FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Wood, LV Wigginton, JM Zuckerman, J Higham, C Loy, S Brouwers, P Lane, HC Townley, E Jankelevich, S Serchuk, L Sei, S Zeichner, S AF Wood, LV Wigginton, JM Zuckerman, J Higham, C Loy, S Brouwers, P Lane, HC Townley, E Jankelevich, S Serchuk, L Sei, S Zeichner, S TI A pilot study of recombinant IL-2 in children and adolescents with human immunodeficiency virus infection. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,HIV AIDS MALIGNANCY BRANCH,BETHESDA,MD 20892. NCI,PEDIAT ONCOL BRANCH,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 433 EP 433 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200431 ER PT J AU SuriPayer, E Shevach, EM AF SuriPayer, E Shevach, EM TI Post-thymectomy autoimmune gastritis (AIG): Pathogenesis and regulation. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 437 EP 437 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200435 ER PT J AU Hague, BF Mahana, W Kindt, TJ AF Hague, BF Mahana, W Kindt, TJ TI HIV-1 infection induces apoptosis in cell lines refractive to apoptosis induced by Fas crosslinking. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 444 EP 444 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200442 ER PT J AU GeaBanacloche, JC Weiskopf, E Lopez, JC Falloon, J Baseler, M Stevens, R Connors, M AF GeaBanacloche, JC Weiskopf, E Lopez, JC Falloon, J Baseler, M Stevens, R Connors, M TI HIV infection induces progressive depletions within the CD4+ T cell repertoire that are not immediately restored by anti-viral or immune-based therapies. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 447 EP 447 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200445 ER PT J AU Lowry, RP Goebel, J Ghosh, P Lempicki, R Mikovits, J Young, H Robey, F AF Lowry, RP Goebel, J Ghosh, P Lempicki, R Mikovits, J Young, H Robey, F TI Interruption of IL-2 receptor signaling by CD3-ligand HIV-gp120 binding. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,FREDERICK,MD. NIH,BETHESDA,MD 20892. UNIV S ALABAMA,DEPT MED,MOBILE,AL 36688. UNIV S ALABAMA,DEPT PEDIAT,MOBILE,AL 36688. RI Lempicki, Richard/E-1844-2012 OI Lempicki, Richard/0000-0002-7059-409X NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 448 EP 448 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200446 ER PT J AU Siegel, CT Spalding, JW Rowley, DA Schreiber, K Dubey, P Tennant, TW Schreiber, H AF Siegel, CT Spalding, JW Rowley, DA Schreiber, K Dubey, P Tennant, TW Schreiber, H TI Cancer-prone mice carrying a mutant ras gene can be immunized against the mutant ras peptide. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NATL INST ENVIRONM HLTH,RES TRIANGLE PK,NC. UNIV CHICAGO,CHICAGO,IL 60637. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 468 EP 468 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200466 ER PT J AU Celis, E Tsai, V Southwood, S Sidney, J Sakaguchi, K Kawakami, Y Appella, E Sette, A AF Celis, E Tsai, V Southwood, S Sidney, J Sakaguchi, K Kawakami, Y Appella, E Sette, A TI Identification of subdominant CTL epitopes of the gp100 melanoma-associated tumor antigen by primary in vitro immunization with peptide-pulsed dendritic cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. CYTEL CORP,SAN DIEGO,CA 92121. NR 0 TC 0 Z9 0 U1 0 U2 2 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 470 EP 470 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200468 ER PT J AU Porgador, A Germain, RN AF Porgador, A Germain, RN TI Monoclonal antibody detection of specific cell-bound peptide-MHC class I complexes with a sensitivity approaching CD8+ T cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LYMPHOCYTE BIOL SECT,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 472 EP 472 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200470 ER PT J AU Worobec, AS Semere, T Nagata, H Metcalfe, DD AF Worobec, AS Semere, T Nagata, H Metcalfe, DD TI The c-kit mutation in patients with mastocytosis: A follow-up study. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 503 EP 503 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200501 ER PT J AU Rivera, J Song, JS HaleemSmith, H Gomez, J Scott, PM Mills, JF AF Rivera, J Song, JS HaleemSmith, H Gomez, J Scott, PM Mills, JF TI Overexpression of p95 Vav in the mast cell line RBL-2H3 results in a constitutive increase in Vav phosphorylation, NFAT activity, and IL-2 mRNA. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAMS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 547 EP 547 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200545 ER PT J AU Choi, OH Kim, JH Kinet, JP AF Choi, OH Kim, JH Kinet, JP TI Calcium mobilization via sphingosine kinase in signaling through Fc receptors. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,ROCKVILLE,MD. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 548 EP 548 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200546 ER PT J AU Zaitoun, FH Meyer, CF Holland, SM Cox, FE Deane, DA Wray, BB AF Zaitoun, FH Meyer, CF Holland, SM Cox, FE Deane, DA Wray, BB TI Fungal pneumonia, elevated serum IgE, and pulmonary hypereosinophilia in a patient with chronic granulomatous disease (CGD). SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 MED COLL GEORGIA,AUGUSTA,GA 30912. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 713 EP 713 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200711 ER PT J AU Han, M Currier, J Kehn, P Robinson, MA AF Han, M Currier, J Kehn, P Robinson, MA TI Patterns of TCRA diversity generated in response to mitogen, superantigen, and nominal antigen. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOGENET LAB,NIH,ROCKVILLE,MD 20852. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 734 EP 734 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200732 ER PT J AU DeRijk, RH Dijkstra, CD Uitdehaag, B Maloni, H Elroy, B McFarland, H Sternberg, EM AF DeRijk, RH Dijkstra, CD Uitdehaag, B Maloni, H Elroy, B McFarland, H Sternberg, EM TI Corticosteroid-resistance of ex vivo IL-6 production in multiple sclerosis. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIMH,NIH,BETHESDA,MD 20892. NINCDS,NIH,BETHESDA,MD 20892. FREE UNIV AMSTERDAM,DEPT HISTOL,AMSTERDAM,NETHERLANDS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 752 EP 752 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200750 ER PT J AU Song, XY Worley, P Jin, WW Pilo, CM Wahl, SM AF Song, XY Worley, P Jin, WW Pilo, CM Wahl, SM TI Apoptosis in streptococcal cell wall-induced arthritis. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 773 EP 773 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200771 ER PT J AU Chen, H Paul, WE AF Chen, H Paul, WE TI NK1.1-, CD4+ T cells from class II-/- mice resemble NK1.1+, CD4+ T cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 802 EP 802 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200800 ER PT J AU Ludviksson, BR Marth, T Neurath, M Strober, W Ehrhardt, RO AF Ludviksson, BR Marth, T Neurath, M Strober, W Ehrhardt, RO TI The role of IL-12 in thymocyte selection. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 806 EP 806 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200804 ER PT J AU Itoh, Y Germain, RN AF Itoh, Y Germain, RN TI Cell response threshold and response hierarchy analyzed at the single cell level. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LYMPHOCYTE BIOL SECT,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 818 EP 818 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200816 ER PT J AU Fernandez, EG Coligan, JE AF Fernandez, EG Coligan, JE TI Differential signaling capabilities of the TCR beta and CD3 epsilon chains of the T cell antigen receptor complex in CD4(+)CD8(+) cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,MOL STRUCT LAB,NIH,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 819 EP 819 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200817 ER PT J AU Plaksin, D Polakova, K Margulies, DH AF Plaksin, D Polakova, K Margulies, DH TI A three domain T-cell receptor is biologically active and specifically stains cell surface MHC/peptide complexes. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,MOL BIOL SECT,IMMUNOL LAB,NIH,BETHESDA,MD 20892. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 824 EP 824 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200822 ER PT J AU Koshiba, M Apasov, S Erb, L Turner, JT Weisman, GA Sitkovsky, MV AF Koshiba, M Apasov, S Erb, L Turner, JT Weisman, GA Sitkovsky, MV TI Transient up-regulation of P2Y(2) nucleotide receptor mRNA expression is an immediate early gene response in activated thymocytes. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LI,NIH,BETHESDA,MD 20892. UNIV MISSOURI,DEPT BIOCHEM & PHARMACOL,COLUMBIA,MO. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 861 EP 861 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200858 ER PT J AU Deng, YJ AF Deng, YJ TI Molecular characterization of a baculovirus-expressed Fab fragment of human polyreactive antibody. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,ORAL MED LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 903 EP 903 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200900 ER PT J AU Matousek, MP Nedrud, JG Cieplak, W Harding, CV AF Matousek, MP Nedrud, JG Cieplak, W Harding, CV TI E-coli heat labile enterotoxin and cholera toxin inhibit class II MHC antigen processing. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. NIAID,ROCKY MT LABS,NIH,HAMILTON,MT 59840. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 938 EP 938 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200935 ER PT J AU Biddison, W Taub, D Cruikshank, W Center, D StetlerStevenson, W Honma, K AF Biddison, W Taub, D Cruikshank, W Center, D StetlerStevenson, W Honma, K TI MIP-1 alpha, MIP-1 beta, IL-16, IP-10 and matrix metalloproteinase secretion by CD8(+) cytotoxic T lymphocytes derived from patients with neurological diseases. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD. BOSTON UNIV,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 959 EP 959 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200956 ER PT J AU McCartneyFrancis, NL Song, XY Worley, P Wahl, SM AF McCartneyFrancis, NL Song, XY Worley, P Wahl, SM TI Selective inhibition of inducible nitric oxide synthase exacerbates erosive joint disease. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 961 EP 961 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200958 ER PT J AU Numerof, R Lin, S Scharenberg, A Yi, T Kinet, JP AF Numerof, R Lin, S Scharenberg, A Yi, T Kinet, JP TI Functional interactions between the high affinity receptor for IgE (Fc epsilon RI) and the tyrosine phosphatase SHP-1. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,MOL ALLERGY & IMMUNOL SECT,NIH,BETHESDA,MD 20892. CLEVELAND CLIN,RES INST,CLEVELAND,OH 44106. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 972 EP 972 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200969 ER PT J AU Abrams, SI Khleif, SN BergmannLeitner, ES Schlom, J AF Abrams, SI Khleif, SN BergmannLeitner, ES Schlom, J TI Development of cell-mediated immunity in carcinoma patients vaccinated with mutant ras oncogene peptides. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,TUMOR IMMUNOL & BIOL LAB,NIH,BETHESDA,MD 20892. NCI,NAVY ONCOL BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 995 EP 995 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14200992 ER PT J AU Feldman, GM Wahl, SM Vachhani, B McCarthy, J AF Feldman, GM Wahl, SM Vachhani, B McCarthy, J TI Regulation of interferon signalling by the extracellular matrix. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 US FDA,DIV CYTOKINE BIOL,BETHESDA,MD 20892. NIDR,IMMUNOL LAB,BETHESDA,MD 20892. UNIV MINNESOTA,DEPT LAB MED PATH,MINNEAPOLIS,MN 55455. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1009 EP 1009 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201006 ER PT J AU Sehgal, D Schiaffella, E Mage, RG AF Sehgal, D Schiaffella, E Mage, RG TI Rabbits lacking the V(H)1a2 gene develop a2(+) B cells in the appendix by gene conversion-like events. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,IMMUNOL LAB,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1010 EP 1010 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201007 ER PT J AU Martin, R Stephanova, I Vergelli, M Germain, RN Hemmer, B AF Martin, R Stephanova, I Vergelli, M Germain, RN Hemmer, B TI Comparison of effector functions and early signalling events in human CD4+ T cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NINCDS,NEUROIMMUNOL BRANCH 1,NATL INST HLTH,BETHESDA,MD 20892. NIAID,LYMPHOCYTE BIOL SECT,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1026 EP 1026 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201023 ER PT J AU Doherty, TM Sher, A AF Doherty, TM Sher, A TI Defects in macrophage effector function inhibit immunopathology induced by Mycobacterium avium infection but fail to alter bacterial growth in vivo. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,PARASIT DIS LAB,IMMUNOBIOL SECT,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1039 EP 1039 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201036 ER PT J AU FrazierJessen, MR Jin, WW Cheever, A Sher, A Kopp, J Wahl, SM AF FrazierJessen, MR Jin, WW Cheever, A Sher, A Kopp, J Wahl, SM TI Schistosoma mansoni infection in murine TGF-beta 1 transgenic models. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 INST BIOMED RES,ROCKVILLE,MD. NIDR,NIH,BETHESDA,MD 20892. NIAID,NIH,BETHESDA,MD 20892. NIDDK,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1040 EP 1040 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201037 ER PT J AU Ortaldo, JR WinklerPickett, R Gregorio, TA Stoll, J Mason, LH AF Ortaldo, JR WinklerPickett, R Gregorio, TA Stoll, J Mason, LH TI The Ly-49 family: Regulation of cytotoxicity and cytokine production in murine NK and CD3(+) cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,LEI,DBS,FREDERICK,MD 21702. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1047 EP 1047 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201044 ER PT J AU Prussin, C Foster, B AF Prussin, C Foster, B TI V alpha 24+, V beta 11+ natural T cells are the human analog of murine NK1.1 T cells and demonstrate a predominant Th1 phenotype. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1049 EP 1049 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201046 ER PT J AU Nelms, K Paul, WE AF Nelms, K Paul, WE TI Characterization and genetic mapping of FRIP-1, a novel signaling molecule specifically expressed in hematopoietic cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1055 EP 1055 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201052 ER PT J AU Gauchat, JF LecoanetHenchoz, S Giliani, S Candotti, F Oakes, SA OShea, JJ Notarangelo, LD Bonnefoy, JY AF Gauchat, JF LecoanetHenchoz, S Giliani, S Candotti, F Oakes, SA OShea, JJ Notarangelo, LD Bonnefoy, JY TI Impairment of IgE germline transcript induction by IL-4, but not IL-13, in B cell lines from JAK-3 and gamma(c) deficient SCID patients. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 GENEVA BIOMED RES INST,GENEVA,SWITZERLAND. UNIV BRESCIA,I-25121 BRESCIA,ITALY. NIH,BETHESDA,MD 20892. RI Notarangelo, Luigi/F-9718-2016 OI Notarangelo, Luigi/0000-0002-8335-0262 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1060 EP 1060 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201057 ER PT J AU Ehrhardt, RO Ludviksson, BR Gray, B Strober, W AF Ehrhardt, RO Ludviksson, BR Gray, B Strober, W TI Induction and regulation of autoimmunity in IL-2-deficient mice. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,MUCOSAL IMMUN SECT,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1073 EP 1073 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201070 ER PT J AU Iglesias, A Zea, AH Egea, E deEgea, G Ochoa, AC AF Iglesias, A Zea, AH Egea, E deEgea, G Ochoa, AC TI Frequent alterations in T cell receptor xi-chain and p56(LCK) are observed in patients with SLE. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV NACL COLOMBIA,BOGOTA,COLOMBIA. UNIV NORTE,BARRANQUILLA,COLOMBIA. NCI,CLIN RES BRANCH,SAIC FREDERICK CANC RES & DEV CTR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1143 EP 1143 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201140 ER PT J AU Ryan, JJ Huang, H McReynolds, LJ Shelburne, C Huff, TF Paul, WE AF Ryan, JJ Huang, H McReynolds, LJ Shelburne, C Huff, TF Paul, WE TI Stem cell factor activates STAT-5 DNA binding in IL-3-derived bone marrow mast cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1183 EP 1183 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201180 ER PT J AU Coligan, JE Brooks, AG Posch, PE Scorezelli, CJ Borrego, F AF Coligan, JE Brooks, AG Posch, PE Scorezelli, CJ Borrego, F TI NKG2A is associated with CD94 on the cell surface of NK cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,MOL STRUCT LAB,NIH,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1195 EP 1195 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201192 ER PT J AU Mason, LH Anderson, SK Gosselin, P Ortaldo, JR McVicar, DW AF Mason, LH Anderson, SK Gosselin, P Ortaldo, JR McVicar, DW TI The murine inhibitory receptors Ly-49A and G are tyrosine phosphorylated following receptor stimulation; Ly-49D, an activation receptor is not. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 SAIC,LEI,DBS,FREDERICK,MD. SAIC,IRSP,FREDERICK,MD. NCI,FCRDC,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1198 EP 1198 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201195 ER PT J AU Fogler, WE Watanabe, M Volker, K McCormick, K Brunda, M Wiltrout, RH Ortaldo, JR AF Fogler, WE Watanabe, M Volker, K McCormick, K Brunda, M Wiltrout, RH Ortaldo, JR TI Induction of NK cell infiltration into hepatic tissue by IL-12, but not IL-2, is dependent on FN-gamma. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,LEI,DBS,FREDERICK,MD 21701. SAIC,IRSP,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. HOFFMANN LA ROCHE,NUTLEY,NJ. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1202 EP 1202 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201199 ER PT J AU Thornton, AM SuriPayer, E Shevach, EM AF Thornton, AM SuriPayer, E Shevach, EM TI Characterization of CD4+CD25+ immunoregulatory T cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1217 EP 1217 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201214 ER PT J AU Topfer, F Rostapshov, V Korty, PE Shevach, EM AF Topfer, F Rostapshov, V Korty, PE Shevach, EM TI Modulation of Th1/Th2 phenotype by immunization with antigen/cytokine DNA. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1229 EP 1229 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201226 ER PT J AU Segal, BM Klinman, DM Shevach, EM AF Segal, BM Klinman, DM Shevach, EM TI Activation of pathogenic Th1 T cells by microbial products is mediated by IL-12. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. US FDA,BETHESDA,MD 20014. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1232 EP 1232 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201229 ER PT J AU McDyer, JF Seder, RA AF McDyer, JF Seder, RA TI Factors regulating IL-12 production from human purified monocytes and PBMCs. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,CLIN INVEST LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1242 EP 1242 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201239 ER PT J AU Hemmer, B Vergelli, M Fleckenstein, B Jung, G McFarland, H Wiesmueller, KH Martin, R AF Hemmer, B Vergelli, M Fleckenstein, B Jung, G McFarland, H Wiesmueller, KH Martin, R TI Combinatorial peptide libraries allow identification of crossreactive exogenous and endogenous ligands for human class II restricted T cells. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NINCDS,NEUROIMMUNOL BRANCH 1,NIH,BETHESDA,MD 20892. UNIV TUEBINGEN,INST ORGAN CHEM,D-72076 TUBINGEN,GERMANY. UNIV TUEBINGEN,NAT WISSENSCH & MED INST,D-72762 REUTLINGEN,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1252 EP 1252 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201249 ER PT J AU Segal, DM Zacharchuk, CM Vance, BA AF Segal, DM Zacharchuk, CM Vance, BA TI Recombinant mouse Bcl-2((1-203)): Two domains connected by a long protease-sensitive linker. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,EXPT IMMUNOL BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1270 EP 1270 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201267 ER PT J AU Memon, SA Moreno, MB Zacharchuk, CM AF Memon, SA Moreno, MB Zacharchuk, CM TI Apoptotic signaling in T cells: The role of ICE-family proteases. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. RI Memon, Sarfraz/E-1198-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1271 EP 1271 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201268 ER PT J AU Hsieh, LS Martin, BM Doherty, AE Lin, Y AF Hsieh, LS Martin, BM Doherty, AE Lin, Y TI Determination of major IgE-binding epitopes of a latex acidic allergen, Hev b 5. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 CBER,BETHESDA,MD. NIMH,BETHESDA,MD 20892. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1395 EP 1395 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201394 ER PT J AU Caspi, RR Silver, PB Agarwal, R Rizzo, LV Chan, CC Tarrant, TK AF Caspi, RR Silver, PB Agarwal, R Rizzo, LV Chan, CC Tarrant, TK TI Systemic administration of IL-12 protects mice from experimental autoimmune uveitis (EAU) through a mechanism involving IFN-gamma. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NEI,IMMUNOL LAB,BETHESDA,MD 20892. HHMI,NIH,RES SCHOLARS PROGRAM,BETHESDA,MD. RI Rizzo, Luiz Vicente/B-4458-2009 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1503 EP 1503 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201498 ER PT J AU Castellino, F Zappacosta, F Germain, RN AF Castellino, F Zappacosta, F Germain, RN TI Identification of large protein fragments as a substrate for antigen capture by MHC class II molecules. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LYMPHOCYTE BIOL SECT,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1505 EP 1505 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201504 ER PT J AU Zhou, P Sieve, MC Tewari, RP Seder, RA AF Zhou, P Sieve, MC Tewari, RP Seder, RA TI Protection against Histoplasma capsulatum infection does not require IL-12 or IFNg in a secondary response. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 SO ILLINOIS UNIV,SCH MED,SPRINGFIELD,IL. NIAID,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1542 EP 1542 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201537 ER PT J AU SchartonKersten, TM Yap, G Sher, A AF SchartonKersten, TM Yap, G Sher, A TI Inducible nitric oxide is not required for IL-12/IFN-gamma dependent innate resistance to the intracellular pathogen, Toxoplasma gondii. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,LPD,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1544 EP 1544 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201544 ER PT J AU Lucas, PJ Wang, FP Loh, DY Gress, RE AF Lucas, PJ Wang, FP Loh, DY Gress, RE TI Induction of anergy in naive T cell populations. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,EIB,NIH,BETHESDA,MD 20892. WASHINGTON UNIV,ST LOUIS,MO. NIPPON ROCHE RES CTR,KAMAKURA,KANAGAWA 247,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1553 EP 1553 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201548 ER PT J AU Vliagoftis, H Oh, CK Metcalfe, DD AF Vliagoftis, H Oh, CK Metcalfe, DD TI Mast cells express connexins and may communicate in vitro with fibroblasts through gap junctions. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 HARBOR UCLA MED CTR,TORRANCE,CA 90509. NIH,BETHESDA,MD 20892. RI Vliagoftis, Harissios/C-6480-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1577 EP 1577 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201573 ER PT J AU Lukacs, NW Strieter, RM Glass, M Taub, DD Kunkel, SL AF Lukacs, NW Strieter, RM Glass, M Taub, DD Kunkel, SL TI Mast cell-fibroblast interaction induces histamine release and C-C chemokine production. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH MED,DEPT PATHOL,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,ANN ARBOR,MI 48109. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1578 EP 1578 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201574 ER PT J AU Hamawy, MM Swieter, M Mergenhagen, SE Siraganian, RP AF Hamawy, MM Swieter, M Mergenhagen, SE Siraganian, RP TI Reconstitution of high affinity IgE receptor (Fc epsilon RI)-mediated secretion by transfecting protein tyrosine kinase pp125(FAK). SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1652 EP 1652 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201648 ER PT J AU Vonakis, BM Chen, HX HaleemSmith, H Metzger, H AF Vonakis, BM Chen, HX HaleemSmith, H Metzger, H TI The SH4 domain of lyn kinase is constitutively associated with the high affinity receptor for IgE (Fc epsilon RI). SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAMS,ARB,NIH,BETHESDA,MD. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1653 EP 1653 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201649 ER PT J AU Rabin, RL Park, M Swofford, R Stephany, D Farber, JM AF Rabin, RL Park, M Swofford, R Stephany, D Farber, JM TI Response of T cell subsets to alpha and beta chemokines. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1720 EP 1720 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201716 ER PT J AU Swieter, M Berenstein, EH Siraganian, RP AF Swieter, M Berenstein, EH Siraganian, RP TI Functional expression of high affinity IgE receptors (Fc epsilon RI) containing the human alpha subunit in a rat mast cell line. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1775 EP 1775 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201769 ER PT J AU Torigoe, C Goldstein, B Wofsy, C Metzger, H AF Torigoe, C Goldstein, B Wofsy, C Metzger, H TI Competition of receptor phosphorylation between discrete aggregates of Fc epsilon RI. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAMS,ARB,NIH,BETHESDA,MD. LOS ALAMOS NATL LAB,DIV THEORET,THEORET BIOL & BIOPHYS GRP,LOS ALAMOS,NM. UNIV NEW MEXICO,DEPT MATH & STAT,ALBUQUERQUE,NM 87131. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1780 EP 1780 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201774 ER PT J AU Kimura, T Kihara, H Bhattacharyya, S Sakamoto, H Appella, E Siraganian, RP AF Kimura, T Kihara, H Bhattacharyya, S Sakamoto, H Appella, E Siraganian, RP TI Downstream signaling molecules bind to different phosphorylated immunoreceptor tyrosine-based activation motif (ITAM) peptides of the high affinity IgE receptor. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1781 EP 1781 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201775 ER PT J AU Sagawa, K Swaim, WD Zhang, J Unsworth, E Siraganian, RP AF Sagawa, K Swaim, WD Zhang, J Unsworth, E Siraganian, RP TI The surface adhesion protein PECAM-1 (CD31) is tyrosine phosphorylated after aggregation of the high affinity IgE receptor. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 US FDA,NIH,BETHESDA,MD 20014. NIDR,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1782 EP 1782 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201776 ER PT J AU Steel, C Nutman, TB AF Steel, C Nutman, TB TI Parasite antigen-driven priming of naive human T-cells: Implications for subsequent secondary responses. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,PARASIT DIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1842 EP 1842 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201836 ER PT J AU Jankovic, D Hieny, S Charest, H Doherty, M SchartonKersten, TM Sher, A AF Jankovic, D Hieny, S Charest, H Doherty, M SchartonKersten, TM Sher, A TI The spleen contains an unusual cell population which produces IL-12 in response to Toxoplasma gondii in the absence of IFN-gamma priming. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,LPD,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1848 EP 1848 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201842 ER PT J AU Vance, BA Wu, W Ribaudo, R Segal, DM Kearse, KP AF Vance, BA Wu, W Ribaudo, R Segal, DM Kearse, KP TI CD69 heterogeneity results from usage of both typical (N-X-T) and atypical (N-X-C) N-linked glycosylation motifs. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NCI,NIH,EIB,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1869 EP 1869 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201863 ER PT J AU Borrego, F Zappacosta, F Brooks, AG Parker, KC Coligan, JE AF Borrego, F Zappacosta, F Brooks, AG Parker, KC Coligan, JE TI Identification of endogenous peptides complexed to HLA-Cw*0304: Functional relevance to NK cell recognition. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID,MOL STRUCT LAB,NIH,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1884 EP 1884 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201878 ER PT J AU Watanabe, C Zhu, Q Liu, T Hollenbaugh, D Blaese, RM Kanner, SB Aruffo, A Ochs, HD AF Watanabe, C Zhu, Q Liu, T Hollenbaugh, D Blaese, RM Kanner, SB Aruffo, A Ochs, HD TI The Wiskott-Aldrich syndrome: WASP-mutations and their effect on gene transcription and protein expression correlate with clinical phenotypes. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 UW PEDIAT,SEATTLE,WA. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,SEATTLE,WA 98121. NCHCR,CLIN GENE THERAPY BRANCH,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1925 EP 1925 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201919 ER PT J AU Chen, M Candotti, F Oakes, SA Vezzoni, P Blaese, RM Notarangelo, LD Villa, A OShea, JJ AF Chen, M Candotti, F Oakes, SA Vezzoni, P Blaese, RM Notarangelo, LD Villa, A OShea, JJ TI JAK3 SCID: Mutations in noncatalytic domain and basis of Jak3 gamma c interaction. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAMS,ARB,BETHESDA,MD. NCHGR,CGTB,BETHESDA,MD. CNR,IST TECNOL BIOMED AVANZATE,I-20131 MILAN,ITALY. UNIV BRESCIA,BRESCIA,ITALY. RI Notarangelo, Luigi/F-9718-2016 OI Notarangelo, Luigi/0000-0002-8335-0262 NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1929 EP 1929 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201923 ER PT J AU Marth, T Strober, W Kelsall, BL AF Marth, T Strober, W Kelsall, BL TI Regulation of IL-12 by CR3 signalling. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1947 EP 1947 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201941 ER PT J AU Paliogianni, FA Balow, JE Boumpas, DT AF Paliogianni, FA Balow, JE Boumpas, DT TI Glucocorticoids modulate the binding of specific proteins to AU-sequences in the 3'-untranslated region (UTR) of interleukin-2 (IL-2) by activating phosphatases 1 and 2. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 UNIV PATRAS,PATRAS,GREECE. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1954 EP 1954 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201948 ER PT J AU Turetskaya, RL Kuprash, DV Udalova, LA Drutskaya, LN Sheflyan, GY Nedospasov, SA AF Turetskaya, RL Kuprash, DV Udalova, LA Drutskaya, LN Sheflyan, GY Nedospasov, SA TI Regulation of TNF transcription in macrophages. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 VA ENGELHARDT MOL BIOL INST,MOSCOW 117984,RUSSIA. BELOZERSKY INST PHYSICOCHEM BIOL,MOSCOW,RUSSIA. LMI,DBS,FREDERICK,MD. IRSP,SAIC,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD. RI Nedospasov, Sergei/J-5936-2013; Nedospasov, Sergei/L-1990-2015; Kuprash, Dmitry/O-4899-2015; Nedospasov, Sergei/Q-7319-2016 OI Kuprash, Dmitry/0000-0002-1488-4148; NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 1985 EP 1985 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14201979 ER PT J AU Leung, DYM Wenzel, S Szefler, SJ Spahn, J Surs, W Chrousos, GP Hamid, Q AF Leung, DYM Wenzel, S Szefler, SJ Spahn, J Surs, W Chrousos, GP Hamid, Q TI Association of steroid resistant (SR) asthma with increased numbers of cells expressing glucocorticoid receptor (GR) beta. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NATL JEWISH CTR IMMUNOL & RESP MED,DENVER,CO 80206. MCGILL UNIV,MONTREAL,PQ,CANADA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1997 VL 99 IS 1 SU S BP 2009 EP 2009 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA WH142 UT WOS:A1997WH14202003 ER PT J AU Wine, RN Chapin, RE AF Wine, RN Chapin, RE TI Evaluation of the binding patterns of eleven FITC-conjugated lectins in fischer 344 rat testes SO JOURNAL OF ANDROLOGY LA English DT Article DE testis; lectin; spermatogenesis; rat ID EPIDIDYMIS; GLYCOPROTEINS; HISTOCHEMISTRY; SURFACE; MOUSE; SEEDS AB The binding patterns of 11 recently commercially available fluorescein isothiocyanate-conjugated lectins that have been uncharacterized or undercharacterized in rat testes and/or have an unknown or complex carbohydrate specificity were evaluated in paraffin sections from Fischer 344 rat testes. Several of the lectins exhibited unique binding patterns that provide information about changes in carbohydrate domains, particularly during germ-cell maturation, that occur during spermatogenesis. Agaricus bisporus (ABA) lectin produced the most striking staining pattern in the cytoplasm of maturing germ cells, increasing in intensity until spermatid elongation, while the nuclei remained negative. In contrast, Cicer arietinum (CPA) strongly stained the nucleus of early leptotene/zygotene spermatocytes, decreasing to moderate intensity during maturation, until staining was irregular and scattered in elongated spermatids. This study describes new patterns of lectin staining during spermatogenesis and provides additional evidence of the complex carbohydrate modifications that occur as germ cells mature within the seminiferous tubule. RP Wine, RN (reprint author), NIEHS,NATL TOXICOL PROGRAM,REPROD TOXICOL GRP,POB 12233,RES TRIANGLE PK,NC 27709, USA. OI Chapin, Robert/0000-0002-5997-1261 NR 22 TC 8 Z9 8 U1 0 U2 0 PU AMER SOC ANDROLOGY, INC PI LAWRENCE PA C/O ALLEN PRESS, INC PO BOX 368, LAWRENCE, KS 66044 SN 0196-3635 J9 J ANDROL JI J. Androl. PD JAN-FEB PY 1997 VL 18 IS 1 BP 71 EP 79 PG 9 WC Andrology SC Endocrinology & Metabolism GA WM444 UT WOS:A1997WM44400010 PM 9089070 ER PT J AU Hybertson, BM Bursten, SL Leff, JA Lee, YM Jepson, EK Dewitt, CR Zagorski, J Cho, HG Repine, JE AF Hybertson, BM Bursten, SL Leff, JA Lee, YM Jepson, EK Dewitt, CR Zagorski, J Cho, HG Repine, JE TI Lisofylline prevents leak, but not neutrophil accumulation, in lungs of rats given IL-1 intratracheally SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE cytokines; cytokine-induced neutrophil chemoattractant; acute respiratory distress syndrome; inflammation; phosphatidic acid; acute lung injury ID RESPIRATORY-DISTRESS SYNDROME; PHOSPHATIDIC-ACID; MESANGIAL CELLS; FATTY-ACIDS; INTERLEUKIN-1; INJURY; EXPRESSION; CHEMOATTRACTANT; TOLERANCE; CYTOKINES AB Interleukin-1 (IL-1) is increased in lung lavages from patients with the acute respiratory distress syndrome, and administering IL-1 intratracheally causes neutrophil accumulation and a neutrophil-dependent oxidative leak in lungs of rats. In the present study, we found that rats pretreated intraperitoneally with lisofylline [(R)-1-(5-hydroxyhexyl)-3,7-dimethylxanthine (LSF)], an inhibitor of lysophosphatidic acid acyl transferase, which reduces the production of unsaturated phosphatidic acid species, did not develop the lung leak or the related ultrastructural abnormalities that occur after intratracheal administration of IL-1. However. rats pretreated with LSF and then given IL-1 intratracheally did develop the same elevations of lung lavage cytokine-induced neutrophil chemoattractant (CINC) levels and the same increased numbers of lung lavage neutrophils as rats given IL-1 intratracheally. Lungs of rats given IL-1 intratracheally also had increased unsaturated phosphatidic acid and free acyl (linoleate, linolenate) concentrations compared with untreated rats, and these Lipid responses were prevented by pretreatment with LSF. Our results reveal that LSF decreases lung leak and lung lipid alterations without decreasing neutrophil accumulation or lung lavage CINC increases in rats given IL-1 intratracheally. C1 UNIV COLORADO, HLTH SCI CTR, DEPT MED, DENVER, CO 80262 USA. CELL THERAPEUT INC, SEATTLE, WA 98119 USA. NIDR, NIH, BETHESDA, MD 20892 USA. YEUNGNAM UNIV, KYONGSAN 712749, SOUTH KOREA. RP Hybertson, BM (reprint author), WEBB WARING INST BIOMED RES, 4200 E 9TH AVE, BOX C-322, DENVER, CO 80262 USA. OI Cho, Hyun Gug/0000-0002-8267-3801 FU NHLBI NIH HHS [HL-40784] NR 27 TC 16 Z9 16 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JAN PY 1997 VL 82 IS 1 BP 226 EP 232 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA WG328 UT WOS:A1997WG32800030 PM 9029220 ER PT J AU Casjens, S vanVugt, R Tilly, K Rosa, PA Stevenson, B AF Casjens, S vanVugt, R Tilly, K Rosa, PA Stevenson, B TI Homology throughout the multiple 32-kilobase circular plasmids present in Lyme disease spirochetes SO JOURNAL OF BACTERIOLOGY LA English DT Article ID OUTER-SURFACE-PROTEIN; FRAGMENT-LENGTH-POLYMORPHISM; POLYMERASE CHAIN-REACTION; RIBOSOMAL-RNA GENES; BACTERIUM BORRELIA-BURGDORFERI; SENSU LATE STRAINS; LINEAR CHROMOSOME; SP-NOV; IXODES-RICINUS; OSPC GENE AB We have characterized seven different 32-kb circular plasmids carried by Borrelia burgdorferi isolate B31. Restriction endonuclease recognition site mapping and partial sequencing of these plasmids indicated that all seven are probably closely I elated to each other throughout their lengths and have substantial relationships to cp8.3, an 8.3-kb circular plasmid of B. burgdorferi sensu late isolate Ip21. With the addition of the seven 32-kb plasmids, this bacterial strain is known to carry at least 10 linear and 9 circular plasmids. Variant cultures of B. burgdorferi B31 lacking one or more of the 32-kb circular plasmids are viable and, at least in some cases, infectious. We have examined a number of different natural isolates of Lyme disease borreliae and found that all of the B. burgdorferi sensu stricto isolates and most of the B. burgdorferi sensu late isolates tested appear to carry multiple 32-kb circular plasmids related to those of B. burgdorferi B31. The ubiquity of these plasmids suggests that they may be important in the natural life cycle of these organisms. They may be highly conjugative plasmids or prophage genomes, which could prole to be useful in genetically manipulating B. burgdorferi. C1 NIAID, ROCKY MT LABS, MICROBIAL STRUCT & FUNCT LAB, HAMILTON, MT 59840 USA. RP Casjens, S (reprint author), UNIV UTAH, DEPT ONCOL SCI, DIV MOL BIOL & GENET, SALT LAKE CITY, UT 84132 USA. NR 81 TC 113 Z9 114 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1997 VL 179 IS 1 BP 217 EP 227 PG 11 WC Microbiology SC Microbiology GA VZ792 UT WOS:A1997VZ79200029 PM 8982001 ER PT J AU Geanacopoulos, M Adhya, S AF Geanacopoulos, M Adhya, S TI Functional characterization of roles of GalR and GalS as regulators of the gal regulon SO JOURNAL OF BACTERIOLOGY LA English DT Article ID ESCHERICHIA-COLI; REPRESSOR PROTEIN; LAC REPRESSORS; RNA-POLYMERASE; TRANSCRIPTION; GALACTOSE; SYSTEM; GENES AB An isorepressor of the gal regulon in Escherichia call, GalS, has been purified to homogeneity. In vitro DNase I protection experiments indicated that among operators of the gal regulon, GalS binds most strongly to the external operator of the mgl operon, which encodes the high-affinity beta-methylgalactoside galactose transport system, and with less affinity to the operators controlling expression of the gal operon, which codes for enzymes of galactose metabolism, GalS has even less affinity for the external operator of galP, which codes for galactose permease, the major low-affinity galactose transporter in the cell, This order of affinities is the reverse of that of GalR, which binds most strongly to the operator of galP and most weakly to that of mgl. Our results also show that GalS, like its homolog, GalR, is a dimeric protein which in binding to the bipartite operators of the gal operon selectively represses its P1 promoter, Consistent with the fact that GalR is the exclusive regulator of the low-affinity galactose transporter, galactose permease, and that the major role of GalS is in regulating expression of the high-affinity galactose transporter encoded by the mgl operon, we found that the DNA binding of GalS is 15-fold more sensitive than that of GalR to galactose. C1 NCI,MOL BIOL LAB,DEV GENET SECT,NIH,BETHESDA,MD 20892. NR 20 TC 43 Z9 45 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1997 VL 179 IS 1 BP 228 EP 234 PG 7 WC Microbiology SC Microbiology GA VZ792 UT WOS:A1997VZ79200030 PM 8982002 ER PT J AU Mann, RW McCutchen, CW AF Mann, RW McCutchen, CW TI A theoretical solution for the frictionless rolling contact of cylindrical biphasic articular cartilage layers - Comment SO JOURNAL OF BIOMECHANICS LA English DT Letter C1 NIDDK,CELL BIOL & GENET LAB,NIH,BETHESDA,MD 20892. RP Mann, RW (reprint author), MIT,77 MASSACHUSETTS AVE,ROOM 3-137,CAMBRIDGE,MA 02139, USA. NR 2 TC 1 Z9 1 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9290 J9 J BIOMECH JI J. Biomech. PD JAN PY 1997 VL 30 IS 1 BP 99 EP 99 DI 10.1016/S0021-9290(96)00098-X PG 1 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA VY603 UT WOS:A1997VY60300015 PM 8970932 ER PT J AU Shi, YB IshizuyaOka, A AF Shi, YB IshizuyaOka, A TI Autoactivation of Xenopus thyroid hormone receptor beta genes correlates with larval epithelial apoptosis and adult cell proliferation SO JOURNAL OF BIOMEDICAL SCIENCE LA English DT Article DE thyroid hormone receptor; Xenopus laevis; metamorphosis; apoptosis; cell proliferation ID AMPHIBIAN METAMORPHOSIS; MOLECULAR MECHANISMS; CONNECTIVE-TISSUE; SMALL-INTESTINE; PROTEIN GENE; EXPRESSION; LAEVIS; ALPHA; EMBRYOGENESIS; SUPERFAMILY AB The thyroid hormone (T-3)-dependent amphibian metamorphosis involves degeneration of larval tissues through programmed cell death (apoptosis) and concurrent proliferation and differentiation of adult cell types. As the mediators of the causative effects of T-3 on metamorphosis, both thyroid hormone receptor (TR) alpha and beta genes have been found to be expressed in different tissues during this process. In particular, the Xenopus TR beta genes have been shown to be regulated by T-3 at the transcriptional level and their expression correlates with organ-specific metamorphosis. We demonstrate here by in situ hybridization that the Xenopus TR beta genes are regulated in a cell-type specific manner that correlates with tissue transformation. In particular, they are found to be expressed in the larval intestinal epithelial cells prior to their apoptotic degeneration and in the proliferating cells of the adult epithelium, connective tissue, and muscles. However, they are repressed again upon the differentiation of these adult cells. These results implicate that TR beta participates both in inducing apoptosis and stimulating cell proliferation during development. C1 DOKKYO UNIV,SCH MED,DEPT ANAT,MIBU,TOCHIGI 32102,JAPAN. RP Shi, YB (reprint author), NICHHD,MOL EMBRYOL LAB,BLDG 18T,RM 101,BETHESDA,MD 20892, USA. NR 38 TC 26 Z9 26 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1021-7770 J9 J BIOMED SCI JI J. Biomed. Sci. PD JAN-FEB PY 1997 VL 4 IS 1 BP 9 EP 18 DI 10.1007/BF02255588 PG 10 WC Cell Biology; Medicine, Research & Experimental SC Cell Biology; Research & Experimental Medicine GA YD086 UT WOS:A1997YD08600002 ER PT J AU Trihn, D Jeang, KT Semmes, OJ AF Trihn, D Jeang, KT Semmes, OJ TI HTLV-1 tax and cytokeratin: Tax-expressing cells show morphological changes in keratin-containing cytoskeletal networks SO JOURNAL OF BIOMEDICAL SCIENCE LA English DT Article DE HTLV-I; cytokeratin; invasive; motility; HAM/TSP; regulatory protein ID VIRUS TYPE-I; EPIDERMOLYSIS-BULLOSA SIMPLEX; SERUM RESPONSE FACTOR; B PRECURSOR P105; NF-KAPPA-B/REL; INTERMEDIATE FILAMENTS; TRANSCRIPTIONAL ACTIVATOR; TRANSACTIVATOR TAX; MOLECULAR-BIOLOGY; C-REL AB Human T cell leukemia virus type I (HTLV-I) has been linked to the development of an aggressive lymphoproliferative disorder (adult T cell leukemia), a chronic neurodegenerative presentation (HTLV-I-associated myelopathy/tropical spastic paraparesis) and numerous less well-defined inflammatory conditions. The viral regulatory protein Tax has been implicated in cellular transformation events leading to the onset of adult T cell leukemia. Details on the stepwise processes through which Tax induces morphological changes in cells are poorly understood. We show here that Tax can bind to a class of intermediate filaments, the cytokeratins (Ker). Tax interacts with the 1B helical coil of keratin 8, a domain critical for higher-order intermediate filament matrix formation. Expression of Tax in epithelial cells visibly altered the structural pattern of the Ker network. In a T lymphocyte cell line, induction of Tax expression resulted in increased cellular adherence/invasion of Matrigel filters. We propose that one aspect of Tax function is the induction of morphological changes in cellular cytoskeletal structures. This finding for Tax-expressing cells might be one factor contributing directly to the pathogenesis of HTLV-I disease(s). C1 UNIV VIRGINIA,MYLES H THALER CTR,DEPT MICROBIOL,CHARLOTTESVILLE,VA 22908. NIAID,MOL VIROL SECT,MOL MICROBIOL LAB,BETHESDA,MD 20892. RI Jeang, Kuan-Teh/A-2424-2008 NR 52 TC 13 Z9 13 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1021-7770 J9 J BIOMED SCI JI J. Biomed. Sci. PD JAN-FEB PY 1997 VL 4 IS 1 BP 47 EP 53 DI 10.1007/BF02255593 PG 7 WC Cell Biology; Medicine, Research & Experimental SC Cell Biology; Research & Experimental Medicine GA YD086 UT WOS:A1997YD08600007 ER PT J AU Walter, MJ Lehky, TJ Levin, MC Fox, CH Jacobson, S AF Walter, MJ Lehky, TJ Levin, MC Fox, CH Jacobson, S TI Detection of HTLV-I in peripheral blood lymphocytes from patients with chronic HTLV-I-associated myelopathy tropical spastic paraparesis and asymptomatic carriers by PCR in situ hybridization SO JOURNAL OF BIOMEDICAL SCIENCE LA English DT Article DE HTLV-I infection; HTLV-I-associated, myelopathy/tropical, spastic paraparesis; PCR in situ hybridization ID VIRUS TYPE-I; POLYMERASE CHAIN-REACTION; MONONUCLEAR-CELLS; PROVIRAL DNA; INSITU HYBRIDIZATION; NEUROLOGICAL DISEASE; CEREBROSPINAL-FLUID; CLINICAL ENTITY; INFECTION; AMPLIFICATION AB Less than 5% of people infected with human T-lymphotropic virus type I (HTLV-I) develop HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic progressive neurologic disease. A number of factors have been implicated in the development of HAM/TSP including heterogeneity of viral sequences, host-genetic background, viral-specific cellular immune responses and viral load. This study examined the presence of HTLV-I tax DNA in peripheral blood lymphocytes (PBL) from 2 chronic HAM/TSP patients and 2 asymptomatic HTLV-I carriers by using PCR-in situ hybridization (PCR-ISH) for the in situ presence of proviral HTLV-I tax DNA. By this technique, rare PBL from these HTLV-I-infected individuals contained HTLV-I DNA. PCR-ISH did not detect any difference in the number of infected cells between HAM/TSP patients and asymptomatic carriers. C1 NINCDS,NEUROIMMUNOL BRANCH,NIH,BETHESDA,MD 20892. MOL HISTOL LABS,GAITHERSBURG,MD. NR 40 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1021-7770 J9 J BIOMED SCI JI J. Biomed. Sci. PD JAN-FEB PY 1997 VL 4 IS 1 BP 54 EP 60 DI 10.1007/BF02255594 PG 7 WC Cell Biology; Medicine, Research & Experimental SC Cell Biology; Research & Experimental Medicine GA YD086 UT WOS:A1997YD08600008 ER PT J AU Carlomagno, T Mantile, G Bazzo, R Miele, L Paolillo, L Mukherjee, AB Barbato, G AF Carlomagno, T Mantile, G Bazzo, R Miele, L Paolillo, L Mukherjee, AB Barbato, G TI Resonance assignment and secondary structure determination and stability of the recombinant human uteroglobin with heteronuclear multidimensional NMR SO JOURNAL OF BIOMOLECULAR NMR LA English DT Article DE secondary structure; uteroglobin; h-cc10kDa ID NUCLEAR-MAGNETIC-RESONANCE; MULTIPLE QUANTUM COHERENCE; ANTIINFLAMMATORY PEPTIDES ANTIFLAMMINS; PLATELET-ACTIVATING-FACTOR; CHEMICAL-SHIFT INDEX; CELL 10-KDA PROTEIN; PROGESTERONE-BINDING; KDA PROTEIN; PHOSPHOLIPASE-A2 ACTIVITY; CORRELATION SPECTROSCOPY AB Human uteroglobin (h-UG) or Clara cell 10kDa (cc10kDa) is a steroid-dependent, 17 kDa homodimeric, secretory protein with potent anti-inflammatory/immunomodulatory properties. However, the exact physiological role still remains to be determined. It has been hypothesised that its activity is exerted through the binding of a specific target represented by a small molecule (still unknown), and that the binding is regulated by the formation/disruption of two cysteine bonds. The binding properties of the reduced UG have been proved in vitro for several different molecules, but no in vivo data are available to date. However, binding has been observed between reduced rabbit UG and a protein of an apparent molecular mass of 90 kDa and, more recently, we found an h-UG-binding protein (putative receptor), of an apparent molecular mass of 190 kDa, on the surface of several cell types. The recognition involves oxidised h-UG. These findings pose the problem of the relevance of the oxidation state in the recognition process. To determine the solution structure of the oxidised h-UG, we produced wild-type as well as uniformly N-15- and N-15/C-13-labelled samples of the recombinant protein. The assignments of the H-1, N-15 and C-13 resonances are presented, based on a series of homonuclear 2D and 3D and heteronuclear 2D and 3D double and triple resonance NMR experiments. Our results indicate that h-UG is an extremely stable protein under a wide range of temperatures and pH conditions. The secondary structure in solution is in general agreement with previously reported crystal structures of rabbit UG, suggesting that cc10kDa and h-UG are indeed the same protein. Small local differences found in the N- and C-terminal helices seem to support the hypothesis that flexibility involves these residues; moreover, it possibly accounts for the residual binding properties observed when the protein is in the oxidised state. C1 IRBM P ANGELETTI SPA,I-00040 POMEZIA,ITALY. UNIV NAPLES FEDERICO II,DEPT CHEM,I-80100 NAPLES,ITALY. NIH,SECT DEV GENET,HERITABLE DISORDERS BRANCH,BETHESDA,MD 20892. RI Barbato, Gaetano/G-4904-2011 NR 76 TC 12 Z9 12 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0925-2738 J9 J BIOMOL NMR JI J. Biomol. NMR PD JAN PY 1997 VL 9 IS 1 BP 35 EP 46 DI 10.1023/A:1018619501038 PG 12 WC Biochemistry & Molecular Biology; Spectroscopy SC Biochemistry & Molecular Biology; Spectroscopy GA WH730 UT WOS:A1997WH73000005 PM 9081543 ER PT J AU Coxon, B Sari, N Mulard, LA Kovac, P Pozsgay, V Glaudemans, CPJ AF Coxon, B Sari, N Mulard, LA Kovac, P Pozsgay, V Glaudemans, CPJ TI Investigation by NMR spectroscopy and molecular modeling of the conformations of some modified disaccharide antigens for Shigella dysenteriae type 1 SO JOURNAL OF CARBOHYDRATE CHEMISTRY LA English DT Article ID O-SPECIFIC ANTIGEN; SPIN-LATTICE RELAXATION; POLYSACCHARIDE; DERIVATIVES; LIPOPOLYSACCHARIDE; OLIGOSACCHARIDES; HEXAACETATE; RATES AB The O-polysaccharide of Shigella dysenteriae type 1 is made up of multiple repeats of the linear tetrasaccharide 3)-alpha-L-Rhap-(1-->2)-alpha-D-Galp-(1-->3)-alpha-D-GlcpNAc-(1-->3)-alpha-L-Rhap-(1-->, for which the antigenic determinant for a murine monoclonal IgM antibody is the disaccharide alpha-L-Rhap-(1-->2)-alpha-D-Galp. This disaccharide and various analogs have been studied by 2D NOESY, POESY, and TOCSY NMR spectroscopy, in conjunction with proton spin-lattice relaxation rate measurements, restrained molecular mechanics, and restrained molecular dynamics with simulated annealing. It has been found that replacement of any single hydroxyl group in the determinant by a hydrogen atom, or replacement of any single hydroxyl group in the Gal residue by a fluorine atom has little if any influence on the conformation of the resulting derivatives. C1 NIDDKD,MED CHEM LAB,NIH,BETHESDA,MD 20892. RP Coxon, B (reprint author), NATL INST STAND & TECHNOL,DIV BIOTECHNOL,GAITHERSBURG,MD 20899, USA. NR 35 TC 7 Z9 7 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 0732-8303 J9 J CARBOHYD CHEM JI J. Carbohydr. Chem. PY 1997 VL 16 IS 6 BP 927 EP 946 DI 10.1080/07328309708006549 PG 20 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA XR831 UT WOS:A1997XR83100013 ER PT J AU Channavajjala, LS Eidsath, A Saxinger, WC AF Channavajjala, LS Eidsath, A Saxinger, WC TI A simple method for measurement of cell-substrate attachment forces: Application to HIV-1 Tat SO JOURNAL OF CELL SCIENCE LA English DT Article DE cell adhesion; buoyant force; HIV-1 Tat ID HUMAN-IMMUNODEFICIENCY-VIRUS; EXTRACELLULAR-MATRIX PROTEINS; INITIAL BINDING; GROWTH-FACTOR; ADHESION; FIBRONECTIN; TYPE-1; EXPRESSION; INTEGRIN; IDENTIFICATION AB In order to understand the importance of cell attachment to HIV-1 Tat, we quantified the strength of cell attachment to immobilized Tat in microtiter plate wells by the application of buoyant force. By replacing the attachment medium with dense medium, and subjecting the attached cells in the microtiter plates to centrifugal force in the conventional upright position, weakly binding and strongly binding cells could be discriminated (and separated) by varying the centrifugal speed. The strength of attachment of HT1080 cells to Tat was compared with that of the well-known extracellular matrix (ECM) proteins fibronectin and vitronectin. We observed that all three proteins mediated significant attachment of HT1080 cells both at 4 degrees C and 37 degrees C. However, unlike the ECM proteins, Tat was unable to engage in higher strength binding when the temperature was raised to 37 degrees C. The relatively weak binding of HT1080 cells to Tat (in the order of 3.0 mu dynes/picomole of coated Tat) and lack of strengthening of binding to Tat at physiologic temperature suggests that this protein does not mimic adhesion molecule function. We anticipate that the methodology developed and described here will be useful in a wide variety of cell-matrix and cell-cell interaction studies. C1 NCI,TUMOR CELL BIOL LAB,NIH,BETHESDA,MD 20892. NIH,NATL CTR RES RESOURCES,BIOMED ENGN & INSTRUMENTAT PROGRAM,BETHESDA,MD 20892. NR 41 TC 24 Z9 25 U1 0 U2 3 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD JAN PY 1997 VL 110 BP 249 EP 256 PN 2 PG 8 WC Cell Biology SC Cell Biology GA WH025 UT WOS:A1997WH02500015 PM 9044055 ER PT J AU Boone, CW Bacus, JW Bacus, JV Steele, VE Kelloff, GJ AF Boone, CW Bacus, JW Bacus, JV Steele, VE Kelloff, GJ TI Properties of intraepithelial neoplasia relevant to the development of cancer chemopreventive agents SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT International Cancer Chemoprevention Conference CY OCT 13-16, 1996 CL BEIJING, PEOPLES R CHINA DE intraepithelial neoplasia; cancer chemoprevention; genomic instability; clonal evolution; gene amplification; computer-assisted image analysis; biomarkers ID SQUAMOUS-CELL CARCINOMA; MAMMALIAN GENE AMPLIFICATION; IN-SITU; TUMOR PROGRESSION; ACTINIC KERATOSIS; BLADDER-CANCER; COLON-CANCER; ALLELIC LOSS; PROLIFERATION; DYSPLASIA AB Cancer chemoprevention is concerned with the development of drugs or diet supplements that will avert the onset or stop the progression of the intraepithelial neoplasia which precedes invasive cancer. Two basic processes underlie the onset and development of intraepithelial neoplasia. First is genomic instability (often associated with chronic diffuse epithelial hyperplasia), which is the increased production of genomic structural variants due to unrepaired DNA breaks with secondary formation of abnormal structures, including "mutator" mutations in genes responsible for genomic stability, gene copy amplification or loss from DNA breakage-fusion-anaphase bridge cycles, unequal sister chromatid exchange, and accumulation of double minutes. Second is the development within an epithelium having genomic instability of multicentric neoplastic lesions that independently progress through each of the following processes at a continuously accelerating rare: clonal evolution, hyperproliferation, production of genomic structural variants, and apoptosis. Recommended chemoprevention strategies based on these mechanisms are (l) early diagnosis and treatment of genomic instability before the appearance of intraepithelial neoplasia, i.e., during the "predysplastic" or "premorphologic" phase, (2) development of multiple agents that block intralesional proliferation at steps along the "command" pathways of mitotic signal transduction and along the "execute" pathways of synthesis of daughter cell components, (3) development of nontoxic antiinflammatory agents, antioxidants, antimutagens, and proapoptotics, (4) avoidance of "clonal escape" through use of drug combinations, and (5) use of computer-assisted quantitative image analysis to assay modulation of surrogate endpoints in chemoprevention clinical trials. (C) 1998 Wiley-Liss, Inc. C1 NCI, Div Canc Prevent & Control, Chemoprevent Branch, NIH, Bethesda, MD 20892 USA. Bacus Labs Imaging Syst, Elmhurst, IL USA. RP Boone, CW (reprint author), NCI, Div Canc Prevent & Control, Chemoprevent Branch, NIH, Bethesda, MD 20892 USA. NR 69 TC 12 Z9 12 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1997 SU 28-29 BP 1 EP 20 PG 20 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ZL634 UT WOS:000073454800003 ER PT J AU Lantry, LE Zhang, ZQ Gao, F Crist, KA Wang, Y Kelloff, GJ Lubet, RA You, M AF Lantry, LE Zhang, ZQ Gao, F Crist, KA Wang, Y Kelloff, GJ Lubet, RA You, M TI Chemopreventive effect of perillyl alcohol on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone induced tumorigenesis in (C3H/Hej x A/J)F-1 mouse lung SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT International Cancer Chemoprevention Conference CY OCT 13-16, 1996 CL BEIJING, PEOPLES R CHINA DE CAAX motif; farnesyltransferase inhibitor; K-ras; lung cancer; monoterpene ID TOBACCO-SPECIFIC NITROSAMINES; RAS ONCOGENES; D-LIMONENE; PROTEIN ISOPRENYLATION; HUMAN CANCER; A/J MICE; INHIBITION; MONOTERPENE; TUMORS; TRANSFORMATION AB This study was designed to test the chemopreventive potential of perillyl alcohol, an inhibitor of farnesyltransferase, in a mouse lung tumor bioassay. Perillyl alcohol is a naturally occurring monoterpene found in lavender, cherries, and mint. We have shown previously that the majority of lung tumors in this bioassay have an activating mutation in the K-ras gene, which occurs early in the development of mouse lung carcinogenesis. The Ras protein undergoes a series of post-translational modifications, the first of which is farnesylation at the cysteine of the C-terminal CAAX motif. These modifications lead to the anchoring of Ras p21 to the plasma membrane in its biologically active state. Activated Ras p21 couples growth regulatory signals from receptor tyrosine kinases to cytoplasmic second messengers. In a preliminary study, we determined the maximum tolerated dose of perillyl alcohol to be 75 mg/kg body weight. For the bioassay, 5-week-old male (C3H/He] X A/J) F1 hybrid mice were randomized into trial groups, and treated with perillyl alcohol three times per week i.p., starting 1 week prior to initiation with the carcinogen NNK, and continuing for 22 weeks after initiation. Our results show a 22% reduction in tumor incidence, and a 58% reduction in tumor multiplicity. Our study demonstrates that perillyl alcohol is an effective chemopreventive compound in the mouse lung tumor bioassay. (C) 1998 Wiley-Liss, Inc. C1 Med Coll Ohio, Dept Pathol, Toledo, OH 43699 USA. Med Coll Ohio, Dept Surg, Toledo, OH 43699 USA. NCI, Rockville, MD USA. RP You, M (reprint author), Med Coll Ohio, Dept Pathol, Hlth Educ Bldg,Room 202,3000 Arlington Ave, Toledo, OH 43699 USA. NR 38 TC 6 Z9 6 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1997 SU 27 BP 20 EP 25 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ZM634 UT WOS:000073559800006 ER PT J AU Bacus, JW Bacus, JV Stoner, GD Moon, RC Kelloff, GJ Boone, CW AF Bacus, JW Bacus, JV Stoner, GD Moon, RC Kelloff, GJ Boone, CW TI Quantitation of preinvasive neoplastic progression in animal models of chemical carcinogenesis SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT International Cancer Chemoprevention Conference CY OCT 13-16, 1996 CL BEIJING, PEOPLES R CHINA DE preinvasive neoplasia; image analysis; chemical carcinogenesis; rat; mouse ID IMAGE-ANALYSIS; BREAST-CANCER; DISCRIMINATION; EXPRESSION; ROCS AB An assay method that precisely quantitates the cellular and tissue changes associated with early, preinvasive neoplasia is much needed as a surrogate endpoint biomarker (SEB) in clinical trials to predict the potential efficacy of chemopreventive agents in bringing about cancer incidence reduction. Quantification of histological changes at the tissue level are potentially powerful SEB's since these visually apparent changes are common in all neoplastic development, regardless of tissue type or neoplastic cause. Currently subjective inspection of the histological appearance of sectioned and stained material, or "grading," by experienced pathologists is used to evaluate neoplastic progression. This has well-known limitations of reproducibility accuracy, and resolution of grading scale. Since neoplastic changes are visually apparent and morphologic in nature, quantification by image analysis is a measurement modality of choice. Image analysis was implemented through the use of high-resolution "tiled" images of complete tissue sections. A histological grading system, or "scale," was developed that could be expressed in terms of normal deviate units of multiple and different morphometric descriptors. Neoplastic growth was characterized quantitatively with multiple measurements on each tissue image tile, which were combined into a single number for each tile, i.e., a histologic grade per tile, and parameters from the distributions of these measurements were used to represent the histologic grade for the entire region considered. This concept provided a uniform final scale in similar units of measurement, regardless of which tissues were graded. Also, the grading scale automatically adjusted measurement variance for different tissues by using normal tissue for each different type to obtain the normalization to standard deviation it) units. This further defined a uniform final scale and maintained standard references. Using this method, results from two weil-known animal models of carcinogenesis, squamous cell carcinoma of SENCAR mouse skin induced by benzo(a)pyrene (B[a]P), and squamous cell carcinoma of the rat esophagus induced by N-nitrosomethylbenzylamine (NMBA), were compared to each other. Image analysis was performed on skin tissue sections from a total of 64 SENCAR mice, and esophagus tissue sections from 96 Fischer-344 rats. In both cases, a quantitative expression of the preinvasive neoplastic response to the carcinogen as a function of time of exposure was expressed along a continuous grading scale in standard deviation units (z). in the SENCAR mouse skin animal model, similar cohorts of 4 mice at 20 weeks showed significant modulation of B[a]P-induced neoplasia by treatment with the antiproliferative agent difluoromethylornithine, P<.05. In the rat esophagus animal model, similar cohorts of 6 rats at 10 and 15 weeks showed significant modulation of NMBA-induced neoplasia by treatment with the antimutagen phenethyl isothiocyanate, P<.05. (C) 1998 Wiley-Liss, Inc. C1 Bacus Labs Inc, Unit 8A, Elmhurst, IL 60126 USA. Ohio State Univ, Ctr Comprehens Canc, Arthur G James Canc Hosp, Columbus, OH 43210 USA. Univ Illinois, Specialized Canc Ctr, Chicago, IL USA. NCI, Div Canc Prevent & Control, Chemoprevent Branch, NIH, Bethesda, MD 20892 USA. RP Bacus, JW (reprint author), Bacus Labs Inc, Unit 8A, 910 Riverside Dr, Elmhurst, IL 60126 USA. NR 35 TC 2 Z9 3 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1997 SU 28-29 BP 21 EP 38 PG 18 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ZL634 UT WOS:000073454800004 ER PT J AU Herzog, CR Lubet, RA You, M AF Herzog, CR Lubet, RA You, M TI Genetic alterations in mouse lung tumors: Implications for cancer chemoprevention SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT International Cancer Chemoprevention Conference CY OCT 13-16, 1996 CL BEIJING, PEOPLES R CHINA DE mouse lung; genetic alteration; aberrant gene expression; surrogate endpoint biomarkers; cancer chemoprevention ID INDUCED PULMONARY ADENOMAS; K-RAS MUTATIONS; SUPPRESSOR GENE; A/J MICE; 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE NNK; BENZOPYRENE-INDUCED NEOPLASIA; RESISTANCE LOCUS; DNA METHYLATION; ALLELIC LOSSES; B6C3F1 MICE AB Specific genetic alterations affecting known tumor suppressor genes and proto-oncogenes occur during mouse lung tumorigenesis. These include mutational activation of the K-ras gene, commonly seen at. a frequency of about 80% in both spontaneously occurring and chemically induced adenomas and adenocarcinomas of the lung, suggesting that it is an early event that persists into malignancy. Allelic loss of the p16 tumor suppressor gene also is a frequent event, occurring in about 50% of mouse lung adenocarcinomas, but rarely in lung adenomas, suggesting that it may play a role in malignant conversion or progression of lung turners. Other genetic alterations detected in mouse lung tumors include reduced expression of Rb and p16, and increased c-myc expression. Alterations of these genes are also common in the genesis of human lung cancer. Genetic linkage analysis to identify human lung cancer susceptibility genes is difficult due to the genetic heterogeneity and exposure to environmental risk factors. The mouse lung tumor model has become a valuable alternative for identifying such genes. Recently, loci responsible for mouse lung tumor susceptibility have been mapped to chromosomes 6, 9, 17, and 19, while those linked to lung tumor resistance have been mapped to chromosomes 4, 11, 12, and 18. Known candidate susceptibility or resistance genes include the K-ras proto-oncogene on chromosome 6, and the p16 tumor supressor gene on chromosome 4. With evidence of considerable overlap between the genetic alterations that underlie human and mouse lung tumorigenesis, the mouse lung tumor model has been expanded to include pre-clinical screening of chemopreventive agents against human lung cancer. Studies on the modulation of genetic defects in mouse lung tumors by known and potential chemopreventive agents should further the goal of developing an effective prevention and treatment of lung cancer. (C) 1998 Wilev-Liss, Inc. C1 Med Coll Ohio, Dept Pathol, Toledo, OH 43614 USA. NCI, Chemoprevent Branch, NIH, Bethesda, MD 20892 USA. RP You, M (reprint author), Med Coll Ohio, Dept Pathol, HEB 202,3055 Arlington Ave, Toledo, OH 43614 USA. NR 99 TC 7 Z9 7 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1997 SU 28-29 BP 49 EP 63 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ZL634 UT WOS:000073454800006 ER PT J AU Dong, G Loukinova, E Smith, CW Chen, Z Van Waes, C AF Dong, G Loukinova, E Smith, CW Chen, Z Van Waes, C TI Genes differentially expressed with malignant transformation and metastatic tumor progression of murine squamous cell carcinoma SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT International Cancer Chemoprevention Conference CY OCT 13-16, 1996 CL BEIJING, PEOPLES R CHINA DE squamous cell carcinoma; differential display; tropomyosin alpha; cytokine KC; ribosomal protein L18a; antigen Sp17 ID GROWTH STIMULATORY ACTIVITY; EPIDERMAL-CELLS; MELANOMA-CELLS; WW DOMAIN; SKIN CARCINOGENESIS; SIGNAL-TRANSDUCTION; EPITHELIAL-CELLS; MESSENGER-RNA; PROTEIN GENE; NUDE-MICE AB Molecular changes occurring with tumor formation and metastasis need to be identified in order to define novel markers and targets for chemoprevention and therapy. Cell lines from a multistage model of murine squamous cell carcinoma were analyzed for differences in gene expression using mRNA differential display. mRNA was isolated from primary keratinocytes, an in vitro transformed keratinocyte line (Pam 212), and three metastatic cell lines derived from Pam 212 following tumor progression in vivo. cDNA was synthesized by reverse transcription and amplified by PCR using 72 primer combinations to screen and compare approximately 3,600 sequences. Five cDNAs with a differential expression pattern confirmed by Northern blot analysis were cloned and sequenced, revealing homology with known genes. The gene encoding tropomyosin alpha was preferentially expressed in primary keratinocytes; genes for tyrosine kinase Yes-associated protein (YAP65) and ribosomal protein L18a were preferentially expressed in transformed and metastatic tumor cell lines; and genes for the Gro-alpha family cytokine KC and antigen Sp17 exhibited increased expression in the three metastatic cell lines. The structure and function of the genes identified suggest that they may possibly be linked to fell shape and motility, signal transduction, protein synthesis, growth, granulocyte chemotaxis, and angiogenesis. This study demonstrates the ability of mRNA differential display to detect altered gene expression in this tumor progression model of murine squamous cell carcinoma, and the potential usefulness of this approach for identification of candidate genes as chemoprevention markers and targets. (C) 1998 Wiley-Liss, Inc. C1 NINCDS, Head & Neck Surg Branch, Tumor Biol Sect, NIH, Bethesda, MD 20892 USA. RP Van Waes, C (reprint author), NINCDS, Head & Neck Surg Branch, Tumor Biol Sect, NIH, Bldg 10,Rm 5D55,MSC-1419, Bethesda, MD 20892 USA. NR 62 TC 9 Z9 9 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1997 SU 28-29 BP 90 EP 100 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ZL634 UT WOS:000073454800010 ER PT J AU Crist, KA Wang, Y Lubet, RA Steele, VE Kelloff, GJ You, M AF Crist, KA Wang, Y Lubet, RA Steele, VE Kelloff, GJ You, M TI Effect of early vs. late administration of 4-hydroxyphenylretinamide (4-HPR) on N-methyl-N-nitrosourea (MNU)-induced mammary tumorigenesis SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT International Cancer Chemoprevention Conference CY OCT 13-16, 1996 CL BEIJING, PEOPLES R CHINA DE chemoprevention; H-ras; PCNA; rat; retinoid ID CELL NUCLEAR ANTIGEN; RETINOIC ACID RECEPTOR; DNA POLYMERASE-DELTA; BREAST-CANCER; AUXILIARY PROTEIN; FEMALE RATS; CARCINOGENESIS; N-(4-HYDROXYPHENYL)RETINAMIDE; DIFFERENTIATION; INHIBITION AB Mammary tumors were induced in 48-52-day-old female Sprague-Dawley rats in metestrus or diestrus with a single jugular injection of MNU (50 mg/kg). Control rats received the saline vehicle (Group 4 n = 9). Rats were fed 4% Teklad diet containing either 0 (Group 3, n = 20) or 782 mg 4-HPR/kg diet. 4-HPR supplementation was initiated either 1 week prior to (Group 1, n = 14) or 4 weeks following MNU administration (Group 2, n = 19). Neither body weight nor food intake differed significantly between treatment groups. Feeding of 4-HPR 1 week prior to tumor induction reduced the number of tumors (0.8+/-.2) when compared to MNU control rats (2.1+/-.4). Immunohistochemical staining of mammary tumor sections for PCNA was quantitated by microdensitometry and expressed as an HSCORE. No differences in HSCORE were observed between tumor groups although the percentage of nuclear area occupied by intermediate and darkly stained nuclei was reduced in the late 4-HPR group. GC-->AT transitions in codon 12 of the H-ras gene were detected in 50% (12/24) of MNU control tumors, 60% (6/10) of early 4-HPR tumors, and 38% (6/16) of late 4-HPR tumors. Mutation rates did not differ significantly between groups. 4-HPR appears to be a more effective chemopreventive when fed during the initiation period. (C) 1908 Wiley-Liss, Inc. C1 Med Coll Ohio, Dept Surg, Toledo, OH 43699 USA. Med Coll Ohio, Dept Pathol, Toledo, OH 43699 USA. NCI, Div Canc Prevent & Control, Chemoprevent Invest Studies Branch, NIH, Bethesda, MD 20892 USA. RP Crist, KA (reprint author), Med Coll Ohio, Dept Surg, POB 10008, Toledo, OH 43699 USA. NR 42 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1997 SU 27 BP 92 EP 99 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ZM634 UT WOS:000073559800015 ER PT J AU Hu, L Lin, L Crist, KA Kelloff, GJ Steele, VE Lubet, RA You, M Wang, Y AF Hu, L Lin, L Crist, KA Kelloff, GJ Steele, VE Lubet, RA You, M Wang, Y TI Detection of differentially expressed genes in methylnitrosourea-induced rat mammary adenocarcinomas SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article; Proceedings Paper CT International Cancer Chemoprevention Conference CY OCT 13-16, 1996 CL BEIJING, PEOPLES R CHINA DE rat; mammary tumor; gene expression; competitive cDNA library screening ID HUMAN BREAST-CANCER; EPITHELIAL-CELLS; CARCINOMAS; MICROARRAY; DISPLAY; MASPIN; IDENTIFICATION; INDUCTION; GENETICS; PATTERNS AB In this study, altered gene expression in five methylnitrosourea (MNU)-induced rat mammary adenocarcinomas was investigated using a newly developed competitive cDNA library screening assay. In order to detect the differentially expressed cDNA transcripts, three cDNA libraries (rat mammary, rat liver, and rat kidney) with over 18,000 clones were differentially screened with competing normal and neoplastic mammary cDNA probes. Ninety-eight clones indicated by competitive hybridization to be differentially expressed in tumors were verified by dot-blot hybridization analysis. Of these clones, 45 were found to be overexpressed while 53 were underexpressed in tumors. Forty-five of the confirmed clones were further analyzed by single-pass cDNA sequence determination. Four clones showed homology with cytochrome oxidase subunit I, polyoma virus PTA noncoding region, cytoplasmic beta-actin, and mouse secretory protein containing thrombospondin motifs. Further investigation into the potential roles of these identified genes should contribute significantly to our understanding of the molecular mechanism(s) of rat mammary tumorigenesis. (C) 1998 Wiley-Liss, Inc. C1 Med Coll Ohio, Dept Pathol, Toledo, OH 43699 USA. NCI, Chemoprevent Branch, Bethesda, MD 20892 USA. RP Wang, Y (reprint author), Med Coll Ohio, Dept Pathol, 3000 Arlington Ave, Toledo, OH 43699 USA. NR 40 TC 3 Z9 3 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1997 SU 28-29 BP 117 EP 124 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA ZL634 UT WOS:000073454800013 ER PT J AU Herrington, EE Ram, TG Salomon, DS Johnson, GR Gullick, WJ Kenney, N Hosick, HL AF Herrington, EE Ram, TG Salomon, DS Johnson, GR Gullick, WJ Kenney, N Hosick, HL TI Expression of epidermal growth factor-related proteins in the aged adult mouse mammary gland and their relationship to tumorigenesis SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID HUMAN-BREAST-CANCER; MESSENGER-RNA; FACTOR-ALPHA; TGF-ALPHA; EPITHELIAL-CELLS; TRANSGENIC MICE; FUNCTIONAL-PROPERTIES; INSITU HYBRIDIZATION; SECONDARY STRUCTURE; FACTOR RECEPTOR AB Mammary glands from female BALB/c mice of different ages and parity were screened for production of three epidermal growth factor (EGF) related transforming growth factors and their corresponding mRNAs. Glands were obtained from 2-26-month-old nulliparous, 4-26-month-old parous, and 2-8-month-old midpregnant mice. Reverse-transcribed polymerase chain reaction (RT-PCR) was used to screen for mRNA from the transforming growth factor alpha (TGF alpha), cripto-1 (CR-1), and amphiregulin (AR) genes in extracts of whole mammary glands. TGF alpha, CR-1, and AR transcripts were detected in all of the mammary glands assayed. in situ hybridization was then used to localize these mRNAs among various cell types in sections of glands. TGF alpha mRNA levels were low in the mammary epithelium from young nulliparous mice, high in the stroma of midpregnant mammary glands, and highest in luminal epithelium of the aged glands. AR mRNA levels were high and remained unchanged in all developmental stages. CR-1 mRNA level increased with age and was detected primarily in epithelium, with some scattered expression in adjacent stroma. Finally, TGF alpha CR-1, and AR proteins were immunolocalized in histological sections of mammary glands from the various developmental stages. TGF alpha was detected sporadically in midpregnant mice, with more conspicuous reactivity seen in 18-26-month-old mice (38% of mice). CR-1 immunoreactivity was detected in 100% of the 18-26-month-old glands but not in any other age groups. Strong AR immunoreactivity was observed in in all glands, including 100% of the 18-26-month-old glands. Staining for all three of these growth factors was observed primarily in the epithelium, with some reactivity detected in the periductal fibroblasts. No significant difference was discerned between glands from nulliparous and parous animals. We also found intense CR-1 and AR mRNA expression and strong immunoreactivity in seven different carcinogen-induced and eight spontaneous mammary tumors. Our results demonstrate that these growth factors accumulate in significant amounts in the old gland of both nulliparous and parous mice. The observations suggest that these growth factors are positioned to contribute to abnormal development in the older mammary gland, predisposing them to tumorigenesis. (C) 1997 Wiley-Liss, Inc. C1 WASHINGTON STATE UNIV,DEPT GENET & CELL BIOL,PULLMAN,WA 99164. NCI,TUMOR IMMUNOL & BIOL LAB,TUMOR GROWTH FACTOR SECT,NIH,BETHESDA,MD 20892. US FDA,DIV CYTOKINE BIOL,BETHESDA,MD 20892. HAMMERSMITH HOSP,IMPERIAL CANC RES FUND,MOL ONCOL UNIT,LONDON W12 0NN,ENGLAND. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. FU NCI NIH HHS [CA 62039] NR 49 TC 30 Z9 30 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JAN PY 1997 VL 170 IS 1 BP 47 EP 56 PG 10 WC Cell Biology; Physiology SC Cell Biology; Physiology GA WA981 UT WOS:A1997WA98100006 PM 9012784 ER PT J AU Horinaka, N Artz, N Jehle, J Takahashi, S Kennedy, C Sokoloff, L AF Horinaka, N Artz, N Jehle, J Takahashi, S Kennedy, C Sokoloff, L TI Examination of potential mechanisms in the enhancement of cerebral blood flow by hypoglycemia and pharmacological doses of deoxyglucose SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article; Proceedings Paper CT XVII International Symposium on Cerebral Blood Flow and Metabolism CY JUL 02-06, 1995 CL COLOGNE, GERMANY DE insulin; [C-14]iodoantipyrine; nitric oxide; glucoprivation ID INSULIN-INDUCED HYPOGLYCEMIA; NITRIC-OXIDE SYNTHASE; UNANESTHETIZED RATS; OXIDATIVE-METABOLISM; VASCULAR-RESISTANCE; RELAXING FACTOR; BRAIN; RECOVERY; INHIBITION; 2-DEOXY-D-GLUCOSE AB Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [C-14]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 mM, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3- concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p, injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 mM) or pharmacological doses of deoxyglucose. C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. RI Takahashi, Shinichi/L-3454-2013 NR 39 TC 26 Z9 26 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JAN PY 1997 VL 17 IS 1 BP 54 EP 63 PG 10 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA VZ028 UT WOS:A1997VZ02800008 PM 8978387 ER PT J AU Spencer, J Suess, P Better, W Herning, RI AF Spencer, J Suess, P Better, W Herning, RI TI Microtremors during a sustained concentration task from boys previously exposed to opiates in-utero SO JOURNAL OF CHILD & ADOLESCENT SUBSTANCE ABUSE LA English DT Article ID INFANTS; TREMOR AB Fourteen boys who were exposed to opiates in-utero (drug exposed) maintained their index finger in a static, weight-forced position while attempting to maintain a stylus at a fix point producing intentional microtremors. After 2.5 minutes, significant increases in tremor were recorded in mean peak (6 Hz) amplitude while accuracy of sustaining this response was significantly reduced. Age matched boys (ages 7-12) who were raised in an environment in which drugs were used but were not directly exposed in-utero (lifestyle group N = 13) or a standard control group (N = 12), did not show similar changes over time. Resting or postural-extended tremor did differ among groups. Alcohol, marihuana, or tobacco usage by the mother or birth weight of the child did not predict subsequent group differences in tremor. Both biological and environmental variables plus type and sensitivity of measurement used are critical elements for describing long-term, potential residual drug effects in children, especially as they relate to sustained attention. C1 NIDA, Mol Neuropychiat Sect, Div Intramural Res, NIH, Baltimore, MD 21224 USA. RP Herning, RI (reprint author), NIDA, Mol Neuropychiat Sect, Div Intramural Res, NIH, POB 5180, Baltimore, MD 21224 USA. NR 15 TC 0 Z9 0 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 1067-828X J9 J CHILD ADOLES SUBST JI J. Child Adolesc. Subst. Abus. PY 1997 VL 7 IS 2 BP 53 EP 63 PG 11 WC Substance Abuse SC Substance Abuse GA YZ925 UT WOS:000072308600004 ER PT J AU Giedd, JN Smith, KG AF Giedd, JN Smith, KG TI Child psychopharmacology on the Internet online access to journal abstracts and articles SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article AB Advances in information technology now offer several options for child and adolescent psychopharmacologists to navigate the increasingly complex terrain of scientific literature and keep abreast of the rapidly changing advances in our field. MEDLINE, the world's largest database of medical literature, can be accessed and searched by a variety of free or fee-based services. In addition to efficient retrieval of citations and abstracts based on subject, author, or title, many of these services now provide, for a fee, the entire text and graphics of articles (displayed on computer screen, fared, or mailed). There are also current awareness services to alert the user when new requested literature become available as well as services to send via e-mail the tables of contents of requested journals (sometimes prior to paper publication). For online citation and abstract retrieval, we found that free services, such as PubMed, performed as good or better than fee-based services. Physicians' Online, sponsored by the pharmaceutical industry, offered the lowest price for full-text manuscript delivery. In this article, we review literature search, delivery, and update services and offer some tips on how to most effectively use these resources. C1 NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA. NIH Lib, Informat & Educ Serv Sect, Natl Ctr Res Resources, Bethesda, MD USA. RP Giedd, JN (reprint author), NIMH, Child Psychiat Branch, 10 Ctr Dr,MSC 1367,Bldg 10,Room 4C110, Bethesda, MD 20892 USA. 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 2 TC 4 Z9 4 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PY 1997 VL 7 IS 3 BP 201 EP 210 DI 10.1089/cap.1997.7.201 PG 10 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA YV225 UT WOS:000071801900005 PM 9466236 ER PT J AU Vitiello, B Hoagwood, K AF Vitiello, B Hoagwood, K TI Pediatric pharmacoepidemiology: Clinical applications and research priorities in children's mental health SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article C1 NIMH, Child & Adolescent Treatment & Prevent Intervent, Div Serv & Intervent Res, Rockville, MD 20857 USA. RP Vitiello, B (reprint author), NIMH, Child & Adolescent Treatment & Prevent Intervent, Div Serv & Intervent Res, 5600 Fishers Lane, Rockville, MD 20857 USA. NR 11 TC 11 Z9 11 U1 1 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PY 1997 VL 7 IS 4 BP 287 EP 290 DI 10.1089/cap.1997.7.287 PG 4 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA ZC844 UT WOS:000072624000007 PM 9542699 ER PT J AU Mahalati, K Dawson, RB Collins, JO Lietman, S Pearlman, S Gulden, D AF Mahalati, K Dawson, RB Collins, JO Lietman, S Pearlman, S Gulden, D TI Characteristics of 73 patients, 1984-1993, treated by plasma exchange for Guillain-Barre syndrome SO JOURNAL OF CLINICAL APHERESIS LA English DT Article DE GBS; Miller-Fisher; CIDP; EAN; CMV; EBV; plasma exchange; hemapheresis; demyelination; wallerian degeneration ID CAMPYLOBACTER-JEJUNI INFECTION; PERIPHERAL-NERVE MYELIN; ANTIBODY; PLASMAPHERESIS; CELLS AB Acute Guillain-Barre syndrome (GBS) is a demyelinating polyneuropathy which responds readily to plasma exchange (PEX). According to the North American Acute GBS PEX study there is a 50% or more reduction in the recovery time if PEX is initiated early in the course of the disease. Demyelinating antibodies are usually IgM. IgA antibodies require prolonged PEX. Patients with predominant IgG antibodies have chronic inflammatory demyelinating polyneuropathy (CIDP), which requires an even longer course of PEX, over weeks to months or years. We reviewed records of 73 patients with the initial diagnosis of GBS treated with PEX. Among these patients, 55 had classic GBS, three had the Miller-Fisher variant, two had CIDP, and 13 had demyelinating-like polyneuropathies associated with other conditions including malignancy, vaccine-related myelitis, steroid-induced myopathy, polymyositis, botulism, gram-negative sepsis, Sjogren's, and AIDS. Hughes grading system was used. Patients were graded 3 to 5, with grade 3 patients being unable to walk 5 m without support, grade 4 patients being bed or chair bound, and grade 5 patients being ventilator dependent. Of 60 unassociated (GBS) demyelinating cases receiving a mean of 6.5 PEX procedures, 13 (21%) were intubated early in thr treatment, with four (6%) remaining ventilator dependent post-PEX. Of 51 non-intubated patients, 15 became ambulatory post-PEX. Patients with the Miller-Fisher variant showed improvement within 6 hours of PEX initiation. We did not investigate correlation of GBS with infection; however, we did observe a rise in CMV titer among 15% of the 58 patients with acute GBS. Considering our results we believe that intensive PEX on a daily basis for a few days is necessary for severely affected individuals. We advise five to nine procedures at consultation unless early, rapid recovery occurs. (C) 1997 Wiley-Liss, Inc. C1 THERAPEUT APHERESIS CTR,BALTIMORE RH TYPING LAB,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,BLOOD RES LAB,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT PATHOL,BALTIMORE,MD 21201. UNIV MARYLAND,SCH MED,DEPT NEUROL,BALTIMORE,MD 21201. NIH,DEPT TRANSFUS MED,CTR CLIN,HEMAPHERESIS SECT,BETHESDA,MD. GREATER BALTIMORE MED CTR,DEPT PATHOL,BALTIMORE,MD 21204. MARYLAND GEN HOSP,BALTIMORE,MD. NR 27 TC 5 Z9 5 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0733-2459 J9 J CLIN APHERESIS JI J. Clin. Apheresis PY 1997 VL 12 IS 3 BP 116 EP 121 PG 6 WC Hematology SC Hematology GA YE216 UT WOS:A1997YE21600003 PM 9365863 ER PT J AU Raghuramulu, N Reddy, V Underwood, B AF Raghuramulu, N Reddy, V Underwood, B TI Anterior segment collagenase activity in children with keratomalacia SO JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION LA English DT Article DE children; collagenase; corneal lesions; malnutrition; tears ID VITAMIN-A-DEFICIENT; CONTROL RATS; CORNEAS; RELEASE AB The total proteins and collagenase activity in tears as well as alpha(2)-macroglobulin (anticollagenase) and vitamin A levels in serum, were estimated in 35 malnourished children with corneal lesions, in 30 malnourished controls (age matched) without corneal lesions, and in 19 normal children. Also eye swabs from some of the children were cultured for bacteria. Significant decreases in the serum vitamin A and alpha(2)-macroglobulin levels and in tear total protein levels were observed in malnourished children when compared with the normal values. Further, the reduction was more pronounced in children with corneal lesions than in those without them. Interestingly, the tear collagenase activity was significantly elevated in malnourished children with corneal lesions as compared with that in those without lesions or in normal children. Similarly, more bacteria could be cultured in samples from malnourished children (with/without corneal lesions) than in those from normal children. These observations clearly indicate that the elevated levels of anterior segment collagenase may play an important role in the pathogenesis of corneal lesions. C1 Indian Council Med Res, Natl Inst Nutr, Hyderabad 500007, Andhra Pradesh, India. NEI, NIH, Bethesda, MD 20892 USA. RP Raghuramulu, N (reprint author), Indian Council Med Res, Natl Inst Nutr, Jamai Osmania Po, Hyderabad 500007, Andhra Pradesh, India. NR 19 TC 0 Z9 0 U1 0 U2 0 PU JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION PI KYOTO PA KYOTO PREFECTURAL UNIV MED, GRAD SCH MEDICAL SCIENCE, DEPT MOLECULAR GASTROENTEROLOGY & HEPATOLOGY, KYOTO, 602-8566, JAPAN SN 0912-0009 EI 1880-5086 J9 J CLIN BIOCHEM NUTR JI J. Clin. Biochem. Nutr. PY 1997 VL 23 IS 3 BP 197 EP 204 PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA ZV417 UT WOS:000074302500007 ER PT J AU OMarcaigh, AS Puck, JM Pepper, AE DeSantes, K Cowan, MJ AF OMarcaigh, AS Puck, JM Pepper, AE DeSantes, K Cowan, MJ TI Maternal mosaicism for a novel interleukin-2 receptor gamma-chain mutation causing X-linked severe combined immunodeficiency in a Navajo kindred SO JOURNAL OF CLINICAL IMMUNOLOGY LA English DT Article DE severe combined immunodeficiency; cytokine receptor; X-linked inheritance; genetics; bone marrow transplantation ID POPULATION; HOTSPOTS; DISEASE AB X-linked severe combined immunodeficiency disease (SCID) results from mutations of IL2RG, the gene encoding the interleukin-2 receptor gamma chain, also known as the common gamma chain (gamma(c)). A distinct form of autosomal recessive SCID, occurs at an increased frequency among the Navajo Native American population. The disease gene responsible for autosomal Navajo SCID remains to be determined. We report the occurrence of X-linked SCID in a Navajo Native American kindred with two affected brothers. X-linked SCID was suggested by the presce ence of circulating B cells and the absence of surface gamma(c) expression in a cell line derived from an affected male. A C-to-T transition was demonstrated in exon 5 of the IL2RG gene, resulting in the substitution of tryptophan for arginine at position 224. This change was not present in the peripheral blood lymphocytes of the mother, thus proving the occurrence of a new mutation in the maternal germline. This report underscores the importance of establishing a specific genetic diagnosis for SCID cases and illustrates the inherent difficulties in providing genetic counseling in cases involving mosaicism. C1 NIH,IMMUNOL GENET SECT,LAB GENE TRANSFER,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. RP OMarcaigh, AS (reprint author), UNIV CALIF SAN FRANCISCO,DIV PEDIAT BONE MARROW TRANSPLANTAT,BOX 1278,505 PARNASSUS AVE,SAN FRANCISCO,CA 94143, USA. FU NIAID NIH HHS [AI28339-03] NR 14 TC 12 Z9 13 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0271-9142 J9 J CLIN IMMUNOL JI J. Clin. Immunol. PD JAN PY 1997 VL 17 IS 1 BP 29 EP 33 DI 10.1023/A:1027332327827 PG 5 WC Immunology SC Immunology GA WJ841 UT WOS:A1997WJ84100004 PM 9049783 ER PT J AU Auerbach, AD Verlander, PC Brown, KE Liu, JM AF Auerbach, AD Verlander, PC Brown, KE Liu, JM TI New molecular diagnostic tests for two congenital forms of anemia SO JOURNAL OF CLINICAL LABORATORY ANALYSIS LA English DT Article DE Fanconi anemia; molecular diagnosis; ARMS assay; aplastic anemia; birth defects; leukemia; genetic disease; B19 parvovirus ID FANCONI-ANEMIA; PRENATAL-DIAGNOSIS; GROUP-C; COMPLEMENTATION; REGISTRY; FACC; SUSCEPTIBILITY; INFECTION; BREAKAGE; MUTATION AB Congenital hypoplastic anemias are a rare and heterogeneous group of disorders. This paper reviews new molecular diagnostic tests in two distinct forms of congenital anemias, anemia due to transplacental infection with B19 parvovirus and Fanconi anemia. In both instances, molecular assays making use of amplification of DNA by the polymerase chain reaction have been used to diagnose either a specific viral infection or gene mutation responsible for a disorder. Recognition of these entities has important prognostic and therapeutic implications. (C) 1997 Wiley-Liss, Inc. C1 NIH,HEMATOL BRANCH,NHLBI,BETHESDA,MD 20892. ROCKEFELLER UNIV,LAB HUMAN GENET & HEMATOL,NEW YORK,NY 10021. OI Auerbach, Arleen/0000-0002-6911-8379 FU NHLBI NIH HHS [R01 HL 32987] NR 27 TC 3 Z9 3 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 0887-8013 J9 J CLIN LAB ANAL JI J. Clin. Lab. Anal. PY 1997 VL 11 IS 1 BP 17 EP 22 PG 6 WC Medical Laboratory Technology SC Medical Laboratory Technology GA WF105 UT WOS:A1997WF10500004 PM 9021520 ER PT J AU Maloney, EM Brown, LM Kurman, CC Fuchs, D Nelson, DL Wachter, H Blattner, WA Tollerud, DJ AF Maloney, EM Brown, LM Kurman, CC Fuchs, D Nelson, DL Wachter, H Blattner, WA Tollerud, DJ TI Temporal variability in immunological parameters: Peripheral blood mononuclear cell subsets, serum immunoglobulins, and soluble markers of immune system activation SO JOURNAL OF CLINICAL LABORATORY ANALYSIS LA English DT Article DE T-cell subsets; soluble factors; CD4 cells ID CIGARETTE-SMOKING; POPULATION; NEOPTERIN; NONSMOKERS AB T-cell subsets and soluble factors of immune system activation are increasingly used as biologic markers of disease and predictors of disease progression. For example, changes in CD4 cells and CD4:CD8 ratio, sIL-2R, B(2)M, neopterin, and IgA have been used in predicting AIDS onset and progression. We examined the temporal variability of T-cell subsets, monocytes, natural killer cells, B cells, immunoglobulins, soluble interleukin-2 receptor (sIL-2R), neopterin, and beta-2 microglobulin (B(2)M) among 135 adults tested at two time points similar to 3 months apart. The purpose of the study was twofold: (1) to assess the stability of these measures at two points in time, and (2) to investigate which parameters tend to track together over time, i.e., show significant longitudinal correlation. Mean population values for these immunologic parameters remained remarkably stable over the 3-month period. However, individual subjects exhibited significant temporal variability for many parameters. Unlike observations in patients with AIDS, changes in immunoglobulins and other soluble factors were not significantly correlated with changes in cellular subsets over the same period. However, change in B(2)M was correlated with change in neopterin (r = .35, P less than or equal to .0001), and change in IgA was correlated with changes in IgG and IgM (r = .44, r = .54, P less than or equal to .001 for both). Characterizing this temporal variability in a healthy population provides important information for researchers applying these tests in clinical and epidemiological studies. (C) 1997 Wiley-Liss, Inc. C1 NCI, EPIDEMIOL & BIOSTAT PROGRAM, BETHESDA, MD 20892 USA. NCI, METAB BRANCH, BETHESDA, MD 20892 USA. UNIV INNSBRUCK, INST MED CHEM & BIOCHEM, A-6020 INNSBRUCK, AUSTRIA. UNIV PITTSBURGH, GRAD SCH PUBL HLTH, DEPT ENVIRONM & OCCUPAT HLTH, PITTSBURGH, PA 15261 USA. RP Maloney, EM (reprint author), NCI, VIRAL EPIDEMIOL BRANCH, 6130 EXECUT BLVD, ROOM 434, ROCKVILLE, MD 20852 USA. NR 17 TC 6 Z9 6 U1 0 U2 2 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0887-8013 J9 J CLIN LAB ANAL JI J. Clin. Lab. Anal. PY 1997 VL 11 IS 4 BP 190 EP 195 PG 6 WC Medical Laboratory Technology SC Medical Laboratory Technology GA XG444 UT WOS:A1997XG44400003 PM 9219059 ER PT J AU Wheeler, CM Yamada, T Hildesheim, A Jenison, SA AF Wheeler, CM Yamada, T Hildesheim, A Jenison, SA TI Human papillomavirus type 16 sequence variants: Identification by E6 and L1 lineage-specific hybridization SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID CERVICAL INTRAEPITHELIAL NEOPLASIA; POLYMERASE CHAIN-REACTION; CYTOLOGICALLY NORMAL WOMEN; EPIDERMODYSPLASIA-VERRUCIFORMIS; GENETIC-HETEROGENEITY; NUCLEOTIDE-SEQUENCE; CONSENSUS PRIMERS; CLINICAL-SAMPLES; DNA-SEQUENCE; RISK-FACTORS AB A catalog of human papillomavirus (HPV) type 16 (HPV-16) E6 and L1 signature nucleotides was used to develop PCR-based oligonucleotide probe systems capable of distinguishing HPV-16 class and subclass variants. Twenty-three E6-specific oligonucleotide probes targeting 13 variant nucleotide positions and 12 L1-specific oligonucleotide probes targeting 6 variant nucleotide positions were used to characterize HPV-16-containing cervicovaginal lavage specimens. Nucleotide positions that could be distinguished included E6 nucleotides 109, 131, 132, 143, 145, 178, 183, 286, 289, 335, 350, 403, and 532 and L1 nucleotides 6695, 6721, 6803, 6854, 6862, and 6994. Combined hybridization patterns were assigned on the basis of the predicted HPV-16 class, subclass, or minor class variants described previously (T. Yamada, C. M. Wheeler, A. L. Halpern, A.-C. M. Stewart, A. Hildesheim, and S. A. Jenison, J. Virol. 69:7743-7753, 1995). The major HPV-16 variant lineages detected included European prototype-like (E-P), Asian (As), Asian-American (AA), and African (Af1 and Af2) lineages. In addition, E-G131, an E-class variant, and AA-G183, an AA-class variant, were also identified. For each clinical specimen, DNA hybridization results were compared to nucleotide sequence determinations. Targeted L1 and E6 marker nucleotides covaried within all HPV-16 variant isolates examined. These hybridization-based methods result in minimal misclassification error, are amenable to targeting additional lineage-specific nucleotide positions, and should facilitate the large-scale, low-cost analysis of HPV-16 variants in epidemiologic investigations. Specifically, these methods will facilitate epidemiologic studies of HPV-16 transmission and natural history, as well as studies of associations between HPV variants, host immune responses, and cervical neoplasia. C1 UNIV NEW MEXICO, CANC RES & TREATMENT CTR, SCH MED, DEPT MED, ALBUQUERQUE, NM 87131 USA. UNIV NEW MEXICO, CANC RES & TREATMENT CTR, SCH MED, DEPT MICROBIOL, ALBUQUERQUE, NM 87131 USA. UNIV NEW MEXICO, CANC RES & TREATMENT CTR, SCH MED, EPIDEMIOL & CANC CONTROL PROGRAM, ALBUQUERQUE, NM 87131 USA. NCI, DIV CANC ETIOL, EPIDEMIOL & BIOSTAT PROGRAM, BETHESDA, MD 20872 USA. RP Wheeler, CM (reprint author), UNIV NEW MEXICO, CANC RES & TREATMENT CTR, SCH MED, DEPT CELL BIOL, 900 CAMINO DE SALUD NE, ALBUQUERQUE, NM 87131 USA. FU NCI NIH HHS [CA57975]; NIAID NIH HHS [AI32917] NR 70 TC 87 Z9 90 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0095-1137 EI 1098-660X J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1997 VL 35 IS 1 BP 11 EP 19 PG 9 WC Microbiology SC Microbiology GA VY566 UT WOS:A1997VY56600003 PM 8968874 ER PT J AU EspinelIngroff, A Bartlett, M Bowden, R Chin, NX Cooper, C Fothergill, A McGinnis, MR Menezes, P Messer, SA Nelson, PW Odds, FC Pasarell, L Peter, J Pfaller, MA Rex, JH Rinaldi, MG Shankland, GS Walsh, TJ Weitzman, I AF EspinelIngroff, A Bartlett, M Bowden, R Chin, NX Cooper, C Fothergill, A McGinnis, MR Menezes, P Messer, SA Nelson, PW Odds, FC Pasarell, L Peter, J Pfaller, MA Rex, JH Rinaldi, MG Shankland, GS Walsh, TJ Weitzman, I TI Multicenter evaluation of proposed standardized procedure for antifungal susceptibility testing of filamentous fungi SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID AMPHOTERICIN-B; BROTH MACRODILUTION; CANDIDA-ALBICANS; FLUCONAZOLE; INFECTIONS; THERAPY AB A multicenter study was conducted to expand the generation and analysis of data that supports the proposal of a reference method for the antifungal susceptibility testing of filamentous fungi. Broth microdilution MICs of amphotericin B and itraconazole were determined in 11 centers against 30 coded duplicate pairs of Aspergillus spp., Fusarium spp., Pseudallescheria boydii, and Rhizopus arrhizus. The effect of inoculum density (approximately 10(3) and 10(4) CFU/ml), incubation time (24, 48, and 72 h), and procedure of MIC determination (conventional and colorimetric [Alamar Blue] evaluation of growth inhibition) on intra- and interlaboratory agreement was analyzed. Based on intra- (97 to 100%) and interlaboratory (94 to 95%) agreement for both drugs, the overall optimal testing conditions identified were determination of colorimetric MICs after 48 to 72 h of incubation with an inoculum density of approximately 10(4) CFU/ml. These testing conditions are proposed as guidelines for a reference broth microdilution method. C1 INDIANA UNIV,SCH MED,INDIANAPOLIS,IN 46202. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. COLUMBIA PRESBYTERIAN MED CTR,NEW YORK,NY 10032. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77555. UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET HOSP,LAB SERV,SAN ANTONIO,TX 78284. UNIV IOWA,COLL MED,DEPT PATHOL,IOWA CITY,IA 52242. UNIV TEXAS,SCH MED,CTR STUDY EMERGING & REEMERGING PATHOGENS,DEPT INTERNAL MED,DIV INFECT DIS,HOUSTON,TX 77030. JANSSEN RES FDN,B-2340 BEERSE,BELGIUM. NCI,MYCOL UNIT,BETHESDA,MD 20892. NCI,IMMUNOCOMPROMISED HOST SECT,PEDIAT BRANCH,BETHESDA,MD 20892. REG MYCOL REFERENCE LAB,GLASGOW,LANARK,SCOTLAND. RP EspinelIngroff, A (reprint author), VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DIV INFECT DIS,BOX 980049,1101 E MARSHALL ST,RICHMOND,VA 23298, USA. NR 20 TC 198 Z9 206 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1997 VL 35 IS 1 BP 139 EP 143 PG 5 WC Microbiology SC Microbiology GA VY566 UT WOS:A1997VY56600024 PM 8968895 ER PT J AU Leibenluft, E AF Leibenluft, E TI Issues in the treatment of women with bipolar illness SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on the Dynamics of Sex - Gender Differences in Psychiatric Disorders at the 149th Annual Meeting of the American-Psychiatric-Association CY MAY 05, 1996 CL NEW YORK, NEW YORK SP Amer Psychiat Assoc ID TREATMENT-RESISTANT DEPRESSION; CYCLING AFFECTIVE-DISORDER; LITHIUM-CARBONATE; ANTIDEPRESSANT EFFICACY; PSYCHIATRIC-DISORDERS; RECURRENT DEPRESSION; FLUOXETINE TREATMENT; PUERPERAL PSYCHOSIS; POSTPARTUM BLUES; MOOD DISORDERS AB Gender differences in bipolar illness have been relatively neglected, but the course of the illness does appear to differ between men and women. Compared with bipolar men, bipolar women are clearly more likely to develop the rapid cycling form of the illness and may also suffer from more episodes of depression. Therefore, the literature concerning the treatment of rapid cycling bipolar disorder and of bipolar depression is reviewed. in addition, effects of bipolar illness on the female reproductive cycle are discussed. Since bipolar women are at high risk to develop postpartum episodes, the use of mood stabilizers in pregnancy is discussed. C1 NIMH, Clin Psychobiol Branch, Bethesda, MD 20892 USA. RP Leibenluft, E (reprint author), 10-4S-239,10 Ctr Dr MSC 1390, Bethesda, MD 20892 USA. NR 90 TC 36 Z9 38 U1 2 U2 2 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1997 VL 58 SU 15 BP 5 EP 11 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA YN783 UT WOS:000071206400002 PM 9427871 ER PT J AU Solomon, SD Davidson, JRT AF Solomon, SD Davidson, JRT TI Trauma: Prevalence, impairment, service use, and cost SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on Repairing the Shattered Self - Recovering From Trauma, at the 149th Annual Meeting of the American-Psychiatric-Association CY MAY 05, 1996 CL NEW YORK, NY SP Amer Psychiat Assoc, US Pharm Grp, Roerig Div, Pfizer Inc ID POSTTRAUMATIC-STRESS-DISORDER; SEXUAL ASSAULT HISTORY; MENTAL-HEALTH-SERVICES; POPULATION; FREQUENCY; VICTIMS; IMPACT; EVENTS; WOMEN AB A review of the literature on the epidemiology of trauma reveals that traumatic events are common: most Americans experience at least one over the course of their lives. According to recent estimates, 5% of men and 10% to 12% of women will suffer from posttraumatic stress disorder (PTSD) sometime in their lives, and for victims of traumas such as rape, the rate may be as high as 60% to 80%. For at least a third of sufferers, PTSD is a persistent condition lasting many years. Over 80% of persons with PTSD suffer from other psychiatric disorders. Many also experience marital, occupational, financial, and health problems. While trauma victims are disproportionate users of the health care system, they are reluctant to seek mental health treatment. Consequences of exposure to trauma are enormously costly, not only to the victims, but also to our health care system and to society as a whole. C1 DUKE UNIV,MED CTR,ANXIETY & TRAUMAT STRESS PROGRAM,DURHAM,NC. RP Solomon, SD (reprint author), NIH,OFF BEHAV & SOCIAL SCI RES,7550 WISCONSIN AVE,ROOM 8C-16,BETHESDA,MD 20892, USA. NR 30 TC 164 Z9 167 U1 3 U2 13 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1997 VL 58 SU 9 BP 5 EP 11 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA XX441 UT WOS:A1997XX44100002 PM 9329445 ER PT J AU Weinberger, DR AF Weinberger, DR TI The biological basis of schizophrenia: New directions SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on Practical Issues in Using Olanzapine CY AUG 01-03, 1996 CL BOSTON, MA SP Eli Lilly & Co, Physicians Postgrad Press Inc ID EXCITOTOXIC HIPPOCAMPAL DAMAGE; SUSCEPTIBILITY GENES; CORTICAL DEVELOPMENT; ENTORHINAL CORTEX; HYPERRESPONSIVENESS; ABNORMALITIES; DISTURBANCES; DYSFUNCTION; BINDING; SEARCH AB The desire to understand the pathophysiology of schizophrenia has inspired an explosion in research over the past decade. This review highlights some key studies that have led to fundamental changes in our understanding of this disorder, focusing on the search for genes in schizophrenia, as well as several recent alternatives to the original dopamine hypothesis of schizophrenia. Advances in genetic methodology have allowed schizophrenia researchers to conduct genome-wide searches for susceptibility genes. Although these studies have identified several regions that demonstrate potential linkage with schizophrenia, a definitive generic cause has not yet been proved. Recent neurochemical hypotheses have focused on the cortical amino acid neurotransmitter systems (i.e., glutamate and GABA), while anatomical studies suggesting abnormal brain development and premorbid functional deficits have led some researchers to propose a neurodevelopmental origin for schizophrenia. A sizable database can be marshaled in support of each of these ideas, but none as yet fully explain the biological basis of schizophrenia. RP Weinberger, DR (reprint author), NIMH,ST ELIZABETHS HOSP,CTR NEUROSCI,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,NIH,WASHINGTON,DC 20032, USA. NR 47 TC 52 Z9 52 U1 1 U2 5 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PY 1997 VL 58 SU 10 BP 22 EP 27 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA XP738 UT WOS:A1997XP73800005 PM 9265913 ER PT J AU Duncan, RP Slavkin, H Holbrook, K Challoner, D Frankl, S Cohen, DW Machen, B AF Duncan, RP Slavkin, H Holbrook, K Challoner, D Frankl, S Cohen, DW Machen, B TI Academic management in an era of change. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD. BOSTON UNIV,BOSTON,MA 02215. UNIV MICHIGAN,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1 EP 1 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000001 ER PT J AU Mangan, D Braveman, N Rubinstein, M Hausch, G Gartland, W Lipton, J Jackson, L AF Mangan, D Braveman, N Rubinstein, M Hausch, G Gartland, W Lipton, J Jackson, L TI Contemporary grantsmanship. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NIH,DIV EXTRAMURAL RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 7 EP 7 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000004 ER PT J AU Nanci, A Zalzal, S Hashimoto, J Slaby, I Krebsbach, PH Hammarstrom, L AF Nanci, A Zalzal, S Hashimoto, J Slaby, I Krebsbach, PH Hammarstrom, L TI Ultrastructural immunolocalization of amelin and ameloblastin in rat incisor ameloblasts. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MONTREAL,MONTREAL,PQ,CANADA. NIDR,BETHESDA,MD 20892. KAROLINSKA INST,S-10401 STOCKHOLM,SWEDEN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 109 EP 109 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000107 ER PT J AU Antonucci, JM Fowler, BO Stansbury, JW AF Antonucci, JM Fowler, BO Stansbury, JW TI Facile synthesis of reactive organosilsesquioxanes for dental applications. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIST,GAITHERSBURG,MD 20899. NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 214 EP 214 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000213 ER PT J AU Eidelman, N Mathew, M Fowler, BO Breuer, E Golomb, G Skrtic, D AF Eidelman, N Mathew, M Fowler, BO Breuer, E Golomb, G Skrtic, D TI The possible role of calcium phosphonates in inhibition of calcium phosphate formation SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. NIDR,NIH,BETHESDA,MD 20892. NIST,AMER DENT ASSOC HLTH FDN,PRC,GAITHERSBURG,MD 20899. RI Breuer, Eli/E-8382-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 270 EP 270 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000269 ER PT J AU Sommer, B IbarakiOConnor, K Satomura, K Xu, T Eanes, ED Young, MF AF Sommer, B IbarakiOConnor, K Satomura, K Xu, T Eanes, ED Young, MF TI Detection of amelogenin mRNA in bones of transgenic mice. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BONE RES BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 274 EP 274 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000275 ER PT J AU Takahashi, K Bringas, P Caton, J Yamane, A Slavkin, HC ZeichnerDavid, M AF Takahashi, K Bringas, P Caton, J Yamane, A Slavkin, HC ZeichnerDavid, M TI IGF's control enamel gene expression during tooth morphogenesis in vivo. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 USCDS,CCMB,LOS ANGELES,CA. NIDR,BETHESDA,MD 20892. RI Zeichner-David, Margarita/A-6567-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 275 EP 275 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000272 ER PT J AU Souza, RD Sunavala, G Ohshima, T Kulkarni, AB MacDougall, M AF Souza, RD Sunavala, G Ohshima, T Kulkarni, AB MacDougall, M TI Differential patterns of expression of mouse dentin proteins. DSP and Dmp1. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,GENE TARGETING RES & CORE FACIL,BETHESDA,MD 20892. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 278 EP 278 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000277 ER PT J AU Parks, MS Eanes, ED Antonucci, JM Skrtic, D AF Parks, MS Eanes, ED Antonucci, JM Skrtic, D TI Mechanical properties of bioactive ACP/methacrylate composites. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. PHIL DENT CLIN,KYUNG KI DO,SOUTH KOREA. NIST,ADAHF,PRC,GAITHERSBURG,MD 20899. NIST,DMMG,GAITHERSBURG,MD 20899. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 504 EP 504 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000502 ER PT J AU Corrigan, JG Hamilton, KAS AF Corrigan, JG Hamilton, KAS TI Links between patented technology and NIDR-funded research. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. CHI RES INC,HADDON HTS,NJ. NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 597 EP 597 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000593 ER PT J AU Schumacher, GE Antonucci, JM Bennett, PS Code, JE AF Schumacher, GE Antonucci, JM Bennett, PS Code, JE TI N-phenyliminodiacetic acid as an etchant/primer for dentin bonding SO JOURNAL OF DENTAL RESEARCH LA English DT Article DE acid etching; adhesion; dental bonding; dentin-bonding agents; self-etching primer ID HARD TOOTH TISSUES; ADHESIVE; PHENYLGLYCINE; SUBSTITUTES; SYSTEMS; RESIN AB Effective composite-to-dentin bonding has been achieved by the sequential use of dilute aqueous nitric acid (HNO3) and acetone solutions of N-phenylglycine and a carboxylic acid monomer, e.g., p-PMDM. Both the HNO3 pre-treatment and the surface-initiated polymerization that results from reaction of infused N-phenylglycine and PMDM have been identified as key elements of this bonding system. In this study, N-phenyliminodiacetic acid, a unique imino acid derivative with acidic and chelating potential, was evaluated as a dual etchant/primer for dentin bonding. A randomized, 2(3) factorial design was used to study the effects of 3 factors on tensile bond strength (TBS): conditioner (HNO3 vs. no HNO3), primer (N-phenylglycine vs. N-phenyliminodiacetic acid), and primer solvent (acetone vs. acetone:H2O). The three-step protocol consisting of HNO3, N-phenylglycine in acetone, and PMDM in acetone served as the control. The hypothesis tested was that N-phenyliminodiacetic acid could act as both an effective conditioner (i.e., etchant) and as a primer. Two-step protocols that included only N-phenyliminodiacetic acid and PMDM were compared with the control. TBS (n = 10 per group) were determined after 24-hour storage in H2O and analyzed by ANOVA and Duncan's Multiple Range test. Primer solvent was critical for obtaining significant bonding to dentin when HNO3 was omitted. N-phenyliminodiacetic acid in acetone without prior HNO3 etching gave the lowest ranking mean TBS (95% CI, 3.8 +/- 1.9 MPa). In contrast, the mean TBS obtained from samples treated with N-phenyliminodiacetic acid in acetone:H2O without prior HNO3 etching was not statistically different (p > 0.05) from the mean TBS for the control (95% CI, 9.3 +/- 1.8 and 9.8 +/- 1.9 MPa, respectively). Due to its dual function as etchant and primer, N-phenyliminodiacetic acid in acetone:H2O provides for a simplified bonding technique that yields strong, PMDM-mediated adhesion to dentin. C1 NATL INST STAND & TECHNOL,DIV POLYMERS,DENT & MED MAT GRP,GAITHERSBURG,MD 20899. NIH,CODC,CTR CLIN,BETHESDA,MD 20892. NATL INST STAND & TECHNOL,PAFFENBARGER RES CTR,AMER DENT ASSOC HLTH FDN,GAITHERSBURG,MD 20899. FU NIDCR NIH HHS [DE05129, DE09322, Y0I DE30001] NR 25 TC 18 Z9 18 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD JAN PY 1997 VL 76 IS 1 BP 602 EP 609 PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WH344 UT WOS:A1997WH34400012 PM 9042084 ER PT J AU Eanes, ED Hailer, AW AF Eanes, ED Hailer, AW TI Fluoride effect on size of apatite crystals grown from physiological-like solutions. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BONE RES BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 672 EP 672 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000669 ER PT J AU Grisius, MM Fox, PC AF Grisius, MM Fox, PC TI Salivary IL-10 in primary Sjogren's syndrome. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 688 EP 688 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000685 ER PT J AU Kozelsky, CS Cisar, JO Yeung, MK AF Kozelsky, CS Cisar, JO Yeung, MK TI Molecular analysis of the cell wall polysaccharide from Streptococcus oralis strain 34. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 722 EP 722 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000722 ER PT J AU Berthold, CW Corey, SE Dionne, RA AF Berthold, CW Corey, SE Dionne, RA TI Triazolam drug levels following sublingually and orally administered premedication. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV PITTSBURGH,PITTSBURGH,PA. NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 804 EP 804 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000803 ER PT J AU White, SN Yu, Z Li, ZC Kipnis, V AF White, SN Yu, Z Li, ZC Kipnis, V TI Cyclic mechanical fatigue behavior of three dental porcelains SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV SO CALIF,LOS ANGELES,CA. NCI,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 995 EP 995 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68000991 ER PT J AU Brunelle, JA Streckfus, CF Kleinman, DV Winn, D Swango, PA AF Brunelle, JA Streckfus, CF Kleinman, DV Winn, D Swango, PA TI Denture-related oral mucosal lesions in US adults. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV MISSISSIPPI,JACKSON,MS 39216. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1031 EP 1031 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001025 ER PT J AU Giba, E Metter, EJ Streckfus, C Baum, B Ship, J AF Giba, E Metter, EJ Streckfus, C Baum, B Ship, J TI Longitudinal influence of menopause and HRT on parotid flow rates. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MICHIGAN,SCH DENT,ANN ARBOR,MI 48109. NIA,BETHESDA,MD 20892. NIDR,BETHESDA,MD. UNIV MISSISSIPPI,SCH DENT,UNIVERSITY,MS 38677. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1037 EP 1037 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001032 ER PT J AU Reid, KI Carlson, CA Rayens, MK Gracely, RH AF Reid, KI Carlson, CA Rayens, MK Gracely, RH TI Facial and thenar thermal thresholds in temporomandibular joint derangement. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV KENTUCKY,MAYO CLIN,LEXINGTON,KY 40506. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1073 EP 1073 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001070 ER PT J AU Wang, S Sun, C Gillanders, E Wang, YF FreasLutz, D Zhang, YJ Burmeister, JA Gunsolley, JC Schenkein, HA Diehl, SR AF Wang, S Sun, C Gillanders, E Wang, YF FreasLutz, D Zhang, YJ Burmeister, JA Gunsolley, JC Schenkein, HA Diehl, SR TI Evidence for susceptibility genes onset periodontitis. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. VIRGINIA COMMONWEALTH UNIV,CRCPD,RICHMOND,VA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1098 EP 1098 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001098 ER PT J AU Albandar, JM Brown, LJ Loe, H AF Albandar, JM Brown, LJ Loe, H TI Putative periodontal pathogens in early-onset periodontitis. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV CONNECTICUT,CTR HLTH,FARMINGTON,CT. NIDR,BETHESDA,MD 20892. AMER DENT ASSOC HLTH FDN,FARMINGTON,CT. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1102 EP 1102 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001100 ER PT J AU Gordon, SM Dionne, RA Brahim, JS Sang, CN Dubner, R AF Gordon, SM Dionne, RA Brahim, JS Sang, CN Dubner, R TI Differential effects of local anesthesia on central hyperalgesia. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1118 EP 1118 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001116 ER PT J AU Gordon, SM Rowan, J Dionne, RA AF Gordon, SM Rowan, J Dionne, RA TI Evaluation of a peripherally administered opioid in the oral surgery model. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1123 EP 1123 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001119 ER PT J AU Taichman, LB Shillitoe, EJ OConnell, BC Cheng, SH Blaese, RM AF Taichman, LB Shillitoe, EJ OConnell, BC Cheng, SH Blaese, RM TI Human gene therapy progress and prospects. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,PATIENT CARE BRANCH,BETHESDA,MD 20892. GENZYME CORP,BOSTON,MA. NIH,CLIN GENE THERAPY BRANCH,BETHESDA,MD 20892. SUNY STONY BROOK,STONY BROOK,NY 11794. SUNY SYRACUSE,SYRACUSE,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1159 EP 1159 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001153 ER PT J AU Watson, MR Horowitz, AM Garcia, I Canto, MT AF Watson, MR Horowitz, AM Garcia, I Canto, MT TI Oral health of Hispanic children and parent's knowledge, opinions and practices. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UNIV MARYLAND,BALTIMORE,MD 21201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1166 EP 1166 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001164 ER PT J AU Forrest, JL Horowitz, AM Bross, T AF Forrest, JL Horowitz, AM Bross, T TI Caries prevention knowledge, opinions and practices of dental hygienists: A pilot-study. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107. NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1613 EP 1613 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001608 ER PT J AU Fitzgerald, BP Kingman, A Hawley, CE Harrold, CQ Garrett, S Rams, TE AF Fitzgerald, BP Kingman, A Hawley, CE Harrold, CQ Garrett, S Rams, TE TI Reproducibility of calculated periodontal attachment level assessment in moderate-deep pockets. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TEMPLE UNIV,SCH DENT,PHILADELPHIA,PA. NIDR,NIH,BETHESDA,MD 20892. UNIV MARYLAND,SCH DENT,BALTIMORE,MD 21201. ATRIX LABS INC,FT COLLINS,CO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1720 EP 1720 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001717 ER PT J AU Kingman, A Albandar, JM AF Kingman, A Albandar, JM TI Validity of partial recording of attachment loss in early-onset periodontitis SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 3 Z9 3 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1722 EP 1722 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001722 ER PT J AU Muro, M Koseki, T Osaki, Y Nonaka, K Kato, S Kowashi, Y Nishihara, T AF Muro, M Koseki, T Osaki, Y Nonaka, K Kato, S Kowashi, Y Nishihara, T TI Suppressive affect of lipopolysaccharide on apoptosis in Actinobacillus actinomycetemcomitans-infected macrophages. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. HOKKAIDO UNIV,HS,SAPPORO,HOKKAIDO 060,JAPAN. KYUSHU UNIV,FUKUOKA 812,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1734 EP 1734 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001732 ER PT J AU Denucci, DJ Dionne, RA Chen, CC Meehan, SC AF Denucci, DJ Dionne, RA Chen, CC Meehan, SC TI SPECT bone scanning in the diagnosis of chronic idiopathic jaw pain. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CC,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1787 EP 1787 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001783 ER PT J AU Vij, K Eliav, E Ruda, MA AF Vij, K Eliav, E Ruda, MA TI The expression of dynorphin in the rat spinal cold following neuritis treatment. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV ILLINOIS,COLL DENT,CHICAGO,IL. NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1806 EP 1806 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001803 ER PT J AU Vissink, A Mitchell, JB OConnell, AC Denny, PC AF Vissink, A Mitchell, JB OConnell, AC Denny, PC TI Symposium: Radiation-induced xerostomia in cancer patients: Current treatments and future therapies. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV GRONINGEN HOSP,GRONINGEN,NETHERLANDS. NCI,BETHESDA,MD 20892. NIDR,BETHESDA,MD 20892. UNIV SO CALIF,LOS ANGELES,CA 90089. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1901 EP 1901 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001895 ER PT J AU Gooch, BF Kaste, LM Lockwood, SL Gift, HC AF Gooch, BF Kaste, LM Lockwood, SL Gift, HC TI Correlates of perceived condition of teeth in US children, 1988-1991. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 CDC,ATLANTA,GA 30333. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1914 EP 1914 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001913 ER PT J AU Canto, MT Goodman, HS Horowitz, AM Watson, MR AF Canto, MT Goodman, HS Horowitz, AM Watson, MR TI Hispanic youths' knowledge of oral cancer risk factors. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 VAMHCS,PERRY POINT,MD. UNIV MARYLAND,BALTIMORE,MD 21201. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1917 EP 1917 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001911 ER PT J AU Horowitz, AM Goodman, HS Yellowitz, JA Moon, HS AF Horowitz, AM Goodman, HS Yellowitz, JA Moon, HS TI Knowledge and behaviors concerning oral cancer among Maryland adults. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. UMAB,DEPT HLTH & MENTAL HGY,BALTIMORE,MD. SNU,SEOUL,SOUTH KOREA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1918 EP 1918 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001915 ER PT J AU Paik, DI Moon, HS Kim, JB Horowitz, AM AF Paik, DI Moon, HS Kim, JB Horowitz, AM TI National Survey of Korean Dentists' Knowledge and Opinions: Caries etiology and prevention. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 SEOUL NATL UNIV,SEOUL 151,SOUTH KOREA. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1919 EP 1919 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001912 ER PT J AU Yellowitz, JA Horowitz, AM Goodman, HS Farooq, NS AF Yellowitz, JA Horowitz, AM Goodman, HS Farooq, NS TI Dentists' knowledge, opinions, and practices related to oral cancer. A pilot survey SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UMAB,SCH DENT,NIDR,BETHESDA,MD. DEPT HLTH & MENTAL HGY,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1920 EP 1920 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001916 ER PT J AU Yamane, A Ohnuki, Y Saeki, Y Slavkin, H AF Yamane, A Ohnuki, Y Saeki, Y Slavkin, H TI Expression of IGF-II and skeletal muscle specific genes during tongue myogenesis. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TSURUMI UNIV,YOKOHAMA,KANAGAWA,JAPAN. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 1942 EP 1942 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68001939 ER PT J AU Thomas, HF Jiang, H Chen, J Macdougall, M Krebsbach, P AF Thomas, HF Jiang, H Chen, J Macdougall, M Krebsbach, P TI Ameloblastin expression by cells of the murine epithelial root sheath. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT PEDIAT DENT,SAN ANTONIO,TX 78284. NIDR,DEV BIOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2018 EP 2018 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002017 ER PT J AU Sun, D EmmertBuck, MR Fox, PC AF Sun, D EmmertBuck, MR Fox, PC TI Cytokine mRNA expression in human labial salivary glands in Sjogren's syndrome. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,NIH,BETHESDA,MD 20892. NCI,LP,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2084 EP 2084 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002082 ER PT J AU Benjavongkulchai, E Caterina, N BirkedalHansen, H Fox, PC AF Benjavongkulchai, E Caterina, N BirkedalHansen, H Fox, PC TI Matrix metalloproteinases in parotid saliva of primary Sjogren's syndrome patients. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 CHULALONGKORN UNIV,BANGKOK,THAILAND. NIDR,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2086 EP 2086 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002083 ER PT J AU Gannot, G Gannot, I Gandjbakhche, AH Bonner, RF Fox, PC AF Gannot, G Gannot, I Gandjbakhche, AH Bonner, RF Fox, PC TI Development of a non invasive method to diagnose Sjogren's syndrome. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,DCRT,NCRR,NIH,CDRH,FDA,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2088 EP 2088 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002084 ER PT J AU Lavigne, GJ DeLaat, A Capra, N Lobbezoo, F Blanchet, P Hallet, M Widmer, C AF Lavigne, GJ DeLaat, A Capra, N Lobbezoo, F Blanchet, P Hallet, M Widmer, C TI Clinical and neuropharmacological aspects of bruxism, Parkinson's disease, and idiopathic cranial-cervical dystonia (Meige's syndrome). SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV MONTREAL,MONTREAL,PQ H3C 3J7,CANADA. CATHOLIC UNIV LEUVEN,B-3000 LOUVAIN,BELGIUM. UNIV MARYLAND,COLLEGE PK,MD 20742. UNIV AMSTERDAM,NL-1012 WX AMSTERDAM,NETHERLANDS. NINCDS,NIH,BETHESDA,MD. UNIV FLORIDA,GAINESVILLE,FL 32611. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2089 EP 2089 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002085 ER PT J AU Hayes, C Lieff, S Dixon, M Strauss, R Slavkin, H AF Hayes, C Lieff, S Dixon, M Strauss, R Slavkin, H TI Current research on oral clefts SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TUFTS UNIV,SCH DENT MED,DEPT GEN DENT,MEDFORD,MA 02155. UNIV N CAROLINA,CHAPEL HILL,NC 27515. UNIV MANCHESTER,DEPT DENT MED & SURG,MANCHESTER M13 9PL,LANCS,ENGLAND. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2090 EP 2090 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002089 ER PT J AU BirkedalHansen, B Parker, M Gluckman, JL Stambrook, P Li, YQ Pavelic, ZP StetlerStevenson, WG AF BirkedalHansen, B Parker, M Gluckman, JL Stambrook, P Li, YQ Pavelic, ZP StetlerStevenson, WG TI Expression of stromelysins and matrilysin in head and neck SCC. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. UNIV CINCINNATI,DEPT OTOLARYNGOL HEAD & NECK SURG,CINCINNATI,OH 45221. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2141 EP 2141 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002135 ER PT J AU Skrtic, D Eanes, ED Breuer, E Golomb, G Alferiev, IS Solomon, V Eidelman, N AF Skrtic, D Eanes, ED Breuer, E Golomb, G Alferiev, IS Solomon, V Eidelman, N TI Effects of novel N-containing bisphosphonates on liposomal calcification. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. NIDR,BETHESDA,MD 20892. PRC,ADAHF,GAITHERSBURG,MD. RI Breuer, Eli/E-8382-2011 NR 0 TC 0 Z9 0 U1 1 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2184 EP 2184 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002180 ER PT J AU Berkman, ME Nuckolls, GI Shum, L Dashner, R Takahashi, I Slavkin, HC AF Berkman, ME Nuckolls, GI Shum, L Dashner, R Takahashi, I Slavkin, HC TI Regulation of the actin cytoskeleton during chondrogenesis, studies with C3 transferase SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIAMSD,CRANIOFACIAL DEV SECT,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2305 EP 2305 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002301 ER PT J AU Selwitz, RH Drury, TF NowjackRaymer, RE Gift, HC AF Selwitz, RH Drury, TF NowjackRaymer, RE Gift, HC TI SES, dental care, and racial patterns of root caries experience SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2552 EP 2552 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002547 ER PT J AU Albertini, TF Drury, TF Selwitz, RH AF Albertini, TF Drury, TF Selwitz, RH TI Evaluation of racial-ethnic patterns of selected tooth conditions. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2553 EP 2553 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002548 ER PT J AU Drury, TF NowjackRaymer, RE Selwitz, RH Gift, HC AF Drury, TF NowjackRaymer, RE Selwitz, RH Gift, HC TI Oral health profiles of US baby boomers. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2555 EP 2555 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002549 ER PT J AU NowjackRaymer, RE Drury, TF Selwitz, RH Gift, HC AF NowjackRaymer, RE Drury, TF Selwitz, RH Gift, HC TI Sociodemographic factors in oral health. Implications for worksite health promotion. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2559 EP 2559 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002551 ER PT J AU Wu, AJ Chen, ZJ Kan, EC Meehan, S Ambudkar, IS AF Wu, AJ Chen, ZJ Kan, EC Meehan, S Ambudkar, IS TI The effect of 2,5-di(tert-butyl)hydroquinone (BHQ) on a human salivary gland cell line. SO JOURNAL OF DENTAL RESEARCH 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 AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2631 EP 2631 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002623 ER PT J AU Lancaster, H OConnell, B Baum, BJ AF Lancaster, H OConnell, B Baum, BJ TI Effect of adenoviral-mediated gene transfer on rat submandibular saliva composition. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CLIN INVEST & PATIENT CARE BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2638 EP 2638 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002634 ER PT J AU Lee, SK Krebsbach, P Ganss, B Slavkin, H Yamada, Y AF Lee, SK Krebsbach, P Ganss, B Slavkin, H Yamada, Y TI Krox 26, a new Kruppel-like zinc finger protein, plays a critical role in tooth development. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. UNIV TORONTO,FAC DENT,MRC,TORONTO,ON M5S 1A1,CANADA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2810 EP 2810 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002807 ER PT J AU Lee, SK Krebsbach, P ZiechnerDavid, M Slavkin, H Yamada, KM Yamada, Y AF Lee, SK Krebsbach, P ZiechnerDavid, M Slavkin, H Yamada, KM Yamada, Y TI Ameloblastin, a new enamel matrix protein: Expression of isoforms and critical role in enamel formation. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. UNIV SO CALIF,CTR CRANIOFACIAL MOL BIOL,LOS ANGELES,CA 90033. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2811 EP 2811 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002804 ER PT J AU Beiraghi, S Gillanders, E MillerChisholm, A Wang, YF FreasLutz, D Storm, A Long, RE Mazaheri, M Diehl, SR AF Beiraghi, S Gillanders, E MillerChisholm, A Wang, YF FreasLutz, D Storm, A Long, RE Mazaheri, M Diehl, SR TI Localization of Van der Woude syndrome to the 1q41-42 region. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV NEBRASKA,OMAHA,NE 68182. NIDR,BETHESDA,MD 20892. UNIV ARIZONA,TUCSON,AZ. LANCASTER CLEFT PALATE CLIN,LANCASTER,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2847 EP 2847 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002838 ER PT J AU Redford, M Drury, TF AF Redford, M Drury, TF TI Gender differences in oral disease patterns among US adults SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2879 EP 2879 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002870 ER PT J AU Rams, TE Brown, LJ Davidson, PL Andersen, RM AF Rams, TE Brown, LJ Davidson, PL Andersen, RM TI Tooth loss patterns in Navajo and Lakota Native American adults SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TEMPLE UNIV,SCH DENT,PHILADELPHIA,PA. AMER DENT ASSOC HLTH POLICY RESOURCES CTR,CHICAGO,IL. NIDR,BETHESDA,MD 20892. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2880 EP 2880 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002874 ER PT J AU Brown, LJ Oldakowski, RJ Rams, TE AF Brown, LJ Oldakowski, RJ Rams, TE TI Tooth loss patterns in USA. Age, gender and ethnic-racial population groups. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 AMER DENT ASSOC HLTH POLICY RESOURCES CTR,CHICAGO,IL. NIDR,NIH,BETHESDA,MD 20892. TEMPLE UNIV,SCH DENT,PHILADELPHIA,PA 19122. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2881 EP 2881 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002875 ER PT J AU Grzesik, WJ Ivanov, B Southerland, J Yamauchi, M AF Grzesik, WJ Ivanov, B Southerland, J Yamauchi, M TI The effects of synthetic integrin ligands on PDL cells. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,CELLULAR DEV & ONCOL LAB,NIH,BETHESDA,MD 20892. UNIV N CAROLINA,DENT RES CTR,CHAPEL HILL,NC 27599. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 2906 EP 2906 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68002903 ER PT J AU Tanaka, O Takahashi, K Nuckolls, GH Shum, L Slavkin, HC AF Tanaka, O Takahashi, K Nuckolls, GH Shum, L Slavkin, HC TI DiI labelling and ectopic gene expression using craniofacial explant cultures. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIAMS,CRANIOFACIAL DEV SECT,NIH,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 3068 EP 3068 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68003063 ER PT J AU Chai, Y Bringas, P Slavkin, HC AF Chai, Y Bringas, P Slavkin, HC TI In vitro studies of CNC cell fate during mandibular morphogenesis. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 UNIV SO CALIF,CTR CRANIOFACIAL MOL BIOL,SCH DENT,LOS ANGELES,CA. NIDR,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 3071 EP 3071 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68003061 ER PT J AU Genco, R Chadda, S Grossi, S Dunford, R Taylor, G Knowler, W Pettitt, D AF Genco, R Chadda, S Grossi, S Dunford, R Taylor, G Knowler, W Pettitt, D TI Periodontal disease is a predictor of cardiovascular disease in a native American population SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 SUNY BUFFALO,PERIODONTAL DIS RES CTR,BUFFALO,NY 14260. NIDDK,PHOENIX,AZ. UNIV MICHIGAN,SCH DENT,ANN ARBOR,MI 48109. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 3158 EP 3158 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68003152 ER PT J AU Wang, YF Gillanders, E Wang, S Sun, C FreasLitz, D Zhang, YJ Koertge, TE Gunsolley, JC Schenkein, HA Diehl, SR AF Wang, YF Gillanders, E Wang, S Sun, C FreasLitz, D Zhang, YJ Koertge, TE Gunsolley, JC Schenkein, HA Diehl, SR TI Mapping genes influencing smoking behavior and IgG2 levels in early onset periodontitis families. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,NIH,BETHESDA,MD 20892. VIRGINIA COMMONWEALTH UNIV,CRCPD,RICHMOND,VA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 3164 EP 3164 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68003159 ER PT J AU Sonnier, K Dalesandro, M Gu, X Diehl, S Miller, G AF Sonnier, K Dalesandro, M Gu, X Diehl, S Miller, G TI Association of superantigens in the development of advanced periodontitis. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 GEOCENTERS INC,BETHESDA,MD. NIDR,USN,DENT RES INST,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 3176 EP 3176 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68003169 ER PT J AU Watson, EL Myers, EM Kim, KS Williams, R AF Watson, EL Myers, EM Kim, KS Williams, R TI Poor survival of African Americans despite early diagnosis of head and neck cancer. SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 NIDR,BETHESDA,MD 20892. HOWARD UNIV HOSP,CTR CANC,WASHINGTON,DC 20059. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PY 1997 VL 76 SI SI BP 3322 EP 3322 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WB680 UT WOS:A1997WB68003318 ER PT J AU Simons-Morton, BG Cummings, SS AF Simons-Morton, BG Cummings, SS TI Evaluation of a local designated driver and responsible server program to prevent drinking and driving SO JOURNAL OF DRUG EDUCATION LA English DT Article ID ALCOHOL AB Point of purchase interventions by beverage alcohol servers provide one promising approach to preventing drinking and driving and many communities now support such programs. To evaluate the impact of a designated driver and responsible server program in Houston, we assessed server training courses, observed and interviewed servers and patrons at five establishments participating in the program, and reviewed the distribution of vouchers awarded for a safe ride home by taxi. The training course for alcoholic beverage servers produced significant improvements in the participants' perceptions about their role in preventing drunk driving. In five participating establishments 15.6 percent of servers wore buttons announcing the establishment's participation in the program; immediately after retraining 26.6 percent wore the buttons. Of the eligible patrons in these establishments 6.6 percent actually participated in the designated driver program. The program provided an average of 0.7 safe ride home vouchers per establishment per month. In one additional establishment an experiment was conducted in which servers always announced the designated driver program to patrons, but no increase in the prevalence of designated drivers occurred. C1 NIH, Publ Hlth Serv, Bethesda, MD 20892 USA. Univ Texas, Hlth Sci Ctr, Houston, TX USA. RP Simons-Morton, BG (reprint author), NIH, Publ Hlth Serv, Bethesda, MD 20892 USA. OI Simons-Morton, Bruce/0000-0003-1099-6617 NR 15 TC 15 Z9 15 U1 0 U2 2 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 USA SN 0047-2379 J9 J DRUG EDUC JI J. Drug Educ. PY 1997 VL 27 IS 4 BP 321 EP 333 DI 10.2190/2RJA-22Y1-R15T-ULM8 PG 13 WC Substance Abuse; Education, Scientific Disciplines SC Substance Abuse; Education & Educational Research GA YV651 UT WOS:000071849100001 PM 9489276 ER PT J AU Russell, MW Law, I Sholinsky, P Fabsitz, RR AF Russell, MW Law, I Sholinsky, P Fabsitz, RR TI Heritability of ECG measurements in adult male twins SO JOURNAL OF ELECTROCARDIOLOGY LA English DT Article; Proceedings Paper CT 22nd Annual ISCE Conference on Research and Technology Transfer in Computerized Electrocardiology CY APR 26-MAY 01, 1997 CL PALM COAST, FLORIDA SP Burdick Inc, Del Mar Avion, Fukuda Denshi, Hewlett Packard Co, Marquette Med Syst Inc, Medicomp Inc, Merck & Co Inc, Mortara Instrument Inc, Nihon Kohden, Nippon Boehringer Ingelheim Co Ltd, Physio Control Corp, Quinton Instrument Co, Rozinn Electr Inc, Schiller AG, Seimens Elema AB DE heritability ECG measurements; heart rate; ventricular repolarization; twins ID HEART-RATE-VARIABILITY; MYOCARDIAL-INFARCTION; GENETIC VARIANCE; NHLBI TWIN; RISK; ELECTROCARDIOGRAM; METHODOLOGY; DISPERSION; DISEASE; DEATH AB To assess the genetic contribution to electrocardiographic (EGG) measurements, heritability analysis tvas performed on ECG data collected on 251 pairs of adult male twins during the second examination of the National Heart, Lung and Blood Institute twin study, a multicenter study of cardiovascular risk factors. Resting 12-lead ECGs were obatained on each twin, pair and, the R-R, QRS, QT and JT intervals were measured. Both the R-R and QT intervals demonstrated significant heritable components, accounting for 77% and 36%, respectively, of the variability. No significant heritable component of the QRS complex could be identified. Although the MZ intraclass correlation was higher than the DZ intraclass correlation, the JT interval did not demonstrate significant heritability. Therefore, in adult males both heart rate and the duration of ventricular repolarization have significant heritable components. These heritable components may need to be considered when using ECG measurements to screen for patients at risk for cardiovascular disorders or sudden cardiac death. C1 Univ Michigan, Dept Pediat, Ann Arbor, MI 48109 USA. NHLBI, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA. RP Russell, MW (reprint author), Div Pediat Cardiol, F1310 MCHC Box 0204,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. NR 24 TC 3 Z9 3 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI PHILADELPHIA PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA SN 0022-0736 J9 J ELECTROCARDIOL JI J. Electrocardiol. PY 1997 VL 30 SU S BP 64 EP 68 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA ZE485 UT WOS:000072797600012 ER PT J AU Ault, GS AF Ault, GS TI Activity of JC virus archetype and PML-type regulatory regions in glial cells SO JOURNAL OF GENERAL VIROLOGY LA English DT Article ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; HUMAN POLYOMAVIRUS-JC; HUMAN-IMMUNODEFICIENCY-VIRUS; DNA-REPLICATION; PROMOTER ENHANCER; BRAIN-CELLS; BK-VIRUS; TRANSCRIPTION; SEQUENCES; PROTEIN AB Sequence variations are seen in the JC virus promoter/enhancer in virus taken from progressive multifocal leukoencephalopathy (PML) brains and it has been hypothesized that the variations arise in the host at some point in the development of PML. These rearrangements may be adaptations for enhanced growth in glial cells; if so, transcription or replication levels should differ between archetypal and rearranged PML-type promoters. The archetype and four PML-type promoters were analysed in human glial cells for early and late transcriptional activity in the absence or presence of virus T antigen, and for DNA replication. CAT reporter expression differed within a fivefold range and the archetype was intermediate in strength to the PML-type regulatory regions. The archetype differed from rearranged promoters in that the late promoter was less responsive to T antigen and the shift from early to late activity with T antigen was less pronounced. All five regulatory regions demonstrated similar levels of DNA replicating activity. Rearrangement of the archetype was not required for activity in glial cells, but the potential for differences in the regulation of the late capsid genes was found. RP Ault, GS (reprint author), NINCDS,LAB MOL MED & NEUROSCI,NATL INST HLTH,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 50 TC 27 Z9 28 U1 0 U2 1 PU SOC GENERAL MICROBIOLOGY PI READING PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING, BERKS, ENGLAND RG7 1AE SN 0022-1317 J9 J GEN VIROL JI J. Gen. Virol. PD JAN PY 1997 VL 78 BP 163 EP 169 PN 1 PG 7 WC Biotechnology & Applied Microbiology; Virology SC Biotechnology & Applied Microbiology; Virology GA WD448 UT WOS:A1997WD44800022 PM 9010300 ER PT J AU Shapiro, J Sciaky, N Lee, J Bosshart, H Angeletti, RH Bonifacino, JS AF Shapiro, J Sciaky, N Lee, J Bosshart, H Angeletti, RH Bonifacino, JS TI Localization of endogenous furin in cultured cell lines SO JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY LA English DT Article DE furin; Golgi; TGN; immunolocalization; video microscopy ID TRANS-GOLGI NETWORK; INTRACELLULAR TRAFFICKING; ENDOPROTEOLYTIC CLEAVAGE; CYTOPLASMIC DOMAIN; SECRETORY PATHWAY; EXPRESSION; PROTEIN; SURFACE; DETERMINANT; ACTIVATION AB Furin is a dibasic endopeptidase responsible for the proteolytic maturation of many precursor proteins in the secretory and endocytic pathways of mammalian cells. The levels of furin expression in most cells are very low, and this has hampered attempts to identify the intracellular compartments in which endogenous furin is localized. We have used a specific antibody reagent to a sequence in the carboxy terminus of furin to perform immunofluorescent staining of mammalian cell lines. This antibody was sensitive enough to detect staining for furin in various cell lines. For the most part, furin staining was confined to a juxtanuclear structure characteristic of the Golgi complex. Analyses by video microscopy and confocal microscopy showed that the distribution of furin was distinct from that Furin of mannosidase II, a marker of the Golgi stack, and most closely resembled that of TGN38, a Golgi marker of the trans-Golgi network. Therefore, our results suggest that endogenous furin is predominantly localized to the area of the Golgi complex, most likely within the trans-Golgi network. C1 NICHHD,CELL BIOL & METAB BRANCH,NIH,BETHESDA,MD 20892. ALBERT EINSTEIN COLL MED,BRONX,NY 10467. OI Bonifacino, Juan S./0000-0002-5673-6370 NR 30 TC 50 Z9 50 U1 0 U2 6 PU HISTOCHEMICAL SOC INC PI SEATTLE PA UNIV WASHINGTON, DEPT BIOSTRUCTURE, BOX 357420, SEATTLE, WA 98195 SN 0022-1554 J9 J HISTOCHEM CYTOCHEM JI J. Histochem. Cytochem. PD JAN PY 1997 VL 45 IS 1 BP 3 EP 12 PG 10 WC Cell Biology SC Cell Biology GA WD500 UT WOS:A1997WD50000002 PM 9010463 ER PT J AU Rojo, S Burshtyn, DN Long, EO Wagtmann, N AF Rojo, S Burshtyn, DN Long, EO Wagtmann, N TI Type I transmembrane receptor with inhibitory function in mouse mast cells and NK cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NATURAL-KILLER-CELL; C-TYPE LECTIN; HLA-B; IMMUNOGLOBULIN-SUPERFAMILY; MOLECULAR-CLONING; RECOGNITION; COMPLEX; CLONES; EXPRESSION; ANTIGEN AB The MHC class I-specific inhibitory receptors on human and mouse NK cells have surprisingly different structures. The mouse receptors (Ly-49) are type II transmembrane glycoproteins of the C-type lectin family, whereas the human receptors (killer cell inhibitory receptors (KIR)) belong to the Ig superfamily. This difference prompted a search for Ig-like inhibitory receptors in mice. Here we show that gp49, a mouse mast cell protein of unknown function but with sequence similarity to KIR, is expressed in NK cells. The gp49 cytoplasmic tail, containing a sequence related to an inhibitory motif shared by KIR and Ly-49, delivered a strong inhibitory signal in both human and mouse NK cells when substituted for a KIR cytoplasmic tail. These data show that Ig-like receptors with inhibitory properties exist in both species and that mouse mast and NK cells may recognize common inhibitory ligands. C1 NIAID,IMMUNOGENET LAB,NIH,ROCKVILLE,MD 20852. RI Long, Eric/G-5475-2011 OI Long, Eric/0000-0002-7793-3728 NR 27 TC 91 Z9 92 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1997 VL 158 IS 1 BP 9 EP 12 PG 4 WC Immunology SC Immunology GA VZ128 UT WOS:A1997VZ12800003 PM 8977169 ER PT J AU Bonney, EA Matzinger, P AF Bonney, EA Matzinger, P TI The maternal immune system's interaction with circulating fetal cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PERIPHERAL-BLOOD; ANTERIOR-CHAMBER; PREGNANT-WOMEN; MESSENGER-RNA; T-CELLS; HLA-G; CHIMERISM; ANTIGEN; RECIPIENTS; ALLOTRANSPLANTATION AB Although female mice readily reject organs from allogeneic or semiallogeneic male donors, they do not reject the fetuses sired by those same donors. An explanation for this that has been made in the past is that the fetus influences its mother's immune response by sending fetal cells into the maternal circulation. To determine the frequency and magnitude of fetal to maternal cell migration, we employed a sensitive quantitative PCR technique to assess the numbers of male cells in the thymus, spleen, liver, lymph nodes, and peripheral blood of normal mice undergoing their first pregnancy. We found that fetal cell migration is not universal but occurs in only a fraction of pregnancies. Using a kinetic analysis of normal mice mated to syngeneic or allogeneic males, a comparison of normal and SCID mice, and testing of multiparous mice for CTL against fetal Ags, we found that migrating fetal cells were cleared by the maternal immune system. Thus the mother is not continuously exposed to circulating fetal cells and, in fact, has the capacity to eliminate them without eliminating the fetus. RP Bonney, EA (reprint author), NIAID,CELLULAR & MOL IMMUNOL LAB,SECT T CELL TOLERANCE,NIH,BLDG 4,ROOM 111,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 58 TC 121 Z9 123 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1997 VL 158 IS 1 BP 40 EP 47 PG 8 WC Immunology SC Immunology GA VZ128 UT WOS:A1997VZ12800007 PM 8977173 ER PT J AU Fuschiotti, P Fitts, MG Pospisil, R Weinstein, PD Mage, RG AF Fuschiotti, P Fitts, MG Pospisil, R Weinstein, PD Mage, RG TI RAG1 and RAG2 in developing rabbit appendix subpopulations SO JOURNAL OF IMMUNOLOGY LA English DT Article ID IMMUNOGLOBULIN GENE CONVERSION; AVIAN B-CELL; V(D)J RECOMBINATION; GERMINAL-CENTERS; T-CELL; POSITIVE SELECTION; PROTEIN RAG-2; BONE-MARROW; EXPRESSION; REARRANGEMENT AB The appendix of young rabbits is a site of primary heavy chain variable region-gene diversification and B cell selection. Appendix cells from 6- to 9-wk-old rabbits were stained and sorted for surface CD43 and IgM. We found that the CD43(+)IgM(-) and double-negative CD43(-)IgM(-) cells contained RAG1 transcripts and RAG2 protein, The presence of RAG gene products in appendix raised the possibility that pro-/pre-B cells were present in young rabbit appendix, Although an early suggestion that RAG2 plays a role in variable region-gene diversification by gene conversion in chicken bursa was not supported by studies of RAG2 protein in this tissue, we produced anti-rabbit RAG2 Abs to determine whether RAG2 protein was present in rabbit appendix, where cells that recently underwent gene conversion are found, We detected RAG2 protein in the four subpopulations of rabbit appendix lymphocytes, distinguished by surface CD43 and IgM markers, The appearance of RAG gene products during different stages of B cell maturation may reflect the function of the young rabbit appendix as a site of both B cell development and diversification. C1 NIAID, IMMUNOL LAB, NIH, BETHESDA, MD 20892 USA. RI Pospisil, Richard/B-7467-2012 NR 60 TC 10 Z9 10 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1997 VL 158 IS 1 BP 55 EP 64 PG 10 WC Immunology SC Immunology GA VZ128 UT WOS:A1997VZ12800009 PM 8977175 ER PT J AU Ludviksson, BR Gray, B Strober, W Ehrhardt, RO AF Ludviksson, BR Gray, B Strober, W Ehrhardt, RO TI Dysregulated intrathymic development in the IL-2-deficient mouse leads to colitis-inducing thymocytes SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL RECEPTOR; INTERLEUKIN-2-DEFICIENT MICE; ULCERATIVE-COLITIS; AUTOIMMUNE-DISEASE; NEGATIVE SELECTION; THYMIC SELECTION; IN-VITRO; EXPRESSION; IL-2; APOPTOSIS AB Gene-targeted mice lacking the IL-2 gene (IL-2 -/- mice) develop various forms of autoimmunity as well as severe colitis, either spontaneously in a conventional environment or after immunization with 2,4,6-trinitrophenol (TNP)-conjugated keyhole limpet hemocyanin (KLH) in a specific pathogen-free environment, We show here that the induction of colitis with TNP-KLH induces a change in the thymocyte population characterized by decreased numbers of double positive (DP; CD4(+)CD8(+)) thymocytes (IL-2 +/+, 45.2 x 10(6) vs IL-2 -/-, 23.6 x 10(6)) and increased numbers of single positive (SP; CD4(+)CD8(-) or CD4(-)CD8(+)) thymocytes (IL-2 +/+, 5.3 x 10(6) VS IL-2 -/-, 20.9 x 10(6)), Th, latter also bear activation markers, In addition, thymocytes from TNP-KLH-immunized IL-2 -/- mice produce more IFN-gamma and less IL-4 than similarly immunized IL-2 +/+ mice, These defects in thymocyte maturation and lymphokine production are IL-12 driven, since they are prevented when immunized IL-2 -/- mice are coadministered with anti-IL-12, Furthermore, we demonstrate that IL-2 -/- mice exhibit decreased cortical apoptosis as determined by thymocyte numbers and detection oi apoptotic cells in situ. Finally, we show that colitis-inducing thymocytes are generated in the immunized IL-2 -/- thymus, since IL-2 +/+ mice develop colitis following injection of small numbers of single positive thymocytes from immunized IL-2 -/- mice but not from IL-2 +/+ mice, Taken together, these data indicate that, in the absence of IL-2, thymocyte maturation is abnormally directed by IL-12 toward the generation of mature, activated Th1-type thymocytes that are capable of mediating colitis. RP Ludviksson, BR (reprint author), NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,NIH,BLDG 10,ROOM 11N238,BETHESDA,MD 20892, USA. OI Ludviksson, Bjorn/0000-0002-6445-148X NR 42 TC 49 Z9 51 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1997 VL 158 IS 1 BP 104 EP 111 PG 8 WC Immunology SC Immunology GA VZ128 UT WOS:A1997VZ12800014 PM 8977180 ER PT J AU Sugiyama, H Chen, P Hunter, MG Sitkovsky, MV AF Sugiyama, H Chen, P Hunter, MG Sitkovsky, MV TI Perturbation of the expression of the catalytic subunit C alpha of cyclic AMP-dependent protein kinase inhibits TCR-triggered secretion of IL-2 by T helper hybridoma cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID REGULATORY SUBUNIT; CAMP-BINDING; EFFECTOR FUNCTIONS; LYMPHOCYTES-T; ACTIVATION; PHOSPHORYLATION; MUTATIONS; ANTIGEN; PATHWAY; GENES AB The role of cAMP-dependent protein kinase (PKA) in the regulation of TCR-triggered IL-2 secretion was studied by transfecting T hybridoma cells with cDNA encoding the inhibitory regulatory subunit (RI alpha) of PKA with mutations in cAMP-binding sites (RI alpha m) or by pretreating T cells with catalytic subunit-alpha (C alpha) antisense mRNA oligonucleotides. Transfected RI alpha m was expected to compete with endogenous regulatory subunits and to irreversibly inactivate the catalytic subunit in RI alpha m-C alpha complexes. It was shown that C alpha and RI alpha are the major PKA subunits in T cells, thereby justifying the choice of RI alpha m and C alpha antisense oligos to modulate PKA activity in T lymphocytes. Perturbation of the expression of PKA subunits by RI alpha m resulted in transfectants with 1) no changes in basal PKA activity but inhibited cAMP-inducible PKA activity or 2) inhibited basal PKA activity but unaffected cAMP-inducible PKA activity, Transfectants with inhibited basal PKA activity had changed (inhibited) levels of TCR-triggered IL-2 production, The anti-C alpha antisense mRNA oligomers also inhibited basal PKA activity and TCR-triggered production of IL-2. The experiments described here and recently reported studies of the effects of C alpha inactivation on CTL effector functions and IFN-gamma secretion suggest that basal PKA activity could be required for the propagation of TCR-triggered signals needed for lymphokine secretion by T cells. C1 NIAID, IMMUNOL LAB, NIH, BETHESDA, MD 20892 USA. NR 50 TC 18 Z9 18 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 EI 1550-6606 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1997 VL 158 IS 1 BP 171 EP 179 PG 9 WC Immunology SC Immunology GA VZ128 UT WOS:A1997VZ12800022 PM 8977188 ER PT J AU Roilides, E Dimitriadou, A Kadiltsoglou, I Sein, T Karpouzas, J Pizzo, PA Walsh, TJ AF Roilides, E Dimitriadou, A Kadiltsoglou, I Sein, T Karpouzas, J Pizzo, PA Walsh, TJ TI IL-10 exerts suppressive and enhancing effects on antifungal activity of mononuclear phagocytes against Aspergillus fumigatus SO JOURNAL OF IMMUNOLOGY LA English DT Article; Proceedings Paper CT 34th Interscience Conference on Antimicrobial Agents and Chemotherapy CY OCT 03-07, 1994 CL ORLANDO, FL ID COLONY-STIMULATING FACTOR; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; CHRONIC GRANULOMATOUS-DISEASE; TUMOR-NECROSIS-FACTOR; T-CELL PROLIFERATION; GROWTH-FACTOR-BETA; INTERFERON-GAMMA; INVASIVE ASPERGILLOSIS; HUMAN MONOCYTES; PULMONARY ASPERGILLOSIS AB Invasive aspergillosis has emerged as a frequent and serious infection in immunocompromised patients, We studied the effects of human IL-10 on antifungal activity of monocytes (MNCs) from healthy adults against Aspergillus fumigatus after incubation with IL-10 at 37 degrees C for 2 to 4 days, IL-10 (2-20 ng/ml)-pretreated MNCs exhibited approximately 40% suppression of superoxide anion (O-2(-)) production in response to PMA and FMLP (p less than or equal to 0.003), and anti-IL-10 containing supernatant neutralized the IL-10 effect, IL-10 (20 ng/ml)-pretreated MNCs exhibited decreased damage of Aspergillus hyphae after 2 to 4 days (55-98% decrease, p less than or equal to 0.04). The MNC phagocytic activity against conidia, as assessed by microscopy (percentage of phagocytosing MNCs and number of intracellular conidia per MNC) as well as by colony counting (colonies grown from intracellular conidia), was enhanced by 127% (p=0.006), 14% (p=0.03), and 23% (p=0.009), respectively. MNC capacity to inhibit intracellular germination was marginally enhanced (p=0.04) and intracellular conidiocidal activity was unaffected by IL-10. IL-4 (5 ng/ml) did not change the up-regulatory IL-10 effect on phagocytosis. IFN-gamma (25 ng/ml) and granulocyte-macrophage CSF (20 ng/ml), but not macrophage CSF (15 ng/ml), appeared to counteract suppressive IL-10 effects, Thus, IL-10 suppresses oxidative burst and antifungal activity of MNCs against Aspergillus hyphae, while increasing their phagocytic activity, These findings further elucidate a potential role of IL-10 in the pathogenesis of invasive aspergillosis, which may lead to new treatment strategies. C1 NCI,PEDIAT BRANCH,INFECT DIS SECT,BETHESDA,MD 20892. UNIV THESSALONIKI,HIPPOKRATIO GEN HOSP,DEPT PEDIAT 3,GR-54006 THESSALONIKI,GREECE. NR 54 TC 98 Z9 99 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1997 VL 158 IS 1 BP 322 EP 329 PG 8 WC Immunology SC Immunology GA VZ128 UT WOS:A1997VZ12800040 PM 8977206 ER PT J AU GuexCrosier, Y Raber, J Chan, CC Kriete, MS Benichou, J Pilson, RS Kerwin, JA Waldmann, TA Hakimi, J Roberge, FG AF GuexCrosier, Y Raber, J Chan, CC Kriete, MS Benichou, J Pilson, RS Kerwin, JA Waldmann, TA Hakimi, J Roberge, FG TI Humanized antibodies against the alpha-chain of the IL-2 receptor and against the beta-chain shared by the IL-2 and IL-15 receptors in a monkey uveitis model of autoimmune diseases SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CARDIAC ALLOGRAFT SURVIVAL; REFRACTORY RHEUMATOID-ARTHRITIS; NONOBESE DIABETIC MICE; CELL GROWTH-FACTOR; ANTI-TAC-H; MONOCLONAL-ANTIBODY; INTERLEUKIN-2 RECEPTOR; GAMMA-CHAIN; T-CELLS; CYNOMOLGUS MONKEYS AB We studied the efficacy and tolerance of humanized Ab interfering with the signal of the IL-2 and IL-15 receptors in a primate model of experimental autoimmune uveoretinitis. The inhibitory effects of humanized anti-Tac (HAT), an anti-IL-2R alpha-chain Ab, and HuMik beta 1, an Ab directed at the beta-chain shared by the receptors of IL-2 and IL-15, were tested in culture on the proliferative response of monkey Con A-blast lymphocytes stimulated with IL-2 or IL-15, Uveitis was induced in cynomolgus monkeys by immunization with human recombinant retinal S-antigen, Treatment was initiated at the first sign of disease and consisted of HAT and HuMik beta 1, alone or in combination, or vehicle control given by i.v, injection twice a week for 4 wk, Disease was evaluated by ocular funduscopy, The results in culture showed a significant dose-dependent inhibition of the IL-2-driven proliferation of lymphocytes by HAT, HuMik beta 1 alone was ineffective against IL-2 stimulation, but had a marked potentiating effect in combination with HAT, independent of IL-15 signaling, IL-15-driven proliferation was inhibited by HuMik beta 1, but not by HAT alone or in combination. In monkeys, experimental autoimmune uveoretinitis evolution was significantly inhibited by HAT treatment. HuMik beta 1 alone had no effect on the disease, However, when used in combination, the two Ab markedly reduced the severity of ocular inflammation. The Ab were well tolerated. Only three monkeys, treated with HAT alone, made an Ab response against the injected Ab. C1 NEI,IMMUNOL LAB,NIH,BETHESDA,MD 20892. NEI,VET RES & RESOURCES SECT,NIH,BETHESDA,MD 20892. NCI,BIOSTAT BRANCH,NIH,BETHESDA,MD 20892. NCI,METAB BRANCH,NIH,BETHESDA,MD 20892. UNIV LAUSANNE,JULES GONIN HOSP,LAUSANNE,SWITZERLAND. HOFFMANN LA ROCHE INC,ROCHE RES CTR,INFLAMMAT & AUTOIMMUNE DIS,NUTLEY,NJ 07110. NR 57 TC 51 Z9 52 U1 1 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1997 VL 158 IS 1 BP 452 EP 458 PG 7 WC Immunology SC Immunology GA VZ128 UT WOS:A1997VZ12800056 PM 8977222 ER PT J AU McDyer, JF Hackley, MN Walsh, TE Cook, JL Seder, RA AF McDyer, JF Hackley, MN Walsh, TE Cook, JL Seder, RA TI Patients with multidrug-resistant tuberculosis with low CD4(+) T cell counts have impaired Th1 responses SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; MEDIATED IMMUNE-RESPONSES; MYCOBACTERIUM-TUBERCULOSIS; INTERFERON-GAMMA; CYTOKINE PRODUCTION; PULMONARY TUBERCULOSIS; HUMAN-MONOCYTES; LYMPHOCYTES-T; FACTOR-ALPHA; IFN-GAMMA AB Multidrug-resistant tuberculosis (MDRTB) has emerged as a challenging clinical problem in both HIV-infected and -uninfected individuals, In this study, immune responses from HIV-negative patients with MDRTB were compared with those of healthy purified protein derivative (PPD)-positive and PPD-negative individuals, These responses were characterized by measuring the proliferation and cytokine production from PBMCs stimulated in vitro with Mycobacterium tuberculosis, PPD, or mitogens. MDRTB patients with CD4 counts > 500/mu l stimulated in vitro with M. tuberculosis had similar immune responses (proliferation, IFN-gamma, and IL-2 production) as the PPD-positive and -negative controls, By contrast, MDRTB patients with CD4 counts < 500/mu l had markedly deficient immune responses to similar stimuli, In these patients, IFN-gamma production could be restored by adding IL-12 to the in vitro cultures, IL-12 also caused a striking increase in the amount of IFN-gamma produced from PBMCs of both PPD-positive and -negative controls. The role of endogenous IL-12 production was also studied, Addition of anti-IL-12 to cultures resulted in a two- to eightfold decrease in IFN-gamma production in response to PHA stimulation. Inhibition of IFN-gamma was also observed when cells were stimulated by M. tuberculosis and PPD, Using Staphylococcus aureus Cowan strain as a mitogenic stimulus, IL-12 p70 was produced in similar amounts in all groups tested, TNF-alpha production was also assessed from cells stimulated by M. tuberculosis. Addition of IL-12 to the cultures did not cause a significant enhancement of TNF-alpha production, Last, production of IL-10 and IL-4 in response to M. tuberculosis and PHA, respectively, was not significantly different among all groups tested. These results suggest that patients with MDRTB tuberculosis with CD4 T cell counts < 500/mu l have impaired IFN-gamma and IL-2 responses and might benefit by adjunctive IL-12 therapy. C1 NIAID,CLIN INVEST LAB,NIH,BETHESDA,MD 20892. NATL JEWISH CTR IMMUNOL & RESP MED,DENVER,CO 80206. MONTGOMERY CTY TB CLIN,SILVER SPRING,MD 20902. FU PHS HHS [N01-A0-42701] NR 47 TC 39 Z9 42 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1997 VL 158 IS 1 BP 492 EP 500 PG 9 WC Immunology SC Immunology GA VZ128 UT WOS:A1997VZ12800061 PM 8977227 ER PT J AU Zhai, YF Yang, JC Spiess, P Nishimura, MI Overwijk, WW Roberts, B Restifo, NP Rosenberg, SA AF Zhai, YF Yang, JC Spiess, P Nishimura, MI Overwijk, WW Roberts, B Restifo, NP Rosenberg, SA TI Cloning and characterization of the genes encoding the murine homologues of the human melanoma antigens MART1 and gp100 SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE cancer vaccine; in vivo model; B16 melanoma; adenovirus; vaccinia virus ID TUMOR-INFILTRATING LYMPHOCYTES; CYTOLYTIC T-LYMPHOCYTES; LUPUS AUTOIMMUNITY; HLA-A2 MELANOMAS; TYROSINASE GENE; SILVER LOCUS; SELF; CELLS; IDENTIFICATION; RECOGNITION AB The recent identification of genes encoding melanoma-associated antigens has opened new possibilities for the development of cancer vaccines designed to cause the rejection of established tumors. To develop a syngeneic animal model for evaluating antigen-specific vaccines in cancer therapy, the murine homologues of the human melanoma antigens MART1 and gp100, which were specifically recognized by tumor-infiltrating lymphocytes from patients with melanoma, were cloned and sequenced from a murine B16 melanoma cDNA library. The open reading frames of murine MART1 and gp100 encode proteins of 113- and 626-amino acids with 68.8 and 77% identity to the respective human proteins. Comparison of the DNA sequences of the murine MART1 genes, derived from normal melanocytes, the immortalized nontumorgenic melanocyte line Melan-a and the B16 melanoma, showed all to be identical. Northern and Western blot analyses confirmed that both genes encoded products that were melanocyte lineage proteins. Mice immunized with murine MART1 or gp100 using recombinant vaccinia virus failed to produce any detectable T-cell responses or protective immunity against B16 melanoma. In contrast, immunization of mice with human gp100 using recombinant adenoviruses elicited T cells specific for hgp100. but these T cells also cross reacted with B16 tumor in vitro and induced significant but weak protection against B16 challenge. Immunization with human and mouse gp100 together [adenovirus type 2 (Ad2)-hgp100 plus recombinant vaccinia virus (rVV)-mgp100], or immunization with human gp100 (Ad2-hgp100) and boosting with heterologous vector (rVV-hgp100 or rVV-mgp100) or homologous vector (Ad2-hgp100), did not significantly enhance the protective response against B16 melanoma. These results may suggest that immunization with heterologous tumor antigen, rather than self, may be more effective as an immunotherapeutic reagent in designing antigen-specific cancer vaccines. C1 GENZYME CORP,FRAMINGHAM,MA 01701. RP Zhai, YF (reprint author), NCI,SURG BRANCH,NIH,BLDG 10,ROOM 2B46,BETHESDA,MD 20892, USA. RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [NIH0010139353, Z99 TW999999, Z01 BC010763-01] NR 28 TC 80 Z9 84 U1 0 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1997 VL 20 IS 1 BP 15 EP 25 DI 10.1097/00002371-199701000-00002 PG 11 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA WK735 UT WOS:A1997WK73500002 PM 9101410 ER PT J AU Akagi, J Hodge, JW McLaughlin, JP Gritz, L Mazzara, G Kufe, D Schlom, J Kantor, JA AF Akagi, J Hodge, JW McLaughlin, JP Gritz, L Mazzara, G Kufe, D Schlom, J Kantor, JA TI Therapeutic antitumor response after immunization with an admixture of recombinant vaccinia viruses expressing a modified MUC1 gene and the murine T-cell costimulatory molecule B7 SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE MUC1; B7; vaccine; costimulation; vaccinia ID ACTIVE-SPECIFIC IMMUNOTHERAPY; CARCINOMA-ASSOCIATED ANTIGEN; TUMOR-ASSOCIATED ANTIGENS; BREAST-CANCER; PROTEIN CORE; ADJUVANT; IMMUNITY; SEQUENCE; DF3; LYMPHOCYTES AB Tumor-associated antigens have considerable promise not only as diagnostic or prognostic markers but also as targe ts for active or passive immunotherapy. DF3/MUC1 is a tumor-associated antigen that is overexpressed with an abnormal glycosylation pattern in breast, ovarian, lung, and pancreatic cancers. The major extracellular portion of MUC1 is composed of tandem repeal units of 20 amino acids. Recombinant vaccinia viruses encoding mucin molecules have been constructed by several groups. However, these recombinants have met with limited success in protecting animals from MUC1-expressing tumors because of the vaccinia genome being subject to high-frequency homologous recombination, therefore being unstable in expression of the tandem repeats. In light of these studies, two concurrent strategies were used to improve immune responses to MUC1: a recombinant vaccinia virus was constructed containing a modified ''mini'' MUC1 gene containing only 10 tandem repeat sequences to minimize vaccinia-mediated rearrangement (designated rV-MUC1); and an admixture was used containing rV-MUC1 and a recombinant vaccinia virus containing the gene for the murine T-cell costimulatory molecule B7-1 (rV-B7). The rV-MUC1 gene product maintained a consistent molecular weight throughout several passages, indicating stability of the inserted gene. Mice inoculated with rV-MUC1 demonstrated MUC1-specific cytolytic responses that were further enhanced by admixture with rV-B7. In a MUC1-expressing pulmonary metastases prevention model, mice inoculated two times with rV-MUC1 were protected from the establishment of metastases. No additive effect on antitumor immunity (>90% with rV-MUC1 alone) was observed in mice primed with an admixture of rV-MUC and rV-B7 and boosted with rV-MUC1. When rV-MUC1 was used to treat established MUC1 positive metastases, however, three administrations of rV-MUC1 were not sufficient to confer antitumor effects. In contrast, when tumor-bearing mice were primed with an admixture of rV-MUC1 and rV-B7, followed by two boosts with rV-MUC1, there was a significant reduction in pulmonary metastases (p = < 0.0001), which correlated to 100% survival. Coexpression of the B7 molecule, although not necessary for the induction of an immune response of sufficient magnitude to prevent MUC1 tumors, tvas thus essential in a treatment setting. C1 NCI, TUMOR IMMUNOL & BIOL LAB, NIH, BETHESDA, MD 20892 USA. KUMAMOTO UNIV, SCH MED, DEPT SURG, KUMAMOTO 860, JAPAN. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV CANC PHARMACOL, BOSTON, MA 02115 USA. THER BIOL CORP, CAMBRIDGE, MA USA. RI Hodge, James/D-5518-2015 OI Hodge, James/0000-0001-5282-3154 NR 32 TC 62 Z9 62 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1997 VL 20 IS 1 BP 38 EP 47 DI 10.1097/00002371-199701000-00004 PG 10 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA WK735 UT WOS:A1997WK73500004 PM 9101412 ER PT J AU Abrams, SI Hodge, JW McLaughlin, JP Steinberg, SM Kantor, JA Schlom, J AF Abrams, SI Hodge, JW McLaughlin, JP Steinberg, SM Kantor, JA Schlom, J TI Adoptive immunotherapy as an in vivo model to explore antitumor mechanisms induced by a recombinant anticancer vaccine SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE recombinant vaccinia virus; carcinoembryonic antigen; CD4(+) and CD8(+) T lymphocytes; adoptive immunotherapy ID CYTOTOXIC T-CELLS; CARCINOEMBRYONIC ANTIGEN GENE; TUMOR-ASSOCIATED ANTIGEN; I-DEFICIENT MICE; VIRUS-VACCINE; IMMUNE-RESPONSE; LYMPHOCYTE; CD8+; PERSPECTIVES; METASTASES AB We have described previously the construction, generation, and in vivo biologic consequences of a recombinant vaccinia virus containing the human CEA gene (rV-CEA) in an experimental murine colon carcinoma model. Immunization of C57BL/6 mice with rV-CEA led to antigen-specific inhibition of tumor growth in both prophylactic and therapeutic settings. Although such antitumor effects were correlated with the induction of CEA-specific T-cell responses, their exact contribution in the tumor rejection mechanism remained unclear. In this study, we examined the mechanism of action of rV-CEA, with emphasis on definition of the immune cells important for such antitumor effects. To that end, a cellular adoptive transfer model was established in vivo, which allowed specific functional analysis of donor-derived immune cells in naive, sublethally irradiated, tumor-bearing recipients, Splenocytes from rV-CEA-immunized donors expressed strong antitumor activity in such tumor-bearing recipients, whereas nonimmune donor cells did not. Depletion of immune T cells before cellular transfer abolished the antitumor response. Moreover, depletion of CD8(+) T cells before transfer resulted in the loss of antitumor activity, despite the presence of CD4(+) T cells, In contrast, antitumor activity was demonstrable with CD8-containing, CD4-depleted effecters, although it was not as effective as with both T-cell subpopulations combined, Finally, in beta(2)-microglobulin/CD8(+) T-cell-deficient mice, rV-CEA immunization exerted only partial antitumor protection, compared with the Immune-competent controls, Overall, we demonstrated that (a) antitumor activity induced by rV-CEA was essentially mediated by CD8(+) effectors; and (b) the combination of both CD8(+) and CD4(+) lymphocytes led to maximal antitumor therapeutic effects, suggesting an important helper or immunoregulatory contribution of the CD4(+) subset, Thus, adoptive cellular transfer strategies may have implications for both the study of recombinant anticancer vaccines and the development of potential clinical applications for cancer immunotherapy. C1 NCI,TUMOR IMMUNOL & BIOL LAB,NIH,BETHESDA,MD 20892. NCI,BIOSTAT & DATA MANAGEMENT SECT,NIH,BETHESDA,MD 20892. RI Hodge, James/D-5518-2015 OI Hodge, James/0000-0001-5282-3154 NR 34 TC 21 Z9 21 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1997 VL 20 IS 1 BP 48 EP 59 DI 10.1097/00002371-199701000-00005 PG 12 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA WK735 UT WOS:A1997WK73500005 PM 9101413 ER PT J AU Fetsch, PA Cormier, J Hijazi, YM AF Fetsch, PA Cormier, J Hijazi, YM TI Immunocytochemical detection of MART-1 in fresh and paraffin-embedded malignant melanomas SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE MART-1; immunocytochemistry; antigen retrieval; melanoma ID ANTIGEN RETRIEVAL; TUMOR AB MART-1 is a transmembrane protein that appears to be melanocyte specific. This study evaluated the use of a new monoclonal antibody, directed against MART-1, in fresh and paraffin-embedded specimens. Twenty-three paraffin-embedded tumors were evaluated for MART-1 immunoreactivity both before and after microwave-based antigen retrieval. After this comparison, 53 fine-needle aspirates from 43 patients with malignant melanoma were assessed for MART-1 immunoreactivity. Immunocytochemistry was performed on both cytospins and paraffin-embedded tissues that were pretreated with antigen retrieval. Seventeen (74%) of 23 tumors evaluated for immunoreactivity before and after antigen retrieval showed a significant increase in both staining intensity and the number of cells stained. When cytospins and antigen-retrieved cell blacks from 53 fine-needle aspirates were compared, 38 (72%) showed good correlation. In 13 (25%) of 53 tumors, MART-1 immunoreactivity was more intense in the cytospins, although the differences were marked in only two cases. Microwave-based antigen retrieval renders paraffin-embedded tissues nearly as sensitive as fresh material for use in the immunocytochemical detection of MART-1. This technique will allow the evaluation of MART-1 immunoreactivity in archival malignant melanomas. C1 NCI,SURG BRANCH,NIH,BETHESDA,MD 20892. RP Fetsch, PA (reprint author), NCI,PATHOL LAB,NIH,BLDG 10 RM 2A19,10 CTR DR,MSC 1500,BETHESDA,MD 20892, USA. NR 8 TC 49 Z9 49 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD JAN PY 1997 VL 20 IS 1 BP 60 EP 64 DI 10.1097/00002371-199701000-00006 PG 5 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA WK735 UT WOS:A1997WK73500006 PM 9101414 ER PT J AU Ugen, KE Srikantan, V Goedert, JJ Nelson, RP Williams, WV Weiner, DB AF Ugen, KE Srikantan, V Goedert, JJ Nelson, RP Williams, WV Weiner, DB TI Vertical transmission of human immunodeficiency virus type 1: Seroreactivity by maternal antibodies to the carboxy region of the gp41 envelope glycoprotein SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 12th Annual Meeting on Molecular Approaches to the Control of Infectious Diseases CY OCT, 1994 CL COLD SPRING HARBOR, NY SP Alafi Capital Co, Amer Cyanamid Co, Amgen Inc, Becton Dickinson & Co, Biogen, Boehringer Mannheim Corp, Bristol Myers Squibb Co, Chugai Pharm Co Ltd, Ciba Geigy Corp, Diagnost Prod Corp, Du Pont Merck Pharm Co, Forest Labs Inc, Genentech Inc, Glaxco, Hoffman La Roche Inc, Johnson & Johnson, Kyowa Hakko Kogyo Co Ltd, Life Technol Inc, Mitsubishi Kasei Inst Life Sci, Monsanto Co, New England BioLabs Inc, Oncogene Sci Inc, Pall Corp, Perkin Elmer Corp, Pfizer Inc, Res Genet, Sandoz Res Inst, Schering Plough Corp, SmithKline Beecham Pharm, Sterling Winthrop Inc, Sumitomo Pharm Co Ltd, Tekeda Chem Ind Ltd, Toyobo Co Ltd, Wyeth Ayerst Res, Zeneca Grp PLC ID PRINCIPAL NEUTRALIZING DETERMINANT; SYNTHETIC PEPTIDES; PERINATAL TRANSMISSION; MONOCLONAL-ANTIBODY; HIV-1 INFECTION; GP120; REACTIVITY; PREVENTION; EPITOPES; CHIMPANZEES AB Maternal antibodies against the envelope glycoprotein of human immunodeficiency virus type 1 (HIV-1) have previously been suggested to be important in influencing the rate of vertical transmission. In this study, serum antibody responses in mothers who did or did not transmit HIV-1 infection to their children were measured against the carboxy region of the transmembrane envelope glycoprotein gp41. Results indicate significantly higher binding reactivity of nontransmitter mothers compared with transmitters to three peptides spanning amino acids 771-810 and 841-856. In addition, high neutralization titers in maternal sera against HIV-1(MN) were associated with a nontransmission status. This is the initial report demonstrating a correlation between maternal antibody binding to epitopes within the carboxy region of gp41 envelope glycoprotein and lack of vertical transmission. Immunodetection that identifies antibodies to these regions in gp41 could therefore be considered a strategy to assess the risk of vertical transmission of HIV-1. C1 UNIV S FLORIDA,COLL MED,ALL CHILDRENS HOSP,DEPT PEDIAT,ST PETERSBURG,FL. UNIFORMED SERV UNIV HLTH SCI,DEPT SURG,ROCKVILLE,MD. NCI,VIRAL EPIDEMIOL BRANCH,ROCKVILLE,MD. UNIV PENN,INST BIOTECHNOL & ADV MOL MED,DEPT MED,PHILADELPHIA,PA. UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. RP Ugen, KE (reprint author), UNIV S FLORIDA,COLL MED,DEPT MED MICROBIOL & IMMUNOL,MDC 10,12901 BRUCE B DOWNS BLVD,TAMPA,FL 33612, USA. RI Ugen, Kenneth/H-6544-2011; Weiner, David/H-8579-2014 NR 36 TC 24 Z9 24 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JAN PY 1997 VL 175 IS 1 BP 63 EP 69 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA WA937 UT WOS:A1997WA93700009 PM 8985197 ER PT J AU Hwu, P AF Hwu, P TI Current challenges in cancer gene therapy SO JOURNAL OF INTERNAL MEDICINE LA English DT Article; Proceedings Paper CT International-Society-of-Haematology XIV Meeting CY AUG 30-SEP 04, 1997 CL STOCKHOLM, SWEDEN SP Int Soc Haematol, European & African Div DE gene therapy; immunotherapy; cancer ID BONE-MARROW TRANSPLANTATION; TUMOR-INFILTRATING LYMPHOCYTES; LASTING ANTITUMOR IMMUNITY; COLONY-STIMULATING FACTOR; CD8+ T-CELLS; RETROVIRAL VECTOR; DENDRITIC CELLS; INTERLEUKIN-2; MELANOMA; INVIVO AB The ability to transfer novel genes into mammalian cells has allowed us to conceive of novel strategies towards cancer therapy. Since the initial gene-transfer clinical trial in 1989, over 300 cancer patients have been enrolled in gene therapy trials. Despite this, an NTH-sponsored panel concluded that 'clinical efficacy has not been definitively demonstrated at this time in any gene therapy protocol' [I]. However, the first 8 pears of gene therapy research have provided us with insights regarding the areas that require further scientific progress. For example, it is now clear that while in vitro assays of gene-modified haemotopoietic progenitor cells suggest high transduction efficiencies, once these cells are infused in vivo, only a small percentage of circulating transduced cells can be detected. While the initial clinical studies have demonstrated that gene transfer in patients can be safe and feasible, they have also indicated that future research is necessary towards the development of improved gene transfer techniques for these approaches to be successful. RP Hwu, P (reprint author), NCI,BLDG 10,ROOM 2B42,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 37 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0954-6820 J9 J INTERN MED JI J. Intern. Med. PY 1997 VL 242 SU 740 BP 109 EP 114 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA XZ563 UT WOS:A1997XZ56300018 ER PT J AU IshidaYamamoto, A Kartasova, T Matsuo, S Kuroki, T Iizuka, H AF IshidaYamamoto, A Kartasova, T Matsuo, S Kuroki, T Iizuka, H TI Involucrin and SPRR are synthesized sequentially in differentiating cultured epidermal cells SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE keratinocytes; keratinization; immunoelectron microscopy; confocal laser scanning microscopy ID PROLINE-RICH PROTEINS; CROSS-LINKED ENVELOPE; ULTRASTRUCTURAL-LOCALIZATION; TERMINAL DIFFERENTIATION; LAMELLAR ICHTHYOSIS; MAMMALIAN EPIDERMIS; HUMAN KERATINOCYTES; ELASTASE INHIBITOR; CORNIFIED ENVELOPE; TRANSGENIC MICE AB Epidermal keratinocytes form cornified cell envelopes during terminal differentiation. These envelopes are composed of several cross-linked molecules, including involucrin, loricrin, and SPRR. We have previously reported that involucrin is synthesized earlier in terminal differentiation than loricrin. To further elucidate the mechanisms of terminal differentiation, we have now examined the expression of the two differentiation markers, involucrin and SPRR, in cultured human epidermal keratinocytes. In confluent nonstratified cultures, many involucrin-immunoreactive cells were detected, but few SPRR1/3-positive cells. Double staining demonstrated that cells containing SPRR1/3 almost always contained involucrin, but involucrin was present in many cells that did not contain SPRR. Light and electron microscopic immunohistochemistry of a stratified culture demonstrated that lower cells (close to the basal layer) were occasionally involucrin-positive, but lacked SPRR1/3, whereas more superficial cells contained both involucrin and SPRR. We conclude that involucrin and SPRR are sequentially induced in this order during keratinocyte differentiation. C1 NIAMS,SKIN BIOL LAB,NIH,BETHESDA,MD. UNIV TOKYO,INST MED SCI,DEPT CANC CELL RES,TOKYO,JAPAN. RP IshidaYamamoto, A (reprint author), ASAHIKAWA MED COLL,DEPT DERMATOL,NISHIKAGURA 4-5-3-11,ASAHIKAWA,HOKKAIDO 078,JAPAN. RI Kuroki, Toshio/A-9500-2011 OI Kuroki, Toshio/0000-0001-6369-4351 NR 40 TC 26 Z9 27 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JAN PY 1997 VL 108 IS 1 BP 12 EP 16 DI 10.1111/1523-1747.ep12285611 PG 5 WC Dermatology SC Dermatology GA VZ789 UT WOS:A1997VZ78900003 PM 8980279 ER PT B AU Biro, T Acs, G Acs, P Modarres, S Blumberg, PM AF Biro, T Acs, G Acs, P Modarres, S Blumberg, PM BE Hauser, C TI Recent advances in understanding of vanilloid receptors: A therapeutic target for treatment of pain and inflammation in skin SO JOURNAL OF INVESTIGATIVE DERMATOLOGY SYMPOSIUM PROCEEDINGS, VOL 2, NO 1, AUGUST 1997 LA English DT Proceedings Paper CT 45th Annual Symposium on the Biology of the Skin - Cutaneous Innervation and Neurobiology of the Skin CY JUL 20-24, 1996 CL SNOWMASS, CO SP Natl Psoriasis Fdn, Orentreich Fdn Adv Sci, Univ Colorado Canc Ctr DE capsaicin; resiniferatoxin AB C-fiber sensory afferent neurons, which contain neuropeptides such as calcitonin-gene related peptide and substance P, mediate a wide variety of physiologic responses, including chemogenic pain, thermoregulation, and neurogenic inflammation. Capsaicin, the pungent constituent in red pepper, functions to activate and then, at higher doses and longer times, desensitize this class of neurons, This latter response provides the basis for the therapeutic application of capsaicin, A major advance in the field has been the identification of resiniferatoxin, a phorbol-related diterpene, as an analog of capsaicin that is ultrapotent but with differential selectivity, In particular, resiniferatoxin is only similar in potency for induction of pain but is much more effective for desensitization, Structure-activity analysis in whole animal experiments provides further evidence for dissociation of biologic endpoints, strongly arguing for the existence of vanilloid receptor subclasses, Using resiniferatoxin, we have been able to define specific, high-affinity receptors for capsaicin both in animal models such as rats and in man, Of great importance, the pharmacologic characterization in cultured dorsal root ganglion cells of the high-affinity resiniferatoxin-binding site and of tile physiologic response believed to be directly coupled to the receptor, viz, calcium uptake, differed in structure-activity and in cooperativity. We conclude that multiple high-affinity vanilloid receptor subclasses mediate vanilloid response; moreover, the resiniferatoxin-selective subclass of vanilloid receptors is not the voltage-independent, cation-nonselective ion channel as previously believed, Optimization of ligands for the individual vanilloid receptor subclasses should revolutionize this therapeutic area. C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20892. RP Blumberg, PM (reprint author), NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,37 CONVENT DR MSC 4255,BLDG 37-3A01,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 4 U2 4 PU BLACKWELL SCIENCE INC PI MALDEN PA COMMERCE PLACE 350 MAIN ST, MALDEN, MA 02148 PY 1997 BP 56 EP 60 PG 5 WC Dermatology SC Dermatology GA BJ37T UT WOS:A1997BJ37T00011 ER PT J AU Musachio, JL Horti, A London, ED Dannals, RF AF Musachio, JL Horti, A London, ED Dannals, RF TI Synthesis of a Radioiodinated Analog of epibatidine: (+/-)-exo-2-(2-iodo-5-pyridyl)-7-azabicyclo[2.2.1]heptane for in vitro and in vivo studies of nicotinic acetylcholine receptors SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE epibatidine; I-123; I-125; copper-assisted halogen-exchange; nicotinic receptors; single photon emission computed tomography; brain imaging ID ANTAGONIST; DISEASE; I-123 AB [I-125] or [I-123] labeled (+/-)-exo-2-(2-iodo-5-pyridyl)-7-azabicyclo-[2.2.1]heptane (IPH), an analog of the high-affinity nicotinic acetylcholine receptor ligand, epibatidine, was prepared by a nucleophilic non-isotopic exchange reaction. Treatment of the 2-bromo pyridyl precursor with radioiodide and in situ generated Cu(I) at high temperature (200 - 220 degrees C) gave [I-125] or [I-123]IPH that was purified by reverse phase HPLC. Radiochemical yields ranged from 31 - 50% for the [I-125] labeling (average = 37%, n = 7) and 20% for [I-123]. Both [I-125]IPH and [I-123]IPH were of high radiochemical purity (> 96%) and high specific activity (average of 1540 mCi/mu mol (57 GBq/mu mol) for [I-125]IPH and > 1750 mCi/mu mol (65 GBq/mu mol) for [I-123]IPH). C1 JOHNS HOPKINS MED INST,DIV RADIAT HLTH SCI,BALTIMORE,MD 21287. NIDA,ADDICT RES CTR,BRAIN IMAGING SECT,INTRAMURAL RES PROGRAM,BALTIMORE,MD 21224. UNIV MARYLAND,SCH MED,DEPT PHARMACOL & EXPT THERAPEUT,BALTIMORE,MD 21201. RP Musachio, JL (reprint author), JOHNS HOPKINS MED INST,DIV NUCL MED,600 N WOLFE ST,NELSON BLDG,RM B1-167,BALTIMORE,MD 21287, USA. NR 26 TC 27 Z9 27 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0362-4803 J9 J LABELLED COMPD RAD JI J. Label. Compd. Radiopharm. PD JAN PY 1997 VL 39 IS 1 BP 39 EP 48 DI 10.1002/(SICI)1099-1344(199701)39:1<39::AID-JLCR945>3.0.CO;2-X PG 10 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA WF389 UT WOS:A1997WF38900005 ER PT J AU Niemela, JE Csako, G Bui, MN Elin, RJ AF Niemela, JE Csako, G Bui, MN Elin, RJ TI Gender-specific correlation of platelet ionized magnesium and serum low-density-lipoprotein cholesterol concentrations in apparently healthy subjects SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Article ID SMOOTH-MUSCLE CELLS; INTRACELLULAR FREE MAGNESIUM; LIPID-PEROXIDATION; MEMBRANE CHOLESTEROL; SKELETAL-MUSCLE; HEART-DISEASE; NITRIC-OXIDE; RATS; DEFICIENCY; CALCIUM AB We previously found an inverse correlation between platelet ionized magnesium concentration ((Mg2+)(i)) and serum total cholesterol concentration in normal male but not female subjects. In the present study, we determined the platelet (Mg2+)(i) by using a fluorescent ionized magnesium (Mg2+) indicator, FURAPTRA, and measured the serum concentrations of the following: total cholesterol; very-low-density lipoprotein cholesterol (VLDL-C); low-density lipoprotein cholesterol (LDL-C); high-density lipoprotein cholesterol (HDL-C); antioxidized low-density lipoprotein (LDL) autoantibodies; lipoprotein(a); apolipoproteins A-I (ape A-I) and B (ape B); triglycerides; estradiol-17 (E(2)); ceruloplasmin (Cp); and selected electrolytes, including total and ionized magnesium and calcium and total protein and albumin. In men, but not in women, platelet (Mg2+)(i) significantly inversely correlated with serum total cholesterol (r = -0.52, p < 0.02), LDL-C (r = -0.54, p < 0.009 by a ''direct'' method; r = -0.40, p < 0.05 by an electrophoretic method), and apo B (r = -0.42, p < 0.04). We found no significant correlations between platelet (Mg2+)(i) and any other variables, including serum total and ionized magnesium, antioxidized LDL autoantibodies, Cp, and E(2). We speculate that decreased platelet (Mg2+)(i) is a possible marker for platelet membrane alterations that may affect platelet involvement in thrombosis and atherogenesis. C1 NIH,DEPT CLIN PATHOL,WARREN GRANT MAGNUSON CLIN CTR,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,DEPT INTERNAL MED,WASHINGTON,DC 20007. OI Niemela, Julie/0000-0003-4197-3792 NR 67 TC 8 Z9 8 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD JAN PY 1997 VL 129 IS 1 BP 89 EP 96 DI 10.1016/S0022-2143(97)90165-7 PG 8 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA WB904 UT WOS:A1997WB90400010 PM 9011595 ER PT J AU Fauci, AS AF Fauci, AS TI Host factors in the pathogenesis of HIV disease. SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NIAID,NIH,BETHESDA,MD 20814. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 1 EP 1 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600001 ER PT J AU Tiffany, HL Alkhatib, G Combadiere, C Berger, EA Murphy, PM AF Tiffany, HL Alkhatib, G Combadiere, C Berger, EA Murphy, PM TI A model system for inducible expression of the CC chemokine receptors CCR1, CCR3, and CCR8. SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NATL INST HLTH,HOST DEF LAB,BETHESDA,MD 20892. NATL INST HLTH,VIRAL 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 3 EP 3 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600002 ER PT J AU Koski, G Weng, D Cohen, P AF Koski, G Weng, D Cohen, P TI Induction of dendritic cell properties in HL-60 cells. SO JOURNAL OF LEUKOCYTE BIOLOGY 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 6 EP 6 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600008 ER PT J AU He, H Wang, X Holbrook, NJ Trush, MA AF He, H Wang, X Holbrook, NJ Trush, MA TI Mononuclear cell differentiation induced by phorbol ester is blocked by the MEK inhibitor PD98059 SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21205. NIA,GENE EXPRESS & AGING SECT,NATL INST HLTH,BALTIMORE,MD 21224. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 12 EP 12 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600014 ER PT J AU McKinney, LC Aquilla, EM Coffin, D Cook, JA Wink, DA Mitchell, JB Vodovotz, Y AF McKinney, LC Aquilla, EM Coffin, D Cook, JA Wink, DA Mitchell, JB Vodovotz, Y TI Ionizing radiation potentiates production of nitric oxide in macrophage cell lines and in tumor-infiltrating leukocytes. Role of tumor necrosis factor-alpha. SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 ARMED FORCES RADIOBIOL RES INST,DEPT RADIAT PATHOPHYSIOL,BETHESDA,MD 20889. NCI,RADIAT BIOL 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 18 EP 18 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600020 ER PT J AU Germolec, D Spalding, J Yu, H Simeonova, P Luster, M AF Germolec, D Spalding, J Yu, H Simeonova, P Luster, M TI Arsenic enhancement of skin neoplasia by chronic stimulation of growth-promoting cytokines SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NIEHS,RES TRIANGLE PK,NC 27709. TOKAI UNIV,KANAGAWA,JAPAN. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 44 EP 44 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600045 ER PT J AU Wuyts, A Gong, W Proost, P VanDamme, J Wang, JM AF Wuyts, A Gong, W Proost, P VanDamme, J Wang, JM TI The human chemokines GCP-2 and ENA-78 activate neutrophils through the receptors CXCR1 and CXCR2 SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 UNIV LEUVEN,REGA INST,LAB MOL IMMUNOL,B-3000 LOUVAIN,BELGIUM. NCI,FREDERICK CANC RES & DEV CTR,MOL IMMUNOREGULAT LAB,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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 49 EP 49 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600048 ER PT J AU Howard, OMZ Grimm, M Tarasova, NI Murphy, W Hollingshead, MG Turpin, JA Rice, WG Oppenheim, JJ AF Howard, OMZ Grimm, M Tarasova, NI Murphy, W Hollingshead, MG Turpin, JA Rice, WG Oppenheim, JJ TI Ureido analog of distamycin blocks chemokine receptor mediated function SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 SAIC,FREDERICK,MD. LMI,FREDERICK,MD. MADDS,ABL,BRP,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. RI Howard, O M Zack/B-6117-2012 OI Howard, O M Zack/0000-0002-0505-7052 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 51 EP 51 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600049 ER PT J AU Vodovotz, Y Kopp, JB Takeguchi, H Shrivastav, S Coffin, D Lucia, MS Webber, R Letterio, J Wink, D Roberts, AB AF Vodovotz, Y Kopp, JB Takeguchi, H Shrivastav, S Coffin, D Lucia, MS Webber, R Letterio, J Wink, D Roberts, AB TI Increased mortality, blunted production of nitric oxide, and increased production of tumor necrosis fartor-alpha in endotoxemic transforming growth factor-beta 1 transgenic mice SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NIDDK,RADIAT BIOL BRANCH,NATL CANC INST,BETHESDA,MD 20892. NIDDK,KIDNEY DIS SECT,METAB DIS BRANCH,BETHESDA,MD 20892. NATL CANC INST,CHEMOPREVENT LAB,NATL INST HLTH,BETHESDA,MD 20892. RES & DIAGNOST ANTIBODIES,RICHMOND,CA 94806. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 56 EP 56 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600057 ER PT J AU Linnekin, D Mou, S DeBerry, C Ortaldo, J AF Linnekin, D Mou, S DeBerry, C Ortaldo, J TI Stem cell factor activates both the JAK/STAT and Src family pathways in hematopoietic cells. SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI,FREDERICK CANC RES & DEV CTR,LAB LEUKOCYTE BIOL,DBS,FREDERICK,MD 21702. IRSP,SAIC,FREDERICK,MD 21702. 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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 66 EP 66 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600068 ER PT J AU Danilkovitch, A Leonard, EJ AF Danilkovitch, A Leonard, EJ TI Regulation of integrin functional activity by macrophage stimulating protein (MSP). SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 NCI,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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 73 EP 73 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600072 ER PT J AU Erwin, RA Kirken, RA Farrar, WL AF Erwin, RA Kirken, RA Farrar, WL TI IL9 induces serine and tyrosine, but not threonine, phosphorylation of STAT5a and STAT5b in PHA-activated human T cells SO JOURNAL OF LEUKOCYTE BIOLOGY LA English DT Meeting Abstract C1 IRSP,SAIC,FREDERICK,MD. NCI,FREDERICK CANC RES & DEV CTR,CYTOKINE MOL MECH SECT,MOL IMMUNOREGULAT LAB,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 0741-5400 J9 J LEUKOCYTE BIOL JI J. Leukoc. Biol. PY 1997 SU S BP 80 EP 80 PG 1 WC Cell Biology; Hematology; Immunology SC Cell Biology; Hematology; Immunology GA YG406 UT WOS:A1997YG40600081 ER PT J AU Hui, RT Everhart, AL Glasgow, WC AF Hui, RT Everhart, AL Glasgow, WC TI Epidermal growth factor-stimulated production of esterified 13(S)-hydroxyoctadecadienoic acid is associated with tumor suppressor phenotype in Syrian hamster embryo fibroblasts SO JOURNAL OF LIPID RESEARCH LA English DT Article DE 15-lipoxygenase; linoleic acid; 13-hydroxyoctadecadienoic acid; tumor suppressor gene; epidermal growth factor; mitogen; cell proliferation ID LOW-DENSITY-LIPOPROTEIN; ARACHIDONIC-ACID; RETICULOCYTE LIPOXYGENASE; ATHEROSCLEROTIC LESIONS; RABBIT RETICULOCYTES; PHOSPHOLIPASE-C; PHORBOL ESTER; MESSENGER-RNA; 15-LIPOXYGENASE; CELLS AB Epidermal growth factor (EGF) stimulates the lipoxygenase metabolism of linoleic acid to 13(S)-hydroxyoctadecadienoic acid (HODE) in Syrian hamster embryo (SHE) fibroblasts. 13(S)-HODE is a potent and specific enhancer of EGF-dependent DNA synthesis in normal phenotypic SHE cells (supB(+)), but is inactive in Variant SHE cells that have lost tumor suppressor gene function (supB(-)). EGF activation of quiescent SHE cells results in increased levels of 13-HODE esterified in cellular phospholipid and triglyceride. Steric analyses suggest that this metabolite is generated in part by direct oxygenation of membrane lipids by an n-6 lipoxygenase. In studies on the uptake and mobilization of 13-HODE in SHE cells, we observed EGF to stimulate a time- and dose-dependent incorporation and reacylation of the monohydroxy linoleate metabolite. The level of 13-HODE uptake in supB(+) cells is twice that of supB(-). Among classes of phospholipids, radiolabeled 13-HODE is esterified pre dominantly into phosphatidylcholine and this distribution pattern is similar for both SHE cell lines. Pretreatment of cells with the tyrosine kinase inhibitor methyl-2,5-dihydroxycinnamate blocks EGF-stimulated HODE incorporation. Inhibition of tyrosine phosphatase activity with vanadate potentiates HODE uptake in supB(+) but not supB(-) cells. Moreover, activation of protein kinase C with phorbol ester stimulates HODE incorporation in the supB(+) line only. The differential effects of EGF on 13-HODE uptake and mobilization in supB(+) and supB(-) cells appear to be related to loss of the tumor suppressor phenotype. EGF-stimulated generation of esterified 13-HODE may be an important biological process in determining the mechanism and site of HODE interaction with the mitogenic signaling pathway. C1 NIEHS,LAB MOL BIOPHYS,NATL INST HLTH,RES TRIANGLE PK,NC 27709. NR 41 TC 2 Z9 2 U1 0 U2 0 PU LIPID RESEARCH INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD JAN PY 1997 VL 38 IS 1 BP 49 EP 60 PG 12 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA WH710 UT WOS:A1997WH71000006 PM 9034199 ER PT J AU Issaq, HJ Horng, PLC Janini, GM Muschik, GM AF Issaq, HJ Horng, PLC Janini, GM Muschik, GM TI Micellar electrokinetic chromatography using mixed sodium dodecyl sulfate and sodium cholate SO JOURNAL OF LIQUID CHROMATOGRAPHY & RELATED TECHNOLOGIES LA English DT Article ID CAPILLARY CHROMATOGRAPHY; ELUTION RANGE; SEPARATION; CORTICOSTEROIDS AB The migration behavior of fifteen dansylated amino acids, two estrogens, and two poly-cyclic aromatic hydrocarbons (PAHs) was studied by micellar electrokinetic chromatography (MEKC) with mixed micelles. The buffer system consisted of 10 mM berate at pH 9.0, containing 50 mM total surfactant concentration. Five different ratios of sodium dodecyl sulfate (SDS) and sodium cholate (SC) surfactants were used, namely. 100:0, 75:25, 50:50, 25:75, and 0:100 (SDS:SC). The numbers refer to molar ratio percent. The migration time window was 50% larger in 50:50 (SDS:SC) compared to 100% SC, and 15% larger than that of 100% SDS. The migration times of PAHs and estrogens exhibited a pattern similar to that of Sudan III in all the SDS/SC mixed micellar systems, due to their hydrophobic property. Although most amino acids are negatively charged at pH 9, their migration patterns were different depending on their R-group. The migration times of amino acids with negatively charged R-groups increased continuously with increasing percent of SC in the SDS/SC mixed micellar systems, while the migration time of amino acids with positively charged R-group continuously decreased with increasing percent of SC in the SDS/SC mixed micellar system. For other groups of amino acids, the migration times in SDS/SC mixed micellar systems exhibited variation without specific pattern. In general, the use of SDS and SC mixed micelles extended the migration time window to some extent, but it was not sufficient to get satisfactory resolution for the amino acids tested in this study. RP Issaq, HJ (reprint author), NCI,FREDERICK CANC RES & DEV CTR,SAIC FREDERICK,POB B,FREDERICK,MD 21702, USA. NR 20 TC 16 Z9 16 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1082-6076 J9 J LIQ CHROMATOGR R T JI J. Liq. Chromatogr. Relat. Technol. PY 1997 VL 20 IS 2 BP 167 EP 182 DI 10.1080/10826079708010645 PG 16 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA WH187 UT WOS:A1997WH18700001 ER PT J AU Beutler, JA AF Beutler, JA TI Separation of high molecular weight saponins of Archidendron ellipticum by hydrophilic interaction chromatography SO JOURNAL OF LIQUID CHROMATOGRAPHY & RELATED TECHNOLOGIES LA English DT Article ID LIQUID-CHROMATOGRAPHY; SILICA; RETENTION; PHASES; PLANTS AB Saponins of high molecular weight (Mr 2,000-2,100) from several species in the plant family Leguminosae were separated at both analytical and preparative scale using wide pore aminopropyl HPLC with acetonitrile-water mixtures, and gradient wide-pore butyl reversed-phase HPLC. The basis for the aminopropyl separation appears to be hydrophilic interaction chromatography, and the pore size of the media appears to play a key role in the separation. RP Beutler, JA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,LAB DRUG DISCOVERY RES & DEV,DEV THERAPEUT PROGRAM,FREDERICK,MD 21702, USA. RI Beutler, John/B-1141-2009 OI Beutler, John/0000-0002-4646-1924 NR 13 TC 10 Z9 10 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1082-6076 J9 J LIQ CHROMATOGR R T JI J. Liq. Chromatogr. Relat. Technol. PY 1997 VL 20 IS 15 BP 2415 EP 2426 DI 10.1080/10826079708002712 PG 12 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA XT074 UT WOS:A1997XT07400008 ER PT J AU Negrusz, A Tolhurst, TA Buehler, PW Woods, EF Crowell, JA Levine, BS AF Negrusz, A Tolhurst, TA Buehler, PW Woods, EF Crowell, JA Levine, BS TI High performance liquid chromatographic determination of fumaric acid in rat plasma, urine, and fecal samples SO JOURNAL OF LIQUID CHROMATOGRAPHY & RELATED TECHNOLOGIES LA English DT Article ID CARBOXYLIC-ACIDS; DOUBLE-BLIND; HEPATOCARCINOGENESIS; DERIVATIVES; PSORIASIS; THERAPY; THIOACETAMIDE; BEVERAGES; WINES; MICE AB Fumaric acid, a Krebs cycle intermediate, is a potential cancer chemoprevention agent. A high performance liquid chromatographic procedure with UV detection for determination of fumaric acid in large numbers of rat plasma, urine and fecal samples was developed. Fumaric acid was extracted from plasma, urine, and fecal samples utilizing solid phase extraction using Clean Up(R) Quaternary. Amine 1 mL (plasma, fecal samples) and 3 mL (urine) extraction columns followed by reverse phase high performance liquid chromatography with UV detection at 215 nn. Standard curves for plasma (1 mu g/mL - 200 mu g/mL), urine (5 mu g/mL - 200 mu g/mL), and fecal material (25 mu g/g - 500 mu g/g) were analyzed and replicate analysis of controls were used to determine intra-day and inter-day variability. Chlorofumaric acid was used as an internal standard for plasma and fecal samples; trans-glutaconic acid for urine samples. Precision and accuracy were studied using control solutions (low and high) prepared in naive rat plasma, urine, and fecal material. Intra-day variability was determined using 3 - 6 replicates of each control solution on a single day. Coefficient of variation (CV) for 20 mu g/mL control (low) in plasma was 6.11% and for 80 mu g/mL (high) was 7.07%; relative accuracy (RA) was 0% and 6.01%, respectively. CV for 15 mu g/mL low control in urine was 38.95% and for 150 mu g/mL high control was 8.84%; RA values were -12.2% and -15.16%, respectively. For the fecal material, CV for low control (100 mu g/g) was 0.92% and for the high control (400 mu g/g) was 4.67%. RA values were -4.02% and 4.14%, respectively. Inter-day variability was determined over a four day period. For the 20 and 80 mu g/mL plasma control solutions, CVs were 12.97% and 9.09%, respectively, and RA values were 1.1% and 4.04%, respectively. For the 15 and 150 mu g/mL urine control solutions, CVs were 26.85% and 14.17%, respectively, and RA values were 33.07% and -1.24%, respectively. For the 100 and 400 mu g/g fecal material controls, CVs were 2.5% and 4.39%, respectively, and RA values were -4.07% and -3.87%, respectively. The standard curves for plasma, urine, and fecal samples were linear over the range of fumaric acid assayed and the means for the regression coefficient were 0.9939, 0.9972, and 0.9956, respectively. The limits of quantitation for plasma, urine, and fecal material were 1 mu g/mL, 5 mu g/mL and 25 mu g/g, respectively. C1 NATL CANC INST,DIV CANC PREVENT & CONTROL,ROCKVILLE,MD 20892. UNIV ILLINOIS,COLL MED,DEPT PHARMACOL,TOXICOL RES LAB,CHICAGO,IL 60612. RP Negrusz, A (reprint author), UNIV ILLINOIS,COLL PHARM,DEPT PHARMACEUT & PHARMACODYNAM,833 S WOOD ST,CHICAGO,IL 60612, USA. NR 21 TC 5 Z9 5 U1 1 U2 3 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 SN 1082-6076 J9 J LIQ CHROMATOGR R T JI J. Liq. Chromatogr. Relat. Technol. PY 1997 VL 20 IS 20 BP 3365 EP 3376 DI 10.1080/10826079708005837 PG 12 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA YL125 UT WOS:A1997YL12500008 ER PT J AU Das, R Vonderhaar, BK AF Das, Rina Vonderhaar, Barbara K. TI Prolactin as a Mitogen in Mammary Cells SO JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA LA English DT Article DE Prolactin; breast cancer; normal mammary gland development; mitogenesis; receptor forms; signal pathways AB Prolactin (PRL) acts as both a mitogen and a differentiating agent in the breast. The decision to respond to PRL as a mitogen by breast cells depends on the hormonal milieu in which the epithelial cell resides. In addition, PRL's action on the breast is regulated (1) at the level of the hormone itself; (2) at the receptor level; (3) at the level of selection of signaling pathway; and, (4) by combinations of these aspects. The development of cell lines containing only one class of the PRL receptors and showing qualitative differences in response and signaling pathways will help in understanding the pleiotropic nature of PRL action. C1 [Das, Rina; Vonderhaar, Barbara K.] NCI, Lab Tumor Immunol & Biol, NIH, Bethesda, MD 20892 USA. RP Vonderhaar, BK (reprint author), Bldg 10,Rm 5B56,9000 Rockville Pike, Bethesda, MD 20892 USA. EM barbarav@helix.nih.gov NR 68 TC 70 Z9 70 U1 0 U2 0 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1083-3021 J9 J MAMMARY GLAND BIOL JI J. Mammary Gland Biol. Neoplasia PD JAN PY 1997 VL 2 IS 1 BP 29 EP 39 DI 10.1023/A:1026369412612 PG 11 WC Oncology; Endocrinology & Metabolism; Physiology SC Oncology; Endocrinology & Metabolism; Physiology GA V25HF UT WOS:000208468400003 PM 10887517 ER PT J AU Mears, D Sheppard, NF Atwater, I Rojas, E Bertram, R Sherman, A AF Mears, D Sheppard, NF Atwater, I Rojas, E Bertram, R Sherman, A TI Evidence that calcium release-activated current mediates the biphasic electrical activity of mouse pancreatic beta-cells SO JOURNAL OF MEMBRANE BIOLOGY LA English DT Article DE islet of Langerhans; stimulus-secretion coupling; endoplasmic reticulum; acute insulin response; mathematical model; glucose ID INSULIN-SECRETION; B-CELLS; INTRACELLULAR CA2+; K+ CHANNEL; GLUCOSE; ISLETS; MEMBRANE; OSCILLATIONS; MECHANISMS; LANGERHANS AB The electrical response of pancreatic beta-cells to step increases in glucose concentration is biphasic, consisting of a prolonged depolarization with action potentials (Phase 1) followed by membrane potential oscillations known as bursts. We have proposed that the Phase 1 response results from the combined depolarizing influences of potassium channel closure and an inward, nonselective cation current (I-CRAN) that activates as intracellular calcium stores empty during exposure to basal glucose (Bertram et al., 1995). The stores refill during Phase 1, deactivating I-CRAN and allowing steady-state bursting to commence. We support this hypothesis with additional simulations and experimental results indicating that Phase 1 duration is sensitive to the filling state of intracellular calcium stores. First, the duration of the Phase 1 transient increases with duration of prior exposure to basal (2.8 mM) glucose, reflecting the increased time required to fill calcium stores that have been emptying for longer periods. Second, Phase 1 duration is reduced when islets are exposed to elevated K+ to refill calcium stores in the presence of basal glucose. Third, when extracellular calcium is removed during the basal glucose exposure to reduce calcium influx into the stores, Phase 1 duration increases. Finally, no Phase 1 is observed following hyperpolarization of the beta-cell membrane with diazoxide in the continued presence of 11 mM glucose, a condition in which intracellular calcium stores remain full. Application of carbachol to empty calcium stores during basal glucose exposure did not increase Phase 1 duration as the model predicts. Despite this discrepancy, the good agreement between most of the experimental results and the model predictions provides evidence that a calcium release-activated current mediates the Phase 1 electrical response of the pancreatic beta-cell. C1 NIDDK,CELL BIOL & GENET LAB,NIH,BETHESDA,MD 20892. NIDDK,MATH RES BRANCH,NIH,BETHESDA,MD 20892. RP Mears, D (reprint author), JOHNS HOPKINS UNIV,DEPT BIOMED ENGN,BALTIMORE,MD 21218, USA. FU NIGMS NIH HHS [5 T32 GM7057] NR 55 TC 21 Z9 22 U1 1 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0022-2631 J9 J MEMBRANE BIOL JI J. Membr. Biol. PD JAN 1 PY 1997 VL 155 IS 1 BP 47 EP 59 PG 13 WC Biochemistry & Molecular Biology; Cell Biology; Physiology SC Biochemistry & Molecular Biology; Cell Biology; Physiology GA WA339 UT WOS:A1997WA33900005 PM 9002424 ER PT J AU Flanders, KC Bhandiwad, AR Winokur, TS AF Flanders, KC Bhandiwad, AR Winokur, TS TI Transforming growth factor-beta s block cytokine induction of catalase and xanthine oxidase mRNA levels in cultured rat cardiac cells SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE catalase; cultured cardiac myocytes; cytokines; enzyme induction; free radicals; TGF-beta; reperfusion injury; xanthine oxidase ID TUMOR NECROSIS FACTOR; AMINO-ACID-SEQUENCE; SUPEROXIDE-DISMUTASE; GENE-EXPRESSION; HYDROGEN-PEROXIDE; ENDOTHELIAL-CELLS; MESSENGER-RNA; IN-VITRO; FIBROBLASTS; PROTEIN AB We examined the effects of transforming growth factor-beta (TGF-beta) on the mRNA expression of the antioxidative enzymes, catalase, manganese superoxide dismutase (MnSOD), and copper-zinc superoxide dismutase (CuZnSOD), as well as the oxidative enzyme, xanthine oxidase (XO), in cultures of cardiomyocytes, cardiac non-myocytes, and fetal bovine heart endothelial cells. TGF-beta s alone had little effect on expression of these enzymes, but treatment with a combination of interleukin-1 beta, interferon-gamma, and tumor necrosis factor-alpha increased expression of MnSOD, catalase, and XO in some cell types with little effect on CuZnSOD expression. When TGF-beta s were added along with these inflammatory cytokines there was a return to control levels of catalase expression, as well as a dramatic reduction in XO expression. In fetal bovine heart endothelial cells, treatment with inflammatory cytokines increased XO mRNA expression 11.5-fold and inclusion of TGF-beta s reduced this 4-5-fold; effects on XO enzyme activity paralleled those seen on mRNA expression. Similar changes in XO expression were seen in cardiomyocytes. In contrast, TGF-beta s did not change cytokine-induced MnSOD expression. All three mammalian isoforms of TGF-beta showed similar effects. In summary, TGF-beta s may be able to decrease superoxide anion production and subsequent tissue damage by decreasing levels of XO. (C) 1997 Academic Press Limited RP Flanders, KC (reprint author), NCI, CHEMOPREVENT LAB, BLDG 41-ROOM C-629, 41 LIBRARY OR MSC5055, BETHESDA, MD 20892 USA. NR 38 TC 14 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD JAN PY 1997 VL 29 IS 1 BP 273 EP 280 DI 10.1006/jmcc.1996.0272 PG 8 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA WK014 UT WOS:A1997WK01400027 PM 9040042 ER PT J AU Johnson, WE OBrien, SJ AF Johnson, WE OBrien, SJ TI Phylogenetic reconstruction of the Felidae using 16S rRNA and NADH-5 mitochondrial genes SO JOURNAL OF MOLECULAR EVOLUTION LA English DT Article DE phylogeny; 16S rRNA; NADH dehydrogenase subunit 5 (NADH-5); mitochondrial sequence data; Felidae ID CODON USAGE; SEQUENCES; DNA; CAT; AMPLIFICATION; EVOLUTION; AMERICAN; PATTERNS; TREES; RNA AB The Felidae family represents a challenge for molecular phylogenetic reconstruction because it consists of 38 living species that evolved from a relatively recent common ancestor (10-15 million years ago). We have determined mitochondrial DNA sequences from two genes that evolve at relatively rapid evolutionary rates, 16S rRNA (379 bp) and NADH dehydrogenase subunit 5 (NADH-5, 318 bp), from multiple individuals of 35 species. Based on separate and combined gene analyses using minimum evolution, maximum parsimony, and maximum likelihood phylogenetic methods, we recognized eight significant clusters or species clades that likely reflect separate monophyletic evolutionary radiations in the history of this family. The clusters include (1) ocelot lineage, (2) domestic cat lineage, (3) Panthera genus, (4) puma group, (5) Lynx genus, (6) Asian leopard cat group, (7) caracal group, and (8) bay cat group. The results confirm and extend previously hypothesized associations in most cases, but in others, e.g., the bay cat group, suggest novel phylogenetic relationships. The results are compared and evaluated with molecular, cytogenetic, and morphological data to derive a phylogenetic synthesis of field evolutionary history. RP Johnson, WE (reprint author), NCI, LAB GEN DIVERS, BLDG 560, ROOM 21-105, FREDERICK, MD 21702 USA. NR 69 TC 80 Z9 85 U1 12 U2 65 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0022-2844 EI 1432-1432 J9 J MOL EVOL JI J. Mol. Evol. PY 1997 VL 44 SU 1 BP S98 EP S116 DI 10.1007/PL00000060 PG 19 WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics & Heredity GA WL081 UT WOS:A1997WL08100015 PM 9071018 ER PT J AU Garraffo, HM Jain, P Spande, TF Daly, JW AF Garraffo, HM Jain, P Spande, TF Daly, JW TI Alkaloid 223A: The first trisubstituted indolizidine from dendrobatid frogs SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID POISON FROGS; 8-METHYLINDOLIZIDINES; DECAHYDROQUINOLINES; PYRROLIZIDINES; QUINOLIZIDINES; PUMILIOTOXINS; PYRROLIDINES; SKIN AB The structure of alkaloid 223A (1), the first member of a new class of amphibian alkaloids, purified by HPLC from a skin extract of a Panamanian population of the frog Dendrobates pumilio Schmidt (Dendrobatidae), has been established as (5R,6S,8R,9S)- or (5S,6R,8S,9R)-6,8-diethyl-5-propylindolizidine, based on GC-MS, GC-FTIR, and H-1-NMR spectral studies. Three higher homologs of 223A, namely alkaloids 237L (2), 251M (3), and 267J (4), have been detected in other extracts, and tentative structures are proposed. C1 NIDDKD,LAB BIOORGAN CHEM,NIH,BETHESDA,MD 20892. NR 14 TC 29 Z9 29 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD JAN PY 1997 VL 60 IS 1 BP 2 EP 5 DI 10.1021/np960522l PG 4 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA WD946 UT WOS:A1997WD94600002 PM 9014346 ER PT J AU Cragg, GM Newman, DJ Snader, KM AF Cragg, GM Newman, DJ Snader, KM TI Natural products in drug discovery and development SO JOURNAL OF NATURAL PRODUCTS LA English DT Review ID MARKET; PLANTS; AGENTS C1 NCI, FREDERICK CANC RES & DEV CTR, DIV CANC BIOL DIAG & CTR,DEV THERAPEUT PROGRAM, NAT PROD BRANCH, FREDERICK, MD 21702 USA. NR 35 TC 690 Z9 719 U1 12 U2 95 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0163-3864 EI 1520-6025 J9 J NAT PROD JI J. Nat. Prod. PD JAN PY 1997 VL 60 IS 1 BP 52 EP 60 DI 10.1021/np9604893 PG 9 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA WD946 UT WOS:A1997WD94600017 PM 9014353 ER PT J AU Braun, AR Laruelle, M Mouradian, MM AF Braun, AR Laruelle, M Mouradian, MM TI Interactions between D1 and D2 dopamine receptor family agonists and antagonists: The effects of chronic exposure on behavior and receptor binding in rats and their clinical implications SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE D1D2 dopamine receptor; behavior chronic stereotypy; locomotion; catalepsy; supersensitivity ID PARKINSONS-DISEASE; SELECTIVE D-1; UP-REGULATION; HALOPERIDOL TREATMENT; NEUROLEPTIC TREATMENT; STEREOTYPED BEHAVIOR; NUCLEUS-ACCUMBENS; BRAIN-REGIONS; SCH-23390; SUPERSENSITIVITY AB Functional interactions between dopamine receptor subtypes may affect behavioral and biochemical responses which serve as models for neuropsychiatric illnesses and the clinical effects of drug therapy. We evaluated the effects of chronic exposure to the selective D1 receptor antagonist SCH 23390, and the selective D2 receptor antagonist metoclopramide, on spontaneous and drug-induced behavior and receptor density in rats, and then determined how these effects would be modified by concurrent administration of antagonists or agonists [SKF 38393, LY 171555 (quinpirole)] selective for the complementary receptor subtype. Administered alone, both the D1 and D2 antagonists had acute cataleptic effects to which animals became tolerant following chronic treatment, but the selective antagonists had opposing effects on spontaneous locomotor activity, Both antagonists produced equivalent, supersensitive behavioral responses to apomorphine, and resulted in an increase in D2 receptor density. Coadministration of the D1 and D2 antagonists had a synergistic effect on catalepsy, attenuated the effects on spontaneous locomotor activity observed with either drug alone, and had an additive effect on both apomorphine-induced stereotypic behavior and D2 receptor proliferation. On the other hand, when either selective antagonist was combined with the agonist selective for the complementary receptor subtype, both D2 receptor proliferation and behavioral supersensitivity were completely blocked. Combined antagonist-agonist treatments had opposing effects on the development of tolerance to antagonist-induced catalepsy. D2 but not D1 - receptor densities were correlated with animals' behavioral responses to apomorphine. There results support and extend the notion that complex functional interactions between D1 and D2 receptor families occur within the central nervous system, and suggest that novel effects might be derived from combined administration of receptor selective agonists and antagonists. C1 NINCDS,EXPT THERAPEUT BRANCH,NATL INST HLTH,BETHESDA,MD 20892. YALE UNIV,DEPT PSYCHIAT,W HAVEN,CT. W HAVEN VA MED CTR,W HAVEN,CT. RP Braun, AR (reprint author), NIDCD,LANGUAGE SECT,VSLB,NATL INST HLTH,BLDG 10,ROOM 5N118A,BETHESDA,MD 20892, USA. OI Mouradian, M. Maral/0000-0002-9937-412X NR 70 TC 36 Z9 36 U1 0 U2 3 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 1997 VL 104 IS 4-5 BP 341 EP 362 DI 10.1007/BF01277656 PG 22 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA XP868 UT WOS:A1997XP86800003 PM 9295170 ER PT J AU Zimmer, R Leucht, S Radler, T Schmauss, F Gebhardt, U Lauter, H AF Zimmer, R Leucht, S Radler, T Schmauss, F Gebhardt, U Lauter, H TI Variability of cerebral blood flow deficits in Tc-99m-HMPAO SPECT in patients with Alzheimer's disease SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE SPECT; Alzheimer's disease; neuropsychological tests ID EMISSION COMPUTED-TOMOGRAPHY; SENILE DEMENTIA; TECHNETIUM-99M-HMPAO SPECT; COGNITIVE PERFORMANCE; FLUORINE-18-FDG PET; PERFUSION; DIAGNOSIS; METABOLISM; PATTERN; HMPAO AB The purpose of this study was to analyse the frequency of the different pathological perfusion patterns in SPECT in a clinical, unselected population of patients with Alzheimer's disease. In 91 patients and 16 control subjects regional cerebral blood flow (rCBF) was measured with Single Photon Emission Computed Tomography (SPECT) using Tc-99m-hexa-methyl-propyleneamine oxime (HMPAO). 95% confidence intervals obtained from the perfusion values of the control subjects were used to define normal perfusion ranges. The frequency of perfusion deficits in the left frontal, temporal, parietal and occipital lobes were 62.2%, 60.4%, 70.3% and 23.1%, respectively. In the right hemisphere the corresponding values were 60.4%, 58.2%, 63.7% and 9.9%. With the exception of the occipital lobes these frequencies were not significantly different. The analysis of the perfusion pattern of each patient revealed 35 different combinations of lobes with perfusion deficits. The temporo-parietal perfusion deficits were not more frequent than the temporofrontal perfusion deficits. These results suggest that in the clinical routine a high variety of heterogeneous rCBF patterns have to be expected. C1 TECH UNIV MUNICH,DEPT NUCL MED,D-81675 MUNICH,GERMANY. KREISKRANKENHAUS WASSERBURG,DEPT INTERNAL MED,WASSERBURG,GERMANY. ST ELIZABETH HOSP,NATL INST MENTAL HLTH,WASHINGTON,DC. RP Zimmer, R (reprint author), TECH UNIV MUNICH,DEPT PSYCHIAT,ISMANINGER STR 22,D-81675 MUNICH,GERMANY. NR 35 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 1997 VL 104 IS 6-7 BP 689 EP 701 DI 10.1007/BF01291886 PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA YB368 UT WOS:A1997YB36800011 PM 9444568 ER PT J AU Hayashi, T Kagaya, A Takebayashi, M Oyamada, T Inagaki, M Tawara, Y Yokota, N Horiguchi, J Su, TP Yamawaki, S AF Hayashi, T Kagaya, A Takebayashi, M Oyamada, T Inagaki, M Tawara, Y Yokota, N Horiguchi, J Su, TP Yamawaki, S TI Effect of dantrolene on KCl- or NMDA-induced intracellular Ca2+ changes and spontaneous Ca2+ oscillation in cultured rat frontal cortical neurons SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE Ca2+-induced Ca2+ release; N-methyl-D-aspartate receptor; primary cultures of rat frontal cortical neurons; intracellular free Ca2+ concentration; intracellular Ca2+ stores; spontaneous Ca2+ oscillation ID NEUROLEPTIC MALIGNANT SYNDROME; METHYL-D-ASPARTATE; BULLFROG SYMPATHETIC NEURONS; CEREBELLAR GRANULE CELLS; INDUCED CA-2+ RELEASE; SARCOPLASMIC-RETICULUM; HIPPOCAMPAL-NEURONS; MOBILIZATION; SODIUM; STORES AB Dantrolene has been known to affect intracellular Ca2+ concentration ([Ca2+](i)) by inhibiting Ca2+ release from intracellular stores in cultured neurons. We were interested in examining this property of dantrolene in influencing the [Ca2+](i) affected by the NMDA receptor ligands, KCl, L-type Ca2+ channel blocker nifedipine, and two other intracellular Ca2+-mobilizing agents caffeine and bradykinin. Effect of dantrolene on the spontaneous oscillation of [Ca2+](i) was also examined. Dantrolene in mu M concentrations dose-dependently inhibited the increase in [Ca2+](i) elicited by NMDA and KCl. AP-5, MK-801 (NMDA an antagonists), and nifedipine respectively reduced the NMDA and KCl-induced increase in [Ca2+](i). Dantrolene, added to the buffer solution together with the antagonists or nifedipine, caused a further reduction in [Ca2+](i) to a degree similar to that seen with dantrolene alone inhibiting the increase in [Ca2+](i) caused by NMDA or KCl. At 30 mu M, dantrolene partially inhibited caffeine-induced increase in [Ca2+](i) whereas it has no effect on the bradykinin-induced change in [Ca2+](i). The spontaneous oscillation of [Ca2+](i) in frontal cortical neurons was reduced both in amplitude and in base line concentration in the presence of 10 mu M dantrolene. Our results indicate that dantrolene's mobilizing effects on intracellular Ca2+ stores operate independently from the influxed Ca2+ and that a component of the apparent increase in [Ca2+](i) elicited by NMDA or KCl represents a dantrolene-sensitive Ca2+ release from intracellular stores. Results also suggest that dantrolene does not affect the IP3-gated release of intracellular Ca2+ and that the spontaneous Ca2+ oscillation is, at least partially, under the control of Ca2+ mobilization from internal stores. C1 HIROSHIMA UNIV,SCH MED,DEPT PSYCHIAT & NEUROSCI,MINAMI KU,HIROSHIMA 734,JAPAN. NIDA,UNIT CELLULAR PATHOBIOL,MOL NEUROPSYCHIAT SECT,NEUROSCI BRANCH,IRP,NIH,BALTIMORE,MD. RI Hayashi, Teruo/A-9690-2008 NR 34 TC 17 Z9 17 U1 1 U2 1 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 1997 VL 104 IS 8-9 BP 811 EP 824 DI 10.1007/BF01285550 PG 14 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA YH660 UT WOS:A1997YH66000004 PM 9451714 ER PT J AU Wenning, GK Jellinger, K Litvan, I AF Wenning, GK Jellinger, K Litvan, I TI Snpranuclear gaze palsy and eyelid apraxia in postencephalitic parkinsonism SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE postencephalitic parkinsonism; ocular abnormalities; progressive supranuclear palsy; clinicopathologic study ID PROGRESSIVE SUPRANUCLEAR PALSY; RICHARDSON-OLSZEWSKI-SYNDROME; SMOOTH-PURSUIT IMPAIRMENT; ENCEPHALITIS LETHARGICA; COGNITIVE IMPAIRMENT; RETICULAR-FORMATION; CRITERIA; BRAIN; ALZHEIMERS; PARALYSIS AB We describe six patients with clinicopathologically confirmed postencephalitic parkinsonism (PEP) in whom oculomotor abnormalities developed several years after suffering the initial episode of encephalitis lethargica. Four of the cases had vertical supranuclear gaze palsy and two eyelid apraxia, features typically associated with progressive supranuclear palsy (PSP). Our findings indicate that the presence of gaze palsy alone may not be a reliable clinical discriminator between PEP and PSP. Involvement of the dorsal central gray nucleus, nucleus centralis pontis oralis, nucleus dorsal raphe interpositus, rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), nucleus interstitialis of Cajal, nucleus of the posterior commissure, pedunculopontine nuclei and frontal cortex was observed in several of our PEP cases and may contribute to the oculomotor abnormalities in this disorder. Whether the dorsal tegmental nucleus, caudal to the supratrochlear nucleus, severely affected in all our PEP cases, has a role in vertical gaze needs to be further studied. C1 NINCDS,NEUROEPIDEMIOL BRANCH,NIH,BETHESDA,MD 20814. UNIV HOSP,DEPT NEUROL,INNSBRUCK,AUSTRIA. LAINZ HOSP,LUDWIG BOLTZMANN INST CLIN NEUROBIOL,A-1130 VIENNA,AUSTRIA. NR 69 TC 23 Z9 24 U1 0 U2 0 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 1997 VL 104 IS 8-9 BP 845 EP 865 DI 10.1007/BF01285553 PG 21 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA YH660 UT WOS:A1997YH66000007 PM 9451717 ER PT J AU Licinio, J AF Licinio, J TI Central nervous system cytokines and their relevance for neurotoxicity and apoptosis SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article; Proceedings Paper CT International Winter Conference on Neurodegeneration CY 1996 CL SPITZINGSEE, GERMANY SP Schering ID INTERLEUKIN-1-BETA CONVERTING-ENZYME; RECEPTOR MESSENGER-RNA; RAT-BRAIN; CELL-DEATH; LOCALIZATION; HIPPOCAMPUS; EXPRESSION; HYPOTHALAMUS; INDUCTION; IL-1-BETA AB Cytokines are molecules that are synthesized not only by the immune system, but also by cells in the central nervous system, including neurons, glia, and brain vascular cells. In the brain, cytokines can be neuroprotective or they can contribute to neurodegeneration. The role of cytokines in the regulation of normal and abnormal brain function represents a rapidly growing frontier in neuroscience. Cytokines are pleiotropic and redundant, and they can modulate the effects of neurotransmitters and neuropeptides; thus, in order to understand the effects of brain cytokines on apoptosis and toxicity, it is necessary to study the temporal and spatial expression of complex networks of cytokines, growth factors, neuropeptides, and neurotransmitters. This effort is currently in progress in many centers. Modulation of cytokine function in the central nervous system represents a new therapeutic strategy for neurodegeneration. RP Licinio, J (reprint author), NIMH,NIH,CLIN NEUROENDOCRINOL BRANCH,BETHESDA,MD 20892, USA. OI Licinio, Julio/0000-0001-6905-5884 NR 28 TC 17 Z9 17 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 1997 IS 49 BP 169 EP 175 PG 7 WC Neurosciences SC Neurosciences & Neurology GA XN650 UT WOS:A1997XN65000019 ER PT J AU Fossom, LH Skolnick, P AF Fossom, LH Skolnick, P TI Chronic administration of a partial agonist at strychnine-insensitive glycine receptors: A novel experimental approach to the treatment of ischemias SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article; Proceedings Paper CT International Winter Conference on Neurodegeneration CY 1996 CL SPITZINGSEE, GERMANY SP Schering ID D-ASPARTATE RECEPTOR; 1-AMINOCYCLOPROPANECARBOXYLIC ACID; NMDA-RECEPTORS; SUBUNIT COMPOSITION; RAT; ANTAGONISTS; GLUTAMATE; COMPLEX; INJURY; CULTURES AB During the past decade, converging lines of evidence have linked the abnormal release or leak of excitatory amino acids to the neurodegeneration associated with a wide range of pathologies including cerebral ischemias, Huntington's disease, and AIDS dementia (Coyle and Robinson, 1987; Lipton, 1994; Meldrum, 1994). Pharmacological studies indicate that activation of both ionotropic and metabotropic glutamate receptors can substantially contribute to excitotoxic cell damage (Choi, 1992; Pizzi et al., 1993; Sheardown et al., 1993; Xue et al., 1994). Based on these findings, therapeutic strategies based on blunting or blocking glutamatergic transmission may be useful in treating a variety of neurodegenerative disorders. C1 NIDDK,NEUROSCI LAB,NIH,BETHESDA,MD 20892. NR 38 TC 5 Z9 5 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 1997 IS 49 BP 235 EP 244 PG 10 WC Neurosciences SC Neurosciences & Neurology GA XN650 UT WOS:A1997XN65000025 PM 9266432 ER PT J AU Toretsky, JA Connell, Y Neckers, L Bhat, NK AF Toretsky, JA Connell, Y Neckers, L Bhat, NK TI Inhibition of EWS-FLI-1 fusion protein with antisense oligodeoxynucleotides SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article; Proceedings Paper CT 3rd Workshop on Biochemistry of NeuroEctodermal Tumours CY JUN 12-14, 1995 CL IST DERMOPAT IMMACOLATA, ROME, ITALY SP IRCCS, IDI HO IST DERMOPAT IMMACOLATA DE Ewing's sarcoma; antisense; oligodeoxynucleotide; translocation; FLI ID DNA-BINDING DOMAIN; CHROMOSOME-TRANSLOCATION; REVERSE-TRANSCRIPTASE; RIBONUCLEASE-H; EWING SARCOMA; ETS-FAMILY; EWS GENE; TUMORS; CELLS; GROWTH AB Ewing's sarcoma family of tumors (EFT) contain reciprocal translocations, of which approximately 90% occur between the long arm of chromosomes 11 and 22, t(11;22)(q24;q12), resulting in the formation of chimeric proteins generated by a fusion of the EWS and FLI-1 genes. To determine if EWS-FLI-1 protein is responsible for the Ewing sarcoma phenotype we have used sequence-specific antisense oligodeoxynucleotides (ODN) to block its expression. We have evaluated a series of antisense ODN directed toward the breakpoint region in an effort to prevent translation of the fusion messenger RNA. ODN were first evaluated in a cell-free in vitro translation system. Exogenously added RNase I-I was found to be required for translation inhibition. bi ODN that showed complete inhibition of translation were electroporated into TC-32 cells, a EFT cell line. Fusion protein and EWS protein levels were evaluated by Western blot analysis. A 40-60% decrease in the fusion protein was observed in TC-32 cells with antisense ODN directed toward the breakpoint region. Cell viability was reduced with antisense sequences in TC-32 cells but not in a prostate cancer cell line. Since inhibition of t(11;22) gene product is correlated to effects on cell viability, reduction of the fusion protein may thus offer insight into the biology of EFT. C1 NCI,CLIN PHARMACOL BRANCH,FREDERICK,MD. NCI,SAIC,FREDERICK CANC RES CTR,FREDERICK,MD 21701. RP Toretsky, JA (reprint author), NCI,PEDIAT BRANCH,BLDG 10,ROOM 13N240,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 23 TC 52 Z9 55 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD JAN PY 1997 VL 31 IS 1-2 BP 9 EP 16 DI 10.1023/A:1005716926800 PG 8 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA WJ074 UT WOS:A1997WJ07400003 PM 9049825 ER PT J AU Melino, G Thiele, CJ Knight, RA Piacentini, M AF Melino, G Thiele, CJ Knight, RA Piacentini, M TI Retinoids and the control of growth/death decisions in human neuroblastoma cell lines SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article; Proceedings Paper CT 3rd Workshop on Biochemistry of NeuroEctodermal Tumours CY JUN 12-14, 1995 CL IST DERMOPAT IMMACOLATA, ROME, ITALY SP IRCCS, IDI HO IST DERMOPAT IMMACOLATA DE neuroblastoma; retinoic acid; programmed cell death; apoptosis; transglutaminase; trk ID HUMAN NEURO-BLASTOMA; N-MYC GENE; ACID-INDUCED DIFFERENTIATION; INTESTINAL POLYPEPTIDE VIP; PERIPHERAL NERVOUS-SYSTEM; METHYL-D-ASPARTATE; TISSUE TRANSGLUTAMINASE; OPIOID RECEPTOR; FACTOR-II; PROLIFERATIVE RESPONSES AB Cell proliferation, the balance between mitosis and apoptosis is the result of the continuous integration of a number of different signal transduction pathways stimulated in a cell at any given point in its life. Neuroblastoma cells regulate the switch between mitosis and death, according both to intrinsic factors and extrinsic factors, such as growth factor withdrawal and action of the vitamin A derivative, retinoic acid. In this review, we describe the balance of some factors regulating growth and death of human neuroblastoma cells in vitro. These dynamic studies are necessarily performed on cell lines, which offer controlled conditions enabling the disection of the complex stimuli mediating survival and growth (IGE trk, BDNF) and death (transglutaminase, free radicals, Bcl-2). Although the conclusions drawn may therefore not be directly applicable to tumour cells in vivo, the results herein discussed are of sufficient significance to warrant in vivo relevance. C1 UNIV AQUILA,DEPT BIOL,I-67100 LAQUILA,ITALY. NCI,MOL & CELLULAR BIOL SECT,PEDIAT BRANCH,NIH,BETHESDA,MD. NATL HEART & LUNG INST,DEPT CYST FIBROSIS,LONDON SW3 6LR,ENGLAND. UNIV ROMA TOR VERGATA,DEPT BIOL,I-00173 ROME,ITALY. RP Melino, G (reprint author), UNIV ROMA TOR VERGATA,DEPT EXPT MED,BIOCHEM LAB,IRCCS,IDI,ROOM F153,I-00133 ROME,ITALY. RI Piacentini, Mauro/I-2411-2016 OI Piacentini, Mauro/0000-0003-2919-1296 NR 133 TC 60 Z9 60 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD JAN PY 1997 VL 31 IS 1-2 BP 65 EP 83 DI 10.1023/A:1005733430435 PG 19 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA WJ074 UT WOS:A1997WJ07400010 PM 9049832 ER PT J AU Cirielli, C Capogrossi, MC Passaniti, A AF Cirielli, C Capogrossi, MC Passaniti, A TI Anti-tumor gene therapy SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article; Proceedings Paper CT 3rd Workshop on Biochemistry of NeuroEctodermal Tumours CY JUN 12-14, 1995 CL IST DERMOPAT IMMACOLATA, ROME, ITALY SP IRCCS, IDI HO IST DERMOPAT IMMACOLATA DE gene therapy; liposome; retrovirus; adenovirus ID THYMIDINE KINASE GENE; MALIGNANT BRAIN-TUMORS; TRANSFER IN-VIVO; RECOMBINANT ADENOVIRUS; EXPERIMENTAL GLIOMAS; RETROVIRAL VECTORS; TRANSGENIC MICE; CANCER CELLS; MOUSE MODEL; HUMAN HEAD AB Gene therapy as an anti-tumor strategy is becoming a powerful tool for cytokine delivery to inhibit the growth of many tumors. Several delivery systems are being utilized and designed for the expression of specific genes to achieve a therapeutic result. Liposomes, retroviral vectors, and adenoviral vectors have all been used and eventual clinical application may depend on the type of tumor, the location, the specific gene carried, and the patient's health status. Novel expression vectors may eventually achieve tissue-specific targeting and low immuno-reactivity. Inactivation of mutated oncogenes, such as ms, or re-expression of inactive suppressor genes, such as p53 have been used as strategies for anti-tumor therapy. Additionally, exogenous genes, such as viral thymidine kinase that metabolize chemotherapeutic agents to achieve local cytotoxicity have also been employed. Neuro-endocrine tumors are targets of these genetic strategies since they are often difficult to treat by conventional methods because of their location (brain tumors) or because they have spread from the primary tumor (melanoma). Further advances in the design of these vectors may achieve safe targeting of a variety of malignant tumors. C1 NIA,GENE THERAPY UNIT,CARDIOVASC SCI LAB,BALTIMORE,MD 21224. NIA,BIOL CHEM LAB,CTR GERONTOL RES,BALTIMORE,MD 21224. RP Cirielli, C (reprint author), IDI,LAB VASC PATHOL,VIA MONTI DI CRETA 104,I-00167 ROME,ITALY. NR 65 TC 3 Z9 3 U1 1 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD JAN PY 1997 VL 31 IS 1-2 BP 217 EP 223 DI 10.1023/A:1005791012205 PG 7 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA WJ074 UT WOS:A1997WJ07400029 PM 9049851 ER PT J AU Appel, NM Hayakawa, T Chang, M Bell, J Seemann, R Rapoport, SI AF Appel, NM Hayakawa, T Chang, M Bell, J Seemann, R Rapoport, SI TI Effect of D-2 dopamine receptor activation on [H-3]arachidonic acid incorporation in rats with unilateral 6-hydroxydopamine lesions SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,LNS,NIH,BETHESDA,MD 20892. US FDA,CDER,OTR,DAPR,LAUREL,MD 20708. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S71 EP S71 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500275 ER PT J AU Baas, D Dalencon, D Fressinaud, C Vitkovic, L Vincendon, G Sarlieve, LL AF Baas, D Dalencon, D Fressinaud, C Vitkovic, L Vincendon, G Sarlieve, LL TI Differential expression and regulation of glutamine synthetase gene in oligodendroglial and astroglial cell cultures SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 CNRS,CTR NEUROCHIM,UPR 416,F-67084 STRASBOURG,FRANCE. NIMH,DIV NEUROSCI & BEHAV SCI,NIH,ROCKVILLE,MD 20857. RI Fressinaud, Catherine/K-4393-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S174 EP S174 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500684 ER PT J AU Brining, SK Jones, CR AF Brining, SK Jones, CR TI Degradation of beta-amyloid by rat brain SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,LNS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S44 EP S44 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500174 ER PT J AU Brodie, C Kuperstein, I Bogi, K Acs, P Blumberg, PM AF Brodie, C Kuperstein, I Bogi, K Acs, P Blumberg, PM TI Role of specific PKC isoforms in glial cell differentiation. Differential regulation of glutamine synthetase (GS) and GFAP by PKC delta SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NCI,MOL MECHANISMS TUMOR PROMOT SECT,LCCTP,NIH,BETHESDA,MD 20892. BAR ILAN UNIV,DEPT LIFE SCI,IL-52900 RAMAT GAN,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S203 EP S203 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500800 ER PT J AU Bruccoleri, A Harry, GJ AF Bruccoleri, A Harry, GJ TI Modulation of trimethyltin-induced cytokine mRNA expression and hippocampal neuropathy by dexamethasone. SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIEHS,TOXICOL LAB,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S178 EP S178 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500699 ER PT J AU Chandross, KJ Spray, DC Dermietzel, R Cohen, RI Kessler, JA AF Chandross, KJ Spray, DC Dermietzel, R Cohen, RI Kessler, JA TI Nerve injury and inflammatory cytokines modulate coordinated changes in Schwann cell phenotype, junctional coupling strength, and CX46 expression. SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,LAB DEV NEUROGENET,NIH,BETHESDA,MD 20892. ALBERT EINSTEIN COLL MED,DEPT NEUROSCI,BRONX,NY 10467. UNIV REGENSBURG,DEPT ANAT,D-8400 REGENSBURG,GERMANY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S126 EP S126 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500495 ER PT J AU Chang, MCJ Rabin, O Grange, E Jones, CR AF Chang, MCJ Rabin, O Grange, E Jones, CR TI Effect of chronic lithium treatment on turnover of fatty acids in brain phospholipids SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S13 EP S13 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500050 ER PT J AU Cohen, RI Chandross, KJ Hudson, LD AF Cohen, RI Chandross, KJ Hudson, LD TI FGF-9 and FGF-2 regulate the expression of fibroblast growth factor receptors and myelin proteins during oligodendrocyte development. SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S89 EP S89 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500349 ER PT J AU Daniel, GA Wang, RY Cruz, NF AF Daniel, GA Wang, RY Cruz, NF TI Channeling of [C-14]glucose into tricarboxylic acid cycle-derived metabolic pools in neurons and glia during & after sensory stimulation. SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. UNIV ARKANSAS MED SCI,DEPT NEUROL,LITTLE ROCK,AR 72205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S274 EP S274 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28501075 ER PT J AU Dobi, AL Palkovits, M Palkovits, CG VonAgoston, D AF Dobi, AL Palkovits, M Palkovits, CG VonAgoston, D TI Molecular tags of glial and neuronal lineages that bend the DNA of the enkephalin gene SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,DEV NEUROBIOL LAB,NIH,BETHESDA,MD 20892. NIMH,CELL BIOL LAB,NIH,BETHESDA,MD 20892. RI Palkovits, Miklos/F-2707-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S25 EP S25 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500097 ER PT J AU Gotoh, J Nakao, Y ShiraishiGotoh, H Stone, S Law, MJ Sokoloff, L AF Gotoh, J Nakao, Y ShiraishiGotoh, H Stone, S Law, MJ Sokoloff, L TI Effects of extracellular K+ levels on glucose utilization in cultured astroglia SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S245 EP S245 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500965 ER PT J AU Grant, P Diggins, M Pant, HC AF Grant, P Diggins, M Pant, HC TI Topographic phosphorylation of neurofilament proteins in the squid giant axon: A multimeric complex hypothesis SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 MARINE BIOL LAB,WOODS HOLE,MA 02543. NINCDS,NEUROCHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S117 EP S117 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500459 ER PT J AU Izenwasser, S Ladenheim, B Cadet, JL Carroll, FI Kunko, PM AF Izenwasser, S Ladenheim, B Cadet, JL Carroll, FI Kunko, PM TI Differential neuroadaptive responses produced by chronic treatment with cocaine versus selective dopamine uptake inhibitors SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIDA,INTRAMURAL RES PROGRAM,PSYCHOBIOL SECT,BALTIMORE,MD 21224. NIDA,INTRAMURAL RES PROGRAM,MOL NEUROPSYCHIAT SECT,BALTIMORE,MD 21224. RES TRIANGLE INST,RES TRIANGLE PK,NC 27709. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S68 EP S68 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500265 ER PT J AU Kuang, TY Wang, R Pak, H Sokoloff, L AF Kuang, TY Wang, R Pak, H Sokoloff, L TI Effects of insulin hypoglycemia or glycolytic blockade by loading dose of 2-deoxyglucose on levels of adenosine and its metabolic products in brain of conscious rats. SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S167 EP S167 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500658 ER PT J AU Malinchik, VI Law, MJ Burlin, T AF Malinchik, VI Law, MJ Burlin, T TI K+-induced neurotoxicity in neuronal cultures: Involvement of calmodulin and calmodulin-dependent enzymes SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S157 EP S157 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500616 ER PT J AU McCarron, RM Strasser, A Kawai, N Stanimirovic, D Spatz, M AF McCarron, RM Strasser, A Kawai, N Stanimirovic, D Spatz, M TI Effect of hypoxia on free radical formation by brain microvascular endothelium SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,STROKE BRANCH,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S152 EP S152 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500597 ER PT J AU Rabin, O Drieu, K Grange, E Chang, M Deutsch, J Rapoport, S Purdon, D AF Rabin, O Drieu, K Grange, E Chang, M Deutsch, J Rapoport, S Purdon, D TI Acceleration of arachidonic acid reincorporation into gerbil brain membranes following ischemia SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIH,NEUROSCI LAB,BETHESDA,MD 20892. INST HENRI BEAUFOUR,PARIS,FRANCE. HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S114 EP S114 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500448 ER PT J AU Russell, JT Simpson, PB AF Russell, JT Simpson, PB TI Cellular mechanisms that support long distance propagation of calcium waves in glial cells. SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NICHHD,LCMN,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S212 EP S212 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500837 ER PT J AU Shetty, HU Siarey, RJ Stoll, J Galdzicki, Z Rapoport, SI AF Shetty, HU Siarey, RJ Stoll, J Galdzicki, Z Rapoport, SI TI Regional increase in brain accumulation of myo-inositol in Ts65Dn mouse (Down syndrome model) SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S30 EP S30 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500118 ER PT J AU Sokoloff, L Cook, M Law, MJ Kaufman, E AF Sokoloff, L Cook, M Law, MJ Kaufman, E TI Developmental changes in cerebral energy metabolism: Ketone body utilization by neurons and astroglia SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S262 EP S262 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28501030 ER PT J AU Sokoloff, L AF Sokoloff, L TI Cerebral energy metabolism and consciousness SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S218 EP S218 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500859 ER PT J AU Stebbins, JW Jaffe, H Moller, JR AF Stebbins, JW Jaffe, H Moller, JR TI Characterization of a myelin associated cathepsin L-like protease SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,DEMYELINATING DISORDERS UNIT,LMCN,NIH,BETHESDA,MD 20892. NINCDS,LNC,PROT PEPTIDE SEQUENCING FACIL,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S84 EP S84 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500329 ER PT J AU Vergelli, M Mazzanti, B Pinet, V Kalbus, M Martin, R Long, EO Liuzzi, GM Massacesi, L Riccio, P AF Vergelli, M Mazzanti, B Pinet, V Kalbus, M Martin, R Long, EO Liuzzi, GM Massacesi, L Riccio, P TI Differential T cell recognition of lipid-bound myelin basic protein SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 UNIV FLORENCE,DEPT NEUROL PSICH,I-50121 FLORENCE,ITALY. NINCDS,NIB,NIH,BETHESDA,MD 20892. NIAID,LIG,NIH,ROCKVILLE,MD. UNIV TUBINGEN,DEPT NEUROL,D-72074 TUBINGEN,GERMANY. UNIV BARI,DEPT BIOCHEM MOL BIOL,I-70121 BARI,ITALY. UNIV BASILICATA,DEPT BIOL,DBDAF,BASILICATA,ITALY. CNR,CSMME,I-00185 ROME,ITALY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S155 EP S155 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500608 ER PT J AU Weiss, M Dalakas, M Willison, H Quarles, R AF Weiss, M Dalakas, M Willison, H Quarles, R TI Variability in the binding of monoclonal IgM anti-MAG/SGPG antibodies from neuropathy patients to nerve glycoconjugates SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S91 EP S91 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500355 ER PT J AU Williams, WM Hayakawa, T Grange, E Rapoport, SI AF Williams, WM Hayakawa, T Grange, E Rapoport, SI TI Arecoline stimulation of radiolabeled arachidonate incorporation from plasma into brain microvessels of awake rat SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIA,NEUROSCI LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S153 EP S153 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500600 ER PT J AU Winsky, L Nagula, S Lester, DS AF Winsky, L Nagula, S Lester, DS TI Calcium dependent association of calretinin with phospholipid vesicles SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NIMH,CLIN SCI LAB,BETHESDA,MD. US FDA,CDER,DAPR,LAUREL,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S182 EP S182 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500717 ER PT J AU Yin, SH Quarles, RH AF Yin, SH Quarles, RH TI Differences in the signal transduction pathways by which platelet derived growth factor and fibroblast growth factor activate MAP kinase during oligodendrocyte differentiation SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract C1 NINCDS,MYELIN & BRAIN DEV SECT,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PY 1997 VL 69 SU S BP S90 EP S90 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA XM285 UT WOS:A1997XM28500351 ER PT J AU Taniwaki, T Hirashima, N Becerra, SP Chader, GJ Etcheberrigaray, R Schwartz, JP AF Taniwaki, T Hirashima, N Becerra, SP Chader, GJ Etcheberrigaray, R Schwartz, JP TI Pigment epithelium-derived factor protects cultured cerebellar granule cells against glutamate-induced neurotoxicity SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE calcium imaging; intracellular calcium; excitotoxicity ID METHYL-D-ASPARTATE; GROWTH-FACTOR; NEURONS; CALCIUM; IDENTIFICATION; INVOLVEMENT; DYSFUNCTION; DEPENDENCE; MECHANISMS; RECEPTOR AB Pigment epithelium-derived factor (PEDF) is a survival factor for cerebellar granule cells in culture. In the present study, we have investigated the ability of a recombinant form of PEDF (rPEDF) to protect against glutamate neurotoxicity. When rPEDF was added to cerebellar granule cell cultures 30 min before addition of 100 mu M glutamate, glutamate-induced neuronal death was significantly reduced. The protective effect of rPEDF was dose-dependent in the range from 0.023 to 7.0 nM (1-500 ng/ml), with a half-maximal dose of 0.47 nM, An antibody to rPEDF blocked this protective effect. Measurement of intraneuronal free calcium levels demonstrated that rPEDF raised the basal calcium content, However, after the elevation of intracellular calcium in response to administration of glutamate, rPEDF reduced the plateau level seen in the presence of glutamate. These data show that PEDF can protect neurons against glutamate-induced neurotoxicity, possibly via a calcium-related pathway. The finding that only 30 min of preincubation is required for the neuroprotective effect, significantly faster than other known neurotrophic factors, suggests that PEDF may be useful clinically as a neuroprotective agent in the CNS. C1 NINCDS,CNB,MGS,NIH,BETHESDA,MD 20892. NINCDS,LAB ADAPT SYST,NIH,BETHESDA,MD 20892. NEI,RETINAL CELL & MOL BIOL LAB,NIH,BETHESDA,MD 20892. NR 33 TC 91 Z9 93 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1997 VL 68 IS 1 BP 26 EP 32 PG 7 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA VY893 UT WOS:A1997VY89300004 PM 8978706 ER PT J AU Yu, OF Chuang, DM AF Yu, OF Chuang, DM TI Neurotrophin protection against toxicity induced by low potassium and nitroprusside in cultured cerebellar granule neurons SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE cerebellar granule cells; nitroprusside; neurotoxicity; neuronal survival; intracellular calcium; neurotrophins; neuroprotection ID NITRIC-OXIDE DONOR; INDUCED CELL-DEATH; SODIUM-NITROPRUSSIDE; CALCIUM-CONCENTRATION; CORTICAL-NEURONS; NERVOUS-SYSTEM; MESSENGER-RNA; FACTOR BDNF; SURVIVAL; GLUTAMATE AB Long-term survival of cultured rat cerebellar granule neurons requires depolarizing concentrations of potassium (high potassium; 25 mM KCI). A high-potassium culturing condition has been reported to increase the intracellular calcium concentration ([Ca2+](i)) and the expression of brain-derived neurotrophic factor (BDNF), which in turn induces the expression of neurotrophin-3 (NT-3) in these neurons, We therefore examined the neurotrophic effect of these two neurotrophins in low-potassium (5 mM) cultures and their neuroprotective capabilities against sodium nitroprusside-induced neurotoxicity in both low- and high-potassium cultures, Neuronal survival and neurotrophic effects were monitored by [H-3]ouabain binding and 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide assays, In low-potassium cultures, the neurotrophic effect of BDNF approached that found in high-potassium cultures but was much more robust than that of NT-3. In contrast, undifferentiated neurons cultured in high-potassium medium were much less responsive to BDNF and not responsive at all to NT-3. Induction of nitroprusside neurotoxicity occurred more readily in low- than in high-potassium cultures. BDNF, NT-3, and a high potassium concentration, alone or in combination, were unable to protect neurons treated with nitroprusside at 50 or 100 mu M. However, the neurotoxicity of a lower dose of nitroprusside (10 mu M) was reversed by the combined actions of these two neurotrophins in low-potassium cultures and by BDNF alone in high-potassium cultures. Because nitroprusside neurotoxicity is less robust in high-potassium cultures, high-potassium-induced BDNF expression and subsequent NT-3 expression may participate in its neuroprotection and neurotrophism in these cultures, Also, we found that toxic doses of nitroprusside antagonized KCl- and NMDA-induced rises in [Ca2+](i), suggesting that this effect is related to nitroprusside-induced neurotoxicity. C1 NIMH,MOL NEUROBIOL SECT,BIOL PSYCHIAT BRANCH,NIH,BETHESDA,MD 20892. NR 53 TC 17 Z9 17 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1997 VL 68 IS 1 BP 68 EP 77 PG 10 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA VY893 UT WOS:A1997VY89300009 PM 8978711 ER PT J AU Bernard, M Iuvone, PM Cassone, VM Roseboom, PH Coon, SL Klein, DC AF Bernard, M Iuvone, PM Cassone, VM Roseboom, PH Coon, SL Klein, DC TI Avian melatonin synthesis: Photic and circadian regulation of serotonin N-acetyltransferase mRNA in the chicken pineal gland and retina SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE serotonin N-acetyltransferase; molecular cloning; melatonin; pineal gland; retina; circadian rhythm; light ID HYDROXYINDOLE-O-METHYLTRANSFERASE; TRYPTOPHAN-HYDROXYLASE ACTIVITY; MESSENGER-RNA; MOLECULAR ANALYSIS; BIOLOGICAL CLOCK; KAINIC ACID; LIGHT; RHYTHM; CELLS; LOCALIZATION AB The circadian rhythms in melatonin production in the chicken pineal gland and retina reflect changes in the activity of serotonin N-acetyltransferase (arylalkylamine N-acetyltransferase; AA-NAT; EC 2.3.1.87). Here we determined that the chicken AA-NAT mRNA is detectable in follicular pineal cells and retinal photoreceptors and that it exhibits a circadian rhythm, with peak levels at night. AA-NAT mRNA was not detected in other tissues. The AA-NAT mRNA rhythm in the pineal gland and retina persists in constant darkness (DD) and constant lighting (LL). The amplitude of the pineal mRNA rhythm is not decreased in LL. Light appears to influence the phase of the clock driving the rhythm in pineal AA-NAT mRNA in two ways: The peak is delayed by similar to 6 h in LL, and it is advanced by >4 h by a 6-h light pulse late in subjective night in DD. Nocturnal AA-NAT mRNA levels do not change during a 20-min exposure to light, whereas this treatment dramatically decreases AA-NAT activity. These observations suggest that the rhythmic changes in chicken pineal AA-NAT activity reflect, at least in part, clock-generated changes in mRNA levels. In contrast, changes in mRNA content are not involved in the rapid light-induced decrease in AA-NAT activity. C1 NICHHD,SECT NEUROENDOCRINOL,DEV NEUROBIOL LAB,NIH,BETHESDA,MD 20892. EMORY UNIV,SCH MED,DEPT PHARMACOL,ATLANTA,GA 30322. TEXAS A&M UNIV,DEPT BIOL,COLLEGE STN,TX 77843. FU NEI NIH HHS [R01 EY004864, EY-04864] NR 56 TC 157 Z9 160 U1 1 U2 6 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1997 VL 68 IS 1 BP 213 EP 224 PG 12 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA VY893 UT WOS:A1997VY89300026 PM 8978728 ER PT J AU Huff, RA Vaughan, RA Kuhar, MJ Uhl, GR AF Huff, RA Vaughan, RA Kuhar, MJ Uhl, GR TI Phorbol esters increase dopamine transporter phosphorylation and decrease transport V-max SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE dopamine transporter; phosphorylation; protein kinase C; phorbol esters; phorbol 12-myristate 13-acetate; cocaine ID PROTEIN-KINASE-C; AGONIST-DEPENDENT PHOSPHORYLATION; BETA-ADRENERGIC-RECEPTOR; SEROTONIN TRANSPORTER; RAT STRIATUM; COCAINE; CLONING; DESENSITIZATION; MODULATION; EXPRESSION AB Sodium- and chloride-coupled transport of dopamine from synapses into presynaptic terminals plays a key role in terminating dopaminergic neurotransmission. Regulation of the function of the dopamine transporter, the molecule responsible for this translocation, is thus of interest. The primary sequence of the dopamine transporter contains multiple potential phosphorylation sites, suggesting that the function of the transporter could be regulated by phosphorylation. Previous work from this laboratory has documented that phorbol ester activation of protein kinase C (PKC) decreases dopamine transport V-max in transiently expressing COS cells. In the present report, we document in vivo phosphorylation of the rat dopamine transporter stably expressed in LLC-PK1 cells and show that phosphorylation is increased threefold by phorbol esters. Dopamine uptake is also regulated by phorbol esters in these cells; phorbol 12-myristate 13-acetate (PMA) reduces transport V-max by 35%. Parallels between the time course, concentration dependency, and staurosporine sensitivity of alterations in transporter phosphorylation and transporter V-max suggest that dopamine transporter phosphorylation involving PKC could contribute to this decreased transporter function. Phosphorylation of the dopamine transporter by PKC or by a PKC-activated kinase could be involved in rapid neuroadaptive processes in dopaminergic neurons. C1 NIDA,MOL NEUROBIOL BRANCH,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. EMORY UNIV,YERKES REG PRIMATE RES CTR,DIV NEUROSCI,ATLANTA,GA 30322. NR 44 TC 146 Z9 146 U1 2 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1997 VL 68 IS 1 BP 225 EP 232 PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA VY893 UT WOS:A1997VY89300027 PM 8978729 ER PT J AU Bing, GY Wang, W Qi, QP Feng, ZH Hudson, P Jin, L Zhang, WQ Bing, RJ Hong, JS AF Bing, GY Wang, W Qi, QP Feng, ZH Hudson, P Jin, L Zhang, WQ Bing, RJ Hong, JS TI Long-term expression of Fos-related antigen and transient expression of Delta FosB associated with seizures in the rat hippocampus and striatum SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE brain; cell death; immunocytochemistry; polymerase chain reaction; transcription factors; northern blot analysis; western blot analysis ID AP-1 DNA-BINDING; CENTRAL-NERVOUS-SYSTEM; MESSENGER-RNA LEVELS; C-FOS; CHRONIC COCAINE; KAINIC ACID; ELECTROCONVULSIVE SEIZURE; TRANSCRIPTION FACTORS; PROTEINS; INDUCTION AB Systemic administration of kainic acid (KA), an analogue of glutamic acid, causes limbic seizures and pathophysiological changes in adult rats that are very similar to human temporal lobe epilepsy. One of the earliest changes in gene expression after treatment with KA is the induction of immediate-early genes. The fos and jun families are frequently studied immediate-early genes that are induced by KA. Several groups, including ours, have recently reported that a 35-kDa Fos-related antigen (FRA) is induced for a protracted time by various stimuli. It has been suggested that this FRA is Delta FosB, which has a molecular mass of similar to 35 kDa, The present study characterizes the long-term expression of FRA and Delta FosB after systemic treatment with KA. Immunocytochemistry and western blot analysis using an antibody that cross-reacts with all known FRAs showed that a 35-kDa FRA was induced at high levels in both the hippocampus and striatum for up to 1 month by KA, A semiquantitative PCR analysis showed that Delta FosB was induced by KA, but its expression lasted for only 6 h. This result was also verified by northern blot analysis, These results suggested that the 35-kDa FRA with long-term elevated levels seen with western blot analysis and immunocytochemistry is a new species of the FRA and not Delta FosB. The long-term expression of FRA in both the hippocampus and striatum may be associated with the pathophysiological changes after KA administration. RP Bing, GY (reprint author), NIEHS,TOXICOL BRANCH,NEUROPHARMACOL SECT,NIH,MD F1-01,POB 12233,RES TRIANGLE PK,NC 27709, USA. RI bing, guoying/F-7084-2012; OI Bing, Guoying/0000-0003-0609-8152 NR 44 TC 20 Z9 20 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1997 VL 68 IS 1 BP 272 EP 279 PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA VY893 UT WOS:A1997VY89300033 PM 8978735 ER PT J AU Heyes, MP Morrison, PF AF Heyes, MP Morrison, PF TI Quantification of local de novo synthesis versus blood contributions to quinolinic acid concentrations in brain and systemic tissues SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE kynurenine pathway; systemic immune activation; endotoxin; cerebral ischemic injury; blood-brain barrier; mass spectrometry ID KYNURENINE PATHWAY METABOLISM; CEREBROSPINAL-FLUID; L-TRYPTOPHAN; RAT-BRAIN; NEUROLOGICAL DISEASE; IMMUNE ACTIVATION; CEREBRAL-ISCHEMIA; 4-CHLORO-3-HYDROXYANTHRANILATE; MECHANISM; 6-CHLOROTRYPTOPHAN AB The source of the neurotoxin quinolinic acid (QUIN) in brain and systemic tissues under normal and pathologic circumstances reflects either de novo synthesis from L-tryptophan and other precursors, or entry of QUIN itself from the blood. To quantify the relative contributions of blood- versus tissue-derived QUIN, [C-13(7)]QUIN was infused subcutaneously via osmotic pumps (0.55 mu l/h, 30 mM) in gerbils, and the fraction of QUIN in tissue (Ti; measured in tissue homogenates) derived from blood (BI; measured in serum) was calculated by the formula ([C-13(7)] QUIN(Ti)/QUIN(Ti))/([C-13(7)]QUIN(BI)/QUIN(BI)). In controls, blood QUIN contributed 38-49% of QUIN in brain, 70% in CSF, between 40 and 70% in kidney, heart, and skeletal muscle, but <5% in spleen, lung, liver, and intestine. Systemic endotoxin (450 mu g/kg) increased blood, brain, CSF, and systemic tissue QUIN levels. Notably, the relative proportion of QUIN derived from blood in brain, spleen, lung, and intestine was unchanged by endotoxin, but increased in kidney, heart, and skeletal muscle. In contrast, cerebral ischemic injury (10 min of bilateral carotid artery occlusion) increased regional brain QUIN concentrations at 4 days post ischemia, with a proportional increase in the amount of QUIN derived from de novo synthesis by brain tissue. In the blood and systemic tissues of postischemic gerbils, there were no changes in systemic tissue or blood QUIN levels, or changes in the relative proportions of blood- versus systemic tissue-derived QUIN. These results establish that the brain normally synthesizes QUIN, that the blood is a significant source of QUIN in controls and during acute systemic immune activation, and that the rate of QUIN formation by brain tissue increases in conditions of brain and systemic immune activation. C1 NIH, NATL CTR RES RESOURCES, BETHESDA, MD 20892 USA. RP Heyes, MP (reprint author), NIMH, LAB NEUROTOXICOL,NIH,BLDG 10,ROOM 3D40, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 33 TC 46 Z9 47 U1 1 U2 5 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD JAN PY 1997 VL 68 IS 1 BP 280 EP 288 PG 9 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA VY893 UT WOS:A1997VY89300034 PM 8978736 ER PT J AU Zhao, GJ Redekop, WK Riddehough, A Li, DKB Cover, K Wolinsky, JS Paty, DW Koopmans, RA Mietlowski, W Scheinberg, LC Traugott, U Aisen, M Robbins, K Hurwitz, BJ Greenberg, SM Fredane, LM Herbstreith, R Hurwitz, JG Burk, J McFarland, HF Goodman, A McFarlin, DE Krebs, H Maloni, H Debronso, J Franklin, GM Burks, JS Nelson, L Wangaard, C Sears, S Nath, A Smith, L McGinnis, J Tourtellote, WW Baumhefner, RW Ellison, G Meyers, L Syndulko, K Newton, L AF Zhao, GJ Redekop, WK Riddehough, A Li, DKB Cover, K Wolinsky, JS Paty, DW Koopmans, RA Mietlowski, W Scheinberg, LC Traugott, U Aisen, M Robbins, K Hurwitz, BJ Greenberg, SM Fredane, LM Herbstreith, R Hurwitz, JG Burk, J McFarland, HF Goodman, A McFarlin, DE Krebs, H Maloni, H Debronso, J Franklin, GM Burks, JS Nelson, L Wangaard, C Sears, S Nath, A Smith, L McGinnis, J Tourtellote, WW Baumhefner, RW Ellison, G Meyers, L Syndulko, K Newton, L TI Clinical and magnetic resonance imaging changes correlate in a clinical trial monitoring cyclosporine therapy for multiple sclerosis SO JOURNAL OF NEUROIMAGING LA English DT Article ID MRI; DISABILITY; SERIAL AB Magnetic resonance imaging (MRI) was used to monitor cyclosporine therapy for chronic progressive multiple sclerosis in a multicenter clinical trial and an analysis was performed to determine whether there was a correlation between clinical changes and MRI changes. MRI was performed on 163 patients at the onset and completion of the 2-year study. Burden of disease (BOD, lesion load) was quantitated by a single observer using a computer program. Active lesions were also identified. The Expanded Disability Status Scale (EDSS) score was determined every 3 months. MRI data did not show any effect of cyclosporine treatment on BOD progression (mean 24.5% increase/yr) or lesion activity. However, there was a statistically significant positive correlation between the baseline total BOD value and the baseline EDSS score (r = 0.221, p = 0.005) and a positive correlation between the percent changes in BOD from baseline to exit and EDSS score (r = 0.186, p = 0.018). The study supports the concepts that MRI is a useful technique in monitoring therapeutic trials and that MRI is a direct measure of pathology. C1 UNIV BRITISH COLUMBIA,VANCOUVER HOSP & HLTH SCI CTR,DEPT MED,DIV NEUROL,VANCOUVER,BC V6T 2B5,CANADA. UNIV BRITISH COLUMBIA,VANCOUVER HOSP & HLTH SCI CTR,DEPT DIAGNOST RADIOL,VANCOUVER,BC V6T 2B5,CANADA. UNIV TEXAS,HLTH SCI CTR,DEPT NEUROL,HOUSTON,TX 77225. SANDOZ PHARMACEUT CORP,E HANOVER,NJ. ALBERT EINSTEIN COLL MED,BRONX,NY. DUKE UNIV,DURHAM,NC 27706. NIH,BETHESDA,MD. UNIV TEXAS,AUSTIN,MN. VET ADM WADSWORTH MED CTR,LOS ANGELES,CA. NR 19 TC 34 Z9 35 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1051-2284 J9 J NEUROIMAGING JI J. Neuroimaging PD JAN PY 1997 VL 7 IS 1 BP 1 EP 7 PG 7 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA WN534 UT WOS:A1997WN53400001 PM 9038425 ER PT J AU Duncan, BB Sharrett, AR Tegeler, C Tyroler, HA Metcalf, P Heiss, G Crouse, JR Li, RL AF Duncan, BB Sharrett, AR Tegeler, C Tyroler, HA Metcalf, P Heiss, G Crouse, JR Li, RL TI Risk factors differ for carotid artery plaque with and without acoustic shadowing SO JOURNAL OF NEUROIMAGING LA English DT Article ID B-MODE ULTRASOUND; DENSITY-LIPOPROTEIN CHOLESTEROL; ACUTE CORONARY SYNDROMES; ATHEROSCLEROSIS RISK; CIGARETTE-SMOKING; DISEASE; ULTRASONOGRAPHY; PREVALENCE; MANIFESTATIONS; ENDARTERECTOMY AB To investigate the association of gender, ethnicity, and several cardiovascular risk factors with carotid artery plaque and plaque with acoustic shadowing in a population-based sample, high-resolution B-mode ultrasonography was used to characterize lesions in the common and internal carotid arteries, and at the carotid bifurcation in 12,796 US men and women, aged 45 to 64 years, participating in the Atherosclerosis Risk in Communities Study (ARIC) baseline survey In multiple logistic regression analyses, male gender (odds ratio and 95% confidence interval: 1.52 [1.39 - 1.67]) and increased total (1.47 [1.32 - 1.63]) and low-density-lipoprotein cholesterol (1.49 [1.34 - 1.65]) levels were statistically significantly associated only with the presence of plaque. In contradistinction, smoking (2.22 [1.79 - 2.75]) and hypertension (1.54 [1.30 - 1.82]) were additionally associated with acoustic shadowing. Hyperfibrinogenemia (1.33 [1.12 - 1.59]) was associated only with lesions accompanied by acoustic shadowing. While ethnicity associations with plaque alone varied across the artery segments, among those with plaque, being white was uniformly associated with acoustic shadowing. After multivariable adjustment, high-density-lipoprotein cholesterol was not associated with either manifestation of atherosclerosis. In conclusion, differences were seen in the associations of established cardiovascular risk factors with discretely characterized carotid artery plaque lesions, according to the presence or absence of acoustic shadowing suggestive of mineralization of plaque. C1 UNIV N CAROLINA,SCH PUBL HLTH,DEPT EPIDEMIOL,CHAPEL HILL,NC. UNIV N CAROLINA,SCH PUBL HLTH,DEPT BIOSTAT,CHAPEL HILL,NC. NHLBI,BETHESDA,MD 20892. BOWMAN GRAY SCH MED,DEPT NEUROL,WINSTON SALEM,NC. RP Duncan, BB (reprint author), UNIV FED RIO GRANDE SUL,FAC MED,DEPT SOCIAL MED,SCH MED,RUA RAMIRO BARCELLOS 2600-414,BR-90035003 PORTO ALEGRE,RS,BRAZIL. FU NHLBI NIH HHS [N01-HC-55018, N01-HC-55016, N01-HC-55015] NR 42 TC 14 Z9 14 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1051-2284 J9 J NEUROIMAGING JI J. Neuroimaging PD JAN PY 1997 VL 7 IS 1 BP 28 EP 34 PG 7 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA WN534 UT WOS:A1997WN53400005 PM 9038429 ER PT J AU Nagasato, K Farris, RW DuboisDalcq, M Voskuhl, RR AF Nagasato, K Farris, RW DuboisDalcq, M Voskuhl, RR TI Exon 2 containing myelin basic protein (MBP) transcripts are expressed in lesions of experimental allergic encephalomyelitis (EAE) SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE myelin basic protein; experimental allergic encephalomyelitis; multiple sclerosis; remyelination ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS; GENE TRANSCRIPTS; REMYELINATION; MOUSE; DEMYELINATION AB Exon 2 containing myelin basic protein (MBP) transcripts are expressed during developmental myelination in mice and humans, and during remyelination subsequent to virally induced demyelination in adult mice. Since remyelination characterizes CNS lesions during experimental allergic encephalomyelitis (EAE) and multiple sclerosis (MS), we investigated whether exon 2 containing isoforms of MBP are expressed in EAE lesions during relapsing disease. Exon 2 containing MBP transcripts were detected by in situ hybridization in 17 of 52 EAE mice and in 16 of 30 mice at the peak of the first or second episode of paralysis. Thus exon 2 containing MBP transcripts are expressed in lesions of the CNS during active phases of chronic relapsing autoimmune disease. Implications of these findings with respect to future therapies aimed toward enhancing remyelination in EAE and, possibly MS, are discussed. C1 NINCDS,VIRAL & MOL PATHOGENESIS LAB,NIH,BETHESDA,MD 20892. NR 15 TC 13 Z9 13 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD JAN PY 1997 VL 72 IS 1 BP 21 EP 25 DI 10.1016/S0165-5728(96)00137-3 PG 5 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA WB856 UT WOS:A1997WB85600004 PM 9003242 ER PT J AU Luck, SJ Chelazzi, L Hillyard, SA Desimone, R AF Luck, SJ Chelazzi, L Hillyard, SA Desimone, R TI Neural mechanisms of spatial selective attention in areas V1, V2, and V4 of macaque visual cortex SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID INFERIOR TEMPORAL CORTEX; AWAKE MACAQUE; NEURONS; MONKEY; RESPONSES; PERCEPTION; PARIETAL; FIXATION; STIMULI; CELLS AB Many neurons in extrastriate visual cortex have large receptive fields, and this may lead to significant computational problems whenever multiple stimuli fall within a single held. Previous studies have suggested that when multiple stimuli fall within a cell's receptive field, they compete for the cell's response in a manner that can be biased in favor of attended stimuli. In the present study we examined this role of attention in areas VI, V2, and V4 of macaque monkeys with the use of a behavioral paradigm in which attention was directed to one of two stimulus locations. When two stimuli were presented simultaneously inside the cell's receptive field (which could be accomplished only in areas V2 and V4), we found that the cell's response was strongly influenced by which of the two stimuli was attended. The size of this attention effect was reduced when the attended and ignored stimuli were presented sequentially rather than simultaneously. In addition, the effects became very weak and inconsistent in these areas when only one of the two stimuli was located inside the receptive held. Attention thus modulated sensory responses primarily when two or more simultaneous stimuli competed for access to a neuron's receptive field. As in areas V2 and V4, attention did not modulate sensory responses in area V1 when only a single stimulus was inside the receptive held. In addition, the small receptive fields in this area precluded the simultaneous presentation of attended and ignored stimuli inside the receptive held, making it impossible to determine whether attention effects would be observed under the conditions that led to consistent attention effects in areas V2 and V4. Spontaneous firing rates in areas V2 and V4 were found to be 30-40% higher when attention was directed inside rather than outside the receptive field, even when no stimulus was present in the receptive held. Spontaneous firing rates also varied according to the particular location within the receptive field that was attended. These shifts in spontaneous activity may reflect a top-down signal that biases responses in favor of stimuli at the attended location. C1 NIMH,NEUROPSYCHOL LAB,BETHESDA,MD 20892. UNIV IOWA,DEPT PSYCHOL,IOWA CITY,IA 52242. UNIV VERONA,DEPT NEUROL & VISUAL SCI,I-37134 VERONA,ITALY. UNIV CALIF SAN DIEGO,DEPT NEUROSCI,LA JOLLA,CA 92093. RI Chelazzi, Leonardo/B-6084-2011 OI Chelazzi, Leonardo/0000-0001-8566-0611 FU NIMH NIH HHS [MH-25594]; NINDS NIH HHS [NS-17778] NR 44 TC 974 Z9 990 U1 7 U2 45 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD JAN PY 1997 VL 77 IS 1 BP 24 EP 42 PG 19 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA WG229 UT WOS:A1997WG22900005 PM 9120566 ER PT J AU Schreurs, BG Tomsic, D Gusev, PA Alkon, DL AF Schreurs, BG Tomsic, D Gusev, PA Alkon, DL TI Dendritic excitability microzones and occluded long-term depression after classical conditioning of the rabbit's nictitating membrane response SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID PURKINJE-CELL DENDRITES; POSITRON-EMISSION TOMOGRAPHY; PARALLEL FIBER SYNAPSES; CEREBELLAR CORTEX; UNCONDITIONED-STIMULUS; ESSENTIAL INVOLVEMENT; INFERIOR OLIVE; LOBULE HVI; MEMORY; STIMULATION AB We made intradendritic recordings in Purkinje cells (n = 164) from parasaggital slices of cerebellar lobule HVI obtained from rabbits given paired presentations of tone and periorbital electrical stimulation (classical conditioning, n = 27) or explicitly unpaired presentations of tone and periorbital stimulation (control, n = 16). Purkinje cell dendritic membrane excitability, assessed by the current required to elicit local dendritic calcium spikes, increased significantly in slices from animals that received classical conditioning. In contrast, membrane potential, input resistance, and amplitude of somatic and dendritic spikes were not different in slices from animals given paired or explicitly unpaired stimulus presentations. The location of cells with low thresholds for local dendritic calcium spikes suggested that there are specific sites for learning-related changes within lobule HVI. These areas may correspond to learning ''microzones'' and are consistent with locations of learning-related in vivo changes in Purkinje cell activity. Application of 4-aminopyridine, an antagonist of the rapidly inactivating potassium current I-A, reduced the threshold for dendritic spikes in slices from naive animals to levels found in slices from trained animals. In cells where thresholds for eliciting parallel fiber-stimulated Purkinje cell excitatory postsynaptic potentials (EPSPs) were measured, levels of parallel fiber stimulation required to elicit a 6-mV EPSP as well as a 4-mV EPSP (n = 30) and a Purkinje cell spike (n = 56) were found to be significantly lower in slices from paired animals than unpaired controls. A classical conditioning procedure was simulated in slices of lobule HVI by pairing a brief, high-frequency train of parallel fiber stimulation (8 pulses, 100 Hz) with a brief, lower frequency train of climbing fiber stimulation (3 pulses, 20 Hz) to the same Purkinje cell. Following paired stimulation of the parallel and climbing fibers, Purkinje cell EPSPs underwent a long-term (>20 min) reduction in peak amplitude (-24%) in cells (n = 12) from animals given unpaired stimulus presentations but to a far less extent (-9%) in cells (n = 20) from animals given in vivo paired training. Whereas 92% of cells from unpaired animals showed pairing-specific depression, 50% of cells from paired animals showed no depression and in several cases showed potentiation. Our data establish that there are localized learning-specific changes in membrane and synaptic excitability of Purkinje cells in rabbit lobule HVI that can be detected in slices 24 h after classical conditioning. Long-term changes within Purkinje cells that effect this enhanced excitability may occlude pairing-specific long-term depression. RP Schreurs, BG (reprint author), NINCDS,LAB ADAPT SYST,NIH,BLDG 36,RM B205,BETHESDA,MD 20892, USA. OI Schreurs, Bernard/0000-0002-5776-0807 NR 53 TC 74 Z9 74 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD JAN PY 1997 VL 77 IS 1 BP 86 EP 92 PG 7 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA WG229 UT WOS:A1997WG22900010 PM 9120599 ER PT J AU Chew, LJ Fleck, MW Wright, P Scherer, SE Mayer, ML Gallo, V AF Chew, LJ Fleck, MW Wright, P Scherer, SE Mayer, ML Gallo, V TI Growth factor-induced transcription of GluR1 increases functional AMPA receptor density in glial progenitor cells SO JOURNAL OF NEUROSCIENCE LA English DT Article DE platelet-derived growth factor; basic fibroblast growth factor; oligodendrocytes; gene transcription; glutamate-gated channels; rectification ID CULTURED HIPPOCAMPAL-NEURONS; RAT CEREBELLAR CULTURES; CENTRAL-NERVOUS-SYSTEM; GLUTAMATE-RECEPTOR; OLIGODENDROCYTE LINEAGE; CORTICAL NEUROGENESIS; INWARD RECTIFICATION; MOLECULAR-CLONING; MACROGLIAL CELLS; GENE-EXPRESSION AB We analyzed the effects of two growth factors that regulate oligodendrocyte progenitor (O-2A) development on the expression of glutamate receptor (GluR) subunits in cortical O-2A cells. In the absence of growth factors, GluR1 was the AMPA subunit mRNA expressed at the lowest relative level. Basic fibroblast growth factor (bFGF) caused an increase in GluR1 and GluR3 steady-state mRNA levels. Platelet-derived growth factor (PDGF) did not modify the mRNA levels for any of the AMPA subunits but selectively potentiated the effects of bFGF on GluR1 mRNA (4.5-fold increase). The kainate-preferring subunits GluR7, KA1, and KA2 mRNAs were increased by bFGF, but these effects were not modified by cotreatment with PDGF. Nuclear run-on assays demonstrated that PDGF+bFGF selectively increased the rate of GluR1 gene transcription (2.5-fold over control). Western blot analysis showed that GluR1 protein levels were increased selectively (sixfold over control) by PDGF+bFGF. Functional expression was assessed by rapid application of AMPA to cultured cells. AMPA receptor current densities (pA/pF) were increased nearly fivefold in cells treated with PDGF+bFGF, as compared with untreated cells. Further, AMPA receptor channels in cells treated with PDGF+bFGF were more sensitive to voltage-dependent block by intracellular polyamines, as expected from the robust and selective enhancement of GluR1 expression. Our combined molecular and electrophysiological findings indicate that AMPA receptor function can be regulated by growth factor-induced changes in the rate of gene transcription. C1 NICHHD,LAB CELLULAR & MOL NEUROPHYSIOL,NIH,BETHESDA,MD 20892. RI Mayer, Mark/H-5500-2013 NR 71 TC 31 Z9 31 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JAN 1 PY 1997 VL 17 IS 1 BP 227 EP 240 PG 14 WC Neurosciences SC Neurosciences & Neurology GA WJ677 UT WOS:A1997WJ67700021 PM 8987751 ER PT J AU Fernandez, PL Merino, MJ Gomez, M Campo, E Medina, T Castronovo, V Sanjuan, X Cardesa, A Liu, FT Sobel, ME AF Fernandez, PL Merino, MJ Gomez, M Campo, E Medina, T Castronovo, V Sanjuan, X Cardesa, A Liu, FT Sobel, ME TI Galectin-3 and laminin expression in neoplastic and non-neoplastic thyroid tissue SO JOURNAL OF PATHOLOGY LA English DT Article DE galectin-3; thyroid; carcinoma; laminin ID IGE-BINDING-PROTEIN; BASEMENT-MEMBRANE; MOLECULAR-CLONING; COLON-CARCINOMA; TUMOR INVASION; LECTIN; MAC-2; CELLS; GENE; IDENTIFICATION AB Galectin-3 is a 31 kD beta-galactoside-binding lectin which is expressed by several types of non-neoplastic and neoplastic cells and which may he involved in cell-extracellular matrix interactions. An immunohistochemical study has been made of the expression of galectin-3, as well as its ligand, laminin, in a spectrum of benign and malignant thyroid neoplasms and in some non-neoplastic conditions. Immunohistochemistry with anti-human recombinant galectin-3 antibody showed consistent, intense positivity in the neoplastic cells of IS cases of papillary carcinoma and less intense staining In the five anaplastic carcinomas studied, Ln addition, two out of three poorly differentiated carcinomas, three out of six medullary carcinomas, and four out of eight follicular carcinomas had less intense or focal positivity, One case of Hurthle cell carcinoma showed scattered strongly positive cells, Eight follicular adenomas, three hyperplastic nodules, five nodular goitres, and normal thyroid tissue were negative, Galectin-3 mRNA expression was also evaluated in three of the papillary carcinomas, two follicular adenomas, and one hyperplastic nodule with matched normal tissue, Northern blot analysis demonstrated mRNA overexpression in the three cases of papillary carcinomas, whereas normal and benign tissues were negative, Laminin distribution in neoplastic and non-neoplastic tissue varied with architectural patterns but did not correlate with galectin3 immunohistochemical expression. We conclude that expression of galectin-3 is limited to inflammatory foci in normal and benign thyroid tissue and is a phenotypic feature of malignant thyroid neoplasms, especially papillary carcinomas. C1 UNIV GRANADA, SCH MED, GRANADA, SPAIN. NCI, SURG PATHOL SECT, PATHOL LAB, NIH, BETHESDA, MD 20892 USA. NCI, MOL PATHOL SECT, PATHOL LAB, NIH, BETHESDA, MD 20892 USA. UNIV LIEGE, METASTASIS RES LAB, LIEGE, BELGIUM. SCRIPPS RES INST, LA JOLLA, CA USA. RP Fernandez, PL (reprint author), UNIV BARCELONA, DEPT ANAT PATOL, SCH MED, HOSP CLIN, VILLARROEL 170, E-08036 BARCELONA, SPAIN. OI Campo, elias/0000-0001-9850-9793 NR 48 TC 119 Z9 128 U1 0 U2 3 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0022-3417 J9 J PATHOL JI J. Pathol. PD JAN PY 1997 VL 181 IS 1 BP 80 EP 86 PG 7 WC Oncology; Pathology SC Oncology; Pathology GA WH724 UT WOS:A1997WH72400014 PM 9072007 ER PT J AU Bottinger, EP Jakubczak, J Roberts, ISD Mumy, M Hemmati, P Roberts, AB Merlino, G Wakefield, LM AF Bottinger, EP Jakubczak, J Roberts, ISD Mumy, M Hemmati, P Roberts, AB Merlino, G Wakefield, LM TI Histopathology of the pancreas in transgenic mice with targeted overexpression of dominant negative mutant TGF beta type II receptors SO JOURNAL OF PATHOLOGY LA English DT Meeting Abstract C1 NCI,CHEMOPREVENT LAB,NIH,BETHESDA,MD 20892. UNIV MANCHESTER,DEPT PATHOL SCI,MANCHESTER M13 9PL,LANCS,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0022-3417 J9 J PATHOL JI J. Pathol. PY 1997 VL 181 SU S BP A10 EP A10 PG 1 WC Oncology; Pathology SC Oncology; Pathology GA WK188 UT WOS:A1997WK18800038 ER PT J AU Sonies, BC AF Sonies, BC TI Swallowing disorders and rehabilitation techniques SO JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION LA English DT Article; Proceedings Paper CT 1st International Symposium on Pediatric NeuroGastroenterology - Gut Interactions with Brain and Environment in Children CY SEP 18-20, 1997 CL CAPRI, ITALY RP Sonies, BC (reprint author), NIH,DEPT REHABIL MED,BETHESDA,MD 20854, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-2116 J9 J PEDIATR GASTR NUTR JI J. Pediatr. Gastroenterol. Nutr. PY 1997 VL 25 SU 1 BP S32 EP S33 PG 2 WC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics SC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics GA XV066 UT WOS:A1997XV06600016 PM 9285863 ER PT J AU Recknor, JC Reigart, JR Darden, PM Goyer, RA Olden, K Richardson, MC AF Recknor, JC Reigart, JR Darden, PM Goyer, RA Olden, K Richardson, MC TI Prenatal care and infant lead exposure SO JOURNAL OF PEDIATRICS LA English DT Article; Proceedings Paper CT 35th Annual Meeting of Ambulatory-Pediatric-Association CY MAY 07-11, 1995 CL SAN DIEGO, CA SP Ambulatory Pediat Assoc ID LOW-BIRTH-WEIGHT; BLOOD LEAD; HEALTH AB Objective: The objective of the study was to determine the relation between prenatal care of mothers and blood lead concentrations in their offspring in the first year of life. Methods: A retrospective survey was conducted of 200 predominantly black infants between the ages of 6 and 22 months (mean age, 13.4 months). The infants had been screened for the first time since birth at the Charleston County (South Carolina) Health Department. They resided in a neighborhood with the highest prevalence of lead poisoning in Charleston. Prenatal care use data were obtained after matching birth records with lead-screening records. Results: Seventy-three infants (37%) had blood lead levels 0.48 mu mol/L (greater than or equal to 10 mu g/dl) or higher, Adequacy of prenatal care, defined by the Modified Kessner Index, showed 11% with intensive care (26% of these with high lead levels), 39% with adequate care (35% high blood lead levels), 35% with intermediate care (40% with high blood lead levels), 13% with inadequate care (42% with high blood lead levels), and 2% with no prenatal care (25% with high blood lead levels), With the exception of the small group with no prenatal care (n = 4), the proportion of infants with a high blood lead level was inversely proportional to the level of care, The logistic regression model that best fit the data included age at screen for lead and birth weight. Low birth weight babies (<2500 gm) were more likely to have a high blood lead level at primary screen than babies who were heavier at birth (odds ratio, 2.60; p = 0.04), and the older the baby at screening, the greater the likelihood of a high blood lead level (odds ratio, 1.23; p = 0.01), There was a trend for black infants to have a high blood lead level more often than white infants (odds ratio, 3.05; p = 0.06). Conclusions: Less than adequate use of prenatal care may reflect an increase in risk factors contributing to lead exposure in infancy, Low birth weight also was related to high blood lead levels, Further studies are required to differentiate among several hypotheses for this effect, Intrauterine lead exposure, which is known to reduce birth weight, may contribute to measured blood lead levels at first screen, Alternatively, low birth weight may increase lead absorption and retention in infancy or may increase risk of lead exposure. C1 NATL INST ENVIRONM HLTH SCI, RES TRIANGLE PK, NC USA. RP Recknor, JC (reprint author), MED UNIV S CAROLINA, DEPT PEDIAT, 171 ASHLEY AVE, CHARLESTON, SC 29425 USA. NR 20 TC 6 Z9 6 U1 0 U2 0 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD JAN PY 1997 VL 130 IS 1 BP 123 EP 127 DI 10.1016/S0022-3476(97)70320-2 PG 5 WC Pediatrics SC Pediatrics GA WD718 UT WOS:A1997WD71800022 PM 9003861 ER PT J AU Witkin, JM Steele, TD Sharpe, LG AF Witkin, JM Steele, TD Sharpe, LG TI Effects of strychnine-insensitive glycine receptor ligands in rats discriminating dizocilpine or phencyclidine from saline SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID D-ASPARTATE RECEPTOR; EXCITATORY AMINO-ACIDS; NMDA-RECEPTOR; BEHAVIORAL PHARMACOLOGY; EXHIBIT ANTIDEPRESSANT; GLUTAMATE ANTAGONISTS; INDUCED HYPERACTIVITY; DRUG DISCRIMINATION; STIMULUS PROPERTIES; D-SERINE AB Several pharmacologically distinct sites are known to modulate the N-methyl-D-aspartate (NMDA) receptor/ion complex, including a site within the ion channel which binds uncompetitive antagonists like phencyclidine (PCP) or dizocilpine. Glycine acts as a co-agonist for activation of the NMDA receptor complex through a strychnine-insensitive receptor, which is a potential target far novel therapeutic agents (e.g., anticonvulsants, antidepressants). We evaluated the behavioral effects of glycine receptor ligands in rats trained to discriminate either dizocilpine or PCP from saline, to predict whether glycine receptor ligands might induce undesirable PCP-like subjective effects in humans. Dizocilpine ([+]-MK-801), (-)-MK-801 and PCP produced dose-dependent substitution in these rats with potencies in accord with NMDA receptor affinity. Pentobarbital and drugs acting at other sites of the NMDA receptor, including competitive antagonists (NPC 12626 and LY 274614) and the polyamine antagonist, ifenprodil, did nat substitute for either dizocilpine or PCP. In contrast to the uncompetitive antagonists like PCP, none of the strychnine-insensitive glycine receptor ligands substituted. Neither the full agonist, glycine; the partial agonists, 1-amino-1-cyclopropanecarboxylic acid, D-cycloserine or (+)-3-amino-1-hydroxypyrrolid-2-one; nor the antagonists, 7-chloro and 5,7-dichlorokynurenic acid, mimicked the discriminative stimulus effects of dizocilpine or PCP. Further, co-administration of 1-amino-1-cyclopropanecarboxylic acid did not significantly enhance the discriminative stimulus effects of dizocilpine. Intracerebroventricular administration of D-serine, a selective agonist of the strychnine-insensitive glycine receptor, neither mimicked nor blocked the discriminative stimulus effects of PCP. These data suggest that functional antagonists of the strychnine-insensitive glycine receptor may be devoid of the subjective side effects characteristic of NMDA channel ligands. RP Witkin, JM (reprint author), NIDA,ADDICT RES CTR,PRECLIN PHARMACOL LAB,DRUG DEV GRP,POB 5180,BALTIMORE,MD 21224, USA. NR 63 TC 27 Z9 27 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD JAN PY 1997 VL 280 IS 1 BP 46 EP 52 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WC041 UT WOS:A1997WC04100007 PM 8996180 ER PT J AU Kong, LY McMillian, MK Hudson, PM Jin, L Hong, JS AF Kong, LY McMillian, MK Hudson, PM Jin, L Hong, JS TI Inhibition of lipopolysaccharide-induced nitric oxide and cytokine production by ultralow concentrations of dynorphins in mixed glia cultures SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID TUMOR-NECROSIS-FACTOR; OPIOID-PEPTIDES; BETA-ENDORPHIN; IMMUNE-SYSTEM; NEUROENDOCRINE HORMONES; PERITONEAL-MACROPHAGES; CORTICAL CULTURES; CELL-CULTURES; BRAIN; EXPRESSION AB Dynorphins (dyn) are a major class of endogenous opioid peptides that modulate the functions of immune cells. However, the effects of dyn on the immune functions of glial cells in the central nervous system (CNS) have not been well characterized. Because nitric oxide (NO) and the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) produced by glial cells are involved in various physiopathological conditions in the CNS, this study examined the effects of dyn on the production of NO and TNF-alpha from mouse glial cells treated with lipopolysaccharide (LPS). LPS induced a concentration-dependent increase in the production of NO or TNF-alpha from the mouse primary mixed glia cultures. Ultralow concentrations (10(-16)-10(-12) M) of dynorphin (dyn) A-(1-8) significantly inhibited the LPS-induced production of NO or TNF-alpha. The inhibitory effects of dyn A-(1-8) were not blocked by nor-binaltorphimine, a selective kappa opioid receptor antagonist. U50-488H, a selective kappa opioid receptor agonist, did not affect the LPS-induced production of NO or TNF-alpha. Ultralow concentrations (10(-16)-10(-12) M) of des[Tyr(1)]-dyn A-(2-17), a nonopioid analog that does not bind to kappa opioid receptors, exhibited the same inhibitory effects as dyn A-(1-17) and dyn A-(1-8). These results suggest that dyn modulate the immune functions of microglia and/or astrocytes in the brain and these modulatory effects of dyn are not mediated by classical kappa opioid receptors. RP Kong, LY (reprint author), NIEHS, NEUROPHARMACOL SECT,TOXICOL LAB,NIH,POB 12233, MD, F1-01, RES TRIANGLE PK, NC 27709 USA. NR 43 TC 55 Z9 57 U1 0 U2 1 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD JAN PY 1997 VL 280 IS 1 BP 61 EP 66 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WC041 UT WOS:A1997WC04100009 PM 8996182 ER PT J AU Zhou, LM Gu, ZQ Costa, AM Yamada, KA Mansson, PE Giordano, T Skolnick, P Jones, KA AF Zhou, LM Gu, ZQ Costa, AM Yamada, KA Mansson, PE Giordano, T Skolnick, P Jones, KA TI (2S,4R)-4-methylglutamic acid (SYM 2081): A selective, high-affinity ligand for kainate receptors SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID CULTURED HIPPOCAMPAL-NEURONS; GLUTAMATE-RECEPTOR; RAT-BRAIN; BINDING-SITES; KAINIC ACID; DRG-NEURONS; AMPA; EXPRESSION; CLONING; SUBUNIT AB Glutamic acid activates ionotropic glutamate receptors that mediate excitatory transmission in the central nervous system. The introduction of a methyl group at position 4 of glutamic acid imparts selectivity for kainate receptors, relative to other (N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) ionotropic glutamate receptors. Among the stereoisomers of 4-methylglutamic acid, the potency of the (2S,4R)-isomer (SYM 2081) to inhibit [H-3]kainic acid binding to both wild-type (rat forebrain) and recombinant (GluR6) kainate receptors (IC50 values of similar to 32 and 19 nM, respectively) was comparable to that of kainic acid (IC50 values of similar to 13 and 28 nM, respectively), SYM 2081 was similar to 800- and 200-fold less potent as an inhibitor of radioligand binding to wild-type (rat forebrain) alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and N-methyl-D-aspartate receptors, respectively. Preexposure of human embryonic kidney 293 cells stably expressing GluR6 receptors to low concentrations of SYM 2081 (30-300 nM) resulted in a reversible blockade of the rapidly desensitizing currents produced by kainate application. At higher concentrations, SYM 2081 (EC(50) of similar to 1 mu M) elicited kainate-like, rapidly desensitizing, inward currents. Pretreatment of recombinant GluR6 receptors with concanavalin A both abolished the effect of SYM 2081 to block kainate-induced currents and revealed nondesensitizing currents induced by SYM 2081 alone. The latter observations provide strong support for the hypothesis that SYM 2081 blocks kainate-induced currents through a process of agonist-induced desensitization. SYM 2081 also activated alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor currents in primary cultures of cerebral cortex and, consistent with data obtained by radioligand binding, was similar to 5-fold less potent than kainate (EC(50) values of 325 and 70 mu M, respectively) in this measure. SYM 2081 is a high-affinity, selective, kainate agonist that may prove useful both as a probe to examine the physiological functions of kainate receptors and as the prototype of a novel class of therapeutic agents. C1 SYMPHONY PHARMACEUT INC,MALVERN,PA. NIDDK,NEUROSCI LAB,NIH,BETHESDA,MD. WASHINGTON UNIV,SCH MED,DEPT NEUROL,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT PEDIAT,ST LOUIS,MO 63110. NR 40 TC 101 Z9 106 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD JAN PY 1997 VL 280 IS 1 BP 422 EP 427 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WC041 UT WOS:A1997WC04100051 PM 8996224 ER PT J AU Pumford, NR Halmes, NC Martin, BM Cook, RJ Wagner, C Hinson, JA AF Pumford, NR Halmes, NC Martin, BM Cook, RJ Wagner, C Hinson, JA TI Covalent binding of acetaminophen to N-10-formyl-tetrahydrofolate dehydrogenase in mice SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID INDUCED HEPATIC NECROSIS; 56-KDA SELENIUM-BINDING; 10-FORMYLTETRAHYDROFOLATE DEHYDROGENASE; LIVER PROTEINS; 3-(CYSTEIN-S-YL)ACETAMINOPHEN ADDUCTS; TREATED MICE; IDENTIFICATION; CYTOSOL; PURIFICATION; QUANTITATION AB The analgesic acetaminophen is frequently used as a model chemical to study hepatotoxicity; however, the critical mechanisms by which it produces toxicity within the cell are unknown. It has been postulated that covalent binding of a toxic metabolite to crucial proteins may inhibit vital cellular functions and may be responsible for, or contribute to, the hepatotoxicity. To further understand the importance of covalent binding in the toxicity, a major cytosolic acetaminophen-protein adduct of 100 kDa has been purified by a combination of anion exchange chromatography and preparative electrophoresis. N-Terminal and internal amino acid sequences of peptides from the purified 100-kDa acetaminophen-protein adduct were found to be homologous with the deduced amino acid sequence from the cDNA of N-10-formyltetrahydrofolate dehydrogenase. Anti-serum specific for N-10-formyltetrahydrofolate dehydrogenase and acetaminophen react in a Western blot with the purified 100-kDa acetaminophen-protein adduct. Administration of a toxic dose of acetaminophen (400 mg/kg) to mice resulted in a 25% decrease in cytosolic N-10-formyltetrahydrofolate dehydrogenase activity at 2 hr. The covalent binding of acetaminophen to proteins such as N-10-formyltetrahydrofolate dehydrogenase and the subsequent decreases in their enzyme activity may play a role in acetaminophen hepatotoxicity. C1 NIH,CLIN NEUROSCI BRANCH,BETHESDA,MD 20892. VANDERBILT UNIV,SCH MED,DEPT BIOCHEM,NASHVILLE,TN 37240. VET ADM MED CTR,NASHVILLE,TN 37203. RP Pumford, NR (reprint author), UNIV ARKANSAS MED SCI HOSP,DIV TOXICOL,4301 W MARKHAM ST,SLOT 638,LITTLE ROCK,AR 72205, USA. FU NIGMS NIH HHS [GM 48749] NR 27 TC 50 Z9 50 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD JAN PY 1997 VL 280 IS 1 BP 501 EP 505 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WC041 UT WOS:A1997WC04100061 PM 8996234 ER PT J AU Chester, AC Levine, PH AF Chester, AC Levine, PH TI The natural history of concurrent sick building syndrome and chronic fatigue syndrome SO JOURNAL OF PSYCHIATRIC RESEARCH LA English DT Article; Proceedings Paper CT 1st Research and Clinical Conference of the American-Association-for-Chronic-Fatigue-Syndrome CY OCT 07-09, 1994 CL FT LAUDERDALE, FL SP Amer Assoc Chron Fatigue Syndrome ID PRIMARY-CARE; GENERAL-PRACTICE; PREVALENCE; ILLNESS; DEFINITION; ATTENDERS AB An outbreak of chronic fatigue syndrome linked with sick building syndrome was recently described as a new association. Whether chronic fatigue syndrome acquired in this setting tends to remit or, as sporadic cases often do, persist, is unknown. To clarify the natural history of chronic fatigue syndrome in association with sick building syndrome the 23 individuals involved in the outbreak were interviewed four years after the onset. In the previous interview one year after the onset of symptoms, 15 (including 5 with chronic fatigue syndrome and 10 with idiopathic chronic fatigue) of the 23 noted fatigue. Three years later 10 of the 15 were ''fatigue free'' or ''much improved''. Five were only ''some better'', ''the same'', or ''worse''. Three of the five people previously diagnosed with chronic fatigue syndrome were ''much improved'' (two) or ''fatigue free'' (one). The remaining two were seriously impaired, homebound and unable to work. The 10 individuals with substantially improved fatigue (three of the five with chronic fatigue syndrome and seven of the 10 with idiopathic chronic fatigue) were more likely to have noted improvement in nasal and sinus symptoms, sore throats, headaches, and tender cervical lymph nodes when compared to those with a lingering significant fatigue (p < 0.001). Upper respiratory symptoms and headaches improved in those with reduced fatigue but remained problematic in those with persisting significant fatigue, We conclude that the fatigue related to sick building syndrome, including chronic fatigue syndrome, is significantly more likely to improve than fatigue identified in sporadic cases of chronic fatigue syndrome. (C) 1997 Elsevier Science Ltd. C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20057. NIH,BETHESDA,MD 20892. NR 35 TC 7 Z9 7 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0022-3956 J9 J PSYCHIAT RES JI J. Psychiatr. Res. PD JAN-FEB PY 1997 VL 31 IS 1 BP 51 EP 57 DI 10.1016/S0022-3956(96)00054-4 PG 7 WC Psychiatry SC Psychiatry GA XD894 UT WOS:A1997XD89400006 PM 9201647 ER PT J AU Knable, MB Weinberger, DR AF Knable, MB Weinberger, DR TI Dopamine, the prefrontal cortex and schizophrenia SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Review DE antipsychotic drugs; dopamine; dopamine receptors; prefrontal cortex; schizophrenia ID VENTRAL TEGMENTAL AREA; HUMAN CEREBRAL-CORTEX; 3,4-DIHYDROXYPHENYLACETIC ACID DOPAC; CHRONIC HALOPERIDOL TREATMENT; RECEPTOR STIMULATION ENABLES; ANTERIOR CINGULATE CORTEX; STRESS-INDUCED INCREASE; FREELY MOVING RATS; C-FOS EXPRESSION; AUTORADIOGRAPHIC LOCALIZATION AB Dysfunction of the prefrontal cortex (PFC) in schizophrenia has been suspected based on observations from clinical, neuropsychological and neuroimaging studies. Since the PFC receives a dense dopaminergic innervation, abnormalities of the mesocortical dopamine system have been proposed to contribute to the pathophysiology of schizophrenia. In this review, aspects of the anatomy, physiology and pharmacology of the mesencephalic-frontal cortical dopamine system as they may relate to schizophrenia are described, and evidence for altered dopaminergic neurotransmission in the frontal cortex of schizophrenic patients is presented. RP Knable, MB (reprint author), NIMH,INTRAMURAL RES PROGRAM,CLIN BRAIN DISORDERS BRANCH,2700 MARTIN LUTHER KING JR AVE SE,WASHINGTON,DC 20032, USA. NR 142 TC 198 Z9 202 U1 1 U2 14 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON, ENGLAND EC2A 4PU SN 0269-8811 J9 J PSYCHOPHARMACOL JI J. Psychopharmacol. PY 1997 VL 11 IS 2 BP 123 EP 131 DI 10.1177/026988119701100205 PG 9 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA XK611 UT WOS:A1997XK61100005 PM 9208376 ER PT J AU Zabora, JR Blanchard, CG Smith, ED Roberts, CS Glajchen, M Sharp, JW BrintzenhofeSzoc, KM Locher, JW Carr, EW BestCastner, S Smith, PM DozierHall, D Polinsky, ML Hedlund, SC AF Zabora, JR Blanchard, CG Smith, ED Roberts, CS Glajchen, M Sharp, JW BrintzenhofeSzoc, KM Locher, JW Carr, EW BestCastner, S Smith, PM DozierHall, D Polinsky, ML Hedlund, SC TI Prevalence of psychological distress among cancer patients across the disease continuum SO JOURNAL OF PSYCHOSOCIAL ONCOLOGY LA English DT Article ID QUALITY; LIFE; DIAGNOSIS AB Psychological distress is considered to be common as patients with cancer move beyond their diagnosis and into intensive treatment. However, the absolute prevalence of elevated psychological distress among patients is reported to be about 30% at the diagnosis and when the disease recurs. In all probability, patients enter their initial experience with cancer with preexisting levels of distress. Without intervention, their level of distress remains elevated, whereas patients with a lower level of distress gradually adapt to the diagnosis and treatment. To target interventions: understanding the relationship between a cancer diagnosis and the level of psychological distress at any point in time is essential. This article describes a study undertaken to determine the prevalence of psychological distress across the disease continuum in a sample of 386 adult cancer patients selected at random from 12 oncology outpatient departments across the United States. Psychological distress was measured with the Brief Symptom Inventory, and quality of life was measured with the Functional Living Index-Cancer. The results indicated that the prevalence of psychological distress did not vary significantly across the disease continuum, with the exception of the terminal phase. C1 ALBANY MED COLL,DIV MED ONCOL,ALBANY,NY 12208. CATHOLIC UNIV AMER,NATL CATHOLIC SCH SOCIAL SERV,WASHINGTON,DC 20064. UNIV S FLORIDA,COLL MED,H LEE MOFFITT CANC CTR & RES INST,TAMPA,FL 33612. MEM SLOAN KETTERING CANC CTR,DEPT SOCIAL WORK,NEW YORK,NY 10021. CLEVELAND CLIN FDN,DEPT SOCIAL WORK,CLEVELAND,OH 44195. JOHNS HOPKINS UNIV,SCH MED,JOHNS HOPKINS ONCOL CTR,DEPT ONCOL SOCIAL WORK,BALTIMORE,MD 21205. UNIV IOWA HOSP & CLIN,DEPT SOCIAL SERV,IOWA CITY,IA 52242. THOMAS JEFFERSON UNIV HOSP,DEPT SOCIAL WORK,PHILADELPHIA,PA 19107. LEGACY GOOD SAMARITAN HOSP,CANC REHABIL SERV,PORTLAND,OR. YALE NEW HAVEN MED CTR,DEPT SOCIAL WORK,NEW HAVEN,CT 06504. NATL INST HLTH CLIN CTR,DEPT SOCIAL WORK,BETHESDA,MD. UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,NEUROPSYCHIAT INST & HOSP,DEPT PSYCHIAT & BIOBEHAV SCI,FAC SOCIAL WORK,LOS ANGELES,CA 90024. OREGON HLTH SCI UNIV,DIV ONCOL & PATIENT RELAT,PORTLAND,OR 97201. RP Zabora, JR (reprint author), DEPT PATIENT & FAMILY SERV,JOANNE ROCKWELL MEM HOUSE,1910 E JEFFERSON ST,BALTIMORE,MD 21205, USA. NR 24 TC 90 Z9 92 U1 1 U2 2 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 SN 0734-7332 J9 J PSYCHOSOC ONCOL JI J. Psychosoc. Oncol. PY 1997 VL 15 IS 2 BP 73 EP 87 DI 10.1300/J077V15N02_05 PG 15 WC Psychology, Social SC Psychology GA YB420 UT WOS:A1997YB42000005 ER PT J AU Austin, HA Patel, AD Cadena, CA Boumpas, DT Balow, JE AF Austin, HA Patel, AD Cadena, CA Boumpas, DT Balow, JE TI Ongoing immunologic activity after short courses of pulse cyclophosphamide in the NZB/W murine model of systemic lupus erythematosus SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE systemic lupus erythematosus; lupus nephritis; cyclophosphamide; immunosuppressive agents; animal disease models ID ANTIBODY-SECRETING CELLS; LYMPHOCYTE-B FUNCTION; RICIN-A-CHAIN; MONOCLONAL-ANTIBODY; BACTERIAL LIPOPOLYSACCHARIDES; INTRAVENOUS CYCLOPHOSPHAMIDE; AUTOIMMUNE-DISEASE; CONTROLLED TRIAL; DNA ANTIBODIES; NEPHRITIS AB Objective, Short courses of intermittent pulse cyclophosphamide (CY) have mitigated ovarian toxicity but have also led to incomplete or unsustained remissions of active systemic lupus erythematosus (SLE) in many patients, prompting an evaluation of the immunologic effects of this regimen in the NZB/W female mouse (B/W) model of human SLE. Methods, Phenotypic and functional characteristics of spleen lymphocytes from B/W mice treated with short courses of intraperitoneal (ip) CY were compared to those from untreated control B/W mice. Results, After a single dose (250 mg/kg) of ip CY, spleen lymphocyte subpopulations fell abruptly but recovered within 4 weeks. Four monthly doses of ip CY (starting at 5 months of age) led to a sustained reduction in spleen lymphocyte subpopulations and a parallel decrease in the number of spleen cells spontaneously secreting immunoglobulin and anti-DNA antibody to about 30% of the number seen in untreated control B/W mice. Lipopolysaccharide induced secretion of total IgG and IgG anti-DNA by cultured spleen cells was not diminished one month after the 4 month course of ip CY. Conclusion. The 4 month course of ip CY produced a marked reduction in the number of activated B cells producing autoantibody, but did not achieve sustained immunomodulation judged by the unaltered proportion of spleen B cells spontaneously secreting immunoglobulin and anti-DNA, as well as the response to polyclonal activators of B cells. These results suggest a continued susceptibility to flares of SLE activity after brief courses of intensive immunosuppressive therapy. RP Austin, HA (reprint author), NIDDKD,KIDNEY DIS SECT,NIH,BLDG 10,ROOM 3N-112,9000 ROCKVILLE PIKE,BETHESDA,MD 20892, USA. NR 57 TC 9 Z9 9 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD JAN PY 1997 VL 24 IS 1 BP 61 EP 68 PG 8 WC Rheumatology SC Rheumatology GA WC496 UT WOS:A1997WC49600012 PM 9002012 ER PT J AU Weeks, DE Davis, S Schroeder, M Goldin, LR AF Weeks, DE Davis, S Schroeder, M Goldin, LR TI Nonparametric simulation based linkage statistics for general pedigrees SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE genetic analysis; identity-by-state; rheumatoid arthritis; identity-by-descent ID MEMBER METHOD AB A common strategy for testing for linkage without posing a disease model is to test for increased marker similarity among the affected pedigree members. We developed a simulation based statistic, SimIBD, which measures marker similarity in terms of identity-by-descent (IBD) when it can be determined whether or not the alleles are IBD, and in terms of the probability of the alleles being IBD when it cannot be determined. The SimIBD statistic is not only more powerful than its precursor, the affected-pedigree-member (APM) method, but it is also less sensitive to the misspecification of marker allele frequencies. C1 UNIV PITTSBURGH,DEPT HUMAN GENET,PITTSBURGH,PA. NIMH,CLIN NEUROGENET BRANCH,BETHESDA,MD 20892. RP Weeks, DE (reprint author), UNIV OXFORD,WELLCOME TRUST CTR HUMAN GENET,WINDMILL RD,OXFORD 0X3 7BN,ENGLAND. RI Weeks, Daniel/B-2995-2012; OI Davis, Sean/0000-0002-8991-6458; Weeks, Daniel/0000-0001-9410-7228 NR 7 TC 1 Z9 1 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD JAN PY 1997 VL 24 IS 1 BP 206 EP 207 PG 2 WC Rheumatology SC Rheumatology GA WC496 UT WOS:A1997WC49600040 PM 9002040 ER PT J AU Bamberger, CM Bamberger, AM Wald, M Chrousos, GP Schulte, HM AF Bamberger, CM Bamberger, AM Wald, M Chrousos, GP Schulte, HM TI Inhibition of mineralocorticoid activity by the beta-isoform of the human glucocorticoid receptor SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article; Proceedings Paper CT 12th International Symposium of the Journal-of-Steroid-Biochemistry-and-Molecular-Biology CY MAY 21-24, 1995 CL BERLIN, GERMANY SP J Steroid Biochem & Molec Biol ID 11-BETA-HYDROXYSTEROID DEHYDROGENASE; PSEUDOHYPOALDOSTERONISM; DNA; SUPERFAMILY; BINDING; HYPERTENSION; ALDOSTERONE; SPECIFICITY; CLONING; SYSTEM AB Mineralocorticoids and glucocorticoids are important regulators of electrolyte homeostasis and arterial blood pressure. Their effects are mediated by the mineralocorticoid (MR) and the glucocorticoid receptor (GR), respectively. The present study was designed to determine how the two isoforms of the human GR, the ''classic'' GR alpha and the non-hormone-binding GR beta, interfere with the transcriptional effects of the hormone-activated human MR. COS-7 monkey kidney cells were transfected with different mineralocorticoid-responsive reporter plasmids and a vector expressing the human MR protein. Different amounts of either control, GR alpha, or GR beta plasmid were co-transfected, and luciferase activity was measured after stimulation with aldosterone and/or dexamethasone. MR-mediated stimulation of transcription was enhanced by co-transfection of the GR alpha expression vector. In contrast, MR-mediated stimulation of transcription was strongly inhibited by co-transfection of equal amounts of the GRP expression vector. Reverse transcription-polymerase chain reaction (RT-PCR) showed expression of both GR isoforms as well as of MR in the human kidney. These data indicate that the two isoforms of the human GR exert opposite effects on mineralocorticoid activity. We conclude that the ratio between GR alpha and GR beta can define the sensitivity of mineralocorticoid target tissues to aldosterone. Imbalances of this ratio may participate in clinical syndromes of impaired or augmented mineralocorticoid sensitivity, such as certain cases of pseudohypoaldosteronism or, possibly, primary arterial hypertension. (C) 1997 Elsevier Science Ltd. C1 UNIV HAMBURG, DEPT MED, D-20246 HAMBURG, GERMANY. NICHHD, DEV ENDOCRINOL BRANCH, NIH, BETHESDA, MD 20892 USA. RP Bamberger, CM (reprint author), UNIV HAMBURG, IHF INST HORMONE & FERTIL RES, D-22529 HAMBURG, GERMANY. NR 39 TC 43 Z9 43 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0960-0760 J9 J STEROID BIOCHEM JI J. Steroid Biochem. Mol. Biol. PD JAN PY 1997 VL 60 IS 1-2 BP 43 EP 50 DI 10.1016/S0960-0760(96)00167-7 PG 8 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA XC696 UT WOS:A1997XC69600006 PM 9182857 ER PT J AU Miyaguchi, K AF Miyaguchi, K TI Ultrastructure of intermediate filaments of nestin- and vimentin-immunoreactive astrocytes in organotypic slice cultures of hippocampus SO JOURNAL OF STRUCTURAL BIOLOGY LA English DT Article ID FIBRILLARY ACIDIC PROTEIN; REACTIVE ASTROCYTES; GLIAL-CELLS; PRECURSOR CELLS; RADIAL GLIA; ORGANIZATION; LOCALIZATION; DIFFERENTIATION; NEUROFILAMENTS; PROLIFERATION AB Glial cells in rat hippocampal slices cultured for 4 weeks were examined with immunocytochemical and cryoelectron microscopical methods. Astrocytes possessing long processes were similarly stained with antibodies against nestin, vimentin, and glial fibrillary acidic protein as seen by confocal microscopy. The three antibodies also labeled intermediate filaments in these astrocytes. In order to examine the fine structure of these intermediate filaments, slices were rapid-frozen for freeze-substitution and freeze-etching. By freeze-substitution the processes of the astrocytes were packed with large bundles of intermediate filaments. In rapid-freeze deep-etched slices, these filaments were often interconnected with filamentous cross-bridges. These cross-bridges were rather uniform in size and shape (mean 2.9 nm thick and 14.8 nm long). These results suggest that the filament network with these cross-linkers is important for shaping the long processes of nestin- and vimentin-immunoreactive astrocytes in slice cultures. (C) 1997 Academic Press. RP Miyaguchi, K (reprint author), NINCDS,NEUROBIOL LAB,NIH,BLDG 36,RM 4D04,BETHESDA,MD 20892, USA. NR 28 TC 14 Z9 14 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 1047-8477 J9 J STRUCT BIOL JI J. Struct. Biol. PY 1997 VL 120 IS 1 BP 61 EP 68 DI 10.1006/jsbi.1997.3900 PG 8 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA YE758 UT WOS:A1997YE75800007 PM 9356292 ER PT J AU Murphy, LD Zimmerman, SB AF Murphy, LD Zimmerman, SB TI Isolation and characterization of spermidine nucleoids from Escherichia coli SO JOURNAL OF STRUCTURAL BIOLOGY LA English DT Article ID HISTONE-LIKE PROTEINS; SALMONELLA-TYPHIMURIUM; PLASMOLYSIS SPACES; FOLDED CHROMOSOME; LIGHT-MICROSCOPY; BINDING-PROTEIN; PROKARYOTIC DNA; PHASE-CONTRAST; CELL-ENVELOPE; H-PROTEIN AB Nucleoids isolated from Escherichia coli at low salt concentrations in the presence of spermidine (Kornberg et al., Proc. Natl. Acad. Sci. USA, 71, 3189-3193 (1974)) retain large amounts of protein and RNA and are, thus, potentially useful in structural and other studies, However, these preparations have neither been visualized nor extensively characterized with regard to their protein and other components. We have investigated this type of nucleoid preparation and here supply both Light and electron microscope appearances and a description of the DNA-associated proteins. Light microscopy is used to follow the stages of nucleoid release and to demonstrate characteristically rounded nucleoids after chloramphenicol treatment of the cells from which the nucleoids were isolated. The nucleoids are ''envelope-associated'' particles. Electron microscopy shows an irregular central core that is partially covered with small, membranous vesicles. A significant fraction of the nucleoids have a characteristic doublet/dumbbell-shaped appearance by light microscopy, The nucleoids contain large amounts of protein and RNA in addition to DNA, The DNA and RNA are rendered acid-soluble by very low levels of nucleases, indicating an open structure. A small group of proteins, including H-NS, FIS, HU, and RNA polymerase, is released from the particles upon enzymatic digestion of the DNA. (C) 1997 Academic Press. C1 NIDDKD,MOL BIOL LAB,NIH,BETHESDA,MD 20892. NR 78 TC 46 Z9 46 U1 1 U2 5 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1047-8477 J9 J STRUCT BIOL JI J. Struct. Biol. PY 1997 VL 119 IS 3 BP 321 EP 335 DI 10.1006/jsbi.1997.3883 PG 15 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA XP435 UT WOS:A1997XP43500007 PM 9245770 ER PT J AU Murphy, LD Zimmerman, SB AF Murphy, LD Zimmerman, SB TI Stabilization of compact spermidine nucleoids from Escherichia coli under crowded conditions: Implications for in vivo nucleoid structure SO JOURNAL OF STRUCTURAL BIOLOGY LA English DT Article ID EXCLUDED VOLUME; DNA; PROTEINS; CHROMOSOME; GENOME AB Nucleoids from Escherichia coli were isolated in the presence of spermidine at low salt concentrations. The nucleoids denature at relatively low temperatures or salt concentrations, yielding broad slowly sedimenting zones and/or macroscopic aggregates upon sucrose gradient centrifugation. Denaturation is accompanied by a loss of a characteristically compact shape as visualized by light and electron microscopy. Addition of polyethylene glycol or dextran prevents these changes, extending the range of stability of the isolated nucleoids to temperatures and ionic conditions like those which commonly occur in vivo. The effects of the polymers are consistent with stabilization by macromolecular crowding. Enzymatic digestion of the nucleoid DNA primarily releases three small proteins (H-NS, FIS, and HU) and RNA polymerase, as well as residual lysozyme from the cell lysis procedure. If isolated nucleoids are extracted with elevated salt concentrations under crowded, stabilized conditions, two of the proteins (HU and lysozyme) are efficiently removed and the compact form of the nucleoids is retained. These extracted nucleoids maintain their compact form upon reisolation into the initial uncrowded low-salt medium, indicating that HU, the most common ''histone-like'' protein off. coil, is not a necessary component for maintaining compaction in these preparations. (C) 1997 Academic Press. C1 NIDDKD,MOL BIOL LAB,NIH,BETHESDA,MD 20892. NR 19 TC 32 Z9 32 U1 1 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1047-8477 J9 J STRUCT BIOL JI J. Struct. Biol. PY 1997 VL 119 IS 3 BP 336 EP 346 DI 10.1006/jsbi.1997.3884 PG 11 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA XP435 UT WOS:A1997XP43500008 PM 9245771 ER PT J AU Allen, JP Mattson, ME Miller, WR Tonigan, JS Connors, GJ Rychtarik, RG Randall, CL Anton, RF Kadden, RM Litt, M Cooney, NL DiClemente, CC Carbonari, J Zweben, A Longabaugh, RH Stout, RL Donovan, D Babor, TF DelBoca, FK Rounsaville, BJ Carroll, KM Wirtz, PW Bailey, S Brady, K Cisler, R Hester, RK Kivlahan, DR Nirenberg, TD Pate, LA Sturgis, E Muenz, L Cushman, P Finney, J Hingson, R Klett, J Townsend, M AF Allen, JP Mattson, ME Miller, WR Tonigan, JS Connors, GJ Rychtarik, RG Randall, CL Anton, RF Kadden, RM Litt, M Cooney, NL DiClemente, CC Carbonari, J Zweben, A Longabaugh, RH Stout, RL Donovan, D Babor, TF DelBoca, FK Rounsaville, BJ Carroll, KM Wirtz, PW Bailey, S Brady, K Cisler, R Hester, RK Kivlahan, DR Nirenberg, TD Pate, LA Sturgis, E Muenz, L Cushman, P Finney, J Hingson, R Klett, J Townsend, M TI Matching alcoholism treatments to client heterogeneity: Project MATCH posttreatment drinking outcomes SO JOURNAL OF STUDIES ON ALCOHOL LA English DT Article ID CARBOHYDRATE-DEFICIENT TRANSFERRIN; APTITUDE TREATMENT INTERACTION; ADDICTION SEVERITY INDEX; SOCIAL INVESTMENT; COPING SKILLS; THERAPIES; PSYCHOTHERAPY; ORIENTATION; MODELS AB Objective: To assess the benefits of matching alcohol dependent clients to three different treatments with reference to a variety of client attributes. Method: Two parallel but independent randomized clinical trials were conducted, one with alcohol dependent clients receiving outpatient therapy (N = 952; 72% male) and one with clients receiving aftercare therapy following inpatient or day hospital treatment (N=774; 80% male). Clients were randomly assigned to one of three 12-week, manual-guided, individually delivered treatments: Cognitive Behavioral Coping Skills Therapy, Motivational Enhancement Therapy or Twelve-Step Facilitation Therapy. Clients were then monitored over a 1-year posttreatment period. Individual differences in response to treatment were modeled as a latent growth process and evaluated for 10 primary matching variables and 16 contrasts specified a priori. The primary outcome measures were percent days abstinent and drinks per drinking day during the 1-year posttreatment period. Results: Clients attended on average two-thirds of treatment sessions offered indicating that substantial amounts of treatment were delivered, and research follow-up rates exceeded 90% of living subjects interviewed at the 1-year posttreatment assessment. Significant and sustained improvements in drinking outcomes were achieved from baseline to 1-year posttreatment by the clients assigned to each of these well-defined and individually delivered psychosocial treatments. There was little difference in outcomes by type of treatment. Only one attribute, psychiatric severity, demonstrated a significant attribute by treatment interaction: In the outpatient study, clients low in psychiatric severity had more abstinent days after 12-step facilitation treatment than after cognitive behavioral therapy. Neither treatment was clearly superior for clients with higher levels of psychiatric severity. Two other attributes showed time-dependent matching effects: motivation among outpatients and meaning-seeking among aftercare clients. Client attributes of motivational readiness, network support for drinking, alcohol involvement gender, psychiatric severity and sociopathy were prognostic of drinking outcomes over time. Conclusions: The findings suggest that psychiatric severity should be considered when assigning clients to outpatient therapies. The lack of other robust matching effects suggests that, aside from psychiatric severity, providers need not take these client characteristics into account when triaging clients to one or the other of these three individually delivered treatment approaches, despite their different treatment philosophies. RP Allen, JP (reprint author), NIAAA, SCI COMMUN BRANCH, WILLCO BLDG, SUITE 409, 6000 EXECUT BLVD, BETHESDA, MD 20892 USA. RI Carroll, Kathleen/A-7526-2009; Cooney, Ned/C-5176-2014; OI Cooney, Ned/0000-0001-6698-8312; Carroll, Kathleen/0000-0003-3263-3374; Litt, Mark/0000-0002-8319-6090 NR 92 TC 1135 Z9 1144 U1 5 U2 76 PU ALCOHOL RES DOCUMENTATION INC CENT ALCOHOL STUD RUTGERS UNIV PI PISCATAWAY PA C/O DEIRDRE ENGLISH, 607 ALLISON RD, PISCATAWAY, NJ 08854-8001 USA SN 0096-882X J9 J STUD ALCOHOL JI J. Stud. Alcohol PD JAN PY 1997 VL 58 IS 1 BP 7 EP 29 PG 23 WC Substance Abuse; Psychology SC Substance Abuse; Psychology GA VZ416 UT WOS:A1997VZ41600002 ER PT J AU Martin, SE AF Martin, SE TI Alcohol and homicide: A deadly combination of two American traditions - Parker,RN, Rebhun,LA SO JOURNAL OF STUDIES ON ALCOHOL LA English DT Book Review RP Martin, SE (reprint author), NIAAA,BETHESDA,MD 20205, USA. NR 1 TC 1 Z9 1 U1 0 U2 1 PU ALCOHOL RES DOCUMENTATION INC CENT ALCOHOL STUD RUTGERS UNIV PI PISCATAWAY PA PO BOX 969, PISCATAWAY, NJ 08855-0969 SN 0096-882X J9 J STUD ALCOHOL JI J. Stud. Alcohol PD JAN PY 1997 VL 58 IS 1 BP 107 EP 107 PG 1 WC Substance Abuse; Psychology SC Substance Abuse; Psychology GA VZ416 UT WOS:A1997VZ41600012 ER PT J AU Faden, VB Hanna, E Graubard, BI AF Faden, VB Hanna, E Graubard, BI TI The effect of positive and negative health behavior during gestation on pregnancy outcome SO JOURNAL OF SUBSTANCE ABUSE LA English DT Article ID PRENATAL EXPOSURE; FETAL GROWTH; ALCOHOL; ADOLESCENT; MARIJUANA; EXERCISE; NEWBORN; CHILD; WOMEN; DRUGS AB This study examined the effects of substance use (alcohol, tobacco and/or drugs (cocaine and/or marijuana)) and healthy maternal behavior (prenatal care, prenatal class, vitamins, regular exercise) during gestation on pregnancy outcome. Live births from the nationally representative 1988 National Maternal and Infant Health Survey were analyzed. Pregnancy outcomes (infant birth weight, weeks gestation, one and five minute Apgar scores, whether or not the infant was transferred to another hospital after delivery and whether or not the infant was rehospitalized) were studied in multiple linear regression and logistic regression models. The relationship of the interaction of substance use and healthy behaviors and outcome was studied in all models. It was found that women engaging in substance use while pregnant were less likely to engage in healthy behavior. However, in general, engaging in healthy behaviors had the largest positive effects on outcome for those women who engaged in multiple substance use while pregnant. Significant interactions between healthy and unhealthy behavior were found for birth weight, weeks gestation and five minute Apgar scores, indicating that engaging in positive health behavior may help moderate some of the deleterious consequences of substance use during pregnancy. C1 NIAAA, Div Biometry & Epidemiol, Bethesda, MD 20892 USA. NCI, Bethesda, MD 20892 USA. RP Faden, VB (reprint author), NIAAA, Div Biometry & Epidemiol, 6000 Execut Blvd,Suite 514, Bethesda, MD 20892 USA. NR 24 TC 14 Z9 17 U1 0 U2 0 PU ABLEX PUBL CORP PI STAMFORD PA 100 PROSPECT ST, PO BOX 811, STAMFORD, CT 06904-0811 USA SN 0899-3289 J9 J SUBST ABUSE JI J. SUBST. ABUSE PY 1997 VL 9 BP 63 EP 76 DI 10.1016/S0899-3289(97)90006-7 PG 14 WC Substance Abuse SC Substance Abuse GA 104LT UT WOS:000075017000005 PM 9494939 ER PT J AU Grant, BF AF Grant, BF TI Convergent validity of DSM-III-R and DSM-IV alcohol dependence: Results from the National Longitudinal Alcohol Epidemiologic Survey SO JOURNAL OF SUBSTANCE ABUSE LA English DT Article ID ABUSE AB The purpose of this study was to separately examine the associations between ethanol intake and alcohol dependence, as defined in the DSM-III-R and DSM-IV, in conjunction with an identical set of external correlates, with a view toward assessing the convergent validity of the two diagnostic definitions of dependence. Although the sociodemographic, alcohol, drug and comorbid profiles of respondents classified as DSM-III-R and DSM-IV dependent were similar, the results of the linear logistic regression analyses differed for each of the diagnostic definitions. The risk of DSM-III-R dependence was reduced among blacks and increased among early onset dl-inkers. Given equivalent levels of ethanol intake, the risk of DSM-III-R dependence was greater for these respondents who had experienced a recent death of close relative compared to those who had not. In contrast, the risk of DSM-IV dependence was greatest among respondents with a current alcoholic spouse or partner relative to those without an alcoholic spouse or partner. Major differences in the content and structure of the two definitions of dependence were useful in predicting the observed discrepancies between the risk gradients associated with the DSM-III-R and DSM-IV classifications. implications of these findings were discussed in terms of differential coverage of the DSM-III-R and DSM-IV diagnostic categories and rite impact of the absence of complete convergent validity on epidemiologic research. C1 NIAAA, Div Biometry & Epidemiol, Bethesda, MD 20892 USA. RP Grant, BF (reprint author), NIAAA, Div Biometry & Epidemiol, Suite 514,6000 Execut Blvd, Bethesda, MD 20892 USA. NR 18 TC 8 Z9 8 U1 1 U2 2 PU ABLEX PUBL CORP PI STAMFORD PA 100 PROSPECT ST, PO BOX 811, STAMFORD, CT 06904-0811 USA SN 0899-3289 J9 J SUBST ABUSE JI J. SUBST. ABUSE PY 1997 VL 9 BP 89 EP 102 DI 10.1016/S0899-3289(97)90008-0 PG 14 WC Substance Abuse SC Substance Abuse GA 104LT UT WOS:000075017000007 PM 9494941 ER PT J AU Grant, BF Dawson, DA AF Grant, BF Dawson, DA TI Age at onset of alcohol use and its association with DSM-IV alcohol abuse and dependence: Results from the National Longitudinal Alcohol Epidemiologic Survey SO JOURNAL OF SUBSTANCE ABUSE LA English DT Article ID YOUNG MEN; ADOLESCENTS; BEHAVIOR AB Data from 27,616 current and former drinkers interviewed in the 1992 National Longitudinal Alcohol Epidemiologic Survey were used to examine the relationship between age at first nse of alcohol and the prevalence of lifetime alcohol abuse and alcohol dependence, among all U.S. adults 18 years of age and over and within subgroups defined hy sex and race. The rates of lifetime dependence declined from more than 40% among individuals who started drinking at ages 14 or younger to roughly 10% among those who started drinking at ages 20 and older. The rates of lifetime abuse declined from just over 11% among those who initiated use of alcohol at ages 16 or younger to approximately 4% among those whose onset of use was at ages 20 or older, After using multivariate logistic regression models to adjust for potential confounders, the odds of dependence decreased by 14% with each increasing year of age at onset of use, and the odds of abuse decreased by 8%. These findings are discussed with respect to their implications for prevention policies and the need to integrate epidemiological and intervention research. C1 NIAAA, Div Biometry & Epidemiol, Rockville, MD 20852 USA. RP Grant, BF (reprint author), NIAAA, Div Biometry & Epidemiol, Suite 514,6000 Execut Blvd,MSC 7003, Rockville, MD 20852 USA. NR 22 TC 964 Z9 970 U1 20 U2 59 PU ABLEX PUBL CORP PI STAMFORD PA 100 PROSPECT ST, PO BOX 811, STAMFORD, CT 06904-0811 USA SN 0899-3289 J9 J SUBST ABUSE JI J. SUBST. ABUSE PY 1997 VL 9 BP 103 EP 110 DI 10.1016/S0899-3289(97)90009-2 PG 8 WC Substance Abuse SC Substance Abuse GA 104LT UT WOS:000075017000008 PM 9494942 ER PT J AU Hanna, EZ Faden, VB Dufour, MC AF Hanna, EZ Faden, VB Dufour, MC TI The effects of substance use during gestation on birth outcome, infant and maternal health SO JOURNAL OF SUBSTANCE ABUSE LA English DT Article ID PREGNANCY-INDUCED HYPERTENSION; DEPRESSIVE SYMPTOMS; PRENATAL-CARE; RISK-FACTORS; ALCOHOL; WEIGHT; POSTPARTUM; EMPLOYMENT AB This study examines the relationship of substance use to birth outcome, infant, and maternal health in a large. nationally representative sample. Multiple regression analyses, accommodating the nature of the survey data using the SUDAAN software package, indicated that drinking and smoking independently and/or interactively with depression account for poor health and serious medical conditions among pregnant women as well as negative birth outcomes or adverse health consequences in those infants who are live births. In addition, African American women and their infants are more likely than those of other racial groups to suffer these adverse outcomes. Given rite risk profiles of individual illnesses, this study suggests the need for developing and targeting health education and preventive efforts specific to those groups that are clearly at greater risk. C1 NIAAA, Div Biometry & Epidemiol, Bethesda, MD 20892 USA. RP Hanna, EZ (reprint author), NIAAA, Div Biometry & Epidemiol, 6000 Execut Blvd,Suite 514, Bethesda, MD 20892 USA. NR 30 TC 14 Z9 14 U1 1 U2 1 PU ABLEX PUBL CORP PI STAMFORD PA 100 PROSPECT ST, PO BOX 811, STAMFORD, CT 06904-0811 USA SN 0899-3289 J9 J SUBST ABUSE JI J. SUBST. ABUSE PY 1997 VL 9 BP 111 EP 125 DI 10.1016/S0899-3289(97)90010-9 PG 15 WC Substance Abuse SC Substance Abuse GA 104LT UT WOS:000075017000009 PM 9494943 ER PT J AU Crowley, MF Darden, TA Cheatham, TE Deerfield, DW AF Crowley, MF Darden, TA Cheatham, TE Deerfield, DW TI Adventures in improving the scaling and accuracy of a parallel molecular dynamics program SO JOURNAL OF SUPERCOMPUTING LA English DT Article DE Ewald; parallel; T3E; simulation; electrostatic; molecular dynamics; PME ID PARTICLE MESH EWALD; SIMULATION; SYSTEMS AB We report our work to parallelize the Particle Mesh Ewald (PME) method to compute the long-range electrostatic interactions in the molecular dynamics program AMBER and to extend the scalability of the PME method to hundreds of processors. C1 NIEHS, RES TRIANGLE PK, NC 27709 USA. RP Crowley, MF (reprint author), PITTSBURGH SUPERCOMP CTR, 4400 5TH AVE, PITTSBURGH, PA 15213 USA. RI crowley, michael/A-4852-2013 OI crowley, michael/0000-0001-5163-9398 NR 20 TC 49 Z9 49 U1 0 U2 4 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0920-8542 J9 J SUPERCOMPUT JI J. Supercomput. PY 1997 VL 11 IS 3 BP 255 EP 278 DI 10.1023/A:1007907925007 PG 24 WC Computer Science, Hardware & Architecture; Computer Science, Theory & Methods; Engineering, Electrical & Electronic SC Computer Science; Engineering GA YE691 UT WOS:A1997YE69100004 ER PT J AU Chen, CY Hanson, SR Keefer, LK Saavedra, JE Davies, KM Hutsell, TC Hughes, JD Ku, DN Lumsden, AB AF Chen, CY Hanson, SR Keefer, LK Saavedra, JE Davies, KM Hutsell, TC Hughes, JD Ku, DN Lumsden, AB TI Boundary layer infusion of nitric oxide reduces early smooth muscle cell proliferation in the endarterectomized canine artery SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT Annual Symposium of the Association-of-Veterans-Administration-Surgeons CY APR 28-30, 1996 CL DETROIT, MI SP Assoc Vet Adm Surgeons ID CONTROLLED BIOLOGICAL RELEASE; RIBONUCLEOTIDE REDUCTASE; ADENOCARCINOMA CELLS; CYCLIC-GMP; INJURY; VASODILATORS; MECHANISMS; INHIBITION; THROMBOSIS; NUCLEOPHILES AB To evaluate the direct effect of nitric oxide (NO) on vascular smooth muscle cell (SMC) proliferation in vivo, we used an expanded polytetrafluoroethylene (ePTFE)-based local infusion device to deliver an NO donor, proline/NO (PROLI/NO), to the luminal boundary layer of endarterectomized artery and the distal anastomosis of the graft in a canine model. Once delivered to the blood, PROLI/NO releases NO by a mechanism involving pH-dependent decomposition. Six dogs underwent bilateral femoral artery endarterectomies. ePTFE infusion devices, blindly primed with PROLI/NO to one artery or proline to the contralateral vessel, were anastomosed proximal to the injured segments so that each animal served as its own control. PROLI/NO or proline was continuously delivered for 7 days from an osmotic reservoir, through the wall of the graft infusion device. Euthanasia was carried out at 7 days, and the processed specimens were blindly analyzed for SMC proliferation at both graft anastomoses and endarterectomized segments by a bromodeoxyuridine index assay. All dogs survived with no clinical side effects. In comparing the treated and control vessels, NO released from PROLI/NO significantly reduced SMC proliferation by 43% (13.24 +/- 1.24% versus 23.24 +/- 1.01%, P = 0.004) at the distal anastomoses and by 68% (10.58 +/- 1.63% versus 25.17 +/- 3.39%, P = 0.007) at endarterectomized segments. However, there was no significant difference in blood flow measurements between treated and control arteries (56.25 +/- 6.50 ml/min versus 46.50 +/- 3.20 ml/min, P = 0.094). These data demonstrate that local boundary layer infusion of NO released from PROLI/NO significantly reduces SMC proliferation in injured arteries with no effect on regional blood flow. This study suggests a new strategy to inhibit early SMC proliferation in injured arteries and probably to control intimal hyperplastic lesion formation in the manipulated vessels. (C) 1997 Academic Press. C1 VET AFFAIRS MED CTR, DEPT SURG, DECATUR, GA 30033 USA. EMORY UNIV, SCH MED, ATLANTA, GA 30322 USA. NCI, FREDERICK CANC RES & DEV CTR, FREDERICK, MD 21702 USA. GEORGE MASON UNIV, DEPT CHEM, FAIRFAX, VA 22030 USA. COMEDICUS INC, COLUMBIA HTS, MN 55421 USA. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 FU NHLBI NIH HHS [HL 48667, HL 31469] NR 41 TC 23 Z9 24 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 0022-4804 J9 J SURG RES JI J. Surg. Res. PD JAN PY 1997 VL 67 IS 1 BP 26 EP 32 DI 10.1006/jsre.1996.4915 PG 7 WC Surgery SC Surgery GA WK047 UT WOS:A1997WK04700006 PM 9070177 ER PT J AU Sharaf, BL Williams, DO Miele, NJ McMahon, RP Stone, PH Bjerregaard, P Davies, R Goldberg, AD Parks, M Pepine, CJ Sopko, G Conti, CR AF Sharaf, BL Williams, DO Miele, NJ McMahon, RP Stone, PH Bjerregaard, P Davies, R Goldberg, AD Parks, M Pepine, CJ Sopko, G Conti, CR TI A detailed angiographic analysis of patients with ambulatory electrocardiographic ischemia: Results from the Asymptomatic Cardiac Ischemia Pilot (ACIP) study angiographic core laboratory SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID SILENT MYOCARDIAL ISCHEMIA; CORONARY-ARTERY DISEASE; STABLE ANGINA-PECTORIS; UNSTABLE ANGINA; PROGNOSTIC-SIGNIFICANCE; INFARCTION; TRANSIENT; MORTALITY; DEATH; ATHEROSCLEROSIS AB Objectives. The purpose of this Asymptomatic Cardiac Ischemia Pilot (ACIP) data bank study was to characterize angiographic features of coronary pathology of patients enrolled in the ACIP study. Background. Ischemia during ambulatory electrocardiographic (AECG) monitoring is associated with increased morbidity and mortality. Reports relating AECG ischemia to severity or complexity of coronary artery disease are few in number and small in size and have produced conflicting results. Methods. Coronary angiograms from patients with asymptomatic AECG ischemia enrolled in the ACIP study were reviewed at a central fore laboratory. Quantitative measurement of percent stenosis and Thrombolysis in Myocardial Infarction how grades were used to assess the severity of coronary artery disease. Lesions were also evaluated for the presence of intracoronary thrombus, ulceration and lumen contour as indicators of stenosis complexity. In addition, comparisons were made with 27 patients screened for the ACIP study, but who were found ineligible because they did not have AECG ischemia on 48-h Holter monitoring. Results. A total of 329 (75%) of 439 patients with AECG ischemia had multivessel coronary artery disease. Proximal stenoses greater than or equal to 50% diameter reduction were common in patients with AECG ischemia (62.2%), as were proximal stenoses greater than or equal to 70% (38.7%). Features suggesting complex plaque were found in 50.1% of patients with AECG ischemia. Conclusions. Multivessel coronary artery disease, severe proximal stenoses and features of complex plaque were observed frequently in patients who exhibited AECG ischemia. The presence of severe and complex coronary artery disease may explain, in part, the increased risk for adverse outcome associated with ischemia during activities of daily life. C1 BROWN UNIV,RHODE ISL HOSP,PROVIDENCE,RI 02903. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. ST LOUIS UNIV,MED CTR,ST LOUIS,MO. OTTAWA HEART INST,OTTAWA,ON,CANADA. HENRY FORD HOSP,DETROIT,MI 48202. UNIV ALABAMA,BIRMINGHAM,AL. UNIV FLORIDA,GAINESVILLE,FL. NHLBI,BETHESDA,MD 20892. RP Sharaf, BL (reprint author), MARYLAND MED RES INST,AC1P CLIN COORDINATING CTR,600 WYNDHURST AVE,BALTIMORE,MD 21210, USA. FU NHLBI NIH HHS [HV-90-07, HV-91-05, HV-90-08] NR 34 TC 47 Z9 49 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JAN PY 1997 VL 29 IS 1 BP 78 EP 84 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA WB902 UT WOS:A1997WB90200012 PM 8996298 ER PT J AU Slavkin, HC AF Slavkin, HC TI Emerging and re-emerging infectious diseases: A biological evolutionary drama SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Article RP Slavkin, HC (reprint author), NIDR,31 CTR DR,MSC 2290,BLDG 31,ROOM 2C39,BETHESDA,MD 20892, USA. NR 0 TC 4 Z9 6 U1 0 U2 0 PU AMER DENTAL ASSN PI CHICAGO PA 211 E CHICAGO AVE, CHICAGO, IL 60611 SN 0002-8177 J9 J AM DENT ASSOC JI J. Am. Dent. Assoc. PD JAN PY 1997 VL 128 IS 1 BP 108 EP & PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA WC302 UT WOS:A1997WC30200026 PM 9002409 ER PT J AU Newman, AB Enright, PL Manolio, TA Haponik, EF Wahl, PW AF Newman, AB Enright, PL Manolio, TA Haponik, EF Wahl, PW TI Sleep disturbance, psychosocial correlates, and cardiovascular disease in 5201 older adults: The cardiovascular health study SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID MINI-MENTAL STATE; HEART-DISEASE; PREVALENCE; BENZODIAZEPINE; DEPRESSION; POPULATION; DISORDERS; WAKING; STROKE; SCALE AB OBJECTIVES: To describe the prevalence of self reported sleep disturbances in older men and women and to describe their relationships with health status and cardiovascular diseases (CVD). DESIGN: Cross-sectional study of sleep disturbance, CVD, general health, psychosocial factors, physical function, and use of psychotropic medications. SETTING: Participants of the Cardiovascular Health Study, 5201 adults aged 65 and older recruited from a random sample of noninstitutionalized Medicare enrollees in four US communities. MEASURES: Self-reported sleep disturbances and standardized questionnaires for cardiopulmonary symptoms and diseases, depression, social support, activities of daily living, physical activity, cognitive function, and current medications, spirometry, EGG, echocardiography, and carotid ultrasound. RESULTS: Women were twice as likely as men to report difficulty falling asleep (30% vs 14%). Daytime sleepiness, difficulty falling asleep, and frequent awakenings increased in prevalence with age. All symptoms were related strongly to depression. Symptoms of daytime sleepiness were also related strongly to poor health and limitations in activities of daily living in men and women. In multivariate analysis, men taking benzodiazepines were likely to report difficulty falling asleep and daytime sleepiness, whereas women taking benzodiazepines reported difficulty falling asleep and waking up too early. After accounting for these factors, the only cardiovascular disease independently associated with sleep disturbances was angina. Men and women with confirmed angina were 1.6 times more likely to report trouble falling asleep. Independent relationships between sleep disturbances and cardiovascular risk factors such as obesity, hypertension, smoking, and diabetes were relatively weak and inconsistent, though smokers were less likely to report frequent awakenings. CONCLUSIONS: Sleep disturbances are relatively common in older men and women and are associated with poor health, depression, angina, limitations in activities of daily living, and the use of benzodiazepines. C1 UNIV ARIZONA,RESP SCI CTR,TUCSON,AZ. NHLBI,DIV EPIDEMIOL & CLIN APPLICAT,BETHESDA,MD 20892. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT MED,WINSTON SALEM,NC 27109. UNIV WASHINGTON,DEPT BIOSTAT,SEATTLE,WA 98195. RP Newman, AB (reprint author), UNIV PITTSBURGH,DIV GERIATR MED,DEPT MED,3520 5TH AVE,KEYSTONE BLDG,SUITE 300,PITTSBURGH,PA 15213, USA. RI Newman, Anne/C-6408-2013 OI Newman, Anne/0000-0002-0106-1150 FU NHLBI NIH HHS [N01-HC-85079] NR 46 TC 186 Z9 195 U1 1 U2 9 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1997 VL 45 IS 1 BP 1 EP 7 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA WB733 UT WOS:A1997WB73300001 PM 8994480 ER PT J AU Santanello, NC Barber, BL Applegate, WB Elam, J Curtis, C Hunninghake, DB Gordon, DJ AF Santanello, NC Barber, BL Applegate, WB Elam, J Curtis, C Hunninghake, DB Gordon, DJ TI Effect of pharmacologic lipid lowering on health-related quality of life in older persons: Results from the cholesterol reduction in seniors program (CRISP) pilot study SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID HIGH BLOOD CHOLESTEROL; OF-LIFE; HYPERTENSION AB OBJECTIVE: To determine the effect of lovastatin therapy on health-related quality of life in older persons. DESIGN: A prospective, randomized, double blind clinical trial. SETTING: Four university medical center research clinics. PARTICIPANTS: There were 431 men and women, primarily 65 years of age or older, with low density lipoprotein levels greater than 159 mg/dL and less than 221 mg/dL. Exclusion criteria included a Mini-Mental state score less than 24 or presence of recent cardiovascular events or other serious chronic disease likely to shorten survival. INTERVENTION: All participants were administered the National Cholesterol Education Program step one diet and were then randomized to placebo, 20 mg lovastatin, or 40 mg lovastatin. MEASUREMENTS: Areas of health-related quality of life assessed in the Cholesterol Reduction in Seniors Program (CRISP) included: (1) physical functioning, (2) sleep behavior, (3) social support, (4) depression, (5) cognitive function, and (6) health perception. Three global change questions asked the patients to judge change in general health since starting the study diet or the study medication and change in ability to function or care for self. Although some patients were followed for a total of 12 months, all participants were followed for 6 months, and 6-month data have been used for the primary analysis in this paper. RESULTS: Patients treated with 20 mg of lovastatin had a 17% and 24% reduction in total cholesterol and LDL-cholesterol, respectively. Patients treated with the 40-mg lovastatin dose achieved reductions of 20% for total cholesterol and 28% for LDL-cholesterol. Complaints of possible adverse events were remarkably similar in the two active treatment groups and the placebo group. At 6 months of follow-up there were no statistically significant differences found in mean change scores from baseline between treatment groups on the health-related quality of life measures (physical functioning, sleep, social support, depression, cognitive function scales, health perception) or global questions. CONCLUSIONS: This study demonstrates that lovastatin was extremely well tolerated in an older cohort, both with regard to symptoms and to health-related quality of life. C1 UNIV TENNESSEE,MEMPHIS,TN. UNIV N CAROLINA,CHAPEL HILL,NC 27515. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NHLBI,DIV HEART & VASC DIS,BETHESDA,MD 20892. RP Santanello, NC (reprint author), MERCK RES LABS,BL2-3,POB 4,W POINT,NY, USA. NR 27 TC 63 Z9 64 U1 2 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1997 VL 45 IS 1 BP 8 EP 14 PG 7 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA WB733 UT WOS:A1997WB73300002 PM 8994481 ER PT J AU Bradley, E Walker, L Blechner, B Wetle, T AF Bradley, E Walker, L Blechner, B Wetle, T TI Assessing capacity to participate in discussions of advance directives in nursing homes: Findings from a study of the patient self determination act SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID INFORMED CONSENT; PREFERENCES; DECISIONS; INCREASE; LIFE AB OBJECTIVE: To better understand the implementation of the Patient Self-Determination Act (PSDA) in long-term care, with a focus on the informing process as it affects advance directives. DESIGN: Retrospective cohort study of nursing home admissions, using medical record reviews, and a companion qualitative survey using key informant interviews. SETTING: Eleven nursing homes in Connecticut. PARTICIPANTS: A total of 600 residents randomly selected from six randomly chosen nursing homes and 19 key informants selected from five purposely sampled nursing homes in Connecticut. MEASURES: Institutional compliance with the PSDA requirement to provide written information about advance directives at admission and aspects of the informing process, including to whom the information is given. RESULTS: Compliance with the PSDA requirement to provide information at admission is high (90.7 of admissions in the post-PSDA cohort received information within 1 week of admission). However, in nearly 70% of admissions in which information was provided, someone other than the residents received the information. Staff often cited the resident's cognitive impairment as a reason for excluding residents from this informing process. However, even among those residents judged to be alert and oriented at admission, someone other than the resident received the information 47.7% of the time. CONCLUSIONS: Substantial numbers of residents may be inappropriately excluded from participating in discussions because of difficulties in determining decisional capacity to discuss future treatment wishes. The research highlights the difficulties of enhancing resident participation and autonomy in long-term care through procedural regulations such as the PSDA. More reliable methods of determining resident decisional capacity are needed to integrate the full intent of the PSDA into clinical practice in long-term care. C1 INST LIVING,BRACELAND CTR MENTAL HLTH & AGING,HARTFORD,CT. UNIV CONNECTICUT,SCH MED,DEPT COMMUNITY MED & HLTH CARE,FARMINGTON,CT. NIA,NIH,BETHESDA,MD 20892. RP Bradley, E (reprint author), YALE UNIV,DEPT EPIDEMIOL & PUBL HLTH,SCH MED,60 COLL ST,NEW HAVEN,CT 06520, USA. FU AHRQ HHS [1T32HS00052] NR 32 TC 20 Z9 20 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1997 VL 45 IS 1 BP 79 EP 83 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA WB733 UT WOS:A1997WB73300014 PM 8994493 ER PT J AU Fried, LP Guralnik, JM AF Fried, LP Guralnik, JM TI Disability in older adults: Evidence regarding significance, etiology, and risk SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID BODY-MASS INDEX; PHYSICAL-DISABILITY; FUNCTIONAL STATUS; ELDERLY PATIENTS; FRAMINGHAM DISABILITY; MAINTAINING MOBILITY; MEDICAL CONDITIONS; RANDOMIZED TRIAL; HIP FRACTURE; LATE-LIFE AB OBJECTIVES: This article synthesizes and assesses current evidence about the importance of physical disability to older adults. It then considers the applications of research findings to clinical geriatrics practice. RESULTS: Physical disability is a major adverse health outcome associated with aging. Certain subgroups of older adults, including individuals with mobility difficulty, with preclinical functional changes, and persons who are hospitalized, are at particularly high risk of becoming disabled or experiencing disability progression. The major underlying causes of physical disability are chronic diseases, including both acute events, such as hip fracture and stroke and slowly progressive diseases such as arthritis and heart disease. These diseases appear to have task-specific effects; understanding this may assist in setting treatment and prevention goals. Comorbidity, particularly certain combinations of chronic diseases, is a strong risk factor for disability in itself. Recent trials indicate that clinical interventions may be able to prevent onset or progression of disability. CONCLUSIONS: Available evidence now suggests clinical approaches to both treatment and prevention of disability and directions for defining optimal clinical care for the future. C1 JOHNS HOPKINS MED INST,DEPT MED & EPIDEMIOL,BALTIMORE,MD 21205. NIA,DEMOG & BIOMETRY PROGRAM,BETHESDA,MD 20892. NR 88 TC 473 Z9 484 U1 3 U2 30 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1997 VL 45 IS 1 BP 92 EP 100 PG 9 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA WB733 UT WOS:A1997WB73300017 PM 8994496 ER PT J AU Ackerman, MJ Humphreys, BL AF Ackerman, MJ Humphreys, BL TI A focus on telehealth SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Editorial Material RP Ackerman, MJ (reprint author), NATL LIB MED,BLDG 38A-B1N-30,8600 ROCKVILLE PIKE,BETHESDA,MD 20894, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PD JAN-FEB PY 1997 VL 4 IS 1 BP 68 EP 68 PG 1 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA WB909 UT WOS:A1997WB90900010 ER PT J AU Hatton, C Woods, J Dhir, R Bastacky, S Epstein, J Miller, G Greenson, J Wojno, K Becich, M AF Hatton, C Woods, J Dhir, R Bastacky, S Epstein, J Miller, G Greenson, J Wojno, K Becich, M TI Application of UMLS indexing systems to a WWW-based tool for indexing of digital images SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article C1 Univ Pittsburgh, Med Ctr, Dept Pathol, Pittsburgh, PA 15260 USA. Natl Lib Med, Cognit Sci Branch, Bethesda, MD 20894 USA. UPMC, Dept Pathol, Pittsburgh, PA USA. Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21218 USA. Univ Colorado, Dept Pathol, Boulder, CO 80309 USA. Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA. RP Hatton, C (reprint author), Univ Pittsburgh, Med Ctr, Dept Pathol, Pittsburgh, PA 15260 USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1997 SU S BP 420 EP 423 PG 4 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA V3182 UT WOS:000171774300085 ER PT J AU Bidgood, WD AF Bidgood, WD TI Documenting the information content of images SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article AB A standards-based message and terminology architecture has been specified to enable large-scale open and non-proprietary interchange of imaging-procedure descriptions and image-interpretation reports providing semantically-rich linkage of linguistic and non-linguistic information. The DICOM Structured Reporting Supplement, now available for trial use, embodies this interdependent message/terminology architecture. A DICOM Structured report object is a self-describing information structure that can be tailored to support diverse clinical observation reporting applications by utilization of templates and context-dependent terminology from an external message/terminology mapping resource such as the SNOMED DICOM Microglossary (SDM), HL7 Vocabulary, or Terminology Resource for Message Standards (TeRMS). C1 Duke Univ, Ctr Healthcare Informat, Durham, NC 27706 USA. US Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD USA. RP Bidgood, WD (reprint author), Duke Univ, Ctr Healthcare Informat, Durham, NC 27706 USA. NR 19 TC 3 Z9 3 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1997 SU S BP 424 EP 428 PG 5 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA V3182 UT WOS:000171774300086 ER PT J AU Korman, LY Bidgood, WD AF Korman, LY Bidgood, WD TI Representation of the Gastrointestinal Endoscopy Minimal Standard Terminology (c) in the SNOMED DICOM Microglossary SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article AB In Gastroenterology, endoscopic images and interpretation reports are essential elements of the patient record. The Digital Imaging and Communications in Medicine (DICOM Visible Light and Structured Reporting Standards provide a standard representation of images and reports. However, the message standards are not sufficient in themselves. Controlled terminology is needed to enable interchange of patient records and to facilitate the pooling of multi-center data for large-scale outcomes studies and clinical research. The ASGE has joined with European and Japanese colleagues to develop and publish a lexicon of endoscopic terminology. The lexicon is being tested now in a multi-center trial. In addition, the ASGE is collaborating with the DICOM Standards Committee to transform the endoscopic lexicon into a database structure that is suitable for use with the DICOM Visible Light and Structured Reporting Standards. The combination of an internationally accepted, tested and non-proprietary lexical standard and a DICOM message standard supporting endoscopic images and reports represents a powerful tool for clinicians to improve communication, research and the quality of care. C1 George Washington Univ, Sch Med, Vet Adm Med Ctr, Washington, DC 20052 USA. Georgetown Univ, Sch Med, Washington, DC USA. Amer Soc Gastrointestinal Endoscopy, Manchester, MA 01944 USA. Duke Univ, Med Ctr, Dept Med Informat, Durham, NC USA. Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, NIH, Bethesda, MD USA. Amer Coll Radiol, Reston, VA 20191 USA. RP Korman, LY (reprint author), George Washington Univ, Sch Med, Vet Adm Med Ctr, Washington, DC 20052 USA. NR 15 TC 0 Z9 0 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1997 SU S BP 434 EP 438 PG 5 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA V3182 UT WOS:000171774300088 ER PT J AU Aronson, AR Rindflesch, TC AF Aronson, AR Rindflesch, TC TI Query expansion using the UMLS (R) Metathesaurus (R) SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article AB Recent work has demonstrated the importance of query expansion for improving retrieval effectiveness when applying statistically-based systems to MEDLINE(R) citations. The research has suggested the use of retrieval feedback for enhancing the original text of users' queries. As an alternative method of query expansion, we propose the use of the MetaMap program for associating UMLS Metathesaurus concepts with the original query. Our experiments show that query expansion based on MetaMap compares favorably with retrieval feedback. We conclude that the optimal strategy would be to combine the two techniques. C1 Natl Lib Med, Bethesda, MD 20894 USA. RP Aronson, AR (reprint author), Natl Lib Med, Bethesda, MD 20894 USA. NR 13 TC 14 Z9 14 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1997 SU S BP 485 EP 489 PG 5 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA V3182 UT WOS:000171774300098 ER PT J AU McCray, AT Cheh, ML Bangalore, AK Rafei, K Razi, AM Divita, G Stavri, PZ AF McCray, AT Cheh, ML Bangalore, AK Rafei, K Razi, AM Divita, G Stavri, PZ TI Conducting the NLM/AHCPR Large Scale Vocabulary Test: A distributed Internet-based experiment SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article AB The Large Scale Vocabulary Test, sponsored by the National Library of Medicine (NLM) and the Agency for Health Care Policy and Research (AHCPR), was conducted to determine the extent to which a combination of existing health-related terminologies cover vocabulary needed in health care information systems. The test was conducted over the Internet using a sophisticated World Wide Web interface with over 60 participants and over 40,000 terms submitted This paper discusses the issues encountered in the design and execution of the experiment, including the design of the interface and the issues of recruitment, training, and guidance of remote participants over the Internet. Test data are currently undergoing expert review. Upon completion of the expert review, the results of the test will be fully reported. C1 Natl Lib Med, Bethesda, MD 20894 USA. RP McCray, AT (reprint author), Natl Lib Med, Bethesda, MD 20894 USA. NR 12 TC 0 Z9 0 U1 0 U2 1 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1997 SU S BP 560 EP 564 PG 5 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA V3182 UT WOS:000171774300113 ER PT J AU Mori, AR Galeazzi, E Consorti, F Bidgood, WD AF Mori, AR Galeazzi, E Consorti, F Bidgood, WD TI Conceptual schemata for terminology: A continuum from headings to values in patient records and messages SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION LA English DT Article AB We developed a technique of reverse engineering to extract a conceptual schema - also called "categorial structure" in the European standard CEN ENV 12264 (MoSe) - from a set of terminological phrases. The technique was originally applied to coding systems, ie. to large value sets. We applied this technique to subsets of two new terminological resources for message standards: headings of patient record from Clinical LOINC and names of "Context Groups" for structured reporting from SNOMED DICOM Microglossary (SDM). Both sources provide context-independent names for message fields and domains of admitted values. Therefore conceptual schemata on the potential content for afield are compatible with the ones on names of the fields themselves. Both kinds of schemata can be compared and integrated with conceptual schemata for the information system that manages the patient record. This continuity in the schemata allows the coupling of applications with different organization of data, and will facilitate mapping from an application to standard messages and viceversa. Moreover, the simplified representation produced according the MoSe approach is easy to understand by healthcare operators, allowing their progressive involvement in cooperative efforts of design, discussion and validation of the schemata. C1 Univ Roma La Sapienza, Clin Chirurg 4, Rome, Italy. Natl Lib Med, Bethesda, MD USA. Duke Univ, Med Ctr, Durham, NC USA. CNR, ITBM, Reparto Informat Med, Rome, Italy. RP Mori, AR (reprint author), CNR, ITBM, Reparto Informat Med, Rome, Italy. NR 14 TC 3 Z9 3 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 USA SN 1067-5027 J9 J AM MED INFORM ASSN JI J. Am. Med. Inf. Assoc. PY 1997 SU S BP 650 EP 654 PG 5 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications; Information Science & Library Science; Medical Informatics SC Computer Science; Information Science & Library Science; Medical Informatics GA V3182 UT WOS:000171774300131 ER PT J AU Brull, LP Heerma, W ThomasOates, J Haverkamp, J Kovacik, V Kovac, P AF Brull, LP Heerma, W ThomasOates, J Haverkamp, J Kovacik, V Kovac, P TI Loss of internal 1->6 substituted monosaccharide residues from underivatized and per-O-methylated trisaccharides SO JOURNAL OF THE AMERICAN SOCIETY FOR MASS SPECTROMETRY LA English DT Article ID FAST-ATOM-BOMBARDMENT; TANDEM MASS-SPECTROMETRY; BETA-GLYCOSIDES; INDUCED DISSOCIATION; OLIGOSACCHARIDE CHARACTERIZATION; (1->6)-BETA-D-GALACTOOLIGOSACCHARIDES; FAB; O-(3-DEOXY-3-FLUORO-BETA-D-GALACTOPYRANOSYL)-(1->6)-O-BETA-D-GALACTOPYRA NOSYL-(.; (1->6)-BETA-D-GALACTO-OLIGOSACCHARIDES; SPECTRA AB The fragmentation behavior of [M + H](+) ions of a series of underivatized and per-O-methylated trisaccharides having 1 --> 6 linked residues, of which one or two is a deoxy-fluoro or deoxy residue and thus has a unique mass, has been studied by using collision-induced dissociation fast-atom bombardment mass spectrometry. In addition to the usual fragment ions resulting from glycosidic bond cleavage, fragment ions were observed which must have been generated following an unusual rearrangement process which can be rationalized in terms of the loss of an internal monosaccharide residue. (C) 1997 American Society for Mass Spectrometry C1 SLOVAK ACAD SCI,INST CHEM,BRATISLAVA,SLOVAKIA. NIDDK,NIH,BETHESDA,MD. RP Brull, LP (reprint author), UNIV UTRECHT,DEPT MASS SPECTROMETRY,FAFC WENTGEBOUW,BIJVOET CTR BIOMOL RES,SORBONNELAAN 16,NL-3584 CA UTRECHT,NETHERLANDS. NR 23 TC 61 Z9 62 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1044-0305 J9 J AM SOC MASS SPECTR JI J. Am. Soc. Mass Spectrom. PD JAN PY 1997 VL 8 IS 1 BP 43 EP 49 DI 10.1016/S1044-0305(96)00134-1 PG 7 WC Chemistry, Analytical; Chemistry, Physical; Spectroscopy SC Chemistry; Spectroscopy GA WA210 UT WOS:A1997WA21000007 ER PT J AU Maunsbach, AB Marples, D Chin, E Ning, G Bondy, C Agre, P Nielsen, S AF Maunsbach, AB Marples, D Chin, E Ning, G Bondy, C Agre, P Nielsen, S TI Aquaporin-1 water channel expression in human kidney SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID PROTEIN; LOCALIZATION; SEGMENTS; FAMILY; CHIP AB The pattern of aquaporin-1 water channel protein (AQP1) expression in the human kidney was analyzed by immunocytochemistry using semi-thin and optimized high-resolution immunoelectron microscopy based on freeze-substituted and Lowicryl HM20 embedded tissue. In addition, in situ hybridization was used to determine AQP1 mRNA distribution. Immunoblots revealed a 28-kd band and a 35- to 45-kd band corresponding to unglycosylated and glycosylated AQP1. Glomerular capillary endothelium exhibited extensive AQP1 labeling, whereas glomerular podocytes and Bowman's capsule epithelium were unlabeled. AQP1 was localized in the proximal tubule, including the neck region directly connected to the glomerulus. However, there was a marked difference in the level of expression between cross-sections of the convoluted part and the proximal straight tubules, the latter displaying the most intense labeling. AQP1 labeling continued uninterrupted from the proximal straight tubule into descending thin limbs in outer medulla. Abrupt transitions from heavily labeled to unlabeled segments of thin Limbs were observed, primarily in the inner medulla. This may represent the transition from the water-permeable thin descending limb to the water-impermeable thin ascending limb. In addition, heavy labeling of fenestrated endothelium was also observed in peritubular capillaries in cortex, outer medulla, and inner medulla. Immunolabeling controls were negative. In situ hybridization documented a marked difference in AQP1 mRNA levels within the proximal tubule, with the greatest AQP1 mRNA expression in straight proximal tubules. Glomeruli also showed marked signals, and descending thin limbs exhibited extensive expression in exact concordance with the immunocytochemical results. It was concluded that: (I) AQP1 is present in all proximal tubule segments, including segment 1 and the neck region, but there is a pronounced difference in expression levels with respect to both protein and mRNA levels; (2) AQP1 labeling is observed in the endothelium of fenestrated peritubular capillaries, as well as fenestrated glomerular capillaries; (3) AQP1 labeling continues directly from proximal tubules to descending thin limbs; and (4) abrupt transitions from labeled to unlabeled thin Limb epithelium are noted. C1 UNIV LEEDS,DEPT PHYSIOL,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND. NICHHD,NIH,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,SCH MED,DEPT MED & BIOL CHEM,BALTIMORE,MD. RP Maunsbach, AB (reprint author), AARHUS UNIV,INST ANAT,DEPT CELL BIOL,DK-800 AARHUS C,DENMARK. NR 27 TC 88 Z9 94 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD JAN PY 1997 VL 8 IS 1 BP 1 EP 14 PG 14 WC Urology & Nephrology SC Urology & Nephrology GA WD255 UT WOS:A1997WD25500001 PM 9013443 ER PT J AU Apostol, E Ecelbarger, CA Terris, J Bradford, AD Andrews, P Knepper, MA AF Apostol, E Ecelbarger, CA Terris, J Bradford, AD Andrews, P Knepper, MA TI Reduced renal medullary water channel expression in puromycin aminonucleoside-induced nephrotic syndrome SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article ID KIDNEY COLLECTING DUCT; RAT-KIDNEY; MOLECULAR-CLONING; AQUAPORIN FAMILY; VASOPRESSIN; PLASMA; PERMEABILITY; PROTEINURIA; EXCRETION; MEMBRANE AB The aquaporins are molecular water channels that mediate transcellular water transport across water-permeable epithelia. To investigate the cause of the concentrating defect in the nephrotic syndrome, immunoblotting using membrane fractions from inner medulla was utilized to assess the level of expression of four aquaporin water channels in vehicle-treated versus puromycin aminonucleoside (PAN)-treated rats. Scanning electron microscopy demonstrating loss of glomerular foot processes and measurements of urinary protein excretion confirmed the efficacy of the PAN treatment. In rats receiving PAN, there was an increase in plasma vasopressin, without a change in plasma sodium concentration. Inner medullary tissue hypertonicity was sustained in PAN-treated rats while the urinary osmolality was low, pointing to defective osmotic equilibration across the collecting ducts in PAN-nephrosis. Among collecting duct aquaporins, there was an 87% decrease in aquaporin-2 expression and a 70% decrease in aquaporin-3 expression in the inner medulla, whereas aquaporin-4 expression was unaltered. Transmission electron microscopy of the inner medullary collecting ducts of PAN-treated rats showed normal-appearing cells. Thus, PAN-nephrosis is associated with an extensive downregulation of collecting duct water channel expression despite increased circulating vasopressin, providing an explanation for the concentrating defect associated with the nephrotic syndrome. C1 NHLBI,KIDNEY & ELECTROLYTE METAB LAB,NIH,BETHESDA,MD 20892. GEORGETOWN UNIV,SCH MED,DEPT CELL BIOL,WASHINGTON,DC. UNIFORMED SERV UNIV HLTH SCI,DEPT PHYSIOL,BETHESDA,MD 20814. FU NHLBI NIH HHS [HL09005]; NIDDK NIH HHS [DK-08832]; PHS HHS [5T346M07651] NR 37 TC 83 Z9 84 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD JAN PY 1997 VL 8 IS 1 BP 15 EP 24 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA WD255 UT WOS:A1997WD25500002 PM 9013444 ER PT J AU Gottschalk, CW Knepper, MA AF Gottschalk, CW Knepper, MA TI Micropuncture study of the mammalian urinary concentrating mechanism: Evidence for the countercurrent hypothesis - Comments SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Editorial Material ID MEDULLARY COLLECTING DUCT; THICK ASCENDING LIMB; MULTIPLICATION SYSTEM; INNER MEDULLA; TRANSPORT; WATER; HENLE; MODEL; NACL; UREA RP Gottschalk, CW (reprint author), NHLBI,KIDNEY & ELECTROLYTE METAB LAB,NIH,BETHESDA,MD 20892, USA. NR 16 TC 5 Z9 5 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD JAN PY 1997 VL 8 IS 1 BP 153 EP & PG 6 WC Urology & Nephrology SC Urology & Nephrology GA WD255 UT WOS:A1997WD25500019 PM 9013460 ER PT J AU Weed, DL AF Weed, DL TI Methodologic guidelines for review papers SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID SYSTEMATIC REVIEWS; ARTICLES; SCIENCE; QUALITY RP Weed, DL (reprint author), NCI,PREVENT ONCOL BRANCH,DIV CANC PREVENT & CONTROL,NIH,EXECUT PLAZA S,RM T-41,BETHESDA,MD 20892, USA. NR 21 TC 48 Z9 49 U1 0 U2 3 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JAN 1 PY 1997 VL 89 IS 1 BP 6 EP 7 PG 2 WC Oncology SC Oncology GA VZ936 UT WOS:A1997VZ93600005 ER PT J AU Lubin, JH Boice, JD AF Lubin, JH Boice, JD TI Lung cancer risk from residential radon: Meta-analysis of eight epidemiologic studies SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID INDOOR RADON; DOSE-RATE; EXPOSURE; MINERS; WOMEN; METAANALYSIS; STATES; RADIATION; ERRORS; BIASES AB Background: Studies of underground miners exposed to radioactive radon and its decay products have found that exposure increases risk of lung cancer, Consequently, when radon was found to accumulate in houses, there was concern about the public health impact from exposure to a known carcinogen, Estimates on the basis of studies of underground miners suggest that indoor radon may account for 6000-36 000 lung cancer deaths each year in the United States, Because of differences between working in underground mines and living in houses, estimates are subject to major uncertainties, Numerous case-control studies were launched to assess directly the lung cancer risk from indoor radon, Some studies report positive or weakly positive findings, while others report no increased risk, Thus, the potential hazard from indoor radon remains answered only indirectly through miner studies, experimental animal studies, and cellular studies, Purpose: To provide more information on the risk of lung cancer from indoor radon, we conducted a metaanalysis of all case-control studies that included at least 200 case subjects each and that used long-term indoor radon measurements, Methods: Eight studies were available and included a total of 4263 lung cancer case subjects and 6612 control subjects, From the published results of each study, confounder-adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for categories of radon concentration were obtained, and weighted linear regression analyses were performed, Results: The combined trend in the RR was significantly different from zero (two-sided P =.03), and an estimated RR of 1.14 (95% CI = 1.0-1.3) at 150 Bq/m(3) was found, An influence analysis indicated that no single study dominated the combined results, The exposure-response trend was similar to model-based extrapolations from miners and to RRs computed directly from miners with low cumulative exposures, However, there were significant differences in the study-specific estimates of the exposure response (two-sided P<.001), which were not explained by study differences in percent of the defined exposure interval covered by radon measurements, mean number of residences per subject, and other factors, Conclusions: Meta-analyses are valuable for identifying differences among studies and for summarizing results, but they should be interpreted cautiously when expected RRs are low as with indoor radon exposure, when there is study heterogeneity and where there is the potential for confounding and exposure misclassification, Nonetheless, the results of this meta-analysis suggest that the risk from indoor radon is not likely to be markedly greater than that predicted from miners and indicate that the negative exposure response reported in some ecologic studies is likely due to model misspecification or uncontrolled confounding and can be rejected, Implications: Until ongoing case-control studies of indoor radon are completed and the data are pooled and analyzed, the studies of underground miners remain the best source of data to use to assess risk from indoor radon. This meta-analysis provides support for their general validity. RP Lubin, JH (reprint author), NCI,EPIDEMIOL & BIOSTAT PROGRAM,DIV CANC EPIDEMIOL & GENET,NIH,EXECUT PLAZA N,RM 403,BETHESDA,MD 20892, USA. NR 49 TC 307 Z9 330 U1 6 U2 34 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 JAN 1 PY 1997 VL 89 IS 1 BP 49 EP 57 DI 10.1093/jnci/89.1.49 PG 9 WC Oncology SC Oncology GA VZ936 UT WOS:A1997VZ93600016 PM 8978406 ER PT J AU Gumerlock, PH Chi, SG Shi, XB Voeller, HJ Jacobson, JW Gelmann, EP White, RWD AF Gumerlock, PH Chi, SG Shi, XB Voeller, HJ Jacobson, JW Gelmann, EP White, RWD TI p53 Abnormalities in primary prostate cancer: Single-strand conformation polymorphism analysis of complementary DNA in comparison with genomic DNA SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID POLYMERASE CHAIN-REACTION; POINT MUTATIONS; SSCP ANALYSIS; GENE; CARCINOMA; ACCUMULATION; PROGRESSION; SENSITIVITY; EXPRESSION; PROTEIN AB Background: The reported frequency of mutation of the p53 tumor suppressor gene (also known as TP53) in human carcinomas of the prostate has varied widely, ranging from 3% to 42%, This variability may be a consequence of tumor heterogeneity and/or the use of different methods of analysis, Since p53 mutation has been associated with clinical outcome for a number of cancer types, determination of its true frequency in primary carcinomas of the prostate is important, Purpose: The principal aims of this study were as follows: 1) to validate the utility of detecting p53 gene mutations by means of polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis of complementary DNA (cDNA) (synthesized from prostate tissue RNA and 2) to study the concordance of RNA- and DNA-based PCR-SSCP assays in detecting p53 mutations in individual tumor fragments, Methods: RNA and genomic DNA were isolated by means of standard techniques from specimens of 19 carcinomas of the prostate, selected on the basis of p53 data obtained in a previous analysis of cDNA (indicating that 14 were mutant and five were wild-type), RNA was converted into cDNA by means of reverse transcription (RT); the cDNA was then amplified by means of nonisotopic (i.e., nonradioactive) PCR, and the PCR products were subjected to SSCP analysis in polyacrylamide gels (RT-PCR-SSCP analysis), Genomic DNA was examined by means of SSCP analysis of isotopically labeled ((PO4)-P-32) PCR products (DNA-PCR-SSCP analysis), In both approaches, the protein coding region of the p53 gene was divided into multiple, smaller fragments for study, PCR products exhibiting abnormal migration in SSCP gels were subjected to direct nucleotide sequencing or to cloning and sequencing of multiple clones, Results: RT-PCR-SSCP and DNA-PCR-SSCP identified p53 gene abnormalities in 15 of the 19 selected carcinomas, including one previously reported to be wild-type for p53, Overall, PCR-SSCP analysis identified 18 p53 fragments with abnormalities; three carcinomas showed two abnormalities each, Six (33%) of the 18 abnormalities were detected by both RT-PCR-SSCP and DNA-PCR-SSCP, 10 (56%) were detected by RT-PCR-SSCP alone, and two (11%) were detected by DNA-PCR-SSCP alone, The 18 abnormalities were caused by 20 changes in the sequence of the p53 gene; in one carcinoma, double mutations in two individual p53 exons were identified, Conclusions and Implications: PCR-SSCP analysis of both RNA and DNA allows the detection of more mutations than the analysis of either alone, Some primary carcinomas of the prostate contain more than one altered p53 gene, consistent with the possibility of intratumoral heterogeneity of mutation of this gene, For comprehensive analysis of p53 mutations in carcinomas of the prostate, and perhaps in other tumor tissues, SSCP analysis of cDNA should be used in combination with SSCP analysis of genomic DNA. C1 UNIV CALIF DAVIS,DAVIS CANC CTR,DEPT UROL,SACRAMENTO,CA 95817. GEORGETOWN UNIV,SCH MED,DEPT HEMATOL ONCOL,WASHINGTON,DC. NCI,DIAG & CTR,DIV CANC TREATMENT,CANC DIAG BRANCH,BETHESDA,MD. NCI,COOPERAT PROSTATE NETWORK,BETHESDA,MD 20892. RP Gumerlock, PH (reprint author), UNIV CALIF DAVIS,DAVIS CANC CTR,DEPT INTERNAL MED,DIV HEMATOL ONCOL,CANC & MOL RES LAB,4501 X ST,SACRAMENTO,CA 95817, USA. FU NCI NIH HHS [CA57183, CA57178, CA60098] NR 27 TC 49 Z9 50 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 JAN 1 PY 1997 VL 89 IS 1 BP 66 EP 71 DI 10.1093/jnci/89.1.66 PG 6 WC Oncology SC Oncology GA VZ936 UT WOS:A1997VZ93600018 PM 8978408 ER PT J AU Li, FP Abramson, DH Tarone, RE Kleinerman, RA Fraumeni, JF Boice, JD AF Li, FP Abramson, DH Tarone, RE Kleinerman, RA Fraumeni, JF Boice, JD TI Hereditary retinoblastoma, lipoma, and second primary cancers SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID TUMORS; SARCOMA; BENIGN; GENE C1 HARVARD UNIV,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. CORNELL UNIV,MED CTR,NEW YORK HOSP,OPHTHALM ONCOL CTR,NEW YORK,NY 10021. NCI,DIV CANC EPIDEMIOL & GENET,BETHESDA,MD 20892. OI Kleinerman, Ruth/0000-0001-7415-2478 FU NCI NIH HHS [N01CP05609, N01CP85604] NR 12 TC 33 Z9 33 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 JAN 1 PY 1997 VL 89 IS 1 BP 83 EP 84 DI 10.1093/jnci/89.1.83 PG 2 WC Oncology SC Oncology GA VZ936 UT WOS:A1997VZ93600021 PM 8978411 ER PT J AU Sammel, MD Ryan, LM Legler, JM AF Sammel, MD Ryan, LM Legler, JM TI Latent variable models for mixed discrete and continuous outcomes SO JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES B-METHODOLOGICAL LA English DT Article DE exponential family; hierarchical models; latent trait; mixed effects ID LONGITUDINAL DATA-ANALYSIS; GENERALIZED LINEAR-MODELS; EM ALGORITHM; MAXIMUM-LIKELIHOOD; BINARY AB We propose a latent variable model for mixed discrete and continuous outcomes. The model accommodates any mixture of outcomes from an exponential family and allows for arbitrary covariate effects, as well as direct modelling of covariates on the latent variable. An EM algorithm is proposed for parameter estimation and estimates of the latent variables are produced as a by-product of the analysis. A generalized likelihood ratio test can be used to test the significance of covariates affecting the latent outcomes. This method is applied to birth defects data, where the outcomes of interest are continuous measures of size and binary indicators of minor physical anomalies. Infants who were exposed in utero to anticonvulsant medications are compared with controls. C1 DANA FARBER CANC INST,BOSTON,MA 02115. NCI,BETHESDA,MD 20892. RP Sammel, MD (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 NR 33 TC 146 Z9 147 U1 1 U2 6 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD, OXON, ENGLAND OX4 1JF SN 0035-9246 J9 J ROY STAT SOC B MET JI J. R. Stat. Soc. Ser. B-Methodol. PY 1997 VL 59 IS 3 BP 667 EP 678 DI 10.1111/1467-9868.00090 PG 12 WC Statistics & Probability SC Mathematics GA XD527 UT WOS:A1997XD52700010 ER PT J AU Fidel, PL Romero, R Cutright, J Wolf, N Gomez, R Araneda, H Ramirez, M Yoon, BH AF Fidel, PL Romero, R Cutright, J Wolf, N Gomez, R Araneda, H Ramirez, M Yoon, BH TI Treatment with the interleukin-1 receptor antagonist and soluble tumor necrosis factor receptor Fc fusion protein does not prevent endotoxin-induced preterm parturition in mice SO JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION LA English DT Article DE preterm parturition; endotoxin; murine model; interleukin-1 receptor antagonist; soluble tumor necrosis factor receptor Fc fusion protein ID GROWTH-FACTOR-BETA; ACUTE PYELONEPHRITIS; T-CELLS; INFECTION; EXPRESSION; INHIBITION; PREGNANCY; LABOR; DELIVERY; FETAL AB OBJECTIVE: To determine whether the administration of anticytokine agents, the interleukin-1 receptor antagonist (IL-1ra) and a soluble tumor necrosis factor receptor Fc fusion protein (sTNFR-Fc), prevents endotoxin-induced preterm delivery in mice. METHODS: C3H/HeN pregnant mice at 15 days of gestation (70% gestation) were randomized to receive phosphate-buffered saline (PBS) or lipopolysaccharide (LPS) (50 mu g/mouse) intraperitoneally (i.p.). Randomly selected PBS- or LPS-treated mice were additionally treated intravenously (i.v.), i.p., or subcutaneously (s.c.) every 3 hours with IL-1ra (1-50 mg) or every 12 hours with sTNFR-Fc (200-400 mu g) beginning 1 hour before LPS injection. Animals were observed for vaginal bleeding and preterm delivery. RESULTS: Mice treated i.p. with 50 mu g LPS (n = 13) had a shorter injection-to-delivery interval than mice treated similarly with PBS (n = 19) (median 13.5 hours, range 10-105 versus median 86.8 hours, range 53-120, respectively, P <.001). Saline-treated mice given 10 mg IL-1ra every 3 hours i.p. (n = 3) or 200 mu g sTNFR-Fc every 12 hours i.v. (n = 4) had similar injection-to-delivery intervals as PBS-treated control mice (median 70 hours, range 70-76 versus median 58 hours, range 50-120, respectively). Similarly, LPS-treated mice given PBS every 3 hours (n = 20) had injection-to-delivery intervals comparable to LPS-treated mice (n = 13) (median 15.5 hours, range 9.8-92 versus median 13.5 hours, range 10-105, respectively). Lipopolysaccharide-treated mice given i.p. injections of 1 (n = 4), 10 (n = 31), or 50 (n = 15) mg of IL-1ra every 3 hours did not have longer injection-to-delivery intervals compared with LPS-treated mice (n = 13) (medians 11.6, 15, 14.5, and 13.5 hours; ranges 10.8-12, 8-95, 11-92, and 10-105, respectively). Lipopolysaccharide-treated mice given i.v. injections of 200 (n = 4) or 400 (n = 9) mu g sTNFR-Fc every 12 hours did not have longer injection-to-delivery intervals compared with LPS-treated mice (n = 8) (medians 23.3, 22.5, and 21.9 hours; ranges 14.8-33, 15-95.5, and 15.5-44, respectively). The median injection-to-delivery interval of LPS-treated mice given both IL-1ra (10 mg) every 3 hours i.p. and sTNFR-Fc (200 mu g) every 12 hours i.v. (n = 5) was riot different from that of LPS-treated mice (median 26 hours, range 24.5-72 versus median 13.5 hours, range 10-105, respectively; P>.05). CONCLUSION: The anticytokine agents IL-1ra and sTNFR-Fc did not prevent preterm delivery or prolong pregnancy in endotoxin-induced preterm labor in mice. Copyright (C) 1997 by the Society for Gynecologic Investigation. C1 WAYNE STATE UNIV,SCH MED,DEPT OBSTET & GYNECOL,DETROIT,MI 48201. NICHHD,PERINATOL RES BRANCH,BETHESDA,MD 20892. SEOUL NATL UNIV,COLL MED,DEPT OBSTET,SEOUL,SOUTH KOREA. SEOUL NATL UNIV,COLL MED,DEPT GYNECOL,SEOUL,SOUTH KOREA. RI Yoon, Bo Hyun/H-6344-2011 NR 43 TC 39 Z9 39 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1071-5576 J9 J SOC GYNECOL INVEST JI J. Soc. Gynecol. Invest. PD JAN-FEB PY 1997 VL 4 IS 1 BP 22 EP 26 DI 10.1016/S1071-5576(96)00060-3 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA WJ697 UT WOS:A1997WJ69700005 PM 9051630 ER PT J AU Pastorino, U Buyse, M Friedel, G Ginsberg, RJ Girard, P Goldstraw, P Johnston, M McCormack, P Pass, H Putnam, JB Cerrina, J Chapelier, A Dartevelle, P Baldeyrou, P Grunenwald, D Bulzebruck, H Schirren, J VogtMoykopf, I Toomes, H vanGeel, AN Cappello, M Rocmans, P Pietraszek, A Sklodowska, M Andreani, S Incarbone, M Ravasi, G Tavecchio, L Ambrogi, V Ricci, C Mineo, T Maggi, G Briccoli, A Gelmini, R Heidari, A Guernelli, N Beltrami, V Bains, MS Burt, ME Martini, N McCormack, PM Rusch, VW Roth, J Holmes, C Temeck, B Marchand, P AF Pastorino, U Buyse, M Friedel, G Ginsberg, RJ Girard, P Goldstraw, P Johnston, M McCormack, P Pass, H Putnam, JB Cerrina, J Chapelier, A Dartevelle, P Baldeyrou, P Grunenwald, D Bulzebruck, H Schirren, J VogtMoykopf, I Toomes, H vanGeel, AN Cappello, M Rocmans, P Pietraszek, A Sklodowska, M Andreani, S Incarbone, M Ravasi, G Tavecchio, L Ambrogi, V Ricci, C Mineo, T Maggi, G Briccoli, A Gelmini, R Heidari, A Guernelli, N Beltrami, V Bains, MS Burt, ME Martini, N McCormack, PM Rusch, VW Roth, J Holmes, C Temeck, B Marchand, P TI Long-term results of lung metastasectomy: Prognostic analyses based on 5206 cases SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article; Proceedings Paper CT 76th Annual Meeting of the American-Association-for-Thoracic-Surgery CY APR 28-MAY 01, 1996 CL SAN DIEGO, CA SP Amer Assoc Thorac Surg ID SOFT-TISSUE SARCOMAS; PULMONARY METASTASES; MEDIAN STERNOTOMY; ADJUVANT CHEMOTHERAPY; SURGICAL-MANAGEMENT; OSTEOGENIC-SARCOMA; RESECTION; SURGERY; TOMOGRAPHY AB Objectives: The International Registry of Lung Metastases was established in 1991 to assess the long-term results of pulmonary metastasectomy, Methods: The Registry has accrued 5206 cases of lung metastasectomy, from 18 departments of thoracic surgery in Europe (n = 13), the United States (n = 4) and Canada (n = 1), Of these patients, 4572 (88%) underwent complete surgical resection. The primary tumor was epithelial in 2260 cases, sarcoma in 2173, germ cell in 363, and melanoma in 328, The disease-free interval was 0 to 11 months in 2199 cases, 12 to 35 months in 1857, and more than 36 months in 1620, Single metastases accounted for 2383 cases and multiple lesions for 2726, Mean follow-up nas 46 months, Analysis was performed by Kaplan-Meier estimates of survival, relative risks of death, and multivariate Cox model, Results: The actuarial survival after complete metastasectomy was 36% at 5 years, 26% at 10 years, and 22% at 15 years (median 35 months); the corresponding values for incomplete resection were 13% at 5 years and 7% at 10 years (median 15 months), Among complete resections, the 5-year survival was 33% for patients with a disease-free interval of 0 to 11 months and 45% for those with a disease-free interval of more than 36 months; 43% for single lesions and 27% for four or more lesions. Multivariate analysis showed a better prognosis for patients with germ cell tumors, disease-free intervals of 36 months or more, and single metastases. Conclusions: These results confirm that lung metastasectomy is a safe and potentially curative procedure, Resectability, disease-free interval, and number of metastases enabled us to design a simple system of classification valid for different tumor types. C1 CTR CHIRURG MARIE LANNELONGUE,INT REGISTRY LUNG METASTASES,PARIS,FRANCE. HOP PORTE CHOISY,INT REGISTRY LUNG METASTASES,PARIS,FRANCE. THORAXKLIN,INT REGISTRY LUNG METASTASES,HEIDELBERG,GERMANY. THORAXCHIRURG CLIN SCILLERHOHE,INT REGISTRY LUNG METASTASES,GERLINGEN,GERMANY. DR DANIEL DEN HOED CANC CTR,INT REGISTRY LUNG METASTASES,NL-3008 AE ROTTERDAM,NETHERLANDS. FREE UNIV BRUSSELS,INT REGISTRY LUNG METASTASES,HOP ERASME,B-1070 BRUSSELS,BELGIUM. IST NAZL TUMORI,INT REGISTRY LUNG METASTASES,I-20133 MILAN,ITALY. UNIV LA SAPIENZA,INT REGISTRY LUNG METASTASES,MILAN,ITALY. UNIV ROMA TOR VERGATA,INT REGISTRY LUNG METASTASES,MILAN,ITALY. UNIV TURIN,INT REGISTRY LUNG METASTASES,OSPED MOLINETTE,TURIN,ITALY. UNIV MODENA,INT REGISTRY LUNG METASTASES,PATOL CHIRURG,I-41100 MODENA,ITALY. OSPED S ORSOLA MALPIGHI,INT REGISTRY LUNG METASTASES,BOLOGNA,ITALY. UNIV G DANNUNZIO,INT REGISTRY LUNG METASTASES,CHIETI,ITALY. MEM SLOAN KETTERING CANC CTR,INT REGISTRY LUNG METASTASES,NEW YORK,NY 10021. UNIV TEXAS,INT REGISTRY LUNG METASTASES,MD ANDERSON CANC CTR,HOUSTON,TX. UNIV CALIF LOS ANGELES,INT REGISTRY LUNG METASTASES,LOS ANGELES,CA. NCI,INT REGISTRY LUNG METASTASES,BETHESDA,MD 20892. MT SINAI HOSP,INT REGISTRY LUNG METASTASES,TORONTO,ON M5G 1X5,CANADA. RP Pastorino, U (reprint author), ROYAL BROMPTON HOSP,INT REGISTRY LUNG METASTASES,SYDNEY ST,LONDON SW3 6NP,ENGLAND. RI Gelmini, Roberta/J-8234-2016; Pastorino, Ugo/C-2712-2017 OI Gelmini, Roberta/0000-0002-8471-710X; Pastorino, Ugo/0000-0001-9974-7902 NR 30 TC 438 Z9 463 U1 1 U2 11 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD JAN PY 1997 VL 113 IS 1 BP 37 EP 47 DI 10.1016/S0022-5223(97)70397-0 PG 11 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA WC267 UT WOS:A1997WC26700005 PM 9011700 ER PT J AU Wahl, SM AF Wahl, SM TI Inflammation and growth factors SO JOURNAL OF UROLOGY LA English DT Article DE inflammation; growth substances; penile induration; fibrosis ID CELL-DEATH APOPTOSIS; FACTOR-BETA; SELECTINS; INTEGRINS; RECEPTORS; MONOCYTES; CYTOKINES; ARTHRITIS; ADHESION; PEPTIDES AB Purpose: Pathways of inflammation culminating in tissue repair and scarring are defined. Materials and Methods: Inflammatory responses were induced in vitro and in vivo to monitor the mechanisms of leukocyte activation, the inflammatory products generated, the resolution of the response and tissue repair. Results: Recruitment and activation of circulating leukocytes at sites of trauma and inflammation are essential to debridement, clearance of infectious organisms and repair of tissue injury. Once activated, infiltrating leukocytes generate a plethora of inflammatory mediators important in host defense. However, failure to clear the original stimulus and resolve the inflammatory response results in persistent release of these mediators, including cytokines, enzymes, eicosanoids, and reactive nitrogen and oxygen intermediates, which can cause tissue damage. Overabundant matrix generation during the chronic repair process may cause fibro-obstructive pathology. Conclusions: Disruption of these pathways, including leukocyte recruitment, may have therapeutic efficacy. RP Wahl, SM (reprint author), NIDR,CELLULAR IMMUNOL SECT,NIH,BETHESDA,MD 20892, USA. NR 22 TC 13 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD JAN PY 1997 VL 157 IS 1 BP 303 EP 305 DI 10.1016/S0022-5347(01)65365-5 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA VW915 UT WOS:A1997VW91500102 PM 8976285 ER PT J AU Hoofnagle, JH Lau, D AF Hoofnagle, JH Lau, D TI New therapies for chronic hepatitis B SO JOURNAL OF VIRAL HEPATITIS LA English DT Article; Proceedings Paper CT Proceedings of the VII International Symposium on Viral Hepatitis CY JAN 25-27, 1996 CL MADRID, SPAIN DE alpha-interferon; cirrhosis; hepatitis B virus; nucleoside analogues; randomized controlled trials ID PLACEBO-CONTROLLED TRIAL; IMMUNODEFICIENCY-VIRUS INFECTION; RANDOMIZED CONTROLLED TRIAL; HUMAN ALPHA-INTERFERON; LYMPHOBLASTOID INTERFERON; LIVER-TRANSPLANTATION; UNITED-STATES; DOUBLE-BLIND; PHASE I/II; REPLICATION AB Currently, the only therapy of proven benefit in chronic hepatitis B is interferon-alpha which leads to a long-term benefit in only one-third of patients. New therapies for hepatitis B fall into three categories: antiviral chemotherapy, immunomodulation with cell-based therapies, vaccines or cytokines, and gene therapy such as with antisense oligonucleotides, ribozymes or viral mutants. The most promising immediate approach to therapy is with the new nucleoside antivirals - lamivudine and famciclovir, These drugs are well absorbed orally, result in profound inhibition of circulating hepatitis B virus, and, in some cases, loss of hepatitis B e antigen and improvement in serum aminotransferases. Controlled trials of long-term famciclovir and lamivudine therapy currently underway aim to show whether these drugs are safe and can provide sustained inhibition of viral replication and attentant improvement in liver disease. RP Hoofnagle, JH (reprint author), NIDDKD, LIVER DIS SECT,DIGEST DIS BRANCH,NIH,BLDG 10, RM 9B16, BETHESDA, MD 20892 USA. NR 71 TC 27 Z9 28 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1352-0504 J9 J VIRAL HEPATITIS JI J. Viral Hepatitis PY 1997 VL 4 SU 1 BP 41 EP 50 DI 10.1111/j.1365-2893.1997.tb00159.x PG 10 WC Gastroenterology & Hepatology; Infectious Diseases; Virology SC Gastroenterology & Hepatology; Infectious Diseases; Virology GA WN971 UT WOS:A1997WN97100007 PM 9097277 ER PT J AU Tabernero, C Zolotukhin, AS Bear, J Schneider, R Karsenty, G Felber, BK AF Tabernero, C Zolotukhin, AS Bear, J Schneider, R Karsenty, G Felber, BK TI Identification of an RNA sequence within an intracisternal-A particle element able to replace Rev-mediated posttranscriptional regulation of human immunodeficiency virus type 1 SO JOURNAL OF VIROLOGY LA English DT Article ID SIMIAN RETROVIRUS TYPE-1; 3' UNTRANSLATED REGION; MOUSE OSTEOCALCIN GENE; VIRAL MESSENGER-RNA; RESPONSIVE ELEMENT; EXPRESSION; PROTEIN; TRANSLATION; PRODUCT; CELLS AB Human immunodeficiency virus type 1 (HIV-1) replication depends on the posttranscriptional regulation by the viral Rev protein and can be replaced with the posttranscriptional RNA control element (CTE) of the type D simian retroviruses. We have identified a sequence which shares only nucleotide sequences of the internal loops and secondary structure with the CTE and which is part of a novel murine intracisternal-A particle (IAP) retroelement, inserted within the transcribed mouse osteocalcin-related gene. This sequence, named CTE(IAP), can replace the Rev-mediated regulation of HIV-1, hence it is a posttranscriptional regulatory element, Related elements have been identified in other IAPs. These results suggest that insertional mutagenesis can affect gene expression by providing a functional posttranscriptional control element. The CTE(IAP) and CTEs of the type D simian retroviruses represent a novel class of RNA elements characterized by unique sequences within the internal loops which are predicted to represent the interaction site,vith cellular factor(s). These findings suggest that such elements may be involved in posttranscriptional regulation of cellular mRNAs. C1 NCI,HUMAN RETROVIRUS PATHOGENESIS GRP,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NCI,HUMAN RETROVIRUS SECT,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT MOL GENET,HOUSTON,TX 77030. NR 48 TC 46 Z9 46 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1997 VL 71 IS 1 BP 95 EP 101 PG 7 WC Virology SC Virology GA VX292 UT WOS:A1997VX29200012 PM 8985327 ER PT J AU Bloom, ME Martin, DA Oie, KL Huhtanen, ME Costello, F Wolfinbarger, JB Hayes, SF AgbandjeMcKenna, M AF Bloom, ME Martin, DA Oie, KL Huhtanen, ME Costello, F Wolfinbarger, JB Hayes, SF AgbandjeMcKenna, M TI Expression of Aleutian mink disease parvovirus capsid proteins in defined segments: Localization of immunoreactive sites and neutralizing epitopes to specific regions SO JOURNAL OF VIROLOGY LA English DT Article ID CANINE HOST-RANGE; B-CELL EPITOPES; NUCLEOTIDE-SEQUENCE; ANTIVIRAL ANTIBODIES; ESCHERICHIA-COLI; VIRUS-STRAINS; IDENTIFICATION; INFECTION; ANTIGEN; SURFACE AB The capsid proteins of the ADV-G isolate of Aleutian mink disease parvovirus (ADV) were expressed in 10 nonoverlapping segments as fusions with maltose-binding protein in pMAL-C2 (pVP1, pVP2a through pVP2i). The constructs were designed to capture the VP1 unique sequence and the portions analogous to the four variable surface loops of canine parvovirus (CPV) in individual fragments (pVP2b, pVP2d, pVP2e, and pVPZg, respectively). The panel of fusion proteins was immunoblotted with sera from mink infected with ADV. Seropositive mink infected with either ADV-TR, ADV-Utah, or ADV-Pullman reacted preferentially against certain segments, regardless of mink genotype or virus inoculum. The most consistently immunoreactive regions were pVP2g, pVP2e, and pVP2f, the segments that encompassed the analogs of CPV surface loops 3 and 4, The VPI unique region was also consistently immunoreactive. These findings indicated that infected mink recognize linear epitopes that localized to certain regions of the capsid protein sequence. The segment containing the hypervariable region (pVP2d), corresponding to CPV loop 2, was also expressed from ADV-Utah, An anti-ADV-G monoclonal antibody and a rabbit anti-ADV-G capsid antibody reacted exclusively with the ADV-G pVP2d segment but not,vith the corresponding segment from ADV-Utah. Mink infected with ADV-TR or ADV-Utah also preferentially reacted with the pVP2d sequence characteristic of that virus. These results suggested that the loop 2 region may contain a type-specific linear epitope and that the epitope may also be specifically recognized by infected mink. Heterologous antisera were prepared against the VP1 unique region and the four segments capturing the variable surface loops of CPV. The antisera against the proteins containing loop 3 or loop 4, as well as the anticapsid antibody, neutralized ADV-G infectivity in vitro and bound to capsids in immune electron microscopy. These results suggested that regions of the ADV capsid proteins corresponding to surface loops 3 and 4 of CPV contain linear epitopes that are located on the external surface of the ADV capsid. Furthermore, these linear epitopes contain neutralizing determinants. Computer comparisons with the CPV crystal: structure suggest that these sequences may be adjacent to the threefold axis of symmetry of the viral particle. C1 NIAID,ROCKY MT LABS,ROCKY MT MICROSCOPY BRANCH,HAMILTON,MT 59840. UNIV WARWICK,DEPT BIOL SCI,COVENTRY CV4 7AL,W MIDLANDS,ENGLAND. RP Bloom, ME (reprint author), NIAID,ROCKY MT LABS,PERSISTENT VIRAL DIS LAB,HAMILTON,MT 59840, USA. NR 60 TC 23 Z9 30 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1997 VL 71 IS 1 BP 705 EP 714 PG 10 WC Virology SC Virology GA VX292 UT WOS:A1997VX29200087 PM 8985402 ER PT J AU Andrews, JM Newbound, GC Oglesbee, M Brady, JN Lairmore, MD AF Andrews, JM Newbound, GC Oglesbee, M Brady, JN Lairmore, MD TI The cellular stress response enhances human T-cell lymphotropic virus type 1 basal gene expression through the core promoter region of the long terminal repeat SO JOURNAL OF VIROLOGY LA English DT Article ID HEAT-SHOCK INDUCTION; TRANSCRIPTIONAL ACTIVATION; LEUKEMIA; LINES AB Viral protein expression is postulated to play a critical role in the pathogenesis of human T-cell lymphotropic virus type 1 (HTLV-1)-associated diseases. Therefore, knowledge of the cellular events which initiate or enhance viral gene expression is important in understanding the mechanism of HTLV-1-induced disease. In this report, we examined the modulation of transcription of the HTLV-1 long terminal repeat (LTR) following induction of the cellular stress response, We demonstrate by both in vitro transcription assays and transient transfections that induction of the stress response increases basal transcription from the LTR. Transient cotransfection assays indicate that stress induction of viral transcription is Tax independent, In addition, we provide evidence that the sequences responsible for the enhanced transcription are -52 through +157 of the U3/R region of the HTLV-I LTR. Finally, our data suggest that the increase in transcription is mediated through an intermediate polymerase II/polymerase III transcriptional complex, demonstrated by the inability to abolish the effect with low concentrations of alpha-amanitin. C1 OHIO STATE UNIV,DEPT VET BIOSCI,COLUMBUS,OH 43210. OHIO STATE UNIV,CTR RETROVIRUS RES,COLUMBUS,OH 43210. OHIO STATE UNIV,ARTHUR JAMES CANC HOSP & RES INST,CTR COMPREHENS CANC,COLUMBUS,OH 43210. NCI,MOL VIROL LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA55185]; NIAID NIH HHS [K11 AI01190] NR 22 TC 14 Z9 14 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JAN PY 1997 VL 71 IS 1 BP 741 EP 745 PG 5 WC Virology SC Virology GA VX292 UT WOS:A1997VX29200094 PM 8985409 ER PT J AU Berardi, A Haxby, JV DeCarli, C Schapiro, MB AF Berardi, A Haxby, JV DeCarli, C Schapiro, MB TI Face and word memory differences are related to patterns of right and left lateral ventricle size in healthy aging SO JOURNALS OF GERONTOLOGY SERIES B-PSYCHOLOGICAL SCIENCES AND SOCIAL SCIENCES LA English DT Article ID CONTINUOUS RECOGNITION MEMORY; AGE-RELATED DIFFERENCES; COMPUTED-TOMOGRAPHY; INTELLECTUAL IMPAIRMENT; HUMAN-BRAIN; ASYMMETRIES; DEMENTIA; ATROPHY; FLUID; TASK AB Discrepancy between face and word memory was measured with experimental continuous recognition tests and compared with right-left asymmetry of lateral ventricle size, measured with volumetric x-ray computed tomography, in 10 young and in 10 elderly subjects. All were right-handed and healthy. Old subjects differed significantly from young subjects on face but not word memory. Old subjects had significantly larger lateral ventricles than did young subjects and more lateral ventricle asymmetry. No group trend toward disproportionate age-related enlargement of the right ventricle relative to the left was noted. In old subjects, however, lateral ventricle asymmetry correlated with face-word memory discrepancies in the expected direction, worse word than face memory being associated with disproportionate enlargement of the left lateral ventricle. These correlations were not significant in young subjects. These results suggest that the group rend toward disproportionate nonverbal/visual, as opposed to verbal, age-related memory differences is not associated with a group trend toward disproportionate enlargement of the right ventricle. Individual deviations from the normative pattern of age-related ventricle enlargement, however, are associated with different patterns of material-specific memory changes. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. RI DeCarli, Charles/B-5541-2009 NR 51 TC 1 Z9 1 U1 0 U2 0 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 1079-5014 J9 J GERONTOL B-PSYCHOL JI J. Gerontol. Ser. B-Psychol. Sci. Soc. Sci. PD JAN PY 1997 VL 52 IS 1 BP P54 EP P61 PG 8 WC Geriatrics & Gerontology; Gerontology; Psychology; Psychology, Multidisciplinary SC Geriatrics & Gerontology; Psychology GA WC118 UT WOS:A1997WC11800005 PM 9008675 ER PT J AU Neumann, HPH Zbar, B AF Neumann, HPH Zbar, B TI Renal cysts, renal cancer and vonHippel-Lindau disease SO KIDNEY INTERNATIONAL LA English DT Review ID TUMOR-SUPPRESSOR GENE; RNA-POLYMERASE-II; TRANSCRIPTION FACTOR-SIII; MULTIPLE ENDOCRINE NEOPLASIA; CELL-CARCINOMA; BRCA1 GENE; CEREBELLAR HEMANGIOBLASTOMA; GERMLINE MUTATIONS; OVARIAN-CANCER; BREAST-CANCER C1 NCI, FREDERICK, MD 21701 USA. RP Neumann, HPH (reprint author), UNIV FREIBURG, MED KLIN, HUGSTETTER STR 55, D-79106 FREIBURG, GERMANY. NR 94 TC 65 Z9 74 U1 0 U2 1 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 EI 1523-1755 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1997 VL 51 IS 1 BP 16 EP 26 DI 10.1038/ki.1997.3 PG 11 WC Urology & Nephrology SC Urology & Nephrology GA WB338 UT WOS:A1997WB33800003 PM 8995713 ER PT J AU Fogo, A Breyer, JA Smith, MC Cleveland, WH Agodoa, L Kirk, KA Glassock, R Faulkner, M Kopple, JD Massry, SG Grim, C Randall, OS Toto, RD Whelton, P Wright, JT AF Fogo, A Breyer, JA Smith, MC Cleveland, WH Agodoa, L Kirk, KA Glassock, R Faulkner, M Kopple, JD Massry, SG Grim, C Randall, OS Toto, RD Whelton, P Wright, JT TI Accuracy of the diagnosis of hypertensive nephrosclerosis in African Americans: A report from the African American Study of Kidney Disease (AASK) Trial SO KIDNEY INTERNATIONAL LA English DT Article ID STAGE RENAL-DISEASE; ANGIOTENSIN-CONVERTING ENZYME; DELETION POLYMORPHISM; BENIGN NEPHROSCLEROSIS; BIOPSY FINDINGS; AGING PROCESSES; UNITED-STATES; FAMILIAL RISK; BLACK; GENE AB African Americans have excess hypertension and end-stage renal disease presumed due to hypertension compared to Caucasians. The AASK was designed to examine the impact of antihypertensive therapies and two levels of blood pressure control on the rate of decline of GFR in African Americans with presumed hypertensive renal disease. During the pilot phase of the trial, eligible participants were requested to undergo renal biopsy to assess the underlying lesions in this population. Eighty-eight hypertensive (diastolic BP > 95 mm Hg) non-diabetic African American patients between the ages of 18 to 70 years, with GFR between 25 to 70 ml/min/1.73 m(2) and without marked proteinuria were assessed for possible renal biopsy. Forty-three patients did not undergo renal biopsy due to refusal or contraindications. Adequate renal biopsies were obtained in 39 of the remaining 46 patients. Biopsy findings were analyzed and then compared to clinical parameters. The 39 patients studied, 29 men and 10 women, were on average 53.0 +/- 11.0 years old, and had a MAP of 109 +/- 15 mm Hg and GFR 51.7 +/- 13.6 ml/min/1.73 m(2) (not significantly different from nonbiopsied patients). Thirty-eight of these 39 biopsies showed arteriosclerosis and/or arteriolosclerosis, severity on average 1.5 +/- 0.9 and 1.5 +/- 0.8, respectively on a 0 to 3+ scale. Interstitial fibrosis was moderate, 1.3 +/- 0.9 (0 to 3+ scale). Segmental glomerulosclerosis was present in five biopsies, and in one patient, biopsy and clinical findings were consistent with idiopathic focal segmental glomerulosclerosis. Additional lesions included mesangiopathic glomerulonephritis in one patient, basement membrane thickening suggestive of diabetic nephropathy in one, and cholesterol emboli in two cases. Arteriolar and arterial sclerosis were tightly linked, and correlated with interstitial fibrosis and the reciprocal of scrum creatinine. Global glomerulosclerosis was extensive, involving on average 43 +/- 26% of glomeruli. The extent of this lesion did not correlate with degree of arteriolar or arterial thickening, but did correlate with systolic blood pressure (P = 0.0174), the reciprocal of serum creatinine (P = 0.0009), serum cholesterol (P = 0.0129) and interstitial fibrosis (P < 0.0001). These data underscore that renal biopsies in non-diabetic hypertensive African-Americans with mild to moderate renal insufficiently in the absence of marked proteinuria are overwhelmingly likely to show renal vascular lesions consistent with the clinical diagnosis of hypertensive nephrosclerosis. C1 VANDERBILT UNIV, MED CTR, DIV NEPHROL, NASHVILLE, TN 37232 USA. CASE WESTERN RESERVE UNIV, DEPT MED, CLEVELAND, OH 44106 USA. MOREHOUSE SCH MED, ATLANTA, GA 30310 USA. NIDDK, DIV KIDNEY UROL & HEMATOL DIS, BETHESDA, MD USA. UNIV ALABAMA, BIRMINGHAM, AL USA. UNIV KENTUCKY, DEPT MED, LEXINGTON, KY 40506 USA. RP Fogo, A (reprint author), VANDERBILT UNIV, MED CTR, DEPT PATHOL, MCN C-3321, NASHVILLE, TN 37232 USA. NR 62 TC 166 Z9 171 U1 1 U2 3 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 EI 1523-1755 J9 KIDNEY INT JI Kidney Int. PD JAN PY 1997 VL 51 IS 1 BP 244 EP 252 DI 10.1038/ki.1997.29 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA WB338 UT WOS:A1997WB33800029 PM 8995739 ER PT J AU Bendon, R AF Bendon, R TI The NICHD-MFMU antibiotic treatment of PPROM: Evaluation of the histopathology of PPROM SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NICHHD,MATERNAL FETAL MED UNITS NETWORK,BETHESDA,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 4 EP 4 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48601113 ER PT J AU Cangiarella, J Jagirdar, J Gutierrez, MC Askin, F Linnoila, RI Goswami, S Greco, MA AF Cangiarella, J Jagirdar, J Gutierrez, MC Askin, F Linnoila, RI Goswami, S Greco, MA TI Congenital cystic adenomatoid malformation of the lung (CCAM): Further insights into pathogenesis. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NYU MED CTR,NEW YORK,NY 10016. HOSP PEREIRA ROSSEL,MONTEVIDEO,URUGUAY. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21287. NCI,ROCKVILLE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 8 EP 8 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48601117 ER PT J AU Fetsch, PA Fetsch, JF Marincola, FM Travis, W Batts, K Abati, A AF Fetsch, PA Fetsch, JF Marincola, FM Travis, W Batts, K Abati, A TI Comparison of melanoma-associated membrane antigen, MART-1, to HMB-45: Further evidence to support a common lineage for angiomyolipoma (AML), lymphangiomyomatosis (LAM) and clear cell ''sugar tumor'' SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. AFIP,WASHINGTON,DC. MAYO CLIN,ROCHESTER,MN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 36 EP 36 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600051 ER PT J AU Alburquerque, A Kennedy, S Bryant, B Liotta, L Merino, MJ AF Alburquerque, A Kennedy, S Bryant, B Liotta, L Merino, MJ TI LOH on chromosome 17p and 17q in the histologic spectrum of DCIS. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. ST VINCENTS HOSP,DEPT PATHOL,DUBLIN 4,IRELAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 68 EP 68 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600083 ER PT J AU Lininger, RA Zhuang, Z Man, YG Pham, T Park, WS MacGrogan, G Tavassoli, FA AF Lininger, RA Zhuang, Z Man, YG Pham, T Park, WS MacGrogan, G Tavassoli, FA TI LOH at 16p13 detected in microdissected papillary neoplasms of the breast and their precursors SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,DEPT GYNECOL & BREAST PATHOL,WASHINGTON,DC 20306. NIH,BETHESDA,MD 20892. INST BERGONIE,BORDEAUX,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 107 EP 107 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600122 ER PT J AU Lininger, RA Zhuang, Z Man, YG Park, WS EmmertBuck, M Tavassoli, FA AF Lininger, RA Zhuang, Z Man, YG Park, WS EmmertBuck, M Tavassoli, FA TI LOH in microdissected apocrine carcinomas of the breast SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,DEPT GYNECOL & BREAST PATHOL,WASHINGTON,DC 20306. NIH,DEPT PATHOL,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 108 EP 108 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600123 ER PT J AU Merino, MJ Albuquerque, A Bryant, B Middleton, L Grases, P Tressera, F Zhuang, Z Liotta, L AF Merino, MJ Albuquerque, A Bryant, B Middleton, L Grases, P Tressera, F Zhuang, Z Liotta, L TI Genetic changes in chromosome 17p in aggressive variants of breast cancer. A marker of poor prognosis. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 113 EP 113 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600128 ER PT J AU Beaty, MW Park, WS EmmertBuck, M Zhuang, Z Lubensky, I Abati, A AF Beaty, MW Park, WS EmmertBuck, M Zhuang, Z Lubensky, I Abati, A TI FNA of metastatic clear cell carcinoma of kidney - Employment of microdissection and the polymerase chain reaction (PCT) for definitive genetic identification. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 167 EP 167 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600182 ER PT J AU Tabbara, SO Sherman, ME Schiffman, MH Glass, AG Cadell, DM Rush, BB Scott, DR Kurman, RJ Lorincz, A Manos, MM AF Tabbara, SO Sherman, ME Schiffman, MH Glass, AG Cadell, DM Rush, BB Scott, DR Kurman, RJ Lorincz, A Manos, MM TI ASCUS vs HSIL: Evaluation of the morphologic features. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. NCI,BETHESDA,MD 20892. KAISER PERMANENTE,PORTLAND,OR. WESTAT CORP,ROCKVILLE,MD. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. DIGENE CORP,ROCKVILLE,MD. CETUS CORP,EMERYVILLE,CA 94608. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 212 EP 212 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600227 ER PT J AU Fetsch, PA Kleiner, D Marincola, FM Abati, A AF Fetsch, PA Kleiner, D Marincola, FM Abati, A TI Analysis of melanoma-associated antigen, MART-1, in normal tissues and in selected non-melanomatous neoplasms SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 235 EP 235 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600250 ER PT J AU Fritsch, M Marincola, FM Rosenberg, SA Duray, PH AF Fritsch, M Marincola, FM Rosenberg, SA Duray, PH TI Cutaneous T-cell and HLA-DR vascular endothelial responses within melanoma following exposure to MART-1 melanoma vaccine. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 237 EP 237 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600252 ER PT J AU Greene, JF Alexander, MA Arguello, F AF Greene, JF Alexander, MA Arguello, F TI Diphtheria toxin mediated differentiation in human melanoma xenografts SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 TEXAS A&M UNIV,SCOTT & WHITE CLIN,TEMPLE,TX 76508. NCI,NIH,FREDERICK,MD 21701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 245 EP 245 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600260 ER PT J AU Orenstein, JM Alkan, S Blauvelt, A Jeang, KT Herndier, B AF Orenstein, JM Alkan, S Blauvelt, A Jeang, KT Herndier, B TI Visualization of human herpesvirus type 8 in Kaposi's sarcoma by light and transmission electron SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. NCI,DERMATOL BRANCH,BETHESDA,MD 20892. NIAID,MOL VIROL LAB,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. RI Jeang, Kuan-Teh/A-2424-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 252 EP 252 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600267 ER PT J AU Park, WS Duray, PH Pack, S Guerami, AA Boni, R Votmeyer, AO EmmertBuck, MR Liotta, L Zhuang, Z AF Park, WS Duray, PH Pack, S Guerami, AA Boni, R Votmeyer, AO EmmertBuck, MR Liotta, L Zhuang, Z TI Allelic deletion at chromosome 9p21(p16 gene locus) in microdissected dysplastic nevus SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. RI Pack, Svetlana/C-2020-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 253 EP 253 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600268 ER PT J AU Wiltshire, RN Duray, P Meltzer, PS Liotta, LA Trent, JM AF Wiltshire, RN Duray, P Meltzer, PS Liotta, LA Trent, JM TI Comparative genomic hybridization analysis of archival biopsies of human cutaneous malignant melanoma. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,NATL CTR HUMAN GENOME RES,CANC GENET LAB,NIH,BETHESDA,MD 20892. NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 264 EP 264 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600279 ER PT J AU Lubensky, IA Pack, S Amada, S Walther, M Linehan, WM Zhuang, Z AF Lubensky, IA Pack, S Amada, S Walther, M Linehan, WM Zhuang, Z TI Multiple neuroendocrine tumors of pancreas in VHL patients: Histopathologic and molecular genetic analysis. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,NIH,BETHESDA,MD 20892. NCI,SURG BRANCH,NIH,BETHESDA,MD 20892. RI Pack, Svetlana/C-2020-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 279 EP 279 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600294 ER PT J AU Park, WS Bryant, B Wang, C Pham, T Zhuang, Z Merino, MJ AF Park, WS Bryant, B Wang, C Pham, T Zhuang, Z Merino, MJ TI Loss of heterozygosity of chromosome 1 in tall cell papillary carcinoma of thyroid. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 284 EP 284 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600299 ER PT J AU Fogt, F Vortmeyer, AO Goldman, H Giordano, TJ Merino, MJ Zhuang, ZP AF Fogt, F Vortmeyer, AO Goldman, H Giordano, TJ Merino, MJ Zhuang, ZP TI Loss of heterozygosity in the development of dysplasia and carcinoma in ulcerative colitis: A genetic characterization. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. DEACONESS HOSP,DEPT PATHOL,BOSTON,MA. UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 308 EP 308 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600323 ER PT J AU Krishnamurthy, S Terninini, B Jensen, RT Dayal, Y AF Krishnamurthy, S Terninini, B Jensen, RT Dayal, Y TI Gastric endocrine cell status in familial and sporadic Zollinger-Ellison syndrome. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 TUFTS UNIV NEW ENGLAND MED CTR,DEPT PATHOL,BOSTON,MA 02111. NIH,DIGEST DIS BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 328 EP 328 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600343 ER PT J AU Quezado, MM Albuquerque, A Bryant, B Merino, MJ Duray, PH AF Quezado, MM Albuquerque, A Bryant, B Merino, MJ Duray, PH TI Alterations near NF2 tumor supressor gene occur in some gastrointestinal stromal tumors SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 353 EP 353 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600368 ER PT J AU SanzOrtega, J SanzEsponera, J Sobel, M Zhengping, Z Merino, MJ AF SanzOrtega, J SanzEsponera, J Sobel, M Zhengping, Z Merino, MJ TI LOH at the APC/MCC gene (5Q21) in preneoplastic and cancerous lesions of stomach SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,NIH,BETHESDA,MD 20892. HOSP SAN CARLOS,MADRID,SPAIN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 360 EP 360 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600375 ER PT J AU Chuaqui, RF Englert, CR Strup, SE Vocke, CD Zhuang, ZP Duray, PH Bostwick, DG Linehan, WM Liotta, LA EmmertBuck, MR AF Chuaqui, RF Englert, CR Strup, SE Vocke, CD Zhuang, ZP Duray, PH Bostwick, DG Linehan, WM Liotta, LA EmmertBuck, MR TI Comparison of gene expression in microdissected prostate normal and tumor epithelium in a patient with clinically aggressive cancer SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. MAYO CLIN,DEPT PATHOL,BETHESDA,MD. NCI,SURG BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 408 EP 408 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600423 ER PT J AU Duray, PH Chuaqui, R EmmertBuck, M Linehan, WM Margolis, L Hatfill, S AF Duray, PH Chuaqui, R EmmertBuck, M Linehan, WM Margolis, L Hatfill, S TI Long term in-vitro maintenance of histologically intact human prostate tissue in a NASA designed rotating wall vessel bioreactor SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. NCI,NICHD,LTPB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 419 EP 419 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600434 ER PT J AU Fogt, F Zhuang, ZP Linehan, M Merino, MJ AF Fogt, F Zhuang, ZP Linehan, M Merino, MJ TI Genetic changes present in collecting duct carcinomas. A comparison with renal cell carcinoma. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 428 EP 428 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600443 ER PT J AU Hughson, MD Schmidt, L Zbar, B Dunn, S Silva, FG AF Hughson, MD Schmidt, L Zbar, B Dunn, S Silva, FG TI Renal cell carcinomas of end-stage renal disease: Histopathology and molecular genetics. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 DVAMC,NORTHPORT,NY. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21701. UNIV OKLAHOMA,HLTH SCI CTR,OKLAHOMA CITY,OK 73104. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 443 EP 443 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600458 ER PT J AU Lapham, RL Ro, JY Ordonez, NG Merino, MJ Ayala, AG AF Lapham, RL Ro, JY Ordonez, NG Merino, MJ Ayala, AG TI Small cell tumor of kidney with features of Ewing's sarcoma (ES)/primitive neuroectodermal tumor (PNET) in adults SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX. UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 455 EP 455 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600470 ER PT J AU Isacson, C Kessis, T MacVille, M Baranyai, J Jones, R Kurman, R Shah, K Ried, T AF Isacson, C Kessis, T MacVille, M Baranyai, J Jones, R Kurman, R Shah, K Ried, T TI Comparative genomic hybridization (CGH) analysis of primary vulvar carcinomas SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NATL WOMENS HOSP,AUCKLAND,NEW ZEALAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 592 EP 592 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600607 ER PT J AU Vargas, MP Mazariegos, J Merino, MJ AF Vargas, MP Mazariegos, J Merino, MJ TI Lymphoepithelioma-like carcinoma of endometrium. An aggressive form of uterine cancer SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MERCY HOSP,BUFFALO,NY. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 620 EP 620 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600635 ER PT J AU Quezado, MM Albuquerque, A Bryant, B Merino, HJ Duray, PH AF Quezado, MM Albuquerque, A Bryant, B Merino, HJ Duray, PH TI Ocular melanoma: Absence of genetic changes support different origin from cutaneous melanomas SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 676 EP 676 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600691 ER PT J AU Abruzzo, LV Griffith, LM Nandedkar, M Aguilera, NS Taubenberger, JK Raffeld, M Stass, SA Abbondanzo, SL Jaffe, ES AF Abruzzo, LV Griffith, LM Nandedkar, M Aguilera, NS Taubenberger, JK Raffeld, M Stass, SA Abbondanzo, SL Jaffe, ES TI Histologically discordant lymphomas with B-cell and T-cell components. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV MARYLAND,BALTIMORE,MD 21201. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 690 EP 690 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600705 ER PT J AU Alkan, S Ortiz, A Detrick, B Brown, E Hooks, JJ Karcher, DS AF Alkan, S Ortiz, A Detrick, B Brown, E Hooks, JJ Karcher, DS TI Interleukin-10 is an autocrine growth factor for primary effusion lymphoma SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,MED CTR,DEPT PATHOL,WASHINGTON,DC 20037. NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 692 EP 692 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600707 ER PT J AU ElenitobaJohnson, KSJ Medeiros, LJ Taubenberger, JK Molldrem, J Fukushima, P StetlerStevenson, M AF ElenitobaJohnson, KSJ Medeiros, LJ Taubenberger, JK Molldrem, J Fukushima, P StetlerStevenson, M TI T-cell large granular lymphocytosis (TLGL): Comparison of clinical criteria and results of immunophenotypic and molecular studies SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. CITY HOPE NATL MED CTR,DUARTE,CA 91010. ARMED FORCES INST PATHOL,WASHINGTON,DC. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 722 EP 722 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600737 ER PT J AU ElenitobaJohnson, KSJ ZarateOsorno, A Meneses, A Krenacs, L Kingma, DW Raffeld, M Jaffe, ES AF ElenitobaJohnson, KSJ ZarateOsorno, A Meneses, A Krenacs, L Kingma, DW Raffeld, M Jaffe, ES TI EBV strain type and LMP-1 oncogene deletions in nasal T/NK-cell lymphomas from Mexico SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. INST NACL CANCEROL,HMC,MEXICO CITY,DF,MEXICO. RI Krenacs, Laszlo/L-8063-2014 OI Krenacs, Laszlo/0000-0001-6541-3031 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 723 EP 723 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600738 ER PT J AU Gocke, CD Benko, FA Sternas, L Kwak, LW Kopreski, MS AF Gocke, CD Benko, FA Sternas, L Kwak, LW Kopreski, MS TI Detection of tumor-specific extracellular DNA (the bcl-2/IgH transgene) in serum of untreated follicular lymphoma patients. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 PENN STATE UNIV,COLL MED,DEPT PATHOL,UNIVERSITY PK,PA 16802. NCI,DIV CLIN SCI,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 733 EP 733 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600748 ER PT J AU Kumar, S Krenacs, L Raffeld, M Jaffe, ES AF Kumar, S Krenacs, L Raffeld, M Jaffe, ES TI Subcutaneous Panniculitis-like T-cell lymphoma is a tumor of cytotoxic T lymphocytes SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 CHILDRENS NATL MED CTR,DEPT PATHOL,WASHINGTON,DC 20010. NCI,HEMATOPATHOL SECT,BETHESDA,MD. RI Krenacs, Laszlo/L-8063-2014 OI Krenacs, Laszlo/0000-0001-6541-3031 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 749 EP 749 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600764 ER PT J AU Lim, MS StetlerStevenson, M ElenitobaJohnson, KSJ Kumar, S Raffeld, M Jaffe, ES AF Lim, MS StetlerStevenson, M ElenitobaJohnson, KSJ Kumar, S Raffeld, M Jaffe, ES TI Analysis of human MIC2 expression in myeloid tumors SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 751 EP 751 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600766 ER PT J AU Mansoor, A BirkedalHansen, B Lim, MS Guedez, L StetlerStevenson, WG StetlerStevenson, M AF Mansoor, A BirkedalHansen, B Lim, MS Guedez, L StetlerStevenson, WG StetlerStevenson, M TI TIMP-1 expression correlates with histologic grade in B-cell lymphomas. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,HEMATOPATHOL SECT,BETHESDA,MD 20892. NIH,EXTRACELLULAR MATRIX PATHOL SECT,PATHOL LAB,BETHESDA,MD 20892. RI Guedez, Liliana/H-4951-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 755 EP 755 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600770 ER PT J AU Riley, C Ried, T Bittner, M Bagg, A Cossman, J AF Riley, C Ried, T Bittner, M Bagg, A Cossman, J TI Reed-Sternberg cell genetics: Single cell CGH SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 GEORGETOWN UNIV,WASHINGTON,DC 20057. NIH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 774 EP 774 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600789 ER PT J AU TeruyaFeldstein, J Jaffe, ES Burd, PR Kingma, DW Tosato, G AF TeruyaFeldstein, J Jaffe, ES Burd, PR Kingma, DW Tosato, G TI Expression of interferon-gamma inducible protein 10 (IP-10) and macrophage interferon-gamma induced gene (Mig) in Hodgkin's disease (HD) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,HEMATOPATHOL SECT,CTR BIOL EVALUAT & RES,FDA,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 787 EP 787 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600802 ER PT J AU Chang, DTW Arayssi, T Pando, JA Schumacher, HR Duray, PH AF Chang, DTW Arayssi, T Pando, JA Schumacher, HR Duray, PH TI Angiogenesis as an early predictor for the development of rheumatoid arthritis. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIAMS,PATHOL LAB,NCI,BETHESDA,MD. UNIV PENN,DEPT MED & RHEUMATOL,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 802 EP 802 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600817 ER PT J AU Orenstein, JM Wahl, SM AF Orenstein, JM Wahl, SM TI Upregulation of HIV in tissues infected with opportunistic pathogens SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 GEORGE WASHINGTON UNIV,DEPT PATHOL,WASHINGTON,DC. NIDR,IMMUNOL LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 821 EP 821 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600836 ER PT J AU Kleiner, DE DiBisceglie, AM Hoofnagle, JH AF Kleiner, DE DiBisceglie, AM Hoofnagle, JH TI Ribavirin therapy for chronic hepatitis C (CHC): A dose-duration dependent improvement in inflammatory activity SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 849 EP 849 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600864 ER PT J AU Vortmeyer, AO Lubensky, IA Khettry, U Fogt, F Linehan, WM Zhuang, Z AF Vortmeyer, AO Lubensky, IA Khettry, U Fogt, F Linehan, WM Zhuang, Z TI VHL gene alterations detected in microcystic adenomas of the pancreas SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,PATHOL LAB,BETHESDA,MD 20892. NIH,SURG BRANCH,BETHESDA,MD 20892. DEACONESS HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 867 EP 867 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600882 ER PT J AU Burke, L Freedman, A ElDeiry, W Bennett, W Guinee, D Rush, W Przygodzki, R Jones, R Borkowski, A Caporaso, N Fleming, MV Travis, W Colby, T Trastek, V Pairolero, P Tazelaar, H Midthun, D Liotta, L Vogelstein, B Harris, C AF Burke, L Freedman, A ElDeiry, W Bennett, W Guinee, D Rush, W Przygodzki, R Jones, R Borkowski, A Caporaso, N Fleming, MV Travis, W Colby, T Trastek, V Pairolero, P Tazelaar, H Midthun, D Liotta, L Vogelstein, B Harris, C TI Cyclin D1, p53 and p21(waf1/cip1) expression predict survival in non-small cell lung cancer (NSCLC). SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. UNIV PENN,PHILADELPHIA,PA 19104. UNIV UTAH,MED CTR,SALT LAKE CITY,UT 84112. AFIP,WASHINGTON,DC. UNIV MARYLAND,BALTIMORE,MD 21201. VET ADM MED CTR,BALTIMORE,MD 21218. MAYO CLIN,SCOTTSDALE,AZ. MAYO CLIN,ROCHESTER,MN. JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 946 EP 946 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600961 ER PT J AU Duray, P Bryant, B Longo, D Duffey, P Tate, DJ Nowels, K Kelley, M AF Duray, P Bryant, B Longo, D Duffey, P Tate, DJ Nowels, K Kelley, M TI Pulmonary carcinoma following Hodgkins Disease SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,LAB PATHOL MED ONCOL,BETHESDA,MD 20892. STANFORD UNIV,STANFORD,CA 94305. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 954 EP 954 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600969 ER PT J AU Fleming, M Brambilla, E Gal, A Falk, R Wei, M Abbondanzo, S Przygodzki, R Finkelstein, S Rush, W Koss, M Travis, W AF Fleming, M Brambilla, E Gal, A Falk, R Wei, M Abbondanzo, S Przygodzki, R Finkelstein, S Rush, W Koss, M Travis, W TI BCL-2/BAX ratio (BBR) in neuroendocrine lung tumors (NET) predicts poor prognosis and P53 abnormalities. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. PATHOL LAB,GRENOBLE,FRANCE. EMORY UNIV,DEPT PATHOL,ATLANTA,GA 30322. NCI,ENVIRONM EPIDEMIOL BRANCH,NIH,BETHESDA,MD 20892. UNIV PITTSBURGH,DEPT PATHOL,PITTSBURGH,PA 15260. RI Brambilla, Elisabeth/L-8796-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 959 EP 959 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600974 ER PT J AU Fleming, M Brambilla, E Freedman, A Przygodzki, R Caporaso, N Bennett, W Travis, W Colby, T Jett, J Tazelaar, H Trastek, V Pairolero, P Liotta, L Harris, C AF Fleming, M Brambilla, E Freedman, A Przygodzki, R Caporaso, N Bennett, W Travis, W Colby, T Jett, J Tazelaar, H Trastek, V Pairolero, P Liotta, L Harris, C TI Bax immunohistochemical staining (IHC) relates to gender, grade, histology, family history, and K-ras mutations in non-small cell carcinomas (NSCC) of the lung. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,DEPT PULM & MEDIASTINAL PATHOL,WASHINGTON,DC 20306. CHRU,PATHOL CELLULAIRE LAB,GRENOBLE,FRANCE. NCI,GENET EPIDEMIOL BRANCH,NIH,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,DEPT CELLULAR PATHOL,WASHINGTON,DC 20306. NCI,HUMAN CARCINOGENESIS LAB,NIH,BETHESDA,MD 20892. MAYO CLIN,ROCHESTER,MN. RI Brambilla, Elisabeth/L-8796-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 960 EP 960 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600975 ER PT J AU Flieder, DB Falk, R Rush, WR Fleming, MV Gal, A Koss, M Travis, W AF Flieder, DB Falk, R Rush, WR Fleming, MV Gal, A Koss, M Travis, W TI Proposed modified histologic criteria for diagnosis of atypical carcinoid tumors. SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NCI,ENVIRONM EPIDEMIOL BRANCH,NIH,BETHESDA,MD 20892. EMORY UNIV,ATLANTA,GA 30322. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 962 EP 962 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600977 ER PT J AU Guinee, DG Brambilla, E Fleming, M Hayashi, T Koss, M Ferrans, V Travis, W AF Guinee, DG Brambilla, E Fleming, M Hayashi, T Koss, M Ferrans, V Travis, W TI Upregulation of proapoptotic BAX protein in diffuse alveolar damage SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV UTAH,DEPT PATHOL,SALT LAKE CITY,UT. CHRU,PATHOL CELLULAIRE LAB,GRENOBLE,FRANCE. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NIH,BETHESDA,MD 20892. RI Brambilla, Elisabeth/L-8796-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 965 EP 965 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600980 ER PT J AU Kumar, V Fraig, M Meduri, GU Mann, L Travis, W StetlerStevenson, WB Eltorky, M AF Kumar, V Fraig, M Meduri, GU Mann, L Travis, W StetlerStevenson, WB Eltorky, M TI Matrix metalloprotease and TIMP in proliferative phase of diffuse alveolar damage (DAD-F) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV TENNESSEE,DEPT PATHOL,MEMPHIS,TN. UNIV TENNESSEE,DEPT MED,MEMPHIS,TN 38104. ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. NIH,BETHESDA,MD 20892. RI Fraig, Mostafa/I-1670-2016 OI Fraig, Mostafa/0000-0003-1119-3672 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 977 EP 977 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48600992 ER PT J AU Rush, W Hayashi, T Suarez, E Chu, W Abbondanzo, S Ferrans, V Travis, W AF Rush, W Hayashi, T Suarez, E Chu, W Abbondanzo, S Ferrans, V Travis, W TI Comparative utility of staining for S-100 protein and CD1a in the evaluation of pulmonary Langerhans' cell granulomatosis (PLCG), Letterer-Siwe disease (LSD) and respiratory bronchiolitis (RB): An immunohistochemical and confocal microscopic study SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 ARMED FORCES INST PATHOL,DEPT PULM & MEDIASTINAL PATHOL,WASHINGTON,DC 20306. NHLBI,PATHOL SECT,NIH,BETHESDA,MD 20892. ARMED FORCES INST PATHOL,DEPT PEDIAT PATHOL,WASHINGTON,DC 20306. ARMED FORCES INST PATHOL,DEPT HEMATOL & LYMPHAT PATHOL,WASHINGTON,DC 20306. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 1004 EP 1004 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48601019 ER PT J AU Wilson, JD Merino, MJ Harris, C Kleiner, DE AF Wilson, JD Merino, MJ Harris, C Kleiner, DE TI Mesothelioma vs adenocarcinoma: Does immunohistochemistry help? SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NCI,PATHOL LAB,BETHESDA,MD 20892. RI Wilson, Jon/H-5148-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 1020 EP 1020 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48601035 ER PT J AU Neumann, RD Panyutin, IG AF Neumann, RD Panyutin, IG TI Sequence-specific DNA breaks from triplex-directed I-125 decay as a tool for gene analysis SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1997 VL 76 IS 1 BP 1078 EP 1078 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA WD486 UT WOS:A1997WD48601093 ER PT B AU Teng, CT Yang, NY AF Teng, CT Yang, NY BE Hutchens, TW Lonnerdal, B TI Estrogen regulation of human lactoferrin gene activity - Transcriptional synergism between estrogen receptor and related orphan receptor SO LACTOFERRIN - INTERACTIONS AND BIOLOGICAL FUNCTIONS: INTERACTIONS AND BIOLOGICAL FUNCTIONS SE EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Proceedings Paper CT 2nd International Symposium on Lactoferrin Structure and Function CY 1995 CL HONOLULU, HI SP Agennix Inc, DMV Int, Milupa AG, Morinaga Milk Ind Co, Wei Chuan Foods, Wyeth Ayerst Res AB Human lactoferrin gene is differentially regulated in different tissues. The 5'-flanking region of the gene contains multiple positive and negative regulatory elements that can contribute to the cell-type-specific expression of the gene. A functional estrogen response element (ERE) is located at nucleotide -354 from the initiation start site. Upstream from the ERE, a DNA sequence (-418 to -378, FP1) is selectively protected from DNase I digestion by nuclear extracts of endometrium (RL95-2) and mammary gland (HB100) cells. Ln the electrophoresis mobility shift assay (EMSA), nuclear proteins of the RL95-2 cells and FP1 formed three protein-DNA complexes (C1, C2, and C3). We have delineated the positions of these proteins by EMSA, site-directed mutagenesis, and DNA methylation interference analyses. Mutation at the C1-binding region, TCAAGGTCATC, abolished the formation of C1 complex and reduced the estrogen responsiveness of the reporter plasmids, which contain the intact lactoferrin ERE in RL95-2 cell. We cloned and sequenced the cDNA encoding the C1-binding protein. The nucleotide sequence of the cDNA shared 99% homology with the hERR1. As a result of several deletions in our clone, the predicated amino acid sequence was 97.5% homology between our clone and the hERR1. From these data, we have cloned a variant form of this receptor. We named its binding element estrogen receptor-related orphan receptor response element (ERRE). To examine the mechanism of hERR1 and ERRE in enhancing the estrogen response, we performed DNase I footprinting, EMSA, and far-Western analyses. The results demonstrated that the presence of hERR1 and ERRE stabilized ER binding to the ERE of human lactoferrin gene. A direct protein-protein contact between ER and hERR1 was shown by far-Western analysis. These observations suggest that hERR1 acid ER acted synergistically in estrogen-stimulated lactoferrin gene activity. RP Teng, CT (reprint author), NIEHS,REPROD & DEV TOXICOL LAB,GENE REGULAT GRP,RES TRIANGLE PK,NC 27709, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DR, STE 208, TOTOWA, NJ 07512-1165 BN 0-89603-366-X J9 EXP BIOL M PY 1997 VL 28 BP 135 EP 153 PG 19 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA BH48E UT WOS:A1997BH48E00010 ER PT J AU Lamb, ME Sternberg, KJ Esplin, PW AF Lamb, ME Sternberg, KJ Esplin, PW TI Assessing the credibility of children's allegations of sexual abuse: A survey of recent research SO LEARNING AND INDIVIDUAL DIFFERENCES LA English DT Article ID STATEMENTS; VALIDITY; MEMORY AB Alarmed by the increasing numbers of alleged incidents of child sexual abuse, forensic psychologists have attempted to learn whether credible and implausible allegations can be discriminated reliably. Most attention has focused on components of Statement Validity Analysis (SVA), particularly Criterion-Based Content Analysis (CBCA). Recent studies have shown that CBCA scores indeed distinguish plausible from implausible accounts, although the precision is still too poor to permit forensic application. Sensitivity may be enhanced by further improvements in the quality of the investigative interviews on which evaluations of credibility are based, and may be additionally enhanced by development and application of techniques like the Validity Checklist, a little studied component of SVA. C1 UNIV HAIFA, IL-31999 HAIFA, ISRAEL. RP Lamb, ME (reprint author), NICHHD, SECT SOCIAL & EMOT DEV, 9190 ROCKVILLE PIKE, BETHESDA, MD 20814 USA. NR 40 TC 31 Z9 32 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1041-6080 J9 LEARN INDIVID DIFFER JI Learn. Individ. Differ. PY 1997 VL 9 IS 2 BP 175 EP 194 DI 10.1016/S1041-6080(97)90005-4 PG 20 WC Psychology, Educational SC Psychology GA XH691 UT WOS:A1997XH69100005 ER PT J AU Funakoshi, S Taub, DD Asai, O Hirano, A Ruscetti, FW Longo, DL Murphy, WJ AF Funakoshi, S Taub, DD Asai, O Hirano, A Ruscetti, FW Longo, DL Murphy, WJ TI Effects of CD40 stimulation in the prevention of human EBV-lymphomagenesis SO LEUKEMIA & LYMPHOMA LA English DT Review DE CD40; B cell; lymphoma; immunotherapy; Epstein-Barr virus; human/mouse chimera ID B-CELL LYMPHOMA; SEVERE COMBINED IMMUNODEFICIENCY; LYMPHOPROLIFERATIVE DISEASE; MONOCLONAL-ANTIBODY; GROWTH-INHIBITION; IN-VITRO; LIGAND; MICE; ACTIVATION; LINES AB CD40 is a molecule present on B lineage cells, both normal and neoplastic. Signalling through CD40 has been demonstrated to promote B cell growth and differentiation in vitro. In contrast to its effects on normal B cells, we have found that CD40 stimulation can inhibit the growth of various aggressive histology human B cell lymphomas both in vitro and in vivo. Moreover, using a human/mouse chimera model in which human EBV-induced B cell lymphomas can spontaneously arise, we have found that CD40 stimulation can prevent the occurrence of this human lymphoma in mice. However, normal human B cell engraftment and function was not adversely affected in these mice by CD40 stimulation. This indicates that CD40 stimulation is selective in its effects on aggressive histology B cell lymphomas. Thus, CD40 stimulation either by antibody or a recombinant soluble ligand, may be of potential clinical use, not only in the treatment of EBV-induced B cell lymphomas, but also in their prevention. C1 NCI,FREDERICK CANC RES & DEV CTR,SAIC,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD 21702. NR 32 TC 12 Z9 12 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-8194 J9 LEUKEMIA LYMPHOMA JI Leuk. Lymphoma PD JAN PY 1997 VL 24 IS 3-4 BP 187 EP & PG 15 WC Oncology; Hematology SC Oncology; Hematology GA WE532 UT WOS:A1997WE53200001 PM 9156649 ER PT J AU Cheson, BD AF Cheson, BD TI Trials and tribulations SO LEUKEMIA RESEARCH LA English DT Editorial Material RP Cheson, BD (reprint author), NCI,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD JAN PY 1997 VL 21 IS 1 BP 1 EP 1 DI 10.1016/S0145-2126(96)00133-6 PG 1 WC Oncology; Hematology SC Oncology; Hematology GA WG609 UT WOS:A1997WG60900001 PM 9029178 ER PT S AU Holm, C Langin, D Manganiello, V Belfrage, P Degerman, E AF Holm, C Langin, D Manganiello, V Belfrage, P Degerman, E BE Rubin, B Dennis, EA TI Regulation of hormone-sensitive lipase activity in adipose tissue SO LIPASES, PT B: ENZYME CHARACTERIZATION AND UTILIZATION SE Methods in Enzymology LA English DT Review ID DEPENDENT PROTEIN-KINASE; ISOLATED RAT ADIPOCYTES; MESSENGER-RNA; CYCLIC-AMP; LIPOPROTEIN-LIPASE; CAMP-PHOSPHODIESTERASE; ADENYLATE-CYCLASE; LIPID-METABOLISM; FAT-CELLS; PHOSPHORYLATION C1 CHU RANGUEIL, INST LOUIS BUGNARD, F-31003 TOULOUSE 4, FRANCE. NHLBI, PULM CRIT CARE MED BRANCH, NIH, BETHESDA, MD 20892 USA. RP LUND UNIV, DEPT CELL & MOL BIOL, SECT MOL SIGNALLING, S-22100 LUND, SWEDEN. NR 73 TC 48 Z9 48 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-182187-0 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1997 VL 286 BP 45 EP 67 PG 23 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BJ65Z UT WOS:A1997BJ65Z00002 PM 9309644 ER PT S AU Harrison, EH Kempner, ES AF Harrison, EH Kempner, ES BE Rubin, B Dennis, EA TI Radiation inactivation studies of hepatic cholesteryl ester hydrolases SO LIPASES, PT B: ENZYME CHARACTERIZATION AND UTILIZATION SE Methods in Enzymology LA English DT Review ID SALT-ACTIVATED LIPASE; RAT-LIVER; PHOSPHOLIPASE A(2); CLONING; ENZYME; CDNA; LYSOPHOSPHOLIPASE; DIFFERENTIATION; PURIFICATION; EXPRESSION C1 NIAMSD, NIH, BETHESDA, MD 20892 USA. RP Harrison, EH (reprint author), MED COLL PENN & HAHNEMANN UNIV, DEPT BIOCHEM, PHILADELPHIA, PA 19129 USA. FU NIDDK NIH HHS [R01 DK044498] NR 37 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-182187-0 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1997 VL 286 BP 116 EP 126 PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BJ65Z UT WOS:A1997BJ65Z00006 PM 9309648 ER PT S AU Rand, RP Parsegian, VA AF Rand, RP Parsegian, VA BE Epand, RM TI Hydration, curvature, and bending elasticity of phospholipid monolayers SO LIPID POLYMORPHISM AND MEMBRANE PROPERTIES SE Current Topics in Membranes LA English DT Review ID HEXAGONAL HII PHASE; STRONGLY CURVED MONOLAYERS; STRUCTURAL TRANSITIONS; INTERMOLECULAR FORCES; PROTEIN SOLVATION; NEUTRAL SURFACE; MEMBRANE-FUSION; OSMOTIC-STRESS; WATER-SYSTEMS; LAMELLAR C1 NICHHD, NIH, BETHESDA, MD 20892 USA. NIH, DIV COMP RES & TECHNOL, BETHESDA, MD 20892 USA. BROCK UNIV, ST CATHARINES, ON L2S 3A1, CANADA. NR 43 TC 20 Z9 20 U1 0 U2 8 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 1063-5823 BN 0-12-153344-1 J9 CURR TOP MEMBR JI Curr. Top. Membr. PY 1997 VL 44 BP 167 EP 189 PG 23 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BJ66B UT WOS:A1997BJ66B00004 ER PT J AU Lu, L Sharma, N Gowda, GAN Khetrapal, CL Weiss, RG AF Lu, L Sharma, N Gowda, GAN Khetrapal, CL Weiss, RG TI Enantiotropic nematic phases of quaternary ammonium halide salts based on trioctadecylamine SO LIQUID CRYSTALS LA English DT Article ID AMPHIPHILES AB The neat phases of a series of quaternary ammonium halides based on trioctadecylamine have been investigated by optical microscopy, differential scanning calorimetry, and H-2 NMR spectroscopy. Phase behaviour depends primarily on the structure of the fourth substituent on nitrogen and the thermal history of the samples. For instance, the iodide salts with methyl, ethyl, or propyl as the fourth substituent form enantiotropic nematic phases, while those with a proton or a longer alkyl substituent exhibit complex phase behaviour that does not include a liquid crystalline phase. Possible reasons are advanced for the unprecedented formation of nematic phases. C1 GEORGETOWN UNIV,DEPT CHEM,WASHINGTON,DC 20057. INDIAN INST SCI,SOPHISTICATED INSTRUMENTS FACIL,BANGALORE 560012,KARNATAKA,INDIA. NIH,BETHESDA,MD 20892. NR 21 TC 27 Z9 27 U1 0 U2 4 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0267-8292 J9 LIQ CRYST JI Liq. Cryst. PD JAN PY 1997 VL 22 IS 1 BP 23 EP 28 PG 6 WC Chemistry, Multidisciplinary; Crystallography; Materials Science, Multidisciplinary SC Chemistry; Crystallography; Materials Science GA WF611 UT WOS:A1997WF61100004 ER PT J AU Belaaouaj, K Walsh, BC Jenkins, NA Copeland, NG Shapiro, SD AF Belaaouaj, K Walsh, BC Jenkins, NA Copeland, NG Shapiro, SD TI Characterization of the mouse neutrophil elastase gene and localization to Chromosome 10 SO MAMMALIAN GENOME LA English DT Article ID 1ST 2 CENTURIES; FUTURE-RESEARCH; LINKAGE MAP; DNA; ORGANIZATION; SUGGESTIONS; EXPRESSION; SEQUENCES; EMPHYSEMA AB Neutrophil elastase (NE), a serine proteinase, is considered to play a role in normal tissue turnover and host defense. NE may also cause tissue damage in acute and chronic inflammatory diseases. We have isolated and characterized the gene for mouse NE and determined its chromosomal location. The mouse NE gene has been localized by interspecific backcross analysis to Chromosome (Chr) 10. The gene for mouse NE is composed of 5 exons and 4 introns, similar to the human NE. Mouse NE shares the highly conserved exon size and intron-exon borders with human NE. The coding exons of the mouse NE gene predict a translation product in a pre-pro form, similar to human NE. Knowledge of the genomic organization and chromosomal location of mouse NE may allow us to further define mechanisms responsible for cell and tissue-specific expression of mouse NE. C1 WASHINGTON UNIV,BARNES JEWISH HOSP,SCH MED,DEPT MED,RESP & CRIT CARE DIV,ST LOUIS,MO 63110. WASHINGTON UNIV,BARNES JEWISH HOSP,SCH MED,DEPT CELL BIOL,ST LOUIS,MO 63110. WASHINGTON UNIV,BARNES JEWISH HOSP,SCH MED,DEPT PHYSIOL,ST LOUIS,MO 63110. NIH,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 16 TC 8 Z9 8 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD JAN PY 1997 VL 8 IS 1 BP 5 EP 8 PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA WA746 UT WOS:A1997WA74600002 ER PT J AU Russell, MW duManoir, S Collins, FS Brody, LC AF Russell, MW duManoir, S Collins, FS Brody, LC TI Cloning of the human NADH: Ubiquinone oxidoreductase subunit B13 localization to Chromosome 7q32 and identification of a pseudogene on 11p15 SO MAMMALIAN GENOME LA English DT Article ID COMPLEX-I; LIBRARY; CHAIN C1 NIH,NATL CTR HUMAN GENOME RES,LAB GENE TRANSFER,BETHESDA,MD 20892. UNIV MICHIGAN,DEPT PEDIAT & COMMUNICABLE DIS,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT HUMAN GENET,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI 48109. NIH,NATL CTR HUMAN GENOME RES,DIAGNOST DEV BRANCH,BETHESDA,MD 20892. NR 13 TC 8 Z9 8 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PD JAN PY 1997 VL 8 IS 1 BP 60 EP 61 PG 2 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA WA746 UT WOS:A1997WA74600015 PM 9021153 ER PT J AU Huppi, K Siwarski, D AF Huppi, K Siwarski, D TI Mouse Chromosome 15 SO MAMMALIAN GENOME LA English DT Article RP Huppi, K (reprint author), NCI,GENET LAB,NIH,BLDG 37,RM 2B-21,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 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1997 VL 7 SI SI BP S251 EP S263 DI 10.1007/s003359900327 PG 13 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA XM207 UT WOS:A1997XM20700015 PM 9233398 ER PT J AU Kozak, C Stephenson, D AF Kozak, C Stephenson, D TI Mouse chromosme 5 SO MAMMALIAN GENOME LA English DT Article C1 UCL, DEPT BIOL, GALTON LAB, LONDON NW1 2HE, ENGLAND. RP Kozak, C (reprint author), NATL INST ALLERGY & INFECT DIS, NIH, ROOM 329, BETHESDA, MD 20892 USA. NR 0 TC 7 Z9 7 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1997 VL 7 SI SI BP S80 EP S99 DI 10.1007/s003359900317 PG 20 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA XM207 UT WOS:A1997XM20700022 PM 9233388 ER PT J AU Mock, BA Neumann, PE Fiedorek, FT AF Mock, BA Neumann, PE Fiedorek, FT TI Mouse Chromosome 4 SO MAMMALIAN GENOME LA English DT Article C1 DALHOUSIE UNIV,DEPT ANAT & NEUROBIOL,HALIFAX,NS B3H 4H7,CANADA. UNIV N CAROLINA,DEPT MED,CHAPEL HILL,NC 27599. RP Mock, BA (reprint author), NCI,GENET LAB,NIH,BLDG 37,RM 2B08,37 CONVENT DR,MSC 4255,BETHESDA,MD 20892, USA. NR 0 TC 4 Z9 4 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1997 VL 7 SI SI BP S60 EP S79 DI 10.1007/s003359900316 PG 20 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA XM207 UT WOS:A1997XM20700005 PM 9233387 ER PT J AU Ferraris, JD Norenburg, JL AF Ferraris, JD Norenburg, JL TI Oxygen uptake during repeated exposure to temperature change: Physiological divergence in Panamanian cognate pairs and latitudinally distant populations of decapod crustacea SO MARINE ECOLOGY-PUBBLICAZIONI DELLA STAZIONE ZOOLOGICA DI NAPOLI I LA English DT Article DE fluctuating temperature; oxygen uptake; invertebrate; Decapoda ID MITOCHONDRIAL-DNA; ISTHMUS AB The emergence of the Isthmus of Panama subdivided the amphi-American biota. In the present study; Pacific and Atlantic populations of four cognate pairs of crabs were used to discern whether exposure to different thermal regimes in habitats, in the putative absence of gene flow, has resulted in physiological divergence. Populations that potentially form a common genetic pool were also used; these were populations of the Atlantic Panama cognate that occur in belize and Florida. Decreases in water temperature occur periodically in Pacific Panama and Florida, but nor in Atlantic Panama or Belize. In this study, physiological divergence in oxygen uptake was assessed in response to repeated exposure to either control and decreased temperature or control and increased temperature. Results indicate that, in only some of the genera tested, exposure to decreases in habitat temperature has resulted in divergence. Partial support is found for the corollary that adaptation to an environment with periods of decreased temperature results in reduced compensation during exposure to elevated temperature. C1 SMITHSONIAN INST,NATL MUSEUM NAT HIST,WASHINGTON,DC 20560. RP Ferraris, JD (reprint author), NHLBI,KIDNEY & ELECTROLYTE METAB LAB,NIH,10 CTR DR MSC 1598,BLDG 10,RM 6N307,BETHESDA,MD 20892, USA. RI Norenburg, Jon/K-3481-2015 OI Norenburg, Jon/0000-0001-7776-1527 NR 26 TC 0 Z9 0 U1 1 U2 1 PU BLACKWELL WISSENSCHAFTS-VERLAG GMBH PI BERLIN PA KURFURSTENDAMM 57, D-10707 BERLIN, GERMANY SN 0173-9565 J9 PSZNI MAR ECOL JI Mar. Ecol.-Pubbl. Stn. Zool. Napoli PY 1997 VL 18 IS 2 BP 127 EP 146 PG 20 WC Marine & Freshwater Biology SC Marine & Freshwater Biology GA XQ578 UT WOS:A1997XQ57800003 ER PT J AU Ferraris, JD Norenburg, JL AF Ferraris, JD Norenburg, JL TI Volume and ion regulation during repeated exposure to temperature change: Physiological divergence in trans-isthmian cognate pairs and latitudinally distant populations of decapod crustacea SO MARINE ECOLOGY-PUBBLICAZIONI DELLA STAZIONE ZOOLOGICA DI NAPOLI I LA English DT Article DE volume regulation; ion regulation; invertebrate; temperature; Decapoda ID INTERTIDAL NEMERTINE; MITOCHONDRIAL-DNA; PANAMA; SALINITY; DECEREBRATION; TIME; K+ AB When the Isthmus of Panama emerged as a land bridge, it set the stage for allopatric speciation in the marine fauna. In the present study Pacific and Atlantic populations of three cognate pairs of crabs were used to discern whether physiological divergence has occurred as a result of exposure to different thermal regimes in habitats and in the putative absence of gene flow. Additional comparison was made with Belize and Florida populations of the Atlantic Panama cognate. This was done to test the strength of correlation between physiological divergence and exposure to different thermal regimes in populations that potentially form a common genetic pool. Water temperatures decrease periodically in Pacific Panama and Florida but not in Atlantic Panama or Belize. Physiological divergence in volume and ion regulation was assessed in response to repeated exposure to either control and decreased temperature or to control and increased temperature. Results indicate that exposure to naturally occurring decreased temperatures in habitats has resulted in divergence. This divergence is demonstrated both in enhanced ability to regulate volume at decreased temperature and impaired ability to regulate volume at elevated temperature. C1 SMITHSONIAN INST,NATL MUSEUM AMER HIST,WASHINGTON,DC 20560. RP Ferraris, JD (reprint author), NHLBI,LKEM,NIH,10 CTR DR MSC 1598,BLDG 10,RM 6N307,BETHESDA,MD 20892, USA. RI Norenburg, Jon/K-3481-2015 OI Norenburg, Jon/0000-0001-7776-1527 NR 32 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL WISSENSCHAFTS-VERLAG GMBH PI BERLIN PA KURFURSTENDAMM 57, D-10707 BERLIN, GERMANY SN 0173-9565 J9 PSZNI MAR ECOL JI Mar. Ecol.-Pubbl. Stn. Zool. Napoli PY 1997 VL 18 IS 3 BP 193 EP 209 PG 17 WC Marine & Freshwater Biology SC Marine & Freshwater Biology GA YD553 UT WOS:A1997YD55300001 ER PT B AU Kawahara, N Belayev, L Orzi, F Colangelo, V Klatzo, I AF Kawahara, N Belayev, L Orzi, F Colangelo, V Klatzo, I BE Ito, U Kirino, T Kuroiwa, T Klatzo, I TI Transneuronal induction of tolerance in cerebral ischemia SO MATURATION PHENOMENON IN CEREBRAL ISCHEMIA II: NEURONAL RECOVERY AND PLASTICITY LA English DT Proceedings Paper CT 2nd International Workshop on the Maturation Phenomenon in Cerebral Ischemia - Neuronal Recovery and Plasticity CY APR, 1996 CL TOKYO, JAPAN AB Development of enhanced tolerance to ischemic injury has been demonstrated when lethal ischemia is preceded by sublethal ischemic exposure. This study demonstrates a transneuronal induction of tolerance in distant areas, unaffected by primary ischemia, but connected by neuronal circuitry. In Model I, the induction of spreading depression in the cerebral cortex of the rat preceded 10-min cardiac arrest cerebral ischemia by 3 days. In Model II, the middle cerebral artery (MCA) occlusion for 2h in rats was followed 3 days later by 10-min clamping of both common carotid arteries, with simultaneous lowering of mean arterial blood pressure to 50 mm Hg. In Model III, 5-min bilateral occlusion of common carotid arteries in gerbils was preceded 3 days earlier by 35-min occlusion of the left common carotid artery in ischemia-sensitive animals. Our observations in Models I and II revealed a marked bilateral preservation of CA1 pyramidal neurons. Gerbils in Model III showed, on the side of the 35-min occlusion, numerous infarcted regions, including hippocampus, whereas the contralateral hippocampus revealed a marked preservation of CA1 neurons. It is assumed that CA1 pyramidal cell protection is transneuronally transmitted via the entorhinal cortex and is associated with early activation of c-fos expression in both hippocampi. RP Kawahara, N (reprint author), NIH,STROKE BRANCH,BLDG 36,ROOM 4A-03,CONVENT DR,MSC 4128,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN 33 PA HEIDELBERGER PLATZ 3, W-1000 BERLIN 33, GERMANY BN 3-540-61673-X PY 1997 BP 99 EP 104 PG 6 WC Neurosciences SC Neurosciences & Neurology GA BH47B UT WOS:A1997BH47B00013 ER PT B AU Kawahara, N Belayev, L Orzi, F Colangelo, V Klatzo, I AF Kawahara, N Belayev, L Orzi, F Colangelo, V Klatzo, I BE Ito, U Kirino, T Kuroiwa, T Klatzo, I TI Transneuronal induction of tolerance in cerebral ischemia SO MATURATION PHENOMENON IN CEREBRAL ISCHEMIA II: NEURONAL RECOVERY AND PLASTICITY LA English DT Proceedings Paper CT 2nd International Workshop on the Maturation Phenomenon in Cerebral Ischemia - Neuronal Recovery and Plasticity CY APR, 1996 CL TOKYO, JAPAN AB Development of enhanced tolerance to ischemic injury has been demonstrated when lethal ischemia is preceded by sublethal ischemic exposure. This study demonstrates a transneuronal induction of tolerance in distant areas, unaffected by primary ischemia, but connected by neuronal circuitry. In Model I, the induction of spreading depression in the cerebral cortex of the rat preceded 10-min cardiac arrest cerebral ischemia by 3 days. In Model II, the middle cerebral artery (MCA) occlusion for 2h in rats was followed 3 days later by 10-min clamping of both common carotid arteries, with simultaneous lowering of mean arterial blood pressure to 50 mm Hg. In Model III, 5-min bilateral occlusion of common carotid arteries in gerbils was preceded 3 days earlier by 35-min occlusion of the left common carotid artery in ischemia-sensitive animals. Our observations in Models I and II revealed a marked bilateral preservation of CA1 pyramidal neurons. Gerbils in Model III showed, on the side of the 35-min occlusion, numerous infarcted regions, including hippocampus, whereas the contralateral hippocampus revealed a marked preservation of CA1 neurons. It is assumed that CA1 pyramidal cell protection is transneuronally transmitted via the entorhinal cortex and is associated with early activation of c-fos expression in both hippocampi. RP Kawahara, N (reprint author), NIH,STROKE BRANCH,BLDG 36,ROOM 4A-03,CONVENT DR,MSC 4128,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN 33 PA HEIDELBERGER PLATZ 3, W-1000 BERLIN 33, GERMANY BN 3-540-61673-X PY 1997 BP 105 EP 111 PG 7 WC Neurosciences SC Neurosciences & Neurology GA BH47B UT WOS:A1997BH47B00014 ER PT B AU Spatz, M Yasuma, Y Strasser, A McCarron, RM AF Spatz, M Yasuma, Y Strasser, A McCarron, RM BE Ito, U Kirino, T Kuroiwa, T Klatzo, I TI The role of endothelin-1 and nitric oxide in cerebral ischemia SO MATURATION PHENOMENON IN CEREBRAL ISCHEMIA II: NEURONAL RECOVERY AND PLASTICITY LA English DT Proceedings Paper CT 2nd International Workshop on the Maturation Phenomenon in Cerebral Ischemia - Neuronal Recovery and Plasticity CY APR, 1996 CL TOKYO, JAPAN AB The effect of cerebral ischemia/reperfusion on vascular responses and endothelin (ET) content in cerebrospinal fluid was investigated in the presence and absence of N omega-nitro-L-arginine (NLA), the nitric oxide (NO) inhibitor. A single intraperitoneal injection of NLA (4 h prior to the induction of ischemia) stereospecifically increased systemic blood pressure (SBP) and reduced the transient, initial (early) recovery of cerebral blood flow (CBF). However, NLA treatment did not significantly affect the late hypoperfusion observed in either Ringer's- or N omega-nitro-D-arginine methyl ester (D-NAME)-treated animals. Both the early and late hypoperfusion coincided with the increased content of ET-1 in the cerebrospinal fluid. These findings strongly suggest that endogenously released ET-1 is responsible for the observed postischemic hypoperfusion. RP Spatz, M (reprint author), NINCDS,STROKE BRANCH,NIH,36 CONVENT DR,MSC 4128,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN 33 PA HEIDELBERGER PLATZ 3, W-1000 BERLIN 33, GERMANY BN 3-540-61673-X PY 1997 BP 189 EP 195 PG 7 WC Neurosciences SC Neurosciences & Neurology GA BH47B UT WOS:A1997BH47B00024 ER PT B AU Watson, JT AF Watson, JT BE Hetzer, R Hennig, E Loebe, M TI Prospects for permanent mechanical circulatory support SO MECHANICAL CIRCULATORY SUPPORT: IN CHILDREN - TOWARDS MYOCARDIAL RECOVERY - PERMANENT LA English DT Proceedings Paper CT Mechanical Circulatory Support Meeting CY OCT 21-22, 1995 CL BERLIN, GERMANY RP Watson, JT (reprint author), NHLBI,NATL INST HLTH,2 ROCKLEGE CTR,STE 9044,6701 ROCKLEGE DR,MSC 7940,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU DR DIETRICH STEINKOPFF VERLAG PI BERLIN 33 PA C/O SPRINGER VERLAG, HEIDELBERGER PLATZ 3, 1000 BERLIN 33, GERMANY BN 3-7985-1046-6 PY 1997 BP 185 EP 189 PG 5 WC Cardiac & Cardiovascular Systems; Engineering, Biomedical; Pediatrics SC Cardiovascular System & Cardiology; Engineering; Pediatrics GA BH83Z UT WOS:A1997BH83Z00016 ER PT J AU Meersseman, G Verschueren, K Nelles, L Blumenstock, C Kraft, H Wuytens, G Remacle, J Kozak, CA Tylzanowski, P Niehrs, C Huylebroeck, D AF Meersseman, G Verschueren, K Nelles, L Blumenstock, C Kraft, H Wuytens, G Remacle, J Kozak, CA Tylzanowski, P Niehrs, C Huylebroeck, D TI The C-terminal domain of Mad-like signal transducers is sufficient for biological activity in the Xenopus embryo and transcriptional activation SO MECHANISMS OF DEVELOPMENT LA English DT Article DE mothers against dpp; serine-threonine kinase receptors; signal transduction; transcription factors; transforming growth factor-beta ID TGF-BETA RECEPTOR; BONE MORPHOGENETIC PROTEIN-4; I RECEPTORS; VENTRALIZING FACTOR; MAMMALIAN-CELLS; KINASE RECEPTOR; THICK VEINS; DROSOPHILA; GENE; EXPRESSION AB We report the characterization of two vertebrate homologs of Drosophila mothers against dpp (Mad) isolated from the mouse and the Xenopus embryo, named MusMLP (mad-like protein) and XenMLP, respectively, together with a summary of their expression patterns in the embryo. Overexpression of XenMLP causes ventralization of Xenopus embryos and we demonstrate that the C-terminal domain is necessary and sufficient to confer this biological effect. This domain also has the potential for transcriptional activation, as shown in one-hybrid assays in mammalian cells. We further demonstrate that MLPs are multidomain proteins by showing a cis-negative effect of the N-terminal domain on the transactivation by the C-terminal domain and that the proline-rich, middle domain maximizes the activity of the C-terminal domain. We also mapped the MusMLP gene to a region on mouse chromosome 13 that corresponds to a region on human chromosome 59 that contains cancer-related genes. (C) 1997 Elsevier Science Ireland Ltd. C1 FLANDERS INTERUNIV INST BIOTECHNOL,DEPT CELL GROWTH DIFFERENTIAT & DEV,VIB,B-3000 LOUVAIN,BELGIUM. UNIV LOUVAIN,MOL BIOL LAB,CELGEN,B-3000 LOUVAIN,BELGIUM. DEUTSCH KREBSFORSCHUNGSZENTRUM,GERMAN CANC RES CTR,DIV MOL EMBRYOL,D-69120 HEIDELBERG,GERMANY. NIAID,MOL MICROBIOL LAB,NIH,BETHESDA,MD 20892. RI Tylzanowski, Przemko/G-8881-2013 NR 72 TC 62 Z9 63 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4773 J9 MECH DEVELOP JI Mech. Dev. PD JAN PY 1997 VL 61 IS 1-2 BP 127 EP 140 DI 10.1016/S0925-4773(96)00629-6 PG 14 WC Developmental Biology SC Developmental Biology GA WK611 UT WOS:A1997WK61100011 PM 9076683 ER PT J AU Fleishman, JA Schneider, DA Garcia, I Hardwick, K AF Fleishman, JA Schneider, DA Garcia, I Hardwick, K TI Dental service use among adults with human immunodeficiency virus infection SO MEDICAL CARE LA English DT Article ID ORAL LESIONS; DENTISTS ATTITUDES; LONGITUDINAL DATA; NATIONAL SURVEY; HIV-INFECTION; PREVALENCE; HEALTH; CARE; AIDS; BEHAVIOR C1 HLTH RESOURCES & SERV ADM,BUR HLTH RESOURCES DEV,ROCKVILLE,MD. NIDR,BETHESDA,MD 20892. RP Fleishman, JA (reprint author), AGCY HLTH CARE POLICY & RES,CTR COST & FINANCING,2101 E JEFFERSON ST,SUITE 502,ROCKVILLE,MD 20852, USA. NR 37 TC 10 Z9 10 U1 3 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD JAN PY 1997 VL 35 IS 1 BP 77 EP 85 DI 10.1097/00005650-199701000-00007 PG 9 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA WB739 UT WOS:A1997WB73900007 PM 8998205 ER PT J AU Sneller, MC Fauci, AS AF Sneller, MC Fauci, AS TI Pathogenesis of vasculitis syndromes SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Review ID TUMOR-NECROSIS-FACTOR; ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES; SYSTEMIC LUPUS-ERYTHEMATOSUS; HUMAN-ENDOTHELIAL-CELLS; INTERCELLULAR-ADHESION MOLECULE-1; BLOOD MONONUCLEAR-CELLS; HEPATITIS-C VIRUS; WEGENERS GRANULOMATOSIS; KAWASAKI-DISEASE; CIRCULATING ICAM-1 AB The pathogenesis of vasculitis is complex and involves a variety of mechanisms acting in concert to bring about necrotizing inflammation of blood vessel walls. Ln recent years, there has been considerable progress in dissecting the immunologic abnormalities present in specific vasculitis syndromes. Although the cause of most vasculitis syndromes remains a mystery, recent advances in molecular and cellular immunology have defined many of the effector mechanisms that mediate inflammatory vascular damage. C1 NIAID,IMMUNOREGULAT LAB,IMMUNOL DIS SECT,NIH,BETHESDA,MD 20892. NR 104 TC 58 Z9 62 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD JAN PY 1997 VL 81 IS 1 BP 221 EP & DI 10.1016/S0025-7125(05)70512-5 PG 23 WC Medicine, General & Internal SC General & Internal Medicine GA WE365 UT WOS:A1997WE36500011 PM 9012762 ER PT J AU Sallie, R AF Sallie, R TI Hepatitis B virus replication and mutation are autoregulated by interactions between surface antigen and HBeAg and the HBV DNA polymerase: A functional model with therapeutic implications SO MEDICAL HYPOTHESES LA English DT Article ID ACUTE VIRAL-HEPATITIS; HEPATOCELLULAR-CARCINOMA; INFECTION; LIVER; PERSISTENCE; INTERFERON; HBSAG; REACTIVATION; LYMPHOCYTES; MECHANISMS AB Infection with hepatitis B virus can result in asymptomatic seroconversion with viral clearance, fulminant hepatic failure and death, or chronic, typically lifelong, transmissible infection. The mechanism(s) of viral persistence are poorly understood but viral clearance and fulminant hepatic failure are generally thought to result from co-ordinated and effective and abnormally vigorous immune responses, respectively, whereas viral persistence results from immunological failure in addition to poorly characterized viral factors promoting persistence. This paper proposes (1) that the predominant viral factor(s) promoting persistence of hepatitis B virus are homeostatic mechanism(s) responsible for modulating its replication and mutation and (2) that chronic hepatitis B results when these mechanisms are successful and other outcomes occur when these homeostatic mechanism(s) fail. Furthermore, it is proposed that seroconversion (e.g. from HBsAg to anti HBsAg positivity), when it occurs, is a consequence facilitated by restricted viral antigenic diversity and reduced viral replication rather than a proximate cause of it. The specific homeostatic mechanisms proposed negative feedback inhibition of hepatitis B virus DNA polymerase/reverse transcriptase mediated by HBs antigen and a hepatitis B virus DNA polymerase fidelity modulating function of HBeAg - are consistent with the available data and resolve many paradoxical clinical observations. But, more importantly, this model has clear implications for therapy, including the rational design of drugs and therapeutic vaccines. RP Sallie, R (reprint author), NIDDK,LIVER UNIT,NIH,ROOM 4D-52,BLDG 10,BETHESDA,MD 20892, USA. NR 32 TC 4 Z9 4 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD JAN PY 1997 VL 48 IS 1 BP 1 EP 10 DI 10.1016/S0306-9877(97)90016-5 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA WH735 UT WOS:A1997WH73500001 PM 9049982 ER PT J AU Yu, QS Greig, NH Holloway, HW Utsuki, T Pei, XF Brossi, A AF Yu, QS Greig, NH Holloway, HW Utsuki, T Pei, XF Brossi, A TI (-)-(3aS)-eseroline carbamate, a close analogue of physostigmine SO MEDICINAL CHEMISTRY RESEARCH LA English DT Article ID ALZHEIMERS-DISEASE; PHARMACOKINETICS; RAT AB (-)-Eseroline 1 on reaction with trimethylsilyl isocyanate in refluxing toluene directly gave the crystalline carbamate 5, which is the simplest carbamate of eseroline whose activity has not previously been reported. Surprisingly, unlike physostigmine and numerous analogs, carbamate 5 was found to possess only low enzyme inhibitory activity against human acetyl-(AChE) and butyrylcholinesterase (BChE) in vitro and only minimal action when administered to rats in in vivo studies. Its synthesis and pharmacology, in comparison to physostigmine and known n-alkyl and aryl carbamates, are reported for the first time. C1 NIDDK,BIOORGAN CHEM LAB,NIH,BETHESDA,MD 20892. UNIV N CAROLINA,SCH PHARM,CHAPEL HILL,NC 27599. RP Yu, QS (reprint author), NIA,GERONTOL RES CTR,CELLULAR & MOL BIOL LAB,NIH,4940 EASTERN AVE,BALTIMORE,MD 21224, USA. NR 17 TC 4 Z9 4 U1 0 U2 0 PU BIRKHAUSER BOSTON INC PI CAMBRIDGE PA 675 MASSACHUSETTS AVE, CAMBRIDGE, MA 02139 SN 1054-2523 J9 MED CHEM RES JI Med. Chem. Res. PY 1997 VL 7 IS 2 BP 116 EP 122 PG 7 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA XA526 UT WOS:A1997XA52600006 ER PT J AU Aggleton, JP Saunders, RC AF Aggleton, JP Saunders, RC TI The relationships between temporal lobe and diencephalic structures implicated in anterograde amnesia SO MEMORY LA English DT Article ID MATCHING-TO-SAMPLE; LASTING MEMORY IMPAIRMENT; MEDIAL THALAMIC LESIONS; VISUAL RECOGNITION; FORNIX TRANSECTION; HIPPOCAMPAL-FORMATION; WORKING-MEMORY; MEDIODORSAL NUCLEUS; PREFRONTAL LESIONS; EPISODIC MEMORY AB The relationship between the anterograde amnesic syndromes associated with diencephalic and temporal lobe pathology is examined in the light of recent findings. It is proposed that a common feature of anterograde amnesia is damage to part of an ''extended hippocampal system'' comprising the hippocampus, the fornix, the mammillary bodies, and the anterior thalamic nuclei. Damage to this system results in deficits in the recall of episodic information, the core symptom of anterograde amnesia. In contrast, lesions in this system need not disrupt tests of recognition memory when they primarily tax familiarity judgements. It is assumed that familiarity judgements depend on other regions (e.g. the rhinal cortex in the case of temporal lobe amnesia) and that the extended hippocampal system is principally involved in those aspects of recognition that are retrieval-based rather than familiarity-based. These proposals arise from new evidence on the performance of delayed nonmatching-to-sample by animals, from a meta-analysis of the performance of amnesic subjects on a test of recognition memory, and from new research into the pattern of connections between the medial temporal lobe and the medial diencephalon in primates. C1 NIMH,BETHESDA,MD 20892. RP Aggleton, JP (reprint author), UNIV WALES COLL CARDIFF,COLL CARDIFF,SCH PSYCHOL,POB 901,CARDIFF CF1 3YG,S GLAM,WALES. OI Aggleton, John/0000-0002-5573-1308 NR 92 TC 74 Z9 75 U1 2 U2 9 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE, EAST SUSSEX, ENGLAND BN3 2FA SN 0965-8211 J9 MEMORY JI Memory PD JAN-MAR PY 1997 VL 5 IS 1-2 BP 49 EP 71 PG 23 WC Psychology, Experimental SC Psychology GA WV187 UT WOS:A1997WV18700004 PM 9156091 ER PT J AU Leyendecker, B Lamb, ME Fracasso, MP Scholmerich, A Larson, C AF Leyendecker, B Lamb, ME Fracasso, MP Scholmerich, A Larson, C TI Playful interaction and the antecedents of attachment: A longitudinal study of Central American and Euro-American mothers and infants SO MERRILL-PALMER QUARTERLY-JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID STRANGE SITUATION; 1ST YEAR; SECURITY; ORIGINS; RESPONSIVENESS; PERSPECTIVES; HISPANICS; BEHAVIOR; DISTRESS; TIME AB Microanalytic procedures were used to explore maternal and infant behaviors, behavioral coordination, maternal response, and nonresponse in relation to security of attachment. Two samples, one of recent immigrants from central America (n = 39) and the other of mothers and infants from middle-class Euro-American backgrounds (n = 40) were videotaped when the infants were ages 4, 8, and 12 months. Individual differences an measures of maternal response and nonresponse were stable over time and strongly related to the security of attachment, as were some measures of infant behavior and behavioral coordination. The maternal response measures reflected similar associations between maternal behavior and attachment security in the two groups. The results are consistent with other findings showing that mothers of insecure infants are most involved with their infants in such contexts. C1 NICHHD,SECT SOCIAL & EMOTIONAL DEV,BETHESDA,MD 20814. RI Schoelmerich, Axel/C-9039-2009 OI Schoelmerich, Axel/0000-0002-9844-3920 NR 47 TC 24 Z9 24 U1 1 U2 3 PU WAYNE STATE UNIV PRESS PI DETROIT PA 4809 WOODWARD AVE, DETROIT, MI 48201-1309 SN 0272-930X J9 MERRILL PALMER QUART JI Merrill-Palmer Q.-J. Dev. Psychol. PD JAN PY 1997 VL 43 IS 1 BP 24 EP 47 PG 24 WC Psychology, Developmental SC Psychology GA WE106 UT WOS:A1997WE10600002 ER PT J AU Vittone, J Blackman, MR BusbyWhitehead, J Tsiao, C Stewart, KJ Tobin, J Stevens, T Bellantoni, MF Rogers, MA Baumann, G Roth, J Harman, SM Spencer, RGS AF Vittone, J Blackman, MR BusbyWhitehead, J Tsiao, C Stewart, KJ Tobin, J Stevens, T Bellantoni, MF Rogers, MA Baumann, G Roth, J Harman, SM Spencer, RGS TI Effects of single nightly injections of growth hormone-releasing hormone (GHRH 1-29) in healthy elderly men SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article; Proceedings Paper CT National Meeting of the American-Federation-for-Clinical-Research CY APR 30-MAY 02, 1994 CL BALTIMORE, MD SP Amer Federat Clin Res ID MAGNETIC-RESONANCE SPECTROSCOPY; FACTOR-I LEVELS; BINDING-PROTEIN; SKELETAL-MUSCLE; DEFICIENT ADULTS; OLD MEN; METABOLISM; RATS; PH; RADIOIMMUNOASSAY AB Age-related reductions in growth hormone IGH) and insulin-like growth factor-I (IGF-I) may contribute to decreased muscle mass and strength in older persons. The relationship of this phenomenon to skeletal muscle bioenergetics has not been reported. We sought to determine whether administration of OH-releasing hormone (GHRH) would sustain increases in GH and IGF-I and improve skeletal muscle function and selected measures of body composition and metabolism. We measured GH secretion, muscle strength, muscle histology, and muscle energy metabolism by phosphorus nuclear magnetic resonance spectroscopy (P-31-NMRS), body composition, and endocrine-metabolic functions before and after 6 weeks of treatment. Eleven healthy, ambulatory, non-obese men aged 64 to 76 years with low baseline IGF-I levels were treated at home as outpatients by nightly subcutaneous self-injections of 2 mg GHRH for 6 weeks. We measured GH levels in blood samples obtained every 20 minutes from 8:00 PM to 8:00 AM; AM serum levels of IGF-I, IGF binding protein-3 (IGFBP-3), and GH binding protein (GHBP); muscle strength; muscle histology; the normalized phosphocreatine abundance, PCr/[PCr + Pi], and intracellular pH in forearm muscle by NMRS during both sustained and ramped exercise; body composition by dual-energy x-ray absorptiometry (DEXA); lipid levels; and glucose, insulin, and GH levels during an oral glucose tolerance test (OGTT). GHRH treatment increased mean nocturnal GH release (P < .02), the area under the GH peak ([AUPGH] P < .006), and GH peak amplitude (P < .05), with no change in GH pulse frequency or in levels oi IGF-I, IGFBP-3, or GHBP. Two of six measures of muscle strength, upright row (P < .02) and shoulder press (P < .04), and a test of muscle endurance, abdominal crunch (P < .03), improved. GHRH treatment did not alter exercise-mediated changes in PCr/[PCr + Pi] or intracellular pH, but decreased or abolished significant relationships between changes in PCr/[PCr + Pi] or pH and indices of muscle strength. GHRH treatment did not change weight, body mass index, waist to hip ratio, DEXA measures of muscle and fat, muscle histology, glucose, insulin, or GH responses to OGTT, or lipids. No significant adverse effects were observed. These data suggest that single nightly doses of GHRH are less effective than multiple daily doses of GHRH in eliciting GH- and/or IGF-I-mediated effects. GHRH treatment may increase muscle strength, and it alters baseline relationships between muscle strength and muscle bioenergetics in a manner consistent with a reduced need for anaerobic metabolism during exercise. Thus, an optimized regimen of GHRH administration might attenuate some of the effects of aging on skeletal muscle function in older persons. Copyright (C) 1997 by W.B. Saunders Company C1 JOHNS HOPKINS BAYVIEW MED CTR,DEPT MED,BALTIMORE,MD 21224. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. NIA,GERONTOL RES CTR,NIH,BALTIMORE,MD 21224. UNIV MARYLAND,DEPT KINESIOL,COLLEGE PK,MD 20742. NORTHWESTERN UNIV,SCH MED,DEPT MED,CHICAGO,IL 60611. OI Bellantoni, Michele/0000-0001-8525-2247 FU NCRR NIH HHS [MO-1-RR-02719]; NIA NIH HHS [R0-1-AG-1102] NR 45 TC 36 Z9 37 U1 0 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD JAN PY 1997 VL 46 IS 1 BP 89 EP 96 DI 10.1016/S0026-0495(97)90174-8 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA WD749 UT WOS:A1997WD74900017 PM 9005976 ER PT J AU Young, HA AF Young, HA TI Interferon expression by B cells SO METHODS-A COMPANION TO METHODS IN ENZYMOLOGY LA English DT Article ID FLAVONE ACETIC-ACID; GAMMA GENE; IFN-GAMMA; LINES; INDUCTION; ALPHA; DIFFERENTIATION; BETA AB Interferons have effects on many facets of immune system development, maturation, and function. B cells are a target for the interferons, causing alterations in cell differentiation and gene expression. However, production of interferons by B cells has not been widely studied. In this review I will discuss the limited literature on B-cell interferon production. In addition I will describe results obtained from a transgenic model in which interferon-gamma production has been targeted to the B-cell compartment. In this animal, B-cell development is blocked, reflecting the deleterious effects that aberrant expression of interferon can have on this cell population. (C) 1997 Academic Press, Inc. RP Young, HA (reprint author), NCI,FREDERICK CANC RES & DEV CTR,HEAD CELLULAR & MOL IMMUNOL SECT,LAB EXPT IMMUNOL,DIV BASIC SCI,FREDERICK,MD 21702, USA. NR 24 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 1046-2023 J9 METHODS JI Methods PD JAN PY 1997 VL 11 IS 1 BP 112 EP 115 DI 10.1006/meth.1996.0394 PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA XT375 UT WOS:A1997XT37500015 PM 8990096 ER PT J AU Rieckmann, P Tuscano, JM Kehrl, JH AF Rieckmann, P Tuscano, JM Kehrl, JH TI Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in B-Lymphocyte function SO METHODS-A COMPANION TO METHODS IN ENZYMOLOGY LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; NF-KAPPA-B; HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-INFECTED INDIVIDUALS; AUTOCRINE GROWTH-FACTOR; T-CELL CLONES; TRANSCRIPTION FACTOR; CASTLEMANS DISEASE; ACTIVATING-FACTOR; CYCLOSPORINE-A AB Two cytokines important in the regulation of B-cell function are tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). They act at different steps in B-cell differentiation and can be produced by the B cells themselves upon appropriate stimulation. Crosslinking of surface Ig and signaling through CD22 or CD40 lead to increased secretion of both cytokines. Neutralization of TNF-alpha or IL-6 biologic activity in B-cell cultures results in a significant reduction in B-cell proliferation and Ig secretion. Increased production of these cytokines is found in several diseases associated with aberrant B-cell function. This review will focus on the role of TNF-alpha and IL-6 in normal and pathophysiological conditions of B-cell function. (C) 1997 Academic Press Inc. C1 NIAID,IMMUNOREGULAT LAB,NIH,BETHESDA,MD 20892. RP Rieckmann, P (reprint author), UNIV WURZBURG,DEPT NEUROL,JOSEF SCHNEIDER STR 2,D-97080 WURZBURG,GERMANY. NR 65 TC 32 Z9 32 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 1046-2023 J9 METHODS JI Methods PD JAN PY 1997 VL 11 IS 1 BP 128 EP 132 DI 10.1006/meth.1996.0396 PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA XT375 UT WOS:A1997XT37500017 PM 8990098 ER PT S AU Pauly, RR Bilato, C Cheng, L Monticone, R Crow, MT AF Pauly, RR Bilato, C Cheng, L Monticone, R Crow, MT BE Emerson, CP Sweeney, HL TI Vascular smooth muscle cell cultures SO METHODS IN CELL BIOLOGY, VOL 52: METHODS IN MUSCLE BIOLOGY SE Methods in Cell Biology LA English DT Review ID HEAVY-CHAIN ISOFORM; BIOLOGICAL-ACTIVITY; ACTIN EXPRESSION; CAROTID ARTERIES; PROTEIN-KINASE; GROWTH-FACTOR; PHENOTYPE; MODULATION; MIGRATION; CALPONIN RP Pauly, RR (reprint author), NIA, NATL INST HLTH, VASC BIOL GRP, LAB CARDIOVASC SCI, BALTIMORE, MD 21224 USA. NR 32 TC 38 Z9 38 U1 0 U2 3 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X BN 0-12-238190-4 J9 METHOD CELL BIOL JI Methods Cell Biol. PY 1997 VL 52 BP 133 EP 154 DI 10.1016/S0091-679X(08)60377-5 PG 22 WC Cell Biology SC Cell Biology GA BJ78C UT WOS:A1997BJ78C00007 PM 9379948 ER PT S AU Federspiel, MJ Hughes, SH AF Federspiel, MJ Hughes, SH BE Emerson, CP Sweeney, HL TI Retroviral gene delivery SO METHODS IN CELL BIOLOGY, VOL 52: METHODS IN MUSCLE BIOLOGY SE Methods in Cell Biology LA English DT Review ID ROUS-SARCOMA VIRUS; AVIAN-LEUKOSIS VIRUS; MURINE LEUKEMIA-VIRUS; CHICKEN-EMBRYO FIBROBLASTS; HUMAN ADENOSINE-DEAMINASE; LONG TERMINAL REPEATS; HIGH-TITER STRAIN; MAMMALIAN-CELLS; MEDIATED TRANSFER; SKELETAL-MUSCLE C1 NCI, FREDERICK CANC RES & DEV CTR, ABL BASIC RES PROGRAM, FREDERICK, MD 21702 USA. RP Federspiel, MJ (reprint author), MAYO CLIN & MAYO FDN, PROGRAM MOL MED, 200 1ST ST SW, ROCHESTER, MN 55905 USA. NR 94 TC 83 Z9 84 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X BN 0-12-238190-4 J9 METHOD CELL BIOL JI Methods Cell Biol. PY 1997 VL 52 BP 179 EP + DI 10.1016/S0091-679X(08)60379-9 PG 0 WC Cell Biology SC Cell Biology GA BJ78C UT WOS:A1997BJ78C00009 PM 9379950 ER PT J AU Lindsberg, PJ Siren, AL Hallenbeck, JM AF Lindsberg, PJ Siren, AL Hallenbeck, JM TI Microvascular perfusion during focal vasogenic brain edema: A scanning laser fluorescence microscopy study SO MICROVASCULAR RESEARCH LA English DT Article ID CEREBRAL BLOOD-FLOW; CAPILLARY NETWORK; MORPHOMETRIC INDEXES; RAT BRAINS; PERMEABILITY; RECRUITMENT; HEMORRHAGE; ISCHEMIA; BARRIER; DAMAGE AB Controversy exists about the effect of tissue edema on cerebral microcirculation. High spatial resolution is required for observation of extravasation and microcirculation during focal vasogenic edema formation. To study the relationship between tissue edema and perfusion, we developed a technique for simultaneous visualization of extravasation and microvessel perfusion in rats. Focal intracortical microvascular injury was generated with a 1-sec Nd-YAG laser pulse. Evans blue albumin (EBA) was infused 30 min before decapitation to study extravasation and FITC-dextran was injected 30 sec prior to decapitation to examine microvessel perfusion. Computerized scanning laser-excited fluorescence microscopy followed by high resolution image analysis permitted quantitative assessment of both parameters on single fresh-frozen brain sections. Studied at 30 min (3.66 +/- 0.15 mm), 2 hr (4.14 +/- 0.08 mm, P < .05), and 8 hr (4.69 +/- 0.18 mm, P < .01) after injury, the diameter of the circular, sharply demarcated zone of EBA-extravasation increased progressively. At 30 min, microvessels at a zone surrounding the area of EBA-extravasation contained 69 +/- 14% (P < .05) more fluorescent FITC-filling than in the control hemisphere, but the density of perfused microvessels was unchanged. At 2 hr, secondary tissue changes had already occurred in a zone surrounding the initial laser lesion. While severe reduction in the density (-76 +/- 13%, P < .05) of perfused microvessels was observed within 400 to 240 mu m inside the border of EBA extravasation, perfusion indexes were normal despite the presence of extravasated plasma constituents within 0-80 mu m from the border. In a narrow zone (80 mu m) outside the border of extravasation, individual microvessels contained 34 +/- 9% (P < .01) less FITC-fluorescence than those in a homologous area of the uninjured contralateral hemisphere. This report demonstrates the feasibility of simultaneous measurement and high-resolution mapping of indices of microvascular perfusion (density, filling) and extravasated plasma constituents in damaged and intact brain areas. In this model, the presence of extravasated plasma constituents the size of proteins did not immediately influence indices of cortical microcirculation. However, microvascular perfusion may be perturbed surrounding such an area of advancing vasogenic edema formation. C1 UNIFORMED SERV UNIV HLTH SCI,F EDWARD HEBERT SCH MED,DEPT NEUROL,BETHESDA,MD 20814. UNIV HELSINKI,CENT HOSP,DEPT NEUROL,SF-00290 HELSINKI,FINLAND. NINCDS,STROKE BRANCH,NIH,BETHESDA,MD 20892. RI Lindsberg, Perttu/F-1271-2010; OI Siren, Anna-Leena/0000-0002-2217-0081 NR 33 TC 6 Z9 6 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 0026-2862 J9 MICROVASC RES JI Microvasc. Res. PD JAN PY 1997 VL 53 IS 1 BP 92 EP 103 DI 10.1006/mvre.1996.1981 PG 12 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA WK468 UT WOS:A1997WK46800009 PM 9056479 ER PT J AU Lewis, EN Levin, IW Crocombe, RA AF Lewis, EN Levin, IW Crocombe, RA TI Applications of infrared imaging with a focal plane array detector and a step-scan FT-IR spectrometer SO MIKROCHIMICA ACTA LA English DT Article; Proceedings Paper CT 10th International Conference on Fourier Transform Spectroscopy (ICOFTS) CY AUG 27-SEP 01, 1995 CL BUDAPEST, HUNGARY SP Fed Eur Chem Soc, Hung Acad Sci, Working Comm Laser Phys Spectro HAS, Minist Cult Educ Hungary, Austrian Soc Anal Chem, Hung Nat Comm Technol Develop, Inst Isotopes HAS, Univ Veszprem, Central Res Inst Chem HAS DE FT-IR; step-scan; focal-plane array; imaging; microscopy AB A powerful new mid-infrared spectroscopic chemical imaging technique combining step-scan Fourier transform (FT) Michelson interferometry with indium antimonide (InSb) focal-plane array (FPA) image detection is described. The coupling of an infrared focal-plane array detector to an interferometer provides an instrumental multiplex/multichannel advantage. Specifically, the multiple detector elements enable spectra at all pixels to be collected simultaneously, while the interferometer allows all the spectral frequencies to be measured concurrently. C1 BIORAD DIGILAB DIV,CAMBRIDGE,MA 02139. NIDDKD,CHEM PHYS LAB,NIH,BETHESDA,MD 20892. NR 3 TC 0 Z9 0 U1 0 U2 3 PU SPRINGER-VERLAG WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0026-3672 J9 MIKROCHIM ACTA JI Mikrochim. Acta PY 1997 SU 14 BP 589 EP 590 PG 2 WC Chemistry, Analytical SC Chemistry GA WW404 UT WOS:A1997WW40400148 ER PT J AU Vargas, MP Vargas, HI Kleiner, DE Merino, MJ AF Vargas, MP Vargas, HI Kleiner, DE Merino, MJ TI The role of prognostic markers (MiB-1, RB, and bcl-2) in the diagnosis of parathyroid tumors SO MODERN PATHOLOGY LA English DT Article DE bcl-2; MiB-1; p53; parathyroid adenoma; parathyroid carcinoma; retinoblastoma ID SUPPRESSOR GENE; PROLIFERATIVE ACTIVITY; THYROID-GLAND; P53 MUTATIONS; CARCINOMA; PROTEIN; ACCUMULATION; ASSOCIATION; EXPRESSION; CYTOMETRY AB Assessment of the malignant potential of parathyroid tumors in the absence of metastasis can be difficult using morphologic criteria alone. The role of prognostic markers that may assist in evaluating aggressive behavior in these tumors has not been fully studied. We performed a retrospective study of 31 parathyroid lesions, including 10 adenomas, 10 atypical lesions, and 11 carcinomas, to evaluate the diagnostic and prognostic role of the MiB-1, p53, RB, and bcl-2 markers by immunohistochemical techniques. The mean tumor proliferative fraction (TPF), expressed as the number of MiB-1-positive nuclei per 1000 cells, was 20.3 in adenomas (range, 5-51), 20.0 in atypical lesions (range, 8-36), and 79.8 in carcinomas (range, 4-133). Only 1 of 20 benign lesions had a TPF more than 40, and only 2 of 11 carcinomas had a TPF less than 40. One atypical lesion and two carcinomas showed scattered cells positive for p53. Patients with the adenoma with increased TPF and the atypical lesion with positive p53 have been free of disease for 16 months. bcl-2 was expressed in 7 (70%) of 10 adenomas, 2 (20%) of 10 atypical lesions, and 4 (36%) of 11 carcinomas. Two Of the 11 carcinomas were RB negative, whereas all of the 20 benign lesions were RB positive. We conclude that high TPF (greater than 40 as measured by staining with MiB-1) strongly correlates with malignancy and, therefore, may be useful in the diagnosis of carcinomas. Negative RB stain, although not a common event, may be helpful to exclude benign lesions. Other tumor markers (p53 and bcl-2) were not useful in distinguishing malignant from benign lesions. C1 NCI,NIH,PATHOL LAB,BETHESDA,MD 20892. NCI,NIH,SURG BRANCH,BETHESDA,MD 20892. OI Kleiner, David/0000-0003-3442-4453 NR 27 TC 45 Z9 46 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD JAN PY 1997 VL 10 IS 1 BP 12 EP 17 PG 6 WC Pathology SC Pathology GA WD752 UT WOS:A1997WD75200003 PM 9021722 ER PT J AU Templeton, TJ Kaslow, DC AF Templeton, TJ Kaslow, DC TI Cloning and cross-species comparison of the thrombospondin-related anonymous protein (TRAP) gene from Plasmodium knowlesi, Plasmodium vivax and Plasmodium gallinaceum SO MOLECULAR AND BIOCHEMICAL PARASITOLOGY LA English DT Article DE thrombospondin-related anonymous protein (TRAP); Plasmodium gallinaceum; Plasmodium knowlesi; Plasmodium vivax ID SPOROZOITE SURFACE PROTEIN-2; HUMAN MALARIA PARASITE; RIBOSOMAL-RNA GENE; CIRCUMSPOROZOITE PROTEIN; FALCIPARUM SPOROZOITES; CRYSTAL-STRUCTURE; SALIVARY-GLANDS; I-DOMAIN; CELLS; HEPATOCYTES AB To examine the structure of the Plasmodium sporozoite micronemal protein, thrombospondin-related anonymous protein (TRAP) we have isolated TRAP genes from three species of Plasmodium: P. gallinaceum (PgTRAP), P. knowlesi (PkTRAP) and P. vivax (PvTRAP). Thus it is now possible to compare the TRAP gene from a total of six species of Plasmodium. The overall structure of TRAP is conserved in all species; specifically, an amino-terminal A-domain similar to magnesium-binding domains of mammalian integrins a thrombospondin-like sulfatide-binding domain similar to region II in Plasmodium circumsporozoite protein. an acidic asparagine/proline-rich repeat region; a trans-membrane domain and a short acidic cytoplasmic region with a highly conserved carboxy terminus. The overall structure of TRAP from P. gallinaceum and P. falciparum (PfTRAP) is conserved and phylogenetic analysis suggests a monophyletic relationship of avian P. gallinaceum and human P. falciparum. Comparison of the amino acid sequences of the A-domain of PgTRAP and PfTRAP indicates a more rapid divergence of this domain with respect to the rest of the protein in these two species. The structural differences of PgTRAP and PfTRAP may relate to the distinct invasion pathways, macrophage and endothelial cell invasion of P. gallinaceum sporozoites versus hepatocyte invasion of P. falciparum. Copyright (C) 1997 Elsevier Science B.V. C1 NIAID,MALARIA VACCINES SECT,PARASIT DIS LAB,NIH,BETHESDA,MD 20892. NR 47 TC 59 Z9 60 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-6851 J9 MOL BIOCHEM PARASIT JI Mol. Biochem. Parasitol. PD JAN PY 1997 VL 84 IS 1 BP 13 EP 24 DI 10.1016/S0166-6851(96)02775-2 PG 12 WC Biochemistry & Molecular Biology; Parasitology SC Biochemistry & Molecular Biology; Parasitology GA WG376 UT WOS:A1997WG37600003 PM 9041517 ER PT J AU Lenczowski, JM Dominguez, L Eder, AM King, LB Zacharchuk, CM Ashwell, JD AF Lenczowski, JM Dominguez, L Eder, AM King, LB Zacharchuk, CM Ashwell, JD TI Lack of a role for Jun kinase and AP-1 in Fas-induced apoptosis SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ACTIVATED PROTEIN-KINASES; SIGNAL-TRANSDUCTION PATHWAYS; DOMINANT-NEGATIVE MUTANT; SERUM RESPONSE ELEMENT; HUMAN T-CELLS; C-JUN; TRANSCRIPTION FACTORS; HA-RAS; BETA-GALACTOSIDASE; DELETION MUTANT AB Cross-linking of Fas (CD95) induces apoptosis, a response that has been reported to depend upon the Ras activation pathway. Since man?; examples of apoptosis have been reported to involve AP-1 and/or the AP-1-activating enzyme Jun kinase (JNK), downstream effecters of Pas or Ras-like small GTP-binding proteins, we evaluated the role of these molecules in Fas-mediated apoptosis. Although cross-linking of Pas an Jurkat T cells did result in JNK activation, increased activity was observed relatively late, being detectable only after 60 min of stimulation. Expression of a dominant negative form of SEK1 that blocked Pas-mediated induction of JNK activity had no effect on Pas-mediated apoptosis, Furthermore, maximally effective concentrations of anti-Pas did not cause JNK activation if apoptosis was blocked by a cysteine protease inhibitor, suggesting that under these conditions, activation of JNK may be secondary to the stress of apoptosis rather than a direct result of Fas engagement, Despite the activation of JNK, there was no induction of AP-I activity as determined by gel shift assay or induction of an AP-1-responsive reporter, The lack of a requirement for AP-1 induction in Pas-mediated death was further substantiated with Jurkat cells that were stably transfected with a dominant negative cJun, TAM-67. While TAM-67 effectively prevented AP-1-dependent transcription of both the interleukin-2 and cJun genes, it had no effect on Pas-induced cell death, even at limiting levels of Pas signaling, Thus, induction of JNK activity in Jurkat cells hy ligation of Pas at levels sufficient to cause cell death is likely a result, rather than a cause, of the apoptotic response, and AP-1 function is not required for Pas-induced apoptosis. C1 NIH,LAB IMMUNE CELL BIOL,BETHESDA,MD 20892. UNIV SANTIAGO DE COMPOSTELA,FAC BIOL,DEPT BIOQUIM & BIOL MOL,SANTIAGO COMPOSTE,SPAIN. NR 80 TC 222 Z9 224 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JAN PY 1997 VL 17 IS 1 BP 170 EP 181 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WA233 UT WOS:A1997WA23300019 PM 8972197 ER PT J AU Rein, T Zorbas, H DePamphilis, ML AF Rein, T Zorbas, H DePamphilis, ML TI Active mammalian replication origins are associated with a high-density cluster of (m)CpG dinucleotides SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DIHYDROFOLATE-REDUCTASE DOMAIN; BIDIRECTIONAL DNA-REPLICATION; XENOPUS EGG EXTRACT; ESCHERICHIA-COLI; INITIATION SITES; GENE-EXPRESSION; NUCLEAR MATRIX; METHYLATED DNA; RIBOSOMAL DNA; START SITES AB ori-beta is a well-characterized origin of bidirectional replication (OBR) located similar to 17 kb downstream of the dihydrofolate reductase gene in hamster cell chromosomes. The similar to 2-kb region of ori-beta that exhibits greatest replication initiation activity also contains 12 potential methylation sites in the form of CpG dinucleotides, To ascertain whether DNA methylation might play a role at mammalian replication origins, the methylation status of these sites was examined with bisulfite to chemically distinguish cytosine (C) from 5-methylcytosine (C-m), All of the CpGs were methylated, and nine of them were located within 356 hp flanking the minimal OBR, creating a high-density cluster of (m)CpGs that was similar to 10 times greater than average for human DNA. However, the previously reported densely methylated island in which all cytosines were methylated regardless of their dinucleotide composition was not detected and appeared to he an experimental artifact, ti second OBR, located at the 5' end of the RPS14 gene, exhibited a strikingly similar methylation pattern, and the organization of CPG dinucleotides at other mammalian origins revealed the potential for high-density CpG methylation, Moreover, analysis of bromodeoxyuridine-labeled nascent DNA confirmed that active replication origins were methylated. These results suggest that a high-density cluster of (m)CpG dinucleotides may play a role in either the establishment or the regulation of mammalian replication origins. C1 UNIV MUNICH,DEPT BIOCHEM,D-81377 MUNICH,GERMANY. RP Rein, T (reprint author), NICHHD,NIH,BLDG 6,ROOM 416,BETHESDA,MD 20892, USA. NR 80 TC 87 Z9 90 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JAN PY 1997 VL 17 IS 1 BP 416 EP 426 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WA233 UT WOS:A1997WA23300044 PM 8972222 ER PT J AU Xu, RH Kim, J Taira, M Lin, JJ Zhang, CH Sredni, D Evans, T Kung, HF AF Xu, RH Kim, J Taira, M Lin, JJ Zhang, CH Sredni, D Evans, T Kung, HF TI Differential regulation of neurogenesis by the two Xenopus GATA-1 genes SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID BONE MORPHOGENETIC PROTEIN-4; TRANSCRIPTION FACTOR GATA-2; NEURAL INDUCTION; VENTRALIZING FACTOR; MESODERM INDUCTION; SPEMANN ORGANIZER; BINDING PROTEINS; EARLY RESPONSE; MESSENGER-RNA; EXPRESSION AB Previously, we have shown that the ventralizing factor bone morphogenetic protein 4 (BMP-4) can inhibit Xenopus neurogenesis. The erythroid transcription factor GATA-1 functions downstream of the BMP-4 signaling pathway and mediates BMP-4-induced erythropoiesis. We hare found that similar to BMP-4, GATA-1b inhibits neuralization of Xenopus animal cap (AC) cells. The neural inhibition is not seen with GATA-1a, although both GATA-1a and GATA-1b RNAs are translated at the same efficiency and induce globin expression equally in AC cells. GATA-1b RNA injection into AC cells neither induces expression of Xbra (a general mesoderm marker) nor affects expression of XK81 (epidermal keratin) or BMP-4 and Xvent-1 (two ventral markers). These data suggest that GATA-1b retains the epidermal fate of the AC. Intact GATA-1b protein is required for both inhibition of neurogenesis and induction of globin expression. Our findings indicate that GATA-1b can function in ectoderm to specifically regulate neural inducing mechanisms, apparently related to the expression of chordin, a neuralizing gene. Furthermore, tadpole stage embryos injected with GATA-1b are devoid of all dorsoanterior structures including neural tissue. This report provides evidence that the two transcription factors, derived from a recent genome duplication, share a common biological activity (stimulation of erythropoiesis) white also exhibiting a distinct function (inhibition of neurogenesis). C1 NCI,FREDERICK CANC RES & DEV CTR,DIV BASIC SCI,LAB BIOCHEM PHYSIOL,FREDERICK,MD 21702. NICHHD,NIH,GENET MOL LAB,BETHESDA,MD 20892. ALBERT EINSTEIN COLL MED,DEPT DEV & MOL BIOL,BRONX,NY 10461. BAR ILAN UNIV,DEPT INTERDISCIPLINARY,IL-52900 RAMAT GAN,ISRAEL. RI Xu, Ren-He/M-3125-2016 NR 47 TC 44 Z9 46 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JAN PY 1997 VL 17 IS 1 BP 436 EP 443 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WA233 UT WOS:A1997WA23300046 PM 8972224 ER PT J AU Kubbutat, MHG Vousden, KH AF Kubbutat, MHG Vousden, KH TI Proteolytic cleavage of human p53 by calpain: A potential regulator of protein stability SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HUMAN PAPILLOMAVIRUS TYPE-16; ACTIVATED NEUTRAL PROTEASE; DNA-DAMAGING AGENTS; WILD-TYPE P53; TRANSCRIPTIONAL ACTIVATION; CELL-LINES; MONOCLONAL-ANTIBODIES; E6 ONCOPROTEIN; HPV E6; EXPRESSION AB The p53 tumor suppressor protein is activated in cells in response to DNA damage and prevents the replication of cells sustaining genetic damage bg inducing a cell cycle arrest or apoptosis. Activation of p53 is accompanied by stabilization of the protein, resulting in accumulation to high levels within the cell. p53 is normally degraded through the proteasome following ubiquitination, although the mechanisms which regulate this proteolysis in normal cells and how the p53 protein becomes stabilized following DNA damage are not well understood. We show here that p53 can also be a substrate for cleavage by the calcium-activated neutral protease, calpain, and that a preferential site for calpain cleavage exists within the N terminus of the p53 protein. Treatment of cells expressing, wild-type p53 with an inhibitor of calpain resulted in the stabilization of the p53 protein. By contrast, in vitro or in vivo degradation mediated by human papillomavirus E6 protein was unaffected by the calpain inhibitor, indicating that the stabilization did not result from inhibition of the proteasome. These results suggest that calpain cleavage plays a role in regulating p53 stability. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 70 TC 240 Z9 242 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JAN PY 1997 VL 17 IS 1 BP 460 EP 468 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WA233 UT WOS:A1997WA23300049 PM 8972227 ER PT J AU Fukasawa, K VandeWoude, GF AF Fukasawa, K VandeWoude, GF TI Synergy between the Mos/mitogen-activated protein kinase pathway and loss of p53 function in transformation and chromosome instability SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID WILD-TYPE P53; CELL-CYCLE CONTROL; SERINE THREONINE KINASES; MAMMALIAN SOMATIC-CELLS; MURINE SARCOMA-VIRUS; NIH 3T3 CELLS; MAP KINASE; XENOPUS-OOCYTES; GROWTH ARREST; IN-VITRO AB Constitutive activation of mitogen-activated protein kinase (MAPK) is a property common to many oncoproteins, including Mos, Ras, and Raf, and is essential for their transforming activities. We have shown that high levels of expression of the Mos/MAPK pathway in Swiss 3T3 fibroblast cause cells in S phase to undergo apoptosis, while cells in G(1) irreversibly growth arrest. Interestingly, cells in G(2) and hi phases also arrest at a G(1)-like checkpoint after proceeding through mitosis. These cells fail to undergo cytokinesis and are binucleated. Thus, constitutive overexpression of Mos and MAPK cannot be tolerated, and fibroblasts transformed by Mos express only low levels of the mos oncogene product. Here, we show that p53 plays a key role in preventing oncogene-mediated activation of MAPK In the absence of p53 (p53(-/-)), the growth arrest normally observed in wild-type p53 (p53(+/+)) mouse embryo fibroblasts (MEFs) is markedly reduced. The mos transformation efficiency in p53(-/-) MEFs is two to three orders of magnitude higher than that in p53(+/+) cells, and p53(-/-) cells tolerate >10-fold higher levels of both R-los and activated MAPK. Moreover, we shaw that, like Mos, both v-ras and v-raf oncogene products induce apoptosis in p53(+/+) MEFs. These oncogenes also display a high transforming activity in p53(-/-) MEFs, as does a gain-of-function MAPK kinase mutant (MEK*). Thus, the p53-dependent checkpoint pathway is responsive to oncogene-mediated MAPK activation in inducing irreversible G(1) growth arrest and apoptosis. Moreover, we show that the chromosome instability induced by the loss of p53 is greatly enhanced by the constitutive activation of the Mos/MAPK pathway. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. NR 100 TC 103 Z9 106 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JAN PY 1997 VL 17 IS 1 BP 506 EP 518 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA WA233 UT WOS:A1997WA23300053 PM 8972231 ER PT S AU Stables, JP Kupferberg, HJ AF Stables, JP Kupferberg, HJ BE Avanzini, G Regesta, G Tanganelli, P Avoli, M TI The NIH Anticonvulsant Drug Development (ADD) Program: preclinical anticonvulsant screening project SO MOLECULAR AND CELLULAR TARGETS FOR ANTI-EPILEPTIC DRUGS SE CURRENT PROBLEMS IN EPILEPSY LA English DT Proceedings Paper CT International Symposium on Molecular Targets and Cellular Mechanisms of Antiepileptic Drugs CY JAN 25-27, 1996 CL GENOA, ITALY SP Italian Leeague Against Epilepsy, Italian Neurol Soc, Italian Soc Hosp Neurologists, Neurosurgeons & Neuroradiologists AB Summ. reports are written for those compounds that have undergone multilevel evaluations. A report analyzes and interprets the generated data, and also compares the candidate compound's pharmacodynamic and pharmacokinetic profile to that of current clinically effective drugs. Annually, approximately ten promising compounds are considered for further development by the ADD Program. If a compound appears to have potential, the ADD Program collaborates with the pharmaceutical or academic sponsor in scheduling further preclinical and clinical evaluations. C1 NINDS, Epilepsy Branch, NIH, Bethesda, MD 20892 USA. RP Stables, JP (reprint author), NINDS, Epilepsy Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 116 Z9 117 U1 2 U2 2 PU JOHN LIBBEY & CO PI LONDON PA 13 SMITHS YARD, SUMMERLEY ST, LONDON SW18 4HR, ENGLAND SN 0950-4591 BN 0-86196-554-X J9 CURR PROB E PY 1997 VL 12 BP 191 EP 198 PG 8 WC Clinical Neurology; Pharmacology & Pharmacy SC Neurosciences & Neurology; Pharmacology & Pharmacy GA BL76P UT WOS:000076655200016 ER PT S AU Nossal Paul Goodnow Melchers Metcalf Hodgkin Williams Dexter Strasser Zinkernagel Morstyn AF Nossal Paul Goodnow Melchers Metcalf Hodgkin Williams Dexter Strasser Zinkernagel Morstyn BE Bock, GR Goode, JA TI Selection versus instruction? SO MOLECULAR BASIS OF CELLULAR DEFENCE MECHANISMS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on the Molecular Basis of Cellular Defence Mechanisms CY MAR 19-21, 1996 CL INST MED RES, WALTER & ELIZA HALL, MELBOURNE, AUSTRALIA SP Ciba Fdn HO INST MED RES, WALTER & ELIZA HALL ID COLONY C1 NIAID, NIH, IMMUNOL LAB, BETHESDA, MD 20892 USA. STANFORD UNIV, SCH MED, HOWARD HUGHES MED INST, STANFORD, CA 94305 USA. STANFORD UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA. BASEL INST IMMUNOL, CH-4005 BASEL, SWITZERLAND. CENTENARY INST CANC MED & CELL BIOL, NEWTOWN, NSW 2042, AUSTRALIA. INDIANA UNIV, SCH MED,HOWARD HUGHES MED INST, RILEY HOSP CHILDREN,DEPT PEDIAT HEMATOL ONCOL, INDIANAPOLIS, IN 46202 USA. CHRISTIE HOSP NHS TRUST, PATERSON INST CANC RES, MANCHESTER M20 4BX, LANCS, ENGLAND. UNIV ZURICH HOSP, INST EXPT IMMUNOL, CH-8091 ZURICH, SWITZERLAND. AMGEN INC, THOUSAND OAKS, CA 91320 USA. RP Nossal (reprint author), ROYAL MELBOURNE HOSP, WALTER & ELIZA HALL INST MED RES, POST OFF, MELBOURNE, VIC 3050, AUSTRALIA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-96567-7 J9 CIBA F SYMP PY 1997 VL 204 BP 33 EP 39 PG 7 WC Cell Biology; Immunology; Medicine, General & Internal SC Cell Biology; Immunology; General & Internal Medicine GA BH80V UT WOS:A1997BH80V00003 ER PT S AU Nossal Zinkernagel Paul Mathis Williams Rajewsky Burgess Dexter Morstyn Metcalf Nicola Davis AF Nossal Zinkernagel Paul Mathis Williams Rajewsky Burgess Dexter Morstyn Metcalf Nicola Davis BE Bock, GR Goode, JA TI Test tube data and in vivo realities SO MOLECULAR BASIS OF CELLULAR DEFENCE MECHANISMS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on the Molecular Basis of Cellular Defence Mechanisms CY MAR 19-21, 1996 CL INST MED RES, WALTER & ELIZA HALL, MELBOURNE, AUSTRALIA SP Ciba Fdn HO INST MED RES, WALTER & ELIZA HALL C1 UNIV ZURICH, INST EXPT IMMUNOL, CH-8091 ZURICH, SWITZERLAND. NIAID, NIH, IMMUNOL LAB, BETHESDA, MD 20892 USA. INST GENET & BIOL MOL & CELLULAIRE, F-67404 ILLKIRCH GRAFFENSTADEN, CU STRASBOURG, FRANCE. INDIANA UNIV, SCH MED,HOWARD HUGHES MED INST, RILEY HOSP CHILDREN,DEPT PEDIAT HEMATOL ONCOL, INDIANAPOLIS, IN 46202 USA. UNIV COLOGNE, INST GENET, D-50931 COLOGNE, GERMANY. ROYAL MELBOURNE HOSP, LUDWIG INST CANC RES, MELBOURNE TUMOUR BIOL BRANCH, MELBOURNE, VIC 3050, AUSTRALIA. CHRISTIE HOSP NHS TRUST, PATERSON INST CANC RES, MANCHESTER M20 4BX, LANCS, ENGLAND. AMGEN INC, THOUSAND OAKS, CA 91320 USA. STANFORD UNIV, SCH MED, BECKMAN CTR, HOWARD HUGHES MED INST, STANFORD, CA 94305 USA. RP Nossal (reprint author), ROYAL MELBOURNE HOSP, WALTER & ELIZA HALL INST MED RES, POST OFF, MELBOURNE, VIC 3050, AUSTRALIA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-96567-7 J9 CIBA F SYMP PY 1997 VL 204 BP 88 EP 93 PG 6 WC Cell Biology; Immunology; Medicine, General & Internal SC Cell Biology; Immunology; General & Internal Medicine GA BH80V UT WOS:A1997BH80V00008 ER PT S AU Nossal Hodgkin Zinkernagel Tarlinton Davis Rajewsky Mathis vonBoehmer Carbone Metcalf Shortman Melchers Strasser Paul Goodnow AF Nossal Hodgkin Zinkernagel Tarlinton Davis Rajewsky Mathis vonBoehmer Carbone Metcalf Shortman Melchers Strasser Paul Goodnow BE Bock, GR Goode, JA TI Immune recognition, control of infections and vaccination strategies SO MOLECULAR BASIS OF CELLULAR DEFENCE MECHANISMS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on the Molecular Basis of Cellular Defence Mechanisms CY MAR 19-21, 1996 CL INST MED RES, WALTER & ELIZA HALL, MELBOURNE, AUSTRALIA SP Ciba Fdn HO INST MED RES, WALTER & ELIZA HALL ID MICE C1 CENTENARY INST CANC MED & CELL BIOL, NEWTOWN, NSW 2042, AUSTRALIA. UNIV ZURICH HOSP, INST EXPT IMMUNOL, CH-8091 ZURICH, SWITZERLAND. STANFORD UNIV, SCH MED, BECKMAN CTR, HOWARD HUGHES MED INST, STANFORD, CA 94305 USA. UNIV COLOGNE, GENET INST, D-50931 COLOGNE, GERMANY. INST GENET & BIOL MOL & CELLULAIRE, F-67404 ILLKIRCH GRAFFENSTADEN, CU STRAUSBOURG, FRANCE. INSERM, INST NECKER, F-75015 PARIS, FRANCE. ALFRED HOSP, MONASH MED SCH, DEPT PATHOL & IMMUNOL, PRAHRAN, VIC 3181, AUSTRALIA. BASEL INST IMMUNOL, CH-4005 BASEL, SWITZERLAND. NIAID, NIH, IMMUNOL LAB, BETHESDA, MD 20892 USA. STANFORD UNIV, SCH MED, HOWARD HUGHES MED INST, STANFORD, CA 94305 USA. STANFORD UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA. RP Nossal (reprint author), ROYAL MELBOURNE HOSP, WALTER & ELIZA HALL INST MED RES, POST OFF, MELBOURNE, VIC 3050, AUSTRALIA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-96567-7 J9 CIBA F SYMP PY 1997 VL 204 BP 142 EP 147 PG 6 WC Cell Biology; Immunology; Medicine, General & Internal SC Cell Biology; Immunology; General & Internal Medicine GA BH80V UT WOS:A1997BH80V00012 ER PT S AU Nossal Mosmann Paul Burgess Miller Melchers Goodnow Hodgkin Zinkernagel AF Nossal Mosmann Paul Burgess Miller Melchers Goodnow Hodgkin Zinkernagel BE Bock, GR Goode, JA TI Cytokine regulation of immune responses and further reflections on self-non-self discrimination SO MOLECULAR BASIS OF CELLULAR DEFENCE MECHANISMS SE CIBA FOUNDATION SYMPOSIA LA English DT Editorial Material CT Symposium on the Molecular Basis of Cellular Defence Mechanisms CY MAR 19-21, 1996 CL INST MED RES, WALTER & ELIZA HALL, MELBOURNE, AUSTRALIA SP Ciba Fdn HO INST MED RES, WALTER & ELIZA HALL C1 UNIV ALBERTA, DEPT MED MICROBIOL & IMMUNOL, EDMONTON, AB T6G 2H7, CANADA. NIAID, NIH, IMMUNOL LAB, BETHESDA, MD 20892 USA. BASEL INST IMMUNOL, CH-4005 BASEL, SWITZERLAND. STANFORD UNIV, SCH MED, HOWARD HUGHES MED INST, STANFORD, CA 94305 USA. STANFORD UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, STANFORD, CA 94305 USA. CENTENARY INST CANC MED & CELL BIOL, NEWTOWN, NSW 2042, AUSTRALIA. UNIV ZURICH HOSP, INST EXPT IMMUNOL, CH-8091 ZURICH, SWITZERLAND. RP Nossal (reprint author), ROYAL MELBOURNE HOSP, WALTER & ELIZA HALL INST MED RES, POST OFF, MELBOURNE, VIC 3050, AUSTRALIA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-96567-7 J9 CIBA F SYMP PY 1997 VL 204 BP 187 EP 189 PG 3 WC Cell Biology; Immunology; Medicine, General & Internal SC Cell Biology; Immunology; General & Internal Medicine GA BH80V UT WOS:A1997BH80V00016 ER PT S AU Paul, WE Melchers Metcalf Burgess Strasser Dexter Nicola AF Paul, WE Melchers Metcalf Burgess Strasser Dexter Nicola BE Bock, GR Goode, JA TI Interleukin 4: Signalling mechanisms and control of T cell differentiation SO MOLECULAR BASIS OF CELLULAR DEFENCE MECHANISMS SE CIBA FOUNDATION SYMPOSIA LA English DT Article; Proceedings Paper CT Symposium on the Molecular Basis of Cellular Defence Mechanisms CY MAR 19-21, 1996 CL INST MED RES, WALTER & ELIZA HALL, MELBOURNE, AUSTRALIA SP Ciba Fdn HO INST MED RES, WALTER & ELIZA HALL ID STIMULATORY FACTOR-I; PROMPTLY PRODUCE INTERLEUKIN-4; RECEPTOR GAMMA-CHAIN; INSULIN-RECEPTOR; B-CELLS; IL-4; DISTINCT; REGION; GROWTH; MOUSE AB Interleukin 4 (IL-4) is a pleiotropic type I cytokine that controls both growth and differentiation among haemopoietic and non-haemopoietic cells. Its receptor is a heterodimer. One chain, the IL-4R alpha chain, binds IL-4 with high affinity and determines the nature of the biochemical signals that are induced. The second chain, gamma c, is required for the induction of such signals. IL-4-mediated growth depends upon activation events that involve phosphorylation of Y497 of IL-4R alpha, leading to the binding and phosphorylation of 4PS/IRS-2 in haemopoietic cells and of IRS-I in non-haemopoietic cells. By contrast, IL-4-mediated differentiation events depend upon more distal regions of the IL-4R alpha chain that include a series of STAT-6 binding sites. The distinctive roles of these receptor domains was verified by receptor-reconstruction experiments. The 'growth' and 'differentiation' domains of the IL-4R alpha chain, independently expressed as chimeric structures with a truncated version of the IL-2R beta chain, were shown to convey their functions to the hybrid receptor. The critical role of STAT-6 in IL-4-mediated gene activation and differentiation was made clear by the finding that lymphocytes from STAT-6 knockout mice are strikingly deficient in these functions but have retained the capacity to grow, at least partially, in response to IL-4. IL-4 plays a central role in determining the phenotype of naive CD4(+) T cells. In the presence of IL-4, newly primed naive T cells develop into IL-4 producers while in its absence they preferentially become gamma-interferon (IFN-gamma) producers. Recently, a specialized subpopulation of T cells, CD4(+)/NK1.1(+) cells, has been shown to produce large amounts of IL-4 upon stimulation. Two examples of mice with deficiencies in these cells are described-beta(2)-microglobulin knockout mice and SJL mice. Both show defects in the development of IL-4-producing cells and in the increase in serum IgE in response to stimulation with the polyclonal stimulant anti-IgD. Both sets of mice have major diminutions in the number of CD4(+)/NK1.1(+) T cells, strongly indicating an important role of these cells in some but not all IgE responses to physiologic stimuli. RP Paul, WE (reprint author), NIAID, NATL INST HLTH, IMMUNOL LAB, 9000 ROCKVILLE PIKE, BETHESDA, MD 20892 USA. NR 40 TC 68 Z9 69 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, WEST SUSSEX, ENGLAND SN 0300-5208 BN 0-471-96567-7 J9 CIBA F SYMP PY 1997 VL 204 BP 208 EP 219 PG 12 WC Cell Biology; Immunology; Medicine, General & Internal SC Cell Biology; Immunology; General & Internal Medicine GA BH80V UT WOS:A1997BH80V00018 PM 9107423 ER PT J AU Shaitan, KV Nemukhin, AV Firsov, DA Bogdan, TV Topol, IA AF Shaitan, KV Nemukhin, AV Firsov, DA Bogdan, TV Topol, IA TI Importance of effective charges in the analysis of electron-conformational interactions in peptides SO MOLECULAR BIOLOGY LA English DT Article DE peptides; electron-conformational interactions; hydrogen bonds; electron transfer; atomic charges ID ATOMIC CHARGES; POTENTIALS; DIPEPTIDE; DENSITY; MODEL AB Dependences of electron distributions on conformations of model dipeptides and their water and glycerol complexes in ground electronic states are studied by nb initio quantum chemistry methods. The influence of conformational distortions, hydrogen bonding, chemical group substitutions, and electron attachment on the effective atomic charges for a number of dipeptides are analyzed. Various approaches to atomic charge determination are considered. It is shown, that the ESP method of charge calculations is the most conformation-dependent approach and that optimization of the molecular geometry reduces charge variations considerably. C1 NCI,FREDERICK BIOMED SUPERCOMP CTR,SAIC,FREDERICK,MD 21702. RP Shaitan, KV (reprint author), MOSCOW MV LOMONOSOV STATE UNIV,MOSCOW 117899,RUSSIA. RI Shaitan, Konstantin/F-2316-2014; Nemukhin, Alexander/P-9662-2015 OI Shaitan, Konstantin/0000-0002-5137-303X; NR 40 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PUBL CORP PI NEW YORK PA CONSULTANTS BUREAU, 233 SPRING ST, NEW YORK, NY 10013 SN 0026-8933 J9 MOL BIOL+ JI Mol. Biol. PD JAN-FEB PY 1997 VL 31 IS 1 BP 90 EP 97 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA XE985 UT WOS:A1997XE98500015 ER PT J AU Langenberg, WG Zhang, LY Court, DL Giunchedi, L Mitra, A AF Langenberg, WG Zhang, LY Court, DL Giunchedi, L Mitra, A TI Transgenic tobacco plants expressing the bacterial mc gene resist virus infection SO MOLECULAR BREEDING LA English DT Article DE ds-RNA binding protein; RNase III; plant transformation; virus resistance ID DOUBLE-STRANDED-RNA; ESCHERICHIA-COLI; PHASEOLUS-VULGARIS; RECOMBINATION; MITOCHONDRIA; RIBONUCLEASE; ACTIVATION; FRAGMENTS; PROTEINS; DISEASES AB A bacterial me gene coding for a double-stranded RNA-dependent RNase III endoribonuclease and a mutant, mc70, were expressed in tobacco plants. The RNase III protein produced in the transgenic plants was the same size as the bacterial protein. Expression of the wild-type gene could cause stunting in some plant lines, but not in others. Expression of the mutant protein did not affect normal growth and development of the transgenic plants. Transgenic plants of the R1 and R2 generations, expressing the wild type, as well as a mutant protein, were resistant to infection by three disparate RNA plant viruses with a divided genome but not against two viruses with a single-stranded RNA genome. Introduction of the me gene in crop plants may provide resistance to economically important virus diseases. C1 UNIV NEBRASKA,CTR BIOTECHNOL,LINCOLN,NE 68583. NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,GENE REGULAT & CHROMOSOME BIOL LAB,FREDERICK,MD 21702. UNIV BOLOGNA,IST PATOL VEGETALE,BOLOGNA,ITALY. RP Langenberg, WG (reprint author), USDA ARS,LINCOLN,NE 68583, USA. NR 45 TC 13 Z9 14 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 1380-3743 J9 MOL BREEDING JI Mol. Breed. PY 1997 VL 3 IS 5 BP 391 EP 399 DI 10.1023/A:1009697507261 PG 9 WC Agronomy; Plant Sciences; Genetics & Heredity; Horticulture SC Agriculture; Plant Sciences; Genetics & Heredity GA YB953 UT WOS:A1997YB95300006 ER PT J AU Tsutsui, T Tanaka, Y Matsudo, Y Hasegawa, K Fujino, T Kodama, S Barrett, JC AF Tsutsui, T Tanaka, Y Matsudo, Y Hasegawa, K Fujino, T Kodama, S Barrett, JC TI Extended lifespan and immortalization of human fibroblasts induced by X-ray irradiation SO MOLECULAR CARCINOGENESIS LA English DT Article DE human fibroblasts; extended lifespan; immortalization ID HUMAN-DIPLOID FIBROBLASTS; CELL NEOPLASTIC TRANSFORMATION; ABNORMAL CLONE FORMATION; ATAXIA TELANGIECTASIA; INDEFINITE DIVISION; GENETIC-ANALYSIS; EMBRYO CELLS; GAMMA-RAYS; SENESCENCE; CHROMOSOME AB The induction of immortalization of human fibroblasts by carcinogens is a very rare process. Hybrids between immortal cells and normal fibroblasts senesce, indicating that immortal cells must lose one or more senescence genes for immortalization. To examine the possible involvement of multiple gene alterations in extended lifespan or immortalization of normal human fibroblasts, normal human fibroblasts (WHE-7 cells) and skin fibroblasts (MDAH 087 cells) derived from a Li-Fraumeni syndrome patient with a mutated p53 allele were periodically irradiated with x rays. All six unirradiated control MDAH 087 cell cultures ceased growing by 37 population doublings (PD) and senesced. In contrast, one of six MDAH 087 cultures irradiated one to three times with x rays (2 or 4 Gy at 2 Gy/min) grew continuously for over 450 PD, indicating that the cells were immortal. All 12 WHE-7 cell cultures that were irradiated under the same conditions and all 20 unirradiated control WHE-7 cultures did not become immortal. Single-stranded DNA conformation analysis and DNA sequencing revealed that no additional mutations were induced by x-ray irradiation in exons 2-10 of the p53 gene of the immortal cells (LCS-4X2 cells) and that loss of the wild-type p53 gene was necessary but not sufficient for immortalization. Karyotypic analysis and chromosome painting analysis demonstrated that a high percentage (more than 98%) of LCS-4X2 cells had lost chromosome 6. Irradiation of WHE-7 cells nine times with x rays (2 Gy at 2 Gy/min) extended the cells' lifespans but did not immortalize them. These cells (X9 cells) exhibited a nonrandom karyotypic alteration, monosomy 6, that was confirmed by loss of heterozygosity for a polymorphic dinucleotide repeat sequence on chromosome 6. DNA analysis showed that X9 cells had no mutations in exons 2-10 of the p53 gene. DNA fingerprint analysis with a multi-locus probe detected DNA rearrangements in LCS-4X2 cells and X9 cells, indicating that both cells could have mutations at a gene or genes other than the p53 gene. The results are consistent with our previous findings that cells with a mutation in one gene involved in cellular senescence (i.e., the p53 gene in Li-Fraumeni fibroblasts) are prone to immortalization. Furthermore, we conclude that immortalization of normal human fibroblasts is a multistep process involving loss or inactivation of multiple genes, such as p53 and a gene on chromosome 6. Loss of a gene on chromosome 6 without p53 alterations extends cellular lifespan without immortalizing the cells. (C) 1997 Wiley-Liss, Inc.dagger C1 NIEHS,MOL CARCINOGENESIS LAB,NIH,RES TRIANGLE PK,NC 27709. NIPPON DENT UNIV TOKYO,SCH DENT,DEPT PHARMACOL,TOKYO,JAPAN. HOKKAIDO UNIV,SCH MED,DEPT OBSTET & GYNECOL,SAPPORO,HOKKAIDO 060,JAPAN. NAGASAKI UNIV,FAC PHARMACEUT SCI,DEPT HLTH SCI,DIV RADIAT BIOL,NAGASAKI 852,JAPAN. NR 41 TC 26 Z9 28 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD JAN PY 1997 VL 18 IS 1 BP 7 EP 18 DI 10.1002/(SICI)1098-2744(199701)18:1<7::AID-MC2>3.0.CO;2-F PG 12 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA WF245 UT WOS:A1997WF24500002 PM 9022808 ER PT J AU Lee, YS Dlugosz, AA McKay, R Dean, NM Yuspa, SH AF Lee, YS Dlugosz, AA McKay, R Dean, NM Yuspa, SH TI Definition by specific antisense oligonucleotides of a role for protein kinase C alpha in expression of differentiation markers in normal and neoplastic mouse epidermal keratinocytes SO MOLECULAR CARCINOGENESIS LA English DT Article DE antisense oligonucleotides; protein kinase C; keratinocytes; ras; differentiation ID CULTURED MURINE KERATINOCYTES; V-RAS ONCOGENE; GENE-EXPRESSION; ORNITHINE DECARBOXYLASE; ULTRASTRUCTURAL-LOCALIZATION; MONOSPECIFIC ANTIBODIES; CHEMICAL CARCINOGENESIS; PHOSPHOLIPID-METABOLISM; THERAPEUTIC AGENTS; TUMOR PROMOTION AB Epidermal keratinocyte differentiation is a tightly regulated, stepwise process that requires protein kinase C (PKC) activation. Studies using cultured mouse keratinocytes induced to differentiate with Ca2+ have indirectly implicated the alpha isoform of PKC in upregulation of ''late'' (granular cell) epidermal differentiation markers. Activation of this isoform is also implicated in the suppression of ''early'' differentiation markers keratin (K) 1 and 10 that characterizes the neoplastic phenotype produced by the v-Ha-ras oncogene. We used antisense oligonucleotides (AS) to directly address the role of PKC alpha in regulating expression of these markers in normal and v-Ha-ras-transduced primary keratinocytes and a keratinocyte cell line (SP-1) containing an activating mutation of the c-Ha-ras gene. Transfection of PKC alpha AS reduced the PKC alpha protein level in a dose-dependent manner, with a maximum effect at doses of 100 nM or higher. Immunoblot analysis with antibodies against PKC alpha, PKC delta, PKC epsilon, and PKC eta confirmed that PKC alpha AS selectively reduced the level of PKC alpha but not the other isoforms. In vitro kinase assays also revealed suppression of Ca2+-dependent PKC activity, which is the PKC alpha activity in this cell type, after transfection of PKC alpha AS. When PKC alpha AS-treated normal keratinocytes were stimulated to terminally differentiate with Ca2+, induction of the late differentiation markers loricrin, filaggrin, and SPR-1, as well as transglutaminase K mRNA, was suppressed when compared with their induction in scrambled AS-treated controls. In neoplastic v-Ha-ras-transduced keratinocytes and SP-1 cells, transfection of PKC alpha AS, but not the scrambled AS control, selectively downregulated PKC alpha and restored differentiation-specific expression of K1. These findings directly confirm that PKC alpha is an important component of the signaling pathway regulating terminal differentiation of normal keratinocytes and that activation of PKC alpha contributes to the altered differentiation program of neoplastic murine keratinocytes. (C) 1997 Wiley-Liss, Inc.dagger C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,NIH,BETHESDA,MD 20892. NCI,TUMOR VIRUS BIOL LAB,NIH,BETHESDA,MD 20892. ISIS PHARMACEUT,DEPT MOL PHARMACOL,CARLSBAD,CA. NR 64 TC 88 Z9 89 U1 1 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD JAN PY 1997 VL 18 IS 1 BP 44 EP 53 DI 10.1002/(SICI)1098-2744(199701)18:1<44::AID-MC6>3.0.CO;2-R PG 10 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA WF245 UT WOS:A1997WF24500006 PM 9022812 ER PT J AU Ramanathan, KV Khetrapal, CL AF Ramanathan, KV Khetrapal, CL TI NMR in liquid crystals spinning at and near magic angle SO MOLECULAR CRYSTALS AND LIQUID CRYSTALS SCIENCE AND TECHNOLOGY SECTION A-MOLECULAR CRYSTALS AND LIQUID CRYSTALS LA English DT Article; Proceedings Paper CT 16th International Liquid Crystal Conference CY JUN 24-28, 1996 CL KENT STATE UNIV, KENT, OH SP Kent State Univ, Dept Phys, Kent State Univ, Dept Chem, Kent State Univ, Liquid Crystal Inst, Int Liquid Crystal Soc, Natl Sci Fdn, Sci & Technol Ctr Adv Liquid Crystalline Opt Mat, Samsung Electr Co Ltd, Gordon & Breach Sci Publ, USN, Off Naval Res, Natl Sci Fdn, Cystaloid Electr, Minolta Ltd, Soc Informat Display, Blake Ind, EM Ind Inc, Instec Inc, Linkam Sci Instruments, ROLIC Ltd, Siemens Energy & Automat Inc, Aerosp Display Syst, McNeil Travel HO KENT STATE UNIV ID ORIENTED MOLECULES; SPECTRA; LIPIDS; ORDER AB NMR spectra of liquid crystalline phases and the molecules dissolved therein, spinning at and near the magic angle provide information on the director dynamics and the order parameter. The studies on the dynamics of the liquid crystal director for sample spinning near magic angle in mesophases with positive and negative diamagnetic susceptibility anisotropies (Delta chi) and their mixtures with near-zero macroscopic diamagnetic susceptibility anisotropies have been reported. In systems with weakly positive Delta chi, the director has been observed to switch from an orientation parallel to the spinning axis at low rotational speeds to one perpendicular to the spinning axis at high rotational speeds, when the angle theta, the axis of rotation makes with the magnetic field is smaller than the magic angle theta(m). For systems with a small negative Delta chi, similar director behaviour has been observed for theta greater than theta(m). At magic angle, the spectra under slow spinning speeds exhibit a centre band and side bands at integral values of the spinning speeds. The intensities of the spinning side bands have been shown to contain information on the sign and the magnitude of the order parameter(s). The results are discussed with illustrative examples. Results on the orientation of the chemical shielding tensor obtained from a combination of the NMR studies in the solid and the liquid crystalline states, have been described. C1 NIH,BETHESDA,MD 20892. RP Ramanathan, KV (reprint author), INDIAN INST SCI,SOPHISTICATED INSTRUMENTS FACIL,BANGALORE 560012,KARNATAKA,INDIA. NR 23 TC 0 Z9 0 U1 0 U2 1 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1058-725X J9 MOL CRYST LIQ CRYS A JI Mol. Cryst. Liq. Cryst. Sci. Technol. Sect. A-Mol. Cryst. Liq. Cryst. PY 1997 VL 303 BP 403 EP 413 DI 10.1080/10587259708039451 PG 11 WC Crystallography SC Crystallography GA YE814 UT WOS:A1997YE81400056 ER PT S AU Cortner, J VandeWoude, S VandeWoude, GF AF Cortner, J VandeWoude, S VandeWoude, GF BE Dodds, WJ Womack, JE TI Genes involved in oncogenesis SO MOLECULAR GENETICS, GENE TRANSFER, AND THERAPY SE ADVANCES IN VETERINARY MEDICINE (ACADEMIC PRESS) LA English DT Review ID HEPATOCYTE GROWTH-FACTOR; RETINOBLASTOMA SUSCEPTIBILITY GENE; MET PROTOONCOGENE PRODUCT; TUMOR-SUPPRESSOR GENE; ADENOVIRUS E1A PROTEINS; FACTOR SCATTER FACTOR; CYSTIC-FIBROSIS GENE; TRANSGENIC MICE; BREAST-CANCER; CELL-CYCLE C1 COLORADO STATE UNIV, LAB ANIM RESOURCES, FT COLLINS, CO 80523 USA. NCI, ABL BASIC RES PROGRAM, FREDERICK CANC RES & DEV CTR, FREDERICK, MD 21702 USA. RP Cortner, J (reprint author), NCI, NIH, DIV BASIC SCI, BETHESDA, MD 20892 USA. NR 171 TC 1 Z9 1 U1 1 U2 1 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0065-3519 BN 0-12-039241-0 J9 ADV VET MED-ACAD PR PY 1997 VL 40 BP 51 EP 102 PG 52 WC Veterinary Sciences SC Veterinary Sciences GA BJ68B UT WOS:A1997BJ68B00002 PM 9395729 ER PT J AU Chowdhury, PS Chang, K Pastan, I AF Chowdhury, PS Chang, K Pastan, I TI Isolation of anti-mesothelin antibodies from a phage display library SO MOLECULAR IMMUNOLOGY LA English DT Article DE mesothelin; cancer antibodies; phage display; megakaryocyte potentiating factor ID MONOCLONAL-ANTIBODY; FILAMENTOUS PHAGE; GENES; IMMUNOTOXINS; EXPRESSION; FRAGMENTS; PROTEINS; CLONING; MICE; K1 AB Phage display has been used to select single-chain Fvs (scFvs) against mesothelin, a surface antigen present on mesothelial cells as well as mesotheliomas and non-mucinous ovarian cancers. Several attempts to produce anti-mesothelin hybridomas from spleen cells of mice immunized with recombinant mesothelin were unsuccessful. This report describes the isolation of anti-mesothelin scFvs from a phage display library made from the mRNA of the same spleens. Panning on recombinant antigen produced in E. coli or on antigen positive cells was employed. Several scFvs which bind specifically to mesothelin were isolated. Panning on recombinant antigen yielded five different scFvs. Fanning on cells selected two different scFvs which also differ from the scFvs selected by recombinant antigen. The heavy chains of the scFvs selected on recombinant antigen are derived from four different heavy chain gene families and the scFvs selected on cells are derived from two of these families. In contrast, the light chains of all of these scFvs are derived from family XI. Moreover, the light chains of the two scFvs selected on cells are very similar to the light chains of two of the scFvs selected by panning on recombinant mesothelin except for a few point mutations. One of these scFvs which have been studied in detail has been shown to bind specifically to mesothelin positive transfected cells. Published by Elsevier Science Ltd. C1 NCI,MOL BIOL LAB,DBS,NIH,BETHESDA,MD 20892. NR 26 TC 22 Z9 26 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD JAN PY 1997 VL 34 IS 1 BP 9 EP 20 DI 10.1016/S0161-5890(97)00011-4 PG 12 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA XC150 UT WOS:A1997XC15000002 PM 9182872 ER PT J AU Zimmerman, PA BucklerWhite, A Alkhatib, G Spalding, T Kubofcik, J Combadiere, C Weissman, D Cohen, O Rubbert, A Lam, G Vaccarezza, M Kennedy, PE Kumaraswami, V Giorgi, JV Detels, R Hunter, J Chopek, M Berger, EA Fauci, AS Nutman, TB Murphy, PM AF Zimmerman, PA BucklerWhite, A Alkhatib, G Spalding, T Kubofcik, J Combadiere, C Weissman, D Cohen, O Rubbert, A Lam, G Vaccarezza, M Kennedy, PE Kumaraswami, V Giorgi, JV Detels, R Hunter, J Chopek, M Berger, EA Fauci, AS Nutman, TB Murphy, PM TI Inherited resistance to HIV-1 conferred by an inactivating mutation in CC chemokine receptor 5: Studies in populations with contrasting clinical phenotypes, defined racial background, and quantified risk SO MOLECULAR MEDICINE LA English DT Article ID INFECTION; IDENTIFICATION; CLONING AB Background: CC chemokine receptor 5 (CCR5) is a cell entry cofactor for macrophage-tropic isolates of human immunodeficiency virus-1 (HIV-1). Recently, an inactive CCR5 allele (designated here as CCR5-2) was identified that confers resistance to HIV-1 infection in homozygotes and slows the rate of progression to AIDS in heterozygotes. The reports conflict on the effect of heterozygous CCR5-2 on HIV-1 susceptibility, and race and risk levels have not yet been fully analyzed. Here we report our independent identification of CCR5-2 and test its effects on HIV-1 pathogenesis in individuals with contrasting clinical outcomes, defined race, and quantified risk. Materials and Methods: Mutant CCR5 alleles were sought by directed heteroduplex analysis of genomic DNA from random blood donors. Genotypic frequencies were then determined in (I) random blood donors from North America, Asia, and Africa; (2) HIV-1 + individuals; and (3) highly exposed-seronegative homosexuals with quantified risk. Results: CCR5-2 was the only mutant allele found. It was common in Caucasians, less common in other North American racial groups, and not detected in West Africans or Tamil Indians. Homozygous CCR5-2 frequencies differed reciprocally in highly exposed-seronegative (4.5%, n = 111) and HIV-1-seropositive (0%, n = 614) Caucasians relative to Caucasian random blood donors (0.8%, n = 387). This difference was highly significant (p < 0.0001). By contrast, heterozygous CCR5-2 frequencies did not differ significantly in the same three groups (21.6, 22.6, and 21.7%, respectively). A 55% increase in the frequency of heterozygous CCR5-2 was observed in both of two cohorts of Caucasian homosexual male, long-term nonprogressors compared with other HIV-1 + Caucasian homosexuals (p = 0.006) and compared with Caucasian random blood donors. Moreover, Kaplan-Meier estimates indicated that CCR5-2 heterozygous seroconvertors had a 52.6% lower risk of developing AIDS than homozygous wild-type seroconvertors. Conclusions: The data suggest that homozygous CCR5-2 is an HIV-1 resistance factor in Caucasians with complete penetrance, and that heterozygous CCR5-2 slows the rate of disease progression in infected Caucasian homosexuals. Since the majority (similar to 96%) of highly exposed-seronegative individuals tested are not homozygous for CCR5-2, other resistance factors must exist. Since CCR5-2 homozygotes have no obvious clinical problems, CCR5 may be a good target for the development of novel antiretroviral therapy. C1 NIAID,PARASIT DIS LAB,NIH,BETHESDA,MD 20892. NIAID,VIRAL DIS LAB,NIH,BETHESDA,MD 20892. NIAID,HOST DEF LAB,NIH,BETHESDA,MD 20892. NIAID,IMMUNOREGULAT LAB,NIH,BETHESDA,MD 20892. GEORGETOWN UNIV,DIV MOL VIROL & IMMUNOL,ROCKVILLE,MD. UNIV MARYLAND,MED SYST,AMER RED CROSS,NATL HLA HISTOCOMPATIBIL LAB,BALTIMORE,MD 21201. TB RES CTR,MADRAS,TAMIL NADU,INDIA. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH PUBL HLTH,DEPT EPIDEMIOL,LOS ANGELES,CA 90024. RI Combadiere, Christophe/I-5639-2013; OI Combadiere, Christophe/0000-0002-1755-4531; VACCAREZZA, Mauro/0000-0003-3060-318X FU NCRR NIH HHS [5-MO1-RR-00722]; NIAID NIH HHS [UO1-AI-35042, UO1-AI-35043] NR 38 TC 314 Z9 326 U1 0 U2 7 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 1076-1551 J9 MOL MED JI Mol. Med. PD JAN PY 1997 VL 3 IS 1 BP 23 EP 36 PG 14 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA WH770 UT WOS:A1997WH77000004 PM 9132277 ER PT J AU Belland, RJ Morrison, SG Carlson, JH Hogan, DM AF Belland, RJ Morrison, SG Carlson, JH Hogan, DM TI Promoter strength influences phase variation of neisserial opa genes SO MOLECULAR MICROBIOLOGY LA English DT Article ID OUTER-MEMBRANE PROTEINS; NORMAL HUMAN SERUM; ESCHERICHIA-COLI; GONOCOCCUS INFECTION; OPACITY PROTEINS; EPITHELIAL-CELLS; LEUKOCYTE ASSOCIATION; ANTIGENIC VARIATION; HELA-CELLS; II GENES AB The opa multigene family of Neisseria gonorrhoeae encodes 11 related outer-membrane proteins which phase vary in vitro and in vivo. Illegitimate recombination within direct pentameric DNA repeats, encoding the signal-peptide region of pre-Opas, leads to switches in expression states. Despite the conserved nature of the variation mechanism, specific genes are expressed at high frequencies in the transition from Opa- to Opa+. The genes which are expressed at elevated frequencies differ from the rest of the family with respect to promoter structure, based on sequence comparisons between the cpa genes of strain MS11mk. We have analysed transcription of the cpa gene family of N. gonorrhoeae MS11mk, focussing on the different promoters found among the 11 genes to determine whether increased levels of expression are associated with increased phase-variation rates. Primer extension and Northern blotting was used to assess the levels of transcription of three representative opa genes (opaA, B and C) in 'on' and 'off' states. Full-length opa mRNA was detected primarily in strains expressing the homologous gene. Truncated opa mRNA was constitutively expressed from all cpa genes regardless of their expression state. Quantitative comparisons in N. gonorrhoeae were complicated by the simultaneous expression of all 11 genes and the cross-reactivity of mRNA probes. Expression levels from the individual promoters were therefore assessed by creating transcriptional and translational lacZ fusions to each of the representative cpa promoters which lacked the DNA repeats responsible for variation. The expression levels were compared to the phase-variation rates of translational opa::phoA fusions containing the same promoters in addition to the corresponding coding repeat regions. A strong correlation was found between expression levels from the different promoters and the variation rates at which 'on' variants appeared from an 'off' population (i.e. opaA > opaB > opaC). These results provide an explanation for the favoured expression of specific Opa proteins and indicate that expression of cpa genes may be regulated at the level of transcription. RP Belland, RJ (reprint author), NIAID,ROCKY MT LABS,MICROBIAL STRUCT & FUNCT LAB,NIH,HAMILTON,MT 59840, USA. NR 52 TC 30 Z9 30 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0NE SN 0950-382X J9 MOL MICROBIOL JI Mol. Microbiol. PD JAN PY 1997 VL 23 IS 1 BP 123 EP 135 DI 10.1046/j.1365-2958.1997.1971556.x PG 13 WC Biochemistry & Molecular Biology; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA VZ831 UT WOS:A1997VZ83100012 PM 9004226 ER PT B AU Iadarola, MJ Lee, S Mannes, AJ AF Iadarola, MJ Lee, S Mannes, AJ BE Borsook, D TI Gene transfer approaches to pain control SO MOLECULAR NEUROBIOLOGY OF PAIN SE PROGRESS IN PAIN RESEARCH AND MANAGEMENT LA English DT Proceedings Paper CT Conference on Molecular Aspects of the Neurobiology of Pain as part of the Celebration to Mark the 150th Anniversary of the First Public Demonstration of Ether CY OCT 15-17, 1996 CL BOSTON, MA SP Massachusetts Gen Hosp, Harvard Med Sch C1 NIDR, Pain & Neurosensory Mechanisms Branch, NIH, Bethesda, MD 20892 USA. RP Iadarola, MJ (reprint author), NIDR, Pain & Neurosensory Mechanisms Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU INT ASSOC STUDY PAIN (IASP) PRESS PI SEATTLE PA 909 NE 43RD ST, SUITE 304, SEATTLE, WA 98105 USA BN 0-931092-19-1 J9 PROG PAIN RES MANAG PY 1997 VL 9 BP 337 EP 359 PG 23 WC Biochemistry & Molecular Biology; Clinical Neurology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA BK46M UT WOS:000072280000018 ER PT J AU Badio, B Padgett, WL Daly, JW AF Badio, B Padgett, WL Daly, JW TI Ibogaine: A potent noncompetitive blocker of ganglionic/neuronal nicotinic receptors SO MOLECULAR PHARMACOLOGY LA English DT Article ID INDUCED LOCOMOTOR STIMULATION; ANTI-ADDICTIVE DRUG; RADIOLIGAND-BINDING; EPIBATIDINE; MECHANISMS; ANTAGONIST; CONGENERS; MICE AB Ibogaine noncompetitively blocked (IC50 similar to 20 nM) (NaCl)-Na-22 influx through ganglionic-type nicotinic receptor channels of rat pheochromocytoma PC12 cells. The major metabolite O-desmethylibogaine was 75-fold less active, and O-t-butyl-O-desmethylibogaine was 20-fold less active. Ibogaine was relatively weak as a blocker (IC50 similar to 2000 nM) of the neuromuscular-type nicotinic receptor channels in human medulloblastoma TE671 cells. The blockade of nicotinic responses by ibogaine was only partially reversible in PC12 cells. In vivo, ibogaine at 10 mg/kg completely blocked epibatidine-elicited antinociception in mice, a response that is mediated by central nicotinic receptor channels. There was no significant blockade of the epibatidine response at 24 hr after the administration of 40 mg/kg ibogaine. The blockade of nicotinic channels could contribute to the antiaddictive properties of ibogaine. C1 NIDDK,BIOORGAN CHEM LAB,NIH,BETHESDA,MD 20892. NR 29 TC 32 Z9 32 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JAN PY 1997 VL 51 IS 1 BP 1 EP 5 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WC872 UT WOS:A1997WC87200001 PM 9016339 ER PT J AU Licinio, J AF Licinio, J TI Molecular psychiatry: Does a new field need to examine strategy? SO MOLECULAR PSYCHIATRY LA English DT Editorial Material RP Licinio, J (reprint author), NIMH,CLIN NEUROENDOCRINOL BRANCH,NIH,INTRAMURAL RES PROGRAM,UNIT CLIN RES,BLDG 10,RM 3S231,BETHESDA,MD 20892, USA. RI Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 7 TC 4 Z9 4 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 1359-4184 J9 MOL PSYCHIATR JI Mol. Psychiatr. PD JAN PY 1997 VL 2 IS 1 BP 3 EP 4 DI 10.1038/sj.mp.4000236 PG 2 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA WJ359 UT WOS:A1997WJ35900001 PM 9154207 ER PT J AU Frye, MA Altshuler, LL AF Frye, MA Altshuler, LL TI Selection of initial treatment for bipolar disorder, manic phase SO MOOD DISORDERS SE MODERN PROBLEMS OF PHARMACOPSYCHIATRY LA English DT Review ID OPEN CLINICAL-TRIAL; LITHIUM-CARBONATE; MIXED MANIA; SCHIZOAFFECTIVE DISORDER; RISPERIDONE TREATMENT; SUBSTANCE-ABUSE; VALPROATE; CARBAMAZEPINE; PROPHYLAXIS; ILLNESS C1 NIMH, BIOL PSYCHIAT BRANCH, BETHESDA, MD 20892 USA. NR 103 TC 8 Z9 8 U1 4 U2 4 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0077-0094 J9 MOD PROBL PHARM PY 1997 VL 25 BP 88 EP 113 DI 10.1159/000061663 PG 26 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA BJ75D UT WOS:A1997BJ75D00007 PM 9344372 ER PT J AU Post, RM Denicoff, KD Frye, MA Leverich, GS AF Post, RM Denicoff, KD Frye, MA Leverich, GS TI Algorithms for bipolar mania SO MOOD DISORDERS SE MODERN PROBLEMS OF PHARMACOPSYCHIATRY LA English DT Review ID TARDIVE-DYSKINESIA; AFFECTIVE-DISORDER; LITHIUM TREATMENT; DOUBLE-BLIND; DEPRESSIVE PSYCHOSIS; CONTROLLED TRIAL; MOOD DISORDERS; MIXED MANIA; CALCIUM-ANTAGONISTS; DYSPHORIC MANIA RP Post, RM (reprint author), NIMH,BIOL PSYCHIAT BRANCH,NIH,BLDG 10,ROOM 3N212,10 CTR DR MSC 1272,BETHESDA,MD 20892, USA. NR 119 TC 7 Z9 7 U1 2 U2 2 PU KARGER PI BASEL PA POSTFACH, CH-4009 BASEL, SWITZERLAND SN 0077-0094 J9 MOD PROBL PHARM PY 1997 VL 25 BP 114 EP 145 DI 10.1159/000061664 PG 32 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA BJ75D UT WOS:A1997BJ75D00008 PM 9344373 ER PT J AU Dutta, C Alexander, NB AF Dutta, C Alexander, NB TI Summary of Work Group II: Small-Scale Clinical Studies SO MUSCLE & NERVE LA English DT Article; Proceedings Paper CT National-Institute-on-Aging Workshop on Sarcopenia and Physical Performance in Old Age CY JUL 09-10, 1996 CL BETHESDA, MD SP NIA C1 UNIV MICHIGAN,DEPT INTERNAL MED,DIV GERIATR MED,ANN ARBOR,MI 48109. DEPT VET AFFAIRS,CTR GERIATR RES EDUC & CLIN,ANN ARBOR,MI. RP Dutta, C (reprint author), NIA,GERIATR PROGRAM,NIH,SUITE 3E-327,GATEWAY BLDG,7201 WISCONSIN AVE,BETHESDA,MD 20892, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PY 1997 SU 5 BP S117 EP S120 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA XY540 UT WOS:A1997XY54000028 ER PT J AU Dutta, C Hadley, EC Lexell, J AF Dutta, C Hadley, EC Lexell, J TI Sarcopenia and physical performance in old age: Overview SO MUSCLE & NERVE LA English DT Editorial Material ID MUSCLE; MEN; EXPRESSION; FITNESS; NEURONS C1 UNIV LUND HOSP,DEPT REHABIL,S-22185 LUND,SWEDEN. RP Dutta, C (reprint author), NIA,GERIATR PROGRAM,NIH,SUITE 3E-327,GATEWAY BLDG,7201 WISCONSIN AVE,BETHESDA,MD 20892, USA. NR 15 TC 0 Z9 0 U1 0 U2 3 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PY 1997 SU 5 BP S5 EP S9 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA XY540 UT WOS:A1997XY54000002 ER PT J AU Guo, SMS Harris, T Studenski, S AF Guo, SMS Harris, T Studenski, S TI Summary of Work Group I: Population-Based Studies SO MUSCLE & NERVE LA English DT Article; Proceedings Paper CT National-Institute-on-Aging Workshop on Sarcopenia and Physical Performance in Old Age CY JUL 09-10, 1996 CL BETHESDA, MD SP NIA ID SARCOPENIA C1 NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,NIH,BETHESDA,MD 20892. UNIV KANSAS,MED CTR,CTR AGING,KANSAS CITY,KS 66103. RP Guo, SMS (reprint author), WRIGHT STATE UNIV,SCH MED,DEPT COMMUNITY HLTH,1005 XENIA AVE,YELLOW SPRINGS,OH 45387, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PY 1997 SU 5 BP S114 EP S116 PG 3 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA XY540 UT WOS:A1997XY54000027 ER PT J AU Guralnik, JM AF Guralnik, JM TI Assessment of physical performance and disability in older persons SO MUSCLE & NERVE LA English DT Article; Proceedings Paper CT National-Institute-on-Aging Workshop on Sarcopenia and Physical Performance in Old Age CY JUL 09-10, 1996 CL BETHESDA, MD SP NIA ID BODY-MASS INDEX; MAINTAINING MOBILITY; FUNCTIONAL STATUS; LATE-LIFE; NHANES-I; LEVEL; TRIAL; CARE RP Guralnik, JM (reprint author), NIA,EPIDEMIOL DEMOG & BIOMETRY PROGRAM,7201 WISCONSIN AVE,ROOM 3C-309,BETHESDA,MD 20892, USA. NR 20 TC 2 Z9 3 U1 1 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PY 1997 SU 5 BP S14 EP S16 PG 3 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA XY540 UT WOS:A1997XY54000004 ER PT J AU Horton, WE Tillman, SF AF Horton, WE Tillman, SF TI Analysis of apoptosis in culture models and intact tissues SO MUSCLE & NERVE LA English DT Article; Proceedings Paper CT National-Institute-on-Aging Workshop on Sarcopenia and Physical Performance in Old Age CY JUL 09-10, 1996 CL BETHESDA, MD SP NIA ID PROGRAMMED CELL-DEATH; BCL-2 PROTOONCOGENE; CHONDROCYTES; MECHANISMS RP Horton, WE (reprint author), NIA,BIOL CHEM LAB,CTR GERONTOL RES,NIH,4940 EASTERN AVE,BETHESDA,MD 21224, USA. NR 17 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PY 1997 SU 5 BP S79 EP S82 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA XY540 UT WOS:A1997XY54000019 ER PT J AU Gornig, M EmmertBuck, M Walsh, TJ AF Gornig, M EmmertBuck, M Walsh, TJ TI Patterns of Candida oesophagitis in cancer and in AIDS patients. Histopathological study of 23 patients SO MYCOSES LA German DT Article; Proceedings Paper CT Scholarly Meeting of the Deutschsprachigen-Mykologischen-Gesellschaft CY SEP 19-22, 1996 CL KIEL, GERMANY SP Deutschsprachigen Mykolog Gesell DE Candida; oesophagitis; cancer; AIDS; neutropenia; histopathology AB Candida oesophagitis is a common concomitant disease in neutropenic cancer patients after chemotherapie as well as in HIV-patients. In order to characterize the features of oesophagitis in each population, we reviewed the medical history and pathology records of 23 patients (18 cancer-patients, 5 HIV-patients) with culture and autopsy-proven Candida oesophagitis. Histopathological patterns of morphology, invasion, angioinvasion and inflammation were evaluated. Virtually all patients, 17/18 cancer- and 5/5 HIV-patients, had a history of previous mucosal candidosis or candidemia. There was a significant difference histopathologically in depth of invasion of the Candida-organisms between cancer and HIV-patients. Only in HIV-patients organisms were observed within the muscularis propria and the adventitia (2/5 vs 0/18; p = 0,04). The frequency of angioinvasion (12/18 vs 3/5) was similar in both groups. Neutropenia (< 500/mu l) was present in 12 (68%) of 18 cancer patients vs 0/5 HIV-patients (p = 0,01). Correspondingly there was a significant higher PMN/MN ratio in the oesophageal inflammatory infiltrate in HIV-patients, reflecting chemotherapy-induced neutropenia in cancer patients (p = 0,02). Oesophageal candidosis in HIV-patients may be highly invasive despite the presence of neutrophils. These findings suggest an impaired inflammatory response of HIV-patients to invasive candidosis, leading to impaired mucosal host defence. C1 NCI,DEPT PATHOL,NIH,BETHESDA,MD 20892. NCI,PEDIAT BRANCH,NIH,BETHESDA,MD 20892. RP Gornig, M (reprint author), UNIV JENA,KLIN HAUTKRANKHEITEN,D-07740 JENA,GERMANY. NR 6 TC 4 Z9 5 U1 1 U2 1 PU BLACKWELL WISSENSCHAFTS-VERLAG GMBH PI BERLIN PA KURFURSTENDAMM 57, D-10707 BERLIN, GERMANY SN 0933-7407 J9 MYCOSES JI Mycoses PY 1997 VL 40 SU 1 BP 81 EP 85 PG 5 WC Dermatology; Mycology SC Dermatology; Mycology GA YF410 UT WOS:A1997YF41000013 PM 9417519 ER PT S AU Kaya, S Yokoyama, A Imagawa, T Taniguchi, K Froehlich, JP Albers, RW AF Kaya, S Yokoyama, A Imagawa, T Taniguchi, K Froehlich, JP Albers, RW BE Beauge, LA Gadsby, DC Garrahan, PJ TI Cloning of the eel electroplax Na+,K+-ATPase alpha subunit SO NA/K-ATPASE AND RELATED TRANSPORT ATPASES: STRUCTURE, MECHANISM, AND REGULATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT VIIIth International Conference on the Na/K-ATPase (and Related Transport ATPases) CY AUG 26-30, 1996 CL MAR DEL PLATA, ARGENTINA ID PROTEIN-KINASE-C; PHOSPHORYLATION; NA,K-ATPASE C1 Hokkaido Univ, Grad Sch Sci, Div Chem, Sapporo, Hokkaido 060, Japan. NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. NINCDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. RP Kaya, S (reprint author), Hokkaido Univ, Grad Sch Sci, Div Chem, N-10,W-8, Sapporo, Hokkaido 060, Japan. RI Imagawa, Toshiaki/A-4255-2012 NR 6 TC 5 Z9 5 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-060-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 834 BP 129 EP 131 DI 10.1111/j.1749-6632.1997.tb52238.x PG 3 WC Biochemistry & Molecular Biology; Biophysics; Multidisciplinary Sciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Biophysics; Science & Technology - Other Topics; Pharmacology & Pharmacy GA BK07V UT WOS:000071090100019 PM 9405797 ER PT S AU Froehlich, JP Taniguchi, K Fendler, K Mahaney, JE Thomas, DD Albers, RW AF Froehlich, JP Taniguchi, K Fendler, K Mahaney, JE Thomas, DD Albers, RW BE Beauge, LA Gadsby, DC Garrahan, PJ TI Complex kinetic behavior in the Na,K- and Ca-ATPases - Evidence for subunit-subunit interactions and energy conservation during catalysis SO NA/K-ATPASE AND RELATED TRANSPORT ATPASES: STRUCTURE, MECHANISM, AND REGULATION SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT VIIIth International Conference on the Na/K-ATPase (and Related Transport ATPases) CY AUG 26-30, 1996 CL MAR DEL PLATA, ARGENTINA ID (NA+ + K+)-ATPASE; SARCOPLASMIC-RETICULUM; ADENOSINE-TRIPHOSPHATASE; STEADY-STATE; MECHANISM; PUMP; ATP; K+; SODIUM; PHOSPHOENZYME C1 NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. Hokkaido Univ, Dept Chem, Sapporo, Hokkaido, Japan. Max Planck Inst Biophys, D-6000 Frankfurt, Germany. W Virginia Univ, Sch Med, Dept Biochem, Morgantown, WV 26506 USA. Univ Minnesota, Sch Med, Dept Biochem, Minneapolis, MN 55455 USA. Natl Inst Comm Disorders & Stroke, NIH, Bethesda, MD 20892 USA. RP Froehlich, JP (reprint author), NIA, Gerontol Res Ctr, 4940 Eastern Ave, Baltimore, MD 21224 USA. RI Thomas, David/B-4257-2012 NR 26 TC 29 Z9 29 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-060-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 834 BP 280 EP 296 DI 10.1111/j.1749-6632.1997.tb52259.x PG 17 WC Biochemistry & Molecular Biology; Biophysics; Multidisciplinary Sciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Biophysics; Science & Technology - Other Topics; Pharmacology & Pharmacy GA BK07V UT WOS:000071090100040 PM 9405815 ER PT S AU Arulanantham, PR Edmonds, ZV Albers, RW AF Arulanantham, PR Edmonds, ZV Albers, RW BE Beauge, LA Gadsby, DC Garrahan, PJ TI Solute effects on the sodium pump - An evaluation of the osmotic dehydration hypothesis SO NA/K-ATPASE AND RELATED TRANSPORT ATPASES: STRUCTURE, MECHANISM, AND REGULATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT VIIIth International Conference on the Na/K-ATPase (and Related Transport ATPases) CY AUG 26-30, 1996 CL MAR DEL PLATA, ARGENTINA C1 NINDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. RP Arulanantham, PR (reprint author), NINDS, Neurochem Lab, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. NR 3 TC 0 Z9 0 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-060-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 834 BP 376 EP 377 DI 10.1111/j.1749-6632.1997.tb52275.x PG 2 WC Biochemistry & Molecular Biology; Biophysics; Multidisciplinary Sciences; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Biophysics; Science & Technology - Other Topics; Pharmacology & Pharmacy GA BK07V UT WOS:000071090100056 PM 9405828 ER PT J AU Dai, JR Cardellina, JH McMahon, JB Boyd, MR AF Dai, JR Cardellina, JH McMahon, JB Boyd, MR TI Zerumbone, an HIV-inhibitory and cytotoxic sesquiterpene of Zingiber aromaticum and Z-zerumbet SO NATURAL PRODUCT LETTERS LA English DT Article DE HIV-inhibitory; sesquiterpene; zerumbone; Zingiber ID SCREEN AB Zerumbone and 3 '',4 ''-O-diacetylafzelin were isolated from organic extracts of rhizomes of Zingiber aromaticum (Zingiberaceae), and zerumbone and 4 ''-O-acetylafzelin were obtained from organic extracts of entire plants of Z. zerumbet. Zerumbone exhibited HIV-inhibitory and cytotoxic activities, while the afzelins were inactive in both assays. C1 NCI,LAB DRUG DISCOVERY RES & DEV,DEV THERAPEUT PROGRAM,DIV CANC TREATMENT DIAGNOSIS & CTR,FREDERICK,MD 21702. NR 9 TC 42 Z9 43 U1 1 U2 2 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1057-5634 J9 NAT PROD LETT JI Nat. Prod. Lett. PY 1997 VL 10 IS 2 BP 115 EP 118 DI 10.1080/10575639708043725 PG 4 WC Biochemistry & Molecular Biology; Chemistry, Medicinal SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA XG348 UT WOS:A1997XG34800006 ER PT J AU Fitzgerald, DJP AF Fitzgerald, DJP TI Antitumor immunotoxin secretion by T cells: ABSolutely FABulous? SO NATURE BIOTECHNOLOGY LA English DT News Item ID PSEUDOMONAS EXOTOXIN; CYTOTOXICITY RP Fitzgerald, DJP (reprint author), NCI,MOL BIOL LAB,BIOTHERAPY SECT,DBS,BLDG 37,4B-03,37 CONVENT DR,MSC 4255,BETHESDA,MD 20892, USA. NR 10 TC 0 Z9 0 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1087-0156 J9 NAT BIOTECHNOL JI Nat. Biotechnol. PD JAN PY 1997 VL 15 IS 1 BP 18 EP 19 DI 10.1038/nbt0197-18 PG 2 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA WA729 UT WOS:A1997WA72900015 PM 9035099 ER PT J AU Kallioniemi, OP AF Kallioniemi, OP TI Linking chromosomal clues SO NATURE GENETICS LA English DT Editorial Material ID PEUTZ-JEGHERS SYNDROME; CANCER RP Kallioniemi, OP (reprint author), NIH,NATL CTR HUMAN GENOME RES,CANC GENET LAB,BETHESDA,MD 20892, USA. RI Kallioniemi, Olli/H-5111-2011; Kallioniemi, Olli/H-4738-2012 OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332 NR 9 TC 5 Z9 5 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD JAN PY 1997 VL 15 IS 1 BP 5 EP 6 DI 10.1038/ng0197-5 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA WA373 UT WOS:A1997WA37300003 PM 8988157 ER PT J AU Howard, TD Paznekas, WA Green, ED Chiang, LC Ma, N DeLuna, RIO Delgado, CG GonzalezRamos, M Kline, AD Jabs, EW AF Howard, TD Paznekas, WA Green, ED Chiang, LC Ma, N DeLuna, RIO Delgado, CG GonzalezRamos, M Kline, AD Jabs, EW TI Mutations in TWIST, a basic helix-loop-helix transcription factor, in Saethre-Chotzen syndrome SO NATURE GENETICS LA English DT Article ID GROWTH-FACTOR RECEPTOR-2; JACKSON-WEISS-SYNDROME; CROUZON-SYNDROME; SYNDROME LOCUS; BALANCED TRANSLOCATIONS; DROSOPHILA EMBRYOS; GENE; CRANIOSYNOSTOSIS; HETEROGENEITY; LOCALIZATION AB Saethre-Chotzen syndrome is one of the most common autosomal dominant disorders of craniosynostosis in humans and is characterized by craniofacial and limb anomalies. The locus for Saethre-Chotzen syndrome maps to chromosome 7p21-p22, We have evaluated TWIST; a basic helix-loop-helix transcription factor, as a candidate gene for this condition because its expression pattern and mutant phenotypes in Drosophila and mouse are consistent with the Saethre-Chotzen phenotype. We mapped TWIST to human chromosome 7p21-p22 and mutational analysis reveals nonsense, missense, insertion and deletion mutations in patients. These mutations occur within the basic DNA binding, helix I and loop domains, or result in premature termination of the protein, Studies in Drosophila indicate that twist may affect the transcription of fibroblast growth factor receptors (FGFRs), another gene family implicated in human craniosynostosis. The emerging cascade of molecular components involved in craniofacial and limb development now includes TWIST, which may function as an upstream regulator of FGFRs. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,CTR MED GENET,BALTIMORE,MD 21287. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,CTR MED GENET,BALTIMORE,MD 21287. JOHNS HOPKINS UNIV,SCH MED,DEPT SURG,CTR MED GENET,BALTIMORE,MD 21287. NIH,GENOME TECHNOL BRANCH,NATL CTR HUMAN GENOME RES,BETHESDA,MD 20892. GENOME THERAPEUT CORP,COLLABORAT RES DIV,WALTHAM,MA 02154. HOSP INFANTIL MEXICO DR FEDERICO GOMEZ,DEPT GENET,MEXICO CITY 06720,DF,MEXICO. SINAI HOSP,DEPT PEDIAT,DIV CLIN GENET,BALTIMORE,MD 21215. OI Jabs, Ethylin/0000-0001-8983-5466 FU NCRR NIH HHS [RR00722]; NICHD NIH HHS [HD24061]; NIDCR NIH HHS [DE11131] NR 41 TC 394 Z9 405 U1 1 U2 8 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD JAN PY 1997 VL 15 IS 1 BP 36 EP 41 DI 10.1038/ng0197-36 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA WA373 UT WOS:A1997WA37300018 PM 8988166 ER PT J AU Lyons, LA Laughlin, TF Copeland, NG Jenkins, NA Womack, JE OBrien, SJ AF Lyons, LA Laughlin, TF Copeland, NG Jenkins, NA Womack, JE OBrien, SJ TI Comparative anchor tagged sequences (CATS) for integrative mapping of mammalian genomes SO NATURE GENETICS LA English DT Article ID GENETIC-LINKAGE MAP; BOVINE GENOME; POLYMORPHISMS; MOUSE; LOCI AB Precise comparisons of mammalian gene maps require common anchor loci as landmarks for conserved chromosomal segments. Using a computer script that automates DNA sequence database alignments. we designed 410 evolutionarily conserved primer pair sequences which are specific for anchor locus gene amplification from any mammalian species' DNA. Primer pairs were designed to span introns for polymorphism ascertainment. and to include sufficient exonic sequence (25-400 bp) to allow for gene identification. A total of 318 primer pairs were optimized for domestic cats, and 86% of the sequenced feline PCR products showed homology to the gene of primer origin. A screen of 20 mammals from 11 orders revealed that 35-52% of the 318 primers yielded a single PCR product without further optimization suggesting that nearly 75% can be optimized for any eutherian mammal. C1 NCI,FREDERICK CANC RES & DEV CTR,LAB GENOM DIVERS,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,BIOL CARCINOGENESIS & DEV PROGRAM,SAIC FREDERICK,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MAMMALIAN GENET LAB,ABL BASIC RES PROGRAM,FREDERICK,MD 21702. TEXAS A&M UNIV,DEPT VET PATHOBIOL,COLLEGE STN,TX 77843. NR 29 TC 285 Z9 292 U1 0 U2 11 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD JAN PY 1997 VL 15 IS 1 BP 47 EP 56 DI 10.1038/ng0197-47 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA WA373 UT WOS:A1997WA37300020 PM 8988168 ER PT J AU Kunst, CB Mezey, E Brownstein, MJ Patterson, D AF Kunst, CB Mezey, E Brownstein, MJ Patterson, D TI Mutations in SOD1 associated with amyotrophic lateral sclerosis cause novel protein interactions SO NATURE GENETICS LA English DT Article ID SUPEROXIDE-DISMUTASE GENE; TRANSFER-RNA-SYNTHETASE; SACCHAROMYCES-CEREVISIAE; WILD-TYPE; AUTOANTIBODIES; COMPLEX; MODEL; CELLS; YEAST; MICE AB A subset of familial and sporadic amyotrophic lateral sclerosis (ALS - a fatal disorder characterised by progressive motor neuron degeneration) cases are due to mutations in the gene encoding Cu,Zn superoxide dismutase (SOD1)(1-4). Two mutations which have been successfully used to generate transgenic mice that develop an ALS-like syndrome are glycine 85 to arginine (G85R) and glycine 93 to alanine (G93A) with the mutant SOD1 allele overexpressed in a normal mouse genetic background(5-7). No ALS-like phenotype is observed in mice overexpressing wild-type SOD1 or mice without any SOD1 activity(6,8,9). These dominant mutations, which do not necessarily decrease SOD1 activity, may confer a gain of function that is selectively lethal to motor neurons(5,10-12). The yeast interaction trap system(13) allowed us to determine whether these mutations in SOD1 caused novel protein interactions not observed with wild-type SOD1 and which might participate in the generation of the ALS phenotype. Two proteins, lysyl-tRNA synthetase and translocon-associated protein delta, interact with mutant forms of SOD1 but not with wild-type SOD1. The specificity of the interactions was confirmed by the coimmunoprecipitation of mutant SOD1 and the expressed proteins. These proteins are expressed in ventral cord, lending support to the relevance of this interaction to motor neuron disease. C1 UNIV COLORADO,HLTH SCI CTR,ELEANOR ROOSEVELT INST CANC RES,DENVER,CO 80206. UNIV COLORADO,HLTH SCI CTR,HUMAN MED GENET PROGRAM,DENVER,CO 80206. UNIV COLORADO,HLTH SCI CTR,DEPT BIOCHEM BIOPHYS & GENET,DENVER,CO 80206. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80206. NIMH,CELL BIOL LAB,BETHESDA,MD 20892. RI Brownstein, Michael/B-8609-2009 FU NIA NIH HHS [AG 00029]; NICHD NIH HHS [HD 07197, HD 17449] NR 31 TC 98 Z9 101 U1 1 U2 4 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD JAN PY 1997 VL 15 IS 1 BP 91 EP 94 DI 10.1038/ng0197-91 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA WA373 UT WOS:A1997WA37300028 PM 8988176 ER PT J AU Vondrasek, J vanBuskirk, CP Wlodawer, A AF Vondrasek, J vanBuskirk, CP Wlodawer, A TI Data base of three-dimensional structures of HIV proteinases SO NATURE STRUCTURAL BIOLOGY LA English DT Editorial Material ID IMMUNODEFICIENCY-VIRUS PROTEASE C1 JOHNS HOPKINS UNIV,KRIEGER MIND BRAIN INST,BALTIMORE,MD 21218. RP Vondrasek, J (reprint author), NCI,MACROMOL STRUCT LAB,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD 21702, USA. RI Vondrasek, JIri/A-4244-2008 NR 10 TC 43 Z9 44 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD JAN PY 1997 VL 4 IS 1 BP 8 EP 8 DI 10.1038/nsb0197-8 PG 1 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA WA810 UT WOS:A1997WA81000004 PM 8989313 ER PT J AU Takahashi, S Yeh, SR Das, TK Chan, CK Gottfried, DS Rousseau, DL AF Takahashi, S Yeh, SR Das, TK Chan, CK Gottfried, DS Rousseau, DL TI Folding of cytochrome c initiated by submillisecond mixing SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID RESONANCE RAMAN; HEME IRON; COORDINATION; MYOGLOBIN; MUTANTS; FLUORESCENCE; EVENTS; STATE; SPIN AB Cytochrome c folding was initiated using a new solution mixer that provides a time window which covers over 90% of the burst phase unresolved by conventional stop-flow measurements, Folding was followed by resonance Raman scattering. Kinetic analysis of the high frequency Raman data indicates that a nascent phase occurs within the mixing dead time of 100 mu s. A significant fraction of the protein was found to be trapped in a misfolded bis-histidine form during the nascent phase at pH 4.5, thereby preventing the protein from folding rapidly and homogeneously. The nascent phase was followed by a haem-ligand exchange phase that populates the native histidjie-methionine coordinated form through a thermodynamically controlled equilibrium. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT PHYSIOL & BIOPHYS,BRONX,NY 10461. RIKEN,INST PHYS & CHEM RES,WAKO,SAITAMA 3510,JAPAN. NIH,CHEM PHYS LAB,BETHESDA,MD 20892. OI Gottfried, David/0000-0002-2729-2504 NR 31 TC 198 Z9 198 U1 0 U2 14 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD JAN PY 1997 VL 4 IS 1 BP 44 EP 50 DI 10.1038/nsb0197-44 PG 7 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA WA810 UT WOS:A1997WA81000014 PM 8989323 ER PT J AU Lubkowski, J Bujacz, G Boque, L Domaille, PJ Handel, TM Wlodawer, A AF Lubkowski, J Bujacz, G Boque, L Domaille, PJ Handel, TM Wlodawer, A TI The structure of MCP-1 in two crystal forms provides a rare example of variable quaternary interactions SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID MONOCYTE CHEMOATTRACTANT PROTEIN-1; 3-DIMENSIONAL STRUCTURE; PLATELET FACTOR-4; INTERLEUKIN-8; CHEMOKINE; RESOLUTION; BINDING; DIMER; NMR; EQUILIBRIA AB The X-ray crystal structure of recombinant human monocyte chemoattractant protein (MCP-1) has been solved in two crystal forms. One crystal form (P), refined to 1.85 Angstrom, resolution, contains a dimer in the asymmetric unit, while the other (I) contains a monomer and was refined at 2.4 Angstrom. Although both crystal forms grow together in the same droplet, the respective quaternary structures of the protein differ dramatically. In addition, both X-ray structures differ to a similar extent from the solution structure of MCP-1. Such extent of variability of quaternary structures is unprecedented, in the crystal structures, the well-ordered N termini of MCP-1 form 3(10)-helices. Comparison of the three MCP-1 structures revealed a direct correlation between the main-chain conformation of the first two cysteine residues and the quaternary arrangements. These data can be used to explain the structural basis for the assignment of residues responsible for biological activity. C1 NCI,MACROMOL STRUCT LAB,FREDERICK CANC RES & DEV CTR,ABL,BASIC RES PROGRAM,FREDERICK,MD 21702. DUPONT MERCK PHARMACEUT CO,CHEM & PHYS SCI,WILMINGTON,DE 19880. UNIV CALIF BERKELEY,DEPT MOL & CELL BIOL,BERKELEY,CA 94720. TECH UNIV LODZ,FAC FOOD CHEM & BIOTECHNOL,PL-90924 LODZ,POLAND. FU NIAID NIH HHS [R01 AI037113] NR 45 TC 116 Z9 122 U1 0 U2 5 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD JAN PY 1997 VL 4 IS 1 BP 64 EP 69 DI 10.1038/nsb0197-64 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA WA810 UT WOS:A1997WA81000017 PM 8989326 ER PT J AU Markus, MA Hinck, AP Huang, SR Draper, DE Torchia, DA AF Markus, MA Hinck, AP Huang, SR Draper, DE Torchia, DA TI High resolution solution structure of ribosomal protein L11-C76, a helical protein with a flexible loop that becomes structured upon binding to RNA SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID ISOTOPICALLY ENRICHED PROTEINS; SIDE-CHAIN RESONANCES; CARBON-J-COUPLINGS; ESCHERICHIA-COLI; NMR-SPECTROSCOPY; CRYSTAL-STRUCTURE; ANTIBIOTIC THIOSTREPTON; C-13-ENRICHED PROTEINS; C-13 MAGNETIZATION; LARGER PROTEINS AB The structure of the C-terminal RNA recognition domain of ribosomal protein L11 has been solved by heteronuclear three-dimensional nuclear magnetic resonance spectroscopy. Although the structure can be considered high resolution in the core, 15 residues between helix alpha(1) and strand beta(1) form an extended, unstructured loop. N-15 transverse relaxation measurements suggest that the loop is moving on a picosecond-to-nanosecond time scale in the free protein but not in the protein bound to RNA. Chemical shifts differences between the free protein and the bound protein suggest that the loop as well as the C-terminal end of helix alpha 3 are involved in RNA binding. C1 NIDR,STRUCT MOL BIOL UNIT,BETHESDA,MD 20892. JOHNS HOPKINS UNIV,DEPT CHEM,BALTIMORE,MD 21218. NR 54 TC 85 Z9 87 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD JAN PY 1997 VL 4 IS 1 BP 70 EP 77 DI 10.1038/nsb0197-70 PG 8 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA WA810 UT WOS:A1997WA81000018 PM 8989327 ER PT J AU Fricker, G Drewe, J Miller, DS AF Fricker, G Drewe, J Miller, DS TI P-glycoprotein-mediated transport of a fluorescent rapamycin derivative in renal proximal tubules SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY LA English DT Meeting Abstract C1 UNIV HEIDELBERG,INST PHARMAZEUT TECHNOL & BIOPHARM,D-69120 HEIDELBERG,GERMANY. UNIV BASEL KLINIKEN,MED POLIKLIN,CH-4031 BASEL,SWITZERLAND. NIEHS,NIH,RES TRIANGLE PK,NC 27709. 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 0028-1298 J9 N-S ARCH PHARMACOL JI Naunyn-Schmiedebergs Arch. Pharmacol. PY 1997 VL 355 IS 4 SU S BP 10 EP 10 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WV420 UT WOS:A1997WV42000034 ER PT J AU Trankle, C Kostenis, E Mohr, K AF Trankle, C Kostenis, E Mohr, K TI G-protein coupling specificity and sensitivity towards allosteric modulation of muscarinic M-2 and M-3 receptors SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY LA English DT Meeting Abstract C1 UNIV BONN,INST PHARM,D-53121 BONN,GERMANY. NIDDKD,BIOORGAN CHEM LAB,NIH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0028-1298 J9 N-S ARCH PHARMACOL JI Naunyn-Schmiedebergs Arch. Pharmacol. PY 1997 VL 355 IS 4 SU S BP 63 EP 63 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WV420 UT WOS:A1997WV42000087 ER PT J AU Schoneberg, T Sandig, V Wess, J Gudermann, T Schultz, G AF Schoneberg, T Sandig, V Wess, J Gudermann, T Schultz, G TI Functional reconstitution of mutant V2 vasopressin receptors by adenovirus-mediated gene transfer of a receptor fragment SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY LA English DT Meeting Abstract C1 MAX DELBRUCK ZENTRUM MOL MED,BERLIN,GERMANY. FREE UNIV BERLIN,INST PHARMAKOL,D-14195 BERLIN,GERMANY. NIH,BIOORGAN CHEM LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0028-1298 J9 N-S ARCH PHARMACOL JI Naunyn-Schmiedebergs Arch. Pharmacol. PY 1997 VL 355 IS 4 SU S BP 200 EP 200 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WV420 UT WOS:A1997WV42000224 ER PT J AU Stopper, H Eckert, I Boos, G Caspary, WJ AF Stopper, H Eckert, I Boos, G Caspary, WJ TI Analysis of loss of heterozygozity and chromosome painting of etoposide-induced mutants SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY LA English DT Meeting Abstract C1 UNIV WURZBURG,DEPT TOXICOL,D-97078 WURZBURG,GERMANY. NIEHS,NIH,RES TRIANGLE PK,NC 27709. 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 0028-1298 J9 N-S ARCH PHARMACOL JI Naunyn-Schmiedebergs Arch. Pharmacol. PY 1997 VL 355 IS 4 SU S BP 621 EP 621 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WV420 UT WOS:A1997WV42000644 ER PT J AU Schleger, C Becker, R Heck, R Oesch, F Harris, CC Steinberg, P AF Schleger, C Becker, R Heck, R Oesch, F Harris, CC Steinberg, P TI Mutant p53 per se does not lead to the malignant transformation of human liver cells SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY LA English DT Meeting Abstract C1 UNIV MAINZ,INST TOXICOL,D-55131 MAINZ,GERMANY. NIH,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0028-1298 J9 N-S ARCH PHARMACOL JI Naunyn-Schmiedebergs Arch. Pharmacol. PY 1997 VL 355 IS 4 SU S BP 624 EP 624 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA WV420 UT WOS:A1997WV42000647 ER PT J AU Genova, L Berke, J Hyman, SE AF Genova, L Berke, J Hyman, SE TI Molecular adaptations to psychostimulants in striatal neurons: Toward a pathophysiology of addiction SO NEUROBIOLOGY OF DISEASE LA English DT Review ID IMMEDIATE-EARLY GENE; TRANSCRIPTION FACTOR GENES; DEPENDENT PROTEIN-KINASE; DOPAMINE RELEASE INVIVO; CAMP-RESPONSIVE ELEMENT; RAT NUCLEUS-ACCUMBENS; C-FOS; NMDA RECEPTORS; NEOSTRIATAL NEURONS; BINDING PROTEIN C1 NINCDS,SECT MOL PLAST,NIH,BETHESDA,MD 20892. NR 72 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0969-9961 J9 NEUROBIOL DIS JI Neurobiol. Dis. PY 1997 VL 4 IS 3-4 BP 239 EP 246 DI 10.1006/nbdi.1997.0154 PG 8 WC Neurosciences SC Neurosciences & Neurology GA YD463 UT WOS:A1997YD46300009 PM 9361300 ER PT J AU Fouquet, F Zhou, JM Ralston, E Murray, K Troalen, F Magal, E Robain, O DuboisDalcq, M Aubourg, P AF Fouquet, F Zhou, JM Ralston, E Murray, K Troalen, F Magal, E Robain, O DuboisDalcq, M Aubourg, P TI Expression of the adrenoleukodystrophy protein in the human and mouse central nervous system SO NEUROBIOLOGY OF DISEASE LA English DT Article ID X-LINKED ADRENOLEUKODYSTROPHY; PEROXISOMAL MEMBRANE-PROTEIN; BONE-MARROW TRANSPLANTATION; TUMOR-NECROSIS-FACTOR; CHAIN FATTY-ACID; ZELLWEGER SYNDROME; HUMAN BRAIN; DEVELOPMENTAL IMMUNOHISTOCHEMISTRY; MONOCLONAL-ANTIBODIES; RAT-LIVER AB The gene mutated in X-linked adrenoleukodystrophy (ALD), a progressive demyelinating disease, codes for a protein (ALDP) involved in very-long-chain fatty acid (VLCFA) transport. The expression of ALDP and of two peroxisomal enzymes involved in beta-oxidation of VLCFA, acyl-CoA oxidase, and catalase was studied in human and mouse brain. The pattern of expression was similar in both species. While acyl-CoA oxidase and catalase are found in all types of CNS cells, including neurons and oligodendrocytes, ALDP expression is restricted mostly to the white matter and endothelial cells. ALDP is highly expressed in astrocytes and microglial cells in vivo and in regenerating oligodendrocytes in vitro. In contrast, in vivo, ALDP is detected in much fewer oligodendrocytes and quantitative Western blot analysis confirmed the lower abundance of ALDP in these cells than in astrocytes, Only oligodendrocytes localized in corpus callosum, internal capsules, and anterior commissure express ALDP at levels comparable to those seen in astrocytes. In ALD, demyelination is first detected in these white matter regions, suggesting that the ALD gene mutation selectively affects those oligodendrocytes strongly expressing ALDP. Because of their failure to express ALDP, microglia and astrocytes may also contribute to demyelination in ALD patients. (C) 1997 Academic Press. C1 INST PASTEUR,DEPT VIROL,UNITE NEUROVIROL & REGENERAT SYST NERVEUX,PARIS,FRANCE. NINCDS,VIRAL & MOL PATHOGENESIS LAB,NIH,BETHESDA,MD 20892. NINCDS,NEUROBIOL LAB,NIH,BETHESDA,MD 20892. INST GUSTAVE ROUSSY,DEPT BIOL CLIN,F-94805 VILLEJUIF,FRANCE. AMGEN INC,THOUSAND OAKS,CA 91320. HOP PORT ROYAL,INSERM,U29,PARIS,FRANCE. RP Fouquet, F (reprint author), HOP ST VINCENT DE PAUL,INSERM,U324,UNITE PATHOL METAB & HORMONALE DEV,F-75674 PARIS,FRANCE. NR 63 TC 73 Z9 73 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 0969-9961 J9 NEUROBIOL DIS JI Neurobiol. Dis. PY 1997 VL 3 IS 4 BP 271 EP 285 DI 10.1006/nbdi.1997.0127 PG 15 WC Neurosciences SC Neurosciences & Neurology GA WV413 UT WOS:A1997WV41300003 PM 9173925 ER PT S AU Stoff, DM Mann, JJ AF Stoff, DM Mann, JJ BE Staff, DM Mann, JJ TI Suicide research - Overview and introduction SO NEUROBIOLOGY OF SUICIDE: FROM THE BENCH TO THE CLINIC SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Editorial Material CT Suicide Research Workshops - From the Bench to the Clinic CY NOV 14-15, 1996 CL WASHINGTON, D.C. SP NIMH, Amer Suicide Fdn ID DEPRESSION; CORTISOL C1 NIMH, Rockville, MD 20857 USA. New York State Psychiat Inst, Dept Neurosci, New York, NY 10032 USA. RP Stoff, DM (reprint author), NIMH, 5600 Fishers Lane,Room 18-101, Rockville, MD 20857 USA. NR 42 TC 13 Z9 13 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-094-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 836 BP 1 EP 11 DI 10.1111/j.1749-6632.1997.tb52352.x PG 11 WC Multidisciplinary Sciences; Psychiatry SC Science & Technology - Other Topics; Psychiatry GA BK30V UT WOS:000071743800001 PM 9616791 ER PT S AU Higley, JD Linnoila, M AF Higley, JD Linnoila, M BE Staff, DM Mann, JJ TI Low central nervous system serotonergic activity is traitlike and correlates with impulsive behavior - A nonhuman primate model investigating genetic and environmental influences on neurotransmission SO NEUROBIOLOGY OF SUICIDE: FROM THE BENCH TO THE CLINIC SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Suicide Research Workshops - From the Bench to the Clinic CY NOV 14-15, 1996 CL WASHINGTON, D.C. SP NIMH, Amer Suicide Fdn ID FLUID 5-HYDROXYINDOLEACETIC ACID; CERCOPITHECUS-AETHIOPS-SABAEUS; OBSESSIVE-COMPULSIVE DISORDER; DIMINISHED SOCIAL COMPETENCE; ADRENERGIC-RECEPTOR BINDING; BIOGENIC-AMINE METABOLISM; CSF MONOAMINE METABOLITE; MONKEYS MACACA-MULATTA; CEREBROSPINAL-FLUID; RHESUS-MONKEYS AB We have used nonhuman primates to examine developmental and behavioral correlates of CNS serotonergic activity, as measured by concentrations of the serotonin metabolite 5-hydroxyin-doleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). These studies show that interindividual differences in CNS serotonin turnover rate exhibit traitlike qualities and are stable across time and settings, with interindividual differences in CSF 5-HIAA concentrations showing positive correlations across repeated sampling. Primates with low CNS serotonergic activity exhibit behaviors indicative of impaired impulse control, unrestrained aggression, social isolation, and low social dominance, Maternal and paternal genetic influences play major roles in producing low CNS serotonin functioning beginning early in life. These genetic influences on serotonin functioning are further influenced by early rearing experiences, particularly parental deprivation. C1 NIAAA, Clin Studies Lab, Primate Unit, DICBR, Poolesville, MD 20837 USA. NIAAA, Clin Studies Lab, Off Director, DICBR, Bethesda, MD 20892 USA. RP Higley, JD (reprint author), NIH Anim Ctr, Bldg 112,POB 529, Poolesville, MD 20837 USA. EM higleyd@lce.nichd.nih.gov NR 144 TC 126 Z9 127 U1 3 U2 7 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-094-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 836 BP 39 EP 56 DI 10.1111/j.1749-6632.1997.tb52354.x PG 18 WC Multidisciplinary Sciences; Psychiatry SC Science & Technology - Other Topics; Psychiatry GA BK30V UT WOS:000071743800003 PM 9616793 ER PT S AU Bachus, SE Hyde, TM Akil, M Weickert, CS Vawter, MP Kleinman, JE AF Bachus, SE Hyde, TM Akil, M Weickert, CS Vawter, MP Kleinman, JE BE Staff, DM Mann, JJ TI Neuropathology of suicide - A review and an approach SO NEUROBIOLOGY OF SUICIDE: FROM THE BENCH TO THE CLINIC SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT Suicide Research Workshops - From the Bench to the Clinic CY NOV 14-15, 1996 CL WASHINGTON, D.C. SP NIMH, Amer Suicide Fdn ID ADRENERGIC-RECEPTOR BINDING; REGIONALLY SELECTIVE INCREASES; TRITIATED IMIPRAMINE BINDING; SEROTONIN UPTAKE SITES; 5-HT UPTAKE SITES; FRONTAL-CORTEX; HUMAN-BRAIN; DEPRESSED SUICIDES; LOCUS-COERULEUS; 5-HYDROXYINDOLEACETIC ACID AB Neuropathology is one approach to the effort to elucidate the pathophysiology of suicide. Initial neurochemical studies focusing on the roles of serotonin (5-HT) and noradrenaline (NE) abnormalities in brains of suicide victims have been somewhat inconsistent. More recently developed methodologies, including quantitative receptor autoradiography, immunoblotting, immunohistochemistry, cell morphometry, in situ hybridization, Northern analysis, solution hybridization/RNase protection assay, reverse transcriptase polymerase chain reaction, and genotyping, which have already been applied successfully in studies of other disorders of brain structure or function, are now increasingly being adopted for postmortem studies of suicide. These new strategies are adding convergent evidence for brain 5-HT and NE dysfunction in the etiology of suicide susceptibility, refining the neuroanatomical localization of this dysfunction, and in addition, implicating heretofore unsuspected candidate neurotransmitter systems in the neuropathological substrates of suicide susceptibility. It is argued here that the confluence of the availability of suitable postmortem samples and this augmentation of our armamentarium of techniques promises the attainment of important new insights into the biological underpinnings of suicide from postmortem research. It is to be hoped that this new knowledge might inspire novel pharmacotherapeutic strategies for the prevention of suicide. C1 NIMH, Neuropathol Sect,Clin Brain Disorders Branch, Intramural Res Programs,NIH,Neurosci Ctr, St Elizabeths Hosp, Washington, DC 20032 USA. RP NIMH, Neuropathol Sect,Clin Brain Disorders Branch, Intramural Res Programs,NIH,Neurosci Ctr, St Elizabeths Hosp, 2700 Martin Luther King Ave SE, Washington, DC 20032 USA. EM bachuss@dirpc.nimh.nih.gov; hydet@dirpc.nimh.nih.gov; akilm@dirpc.nimh.nih.gov; shannowc@dirpc.nimh.nih.gov; vawterm@dirpc.nimh.nih.gov; kleinmaj@dirpc.nimh.nih.gov RI Shannon Weickert, Cynthia/G-3171-2011 NR 95 TC 13 Z9 13 U1 21 U2 23 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-095-6; 1-57331-094-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 836 BP 201 EP 219 DI 10.1111/j.1749-6632.1997.tb52361.x PG 19 WC Multidisciplinary Sciences; Psychiatry SC Science & Technology - Other Topics; Psychiatry GA BK30V UT WOS:000071743800010 PM 9616800 ER PT S AU Arango, V Underwood, MD Mann, JJ AF Arango, V Underwood, MD Mann, JJ BE Staff, DM Mann, JJ TI Postmortem findings in suicide victims - Implications for in vivo imaging studies SO NEUROBIOLOGY OF SUICIDE: FROM THE BENCH TO THE CLINIC SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Suicide Research Workshops - From the Bench to the Clinic CY NOV 14-15, 1996 CL WASHINGTON, D.C. SP NIMH, Amer Suicide Fdn ID SEROTONIN UPTAKE SITES; H-3 PAROXETINE BINDING; ADRENERGIC-RECEPTOR BINDING; NORMAL HUMAN CORTEX; 5-HT UPTAKE SITES; HUMAN-BRAIN; POST-MORTEM; RAT-BRAIN; MONOAMINE METABOLITES; CEREBROSPINAL-FLUID AB Alterations in serotonergic and noradrenergic receptor binding in membrane homogenates from the brain of suicide victims suggest a biological substrate for the vulnerability to commit suicide. We and others have employed high-resolution quantitative autoradiography of full coronal sections of the prefrontal cortex to map the locus of maximal change in receptor binding. We found alterations in binding to the serotonin transporter, the 5-HT1A, and the 5-HT2A receptors primarily in the ventral and ventrolateral prefrontal cortex of suicide victims. Importantly, these changes are often modest in magnitude and anatomically restricted to one or two Brodmann areas. Furthermore, we have found that care in case selection is essential, because sex, age, drugs, and comorbid diagnoses contribute to receptor binding. The implications for in vivo imaging are considerable, directing the focus of such studies toward the ventrolateral prefrontal cortex. However, because ligands are limited, as is the resolution of current methods, including PET, automated analyses that produce statistical images, rather than manual selection of individual slices, will likely lack the ability to detect the discrete receptor changes found postmortem. Alternatively, the advantages of examining large numbers of subjects, imaging the entire brain, obtaining detailed clinical information in the living patient, and magnifying the changes with neuropharmacological challenges present a promising outlook for making major advances into the identification of brain abnormalities associated with suicide risk. C1 Columbia Univ Coll Phys & Surg, New York State Psychiat Inst, Dept Psychiat, NIMH,Clin Res Ctr Study Suicidal Behav, New York, NY 10032 USA. Columbia Univ Coll Phys & Surg, Dept Neurosci, New York State Psychiat Inst, New York, NY 10032 USA. RP Arango, V (reprint author), Columbia Univ Coll Phys & Surg, Dept Neurosci, New York State Psychiat Inst, 722 W 168th St,Box 28, New York, NY 10032 USA. EM varango@neuron.cpmc.columbia.edu RI Arango, Victoria/K-9377-2015; Underwood, Mark/N-1412-2015 OI Arango, Victoria/0000-0001-8811-400X; Underwood, Mark/0000-0003-0595-8712 FU NIAAA NIH HHS [AA09004]; NIMH NIH HHS [MH46745, MH40210] NR 77 TC 78 Z9 78 U1 0 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-094-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 836 BP 269 EP 287 DI 10.1111/j.1749-6632.1997.tb52365.x PG 19 WC Multidisciplinary Sciences; Psychiatry SC Science & Technology - Other Topics; Psychiatry GA BK30V UT WOS:000071743800014 PM 9616804 ER PT B AU Cadet, JL AF Cadet, JL BE Teelken, A Korf, J TI The possible involvement of death-related genes in methamphetamine-induced apoptosis SO NEUROCHEMISTRY: CELLULAR, MOLECULAR, AND CLINICAL ASPECTS LA English DT Proceedings Paper CT 11th Meeting of the European-Society-for-Neurochemistry CY JUN 15-20, 1996 CL GRONINGEN, NETHERLANDS SP European Soc Neurochem C1 NIDA, Mol Neuropsychiat Sect, NIH, AIRP, Baltimore, MD 21224 USA. RP Cadet, JL (reprint author), NIDA, Mol Neuropsychiat Sect, NIH, AIRP, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA BN 0-306-45705-9 PY 1997 BP 323 EP 325 PG 3 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA BK43L UT WOS:000072167400054 ER PT B AU Goldberg, SR Yasar, S AF Goldberg, SR Yasar, S BE Teelken, A Korf, J TI Methamphetamine administration and associated neurotoxicity - Effects of selegiline (l-deprenyl) SO NEUROCHEMISTRY: CELLULAR, MOLECULAR, AND CLINICAL ASPECTS LA English DT Proceedings Paper CT 11th Meeting of the European-Society-for-Neurochemistry CY JUN 15-20, 1996 CL GRONINGEN, NETHERLANDS SP European Soc Neurochem C1 Preclin Pharmacol Lab, Nida Intramur Res Progr, Baltimore, MD 21224 USA. RP Goldberg, SR (reprint author), Preclin Pharmacol Lab, Nida Intramur Res Progr, 4940 Eastern Ave Bldg C,POB 5180, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PLENUM PRESS DIV PLENUM PUBLISHING CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA BN 0-306-45705-9 PY 1997 BP 327 EP 330 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA BK43L UT WOS:000072167400055 ER PT J AU Martinez-Lage, JF Poza, M Brown, P Cervenakova, L Bremon, AR de Pedro, J AF Martinez-Lage, JF Poza, M Brown, P Cervenakova, L Bremon, AR de Pedro, J TI Creutzfeldt-Jakob disease in neurosurgery: a review of risks and prevention measures SO NEUROCIRUGIA LA Spanish DT Review DE complications in neurosurgery; dura mater grafts; iatrogenic Creutzfeldt-Jakob disease; prion infection; slow-virus infection; spongiform encephalopathy ID DURA-MATER GRAFT; SPONGIFORM ENCEPHALOPATHY; PERSON TRANSMISSION; EPIDEMIOLOGY; MEDICINE; ENGLAND; PATIENT; TISSUE; WALES AB From 1988 to 1996 there have been at least 17 reports on Creutzfeldt-Jakob disease (CJD) related to the placement of dura mater grafts of cadaveric origin during the course of neurosurgical procedures. The knowledge of means of transmission in the neurosurgical milieu, the changes introduced in the procurement and sterilization of grafts of human origin, and especially the widespread utilization of autologous tissues in dural repair, seems to have put to an end to this feared neurosurgical complication. Probably, we will see in the future only sporadic and infrequent cases of this entity. The authors review their personal experience, published and unpublished data on iatrogenic CJD cases, and the methods in use for eradication of this disease, in which the neurosurgeons have been involuntary protagonists and vectors. We also note the role played by neurosurgeons in the active investigation of most cases, and in contributing to halt CJD spread in the surgical environment. C1 Hosp Univ Virgen Arrixaca, Serv Neurocirugia, Murcia, Spain. NINDS, Cent Nervous Syst Studies Lab, Bethesda, MD 20892 USA. Inst Salud Carlos III, Ctr Vigilancia Epidemiol, Madrid, Spain. NR 48 TC 1 Z9 1 U1 0 U2 1 PU SOCIEDAD LUSO-ESPANOLA NEUROCIRUGIA PI SANTANDER PA C/O J M IZQUIERDO HOSPITAL VALDECILLA, 39908 SANTANDER, SPAIN SN 1130-1473 J9 NEUROCIRUGIA JI Neurocirugia PY 1997 VL 8 IS 4 BP 284 EP 293 PG 10 WC Neurosciences; Surgery SC Neurosciences & Neurology; Surgery GA YQ140 UT WOS:000071352500002 ER PT J AU Harrison, LH Vaz, B Taveira, DM Quinn, TC Gibbs, CJ deSouza, SH McArthur, JC Schechter, M AF Harrison, LH Vaz, B Taveira, DM Quinn, TC Gibbs, CJ deSouza, SH McArthur, JC Schechter, M TI Myelopathy among Brazilians coinfected with human T-cell lymphotropic virus type I and HIV SO NEUROLOGY LA English DT Article ID INTRAVENOUS-DRUG-USERS; HTLV-I; VACUOLAR MYELOPATHY; PROGRESSIVE MYELOPATHY; INFECTION; DISEASE; LEUKEMIA; PATIENT; AIDS; TRANSPLANTATION AB Objective: To determine whether subjects coinfected with HTLV-I and HIV have a higher frequency of myelopathy than subjects singly infected with HIV. Design: A prospective, nested case-control study of HTLV-I and HIV coinfected (cases) and HIV singly infected adults (controls) participating in a prospective HIV cohort study at a university hospital outpatient HIV clinic in Rio de Janeiro, Brazil. Measurements: Subjects were evaluated for evidence of myelopathy by a neurologist unaware of their HTLV serologic status. Patients with at least two pyramidal signs, such as paresis, hypertonicity or spasticity, hyperreflexia, clonus, diminished or absent superficial reflexes, or the presence of pathologic reflexes (e.g., Babinski or Hoffmann), were defined as having myelopathy. Myelopathy severity was quantified using the Kurtzke Functional Disability Scale (FDS); patients with FDS scores greater than or equal to 4 were considered to have significant myelopathy. Selected patients with myelopathy underwent lumbar puncture for the evaluation of intrathecal synthesis of HTLV-I antibodies. Results: Of 15 coinfected subjects, 11 (73%) had evidence of myelopathy versus 10 of 62 subjects (16%) with HIV single infection (adjusted odds ratio [OR] = 13.0, p = 0.00002). When only myelopathy patients with FDS scores of greater than or equal to 2 or greater than or equal to 4 were included, the association between coinfection and the presence of myelopathy remained (OR = 7.3, p = 0.0003 for scores greater than or equal to 2; and OR = 8.9 for scores greater than or equal to 4, p = 0.04). In addition, a higher proportion of coinfected subjects had peripheral neuropathy (40%) than controls (16%) (OR = 3.5, p = 0.07). Conclusion: Coinfection with HTLV-I was strongly associated with myelopathy among subjects infected with HIV. The relative contribution of HTLV-I versus HN in the pathogenesis of coinfection-associated myelopathy is not known. Coinfection may also be associated with peripheral neuropathy. Further studies are needed to elucidate the mechanisms of coinfection-associated neurologic conditions. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT INT HLTH,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT NEUROL,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,DEPT INT HLTH,BALTIMORE,MD. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205. UNIV FED RIO DE JANEIRO,HOSP UNIV CLEMENTINO FRAGA FILHO,INFECT DIS SERV,RIO JANEIRO,BRAZIL. UNIV FED RIO DE JANEIRO,HOSP UNIV CLEMENTINO FRAGA FILHO,NEUROL SERV,RIO JANEIRO,BRAZIL. NIAID,NIH,BETHESDA,MD 20892. NINCDS,NIH,BETHESDA,MD 20892. FU NINDS NIH HHS [NS26643] NR 38 TC 41 Z9 45 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1997 VL 48 IS 1 BP 13 EP 18 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA WC676 UT WOS:A1997WC67600004 PM 9008486 ER PT J AU Luciano, CA Dalakas, MC AF Luciano, CA Dalakas, MC TI Inclusion body myositis: No evidence for a neurogenic component SO NEUROLOGY LA English DT Article; Proceedings Paper CT 47th Annual Meeting of the American-Academy-of-Neurology CY MAY 11, 1995 CL SEATTLE, WA SP Amer Acad Neurol ID MOTOR UNIT POTENTIALS; MACRO-EMG; INFLAMMATORY MYOPATHY; MUSCULAR-DYSTROPHY; SCANNING EMG; ELECTROMYOGRAPHY; SIMULATION AB Because electrophysiologic, clinical, and histopathologic observations have suggested that inclusion body myositis (IBM) may have a coexistent neurogenic component, we used macro-electromyography (macro-EMG) to search for changes in the motor unit territory and signs of reinnervation. We studied 11 patients, aged 53 to 77 years (mean, 65.2 years), with typical, nonfamilial IBM lasting a mean of 8.5 years, and eight healthy volunteers aged 54 to 70 years (mean, 64.6 years), as control subjects. Nerve conduction studies showed focal abnormalities in 5 of the patients, but no evidence of a polyneuropathy. Concentric needle EMG in various proximal and distal muscles of the upper and lower Limbs revealed short- or long-duration complex motor unit potentials (MUPs) or a mixture of both types of MUPs. Macro-EMG studies in the tibialis anterior muscle showed smaller macro-MUP amplitudes and areas in patients than in normal subjects. Four patients had abnormal macro-EMG studies with an increased number of small macro-MUPs, 1 patient had an equivocal study with large-amplitude but normal-area macro-MUPs, and the remaining 6 patients had normal studies. These findings are consistent with a primary muscle disorder similar to those seen in other myopathies. We conclude that macro-EMG does not support a coexistent neurogenic component in patients with IBM compared with normal subjects of similar age. C1 NINCDS,ELECTROMYOG SECT,NIH,BETHESDA,MD 20892. RP Luciano, CA (reprint author), NINCDS,NEUROMUSCULAR DIS SECT,NIH,BLDG 10,ROOM 4N248,10 CTR DR MSC 1382,BETHESDA,MD 20892, USA. NR 24 TC 25 Z9 27 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1997 VL 48 IS 1 BP 29 EP 33 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA WC676 UT WOS:A1997WC67600007 PM 9008489 ER PT J AU Litvan, I Agid, Y Goetz, C Jankovic, J Wenning, GK Brandel, JP Lai, EC Verny, M RayChaudhuri, K McKee, A Jellinger, K Pearce, RKB Bartko, JJ AF Litvan, I Agid, Y Goetz, C Jankovic, J Wenning, GK Brandel, JP Lai, EC Verny, M RayChaudhuri, K McKee, A Jellinger, K Pearce, RKB Bartko, JJ TI Accuracy of the clinical diagnosis of corticobasal degeneration: A clinicopathologic study SO NEUROLOGY LA English DT Article; Proceedings Paper CT Movement Disorder Society Symposium on Cortical-Basal Ganglionic Degeneration(CBGD) and Its Relationship to Other Asymmetrical Cortical Degeneration Syndromes(ACDs) CY OCT, 1995 CL WASHINGTON, DC SP Movement Disorder Soc ID PROGRESSIVE SUPRANUCLEAR PALSY; BASAL GANGLIONIC DEGENERATION; MULTIPLE SYSTEM ATROPHY; NEURONAL ACHROMASIA; NATURAL-HISTORY; CORTICONIGRAL DEGENERATION; NEUROFIBRILLARY TANGLES; PARKINSONS-DISEASE; KAPPA-COEFFICIENT; CATEGORICAL-DATA AB The accuracy of the clinical diagnosis of corticobasal degeneration (CBD) is unknown. To determine its diagnostic accuracy, we presented 105 cases with known neuropathologic diagnoses, including CBD (n = 10), progressive supranuclear palsy (PSP, n = 24), Parkinson's disease (n = 15), diffuse Lewy body disease (n = 14), multiple system atrophy (n = 16), postencephalitic parkinsonism (n = 7), Pick's disease (n = 7), Creutzfeldt-Jacob disease (n = 4), Alzheimer's disease (n = 4), vascular parkinsonism (n = 3), and Whipple's disease (n = 1), as clinical vignettes to six neurologists unaware of the autopsy findings. Reliability was measured with the kappa statistics. The neurologists' clinical diagnoses were compared with clinicopathologic diagnoses for sensitivity, specificity, and positive predictive values at first and last clinic visits. The group reliability for the diagnosis of CBD significantly improved from moderate for the first visit (mean = 34 months after onset) to substantial for the last (68 months after onset). For the first visit, mean sensitivity for CBD was low (35%), but specificity was near-perfect (99.6%). For the last visit, mean sensitivity minimally increased (48.3%), and specificity remained stable. False-negative misdiagnoses mainly occurred with PSP. False-positive diagnoses were rare. The extremely low sensitivity of the clinical diagnosis of CBD suggests that this disorder is markedly underdiagnosed. Although the validity of the clinical diagnosis might have been improved if neurologists could have examined these patients, more important is that this disorder was misdiagnosed by the primary neurologists. In our data set, the best predictors for the diagnosis of CBD included limb dystonia, ideomotor apraxia, myoclonus, and asymmetric akinetic-rigid syndrome with late onset of gait or balance disturbances. C1 HOP LA PITIE SALPETRIERE,FED NEUROL,PARIS,FRANCE. HOP LA PITIE SALPETRIERE,INSERM,U289,PARIS,FRANCE. RUSH MED COLL,DEPT NEUROL,CHICAGO,IL 60612. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. NEUROL INST,PARKINSONS DIS SOC BRAIN TISSUE BANK,LONDON,ENGLAND. INST PSYCHIAT,DEPT NEUROL,LONDON SE5 8AF,ENGLAND. HOP LA PITIE SALPETRIERE,RAYMOND ESCOUROLLE NEUROPATHOL LAB,INSERM,U360,PARIS,FRANCE. MASSACHUSETTS GEN HOSP,DEPT NEUROPATHOL,BOSTON,MA 02114. LAINZ HOSP,LUDWIG BOLTZMANN INST CLIN NEUROBIOL,A-1130 VIENNA,AUSTRIA. NIMH,DIV EPIDEMIOL & RES STUDIES,BETHESDA,MD 20892. RP Litvan, I (reprint author), NINCDS,NEUROEPIDEMIOL BRANCH,NIH,FED BLDG,ROOM 714,BETHESDA,MD 20892, USA. OI Litvan, Irene/0000-0002-3485-3445; Ray Chaudhuri, K/0000-0003-2815-0505 NR 73 TC 282 Z9 286 U1 0 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1997 VL 48 IS 1 BP 119 EP 125 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA WC676 UT WOS:A1997WC67600024 PM 9008506 ER PT J AU Fouad, G Dalakas, M Servidei, S Mendell, JR VandenBergh, P Angelini, C Alderson, K Griggs, RC Tawil, R Gregg, R Hogan, K Powers, PA Weinberg, N Malonee, W Ptacek, LJ AF Fouad, G Dalakas, M Servidei, S Mendell, JR VandenBergh, P Angelini, C Alderson, K Griggs, RC Tawil, R Gregg, R Hogan, K Powers, PA Weinberg, N Malonee, W Ptacek, LJ TI Genotype-phenotype correlations of DHP receptor alpha(1)-subunit gene mutations causing hypokalemic periodic paralysis SO NEUROMUSCULAR DISORDERS LA English DT Article DE hypokalemic periodic paralysis; muscle weakness; mutation ID PARAMYOTONIA-CONGENITA; CALCIUM; FAMILIES; HYPOPP AB Hypokalemic periodic paralysis (hypoKPP) is an autosomal dominant or sporadic disorder characterized by periodic, reversible attacks of muscle weakness. Mutations in the skeletal muscle dihydropyridine receptor alpha(1)-subunit that functions as a calcium channel (CACNLIA3) cause hypoKPP. We studied a group of 45 hypoKPP probands and demonstrated mutations in 30 of them. When compared with patients in whom CACNL1A3 mutations were not identified, those with mutations had an earlier age of onset and more often had a family history of hypoKPP. To date, three mutations have been identified. The R1239G mutation has only been found in one family. Of the 30 probands with recognized mutations, R528H accounted for 43% and R1239H was seen in 53%. Age of onset and potassium levels during attacks were lower in patients with the R1239H mutation than those with R528H. Cardiac dysrhythmias co-segregated with hypoKPP in one small kindred with the R528 H mutation. No mutations were identified in exons of the gene encoding the S4 segments of domains one and three or the cytoplasmic loop between domains two and three. In addition to the 45 hypoKPP probands, an additional 11 probands with clinical variants of hypoKPP (three thyrotoxic hypoKPP and eight Andersen syndrome patients) were examined for CACNLIA3 mutations and none were found. (C) 1997 Elsevier Science B.V. C1 UNIV UTAH,DEPT NEUROL,SALT LAKE CITY,UT 84112. UNIV UTAH,DEPT HUMAN GENET,SALT LAKE CITY,UT 84112. UNIV UTAH,PROGRAM HUMAN MOL BIOL & GENET,SALT LAKE CITY,UT 84112. NINCDS,NIH,BETHESDA,MD 20892. UNIV CATTOLICA SACRO CUORE,FAC MED & CHIRURG AGOSTINO GEMELLI,ROME,ITALY. OHIO STATE UNIV,DEPT NEUROL,COLUMBUS,OH 43210. UNIV BRUSSELS,CLIN ST LUC,SERV NEUROL,BRUSSELS,BELGIUM. UNIV PADUA,PADUA,ITALY. NEUROMUSCULAR ASSOCIATES INC,SALT LAKE CITY,UT 84112. UNIV ROCHESTER,MED CTR,NEUROMUSCULAR DIS CTR,ROCHESTER,NY 14642. UNIV WISCONSIN,WAISMAN CTR MENTAL RETARDAT & HUMAN DEV,MADISON,WI 53706. UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,MADISON,WI 53706. UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53706. PEDIAT HLTH CARE ASSOCIATES,YPSILANTI,MI 48197. HUTCHINSON CLIN,HUTCHINSON,KS. OI Angelini, Corrado/0000-0002-9554-8794 FU NCRR NIH HHS [M01-RR00064]; NHGRI NIH HHS [8 R01 HG00367]; NICHD NIH HHS [HD00940]; Telethon [0916C] NR 20 TC 69 Z9 73 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-8966 J9 NEUROMUSCULAR DISORD JI Neuromusc. Disord. PD JAN PY 1997 VL 7 IS 1 BP 33 EP 38 DI 10.1016/S0960-8966(96)00401-4 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA WN036 UT WOS:A1997WN03600006 PM 9132138 ER PT S AU Gressens, P Paindaveine, B Hill, JM Brenneman, DE Evrard, P AF Gressens, P Paindaveine, B Hill, JM Brenneman, DE Evrard, P BE Beckwith, BE Saria, A Chronwall, BM Sandman, CA Strand, FL TI Growth factor properties of VIP during early brain development - Whole embryo culture and in vivo studies SO NEUROPEPTIDES IN DEVELOPMENT AND AGING SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Neuropeptides in Development and Aging, 1st Joint Meeting of the European-Neuropeptide-Club / 17th Winter Neuropeptide Conference CY FEB 03-06, 1996 CL BRECKENRIDGE, COLORADO SP European Neuropeptide Club, New York Acad Sci, Biomeasure Inc, Burroughs Wellcome, Cephalon Inc, Merck, Pfizer Inc, Smith Kline Beecham Pharmaceuticals, Council Tobacco Res, Upjohn Co ID VASOACTIVE-INTESTINAL-PEPTIDE; MOUSE EMBRYOS; NEUROTROPHIC ACTION; ANTAGONIST C1 Hop Robert Debre, Lab Neurol Dev, F-75019 Paris, France. Hop Robert Debre, Serv Neuropediat, F-75019 Paris, France. NICHHD, Sect Mol & Dev Pharmacol, NIH, Bethesda, MD 20892 USA. RP Gressens, P (reprint author), Hop Robert Debre, Lab Neurol Dev, 48 Blvd Serurier, F-75019 Paris, France. EM Gressens@msn.com NR 26 TC 28 Z9 28 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-066-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 814 BP 152 EP 160 DI 10.1111/j.1749-6632.1997.tb46153.x PG 9 WC Geriatrics & Gerontology; Multidisciplinary Sciences; Neurosciences SC Geriatrics & Gerontology; Science & Technology - Other Topics; Neurosciences & Neurology GA BM45V UT WOS:000078790100015 PM 9160967 ER PT S AU Gozes, I Bardea, A Bechar, M Pearl, O Reshef, A Zamostiano, R Davidson, A Rubinraut, S Giladi, E Fridkin, M Brenneman, DE AF Gozes, I Bardea, A Bechar, M Pearl, O Reshef, A Zamostiano, R Davidson, A Rubinraut, S Giladi, E Fridkin, M Brenneman, DE BE Beckwith, BE Saria, A Chronwall, BM Sandman, CA Strand, FL TI Neuropeptides and neuronal survival: Neuroprotective strategy for Alzheimer's disease SO NEUROPEPTIDES IN DEVELOPMENT AND AGING SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Neuropeptides in Development and Aging, 1st Joint Meeting of the European-Neuropeptide-Club / 17th Winter Neuropeptide Conference CY FEB 03-06, 1996 CL BRECKENRIDGE, COLORADO SP European Neuropeptide Club, New York Acad Sci, Biomeasure Inc, Burroughs Wellcome, Cephalon Inc, Merck, Pfizer Inc, Smith Kline Beecham Pharmaceuticals, Council Tobacco Res, Upjohn Co ID VASOACTIVE-INTESTINAL-PEPTIDE; FUNCTIONAL IMPLICATIONS; MESSENGER PLASTICITY; CORTICAL-NEURONS; ENVELOPE PROTEIN; VIP; ASTROCYTES; GROWTH; PREVENTION; EXPRESSION C1 Tel Aviv Univ, Sackler Sch Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. Weizmann Inst Sci, Dept Organ Chem, IL-76100 Rehovot, Israel. NICHHD, Sect Dev & Mol Pharmacol, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA. NIH, Fogarty Int Ctr Adv Study Hlth Sci, Bethesda, MD 20892 USA. RP Gozes, I (reprint author), Tel Aviv Univ, Sackler Sch Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. NR 33 TC 17 Z9 17 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-066-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 814 BP 161 EP 166 DI 10.1111/j.1749-6632.1997.tb46154.x PG 6 WC Geriatrics & Gerontology; Multidisciplinary Sciences; Neurosciences SC Geriatrics & Gerontology; Science & Technology - Other Topics; Neurosciences & Neurology GA BM45V UT WOS:000078790100016 PM 9160968 ER PT S AU Brenneman, DE Phillips, TM Festoff, BW Gozese, I AF Brenneman, DE Phillips, TM Festoff, BW Gozese, I BE Beckwith, BE Saria, A Chronwall, BM Sandman, CA Strand, FL TI Identity of neurotrophic molecules released from astroglia by vasoactive intestinal peptide SO NEUROPEPTIDES IN DEVELOPMENT AND AGING SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Neuropeptides in Development and Aging, 1st Joint Meeting of the European-Neuropeptide-Club / 17th Winter Neuropeptide Conference CY FEB 03-06, 1996 CL BRECKENRIDGE, COLORADO SP European Neuropeptide Club, New York Acad Sci, Biomeasure Inc, Burroughs Wellcome, Cephalon Inc, Merck, Pfizer Inc, Smith Kline Beecham Pharmaceuticals, Council Tobacco Res, Upjohn Co ID LUNG-CANCER GROWTH; NEURONAL SURVIVAL; NERVOUS-SYSTEM; TERM SURVIVAL; PREVENTION; ANTAGONIST; RECEPTORS; CYTOKINES; CULTURE; SERPIN C1 NICHHD, Sect Dev & Mol Pharmacol, NIH, Bethesda, MD 20892 USA. George Washington Univ, Sch Med, Dept Med, Washington, DC USA. Univ Kansas, Med Ctr, Dept Neurol, Kansas City, KS 66103 USA. Tel Aviv Univ, Sackler Sch Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. RP Brenneman, DE (reprint author), NICHD, SDMP, LDN, NIH, Bldg 49,Room 5A38, Bethesda, MD 20892 USA. NR 30 TC 42 Z9 45 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-066-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 814 BP 167 EP 173 DI 10.1111/j.1749-6632.1997.tb46155.x PG 7 WC Geriatrics & Gerontology; Multidisciplinary Sciences; Neurosciences SC Geriatrics & Gerontology; Science & Technology - Other Topics; Neurosciences & Neurology GA BM45V UT WOS:000078790100017 PM 9160969 ER PT S AU Hill, JM Gressens, P Brenneman, DE AF Hill, JM Gressens, P Brenneman, DE BE Beckwith, BE Saria, A Chronwall, BM Sandman, CA Strand, FL TI Growth of the early postimplantation embryo - Regulation by high-affinity, GTP-insensitive VIP receptors SO NEUROPEPTIDES IN DEVELOPMENT AND AGING SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Neuropeptides in Development and Aging, 1st Joint Meeting of the European-Neuropeptide-Club / 17th Winter Neuropeptide Conference CY FEB 03-06, 1996 CL BRECKENRIDGE, COLORADO SP European Neuropeptide Club, New York Acad Sci, Biomeasure Inc, Burroughs Wellcome, Cephalon Inc, Merck, Pfizer Inc, Smith Kline Beecham Pharmaceuticals, Council Tobacco Res, Upjohn Co ID VASOACTIVE-INTESTINAL-PEPTIDE; NEUROTROPHIC ACTION; RAT-BRAIN; EXPRESSION; MOUSE C1 NIH, Sect Dev & Mol Pharmacol, Dev Neurobiol Lab, Bethesda, MD 20892 USA. Hop Robert Debre, Lab Neurol Dev, F-75019 Paris, France. Hop Robert Debre, Serv Neuropediat, F-75019 Paris, France. RP Hill, JM (reprint author), NICHD, LDN, Bldg 49,Room 5A38,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 14 TC 2 Z9 2 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-066-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 814 BP 174 EP 180 DI 10.1111/j.1749-6632.1997.tb46156.x PG 7 WC Geriatrics & Gerontology; Multidisciplinary Sciences; Neurosciences SC Geriatrics & Gerontology; Science & Technology - Other Topics; Neurosciences & Neurology GA BM45V UT WOS:000078790100018 PM 9160970 ER PT S AU Abbracchio, MP Ceruti, S Brambilla, R Franceschi, C Malorni, W Jacobson, KA vonLubitz, DKJE Cattabeni, F AF Abbracchio, MP Ceruti, S Brambilla, R Franceschi, C Malorni, W Jacobson, KA vonLubitz, DKJE Cattabeni, F BE Slikker, W TI Modulation of apoptosis by adenosine in the central nervous system: a possible role for the A(3) receptor - Pathophysiological significance and therapeutic implications for neurodegenerative disorders SO NEUROPROTECTIVE AGENTS - THIRD INTERNATIONAL CONFERENCE SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT 3rd International Conference on Neuroprotective Agents - Clinical and Experimental Aspects CY SEP 09-12, 1996 CL VARENNA, ITALY SP New York Acad Sci, FDA, Natl Ctr Toxicol Res, Arkansas, Dept Vet Affairs Med Ctr, Togus, Maine ID LEUKEMIA-CELLS; RAT-BRAIN; TRANSDUCTIONAL MECHANISMS; DEAMINASE DEFICIENCY; PRIMARY CULTURES; DNA-SYNTHESIS; C-FOS; DEATH; 2-CHLORODEOXYADENOSINE; AGONISTS C1 UNIV MODENA, INST GEN PATHOL, I-41100 MODENA, ITALY. INRCA ANCONA, DEPT GERONTOL, ANCONA, ITALY. IST SUPER SANITA, DEPT ULTRASTRUCT, I-00161 ROME, ITALY. NIDDKD, MOL RECOGNIT SECT, BIOORGAN CHEM LAB, NIH, BETHESDA, MD 20892 USA. RP Abbracchio, MP (reprint author), UNIV MILAN, INST PHARMACOL SCI, VIA BALZARETTI 9, I-20133 MILAN, ITALY. RI Ceruti, Stefania/A-6376-2008; Jacobson, Kenneth/A-1530-2009; Abbracchio, Maria Pia/B-9342-2014; Malorni, Walter/G-5874-2016 OI Ceruti, Stefania/0000-0003-1663-4211; Jacobson, Kenneth/0000-0001-8104-1493; Abbracchio, Maria Pia/0000-0002-7833-3388; FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999] NR 52 TC 64 Z9 66 U1 0 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-093-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 825 BP 11 EP 22 DI 10.1111/j.1749-6632.1997.tb48410.x PG 12 WC Multidisciplinary Sciences; Neurosciences; Pharmacology & Pharmacy SC Science & Technology - Other Topics; Neurosciences & Neurology; Pharmacology & Pharmacy GA BJ99G UT WOS:A1997BJ99G00002 PM 9369971 ER PT S AU Bischofberger, N Jacobson, KA vonLubitz, DKJE AF Bischofberger, N Jacobson, KA vonLubitz, DKJE BE Slikker, W TI Adenosine A(1) receptor agonists as clinically viable agents for treatment of ischemic brain disorders SO NEUROPROTECTIVE AGENTS - THIRD INTERNATIONAL CONFERENCE SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT 3rd International Conference on Neuroprotective Agents - Clinical and Experimental Aspects CY SEP 09-12, 1996 CL VARENNA, ITALY SP New York Acad Sci, FDA, Natl Ctr Toxicol Res, Arkansas, Dept Vet Affairs Med Ctr, Togus, Maine ID CEREBRAL-ISCHEMIA; RAT-BRAIN; NEURONS; CELLS; CONDUCTANCE; ANTAGONIST; AFFINITY; GERBILS; RELEASE; INVITRO C1 NIDDK, MOL RECOGNIT SECT, BIOORGAN CHEM LAB, NIH, BETHESDA, MD 20892 USA. RP Bischofberger, N (reprint author), GILEAD SCI INC, 353 LAKESIDE DR, FOSTER CITY, CA 94404 USA. RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031117-20, Z99 DK999999] NR 34 TC 33 Z9 34 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-093-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 825 BP 23 EP 29 DI 10.1111/j.1749-6632.1997.tb48411.x PG 7 WC Multidisciplinary Sciences; Neurosciences; Pharmacology & Pharmacy SC Science & Technology - Other Topics; Neurosciences & Neurology; Pharmacology & Pharmacy GA BJ99G UT WOS:A1997BJ99G00003 PM 9369972 ER PT S AU vonLubitz, DKJE AF vonLubitz, DKJE BE Slikker, W TI Adenosine A(3) receptor and brain - A culprit, a hero, or merely yet another receptor? SO NEUROPROTECTIVE AGENTS - THIRD INTERNATIONAL CONFERENCE SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT 3rd International Conference on Neuroprotective Agents - Clinical and Experimental Aspects CY SEP 09-12, 1996 CL VARENNA, ITALY SP New York Acad Sci, FDA, Natl Ctr Toxicol Res, Arkansas, Dept Vet Affairs Med Ctr, Togus, Maine ID SPECIES-DIFFERENCES; MOLECULAR-CLONING; MAST-CELLS; RAT; ACTIVATION; AGONISTS; RELEASE; EXPRESSION; ANTAGONISTS; HYPOTENSION RP vonLubitz, DKJE (reprint author), NIDDKD, MOL RECOGNIT SECT,BIOORGAN CHEM LAB,NIH,BLDG 8, ROOM 1A15, BETHESDA, MD 20892 USA. NR 58 TC 19 Z9 19 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-093-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 825 BP 49 EP 67 PG 19 WC Multidisciplinary Sciences; Neurosciences; Pharmacology & Pharmacy SC Science & Technology - Other Topics; Neurosciences & Neurology; Pharmacology & Pharmacy GA BJ99G UT WOS:A1997BJ99G00005 PM 9369974 ER PT S AU Herning, RI King, DE Better, W Cadet, JL AF Herning, RI King, DE Better, W Cadet, JL BE Slikker, W TI Cocaine dependence - A clinical syndrome requiring neuroprotection SO NEUROPROTECTIVE AGENTS - THIRD INTERNATIONAL CONFERENCE SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT 3rd International Conference on Neuroprotective Agents - Clinical and Experimental Aspects CY SEP 09-12, 1996 CL VARENNA, ITALY SP New York Acad Sci, FDA, Natl Ctr Toxicol Res, Arkansas, Dept Vet Affairs Med Ctr, Togus, Maine ID PERFUSION; ABUSE; TECHNETIUM-99M-HMPAO; COMPLICATIONS; ABSTINENCE; SPECT RP Herning, RI (reprint author), NIDA, MOL NEUROPSYCHIAT SECT, DIV INTRAMURAL RES, NIH, POB 5180, BALTIMORE, MD 21224 USA. NR 22 TC 2 Z9 2 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-093-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 825 BP 323 EP 327 DI 10.1111/j.1749-6632.1997.tb48442.x PG 5 WC Multidisciplinary Sciences; Neurosciences; Pharmacology & Pharmacy SC Science & Technology - Other Topics; Neurosciences & Neurology; Pharmacology & Pharmacy GA BJ99G UT WOS:A1997BJ99G00028 PM 9369997 ER PT S AU King, DE Herning, RI Cadet, JL AF King, DE Herning, RI Cadet, JL BE Slikker, W TI Subclinical neurological and neurovascular deficits in cocaine dependence - Gender and psychosocial considerations SO NEUROPROTECTIVE AGENTS - THIRD INTERNATIONAL CONFERENCE SE Annals of the New York Academy of Sciences LA English DT Article; Proceedings Paper CT 3rd International Conference on Neuroprotective Agents - Clinical and Experimental Aspects CY SEP 09-12, 1996 CL VARENNA, ITALY SP New York Acad Sci, FDA, Natl Ctr Toxicol Res, Arkansas, Dept Vet Affairs Med Ctr, Togus, Maine ID TECHNETIUM-99M-HMPAO; PERFUSION C1 NIDA, MOL NEUROPSYCHIAT SECT, DIV INTRAMURAL RES, NIH, BALTIMORE, MD 21224 USA. NR 3 TC 6 Z9 6 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-093-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1997 VL 825 BP 328 EP 331 DI 10.1111/j.1749-6632.1997.tb48443.x PG 4 WC Multidisciplinary Sciences; Neurosciences; Pharmacology & Pharmacy SC Science & Technology - Other Topics; Neurosciences & Neurology; Pharmacology & Pharmacy GA BJ99G UT WOS:A1997BJ99G00029 PM 9369998 ER PT J AU Greenwood, PM Parasuraman, R Alexander, GE AF Greenwood, PM Parasuraman, R Alexander, GE TI Controlling the focus of spatial attention during visual search: Effects of advanced aging and Alzheimer disease SO NEUROPSYCHOLOGY LA English DT Article ID VISUOSPATIAL ATTENTION; SELECTIVE ATTENTION; AGE-DIFFERENCES; FEATURE-INTEGRATION; ALLOCATION; PARALLEL; DEMENTIA; DEFICIT; CONJUNCTION; PERFORMANCE AB It was hypothesized that slowed visual search in healthy adult aging arises from reduced ability to adjust the size of the attentional focus. A novel, cued-visual search task manipulated the scale of spatial attention in a complex field in healthy elderly individuals and patients with dementia of the Alzheimer type (DAT). Precues indicated with varying validity the size and location of the area to be searched. Location precues exerted the strongest effects on conjunction search and the weakest effects on feature search. As the size of valid location cues decreased, conjunction search was facilitated. These effects declined progressively with advanced age and the onset of DAT. As the size of invalid cues increased, conjunction search was first facilitated, then slowed, but neither age nor DAT altered this effect. These results indicate that both Alzheimer's disease and, to a lesser degree, advanced aging, reduce control of the spatial focus of attention. C1 NIA,NEUROSCI LAB,BETHESDA,MD 20892. RP Greenwood, PM (reprint author), CATHOLIC UNIV AMER,DEPT PSYCHOL,COGNIT SCI LAB,WASHINGTON,DC 20064, USA. FU NIA NIH HHS [AG07569, AG123987] NR 60 TC 79 Z9 84 U1 2 U2 8 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0894-4105 J9 NEUROPSYCHOLOGY JI Neuropsychology PD JAN PY 1997 VL 11 IS 1 BP 3 EP 12 DI 10.1037/0894-4105.11.1.3 PG 10 WC Psychology, Clinical; Neurosciences; Psychology SC Psychology; Neurosciences & Neurology GA WE359 UT WOS:A1997WE35900001 PM 9055265 ER PT J AU Vitiello, B Martin, A Hill, J Mack, C Molchan, S Martinez, R Murphy, DL Sunderland, T AF Vitiello, B Martin, A Hill, J Mack, C Molchan, S Martinez, R Murphy, DL Sunderland, T TI Cognitive and behavioral effects of cholinergic, dopaminergic, and serotonergic blockade in humans SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE scopolamine; haloperidol; metergoline; cognition ID ALZHEIMERS-DISEASE; HEALTHY-VOLUNTEERS; MEMORY FAILURE; SCOPOLAMINE; HALOPERIDOL; DEMENTIA; DYSFUNCTION; AGE; ENHANCEMENT; ANTAGONISTS AB The purpose of this study teas to investigate the cognitive and behavioral effects of anticholinergic, antidopaminergic, and antiserotonergic agents given alone and in combination to normal volunteers. Twelve young male volunteers took part in this double-blind, randomized, placebo-controlled, crossover study of six drug conditions, each administered on separate days [haloperidol (2 mg PO) +/- scopolamine (0.5 mg IV), metergoline (4 mg PO) +/- scopolamine (0.5 mg IV), placebo, and scopolamine alone (0.5 mg IV)]. Scopolamine-induced sedation (p < .01), slowed information processing (p < .01) and impaired ne so learning and memory (p < .01), but did not affect attention or retrieval from semantic memory. Given alone, haloperidol selectively impaired the ability to rapidly switch cognitive sets (p < .05), and metergoline decreased pupil size (p < .01) but did not induce cognitive deficits. In combination with scopolamine, neither haloperidol nor metergoline produced a worsening of the subjects' cognitive performance above and beyond that seen with scopolamine alone. On the contrary a trend (p < .10) for haloperidol to reverse some of the scopolamine-induced exacerbation of verbal short-term forgetting was observed. The data indicate that scopolamine and haloperidol can independently and selectively affect cognition and that at the doses tested in this study no synergistic exacerbation of cognitive functioning was found when cholinergic blockage was coupled with dopaminergic or serotonergic blockade. (C) 1997 American College of Neuropsychopharmacology. C1 NIMH,LCS,NIH,SECT GERIATR PSYCHIAT,LAB CLIN SCI,BETHESDA,MD 20892. NIMH,LCS,NIH,COGNIT STUDIES UNIT,LAB CLIN SCI,BETHESDA,MD 20892. RI martin, alex/B-6176-2009 NR 54 TC 65 Z9 67 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD JAN PY 1997 VL 16 IS 1 BP 15 EP 24 DI 10.1016/S0893-133X(96)00134-0 PG 10 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA WW631 UT WOS:A1997WW63100003 PM 8981385 ER PT J AU Vawter, MP DillonCarter, O Issa, F Wyatt, RJ Freed, WJ AF Vawter, MP DillonCarter, O Issa, F Wyatt, RJ Freed, WJ TI Transforming growth factors beta 1 and beta 2 in the cerebrospinal fluid of chronic schizophrenic patients SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE schizophrenia; transforming growth factor beta 1; transforming growth factor beta 2; ELISA; CSF ID MIDBRAIN DOPAMINERGIC-NEURONS; EXPRESSION; SURVIVAL; FACTOR-BETA-1; PROLIFERATION; INTERLEUKIN-2; GLIOBLASTOMA; ASTROCYTES; TOXICITY; CELLS AB Transforming growth factor betas (TGF beta s) are potent immunosuppressive molecules released in the brain after injury. We hypothesized that TGF beta levels in cerebrospinal fluid (CSF) of schizophrenic patients would be altered because TGF beta can influence neural cell adhesion moelecule (N-CAM) expression in vitro. The levels of TGF beta 1 and beta 2 in CSF of patients with schizophrenia and normal controls measured by ELISA showed no differences. There was evidence that the stability of TGF beta in CSF may be altered in schizophrenia. For a limited sample, TGF beta 1 and N-CAM concentrations were significantly correlated in normal patients (r = 0.98) but not in schizophrenics. The results do not support an active neurodegeneration or anti-inflammatory response in the central nervous system, which is reflected in the CSF of chronic schizophrenics. (C) 1997 American College of Neuropsychopharmacology. RP Vawter, MP (reprint author), NIMH,NEUROSCI CTR ST ELIZABETHS,SECT PRECLIN NEUROSCI,NEUROPSYCHIAT BRANCH,WASHINGTON,DC 20032, USA. NR 21 TC 15 Z9 15 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD JAN PY 1997 VL 16 IS 1 BP 83 EP 87 DI 10.1016/S0893-133X(96)00143-1 PG 5 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA WW631 UT WOS:A1997WW63100010 PM 8981392 ER PT J AU Daniel, DG Egan, M Issa, F AF Daniel, DG Egan, M Issa, F TI Untitled SO NEUROPSYCHOPHARMACOLOGY LA English DT Letter C1 GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. ST ELIZABETH HOSP,NIMH,CTR NEUROSCI,WASHINGTON,DC. RP Daniel, DG (reprint author), WASHINGTON CLIN RES CTR,FALLS CHURCH,VA, USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD JAN PY 1997 VL 16 IS 1 BP 88 EP 88 DI 10.1016/S0893-133X(97)82241-5 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA WW631 UT WOS:A1997WW63100011 PM 8981393 ER PT J AU Ashur-Fabian, O Giladi, E Brenneman, DE Gozes, I AF Ashur-Fabian, O Giladi, E Brenneman, DE Gozes, I TI Molecular identification of the VIP/PACAP neuroprotection receptor SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Tel Aviv Univ, Sackler Fac Med, Lilly & Avraham Gildor Chair Invest Growth Factor, IL-69978 Tel Aviv, Israel. NICHD, LDN, Sect Dev & Mol Pharmacol, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S4 EP S4 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000016 ER PT J AU Bayewitch, ML Avidor-Reiss, T Levy, R Nevo, I Simonds, WF Vogel, Z AF Bayewitch, ML Avidor-Reiss, T Levy, R Nevo, I Simonds, WF Vogel, Z TI Modulation of adenylyl cyclase isoforms I, II, V and VI by various G(BG) subunits SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel. NIDDK, Metab Dis Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S8 EP S8 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000032 ER PT J AU Beni-Adani, L Pomeranz, S Gozes, I Bassan, M Brenneman, DE Shohami, E AF Beni-Adani, L Pomeranz, S Gozes, I Bassan, M Brenneman, DE Shohami, E TI The neuroprotective effect of activity dependent neurotrophic protein in mice after closed head injury SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Neurosurg, Jerusalem, Israel. Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Pharmacol, Jerusalem, Israel. Tel Aviv Univ, Sackler Sch Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. NICHD, Sect Dev & Mol Pharmacol, LDN, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S9 EP S10 PG 2 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000039 ER PT J AU Brodie, C Bogi, K Acs, P Lorenzo, P Baskin, L Blumberg, PM AF Brodie, C Bogi, K Acs, P Lorenzo, P Baskin, L Blumberg, PM TI The regulatory domain of PKC delta mediates its inhibitory effect on glutamine synthetase expression in C6 glial cells: Role of tyrosine phosphorylation SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Bar Ilan Univ, Dept Life Sci, Ramat Gan, Israel. NCI, Mol Mechanisms Tumor Promot Sect, LCCTP, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S12 EP S12 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000047 ER PT J AU Giladi, E Davidson, A Bachar, M Bardea, A Rubinraut, S Fridkin, M Brenneman, DE Gozes, I AF Giladi, E Davidson, A Bachar, M Bardea, A Rubinraut, S Fridkin, M Brenneman, DE Gozes, I TI Protection against developmental and learning impairments in apolipoprotein E-deficient mice by activity-dependent femtomolar-acting peptides SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel. Weizmann Inst Sci, IL-76100 Rehovot, Israel. NICHD, SDMP, LDN, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S19 EP S19 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000078 ER PT J AU Gozes, I Bassan, M Zamostiano, R Davidson, A Perl, O Bassan, H Blat, C Giladi, E Gibney, G Glazner, G Brenneman, DE AF Gozes, I Bassan, M Zamostiano, R Davidson, A Perl, O Bassan, H Blat, C Giladi, E Gibney, G Glazner, G Brenneman, DE TI A femtomolar-acting activity-dependent neuroprotective protein (ADNP) SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Tel Aviv Univ, Sackler Sch Med, Lilly & Avraham Gildor Chair Invest Growth Factor, IL-69978 Tel Aviv, Israel. NICHD, Sect Dev & Mol Pharmacol, LDN, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S21 EP S21 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000087 ER PT J AU Heller, H Deutsch, J Purdon, AD Rapoport, SI Horowitz, M Shohami, E AF Heller, H Deutsch, J Purdon, AD Rapoport, SI Horowitz, M Shohami, E TI Long-chain acyl CoAs and free fatty acids in rat brain after head injury SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Hebrew Univ Jerusalem, Fac Med, Dept Pharmacol, Jerusalem, Israel. Hebrew Univ Jerusalem, Fac Med, Dept Pharmaceut Chem, Jerusalem, Israel. Hebrew Univ Jerusalem, Fac Med, Dept Physiol, Jerusalem, Israel. NIA, Neurosci Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S25 EP S25 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000100 ER PT J AU Ishai, A Ungerleider, LG Martin, A Haxby, JV AF Ishai, A Ungerleider, LG Martin, A Haxby, JV TI FMRI reveals differential activation in the ventral vision pathway during the perception of objects SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 NIMH, Lab Brain & Cognit, Bethesda, MD USA. RI martin, alex/B-6176-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S25 EP S26 PG 2 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000104 ER PT J AU Lazarovici, P Jiang, H St Ulme, D Dickens, G Chabuck, A Lavarreda, M Guroff, G AF Lazarovici, P Jiang, H St Ulme, D Dickens, G Chabuck, A Lavarreda, M Guroff, G TI Both p140(trk) and p75(NGFR) nerve growth factor receptors mediate nerve growth factor-stimulated calcium uptake SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Hebrew Univ Jerusalem, Sch Pharm, Dept Pharmacol, IL-91120 Jerusalem, Israel. NICHHD, Growth Factors Sect, NIH, Bethesda, MD 20892 USA. RI Shibutani, Makoto/C-2510-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S31 EP S31 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000128 ER PT J AU Lazarovici, P Jiang, H Movsesyan, V Fink, DW Fasler, M Whalin, M Monshipouri, M Dickens, G Lelkes, P Guroff, G AF Lazarovici, P Jiang, H Movsesyan, V Fink, DW Fasler, M Whalin, M Monshipouri, M Dickens, G Lelkes, P Guroff, G TI Expression of human pl40trk receptors in p140(trk)-deficient PC12/endothelial (PpC12EN) cells results in nerve growth factor (NGF)-induced signal transduction and DNA synthesis SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Hebrew Univ Jerusalem, Sch Pharm, IL-91120 Jerusalem, Israel. NICHD, Growth Factors Sect, NIH, Bethesda, MD USA. Univ Wisconsin, Dept Med, Milwaukee, WI 53201 USA. RI Shibutani, Makoto/C-2510-2013 NR 1 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S31 EP S31 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000129 ER PT J AU Lazarovici, P Oshima, M Shavit, D Shibutani, M Jiang, H Monshipouri, M Fink, D Movsesyan, V Guroff, G AF Lazarovici, P Oshima, M Shavit, D Shibutani, M Jiang, H Monshipouri, M Fink, D Movsesyan, V Guroff, G TI Down-regulation of epidermal growth factor (EGF) receptors by nerve growth factor (NGF) in PC12 cells is P140(TRK)-, Ras-, and Src-dependent SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Hebrew Univ Jerusalem, Sch Pharm, Dept Pharmacol, IL-91120 Jerusalem, Israel. NICHD, Growth Factors Sect, NIH, Bethesda, MD USA. US FDA, Div Cytokines Biol, Bethesda, MD 20892 USA. RI Shibutani, Makoto/C-2510-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S31 EP S31 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000127 ER PT J AU Ohnona, S Wallin, M Jiang, H Movsesyan, V Shaffer, EM Fink, D Kaplan, D Guroff, G Lazarovici, P AF Ohnona, S Wallin, M Jiang, H Movsesyan, V Shaffer, EM Fink, D Kaplan, D Guroff, G Lazarovici, P TI Staurosporine induces neurite outgrowth in PC12 variant cell lines by trkA-, ras-, and src-independent signal transduction pathways SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Hebrew Univ Jerusalem, Sch Pharm, Dept Pharmacol, IL-91120 Jerusalem, Israel. NICHD, Growth Factors Sect, NIH, Bethesda, MD USA. Promega Corp, Madison, WI USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S38 EP S38 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000157 ER PT J AU Simon, ES Burke, RE AF Simon, ES Burke, RE TI Oscillator mice as a model for certain hyperkinetic movement disorders: An in vitro physiological study SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Tel Aviv Med Ctr, Dept Neurol, Tel Aviv, Israel. NINDS, Lab Neural Control, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S48 EP S48 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000196 ER PT J AU Zamostiano, R Bassan, M Davidson, A Brenneman, DE Gozes, I AF Zamostiano, R Bassan, M Davidson, A Brenneman, DE Gozes, I TI A human homologue for activity-dependent neuroprotective protein SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Tel Aviv Univ, Sackler Sch Med, Lily & Avraham Gildor Chair Invest Growth Factors, IL-69978 Tel Aviv, Israel. NICHD, Sect Dev & Mol Pharmacol, LDN, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S54 EP S54 PG 1 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000224 ER PT J AU Zangen, A Herzberg, U Vogel, Z Yadid, G AF Zangen, A Herzberg, U Vogel, Z Yadid, G TI Pain induces release of endogenous B-endorphin in the arcuate nucleus SO NEUROSCIENCE LETTERS LA English DT Meeting Abstract C1 Bar Ilan Univ, Dept Life Sci, Ramat Gan, Israel. NINDS, NIH, Bethesda, MD 20892 USA. Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel. NR 0 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PY 1997 SU 48 BP S54 EP S55 PG 2 WC Neurosciences SC Neurosciences & Neurology GA ZB328 UT WOS:000072460000225 ER EF