FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Leferson, JD Kleiner, DE StetlerStevenson, WG AF Leferson, JD Kleiner, DE StetlerStevenson, WG TI Macromolecular substrate inhibition of matrix metalloproteinases demonstrated using a competing thiopeptolide assay. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 765 EP 765 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86100997 ER PT J AU Johnson, AC Reed, AL AF Johnson, AC Reed, AL TI Molecular cloning and characterization of a eukaryotic transcriptional repressor SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,DIV BASIC SCI,MOLEC BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 824 EP 824 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101054 ER PT J AU Kopantzev, E Roschke, V Rudikoff, S AF Kopantzev, E Roschke, V Rudikoff, S TI Immunomodulatory effects of murine plasmacytoma cells transfected with a retroviral vector encoding interleukin-2 cDNA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 852 EP 852 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101082 ER PT J AU Roschke, V Kopantzev, E Hausner, P Rudikoff, S AF Roschke, V Kopantzev, E Hausner, P Rudikoff, S TI Dissemination pattern of murine plasmacytoma. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 854 EP 854 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101086 ER PT J AU Yu, W Sipowicz, MA Kasprzak, KS Haines, D Anderson, LM AF Yu, W Sipowicz, MA Kasprzak, KS Haines, D Anderson, LM TI Pathological effects of preconception exposure to urethane or chromium SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,COMPARAT CARCINOGENESIS LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 858 EP 858 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101088 ER PT J AU Quan, X Akiyama, SK Godfrey, HP AF Quan, X Akiyama, SK Godfrey, HP TI Activation of endothelial cells by T cell fibronectin (FN). SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEW YORK MED COLL,VALHALLA,NY 10595. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 874 EP 874 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101105 ER PT J AU Medin, JA Tudor, M Simovitch, R Quirk, JM Jacobson, S Murray, GJ Brady, RO AF Medin, JA Tudor, M Simovitch, R Quirk, JM Jacobson, S Murray, GJ Brady, RO TI Gene therapy for fabry disease: Expression, secretion and uptake of alpha-galactosidase A (alpha-gal A) driven by a high titer recombinant retroviral SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS,UNIT THERAPEUT GENE TRANSFER,DEV & METAB NEUROL BRANCH,NEUROIMMUNOL BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 885 EP 885 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101114 ER PT J AU Curiel, RE Lahesmaa, R Cippitelli, M Subleski, J Young, HA Ghosh, P AF Curiel, RE Lahesmaa, R Cippitelli, M Subleski, J Young, HA Ghosh, P TI Identification of an IL-4-responsive element in the promoter of human IL-4 gene. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,EXPTL IMMUNOL LAB,DBS,FREDERICK,MD 21702. SYNTEX RES,DEPT LEUKO BIOL,PALO ALTO,CA 94304. SAIC FREDERICK,BCDP,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 890 EP 890 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101119 ER PT J AU Choudhury, BK Mannen, H Sharief, FS Hou, EW Li, SSL AF Choudhury, BK Mannen, H Sharief, FS Hou, EW Li, SSL TI Cloning, structure and evolution of the enhancer of split groucho and related genes from human, mouse, alligator, Xenopus and nematode SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,GENET MOLEC LAB,NIH,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 896 EP 896 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101124 ER PT J AU Park, SI Lee, BJ Hatfield, DL AF Park, SI Lee, BJ Hatfield, DL TI Drosophila as a model to study the effects of selenium on aging, cancer and heart disease. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,LEC,NIH,BETHESDA,MD 20892. SEOUL NATL UNIV,INST MOLEC BIOL & GENET,LMG,SEOUL,SOUTH KOREA. NR 0 TC 0 Z9 0 U1 2 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 904 EP 904 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101134 ER PT J AU Burshtyn, DN Scharenberg, AM Wagtmann, N Rajagopalan, S Berrada, K Yi, T Kinet, JP Long, EO AF Burshtyn, DN Scharenberg, AM Wagtmann, N Rajagopalan, S Berrada, K Yi, T Kinet, JP Long, EO TI Signal transduction by killer cell inhibitory receptors involves recruitment of tyrosine phosphatase SHP-1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,NIH,ROCKVILLE,MD 20852. CLEVELAND CLIN FDN,RES INST,DEPT CANC BIOL,CLEVELAND,OH 44195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 915 EP 915 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101145 ER PT J AU Marth, T Seder, RA Strober, W Kelsall, BL AF Marth, T Seder, RA Strober, W Kelsall, BL TI Regulation of transforming growth factor B production by interleukin-12. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,MUCOSAL IMMUN SECT,LCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 937 EP 937 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101167 ER PT J AU Asai, O Funakoshi, S Beckwith, M Fanslow, W Longo, DL Murphy, WJ AF Asai, O Funakoshi, S Beckwith, M Fanslow, W Longo, DL Murphy, WJ TI Inhibition of murine B-cell lymphoma growth by soluble recombinant murine CD40 ligand SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BCDP,FREDERICK,MD 21702. NCI,DBS,LLB,FREDERICK,MD 21702. IMMUNEX CORP,SEATTLE,WA. NIA,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 944 EP 944 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101174 ER PT J AU Pospisil, R Fitts, M Mage, RG AF Pospisil, R Fitts, M Mage, RG TI CD5 on rabbit appendix B-lymphocytes is a potential selecting ligand for B-cell surface immunoglobulin framework region sequences SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,NIH,BETHESDA,MD. RI Pospisil, Richard/B-7467-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 951 EP 951 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101180 ER PT J AU Zhang, J Berenstein, EH Evans, RL Siraganian, RP AF Zhang, J Berenstein, EH Evans, RL Siraganian, RP TI Transfection of Syk reconstitutes high affinity IgE mediated degranulation in Syk negative variants of rat basophilic leukemia RBL-2H3 cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 959 EP 959 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101189 ER PT J AU Song, JS HaleemSmith, H Szallasi, Z Blumberg, PM Rivera, J AF Song, JS HaleemSmith, H Szallasi, Z Blumberg, PM Rivera, J TI Association of PKC-delta with Src kinase family members in the RBL-2H3 mucosal mast cell line: Implications on the regulation of PKC-delta activity. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAMS,BETHESDA,MD 20892. NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 961 EP 961 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101190 ER PT J AU SchartonKersten, T Butcher, B Denkers, E Gazzinelli, R Grunvald, E Sher, A AF SchartonKersten, T Butcher, B Denkers, E Gazzinelli, R Grunvald, E Sher, A TI Endogenous IFN-gamma is not required for the induction of macrophage and granulocyte IL-12 responses during acute infection with Toxoplasma gondii. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 966 EP 966 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101198 ER PT J AU Chen, HT Alexander, CB Chen, FF Mage, RG AF Chen, HT Alexander, CB Chen, FF Mage, RG TI Rabbit DQ52 and D-H gene rearrangements in early B-cell development. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1004 EP 1004 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101232 ER PT J AU Zhu, XJ SadeghNasseri, S Bavari, S Ulrich, RG Mage, M AF Zhu, XJ SadeghNasseri, S Bavari, S Ulrich, RG Mage, M TI Recombinant single chain human HLA-DR1 molecules as biologically active covalently linked heterotrimers of antigenic peptide, beta chain, and alpha chain. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. AMER RED CROSS,ROCKVILLE,MD. ARMY MED RES INST,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1013 EP 1013 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101245 ER PT J AU Han, M Robinson, M Kindt, TJ AF Han, M Robinson, M Kindt, TJ TI Mapping of the rabbit MHC. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LIG,NIH,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1019 EP 1019 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101251 ER PT J AU Currier, JR Robinson, MA AF Currier, JR Robinson, MA TI Distinctive patterns of TCR diversity generated in response to mitogen, superantigen and nominal antigen. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1029 EP 1029 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101259 ER PT J AU Hieny, S Grunvald, E Morita, Y Englund, PT Gazzinelli, RT Sher, A AF Hieny, S Grunvald, E Morita, Y Englund, PT Gazzinelli, RT Sher, A TI Characterization of IL-12 and TNF-alpha inducing activities in Toxoplasma gondii as protein-associated glycolipids. SO FASEB JOURNAL LA English DT Meeting Abstract C1 JOHNS HOPKINS SCH MED,BALTIMORE,MD 21205. NIAID,LPD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1045 EP 1045 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101275 ER PT J AU Zhou, P Sieve, MC Tewari, RP Seder, RA AF Zhou, P Sieve, MC Tewari, RP Seder, RA TI IL-12 and amphotericin B prolong survival in SCID mice infected with Histoplasma capsulatum. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. SO ILLINOIS MED SCH,SPRINGFIELD,IL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1050 EP 1050 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101278 ER PT J AU Camargo, M Almeida, IC Rizzo, LV Travassos, LR Gazzinelli, RT AF Camargo, M Almeida, IC Rizzo, LV Travassos, LR Gazzinelli, RT TI A Trypanosoma cruzi derived glycoconjugate is potent inducer of IL-12 synthesis by macrophages. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV FED MINAS GERAIS,DEPT BIOCHEM & IMMUNOL,BR-30161 BELO HORIZONT,MG,BRAZIL. FIOCRUZ MS,CTR PESQUISAS RENE RACHOU,LAB CHAGAS DIS,BR-30161 BELO HORIZONT,MG,BRAZIL. EPM,DISC CELLULAR BIOL,SAO PAULO,BRAZIL. NEI,NIH,BETHESDA,MD 20982. RI Rizzo, Luiz Vicente/B-4458-2009; Travassos, Luiz/J-3631-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1052 EP 1052 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101282 ER PT J AU McDyer, JF Seder, RA AF McDyer, JF Seder, RA TI Characterization of cytokine production from patients with multi-drug resistant tuberculosis SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1063 EP 1063 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101293 ER PT J AU Peruzzi, M Wagtmann, N Malnati, M Parker, K Long, EO AF Peruzzi, M Wagtmann, N Malnati, M Parker, K Long, EO TI A single killer cell inhibitory receptor (KIR) can discriminate among peptides bound to HLA-B*2705. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,MOLEC STRUCT LAB,IMMUNOGENET LAB,NIH,ROCKVILLE,MD 20852. RI Long, Eric/G-5475-2011 OI Long, Eric/0000-0002-7793-3728 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1076 EP 1076 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101305 ER PT J AU Sconocchia, G Titus, IA Pericle, F Segal, DM AF Sconocchia, G Titus, IA Pericle, F Segal, DM TI A tyrosine phosphorylated protein may link CD44 to NK cytotoxicity SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1085 EP 1085 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101315 ER PT J AU Jakob, T Udey, MC AF Jakob, T Udey, MC TI E-cadherin-associated proteins and tyrosinephosphorylation status in Langerhans cell-like dendritic cells (FSDC) propagated from fetal murine skin SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,DERMATOL BRANCH,NIH,BETHESDA,MD. RI Jakob, Thilo/J-1621-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1182 EP 1182 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101411 ER PT J AU Yamashita, Y Hodes, RJ AF Yamashita, Y Hodes, RJ TI Regulation of mouse CD44 epitopes associated with expression of variable exon-containing isoforms. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NIA,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1183 EP 1183 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101414 ER PT J AU Caspi, RR Jones, LS Agarwal, R Silver, PB Chan, CC Rizzo, LV AF Caspi, RR Jones, LS Agarwal, R Silver, PB Chan, CC Rizzo, LV TI Interferon gamma (IFN-gamma)-deficient mice are susceptible to induction of experimental autoimmune uveitis (EAU) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. HHMI,NIH,RES SCHOLARS PROG,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1188 EP 1188 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101417 ER PT J AU Silver, P Hathcock, K Chan, CC Green, JM Thompson, CB Caspi, R AF Silver, P Hathcock, K Chan, CC Green, JM Thompson, CB Caspi, R TI CD28 costimulation is required for induction of autoimmune, but not for endotoxin-induced, uveitis. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEI,NIH,BETHESDA,MD 20892. NCI,NIH,BETHESDA,MD 20892. UNIV CHICAGO,GWEN KNAPP CTR,CHICAGO,IL 60637. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1189 EP 1189 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101420 ER PT J AU Tuscano, J Tedder, TF Kehrl, JH AF Tuscano, J Tedder, TF Kehrl, JH TI Engagement of the adhesion receptor CD22 triggers a potent stimulatory signal for B cells and blocking CD22/CD22L interactions impairs T-cell proliferation. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LIR,NIH,BETHESDA,MD 20892. DUKE UNIV,MED CTR,DEPT IMMUNOL,DURHAM,NC 27710. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1213 EP 1213 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101441 ER PT J AU Chen, ZJ Shimizu, F Wheeler, J Notkins, AL AF Chen, ZJ Shimizu, F Wheeler, J Notkins, AL TI Properties of polyreactive antigen-binding B cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,DEPT ORAL MED,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1217 EP 1217 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101446 ER PT J AU Bouloc, A Walker, P Grivel, JC Vogel, J Katz, SL AF Bouloc, A Walker, P Grivel, JC Vogel, J Katz, SL TI A role for Langerhans cells in intracutaneous DNA immunization. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1232 EP 1232 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101459 ER PT J AU Swieter, M Berenstein, EH Siraganian, RP AF Swieter, M Berenstein, EH Siraganian, RP TI Protein tyrosine phosphatases in RBL-2H3 cells and their possible involvement in IgE receptor (Fc epsilon RI) signaling. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20893. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1242 EP 1242 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101470 ER PT J AU Hamawy, MM Sagawa, K Zhang, J Mergenhagen, SE Siraganian, RP AF Hamawy, MM Sagawa, K Zhang, J Mergenhagen, SE Siraganian, RP TI A 72 kDa protein downstream of Syk that is tyrosine phosphorylated by the aggregation of the high affinity IgE receptor (Fc epsilon RI). SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1243 EP 1243 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101473 ER PT J AU Berenstein, EH Swieter, M Siraganian, RP AF Berenstein, EH Swieter, M Siraganian, RP TI CD45 and signaling through the Fc epsilon RI in RBL-2H3 mast cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1245 EP 1245 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101474 ER PT J AU Kimura, T Sakamoto, H Apella, E Siraganian, RP AF Kimura, T Sakamoto, H Apella, E Siraganian, RP TI Conformational changes induced in protein tyrosine kinase Syk by tyrosine phosphorylation or by binding of phosphorylated ITAM peptides. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1252 EP 1252 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101481 ER PT J AU Amichay, D Gazzinelli, R Karupiah, G Sher, A Farber, I AF Amichay, D Gazzinelli, R Karupiah, G Sher, A Farber, I TI Chemokine expression patterns suggest unique biological roles in-vivo. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1290 EP 1290 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101520 ER PT J AU Kioka, N Humphries, MJ Akiyama, SK AF Kioka, N Humphries, MJ Akiyama, SK TI Effects of integrin activation on cell proliferation and the cell cycle. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV MANCHESTER,SCH BIOL SCI,MANCHESTER,LANCS,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1326 EP 1326 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101555 ER PT J AU Yang, LH Ahmed, SA Miles, EW AF Yang, LH Ahmed, SA Miles, EW TI Roles of conserved and variable C-terminal residues in the beta subunit of tryptophan synthase. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1374 EP 1374 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101605 ER PT J AU Gladyshev, VN Jeang, KT Stadtman, TC AF Gladyshev, VN Jeang, KT Stadtman, TC TI Selenium in normal and HIV-infected human T-cells: Selenocysteine in a C-terminal tripeptide of T-cell thioredoxin reductase corresponds to TGA in the gene. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,BETHESDA,MD 20892. NIAID,NIH,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1405 EP 1405 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101632 ER PT J AU Kang, JH Yim, HS Kwak, HS Chock, PB Stadtman, ER Yim, MB AF Kang, JH Yim, HS Kwak, HS Chock, PB Stadtman, ER Yim, MB TI A gain-of-function of an amyotrophic lateral sclerosis-associated Cu,Zn-superoxide dismutase mutant. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1422 EP 1422 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101652 ER PT J AU Qin, KF Wang, YX Huang, CY AF Qin, KF Wang, YX Huang, CY TI Characteristics of a novel Mg2+-dependent, Ca2+-inhibitable serine/threonine phosphatase revealed by molecular cloning. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1457 EP 1457 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101686 ER PT J AU Huang, K Sommers, CL Grinberg, A Kozak, CA Love, PE AF Huang, K Sommers, CL Grinberg, A Kozak, CA Love, PE TI Cloning and characterization of PTPK1, a novel nonreceptor protein tyrosine phosphatase highly expressed in bone marrow. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,NIH,BETHESDA,MD 20892. NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1463 EP 1463 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101692 ER PT J AU deMendez, I Leto, T AF deMendez, I Leto, T TI The molecular basis of p47(phox) SH3 domain binding specificities. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1515 EP 1515 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101744 ER PT J AU Leto, TL AF Leto, TL TI The p67-phox NADPH oxidase component is comprised of several tetratricopeptide repeats (TPR) that are disrupted in a rare form of chronic granulomatous disease SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1516 EP 1516 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101745 ER PT J AU Roche, PA Chawla, A Ravichandran, V AF Roche, PA Chawla, A Ravichandran, V TI Identification and characterization of SNAP-23, the non-neuronal homolog of the membrane fusion protein receptor SNAP-25. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1530 EP 1530 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101758 ER PT J AU Kong, SK Chock, PB AF Kong, SK Chock, PB TI Ubiquitin carrier protein kinase activity of normal rat tissues. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1549 EP 1549 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101779 ER PT J AU MacGregor, D Marrogi, AJ Lockyer, JM Gendelman, R Lu, M Ensoli, B AF MacGregor, D Marrogi, AJ Lockyer, JM Gendelman, R Lu, M Ensoli, B TI Expression of Bcl-2 in AIDS-associated and classical Kaposi's Sarcoma. SO FASEB JOURNAL LA English DT Meeting Abstract C1 TULANE UNIV,MED CTR,NEW ORLEANS,LA 70112. NCI,NIH,BETHESDA,MD 20892. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1571 EP 1571 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101801 ER PT J AU Oliver, GW EmmertBuck, M StetlerStevenson, WG Lim, MS Kleiner, DE AF Oliver, GW EmmertBuck, M StetlerStevenson, WG Lim, MS Kleiner, DE TI Quantitative analysis of picogram amounts of metalloproteinase inhibitors in human tumor tissues. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1579 EP 1579 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101808 ER PT J AU Utz, U Banks, D McFarland, HF Jacobson, S Biddison, WE AF Utz, U Banks, D McFarland, HF Jacobson, S Biddison, WE TI TCR usage in human demyelinating diseases: MBP-reactive TCR in MS versus HTLV-I tax-reactive TCR in HAM/TSP. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS,NEUROIMMUNOL BRANCH,NIH,BETHESDA,MD 20892. INST RECH CLIN MONTREAL,IMMUNOL LAB,MONTREAL,PQ H2W 1R7,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1589 EP 1589 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101819 ER PT J AU Omori, M Evarts, RP Hu, Z Omori, N Marsden, ER Thorgeirsson, SS AF Omori, M Evarts, RP Hu, Z Omori, N Marsden, ER Thorgeirsson, SS TI Activation of stem cell compartment in bile duct ligated young rats. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,LEC,DBS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1629 EP 1629 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101857 ER PT J AU Omori, N Evarts, RP Omori, M Hu, Z Marsden, ER Thorgeirsson, SS AF Omori, N Evarts, RP Omori, M Hu, Z Marsden, ER Thorgeirsson, SS TI Expression of leukemia inhibitory factor and its receptor during liver regeneration in the adult rat SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,LEC,DBS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1637 EP 1637 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101864 ER PT J AU Schweighoffer, E Fowlkes, BJ AF Schweighoffer, E Fowlkes, BJ TI alpha beta/gamma delta lineage decisions in T cell development SO FASEB JOURNAL LA English DT Meeting Abstract C1 NATL INST HLTH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1739 EP 1739 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101968 ER PT J AU Magner, WJ Chang, AC Hong, MJP Brooks, A Owens, J Coligan, JE AF Magner, WJ Chang, AC Hong, MJP Brooks, A Owens, J Coligan, JE TI Aberrant differentiation of thymocytes in mice lacking laminin-2 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,MOLEC STRUCT LAB,ROCKVILLE,MD 20852. NCRR,NIH,LAB SCI SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1740 EP 1740 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101970 ER PT J AU Parker, K Turner, R Coligan, J Biddison, W AF Parker, K Turner, R Coligan, J Biddison, W TI HLA-A2/HTLV-1 tax peptide single-chain molecules are recognized by tax-specific and HLA-A2 allo-specific T cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,ROCKVILLE,MD 20852. NINCDS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1750 EP 1750 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101981 ER PT J AU Fenske, TS Farner, NL deJong, JLO OShea, JJ Sondel, PM AF Fenske, TS Farner, NL deJong, JLO OShea, JJ Sondel, PM TI Interleukin-2 mediated activation of JAK3 in the absence of a detectable 64 kDa common gamma chain. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV WISCONSIN,MADISON,WI 53706. NIAMSD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1752 EP 1752 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101982 ER PT J AU Drew, PD Franzoso, G Biddison, WE Siebenlist, U Ozato, K AF Drew, PD Franzoso, G Biddison, WE Siebenlist, U Ozato, K TI Interferon regulatory factor and NF kappa B proteins physically interact and coordinately regulate major histocompatibility class I gene expression. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1755 EP 1755 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101984 ER PT J AU Tagaya, Y Burton, JD Miyamoto, Y Waldmann, TA AF Tagaya, Y Burton, JD Miyamoto, Y Waldmann, TA TI Interleukin-15/T utilizes a novel receptor signal transduction pathway in mast cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,METAB BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1757 EP 1757 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101985 ER PT J AU Segal, BM Shevach, EM AF Segal, BM Shevach, EM TI The role of cytokines in resistance to an autoimmune disease. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1759 EP 1759 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101988 ER PT J AU Weiss, RA Madaio, MP Schwartz, RH AF Weiss, RA Madaio, MP Schwartz, RH TI Cadmium chloride induces B7.1 expression in murine renal tubular cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20894. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1765 EP 1765 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101994 ER PT J AU Wu, AJ Shimizu, F Baum, BJ Fox, PC Notkins, AL Chen, ZJ AF Wu, AJ Shimizu, F Baum, BJ Fox, PC Notkins, AL Chen, ZJ TI Interferon-gamma induces the expression of B7 on a human salivary gland cell line. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,CIPCB,BETHESDA,MD 20892. NIDR,LOM,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1766 EP 1766 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86101997 ER PT J AU Schwartz, LB Sakai, K Worobec, A Metcalfe, D Ren, S AF Schwartz, LB Sakai, K Worobec, A Metcalfe, D Ren, S TI A novel heparin-dependent processing pathway for human tryptase may account for different mechanisms of release of alpha and beta forms of this enzyme SO FASEB JOURNAL LA English DT Meeting Abstract C1 VIRGINIA COMMONWEALTH UNIV,RICHMOND,VA 23298. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1773 EP 1773 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102003 ER PT J AU Rumsaeng, V Cruikshank, WW Foster, B Kornfeld, H Center, DM Metcalfe, DD AF Rumsaeng, V Cruikshank, WW Foster, B Kornfeld, H Center, DM Metcalfe, DD TI Interleukin-16 production by human leukemic mast cells (HMC-1) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. BOSTON UNIV,BOSTON,MA 02118. NR 0 TC 1 Z9 1 U1 0 U2 5 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1776 EP 1776 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102005 ER PT J AU Huang, H HuLi, J BenSasson, SZ Seder, R Li, WEP AF Huang, H HuLi, J BenSasson, SZ Seder, R Li, WEP TI A STAT-6-binding element in the IL-4 promoter SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1793 EP 1793 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102022 ER PT J AU Tarrant, T Rizzo, LV Silver, PB Caspi, RR AF Tarrant, T Rizzo, LV Silver, PB Caspi, RR TI TGF-beta suppresses antigen stimulation of a uveitogenic T cell line through an effect on antigen-presenting cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,HHMI,RES SCHOLARS PROGRAM,LAB IMMUNOL,NEI,BETHESDA,MD 20892. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1799 EP 1799 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102030 ER PT J AU Nishimura, MI McKee, MD Rosenberg, SA AF Nishimura, MI McKee, MD Rosenberg, SA TI Use of competitive PCR to quantitate TCR V beta gene usage in cultured T cell lines and patient samples. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,SURG BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1822 EP 1822 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102051 ER PT J AU SuriPayer, E Shevach, E AF SuriPayer, E Shevach, E TI Identification of H/K ATP'ase-reactive T cells in autoimmune gastritis SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1827 EP 1827 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102056 ER PT J AU Deulofeut, H Robinson, MA AF Deulofeut, H Robinson, MA TI Characterization of the TCRBV repertoire utilized in response to HBsAg. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1829 EP 1829 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102060 ER PT J AU Apasov, SG Koshiba, M Chused, TM Sitkovsky, MV AF Apasov, SG Koshiba, M Chused, TM Sitkovsky, MV TI Differential susceptibility of T cell subsets to effects of extracellular adenosine and ATP: Possible role for purinergic receptors. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1843 EP 1843 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102073 ER PT J AU Ryan, JJ McReynolds, LJ Paul, WE AF Ryan, JJ McReynolds, LJ Paul, WE TI A movable IL-4 receptor sequence capable of enhancing CD23 expression. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1873 EP 1873 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102100 ER PT J AU Melillo, G Taylor, LS Brook, A Cox, GW Varesio, L AF Melillo, G Taylor, LS Brook, A Cox, GW Varesio, L TI Cooperative interaction between hypoxia and lipopolysaccharide (LPS) in the activation of the inducible nitric oxide synthase (iNOS) promoter. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BCDP,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,DBS,EXPTL IMMUNOL LAB,FREDERICK,MD. RI varesio, luigi/J-8261-2016 OI varesio, luigi/0000-0001-5659-2218 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1878 EP 1878 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102108 ER PT J AU Nelms, K Paul, WE AF Nelms, K Paul, WE TI The I4R motif of the IL-4 receptor: Critical residues and novel interactions. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1879 EP 1879 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102106 ER PT J AU Kuhns, DB Gallin, EK Gallin, JI AF Kuhns, DB Gallin, EK Gallin, JI TI Thapsigargin induces Ca2+-dependent production and release of IL-8 in human neutrophils (PMNs) SO FASEB JOURNAL LA English DT Meeting Abstract C1 SAIC FREDERICK,FREDERICK,MD 21702. NIAID,NIH,HOST DEF LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1915 EP 1915 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102144 ER PT J AU Druey, KM Blumer, KJ Kang, VH Kehrl, JH AF Druey, KM Blumer, KJ Kang, VH Kehrl, JH TI A novel mammalian gene family that regulates G protein-mediated signal transduction. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. NR 0 TC 1 Z9 1 U1 1 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 APR 30 PY 1996 VL 10 IS 6 BP 1919 EP 1919 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102146 ER PT J AU Bosco, MC Zea, A Rowe, T Ortaldo, J Varesio, L EspinozaDelgado, I AF Bosco, MC Zea, A Rowe, T Ortaldo, J Varesio, L EspinozaDelgado, I TI Involvement of protein tyrosine kinases in IL-2-induced activation of human monocytes. SO FASEB JOURNAL LA English DT Meeting Abstract C1 SAIC,BCDP,FREDERICK,MD 21702. SAIC,CSP,FREDERICK,MD 21702. FCRDC,NCI,DBS,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. RI Bosco, Maria Carla/J-7928-2016; varesio, luigi/J-8261-2016 OI Bosco, Maria Carla/0000-0003-1857-7193; varesio, luigi/0000-0001-5659-2218 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1960 EP 1960 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102187 ER PT J AU Ito, N Li, Y Dileepan, KN Stechschulte, DJ Rice, N Suzuki, T AF Ito, N Li, Y Dileepan, KN Stechschulte, DJ Rice, N Suzuki, T TI Phagocytosis of mast cell granules (MCG) leads to degradation of NF-kappa B proteins in mouse macrophages. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV KANSAS,MED CTR,KANSAS CITY,KS 66160. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1968 EP 1968 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102197 ER PT J AU EspinozaDelgado, I Rottschafer, S Bosco, MC Ortaldo, JR AF EspinozaDelgado, I Rottschafer, S Bosco, MC Ortaldo, JR TI Interleukin-2 enhances B7-1 mRNA and protein expression. SO FASEB JOURNAL LA English DT Meeting Abstract C1 SAIC,BCDP,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,DBS,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. RI Bosco, Maria Carla/J-7928-2016 OI Bosco, Maria Carla/0000-0003-1857-7193 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1973 EP 1973 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102202 ER PT J AU Jankovic, D Kullberg, M Yap, G Epstein, M Cheever, A Sher, A AF Jankovic, D Kullberg, M Yap, G Epstein, M Cheever, A Sher, A TI B cell-deficient mice exposed to Schistosoma mansoni develop exacerbated egg pathology which fails to down-modulate during chronic infection. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOBIOL SECT,PARASIT DIS LAB,BETHESDA,MD 20892. NIAID,CELLULAR & MOLEC IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 1995 EP 1995 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102225 ER PT J AU PitchekianHalabi, H Kim, S MackenzieGraham, A McFarland, HF Raine, CS Voskuhl, RR AF PitchekianHalabi, H Kim, S MackenzieGraham, A McFarland, HF Raine, CS Voskuhl, RR TI Gender differences in autoimmune demyelination in the mouse; Implications for multiple sclerosis. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90095. NIH,BETHESDA,MD 20892. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2038 EP 2038 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102267 ER PT J AU Smith, ME Eller, NL AF Smith, ME Eller, NL TI Gender influences EAE both before and after sexual maturation. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,PEDIAT MED BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2039 EP 2039 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102268 ER PT J AU Qui, JX Murozono, M Weng, N Marcus, DM Padian, EA AF Qui, JX Murozono, M Weng, N Marcus, DM Padian, EA TI Molecular models of antibodies against GM1 ganglioside and related structures. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. BAYLOR COLL MED,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2071 EP 2071 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102301 ER PT J AU Bonney, EA Matzinger, P AF Bonney, EA Matzinger, P TI Beyond fetal cell migration into the maternal circulation. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,SECT T CELL TOLERANCE,CELLULAR & MOLEC IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2104 EP 2104 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102333 ER PT J AU Ubagai, T Chamberlin, ME Mudd, SH Chou, JY AF Ubagai, T Chamberlin, ME Mudd, SH Chou, JY TI Demyelination of the brain is associated with defects in the hepatic form of methionine adenosyl transferase SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,HERITABLE DISORDERS BRANCH,NIH,BETHESDA,MD 20892. NIMH,LAB GEN & COMPARAT BIOCHEM,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2147 EP 2147 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102375 ER PT J AU Napolitano, M Hockman, S Taira, M Pepin, L Degerman, E Manganiello, V AF Napolitano, M Hockman, S Taira, M Pepin, L Degerman, E Manganiello, V TI Molecular cloning and expression of mouse adipocyte cGMP-inhibited cyclic nucleotides phosphodiesterase (cGI PDE) SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2160 EP 2160 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102390 ER PT J AU Warner, DR Fishman, PH AF Warner, DR Fishman, PH TI A human G(s)alpha mutant that is is unable to couple to adenylate cyclase and associate with membranes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS,MBS,LMCN,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2161 EP 2161 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102388 ER PT J AU Basi, NS Rebois, RV AF Basi, NS Rebois, RV TI Fast rate zonal sedimentation of GTP gamma S-activated Gs. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NINCDS,MEMBRANE BIOCHEM SECT,LMCN,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2163 EP 2163 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102392 ER PT J AU Garcia, MC Kim, HY AF Garcia, MC Kim, HY TI Activation of serotonin receptors is coupled to the release of polyunsaturated fatty acids from C6 glioma cells SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,LMBB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2199 EP 2199 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102430 ER PT J AU Wolff, EC Joe, YA Park, MH Folk, JE AF Wolff, EC Joe, YA Park, MH Folk, JE TI Specific labeling of deoxyhypusine synthase by [H-3]spermidine SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,LCDO,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2207 EP 2207 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102434 ER PT J AU Liu, SY Stadtman, TC AF Liu, SY Stadtman, TC TI Two types of selenium-containing thioredoxin reductase from human lung tumor and HeLa cell lines. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2208 EP 2208 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102437 ER PT J AU Joe, YA Wolff, E Park, MH AF Joe, YA Wolff, E Park, MH TI Site-directed mutagenesis studies of the recombinant human deoxyhypusine synthase SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2209 EP 2209 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102438 ER PT J AU Ciotti, M Owens, IS AF Ciotti, M Owens, IS TI Comparison of bilirubin and 17 alpha-ethynylestradiol glucuronidation by HUG-Br1 and some of its mutants. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,DISORDERS BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2212 EP 2212 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102442 ER PT J AU Webster, JC Oakley, RH Sar, M Cidlowski, JA AF Webster, JC Oakley, RH Sar, M Cidlowski, JA TI Regulation of the alpha and beta isoforms of the human glucocorticoid receptor by TNF-alpha SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,MOL ENDOCRINOL GRP,LAB INTEGRAT BIOL,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2249 EP 2249 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102478 ER PT J AU Pak, JH Mahoney, CW Huang, FL Huang, KP AF Pak, JH Mahoney, CW Huang, FL Huang, KP TI Nitric oxide oxidation of neurogranin attenuates its phosphorylation by protein kinase C and affinity for calmodulin. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2298 EP 2298 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102526 ER PT J AU Saito, H Oka, T AF Saito, H Oka, T TI Hormonally regulated double- and single-stranded DNA binding complexes involved in mouse beta-casein gene transcription SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,LMCB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2311 EP 2311 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102538 ER PT J AU Friguet, B Conconi, M Szweda, LI Levine, RL Stadtman, ER AF Friguet, B Conconi, M Szweda, LI Levine, RL Stadtman, ER TI Multicatalytic proteinase activity: Age-related decline and protection from oxidative inactivation by Hsp 90. SO FASEB JOURNAL LA English DT Meeting Abstract C1 INST PASTEUR,UNITE BIOCHIM CELLULAIRE,F-75015 PARIS,FRANCE. CASE WESTERN RESERVE UNIV,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106. NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. RI Levine, Rodney/D-9885-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2320 EP 2320 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102551 ER PT J AU Corcoran, ML StetlerStevenson, WG AF Corcoran, ML StetlerStevenson, WG TI TIMP-2 suppresses cell growth by stimulating tyrosine phosphatase activity SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,EXTRACELLULAR MATRIX PATHOL SECT,PATHOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2352 EP 2352 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102579 ER PT J AU Yamada, KM Miyamoto, S Aota, S Katz, BZ AF Yamada, KM Miyamoto, S Aota, S Katz, BZ TI Fibronectin and integrin signaling and cytoskeletal regulation. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,DEV BIOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2433 EP 2433 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102661 ER PT J AU Wlodawer, A Bujacz, G Jaskolski, M Alexandratos, J Merkel, G Katz, RA Skalka, AM AF Wlodawer, A Bujacz, G Jaskolski, M Alexandratos, J Merkel, G Katz, RA Skalka, AM TI Retroviral integrase - Crystal structure of a new target for designing drugs against AIDS. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2440 EP 2440 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102667 ER PT J AU Kiss, A Thorgeirsson, SS AF Kiss, A Thorgeirsson, SS TI Analysis of TGF-alpha/EGFR, HGF/c-met, TGF-beta-RII and p53 expression in 85 human hepatocellular carcinomas (HCCs) from Chinese patients. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,DBS,LEC,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2475 EP 2475 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102704 ER PT J AU Yap, G Cheever, A Jankovic, D Sher, A AF Yap, G Cheever, A Jankovic, D Sher, A TI Immunomodulation of the granulomatous response to schistosome eggs proceeds normally IFN-gamma and beta-2 microglobulin-deficient mice. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2500 EP 2500 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102730 ER PT J AU Murphy, WJ Asai, O Tian, Z Hornung, R Longo, DL AF Murphy, WJ Asai, O Tian, Z Hornung, R Longo, DL TI Activated natural killer (NK) cells mediate graft-versus-tumor (GVT) effects but inhibit graft-versus-host disease (GVHD) after allogeneic bone marrow transplantation (BMT). SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,LLB,DBS,FREDERICK,MD 21702. NCI,BCDP,SAIC FREDERICK,FCRDC,FREDERICK,MD 21702. NIA,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2509 EP 2509 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102737 ER PT J AU Karp, CL Wysocka, M Wahl, LM Cuomo, PJ Ahearn, JM Trinchieri, G Griffin, DE AF Karp, CL Wysocka, M Wahl, LM Cuomo, PJ Ahearn, JM Trinchieri, G Griffin, DE TI Inhibition of interleukin-12 production by measles virus SO FASEB JOURNAL LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21287. SCH HYG & PUBL HLTH,BALTIMORE,MD 21287. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2515 EP 2515 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102745 ER PT J AU Goletz, TJ Zhan, S Pendleton, CD Helman, LJ Berzofsky, JA AF Goletz, TJ Zhan, S Pendleton, CD Helman, LJ Berzofsky, JA TI Generation of cytotoxic T cells against tumor-specific translocations: Potential anti-cancer vaccines for Ewing's sarcoma and alveolar rhabdomyosarcoma. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2521 EP 2521 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102751 ER PT J AU Chen, W Chesebro, B Qin, H Cheever, MA AF Chen, W Chesebro, B Qin, H Cheever, MA TI Cytotoxic T lymphocytes elicited by priming with tumor-associated peptide can eradicate established leukemia. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV WASHINGTON,DIV ONCOL,SEATTLE,WA 98195. NIAID,ROCKY MT LABS,LPVD,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2522 EP 2522 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102749 ER PT J AU Anderson, H Roche, P AF Anderson, H Roche, P TI Role of invariant chain phosphorylation in intracellular transport. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,EXPTL IMMUNOL BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2530 EP 2530 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102756 ER PT J AU Reeves, ME Rosenberg, SA Hwu, P AF Reeves, ME Rosenberg, SA Hwu, P TI Transduction and differentiation of dendritic cells from human hematopoietic progenitor cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,SURG BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2552 EP 2552 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102779 ER PT J AU Chen, H Paul, WE AF Chen, H Paul, WE TI Cultured splenic NK1.1+, CD4+ T cells produce IL4. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2560 EP 2560 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102790 ER PT J AU Smith, P Apasov, S Jelonik, M Margulies, D Sitkovsky, MV AF Smith, P Apasov, S Jelonik, M Margulies, D Sitkovsky, MV TI Constitutive intracellular Ser/Thr phosphorylation of the extracellular domain of alpha beta TCR. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2569 EP 2569 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102795 ER PT J AU Huang, S Smith, P Apasov, S Sitkovsky, M AF Huang, S Smith, P Apasov, S Sitkovsky, M TI T-cell plasma membrane association of PP2A protein phosphatase. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2589 EP 2589 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102817 ER PT J AU Correa, MR Ghosh, P Longo, DL Ochoa, AC AF Correa, MR Ghosh, P Longo, DL Ochoa, AC TI Alterations in signal transduction and nuclear transcription factors in chronically stimulated T cells through the TCR. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,IMMUNOTHERAPY LAB,FREDERICK,MD 21702. ONCOTHERAPEUT INC,CRANBURY,NJ 08512. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2599 EP 2599 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102825 ER PT J AU Ishaq, M Natarajan, V AF Ishaq, M Natarajan, V TI Down regulation of an RXR alpha related gene expression during T cell receptor (TCR) mediated activation of human T cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2600 EP 2600 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102828 ER PT J AU Luo, G Kazansky, A Liu, X Henninghausen, L YuLee, L AF Luo, G Kazansky, A Liu, X Henninghausen, L YuLee, L TI Structure and function analysis of a prolactin-inducible Stat factor, Stat 5b, in T cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOUSTON,TX 77030. NIDDK,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2604 EP 2604 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102833 ER PT J AU Koshiba, M Apasov, S Sverdlov, V Erb, L Turner, J Weisman, G Sitkovsky, MV AF Koshiba, M Apasov, S Sverdlov, V Erb, L Turner, J Weisman, G Sitkovsky, MV TI Transient up-regulation of the expression of p2y(2) purinergic receptors in thymocytes as an immediate early gene response. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,LI,BETHESDA,MD 20892. UNIV MISSOURI,DEPT BIOCHEM,COLUMBIA,MO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2606 EP 2606 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102834 ER PT J AU Kwon, TK Nagel, J Buchholz, M Nordin, A AF Kwon, TK Nagel, J Buchholz, M Nordin, A TI Characterization of the murine cyclin-dependent kinase inhibitor gene p27(Kip). SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2608 EP 2608 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102838 ER PT J AU Matsubara, H Shearer, GM AF Matsubara, H Shearer, GM TI Suggestion or a unique CD28 costimulatory mechanism in human T cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,EIB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2619 EP 2619 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102847 ER PT J AU Palmer, L Saha, B Hodes, R Abe, R AF Palmer, L Saha, B Hodes, R Abe, R TI Immune-mediated responses against mouse mammary tumor virus (MMTV) in CD28-deficient mice. SO FASEB JOURNAL LA English DT Meeting Abstract C1 USN,RES INST,NATL NAVAL MED CTR,BETHESDA,MD 20892. NIA,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2639 EP 2639 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102866 ER PT J AU Cole, DJ Wilson, M Rivoltini, L Custer, M Nishimura, MI AF Cole, DJ Wilson, M Rivoltini, L Custer, M Nishimura, MI TI T-cell response in matched MART-1 peptide stimulated peripheral blood lymphocytes and tumor infiltrating lymphocytes. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NATL TUMOR INST MILAN,I-20133 MILAN,ITALY. MED UNIV S CAROLINA,DEPT SURG,CHARLESTON,SC 29425. NCI,SURG BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2687 EP 2687 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102915 ER PT J AU Pericle, F Sconocchia, G Segal, DM AF Pericle, F Sconocchia, G Segal, DM TI Hyaluronan binding to CD44 on human neutrophils induces PMN tumoricidal activity. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,EXPTL IMMUNOL BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2696 EP 2696 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102929 ER PT J AU Loftus, D Castelli, C Marincola, F Parmiani, G Appella, E Rivoltini, L AF Loftus, D Castelli, C Marincola, F Parmiani, G Appella, E Rivoltini, L TI A possible role for epitope mimicry in shaping the CTL response to melanoma antigen MART-1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. IST NAZL TUMORI,I-20133 MILAN,ITALY. RI castelli, chiara/K-6899-2012 OI castelli, chiara/0000-0001-6891-8350 NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2705 EP 2705 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102933 ER PT J AU Rivoltini, L Loftus, DJ Barracchini, K Arienti, F Mazzocchi, A Squarcina, P Biddison, WE Appella, E Parmiani, G Marincola, FM AF Rivoltini, L Loftus, DJ Barracchini, K Arienti, F Mazzocchi, A Squarcina, P Biddison, WE Appella, E Parmiani, G Marincola, FM TI Binding, presentation and immunogenicity of peptides derived from melanoma antigens MART-1 and GP100 by HLA-A2 subtypes SO FASEB JOURNAL LA English DT Meeting Abstract C1 NATL TUMOR INST MILAN,DIV EXPT ONCOL D,I-20133 MILAN,ITALY. NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2706 EP 2706 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102931 ER PT J AU Irvine, KR Chamberlain, RS Bronte, V Rosenberg, SA Restifo, NP AF Irvine, KR Chamberlain, RS Bronte, V Rosenberg, SA Restifo, NP TI The route of administration of recombinant vaccinia virus (rVV) vaccines effects the active treatment of cancer. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,SURG BRANCH,NIH,BETHESDA,MD 20892. RI Restifo, Nicholas/A-5713-2008 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2711 EP 2711 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102939 ER PT J AU Cain, SA Padlan, EA Helm, BA AF Cain, SA Padlan, EA Helm, BA TI Expression of human IgE-Fc and the extracellular domains of the alpha-chain of the high affinity receptor for IgE in Pichia pastoris. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV SHEFFIELD,DEPT MOLEC BIOL & BIOTECHNOL,KREBS INST,SHEFFIELD S10 2UH,S YORKSHIRE,ENGLAND. NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2746 EP 2746 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102973 ER PT J AU Helm, BA Sayers, I Machado, DC Padlan, EA AF Helm, BA Sayers, I Machado, DC Padlan, EA TI Potential applications of hIgE-Fc derived peptides as rational antagonists of the allergic response. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV SHEFFIELD,KREBS INST,DEPT MOLEC BIOL & BIOTECHNOL,SHEFFIELD S10 2UH,S YORKSHIRE,ENGLAND. NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2747 EP 2747 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102971 ER PT J AU Sayers, I Machado, DC Ahmad, K Padlan, EA Helm, BA AF Sayers, I Machado, DC Ahmad, K Padlan, EA Helm, BA TI Identification of the sites(s) on human IgE that are involved in the interaction with its high (Fc epsilon RI) and low (Fc epsilon RII) affinity receptors. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV SHEFFIELD,KREBS INST,DEPT MOL BIOL & BIOTECH,SHEFFIELD S10 2UH,S YORKSHIRE,ENGLAND. NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2748 EP 2748 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86102981 ER PT J AU Su, HC Kulkarni, AB Karlsson, S Biron, CA AF Su, HC Kulkarni, AB Karlsson, S Biron, CA TI Aberrant NK cell responses in TGF-beta 1-deficient mice SO FASEB JOURNAL LA English DT Meeting Abstract C1 BROWN UNIV,PROVIDENCE,RI 02912. NINCDS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2800 EP 2800 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103033 ER PT J AU Veech, RL Kashiwaya, Y Keon, CA Radda, GK Clarke, K AF Veech, RL Kashiwaya, Y Keon, CA Radda, GK Clarke, K TI A new P-31 NMR method to measure intracellular free [Mg2+] SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAAA,LMBB,ROCKVILLE,MD 20852. UNIV OXFORD,DEPT BIOCHEM,OXFORD OX1 3QU,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2858 EP 2858 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103082 ER PT J AU Zimmerman, SB Murphy, LD AF Zimmerman, SB Murphy, LD TI Stabilization of isolated nucleoids from Escherichia coli under crowded conditions. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2861 EP 2861 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103091 ER PT J AU Rabinovitz, M AF Rabinovitz, M TI Consequences of amino acid deprivation: A unifying theory SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2898 EP 2898 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103125 ER PT J AU Venkatachalam, KV Strott, CA AF Venkatachalam, KV Strott, CA TI Isolation of a 55 kD protein from the guinea pig adrenal that catalyzes production of the sulfotransferase sulfonate donor molecule 3'-phosphoadenosine 5'-phosphosulfate (PAPS): Evidence for intrinsic sulfatase activity. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2951 EP 2951 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103178 ER PT J AU Kallarakal, AT Jeng, J Popov, KM Song, BJ AF Kallarakal, AT Jeng, J Popov, KM Song, BJ TI Naturally occurring mutant (H263L) of pyruvate dehydrogenase complex E1 alpha subunit: Implications in thiamine binding and phosphorylation. SO FASEB JOURNAL LA English DT Meeting Abstract C1 INDIANA UNIV,SCH MED,DEPT BIOCHEM & MOLEC BIOL,INDIANAPOLIS,IN 46202. NIAAA,NIH,NEUROGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2952 EP 2952 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103176 ER PT J AU Srivastava, RK ChoChung, YS AF Srivastava, RK ChoChung, YS TI Protein kinase A RII beta regulatory subunit binds to cAMP-response element in reverse transformation. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2967 EP 2967 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103192 ER PT J AU Nesterova, M Noguchi, K Srivastava, RK ChoChung, YS AF Nesterova, M Noguchi, K Srivastava, RK ChoChung, YS TI Protein kinase A type I - Directed antisense restrains tumor growth: Sequence specific inhibition of gene expression. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2968 EP 2968 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103195 ER PT J AU Sweitzer, TD Hanover, JA AF Sweitzer, TD Hanover, JA TI A calmodulin-dependent pathway for nuclear protein import that does not require GTP in vitro. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDDK,NIH,LAB CELL BIOL & BIOCHEM,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 2995 EP 2995 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103224 ER PT J AU Ponsalle, P Buchholz, M Nordin, A AF Ponsalle, P Buchholz, M Nordin, A TI Decreased G(1) cdk2 kinase activity in activated T cells from old mice. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIA,GERONTOL RES CTR,CLIN IMMUNOL SECT,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 3002 EP 3002 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103231 ER PT J AU Patton, WA Moss, J Vaughan, M Colombo, MI Stahl, PD AF Patton, WA Moss, J Vaughan, M Colombo, MI Stahl, PD TI Evidence for cholera toxin and beta gamma subunit interaction domains in ARF, a regulator of vesicular trafficking. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,NIH,PULM CRIT CARE MED BRANCH,BETHESDA,MD 20892. WASHINGTON UNIV,SCH MED,DEPT CELL BIOL & PHYSIOL,ST LOUIS,MO 63110. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 3008 EP 3008 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103233 ER PT J AU Cieplak, W Mead, DJ AF Cieplak, W Mead, DJ TI Inhibition of endosomal acidification or microtubule function potentiates the cytotoxic activity of Escherichia coli heat-labile toxin in CHO-K1 cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,NIH,ROCKY MT LABS,HAMILTON,MT 59840. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 3009 EP 3009 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103236 ER PT J AU Zhang, ZI Panda, D Mukherjee, AB AF Zhang, ZI Panda, D Mukherjee, AB TI Is human uteroglobin gene a tumor suppressor? SO FASEB JOURNAL LA English DT Meeting Abstract C1 NICHHD,HERITABLE DISORDERS BRANCH,SECT DEV GENET,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP 3028 EP 3028 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86103252 ER PT J AU Torchia, DA AF Torchia, DA TI Flexibility and function in HIV protease. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP C10 EP C10 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86100060 ER PT J AU Umar, A Koi, M Risinger, JI Barrett, JC Kunkel, TA AF Umar, A Koi, M Risinger, JI Barrett, JC Kunkel, TA TI Correction of mismatch repair defective lines via chromosome transfer. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP D14 EP D14 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86100014 ER PT J AU Cissel, DS Fraundorfer, PF Beaven, MA AF Cissel, DS Fraundorfer, PF Beaven, MA TI A requirement for phospholipase (PL) D for mediation of Ca2+/protein kinase C (PKC)-dependent secretion in a mast cell line. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NHLBI,LMI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP L46 EP L46 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86100137 ER PT J AU Burshtyn, DN Scharenberg, AM Wagtmann, N Rajagopalan, S Berrada, K Yis, T Kinet, JP Long, EO AF Burshtyn, DN Scharenberg, AM Wagtmann, N Rajagopalan, S Berrada, K Yis, T Kinet, JP Long, EO TI Signal transduction by killer cell inhibitory receptors involves recruitment of the tyrosine phosphatase SHP-1. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. CLEVELAND CLIN FDN,RES INST,DEPT CANC BIOL,CLEVELAND,OH 44195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD APR 30 PY 1996 VL 10 IS 6 BP P29 EP P29 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA UK861 UT WOS:A1996UK86100192 ER PT J AU Chung, KW Lee, YM Park, TK Kim, SJ Lee, CC AF Chung, KW Lee, YM Park, TK Kim, SJ Lee, CC TI Cooperative transcriptional activation by two glutamine-rich regions of twist product in Drosophila melanogaster SO MOLECULES AND CELLS LA English DT Article ID DNA-BINDING; DORSAL; PROTEIN; MESODERM; GENE; SEQUENCE; DOMAINS; EMBRYO; MOTIF; DAUGHTERLESS AB twist is one of the important genes that determine dorsal-ventral (D-V) axis during embryogenesis in Drosophila. The twist which is expressed in the ventral part of an embryo encodes a transcription factor which contains a basic helix-loop-helix (bHLH) domain. Twist (twist product) has two distinct glutamine-rich regions (QRs) on the upstream of the bHLH domain (major QR: QR-A, minor QR: QR-B). Domain analysis on the QRs using modified yeast two-hybrid assay has revealed that the QR-A has the function of a transcriptional activation domain. Although the QR-A alone could play the role of transcriptional activation domain, the QR-B may be required for stronger transcriptional activation. C1 NHLBI, NIH, MOLEC CARDIOL LAB, BETHESDA, MD 20892 USA. KONKUK UNIV, DEPT MOLEC BIOL, CHUNGJU 380701, SOUTH KOREA. CHEJU NATL UNIV, DEPT BIOL, CHEJU 690756, SOUTH KOREA. SEOUL NATL UNIV, DEPT BIOL, SEOUL 151742, SOUTH KOREA. SEOUL NATL UNIV, RES CTR CELL DIFFERENTIAT, SEOUL 151742, SOUTH KOREA. RP Chung, KW (reprint author), KONGJU NATL UNIV, DEPT BIOL, KONG JU 314701, SOUTH KOREA. NR 29 TC 3 Z9 3 U1 0 U2 1 PU KOREAN SOC MOLECULAR & CELLULAR BIOLOGY PI SEOUL PA 635-4, YUCKSAM-DONG, GANGNAM-GU, SEOUL 135-703, SOUTH KOREA SN 1016-8478 J9 MOL CELLS JI Mol. Cells PD APR 30 PY 1996 VL 6 IS 2 BP 197 EP 202 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UG984 UT WOS:A1996UG98400012 ER PT J AU AlexanderMiller, MA Leggatt, GR Berzofsky, JA AF AlexanderMiller, MA Leggatt, GR Berzofsky, JA TI Selective expansion of high- or low-avidity cytotoxic T lymphocytes and efficacy for adoptive immunotherapy SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE viral immunity; virus clearance; T-cell therapy; determinant density; antigen dose ID TUMOR-INFILTRATING LYMPHOCYTES; INFECTED TARGET-CELLS; ENVELOPE GLYCOPROTEIN; VIRUS; INVIVO; PEPTIDE; INDUCTION; CLONES; PROTECTION; ANTIGEN AB The conventional approach to cytotoxic T-lymphocyte (CTL) induction uses maximal antigen concentration with the intent of eliciting more CTL. However, the efficacy of this approach has not been systematically explored with regard to the quality of the CTLs elicited or their in vivo functionality. Here, we show that a diametrically opposite approach elicits CTLs that are much more effective at clearing virus. CTLs specific for a defined peptide epitope were selectively expanded with various concentrations of peptide antigen. CTLs generated with exceedingly low-dose peptide lysed targets sensitized with >100-fold less peptide than CTLs generated with high-dose peptide. Differences in expression of T-cell antigen receptors or a number of other accessory molecules did not account for the functional differences. Further, high-avidity CTLs adoptively transferred into severe combined immunodeficient mire were 100- to 1000-fold more effective at viral clearance than the low-avidity CTLs, despite the fact that all CTL lines lysed virus-infected targets in vitro. Thus, the quality of CTLs is as important as the quantity of CTLs for adoptive immunotherapy, and the ability to kill virally infected targets in vitro is not predictive of in vivo efficacy, whereas the determinant density requirement described here is predictive. Application of these principles may be critical in developing effective adoptive cellular immunotherapy for viral infections and cancer. C1 NCI, METAB BRANCH, NIH, BETHESDA, MD 20892 USA. RI Leggatt, Graham/G-1924-2010; OI Leggatt, Graham/0000-0002-4078-5653 NR 28 TC 416 Z9 418 U1 1 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4102 EP 4107 DI 10.1073/pnas.93.9.4102 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700068 PM 8633023 ER PT J AU Sekido, Y Bader, S Latif, F Chen, JY Duh, FM Wei, MH Albanesi, JP Lee, CC Lerman, MI Minna, JD AF Sekido, Y Bader, S Latif, F Chen, JY Duh, FM Wei, MH Albanesi, JP Lee, CC Lerman, MI Minna, JD TI Human semaphorins A(V) and IV reside in the 3p21.3 small cell lung cancer deletion region and demonstrate distinct expression patterns SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE growth cone guidance; collapsin; recessive oncogene; G protein ID GROWTH; GENE; CHROMOSOME-3; 3P(14-23); SEQUENCE; PROTEIN; LINES AB Semaphorins acid collapsins make up a family of conserved genes that encode nerve growth cone guidance signals. We have identified two additional members of the human semaphorin family [human semaphorin A(V) and human semaphorin IV] in chromosome region 3p21.3, where several small cell lung cancer (SCLC) cell lines exhibit homozygous deletions indicative of a tumor suppressor gene. Human semaphorin A(V) has 86% amino acid homology with murine semaphorin A, whereas semaphorin IV is most closely related to murine semaphorin E, with 50% homology. These semaphorin genes are approximate to 70 kb apart flanking two GTP-binding protein genes, GNAI-2 and GNAT-1. In contrast, other human semaphorin gene sequences (human semaphorin LII and homologues of murine semaphorins B and C) are not located on chromosome 3. Human semaphorin A(V) is translated in vitro into a 90-kDa protein, which accumulates at the endoplasmic reticulum. The human semaphorin A(V) (3.4-kb mRNA) and IV (3.9- and 2.9-kb mRNAs) genes are expressed abundantly but differentially in a variety of human neural and nonneural tissues. Human semaphorin A(V) was expressed in only 1 out of 23 SCLCs and 7 out of 16 non-SCLCs, whereas semaphorin IV was expressed in 19 out of 23 SCLCs and 13 out of 16 non-SCLCs. Mutational analysis in semaphorin A(V) revealed mutations (germ line in one case) in 3 of 40 lung cancers. Our data suggest the need to determine the function of human semaphorins A(V) and IV in nonneural tissues and their role in the pathogenesis of lung cancer. C1 UNIV TEXAS,SW MED CTR,DEPT PHARMACOL,DALLAS,TX 75235. UNIV TEXAS,SW MED CTR,DEPT INTERNAL MED,DALLAS,TX 75235. NCI,FREDERICK CANC RES & DEV CTR,SCI APPLICAT INT CORP,IMMUNOBIOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,SCI APPLICAT INT CORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. BAYLOR COLL MED,DEPT MOL & HUMAN GENET,HOUSTON,TX 77030. RP Sekido, Y (reprint author), UNIV TEXAS,SW MED CTR,HAMON CTR THERAPEUT ONCOL RES,DALLAS,TX 75235, USA. RI Sekido, Yoshitaka/P-9756-2015 FU NCI NIH HHS [P20 CA58220] NR 30 TC 205 Z9 213 U1 0 U2 9 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4120 EP 4125 DI 10.1073/pnas.93.9.4120 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700071 PM 8633026 ER PT J AU Lane, MA Baer, DJ Rumpler, WV Weindruch, R Ingram, DK Tilmont, EM Cutler, RG Roth, GS AF Lane, MA Baer, DJ Rumpler, WV Weindruch, R Ingram, DK Tilmont, EM Cutler, RG Roth, GS TI Calorie restriction lowers body temperature in rhesus monkeys, consistent with a postulated anti-aging mechanism in rodents SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE aging; Macaca mulatta; locomotor activity; circadian rhythm; heart rate ID DIETARY RESTRICTION; FOOD RESTRICTION; METABOLIC-RATE; DEOXYRIBONUCLEIC-ACID; ENERGY-METABOLISM; FISCHER-344 RATS; MICE; ADULT; VARIABLES; LONGEVITY AB Many studies of caloric restriction (CR) in rodents and lower animals indicate that this nutritional manipulation retards aging processes, as evidenced by increased longevity, reduced pathology, and maintenance of physiological function in a more youthful state. The anti-aging effects of CR are believed to relate, at least in part, to changes in energy metabolism. We are attempting to determine whether similar effects occur in response to CR in nonhuman primates. Core (rectal) body temperature decreased progressively with age from 2 to 30 years in rhesus monkeys fed ad lib (controls) and is reduced by approximate to 0.5 degrees C in age-matched monkeys subjected to 6 years of a 30% reduction in caloric intake. A short-term (1 month) 30% restriction of 2.5-year-old monkeys lowered subcutaneous body temperature by 1.0 degrees C. Indirect calorimetry showed that 24-hr energy expenditure was reduced by approximately 24% during short-term CR. The temporal association between reduced body temperature and energy expenditure suggests that reductions in body temperature relate to the induction of an energy conservation mechanism during CR. These reductions in body temperature and energy expenditure are consistent with findings in rodent studies in which aging rate was retarded by CR, now strengthening the possibility that CR may exert beneficial effects in primates analogous to those observed in rodents. C1 USDA ARS,BELTSVILLE HUMAN NUTR RES CTR,DIET & HUMAN PERFORMANCE LAB,BELTSVILLE,MD 20705. UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI 53706. RP Lane, MA (reprint author), NIA,MOLEC PHYSIOL & GENET SECT,NATHAN W SHOCK LABS,GERONTOL RES CTR,NIH,BAYVIEW MED CTR,BALTIMORE,MD 21224, USA. NR 43 TC 204 Z9 207 U1 0 U2 10 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4159 EP 4164 DI 10.1073/pnas.93.9.4159 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700078 PM 8633033 ER PT J AU Cabiscol, E Levine, RL AF Cabiscol, E Levine, RL TI The phosphatase activity of carbonic anhydrase III is reversibly regulated by glutathiolation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID S-THIOLATION; RAT-LIVER; TYROSINE KINASE; PROTEIN; REDUCTION; SITE; DETHIOLATION; SPECIFICITY; DISULFIDES; BINDING AB Carbonic anhydrase isozyme III (CAIII) is unique among the carbonic anhydrases because it demonstrates phosphatase activity. CAIII forms a disulfide link between glutathione and two of its five cysteine residues, a profess termed S-glutathiolation. Glutathiolation of CAIII occurs in Fire and is increased during aging and under acute oxidative stress. We show that glutathiolation serves to reversibly regulate the phosphatase activity of CAIII. Glutathiolation of Cys-186 is required for phosphatase activity, while glutathiolation of Cys-181 blocks activity. Phosphotyrosine is the preferred substrate, although phosphoserine and phosphothreonine can also be cleaved. Thus, glutathiolation is a reversible covalent modification that can regulate CAIII, a phosphatase that may function in the cellular response to oxidative stress. C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. RI Cabiscol, Elisa/A-4584-2009; Levine, Rodney/D-9885-2011 OI Cabiscol, Elisa/0000-0003-2795-7999; NR 37 TC 106 Z9 115 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4170 EP 4174 DI 10.1073/pnas.93.9.4170 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700080 PM 8633035 ER PT J AU Podgornik, R Strey, HH Gawrisch, K Rau, DC Rupprecht, A Parsegian, VA AF Podgornik, R Strey, HH Gawrisch, K Rau, DC Rupprecht, A Parsegian, VA TI Bond orientational order, molecular motion, and free energy of high-density DNA mesophases SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DOUBLE HELICES; INTERMOLECULAR FORCES; HYDRATION FORCES; PHASES; FLUCTUATIONS; DYNAMICS; INVITRO; INVIVO AB By equilibrating condensed DNA arrays against reservoirs of known osmotic stress and examining them with several structural probes, it has been possible to achieve a detailed thermodynamic and structural characterization of the change between two distinct regions on the liquid-crystalline phase diagram: (i) a higher density hexagonally packed region with long-range bond orientational order in the plane perpendicular to the average molecular direction and (ii) a lower density cholesteric region with fluid-like positional order. X-ray scattering on highly ordered DNA arrays at high density and with the helical axis oriented parallel to the incoming beam showed a sixfold azimuthal modulation of the first-order diffraction peak that reflects the macroscopic bond-orientational order. Transition to the less-dense cholesteric phase through osmotically controlled swelling shows the loss of this bond orientational order, which had been expected from the change in optical birefringence patterns and which is consistent with a rapid onset of molecular positional disorder. This change in order was previously inferred from intermolecular force measurements and is now confirmed by P-31 NMR. Controlled reversible swelling and compaction under osmotic stress, spanning a range of densities between approximate to 120 mg/ml to approximate to 600 mg/ml, allow measurement of the free-energy changes throughout each phase and at the phase transition, essential information for theories of liquid-crystalline states. C1 NIDDKD, STRUCT BIOL LAB, DIV COMP RES & TECHNOL, NIH, BETHESDA, MD 20892 USA. NIDDKD, OFF DIRECTOR, DIV INTRAMURAL RES, NIH, BETHESDA, MD 20892 USA. NIAAA, DIV INTRAMURAL CLIN & BIOL RES, NIH, BETHESDA, MD 20892 USA. UNIV STOCKHOLM, ARRHENIUS LAB, STOCKHOLM, SWEDEN. RI Strey, Helmut/B-5456-2009; Podgornik, Rudolf/C-6209-2008; OI Podgornik, Rudolf/0000-0002-3855-4637; Rupprecht, Allan/0000-0002-2772-1620 NR 29 TC 81 Z9 83 U1 0 U2 7 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4261 EP 4266 DI 10.1073/pnas.93.9.4261 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700097 PM 8633052 ER PT J AU Yap, N Yu, CL Cheng, SY AF Yap, N Yu, CL Cheng, SY TI Modulation of the transcriptional activity of thyroid hormone receptors by the tumor suppressor p53 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE gene regulation; transcription factors; protein-protein interaction ID RETINOID-X-RECEPTOR; WILD-TYPE P53; NUCLEAR RECEPTOR; BINDING ACTIVITY; GENE-EXPRESSION; RXR-BETA; ACID; PROMOTER; PROTEIN; FORMS AB Thyroid hormone nuclear receptors (TRs) are ligand-dependent transcriptional factors that regulate growth, differentiation, and development. The molecular mechanisms by which TRs mediate these effects are unclear. One prevailing hypothesis suggests that TRs may cooperate with other transcriptional factors to mediate their biological effects. In this study, we tested this hypothesis by examining whether the activity of TRs is modulated by the tumor suppressor p53. p53 is a nuclear protein that regulates gene expression via sequence-specific DNA binding and/or direct protein-protein interaction. We found that the human TR subtype beta 1 (h-TR beta 1) physically interacted with p53 via its DNA binding domain. As a result of this physical interaction, binding of h-TR beta 1 to its hormone response elements either as homodimer or as a heterodimer with the retinoic X receptor was inhibited by p53 in a concentration-dependent manner. In transfected cells, wild-type p53 repressed the hormone-dependent transcriptional activation of h-TR beta 1. In contrast, mutant p53 either had no effect or activated the transcriptional activity of h-TR beta 1 depending on the type of hormone response elements. These results indicate the gene regulating activity of TRs was modulated by p53, suggesting that the cross talk between these two transcriptional factors may play an important role in the biology of normal and cancer cells. C1 NCI,GENE REGULAT SECT,MOLEC BIOL LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892. NR 40 TC 73 Z9 73 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4273 EP 4277 DI 10.1073/pnas.93.9.4273 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700099 PM 8633054 ER PT J AU Butt, J Kim, HY Basilion, JP Cohen, S Iwai, K Philpott, CC Altschul, S Klausner, RD Rouault, TA AF Butt, J Kim, HY Basilion, JP Cohen, S Iwai, K Philpott, CC Altschul, S Klausner, RD Rouault, TA TI Differences in the RNA binding sites of iron regulatory proteins and potential target diversity SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID FERRITIN MESSENGER-RNA; RESPONSIVE ELEMENT; TRANSFERRIN RECEPTOR; UNTRANSLATED REGION; HEART ACONITASE; IDENTIFICATION; DNA; POLYMERASE; SYNTHASE; CLONING AB Posttranscriptional regulation of genes of mammalian iron metabolism is mediated by the interaction of iron regulatory proteins (IRPs) with RNA stem-loop sequence elements known as iron-responsive elements (IREs). There are two identified IRPs, IRP1 and IRP2, each of which binds consensus IREs present in eukaryotic transcripts with equal affinity. Site-directed mutagenesis of IRP1 and IRP2 reveals that, although the binding affinities for consensus IREs are indistinguishable, the contributions of arginine residues in the active-site cleft to the binding affinity are different in the two RNA binding sites. Furthermore, although each IRP binds the consensus IRE with high affinity, each IRP also binds a unique alternative ligand, which was identified in an in vitro systematic evolution of ligands by exponential enrichment procedure. Differences in the two binding sites may be important in the function of the IRE-IRP regulatory system. C1 NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892. NR 37 TC 105 Z9 106 U1 2 U2 7 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4345 EP 4349 DI 10.1073/pnas.93.9.4345 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700113 PM 8633068 ER PT J AU Khleif, SN DeGregori, J Yee, CL Otterson, GA Kaye, FJ Nevins, JR Howley, PM AF Khleif, SN DeGregori, J Yee, CL Otterson, GA Kaye, FJ Nevins, JR Howley, PM TI Inhibition of cyclin D-CDK4/CDK6 activity is associated with an E2F-mediated induction of cyclin kinase inhibitor activity SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE human papillomaviruses; cervical cancer; E7 oncoprotein; retinoblastoma protein ID RETINOBLASTOMA GENE-PRODUCT; HUMAN PAPILLOMAVIRUS TYPE-16; CARCINOMA CELL-LINES; CERVICAL-CARCINOMA; DEPENDENT REGULATION; PROTEIN; PHOSPHORYLATION; EXPRESSION; TRANSCRIPTION; BINDING AB Alterations of various components of the cell cycle regulatory machinery that controls the progression of cells from a quiescent to a growing state contribute to the development of many human cancers. Such alterations include the deregulated expression of G(1) cyclins, the loss of function of activities such as those of protein p16(INK4a) that control G(1) cyclin-dependent kinase activity, and the loss of function of the retinoblastoma protein (RB),which is normally regulated by the G(1) cyclin-dependent kinases. Various studies have revealed an inverse relationship in the expression of p16(INK4a) protein and the presence of functional RB in many cell lines. In this study we show that p16(INK4a) is expressed in cervical cancer cell lines in which the RB gene, Rb, is not functional, either as a consequence of Rb mutation or expression of the human papillomavirus E7 protein. We also demonstrate that p16(INK4a) levels are increased in primary cells in which RB has been inactivated by DNA tumor virus proteins. Given the role of RB in controlling E2F transcription factor activity, we investigated the role of E2F in controlling p16(INK4a) expression. We found that E2F1 overexpression leads to an inhibition of cyclin D1-dependent kinase activity and induces the expression of a p16-related transcript. We conclude that the accumulation of G(1) cyclin-dependent kinase activity during normal G(1) progression leads to E2F accumulation through the inactivation of RB, and that this then leads to the induction of cyclin kinase inhibitor activity and a shutdown of G(1) kinase activity. C1 USN,NCI,MED ONCOL BRANCH,BETHESDA,MD 20889. UNIFORMED SERV UNIV HLTH SCI,BETHESDA,MD 20814. DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT GENET,DURHAM,NC 27710. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RI kaye, frederic/E-2437-2011 NR 59 TC 232 Z9 241 U1 0 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4350 EP 4354 DI 10.1073/pnas.93.9.4350 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700114 PM 8633069 ER PT J AU Tellier, R Bukh, J Emerson, SU Purcell, RH AF Tellier, R Bukh, J Emerson, SU Purcell, RH TI Amplification of the full-length hepatitis A virus genome by long reverse transcription-PCR and transcription of infectious RNA directly from the amplicon SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; A VIRUS; POLIOVIRUS RNA; CELL-CULTURE; POLYMERASE; CDNA; DNA; INHIBITION; TEMPLATES; INVITRO AB The genetic study of RNA viruses is greatly facilitated by the availability of infectious cDNA clones. However, their construction has often been difficult. While exploring ways to simplify the construction of infectious clones, we have successfully modified and applied the newly described technique of ''long PCR'' to the synthesis of a full-length DNA amplicon from the RNA of a cytopathogenic mutant (HM 175/24a) of the hepatitis A virus (HAV). Primers were synthesized to match the two extremities of the HAV genome. The antisense primer, homologous to the 3' end, was used in both the reverse transcription (RT) and the PCR steps. With these primers we reproducibly obtained a full-length amplicon of approximate to 7.5 kb. Further, since we engineered a T7 promoter in the sense primer, RNA could be transcribed directly from the amplicon with T7 RNA polymerase. Following transfection of cultured fetal rhesus kidney cells with the transcription mixture containing both the HAV cDNA and the transcribed RNA, replicating HAV was detected by immunofluorescence microscopy and, following passage to other cell cultures, by focus formation. The recovered virus displayed the cytopathic effect and targe plaque phenotype typical of the original virus; this result highlights the fidelity of the modified long reverse transcription-PCR procedure and demonstrates the potential of this method for providing cDNAs of viral genomes and simplifying the construction of infectious clones. C1 NIAID,INFECT DIS LAB,HEPATITIS VIRUSES SECT,NIH,BETHESDA,MD 20892. NR 30 TC 32 Z9 36 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4370 EP 4373 DI 10.1073/pnas.93.9.4370 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700118 PM 8633073 ER PT J AU Graziosi, C Gantt, KR Vaccarezza, M Demarest, JF Daucher, M Saag, MS Shaw, GM Quinn, TC Cohen, OJ Welbon, CC Pantaleo, G Fauci, AS AF Graziosi, C Gantt, KR Vaccarezza, M Demarest, JF Daucher, M Saag, MS Shaw, GM Quinn, TC Cohen, OJ Welbon, CC Pantaleo, G Fauci, AS TI Kinetics of cytokine expression during primary human immunodeficiency virus type 1 infection SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID PRIMARY HIV-1 INFECTION; STEP AB In the present study, se have determined the kinetics of constitutive expression of a panel of cytokines [interleukin (IL) 2, IL-4, IL-6, IL-10, interferon gamma (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha)] in sequential peripheral blood mononuclear cell samples from nine individuals with primary human immunodeficiency virus infection. Expression of IL-2 and IL-4 was barely detected in peripheral blood mononuclear cells. However, substantial levels of IL-2 expression were found in mononuclear cells isolated from lymph node. Expression of IL-6 was detected in only three of nine patients, and IL-6 expression was observed when transition from the acute to the chronic phase had already occurred. Expression of IL-10 and TNF-alpha was consistently observed in all patients tested, and levels of both cytokines were either stable or progressively increased over time. Similar to IL-10 and TNF-alpha, IFN-gamma expression was detected in all patients; however, in five of nine patients, IFN-gamma expression peaked very early during primary infection. The early peak in IFN-gamma expression coincided with oligoclonal expansions of CD8(+) T cells in five of six patients, and CD8(+) T cells mostly accounted for the expression of this cytokine. These results indicate that high levels of expression of proinflammatory cytokines are associated with primary infection and that the cytokine response during this phase of infection is strongly influenced by oligoclonal expansions of CD8(+) T cells. C1 UNIV ALABAMA,BIRMINGHAM,AL 35294. RP Graziosi, C (reprint author), NIAID,IMMUNOREGULAT LAB,NIH,BLDG 10,BETHESDA,MD 20892, USA. RI Quinn, Thomas/A-2494-2010; Pantaleo, Giuseppe/K-6163-2016; OI VACCAREZZA, Mauro/0000-0003-3060-318X NR 32 TC 107 Z9 107 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4386 EP 4391 DI 10.1073/pnas.93.9.4386 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700121 PM 8633076 ER PT J AU Arya, SK Gallo, RC AF Arya, SK Gallo, RC TI Human immunodeficiency virus (HIV) type 2-mediated inhibition of HIV type 1: A new approach to gene therapy of HIV infection SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AIDS; transcriptional downmodulation; mutational analysis; chimeric genomes; retroviral vectors ID TRANS-ACTIVATOR GENE; TRANSACTIVATOR TAT; HTLV-III; CD4; TRANSMISSION; ORGANIZATION; RETROVIRUSES; REPLICATION; EXPRESSION; ISOLATE AB Human immunodeficiency virus (HIV) type 2, the second AIDS-associated human retrovirus, differs from HIV-1 in its natural history, infectivity, and pathogenicity, as Kell as in details of its genomic structure and molecular behavior. We report here that HIV-2 inhibits the replication of HIV-I at the molecular level. This inhibition was selective, dose-dependent, and nonreciprocal. The closely related simian immunodeficiency provirus also inhibited HIV-1. The selectivity of inhibition was shown by the observation that HIV-2 did not significantly downmodulate the expression of the unrelated murine leukemia virus; neither did the murine leukemia virus markedly affect HIV-1 or HIV-2 expression. Moreover, while HIV-2 potently inhibited HIV-I, the reverse did not happen, thus identifying Set another and remarkable difference between HIV-I and HIV-2. Mutational analysis of the HIV-1, genome suggested that the inhibition follows a complex pathway, possibly involving multiple genes and redundant mechanisms. Introduction of inactivating mutations into the structural and regulatory/accessory genes did not render the HIV-2 provirus ineffective. Some of the HIV-2 gene defects, such as that of tat and rev genes, were phenotypically transcomplemented by HIV-1. The HIV-2 proviruses,vith deletions in the putative packaging signal and defective for virus replication were effective in inducing the suppressive phenotype. Though the exact mechanism remains to be defined, the inhibition appeared to be mainly due to an intracellular molecular event because it could not be explained solely on the basis of cell surface receptor mediated interference. The results support the notion that the inhibition likely occurred at the level of viral RNA, possibly involving competition between viral RNAs for some transcriptional factor essential for virus replication. Induction of a cytokine is another possibility. These findings might be relevant to the clinical-epidemiological data suggesting that infection with HIV-2 may offer some protection against HIV-1 infection. RP Arya, SK (reprint author), NCI,TUMOR CELL BIOL LAB,NIH,BLDG 37,ROOM 6C24,37 CONVENT DR,BETHESDA,MD 20892, USA. NR 32 TC 32 Z9 33 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 30 PY 1996 VL 93 IS 9 BP 4486 EP 4491 DI 10.1073/pnas.93.9.4486 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UK557 UT WOS:A1996UK55700139 PM 8633095 ER PT J AU Guerrini, R Capasso, A Sorrentino, L Anacardio, R Bryant, SD Lazarus, LH Attila, M Salvadori, S AF Guerrini, R Capasso, A Sorrentino, L Anacardio, R Bryant, SD Lazarus, LH Attila, M Salvadori, S TI Opioid receptor selectivity alteration by single residue replacement: Synthesis and activity profile of [Dmt]deltorphin B SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE antinociception; bioassay; deltorphin; opioid receptor; peptide synthesis ID MORPHINE ANTINOCICEPTION; HIGH-AFFINITY; MU-RECEPTOR; DEXAMETHASONE; ANALGESIA; PEPTIDE; MICE; AGONIST; DESIGN AB The single amino acid replacement of 2',6'-dimethyl-L-tyrosine in deltorphin B (H-Dmt-D-Ala-Phe-Glu-Val-Val-Gly-NH2) yielded high affinity for mu- and delta-binding sites. [Dmt(1)]Deltorphin B lacks activity at kappa-opioid binding sites. Bioactivity in vitro with guinea-pig ileum confirmed that [Dmt(1)]deltorphin B interacted with mu-opioid receptors by reducing electrically induced contractions in a naloxone-reversible manner and was 150-fold more potent than morphine and comparable to [D-Ala(2),NMePhe(4),Gly-ol(5)]enkephalin (DAGO). The inhibition of spontaneous contractions of rabbit jejunum provided evidence for delta-opioid receptor interaction. Analgesia (hot plate and tail flick tests) revealed that [Dmt(1)]deltorphin B was 180- to 200-fold more potent than morphine. Pretreatment with naloxone, naltrindole or H-Dmt-Tic-Ala-OH (a highly selective delta-opioid receptor antagonist) prevented [Dmt(1)]deltorphin B antinociception. Thus, [Dmt(1)]deltorphin B exhibited remarkably high dual affinity and bioactivity toward delta- and mu-opioid receptors. C1 UNIV FERRARA,DIPARTIMENTO SCI FARMACEUT,I-44100 FERRARA,ITALY. UNIV SALERNO,SCH PHARM,I-84084 SALERNO,ITALY. UNIV NAPLES FEDERICO II,DEPT EXPTL PHARMACOL,I-80131 NAPLES,ITALY. DOMPE SPA,I-67100 LAQUILA,ITALY. NIEHS,RES TRIANGLE PK,NC 27709. HELSINKI UNIV,DEPT PHARMACOL,DIV PHARMACOL & TOXICOL,SF-00014 HELSINKI,FINLAND. OI Guerrini, Remo/0000-0002-7619-0918 NR 29 TC 43 Z9 44 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD APR 29 PY 1996 VL 302 IS 1-3 BP 37 EP 42 DI 10.1016/0014-2999(96)00067-2 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UQ817 UT WOS:A1996UQ81700006 PM 8790989 ER PT J AU VonLubitz, DKJE Beenhakker, M Lin, RCS Carter, MF Paul, IA Bischofberger, N Jacobson, KA AF VonLubitz, DKJE Beenhakker, M Lin, RCS Carter, MF Paul, IA Bischofberger, N Jacobson, KA TI Reduction of postischemic brain damage and memory deficits following treatment with the selective adenosine A(1) receptor a agonist SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE cerebral ischemia; adenosine receptor; spatial memory; water maze; (gerbil) ID FOREBRAIN ISCHEMIA; CEREBRAL-ISCHEMIA; HIPPOCAMPUS; GERBILS; RATS AB Agonists of adenosine A(1) receptors have been frequently proposed as candidate, for clinical development in treatment of cerebral ischemia and stroke, Numerous experimental studies have shown that pre- and postischemic administration of these drugs results in a very significant reduction of postischemic brain damage. However, only a few studies determined the impact of cerebral ischemia and drug treatment on postischemic recovery of spatial memory. Thr present paper demonstrates that preischemic i.p. administration of adenosine amine congener(ADAC) at 100 mu g/kg in gerbils results in a significant (P < 0.05) reduction of postischemic mortality and hippocampal, cortical and striatal morbidity. Postischemic Morris' water maze tests show that preischemic treatment with ADAC also leads to a very significant (P < 0.001) reduction of postischemic spatial memory loss, Our results indicate feasibility of further consideration of adenosine A(1) receptor agonists as a clinically applicable acute treatment of brain ischemia. Recent development of neuroprotective adenosine A(1) receptor agonists that are free of cardiovascular side effects supports such development. C1 MED COLL PENN & HAHNEMANN UNIV, DEPT ANAT & NEUROBIOL, PHILADELPHIA, PA 19102 USA. UNIV MISSISSIPPI, MED CTR, LAB NEUROBEHAV PHARMACOL & IMMUNOL, JACKSON, MS 39216 USA. GILEAD SCI INC, FOSTER CITY, CA 94404 USA. RP VonLubitz, DKJE (reprint author), NIDDK, MOLEC RECOGNIT SECT, BLDG 8, ROOM 1A15, BETHESDA, MD 20892 USA. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z99 DK999999, Z01 DK031117-20] NR 34 TC 35 Z9 36 U1 0 U2 1 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 APR 29 PY 1996 VL 302 IS 1-3 BP 43 EP 48 DI 10.1016/0014-2999(96)00101-X PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UQ817 UT WOS:A1996UQ81700007 PM 8790990 ER PT J AU Wynn, TA Sher, A AF Wynn, TA Sher, A TI Hot Papers - Immunology Parasitology - Endogenous interleukin 12 (IL-12) regulates granuloma formation induced by eggs of Schistosoma mansoni and exogenous IL-12 both inhibits and prophylactically immunizes against egg pathology by T.A. Wynn, I. Eltoum, I.P. Oswald, A.W. Cheever, A. Sher - Comments SO SCIENTIST LA English DT Editorial Material AB Hot papers: Parasitologist Thomas A. Wynn and Alan Sher report on use of interleukin 12 to regulate granuloma formation induced by eggs of Schistosoma mansoni. RP Wynn, TA (reprint author), NIAID,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Wynn, Thomas/C-2797-2011 NR 3 TC 0 Z9 0 U1 0 U2 0 PU SCIENTIST INC PI PHILADELPHIA PA 3600 MARKET ST SUITE 450, PHILADELPHIA, PA 19104 SN 0890-3670 J9 SCIENTIST JI Scientist PD APR 29 PY 1996 VL 10 IS 9 BP 14 EP 14 PG 1 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA UH057 UT WOS:A1996UH05700013 ER PT J AU Bigbee, WL Jensen, RH Veidebaum, T Tekkel, M Rahu, M Stengrevics, A Kesminiene, A Kurtinaitis, J Auvinen, A Hakulinen, T Servomaa, E Rytomaa, T Obrams, GI Boice, JD AF Bigbee, WL Jensen, RH Veidebaum, T Tekkel, M Rahu, M Stengrevics, A Kesminiene, A Kurtinaitis, J Auvinen, A Hakulinen, T Servomaa, E Rytomaa, T Obrams, GI Boice, JD TI Glycophorin A biodosimetry in Chernobyl cleanup workers from the Baltic countries SO BRITISH MEDICAL JOURNAL LA English DT Article C1 UNIV PITTSBURGH,INST CANC,MOL CARCINOGENESIS PROGRAM,PITTSBURGH,PA 15238. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. INST EXPT & CLIN MED,DEPT EPIDEMIOL & BIOSTAT,TALLINN,ESTONIA. LATVIA CANC REGISTRY,RIGA,LATVIA. LITHUANIAN CHERNOBYL MED CTR,VILNIUS,LITHUANIA. LITHUANIAN CANC REGISTRY,MITHUANIAN ONCOL CTR,VILNIUS,LITHUANIA. FINNISH CTR RADIAT & NUCL SAFETY,HELSINKI,FINLAND. FINNISH CANC REGISTRY,SF-00170 HELSINKI,FINLAND. NCI,EXTRAMURAL PROGRAMS BRANCH,BETHESDA,MD 20892. NCI,RADIAT EPIDEMIOL BRANCH,BETHESDA,MD 20892. RP Bigbee, WL (reprint author), UNIV PITTSBURGH,CTR ENVIRONM & OCCUPAT HLTH & TOXICOL,GRAD SCH PUBL HLTH,PITTSBURGH,PA 15238, USA. RI Rahu, Mati/A-9981-2008; OI Auvinen, Anssi/0000-0003-1125-4818 FU NCI NIH HHS [N01-CP-50520] NR 5 TC 23 Z9 23 U1 1 U2 4 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0959-8138 J9 BRIT MED J JI Br. Med. J. PD APR 27 PY 1996 VL 312 IS 7038 BP 1078 EP 1079 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA UH816 UT WOS:A1996UH81600027 PM 8616416 ER PT J AU Dong, ZG Xu, RH Kim, JB Zhan, SN Ma, WY Colburn, NH Kung, HF AF Dong, ZG Xu, RH Kim, JB Zhan, SN Ma, WY Colburn, NH Kung, HF TI AP-1/jun is required for early Xenopus development and mediates mesoderm induction by fibroblast growth factor but not by activin SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR; JUN; RECEPTOR; FOS; EXPRESSION; EMBRYOS; FGF; ONCOGENE; ENHANCER; KINASE AB In Xenopus, normal mesoderm formation depends on signaling through the fibroblast growth factor (FGF) tyrosine kinase receptor. An important signaling pathway from receptor tyrosine kinases involves Ras/Raf/MAP kinase, However, the downstream pathway that occurs in the nucleus to finally trigger gene expression for mesoderm formation remains unknown, We report here that a high level of activator protein-1 (AP-1)-dependent transcriptional activity is detected during the early development of Xenopus embryos. Injection of a dominant negative mutant jun (DNM-jun or TAM67) RNA into the two-cell stage embryos inhibited endogenous AP-1 activity and blocked normal embryonic development with severe posterior truncation in tadpoles. The inhibition of AP-1 activity and the phenotypic change induced by TAM67 was rescued by co-injection of wild-type c-jun RNA, but not by the control beta-galactosidase RNA. The FGF-stimulated mesoderm induction was markedly inhibited in animal cap explants from the embryos injected with TAM67. Activin induction of mesoderm, on the other hand, was normal in the embryos injected with TAM67 RNA. These findings suggest that AP-1 mediates FGF, but not activin, receptor signaling during mesoderm induction and the AP-1/Jun is a key signaling molecule in the development of posterior structure. C1 SAIC,LAB BIOCHEM PHYSIOL,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,NIH,CELL BIOL SECT,DIV BASIC SCI,FREDERICK,MD 21702. RP Dong, ZG (reprint author), UNIV MINNESOTA,HORMEL INST,801 16TH AVE NE,AUSTIN,MN 55912, USA. RI Xu, Ren-He/M-3125-2016 NR 38 TC 42 Z9 42 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 26 PY 1996 VL 271 IS 17 BP 9942 EP 9946 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG257 UT WOS:A1996UG25700015 PM 8626631 ER PT J AU Sackett, DL KoskKosicka, D AF Sackett, DL KoskKosicka, D TI The active species of plasma membrane Ca2+-ATPase are a dimer and a monomer-calmodulin complex SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ERYTHROCYTE CA-2+-ATPASE; MOLECULAR-CLONING; OLIGOMERIZATION; FLUORESCENCE; ASSOCIATION; ACTIVATION; ISOFORMS; BINDING; ATPASE; STATES AB The purified plasma membrane Ca2+-ATPase is fully activated through the enzyme concentration-dependent self-association at physiologically relevant Ca2+ concentrations (Kosk-Kosicka, D., and Bzdega, T. (1988) J. Biol. Chem. 263, 18184-18189; Kosk-Kosicka, D., Bzdega, T., and Wawrzynow, A. (1989) J. Biol. Chem. 264, 19495-19499). We have previously shown that the Ca2+-ATPase activity of the oligomeric enzyme is independent of calmodulin, in contrast to another active enzyme species, a presumable monomer, that is activated by calmodulin binding, Presently, we have succeeded in determining the molecular mass of the two active enzyme species by equilibrium ultracentrifugation. For the calmodulin dependent species, the molecular mass is 170 +/- 30 kDa, which is consistent with predominantly monomeric Ca2+-ATPase with bound calmodulin, The molecular mass of calmodulin-independent oligomers is 260 +/- 34 kDa, indicating that they are dimers, Results of experiments performed under different calcium and potassium concentrations and in the presence of dextran that causes molecular crowding verify a strict Ca2+ requirement of the dimerization process, We conclude that the active species of the Ca2+-ATPase are a monomer-calmodulin complex and a dimer. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21287. NIDDK,NIH,BIOCHEM PHARMACOL LAB,BETHESDA,MD 20892. FU NIGMS NIH HHS [GM 447130] NR 24 TC 21 Z9 22 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 26 PY 1996 VL 271 IS 17 BP 9987 EP 9991 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG257 UT WOS:A1996UG25700022 PM 8626638 ER PT J AU Frederikse, PH Garland, D Zigler, JS Piatigorsky, J AF Frederikse, PH Garland, D Zigler, JS Piatigorsky, J TI Oxidative stress increases production of beta-amyloid precursor protein and beta-amyloid (A beta) in mammalian lenses, and A beta has toxic effects on lens epithelial cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ALPHA-B-CRYSTALLIN; ALZHEIMERS-DISEASE; PHASE-SEPARATION; CATARACT FORMATION; ACTIVATION; MOUSE; OPACIFICATION; FIBROBLASTS; DEPOSITION; MECHANISM AB Many amyloid diseases are characterized by protein aggregations linked to oxidative stress. Such diseases including those of the brain, muscle, and blood vessels exhibit plaques containing beta-amyloid (A beta). Here we demonstrate that Alzheimer's precursor protein (beta APP) and A beta are present at low levels in normal lenses and increase in intact cultured monkey lenses treated with H2O2 or UV radiation (known cataractogenic agents), and with phorbol 12-myristate 13-acetate. AP-1 factor binding, shown by others to up-regulate beta APP expression, increased in the monkey lenses treated with H2O2, UV radiation, or phorbol 12-myristate 13-acetate and paralleled the increase in beta APP expression. Rat lenses exposed to oxidative stress showed increased beta APP in the anterior epithelium and cortex. Incubation of cultured rabbit lens N/N1003A epithelial cells with A beta induced inclusions and vacuoles and was cytotoxic. A beta cross-reacting protein was readily detected in the cortex of a cataractous human lens. Our data show that beta APP and A beta increase in mammalian lenses as part of a response to H2O2 or UV radiation and suggest that they may contribute to the mechanism by which oxidative damage leads to lens opacification. C1 NEI,LAB MECHANISMS OCULAR DIS,NIH,BETHESDA,MD 20892. RP Frederikse, PH (reprint author), NEI,MOLEC & DEV BIOL LAB,NIH,6 CTR DR,MSC 2730,BETHESDA,MD 20892, USA. NR 79 TC 138 Z9 143 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 26 PY 1996 VL 271 IS 17 BP 10169 EP 10174 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG257 UT WOS:A1996UG25700050 PM 8626578 ER PT J AU Hu, ZZ Zhuang, L Dufau, ML AF Hu, ZZ Zhuang, L Dufau, ML TI Multiple and tissue-specific promoter control of gonadal and non-gonadal prolactin receptor gene expression SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RAT OVARY; CELLS AB Prolactin receptors (PRLRs) are widely expressed, and multiple mRNA transcripts encoding PRLRs are present in prolactin target tissues. The molecular basis for the control of the PRLR gene expression is currently unknown. Analyses of the 5'-untranslated regions of PRLR mRNAs expressed in gonadal and non-gonadal tissues and their genomic organization revealed three alternative first exons designated as El(1), El(2), and El(3). Each of these exons is alternatively spliced to a common noncoding exon (exon 2, nucleotides -115 to -56) that precedes the third exon containing the translation initiation codon. Alternative utilization of exons El(1), El(2), and El(3), as well as alternative splicing of exon 2, generates multiple 5'-untranslated regions in PRLR transcripts. These alternative first exons (El(1), El(2), and El(3)) were found to be utilized in a tissue-specific manner in vivo. El(1) is predominantly expressed in the ovary, El(2) is specifically expressed in the liver, and El(3) is expressed as a predominant form in the Leydig cell and as a minor form in the ovary and liver. Genomic 5'-flanking regions containing the three putative PRLR gene promoters (PI, PII, and PIII) that initiate the transcription of El(1), El(2), and El(3), respectively, were identified. El(1) was found to initiate from a single site at -549, El(2) from multiple sites at -405, -461, and -506, and El(3) from two major sites at -340 and -351. These findings indicate that multiple promoters control transcription of the PRLR gene and provide a molecular basis for the differential regulation of PRLR expression in diverse tissues. C1 NICHHD,SECT MOL ENDOCRINOL,ENDOCRINOL & REPROD RES BRANCH,NIH,BETHESDA,MD 20892. NR 19 TC 54 Z9 54 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 26 PY 1996 VL 271 IS 17 BP 10242 EP 10246 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG257 UT WOS:A1996UG25700062 PM 8626590 ER PT J AU Choi, D Stables, JP Kohn, H AF Choi, D Stables, JP Kohn, H TI Synthesis and anticonvulsant activities of N-benzyl-2-acetamidopropionamide derivatives SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID AMINO-ACIDS; SERIES AB Studies have demonstrated that 2-substituted N-benzyl-2-acetamidoacetamides (2) are potent anticonvulsants. A recent investigation has led to the hypothesis that an important structural feature in 2 for maximal anticonvulsant activity is the placement of a small, substituted heteroatom moiety one atom from the C(2) sate. This paper validates this hypothesis. Twelve derivatives of N-benzyl-2-acetamidopropionamide have been prepared in which six different heteroatom substituents (chloro, bromo, iodo, oxygen, nitrogen, and sulfur) were incorporated at the C(3) site. Highly potent activities were observed for the two oxygen-substituted derivatives, N-benzyl-2-acetamido-3-methoxypropionamide (18) and N-benzyl-2-acetamido-3-ethoxypropionamide (19). The ED(50) values in mice following intraperitoneal (ip) dosing for the maximal electroschock-induced seizure test for 18 and 19 were 8.3 and 17.3 mg/kg, respectively. These values compared favorably to the ED(50) value found for phenytoin (ED(50) = 6.5 mg/kg). Comparable activities were observed for 18 and 19 upon oral (po) administration to rats (18, ED(50) = 3.9 mg/kg; 19, ED(50) = 19 mg/kg; phenytoin, ED(50) = 23 mg/kg). Evaluation of the individual stereoisomers for 18 demonstrated that the principal anticonvulsant activity resided in the (R)-stereoisomer. The ED(50) value for (R)-18 was 4.5 mg/kg, and the ED(50) for (S)-18 exceeded 100 mg/kg. This difference in activity for the two stereochemical isomers surpassed comparable values for other members within this class of compounds. The protective indices (PI = TD50/ED(50)) (where TD50 represents a neurotoxic dose impairing rotorod performance) for (R)-18 in mice (ip) and in rats (po) were 6.0 and >130, respectively. C1 UNIV HOUSTON, DEPT CHEM, HOUSTON, TX 77204 USA. NINCDS, EPILEPSY BRANCH, NIH, BETHESDA, MD 20892 USA. NR 33 TC 96 Z9 102 U1 3 U2 9 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 26 PY 1996 VL 39 IS 9 BP 1907 EP 1916 DI 10.1021/jm9508705 PG 10 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA UJ112 UT WOS:A1996UJ11200019 PM 8627614 ER PT J AU Liu, RY Hu, RJ Zhang, PW Skolnick, P Cook, JM AF Liu, RY Hu, RJ Zhang, PW Skolnick, P Cook, JM TI Synthesis and pharmacological properties of novel 8-substituted imidazobenzodiazepines: High-affinity, selective probes for alpha 5-containing GABA(A) receptors SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID BENZODIAZEPINE RECEPTORS; A RECEPTORS; PHARMACOPHORE; SUBUNIT; BRAIN; ANXIETY; CLONING; SITE AB The synthesis and pharmacological properties of imidazobenzodiazepines with both high affinity and selectivity for alpha 5-containing GABAA receptors are described. Four of these compounds (5, 6, 8, and 9) inhibited [H-3]flunitrazepam binding to recombinant alpha 5 beta 2 gamma 2 GABA(A) receptors with IC50 values between similar to 0.4 and 5 nM. These compounds were greater than or equal to 24-75-fold more selective for recombinant receptors containing alpha 5 subunits compared to other, ''diazepam-sensitive'' GABA(A) receptors containing either alpha 1, alpha 2, or alpha 3 subunits. Imidazobenzodiazepine 9 (used as the prototypical alpha 5 selective ligand) inhibited [H-3]flunitrazepam binding to hippocampal membranes with high- and low-affinity components (IC50 0.6 +/- 0.2 and 85.6 +/- 13.1 nM, respectively), representing similar to 16% and similar to 84% of the receptor pool. Inhibition of [H-3]flunitrazepam binding to cerebellar membranes with imidazobenzodiazepine 9 was best fitted to a single population of sites with an IC50 of 79.8 +/- 18.3 nM. These imidazobenzodiazepines behaved as GABA negative ligands in recombinant GABA(A) receptors expressed in Xenopus oocytes and were convulsant in mice after parenteral administration. The relative potencies of flumazenil and zolpidem in blocking convulsions induced by 9 and DMCM, respectively, indicated that occupation of alpha 5-containing GABA(A) receptors substantially contributed to the convulsant properties of acetylene analog 9. These 8-substituted imidazobenzodiazepines (5, 6, 8, and 9) should prove useful in examining the physiological roles of GABA(A) receptors bearing an alpha 5 subunit and may also lead to the development of novel, subtype selective therapeutic agents. C1 UNIV WISCONSIN, DEPT CHEM, MILWAUKEE, WI 53201 USA. NIDDK, NEUROSCI LAB, NIH, BETHESDA, MD 20892 USA. NR 37 TC 72 Z9 73 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 26 PY 1996 VL 39 IS 9 BP 1928 EP 1934 DI 10.1021/jm950887n PG 7 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA UJ112 UT WOS:A1996UJ11200022 PM 8627617 ER PT J AU Kiser, R Makovsky, S Terpening, SJ Laing, N Clanton, DJ AF Kiser, R Makovsky, S Terpening, SJ Laing, N Clanton, DJ TI Assessment of a cytoprotection assay for the discovery and evaluation of anti-human immunodeficiency virus compounds utilizing a genetically-impaired virus SO JOURNAL OF VIROLOGICAL METHODS LA English DT Article DE human immunodeficiency virus; cytoprotection assay; antiviral activity ID REVERSE-TRANSCRIPTASE; NATURAL-PRODUCTS; TYPE-1; HIV-1; RETROVIRUSES; REPLICATION; INHIBITORS; MECHANISM; AIDS AB A biologically contained cytoprotection assay was developed to screen inhibitors of the human immunodeficiency virus without the need for high level containment or practices. The virus used has multiple point mutations that have destroyed its ability to produce both Rev and Tat, proteins essential for virus replication in vitro. The original cell line employed (CEM-SSTART) contains a genetic construct that allows for the continuous expression of both Rev and Tat, and a subclone (1A2) was developed that provides for maximum acute cytopathic effect. The National Cancer Institute's AIDS drug screening assay was used to rest known drugs with both HIVIIIB virus in the T4 lymphocytic cell line CEM-SS and mutant virus in the 1A2 subclone. This cell-based assay uses the tetrazolium salt, XTT, as an indicator of cellular metabolism after the cells have been infected with virus. The results of extensive testing have shown that the assay using mutant virus is comparable to the current NCI AIDS drug screen. After 42 days in 1A2 or CEM-SS cell culture, the virus or the integrated genome did not revert to wild-type, and the virus produced in 1A2 cells was unable to replicate in PBMCs. Mutant viral stocks were devoid of wild-type virus as determined by a PCR assay that would have found 60-600 copies of mutant RNA. These materials, which are now available to the scientific community (NIH AIDS Research and Reference Reagent Program), should be useful tools to screen and test compounds for potential inhibition of HIV in laboratories not equipped to maintain and use wild-type infectious virus. C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,AIDS DRUG SCREENING & DEV LAB,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-56000] NR 29 TC 26 Z9 26 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-0934 J9 J VIROL METHODS JI J. Virol. Methods PD APR 26 PY 1996 VL 58 IS 1-2 BP 99 EP 109 DI 10.1016/0166-0934(95)01998-7 PG 11 WC Biochemical Research Methods; Biotechnology & Applied Microbiology; Virology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Virology GA UQ674 UT WOS:A1996UQ67400011 PM 8783155 ER PT J AU Mellon, I Rajpal, DK Koi, M Boland, CR Champe, GN AF Mellon, I Rajpal, DK Koi, M Boland, CR Champe, GN TI Transcription-coupled repair deficiency and mutations in human mismatch repair genes SO SCIENCE LA English DT Article ID NONPOLYPOSIS COLORECTAL-CANCER; NUCLEOTIDE EXCISION REPAIR; ESCHERICHIA-COLI; COCKAYNE-SYNDROME; DNA DAMAGE; PREFERENTIAL REPAIR; SELECTIVE REPAIR; STRAND; YEAST; MECHANISM AB Deficiencies in mismatch repair have been linked to a common cancer predisposition syndrome in humans, hereditary nonpolyposis colorectal cancer (HNPCC), and a subset of sporadic cancers. Here, several mismatch repair-deficient tumor cell lines and HNPCC-derived lymphoblastoid cell lines were found to be deficient in an additional DNA repair process termed transcription-coupled repair (TCR). The TCR defect was corrected in a mutant cell line whose mismatch repair deficiency had been corrected by chromosome transfer. Thus, the connection between excision repair and mismatch repair previously described in Escherichia coli extends to humans. These results imply that deficiencies in TCR and exposure to carcinogens present in the environment may contribute to the etiology of tumors associated with genetic defects in mismatch repair. C1 NIEHS,MOLEC CARCINOGENESIS LAB,RES TRIANGLE PK,NC 27706. UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. RP Mellon, I (reprint author), UNIV KENTUCKY,MARKEY CANC CTR,TOXICOL PROGRAM,DEPT PATHOL,LEXINGTON,KY 40536, USA. RI Koi, Minoru/C-3489-2012; Koi, Minoru/G-9197-2014 FU NIGMS NIH HHS [GM45535-03] NR 46 TC 238 Z9 238 U1 0 U2 3 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 26 PY 1996 VL 272 IS 5261 BP 557 EP 560 DI 10.1126/science.272.5261.557 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UG826 UT WOS:A1996UG82600047 PM 8614807 ER PT J AU Oh, CK Metcalfe, DD AF Oh, CK Metcalfe, DD TI Activated lymphocytes induce promoter activity of the TCA3 gene in mast cells following cell-to-cell contact SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID DE-GRANULATION; HYPERSENSITIVITY; INVITRO AB Aggregates of mast cells and lymphocytes have been found in inflamed tissues suggesting that lymphocytes may have the ability to activate mast cells through cell-to-cell contact. To examine this hypothesis, murine mast cells were transfected with a T cell activation gene-3 (TCA3)-chloramphenicol acetyl transferase (CAT) construct, and these cells co-cultured with murine EL-4 (T), CH12.LX (B), WEHI-3 (myelomonocytic) or 3T3(fibroblast) cell lines. Go-culture of activated EL-4 or CH12.LX cells, but not WEHI-3 or 3T3 cells, with transfected mast cells induced a 5 to 7 fold increase in CAT expression which was dependent on the lymphocyte to mast cell ratio. Supernatants from activated EL-4 or CH12.LX cells did not induce CAT expression in transfected mast cells. These data demonstrate that activated lymphocytes have the ability to induce the promoter of the TCA3 gene in mast cells through a mechanism requiring cell-to-cell contact, and suggest the possibility that activated lymphocytes may effect other biologic processes in mast cells as well through such heterotypic activation. (C) 1996 Academic Press, Inc. RP Oh, CK (reprint author), NIAID,LAB ALLERG DIS,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 11 TC 11 Z9 11 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 APR 25 PY 1996 VL 221 IS 3 BP 510 EP 514 DI 10.1006/bbrc.1996.0627 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA UH698 UT WOS:A1996UH69800004 PM 8629992 ER PT J AU McDermott, JB Cvekl, A Piatigorsky, J AF McDermott, JB Cvekl, A Piatigorsky, J TI Lens-specific expression of a chicken beta A3/Al-crystallin promoter fragment in transgenic mice SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID A-CRYSTALLIN PROMOTER; CHLORAMPHENICOL ACETYLTRANSFERASE; GENE-EXPRESSION; ELEMENTS; PROTEINS; SITES; CELLS AB beta A3/A1-crystallin is one of the major refractive proteins of the chicken eye lens. Previously we showed that a fragment from -382 to +22 bp of the beta A3/A1-crystallin gene functions as a promoter in transfected lens cells. Here we show by use of the bacterial chloramphenicol acetyltransferase reporter gene that the -143/+22 fragment is sufficient for lens-specific promoter activity in transgenic mice. DNase I footprinting shows that lens nuclear proteins protect several regions within the minimal promoter fragment. (C) 1996 Academic Press, Inc. C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. RI Cvekl, Ales/B-2427-2013 NR 28 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 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 25 PY 1996 VL 221 IS 3 BP 559 EP 564 DI 10.1006/bbrc.1996.0635 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA UH698 UT WOS:A1996UH69800012 PM 8630000 ER PT J AU Haxby, JV AF Haxby, JV TI Memory - Medial temporal lobe imaging SO NATURE LA English DT Editorial Material RP Haxby, JV (reprint author), NIMH,SECT FUNCT BRAIN IMAGING,BETHESDA,MD 20892, USA. NR 10 TC 16 Z9 16 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 25 PY 1996 VL 380 IS 6576 BP 669 EP 670 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UG827 UT WOS:A1996UG82700024 PM 8614458 ER PT J AU Peat, TS Frank, EG McDonald, JP Levine, AS Woodgate, R Hendrickson, WA AF Peat, TS Frank, EG McDonald, JP Levine, AS Woodgate, R Hendrickson, WA TI Structure of the UmuD' protein and its regulation in response to DNA damage SO NATURE LA English DT Article ID RECA-MEDIATED CLEAVAGE; MUTANT LEXA PROTEINS; ANOMALOUS DIFFRACTION; DEPENDENT CLEAVAGE; ESCHERICHIA-COLI; SOS MUTAGENESIS; AUTODIGESTION; POLYMERASE AB FOR life to be sustained, mistakes in DNA repair must be tolerated when damage obscures the genetic information. In bacteria such as Escherichia coli, DNA damage elicits the well regulated 'SOS response' (reviewed in ref. 1). For the extreme case of damage that cannot be repaired by conventional enzymes, there are proteins that allow the replication of DNA through such lesions, but with a reduction in the fidelity of replication(2). Essential proteins in this mutagenic process are RecA, DNA polymerase III, UmuD, UmuD' and UmuC (umu: UV mutagenesis)(1-3). Regulation of this response involves a RecA-mediated self-cleavage of UmuD to produce UmuD'. To understand this system in more detail, we have determined the crystal structure of the E. coli UmuD' mutagenesis protein at 2.5 Angstrom resolution. Globular heads folded in an unusual beta-structure associate to form molecular dimers, and extended amino-terminal tails associate to produce crystallized filaments. The structure provides insight into the mechanism of the self-cleavage reaction that UmuD-like proteins undergo as part of the global SOS response(4-8). C1 COLUMBIA UNIV,DEPT BIOCHEM & MOLEC BIOPHYS,NEW YORK,NY 10032. COLUMBIA UNIV,HOWARD HUGHES MED INST,NEW YORK,NY 10032. NICHHD,SECT DNA REPLICAT REPAIR & MUTAGENESIS,NIH,BETHESDA,MD 20892. RI Peat, Thomas/F-9817-2010 OI Peat, Thomas/0000-0002-6488-0831 NR 30 TC 134 Z9 136 U1 0 U2 3 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 25 PY 1996 VL 380 IS 6576 BP 727 EP 730 DI 10.1038/380727a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UG827 UT WOS:A1996UG82700056 PM 8614470 ER PT J AU Hoofnagle, J McKenzie, R Straus, S AF Hoofnagle, J McKenzie, R Straus, S TI Severe toxicity of fialuridine (FIAU) - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP Hoofnagle, J (reprint author), NIH,BETHESDA,MD 20892, USA. NR 4 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 APR 25 PY 1996 VL 334 IS 17 BP 1137 EP 1137 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA UG457 UT WOS:A1996UG45700021 ER PT J AU Fiore, MC Wetter, DW Bailey, WC Bennett, G Cohen, SJ Dorfman, SF Goldstein, MG Gritz, ER Hasselblad, V Henningfield, JE Heyman, RB Holbrook, J Husten, C Jaen, CR Kohler, C Kottke, TE Lando, HA Manley, M Mecklenburg, R Melvin, C Mullen, PD Nett, LM Piasecki, TM Robinson, L Rothstein, D Schriger, DL Stitzer, ML Stachenko, S Tommasello, A Villejo, L Wewers, ME Baker, TB AF Fiore, MC Wetter, DW Bailey, WC Bennett, G Cohen, SJ Dorfman, SF Goldstein, MG Gritz, ER Hasselblad, V Henningfield, JE Heyman, RB Holbrook, J Husten, C Jaen, CR Kohler, C Kottke, TE Lando, HA Manley, M Mecklenburg, R Melvin, C Mullen, PD Nett, LM Piasecki, TM Robinson, L Rothstein, D Schriger, DL Stitzer, ML Stachenko, S Tommasello, A Villejo, L Wewers, ME Baker, TB TI The Agency for Health Care Policy and Research Smoking Cessation Clinical Practice Guideline SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID WEIGHT-GAIN; NICOTINE REPLACEMENT; CIGARETTE-SMOKING; UNITED-STATES; QUIT SMOKING; BODY-WEIGHT; WOMEN; INTERVENTION; POPULATION; PHYSICIAN AB Objective.-To summarize the Smoking Cessation Clinical Practice Guideline that provides recommendations for 3 groups of professionals: primary care clinicians, smoking cessation specialists, and health care administrators, insurers, and purchasers. Participants.-An independent panel of scientists, clinicians, consumers, and methodologists selected by the US Agency for Health Care Policy and Research. Evidence.-English-language, peer-reviewed literature published between 1975 and 1994 that addresses the assessment and treatment of tobacco dependence, nicotine addiction, and clinical practice. Consensus Process.-Four panel meetings were held over 2 years to evaluate meta-analytic and other results, to synthesize the results, and to develop recommendations. The Guideline was repeatedly reviewed and revised. Conclusions.-The panel recommendations address 3 audiences, Major recommendations for primary care clinicians are to use officewide systems to identify smokers, treat every smoker with a cessation or motivational intervention, offer nicotine replacement except in special circumstances, and schedule follow-up contact to occur after cessation, Major recommendations to smoking cessation specialists are to use multiple individual or group counseling sessions lasting at least 20 minutes each with sessions spanning multiple weeks, offer nicotine replacement, and provide problem-solving and social support counseling, Major recommendations for health care administrators, insurers, and purchasers are that tobacco-user identification systems be used in all clinics and that smoking cessation treatment be supported through staff education and training, dedicated staff, changes in hospital policies, and the provision of reimbursement for tobacco-dependence treatment. C1 UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX. UNIV ALABAMA,BIRMINGHAM,AL. NHLBI,NIH,BETHESDA,MD 20892. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC. BROWN UNIV,SCH MED,MIRIAM HOSP,PROVIDENCE,RI 02912. DUKE UNIV,DURHAM,NC. NIDA,NIH,BALTIMORE,MD. AMER ACAD PEDIAT,CINCINNATI,OH. UNIV UTAH,SCH MED,SALT LAKE CITY,UT. CTR DIS CONTROL & PREVENT,OFF SMOKING & HLTH,ATLANTA,GA 30341. SUNY BUFFALO,CTR URBAN RES PRIMARY CARE,BUFFALO,NY. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NCI,NIH,ROCKVILLE,MD. NCI,POTOMAC,MD. UNIV TEXAS,CTR HLTH PROMOT RES & DEV,HOUSTON,TX. CTR HLTH SCI STUDIES,PSL HLTH ONE,DENVER,CO. UNIV WISCONSIN,SCH MED,CTR TOBACCO RES & INTERVENT,MADISON,WI. OFF DIS PREVENT & HLTH PROMOT,WASHINGTON,DC. DEPT PUBL HLTH,WASHINGTON,DC. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. JOHNS HOPKINS UNIV HOSP,BAYVIEW MED CTR,BALTIMORE,MD. HLTH CANADA,OTTAWA,ON,CANADA. UNIV MARYLAND,SCH PHARM,BALTIMORE,MD 21201. OHIO STATE UNIV,COLL NURSING,COLUMBUS,OH 43210. RP Fiore, MC (reprint author), UNIV WISCONSIN,SCH MED,CTR TOBACCO RES & INTERVENT,1300 UNIV AVE,MADISON,WI 53706, USA. NR 68 TC 222 Z9 222 U1 2 U2 3 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD APR 24 PY 1996 VL 275 IS 16 BP 1270 EP 1280 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA UF478 UT WOS:A1996UF47800032 ER PT J AU Lee, H Darden, TA Pedersen, LG AF Lee, H Darden, TA Pedersen, LG TI An ab initio quantum mechanical model for the catalytic mechanism of HIV-1 protease SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID IMMUNODEFICIENCY VIRUS-1 PROTEASE; ASPARTIC PROTEINASES; CHEMICAL MECHANISM; ELUCIDATE DETAILS; ACTIVE-SITE; INHIBITOR; RESONANCE; BARRIERS AB The catalytic mechanism of the HIV-1 protease (HIV-PR) is studied through ab initio theoretical model calculations. This model consists of a formate/formic acid pair, a structurally important water molecule, and a formamide molecule. The proposed catalytic mechanism is composed of five steps, two of which are transition states separated by a third step (an intermediate state). The remaining two steps are related to product release. The overall forward hydrolysis reaction barrier is approximately 22 kcal/mol, with a reverse hydrolysis barrier of approximately 34 kcal/mol at the RHF/6-31G* level. The second transition state is related to a nucleophilic attack of the water molecule on the carbon atom of the substrate scissile bond, and is essential for the collapse of the substrate. That the transition state structures of HIV-PR have not been identified makes a theoretical study of this kind particularly valuable for understanding the HIV-PR mechanism. C1 UNIV N CAROLINA,DEPT CHEM,CHAPEL HILL,NC 27599. RP Lee, H (reprint author), NIEHS,LAB QUANTITAT & COMPUTAT BIOL,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI Pedersen, Lee/E-3405-2013 OI Pedersen, Lee/0000-0003-1262-9861 NR 33 TC 32 Z9 33 U1 0 U2 2 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 APR 24 PY 1996 VL 118 IS 16 BP 3946 EP 3950 DI 10.1021/ja9513188 PG 5 WC Chemistry, Multidisciplinary SC Chemistry GA UG695 UT WOS:A1996UG69500019 ER PT J AU Siebler, T Kiess, W Linder, B Kessler, U Schwarz, HP Nissley, SP AF Siebler, T Kiess, W Linder, B Kessler, U Schwarz, HP Nissley, SP TI Pertussis toxin sensitive G-proteins are not involved in the mitogenic signaling pathway of insulin-like growth factor-I in normal rat kidney epithelial (NRKE) cells SO REGULATORY PEPTIDES LA English DT Article DE IGF-I; IGF-II; G-protein; signal transduction; pertussis toxin; NRKE cell ID MANNOSE 6-PHOSPHATE RECEPTOR; PHENOTYPIC TRANSFORMATION; GENE-EXPRESSION; CALCIUM INFLUX; IGF BINDING; TRANSDUCTION AB There is controversy as to whether or not a pertussis toxin sensitive G-protein is involved in the signaling pathway of insulin-like growth factor-I. We have used normal rat kidney epithelial (NRKE) cells to ask whether or not a pertussis toxin sensitive G-protein was involved in IGF-I stimulated DNA synthesis. NRKE cells express both IGF-I and IGF-II/M6P receptors and respond to IGF-I with increased thymidine incorporation into DNA. Under many circumstances incubation of cells/cell membranes with GTP analogues will inhibit binding of ligands that are linked to a G-protein-receptor pathway, However, when NRKE membrane preparations were incubated with I-125-IGF-I or I-125-IGF-II in the presence or absence of GTP gamma S, ATP and GTP, binding of the radioligands was not affected by the GTP-analogue. IGF-I and factors from serum of hypophysectomized rats (HRS) stimulated [H-3]thymidine incorporation into DNA of NRKE cells. Under serum-free conditions in the presence of EGF (2 ng/ml) and PDGF (1 ng/ml) pertussis toxin over a wide range of doses had no effect upon IGF-I stimulated [H-3]thymidine incorporation into DNA of NRKE cells, In addition, PT at a dose of 100 ng/ml had no effect on IGF-I (0.2-50 ng/ml) stimulated DNA synthesis of NRKE cells, However, PT at doses of 5, 50, 500, 5000 and 50 000 ng/ml was capable to ADP-ribosylate a 40 kDa protein in NRKE cell plasma membrane preparations corresponding to known PT-sensitive G-proteins. We conclude, that (1) PT-sensitive G-proteins and both IGF-I and IGF-II/M6P receptors are present in NRKE cell plasma membrane preparations, and most importantly, that (2) PT-sensitive G-proteins are not involved in the mitogenic signaling pathway of IGF-I in NRKE cells. C1 UNIV MUNICH,CHILDRENS HOSP,D-80336 MUNICH,GERMANY. NCI,NIH,METAB BRANCH,BETHESDA,MD 20892. NR 26 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-0115 J9 REGUL PEPTIDES JI Regul. Pept. PD APR 23 PY 1996 VL 62 IS 2-3 BP 65 EP 71 DI 10.1016/0167-0115(95)00159-X PG 7 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA UR476 UT WOS:A1996UR47600001 PM 8795068 ER PT J AU Matsumoto, RR Bowen, WD Walker, JM Patrick, SL Zambon, AC Vo, VN Truong, DD DeCosta, BR Rice, KC AF Matsumoto, RR Bowen, WD Walker, JM Patrick, SL Zambon, AC Vo, VN Truong, DD DeCosta, BR Rice, KC TI Dissociation of the motor effects of (+)-pentazocine from binding to sigma(1) sites SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE opiate; (+)-pentazocine; sigma site; red nucleus; substantia nigra ID GUINEA-PIG BRAIN; RAT-BRAIN; AUTORADIOGRAPHIC LOCALIZATION; H-3 (+)-PENTAZOCINE; LOW-AFFINITY; RECEPTORS; FOREBRAIN; SUGGEST; POTENT; LIGAND AB Radioligand binding and behavioral studies were conducted to determine whether a relationship existed between the motor effects produced by (+)-pentazocine and its binding to sigma sites. Scatchard analyses revealed decreased [H-3](+)-pentazocine binding in middle aged rats (5-6 months old) compared to young adult rats (2-3 months old). However, there was no difference between the extent of circling behavior or dystonia produced by microinjection of (+)-pentazocine into the substantia nigra or red nucleus in the older animals compared to the young adult rats. There was also a significant decrease in [H-3](+)-pentazocine binding in rats chronically treated with haloperidol. Again, however, despite the reduction in [H-3](+)-pentazocine binding, there was no difference between the extent of dystonia produced by unilateral intrarubral microinjection of (+)-pentazocine into animals chronically treated with haloperidol vs. saline. The postural changes produced by (+)-pentazocine could not be attenuated with coadministration of the putative sigma receptor antagonist BD1047 (N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(dimethylamino)ethylamine), or the opiate receptor antagonist naloxone. However, the (+)-opiate, (+)-nordihydrocodeinone, partially attenuated the postural effects of(+)-pentazocine, despite its very low affinity for sigma(1), sigma(2) or opiate receptors. Taken together with previous studies, the results suggest that [H-3](+)-pentazocine is a potent and selective probe for sigma(1) binding sites, but the in vivo effects of (+)-pentazocine cannot be fully attributed to actions through these sites. Some of the in vivo effects of (+)-pentazocine appear to involve other binding sites that are not detected under the conditions normally used in in vitro assays. C1 BROWN UNIV,DEPT PSYCHOL,PROVIDENCE,RI 02912. BROWN UNIV,DEPT PSYCHOL,PROVIDENCE,RI 02912. BROWN UNIV,DIV BIOL & MED,BIOCHEM SECT,PROVIDENCE,RI 02912. NIDDK,MED CHEM LAB,NIH,BETHESDA,MD 20892. RP Matsumoto, RR (reprint author), UNIV CALIF IRVINE,DEPT NEUROL,154 MED SURGE 1,IRVINE,CA 92717, USA. FU NIDA NIH HHS [DA04988]; NIMH NIH HHS [MH50564] NR 37 TC 13 Z9 13 U1 0 U2 1 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 APR 22 PY 1996 VL 301 IS 1-3 BP 31 EP 40 DI 10.1016/0014-2999(96)00008-8 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UP247 UT WOS:A1996UP24700005 PM 8773444 ER PT J AU Yoshiji, H Gomez, DE Thorgeirsson, UP AF Yoshiji, H Gomez, DE Thorgeirsson, UP TI Enhanced RNA expression of tissue inhibitor of metalloproteinases-1 (TIMP-1) in human breast cancer SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID ERYTHROID-POTENTIATING ACTIVITY; LOCALIZATION; INVASION; PROTEINASES; LYMPHOMAS; MEMBER; FAMILY; CELLS AB Tissue inhibitor of metalloproteinases-1 (TIMP-1) is known to have at least 2 distinct types of activity, i.e., as a regulator of collagenolytic activity, and erythroid potentiating activity (ERA). In this study, we examined the expression of TIMP-1 in human mammary carcinomas, non-malignant breast tissues and benign breast tumors. A total of 53 samples were subjected to Northern-blot analysis, including 23 of primary breast cancer, 26 of non-malignant breast tissues, and 4 of benign tumors. Of the 53 samples, 10 were paired malignant and non-malignant breast-tissue samples from the same patient. TIMP-1 RNA expression was significantly higher in the malignant tumor tissues than in the non-malignant counterpart. Similar differences were observed in the level of TIMP-1 protein expression in the paired breast samples examined. Moreover, breast-cancer cell lines secreted larger amounts of TIMP-1 in vitro than non-neoplastic breast epithelial lines. The up-regulation of TIMP-1 expression in breast cancer may suggest that TIMP-1 has an additional role to that of metalloproteinase inhibitor. (C) 1996 Wiley-Liss, Inc.* C1 NCI,DIV BASIC SCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,TUMOR BIOL & CARCINOGENESIS SECT,BETHESDA,MD 20892. OI Gomez, Daniel E/0000-0002-8629-0787 NR 22 TC 60 Z9 60 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 22 PY 1996 VL 69 IS 2 BP 131 EP 134 DI 10.1002/(SICI)1097-0215(19960422)69:2<131::AID-IJC11>3.0.CO;2-C PG 4 WC Oncology SC Oncology GA UH135 UT WOS:A1996UH13500011 PM 8608981 ER PT J AU Pahor, M Guralnik, JM Furberg, CD Carbonin, P Havlik, RJ AF Pahor, M Guralnik, JM Furberg, CD Carbonin, P Havlik, RJ TI Risk of gastrointestinal haemorrhage with calcium antagonists in hypertensive persons over 67 years old SO LANCET LA English DT Article ID PLATELET-AGGREGATION; CLINICAL-TRIAL; DIHYDROPYRIDINES; HEMORRHAGE AB Background Calcium antagonists are used frequently in management of hypertension, In addition to their cardiovascular effects, these drugs inhibit platelet aggregation. Therefore we examined whether the use of calcium antagonists was associated with an increased risk of gastrointestinal haemorrhage (GIH). Methods A prospective cohort study was conducted from 1985 through 1992 on 1636 hypertensive persons aged greater than or equal to 68 years living in three communities. The participants were taking beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, or calcium antagonists; those taking combinations of these drugs were excluded, The incidence of GIH was assessed by surveying hospital discharge deaths. Age, gender, disability, arterial pressure, other drugs, and comorbid conditions were examined as confounders. Findings Compared with beta-blockers (4819 person-years, 65 events), after adjustment for confounders the relative risk for GIH associated with ACE inhibitors (772 person-years, 13 events) was 1 . 23 (95% CI 0 . 66-2 . 28) and with calcium antagonists (1510 person-years, 42 events) it was 1 . 86 (1 . 22-2 . 82). The risks for verapamil, diltiazem, and nifedipine did not differ significantly. The results were unchanged when the analyses were restricted to severe events (GIH in conjunction with blood transfusion or death). Interpretation Calcium antagonists were associated with an increased risk of GIH in this population. Therefore caution is needed in prescription of these agents to old patients who have other risk factors for gastrointestinal bleeding. C1 NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,WINSTON SALEM,NC 27103. RP Pahor, M (reprint author), UNIV CATTOLICA SACRO CUORE,IST MED INTERNA & GERIATRIA,LARGO F VITO 1,I-00168 ROME,ITALY. NR 30 TC 203 Z9 205 U1 0 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 20 PY 1996 VL 347 IS 9008 BP 1061 EP 1065 DI 10.1016/S0140-6736(96)90276-7 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA UG042 UT WOS:A1996UG04200009 PM 8602055 ER PT J AU Quintero, RA Romero, R Dzieczkowski, J Mammen, E Evans, MI AF Quintero, RA Romero, R Dzieczkowski, J Mammen, E Evans, MI TI Sealing of ruptured amniotic membranes with intra-amniotic platelet-cryoprecipitate plug SO LANCET LA English DT Letter ID PREMATURE RUPTURE C1 HUTZEL HOSP,DEPT PATHOL & MED,DETROIT,MI 48201. HUTZEL HOSP,DEPT PHYSIOL,DETROIT,MI 48201. NICHHD,PERINATOL BRANCH,BETHESDA,MD 20892. RP Quintero, RA (reprint author), WAYNE STATE UNIV,HUTZEL HOSP,DEPT OBSTET & GYNECOL,FETAL ENDOSCOPY PROGRAM,DETROIT,MI 48201, USA. NR 5 TC 42 Z9 44 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 APR 20 PY 1996 VL 347 IS 9008 BP 1117 EP 1117 DI 10.1016/S0140-6736(96)90316-5 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA UG042 UT WOS:A1996UG04200056 PM 8602087 ER PT J AU Dunnick, JK Elwell, MR Haseman, JK AF Dunnick, JK Elwell, MR Haseman, JK TI Decreased incidence of spontaneous mammary gland neoplasms in female F344 rats treated with amphetamine, methylphenidate, or codeine SO CANCER LETTERS LA English DT Article DE mammary gland neoplasm; amphetamine; methylphenidate; codeine; F344 rats ID SPONTANEOUS TUMORS; EXPRESSION; RECEPTOR; MICE; GROWTH AB Three drugs that affect the neuroendocrine system (amphetamine, methylphenidate, and codeine) caused decreases in body weights and in the incidence of spontaneously occurring mammary gland neoplasms in the female F344/N rat in 2-year carcinogenicity studies. Using a mathematical model that relates body weight changes to the incidence of mammary gland neoplasms, we find that the decrease in mammary gland tumors seen in female rats cannot be fully explained by body weight decreases relative to control animals. Further, the observed decreases in body weight in treated female rats were not a function of differences in feed consumption between treated and control groups. These pharmaceuticals are thought to affect the biologic system through interaction with membrane receptors. This interaction and/or subsequent cell signaling events may play a role in the observed decrease in spontaneously occurring mammary gland neoplasms in the female rat treated with amphetamine, methylphenidate, or codeine. RP Dunnick, JK (reprint author), NIEHS,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 28 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD APR 19 PY 1996 VL 102 IS 1-2 BP 77 EP 83 DI 10.1016/0304-3835(96)04168-7 PG 7 WC Oncology SC Oncology GA UB974 UT WOS:A1996UB97400011 PM 8603383 ER PT J AU Craigie, R AF Craigie, R TI Quality control in Mu DNA transposition SO CELL LA English DT Review ID RECOMBINATION RP Craigie, R (reprint author), NIDDK,NIH,BLDG 5,ROOM 301,BETHESDA,MD 20892, USA. NR 9 TC 17 Z9 17 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 APR 19 PY 1996 VL 85 IS 2 BP 137 EP 140 DI 10.1016/S0092-8674(00)81089-2 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UG255 UT WOS:A1996UG25500001 PM 8612265 ER PT J AU Savilahti, H Mizuuchi, K AF Savilahti, H Mizuuchi, K TI Mu transpositional recombination: Donor DNA cleavage and strand transfer in trans by the Mu transposase SO CELL LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; POLYNUCLEOTIDYL TRANSFER; INTEGRASE PROTEIN; INVITRO PROCEEDS; BACTERIOPHAGE-MU; SITE; MECHANISM; DOMAINS; IDENTIFICATION; COMPLEX AB Central to the Mu transpositional recombination are the two chemical steps; donor DNA cleavage and strand transfer. These reactions occur within the Mu transpososome that contains two Mu DNA end segments bound to a tetramer of MuA, the transposase. To investigate which MuA-monomer catalyzes which chemical reaction, we made transpososomes containing wild-type and active site mutant MuA. By preloading the MuA variants onto Mu end DNA fragments of different length prior to transpososome assembly, we could track the catalysis by MuA bound to each Mu end segment. The donor DNA end that underwent the chemical reaction was identified. Both the donor DNA cleavage and strand transfer were catalyzed in trans by the MuA monomers bound to the partner Mu end. This arrangement explains why the transpososome assembly is a prerequisite for the chemical steps. C1 NIDDKD, MOLEC BIOL LAB, NIH, BETHESDA, MD 20892 USA. NR 59 TC 80 Z9 81 U1 1 U2 2 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0092-8674 EI 1097-4172 J9 CELL JI Cell PD APR 19 PY 1996 VL 85 IS 2 BP 271 EP 280 DI 10.1016/S0092-8674(00)81103-4 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UG255 UT WOS:A1996UG25500015 PM 8612279 ER PT J AU BeitnerJohnson, D Blakesley, VA ShenOrr, Z Jimenez, M Stannard, B Wang, LM Pierce, J LeRoith, D AF BeitnerJohnson, D Blakesley, VA ShenOrr, Z Jimenez, M Stannard, B Wang, LM Pierce, J LeRoith, D TI The proto-oncogene product c-Crk associates with insulin receptor substrate-1 and 4PS - Modulation by insulin growth factor-1 (IGF) and enhanced IGF-1 signaling SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PHOSPHATIDYLINOSITOL 3'-KINASE; HEMATOPOIETIC-CELLS; IRS-1; SH2; PHOSPHORYLATION; PROTEINS; ELEMENTS; PATHWAYS; DOMAINS; BINDING AB The Crk proto-oncogene product is an SH2 and SH3 domain-containing adaptor protein which we have previously shown to become rapidly tyrosine phosphorylated in response to stimulation with insulin-like growth factor I (IGF-I) in NIH-3T3 cells, In order to further characterize the role of Crk in the IGF-I signaling pathway, NIH-3T3 and 293 cells were stably transfected with an expression vector containing the Crk cDNA, The various resultant 3T3-Crk clones expressed Crk at approximately 2-15-fold higher levels than parental 3T3 cells, In 3T3-Crk cells, Crk immunoreactivity was detected in insulin receptor substrate-1 (IRS-1) immunoprecipitates, Stimulation with IGF-I resulted in a dissociation of Crk protein from IRS-1, In contrast, the association of the related adaptor protein Grb2 with IRS-1 was enhanced by IGF-I stimulation. Similar results were obtained in stably transfected 293-Crk cells, which express both IRS-I and the IRS-1-related signaling protein 4PS. In these cells, IRS-1 and 4PS both associated with Crk, and this association was also decreased by IGF-I treatment, whereas the association of Grb2 with IRS-1 and 4PS was enhanced by IGF-I. Overexpression of Crk also enhanced IGF-I-induced mitogenesis of NIH-3T3 cells, as measured by [H-3]thymidine incorporation. The levels of IGF-I-induced mitogenesis were proportional to the level of Crk expression, These results suggest that Crk is a positive effector of IGF-I signaling, and may mediate its effects via interaction with IRS-1 and/or 4PS. C1 NIDDK,DIABET BRANCH,CELLULAR & MOLEC BIOL LAB,BETHESDA,MD 20892. NCI,NIH,BETHESDA,MD 20892. NR 31 TC 69 Z9 70 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 19 PY 1996 VL 271 IS 16 BP 9287 EP 9290 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG044 UT WOS:A1996UG04400021 PM 8621590 ER PT J AU Oakley, RH Sar, M Cidlowski, JA AF Oakley, RH Sar, M Cidlowski, JA TI The human glucocorticoid receptor beta isoform - Expression, biochemical properties, and putative function SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HORMONE-BINDING DOMAIN; HUMAN PROGESTERONE-RECEPTOR; 3' UNTRANSLATED REGION; GENE-EXPRESSION; DNA-BINDING; MULTIPLE; TRANSCRIPTION; LOCALIZATION; ACTIVATION; RESISTANCE AB Alternative splicing of the human glucocorticoid receptor (hGR) primary transcript produces two receptor isoforms, hGR alpha and hGR beta, which differ at their carboxyl termini. The hGR alpha isoform conveys endocrine information to target tissues by altering patterns of gene expression in a hormone-dependent fashion, In contrast to hGR alpha, very little is known about the hGR beta splice variant. Using hGR alpha- and hGR beta-specific riboprobes on human multiple tissue Northern blots, we show that the hGR beta message has a widespread tissue distribution. We also prove by reverse transcriptase-polymerase chain reaction that the alternative splicing event underlying the formation of the hGR beta message occurs in these tissues. Because the hGR beta protein differs from hGR alpha at the extreme COOH terminus, we investigated several of the biochemical properties of hGR beta expressed in transfected cells. hGR beta does not bind the glucocorticoid agonist dexamethasone nor the glucocorticoid antagonist RU38486 in vivo. Moreover, in contrast to hGR beta, hGR beta is located primarily in the nucleus of transfected cells independent of hormone administration, Finally, in the absence of hGR alpha, hGR beta is transcriptionally inactive on a glucocorticoid-responsive enhancer. However, when both isoforms are expressed in the same cell, hGR beta inhibits the hormone-induced, hGR alpha-mediated stimulation of gene expression. Thus, hGR beta potentially functions as a dominant negative inhibitor of hGR alpha activity. C1 NIEHS,LAB INTEGRAT BIOL,RES TRIANGLE PK,NC 27709. UNIV N CAROLINA,DEPT PHYSIOL,CHAPEL HILL,NC 27599. NR 53 TC 379 Z9 410 U1 0 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 19 PY 1996 VL 271 IS 16 BP 9550 EP 9559 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG044 UT WOS:A1996UG04400059 PM 8621628 ER PT J AU vanLeeuwen, JEM Kearse, KP AF vanLeeuwen, JEM Kearse, KP TI Calnexin associates exclusively with individual CD3 delta and T cell antigen receptor (TCR) alpha proteins containing incompletely trimmed glycans that are not assembled into multisubunit TCR complexes SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ENDOPLASMIC-RETICULUM; MONOCLONAL-ANTIBODY; TRANSGENIC MICE; DELTA-CHAIN; IDENTIFICATION; CHAPERONE; IP90 AB Most T lymphocytes express on their surfaces an oligomeric protein complex consisting of clonotypic alpha beta polypeptides associated with invariant CD3-gamma delta epsilon and zeta chains, designated the T cell antigen receptor (TCR) complex. Assembly and intracellular transport of nascent TCR proteins is believed to be assisted by their interaction with the molecular chaperone calnexin, which for certain molecules functions as a lectin for monoglucosylated glycans. However, as most of our knowledge about calnexin-TCR protein associations has been obtained under conditions of limited TCR assembly, the role of calnexin in the formation of nascent TCR complexes is unclear, Here, we studied the role of glucose (Glc) trimming and calnexin association in the oligomerization of TCR alpha and CD3 delta glycoproteins in murine splenic T lymphocytes, a model cell type for efficient assembly of complete TCR complexes. We show that removal of Glc residues from both CD3 delta proteins and TCR alpha proteins occurred prior to their association with any other TCR components and that calnexin specifically interacted with unassembled TCR alpha and CD3 delta proteins containing incompletely trimmed oligosaccharides, Interestingly, we found that removal of Glc residues from glycan chains was necessary for efficient association of calnexin with TCR alpha glycoproteins but not with CD3 delta glycoproteins. These studies define Glc trimming and calnexin association as initial molecular events in the translation of CD3 delta and TCR alpha proteins, occurring coincident with or immediately after their translocation into the endoplasmic reticulum and preceding the ordered pairing of TCR chains, In addition, these data document that calnexin assembly with CD36 and TCR alpha glycoproteins involves both glycan-dependent and glycan-independent mechanisms. C1 NCI,EXPTL IMMUNOL BRANCH,NIH,BETHESDA,MD 20892. RI van Leeuwen, Jeroen/G-3555-2010 NR 33 TC 41 Z9 41 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 19 PY 1996 VL 271 IS 16 BP 9660 EP 9665 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG044 UT WOS:A1996UG04400072 PM 8621641 ER PT J AU ODea, MH Tamura, JK Gellert, M AF ODea, MH Tamura, JK Gellert, M TI Mutations in the B subunit of Escherichia coli DNA gyrase that affect ATP-dependent reactions SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID N-TERMINAL FRAGMENT; NUCLEOTIDE BINDING; TOPOISOMERASE-II; NALIDIXIC-ACID; BASE-PAIRS; PROTEIN; MECHANISM; ENERGY; ENZYME; SITE AB We have previously reported specific labeling of Escherichia coli DNA gyrase by the ATP affinity analog pyridoxal 5'-diphospho-5'adenosine (PLP-AMP), which resulted in inhibition of ATP-dependent reactions,The analog was found to be covalently bound at Lys(103) and Lys(110) on the gyrase B subunit (Tamura, J, K,, and Gellert, M, (1990) J, Biol, Chem, 265, 21342-21349), In this study, the importance of these two lysine residues is examined by site-directed mutagenesis. Substitutions of Lys(103) result in the loss of ATP-dependent functions, These mutants are unable to supercoil DNA, to hydrolyze ATP, or to bind a nonhydrolysable ATP analog, 5'-adenylyl-beta, gamma-imidodiphosphate (ADPNP), The ATP-independent functions of gyrase, such as relaxation of negatively supercoiled DNA and oxolinic acid induced cleavage of double-stranded DNA, are unaffected by these mutations, suggesting that the mutant B subunits are assembling correctly with the A subunits, Gyrase with substitutions of Lys(110) retains all activities, However, the affinity of ATP is decreased, The DNA supercoiling activity of gyrase A(2)B(2) tetramers reconstituted with varying ratios of inactive mutant and wild-type gyrase B subunits is consistent with a mechanism of DNA supercoiling that requires the interdependent activity of both B subunits in ATP binding and hydrolysis. C1 NIDDK,MOLEC BIOL LAB,NIH,BETHESDA,MD 20892. NR 35 TC 28 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 APR 19 PY 1996 VL 271 IS 16 BP 9723 EP 9729 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG044 UT WOS:A1996UG04400081 PM 8621650 ER PT J AU Semmes, OJ Barrett, JF Dang, CV Jeang, KT AF Semmes, OJ Barrett, JF Dang, CV Jeang, KT TI Human T-cell leukemia virus type I Tax masks c-myc function through a cAMP-dependent pathway SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LONG TERMINAL REPEAT; PRIMARY HUMAN-LYMPHOCYTES; RECEPTOR GENE-EXPRESSION; PROTEIN-KINASE-A; HTLV-I; CYCLIC-AMP; DNA-BINDING; NEOPLASTIC TRANSFORMATION; TRANSCRIPTION FACTOR; ACTIVATES TRANSCRIPTION AB Human T-cell leukemia virus type I Tax is a pleiotropic gene regulator that functions through CREB/ATF- and NF-kappa B-mediated pathways, In most contexts, Tax is a potent gene activator. Here, we describe an unexpected finding of Myc repression by Tax. In cells that overexpress human T-cell leukemia virus type I Tax, the detection of c-Myc protein in the nucleus by a monoclonal antibody was masked. Tax prevented immunological visualization of a Myc epitope contained within amino acids 45-104, resulting in interference with Myc function in transcription and in anchorage-independent cell growth, Tax did not affect steady-state protein levels since detection of c-Myc with other antibodies was unperturbed. Four observations suggest that this Tax-Myc interaction is mediated through CREB/ATF signal transduction. 1) Tax point mutants, selectively defective for activation of CREB/ATF but not NF-kappa B, failed to mask. c-Myc; 2) masking of Myc was abolished when Tax-expressing cells were treated with protein kinase inhibitor H-9; 3) Tax-specific shielding of Myc is absent in cells (B1R) that are genetically defective for cAMP signaling; and 4) forskolin treatment of cells mimicked Tax in masking the Myc epitope, Considered collectively, these findings suggest a regulation of Myc function at the level of localized protein conformation. C1 NIAID,MOL VIROL SECT,MOLEC MICROBIOL LAB,NIH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV HEMATOL,BALTIMORE,MD 21205. RI Jeang, Kuan-Teh/A-2424-2008 NR 95 TC 24 Z9 24 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 19 PY 1996 VL 271 IS 16 BP 9730 EP 9738 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG044 UT WOS:A1996UG04400082 PM 8621651 ER PT J AU Honkakoski, P Moore, R Gynther, J Negishi, M AF Honkakoski, P Moore, R Gynther, J Negishi, M TI Characterization of phenobarbital-inducible mouse Cyp2b10 gene transcription in primary hepatocytes SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ADULT-RAT HEPATOCYTES; TISSUE-SPECIFIC EXPRESSION; CYTOCHROME-P-450 GENE; GROWTH-HORMONE; MESSENGER-RNA; TESTOSTERONE 16-ALPHA-HYDROXYLASE; CHROMOSOME LOCALIZATION; INVITRO TRANSCRIPTION; GLYCOPROTEIN GENE; LIVER-MICROSOMES AB The mouse phenobarbital (PB)-inducible Cyp2b10 gene promoter has been isolated and sequenced, and control of its expression has been characterized, The 1405-base pair (bp) Cyp2b10 promoter sequence is 83% identical to the corresponding region from the rat CYP2B2 gene. In addition to the lack of CA repeats, differences include insertion of 42 base pairs (-123/-82 bp) into the middle of a consensus sequence to the so called ''Barbie box.'' In this report, we have developed a primary mouse hepatocyte culture system in which endogenous 2B10 mRNA as well as Cyp2b10-driven CAT activity were induced by PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP), but not by the 3-chloro derivative of TCPOBOP, Deletion analysis of the Cyp2b10 promoter identified a basal transcription element at -64/-34 bp and a negative element at -971/-775 bp. Sequences contained within the -1404/-971 bp region are responsible for the induced CAT activity. DNase I protection and gel shift assays detected five major protein binding sites within the -1404/-971 bp fragment, one of which shared high sequence identity with a portion of a regulatory element in CYP2B2 gene (Trottier, E,, Belzil, A., Stoltz, C,, and Anderson, A, (1995) Gene 158, 263-268). Our results indicate that sequences important for PB-induced transcription of Cyp2b10 gene are located in the distal promoter. C1 NIEHS,PHARMACOGENET SECT,REPROD & DEV TOXICOL LAB,NIH,RES TRIANGLE PK,NC 27709. UNIV KUOPIO,DEPT PHARMACEUT CHEM,SF-70211 KUOPIO,FINLAND. OI Honkakoski, Paavo/0000-0002-4332-3577 NR 68 TC 103 Z9 104 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 19 PY 1996 VL 271 IS 16 BP 9746 EP 9753 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG044 UT WOS:A1996UG04400084 PM 8621653 ER PT J AU Boix, E Wu, YN Vasandani, VM Saxena, SK Ardelt, W Ladner, J Youle, RJ AF Boix, E Wu, YN Vasandani, VM Saxena, SK Ardelt, W Ladner, J Youle, RJ TI Role of the N terminus in RNase a homologues: Differences in catalytic activity, ribonuclease inhibitor interaction and cytotoxicity SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE human pancreatic RNase; Rana pipiens RNase; pyroglutamic acid; ribonuclease inhibitor; cytotoxicity ID BOVINE PANCREATIC RIBONUCLEASE; HUMAN PLACENTAL RIBONUCLEASE; AMINO-ACID-SEQUENCE; C-PEPTIDE HELIX; SEMINAL RIBONUCLEASE; LIVER RIBONUCLEASE; RANA-CATESBEIANA; P-30 PROTEIN; ANGIOGENIN; SUPERFAMILY AB A number of biochemical properties differ dramatically among homologues within the pancreatic ribonuclease superfamily Human pancreatic ribonuclease (hRNase) has high enzyme activity, extreme sensitivity to ribonuclease inhibitor (RI) and is non-toxic, whereas a homologous RNase from frog eggs, called onconase, has much lower enzyme activity, is not sensitive to RI and is cytotoxic to cancer cell lines and animals. To explore the structural basis of these differences among members in the RNase family we synthesized genes for onconase, hRNase, a mutant onconase (K9Q) and onconase-hRNase N-terminal hybrids and expressed the proteins in Escherichia coli with final yields of 10 to 50 mg per liter of culture after purification. A recombinant version of onconase with an N-terminal methionine instead of the native pyroglutamyl residue had decreased cytotoxicity and enzyme activity. Cleavage of the recombinant onconase Met-1 residue, and cyclization of the Gln1 residue to reform the pyroglutamyl N terminus, reconstituted cytotoxicity and enzyme activity Thus a unique role of the pyroglutamyl residue in the active site of amphibian RNases is indicated. Replacement of one to nine residues of onconase with the homologous residues of hRNase increased the enzymatic activity against most of the substrates tested with a simultaneous shift in the enzyme specificity from high preference for poly(U) to slight preference for poly(C). Cytotoxicity of the chimera decreased, dissociating cytotoxicity from enzymatic activity: The molecular basis for the low binding affinity of onconase for RI has been examined experimentally with the recombinant RNases and by fitting onconase and RNase A structures to the coordinates from the recently published RNase A-RI complex. (C) 1996 Academic Press Limited C1 NINCDS,BIOCHEM SECT,SURG NEUROL BRANCH,NIH,BETHESDA,MD 20892. ALFACELL CORP,BLOOMFIELD,NJ 07003. UNIV MARYLAND,MARYLAND BIOTECHNOL INST,CTR ADV RES BIOTECHNOL,ROCKVILLE,MD 20850. NATL INST STAND & TECHNOL,ROCKVILLE,MD 20850. RI Boix, Ester/B-9038-2012; OI Boix, Ester/0000-0003-1790-2142; Saxena, Shailendra K/0000-0003-2856-4185 NR 77 TC 164 Z9 168 U1 2 U2 6 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD APR 19 PY 1996 VL 257 IS 5 BP 992 EP 1007 DI 10.1006/jmbi.1996.0218 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UG014 UT WOS:A1996UG01400010 PM 8632481 ER PT J AU Vondrasek, J Wlodawer, A AF Vondrasek, J Wlodawer, A TI New database SO SCIENCE LA English DT Letter RP Vondrasek, J (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MACROMOLEC STRUCT LAB,FREDERICK,MD 21702, USA. RI Vondrasek, JIri/A-4244-2008 NR 3 TC 6 Z9 6 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 19 PY 1996 VL 272 IS 5260 BP 337 EP 338 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UG252 UT WOS:A1996UG25200009 PM 8602518 ER PT J AU Wolffe, AP AF Wolffe, AP TI Histone deacetylase: A regulator of transcription SO SCIENCE LA English DT Editorial Material ID DNA; ACETYLATION; INVITRO; YEAST RP Wolffe, AP (reprint author), NICHHD,MOLEC EMBRYOL LAB,NIH,BETHESDA,MD 20892, USA. NR 16 TC 227 Z9 233 U1 1 U2 12 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 19 PY 1996 VL 272 IS 5260 BP 371 EP 372 DI 10.1126/science.272.5260.371 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UG252 UT WOS:A1996UG25200036 PM 8602525 ER PT J AU Shimoda, K vanDeursen, J Sangster, MY Sarawar, SR Carson, RT Tripp, RA Chu, C Quelle, FW Nosaka, T Vignali, DAA Doherty, PC Grosveld, G Paul, WE Ihle, JN AF Shimoda, K vanDeursen, J Sangster, MY Sarawar, SR Carson, RT Tripp, RA Chu, C Quelle, FW Nosaka, T Vignali, DAA Doherty, PC Grosveld, G Paul, WE Ihle, JN TI Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted Stat6 gene SO NATURE LA English DT Article ID IL-4; GENERATION; INVIVO; CELLS AB Signal transducers and activators of transcription (Stats) are activated by tyrosine phosphorylation in response to cytokines, and are thought to mediate many of their functional responses(1-4) Stat6 is activated in response to interleukin (IL)-4 (refs 5,6) and may contribute to various functions including mitogenesis, T-helper cell differentiation and immunoglobulin isotype switching(7). To evaluate the role of Stat6, we generated Stat6-null mice (Stat6(-/-)) by gene disruption in embryonic stem cells. The mice were viable, indicating the lack of a non-redundant function in normal development. Although naive lymphoid cell development was normal, Stat6(-/-) mice were deficient in IL-4-mediated functions including Th2 helper T-cell differentiation, expression of cell surface markers, and immunoglobulin class switching to IgE. In contrast, IL-4-mediated proliferation was only partly affected. C1 ST JUDE CHILDRENS RES HOSP, DEPT BIOCHEM, MEMPHIS, TN 38105 USA. ST JUDE CHILDRENS RES HOSP, DEPT GENET, MEMPHIS, TN 38105 USA. ST JUDE CHILDRENS RES HOSP, DEPT IMMUNOL, MEMPHIS, TN 38105 USA. NIAID, IMMUNOL LAB, NIH, BETHESDA, MD 20892 USA. RI Doherty, Peter Charles/C-4185-2013; OI Doherty, Peter Charles/0000-0002-5028-3489; Tripp, Ralph/0000-0002-2924-9956 NR 29 TC 975 Z9 989 U1 3 U2 22 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD APR 18 PY 1996 VL 380 IS 6575 BP 630 EP 633 DI 10.1038/380630a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF741 UT WOS:A1996UF74100047 PM 8602264 ER PT J AU Choi, OH Kim, JH Kinet, JP AF Choi, OH Kim, JH Kinet, JP TI Calcium mobilization via sphingosine kinase in signalling by the Fc epsilon RI antigen receptor SO NATURE LA English DT Article ID CELL; TRANSDUCTION; PLATELETS AB Calcium mobilization through antigen receptors, including high-affinity IgE receptors (Fc epsilon RI), is thought to be mediated by inositol-1,4,5-trisphosphate production (InsP(3))(1-4). Here we show that antigen clustering of Fc epsilon RI on the rat mast-cell line (RBC 2H3) activates a sphingosine kinase (SK) and produces sphingosine-l-phosphate (S1P), an alternative second messenger for intracellular calcium mobilization, The sphingosine analogue, D-L-threo-dihydrosphingosine (DHS), inhibits the SK enzyme competitively with a dissociation constant, K-i, of 5 to 18 mu M. This inhibition substantially suppresses the Fc epsilon RI-mediated calcium signal, but leaves intact the syk tyrosine kinase activation and the small InsP(3) production. The entire InsP(3)-dependent pathway activated by a transfected G-protein coupled receptor, used here as a positive control, also remained intact. Thus Fc epsilon RI principally utilizes a SK pathway to mobilize calcium. C1 BETH ISRAEL HOSP,LAB ALLERGY & IMMUNOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02215. RP Choi, OH (reprint author), NIAID,LAB ALLERG DIS,NIH,ROCKVILLE,MD 20852, USA. NR 17 TC 350 Z9 357 U1 0 U2 8 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 18 PY 1996 VL 380 IS 6575 BP 634 EP 636 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF741 UT WOS:A1996UF74100048 PM 8602265 ER PT J AU Collier, AC Coombs, RW Schoenfeld, DA Bassett, RL Timpone, J Baruch, A Jones, M Facey, K Whitacre, C McAuliffe, VJ Friedman, HM Merigan, TC Reichman, RC Hooper, C Corey, L AF Collier, AC Coombs, RW Schoenfeld, DA Bassett, RL Timpone, J Baruch, A Jones, M Facey, K Whitacre, C McAuliffe, VJ Friedman, HM Merigan, TC Reichman, RC Hooper, C Corey, L TI Treatment of human immunodeficiency virus infection with saquinavir, zidovudine, and zalcitabine SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; REVERSE-TRANSCRIPTASE; AZIDOTHYMIDINE AZT; PROTEASE INHIBITOR; NATURAL-HISTORY; HIV PROTEINASE; DOUBLE-BLIND; RO 31-8959; RESISTANCE AB Background. In patients with human immunodeficiency virus (HIV) infection, combined treatment with several agents may increase the effectiveness of antiviral therapy. We studied the safety and efficacy of saquinavir, an HIV-protease inhibitor, given with one or two nucleoside antiretroviral agents, as compared with the safety and efficacy of a combination of two nucleosides alone. Methods. In this double-blind trial, patients with HIV infection were randomly assigned to receive either saquinavir (1800 mg per day) plus both zidovudine (600 mg per day) and zalcitabine (2.25 mg per day) or zidovudine plus either saquinavir or zalcitabine. The 302 patients enrolled had CD4+ counts of 50 to 300 cells per cubic millimeter and had previously received zidovudine for a median of 27 months. The study lasted 24 weeks, with an optional double-blind extension period of an additional 12 to 32 weeks. Results. Ninety-six percent of the patients completed the 24-week study. In all three treatment groups, CD4+ cell counts rose at first and then fell gradually. The normalized area under the curve for the CD4+ cell count was greater with the three-drug combination than with either saquinavir and zidovudine (P=0.017) or zalcitabine and zidovudine (P<0.001). There were significantly greater reductions in plasma HIV with the three-drug combination than with the other regimens when peripheral-blood mononuclear cells were cultured for HIV and HIV RNA was assessed, and there were greater decreases in serum neopterin and beta(2)-microglobulin levels. There were no major differences in toxic effects among the three treatments. Conclusions. Treatment with saquinavir, zalcitabine, and zidovudine was well tolerated. This drug combination reduced HIV-1 replication, increased CD4+ cell counts, and decreased levels of activation markers in serum more than did treatment with zidovudine and either saquinavir or zalcitabine. Studies are warranted to evaluate whether the three-drug combination will reduce morbidity and mortality. C1 UNIV WASHINGTON,SCH MED,SEATTLE,WA. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NIAID,BETHESDA,MD 20892. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. ROCHE PROD,WELWYN GARDEN CIT,HERTS,ENGLAND. OHIO STATE UNIV,COLUMBUS,OH 43210. NYU,NEW YORK,NY. UNIV PENN,PHILADELPHIA,PA 19104. STANFORD UNIV,PALO ALTO,CA 94304. UNIV ROCHESTER,ROCHESTER,NY. FU NCRR NIH HHS [RR00044]; NIAID NIH HHS [AI-27658, AI-27664] NR 42 TC 561 Z9 567 U1 5 U2 17 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 18 PY 1996 VL 334 IS 16 BP 1011 EP 1017 DI 10.1056/NEJM199604183341602 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA UE733 UT WOS:A1996UE73300002 PM 8598838 ER PT J AU Lindpaintner, K Lee, MA Larson, MG Rao, VS Pfeffer, MA Ordovas, JM Schaefer, EJ Wilson, AF Wilson, PWF Vasan, RS Myers, RH Levy, D AF Lindpaintner, K Lee, MA Larson, MG Rao, VS Pfeffer, MA Ordovas, JM Schaefer, EJ Wilson, AF Wilson, PWF Vasan, RS Myers, RH Levy, D TI Absence of association or genetic linkage between the angiotensin-converting-enzyme gene and left ventricular mass SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID HEART-FAILURE; HYPERTROPHY; TWINS; CELLS; CAPTOPRIL; RATS; POLYMORPHISM; HYPERTENSION; DYSFUNCTION; EXPRESSION AB Background. Homozygous carriers of the D allele of the angiotensin-converting-enzyme (ACE) gene have been reported to be at increased risk for various cardiovascular disorders, including left ventricular hypertrophy. We investigated the potential role of the ACE gene in influencing left ventricular mass. Methods. Quantitative echocardiographic data and DNA samples were available for 2439 subjects from the Framingham Heart Study. ACE genotypes were determined by an assay based on the polymerase chain reaction. (The D allele of the ACE gene contains a deletion, whereas the I [insertion] allele does not.) Left ventricular mass and the prevalence of left ventricular hypertrophy, adjusted for clinical covariates, were analyzed according to genotype, Genetic linkage between the ACE locus and left ventricular mass was evaluated by quantitative analysis of pairs of siblings. Results. The ACE genotype was associated neither with left ventricular mass nor with the prevalence of left ventricular hypertrophy. Mean (+/-SE) left ventricular mass (adjusted for sex) among subjects carrying the DD, DI, and II genotypes was 165+/-1.6, 165+/-1.3, and 166+/-2.0 g, respectively (P=0.90). The prevalence of left ventricular hypertrophy among the three genotype groups was 15.6 percent, 13.6 percent, and 15.6 percent, respectively (P=0.36), and the adjusted relative risk of left ventricular hypertrophy associated with the DD genotype was 1.10 (95 percent confidence interval, 0.86 to 1.19). Linkage analysis in 759 pairs of siblings using both the ACE D/I marker and a microsatellite polymorphism at the neighboring locus for the human growth hormone gene failed to support any role of ACE in influencing left ventricular mass. Conclusions. The ACE genotype showed no association with echocardiographically determined left ventricular mass, nor did it confer an increased risk of left ventricular hypertrophy. We found no appreciable role of the ACE gene in influencing left ventricular mass. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT CARDIOL,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV CARDIOL,BOSTON,MA. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,DIV CLIN EPIDEMIOL,BOSTON,MA. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DIV EPIDEMIOL,BOSTON,MA. BOSTON UNIV,SCH MED,DEPT MED,DIV PREVENT MED,BOSTON,MA 02118. TUFTS UNIV,SCH MED,HUMAN NUTR RES CTR AGING,USDA,LIPID METAB LAB,BOSTON,MA. FRAMINGHAM HEART DIS EPIDEMIOL STUDY,FRAMINGHAM,MA. LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,NEW ORLEANS,LA 70112. NHLBI,BETHESDA,MD 20892. RP Lindpaintner, K (reprint author), HARVARD UNIV,DIV CARDIOVASC DIS,DEPT MED,BRIGHAM & WOMENS HOSP,SCH MED,75 FRANCIS ST,BOSTON,MA 02115, USA. RI Wilson, Alexander/C-2320-2009; OI Ramachandran, Vasan/0000-0001-7357-5970; Ordovas, Jose/0000-0002-7581-5680 FU NCRR NIH HHS [RR03655]; NHLBI NIH HHS [K04-HL03138-01]; PHS HHS [N01-38038] NR 52 TC 219 Z9 225 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 APR 18 PY 1996 VL 334 IS 16 BP 1023 EP 1028 DI 10.1056/NEJM199604183341604 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA UE733 UT WOS:A1996UE73300004 PM 8598840 ER PT J AU Okimoto, T Kohno, K Kuwano, M Gopas, J Kung, HF Ono, M AF Okimoto, T Kohno, K Kuwano, M Gopas, J Kung, HF Ono, M TI Regulation of epidermal growth factor receptor by activated H-ras and V-myc oncogenes in mouse Balb/3T3 cells: Possible roles of AP-1 SO ONCOGENE LA English DT Article DE H-ras; EGF receptor; AP-1; dominant negative c-jun ID DENSITY-LIPOPROTEIN RECEPTOR; TRANSCRIPTION FACTOR AP-1; TUMOR-NECROSIS-FACTOR; MIDDLE T-ANTIGEN; C-FOS GENE; PROTO-ONCOGENE; MALIGNANT TRANSFORMATION; CHEMICAL CARCINOGENS; MOLECULAR-CLONING; TYROSINE KINASE AB We previously reported that introduction of H-ras oncogene decreases the epidermal growth factor (EGF) binding activity to cell surface EGF receptor in mouse Balb/3T3, In this study, we have further isolated four H-ras transfectants, four v-myc transfectants and three both H-ras and v-myc (H-ras/v-myc) transfectants of mouse Balb/3T3 cells. In comparison with introduction of v-myc alone or both H-ras and v-myc oncogenes, introduction of H-ras alone resulted in a loss of [I-125]EGF binding activity to the cell surface EGF receptor, RT-PCR analysis also showed much lower levels of EGF receptor gene expression in H-ras transfectants compared to that of parental untransformed cells (Balb-Neo1), v-myc and H-ras/v-myc transfectants, Our results demonstrated the activated binding of a transcription factor, Stat1 p84/p91, which directly interacts with EGF receptor, to c-sis-inducible element (SIE) in both v-myc and H-ras/v-myc transfectants, but not in H-ras transfectants, Among transcription factors which we have analysed, activator protein 1 (AP-1) but not SP-1 was modulated by H-ras. Gel shift assays demonstrated the mobility pattern of TPA-responsive element (TRE) binding complex with AP-1 derived from H-ras transfectants migrated faster than those from Balb-Neo1, v-myc and H-ras/v-myc. Expression of c-Jun and Fra-1 was increased more than threefold in H-ras transfectants compared with Balb-Neo1, v-myc and H-ras/v-myc transfectants, but that of c-Fos, Jun B and SP-1 was unchanged, Both transient and permanent expression of H-ras enhanced AP-1 activity in mouse cells, but further co-introduction of dominant negative c-jun mutant encoding a transcriptionally inactive product inhibited the H-ras dependent AP-1 induction, Transfection of the dominant negative c-jun mutant also restored down-regulation of EGF binding by activated H-ras oncogene, Down-regulation of EGF receptor by activated H-ras and the possible involvement of a transcription factor, AP-1, will be discussed. C1 KYUSHU UNIV,SCH MED,DEPT BIOCHEM,FUKUOKA 81282,JAPAN. SOROKA MED CTR,LAB ONCOL,IL-84101 BEER SHEVA,ISRAEL. BEN GURION UNIV NEGEV,FAC HLTH SCI,DEPT MICROBIOL & IMMUNOL,IL-84105 BEER SHEVA,ISRAEL. NCI,FREDERICK CANC RES & DEV CTR,LAB BIOCHEM PHYSIOL,FREDERICK,MD 21702. NR 59 TC 22 Z9 22 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR 18 PY 1996 VL 12 IS 8 BP 1625 EP 1633 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA UG458 UT WOS:A1996UG45800004 PM 8622882 ER PT J AU Lee, JE Beck, TW Wojnowski, L Rapp, UR AF Lee, JE Beck, TW Wojnowski, L Rapp, UR TI Regulation of A-raf expression SO ONCOGENE LA English DT Article DE A-raf; steroid hormones; glucocorticoid receptor; transcription ID MAMMARY-TUMOR VIRUS; DNA-BINDING DOMAIN; ESTROGEN-RESPONSIVE ELEMENT; STEROID-HORMONE RECEPTORS; GLUCOCORTICOID RECEPTOR; GENE-EXPRESSION; TRANSCRIPTION FACTORS; MMTV PROMOTER; GROWTH-FACTOR; AMINO-ACIDS AB The Raf family proto-oncogenes encode cytoplasmic protein serine/threonine kinases which play a critical role in cell growth and development, A-raf shares several functional properties with Raf-1 including transforming activity, stimulation of the Raf/MAPK pathway and the ability of dominant negative versions to functionally block Ras signalling, A-raf transcripts are predominantly expressed in the mouse urogenital tissues, Interestingly, the human A-raf promoter region contains three potential glucocorticoid response elements GRE-1, GRE-2 and GRE-3, at positions -17, -34 and -168 respectively from the transcriptional start site, DNA sequence analysis of the mouse A-raf promoter region demonstrated that GRE-1 and -2 were conserved evolutionarily, To determine whether the human A-raf GREs represent functional motifs, an expression vector for the glucocorticoid receptor was cotransfected with A-raf promoter/reporter constructs into HeLa cells, A fivefold dexamethasone-dependent induction of A-raf promoter activity was observed using constructs containing all three GRE motifs whereas point mutations in the GREs either diminished or abolished dexamethasone induction, Electrophoretic mobility shift assays (EMSAs) using purified glucocorticoid receptor DNA binding domain (DBD) demonstrated that both GRE-2 and -3 motifs interact with DBD and oligonucleotide competition experiments established that these have different affinities for DBD, Using nuclear extracts from human and rodent cell lines in EMSAs, a specific protein-DNA complex was observed with GRE-1 which displayed binding properties unlike that of glucocorticoid receptor, These results demonstrate that the A-raf promoter is regulated in part by members of the glucocorticoid family of steroid hormone receptors and suggest a model for the regulation of A-raf expression in urogenital tissues. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,DYN CORP,PROGRAM RESOURCES,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,VIRAL PATHOL SECT,FREDERICK,MD 21702. NR 41 TC 14 Z9 16 U1 0 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR 18 PY 1996 VL 12 IS 8 BP 1669 EP 1677 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA UG458 UT WOS:A1996UG45800009 PM 8622887 ER PT J AU Cobb, JP Danner, RL AF Cobb, JP Danner, RL TI Nitric oxide and septic shock SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID VASCULAR SMOOTH-MUSCLE; METHYL-L-ARGININE; INDUCED HYPOTENSION; HEMODYNAMIC-CHANGES; INHIBITION; SYNTHASE; SEPSIS; ENDOTOXIN; EXPRESSION; REVERSAL C1 NIH,DEPT CRIT CARE MED,WARREN G MAGNUSON CLIN CTR,BETHESDA,MD 20892. NR 59 TC 125 Z9 132 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 APR 17 PY 1996 VL 275 IS 15 BP 1192 EP 1196 DI 10.1001/jama.275.15.1192 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA UE625 UT WOS:A1996UE62500032 PM 8609688 ER PT J AU Lancaster, JM Cochran, CJ Brownlee, HA Evans, AC Berchuck, A Futreal, PA Wiseman, RW AF Lancaster, JM Cochran, CJ Brownlee, HA Evans, AC Berchuck, A Futreal, PA Wiseman, RW TI Detection of BRCA1 mutations in women with early-onset ovarian cancer by use of the protein truncation test SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article C1 DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DIV GYNECOL ONCOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT SURG,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT GENET,DURHAM,NC 27710. RP Lancaster, JM (reprint author), NIEHS,MOLEC CARCINOGENESIS LAB,MAIL DROP C4-06,111 ALEXANDER DR,RES TRIANGLE PK,NC 27709, USA. NR 21 TC 11 Z9 11 U1 0 U2 2 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 17 PY 1996 VL 88 IS 8 BP 552 EP 554 DI 10.1093/jnci/88.8.552 PG 3 WC Oncology SC Oncology GA UE732 UT WOS:A1996UE73200017 PM 8606385 ER PT J AU Barnes, KM Dickstein, B Cutler, GB Fojo, T Bates, SE AF Barnes, KM Dickstein, B Cutler, GB Fojo, T Bates, SE TI Steroid transport, accumulation, and antagonism of P-glycoprotein in multidrug-resistant cells SO BIOCHEMISTRY LA English DT Article ID REDUCED DRUG ACCUMULATION; BREAST CANCER-CELLS; HUMAN-KB CELLS; SECRETORY EPITHELIUM; EXPRESSION; GENE; PROGESTERONE; PHOSPHORYLATION; LINES; CYTOTOXICITY AB According to multiple reports, progesterone is not transported by P-glycoprotein (Pgp), which mediates multidrug resistance through active drug efflux. However, progesterone has been shown to block Pgp-mediated efflux of other drugs. To extend these observations, and to examine the effect of modulating Pgp phosphorylation, the accumulation of progesterone and 14 other steroids in untreated and calphostin C-treated multidrug-resistant human colon carcinoma SW620 Ad300 cells was compared to the accumulation in parental SW620 cells. The accumulation of progesterone in untreated multidrug resistant cells expressing Pgp was not reduced compared to parental cells. However, the accumulation of more hydrophilic steroids was reduced by as much as 50%. Progesterone and progesterone-like compounds, however, were potent inhibitors of Pgp-mediated vinblastine efflux; increased antagonism correlated with increased steroid hydrophobicity. Treatment with calphostin C, a PKC inhibitor which decreases Pgp phosphorylation, increased progesterone efflux, modulated Pgp antagonism by steroids, and inhibited photoaffinity labeling of Pgp by progesterone. These results extend previous observations that Pgp can mediate the transport of, and be antagonized by, a variety of steroids and that these properties vary with both a steroid's hydrophobicity and the phosphorylated state of Pgp. C1 NICHHD,DEV ENDOCRINOL BRANCH,NIH,BETHESDA,MD 20892. NCI,MED BRANCH,DCS,BETHESDA,MD 20892. NR 50 TC 140 Z9 144 U1 3 U2 14 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 16 PY 1996 VL 35 IS 15 BP 4820 EP 4827 DI 10.1021/bi952380k PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UF521 UT WOS:A1996UF52100020 PM 8664272 ER PT J AU Reeves, R Wolffe, AP AF Reeves, R Wolffe, AP TI Substrate structure influences binding of the non-histone protein HMG-I(Y) to free and nucleosomal DNA SO BIOCHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR ACCESS; BOVINE INTERLEUKIN-2 CDNA; SEQUENCE-SPECIFIC BINDING; CHROMATIN CORE PARTICLES; TUMOR VIRUS PROMOTER; HMG-I; B-DNA; POSITIONED NUCLEOSOMES; HELICAL PERIODICITY; BASE-PAIRS AB High mobility group protein HMG-I(Y) selectively binds to stretches of A . T-rich B-form DNA in vitro by recognition of substrate structure rather nucleotide sequence. Recognition of altered DNA structures has also been proposed to explain the preferential binding of this non-histone protein to four-way junction DNA as well as to restricted regions of DNA on random-sequence nucleosome core particles. Here we describe experiments that examine the influence of intrinsic DNA structure, and of structure imposed by folding of DNA around histone cores, on the binding of HMG-I(Y). As substrates for binding, we chose defined-sequence DNA molecules containing A . T-rich segments demonstrated previously to have very different structures in solution. These segments are either intrinsically bent (phased A . T tracts), flexible (oligo[d(A-T)]), or straight and rigid [oligo(dA). oligo(dT)]. DNase-I and hydroxyl radical footprinting techniques were employed to analyze protein binding to these DNAs either free in solution or when they were reconstituted into monomer or dinucleosomes in vitro. Results indicate that the DNA structure exerts a significant influence on HMG-I(Y) binding both when substrates are free in solution and when they are wrapped into nucleosomal structures. For example, when DNA is free in solution, HMG-I(Y) prefers to bind to the narrow minor groove of A . T sequences but sometimes also binds to certain GpC residues having narrowed major grooves that are embedded in such sequences. On the other hand, depending on the structure and/or orientation assumed by particular A . T-rich segments on the surface of reconstituted histone octamers, HMG-I(Y) binding site selection on individual nucleosomes differs considerably. Two observations are of particular importance: (i) HMG-I(Y) can preferentially bind to certain types of A . T-DNA located on the surface of nucleosomes; and (ii) HMG-I(Y) binding can induce localized alterations in the helical periodicity and/or rotational setting of DNA on the surface of some nucleosomes. These abilities of HMG-I(Y) suggests that in vivo the protein may play an important role in recognizing and altering the structure of localized regions of chromatin. C1 WASHINGTON STATE UNIV,DEPT GENET & CELL BIOL,PULLMAN,WA 99164. NICHHD,MOLEC EMBRYOL LAB,NIH,BETHESDA,MD 20892. RP Reeves, R (reprint author), WASHINGTON STATE UNIV,DEPT BIOCHEM BIOPHYS,PULLMAN,WA 99164, USA. NR 95 TC 62 Z9 62 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 APR 16 PY 1996 VL 35 IS 15 BP 5063 EP 5074 DI 10.1021/bi952424p PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UF521 UT WOS:A1996UF52100047 PM 8664299 ER PT J AU Zolkiewski, M Redowicz, MJ Korn, ED Ginsburg, A AF Zolkiewski, M Redowicz, MJ Korn, ED Ginsburg, A TI Thermal unfolding of Acanthamoeba myosin 11 and skeletal muscle myosin SO BIOPHYSICAL CHEMISTRY LA English DT Article DE protein unfolding; myosin; muscle, skeletal; unfolding, thermal; Acanthamoeba ID DIFFERENTIAL SCANNING CALORIMETRY; 3 PHOSPHORYLATION SITES; ACTIN-ACTIVATED ATPASE; AMINO-ACID-SEQUENCE; HEAVY-CHAIN; LIGHT-MEROMYOSIN; SUBFRAGMENT-1; STABILITY; PROTEINS; DOMAINS AB Studies on the thermal unfolding of monomeric Acanthamoeba myosin II and other myosins, in particular skeletal muscle myosin, using differential scanning calorimetry (DSC) are reviewed. The unfolding transitions for intact myosin or its head fragment are irreversible, whereas those of the rod part and its fragments are completely reversible, Acanthamoeba myosin II unfolds with a high degree of cooperativity from ca, 40-45 degrees C at pH 7.5 in 0.6 M KCl, producing a single, sharp endotherm in DSC. In contrast, thermal transitions of rabbit skeletal muscle myosin occur over a broader temperature range (ca, 40-60 degrees C) under the same conditions, The DSC studies on the unfolding of the myosin rod and its fragments allow identification of cooperative domains, each of which unfolds according to a two-state mechanism, Also, DSC data show the effect of the nucleotide-induced conformational changes in the myosin head on the protein stability. C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. RI Korn, Edward/F-9929-2012; Redowicz, Maria Jolanta/R-4083-2016 NR 45 TC 8 Z9 8 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0301-4622 J9 BIOPHYS CHEM JI Biophys. Chem. PD APR 16 PY 1996 VL 59 IS 3 BP 365 EP 371 DI 10.1016/0301-4622(95)00129-8 PG 7 WC Biochemistry & Molecular Biology; Biophysics; Chemistry, Physical SC Biochemistry & Molecular Biology; Biophysics; Chemistry GA UK319 UT WOS:A1996UK31900015 PM 8672724 ER PT J AU Merril, CR Biswas, B Carlton, R Jensen, NC Creed, GJ Zullo, S Adhya, S AF Merril, CR Biswas, B Carlton, R Jensen, NC Creed, GJ Zullo, S Adhya, S TI Long-circulating bacteriophage as antibacterial agents SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE phage; bacteria; reticuloendothelial system; toxins; antibiotic resistance ID PROTEIN AB The increased prevalence of multidrug-resistant bacterial pathogens motivated us to attempt to enhance the therapeutic efficacy of bacteriophages. The therapeutic application of phages as antibacterial agents was impeded by several factors: (i) the failure to recognize the relatively narrow host range of phages; (ii) the presence of toxins in crude phage lysates; and (iii) a lack of appreciation for the capacity of mammalian host defense systems, particularly the organs of the reticuloendothelial system, to remove phage particles from the circulatory system, In our studies involving bacteremic mice, the problem of the narrow host range of phage was dealt with by using selected bacterial strains and virulent phage specific for them, Toxin levels were diminished by purifying phage preparations, To reduce phage elimination by the host defense system, we developed a serial-passage technique in mice to select for phage mutants able to remain in the circulatory system for longer periods of time, By this approach we isolated long-circulating mutants of Escherichia coli phage lambda and of Salmonella typhimurium phage P22. We demonstrated that the long-circulating lambda mutants also have greater capability as antibacterial agents than the corresponding parental strain in animals infected with lethal doses of bacteria, Comparison of the parental and mutant lambda capsid proteins revealed that the relevant mutation altered the major phage head protein E. The use of toxin free, bacteria-specific phage strains, combined with the serial-passage technique, may provide insights for developing phage into therapeutically effective antibacterial agents. C1 EXPONENTIAL BIOTHERAPIES INC, NEW YORK, NY 10001 USA. NCI, MOLEC BIOL LAB, NIH, BETHESDA, MD 20892 USA. RP Merril, CR (reprint author), NIMH, NEUROSCI CTR ST ELIZABETHS, LAB BIOCHEM GENET, WASHINGTON, DC 20032 USA. NR 21 TC 228 Z9 249 U1 5 U2 47 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 16 PY 1996 VL 93 IS 8 BP 3188 EP 3192 DI 10.1073/pnas.93.8.3188 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF740 UT WOS:A1996UF74000007 PM 8622911 ER PT J AU Moskovitz, J Jenkins, NA Gilbert, DJ Copeland, NG Jursky, F Weissbach, H Brot, N AF Moskovitz, J Jenkins, NA Gilbert, DJ Copeland, NG Jursky, F Weissbach, H Brot, N TI Chromosomal localization of the mammalian peptide-methionine sulfoxide reductase gene and its differential expression in various tissues SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID RETINAL-PIGMENT EPITHELIUM; ENZYMATIC REDUCTION; PROTEINS; RESIDUES; CLONING; DAMAGE; MOUSE AB Peptide methionine sulfoxide reductase (MsrA; EC 1.8.4.6) is a ubiquitous protein that can reduce methionine sulfoxide residues in proteins as well as in a large number of methyl sulfoxide compounds, The expression of MsrA in various rat tissues was determined by using immunocytochemical staining. Although the protein was found in all tissues examined, it,vas specifically localized to renal medulla and retinal pigmented epithelial cells, and it was prominent in neurons and throughout the nervous system. In addition, blood and alveolar macrophages showed high expression of the enzyme, The msrA gene was mapped to the central region of mouse chromosome 14, in a region of homology with human chromosomes 13 and 8p21. C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA. RP Moskovitz, J (reprint author), ROCHE INST MOLEC BIOL, ROCHE RES CTR, NUTLEY, NJ 07110 USA. NR 27 TC 115 Z9 118 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 16 PY 1996 VL 93 IS 8 BP 3205 EP 3208 DI 10.1073/pnas.93.8.3205 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF740 UT WOS:A1996UF74000010 PM 8622914 ER PT J AU Dix, DJ Allen, JW Collins, BW Mori, C Nakamura, N PoormanAllen, P Goulding, EH Eddy, EM AF Dix, DJ Allen, JW Collins, BW Mori, C Nakamura, N PoormanAllen, P Goulding, EH Eddy, EM TI Targeted gene disruption of Hsp70-2 results in failed meiosis, germ cell apoptosis, and male infertility SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE gametogenesis; heat shock protein; programmed cell death; spermatogenesis; stress protein ID MOUSE SPERMATOGENIC CELLS; HEAT-SHOCK PROTEINS; NUCLEOTIDE-SEQUENCE; EXPRESSION; CLONING; FAMILY; IDENTIFICATION; MEMBER; P70 AB In addition to the five 70-kDa heat shock proteins (HSP70) common to germ cells and somatic tissues of mammals, spermatogenic cells synthesize HSP70-2 during meiosis, To determine if this unique stress protein has a critical role in meiosis, we used gene-targeting techniques to disrupt Hsp70-2 in mice. Male mice homozygous for the mutant allele (Hsp70-2(-/-)) did not synthesize HSP70-2, lacked postmeiotic spermatids and mature sperm, and were infertile, However, neither meiosis nor fertility was affected in female Hsp70-2(-/-) mice, We previously found that HSP70-2 is associated with synaptonemal complexes in the nucleus of meiotic spermatocytes from mice and hamsters. While synaptonemal complexes assembled in Hsp70-2(-/-) spermatocytes, structural abnormalities became apparent in these cells by late prophase, and development rarely progressed to the meiotic divisions, Furthermore, analysis of nuclei and genomic DNA indicated that the failure of meiosis in Hsp70-2(-/-) mice was coincident with a dramatic increase in spermatocyte apoptosis. These results suggest that HSP70-2 participates in synaptonemal complex function during meiosis in male germ cells and is linked to mechanisms that inhibit apoptosis. C1 US EPA,DIV ENVIRONM CARCINOGENESIS,NATL HLTH & ENVIRONM EFFECTS RES LAB,RES TRIANGLE PK,NC 27711. NIEHS,GAMETE BIOL SECT,REPROD & DEV TOXICOL LAB,NIH,RES TRIANGLE PK,NC 27709. KYOTO UNIV,FAC MED,DEPT ANAT,KYOTO 60601,JAPAN. GLAXO INC,DIV MED SAFETY EVALUAT,RES TRIANGLE PK,NC 27709. RP Dix, DJ (reprint author), US EPA,REPROD TOXICOL DIV,GAMETE & EARLY EMBRYO BIOL BRANCH,MAIL DROP 72,RES TRIANGLE PK,NC 27711, USA. NR 35 TC 384 Z9 403 U1 1 U2 12 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 16 PY 1996 VL 93 IS 8 BP 3264 EP 3268 DI 10.1073/pnas.93.8.3264 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF740 UT WOS:A1996UF74000021 PM 8622925 ER PT J AU Kong, SK Yim, MB Stadtman, ER Chock, PB AF Kong, SK Yim, MB Stadtman, ER Chock, PB TI Peroxynitrite disables the tyrosine phosphorylation regulatory mechanism: Lymphocyte-specific tyrosine kinase fails to phosphorylate nitrated cdc2(6-20)NH2 peptide SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE tyrosine nitration; tyrosine kinase; signal transduction; cell cycle ID NITRIC-OXIDE; SUPEROXIDE-DISMUTASE; SUBSTRATE; ACID; NO AB To determine if nitration of tyrosine residues by peroxynitrite (PN), which can be generated endogenously, can disrupt the phosphorylation of tyrosine residues in proteins involved in cell signaling networks, we studied the effect of PN-promoted nitration of tyrosine residues in a penta-decameric peptide, cdc2(6-20)NH2, on the ability of the peptide to be phosphorylated, cdc2(6-20)NH2 corresponds to the tyrosine phosphorylation site of p34(cdc2) kinase, which is phosphorylated by lck kinase (lymphocyte-specific tyrosine kinase, p56(lck)). PN nitrates both Tyr-15 and Tyr-19 of the peptide in phosphate buffer (pH 7.5) at 37 degrees C. Nitration of Tyr-15, which is the phosphorylated amino acid residue, inhibits completely the phosphorylation of the peptide. The nitration reaction is enhanced by either Fe(III)EDTA or Cu(II)-Zn(II)-superoxide dismutase (Cu,Zn-SOD). The kinetic data are consistent with the view that reactions of Fe(III)EDTA or Cu,Zn-SOD with the cis form of PN yield complexes in which PN decomposes more slowly to form NO2+, the nitrating agent, Thus, the nitration efficiency of PN is enhanced, These results are discussed from the point of view that PN-promoted nitration will result in permanent impairment of cyclic cascades that control signal transduction processes and regulate cell cycles. C1 NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. NR 27 TC 269 Z9 273 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 16 PY 1996 VL 93 IS 8 BP 3377 EP 3382 DI 10.1073/pnas.93.8.3377 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF740 UT WOS:A1996UF74000043 PM 8622943 ER PT J AU Maraia, RJ AF Maraia, RJ TI Transcription termination factor La is also an initiation factor for RNA polymerase III SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE autoimmune antigen; ribonucleoprotein; transcription complexes ID GENE-TRANSCRIPTION; PROTEIN; COMPLEXES; INVITRO; BINDING; INTERMEDIATE; ANTIBODIES; FRACTION; ANTIGEN AB La RNA-binding protein is a transcription termination factor that facilitates recycling of template and RNA polymerase (pot) III. Transcription complexes preassembled on immobilized templates were depleted of pol III after a single round of RNA synthesis in the presence of heparin and sarkosyl. The isolated complexes could then be complemented with highly purified pol III and/or recombinant La to test if La is required for transcription reinitiation. VA1, 7SL, and B1 transcription complexes cannot be transcribed by supplemental pol III in single or multiple-round transcription assays unless La is also provided, La mediates concentration-dependent activation of pol III initiation and thereby controls the use of preassembled stable transcription complexes. The initiation factor activity of La augments its termination factor activity to produce a novel mechanism of activated reinitiation. A model in which La serves pol III upon transcription initiation and again at termination is discussed. RP Maraia, RJ (reprint author), NICHHD,LAB MOLEC GROWTH REGULAT,NIH,BLDG 6,ROOM 416,BETHESDA,MD 20892, USA. NR 30 TC 90 Z9 90 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 16 PY 1996 VL 93 IS 8 BP 3383 EP 3387 DI 10.1073/pnas.93.8.3383 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF740 UT WOS:A1996UF74000044 PM 8622944 ER PT J AU Weihe, E TaoCheng, JH Schafer, MKH Erickson, JD Eiden, LE AF Weihe, E TaoCheng, JH Schafer, MKH Erickson, JD Eiden, LE TI Visualization of the vesicular acetylcholine transporter in cholinergic nerve terminals and its targeting to a specific population of small synaptic vesicles SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE vesicular monoamine transporter; immunohistochemistry; small synaptic vesicles; large dense-core vesicles; regulated secretion ID ADRENAL PHEOCHROMOCYTOMA CELLS; GROWTH-FACTOR; MONOAMINE TRANSPORTER; CLONAL LINE; IDENTIFICATION; MICROVESICLES; CLONING; RESPOND AB Immunohistochemical visualization of the rat vesicular acetylcholine transporter (VAChT) in cholinergic neurons and nerve terminals has been compared to that for choline acetyltransferase (ChAT), heretofore the most specific marker for cholinergic neurons, VAChT-positive cell bodies were visualized in cerebral cortex, basal forebrain, medial habenula, striatum, brain stem, and spinal cord by using a polyclonal anti-VAChT antiserum, VAChT-immunoreactive fibers and terminals were also visualized in these regions and in hippocampus, at neuromuscular junctions within skeletal muscle, and in sympathetic and parasympathetic autonomic ganglia and target tissues, Cholinergic nerve terminals contain more VAChT than ChAT immunoreactivity after routine fixation, consistent with a concentration of VAChT within terminal neuronal arborizations in which secretory vesicles are clustered. These include VAChT-positive terminals of the median eminence of the hypothalamus, not observed with ChAT antiserum after routine fixation, Subcellular localization of VAChT in specific organelles in neuronal cells was examined by immunoelectron microscopy in a rat neuronal cell line (PC12-c4) expressing VAChT as well as the endocrine and neuronal forms of the vesicular monoamine transporters (VMAT1 and VMAT2). VAChT is targeted to small synaptic vesicles, while VMAT1 is found mainly but not exclusively on large dense-core vesicles. VMAT2 is found on large dense-core vesicles but not on the small synaptic vesicles that contain VAChT in PC12-c4 cells, despite the presence of VMAT2 immunoreactivity in central and peripheral nerve terminals known to contain monoamines in small synaptic vesicles, Thus, VAChT and VMATZ may be specific markers for ''cholinergic'' and ''adrenergic'' small synaptic vesicles, with the latter not expressed in nonstimulated neuronally differentiated PC12-c4 cells. C1 NIMH,NIH,CELL BIOL LAB,MOLEC NEUROSCI SECT,BETHESDA,MD 20892. UNIV MARBURG,DEPT ANAT & CELL BIOL,W-3550 MARBURG,GERMANY. NINCDS,NIH,NEUROBIOL LAB,BETHESDA,MD 20892. OI Eiden, Lee/0000-0001-7524-944X NR 32 TC 237 Z9 241 U1 4 U2 6 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 16 PY 1996 VL 93 IS 8 BP 3547 EP 3552 DI 10.1073/pnas.93.8.3547 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF740 UT WOS:A1996UF74000074 PM 8622973 ER PT J AU Levine, M ConryCantilena, C Wang, YH Welch, RW Washko, PW Dhariwal, KR Park, JB Lazarev, A Graumlich, JF King, J Cantilena, LR AF Levine, M ConryCantilena, C Wang, YH Welch, RW Washko, PW Dhariwal, KR Park, JB Lazarev, A Graumlich, JF King, J Cantilena, LR TI Vitamin C pharmacokinetics in healthy volunteers: Evidence for a recommended dietary allowance SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ascorbic acid; bioavailability ID COULOMETRIC ELECTROCHEMICAL DETECTION; PERFORMANCE LIQUID-CHROMATOGRAPHY; ASCORBIC-ACID; DEHYDROASCORBIC ACID; CHROMAFFIN GRANULES; INSITU KINETICS; HEART-DISEASE; PLASMA; DEPLETION; TRANSPORT AB Determinants of the recommended dietary allowance (RDA) for vitamin C include the relationship between vitamin C dose and steady state plasma concentration, bioavailability, urinary excretion, cell concentration, and potential adverse effects. Because current data are inadequate, an in-hospital depletion-repletion study was conducted. Seven healthy volunteers were hospitalized for 4-6 months and consumed a diet containing <5 mg of vitamin C daily. Steady-state plasma and tissue concentrations were determined at seven daily doses of vitamin C from 30 to 2500 mg. Vitamin C steady-state plasma concentrations as a function of dose displayed sigmoid kinetics. The steep portion of the curve occurred between the 30- and 100-mg daily dose, the current RDA of 60 mg daily was on the lower third of the curve, the first dose beyond the sigmoid portion of the curve was 200 mg daily, and complete plasma saturation occurred at 1000 mg daily. Neutrophils, monocytes, and lymphocytes saturated at 100 mg daily and contained concentrations at least 14-fold higher than plasma. Bioavailability was complete for 200 mg of vitamin C as a single dose. No vitamin C was excreted in urine of six of seven volunteers until the 100-mg dose. At single doses of 500 mg and higher, bioavailability declined and the absorbed amount was excreted. Oxalate and urate excretion were elevated at 1000 mg of vitamin C daily compared to lower doses. Based on these data and Institute of Medicine criteria, the current RDA of 60 ng daily should be increased to 200 mg daily, which can be obtained from fruits and vegetables. Safe doses of vitamin C are less than 1000 mg daily, and vitamin C daily doses above 400 mg have no evident value. C1 NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT TRANSFUS MED,BETHESDA,MD 20892. UNIFORMED SERV UNIV HLTH SCI,DIV CLIN PHARMACOL,BETHESDA,MD 20814. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT NUTR,BETHESDA,MD 20892. RP Levine, M (reprint author), NIDDKD,MOL & CLIN NUTR SECT,NIH,BLDG 10,ROOM 4D52,MSC 1372,BETHESDA,MD 20892, USA. NR 56 TC 629 Z9 645 U1 2 U2 36 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 16 PY 1996 VL 93 IS 8 BP 3704 EP 3709 DI 10.1073/pnas.93.8.3704 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UF740 UT WOS:A1996UF74000103 PM 8623000 ER PT J AU Licinio, J Magistretti, P Bolis, CL AF Licinio, J Magistretti, P Bolis, CL TI The World Health Organization sponsored study group on anorexia nervosa (AN): Basic mechanisms, clinical approaches and treatment - Introduction SO PSYCHIATRY RESEARCH LA English DT Editorial Material C1 UNIV LAUSANNE,INST PHYSIOL,CH-1005 LAUSANNE,SWITZERLAND. WHO,CH-1211 GENEVA,SWITZERLAND. UNIV MILAN,MILAN,ITALY. RP Licinio, J (reprint author), NIMH,NIH,CLIN NEUROENDOCRINOL BRANCH,UNIT CLIN RES,BLDG 10,RM 3S231,10 CTR DR MSC 1284,BETHESDA,MD 20892, USA. RI Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 10 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD APR 16 PY 1996 VL 62 IS 1 BP 1 EP 2 DI 10.1016/0165-1781(96)01007-4 PG 2 WC Psychiatry SC Psychiatry GA UL142 UT WOS:A1996UL14200001 ER PT J AU Licinio, J Wong, ML Gold, PW AF Licinio, J Wong, ML Gold, PW TI The hypothalamic-pituitary-adrenal axis in anorexia nervosa SO PSYCHIATRY RESEARCH LA English DT Article; Proceedings Paper CT WHO Study Group on Anorexia Nervosa (AN) Meeting - Basic Mechanisms, Clinical Approaches and Treatment CY SEP 27-29, 1993 CL GENEVA, SWITZERLAND SP WHO, Study Grp Anorexia Nervosa DE cortisol; adrenocorticotropic hormone; corticotropin-releasing hormone; circadian rhythms; depression ID CORTICOTROPIN-RELEASING-FACTOR; PRIMARY CORTISOL RESISTANCE; GLUCOCORTICOID RECEPTORS; ARGININE VASOPRESSIN; WEIGHT-LOSS; HORMONE; DEPRESSION; SECRETION; SYSTEM; PLASMA AB Studies examining the function of the hypothalamic-pituitary-adrenal (HPA) axis in anorexia nervosa are reviewed. A principal finding is that of hypercortisolism, associated with increased central corticotropin-releasing hormone levels and normal circulating levels of adrenocorticotropic hormone. Similarities between neuroendocrine findings in anorexia nervosa and in affective disorder are reviewed. The contribution of circadian rhythm disturbances and malnutrition to observed HPA axis abnormalities in anorexia nervosa is also considered. Directions for future research are discussed. RP Licinio, J (reprint author), NIMH,CLIN NEUROENDOCRINOL BRANCH,INTRAMURAL RES PROGRAM,BLDG 10,RM 3S231,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. RI Wong, Ma-Li/D-7903-2011; Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 46 TC 93 Z9 93 U1 2 U2 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD APR 16 PY 1996 VL 62 IS 1 BP 75 EP 83 DI 10.1016/0165-1781(96)02991-5 PG 9 WC Psychiatry SC Psychiatry GA UL142 UT WOS:A1996UL14200010 PM 8739117 ER PT J AU Chyou, PH White, LR Yano, K Sharp, DS Burchfiel, CM Chen, R Rodriguez, BL Curb, JD AF Chyou, PH White, LR Yano, K Sharp, DS Burchfiel, CM Chen, R Rodriguez, BL Curb, JD TI Pulmonary function measures as predictors and correlates of cognitive functioning in later life SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE aging; cognition; forced expiratory volume ID SLEEP-APNEA; DISEASE; PERFORMANCE; RISK; MEN; POPULATION; HAWAII AB The relation between pulmonary function and cognitive functioning was investigated in a cohort of 3,036 Japanese-American men living in Hawaii. Pulmonary function, as indicated by forced expiratory volume in 1 second (FEV(1)), was measured at the baseline examination from 1965 to 1968. Cognitive function was assessed by the Cognitive Abilities Screening Instrument (CASI) test at least 23 years later (1991-1993). Baseline FEV(1) was significantly correlated with follow-up CASI score (r = 0.22, p = 0.0001). Although the strength of the association was reduced by controlling for the effects of other factors, stepwise multiple linear regression showed that FEV(1) during middle age was a significant predictor of CASI in later life, after taking into account the effects of age, education, stroke, sedentary job activity, nonmanual occupation, height, generation, and Japanese speaking ability. The mean CASI value was significantly greater for men whose FEV(1) exceeded 2.8 liter compared with those whose FEV(1) levels were in the lowest (<2.5 liters) quartile. Furthermore, the test on the effect of interaction between FEV(1) and age was statistically significant (p = 0.0024), with subjects less than 55 years of age at the baseline examination showing a stronger direct association of FEV(1) with CASI than the men aged 55 or older. These findings suggest that pulmonary function impairment may be associated with cognitive function impairment in later life. C1 MARSHFIELD MED RES FDN,MARSHFIELD CLIN,DEPT EPIDEMIOL & BIOSTAT,MARSHFIELD,WI 54449. NIA,HONOLULU,HI. HONOLULU ASIA AGING STUDY,HONOLULU,HI. KUAKINI MED CTR,HONOLULU HEART PROGRAM,HONOLULU,HI 96817. NHLBI,HONOLULU EPIDEMIOL RES UNIT,EPIDEMIOL & BIOMETRY PROGRAM,DIV EPIDEMIOL & CLIN APPLICAT,NIH,BETHESDA,MD 20892. FU NHLBI NIH HHS [N01-HC-05102] NR 32 TC 53 Z9 53 U1 0 U2 1 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 15 PY 1996 VL 143 IS 8 BP 750 EP 756 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UE759 UT WOS:A1996UE75900002 PM 8610684 ER PT J AU Beckett, LA Brock, DB Lemke, JH deLeon, CFM Guralnik, JM Fillenbaum, GG Branch, LG Wetle, TT Evans, DA AF Beckett, LA Brock, DB Lemke, JH deLeon, CFM Guralnik, JM Fillenbaum, GG Branch, LG Wetle, TT Evans, DA TI Analysis of change in self-reported physical function among older persons in four population studies SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE activities of daily living; aging; longitudinal studies; population surveillance ID ELDERLY FINNISH MEN; PREVALENCE RATES; ALAMEDA COUNTY; FOLLOW-UP; DISABILITY; PREDICTORS; MORTALITY; MODELS; LIFE AB Change in self-reported physical function was examined using baseline and 5 years of follow-up data between 1982 and 1991 from the four Established Populations for Epidemiologic Studies of the Elderly studies. In East Boston, Massachusetts (n = 3,809), Iowa and Washington Counties, Iowa (n = 3,673), New Haven, Connecticut (n = 2,812), and North Carolina (n = 4,163), noninstitutionalized persons aged 65 years and older were asked a series of questions to assess their physical function: a modified Katz Activities of Daily Living (ADL) scale, three items from the Rosow-Breslau Functional Health Scale, and questions on physical performance, adapted from Nagi, as well as information on demographic, social, and health characteristics. Longitudinal statistical analyses (random effects and Markov transition models) were used to evaluate improvement, stability, and deterioration in functional ability at both an individual and a population level over multiple years of data. The average decline in physical function associated with age was found to be greater than previous cross-sectional studies have suggested, and the rate of decline increased with increasing age. Considerable individual variation was evident. Although many people experienced declines, a smaller but substantial portion experienced recovery. Women reported a greater rate of decline in physical function and were less likely to recover from disability. C1 RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892. UNIV IOWA,DEPT PREVENT MED & ENVIRONM HLTH,IOWA CITY,IA 52242. YALE UNIV,SCH MED,DEPT EPIDEMIOL & PUBL HLTH,NEW HAVEN,CT 06510. DUKE UNIV,MED CTR,CTR STUDY AGING & HUMAN DEV,DURHAM,NC 27710. ABT ASSOCIATES INC,CAMBRIDGE,MA 02138. BOSTON UNIV,SCH MED,BOSTON,MA 02118. UNIV CONNECTICUT,SCH MED,INST LIVING,BRACELAND CTR MENTAL HLTH & AGING,HARTFORD,CT 06112. UNIV CONNECTICUT,SCH MED,DEPT COMMUNITY MED & HLTH CARE,HARTFORD,CT 06112. RP Beckett, LA (reprint author), RUSH UNIV,RUSH INST AGING,1645 W JACKSON BLVD,CHICAGO,IL 60612, USA. FU NIA NIH HHS [N01AG02105, N01AG02106, N01AG02107] NR 41 TC 202 Z9 204 U1 2 U2 5 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 15 PY 1996 VL 143 IS 8 BP 766 EP 778 PG 13 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UE759 UT WOS:A1996UE75900004 PM 8610686 ER PT J AU Fest, T Pron, B Lefranc, MP Pierre, C Angonin, R deWazieres, B Soua, Z Dupond, JL AF Fest, T Pron, B Lefranc, MP Pierre, C Angonin, R deWazieres, B Soua, Z Dupond, JL TI Detection of a clonal BCL2 gene rearrangement in tissues from a patient with Whipple disease SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID FOLLICULAR LYMPHOMAS; IMMUNE-RESPONSE; MUCOSA; PYLORI C1 HOP NECKER ENFANTS MALAD,MICROBIOL SERV,F-75743 PARIS 15,FRANCE. INST GENET MOLEC,UMR CNRS 9942,IMMUNOGENET MOLEC LAB,F-34033 MONTPELLIER 1,FRANCE. HOP UNIV JEAN MINJOZ,SERV ANATOMOPATHOL,F-25030 BESANCON,FRANCE. HOP UNIV JEAN MINJOZ,SERV MED INTERNE,F-25030 BESANCON,FRANCE. RP Fest, T (reprint author), NEI,PATHOL LAB,9000 ROCKVILLE PIKE,BLDG 10,ROOM 2N109,BETHESDA,MD 20892, USA. NR 11 TC 10 Z9 10 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 APR 15 PY 1996 VL 124 IS 8 BP 738 EP 740 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA UD936 UT WOS:A1996UD93600006 PM 8633834 ER PT J AU Candotti, F Johnston, JA Puck, JM Sugamura, K OShea, JJ Blaese, M AF Candotti, F Johnston, JA Puck, JM Sugamura, K OShea, JJ Blaese, M TI Retroviral-mediated gene correction for X-linked severe combined immunodeficiency SO BLOOD LA English DT Article ID RECEPTOR GAMMA-CHAIN; BONE-MARROW TRANSPLANTATION; HUMAN ADENOSINE-DEAMINASE; FUNCTIONAL COMPONENT; CELLS; EXPRESSION; VIRUS AB X-linked severe combined immunodeficiency (XSCID) is a lethal disease caused by a defect in the gene encoding the common gamma chain (gamma(c)) of the receptor for interleukin-2 (IL-2), IL-4, IL-7, IL-9, and IL-15. Allogeneic bone marrow transplantation, the current therapy of choice for this defect, is often complicated by graft-versus-host disease and/or incomplete reconstitution of B-lymphocyte functions. Correction of the gene defect at the level of the autologous lymphohematopoietic progenitors could therefore represent an improvement in the medical management of these patients. To study the feasibility of a gene therapy approach for XSCID, a retroviral vector expressing gamma(c) was used to transduce Epstein-Barr virus-transformed B-cell lines derived from patients with XSCID. After transduction, XSCID cells newly expressed gamma(c) on the cell surface at levels comparable to those observed on B-cell lines obtained from normal donors. Moreover, the reconstituted gamma(c) restored function to the IL-2 and IL-4 receptors as shown by signal transduction mediated by phosphorylation of the JAK1 and JAK3 members of the Janus family of tyrosine kinases and by restoration of cellular proliferation in response to IL-2. This is a US government work. There are no restrictions on its use. C1 NIAMS,LEUKOCYTE CELL BIOL SECT,NIH,BETHESDA,MD. NIH,IMMUNOL GENET SECT,NCHGR,BETHESDA,MD 20892. TOHOKU UNIV,SCH MED,DEPT MICROBIOL,SENDAI,MIYAGI 980,JAPAN. RP Candotti, F (reprint author), NIH,CLIN GENE THERAPY BRANCH,NCHGR,BLDG 10-ROOM 10C103,10 CTR DR,BETHESDA,MD 20892, USA. NR 47 TC 60 Z9 61 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1996 VL 87 IS 8 BP 3097 EP 3102 PG 6 WC Hematology SC Hematology GA UF381 UT WOS:A1996UF38100004 PM 8605322 ER PT J AU Hernandez, L Fest, T Cazorla, M TeruyaFeldstein, J Bosch, F Peinado, MA Piris, MA Montserrat, E Cardesa, A Jaffe, ES Campo, E Raffeld, M AF Hernandez, L Fest, T Cazorla, M TeruyaFeldstein, J Bosch, F Peinado, MA Piris, MA Montserrat, E Cardesa, A Jaffe, ES Campo, E Raffeld, M TI p53 gene mutations and protein overexpression are associated with aggressive variants of mantle cell lymphomas SO BLOOD LA English DT Article ID LYMPHOCYTIC LYMPHOMA; CENTROCYTIC LYMPHOMA; INTERMEDIATE DIFFERENTIATION; GEL-ELECTROPHORESIS; CYCLIN D1; EXPRESSION; PROGRESSION; ONCOGENE; CANCER; REARRANGEMENT AB Mantle cell lymphoma (MCL) is molecularly characterized by bcl-1 rearrangement and cyclin D1/PRAD-1 gene overexpression. Some aggressive variants have been recognized with a blastic or large cell morphology, higher proliferative activity, and shorter survival. p53 gene mutations in lymphoid neoplasms have been detected mainly in high grade lymphomas and have been associated with tumor progression in follicular and small lymphocytic lymphomas. To determine the role of p53 alterations in MCL, we examined 35 typical and 8 aggressive variants (5 blastic and 3 large cell) of MCLs by a combination of immunohistochemistry. single-strand conformational polymorphism analysis of genomic DNA and/or cDNA obtained by reverse transcriptase-polymerase chain reaction, denaturing gradient gel electrophoresis, and sequencing. Of the 8 aggressive MCLs, 3 (38%) contained missense point mutations in exon 8 codon 278 (Pro --> Leu), exon 8 codon 273 (Arg --> His), and exon 5 codon 151 (Pro --> Ser), respectively. A diffuse p53 protein overexpression was observed in more than 50% of the tumor cells in these 3 cases. A fourth blastic MCL also showed strong p53 immunoreactivity. However, no mutations were detected in exons 5-9 in this case. p53 expression was also detected in 10% of the cells in an additional large cell type of MCL and in less than 1% of the cells in 6 typical cases. No mutations were detected in any of these cases or in the remaining cases with no expression of the protein. Four nucleotide changes were observed by single-strand conformational polymorphism analysis in 4 typical MCLs with no overexpression of the protein. Direct sequencing showed that these nucleotide changes were located at exon 6 (1 case), intron 7 (2 cases), and intron 8 (1 case). The changes in exon 6 and intron 7 were known polymorphisms. The nucleotide change in intron 8 was outside splicing sites of the neighboring exons. The overall survival of the 3 patients with p53 mutations (median, 18.3 months) was significantly shorter than that of pateints with the nonmutated MCLs (median, 49 months; P < .01). These findings indicate that p53 gene mutations are an infrequent phenomenon in MCLs and are associated with a subset of aggressive variants. This is a US government work. There are no restrictions on its use. C1 UNIV BARCELONA,ANAT PATHOL LAB,HOSP CLIN PROV,E-08036 BARCELONA,SPAIN. UNIV BARCELONA,HOSP CLIN PROV,POSTGRAD SCH HEMATOL FARRERAS VALENTI,BARCELONA,SPAIN. INST RECERCA ONCOL,BARCELONA,SPAIN. HOSP VIRGEN DE LA SALUD,DEPT PATHOL ANAT,TOLEDO,SPAIN. UNIV LLEIDA,SCH MED,DEPT BASIC MED SCI,LLEIDA,SPAIN. NCI,HEMATOPATHOL SECT,PATHOL LAB,NIH,BETHESDA,MD 20892. RI Peinado, Miguel A./A-5591-2008; OI Peinado, Miguel A./0000-0002-4090-793X; Bosch, Francesc/0000-0001-9241-2886; Piris, Miguel A/0000-0001-5839-3634; Campo, elias/0000-0001-9850-9793 NR 47 TC 206 Z9 207 U1 1 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1996 VL 87 IS 8 BP 3351 EP 3359 PG 9 WC Hematology SC Hematology GA UF381 UT WOS:A1996UF38100034 PM 8605352 ER PT J AU Gamel, JW Meyer, JS Feuer, E Miller, BA AF Gamel, JW Meyer, JS Feuer, E Miller, BA TI The impact of stage and histology on the long-term clinical course of 163,808 patients with breast carcinoma SO CANCER LA English DT Article DE breast cancer; histologic type; cured fraction; survival time; stage ID CELL-KINETICS; CANCER AB BACKGROUND, Stage and histologic type have a significant impact on the long term clinical course of breast carcinoma. Clinical course is governed by two components: likelihood of cure and median tumor-related survival time among uncured patients. Estimates of these components can be derived only by using survival models that incorporate cured fraction as a specific parameter. METHODS. The prognostic value of stage and histologic type was determined for 163,808 patients with breast carcinoma using the log normal and log legit cure-based survival models. Follow-up ranged from 1 month to 19 years and was obtained from the SEER Program. RESULTS, In approximate terms, ductal carcinoma was diagnosed in 70% of the patients, with estimated cured fractions of 2/3 and 1/3 for local, and regional disease, respectively. Estimates of median survival times for uncured patients were 10 and 5 years. Findings were similar for patients with tumors of miscellaneous histologic types. For patients with medullary carcinoma, cured fractions were relatively high at 82% and 64%, but median survival times were relatively short at 4 and 3 years. Corresponding values for patients with invasive comedo carcinoma were 82% and 50%, with median survival rimes of 6 and 4 years. For patients with mucinous, lobular, and ductolobular carcinomas, parametric analysis gave inconsistent estimates of cured fraction, but findings suggested unusually long tumor-related survival times. CONCLUSIONS, Cure-based parametric survival models offer valuable insight into the impact of stage and histology on the clinical course of breast cancer. (C) 1996 American Cancer Society. C1 UNIV LOUISVILLE,SCH MED,VET ADM MED CTR,LOUISVILLE,KY 40292. UNIV LOUISVILLE,SCH MED,DEPT OPHTHALMOL,LOUISVILLE,KY 40292. ST LUKES HOSP,ST LOUIS,MO. NCI,NIH,SURVEILLANCE PROGRAM,BETHESDA,MD 20892. NR 17 TC 41 Z9 41 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 15 PY 1996 VL 77 IS 8 BP 1459 EP 1464 DI 10.1002/(SICI)1097-0142(19960415)77:8<1459::AID-CNCR6>3.0.CO;2-7 PG 6 WC Oncology SC Oncology GA UD430 UT WOS:A1996UD43000006 PM 8608529 ER PT J AU Kato, S Onda, M Matsukura, N Tokunaga, A Matsuda, N Yamashita, K Shields, PG AF Kato, S Onda, M Matsukura, N Tokunaga, A Matsuda, N Yamashita, K Shields, PG TI Genetic polymorphisms of the cancer related gene and Helicobacter pylori infection in Japanese gastric cancer patients an age and gender matched case-control study SO CANCER LA English DT Article; Proceedings Paper CT 7th Annual Meeting of the Japanese-Research-Society-for-Gastroenterological-Carcinogenesis CY SEP 08-09, 1995 CL OITA, JAPAN SP Japanese Res Soc Gastroenterol Carcinogenesis DE genetic polymorphism; cytochrome p450; Helicobacter pylori; gastric cancer susceptibility; glutathione-S-transferase; L-myc protooncogene ID FRAGMENT-LENGTH-POLYMORPHISM; SERUM PEPSINOGEN-I; L-MYC GENE; LUNG-CANCER; STOMACH-CANCER; CYTOCHROME-P450IIE1; METASTASIS; RISK; CARCINOGENESIS; SUSCEPTIBILITY AB BACKGROUND. Gastric cancer is a multistage process, each caused by numerous factors. The objective of this study was to elucidate the risk factors for gastric cancer by using molecular epidemiologic techniques and serum markers. METHODS. Serum pepsinogen I levels, pepsinogen I/pepsinogen II (I/II) ratios, serum IgG antibody against Helicobacter pylori (H. pylori), and genetic polymorphisms of cytochrome p450 2E1 (CYP2E1), glutathione-S-transferase M1 (GSTM1), and L-myc protooncogenes were analyzed in 82 persons with gastric cancer and in 151 age- and sex-matched controls, who were selected from 208 gastric cancer patients and 375 noncancer patients, respectively. Statistical analysis was performed to elucidate which risk factors for gastric cancer were contributing the most to gastric carcinogenicity. RESULTS. Serum pepsinogen I level (odds ratio [OR] = 1.81; 95% confidence interval [CI], 1.04-3.16) and pepsinogen I/II ratios (OR = 3.09; 95% CI, 1.74-5.49) were significantly associated with gastric cancer risk in a case-control study. Seropositivity of serum IgG antibody against H. pylori (OR = 1.25; 95% CI, 0.84-1.85) and specific genotypes of a L-myc genetic polymorphism (OR = 1.33; 95% CI, 0.59-2.99) were more commonly observed in gastric cancer cases, but this was not statistically significant. Specific genotypes of the CYP2E1 RsaI polymorphism and GSTM1 gene deletion were not associated with gastric cancer. CONCLUSIONS. Atrophic mucosal change, indicated by serum pepsinogen levels, is possible a risk factor for gastric cancer. X. pylori infection and genetic polymorphisms of CYP2E1, L-myc, and GSTM1 genetic polymorphisms were not risk factors in this study. (C) 1996 American Cancer Society. C1 NCI,HUMAN CARCINOGENESIS LAB,DIV CANC ETIOL,NIH,BETHESDA,MD 20892. RP Kato, S (reprint author), NIPPON MED COLL,DEPT SURG 1,BUNKYO KU,1-1-5 SENDAGI,TOKYO 113,JAPAN. RI Shields, Peter/I-1644-2012 NR 39 TC 67 Z9 68 U1 0 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 15 PY 1996 VL 77 IS 8 SU S BP 1654 EP 1661 DI 10.1002/(SICI)1097-0142(19960415)77:8+<1654::AID-CNCR11>3.0.CO;2-X PG 8 WC Oncology SC Oncology GA UE554 UT WOS:A1996UE55400011 PM 8608558 ER PT J AU McCormick, DL Rao, KVN Johnson, WD BowmanGram, TA Steele, VE Lubet, RA Kelloff, GJ AF McCormick, DL Rao, KVN Johnson, WD BowmanGram, TA Steele, VE Lubet, RA Kelloff, GJ TI Exceptional chemopreventive activity of low-dose dehydroepiandrosterone in the rat mammary gland SO CANCER RESEARCH LA English DT Article ID LONG-TERM TREATMENT; INHIBITION; MICE; 7,12-DIMETHYLBENZANTHRACENE; CARCINOGENESIS; 3-BETA-METHYLANDROST-5-EN-17-ONE; SUSCEPTIBILITY; TUMORIGENESIS; METABOLISM; DHEA AB To determine if the chemopreventive activity of dehydroepiandrosterone (DHEA) in the rat mammary gland can be dissociated from its toxicity, two studies were conducted in which low doses of DHEA were administered alone and in combination with other agents to rats treated with N-methyl-N-nitrosourea, Beginning 1 week prior to administration of 35 mg N-methyl-N-nitrosourea per kg body weight, groups of 20 female Sprague-Dawley rats were fed AIN-76A diet supplemented with DHEA alone (800 or 400 mg/kg diet), DHEA + tamoxifen (80 or 40 mu g/kg diet), DHEA + carbenoxolone (3500 or 1750 mg/kg diet), or DHEA + tamoxifen + carbenoxolone. When administered alone at either 800 or 100 mg/kg diet, DHEA reduced mammary cancer incidence from >70% in dietary controls to 0%; mammary cancer incidence in all DHEA combination regimens was also less than or equal to 5%. The dose levels of DHEA used induced no toxicity or alteration in body weight gain, These results indicate that dietary supplementation with low doses of DHEA has chemopreventive efficacy greater than or equal to that of endocrine ablation, This protection may be mediated by the induction of differentiation in the mammary parenchyma. C1 NCI,CHEMOPREVENT INVEST STUDIES BRANCH,BETHESDA,MD 20852. RP McCormick, DL (reprint author), IIT,DEPT LIFE SCI,10 W 35TH ST,CHICAGO,IL 60616, USA. FU NCI NIH HHS [CA-30646, N01-CN-85097-11] NR 24 TC 47 Z9 49 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1996 VL 56 IS 8 BP 1724 EP 1726 PG 3 WC Oncology SC Oncology GA UE735 UT WOS:A1996UE73500005 PM 8620482 ER PT J AU Steller, MA Delgado, CH Bartels, CJ Woodworth, CD Zou, ZQ AF Steller, MA Delgado, CH Bartels, CJ Woodworth, CD Zou, ZQ TI Overexpression of the insulin-like growth factor-1 receptor and autocrine stimulation in human cervical cancer cells SO CANCER RESEARCH LA English DT Article ID FACTOR-I RECEPTOR; PAPILLOMAVIRUS TYPE-16; DNA AB We characterized mechanisms of growth control involving insulin-like growth factor-1 (IGF-I), IGF-2, and IGF-I receptor (IGF-IR) by investigating their expression in human cervical cancer cell lines, primary cervical tumor cell cultures, and normal ectocervical epithelial cells maintained in short-term culture, By reverse transcription followed by PCR, IGF-1 mRNA was not detected in any of the cell lines, whereas IGF-2-mRNA transcripts were detected in all of them, Using the RNase protection assay, low levels of IGF-2 mRNA were also detected in all of the cervical cancer cell lines, primary cervical tumor cell cultures, and normal ectocervical cultures tested, but no IGF-1 transcripts were detected, Scatchard analysis revealed 3- and 5-fold increases in IGF-1R expression by the primary cervical cancer cell cultures and cervical cancer cell lines, respectively, compared with the normal ectocervical cells, In proliferation assays, epidermal growth factor (EGF) consistently enhanced cervical cancer cell growth, but an antisense oligonucleotide to IGF-2 uniformly inhibited the EGF-induced mitogenic effect, These studies suggest that autocrine production of IGF-2 and overexpression of the IGF-1R are important components controlling the proliferation of cervical carcinoma cells, and that autocrine IGF-2 production in cervical cancer cells may participate in the mitogenic signaling of EGF. C1 NCI,BIOL LAB,BETHESDA,MD 20892. RP Steller, MA (reprint author), NCI,GYNECOL ONCOL SECT,SURG BRANCH,BLDG 10,ROOM 2B-42,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 30 TC 63 Z9 66 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1996 VL 56 IS 8 BP 1761 EP 1765 PG 5 WC Oncology SC Oncology GA UE735 UT WOS:A1996UE73500013 PM 8620490 ER PT J AU Gallahan, D Jhappan, C Robinson, G Hennighausen, L Sharp, R Kordon, E Callahan, R Merlino, G Smith, GH AF Gallahan, D Jhappan, C Robinson, G Hennighausen, L Sharp, R Kordon, E Callahan, R Merlino, G Smith, GH TI Expression of a truncated Int3 gene in developing secretory mammary epithelium specifically retards lobular differentiation resulting in tumorigenesis SO CANCER RESEARCH LA English DT Article ID TRANSGENIC MICE; TGF-ALPHA; GLAND; OVEREXPRESSION; CELLS AB Insertional mutation of the Int3 gene, a member of the Notch gene family, is frequently associated with primary mouse mammary tumors induced by the mouse mammary tumor virus (MMTV). A major consequence of these mutations Is the production of a shortened 2,4-kb tumor-specific Int3 RNA transcript that encodes the entire intracellular domain of the Int3 protein, Previous studies have demonstrated that mammary gland development and function was severely impaired in transgenic mice expressing the truncated Int3 gene product from the MMTV viral promoter, Both mammary ductal growth and secretory lobule development were curtailed in these mice, These results were attributed to a gain of function modification of the Int3 gene, which led to a restriction of cell fate selection in the affected mammary epithelial cells, To confirm and extend these findings, truncated Int3 was expressed from the whey acidic protein (WAP) promoter, the activity of which, unlike that of the MMTV long terminal repeat, is restricted to the secretory mammary epithelial population, In transgenic mice carrying the WAP/Int3 construct, mammary ductal growth was unaffected in virgin females, but growth and differentiation of secretory lobules during gestation was profoundly inhibited, Coincidental with the block in lobular secretory differentiation, mammary dysplasia and tumorigenesis occurred in all breeding females by 25 weeks of age, In nonbreeding WAP/Int3 females, mammary tumor incidence also reached 100%, but only after 70 weeks. The WAP/Int3 mammary tumors were highly malignant, and most tumor-bearing females, irrespective of breeding history, developed metastatic lung lesions, These results suggest that WAP promoter-targeted Int3 function is associated with mammary secretory cell differentiation and maintenance in this transgenic model, Consistent with the conclusion that WAP-driven truncated Int3 expression influenced only lobular differentiation and not ductal growth and extension during mammary gland development, transplants of I VAP/Int3 gland into nontransgenic mammary fat pads produced complete mammary ductal outgrowths in virgin FVB/N mice but failed to develop secretory lobules when the females were impregnated. C1 NCI,TUMOR IMMUNOL & BIOL LAB,BETHESDA,MD 20892. NIDDK,BIOCHEM & METAB LAB,NIH,BETHESDA,MD 20892. RI Robinson, Gertraud/I-2136-2012 NR 26 TC 134 Z9 138 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1996 VL 56 IS 8 BP 1775 EP 1785 PG 11 WC Oncology SC Oncology GA UE735 UT WOS:A1996UE73500016 PM 8620493 ER PT J AU Blagosklonny, MV Schulte, T Nguyen, P Trepel, J Neckers, LM AF Blagosklonny, MV Schulte, T Nguyen, P Trepel, J Neckers, LM TI Taxol-induced apoptosis and phosphorylation of Bcl-2 protein involves c-Raf-1 and represents a novel c-Raf-1 signal transduction pathway SO CANCER RESEARCH LA English DT Article ID KINASE; RAF-1 AB c-Raf-l (Raf-l) is a central component of signal transduction pathways stimulated by various growth factors, protein kinase C, and other protein kinases. Raf-l activation is thought to be initiated at the plasma membrane after its recruitment by Ras, Raf-l activation is associated primarily with proliferation and cell survival, but it has also been implicated in apoptosis, Raf-l has also been shown to form complexes with both R-Ras and Bcl-2, raising the possibility that this component of cellular Raf-l plays a role in apoptosis, Recently, taxol was reported to induce Bcl-2 phosphorylation and inactivation, We have previously demonstrated Raf-l activation following taxol in MCF7 cells, We now present evidence that taxol fails to stimulate either apoptosis or phosphorylation of Bcl-2 in the absence of Raf-l, Moreover, Raf-l activation by taxol coincided with Bcl-2 phosphorylation, showing similar dose and time dependence, Thus, our data support a role for a distinct subcellular component of Raf-l, which is taxol but not phorbol myristate acetate sensitive, in mediating an apoptotic pathway involving Bcl-2. C1 NCI,CLIN PHARMACOL BRANCH,NIH,BETHESDA,MD 20892. NR 27 TC 355 Z9 368 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1996 VL 56 IS 8 BP 1851 EP 1854 PG 4 WC Oncology SC Oncology GA UE735 UT WOS:A1996UE73500026 PM 8620503 ER PT J AU vanderPluijm, G Vloedgraven, HJM Ivanov, B Robey, FA Grzesik, WJ Robey, PG Papapoulos, SE Lowik, CWGM AF vanderPluijm, G Vloedgraven, HJM Ivanov, B Robey, FA Grzesik, WJ Robey, PG Papapoulos, SE Lowik, CWGM TI Bone sialoprotein peptides are potent inhibitors of breast cancer cell adhesion to bone SO CANCER RESEARCH LA English DT Article ID CYCLIC RGD PEPTIDE; MESSENGER-RNA; DEVELOPMENTAL EXPRESSION; VITRONECTIN RECEPTOR; TUMOR-METASTASIS; RAT OSTEOCLASTS; MATRIX; OSTEOPONTIN; INTEGRINS; RESORPTION AB Bone and bone marrow are important sites of metastasis formation in breast cancer. Extracellular matrix proteins with attachment properties are generally believed to play a key role in tumorigenesis and metastasis formation, We have investigated whether mammary carcinoma cells (MDA-MB-231) can recognize constructs of the fairly bone-specific human bone sialoprotein, which encompass the RGD sequence (EPRGDNYR), Exogenously added bone sialoprotein peptides with this amino acid sequence in their backbone structure, but not the more common fibronectin-derived GRGDS peptide, strongly inhibited breast cancer cell adhesion to extracellular bone matrix at micromolar concentrations, Most cyclic derivatives with the EPRGDNYR sequence were more effective inhibitors of tumor cell adhesion to bone than their linear equivalents, Furthermore, changes in the RGD-tripeptide of the backbone structure of the constructs, removal of the NYR flanking sequence, or a different tertiary cyclic structure significantly decreased their inhibitory potencies, In addition, the RGE-analogue EPRGENYR was capable of inhibiting breast cancer cell adhesion to bone, albeit to a lesser extent. We conclude, therefore, that the inhibitory potency of the bone sialoprotein-derived peptides on breast cancer cell adhesion to bone is not solely due to a properly positioned RGD-motif alone but is also determined by its flanking regions, together with the tertiary structure of the EPRGDNYR peptide, Synthetic cyclic constructs with the EPRGDNYR sequence may, therefore, be potentially useful as antiadhesive agents for cancer cells to bone in vivo. C1 NIDR, CELLULAR DEV & ONCOL LAB, PEPTIDE & IMMUNOCHEM UNIT, NIH, BETHESDA, MD 20892 USA. RP vanderPluijm, G (reprint author), LEIDEN UNIV HOSP, DEPT ENDOCRINOL & METAB DIS C489, POB 9600, 2300 RC LEIDEN, NETHERLANDS. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 59 TC 56 Z9 57 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1996 VL 56 IS 8 BP 1948 EP 1955 PG 8 WC Oncology SC Oncology GA UE735 UT WOS:A1996UE73500041 PM 8620518 ER PT J AU Lauer, MS Okin, PM Larson, MG Evans, JC Levy, D AF Lauer, MS Okin, PM Larson, MG Evans, JC Levy, D TI Impaired heart rate response to graded exercise - Prognostic implications of chronotropic incompetence in the Framingham Heart Study SO CIRCULATION LA English DT Article DE mortality; heart rate; exercise testing; coronary heart disease ID PHYSICAL-ACTIVITY; DISEASE; RISK; MEN AB Background Previous reports have suggested that an attenuated exercise heart rate response may be associated with coronary heart disease risk and with mortality. These observations may parallel the association between reduced heart rate variability during normal activities and adverse outcome. This investigation was designed to look at the prognostic implications of exercise heart rate response in a population-based sample. Methods and Results In this prospective cohort investigation, 1575 male participants (mean age, 43 years) in the Framingham Offspring Study who were free of coronary heart disease, who were not taking beta-blockers, and who underwent submaximal treadmill exercise testing (Bruce protocol) were studied. Heart rate response was assessed in three ways: (1) failure to achieve 85% of the age-predicted maximum heart rate, which has been the traditional definition of chronotropic incompetence; (2) the actual increase in heart rate from rest to peak exercise; and (3) the ratio of heart rate to metabolic reserve used by stage 2 of exercise (''chronotropic response index''). Proportional hazards analyses were used to evaluate the associations of heart rate responses with all-cause mortality and with coronary heart disease incidence during 7.7 years of follow-up. Failure to achieve target heart rate occurred in 327 (21%) subjects. During follow-up there were 55 deaths (14 caused by coronary heart disease) and 95 cases of incident coronary heart disease. Failure to achieve target heart rate, a smaller increase in heart rate with exercise, and the chronotropic response index were predictive of total mortality and incident coronary heart disease (P<.01). Failure to achieve target heart rate remained predictive of incident coronary heart disease even after adjusting for age, ST-segment response, physical activity, and traditional coronary disease risk factors (adjusted hazard ratio, 1.75; 95% confidence interval, 1.11 to 2.74; P=.02). After adjusting for the same factors, the increase in exercise heart rate remained inversely predictive of total mortality (P=.04) and coronary heart disease incidence (P=.0003). The chronotropic response index also was predictive of total mortality (P=.05) and incident coronary heart disease (P=.001) after adjusting for age and other risk factors. Conclusions An attenuated heart rate response to exercise, a manifestation of chronotropic incompetence, is predictive of increased mortality and coronary heart disease incidence. C1 NEW YORK HOSP,CORNELL MED CTR,DEPT CARDIOL,NEW YORK,NY. BOSTON UNIV,SCH MED,DEPT EPIDEMIOL & PREVENT MED,BOSTON,MA. NHLBI,FRAMINGHAM HEART STUDY,FRAMINGHAM,MA. RP Lauer, MS (reprint author), CLEVELAND CLIN FDN,DEPT CARDIOL,DESK F-15,9500 EUCLID AVE,CLEVELAND,OH 44195, USA. RI Lauer, Michael/L-9656-2013 OI Lauer, Michael/0000-0002-9217-8177 NR 26 TC 306 Z9 322 U1 1 U2 14 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR 15 PY 1996 VL 93 IS 8 BP 1520 EP 1526 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA UE620 UT WOS:A1996UE62000009 PM 8608620 ER PT J AU Antinore, MJ Birrer, MJ Patel, D Nader, L McCance, DJ AF Antinore, MJ Birrer, MJ Patel, D Nader, L McCance, DJ TI The human papillomavirus type 16 E7 gene product interacts with and trans-activates the AP1 family of transcription factors SO EMBO JOURNAL LA English DT Article DE AP1; E7; human papillomavirus; Jun ID DNA-BINDING ACTIVITY; ADENOVIRUS E1A PROTEINS; CASEIN KINASE-II; EPITHELIAL-CELL DIFFERENTIATION; OPEN READING FRAME; RAT EMBRYO CELLS; C-JUN; HUMAN KERATINOCYTES; CERVICAL-CARCINOMA; NUCLEAR-PROTEIN AB The E7 gene product of human papillomavirus type 16 (HPV16) binds to the retinoblastoma gene product (pRb) and dissociates pRb-E2F complexes. However, the observation that the ability of E7 to bind pRb is not required for the HPV16-induced immortalization of primary keratinocytes prompted a search for other cellular factors bound by E7. Using a glutathione-S-transferase (GST) fusion protein system, we show that E7 complexes with AP1 transcription factors including c-Jun, JunB, JunD and c-Fos. The ability of E7 to complex with c-Jun in vivo is demonstrated by co-immunoprecipitation and the yeast two-hybrid system. An analysis of E7 point mutants in the GST system indicates that the E7 zinc-finger motif, but not the pRb binding domain, is involved in these interactions. Using c-Jun deletion mutants, E7 binding maps between amino acids 224 and 286 of c-Jun. E7 trans-activates c-Jun-induced transcription from a Jun responsive promoter, and this activity correlates with the ability of E7 mutants to bind Jun proteins. Finally, a transcriptionally inactive c-Jun deletion, which can bind E7, interferes with the E7-induced transformation of rat embryo fibroblasts in cooperation with an activated ras, indicating that the Jun-E7 interaction is physiologically relevant and that Jun factors may be targeted in the E7 transformation pathway. C1 UNIV ROCHESTER,DEPT MICROBIOL & IMMUNOL,ROCHESTER,NY 14642. NCI,BIOMARKERS & PREVENT RES BRANCH,DIV CANC PREVENT & CONTROL,ROCKVILLE,MD 20850. FU NIAID NIH HHS [AI 30798-05, T32 AI07362-01] NR 72 TC 156 Z9 158 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR 15 PY 1996 VL 15 IS 8 BP 1950 EP 1960 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UG748 UT WOS:A1996UG74800023 PM 8617242 ER PT J AU Tuomisto, J Sewall, CH Unkila, M Pohjanvirta, R Clark, GC Viluksela, M Rozman, K Lucier, GW AF Tuomisto, J Sewall, CH Unkila, M Pohjanvirta, R Clark, GC Viluksela, M Rozman, K Lucier, GW TI Differences in binding of epidermal growth factor to liver membranes of TCDD-resistant and TCDD-sensitive rats after a single dose of TCDD SO ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY LA English DT Article DE dioxin; TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin); EGF (epidermal growth factor); EGF receptor; phosphoenolpyruvate carboxykinase (PEPCK); TCDD-resistant rat; TCDD-sensitive rat; strain difference; liver, rat ID HEPATIC PLASMA-MEMBRANE; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; FACTOR RECEPTOR; PHOSPHOENOLPYRUVATE CARBOXYKINASE; EGF RECEPTOR; EXPRESSION; INVIVO; STRAIN; TOXICITY; INCREASE AB Epidermal growth factor (EGF) receptor has been implied as having a role in certain actions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). After a single dose of TCDD, the receptor has been shown to be downregulated in several tissues including the liver. Two rat substrains, the Han/Wistar (Kuopio; H/W) rat and the Long-Evans (Turku AB; L-E) rat exhibit over a 1000-fold difference in their sensitivity to the lethal effect of TCDD, This large sensitivity difference was utilized in the current study to investigate whether or not a correlation exists between TCDD lethality and biochemical endpoints related to the hepatic EGF receptor. In the TCDD-sensitive L-E strain both the B-max of the EGF receptor and the receptor protein as measured by Western blots, decreased dose and time dependently. Ten days after a lethal dose of TCDD (50 mu g/kg), the downregulation was 80%. In the resistant H/W strain, two non-lethal doses were used (50 and 500 mu g/kg), since the lethal dose is not known, These doses caused a downregulation already at 4 days after dosing, but no further decrease by day 10. The activity of phosphoenolpyruvate carboxykinase (PEPCK, the main gluconeogenetic enzyme in the liver and a proposed target of TCDD) decreased in H/W rats at least to the same extent as in L-E rats at both 4 and 10 days, It is concluded that EGF receptor downregulation is different in the two rat strains studied, despite the fact that a classical Ah receptor-regulated response (CYP1Al induction) is similar. The results demonstrate that downregulation of the EGF receptor by TCDD is strain-dependent as well as dose- and time-dependent. C1 NATL INST ENVIRONM HLTH,BIOCHEM RISK ANAL LAB,RES TRIANGLE PK,NC 27709. UNIV KANSAS,MED CTR,DEPT PHARMACOL TOXICOL & THERAPEUT,KANSAS CITY,KS 66160. RP Tuomisto, J (reprint author), NATL PUBL HLTH INST,DEPT TOXICOL,DIV ENVIRONM HLTH,POB 95,FIN-70701 KUOPIO,FINLAND. NR 33 TC 3 Z9 3 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1382-6689 J9 ENVIRON TOXICOL PHAR JI Environ. Toxicol. Pharmacol. PD APR 15 PY 1996 VL 1 IS 2 BP 109 EP 116 DI 10.1016/1382-6689(95)00016-X PG 8 WC Environmental Sciences; Pharmacology & Pharmacy; Toxicology SC Environmental Sciences & Ecology; Pharmacology & Pharmacy; Toxicology GA UT284 UT WOS:A1996UT28400004 PM 21781670 ER PT J AU Mermelstein, F Yeung, K Cao, J Inostroza, JA ErdjumentBromage, H Eagelson, K Landsman, D Levitt, P Tempst, P Reinberg, D AF Mermelstein, F Yeung, K Cao, J Inostroza, JA ErdjumentBromage, H Eagelson, K Landsman, D Levitt, P Tempst, P Reinberg, D TI Requirement of a corepressor for Dr1-mediated repression of transcription SO GENES & DEVELOPMENT LA English DT Article DE Dr1-mediated repression; corepression of transcription; HeLa cells; heterodimer formation ID RNA POLYMERASE-II; TATA-BINDING-PROTEIN; SACCHAROMYCES-CEREVISIAE; PREINITIATION COMPLEX; PROMOTER INTERACTIONS; GENE-TRANSCRIPTION; LESS PROMOTER; TFIID COMPLEX; PURIFICATION; ACTIVATION AB A Dr1-associated polypeptide (DRAP1) was isolated from HeLa cells and found to function as a corepressor of transcription. Corepressor function requires an interaction between DRAP1 and Dr1. Heterodimer formation was dependent on a histone fold moth present at the amino terminus of both polypeptides. Association of DRAP1 with Dr1 results in higher stability of the Dr1-TBP-TATA moth complex and precluded the entry of TPIIA and/or TFIIB to preinitiation complexes. DRAP1 was found to be expressed in all tissues analyzed with higher levels in tissues with a low mitotic index. Analysis of DRAP1 in the developing brain of rat demonstrated undetectable levels of DRAP1 in actively dividing cells but high levels of DRAP1 expression in differentiated non dividing cells. Dr1 was immunodetected in all cells analyzed. A model for DRAP1-dependent, Dr1-mediated repression of transcription is proposed. C1 UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT BIOCHEM,HOWARD HUGHES MED INST,PISCATAWAY,NJ 08854. MEM SLOAN KETTERING CANC CTR,PROGRAM MOLEC BIOL,NEW YORK,NY 10021. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT NEUROBIOL,PISCATAWAY,NJ 08854. NATL LIB MED,NATL CTR BIOTECHNOL INFORMAT,NIH,BETHESDA,MD 20894. RI Landsman, David/C-5923-2009; OI Landsman, David/0000-0002-9819-6675 NR 82 TC 105 Z9 108 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD APR 15 PY 1996 VL 10 IS 8 BP 1033 EP 1048 DI 10.1101/gad.10.8.1033 PG 16 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA UJ343 UT WOS:A1996UJ34300011 PM 8608938 ER PT J AU Wang, JY Walker, H Lin, Q Jenkins, N Copeland, NG Watanabe, T Burrows, PD Cooper, MD AF Wang, JY Walker, H Lin, Q Jenkins, N Copeland, NG Watanabe, T Burrows, PD Cooper, MD TI The mouse BP-1 gene: Structure, chromosomal localization, and regulation of expression by type I interferons and interleukin-7 SO GENOMICS LA English DT Article ID TRANSFORMATION-ASSOCIATED ANTIGEN; PRE-B-CELLS; MURINE INTERLEUKIN-7; MOLECULAR-CLONING; AMINOPEPTIDASE-A; BONE-MARROW; DIFFERENTIATION; ORGANIZATION; RECEPTOR; DISTINCT AB The BP-1/6C3 antigen is a homodimeric, phosphorylated type II membrane integral glycoprotein expressed on immature B-lineage cells, bone marrow stromal cells, thymic cortical epithelial cells, endothelial cells, enterocytes, and renal proximal tubular cells. Biochemical and molecular analysis identified BP-1 as glutamyl aminopeptidase, an ectoenzyme that catalyzes the hydrolysis of acidic amino acid residues from the amino termini of regulatory peptides. We have isolated genomic clones that encode the BP-1 gene (gene symbol Enpep). The gene spans more than 110 kb and contains 20 exons. Except for the first and the last exons, it is composed of small exons ranging from 56 to 171 bp that are separated by introns ranging from less than 100 bp to approximately 10 kb. The zinc binding motif HEXXH and the glutamic acid residue 19 amino acids downstream, which also binds zinc, are encoded in exons 5 and 6. Primer extension analysis revealed a common major transcriptional start site in a pre-B cell line, in a bone marrow stromal cell line, and in kidney cells. The promoter region contains a TATA-like element and potential DNA-binding motifs for lymphocyte-specific transcription factors including Ikaros, BSAP, PU.1, and octamer binding proteins, as well as DNA binding motifs for several ubiquitous transcription factors. An interferon responsive element also located in the promoter region appeared to be functional, since type I interferons (IFN-alpha/IFN-beta) upregulated BP-1 expression in pre-B cell lines. A 2.1-kb promoter fragment, when fused to a luciferase reporter gene, was able to drive luciferase expression in pre-B cells, which normally express BP-1, and ill Ag8 cells, in which BP-1 expression is extinguished. The BP-1/Enpep gene was localized to a distal region of mouse chromosome 3 in a region homologous to human chromosome 4q25. Interestingly, while interleukin-7 (IL-7) induced both cell growth and increased BP-1 expression, IFN-alpha/IFN-beta upregulated BP-1 expression but inhibited IL-7-induced proliferation. This finding indicates that the upregulated BP-1 expression can be disassociated from the cell growth signal. (C) 1996 Academic Press, Inc. C1 UNIV ALABAMA,WALLACE TUMOR INST 386,HOWARD HUGHES MED INST,BIRMINGHAM,AL 35294. UNIV ALABAMA,DIV DEV & CLIN IMMUNOL,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT PEDIAT,BIRMINGHAM,AL 35294. UNIV ALABAMA,DEPT MICROBIOL,BIRMINGHAM,AL 35294. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. KYUSHU UNIV,MED INST BIOREGULAT,FUKUOKA 81282,JAPAN. FU NCI NIH HHS [N01-CO-46000]; NIAID NIH HHS [AI 34568, AI 39816] NR 48 TC 32 Z9 32 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR 15 PY 1996 VL 33 IS 2 BP 167 EP 176 DI 10.1006/geno.1996.0180 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA UH006 UT WOS:A1996UH00600003 PM 8660964 ER PT J AU Long, GL Winfield, S Adolph, KW Ginns, EI Bornstein, P AF Long, GL Winfield, S Adolph, KW Ginns, EI Bornstein, P TI Structure and organization of the human metaxin gene (MTX) and pseudogene SO GENOMICS LA English DT Article ID GLUCOCEREBROSIDASE GENE; GAUCHER DISEASE; TARGETED DISRUPTION; LEADER SEQUENCE; EVOLUTION; MODEL; EXPRESSION; MURINE; MUCIN AB Metaxin encodes a mitochondrial protein and is an essential nuclear gene in mice. The cDNA sequence and genomic organization of the human metaxin gene (MIX) have now been determined, MIX is 6 kb and consists of eight protein-encoding exons, The gene is contiguous to thrombospondin 3 (THBS3) and to the pseudogene for glucocerebrosidase (psGBA), but is transcribed in a direction opposite to the latter two genes. Thus, MIX and THBS3 share a common promoter region and are transcribed divergently, whereas MIX and psGBA are transcribed convergently and have closely apposed polyadenylation sites, Human metaxin contains 317 amino acids and is 91.5% identical to mouse metaxin. Metaxin is rich in leucine (14.2%) and in basic (12.9%) and acidic (12.0%) amino acids, The predicted protein lacks an amino-terminal signal sequence and N-glycosylation sites, but contains a putative transmembrane domain near its carboxy terminus, A DNA duplication has led to a direct repeat and the evolution of a pseudogene for GBA. A pseudogene for metaxin (psMTX) is also located within the 16 kb of DNA separating GBA from psGBA. The psMTX sequence is nearly identical to the 3' part of exon 2 through exon 8 of MTX, and both the intronic and the 3'-flanking sequences are highly conserved, Thus, there is a 278 amino acid open reading frame that is 97.8% identical to metaxin. However, psMTX lacks the first intron and promoter present in MIX and at least in liver, the pseudogene is not expressed. (C) 1996 Academic Press, Inc. C1 UNIV WASHINGTON,DEPT BIOCHEM,SEATTLE,WA 98195. NIMH,CLIN NEUROSCI BRANCH,IRP,BETHESDA,MD 20892. FU NCI NIH HHS [CO6-HL39745]; NIDCR NIH HHS [DE 08229] NR 24 TC 32 Z9 33 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 0888-7543 J9 GENOMICS JI Genomics PD APR 15 PY 1996 VL 33 IS 2 BP 177 EP 184 DI 10.1006/geno.1996.0181 PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA UH006 UT WOS:A1996UH00600004 PM 8660965 ER PT J AU Savitsky, K Ziv, Y BarShira, A Gilad, S Tagle, DA Smith, S Uziel, T Sfez, S Nahmias, J Sartiel, A Eddy, RL Shows, TB Collins, FS Shiloh, Y Rotman, G AF Savitsky, K Ziv, Y BarShira, A Gilad, S Tagle, DA Smith, S Uziel, T Sfez, S Nahmias, J Sartiel, A Eddy, RL Shows, TB Collins, FS Shiloh, Y Rotman, G TI A human gene (DDX10) encoding a putative DEAD-box RNA helicase at 11q22-q23 SO GENOMICS LA English DT Article ID TRANSLATION INITIATION FACTOR-4A; A-D BOX; ESCHERICHIA-COLI; RIBOSOMAL-RNA; PROTEIN; DROSOPHILA; SEQUENCE; SIMILARITY; DISEASE; HYBRIDS AB A human gene encoding a putative RNA helicase, designated DDX10, was identified 400 kb telomeric to the ataxia-telangiectasia gene at chromosome 11q22-q23. The predicted amino acid sequence shows very high similarity to a subgroup of DEAD-box RNA helicases involved in ribosome biogenesis. This novel gene encodes a 3.2-kb transcript in a variety of human tissues. A processed pseudogene of DDX10 was detected at chromosome 9q21-q22. We observed a rare trinucleotide repeat length polymorphism within the coding sequence of DDX10. (C) 1996 Academic Press, Inc. C1 TEL AVIV UNIV, SACKLER SCH MED, DEPT HUMAN GENET, IL-69978 RAMAT AVIV, ISRAEL. NIH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA. UCL, GALTON LAB, MRC, HUMAN BIOCHEM GENET UNIT, LONDON NW1 2HE, ENGLAND. NEW YORK STATE DEPT HLTH, ROSWELL PK CANC INST, DEPT HUMAN GENET, BUFFALO, NY 14263 USA. FU NINDS NIH HHS [NS31763] NR 39 TC 40 Z9 42 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD APR 15 PY 1996 VL 33 IS 2 BP 199 EP 206 DI 10.1006/geno.1996.0184 PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA UH006 UT WOS:A1996UH00600007 PM 8660968 ER PT J AU Lopez, JV Cevario, S OBrien, SJ AF Lopez, JV Cevario, S OBrien, SJ TI Complete nucleotide sequences of the domestic cat (Felis catus) mitochondrial genome and a transposed mtDNA tandem repeat (Numt) in the nuclear genome SO GENOMICS LA English DT Article ID D-LOOP REGION; MOLECULAR PHYLOGENY; DNA DAMAGE; FIN WHALE; EVOLUTION; GENES; MUTATION; ORGANIZATION; HETEROPLASMY; SUBSTITUTION AB The complete 17,009-bp mitochondrial genome of the domestic cat, Felis catus, has been sequenced and conforms largely to the typical organization of previously characterized mammalian mtDNAs. Codon usage and base composition also followed canonical vertebrate patterns, except for an unusual ATC (non-AUG) codon initiating the NADH dehydrogenase subunit 2 (ND2) gene. Two distinct repetitive motifs at opposite ends of the control region contribute to the relatively large size (1559 bp) of this carnivore mtDNA. Alignment of the feline mtDNA genome to a homologous 7946-bp nuclear mtDNA tandem repeat DNA sequence in the cat, Numt, indicates simple repeat motifs associated with insertion/deletion mutations. Overall DNA sequence divergence between Numt and cytoplasmic mtDNA sequence was only 5.1%. Substitutions predominate at the third codon position of homologous feline protein genes. Phylogenetic analysis of mitochondrial gene sequences confirms the recent transfer of the cytoplasmic mtDNA sequences to the domestic cat nucleus and recapitulates evolutionary relationships between mammal species. (C) 1996 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,SAIC FREDERICK,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. GEORGE MASON UNIV,DEPT BIOL,FAIRFAX,VA 22030. RI Lopez, Jose/F-8809-2011 OI Lopez, Jose/0000-0002-1637-4125 NR 86 TC 180 Z9 204 U1 1 U2 15 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR 15 PY 1996 VL 33 IS 2 BP 229 EP 246 DI 10.1006/geno.1996.0188 PG 18 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA UH006 UT WOS:A1996UH00600011 PM 8660972 ER PT J AU Cerretti, DP Lyman, SD Kozlosky, CJ Copeland, NG Gilbert, DJ Jenkins, NA Valentine, V Kirstein, MN Shapiro, DN Morris, SW AF Cerretti, DP Lyman, SD Kozlosky, CJ Copeland, NG Gilbert, DJ Jenkins, NA Valentine, V Kirstein, MN Shapiro, DN Morris, SW TI The genes encoding the Eph-related receptor tyrosine kinase ligands LERK-1 (EPLG1, Epl1), LERK-3 (EPLG3, Epl3), and LERK-4 (EPLG4, EPl4) are clustered on human chromosome 1 and mouse chromosome 3 SO GENOMICS LA English DT Article ID FAMILY; IDENTIFICATION; EXPRESSION; HINDBRAIN; CLONING; CHICKEN; TUMOR; ELK AB Hek and elk are members of the eph-related family of receptor tyrosine kinases. Recently, we isolated five cDNAs encoding membrane-bound ligands to hek and elk. Because of the promiscuous nature of their binding, we have termed these proteins ligands of the ephrelated kinases or LERKs. The LERKs can be divided into two subgroups by virtue of their sequence identity, binding properties, and mode of cell membrane attachment. For example, LERK-2 (EPLG2, Ep12) and LERK-5 (EPLG5, Epl5) are type 1 transmembrane proteins, while LERK-1 (EPLG1, Epl1), LERK-3 (EPLG3, Epl3), and LERK-4 (EPLG4, Epl4) are anchored to the membrane by glycosyl-phosphatidylinositol (GPI) linkage. Using Southern hybridization analysis of human x rodent somatic cell hybrid DNAs, we have assigned the genes that encode the GPI-anchored LERKs (EPLG1, EPLG3, and EPLG4) to human chromosome 1. Fluorescence in situ hybridization to metaphase chromosome preparations using genomic clones from each locus refined this localization to chromosome 1, bands q21-q22. In addition, Southern blot analysis of DNA from interspecific backcross mice indicated that the mouse homologues Epl1, Epl3, and Epl4 map to a homologous region on mouse chromosome 3. (C) 1996 Academic Press, Inc. C1 NCI, FREDERICK CANC RES & DEV CTR, MAMMALIAN GENET LAB, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA. ST JUDE CHILDRENS RES HOSP, DEPT EXPTL ONCOL, MEMPHIS, TN 38101 USA. ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, MEMPHIS, TN 38101 USA. RP Cerretti, DP (reprint author), IMMUNEX RES & DEV CORP, 51 UNIV ST, SEATTLE, WA 98101 USA. FU NCI NIH HHS [CA23099, CA01702, CA21765] NR 36 TC 14 Z9 14 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 J9 GENOMICS JI Genomics PD APR 15 PY 1996 VL 33 IS 2 BP 277 EP 282 DI 10.1006/geno.1996.0192 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA UH006 UT WOS:A1996UH00600015 PM 8660976 ER PT J AU Carrington, M Martin, M Newell, W Beck, S Klitz, W AF Carrington, M Martin, M Newell, W Beck, S Klitz, W TI Association of alleles at loci located throughout the HLA complex SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,BCDP,FREDERICK,MD. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. UNIV CALIF BERKELEY,BERKELEY,CA. RI Newell, William/C-7995-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP O06 EP O06 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500007 ER PT J AU Cullen, M Noble, J Erlich, H Thorpe, K Beck, S Trowsdale, J Carrington, M AF Cullen, M Noble, J Erlich, H Thorpe, K Beck, S Trowsdale, J Carrington, M TI Mapping recombination sites in the HLA class II region. SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,FREDERICK,MD 21702. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. ROCHE MOL SYST,ALAMEDA,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP O02 EP O02 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500005 ER PT J AU Mann, DL Nelson, G Carrington, M Geodert, J Kaslow, R AF Mann, DL Nelson, G Carrington, M Geodert, J Kaslow, R TI Combinations of mhc genes influence HIV-1 disease course SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,SIAC INC,BETHESDA,MD 20892. NIAID,ROCKVILLE,MD. NIAID,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP O647 EP O647 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500648 ER PT J AU Wade, JA Ng, CM Harding, A Malasky, M Carrington, M AF Wade, JA Ng, CM Harding, A Malasky, M Carrington, M TI Stratified testing for HLA matching: Selection of identical SIB pairs using microsatellite loci across HLA SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV TORONTO,TTH REG HISTOCOMPATIBIL LAB,TORONTO,ON,CANADA. NCI,FRDC,SAIC,FREDERICK,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP O439 EP O439 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500438 ER PT J AU Assefi, N Kim, E Hodgson, W Ribaudo, R AF Assefi, N Kim, E Hodgson, W Ribaudo, R TI Engineering higher affinity variants of beta 2-microglobulin SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 NATL CANC INST,NIH,BETHESDA,MD. HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,COCONUT GROVE,FL 33133. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP P502 EP P502 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500502 ER PT J AU Begovich, AB Chang, JD Steiner, LL Aldrich, CA Zimmerman, PA AF Begovich, AB Chang, JD Steiner, LL Aldrich, CA Zimmerman, PA TI A comparison of HLA class II allele frequencies within Africa: Implications for vaccine development SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 ROCHE MOLEC SYST,ALAMEDA,CA. NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP P574 EP P574 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500577 ER PT J AU Hackett, JA Simonis, TB Mixon, A Wunderlich, J Ferrone, S Marincola, FM AF Hackett, JA Simonis, TB Mixon, A Wunderlich, J Ferrone, S Marincola, FM TI Variability in HLA-A2 antigen expression by melanoma cell lines. Functional implications SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NEW YORK MED COLL,VALHALLA,NY 10595. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP P110 EP P110 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500110 ER PT J AU Hollenbach, JA Barcellos, LF Thomson, G Winkler, C Winter, M Klitz, W AF Hollenbach, JA Barcellos, LF Thomson, G Winkler, C Winter, M Klitz, W TI HLA differentiation among Mesoamerican natives SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK,MD 21701. UNIV CALIF BERKELEY,BERKELEY,CA 94720. INST NATL ANTROPOL & HIST,OAXACA,MEXICO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP P329 EP P329 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500330 ER PT J AU Manns, A Mann, D Wilks, R Carrington, M Cranston, B Hanchard, B Blattner, W AF Manns, A Mann, D Wilks, R Carrington, M Cranston, B Hanchard, B Blattner, W TI HLA associated with HTLV-I seroconversion after transfusion SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV W INDIES,KINGSTON 7,JAMAICA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP P660 EP P660 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500663 ER PT J AU Martayan, A Fiscella, M Setini, A Ciccarelli, G Gambari, R Beretta, A Siccardi, A Appella, E Giacomini, P AF Martayan, A Fiscella, M Setini, A Ciccarelli, G Gambari, R Beretta, A Siccardi, A Appella, E Giacomini, P TI Conformation and surface expression of free HLA-CW1 heavy chains in beta(2)m defective cells SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 IST REGINA ELENA,I-00161 ROME,ITALY. UNIV FERRARA,I-44100 FERRARA,ITALY. DIBIT,HSR,MILAN,ITALY. NCI,NIH,BETHESDA,MD 20892. RI Gambari, Roberto/F-9555-2015 OI Gambari, Roberto/0000-0001-9205-6033 NR 0 TC 0 Z9 0 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP P503 EP P503 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500505 ER PT J AU Thomsen, M Cullen, M Carrington, M Foissac, A Abbal, M dePreval, C CrouauRoy, B CambonThomsen, A AF Thomsen, M Cullen, M Carrington, M Foissac, A Abbal, M dePreval, C CrouauRoy, B CambonThomsen, A TI Localisation of the recombination points in a family with two DR/DP recombinations SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 CHU PURPAN,INSERM U395,TOULOUSE,FRANCE. CHU PURPAN,CNRS UPR 8291,TOULOUSE,FRANCE. CHU RANGUEIL,IMMUNOL LAB,F-31054 TOULOUSE,FRANCE. NCI,FREDERICK,MD 21701. RI Thomsen, Mogens/B-7651-2011 OI Thomsen, Mogens/0000-0002-4546-0129 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP P359 EP P359 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500361 ER PT J AU Wang, ZG Marincola, FM Ferrone, S AF Wang, ZG Marincola, FM Ferrone, S TI Molecular analysis of the selective loss of HLA-A2 antigen expression by melanoma cells 624MEL28 SO HUMAN IMMUNOLOGY LA English DT Meeting Abstract C1 NEW YORK MED COLL,VALHALLA,NY 10595. NATL CANC INST,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD APR 15 PY 1996 VL 47 IS 1-2 BP P108 EP P108 PG 1 WC Immunology SC Immunology GA UM455 UT WOS:A1996UM45500109 ER PT J AU Brousseau, ME SantamarinaFojo, S Zech, LA Berard, AM Vaisman, BL Meyn, SM Powell, D Brewer, HB Hoeg, JM AF Brousseau, ME SantamarinaFojo, S Zech, LA Berard, AM Vaisman, BL Meyn, SM Powell, D Brewer, HB Hoeg, JM TI Hyperalphalipoproteinemia in human lecithin cholesterol acyltransferase transgenic rabbits - In vivo apolipoprotein A-I catabolism is delayed in a gene dose-dependent manner SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE high density lipoproteins; lipoproteins; apolipoprotein A-I; metabolism; cholesterol ID HIGH-DENSITY-LIPOPROTEIN; ESTER TRANSFER PROTEIN; HEPATIC LIPASE; PARTICLE-SIZE; PLASMA; METABOLISM; DEFICIENCY; RECEPTOR; KINETICS; LCAT AB Lecithin cholesterol acyltransferase (LCAT) is an enzyme involved in the intravascular metabolism of high density lipoproteins (HDLs). Overexpression of human LCAT (hLCAT) in transgenic rabbits leads to gene dose-dependent increases of total and HDL cholesterol concentrations. To elucidate the mechanisms responsible for this effect, I-131-HDL apoA-I kinetics were assessed in age- and sex-matched groups of rabbits (n = 3 each) with high, low, or no hLCAT expression. Mean total and HDL cholesterol concentrations (mg/dl), respectively, were 162 +/- 18 and 121 +/- 12 for high expressors (HE), 55 +/- 6 and 55 +/- 10 for low expressors (LE), and 29 +/- 2 and 28 +/- 4 for controls. Fast protein liquid chromatography analysis of plasma revealed that the HDL of both HE and LE were cholesteryl ester and phospholipid enriched, as compared with controls, with the greatest differences noted between HE and controls. These compositional changes resulted in an incremental shift in apparent HDL particle size which correlated directly with the level of hLCAT expression, such that HE had the largest HDL particles and controls the smallest. In vivo kinetic experiments demonstrated that the fractional catabolic rate (FCR, d(-1)) of apoA-I was slowest in HE (0.328 +/-0.03) followed by LE (0.408 +/- 0.01) and, lastly, by controls (0.528 +/- 0.04). ApoA-I FCR was inversely associated with HDL cholesterol level (r = -0.851, P < 0.01) and hLCAT activity (r = -0.816, P < 0.01). These data indicate that fractional catabolic rate is the predominant mechanism by which hLCAT overexpression differentially modulates HDL concentrations in this animal model. We hypothesize that LCAT-induced changes in HDL composition and size ultimately reduce apoA-I catabolism by altering apoA-I conformation and/or HDL particle regeneration. C1 NHLBI,LAB ANIM MED & SURG,NIH,BETHESDA,MD 20892. RP Brousseau, ME (reprint author), NHLBI,MOLEC DIS BRANCH,NIH,BLDG 10-ROOM 7N116,10 CTR DR MSC 1666,BETHESDA,MD 20892, USA. NR 56 TC 37 Z9 37 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR 15 PY 1996 VL 97 IS 8 BP 1844 EP 1851 DI 10.1172/JCI118614 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA UG083 UT WOS:A1996UG08300008 PM 8621767 ER PT J AU Taub, DD Anver, M Oppenheim, JJ Longo, DL Murphy, WJ AF Taub, DD Anver, M Oppenheim, JJ Longo, DL Murphy, WJ TI T lymphocyte recruitment by interleukin-8 (IL-8) - IL-8-induced degranulation of neutrophils releases potent chemoattractants for human T lymphocytes both in vitro and in vivo SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE chemotaxis; T lymphocytes; neutrophils; granules ID HUMAN POLYMORPHONUCLEAR LEUKOCYTES; PHORBOL MYRISTATE ACETATE; LYSOSOMAL ENZYME RELEASE; DELAYED-TYPE HYPERSENSITIVITY; HOST DEFENSE CYTOKINES; INVIVO IMMUNE-RESPONSE; TUMOR-NECROSIS-FACTOR; RED-BLOOD-CELLS; MESSENGER-RNA; RABBIT SKIN AB IL-8 has been shown to be a human neutrophil and T cell chemoattractant in vitro. In an effort to assess the in vivo effects of IL-8 on human leukocyte migration, we examined the ability of rhIL-8 to induce human T cell infiltration using a human/mouse model in which SCID mice were administered human peripheral blood lymphocytes intraperitoneally, followed by subcutaneous injections of rhIL-8. rhIL-8 induced predominantly murine neutrophil accumulation by 4 h after administration while recombinant human macrophage inflammatory protein-1 beta (rhMIP-1 beta)induced both murine monocytes and human T cell infiltration during the same time period as determined by immunohistology, Interestingly, 72 h after chemokine administration, a marked human T cell infiltrate was observed in the IL-8 injection site suggesting that rhIL-8 may be acting indirectly possibly through a murine neutrophil-derived T cell chemoattractant, This hypothesis was confirmed using granulecyte-depleted SCID mice. Moreover, human neutrophils stimulated in vitro with IL-8 were found to release granule-derived factor(s) that induce in vitro T cell and monocyte chemotaxis and chemokinesis. This T cell and monocyte chemotactic activity was detected in extracts of both azurophilic and specific granules. Together, these results demonstrate that neutrophils store and release, upon stimulation with IL-8 or other neutrophil activators, chemoattractants that mediate T cell and monocyte accumulation at sites of inflammation. C1 NCI, FREDERICK CANC RES & DEV CTR, BIOL CARCINOGENESIS & DEV PROGRAM, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, PATHOL HISTOTECHNOL LAB, FREDERICK, MD 21702 USA. NCI, FREDERICK CANC RES & DEV CTR, MOLEC IMMUNOREGULAT LAB, FREDERICK, MD 21702 USA. NIA, OFF SCI DIRECTOR, BALTIMORE, MD 21224 USA. RP Taub, DD (reprint author), NCI, FREDERICK CANC RES & DEV CTR,SAIC FREDERICK, CLIN SERV PROGRAM,BLDG 560, RM 11-23, FREDERICK, MD 21702 USA. NR 59 TC 177 Z9 179 U1 0 U2 3 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR 15 PY 1996 VL 97 IS 8 BP 1931 EP 1941 DI 10.1172/JCI118625 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA UG083 UT WOS:A1996UG08300019 PM 8621778 ER PT J AU Marples, D Frokiaer, J Dorup, J Knepper, MA Nielsen, S AF Marples, D Frokiaer, J Dorup, J Knepper, MA Nielsen, S TI Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE aquaporins; water channels; vasopressin; nephrogenic diabetes insipidus; polyuria ID INVIVO AB Prolonged hypokalemia causes vasopressin-resistant polyuria. We have recently shown that another cause of severe polyuria, chronic lithium therapy, is associated with decreased aquaporin-2 (AQP2) water channel expression (Marples, D., S. Christensen, E.I, Christensen, P.D, OttoSen, and S. Nielsen, 1995. J. Clin. Invest., 95: 1838-1845), Consequently, we studied the effect in rats of 11 days' potassium deprivation on urine production and AQP2 expression and distribution, Membrane fractions were prepared from one kidney, while the contralateral kidney was perfusion-fixed for immunocytochemistry. Immunoblotting and densitometry revealed a decrease in AQP2 levels to 27 +/- 3.4% of control levels (n = 11, P < 0.001) in inner medulla, and 34 +/- 15% of controls (n = 5, P < 0.05) in cortex. Urine production increased in parallel, from 11 +/- 1.4 to 30 +/- 4.4 ml/day (n = 11, P < 0.01), After return to a potassium-containing diet both urine output and AQP2 levels normalized within 7 d. Immunocytochemistry confirmed decreased AQP2 labeling in principal cells of both inner medullary and cortical collecting ducts, AQP2 labeling was predominantly associated with the apical plasma membrane and intracellular vesicles. Lithium treatment for 24 d caused a more extensive reduction of AQP2 levels, to 4 +/- 1% of control levels in the inner medulla and 4 +/- 2% in cortex, in association with severe polyuria, The similar degree of downregulation in medulla and cortex suggests that interstitial tonicity is not the major factor in the regulation of AQP2 expression, Consistent with this furosemide treatment did not alter AQP2 levels. In summary, hypokalemia, like lithium treatment, results in a decrease in AQP2 expression in rat collecting ducts, in parallel with the development of polyuria, and the degree of downregulation is consistent with the level of polyuria induced, supporting the view that there is a causative link. C1 AARHUS UNIV,INST ANAT,DEPT CELL BIOL,DK-8000 AARHUS,DENMARK. AARHUS UNIV HOSP,DEPT CLIN PHYSIOL,DK-8000 AARHUS,DENMARK. AARHUS UNIV,INST EXPTL CLIN RES,DK-8000 AARHUS,DENMARK. NHLBI,NIH,BETHESDA,MD 20892. NR 30 TC 190 Z9 191 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR 15 PY 1996 VL 97 IS 8 BP 1960 EP 1968 DI 10.1172/JCI118628 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA UG083 UT WOS:A1996UG08300022 PM 8621781 ER PT J AU Tsui, CC Copeland, NG Gilbert, DJ Jenkins, NA Barnes, C Worley, PF AF Tsui, CC Copeland, NG Gilbert, DJ Jenkins, NA Barnes, C Worley, PF TI Narp, a novel member of the pentraxin family, promotes neurite outgrowth and is dynamically regulated by neuronal activity SO JOURNAL OF NEUROSCIENCE LA English DT Article DE growth factors; immediate-early genes; lectins; long-term potentiation; neurite outgrowth; pentraxins ID LONG-TERM POTENTIATION; AMYLOID-P-COMPONENT; C-REACTIVE PROTEIN; IMMEDIATE-EARLY GENES; FACTOR MESSENGER-RNAS; CONCANAVALIN-A; RAT-BRAIN; NICOTINIC TRANSMISSION; SELECTIVE EXPRESSION; HIPPOCAMPAL-NEURONS AB Stimulus-linked RNA and protein synthesis is required for establishment of long-term neuroplasticity. To identify molecular mechanisms underlying long-term neuroplasticity, we have used differential cDNA techniques to clone a novel immediate-early gene (IEG) that is rapidly induced in neurons of the hippocampus and cortex by physiological synaptic activity. Analysis of the deduced amino acid sequence indicates homology to members of the pentraxin family of secreted lectins that include C-reactive protein and serum amyloid P component. Regions of homology include an 8 amino acid ''pentraxin signature'' sequence and a characteristic pentraxin calcium-binding domain. We have termed this gene and the encoded protein Narp (from neuronal activity-regulated pentraxin). Biochemical analyses confirm the presence of a functional signal sequence, and Narp is secreted by transfected COS-1 cells in culture. Additionally, Narp binds to agar matrix in a calcium-dependent manner consistent with the lectin properties of the pentraxin family. When cocultured with Narp-secreting COS-1 cells, neurons of cortical explants exhibit enhanced growth of neuronal dendritic processes. Neurite outgrowth-promoting activity is also observed using partially purified Narp and can be specifically immunodepleted, demonstrating that Narp is the active principle. Narp is fully active at a concentration of similar to 40 ng/ml, indicating a potency similar to known peptide growth factors. Because Narp is rapidly regulated by neuronal activity, its lectin and growth-promoting activities are likely to play role in the modification of cellular properties that underlie long-term plasticity. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. UNIV ARIZONA,DEPT PSYCHOL NEUROL,TUCSON,AZ 85724. UNIV ARIZONA,DIV NEURONAL SYST MEMORY & AGING,TUCSON,AZ 85724. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. FU NCI NIH HHS [N01-CO-74101]; NIA NIH HHS [AG09219]; NIMH NIH HHS [MH53608] NR 90 TC 186 Z9 192 U1 0 U2 5 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR 15 PY 1996 VL 16 IS 8 BP 2463 EP 2478 PG 16 WC Neurosciences SC Neurosciences & Neurology GA UD671 UT WOS:A1996UD67100005 PM 8786423 ER PT J AU Gallo, V Zhou, JM McBain, CJ Wright, P Knutson, PL Armstrong, RC AF Gallo, V Zhou, JM McBain, CJ Wright, P Knutson, PL Armstrong, RC TI Oligodendrocyte progenitor cell proliferation and lineage progression are regulated by glutamate receptor-mediated K+ channel block SO JOURNAL OF NEUROSCIENCE LA English DT Article DE AMPA receptors; O-2A cells; glia; cell migration; tetraethylammonium; delayed rectifier K+ channels ID CENTRAL NERVOUS-SYSTEM; RAT CEREBELLAR CULTURES; EXCITATORY AMINO-ACIDS; TYPE-2 ASTROCYTES; MACROGLIAL CELLS; DEVELOPMENTAL CLOCK; POTASSIUM CHANNELS; GLIAL PROGENITORS; NMDA RECEPTORS; GROWTH-FACTOR AB We have analyzed the role of glutamate and its receptors (GluRs) in regulating the development of oligodendrocytes. Activation of AMPA-preferring GluRs with selective agonists inhibited proliferation of purified cortical oligodendrocyte progenitor (O-2A) cells cultured with different mitogens, as measured by [H-3]thymidine incorporation or bromodeoxyuridine staining. In contrast, activation of GABA or muscarinic receptors did not affect O-2A proliferation. Cell viability and apoptosis assays demonstrated that the inhibition of O-2A proliferation was not attributable to a cytotoxic action of GluR agonists, and was reversible. Activation of GluRs prevented lineage progression from the O-2A (GD3(+)/nestin(+)) stage to the pro-oligodendroblast (O4(+)) stage, but did not affect O-2A migration. Additional experiments examined the membrane ionic channels mediating these GlUR activation effects. We found that proliferating O-2A cells expressed functional delayed rectifier K+ channels, which were absent in pro-oligodendroblasts. GluR agonists and the K+ channel blocker tetraethylammonium (TEA) strongly inhibited delayed rectifier K+ currents in O-2A cells. TEA reproduced the effects of GluR activation on O-2A proliferation and lineage progression in the same concentration range that blocked delayed rectifier K+ currents. These results indicate that glutamate regulates oligodendrogenesis specifically at the O-2A stage by modulating K+ channel activity. C1 UNIFORMED SERV UNIV HLTH SCI,DEPT ANAT & CELL BIOL,BETHESDA,MD 20814. RP Gallo, V (reprint author), NICHHD,NATL INST HLTH,LAB CELLULAR & MOL NEUROPHYSIOL,BLDG 49,ROOM 5A78,BETHESDA,MD 20892, USA. RI Messier, Claude/A-2322-2008 OI Messier, Claude/0000-0002-4791-1763 FU NCI NIH HHS [R070CB] NR 70 TC 266 Z9 267 U1 2 U2 6 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR 15 PY 1996 VL 16 IS 8 BP 2659 EP 2670 PG 12 WC Neurosciences SC Neurosciences & Neurology GA UD671 UT WOS:A1996UD67100024 PM 8786442 ER PT J AU Sadato, N Campbell, G Ibanez, V Deiber, MP Hallett, M AF Sadato, N Campbell, G Ibanez, V Deiber, MP Hallett, M TI Complexity affects regional cerebral blood flow change during sequential finger movements SO JOURNAL OF NEUROSCIENCE LA English DT Article DE regional cerebral blood flow; sequential finger movements; positron emission tomography; sensorimotor cortex; premotor cortex; supplementary motor area ID POSITRON EMISSION TOMOGRAPHY; SUPPLEMENTARY MOTOR AREA; NEURONAL-ACTIVITY; PREMOTOR CORTEX; CORTICOSPINAL PROJECTIONS; WORKING-MEMORY; CORTICAL AREAS; FRONTAL-LOBE; PET IMAGES; MONKEY AB Brain regions activated with complex sequential finger movements were localized by measuring regional cerebral blood flow (rCBF) with positron emission tomography. Whereas the total number and frequency of finger movements were kept constant, the complexity of auditory cued sequential finger movements of the right hand varied, with sequence length as the independent variable. In four conditions of differing complexity, the bilateral primary sensorimotor area, left ventral premotor cortex, posterior supplementary motor area, right superior part of the cerebellum, and left putamen were consistently and equally activated. This finding suggests an executive role in running sequences, regardless of their length. The right dorsal premotor cortex (Brodmann area 6) and the right precuneus (Brodmann area 7) showed a linear increase of rcBF as sequence complexity increased. This finding is consistent with the hypothesis that these areas function in the storage of motor sequences in spatial working memory and the production of ongoing sequential movement with reference to that of buffered memory. A similar increase in the cerebellar vermis and the left thalamus likewise suggests a role of these subcortical structures in complexity of sequential finger movements. Conversely, the left inferior parietal lobule showed a decrease of rCBF as complexity increased. Because short-term phonological storage is localized to this area, we suggest that the visuospatial working memory system may suppress other systems not in use. Our findings suggest that complex sequential finger movements recruit a discrete set of brain areas, in addition to areas underlying the execution of simple movement sequences. C1 NINDS,NIH,HUMAN MOTOR CONTROL SECT,MED NEUROL BRANCH,BETHESDA,MD 20892. NINDS,NIH,BIOMETRY & FIELD STUDIES BRANCH,BETHESDA,MD 20892. RI Deiber, Marie-Pierre/M-5949-2014 NR 67 TC 76 Z9 78 U1 0 U2 3 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR 15 PY 1996 VL 16 IS 8 BP 2693 EP 2700 PG 8 WC Neurosciences SC Neurosciences & Neurology GA UD671 UT WOS:A1996UD67100027 ER PT J AU Su, XZ Wu, YM Sifri, CD Wellems, TE AF Su, XZ Wu, YM Sifri, CD Wellems, TE TI Reduced extension temperatures required for PCR amplification of extremely A+T-rich DNA SO NUCLEIC ACIDS RESEARCH LA English DT Article ID PLASMODIUM-FALCIPARUM; SEQUENCE; GENERATION; GENOME C1 NIAID,NIH,PARASIT DIS LAB,BETHESDA,MD 20892. OI Su, Xinzhuan/0000-0003-3246-3248 NR 17 TC 74 Z9 76 U1 1 U2 10 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD APR 15 PY 1996 VL 24 IS 8 BP 1574 EP 1575 DI 10.1093/nar/24.8.1574 PG 2 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UH370 UT WOS:A1996UH37000026 PM 8628694 ER PT J AU Hjalmars, U Kulldorff, M Gustafsson, G Nagarwalla, N AF Hjalmars, U Kulldorff, M Gustafsson, G Nagarwalla, N TI Childhood leukaemia in Sweden: Using GIS and a spatial scan-statistic for cluster detection SO STATISTICS IN MEDICINE LA English DT Article; Proceedings Paper CT Conference on Statistics and Computing in Disease Clustering CY JUL 21-22, 1994 CL UNIV BRITISH COLUMBIA, VANCOUVER, CANADA SP BioMedware, Elect Power Res Inst, Natl Canc Inst HO UNIV BRITISH COLUMBIA ID ACUTE LYMPHOBLASTIC-LEUKEMIA; BRITAIN; POWER AB The study of disease clustering is becoming increasingly common in the field of medical epidemiology. There is great public concern and numerous reports on perceived clusters of various diseases, with cancers, and especially leukaemia, being the most commonly studied. We present a population based study on acute childhood leukaemia in Sweden 1973-1993, illustrating the possibility of a system for full-scale spatial epidemiological study design. The aim of the study is to test a large set of childhood leukaemia cases for the presence of geographical clusters. Necessary prerequisites, in the form of extensive population and disease data, a tool for geographical spatial analysis and a proper statistical method were fulfilled. No significant clusters were found. C1 NCI,BIOMETRY BRANCH,DCPC,BETHESDA,MD 20892. UNIV UPPSALA,DEPT STAT,S-75120 UPPSALA,SWEDEN. KAROLINSKA INST,REG ONCOL CTR,S-10401 STOCKHOLM,SWEDEN. HARVARD UNIV,SCH DENT MED,DEPT ORAL PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP Hjalmars, U (reprint author), OSTERSUND CENT HOSP,DEPT PAEDIAT,S-83183 OSTERSUND,SWEDEN. RI Kulldorff, Martin/H-4282-2011; OI Kulldorff, Martin/0000-0002-5284-2993 NR 26 TC 86 Z9 89 U1 2 U2 9 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR 15 PY 1996 VL 15 IS 7-9 BP 707 EP 715 DI 10.1002/(SICI)1097-0258(19960415)15:7/9<707::AID-SIM242>3.3.CO;2-W PG 9 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA UG357 UT WOS:A1996UG35700004 PM 9132898 ER PT J AU Melnick, RL Elwell, MR Roycroft, JH Chou, BJ Ragan, HA Miller, RA AF Melnick, RL Elwell, MR Roycroft, JH Chou, BJ Ragan, HA Miller, RA TI Toxicity of inhaled chloroprene (2-chloro-1,3-butadiene) in F344 rats and B6C3F(1) mice SO TOXICOLOGY LA English DT Article DE chloroprene; butadiene; inhalation toxicology; hepatocellular necrosis; anemia; olfactory epithelial degeneration ID INHALATION EXPOSURE; 1,3-BUTADIENE; CARCINOGENICITY; TOXICOLOGY; ISOPRENE; TISSUE; RODENT AB Chloroprene (2-chloro-1,3-butadiene) is a high production chemical used almost exclusively in the production of polychloroprene (neoprene) elastomer. Because of its structural similarity to isoprene (2-methyl-1,3-butadiene) and to 1,3-butadiene, a potent trans-species carcinogen, inhalation studies were performed on chloroprene to characterize its toxicological potential and to provide a basis for selecting exposure concentrations for chronic toxicity and carcinogenicity studies. Thirteen-week inhalation toxicology studies were conducted in male and female F344 rats and B6C3F(1) mice at exposure concentrations of 0, 5, 12, 32 or 80 ppm (6 h/day; 5 days/week). A 200 ppm exposure group was also included for rats only, because a previous study showed that this concentration of chloroprene is lethal to mice. In mice, exposure to 80 ppm chloroprene caused a marginal decrease in body weight gain in males and epithelial hyperplasia of the forestomach in males and females. This lesion has been observed in mice exposed to isoprene or 1,3-butadiene. In rats, exposure to 80 ppm chloroprene or higher concentrations caused degeneration and metaplasia of the olfactory epithelium and exposure to 200 ppm caused anemia, hepatocellular necrosis and reduced sperm motility. These lesions have not been observed in rats exposed to isoprene or 1,3-butadiene. The profile of toxic effects of chloroprene is considerably different from that of isoprene or 1,3-butadiene; this may be due to differences in exposure concentrations that were used in toxicology studies of these compounds and/or to the influence of the chlorine substitution on the toxicokinetics of these compounds, on their biotransformation, or on the reactivity of metabolic intermediates with tissue macromolecules. C1 NIEHS, RES TRIANGLE PK, NC 27709 USA. PACIFIC NW LAB, RICHLAND, WA 99352 USA. NR 36 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 APR 15 PY 1996 VL 108 IS 1-2 BP 79 EP 91 DI 10.1016/0300-483X(95)03286-O PG 13 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA UC593 UT WOS:A1996UC59300011 PM 8644121 ER PT J AU Vowells, SJ Fleisher, TA Malech, HL AF Vowells, SJ Fleisher, TA Malech, HL TI Testing for chronic granulomatous disease SO LANCET LA English DT Letter RP Vowells, SJ (reprint author), NIH,BETHESDA,MD 20892, USA. NR 3 TC 18 Z9 19 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 APR 13 PY 1996 VL 347 IS 9007 BP 1048 EP 1049 DI 10.1016/S0140-6736(96)90189-0 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA UF380 UT WOS:A1996UF38000060 PM 8606593 ER PT J AU Lee, MD Bhakta, KY Raina, S Yonescu, R Griffin, CA Copeland, NG Gilbert, DJ Jenkins, NA Preston, GM Agre, P AF Lee, MD Bhakta, KY Raina, S Yonescu, R Griffin, CA Copeland, NG Gilbert, DJ Jenkins, NA Preston, GM Agre, P TI The human aquaporin-5 gene - Molecular characterization and chromosomal localization SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RNA POLYMERASE-II; WATER CHANNEL; DNA-SEQUENCES; LINKAGE MAP; RAT-KIDNEY; TRANSCRIPTION; INITIATOR; ORGANIZATION; ELEMENTS; CLONING AB The cDNA for the fifth mammalian aquaporin (AQP5) was isolated from rat, and expression was demonstrated in rat salivary and lacrimal glands, cornea, and lung (Raina, S., Preston, G. M., Guggino, W. B., and Agre, P. (1995) J. Biol. Chem. 270, 1908-1912). Here we report the isolation and characterization of the human AQP5 cDNA and gene. The AQP5 cDNA from a human submaxillary gland library contains a 795-base pair open reading frame encoding a 265-amino acid protein. The deduced amino acid sequences of human and rat AQP5 are 91% identical with 6 substitutions in the 22-amino acid COOH-terminal domain. Expression of human AQP5 in Xenopus oocytes conferred mercurial-sensitive osmotic water permeability (Pf) equivalent to other aquaporins. The human AQP5 structural gene resides within a 7.4-kilobase SalI-EcoRI fragment with four exons corresponding to amino acids 1-121, 122-176, 177-204, and 205-265 separated by introns of 1.2, 0.5, and 0.9 kilobases. A transcription initiation site was identified 518 base pairs upstream of the initiating methionine. Genomic Southern analysis indicated that AQP5 is a single copy gene which localized to human chromosome 12q13; this coincides with the chromosomal locations of the homologous human genes MIP and AQP2, thus confirming 12q13 as the site of an aquaporin gene cluster. The mouse gene localized to distal chromosome 15. This information may permit molecular characterization of AQP5 expression during normal development and in clinical disorders. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV PULM & CRIT CARE MED,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT PATHOL,BALTIMORE,MD 21205. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,MAMMALIAN GENET LAB,NIH,FREDERICK,MD 21702. FU NEI NIH HHS [EY11239]; NHLBI NIH HHS [HL33991, HL48268] NR 43 TC 60 Z9 63 U1 1 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 12 PY 1996 VL 271 IS 15 BP 8599 EP 8604 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE730 UT WOS:A1996UE73000020 PM 8621489 ER PT J AU Ahmed, SA McPhie, P Miles, EW AF Ahmed, SA McPhie, P Miles, EW TI A thermally induced reversible conformational transition of the tryptophan synthase beta(2) subunit probed by the spectroscopic properties of pyridoxal phosphate and by enzymatic activity SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; L-SERINE; 5'-PHOSPHATE; ALPHA; SYNTHETASE; MECHANISM; SPECTRA; INDOLE; BASES AB A reversible thermally induced conformational transition of the beta(2) subunit of tryptophan synthase from Salmonella typhimurium has been detected by use of the pyridoxal 5'-phosphate coenzyme as a spectroscopic probe. Increasing the temperature converts the major form of pyridoxal 5'-phosphate bound to the beta(2) subunit from a ketoenamine species with lambda(max) at 410 nm to a enolimine species with lambda(max) at 336 nm (T-m = similar to 43 degrees C) and results in loss of the circular dichroism signal at 410 nm and of fluorescence emission at 510 nm, The results indicate that increasing the temperature favors a conformer of the enzyme that binds pyridoxal 5'-phosphate in a more nonpolar environment and leads to loss of asymmetric pyridoxal 5'-phosphate binding. The internal aldimine between pyridoxal 5'-phosphate and the E-amino group of lysine 87 is not disrupted by increased temperature because sodium borohydride treatment of the enzyme at either 15 or 60 degrees C results in covalent attachment of [4'-H-3]pyridoxal 5'-phosphate. The thermal transition of the beta(2) subunit below 60 degrees C produces reversible thermal inactivation (T-i = similar to 52 degrees C) and occurs at a much lower temperature than the major reversible unfolding at similar to 80 degrees C (Remeta, D. P., Miles, E. W., and Ginsburg, A. (1995) Pure Appl. Chem. 67, 1859-1866). Our new results indicate that the 410 nm absorbing species of pyridoxal 5'-phosphate is the catalytically active form of the cofactor in the beta(2) subunit and that the low temperature reversible conformational transition disturbs the active site and causes loss of catalytic activity. C1 NIDDKD, BIOCHEM PHARMACOL LAB, NIH, BETHESDA, MD 20892 USA. NR 32 TC 9 Z9 9 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD APR 12 PY 1996 VL 271 IS 15 BP 8612 EP 8617 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE730 UT WOS:A1996UE73000022 PM 8621491 ER PT J AU Cenciarelli, C Wilhelm, KG Guo, A Weissman, AM AF Cenciarelli, C Wilhelm, KG Guo, A Weissman, AM TI T cell antigen receptor ubiquitination is a consequence of receptor-mediated tyrosine kinase activation SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FACTOR BETA-RECEPTOR; SIGNAL TRANSDUCTION; ZETA-CHAIN; LYMPHOCYTES-T; PHOSPHORYLATION; COMPLEX; PATHWAY; CD45; INHIBITOR; INVITRO AB Engagement of the T cell antigen receptor results in both its phosphorylation and its ubiquitination. T cell antigen receptor ubiquitination was evaluated in Jurkat, a well characterized human T leukemia cell line. Treatment of cells with the tyrosine kinase inhibitor herbimycin A resulted in an inhibition of receptor ubiquitination, Consistent with this, pervanadate, which increases cellular tyrosine phosphorylation, enhanced receptor ubiquitination, A requirement for receptor-mediated tyrosine kinase activity for ubiquitination was confirmed in cells lacking the tyrosine kinase p56(lck) and also in cells that are defective in expression of CD45, a tyrosine phosphatase that regulates the activity of p56(lck). The need for tyrosine kinase activation for ubiquitination was not bypassed by directly activating protein kinase C and stimulating endocytosis of receptors. These observations establish ubiquitination of the T cell antigen receptor as a tyrosine kinase-dependent manifestation of transmembrane signaling and suggest a role for tyrosine phosphorylation in the ligand-dependent ubiquitination of mammalian transmembrane receptors. C1 NCI,NIH,DIV BASIC SCI,LAB IMMUNE CELL BIOL,BETHESDA,MD 20892. NR 54 TC 71 Z9 71 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 12 PY 1996 VL 271 IS 15 BP 8709 EP 8713 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE730 UT WOS:A1996UE73000034 PM 8621503 ER PT J AU Liu, J Wess, J AF Liu, J Wess, J TI Different single receptor domains determine the distinct G protein coupling profiles of members of the vasopressin receptor family SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID 3',5'-CYCLIC ADENOSINE-MONOPHOSPHATE; BETA-ADRENERGIC RECEPTORS; MOLECULAR-CLONING; MUSCARINIC RECEPTOR; BINDING PROTEINS; EXPRESSION; SIGNAL; GENES; RAT; IDENTIFICATION AB The vasopressin receptor family is unique among all classes of peptide receptors in that its individual members couple to different subsets of G proteins. The V-1n vasopressin receptor, for example, is preferentially linked to G proteins of the G(q/11) class (biochemical response: stimulation of phosphatidylinositol hydrolysis), whereas the V-2 vasopressin receptor is selectively coupled to G(s) (biochemical response: stimulation of adenylyl cyclase). To elucidate the structural basis underlying this functional heterogeneity, we have systematically exchanged different intracellular domains between the V-1a and V-2 receptors. Transient expression of the resulting hybrid receptors in COS-7 cells showed that all mutant receptors containing V-1a receptor sequence in the second intracellular loop were able to activate the phosphatidylinositol pathway with high efficiency. On the other hand, only those hybrid receptors containing V-2 receptor sequence in the third intracellular loop were capable of efficiently stimulating cAMP production. These findings suggest that the differential G protein coupling profiles of individual members of a structurally closely related receptor subfamily can be determined by different single intracellular receptor domains. C1 NIDDK, NIH, BIOORGAN CHEM LAB, BETHESDA, MD 20892 USA. NR 53 TC 111 Z9 111 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD APR 12 PY 1996 VL 271 IS 15 BP 8772 EP 8778 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE730 UT WOS:A1996UE73000044 PM 8621513 ER PT J AU Toyoshige, M Basi, NS Rebois, RV AF Toyoshige, M Basi, NS Rebois, RV TI Chloride effects on G(s) subunit dissociation - Fluoroaluminate binding to G(s) does not cause subunit dissociation in the absence of chloride ion SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ADENYLATE-CYCLASE; REGULATORY COMPONENT; G-PROTEINS; CONFORMATIONAL-CHANGES; GUANINE-NUCLEOTIDES; ALPHA-SUBUNIT; RECEPTOR; PURIFICATION AB The stimulatory guanine nucleotide binding protein (G(s)) is heterotrimeric (alpha beta gamma), and mediates activation of adenylyl cyclase by a ligand-receptor complex. The cu subunit of G(s) (G(s) alpha) has a guanine nucleotide binding site, and activation occurs when tightly bound GDP is displaced by GTP. Together, GDP and fluoroaluminate (AlF4-) form a transition state analog of GTP that activates G(s). The work of other investigators suggests that AlF4- causes subunit dissociation when it activates G(s). We have observed that in solution AlF4- did not cause G(s) subunits to dissociate unless NaCl was also present. The effect of NaCl was concentration dependent (10-200 mM). Omitting F-, Al3+, or Mg2+ prevented the NaCl-induced dissociation of G(s) subunits. Na2SO4 could not substitute for NaCl in causing subunit dissociation, but KCl could, suggesting that the anion was responsible for the effect. G(s) subunit reassociation occurred when the concentration of Cl- was reduced even though the concentrations of AlF4- and Mg2+ were maintained. The absence of Cl- did not prevent AlF4- binding to G(s) alpha. We have concluded that AlF4- a ligand which is capable of activating G proteins, can bind to G(s) in solution without causing subunit dissociation. C1 NINCDS,NIH,MEMBRANE BIOCHEM SECT,LAB MOL & CELLULAR NEUROBIOL,BETHESDA,MD 20892. NR 29 TC 14 Z9 14 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 12 PY 1996 VL 271 IS 15 BP 8791 EP 8795 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE730 UT WOS:A1996UE73000047 PM 8621516 ER PT J AU Najjar, SM Boisclair, YR Nabih, ZT Phillippe, N Imai, Y Suzuki, Y Suh, DS Ooi, GT AF Najjar, SM Boisclair, YR Nabih, ZT Phillippe, N Imai, Y Suzuki, Y Suh, DS Ooi, GT TI Cloning and characterization of a functional promoter of the rat pp120 gene, encoding a substrate of the insulin receptor tyrosine kinase SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MEMBRANE ECTO-ATPASE; LIVER-SPECIFIC GENES; RNA POLYMERASE-II; ENDOGENOUS SUBSTRATE; TRANSCRIPTION FACTOR; GROWTH-FACTOR; CARCINOEMBRYONIC ANTIGEN; ADHESION MOLECULE; PROTEIN-KINASE; LESS PROMOTER AB Cloning of the 5'-flanking region of the rat pp120 gene has indicated that it is a housekeeping gene: it lacks a functional TATA bog and contains several Spl binding sites and multiple transcription initiation sites at nucleotides -101, -71, -41, and -27 spread over a GC-rich area, A fragment between nucleotides -21 and -1609 exhibited promoter activity when ligated in a sense orientation into a promoterless luciferase reporter plasmid and transiently transfected into rat H4-II-E hepatoma cells, 5' progressive deletion and block substitution analyses revealed that the three proximal Spl boxes (boxes 3, 5, and 6) are required for basal transcription of the pp120 gene. Promoter activity was stimulated 2-3-fold in response to insulin, dexamethasone, insulin plus dexamethasone, and cAMP. Although unaltered by phorbol esters alone, promoter activity was stimulated 4-5-fold in response to phorbol esters plus cAMP. Several motifs resembling response elements for insulin (in the rat phosphoenolpyruvate carboxykinase gene), glucocorticoids, cAMP, and phorbol esters as well as a number of putative binding sites for activating proteins-1 (Jun/Fos) and -2, and liver-specific factors were detected, The role of these sites in tissue-specific expression of pp120 remains to be investigated. C1 NIDDK,NIH,MOLEC & CELLULAR ENDOCRINOL BRANCH,BETHESDA,MD 20892. CORNELL UNIV,DEPT ANIM SCI,ITHACA,NY 14853. RP Najjar, SM (reprint author), MED COLL OHIO,DEPT PHARMACOL & THERAPEUT,HLTH SCI BLDG,RM 270,TOLEDO,OH 43614, USA. NR 55 TC 22 Z9 22 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 12 PY 1996 VL 271 IS 15 BP 8809 EP 8817 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE730 UT WOS:A1996UE73000050 PM 8621519 ER PT J AU Saito, H Oka, T AF Saito, H Oka, T TI Hormonally regulated double- and single-stranded DNA-binding complexes involved in mouse beta-casein gene transcription SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MAMMARY EPITHELIAL-CELLS; MULTIGENE FAMILY; NUCLEAR FACTOR; FINE-STRUCTURE; PROTEINS; GROWTH; PROMOTER; IDENTIFICATION; EXPRESSION; INDUCTION AB Transcription of the 252-base pair-long mouse beta-casein gene promoter is induced by the synergistic action of insulin, prolactin, and glucocorticoid in a primary mammary epithelial cell culture, The promoter contains a region termed block C having a highly conserved sequence and position among many casein genes, Mutation of block C reduced the response of the promoter to lactogenic hormones 84%. Nuclear extracts from lactating mouse mammary glands contained both a double-stranded and a single-stranded DNA binding protein complex (DS1 and SS), which specifically bind to the sequences AAATTAGCATGT and CCACAA of block C, respectively, The DS1 and the SS protein complexes were approximately 400 and 280 kDa, respectively, Each complex contained a DNA-binding component(s) having a molecular mass of approximately 120 kDa for DS1 and 80 and 65 kDa for SS, Deoxycholate, which interferes with the protein-protein interactions, inhibited the binding activities of DS1 and SS, The maximal increase in the binding activity of DS1 and SS in the mammary gland occurred during pregnancy and during lactation, respectively. In organ culture, the DSI activity is increased by epidermal growth factor or prolactin in combination with insulin, whereas the SS activity is enhanced by insulin, prolactin, and glucocorticoid, These results suggest that multiprotein complexes binding to the double- and single-stranded DNA of block C mediate hormonal induction of beta-casein gene transcription. C1 NIDDK,LMCB,BETHESDA,MD 20892. NR 38 TC 25 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 APR 12 PY 1996 VL 271 IS 15 BP 8911 EP 8918 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE730 UT WOS:A1996UE73000065 PM 8621534 ER PT J AU Driscoll, JS Siddiqui, MA Ford, H Kelley, JA Roth, JS Mitsuya, H Tanaka, M Marquez, VE AF Driscoll, JS Siddiqui, MA Ford, H Kelley, JA Roth, JS Mitsuya, H Tanaka, M Marquez, VE TI Lipophilic, acid-stable, adenosine deaminase-activated anti-HIV prodrugs for central nervous system delivery .3. 6-Amino prodrugs of 2'-beta-fluoro-2',3'-dideoxyinosine SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID NUCLEOSIDES; INFECTION; 2',3'-DIDEOXYADENOSINE; THERAPY; ANALOGS; AGENTS AB A series of 6-substituted amino analogs of 9-(2,3-dideoxy-2-fluoro-beta-D-threo-pentofuranosyl) purines (F-ddN) has been synthesized and characterized with the objective of finding compounds which might be superior to existing chugs for the treatment of HIV in the central nervous system. These compounds are intended to be more lipophilic than the currently approved anti-HIV drugs for better blood-brain barrier penetration. Subsequent adenosine deaminase (ADA)-catalyzed hydrolysis of these prodrugs in the brain is expected to produce the anti-HIV agent, 9-(2,3-dideoxy-2-fluoro-beta-D-threo-pentofuranosyl)hypoxanthine (F-ddI). The new compounds, synthesized from the corresponding 6-chloro analog, include F-ddN which contain methylamino, ethylamino, dimethylamino, hydroxylamino, methoxyamino, benzyloxyamino, hydrazino, and nitro substituents in the 6-position. The 6-nitro analog was isolated as an unexpected product during the preparation of the 6-chloro derivative. Among the analogs with anti-HIV activity, the ethylamino and dimethylamino compounds are ca. 100 times more Lipophilic than ddI or F-ddI. As expected, 2'-fluoro substitution protects the compounds from acid-catalyzed glycosylic cleavage. Only the hydroxylamino and nitro analogs underwent any nonenzymatic hydrolysis at pH 1.0 or 7.4. This reaction, however, results in hydrolysis of the group in the 6-position rather than glycosylic bond cleavage. ADA catalyzes the hydrolysis of the 6-substituents at rates which vary from slightly slower (NO2, 1.7x) to much slower (NHEt, 5000 x) than F-ddA. The 6-dimethylamino analog is the only compound which possesses anti-HIV activity (ED(50) is mu M) without ADA hydrolysis. With the exception of the two inactive alkoxyamino compounds, the other prodrugs exhibited cellular protection in the HIV-1/PHA-PBM system with IC50 potencies of 7-40 mu M. C1 NCI, NIH, DIV CLIN SCI, EXPTL RETROVIROL SECT, BETHESDA, MD 20892 USA. RP Driscoll, JS (reprint author), NCI, NIH, DIV BASIC SCI, MED CHEM LAB, BETHESDA, MD 20892 USA. NR 41 TC 20 Z9 21 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 12 PY 1996 VL 39 IS 8 BP 1619 EP 1625 DI 10.1021/jm9509197 PG 7 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA UE818 UT WOS:A1996UE81800007 PM 8648601 ER PT J AU Gussio, R Pattabiraman, N Zaharevitz, DW Kellogg, GE Topol, IA Rice, WG Schaeffer, CA Erickson, JW Burt, SK AF Gussio, R Pattabiraman, N Zaharevitz, DW Kellogg, GE Topol, IA Rice, WG Schaeffer, CA Erickson, JW Burt, SK TI All-atom models for the non-nucleoside binding site of HIV-1 reverse transcriptase complexed with inhibitors: A 3D QSAR approach SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; NONNUCLEOSIDE INHIBITORS; ANTIVIRAL ACTIVITY; REPLICATION; DERIVATIVES; NEVIRAPINE; ZIDOVUDINE; INVITRO; POTENT; SERIES AB Several molecular modeling techniques were used to generate an all-atom molecular model of a receptor binding site starting only from Ca atom coordinates. The model consists of 48 noncontiguous residues of the non-nucleoside binding site of HIV-1 reverse transcriptase and was generated using a congeneric series of nevirapine analogs as structural probes. On the basis of the receptor-ligand atom contacts, the program HINT was used to develop a 3D quantitative structure activity relationship that predicted the rank order of binding affinities for the series of inhibitors. Electronic profiles of the ligands in their docked conformations were characterized using electrostatic potential maps and frontier orbital calculations. These results led to the development of a 3D stereoelectronic pharmacophore which was used to construct 3D queries for database searches. A search of the National Cancer Institute's open database identified a lead compound that exhibited moderate antiviral activity. C1 SAIC FREDERICK,NCI,FREDERICK CANC RES & DEV CTR,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702. SAIC FREDERICK,NCI,FREDERICK CANC RES & DEV CTR,FREDERICK BIOMED SUPERCOMP CTR,FREDERICK,MD 21702. VIRGINIA COMMONWEALTH UNIV,SCH PHARM,DEPT MED CHEM,RICHMOND,VA 23298. RI Kellogg, Glen/A-8008-2011 NR 37 TC 50 Z9 51 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 12 PY 1996 VL 39 IS 8 BP 1645 EP 1650 DI 10.1021/jm9508088 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA UE818 UT WOS:A1996UE81800010 PM 8648604 ER PT J AU Drgonova, J Drgon, T Tanaka, K Kollar, R Chen, GC Ford, RA Chan, CSM Takai, Y Cabib, E AF Drgonova, J Drgon, T Tanaka, K Kollar, R Chen, GC Ford, RA Chan, CSM Takai, Y Cabib, E TI Rho1p, a yeast protein at the interface between cell polarization and morphogenesis SO SCIENCE LA English DT Article ID RAS SUPERFAMILY GENES; SACCHAROMYCES-CEREVISIAE; BETA-(1->3)GLUCAN SYNTHETASE; WALL; BIOSYNTHESIS; GROWTH; DEFECT; GTP AB The enzyme that catalyzes the synthesis of the major structural component of the yeast cell wall, beta(1-->3)-D-glucan synthase (also known as 1,3-beta-glucan synthase), requires a guanosine triphosphate (GTP) binding protein for activity. The GTP binding protein was identified as Rho1p. The rho1 mutants were defective in GTP stimulation of glucan synthase, and the defect was corrected by addition of purified or recombinant Rho1p. A protein missing in purified preparations from a rho1 strain was identified as Rho1p. Rho1p also regulates protein kinase C, which controls a mitogen-activated protein kinase cascade. Experiments with a dominant positive PKC1 gene showed that the two effects of Rho1p are independent of each other. The colocalization of Rho1p with actin patches at the site of bud emergence and the role of Rho1p in cell wall synthesis emphasize the importance of Rho1p in polarized growth and morphogenesis. C1 NIDDKD,BIOCHEM & METAB LAB,BETHESDA,MD 20892. OSAKA UNIV,SCH MED,DEPT MOLEC BIOL & BIOCHEM,SUITA,OSAKA 565,JAPAN. UNIV TEXAS,DEPT MICROBIOL,AUSTIN,TX 78712. RI Drgonova, Jana/B-2903-2008; OI Drgonova, Jana/0000-0002-4623-8466 NR 24 TC 275 Z9 279 U1 0 U2 5 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD APR 12 PY 1996 VL 272 IS 5259 BP 277 EP 279 DI 10.1126/science.272.5259.277 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UE729 UT WOS:A1996UE72900044 PM 8602514 ER PT J AU Sadato, N PascualLeone, A Grafman, J Ibanez, V Deiber, MP Dold, G Hallett, M AF Sadato, N PascualLeone, A Grafman, J Ibanez, V Deiber, MP Dold, G Hallett, M TI Activation of the primary visual cortex by Braille reading in blind subjects SO NATURE LA English DT Article ID MONKEY; MACAQUE AB PRIMARY visual cortex receives visual input from the eyes through the lateral geniculate nuclei, but is not known to receive input from other sensory modalities'. Its level of activity, both at rest and during auditory or tactile tasks, is higher in blind subjects than in normal controls(2), suggesting that it can subserve nonvisual functions; however, a direct effect of non-visual tasks on activation has not been demonstrated(2-4). To determine whether the visual cortex receives input from the somatosensory system(5-8), we used positron emission tomography (PET) to measure activation during tactile discrimination tasks in normal subjects and in Braille readers blinded in early life. Blind subjects showed activation of primary and secondary visual cortical areas during tactile tasks, whereas normal controls showed deactivation, A simple tactile stimulus that did not require discrimination produced no activation of visual areas in either group. Thus, in blind subjects, cortical areas normally reserved for vision may be activated by other sensory modalities. C1 NINCDS,HUMAN MOTOR CONTROL SECT,NIH,BETHESDA,MD 20892. NINCDS,COGNIT NEUROSCI SECT,MED NEUROL BRANCH,NIH,BETHESDA,MD 20892. FUKUI MED SCH,BIOMED IMAGING RES CTR,MATUOKA,FUKUI 91011,JAPAN. RI Deiber, Marie-Pierre/M-5949-2014; OI Grafman, Jordan H./0000-0001-8645-4457 NR 24 TC 624 Z9 632 U1 5 U2 54 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 11 PY 1996 VL 380 IS 6574 BP 526 EP 528 DI 10.1038/380526a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UE663 UT WOS:A1996UE66300049 PM 8606771 ER PT J AU Kirschstein, RL AF Kirschstein, RL TI Women physicians - Good news and bad news SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material RP Kirschstein, RL (reprint author), NIH,BETHESDA,MD 20892, USA. NR 8 TC 4 Z9 4 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 APR 11 PY 1996 VL 334 IS 15 BP 982 EP 983 DI 10.1056/NEJM199604113341510 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA UD596 UT WOS:A1996UD59600010 ER PT J AU Mireskandari, A Reid, RL Kashanchi, F Dittmer, J Li, WB Brady, JN AF Mireskandari, A Reid, RL Kashanchi, F Dittmer, J Li, WB Brady, JN TI Isolation of a cDNA clone, TRX, encoding a human T-cell lymphotrophic virus type-I Tax(1) binding protein SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE HTLV-1 Tax(1); Tax(1) binding protein ID TRANSCRIPTIONAL ACTIVATOR TAX; HTLV-I; REGULATORY ELEMENTS; TRANSACTIVATION; MYELOPATHY; SEQUENCES; PROMOTER; ENHANCER; REPEATS; BLOOD AB Tax, is essential for human T-cell lymphotropic virus type I (HTLV-I) virus replication and transformation. We have identified and characterized a Tax(1) binding protein, TRX, by cDNA screening of a Jurkat T-cell cDNA library. TRX mRNA is ubiquitously expressed in human tissues tested and cell lines analyzed. C1 NCI,MOLEC VIROL LAB,NIH,BETHESDA,MD 20892. US FDA,ONCOL BRANCH,DIB CLIN TRIAL DESIGN & ANAL,CTR BIOL & RES,ROCKVILLE,MD 20852. LIFE TECHNOL,GAITHERSBURG,MD. RI Dittmer, Juergen/G-1160-2011 NR 19 TC 8 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD APR 10 PY 1996 VL 1306 IS 1 BP 9 EP 13 DI 10.1016/0167-4781(96)00012-7 PG 5 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA UF670 UT WOS:A1996UF67000003 PM 8611628 ER PT J AU Fisher, GH Lenardo, MJ ZunigaPflucker, JC AF Fisher, GH Lenardo, MJ ZunigaPflucker, JC TI Synergy between T cell receptor and Fas (CD95/APO-1) signaling in mouse thymocyte death SO CELLULAR IMMUNOLOGY LA English DT Article ID CLONAL DELETION; MONOCLONAL-ANTIBODIES; IMMATURE THYMOCYTES; NEGATIVE SELECTION; CD4+8+ THYMOCYTES; AUTOIMMUNE MICE; LYMPHOCYTES-T; EXPRESSION; ANTIGEN; APOPTOSIS AB Administration of anti-TCR/CD3 epsilon antibody in vivo or in thymic organ culture results in the apoptotic death of CD4(+)/CD8(+) thymocytes. In contrast, purified thymocytes in suspension culture are resistant to TCR/CD3 epsilon-induced apoptotic death. We show that induction of thymocyte death, in suspension culture, can be induced by the combination of TCR/CD3 epsilon and Fas (CD95/Apo-1) signaling. No significant thymocyte death was observed after in vitro Fas cross-linking unless TCR/CD3 epsilon was simultaneously co-cross-linked or metabolic inhibitors such as actinomycin D were added. Furthermore, TCR/CD3 epsilon and Fas synergy did not operate through upregulation of Fas but by facilitation of the Fas-mediated death signal. Both TCR(mid/lo)/HSA(hi)/CD4(+)/CD8(+) (double positive) and TCR(hi)/HSA(lo)/CD4(+)/CD8(-) or CD4(-)/CD8(+) (single positive) thymocytes were susceptible to death induced by co-cross-linking of TCR/CD3 epsilon and Fas. Our results reveal a signaling synergy between the Fas and TCR/CD3 epsilon complex that has important implications for our understanding of in vivo vs in vitro models of thymocyte deletion. (C) 1996 Academic Press, Inc. C1 UNIV TORONTO,DEPT IMMUNOL,TORONTO,ON M5S 1A8,CANADA. RP Fisher, GH (reprint author), NIAID,IMMUNOL LAB,NIH,BETHESDA,MD 20892, USA. RI Zuniga-Pflucker, Juan/H-1295-2012; OI Zuniga-Pflucker, Juan Carlos/0000-0003-2538-3178 NR 47 TC 17 Z9 17 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD APR 10 PY 1996 VL 169 IS 1 BP 99 EP 106 DI 10.1006/cimm.1996.0096 PG 8 WC Cell Biology; Immunology SC Cell Biology; Immunology GA UF065 UT WOS:A1996UF06500014 PM 8612301 ER PT J AU Ujike, H Akiyama, K Kuroda, S AF Ujike, H Akiyama, K Kuroda, S TI [H-3]YM-09151-2 (nemonapride), a potent radioligand for both sigma(1) and sigma(2) receptor subtypes SO NEUROREPORT LA English DT Article DE sigma receptors; nemonapride; [H-3]YM-09151-2; (+)-[H-3]SKF-10047; [H-3]DTG, (+)-[H-3]3-PPP; (+)-[H-3]pentazocine; binding study; autoradiography; rat ID GUINEA-PIG BRAIN; BINDING-SITES; H-3 YM-09151-2; RAT; ANTAGONISTS; AFFINITY; LIGANDS; CELLS AB USING K+ phosphate buffer with 25 nM spiperone, [H-3]YM-09151-2 binding showed a high affinity for sigma receptors but no affinity for D-2 dopamine or 5-HT1A receptors in rat brain. The order of pK(i) values of various sigma compounds at [H-3]YM-09151-2 binding sites and stereoisomer selectivity were consistent with previous studies using other sigma ligands such as (+)-[H-3]SKF-10047, [H-3]DTG and (+)-[H-3]3-PPP. Although Scatchard analysis fitted a one-site model, competition between [H-3]YM-09151-2 and (+)-pentazocine revealed two sites, sigma(1) and sigma(2) receptors, at which the K-i values of YM-09151-2 were 8.4nM and 9.6nM, respectively. Autoradiography using [H-3]YM-09151-2 also showed a characteristic distribution of sigma receptors in rat brain. [H-3]YM-09151-2 is, therefore, a potent and useful radioligand for sigma(1)/sigma(2) receptor subtypes. C1 NIDA,MOL NEUROBIOL BRANCH,BALTIMORE,MD 21224. RP Ujike, H (reprint author), OKAYAMA UNIV,SCH MED,DEPT NEUROPSYCHIAT,2-5-1 SHIKATA CHO,OKAYAMA 700,JAPAN. NR 19 TC 18 Z9 19 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD APR 10 PY 1996 VL 7 IS 5 BP 1057 EP 1061 DI 10.1097/00001756-199604100-00021 PG 5 WC Neurosciences SC Neurosciences & Neurology GA VF117 UT WOS:A1996VF11700021 PM 8804051 ER PT J AU Winokur, G Coryell, W Endicott, J Keller, M Akiskal, H Solomon, D AF Winokur, G Coryell, W Endicott, J Keller, M Akiskal, H Solomon, D TI Familial alcoholism in manic-depressive (bipolar) disease SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE familial alcoholism; bipolar; mania; hyperactivity ID HYPERACTIVE CHILD SYNDROME; DISORDER; CRITERIA AB A previous analysis found a relatively high rate of alcoholism in a cohort of bipolar I subjects, and a trend for increased rates of alcoholism in relatives of subjects with both bipolar I disorder and alcoholism, compared to relatives of subjects with bipolar I disorder and no alcoholism. The sample of subjects with bipolar I disorder has been enlarged through continued follow-up, permitting new analyses to address the association and heritability of bipolar I disorder with alcoholism. Probands with bipolar I disorder were followed for 10 years as part of the NIMH Collaborative Depression Study. The rate of alcoholism in relatives of probands with both bipolar I disorder and alcoholism was compared to the rate of alcoholism in relatives of probands with bipolar disorder and no alcoholism. The prevalence of alcoholism in relatives of subjects with bipolar I disorder was compared to the rate of alcoholism in relatives of control subjects, Relatives of probands with bipolar I disorder showed a higher rate of alcoholism than relatives of controls. Relatives of probands with bipolar I disorder and alcoholism showed a higher rate of alcoholism than relatives of probands with bipolar I disorder without alcoholism. These data suggest that familial alcoholism may contribute to a vulnerability to bipolar I disorder, and that there is a shared heritability for the two disorders. (C) 1996 Wiley-Liss, Inc. C1 NIMH,COLLABORAT PROGRAM PSYCHOBIOL DEPRESS CLIN STUDIE,WASHINGTON,DC. FU NIMH NIH HHS [R01 MH025478] NR 18 TC 39 Z9 39 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD APR 9 PY 1996 VL 67 IS 2 BP 197 EP 201 DI 10.1002/(SICI)1096-8628(19960409)67:2<197::AID-AJMG10>3.0.CO;2-E PG 5 WC Genetics & Heredity SC Genetics & Heredity GA UH661 UT WOS:A1996UH66100012 PM 8723047 ER PT J AU Gershon, ES Badner, JA DeteraWadleigh, SD Ferraro, TN Berrettini, WH AF Gershon, ES Badner, JA DeteraWadleigh, SD Ferraro, TN Berrettini, WH TI Maternal inheritance and chromosome 18 allele sharing in unilineal bipolar illness pedigrees SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE genetic linkage; affected-sib-pairs; manic-depressive illness AB We have replicated the observation of McMahon et al, [1995] that there is excess maternal transmission of illness in a series of previously described unilineal Bipolar manic-depressive illness extended pedigrees [Berrettini et al., 1991], (''Transmission'' is defined for any ill person in a pedigree when father or mother has a personal or immediate family history of major affective disorder.) We divided our pedigrees into exclusively maternal transmission (Mat) and mixed maternal-paternal transmission (in different pedigree branches) (Pat). Using affected sib-pair-analysis, linkage to a series of markers on chromosome 18p-cen was observed in the Pat but not the Mat pedigrees, with significantly greater identity by descent (IBD) at these markers in the Pat pedigrees. As compared with the pedigree series as a whole, the proportion of alleles IBD in the linkage region is much increased in the Pat pedigrees. As shown by Kruglyak and Lander [1995], as the sharing proportion of alleles in affected relative pairs increases, the number of such pairs needed to resolve the linkage region to a 1 cM interval becomes smaller. Genetic subdivision of an illness by clinical or pedigree configuration criteria may thus play an important role in discovery of disease susceptibility mutations (C) 1996 Wiley-Liss, Inc. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. RP Gershon, ES (reprint author), NIMH,BETHESDA,MD 20892, USA. FU PHS HHS [49181] NR 10 TC 105 Z9 106 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD APR 9 PY 1996 VL 67 IS 2 BP 202 EP 207 DI 10.1002/(SICI)1096-8628(19960409)67:2<202::AID-AJMG11>3.0.CO;2-N PG 6 WC Genetics & Heredity SC Genetics & Heredity GA UH661 UT WOS:A1996UH66100013 PM 8723048 ER PT J AU Rothschild, LG Badner, J Cravchik, A Gershon, ES Gejman, PV AF Rothschild, LG Badner, J Cravchik, A Gershon, ES Gejman, PV TI No association detected between a D-3 receptor gene-expressed variant and schizophrenia SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE schizophrenia; dopamine D-3 receptor gene; DRD3; polymorphism; transmission for linkage disequilibrium test; TDT ID DOPAMINE D3 RECEPTOR; SCHIZOAFFECTIVE DISORDER; HOMOZYGOSITY; LINKAGE; FAMILY AB A missense polymorphism (glycine to serine) in the first exon of the dopamine D-3 (DRDS) gene was examined in a sib-pairs schizophrenia collection by the transmission test for linkage disequilibrium (TDT). No association due to linkage disequilibrium was detected using TDT. Additionally, no evidence for excess homozygosity was found. (C) 1996 Wiley-Liss, Inc. C1 NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. NR 26 TC 21 Z9 21 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 APR 9 PY 1996 VL 67 IS 2 BP 232 EP 234 DI 10.1002/(SICI)1096-8628(19960409)67:2<232::AID-AJMG18>3.0.CO;2-K PG 3 WC Genetics & Heredity SC Genetics & Heredity GA UH661 UT WOS:A1996UH66100020 PM 8723055 ER PT J AU Warner, DR Hoffman, JL AF Warner, DR Hoffman, JL TI Suicide inactivation of thioether S-methyltransferase by ethyl vinyl sulfide SO BIOCHEMISTRY LA English DT Article ID SULFONIUM; PROTEIN; ENZYME; SULFUR AB Thioether S-methyltransferase is an important enzyme in the metabolism of sulfur and selenium-containing compounds in animals. Ethyl vinyl sulfide was previously shown to be a substrate for this enzyme yielding methyl ethyl vinyl sulfonium ion (MEVS(+)) upon reaction with S-adenosylmethionine. Since vinyl sulfonium ions are reactive toward nucleophiles, the inactivation of thioether S-methyltransferase as a result of its methylation of ethyl vinyl sulfide was investigated, Ethyl vinyl sulfide was found to inactivate thioether S-methyltransferase in a time-dependent, pseudo-first-order process with k(inact) and K-I values of 0.05 min(-1) and 0.275 mM, respectively, Calculation of the partition ratio revealed one inactivation event for every 100 turnovers, Dimethyl sulfide, an alternate substrate for thioether S-methyltransferase which yields the nonreactive product trimethyl sulfonium ion, protected the enzyme from inactivation by ethyl vinyl sulfide. The inactivation is a result of covalent reaction of methyl ethyl vinyl sulfonium ion with the enzyme as shown by comigration of radioactivity with the enzyme during denaturing gel filtration of reaction mixtures containing thioether S-methyltransferase, ethyl vinyl sulfide, and S-adenosyl[methyl-H-3]methionine, Using this method the stoichiometry of inactivation was determined to be 1 mel of [H-3]-methyl group/mol of thioether S-methyltransferase inactivated, Both the alternate substrate, dimethyl sulfide, and the competitive product inhibitor, S-adenosylhomocysteine, inhibited such covalent labeling of the enzyme by ethyl vinyl sulfide and S-adenosyl[methyl-H-3]methionine, Chemically synthesized MEVS(+) inactivated thioether S-methyltransferase, and [methyl-C-14]MEVS(+) covalently labeled the enzyme with C-14. These results reveal a previously unrecognized mechanism for biochemical activation of vinyl thioethers by methylation to form reactive vinyl sulfonium ions. C1 UNIV LOUISVILLE,DEPT BIOCHEM,SCH MED,LOUISVILLE,KY 40292. NINCDS,MEMBRANE BIOCHEM SECT,NIH,BETHESDA,MD 20892. FU NIEHS NIH HHS [ES-4887] NR 17 TC 5 Z9 5 U1 2 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 9 PY 1996 VL 35 IS 14 BP 4480 EP 4484 DI 10.1021/bi9600815 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE612 UT WOS:A1996UE61200025 PM 8605197 ER PT J AU Barnett, SM Dracheva, S Hendler, RW Levin, IW AF Barnett, SM Dracheva, S Hendler, RW Levin, IW TI Lipid-induced conformational changes of an integral membrane protein: An infrared spectroscopic study of the effects of triton X-100 treatment on the purple membrane of Halobacterium halobium ET1001 SO BIOCHEMISTRY LA English DT Article ID X-RAY-DIFFRACTION; BACTERIORHODOPSIN PHOTOCYCLE; PROTON TRANSLOCATION; SECONDARY STRUCTURE; REVISED STRUCTURE; RAMAN; MODEL; INTERMEDIATE; SPECTRA; RECONSTITUTION AB Exposure of purple membrane from Halobacterium halobium to sublytic concentrations of Triton X-100 results in significant changes in the bacteriorhodopsin (BR) photocycle (Mukhopadhyay et al., 1994). Infrared spectra of purple membrane samples exposed briefly to Triton indicate that this change in protein function accompanies the preferential release of purple membrane glycolipids and squalenes, an association of Triton with purple membrane, and a perturbation of specific lipid headgroup interactions within the membrane. Specifically, the bilayer alterations induced by Triton entail a disruption of lipid headgroup hydrogen bonding in addition to protein conformational changes involving a loss in beta-turn and alpha(II)-helical structures in BR. We propose that the purple membrane glycolipids and squalenes are critical for the normal functioning of the BR photocycle and that perturbations of these lipids cause the profound photocycle changes induced by exposure to Triton. Lipid reconstitution studies demonstrated that although several of the infrared spectral parameters characteristic of the structural changes induced by Triton were reversed, the photocycle characteristics of BR in native purple membrane were not regained. The observed changes in the vibrational spectra induced by lipid-mediated bilayer perturbations suggest a useful approach for clarifying structure-function relationships of intrinsic membrane proteins exhibiting transmembrane helices. C1 NIDDKD,CHEM PHYS LAB,BETHESDA,MD 20892. NHLBI,CELL BIOL LAB,NIH,BETHESDA,MD 20892. NR 80 TC 33 Z9 33 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 9 PY 1996 VL 35 IS 14 BP 4558 EP 4567 DI 10.1021/bi952258l PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UE612 UT WOS:A1996UE61200034 PM 8605206 ER PT J AU Bowen, T Planalp, RP Brechbiel, MW AF Bowen, T Planalp, RP Brechbiel, MW TI An improved synthesis of cis,cis-1,3,5-triaminocyclohexane. Synthesis of novel hexadentate ligand derivatives for the preparation of gallium radiopharmaceuticals SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID METAL-IONS; COMPLEXES; DESIGN; PET AB An improved synthesis of cis,cis-1,3,5-triaminocyclohexane in 82% yield involves reaction of the commercially available cis,cis-1,3,5-cyclohexanetricarboxylic acid with DPPA to afford the tri(benzylcarbamate) as the Curtius rearrangement product Deprotection yields the triamine which serves as a platform from which a variety of chelating structures may be assembled. Novel tris(2-methylenepyridyl)triamine and tris(2-methylenethienyl)triamine ligands are prepared to investigate their suitability for use as gallium radiopharmaceuticals. C1 UNIV NEW HAMPSHIRE,DEPT CHEM,DURHAM,NH 03824. RP Bowen, T (reprint author), NIH,RADIAT ONCOL BRANCH,CHEM SECT,BETHESDA,MD 20892, USA. NR 25 TC 61 Z9 61 U1 2 U2 11 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 APR 9 PY 1996 VL 6 IS 7 BP 807 EP 810 DI 10.1016/0960-894X(96)00110-2 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA UG180 UT WOS:A1996UG18000015 ER PT J AU Ichikawa, H Deguchi, T Fujiyoshi, Y Nakago, T Jacobowitz, DM Sugimoto, T AF Ichikawa, H Deguchi, T Fujiyoshi, Y Nakago, T Jacobowitz, DM Sugimoto, T TI Calbindin-D28k-immunoreactivity in the trigeminal ganglion neurons and molar tooth pulp of the rat SO BRAIN RESEARCH LA English DT Article DE calbindin-D28k; calretinin; carbonic anhydrase; trigeminal ganglion; tooth pulp; immunohistochemistry; rat ID GENE-RELATED-PEPTIDE; CARBONIC-ANHYDRASE ACTIVITY; DORSAL-ROOT GANGLIA; PRIMARY SENSORY NEURONS; CENTRAL NERVOUS-SYSTEM; SUBSTANCE-P; HORSERADISH-PEROXIDASE; CYTOCHEMICAL-LOCALIZATION; TRANSGANGLIONIC TRANSPORT; CENTRAL PROJECTIONS AB The cell body size and coexpression of carbonic anhydrase (CA), calretinin (CR) and calcitonin gene-related peptide (CGRP) of primary neurons with calbindin-D28k (CB) was examined in the trigeminal ganglion (TG) of the rat. CB-immunoreactive (-ir) cells were mostly large and preferentially distributed in the maxillary and mandibular divisions of the TG. 48% of CB-ir TG cells exhibited enzyme CA activity. 10% of CB-ir TG cells contained CR-ir. Most TC cells coexpressing CB- and CR-irs were localized to the maxillary and mandibular divisions and exhibited CA activity. 6.5% of CB-ir TG cells coexisted with CGRP-ir. 46% of TG cells coexpressing CB and CGRP exhibited CA activity, The innervation of the molar tooth pulp by CB-ir TG primary neurons was also examined. CB-ir thick and smooth nerve fibers projected from the root pulp to the pulp horn and the roof of the pulp chamber, where they became thinner and rarely entered the subodontoblastic layer. However, they could not be traced to the odontoblastic layer, predentin or dentine. The distribution pattern of CB-ir pulpal fibers was different from that of CR-ir ones. The trigeminal neuronal cells retrogradely labeled with fast blue (FB) from the maxillary molar tooth pulp contained CB- and CR-irs. 23% and 1% of the labeled cells were immunoreactive for CB and CR, respectively. The coexpression of CB- and CR-immunoreactivities (-irs) in FB-labeled cells was negligible. An immunoelectron microscopic method revealed that 21% of pulpal nerve fibers were immunoreactive for CB, and that all CB-ir nerve fibers in the root pulp were myelinated. The present study indicated that the tooth pulp primary neurons contained CB-ir but did not coexpress CB- and CR-irs and that these neurons projected their myelinated axons to the pulp. C1 OKAYAMA UNIV,SCH DENT,DEPT ORTHODONT,OKAYAMA 700,JAPAN. NIMH,CLIN SCI LAB,BETHESDA,MD 20892. RP Ichikawa, H (reprint author), OKAYAMA UNIV,SCH DENT,DEPT ORAL ANAT 2,2-5-1 SHIKATA CHO,OKAYAMA 700,JAPAN. NR 40 TC 30 Z9 30 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 9 PY 1996 VL 715 IS 1-2 BP 71 EP 78 DI 10.1016/0006-8993(95)01550-7 PG 8 WC Neurosciences SC Neurosciences & Neurology GA UK609 UT WOS:A1996UK60900009 PM 8739624 ER PT J AU Jain, R Cohen, LA AF Jain, R Cohen, LA TI Regiospecific alkylation of histidine and histamine at N-1 (tau) SO TETRAHEDRON LA English DT Article ID 3-SUBSTITUTED L-HISTIDINES; SIDE-CHAINS; METHYLHISTIDINE AB Series of 1-alkyl histidines and histamines have been synthesized by the alkylation of the corresponding 5,6,7,8-tertrahydro-5-oxoimidazo[1,5-c]pyrimidines with alkyl halides in aprotic solvents. The method of conversion of the intermediate quaternary salt to the aminoacid or amine depends oil the nature of the alkyl group. C1 NIDDK,BIOORGAN CHEM LAB,NIH,BETHESDA,MD 20892. NR 21 TC 43 Z9 43 U1 0 U2 7 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0040-4020 J9 TETRAHEDRON JI Tetrahedron PD APR 8 PY 1996 VL 52 IS 15 BP 5363 EP 5370 DI 10.1016/0040-4020(96)00187-1 PG 8 WC Chemistry, Organic SC Chemistry GA UD909 UT WOS:A1996UD90900006 ER PT J AU Hasbahceci, M Kiyan, M Eyol, E Ewalt, LC Lodmell, DL AF Hasbahceci, M Kiyan, M Eyol, E Ewalt, LC Lodmell, DL TI Human diploid-cell rabies vaccine: Efficacy of four doses SO LANCET LA English DT Letter C1 NIAID,ROCKY MT LABS,LAB PERSISTENT DIS,HAMILTON,MT. RP Hasbahceci, M (reprint author), HACETTEPE UNIV HOSP,DEPT SURG,CENT CAMPUS SIHHIYE,ANKARA,TURKEY. RI Kiyan, Mehmet/D-2527-2015 OI Kiyan, Mehmet/0000-0002-6748-2070 NR 3 TC 4 Z9 5 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 6 PY 1996 VL 347 IS 9006 BP 976 EP 977 DI 10.1016/S0140-6736(96)91467-1 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA UD591 UT WOS:A1996UD59100067 PM 8598794 ER PT J AU Angeles, TS Steffler, C Bartlett, BA Hudkins, RL Stephens, RM Kaplan, DR Dionne, CA AF Angeles, TS Steffler, C Bartlett, BA Hudkins, RL Stephens, RM Kaplan, DR Dionne, CA TI Enzyme-linked immunosorbent assay for trkA tyrosine kinase activity SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID NERVE GROWTH-FACTOR; PHOSPHOLIPASE-C-GAMMA; FACTOR RECEPTOR; EGF RECEPTOR; NEUROTROPHIN RECEPTORS; SELECTIVE INHIBITOR; INSULIN-RECEPTOR; CELLULAR ACTIONS; BINDING-SITE; PROTEIN AB A 96-well microtiter enzyme-linked immunosorbent assay was developed to assay the activity of the cytoplasmic domain of trkA tyrosine kinase. The assay involves immobilization of phospholipase C-gamma/glutathione S-transferase fusion protein on a microtiter plate, addition of the kinase reaction mixture, and detection by an antibody to phosphotyrosine followed by an alkaline phosphatase-conjugated second antibody. The substrate used in this system, phospholipase C-gamma, is one of several biologically important substrates for the phosphorylation reaction of receptor-linked tyrosine kinases. The assay was then used to characterize kinase inhibitory activities of various small molecules including analogs of K-252a. (C) 1996 Academic Press, Inc. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,EUKARYOT SIGNAL TRANSDUCT SECT,FREDERICK,MD 21702. CEPHALON INC,DEPT CHEM,W CHESTER,PA 19380. RP Angeles, TS (reprint author), CEPHALON INC,DEPT CELL BIOL,145 BRANDYWINE PKWY,W CHESTER,PA 19380, USA. NR 31 TC 40 Z9 40 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD APR 5 PY 1996 VL 236 IS 1 BP 49 EP 55 DI 10.1006/abio.1996.0130 PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA UE209 UT WOS:A1996UE20900008 PM 8619495 ER PT J AU Pergami, P Jaffe, H Safar, J AF Pergami, P Jaffe, H Safar, J TI Semipreparative chromatographic method to purify the normal cellular isoform of the prion protein in nondenatured form SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID SODIUM DODECYL-SULFATE; MEMBRANE-PROTEINS; LIQUID-CHROMATOGRAPHY; PRECURSOR PROTEIN; MOLTEN GLOBULE; SCRAPIE AGENT; PURIFICATION; BRAIN; SIZE; PRP AB A fundamental step in the pathogenesis of spongiform encephalopathies (prion diseases) is the conversion of the cellular isoform of prion protein (PrPC) into the infectious form (scrapie isoform, PrPSc), apparently by a conformational mechanism, Comparison of the native secondary and tertiary structures of both proteins is essential to elucidate the molecular basis of this transformation, To obtain sufficient quantities of native-like PrPC, we have developed a semipreparative method to purify PrPC from hamster brains, PrPC was solubilized from purified synaptosomal and microsomal membranes by the nonionic detergent n-octyl-beta-glucopyranoside; the soluble fraction was loaded at pH 7.5 onto a semipreparative cation-exchange TSK-SP-BPW (HPLC) column, The fr actions eluted by linear NaCl gradient and enriched for PrPC were sequentially purified using an immobilized ion-affinity HPLC column charged by Co2+, followed by wheat germ agglutinin (WGA)-affinity HPLC or size-exclusion HPLC (SE-HPLC) using a TSK G3000SW column, More than 95% purity was achieved after SE-HPLC as estimated by quantitative densitometry of the silver-stained SDS-PAGE gel; the recovery of total brain PrPC was greater than or equal to 8%. The purified PrPC was a monomer with an intact N-terminus, and with a Stoke's radius of 26 Angstrom, corresponding to that expected from the molecular weight for a native protein, The presence of the native-like conformation was further verified by peptide mapping after limited trypsin proteolysis, and by the apparent unfolding in guanidine hydrochloride, as detected by SE-HPLC. (C) 1906 Academic Press, Inc. C1 NINCDS,NIH,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. NINCDS,NIH,DIV INTRAMURAL RES,PROT PEPTIDE SEQUENCING FACIL,BETHESDA,MD 20892. RI Safar, Jiri/G-6512-2013 NR 40 TC 67 Z9 70 U1 0 U2 3 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD APR 5 PY 1996 VL 236 IS 1 BP 63 EP 73 DI 10.1006/abio.1996.0132 PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA UE209 UT WOS:A1996UE20900010 PM 8619497 ER PT J AU Steinert, PM Chung, SI Kim, SY AF Steinert, PM Chung, SI Kim, SY TI Inactive zymogen and highly active proteolytically processed membrane-bound forms of the transglutaminase 1 enzyme in human epidermal keratinocytes SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID ANCHORAGE REGION; ENVELOPE; EXPRESSION; DIFFERENTIATION; INVOLUCRIN; PROTEIN; CELLS; GENE AB The transglutaminase 1 enzyme is important for the formation of a cornified cell envelope in terminally differentiating keratinocytes. We show here that it is present in low levels in proliferating foreskin or cultured epidermal cells as an inactive zymogen full length form of 106 kDa, of which >95% is attached to membranes. In terminally differentiating keratinocytes, there is a greater than or equal to 100-fold induction of mRNA and protein. In addition to some cytosolic protein, most of the newly expressed protein is attached to membranes, of which about half exists in the zymogen form. Other protein consists of a 67/33/10 kDa complex formed by proteolytic processing at specific sites, and is anchored by way of the 10 kDa fragment. This processed form is very highly active and thus accounts for almost all transglutaminase 1 activity in keratinocytes. (C) 1996 Academic Press, Inc. C1 GREEN CROSS CO,KIHEUNG EUP,SOUTH KOREA. PACIFIC CORP,KYOUNGGI DO 449900,SOUTH KOREA. RP Steinert, PM (reprint author), NIAMSD,SKIN BIOL LAB,NIH,BLDG 6,ROOM 425,BETHESDA,MD 20892, USA. NR 25 TC 57 Z9 57 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 APR 5 PY 1996 VL 221 IS 1 BP 101 EP 106 DI 10.1006/bbrc.1996.0552 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA UF049 UT WOS:A1996UF04900019 PM 8660317 ER PT J AU vanGent, DC Ramsden, DA Gellert, M AF vanGent, DC Ramsden, DA Gellert, M TI The RAG1 and RAG2 proteins establish the 12/23 rule in V(D)J recombination SO CELL LA English DT Article ID MOUSE THYMOCYTES; SIGNALS; DNA AB V(D)J recombination requires a pair of signal sequences with spacer lengths of 12 and 23 base pairs. Cleavage by the RAG1 and RAG2 proteins was previously shown to demand only a single signal sequence. Here, we establish conditions where 12- and 23-spacer signal sequences are both necessary for cleavage. Coupled cutting at both sites requires only the RAG1 and RAG2 proteins, but depends on the metal ion. In Mn2+, a single signal sequence supports efficient double strand cleavage, but cutting in Mg2+ requires two signal sequences and is best with the canonical 12/23 pair. Thus, the RAG proteins determine both aspects of the specificity of V(D)J recombination, the recognition of a single signal sequence and the correct 12/23 coupling in a pair of signals. RP vanGent, DC (reprint author), NIDDKD,MOLEC BIOL LAB,NIH,BETHESDA,MD 20892, USA. NR 18 TC 223 Z9 224 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 0092-8674 J9 CELL JI Cell PD APR 5 PY 1996 VL 85 IS 1 BP 107 EP 113 DI 10.1016/S0092-8674(00)81086-7 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UE559 UT WOS:A1996UE55900013 PM 8620529 ER PT J AU Phelps, DE Dressler, GR AF Phelps, DE Dressler, GR TI Identification of novel Pax-2 binding sites by chromatin precipitation SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR BSAP; B-CELL DIFFERENTIATION; HOMEOTIC GENE-CONTROL; PAIRED BOX GENE; EARLY NEUROGENESIS; SWITCH REGIONS; IN-VIVO; EXPRESSION; PROTEIN; DROSOPHILA AB The Pax genes encode a family of developmental transcription factors that bind to specific DNA sequences via the paired domain and are necessary for the morphogenesis of a variety of tissues, The murine Pax-2 gene, through alternative splicing, encodes two nuclear proteins, Pax-2A and Pax-2B, which are transiently expressed during the differentiation of specific neural cell types and early kidney formation. In order to identify potential in vivo Pax-2 target sequences, chromatin from embryonic neural tube was immunoprecipitated with Pax-2 specific antibodies and cloned. Two unique immunoprecipitated clones containing three specific Pax-2 binding sites were identified by functional binding assays using Pax-2 proteins produced in both Escherichia coli and eukaryotic cells. In vitro DNA binding assays, using Pax-5 and Pax-8 DNA recognition sequences as well as the three immunopurified Pax-2 binding sites, demonstrated that both forms of the Pax-2 protein bind DNA with a similar specificity and that this binding is mediated by the paired domain. The binding sites identified in this report share significant homology among themselves and with previously defined consensus sequences for Pax-5 and Pax-2. The genomic clones can now be used as sequence tags to identify potential target loci. C1 NICMD, NIH, BETHESDA, MD 20892 USA. NR 58 TC 52 Z9 52 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1996 VL 271 IS 14 BP 7978 EP 7985 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UD600 UT WOS:A1996UD60000018 PM 8626478 ER PT J AU Roesler, WJ Crosson, SM Vinson, C McFie, PJ AF Roesler, WJ Crosson, SM Vinson, C McFie, PJ TI The alpha-isoform of the CCAAT/enhancer-binding protein is required for mediating cAMP responsiveness of the phosphoenolpyruvate carboxykinase promoter in hepatoma cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID 3 C/EBP ISOFORMS; GTP GENE; TRANSCRIPTIONAL REGULATION; RESPONSE ELEMENT; KINASE-C; EXPRESSION; ACTIVATION; ENHANCER; FAMILY; IDENTIFICATION AB The gene coding for phosphoenolpyruvate carboxykinase (GTP) (EC 4.1.1.32) is expressed in all gluconeogenic tissues, but stimulation of its rate of transcription by cAMP is robust only in liver, Evidence has accumulated which suggests that a liver-enriched transcription factor, likely a member of the CCAAT/enhancer binding protein (C/EBP) family, is required along with other ubiquitously expressed transcription factors to mediate this liver-specific response to cAMP. In this study, we examined the ability of C/EBP to participate in the cAMP-mediated activation of phosphoenolpyruvate carboxykinase (PEPCK) gene transcription in hepatoma cells, Expression of a dominant repressor of C/EBP in hepatoma cells significantly inhibited the protein kinase A-stimulated transcription of the PEPCK promoter, suggesting that a C/EBP family member was required for maximal transcriptional activation by protein kinase A. To provide additional support for this hypothesis, we prepared GAL4 fusion proteins containing C/EBP domains. Both C/EBP alpha and C/EBP beta GAL4 fusion proteins were capable of stimulating transcription from promoters containing binding sites for the DNA-binding domain of GAL4, However, only the GAL4-C/EBP alpha fusion protein demonstrated the ability to synergize with the other transcription factors bound to the PEPCK promoter which are required to mediate cAMP responsiveness, The DNA-binding domain of C/EBP alpha was not required for this activity in hepatoma cells, although in non-hepatoma cells the basic region leucine zipper domain appeared to inhibit the ability of C/EBP alpha to participate in mediating cAMP responsiveness, These results suggest that the liver-specific nature of the cAMP responsiveness of the PEPCK promoter involves the recruitment of C/EBP alpha to the cAMP response unit. C1 NCI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. RP Roesler, WJ (reprint author), UNIV SASKATCHEWAN,DEPT BIOCHEM,SASKATOON,SK S7N 5E5,CANADA. NR 43 TC 50 Z9 50 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1996 VL 271 IS 14 BP 8068 EP 8074 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UD600 UT WOS:A1996UD60000031 PM 8626491 ER PT J AU Gladyshev, VN Boyington, JC Khangulov, SV Grahame, DA Stadtman, TC Sun, PD AF Gladyshev, VN Boyington, JC Khangulov, SV Grahame, DA Stadtman, TC Sun, PD TI Characterization of crystalline formate dehydrogenase H from Escherichia coli - Stabilization, EPR spectroscopy, and preliminary crystallographic analysis SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MOLYBDENUM COFACTORS; HYDROGEN-LYASE; SELENOCYSTEINE; SEQUENCE; BIOCHEMISTRY; SELENIUM; ENZYMES AB The selenocysteine-containing formate dehydrogenase H (FDH) is an 80-kDa component of the Escherichia coli formate-hydrogen lyase complex. The molybdenum-coordinated selenocysteine is essential for catalytic activity of the native enzyme, FDH in dilute solutions (30 mu g/ml) was rapidly inactivated at basic pH or in the presence of formate under anaerobic conditions, but at higher enzyme concentrations (greater than or equal to 3 mg/ml) the enzyme was relatively stable, The formate-reduced enzyme was extremely sensitive to air inactivation under all conditions examined. Active formate-reduced FDH was crystallized under anaerobic conditions in the presence of ammonium sulfate and PEG 400. The crystals diffract to 2.6 Angstrom resolution and belong to a space group of P4(1)2(1)2 or P4(3)2(1)2 with unit cell dimensions a = b = 146.1 Angstrom and c = 82.7 Angstrom. There is one monomer of FDH per crystallographic asymmetric unit. Similar diffraction quality crystals of oxidized FDH could be obtained by oxidation of crystals of formate-reduced enzyme with benzyl viologen. By EPR spectroscopy, a signal of a single reduced FeS cluster was found in a crystal of reduced FDH, but not in a crystal of oxidized enzyme, whereas Mo(V) signal was not detected in either form of crystalline FDH. This suggests that Mo(IV)- and the reduced FeS cluster-containing form of the enzyme was crystallized and this could be converted into Mo(VI)- and oxidized FeS cluster form upon oxidation. A procedure that combines anaerobic and cryocrystallography has been developed that is generally applicable to crystallographic studies of oxygen-sensitive enzymes. These data provide the first example of crystallization of a substrate-reduced form of a Se- and Mo-containing enzyme. C1 NHLBI,NIH,LB,BETHESDA,MD 20892. NIAID,MOLEC STRUCT LAB,NIH,ROCKVILLE,MD 20852. UNIFORMED SERV UNIV HLTH SCI,DEPT BIOCHEM,BETHESDA,MD 20814. NR 26 TC 34 Z9 35 U1 1 U2 6 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1996 VL 271 IS 14 BP 8095 EP 8100 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UD600 UT WOS:A1996UD60000035 PM 8626495 ER PT J AU Nashed, EM Glaudemans, CPJ AF Nashed, EM Glaudemans, CPJ TI Observations on the binding of four anti-carbohydrate monoclonal antibodies to their homologous ligands SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MYELOMA PROTEINS; CHEMICAL SYNTHESIS; O-ANTIGEN; OLIGOSACCHARIDES; GLYCOSIDES; SUBSITES; DEXTRAN; THERMODYNAMICS; SPECIFICITY; SALMONELLA AB The binding of four monoclonal immunoglobulins, two with specificity for beta(1-->6)-linked D-galactopyranans (IgA X24 and IgA J539) and two with specificity for the chain terminus of alpha(1-->6)-linked D-glucopyranans (IgA W3129 and IgA 16.4.12E), was measured with a number of their homologous oligosaccharide ligands at different temperatures. The results show a linear relationship between lnk(alpha) and 1/T, where K-alpha is the affinity constant and T is the absolute temperature. The unitary free energy of binding, Delta G(u), is virtually independent of T, and the Delta S-u is small when compared with Delta G(u). The enthalpy changes derived from van't Hoff plots are large and negative, indicating an exothermic binding effect, whereas the entropy changes are small and negative, indicating minor overall hydrophobic contributions. Measurements of the free energies of binding, in low and high salt buffers, of methyl beta-D-galactopyranoside and the methyl glycoside of beta(1-->6)-D-galactopyranotetraose with anti-galactan IgA X24 indicate that the monosaccharide has no hydrophobic interaction with the highest affinity subsite of IgA, whereas the tetraoside might have a modest hydrophobic interaction with the three other hapten-binding subsites of IgA. The standard entropy change of binding of the two groups (galactosyl and glucosyl) of oligosaccharides to the two respective sets (anti-galactan and anti-dextran) of antibodies shows a distinct, differing correlation with the hapten chain length within each set. This correlation agrees with the type of association previously established between the antibodies and either the interior determinants of the antigen (in the case of the anti-galactans) or the chain terminus (in the case of the anti-dextrans). RP Nashed, EM (reprint author), NIDDK,NIH,BETHESDA,MD 20892, USA. NR 33 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1996 VL 271 IS 14 BP 8209 EP 8214 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UD600 UT WOS:A1996UD60000053 PM 8626513 ER PT J AU Funada, M Schutz, CG Shippenberg, TS AF Funada, M Schutz, CG Shippenberg, TS TI Role of delta-opioid receptors in mediating the aversive stimulus effects of morphine withdrawal in the rat SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE naltrindole; naltriben; delta-opioid receptor; opioid withdrawal ID STRESS-INDUCED ANTINOCICEPTION; ANTAGONIST NALTRINDOLE; YOUNG-RATS; DEPENDENCE; NALOXONE; MAINTENANCE; PEPTIDES; BINDING; POTENT; DRUGS AB An unbiased place preference conditioning procedure was used to examine the role of delta-opioid receptors in mediating the aversive effects of opioid withdrawal. Rats were implanted s.c. with two pellets each containing placebo or 75 mg morphine. Single-trial conditioning sessions with saline and the opioid receptor antagonists naloxone (0.001-1.0 mg/kg, s.c.), naltrindole (0.01-3.0 mg/kg, s.c.) or naltriben (0.01-3.0 mg/kg, s.c.) commenced 4 days later. During these conditioning sessions, physical signs of withdrawal were also quantified. Tests of conditioning were conducted on day 5. Naloxone in doses of 0.01-1.0 mg/kg produced significant conditioned place aversions in morphine-implanted animals. A dose of 0.01 mg/kg produced few physical withdrawal signs whereas higher doses resulted in marked wet dog shakes, body weight loss, ptosis and diarrhea. No such effects were observed in control (placebo-implanted) animals. Administration of the selective delta-opioid receptor antagonists naltrindole and naltriben produced dose-related place aversions in morphine-implanted animals. The magnitude of these effects did not differ from that observed with naloxone. The minimum effective doses of naltrindole and naltriben were 0.1 mg/kg. Doses of 0.1-1.0 mg/kg produced few, if any, somatic signs of withdrawal whereas higher doses of these antagonists only produced diarrhea and wet-dog shakes. Other withdrawal signs were absent. In contrast to the opioid receptor antagonists tested, the dopamine D-1 receptor antagonist SCH23390 failed to produced conditioned place aversions or physical signs of withdrawal in morphine-pelleted animals. These data demonstrate that the selective blockade of either delta- or mu-opioid receptors is sufficient to induce conditioned aversive effects in morphine-dependent animals. They also indicate that physical symptoms associated with precipitated morphine withdrawal differ depending upon the opioid receptor antagonist employed. C1 NIDA,DIV INTRAMURAL RES,PRECLIN PHARMACOL BRANCH,BALTIMORE,MD 21224. RP Funada, M (reprint author), NIDA,DIV INTRAMURAL RES,CLIN PHARMACOL BRANCH,POB 5180,BALTIMORE,MD 21224, USA. NR 34 TC 20 Z9 20 U1 0 U2 1 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 APR 4 PY 1996 VL 300 IS 1-2 BP 17 EP 24 DI 10.1016/0014-2999(95)00860-8 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UG949 UT WOS:A1996UG94900003 PM 8741160 ER PT J AU Silberman, JD Sogin, ML Leipe, DD Clark, CG AF Silberman, JD Sogin, ML Leipe, DD Clark, CG TI Human parasite finds taxonomic home SO NATURE LA English DT Letter ID BLASTOCYSTIS-HOMINIS C1 NIH, NCBI GENBANK, NATL LIB MED, BETHESDA, MD 20984 USA. UNIV LONDON LONDON SCH HYG & TROP MED, DEPT MED PARASITOL, LONDON WC1E 7HT, ENGLAND. RP Silberman, JD (reprint author), MARINE BIOL LAB, CTR MOLEC EVOLUT, WOODS HOLE, MA 02543 USA. RI Clark, C Graham/H-3683-2011 OI Clark, C Graham/0000-0002-0521-0977 NR 13 TC 130 Z9 136 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 EI 1476-4687 J9 NATURE JI Nature PD APR 4 PY 1996 VL 380 IS 6573 BP 398 EP 398 DI 10.1038/380398a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD590 UT WOS:A1996UD59000045 PM 8602239 ER PT J AU Chackalaparampil, I Peri, A Nemir, M Mckee, MD Lin, PH Mukherjee, BB Mukherjee, AB AF Chackalaparampil, I Peri, A Nemir, M Mckee, MD Lin, PH Mukherjee, BB Mukherjee, AB TI Cells in vivo and in vitro from osteopetrotic mice homozygous for c-src disruption show suppression of synthesis of osteopontin, a multifunctional extracellular matrix protein SO ONCOGENE LA English DT Article DE osteopontin; src-deficient; epidermal growth factor (EGF); homozygous; osteopetrosis ID TYROSINE KINASE; GROWTH-FACTOR; PHOSPHOPROTEIN; BONE; OSTEOCLASTS; EXPRESSION; ACTIVATION; INDUCTION; PATHWAYS AB Mice carrying homozygous disruption of the c-src protooncogene (Src-/-) develop osteopetrosis due to an impaired ability of osteoclasts to adhere to the bone surface and/or to form bone-resorbing ruffled border. It has also been reported that osteopontin (OPN), a secreted phosphoprotein, mediates osteoclast adherence to the bone matrix. We report here that cells from Src-/- mice, both in vitro and in vivo, express OPN mRNA and protein at a significantly reduced level as compared to cells from Src+/- and +/+ animals, suggesting a potential role for the proto-oncogene c-src in the regulation of OPN gene expression. Our data also show that OPN gene expression can be induced by treatment of Src -/- cells with epidermal growth factor (EGF) and 12-O-tetradecanoyl phorbol-13-acetate (TPA). Results obtained from studies using inhibitors of receptor tyrosine kinases (RTKs) and protein kinase C (PKC) suggest that PKC and RTK are positioned in a pathway with PKC as the downstream effector for the EGF-induced OPN gene expression in Src-/- cells, and that pp60(c-src) and EGF may regulate OPN gene expression through a common signalling pathway. Furthermore, contrary to published reports, our study shows that EGF-mediated cell signalling does not require functional interaction between the EGF-receptor and pp60(c-src). C1 MCGILL UNIV,DEPT BIOL,MONTREAL,PQ H3A 1B1,CANADA. NICHHD,SECT DEV GENET,HERITABLE DISORDERS BRANCH,NIH,BETHESDA,MD 20892. UNIV MONTREAL,FAC DENT,DEPT STOMATOL,MONTREAL,PQ H3C 3J7,CANADA. RUTGERS STATE UNIV,WAKSMAN INST,DEPT MICROBIOL,PISCATAWAY,NJ 08855. RI Lin, Pei-Hui/I-3011-2015 OI Lin, Pei-Hui/0000-0002-3894-5099 NR 38 TC 39 Z9 40 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD APR 4 PY 1996 VL 12 IS 7 BP 1457 EP 1467 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA UF076 UT WOS:A1996UF07600010 PM 8622862 ER PT J AU Murphy, EL Bryzman, S Williams, AE CoChien, H Schreiber, GB Ownby, HE Gilcher, RO Kleinman, SH Matijas, L Thomson, RA Nemo, GJ AF Murphy, EL Bryzman, S Williams, AE CoChien, H Schreiber, GB Ownby, HE Gilcher, RO Kleinman, SH Matijas, L Thomson, RA Nemo, GJ TI Demographic determinants of hepatitis C virus seroprevalence among blood donors SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID RISK-FACTORS; UNITED-STATES; INFECTION; ANTIBODIES; ASSOCIATION; SEROEPIDEMIOLOGY; EPIDEMIOLOGY; PREVALENCE; VIREMIA; DISEASE AB Objective.-To measure demographic determinants of hepatitis C virus (HCV) seroprevalence among blood donors in the United States. Design.-Cross-sectional epidemiological study. Setting.-Five blood centers in different regions of the United States. Subjects.-A total of 862 398 consecutive volunteer blood donors with one or more nonautologous donations from March 1992 through December 1993. Methods.-Demographic data collection, serological screening with second-generation anti-HCV enzyme immunoassay, and confirmation with anti-HCV recombinant immunoblot. Results.-There were 3126 donors with at least one blood donation confirmed HCV-seropositive, for a crude prevalence of 3.6 per 1000. Age-specific HCV seroprevalence rose from 0.5 per 1000 in donors younger than 20 years to a maximum of 6.9 per 1000 in donors aged 30 to 39 years and declined in older age groups. There was interaction between age and educational attainment, with 30- to 49-year-olds with less than a high school diploma at highest risk of HCV infection (odds ratio [OR], 33.0; 95% confidence interval [CI], 23.0 to 47.2 compared with those younger than 30 years with a bachelor's degree or higher degree), Other independent risk factors for HCV seropositivity included male sex (OR, 1.9, 95% CI, 1.8 to 2.1), black race (OR, 1.7, 95% CI, 1.6 to 1.9), Hispanic ethnicity (OR, 1.3, 95% CI, 1.1 to 1.5), previous blood transfusion (OR, 2.8; 95% CI, 2.5 to 3.1), and first/only time donor status (OR, 4.2; 95% CI, 3.9 to 4.5, compared with repeat donors), Seropositivity for human T-lymphotropic virus types I and II, human immunodeficiency virus, or hepatitis B core antigen was highly associated with HCV seropositivity (OR, 10.4; 95% CI, 9.6 to 11.4 for one vs no marker). Conclusions.-Despite a low overall HCV prevalence in blood donors in the United States, there is marked variation in HCV seroprevalence by demographic subgroup, even after controlling for prior blood transfusion, a recognized risk factor for HCV. Further study of the prevalence of other parenteral risk factors such as past injection drug use among blood donors is needed. C1 HIGHLAND GEN HOSP,OAKLAND,CA. AMER RED CROSS,JEROME H HOLLAND LAB,ROCKVILLE,MD. WESTAT CORP,ROCKVILLE,MD. AMER RED CROSS,BLOOD SERV,DETROIT,MI. OKLAHOMA BLOOD INST,OKLAHOMA CITY,OK. UNIV CALIF LOS ANGELES,BLOOD & PLATELET CTR,LOS ANGELES,CA 90024. NHLBI,BETHESDA,MD 20892. RP Murphy, EL (reprint author), UNIV CALIF SAN FRANCISCO,DEPT LAB MED,BOX 0884,SAN FRANCISCO,CA 94143, USA. FU NHLBI NIH HHS [N01-HB-97079, N01-HB-97078, N01-HB-97077] NR 33 TC 95 Z9 97 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 APR 3 PY 1996 VL 275 IS 13 BP 995 EP 1000 DI 10.1001/jama.275.13.995 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA UC123 UT WOS:A1996UC12300026 PM 8596257 ER PT J AU Smith, MA McCaffrey, RP Karp, JE AF Smith, MA McCaffrey, RP Karp, JE TI The secondary leukemias: Challenges and research directions SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Review ID ACUTE MYELOID-LEUKEMIA; ACUTE NONLYMPHOCYTIC LEUKEMIA; DNA-TOPOISOMERASE-II; CELL NUCLEAR ANTIGEN; DEBRISOQUINE METABOLIC PHENOTYPE; ACUTE LYMPHOBLASTIC-LEUKEMIA; BREAKAGE-REUNION REACTION; WILD-TYPE P53; LUNG-CANCER; HODGKINS-DISEASE AB Acute myelogenous leukemia (AML) arising following exposure to genotoxic agents has been recognized as a distinctive entity for more than 40 years. Secondary, or therapy-related, AML accounts for 10%-20% of all AML cases. This review addresses four overarching areas of investigation focused on secondary AMLs: 1) dissection of the molecular structure of the induced genetic lesions and identification of the functional consequences of these changes, thereby providing clues to the pathogenesis of secondary AML and potentially serving as a basis for innovative therapeutic interventions; 2) identification and characterization of mechanisms of DNA damage and the orderly repair of such damage; 3) identification and application of accurate biomarkers of leukemogenesis for the purpose of risk prediction and quantification, potentially allowing recognition of patients especially susceptible to the leukemogenic effects of chemotherapy (for genetic or acquired reasons) and allowing their treatment for cancer to be modified on the basis of this susceptibility; and 4) design and implementation of longitudinal clinical and genetic monitoring of high-risk populations (i.e., individuals undergoing cytotoxic therapies for primary cancers). This review of the literature relating to these areas builds upon these themes and attempts to synthesize these seemingly disparate areas of research so that they can be more effectively utilized together to address the problem of secondary AML. Ultimately, the evaluation of these areas will improve our understanding of de novo leukemia and will serve as a springboard for the development of new concepts of therapy and prevention. C1 NCI, NIH, CLIN TRIALS EVALUAT PROGRAM, DIV CANC TREATMENT DIAGNOSIS & CTR, BETHESDA, MD 20892 USA. NCI, NIH, CHEMOPREVENT BRANCH, DIV CANC PREVENT & CONTROL, BETHESDA, MD 20892 USA. BOSTON UNIV, EVANS DEPT CLIN RES, SECT MED ONCOL, BOSTON, MA 02215 USA. NR 201 TC 141 Z9 145 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 EI 1460-2105 J9 JNCI-J NATL CANCER I JI JNCI-. Natl. Cancer Inst. PD APR 3 PY 1996 VL 88 IS 7 BP 407 EP 418 DI 10.1093/jnci/88.7.407 PG 12 WC Oncology SC Oncology GA UD518 UT WOS:A1996UD51800010 PM 8618232 ER PT J AU Popescu, NC Zimonjic, DB LeventonKriss, S Bryant, JL LunardiIskandar, Y Gallo, RC AF Popescu, NC Zimonjic, DB LeventonKriss, S Bryant, JL LunardiIskandar, Y Gallo, RC TI Deletion and translocation involving chromosome 3(p14) in two tumorigenic Kaposi's sarcoma cell lines SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; SHORT ARM; CANCER; CARCINOMA; HETEROZYGOSITY; ABERRATIONS; GENE AB Background: Two neoplastic Kaposi's sarcoma (KS) cell lines, KS Y-1 (derived from a patient with KS associated with acquired immunodeficiency syndrome) and KS SLK (derived from an immunosuppressed patient with a renal transplant and KS or iatrogenic KS), have been shown to have abnormal chromosome constitution and to require no exogenous growth factors. They produce malignant tumors in immunodeficient mice. In contrast, all other cell cultures prepared in the past from KS specimens have been shown to have normal diploid characteristics, are hyperplastic, and depend on cytokines for growth, but they do not produce malignant tumors in immunodeficient mice. Purpose: We investigated whether the chromosomal changes that occurred in these KS cell lines were random or nonrandom and if such changes contribute to the pathogenesis of KS. Methods: We used the conventional G-banding technique and fluorescence in situ hybridization to identify structural and numerical chromosomal changes in the KS cell lines. Results: We demonstrated that both cell lines are aneuploid and have some additional features in common, i.e., loss of copies of chromosomes 14 and 21 and nonrandom translocations and deletions in the short arm of chromosome 3 at region 3p14. These KS cell lines also exhibit loss of heterozygosity of loci at region 3p14-ter. Conclusion: This is the first time nonrandom chromosomal alterations have been described in KS neoplastic cells. On the basis of information available on other cancers, the chromosome 3 alterations observed here can be expected to contribute to the neoplastic process in KS. Implications: Future research should focus on the identification of cytogenetic markers, thus facilitating generation of specific molecular probes for detecting neoplastic cells early in the disease process. C1 TEL AVIV UNIV,SCH MED,CHAIM SHEBA MED CTR,CENT VIRUS LAB,TEL HASHOMER,ISRAEL. NIDR,ANIM CARE UNIT,BETHESDA,MD 20892. NCI,BIOL LAB,DIV BASIC SCI,BETHESDA,MD. NCI,TUMOR CELL BIOL LAB,DIV BASIC SCI,BETHESDA,MD 20892. NR 36 TC 23 Z9 24 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 3 PY 1996 VL 88 IS 7 BP 450 EP 455 DI 10.1093/jnci/88.7.450 PG 6 WC Oncology SC Oncology GA UD518 UT WOS:A1996UD51800015 PM 8618237 ER PT J AU Clerici, M Clerici, E Shearer, GM AF Clerici, M Clerici, E Shearer, GM TI The tumor enhancement phenomenon: Reinterpretation from a Th1/Th2 perspective SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter ID INTERLEUKIN-12 C1 UNIV MILAN,CATTEDRA IMMUNOL,MILAN,ITALY. NCI,EXPTL IMMUNOL BRANCH,DIV BASIC SCI,BETHESDA,MD 20892. NR 20 TC 29 Z9 30 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 APR 3 PY 1996 VL 88 IS 7 BP 461 EP 462 DI 10.1093/jnci/88.7.461 PG 2 WC Oncology SC Oncology GA UD518 UT WOS:A1996UD51800017 PM 8618239 ER PT J AU Rhee, S Parris, KD Ahmed, SA Miles, EW Davies, DR AF Rhee, S Parris, KD Ahmed, SA Miles, EW Davies, DR TI Exchange of K+ or Cs+ for Na+ induces local and long-range changes in the three-dimensional structure of the tryptophan synthase alpha(2)beta(2) complex SO BIOCHEMISTRY LA English DT Article ID D-SERINE DEHYDRATASE; ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; BIENZYME COMPLEX; ALPHA-SUBUNIT; HINGE REGION; BETA-SUBUNIT; MECHANISM; SYNTHETASE; SUBSTRATE AB Monovalent cations activate the pyridoxal phosphate-dependent reactions of tryptophan synthase and affect intersubunit communication in the alpha(2) beta(2) complex. We report refined crystal structures of the tryptophan synthase alpha(2) beta(2) complex from Salmonella typhimurium in the presence of K+ at 2.0 Angstrom and of Cs+ at 2.3 Angstrom. Comparison of these structures with the recently refined structure in the presence of Na+ shows that each monovalent cation binds at approximately the same position about 8 Angstrom from the phosphate of pyridoxal phosphate. Na+ and K+ are coordinated to the carbonyl oxygens of beta Phe-306, beta Ser-308, and beta Gly-232 and to two or one water molecule, respectively. Cs+ is coordinated to the carbonyl oxygens of beta Phe-306, beta Ser-308, beta Gly-232, beta Val-231, beta Gly-268, and beta Leu-304. A second binding site for Cs+ is located in the pip interface on the 2-fold axis with four carbonyl oxygens in the coordination sphere. In addition to local changes in structure close to the cation binding site, a number of long-range changes are observed. The K+ and Cs+ structures differ from the Na+ structure with respect to the positions of beta Asp-305, beta Lys-167, and alpha Asp-56. One unexpected result of this investigation is the movement of the side chains of beta Phe-280 and beta Tyr-279 from a position partially blocking the tunnel in the Na+ structure to a position lining the surface of the tunnel in the K+ and Cs+ structures. The results provide a structural basis for understanding the effects of cations on activity and intersubunit communication. C1 NIDDK, NIH, MOLEC BIOL LAB, BETHESDA, MD 20892 USA. NIDDK, NIH, BIOCHEM PHARMACOL LAB, BETHESDA, MD 20892 USA. NR 70 TC 118 Z9 119 U1 2 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 2 PY 1996 VL 35 IS 13 BP 4211 EP 4221 DI 10.1021/bi952506d PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UC977 UT WOS:A1996UC97700042 PM 8672457 ER PT J AU Scherf, U Pastan, I Willingham, MC Brinkmann, U AF Scherf, U Pastan, I Willingham, MC Brinkmann, U TI The human CAS protein which is homologous to the CSE1 yeast chromosome segregation gene product is associated with microtubules and mitotic spindle SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE Pseudomonas exotoxin; tumor necrosis factor; microtubule-associated protein; apoptosis; cyclin B AB Human CAS cDNA contains a 971-aa open reading frame that is homologous to the essential yeast gene CSE1. CSE1 is involved in chromosome segregation and is necessary for B-type cyclin degradation in mitosis, Using antibodies to GAS, it was shown that CAS levels are high in proliferating and low in nonproliferating cells, Here we describe the distribution of GAS in cells and tissues analyzed with antibodies against GAS. CAS is an approximate to 100-kDa protein present in the cytoplasm of proliferating cells at levels between 2 x 10(5) and 1 x 10(6) molecules per cell. The intracellular distribution of CAS resembles that of tubulin, In interphase cells, anti-GAS antibody shows microtubule-like patterns and in mitotic cells it labels the mitotic spindle. CAS Is removed from microtubules by mild detergent treatment (cytoskeleton preparations) and in vincristine- or taxol-treated cells, CAS is diffusely distributed in the cytoplasm with only traces present in tubulin paracrystals or bundles, Thus, CAS appears to be associated with but not to be an integral part of microtubules. Immunohistochemical staining of frozen tissues shows elevated amounts of GAS in proliferating cells such as testicular spermatogonia and cells in the basal layer cells of the colon, CAS was also concentrated in the respiratory epithelium of the trachea and in axons and Purkinje cells in the cerebellum, These cells contain many microtubules. The cellular location of CAS is consistent with an important role in cell division as well as in ciliary movement and vesicular transport. C1 NCI,MOLEC BIOL LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892. MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. NR 20 TC 51 Z9 52 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2670 EP 2674 DI 10.1073/pnas.93.7.2670 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500009 PM 8610099 ER PT J AU Neel, JV Major, EO Awa, AA Glover, T Burgess, A Traub, R Curfman, B Satoh, C AF Neel, JV Major, EO Awa, AA Glover, T Burgess, A Traub, R Curfman, B Satoh, C TI Hypothesis: ''Rogue cell''-type chromosomal damage in lymphocytes is associated with infection with the JC human polyoma virus and has implications for oncopenesis SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE viral chromosome damage; JC viral oncogenesis ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; HUMAN-DIPLOID FIBROBLASTS; LARGE T-ANTIGEN; CHERNOBYL ACCIDENT; SIMIAN VIRUS-40; SV40-T ANTIGEN; ABERRATIONS; TRANSFORMATION; PATHOGENESIS; FALLOUT AB The hemagglutination inhibition antibody titers against the JC and BK polyoma viruses (JCV and BKV, respectively) are significantly elevated in individuals exhibiting ''rogue'' cells among their cultured lymphocytes. However, the elevation is so much greater with respect to JCV that the BKV elevation could readily be explained by cross reactivity to the capsid protein of these two closely related viruses, The JCV exhibits high sequence homology with the simian papovavirus, simian virus 40 (SV40), and Inoculation of human fetal brain cells with JCV produces polyploidy and chromosomal damage very similar to that produced by SV40. We suggest, by analogy with the effects of SV40, that these changes are due to the action of the viral large tumor antigen, a pluripotent DNA binding protein that acts in both transcription and replication, The Implications of these findings for oncogenesis are briefly discussed. C1 NINCDS,MOLEC MED & VIROL SECT,LAB MOLEC MED & NEUROSCI,NIH,BETHESDA,MD 20892. RADIAT EFFECTS RES FDN,MINAMI KU,HIROSHIMA 732,JAPAN. RP Neel, JV (reprint author), UNIV MICHIGAN,SCH MED,DEPT HUMAN GENET,ANN ARBOR,MI 48109, USA. NR 45 TC 99 Z9 103 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2690 EP 2695 DI 10.1073/pnas.93.7.2690 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500013 PM 8610102 ER PT J AU Yoritaka, A Hattori, N Uchida, K Tanaka, M Stadtman, ER Mizuno, Y AF Yoritaka, A Hattori, N Uchida, K Tanaka, M Stadtman, ER Mizuno, Y TI Immunohistochemical detection of 4-hydroxynonenal protein adducts in Parkinson disease SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID SUBSTANTIA-NIGRA; CELL-DEATH; COMPLEX-I; LIPID-PEROXIDATION; IRON; GLUTATHIONE; DEFICIENCY; NEURONS; BRAINS AB There is growing evidence that oxidative stress and mitochondrial respiratory failure with attendant decrease in energy output are implicated in nigral neuronal death in Parkinson disease (PD), It is not known, however, which cellular elements (neurons or glial cells) are major targets of oxygen-mediated damage, 4-Hydroxy-2-nonenal (HNE) was shown earlier to react with proteins to form stable adducts that can be used as markers of oxidative stress-induced cellular damage, We report here results of immunochemical studies using polyclonal antibodies directed against HNE-protein conjugates to label the site of oxidative damage in control subjects (ages 18-99 years) and seven patients that died of PD (ages 57-78 years), All the nigral melanized neurons in one of the midbrain sections were counted and classified into three groups according to the intensity of immunostaining for HNE-modified proteins-i.e., no staining, weak staining, and intensely positive staining, On average, 58% of nigral neurons were positively stained for HNE-modified proteins in PD; in contrast only 9% of nigral neurons were positive in the control subjects; the difference was statistically significant (Mann-Whitney U test; P < 0.01), In contrast to the substantia nigra, the oculomotor neurons in the same midbrain sections showed no or only weak staining for HNE-modified proteins in both PD and control subjects; young control subjects did not show any immunostaining; however, aged control subjects showed weak staining in the oculomotor nucleus, suggesting age-related accumulation of HNE-modified proteins in the neuron, Our results indicate the presence of oxidative stress within nigral neurons in PD, and this oxidative stress may contribute to nigral cell death. C1 JUNTENDO UNIV,SCH MED,DEPT NEUROL,BUNKYO KU,TOKYO 113,JAPAN. NAGOYA UNIV,FAC MED,DEPT BIOMED CHEM,SHOWA KU,NAGOYA,AICHI 46401,JAPAN. NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. NR 28 TC 672 Z9 688 U1 3 U2 23 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2696 EP 2701 DI 10.1073/pnas.93.7.2696 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500014 PM 8610103 ER PT J AU deAzevedo, WF MuellerDieckmann, HJ SchulzeGahmen, U Worland, PJ Sausville, E Kim, SH AF deAzevedo, WF MuellerDieckmann, HJ SchulzeGahmen, U Worland, PJ Sausville, E Kim, SH TI Structural basis for specificity and potency of a flavonoid inhibitor of human CDK2, a cell cycle kinase SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE cyclin-dependent kinase; protein kinase inhibitors; cancer; drug design; flavopiridol ID CATALYTIC SUBUNIT; PROTEIN-KINASE; DEPENDENT KINASE-2; CRYSTAL-STRUCTURE; CRYSTALLIZATION; P21 AB The central role of cyclin-dependent kinases (CDKs) in cell cycle regulation makes them a promising target for studying inhibitory molecules that can modify the degree of cell proliferation, The discovery of specific inhibitors of CDKs such as polyhydroxylated flavones has opened the way to investigation and design of antimitotic compounds, A novel flavone, (-)-cis-5,7-dihydroxyphenyl-8-[4-(3-hydroxy-1-methyl)piperidinyl]-4H-1-benzopyran-4-one hydrochloride hemihydrate (L868276), is a potent inhibitor of CDKs. A chlorinated form, flavopiridol, is currently in phase I clinical trials as a drug against breast tumors, We determined the crystal structure of a complex between CDK2 and L868276 at 2.33-Angstrom resolution and refined to an R(factor) of 20.3%. The aromatic portion of the inhibitor binds to the adenine-binding pocket of CDK2, and the position of the phenyl group of the inhibitor enables the inhibitor to make contacts with the enzyme not observed in the ATP complex structure, The analysis of the position of this phenyl ring not only explains the great differences of kinase inhibition among the flavonoid inhibitors but also explains the specificity of L868276 to inhibit CDK2 and CDC2. C1 UNIV CALIF BERKELEY,DEPT CHEM,BERKELEY,CA 94720. UNIV CALIF BERKELEY,LAWRENCE BERKELEY LAB,BERKELEY,CA 94720. NCI,DIV CANC TREATMENT,BIOL CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. NR 36 TC 328 Z9 333 U1 1 U2 11 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2735 EP 2740 DI 10.1073/pnas.93.7.2735 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500021 PM 8610110 ER PT J AU Botos, I Scapozza, L Zhang, DC Liotta, LA Meyer, EF AF Botos, I Scapozza, L Zhang, DC Liotta, LA Meyer, EF TI Batimastat, a potent matrix metalloproteinase inhibitor, exhibits an unexpected mode of binding SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE metastasis; drug design; crystallography; molecular modelling ID CARCINOMA; MACROMOLECULES; ASSOCIATION; EXPRESSION; GELATINASE; MOLECULES; INVASION; PROGRAM; VENOM AB Matrix metalloproteinase enzymes have been implicated in degenerative processes like tumor cell invasion, metastasis, and arthritis, Specific metalloproteinase inhibitors have been used to block tumor cell proliferation. We have examined the interaction of batimastat (BB-94) with a metalloproteinase [atrolysin C (Ht-d), EC 3.4.24.42] active site at 2.0-Angstrom resolution (R = 16.8%). The title structure exhibits an unexpected binding geometry, with the thiophene ring deeply inserted into the primary specificity site, This unprecedented binding geometry dramatizes the significance of the cavernous primary specificity site, pointing the way for the design of a new generation of potential antitumor drugs. C1 TEXAS A&M UNIV,DEPT BIOCHEM & BIOPHYS,BIO LAB,COLLEGE STN,TX 77843. NCI,PATHOL LAB,BETHESDA,MD 20892. NR 36 TC 109 Z9 110 U1 0 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2749 EP 2754 DI 10.1073/pnas.93.7.2749 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500024 PM 8610113 ER PT J AU Pedone, PV Ghirlando, R Clore, GM Gronenborn, AM Felsenfeld, G Omichinski, JG AF Pedone, PV Ghirlando, R Clore, GM Gronenborn, AM Felsenfeld, G Omichinski, JG TI The single Cys(2)-His(2) zinc finger domain of the GAGA protein flanked by basic residues is sufficient for high-affinity specific DNA binding SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE gene expression; DNA-protein interaction ID NITROGEN REGULATORY GENE; TRANSCRIPTION FACTOR; CRYSTAL-STRUCTURE; SACCHAROMYCES-CEREVISIAE; DISTINCT ROLES; SEQUENCE; COMPLEX; RECOGNITION; ACTIVATION; EXPRESSION AB Specific DNA binding to the core consensus site GAGAGAG has been shown with an 82-residue peptide (residues 310-391) taken from the Drosophila transcription factor GAGA. Using a series of deletion mutants, it was demonstrated that the minimal domain required for specific binding (residues 310-372) includes a single zinc finger of the Cys(2)-His(2) family and a stretch of basic amino acids located on the N-terminal end of the zinc finger, In gel retardation assays, the specific binding seen with either the peptide or the whole protein Is zinc dependent and corresponds to a dissociation constant of approximate to 5 x 10(-9) M for the purified peptide. It has previously been thought that a single zinc finger of the Cys(2)-His(2) family is incapable of specific, high-affinity binding to DNA. The combination of an N-terminal basic region with a single Cys(2)-His(2) zinc finger in the GAGA protein can thus be viewed as a novel DNA binding domain. This raises the possibility that other proteins carrying only one Cys(2)-His(2) finger are also capable of high-affinity specific binding to DNA. C1 NIH,MOLEC BIOL LAB,BETHESDA,MD 20892. NIH,PHYS CHEM LAB,BETHESDA,MD 20892. RI Clore, G. Marius/A-3511-2008; Ghirlando, Rodolfo/A-8880-2009 OI Clore, G. Marius/0000-0003-3809-1027; NR 33 TC 106 Z9 107 U1 0 U2 4 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2822 EP 2826 DI 10.1073/pnas.93.7.2822 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500038 PM 8610125 ER PT J AU Fijalkowska, IJ Schaaper, RM AF Fijalkowska, IJ Schaaper, RM TI Mutants in the Exo I motif of Escherichia coli dnaQ: Defective proofreading and inviability due to error catastrophe SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE fidelity of DNA replication; dnaQ and dnaE genes; mutD5 mutator; dnaE antimutators; saturation of mismatch repair ID POLYMERASE-III HOLOENZYME; MISMATCH REPAIR; MUTATOR MUTD5; SALMONELLA-TYPHIMURIUM; REPLICATION ERRORS; 3'-5' EXONUCLEASE; CODING PROPERTIES; LAC REPRESSOR; ACTIVE-SITE; AMINO-ACID AB The Escherichia coli dnaQ gene encodes the proofreading 3' exonuclease (epsilon subunit) of DNA polymerase III holoenzyme and is a critical determinant of chromosomal replication fidelity, We constructed by site-specific mutagenesis a mutant, dnaQ926, by changing two conserved amino acid residues (Asp-12-->Ala and Glu-14-->Ala) in the Exo I motif, which, by analogy to other proofreading exonucleases, is essential for the catalytic activity, When residing on a plasmid, dnaQ926 confers a strong, dominant mutator phenotype, suggesting that the protein, although deficient in exonuclease activity, still binds to the polymerase subunit (cu subunit or dnaE gene product), When dnaQ926 was transferred to the chromosome, replacing the wild-type gene, the cells became inviable, However, viable dnaQ926 strains could be obtained if they contained one of the dnaE alleles previously characterized in our laboratory as antimutator alleles or if it carried a multicopy plasmid containing the E. coli mutL(+) gene, These results suggest that loss of proofreading exonuclease activity in dnaQ926 is lethal due to excessive error rates (error catastrophe), Error catastrophe results from both the loss of proofreading and the subsequent saturation of DNA mismatch repair, The probability of lethality by excessive mutation is supported by calculations estimating the number of inactivating mutations in essential genes per chromosome replication. C1 NIEHS,MOLEC GENET LAB,RES TRIANGLE PK,NC 27709. RI Fijalkowska, Iwona/I-7796-2016 NR 45 TC 105 Z9 107 U1 2 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2856 EP 2861 DI 10.1073/pnas.93.7.2856 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500044 PM 8610131 ER PT J AU Bamford, RN Battiata, AP Burton, JD Sharma, H Waldmann, TA AF Bamford, RN Battiata, AP Burton, JD Sharma, H Waldmann, TA TI Interleukin (IL) 15/IL-T production by the adult T-cell leukemia cell line HuT-102 is associated with a human T-cell lymphotrophic virus type I R region/IL-15 fusion message that lacks many upstream AUGs that normally attenuate IL-15 mRNA translation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MESSENGER-RNA; UNTRANSLATED REGION; HTLV-I; INTEGRATION; ACTIVATION; SEQUENCES; PROVIRUS AB We reported previously that the human T-cell lymphotrophic virus type I (HTLV-I)-associated adult T-cell leukemia line HuT-102 produces a cytokine designated interleukin (IL) T that requires interleukin (IL) 2 receptor beta-subunit expression for its action, Using anti-cytokine antibodies, we demonstrated that IL-T is identical to the simultaneously described IL-15, When compared to activated monocytes, IL-15 mRNA expression was 6- to 10-fold greater in HuT-102 cells, The predominant IL-15 message from HuT-102 is a chimeric mRNA joining a segment of the R region of the long terminal repeat of HTLV-I and the 5'-untranslated region (UTR) of IL-15, Normally, by alternative splicing, this 118-nucleotide R element represents the most 5' region of several HTLV-I transcripts including tax, rex, and env, The introduction of the R element eliminated over 200 nucleotides of the IL-15 5'-UTR, including 8 of 10 upstream AUGs that are present in normal IL-15 messages, On analysis of the 5'-UTR of normal IL-15, we demonstrated that the presence of these 10 upstream AUGs interferes with IL-15 mRNA translation, Thus, IL-15 synthesis by the adult T-cell leukemia line HuT-102 involves an increase in IL-15 mRNA transcription and translation secondary to the production of an HTLV-I R element fusion message that lacks many upstream AUGs. C1 GENZYME CORP,CAMBRIDGE,MA 02139. RP Bamford, RN (reprint author), NCI,NIH,METAB BRANCH,BETHESDA,MD 20892, USA. NR 26 TC 173 Z9 175 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2897 EP 2902 DI 10.1073/pnas.93.7.2897 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500052 PM 8610139 ER PT J AU Kundu, GC Mantile, G Miele, L CordellaMiele, E Mukherjee, AB AF Kundu, GC Mantile, G Miele, L CordellaMiele, E Mukherjee, AB TI Recombinant human uteroglobin suppresses cellular invasiveness via a novel class of high-affinity cell surface binding site SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE Clara cell 10-kDa protein; invasion; extracellular matrix; metastasis ID KDA PROTEIN; PHOSPHOLIPASE-A2 ACTIVITY; RABBIT UTEROGLOBIN; 10-KDA PROTEIN; EXPRESSION; GENE; PEPTIDES; REGION; CC10; RAT AB The mechanism(s) that regulates invasion of trophoblasts through the uterine epithelium during embryo implantation and nidation in hemochorial placental mammals is poorly understood. While limited trophoblast invasion is essential for the establishment of normal pregnancy, dysregulation of this process may contribute to the pathogenesis of choriocarcinoma, a highly invasive and lethal form of cancer arising from the trophoblasts. We have previously demonstrated that rabbit uteroglobin (UG), a cytokine-like, antiinflammatory protein, produced by the endometrial epithelium during pregnancy, has a potent antichemotactic effect on neutrophils and monocytes in vitro. Here, we report that recombinant human UG (hUG) dramatically suppresses invasion of human trophoblasts and NIH 3T3 cells through an artificial basement membrane (Matrigel) in vitro but has no effect on that of human choriocarcinoma cells. We identified a previously unreported high-affinity, high molecular weight (approximate to 190 kDa), nonglycosylated hUG-binding protein, readily detectable on human trophoblasts and NIH 3T3 cells but totally lacking on choriocarcinoma cells. Taken together, these results raise the possibility that (i) hUG plays a critical role in regulating cellular invasiveness, at least in part, via its previously unrecognized cell surface binding site, and (ii) some of the numerous biological activities of proteins of the UG family, reported so far, may be mediated via this binding site. C1 NICHHD,NIH,SECT DEV GENET,HUMAN GENET BRANCH,BETHESDA,MD 20892. NR 35 TC 59 Z9 61 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2915 EP 2919 DI 10.1073/pnas.93.7.2915 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500055 PM 8610142 ER PT J AU Wimley, WC Gawrisch, K Creamer, TP White, SH AF Wimley, WC Gawrisch, K Creamer, TP White, SH TI Direct measurement of salt-bridge solvation energies using a peptide model system: Implications for protein stability SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE protein folding; electrostatics; hydrophobicity; octanol partitioning; C-13 NMR) ID T4 LYSOZYME; HYDROPHOBIC CORE; PACKING; ACIDS AB The solvation energies of salt bridges formed between the terminal carboxyl of the host pentapeptide AcWL-X-LL and the side chains of Arg or Lys in the guest (X) position have been measured. The energies were derived from octanol-to-buffer transfer free energies determined between pH 1 and pH 9, C-13 NMR measurements show that the salt bridges form in the octanol phase, but not in the buffer phase, when the side chains and the terminal carboxyl group are charged. The free energy of salt-bridge formation in octanol is approximately -4 kcal/mol (1 cal = 4.184 J), which is equal to or slightly larger than the sum of the solvation energies of noninteracting pairs of charged side chains, This is about one-half the free energy that would result from replacing a charge pair in octanol with a pair of hydrophobic residues of moderate size. Therefore, salt bridging in octanol can change the favorable aqueous solvation energy of a pair of oppositely charged residues to neutral or slightly unfavorable but cannot provide the same free energy decrease as hydrophobic residues. This is consistent with recent computational and experimental studies of protein stability. C1 UNIV CALIF IRVINE,DEPT PHYSIOL & BIOPHYS,IRVINE,CA 92717. NIAAA,NIH,NMR STUDIES SECT,MEMBRANE BIOPHYS & BIOCHEM LAB,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT BIOPHYS & BIOPHYS CHEM,BALTIMORE,MD 21205. RI Creamer, Trevor/A-5252-2008; White, Stephen/B-1053-2009 OI White, Stephen/0000-0001-8540-7907 FU NIGMS NIH HHS [GM29458, GM46823] NR 33 TC 101 Z9 102 U1 0 U2 8 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 2 PY 1996 VL 93 IS 7 BP 2985 EP 2990 DI 10.1073/pnas.93.7.2985 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UD375 UT WOS:A1996UD37500068 PM 8610155 ER PT J AU Shulman, LE AF Shulman, LE TI Clinical research 1996: Stirrings from the academic health centers SO ACADEMIC MEDICINE LA English DT Editorial Material RP Shulman, LE (reprint author), NIAMSD,NIH,BETHESDA,MD 20892, USA. NR 0 TC 20 Z9 20 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD APR PY 1996 VL 71 IS 4 BP 362 EP & DI 10.1097/00001888-199604000-00013 PG 3 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA UF246 UT WOS:A1996UF24600016 PM 8645401 ER PT J AU Stein, DH Salive, ME AF Stein, DH Salive, ME TI Adequacy of training in preventive medicine and public health: A national survey of residency graduates SO ACADEMIC MEDICINE LA English DT Article AB Purpose. To evaluate training in general preventive medicine and public health, determining which experiences and institutional sponsors best prepare residents for practice and where improvements are most needed. Method. A 1991 survey of the 1,070 graduates of preventive medicine residencies from 1979 through 1989 asked the graduates to measure the adequacy of their training in preventive medicine topic areas by using a Likert-type scale of 1 (poor) to dr (excellent), Adequacy was analyzed for variation against practice emphasis during training, training program sponsor, and other variables. The statistical methods included Student's t-test, analysis of variance, and linear regression. Results. A total of 797 graduates (74.5%) responded. The overall mean ratings of adequacy of training were 3.1 (SD, 0.9) for epidemiology, 2.5 (SD, 1.0) for clinical preventive medicine, 2.4 (SD, 0.9) for environmental health, 2.3 (SD, 0.9) for health administration, 2.3 (SD, 0.9) for health education and behavioral sciences, and 2.2 (SD, 0.9) for occupational medicine. Training was rated highest for topics emphasized during practice experiences. Adequacy varied by type of institution sponsoring the residency. Women rated their training as being less adequate than did men in all areas except clinical preventive medicine. The graduates tended ultimately to practice in topic areas emphasized during training. Conclusion. The graduates' ratings suggest that improvements are most needed in health administration, environment health, health education, and occupational medicine. Potential improvement strategies include highly focused practice experiences and increased emphasis on training in actual practice settings and community sites. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT HLTH POLICY & MANAGEMENT,BALTIMORE,MD. NIA,NIH,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892. NR 17 TC 7 Z9 7 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD APR PY 1996 VL 71 IS 4 BP 375 EP 380 DI 10.1097/00001888-199604000-00016 PG 6 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA UF246 UT WOS:A1996UF24600020 PM 8645404 ER PT J AU Shtern, F AF Shtern, F TI Technology assessment: A perspective from the National Cancer Institute SO ACADEMIC RADIOLOGY LA English DT Article; Proceedings Paper CT International Symposium on Costs and Benefits of Radiology CY 1995 CL OXFORD, ENGLAND ID DIAGNOSTIC-ONCOLOGY-GROUP; CLINICAL-EXPERIENCE; BREAST; CT RP Shtern, F (reprint author), NCI,DIAGNOST IMAGING RES BRANCH,RADIAT RES PROGRAM,DEPT HLTH & HUMAN SERV,DIV CANC TREATMENT,ROCKVILLE,MD 20852, USA. NR 23 TC 2 Z9 2 U1 0 U2 0 PU ASSOC UNIV RADIOLOGISTS PI RESTON PA 1891 PRESTON WHITE DR, RESTON, VA 22091 SN 1076-6332 J9 ACAD RADIOL JI Acad. Radiol. PD APR PY 1996 VL 3 SU 1 BP S84 EP S87 DI 10.1016/S1076-6332(96)80494-6 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UE519 UT WOS:A1996UE51900033 PM 8796524 ER PT J AU Verny, M Jellinger, KA Hauw, JJ Bancher, C Litvan, I Agid, Y AF Verny, M Jellinger, KA Hauw, JJ Bancher, C Litvan, I Agid, Y TI Progressive supranuclear palsy: A clinicopathological study of 21 cases SO ACTA NEUROPATHOLOGICA LA English DT Article DE progressive supranuclear palsy; symptoms; diagnostic criteria ID DISEASE AB The symptoms and signs used to diagnose progressive supranuclear palsy (PSP) should be easily identifiable by neuropathologists and neurologists as well as by movement disorder experts. The presence, at the time of death, of symptoms and signs that are used in published clinical criteria for the diagnosis of this disorder was searched for in 21 pathologically confirmed typical PSP cases. The following items, present in at least 80% of pathologically confirmed cases, can be considered as the most accurate clinical data for the diagnosis of PSP: nonfamilial parkinsonism, not improved by L-dopa therapy, with vertical voluntary gaze palsy; postural instability and falls; pseudobulbar palsy and dementia with frontal lobelike syndrome; and a progressive course of less than 10 years. The definite diagnosis of PSP must be clinicopathological, and these minimal clinical data may be used for this purpose. C1 HOP LA PITIE SALPETRIERE,DIV MAZARIN,DEPT NEUROL,PARIS,FRANCE. KRANKENHAUS STADT WIEN LAINZ,LUDWIG BOLTZMANN INST CLIN NEUROBIOL,A-1130 VIENNA,AUSTRIA. NINCDS,NIH,NEUROEPIDEMIOL BRANCH,BETHESDA,MD 20892. HOP LA PITIE SALPETRIERE,INSERM U289,F-75651 PARIS,FRANCE. HOP LA PITIE SALPETRIERE,FEDERAT NEUROL,F-75651 PARIS,FRANCE. RP Verny, M (reprint author), HOP LA PITIE SALPETRIERE,INSERM U360,LAB NEUROPATHOL R ESCOUROLLE,ASSOC CLAUDE BERNARD,F-75651 PARIS 13,FRANCE. OI Litvan, Irene/0000-0002-3485-3445 NR 29 TC 60 Z9 61 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0001-6322 J9 ACTA NEUROPATHOL JI Acta Neuropathol. PD APR PY 1996 VL 91 IS 4 BP 427 EP 431 PG 5 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA UB191 UT WOS:A1996UB19100015 PM 8928621 ER PT J AU Johanson, CE Duffey, FF Anthony, JC AF Johanson, CE Duffey, FF Anthony, JC TI Associations between drug use and behavioral repertoire in urban youths SO ADDICTION LA English DT Article ID SUBSTANCE USE; COCAINE; SCHOOL; DRINKING; STUDENTS; SMOKING; MONKEYS; ABUSE AB Converging with psyche-social research findings, animal and human laboratory studies indicate that behavioral alternatives are important determinants of drug-taking. To investigate associations between how early adolescents spend their time, i.e. their behavioral repertoire and drug use (use of marijuana, crack/cocaine or inhalants), we analyzed data from an epidemiological sample of 1516 urban middle-school students who had completed private interviews in spring 1993. The interview included a 36-item questionnaire to assess how frequently the youth engaged in different activities; history of drug-taking was assessed separately. Multiple logistic regression was wed to estimate associations between drug we and each of seven behavioral domains as well as sex, age and racial-ethnic status. Youths spending a great deal of time working for pay and assuming other adult-like roles were more likely to have initiated drug use (estimated odds ratio, OR = 3.49; p = 0.002). Those who spent much time in religious activities were less likely (OR = 0.2, p < 0.001). An exploratory search for interactions disclosed other associations that merit attention in future research. These results corroborate evidence on the potential etiological significance of behavioral repertoire in relation to risk of drug use. C1 NIDA,ETIOL BRANCH,INTRAMURAL RES PROGRAM,BALTIMORE,MD. NR 40 TC 18 Z9 18 U1 8 U2 15 PU CARFAX PUBL CO PI ABINGDON PA PO BOX 25, ABINGDON, OXFORDSHIRE, ENGLAND OX14 3UE SN 0965-2140 J9 ADDICTION JI Addiction PD APR PY 1996 VL 91 IS 4 BP 523 EP 534 DI 10.1111/j.1360-0443.1996.tb02310.x PG 12 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA UE993 UT WOS:A1996UE99300012 PM 8857378 ER PT J AU Corti, MC Guralnik, JM Bilato, C AF Corti, MC Guralnik, JM Bilato, C TI Coronary heart disease risk factors in older persons SO AGING CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Review DE aged; atherosclerosis; cardiovascular disease; coronary heart disease; risk factors ID POSTMENOPAUSAL ESTROGEN USE; HIGH BLOOD CHOLESTEROL; BODY-MASS INDEX; SERUM URIC-ACID; FACTOR INTERVENTION TRIAL; 10-YEAR FOLLOW-UP; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; PHYSICAL-ACTIVITY; SYSTOLIC HYPERTENSION AB In most Western nations, coronary heart disease (CHD) is the leading cause of death and one of the most important causes of physical disability in persons over 65 years of age. The importance of traditional CHD risk factors has been well documented in middle-aged populations, whereas their role in older populations is still under debate. This paper reviews the epidemiologic evidence from observational studies and randomized clinical trials that established risk factors for CHD predict level of risk of CHD, and identify high risk individuals among older men and women. Hypertension and cigarette smoking have been clearly associated with an increased risk of CHD events, and their modification has been proven to be highly effective in the primary and secondary prevention of CHD in older persons. For other highly prevalent risk factors, such as lipid abnormalities, obesity and physical inactivity, evidence of an independent association with CHD risk has been demonstrated by the majority of observational studies. However, definitive proof from controlled clinical trials of the beneficial effects of their modification is still lacking in the older population. The role of estrogen replacement therapy in the primary and secondary prevention of CHD in older women is still an open question. In evaluating the impact of these risk factors in older persons, elements such as comorbidity, frailty, and age-related changes in risk profile should also be taken into consideration; Given the complexity of the relationship between risk factors and multiple disease statuses, other important outcomes, such as osteoporosis, cancer, falls and physical disability, should be considered when evaluating the risks and benefits of risk factor modifications in older persons. RP NIA, EPIDEMIOL DEMOG BIOMETRY PROGRAM, NIH, 7201 WISCONSIN AVE, RM 3C309, BETHESDA, MD 20892 USA. NR 154 TC 17 Z9 17 U1 4 U2 6 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1594-0667 EI 1720-8319 J9 AGING CLIN EXP RES JI Aging Clin. Exp. Res. PD APR PY 1996 VL 8 IS 2 BP 75 EP 89 PG 15 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA UJ079 UT WOS:A1996UJ07900002 PM 8737605 ER PT J AU Faris, M Ensoli, B Stahl, N Yancopoulos, G Nguyen, A Wang, S Nel, AE AF Faris, M Ensoli, B Stahl, N Yancopoulos, G Nguyen, A Wang, S Nel, AE TI Differential activation of the extracellular signal-regulated kinase, Jun Kinase and Janus Kinase-Stat pathways by oncostatin M and basic fibroblast growth factor in AIDS-derived Kaposi's sarcoma cells SO AIDS LA English DT Article DE JAK-Stat; ERK; Kaposi's sarcoma ID RECEPTOR TYROSINE KINASES; PROTEIN-KINASE; FOS; PHOSPHORYLATION; IDENTIFICATION; PATHOGENESIS; TRANSDUCTION; CYTOKINES; PROMOTER; COMPLEX AB Objectives: To determine the integration of signalling pathways associated with two recognized Kaposi's sarcoma (KS) growth factors, oncostatin M (OSM) and basic fibroblast growth factor (bFGF), in the induction of KS cell proliferation. Design and methods: We used protein kinase assays, protein-DNA interactions and AP-1 luciferase assays to study the extracellular signal-regulated kinase (ERK), janus kinase (JAK)-Stat and Jun kinase (JNK) pathways in AIDS-derived KS cells during stimulation with OSM and bFGF. Results: Treatment with OSM-induced activation of receptor-associated JAK and phosphorylation of Stat1 and Stat3. Stat1/Stat3 heterodimers interacted with known gamma-interferon-activated sites like elements such as the sis-inducible element (SIE) in the c-fos promoter. In contrast, ligation of the bFGF receptor induced Stat3 phosphorylation and its association with the bFGF receptor, but failed to induce IAK activity or protein complexes which interact with GAS-like oligonucleotides. OSM also induced the activation of ERK2 by activating the serine/threonine kinases Raf-1 and [mitogen-activated protein kinase (MAPK) ERK kinase (MEK1)]-1, while bFGF failed to activate any of the above components. Both OSM and bFGF activated the JNK pathway, along with the activation of MEKkinase (MEKK)-1.JNK control the transcriptional activation of c-Jun. Because the above pathways exert an effect on the expression or activation of activation protein (AP)-1 components, we confirm that OSM and bFGF induce TPA response element (TRE)-luciferase activity synergistically. Conclusion We demonstrate that OSM and bFGF activate distinct as well as shared signalling cascades in KS cells, which integrate to provide a synergistic AP-1 response by which OSM and bFGF may sustain KS cell growth. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,CIA,LOS ANGELES,CA 90024. NCI,NIH,TUMOR CELL BIOL LAB,BETHESDA,MD 20892. REGENERON PHARMACEUT INC,TARRYTOWN,NY 10591. RI Nel, Andre/J-2808-2012; Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 FU CSR NIH HHS [02104-15-RG]; NCI NIH HHS [CA6532901, CA09120-20] NR 58 TC 34 Z9 34 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD APR PY 1996 VL 10 IS 4 BP 369 EP 378 DI 10.1097/00002030-199604000-00004 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA UE997 UT WOS:A1996UE99700004 PM 8728040 ER PT J AU Hitchcock, PJ AF Hitchcock, PJ TI Adolescents and sexually transmitted diseases SO AIDS PATIENT CARE AND STDS LA English DT Article ID HIV INFECTION; RISK; TRANSMISSION; HERPES AB This paper presents a brief overview of sexually transmitted diseases (STDs), including acquired immunodeficiency syndrome (AIDS), in adolescent populations. Using the framework of a mathematical model (which considers how, why, and whether an infection spreads within a population), the epidemic of STDs among adolescent populations is considered. The unique aspects of adolescent behavior, adolescent biology, and the social context of adolescents' lives are highlighted. RP Hitchcock, PJ (reprint author), NIAID,SEXUALLY TRANSMITTED DIS BRANCH,9000 ROCKVILLE PIKE,SOLAR BLDG 3A24,BETHESDA,MD 20892, USA. NR 26 TC 3 Z9 3 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1087-2914 J9 AIDS PATIENT CARE ST JI Aids Patient Care STDS PD APR PY 1996 VL 10 IS 2 BP 79 EP 85 DI 10.1089/apc.1996.10.79 PG 7 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA UN022 UT WOS:A1996UN02200004 PM 11361711 ER PT J AU Grant, BF AF Grant, BF TI Toward an alcohol treatment model: A comparison of treated and untreated respondents with DSM-IV alcohol use disorders in the general population SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE alcohol treatment; help-seeking for alcohol problems; alcohol treatment utilization; access to alcohol treatment ID PROBLEM DRINKERS; DRINKING; HELP AB The purpose of this study was to compare characteristics of person with alcohol use disorders who sought alcohol treatment with those who did not using data from a nationally representative sample of the United States. Applying an organizing framework from the larger literature on service utilization, a logistic regression analysis was conducted to examine the interaction among factors influencing treatment, The results identified unemployment status and lower educational level as barriers to alcohol treatment, but the impact of these factors differed depending on whether the respondent had previous experience with alcohol treatment. The major findings of this study are discussed in terms of consumer satisfaction, minimizing barriers to alcohol treatment services, and the need to examine individual determinants of alcohol treatment within the larger context of organizational and sociopolitical factors. RP Grant, BF (reprint author), NIAAA,DEPT BIOMETRY & EPIDEMIOL,BIOMETRY BRANCH,SUITE 514,6000 EXECUT BLVD,MSC 7003,BETHESDA,MD 20892, USA. NR 25 TC 80 Z9 80 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD APR PY 1996 VL 20 IS 2 BP 372 EP 378 DI 10.1111/j.1530-0277.1996.tb01655.x PG 7 WC Substance Abuse SC Substance Abuse GA UE737 UT WOS:A1996UE73700027 PM 8730232 ER PT J AU Kalkwarf, HJ Specker, BL Heubi, JE Vieira, NE Yergey, AL AF Kalkwarf, HJ Specker, BL Heubi, JE Vieira, NE Yergey, AL TI Intestinal calcium absorption of women during lactation and after weaning SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE intestinal calcium absorption; lactation; weaning; stable isotopes ID METABOLISM; PREGNANCY AB We investigated whether intestinal calcium absorption and serum 1,25-dihydroxycholecalciferol (calcitriol) concentrations are higher in women during lactation and after weaning to compensate for calcium lost in breast milk. Measurements were obtained at 4.6 mo postpartum in 24 lactating women and 24 nonlactating women, at 9.6 mo postpartum in 24 lactating women (2.6 mo after complete weaning) and 24 nonlactating women. One-half of the women in each group were randomly assigned to receive 1 g supplemental Ca/d as calcium carbonate. Fractional calcium absorption was measured by using stable isotopic tracers Ca-42 and Ca-44. Fractional absorption was 0.32 +/- 0.02 (+/- SEM) in both lactating and nonlactating women, but was higher in lactating women after weaning (0.37 +/- 0.02) compared with nonlactating postpartum control subjects (0.31 +/- 0.02). These effects were independent of calcium intake. Changes in serum calcitriol paralleled changes in fractional absorption. There were no differences in calcitriol concentrations between lactating and nonlactating women, but calcitriol was greater in women after weaning compared with postpartum control subjects. Lactating women who had resumed menses had higher fractional absorption and serum calcitriol than did lactating women who had not. Serum calcium and phosphorus concentrations were greater in lactating compared with nonlactating women; there were no differences between groups after weaning. We conclude that lactation stimulates increases in fractional calcium absorption and serum calcitriol, but the responses are only apparent after weaning or the resumption of menses. C1 NICHHD,NIH,BETHESDA,MD 20892. RP Kalkwarf, HJ (reprint author), CHILDRENS HOSP,MED CTR,DIV NEONATOL,ML-0541,3333 BURNET AVE,CINCINNATI,OH 45229, USA. FU NCRR NIH HHS [MO1 RR 08084]; NIAMS NIH HHS [R01 AR41366] NR 16 TC 59 Z9 61 U1 0 U2 4 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1996 VL 63 IS 4 BP 526 EP 531 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA UC185 UT WOS:A1996UC18500008 PM 8599316 ER PT J AU Mark, SD Wang, W Fraumeni, JF Li, JY Taylor, PR Wang, GQ Guo, W Dawsey, SM Li, B Blot, WJ AF Mark, SD Wang, W Fraumeni, JF Li, JY Taylor, PR Wang, GQ Guo, W Dawsey, SM Li, B Blot, WJ TI Lowered risks of hypertension and cerebrovascular disease after vitamin mineral supplementation - The Linxian nutrition intervention trial SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE antioxidants; cerebrovascular disorders; hypertension; minerals; nutrition; randomized controlled trials; stroke; vitamins ID BLOOD-PRESSURE; CANCER INCIDENCE; VEGETABLES PROTECT; SERUM SELENIUM; UNITED-STATES; HEART-DISEASE; DIETARY FATS; FOLLOW-UP; STROKE; MORTALITY AB A total of 3,318 men and women from a region in rural China were randomized to receive daily either a multiple vitamin/mineral supplement or a placebo. Deaths that occurred in the participants were ascertained and classified according to cause over the 6-year period from 1985 to 1991, At the end of supplementation, blood pressure readings were taken, and the prevalence of hypertension was determined, There was a slight reduction in overall mortality in the supplement group (relative risk (RR) = 0.93, 95% confidence interval (CI) 0.75-1.16), with the decreased relative risk most pronounced for cerebrovascular disease deaths (RR = 0.63, 95% CI 0.37-1.07). This benefit was greater for men (RR = 0.42, 95% CI 0.19-0.93) than for women (RR = 0.93, 95% CI 0.44-1.98). Among the survivors, the presence of elevations in both systolic and diastolic blood pressures was less common in those who received the supplement (RR for men = 0.43, 95% CI 0.28-0.65; RR for women = 0.92, 95% CI 0.68-1.24). This study indicates that supplementation with a multivitamin/mineral combination may have reduced mortality from cerebrovascular disease and the prevalence of hypertension in this rural population with a micronutrient-poor diet. C1 CHINESE ACAD MED SCI, INST CANC, BEIJING 100021, PEOPLES R CHINA. INT EPIDEMIOL INST, ROCKVILLE, MD USA. RP Mark, SD (reprint author), NCI, BETHESDA, MD 20892 USA. NR 47 TC 79 Z9 91 U1 0 U2 4 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 1 PY 1996 VL 143 IS 7 BP 658 EP 664 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UD948 UT WOS:A1996UD94800002 PM 8651227 ER PT J AU Cushman, M Yanez, D Psaty, BM Fried, LP Heiss, G Lee, M Polak, JF Savage, PJ Tracy, RP AF Cushman, M Yanez, D Psaty, BM Fried, LP Heiss, G Lee, M Polak, JF Savage, PJ Tracy, RP TI Association of fibrinogen and coagulation factors VII and VIII with cardiovascular risk factors in the elderly - The cardiovascular health study SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE aged; blood coagulation factors; cardiovascular disease; risk factors ID POSTMENOPAUSAL ESTROGEN THERAPY; ISCHEMIC-HEART-DISEASE; VON-WILLEBRAND-FACTOR; PLASMA-FIBRINOGEN; INDUSTRIAL-POPULATION; HEMOSTATIC FUNCTION; BASELINE DATA; ATHEROSCLEROSIS; CHOLESTEROL; MENOPAUSE AB The cross-sectional correlates of three hemostatic factors-fibrinogen, factor VII, and factor VIII-were examined in the Cardiovascular Health Study, a population-based cohort study of 5,201 subjects over age 65 years. Subjects were recruited in 1989-1990 in Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh, Pennsylvania. In multivariate linear regression models, cardiac risk factors significantly associated with fibrinogen were current smoking, race, lipids, and white blood count. In women, alcohol use, obesity, physical activity, and insulin level were also significant, while in men hypertension was correlated. The significant correlates of factor VII were lipids and white blood count in men and estrogen use, alcohol use, race, lipids, insulin level, white blood count, and obesity in women. The independent correlates of factor VIII were insulin, glucose, and race in both sexes; low density lipoprotein cholesterol, white blood count, and diuretic use in men; and alcohol use in women. In multivariate models, factors known to be modifiable risk factors for cardiovascular disease accounted for more of the population variance of these hemostatic factors in women than in men, especially for factor VII. The hemostatic factors may mediate some effects of risk factors on disease, and this should be considered in longitudinal studies. C1 UNIV VERMONT,DEPT PATHOL & MED,BURLINGTON,VT. UNIV WASHINGTON,DEPT BIOSTAT,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT EPIDEMIOL,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT HLTH SERV,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. JOHNS HOPKINS UNIV,DEPT MED,BALTIMORE,MD. JOHNS HOPKINS UNIV,DEPT EPIDEMIOL,BALTIMORE,MD. UNIV N CAROLINA,DEPT EPIDEMIOL,CHAPEL HILL,NC. UNIV CALIF DAVIS,DEPT MED,DAVIS,CA 95616. BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115. NHLBI,EPIDEMIOL & BIOMETRY PROGRAM,BETHESDA,MD 20892. UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405. UNIV VERMONT,DEPT BIOCHEM,BURLINGTON,VT 05405. FU NHLBI NIH HHS [N01-HC-85081, N01-HC-85079, N01-HC-85080] NR 56 TC 97 Z9 99 U1 0 U2 1 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 1 PY 1996 VL 143 IS 7 BP 665 EP 676 PG 12 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UD948 UT WOS:A1996UD94800003 PM 8651228 ER PT J AU Hayes, RB Brown, LM Schoenberg, JB Greenberg, RS Silverman, DT Schwartz, AG Swanson, GM Benichou, J Liff, JM Hoover, RN Pottern, LM AF Hayes, RB Brown, LM Schoenberg, JB Greenberg, RS Silverman, DT Schwartz, AG Swanson, GM Benichou, J Liff, JM Hoover, RN Pottern, LM TI Alcohol use and prostate cancer risk in US blacks and whites SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE alcohol; case-control studies; prostatic neoplasms ID CHRONIC ETHANOL; GROWTH-HORMONE; CONSUMPTION; LIVER; RAT; PERSPECTIVE; SECRETION; INGESTION; TOBACCO; COHORT AB Prostate cancer is the most common malignancy in US men (more than 165,000 cases per annum) and occurs substantially more frequently in blacks than in whites. The causes of this disease are, however, poorly understood. Alcohol consumption, which has been clearly related to malignancies of the upper aerodigestive tract, may also increase risk of cancer at other sites, including the prostate. The authors investigated alcohol use as a risk factor for prostate cancer among US blacks and whites. A population-based, case-control study was carried out among 981 men (479 blacks and 502 whites) with pathologically confirmed prostate cancer diagnosed between August 1, 1986, and April 30, 1989, and 1,315 controls (594 blacks and 721 whites) who resided in Atlanta, Georgia; Detroit, Michigan; and 10 counties in New Jersey, geographic areas covered by three population-based cancer registries. In-person interviews elicited information on alcohol use and other factors possibly related to prostate cancer. Compared with never-users, risk for prostate cancer increased with amount of alcohol drunk (chi(trend)(2), p < 0.001), with significantly elevated risks seen for those who had 22-56 drinks per week (odds ratio = 1.4; 95% confidence interval 1.0-1.8) and 57 or more drinks per week (odds ratio = 1.9; 95% confidence interval 1.3-2.7). The finding was consistent among blacks (chi(trend)(2), p < 0.01) and whites (chi(trend)(2), p < 0.05), and among young and old subjects; it was not restricted to a specific type of alcoholic beverage. In this first large study among US blacks and whites, increased risk for prostate cancer was associated with increased alcohol use. The risk was similar for whites and blacks and could not be attributed to tobacco use or to a number of other potential confounders. C1 NCI,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. NEW JERSEY STATE DEPT HLTH,SPECIAL EPIDEMIOL PROGRAM,TRENTON,NJ 08625. EMORY UNIV,SCH PUBL HLTH,DIV EPIDEMIOL,ATLANTA,GA. UNIV PITTSBURGH,SCH MED & FAMILY MED,DEPT CLIN EPIDEMIOL,PITTSBURGH,PA. MICHIGAN STATE UNIV,COLL HUMAN MED,E LANSING,MI 48824. FU NCI NIH HHS [N01-CP-51089, N01-CN-05225, N01-CP-5109] NR 41 TC 55 Z9 56 U1 0 U2 1 PU AMER J EPIDEMIOLOGY PI BALTIMORE PA 624 N BROADWAY RM 225, BALTIMORE, MD 21205 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 1 PY 1996 VL 143 IS 7 BP 692 EP 697 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UD948 UT WOS:A1996UD94800006 PM 8651231 ER PT J AU Swanson, CA Coates, RJ Schoenberg, JB Malone, KE Gammon, MD Stanford, JL Shorr, IJ Potischman, NA Brinton, LA AF Swanson, CA Coates, RJ Schoenberg, JB Malone, KE Gammon, MD Stanford, JL Shorr, IJ Potischman, NA Brinton, LA TI Body size and breast cancer risk among women under age 45 years SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE anthropometry; body height; body weight; breast neoplasms ID FAT DISTRIBUTION; PREMENOPAUSAL WOMEN; MENSTRUAL EVENTS; RELATIVE WEIGHT; HEIGHT; OBESITY; MASS AB In a multicenter population-based case-control study that included 1,588 cases and 1,394 controls less than age 45 years, the authors examined the relation of adult body size and breast cancer risk among young women. Breast cancer patients and healthy controls were identified in Atlanta, Georgia; Seattle/Puget Sound, Washington; and central New Jersey. Cases were newly diagnosed with in situ or invasive breast cancer during the period of May 1, 1990, through December 31, 1992. Anthropometric variables thought to reflect early environmental factors (e.g., height, sitting height, frame size), obesity, and body fat distribution were measured directly. Height, but not sitting height or frame size, was a breast cancer risk factor. Risk of the disease was increased 46 percent among women in the fourth quartile of height (>167 cm) compared with women in the first quartile (<159 cm). Body weight, but not body fat distribution, was related to breast cancer risk. Risk of the disease was 35 percent lower among women in the highest quartile of Quetelet index (>28.8 kg/m(2)) compared with women in the lowest quartile (<22.0 kg/m(2)). Risk of the disease was increased about 2.1-fold (95 percent confidence interval 1.2-3.8) among women who were thin and tall compared with women who were heavy and short. Thus, breast cancer risk was increased substantially among younger women with a linear body type. C1 EMORY UNIV, ROLLINS SCH PUBL HLTH, DEPT EPIDEMIOL, ATLANTA, GA 30322 USA. NEW JERSEY STATE DEPT HLTH, SPECIAL EPIDEMIOL PROGRAM, TRENTON, NJ 08625 USA. FRED HUTCHINSON CANC RES CTR, SEATTLE, WA 98104 USA. COLUMBIA UNIV, SCH PUBL HLTH, DIV EPIDEMIOL, NEW YORK, NY USA. RP Swanson, CA (reprint author), NCI, NUTR EPIDEMIOL SECT,ENVIRONM EPIDEMIOL BRANCH, DIV CANC EPIDEMIOL & GENET,NIH, EPN ROOM 443, BETHESDA, MD 20892 USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 39 TC 88 Z9 89 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 EI 1476-6256 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD APR 1 PY 1996 VL 143 IS 7 BP 698 EP 706 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UD948 UT WOS:A1996UD94800007 PM 8651232 ER PT J AU Cohen, MR Anderson, RW Attilio, RM Green, L Muller, RJ Pruemer, JM AF Cohen, MR Anderson, RW Attilio, RM Green, L Muller, RJ Pruemer, JM TI Preventing medication errors in cancer chemotherapy SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY LA English DT Article ID INTRATHECAL VINCRISTINE; OVERDOSE; MYELOENCEPHALOPATHY; CISPLATIN AB Recommendations for preventing medication errors in cancer chemotherapy are made. Before a health care provider is granted privileges to prescribe, dispense, or administer antineoplastic agents, he or she should undergo a tailored educational program and possibly testing or certification. Appropriate reference materials should be developed. Each institution should develop a dose-verification process with as many independent checks as possible. A detailed checklist covering prescribing, transcribing, dispensing, and administration should be used. Oral orders are not acceptable. All doses should be calculated independently by the physician, the pharmacist, and the nurse. Dosage limits should be established and a review process set up for doses that exceed the limits. These limits should be entered into pharmacy computer systems, listed on preprinted order forms, stated on the product packaging, placed in strategic locations in the institution, and communicated to employees. The prescribing vocabulary must be standardized. Acronyms, abbreviations, and brand names must be avoided and steps taken to avoid other sources of confusion in the written orders, such as trailing zeros. Preprinted anti neoplastic drug order forms containing checklists can help avoid errors. Manufacturers should be encouraged to avoid or eliminate ambiguities in drug names and dosing information. Patients must be educated about all aspects of their cancer chemotherapy, as patients represent a last line of defense against errors. An interdisciplinary team at each practice site should review every medication error reported. Pharmacists should be involved at all sites where antineoplastic agents are dispensed. Although it may not be possible to eliminate all medication errors in cancer chemotherapy, the risk can be minimized through specific steps. Because of their training and experience, pharmacists should take the lead in this effort. C1 UNIV TEXAS,MD ANDERSON CANC CTR,DIV PHARM,HOUSTON,TX. LEHIGH VALLEY HOSP,JOHN & DOROTHY MORGAN CANC CTR,DEPT PHARM,ALLENTOWN,PA. NIH,WARREN GRANT MAGNUSON CLIN CTR,DEPT PHARM,BETHESDA,MD 20892. MEM SLOAN KETTERING CANC CTR,DIV PHARM SERV,NEW YORK,NY. UNIV CINCINNATI,DEPT PHARM,CINCINNATI,OH. RP Cohen, MR (reprint author), INST SAFE MEDICAT PRACTICES,320 W ST RD,WARMINSTER,PA 18974, USA. NR 66 TC 44 Z9 46 U1 0 U2 2 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 1079-2082 J9 AM J HEALTH-SYST PH JI Am. J. Health-Syst. Pharm. PD APR 1 PY 1996 VL 53 IS 7 BP 737 EP 746 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UD644 UT WOS:A1996UD64400006 PM 8697025 ER PT J AU Rick, ME Krizek, DM AF Rick, ME Krizek, DM TI Identification of a His54Gln substitution in von Willebrand factor from a patient with defective binding of factor VIII SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE von Willebrand factor; Normandy variant; genetic defect; factor VIII binding defect ID VONWILLEBRAND-FACTOR GENE; ACTIVATED PROTEIN-C; AMINO-ACID-RESIDUES; FACTOR VWF; NORMANDY VARIANT; POINT MUTATIONS; DISEASE; PLASMA; DOMAIN; INACTIVATION AB A patient with type 2N (''Normandy'' variant) von Willebrand's disease is described. Her von Willebrand factor level was borderline low, while her factor VIII was markedly decreased to 7%. Her plasma von Willebrand factor demonstrated a decreased ability to complex with factor VIII in vitro, binding less than 10% when compared to normal plasma von Willebrand factor. The factor VIII released into the circulation after the patient received DDAVP had a shortened survival in vivo. Nucleotide sequence analysis revealed a T-to-A transition at nucleotide 2451 on both alleles. This transition results in a substitution of Gln for His at amino acid 54 in the mature subunit of von Willebrand factor. (C) lees Wiley Liss, Inc.* RP Rick, ME (reprint author), NIH,HEMATOL SECT,WARREN GRANT MAGNUSON CLIN CTR,BLDG 10,ROOM 2C 390,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 39 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 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD APR PY 1996 VL 51 IS 4 BP 302 EP 306 PG 5 WC Hematology SC Hematology GA UC620 UT WOS:A1996UC62000009 PM 8602631 ER PT J AU Davis, S Schroeder, M Goldin, LR Weeks, DE AF Davis, S Schroeder, M Goldin, LR Weeks, DE TI Nonparametric simulation-based statistics for detecting linkage in general pedigrees SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID MEMBER METHOD; TRAITS; PAIRS AB We present here four nonparametric statistics for linkage analysis that test whether pairs of affected relatives share marker alleles more often than expected. These statistics are based on simulating the null distribution of a given statistic conditional on the unaffecteds' marker genotypes. Each statistic uses a different measure of marker sharing: the SimAPM statistic uses the simulation-based affected-pedigree-member measure based on identity-by-state (IBS) sharing. The SimKIN (kinship) measure is 1.0 for identity-by-descent (IBD) sharing, 0.0 for no IBD sharing, and the kinship coefficient when the IBD status is ambiguous. The simulation-based IBD (SimIBD) statistic uses a recursive algorithm to determine the probability of two affecteds sharing a specific allele IBD. The SimISO statistic is identical to SimIBD, except that it also measures marker similarity between unaffected pairs. We evaluated our statistics on data simulated under different two-locus disease models, comparing our results to those obtained with several other nonparametric statistics. Use of IBD information produces dramatic increases in power over the SimAPM method, which uses only IBS information. The power of our best statistic in most cases meets or exceeds the power of the other nonparametric statistics. Furthermore, our statistics perform comparisons between all affected relative pairs within general pedigrees and are not restricted to sib pairs or nuclear families. C1 UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA 15261. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. UNIV OXFORD,WELLCOME TRUST CTR HUMAN GENET,OXFORD,ENGLAND. RI Weeks, Daniel/B-2995-2012; OI Davis, Sean/0000-0002-8991-6458; Weeks, Daniel/0000-0001-9410-7228 FU NCRR NIH HHS [1 P41 RR03655]; NHGRI NIH HHS [HG00719]; Wellcome Trust NR 32 TC 94 Z9 95 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD APR PY 1996 VL 58 IS 4 BP 867 EP 880 PG 14 WC Genetics & Heredity SC Genetics & Heredity GA UA380 UT WOS:A1996UA38000025 PM 8644751 ER PT J AU Cannon, RO AF Cannon, RO TI The heart in hypertension - Thinking small SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Editorial Material ID LEFT-VENTRICULAR HYPERTROPHY; DIPYRIDAMOLE-ECHOCARDIOGRAPHY TEST; NORMAL CORONARY-ARTERIES; ANGINA-PECTORIS; CHEST PAIN; SYNDROME-X; DISEASE; CIRCULATION; RESERVE RP Cannon, RO (reprint author), NHLBI,CARDIOL BRANCH,NIH,BLDG 10,ROOM 7B15,10 CTR DR MSC-1650,BETHESDA,MD 20892, USA. NR 19 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD APR PY 1996 VL 9 IS 4 BP 406 EP 408 PN 1 PG 3 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA UF251 UT WOS:A1996UF25100017 PM 8722445 ER PT J AU Alciati, MH AF Alciati, MH TI Intervention research: A model from the national cancer institute's smoking and tobacco control program SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE cancer control; intervention research tobacco control; disease prevention AB Recognizing that the scientific method is as critical to cancer control as it is to basic laboratory research, the National Cancer Institute (NCI) established a well-defined, systematic strategy for attaining its cancer control goals and objectives. This strategy, operationalized in the early 1980s as a five-phase process, emphasized cancer control as a research science rather than a demonstration science. The five phases of NCI's cancer control research strategy progress from hypothesis development, to methods development to controlled intervention trials, to defined population studies, and finally to demonstration and implementation programs. This research base provides the foundation for nationwide prevention and health services programs. The application of this five-phase approach to NCI's efforts to reduce morbidity and mortality attributable to tobacco use is described and some of the challenges that faced the Institute in this process ale identified. These experiences provide an important framework for other disciplines faced with the challenge of translating science into practice. (C) 1996 Wiley-Liss, Inc.* C1 NCI,PUBL HLTH AGCY SECT,ROCKVILLE,MD. OI Alciati, Marianne/0000-0001-6294-1090 NR 23 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD APR PY 1996 VL 29 IS 4 BP 324 EP 328 PG 5 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UD075 UT WOS:A1996UD07500009 PM 8728133 ER PT J AU Striker, GE AF Striker, GE TI NIDDK goes on-line SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT News Item RP Striker, GE (reprint author), NIDDKD,DIV KIDNEY UROL & HEMATOL DIS,BETHESDA,MD 20892, USA. 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 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD APR PY 1996 VL 27 IS 4 BP 603 EP 603 DI 10.1016/S0272-6386(96)90175-4 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA UC864 UT WOS:A1996UC86400021 ER PT J AU Regan, JA Klebanoff, MA Nugent, RP Eschenbach, DA Blackwelder, WC Lou, Y Gibbs, RS Rettig, PJ Martin, DH Edelman, R AF Regan, JA Klebanoff, MA Nugent, RP Eschenbach, DA Blackwelder, WC Lou, Y Gibbs, RS Rettig, PJ Martin, DH Edelman, R TI Colonization with group B streptococci in pregnancy and adverse outcome SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE Group B streptococci; Streptococcus agalactiae; low birth weight; preterm birth ID SELECTIVE INTRAPARTUM CHEMOPROPHYLAXIS; EARLY-ONSET DISEASE; CHLAMYDIA-TRACHOMATIS; PREMATURE RUPTURE; PRETERM LABOR; VAGINAL FLORA; MEMBRANES; INFECTION; PREVENTION; DELIVERY AB OBJECTIVE: Our purpose was to study the association of cervicovaginal colonization with group B streptococci with pregnancy and neonatal outcome. STUDY DESIGN: A prospective study was conducted at seven medical centers between 1984 and 1989. Genital tract cultures were obtained at 23 to 26 weeks' gestation and at delivery. Prematurity and neonatal sepsis rates were compared between group B streptococci positive and negative women. RESULTS: Group B streptococci was recovered from 2877 (21%) of 13,646 women at enrollment. Heavy colonization was associated with a significant risk of delivering a preterm infant who had a low birth weight (odds ratio = 1.5, 95% confidence interval 1.1 to 1.9). Heavily colonized women given antibiotics effective against group B streptococci had little increased risk of a preterm, low-birth-weight birth. Women with light colonization were at the same risk of adverse outcome as the uncolonized women. Neonatal group B streptococci sepsis occurred in 2.6 of 1000 live births in women with and 1.6 of 1000 live births in women without group B streptococci at 23 to 26 weeks' gestation (p = 0.11). However, sepsis occurred in 16 of 1000 live births to women with and 0.4 of 1000 live births to women without group B streptococci at delivery (p < 0.001). CONCLUSIONS: Heavy group B streptococci colonization at 23 to 26 weeks' gestation was associated with an increased risk of delivering a preterm, low-birth-weight infant. Cervicovaginal colonization with group B streptococci at 23 to 26 weeks' gestation was not a reliable predictor of neonatal group B streptococci sepsis. Colonization at delivery was associated with sepsis. C1 NICHHD,NIH,DESPR,BETHESDA,MD 20892. COLUMBIA UNIV,DEPT PEDIAT,NEW YORK,NY 10027. UNIV WASHINGTON,DEPT OBSTET & GYNECOL,SEATTLE,WA 98195. NIAID,NIH,BETHESDA,MD 20892. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. UNIV TEXAS,DEPT OBSTET & GYNECOL,SAN ANTONIO,TX. UNIV OKLAHOMA,DEPT PEDIAT,NORMAN,OK 73019. LOUISIANA STATE UNIV,DEPT MED,NEW ORLEANS,LA. TULANE UNIV,NEW ORLEANS,LA 70118. HARLEM HOSP MED CTR,NEW YORK,NY. FU NICHD NIH HHS [HD-3-2833, HD-3-2832, HD-3-2834] NR 25 TC 127 Z9 143 U1 0 U2 8 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD APR PY 1996 VL 174 IS 4 BP 1354 EP 1360 DI 10.1016/S0002-9378(96)70684-1 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA UH184 UT WOS:A1996UH18400052 PM 8623869 ER PT J AU deSmet, MD StarkVancs, V Kohler, DR Smith, J Wittes, R Nussenblatt, RB AF deSmet, MD StarkVancs, V Kohler, DR Smith, J Wittes, R Nussenblatt, RB TI Intraocular levels of methotrexate after intravenous administration SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID LYMPHOMA; THERAPY AB PURPOSE: To determine if adequate intraocular levels of methotrexate are achieved after intravenous administration. METHODS: After intravenous administration, methotrexate levels were determined in the serum, the anterior chamber, and the cerebrospinal fluids of a patient with recurrent ocular lymphoma. A fluorescence polarization immunoassay was used to make the determinations. RESULTS: At seven hours into a 24-hour intravenous infusion, methotrexate was at cytotoxic level in all samples. At 74 hours, cytotoxic levels were present only in the aqueous humor. CONCLUSION: Sustained cytotoxic ocular methotrexate levels are achievable after systemic administration. C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NCI,DIV CANC TREATMENT,NIH,BETHESDA,MD. NIH,DEPT PHARM,WARREN G MAGNUSON CLIN CTR,BETHESDA,MD. RP deSmet, MD (reprint author), NEI,CLIN IMMUNOL SECT,NIH,BLDG 10,RM 10N112,10 CTR DR,MSC 1858,BETHESDA,MD 20892, USA. OI de Smet, Marc/0000-0002-9217-5603 NR 5 TC 29 Z9 31 U1 0 U2 1 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 APR PY 1996 VL 121 IS 4 BP 442 EP 444 PG 3 WC Ophthalmology SC Ophthalmology GA UD610 UT WOS:A1996UD61000014 PM 8604740 ER PT J AU Baumrind, S Korn, EL Boyd, RL Maxwell, R AF Baumrind, S Korn, EL Boyd, RL Maxwell, R TI The decision to extract .2. Analysis of clinicians' stated reasons for extraction SO AMERICAN JOURNAL OF ORTHODONTICS AND DENTOFACIAL ORTHOPEDICS LA English DT Article AB In a recently reported study, the pretreatment records of each subject in a randomized clinical trial of 148 patients with Class I and Class II malocclusions presenting for orthodontic treatment were evaluated independently by five experienced clinicians (drawn from a panel of 14). The clinicians displayed a higher incidence of agreement with each other than had been expected with respect to the decision as to whether extraction was indicated in each specific case. To improve our understanding of how clinicians made their decisions on whether to extract or not, the records of a subset of 72 subjects randomly selected from the full sample of 148, have now been examined in greater detail. In 21 of these cases, all five clinicians decided to treat without extraction. Among the remaining 51 cases, there were 202 decisions to extract (31 unanimous decision cases and 20 split decision cases). The clinicians cited a total of 469 reasons to support these decisions. Crowding was cited as the first reason in 49% of decisions to extract, followed by incisor protrusion (14%), need for profile correction (8%), Class II severity (5%), and achievement of a stable result (5%). When all the reasons for extraction in each clinician's decision were considered as a group, crowding was cited in 73% of decisions, incisor protrusion in 35%, need for profile correction in 27%, Class II severity in 15% and posttreatment stability in 9%. Tooth size anomalies, midline deviations, reduced growth potential, severity of overjet, maintenance of existing profile, desire to close the bite, periodontal problems, and anticipation of poor cooperation accounted collectively for 12% of the first reasons and were mentioned in 54% of the decisions, implying that these considerations play a consequential, if secondary, role in the decision-making process. All other reasons taken together were mentioned in fewer than 20% of cases. In this sample at least, clinicians focused heavily on appearance-related factors that are qualitatively determinable by physical examination of the surface structures of the face and teeth. They appear to have made primary use of indicators available on study casts and facial photographs and relatively little use of information that is available only on cephalograms or that involves the application of specialized orthodontic theories. C1 UNIV CALIF SAN FRANCISCO,DEPT GROWTH & DEV,DIV ORTHODONT,SAN FRANCISCO,CA 94143. UNIV MED & DENT NEW JERSEY,NEWARK,NJ 07103. NCI,CLIN TRIALS SECT,BIOMETR RES BRANCH,BETHESDA,MD 20892. FU NIDCR NIH HHS [DE08713] NR 9 TC 20 Z9 25 U1 0 U2 0 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 APR PY 1996 VL 109 IS 4 BP 393 EP 402 DI 10.1016/S0889-5406(96)70121-X PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA UF041 UT WOS:A1996UF04100010 PM 8638581 ER PT J AU Smith, ML Fornace, AJ AF Smith, ML Fornace, AJ TI The two faces of tumor suppressor p53 SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID CELL RP Smith, ML (reprint author), NCI,MOLEC PHARMACOL LAB,DEV THERAPEUT PROGRAM,DIV CANC TREATMENT,NIH,BLDG 37,ROOM 5C09,BETHESDA,MD 20892, USA. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 39 TC 52 Z9 54 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 APR PY 1996 VL 148 IS 4 BP 1019 EP 1022 PG 4 WC Pathology SC Pathology GA UD966 UT WOS:A1996UD96600001 PM 8644842 ER PT J AU Morris, CB Gendelman, R Marrogi, AJ Lu, M Lockyer, JM AlperinLea, W Ensoli, B AF Morris, CB Gendelman, R Marrogi, AJ Lu, M Lockyer, JM AlperinLea, W Ensoli, B TI Immunohistochemical detection of bcl-2 in AIDS-associated and classical Kaposi's sarcoma SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; PROGRAMMED CELL-DEATH; YOUNG HOMOSEXUAL MEN; TAT PROTEIN; TUMOR-SUPPRESSOR; WILD-TYPE; P53; GROWTH; EXPRESSION; APOPTOSIS AB Kaposi's Sarcoma (KS) is an angioproliferative disease that is characterized by, proliferation of spindle-shaped cells predominantly of vascular endothelial cell origin, neoangiogenesis, inflammatory cell infiltration, and edema. Although the lesions of classical KS and AIDS-associated KS (AIDS-KS) share common histological features, AIDS-KS occurs at a markedly higher frequency with a more aggressive clinical course Immunohistochemical analyses of 26 evolutionarily staged AIDS-KS lesions derived from HIV-infected patients demonstrate significant cytoplasmic levels of Bcl-2, a protooncogene known to prolong cellular viability and to antagonize apoptosis. Bcl-2 expression increases as the pathological stage of KS advances. Immunohistochemical analyses of classical KS lesions demonstrate prevalent expression of Bcl-2 as well, indicating that upregulation of Bcl-2 may be important in the pathogenesis of both classical and AIDS-associated KS. Coexpression of Bcl-2 and factor VIII-related antigen in spindle-shaped cells present within RS lesions suggests that Bcl-2 is upregulated within the vascular endothelial spindle-shaped cells of KS. The consequences of upregulated Bcl-2 expression within RS lesions may be prolonged spindle cell viability which, when coupled with dysregulated cellular proliferation due in part to synergistic activities of inflammatory and angiogenic cytokines and NN-I Tat protein, may result in the maintenance, growth, and progression of KS. C1 TULANE UNIV,MED CTR,DEPT PATHOL & LAB MED,TULANE CANC CTR,MOL & CELLULAR BIOL PROGRAM,NEW ORLEANS,LA. NCI,TUMOR CELL BIOL LAB,NIH,BETHESDA,MD 20892. TULANE UNIV,MED CTR,DEPT MED,SECT CARDIOL,MOL & CELLULAR BIOL PROGRAM,NEW ORLEANS,LA 70112. RI Ensoli, Barbara/J-9169-2016 OI Ensoli, Barbara/0000-0002-0545-8737 FU NIAID NIH HHS [AI 32880] NR 39 TC 34 Z9 35 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 APR PY 1996 VL 148 IS 4 BP 1055 EP 1063 PG 9 WC Pathology SC Pathology GA UD966 UT WOS:A1996UD96600006 PM 8644847 ER PT J AU Tseng, CC Boylan, MO Jarboe, LA Usdin, TB Wolfe, MM AF Tseng, CC Boylan, MO Jarboe, LA Usdin, TB Wolfe, MM TI Chronic desensitization of the glucose-dependent insulinotropic polypeptide receptor in diabetic rats SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE downregulation; non-insulin-dependent diabetes mellitus ID GASTRIC-INHIBITORY POLYPEPTIDE; PANCREATIC ALPHA-CELL; PEPTIDE-1 7-36 AMIDE; HOMOLOGOUS DESENSITIZATION; ADENYLATE-CYCLASE; GIP; RELEASE; BLOOD AB Rats were rendered diabetic by streptozotocin, after which serum glucose-dependent insulinotropic polypeptide (GIP) levels, duodenal mucosal GIP content, and GIP mRNA levels were nine times, 50%, and 80%, respectively, greater than in control rats. To determine whether an increase in GIP gene expression might induce chronic desensitization of its receptor, normal rats were subjected to continuous intravenous GIP infusion. Serum GIP levels increased gradually in GIP-infused rats, and by 4 h a threefold increase was detected. In response to GIP infusion, the serum insulin concentration increased at 30 min, followed by a gradual decrease, and at 4 h, no increase in insulin levels was detected despite a sustained elevated serum GIP level. The response to glucagon-like peptide-1 (GLP-1) was preserved, indicating that desensitization was ligand specific. To determine the mechanisms governing desensitization of this receptor, a reporter cell line (LGIPR2) stably transfected with rat GIP receptor cDNA was studied. GIP stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production in LGIPR2 cells, which was first detected after 1 h of stimulation, reached maximum level at 4 h, and returned to basal concentrations by 16 h. Additional stimulation with GIP at 16 h did not affect cAMP generation, indicating desensitization of the GIP receptor by the ligand. In contrast, a response to prostaglandin E(1) or forskolin in GIP-desensitized LGIPR2 cells was unchanged, suggesting that desensitization was a receptor-specific process. The results of these studies indicate that GIP gene expression is enhanced in diabetic animals and that elevated serum GIP level induces chronic desensitization of the GIP receptor in vivo and in a stably transfected cell line. C1 HARVARD UNIV, SCH MED, DIV GASTROENTEROL, HARVARD DIGEST DIS CTR, BOSTON, MA 02115 USA. NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA. RP Tseng, CC (reprint author), BRIGHAM & WOMENS HOSP, DIV GASTROENTEROL, 75 FRANCIS ST, BOSTON, MA 02115 USA. FU NIDDK NIH HHS [DK-02277, DK-48042, P30-DK-34854] NR 30 TC 45 Z9 47 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD APR PY 1996 VL 270 IS 4 BP E661 EP E666 PG 6 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA UE561 UT WOS:A1996UE56100018 PM 8928774 ER PT J AU Ecelbarger, CA Chou, CL Lolait, SJ Knepper, MA DiGiovanni, SR AF Ecelbarger, CA Chou, CL Lolait, SJ Knepper, MA DiGiovanni, SR TI Evidence for dual signaling pathways for V-2 vasopressin receptor in rat inner medullary collecting duct SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE water permeability; V-1a receptor; adenosine 3',5'-cyclic monophosphate; intracellular calcium; secondary messengers; signaling; vasopressin analogues; oxytocin ID POLYMERASE CHAIN-REACTION; WATER PERMEABILITY; ADENYLYL CYCLASE; PHOSPHOLIPASE-C; CA2+ MOBILIZATION; NEPHRON SEGMENTS; V2 RECEPTOR; CELLS; OXYTOCIN; TUBULES AB Previous studies have demonstrated that both the V-2-receptor agonist, 1-desamino-8-D-arginine vasopressin (dDAVP), and the V-1a-receptor agonist, [Phe(2),Orm(8)]vasotocin (PO-VT), increase intracellular calcium concentration( [Ca2+](i)) in the rat inner medullary collecting duct (IMCD). The present studies were done to clarify the receptor subtype(s) responsible for calcium mobilization. Measurements of [Ca2+](i) using fura 2 in microdissected IMCD segments, confirmed that arginine vasopressin (AVP), dDAVP, and PO-VT stimua late an increase in [Ca2+](i) and that the response to all three agents could be blocked by the specific V-2-receptor antagonist, [d(CH2)(5)(1),D-Ile(2),Ile(4),Arg(8)]vasopressin (II-VP). These results would suggest that all three agents acted through the V-2 receptor. Furthermore, we showed that PO-VT increased cAMP production in IMCD suspensions and water permeability in isolated perfused tubules. These responses were also blocked by II-VP, indicating that PO-VT is also a V-2 agonist in the IMCD. Finally, we utilized the quantitative reverse transcription-polymerase chain reaction technique of Wiesner (Nucleic Acids Res. 20: 5863-5864, 1992) to evaluate V-1a and V-2 mRNA levels in rat collecting duct. In terminal IMCD, we estimated >30 copies/cell for V-2 receptor mRNA but less than 1 copy/cell of V-1a receptor mRNA, thus there is little or no V-1a mRNA expression in the terminal IMCD. These results suggest that calcium mobilization in response to vasopressin analogues is associated with the V-2 receptor and that the V-2 receptor is linked to both adenylyl cyclase and calcium mobilization in the rat IMCD. C1 NHLBI, KIDNEY & ELECTROLYTE METAB LAB, NIH, BETHESDA, MD 20892 USA. NIMH, CELL BIOL LAB, BETHESDA, MD 20892 USA. FU NIDDK NIH HHS [DK-00832] NR 40 TC 81 Z9 82 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrolyte Physiol. PD APR PY 1996 VL 270 IS 4 BP F623 EP F633 PG 11 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA UE696 UT WOS:A1996UE69600007 PM 8967340 ER PT J AU Frokiaer, J Marples, D Knepper, MA Nielsen, S AF Frokiaer, J Marples, D Knepper, MA Nielsen, S TI Bilateral ureteral obstruction downregulates expression of vasopressin-sensitive AQP-2 water channel in rat kidney SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE polyuria; nephrongenic diabetes insipidus; postobstructive diuresis ID POSTOBSTRUCTIVE DIURESIS; TRANSPORT DEFECTS; DEEP NEPHRON; YOUNG RAT; SEGMENTS; PROTEIN; CELLS AB Polyuria after release of bilateral ureteral obstruction (BUO) is frequently seen in patients with urological disorders. In this study, we examined the effect of BUO and release of BUO on the expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in rat kidney. Ureters were obstructed for 24 h in all experiments, and BUO was either not released or released for 24 or 48 h or 7 days. Each group of experimental rats were matched with sham-operated controls. One kidney was used for membrane fractionation and immunoblotting, whereas the contralateral was fixed for immunocytochemistry. Immunoblotting demonstrated a significant reduction in AQP-2 expression in inner medulla during 24 h of BUO to 26 +/- 8% (P < 0.001). Release of BUO was associated with immediate onset of a predominant osmotic-dependent polyuria. Forty-eight hours after release of BUO, the reduction in AQP-2 expression persisted (19 +/- 8%, P < 0.001), concurrent with a marked nonosmotic postobstructive polyuria, as determined by a significant reduction in free-water clearance (-50 +/- 7 vs. -85 +/- 10 mu l . min(-1). kg(-1), P < 0.05). Immunofluorescence and immunoelectron microscopy confirmed the reduced levels of AQP-2 in collecting duct principal cells. Seven days after release, the renal excretion of water and electrolytes had almost normalized. However, the downregulation of AQP-2 was only partly reversed (49 +/- 14%, P < 0.001), and, consistent with this, the urinary concentrating capacity was significantly reduced 7 days after release of BUO compared with sham-operated rats in response to an 18-h period of thirst. This strongly suggests that the persistent downregulation of AQP-2 is the cause of the slow recovery in concentrating capacity. In conclusion, BUO and release of BUO were associated with a marked reduction in expression of AQP-2, coincident with the development and maintenance of postobstructive polyuria. Thus reduced AQP-2 levels may represent an important factor in the slow recovery from postobstructive diuresis. C1 AARHUS UNIV, INST ANAT, DEPT CELL BIOL, DK-8000 AARHUS C, DENMARK. AARHUS UNIV HOSP, DEPT CLIN PHYSIOL, DK-8000 AARHUS, DENMARK. AARHUS UNIV, INST EXPTL CLIN RES, DK-8000 AARHUS C, DENMARK. NHLBI, KIDNEY & ELECTROLYTE METAB LAB, BETHESDA, MD 20892 USA. NR 37 TC 134 Z9 138 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrolyte Physiol. PD APR PY 1996 VL 270 IS 4 BP F657 EP F668 PG 12 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA UE696 UT WOS:A1996UE69600011 PM 8967344 ER PT J AU Liu, LT Khastgir, A McCauley, JM Dunn, ST Morrissey, JH Christakos, S Hughes, MR Bourdeau, JE AF Liu, LT Khastgir, A McCauley, JM Dunn, ST Morrissey, JH Christakos, S Hughes, MR Bourdeau, JE TI RT-PCR microlocalization of mRNAS for calbindin D-28k and vitamin D receptor in the murine nephron SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE reverse transcription; polymerase chain reaction; messenger ribonucleic acid ID CALCIUM-BINDING PROTEINS; MOUSE KIDNEY; GENE-EXPRESSION; RAT-KIDNEY; LOCALIZATION; VERTEBRATES AB The spatial relationship between vitamin D receptor (VDR) and calbindin D-28k [calcium binding protein D-28k (CaBP-D-28k)] gene expression within the murine kidney was studied by localizing their mRNAs in discrete nephron structures using reverse transcription-polymerase chain reaction (RT-PCR). Primers for beta-actin mRNA were used as a control for the presence of tissue during RT-PCR for CaBP-D-28k mRNA. mRNA for CaBP-D-28k was found only in distal convoluted tubules (DCTs), connecting tubules (CNTs), and cortical collecting ducts (CCDs). In contrast, VDR mRNA was detected in glomeruli, S2 proximal convoluted tubules, cortical thick ascending limbs of Henle's loop, DCTs, CNTs, and initial CCDs. The presence of both VDR and CaBP-D-28k mRNA in DCTs, CNTs, and CCDs is consistent with the hypothesis that calcitriol acts via the VDR to stimulate CaBP-D-28k synthesis. Conversely, the presence of VDR mRNA in other parts of the nephron suggests that calcitriol has genomically mediated actions within the kidney in addition to stimulation of CaBP-D-28k synthesis. C1 UNIV OKLAHOMA, HLTH SCI CTR, DEPT MED, NEPHROL SECT, OKLAHOMA CITY, OK USA. UNIV OKLAHOMA, HLTH SCI CTR, DEPT PATHOL, OKLAHOMA CITY, OK USA. UNIV OKLAHOMA, HLTH SCI CTR, DEPT PHYSIOL & BIOPHYS, OKLAHOMA CITY, OK USA. DEPT VET AFFAIRS MED CTR, MED SERV, OKLAHOMA CITY, OK USA. OKLAHOMA MED RES FDN, CARDIOVASC BIOL PROGRAM, OKLAHOMA CITY, OK 73104 USA. NIH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA. UNIV MED & DENT NEW JERSEY, NEW JERSEY MED SCH, DEPT BIOCHEM & MOLEC BIOL, NEWARK, NJ 07103 USA. FU NIDDK NIH HHS [DK-41427, DK-35985, DK-38961] NR 22 TC 16 Z9 18 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrolyte Physiol. PD APR PY 1996 VL 270 IS 4 BP F677 EP F681 PG 5 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA UE696 UT WOS:A1996UE69600013 PM 8967346 ER PT J AU Coryell, W Leon, A Winokur, G Endicott, J Keller, M Akiskal, H Solomon, D AF Coryell, W Leon, A Winokur, G Endicott, J Keller, M Akiskal, H Solomon, D TI Importance of psychotic features to long-term course in major depressive disorder SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DEXAMETHASONE SUPPRESSION TEST; FOLLOW-UP; DELUSIONAL DEPRESSION; UNIPOLAR DEPRESSION; SEPARATE ENTITY; SUICIDE; SUBTYPES AB Objective: Most efforts to describe the prognostic significance of psychotic features in depression have been limited to single assessments 1 year or less after the initial evaluation. However, the various biological and treatment response differences between patients with psychotic and nonpsychotic depression suggest that prognostic differences may be very long-term. Method: The 787 patients described here entered the study as they sought treatment at one of five academic medical centers; they had either RDC major depressive disorder or schizoaffective depression (other than the mainly schizophrenic subtype) and completed at least 6 months of follow-up. Of these, 144 (18.3%) had psychotic depression as defined here. Patients provided follow-up interviews at 6-month intervals for 5 years and annually thereafter; 98 of those with psychotic depression and 434 of those with nonpsychotic depression were followed for 10 years. Results: Those who began follow-up with psychotic depression had fewer weeks with minimal symptoms in each of the 10 years of follow-up and reported more psychosocial impairment at both 5 and 10 years. Both the index episode and the first recurrence of psychotic depression lasted longer than nonpsychotic episodes, but nonpsychotic episodes among previously psychotic individuals were relatively brief. Intervals between episodes were significantly shorter for patients who had ever been psychotic. Conclusions: Together with evidence that psychotic features are highly recurrent, these data show 1) that psychotic features denote a lifetime illness of greater severity and 2) that within individuals, psychotic features may emerge in only the more severe episodes. C1 NIMH,COLLABORAT PROGRAM PSYCHOBIOL DEPRESSION CLIN STU,BETHESDA,MD 20892. RP Coryell, W (reprint author), UNIV IOWA,DEPT PSYCHIAT,200 HAWKINS DR,IOWA CITY,IA 52242, USA. FU NIMH NIH HHS [R01 MH025478] NR 38 TC 115 Z9 117 U1 2 U2 4 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1996 VL 153 IS 4 BP 483 EP 489 PG 7 WC Psychiatry SC Psychiatry GA UC478 UT WOS:A1996UC47800006 PM 8599395 ER PT J AU Frazier, JA Giedd, JN Kaysen, D Albus, K Hamburger, S AlaghbandRad, J Lenane, MC McKenna, K Breier, A Rapoport, JL AF Frazier, JA Giedd, JN Kaysen, D Albus, K Hamburger, S AlaghbandRad, J Lenane, MC McKenna, K Breier, A Rapoport, JL TI Childhood-onset schizophrenia: Brain MRI rescan after 2 years of clozapine maintenance treatment SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID CORTEX AB Objective: The effect of clozapine on striatal morphology was examined in adolescents with childhood-onset schizophrenia. Method: Eight adolescent patients with onset of psychosis before age 12 and eight matched comparison subjects had initial and 2-year follow-up brain magnetic resonance imaging scans. Basal ganglia and lateral ventricle volumes were measured. The patients were on a clozapine regimen during the 2-year interim. Results: Caudate volume was larger in the patients at the initial scanning, decreased in the patients between scans, and did not differ significantly between the patients and the comparison subjects at the second scanning. Conclusions: Caudate enlargement in patients with childhood-onset schizophrenia who are taking typical neuroleptics appears to be secondary to medication exposure. Rescanning to examine basal ganglia morphology is indicated for these patients when they are taking an atypical neuroleptic. C1 NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. NIMH,EXPTL THERAPEUT BRANCH,BETHESDA,MD 20892. RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015 OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978 NR 15 TC 103 Z9 105 U1 0 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 1996 VL 153 IS 4 BP 564 EP 566 PG 3 WC Psychiatry SC Psychiatry GA UC478 UT WOS:A1996UC47800021 PM 8599409 ER PT J AU Avila, NA Worobec, AS Ling, A Hijazi, Y Metcalfe, DD AF Avila, NA Worobec, AS Ling, A Hijazi, Y Metcalfe, DD TI Pulmonary and ovarian manifestations of systemic mastocytosis SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID MAST-CELL DISEASE C1 NIAID,ALLERG DIS SECT,NIH,BETHESDA,MD 20892. NIH,DEPT PATHOL,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD 20892. RP Avila, NA (reprint author), NIH,DEPT DIAGNOST RADIOL,HENRY M JACKSON FDN,WARREN GRANT MAGNUSON CLIN CTR,BLDG 10,RM 1C660,BETHESDA,MD 20892, USA. NR 8 TC 6 Z9 6 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD APR PY 1996 VL 166 IS 4 BP 969 EP 970 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UB521 UT WOS:A1996UB52100040 PM 8610583 ER PT J AU Zhong, M McCarthy, J Bierwert, L LizotteWaniewski, M Chanteau, S Nutman, TB Ottesen, EA Williams, SA AF Zhong, M McCarthy, J Bierwert, L LizotteWaniewski, M Chanteau, S Nutman, TB Ottesen, EA Williams, SA TI A polymerase chain reaction assay for detection of the parasite Wuchereria bancrofti in human blood samples SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID SPECIES-SPECIFIC DETECTION; REPEATED DNA-SEQUENCES; OLIGONUCLEOTIDE PROBES; BRUGIA-PAHANGI; FILARIASIS; MALAYI AB To identify Wuchereria bancrofti DNA sequences that could be used as the basis for a simple and rapid parasite detection assay, a genomic library of W. bancrofti was constructed and screened for highly repeated DNA. The repeat found with the highest copy number was 195 basepairs (bps) long, 77% AT, and 300 copies per haploid genome. This sequence was designated the Ssp I repeat because it has a unique recognition site for that restriction endonuclease in all or most of the repeat copies. The Ssp I repeat DNA family is dispersed, genus-specific, and exists in all of the different geographic isolates of W. bancrofti tested. Based on DNA sequence analysis of this repeat, we have developed an assay to detect very small quantities of W. bancrofti DNA using the polymerase chain reaction (PCR). With this PCR assay, the Ssp I repeat was detected in as little as 1 pg of W. bancrofti genomic DNA (about 1% of the DNA in one microfilaria) added to 100 mu l of human blood. The PCR assay also amplified Ssp I repeat DNA from geographic isolates of W. bancrofti from around the world but not from other species of filariae or from human or mosquito DNA. Microfilaria-positive human blood samples collected in Mauke, Cook Islands were shown to be Ssp I PCK-positive, while microfilaria-negative samples were PCR-negative. The specificity and sensitivity of the Ssp I PCR assay indicates that this approach has significant potential for improved screening of large human populations for active W. bancrofti infection. C1 INST TERRITORIAL RECH MED LOUIS MALARDE,PAPEETE,TAHITI,FR POLYNESIA. NIAID,NATL INST HLTH,PARASIT DIS LAB,BETHESDA,MD 20892. RP Zhong, M (reprint author), SMITH COLL,CLARK SCI CTR,DEPT BIOL SCI,NORTHAMPTON,MA 01063, USA. RI McCarthy, James/C-1681-2009; yu, yan/C-2322-2012 FU PHS HHS [636005] NR 12 TC 81 Z9 82 U1 0 U2 2 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD APR PY 1996 VL 54 IS 4 BP 357 EP 363 PG 7 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA UJ490 UT WOS:A1996UJ49000009 PM 8615447 ER PT J AU Vernick, KD Keister, DB Toure, A Toure, YT AF Vernick, KD Keister, DB Toure, A Toure, YT TI Quantification of Plasmodium falciparum sporozoites by ribosomal RNA detection SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE LA English DT Article ID CIRCUMSPOROZOITE PROTEIN; MALARIA SPOROZOITES; ANTIBODIES; TARGET; GENES AB We used sequences specific to the small subunit ribosomal RNA (SSU rRNA) of the sporogonic stages of Plasmodium falciparum to design a reverse transcriptase-polymerase chain reaction (RT-PCR) assay that can detect 0.1 sporozoites in total RNA purified from potentially infected mosquitoes. We made a synthetic RNA that is amplified in the RT-PCR by the same primers as the parasite SSU rRNA and that serves as an internal control and competitive quantitation standard. We calibrated the assay for quantitation of sporozoites by making a standard curve with RNA from purified and counted sporozoites. The assay accurately measured sporozoite number with a linear range of at least three orders of magnitude in a single reaction. Some applications and limitations of the assay are discussed. C1 ECOLE NATL MED & PHARM,DEPT EPIDEMIOL AFFECTAT PARASITAIRES,BAMAKO,MALI. RP Vernick, KD (reprint author), NIAID,NATL INST HLTH,PARASIT DIS LAB,BETHESDA,MD 20892, USA. NR 15 TC 14 Z9 16 U1 0 U2 0 PU AMER SOC TROP MED & HYGIENE PI MCLEAN PA 8000 WESTPARK DRIVE SUITE 130, MCLEAN, VA 22101 SN 0002-9637 J9 AM J TROP MED HYG JI Am. J. Trop. Med. Hyg. PD APR PY 1996 VL 54 IS 4 BP 430 EP 438 PG 9 WC Public, Environmental & Occupational Health; Tropical Medicine SC Public, Environmental & Occupational Health; Tropical Medicine GA UJ490 UT WOS:A1996UJ49000022 PM 8615460 ER PT J AU Ma, Y Ito, Y AF Ma, Y Ito, Y TI Affinity countercurrent chromatography using a ligand in the stationary phase SO ANALYTICAL CHEMISTRY LA English DT Article AB In countercurrent chromatography (CCC), an addition of a ligand to the liquid stationary phase remarkably improved both retention time and peak resolution of the analytes: various amino acid derivatives were separated by N-dodecanoyl-L-proline-3,5-dimethylanilide, while polar catecholamines and dipeptides were separated by bis(2-ethylhexyl)phosphoric acid. By selecting an appropriate ligand and dissolving it in the liquid stationary phase, the present CCC technique can perform a variety of separations comparable to chiral chromatography, ion chromatography, and affinity chromatography. Leakage of the ligand from the column can be entirely eliminated by introducing a small volume of a ligand-free stationary phase at the end of the column as an absorbent. The method further facilitates application of pH-zone-refining CCC and can uncrease the sample loading capacity over 10 times for a given column. C1 NHLBI,NATL INST HLTH,BIOPHYS CHEM LAB,BETHESDA,MD 20892. NR 13 TC 22 Z9 24 U1 4 U2 11 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0003-2700 J9 ANAL CHEM JI Anal. Chem. PD APR 1 PY 1996 VL 68 IS 7 BP 1207 EP 1211 DI 10.1021/ac9509263 PG 5 WC Chemistry, Analytical SC Chemistry GA UC182 UT WOS:A1996UC18200028 PM 8651493 ER PT J AU Kirch, W Horneber, M Tamm, ER AF Kirch, W Horneber, M Tamm, ER TI Characterization of Meibomian gland innervation in the cynomolgus monkey (Macaca fascicularis) SO ANATOMY AND EMBRYOLOGY LA English DT Article DE neuropeptide; nitric oxide; eyelid; double-labeling method; immunocytochemistry ID GENE-RELATED PEPTIDE; VASOACTIVE INTESTINAL POLYPEPTIDE; NITRIC-OXIDE SYNTHASE; CRANIAL PARASYMPATHETIC NEURONS; IMMUNOREACTIVE NERVE-FIBERS; SUBSTANCE-P; NEUROPEPTIDE-Y; GUINEA-PIG; TRIGEMINAL GANGLION; NADPH DIAPHORASE AB To characterize the innervation of the cynomolgus monkey (Macaca fascicularis) Meibomian (tarsal) glands, upper lids of six cynomolgus monkeys were investigated with electronmicroscopical and double-labeling immunocytochemical methods. Antibodies against calcitonin gene-related peptide (CGRP), dopamine-beta-hydroxylase (DBH), neuropeptide Y (NPY), nitric oxide synthase (NOS), protein gene product 9.5 (PGP 9.5), substance P (SP), tyrosine hydroxylase (TH), and vasoactive intestinal peptide (VIP) were used. In addition, sections were processed for NADPH-diaphorase (NADPH-d) histochemistry. Staining for PGP 9.5 and electron microscopy showed that Meibomian gland acini were surrounded by a network of unmyelinated nerves and terminal varicose axons. The terminals contained small agranular (30-60 nm) and large granular vesicles (65-110 nm), and were observed in close contact with the basal lamina of the acini, but never internally to the basal lamina. Meibomian axons showed like-immunoreactivity (LI) for the neuropeptides SP, CGRP, NPY, and VIP. In addition, the axons stained for TH, DBH, NOS, and NADPH-d. VIP-LI, NOS- and NADPH-d-positive axons appeared to be more numerous, TH- and DBH-positive axons more rare than others. Most SP-LI axons were double-labelled for CGRP-LI, some for VIP-LI or NPY-LI. In addition, some VIP-LI axons were double-labeled for NPY-LI. NPY/VIP-LI and NPY/SP-LI axons were only observed close to the Meibomian acini. Conversely, NPY-LI colocalized with TH-IR or DBH-IR predominated in perivascular nerves of Meibomian gland vasculature. The close association of varicose axons with the acini of Meibomian glands indicates that nervous signals modulate meibomian secretion. Meibomian gland nerve fibers in the cynomolgus monkey appear to utilize various neuropeptides, catecholamines and nitric oxide as transmitter substances, and seem to derive from the pterygopalatine, superior cervical and trigeminal ganglion respectively. C1 NEI,MOLEC & DEV BIOL LAB,BETHESDA,MD 20892. UNIV ERLANGEN NURNBERG,DEPT ANAT 2,UNIVERSITATSSTR 19,D-91054 ERLANGEN,GERMANY. NR 74 TC 20 Z9 20 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-2061 J9 ANAT EMBRYOL JI Anat. Embryol. PD APR PY 1996 VL 193 IS 4 BP 365 EP 375 PG 11 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA UC857 UT WOS:A1996UC85700006 PM 8694272 ER PT J AU Martin, JL Laster, MJ Kandel, L Kerschmann, RL Reed, GF Eger, EI AF Martin, JL Laster, MJ Kandel, L Kerschmann, RL Reed, GF Eger, EI TI Metabolism of compound A by renal cysteine-S-conjugate beta-lyase is not the mechanism of compound A-induced renal injury in the rat SO ANESTHESIA AND ANALGESIA LA English DT Article ID GLUTATHIONE DEPLETION; DEGRADATION PRODUCTS; SEVOFLURANE; NEPHROTOXICITY; KIDNEY AB Compound A [CF2=C(CF3)OCH2F], a vinyl ether produced by CO2 absorbents acting on sevoflurane, can produce corticomedullary junction necrosis (injury to the outer stripe of the outer medullary layer, i.e., corticomedullary junction) in rats. Several halogenated alkenes produce a histologically similar corticomedullary necrosis by converting glutathione conjugates of these alkenes to halothionoacetyl halides. To test whether this mechanism explained the nephrotoxicity of Compound A, we blocked three metabolic steps which would lead to formation of a halothionoacetyl halide: 1) we depleted glutathione by administering dl-buthionine-S,R-sulfoximine (BSO); 2) we blocked cysteine S-conjugate formation by administering acivicin (AT-125); and 3) we inhibited subsequent metabolism by renal cysteine conjugate beta-lyase to the nephrotoxic acetic acid (AOAA). These treatments were given alone or in combination to separate groups of 10 or 20 Wistar rats before their exposure to Compound A. We hypothesized that blocking these metabolic steps should decrease the injury produced by breathing 150 ppm of Compound A for 3 h. However, we found either no change or an increase in renal injury, suggesting that this pathway mediates detoxification rather than toxicity. Our findings suggest that the cysteine-S-conjugate-mediated pathway is not the mechanism of Compound A nephrotoxicity and, therefore, observed interspecies differences in the activity of this activating pathway may not be relevant in the prediction of the nephrotoxic potential of Compound A in clinical practice. C1 JOHNS HOPKINS MED INST,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205. NIAID,NIH,DIV MICROBIOL & INFECT DIS,BIOMETRY BRANCH,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT ANESTHESIA,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT ANESTHESIA,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PATHOL,SAN FRANCISCO,CA 94143. NR 25 TC 35 Z9 35 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD APR PY 1996 VL 82 IS 4 BP 770 EP 774 DI 10.1097/00000539-199604000-00017 PG 5 WC Anesthesiology SC Anesthesiology GA UC482 UT WOS:A1996UC48200017 PM 8615496 ER PT J AU Cohen, SG Settipane, GA AF Cohen, SG Settipane, GA TI Hymenoptera honored again SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY LA English DT Letter C1 BROWN UNIV,PROVIDENCE,RI 02912. RP Cohen, SG (reprint author), NIAID,NIH,BETHESDA,MD 20892, USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY PI ARLINGTON HTS PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 SN 1081-1206 J9 ANN ALLERG ASTHMA IM JI Ann. Allergy Asthma Immunol. PD APR PY 1996 VL 76 IS 4 BP 379 EP 380 PG 2 WC Allergy; Immunology SC Allergy; Immunology GA UF806 UT WOS:A1996UF80600016 ER PT J AU Cohen, SG Bianchini, PJ AF Cohen, SG Bianchini, PJ TI Hymenoptera honored again SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY LA English DT Letter C1 BROWN UNIV,PROVIDENCE,RI 02912. RP Cohen, SG (reprint author), NIAID,NIH,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER COLL ALLERGY ASTHMA IMMUNOLOGY PI ARLINGTON HTS PA 85 WEST ALGONQUIN RD SUITE 550, ARLINGTON HTS, IL 60005 SN 1081-1206 J9 ANN ALLERG ASTHMA IM JI Ann. Allergy Asthma Immunol. PD APR PY 1996 VL 76 IS 4 BP 379 EP 379 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA UF806 UT WOS:A1996UF80600015 ER PT J AU Licht, T Pastan, I Gottesman, MM Herrmann, F AF Licht, T Pastan, I Gottesman, MM Herrmann, F TI The multidrug-resistance gene in gene therapy of cancer and hematopoietic disorders SO ANNALS OF HEMATOLOGY LA English DT Review DE chemotherapy; myelosuppression; hematopoietic stem cells; P-glycoprotein; dihydrofolate reductase ID BONE-MARROW CELLS; DIHYDROFOLATE-REDUCTASE GENE; ADENOSINE-DEAMINASE GENE; MDR1 MESSENGER-RNA; P-GLYCOPROTEIN; TRANSGENIC MICE; STEM-CELLS; MONOCLONAL-ANTIBODIES; DRUG-RESISTANCE; RETROVIRAL TRANSFER AB Chemoresistance genes have been identified as an impediment to anticancer drug treatment. In particular, P-glycoprotein, the product of the multidrug-resistance (MDR1) gene, plays a major role in clinical treatment failure. Conversely, expression of an MDR1 cDNA in bone marrow of transgenic animals renders hematopoietic cells chemoresistant. Efficient transfer of drug-resistance genes to normal hematopoietic progenitor cells has been achieved with the use of retroviral vectors. In this article we review approaches which use the multidrug-resistance gene to protect bone marrow from myelosuppression following chemotherapy and as a selectable markerin vivo to increase the expression of nonselectable genes which correct hereditary diseases of the hematopoietic system. C1 NCI,MOLEC BIOL LAB,DIV CANC BIOL DIAG & CTR,NIH,BETHESDA,MD 20892. RP Licht, T (reprint author), UNIV ULM,DEPT INTERNAL MED 3,ROBERT KOCH STR 8,D-89081 ULM,GERMANY. NR 119 TC 20 Z9 22 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0939-5555 J9 ANN HEMATOL JI Ann. Hematol. PD APR PY 1996 VL 72 IS 4 BP 184 EP 193 DI 10.1007/s002770050159 PG 10 WC Hematology SC Hematology GA UG571 UT WOS:A1996UG57100005 PM 8624371 ER PT J AU Lenders, JWM Keiser, HR Eisenhofer, G AF Lenders, JWM Keiser, HR Eisenhofer, G TI Plasma metanephrines in the diagnosis of pheochromocytoma - In response SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP Lenders, JWM (reprint author), NIH,BLDG 10,BETHESDA,MD 20892, USA. NR 1 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 APR 1 PY 1996 VL 124 IS 7 BP 695 EP 695 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA UB513 UT WOS:A1996UB51300020 ER PT J AU Dalakas, MC Quarles, RH AF Dalakas, MC Quarles, RH TI Autoimmune ataxic neuropathies (sensory ganglionopathies): Are glycolipids the responsible autoantigens? SO ANNALS OF NEUROLOGY LA English DT Editorial Material ID MONOCLONAL IGM; PATIENT; POLYNEUROPATHY; GANGLIOSIDES; BINDS C1 NINCDS,MOLEC & CELLULAR NEUROBIOL LAB,NIH,BETHESDA,MD 20892. RP Dalakas, MC (reprint author), NINCDS,NEUROMUSCULAR DIS SECT,NIH,BETHESDA,MD 20892, USA. NR 17 TC 46 Z9 47 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1996 VL 39 IS 4 BP 419 EP 422 DI 10.1002/ana.410390402 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA UF808 UT WOS:A1996UF80800001 PM 8619518 ER PT J AU Goldfarb, LG Vasconcelos, O Platonov, FA Lunkes, A Kipnis, V Kononova, S Chabrashvili, T Vladimirtsev, VA Alexeev, VP Gajdusek, DC AF Goldfarb, LG Vasconcelos, O Platonov, FA Lunkes, A Kipnis, V Kononova, S Chabrashvili, T Vladimirtsev, VA Alexeev, VP Gajdusek, DC TI Unstable triplet repeat and phenotypic variability of spinocerebellar ataxia type 1 SO ANNALS OF NEUROLOGY LA English DT Article ID HEREDITARY ATAXIA; CAG REPEAT; HLA; SIBERIA; LINKAGE AB A Siberian kindred with spinocerebellar ataxia genetically linked to the SCA1 locus on chromosome 6p has been screened for the CAG triplet expansion within the coding region of the SCA1 gene. The kindred includes 1,484 individuals, 225 affected and 656 at risk, making this collection the largest spinocerebellar ataxia type 1 (SCA1) pedigree known. Each of the studied 78 SCA1 patients carried an expanded allele containing a stretch of 39 to 72 uninterrupted CAG repeats. Normal alleles had 25 to 37 trinucleotide repeats. Expanded alleles containing 40 to 55 repeats were found in 26 at-risk relatives. The number of CAG repeats in the mutated allele was inversely correlated with age at disease onset. Cerebellar deficiency was present in each patient and its severity was moderately affected by the number of CAG repeats. In contrast, the associated signs, dysphagia, diffuse skeletal muscle atrophy with fasciculations, and tongue atrophy were absent or mild in patients with low CAG repeat numbers, but severely complicated the course of illness in patients with a larger number of repeat units. One female mutation carrier was asymptomatic at age 66, more than 2 standard deviations beyond the average age of risk, suggesting incomplete penetrance. In 2 symptomatic individuals who had an expanded number of CAG repeats on both chromosomes, age at onset, rate of progression, and clinical manifestation corresponded to the size of the larger allele. C1 NINDS,CLIN NEUROGENET UNIT,MED NEUROL BRANCH,BETHESDA,MD 20892. NINDS,CENT NERVOUS SYST STUDIES LAB,BETHESDA,MD 20892. NCI,BIOMETRY BRANCH,NIH,BETHESDA,MD 20892. RES CTR NEURODEGENERAT DISORDERS,YAKUTSK,SAKHA REPUBL,RUSSIA. UNIV DUSSELDORF,DEPT NEUROL,W-4000 DUSSELDORF,GERMANY. NR 25 TC 52 Z9 58 U1 2 U2 4 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1996 VL 39 IS 4 BP 500 EP 506 DI 10.1002/ana.410390412 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA UF808 UT WOS:A1996UF80800011 PM 8619528 ER PT J AU DeJonge, BLM Handwerger, S Gage, D AF DeJonge, BLM Handwerger, S Gage, D TI Altered peptidoglycan composition in vancomycin-resistant Enterococcus faecalis SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID STAPHYLOCOCCUS-AUREUS STRAIN; ALANYL-D-ALANINE; FAECIUM BM4147; ESCHERICHIA-COLI; GLYCOPEPTIDE RESISTANCE; PENICILLIN; PRECURSORS; BIOSYNTHESIS; CARBOXYPEPTIDASE; PROTEINS AB The muropeptide compositions of isogenic vancomycin-resistant and -susceptible Enterococcus faecalis strains were analyzed by reverse-phase high-performance liquid chromatography combined with amino acid analysis and fast atom bombardment mass spectrometry, Peptidoglycan of the susceptible strain contained pentapeptides as stem peptides, whereas peptidoglycan of the isogenic resistant strain was composed of muropeptides with tetrapeptide stem peptides. Despite the synthesis of lactate-terminating peptidoglycan precursors, no lactate-containing muropeptides were detected In peptidoglycan of the resistant strain. These findings indicate that either lactate-terminating precursors are not incorporated into peptidoglycan of the resistant strain or that the lactate residues are removed from peptidoglycan during synthesis. C1 MICHIGAN STATE UNIV,DEPT BIOCHEM,NIH,MASS SPECTROMETRY FACIL,E LANSING,MI 48824. RP DeJonge, BLM (reprint author), ROCKEFELLER UNIV,MICROBIOL LAB,BOX 152,1230 YORK AVE,NEW YORK,NY 10021, USA. FU NCRR NIH HHS [RR00480]; NIAID NIH HHS [R01 AI31612] NR 41 TC 18 Z9 18 U1 2 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD APR PY 1996 VL 40 IS 4 BP 863 EP 869 PG 7 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA UD248 UT WOS:A1996UD24800007 PM 8849241 ER PT J AU Gandjbakhche, AH Bonner, RF Nossal, R Weiss, GH AF Gandjbakhche, AH Bonner, RF Nossal, R Weiss, GH TI Absorptivity contrast in transillumination imaging of tissue abnormalities SO APPLIED OPTICS LA English DT Article DE random walks; optical imaging; detectability; optical contrast ID SCATTERING MEDIA; TIME AB We calculate the time-resolved flux of photons transmitted across an optically turbid slab containing a partially absorbing inclusion. An analytical expression is obtained for the flux at a detector positioned opposite a point source (at a distance equal to the thickness of the slab) when the center of the inclusion lies on the line connecting those points. The calculation employs a discrete-time lattice random-walk model of photon transport. The resulting expression is used to assess the affects of time resolution on the detectability of the inclusion. C1 NIH,PHYS SCI LAB,DIV COMP RES & TECHNOL,BETHESDA,MD 20892. RP Gandjbakhche, AH (reprint author), NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892, USA. RI Bonner, Robert/C-6783-2015 NR 30 TC 29 Z9 30 U1 0 U2 0 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 SN 0003-6935 J9 APPL OPTICS JI Appl. Optics PD APR 1 PY 1996 VL 35 IS 10 BP 1767 EP 1774 DI 10.1364/AO.35.001767 PG 8 WC Optics SC Optics GA UC179 UT WOS:A1996UC17900025 PM 21085300 ER PT J AU Cohn, JA Tsai, L Friguet, B Szweda, LI AF Cohn, JA Tsai, L Friguet, B Szweda, LI TI Chemical characterization of a protein-4-hydroxy-2-nonenal cross-link: Immunochemical detection in mitochondria exposed to oxidative stress SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE free radicals; lipid peroxidation; 4-hydroxy-2-nonenal; protein cross-linking; Mitochondria ID LOW-DENSITY-LIPOPROTEIN; LIPID-PEROXIDATION; ISCHEMIA REPERFUSION; APOLIPOPROTEIN-B; PROTEIN ADDUCTS; FREE-RADICALS; OXIDIZED LDL; MACROPHAGES; OXYGEN; PRODUCTS AB We have previously shown that incubation of the model protein glucose-6-phosphate dehydrogenase (Glu-6-PDH) from the bacterium Leuconostoc mesenteroides with 4-hydroxy-2-nonenal (HNE), a major product of lipid peroxidation, results in the formation of cross-linked protein, HNE-modified protein is resistant to proteolytic degradation and acts as an inhibitor of the multicatalytic proteinase, It was therefore important to establish the chemistry of the cross-linking reaction. The formation of cross-linked Glu-6-PDH is associated with the nearly exclusive loss of lysine residues, For this reason the reaction of N-acetyllysine with HNE has been investigated. The E-amino group of lysine reacts with the double bond (C3) and the carbonyl (C1) functions of HNE via Michael addition and Schiff base formation resulting in the production of a 2:1 amino acid-HNE cross-link. Chromatographic detection of this adduct in the acid hydrolysate of HNE-treated Glu-6-PDH reveals that this chemistry is responsible for the formation of cross-linked protein. Antibody to the reduced form of the 2:1 lysine-HNE adduct was prepared, The antibody was used to demonstrate that exposure of isolated liver mitochondria to oxidative stress led to the formation of intra- and intermolecular protein-HNE cross-links. The results of the present study indicate that modifications to protein by lipid peroxidation products may be physiologically relevant and could contribute to the disease- and age-related buildup of damaged protein. (C) 1996 Academic Press, Inc. C1 CASE WESTERN RESERVE UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106. NHLBI,BIOCHEM LAB,NIH,BETHESDA,MD 20892. INST PASTEUR,UNITE BIOCHIM CELLULAIRE,F-75724 PARIS 15,FRANCE. NR 43 TC 111 Z9 115 U1 0 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD APR 1 PY 1996 VL 328 IS 1 BP 158 EP 164 DI 10.1006/abbi.1996.0156 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA UD396 UT WOS:A1996UD39600022 PM 8638925 ER PT J AU Shou, MG Krausz, KW Gonzalez, FJ Gelboin, HV AF Shou, MG Krausz, KW Gonzalez, FJ Gelboin, HV TI Metabolic activation of the potent carcinogen dibenzo[a,h]anthracene by cDNA-expressed human cytochromes P450 SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE dibenzo[a,h]anthracene; cytochrome P450; cDNA expression; human liver microsomes; metabolism; high-performance liquid chromatography ID VACCINIA VIRUS; HUMAN-TISSUES; DIHYDRODIOLS; DIBENZO(A,H)ANTHRACENE; DIBENZANTHRACENE; INDUCTION; ENZYMES AB The metabolic activation of the potent carcinogen dibenzo[a,h] anthracene (DB[a,h]A) was investigated with recombinant human cytochrome P450 enzymes 1A2, 2B6, 2C8, 2C9, 2E1, 3A3, 3A4, and 3A5 expressed in hepatoma G2 cells and with 14 different human liver microsomes. Three dihydrodiols, three phenols, and one diphenol were formed and separated by high-performance liquid chromatography and identified by UV absorption and mass spectra. Of all P450s tested, 1A2 and 2C9 were the most active and 2B6 was moderately active in the rate of total DB[a,h]A metabolism (2.5- to 12-fold greater activity than that for other P450s). The trans-3,4-dihydrodiol, generally recognized as a precursor of the ultimate carcinogenic 3,4-diol-1,2-epoxides, was produced most actively by 2C9, then 1A2 and 2B6. The values of enzymatic kinetics (K-m and V-max) indicated that 2C9 had the highest catalytic efficiency (V-max/K-m = 9.7) in the formation of 3,4-dihydrodiol, in contrast to 1A2 (5.9) and 2B6 (4.4). 1A2 had the highest activity toward production of the 1,2-dihydrodiol, which is considered to be a weakly carcinogenic metabolite. Although specific activities of human liver microsomes in overall metabolism of DB[a,h]A markedly differed between individuals, metabolic patterns were observed similar to that generated from 1A2. Since human 1A1, a predominant enzyme for metabolism of polycyclic aromatic hydrocarbons, is not significantly expressed in the liver, hepatic microsomal 2C9, 1A2, and 2B6 all probably contribute to the metabolic activation of DB[a,h]A. (C) 1996 Academic Press, Inc. RP Shou, MG (reprint author), NCI,MOLEC CARCINOGENESIS LAB,NIH,BLDG 37,BETHESDA,MD 20892, USA. NR 26 TC 35 Z9 37 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 APR 1 PY 1996 VL 328 IS 1 BP 201 EP 207 DI 10.1006/abbi.1996.0161 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA UD396 UT WOS:A1996UD39600027 PM 8638931 ER PT J AU Hommer, D Momenan, R Rawlings, R Ragan, P Williams, W Rio, D Eckardt, M AF Hommer, D Momenan, R Rawlings, R Ragan, P Williams, W Rio, D Eckardt, M TI Decreased corpus callosum size among alcoholic women SO ARCHIVES OF NEUROLOGY LA English DT Article ID LIVER-DISEASE; WHITE MATTER; SEX; MRI; CONSUMPTION; INSTRUMENT; METABOLISM; HISTORY; ATROPHY; DAMAGE AB Background: Although females appear to be more sensitive to the hepatic consequences of alcoholism, it is not clear if women are more sensitive to the effects of excessive alcohol consumption on the brain than men. Subjects and Methods: We compared the cross-sectional area of the corpus callosum in a group of 14 hospitalized alcoholic women and 13 hospitalized alcoholic men with a group of nine nonalcoholic women and 10 nonalcoholic men. All subjects were between the ages of 30 and 50 years. The cross-sectional areas of the corpus callosum and the inner table of the skull were measured on midsagittal T-1-weighted magnetic resonance images. Results: Females had smaller intracranial areas than males, but there was no difference in intracranial area between the alcoholics and nonalcoholics. The corpus callosum area was significantly smaller among the alcoholic women compared with either. the control women or the alcoholic men. Alcoholic men did not differ from control men in the corpus callosum area. These results did not change when the corpus callosum area was adjusted for intracranial area by analysis of covariance. When the corpus callosum was divided into four segments of equal length, the reduction in area was not localized to any particular region. Conclusion: These results suggest an increased sensitivity to alcohol-induced brain damage among alcoholic women compared with alcoholic men. C1 NIAAA,DIV INTRAMURAL CLIN & BIOL RES,CLIN STUDIES LAB,NIH,BETHESDA,MD 20892. NR 27 TC 105 Z9 107 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD APR PY 1996 VL 53 IS 4 BP 359 EP 363 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA UD631 UT WOS:A1996UD63100013 PM 8929159 ER PT J AU Sternberg, P Brown, JM Curtis, L Fremstad, A Gibbs, D Gilman, J Swords, R Waldron, RG Bressler, NM Belt, J Bressler, SB Muth, T Elman, MJ George, T Haller, JA Herring, M Orr, PR Schachat, AP Sotirakos, P Starr, J Singerman, LJ Brown, P Coreno, K DeLisio, M Novak, M Pinter, AS Rice, TA SmithBrewer, S Fish, GE Aguado, H Anderson, T Crockett, E Jost, BF Nork, CP Orth, DH Baczewski, D Bryant, D Doherty, D Fitzgerald, J Flood, TP Graff, S Kwiatkowski, K Packo, KH Garcia, CA Bloome, MA Foreman, J Horton, J Matheny, J Ruiz, RS Folk, JC Fountain, C Griffin, M Heffron, E Kimura, AE Northway, R Vogel, C Ward, B Chandra, SR Harrison, R Knutson, G Lewis, B Lyngaas, H Myers, RL Quackenboss, D Saine, PJ Somers, G Stevens, TS Weber, GB Gass, JDM Cubillas, T Chuang, E Duria, L HessJacobsen, D Lewis, ML Pall, M Rams, I Soler, A Burton, TC Laabs, J Mieler, WF Phillips, J Wipplinger, W Zarling, D Gitter, K Schomacker, K Wilkinson, CP Wheeler, A Klein, ML Evans, M Nolte, SK Vahrenwald, D Wallace, P Watzke, RC Wilson, DJ Margherio, RR Bridges, C Cox, S Cumming, K Huston, G Johnson, JL Murphy, PL Regan, VS Stenic, C Streasik, P Burgess, DB Blank, J Breeding, L Dahl, J Hoffmeyer, G Kacizak, R Meredith, TA Olk, RJ Ort, E Wilder, A Fine, SL Fatula, E Hawkins, BS Maguire, MG Cramer, LD Goldsborough, IL Keller, JA Marsh, MJ McCaffrey, L MillerHart, A Newhouse, MM White, VL Alexander, J EureCooper, R Hiner, CJ Javornik, NB Phillips, DA Tian, Y Walker, VG Ward, RG Whitehead, GR McLaughlin, JA Donald, J Gass, M Meinert, CL McCormick, P Hillis, AI Jampol, LM McLean, EB Rosner, B Safriet, B AF Sternberg, P Brown, JM Curtis, L Fremstad, A Gibbs, D Gilman, J Swords, R Waldron, RG Bressler, NM Belt, J Bressler, SB Muth, T Elman, MJ George, T Haller, JA Herring, M Orr, PR Schachat, AP Sotirakos, P Starr, J Singerman, LJ Brown, P Coreno, K DeLisio, M Novak, M Pinter, AS Rice, TA SmithBrewer, S Fish, GE Aguado, H Anderson, T Crockett, E Jost, BF Nork, CP Orth, DH Baczewski, D Bryant, D Doherty, D Fitzgerald, J Flood, TP Graff, S Kwiatkowski, K Packo, KH Garcia, CA Bloome, MA Foreman, J Horton, J Matheny, J Ruiz, RS Folk, JC Fountain, C Griffin, M Heffron, E Kimura, AE Northway, R Vogel, C Ward, B Chandra, SR Harrison, R Knutson, G Lewis, B Lyngaas, H Myers, RL Quackenboss, D Saine, PJ Somers, G Stevens, TS Weber, GB Gass, JDM Cubillas, T Chuang, E Duria, L HessJacobsen, D Lewis, ML Pall, M Rams, I Soler, A Burton, TC Laabs, J Mieler, WF Phillips, J Wipplinger, W Zarling, D Gitter, K Schomacker, K Wilkinson, CP Wheeler, A Klein, ML Evans, M Nolte, SK Vahrenwald, D Wallace, P Watzke, RC Wilson, DJ Margherio, RR Bridges, C Cox, S Cumming, K Huston, G Johnson, JL Murphy, PL Regan, VS Stenic, C Streasik, P Burgess, DB Blank, J Breeding, L Dahl, J Hoffmeyer, G Kacizak, R Meredith, TA Olk, RJ Ort, E Wilder, A Fine, SL Fatula, E Hawkins, BS Maguire, MG Cramer, LD Goldsborough, IL Keller, JA Marsh, MJ McCaffrey, L MillerHart, A Newhouse, MM White, VL Alexander, J EureCooper, R Hiner, CJ Javornik, NB Phillips, DA Tian, Y Walker, VG Ward, RG Whitehead, GR McLaughlin, JA Donald, J Gass, M Meinert, CL McCormick, P Hillis, AI Jampol, LM McLean, EB Rosner, B Safriet, B TI Occult choroidal neovascularization - Influence on visual outcome in patients with age-related molecular degeneration SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID MACULAR DEGENERATION AB Objective: To determine whether the presence of occult choroidal neovascularization (CNV) influenced the anatomic and visual acuity outcomes in a randomized clinical trial of krypton red laser photocoagulation to treat juxtafoveal neovascular lesions in age-related macular degeneration. Design, getting, and Patients: The fluorescein angiograms obtained at the baseline examination at tertiary retinal referral centers between April 1, 1981, and December 31, 1987, as part of the Macular Photocoagulation Study (MPS) Age-Related Macular Degeneration Study-Krypton Laser were evaluated retrospectively at the MPS Fundus Photograph Reading Center by two senior readers independently (with open adjudication of any differences) from 1992 to 1994. Criteria for classifying classic and occult CNV by the MPS Group were established by 1989, 2 years after the last patient had been assigned randomly to treatment or observation in the krypton laser study. Main Outcome Measures: Treatment coverage of classic and occult CNV, persistent CNV, recurrent CNV, and visual acuity from scheduled follow-up examinations for up to 5 years were analyzed for the absence or presence of occult CNV at baseline. Results: The number of eyes with classic CNV but no occult CNV, classic and occult CNV, and occult CNV but no classic CNV were almost identical for the eyes assigned randomly to treatment or observation. Classic CNV almost always was covered completely with intense laser treatment; nevertheless, recurrent CNV developed in more than half of these eyes within 1 year after initial laser treatment. In contrast, in more than half of the eyes with occult CNV, more than 50% of the occult CNV was not covered with heavy laser treatment. Laser treatment was clearly beneficial for eyes with classic CNV but no occult CNV and almost equivalent to no treatment for eyes with classic and occult CNV. The few eyes with occult CNV but no classic CNV precluded conclusions about the value of treatment in this subgroup. Conclusions: These results strengthen previous reports that laser treatment is beneficial for eyes with juxtafoveal choroidal neovascular lesions when classic CNV is present, even though CNV often recurs. Treatment of classic CNV alone in eyes with classic and occult CNV was not beneficial in this study. Distinguishing classic CNV from occult CNV can aid in the selection of patients who will benefit most from laser treatment. C1 JOHNS HOPKINS UNIV,SCH MED,WILMER OPHTHALMOL INST,BALTIMORE,MD 21205. EMORY EYE CTR,ATLANTA,GA. RETINA ASSOCIATES,CLEVELAND,OH. TEXAS RETINA ASSOCIATES,DALLAS,TX. INGALLS MEM HOSP,HARVEY,IL. INGALLS MEM HOSP,CHICAGO,IL. HERMANN EYE CTR,HOUSTON,TX. UNIV IOWA,IOWA CITY,IA. UNIV WISCONSIN,MADISON,WI. UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,MIAMI,FL. MED COLL WISCONSIN,MILWAUKEE,WI 53226. TOURO INFIRM,NEW ORLEANS,LA. UNIV OKLAHOMA,MCGEE EYE INST,OKLAHOMA CITY,OK. OREGON HLTH SCI UNIV,PORTLAND,OR. WILLIAM BEAUMONT HOSP,ROYAL OAK,MI 48072. RETINA CONSULTANTS LTD,ST LOUIS,MO. UNIV PENN,SCHEIE EYE INST,PHILADELPHIA,PA 19104. NEI,NIH,BETHESDA,MD 20892. NR 25 TC 104 Z9 104 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD APR PY 1996 VL 114 IS 4 BP 400 EP 412 PG 13 WC Ophthalmology SC Ophthalmology GA UD951 UT WOS:A1996UD95100005 ER PT J AU Elsas, FJ Braune, K Jones, J Kimble, JA Kline, L Lampton, G Witherspoon, D Roth, AM Erickson, R Gilbert, WS Chrousos, GA Friendly, DS Jaafar, M Keys, MP Kolsky, MP Mercer, PA ONeill, JF Parelhoff, ES Perraut, E Pilkerton, AR Plotsky, D Flynn, JT Bancalari, E Clarkson, J Vandenbroucke, R Warman, R Miller, MT Cronin, C Daily, M Gieser, R Mittelman, D Squires, P Vygantas, C Kaufman, LM Santiago, N Shapiro, M Ellis, FD Helveston, EM Plager, D Schreiner, R Sprunger, DT Barr, CC Douglas, CH Fishman, PH Whittington, GK Gordon, RA Bushaw, C Haik, BG Repka, MX Loupe, DN Haller, JA Baker, JD Trese, MT Manatrey, P Summers, CG Balles, MW Egbert, JE Knobloch, DK Knobloch, WH Lavoie, JD Maxwell, M Ramsay, RC Phelps, DL Reynolds, JD Torrisi, P Asselin, D Esposito, P Gardner, K Guillet, E Hampton, R Merriam, W Metz, HS Olsen, R Platt, C Simon, R Spalding, SC Tingley, D Vanderlinde, RE Wood, NE Buckley, EG Anderson, MM Machemer, R Valentine, G Burke, MJ Johnson, JC Lipman, M Szmyd, SM Rogers, GL Bremer, DL Fellows, RR Letson, AD McGregor, MLK Palmer, EA Chao, J LaFrance, SB Robertson, J Brown, GC Hertle, RW Kubacki, JJ Menacker, SJ Miller, DL Schaffer, DB Tasman, W Biglan, AW Cheng, KP Schramm, M Saunders, RA Bluestein, E King, LP McPherson, J Wilson, ME Feman, SS Law, AB Spencer, R Arnwine, J Berry, PM Leffler, JN Stager, DR vanHeuven, WAJ Montez, MG Hoffman, RO Bracken, S Teske, M Mowery, RL Krom, CP Phillips, CL Hardy, RJ Davis, BR Tung, B Foos, RY Dobson, V Quinn, GE Bartholomew, P Evans, J Hammel, N Trueb, L Verness, J Scher, S Connett, J Davis, M Hillis, A Robb, R Safriet, B Saigal, S Silverman, W Roth, A Palmer, EA AF Elsas, FJ Braune, K Jones, J Kimble, JA Kline, L Lampton, G Witherspoon, D Roth, AM Erickson, R Gilbert, WS Chrousos, GA Friendly, DS Jaafar, M Keys, MP Kolsky, MP Mercer, PA ONeill, JF Parelhoff, ES Perraut, E Pilkerton, AR Plotsky, D Flynn, JT Bancalari, E Clarkson, J Vandenbroucke, R Warman, R Miller, MT Cronin, C Daily, M Gieser, R Mittelman, D Squires, P Vygantas, C Kaufman, LM Santiago, N Shapiro, M Ellis, FD Helveston, EM Plager, D Schreiner, R Sprunger, DT Barr, CC Douglas, CH Fishman, PH Whittington, GK Gordon, RA Bushaw, C Haik, BG Repka, MX Loupe, DN Haller, JA Baker, JD Trese, MT Manatrey, P Summers, CG Balles, MW Egbert, JE Knobloch, DK Knobloch, WH Lavoie, JD Maxwell, M Ramsay, RC Phelps, DL Reynolds, JD Torrisi, P Asselin, D Esposito, P Gardner, K Guillet, E Hampton, R Merriam, W Metz, HS Olsen, R Platt, C Simon, R Spalding, SC Tingley, D Vanderlinde, RE Wood, NE Buckley, EG Anderson, MM Machemer, R Valentine, G Burke, MJ Johnson, JC Lipman, M Szmyd, SM Rogers, GL Bremer, DL Fellows, RR Letson, AD McGregor, MLK Palmer, EA Chao, J LaFrance, SB Robertson, J Brown, GC Hertle, RW Kubacki, JJ Menacker, SJ Miller, DL Schaffer, DB Tasman, W Biglan, AW Cheng, KP Schramm, M Saunders, RA Bluestein, E King, LP McPherson, J Wilson, ME Feman, SS Law, AB Spencer, R Arnwine, J Berry, PM Leffler, JN Stager, DR vanHeuven, WAJ Montez, MG Hoffman, RO Bracken, S Teske, M Mowery, RL Krom, CP Phillips, CL Hardy, RJ Davis, BR Tung, B Foos, RY Dobson, V Quinn, GE Bartholomew, P Evans, J Hammel, N Trueb, L Verness, J Scher, S Connett, J Davis, M Hillis, A Robb, R Safriet, B Saigal, S Silverman, W Roth, A Palmer, EA TI Multicenter trial of cryotherapy for retinopathy of prematurity - Snellen visual acuity and structural outcome at 5 1/2 years after randomization SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article AB Objective: To evaluate outcome at 5 1/2 years after randomization in eyes that underwent cryotherapy and in control eyes of patients in the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity. Design: During infancy, patients with bilateral threshold retinopathy of prematurity (ROP) were assigned to receive cryotherapy for one eye and no cryotherapy for the other eye. Those with threshold ROP in only one eye (asymmetric) were randomly assigned to cryotherapy or no cryotherapy for that eye. Then, 5 1/2 years later, testers who were masked to the treatment status of each eye measured the patients' monocular visual acuity by using the log of the minimum angle of resolution visual acuity chart that was used in the Early Treatment Diabetic Retinopathy Study. This was the most refined visual acuity testing yet performed on this cohort. Structural outcome was evaluated by participating ophthalmologists' assessment of ROP residua in the posterior pole of the fundus. Patients: Patients were 291 children who had been preterm infants with birth weights of less than 1251 g in whom threshold ROP had developed. Two hundred forty patients had bilateral threshold ROP, and 51 had threshold ROP in only one eye. Results: For the 234 children examined, both visual acuity and fundus structure showed a reduction in unfavorable outcomes in treated vs control eyes: 47.1% vs 61.7%, respectively (P<.005), for visual acuity and 26.9% vs 45.4%, respectively (P<.001), for fundus status. Detailed analysis uf visual acuity outcomes for all eyes revealed that while fewer treated eyes (31.5%) than control eyes (48%) were blind (P<.001), there was a slight trend toward fewer eyes with a visual acuity of 20/40 or better in the treated (13%) vs control (17%) groups (P=.19). Conclusions: The results support the long-term efficacy and safety of cryotherapy in the treatment of severe ROP. However, the data show preliminary evidence of a possible adverse effect of this treatment on visual acuity. C1 OREGON HLTH SCI UNIV,CASEY EYE INST,CRYO ROP HEADQUARTERS,PORTLAND,OR 97201. CHILDRENS HOSP,BIRMINGHAM,AL. UNIV CALIF DAVIS,MED CTR,SUTTER MEM HOSP,SACRAMENTO,CA 95817. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. CHILDRENS HOSP,NATL MED CTR,WASHINGTON,DC 20010. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. WASHINGTON HOSP CTR,WASHINGTON,DC 20010. JACKSON MEM HOSP,MIAMI,FL 33136. UNIV ILLINOIS,EYE & EAR INFIRM,CHICAGO,IL 60612. LOYOLA UNIV,MAYWOOD,IL 60153. LUTHERAN GEN HOSP,PARK RIDGE,IL 60068. RILEY HOSP,WISHARD MEM HOSP,INDIANAPOLIS,IN. UNIV HOSP,INDIANAPOLIS,IN. UNIV LOUISVILLE HOSP,LOUISVILLE,KY. NORTON KOSAIR CHILDRENS HOSP,LOUISVILLE,KY. TULANE UNIV,MED CTR,NEW ORLEANS,LA. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21287. WILLIAM BEAUMONT HOSP,DETROIT,MI. CHILDRENS HOSP MICHIGAN,DETROIT,MI. UNIV MINNESOTA HOSP,MINNEAPOLIS CHILDRENS MED CTR,MINNEAPOLIS,MN. UPSTATE NEW YORK CTR,ROCHESTER,NY. UPSTATE NEW YORK CTR,SYRACUSE,NY. UPSTATE NEW YORK CTR,BUFFALO,NY. STRONG MEM HOSP,BUFFALO,NY. CHILDRENS HOSP BUFFALO,BUFFALO,NY. RETINA RES INST CENT NEW YORK,SYRACUSE,NY. DUKE EYE CTR,DURHAM,NC. UNIV HOSP,CHILDRENS HOSP MED CTR,CINCINNATI,OH. CHILDRENS HOSP,COLUMBUS,OH 43205. UNIV HOSP,COLUMBUS,OH. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA 19104. UNIV PITTSBURGH,PITTSBURGH,PA. INST EYE & EAR,PITTSBURGH,PA. MED UNIV HOSP,CHARLESTON,SC. VANDERBILT UNIV SCH MED,NASHVILLE,TN. METHODIST MED CTR,DALLAS,TX. PARKLAND MEM HOSP & AFFILIATED INST,DALLAS,TX. ST PAULS HOSP,DALLAS,TX. MED CITY DALLAS HOSP,DALLAS,TX. PRESBYTERIAN MED CTR,DALLAS,TX. UNIV TEXAS,HLTH SCI CTR,MED CTR,SAN ANTONIO,TX. UNIV UTAH HOSP,SALT LAKE CITY,UT. NEI,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,COORDINATING CTR CLIN TRIALS,HOUSTON,TX. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. NR 20 TC 131 Z9 137 U1 0 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD APR PY 1996 VL 114 IS 4 BP 417 EP 424 PG 8 WC Ophthalmology SC Ophthalmology GA UD951 UT WOS:A1996UD95100007 ER PT J AU Pattatucci, AML AF Pattatucci, AML TI Heterosexuality: A feminism & psychology reader - Wilkinson,S, Kitzinger,C SO ARCHIVES OF SEXUAL BEHAVIOR LA English DT Book Review RP Pattatucci, AML (reprint author), NCI,LB,NIH,BLDG 37,ROOM 4A13,BETHESDA,MD 20892, USA. NR 4 TC 0 Z9 0 U1 1 U2 1 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 APR PY 1996 VL 25 IS 2 BP 221 EP 225 PG 5 WC Psychology, Clinical; Social Sciences, Interdisciplinary SC Psychology; Social Sciences - Other Topics GA UJ516 UT WOS:A1996UJ51600007 ER PT J AU Tayebi, N Herman, J Ginns, EI Sidransky, E AF Tayebi, N Herman, J Ginns, EI Sidransky, E TI Genotype D399N/R463C in a patient with type 3 Gaucher disease previously assigned genotype N370S/R463C SO BIOCHEMICAL AND MOLECULAR MEDICINE LA English DT Article ID GLUCOCEREBROSIDASE GENE AB A patient with type 3 Gaucher disease is described with a novel genotype, D399N/R463C, established by DNA sequencing. This patient was previously reported as having genotype N370S/R463C. This communication now establishes that no patients reported with mutation N370S have the neuronopathic forms of Gaucher disease and has important implications for genetic counseling. (C) 1996 Academic Press, Inc. RP Tayebi, N (reprint author), NIMH,CLIN NEUROSCI BRANCH,NIH,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 1077-3150 J9 BIOCHEM MOL MED JI Biochem. Mol. Med. PD APR PY 1996 VL 57 IS 2 BP 149 EP 151 DI 10.1006/bmme.1996.0021 PG 3 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA UJ835 UT WOS:A1996UJ83500010 PM 8733893 ER PT J AU OmatsuKanbe, M Zarnowski, MJ Cushman, SW AF OmatsuKanbe, M Zarnowski, MJ Cushman, SW TI Hormonal regulation of glucose transport in a brown adipose cell preparation isolated from rats that shows a large response to insulin SO BIOCHEMICAL JOURNAL LA English DT Article ID UNCOUPLING PROTEIN; SKELETAL-MUSCLE; TRANSGENIC MICE; PLASMA-MEMBRANE; ADIPOCYTES; TISSUE; EXPRESSION; GLUT4; STIMULATION; NOREPINEPHRINE AB Isolated brown adipose cells from rats are prepared whose viability is indicated by the expected stimulation of oxygen consumption by noradrenaline and counter-regulation of this oxygen consumption response by insulin. Insulin stimulates 3-O-methyl-D-glucose transport by approx. 15-fold in the absence of adenosine, and adenosine augments this response at least 2-fold. The insulin-stimulated translocation of the glucose transporter GLUT4 from an intracellular compartment to the plasma membrane is readily detected by subcellular fractionation and Western blotting, and the appearance of GLUT4 on the cell surface in response to insulin is demonstrated by bis-mannose photolabelling. Isoprenaline also stimulates glucose transport activity but only by approx, 3-fold; this effect is not altered by adenosine. Isoprenaline increases insulin-stimulated glucose transport activity in the absence of adenosine but decreases it in the presence of adenosine. These results demonstrate that although the regulation of glucose transport by insulin in brown adipose cells is qualitatively similar to that in white adipose cells, counter-regulation by adenosine and isoprenaline is at least quantitatively and may be qualitatively different. Isolated brown adipose cells from rats thus represent an excellent model for further examination of the mechanism by which multiple hormone signalling pathways interact to control glucose transport and GLUT4 subcellular trafficking. C1 NIDDK,NATL INST HLTH,DIABET BRANCH,EXPTL DIABET METAB & NUTR SECT,BETHESDA,MD 20892. NR 31 TC 21 Z9 22 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD APR 1 PY 1996 VL 315 BP 25 EP 31 PN 1 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UF053 UT WOS:A1996UF05300005 PM 8670115 ER PT J AU Zang, LY Shi, XL Misra, HP AF Zang, LY Shi, XL Misra, HP TI EPR-spin trapping kinetic studies of superoxide radicals produced by photosensitized hypocrellin A, a photodynamic therapeutic agent SO BIOCHEMISTRY AND MOLECULAR BIOLOGY INTERNATIONAL LA English DT Article DE kinetics; superoxide radicals; hypocrellin A; EPR; spin trapping ID GENERATION; PHOTOLYSIS AB Kinetics of superoxide radicals generation by a photodynamic therapeutic agent, Hypocrellin A has been studied by EPR-spin trapping technique. The rate constant (k(g)) for superoxide radicals generation by Hypocrellin A was found to be 5.0 x 10(-3) s(-1). The first-order rate constant (k(1)) and the half-life time (t(0.5)) for DMPO-O-2(-) decay were 2.86 x 10(-3) s(-1) and 242.3 s, respectively. It appears that oxyradicals, generated during the photodynamic process, may be associated with the treatment of various skin diseases by photodynamic therapy of Hypocrellin A. C1 VIRGINIA TECH,VIRGINIA MARYLAND REG COLL VET MED,DEPT BIOMED SCI,BLACKSBURG,VA 24061. NCI,LAB EXPT PATHOL,BETHESDA,MD 20892. RI Shi, Xianglin/B-8588-2012 NR 11 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 1039-9712 J9 BIOCHEM MOL BIOL INT JI Biochem. Mol. Biol. Int. PD APR PY 1996 VL 38 IS 4 BP 685 EP 691 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA VG882 UT WOS:A1996VG88200006 PM 8728097 ER PT J AU Kaye, W Halmi, K Berrettini, W Goldman, D Fichter, M Strober, M Treasurer, J Kaplan, A Woodside, B Plotnikov, K Pollice, C Lilenfeld, L AF Kaye, W Halmi, K Berrettini, W Goldman, D Fichter, M Strober, M Treasurer, J Kaplan, A Woodside, B Plotnikov, K Pollice, C Lilenfeld, L TI Clinical studies supporting genetic research in anorexia nervosa SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV PITTSBURGH,PITTSBURGH,PA 15213. CORNELL UNIV,COLL MED,NEW YORK,NY 10605. THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107. NIAAA,NIH,BETHESDA,MD 20852. UNIV MUNICH,MUNICH,GERMANY. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. INST PSYCHIAT,LONDON,ENGLAND. UNIV TORONTO,TORONTO,ON,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 17 EP 17 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300013 ER PT J AU Hitri, A Wyatt, RJ AF Hitri, A Wyatt, RJ TI Dopamine transporter in schizophrenia: A progressive loss with age in the cingulate cortex SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 VET ADM MED CTR,RES & DEV,WASHINGTON,DC 20422. NIMH,CTR NEUROSCI,NPB,WASHINGTON,DC 20422. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 22 EP 22 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300018 ER PT J AU Rapoport, JL AF Rapoport, JL TI Childhood onset schizophrenia: New research SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 27 EP 27 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300023 ER PT J AU Putnam, F AF Putnam, F TI Post-traumatic stress disorder: A developmental perspective SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 28 EP 28 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300024 ER PT J AU London, ED Grant, S Newlin, D Villemagne, V Phillips, RL Liu, X Kimes, AS Contoreggi, C Margolin, A AF London, ED Grant, S Newlin, D Villemagne, V Phillips, RL Liu, X Kimes, AS Contoreggi, C Margolin, A TI Cocaine-related cues elicit craving and activate cortical circuits relevant to episodic memory SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIDA,INTRAMURAL RES PROGRAM,NEUROSCI BRANCH,BALTIMORE,MD 21224. YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06519. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 35 EP 35 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300031 ER PT J AU Rosenthal, NE AF Rosenthal, NE TI The use of light therapy in psychiatry SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,SECT ENVIRONM PSYCHIAT,CPB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 45 EP 45 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300041 ER PT J AU Breier, A Su, TP Weisenfeld, N Elman, I Adler, C Malhotra, AK Pickar, D AF Breier, A Su, TP Weisenfeld, N Elman, I Adler, C Malhotra, AK Pickar, D TI Assessment of striatal dopamine function in schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,EXPTL THERAPEUT BRANCH,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 48 EP 48 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300044 ER PT J AU Su, TP Breier, A Coppola, R Hadd, K Elman, I Adler, C Malhotra, AK Watsky, E Gorey, J Weinberger, D Pickar, D AF Su, TP Breier, A Coppola, R Hadd, K Elman, I Adler, C Malhotra, AK Watsky, E Gorey, J Weinberger, D Pickar, D TI D2 receptor occupancy in risperidone and clozapine-treated schizophrenics SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,EXPTL THERAPEUT BRANCH,NIH,BETHESDA,MD. NIMH,CLIN BRAIN DISORDERS BRANCH,ST ELIZABETHS HOSP,NIH,NEUROSCI CTR,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 51 EP 51 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300047 ER PT J AU Knable, MB Heinz, A Coppola, R Gorey, J Weinberger, DR AF Knable, MB Heinz, A Coppola, R Gorey, J Weinberger, DR TI IBZM SPECT measurement of D2 receptor occupancy by haloperidol and risperidone SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 56 EP 56 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300052 ER PT J AU Bahro, M Schreurs, BG McIntosh, AR Sunderland, T Molchan, SE AF Bahro, M Schreurs, BG McIntosh, AR Sunderland, T Molchan, SE TI Scopolamine effects on rCBF during human eyeblink conditioning SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,SECT GERIATR PSYCHIAT,NIH,BETHESDA,MD 20892. NINCDS,LAB ADAPT SYST,NIH,BETHESDA,MD 20892. UNIV TORONTO,TORONTO,ON M6A 2E1,CANADA. RI McIntosh, Anthony/G-4955-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 60 EP 60 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300056 ER PT J AU Jacobsen, LK Giedd, JN Rajapakse, JC Hamburger, SD Vaituzis, AC Frazier, JA Lenane, MC Rapoport, JL AF Jacobsen, LK Giedd, JN Rajapakse, JC Hamburger, SD Vaituzis, AC Frazier, JA Lenane, MC Rapoport, JL TI The corpus callosum in childhood onset schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA. NIMH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. RI Giedd, Jay/A-3080-2008; Rajapakse, Jagath/B-8485-2008; Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015 OI Rajapakse, Jagath/0000-0001-7944-1658; Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 66 EP 66 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300062 ER PT J AU Kumra, S Jacobsen, LK Frazier, JA McKenna, K Gordon, CT Smith, AK Rapoport, JL AF Kumra, S Jacobsen, LK Frazier, JA McKenna, K Gordon, CT Smith, AK Rapoport, JL TI Clozapine treatment of childhood-onset schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,NIH,CHILD PSYCHIAT BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 106 EP 106 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300102 ER PT J AU Shoaf, SE Schmall, B AF Shoaf, SE Schmall, B TI Lumped constant for pharmacokinetic estimation of brain serotonin synthesis rates SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,BETHESDA,MD 20892. NIH,CTR CLIN,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 115 EP 115 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300111 ER PT J AU George, DT Ragan, PW Rawlings, R Umhau, J Phillips, M Shoaf, S Linnoila, M AF George, DT Ragan, PW Rawlings, R Umhau, J Phillips, M Shoaf, S Linnoila, M TI Cerebrospinal fluid 5-HIAA is low in perpetrators of domestic violence SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,NIH,DICBR,CLIN STUDIES LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 123 EP 123 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300119 ER PT J AU Williams, W Andreason, P Ruttimann, U Kerich, M Rio, D Rawlings, R Brown, G Hommer, D Linnoila, M AF Williams, W Andreason, P Ruttimann, U Kerich, M Rio, D Rawlings, R Brown, G Hommer, D Linnoila, M TI Brain glucose metabolic rates in alcoholic patients SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,NIH,DICBR,CLIN STUDIES LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 125 EP 125 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300121 ER PT J AU Hibbeln, JR Umhau, JC Salem, N Rawlings, R George, DT Linnoila, M AF Hibbeln, JR Umhau, JC Salem, N Rawlings, R George, DT Linnoila, M TI Plasma fatty acids predict CSF 5-HIAA and HVA in normals, early and late onset alcoholics SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,MEMBRANE BIOPHYS LAB,BETHESDA,MD 20892. NIAAA,BIOCHEM LAB,BETHESDA,MD 20892. NIAAA,CLIN STUDIES LAB,BETHESDA,MD 20892. NIAAA,DIV INTRAMURAL CLIN & BIOL RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 126 EP 126 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300122 ER PT J AU Feltner, DE Hermesz, E Grinberg, A Mahon, KA AF Feltner, DE Hermesz, E Grinberg, A Mahon, KA TI Targeted disruption of the mouse Rpx gene SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NICHHD,NIH,MAMMALIAN GENES & DEV LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 145 EP 145 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300141 ER PT J AU Heinz, A Knable, MB Pietzcker, A Schmidt, LG Weinberger, DR AF Heinz, A Knable, MB Pietzcker, A Schmidt, LG Weinberger, DR TI Positive symptoms in dopaminergic psychosis - Implications for the dopamine hypothesis of schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,NIH,CLIN BRAIN DISORDERS BRANCH,BETHESDA,MD 20892. FREE UNIV BERLIN,DEPT PSYCHIAT,W-1000 BERLIN,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 151 EP 151 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300147 ER PT J AU Waltrip, RW Torrey, EF King, LR Weinberger, DR Rickler, KC Rubin, SA Carbone, KM AF Waltrip, RW Torrey, EF King, LR Weinberger, DR Rickler, KC Rubin, SA Carbone, KM TI Schizophrenia, borna disease, and neurological signs in a monozygotic twin study cohort SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MARYLAND PSYCHIAT RES CTR,BALTIMORE,MD 21228. JOHNS HOPKINS UNIV,DEPT MED,VIRAL IMMUNOPATHOGENESIS LAB,BALTIMORE,MD 21218. NIMH,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 152 EP 152 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300148 ER PT J AU Daniel, DG Egan, M Hyde, T AF Daniel, DG Egan, M Hyde, T TI Probable neuroleptic induced tardive dyskinesia in association with combined fluoxetine and risperidone treatment SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 WASHINGTON CLIN RES CTR,FALLS CHURCH,VA 22044. NIMH,DIRP,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 182 EP 182 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300178 ER PT J AU Skolnick, P AF Skolnick, P TI Adaptation of NMDA receptors following antidepressant treatments SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIDDK,NIH,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 203 EP 203 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300195 ER PT J AU Goldman, D Nielsen, D Okada, M Adamson, M Lappalainen, J Malhotra, N Pesonen, U Koulu, M Eggert, M Virkkunen, M Ozaki, N Linnoila, M AF Goldman, D Nielsen, D Okada, M Adamson, M Lappalainen, J Malhotra, N Pesonen, U Koulu, M Eggert, M Virkkunen, M Ozaki, N Linnoila, M TI Molecular genetics of impaired impulse control and early onset alcoholism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,NEUROGENET LAB,ROCKVILLE,MD 20852. RI Nielsen, David/B-4655-2009 NR 0 TC 0 Z9 0 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 212 EP 212 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300204 ER PT J AU Higley, JD Mehlman, P Suomi, SJ Linnoila, M AF Higley, JD Mehlman, P Suomi, SJ Linnoila, M TI A nonhuman primate model of type II excessive alcohol consumption SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,CLIN STUDIES LAB,PRIMATE UNIT,NIH,ANIM CTR,POOLESVILLE,MD 20837. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 213 EP 213 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300205 ER PT J AU Altemus, M Paletzki, R Gerfen, CR Murphy, DL AF Altemus, M Paletzki, R Gerfen, CR Murphy, DL TI Differential activation of ZIF268 in the amygdala in response to MCPP SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN SCI LAB,BETHESDA,MD 20892. NIMH,NEUROPHYSIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 285 EP 285 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300277 ER PT J AU Malhotra, AK Pinals, DA Weisenfeld, N Pickar, D Breier, A AF Malhotra, AK Pinals, DA Weisenfeld, N Pickar, D Breier, A TI NMDA receptor function and schizophrenia: Studies with ketamine SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,EXPTL THERAPEUT BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 296 EP 296 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300288 ER PT J AU Butler, PD Printz, DJ DeSanti, L Issa, F Gorman, JM Carraway, RE AF Butler, PD Printz, DJ DeSanti, L Issa, F Gorman, JM Carraway, RE TI Neurotensin and metabolites in CSF of patients with schizophrenia and controls SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 DVAMC,PSYCHIAT SERV,NEW YORK,NY 10010. NEW YORK STATE PSYCHIAT INST & HOSP,DEPT CLIN PSYCHOBIOL,NEW YORK,NY 10032. NIMH,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA 01604. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 300 EP 300 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300292 ER PT J AU Mosnaim, AD Freitag, F Karoum, F Wolf, ME Diamond, S Salas, MA AF Mosnaim, AD Freitag, F Karoum, F Wolf, ME Diamond, S Salas, MA TI Migraine and the contents of tyramine and phenylethylamine in food SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV HLTH SCI CHICAGO MED SCH,N CHICAGO,IL 60064. N CHICAGO UAMO,DIAMOND HEADACHE CLIN,N CHICAGO,IL. ST ELIZABETH HOSP,NIMH,NPB,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 325 EP 325 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300317 ER PT J AU Frye, MA Mathe, AA Gary, KA George, MS CoraLocatelli, G Huggins, T Pazzaglia, PJ Callahan, AM Davis, C Marangell, L Rubinow, D Winokur, A Post, RM AF Frye, MA Mathe, AA Gary, KA George, MS CoraLocatelli, G Huggins, T Pazzaglia, PJ Callahan, AM Davis, C Marangell, L Rubinow, D Winokur, A Post, RM TI CSF neuropeptide dysregulation in patients with affective disorder SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BIOL PSYCHIAT BRANCH,BETHESDA,MD 20892. KAROLINSKA INST,STOCKHOLM,SWEDEN. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. MED UNIV S CAROLINA,CHARLESTON,SC 29425. UNIV MISSISSIPPI,SCH MED,JACKSON,MS. MT SINAI MED CTR,NEW YORK,NY 10029. VET ADM MED CTR,BRONX,NY 10468. BAYLOR COLL MED,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 327 EP 327 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300319 ER PT J AU Bigelow, LB Torrey, EF Kleinman, JE AF Bigelow, LB Torrey, EF Kleinman, JE TI Problems in post-mortem diagnosis can be solved SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CTR NEUROSCI,CLIN BRAIN DISORDERS BRANCH,WASHINGTON,DC 20032. NIMH,CTR NEUROSCI,STANLEY RES FDN,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 328 EP 328 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300320 ER PT J AU Elman, I Wiesenfeld, N Su, TP Malhotra, AK Pickar, D Breier, A AF Elman, I Wiesenfeld, N Su, TP Malhotra, AK Pickar, D Breier, A TI The effects of metabolic and cognitive stress on cerebral blood flow SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,NIH,EXPTL THERAPEUT BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 354 EP 354 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300346 ER PT J AU Wyatt, RJ AF Wyatt, RJ TI Early intervention in schizophrenia improves the long-term course of the illness SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,NIH,DIV INTRAMURAL RES,NEUROPSYCHIAT BRANCH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 384 EP 384 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300372 ER PT J AU Rubinow, DR Schmidt, PJ AF Rubinow, DR Schmidt, PJ TI Reproductive hormones and mood in women SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 386 EP 386 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300374 ER PT J AU Baumann, MH Rothman, RB AF Baumann, MH Rothman, RB TI Withdrawal from chronic cocaine in rats: A model of depression SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIDA,CLIN PSYCHOPHARMACOL SECT,NIH,IRP,BALTIMORE,MD 21224. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 399 EP 399 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300386 ER PT J AU Ragan, PW George, DT Shoaf, S Eckardt, M Linnoila, M AF Ragan, PW George, DT Shoaf, S Eckardt, M Linnoila, M TI CSF monoamine metabolites in alcoholics with and without nicotine addiction SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA,CLIN STUDIES LAB,DICBR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 437 EP 437 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300422 ER PT J AU Bachus, SE Hyde, TM Herman, MM Kleinman, JE AF Bachus, SE Hyde, TM Herman, MM Kleinman, JE TI Elevated cholecystokinin mRNA in dorsolateral prefrontal cortex in suicides SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN BRAIN DISORDERS BRANCH,NEUROSCI CTR ST ELIZABETHS,WASHINGTON,DC 20032. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 447 EP 447 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300432 ER PT J AU Bertolino, A Callicott, JH Elman, I Duyn, JH Tedeschi, G Frank, JA Pickar, D Weinberger, DR AF Bertolino, A Callicott, JH Elman, I Duyn, JH Tedeschi, G Frank, JA Pickar, D Weinberger, DR TI Proton magnetic resonance spectroscopic imaging in drug free patients with schizophrenia: Regional neuronal damage SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN BRAIN DISORDERS BRANCH,NIH,BETHESDA,MD 20892. RI Duyn, Jozef/F-2483-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 460 EP 460 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300445 ER PT J AU Bertolino, A Callicott, JH Nawroz, S Knable, MB Mattay, VS Duyn, JH Tedeschi, G Frank, JA Weinberger, DR AF Bertolino, A Callicott, JH Nawroz, S Knable, MB Mattay, VS Duyn, JH Tedeschi, G Frank, JA Weinberger, DR TI Reproducibility of proton magnetic resonance spectroscopic imaging in patients with schizophrenia and normal controls SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN BRAIN DISORDERS BRANCH,NIH,BETHESDA,MD 20892. RI Duyn, Jozef/F-2483-2010 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 461 EP 461 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300446 ER PT J AU Bertolino, A Saunders, RC Frank, JA Weinberger, DR AF Bertolino, A Saunders, RC Frank, JA Weinberger, DR TI Proton magnetic resonance spectroscopic imaging in a monkey model of schizophrenia: Preliminary results SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN BRAIN DISORDERS BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 463 EP 463 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300448 ER PT J AU Callicott, JH Tallent, K Bertolino, A Ramsey, N Santha, A Knable, M Coppola, R Goldberg, T Mattay, V vanGelderen, P Frank, JA Moonen, CTW Weinberger, DR AF Callicott, JH Tallent, K Bertolino, A Ramsey, N Santha, A Knable, M Coppola, R Goldberg, T Mattay, V vanGelderen, P Frank, JA Moonen, CTW Weinberger, DR TI 3-D fMRI of working memory in schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,CLIN BRAIN DISORDERS BRANCH,IRP,WASHINGTON,DC 20032. NIH,INVIVO NMR CTR,BETHESDA,MD 20892. NIH,LAB DIAGNOST RADIOL RES,BETHESDA,MD 20892. RI Moonen, Chrit/K-4434-2016 OI Moonen, Chrit/0000-0001-5593-3121 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 466 EP 466 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300451 ER PT J AU Elman, I Bir, C Pickar, D Breier, A AF Elman, I Bir, C Pickar, D Breier, A TI Neuroendocrinological impacts of glucoprivic stress SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,EXPTL THERAPEUT BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 494 EP 494 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300479 ER PT J AU Roca, CA Rosenstein, DL Schmidt, PJ Danaceau, MA Greenberg, B Murphy, DL Rubinow, DR AF Roca, CA Rosenstein, DL Schmidt, PJ Danaceau, MA Greenberg, B Murphy, DL Rubinow, DR TI Mechanism of efficacy of fluoxetine in premenstrual syndrome SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 497 EP 497 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300482 ER PT J AU Bloch, M Schmidt, PJ Su, TP Tobin, MB Rubinow, DR AF Bloch, M Schmidt, PJ Su, TP Tobin, MB Rubinow, DR TI ACTH & beta-endorphin over the menstrual cycle in women with PMS & controls SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIMH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 506 EP 506 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300491 ER PT J AU Pietrini, P Dani, A Furey, ML Freo, U Horwitz, B Mentis, M Alexander, GE Grady, C Schapiro, MB Rapoport, SI AF Pietrini, P Dani, A Furey, ML Freo, U Horwitz, B Mentis, M Alexander, GE Grady, C Schapiro, MB Rapoport, SI TI Brain stimulation reverses cerebral metabolic reductions in Alzheimer disease SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 544 EP 544 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300529 ER PT J AU Mentis, MJ Horwitz, B Grady, C Alexander, GE Furey, ML Schapiro, MB Rapoport, SI AF Mentis, MJ Horwitz, B Grady, C Alexander, GE Furey, ML Schapiro, MB Rapoport, SI TI Visual processing is abnormal in striate and association areas in Alzheimer's disease SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 549 EP 549 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300534 ER PT J AU Shingarova, LN Sagaidak, LN Turetskaya, RL Nedospasov, SA Esipov, DS Korobko, VG AF Shingarova, LN Sagaidak, LN Turetskaya, RL Nedospasov, SA Esipov, DS Korobko, VG TI Mutants of human tumor necrosis factor: Preparation and properties SO BIOORGANICHESKAYA KHIMIYA LA Russian DT Article DE human tumor necrosis factor (TNF-alpha); mutants; polymerase chain reaction; expression in E-coli ID FACTOR-ALPHA; TNF RECEPTORS; MOLECULAR-CLONING; HUMAN LYMPHOTOXIN; EXPRESSION; BETA; ACTIVATION; PROTEINS; INVITRO; FAMILY AB Using polymerase chain reaction, a number of mutant genes encoding human tumor necrosis factor (TNF-alpha) with amino acid substitutions and a deletion were obtained. The mutant proteins (muteins) contained point mutations R32H, A33S, F144L, I118M, and I118A; double mutation R32H-F144L; and deletion of four amino acid residues 67-70. The mutant genes were expressed in E. coli under the control of constitutive promoters. A simple purification method for the muteins was developed and their physicochemical properties were studied. All the muteins obtained, except F144L and I118A, were shown by CD and cross-linking to form a spatial structure similar to that of the native TNF-alpha. The collection of muteins was characterized by their biological activity. Mutants R32H and A33S exerted a decreased cytotoxicity against murine fibroblast cell line L929, whereas point mutant F144L and double mutant R32H-F144L were essentially inactive. C1 RUSSIAN ACAD SCI,SHEMYAKIN OVCHINNIKOV INST BIOORGAN CHEM,MOSCOW 117871,RUSSIA. NCI,FREDERICK,MD 21701. VA ENGELHARDT MOLEC BIOL INST,MOSCOW 117984,RUSSIA. RI Nedospasov, Sergei/J-5936-2013; Esipov, Dmitriy/J-9434-2012; Nedospasov, Sergei/L-1990-2015; Nedospasov, Sergei/Q-7319-2016 OI Esipov, Dmitriy/0000-0003-3973-0898; NR 36 TC 15 Z9 20 U1 0 U2 1 PU MEZHDUNARODNAYA KNIGA PI MOSCOW PA 39 DIMITROVA UL., 113095 MOSCOW, RUSSIA SN 0132-3423 J9 BIOORG KHIM+ JI Bioorg. Khim. PD APR PY 1996 VL 22 IS 4 BP 243 EP 251 PG 9 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA UV957 UT WOS:A1996UV95700001 PM 8768260 ER PT J AU Wilbur, WJ Major, F Spouge, J Bryant, S AF Wilbur, WJ Major, F Spouge, J Bryant, S TI The statistics of unique native states for random peptides SO BIOPOLYMERS LA English DT Article ID PROTEIN; CONFORMATIONS; SEQUENCES AB Given a probability distribution from which the energy spectrum of a random peptide is to be sampled, we derive a general expression for the probability that such a peptide will fold to a unique native state and for the probability distribution of the native energy. This latter results allows us to localize the energy of folding based on the model parameters and is one advantage of our formulation. Evidence from both the lattice theory of proteins and protein threading experiments suggest that the energy spectrum for the compact states of a peptide chain is Gaussian in form. For this reason we have derived from the more general framework the specific formulas that apply in the Gaussian case, where one requires only the number of states and the variance of the Gaussian distribution in order to apply the theory. This simplicity allows us to perform calculations that we compare with calculations previously made by others based on statistical thermodynamics. We find qualitative agreement, but a significant correction to prior estimates of folding probability derived from the Gaussian assumption is necessary. (C) 1996 John Wiley & Sons, Inc. RP Wilbur, WJ (reprint author), NIH,NATL CTR BIOTECHNOL INFORMAT,NATL LIB MED,BLDG 38A,RM 8S806,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 21 TC 4 Z9 4 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PD APR PY 1996 VL 38 IS 4 BP 447 EP 459 DI 10.1002/(SICI)1097-0282(199604)38:4<447::AID-BIP2>3.3.CO;2-Y PG 13 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA UA092 UT WOS:A1996UA09200003 PM 8867208 ER PT J AU BakerCairns, B Meyers, K Hamilton, R Smith, C Tornatore, C AF BakerCairns, B Meyers, K Hamilton, R Smith, C Tornatore, C TI Immunohistochemical staining of fixed tissue using antigen retrieval and a thermal cycler SO BIOTECHNIQUES LA English DT Article ID PARAFFIN SECTIONS; CELLS AB The use of monoclonal antibodies to identify antigens in perfused fixed tissue is currently very challenging, Recently, many antigen retrieval methods have been described that require heating the tissue on slides using a microwave oven. Here, we describe a protocol for antigen retrieval that uses a commercially available solution called Citra and a DNA thermal cycler to heat the tissue sections. This method (i) allows for precise control of the temperature and time (unlike the microwave oven), (ii) uses very small quantities of the antigen retrieval solution, (iii) stains either free-floating sections or sections mounted on slides and (iv) achieves uniform staining throughout the tissue. In the paraformaldehyde-perfused fired rat cerebellum, the monoclonal antibody glial fibrillary acidic protein conveys the clarity of the Bergmann and stellate glia in the strata. Scanning confocal images through the center of the tissue demonstrates the depth of antibody penetration achieved using this method. Finally, using a monoclonal antibody against the simian virus 40 (SV40) T antigen allowed positive, unequivocal identification of a grafted cell fine, immortalized using SV40 T protein, thus demonstrating the true value of this method in an experimental paradigm. C1 NINCDS,NIH,LAB MOL MED & NEUROSCI,MOL THERAPEUT SECT,BETHESDA,MD 20892. NR 13 TC 3 Z9 3 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD APR PY 1996 VL 20 IS 4 BP 641 EP & PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UD717 UT WOS:A1996UD71700020 PM 8800684 ER PT J AU Schwarzenberger, P Spence, S Lohrey, N Kmiecik, T Longo, DL Murphy, WJ Ruscetti, FW Keller, JR AF Schwarzenberger, P Spence, S Lohrey, N Kmiecik, T Longo, DL Murphy, WJ Ruscetti, FW Keller, JR TI Gene transfer of multidrug resistance into a factor-dependent human hematopoietic progenitor cell line: In vivo model for genetically transferred chemoprotection SO BLOOD LA English DT Article ID BONE-MARROW CELLS; HUMAN MDR1; TRANSGENIC MICE; DRUG-RESISTANCE; EXPRESSION; AGENTS; CDNA AB To develop a rapid preclinical in vivo model to study gene transfer into human hematopoietic progenitor cells, MO-7e cells (CD-34(+), c-kit(+)) were infected with multidrug resistance (MDR1)-containing retroviruses and then transplanted into nonobese diabetic severe combined immunodeficient mice (NOD SCID), MO-7e cells infected with a retrovirus encoding the human MDR1 cDNA showed integration, transcription, and expression of the transfered MDR1 gene. This resulted in a 20-fold increase in the resistance of MO-7e cells to paclitaxel in vitro. The expression of the MDR1 gene product was stable over a 6-month period in vitro without selection in colchicine, MO-7e and MDR1-infected MO-7e cells were transplanted into NOD SCID mice to determine whether MDR1 could confer drug resistance in vivo. A sensitive polymerase chain reaction method specific for human sequences was developed to quantitate the level of human cell engraftment in NOD SCID bone marrow (BM) cells. The percentage of human DNA in BM cells from MO-7e-transplanted mice was 10.9% and decreased to 0.7% in mice treated with paclitaxel, The percentage of human DNA in infected-MO-7e transplanted mice was 7.6% and that level was unchanged in mice treated with paclitaxel. These results show that expression of the MDR1 gene in human hematopoietic progenitor cells can confer functional drug resistance in an in vivo model. (C) 1996 by The American Society of Hematology. C1 NCI,BIOL CARCINOGENESIS & DEV PROGRAM,SAIC,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NCI,LAB LEUKOCYTE BIOL,BIOL RESPONSE MODIFIERS PROGRAM,DIV CANC TREATMENT,FREDERICK,MD 21701. FU NCI NIH HHS [N01-CO-56000] NR 22 TC 17 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 APR 1 PY 1996 VL 87 IS 7 BP 2723 EP 2731 PG 9 WC Hematology SC Hematology GA UC776 UT WOS:A1996UC77600013 PM 8639888 ER PT J AU Kwak, LW Pennington, R Longo, DL AF Kwak, LW Pennington, R Longo, DL TI Active immunization of murine allogeneic bone marrow transplant donors with B-cell tumor-derived idiotype: A strategy for enhancing the specific antitumor effect of marrow grafts SO BLOOD LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; CHRONIC MYELOGENOUS LEUKEMIA; MULTIPLE-MYELOMA; HOST-DISEASE; T-CELLS; LYMPHOMA; IMMUNOTHERAPY; INDUCTION; IMMUNITY; ANTIGEN AB Persistence of the underlying malignancy remains the major obstacle limiting the success of high-dose chemoradiotherapy with allogeneic bone marrow transplantation (BMT) for lymphomas and multiple myeloma, We used the C3H 38C13 murine B-cell lymphoma, which expresses and secretes clonally derived Ig, the idiotype of which can serve as a tumor-specific antigen, to test the principle of transfer of tumor idiotype-specific immunity with BM. BALB/c marrow donors were twice immunized with 38C13-derived Ig, or with an isotype-matched control Ig, conjugated to keyhole limpet hemocyanin. Lethally irradiated C3H recipients reconstituted with marrow from idiotype immune, but not nonspecifically immune, donors demonstrated protection against subsequent lethal tumor challenge. The immunoprotective effect of immune allogeneic marrow was abrogated by T-cell depletion of the marrow graft before infusion, Low levels of serum anti-idiotypic antibody remained unaltered in recipients of T-cell-depleted immune marrow, consistent with a primary role for T-cell immunity in the cellular mechanism of this phenomenon. A modest therapeutic effect of immune allogeneic marrow was observed against 10 day, 1 cm established subcutaneous tumors, but only in combination with a booster immunization of the recipient post-BMT. These results provide the rationale for a novel strategy for enhancing the specific antitumor effect of allogeneic marrow grafts. C1 SAIC FREDERICK,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. RP Kwak, LW (reprint author), NCI,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK CANC RES & DEV CTR,DIV CLIN SCI,BLDG 567,ROOM 205,FREDERICK,MD 21702, USA. NR 36 TC 33 Z9 34 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1996 VL 87 IS 7 BP 3053 EP 3060 PG 8 WC Hematology SC Hematology GA UC776 UT WOS:A1996UC77600054 PM 8639929 ER PT J AU Pines, M Fukayama, S Costas, K Meurer, E Goldsmith, PK Xu, X Muallem, S Behar, V Chorev, M Rosenblatt, M Tashjian, AH Suva, LJ AF Pines, M Fukayama, S Costas, K Meurer, E Goldsmith, PK Xu, X Muallem, S Behar, V Chorev, M Rosenblatt, M Tashjian, AH Suva, LJ TI Inositol 1-,4-,5-trisphosphate-dependent Ca2+ signaling by the recombinant human PTH/PTHrP receptor stably expressed in a human kidney cell line SO BONE LA English DT Article DE PTH/PTHrP receptor; hormone; intracellular calcium; signal transduction ID OSTEO-SARCOMA CELLS; THYROTROPIN-RELEASING-HORMONE; ALKALINE-PHOSPHATASE ACTIVITY; CYTOSOLIC FREE CALCIUM; PROTEIN KINASE-C; PARATHYROID-HORMONE; OSTEOSARCOMA CELLS; BINDING PROTEINS; UMR-106-01 CELLS; PERTUSSIS TOXIN AB We previously reported the preparation and partial characterization of a series of human embryonic kidney cell lines (HEK-293) stably expressing various numbers of the recombinant human (h) parathyroid hormone (PTH)/PTH-related protein (PTHrP) receptor (Rc), Using this expression system we examined ligand (PTH or PTHrP) binding characteristics and cyclic AMP responsiveness, We have now extended these studies to investigate the calcium signal transduction pathways activated by the hPTH/PTHrP Rc. In parental HEK-293 cells, which lack endogenous PTH/PTHrP Rc, incubation with hPTH(1-34) had no effect on cytosolic free Ca2+ concentration [Ca2+](i). In HEK-293 clone C-21, stably expressing similar to 400,000 Rc/cell, PTH stimulated an increase in [Ca2+](i) by Ca2+ release from intracellular stores; PTH released Ca2+ exclusively from the IP3 sensitive Ca2+ pool, Unlike previous studies, the ability of PTH to elicit both cAMP responses and [Ca2+](i) transients occurred over a wide range of Rc numbers (between 400,000 and 3000 Rc/cell); both responses were always observed at PTH concentrations in the same dose range although the magnitude of the responses decrease with Rc number, Pretreatment of C-21 cells with pertussis toxin for 24 h, which significantly enhanced PTH-stimulated cAMP accumulation, did not modulate PTH-stimulated [Ca2+](i) transients, At each PTH concentration tested which resulted in increased cAMP levels, there was also an increase in [Ca2+](i) transients. Treatment of C-21 cells with a battery of midregion and C-terminal PTH or PTHrP peptides showed no effect on either [Ca2+](i) transients or cAMP accumulation, indicating a lack of functional interactions between these peptides and the form of the hPTH/PTHrP Rc stably expressed in these cells, Immunological analysis of G-protein expression demonstrated the presence of G(s), G(i), and G(q) in all parental and transfected cell lines examined, Taken together, these data demonstrate that the hPTH/PTHrP Rc, stably expressed in HEK-293 cells, elicits responses in both the cAMP and IP3-dependent [Ca2+](i) pathways and is responsive only to N-terminal PTH/PTHrP peptides. C1 BETH ISRAEL HOSP,HARVARD THORNDIKE LAB,DIV BONE & MINERAL METAB,DEPT MED,BOSTON,MA 02215. BETH ISRAEL HOSP,CHARLES A DANA LABS,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH PUBL HLTH,DEPT MOLEC & CELLULAR TOXICOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NIDDKD,METAB DIS BRANCH,BETHESDA,MD 20892. UNIV TEXAS,SW MED CTR,DEPT PHYSIOL,DALLAS,TX 75235. FU NIDDK NIH HHS [DK47940, DK46655] NR 61 TC 51 Z9 51 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 8756-3282 J9 BONE JI Bone PD APR PY 1996 VL 18 IS 4 BP 381 EP 389 DI 10.1016/8756-3282(96)00008-7 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UG174 UT WOS:A1996UG17400015 PM 8726398 ER PT J AU Schmidt, EM Bak, MJ Hambrecht, FT Kufta, CV ORourke, DK Vallabhanath, P AF Schmidt, EM Bak, MJ Hambrecht, FT Kufta, CV ORourke, DK Vallabhanath, P TI Feasibility of a visual prosthesis for the blind based on intracortical microstimulation of the visual cortex SO BRAIN LA English DT Article DE human; electrical stimulation; visual cortex ID HUMAN OCCIPITAL CORTEX; ELECTRICAL-STIMULATION; VISION AB The feasibility of producing a visual prosthesis for the blind using intracortical microstimulation (ICMS) of the visual cortex was studied in a 42-year-old woman who had been totally blind for 22 years secondary to glaucoma. Thirty-eight microelectrodes were implanted in the right visual cortex, near the occipital pole, for a period of 4 months. Percepts reported as small spots of light, called phosphenes, were produced with 34 of the 38 implanted microelectrodes. Threshold currents for phosphene generation with trains of biphasic pulses were as low as 1.9 mu A, and most of the microelectrodes had thresholds below 25 mu A. Phosphene brightness could be modified with stimulus amplitude, frequency and pulse duration. Repeated stimulation over a period of minutes produced a gradual decrease in phosphene brightness. Phosphenes did not flicker. The apparent size of phosphenes ranged from a 'pin-point' to a 'nickel' (20 mm diameter coin) held at arm's length. Phosphene size usually decreased as stimulation current was increased but increased slightly as the train length (TL) was increased. At levels of stimulation near threshold, the phosphenes were often reported to have colours. As the stimulation level was increased, the phosphenes generally became white, greyish or yellowish. Individual phosphenes appeared at different distances from the subject. When two phosphenes were simultaneously generated, the apparent distances of the individual phosphenes sometimes changed to make them appear to be at about the same distance. When three or more phosphenes were simultaneously generated, they became coplanar Except for rave occasions, phosphenes extinguished rapidly at the termination of the stimulation train. When stimulation TLs were increased beyond 1 s, phosphenes usually disappeared before the end of the train. The duration of phosphene perception could be increased by interrupting a long stimulation train with brief pauses in stimulation. Intracortical microelectrodes spaced 500 mu m apart generated separate phosphenes, but microelectrodes spaced 250 mu m typically did not. This two-point resolution was about Jive times closer than has typically been achieved with surface stimulation. With some individual microelectrodes, a second closely spaced phosphene was sometimes produced by increasing the stimulation current Phosphenes moved with eye movements. When up to six phosphenes were simultaneously elicited, they all moved with the same relative orientation during eye movements. All phosphenes were located in the left hemi-field with the majority above the horizontal meridian There was a clustering of most of the phosphenes within a relatively small area of visual space. The potentially greater microelectrode density and lower power requirements of ICMS compared with surface stimulation appears encouraging for a visual prosthesis. However, further studies with blind subjects are required to optimize stimulation parameters and test complex image recognition before the feasibility of a visual prosthesis based on ICMS can be established. C1 NINCDS,NEURAL PROSTHESIS PROGRAM,NIH,BETHESDA,MD 20892. NINCDS,SURG NEUROL BRANCH,NIH,BETHESDA,MD 20892. HOWARD HUGHES MED INST,BETHESDA,MD 20817. RP Schmidt, EM (reprint author), NINCDS,NEURAL CONTROL LAB,NIH,BLDG 49,ROOM 3A50,BETHESDA,MD 20892, USA. NR 21 TC 335 Z9 350 U1 0 U2 23 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0006-8950 J9 BRAIN JI Brain PD APR PY 1996 VL 119 BP 507 EP 522 DI 10.1093/brain/119.2.507 PN 2 PG 16 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA UN423 UT WOS:A1996UN42300015 PM 8800945 ER PT J AU Berardelli, A Hallett, M Rothwell, JC Agostino, R Manfredi, M Thompson, PD Marsden, CD AF Berardelli, A Hallett, M Rothwell, JC Agostino, R Manfredi, M Thompson, PD Marsden, CD TI Single-joint rapid arm movements in normal subjects and in patients with motor disorders SO BRAIN LA English DT Review DE rapid movements; arm; normal subjects; motor disorders ID ELBOW FLEXION MOVEMENTS; STEREOTYPED VOLUNTARY MOVEMENTS; ANTAGONIST MUSCLE-ACTIVITY; AGONIST EMG BURST; PARKINSONS-DISEASE; ORGANIZING PRINCIPLES; POSTURAL ADJUSTMENTS; ABDUCTION MOVEMENTS; HUNTINGTONS-DISEASE; BALLISTIC MOVEMENT AB In normal subjects the execution of single rapid one-joint movements is characterized by an electromyographic (EMG) pattern composed of three discrete bursts of activity: two bursts (first and second agonist bursts, or AG1 and AG2) are present in the agonist muscle separated by an almost complete period of electrical silence. During this pause, another burst (antagonist burst or ANT) occurs in the antagonist muscle. If a rapid movement is executed during tonic activation of the agonist muscle, tonic activity is inhibited just prior to AG1 onset (agonist inhibition). Similarly, if the movement is performed during tonic activation of the antagonist muscle, such activity is also inhibited prior to AG1 onset (antagonist inhibition). Antagonist inhibition also starts prior to AG1 onset and lasts until ANT onset. A general descriptor of the kinematic features related to the EMG pattern described above is a symmetrical and unimodal velocity profile that is bell-shaped and shows an acceleration time roughly equal to the deceleration time. This holds true for movements performed under low accuracy constraints; as accuracy demands become stricter and stricter the peak velocity decreases but as long as the movement is made with one continuous trajectory the velocity profile remains roughly symmetrical. In general terms, the function of AG1 is to provide the impulsive force to start the movement; the function of ANT is to halt the movement at the desired end-point; and the function of AG2 is to dampen out the oscillations which might occur at the end of the movement. The timing and size of the bursts vary according to the speed and amplitude of the movement. The origin of the EMG pattern is a central programme, but afferent inputs can modulate the voluntary activity. In this paper we also review the EMG and kinematic abnormalities that are present during the execution of single-joint, rapid arm movements in patients with Parkinson's disease, Huntington's disease, Sydenham's chorea, dystonia, athetosis, cerebellar deficits, upper motor neuron syndrome, essential tremor and large-fibre sensory neuropathy. The data from these studies lead us to the following conclusions: (i) the basal ganglia have a role in scaling the size of AG1, reinforcing the voluntary command and inhibiting inappropriate EMG activity; (ii) the cerebellum has a role in timing the voluntary bursts and probably in implementing muscle force phasically; (iii) the corticospinal tract has a role in determining spatial and temporal recruitment of motor units; (iv) proprioceptive feedback is not necessary reproduce the triphasic pattern but it contributes to the accuracy of both the trajectory and the end-point of rapid movements. C1 NATL INST HLTH, BETHESDA, MD USA. UCL NATL HOSP NEUROL & NEUROSURG, DEPT NEUROL, LONDON WC1N 3BG, ENGLAND. UNIV ADELAIDE, DEPT MED, ADELAIDE, SA 5001, AUSTRALIA. RP Berardelli, A (reprint author), UNIV ROMA LA SAPIENZA, DIPARTIMENTO SCI NEUROL, VIALE UNIV 30, I-00185 ROME, ITALY. OI Rothwell, John/0000-0003-1367-6467 NR 76 TC 152 Z9 152 U1 2 U2 13 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD APR PY 1996 VL 119 BP 661 EP 674 DI 10.1093/brain/119.2.661 PN 2 PG 14 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA UN423 UT WOS:A1996UN42300025 PM 8800955 ER PT J AU Brown, P Tateishi, J Budka, H AF Brown, P Tateishi, J Budka, H TI Inactivation of the causal agents of Creutzfeldt-Jakob disease and other human prion diseases - Reply SO BRAIN PATHOLOGY LA English DT Letter C1 KYUSHU UNIV,INST NEUROL,FUKUOKA 812,JAPAN. UNIV VIENNA,INST NEUROL,VIENNA,AUSTRIA. RP Brown, P (reprint author), NINCDS,CNS STUDIES LAB,NIH,BLDG 36,RM 4D04,BETHESDA,MD 20892, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU INT SOC NEUROPATHOLOGY PI ZURICH PA ISN JOURNAL PO BOX, CH-8033 ZURICH, SWITZERLAND SN 1015-6305 J9 BRAIN PATHOL JI Brain Pathol. PD APR PY 1996 VL 6 IS 2 BP 198 EP 198 DI 10.1111/j.1750-3639.1996.tb00801.x PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA UF671 UT WOS:A1996UF67100015 ER PT J AU Hirata, H Ladenheim, B Carlson, E Epstein, C Cadet, JL AF Hirata, H Ladenheim, B Carlson, E Epstein, C Cadet, JL TI Autoradiographic evidence for methamphetamine-induced striatal dopaminergic loss in mouse brain: Attenuation in CuZn-superoxide dismutase transgenic mice SO BRAIN RESEARCH LA English DT Article DE methamphetamine; transgenic mouse; superoxide dismutase; superoxide radical; dopamine uptake site; striatum; gender ID PARKINSONS-DISEASE; CAUDATE-NUCLEUS; NITRIC-OXIDE; RAT-BRAIN; AMPHETAMINE; NEUROTOXICITY; 6-HYDROXYDOPAMINE; GLUTAMATE; TOXICITY; RELEASE AB Methamphetamine (METH) has long-lasting neurotoxic effects on the nigrostriatal dopamine (DA) system of rodents. METH-induced neurotoxicity is thought to involve release of DA in presynaptic DA terminals, which is associated with increased formation of oxygen-based free radicals. We have recently shown that METH-induced striatal DA depletion is attenuated in transgenic (Tg) mice that express the human CuZn-superoxide dismutase (SOD) enzyme. That study did not specifically address the issue of loss of DA terminals. In the present study, we have used receptor autoradiographic studies of [I-125]RTI-121-labeled DA uptake sites to evaluate the effects of several doses of METH on striatal DA terminals of Non-Tg as well as of heterozygous and homozygous SOD-Tg mice. In Non-Tg mice, METH caused decreases in striatal DA uptake sites in a dose-dependent fashion. The loss of DA terminals was more prominent in the lateral region than in the medial subdivisions of the striatum. In SOD-Tg mice, the loss of DA terminals caused by METH was attenuated in a gene dosage-dependent fashion, with the homozygous mice showing the greatest protection. Female mice were somewhat more resistant than male mice against these deleterious effects of METH. These results provide further evidence for a role of superoxide radicals in the long-term effects of METH. They also suggest the notion of a gender-specific handling of oxidative stress. C1 NIDA,MOLEC NEUROPSYCHIAT SECT,NIH,DIV INTRAMURAL RES,BALTIMORE,MD 21224. UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. FU NIA NIH HHS [AG-08938] NR 43 TC 91 Z9 92 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD APR 1 PY 1996 VL 714 IS 1-2 BP 95 EP 103 DI 10.1016/0006-8993(95)01502-7 PG 9 WC Neurosciences SC Neurosciences & Neurology GA UF668 UT WOS:A1996UF66800011 PM 8861613 ER PT J AU Melbye, M Cote, TR West, D Kessler, L Biggar, RJ Lemp, G Singleton, J Young, J Kerndt, P Deapen, D Ginzberg, M AntonCulver, H Lieb, S Hopkins, R Williams, B Liff, J Morgan, D Parkin, W AF Melbye, M Cote, TR West, D Kessler, L Biggar, RJ Lemp, G Singleton, J Young, J Kerndt, P Deapen, D Ginzberg, M AntonCulver, H Lieb, S Hopkins, R Williams, B Liff, J Morgan, D Parkin, W TI Nasopharyngeal carcinoma: An EBV-associated tumour not significantly influenced by HIV-induced immunosuppression SO BRITISH JOURNAL OF CANCER LA English DT Article DE human immunodeficiency virus; immunosuppression; nasopharyngeal carcinoma; Epstein-Barr virus; registry linkage ID RENAL-TRANSPLANT RECIPIENTS; HODGKINS-DISEASE; KAPOSIS-SARCOMA; CANCER; RISK AB We used a link between cancer (859 398 reports) and AIDS (50 050 reports) registries in the United States to study whether nasopharyngeal carcinoma (NPC) was increased in the population with AIDS. There was no indication of a significantly increased risk up to or after the AIDS diagnosis, which argues against progressively failing immunity being important in the development of this malignancy. C1 NCI,DIV CANC ETIOL,VIRAL EPIDEMIOL BRANCH,ROCKVILLE,MD 20852. SAN FRANCISCO CANC REGISTRY,SAN FRANCISCO,CA. NCI,DIV CANC PREVENT & CONTROL,APPL RES BRANCH,ROCKVILLE,MD 20852. RP Melbye, M (reprint author), STATENS SERUM INST,DANISH EPIDEMIOL SCI CTR,COPENHAGEN,DENMARK. NR 17 TC 9 Z9 9 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD APR PY 1996 VL 73 IS 8 BP 995 EP 997 DI 10.1038/bjc.1996.194 PG 3 WC Oncology SC Oncology GA UE606 UT WOS:A1996UE60600019 PM 8611438 ER PT J AU Mellemkjaer, L Gridley, G Moller, H Hsing, AW Linet, MS Brinton, LA Olsen, JH AF Mellemkjaer, L Gridley, G Moller, H Hsing, AW Linet, MS Brinton, LA Olsen, JH TI Pernicious anaemia and cancer risk in Denmark SO BRITISH JOURNAL OF CANCER LA English DT Article DE pernicious anaemia; cancer risk; cohort study ID ANEMIA AB A cohort of 5072 patients with pernicious anaemia was identified in the Danish Hospital Discharge Register from 1977 to 1989 and, through linkage to the Danish Cancer Registry, the occurrence of cancer in the cohort was determined up to 1991. Observed numbers of cancer cases during 1-15 years of follow-up were compared with expected numbers based on national incidence rates. Besides the well-established increased risk for stomach cancer, the analysis also revealed a 2-fold increase in the relative risk for cancer of the buccal cavity and pharynx among pernicious anaemia patients in accordance with previous studies; previously reported elevated risks for other digestive tract cancers were not confirmed. There was a non-significantly increased risk for lymphatic and haematological malignancy but the risk tended to disappear after 5 years of follow-up, indicating a possible selection bias. Decreased risks for cervical cancer and non-melanoma skin cancer were also seen. C1 NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. CTR RES HLTH & SOCIAL STAT,DK-2100 COPENHAGEN O,DENMARK. RP Mellemkjaer, L (reprint author), DANISH CANC SOC,DIV CANC EPIDEMIOL,STRANDBLVD 49,DK-2100 COPENHAGEN O,DENMARK. RI Brinton, Louise/G-7486-2015; OI Brinton, Louise/0000-0003-3853-8562; Moller, Henrik/0000-0001-8200-5929 FU NCI NIH HHS [N01-CP-85639-04] NR 11 TC 20 Z9 20 U1 1 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD APR PY 1996 VL 73 IS 8 BP 998 EP 1000 DI 10.1038/bjc.1996.195 PG 3 WC Oncology SC Oncology GA UE606 UT WOS:A1996UE60600020 PM 8611439 ER PT J AU Coceani, F Kelsey, L Seidlitz, E Korzekwa, Z AF Coceani, F Kelsey, L Seidlitz, E Korzekwa, Z TI Inhibition of the contraction of the ductus arteriosus to oxygen by 1-aminobenzotriazole, a mechanism-based inactivator of cytochrome P450 SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE foetus ductus arteriosus closure; oxygen; cytochrome P450; endothelin-1; 1-aminobenzotriazole ID PROSTAGLANDIN-E2; EXPRESSION; TENSION; METABOLISM; CLOSURE; CELLS AB 1 We have proposed that contractile tension of the ductus arteriosus is sustained by a cytochrome P450-linked mechanism acting as a limiting step in the synthesis of endothelin-1 (ET-1). In the present study, we have used the isolated ductus from near-term foetal lambs and guinea-pigs to investigate the effect on both muscle tone and ET-1 formation of 1-aminobenzotriazole (ABT), a suicide substrate for mono-oxygenase reactions. 2 ABT relaxed the lamb ductus at rest (2.5% O-2) and during the oxygen contraction (ii to 95% O-2) The effect was seen at 40 mu M, and at 0.8 mM active tone was almost completely abolished. ABT (1 mM) also reversed the oxygen contraction in the guinea-pig ductus. 3 In the lamb ductus, the ABT response was not affected by removal of the endothelium or by treatment with 2.8 mu M indomethacin (al 2.5% O-2) and the ensuing contraction. 4 At both low and high concentration, ABT relaxed marginally, or not at all, the potassium-contracted (55 mM) ductus from either species. 5 ET-1 release from either the intact or endothelium-denuded lamb ductus tended to decrease in the presence of ABT (1 mM), whilst during the same treatment cyclic GMP content of the tissue remained unchanged. 6 We conclude that ABT relaxation is due to suppression of a contractile mechanism and not to activation of prostaglandin- and NO-mediated relaxing mechanisms. This contractile mechanism has a cytochrome P450-based mono-oxygenase reaction as a key component. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. RP Coceani, F (reprint author), HOSP SICK CHILDREN,RES INST,555 UNIV AVE,TORONTO,ON M5G 1X8,CANADA. RI Seidlitz, Eric/K-6765-2013 OI Seidlitz, Eric/0000-0001-9760-1133 NR 40 TC 22 Z9 26 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD APR PY 1996 VL 117 IS 7 BP 1586 EP 1592 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UF138 UT WOS:A1996UF13800033 PM 8730758 ER PT J AU Jordan, NJ Watson, ML Williams, RJ Roach, AG Yoshimura, T Westwick, J AF Jordan, NJ Watson, ML Williams, RJ Roach, AG Yoshimura, T Westwick, J TI Chemokine production by human vascular smooth muscle cells: Modulation by IL-13 SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Meeting Abstract C1 UNIV BATH,DEPT PHARMACOL,BATH BA2 7AY,AVON,ENGLAND. RHONE POULENC RORER,DAGENHAM RES CTR,DAGENHAM RM10 7XS,ESSEX,ENGLAND. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. RI Jordan, Nicola/B-3341-2013 NR 3 TC 0 Z9 0 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 APR PY 1996 VL 117 SU S BP P113 EP P113 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UD162 UT WOS:A1996UD16200113 ER PT J AU Wise, SP diPellegrino, G Boussaoud, D AF Wise, SP diPellegrino, G Boussaoud, D TI The premotor cortex and nonstandard sensorimotor mapping SO CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY LA English DT Article; Proceedings Paper CT Symposium on Visuomotor Control - Planning and Execution CY MAY 11-12, 1995 CL MONTREAL, CANADA SP Univ Montreal, Ctr Rech Sci Neurol DE premotor cortex; frontal cortex; sensorimotor mapping; behavioral neurophysiology ID MOTOR CORTICAL ACTIVITY; VISUALLY GUIDED ARM; STIMULUS-RESPONSE COMPATIBILITY; MONKEY SUPERIOR COLLICULUS; MOVEMENT-RELATED ACTIVITY; PRIMATE FRONTAL-CORTEX; NEURONAL-ACTIVITY; REACHING MOVEMENTS; HAND MOVEMENTS; RHESUS-MONKEYS AB We often gaze at and attend to an object while preparing to reach toward and grasp it, and continue doing so when the plan is executed. Elaborate machinery, much of it in the brainstem and spinal cord, provides control systems for the spatially congruent guidance of the eyes, limbs, and body toward targets in visual space. We will use the term standard mapping for the sensorimotor transformations that underlie such behavior. Despite the commonsense character of standard mapping, the targets of gaze, attention, and reaching can be dissociated from each other. We can attend to stimuli in locations that differ from the target of action. We can gaze in one direction while reaching in another. And we can guide spatial action with nonspatial stimuli, such as when, in conditional motor tasks, the color of an object instructs a movement elsewhere in space. All of these situations, and many others, call for a process that we term nonstandard mapping, wherein the central nervous system must reject the commonplace correspondences among visuospatial stimuli, gaze, attention, and reaching movements. We focus in this article on the possibility that premotor cortex underlies nonstandard mapping and, therefore, the behavioral flexibility that such a process allows. RP Wise, SP (reprint author), NIMH, NEUROPHYSIOL LAB, POB 608, POOLESVILLE, MD 20837 USA. RI Boussaoud, Driss/B-6932-2008; OI di Pellegrino, Giuseppe/0000-0001-7080-4758 NR 92 TC 173 Z9 174 U1 1 U2 6 PU CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS PI OTTAWA PA 1200 MONTREAL ROAD, BUILDING M-55, OTTAWA, ON K1A 0R6, CANADA SN 0008-4212 J9 CAN J PHYSIOL PHARM JI Can. J. Physiol. Pharmacol. PD APR PY 1996 VL 74 IS 4 BP 469 EP 482 DI 10.1139/cjpp-74-4-469 PG 14 WC Pharmacology & Pharmacy; Physiology SC Pharmacology & Pharmacy; Physiology GA UY560 UT WOS:A1996UY56000013 PM 8828893 ER PT J AU Cavazza, A Travis, LB Travis, WD Wolfe, JT Foo, ML Gillespie, DJ Weidner, N Colby, TV AF Cavazza, A Travis, LB Travis, WD Wolfe, JT Foo, ML Gillespie, DJ Weidner, N Colby, TV TI Post-irradiation malignant mesothelioma SO CANCER LA English DT Article DE mesothelioma; radiotherapy; Hodgkin's disease; breast carcinoma ID PERITONEAL MESOTHELIOMA; PLEURAL MESOTHELIOMA; HODGKINS-DISEASE; UNITED-STATES; WILMS TUMOR; CANCER; RADIATION; RADIOTHERAPY; EXPERIENCE; THOROTRAST AB BACKGROUND. Approximately 30 patients with malignant mesothelioma following radiotherapy have been described. Population-based studies of this occurrence have not been reported. METHODS. Patients with malignant mesothelioma of the pleura were collected. All of the patients had a prior cancer and had received radiotherapy to the region in which the malignant mesothelioma developed. Data from the National Cancer Institute's Surveillance, Epidemiology and End Results Program and the Connecticut Tumor Registry were evaluated for cases of malignant mesothelioma of the pleura occurring in patients with a previous cancer. The literature on post-irradiation malignant mesotheliomas was reviewed. RESULTS. Eight patients (4 men, 4 women) with malignant mesothelioma occurring in sites of radiotherapy for a prior tumor were identified. The mean age at diagnosis of mesothelioma was 45 years (range: 22-78 years), and the average interval between radiotherapy and the mesothelioma was 21 years (range: 11-29 years). Three of the patients had also received chemotherapy. Histologically, the mesotheliomas were epithelial in five cases, biphasic in one, and sarcomatous in one. One hundred forty-two patients were identified in the epidemiologic survey. The majority were men (89%), with a median age for all patients of 68.5 years (range: 35-86 years) and a median latency between first cancer and mesothelioma of 4.3 pears (range: 2 months-29.9 years). CONCLUSIONS. Mesotheliomas rarely develop as second malignant neoplasms. Within a large, population-based survey of patients with cancer, temporal patterns and demographic features of most second primary mesotheliomas were similar to asbestos-related tumors, although the late effects of cancer treatment might have contributed to the occurrence of cancer in some patients. (C) 1996 American Cancer Society. C1 NCI,RADIAT EPIDEMIOL BRANCH,NIH,BETHESDA,MD. ARMED FORCES INST PATHOL,DEPT PULM & MEDIASTINAL PATHOL,WASHINGTON,DC 20306. MAYO CLIN SCOTTSDALE,DEPT LAB MED & PATHOL,SCOTTSDALE,AZ. MAYO CLIN JACKSONVILLE,DEPT PATHOL,JACKSONVILLE,FL 32224. MAYO CLIN JACKSONVILLE,DEPT RADIAT ONCOL,JACKSONVILLE,FL 32224. MAYO CLIN,DEPT THORAC DIS,ROCHESTER,MN. UNIV CALIF SAN FRANCISCO,MED CTR,SAN FRANCISCO,CA 94143. NR 33 TC 55 Z9 57 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD APR 1 PY 1996 VL 77 IS 7 BP 1379 EP 1385 DI 10.1002/(SICI)1097-0142(19960401)77:7<1379::AID-CNCR24>3.3.CO;2-5 PG 7 WC Oncology SC Oncology GA UA645 UT WOS:A1996UA64500024 PM 8608519 ER PT J AU Goto, M Miller, RW Ishikawa, Y Sugano, H AF Goto, M Miller, RW Ishikawa, Y Sugano, H TI Excess of rare cancers in Werner syndrome (adult progeria) SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Review ID MELANOMA; TISSUE; CARCINOMA; CELLS; GENE AB The association between genetic disorders and diverse cancers has provided clues for laboratory research into carcinogenesis, Such an opportunity now arises from studies of cancer in Werner syndrome (WRN). Soft-tissue sarcoma (STS) and benign meningioma have been associated with WRN, an autosomal recessive disorder characterized by premature aging, more commonly reported in Japan than elsewhere, in part because of inbreeding, In the literature we found 124 case-reports of neoplasia and WRN from Japan and 34 from outside Japan, 1939-August 1995, They reveal a greater diversity of neoplasia in WRN than was previously known, In Japanese, there were 127 cancers, 14 benign meningioma, and 5 myeloid disorders, as compared with 30, 7 and 2 respectively in non-Japanese, The ratio of epithelial to non-epithelial cancers was about 1:1 for Japanese and for non-Japanese instead of the usual 10:1, Both series had excesses of STS, osteosarcoma, myeloid disorders, and benign meningioma. In addition, the Japanese had an excess of thyroid cancer (20 versus 2 cases in non-Japanese) and melanoma (21 versus 3 cases), including 5 intranasal and 13 of the feet, STS, osteosarcoma, melanoma, and thyroid carcinoma accounted for 57% of all cancer in WRN as compared with 2% expected based on the Osaka population at 25-64 years of age, Multiple tumors were reported in 19 Japanese and 5 non-Japanese. In Japan, nine first-degree relatives had WRN and cancer, six of whom were concordant as to site and/or cell type, The WRN gene has been mapped to chromosome 8p, The high frequency of thyroid cancer and melanoma in Japanese, not found in Caucasians, may be related to a report of linkage disequilibrium with the WRN gene in Japanese but not in Caucasians and to haplotype differences within and between the two races, suggesting multiple independent mutations. C1 NCI,GENET EPIDEMIOL BRANCH,BETHESDA,MD 20892. INST CANC RES,TOSHIMA KU,TOKYO 170,JAPAN. TOKYO METROPOLITAN OTSUKA HOSP,DEPT RHEUMAT DIS,TOSHIMA KU,TOKYO 170,JAPAN. NR 164 TC 280 Z9 287 U1 2 U2 5 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD APR PY 1996 VL 5 IS 4 BP 239 EP 246 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA UE615 UT WOS:A1996UE61500001 PM 8722214 ER PT J AU Weed, DL Gorelic, LS AF Weed, DL Gorelic, LS TI The practice of causal inference in cancer epidemiology SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Review ID ALCOHOLIC-BEVERAGE CONSUMPTION; UNITED-STATES MEN; BREAST-CANCER; PROSTATE-CANCER; CIGARETTE-SMOKING; RISK-FACTORS; RETROSPECTIVE COHORT; VASECTOMY; DIET; HEALTH AB Causal inference is an important link between the practice of cancer epidemiology and effective cancer prevention, Although many papers and epidemiology textbooks have vigorously debated theoretical issues in causal inference, almost no attention has been paid to the issue of how causal inference is practiced, In this paper, we review two series of review papers published between 1985 and 1994 to find answers to the following questions: which studies and prior review papers were cited, which causal criteria were used, and what causal conclusions and public health recommendations ensued, Fourteen published reviews on alcohol and breast cancer and 6 published reviews on vasectomy and prostate cancer were examined, For both series of reviews, nearly all available published studies were cited except for ecological studies and prior reviews, Sources of causal criteria were often not provided, When they appeared, all citations were either the 1964 Surgeon General's report or works of Austin Bradford Hill, Reviews often excluded and sometimes altered criteria without giving reasons for these changes, The criteria of consistency and strength of association were almost always used accompanied by dose-response and biological plausibility in a majority of reviews, The criterion of temporality, considered by many methodologists to be a necessary causal condition, was infrequently used, Confounding and bias were often added considerations. Public health recommendations were not discussed in nearly one-half of the reviews. C1 NCI,COMPREHENS MINOR BIOMED PROGRAM,BETHESDA,MD 20892. RP Weed, DL (reprint author), NCI,PREVENT ONCOL BRANCH,EPS T-41,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 175 TC 59 Z9 61 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 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD APR PY 1996 VL 5 IS 4 BP 303 EP 311 PG 9 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA UE615 UT WOS:A1996UE61500010 PM 8722223 ER PT J AU DeLaPena, L WooleryAntill, M Tomaszewski, JG Gantz, S DiLorenzo, K Kryk, JA AF DeLaPena, L WooleryAntill, M Tomaszewski, JG Gantz, S DiLorenzo, K Kryk, JA TI Programmed instruction: Biotherapy module .5. Hematopoietic growth factors SO CANCER NURSING LA English DT Article RP DeLaPena, L (reprint author), NIH,CTR CLIN,DEPT NURSING,BETHESDA,MD 20892, USA. NR 12 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0162-220X J9 CANCER NURS JI Cancer Nurs. PD APR PY 1996 VL 19 IS 2 BP 135 EP 150 DI 10.1097/00002820-199604000-00008 PG 16 WC Oncology; Nursing SC Oncology; Nursing GA UE722 UT WOS:A1996UE72200008 PM 8635167 ER PT J AU Wei, MH Latif, F Bader, S Kashuba, V Chen, JY Duh, FM Sekido, Y Lee, CC Geil, L Kuzmin, I Zabarovsky, E Klein, G Zbar, B Minna, JD Lerman, MI AF Wei, MH Latif, F Bader, S Kashuba, V Chen, JY Duh, FM Sekido, Y Lee, CC Geil, L Kuzmin, I Zabarovsky, E Klein, G Zbar, B Minna, JD Lerman, MI TI Construction of a 600-kilobase cosmid clone contig and generation of a transcriptional map surrounding the lung cancer tumor suppressor gene (TSG) locus on human chromosome 3p21.3: Progress toward the isolation of a lung cancer TSG SO CANCER RESEARCH LA English DT Article ID 3P(14-23); DELETION; REGION; DNA AB The critical region on human chromosome 3p21.3 harboring a putative lung cancer tumor suppressor gene (TSG) was previously defined by allelotyping and recently refined by overlapping homozygous deletions. We report the construction of a 700-kb (cosmid and one P1 phage) clone contig covering the deletion overlap and its flanks. The minimal set of 23 cosmids comprises 600 kb and is extended by one P1 phage to 700 kb to cover the distal breakpoint of the overlap. The clone contig was extensively characterized by restriction and expression mapping to produce high resolution physical and transcription maps of the cloned region, Potential transcribed fragments were detected by hybridization with PCR-amplified cDNA libraries, direct cDNA selection, ''zoo'' blotting, cDNA screening, and identification of 24 CpG islands. Thus far, 15 new genes represented hy partial or full-length cDNAs were isolated, characterized, and precisely positioned on the contig. Two previously cloned genes, namely GNAI-2 and GNAT-1, mere also positioned, In addition, the telomeric breakpoint of the NCI H740 deletion and the centromeric breakpoint of the overlapping GLC20 deletion were discovered and mapped to define precisely the candidate TSG region. This large cosmid clone contig and high resolution maps will prove crucial in the identification of the lung cancer TSG(s). C1 NCI,FREDERICK CANC RES & DEV CTR,IMMUNOBIOL LAB,FREDERICK,MD 21702. SCI APPLICAT INT CORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. UNIV TEXAS,SW MED CTR,SIMMONS CANC CTR,DALLAS,TX 75235. KAROLINSKA INST,DEPT TUMOR BIOL,S-17177 STOCKHOLM,SWEDEN. BAYLOR COLL MED,DEPT MOLEC & HUMAN GENET,HOUSTON,TX 77030. RI Zabarovsky, Eugene/A-6645-2010; Sekido, Yoshitaka/P-9756-2015 FU NCI NIH HHS [P20 CA58220] NR 23 TC 144 Z9 151 U1 0 U2 9 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1996 VL 56 IS 7 BP 1487 EP 1492 PG 6 WC Oncology SC Oncology GA UC167 UT WOS:A1996UC16700006 PM 8603390 ER PT J AU Kondratyev, AD Chung, KN Jung, MO AF Kondratyev, AD Chung, KN Jung, MO TI Identification and characterization of a radiation-inducible glycosylated human early-response gene SO CANCER RESEARCH LA English DT Article ID PROTEIN-KINASE-C; FACTOR-KAPPA-B; IONIZING-RADIATION; LEUKEMIA-CELLS; PLASMACYTOID DIFFERENTIATION; HYDROGEN-PEROXIDE; MESSENGER-RNA; EXPRESSION; ACTIVATION; SEQUENCE AB A radiation-inducible immediate-early gene, IEX-1, was identified and characterized in human squamous carcinoma cells. Sequence analysis revealed 156-amino acid nucleotides, encoding a protein of M(r) 20,000. The protein is glycosylated (M(r) similar to 27,000) in the presence of microsomal membranes, Northern analysis reveals a 1.2-kb transcript. Treatment with cycloheximide was associated with superinduction of this transcript, suggesting that it is an immediate-early gene. The abundance of IEX-1 mRNA increased rapidly after exposure of the cells to ionizing radiation (2-10 Gy), reaching a maximum by 15 min and returning subsequently to basal levels by 4 h. Expression of IEX-1 was also induced significantly by the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol-13-acetate (TPA), the protein phosphatase inhibitor okadaic acid, and tumor necrosis factor-alpha, whereas treatment of cells with UV light and H2O2 had little effect on IEX-1 expression. Cells depleted of PKC by prolonged incubation with TPA showed no attenuated IEX-1 response to tumor necrosis factor-alpha. This is the first report of IEX-1, a radiation-inducible glycosylated human protein, whose expression can be mediated through multisignal transduction pathways. C1 GEORGETOWN UNIV,MED CTR,DEPT RADIAT MED,DIV RADIAT RES,WASHINGTON,DC 20007. NIH,NCI,MED BRANCH,BETHESDA,MD 20892. NR 32 TC 81 Z9 84 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1996 VL 56 IS 7 BP 1498 EP 1502 PG 5 WC Oncology SC Oncology GA UC167 UT WOS:A1996UC16700008 PM 8603392 ER PT J AU Travis, LB Curtis, RE Boice, JD Platz, CE Hankey, BF Fraumeni, JF AF Travis, LB Curtis, RE Boice, JD Platz, CE Hankey, BF Fraumeni, JF TI Second malignant neoplasms among long-term survivors of ovarian cancer SO CANCER RESEARCH LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; BREAST-CANCER; MUCINOUS TUMORS; COLON-CANCER; RISK; CARCINOMA; APPENDIX; CYCLOPHOSPHAMIDE; TRANSLOCATION; CHEMOTHERAPY AB Second malignant neoplasms were evaluated among 32,251 women with ovarian cancer, including 4,402 10-year survivors, within the nine population-based registries of the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute (1973-1992) and the Connecticut Tumor Registry (1935-1972). Overall, 1,296 second cancers occurred against 1,014 expected [observed/expected (O/E), 1.28; 95% confidence interval (CI), 1.21-1.35]. Sites contributing 25 or more excess cancers included leukemia (O/E, 4.17; O, 111; 95% CI, 3.43-5.03) and malignancies of colon (O/E, 1.33; O, 188; 95% CI, 1.15-1.51), rectum (O/E, 1.43; O, 76; 95% CI, 1.13-1.79), breast (O/E, 1.18; O, 404; 95%, CI 1.07-1.30), and bladder (O/E, 2.07; O, 65; 95% CI, 1.59-2.63). Ocular melanoma (O/E, 4.45; O, 8; 95% CI, 1.92-8.77) was also significantly increased. Second cancer risk was high during all follow-up intervals, and cumulative risk at 20 years was 18.2%, compared with a population expected risk of 11.5%, Statistically significant relationships existed between serous adenocarcinoma of the ovary and breast cancer (O/E, 1.29; 95% CI, 1.06-1.56) and mucinous ovarian adenocarcinoma and rectal cancer (O/E, 1.95; 95% CI, 1.09-3.22), Secondary leukemia appeared linked with antecedent chemotherapy, whereas radiotherapy was associated with cancers of connective tissue, bladder, and possibly pancreas, Genetic and reproductive factors predisposing to ovarian cancer may have contributed to the elevated risk of breast and colorectal neoplasms and possibly ocular melanoma, Thus, excess malignancies following ovarian cancer represent complications of curative therapies and/or underlying susceptibility states that have etiological and clinical ramifications. C1 NCI,NIH,DIV CANC PREVENT & CONTROL,SURVEILLANCE PROGRAM,CANC STAT BRANCH,BETHESDA,MD 20892. UNIV IOWA,DEPT PATHOL,IOWA CITY,IA 52242. RP Travis, LB (reprint author), NCI,NIH,DIV CANC EPIDEMIOL & GENET,EPN 408,BETHESDA,MD 20892, USA. NR 60 TC 81 Z9 81 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1996 VL 56 IS 7 BP 1564 EP 1570 PG 7 WC Oncology SC Oncology GA UC167 UT WOS:A1996UC16700019 PM 8603403 ER PT J AU Buckwalter, CA Lin, AH Tanizawa, A Pommier, YG Cheng, YC Kaufmann, SH AF Buckwalter, CA Lin, AH Tanizawa, A Pommier, YG Cheng, YC Kaufmann, SH TI RNA synthesis inhibitors alter the subnuclear distribution of DNA topoisomerase I SO CANCER RESEARCH LA English DT Article ID HELA-CELLS; PROTEIN B23; CAMPTOTHECIN ANALOGS; CATALYTIC ACTIVITY; ANTITUMOR AGENTS; NUCLEAR MATRIX; TRANSCRIPTION; LOCALIZATION; TRANSLOCATION; NUCLEOLUS AB The acute effect of RNA and DNA synthesis inhibitors on DNA topoisomerase (topo)I localization within cells was examined. Indirect immunofluorescence revealed that topo I was distributed throughout the nuclei but was concentrated in nucleoli of untreated K562 leukemia cells and A549 non-small cell lung cancer cells, Treatment with the DNA polymerase inhibitor aphidicolin did not alter this distribution. In contrast, 30-60 min after addition of the RNA synthesis inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) at concentrations that inhibited [H-3]uridine incorporation into RNA by greater than or equal to 50%, topo I was visible throughout the nuclei without nucleolar accentuation, Western blotting and activity assays confirmed that the amount of topo I polypeptide and topo I activity were unaltered by the brief DRB treatment, Within 30 min of DRB removal, topo I relocalized to the nucleoli in the absence or presence of the protein synthesis inhibitor cycloheximide. Collectively, these results suggest a reversible translocation of topo I out of the nucleoli when RNA synthesis is inhibited, Treatment with the topo I poisons topotecan or camptothecin, agents that also inhibit RNA synthesis, likewise caused redistribution of topo I to nonnucleolar regions of the nucleus in a variety of cell types, In DC3F hamster lung fibroblasts, 2.5 mu M topotecan or 1.25 mu M camptothecin was sufficient to cause this topo I redistribution, In DC3F/C-10 cells that contain a mutant camptothecin-resistant topo I, topo I relocalization required 50-fold higher concentrations of topotecan or camptothecin but not DRB, These observations not only suggest that accumulation of topo I in the nucleolus is related to ongoing RNA synthesis but also raise the possibility of screening for some types of camptothecin resistance at the single-cell level using a rapid immunofluorescence-based assay. C1 MAYO CLIN,DIV ONCOL RES,ROCHESTER,MN 55905. MAYO CLIN & MAYO FDN,MAYO MED SCH,DEPT PHARMACOL,ROCHESTER,MN 55905. JOHNS HOPKINS UNIV,BALTIMORE,MD 21203. NCI,MOLEC PHARMACOL LAB,BETHESDA,MD 20892. YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06510. FU NCI NIH HHS [CA44358] NR 57 TC 63 Z9 64 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1996 VL 56 IS 7 BP 1674 EP 1681 PG 8 WC Oncology SC Oncology GA UC167 UT WOS:A1996UC16700035 PM 8603419 ER PT J AU Lowry, DT Li, LW Hennings, H AF Lowry, DT Li, LW Hennings, H TI Thapsigargin, a weak skin tumor promoter, alters the growth and differentiation of mouse keratinocytes in culture SO CARCINOGENESIS LA English DT Article ID ORNITHINE DECARBOXYLASE ACTIVITY; EPIDERMAL-CELLS; TERMINAL DIFFERENTIATION; MURINE KERATINOCYTES; GENE-EXPRESSION; CALCIUM-ENTRY; INVITRO; 12-0-TETRADECANOYLPHORBOL-13-ACETATE; CARCINOGENESIS; ACTIVATION AB Thapsigargin (Tg), applied twice weekly to the backs of CD-1 mice initiated with 7,12-dimethylbenz[a]anthracene, promoted papillomas on the skin of similar to 50% of the mice, Tg alone induced papillomas in 10% of the mice, Although Tg and 12-O-tetradecanoylphorbol-13-acetate (TPA) are synergistic in a keratinocyte co-culture assay for promotion, skin tumor promotion by TPA was inhibited by co-treatment with Tg, Treatment of cultured keratinocytes with non-toxic doses of Tg increased the level of intracellular free Ca2+ and delayed Ca2+-induced stratification, Tg blocked expression of the spinous layer differentiation marker keratin 1 (K1), while inducing cornification, a marker of differentiation in the granular layer/stratum corneum, In medium with 1.4 mM Ca2+, Tg prolonged keratinocyte proliferation and selected foci of monolayer cells. A Tg-independent cell line, TK-1, was developed from a single dish in which foci continued to expand after Tg removal, Grafting TK-1 cells on to the backs of nude mice as part of a reconstituted skin resulted in the development of dysplastic papillomas with a high rate of progression to squamous cell carcinomas. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. NR 36 TC 10 Z9 11 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1996 VL 17 IS 4 BP 699 EP 706 DI 10.1093/carcin/17.4.699 PG 8 WC Oncology SC Oncology GA UG814 UT WOS:A1996UG81400013 PM 8625480 ER PT J AU Blomeke, B Greenblatt, MJ Doan, VD Bowman, ED Murphy, SE Chen, CC Kato, S Shields, PG AF Blomeke, B Greenblatt, MJ Doan, VD Bowman, ED Murphy, SE Chen, CC Kato, S Shields, PG TI Distribution of 7-alkyl-2'-deoxyguanosine adduct levels in human lung SO CARCINOGENESIS LA English DT Article ID TOBACCO-SPECIFIC NITROSAMINES; NON-ENZYMATIC METHYLATION; HYDROCARBON-DNA ADDUCTS; P-32 POSTLABELING ASSAY; HUMAN CANCER; CARCINOGEN METABOLISM; F344 RATS; II CELLS; SMOKING; EXPOSURE AB Human lung tissue is frequently studied as a target organ for DNA damage from carcinogen-DNA adducts, In order to assess the distribution of carcinogen-DNA adducts in human lung, we measured 7-methyl-2'-deoxyguanosine-3'-monophosphate (7-methyl-dGp), 7-ethyl-2'-deoxyguanosine-3'-monophosphate (7-ethyl-dGp) and 4-hydroxy-(3-pyridyl)-1-butanone (HPB)-releasing DNA adducts in different lobes, The first two result from exposure to N-nitrosamines, including tobacco-specific nitrosamines, and the latter only from tobacco-specific nitrosamines. Using a chemically-specific P-32-postlabeling assay for 7-alkyl-2'-deoxyguanosines, adducts were measured in eight separate lung segments of ten autopsy donors, 7-Methyl-dGp levels were detected in all eighty samples (range from 0.3 to 11.5 adducts/10(7) dGp; mean 2.5 +/- 2.3 adducts/10(7) dGp), 7-Ethyl-dGp were detected in all but five of the samples (range from <0.1 to 7.1 adducts/10(7) dGp; mean 1.6 +/- 1.7 adducts/10(7) dGp). 7-Methyl-dGp levels were approximately 1.5-fold higher than 7-ethyl-dGp levels, and they were positively correlated with each other in most individuals. There was no consistent pattern of adduct distribution in the different lobar segments, Most individuals, especially those with the lowest levels, had similar levels among the lobes, while those with the highest levels had a widely variable pattern ranging as much as ten-fold, Moreover, 7-methyl-dGp and 7-ethyl-dGp levels in all people showed a highly significant inter-individual variation (P = 0.0001), The levels of 7-alkyl-2'-deoxyguanosine among individuals could not be explained by differences in tobacco exposure (measured by serum cotinine), onset of death, gender, age, race, blood ethanol, or ventilation and perfusion variability, In an effort to corroborate 7-alkyl-2'-deoxyguanosine adducts variability among lobes or individuals, we sought to determine a correlation with HPB-releasing DNA adducts as an independent marker of tobacco exposure. However, this tobacco-specific carcinogen-DNA adduct could not be detected in four individuals tested (detection limit: 0.3 adducts per 10(7) dGp), Based upon the lack of 7-alkyl-2'-deoxyguanosine discernible adduct patterns, no conclusions could be drawn regarding a potential relationship to lobar cancer incidence. The results indicate that in studies of carcinogen-DNA adducts, such as 7-alkyl-dGp in human lungs, for most individuals a random lung sample would be representative of other parts of the lungs, Some individuals however might be misclassified due to highly variable 7-alkyl-dGp levels. C1 NCI,HUMAN CARCINOGENESIS LAB,NIH,BETHESDA,MD 20892. RI Shields, Peter/I-1644-2012 NR 61 TC 33 Z9 34 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1996 VL 17 IS 4 BP 741 EP 748 DI 10.1093/carcin/17.4.741 PG 8 WC Oncology SC Oncology GA UG814 UT WOS:A1996UG81400018 PM 8625485 ER PT J AU Bishop, RE Pauly, GT Moschel, RC AF Bishop, RE Pauly, GT Moschel, RC TI O-6-ethylguanine and O-6-benzylguanine incorporated site-specifically in codon 12 of the rat H-ras gene induce semi-targeted as well as targeted mutations in Rat4 cells SO CARCINOGENESIS LA English DT Article ID O6-ETHYLGUANINE CARCINOGENIC LESIONS; MOLECULAR MECHANICS CALCULATIONS; APURINIC APYRIMIDINIC SITE; MAMMALIAN-CELLS; ABASIC SITE; O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE; DODECANUCLEOTIDE DUPLEXES; DEOXYADENOSINE STACKS; MUTAGENIC PROPERTIES; ADJACENT POSITIONS AB To examine the miscoding properties of modified guanine residues bearing increasingly bulky O-6-substituents, Rat4 cells, grown in the presence of O-6-benzylguanine to deplete the DNA. repair protein O-6-alkylguanine-DNA alkyltransferase, were transfected with plasmids carrying H-ras genes in which O-6-methyl, O-6-ethyl- and O-6-benzylguanine were substituted for the first, second or both the first and second guanine residues of codon 12 (GGA). DNA from isolated transformed colonies was amplified by PCR and directly sequenced by high-temperature manual and automated methods, The results show that O-6-ethylguanine and O-6-benzylguanine induced semi-targeted as well as targeted mutations, in contrast to O-6-methylguanine, which induced only targeted mutations, When incorporated in place of the first guanine of H-ras codon 12, the targeted mutations induced by all these modified guanines were exclusively G-->A transitions. When incorporated at the second position of codon 12, O-6-benzylguanine induced G-->A, G-->T and G-->C mutations, O-6-Ethylguanine at the second position induced chiefly G-->A transitions, and O-6-methylguanine induced G-->A transitions exclusively, Semi-targeted mutations were strictly G-->A at the base 3' to a position 1 adduct or 5' to a position 2 adduct, The mechanism for induction of targeted mutations probably involves decreasing preference for thymidine incorporation opposite an O-6-modified guanine as the size of the O-6-substituent increases, while the mechanism for non-targeted mutations may be related to abasic site formation or to translesion synthesis which might be made error-prone by obstructive DNA lesions in this context. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702. NR 53 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 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1996 VL 17 IS 4 BP 849 EP 856 DI 10.1093/carcin/17.4.849 PG 8 WC Oncology SC Oncology GA UG814 UT WOS:A1996UG81400033 PM 8625500 ER PT J AU Deakin, M Elder, J Hendrickse, C Peckham, D Baldwin, D Pantin, C Wild, N Leopard, P Bell, DA Jones, P Duncan, H Brannigan, K Alldersea, J Fryer, AA Strange, RC AF Deakin, M Elder, J Hendrickse, C Peckham, D Baldwin, D Pantin, C Wild, N Leopard, P Bell, DA Jones, P Duncan, H Brannigan, K Alldersea, J Fryer, AA Strange, RC TI Glutathione S-transferase GSTT1 genotypes and susceptibility to cancer: Studies of interactions with GSTM1 in lung, oral, gastric and colorectal cancers SO CARCINOGENESIS LA English DT Article ID CLASS-MU; CARCINOMA; PHENOTYPE; JAPANESE; MARKER AB Allelism in glutathione S-transferase GSTM1 and GSTT1 has been suggested as a risk factor in various cancers, Accordingly, we describe a group of case-control studies carried out to identify associations between GSTT1 genotypes and susceptibility to lung, oral, gastric and colorectal cancers, The frequencies of the putatively high risk GSTT1 null genotype were not increased in the lung, oral or gastric cancer cases compared with controls but the frequency of this genotype was significantly increased (P = 0.0011, odds ratio = 1.88) in the colorectal cancer cases, No significant interactions between the GSTT1 and GSTM1 null genotypes were identified in the cancer groups studied, Indeed, no significant associations between GSTM1 genotypes and susceptibility were identified though further evidence was obtained that the protective effect of GSTM1*A and GSTM1*B is not equal, The data complement studies showing that GSTT1 null is associated with an increased susceptibility to total ulcerative colitis and suggests that this enzyme is important in the detoxification of unidentified xenobiotics in the large intestine. C1 KEELE UNIV,N STAFFORDSHIRE HOSP,POSTGRAD MED SCH,DEPT SURG,KEELE,STAFFS,ENGLAND. N STAFFORDSHIRE HOSP,DEPT RESP MED,STOKE ON TRENT,STAFFS,ENGLAND. N STAFFORDSHIRE HOSP,DEPT ORAL & MAXILLOFACIAL SURG,STOKE ON TRENT,STAFFS,ENGLAND. NIEHS,RES TRIANGLE PK,NC 27709. KEELE UNIV,DEPT MATH,KEELE,STAFFS,ENGLAND. NR 28 TC 274 Z9 287 U1 0 U2 3 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD APR PY 1996 VL 17 IS 4 BP 881 EP 884 DI 10.1093/carcin/17.4.881 PG 4 WC Oncology SC Oncology GA UG814 UT WOS:A1996UG81400038 PM 8625505 ER PT J AU Packard, B AF Packard, B TI Prescription for the 21st century SO CARDIOVASCULAR RISK FACTORS LA English DT Editorial Material RP Packard, B (reprint author), NHLBI,INFORMAT CTR,SCI PROGRAM OPERAT,NIH,POB 30105,BETHESDA,MD 20824, USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1130-7501 J9 CARDIOVASC RISK FACT JI Cardiovasc. Risk Factors PD APR PY 1996 VL 6 IS 2 BP 63 EP 65 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA UP304 UT WOS:A1996UP30400001 ER PT J AU Higgins, M AF Higgins, M TI Cardiovascular diseases in women: A public health problem SO CARDIOVASCULAR RISK FACTORS LA English DT Article DE heart; risk factors; women ID CORONARY AB Cardiovascular diseases (CVDs) are the leading causes of death and major causes of illness and disability in women. Forty-six percent of all deaths in U.S. women are attributed to CVD; 22% to coronary heart disease (CHD) and 8% to stroke. Although death and incidence rates are 2 to 3 times higher in men than in women during middle age, and CHD tends to occur similar to 10 years later in women, a higher proportion of women die soon after a heart attack, and more women who survive a heart attack have a recurrent event. Diagnostic procedures and surgical treatment may be delayed and are performed less frequently in women. Risk factors for CVD are highly prevalent among women. Recent national surveys estimate that: 23% have high levels of serum cholesterol, 25% have hypertension, 37% are overweight, and 25% smoke cigarettes. Obesity and diabetes mellitus are more prevalent in than in men. Premature menopause, oophorectomy, and oral contraceptive use are risk factors unique to women. There is substantial evidence that reducing cholesterol, blood pressure, and cigarette smoking and controlling weight are effective strategies for reducing CVD risk in women. Failure to prevent, diagnose, and treat CVD and to reduce prevalence of risk factors in women to the maximum extent possible should be considered a public health problem. RP Higgins, M (reprint author), NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,NIH,2 ROCKLEDGE CTR,ROOM 8104,6701 ROCKLEDGE DR,BETHESDA,MD 20892, USA. NR 23 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1130-7501 J9 CARDIOVASC RISK FACT JI Cardiovasc. Risk Factors PD APR PY 1996 VL 6 IS 2 BP 66 EP 73 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA UP304 UT WOS:A1996UP30400002 ER PT J AU Bian, XP Bird, GSJ Putney, JW AF Bian, XP Bird, GSJ Putney, JW TI cGMP is not required for capacitative Ca2+ entry in Jurkat T-lymphocytes SO CELL CALCIUM LA English DT Article ID PANCREATIC ACINAR CELL; CALCIUM ENTRY; STORES; DEPLETION; MESSENGER AB In this study, we have addressed the potential role of cGMP in regulating calcium entry in Jurkat T-lymphocytes. These cells display capacitative Ca2+-entry in response to the intracellular Ca2+-ATPase inhibitor, thapsigargin (TG). In the presence of extracellular Ca2+, TG stimulates a sustained elevation of intracellular cGMP levels. In the absence of extracellular Ca2+, TG induces no apparent increase in the levels of cGMP. However, experiments using Mn2+, as a. surrogate for Ca2+, demonstrated that TG increased the rate of divalent cation entry in the absence of extracellular Ca2+. Treatment of Jurkat cells with the guanylyl cyclase inhibitor, LY83583 (20 mu M), completely blocked cGMP formation in response to TG. However, LY83583 treated cells still exhibited a sustained, albeit partially reduced, Ca2+ response induced by TG. These data demonstrate that, in Jurkat cells, the sustained formation of cGMP is dependent on elevated intracellular Ca2+, and that elevated levels of cGMP are not necessary for the activation of capacitative Ca2+ entry. C1 NIEHS,NIH,CELLULAR & MOLEC PHARMACOL LAB,CALCIUM REGULAT SECT,RES TRIANGLE PK,NC 27709. NR 21 TC 13 Z9 14 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0143-4160 J9 CELL CALCIUM JI Cell Calcium PD APR PY 1996 VL 19 IS 4 BP 351 EP 354 DI 10.1016/S0143-4160(96)90075-5 PG 4 WC Cell Biology SC Cell Biology GA UM872 UT WOS:A1996UM87200008 PM 8983855 ER PT J AU Baez, A Torres, K Tan, EM Pommier, Y Casiano, CA AF Baez, A Torres, K Tan, EM Pommier, Y Casiano, CA TI Expression of proliferation-associated nuclear autoantigens, p330(d)/CENP-F and PCNA, in differentiation and in drug-induced growth inhibition using two-parameter flow cytometry SO CELL PROLIFERATION LA English DT Article ID MONOCLONAL-ANTIBODY KI-67; DNA POLYMERASE-DELTA; CELL-CYCLE ANALYSIS; S-PHASE; HL-60 CELLS; CLINICAL-APPLICATIONS; AUXILIARY PROTEIN; LENS REGENERATION; TOPOISOMERASE-I; RETINOIC ACID AB p330(d)/CENP-F is a recently described nuclear autoantigen that was detected in PHA-stimulated but not in resting peripheral lymphocytes. This protein accumulates in the nucleus during S-phase and reaches maximum levels during the G(2) and M phases of the cell cycles. We compared the expression of p330(d)/CENP-F and proliferating cell nuclear antigen (PCNA) during the induction of terminal myeloid differentiation of HL-60 tumour cells. HL-60 cells were induced to differentiate with retinoic acid (RA), dimethyl sulfoxide (DMSO), and 3-nitrobenzothiazolo [3,2-]quinolinium (NBQ), and collected at different intervals. Control and treated cells were analyzed by two-parameter flow cytometry using propidium iodide and antibodies to p330(d)/CENP-F and PCNA. The percentage of p330(d)/CENP-F and PCNA positive cells was found to be proportional to the percentage of proliferating cells. After two cell cycles (65 h), the percentage of p330(d)/CENP-F and PCNA positive cells was reduced proportionately to the number of cells that had differentiated. Reduction in the expression of both antigens was completed after 120 h when 80% to 85% of the cells were arrested in G(1) and displayed the mature phenotype. The expression of p330(d)/CENP-F and PCNA was also assessed in the growth inhibition of HT-29 cells induced by various concentrations of camptothecin (CPT), etoposide (VP-16), and aphidicolin (APH). There was a dose-dependent displacement of cells to late S-phase by CPT while VP-16 induced cells to accumulate in G(2) + M, and as expected these effects caused a strong increase in the cellular levels of both antigens. The arrest of cells in G(1) by APH led to a significant decrease in their expression. The dramatic reduction in p330(d)/CENP-F levels during differentiation, and the correlation of its expression with the cell cycle effects of the cytotoxic drugs are consistent with the behaviour expected for a proliferation marker. C1 WM KECK AUTOIMMUNE DIS CTR, DEPT MOLEC & EXPTL MED SRB6, SCRIPPS RES INST, LA JOLLA, CA USA. NCI, MOLEC PHARMACOL LAB, DPT, DCT, NIH, BETHESDA, MD 20892 USA. RP Baez, A (reprint author), UNIV PUERTO RICO, SCH MED, DEPT PHARMACOL, BOX 365067, SAN JUAN, PR 00936 USA. FU NCI NIH HHS [CA569056]; NIAMS NIH HHS [AR320063]; NIGMS NIH HHS [GM08224] NR 39 TC 9 Z9 10 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0960-7722 J9 CELL PROLIFERAT JI Cell Prolif. PD APR PY 1996 VL 29 IS 4 BP 183 EP 196 DI 10.1111/j.1365-2184.1996.tb00105.x PG 14 WC Cell Biology SC Cell Biology GA UZ205 UT WOS:A1996UZ20500002 PM 8695747 ER PT J AU Lopez, FJ Merchenthaler, I Liposits, Z NegroVilar, A AF Lopez, FJ Merchenthaler, I Liposits, Z NegroVilar, A TI Steroid imprinting and modulation of sexual dimorphism in the luteinizing hormone-releasing hormone neuronal system SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Article DE luteinizing hormone-releasing hormone; sexual dimorphism; galanin; estrogen ID IMMORTALIZED HYPOTHALAMIC NEURONS; ESTROGEN-RECEPTOR; GALANIN; EXPRESSION; RAT; GONADOTROPIN; SEQUENCE; BRAIN AB 1. Sex differences in the control of gonadotropin secretion and reproductive functions are a distinct characteristic in all mammalian species, including humans. Ovulation and cyclicity are among the most distinct neuroendocrine markers of female brain differentiation, along with sex behavioral traits that are also evident in different species. 2. The luteinizing hormone-releasing hormone (LHRH) neuronal system is the prime regulator of neuroendocrine events leading to ovulation and hormonal changes during the menstrual cycle and, as such, is the potential site where many of these sex differences may be expressed or, at the very least, integrated. However, until recently, no significant differences were seen in LHRH neurons between male and female brains, including cell number, pattern of distribution, and expression of message or peptide (LHRH) levels. 3. Recently, we reported that galanin (GAL), a brain-gut peptide, is coexpressed in LHRH neurons and that this coexpression is sexually dimorphic. When GAL is used as a marker for this neuronal system, it is clear that estradiol as well as progesterone profoundly affects the message and expression of the peptide and that this regulation, at least in rodents, is neonatally predetermined by gonadal steroid imprinting. 4. Changes in GAL expression and message can also be seen at puberty, during pregnancy and lactation, and in aging, all situations that affect the function of the LHRH neuronal system. Using an immortalized LHRH neuronal cell line (GT1) we have recently observed that these neurons express estrogen receptor (ER) and GAL and that estradiol can increase the expression of GAL, indicating functional activation of the endogenous ER. C1 WYETH AYERST RES,WOMENS HLTH RES INST,RADNOR,PA 19087. NIEHS,NIH,RADNOR,PA. NR 25 TC 15 Z9 15 U1 0 U2 2 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0272-4340 J9 CELL MOL NEUROBIOL JI Cell. Mol. Neurobiol. PD APR PY 1996 VL 16 IS 2 BP 129 EP 141 DI 10.1007/BF02088172 PG 13 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA UN346 UT WOS:A1996UN34600004 PM 8743965 ER PT J AU Agarwal, R Canella, KA Yagi, H Jerina, DM Dipple, A AF Agarwal, R Canella, KA Yagi, H Jerina, DM Dipple, A TI Benzo[c]phenanthrene-DNA adducts in mouse epidermis in relation to the tumorigenicities of four configurationally isomeric 3,4-dihydrodiol 1,2-epoxides SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID REGION DIOL-EPOXIDES; EMBRYO CELL-CULTURES; DIHYDRODIOL-EPOXIDE; MAMMALIAN-CELLS; DNA ADDUCTS; BENZO(C)PHENANTHRENE; 3,4-DIOL-1,2-EPOXIDES; SKIN; 7,12-DIMETHYLBENZ(A)ANTHRACENE; BINDING AB P-32-Postlabeling assays were used to monitor the binding to epidermal DNA that resulted from the application of each of the four configurational isomers of benzo[c]phenanthrene 3,4-dihydrodiol 1,2-epoxide to mouse skin in vivo. For three of these configurational isomers, there was a reasonable correlation between the relative level of binding to epidermal DNA and the known tumorigenic effects of these compounds. However, for the 4(S),3(R)-dihydrodiol a(S),1(R)-epoxide, the tumorigenic response was considerably greater in relation to the level of DNA modification than was the case for the other isomers. This greater tumorigenic response was consistent with previous observations indicating that this isomer was more mutagenic, at equivalent levels of DNA modification, than the other two tumorigenic dihydrodiol epoxides. Additionally, the 4(S),3(R)-dihydrodiol 2(S),1(R);epoxide reacts with DNA to generate predominantly (similar to 80%) adducts on the amino group of adenine residues. These findings might imply a greater intrinsic biological effect of such adenine adducts with respect to the other major adduct formed on the amino group of guanine residues. C1 NIDDKD,NIH,BIOORGAN CHEM LAB,BETHESDA,MD 20892. RP Agarwal, R (reprint author), NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CHEM CARCINOGENESIS LAB,FREDERICK,MD 21702, USA. NR 27 TC 28 Z9 28 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD APR-MAY PY 1996 VL 9 IS 3 BP 586 EP 592 DI 10.1021/tx950148+ PG 7 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA UF846 UT WOS:A1996UF84600005 PM 8728502 ER PT J AU Putnam, FW AF Putnam, FW TI A brief history of multiple personality disorder SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID SATANIC RITUAL ABUSE; CLINICAL PHENOMENOLOGY; DISSOCIATIVE DISORDERS; POSTTRAUMATIC-STRESS; CHILDHOOD; SCHIZOPHRENIA; CHILDREN AB This brief review of multiple personality disorder (MPD) focuses on a number of historical threads of inquiry spanning the past century. Nineteenth-century investigations of dissociation paved the way for multilevel models of the mind and the development of dynamic psychiatry. Modern controversies, such as the role of trauma in dissociation, cultural influences on the expression of dissociation, the portrayal of MPD in the popular media, and the validity of MPD, grow out of nineteenth-century debates. The recognition of child and adolescent dissociative disorders and the adoption of a developmental focus of investigation offers an opportunity to resolve many of these contentious issues. RP Putnam, FW (reprint author), NIMH,UNIT DEV TRAUMATOL,BIOL PSYCHOL BRANCH,DIV INTRAMURAL RES,BLDG 15K,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 61 TC 2 Z9 2 U1 2 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD APR PY 1996 VL 5 IS 2 BP 263 EP & PG 10 WC Psychiatry SC Psychiatry GA UZ891 UT WOS:A1996UZ89100003 ER PT J AU Putnam, FW AF Putnam, FW TI Child development and dissociation SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID MULTIPLE PERSONALITY-DISORDER; POSTTRAUMATIC-STRESS-DISORDER; SEXUAL ABUSE; CLINICAL PHENOMENOLOGY; FAMILY ENVIRONMENT; EXPERIENCES SCALE; SYMPTOMS; VALIDITY; INTERVIEW; VETERANS AB Increased recognition of dissociative symptoms and phenomena in children and adolescents has confronted clinicians with the challenge of differentiating normal from abnormal or pathologic dissociation. Reliable and valid measures of dissociation are increasingly being used both clinically and for research. These data strongly link pathologic dissociation with traumatic antecedents. They also point to family environmental experiences and attachment as important contributors to an individual's dissociativity. High levels of dissociation are linked with behavioral problems and psychopathology in maltreated children and adults. RP Putnam, FW (reprint author), NIMH, UNIT DEV TRAUMATOL,BIOL PSYCHIAT BRANCH, DIV INTRAMURAL RES,BLDG 15K, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 89 TC 20 Z9 20 U1 2 U2 10 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 1056-4993 EI 1558-0490 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD APR PY 1996 VL 5 IS 2 BP 285 EP + PG 0 WC Psychiatry SC Psychiatry GA UZ891 UT WOS:A1996UZ89100005 ER PT J AU Putnam, FW Hornstein, N Peterson, G AF Putnam, FW Hornstein, N Peterson, G TI Clinical phenomenology of child and adolescent dissociative disorders - Gender and age effects SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID MULTIPLE PERSONALITY-DISORDER AB Clinicians have noted age and gender differences in the presentations of children and adolescents with dissociative disorders. This study uses a composite sample of 177 cases to explore developmental and gender differences in youth with pathologic dissociation. Females proved to be more symptomatic than males in five areas: anxiety and phobic symptoms, post-traumatic stress disorder symptoms, sleep problems, sexual acting out, and somatization. In general, there were more dissociative and comorbid symptoms with increasing age, although most age differences did not achieve statistical significance. Internalized auditory hallucinations, conversion symptoms, amnesias,suicidal ideation, and self-mutilation increased significantly with age. Preschool cases were essentially equally divided between males and females. By late adolescence, 83% of cases were female. Cases diagnosed with dissociative identity disorder/multiple personality disorder were significantly more symptomatic than those diagnosed with dissociative disorder not otherwise specified. C1 UNIV ILLINOIS,DIV CHILD PSYCHIAT,CHICAGO,IL. SO CALIF PSYCHOANAL INST,LOS ANGELES,CA. UNIV N CAROLINA,DEPT PSYCHIAT,CHAPEL HILL,NC. RP Putnam, FW (reprint author), NIMH,UNIT DEV TRAUMATOL,BIOL PSYCHIAT BRANCH,DIV INTRAMURAL RES,BLDG 15K,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 15 TC 15 Z9 15 U1 3 U2 12 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD APR PY 1996 VL 5 IS 2 BP 351 EP & PG 12 WC Psychiatry SC Psychiatry GA UZ891 UT WOS:A1996UZ89100008 ER PT J AU Lewis, DO Putnam, FW AF Lewis, DO Putnam, FW TI Dissociative identity disorder/multiple personality disorder - Preface SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Editorial Material C1 NIMH,UNIT DEV TRAUMATOL,BETHESDA,MD 20892. RP Lewis, DO (reprint author), NYU,SCH MED,DEPT PSYCHIAT,NEW BELLEVUE 21S25,550 1ST AVE,NEW YORK,NY 10016, 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 1056-4993 J9 CHILD ADOL PSYCH CL JI Child Adolesc. Psychiatr. N. Am. PD APR PY 1996 VL 5 IS 2 BP R13 EP R14 PG 2 WC Psychiatry SC Psychiatry GA UZ891 UT WOS:A1996UZ89100002 ER PT J AU Dunn, PF Newman, KD Jones, M Yamada, I Shayani, V Virmani, R Dichek, DA AF Dunn, PF Newman, KD Jones, M Yamada, I Shayani, V Virmani, R Dichek, DA TI Seeding of vascular grafts with genetically modified endothelial cells - Secretion of recombinant TPA results in decreased seeded cell retention in vitro and in vivo SO CIRCULATION LA English DT Article DE carotid arteries; cells; plasminogen activators; viruses ID MEDIATED GENE-TRANSFER; TISSUE PLASMINOGEN-ACTIVATOR; HUMAN UMBILICAL VEIN; PROSTHESES; POLYTETRAFLUOROETHYLENE; EXPRESSION; UROKINASE; MEMBRANE; INVITRO; BYPASS AB Background Seeding of Small-diameter vascular grafts with endothelial cells (ECs) genetically engineered to secrete fibrinolytic or antithrombotic proteins offers the potential to improve graft patency rates. Methods and Results Sheep venous ECs were transduced with a retroviral vector encoding human tissue plasminogen activator (TPA). The ECs were seeded onto 4-mm-ID synthetic (Dacron) grafts. Retention of the seeded ECs was measured 2 hours after placement of the seeded grafts both in vitro in a nonpulsatile flow system and in vivo (in sheep) as femoral and carotid interposition grafts. On exposure to flow in vitro, ECs transduced with TPA were retained at a significantly lower rate (median, 67%) than either untransduced ECs (81%)or ECs transduced with a control retroviral vector producing beta-galactosidase (beta-Gal) (80%) (P<.05 for TPA versus either control). On implantation in vivo, ECs transduced with TPA were retained at a very low rate (median, 0%), significantly less than the retention of ECs transduced with the beta-Gal vector (32%; P<.00001). Decreased in vivo retention of ECs transduced with TPA correlated modestly with increased in vitro cellular passage level (r(2)=.48; P<.0001) but not with in vivo blood flow rate (P=.45). Addition of the protease inhibitor aprotinin to the cell culture and graft perfusion media resulted in a significant (P<.05) increase in in vitro retention of ECs transduced with TPA. Conclusions Increased TPA expression significantly decreases seeded EC adherence in vitro and in vivo. Gene therapy strategies for decreasing graft thrombosis may require expression of antithrombotic molecules that lack proteolytic activity. C1 UNIV CALIF SAN FRANCISCO,GLADSTONE INST CARDIOVASC DIS,SAN FRANCISCO,CA 94141. NHLBI,MOLEC HEMATOL BRANCH,BETHESDA,MD 20892. NHLBI,LAB ANIM MED & SURG,BETHESDA,MD 20892. CHILDRENS NATL MED CTR,DEPT SURG,WASHINGTON,DC 20010. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NR 52 TC 68 Z9 74 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR 1 PY 1996 VL 93 IS 7 BP 1439 EP 1446 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA UC189 UT WOS:A1996UC18900018 PM 8641034 ER PT J AU Zheng, JS Boluyt, MO Long, XL ONeill, L Lakatta, EG Crow, MT AF Zheng, JS Boluyt, MO Long, XL ONeill, L Lakatta, EG Crow, MT TI Extracellular ATP inhibits adrenergic agonist-induced hypertrophy of neonatal cardiac myocytes SO CIRCULATION RESEARCH LA English DT Article DE ATP; purinergic receptors; cardiac hypertrophy; norepinephrine; cardiac myocytes ID SARCOPLASMIC-RETICULUM CA-2+-ATPASE; RAT MYOCARDIAL-CELLS; PROTEIN-KINASE-C; GENE-EXPRESSION; VENTRICULAR MYOCYTES; SIGNAL-TRANSDUCTION; MESSENGER-RNA; JUN PROTEINS; GROWTH; HEART AB We have previously shown that extracellular ATP, like norepinephrine (NE) and many other hypertrophy-inducing agents, increases expression of the immediate-early genes c-Sos and junB in cultured neonatal cardiac myocytes but that the intracellular signaling pathways activated by ATP and responsible for these changes differ from those stimulated by NE. Furthermore, whereas NE increases incorporation of [C-14]phenylalanine (C-14-Phe) and cell size in neonatal cardiomyocytes, ATP does not. Since ATP is coreleased with NE from sympathetic nerve endings in the heart, we investigated whether ATP could modulate cardiac hypertrophy induced by adrenergic agonists, such as NE. We report in the present study that extracellular ATP inhibited the increase in incorporation of C-14-Phe into cellular protein and the increase in cell size in neonatal rat cardiac myocytes that was induced by NE, phenylephrine (PE), basic fibroblast growth factor, or endothelin-1. This inhibition was dose dependent, occurred predominantly through P-2 purinergic receptors, and was observed even when cells were treated with ATP for as little as 1 hour before the addition of the hypertrophy-inducing agent. ATP also selectively affected changes in gene expression associated with hypertrophy. It prevented PE-stimulated increases in atrial natriuretic factor and myosin light chain-2 mRNA levels, while appearing to augment basal and PE-stimulated skeletal cr-actin mRNA levels. ATP alone increased sarcoplasmic reticulum Ca2+-ATPase mRNA levels but had no effect when added with PE. ATP did not significantly affect the level of the constitutively expressed mRNA for GAPDH. Neither the PE-stimulated increase in immediate-early gene expression nor the initial induction of mitogen-activated protein kinase activity by PE was inhibited by ATP. These results demonstrate that extracellular ATP can inhibit hypertrophic growth of neonatal cardiac myocytes and differentially alter the changes in gene expression that accompany hypertrophy. C1 NIA,NIH,CTR GERONTOL RES,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. NR 49 TC 47 Z9 47 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD APR PY 1996 VL 78 IS 4 BP 525 EP 535 PG 11 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA UC176 UT WOS:A1996UC17600003 PM 8635209 ER PT J AU Whelton, PK Williamson, JD Louis, GT Davis, BR Cutler, JA AF Whelton, PK Williamson, JD Louis, GT Davis, BR Cutler, JA TI Experimental approaches to determining the choice of first-step therapy for patients with hypertension SO CLINICAL AND EXPERIMENTAL HYPERTENSION LA English DT Article; Proceedings Paper CT 3rd WHO/ISH Meeting on Prevention of Hypertension and Cardiovascular Disease CY JUN 15-17, 1995 CL PORTO CERVO, ITALY SP WHO, Int Soc Hypertens DE hypertension; high blood pressure; clinical trials; prevention; epidemiology; cardiovascular disease; pharmacology ID MYOCARDIAL-INFARCTION; DRUG-THERAPY; ANGINA; MILD AB Detection, treatment and control of hypertension is one of the best proven approaches to prevention of cardiovascular disease. Antihypertensive treatment trials have convincingly demonstrated that diuretics and beta-blockers reduce the risk of stroke and coronary heart disease. Corresponding information is not yet available for newer classes of antihypertensive drug therapy such as calcium channel blockers, angiotensin converting enzyme inhibitors and alpha, receptor blockers. Several experimental studies are now addressing this question. The largest such trial (n=40,000) is the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). This manuscript describes two studies (TOMHS and the VA study on antihypertensive agents) that compared several classes of antihypertensive drugs with regard to blood pressure outcomes and ALLHAT, which is comparing the effect of four first-step approaches to antihypertensive therapy on combined incidence of fatal coronary heart disease and non-fatal myocardial infarction. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT EPIDEMIOL,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD. UNIV TEXAS,SCH PUBL HLTH,CTR HLTH SCI,HOUSTON,TX. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,NIH,BETHESDA,MD 20892. RP Whelton, PK (reprint author), JOHNS HOPKINS MED INST,WELCH CTR PREVENT EPIDEMIOL & CLIN RES,2024 E MONUMENT ST,SUITE 2-600,BALTIMORE,MD 21205, USA. NR 17 TC 17 Z9 17 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1064-1963 J9 CLIN EXP HYPERTENS JI Clin. Exp. Hypertens. PD APR-MAY PY 1996 VL 18 IS 3-4 BP 569 EP 579 DI 10.3109/10641969609088986 PG 11 WC Pharmacology & Pharmacy; Peripheral Vascular Disease SC Pharmacology & Pharmacy; Cardiovascular System & Cardiology GA UF358 UT WOS:A1996UF35800026 PM 8743044 ER PT J AU Goldwasser, F Valenti, M Torres, R Kohn, KW Pommier, Y AF Goldwasser, F Valenti, M Torres, R Kohn, KW Pommier, Y TI Potentiation of cisplatin cytotoxicity by 9-aminocamptothecin SO CLINICAL CANCER RESEARCH LA English DT Article ID DNA TOPOISOMERASE-I; OVARIAN-CARCINOMA CELLS; CROSS-LINKING; CYTO-TOXICITY; CIS-DIAMMINEDICHLOROPLATINUM(II); REPAIR; CAMPTOTHECIN; RESISTANCE; LINE; MECHANISM AB Camptothecin (CPT) derivatives are presently in ongoing Phase I/II clinical trials. The interactions between 9-aminocamptothecin (9AC) and cisplatin (CDDP) have been studied in the IGROV-1 human ovarian cancer cell line used in the National Cancer Institute Drug Discovery Anticancer Screen, One-h simultaneous treatment with 9AC and CDDP produced synergistic cytotoxicity. Under these conditions, 9AC delayed the reversal of CDDP-induced DNA interstrand cross-links (ISCs) without modifying the maximum ISC frequency at 6 h after drug treatment, CDDP did not affect the amount and the kinetics of reversion of 9AC-induced DNA single-strand breaks, Simultaneous treatment with CDDP and 9AC prolonged the DNA synthesis inhibition produced by each drug alone, Consistently, flow cytometry analyses showed enhanced S-phase arrest in cells treated with the CDDP-9AC combination, The DNA polymerase inhibitor aphidicolin also increased the residual CDDP-induced ISCs. These results suggest that prolonged inhibition of DNA synthesis by CPTs potentiate the cytotoxicity of CDDP by inhibiting the reversal of CDDP-induced DNA damage, Therefore, the combination of CPTs and CDDP appears to be worthwhile in cancer chemotherapy. C1 NCI,MOLEC PHARMACOL LAB,DIV BASIC SCI,NIH,BETHESDA,MD 20892. NR 51 TC 34 Z9 34 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD APR PY 1996 VL 2 IS 4 BP 687 EP 693 PG 7 WC Oncology SC Oncology GA UD929 UT WOS:A1996UD92900010 PM 9816219 ER PT J AU Contois, JH McNamara, JR LammiKeefe, CJ Wilson, PWF Massov, T Schaefer, EJ AF Contois, JH McNamara, JR LammiKeefe, CJ Wilson, PWF Massov, T Schaefer, EJ TI Reference intervals for plasma apolipoprotein A-I determined with a standardized commercial immunoturbidimetric assay: Results from the framingham offspring study SO CLINICAL CHEMISTRY LA English DT Article DE lipids; lipoproteins; epidemiology; coronary heart disease; standardization ID HIGH-DENSITY-LIPOPROTEIN; CORONARY HEART-DISEASE; ARTERY DISEASE; INTERNATIONAL-FEDERATION; MYOCARDIAL-INFARCTION; HDL-CHOLESTEROL; CIGARETTE-SMOKING; SERUM-LIPIDS; MEN; WOMEN AB We have evaluated a commercially available, standardized immunoturbidimetric assay of apolipoprotein (ape) A-I, the major protein constituent of high-density lipoproteins (HDL). We determined the reference ranges of plasma apo A-I concentration for white men and women and related these values to the risk of coronary heart disease (CHD). The mean between-run CV for this assay was 2.9%. As determined with individuals participating in cycle 4 of the Framingham Offspring Study, the mean (+/- SD) apo A-I concentration was 13 % lower in 1879 men (1.34 +/- 0.23 g/L) than in 1939 women (1.54 +/- 0.28 g/L) (P <0.001). An apo A-I concentration of 1.20 g/L roughly corresponded to the 25th percentile value in men and the 5th percentile in women, and subjects with a concentration below this value were significantly more likely to have CHD than subjects with a higher concentration (P <0.001). C1 TUFTS UNIV,USDA,JEAN MAYER HUMAN NUTR RES CTR AGING,LIPID METAB LAB,BOSTON,MA 02111. UNIV CONNECTICUT,DEPT NUTR SCI,STORRS,CT 06269. NHLBI,FRAMINGHAM HEART STUDY,FRAMINGHAM,MA 01701. FU NHLBI NIH HHS [HV-83-03] NR 43 TC 103 Z9 110 U1 1 U2 1 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 APR PY 1996 VL 42 IS 4 BP 507 EP 514 PG 8 WC Medical Laboratory Technology SC Medical Laboratory Technology GA UD765 UT WOS:A1996UD76500006 PM 8605666 ER PT J AU Contois, JH McNamara, JR LammiKeefe, CJ Wilson, PWF Massov, T Schaefer, EJ AF Contois, JH McNamara, JR LammiKeefe, CJ Wilson, PWF Massov, T Schaefer, EJ TI Reference intervals for plasma apolipoprotein B determined with a standardized commercial immunoturbidimetric assay: Results from the Framingham Offspring Study SO CLINICAL CHEMISTRY LA English DT Article DE lipids; lipoproteins; coronary heart disease; epidemiology; standardization ID CORONARY HEART-DISEASE; DENSITY-LIPOPROTEIN CHOLESTEROL; MIDDLE-AGED MEN; A-I; ARTERY DISEASE; INTERNATIONAL-FEDERATION; MYOCARDIAL-INFARCTION; SUBCLASS PATTERNS; SERUM-LIPIDS; RISK AB We evaluated a commercially available, standardized immunoturbidimetric assay for apolipoprotein (ape) B, the protein constituent of low-density lipoprotein (LDL), to establish reference ranges for men and women, and to determine the concentrations associated with increased risk of coronary heart disease (CHD). The between-run CV for assay of a normal-concentration control for this assay was 6.60%. The mean (+/- SD) apo B concentration was 1.03 +/- 0.24 g/L in 1880 men, significantly higher than the mean for 1944 women (0.96 +/- 0.26 g/L) participating in cycle 4 of the Framingham Offspring Study (P <0.001). An apo B value of 1.20 g/L corresponded roughly to the 75th percentile in men, similar to an LDL cholesterol concentration of 1.60 g/L, and subjects with concentrations greater than this were significantly more likely to have CHD than subjects with apo B concentrations less than 1.00 g/L, the approximate 50th percentile (P <0.05 in men and P <0.001 in women). C1 TUFTS UNIV, USDA, JEAN MAYER HUMAN NUTR RES CTR AGING, LIPID METAB LAB, BOSTON, MA 02111 USA. UNIV CONNECTICUT, DEPT NUTR SCI, STORRS, CT 06269 USA. NHLBI, FRAMINGHAM HEART STUDY, FRAMINGHAM, MA 01701 USA. FU NHLBI NIH HHS [HV-83-03] NR 55 TC 137 Z9 144 U1 1 U2 2 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA SN 0009-9147 EI 1530-8561 J9 CLIN CHEM JI Clin. Chem. PD APR PY 1996 VL 42 IS 4 BP 515 EP 523 PG 9 WC Medical Laboratory Technology SC Medical Laboratory Technology GA UD765 UT WOS:A1996UD76500007 PM 8605667 ER PT J AU Magiakou, MA Mastorakos, G Rabin, D Margioris, AN Dubbert, B Calogero, AE Tsigos, C Munson, PJ Chrousos, GP AF Magiakou, MA Mastorakos, G Rabin, D Margioris, AN Dubbert, B Calogero, AE Tsigos, C Munson, PJ Chrousos, GP TI The maternal hypothalamic-pituitary-adrenal axis in the third trimester of human pregnancy SO CLINICAL ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING HORMONE; INSULIN-INDUCED HYPOGLYCEMIA; PLASMA-CORTISOL; ARGININE VASOPRESSIN; MEDIAN-EMINENCE; BINDING-PROTEIN; BETA-ENDORPHIN; HUMAN-PLACENTA; SECRETION; ADRENOCORTICOTROPIN AB OBJECTIVE The third trimester of pregnancy is characterized by a mildly hyperactive hypothalamic-pituitary-adrenal (HPA) axis, possibly driven by elevated circulating levels of corticotrophin releasing hormone (CRH) of placental origin. In-vitro studies have demonstrated that glucocorticoids and oestrogen stimulate while progesterone inhibits the expression of CRH mRNA and/or protein, suggesting that several potential interactions between the placenta and the HPA axis may exist. DESIGN AND PATIENTS To investigate the detailed pattern of circulating immunoreactive (ir) CRH, ACTH, cortisol, oestradiol and progesterone during the third trimester of pregnancy, plasma samples were drawn serially every 30 minutes from 22 healthy pregnant women (age 32.0 +/- 1.1 years, mean +/- SE) between the 34th and 36th week of gestation. Ten women had plasma samples drawn between 0800 h and 2000 h (daytime group), and 12 between 2000 h and 0300 h (night-time group). The hormone concentrations obtained were analysed for pulsatility by the Detect program, for detection of circadian rhythmicity by comparison between the first and second 6-hour periods within each group by Student's t-test, and for time-dependent correlations by cross-correlation analysis. RESULTS All five hormones were secreted in a pulsatile fashion. There was no apparent circadian rhythm of CRH or oestradiol secretion, whereas there was a clear circadian rhythm in plasma ACTH, cortisol and progesterone secretion, with the latter in reverse phase (P<0.05). No significant correlations were observed between CRH and ACTH, whereas, as expected, ACTH and cortisol concentrations were strongly correlated with each other over time (r = 0.32 and 0.70 at lag time 30 minutes for the daytime and night-time groups, respectively), with ACTH leading cortisol. A weak positive correlation was observed between CRH and cortisol concentrations for the night-time group at lag time 0 minute, suggesting that the latter may have a positive effect on the former in vivo. CONCLUSIONS These data suggest that placental CRH, although pulsatile, drives quantitatively the maternal HPA axis in the third trimester of pregnancy in a non-circadian, non-pulsatile fashion. The maternal HPA axis is probably driven in a circadian and pulsatile fashion by another major ACTH secretagogue, most likely AVP of parvocellular paraventricular nucleus origin. C1 NICHHD,DEV ENDOCRINOL BRANCH,BETHESDA,MD 20892. NIH,ANALYT BIOSTAT SECT,STRUCT BIOL LAB,DCRT,BETHESDA,MD 20892. NR 54 TC 87 Z9 87 U1 1 U2 5 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0300-0664 J9 CLIN ENDOCRINOL JI Clin. Endocrinol. PD APR PY 1996 VL 44 IS 4 BP 419 EP 428 DI 10.1046/j.1365-2265.1996.683505.x PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UH463 UT WOS:A1996UH46300008 PM 8706308 ER PT J AU TreiberHeld, S Stewart, DM Kurman, CC Nelson, DL AF TreiberHeld, S Stewart, DM Kurman, CC Nelson, DL TI IL-15 induces the release of soluble IL-2R alpha from human peripheral blood mononuclear cells SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID RECEPTOR-BETA-CHAIN; HUMAN INTERLEUKIN-2 RECEPTOR; GAMMA-CHAIN; MULTIPLE-SCLEROSIS; CLONING; EXPRESSION; INVITRO; CDNAS; P64 AB The recently identified and cloned cytokine IL-15 shares many of the T-cell and B-cell stimulatory activities of IL-2 and utilizes the beta and gamma chains of the IL-2R for binding and signaling. The present report shows that, like IL-2, IL-15 in a concentration and time-dependent manner causes the release of sIL-2R alpha from PHA-activated human peripheral blood mononuclear cells. This effect of IL-15 is largely direct and independent of IL-2. Blocking of the IL-2R beta chain with the antibody Mik-beta 1 prevented the release of sIL-2R alpha by IL-15 but not by IL-2. IL-7, another cytokine utilizing the gamma chain of the IL-2R, drove the release of sIL-2R alpha as well. Several clinical conditions are associated with abnormal serum sIL-2R alpha levels and are also monitored by the measurement of sIL-2R alpha. The reason for siL-2R alpha release is not fully understood. In this study, IL-15, like IL-2 was shown to be a potent inducer of sIL-2R alpha release in vitro. (C) 1996 Academic Press, Inc. RP TreiberHeld, S (reprint author), NCI,IMMUNOL SECT,METAB BRANCH,NIH,BETHESDA,MD 20982, USA. NR 36 TC 10 Z9 10 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1996 VL 79 IS 1 BP 71 EP 78 DI 10.1006/clin.1996.0052 PG 8 WC Immunology; Pathology SC Immunology; Pathology GA UJ249 UT WOS:A1996UJ24900009 PM 8612353 ER PT J AU Yahnke, CJ Johnson, WE Geffen, E Smith, D Hertel, F Roy, MS Bonacic, CF Fuller, TK vanValkenburgh, B Wayne, RK AF Yahnke, CJ Johnson, WE Geffen, E Smith, D Hertel, F Roy, MS Bonacic, CF Fuller, TK vanValkenburgh, B Wayne, RK TI Darwin's fox: A distinct endangered species in a vanishing habitat SO CONSERVATION BIOLOGY LA English DT Article ID HUMAN MITOCHONDRIAL-DNA; POPULATION; CHILE; CONSERVATION; DIVERSITY; SEQUENCES; EVOLUTION; GENETICS; TAXONOMY; FULVIPES AB The temperate rain forest of Chiloe Island, Chile, is inhabited by an endemic fox (Dusicyon fulvipes) first described by Charles Darwin and now designated Darwin's fox. Despite morphological differences, Darwin's fox has been considered only an insular subspecies of the mainland chilla fox (D. griseus). This follows the assumption that the island population, with an estimated population of less than 500, has been separated from the mainland chilla fox for only about 15,000 years and may have received occasional immigrants from the mainland. Consequently, this island population has not been protected as endangered or bred in captivity. Recently, a population of Darwin's fox was discovered on the Chilena mainland 600 km north of Chiloe Island. This population exists in sympatry with chilla and possibly culpeo (D. culpaeus) foxes, which suggests that Darwin's fox may be reproductivity isolated. To clarify the phylogenetic position of Darwin's fox, we analyzed 344 bp of mitochondrial DNA control-region sequence of the three species of Chilean foxes. Darwin's foxes from the island and mainland populations compose a monophyletic group distinct from the two other Chilean fox species. This indicates that Darwin's fox was probably an early inhabitant of central Chile, and that its present distribution on the mainland may be a relict of a once much wider distribution. Our results highlight the ability of molecular genetic techniques to uncover historical relationships masked by recent events, such as local extinctions. The ''rediscovery'' of Darwin's fox as a distinct species implies that greater significance should be given to the protection of this species and its unique habitat and to documenting the extent of its mainland distribution. C1 UNIV CALIF LOS ANGELES,DEPT BIOL,LOS ANGELES,CA 90024. NO ILLINOIS UNIV,DEPT BIOL SCI,DE KALB,IL 60115. NCI,VIRAL CARCINOGENESIS LAB,FREDERICK,MD 21702. UNIV COPENHAGEN,DEPT POPULAT BIOL,DK-2100 COPENHAGEN,DENMARK. PONTIFICIA UNIV CATOLICA CHILE,DEPT INGN FORESTAI,SANTIAGO,CHILE. UNIV MASSACHUSETTS,DEPT FORESTRY & WILDLIFE MANAGEMENT,AMHERST,MA 01003. RI Johnson, Warren/D-4149-2016 OI Johnson, Warren/0000-0002-5954-186X NR 71 TC 17 Z9 19 U1 3 U2 14 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0888-8892 J9 CONSERV BIOL JI Conserv. Biol. PD APR PY 1996 VL 10 IS 2 BP 366 EP 375 DI 10.1046/j.1523-1739.1996.10020366.x PG 10 WC Biodiversity Conservation; Ecology; Environmental Sciences SC Biodiversity & Conservation; Environmental Sciences & Ecology GA UK801 UT WOS:A1996UK80100017 ER PT J AU Koonin, EV Mushegian, AR Rudd, KE AF Koonin, EV Mushegian, AR Rudd, KE TI Sequencing and analysis of bacterial genomes SO CURRENT BIOLOGY LA English DT Review ID ESCHERICHIA-COLI GENOME; POLYNUCLEOTIDE PHOSPHORYLASE; RIBOSOMAL PROTEIN-S1; NUCLEOTIDE-SEQUENCE; GENE; DATABASE; REGIONS; SEARCH AB The complete sequences of two small bacterial genomes have recently become available, and those of several more species should follow within the next two years. Sequence comparisons show that the most bacterial proteins are highly conserved in evolution, allowing predictions to be made about the functions of most products of an uncharacterized genome. Bacterial genomes differ vastly in their gene repertoires. Although genes for components of the translation and transcription machinery, and for molecular chaperones, are typically maintained, many regulatory and metabolic systems are absent in bacteria with small genomes. Mycoplasma genitalium, with the smallest known genome of any cellular life form, lacks virtually all known regulatory genes, and its gene expression may be regulated differently than in other bacteria, Genome organization is evolutionarily labile: extensive gene shuffling leaves only very few conserved gene arrays in distantly related bacteria. RP NATL LIB MED, NATL CTR BIOTECHNOL INFORMAT, NIH, BETHESDA, MD 20894 USA. OI Mushegian, Arcady/0000-0002-6809-9225 NR 81 TC 71 Z9 72 U1 0 U2 3 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0960-9822 EI 1879-0445 J9 CURR BIOL JI Curr. Biol. PD APR 1 PY 1996 VL 6 IS 4 BP 404 EP 416 DI 10.1016/S0960-9822(02)00508-0 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UH684 UT WOS:A1996UH68400022 PM 8723345 ER PT J AU Lou, MF Xu, GT Zigler, S York, B AF Lou, MF Xu, GT Zigler, S York, B TI Inhibition of naphthalene cataract in rats by aldose reductase inhibitors SO CURRENT EYE RESEARCH LA English DT Article DE naphthalene; cataract; aldose reductase inhibitor; rat ID DIABETIC RATS; LENS; MECHANISM AB Naphthalene-induced cataract in rat lenses can be completely prevented by AL01576, an aldose reductase inhibitor (ARI). In an attempt to understand the mechanism of this inhibition, several ARIs were examined to compare their efficacies in preventing naphthalene cataract, using both in vitro and in vivo models. Two classes of ARIs were tested: One group including AL01576, AL04114 (a AL01576 analog) and Sorbinil contained the spirohydantoin group, while Tolrestat contained a carboxylic acid group. Furthermore, to clarify if aldose reductase played a role in naphthalene-induced cataractogenesis in addition to its role in sugar cataract formation, a new dual cataract model was established for ARI evaluations. This was achieved by feeding rats simultaneously with high galactose and naphthalene or incubating rat lenses in culture media containing high galactose and naphthalene dihydrodiol. Under these conditions, both cortical cataract and perinuclear cataract developed in the same lens. It was found that at the same dosage of 10 mg/kg/day, both AL01576 and AL04114 completely prevented all morphological and biochemical changes in the lenses of naphthalene-fed rats. Sorbinil was less efficacious, while Tolrestat was inactive. AL01576 showed a dose-response effect in preventing naphthalene cataract and at 10 mg/kg/day, it was also effective as an intervention agent after cataractogenesis had begun. With the dual cataract model, Tolrestat prevented the high galactose-induced cortical cataract but showed no protection against the naphthalene-induced peri nuclear cataract. AL01576, on the other hand, prevented both cataract formations. Results for dulcitol and glutathione levels were in good agreement with the morphological findings. AL04114, an ARI as potent as AL01576 but without its property for cytochrome P-450 inhibition, displayed similar efficacy in preventing naphthalene cataract. Based on these results, it was concluded that the prevention of the naphthalene cataract probably results from inhibition of the conversion of naphthalene dihydrodiol to 1,2-dihydroxynaphthalene and that the effect of the ARIs cannot be explained by their inhibition of the dihydrodiol dehydrogenase activity of aldose reductase. C1 UNIV NEBRASKA,MED CTR,DEPT OPHTHALMOL,OMAHA,NE 68198. N TEXAS STATE UNIV,MED CTR,DEPT ANAT & CELL BIOL,FT WORTH,TX 76107. ALCOA LABS,FT WORTH,TX 76134. NEI,BETHESDA,MD 20892. RP Lou, MF (reprint author), UNIV NEBRASKA,DEPT VET & BIOMED SCI,CTR BIOTECHNOL,LINCOLN,NE 68583, USA. FU NEI NIH HHS [EY 10595] NR 26 TC 11 Z9 11 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD APR PY 1996 VL 15 IS 4 BP 423 EP 432 DI 10.3109/02713689608995833 PG 10 WC Ophthalmology SC Ophthalmology GA UG505 UT WOS:A1996UG50500009 PM 8670742 ER PT J AU ZunigaPflucker, JC Lenardo, MJ AF ZunigaPflucker, JC Lenardo, MJ TI Regulation of thymocyte development from immature progenitors SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID T-CELL DEVELOPMENT; HEMATOPOIETIC STEM-CELLS; FETAL THYMUS DEVELOPMENT; C-KIT; PRECURSOR CELLS; ANTIGEN RECEPTORS; LYMPHOCYTES-T; MICE; DIFFERENTIATION; MOUSE AB T lymphocytes differentiate from hematopoietic stem cells that settle in the microenvironment of the thymus. The earliest stages of mouse alpha/beta T-cell differentiation occurring before surface expression of the TCR include three important events: proliferation, commitment to the T lineage, and rearrangement and expression of the TCR loci. Recent evidence suggests that the survival as well as differentiation of early thymocytes depends critically on molecular signals such as those generated by the recently described pre-TCR complex. C1 NIAID,IMMUNOL LAB,NIH,BETHESDA,MD 20892. RP ZunigaPflucker, JC (reprint author), UNIV TORONTO,DEPT IMMUNOL,TORONTO,ON M5S 1A8,CANADA. RI Zuniga-Pflucker, Juan/H-1295-2012; OI Zuniga-Pflucker, Juan Carlos/0000-0003-2538-3178 NR 96 TC 136 Z9 138 U1 0 U2 5 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD APR PY 1996 VL 8 IS 2 BP 215 EP 224 DI 10.1016/S0952-7915(96)80060-4 PG 10 WC Immunology SC Immunology GA UM874 UT WOS:A1996UM87400009 PM 8725945 ER PT J AU Margulies, DH Plaksin, D Khilko, SN Jelonek, MT AF Margulies, DH Plaksin, D Khilko, SN Jelonek, MT TI Studying interactions involving the T-cell antigen receptor by surface plasmon resonance SO CURRENT OPINION IN IMMUNOLOGY LA English DT Review ID BIOSPECIFIC INTERACTION ANALYSIS; CLASS-I MOLECULE; ENDOGENOUS PEPTIDES; MHC MOLECULE; BINDING; COMPLEX; PROTEIN; AFFINITY; IMMOBILIZATION; RECOGNITION AB T-lymphocyte activation is initiated by the interaction of the alpha beta TCR with a complex consisting of a class I or class II MHC-encoded molecule and an antigenic peptide, displayed on the surface of an antigen-presenting cell. Real-time binding measurements using surface plasmon resonance have revealed kinetic and equilibrium parameters for the interactions between purified MHC molecules and peptides, between TCR and MHC-peptide complexes, and between TCR and superantigens. The MHC-peptide interaction is characterized by its high affinity and long half-life, the TCR-MHC/peptide interaction by its low affinity and short half-life, and the TCR-superantigen interaction by its low-to-moderate affinity, which is dependent on the particular superantigen involved. The consistent finding is that both MHC-peptide complexes and superantigens interact with TCR with a low affinity attributable to rapid dissociation. That an MHC-peptide complex that encounters a single TCR only briefly can still deliver the necessary activation signals offers a mechanistic conundrum for which several solutions have been proposed. RP Margulies, DH (reprint author), NIAID,MOLEC BIOL SECT,IMMUNOL LAB,NIH,BLDG 10,ROOM 11N311,BETHESDA,MD 20892, USA. RI Margulies, David/H-7089-2013; OI Margulies, David/0000-0001-8530-7375 NR 56 TC 26 Z9 28 U1 0 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0952-7915 J9 CURR OPIN IMMUNOL JI Curr. Opin. Immunol. PD APR PY 1996 VL 8 IS 2 BP 262 EP 270 DI 10.1016/S0952-7915(96)80066-5 PG 9 WC Immunology SC Immunology GA UM874 UT WOS:A1996UM87400015 PM 8725950 ER PT J AU Suzuki, WA AF Suzuki, WA TI The anatomy, physiology and functions of the perirhinal cortex SO CURRENT OPINION IN NEUROBIOLOGY LA English DT Article ID INFERIOR TEMPORAL CORTEX; SHORT-TERM-MEMORY; HIPPOCAMPAL-FORMATION; CORTICAL AFFERENTS; VISUAL RECOGNITION; ENTORHINAL CORTEX; LESIONS; IMPAIRMENT; ANTERIOR; STIMULUS AB The perirhinal cortex is a polymodal association area that contributes importantly to normal recognition memory. A convergence of recent findings from lesion and electrophysiological studies has provided new evidence that this area participates in an even broader range of memory functions than previously thought, including associative memory and emotional memory, as well as consolidation functions. These results are consistent with neuroanatomical research showing that this area has strong and reciprocal connections with widespread cortical sensory areas and with other memory-related structures, including the hippocampal formation and amygdala. RP Suzuki, WA (reprint author), NIMH,NEUROPSYCHOL LAB,BLDG 49,ROOM 1B80,49 CONVENT DR,BETHESDA,MD 20892, USA. NR 60 TC 150 Z9 151 U1 7 U2 13 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-4388 J9 CURR OPIN NEUROBIOL JI Curr. Opin. Neurobiol. PD APR PY 1996 VL 6 IS 2 BP 179 EP 186 DI 10.1016/S0959-4388(96)80071-7 PG 8 WC Neurosciences SC Neurosciences & Neurology GA UN151 UT WOS:A1996UN15100005 PM 8725959 ER PT J AU Theodore, WH AF Theodore, WH TI Positron emission tomography and single photon emission computed tomography SO CURRENT OPINION IN NEUROLOGY LA English DT Article AB Neuroimaging techniques have had a dramatic impact on the evaluation and treatment of patients with epilepsy. In order to take full advantage of their potential, it is important to place them in clinical and electrophysiological context and to understand their technical limitations. Positron emission tomography with F-18-2-deoxyglucose and single photon emission computed tomography can provide valuable data for presurgical localization of epileptogenic zones. Interictal cerebral blood flow studies, however, using either positron emission tomography or simple photon emission computed tomography are unreliable. Positron emission tomography cerebral blood flow activation studies, on the other hand, are becoming very useful for presurgical cognitive mapping and may be able to replace the intracarotid amytal test for language and memory lateralization. There are a number of receptor ligands available for both positron emission tomography and simple photon emission computed tomography studies, including benzodiazepine, opiate, and cholinergic tracers. Increased mu opiate, decreased benzodiazepine, and increased monoamine oxidase B receptor binding have been reported. RP Theodore, WH (reprint author), NIH,CLIN EPILEPSY SECT,BLDG 10,5C-205,BETHESDA,MD 20892, USA. NR 37 TC 6 Z9 6 U1 1 U2 1 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 1350-7540 J9 CURR OPIN NEUROL JI Curr. Opin. Neurol. PD APR PY 1996 VL 9 IS 2 BP 89 EP 92 DI 10.1097/00019052-199604000-00005 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA UN971 UT WOS:A1996UN97100005 PM 8782973 ER PT J AU Jernigan, RL Bahar, I AF Jernigan, RL Bahar, I TI Structure-derived potentials and protein simulations SO CURRENT OPINION IN STRUCTURAL BIOLOGY LA English DT Article ID GLOBULAR-PROTEINS; MEAN FORCE; MODELS; CONFORMATIONS; PREDICTION; SEQUENCES; CRITERIA; FOLDS AB There has recently been an explosion in the number of structure-derived potential functions that are based on the increasing number of high-resolution protein crystal structures. These functions differ principally in their reference states; the usual two classes correspond either to initial solvent exposure or to residue exposure of residues. Reference states are critically important for applications of these potentials functions. Inspection of the potential functions and their derivation can tell us not only about protein interaction strengths themselves, but can also provide suggestions for the design of better folding simulations. An appropriate goal in this field is achieving self-consistency between the details in the derivation of potentials and the applied simulations. C1 BOGAZICI UNIV, ISTANBUL, TURKEY. TUBITAK, POLYMER RES CTR, ISTANBUL, TURKEY. RP Jernigan, RL (reprint author), NIH, MATH BIOL LAB, MSC 5677, ROOM B-116, BLDG 12A, BETHESDA, MD 20892 USA. RI Jernigan, Robert/A-5421-2012 NR 92 TC 220 Z9 225 U1 2 U2 15 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0959-440X J9 CURR OPIN STRUC BIOL JI Curr. Opin. Struct. Biol. PD APR PY 1996 VL 6 IS 2 BP 195 EP 209 DI 10.1016/S0959-440X(96)80075-3 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UF605 UT WOS:A1996UF60500010 PM 8728652 ER PT J AU Lai, JC Wawrousek, EF Sipe, JD Whitcup, SM Gery, I AF Lai, JC Wawrousek, EF Sipe, JD Whitcup, SM Gery, I TI Reduced susceptibility to IL-1 and endotoxin in transgenic mice expressing IL-1 in their lens SO CYTOKINE LA English DT Article DE endotoxin effects; IL-1 transgene; responses to IL-1; transgenic mice ID TUMOR-NECROSIS-FACTOR; INTERLEUKIN-1; LETHALITY; RATS AB To learn about the effects of chronic exposure to IL-1 we generated a transgenic (Tg) mouse line that expresses human IL-1 beta under the control of the lens alpha A crystallin promoter. Expression of human IL-1 beta was restricted to the eye; neither the protein nor its mRNA were detected in various other organs of the Tg mice, The Tg mice develop severe ocular inflammation shortly after birth, which affects the lens and other eye tissues and apparently allows the release of IL-1 into the circulation. Here we report that the Tg mice exhibit decreased responsiveness to IL-1 and lipopolysaccharide (LPS), as compared to their wildtype littermate controls: (1) when injected with IL-1 the Tg mice produced lower levels of serum amyloid A than their controls; (2) thymocytes of the Tg mice responded less vigorously in culture to stimulation with IL-1; and (3) Tg mice showed lower morbidity and mortality than their controls when injected with toxic amounts of LPS, These data suggest that chronic exposure to IL-1 in the Tg mice induces partial resistance to this cytokine, analogous to the reduced responsiveness to IL-1 in animals pretreated with this proinflammatory cytokine. (C) 1996 Academic Press Limited C1 NEI, NIH, IMMUNOL LAB, BETHESDA, MD 20892 USA. NEI, NIH, MOLEC & DEV BIOL LAB, BETHESDA, MD 20892 USA. NEI, NIH, CLIN BRANCH, BETHESDA, MD 20892 USA. BOSTON UNIV, SCH MED, DEPT BIOCHEM, BOSTON, MA 02118 USA. NIH, HOWARD HUGHES MED INST, RES SCHOLARS PROGRAM, BETHESDA, MD 20814 USA. RI Wawrousek, Eric/A-4547-2008 NR 30 TC 7 Z9 7 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 1043-4666 J9 CYTOKINE JI Cytokine PD APR PY 1996 VL 8 IS 4 BP 288 EP 293 DI 10.1006/cyto.1996.0038 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA UF850 UT WOS:A1996UF85000003 PM 9162217 ER PT J AU BarrettConnor, E Schrott, HG Greendale, G KritzSilverstein, D Espeland, MA Stern, MP Bush, T Perlman, JA AF BarrettConnor, E Schrott, HG Greendale, G KritzSilverstein, D Espeland, MA Stern, MP Bush, T Perlman, JA TI Factors associated with glucose and insulin levels in wealthy postmenopausal women SO DIABETES CARE LA English DT Article ID CARDIOVASCULAR RISK-FACTORS; DEPENDENT DIABETES-MELLITUS; CARBOHYDRATE-METABOLISM; ALCOHOL-CONSUMPTION; PHYSICAL-ACTIVITY; HEART-DISEASE; TOLERANCE; RESISTANCE; POPULATION; NIDDM AB OBJECTIVE - Little is known about the covariates of hyperglycemia and hyperinsulinemia. We examined candidate factors in postmenopausal women. RESEARCH DESIGN AND METHODS - We determined the cross-sectional associations of sociodemographic, body size, lifestyle, reproductive, and menopausal factors with pre-trial fasting and postchallenge glucose and insulin levels in 869 postmenopausal women aged 45-65 years. Women were participants in the Postmenopausal Estrogen/Progestin Interventions study who were not taking estrogen or insulin. RESULTS - Plasma glucose levels increased significantly with age; serum insulin levels did not. BMI and waist-to-hip ratio (WHR) each showed graded positive and independent associations with glucose and insulin levels. Alcohol intake, cigarette smoking, physical activity, parity, education, and income were also associated with insulin or glucose in age-adjusted models. In multivariable models, BMI and WHR explained 18% of the variability in fasting glucose, 16% in postchallenge glucose, 28% in fasting insulin, and 17% in postchallenge insulin. Age and all other factors combined accounted for <6% of the variance in glucose or insulin. In multiply adjusted models, African-American and Hispanic women had higher fasting and 2-h insulin levels than non-Hispanic white women. CONCLUSIONS - Most of the variance in glycemia and insulin is unexplained. Measures of obesity and fat distribution account for nearly all the explained variance. C1 UNIV CALIF LOS ANGELES,LOS ANGELES,CA. UNIV IOWA,IOWA CITY,IA. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. JOHNS HOPKINS UNIV,BALTIMORE,MD. NCI,BETHESDA,MD 20892. RP BarrettConnor, E (reprint author), UNIV CALIF SAN DIEGO,DEPT FAMILY & PREVENT MED,9500 GILMAN DR,LA JOLLA,CA 92093, USA. FU NHLBI NIH HHS [HL40154, U01-HL40185, HL40195] NR 45 TC 28 Z9 28 U1 1 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD APR PY 1996 VL 19 IS 4 BP 333 EP 340 DI 10.2337/diacare.19.4.333 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB885 UT WOS:A1996UB88500006 PM 8729156 ER PT J AU Nelson, RG Pettitt, DJ deCourten, MP Hanson, RL Knowler, WC Bennett, PH AF Nelson, RG Pettitt, DJ deCourten, MP Hanson, RL Knowler, WC Bennett, PH TI Parental hypertension and proteinuria in Pima Indians with NIDDM SO DIABETOLOGIA LA English DT Article DE diabetic nephropathy; hypertension; familial predisposition; non-insulin-dependent diabetes mellitus; Pima Indians ID SODIUM-LITHIUM COUNTERTRANSPORT; DEPENDENT DIABETES-MELLITUS; INCREASED BLOOD-PRESSURE; RED-CELLS; FAMILIAL AGGREGATION; RENAL-DISEASE; URINE SAMPLES; NEPHROPATHY; PREDISPOSITION; CHILDREN AB To determine if parental hypertension is associated with proteinuria in offspring with non-insulin-dependent diabetes mellitus (NIDDM), 438 diabetic Pima Indians (172 men, 266 women) aged 20 years or more and both of their parents were examined. Hypertension was defined as a systolic blood pressure 140 mm Hg or more, diastolic blood pressure 90 mm Hg or more, or treatment with antihypertensive medicine. Sixty-three percent of the fathers and 80 % of the mothers had diabetes at the time their blood pressure was measured. Families in which either parent had proteinuria, defined as a urine protein-to-creatinine ratio greater than or equal to 0.5 g/g were excluded; 73 (16.7 %) of the offspring had proteinuria. The prevalence rates of proteinuria in the offspring were similar if neither parent or only one parent had hypertension (8.9 and 9.4%, respectively), but was significantly higher if both parents had hypertension (18.8 %), after adjustment for age, sex, duration of diabetes, and 2-h post-load plasma glucose concentration in the offspring and diabetes in the parents by logistic regression. The odds for proteinuria being present in the offspring if both parents had hypertension was 2.2 times (95 % confidence interval, 1.2 to 4.2) that if only one parent had hypertension. When mean arterial pressure and blood pressure treatment in the offspring were added to the model the relationship remained (odds ratio = 2.2; 95 % confidence interval, 1.1 to 4.3). Hypertension in both parents is associated with the development of proteinuria in offspring with NIDDM. This relationship was present even when controlled for the effects of blood pressure and its treatment in the offspring. RP Nelson, RG (reprint author), NIDDK,PHOENIX EPIDEMIOL & CLIN RES BRANCH,NIH,1550 E INDIAN SCH RD,PHOENIX,AZ 85014, USA. RI Nelson, Robert/B-1470-2012; Hanson, Robert/O-3238-2015; de Courten, Maximilian/B-3300-2012 OI Hanson, Robert/0000-0002-4252-7068; de Courten, Maximilian/0000-0001-9997-9359 NR 32 TC 25 Z9 26 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD APR PY 1996 VL 39 IS 4 BP 433 EP 438 DI 10.1007/BF00400674 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB882 UT WOS:A1996UB88200007 PM 8777992 ER PT J AU Ghanayem, BI Burka, LT AF Ghanayem, BI Burka, LT TI Excretion and identification of methacrylonitrile metabolites in the bile of male F344 rats SO DRUG METABOLISM AND DISPOSITION LA English DT Article ID 2-CYANOETHYLENE OXIDE; ACRYLONITRILE; INVITRO; CYANIDE; GLUTATHIONE; MICE AB Methacrylonitrile (MAN) is structurally similar to the known carcinogen acrylonitrile (AN), has similar industrial uses, and is occasionally used as its replacement, In contrast to AN, minimal information is available on the toxicity, carcinogenicity, or metabolism of MAN, Earlier work in this laboratory demonstrated that, in rats, MAN is primarily eliminated in the expired air as unchanged MAN, acetone, and CO2. Two mercapturic acids were identified in the urine of rats and mice treated with MAN, In the present work, the common bile duct of anesthetized rats was cannulated, The animals received a single gavage dose of 58 mg/kg 2-[C-14]MAN, Bile was collected before and after MAN administration, Bile flow and MAN-derived radioactivity were determined at each time point. MAN had a minimal effect on bile flow and 4 to 6% of the administered MAN dose was excreted in the bile within 6 hr after dosing, HPLC analysis of bile showed two major metabolites, which were identified as 1-(S-glutathionyl)-2-propanene and 1-(S-glutathionyl)-2-cyanopropane by using NMR spectra and chemical synthesis, The ratio of the two metabolites in MAN-treated rats was approximately 2:1. Pretreatment of rats with sodium phenobarbital caused minimal quantitative or qualitative changes in the biliary excretion of MAN metabolites. In contrast, pretreatment of rats with beta-diethylaminoethyl diphenylpropylacetate before MAN administration resulted in a significant decrease in the ratio of 1-(S-glutathionyl)-2-propanone to 1-(S-glutathionyl)-2-cyanopropane (1:2). These data, especially the identification of 1-(S-glutathionyl)-2-propanone, indirectly demonstrated that MAN is metabolized via an epoxide intermediate (1-cyano-1-methyloxirane), Modulation of MAN metabolism by the P450 modulators suggested that this metabolic pathway is catalyzed via the cytochrome P450 enzymes, This work also confirms that MAN undergoes direct reaction with reduced glutathione via a Michael addition, Because earlier work demonstrated that AN undergoes similar metabolism, MAN might have a qualitative toxicity profile similar to that of acryonitrile. RP Ghanayem, BI (reprint author), NIEHS,NIH,POB 12233,RES TRIANGLE PK,NC 27709, USA. NR 14 TC 11 Z9 11 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-9556 J9 DRUG METAB DISPOS JI Drug Metab. Dispos. PD APR PY 1996 VL 24 IS 4 BP 390 EP 394 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UE830 UT WOS:A1996UE83000003 PM 8801052 ER PT J AU Bunnell, BA Morgan, RA AF Bunnell, BA Morgan, RA TI Gene therapy for HIV infection SO DRUGS OF TODAY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; CYTOTOXIC LYMPHOCYTES-T; HUMAN ADENOSINE-DEAMINASE; LONG-TERM EXPRESSION; WILD-TYPE VIRUS; ANTISENSE RNA; RETROVIRAL VECTORS; INTRACELLULAR IMMUNIZATION; SEROPOSITIVE INDIVIDUALS; TRANSDOMINANT MUTANTS AB The ultimate goal of gene theray for HIV-I is to inhibit viral replication and the resultant AIDS pathogenesis. Gene therapy for HIV-1 requires the introduction of genes that effectively inhibit viral replication by blocking expression of viral genes or altering the normal function of HIV-1 associated proteins. This review details the various anti-HIV-1 gene therapy strategies that have been developed to effectively inhibit HIV-1 replication. The review covers three broad categories: i) gene tehrapy using nucleic acid moieties such as gene vaccines, antisense DNA/RNA, RNA decoys, and ribozymes; ii) protein approaches such as trans-dominant negative proteins and single chain antibodies; and iii) immunotherapy using HIV-1 specific cytotoxic T cells. The discussion focuses on the effectiveness of the various techniques in preclinical experiments and in animal models. Also, the status of all of the current RAC/FDA approved clinical protocols for anti-HIV-1 gene therapy strategies is reviewed. RP Bunnell, BA (reprint author), NIH, CLIN GENE THERAPY BRANCH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA. NR 109 TC 3 Z9 4 U1 0 U2 1 PU PROUS SCIENCE, SA-THOMSON REUTERS PI BARCELONA PA PO BOX 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 1699-3993 J9 DRUG TODAY JI Drugs Today PD APR-MAY PY 1996 VL 32 IS 3 BP 209 EP 224 PG 16 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UT113 UT WOS:A1996UT11300002 ER PT J AU Chen, N Chrambach, A AF Chen, N Chrambach, A TI Enhanced field strength and resolution in gel electrophoresis upon substitution of buffer by histidine at its isoelectric point SO ELECTROPHORESIS LA English DT Article DE electrophoresis; isoelectric histidine; field strength; dispersion coefficient; resolution AB Gel electrophoresis in isoelectric buffers, recently introduced by R. Westermeier and H. Schickle (Electrophoresis '95, Paris, Abstract No. 3, 1995), was applied to the automated HPGE-1000 apparatus in the expectation to be able to increase the field strength under the limiting conditions of heat dissipation capacity and voltage of that apparatus. A previous attempt to achieve that aim by reduction of gel thickness had not yielded more than a twofold increment in resolving power. Replacing 0.2 X Tris-boric acid-EDTA (TEE) buffer, conventionally applied in the apparatus at 15 V/cm, by 0.05 M histidine, pH 7.6 (close to the pI of 7.47), allows one to increase the field strength to 60 V/cm, thus providing a nearly fivefold increment in resolution under otherwise identical conditions (fluorescein carboxylate-labeled conalbumin-sodium dodecyl sulfate (SDS) and soybean trypsin inhibitor-SDS samples, 10 degrees C, 4% MetaPhor agarose). An additional decrease in band dispersion can be obtained by decreasing the starting zone width through buffer dilution in the sample phase. C1 NICHHD,MACROMOLEC ANAL SECT,THEORET & PHYS BIOL LAB,NIH,BETHESDA,MD 20892. NR 10 TC 13 Z9 13 U1 1 U2 4 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD APR PY 1996 VL 17 IS 4 BP 699 EP 703 DI 10.1002/elps.1150170413 PG 5 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA UP016 UT WOS:A1996UP01600012 PM 8738330 ER PT J AU Chang, HT Zakharov, SF Chrambach, A AF Chang, HT Zakharov, SF Chrambach, A TI Separation and isolation of subcellular-sized particles by electrophoresis in polymer solution using the commercial scanning apparatus SO ELECTROPHORESIS LA English DT Article DE subcellular-sized particles; isolation; scanning apparatus AB Electrophoresis of fluorescently labeled rat liver microsomes and polystyrene carboxylates of 10 and 30 nm radius was conducted in buffered 10-15% polyvinylpyrrolidone (M(r) = 10(6)) solutions, using a horizontal gel electrophoresis apparatus with intermittent scanning of fluorescence (HPGE-1000, LabIntelligence). Banding, constant migration rates and Ferguson plots were obtained in these polymer solutions. The major microsome band detected by the automated scan was located visually on the gel by means of its fluorescein label and was isolated by volumetric withdrawal; recovery was monitored by scanning and ascertained to be near quantitative after three consecutive steps, in each of which 30 mu L were withdrawn. This preparative method promises to be generally applicable to particles that are too large to enter into gels. C1 NICHHD,MACROMOLEC ANAL SECT,THEORET & PHYS BIOL LAB,NIH,BETHESDA,MD 20892. RI Chang, Huan-Tsung/C-1183-2011 NR 11 TC 9 Z9 9 U1 0 U2 2 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD APR PY 1996 VL 17 IS 4 BP 776 EP 780 DI 10.1002/elps.1150170426 PG 5 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA UP016 UT WOS:A1996UP01600025 PM 8738343 ER PT J AU Weissenhorn, W Wharton, SA Calder, LJ Earl, PL Moss, B Aliprandis, E Skehel, JJ Wiley, DC AF Weissenhorn, W Wharton, SA Calder, LJ Earl, PL Moss, B Aliprandis, E Skehel, JJ Wiley, DC TI The ectodomain of HIV-1 env subunit gp41 forms a soluble, alpha-helical, rod-like oligomer in the absence of gp120 and the N-terminal fusion peptide SO EMBO JOURNAL LA English DT Article DE conformational change; envelope glycoprotein gp41; HIV-1; membrane fusion ID IMMUNODEFICIENCY-VIRUS TYPE-1; MURINE LEUKEMIA-VIRUS; ENVELOPE GLYCOPROTEIN; TRANSMEMBRANE PROTEIN; CD4 BINDING; STRUCTURAL PROTEINS; MEMBRANE-FUSION; HTLV-III; HEMAGGLUTININ; RECEPTOR AB The human immunodeficiency virus-1 (HIV-1) envelope glycoprotein is composed of a soluble glycopolypeptide gp120 and a transmembrane glycopolypeptide gp41, These subunits form non-covalently linked oligomers on the surface of infected cells, virions and cells transfected with the complete env gene. Two length variants of the extracellular domain of gp41 (aa 21-166 and aa 39-166), that both lack the N-terminal fusion peptide and the C-terminal membrane anchor and cytoplasmic domain, have been expressed in insect cells to yield soluble oligomeric gp41 proteins. Oligomerization was confirmed by chemical cross-linking and gel filtration. Electron microscopy and circular dichroism measurements indicate a rod-like molecule with a high alpha-helical content and a high melting temperature (78 degrees C). The binding of monoclonal antibody Fab fragments dramatically increased the solubility of both gp41 constructs, We propose that gp41 folds into its membrane fusion-active conformation, when expressed alone. C1 CHILDRENS HOSP,HOWARD HUGHES MED INST,MOLEC MED LAB,BOSTON,MA 02215. NIAID,NIH,BETHESDA,MD 20892. HARVARD UNIV,HOWARD HUGHES MED INST,DEPT MOLEC & CELLULAR BIOL,CAMBRIDGE,MA 02138. NATL INST MED RES,LONDON NW7 1AA,ENGLAND. FU NIGMS NIH HHS [GM39589] NR 37 TC 125 Z9 126 U1 0 U2 4 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR 1 PY 1996 VL 15 IS 7 BP 1507 EP 1514 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UF658 UT WOS:A1996UF65800004 PM 8612573 ER PT J AU McSweegan, E AF McSweegan, E TI The infectious diseases impact statement: A mechanism for addressing emerging diseases SO EMERGING INFECTIOUS DISEASES LA English DT Article ID EPIDEMIOLOGY; HEALTH AB The use of an Infectious Diseases Impact Statement (IDIS) is proposed for predictive assessments of local changes in infectious diseases arising from human-engineered activities. IDIS is intended to be analogous to an Environmental Impact Statement. The drafting of an IDIS for specific activities, particularly in developing nations, would provide a formal mechanism for examining potential changes in local health conditions, including infected and susceptible populations, diseases likely to fluctuate in response to development, existing control measures, and vectors likely to be affected by human activities. The resulting survey data could provide a rational basis and direction for development, surveillance, and prevention measures. An IDIS process that balances environmental alterations, local human health, and economic growth could substantially alter the nature of international development efforts and infectious disease outbreaks. RP McSweegan, E (reprint author), NIAID,NIH,SOLAR BLDG,RM 3A34,BETHESDA,MD 20892, USA. NR 20 TC 6 Z9 6 U1 1 U2 2 PU CENTER DISEASE CONTROL PI ATLANTA PA ATLANTA, GA 30333 SN 1080-6040 J9 EMERG INFECT DIS JI Emerg. Infect. Dis PD APR-JUN PY 1996 VL 2 IS 2 BP 103 EP 108 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UM787 UT WOS:A1996UM78700004 PM 8903209 ER PT J AU Pu, LP Ma, W Barker, JL Loh, YP AF Pu, LP Ma, W Barker, JL Loh, YP TI Differential coexpression of genes encoding prothyrotropin-releasing hormone (Pro-TRH) and prohormone convertases (PC1 and PC2) in rat brain neurons: Implications for differential processing of Pro-TRH SO ENDOCRINOLOGY LA English DT Article ID MESSENGER RIBONUCLEIC-ACID; CENTRAL-NERVOUS-SYSTEM; PROPROTEIN CONVERTASE; INSITU HYBRIDIZATION; IDENTIFICATION; EXPRESSION; PEPTIDES; KEX2; LOCALIZATION; ENDOPROTEASE AB Pro-TRH is cleaved at paired basic residues to yield five copies of TRH and cryptic peptides. Recent studies have shown that the prohormone convertases, PC1 and PC2, can process pro-TRH correctly. To determine whether these two enzymes could play a role in pro-TRH processing in vivo, the regional and cellular colocalization of pro-TRH messenger RNA (mRNA) with the mRNAs encoding the prohormone convertases PC1 and PC2 was examined in rat brain, using in situ hybridization histochemistry. Differential regional distribution of pro-TRH mRNA with PC1 and/or PC2 mRNA was found in several brain regions. For example, in the olfactory regions, there was coexpression of pro-TRH mRNA in the glomerular layer with PC2 mRNA, but not PC1 mRNA, whereas in the tenia tecta, coexpression of pro-TRH and PC1 mRNAs was evident, but PC2 mRNA was absent. Pro-TRH mRNA in the paraventricular nucleus was coexpressed with both PC1 and PC2 mRNAs, whereas the basal lateral hypothalamus showed coexistence of pro-TRH mRNA with PC2 mRNA, but not PC1 mRNA. Interestingly, pro-TRH was expressed in the thalamic reticular nucleus, but neither PC1 nor PC2 was detectable in this region. Cellular colocalization studies using double in situ hybridization histochemistry showed the presence of PC2 mRNA in the pro-TRH neurons of the olfactory glomerular layer and basal lateral hypothalamus, and PC1 mRNA in the pro-TRH neurons in the paraventricular nucleus. These results suggest that PC1 and PC2 are enzyme candidates for the processing of pro-TRH in vivo. Moreover, the differential distribution of PC1 and PC2 mRNAs with pro-TRH mRNA may be responsible for the differential processing of this prohormone in the central nervous system. The absence of PC1 and PC2 mRNAs in certain TRH neurons raises the possibility that prohormone convertases other than PC1 and PC2 may be involved in the processing of brain pro-TRH. C1 NICHHD, CELLULAR NEUROBIOL SECT, DEV NEUROBIOL LAB, NIH, BETHESDA, MD 20892 USA. NINCDS, NEUROPHYSIOL LAB, NIH, BETHESDA, MD 20892 USA. NR 39 TC 35 Z9 35 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1996 VL 137 IS 4 BP 1233 EP 1241 DI 10.1210/en.137.4.1233 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB891 UT WOS:A1996UB89100013 PM 8625894 ER PT J AU Moy, E Kimzey, LM Nelson, LM Blithe, DL AF Moy, E Kimzey, LM Nelson, LM Blithe, DL TI Glycoprotein hormone alpha-subunit functions synergistically with progesterone to stimulate differentiation of cultured human endometrial stromal cells to decidualized cells: A novel role for free alpha-subunit in reproduction SO ENDOCRINOLOGY LA English DT Article ID HUMAN CHORIONIC-GONADOTROPIN; FACTOR-BINDING PROTEIN-1; INVITRO DECIDUALIZATION; PREMATURE LUTEINIZATION; LEUPROLIDE ACETATE; HUMAN PROLACTIN; PREGNANCY; GROWTH; SECRETION; SERUM AB Glycoprotein hormone-free alpha subunit is secreted by the pituitary throughout the menstrual cycle and by the placenta during pregnancy. We showed previously that free a subunit stimulated PRL secretion from term pregnancy decidual cells, suggesting a function for free alpha in pregnancy. However, no role has been ascribed to free alpha in the normal menstrual cycle. Using an in vitro model, we examined the role of alpha subunit in regulating human endometrial stromal cell differentiation (decidualization). PRL and insulin-like growth factor binding protein-1 (IGFBP-1), specific decidual secretory products, were used as markers of decidualization. We found that alpha subunit acted synergistically with progesterone (P) to induce more rapid decidualization with higher output (2- to 6-fold) of PRL and IGFBP-1, compared with P alone (P < 0.01). The effect of a was dose dependent, with stimulatory activity starting at 0.05 ng/ml and reaching maximal levels at 1-2 ng/ml. These levels correspond to serum concentrations of free alpha found during the luteal phase of the menstrual cycle when endometrial decidualization occurs in vivo. These findings demonstrate new biological activity for a subunit in the regulation of human endometrial decidualization and indicate that free alpha plays a role in human reproduction. Furthermore, demonstration of potential bioactivities of free a subunit has important implications for understanding normal endocrine function and various pathological conditions. C1 NIH, CTR CLIN, DEPT NURSING, BETHESDA, MD 20892 USA. NICHHD, DEV ENDOCRINOL BRANCH, SECT GYNECOL RES, BETHESDA, MD 20892 USA. NICHHD, DEV ENDOCRINOL BRANCH, UNIT GLYCOBIOL, BETHESDA, MD 20892 USA. NR 48 TC 36 Z9 36 U1 2 U2 3 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1996 VL 137 IS 4 BP 1332 EP 1339 DI 10.1210/en.137.4.1332 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB891 UT WOS:A1996UB89100027 PM 8625908 ER PT J AU Gomez, G Padilla, L Udupi, V Tarasova, N Sundler, F Townsend, CM Thompson, JC Greeley, GH AF Gomez, G Padilla, L Udupi, V Tarasova, N Sundler, F Townsend, CM Thompson, JC Greeley, GH TI Regulation of peptide YY homeostasis by gastric acid and gastrin SO ENDOCRINOLOGY LA English DT Article ID RELEASE; SECRETION; GUT; DOG; PANCREAS; RAT AB Peptide YY (PYY) is a gut hormone localized primarily in the distal bowel. Because circulating PW inhibits gastric acid secretion, we investigated the effects of gastric acid secretion and gastrin on gene expression and secretion of PW. In conscious dogs, PYY release in response to oral food was inhibited (P < 0.05) by pharmacologic inhibition of gastric acid secretion (omeprazole, famotidine). In rats, omeprazole treatment resulted in a significant elevation in serum gastrin concentrations and a simultaneous decrease in PYY messenger RNA (mRNA) and peptide levels in the colon; administration of a gastrin receptor antagonist (L365, 260) prevented the inhibitory actions of omeprazole on colonic PYY mRNA levels. In athymic-nude mice, implantation of a human gastrinoma resulted in an elevation of serum gastrin concentrations and a concomitant depression of colonic PYY mRNA levels. We conclude that endogenous gastric acid secretion up-regulates PYY release and PYY mRNA expression. Circulating gastrin acts to down-regulate PYY release and PYY mRNA expression. This study provides evidence that foregut functions (i.e., gastric acid secretion and gastrin release) exert control over an antiacid signal (e.g. PYY release) emanating from the hindgut. C1 UNIV TEXAS, MED BRANCH, DEPT SURG, GALVESTON, TX 77555 USA. NCI, MOLEC ASPECTS DRUG DESIGRN SECT, FREDERICK, MD 21702 USA. LUND UNIV, DEPT MED CELL RES, S-22362 LUND, SWEDEN. FU NIDDK NIH HHS [DK-15241] NR 24 TC 12 Z9 12 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1996 VL 137 IS 4 BP 1365 EP 1369 DI 10.1210/en.137.4.1365 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB891 UT WOS:A1996UB89100031 PM 8625912 ER PT J AU Malik, KF Young, WS AF Malik, KF Young, WS TI Localization of binding sites in the central nervous system for leptin (OB protein) in normal, obese (ob/ob), and diabetic (db/db) C57BL/6J mice. SO ENDOCRINOLOGY LA English DT Article ID RECEPTORS; BRAIN AB Leptin (OB protein) fused to the FLAG epitope and a kinase recognition site was expressed in bacteria, immunopurified, and phosphorylated using [gamma-(33)p] ATP. The resulting probe was used to characterize the distribution of leptin binding sites within brain sections of normal, ob/ob, and db/db C57BL/6J male mice. Leptin binding sites were found in leptomeninges and choroid plexus. Leptin binding within the choroid plexus is slightly elevated in ob/ob mice when compared to normal males (p<0.05). Binding of leptin by the choroid plexus of db/db male mice is lower than in normal males (p<0.05), but normally distributed. Based on the association and dissociation rates of leptin binding on tissue sections, we estimate the KD of the choroid plexus site at 0.25x10(-9) M. From our results, we hypothesize that the binding of leptin to its site may cause the release or transport of uncharacterized factor(s) into the cerebral spinal fluid (CSF) to affect neuronal populations controlling feeding and metabolism. RP Malik, KF (reprint author), NIMH, CELL BIOL LAB, NIH, BETHESDA, MD 20892 USA. RI Young, W Scott/A-9333-2009 OI Young, W Scott/0000-0001-6614-5112 NR 11 TC 98 Z9 99 U1 0 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1996 VL 137 IS 4 BP 1497 EP 1500 DI 10.1210/en.137.4.1497 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB891 UT WOS:A1996UB89100048 PM 8625929 ER PT J AU Hattis, D Glowa, J Tilson, H Ulbrich, B AF Hattis, D Glowa, J Tilson, H Ulbrich, B TI Risk assessment for neurobehavioral toxicity: SGOMSEC Joint Report SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT 11th SGOMSEC Workshop/19th Rochester International Conference on Environmental Toxicity - Risk Assessment for Neurobehavioral Toxicity CY JUN 12-17, 1994 CL ROCHESTER, NY SP Sci Grp Methodol Safety Evaluat Chem, Sci Comm Problems Environm, Int Programme Chem Safety, WHO, NIEHS, Univ Rochester DE benchmark dose; effect levels; identification of neurotoxicity; interindividual variability; quantitative models; reference doses; regulatory activity; reversibility ID NEUROTOXICOLOGY; CHEMICALS; HAIR; TIME AB Behavioral end points for neurotoxicity risk assessment have been developed and examined over the past three decades. They are now ready to move from simple qualitative guidelines, such as exemplified by reference doses, to more quantitative models, such as benchmark doses, based on dose-response information. Risk assessors, confronted by a wider array of methodologies and data than in the past, should be offered guidance in interpretation because now they have to deal with unaccustomed questions and problems. These include reversibility, susceptible populations, multiple end points, and the details of dose-response and dose-effect distributions. C1 NIDDKD,LMC,NIH,BETHESDA,MD 20892. US EPA,RES TRIANGLE PK,NC 27711. BUNDESGESUNDHEITSAMT,INST ARZBEUNUTTEK,W-1000 BERLIN,GERMANY. RP Hattis, D (reprint author), CLARK UNIV,MARSH INST CTR TECHNOL ENVIRONM & DEV,950 MAIN ST,WORCESTER,MA 01610, USA. NR 44 TC 4 Z9 4 U1 0 U2 1 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1996 VL 104 SU 2 BP 217 EP 226 DI 10.2307/3432643 PG 10 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA UL607 UT WOS:A1996UL60700006 PM 8860324 ER PT J AU Alavanja, MCR Sandler, DP McMaster, SB Zahm, SH McDonnell, CJ Lynch, CF Pennybacker, M Rothman, N Dosemeci, M Bond, AE Blair, A AF Alavanja, MCR Sandler, DP McMaster, SB Zahm, SH McDonnell, CJ Lynch, CF Pennybacker, M Rothman, N Dosemeci, M Bond, AE Blair, A TI The agricultural health study SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE cancers; exposure assessment; farmers; lymphoma; noncancer toxicity; pesticides; prospective cohort ID CANCER MORTALITY; FARMERS; CANADA; RISKS AB The Agricultural Health Study, a large prospective cohort study, has been initiated in North Carolina and Iowa. The objectives of this study are to: 1) identify and quantify cancer risks among men, women, whites, and minorities associated with direct exposure to pesticides and other agricultural agents; 2) evaluate noncancer heath risks including neurotoxicity, reproductive effects, immunologic effects, nonmalignant respiratory disease, kidney disease, and growth and development among children; 3) evaluate disease risks among spouses and children of farmers that may arise from direct contact with pesticides and agricultural chemicals used in the home, lawns and gardens, and from indirect contact, such as spray drift, laundering work clothes, or contaminated food or water; 4) assess current and past occupational and nonoccupational agricultural exposures using periodic interviews and environmental and biologic monitoring, 5) study the relationship between agricultural exposures, biomarkers of exposure, biologic effect, and genetic susceptibility factors relevant to carcinogenesis; and 6) identify and quantify cancer and other disease risks associated with lifestyle factors such as diet, cooking practices, physical activity, smoking and alcohol consumption, and hair dye use. In the first year of a 3-year enrollment period, 26,235 people have been enrolled in the study including 19,776 registered pesticide applicators and 6,459 spouses of registered farmer applicators. It is estimated that when the total cohort is assembled in 1997 it will include approximately 75,000 adult study subjects. Farmers, the largest group of registered pesticide applicators, comprise 77% of the target population enrolled in the study. This experience compares favorably with enrollment rates of previous prospective studies. C1 NIEHS,RES TRIANGLE PK,NC 27709. SRA TECHNOL INC,FALLS CHURCH,VA 22042. UNIV IOWA,IOWA CITY,IA 52242. SURVEY RES ASSOCIATES,DURHAM,NC 27713. US EPA,RES TRIANGLE PK,NC 27711. RP Alavanja, MCR (reprint author), NCI,DIV CANC EPIDEMIOL & GENET,EPN-418,6130 EXECUT BLVD,BETHESDA,MD 20892, USA. RI Zahm, Shelia/B-5025-2015; OI Sandler, Dale/0000-0002-6776-0018 FU NCI NIH HHS [N01-CP-21095, N01-CP-33047, N01-CP-33048] NR 40 TC 288 Z9 292 U1 6 U2 41 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1996 VL 104 IS 4 BP 362 EP 369 DI 10.2307/3432672 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA UH994 UT WOS:A1996UH99400008 PM 8732939 ER PT J AU Glowa, JR AF Glowa, JR TI Dose-response analysis in risk assessment: Evaluation of behavioral specificity SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article; Proceedings Paper CT 11th SGOMSEC Workshop/19th Rochester International Conference on Environmental Toxicity - Risk Assessment for Neurobehavioral Toxicity CY JUN 12-17, 1994 CL ROCHESTER, NY SP Sci Grp Methodol Safety Evaluat Chem, Sci Comm Problems Environm, Int Programme Chem Safety, WHO, NIEHS, Univ Rochester DE risk assessment; drug abuse; rhesus monkeys; GBR 12909; schedule-controlled behavior; neurotoxicology ID MOLECULAR MECHANISMS; RHESUS-MONKEYS; COCAINE; INHIBITORS; FOOD AB Several methods of quantitative risk assessment that have been described recently are particularly applicable to neurotoxic end points. These methods can be broadly divided into two types of approaches based on their treatment of dose-response data to estimate risks. Benchmark approaches estimate risks using variability in response to a fixed dose level in comparison with background control variability. Probabilistic approaches estimate risks using the variability in the dose to produce a small effect in the sample population. The current report seeks to extend the development of probabilistic approaches for neurotoxic end points. Because behavioral data are often used to assess therapeutic efficacy as well as toxicity (unwanted effects), this analysis focused on the relative risks of producing these effects with the same agent. The therapeutic potential of GBR 12909 was determined by its ability to decrease cocaine-maintained responding in monkeys. The effects of this agent were also assessed in the same monkeys using food-maintained responding to provide an indication of behavioral toxicity. GBR 12909 decreased both behaviors, with complete decreases on drug-seeking behavior occurring al doses that had minimal effects on food-maintained responding. The difference in the estimates of doses to decrease drug-seeking and food-maintained behavior suggested that specific therapeutic effects could be obtained in the absence of unwanted side effects for a definable proportion of the population. These results also suggest that multiple behavioral end points can be useful for identifying specific effects of chemicals for the purposes of risk assessment. RP Glowa, JR (reprint author), NIDDK, NIH,LMC,BEHAV PHARMACOL UNIT,BLDG 14D, ROOM 311, BETHESDA, MD 20892 USA. FU ONDIEH CDC HHS [RA-ND-94-24] NR 36 TC 4 Z9 4 U1 1 U2 1 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 EI 1552-9924 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD APR PY 1996 VL 104 SU 2 BP 391 EP 396 DI 10.2307/3432659 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA UL607 UT WOS:A1996UL60700022 PM 9182046 ER PT J AU Ford, PA Arbuck, SG Minniti, C Miller, LL DeMaria, D ODwyer, PJ AF Ford, PA Arbuck, SG Minniti, C Miller, LL DeMaria, D ODwyer, PJ TI Phase I trial of etoposide, doxorubicin and cisplatin (EAP) in combination with GM-CSF SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE phase I trial; GM-CSF; etoposide; doxorubicin; cisplatin ID COLONY-STIMULATING FACTOR; HIGH-DOSE CHEMOTHERAPY; NON-HODGKINS-LYMPHOMA; GASTRIC-CANCER; BREAST-CANCER; GRANULOCYTE AB The aim of this study was to ameliorate the toxicity of the etoposide, doxorubicin and cisplatin (EAP) regimen and to investigate the feasibility of dose escalation, using the molgramostim form of granulocyte macrophage-colony stimulating factor (GM-CSF) 10 mu g/kg/day s.c. into the regimen. The design of the trial allowed for amended scheduling of the agents in the event of suboptimal results. Initially the regimen comprised etoposide 120 mg/m(2), days 1-3, doxorubicin 40 mg/m(2), day 1, and cisplatin 40 mg/m(2), days 2 and 8. GM-CSF was begun on day 4 and continued until recovery of granulocyte counts. Courses were repeated every 21 days. 3 patients were treated at these doses. 5 patients received escalated doses (etoposide 180 mg/m(2); doxorubicin 60 mg/m(2) cisplatin 60 mg/m(2)) on this schedule; 4 out of 5 had intolerable myelosuppression (grade IV neutropenia or thrombocytopenia lasting greater than or equal to 7 days). These results prompted the administration of the day 8 cisplatin dose on day 3, with GM-CSF beginning on day 4. At the lowest doses of each agent (etoposide 120-doxorubicin 40-cisplatin 40), 3 of 6 patients had intolerable myelosuppression, and 3 patients had febrile neutropenia. Dose escalation of all of the drugs to etoposide 180 mg/m(2), doxorubicin 60 mg/m(2), cisplatin 60 mg/m(2) resulted in documented infections in 4 out of 4 patients. GM-CSF toxicity included rash, dyspnoea, arrhythmias and pericardial effusions. The conclusion was that the use of GM-CSF does not permit escalation of drug doses on either schedule of EAP administration, and that these results do not support the combined use of GM-CSF and EAP. (C) 1996 Elsevier Science Ltd C1 FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. ROSWELL PK MEM INST,BUFFALO,NY. NCI,BETHESDA,MD 20892. FU NCI NIH HHS [CA 06972, CA 49820] NR 33 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD APR PY 1996 VL 32A IS 4 BP 631 EP 635 DI 10.1016/0959-8049(95)00602-8 PG 5 WC Oncology SC Oncology GA UJ370 UT WOS:A1996UJ37000018 PM 8695266 ER PT J AU Mannisto, S Pietinen, P Haukka, J Ovaskainen, ML Albanes, D Virtamo, J AF Mannisto, S Pietinen, P Haukka, J Ovaskainen, ML Albanes, D Virtamo, J TI Reported alcohol intake, diet and body mass index in male smokers SO EUROPEAN JOURNAL OF CLINICAL NUTRITION LA English DT Article ID UNITED-STATES ADULTS; DRINKING PATTERN; NUTRIENT INTAKE; SMOKING-HABITS; CONSUMPTION; MEN; POPULATION; PREVALENCE; DISEASE; ETHANOL AB Objective: The study was carried out to determine associations of reported alcohol intake with diet and body mass index. Type and frequency of consumed alcohol were also considered. Design: A cross-sectional study. Setting: The baseline examination of the participants of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study in 1985-1988. Subjects: 27 215 middle-aged Finnish male smokers. Interventions: The diet was assessed by a self-administered food use questionnaire: Subject's habitual diet and alcohol intake over the previous 12 months were asked. Body mass index was used as the measure of adiposity. Results: Energy intake from food was not related to alcohol intake. Although alcohol consumption was associated with food selection (eg berry and coffee consumption), this only slightly influenced daily nutrient intakes. Intake of spirits was more consistently related to higher body mass index than that of other alcoholic beverages. Daily alcohol intake had a much smaller association with body mass index than less frequent use, independently of the total consumption. Conclusions: The differences in nutrient intake between abstainers, light and moderate alcohol consumers were small although the consumption of many foods varied with alcohol consumption. Even if alcohol consumption is one noteworthy factor associated with weight, the energy from alcohol increases body weight less than expected; both the type and frequency of consumed alcohol may explain why energy from alcohol is utilized less efficiently than nonalcoholic energy. C1 NATL PUBL HLTH INST,CANC PREVENT UNIT,HELSINKI,FINLAND. NCI,CANC PREVENT STUDIES BRANCH,BETHESDA,MD 20892. RP Mannisto, S (reprint author), NATL PUBL HLTH INST,DEPT NUTR,HELSINKI,FINLAND. RI Albanes, Demetrius/B-9749-2015; Haukka, Jari/G-1484-2014 OI Haukka, Jari/0000-0003-1450-6208 FU NCI NIH HHS [N01-CN-45165] NR 33 TC 15 Z9 15 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0954-3007 J9 EUR J CLIN NUTR JI Eur. J. Clin. Nutr. PD APR PY 1996 VL 50 IS 4 BP 239 EP 245 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA UD595 UT WOS:A1996UD59500007 PM 8730611 ER PT J AU Newmann, RD AF Newmann, RD TI Findings of the Advisory Committee on human radiation experiments SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material RP Newmann, RD (reprint author), NIH,BLDG 10,BETHESDA,MD 20892, USA. 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 APR PY 1996 VL 23 IS 4 BP 476 EP 477 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UE802 UT WOS:A1996UE80200022 ER PT J AU Wassermann, EM Samii, A Mercuri, B Ikoma, K Oddo, D Grill, SE Hallett, M AF Wassermann, EM Samii, A Mercuri, B Ikoma, K Oddo, D Grill, SE Hallett, M TI Responses to paired transcranial magnetic stimuli in resting, active, and recently activated muscles SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE motor cortex; exercise; transcranial magnetic stimulation; inhibition; paired stimuli; human ID MOTOR CORTEX; BRAIN-STIMULATION; CORTICAL STIMULI; SILENT PERIOD; POTENTIALS AB Transcranial magnetic stimulation (TMS) causes the corticospinal system to become refractory to subsequent stimuli for up to 200 ms. We examined the phenomenon of paired pulse inhibition with TMS under conditions of rest, ongoing voluntary activation (isometric force generation), and at variable delays following activation (postactivation) of the wrist extensors of seven normal subjects, Paired stimuli were delivered to the motor cortex with a circular coil at 1.1 times motor evoked potential (MEP) threshold, with various interstimulus intervals. Voluntary activation caused a marked decrease in the variability of the ratio of the amplitude of the MEP evoked by the test pulse to that of the MEP evoked by the conditioning pulse. Marked inhibition of the MEP evoked by the test pulse was still present. Postactivation, however, caused a dramatic reversal of the inhibitory effect of the conditioning pulse in all subjects at interstimulus intervals ranging from 40 to 120 ms. This effect lasted for up to 10 s following the cessation of activation. MEPs to transcranial electrical stimulation were also inhibited by conditioning TMS, but postactivation did not reverse this inhibition, indicating that the reversal of paired pulse inhibition is intracortical. We conjecture that paired pulse inhibition reflects activity of inhibitory interneurons or inhibitory connections between cortical output cells that are inactivated in the postactivation state. C1 NINCDS,NIH,MED NEUROL BRANCH,HUMAN MOTOR CONTROL SECT,BETHESDA,MD 20892. RI Ikoma, Katsunori/D-8158-2012 NR 21 TC 120 Z9 121 U1 1 U2 9 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PD APR PY 1996 VL 109 IS 1 BP 158 EP 163 PG 6 WC Neurosciences SC Neurosciences & Neurology GA UG931 UT WOS:A1996UG93100019 PM 8740220 ER PT J AU Heindel, JJ Bates, HK Price, CJ Marr, MC Myers, CB Schwetz, BA AF Heindel, JJ Bates, HK Price, CJ Marr, MC Myers, CB Schwetz, BA TI Developmental toxicity evaluation of sodium fluoride administered to rats and rabbits in drinking water SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID ZERO DOSE CONTROL; ENAMEL FLUORIDE; ETHYLENE-GLYCOL; REPRODUCTION; EXPOSURE; PLASMA; MICE; CORD AB Sodium fluoride (NaF; Cas No. 7681-49-4) is used in fluoridating municipal water supplies, resulting in chronic exposure of millions of people worldwide. Because of a lack of pertinent developmental toxicity studies in the literature, sodium fluoride was administered ad libitum in deionized/filtered drinking water (to mimic human exposure) to Sprague-Dawley-derived rats (26/group) on Gestation Days (GD) 6 through 15 at levels of 0, 50, 150, or 300 ppm and New Zealand White rabbits (26/group) on GD 6 through 19 at levels of 0, 100, 200, or 400 ppm. Higher concentrations via drinking water were not practicable due to the poor palatability of sodium fluoride. Drinking water (vehicle) contained less than 0.6 ppm sodium fluoride (limit of detection) and sodium fluoride content of the feed was 12.4 ppm fluoride (rats) and 15.6 ppm fluoride (rabbits). Maternal food, water, body weights, and clinical signs were recorded at regular intervals throughout these studies. Animals were killed on GD 20 (rats) or 30 (rabbits) and examined for implant status, fetal weight, sex, and morphological development. In the high-dose group of both studies there was an initial decreased maternal body weight gain which recovered over time and a decreased water consumption-attributed to decreased palatability. No clear clinical signs of toxicity were observed. Maternal exposure to sodium fluoride during organogenesis did not significantly affect the frequency of postimplantation loss, mean fetal body weight/litter, or external, visceral or skeletal malformations in either the rat or the rabbit. The NOAEL for maternal toxicity was 150 ppm sodium fluoride in drinking water (similar to 18 mg/kg/day) for rats, and 200 ppm (similar to 18 mg/kg/day) for rabbits. The NOAEL for developmental toxicity was greater than or equal to 300 ppm sodium fluoride (similar to 27 mg/kg/day) for rats and greater than or equal to 400 ppm (similar to 29 mg/kg/day) for rabbits administered during organogenesis in drinking water. The total exposure to fluoride (mg F/kg body weight/day from food and drinking water combined) in the mid- and high-dose groups for both species was >100-fold higher than the range at 0.014-0.08 mg F/kg/day estimated for a 70-kg person from food and fluoridated (1 ppm) drinking water. (C) 1996 Society of Toxicology C1 NIEHS, NATL TOXICOL PROGRAM, RES TRIANGLE PK, NC 27709 USA. RP Heindel, JJ (reprint author), RES TRIANGLE INST, CTR LIFE SCI & TOXICOL, RES TRIANGLE PK, NC 27709 USA. FU NIEHS NIH HHS [N01-ES-95255] NR 56 TC 23 Z9 24 U1 2 U2 4 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1996 VL 30 IS 2 BP 162 EP 177 DI 10.1006/faat.1996.0053 PG 16 WC Toxicology SC Toxicology GA UF098 UT WOS:A1996UF09800002 PM 8812262 ER PT J AU Zenilman, ME Magnuson, TH Swinson, K Egan, J Perfetti, R Shuldiner, AR AF Zenilman, ME Magnuson, TH Swinson, K Egan, J Perfetti, R Shuldiner, AR TI Pancreatic thread protein is mitogenic to pancreatic-derived cells in culture SO GASTROENTEROLOGY LA English DT Article ID CHRONIC CALCIFYING PANCREATITIS; MESSENGER-RNA; STONE PROTEIN; REGENERATING ISLETS; ENDOCRINE PANCREAS; EXPRESSION; SEQUENCE; EXOCRINE; GENE; ACINAR AB Background & Aims: Pancreatic thread proteins (PTPs) ave acinar cell products and members of the regenerating gene (reg) family. reg expression increases during islet regeneration, is depressed during aging-related islet dysfunction, and may be important in p-cell growth and maintenance. The aim of this study was to examine the genetic expression of reg in pancreatic-derived cells in vitro and the mitogenic effect of PTP/reg protein on these cells. Methods: reg gene expression was measured by Northern analysis in three rat pancreatic cell lines: ARIP (ductal), AR42J (acinar), and RIN (beta-cell). PTP/reg protein was isolated from bovine and human pancreas. Cells were cultured with PTP/reg for 72 hours, and thymidine incorporation was measured. Results: reg messenger RNA was detected in AR42J but not in ARIP or RIN. PTP/reg protein was mitogenic to RIN and ARIP in a dose-related fashion but not to AR42J. It was not mitogenic to cultured mature rat islets. Conclusions: reg messenger RNA is expressed in acinar but not in beta-cell or ductal pancreatic cell lines. PTP/reg protein was mitogenic to both beta-cell and ductal cell lines but not to mature, nondividing islets. This supports the hypothesis that PTP/reg protein is an acinar cell-derived mediator of beta-cell growth and may be involved in modulating the duct-to-islet axis. C1 NIA,NIH,LAB CLIN PHYSIOL,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT SURG,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. NR 39 TC 58 Z9 59 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 BP 1208 EP 1214 DI 10.1053/gast.1996.v110.pm8613011 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UD846 UT WOS:A1996UD84600029 PM 8613011 ER PT J AU Carethers, JM Koi, M Chauhan, DP Boland, CR AF Carethers, JM Koi, M Chauhan, DP Boland, CR TI The human mismatch repair system recognizes the O-6-methylguanine (O-6-meG) mispair after the first S phase to cause G2/M cell cycle arrest SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO, SAN DIEGO, CA 92103 USA. VAMC, SAN DIEGO, CA USA. NIEHS, RES TRIANGLE PK, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A498 EP A498 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701979 ER PT J AU Corleto, VD Jensen, RT Weber, HC AF Corleto, VD Jensen, RT Weber, HC TI Somatostatin receptor subtype expression in guinea pig colonic smooth muscle cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK, DIGEST DIS BRANCH, NIH, BETHESDA, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A650 EP A650 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702584 ER PT J AU Dickson, RC Everhart, JE AF Dickson, RC Everhart, JE TI Transmission of hepatitis B by transplantation of livers from donors positive for antibody to hepatitis B core antigen. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK, LIVER TRANSPLANTAT DATABASE, GAINESVILLE, FL USA. UNIV FLORIDA, GAINESVILLE, FL 32611 USA. NIDDKD, BETHESDA, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1182 EP A1182 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704706 ER PT J AU Everhart, JE AF Everhart, JE TI Incidence of self-reported peptic ulcer in the United States. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV NEW MEXICO, ALBUQUERQUE, NM 87131 USA. NIDDKD, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A105 EP A105 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73700414 ER PT J AU Felley, CP Saraga, E Ambs, S Friess, H Diezi, J Blum, AL FelleyBosco, E AF Felley, CP Saraga, E Ambs, S Friess, H Diezi, J Blum, AL FelleyBosco, E TI Nitric oxide synthases and oxidant stress in human stomach cancer and peritumoral tissue SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NATL CANC INST, BETHESDA, MD USA. UNIV HOSP BERN, DEPT SURG, CH-3010 BERN, SWITZERLAND. UNIV LAUSANNE HOSP, DEPT GASTROENTEROL & PATHOL, LAUSANNE, SWITZERLAND. UNIV LAUSANNE, INST PHARMACOL & TOXICOL, CH-1015 LAUSANNE, SWITZERLAND. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A511 EP A511 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702032 ER PT J AU Ferrin, LJ CameriniOtero, RD Fleischer, D Tio, L AF Ferrin, LJ CameriniOtero, RD Fleischer, D Tio, L TI An integrated approach to the rapid analysis of DNA rearrangements in GI malignancies. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK, GENET & BIOCHEM BRANCH, BETHESDA, MD USA. GEORGETOWN UNIV, MED CTR, DIV GASTROENTEROL, WASHINGTON, DC 20007 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1190 EP A1190 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704736 ER PT J AU Fuss, I Kelsall, B Strober, W Neurath, M AF Fuss, I Kelsall, B Strober, W Neurath, M TI TNBS-induced experimental granulomatous colitis in mice is abrogated by the induction of TGF-beta mediated oral tolerance. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH, MUCOSAL IMMUN SECT, BETHESDA, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A912 EP A912 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703628 ER PT J AU Garcia, LJ Rosado, JA Tsuda, T Jensen, RT AF Garcia, LJ Rosado, JA Tsuda, T Jensen, RT TI Both low and high affinity CCK receptor states mediate CCK stimulation of p125 focal adhesion kinase and paxillin tyrosine phosphorylation in rat pancreatic acinar cells SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV EXTREMADURA, DEPT PHYSIOL, E-10080 CACERES, SPAIN. NIDDK, NIH, DIGEST DIS BRANCH, BETHESDA, MD USA. RI rosado, juan/H-3488-2015 OI rosado, juan/0000-0002-9749-2325 NR 0 TC 3 Z9 3 U1 1 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A390 EP A390 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701553 ER PT J AU Gibril, F Termanini, B Stewart, CA Sutliff, VE Jensen, RT AF Gibril, F Termanini, B Stewart, CA Sutliff, VE Jensen, RT TI Prospective study of the occurrence of metastases to bone in patients with Zollinger-Ellison syndrome (ZES). SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIDDK, DIGEST DIS BRANCH, NIH, BETHESDA, MD USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1073 EP A1073 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704272 ER PT J AU Gibril, F Fraker, DL Alexander, HR Termanini, B Stewart, CA Sutliff, VE Jensen, RT AF Gibril, F Fraker, DL Alexander, HR Termanini, B Stewart, CA Sutliff, VE Jensen, RT TI Does the use of preoperative somatostatin receptor scintigraphy (SRS) have an impact in improving postoperative cure rate in patients undergoing surgery with Zollinger Ellison syndrome (ZES): A prospective study SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NIH, BETHESDA, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A391 EP A391 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701556 ER PT J AU Guo, YS Evers, BM Ives, K Battey, JF Thompson, JC Townsend, CM AF Guo, YS Evers, BM Ives, K Battey, JF Thompson, JC Townsend, CM TI Effect of transfection of gastrin releasing peptide-receptors (GRP-R) on the expression of neurotensin receptors (NT-R) in BON cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UTMB, DEPT SURG, GALVESTON, TX USA. NIDOCD, ROCKVILLE, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1076 EP A1076 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704286 ER PT J AU Harris, PR Weber, HC Wilcox, CM Kawabata, S Kiyono, H Jensen, RT Smith, PD AF Harris, PR Weber, HC Wilcox, CM Kawabata, S Kiyono, H Jensen, RT Smith, PD TI Cytokine profile in gastric tissue from patients with Helicobacter pylori infection and Zollinger-Ellison syndrome by quantitative PCR. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV ALABAMA, DEPT PEDIAT, BIRMINGHAM, AL USA. UNIV ALABAMA, DEPT MICROBIOL, BIRMINGHAM, AL 35294 USA. UNIV ALABAMA, DEPT MED, BIRMINGHAM, AL 35294 USA. NIDDK, DIGEST DIS BRANCH, NIH, BETHESDA, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A922 EP A922 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703668 ER PT J AU Hirayama, T Miyake, M Wada, A Nagata, H Makiyama, K Moss, J Noda, M AF Hirayama, T Miyake, M Wada, A Nagata, H Makiyama, K Moss, J Noda, M TI ADP-ribosyltransferase activin of Helicobacter pylori SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NAGASAKI UNIV, INST TROP MED, DEPT BACTERIOL, NAGASAKI, JAPAN. CHIBA UNIV, SCH MED, DEPT MICROBIOL 2, CHIBA 260, JAPAN. NAGASAKI UNIV, SCH MED, DEPT MED 2, NAGASAKI, JAPAN. NHLBI, PULM CRIT CARE MED BRANCH, NIH, BETHESDA, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A134 EP A134 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73700529 ER PT J AU Hong, MK Montgomery, EA Lewis, JH Sobin, LH Allegra, CJ Johnston, PG AF Hong, MK Montgomery, EA Lewis, JH Sobin, LH Allegra, CJ Johnston, PG TI Correlation of Ki-67 staining pattern, p53 staining, flow cytometry with routine histologic assessment for dysplasia in Barrett's esophagus (BE) SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GEORGETOWN UNIV, DEPT MED, WASHINGTON, DC USA. GEORGETOWN UNIV, DEPT PATHOL, WASHINGTON, DC USA. ARMED FORCES INST PATHOL, WASHINGTON, DC 20306 USA. NCI, NMOB, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A531 EP A531 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702110 ER PT J AU Jacoby, RF Marshall, DJ Newton, M Tutsch, K Cole, CE Lubet, RA Kelloff, GJ Verma, A Moser, AR Dove, WF AF Jacoby, RF Marshall, DJ Newton, M Tutsch, K Cole, CE Lubet, RA Kelloff, GJ Verma, A Moser, AR Dove, WF TI Chemoprevention of spontaneous intestinal adenomas in the Apc mutant Min mouse model by the nonsteroidal anti-inflammatory drug piroxicam. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV WISCONSIN, DEPT MED, MADISON, WI 53706 USA. UNIV WISCONSIN, DEPT BIOSTAT, MADISON, WI 53706 USA. UNIV WISCONSIN, DEPT ONCOL, MADISON, WI 53706 USA. UNIV WISCONSIN, DEPT GENET, MADISON, WI 53706 USA. WM S MIDDLETON MEM VET HOSP, MADISON, WI USA. NCI, DIV CANC PREVENT & CONTROL, CHEMOPREVENT BRANCH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A535 EP A535 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702127 ER PT J AU Joshi, SN Xu, ZQ Wank, SA Gardner, JD AF Joshi, SN Xu, ZQ Wank, SA Gardner, JD TI CCK-8 regulates the distribution of its own receptor affinity states in COS cells transfected with the CCK-A receptor. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST LOUIS UNIV, ST LOUIS, MO 63104 USA. NATL INST HLTH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1085 EP A1085 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704321 ER PT J AU Joshi, SN Xu, ZQ Wank, SA Gardner, JD AF Joshi, SN Xu, ZQ Wank, SA Gardner, JD TI Differential biochemical regulation of CCK-A and CCK-B receptors is accompanied by differential coupling of the receptors to signal transduction mechanisms. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 ST LOUIS UNIV, ST LOUIS, MO 63104 USA. NATL INST HLTH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1085 EP A1085 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704320 ER PT J AU Joshi, SN Xu, ZQ Wank, SA Gardner, JD AF Joshi, SN Xu, ZQ Wank, SA Gardner, JD TI CCK-8 activation of individual signal transduction mechanisms is mediated by specific affinity states of the CCK-A receptor. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NATL INST HLTH, BETHESDA, MD 20892 USA. ST LOUIS UNIV, ST LOUIS, MO 63104 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1085 EP A1085 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704319 ER PT J AU Josovitz, KN Holland, SM Malech, HL Lewis, JH Gallin, JI AF Josovitz, KN Holland, SM Malech, HL Lewis, JH Gallin, JI TI Endoscopic findings in chronic granulomatous disease SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GEORGETOWN UNIV, MED CTR, DIV GASTROENTEROL, WASHINGTON, DC 20007 USA. NIAID, NIH, HOST DEF LAB, BETHESDA, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A933 EP A933 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703715 ER PT J AU Josoyitz, KN Herion, DW Weber, HC Lewis, JH Hoofnagle, JH AF Josoyitz, KN Herion, DW Weber, HC Lewis, JH Hoofnagle, JH TI Prospective evaluation of routine endoscopy in patients with primary biliary cirrhosis SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 GEORGETOWN UNIV, MED CTR, DIV GASTROENTEROL, WASHINGTON, DC USA. NIDDK, LIVER DIS SECT, BETHESDA, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1224 EP A1224 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704873 ER PT J AU Krishnamurthy, S Dayal, Y Termanini, B Gibril, F Jensen, RT AF Krishnamurthy, S Dayal, Y Termanini, B Gibril, F Jensen, RT TI Correlation of gastric mucosal changes with disease activity and treatment in patients with Zollinger-Ellison syndrome (ZES): A prospective study SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NEMCH, DEPT PATHOL, BOSTON, MA USA. NIH, BETHESDA, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A162 EP A162 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73700644 ER PT J AU Kronenberg, SA Hyde, TM Mulberg, AE AF Kronenberg, SA Hyde, TM Mulberg, AE TI Expression of the cystic fibrosis transmembrane conductance regulator mRNA in human hypothalamus. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 CHILDRENS HOSP PHILADELPHIA, DEPT PEDIAT, DIV PEDIAT GASTROENTEROL & NUTR, PHILADELPHIA, PA 19104 USA. NIMH, CTR NEUROSCI, NIH, BETHESDA, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A814 EP A814 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703237 ER PT J AU Laghi, L Chauhan, DP Marra, G Major, EO Neel, JV Boland, CR AF Laghi, L Chauhan, DP Marra, G Major, EO Neel, JV Boland, CR TI Amplification of JC virus (JCV) sequences from human colorectal cancers. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF SAN DIEGO, LA JOLLA, CA 92093 USA. NIH, BETHESDA, MD 20892 USA. UNIV MICHIGAN, ANN ARBOR, MI USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A548 EP A548 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702181 ER EF