM LEVELS; CELL-GROWTH; INFECTION; CACHECTIN; PLASMA; INDUCTION AB To investigate whether interleukin 6 (IL-6) might be a potential mediator of the depleted fat reserves observed in malignancy-associated cachexia, we measured lipoprotein lipase (LPL) activity in adipose tissue of mice after administration of IL-6 or tumor necrosis factor and in cultured adipocytes after addition of these cytokines. Injection of IL-6 i.p. reduced adipose tissue LPL activity by 53% within 4.5 to 5.5 h. Injection of tumor necrosis factor elevated serum IL-6 levels and reduced adipose tissue LPL activity by 70%. Both human and murine IL-6 reduced heparin-releasable LPL activity in 3T3-L1 adipocytes in a dose-dependent manner; half-maximal inhibition of LPL activity was achieved with 5000 hybridoma growth factor units/ml. Thus, IL-6 reduces adipose LPL activity and may contribute to the loss of body fat stores associated with some cases of cancer cachexia. Since tumor necrosis factor increases circulating IL-6, some of its effects may be mediated or potentiated by IL-6. C1 NCI,GENET LAB,BETHESDA,MD 20892. NCI,SURG BRANCH,BETHESDA,MD 20892. NICHHD,THEORET & PHYS BIOL LAB,BETHESDA,MD 20892. RP GREENBERG, AS (reprint author), NIDDKD,CELLULAR & DEV BIOL LAB,BLDG 6,RM B1-13,BETHESDA,MD 20892, USA. NR 41 TC 218 Z9 225 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 AUG 1 PY 1992 VL 52 IS 15 BP 4113 EP 4116 PG 4 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600008 PM 1638523 ER PT J AU WINTER, SF MINNA, JD JOHNSON, BE TAKAHASHI, T GAZDAR, AF CARBONE, DP AF WINTER, SF MINNA, JD JOHNSON, BE TAKAHASHI, T GAZDAR, AF CARBONE, DP TI DEVELOPMENT OF ANTIBODIES AGAINST P53 IN LUNG-CANCER PATIENTS APPEARS TO BE DEPENDENT ON THE TYPE OF P53 MUTATION SO CANCER RESEARCH LA English DT Article ID CLASS-II REGION; CELLULAR PROTEIN P53; FREE DEFINED MEDIUM; ELECTROPHORETIC TRANSFER; CIRCULATING ANTIBODIES; SV40-TRANSFORMED CELLS; POLYACRYLAMIDE GELS; CLINICAL SPECIMENS; ONCOGENE PRODUCT; GENE AB Using immunoblotting techniques we studied the sera from small cell lung cancer and non-small cell lung cancer patients for antibodies directed against p53. We have also characterized the majority of these patients' tumors for p53 mutations. In the sera of 13% of the patients (4 of 40 small cell lung cancer and 2 of 6 non-small cell lung cancer) we found antibodies specific for the p53 tumor suppressor gene product. All of the antibody-positive patients tested had p53 missense mutations and expressed detectable p53 antigen in their tumor cell lines. No anti-p53 antibodies were detected in sera from patients whose tumor had p53 stop, splice/stop, splice, or frameshift mutations (n = 10). Thus, while we find that the ability of lung cancer patients to develop anti-p53 antibodies is correlated with the type of p53 mutation, many patients have tumors with missense p53 mutations and did not develop anti-p53 antibodies. The presence of p53 antibodies was not correlated to stage, prior treatment, sex, or survival. None of these lung cancer patient sera had measurable amounts of p53 antigen. By immunoblotting all six anti-p53 antisera we were able to detect a variety of mutant p53 proteins (including those from antibody-negative patients) and detected wild-type p53 protein. The development of anti-p53 antibodies represents an interesting model system for studying immune responses in cancer patients against mutant oncogene products. C1 UNIV TEXAS,SW MED CTR,SIMMONS CANC CTR,5323 HARRY HINES BLVD,DALLAS,TX 75235. NCI,USN,MED ONCOL BRANCH,BETHESDA,MD 20889. RI Takahashi, Takashi/I-7262-2014 NR 35 TC 317 Z9 323 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 AUG 1 PY 1992 VL 52 IS 15 BP 4168 EP 4174 PG 7 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600017 PM 1322237 ER PT J AU SNYDERWINE, EG BOHR, VA AF SNYDERWINE, EG BOHR, VA TI GENE-SPECIFIC AND STRAND-SPECIFIC DAMAGE AND REPAIR IN CHINESE-HAMSTER OVARY CELLS TREATED WITH 4-NITROQUINOLINE 1-OXIDE SO CANCER RESEARCH LA English DT Article ID DIHYDROFOLATE-REDUCTASE GENE; PREFERENTIAL DNA-REPAIR; ALKALI-LABILE SITES; XERODERMA PIGMENTOSUM-CELLS; PYRIMIDINE DIMERS; ESCHERICHIA-COLI; EXCISION REPAIR; ACTIVE GENE; DHFR GENE; ADDUCTS AB 4-Nitroquinoline 1-oxide (4NQO) is a model chemical carcinogen that has often been referred to as a UV mimetic agent. Previous studies have indicated that UV-induced pyrimidine dimers are repaired preferentially and strand-specifically in actively transcribing genes. In the current study we have examined the gene-specific and strand-specific repair of 4NQO in Chinese hamster ovary B-11 cells treated with 2.5-mu-M 4NQO. The methodology used for detecting adducts involved the treatment of DNA from 4NQO-exposed cells with uvrABC excinuclease, which incises DNA at adduct sites, followed by denaturing gel electrophoresis of DNA, Southern hybridization, and probing for the sequence of interest. We examined the active and inactive coding regions of the DHFR gene, the active adenine phosphoribosyltransferase gene, relatively inactive c-fos oncogene, and the mitochondrial genome for 4NQO adducts. Initial 4NQO adduct levels found in these genes varied from 1.10 to 1.52 adducts/10 kilobases. Little difference in repair was found between active coding and inactive regions of the DHFR gene, or between DHFR, adenine phosphoribosyltransferase, and c-fos genes, which are transcribed at different levels. Approximately 71% of 4NQO adducts were repaired within 24 h in all gene sequences examined. During this same time period, approximately 51% of adducts were repaired from the genome overall, as determined by comparing the removal of bound radiolabeled 4NQO to total DNA. The results indicate that 4NQO adducts, unlike UV light-induced cyclobutane pyrimidine dimers (UV dimers), are not preferentially repaired in transcriptionally active genes. However, there may be regions of the genome that are not repaired with the same efficiency as the specific genes examined here. In addition, little to no difference was observed in the repair of 4NQO adducts in the transcribed and nontranscribed strands of the DHFR gene, a finding which is also in contrast to results with UV dimers. Interestingly, 4NQO adducts, unlike UV dimers, were removed from the mitochondrial genome, suggesting that repair of select lesions occurs in this organelle. Thus, there appear to be some differences in the repair pathways operating for 4NQO adducts and UV dimers, particularly with respect to gene- and strand-specific DNA repair. C1 NCI,DIV CANC TREATMENT,BETHESDA,MD 20892. RP SNYDERWINE, EG (reprint author), NCI,DIV CANC ETIOL,EXPTL CARCINOGENISIS LAB,BLDG 37,ROOM 3C28,BETHESDA,MD 20892, USA. NR 42 TC 63 Z9 65 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 AUG 1 PY 1992 VL 52 IS 15 BP 4183 EP 4189 PG 7 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600019 PM 1638532 ER PT J AU YAGINUMA, Y WESTPHAL, H AF YAGINUMA, Y WESTPHAL, H TI ABNORMAL STRUCTURE AND EXPRESSION OF THE P53 GENE IN HUMAN OVARIAN-CARCINOMA CELL-LINES SO CANCER RESEARCH LA English DT Article ID TUMOR SUPPRESSOR GENES; MUTANT P53; CANCER; MUTATIONS; FREQUENT; ONCOGENE; OCCUR AB In an effort to analyze molecular mechanisms of human ovarian carcinogenesis, we studied the structure and expression of the p53 gene in different cell lines established from human ovarian carcinomas. In all six lines (PA-1, Caov-3 and -4, OVCAR-3, SK-OV-3, and Kuramochi), p53 abnormalities were detected. In the SK-OV-3 cell line, Southern analysis suggested the presence of sequence deletions/rearrangements in at least one allele of the p53 gene, and transcripts were not detectable by either Northern or polymerase chain reaction analysis. Sequence analysis of the entire coding region of the p53 gene revealed point mutations resulting in codon changes of a highly conserved region of the protein in four cell lines, Caov-3 and -4, OVCAR-3, and Kuramochi. In the Caov-3 cell line, the point mutation resulted in chain termination at codon 136. Quantitation of p53 protein by immunoprecipitation analysis revealed a 6-fold higher than control cell level in PA-1. By contrast, p53 protein was not detectable in lines Caov-3 and SK-OV-3. We conclude that altered levels of p53 gene expression and/or mutant forms of the p53 gene product are associated with all human ovarian cancer cells tested. RP YAGINUMA, Y (reprint author), NICHHD,MAMMALIAN GENES & DEV LAB,BETHESDA,MD 20892, USA. NR 35 TC 182 Z9 188 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD AUG 1 PY 1992 VL 52 IS 15 BP 4196 EP 4199 PG 4 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600021 PM 1638534 ER PT J AU BUTTA, A MACLENNAN, K FLANDERS, KC SACKS, NPM SMITH, I MCKINNA, A DOWSETT, M WAKEFIELD, LM SPORN, MB BAUM, M COLLETTA, AA AF BUTTA, A MACLENNAN, K FLANDERS, KC SACKS, NPM SMITH, I MCKINNA, A DOWSETT, M WAKEFIELD, LM SPORN, MB BAUM, M COLLETTA, AA TI INDUCTION OF TRANSFORMING GROWTH FACTOR-BETA(1) IN HUMAN BREAST-CANCER INVIVO FOLLOWING TAMOXIFEN TREATMENT SO CANCER RESEARCH LA English DT Note ID ESTROGEN-RECEPTOR; FACTOR-BETA; ANTIESTROGENS; LOCALIZATION; ANTIBODIES; BINDING; CELLS AB We have investigated the ability of tamoxifen to regulate members of the transforming growth factor-beta (TGF-beta) family in human breast cancers in vivo. Using immunohistochemical techniques, we find that 3 months of tamoxifen treatment causes a consistent induction of extracellular TGF-beta-1 in breast cancer biopsies, compared with matched pretreatment samples from the same patient. The induced TGF-beta is localized between and around stromal fibroblasts and appears to be derived from these cells. Lower levels of TGF-beta-1,-beta-2, and -beta-3 seen in epithelial cells were not altered by tamoxifen treatment. The increased stromal staining of TGF-beta-1 occurred in estrogen receptor-negative as well as estrogen receptor-positive tumors. These results provide in vivo evidence for a novel, estrogen receptor-independent mechanism of action for tamoxifen, involving the stromal induction of a potent growth inhibitor for epithelial cells. C1 ROYAL MARSDEN HOSP,INST CANC RES,HARTWELL LAB,ACAD SURG SECT,FULHAM RD,LONDON SW3 6JJ,ENGLAND. INST CANC RES,DEPT HISTOPATHOL,LONDON SW3 6JJ,ENGLAND. INST CANC RES,DEPT MED,LONDON SW3 6JJ,ENGLAND. INST CANC RES,DEPT SURG,LONDON SW3 6JJ,ENGLAND. INST CANC RES,DEPT BIOCHEM,LONDON SW3 6JJ,ENGLAND. NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. NR 24 TC 329 Z9 338 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 AUG 1 PY 1992 VL 52 IS 15 BP 4261 EP 4264 PG 4 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600031 PM 1322240 ER PT J AU BHATIA, KG GUTIERREZ, MI HUPPI, K SIWARSKI, D MAGRATH, IT AF BHATIA, KG GUTIERREZ, MI HUPPI, K SIWARSKI, D MAGRATH, IT TI THE PATTERN OF P53 MUTATIONS IN BURKITTS-LYMPHOMA DIFFERS FROM THAT OF SOLID TUMORS SO CANCER RESEARCH LA English DT Note ID WILD-TYPE; GENE; ASSOCIATION; EXPRESSION; CANCER AB Available evidence suggests that, among hematological malignancies, p53 is most often mutated in Burkitt's lymphoma (BL). However, much of the published data is based on cell lines. We have, therefore, analyzed BL biopsies to determine more accurately the frequency and pattern of p53 mutations in primary tumors and to determine whether there are differences among the various subtypes of BL. Among 27 BL biopsies from South America, we have observed mutations in the p53 gene (exons 5 through 8) in 37% of tumors. The higher frequency of mutations in cell lines (70%) suggests that mutation of p53 may be associated with tumor progression. Summarizing available data we conclude that the presence of mutated p53 in BL is independent of the geographic origin of the tumor, the 8;14 chromosomal breakpoint locations and Epstein-Barr virus association. We also find that the mutational spectrum of p53 in BL differs from that observed in nonlymphoid tumors. More than 50% of mutations in BL are clustered in a small stretch of 33 amino acids (codons 213 to 248). Interestingly, codon 213 appears to be as frequently mutated as codon 248. Conversely, codon 273, often mutated in solid tumors, is rarely involved in BL. C1 NCI,GENET LAB,MOLEC GENET SECT,BETHESDA,MD 20892. RP BHATIA, KG (reprint author), NCI,CLIN ONCOL PROGRAM,PEDIAT BRANCH,BLDG 10,ROOM 13N240,BETHESDA,MD 20892, USA. NR 21 TC 101 Z9 102 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 AUG 1 PY 1992 VL 52 IS 15 BP 4273 EP 4276 PG 4 WC Oncology SC Oncology GA JF746 UT WOS:A1992JF74600034 PM 1638540 ER PT J AU DIWAN, BA KASPRZAK, KS RICE, JM AF DIWAN, BA KASPRZAK, KS RICE, JM TI TRANSPLACENTAL CARCINOGENIC EFFECTS OF NICKEL(II) ACETATE IN THE RENAL-CORTEX, RENAL PELVIS AND ADENOHYPOPHYSIS IN F344/NCR RATS SO CARCINOGENESIS LA English DT Article ID ETHYL-N-HYDROXYETHYLNITROSAMINE; DNA-SYNTHESIS; BARBITAL SODIUM; CELL TUMORS; TOXICITY; KIDNEY; PROLIFERATION; INITIATION; PROMOTION; CHLORIDE AB Nickel(II) acetate (NiAcet), a soluble nickel salt known to be an effective initiator of renal epithelial tumors in adult rats, was studied for possible transplacental carcinogenicity. Pregnant F344/NCr rats were given NiAcet i.p. either once a day on day 17 (90-mu-mol/kg body wt; group 1) or twice on days 16 and 18 of gestation (45-mu-mol/kg body wt/day; group 2). Offspring of these rats were further subdivided into groups 1A and B and 2A and B, respectively. Groups 1A and 2A received ordinary tap water while groups 1B and 2B received drinking water containing 500 p.p.m. sodium barbital (NaBB) during weeks 4 - 85 of age. Renal cortical epithelial and renal pelvic transitional epithelial tumors occurred in male offspring given NiAcet prenatally followed by NaBB postnatally (group 1B, 15 tumors in 8/15 rats; group 2B, 10 tumors in 7/15), but not in male offspring given NiAcet only (0/32) or in controls given prenatal sodium acetate (NaAcet) only (0/15) and rarely in males given NaAcet followed by the promoter NaBB (1/15). No renal tumors occurred in females. Pituitary tumor incidence was significantly higher in offspring of both sexes given NiAcet prenatally (NaAcet controls, 4/31, both sexes combined; group 1A, 14/33, P = 0.012; group 2A, 14/31, P = 0.008). Pituitary tumors appeared much earlier in rats given NiAcet prenatally, with or without postnatal NaBB, and often were malignant by cytologic and histologic criteria including pleomorphism and invasion of adjacent structures, unlike the well-differentiated adenomas that occurred less frequently in untreated rats. These results are the first evidence that Ni(II) is a potent transplacental initiator of epithelial tumors in fetal rat kidney and a complete transplacental carcinogen for rat pituitary. C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. RP DIWAN, BA (reprint author), PRI DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74102] NR 46 TC 32 Z9 32 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 AUG PY 1992 VL 13 IS 8 BP 1351 EP 1357 DI 10.1093/carcin/13.8.1351 PG 7 WC Oncology SC Oncology GA JH652 UT WOS:A1992JH65200009 PM 1499087 ER PT J AU GABRIELSON, EW VANDERMEEREN, A REDDEL, RR REDDEL, H GERWIN, BI HARRIS, CC AF GABRIELSON, EW VANDERMEEREN, A REDDEL, RR REDDEL, H GERWIN, BI HARRIS, CC TI HUMAN MESOTHELIOMA CELLS AND ASBESTOS-EXPOSED MESOTHELIAL CELLS ARE SELECTIVELY RESISTANT TO AMOSITE TOXICITY - A POSSIBLE MECHANISM FOR TUMOR PROMOTION BY ASBESTOS SO CARCINOGENESIS LA English DT Article ID BRONCHIAL EPITHELIAL-CELLS; TRANSFORMING GROWTH-FACTOR; MINERAL FIBERS; DNA-SYNTHESIS; FACTOR-BETA; 12-O-TETRADECANOYLPHORBOL-13-ACETATE; CARCINOGENESIS; INDUCTION; DISEASE; SERUM AB To determine if asbestos exposure could contribute to mesothelial cell carcinogenesis by selection and/or expansion of an initiated cell population, we compared normal human pleural mesothelial cells to either human mesothelioma cell lines or mesothelial cells transfected with cancer-related genes for sensitivity to amosite fibers in vitro. Neither normal nor mesothelioma cells were directly stimulated to replicate or increase DNA synthesis by any of the asbestos exposure conditions tested. The potential selective effect of asbestos exposure was demonstrated by a differential sensitivity of normal mesothelial cells and mesothelioma cells to amosite: for example, up to 20-fold higher concentrations of amosite fibers were required to inhibit replication of mesothelioma cell lines than normal mesothelial cells. In addition, a significant resistance (4-fold) to amosite toxicity was observed for SV40 immortalized mesothelial cell lines that had previously been selected in vitro for resistance to asbestos. SV40 immortalized cells that have become tumorigenic after transfection with either Ha-ras or PDGF A-chain genes were not significantly more resistant to the cytotoxic effects of amosite than primary normal cells, and the primary cells were equally sensitive to amosite as mesothelial cells that were only immortalized by SV40. The sensitivity of normal mesothelial cells to asbestos does not appear to be simply a result of general fragility of the mesothelial cells, since similar levels of hydrogen peroxide and silica were cytotoxic for normal mesothelial cells and mesothelioma cell lines. Because mesothelioma cells have a greater resistance to asbestos cytotoxicity than normal mesothelial cells, we hypothesize that a differential resistance to cell killing by asbestos fibers in vivo may result in a selective expansion of an initiated or transformed cell population and thus contribute to the carcinogenesis process. Since tumorigenicity and asbestos resistance occur independently of one another in genetically altered mesothelial cell lines, genotypic and phenotypic alterations that lead to tumorigenic conversion may not be the same changes that provide resistance to cell killing by asbestos. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. NCI,DIV CANC ETIOL,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. RI Reddel, Roger/A-6635-2014 OI Reddel, Roger/0000-0002-6302-6107 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 AUG PY 1992 VL 13 IS 8 BP 1359 EP 1363 DI 10.1093/carcin/13.8.1359 PG 5 WC Oncology SC Oncology GA JH652 UT WOS:A1992JH65200010 PM 1323425 ER PT J AU DRAGAN, YP XU, XH GOLDSWORTHY, TL CAMPBELL, HA MARONPOT, RR PITOT, HC AF DRAGAN, YP XU, XH GOLDSWORTHY, TL CAMPBELL, HA MARONPOT, RR PITOT, HC TI CHARACTERIZATION OF THE PROMOTION OF ALTERED HEPATIC FOCI BY 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN IN THE FEMALE RAT SO CARCINOGENESIS LA English DT Article ID TISSUE DISTRIBUTION; TUMOR PROMOTION; "2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; QUANTITATIVE STEREOLOGY; HYPERPLASTIC NODULES; PHENOTYPIC STABILITY; LIVER; HEPATOCARCINOGENESIS; INDUCTION; DIETHYLNITROSAMINE AB Previous studies have suggested that 2,3,7,8-tetrachlorodi-benzo-p-dioxin (TCDD) acts as a promoting agent in various organ systems including the rat liver. Since a major characteristic of the stage of tumor promotion is its operational reversibility, we have assessed whether TCDD-induced promotion is reversible in a two-stage model of hepatocarcinogenesis. In this model, female Fischer F344 rats were administered a single, intragastric dose of the initiating agent, diethylnitrosamine (DEN, 10 mg/kg), at the peak of proliferation induced by a partial hepatectomy. TCDD was then administered biweekly (0. 14-mu-g/kg, s.c.) for 1, 3 or 5 months. One group of animals was killed at each of these time points, while a second group was maintained for each time point for an additional 6 months in the absence of further TCDD. Four serial frozen sections of liver were each stained with a different enzyme marker of altered hepatic foci (AHF). The AHF were identified and the number and volume fraction determined by quantitative stereology. Exposure to TCDD resulted in an increase in the number and size of AHF in the initiated relative to the uninitiated rats. Increasing the duration of promotion with TCDD led to an increase in the number of AHF per liver, the volume fraction of the liver occupied by AHF and the number of markers expressed aberrantly by a single AHF. Discontinuation of TCDD administration for 6 months before killing the animals resulted in a decrease in the total number of AHF observed, but those AHF that remained increased in size with an overall increase in volume fraction of AHF. Analysis of the size class distribution for AHF for each of the periods of TCDD promotion revealed an increase in the larger AHF but a decrease in the smaller, thereby resulting in an overall decrease in number of AHF with an increase in the volume fraction of AHF. Increasing the duration of the TCDD exposure prior to its withdrawal led to an increased AHF size, phenotypic complexity and number of AHF remaining after cessation of TCDD administration. Although the levels of TCDD in livers of rats 6 months after cessation of TCDD administration were still greater than background, they were markedly reduced compared to immediately after administration. Thus, cessation of exposure to TCDD after a brief duration led to a reversal of its promotional effects on the majority of AHF, while prolonged exposure led to maintained promotion of a minority of AHF. C1 NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. CHEM IND INST TOXICOL,RES TRIANGLE PK,NC 27709. RP DRAGAN, YP (reprint author), UNIV WISCONSIN,MCARDLE LAB CANC RES,MADISON,WI 53706, USA. FU NCI NIH HHS [CA-07175, CA-45700, CA-22484] NR 69 TC 36 Z9 36 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 AUG PY 1992 VL 13 IS 8 BP 1389 EP 1395 DI 10.1093/carcin/13.8.1389 PG 7 WC Oncology SC Oncology GA JH652 UT WOS:A1992JH65200015 PM 1354083 ER PT J AU VANNELLI, GB BARNI, T FORTI, G NEGROVILAR, A VALE, W SERIO, M BALBONI, GC AF VANNELLI, GB BARNI, T FORTI, G NEGROVILAR, A VALE, W SERIO, M BALBONI, GC TI IMMUNOLOCALIZATION OF INHIBIN ALPHA-SUBUNIT IN THE HUMAN TESTIS - A LIGHT-MICROSCOPY AND ELECTRON-MICROSCOPY STUDY SO CELL AND TISSUE RESEARCH LA English DT Article DE TESTIS; INHIBIN; INHIBIN SUBUNITS; SERTOLI CELLS; GERM CELLS; LEYDIG CELLS; HUMAN ID FOLLICLE-STIMULATING-HORMONE; SERTOLI CELLS; SEMINIFEROUS TUBULES; NORMAL MEN; MALE-RATS; SECRETION; FSH; EXPRESSION; PROTEINS; CULTURES AB The localization of inhibin alpha-subunit in the human testis was studied at the light- and electron-microscope level with immunostaining techniques. Antibodies against specific fragments of porcine and human inhibin-alpha-subunits were utilized. At light microscopy, inhibin-alpha-subunit immunoreactivity was detected in Sertoli cells, spermatocytes and in some Leydig cells. At electron microscopy, gold labeling was found in the cisternae of the Golgi apparatus and in the endoplasmic reticulum of Sertoli and Leydig cells. Gold labeling for inhibin was also found in coated vesicles in the cytoplasm of Sertoli cells as well as in coated pits and coated vesicles in the cytoplasm of some spermatocytes. The results of the present study suggest that, in the human testis, inhibin is produced by Sertoli and Leydig cells and is taken up by spermatocytes, on which it might act in a paracrine manner. C1 UNIV FLORENCE,DEPT CLIN PHYSIOPATHOL,ENDOCRINOL UNIT,VIALE MORGAGNI 85,I-50134 FLORENCE,ITALY. UNIV FLORENCE,DEPT HUMAN ANAT & HISTOL,I-50121 FLORENCE,ITALY. NATL INST GERIATR STUDIES,INRCA,FLORENCE,ITALY. NIEHS,MOLEC & INTEGRAT NEUROSCI LAB,RES TRIANGLE PK,NC 27709. SALK INST BIOL STUDIES,CLAYTON FDN LABS PEPTIDE BIOL,LA JOLLA,CA 92037. NR 29 TC 19 Z9 19 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 AUG PY 1992 VL 269 IS 2 BP 221 EP 227 DI 10.1007/BF00319612 PG 7 WC Cell Biology SC Cell Biology GA JD537 UT WOS:A1992JD53700005 PM 1423490 ER PT J AU KUIJPERS, GAJ LEE, G POLLARD, HB AF KUIJPERS, GAJ LEE, G POLLARD, HB TI IMMUNOLOCALIZATION OF SYNEXIN (ANNEXIN-VII) IN ADRENAL CHROMAFFIN GRANULES AND CHROMAFFIN CELLS - EVIDENCE FOR A DYNAMIC ROLE IN THE SECRETORY PROCESS SO CELL AND TISSUE RESEARCH LA English DT Article DE CHROMAFFIN CELL; SECRETION; SYNEXIN; ANNEXINS; MEMBRANE FUSION; CA-2+-BINDING PROTEINS; BOVINE ID INDUCED MEMBRANE-FUSION; FACTOR RECEPTOR-KINASE; BINDING PROTEINS; PHOSPHOLIPID-BINDING; LIPOCORTIN-I; CALCIUM; EXOCYTOSIS; CALPACTIN; PHOSPHORYLATION; SECTIONS AB Synexin (annexin VII) is a Ca2+- and phospholipid-binding protein which has been proposed to play a role in Ca2+-dependent membrane fusion processes. Using a monoclonal antibody against synexin, Mab 10E7, and immunogold, we carried out a semiquantitative localization study of synexin in bovine adrenal medullary chromaffin granules, and in resting and nicotine-stimulated adrenal chromaffin cells. Isolated chromaffin granules contained very little synexin, whereas chromaffin granules aggregated with synexin (24-mu-g/mg) and Ca2+ (1 mM) clearly showed synexin-associated immunogold particles in the vicinity of the granule membrane (1.88 gold particles per granule profile). In isolated, cultured adrenal chromaffin cells, synexin was present in the nucleus (5.5 particles/mu-m2) and in the cytosol (5.3 particles/mu-m2), but mainly around the granule membrane in the granular cell area (11.7 particles/mu-m2). During the active phase of cholinergically stimulated catecholamine secretion, the amount of synexin label was reduced by 33% in the nucleus, by 23% in the cytosol, and by 51% in the granule area. The plasma membrane contained a small amount of synexin, which did not significantly change upon stimulation of the cells. We conclude that synexin is involved in the secretory process in chromaffin cells. RP KUIJPERS, GAJ (reprint author), NIDDKD,CELL BIOL & GENET LAB,BETHESDA,MD 20892, USA. NR 39 TC 29 Z9 29 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 AUG PY 1992 VL 269 IS 2 BP 323 EP 330 DI 10.1007/BF00319624 PG 8 WC Cell Biology SC Cell Biology GA JD537 UT WOS:A1992JD53700017 PM 1423500 ER PT J AU MILLER, MW HANOVER, JA AF MILLER, MW HANOVER, JA TI REGULATION OF MACROMOLECULAR TRAFFIC MEDIATED BY THE NUCLEAR-PORE COMPLEX SO CELL BIOLOGY INTERNATIONAL REPORTS LA English DT Article ID CELL-FREE SYSTEM; MESSENGER-RNA; INTERPHASE NUCLEI; 3-DIMENSIONAL DISTRIBUTION; TRANSPORT; ENVELOPE; PROTEIN; TRANSLOCATION; RECONSTITUTION; INVITRO RP MILLER, MW (reprint author), NIDDK,BIOCHEM & METAB LAB,BETHESDA,MD 20892, USA. NR 50 TC 1 Z9 1 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0309-1651 J9 CELL BIOL INT REP PD AUG PY 1992 VL 16 IS 8 BP 791 EP 798 DI 10.1016/S0309-1651(05)80022-0 PG 8 WC Cell Biology SC Cell Biology GA JK763 UT WOS:A1992JK76300011 PM 1280187 ER PT J AU RYBAK, SM HOOGENBOOM, HR NEWTON, DL RAUS, JCM YOULE, RJ AF RYBAK, SM HOOGENBOOM, HR NEWTON, DL RAUS, JCM YOULE, RJ TI RATIONAL IMMUNOTHERAPY WITH RIBONUCLEASE CHIMERAS - AN APPROACH TOWARD HUMANIZING IMMUNOTOXINS SO CELL BIOPHYSICS LA English DT Proceedings Paper CT 8th International Hammersmith Meeting on Advances in the Applications of Monoclonal Antibodies in Clinical Oncology CY MAY 04-06, 1992 CL PORTO CARRAS, GREECE DE RIBONUCLEASES; IMMUNOTOXINS; CANCER; IMMUNOTHERAPY RP RYBAK, SM (reprint author), NCI,BIOCHEM PHYSIOL,FREDERICK,MD 21702, USA. NR 0 TC 12 Z9 12 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA TOTOWA SN 0163-4992 J9 CELL BIOPHYS JI Cell Biophys. PD AUG-DEC PY 1992 VL 21 IS 1-3 BP 121 EP 138 PG 18 WC Biophysics; Cell Biology SC Biophysics; Cell Biology GA MM033 UT WOS:A1992MM03300012 PM 1285324 ER PT J AU PRASAD, GL VALVERIUS, EM MCDUFFIE, E COOPER, HL AF PRASAD, GL VALVERIUS, EM MCDUFFIE, E COOPER, HL TI COMPLEMENTARY-DNA CLONING OF A NOVEL EPITHELIAL-CELL MARKER PROTEIN, HME1, THAT MAY BE DOWN-REGULATED IN NEOPLASTIC MAMMARY CELLS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID EGF RECEPTOR HOMOLOG; 14-3-3 PROTEIN; MEMBRANE ANTIGEN; EXPRESSION; PURIFICATION; TYROSINE; SEQUENCE; GROWTH; BRAIN; LINE AB A full-length complementary DNA clone from a normal human mammary epithelial cell (strain 184) encoding a 25-kilodalton protein, HME1, was isolated. Expression of HME1 RNA appears to be limited to epithelial cells. The HME1 sequence has extensive sequence homology with bovine 14-3-3 protein, which is an activator of tyrosine and tryptophan hydroxylase. However, the tissue distribution, arrangement of charged amino acids, and location of potential phosphorylation sites of HME1 differ from those of 14-3-3. Compared with normal mammary epithelial cells, expression of HME1 RNA was dramatically low in two cell lines derived from human mammary carcinoma that were examined, and in a line of normal mammary epithelial cells transformed by oncogenes. HME1 therefore appears to be a cellular differentiation marker that may be down-regulated during neoplastic transformation. RP PRASAD, GL (reprint author), NCI,TUMOR IMMUNOL & BIOL LAB,CELL & MOLEC PHYSIOL SECT,BETHESDA,MD 20892, USA. NR 22 TC 141 Z9 147 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 AUG PY 1992 VL 3 IS 8 BP 507 EP 513 PG 7 WC Cell Biology SC Cell Biology GA JH381 UT WOS:A1992JH38100004 PM 1390337 ER PT J AU LICHY, JH MODI, WS SEUANEZ, HN HOWLEY, PM AF LICHY, JH MODI, WS SEUANEZ, HN HOWLEY, PM TI IDENTIFICATION OF A HUMAN CHROMOSOME-11 GENE WHICH IS DIFFERENTIALLY REGULATED IN TUMORIGENIC AND NONTUMORIGENIC SOMATIC-CELL HYBRIDS OF HELA-CELLS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID WILD-TYPE P53; SUPPRESSES TUMORIGENICITY; EXPRESSION; TRANSFORMATION; GROWTH; DNA; PHENOTYPES; MALIGNANCY; CANCER AB The tumorigenicity of HeLa cells in nude mice can be suppressed by the addition of a normal human chromosome 11 in somatic cell hybrids. We have attempted to identify specific genes involved in this phenomenon by transfecting a complementary DNA expression library into a tumorigenic HeLa-fibroblast hybrid. A cell line designated F2 was isolated which displayed morphological features of the nontumorigenic hybrids demonstrated reduced tumorigenicity in nude mice, and showed an 85% reduction in alkaline phosphatase, a consistent marker of the tumorigenic phenotype in these cells. F2 contained a single exogenous complementary DNA, which was recovered by polymerase chain reaction and designated HTS1 because of its potential association with "HeLa tumor suppression." Northern blot studies suggested differential regulation of the HTS1 gene dependent on the tumorigenicity of the cell. In nontumorigenic hybrids, RNA species of 2.8, 3.1, and 4.6 kilobases were identified. In two tumorigenic hybrid lines, the 2.8-kilobase species was markedly reduced or absent. Similarly, three nontumorigenic human keratinocyte lines expressed all three RNA species, whereas several tumorigenic cervical carcinoma cell lines lacked the 2.8-kilobase species. Chromosome localization studies mapped the HTS1 gene to chromosome 11p15, a region of chromosome 11 that is believed to contain a tumor suppressor gene. These findings indicate that HTS1 represents a novel chromosome 11 gene which may be a target of the tumor suppressor gene active in this system. C1 NCI,FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. RP LICHY, JH (reprint author), NCI,TUMOR VIRUS BIOL LAB,BETHESDA,MD 20892, USA. NR 37 TC 31 Z9 33 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 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD AUG PY 1992 VL 3 IS 8 BP 541 EP 548 PG 8 WC Cell Biology SC Cell Biology GA JH381 UT WOS:A1992JH38100008 PM 1390339 ER PT J AU JETTEN, AM BERNACKI, SH FLOYD, EE SAUNDERS, NA PIENIAZEK, J LOTAN, R AF JETTEN, AM BERNACKI, SH FLOYD, EE SAUNDERS, NA PIENIAZEK, J LOTAN, R TI EXPRESSION OF A PREPRORELAXIN-LIKE GENE DURING SQUAMOUS DIFFERENTIATION OF RABBIT TRACHEOBRONCHIAL EPITHELIAL-CELLS AND ITS SUPPRESSION BY RETINOIC ACID SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID MESSENGER-RNA LEVELS; HUMAN RELAXIN; PORCINE RELAXIN; INVITRO; RECEPTOR; BINDING; SECRETION; HOMOLOGY; SEQUENCE; CLONING AB Squamous cell differentiation in tracheobronchial epithelial cells is accompanied by many biochemical and molecular changes. One of the molecular changes in rabbit tracheal epithelial (RbTE) cells is the differential expression of a squamous cell-specific mRNA encoded by the complementary DNA SQ10. In this study, we sequenced SQIO complementary DNA and showed that this gene encodes a preprorelaxin-like protein. The DNA sequence of the coding region of SQIO has 68% identity with the human preprorelaxin mRNA, whereas the deduced amino acid sequence exhibits 46% identity with human preprorelaxin. An antiserum (pepIV-Ab) was raised against a synthetic 22-amino acid oligopeptide of the protein encoded by SQ10. Immunoblot analysis of cellular extracts of squamous-differentiated cells showed that this antiserum reacted with proteins of 22 and 20 kilodaltons, possibly constituting prepro- and pro-forms of this protein. These proteins were undetectable in undifferentiated RbTE cells. In agreement with these observations, PepIV-Ab specifically stained the cytosol of squamous-differentiated RbTE cells but failed to stain undifferentiated cells. PepIV-Ab recognized a 20 and 16 kilodalton polypeptide in medium conditioned by squamous-differentiated RbTE cells, indicating that the prorelaxin-like protein is secreted. The amino acid sequences of three peptides that were obtained after tryptic digestion of the secreted 16 kilodalton protein were identical to sequences encoded by SQ10. Retinoids which have been shown to inhibit squamous differentiation suppressed the induction of SQ10 protein as well as mRNA in a concentration-dependent manner. The concentration at which retinoic acid caused a 50% inhibition of SQ10 mRNA levels was approximately 5 nm. The analogue Ch55 was about 100-fold more effective than retinoic acid and exhibited a 50% effective concentration of about 50 pM. Retinoic acid treatment did not significantly alter the stability of the MRNA encoded by SQ10. Our study identifies a preprorelaxin-like protein as a new marker for squamous cell differentiation and suggests a role for this hormone in this differentiation process. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DEPT TUMOR BIOL,HOUSTON,TX 77030. RP JETTEN, AM (reprint author), NIEHS,PULM PATHOBIOL LAB,CELL BIOL SECT,RES TRIANGLE PK,NC 27709, USA. RI saunders, nicholas/E-1544-2014; McTaggart, Jill/G-4696-2010; OI saunders, nicholas/0000-0002-2478-3420; McTaggart, Jill/0000-0002-9000-8529; Jetten, Anton/0000-0003-0954-4445 FU NCI NIH HHS [CA 16672] NR 45 TC 23 Z9 24 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 AUG PY 1992 VL 3 IS 8 BP 549 EP 556 PG 8 WC Cell Biology SC Cell Biology GA JH381 UT WOS:A1992JH38100009 PM 1339318 ER PT J AU TSANG, WK MIZUGUCHI, J ISHIDA, Y WATSON, C CHUSED, T INMAN, J MARGULIES, DH PAUL, WE AF TSANG, WK MIZUGUCHI, J ISHIDA, Y WATSON, C CHUSED, T INMAN, J MARGULIES, DH PAUL, WE TI FAILURE OF SIGNALING THROUGH A CHIMERIC CLASS I-IMMUNOGLOBULIN MOLECULE EXPRESSED ON THE SURFACE OF TRANSFECTED B-LYMPHOMA CELLS AND CELLS OF TRANSGENIC MICE SO CELLULAR IMMUNOLOGY LA English DT Article ID PROTEIN TYROSINE PHOSPHORYLATION; ANTIGEN RECEPTOR COMPLEX; MURINE LYMPHOCYTES-B; HISTOCOMPATIBILITY ANTIGEN; TRANSPLANTATION ANTIGENS; NUCLEOTIDE-SEQUENCE; PHORBOL ESTER; CROSS-LINKING; KINASE-C; MU-CHAIN C1 NIAID,IMMUNOL LAB,9000 ROCKVILLE PIKE,BLDG 10,ROOM 11N311,BETHESDA,MD 20892. NATL INST HLTH,DEPT IMMUNOL,SHINAGAWA KU,TOKYO 141,JAPAN. RI Margulies, David/H-7089-2013; OI Margulies, David/0000-0001-8530-7375 NR 56 TC 1 Z9 1 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 AUG PY 1992 VL 143 IS 1 BP 80 EP 96 DI 10.1016/0008-8749(92)90007-C PG 17 WC Cell Biology; Immunology SC Cell Biology; Immunology GA JD666 UT WOS:A1992JD66600007 PM 1623567 ER PT J AU BORNSTEIN, MH TAMISLEMONDA, CS TAL, J LUDEMANN, P TODA, S RAHN, CW PECHEUX, MG AZUMA, H VARDI, D AF BORNSTEIN, MH TAMISLEMONDA, CS TAL, J LUDEMANN, P TODA, S RAHN, CW PECHEUX, MG AZUMA, H VARDI, D TI MATERNAL RESPONSIVENESS TO INFANTS IN 3 SOCIETIES - THE UNITED-STATES, FRANCE, AND JAPAN SO CHILD DEVELOPMENT LA English DT Article ID TO-FACE INTERACTION; MOTHER-INFANT; PSYCHOLOGY; PERFORMANCE; BEHAVIOR; CULTURE; COMMUNICATION; STABILITY; CHILD; HOME AB This study examines and compares prominent characteristics of maternal responsiveness to infant activity during home-based naturalistic interactions of mother-infant dyads in New York City, Paris, and Tokyo. Both culture-general and culture-specific patterns of responsiveness emerged. For example, in all 3 locales infants behaved similarly, mothers also behaved similarly with respect to a hierarchy of response types, and mothers and infants manifest both specificity and mutual appropriateness in their interactions: Mothers responded to infants' exploration of the environment with encouragement to the environment, to infants' vocalizing nondistress with imitation, and to infants' vocalizing distress with nurturance. Differences in maternal responsiveness among cultures occurred to infant looking rather than to infant vocalizing and in mothers' emphasizing dyadic versus extradyadic loci of interaction. Universals of maternal responsiveness, potential sources of cultural variation, and implications of similarities and differences in responsiveness for child development in different cultural contexts are discussed. C1 UNIV TOKYO,TOKYO 113,JAPAN. CNRS,F-75005 PARIS,FRANCE. NYU,NEW YORK,NY 10003. SHIRAYURI COLL,CHOFU,JAPAN. UNIV PARIS 05,F-75270 PARIS 06,FRANCE. RP BORNSTEIN, MH (reprint author), NICHHD,BLDG 31,ROOM B2B15,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. FU NICHD NIH HHS [HD00521, HD20559, HD20807] NR 85 TC 113 Z9 115 U1 4 U2 13 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0009-3920 J9 CHILD DEV JI Child Dev. PD AUG PY 1992 VL 63 IS 4 BP 808 EP 821 DI 10.2307/1131235 PG 14 WC Psychology, Educational; Psychology, Developmental SC Psychology GA JH266 UT WOS:A1992JH26600005 PM 1505242 ER PT J AU EPSTEIN, ND COHN, GM CYRAN, F FANANAPAZIR, L AF EPSTEIN, ND COHN, GM CYRAN, F FANANAPAZIR, L TI DIFFERENCES IN CLINICAL EXPRESSION OF HYPERTROPHIC CARDIOMYOPATHY ASSOCIATED WITH 2 DISTINCT MUTATIONS IN THE BETA-MYOSIN HEAVY-CHAIN GENE - A 908LEU-]VAL MUTATION AND A 403ARG-]GLN MUTATION SO CIRCULATION LA English DT Article DE CARDIOMYOPATHY, HYPERTROPHIC; BETA-MYOSIN HEAVY CHAIN GENE MUTATIONS ID MOLECULAR-BASIS; COMPLETE SEQUENCE; DNA AB Background. The disease gene for hypertrophic cardiomyopathy (HCM) has been identified as the beta-myosin heavy chain (beta-MHC) gene in some HCM families. We describe extensive clinical evaluations in two kindreds with two distinct point mutations in the beta-MHC gene. Methods and Results. We used single-strand confirmation polymorphism (SSCP) gel analysis of polymerase chain reaction-amplified products capturing each of the 40 beta-MHC gene exons to identify distinct missense mutations in two HCM kindreds. Clinical, ECG, and echocardiographic studies were performed in the two kindreds: kindred 2755 with amino acid 908(Leu-->Val) mutation and kindred 2002 with amino acid 403(Arg-->Gln) mutation. The morphological appearances of HCM were similar in these two kindreds. However, the two kindreds differed with respect to disease penetrance, age of onset of disease, and incidence of premature sudden death. Twelve of 31 adults (greater-than-or-equal-to 17 years) with the disease gene in kindred 2755 did not have left ventricular hypertrophy (LVH), and only five of these had ECG abnormalities. Thus, the disease penetrance in adults with this mutation was only 61%. None of 11 children aged < 16 years had LVH. The 908 mutation was associated with a low incidence of cardiac events: Only two sudden deaths and one syncope occurred in 46 individuals with the mutant allele. In contrast, LVH was present in all 11 adults in kindred 2002 with the 403 mutation (100% disease penetrance). In addition, three of four affected children were symptomatic and had clinical evidence of HCM. The disease in this kindred was severe and resulted in six premature sudden deaths. Seven additional patients had syncope or presyncope. Conclusions. In some kindreds, the HCM disease gene is more prevalent than indicated by echocardiography and ECG. Some point mutations may be associated with a more malignant prognosis. Preclinical identification of children with mutations associated with a high incidence of sudden death and syncope provides the opportunity to evaluate efficacy of early therapeutic interventions. C1 NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892. RP EPSTEIN, ND (reprint author), NHLBI,CLIN HEMATOL BRANCH,ROOM 7C-103,BLDG 10,BETHESDA,MD 20892, USA. NR 18 TC 190 Z9 200 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD AUG PY 1992 VL 86 IS 2 BP 345 EP 352 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA JH009 UT WOS:A1992JH00900001 PM 1638703 ER PT J AU KONSTAM, MA ROUSSEAU, MF KRONENBERG, MW UDELSON, JE MELIN, J STEWART, D DOLAN, N EDENS, TR AHN, S KINAN, D HOWE, DM KILCOYNE, L METHERALL, J BENEDICT, C YUSUF, S POULEUR, H AF KONSTAM, MA ROUSSEAU, MF KRONENBERG, MW UDELSON, JE MELIN, J STEWART, D DOLAN, N EDENS, TR AHN, S KINAN, D HOWE, DM KILCOYNE, L METHERALL, J BENEDICT, C YUSUF, S POULEUR, H TI EFFECTS OF THE ANGIOTENSIN CONVERTING-ENZYME-INHIBITOR ENALAPRIL ON THE LONG-TERM PROGRESSION OF LEFT-VENTRICULAR DYSFUNCTION IN PATIENTS WITH HEART-FAILURE SO CIRCULATION LA English DT Article DE VASODILATION; VENTRICULAR FUNCTION; CARDIOMYOPATHIES; EJECTION FRACTION ID IDIOPATHIC DILATED CARDIOMYOPATHY; ACUTE MYOCARDIAL-INFARCTION; CAPTOPRIL THERAPY; CONTROLLED TRIAL; NATURAL-HISTORY; DOUBLE-BLIND; DISEASE; RATS; DILATATION; STIFFNESS AB Background. In patients with heart failure, activation of the renin-angiotensin system is common an has been postulated to provide a stimulus for further left ventricular (LV) structural and functional derangement. We tested the hypothesis that chronic administration of the angiotensin converting enzyme (ACE) inhibitor enalapril prevents or reverses LV dilatation and systolic dysfunction among patients with depressed ejection fraction (EF) and symptomatic heart failure. Methods and Results. We examined subsets of patients enrolled in the Treatment Trial of Studies of Left Ventricular Dysfunction (SOLVD). Fifty-six patients with mild to moderate heart failure underwent serial radionuclide ventriculograms, and 16 underwent serial left heart catheterizations, before and after randomization to enalapril (2.5-20 mg/day) or placebo. At 1 year, there were significant treatment differences in LV end-diastolic volume (EDV; p<0.01), end-systolic volume (ESV; p<0.005), and EF (p<0.05). These effects resulted from increases in EDV (mean +/- SD, 136+/-27 to 151+/-38 ml/m2) and ESV (103+/-24 to 116+/-24 ml/m2) in the placebo group and decreases in EDV (140+/-44 to 127+/-37 ml/m2) and ESV (106+/-42 to 93+/-37 ml/m2) in the enalapril group. Mean LVEF increased in enalapril patients from 0.25+/-0.07 to 0.29+/-0.08 (p<0.01). There was a significant treatment difference in LV end-diastolic pressure at 1 year (p<0.05), with changes paralleling those of EDV. The time constant of LV relaxation changed only in the placebo group (p<0.01 versus enalapril), increasing from 59.2+/-8.0 to 67.8+/-7.2 msec. Serial radionuclide studies over a period of 33 months showed increases in LV volumes only in the placebo group. Two weeks after withdrawal of enalapril, EDV and ESV increased to baseline levels but not to the higher levels observed with placebo. Conclusions. In patients with heart failure and reduced LVEF, chronic ACE inhibition with enalapril prevents progressive LV dilatation and systolic dysfunction (increased ESV). These effects probably result from a combination of altered remodeling and sustained reduction in preload and afterload. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT MED,NASHVILLE,TN 37232. VANDERBILT UNIV,MED CTR,SCH MED,DEPT RADIOL,NASHVILLE,TN 37232. UNIV TEXAS,HLTH SCI CTR,DEPT MED,HOUSTON,TX 77225. NHLBI,CLIN TRIALS BRANCH,BETHESDA,MD 20892. TUFTS UNIV,NEW ENGLAND MED CTR,DEPT RADIOL,BOSTON,MA 02111. CATHOLIC UNIV LOUVAIN,SCH MED,DIV CARDIOL,B-1200 BRUSSELS,BELGIUM. CATHOLIC UNIV LOUVAIN,SCH MED,DIV NUCL MED,B-1200 BRUSSELS,BELGIUM. UNIV N CAROLINA,DEPT BIOSTAT,CTR COLLABORAT STUDIES,CHAPEL HILL,NC 27514. RP KONSTAM, MA (reprint author), TUFTS UNIV,NEW ENGLAND MED CTR,DEPT MED,BOX 108,750 WASHINGTON ST,BOSTON,MA 02111, USA. FU NHLBI NIH HHS [N01-HC55010] NR 38 TC 335 Z9 345 U1 1 U2 5 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD AUG PY 1992 VL 86 IS 2 BP 431 EP 438 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA JH009 UT WOS:A1992JH00900011 PM 1638712 ER PT J AU SPEIR, E EPSTEIN, SE AF SPEIR, E EPSTEIN, SE TI INHIBITION OF SMOOTH-MUSCLE CELL-PROLIFERATION BY AN ANTISENSE OLIGODEOXYNUCLEOTIDE TARGETING THE MESSENGER-RNA ENCODING PROLIFERATING CELL NUCLEAR ANTIGEN SO CIRCULATION LA English DT Article DE PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY; RESTENOSIS ID FIBROBLAST GROWTH-FACTOR; PROTEIN CYCLIN; PCNA CYCLIN; FACTOR-I; EXPRESSION; DNA; ATHEROSCLEROSIS; INDUCTION; RECEPTORS; AORTA AB Background. The process by which normally quiescent vascular smooth muscle cells (SMCs) change into proliferating cells, which express and respond to multiple growth factors, plays a major role in restenosis after coronary angioplasty. We are attempting to inhibit SMC proliferation by interventions that inhibit specific factors involved in signal transduction pathways leading to cell division. To date, all studies taking this approach have attempted to block the effects of mitogens acting on the cell surface. In contrast, we have focused on a strategy that bypasses cell surface-mediated events by directly inhibiting the expression of proliferating cell nuclear antigen (PCNA), an intranuclear protein that functions in a final common pathway shared by diverse mitogen-induced signals. In the present investigation, we determined whether antisense oligodeoxynucleotides (ODNs) complementary to the messenger RNA of PCNA will inhibit PCNA expression and thereby reduce SMC proliferation. Methods and Results. When antisense ODNs (15- or 18-mer), modified to inhibit their degradation, are introduced into the medium of rat aortic SMCs in concentrations ranging from 10 to 100-mu-M, the 18-mer ODN, in a concentration-related manner, decreases SMC growth (as assessed by cell counting) by more than 50%. This effect persists for at least 9 days. An ODN with the same nucleotides but a scrambled sequence has little effect. Western blots and immunocytochemistry indicate that the antisense ODN reduces expression of PCNA protein. Conclusions. Our results demonstrate that an antisense ODN directed at the messenger RNA of PCNA decreases expression of the PCNA gene product and reduces SMC proliferation. In addition, these results provide an important impetus to initiating in vivo studies to determine the feasibility of antisense strategies in the prevention of coronary restenosis. RP SPEIR, E (reprint author), NHLBI,CARDIOL BRANCH,BETHESDA,MD 20892, USA. NR 25 TC 97 Z9 105 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD AUG PY 1992 VL 86 IS 2 BP 538 EP 547 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA JH009 UT WOS:A1992JH00900024 PM 1353419 ER PT J AU SPEIR, E TANNER, V GONZALEZ, AM FARRIS, J BAIRD, A CASSCELLS, W AF SPEIR, E TANNER, V GONZALEZ, AM FARRIS, J BAIRD, A CASSCELLS, W TI ACIDIC AND BASIC FIBROBLAST GROWTH-FACTORS IN ADULT-RAT HEART MYOCYTES - LOCALIZATION, REGULATION IN CULTURE, AND EFFECTS ON DNA-SYNTHESIS SO CIRCULATION RESEARCH LA English DT Article DE HEART-DERIVED FIBROBLAST GROWTH FACTORS; TISSUE; CARDIOCYTES; NUCLEAR FIBROBLAST GROWTH FACTORS; POSTMITOTIC CELLS; FIBROBLAST GROWTH FACTOR RECEPTORS ID CARDIAC-MUSCLE-CELLS; TERMINAL DIFFERENTIATION; EXTRACELLULAR-MATRIX; SURVIVAL; BOVINE; PROTEIN; NUCLEI; FORMS AB Basic fibroblast growth factor (bFGF) and acidic fibroblast growth factor (aFGF) are involved in the induction of embryonic mesoderm, angiogenesis, neuronal differentiation, and proliferation and survival of many cell types. In cardiac myocytes their roles are not well understood. Effects of fibroblast growth factors on reexpression of fetal actin genes have been reported. In freshly isolated adult rat cardiac myocytes, bFGF mRNA was not detectable by in situ hybridization, although the cells contained significant amounts of bFGF and aFGF as quantified by radioimmunoassays, mitogen assays with immunoneutralization, and Western blotting. After culturing, bFGF mRNA was detected (aFGF mRNA was not studied), and the cells contained 2.5-fold more bFGF and 60% more aFGF than freshly isolated cells. The FGFs were not found in conditioned medium. They were localized, especially in cultured cells, to the nucleus. Cultured myocytes bound fourfold more I-125-FGF than freshly isolated cells and expressed the fibroblast growth factor R-1 (flg) gene. The addition of bFGF or aFGF in serum-free medium to pure populations of myocytes (after 10 days in culture, at which time they are spread, beating, and multinucleated) led to increased thymidine incorporation. Expression of fibroblast growth factors and fibroblast growth factor receptors by adult cardiac myocytes that survive the shock and "dedifferentiation" of culturing may contribute to DNA synthesis and, by analogy, to other cell types, to regulation of ribosomal and actin genes, and to cell survival. These possibilities and their in vivo relevance will require further study. C1 WHITTIER INST,LA JOLLA,CA. RP SPEIR, E (reprint author), NHLBI,CARDIOL BRANCH,BLDG 10,ROOM 7B-15,BETHESDA,MD 20892, USA. NR 31 TC 83 Z9 83 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD AUG PY 1992 VL 71 IS 2 BP 251 EP 259 PG 9 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA JE935 UT WOS:A1992JE93500003 PM 1378359 ER PT J AU ZWEIG, MH BROSTE, SK REINHART, RA AF ZWEIG, MH BROSTE, SK REINHART, RA TI ROC CURVE ANALYSIS - AN EXAMPLE SHOWING THE RELATIONSHIPS AMONG SERUM-LIPID AND APOLIPOPROTEIN CONCENTRATIONS IN IDENTIFYING PATIENTS WITH CORONARY-ARTERY DISEASE SO CLINICAL CHEMISTRY LA English DT Article ID DIAGNOSTIC-ACCURACY; ASSAYS AB Clinical accuracy, defined as the ability to discriminate between states of health, is the fundamental property of any diagnostic test or system. It is readily expressed as clinical sensitivity and specificity, and elegantly represented by the receiver operating characteristic (ROC) curve. To demonstrate the use of ROC curves, we reexamine a study of the ability of serum lipid and apolipoprotein measures to discriminate among degrees of coronary artery disease in patients undergoing coronary angiography. ROC curve analysis reveals that none of these indexes is highly accurate, but demonstrates a modest increase in the accuracy of apolipoprotein over lipid indexes. C1 MARSHFIELD MED RES FDN,DEPT EPIDEMIOL & BIOSTAT,MARSHFIELD,WI 54449. MARSHFIELD CLIN FDN MED RES & EDUC,DEPT CARDIOL,MARSHFIELD,WI 54449. RP ZWEIG, MH (reprint author), NIH,WARREN G MAGNUSON CLIN CTR,DEPT CLIN PATHOL,BETHESDA,MD 20892, USA. NR 9 TC 36 Z9 38 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD AUG PY 1992 VL 38 IS 8 BP 1425 EP 1428 PN 1 PG 4 WC Medical Laboratory Technology SC Medical Laboratory Technology GA JH683 UT WOS:A1992JH68300007 PM 1643709 ER PT J AU ROBBINS, JB CHU, CY SCHNEERSON, R AF ROBBINS, JB CHU, CY SCHNEERSON, R TI HYPOTHESIS FOR VACCINE DEVELOPMENT - PROTECTIVE IMMUNITY TO ENTERIC DISEASES CAUSED BY NONTYPHOIDAL SALMONELLAE AND SHIGELLAE MAY BE CONFERRED BY SERUM IGG ANTIBODIES TO THE O-SPECIFIC POLYSACCHARIDE OF THEIR LIPOPOLYSACCHARIDES SO CLINICAL INFECTIOUS DISEASES LA English DT Review ID ENTEROINVASIVE ESCHERICHIA-COLI; VI-CAPSULAR POLYSACCHARIDE; GENETIC POPULATION-STRUCTURE; LINKED IMMUNOSORBENT-ASSAY; HEMOLYTIC-UREMIC SYNDROME; SHIGA-LIKE TOXINS; DYSENTERIAE TYPE-1; ACUTE DIARRHEA; UNITED-STATES; VIBRIO-CHOLERAE AB Immunoprophylaxis for bacterial enteric diseases is hindered because the protective immune mechanism(s) against nontyphoidal salmonellae or shigellae in humans are not established. On the basis of the similarities between the clinical signs, epidemiology, pathogenesis, and pathology of as well as protective immunity to salmonellae and shigellae, we propose that serum IgG antibodies to the O-specific polysaccharide (O-SP) of their lipopolysaccharides (LPSs) will confer protective immunity to these two pathogens. Critical to this notion is that (1) the virulence of these two pathogens requires full expression of their LPS; (2) active or passive immunization with serum IgG O-SP antibodies confers protection of mice against Salmonella typhimurium (there are no comparable data for humans); and (3) in humans, convalescence from shigellosis confers type (O-SP) -specific protective immunity, and indirect evidence shows a correlation between the level of serum LPS antibodies and resistance to shigellosis. We designed conjugate vaccines to elicit high levels of long-lived serum IgG O-SP antibodies to nontyphoidal salmonellae and shigellae to test this hypothesis. RP ROBBINS, JB (reprint author), NICHHD,DEV & MOLEC IMMUN LAB,BLDG 6,ROOM 145,BETHESDA,MD 20892, USA. NR 289 TC 122 Z9 127 U1 1 U2 4 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 AUG PY 1992 VL 15 IS 2 BP 346 EP 361 PG 16 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA JF190 UT WOS:A1992JF19000020 PM 1381621 ER PT J AU YOUNG, MF KERR, JM IBARAKI, K HEEGAARD, AM ROBEY, PG AF YOUNG, MF KERR, JM IBARAKI, K HEEGAARD, AM ROBEY, PG TI STRUCTURE, EXPRESSION, AND REGULATION OF THE MAJOR NONCOLLAGENOUS MATRIX PROTEINS OF BONE SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Review ID TRANSFORMING GROWTH-FACTOR; OSTEO-SARCOMA CELLS; HUMAN OSTEOCALCIN GENE; MESSENGER-RNA LEVELS; DERMATAN SULFATE PROTEOGLYCAN; ACID (GLA)-CONTAINING PROTEIN; GLA-PROTEIN; VITAMIN-D; SECRETED PHOSPHOPROTEIN; EXTRACELLULAR-MATRIX AB The noncollagenous proteins (NCPs) that predominate the bone matrix have recently been the focus of intense investigation because of their potential influence on cell attachment, Ca2+ and hydroxyapatite binding, and the mineralization of bone tissue. With the advent of molecular biology, all of the major NCPs of bone have been cloned and their amino acid sequences completely determined. While each of the proteins has distinct structural properties, some proteins appear to be part of gene families. Examples include the small proteoglycans, decorin and biglycan, as well as the gamma carboxyglutamic acid proteins, such as matrix gla protein and osteocalcin (bone gla protein). Some of the NCPs that are clearly not members of any known gene family still share several common characteristics. One such example of this "convergent evolution" is bone sialoprotein and osteopontin. Both are highly posttranslationally modified glycoproteins that share the cell attachment amino acid sequence RGD (arginine-glycine-aspartic acid), which facilitates the attachment of bone cells in vitro, yet they are clearly not related genetically. Using cDNAs and antisera as probes, the precise temporal localization of NCP expression has been determined, and it has been shown that NCPs are produced in skeletal, and in most cases, nonskeletal tissue as well. This observation implies that the functions of the NCPs are not necessarily limited to bone tissue. Many of the promoters for these genes have been isolated and functional domains determined by a combination of chloramphenicol acetyltransferase assay, gel shift, and footprint analyses. The most extensively studied promoter in the NCP category is osteocalcin, whose sensitivity to 1,25-dihydroxycholecalciferol has been delineated in detail. Future studies on the individual and cooperative activities of the NCPs in bone are likely to involve site-directed mutagenesis of cloned DNA and a combination of in vitro and in vivo functional analyses. RP YOUNG, MF (reprint author), NIDR,BONE RES BRANCH,BLDG 30,ROOM 106,BETHESDA,MD 20892, USA. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 125 TC 120 Z9 121 U1 3 U2 13 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD AUG PY 1992 IS 281 BP 275 EP 294 PG 20 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JG977 UT WOS:A1992JG97700042 ER PT J AU SHAH, SA AF SHAH, SA TI INSANITY ON TRIAL - FINKEL,NJ SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review RP SHAH, SA (reprint author), NIMH,DIV APPL & SERV RES,BETHESDA,MD 20892, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD AUG PY 1992 VL 37 IS 8 BP 749 EP 752 PG 4 WC Psychology, Multidisciplinary SC Psychology GA JJ397 UT WOS:A1992JJ39700008 ER PT J AU XU, JC FOLKERS, K BOWERS, C LJUNGQVIST, A FENG, DM HOOK, WA AF XU, JC FOLKERS, K BOWERS, C LJUNGQVIST, A FENG, DM HOOK, WA TI DESIGN, SYNTHESIS AND BIOLOGICAL EVALUATION OF ANTAGONISTS OF LHRH INCLUDING SUBSTITUTIONS WITH L-AZETIDINE 2-2-CARBOXYLIC ACID SO CONTRACEPTION LA English DT Article C1 SHANGHAI INST ORGAN CHEM,SHANGHAI 200032,PEOPLES R CHINA. TULANE UNIV,SCH MED,ENDOCRINE UNIT,NEW ORLEANS,LA 70112. NIDR,BETHESDA,MD 20892. RP XU, JC (reprint author), UNIV TEXAS,INST BIOMED RES,AUSTIN,TX 78712, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0010-7824 J9 CONTRACEPTION JI Contraception PD AUG PY 1992 VL 46 IS 2 BP 113 EP 115 DI 10.1016/0010-7824(92)90015-L PG 3 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA JH893 UT WOS:A1992JH89300004 ER PT J AU ELLENBERG, SS COOPER, E EIGO, J FINKELSTEIN, DM HOTH, DF NUSINOFFLEHRMAN, S SACKS, H AF ELLENBERG, SS COOPER, E EIGO, J FINKELSTEIN, DM HOTH, DF NUSINOFFLEHRMAN, S SACKS, H TI STUDYING TREATMENTS FOR AIDS - NEW CHALLENGES FOR CLINICAL-TRIALS - A PANEL DISCUSSION AT THE 1990 ANNUAL-MEETING OF THE SOCIETY-FOR-CLINICAL-TRIALS SO CONTROLLED CLINICAL TRIALS LA English DT Article ID PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; AZIDOTHYMIDINE AZT; HIV-INFECTION; ZIDOVUDINE; EFFICACY; COMPLEX; DESIGN C1 US FDA,DIV ANTIRETROVIRAL DRUG PROD,ROCKVILLE,MD 20857. ACT UP,COMM TREATMENT & DATA,NEW YORK,NY. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. BURROUGHS WELLCOME CO,DEPT INFECT DIS,RES TRIANGLE PK,NC 27709. MT SINAI HOSP,DIV INFECT DIS,NEW YORK,NY. RP ELLENBERG, SS (reprint author), NIAID,DIV AIDS,6003 EXECUT BLVD,BETHESDA,MD 20892, USA. NR 24 TC 5 Z9 5 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 AUG PY 1992 VL 13 IS 4 BP 272 EP 292 DI 10.1016/0197-2456(92)90011-N PG 21 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA JK567 UT WOS:A1992JK56700003 PM 1330433 ER PT J AU SHEARER, GM CLERICI, M AF SHEARER, GM CLERICI, M TI HOW HUMAN-IMMUNODEFICIENCY-VIRUS RAVAGES THE IMMUNE-SYSTEM SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID T-HELPER; CELL DYSFUNCTION; INFECTION; TYPE-1; HIV; ANTIBODIES; RESERVOIRS; DEPLETION; DEATH; AIDS AB The immune system of individuals infected with human immunodeficiency virus is affected in two distinct ways: by loss of CD4+ cells and by loss of T-helper-cell function. Neither of these processes is yet fully understood. Research during 1991 that investigated the interaction between human immunodeficiency virus and the immune system has raised as many questions as it answered. Nevertheless, many of the issues raised are relevant to mechanisms responsible for the ravaging of the immune system by human immunodeficiency virus. RP SHEARER, GM (reprint author), NCI,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892, USA. NR 19 TC 9 Z9 9 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD AUG PY 1992 VL 4 IS 4 BP 463 EP 465 DI 10.1016/S0952-7915(06)80040-3 PG 3 WC Immunology SC Immunology GA JJ844 UT WOS:A1992JJ84400015 PM 1356347 ER PT J AU LANE, HC AF LANE, HC TI CURRENT STATUS OF THERAPY FOR HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID ZIDOVUDINE; INFECTION; AIDS AB The past year has seen refinement in our ability to delay the progression of human immunodeficiency virus type 1 infection through the use of nucleoside analogues, singly or in combination. Progress has also been made in our ability to detect drug-resistant isolates of human immunodeficiency virus type 1 and to begin to put the laboratory observations of resistance into a clinical context. RP LANE, HC (reprint author), NIAID,IMMUNOREGULAT LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 11 TC 3 Z9 3 U1 0 U2 0 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD AUG PY 1992 VL 4 IS 4 BP 486 EP 489 DI 10.1016/S0952-7915(06)80044-0 PG 4 WC Immunology SC Immunology GA JJ844 UT WOS:A1992JJ84400019 PM 1356350 ER PT J AU LUNDGREN, JD AF LUNDGREN, JD TI MUCUS PRODUCTION IN THE LOWER AIRWAYS - A REVIEW OF EXPERIMENTAL STUDIES SO DANISH MEDICAL BULLETIN LA English DT Review ID PLATELET-ACTIVATING-FACTOR; GASTRIN-RELEASING PEPTIDE; HUMAN NEUTROPHIL ELASTASE; SECRETORY-CELL METAPLASIA; TRACHEAL EPITHELIAL-CELLS; HUMAN NASAL-MUCOSA; PROTEIN-KINASE-C; ARACHIDONIC-ACID METABOLISM; FACTOR STIMULATES SECRETION; BOMBESIN-LIKE PEPTIDES C1 NIH,CTR CLIN,DEPT CRIT CARE MED,BETHESDA,MD 20892. PANUM INST,DEPT ANAT B,COPENHAGEN,DENMARK. GENTOFTE HOSP,DEPT OTORHINOLARYNGOL,DK-2900 COPENHAGEN,DENMARK. HVIDOVRE UNIV HOSP,DEPT INFECT DIS,DK-2650 HVIDOVRE,DENMARK. NR 157 TC 2 Z9 3 U1 0 U2 0 PU DANISH MEDICAL ASSN PI COPENHAGEN PA TRONDHJEMSGADE 9, DK-2100 COPENHAGEN, DENMARK SN 0011-6092 J9 DAN MED BULL JI Dan. Med. Bull. PD AUG PY 1992 VL 39 IS 4 BP 289 EP 303 PG 15 WC Medicine, General & Internal SC General & Internal Medicine GA JL211 UT WOS:A1992JL21100002 PM 1526182 ER PT J AU MINIE, ME KIMURA, T FELSENFELD, G AF MINIE, ME KIMURA, T FELSENFELD, G TI THE DEVELOPMENTAL SWITCH IN EMBRYONIC RHO-GLOBIN EXPRESSION IS CORRELATED WITH ERYTHROID LINEAGE-SPECIFIC DIFFERENCES IN TRANSCRIPTION FACTOR LEVELS SO DEVELOPMENT LA English DT Article DE HEMOGLOBIN SWITCHING; ERYTHROID LINEAGES; SPL; GATA-1; CHICKEN ERYTHROPOIESIS; RHO-GLOBIN; TRANSCRIPTION FACTORS ID CHICKEN-BETA-GLOBIN; I-HYPERSENSITIVE SITES; DNA-BINDING FACTOR; NUCLEOTIDE-SEQUENCE; GENE-TRANSCRIPTION; HEMOGLOBIN SWITCH; PROTEIN-BINDING; TRANSGENIC MICE; NUCLEAR FACTORS; FACTOR GATA-1 AB During chicken embryogenesis, the rho-globin gene is expressed only in the early developmental stages. We have examined the mechanisms that are responsible for this behavior. The transcription of the rho-globin gene is strongly correlated with the presence during development of primitive erythroid lineage cells, consistent with the idea that the expression of the rho-globin gene is restricted to that lineage. The "switching off" of rho-globin during development thus reflects the change from primitive to definitive cell lineages which occurs during erythropoiesis in chicken. We use transient expression assays in primary erythroid and other cells to show that the information for lineage- and tissue-specific expression of the rho-globin gene is contained in a 456 bp region upstream of the gene's translational start site. DNA-binding studies, coupled with analysis of the effect on expression of deletions and binding site mutations, were used to identify important control elements within this 456 bp region. We find that binding sites for the ubiquitous transcription factor Sp1, and the specific hematopoietic factor GATA-1, are crucial for expression of the gene in primitive erythroid cells. Quantitative analysis shows that nuclei of the primitive erythroid lineage contain 10-fold more of these factors than do the nuclei of definitive cells. We show that in principle these differences in factor concentration are sufficient to explain the lineage-specific behavior that we observe in our assays. We suggest that this may be an important part of the mechanism for lineage-restricted rho-globin expression during chicken erythroid development. Similar mechanisms may be involved in regulation of other (but not all) members of the globin family. C1 NIDDKD,PHYS CHEM SECT,MOLEC BIOL LAB,BETHESDA,MD 20892. NR 73 TC 52 Z9 52 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD AUG PY 1992 VL 115 IS 4 BP 1149 EP 1164 PG 16 WC Developmental Biology SC Developmental Biology GA JK993 UT WOS:A1992JK99300023 PM 1451662 ER PT J AU BREWITT, B TALIAN, JC ZELENKA, PS AF BREWITT, B TALIAN, JC ZELENKA, PS TI CELL-CYCLE SYNCHRONY IN THE DEVELOPING CHICKEN LENS EPITHELIUM SO DEVELOPMENTAL BIOLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; SERUM-FREE MEDIUM; MESSENGER-RNA; GROWTH-FACTOR; DNA; QUANTITATION; INVITRO; INSULIN; MOUSE; PDGF RP BREWITT, B (reprint author), NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892, USA. NR 45 TC 12 Z9 12 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD AUG PY 1992 VL 152 IS 2 BP 315 EP 322 DI 10.1016/0012-1606(92)90138-7 PG 8 WC Developmental Biology SC Developmental Biology GA JE961 UT WOS:A1992JE96100010 PM 1644222 ER PT J AU SILBERSTEIN, GB FLANDERS, KC ROBERTS, AB DANIEL, CW AF SILBERSTEIN, GB FLANDERS, KC ROBERTS, AB DANIEL, CW TI REGULATION OF MAMMARY MORPHOGENESIS - EVIDENCE FOR EXTRACELLULAR MATRIX-MEDIATED INHIBITION OF DUCTAL BUDDING BY TRANSFORMING GROWTH FACTOR-BETA-1 SO DEVELOPMENTAL BIOLOGY LA English DT Article ID FACTOR-BETA; BASAL LAMINA; BRANCHING MORPHOGENESIS; GLYCOSAMINOGLYCANS; DIFFERENTIATION; PROTEOGLYCANS; FIBRONECTIN; ANTIBODIES; EXPRESSION; GLAND C1 NCI,CHEMOPREVENT LAB,BETHESDA,MD 20892. RP SILBERSTEIN, GB (reprint author), UNIV CALIF SANTA CRUZ,SINSHEIMER LABS,DEPT BIOL,SANTA CRUZ,CA 95064, USA. FU NICHD NIH HHS [HD 27845] NR 24 TC 112 Z9 112 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD AUG PY 1992 VL 152 IS 2 BP 354 EP 362 DI 10.1016/0012-1606(92)90142-4 PG 9 WC Developmental Biology SC Developmental Biology GA JE961 UT WOS:A1992JE96100014 PM 1644225 ER PT J AU FONTVIEILLE, AM LILLIOJA, S FERRARO, RT SCHULZ, LO RISING, R RAVUSSIN, E AF FONTVIEILLE, AM LILLIOJA, S FERRARO, RT SCHULZ, LO RISING, R RAVUSSIN, E TI 24-HOUR ENERGY-EXPENDITURE IN PIMA-INDIANS WITH TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS SO DIABETOLOGIA LA English DT Article DE ENERGY EXPENDITURE; TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS; INDIRECT CALORIMETRY; OBESITY; BODY COMPOSITION; HEPATIC GLUCOSE PRODUCTION ID HEPATIC GLUCOSE-PRODUCTION; OBESE SUBJECTS; SULFONYLUREA THERAPY; PHYSICAL-ACTIVITY; GLUCONEOGENESIS; RESISTANCE; SECRETION; INVIVO; MAINTENANCE; RATES AB To assess the impact of Type 2 (non-insulin-dependent) diabetes mellitus on energy metabolism, 24-h energy expenditure, basal metabolic rate and sleeping metabolic rate were measured in a respiratory chamber in 151 Pima Indians. 102 with normal glucose tolerance (67 male/35 female, (mean +/- SD) 28 +/- 7 years, 99 +/- 24 kg, 32 +/- 9 % body fat) and in 49 with Type 2 diabetes (22 male/27 female, 35 +/- 11 years, 107 +/- 33 kg, 39 +/- 7 % body fat), after at least 3 days on a weight maintaining diet. After adjustment for differences in fat-free mass, fat mass, age and sex, 24-h energy expenditure, basal metabolic rate and sleeping metabolic rate were significantly higher in diabetic patients than in control subjects (72 kcal/day, p < 0.05; 99 kcal/day, p < 0.005, 99 kcal/day < 0.001 respectively). Spontaneous physical activity was similar in both groups whereas the thermic effect of food, calculated as the mean energy expenditure corrected for activity throughout the day above sleeping metabolic rate and expressed as a percentage of energy intake, was significantly lower in Type 2 diabetic patients (17.1 +/- 7.1 vs 19.8 +/- 5.6 %, p < 0.05). Adjusted values of 24-h energy expenditure. basal metabolic rate and sleeping metabolic rate were correlated with hepatic endogenous glucose production (r = 0.22, p < 0.05; r = 0.22, p < 0.05; r = 0.31, p < 0.01 respectively). Therefore, increased basal and sleeping metabolic rates, resulting in increased 24-h sedentary energy expenditure may play a role in the weight loss so often observed in Type 2 diabetic subjects in addition to the energy loss from glycosuria. RP FONTVIEILLE, AM (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,ROOM 541,PHOENIX,AZ 85016, USA. RI Lillioja, Stephen/A-8185-2012 NR 48 TC 32 Z9 32 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1992 VL 35 IS 8 BP 753 EP 759 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JE632 UT WOS:A1992JE63200009 PM 1511802 ER PT J AU CELI, FS ROTH, A ROTH, A TANNER, K SHULDINER, AR AF CELI, FS ROTH, A ROTH, A TANNER, K SHULDINER, AR TI COORDINATE REGULATION OF THE 2 XENOPUS NONALLELIC INSULIN GENES IN ADULT PANCREAS SO DIABETOLOGIA LA English DT Meeting Abstract C1 NIA,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. 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 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1992 VL 35 SU 1 BP A67 EP A67 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500257 ER PT J AU KADOR, PF TAKAHASHI, Y WYMAN, M AF KADOR, PF TAKAHASHI, Y WYMAN, M TI RETINAL VESSEL CHANGES IN GALACTOSE-FED DOGS - ALDOSE REDUCTASE INHIBITOR EFFECTS SO DIABETOLOGIA LA English DT Meeting Abstract C1 NIH,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 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1992 VL 35 SU 1 BP A143 EP A143 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500551 ER PT J AU PETTITT, DJ KNOWLER, WC JACOBSSON, LTH MCCANCE, DR HANSON, RL CHARLES, MA NELSON, RG LIU, QZ BENNETT, PH AF PETTITT, DJ KNOWLER, WC JACOBSSON, LTH MCCANCE, DR HANSON, RL CHARLES, MA NELSON, RG LIU, QZ BENNETT, PH TI LOWER DIABETES INCIDENCE AFTER IMPAIRED GLUCOSE-TOLERANCE IN PREGNANT THAN IN NONPREGNANT WOMEN SO DIABETOLOGIA LA English DT Meeting Abstract C1 CLEVELAND CLIN,PHOENIX,AZ. NIAMS,PHOENIX,AZ. NIDDK,PHOENIX,AZ. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1992 VL 35 SU 1 BP A179 EP A179 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500692 ER PT J AU WERTHEIMER, E LITVIN, Y EBSTEIN, RP BENNETT, ER BARBETTI, F ACCILI, D TAYLOR, SI AF WERTHEIMER, E LITVIN, Y EBSTEIN, RP BENNETT, ER BARBETTI, F ACCILI, D TAYLOR, SI TI AN INSULIN-RECEPTOR GENE DELETION IN A KINDRED WITH A FAMILIAL FORM OF INSULIN RESISTANCE SO DIABETOLOGIA LA English DT Meeting Abstract C1 SARAH HERZOG MEM HOSP,JERUSALEM,ISRAEL. NIH,DIABET 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 0012-186X J9 DIABETOLOGIA JI Diabetologia PD AUG PY 1992 VL 35 SU 1 BP A81 EP A81 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JJ555 UT WOS:A1992JJ55500311 ER PT J AU FRUCHT, HA JENSEN, RT AF FRUCHT, HA JENSEN, RT TI BODY-WEIGHT AND ZES SO DIGESTIVE DISEASES AND SCIENCES LA English DT Letter RP FRUCHT, HA (reprint author), NIH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD AUG PY 1992 VL 37 IS 8 BP 1309 EP 1309 DI 10.1007/BF01296582 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JH807 UT WOS:A1992JH80700030 ER PT J AU NILSSON, J PANIZZA, M ROTH, BJ BASSER, PJ COHEN, LG CARUSO, G HALLETT, M AF NILSSON, J PANIZZA, M ROTH, BJ BASSER, PJ COHEN, LG CARUSO, G HALLETT, M TI DETERMINING THE SITE OF STIMULATION DURING MAGNETIC STIMULATION OF A PERIPHERAL-NERVE SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE MAGNETIC STIMULATION; MATHEMATICAL MODELING; NERVE CONDUCTION VELOCITY STUDIES; VIRTUAL CATHODE ID ELECTROMAGNETIC INDUCTION; COIL; SYSTEM; VOLUME; MODEL; FIBER AB Magnetic stimulation has not been routinely used for studies of peripheral nerve conduction primarily because of uncertainty about the location of the stimulation site. We performed several experiments to locate the site of nerve stimulation. Uniform latency shifts, similar to those that can be obtained during electrical stimulation, were observed when a magnetic coil was moved along the median nerve in the region of the elbow, thereby ensuring that the properties of the nerve and surrounding volume conductor were uniform. By evoking muscle responses both electrically and magnetically and matching their latencies, amplitudes and shapes, the site of stimulation was determined to be 3.0 +/- 0.5 cm from the center of an 8-shaped coil toward the coil handle. When the polarity of the current was reversed by rotating the coil, the latency of the evoked response shifted by 0.65 +/- 0.05 msec, which implies that the site of stimulation was displaced 4.1 +/- 0.5 cm. Additional evidence of cathode- and anode-like behavior during magnetic stimulation comes from observations of preferential activation of motor responses over H-reflexes with stimulation of a distal site, and of preferential activation of H-reflexes over motor responses with stimulation of a proximal site. Analogous behavior is observed with electrical stimulation. These experiments were motivated by, and are qualitatively consistent with, a mathematical model of magnetic stimulation of an axon. C1 NINCDS, HUMAN CORT PHYSIOL UNIT, HUMAN MOTOR CONTROL SECT, MED NEUROL BRANCH, BETHESDA, MD 20892 USA. FDN CLIN LAVORO, CLIN NEUROPHYSIOL LAB, CASTEL GOFFREDO, ITALY. NIH, NATL CTR RES RESOURCES, BIOMED ENGN & INSTRUMENTAT PROGRAM, BETHESDA, MD 20892 USA. FDN CLIN LAVORO, EMG LAB, CAMPOLI MT, ITALY. RI Roth, Bradley/A-4920-2008; Basser, Peter/H-5477-2011 NR 29 TC 59 Z9 59 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 AUG PY 1992 VL 85 IS 4 BP 253 EP 264 DI 10.1016/0168-5597(92)90114-Q PG 12 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA JM142 UT WOS:A1992JM14200005 PM 1380913 ER PT J AU ROCHE, PA TELETSKI, CL KARP, DR PINET, V BAKKE, O LONG, EO AF ROCHE, PA TELETSKI, CL KARP, DR PINET, V BAKKE, O LONG, EO TI STABLE SURFACE EXPRESSION OF INVARIANT CHAIN PREVENTS PEPTIDE PRESENTATION BY HLA-DR SO EMBO JOURNAL LA English DT Article DE ANTIGEN PRESENTATION; ENDOSOME; HLA-DR; INTRACELLULAR TRAFFIC; INVARIANT CHAIN ID CLASS-II MOLECULES; BETA-CHAIN; ANTIGENS; CELLS; ASSOCIATION; TRANSPORT; ABSENCE; FORMS; GENE AB Class II major histocompatibility complex (MHC) molecules are cell surface glycoproteins that bind and present immunogenic peptides to T cells. Intracellularly, class II molecules associate with a polypeptide referred to as the invariant (Ii) chain. Ii is proteolytically degraded and dissociates from the class II complex prior to cell surface expression of the mature class II alpha-beta-heterodimer. Using human fibroblasts transfected with HLA-DR1 and Ii cDNAs, we now demonstrate that truncation of the cytoplasmic domain of Ii results in the failure of Ii to dissociate from the alpha-beta-Ii complex and leads to stable expression of class II alpha-beta-Ii complexes on the cell surface. Furthermore, biochemical analysis and peptide presentation assays demonstrated that transfectants with stable surface alpha-beta-Ii complexes expressed very few free alpha-beta heterodimers at the surface and were very inefficient in their ability to present immunogenic peptides to T cells. These results support the hypothesis that the cytoplasmic domain of Ii is responsible for endosomal targeting of alpha-beta-Ii and directly demonstrate that association with Ii interferes with the antigen presentation function of class II molecules. C1 NIAID,IMMUNOGENET LAB,TWINBROOK II FACIL,12441 PARKLAWN DR,ROCKVILLE,MD 20852. UNIV OSLO,DEPT BIOL,N-0316 OSLO,NORWAY. RI Long, Eric/G-5475-2011; PINET, Valerie/G-6085-2012 OI Long, Eric/0000-0002-7793-3728; NR 29 TC 102 Z9 102 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD AUG PY 1992 VL 11 IS 8 BP 2841 EP 2847 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JE537 UT WOS:A1992JE53700008 PM 1639058 ER PT J AU JANE, SM NEY, PA VANIN, EF GUMUCIO, DL NIENHUIS, AW AF JANE, SM NEY, PA VANIN, EF GUMUCIO, DL NIENHUIS, AW TI IDENTIFICATION OF A STAGE SELECTOR ELEMENT IN THE HUMAN GAMMA-GLOBIN GENE PROMOTER THAT FOSTERS PREFERENTIAL INTERACTION WITH THE 5' HS2 ENHANCER WHEN IN COMPETITION WITH THE BETA-PROMOTER SO EMBO JOURNAL LA English DT Article DE BETA-GLOBIN; ENHANCER; HYPERSENSITIVITY SITE; PROMOTER; TRANS-ACTING FACTOR ID DOMINANT CONTROL REGION; ERYTHROID-SPECIFIC EXPRESSION; TRANSGENIC MICE; DEVELOPMENTAL REGULATION; MAMMALIAN-CELLS; K562 CELLS; PROTEIN; SEQUENCES; BINDING; SITES AB The erythroid-specific enhancer within hypersensitivity site 2 (HS2) of the human beta-globin locus control region is required for high level globin gene expression. We investigated interaction between HS2 and the gamma- and beta-promoters using reporter constructs in transient assays in human erythroleukemia (K562) cells. The beta-promoter, usually silent in K562 cells, was activated by HS2. This activity was abolished when a gamma-promoter was linked in cis. Analysis of truncation mutants suggested that sequences conveying the competitive advantage of the gamma-promoter for HS2 included those between positions -53 and -35 relative to the transcriptional start site. This sequence, when used to replace the corresponding region of the beta-promoter, increased beta-promoter activity 10-fold when linked to HS2. The modified beta-promoter was also capable of competing with gamma-promoter modified internally in the -53 to -35 region, when the two promoters were linked to HS2 in a single plasmid. The corresponding sequences from the Galago gamma-promoter, a species which lacks fetal gamma-gene expression, were inactive in analogous assays. We have identified and partially purified a nuclear protein found in human (fetal stage) erythroleukemia cells, but present in much lower concentration in murine (adult stage) erythroleukemia cells, that binds the -53 to -35 sequence of the gamma-promoter. We speculate that this region of the gamma-promoter functions as a stage selector element in the regulation of hemoglobin switching in humans. C1 UNIV MICHIGAN,DEPT ANAT & CELL BIOL,ANN ARBOR,MI 48109. GENET THERAPY INC,GAITHERSBURG,MD 20878. RP JANE, SM (reprint author), NHLBI,BETHESDA,MD 20892, USA. RI Jane, Stephen/D-6659-2011 NR 50 TC 124 Z9 124 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD AUG PY 1992 VL 11 IS 8 BP 2961 EP 2969 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JE537 UT WOS:A1992JE53700023 PM 1639067 ER PT J AU SPIEGEL, AM SHENKER, A WEINSTEIN, LS AF SPIEGEL, AM SHENKER, A WEINSTEIN, LS TI RECEPTOR-EFFECTOR COUPLING BY G-PROTEINS - IMPLICATIONS FOR NORMAL AND ABNORMAL SIGNAL TRANSDUCTION SO ENDOCRINE REVIEWS LA English DT Review ID GUANINE-NUCLEOTIDE-BINDING; STIMULATORY G-PROTEIN; BETA-ADRENERGIC RECEPTORS; PERTUSSIS TOXIN-SUBSTRATE; MCCUNE-ALBRIGHT SYNDROME; EPIDERMAL GROWTH-FACTOR; CATALYZED ADP-RIBOSYLATION; ADENYLATE-CYCLASE ACTIVITY; ISLET-ACTIVATING PROTEIN; MUSCARINIC ACETYLCHOLINE-RECEPTOR RP SPIEGEL, AM (reprint author), NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BLDG 10,ROOM 9N-222,BETHESDA,MD 20892, USA. OI Weinstein, Lee/0000-0002-1899-5152 NR 423 TC 313 Z9 320 U1 1 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0163-769X J9 ENDOCR REV JI Endocr. Rev. PD AUG PY 1992 VL 13 IS 3 BP 536 EP 565 DI 10.1210/er.13.3.536 PG 30 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JK742 UT WOS:A1992JK74200009 PM 1425488 ER PT J AU TAYLOR, SI CAMA, A ACCILI, D BARBETTI, F QUON, MJ SIERRA, MD SUZUKI, Y KOLLER, E LEVYTOLEDANO, R WERTHEIMER, E MONCADA, VY KADOWAKI, H KADOWAKI, T AF TAYLOR, SI CAMA, A ACCILI, D BARBETTI, F QUON, MJ SIERRA, MD SUZUKI, Y KOLLER, E LEVYTOLEDANO, R WERTHEIMER, E MONCADA, VY KADOWAKI, H KADOWAKI, T TI MUTATIONS IN THE INSULIN-RECEPTOR GENE SO ENDOCRINE REVIEWS LA English DT Review ID GROWTH FACTOR-I; TYROSINE KINASE-ACTIVITY; HAMSTER OVARY CELLS; POLYMERASE CHAIN-REACTION; COOH-TERMINAL TRUNCATION; SITE-SITE INTERACTIONS; MONOCLONAL-ANTIBODIES; BETA-SUBUNIT; LIGAND-BINDING; MESSENGER-RNA 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 191 TC 232 Z9 236 U1 0 U2 4 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0163-769X J9 ENDOCR REV JI Endocr. Rev. PD AUG PY 1992 VL 13 IS 3 BP 566 EP 595 DI 10.1210/er.13.3.566 PG 30 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JK742 UT WOS:A1992JK74200010 PM 1330507 ER PT J AU ROBBINS, J AF ROBBINS, J TI THYROXINE TRANSPORT AND THE FREE HORMONE HYPOTHESIS SO ENDOCRINOLOGY LA English DT Editorial Material ID BINDING GLOBULIN; HOMOLOGY RP ROBBINS, J (reprint author), NIDDKD,BETHESDA,MD, USA. NR 22 TC 11 Z9 12 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 AUG PY 1992 VL 131 IS 2 BP 546 EP 547 DI 10.1210/en.131.2.546 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JG581 UT WOS:A1992JG58100002 PM 1639006 ER PT J AU BAN, T KOSUGI, S KOHN, LD AF BAN, T KOSUGI, S KOHN, LD TI SPECIFIC ANTIBODY TO THE THYROTROPIN RECEPTOR IDENTIFIES MULTIPLE RECEPTOR FORMS IN MEMBRANES OF CELLS TRANSFECTED WITH WILD-TYPE RECEPTOR COMPLEMENTARY DEOXYRIBONUCLEIC-ACID - CHARACTERIZATION OF THEIR RELEVANCE TO RECEPTOR SYNTHESIS, PROCESSING, STRUCTURE, AND FUNCTION SO ENDOCRINOLOGY LA English DT Article ID IDIOPATHIC MYXEDEMA PATIENTS; THYROID PLASMA-MEMBRANES; GRAVES-DISEASE; AFFINITY-CHROMATOGRAPHY; GONADOTROPIN RECEPTORS; COVALENT CROSSLINKING; MONOCLONAL-ANTIBODIES; EXTRACELLULAR DOMAIN; BLOCKING ANTIBODIES; LIGAND-BINDING AB An antibody to a peptide of the TSH receptor, residues 352-366 which are not present in gonadotropin receptors, specifically identifies three major forms of the receptor on Western blots of detergent-solubilized membrane preparations from Cos-7 cells transfected with full-length rat and human TSH receptor cDNA: 230, 180, and 95-100 kilodaltons (kDa), based on simultaneously run protein standards. The 95- to 100-kDa protein is absent in cells transfected with a mutant receptor with no signal peptide and is sensitive to endoglycosidase-F. Its size is consistent with the sum of amino acids predicted from its cDNA sequence (84 kDa after subtracting the signal peptide) plus its carbohydrate content (14 kDa estimated from glycosylation mutants). It alone is absent in two deletion mutants that have lost TSH binding and activity after transfection: M1 missing residues 37-121 and M2 missing residues 110-307. It, thus, appears to be the processed glycosylated functional receptor on the cell surface. The 230-kDa protein is a nonprocessed form of the receptor, as evidenced by its insensitivity to endoglycosidase-F and its continued presence in cells transfected with a mutant receptor with no signal peptide. It is the primary form identified in rat FRTL-5 thyroid cells that have a functioning TSH receptor; it is not present in rat FRT thyroid cells with no functioning TSH receptor or receptor RNA. It appears, therefore, to be a early synthetic form of the functional TSH receptor. The 180-kDa protein is endoglycosidase-F sensitive and appears to be a processed intermediate between the 230-kDa early synthetic form and the 95- to 100-kDa functional receptor, rather than a dimer of the latter. Thus, with decreases in size appropriate to a receptor monomer, it remains present in membranes from the M1 and M2 deletion mutants that contain the 230-kDa protein but are missing the 95- to 100-kDa receptor form in association with lost TSH binding and activity after transfection. Minor receptor forms (54 kDa in rat receptor transfectants, 54 and 48 kDa in human receptor transfectants) appear to be degraded forms of the processed and glycosylated 95- to 100-kDa receptor. The presence or absence of reducing agents in the detergent solubilization mixture does not change the pattern or amount of the receptor forms recognized by the antibody, including the 54-kDa form; however, boiling does. The presence of these proteins in membrane preparations from cells transfected with mutant receptors can be used to establish that the receptor is normally synthesized, processed, and integrated in the membrane, even if the mutant results in a receptor with no TSH binding or function. In addition, the presence of all forms in association with losses in TSH binding or function reflects a defect in a subsequent step, i.e. altered receptor conformation in the membrane. Applied to studies of two cysteine mutations, 41 and 398, and a chimeric TSH receptor in which residues 90-260 are replaced by comparable residues in the LH/CG receptor, the antibody data can, as a consequence, offer new insights into receptor structure and function. C1 NIDDKD, DEPT BIOCHEM & METAB,CELL REGULAT SECT, BIOCHEM & METAB LAB,BLDG 10,ROOM 9B13, BETHESDA, MD 20892 USA. NR 59 TC 76 Z9 76 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD AUG PY 1992 VL 131 IS 2 BP 815 EP 829 DI 10.1210/en.131.2.815 PG 15 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JG581 UT WOS:A1992JG58100041 PM 1639025 ER PT J AU MERELLI, F STOJILKOVIC, SS IIDA, T KRSMANOVIC, LZ ZHENG, LX MELLON, PL CATT, KJ AF MERELLI, F STOJILKOVIC, SS IIDA, T KRSMANOVIC, LZ ZHENG, LX MELLON, PL CATT, KJ TI GONADOTROPIN-RELEASING HORMONE-INDUCED CALCIUM SIGNALING IN CLONAL PITUITARY GONADOTROPHS SO ENDOCRINOLOGY LA English DT Article ID CYTOSOLIC FREE CALCIUM; SECRETORY RESPONSES; CHANNELS; CELLS; MOBILIZATION; METABOLISM; DEPENDENCE; ACTIVATION; LINEAGE; INFLUX AB In agonist-stimulated clonal pituitary gonadotrophs (alpha-T3-1 cells), cytoplasmic calcium ([Ca2+]i) exhibited rapid and prominent peak increases, followed by lower, but sustained, elevations for up to 15 min. The [Ca2+]i response to GnRH was rapidly inhibited by prior addition of a potent GnRH antagonist. In the absence of extracellular Ca2+ the initial peak [Ca2+]i response was only slightly decreased, but the prolonged increase in [Ca2+]i was abolished, indicating that the peak is derived largely from intracellular calcium mobilization and the sustained phase from Ca2+ influx. Application of the endoplasmic reticulum Ca2+-ATPase blocker thapsigargin caused progressive and dose-dependent elevation of [Ca2+]i and decreased the peak amplitude of the GnRH-induced Ca2+ response. On the other hand, addition of dihydropyridine calcium channel antagonists before or after GnRH treatment prevented or terminated the plateau phase, respectively, consistent with entry of Ca2+ through L-type voltage-sensitive Ca2+ channels (VSCC) as the major Ca2+ influx pathway during GnRH action. The presence of L-type VSCC in alpha-T3-1 cells was further indicated by the ability of elevated extracellular K+ levels and the dihydropyridine calcium channel agonist Bay K 8644 to elevate [Ca2+]i in an extracellular calcium-dependent manner. These actions of depolarization and Bay K 8644 were inhibited by nifedipine, with an IC50 of 10 nM. High extracellular K+- and GnRH-induced Ca2+ entry was also attenuated by phorbol esters and permeant diacylglycerols, indicating that protein kinase-C exerts inhibitory modulation of VSCC activity. In contrast to normal pituitary gonadotrophs, in which GnRH induces a frequency-modulated oscillatory [Ca2+]i response, single alpha-T3-1 cells exhibited a nonoscillatory amplitude-modulated signal during agonist stimulation. The [Ca2+]i responses observed in alpha-T3-1 gonadotrophs indicate that the immortalized cells retain functional GnRH receptors and their coupling to the Ca2+ signaling pathway. Ca2+ influx through L-type channels maintains the plateau phase of the [Ca2+]i response during agonist stimulation and is inhibited by activation of protein kinase-C. C1 NICHHD,ENDOCRINOL & REPROD RES BRANCH,BLDG 10,ROOM B1-L400,BETHESDA,MD 20892. UNIV CALIF SAN DIEGO,DEPT REPROD MED,LA JOLLA,CA 92093. FU NICHD NIH HHS [R01 HD072754, R01 HD020377] NR 30 TC 60 Z9 60 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 AUG PY 1992 VL 131 IS 2 BP 925 EP 932 DI 10.1210/en.131.2.925 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JG581 UT WOS:A1992JG58100057 PM 1379169 ER PT J AU VANECEK, J KLEIN, DC AF VANECEK, J KLEIN, DC TI SODIUM-DEPENDENT EFFECTS OF MELATONIN ON MEMBRANE-POTENTIAL OF NEONATAL RAT PITUITARY-CELLS SO ENDOCRINOLOGY LA English DT Article ID GONADOTROPIN-RELEASING HORMONE; FREE CA-2+ CONCENTRATION; INSULIN-SECRETING CELLS; CYTOSOLIC FREE CALCIUM; SENSITIVE K+ CHANNELS; LUTEINIZING-HORMONE; G-PROTEIN; INHIBITION; INVITRO; RECEPTORS AB Melatonin inhibits GnRH-stimulated release of LH from neonatal rat pituitary cells, probably by inhibiting GnRH-induced elevation of intracellular Ca2+. This effect of melatonin seems to involve inhibition of Ca2+ influx through voltage-sensitive channels. Accordingly, it is possible that melatonin could act by hyperpolarizing pituitary cells, which would close these channels. This issue was addressed here by determining if melatonin influences membrane potential. Membrane potential and intracellular Ca2+ were studied in neonatal rat pituitary cells in suspension, using bis-oxonol and Fluo-3 as fluorescent indicators, respectively. It was found that treatment with melatonin alone causes membrane hyperpolarization and that it has a repolarizing effect after GnRH-induced membrane depolarization. This effect on membrane potential appears to be mediated by high affinity melatonin receptors and a pertussis toxin-sensitive Na+-dependent mechanism; it is not dependent upon Ca2+, Cl-, or bicarbonate. This may be the molecular basis of action of melatonin in other tissues with high affinity melatonin receptors. C1 NICHHD,NEUROENDOCRINOL SECT,DEV NEUROBIOL LAB,BLDG 36,ROOM 4A07,BETHESDA,MD 20892. CZECHOSLOVAK ACAD SCI,INST PHYSIOL,PRAGUE 4,CZECHOSLOVAKIA. NR 38 TC 39 Z9 39 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 AUG PY 1992 VL 131 IS 2 BP 939 EP 946 DI 10.1210/en.131.2.939 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JG581 UT WOS:A1992JG58100059 PM 1322288 ER PT J AU MULUK, SC HAKIM, FT SHEARER, GM AF MULUK, SC HAKIM, FT SHEARER, GM TI REGULATION OF GRAFT-VERSUS-HOST-REACTION BY MLS(A)-REACTIVE DONOR T-CELLS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; PARENTAL LYMPHOCYTES; IMMUNE-DEFICIENCY; MLS DETERMINANTS; GENE-PRODUCTS; LETHAL GRAFT; I-A; RECEPTOR; DISEASE; ALLOSUPPRESSOR AB Injection of A/J splenocytes (H-2D(d), Mls(c)) into unirradiated (A/J x CBA)F1 (BAF1) host mice (H-2D(d/k), Mls(d)) results in an acute suppressive graft-vs.-host reaction (GVHR), characterized by immune dysfunction and appreciable donor cell engraftment; injection of the CBA/J parent (H-2D(k), Mls(d)), which recognizes no Mls disparity in the host, results in little or no GVHR. Furthermore, the Mls(a)-reactive V(beta-6) and V(beta-8.1) T cell subsets in A/J T cells expand significantly in the GVHR host. Finally, depletion of V(beta-6)+ and V(beta-8.1)+ from the A/J population abrogates the proliferative response to BAF1 in vitro and the development of GVHR in vivo. Thus, the response to Mls determinants can contribute to the generation of a GVHR. C1 NCI,EXPTL IMMUNOL BRANCH,BLDG 10,RM4B17,BETHESDA,MD 20892. NR 35 TC 12 Z9 12 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD AUG PY 1992 VL 22 IS 8 BP 1967 EP 1973 DI 10.1002/eji.1830220803 PG 7 WC Immunology SC Immunology GA JH919 UT WOS:A1992JH91900002 PM 1639099 ER PT J AU FARGEAS, C WU, CY NAKAJIMA, T COX, D NUTMAN, T DELESPESSE, G AF FARGEAS, C WU, CY NAKAJIMA, T COX, D NUTMAN, T DELESPESSE, G TI DIFFERENTIAL EFFECT OF TRANSFORMING GROWTH-FACTOR-BETA ON THE SYNTHESIS OF T(H)1-LYMPHOKINES AND T(H)2-LIKE LYMPHOKINES BY HUMAN LYMPHOCYTES-T SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Note ID ENHANCES IGA PRODUCTION; CELL PROLIFERATION; MONONUCLEAR-CELLS; INTERFERON-GAMMA; GENE-EXPRESSION; NON-B; INTERLEUKIN-4; FACTOR-BETA-1; INHIBITION; GLUCOCORTICOIDS AB (TGF)-beta is a pluripotent cytokine exerting differential effects on distinct components of the immune response. The present report, based on lymphokine determination in culture supernatants and Northern blot analysis of lympokine mRNA, demonstrates that TGF-beta-2 markedly inhibits interleukin (IL)-4 and IL-5 synthesis by polyclonally activated human T cells in the absence of any significant effect on (IFN)-gamma, lymphotoxin or IL-2, suggesting a modulatory effect of TGF-beta-2 on the interferon T(h)1/T(h)2) balance of immune responses. The inhibitory effect of TGF-beta on IFN-gamma production by unfractionated peripheral blood mononuclear cells is likely to reflect the blunting of natural killer cell activation by TGF-beta. C1 UNIV MONTREAL,NOTRE DAME HOSP,ALLERGY RES LAB,1560 SHERBROOKE ST E,MONTREAL H2L 4M1,QUEBEC,CANADA. NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. CIBA GEIGY PHARMACEUT CORP,BASEL,SWITZERLAND. NR 37 TC 123 Z9 126 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD AUG PY 1992 VL 22 IS 8 BP 2173 EP 2176 DI 10.1002/eji.1830220833 PG 4 WC Immunology SC Immunology GA JH919 UT WOS:A1992JH91900032 PM 1386318 ER PT J AU LUCIGNANI, G SCHMIDT, K MORESCO, RM TURKHEIMER, F STRIANO, G SOKOLOFF, L FAZIO, F AF LUCIGNANI, G SCHMIDT, K MORESCO, RM TURKHEIMER, F STRIANO, G SOKOLOFF, L FAZIO, F TI OPTIMAL TIME FRAME AND ANALYTICAL PROCEDURE FOR DETERMINATION OF CEREBRAL GLUCOSE-UTILIZATION IN HETEROGENEOUS TISSUES WITH [F-18] FDG AND PET SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 UNIV MILAN,INST HS RAFFAELE,INB,CNR,I-20122 MILAN,ITALY. NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. RI Lucignani, Giovanni/C-6773-2008 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 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PD AUG PY 1992 VL 19 IS 8 BP 646 EP 646 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JL496 UT WOS:A1992JL49600299 ER PT J AU SCOTT, AM DIVGI, CR WELT, S KEMENY, N FINN, RD PENTLOW, K OLD, LJ SCHLOM, J LARSON, SM AF SCOTT, AM DIVGI, CR WELT, S KEMENY, N FINN, RD PENTLOW, K OLD, LJ SCHLOM, J LARSON, SM TI RADIOIMMUNOTHERAPY WITH I-131-LABELED MONOCLONAL-ANTIBODY CC49 IN COLORECTAL-CANCER SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. NIH,BETHESDA,MD 20892. NR 0 TC 11 Z9 11 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PD AUG PY 1992 VL 19 IS 8 BP 709 EP 709 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JL496 UT WOS:A1992JL49600553 ER PT J AU CARTER, CA ALBRIGHT, CD KAUFMAN, DG AF CARTER, CA ALBRIGHT, CD KAUFMAN, DG TI DIFFERENTIAL-EFFECTS OF DIOCTANOYLGLYCEROL ON FIBRONECTIN LOCALIZATION IN NORMAL, PARTIALLY TRANSFORMED, AND MALIGNANT HUMAN ENDOMETRIAL STROMAL CELLS SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID PROTEIN-KINASE-C; PHORBOL ESTER; RAS ONCOGENE; FOCAL CONTACTS; GROWTH-CONTROL; FIBROBLASTS; ADHESION; TUMORIGENICITY; DIACYLGLYCEROL; IDENTIFICATION C1 UNIV CAROLINA,DEPT PATHOL,CHAPEL HILL,NC 27599. UNIV N CAROLINA,LINEBERGER COMPREHENS CANC CTR,CHAPEL HILL,NC 27599. RP CARTER, CA (reprint author), NIEHS,ENVIRONM TOXICOL BRANCH,POB 12233,RES TRIANGLE PK,NC 27709, USA. FU NCI NIH HHS [CA31733]; NIEHS NIH HHS [ES07017] NR 50 TC 7 Z9 7 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 AUG PY 1992 VL 201 IS 2 BP 262 EP 272 DI 10.1016/0014-4827(92)90273-B PG 11 WC Oncology; Cell Biology SC Oncology; Cell Biology GA JH390 UT WOS:A1992JH39000003 PM 1322312 ER PT J AU PARRIS, CN KRAEMER, KH AF PARRIS, CN KRAEMER, KH TI ULTRAVIOLET MUTAGENESIS IN HUMAN-LYMPHOCYTES - THE EFFECT OF CELLULAR-TRANSFORMATION SO EXPERIMENTAL CELL RESEARCH LA English DT Article ID SHUTTLE VECTOR PLASMID; XERODERMA-PIGMENTOSUM; RAS ONCOGENES; MUTATIONAL SPECTRUM; POINT MUTATIONS; SKIN-CANCER; CELLS; FIBROBLASTS; DNA; REPAIR C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. FU Intramural NIH HHS [Z01 BC004517-31] NR 41 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD AUG PY 1992 VL 201 IS 2 BP 462 EP 469 DI 10.1016/0014-4827(92)90295-J PG 8 WC Oncology; Cell Biology SC Oncology; Cell Biology GA JH390 UT WOS:A1992JH39000025 PM 1322318 ER PT J AU POLTORAK, M SHIMODA, K FREED, WJ AF POLTORAK, M SHIMODA, K FREED, WJ TI L1 SUBSTRATE ENHANCES OUTGROWTH OF TYROSINE HYDROXYLASE-IMMUNOREACTIVE NEURITES IN MESENCEPHALIC CELL-CULTURE SO EXPERIMENTAL NEUROLOGY LA English DT Article ID NEURONAL PROCESS OUTGROWTH; MYELIN-ASSOCIATED GLYCOPROTEIN; PERIPHERAL NERVOUS-SYSTEM; ADRENAL-MEDULLA GRAFTS; ADHESION MOLECULES; EXTRACELLULAR-MATRIX; N-CAM; DOPAMINERGIC-NEURONS; SUBSTANTIA-NIGRA; DEVELOPMENTAL EXPRESSION C1 ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,BIOCHEM GENET LAB,WASHINGTON,DC 20032. RP POLTORAK, M (reprint author), ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,NEUROPSYCHIAT BRANCH,PRECLIN NEUROSCI SECT,WASHINGTON,DC 20032, USA. NR 61 TC 14 Z9 14 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD AUG PY 1992 VL 117 IS 2 BP 176 EP 184 DI 10.1016/0014-4886(92)90124-9 PG 9 WC Neurosciences SC Neurosciences & Neurology GA JH927 UT WOS:A1992JH92700006 PM 1354165 ER PT J AU ALBRIGHT, JF OPPENHEIM, JJ AF ALBRIGHT, JF OPPENHEIM, JJ TI CONTEMPORARY TOPICS IN IMMUNOLOGY - APPROACHES TO IMMUNOTHERAPY EMERGING FROM BASIC RESEARCH SO FASEB JOURNAL LA English DT Article DE T-CELL RECEPTOR MHC PEPTIDE INTERACTIONS; B-CELL TOLERANCE; ANERGY-INFLAMMATORY DISEASE; TRANSGENIC RATS; INTERLEUKIN-10; TRANSFORMING GROWTH FACTOR-BETA ID CELL STIMULATORY FACTOR; B-CELLS AB The seventh symposium in thc series "Contemporary Topics in Immunology" was held on April 21, 1991, at the FASEB meeting in Atlanta, Georgia. It was sponsored by the National Institute of Allergy and Infectious Diseases, The American Association of Immunologists, and the Clinical Immunology Society. Five topics were discussed by leading researchers in areas of immunology that currently are of exceptional interest and show promise of leading to new advances in the prevention and treatment of human diseases. The topics included: the interactions between immunogenic peptides, class I MHC molecules and T cell receptors; initiation, maintenance, and breakdown of self-tolerance in B lymphocytes; inflammatory disease in HLA-B27 transgenic rats; properties and functions of interleukin-10; and transforming growth factor-beta in reproductive immunology. The exceptional quality of the presentations in this seventh symposium exemplified perfectly the path of basic research that often leads from the laboratory to the clinic. C1 NCI,FREDERICK CANC RES FACIL,MOLEC IMMUNOREGULAT LAB,FREDERICK,MD 21701. RP ALBRIGHT, JF (reprint author), NIAID,DIV ALLERGY IMMUNOL & TRANSPLANTAT,BASIC IMMUNOL BRANCH,BETHESDA,MD 20892, USA. NR 6 TC 3 Z9 3 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD AUG PY 1992 VL 6 IS 11 BP 2890 EP 2894 PG 5 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA JJ665 UT WOS:A1992JJ66500002 PM 1644254 ER PT J AU HEYES, MP SAITO, K JACOBOWITZ, D MARKEY, SP TAKIKAWA, O VICKERS, JH AF HEYES, MP SAITO, K JACOBOWITZ, D MARKEY, SP TAKIKAWA, O VICKERS, JH TI POLIOVIRUS INDUCES INDOLEAMINE-2,3-DIOXYGENASE AND QUINOLINIC ACID SYNTHESIS IN MACAQUE BRAIN SO FASEB JOURNAL LA English DT Article DE ENTEROVIRUS; INFLAMMATION; NEURODEGENERATION; EXCITOTOXIN; KYNURENINE PATHWAY; INDOLEAMINE 2,3-DIOXYGENASE; CYTOKINES ID CENTRAL NERVOUS-SYSTEM; CEREBROSPINAL-FLUID; INTERFERON-GAMMA; KYNURENIC ACID; INDOLEAMINE 2,3-DIOXYGENASE; HUNTINGTONS-DISEASE; RAT-BRAIN; ALZHEIMERS-DISEASE; RHESUS MACAQUES; REGIONAL BRAIN AB Accumulation of the neurotoxin quinolinic acid within the brain occurs in a broad spectrum of patients with inflammatory neurologic disease and may be of neuropathologic significance. The production of quinolinic acid was postulated to reflect local induction of indoleamine 2,3-dioxygenase by cytokines in reactive cells and inflammatory cell infiltrates within the central nervous system. To test this hypothesis, macaques received an intraspinal injection of poliovirus as a model of localized inflammatory neurologic disease. Seventeen days later, spinal cord indoleamine 2,3-dioxygenase activity and quinolinic acid concentrations in spinal cord and cerebrospinal fluid were both increased in proportion to the degree of inflammatory responses and neurologic damage in the spinal cord, as well as the severity of motor paralysis. The absolute concentrations of quinolinic acid achieved in spinal cord and cerebrospinal fluid exceeded levels reported to kill spinal cord neurons in vitro. Smaller increases in indoleamine 2,3-dioxygenase activity and quinolinic acid concentrations also occurred in parietal cortex, a poliovirus target area. In frontal cortex, which is not a target for poliovirus, indoleamine 2,3-dioxygenase was not affected. A monoclonal antibody to human indoleamine 2,3-dioxygenase was, used to visualize indoleamine 2,3-dioxygenase predominantly in grey matter of poliovirus-infected spinal cord, in conjunction with local inflammatory lesions. Macrophage/monocytes in vitro synthesized [C-13(6)]quinolinic acid from [C-13(6)]L-tryptophan, particularly when stimulated by interferon-gamma. Spinal cord slices from poliovirus-inoculated macaques in vitro also converted [C-13(6)]L-tryptophan to [C-13(6)]quinolinic acid. We conclude that local synthesis of quinolinic acid from L-tryptophan within the central nervous system follows the induction of indoleamine-2,3-dioxygenase, particularly within macrophage/microglia. In view of this link between immune stimulation and the synthesis of neurotoxic amounts of quinolinic acid, we propose that attenuation of local inflammation, strategies to reduce the synthesis of neuroactive kynurenine pathway metabolites, or drugs that interfere with the neurotoxicity of quinolinic acid offer new approaches to therapy in inflammatory neurologic disease. C1 NIMH, CLIN SCI LAB, HISTOPHARMACOL SECT, BETHESDA, MD 20892 USA. OSAKA BIOSCI INST, DEPT CELL BIOL, OSAKA 565, JAPAN. US FDA, CTR BIOL EVALUAT & RES, PATHOBIOL & PRIMATOL LAB, BETHESDA, MD 20892 USA. RP HEYES, MP (reprint author), NIMH, CLIN SCI LAB, ANALYT BIOCHEM SECT, BLDG 10, ROOM 3D40, BETHESDA, MD 20892 USA. NR 55 TC 96 Z9 98 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 AUG PY 1992 VL 6 IS 11 BP 2977 EP 2989 PG 13 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA JJ665 UT WOS:A1992JJ66500012 PM 1322853 ER PT J AU SEI, Y ARORA, PK SKOLNICK, P PAUL, IA AF SEI, Y ARORA, PK SKOLNICK, P PAUL, IA TI SPATIAL-LEARNING IMPAIRMENT IN A MURINE MODEL OF AIDS SO FASEB JOURNAL LA English DT Article DE SPATIAL LEARNING AND MEMORY; HUMAN IMMUNODEFICIENCY VIRUS; HIV-1; AIDS; AIDS DEMENTIA COMPLEX; MICE ID INDUCED IMMUNODEFICIENCY SYNDROME; MICE; RETROVIRUS; INFECTION; VIRUS; ANTIDEPRESSANTS; LOCALIZATION; BRAINS; MAIDS AB Mice infected with an immunosuppressive murine leukemia virus (MuLV) mixture, LP-BM5, displayed profound and selective deficits in spatial learning in a modified Morris water maze. These deficits appeared before the appearance of gross neurological impairment or histopathological changes in the central nervous system. Thus, LP-BM5-infected mice displayed deficits in several aspects of trained performance compared to controls. Furthermore, a failure to exhibit any evidence of task acquisition in this maze was observed almost twice as frequently (P < 0.0005) in infected mice as in uninfected controls. Moreover, in the absence of gross visual, motoric, or motivational impairment, LP-BM5 MuLV-infected animals exhibited neither the target directed search pattern nor the spatial preference characteristic of controls. The spatial learning and memory deficit described here is the first report of cognitive impairment accompanying viral-induced immunosuppression in a nonprimate species. C1 NIDDK,NEUROSCI LAB,BLDG 8,ROOM 111,BETHESDA,MD 20892. NR 28 TC 48 Z9 48 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD AUG PY 1992 VL 6 IS 11 BP 3008 EP 3013 PG 6 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA JJ665 UT WOS:A1992JJ66500016 PM 1644264 ER PT J AU SENTJURC, M MASON, RP AF SENTJURC, M MASON, RP TI INHIBITION OF RADICAL ADDUCT REDUCTION AND REOXIDATION OF THE CORRESPONDING HYDROXYLAMINES IN INVIVO SPIN TRAPPING OF CARBON TETRACHLORIDE-DERIVED RADICALS SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE CARBON TETRACHLORIDE; FREE RADICALS; CCL4 METABOLISM; BILE; SPIN TRAPPING ID PERFUSED RAT-LIVER; SOLUBLE NITROXIDES; CONTRAST AGENTS; LIVING CELLS; METABOLISM; LABELS; OXYGEN; HEPATOCYTES; HEMOGLOBIN; FRACTIONS AB In vivo spin trapping of radical metabolites has become a promising tool in understanding and predicting toxicities caused by different xenobiotics. However, in biological systems radical adducts can be reduced to electron paramagnetic resonance (EPR)-silent hydroxylamines. To overcome this difficulty, different procedures for reoxidation of the reduced radical adducts were systematically investigated and some metabolic inhibitors of nitroxide reduction were tested. As a test system, carbon tetrachloride (CCl4), a known hepatotoxic substance, was used. CCl4 is metabolized by liver to .CCl3 and, in the presence of the spin trap phenyl N-t-butylnitrone (PBN), forms the PBN/.CCl3 and PBN/.CO2- radical adducts. These radical adducts were measured in the bile using electron paramagnetic resonance after administration of CCl4 and PBN to the rat. We have shown that these radical adducts were reduced to the corresponding hydroxylamines in vivo. since immediately after the collection of bile only traces of the radical adducts could be detected, but after oxidation by different procedures such as bubbling with oxygen, addition of mild oxidant potassium ferricyanide or autoxidation the EPR spectra intensity increases. indicating that the hydroxylamines had been re-oxidized back to nitroxides. The collection of bile into plastic Eppendorf tubes containing the sulfhydryl reagent N-ethylmaleimide (NEM) or the enzyme ascorbate oxidase did not increase the intensity of the spectra significantly, demonstrating that neither reduction by reduced glutathione (GSH) nor ascorbic acid occurred ex vivo. However in the presence of NEM faster re-oxidation was observed. A new radical adduct that was not observed previously in any in vivo experiment and which exhibited C-13 hyperfine coupling was detected when the rats were injected with (CCl4)-C-13. We have proven that this is the same adduct detected previously in vitro in microsomal incubations of CCl4, PBN, GSH, and reduced nicotinamide adenine dinucleotide phosphate (NADPH). As a general rule. we have shown that a variety of oxidation procedures should be tried to detect the different radical adducts which are otherwise not observable due to the in vivo reduction of radical adducts. C1 NIEHS,MOLEC BIOPHYS LAB,RES TRIANGLE PK,NC 27709. NR 42 TC 42 Z9 42 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD AUG PY 1992 VL 13 IS 2 BP 151 EP 160 DI 10.1016/0891-5849(92)90077-T PG 10 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA JD557 UT WOS:A1992JD55700011 PM 1325396 ER PT J AU GAWORSKI, CL ARANYI, C HALL, A LEVINE, BS JACKSON, CD ABDO, KM AF GAWORSKI, CL ARANYI, C HALL, A LEVINE, BS JACKSON, CD ABDO, KM TI PRECHRONIC INHALATION TOXICITY STUDIES OF ISOBUTYL NITRITE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID VOLATILE NITRITES; KAPOSIS SARCOMA; BUTYL; INVITRO; MICE C1 IIT,RES INST,10 W 35TH ST,CHICAGO,IL 60616. PATHOL ASSOCIATES INC,CHICAGO,IL 60616. UNIV ILLINOIS,CHICAGO,IL 60612. NATL CTR TOXICOL RES,JEFFERSON,AR 72079. NIEHS,NATL TOXICOL PROGRAM,RES TRIANGLE PK,NC 27709. FU NIEHS NIH HHS [N0S-ES-65143] NR 20 TC 12 Z9 12 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD AUG PY 1992 VL 19 IS 2 BP 169 EP 175 DI 10.1016/0272-0590(92)90148-B PG 7 WC Toxicology SC Toxicology GA JG896 UT WOS:A1992JG89600002 PM 1516772 ER PT J AU HARRIS, MW CHAPIN, RE LOCKHART, AC JOKINEN, MP ALLEN, JD HASKINS, EA AF HARRIS, MW CHAPIN, RE LOCKHART, AC JOKINEN, MP ALLEN, JD HASKINS, EA TI ASSESSMENT OF A SHORT-TERM REPRODUCTIVE AND DEVELOPMENTAL TOXICITY SCREEN SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID ETHYLENE-GLYCOL MONOMETHYL; MONOETHYL ETHER; MICE; RATS; THEOPHYLLINE; TERATOLOGY; MOUSE C1 NIEHS,DEV & REPROD TOXICOL GRP,MAIL DROP E1-02,POB 12233,RTP,RES TRIANGLE PK,NC 27709. NIEHS,COMP SCI CORP,RES TRIANGLE PK,NC 27709. NIEHS,CHEM CARCINOGENESIS BRANCH,RES TRIANGLE PK,NC 27709. OI Chapin, Robert/0000-0002-5997-1261 NR 25 TC 25 Z9 25 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 AUG PY 1992 VL 19 IS 2 BP 186 EP 196 DI 10.1016/0272-0590(92)90150-G PG 11 WC Toxicology SC Toxicology GA JG896 UT WOS:A1992JG89600004 PM 1516774 ER PT J AU HASEMAN, JK SEILKOP, SK AF HASEMAN, JK SEILKOP, SK TI AN EXAMINATION OF THE ASSOCIATION BETWEEN MAXIMUM-TOLERATED DOSE AND CARCINOGENICITY IN 326 LONG-TERM STUDIES IN RATS AND MICE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID NATIONAL-TOXICOLOGY-PROGRAM; GENETIC TOXICITY ASSAYS; RODENT CARCINOGENICITY; POTENCY; BIOASSAYS; CHEMICALS; RISK C1 ANALYT SCI INC,DURHAM,NC 27713. RP HASEMAN, JK (reprint author), NIEHS,DIV BIOMETRY & RISK ASSESSMENT,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 27 TC 27 Z9 27 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD AUG PY 1992 VL 19 IS 2 BP 207 EP 213 DI 10.1016/0272-0590(92)90153-9 PG 7 WC Toxicology SC Toxicology GA JG896 UT WOS:A1992JG89600007 PM 1516777 ER PT J AU KRAWCZYNSKI, K BEACH, MJ BRADLEY, DW KUO, G DIBISCEGLIE, AM HOUGHTON, M REYES, GR KIM, JP CHOO, QL ALTER, MJ AF KRAWCZYNSKI, K BEACH, MJ BRADLEY, DW KUO, G DIBISCEGLIE, AM HOUGHTON, M REYES, GR KIM, JP CHOO, QL ALTER, MJ TI HEPATITIS-C VIRUS-ANTIGEN IN HEPATOCYTES - IMMUNOMORPHOLOGICAL DETECTION AND IDENTIFICATION SO GASTROENTEROLOGY LA English DT Article ID NON-B-HEPATITIS; EXPERIMENTAL NON-A; TRANSMITTED NON-A; VIRAL SEQUENCES; CHIMPANZEES; ANTIBODIES; INTERFERON; GENOME; IMMUNOFLUORESCENCE; THERAPY C1 CHIRON CORP,EMERYVILLE,CA. NIDDKD,LIVER DIS SECT,BETHESDA,MD. GENELABS INC,REDWOOD CITY,CA. RP KRAWCZYNSKI, K (reprint author), CTR DIS CONTROL,HEPATITIS BRANCH,BLDG 6,ROOM 192,ATLANTA,GA 30333, USA. NR 30 TC 151 Z9 151 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 AUG PY 1992 VL 103 IS 2 BP 622 EP 629 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JF014 UT WOS:A1992JF01400035 PM 1378804 ER PT J AU SWAIN, MG ROTHMAN, RB XU, H VERGALLA, J BERGASA, NV JONES, EA AF SWAIN, MG ROTHMAN, RB XU, H VERGALLA, J BERGASA, NV JONES, EA TI ENDOGENOUS OPIOIDS ACCUMULATE IN PLASMA IN A RAT MODEL OF ACUTE CHOLESTASIS SO GASTROENTEROLOGY LA English DT Article ID PRIMARY BILIARY-CIRRHOSIS; BLOOD-BRAIN-BARRIER; MET-ENKEPHALIN; BINDING; IMMUNOREACTIVITY; RECEPTORS; TRANSPORT; PEPTIDES; LIGAND; SITE C1 NIDDKD,MED CHEM LAB,BETHESDA,MD 20892. NIDA,RES CTR,BALTIMORE,MD. RP SWAIN, MG (reprint author), NIDDKD,LIVER DIS SECT,BLDG 10,ROOM 4D-52,BETHESDA,MD 20892, USA. NR 30 TC 144 Z9 146 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 AUG PY 1992 VL 103 IS 2 BP 630 EP 635 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JF014 UT WOS:A1992JF01400036 PM 1634078 ER PT J AU PARRIS, CN SEIDMAN, MM AF PARRIS, CN SEIDMAN, MM TI A SIGNATURE ELEMENT DISTINGUISHES SIBLING AND INDEPENDENT MUTATIONS IN A SHUTTLE VECTOR PLASMID SO GENE LA English DT Article DE RANDOM SEQUENCE OLIGODEOXYRIBONUCLEOTIDE; MAMMALIAN MUTAGENESIS; MUTATIONAL HOTSPOTS ID XERODERMA PIGMENTOSUM-CELLS; ESCHERICHIA-COLI; MAMMALIAN-CELLS; MUTAGENESIS; GENE AB We have developed a new shuttle vector plasmid for studying mutagenesis in mammalian cells that permits proof of independence of identical mutations. Mutations occur more frequently at some sites in a gene than in others, and in a collection of mutant plasmids from a single transfection of mammalian cells the same mutation may appear several times. However, those arising from independent events cannot be distinguished from siblings of an initial event. The new vector system (pSP189) is a population of plasmids, each of which contains an 8-bp `signature sequence'. This sequence confers a unique identification tag to each plasmid and allows individual members to be identified by a distinctive signature. The plasmid also carries the Escherichia coli bacterial supF gene as a marker for mutagenesis, as well as sequences which support replication in primate (including human) cells and E. coli. We have used the pSP189 system to generate a UV-induced spectrum of mutations in supF following replication in a single plate of human DNA-repair-deficient cells (xeroderma pigmentosum, complementation group A). With the signature sequence, we were able to determine whether identical mutations derived from the transfection were of independent or sibling origin. There were eight identical mutations at the strongest hotspot, all of which had different signature sequences. Only one of these events would have been reported in previous experiments. This plasmid reduces the effort required to generate a spectrum of mutations caused by a DNA-damaging agent and allows a more accurate assessment of mutational hotspot intensity. C1 OTSUKA PHARMACEUT CO LTD,9900 MED CTR DR,ROCKVILLE,MD 20850. NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 15 TC 112 Z9 112 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD AUG 1 PY 1992 VL 117 IS 1 BP 1 EP 5 DI 10.1016/0378-1119(92)90482-5 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA JG912 UT WOS:A1992JG91200001 PM 1644298 ER PT J AU GERSHON, PD MOSS, B AF GERSHON, PD MOSS, B TI TRANSITION FROM RAPID PROCESSIVE TO SLOW NONPROCESSIVE POLYADENYLATION BY VACCINIA VIRUS POLY(A) POLYMERASE CATALYTIC SUBUNIT IS REGULATED BY THE NET LENGTH OF THE POLY(A) TAIL SO GENES & DEVELOPMENT LA English DT Article DE POLY(A) POLYMERASE; POLYADENYLATION; MESSENGER RNA; 3'-POLY(A) TAIL; VACCINIA ID YEAST SACCHAROMYCES-CEREVISIAE; MESSENGER-RNA POLYADENYLATION; 3' END; TRANSCRIPTION TERMINATION; SPECIFICITY FACTOR; EARLY GENES; EXPRESSION; CLEAVAGE; INVITRO; SEQUENCE AB The mRNA of vaccinia virus, like that of eukaryotes, possesses a poly(A) tail. VP55, the catalytic subunit of the heterodimeric vaccinia virus poly(A) polymerase, was overexpressed and purified to near homogeneity. VP55 polyadenylated a 30-mer primer representing the 3' end of a vaccinia virus mRNA bimodally: 30-35 adenylates were added in a rapid, processive, initial burst, after which polyadenylation decelerated dramatically and became nonprocessive. Polyadenylation of variants of the 30-mer primer, which contained preformed 3'-oligo(A) extensions, showed that the transition between the two modes of polyadenylation was regulated by the net length of the 3'-oligo(A) tail rather than the number of adenylate additions catalyzed by VP55. Primers comprising oligo(A) alone were polyadenylated only if they were >34 nucleotides in length and, then, only in the slow nonprocessive mode. These data support a dynamic model whereby the mode of polyadenylation by VP55 is regulated by sequences within the 3' 30-35 nucleotides of the mRNA: Polyadenylation is rapid and processive until a net 3'-oligo(A) length of 30-35 nucleotides is achieved. Consistent with this, excess oligo(A) did not compete with the 30-mer primer for rapid processive polyadenylation. The primer specificity of VP55 may contribute to the selective polyadenylation of newly formed mRNA. C1 NIAID,VIRAL DIS LAB,BETHESDA,MD 20892. NR 41 TC 37 Z9 37 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD AUG PY 1992 VL 6 IS 8 BP 1575 EP 1586 DI 10.1101/gad.6.8.1575 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA JH599 UT WOS:A1992JH59900018 PM 1353739 ER PT J AU KAWAKAMI, K SHAFER, BK GARFINKEL, DJ STRATHERN, JN NAKAMURA, Y AF KAWAKAMI, K SHAFER, BK GARFINKEL, DJ STRATHERN, JN NAKAMURA, Y TI TY ELEMENT-INDUCED TEMPERATURE-SENSITIVE MUTATIONS OF SACCHAROMYCES-CEREVISIAE SO GENETICS LA English DT Article ID YEAST RETROTRANSPOSON TY; CELL-DIVISION CYCLE; HEAT-SHOCK PROTEIN; MITOCHONDRIAL PROTEIN; MULTIGENE FAMILY; ESCHERICHIA-COLI; DELTA-SEQUENCES; DNA-POLYMERASE; PEP4 GENE; GROWTH AB Temperature-sensitive mutants of Saccharomyces cerevisiae were isolated by insertional mutagenesis using the HIS3 marked retrotransposon TyH3HIS3. In such mutants, the TyHIS3 insertions are expected to identify loci which encode genes essential for cell growth at high temperatures but dispensable at low temperatures. Five mutations were isolated and named hit for high temperature growth. The hit1-1 mutation was located on chromosome X and conferred the pet phenotype. Two hit2 mutations, hit2-1 and hit2-2, were located on chromosome III and caused the deletion of the PET18 locus which has been shown to encode a gene required for growth at high temperatures. The hit3-1 mutation was located on chromosome VI and affected the CDC26 gene. The hit4-1 mutation was located on chromosome XIII. These hit mutations were analyzed in an attempt to identify novel genes involved in the heat shock response. The hit1-1 mutation caused a defect in synthesis of a 74-kD heat shock protein. Western blot analysis revealed that the heat shock protein corresponded to the SSC1 protein, a member of the yeast hsp70 family. In the hit1-1 mutant, the TyHIS3 insertion caused a deletion of a 3-kb DNA segment between the delta-1 and delta-4 sequences near the SUP4 locus. The 1031-bp wild-type HIT1 DNA which contained an open reading frame encoding a protein of 164 amino acids and the AGG arginine tRNA gene complemented all hit1-1 mutant phenotypes, indicating that the mutant phenotypes were caused by the deletion of these genes. The pleiotropy of the HIT1 locus was analyzed by constructing a disruption mutation of each gene in vitro and transplacing it to the chromosome. This analysis revealed that the HIT1 gene essential for growth at high temperatures encodes the 164-amino acid protein. The arginine tRNA gene, named HSX1, is essential for growth on a nonfermentable carbon source at high temperatures and for synthesis of the SSC1 heat shock protein. C1 FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,EUKARYOT GENE EXPRESS LAB,FREDERICK,MD 21701. RP KAWAKAMI, K (reprint author), UNIV TOKYO,INST MED SCI,DEPT TUMOR BIOL,MINATO KU,TOKYO 108,JAPAN. FU NCI NIH HHS [N01-CO-74101] NR 55 TC 27 Z9 29 U1 0 U2 0 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD AUG PY 1992 VL 131 IS 4 BP 821 EP 832 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA JF933 UT WOS:A1992JF93300007 PM 1325386 ER PT J AU COLE, TJ COPELAND, NG GILBERT, DJ JENKINS, NA SCHUTZ, G RUPPERT, S AF COLE, TJ COPELAND, NG GILBERT, DJ JENKINS, NA SCHUTZ, G RUPPERT, S TI THE MOUSE CREB (CAMP RESPONSIVE ELEMENT BINDING-PROTEIN) GENE - STRUCTURE, PROMOTER ANALYSIS, AND CHROMOSOMAL LOCALIZATION SO GENOMICS LA English DT Article ID TRANSCRIPTION FACTOR CREB; CYCLIC-AMP; LEUCINE ZIPPER; SOMATOSTATIN GENE; EXPRESSION; REGION; DOMAINS; FAMILY; BRAIN; PHOSPHORYLATION C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. RP COLE, TJ (reprint author), GERMAN CANC RES CTR,INST CELL & TUMOR BIOL,NEUENHEIMER FELD 280,W-6900 HEIDELBERG,GERMANY. FU NCI NIH HHS [N01-CO-74101] NR 58 TC 34 Z9 35 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD AUG PY 1992 VL 13 IS 4 BP 974 EP 982 DI 10.1016/0888-7543(92)90010-P PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800010 PM 1387109 ER PT J AU LICHTER, P BRAY, P RIED, T DAWID, IB WARD, DC AF LICHTER, P BRAY, P RIED, T DAWID, IB WARD, DC TI CLUSTERING OF C2-H2 ZINC FINGER MOTIF SEQUENCES WITHIN TELOMERIC AND FRAGILE SITE REGIONS OF HUMAN-CHROMOSOMES SO GENOMICS LA English DT Article ID TRANSCRIPTION FACTOR-IIIA; INSITU HYBRIDIZATION; MULTIGENE FAMILY; PROTEIN GENES; HUMAN GENOME; CELL-LINES; MOUSE; DNA; LOCALIZATION; KRUPPEL C1 YALE UNIV,SCH MED,DEPT GENET,333 CEDAR ST,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT MOLEC BIOPHYS & BIOCHEM,NEW HAVEN,CT 06510. NICHHD,MOLEC GENET LAB,BETHESDA,MD 20892. DEUTSCH KREBSFORSCHUNGSZENTRUM,INST VIRUSFORSCH,W-6900 HEIDELBERG,GERMANY. FU NHGRI NIH HHS [HG-00242, HG-00272] NR 48 TC 50 Z9 58 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 AUG PY 1992 VL 13 IS 4 BP 999 EP 1007 DI 10.1016/0888-7543(92)90013-I PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800013 PM 1505991 ER PT J AU HANLEYHYDE, J MUSHINSKI, JF SADOFSKY, M HUPPI, K KRALL, M KOZAK, CA MOCK, B AF HANLEYHYDE, J MUSHINSKI, JF SADOFSKY, M HUPPI, K KRALL, M KOZAK, CA MOCK, B TI EXPRESSION OF MURINE CYCLIN-B1 MESSENGER-RNAS AND GENETIC-MAPPING OF RELATED GENOMIC SEQUENCES SO GENOMICS LA English DT Article ID 3' UNTRANSLATED REGION; CELL-CYCLE CONTROL; PROTEIN-KINASE; M-PHASE; SACCHAROMYCES-CEREVISIAE; PROMOTING FACTOR; MOUSE; CDNA; MITOSIS; VIRUS C1 NIDDKD,BETHESDA,MD 20892. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RP HANLEYHYDE, J (reprint author), NCI,GENET LAB,BLDG 37,ROOM 2B23,BETHESDA,MD 20892, USA. NR 86 TC 36 Z9 37 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 AUG PY 1992 VL 13 IS 4 BP 1018 EP 1030 DI 10.1016/0888-7543(92)90015-K PG 13 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800015 PM 1387105 ER PT J AU BRANNAN, CI GILBERT, DJ CECI, JD MATSUDA, Y CHAPMAN, VM MERCER, JA EISEN, H JOHNSTON, LA COPELAND, NG JENKINS, NA AF BRANNAN, CI GILBERT, DJ CECI, JD MATSUDA, Y CHAPMAN, VM MERCER, JA EISEN, H JOHNSTON, LA COPELAND, NG JENKINS, NA TI AN INTERSPECIFIC LINKAGE MAP OF MOUSE CHROMOSOME-15 POSITIONED WITH RESPECT TO THE CENTROMERE SO GENOMICS LA English DT Article ID GROWTH-HORMONE RECEPTOR; MYOSIN HEAVY-CHAIN; C-MYC ONCOGENE; MURINE CHROMOSOME-15; INSITU HYBRIDIZATION; GENETIC CONSTITUTION; THYROGLOBULIN GENE; ACID SEQUENCES; MESSENGER-RNA; LOCALIZATION C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,POB B,BLDG 539,FREDERICK,MD 21702. ROSWELL PK CANC INST,DEPT MOLEC & CELLULAR BIOL,BUFFALO,NY 14263. UNIV TEXAS,SW MED CTR,DEPT PHYSIOL,DALLAS,TX 75235. FRED HUTCHINSON CANC RES CTR,DEPT GENET,SEATTLE,WA 98104. UNIV WASHINGTON,DEPT PATHOL,SEATTLE,WA 98195. FU NCI NIH HHS [N01-CO-74101] NR 57 TC 44 Z9 44 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 AUG PY 1992 VL 13 IS 4 BP 1075 EP 1081 DI 10.1016/0888-7543(92)90021-J PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800021 PM 1354638 ER PT J AU JUSTICE, MJ GILBERT, DJ KINZLER, KW VOGELSTEIN, B BUCHBERG, AM CECI, JD MATSUDA, Y CHAPMAN, VM PATRIOTIS, C MAKRIS, A TSICHLIS, PN JENKINS, NA COPELAND, NG AF JUSTICE, MJ GILBERT, DJ KINZLER, KW VOGELSTEIN, B BUCHBERG, AM CECI, JD MATSUDA, Y CHAPMAN, VM PATRIOTIS, C MAKRIS, A TSICHLIS, PN JENKINS, NA COPELAND, NG TI A MOLECULAR GENETIC-LINKAGE MAP OF MOUSE CHROMOSOME-18 REVEALS EXTENSIVE LINKAGE CONSERVATION WITH HUMAN CHROMOSOME-5 AND CHROMOSOME-18 SO GENOMICS LA English DT Article ID MYELIN-BASIC-PROTEIN; MURINE LEUKEMIA-VIRUS; AMINO-ACID SEQUENCE; INTERSPECIFIC BACKCROSS; GROWTH-FACTOR; MYELOBLASTIC LEUKEMIAS; COLORECTAL CANCERS; C-FMS; LOCALIZATION; IDENTIFICATION C1 ROSWELL PK CANC INST, DEPT MOLEC & CELLULAR BIOL, BUFFALO, NY 14263 USA. JOHNS HOPKINS ONCOL CTR, BALTIMORE, MD 21231 USA. FOX CHASE CANC INST, DEPT MOLEC ONCOL, PHILADELPHIA, PA 19111 USA. RP JUSTICE, MJ (reprint author), NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MAMMALIAN GENET LAB, POB B, FREDERICK, MD 21702 USA. FU NCI NIH HHS [5F32CA08853-03, N01-CO-74101] NR 66 TC 53 Z9 53 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 AUG PY 1992 VL 13 IS 4 BP 1281 EP 1288 DI 10.1016/0888-7543(92)90047-V PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800047 PM 1354644 ER PT J AU WEINSTEIN, LS GEJMAN, PV DEMAZANCOURT, P AMERICAN, N SPIEGEL, AM AF WEINSTEIN, LS GEJMAN, PV DEMAZANCOURT, P AMERICAN, N SPIEGEL, AM TI A HETEROZYGOUS 4-BP DELETION MUTATION IN THE G(S)ALPHA GENE (GNAS1) IN A PATIENT WITH ALBRIGHT HEREDITARY OSTEODYSTROPHY SO GENOMICS LA English DT Note ID GRADIENT GEL-ELECTROPHORESIS; NUCLEOTIDE-BINDING PROTEIN; STIMULATORY G-PROTEIN; ALPHA-SUBUNIT GENE; TAY-SACHS DISEASE; RNA; PSEUDOHYPOPARATHYROIDISM; ENDOCRINE; CARRIERS C1 NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. RP WEINSTEIN, LS (reprint author), NIDDKD,MOLEC PATHOPHYSIOL BRANCH,BETHESDA,MD 20892, USA. RI Weinstein, Lee/I-5575-2015; OI Weinstein, Lee/0000-0002-1899-5152 NR 17 TC 77 Z9 78 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD AUG PY 1992 VL 13 IS 4 BP 1319 EP 1321 DI 10.1016/0888-7543(92)90056-X PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800056 PM 1505964 ER PT J AU CHIN, HM MOCK, B KIM, HL KIM, H KOZAK, CA AF CHIN, HM MOCK, B KIM, HL KIM, H KOZAK, CA TI THE GENE FOR THE DIHYDROPYRIDINE-SENSITIVE CALCIUM-CHANNEL ALPHA-2-SUBUNIT (CCHL2A) MAPS TO THE PROXIMAL REGION OF MOUSE CHROMOSOME-5 SO GENOMICS LA English DT Note ID ALPHA-1 SUBUNIT C1 NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. NCI,GENET LAB,BETHESDA,MD 20892. RP CHIN, HM (reprint author), NINCDS,MOLEC BIOL LAB,BLDG 36,ROOM 3D-02,BETHESDA,MD 20892, USA. NR 20 TC 12 Z9 12 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 AUG PY 1992 VL 13 IS 4 BP 1325 EP 1327 DI 10.1016/0888-7543(92)90058-Z PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800058 PM 1324224 ER PT J AU COPELAND, NG GILBERT, DJ CHRETIEN, M SEIDAH, NG JENKINS, NA AF COPELAND, NG GILBERT, DJ CHRETIEN, M SEIDAH, NG JENKINS, NA TI REGIONAL LOCALIZATION OF 3 CONVERTASES, PC1 (NEC-1), PC2 (NEC-2), AND FURIN (FUR), ON MOUSE CHROMOSOMES SO GENOMICS LA English DT Note ID GENETIC-LINKAGE MAP; CLOSE LINKAGE; CDNA SEQUENCE; MURINE; ONCOGENE; PROTEIN; CLONING; LOCI; KEX2; GAP C1 CLIN RES INST MONTREAL, JA DESEVE LABS MOLEC NEUROENDOCRINOL, MONTREAL H2W 1R7, QUEBEC, CANADA. CLIN RES INST MONTREAL, JA DESEVE LABS BIOCHEM NEUROENDOCRINOL, MONTREAL H2W 1R7, QUEBEC, CANADA. RP COPELAND, NG (reprint author), NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, MAMMALIAN GENET LAB, POB B, FREDERICK, MD 21702 USA. RI Seidah, Nabil/I-3596-2013 OI Seidah, Nabil/0000-0001-6503-9342 FU PHS HHS [N01-C0-74101] NR 20 TC 26 Z9 26 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 EI 1089-8646 J9 GENOMICS JI Genomics PD AUG PY 1992 VL 13 IS 4 BP 1356 EP 1358 DI 10.1016/0888-7543(92)90069-5 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800069 PM 1354647 ER PT J AU DEGEN, SJF GILBERT, DJ JENKINS, NA COPELAND, NG AF DEGEN, SJF GILBERT, DJ JENKINS, NA COPELAND, NG TI ASSIGNMENT OF THE GENE CODING FOR HEPATOCYTE GROWTH FACTOR-LIKE PROTEIN TO MOUSE CHROMOSOME-9 SO GENOMICS LA English DT Note ID BETA-GALACTOSIDASE; LINKAGE MAP; AMINOACYLASE-1; EXPRESSION; LOCI C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,FREDERICK,MD 21702. UNIV CINCINNATI,CINCINNATI,OH 45229. RP DEGEN, SJF (reprint author), CHILDRENS HOSP RES FDN,DIV BASIC SCI RES,CINCINNATI,OH 45229, USA. FU NCI NIH HHS [N01-CO-74101]; NHLBI NIH HHS [HL38232] NR 11 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD AUG PY 1992 VL 13 IS 4 BP 1368 EP 1369 DI 10.1016/0888-7543(92)90073-2 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA JH148 UT WOS:A1992JH14800073 PM 1354648 ER PT J AU PERSHAGEN, G LIANG, ZH HRUBEC, Z SVENSSON, C BOICE, JD AF PERSHAGEN, G LIANG, ZH HRUBEC, Z SVENSSON, C BOICE, JD TI RESIDENTIAL RADON EXPOSURE AND LUNG-CANCER IN SWEDISH WOMEN SO HEALTH PHYSICS LA English DT Article DE RADON; CANCER; LUNGS, HUMAN; RISK ANALYSIS ID RADIATION EXPOSURE; INDOOR EXPOSURE; CARCINOMA; SMOKING AB A case-control study was undertaken to investigate the role of residential radon exposure for lung cancer. The study included 210 women with lung cancer diagnosed from 1983-1986 in the county of Stockholm and 191 hospital and 209 population controls. Interviews provided information on lifetime residences and smoking. Radon concentrations measured in 1,573 residences of the study subjects showed a lognormal distribution with arithmetic and geometric means of 127.7 and 96.0 Bq m-3, respectively. Lung cancer risks tended to increase with estimated radon exposure, reaching a relative risk of 1.7 (95% confidence interval: 1.0-2.9) in women having an average radon level exceeding 150 Bq m-3 (4 pCi L-1). Stronger associations were suggested in younger persons and risk estimates appeared to be within the same range as those projected for miners. However, further studies are needed to clarify the level of risk associated with exposure to residential radon. C1 KAROLINSKA HOSP, DEPT ENVIRONM HLTH & INFECT DIS CONTROL, S-10401 STOCKHOLM 60, SWEDEN. NCI, RADIAT EPIDEMIOL BRANCH, BETHESDA, MD 20892 USA. RP PERSHAGEN, G (reprint author), KAROLINSKA INST, INST ENVIRONM MED, DEPT EPIDEMIOL, BOX 60208, S-10401 STOCKHOLM 60, SWEDEN. NR 24 TC 104 Z9 113 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PD AUG PY 1992 VL 63 IS 2 BP 179 EP 186 DI 10.1097/00004032-199208000-00004 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA JE630 UT WOS:A1992JE63000005 PM 1399616 ER PT J AU BERGASA, NV HOOFNAGLE, JH KLEINER, D PARK, Y JONES, EA AF BERGASA, NV HOOFNAGLE, JH KLEINER, D PARK, Y JONES, EA TI METHOTREXATE (MTX) FOR PRIMARY BILIARY-CIRRHOSIS (PBC) - INTERIM EVALUATION OF AN OPEN LABEL STUDY SO HEPATOLOGY LA English DT Meeting Abstract C1 NIDDK,LIVER DIS SECT,BETHESDA,MD. NCI,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD AUG PY 1992 VL 16 IS 2 BP 516 EP 516 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JH147 UT WOS:A1992JH14700050 ER PT J AU DIBISCEGLIE, AM SIMPSON, LH LOTZE, MT HOOFNAGLE, JH AF DIBISCEGLIE, AM SIMPSON, LH LOTZE, MT HOOFNAGLE, JH TI DEVELOPMENT OF HEPATOCELLULAR-CARCINOMA AFTER PROLONGED HEPATITIS-C VIRAL-INFECTION SO HEPATOLOGY LA English DT Meeting Abstract C1 NIDDK,LIVER DIS SECT,BETHESDA,MD. NCI,SURG 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD AUG PY 1992 VL 16 IS 2 BP 530 EP 530 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JH147 UT WOS:A1992JH14700104 ER PT J AU SNG, I LEVIN, A JAFFE, ES NG, HW SIM, CS BLATTNER, WB AF SNG, I LEVIN, A JAFFE, ES NG, HW SIM, CS BLATTNER, WB TI T-CELL LYMPHOMA IN SINGAPORE - PATHOLOGY, CLINICAL FINDINGS AND ASSOCIATION WITH HTLV-1 ANTIBODIES SO HISTOPATHOLOGY LA English DT Article DE MALIGNANT LYMPHOMA; T-CELL LYMPHOMA; HTLV-1 ID UPDATED KIEL CLASSIFICATION; LEUKEMIA-LYMPHOMA; MONOCLONAL-ANTIBODIES; EMBEDDED TISSUES; HUMAN-SERA; VIRUS; MALIGNANCIES; IDENTIFICATION; RETROVIRUS; ANTIGEN AB Of 128 cases of malignant lymphomas studied in Singapore between 1986 and 1988, 28 were identified as peripheral T-cell lymphomas. Sera from two of the 128 cases were positive for HTLV-1 antibodies and both cases had the clinical and pathological features of adult T-cell leukaemia/lymphoma. The pathological and clinical features of the 2 8 cases of peripheral T-cell lymphoma are presented in detail. Survival data indicated no significant difference between the low grade and high grade histological types. Three of the patients had previous or concomitant malignancies. The percentage of T-cell lymphomas associated with HTLV-1 infection in Singapore is low compared to those areas in which HTLV-1 is endemic. C1 SINGAPORE GEN HOSP,DEPT HAEMATOL,SINGAPORE,SINGAPORE. SINGAPORE GEN HOSP,RES TRIANGLE INST UNIT,SINGAPORE,SINGAPORE. NCI,BETHESDA,MD 20892. RP SNG, I (reprint author), SINGAPORE GEN HOSP,DEPT PATHOL,SINGAPORE,SINGAPORE. FU NCI NIH HHS [N01-CP-51030, N01-CP-85603] NR 49 TC 9 Z9 9 U1 1 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0309-0167 J9 HISTOPATHOLOGY JI Histopathology PD AUG PY 1992 VL 21 IS 2 BP 101 EP 113 DI 10.1111/j.1365-2559.1992.tb00358.x PG 13 WC Cell Biology; Pathology SC Cell Biology; Pathology GA JH517 UT WOS:A1992JH51700001 PM 1505928 ER PT J AU EICHMANN, MA GRIFFIN, BP LYONS, JS LARSON, DB FINKEL, S AF EICHMANN, MA GRIFFIN, BP LYONS, JS LARSON, DB FINKEL, S TI AN ESTIMATION OF THE IMPACT OF OBRA-87 ON NURSING-HOME CARE IN THE UNITED-STATES SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article ID RESIDENTS AB The Omnibus Budget Reconciliation Act of 1987 (OBRA-87) established criteria for Medicare- or Medicaid-certified nursing homes to use in admitting or retaining mentally ill patients. In effect, the law created five dispositional categories for residents or potential residents of nursing homes. Using data from the 1985 National Nursing Home Survey conducted by the National Center for Health Statistics, the authors estimate what proportion of nursing home residents would fall into each of the categories. They suggest that the initial impact of the law will be to shift costs from federal programs to the states. Nursing homes will be expected to provide more mental health services. In the absence of other services, the regulations have a high potential for creating homelessness and continuing a pattern of failure to adequately serve patients with serious mental illness. C1 NORTHWESTERN UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,CHICAGO,IL 60611. NIMH,ROCKVILLE,MD 20857. NR 28 TC 14 Z9 14 U1 4 U2 4 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD AUG PY 1992 VL 43 IS 8 BP 781 EP 789 PG 9 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA JF777 UT WOS:A1992JF77700005 PM 1427676 ER PT J AU ANDERSON, WF AF ANDERSON, WF TI THE 1ST SIGNS OF DANGER SO HUMAN GENE THERAPY LA English DT Editorial Material RP ANDERSON, WF (reprint author), NHLBI,MOLEC HEMATOL BRANCH,BLDG 10,70-18,BETHESDA,MD 20892, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD AUG PY 1992 VL 3 IS 4 BP 359 EP 360 DI 10.1089/hum.1992.3.4-359 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA JJ926 UT WOS:A1992JJ92600001 PM 1525207 ER PT J AU HUNTER, L STATES, DJ AF HUNTER, L STATES, DJ TI BAYESIAN CLASSIFICATION OF PROTEIN-STRUCTURE SO IEEE EXPERT-INTELLIGENT SYSTEMS & THEIR APPLICATIONS LA English DT Article RP HUNTER, L (reprint author), NATL LIB MED,BLDG 38A,MAIL STOP 54,BETHESDA,MD 20894, USA. NR 10 TC 8 Z9 8 U1 0 U2 1 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 SN 0885-9000 J9 IEEE EXPERT JI IEEE Expert-Intell. Syst. Appl. PD AUG PY 1992 VL 7 IS 4 BP 67 EP 75 DI 10.1109/64.153466 PG 9 WC Computer Science, Artificial Intelligence; Engineering, Electrical & Electronic SC Computer Science; Engineering GA JH885 UT WOS:A1992JH88500009 ER PT J AU BARNER, M MESSING, LT SEGAL, S AF BARNER, M MESSING, LT SEGAL, S TI INHIBITION OF MURINE ERYTHROLEUKEMIA CELL-DIFFERENTIATION BY NORMAL AND PARTIALLY DELETED C-MYC GENES SO IMMUNOBIOLOGY LA English DT Article; Proceedings Paper CT 7TH SYMP ON SIGNALS AND SIGNAL PROCESSING IN THE IMMUNE SYSTEM CY SEP, 1991 CL KOSZEG, HUNGARY ID DNA-BINDING; TRANSFORMING ACTIVITY; EMBRYO FIBROBLASTS; LEUCINE ZIPPER; N-MYC; PROTEIN; EXPRESSION; RAS; ONCOGENES; COTRANSFORMATION AB In our study of normal and partially deleted myc genes we found that N-myc, similarly to L-myc, can substitute for c-myc and inhibit MEL cell differentiation. All of the known putative functional domains of c-myc seem to be required for this inhibition. It is conceivable that c-myc inhibits differentiation by a mechanism that is related to its normal role in the cell, possibly by regulating transcription of genes involved in growth promotion. As was previously found for all of the other known activities of c-Mvc, the HLH and LZ dimerization motifs are absolutely necessary for inhibition of MEL cell differentiation. Heterodimerization of Myc with Max or Max-like proteins could be a prerequisite for such inhibition. It is, therefore, of interest to study the regulation of max in MEL cells expressing normal and deregulated myc genes. C1 NCI,USN,MED ONCOL BRANCH,BETHESDA,MD 20889. UNIFORMED SERV UNIV HLTH SCI,USN,NATL MED CTR,DEPT MED,BETHESDA,MD 20889. NR 34 TC 2 Z9 2 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0171-2985 J9 IMMUNOBIOLOGY JI Immunobiology PD AUG PY 1992 VL 185 IS 2-4 BP 150 EP 158 PG 9 WC Immunology SC Immunology GA JL906 UT WOS:A1992JL90600003 PM 1452198 ER PT J AU SEGAL, DM QIAN, JH MEZZANZANICA, D GARRIDO, MA TITUS, JA ANDREW, SM GEORGE, AJT JOST, CR PEREZ, P WUNDERLICH, JR AF SEGAL, DM QIAN, JH MEZZANZANICA, D GARRIDO, MA TITUS, JA ANDREW, SM GEORGE, AJT JOST, CR PEREZ, P WUNDERLICH, JR TI TARGETING OF ANTITUMOR RESPONSES WITH BISPECIFIC ANTIBODIES SO IMMUNOBIOLOGY LA English DT Article; Proceedings Paper CT 7TH SYMP ON SIGNALS AND SIGNAL PROCESSING IN THE IMMUNE SYSTEM CY SEP, 1991 CL KOSZEG, HUNGARY ID PERIPHERAL-BLOOD LYMPHOCYTES; HUMAN OVARIAN-CARCINOMA; T-CELLS; MONOCLONAL-ANTIBODIES; CYTOTOXIC LYMPHOCYTES; RECEPTOR ANTIBODIES; COLORIMETRIC ASSAY; CYTO-TOXICITY; X ANTI-CD3; GROWTH AB T cells can be induced to specifically lyse tumor cells with bispecific antibodies containing anti-T cell receptor mAbs crosslinked to anti-tumor mAbs. Such <> requires that the target cell be bound directly to the cytotoxic cell. In addition, targeted T cells mediate a second activity, the secretion of factors that can block the growth of both tumor target cells and bystander tumor cells. When given to nude mice bearing intraperitoneal human ovarian carcinoma, targeted human T cells cause the rapid removal of most tumor cells from the peritoneum, and markedly prolong the times of survival of treated mice. The efficacy of targeted T cells for treating human cancer is currently being tested in clinical trials. RP SEGAL, DM (reprint author), NIMH,EXPTL IMMUNOL BRANCH,BLDG 10,ROOM 4B17,BETHESDA,MD 20892, USA. RI Perez, Pilar/B-4948-2010; Mezzanzanica, Delia/C-2607-2017; OI Perez, Pilar/0000-0003-3557-2247; Mezzanzanica, Delia/0000-0002-9664-6871; George, Andrew/0000-0002-2866-0241 NR 32 TC 10 Z9 10 U1 0 U2 2 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0171-2985 J9 IMMUNOBIOLOGY JI Immunobiology PD AUG PY 1992 VL 185 IS 2-4 BP 390 EP 402 PG 13 WC Immunology SC Immunology GA JL906 UT WOS:A1992JL90600021 PM 1452212 ER PT J AU GUPTA, RK SZU, SC FINKELSTEIN, RA ROBBINS, JB AF GUPTA, RK SZU, SC FINKELSTEIN, RA ROBBINS, JB TI SYNTHESIS, CHARACTERIZATION, AND SOME IMMUNOLOGICAL PROPERTIES OF CONJUGATES COMPOSED OF THE DETOXIFIED LIPOPOLYSACCHARIDE OF VIBRIO-CHOLERAE O1 SEROTYPE INABA BOUND TO CHOLERA-TOXIN SO INFECTION AND IMMUNITY LA English DT Article ID FIELD TRIAL; ANTIBODY-RESPONSES; MUCOSAL IMMUNITY; BREAST-MILK; POLYSACCHARIDE; VACCINES; BANGLADESH; IMMUNOGENICITY; IMMUNIZATION; DISEASE AB Protection against cholera has been correlated with the level of serum vibriocidal antibodies. The specificity of these vibriocidal antibodies was mostly to the lipopolysaccharide (LPS). We synthesized conjugates of detoxified LPS with cholera toxin (CT) and other proteins in order to elicit serum LPS antibodies with vibriocidal activity. Treatment with hydrazine (deacylated LPS) reduced the endotoxic properties of the LPS to clinically acceptable levels and resulted in a molecule larger and more antigenic than the saccharide produced by acid hydrolysis. More immunogenic conjugates resulted from multipoint compared with single-point attachment of the deacylated LPS to the protein. The conjugates containing CT had low levels of pyrogen and no toxic activity upon Chinese hamster ovary cells and elicited booster responses of vibriocidal and CT antibodies when injected subcutaneously as saline solutions into mice; the vibriocidal titers were similar to those elicited by comparable doses of cellular vaccines. We suggest how serum vibriocidal antibodies might prevent cholera. C1 NICHHD,DEV & MOLEC IMMUN LAB,BETHESDA,MD 20892. UNIV MISSOURI,DEPT MOLEC MICROBIOL & IMMUNOL,COLUMBIA,MO 65212. FU NIAID NIH HHS [AI 17312] NR 61 TC 80 Z9 83 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD AUG PY 1992 VL 60 IS 8 BP 3201 EP 3208 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JG023 UT WOS:A1992JG02300026 PM 1639490 ER PT J AU SACKS, DL AF SACKS, DL TI THE STRUCTURE AND FUNCTION OF THE SURFACE LIPOPHOSPHOGLYCAN ON DIFFERENT DEVELOPMENTAL STAGES OF LEISHMANIA PROMASTIGOTES SO INFECTIOUS AGENTS AND DISEASE-REVIEWS ISSUES AND COMMENTARY LA English DT Review DE LEISHMANIA; LIPOPHOSPHOGLYCAN; COMPLEMENT; METACYCLOGENESIS; SAND FLY ID SANDFLY PHLEBOTOMUS-PAPATASI; MAJOR PROMASTIGOTES; INFECTIVE STAGE; COMPLEMENT; EXPRESSION; DONOVANI; GLYCOCONJUGATE; AGGLUTINATION; AMASTIGOTES; MACROPHAGE AB The differentiation of Leishmania promastigotes from a noninfective procyclic stage to an infective metacyclic stage during growth within the midgut of their sand fly vectors or within axenic culture is accompanied by structural modifications of the surface lipophosphoglycan (LPG). The modifications are of two sorts: (a) a two- to three fold increase in size due to an increase in the number of phosphorylated saccharide units expressed and (b) a change in the composition of the terminal sugars of some of these units. The elongation of LPG on metacyclics promotes complement activation and C3 deposition in a nonlethal manner, thus opsonizing the promastigotes for attachment and uptake via macrophage receptors appropriate for subsequent intracellular survival. The down-regulation of terminally exposed galactose residues on metacyclic LPG appears to permit the selective release of infective-stage organisms from adhesion to midgut epithelial cells so as to make them available for subsequent transmission by bite. RP SACKS, DL (reprint author), NIAID,PARASIT DIS LAB,CELL BIOL & IMMUNOL SECT,BLDG 4,RM 126,BETHESDA,MD 20892, USA. NR 35 TC 24 Z9 25 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1056-2044 J9 INFECT AGENT DIS JI Infect. Agents Dis.-Rev. Issues Comment. PD AUG PY 1992 VL 1 IS 4 BP 200 EP 206 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JW595 UT WOS:A1992JW59500004 PM 1365546 ER PT J AU KATKIN, JP MALECH, HL LETO, TL AF KATKIN, JP MALECH, HL LETO, TL TI BACULOVIRUS MEDIATED EXPRESSION OF HUMAN PHAGOCYTIC CELL OXIDASE CYTOCHROME-B558 IN SF9 INSECT CELLS SO INFLAMMATION LA English DT Article ID CHRONIC GRANULOMATOUS-DISEASE; CHROMOSOMAL LOCATION; MICROBICIDAL OXIDASE; HUMAN-NEUTROPHILS; PLASMA-MEMBRANE; LIGHT CHAIN; SUBUNIT; IDENTIFICATION; DEFICIENCY; RECEPTOR AB Chronic granulomatous disease (CGD) results from deficient production of components of the phagocyte NADPH oxidase. Most commonly affected is cytochrome b558, a heterodimer composed of a 22-kDa protein (p22phox) noncovalently bound to a 91-kDa transmembrane glycoprotein (gp91phox). CGD phagocytes lack both p22phox and gp91phox peptides when either gene is affected, suggesting that both peptides must be produced for individual subunit stability. Both genes have been cloned, but eukaryotic expression of recombinant gp91phox has not been reported. To investigate the stability and interaction of cytochrome b558 subunits, we introduced p22phox and gp91phox cDNA into recombinant baculoviruses. Recombinant gp91phox (rgp91phox) and p22phox (rp22phox) were detected individually and together in the same cells by in situ immunofluorescence and by SDS-PAGE immunoblotting of membranes from sf9 cells infected with baculovirus constructs. Formation of rp22phox/rgp91phox complexes was demonstrated by coprecipitation using subunit-specific antibodies. This study demonstrates for the first time that cDNA encoding either subunit is capable of initiating production of stable recombinant cytochrome b558 subunits in eukaryotic cells. RP KATKIN, JP (reprint author), NIAID,HOST DEF LAB,9000 ROCKVILLE PIKE,BETHESDA,MD 20910, USA. NR 29 TC 5 Z9 5 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0360-3997 J9 INFLAMMATION JI Inflammation PD AUG PY 1992 VL 16 IS 4 BP 393 EP 410 DI 10.1007/BF00917630 PG 18 WC Cell Biology; Immunology SC Cell Biology; Immunology GA JD224 UT WOS:A1992JD22400010 PM 1526667 ER PT J AU KUDO, A THALMANN, P SAKAGUCHI, N DAVIDSON, WF PIERCE, JH KEARNEY, JF RETH, M ROLINK, A MELCHERS, F AF KUDO, A THALMANN, P SAKAGUCHI, N DAVIDSON, WF PIERCE, JH KEARNEY, JF RETH, M ROLINK, A MELCHERS, F TI THE EXPRESSION OF THE MOUSE V PREB/LAMBDA-5 LOCUS IN TRANSFORMED-CELL LINES AND TUMORS OF THE B-LINEAGE DIFFERENTIATION PATHWAY SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE B-LINEAGE DIFFERENTIATION; VPREB; LAMBDA-5 ID IMMUNOGLOBULIN GENE REARRANGEMENT; MURINE HEMATOPOIETIC-CELLS; LYMPHOCYTES-PRE-B; LIGHT-CHAIN; SURFACE-ANTIGEN; FETAL LIVER; LAMBDA-5; LYMPHOMA; INVITRO; INVIVO AB The expression of RNA transcripts from two pre B lymphocyte related genes, V(preB) and lambda-5, has been studied in a series of transformed cell lines which appear frozen at different states of B lineage differentiation, from early progenitors to surface Ig positive B cells. In the HAFTL-1 cell line, which arose from fetal liver by transformation with a retrovirus containing the Hras oncogene, Northern analysis of poly A+ mRNA as well as in situ hybridization of RNA in single cells revealed that lambda-5 and V(preB) are already expressed at the progenitor stage and increase in expression as the progenitors differentiate to precursor (preB) cells, or are turned off as the progenitors differentiate to myeloid cells. Continued rearrangements of Ig genes in pre B cell lines leading to Ig expression on the surface of NFS-5 pre B cells do not influence the continued expression of V(preB) and lambda-5. Surface Ig-positive B lineage cell lines also express the pre B-related genes. Both Ly1+ as well as Ly1- pre B cells are V(preB-) and lambda-5-positive. Lipopolysaccharide (LPS) stimulation of 70Z/3 pre B cells does not turn Off lambda-5 expression. It therefore appears that, at least in transformed cell lines, the expression of V(preB) and lambda-5 is not directly regulated by the expression of mu-H, kappa-L, or lambda-L chains, LPS reactivity, or the Ly1 surface antigen. Fusion of plasmacytoma cells with normal pre B cells to generate pre B hybridomas leads to down-regulation of V(preB)/lambda-5 expression. These results suggest that different trans-acting factors in more mature cells might down-regulate the expression Of V(preB)/lambda-5. C1 BASEL INST IMMUNOL,CH-4005 BASEL,SWITZERLAND. NCI,GENET LAB,BETHESDA,MD 20892. NCI,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. UNIV ALABAMA,DEPT MICROBIOL,DIV DEV & CLIN IMMUNOL,BIRMINGHAM,AL 35294. UNIV ALABAMA,CTR COMPREHENS CANC,BIRMINGHAM,AL 35294. MAX PLANCK INST IMMUNOL,FREIBURG,GERMANY. RI Kudo, Akira/C-7340-2015 OI Kudo, Akira/0000-0001-6289-3391 FU NCI NIH HHS [CA 13148]; NIAID NIH HHS [AI 18742, AI 30879, R01 AI014782] NR 40 TC 28 Z9 29 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD AUG PY 1992 VL 4 IS 8 BP 831 EP 840 DI 10.1093/intimm/4.8.831 PG 10 WC Immunology SC Immunology GA JH232 UT WOS:A1992JH23200001 PM 1419955 ER PT J AU FONTVIEILLE, AM DWYER, J RAVUSSIN, E AF FONTVIEILLE, AM DWYER, J RAVUSSIN, E TI RESTING METABOLIC-RATE AND BODY-COMPOSITION OF PIMA INDIAN AND CAUCASIAN CHILDREN SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE ENERGY EXPENDITURE; INDIRECT CALORIMETRY; GROWTH ID ENERGY-EXPENDITURE; PHYSICAL-ACTIVITY; BIRTH-WEIGHT; RISK FACTOR; OBESITY; VALIDATION; ADOLESCENTS; FATNESS; PARENTS; TWINS AB Since a low metabolic rate (for a given body size and body composition) is a risk factor for body weight gain and obesity is prevalent among Pima Indians, we have tested whether Pima Indian children have a low resting metabolic rate (RMR) as compared to Caucasian children. Body composition (bioelectrical resistance) and RMR were measured in 43 Pima Indian children (22 male/21 female, mean +/- s.d. 9.9 +/- 1.1 years) and 42 Caucasian children (21 male/21 female, 9.7 +/- 1.2 years). Pima children were taller (143 +/- 9 vs. 137 +/- 8 cm, P < 0.001), heavier (48.6 +/- 15.8 vs. 32.9 +/- 7.8 kg, P < 0.001) and fatter (39 +/- 10 vs. 24 +/- 7% fat, P < 0.001) than Caucasians. Absolute values of RMR were higher in Pimas than in Caucasians (6234 +/- 1201 vs. 5171 +/-715 kJ/day, P < 0.001), but similar when adjusted for differences in body size, body composition and sex. Contrary to our hypothesis, we did not find a decreased RMR in Pima children when compared to Caucasian children. Therefore, the high prevalence of obesity in Pima children at age 10 suggests that excess energy intake and/or low levels of physical activity might be the major aetiological factor. However, this study does not exclude the possibility that a low metabolic rate might be a predisposing factor at an earlier age. RP FONTVIEILLE, AM (reprint author), NIDDKD,CLIN DIABET & NUTR SECT,4212 N 16TH ST,ROOM 541,PHOENIX,AZ 85016, USA. NR 42 TC 39 Z9 39 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD AUG PY 1992 VL 16 IS 8 BP 535 EP 542 PG 8 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA JH730 UT WOS:A1992JH73000001 PM 1326483 ER PT J AU WHITCUP, SM WAKEFIELD, D LI, Q NUSSENBLATT, RB CHAN, CC AF WHITCUP, SM WAKEFIELD, D LI, Q NUSSENBLATT, RB CHAN, CC TI ENDOTHELIAL LEUKOCYTE ADHESION MOLECULE-1 IN ENDOTOXIN-INDUCED UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE ELAM-1; CELL ADHESION MOLECULES; ENDOTOXIN-INDUCED UVEITIS; OCULAR INFLAMMATION; ENDOTHELIUM AB Expression of endothelial leukocyte adhesion molecule-1 (ELAM-1) on endothelial cells leads to the attachment of polymorphonuclear leukocytes. The sequential expression of ELAM-1 and major histocompatibility complex (MHC) class II antigen was examined in the eves of 59 Lewis rats with endotoxin-induced uveitis (EIU) after the injection of Salmonella typhimurium endotoxin. The eyes were enucleated at 2-hr intervals. Hematoxylin and eosin-stained paraffin-embedded sections and immunohistochemically stained cryostat sections were graded by two masked observers. The MHC class II antigen was expressed on cells in the iris and ciliary body 4 hr after injection of endotoxin and on the corneal endothelium, 8 hr postinjection. It was found that ELAM-1 was expressed first on cells of the ciliary body and iris 10 hr after the injection of endotoxin and on the corneal endothelium, 22 hr postinjection. Clinical and histopathologic disease developed 16 hr postinjection. Adherence of polymorphonuclear cells to the corneal endothelium was observed at the time of ELAM-1 expression. In conclusion, expression of ELAM-1 on ocular tissue occurred in EIU and appeared to promote polymorphonuclear cell accumulation in the anterior segment of the eye. RP WHITCUP, SM (reprint author), NEI,IMMUNOL LAB,BLDG 10,ROOM 10N 202,BETHESDA,MD 20892, USA. NR 10 TC 25 Z9 25 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD AUG PY 1992 VL 33 IS 9 BP 2626 EP 2630 PG 5 WC Ophthalmology SC Ophthalmology GA JG614 UT WOS:A1992JG61400007 PM 1379217 ER PT J AU SASAMOTO, Y KAWANO, YI BOULIGNY, R WIGGERT, B CHADER, GJ GERY, I AF SASAMOTO, Y KAWANO, YI BOULIGNY, R WIGGERT, B CHADER, GJ GERY, I TI IMMUNOMODULATION OF EXPERIMENTAL AUTOIMMUNE UVEORETINITIS BY INTRAVENOUS-INJECTION OF UVEITOGENIC PEPTIDES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE EXPERIMENTAL AUTOIMMUNE UVEORETINITIS (EAU); INTERPHOTORECEPTOR RETINOID-BINDING PROTEIN (IRBP); IRBP-DERIVED PEPTIDES; IMMUNODOMINANCE OF PEPTIDES; IMMUNOMODULATION IMMUNOTOLERANCE ID RETINOID-BINDING PROTEIN; EXPERIMENTAL ALLERGIC UVEITIS; MYELIN BASIC-PROTEIN; S-ANTIGEN; IMMUNE-RESPONSES; IMMUNOLOGICAL PROPERTIES; IMMUNODOMINANT; IRBP; IDENTIFICATION; DETERMINANTS AB Intravenous (IV) injection of antigenic proteins induces specific unresponsiveness, as shown by the diminished response to a challenge with these proteins in complete Freund's adjuvant. This study examined the effect of IV treatment with uveitogenic peptides on the development of experimental autoimmune uveoretinitis (EAU). The peptides used were derived from the sequence of bovine interphotoreceptor retinoid-binding protein (IRBP) and included R16 (sequence, 1177-1191), which is immunodominant and highly uveitogenic, and R4 (sequence, 1158-1180), which is nondominant and weakly uveitogenic. The efficacy of this treatment was found to depend on both the dose used for the IV injection and that used for the challenge. Thus, EAU induced by R16 at a dose of 0.2 nmol/rat was inhibited completely in all rats treated with the peptide at doses of 400 or 133 nmol and partially by the low dose of 5 nmol/rat. However, the EAU induced by a R16 challenge of 40 nmol/rat was inhibited only partially by the high treatment dose of 400 nmol/rat. The IV treatment was found to be effective in inhibiting the EAU induced by peptide R4. A large dose of R4 was needed to induce EAU (40 nmol/rat), and the disease was inhibited completely in all rats treated IV with this peptide at doses of 800, 400, or 133 nmol. In most animals injected with the 44-nmol dose, also, inhibition was complete. These data show that there is a correlation between the doses needed for achieving inhibition and those used for the challenge. The ratios between these doses in all experiments were found within the range 1-20. The IV treatment of rats with the dominant peptide R16 effectively inhibited the development of EAU induced by whole IRBP. By contrast, treatment with peptide R4 had no effect on the disease induced by the native protein. These data therefore show the effectiveness of IV treatment with uveitogenic peptides as a procedure to inhibit EAU. This study also established a new relationship between the immunodominance of peptide determinants and their capacity to induce immune unresponsiveness. C1 NEI,RETINAL CELL & MOLEC BIOL,BETHESDA,MD 20892. HOWARD HUGHES MED INST,BETHESDA,MD. RP SASAMOTO, Y (reprint author), NEI,IMMUNOL LABS,BLDG 10,ROOM 10N210,BETHESDA,MD 20892, USA. NR 37 TC 23 Z9 23 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD AUG PY 1992 VL 33 IS 9 BP 2641 EP 2649 PG 9 WC Ophthalmology SC Ophthalmology GA JG614 UT WOS:A1992JG61400009 PM 1639611 ER PT J AU GOLD, JM RANDOLPH, C CARPENTER, CJ GOLDBERG, TE WEINBERGER, DR AF GOLD, JM RANDOLPH, C CARPENTER, CJ GOLDBERG, TE WEINBERGER, DR TI FORMS OF MEMORY FAILURE IN SCHIZOPHRENIA SO JOURNAL OF ABNORMAL PSYCHOLOGY LA English DT Article ID MILDLY DISTURBED SCHIZOPHRENICS; MONOZYGOTIC TWINS DISCORDANT; COMPLEX PARTIAL SEIZURES; TEMPORAL-LOBE ORIGIN; ANTICHOLINERGIC MEDICATION; WORKING-MEMORY; MATCHED TASKS; RECALL; FREQUENCY; RECOGNITION AB Effortful and automatic memory task performances were examined in 36 schizophrenic patients and 18 normal control Ss. Tasks included free recall, recognition, and frequency estimation. Patients demonstrated impairment in recall, in recognition, in semantic encoding, and in frequency estimation. Deficits were observed across tasks despite differences in attentional demands. The results suggest a basic compromise of memory function, which is consistent with recent neuro-imaging evidence of structural or physiological abnormalities in frontal and temporal lobe structures in schizophrenia. C1 NIMH,DIV INTRAMURAL RES PROGRAMS,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. RP GOLD, JM (reprint author), ST ELIZABETH HOSP,CTR NEUROSCI,NIMH,2700 MARTIN LUTHER KING AVE SE,WASHINGTON,DC 20032, USA. NR 67 TC 223 Z9 226 U1 0 U2 1 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0021-843X J9 J ABNORM PSYCHOL JI J. Abnorm. Psychol. PD AUG PY 1992 VL 101 IS 3 BP 487 EP 494 DI 10.1037/0021-843X.101.3.487 PG 8 WC Psychology, Clinical; Psychology, Multidisciplinary SC Psychology GA JF698 UT WOS:A1992JF69800013 PM 1500605 ER PT J AU CLANTON, DJ MORAN, RA MCMAHON, JB WEISLOW, OS BUCKHEIT, RW HOLLINGSHEAD, MG CIMINALE, V FELBER, BK PAVLAKIS, GN BADER, JP AF CLANTON, DJ MORAN, RA MCMAHON, JB WEISLOW, OS BUCKHEIT, RW HOLLINGSHEAD, MG CIMINALE, V FELBER, BK PAVLAKIS, GN BADER, JP TI SULFONIC-ACID DYES - INHIBITION OF THE HUMAN-IMMUNODEFICIENCY-VIRUS AND MECHANISM OF ACTION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE SULFONIC ACID DYES; HIV-1; CHICAGO SKY BLUE; CELL KILLING ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; REVERSE-TRANSCRIPTASE; ESCHERICHIA-COLI; AZIDOTHYMIDINE AZT; NUCLEOSIDE ANALOGS; ANTIVIRAL ACTIVITY; POTENT INHIBITOR; DEXTRAN SULFATE; ZIDOVUDINE AZT AB Over 50 different commercially available sulfonic acid-containing dyes were analyzed for their ability to prevent HIV-1-induced cell killing and in inhibiting HIV-1 replication. Compounds of remarkably similar structure, but with differing patterns of sulfonic acid group substitutions, had a wide range of potency in inhibiting HIV-1. Chicago sky blue (CSB) was highly effective in the inhibition of HIV-1 with less toxicity to CEM-SS cells than most of the other sulfonated dyes tested. Synthesis of CSB was undertaken to produce a product greater than 98% pure and this compound was used to elucidate the possible mechanisms by which this class of structurally related compounds inhibits HIV-1. Addition of CSB to cells infected at high multiplicity at any time up to 24 h after infection, unlike dideoxycytidine (ddC) or oxathiin carboxanilide (OC), inhibited HIV-1-induced cell killing. Other postinfection time course studies revealed that CSB had to be present for 24 h or longer immediately after infection to be protective. Virus binding to cells occurred in the presence of CSB, but the requirement for virion envelope-cell membrane fusion was delayed. CSB was a potent inhibitor of the reverse transcriptase (RT) of both HIV-1 and HIV-2, although it was less active against HIV-2 in a cell killing-based assay. CSB also inhibited Rauscher and LP-BM5 murine leukemia viruses. CSB appears to disrupt the interaction between viral proteins and cell membranes, both in the fusion step early in the infection cycle, and in the development of syncytia in the late stages of virus infection. C1 NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,ANTIVIRAL EVALUAT BRANCH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,DEV THERAPEUT PROGRAM,DRUG DISCOVERY RES & DEV LAB,FREDERICK,MD 21701. FREDERICK CANC RES & DEV CTR,PROGRAM RESOURCES INC,FREDERICK,MD. SO RES INST,BIRMINGHAM,AL 35255. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21701. FU NCI NIH HHS [N01 CM-87274] NR 40 TC 33 Z9 33 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD AUG PY 1992 VL 5 IS 8 BP 771 EP 781 PG 11 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JE582 UT WOS:A1992JE58200003 PM 1517963 ER PT J AU VASUDEVACHARI, MB UFFELMAN, KW KOVACS, J YEH, CK LANE, HC SALZMAN, NP AF VASUDEVACHARI, MB UFFELMAN, KW KOVACS, J YEH, CK LANE, HC SALZMAN, NP TI ENVELOPE-SPECIFIC ANTIBODIES IN THE SALIVA OF INDIVIDUALS VACCINATED WITH RECOMBINANT HIV-1 GP160 SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1 GP160 VACCINE; SALIVA; IGG ANTIBODIES; ELISA; WESTERN BLOT ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; CONFERS PROTECTION; MUCOSAL IMMUNITY; PAROTID-SALIVA; IGA ANTIBODIES; BODY-FLUIDS; HTLV-III; GLYCOPROTEIN; INFECTION AB HIV-1-specific antibodies have been detected in the saliva of seropositive individuals and may play a role in preventing oral transmission of the virus. We have analyzed saliva samples obtained from HIV-1-seronegative individuals who were immunized with various dosages of a recombinant HIV-1 envelope glycoprotein (gp160) vaccine for the presence of antibodies to HIV-1. Antibodies specific for envelope glycoproteins were detected in saliva from all of the volunteers, with those vaccinated with the higher doses of 640 and 1,280-mu-g showing the strongest responses. Peak salivary antibody titers were obtained 4-14 weeks after vaccination; they then gradually dropped in parallel with serum antibody titers. These envelope-specific antibodies were detected in whole saliva and in submandibular saliva but not in parotid saliva, suggesting that the source of antibodies in saliva is from serum transudation. The class of reactive antibodies was found to be IgG. The HIV-1-specific antibodies in the saliva of vaccinated individuals may offer local protection against HIV-1 infection. C1 NIDR,CTR CLIN,DEPT CRIT CARE MED,BETHESDA,MD 20892. NIDR,CLIN INVEST & PATIENT CARE BRANCH,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,CLIN & MOLEC RETROVIROL SECT,BETHESDA,MD 20892. RP VASUDEVACHARI, MB (reprint author), GEORGETOWN UNIV,SCH MED,DEPT MICROBIOL,MOLEC RETROVIROL LAB,ROOM LM-12,PRECLIN SCI BLDG,WASHINGTON,DC 20057, USA. FU NIAID NIH HHS [N01-AI-05058] NR 38 TC 16 Z9 16 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD AUG PY 1992 VL 5 IS 8 BP 817 EP 821 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JE582 UT WOS:A1992JE58200008 PM 1517967 ER PT J AU DEWAR, RL SARMIENTO, MD LAWTON, ES CLARK, HM KENNEDY, PE SHAH, A BASELER, M METCALF, JA LANE, HC SALZMAN, NP AF DEWAR, RL SARMIENTO, MD LAWTON, ES CLARK, HM KENNEDY, PE SHAH, A BASELER, M METCALF, JA LANE, HC SALZMAN, NP TI ISOLATION OF HIV-1 FROM PLASMA OF INFECTED INDIVIDUALS - AN ANALYSIS OF EXPERIMENTAL CONDITIONS AFFECTING SUCCESSFUL VIRUS PROPAGATION SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE HIV-1; PLASMA VIREMIA; VIRUS CULTIVATION; P24 ANTIGEN ID HUMAN-IMMUNODEFICIENCY-VIRUS; BLOOD MONONUCLEAR-CELLS; VIREMIA; VIRIONS; TYPE-1; AIDS; RETROVIRUS; PATIENT; FRESH AB Experimental conditions affecting the successful propagation of HIV-1 from the plasma of seropositive individuals were examined. It was determined that whole blood samples collected with lithium heparin as the anticoagulant, immediate plasma separation, and immediate culturing were best suited for obtaining viable virus from plasma. Virus was isolated by infecting fresh phytohemagglutinin-stimulated normal donor peripheral blood mononuclear cells (PBMCs) with plasma followed by weekly cocultivation with new target cells. The plasma virus isolation rate was the greatest and HIV-1 titers were the highest for those individuals with < 200 CD4+ cells/mm3 and decreased as the level of CD4+ cells approached normal values. We were able to obtain positive cultures from 29.5% of those patients with CD4+ counts > 500/mm3. HIV-1 titers in plasma also correlated with high serum p24 antigen levels when serum was treated with glycine to dissociate antigen-antibody complexes. C1 NIAID,BETHESDA,MD 20892. PROGRAM RESOURCES INC DYNCORP,FREDERICK,MD. RP DEWAR, RL (reprint author), GEORGETOWN UNIV,SCH MED,MOLEC RETROVIROL LAB,PRECLIN SCI BLDG,ROOM LM-12,WASHINGTON,DC 20007, USA. FU NCI NIH HHS [N01-CO-74102]; NIAID NIH HHS [N01-AI-05058] NR 22 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD AUG PY 1992 VL 5 IS 8 BP 822 EP 828 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA JE582 UT WOS:A1992JE58200009 PM 1355557 ER PT J AU KHAN, S IVEY, DM KRULWICH, TA AF KHAN, S IVEY, DM KRULWICH, TA TI MEMBRANE ULTRASTRUCTURE OF ALKALIPHILIC BACILLUS SPECIES STUDIED BY RAPID-FREEZE ELECTRON-MICROSCOPY SO JOURNAL OF BACTERIOLOGY LA English DT Note ID FLAGELLAR MOTOR; DRIVEN; PH AB Cells of Bacillus firmus OF4 and Bacillus alcalophilus were examined by rapid-freeze freeze-fracture and freeze-substitution electron microscopy. No special vesicular structures linked to growth at alkaline pH were found, either within or associated with the cytoplasmic membrane. The cytoplasmic membranes of the alkaliphilic bacilli and the neutrophilic Bacillus subtilis BD99 were indistinguishable. Distinctive intramembrane particle rings, presumed to be flagellar structures on the basis of distribution and morphological characteristics, were found in all of these species. These observations indicate that the adaptations required to effect oxidative phosphorylation and flagellar rotation at extreme alkaline pH occur without gross morphological rearrangement. C1 CUNY MT SINAI SCH MED, DEPT BIOCHEM, NEW YORK, NY 10029 USA. YESHIVA UNIV ALBERT EINSTEIN COLL MED, DEPT ANAT & STRUCT BIOL, BRONX, NY 10461 USA. YESHIVA UNIV ALBERT EINSTEIN COLL MED, DEPT PHYSIOL & BIOPHYS, BRONX, NY 10461 USA. MARINE BIOL LAB, NINDS, NEUROBIOL LAB, WOODS HOLE, MA 02543 USA. FU NCRR NIH HHS [S10-RR04877]; NIGMS NIH HHS [GM28454, GM36936] NR 19 TC 24 Z9 24 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0021-9193 EI 1098-5530 J9 J BACTERIOL JI J. Bacteriol. PD AUG PY 1992 VL 174 IS 15 BP 5123 EP 5126 PG 4 WC Microbiology SC Microbiology GA JF345 UT WOS:A1992JF34500035 PM 1629169 ER PT J AU AUSTIN, SJ EICHORN, BG AF AUSTIN, SJ EICHORN, BG TI RANDOM DIFFUSION CAN ACCOUNT FOR TOPA-DEPENDENT SUPPRESSION OF PARTITION DEFECTS IN LOW-COPY-NUMBER PLASMIDS SO JOURNAL OF BACTERIOLOGY LA English DT Article ID CENTROMERE-LIKE SITE; P1 PLASMID; ESCHERICHIA-COLI; DAUGHTER CELLS; PSC101 PLASMID; HOST FACTOR; PAR REGION; F-PLASMID; REPLICATION; MINIPLASMIDS AB The maintenance of partition-defective (Par-) mini-P1 and mini-F plasmids was studied in topA strains of Escherichia coli, which are defective in topoisomerase I activity. The partition defects were substantially but not completely suppressed in broth-grown cultures. This suppression was not due to a large increase in copy number. However, the absolute number of copies of Par- mini-P1 plasmids per average dividing cell is sufficiently high to account for the modest stability observed if a random distribution of the copies to daughter cells is assumed. The similar number of Par- plasmid copies in wild-type cells are distributed in a considerably worse-than-random fashion. Thus, it is unnecessary to propose, as was suggested previously, that an active, par-independent pathway operates in topA strains to ensure proper segregation of the plasmids to daughter cells. Rather, it seems likely that the lack of topoisomerase I activity aids the random distribution of the partition-defective plasmids, perhaps by facilitating their separation after replication. The results of studies carried out at reduced growth rates were consistent with this view; when topA cells containing Par- mini-P1 plasmids were cultured in minimal medium, in which the copy number of the plasmids per average cell is sharply reduced, very little suppression of the partition defect was observed. RP AUSTIN, SJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,BASIC RES PROGRAM,ABL,CHROMOSOME BIOL LAB,FREDERICK,MD 21702, USA. FU NCI NIH HHS [N01-CO-74101] NR 32 TC 23 Z9 23 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD AUG PY 1992 VL 174 IS 16 BP 5190 EP 5195 PG 6 WC Microbiology SC Microbiology GA JH979 UT WOS:A1992JH97900003 PM 1322881 ER PT J AU TOONE, WM RUDD, KE FRIESEN, JD AF TOONE, WM RUDD, KE FRIESEN, JD TI MUTATIONS CAUSING AMINOTRIAZOLE RESISTANCE AND TEMPERATURE SENSITIVITY RESIDE IN GYRB, WHICH ENCODES THE B-SUBUNIT OF DNA GYRASE SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; PHYSICAL MAP; GENE; TOPOISOMERASES; TRANSCRIPTION; CLONING AB Certain mutations in gyrA and gyrB, the genes encoding the two subunits of DNA gyrase, are known to influence expression of the his operon (K. E. Rudd and R. Menzel, Proc. Natl. Acad. Sci. USA 84:517-521, 1987). Such mutations lead to a decrease in tRNA(His) levels and consequently to an attenuator-dependent increase in his operon expression. This effect presumably is due to the dependence of the hisR promoter (hisR encodes tRNA(His)) on supercoiling for maximal activity. We used a relaxed (Rel-) strain of Escherichia coli to isolate gyrB mutants by selecting for resistance to the histidine antimetabolite 3-amino-1,2,4-triazole and then screening for temperature-sensitive growth on rich medium. Rel- mutants, which generally have lower basal levels of ppGpp (a positive regulator of his operon transcription), are more sensitive than wild-type E. coli to aminotriazole. The chance of isolating spoT mutants, which can be selected with a similar procedure, was decreased by selecting in the presence of a multicopy plasmid that carries the wild-type spot gene. Under these conditions, gyrB mutants were isolated preferentially. This scheme selects for loss of function of DNA gyrase, rather than for its alteration due to resistance to specific gyrase inhibitors, and thus a greater variety of gyrase mutations might be obtainable. C1 HOSP SICK CHILDREN,RES INST,DEPT GENET,555 UNIV AVE,TORONTO M5G 1X8,ONTARIO,CANADA. UNIV TORONTO,DEPT MOLEC & MED GENET,TORONTO M5S 1A8,ONTARIO,CANADA. NIH,NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,BETHESDA,MD 20894. NR 24 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD AUG PY 1992 VL 174 IS 16 BP 5479 EP 5481 PG 3 WC Microbiology SC Microbiology GA JH979 UT WOS:A1992JH97900044 PM 1322887 ER PT J AU FEDARKO, NS MOERIKE, M BRENNER, R ROBEY, PG VETTER, U AF FEDARKO, NS MOERIKE, M BRENNER, R ROBEY, PG VETTER, U TI EXTRACELLULAR-MATRIX FORMATION BY OSTEOBLASTS FROM PATIENTS WITH OSTEOGENESIS IMPERFECTA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID BONE-CELLS-INVITRO; I COLLAGEN; PROTEOGLYCAN; DECORIN; OSTEONECTIN; EXPRESSION; PROTEINS; TISSUES; FORM; FIBROBLASTS AB Extracellular matrix proteins synthesized by bone cells isolated from 16 patients with different forms of osteogenesis imperfects (OI) were analyzed in vitro. Specific components of the extracellular matrix by OI and age-matched cultures were investigated by steady-state radiolabeling followed by quantitation of label into specific proteins and comparison of 01 cultures to those of age-matched controls. The in vitro proliferation of OI bone cells was found to be lower than that of control cells. In seven patients, abnormalities of the alpha-1(I) and/or alpha-2(I) chains of type I collagen were detected by gel electrophoresis. In two of these patients, the mutations in the COLIA1 and COLIA2 genes have been previously identified. Although the amount of total protein synthesized by the cells in culture was the same for OI bone cells and age-matched control cells, OI bone cells showed a significantly reduced synthesis of not only collagen but also other bone matrix glycoproteins. The synthesis of osteonectin (SPARC/BM40) and three proteoglycans [a large chondroitin sulfate proteoglycan, biglycan (PGI), and decorin (PGII)] was found to be decreased in OI cells. The reduction was most pronounced at the developmental age at which these macromolecules reach maximal levels during normal development. C1 UNIV ULM,KINDERKLIN,BINDEWEBSLAB,W-7900 ULM,GERMANY. RP FEDARKO, NS (reprint author), NIDR,BONE RES BRANCH,BLDG 30,ROOM 106,BETHESDA,MD 20892, USA. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 43 TC 55 Z9 55 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 IS 8 BP 921 EP 930 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JH995 UT WOS:A1992JH99500008 PM 1442206 ER PT J AU BARSONY, J SHAPIRO, JR MATTER, S LIEBERMAN, ME AF BARSONY, J SHAPIRO, JR MATTER, S LIEBERMAN, ME TI DIFFERENTIAL-EFFECTS OF ALUMINUM FLUORIDE ON GENOMIC AND NONGENOMIC VITAMIN-D RECEPTOR FUNCTIONS IN PRIMARY CULTURES OF CHICKEN OSTEOBLASTS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 NIDDK, MINERAL METAB SECT, BETHESDA, MD 20892 USA. JOHNS HOPKINS MED UNIV, BONE METAB RES LAB, BALTIMORE, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S162 EP S162 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500279 ER PT J AU BELL, NH YERGEY, AL VIEIRA, N SHARY, JR AF BELL, NH YERGEY, AL VIEIRA, N SHARY, JR TI CALCIUM-ABSORPTION IS THE SAME AND URINARY CALCIUM IS LOWER IN BLACK THAN WHITE-CHILDREN - MECHANISM FOR CALCIUM RETENTION AND GREATER BONE MASS IN BLACKS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,CHARLESTON,SC 29403. MED UNIV S CAROLINA,CHARLESTON,SC 29425. NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S150 EP S150 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500232 ER PT J AU BIANCO, P RIMINUCCI, M SILVESTRINI, G TERMINE, JD FISHER, LW ROBEY, PG AF BIANCO, P RIMINUCCI, M SILVESTRINI, G TERMINE, JD FISHER, LW ROBEY, PG TI LOCALIZATION OF BONE SIALOPROTEIN AT THE EM LEVEL - EVIDENCE FOR SECRETORY QUANTA OF BSP IN OSTEOBLASTS AND MATRIX SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV ROME LA SAPIENZA,I-00185 ROME,ITALY. ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. NIDR,BETHESDA,MD 20892. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S121 EP S121 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500113 ER PT J AU BIANCO, P RIMINUCCI, M TERMINE, JD ROBEY, PG AF BIANCO, P RIMINUCCI, M TERMINE, JD ROBEY, PG TI EVIDENCE FOR SECRETION OF BONE SIALOPROTEIN AT A SPECIFIC TIME POINT IN THE OSTEOBLAST LIFE-SPAN SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV ROME LA SAPIENZA,I-00185 ROME,ITALY. ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. NIDR,BETHESDA,MD 20892. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S103 EP S103 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500042 ER PT J AU FEDARKO, NS ROBEY, PG VETTER, UK AF FEDARKO, NS ROBEY, PG VETTER, UK TI AN ALTERED BONE-MATRIX COMPONENT STOICHIOMETRY IS ASSOCIATED WITH OSTEOGENESIS IMPERFECTA SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. UNIV FRANKFURT,KINDERKLIN,W-6000 FRANKFURT,GERMANY. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S98 EP S98 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500024 ER PT J AU FIORELLI, G WAKEFIELD, L BALLOCK, T SPORN, MB MASI, L FREDIANI, U TANINI, A BRANDI, ML AF FIORELLI, G WAKEFIELD, L BALLOCK, T SPORN, MB MASI, L FREDIANI, U TANINI, A BRANDI, ML TI TGF-BETA(1) MODULATES THE DIFFERENTIATION OF A HUMAN PREOSTEOCLASTIC CELL-LINE IN AN AUTOCRINE FASHION SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Meeting Abstract C1 UNIV FLORENCE,I-50121 FLORENCE,ITALY. NCI,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD AUG PY 1992 VL 7 SU 1 BP S314 EP S314 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JL595 UT WOS:A1992JL59500882 ER EF