FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Belnap, D Filman, D Trus, B Booy, F Cheng, N Curry, S Hiremath, C Tsang, S Hogle, J Steven, A AF Belnap, D Filman, D Trus, B Booy, F Cheng, N Curry, S Hiremath, C Tsang, S Hogle, J Steven, A TI Springing the trap: Conformational changes when poliovirus switches into cell-entry intermediate and RNA-released states SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, Struct Biol Res Lab, NIH, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA. NIH, CBEL, CIT, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A27 EP A27 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900157 ER PT J AU Bicout, DJ Szabo, A AF Bicout, DJ Szabo, A TI Diffusion in a sphere and protein folding kinetics SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A8 EP A8 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900042 ER PT J AU Carragher, BO Cheng, N Wang, ZY Hammer, JA Korn, ED Reilein, A Belnap, DM Steven, AC AF Carragher, BO Cheng, N Wang, ZY Hammer, JA Korn, ED Reilein, A Belnap, DM Steven, AC TI Structural comparison of Acanthamoeba myosin ic mutants with constitutively active and inactive ATPase bound to F-actin in rigor and ADP-bound states SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Illinois, Beckman Inst, Chicago, IL 60680 USA. NHLB, LCB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A166 EP A166 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900971 ER PT J AU Chen, V Bass, AH Wang, K AF Chen, V Bass, AH Wang, K TI Real time visualization of desmin lattice in fish sonic muscle by dual disk confocal fluorescene microscopy. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, LPB, NIH, Bethesda, MD 20892 USA. Cornell Univ, Neurobiol & Behav Sect, Ithaca, NY 14853 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A95 EP A95 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900553 ER PT J AU Chen, YR Gunther, MR Mason, RP AF Chen, YR Gunther, MR Mason, RP TI An ESR spin-trapping investigation of reaction of mitochondrial cytochrome c oxidase with H2O2 SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A256 EP A256 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901496 ER PT J AU Chen, YR Sturgeon, BE Gunther, MR Mason, RP AF Chen, YR Sturgeon, BE Gunther, MR Mason, RP TI ESR spin trapping of the cyanyl radical in cyanide cytochrome c oxidase and azidyl radical in azide cytochrome c oxidase/H2O2 system SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A257 EP A257 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901500 ER PT J AU Chen-Izu, Y Xiao, RP Izu, LT Cheng, H Spurgeon, H Lakatta, EG AF Chen-Izu, Y Xiao, RP Izu, LT Cheng, H Spurgeon, H Lakatta, EG TI G(i)-protein dependent localization of beta(2)-adrenergic receptor (beta(2)ar) signaling to L-type Ca2+ channels: A single channel study SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A363 EP A363 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902124 ER PT J AU Cheng, N Conway, JF Watts, N Hainfeld, JF Powell, RD Joshi, V Stahl, SJ Wingfield, PT Steven, AC AF Cheng, N Conway, JF Watts, N Hainfeld, JF Powell, RD Joshi, V Stahl, SJ Wingfield, PT Steven, AC TI Mapping sites on the surface of the hepatitis B virus capsid by cryo-electron microscopy with tetra-iridium clusters SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, NIH, Bethesda, MD 20892 USA. Brookhaven Natl Lab, Upton, NY 11973 USA. Nanoprobes Inc, Stony Brook, NY 11790 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A457 EP A457 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902670 ER PT J AU Chik, JK Rau, DC Parsegian, VA AF Chik, JK Rau, DC Parsegian, VA TI The effects of solutes on the reversible heat-induced aggregation of hydroxypropylcellulose SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHD, LPSB, Bethesda, MD 20892 USA. NIDDK, OD, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A320 EP A320 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901869 ER PT J AU Chik, JK Hanson, P Parsegian, VA AF Chik, JK Hanson, P Parsegian, VA TI The entropically driven collapse of sickle cell hemoglobin gels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHD, LSPB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A319 EP A319 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901868 ER PT J AU Clay, JR Kuzirian, A AF Clay, JR Kuzirian, A TI Localization of intracellular K+ channels in squid giant axons. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Marine Biol Lab, Woods Hole, MA 02543 USA. NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0006-3495 EI 1542-0086 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A223 EP A223 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901305 ER PT J AU Colden-Stanfield, M AF Colden-Stanfield, M TI Very late antigen-4 (VLA-4) engagement induces inwardly rectifying potassium currents (Kir) in monocytes. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A222 EP A222 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901296 ER PT J AU Dai, R Robinson, RC Friedman, FK AF Dai, R Robinson, RC Friedman, FK TI Homology modeling of cytochromes P450 SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, Mol Carcinogenesis Lab, Bethesda, MD 20892 USA. RI Friedman, Fred/D-4208-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A423 EP A423 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902474 ER PT J AU Davis, JS AF Davis, JS TI The Huxley-Simmons phase 2 and force generation: A comparative study. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A269 EP A269 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901575 ER PT J AU Drose, S Froehlich, J Fendler, K Bamberg, E Epstein, W Altendorf, K AF Drose, S Froehlich, J Fendler, K Bamberg, E Epstein, W Altendorf, K TI Phosphorylation, ATP hydrolysis and charge translocation in E-coli Kdp-ATPase. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Osnabruck, Dept Microbiol, D-49069 Osnabruck, Germany. Max Planck Inst Biophys, D-60596 Frankfurt, Germany. Univ Chicago, Dept Mol Genet & Cellular Biol, Chicago, IL 60637 USA. NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A451 EP A451 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902638 ER PT J AU Durell, SR Hao, H Guy, HR AF Durell, SR Hao, H Guy, HR TI Three-dimensional models of K+ transport proteins based on the structure of the KcsA K+ channel. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, LECB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A436 EP A436 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902547 ER PT J AU Durell, SR Guy, HR AF Durell, SR Guy, HR TI Evaluation of structural models of K+ channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, LECB, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A333 EP A333 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901949 ER PT J AU Ehrenstein, G Galdicki, Z Lange, GD AF Ehrenstein, G Galdicki, Z Lange, GD TI Interactions between beta-amyloid and acetylcholine in the development of Alzheimer's disease SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, Biophys Sect, Bethesda, MD 20892 USA. USUHS, Dept Physiol, Bethesda, MD USA. NINDS, Instrumentat & Comp Sect, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A54 EP A54 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900312 ER PT J AU Ellison, PA Sellers, JR Cremo, CR AF Ellison, PA Sellers, JR Cremo, CR TI Kinetic properties of smooth muscle heavy meromyosin (SM-HMM) with one head phosphorylated. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Washington State Univ, Dept Biochem & Biophys, Pullman, WA 99164 USA. NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A48 EP A48 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900278 ER PT J AU Fan, J Kingsley, D Zimmerberg, J AF Fan, J Kingsley, D Zimmerberg, J TI The effect of fusion protein surface density on fusion pore phenotype mediated by baculovirus GP64. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHD, Lab Cellular & Mol Biophys, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A440 EP A440 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902571 ER PT J AU Fitch, CA Fowler, B Garcia-Moreno, B Hacker, EDL Silva, AM Wirtz, D AF Fitch, CA Fowler, B Garcia-Moreno, B Hacker, EDL Silva, AM Wirtz, D TI Molecular basis of proton and salt-linked conformational transitions in southern bean mosaic virus. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Johns Hopkins Univ, Dept Biophys, Baltimore, MD USA. Univ Tennessee, Dept Microbiol, Knoxville, TN 37996 USA. Natl Canc Inst, Frederick, MD USA. RI Wirtz, Denis/A-3257-2010 NR 0 TC 0 Z9 0 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A133 EP A133 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900773 ER PT J AU Forbes, JG Yim, PB Wang, F Sellers, JR AF Forbes, JG Yim, PB Wang, F Sellers, JR TI Characterization of a myosin S1-like construct of human non-muscle myosin II-A. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Maryland, Dept Chem & Biochem, College Pk, MD 20742 USA. NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A165 EP A165 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900967 ER PT J AU Gawrisch, K Huster, D Yau, WM Polozov, I Holte, LL AF Gawrisch, K Huster, D Yau, WM Polozov, I Holte, LL TI New insights into biomembrane structure from two-dimensional nuclear overhauser enhancement spectroscopy. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A391 EP A391 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902284 ER PT J AU Gonzalez, A Shirokova, N Kirsch, WG Pizarro, G Stern, MD Cheng, H Rios, E AF Gonzalez, A Shirokova, N Kirsch, WG Pizarro, G Stern, MD Cheng, H Rios, E TI Size distribution of Ca2+ sparks in caffeine-stimulated skeletal muscle. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Rush Univ, Chicago, IL 60612 USA. Univ Republ, Montevideo, Uruguay. NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A465 EP A465 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902720 ER PT J AU Gonzalez, M Weiler, S Ferretti, JA Ginsburg, A AF Gonzalez, M Weiler, S Ferretti, JA Ginsburg, A TI Reversible, thermal unfolding of a vnd/NK-2 (ventral nervous system defective) homeodomain mutant protein. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A107 EP A107 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900621 ER PT J AU Gu, J Xu, S Malinchik, S Yu, LC AF Gu, J Xu, S Malinchik, S Yu, LC TI Model of the patterns of cross-bridges binding to actin in rigor skeletal muscle SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A33 EP A33 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900193 ER PT J AU Hattery, DW Chernomordik, VV Loew, MH Gandjbakhche, AH AF Hattery, DW Chernomordik, VV Loew, MH Gandjbakhche, AH TI Quantitative diffuse fluorescent imaging SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 George Washington Univ, Washington, DC 20052 USA. NICHD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A360 EP A360 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902104 ER PT J AU Hawkins, M Moser, AM Patel, M Balis, FM AF Hawkins, M Moser, AM Patel, M Balis, FM TI Use of 3-methyl isoxanthopterin (3-MI) a fluorescent guanosine analog, in a coupled, single step, real time assay for O-6-alkyl transferase (AT) SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Natl Canc Inst, Pediat Oncol Branch, San Antonio, TX 78229 USA. Childrens Canc Ctr, San Antonio, TX 78229 USA. RI MOSER, ASHER/F-1873-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A326 EP A326 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901903 ER PT J AU Herman, MA Arispe, N Alkon, D AF Herman, MA Arispe, N Alkon, D TI A ryanodine sensitive cation channel from squid optic lobe. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, Lab Adapt Syst, NIH, Bethesda, MD 20892 USA. Uniformed Serv Univ Hlth Sci, Fac Med, Dept Anat & Cell Biol, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A377 EP A377 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902205 ER PT J AU Huster, D Feller, SE Gawrisch, K AF Huster, D Feller, SE Gawrisch, K TI Noesy NMR crosspeaks between lipid headgroups and hydrocarbon chains - Spin diffusion or molecular disorder? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. Univ Leipzig, Inst Med Phys & Biophys, D-04103 Leipzig, Germany. Wabash Coll, Crawfordsville, IN 47933 USA. NR 0 TC 2 Z9 2 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A354 EP A354 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902072 ER PT J AU Huster, D Paasche, G Dietrich, U Zschornig, O Gutberlet, T Gawrisch, K Arnold, K AF Huster, D Paasche, G Dietrich, U Zschornig, O Gutberlet, T Gawrisch, K Arnold, K TI Comparison of polyelectrolyte binding to charged and zwitterionic phospholipid surfaces SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Leipzig, Inst Med Phys & Biophys, D-7010 Leipzig, Germany. NIAAA, LMBB, NIH, Rockville, MD 20852 USA. Univ Leipzig, Inst Expt Phys 1, Leipzig, Germany. RI Gutberlet, Thomas/D-5613-2014 OI Gutberlet, Thomas/0000-0002-6194-2259 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A61 EP A61 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900351 ER PT J AU Iwasa, KH Adachi, M AF Iwasa, KH Adachi, M TI Effect of mechanical constraint on the membrane capacitance in trypsin-treated outer hair cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A46 EP A46 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900266 ER PT J AU Jas, GS Munoz, V Hofrichter, J Eaton, WA AF Jas, GS Munoz, V Hofrichter, J Eaton, WA TI Effect of viscosity on the kinetics of the helix-coil transition. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A175 EP A175 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901025 ER PT J AU Jia, Y Talaga, DS Wei, L Lu, HSM DeGrado, WF Hochstrasser, RM AF Jia, Y Talaga, DS Wei, L Lu, HSM DeGrado, WF Hochstrasser, RM TI Observation of folding dynamics of single GCN-4 peptides by fluorescence energy transfer confocal microscopy. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Penn, Dept Chem, NIH, Reg Laser Labs, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A10 EP A10 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900057 ER PT J AU Jin, AJ Wang, K AF Jin, AJ Wang, K TI Nebulin peptides and calmodulin interaction investigated via isothermal titration calorimetry SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, LPB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A157 EP A157 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900918 ER PT J AU Jin, AJ Edidin, M Nossal, R Gershfeld, NL AF Jin, AJ Edidin, M Nossal, R Gershfeld, NL TI Anomalous diffusion in membrane bilayers at their growth temperatures. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA. NIAMS, LPB, Bethesda, MD USA. NICHD, LIMB, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A58 EP A58 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900337 ER PT J AU Jones, BE Veech, RL Radda, GK Clarke, K AF Jones, BE Veech, RL Radda, GK Clarke, K TI Fatty acids decrease efficiency in the working hyperthyroid rat heart. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Oxford, Dept Biochem, Oxford OX1 2JD, England. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A29 EP A29 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900169 ER PT J AU Joshi, MK Bose, S Hendler, RW AF Joshi, MK Bose, S Hendler, RW TI Comparison of bacteriorhodopsin photocycles in whole cells and purple membrane patches from Halobacteria salinarium SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A241 EP A241 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901410 ER PT J AU Joshi, MK Dracheva, S Mukhopadhyay, AK Bose, S Hendler, RW AF Joshi, MK Dracheva, S Mukhopadhyay, AK Bose, S Hendler, RW TI Importance of specific native lipids in controlling the photocycle of bacteriorhodopsin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A241 EP A241 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901408 ER PT J AU Kawahara, M Arispe, N Kuroda, Y Rojas, E AF Kawahara, M Arispe, N Kuroda, Y Rojas, E TI Alzheimer's beta-amyloid, human islet amylin and prion protein fragment evoke intracellular free-calcium elevations by a common mechanism in a hypothalamic GnRH neuronal cell-line SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Dept Mol & Cel Neurobiol, Tokyo, Japan. USUHS, Dept Anat & Cell Biol, Bethesda, MD USA. NIDDK, LCBB, NIH, Bethesda, MD USA. Univ Chile, Fac Med, IBS, Santiago 7, Chile. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A396 EP A396 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902312 ER PT J AU Keskin, O Bahar, I Jernigan, R Covell, D AF Keskin, O Bahar, I Jernigan, R Covell, D TI Characterization of anticancer agents and their growth-inhibitory potency: Relationships between potency and chemical substructure. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Bogazici Univ, Polymer Res Ctr, TR-80815 Bebek, Turkey. NCI, Lab Expt & Computat Biol, NIH, Bethesda, MD 20892 USA. RI Jernigan, Robert/A-5421-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A384 EP A384 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902243 ER PT J AU Kloczkowski, A Jernigan, RL AF Kloczkowski, A Jernigan, RL TI Transfer matrix method for compact protein lattice conformations. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, NIH, Bethesda, MD 20892 USA. RI Jernigan, Robert/A-5421-2012; Kloczkowski, Andrzej/B-9868-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A199 EP A199 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901165 ER PT J AU Koenig, BW Ferretti, JA Gawrisch, K AF Koenig, BW Ferretti, JA Gawrisch, K TI Folding and membrane interaction of the amphipathic peptide p828s from HIV-1 gp41 SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI, Biophys Chem Lab, NIH, Bethesda, MD 20892 USA. NIAAA, Lab Membrane Biochem & Biophys, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A215 EP A215 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901258 ER PT J AU Kornyshev, AA Leikin, S AF Kornyshev, AA Leikin, S TI Electrostatic interaction between dna helices in dense aggregates. An impetus for DNA poly- and meso-morphism SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Res Ctr Juelich, D-52425 Julich, Germany. NICHD, LPSB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A263 EP A263 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901538 ER PT J AU Kovbasnjuk, ON Everett, CA Spring, KR AF Kovbasnjuk, ON Everett, CA Spring, KR TI Near-membrane pH buffering by the glycocalyx of MDCK cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A235 EP A235 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901371 ER PT J AU Kumar, S Tsai, CJ Ma, B Nussinov, R AF Kumar, S Tsai, CJ Ma, B Nussinov, R TI Why salt bridges in thermophilic proteins? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, IRSP, SAIC, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, LECB, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A108 EP A108 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900629 ER PT J AU Kuznetsova, N Leikin, S AF Kuznetsova, N Leikin, S TI The role of telopeptides in collagen fibrillogenesis revisited. Pronase inhibits fibrillogenesis by cleaving the triple helix. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHD, LPSB, NIH, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A319 EP A319 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901867 ER PT J AU Lata, KR Cheng, N Duda, R Hendrix, R Conway, J Steven, A AF Lata, KR Cheng, N Duda, R Hendrix, R Conway, J Steven, A TI Visualization of conformational intermediates in phage HK97 capsid maturation by time-resolved cryo-EM. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, LSBR, Bethesda, MD 20892 USA. Univ Pittsburgh, Dept Sci Biol, Pittsburgh, PA 15260 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A26 EP A26 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900153 ER PT J AU Leuba, SH Zlatanova, J Bash, R Liu, YZ Harrington, RE Lohr, D Lindsay, SM AF Leuba, SH Zlatanova, J Bash, R Liu, YZ Harrington, RE Lohr, D Lindsay, SM TI It takes more than 650 piconewtons to remove DNA from the histone octamer: MAC Mode AFM measurement of the stretching of single chromatin fibers. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, LRBGE, NIH, Bethesda, MD 20892 USA. Argonne Natl Lab, Argonne, IL 60439 USA. Arizona State Univ, Tempe, AZ 85287 USA. RI Zlatanova, Jordanka/B-3273-2009 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A389 EP A389 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902270 ER PT J AU Lewis, MS Dimitriadis, EK AF Lewis, MS Dimitriadis, EK TI Protein-nucleic acid interactions: Multi-wavelength analysis using ultracentrifugal intensity data. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, OD, ORS, BEPS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A132 EP A132 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900769 ER PT J AU Li-Smerin, Y Swartz, KJ AF Li-Smerin, Y Swartz, KJ TI Structural determinants of the hanatoxin receptors on the DRK1 voltage-gated K+ channel. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A328 EP A328 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901919 ER PT J AU Linse, K Gutierrez, G Wang, K AF Linse, K Gutierrez, G Wang, K TI Interaction of nebulin peptides with calcium and calmodulin investigated via capillary electrophoresis SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, LPB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A157 EP A157 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900915 ER PT J AU Lio, YF Nagle, JF Petrache, HI Gouliaev, N Tristram-Nagle, S Suter, RM Gawrisch, K AF Lio, YF Nagle, JF Petrache, HI Gouliaev, N Tristram-Nagle, S Suter, RM Gawrisch, K TI Multiple mechanisms for critical behavior in the biologically relevant phase of lipid bilayers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Carnegie Mellon Univ, Pittsburgh, PA 15213 USA. NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. RI Suter, Robert/P-2541-2014; Nagle, John/B-1917-2015 OI Suter, Robert/0000-0002-0651-0437; Nagle, John/0000-0002-9844-5934 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A432 EP A432 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902525 ER PT J AU Ma, BY Nussinov, R AF Ma, BY Nussinov, R TI Explicit water and implicit water simulation of a beta-hairpin peptide: Indications for fatal negligence of hydrophobic interaction in the continuum solvation model SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, LECB, FCRDC, Frederick, MD 21702 USA. SAIC, IRSP, LECB, Frederick, MD 21702 USA. Tel Aviv Univ, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A170 EP A170 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900993 ER PT J AU Malkov, VA Panyutin, IG Neumann, RD Zhurkin, VB Camerini-Otero, RD AF Malkov, VA Panyutin, IG Neumann, RD Zhurkin, VB Camerini-Otero, RD TI The arrangement of the three DNA strands within the RecA protein mediated synaptic complexes. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A130 EP A130 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900756 ER PT J AU Maynard, A Covell, D AF Maynard, A Covell, D TI Applications of molecular modeling and density functional theory for the design of retroviral nucleocapsid zinc finger inhibitors SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, LECB, SAIC, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A113 EP A113 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900660 ER PT J AU McGrath, CF Urbaneja, MA Michaels, G Casas-Finet, JR AF McGrath, CF Urbaneja, MA Michaels, G Casas-Finet, JR TI Homology modeling and hydropathic field analysis of retroviral zinc finger structures SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, AVP, SAIC Frederick, Frederick, MD 21702 USA. George Mason Univ, Fairfax, VA 22030 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A153 EP A153 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900893 ER PT J AU Melikov, KC Frolov, VA Chizmadzhev, YA Chernomordik, LV AF Melikov, KC Frolov, VA Chizmadzhev, YA Chernomordik, LV TI Voltage-induced single pores in unmodified planar lipid bilayer SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 RAS, AN Frumkin Electrochem Inst, Moscow 117901, Russia. NICHD, LCMB, NIH, Bethesda, MD 20892 USA. RI Chizmadzhev, Yuri/L-1984-2013 NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A439 EP A439 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902569 ER PT J AU Mirotznik, RR Zheng, X Stanley, EF AF Mirotznik, RR Zheng, X Stanley, EF TI Localization of G-protein classes at a cholinergic presynaptic terminal. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, Synapt Mechanisms Sect, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A345 EP A345 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902017 ER PT J AU Mitchell, DC Litman, BJ AF Mitchell, DC Litman, BJ TI Effects of water activity on receptor conformation changes and acyl chain packing SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A242 EP A242 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901414 ER PT J AU Mitchell, DC Ali, S Litman, BJ AF Mitchell, DC Ali, S Litman, BJ TI How much docosahexaenoic acid is required to eliminate the effects of cholesterol? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A63 EP A63 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900365 ER PT J AU Moncman, CL Wang, K AF Moncman, CL Wang, K TI GFP-nebulette expression alters contractile activity in cardiomyocytes. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Texas, Dept Chem, Austin, TX 78712 USA. NIAMS, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A311 EP A311 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901818 ER PT J AU Niu, SL Litman, BJ AF Niu, SL Litman, BJ TI The lipid dependence of G-protein mediated signal transduction SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A214 EP A214 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901250 ER PT J AU Nourse, A Millar, DB Minton, AP AF Nourse, A Millar, DB Minton, AP TI PAMAM dendrimers as protein mimics SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A127 EP A127 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900739 ER PT J AU Ozarowski, A Maki, AH Urbaneja, MA Henderson, LE Casas-Finet, JR AF Ozarowski, A Maki, AH Urbaneja, MA Henderson, LE Casas-Finet, JR TI Luminescence and ODMR study of HIV-1 nucleocapsid protein (NCp7) bound to psi-site stem loops SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 UC Davis, Dept Chem, Davis, CA 95616 USA. FCRDC, NCI, SAIC Frederick, AVP, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A133 EP A133 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900776 ER PT J AU Packard, BZ Brown, MJ Wu, ML Komoriya, A Henkart, PA AF Packard, BZ Brown, MJ Wu, ML Komoriya, A Henkart, PA TI Intramolecular excitonic H-dimers in protease substrates: Fluorescence measurements of intracellular caspase activities in apoptotic cells. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, EIB, NIH, Bethesda, MD USA. Oncolmmunin Inc, College Pk, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A260 EP A260 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901517 ER PT J AU Panchenko, AR Machler-Bauer, A Bryant, SH AF Panchenko, AR Machler-Bauer, A Bryant, SH TI Combining evolutionary conservation with threading scores. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCBI, NIH, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A381 EP A381 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902226 ER PT J AU Parks, WT Letterio, J Campbell, A Geiser, D Williams, A Tang, B Guarino, J Knapton, A Lucero, T Roche, N Territo, P Roberts, A AF Parks, WT Letterio, J Campbell, A Geiser, D Williams, A Tang, B Guarino, J Knapton, A Lucero, T Roche, N Territo, P Roberts, A TI A novel role for TGF-beta 1 in control of cellular energetics SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A239 EP A239 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901395 ER PT J AU Parsegian, VA AF Parsegian, VA TI The natural thickness of a charged surface in salt water SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A128 EP A128 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900743 ER PT J AU Podgornik, RI Parsegian, VA Girvin, SM AF Podgornik, RI Parsegian, VA Girvin, SM TI Pairwise non-additivity of ion-ion fluctuation correlation forces between spheres or cylinders. Forces between particles near a substrate. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHD, NIH, Bethesda, MD USA. Indiana Univ, Bloomington, IN 47405 USA. RI Podgornik, Rudolf/C-6209-2008 OI Podgornik, Rudolf/0000-0002-3855-4637 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A245 EP A245 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901432 ER PT J AU Polozov, IV Krishnamurthy, A Polozova, AI Litman, BJ Gawrisch, K AF Polozov, IV Krishnamurthy, A Polozova, AI Litman, BJ Gawrisch, K TI MAS-NOESY NMR studies of lateral organization of binary lipid mixtures. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. RI Polozova, Alla/C-2395-2008 NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A356 EP A356 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902079 ER PT J AU Polozova, A Litman, BJ AF Polozova, A Litman, BJ TI Correlation between membrane receptor stability and function: Interaction of rhodopsin with lipids SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA, LMBB, NIH, Rockville, MD 20852 USA. RI Polozova, Alla/C-2395-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A214 EP A214 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901252 ER PT J AU Preusch, PC Norvell, JC Cassatt, JC Cassman, M AF Preusch, PC Norvell, JC Cassatt, JC Cassman, M TI Structural biology of membrane proteins program announcement reissued. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIGMS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A351 EP A351 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902051 ER PT J AU Raab, A Han, E Badt, D Smith-Gill, SJ Lindsay, SM Schindler, H Hinterdorfer, P AF Raab, A Han, E Badt, D Smith-Gill, SJ Lindsay, SM Schindler, H Hinterdorfer, P TI Localization of antigenic sites by magnetic AC force microscopy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Linz, Inst Biophys, A-4040 Linz, Austria. Mol Imaging Corp, Phoenix, AZ 85044 USA. NCI, Genet Lab, NIH, Bethesda, MD 20892 USA. Arizona State Univ, Dept Phys & Astron, Tempe, AZ 85287 USA. RI Hinterdorfer, Peter/C-4235-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A264 EP A264 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901543 ER PT J AU Raviv, Y Puri, A Blumenthal, R AF Raviv, Y Puri, A Blumenthal, R TI Multidrug resistant cells overexpressing P-glycoprotein are resistant to infection by envelope viruses that enter via the plasma membrane. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, IRSP, SAIC Frederick, FCRDC, Bethesda, MD 20892 USA. NCI, LECB, FCRDC, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A122 EP A122 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900713 ER PT J AU Rifkind, JM Nagababu, E Tarien, E AF Rifkind, JM Nagababu, E Tarien, E TI Formation of a free radical during the reaction of ferrylhemoglobin with hydrogen peroxide SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA, MDS, LCMB, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A23 EP A23 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900135 ER PT J AU Rivas, G Minton, AP AF Rivas, G Minton, AP TI Characterization of attractive and repulsive interactions between macromolecules via measurement of tracer sedimentation equilibrium SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 CSIC, CIB, E-28006 Madrid, Spain. NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A455 EP A455 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902661 ER PT J AU Rostovtseva, TK Berzrukov, SM AF Rostovtseva, TK Berzrukov, SM TI Transport of nucleotides through the mitochondrial channel, VDAC. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NICHD, LPSB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A144 EP A144 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900837 ER PT J AU Sackett, D Chernomordik, V Krueger, S Nossal, R AF Sackett, D Chernomordik, V Krueger, S Nossal, R TI SANS studies of microtubule protofilament numbers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, DCT, NIH, Bethesda, MD 20892 USA. NICHD, LIMB, NIH, Bethesda, MD 20892 USA. NIST, RRD, Gaithersburg, MD 20899 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A42 EP A42 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900242 ER PT J AU Sham, JSK Song, LS Stern, MD Lakatta, EG Cheng, H AF Sham, JSK Song, LS Stern, MD Lakatta, EG Cheng, H TI Inactivation of cardiac ryanodine receptor (RyR): Evidence from restitution of Ca2+ release SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Johns Hopkins Univ, Div Pulm Med, Baltimore, MD USA. NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. RI Song, Long-Sheng/D-5899-2012 NR 0 TC 4 Z9 4 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A385 EP A385 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902250 ER PT J AU She, L Yu, LC Chalovich, JM AF She, L Yu, LC Chalovich, JM TI Exchange of troponin from the troponin-tropomyosin complex: Effects of actin, pH and temperature. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, Bethesda, MD 20892 USA. E Carolina Univ, Sch Med, Greenville, NC 27834 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A158 EP A158 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900926 ER PT J AU She, M Gu, J Xu, S Chalovich, JM Yu, LC AF She, M Gu, J Xu, S Chalovich, JM Yu, LC TI X-ray diffraction study of skeletal, muscle labeled with troponin T antibody SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. E Carolina Univ, Greenville, NC 27834 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A32 EP A32 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900185 ER PT J AU Siarey, RJ Waterman, W Maccecchini, ML Rapoport, SI Galdzicki, Z AF Siarey, RJ Waterman, W Maccecchini, ML Rapoport, SI Galdzicki, Z TI Effects of SYM 2081 on kainate-induced responses in the mouse immature hemisected spinal cord. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Uniformed Serv Univ Hlth Sci, Neurosci Lab, NIA, NIH,Dept Physiol, Bethesda, MD 20814 USA. Bearsden Bio Inc, Aston, PA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A337 EP A337 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901971 ER PT J AU Sidorova, NY Rau, DC AF Sidorova, NY Rau, DC TI Kinetic approach to the measurement of water release from the EcoRI-DNA complex. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, NICHD, LPSB, Bethesda, MD 20892 USA. NIH, NIDDK, OD, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A131 EP A131 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900760 ER PT J AU Smith, SV Robinson, RC Koley, AP Dai, R Friedman, FK AF Smith, SV Robinson, RC Koley, AP Dai, R Friedman, FK TI Effects of ethanol and other substrates on the conformation and dynamics of cytochrome P450 2E1 SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, NIH, Bethesda, MD 20892 USA. RI Friedman, Fred/D-4208-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A119 EP A119 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900691 ER PT J AU Song, LS Shou, W Boheler, KR Xiao, RP Stern, MD Lakatta, EG Cheng, H AF Song, LS Shou, W Boheler, KR Xiao, RP Stern, MD Lakatta, EG Cheng, H TI Ca2+ sparks and coupled gating of ryanodine receptors in prenatal FKBP12 knockout mouse cardiac myocytes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Baylor Coll Med, Dept Mol Physiol & Biophys, Houston, TX 77030 USA. RI Song, Long-Sheng/D-5899-2012 NR 0 TC 1 Z9 1 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A385 EP A385 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902248 ER PT J AU Stanley, EF AF Stanley, EF TI Double voltage clamp analysis of presynaptic ice and transmitter release at the isolated chick ciliary ganglion calyx synapse SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, Synapt Mech Sect, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A89 EP A89 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900516 ER PT J AU Stern, MD Song, LS Cheng, H Sham, JSK Rios, E AF Stern, MD Song, LS Cheng, H Sham, JSK Rios, E TI Stochastic simulation of cardiac EC coupling: A possible role for allosteric interactions between ryanodine receptors SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA, NIH, Cardiovasc Sci Lab, Chicago, IL USA. Johns Hopkins Med Inst, Div Pulm & Crit Care Med, Chicago, IL USA. Rush Univ, Dept Mol Biophys & Physiol, Chicago, IL 60612 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A459 EP A459 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902682 ER PT J AU Sudhakar, K Morcock, DR Kane, BP Casas-Finet, JN AF Sudhakar, K Morcock, DR Kane, BP Casas-Finet, JN TI Spectroscopic characterization of the bovine leukemia virus (BLV) nucleocapsid (NC) protein. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 FCRDC, NCI, SAIC Frederick, AVP, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A132 EP A132 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900770 ER PT J AU Sukhareva, M Vautrin, J Maric, D Maric, I Barker, J AF Sukhareva, M Vautrin, J Maric, D Maric, I Barker, J TI GABA and tetanus toxin fragment C bind to GT1B ganglioside-containing liposomes. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A222 EP A222 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901297 ER PT J AU Swartz, KJ AF Swartz, KJ TI Inhibition of voltage-gated K+ channel gating currents by hanatoxin. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, Mol Physiol & Biophys Unit, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A150 EP A150 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900873 ER PT J AU Tarasov, SG Casas-Finet, JR Cholody, WM Michejda, CJ AF Tarasov, SG Casas-Finet, JR Cholody, WM Michejda, CJ TI A physico-chemical study of imidazoacridone-DNA interactions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A128 EP A128 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900747 ER PT J AU Terakawa, S Feller, MB Mannuzzu, LM Isacoff, EY AF Terakawa, S Feller, MB Mannuzzu, LM Isacoff, EY TI Single fluorophore visualization of ion channel gating by evanescence microscopy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Hamamatsu Univ Sch Med, Photon Med Res Ctr, Hamamatsu, Shizuoka 4313192, Japan. NIMH, Mol Neurobiol Lab, Bethesda, MD 20892 USA. Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A413 EP A413 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902415 ER PT J AU Territo, PR Mootha, VK French, SA Balaban, RS AF Territo, PR Mootha, VK French, SA Balaban, RS TI Calcium activation of cardiac oxidative phosphorylation: Direct evidence for actication of the F-o/F(1)ATPase. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A295 EP A295 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901726 ER PT J AU Thompson, PA Munoz, V Jas, GS Henry, ER Eaton, WA Hofrichter, J AF Thompson, PA Munoz, V Jas, GS Henry, ER Eaton, WA Hofrichter, J TI Using tryptophan fluorescence to probe helix-coil kinetics SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A175 EP A175 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901022 ER PT J AU Tullio, AN Hara, Y Conti, MA Tresser, N Chan, CC Adelstein, RS AF Tullio, AN Hara, Y Conti, MA Tresser, N Chan, CC Adelstein, RS TI Ablation of the nonmuscle myosin II-B heavy chain in mice results in structural abnormalities in the brain, retina and spinal cord SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A47 EP A47 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900274 ER PT J AU Uren, D Tullio, AN Hwang, H Kawamoto, S Takeda, K Yu, ZX Ferrans, VJ Hara, Y Tresser, N Preston, YA Adelstein, RS AF Uren, D Tullio, AN Hwang, H Kawamoto, S Takeda, K Yu, ZX Ferrans, VJ Hara, Y Tresser, N Preston, YA Adelstein, RS TI Gene dosage affects the cardiac and brain phenotype in nonmuscle myosin II-B depleted mice SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A47 EP A47 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900272 ER PT J AU Vautrin, J Schaffner, A Maric, D Sukhareva, M Barker, J AF Vautrin, J Schaffner, A Maric, D Sukhareva, M Barker, J TI GABA release from presynaptic surface. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A222 EP A222 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901299 ER PT J AU Veigel, C Kendrick-Jones, J Sellers, JR Sparrow, JC Molloy, JE AF Veigel, C Kendrick-Jones, J Sellers, JR Sparrow, JC Molloy, JE TI Cardiac and smooth muscle myosins: a power-stroke in two phases? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ York, Dept Biol, York YO1 5YW, N Yorkshire, England. MRC, Mol Biol Lab, Cambridge CB2 2QH, England. NHLBI, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A145 EP A145 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900847 ER PT J AU Velan, SS Kuppusamy, P Petersen, E Zweier, JL Fishbein, KW Spencer, RGS AF Velan, SS Kuppusamy, P Petersen, E Zweier, JL Fishbein, KW Spencer, RGS TI EPR oximetry mapping (EPROM) of cartilage formed in a hollow fiber bioreactor SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA, NMR Unit, NIH, Baltimore, MD USA. Johns Hopkins Univ, Dept Med, EPR Ctr, Baltimore, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A357 EP A357 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902088 ER PT J AU Velan, SS Spencer, RGS Zweier, JL Kuppusamy, P AF Velan, SS Spencer, RGS Zweier, JL Kuppusamy, P TI Electron paramagnetic resonance in oximetry mapping (EPROM): A technique for in vivo measurement and visualization of oxygen gradients in tissues SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA, Nucl Magnet Resonance Unit, NIH, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, EPR Ctr, Baltimore, MD 21205 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A357 EP A357 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902086 ER PT J AU Wang, H McCarthy, PK Litman, BJ Levin, IW AF Wang, H McCarthy, PK Litman, BJ Levin, IW TI Microdomain formation in polyunsaturated lipid bilayer assemblies: Infrared spectroscopic studies of didocosahexanenoylphosphatidylcholine (DDPC) and disteroylpnospnatidylcholine (DSPC-d(70)) binary mixtures SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIDDK, Chem Phys Lab, Bethesda, MD 20892 USA. NIAAA, Lab Membrane Biophys & Biochem, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A58 EP A58 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900339 ER PT J AU Wei, Q Adelstein, RS AF Wei, Q Adelstein, RS TI A role for nonmuscle myosin A in the regulation of cell morphology SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NHLBI, LMC, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A47 EP A47 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900275 ER PT J AU West, FW Seo, HS Bradrick, TD Xiao, JM Howell, EE AF West, FW Seo, HS Bradrick, TD Xiao, JM Howell, EE TI Folding kinetics and time-resolved fluorescence characterization of R67 dihydrofolate reductase. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Tennessee, Dept Biochem & Cell & Mol Biol, Knoxville, TN 37996 USA. NHLBI, Opt Spect Sect, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A359 EP A359 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902100 ER PT J AU Winkler, U Tang, Y Torrey, TA Morse, HC AF Winkler, U Tang, Y Torrey, TA Morse, HC TI Interaction between the cellular motor protein KIF-4 and HIV Gag. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAID, Immunopathol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A46 EP A46 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900265 ER PT J AU Winterhalter, M Van Gelder, P Bezrukov, SM AF Winterhalter, M Van Gelder, P Bezrukov, SM TI Probing sugar translocation through maltoporin on a single channel level. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Basel, Biozentrum, CH-4056 Basel, Switzerland. Inst Natl Polytech Toulouse, CNRS, F-31077 Toulouse, France. NICHD, LPSB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A138 EP A138 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900804 ER PT J AU Wojtuszewski, K Hawkins, M Khoo, D Mukerji, L AF Wojtuszewski, K Hawkins, M Khoo, D Mukerji, L TI HU-DNA complex formation studied by fluorescence anisotropy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Wesleyan Univ, Dept Mol Biol & Biochem, Middletown, CT 06457 USA. NCI, Pediat Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A134 EP A134 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900779 ER PT J AU Wong, JY Kuhl, TL Israelachvili, JN Mullah, N Zalipsky, S Jeppesen, C Marques, CM AF Wong, JY Kuhl, TL Israelachvili, JN Mullah, N Zalipsky, S Jeppesen, C Marques, CM TI Direct measurements of a tethered ligand-receptor interaction potential SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, LCB, NIH, Bethesda, MD 20892 USA. NCI, LMB, NIH, Bethesda, MD 20892 USA. NIAMS, LSBR, NIH, Bethesda, MD 20892 USA. RI Wong, Joyce/F-3732-2011 OI Wong, Joyce/0000-0002-3526-6381 NR 0 TC 0 Z9 0 U1 0 U2 3 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A401 EP A401 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902346 ER PT J AU Wu, M Urbaneja, MA Casas-Finet, JR Karpel, RL AF Wu, M Urbaneja, MA Casas-Finet, JR Karpel, RL TI Nucleic acid helix-destabilizing properties and structural binding specificity of HIV-1 nucleocapsid (NC) protein SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Univ Maryland Baltimore Cty, Baltimore, MD 21250 USA. SAIC, AVP, Frederick, MD USA. NCI, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A27 EP A27 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900155 ER PT J AU Xu, S Gu, J Yu, LC AF Xu, S Gu, J Yu, LC TI Characterizing and modeling the structure of weakly attached cross-bridges in the A center dot M center dot ATP state in skinned rabbit psoas muscle. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A33 EP A33 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900190 ER PT J AU Xu, S Gu, J Yu, LC AF Xu, S Gu, J Yu, LC TI Conformational changes in cross-bridges induced by MgADP+VO4 as a function of temperature in skinned rabbit psoas muscle fibers. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAMS, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A164 EP A164 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900957 ER PT J AU Yang, F Gustafson, KR Boyd, MR Clore, M Gronenborn, A Wlodawer, A AF Yang, F Gustafson, KR Boyd, MR Clore, M Gronenborn, A Wlodawer, A TI Crystal structure of a potent HIV-inactivating protein cyanovirin-N shows domain-swapping SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Macromol Struct Lab, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A137 EP A137 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085900799 ER PT J AU Yau, WM Gawrisch, K AF Yau, WM Gawrisch, K TI Two-dimensional NOESY MAS NMR as a tool to locate tryptophan analogs in lipid bilayers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A355 EP A355 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902073 ER PT J AU Zhang, FL Lucke, C Baier, LJ Sacchettini, C Hamilton, JA AF Zhang, FL Lucke, C Baier, LJ Sacchettini, C Hamilton, JA TI NMR studies of T54 allele and normal A54 allele of human intestinal fatty acid binding protein SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 Boston Univ, Sch Med, Dept Biophys, Boston, MA 02118 USA. Univ Frankfurt, D-60439 Frankfurt, Germany. NIDDK, Phoenix Epidemiol & Clin Res Branch, NIH, Phoenix, AZ 85016 USA. Texas A&M Univ, Dept Biochem & Biophys, College Stn, TX 77845 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A247 EP A247 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901443 ER PT J AU Zhou, YY Song, LS Koch, WC Lakatta, EG Xiao, RP Cheng, H AF Zhou, YY Song, LS Koch, WC Lakatta, EG Xiao, RP Cheng, H TI Enhanced SR Ca2+ recycling but not L-type Ca2+ current augments cardiac contractility in transgenic mice overexpressing beta(2)-adrenoceptor SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Duck Univ, Med Ctr, Dept Surg, Durham, NC USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A461 EP A461 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085902697 ER PT J AU Zohar, O Pacini, Z Tandon, A Yoshioka, T Alkon, D AF Zohar, O Pacini, Z Tandon, A Yoshioka, T Alkon, D TI Activated signal transduction pathway generate heat in confined intracellular compartments SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract C1 NINDS, LAS, NIH, Bethesda, MD 20892 USA. Waseda Univ, Dept Mol Neurobiol, Tokyo 160, Japan. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JAN PY 1999 VL 76 IS 1 BP A227 EP A227 PN 2 PG 1 WC Biophysics SC Biophysics GA 210BU UT WOS:000081085901328 ER PT J AU Noronha, S Kaufman, J Shiloach, J AF Noronha, S Kaufman, J Shiloach, J TI Use of Streamline chelating for capture and purification of poly-His-tagged recombinant proteins SO BIOSEPARATION LA English DT Article DE EBA; IMAC; 6xHis; TBV25H; CRM H21G ID BLOCKING VACCINE CANDIDATE; YEAST AB Expression of recombinant proteins with poly-histidine tags enables their convenient capture and purification using immobilized metal affinity chromatography (IMAC). The 6xHis-tagged protein binds to a chelating resin charged with metal ions such as Ni2+, Cu2+ or Zn2+, and can therefore be separated from proteins which have lower, or no, affinity for the resin. Two recombinant proteins, a malaria transmission-blocking vaccine candidate secreted extracellularly by S. cerevisiae and a modified diphtheria toxin produced intracellularly by E. coli, were expressed with 6xHis tags and could therefore be purified using IMAC. In an effort to further simplify the initial capture of these proteins, an expanded bed adsorption technique using a chelating resin (Streamline Chelating) was introduced. It was possible to capture the intracellular diphtheria protein from E. coli directly after cell lysis, without prior centrifugation or filtration. The extracellular malaria vaccine candidate was also directly captured from a high cell density yeast culture. Detailed information on the experimental work performed, and the capture processes developed, is provided. C1 NIDDK, Biotechnol Unit, LCDB, NIH, Bethesda, MD 20892 USA. NR 10 TC 14 Z9 14 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0923-179X J9 BIOSEPARATION JI Bioseparation PY 1999 VL 8 IS 1-5 BP 145 EP 151 DI 10.1023/A:1008006013469 PG 7 WC Biochemical Research Methods; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA 257WZ UT WOS:000083806700017 PM 10734566 ER PT J AU Barlogie, B Jagannath, S Desikan, KR Mattox, S Vesole, D Siegel, D Tricot, G Munshi, N Fassas, A Singhal, S Mehta, J Anaissie, E Dhodapkar, D Naucke, S Cromer, J Sawyer, J Epstein, J Spoon, D Ayers, D Cheson, B Crowley, J AF Barlogie, B Jagannath, S Desikan, KR Mattox, S Vesole, D Siegel, D Tricot, G Munshi, N Fassas, A Singhal, S Mehta, J Anaissie, E Dhodapkar, D Naucke, S Cromer, J Sawyer, J Epstein, J Spoon, D Ayers, D Cheson, B Crowley, J TI Total therapy with tandem transplants for newly diagnosed multiple myeloma SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; HIGH-DOSE CHEMORADIOTHERAPY; STEM-CELL TRANSPLANTATION; AUTOLOGOUS TRANSPLANTATION; INTRAVENOUS MELPHALAN; INTENSIVE TREATMENT; STAGING SYSTEM; CLASSIFICATION; CHEMOTHERAPY; REMISSION AB Between August 1990 and August 1995, 231 patients (median age 51, 53% Durie-Salmon stage III, median serum beta-2-microglobulin 3.1 g/L, median C-reactive protein 4 g/L) with symptomatic multiple myeloma were enrolled in a program that used a series of induction regimens and two cycles of high-dose therapy ("Total Therapy"). Remission induction utilized non-cross-resistant regimens (vincristine-doxorubicin-dexamethasone [VAD], high-dose cyclophosphamide and granulocyte-macrophage colony-stimulating factor with peripheral blood stem cell collection, and etoposide-dexamethasone-cytarabine-cisplatin). The first high-dose treatment comprised melphalan 200 mg/m(2) and was repeated if complete (CR) or partial (PR) remission was maintained after the first transplant; in case of less than PR, total body irradiation or cyclophosphamide was added. Interferon-alpha-2b maintenance was used after the second autotransplant. Fourteen patients with HLA-compatible donors underwent an allograft as their second high-dose therapy cycle. Eighty-eight percent completed induction therapy whereas first and second transplants were performed in 84% and 71% (the majority within 8 and 15 months, respectively). Eight patients (3%) died of toxicity during induction, and 2 (1%) and 6 (4%) during the two transplants. True CR and at least a PR (PR plus CR) were obtained in 5% (34%) after VAD, 15% (65%) at the end of induction, and 26% (75%) after the first and 41% (83%) after the second transplants (intent-to-treat). Median overall (OS) and event-free (EFS) survival durations were 68 and 43 months, respectively. Actuarial 5-year OS and EFS rates were 58% and 42%, respectively. The median time to disease progression or relapse was 52 months. Among the 94 patients achieving CR, the median CR duration was 50 months. On multivariate analysis, superior EFS and OS were observed in the absence of unfavorable karyotypes (11q breakpoint abnormalities, -13 or 13-q) and with low beta-2-microglobulin at diagnosis. CR duration was significantly longer with early onset of CR and favorable karyotypes. Time-dependent covariate analysis suggested that timely application of a second transplant extended both EFS and OS significantly, independent of cytogenetics and beta-2-microglobulin. Total Therapy represents a comprehensive treatment approach for newly diagnosed myeloma patients, using multi-regimen induction and tandem transplantation followed by interferon maintenance. As a result, the proportion of patients attaining CR increased progressively with continuing therapy. This observation is particularly important because CR is a sine qua non for long-term disease control and, eventually, cure. (C) 1999 by The American Society of Hematology. C1 Univ Arkansas Med Sci, Myeloma & Transplantat Res Ctr, Arkansas Canc Res Ctr, Little Rock, AR 72205 USA. St Vincent Comprehens Canc Ctr, New York, NY USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. Greenbaum Canc Ctr, Baltimore, MD USA. NCI, CTEP, Bethesda, MD 20892 USA. SW Oncol Grp, Seattle, WA USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. RP Barlogie, B (reprint author), Univ Arkansas Med Sci, Myeloma & Transplantat Res Ctr, Arkansas Canc Res Ctr, 4301 W Markham Slot 776, Little Rock, AR 72205 USA. FU NCI NIH HHS [CA55819] NR 44 TC 440 Z9 456 U1 0 U2 4 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1200 19TH ST, NW, STE 300, WASHINGTON, DC 20036-2422 USA SN 0006-4971 J9 BLOOD JI Blood PD JAN 1 PY 1999 VL 93 IS 1 BP 55 EP 65 PG 11 WC Hematology SC Hematology GA 153AE UT WOS:000077809900007 PM 9864146 ER PT J AU Robey, R Bakke, S Stein, W Meadows, B Litman, T Patil, S Smith, T Fojo, T Bates, S AF Robey, R Bakke, S Stein, W Meadows, B Litman, T Patil, S Smith, T Fojo, T Bates, S TI Efflux of rhodamine from CD56(+) cells as a surrogate marker for reversal of P-glycoprotein-mediated drug efflux by PSC 833 SO BLOOD LA English DT Article ID PERIPHERAL-BLOOD LYMPHOCYTES; MULTIDRUG-RESISTANCE; COOPERATIVE INTERACTIONS; SDZ PSC-833; PHASE-I; EXPRESSION; MODULATORS; ASSAY; PHARMACOKINETICS; DOXORUBICIN AB The expression of high levels of P-glycoprotein (Pgp) in circulating mononuclear cells allowed us to use an ex vivo assay as a surrogate measure of Pgp antagonism. Efflux of rhodamine from CD56(+) cells was measured before the start of PSC 833 and at varying times thereafter. Patients receiving PSC 833 had decreased rhodamine efflux from their circulating CD56(+) cells. Time course studies showed that following a single oral dose of PSC 833, decreased rhodamine efflux was found in some patients within 15 minutes of treatment. Maximal inhibition was observed at times ranging from 45 minutes to 60 minutes, A dose-response relationship was shown between the concentration of PSC 833 in the blood and the inhibition of rhodamine efflux, with an apparent plateau of the inhibition of rhodamine efflux at approximately 1,000 ng/mL. The Ki, defined as the concentration required for half-maximal inhibition of Pgp-mediated rhodamine efflux, was determined to be in the range of 29 to 181 ng/mL; although results in two patients were distinctly different, with Ki values of 914 and 916 ng/mL. MRK-16 staining was similar among all patients. We conclude that measurement of rhodamine efflux from CD56(+) cells provides a surrogate assay with the potential for monitoring Pgp antagonism in clinical trials. This is a US government work. There are no restrictions on its use. C1 NCI, Med Branch, NIH, Bethesda, MD 20892 USA. Hebrew Univ Jerusalem, Jerusalem, Israel. Novartis Pharmaceut, E Hanover, NJ USA. RP Bates, S (reprint author), NCI, Med Branch, NIH, 9000 Rockville Pike,Bldg 10 Room 12N226, Bethesda, MD 20892 USA. EM sebates@helix.nih.gov NR 47 TC 61 Z9 61 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD JAN 1 PY 1999 VL 93 IS 1 BP 306 EP 314 PG 9 WC Hematology SC Hematology GA 153AE UT WOS:000077809900036 PM 9864175 ER PT J AU Colman, RJ Lane, MA Binkley, N Wegner, FH Kemnitz, JW AF Colman, RJ Lane, MA Binkley, N Wegner, FH Kemnitz, JW TI Skeletal effects of aging in male rhesus monkeys SO BONE LA English DT Article DE rhesus monkey; osteoporosis; osteoarthritis; bone mineral content; age-related bone loss ID BONE-MINERAL DENSITY; X-RAY ABSORPTIOMETRY; DEGENERATIVE JOINT DISEASE; AGE-RELATED-CHANGES; CYNOMOLGUS MACAQUES; MUSCULOSKELETAL SYSTEM; MACACA-FASCICULARIS; SERUM OSTEOCALCIN; SEX; OSTEOARTHRITIS AB Age-related bone loss in men is receiving increased attention. In light of this, animal models for male hone loss are desirable, This study examined the effects of age and osteoarthritis (OA) on bone mineral content (BMC), bone mineral density (BMD), and markers of bone turnover and skeletal relevance in 56 male rhesus monkeys 4-34 years of age. BMC and BMD increased at all sites from 4 to 10 years of age, Male rhesus monkeys reach peak bone mass at approximately 10 years of age after which bone mass is lower at the lateral spine and distal radius, Markers of bone turnover (osteocalcin and carboxyterminal telopeptide of type I collagen [ICTP]) decreased with age, There was no relationship between PTH, 25-hrdroxyvitamin D, FSH, or testosterone and age, With advancing age, the prevalence of lumbar spine OA increases dramatically, masking decreases ill posteroanterior spine bone mass that are clear in the lateral projection. These data suggest that male rhesus monkeys sustain age-related bone loss in the absence of nutritional or gonadal steroid deficiencies. These animals may prove useful in studying the mechanisms of age-related hone loss. (C) 1999 by Elsevier Science Inc. C1 Univ Wisconsin, Wisconsin Reg Primate Res Ctr, Madison, WI 53715 USA. Univ Wisconsin, Dept Anthropol, Madison, WI 53715 USA. Univ Wisconsin, Dept Med, Madison, WI 53715 USA. Univ Wisconsin, Inst Aging, Madison, WI 53715 USA. NIA, Gerontol Res Ctr, Mol Physiol & Genet Sect, Intramural Res Program,NIH, Baltimore, MD 21224 USA. RP Kemnitz, JW (reprint author), Univ Wisconsin, Wisconsin Reg Primate Res Ctr, 1223 Capitol Court, Madison, WI 53715 USA. EM kemnitz@primate.wisc.edu FU NCRR NIH HHS [P51 RR 00167]; NIA NIH HHS [P01 AG 11915] NR 43 TC 46 Z9 49 U1 0 U2 4 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 8756-3282 J9 BONE JI Bone PD JAN PY 1999 VL 24 IS 1 BP 17 EP 23 DI 10.1016/S8756-3282(98)00147-1 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 152CM UT WOS:000077758100003 PM 9916779 ER PT J AU Hensel, N Agarwala, V Jiang, YZ Mavroudis, D Molldrem, J Barrett, AJ AF Hensel, N Agarwala, V Jiang, YZ Mavroudis, D Molldrem, J Barrett, AJ TI A technique for dual determination of cytotoxic and helper lymphocyte precursor frequency by a miniaturized dye release method SO BONE MARROW TRANSPLANTATION LA English DT Article DE lymphocyte; precursor frequency assays; Calcein-AM; bone marrow transplantation; histocompatibility testing; CTLP, HTLP ID BONE-MARROW TRANSPLANTATION; LIMITING DILUTION ANALYSIS; CHRONIC MYELOID-LEUKEMIA; T-CELLS; HOST-DISEASE; GRAFT; SELECTION; RESPONSES; IMMUNITY; INVITRO AB Helper (HTLPf) and cytotoxic (CTLPf) lymphocyte precursor frequency assays are increasingly used in bone marrow stem cell and organ transplant compatibility testing, Current techniques require large cell numbers and radioisotopes. To improve the technique, we developed a miniaturized fluorescent read-out combined HTLPf/CTLPf limiting dilution assay. The assay requires only 5 x 10(6) stimulators, 2 x 10(6) responders and 0.24 x 10(6) target cells in Terasaki plates (40 mu l/well). For the HTLPf, culture supernatants from each well were assayed for IL-2 production. The IL-2-dependent proliferation of the mouse 9.12 cell line was detected by a semi-automated fluorescent dye technique. After addition of rhIL-2 (recombinant human IL-2) on days 3 and 7, CTLPs were detected on day 10 by measuring the lysis of dye-labeled targets, Results were comparable to standard radioisotope-based techniques. The assay had a coefficient of variation of approximately 30%, The assay detected helper CD4 cells, pure cytotoxic CD8, helper CD8 cells and helper/cytotoxic CDS cells. Discrimination was demonstrated between HLA-matched related and non-related pairs. The ease of testing and small cell numbers required should facilitate further evaluation of HTLPf and CTLPf for compatibility testing in unrelated donor transplantation and monitoring immune responses following adoptive transfer of lymphocytes. C1 NHLBI, Bone Marrow Transplantat Unit, Hematol Branch, NIH, Bethesda, MD 20892 USA. RP Hensel, N (reprint author), NHLBI, Bone Marrow Transplantat Unit, Hematol Branch, NIH, 10,7C103,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 23 TC 7 Z9 7 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD JAN PY 1999 VL 23 IS 1 BP 71 EP 78 DI 10.1038/sj.bmt.1701528 PG 8 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA 161YV UT WOS:000078318800011 PM 10037053 ER PT J AU Harris, DT Sakiestewa, D Lyons, C Kreitman, RJ Pastan, I AF Harris, DT Sakiestewa, D Lyons, C Kreitman, RJ Pastan, I TI Prevention of graft-versus-host disease (GVHD) by elimination of recipient-reactive donor T cells with recombinant toxins that target the interleukin 2 (IL-2) receptor SO BONE MARROW TRANSPLANTATION LA English DT Article DE GVHD; graft-versus-host disease; T cells; immunotoxin ID BONE-MARROW TRANSPLANTATION; UMBILICAL-CORD BLOOD; LYMPHOCYTES-T; CHAIN IMMUNOTOXIN; MYELOID-LEUKEMIA; DEPLETION; PROPHYLAXIS; FREQUENCIES; EXPRESSION; RELAPSE AB Graft-versus-host disease (GVHD), due to the presence of recipient-reactive T cells, limits the usefulness of bone marrow transplantation (BMT) and is a major contributor to patient mortality. To prevent GVHD, murine and human T cells were activated by antigen or mitogens and treated with a genetically engineered form of Pseudomonas exotoxin A (PE) directed against the IL-2 receptor. Treatment with the chimeric toxin eliminated alloreactive cytotoxic T lymphocytes (CTL) as determined by cytotoxicity and mixed lymphocyte culture assays. Precursor frequencies of alloreactive cytotoxic T cells and proliferative T cells were reduced up to 100-fold as shown by limiting dilution assays. Flow cytometric analyses revealed that treatment with the chimeric toxin completely eliminated CD25(+) cells from the cultures, Toxin treatment had no significant effect on hematopoietic stem and progenitor cells as determined in vitro by colony-forming assays and in vivo by long-term hematopoietic recovery after 950 rad irradiation. Toxin treatment decreased GVHD in transplanted mice to less than 10% (as compared to 88% in untreated controls). Thus, it is possible to prevent life-threatening GVHD after BMT by using a CD25 receptor-directed toxin to eliminate host-reactive T cells from bane marrow grafts. C1 Univ Arizona, Dept Microbiol & Immunol, Tucson, AZ 85721 USA. NCI, Div Basic Sci, Mol Biol Lab, Bethesda, MD 20892 USA. RP Harris, DT (reprint author), Univ Arizona, Dept Microbiol & Immunol, Bldg 90 Main Campus, Tucson, AZ 85721 USA. NR 38 TC 23 Z9 29 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD JAN PY 1999 VL 23 IS 2 BP 137 EP 144 DI 10.1038/sj.bmt.1701535 PG 8 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA 163LT UT WOS:000078407700007 PM 10197798 ER PT S AU Youle, RJ AF Youle, RJ BE Paulson, OB Knudsen, GM Moos, T TI Immunotoxins for brain tumor therapy SO BRAIN BARRIER SYSTEMS SE ALFRED BENZON SYMPOSIUM SERIES LA English DT Proceedings Paper CT Alfred Benzon Symposium 45 on Brain Barrier Systems CY AUG 23-27, 1998 CL ROYAL DANISH ACAD SCI & LETTERS, COPENHAGEN, DENMARK SP Alfred Benzon Fdn HO ROYAL DANISH ACAD SCI & LETTERS ID TRANSFERRIN RECEPTOR; LEPTOMENINGEAL NEOPLASIA; PURKINJE NEURONS; EFFICACY; ANTIBODY C1 NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA. RP Youle, RJ (reprint author), NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. NR 17 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD PI COPENHAGEN K PA 35 NORRE SOGADE POSTBOX 2148, DK-1016 COPENHAGEN K, DENMARK SN 0105-3639 BN 87-16-12177-5 J9 ALFRED BENZON SYMP S PY 1999 VL 45 BP 225 EP 230 PG 6 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA BN33T UT WOS:000081658600024 ER PT S AU Youle, RJ Huwyler, J Drewes, LR Keep, RF Gjedde, A Pardridge, WM Saunders, NR Blasberg, R Smith, Q AF Youle, RJ Huwyler, J Drewes, LR Keep, RF Gjedde, A Pardridge, WM Saunders, NR Blasberg, R Smith, Q BE Paulson, OB Knudsen, GM Moos, T TI Brain targeting using immunoliposomes - Discussion SO BRAIN BARRIER SYSTEMS SE ALFRED BENZON SYMPOSIUM SERIES LA English DT Proceedings Paper CT Alfred Benzon Symposium 45 on Brain Barrier Systems CY AUG 23-27, 1998 CL ROYAL DANISH ACAD SCI & LETTERS, COPENHAGEN, DENMARK SP Alfred Benzon Fdn HO ROYAL DANISH ACAD SCI & LETTERS ID MONOCLONAL-ANTIBODY; BARRIER TRANSPORT; DRUG-DELIVERY; PHARMACOKINETICS; RECEPTOR C1 NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA. RP Youle, RJ (reprint author), NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 10 TC 0 Z9 0 U1 0 U2 3 PU MUNKSGAARD PI COPENHAGEN K PA 35 NORRE SOGADE POSTBOX 2148, DK-1016 COPENHAGEN K, DENMARK SN 0105-3639 BN 87-16-12177-5 J9 ALFRED BENZON SYMP S PY 1999 VL 45 BP 519 EP 524 PG 6 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA BN33T UT WOS:000081658600061 ER PT J AU Stoner, G AF Stoner, G TI Is SV40 a tumorigenic human pathogen? SO BRAIN PATHOLOGY LA English DT Editorial Material ID JC-VIRUS; CHOROID-PLEXUS; BK-VIRUS; SIMIAN-VIRUS-40; TUMORS; SEQUENCES; URINE; DNA C1 NIH, Bethesda, MD 20892 USA. RP Stoner, G (reprint author), NIH, 36 Convent Dr,Bldg 36,Room 4A29, Bethesda, MD 20892 USA. NR 23 TC 1 Z9 1 U1 0 U2 0 PU INT SOC NEUROPATHOLOGY PI PITTSBURGH PA 200 LOTHROP ST A506, PITTSBURGH, PA 15213 USA SN 1015-6305 J9 BRAIN PATHOL JI Brain Pathol. PD JAN PY 1999 VL 9 IS 1 BP 43 EP 44 PG 2 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 164TG UT WOS:000078479200004 PM 9989449 ER PT J AU Narita, M Mizoguchi, H Narita, M Sora, I Uhl, GR Tseng, LF AF Narita, M Mizoguchi, H Narita, M Sora, I Uhl, GR Tseng, LF TI Absence of G-protein activation by mu-opioid receptor agonists in the spinal cord of mu-opioid receptor knockout mice SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE knockout mice; endomorphins; G-proteins; homologous recombination; opioid peptides; mu-opioid receptors; signal transduction; spinal cord ID MORPHINE-INDUCED ANALGESIA; OPIATE RECEPTOR; RAT-BRAIN; BINDING AB 1 The ability of mu-opioid receptor agonists to activate G-proteins in the spinal cord of mu-opioid receptor knockout mice was examined by monitoring the binding to membranes of the nonhydrolyzable analogue of GTP, guanosine-5'-O-(3-[S-35]thio)triphosphate ([S-35]GTP gamma S). 2 In the receptor binding study, Scatchard analysis of [H-3][D-Ala(2),NHPhe(4),Gly-ol]enkephalin ([H-3]DAMGO; mu-opioid receptor ligand) binding revealed that the heterozygous mu-knockout mice displayed approximately 40% reduction in the number of mu-receptors as compared to the wild-type mice. The homozygous mu-knockout mice showed no detectable mu-binding sites. 3 The newly isolated mu-opioid peptides endomorphin-1 and -2, the synthetic selective mu-opioid receptor agonist DAMGO and the prototype of mu-opioid receptor agonist morphine each produced concentration-dependent increases in [S-35]GTP gamma S binding in wild-type mice. This stimulation was reduced by 55-70% of the wild-type level in heterozygous, and virtually eliminated in homozygous knockout mice. 4 No differences in the [S-35]GTP gamma S binding stimulated by specific delta(1)- ([D-Pen(2,5)]enkephalin), delta(2)- ([D-Ala(2)]deltorphin II) or kappa(1)- (U50,488H) opioid receptor agonists were noted in mice of any of the three genotypes. 5 The data clearly indicate that mu-opioid receptor gene products play a key role in G-protein activation by endomorphins, DAMGO and morphine in the mouse spinal cord. They support the idea that mu-opioid receptor densities could be rate-limiting steps in the G-protein activation by mu-opioid receptor agonists in the spinal cord. These thus indicate a limited physiological mu-receptor reserve. Furthermore, little change in delta(1)-, delta(2)- or kappa(1)-opioid receptor-G-protein complex appears to accompany mu-opioid receptor gene deletions in this region. C1 Med Coll Wisconsin, Dept Anesthesiol, Milwaukee, WI 53226 USA. NIDA, Mol Neurobiol Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA. Johns Hopkins Univ, Sch Med, Dept Neurol & Neurosci, Baltimore, MD 21224 USA. RP Tseng, LF (reprint author), Med Coll Wisconsin, Dept Anesthesiol, Med Educ Bldg,Room 462C,8701 Watertown Plank Rd, Milwaukee, WI 53226 USA. FU NIDA NIH HHS [DA03811] NR 21 TC 46 Z9 46 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD JAN PY 1999 VL 126 IS 2 BP 451 EP 456 DI 10.1038/sj.bjp.0702330 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 162JY UT WOS:000078343600009 PM 10077238 ER PT J AU Kotloff, KL Winickoff, JP Ivanoff, B Clemens, JD Swerdlow, DL Sansonetti, PJ Adak, GK Levine, MM AF Kotloff, KL Winickoff, JP Ivanoff, B Clemens, JD Swerdlow, DL Sansonetti, PJ Adak, GK Levine, MM TI Global burden of Shigella infections: implications for vaccine development and implementation of control strategies SO BULLETIN OF THE WORLD HEALTH ORGANIZATION LA English DT Review ID DAY-CARE-CENTERS; SHIGA-BACILLUS DYSENTERY; ORAL REHYDRATION THERAPY; ACUTE DIARRHEAL DISEASE; SAUDI-ARABIA; RISK-FACTORS; ANTIMICROBIAL RESISTANCE; CHILDHOOD MORTALITY; ENTERIC PATHOGENS; CLINICAL-FEATURES AB Few studies provide data on the global morbidity and mortality caused by infection with Shigella spp.; such estimates are needed, however, to plan strategies of prevention and treatment. Here we report the results of a review of the literature published between 1966 and 1997 on Shigella infection. The data obtained permit calculation of the number of cases of Shigella infection and the associated mortality occurring worldwide each year, by age, and (as a proxy for disease severity) by clinical category, i.e. mild cases remaining at home, moderate cases requiring outpatient care, and severe cases demanding hospitalization. A sensitivity analysis was performed to estimate the high and low range of morbid and fatal cases in each category. Finally, the frequency distribution of Shigella infection, by serogroup and serotype and by region of the world, was determined. The annual number of Shigella episodes throughout the world was estimated to be 164.7 million, of which 163.2 million were in developing countries (with 1.1 million deaths) and 1.5 million in industrialized countries. A total of 69% of ail episodes and 61% of all deaths attributable to shigellosis involved children under 5 years of age. The median percentages of isolates of S. flexneri, S. sonnei, S. boydii, and S. dysenteriae were, respectively, 60%, 15%, 6%, and 6% (30% of 5 dysenteriae cases were type 1) in developing countries; and 16%, 77%, 2%, and 1% in industrialized countries. In developing countries, the predominant serotype of S. flexneri is 2a, followed by 1b, 3a, 4a, and 6. In industrialized countries, most isolates are 5 flexneri 2a or other unspecified type 2 strains. Shigellosis, which continues to have an important global impact, cannot be adequately controlled with the existing prevention and treatment measures. Innovative strategies, including development of vaccines against the most common serotypes, could provide substantial benefits. C1 Univ Maryland, Sch Med,Dept Pediat, Ctr Vaccine Dev,Domest Epidemiol Sect, Div Infect Dis & Trop Pediat, Baltimore, MD 21201 USA. Childrens Hosp, Dept Med, Boston, MA 02115 USA. WHO, Steering Comm Diarrhoeal Dis Vaccines, CH-1211 Geneva, Switzerland. NICHHD, Epidemiol Branch, NIH, Rockville, MD USA. Ctr Dis Control & Prevent, Natl Ctr Infect Dis, Foodborne Dis Epidemiol Sect, Foodborne & Diarrheal Dis Branch, Atlanta, GA USA. Inst Pasteur, Unite Pathogenie Microbienne Mol, Paris, France. Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Div Epidemiol, London NW9 5EQ, England. Univ Maryland, Sch Med, Ctr Vaccine Dev, Div Infect Dis, Baltimore, MD 21201 USA. RP Kotloff, KL (reprint author), Univ Maryland, Sch Med,Dept Pediat, Ctr Vaccine Dev,Domest Epidemiol Sect, Div Infect Dis & Trop Pediat, Baltimore, MD 21201 USA. RI kotloff, karen/E-7768-2012 OI kotloff, karen/0000-0003-1808-6431 NR 119 TC 729 Z9 789 U1 5 U2 41 PU WORLD HEALTH ORGANIZATION PI GENEVA 27 PA MARKETING AND DISSEMINATION, CH-1211 GENEVA 27, SWITZERLAND SN 0042-9686 EI 1564-0604 J9 B WORLD HEALTH ORGAN JI Bull. World Health Organ. PY 1999 VL 77 IS 8 BP 651 EP 666 PG 16 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 236UG UT WOS:000082617100005 PM 10516787 ER PT J AU Illei, GG Klippel, JH AF Illei, GG Klippel, JH TI Why is the ANA result positive? SO BULLETIN ON THE RHEUMATIC DISEASES LA English DT Article ID CHRONIC HEPATITIS-C; ANTINUCLEAR ANTIBODIES; AUTOIMMUNE HEPATITIS; AUTOANTIBODIES; PREVALENCE; DISEASE; SERUM; INDIVIDUALS; LEUKEMIA; PROFILE C1 NIAMSD, Arthrit & Rheumatism Branch, Bethesda, MD 20892 USA. RP Illei, GG (reprint author), NIAMSD, Arthrit & Rheumatism Branch, Bethesda, MD 20892 USA. NR 18 TC 4 Z9 5 U1 0 U2 0 PU ARTHRITIS FOUNDATION PI ATLANTA PA 1314 SPRING STREET NW, ATLANTA, GA 30309 USA SN 0007-5248 J9 B RHEUM DIS JI Bull. Rheum. Dis. PD JAN PY 1999 VL 48 IS 1 BP 1 EP 4 PG 8 WC Rheumatology SC Rheumatology GA 167YV UT WOS:000078663600001 PM 10028188 ER PT J AU Sommer, B Kuznetsov, SA Robey, PG O'Connell, B Cristiano, RJ Young, MF AF Sommer, B Kuznetsov, SA Robey, PG O'Connell, B Cristiano, RJ Young, MF TI Efficient gene transfer into normal human skeletal cells using recombinant adenovirus and conjugated adenovirus-DNA complexes SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE transfection; gene transfer; adenovirus; polylysine-conjugate; skeletal cells ID MARROW STROMAL FIBROBLASTS; IN-VIVO; DELIVERY; BONE; EXPRESSION; VECTORS; THERAPY AB In order to assess efficient DNA gene transfer into human primary cell cultures derived from the skeleton we tested two viral-based procedures. First, replication-deficient recombinant adenoviruses (ADV) were used to infect post-confluent human marrow stromal fibroblasts (HMSF) and human trabecular bone (HTB) cells. Both cell types were readily infected by modified adenoviral vectors carrying a reporter gene making this virus an attractive candidate to facilitate DNA gene transfer. In a second approach we coincubated DNA with ADV that had polylysine (PLL) covalently attached. With this ADV/PLL/DNA complex, very efficient gene transfer into multilayered HMSF and HTB cell cultures was observed, and DNA coincubated with unmodified ADV failed to be effectively transferred. These data imply that the covalently bound PLL more effectively binds exogenous DNA, resulting in a highly efficient internalization event in both cell types. Thus, this latter method has many advantages over conventional ADV gene transfer procedures. It is simple, rapid, and it does not require engineering of DNA into the viral genome, thereby allowing transfer of large fragments of DNA. C1 NIDR, Craniofacial & Skeletal Dis Branch, Bethesda, MD 20892 USA. NIDR, Gene Therapy & Therapy Branch, Bethesda, MD 20892 USA. Univ Texas, MD Anderson Cancer Ctr, Dept Thorac & Cardiovasc Surg, Houston, TX 77030 USA. RP Sommer, B (reprint author), NIDR, Craniofacial & Skeletal Dis Branch, Bldg 30,Room 228, Bethesda, MD 20892 USA. RI Robey, Pamela/H-1429-2011; OI Robey, Pamela/0000-0002-5316-5576; O'Connell, Brian/0000-0003-4529-7664 NR 15 TC 6 Z9 8 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD JAN PY 1999 VL 64 IS 1 BP 45 EP 49 DI 10.1007/s002239900577 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 152QX UT WOS:000077789200008 PM 9868283 ER PT J AU Kotoula, V Hytiroglou, P Thung, SN Tsokos, M Fiel, MI Papadimitriou, CS AF Kotoula, V Hytiroglou, P Thung, SN Tsokos, M Fiel, MI Papadimitriou, CS TI Telomerase activity in precancerous hepatic nodules - Reply SO CANCER LA English DT Letter ID HEPATOCELLULAR-CARCINOMA; DIAGNOSIS C1 Aristotelian Univ Salonika, Sch Med, Dept Pathol, GR-54006 Salonika, Greece. NCI, Pathol Lab, Sect Pediat Pathol & Electron Microscopy, NIH, Bethesda, MD 20892 USA. Mt Sinai Sch Med, Lillian & Henry M Stratton Hans Popper Dept Patho, New York, NY USA. RP Kotoula, V (reprint author), Aristotelian Univ Salonika, Sch Med, Dept Pathol, GR-54006 Salonika, Greece. NR 8 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 0008-543X J9 CANCER JI Cancer PD JAN 1 PY 1999 VL 85 IS 1 BP 247 EP 248 PG 2 WC Oncology SC Oncology GA 157LV UT WOS:000078064100038 ER PT J AU Potischman, N Troisi, R AF Potischman, N Troisi, R TI In-utero and early life exposures in relation to risk of breast cancer SO CANCER CAUSES & CONTROL LA English DT Article DE adolescent; breast cancer; breast fed; epidemiology; maternal age; preeclampsia; prenatal ID HUMAN PLACENTAL-LACTOGEN; MATERNAL AGE; BIRTH-WEIGHT; YOUNG-WOMEN; REPRODUCTIVE FACTORS; PERINATAL FACTORS; ESTROGEN-LEVELS; AMERICAN WOMEN; HEART-DISEASE; PREGNANCY AB Objectives: In response to a hypothesis by Trichopoulos that risk of adult breast cancer is related to high estrogen exposure in utero, studies have been undertaken using proxy indicators of prenatal estrogens. The epidemiologic studies addressing these early factors will be reviewed, consistency with proposed biologic mechanisms will be addressed and recommendations for future research will be presented. Methods: All studies identified in the literature addressing these in utero and early life factors related to adult breast cancer will be included in the review. The study results will be summarized by risk factor, followed by commentary on the findings. Results: Review of epidemiologic studies suggests strong risks related to having been born of a twin pregnancy and reduced risks from a preeclamptic or eclamptic pregnancy. Birthweights greater than 4000 grams have been associated with relative risks of 1.5-1.7 for breast cancer compared with normal birthweights (2500-2999 grams). Having been breastfed as an infant has been associated with a 20-35% reduction in risk of premenopausal breast cancer in four of six studies evaluating this factor. Some studies suggest an influence of older maternal age, perhaps only for firstborn offspring, but the data are not consistent. Smoking during the pregnancy does not seem to impart any risk for the daughter, severe nausea for two or three trimesters may be related to increased risk, and results are inconsistent for birth length, placental weight and gestational age. Conclusion: Although the results from epidemiologic studies assessing prenatal exposures are consistent with the hypothesis concerning estrogen exposure, the specific biologic mechanisms remain largely unknown. Relatively few epidemiologic studies have been published addressing these novel hypotheses; more studies with innovative research methods and analytic approaches are warranted to evaluate these exposures in the distant past. C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Potischman, N (reprint author), Univ Massachusetts, Sch Publ Hlth & Hlth Sci, Dept Biostat & Epidemiol, Arnold House, Amherst, MA 01003 USA. NR 91 TC 120 Z9 122 U1 1 U2 4 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PY 1999 VL 10 IS 6 BP 561 EP 573 DI 10.1023/A:1008955110868 PG 13 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 255WJ UT WOS:000083692900009 PM 10616825 ER PT J AU Franceschi, S Preston-Martin, S Maso, LD Negri, E La Vecchia, C Mack, WJ McTiernan, A Kolonel, L Mark, SD Mabuchi, K Jin, F Wingren, G Galanti, R Hallquist, A Glattre, E Lund, E Levi, F Linos, D Ron, E AF Franceschi, S Preston-Martin, S Maso, LD Negri, E La Vecchia, C Mack, WJ McTiernan, A Kolonel, L Mark, SD Mabuchi, K Jin, F Wingren, G Galanti, R Hallquist, A Glattre, E Lund, E Levi, F Linos, D Ron, E TI A pooled analysis of case-control studies of thyroid cancer. IV. Benign thyroid diseases SO CANCER CAUSES & CONTROL LA English DT Article DE goiter; hyperthyroidism; hypothyroidism; thyroid adenoma; thyroid cancer ID RISK; POPULATION; CARCINOMA; EPIDEMIOLOGY; RADIATION; HISTORY; IODINE; WOMEN; HYPERTHYROIDISM; PAPILLARY AB Objective: To obtain more precise estimates of the association between thyroid cancer and benign thyroid diseases and to elucidate the role of potential confounders or effect modifiers. Methods: The original data from 12 case-control studies from the United States, Asia, and Europe were pooled. Based on 2094 women and 425 men with cancer of the thyroid and, respectively, 3248 and 928 control subjects, odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were obtained by conditional regression models, conditioning on study and age at diagnosis, and adjusting for age and radiotherapy. Results: A history of hypothyroidism was not associated with cancer risk (pooled ORs = 0.9, 95% confidence interval, CI: 0.7-1.3 in women and 1.7, 95% CI: 0.3-11.7 in men). ORs for hyperthyroidism were 1.4 (95% CI: 1.0-2.1) in women and 3.1 (95% CI: 1.0-9.8) in men. In women, however, risk was lower in the absence of or after allowance for history of goiter. Pooled ORs for a history of goiter were 5.9 (95% CI: 4.2-8.1) in women and 38.3 (95% CI: 5.0-291.2) in men. Risk for a history of benign nodules/adenomas was especially high (OR = 29.9, 95% CI: 14.5-62.0, in women; 18 cases versus 0 controls in men). The excess risk for goiter and benign nodules/adenomas was greatest within 2-4 years prior to thyroid cancer diagnosis, but an elevated OR was present 10 years or more before cancer. Conclusions: Goiter and benign nodules/adenomas are the strongest risk factors for thyroid cancer, apart from radiation in childhood. C1 Ctr Riferimento Oncol, Serv Epidemiol, I-33081 Aviano, PN, Italy. Univ So Calif, Dept Prevent Med, Los Angeles, CA 90089 USA. Ist Ric Farmacol Mario Negri, Milan, Italy. Univ Milan, Ist Stat Med & Biometria, I-20122 Milan, Italy. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Hawaii Manoa, Ctr Canc Res, Honolulu, HI 96822 USA. NCI, Div Canc Epidemiol & Genet, Rockville, MD USA. Radiat Effects Res Fdn, Hiroshima, Japan. Shanghai Canc Inst, Shanghai, Peoples R China. Linkoping Univ, Dept Hlth & Environm, Div Environm & Occupat Med, Linkoping, Sweden. Ctr Tobakprevent, Huddinge, Sweden. Stockholm Sjukhem, Stockholm, Sweden. Canc Registry Norway, Montebello, Norway. Univ Tromso, Inst Community Med, Tromso, Norway. Registre Vaudois Tumeurs, Lausanne, Switzerland. NCI, Radiat Epidemiol Branch, Rockville, MD USA. RP Franceschi, S (reprint author), Ctr Riferimento Oncol, Serv Epidemiol, Via Pedemontana, I-33081 Aviano, PN, Italy. RI Negri, Eva/B-7244-2013; OI Negri, Eva/0000-0001-9712-8526; La Vecchia, Carlo/0000-0003-1441-897X NR 38 TC 95 Z9 98 U1 0 U2 6 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PY 1999 VL 10 IS 6 BP 583 EP 595 DI 10.1023/A:1008907227706 PG 13 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 255WJ UT WOS:000083692900011 PM 10616827 ER PT J AU Friedman, HS Pegg, AE Johnson, SP Loktionova, NA Dolan, ME Modrich, P Moschel, RC Struck, R Brent, TP Ludeman, S Bullock, N Kilborn, C Keir, S Dong, Q Bigner, DD Colvin, OM AF Friedman, HS Pegg, AE Johnson, SP Loktionova, NA Dolan, ME Modrich, P Moschel, RC Struck, R Brent, TP Ludeman, S Bullock, N Kilborn, C Keir, S Dong, Q Bigner, DD Colvin, OM TI Modulation of cyclophosphamide activity by O-6-alkylguanine-DNA alkyltransferase SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE alkylating agents; antineoplastic agents; cyclophosphamide; drug resistance; nitrogen mustard compounds ID MEDULLOBLASTOMA CELL-LINES; ALKYLATING-AGENTS; O-6-METHYLGUANINE-DNA METHYLTRANSFERASE; DNA; INHIBITION; DEPLETION; TOXICITY; PROTEIN; REPAIR AB Purpose: The human medulloblastoma cell line D283 Med (4-HCR), a line resistant to 4-hydroperoxycyclophosphamide (4-HC), displays enhanced repair of DNA interstrand crosslinks induced by phosphoramide mustard. D283 Med (4-HCR) cells are cross-resistant to 1,3-bis(2-chloroethyl)-1-nitrosourea, bur partial sensitivity is restored after elevated levels of O-6-alkylguanine-DNA alkyltransferase (AGT) are depleted by O-6-benzylguanine (O-6-BG). Studies were conducted to define the activity of 4-HC and 4-hydroperoxyidechlorocyclophosphamide against D283 Med (4-HCR) after AGT is depleted by O-6-BG, Methods: Limiting dilution and xenograft studies were conducted to define the activity of 4-HC and 4-hydroperoxyidechlorocyclophosphamide with or without O-6-BG. Results: The activity of 4-HC and 4-hydroperoxydidechlorocyclophosphamide against D283 Med (4-HCR) was increased after AGT depletion by O-6-BG preincubation. Similar studies with Chinese hamster ovary cells, with or without stable transfection with a plasmid expressing the human AGT protein, revealed that the AGT-expressing cells were significantly less sensitive to 4-HC and 4-hydroperoxydidechlorocyclophosphamide. Reaction of DNA with 4-HC, phosphoramide mustard, or acrolein revealed that only 4-HC and acrolein caused a decrease in AGT levels, Conclusions: We propose that a small but potentially significant part of the cellular toxicity of cyclophosphamide in these cells is due to acrolein, and that this toxicity is abrogated by removal of the acrolein adduct from DNA by AGT. C1 Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Biochem, Durham, NC 27710 USA. Penn State Univ, Milton S Hershey Med Ctr, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA. Univ Chicago, Dept Med, Chicago, IL 60637 USA. So Res Inst, Birmingham, AL 35255 USA. St Jude Childrens Res Ctr, Dept Mol Pharmacol, Memphis, TN 38101 USA. NCI, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. RP Friedman, HS (reprint author), Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. FU NCI NIH HHS [CA 67266, CA 57725]; NINDS NIH HHS [NS 20023] NR 21 TC 43 Z9 43 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD JAN PY 1999 VL 43 IS 1 BP 80 EP 85 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 144ZU UT WOS:000077347000012 PM 9923545 ER PT J AU Riker, AI Panelli, MC Kammula, US Wang, E Wunderlich, J Abati, A Fetsch, P Rosenberg, SA Marincola, FM AF Riker, AI Panelli, MC Kammula, US Wang, E Wunderlich, J Abati, A Fetsch, P Rosenberg, SA Marincola, FM TI Development and characterization of melanoma cell lines established by fine-needle aspiration biopsy: Advances in the monitoring of patients with metastatic melanoma SO CANCER DETECTION AND PREVENTION LA English DT Article DE fine-needle aspiration biopsy; melanoma; tumor antigens ID MONOCLONAL-ANTIBODIES; HETEROGENEOUS EXPRESSION; LYMPH-NODES; IN-VIVO; DIAGNOSIS; ANTIGENS; MART-1; GP100; VACCINATION; CARCINOMA AB The establishment of melanoma cell lines from fine-needle aspiration biopsies (FNAB) has allowed for an enhanced understanding of the complex interactions that occur between T cells and tumor cells. The technique of FNAB offers the advantage of providing a sequential analysis of the same tumor nodules throughout treatment. The expression of melanoma antigens (MAs) was assessed in fresh melanoma FNAB samples and from tumor cell lines derived from these samples using several different approaches. Cytospin preparations of freshly isolated tumor cell explants were analyzed by immunocytochemistry (ICC), while the daughter cell line was analyzed by fluorescent activated cell sorting (FACS) analysis, and semiquantitative and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR, qRT-PCR). As assessed by these methods, the level of MA expression by the original tumor cell explants correlated with the expression in established in vitro cell lines. Molecular analysis of the established cell lines utilizing PCR technology improved the sensitivity of detection of MA expression. Thus FNAB of melanoma is an efficient and effective method of tissue procurement, capable of generating, sequentially and from the same lesion, fresh tumor cells, tumor infiltrating lymphocytes (TIL), and long-term melanoma cell lines. C1 NCI, NIH, Surg Branch, Bethesda, MD 20892 USA. RP Marincola, FM (reprint author), NCI, NIH, Surg Branch, Ctr Dr,Bldg 10,Rm 2B58, Bethesda, MD 20892 USA. RI Riker, Adam/A-6065-2011 NR 25 TC 19 Z9 21 U1 1 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 1999 VL 23 IS 5 BP 387 EP 396 DI 10.1046/j.1525-1500.1999.99045.x PG 10 WC Oncology SC Oncology GA 231GX UT WOS:000082300700004 PM 10468890 ER PT J AU Greenwald, P AF Greenwald, P TI Role of dietary fat in the causation of breast cancer: Point SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID NUTRITION EXAMINATION SURVEY; PHYSICAL-ACTIVITY; MEASUREMENT ERROR; NATIONAL-HEALTH; ENERGY-INTAKE; FOLLOW-UP; BODY-MASS; OLIVE OIL; RISK; WOMEN C1 NCI, Div Canc Prevent, Bethesda, MD 20892 USA. RP Greenwald, P (reprint author), NCI, Div Canc Prevent, Bldg 31,Room 10A52,31 Ctr Dr,MSC 2580, Bethesda, MD 20892 USA. NR 65 TC 40 Z9 41 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 1999 VL 8 IS 1 BP 3 EP 7 PG 5 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 158LC UT WOS:000078116100001 PM 9950233 ER PT J AU Hayes, RB Ziegler, RG Gridley, G Swanson, C Greenberg, RS Swanson, GM Schoenberg, JB Silverman, DT Brown, LM Pottern, LM Liff, J Schwartz, AG Fraumeni, JF Hoover, RN AF Hayes, RB Ziegler, RG Gridley, G Swanson, C Greenberg, RS Swanson, GM Schoenberg, JB Silverman, DT Brown, LM Pottern, LM Liff, J Schwartz, AG Fraumeni, JF Hoover, RN TI Dietary factors and risks for prostate cancer among blacks and whites in the United States SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID BETA-CAROTENE; ENERGY ADJUSTMENT; PHYSICAL-ACTIVITY; FAT CONSUMPTION; NUTRITION; POPULATION; CARCINOMA; TOBACCO; HEIGHT; WEIGHT AB Prostate cancer is the most common malignancy in men in the United States, with substantially higher rates among American blacks than whites. We carried out a population-based case-control study in three geographic areas of the United States to evaluate the reasons for the racial disparity in incidence rates. A total of 932 men (449 black men and 483 white men) who had been newly diagnosed with pathologically confirmed prostate cancer and 1201 controls (543 black men and 658 white men) were interviewed in person to elicit information on potential risk factors. This report evaluates the impact of dietary factors, particularly the consumption of animal products and animal fat, on the risk of prostate cancer among blacks and whites in the United States. Increased consumption (grams/day) of foods high in animal fat was linked to prostate cancer (independent of intake of other calories) among American blacks [by quartile of intake, odds ratio (OR) = 1.0 (referent), 1.5, 2.1, and 2.0; P-trend = 0.007], but not among American whites [by quartile of intake, OR = 1.0 (referent), 1.6, 1.5, and 1.1; P-trend = 0.90]. However, risks for advanced prostate cancer were higher with greater intake of foods high in animal fat among blacks [by quartile of intake, OR = 1.0 (referent), 2.2, 4.2, and 3.1; P-trend = 0.006] and whites [by quartile of intake, OR = 1.0 (referent), 2.2, 2.6, and 2.4; P-trend = 0.02]. Increased intake of animal fat as it proportion of total caloric intake also showed positive but weaker associations with advanced prostate cancer among blacks (P-trend = 0.13) and whites (P-trend = 0.08). No clear associations were found with vitamin A, calcium, or specific lycopene-rich foods. The study linked greater consumption of fat from animal sources to increased risk for prostate cancer among American blacks and to advanced prostate cancer among American blacks and whites. A reduction of fat from animal sources in the diet could lead to decreased incidence and mortality rates for prostate cancer, particularly among American blacks. C1 NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30329 USA. Michigan Canc Fdn, Detroit, MI 48201 USA. New Jersey State Dept Hlth, Special Epidemiol Program, Trenton, NJ 08625 USA. NIH, Off Director, Bethesda, MD 20892 USA. RP Hayes, RB (reprint author), NCI, Div Canc Epidemiol & Genet, Execut Plaza N,EPN 418, Bethesda, MD 20892 USA. EM hayesr@epndce.nci.nih.gov FU NCI NIH HHS [N01-CP-51089, N01-CN-05225, N01-CP-5109] NR 50 TC 186 Z9 190 U1 2 U2 7 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 1999 VL 8 IS 1 BP 25 EP 34 PG 10 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 158LC UT WOS:000078116100004 PM 9950236 ER PT J AU Moysich, KB Shields, PG Freudenheim, JL Schisterman, EF Vena, JE Kostyniak, P Greizerstein, H Marshall Jr Graham, S Ambrosone, CB AF Moysich, KB Shields, PG Freudenheim, JL Schisterman, EF Vena, JE Kostyniak, P Greizerstein, H Marshall, JR Graham, S Ambrosone, CB TI Polychlorinated biphenyls, cytochrome P4501A1 polymorphism, and postmenopausal breast cancer risk SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID LUNG-CANCER; CYP1A1; WOMEN; PESTICIDES; RESIDUES; SERUM; PCBS AB In experimental systems, polychlorinated biphenyls (PCBs) induce cytochrome P4501A1 (CYP1A1), which is involved in metabolism of steroid hormones and polycyclic aromatic hydrocarbons in humans. A genetic polymorphism coding for a valine to isoleucine substitution in exon 7 has been associated with lung cancer risk in Japanese populations. In a previous study, we found no association between CYP1A1 genotype and breast cancer risk. However, we were interested in determining whether genotype would relate to risk when PCB body burden was taken into account. In a subset of a ease-control study in western New York, 154 postmenopausal women with incident, primary, histologically confirmed postmenopausal breast cancer and 192 community controls were interviewed and underwent phlebotomy. Serum levels of 56 PCB peaks were determined by high resolution gas chromatography with electron capture. PCR-RFLP analyses of the CYP1A1 polymorphism were performed. Unconditional logistic regression was used to compute adjusted odds ratios and 95% confidence intervals. Among women with serum PCB levels above the median of the distribution in the control group, there was increased risk of breast cancer associated with the presence of at least one valine allele, compared with women who were homozygous for the isoleucine alleles (odds ratio, 2.93; 95% confidence interval, 1.17-7.36), Among women with low PCB body burden, no association between CYP1A1 genotype and breast cancer risk was observed, Adjustment for serum lipids and body mass index did not affect the magnitude of the observed associations. PCB body burden may modify the effect of the polymorphism on postmenopausal breast cancer risk through increased CYP1A1 enzyme induction or by activation by specific PCB congeners, These results should be considered preliminary, pending replication by other studies. C1 SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14214 USA. SUNY Buffalo, Toxicol Res Ctr, Buffalo, NY 14214 USA. Univ Arizona, Arizona Canc Ctr, Tucson, AZ 85724 USA. NCI, Bethesda, MD 20892 USA. Natl Ctr Toxicol Res, Jefferson, AR 72079 USA. RP Moysich, KB (reprint author), New York State Dept Hlth, Roswell Pk Canc Inst, Dept Canc Prevent Epidemiol & Biostat, Elm & Carlton St, Buffalo, NY 14263 USA. EM kmoysich@sc3103.med.buffalo.edu RI Shields, Peter/I-1644-2012; OI Schisterman, Enrique/0000-0003-3757-641X FU NCI NIH HHS [CA11535]; NIDA NIH HHS [DAMD1 7-94-J-4108, DAMD-95-1-5022] NR 29 TC 101 Z9 106 U1 2 U2 9 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 1999 VL 8 IS 1 BP 41 EP 44 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 158LC UT WOS:000078116100006 PM 9950238 ER PT J AU Cerhan, JR Parker, AS Putnam, SD Chiu, BCH Lynch, CF Cohen, MB Torner, JC Cantor, KP AF Cerhan, JR Parker, AS Putnam, SD Chiu, BCH Lynch, CF Cohen, MB Torner, JC Cantor, KP TI Family history and prostate cancer risk in a population-based cohort of Iowa men SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID ANDROGEN RECEPTOR GENE; BREAST-CANCER; DIETARY-INTAKE; RELATIVES; ASSOCIATION; CARCINOMA; SWEDEN; MALIGNANCIES; EPIDEMIOLOGY; INHERITANCE AB A family history of prostate cancer has been associated with prostate cancer risk in most prior studies, and more limited data suggest that a family history of breast cancer may also be important; however, there are no data from a population-based cohort study of prostate cancer incidence that adjusts for major confounders. We conducted follow-up through 1995 on 1557 men, ages 40-86 years, who were randomly selected (81% response rate) as cancer-free controls for a population-based case-control study conducted in Iowa from 1987-1989, Family history of cancer in parents and siblings was obtained using a mailed questionnaire. Incident cancers and deaths were ascertained through linkages to state and national databases; 101 incident cases of prostate cancer were identified, At baseline, 4.6% of the cohort reported a family history of prostate cancer in a brother or father, and this was positively associated,vith prostate cancer risk after adjustment for age [relative risk (RR) = 3.2; 95% confidence interval (CI), 1.8-5.7] or after multivariate adjustment for age, alcohol, and dietary factors (RR = 3.7; 95% CI, 1.9-7.2). Risk was greater if a brother had prostate cancer (RR = 4.5; 95% CI, 2.1-9.7) than if a father had prostate cancer (RR = 2.3; 95% CI, 1.0-5.3), Also at baseline, 9.6% of the cohort had a family history of breast and/or ovarian cancer in a mother or sister, and this was positively associated with prostate cancer risk (age-adjusted RR = 1.7; 95% CI, 1.0-3.0; multivariate RR = 1.7; 95% CI, 0.9-3.2). Men with a family history of both prostate and breast/ovarian cancer were also at increased risk of prostate cancer (RR = 5.8; 95% CI, 2.4-14), There was no association with a family history of colon cancer. Exclusion of well-differentiated, localized tumors did not alter these findings. These data from an incidence study confirm that a family history of prostate cancer is a strong prostate cancer risk factor after adjustment for dietary and other risk factors, and suggest that selection and recall bias have not had an important influence on most case-control study results. These data also support the idea that a family history of breast cancer may also be a prostate cancer risk factor. C1 Univ Iowa, Coll Med, Dept Prevent Med & Environm Hlth, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Dept Pathol & Urol, Iowa City, IA 52242 USA. NCI, Div Canc Epidemiol & Genet, Occupat Epidemiol Branch, Bethesda, MD 20892 USA. RP Cerhan, JR (reprint author), Mayo Clin & Mayo Fdn, Dept Hlth Sci Res, 200 1st St SW, Rochester, MN 55905 USA. EM cerhan.james@mayo.edu FU NCI NIH HHS [N01-CP-85614, N01-CP-51026, R21 CA/ES69838] NR 56 TC 82 Z9 82 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1055-9965 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 1999 VL 8 IS 1 BP 53 EP 60 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 158LC UT WOS:000078116100008 PM 9950240 ER PT J AU Sanford, KK Parshad, R AF Sanford, KK Parshad, R TI The contribution of deficient DNA repair to chromosomal radiosensitivity of CHO cells after G(2) irradiation SO CANCER GENETICS AND CYTOGENETICS LA English DT Article ID PHASE X-IRRADIATION; COMPLEMENTATION GROUPS; CYCLE PERIOD; CANCER; UV; INDIVIDUALS; FIBROBLASTS; INDUCTION; MUTATION; LESIONS AB We compared cytogenetic responses of the parental Chinese hamster ovary (CHO) cell line and its DNA repair-deficient strains to irradiation during the G(2) phase. Chromatid breaks were quantified in cells entering metaphase in the presence or absence of cytosine arabinoside (ara-C) 0.5-1.5 hours after exposure to x-rays or UV-C. Addition of ara-C, an inhibitor of DNA repair replication, significantly increased chromatid break frequency (CBF) in the parental line, but not in the strains deficient in nucleotide excision repair (NER). This increase (ara-C effect) was comparable to that in repair-proficient normal human lymphocytes. We conclude that CBF in cells entering metaphase in the presence of ara-C 0.5-1.5 hours after DNA damage represents a functional in vitro assay for evaluating the DNA repair capacity of mammalian cells in culture. Published by Elsevier Science Inc. C1 NCI, Cellular & Mol Biol Lab, Bethesda, MD 20892 USA. Howard Univ, Coll Med, Dept Pathol, Washington, DC USA. RP Sanford, KK (reprint author), 101 Stuart Dr, Sagamiko, Kanagawa 19901, Japan. NR 21 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0165-4608 J9 CANCER GENET CYTOGEN JI Cancer Genet. Cytogenet. PD JAN 1 PY 1999 VL 108 IS 1 BP 38 EP 41 DI 10.1016/S0165-4608(98)00108-3 PG 4 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA 151VQ UT WOS:000077741700007 PM 9973922 ER PT J AU Cragg, GM Newman, DJ AF Cragg, GM Newman, DJ TI Discovery and development of antineoplastic agents from natural sources SO CANCER INVESTIGATION LA English DT Article DE natural products; cancer; drugs ID NATIONAL-CANCER-INSTITUTE; DRUG-DISCOVERY; PRODUCTS; ANTICANCER; THERAPY; PLANTS; DEEP AB Nature has provided many effective anticancer. agents in current use, such as the microbially derived drugs; dactinomycin, bleomycin ann doxorubicin; and the plant-derived drugs, vinblastine, irinotecan, topotecan, etoposide, and paclitaxel. The search for novel antitumor agents front natural sources continues through collaboration among scientists worldwide in the investigation of coral reefs, rainforests, and deep subsurface thermal vents for novel bioactive compounds. The potential for drug discovery is being further enhanced by recent advances in procedures for microbial cultivation and the extraction of nucleic acids from environmental samples, resulting in the identification of novel microbes that provide a vast untapped reservoir of generic and metabolic diversity. Manipulation of the biosynthetic pathways of microbial polyketides through genetic engineering permits the biosynthesis of bioactive polyketides not generated naturally. C1 NCI, Frederick Canc Res & Dev Ctr, Nat Prod Branch,Dev Therapeut Program, Div Canc Treatment & Diag, Frederick, MD 21701 USA. RP Cragg, GM (reprint author), NCI, Frederick Canc Res & Dev Ctr, Nat Prod Branch,Dev Therapeut Program, Div Canc Treatment & Diag, Fairview Ctr,POB B, Frederick, MD 21701 USA. NR 32 TC 80 Z9 89 U1 3 U2 10 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0735-7907 J9 CANCER INVEST JI Cancer Invest. PY 1999 VL 17 IS 2 BP 153 EP 163 PG 11 WC Oncology SC Oncology GA 171YK UT WOS:000078892000009 PM 10071600 ER PT J AU Lee, L Wang, RF Wang, XA Mixon, A Johnson, BE Rosenberg, SA Schrump, DS AF Lee, L Wang, RF Wang, XA Mixon, A Johnson, BE Rosenberg, SA Schrump, DS TI NY-ESO-1 may be a potential target for lung cancer immunotherapy SO CANCER JOURNAL FROM SCIENTIFIC AMERICAN LA English DT Article DE NY-ESO-1; tumor antigen; lung cancer; tumor immunology; demethylation; 5-aza-2 '-deoxycytidine ID CYTOLYTIC T-LYMPHOCYTES; HUMAN GENE MAGE-3; TUMOR-ANTIGENS; CELL-LINES; EXPRESSION; IDENTIFICATION; MELANOMA; RESECTION; RESPONSES; DEFICIENT AB PURPOSE To evaluate the frequency of NY-ESO-1 expression in cultured lung cancer cells and to determine if this cancer-testis antigen can be presented for recognition by an HLA-restricted cytolytic T-cell clone specific for NY-ESO-1. METHODS AND RESULTS Reverse transcriptase and polymerase chain reaction amplification techniques were utilized to screen a panel of lung and esophageal cancer cell lines for expression of NY-ESO-1 encoding a recently identified cancer-testis antigen. NY-ESO-1 expression was detected in 11 of 16 small cell lung cancer lines, three of seven non-small cell lung cancer lines, and zero of 12 esophageal cancer lines. 5-Aza-2'-deoxycytidine induced expression of NY-ESO-1 in lung cancer cells. Expression of HLA-A31 by plasmid transfection or retroviral transduction enabled recognition of lung cancer cells by an HLA-A31-restricted cytotoxic T lymphocyte clone specific for NY-ESO-1. CONCLUSIONS NY-ESO-1 expression may be analagous to MAGE gene expression in lung cancer lines in terms of frequency and mechanism of transcriptional regulation. Furthermore, NY-ESO-1 can be presented on lung cancer cells for recognition by HLA-restricted cytotoxic T lymphocytes. Further investigation is warranted to determine if NY-ESO-1 can be exploited for the immunotherapy for lung cancer. C1 NCI, Surg Branch, NIH, Bethesda, MD 20892 USA. NCI, Med Oncol Branch, Bethesda, MD 20892 USA. RP Schrump, DS (reprint author), NCI, Surg Branch, NIH, Bldg 10,Room 2B-07, Bethesda, MD 20892 USA. NR 31 TC 40 Z9 42 U1 0 U2 0 PU SCI AMERICAN INC PI NEW YORK PA 415 MADISON AVE, NEW YORK, NY 10017 USA SN 1081-4442 J9 CANCER J SCI AM JI Cancer J. Sci. Am. PD JAN-FEB PY 1999 VL 5 IS 1 BP 20 EP 25 PG 6 WC Oncology SC Oncology GA 172AL UT WOS:000078899100004 PM 10188057 ER PT S AU Kelloff, GJ Crowell, JA Steele, VE Lubet, RA Boone, CW Malone, WA Hawk, ET Lieberman, R Lawrence, JA Kopelovich, L Ali, I Viner, JL Sigman, CC AF Kelloff, GJ Crowell, JA Steele, VE Lubet, RA Boone, CW Malone, WA Hawk, ET Lieberman, R Lawrence, JA Kopelovich, L Ali, I Viner, JL Sigman, CC BE Bradlow, HL Fishman, J Osborne, MP TI Progress in cancer chemoprevention SO CANCER PREVENTION: NOVEL NUTRIENT AND PHARMACEUTICAL DEVELOPMENTS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Cancer Prevention - Novel Nutrient and Pharmaceutical Developments CY NOV 13-14, 1998 CL NEW YORK, NEW YORK SP Cornell Univ, Coll Med, Ctr Strang Canc Prevent, Int Soc Canc Chemoprevent, Amer Canc Soc, Amer Italian Canc Fdn, AmerMedia Inc, Donald Beldock, Merck & Co Inc, Weill Med Coll Cornell Univ, Irving Weinstein Fdn ID PROSTATE-CANCER; PREVENTION; TRIAL; SUPPLEMENTATION; CARCINOGENESIS; CYCLOOXYGENASE; INHIBITORS; DRUGS; RISK; MICE AB More than 40 promising agents and agent combinations are being evaluated clinically as chemopreventive drugs for major cancer targets. A few have been in vanguard, large-scale intervention trials-for example, the studies of tamoxifen and fenretinide in breast, 13-cis-retinoic acid in head and neck, vitamin E and selenium in prostate, and calcium in colon. These and other agents are currently in phase II chemoprevention trials to establish the scope of their chemopreventive efficacy and to develop intermediate biomarkers as surrogate end points for cancer incidence in future studies. In this group are fenretinide, 2-difluoromethylornithine, and oltipraz, Nonsteroidal anti-inflammatories (NSAID) are also in this group because of their colon cancer chemopreventive effects in clinical intervention, epidemiological, and animal studies. New agents are continually considered for development as chemopreventive drugs. Preventive strategies with antiandrogens are evolving for prostate cancer, Antiinflammatories that selectively inhibit inducible cyclooxygenase (COX)-2 are being investigated in colon as alternatives to the NSAID, which inhibit both COX-1 and COX-2 and derive their toxicity from COX-1 inhibition. Never retinoids with reduced toxicity, increased efficacy, or both (e.g., 9-cis-retinoic acid) are being investigated. Promising chemopreventive drugs are also being developed from dietary substances (e.g., green and black tea polyphenols, soy isoflavones, curcumin, phenethyl isothiocyanate, sulforaphane, lycopene, indole-3-carbinol, perillyl alcohol). Basic and translational research necessary to progress in chemopreventive agent development includes, for example, (1) molecular and genomic biomarkers that can be used for risk assessment and as surrogate end points in clinical studies, (2) animal carcinogenesis models that mimic human disease (including transgenic and gene knockout mice), and (3) novel agent treatment regimens (e.g., local delivery to cancer targets, agent combinations, and pharmacodynamically guided dosing). C1 NCI, Div Canc Prevent, Bethesda, MD 20892 USA. CSS Associates, Mt View, CA 94043 USA. RP Kelloff, GJ (reprint author), NCI, Chemoprevent Branch, Div Canc Prevent, 6130 Execut Blvd,EPN 201, Rockville, MD 20852 USA. NR 38 TC 97 Z9 97 U1 2 U2 14 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-198-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 889 BP 1 EP 13 DI 10.1111/j.1749-6632.1999.tb08718.x PG 13 WC Medicine, Research & Experimental; Multidisciplinary Sciences; Nutrition & Dietetics; Pharmacology & Pharmacy SC Research & Experimental Medicine; Science & Technology - Other Topics; Nutrition & Dietetics; Pharmacology & Pharmacy GA BP49R UT WOS:000085323100001 PM 10668477 ER PT S AU Langenbach, R Loftin, CD Lee, C Tiano, H AF Langenbach, R Loftin, CD Lee, C Tiano, H BE Bradlow, HL Fishman, J Osborne, MP TI Cyclooxygenase-deficient mice - A summary of their characteristics and susceptibilities to inflammation and carcinogenesis SO CANCER PREVENTION: NOVEL NUTRIENT AND PHARMACEUTICAL DEVELOPMENTS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Cancer Prevention - Novel Nutrient and Pharmaceutical Developments CY NOV 13-14, 1998 CL NEW YORK, NEW YORK SP Cornell Univ, Coll Med, Ctr Strang Canc Prevent, Int Soc Canc Chemoprevent, Amer Canc Soc, Amer Italian Canc Fdn, AmerMedia Inc, Donald Beldock, Merck & Co Inc, Weill Med Coll Cornell Univ, Irving Weinstein Fdn ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ENDOPEROXIDE SYNTHASE CYCLOOXYGENASE; INDUCED COLON CARCINOGENESIS; PROSTAGLANDIN-G/H SYNTHASE; ACTIVATED RECEPTOR-ALPHA; EPITHELIAL-CELLS; TUMOR PROMOTION; MESSENGER-RNA; H SYNTHASE; MULTISTAGE CARCINOGENESIS AB Cyclooxygenase (COX)-1- and COX-2-deficient mice have unique physiological differences that have allowed investigation into the individual biological roles of the COX isoforms, In the following, the phenotypes of the two COX knockout mice are summarized, and recent studies to investigate the effects of COX deficiency on inflammatory responses and cancer susceptibility are discussed. The data suggest that both isoforms have important roles in the maintenance of physiological homeostasis and that such designations as housekeeping and/or response gene may not be entirely accurate, Furthermore, data from COX-deficient mice indicate that both isoforms can contribute to the inflammatory response and that both isoforms have significant roles in carcinogenesis. C1 NIEHS, Res Triangle Pk, NC 27709 USA. RP Langenbach, R (reprint author), NIEHS, 101 Alexander Dr,POB 12233, Res Triangle Pk, NC 27709 USA. NR 70 TC 115 Z9 124 U1 2 U2 5 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-198-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 889 BP 52 EP 61 DI 10.1111/j.1749-6632.1999.tb08723.x PG 10 WC Medicine, Research & Experimental; Multidisciplinary Sciences; Nutrition & Dietetics; Pharmacology & Pharmacy SC Research & Experimental Medicine; Science & Technology - Other Topics; Nutrition & Dietetics; Pharmacology & Pharmacy GA BP49R UT WOS:000085323100006 PM 10668482 ER PT S AU Forman, MR Zhang, J Gunter, E Yao, SX Gross, M Qiao, YL Graubard, BI Taylor, PR Keith, S Maher, M AF Forman, MR Zhang, J Gunter, E Yao, SX Gross, M Qiao, YL Graubard, BI Taylor, PR Keith, S Maher, M BE Bradlow, HL Fishman, J Osborne, MP TI Season-specific correlation between dietary intake of fruits and vegetables and levels of serum biomarkers among Chinese tin miners at high risk for lung cancer SO CANCER PREVENTION: NOVEL NUTRIENT AND PHARMACEUTICAL DEVELOPMENTS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Cancer Prevention - Novel Nutrient and Pharmaceutical Developments CY NOV 13-14, 1998 CL NEW YORK, NEW YORK SP Cornell Univ, Coll Med, Ctr Strang Canc Prevent, Int Soc Canc Chemoprevent, Amer Canc Soc, Amer Italian Canc Fdn, AmerMedia Inc, Donald Beldock, Merck & Co Inc, Weill Med Coll Cornell Univ, Irving Weinstein Fdn ID PLASMA CAROTENOID CONCENTRATIONS; BETA-CAROTENE; ALPHA-TOCOPHEROL; ALCOHOL-CONSUMPTION; VITAMIN-C; RETINOL; WOMEN; SMOKING; DATABASE; LYCOPENE C1 NCI, Div Clin Sci, Canc Prevent Studies Branch, Bethesda, MD 20892 USA. Yunnan Tin Mine Corp, Labor Protect Inst, Gejiu, Yunnan, Peoples R China. NHANES, Lab Biochem Analyses, Ctr Dis Control & Prevent, Atlanta, GA USA. Univ Minnesota, Sch Publ Hlth, Dept Epidemiol, Minneapolis, MN USA. Chinese Acad Med Sci, Inst Canc, Dept Canc Epidemiol, Beijing 1000021, Peoples R China. NCI, Div Canc Epidemiol & Genet, Biostat Branch, Bethesda, MD 20892 USA. Informat Management Sci, Silver Spring, MD USA. RP Forman, MR (reprint author), NCI, Div Clin Sci, Canc Prevent Studies Branch, 6006 Execut Blvd,Suite 321,MSC 7058, Bethesda, MD 20892 USA. RI Qiao, You-Lin/B-4139-2012 OI Qiao, You-Lin/0000-0001-6380-0871 NR 35 TC 3 Z9 3 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 1-57331-198-7 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 889 BP 230 EP 239 DI 10.1111/j.1749-6632.1999.tb08739.x PG 10 WC Medicine, Research & Experimental; Multidisciplinary Sciences; Nutrition & Dietetics; Pharmacology & Pharmacy SC Research & Experimental Medicine; Science & Technology - Other Topics; Nutrition & Dietetics; Pharmacology & Pharmacy GA BP49R UT WOS:000085323100022 PM 10668498 ER PT J AU Miyake, K Mickley, L Litman, T Zhan, ZR Robey, R Cristensen, B Brangi, M Greenberger, L Dean, M Fojo, T Bates, SE AF Miyake, K Mickley, L Litman, T Zhan, ZR Robey, R Cristensen, B Brangi, M Greenberger, L Dean, M Fojo, T Bates, SE TI Molecular cloning of cDNAs which are highly overexpressed in mitoxantrone-resistant cells: Demonstration of homology to ABC transport genes SO CANCER RESEARCH LA English DT Article ID DROSOPHILA WHITE GENE; MULTIDRUG-RESISTANCE; RAT-LIVER; MEMBRANE; PROTEIN; GLYCOPROTEIN; EXPRESSION; ACID; LINE AB Reports of multiple distinct mitoxantrone-resistant sublines without overexpression of P-glycoprotein or the multidrug-resistance associated protein have raised the possibility of the existence of another major transporter conferring drug resistance, In the present study, a cDNA library from mitoxantrone-resistant S1-M1-80 human colon carcinoma cells was screened by differential hybridization, Two cDNAs of different lengths were isolated and designated MXR1 and MXR2. Sequencing revealed a high degree of homology for the cDNAs with Expressed Sequence Tag sequences previously identified as belonging to an ATP binding cassette transporter. Homology to the Drosophila white gene and its homologues was found for the predicted amino acid sequence, Using either cDNA as a probe in a Northern analysis demonstrated high levels of expression in the S1-M1-80 cells and in the human breast cancer subline, MCF-7 AdVp3000. Levels were lower in earlier steps of selection, and in partial revertants. The gene is amplified 10-12-fold in the MCF-7 AdVp3000 cells, but not in the S1-M1-80 cells, These studies are consistent with the identification of a new ATP binding cassette transporter, which is overexpressed in mitoxantrone-resistant cells. C1 NCI, Med Branch, NIH, Bethesda, MD 20892 USA. NCI, Frederick Canc Res & Dev Ctr, Lab Genom Divers, Frederick, MD 21702 USA. Wyeth Ayerst Pharmaceut, Pearl River, NY 10965 USA. RP Bates, SE (reprint author), NCI, Med Branch, NIH, Bldg 10,Room 12N226,9000 Rockville Pike, Bethesda, MD 20892 USA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 NR 19 TC 566 Z9 588 U1 1 U2 10 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1999 VL 59 IS 1 BP 8 EP 13 PG 6 WC Oncology SC Oncology GA 156AM UT WOS:000077979300003 PM 9892175 ER PT J AU Chappell, DB Zaks, TZ Rosenberg, SA Restifo, NP AF Chappell, DB Zaks, TZ Rosenberg, SA Restifo, NP TI Human melanoma cells do not express Fas (Apo-1/CD95) ligand SO CANCER RESEARCH LA English DT Article ID CONFER IMMUNE PRIVILEGE; CD95 LIGAND; IN-VIVO; T-CELLS AB A recent report described the expression of Fas ligand (FasL) by melanoma cells as an important mechanism involved in the immune evasion by tumors [M, Hahne et al., Science (Washington DC), 274: 1363-1366, 1996], To investigate the expression of Fast by melanomas, we screened a panel of early-passage cell lines by functional assay and reverse transcriptase-PCR. Using conditions designed to replicate those in the original report, we did not find functional Fast on any of the 19 human melanoma lines established at the National Cancer Institute. Furthermore, we additionally evaluated our melanoma lines using reverse transcriptase-PCR and found that 0 of the 26 human melanoma cell lines expressed Fast mRNA, Fast mRNA was abundantly expressed by antimelanoma T-cell lines after activation. These data do not support a role for Fast expression in the escape of melanoma cells from immune destruction. C1 NCI, Surg Branch, NIH, Bethesda, MD 20892 USA. Howard Hughes Med Inst, NIH, Res Scholars Program, Bethesda, MD 20814 USA. RP Restifo, NP (reprint author), NCI, Surg Branch, NIH, 10 Ctr Dr MSC 1502, Bethesda, MD 20892 USA. RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z01 BC010763-01, Z99 CA999999] NR 23 TC 110 Z9 111 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1999 VL 59 IS 1 BP 59 EP 62 PG 4 WC Oncology SC Oncology GA 156AM UT WOS:000077979300013 PM 9892185 ER PT J AU Zhu, WY Jones, CS Amin, S Matsukuma, K Haque, M Vuligonda, V Chandraratna, RAS De Luca, LM AF Zhu, WY Jones, CS Amin, S Matsukuma, K Haque, M Vuligonda, V Chandraratna, RAS De Luca, LM TI Retinoic acid increases tyrosine phosphorylation of focal adhesion kinase and paxillin in MCF-7 human breast cancer cells SO CANCER RESEARCH LA English DT Article ID SMOOTH-MUSCLE CELLS; SWISS 3T3 CELLS; GROWTH-FACTOR; CARCINOMA-CELLS; PROTEIN-KINASE; INHIBITION; RECEPTOR; DIFFERENTIATION; PROLIFERATION; EXPRESSION AB Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. In contrast, ER- MDA-MB-231 cells failed to respond. Western blot analysis showed that tyrosine phosphorylation of two major bands at M-r 125,000 and M-r 68,000 was induced by RA in ER+ MCF-7 human breast carcinoma cells. However, this induction was a late phenomenon detectable at 12 and 24 h, but not within 3 h, A similar increase of tyrosine phosphorylation by RA was observed in ER+ human breast cancer cell lines T-47D and ZR-75-1, but not in the ER- cell lines MDA-MB-231, MDA-MB-453, and MDA-MB-468. Focal adhesion kinase and paxillin, which localize in focal adhesion plaques and may play important roles in the integrin signaling pathway, were identified as the major proteins showing IU-induced tyrosine phosphorylation. The retinoid X receptor-selective compound SR11237 failed to induce tyrosine phosphorylation, indicating that retinoid X receptor activation is not involved in this phenomenon. In contrast, stable overexpression of a truncated RA receptor (RAR) alpha cDNA, RAR alpha 403, with strong RAR dominant negative activity prevented the increase in tyrosine phosphate, suggesting that RAR signaling is involved in RA-induced tyrosine phosphorylation. Tyrosine phosphorylation was induced the most by the RAR-alpha (193836), followed by RAR-gamma (194433), but was not significantly induced by RAR-beta (193174)-selective retinoids, This study demonstrates a coordinated albeit relatively late effect of RA on cell adhesion and tyrosine phosphorylation in ER+ human breast cancer cells and suggests RAR-alpha as the major responsible retinoid receptor. C1 NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bethesda, MD 20892 USA. RP De Luca, LM (reprint author), NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bldg 37,Room 3A-17,37 Convent Dr, Bethesda, MD 20892 USA. NR 43 TC 24 Z9 25 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1999 VL 59 IS 1 BP 85 EP 90 PG 6 WC Oncology SC Oncology GA 156AM UT WOS:000077979300018 PM 9892191 ER PT J AU Chen, SC Wang, XJ Xu, GP Zhou, L Vennerstrom, JL Gonzalez, F Gelboin, HV Mirvish, SS AF Chen, SC Wang, XJ Xu, GP Zhou, L Vennerstrom, JL Gonzalez, F Gelboin, HV Mirvish, SS TI Depentylation of [H-3-pentyl]methyl-n-amylnitrosamine by rat esophageal and liver microsomes and by rat and human cytochrome p450 isoforms SO CANCER RESEARCH LA English DT Article ID METHYL-N-AMYLNITROSAMINE; MONOCLONAL-ANTIBODIES; 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE NNK; COUMARIN 7-HYDROXYLASE; METABOLIC-ACTIVATION; DNA METHYLATION; NASAL-MUCOSA; HUMAN CYP2A6; DEALKYLATION; SPECIFICITY AB Methyl-n-amylnitrosamine (MNAN) induces esophageal cancer in rats, probably involving activation by cytochromes P450, We studied the metabolic depentylation of MNAN. [H-3-4,5-pentyl]MNAN and [H-3-2,3-pentyl]-MNAN were synthesized, purified, and incubated with rat esophageal microsomes (REM) or rat liver microsomes (RLM) to give [H-3]pentaldehyde (depentylation), an indicator of MNAN activation. [H-3]Pentaldehyde was determined by high-performance liquid chromatography of its 2,4-dinitrophenylhydrazone. Adding 5 mM semicarbazide to incubations increased the observed depentylation (except that due to CYP2E1) by >60%, MNAN depentylation by REM and uninduced and induced RLM showed K-m values of 64, 610, and 170-330 mu M, respectively (V-max: 20, 220, and 160-1270 pmol/mg protein/min, respectively). The depentylation of 100 mu M MNAN by REM was inhibited 98% by CO and 65% by coumarin preincubated for 15 min with REM (K-i, 120 mu M) but was unaffected by antibodies inhibitory to various P450s. MNAN inhibited coumarin 7-hydroxylation by RLM and CYP2A6 (K-i, 3000 and 320 mu M, respectively). REM showed slight coumarin 7-hydroxylase activity. MNAN depentylation by RLM was 41% inhibited by an antibody to CYP2C11. K-m for rat CYP2E1, human CYP2E1, and human CYP2A6 was 210, 115, and 17 mu M, respectively (V-max: 900, 570, and 120 pmol/nmol P450/min, respectively). We conclude that MNAN activation by REM is probably due to a P450 related to CYP2A3, a rodent nasal P450. C1 Univ Nebraska, Med Ctr, Eppley Inst Res Canc, Omaha, NE 68198 USA. Univ Nebraska, Med Ctr, Dept Pharmaceut Sci, Omaha, NE 68198 USA. Univ Nebraska, Med Ctr, Dept Biochem & Mol Biol, Omaha, NE 68198 USA. NCI, Bethesda, MD 20892 USA. RP Mirvish, SS (reprint author), Univ Nebraska, Med Ctr, Eppley Inst Res Canc, 600 S 42Nd St, Omaha, NE 68198 USA. FU NCI NIH HHS [R01-CA-35628, P30-CA-36727] NR 51 TC 23 Z9 23 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1999 VL 59 IS 1 BP 91 EP 98 PG 8 WC Oncology SC Oncology GA 156AM UT WOS:000077979300019 PM 9892192 ER PT J AU Macville, M Schrock, E Padilla-Nash, H Keck, C Ghadimi, BM Zimonjic, D Popescu, N Ried, T AF Macville, M Schrock, E Padilla-Nash, H Keck, C Ghadimi, BM Zimonjic, D Popescu, N Ried, T TI Comprehensive and definitive molecular cytogenetic characterization of HeLa cells by spectral karyotyping SO CANCER RESEARCH LA English DT Article ID COMPARATIVE GENOMIC HYBRIDIZATION; TUMOR-SUPPRESSOR GENE; CERVICAL-CARCINOMA; INSITU HYBRIDIZATION; HUMAN CHROMOSOME-11; INTEGRATION SITES; FHIT GENE; DNA; IDENTIFICATION; LOCALIZATION AB We revisited the cytogenetic alterations of the cervical adenocarcinoma cell Line HeLa through the use of spectral karyotyping (SKY), comparative genomic hybridization (CGH), and fluorescence in situ hybridization (FISH), SKY analysis unequivocally characterized all abnormal chromosomes. Chromosomal breakpoints were primarily assigned by simultaneous assessment of SKY painted chromosomes and inverted il,4,6-diamidino-2-phenylindole banding from the same cell. Twenty clonally abnormal chromosomes were found. Comparison with previously reported HeLa G-banding karyotypes revealed a remarkably stable cytogenetic constitution because 18 of 20 markers that were found were present before. The classification of 12 markers was refined in this study. Our assignment of the remaining six markers was consistent with those described in the literature, The CGH map of chromosomal copy number gains and losses strikingly matched the SKY results and was, in a few instances, decisive for assigning breakpoints. The combined use of molecular cytogenetic methods SKY, CGH, and FISH with site-specific probes, in addition to inverted 4,6-diamidino-2-phenylindole or conventional G-banding analysis, provides the means to fully assess the genomic abnormalities in cancer cells. Human papillomaviruses (HPVs) are frequently integrated into the cellular DNA in cervical cancers, We mapped by FISH five HPV18 integration sites: three on normal chromosomes 8 at 8q24 and two on derivative chromosomes, der(5)t(5;22;8)(q11;q11q13;q24) and der(22)t(8; 22)(q24;q13), which have chromosome 8q24 material. An 8q24 copy number increase was detected by CGH, Dual-color FISH with a c-MYC probe mapping to 8q24 revealed colocalization with HPV18 at all integration sites, indicating that dispersion and amplification of the c-MYC gene sequences occurred after and was most likely triggered by the viral insertion at a single integration site. Numerical and structural chromosomal aberrations identified by SKY, genomic imbalances detected by CGH, as well as FISH localization of HPV18 integration at the c-MYC locus in HeLa cells are common and representative for advanced stage cervical cell carcinomas. The HeLa genome has been remarkably stable after years of continuous cultivation; therefore, the genetic alterations detected may have been present in the primary tumor and reflect events that are relevant to the development of cervical cancer. C1 Natl Human Genome Res Inst, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. RP Ried, T (reprint author), Natl Human Genome Res Inst, Genome Technol Branch, NIH, NIH Bldg 49,Room 4A28,49 Convent Dr, Bethesda, MD 20892 USA. NR 37 TC 181 Z9 186 U1 2 U2 22 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1999 VL 59 IS 1 BP 141 EP 150 PG 10 WC Oncology SC Oncology GA 156AM UT WOS:000077979300026 PM 9892199 ER PT J AU Wu, PC Alexander, HR Huang, J Hwu, P Gnant, M Berger, AC Turner, E Wilson, O Libutti, SK AF Wu, PC Alexander, HR Huang, J Hwu, P Gnant, M Berger, AC Turner, E Wilson, O Libutti, SK TI In vivo sensitivity of human melanoma to tumor necrosis factor (TNF)-alpha, is determined by tumor production of the novel cytokine endothelial-monocyte activating polypeptide II (EMAPII) SO CANCER RESEARCH LA English DT Article ID ISOLATED LIMB PERFUSION; TISSUE FACTOR; ANGIOGENIC SWITCH; FACTOR CACHECTIN; GROWTH-FACTOR; FACTOR-ALPHA; CELLS; EXPRESSION; MECHANISMS; MELPHALAN AB Tumor necrosis factor (TNF)-alpha is a potent anticancer agent that seems to selectively target tumor-associated vasculature resulting in hemorrhagic necrosis of tumors without injury to surrounding tissues. The major limitation in the clinical use of TNF has been severe dose-limiting toxicity when administered systemically, However, when administered in isolated organ perfusion it results in regression of advanced bulky tumors. A better understanding of the mechanisms of TNF-induced antitumor effects may provide valuable information into how its clinical use in cancer treatment may be expanded. We describe here that the release of a novel tumor-derived cytokine endothelial-monocyte-activating polypeptide II (EMAPII) renders the tumor-associated vasculature sensitive to TNF, EMAPII has the unique ability to induce tissue factor production by tumor vascular endothelial cells that initiates thrombogenic cascades, which may play a role in determining tumor sensitivity to TNF, We demonstrate here that constituitive overexpression of EMAPII in a TNF-resistant human melanoma line by retroviral-mediated transfer of EMAPII cDNA renders the tumor sensitive to the effects of systemic TNF in vivo, but not in vitro. This interaction between tumors and their associated neovasculature provides an explanation for the focal effects of TNF on tumors and possibly for the variable sensitivity of tumors to bioactive agents. C1 NCI, Surg Metab Sect, Surg Branch, NIH, Bethesda, MD 20892 USA. NIH, Ctr Clin, Hematol Sect, Bethesda, MD 20892 USA. RP Libutti, SK (reprint author), NCI, Surg Metab Sect, Surg Branch, NIH, Bldg 10,Room 2B17,10 Ctr Dr MSC 1502, Bethesda, MD 20892 USA. OI Gnant, Michael/0000-0003-1002-2118 NR 29 TC 47 Z9 50 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1999 VL 59 IS 1 BP 205 EP 212 PG 8 WC Oncology SC Oncology GA 156AM UT WOS:000077979300035 PM 9892208 ER PT J AU Boland, CR Thibodeau, SN Hamilton, SR Sidransky, D Burt, RW Meltzer, SJ Rodriguez-Bigas, MA Fodde, R Ranzani, GN Srivastava, S AF Boland, CR Thibodeau, SN Hamilton, SR Sidransky, D Burt, RW Meltzer, SJ Rodriguez-Bigas, MA Fodde, R Ranzani, GN Srivastava, S TI Correspondence re: C. R. Boland et al., a National Cancer Institute Workshop on Microsatellite Instability for Cancer Detection and Familial Predisposition: Development of International Criteria for the Determination of Microsatellite Instability in Colorectal Cancer. Cancer Res., 58 : 5248-5257, 1998. Reply SO CANCER RESEARCH LA English DT Letter ID GERMLINE MUTATIONS; GENE; PTEN; HETEROZYGOSITY; CARCINOMAS; EXPRESSION; FREQUENT; RECEPTOR; TUMORS; BREAST C1 Univ Calif La Jolla, La Jolla, CA 92093 USA. Mayo Clin, Rochester, MN 55905 USA. Univ Texas, Md Anderson Canc Ctr, Houston, TX 77030 USA. Johns Hopkins Univ, Baltimore, MD 21205 USA. Univ Utah, Hlth Sci Ctr, Salt Lake City, UT 84132 USA. Univ Maryland Hosp, Baltimore, MD 21201 USA. New York State Dept Hlth, Roswell Pk Canc Inst, Buffalo, NY 14263 USA. Leiden Univ, NL-2333 AL Leiden, Netherlands. Univ Pavia, I-27100 Pavia, Italy. NCI, Bethesda, MD 20892 USA. RP Boland, CR (reprint author), Univ Calif La Jolla, La Jolla, CA 92093 USA. NR 23 TC 0 Z9 0 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 1999 VL 59 IS 1 BP 254 EP 255 PG 2 WC Oncology SC Oncology GA 156AM UT WOS:000077979300042 ER PT J AU Phillips, AC Vousden, KH AF Phillips, AC Vousden, KH TI Human papillomavirus and cancer: The viral transforming genes SO CANCER SURVEYS LA English DT Review ID TUMOR-SUPPRESSOR GENE; TYPE-16 E7 ONCOPROTEIN; E1A-ASSOCIATED PROTEIN P300; CYCLIN-DEPENDENT KINASES; CARCINOMA CELL-LINES; BOX-BINDING PROTEIN; RETINOBLASTOMA PROTEIN; HUMAN KERATINOCYTES; CERVICAL-CARCINOMA; E6 ONCOPROTEIN C1 NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA. RP Phillips, AC (reprint author), NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Bldg 560,Room 22-96,W 7th St, Frederick, MD 21702 USA. NR 103 TC 9 Z9 9 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1999 VL 33 BP 55 EP 74 PG 20 WC Oncology SC Oncology GA 190QB UT WOS:000079974500005 ER PT J AU Sanders, S Thorgeirsson, SS AF Sanders, S Thorgeirsson, SS TI Phenobarbital promotes liver growth in c-myc/TGF-alpha transgenic mice by inducing hypertrophy and inhibiting apoptosis SO CARCINOGENESIS LA English DT Article ID HEPATIC TUMOR PROMOTERS; NF-KAPPA-B; CELL-DEATH; RAT HEPATOCYTES; TGF-ALPHA; NEOPLASTIC DEVELOPMENT; MAMMARY TUMORIGENESIS; SIGNAL-TRANSDUCTION; BCL-2 PROTEIN; DNA-SYNTHESIS AB Phenobarbital (PB) is a non-genotoxic liver tumor promoter used extensively in initiation-promotion protocols. To determine the mode of PB action, double transgenic mice overexpressing both the c-myc and transforming growth factor (TGF)-alpha genes were treated with PB in the food for 10 weeks, from 3 weeks of age. After 3-4 weeks on PB a peak in liver mass was noted, which subsequently leveled off at a value similar to 30% above untreated animals. The mitotic index in mice given PB peaked at 1 week of treatment and was significantly elevated compared with untreated animals. No significant difference between treated and untreated animals was seen thereafter, although a trend of PB-associated mitotic suppression was noticeable. The apoptotic index also showed a trend of suppression compared with untreated animals, significant after prolonged PB administration. Dysplastic hepatocytes were more prominent in PB-treated mice than untreated animals, particularly pericentrally. Removal of PB from the diet at 4 weeks of treatment led to a dramatic increase in apoptosis. This accompanied a drop in the liver mass to the level of untreated controls by 10 days. Throughout the study, PB-treated animals showed markedly lower levels of TGF-beta 1 ligand, coincident with an elevated level of the anti-apoptotic protein Bcl-2. On withdrawal of PB, the levels of all these proteins rapidly changed to mirror those seen in untreated mice. In all treatment groups, no change in the levels of epidermal growth factor receptor, TGF-beta receptors I and II or Bcl-x(S/L) were seen. We conclude from our data that PB stimulates liver growth in double transgenic c-myc/TGF-alpha mice by induction of liver hypertrophy and inhibition of apoptosis, brought about by both a decrease in signaling through the TGF-beta pathway and an increase in Bcl-2. The data support the hypothesis that PB promotes neoplastic development through a reduction in the incidence of cell death. C1 NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. RP Thorgeirsson, SS (reprint author), NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. NR 62 TC 25 Z9 25 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1999 VL 20 IS 1 BP 41 EP 49 DI 10.1093/carcin/20.1.41 PG 9 WC Oncology SC Oncology GA 158RH UT WOS:000078129600006 PM 9934848 ER PT J AU Waalkes, MP Diwan, BA AF Waalkes, MP Diwan, BA TI Cadmium-induced inhibition of the growth and metastasis of human lung carcinoma xenografts: role of apoptosis SO CARCINOGENESIS LA English DT Article ID SUBRENAL CAPSULE ASSAY; RENAL-CELL CARCINOMA; B6C3F1 MOUSE-LIVER; BLADDER-CANCER; MESSENGER-RNA; TUMOR-GROWTH; NUDE-MICE; METALLOTHIONEIN; BCL-2; EXPRESSION AB Our previous studies indicate that cadmium in mice can inhibit the formation of chemically induced and spontaneously occurring tumors in the liver and lung. Cadmium is an effective anti-tumor agent when given at non-toxic doses and even when given well after tumor formation, implying a unique sensitivity in certain tumor cells. The present studies tested the ability of cadmium to inhibit growth and progression of transplanted human pulmonary tumor xenografts. Male athymic nude mice were inoculated with either H460 cells, originally derived from a non-small cell pulmonary carcinoma, or DMS 114 cells, originally derived from a small cell lung carcinoma, under the left renal capsule. Starting 1 week later mice received 0, 125 or 250 p.p.m. cadmium in the drinking water, levels without effect on host animal growth or survival, and were observed over the next 4 weeks (H460 cells) or 100 days (DMS 114 cells). An additional experiment gave cadmium as an i.v. loading dose (20 mu mol/kg) 4 days after renal inoculation with H460 cells and 200 p.p.m. cadmium in the drinking water from 7 days onward, with an observation period of 28 days. Cadmium caused dose-related reductions in the growth of tumors resulting from the inoculation of either H460 or DMS 114 cells of up to 83 %. Additionally, cadmium reduced the rate of tumor metastasis to the lung by up to 58%. Cadmium treatment had no effects on either Bcl-2 or Bar protein expression in tumor xenografts, indicating that apoptotic pathways probably do not contribute to this anti-neoplastic effect. These studies show cadmium can effectively reduce growth and progression of human lung carcinoma xenografts in a fashion that is probably independent of apoptosis. C1 NIEHS, Inorgan Carcinogensis Sect, Comparat Carcinogenesis Lab, NCI, Res Triangle Pk, NC 27709 USA. SAIC Frederick, Intramural Res Support Program, Frederick, MD 21702 USA. RP Waalkes, MP (reprint author), NIEHS, Inorgan Carcinogensis Sect, Comparat Carcinogenesis Lab, NCI, 111 Alexander Dr,POB 12233,MD F0-09, Res Triangle Pk, NC 27709 USA. EM waalkes@niehs.nih.gov NR 48 TC 28 Z9 29 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1999 VL 20 IS 1 BP 65 EP 70 DI 10.1093/carcin/20.1.65 PG 6 WC Oncology SC Oncology GA 158RH UT WOS:000078129600009 PM 9934851 ER PT J AU Rodriguez-Burford, C Lubet, RA Eto, I Juliana, MM Kelloff, GJ Grubbs, CJ Steele, VE AF Rodriguez-Burford, C Lubet, RA Eto, I Juliana, MM Kelloff, GJ Grubbs, CJ Steele, VE TI Effect of reduced body weight gain on the evaluation of chemopreventive agents in the methylnitrosourea-induced mammary cancer model SO CARCINOGENESIS LA English DT Article ID CHEMICALLY-INDUCED MAMMARY; CALORIC RESTRICTION; DIETARY RESTRICTION; TUMOR PROMOTION; RETINYL ACETATE; GROWTH-FACTOR; RATS; CARCINOGENESIS; FAT; INHIBITION AB These studies examined whether the small to moderate reductions in body weight gain (less than or equal to 15%) affect mammary carcinogenesis. Beginning 1 week prior to methylnitrosourea (MNU) administration (experiment 1), rats received diets supplemented with 4-hydroxyphenylretinamide (4-HPR) (782 mg/kg of diet) and retinyl acetate (328 mg/kg of diet) or underwent food restrictions. Rats were administered an i.v. dose of MNU (50 mg/kg body wt) at 50 days of age. Although the final body weights were similarly depressed by 4-HPR (8%) and by retinyl acetate (11%) from rats fed ad libitum, the kinetics of inhibition were quite different. Whereas 4-HPR caused an acute decrease in body weight at the time it was administered, the effect of retinyl acetate was more chronic. At 110 days after the administration of MNU, the average number of mammary cancers per rat was 4.9 for rats fed ad libitum, 1.3 for rats fed 4-HPR, 3.1 when body weights were matched to 4-HPR-treated rats, 1.9 for retinyl acetate and 3.2 when body weights were matched to retinyl acetate, Experiment II was performed to determine the minimal degree of acute body weight gain reduction that would alter MNU-induced mammary carcinogenesis. Body weight gain depressions of 3, 6, 9, 12 and 15% were initiated at 43 days of age by dietary restrictions and MNU was administered at 50 days of age. At 120 days after MNU, the percentage decreases in mammary cancer multiplicity in the various groups were 14, 15, 41, 44 and 55%, respectively. These data demonstrate that moderate reductions (9-15%) in body weight gain, in particular when occurring during the initiation and early promotion stages can greatly affect cancer multiplicity. C1 Univ Alabama, Chemoprevent Ctr, Birmingham, AL 35294 USA. NCI, Div Canc Prevent, Bethesda, MD 20892 USA. Univ Florida, Dept Comparat & Expt Pathol, Gainesville, FL 32610 USA. RP Grubbs, CJ (reprint author), Univ Alabama, Chemoprevent Ctr, 1675 Univ Blvd, Birmingham, AL 35294 USA. FU NCI NIH HHS [N01-CN-55148-MAO, N01-CN-25454-04] NR 32 TC 17 Z9 17 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1999 VL 20 IS 1 BP 71 EP 76 DI 10.1093/carcin/20.1.71 PG 6 WC Oncology SC Oncology GA 158RH UT WOS:000078129600010 PM 9934852 ER PT J AU Dantzer, F Menissier-de Murcia, J Barlow, C Wynshaw-Boris, A de Murcia, G AF Dantzer, F Menissier-de Murcia, J Barlow, C Wynshaw-Boris, A de Murcia, G TI Poly(ADP-ribose) polymerase activity is not affected in ataxia telangiectasia cells and knockout mice SO CARCINOGENESIS LA English DT Article ID STRAND BREAKS; GENE; PRODUCT; KINASE; REPAIR AB Poly(ADP-ribose) polymerase (PARP) is a constitutive factor of the DNA damage surveillance network in dividing cells, Based on its capacity to bind to DNA strand breaks, PARP plays a regulatory role in their resolution in vivo. ATM belongs to a large family of proteins involved in cell cycle progression and checkpoints in response to DNA damage. Both proteins may act as sensors of DNA damage to induce multiple signalling pathways leading to activation of cell cycle checkpoints and DNA repair. To determine a possible relationship between PARP and ATM, we examined the PARP response in an ATM-null background. We demonstrated that ATM deficiency does not affect PARP activity in human cell lines or Atm-deficient mouse tissues, nor does it alter PARP activity induced by oxidative damage or gamma-irradiation, Our results support a model in which PARP and ATM could be involved in distinct pathways, both effecters transducing the damage signal to cell cycle regulators. C1 Ecole Super Biotechnol Strasbourg, CEA, Lab Conventionne Avec, CNRS,Unite 9003, F-67400 Illkirch Graffenstaden, France. Natl Human Genome Res Inst, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA. RP de Murcia, G (reprint author), Ecole Super Biotechnol Strasbourg, CEA, Lab Conventionne Avec, CNRS,Unite 9003, Blvd Sebastien Brant, F-67400 Illkirch Graffenstaden, France. RI Dantzer, Francoise/O-2126-2016 NR 19 TC 10 Z9 10 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 1999 VL 20 IS 1 BP 177 EP 180 DI 10.1093/carcin/20.1.177 PG 4 WC Oncology SC Oncology GA 158RH UT WOS:000078129600025 PM 9934867 ER PT J AU Nagai, Y Earley, CJ Kemper, MK Bacal, CS Metter, EJ AF Nagai, Y Earley, CJ Kemper, MK Bacal, CS Metter, EJ TI Influence of age and postmenopausal estrogen replacement therapy on carotid arterial stiffness in women SO CARDIOVASCULAR RESEARCH LA English DT Article DE arteries; aging; gender; hormones; ultrasound ID TREATED HYPERTENSIVE PATIENTS; AORTIC DISTENSIBILITY; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION; ELASTIC PROPERTIES; SYSTEMIC ARTERIES; FOLLOW-UP; ATHEROSCLEROSIS; YOUNG; RISK AB Objective: This study examines the influence of age and current estrogen replacement therapy (ERT) on common carotid arterial (CCA) stiffness in women. Methods: The subjects comprised 172 women (age 55.6+/-16.4 years) from the Baltimore Longitudinal Study of Aging, including 37 current postmenopausal ERT users. The ERT users included 18 women taking estrogen alone and 19 women taking estrogen and progesterone. Bilateral CCA were examined by B-mode carotid ultrasonography, and the stiffness index was defined as the logarithm of the ratio of systolic to diastolic blood pressure (BP) divided by the fractional diameter increase during the cardiac cycle. Results: The stiffness index increased linearly with age (r=0.69, p<0.001), and was lower in ERT users than in postmenopausal nonusers (8.0+/-2.0 vs 9.7+/-3.1, p<0.01). Furthermore, the effects of age (beta=0.67, p<0.0001) and ERT (beta=-0.23, p<0.001) on the stiffness index persisted after adjustments for systolic BP (beta=0.23, p<0.01), diastolic BP (beta=-0.26, p<0.001) and other cardiovascular risk factors (model r(2)=0.59, p<0.0001). The stiffness index was similar in both ERT users with and without progesterone and lower than in postmenopausal nonusers (p<0.05) after considering the age effects. Conclusion: Age-associated increases in CCA stiffness are reduced by postmenopausal ERT. (C) 1999 Elsevier Science B.V. All rights reserved. C1 NIA, Gerontol Res Ctr, NIH, Longitudinal Studies Sect, Baltimore, MD 21224 USA. Johns Hopkins Univ, Bayview Med Ctr, Dept Neurol, Baltimore, MD 21224 USA. Johns Hopkins Univ, Bayview Med Ctr, Dept Med, Baltimore, MD 21224 USA. RP Metter, EJ (reprint author), NIA, Gerontol Res Ctr, NIH, Longitudinal Studies Sect, Box 06,5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 32 TC 48 Z9 48 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6363 J9 CARDIOVASC RES JI Cardiovasc. Res. PD JAN PY 1999 VL 41 IS 1 BP 307 EP 311 DI 10.1016/S0008-6363(98)00219-3 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 158YN UT WOS:000078145200036 PM 10325979 ER PT J AU Teng, CT AF Teng, CT TI Regulation of lactoferrin gene expression by estrogen and epidermal growth factor - Molecular mechanism SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE lactoferrin gene promoter; estrogen; epidermal growth factor (EGF); response elements ID REPRODUCTIVE-TRACT; MOUSE UTERUS; COUP-TF; PREIMPLANTATION PERIOD; TRANSCRIPTION FACTOR; PROMOTER; RECEPTOR; ACTIVATION; ELEMENTS; DIFFERENTIATION AB Lactoferrin (LF) is a member of the transferrin gene family. Its expression in the mouse uterus is regulated by estrogen and epidermal growth factor (EGF). The author et al. cloned the LF gene promoter/enhancer region, and demonstrated that multihormone signaling pathways are involved in modulating LF gene activity. Three short but complex modules, within 400 bp from the transcription initiation site of the mouse LF gene, contain the response elements that are responsible for estrogen, retinoic acid, mitogen, and growth factor stimulation. These elements have been identified and characterized, using reporter constructs transiently transfected into human endometrial carcinoma RL95-2 cells. The author et al. used molecular approaches, such as deletion, insertion, and site-directed mutagenesis, to determine the relationship between the response elements, and to fine-map the crucial nucleotides within them. This article reviews the characterization of the estrogen and EGF response elements of the mouse LF gene promoter. C1 NIEHS, Gene Regulat Grp, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA. RP Teng, CT (reprint author), NIEHS, Gene Regulat Grp, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA. EM Teng@niehs.nih.gov NR 66 TC 29 Z9 29 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1085-9195 J9 CELL BIOCHEM BIOPHYS JI Cell Biochem. Biophys. PY 1999 VL 31 IS 1 BP 49 EP 64 DI 10.1007/BF02738154 PG 16 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 282ZJ UT WOS:000085251400003 PM 10505667 ER PT J AU Sweet, DH Pritchard, AB AF Sweet, DH Pritchard, AB TI The molecular biology of renal organic anion and organic cation transporters SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE kidney; liver; transport; organic anion; organic cation; expression cloning ID BRUSH-BORDER MEMBRANES; AMINO-ACID-SEQUENCE; FUNCTIONAL-CHARACTERIZATION; EXPRESSION CLONING; RAT-KIDNEY; INTRACELLULAR COMPARTMENTATION; APICAL MEMBRANE; PROXIMAL TUBULE; CDNA CLONING; HUMAN LIVER C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. RP Sweet, DH (reprint author), NIEHS, Lab Pharmacol & Chem, POB 12233, Res Triangle Pk, NC 27709 USA. RI Sweet, Douglas/H-7914-2013 OI Sweet, Douglas/0000-0002-8911-9184 NR 77 TC 55 Z9 55 U1 0 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1085-9195 J9 CELL BIOCHEM BIOPHYS JI Cell Biochem. Biophys. PY 1999 VL 31 IS 1 BP 89 EP 118 DI 10.1007/BF02738157 PG 30 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 282ZJ UT WOS:000085251400006 PM 10505670 ER PT J AU Baumann, CT Lim, CS Hager, GL AF Baumann, CT Lim, CS Hager, GL TI Intracellular localization and trafficking of steroid receptors SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID HUMAN ANDROGEN RECEPTOR; GLUCOCORTICOID-RECEPTOR; PROGESTERONE-RECEPTOR; LIVING CELLS; MINERALOCORTICOID RECEPTOR; NUCLEAR-LOCALIZATION; ESTROGEN-RECEPTOR; TRANSCRIPTIONAL ACTIVATION; TARGET-CELLS; PROTEIN C1 NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA. RP Hager, GL (reprint author), NCI, Lab Receptor Biol & Gene Express, Bldg 41,Room B602, Bethesda, MD 20892 USA. NR 47 TC 35 Z9 36 U1 0 U2 2 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1085-9195 J9 CELL BIOCHEM BIOPHYS JI Cell Biochem. Biophys. PY 1999 VL 31 IS 2 BP 119 EP 127 DI 10.1007/BF02738167 PG 9 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 282ZK UT WOS:000085251500001 PM 10593254 ER PT J AU Kumar, S Ma, BY Tsai, CJ Wolfson, H Nussinov, R AF Kumar, S Ma, BY Tsai, CJ Wolfson, H Nussinov, R TI Folding funnels and conformational transitions via hinge-bending motions SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article DE hinge-bending; lock-and-key vs induced-fit; conformational ensembles; binding; folding ID YEAST PHOSPHOGLYCERATE KINASE; NORMAL-MODE ANALYSIS; CRYSTAL-STRUCTURE; TRIOSEPHOSPHATE ISOMERASE; TRIGLYCERIDE LIPASE; ADENYLATE KINASE; DOMAIN MOTIONS; FUNCTIONAL COMPLEMENTATION; 3-DIMENSIONAL STRUCTURES; ENGINEERED FRAGMENTS AB In this article we focus on presenting a broad range of examples illustrating low-energy transitions via hinge-bending motions. The examples are divided according to the type of hinge-bending involved; namely, motions involving fragments of the protein chains, hinge-bending motions involving protein domains, and hinge-bending motions between the covalently unconnected subunits. We further make a distinction between allosterically and nonallosterically regulated proteins. These transitions are discussed within the general framework of folding and binding funnels. We propose that the conformers manifesting such swiveling motions are not the outcome of "induced fit" binding mechanism; instead, molecules exist in an ensemble of conformations that are in equilibrium in solution. These ensembles, which populate the bottoms of the funnels, a priori contain both the "open" and the "closed" conformational isomers. Furthermore, we argue that there are no fundamental differences among the physical principles behind the folding and binding funnels. Hence, there is no basic difference between funnels depicting ensembles of conformers of single molecules with fragment, or domain motions, as compared to subunits in multimeric quaternary structures, also showing such conformational transitions. The difference relates only to the size and complexity of the system. The larger the system, the more complex its corresponding fused funnel(s). in particular, funnels associated with allosterically regulated proteins are expected to be more complicated, because allostery is frequently involved with movements between subunits, and consequently is often observed in multichain and multimolecular complexes. This review centers on the critical role played by flexibility and conformational fluctuations in enzyme activity. Internal motions that extend over different time scales and with different amplitudes are known to be essential for the catalytic cycle. The conformational change observed in enzyme-substrate complexes as compared to the unbound enzyme state, and in particular the hinge-bending motions observed in enzymes with two domains, have a substantial effect on the enzymatic catalytic activity. The examples we review span the lipolytic enzymes that are particularly interesting, owing to their activation at the water-oil interface; an allosterically controlled dehydrogenase (lactate dehydrogenase); a DNA methyltransferase, with a covalently-bound intermediate; large-scale flexible loop motions in a glycolytic enzyme (TIM); domain motion in PGK, an enzyme which is essential in most cells, both for Am generation in aerobes and for fermentation in anaerobes; adenylate kinase, showing large conformational changes, owing to their need to shield their catalytic centers from water; a calcium-binding protein (calmodulin), involved in a wide range of cellular calcium-dependent signaling; diphtheria toxin, whose large domain motion has been shown to yield "domain swapping;" the hexameric glutamate dehydrogenase, which has been studied both in a thermophile and in a mesophile; an allosteric enzyme, showing subunit motion between the R and the T states (aspartate transcarbamoylase), and the historically well-studied lac represoor. Nonallosteric subunit transitions are also addressed, with some examples (aspartate receptor and BamHI endonuclease). Hence, using this enzyme-catalysis-centered discussion, we address energy funnel landscapes of large-scale conformational transitions, rather than the faster, quasi-harmonic, thermal fluctuations. C1 NCI, Frederick Canc Res & Dev Ctr, Lab Expt & Computat Biol, SAIC,Intramural Res Support Program, Frederick, MD 21702 USA. Tel Aviv Univ, Comp Sci Sch Math Sci, IL-69978 Tel Aviv, Israel. Tel Aviv Univ, Sackler Fac Med, Sackler Inst Mol Med, IL-69978 Tel Aviv, Israel. RP Nussinov, R (reprint author), NCI, Frederick Canc Res & Dev Ctr, Lab Expt & Computat Biol, SAIC,Intramural Res Support Program, Frederick, MD 21702 USA. RI Wolfson, Haim/A-1837-2011; Ma, Buyong/F-9491-2011 OI Ma, Buyong/0000-0002-7383-719X FU NCI NIH HHS [N01-CO-56000] NR 72 TC 45 Z9 47 U1 1 U2 6 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1085-9195 J9 CELL BIOCHEM BIOPHYS JI Cell Biochem. Biophys. PY 1999 VL 31 IS 2 BP 141 EP 164 DI 10.1007/BF02738169 PG 24 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 282ZK UT WOS:000085251500003 PM 10593256 ER PT J AU Jones, S Yakel, JL AF Jones, S Yakel, JL TI Inhibitory interneurons in hippocampus - Sites for rapid regulation of information flow by neurotransmitters SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID NICOTINIC ACETYLCHOLINE-RECEPTORS; LACUNOSUM-MOLECULARE INTERNEURONS; CIRCUIT SYNAPTIC-INTERACTIONS; LONG-TERM POTENTIATION; GUINEA-PIG HIPPOCAMPUS; FREELY MOVING RAT; DENTATE GYRUS; PYRAMIDAL CELLS; CA1 REGION; 5-HT3 RECEPTORS C1 NIEHS, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA. RP Yakel, JL (reprint author), NIEHS, Lab Signal Transduct, POB 12233, Res Triangle Pk, NC 27709 USA. NR 80 TC 5 Z9 5 U1 0 U2 0 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 1085-9195 J9 CELL BIOCHEM BIOPHYS JI Cell Biochem. Biophys. PY 1999 VL 31 IS 2 BP 207 EP 218 DI 10.1007/BF02738173 PG 12 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 282ZK UT WOS:000085251500007 PM 10593260 ER PT J AU Kalinec, F Kalinec, G Boukhvalova, M Kachar, B AF Kalinec, F Kalinec, G Boukhvalova, M Kachar, B TI Establishment and characterization of conditionally immortalized organ of Corti cell lines SO CELL BIOLOGY INTERNATIONAL LA English DT Article DE cochlea; organ of Corti; cell lines; transgenic mice; Immortomouse ID NEURAL STEM-CELLS; AVIAN INNER-EAR; HAIR-CELLS; SUPPORTING CELL; ACOUSTIC TRAUMA; REGENERATIVE PROLIFERATION; TRANSGENIC MOUSE; BASILAR PAPILLA; NERVOUS-SYSTEM; GERBIL COCHLEA AB A culture of cells was isolated from the organ of Corti of 2-week-old H-2Kb-tsA58 (Immortomouse) transgenic mice. All cells of these mice harbor a mutant of the simian virus 40 A-gene, encoding a thermolabile large T-antigen (Tag) protein. At 33 degrees C the Tag protein is functional and induces cell proliferation, but at 39 degrees C it is rapidly denatured and inactivated. Isolated organ of Corti cells growing at 33 degrees C were predominantly small, rounded or fusiform and proliferated rapidly. When moved to 39 degrees C, the cells reduced their rate of proliferation and differentiated into specific morphological phenotypes; Four cell lines were cloned by limiting dilution and characterized by immunofluorescence microscopy and Western blot. The cell lines, named OC-k1, OC-k2, OC-k3 and OC-k4, have been passaged at least 50 times with retention of a stable phenotype. These cell lines were all positive for the neuroepithelial precursor cell marker nestin and for the inner ear cell marker OCP2. In addition, the cells showed reactivity to epithelial and neuronal cell markers, but with a pattern of protein expression different for each clone and different between cells of the same clone growing at 33 degrees C or 39 degrees C. Some of the clones exhibited asymmetric cell division which is a characteristic commonly ascribed to stem cells. These cell lines can be used advantageously to study mechanisms and signals involved in the control of cell differentiation and morphogenesis of the mammalian inner ear and to isolate inner ear specific proteins. (C) 1999 Academic Press. C1 House Ear Inst, Dept Cell & Mol Biol, Sect Cell Struct & Funct, Los Angeles, CA 90057 USA. Natl Inst Deafness & Other Commun Disorders, Lab Cellular Biol, Sect Struct Cell Biol, NIH, Rockville, MD 20850 USA. RP Kachar, B (reprint author), NIDCD, Sect Struct Cell Biol, NIH, Bldg 36,Rm 5D-15, Bethesda, MD 20892 USA. NR 37 TC 39 Z9 44 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 1065-6995 J9 CELL BIOL INT JI Cell Biol. Int. PY 1999 VL 23 IS 3 BP 175 EP 184 DI 10.1006/cbir.1998.0339 PG 10 WC Cell Biology SC Cell Biology GA 253PB UT WOS:000083564000003 PM 10562438 ER PT J AU Halverson, DO Resau, J Faletto, D Fisher, R Anver, M Rong, S May, JA Tsarfaty, I Blair, DG AF Halverson, DO Resau, J Faletto, D Fisher, R Anver, M Rong, S May, JA Tsarfaty, I Blair, DG TI A mouse fibroblast line cycles between monolayer and spheroid forms, regulates Met and HGF expression, and releases an attachment and growth-promoting substance SO CELL BIOLOGY INTERNATIONAL LA English DT Article DE NIH3T3 fibroblast; attachment factor; met; SF-HGF factor ID HUMAN BREAST-CARCINOMA; MULTICELLULAR TUMOR SPHEROIDS; SCATTER FACTOR-RECEPTOR; SHED MEMBRANE-VESICLES; EPITHELIAL-CELL LINES; SERUM-FREE MEDIUM; IN-VITRO; FIBROSARCOMA CELLS; RAT HEPATOCYTES; LUMEN FORMATION AB A subline of mesoderm-derived mouse NIH3T3 fibroblasts was selected for its ability to proliferate in serum-free media. This cell line (SFDH) grows as a monolayer at low density and spontaneously forms dense, multicellular spheroids at high density. Spheroid formation can also be induced by the addition of dexamethasone, polybrene, or heparin. Spheroids eventually detach from the substrate, but will reattach and re-form monolayers when transferred to fresh culture vessels and media, repeating the cycle again upon reaching high density. Thin section analysis of spheroids shows morphologically-distinct regions of cells, including an attenuated outer surface and a cuboidal interior with occasional lumen-like areas. Over time in culture, spheroids express increasing levels of met, the Met ligand-SF/HGF and cytokeratin, an epithelial marker, in comparison to monolayers. Both monolayer and spheroid-derived cells are rapidly tumorigenic in nude mice. Media conditioned by SFDH cells contain factors that stimulate growth and attachment of a variety of tumorigenic and non-tumorigenic cell lines, inducing cells to divide in serum-free media for up to 14 days when plated on tissue culture-treated and nontreated plastic surfaces pre-coated with SFDH conditional media. The growth-stimulating activity fractionates as a single peak over a sepharose column in the presence of 6 M urea, and sediments as a high molecular weight complex. Growth-stimulating activity can be neutralized by several antisera specific for hepatocyte growth factor, and the same sera recognize a novel similar to 37 kD protein in active supernatants. The cyclic, continuous nature of alternating monolayer and spheroid forms makes this cell line appropriate for studying changing gene expression patterns in progressive cell-cell/cell-matrix interactions. C1 NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, SAIC Frederick, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Pathol Histotechnol Lab, SAIC Frederick, Frederick, MD 21702 USA. NCI, Basic Res Lab, Frederick, MD 21702 USA. RP Blair, DG (reprint author), NCI, Frederick Canc Res & Dev Ctr, Intramural Res Support Program, SAIC Frederick, Frederick, MD 21702 USA. FU NCI NIH HHS [N01-CO-56000] NR 81 TC 3 Z9 3 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 1065-6995 J9 CELL BIOL INT JI Cell Biol. Int. PY 1999 VL 23 IS 4 BP 257 EP 274 DI 10.1006/cbir.1999.0346 PG 18 WC Cell Biology SC Cell Biology GA 258PW UT WOS:000083848400004 PM 10600235 ER PT J AU Momchilova, A Markovska, T Pankov, R AF Momchilova, A Markovska, T Pankov, R TI Ha-ras-transformation alters the metabolism of phosphatidylethanolamine and phosphatidylcholine in NIH 3T3 fibroblasts SO CELL BIOLOGY INTERNATIONAL LA English DT Article DE phosphatidylcholine; phosphatidylethanolamine; phospholipid metabolism; ras ID CTP-PHOSPHOCHOLINE CYTIDYLYLTRANSFERASE; GTPASE-ACTIVATING PROTEIN; SERUM STIMULATION; CELLS; ETHANOLAMINE; KINASE; PHOSPHOLIPASE; BIOSYNTHESIS; ONCOGENE; PATHWAYS AB Cultured NIH 3T3 fibroblasts were employed to investigate the changes in the phospholipid metabolism induced by Ha-ras transformation. All phospholipid fractions were reduced in ras-transformed fibroblasts except phosphatidylethanolamine (PE). The incorporation of labeled choline and ethanolamine into phosphatidylcholine (PC), PE and their corresponding metabolites were elevated in a similar manner in the transformed cells. The enhanced uptake of choline and ethanolamine correlated with the activation of choline kinase and ethanolamine kinase. Similarly, the uptake of arachidonic, oleic and palmitic acids by PC and PE was higher in ras-cells. Acyl-CoA synthetases, which esterify fatty acid before their incorporation into lysophospholipids, were also activated. However, both CTP:phosphocholine-cytidylyltransferase and CTP:phpsphoethanolamine-chytidyltransferase were inhibited in the transformed cells. This fact, taken together with the observed activation of choline- and ethanolamine kinases, led to accumulation of phosphocholine and phosphoethanolamine, which have been presumed to participate in the processes of tumor development. PC biosynthesis seemed to be carried out through the CDP-choline pathway, which was stimulated in the oncogenic cells, whereas PE was more likely, a product of phosphatidylserine decarboxylation rather than the CDP-ethanolamine pathway. (C) 1999 Academic Press. C1 NIDR, Dev Biol Lab, NIH, Bethesda, MD 20892 USA. Bulgarian Acad Sci, Inst Biophys, BU-1113 Sofia, Bulgaria. RP Pankov, R (reprint author), NIDR, Dev Biol Lab, NIH, Bethesda, MD 20892 USA. RI Pankov, Roumen/B-3284-2014 OI Pankov, Roumen/0000-0002-3157-3659 NR 28 TC 23 Z9 23 U1 0 U2 4 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 1065-6995 J9 CELL BIOL INT JI Cell Biol. Int. PY 1999 VL 23 IS 9 BP 603 EP 610 DI 10.1006/cbir.1999.0430 PG 8 WC Cell Biology SC Cell Biology GA 287WJ UT WOS:000085529400002 PM 10728571 ER PT J AU Mears, D Leighton, X Atwater, I Rojas, E AF Mears, D Leighton, X Atwater, I Rojas, E TI Tetracaine stimulates insulin secretion from the pancreatic beta-cell by release of intracellular calcium SO CELL CALCIUM LA English DT Article ID B-CELLS; SARCOPLASMIC-RETICULUM; ELECTRICAL-ACTIVITY; RYANODINE RECEPTOR; SKELETAL-MUSCLE; CA2+ ENTRY; TRANSIENTS; GLUCOSE; ISLETS; K+ AB The role of intracellular calcium stores in stimulus-secretion coupling in the pancreatic beta-cell is largely unknown. We report here that tetracaine stimulates insulin secretion from collagenase-isolated mouse islets of Langerhans in the absence of glucose or extracellular calcium. We also found that the anesthetic evokes a dose-dependent rise of the intracellular free-calcium concentration ([Ca2+](i)) in cultured rat and mouse beta-cells. The tetracaine-specific [Ca2+]i rise also occurs in the absence of glucose, or in beta-cells depolarized by exposure to a Ca2+-deficient medium (<1 mu M) or elevated [K+](o). Furthermore, tetracaine (greater than or equal to 300 mu M) depolarized the beta-cell membrane in mouse pancreatic islets, but inhibited Ca2+ entry through voltage-gated Ca2+ channels in HIT cells, an insulin-secreting cell line. From these data we conclude that tetracaine-enhancement of insulin release occurs by mechanisms that are independent of Ca2+ entry across the cell membrane. The tetracaine-induced [Ca2+], rise in cultured rat beta-cells and insulin secretion from mouse islets is insensitive to dantrolene (20 mu M), a drug that inhibits Ca2+ release evoked by cholinergic agonists in the pancreatic beta-cell, and thapsigargin (3 mu M), a blocker of the endoplasmic reticulum (ER) Ca2+ pump. We conclude that the Ca2+ required for tetracaine-potentiated insulin secretion is released from intracellular Ca2+ stores other than the ER. Furthermore, tetracaine-induced Ca2+ release was unaffected by the mitochondrial electron transfer inhibitors NaN3 and rotenone. Taken together, these data show that a calcium source other than the ER and mitochondria can affect beta-cell insulin secretion. C1 Univ Chile, Fac Med, ICBM, Inst Biomed Sci, Santiago, Chile. NIDDK, Lab Cell Biochem & Biol, NIH, Bethesda, MD USA. RP Rojas, E (reprint author), Univ Chile, Fac Med, ICBM, Inst Biomed Sci, Santiago, Chile. NR 43 TC 9 Z9 9 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 0143-4160 J9 CELL CALCIUM JI Cell Calcium PD JAN PY 1999 VL 25 IS 1 BP 59 EP 68 DI 10.1054/ceca.1998.0007 PG 10 WC Cell Biology SC Cell Biology GA 167AG UT WOS:000078609900006 PM 10191960 ER PT J AU Satoh, MI Hayes, SF Coe, JE AF Satoh, MI Hayes, SF Coe, JE TI Estrogen induces cytokeratin aggregation in primary cultures of Armenian hamster hepatocytes SO CELL MOTILITY AND THE CYTOSKELETON LA English DT Article DE intermediate filaments; beta-estradiol; isolated hepatocytes; immunocytochemistry; Mallory body ID EPIDERMAL GROWTH-FACTOR; GRISEOFULVIN-TREATED MICE; MALLORY BODY; INTERMEDIATE FILAMENTS; HEPATIC NEOPLASIA; FACTOR RECEPTOR; LIVER; INDUCTION; DIFFERENTIATION; PROTEINS AB The effect of estrogen administration to cultured Armenian hamster was studied. Isolated Armenian hamster hepatocytes were cultured in RPMI medium supplemented with beta-estradiol (E-2) beta-estradiol treatment for 24-48 hr induced cytoplasmic inclusion bodies which by immunocytochemistry were positive for cytokeratin (CK) 8, CK 18, and ubiquitin but negative for CK 7 and CK 19. These inclusion bodies appeared as filamentous tangles or amorphous aggregates when observed by electron microscopy. F-actin, tubulin, and desmosomes were not influenced by the presence of the inclusion bodies. Addition of ethanol to culture medium increased the incidence of the inclusion formation. In combination with 0.5% ethanol 1 mu M of E-2 induced five to six times more inclusion bodies, while the number of inclusion bodies decreased when epidermal growth factor (EGF) was added to the medium in combination with E-2. This reduction effect was nullified by treatment with anti-EGF receptor antibody. These findings suggest that E-2 treatment to Armenian hamster hepatocytes in vitro induces Mallory body-like inclusions whose incidence can be influenced by addition of ethanol or EGF to the culture medium. Cell Motil. Cytoskeleton 43:35-42, 1999. (C) 1999 Wiley-Liss, Inc. C1 NIAID, US Dept HHS, Publ Hlth Serv, NIH,Rocky Mt Labs, Hamilton, MT USA. RP Satoh, MI (reprint author), Univ Quebec, Dept Chim Biol, CP 500, Trois Rivieres, PQ G9A 5H7, Canada. NR 29 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0886-1544 J9 CELL MOTIL CYTOSKEL JI Cell Motil. Cytoskeleton PY 1999 VL 43 IS 1 BP 35 EP 42 PG 8 WC Cell Biology SC Cell Biology GA 193HL UT WOS:000080129800004 PM 10340701 ER PT J AU Knipling, L Hwang, J Wolff, J AF Knipling, L Hwang, J Wolff, J TI Preparation and properties of pure tubulin S SO CELL MOTILITY AND THE CYTOSKELETON LA English DT Article DE limited proteolysis; subtilisin; microtubule bundles; critical concentration ID CARBOXYL-TERMINAL DOMAIN; ALPHA-TUBULIN; POLYMERIZATION; MICROTUBULE; PROMOTION; SUBUNIT; PROBE; BRAIN AB Limited proteolysis of the tubulin dimer (alpha beta) by subtilisin occurs more rapidly with beta than with alpha tubulin. This leads to the formation of an intermediate hybrid dimer, alpha beta(s), before both C termini are cleaved to form tubulin S(alpha(s)beta(s)). The three forms of tubulin usually coexist in subtilisin-treated preparations and such cross-contamination can be reliably detected only by running SDS-polyacrylamide gels well beyond expulsion of the dye front. Previously published preparations have not ruled out such contamination or have formed poorly reversible polymers. Because ion exchange separation incurred substantial protein losses, we have developed a new protocol for rapid preparation of tubulin S (alpha(s)beta(s), free of alpha beta or alpha beta(s)) that is based on proteolysis at low ionic strength. This increases the relative rate of C terminal cleavage of beta tubulin. The product forms sheers, bundles, or rings that are depolymerized by cold, salt, and podophyllotoxin, partially depolymerized by Ca2+, and has a decreased critical concentration for polymerization that can be further decreased by taxol. We have also found a method for forming nearly pure alpha beta(s) dimers by using methods that retard proteolysis of the C terminus of alpha tubulin. Cell Motil. Cytoskeleton 43:63-71, 1999. Published 1999 Wiley-Liss, Inc. C1 NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. RP Wolff, J (reprint author), NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. NR 36 TC 27 Z9 28 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0886-1544 J9 CELL MOTIL CYTOSKEL JI Cell Motil. Cytoskeleton PY 1999 VL 43 IS 1 BP 63 EP 71 DI 10.1002/(SICI)1097-0169(1999)43:1<63::AID-CM7>3.0.CO;2-Z PG 9 WC Cell Biology SC Cell Biology GA 193HL UT WOS:000080129800007 PM 10340704 ER PT J AU Borlongan, CV Stahl, CE Fujisaki, T Sanberg, PR Watanabe, S AF Borlongan, CV Stahl, CE Fujisaki, T Sanberg, PR Watanabe, S TI Cyclosporine A-induced hyperactivity in rats: Is it mediated by immunosuppression, neurotrophism, or both? SO CELL TRANSPLANTATION LA English DT Article; Proceedings Paper CT 5th Meeting of the American-Society-for-Neural-Transplantation CY APR 23-25, 1998 CL CLEARWATER, FLORIDA SP Amer Soc Neural Transplantat DE immunosuppression; dopamine; substantia nigra; calcineurin; locomotor activity; neuroprotection; Parkinson's disease ID CENTRAL-NERVOUS-SYSTEM; DOPAMINERGIC-NEURONS; PARKINSONS-DISEASE; BRAIN; GDNF; INJURY; 6-HYDROXYDOPAMINE; CALCINEURIN; INHIBITION; INJECTION AB Cyclosporine A (CsA) immunosuppressive treatment has become an adjunctive therapy in neural transplantation of dopamine-secreting cells for treatment of Parkinson's disease (PD). Recently, CsA and its analogues have been shown to promote trophic effects against neurodegenerative disorders, and therefore CsA may have direct beneficial effects on dopaminergic neurons and dopamine-mediated behaviors. The present study examined the interaction between the reported CsA-induced hyperactivity and the possible alterations in nigral tyrosine hydroxylase (TH)-immunoreactive neurons in rats with damaged blood-brain barrier. CsA was administered at a therapeutic dose (10 mg/kg/day, IP, for 9 days) used in neural transplantation protocol for PD animal models. CsA-treated animals displayed significantly higher general spontaneous locomotor activity than control animals at drug injection days 7 and 9. Histological assays at day 9 revealed that there was a significant increase in TH-immunoreactive neurons in the nigra of CsA-treated rats compared to that of the vehicle-treated rats. The nigral TH elevation was accompanied by suppressed calcium-phosphotase calcineurin activity, indicating an inhibition of host immune response. This is the first report of CsA exerting simultaneous immunosuppressive and neurotrophic effects, as well as increasing general spontaneous locomotor behavior. These results support the utility of CsA as a therapeutic agent for PD and other movement disorders. C1 NIH, Natl Inst Drug Abuse, Intramural Res Program, Baltimore, MD 21224 USA. Univ S Florida, Coll Med, Dept Surg, Tampa, FL 33612 USA. Univ S Florida, Coll Med, Program Neurosci, Tampa, FL 33612 USA. Keio Univ, Dept Psychol, Minato Ku, Tokyo 108, Japan. RP Borlongan, CV (reprint author), NIH, Natl Inst Drug Abuse, Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. OI Borlongan, Cesar/0000-0002-2966-9782 NR 30 TC 18 Z9 18 U1 0 U2 0 PU COGNIZANT COMMUNICATION CORP PI ELMSFORD PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA SN 0963-6897 J9 CELL TRANSPLANT JI Cell Transplant. PD JAN-FEB PY 1999 VL 8 IS 1 BP 153 EP 159 PG 7 WC Cell & Tissue Engineering; Medicine, Research & Experimental; Transplantation SC Cell Biology; Research & Experimental Medicine; Transplantation GA 194TY UT WOS:000080210700014 PM 10338283 ER PT J AU Boheler, KR Fiszman, MY AF Boheler, KR Fiszman, MY TI Can exogenous stem cells be used in transplantation? SO CELLS TISSUES ORGANS LA English DT Article DE embryonic stem cells; cell replacement therapy ID DIFFERENTIATED IN-VITRO; ES CELLS; SKELETAL-MUSCLE; MOUSE EMBRYOS; GENE; EXPRESSION; CARDIOMYOCYTES; LINEAGES; GRAFTS; MODEL AB Today's most urgent problem in transplantation is the lack of suitable donor organs and tissues and as the population ages, demands for organs and tissue therapies will only increase. One alternative to organ transplantation is cell therapy whose aim is to replace, repair or enhance the biological function of damaged tissue or diseased organs. One goal of cellular transplantation thus has been to find a renewable source of cells that could be used in humans. Embryonic stem (ES) cells have the potential to proliferate in vitro in an undifferentiated and pluripotent state. Theoretically, ES cells are capable of unlimited proliferation in vitro. ES cells spontaneously differentiate into derivatives of all three primary germ layers: endoderm, ectoderm and mesoderm, hence providing cells in vitro which can theoretically be isolated and used for transplantation. Furthermore, these pluripotent stem cells can potentially be used to produce large numbers of cells that can be genetically modified in vitro. Once available, this source of cells may obviate some of the critical needs for organ transplantation. Murine ES cells have been extensively studied and all available evidence indicates that all aforementioned expectations are indeed fulfilled by ES cells. ES cells as well as embryonic germ cells have recently been isolated and maintained in culture. The recent descriptions of human ES cells portend the eventual use of allogeneic in vitro differentiated cells for human therapy. This goal, however, is fraught with obstacles. Our aim is first to review the recent advances made with murine ES cells and then to point out potentials and difficulties associated with the use of human ES cells for transplantation. Copyright (C) 1999 S. Karger AG, Basel. C1 Hop La Pitie Salpetriere, Inst Myol, INSERM, U523, F-75651 Paris, France. NIA, Intramural Res Program, Gerontol Res Ctr, Cardiovasc Sci Lab, Baltimore, MD 21224 USA. RP Fiszman, MY (reprint author), Hop La Pitie Salpetriere, Inst Myol, INSERM, U523, 47 Blvd Hop, F-75651 Paris, France. NR 44 TC 17 Z9 17 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1422-6405 J9 CELLS TISSUES ORGANS JI Cells Tissues Organs PY 1999 VL 165 IS 3-4 BP 237 EP 245 DI 10.1159/000016684 PG 9 WC Anatomy & Morphology; Cell Biology; Developmental Biology SC Anatomy & Morphology; Cell Biology; Developmental Biology GA 263NE UT WOS:000084130100012 PM 10592395 ER PT J AU Bates, S Vousden, KH AF Bates, S Vousden, KH TI Mechanisms of p53-mediated apoptosis SO CELLULAR AND MOLECULAR LIFE SCIENCES LA English DT Review DE p53; apoptosis; transcription; Bax; death receptors; tumours ID WILD-TYPE P53; MYC-INDUCED APOPTOSIS; CYCLIN-DEPENDENT KINASES; DNA-BINDING FUNCTION; TRANSCRIPTION ACTIVATION FUNCTION; P53-DEPENDENT G(1) ARREST; TUMOR-SUPPRESSOR GENE; PROGRAMMED CELL-DEATH; HUMAN CANCER-CELLS; GROWTH ARREST AB The loss of p53-mediated apoptosis (programmed cell death) has been implicated as an important event in tumour progression in a number of systems. p53 can induce or potentiate apoptosis through several mechanisms, both by regulating the expression of genes which can participate in the apoptotic response and through transcriptionally independent means. There appears to be cell type variability in both the response to p53 expression and in the requirement for p53 transcriptional transactivation for the induction of apoptosis. It seems clear, however, that the induction of p53 in untransformed cells is more likely to result in cell-cycle arrest, whereas the expression of p53 in their transformed counterparts is more likely to result in the induction of apoptosis, and this may, in part, reflect the deregulated expression of E2F-1 in tumour cells. The synergistic action of p53 and E2F-1 in the induction of apoptosis has raised the possibility that the reactivation of p53 in transformed cells can be an effective tumour therapy. C1 NCI, ABL Basic Res Program, FCRDC, Frederick, MD 21702 USA. RP Vousden, KH (reprint author), NCI, ABL Basic Res Program, FCRDC, Bldg 560,Room 22-96,W 7th St, Frederick, MD 21702 USA. EM vousden@ncifcrf.gov NR 104 TC 225 Z9 238 U1 0 U2 7 PU BIRKHAUSER VERLAG AG PI BASEL PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND SN 1420-682X J9 CELL MOL LIFE SCI JI Cell. Mol. Life Sci. PD JAN PY 1999 VL 55 IS 1 BP 28 EP 37 DI 10.1007/s000180050267 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 165WD UT WOS:000078544100004 PM 10065149 ER PT J AU Steffgen, J Rohrbach, S Beery, E Ersoy, D Jarry, H Metten, M Bornstein, SR Muller, GA Burckhardt, G AF Steffgen, J Rohrbach, S Beery, E Ersoy, D Jarry, H Metten, M Bornstein, SR Muller, GA Burckhardt, G TI Demonstration of a probenecid-inhibitable anion exchanger involved in the release of cortisol and cAMP and in the uptake of p-aminohippurate in bovine adrenocortical cells SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY LA English DT Article DE p-aminohippurate (PAH) uptake; cortisol release; cyclic adenosine monophosphate release probenecid; anion exchanger; adrenocortical cells ID BASOLATERAL MEMBRANE-VESICLES; RAT-KIDNEY; EXPRESSION CLONING; PROXIMAL TUBULE; TRANSPORT; ENZYMES; STEROIDOGENESIS; LIVER; ACTH AB Recently we provided evidence for the involvement of a probenecid-inhibitable anion exchanger in cortisol release from primary cultures of bovine adrenocortical cells. In the present study, we further characterized this exchange transporter. Adrenocorticotropic hormone stimulated H-3-p-aminohippurate (H-3-PAH) uptake into as well as cortisol release from the cells about two- and tenfold, respectively. Probenecid inhibited both H-3-PAH uptake and cortisol release by about 55 and 63%. Preincubation of the cells with 1 mM PAH trans-stimulated H-3-PAH uptake by 30%, whereas cortisol release was inhibited by 30%. H-3-PAH uptake was cis-inhibited by 1 mM glutarate or by 1 mM cortisol in the medium, while cortisol release was trans-stimulated by glutarate. PAH in the incubation medium showed saturable cis-inhibition of H-3-PAH uptake. The release of cyclic adenosine monophosphate, a substrate of the renal PAH exchanger, was also inhibited by probenecid and trans-stimulated by glutarate. In summary, the trans-stimulation and cis-inhibition experiments support the concept of an anion exchanger involved in cortisol and cyclic adenosine monophosphate release from and PAH uptake into adrenocortical cells. C1 Univ Gottingen, Abt Nephrol & Rheumatol, D-37075 Gottingen, Germany. NIH, Dev Endocrinol Branch, Bethesda, MD 20892 USA. RP Steffgen, J (reprint author), Univ Gottingen, Abt Nephrol & Rheumatol, Robert Koch Str 40, D-37075 Gottingen, Germany. NR 29 TC 8 Z9 8 U1 2 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-8987 J9 CELL PHYSIOL BIOCHEM JI Cell. Physiol. Biochem. PY 1999 VL 9 IS 2 BP 72 EP 80 DI 10.1159/000016303 PG 9 WC Cell Biology; Physiology SC Cell Biology; Physiology GA 223VY UT WOS:000081863300002 PM 10394000 ER PT J AU Callicott, JH Mattay, VS Bertolino, A Finn, K Coppola, R Frank, JA Goldberg, TE Weinberger, DR AF Callicott, JH Mattay, VS Bertolino, A Finn, K Coppola, R Frank, JA Goldberg, TE Weinberger, DR TI Physiological characteristics of capacity constraints in working memory as revealed by functional MRI SO CEREBRAL CORTEX LA English DT Article ID DORSOLATERAL PREFRONTAL CORTEX; POSITRON EMISSION TOMOGRAPHY; INDIVIDUAL-DIFFERENCES; BRAIN; TASK; ACTIVATION; SCHIZOPHRENIA; PARADIGM AB A fundamental characteristic of working memory is that its capacity to handle information is limited. While there have been many brain mapping studies of working memory, the physiological basis of its capacity limitation has not been explained. We identified characteristics of Corking memory capacity using functional magnetic resonance imaging (fMRI) in healthy subjects. Working memory capacity was studied using a parametric 'n-back' working memory task involving increasing cognitive load and ultimately decreasing task performance. Loci within dorsolateral prefrontal cortex (DLPFC) evinced exclusively an 'inverted-U' shaped neurophysiological response from lowest to highest toad, consistent with a capacity-constrained response. Regions outside of DLPFC, in contrast, were more heterogeneous in response and often showed early plateau or continuously increasing responses, which did not reflect capacity constraints. However, sporadic loci, including in the premotor cortex, thalamus and superior parietal lobule, also demonstrated putative capacity-constrained responses, perhaps arising as an upstream effect of DLPFC limitations or as part of a broader network-wide capacity limitation. These results demonstrate that regionally specific nodes within the working memory network are capacity-constrained in the physiological domain, providing a missing link in current explorations of the capacity characteristics of working memory. C1 NIMH, Clin Brain Disorders Branch, Intramural Res Program, Bethesda, MD 20892 USA. NIH, Lab Diagnost Radiol Res, OIRR, Bethesda, MD 20892 USA. RP Callicott, JH (reprint author), NIMH, Clin Brain Disorders Branch, Intramural Res Program, 10 Ctr Dr,Room 4S235 MSC 1379, Bethesda, MD 20892 USA. RI Callicott, Joseph/C-9102-2009; Bertolino, Alessandro/O-6352-2016 OI Callicott, Joseph/0000-0003-1298-3334; Bertolino, Alessandro/0000-0002-1251-1380 NR 49 TC 471 Z9 480 U1 7 U2 52 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 1047-3211 J9 CEREB CORTEX JI Cereb. Cortex PD JAN-FEB PY 1999 VL 9 IS 1 BP 20 EP 26 DI 10.1093/cercor/9.1.20 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 158KR UT WOS:000078115100003 PM 10022492 ER PT J AU Watson, JC Myseros, JS Bullock, MR AF Watson, JC Myseros, JS Bullock, MR TI True fungal mycotic aneurysm of the basilar artery: A clinical and surgical dilemma SO CEREBROVASCULAR DISEASES LA English DT Article DE intracranial aneurysm; subarachnoid hemorrhage; mycotic aneurysm; Scedosporium apiospermum; Pseudallescheria boydii ID PSEUDALLESCHERIA-BOYDII INFECTION; INTRACRANIAL ANEURYSMS; SINUSITIS; HOST AB Mycotic aneurysms of the intracranial circulation of true fungal etiology are extremely rare and are associated with a very high mortality. We report a case of a fatal aneurysm of the basilar artery secondary to Scedosporium apiospermum infection. The medical and surgical treatments are presented to demonstrate the difficulties associated with these lesions. C1 Virginia Commonwealth Univ, Med Coll Virginia, Div Neurosurg, Richmond, VA 23298 USA. RP Watson, JC (reprint author), NINDS, NIH, 10 Ctr Dr,Room 5D37, Bethesda, MD 20892 USA. NR 26 TC 22 Z9 22 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-9770 J9 CEREBROVASC DIS JI Cerebrovasc. Dis. PD JAN-FEB PY 1999 VL 9 IS 1 BP 50 EP 53 DI 10.1159/000015896 PG 4 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA 159DT UT WOS:000078157100008 PM 9873163 ER PT S AU Fischbeck, KH Abel, A Lin, GS Scherer, SS AF Fischbeck, KH Abel, A Lin, GS Scherer, SS BE Shy, ME Kamholz, J Lovelace, RE TI X-linked Charcot-Marie-Tooth disease and connexin32 SO CHARCOT-MARIE-TOOTH DISORDERS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 3rd International Conference on Charcot-Marie-Tooth Disorders CY OCT 21-24, 1999 CL ST ADELE, CANADA SP New York Acad Sci, Charcot Marie Tooth Assoc ID GAP JUNCTION PROTEIN; NERVE-CONDUCTION VELOCITIES; SENSORY NEUROPATHY; HEREDITARY MOTOR; MUTATIONS; GENE; MYELIN; MICE; FAMILIES; EXPRESSION AB X-linked Charcot-R Marie-Tooth disease is caused bg mutations in the gene for the gap junction protein connexin32. This protein is expressed in peripheral nerve and present in noncompacted myelin, where it likely forms channels around and across the myelin sheath. Studies in cell culture and in transgenic mice show that connexin32 mutations can cause a loss of channel function or a gain of toxic effects on myelinating Schwann cells or both, with resulting peripheral nerve degeneration. C1 NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA. Univ Penn, Sch Med, Dept Neurol, Philadelphia, PA 19104 USA. RP Fischbeck, KH (reprint author), NINDS, Neurogenet Branch, NIH, Bldg 10,Rm 3B14,10 Ctr Dr, Bethesda, MD 20892 USA. NR 40 TC 13 Z9 14 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 1-57331-182-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 883 BP 36 EP 41 DI 10.1111/j.1749-6632.1999.tb08564.x PG 6 WC Multidisciplinary Sciences; Clinical Neurology; Neurosciences SC Science & Technology - Other Topics; Neurosciences & Neurology GA BP09A UT WOS:000084086800006 PM 10586227 ER PT S AU Lin, GS Glass, JD Shumas, S Scherer, SS Fischbeck, KH AF Lin, GS Glass, JD Shumas, S Scherer, SS Fischbeck, KH BE Shy, ME Kamholz, J Lovelace, RE TI A unique mutation in connexin32 associated with severe, early onset CMTX in a heterozygous female SO CHARCOT-MARIE-TOOTH DISORDERS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 3rd International Conference on Charcot-Marie-Tooth Disorders CY OCT 21-24, 1999 CL ST ADELE, CANADA SP New York Acad Sci, Charcot Marie Tooth Assoc ID MARIE-TOOTH DISEASE; GENE C1 NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA. Univ Penn, Med Ctr, Dept Neurol, Philadelphia, PA 19104 USA. Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA. RP Fischbeck, KH (reprint author), NINDS, Neurogenet Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. NR 8 TC 14 Z9 14 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 1-57331-182-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 883 BP 481 EP 484 DI 10.1111/j.1749-6632.1999.tb08616.x PG 4 WC Multidisciplinary Sciences; Clinical Neurology; Neurosciences SC Science & Technology - Other Topics; Neurosciences & Neurology GA BP09A UT WOS:000084086800058 PM 10586279 ER PT J AU Beland, FA Doerge, DR Churchwell, MI Poirier, MC Schoket, B Marques, MM AF Beland, FA Doerge, DR Churchwell, MI Poirier, MC Schoket, B Marques, MM TI Synthesis, characterization, and quantitation of a 4-aminobiphenyl-DNA adduct standard SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID CARCINOGEN-DNA ADDUCTS; P-32 POSTLABELING ASSAY; P-32-POSTLABELING ANALYSIS; SENSITIVITY; RADIOIMMUNOASSAY; CHROMATOGRAPHY; ENHANCEMENT; METABOLITES; INVIVO; CELLS AB P-32-Postlabeling is a powerful technique for the detection of DNA adducts; however, quantitation of DNA adducts by this method can result in errors due to differences in hydrolysis and labeling efficiencies between adducted and normal nucleotides. We have synthesized a DNA sample modified with 4-aminobiphenyl to serve as a quantitation standard for P-32- postlabeling and other DNA adduct detection methodologies. [2,2'-H-3]-N-Hydroxy-4-aminobiphenyl was reacted with calf thymus DNA at pH 5 to give 62 +/- 0.8 adducts/10(8) nucleotides (mean +/- SD) on the basis of H-3 content. HPLC analyses following enzymatic hydrolysis to nucleosides indicated one major adduct, N-(deoxyguanosin-8-yl)-4-aminobiphenyl (dG-C8-4-ABP). The adduct identity was confirmed by HPLC/electrospray ionization mass spectrometry, which indicated a modification level of 19 +/- 1.7 dG-C8-4-ABP/10(8) nucleotides. P-32-Postlabeling analysis gave a value of 0.84 dG-C8-4-ABP/10(8) nucleotides, while a dissociation-enhanced lanthanide fluoroimmunoassay (DELFIA) indicated levels of 82 +/- 26 and 63 +/- 20 dG-C8-4ABP/10(8) nucleotides after enzymatic hydrolysis to nucleotides and nucleosides, respectively. The utility of the DNA adduct standard was determined by assessing the level of dG-C8-4-ABP in liver DNA from mice treated with [2,2'-H-3]-4-aminobiphenyl. P-32-Postlabeling analyses, based upon measuring the extent of the P-32 incorporation, underestimated the levels of dG-C8-4-ABP, while DELFIA, using a G-C8-4-ABP quantitation standard, overestimated the adduct levels. The adduct levels determined by HPLC/electrospray ionization mass spectrometry best; reflected those obtained from H-3 incorporation. When the P-32-postlabeling analyses and the DELFIA were conducted using the DNA modified in vitro with dG-C8-4-ABP as a quantitation standard, accurate estimations of the extent of in vivo formation of dG-C8-4-ABP were obtained. C1 Natl Ctr Toxicol Res, Div Biochem Toxicol, Jefferson, AR 72079 USA. NCI, Cellular Carcinogenesis & Tumor Promot Lab, Bethesda, MD 20892 USA. Natl Inst Environm Hlth, Dept Biochem, H-1097 Budapest, Hungary. Univ Tecn Lisboa, Ctr Quim Estrutural, Inst Super Tecn, P-1049001 Lisbon, Portugal. RP Beland, FA (reprint author), Natl Ctr Toxicol Res, Div Biochem Toxicol, HFT-110, Jefferson, AR 72079 USA. EM fbeland@nctr.fda.gov RI Marques, M. Matilde/E-2535-2012 OI Marques, M. Matilde/0000-0002-7526-4962 NR 30 TC 55 Z9 55 U1 1 U2 5 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0893-228X J9 CHEM RES TOXICOL JI Chem. Res. Toxicol. PD JAN PY 1999 VL 12 IS 1 BP 68 EP 77 DI 10.1021/tx980172y PG 10 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA 159FE UT WOS:000078160600008 PM 9894020 ER PT J AU Wilken, J Hoover, D Thompson, DA Barlow, PN McSparron, H Picard, L Wlodawer, A Lubkowski, J Kent, SBH AF Wilken, J Hoover, D Thompson, DA Barlow, PN McSparron, H Picard, L Wlodawer, A Lubkowski, J Kent, SBH TI Total chemical synthesis and high-resolution crystal structure of the potent anti-HIV protein AOP-RANTES SO CHEMISTRY & BIOLOGY LA English DT Article DE chemical protein synthesis; chemokine; crystal structure; HIV-1; RANTES ID CC-CHEMOKINE RECEPTOR; MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; FUNCTIONAL EXPRESSION; MOLECULAR-CLONING; T-CELLS; MIP-1-ALPHA; MIP-1-BETA; IDENTIFICATION; INFECTIVITY; LYMPHOCYTES AB Background: RANTES is a CC-type chemokine protein that acts as a chemoattractant for several kinds of leukocytes, playing an important proinflammatory role. Entry of human immunodeficiency virus-1 (HIV-1) into cells depends on the chemokine receptor CCR5. RANTES binds CCR5 and inhibits HIV-1 entry into peripheral blood cells. Interaction with chemokine receptors involves a distinct set of residues at the amino terminus of RANTES. This finding was utilized in the development of a chemically modified aminooxypentane derivative of RANTES, AOP-RANTES, that was originally produced from the recombinant protein using semisynthetic methods. Results: AOP-RANTES has been produced by a novel total chemical synthesis that provides efficient, direct access to large amounts of this anti-HIV protein analog. The crystal structure of chemically synthesized AOP-RANTES has been solved and refined at 1.6 Angstrom resolution. The protein is a dimer, with the aminoterminal pentane oxime moiety clearly defined. Conclusions: Total chemical synthesis of AOP-RANTES provides a convenient method of producing the multi-milligram quantities of this protein needed to investigate the molecular basis of receptor binding and antiviral activity. This work provides the first truly high-resolution structure of a RANTES protein, although the structure of RANTES was known from previous nuclear magnetic resonance (NMR) determinations. C1 NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Macromol Struct Lab, Frederick, MD 21702 USA. Gryphon Sci, S San Francisco, CA 94080 USA. Univ Edinburgh, Edinburgh Ctr Prot Technol, Edinburgh EH9 3JJ, Midlothian, Scotland. Inst Cochin Genet Mol, INSERM, U332, F-75014 Paris, France. RP Kent, SBH (reprint author), NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Macromol Struct Lab, Frederick, MD 21702 USA. RI Barlow, Paul/G-2853-2011; OI Thompson, Darren/0000-0002-3725-7112 NR 41 TC 61 Z9 62 U1 0 U2 5 PU CURRENT BIOLOGY LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1074-5521 J9 CHEM BIOL JI Chem. Biol. PD JAN PY 1999 VL 6 IS 1 BP 43 EP 51 DI 10.1016/S1074-5521(99)80019-2 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 235WA UT WOS:000082564500008 PM 9889151 ER PT B AU Caporaso, N Landi, MT AF Caporaso, N Landi, MT BE BallarinDenti, A Bertazzi, PA Facchetti, S Fanelli, R Mocarelli, P TI Molecular epidemiology and its application to the study of dioxin effects in the Seveso population SO CHEMISTRY, MAN AND ENVIRONMENT: THE SEVESO ACCIDENT 20 YEARS ON - MONITORING, EPIDEMIOLOGY AND REMEDIATION LA English DT Proceedings Paper CT Meeting on Chemistry, Man and Environment CY OCT 21-22, 1996 CL MILAN, ITALY SP Fdn Lombardia Ambiente ID BIOLOGICAL MARKERS; LUNG-CANCER; SUSCEPTIBILITY; RISK AB We measured 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) levels in a sample of individuals from Seveso, Italy, almost two decades after an industrial accident contaminated the area with the toxicant in 1976. Plasma TCDD and other polychlorinated dioxins and furans were determined in a population-based sample of 62 subjects from the highly contaminated area (zones A (7 subjects) and B (55 subjects)), and 59 subjects from the surrounding noninvolved area. Exposed and unexposed individuals were loosely matched according to age, gender and smoking habits. Serum TCDD levels measured almost 20 years after the accident corresponded to zone categorization based on TCDD soil levels measured at the time of the accident. Within zone B, where most of the exposed subjects were found, TCDD levels were higher in elderly subjects. Levels in women were significantly higher when compared to men in both zone B and the uninvolved areas. The gender difference persisted after the adjustment for age, zone (including more precise levels in women) were significantly higher when compared to men in both zone B and the uninvolved areas: The gender difference persisted after the adjustment for age, zone (including more precise adjustment for local area within the zone), body-mass index, cigarette smoking and consumption of meat derived from locally raised animals. Higher levels in women have important implications because of the potential developmental, reproductive and hormonal effects. C1 NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA. RP Caporaso, N (reprint author), NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA. NR 18 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-08-043644-7 PY 1999 BP 65 EP 74 PG 10 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA BP15G UT WOS:000084237800006 ER PT B AU Landi, MT Caporaso, N AF Landi, MT Caporaso, N BE BallarinDenti, A Bertazzi, PA Facchetti, S Fanelli, R Mocarelli, P TI Elevated levels in females, 20 years after the Seveso accident SO CHEMISTRY, MAN AND ENVIRONMENT: THE SEVESO ACCIDENT 20 YEARS ON - MONITORING, EPIDEMIOLOGY AND REMEDIATION LA English DT Proceedings Paper CT Meeting on Chemistry, Man and Environment CY OCT 21-22, 1996 CL MILAN, ITALY SP Fdn Lombardia Ambiente ID HIGHER CHLORINATED DIOXINS; SOFT-TISSUE SARCOMA; POTENTIAL EXPOSURE; CHEMICAL WORKERS; CANCER MORTALITY; TUMOR PROMOTION; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN; VIETNAM; SERUM; RISK AB We measured 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) plasma levels in a sample of 62 healthy individuals from Seveso, Italy, almost two decades after the 1976 industrial accident. TCDD was also determined in a population-based sample of 59 subjects from the surrounding noncontaminated area. Exposed and unexposed individuals were loosely matched for age, gender and smoking. Elevated TCDD levels were present in subjects in the exposed zones, while population values were found in the surrounding area. Measured plasma levels corresponded to soil levels that were used in 1976 to define the original zones. Levels in women were significantly higher compared to men in both zone B and the surrounding area (the small numbers in zone A precluded a gender comparison). The gender difference persists after adjustment for age, zone (including more precise adjustment for local area within the zone, based on the distance from industrial source point), body-mass index, cigarette smoking, and consumption of meat derived from locally raised animals. Higher levels in women have important implications because of potential developmental, reproductive and hormonal effects. C1 NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA. RP Landi, MT (reprint author), NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA. NR 26 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-08-043644-7 PY 1999 BP 75 EP 82 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA BP15G UT WOS:000084237800007 ER PT J AU Sullivan, EJ Beck, GJ Peavy, HH Fanburg, BL AF Sullivan, EJ Beck, GJ Peavy, HH Fanburg, BL TI Lymphangioleiomyomatosis registry SO CHEST LA English DT Letter C1 Cleveland Clin Fdn, LAM Data Coordinating Ctr, Cleveland, OH 44195 USA. NHLBI, Div Lung Dis, Bethesda, MD 20892 USA. New England Med Ctr, Steering Comm LAM Registry, Boston, MA 02111 USA. RP Sullivan, EJ (reprint author), Cleveland Clin Fdn, LAM Data Coordinating Ctr, 9500 Euclid Ave, Cleveland, OH 44195 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA SN 0012-3692 J9 CHEST JI Chest PD JAN PY 1999 VL 115 IS 1 BP 301 EP 301 DI 10.1378/chest.115.1.301 PG 1 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 157QY UT WOS:000078074200056 PM 9925106 ER PT J AU Orbach, Y Lamb, ME AF Orbach, Y Lamb, ME TI Assessing the accuracy of a child's account of sexual abuse: A case study SO CHILD ABUSE & NEGLECT LA English DT Article DE sexual abuse; memory; credibility; child witness; accuracy ID INVESTIGATIVE UTTERANCE TYPES; EYEWITNESS TESTIMONY; MEMORY; WITNESSES; SUGGESTIBILITY; CREDIBILITY; EXPERIENCES; RESPONSES; QUESTIONS; EVENTS AB Objective: The objective of the case study reported in this paper was to examine the accuracy of one child's account of a sexually abusive incident. The availability of an audio recording of the last in a series of abusive incidents enabled us to assess accuracy in greater detail than has hitherto been possible in forensic contexts. Methods: Information given by the victim during an investigative interview was compared with an audio-taped record of the incident. Content analyses of the interview involved quantitative and qualitative analyses of the victim's account, and a qualitative analysis of the eliciting utterances. A CBCA analysis was performed on the victim's account to assess its purported credibility. Results: Over 50% of the informative details reported by the victim were corroborated by the audio-recorded account (of which 98% were central, i.e., allegation related and 64% were confirmed by more than one source (audio-recording, suspect, witness). A total of 10 CBCA criteria were present in the victim's free-narrative account of the last abusive incident. Conclusions: Our findings confirm that children can indeed provide remarkably detailed and accurate accounts of their experiences. Published by Elsevier Science Ltd. C1 NICHHD, Sect Social & Emot Dev, Bethesda, MD 20814 USA. RP Lamb, ME (reprint author), NICHHD, Sect Social & Emot Dev, 9190 Rockville Pike, Bethesda, MD 20814 USA. NR 44 TC 38 Z9 38 U1 1 U2 10 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PD JAN PY 1999 VL 23 IS 1 BP 91 EP 98 DI 10.1016/S0145-2134(98)00114-8 PG 8 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA 151UW UT WOS:000077739900008 PM 10075196 ER PT S AU Alfieri, JA Clark, DJ AF Alfieri, JA Clark, DJ BE Wassarman, PM Wolffe, AP TI Isolation of minichromosomes from yeast cells SO CHROMATIN SE Methods in Enzymology LA English DT Review ID 2-MU-M DNA PLASMID; SACCHAROMYCES-CEREVISIAE; CHROMATIN; GENE; CIRCLE; TRANSFORMATION; CONSTRUCTION; ORGANIZATION; REPLICATION; EXPRESSION C1 NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. Univ Calif Davis, Davis, CA 95616 USA. RP NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. NR 32 TC 6 Z9 6 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 0-12-182205-2 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 304 BP 35 EP 49 PG 15 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12X UT WOS:000087254800003 PM 10372354 ER PT J AU Postnikov, YV Bustin, M AF Postnikov, YV Bustin, M TI Reconstitution of high mobility group 14/17 proteins into nucleosomes and chromatin SO CHROMATIN SE METHODS IN ENZYMOLOGY LA English DT Review ID NASCENT CHROMATIN; CORE PARTICLES; DNA-SYNTHESIS; HMG-17; EFFICIENCY; CONTACTS; BINDING; REGION; DOMAIN C1 NCI, Div Basic Sci, Prot Sect, NIH, Bethesda, MD 20892 USA. RP Postnikov, YV (reprint author), NCI, Div Basic Sci, Prot Sect, NIH, Bethesda, MD 20892 USA. RI Bustin, Michael/G-6155-2015 NR 30 TC 7 Z9 7 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 304 BP 133 EP 155 PG 23 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12X UT WOS:000087254800008 PM 10372359 ER PT J AU Li, Q Bjork, U Wrange, O AF Li, Q Bjork, U Wrange, O TI Assays for interaction of transcription factor with nucleosome SO CHROMATIN SE METHODS IN ENZYMOLOGY LA English DT Review ID MAMMARY-TUMOR VIRUS; GLUCOCORTICOID RESPONSE ELEMENT; FACTOR ACCESS; DNA; RECEPTOR; BINDING; PROMOTER; ACCESSIBILITY; ORGANIZATION; AFFINITY C1 NIH, Mol Embryol Lab, Bethesda, MD 20892 USA. Karolinska Inst, Dept Cell & Mol Biol, S-17177 Stockholm, Sweden. RP Li, Q (reprint author), NIH, Mol Embryol Lab, Bldg 37, Bethesda, MD 20892 USA. NR 29 TC 4 Z9 4 U1 0 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 304 BP 313 EP 332 PG 20 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12X UT WOS:000087254800017 PM 10372368 ER PT J AU Archer, TK Ricci, AR AF Archer, TK Ricci, AR TI Exonuclease III as a probe of chromatin structure in vivo SO CHROMATIN SE METHODS IN ENZYMOLOGY LA English DT Review ID TRANSCRIPTION FACTOR ACCESS; PROMOTER IN-VIVO; MMTV PROMOTER; SACCHAROMYCES-CEREVISIAE; NUCLEAR EXTRACTS; BINDING-SITES; DNA; NUCLEOSOMES; ACTIVATION; MECHANISM C1 Univ Western Ontario, London Reg Canc Ctr, London, ON N6A 4L6, Canada. NIEHS, Reprod & Dev Toxicol Lab, Chromatin & Gene Express Sect, NIH, Res Triangle Pk, NC 27709 USA. Univ Western Ontario, Dept Biochem, London, ON N6A 4L6, Canada. RP Archer, TK (reprint author), Univ Western Ontario, London Reg Canc Ctr, London, ON N6A 4L6, Canada. NR 43 TC 6 Z9 6 U1 0 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 304 BP 584 EP 599 PG 16 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12X UT WOS:000087254800032 PM 10372383 ER PT J AU Hager, GL Fragoso, G AF Hager, GL Fragoso, G TI Analysis of nucleosome positioning in mammalian cells SO CHROMATIN SE METHODS IN ENZYMOLOGY LA English DT Review ID LIGATION-MEDIATED PCR; IN-VIVO; DNA FRAGMENTS; TRANSCRIPTION FACTORS; CHROMATIN-STRUCTURE; IONIC-STRENGTH; MMTV PROMOTER; INVITRO; DEOXYRIBONUCLEASE; SEQUENCES C1 Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA. RP Hager, GL (reprint author), NCI, Lab Receptor & Gene Express, NIH, Bethesda, MD 20892 USA. NR 63 TC 7 Z9 7 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 304 BP 626 EP 638 PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12X UT WOS:000087254800035 PM 10372386 ER PT J AU Kramer, PR Bat, O Sinden, RR AF Kramer, PR Bat, O Sinden, RR TI Measurement of localized DNA supercoiling and topological domain size in eukaryotic cells SO CHROMATIN SE METHODS IN ENZYMOLOGY LA English DT Review ID ESCHERICHIA-COLI-CELLS; SHOCK GENE LOCUS; TORSIONAL TENSION; CHROMATIN STRUCTURE; IN-VIVO; PSORALEN; INVIVO; TRIMETHYLPSORALEN; CHROMOSOMES; EXPRESSION C1 NINDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. Univ Texas, Hlth Sci Ctr, Inst Mol Med, Houston, TX 77030 USA. Texas A&M Univ, Inst Biosci & Technol, Ctr Genome Res, Houston, TX 77030 USA. RP Kramer, PR (reprint author), NINDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. OI Kramer, Phillip/0000-0003-0117-542X NR 26 TC 10 Z9 10 U1 0 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 304 BP 639 EP 650 PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12X UT WOS:000087254800036 PM 10372387 ER PT J AU Wade, PA Jones, PL Vermaak, D Wolffe, AP AF Wade, PA Jones, PL Vermaak, D Wolffe, AP TI Purification of a histone deacetylase complex from Xenopus laevis: Preparation of substrates and assay procedures SO CHROMATIN SE METHODS IN ENZYMOLOGY LA English DT Review ID CHROMATIN; ACETYLTRANSFERASE; ACETYLATION C1 NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. RP Wade, PA (reprint author), NICHHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. NR 13 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 304 BP 715 EP 725 PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12X UT WOS:000087254800041 PM 10372392 ER PT J AU Sandaltzopoulos, R Ossipow, V Gdula, DA Tsukiyama, T Wu, C AF Sandaltzopoulos, R Ossipow, V Gdula, DA Tsukiyama, T Wu, C TI Purification of Drosophila nucleosome remodeling factor SO CHROMATIN SE METHODS IN ENZYMOLOGY LA English DT Review ID CHROMATIN; COMPLEX; ISWI; NURF C1 NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA. RP Sandaltzopoulos, R (reprint author), NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. NR 12 TC 4 Z9 4 U1 0 U2 1 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 304 BP 757 EP 765 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12X UT WOS:000087254800044 PM 10372395 ER PT J AU Nuckolls, GH Shum, L Slavkin, HC AF Nuckolls, GH Shum, L Slavkin, HC TI Progress toward understanding craniofacial malformations SO CLEFT PALATE-CRANIOFACIAL JOURNAL LA English DT Review DE genetics; craniofacial disorders; development ID SAETHRE-CHOTZEN-SYNDROME; GROWTH-FACTOR RECEPTOR; AUTOSOMAL-DOMINANT CRANIOSYNOSTOSIS; BONE MORPHOGENETIC PROTEINS; IMMUNOGLOBULIN-LIKE DOMAIN; NONSYNDROMIC ORAL CLEFTS; DEVELOPING CHICK LIMB; NEURAL-TUBE DEFECTS; SONIC-HEDGEHOG; FACTOR-ALPHA AB Significant advances in the study of the human face have revealed the genetic and gene-environment bases of numerous common and rare craniofacial disorders. Classification of craniofacial malformations based on clinical phenotypes is sometimes quite different from the genetic findings of patients. Different mutations in a single gene can cause distinct syndromes, and mutations in different genes can cause the same syndrome. The extracellular signaling molecule SHH, fibroblast growth factor receptors, and transcription factors GLI3, MSX2, and TWIST are discussed as examples of molecules involved in interrelated signal transduction networks regulating craniofacial development. Progress in the understanding of normal and abnormal craniofacial development, through the study of morphoregulatory signaling pathways, has benefited from multifactorial approaches recommended 40 years ago at the National Institute of Dental Research-sponsored landmark Gatlinburg Conference. The utilization of biochemistry, protein structure analyses, tissue culture, and animal model systems for developmental genetics has resulted in remarkable scientific advances. The evolutionary conservation of morphoregulatory pathways has revealed the homology of genes associated with human craniofacial malformations and their counterparts that regulate the morphogenesis of fruit flies. The continued investments in basic, translational, and patient-oriented research regarding normal and abnormal craniofacial development will translate into substantial improvements in the prevention, diagnosis, and treatment of craniofacial diseases and disorders. C1 NIAMSD, Craniofacial Dev Sect, NIH, Bethesda, MD 20892 USA. Natl Inst Dent & Cranofacial Res, NIH, Bethesda, MD USA. RP Nuckolls, GH (reprint author), NIAMSD, Craniofacial Dev Sect, NIH, 6 Ctr Dr,Room 324 MSC2745, Bethesda, MD 20892 USA. EM gn18s@nih.gov NR 112 TC 25 Z9 27 U1 0 U2 3 PU ALLIANCE COMMUNICATIONS GROUP DIVISION ALLEN PRESS PI LAWRENCE PA 810 EAST 10TH STREET, LAWRENCE, KS 66044 USA SN 1545-1569 J9 CLEFT PALATE-CRAN J JI Cleft Palate-Craniofac. J. PD JAN PY 1999 VL 36 IS 1 BP 12 EP 26 DI 10.1597/1545-1569(1999)036<0012:PTUCM>2.3.CO;2 PG 15 WC Dentistry, Oral Surgery & Medicine; Surgery SC Dentistry, Oral Surgery & Medicine; Surgery GA 185XQ UT WOS:000079696600003 PM 10067756 ER PT J AU Ueyama, T Gu, XX Tsai, CM Karpas, AB Lim, DJ AF Ueyama, T Gu, XX Tsai, CM Karpas, AB Lim, DJ TI Identification of common lipooligosaccharide types in isolates from patients with otitis media by monoclonal antibodies against nontypeable Haemophilus influenzae 9274 SO CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY LA English DT Article ID NONTYPABLE HEMOPHILUS-INFLUENZAE; DETOXIFIED LIPOOLIGOSACCHARIDE; NEISSERIA-MENINGITIDIS; LIPOPOLYSACCHARIDES; PROTEINS; STRAIN; CELLS AB Twenty-one murine monoclonal antibodies (MAbs) were induced by nontypeable Haemophilus influenzae (NTHi) 9274, Nineteen MAbs were specific for the lipooligosaccharide (LOS) as determined by enzyme-linked immunosorbent assay (ELISA) and Western blot analysis. When the MAbs were assayed with five LOS prototype strains by ELISA, all bound to strain 3198 LOS (type III), while six of the MAbs were also reactive with LOSs from strain 1479 (type I), 5657 (type IV), or 7502 (type V). Ten MAbs had complement-mediated bactericidal activity, and three MAbs were opsonophagocytic against the homologous strain. Five LOS MAbs with different specificities were used to analyze 155 NTHi clinical isolates from the United States and from Japan. These isolates were classified into nine groups by ELISA. Only four isolates (2.6%) were not recognized by any of the five MAbs. Most of the isolates (91.6%) were in four groups which bound three of the live MAbs. One of three MAbs, 6347C11, had strong activity against the homologous strain and was also bactericidal to 45 clinical isolates (29%) which belonged to the four common patterns (25 belonged to pattern 1). These data indicate that these MAbs can be used for LOS typing in which almost all NTNi strains can be typed according to the LOS antigenicity. Among NTHi, at least one conserved LOS epitope which is a target of bactericidal antibodies exists. We conclude that strain 9274 LOS, which is the target for bactericidal antibodies, is a candidate for LOS-based NTHi vaccines. C1 NIDCD, Immunol Lab, NIH, Rockville, MD 20850 USA. US FDA, Ctr Biol Evaluat & Res, Bethesda, MD USA. NICHHD, Dev & Mol Immun Lab, Bethesda, MD 20892 USA. RP Gu, XX (reprint author), NIDCD, Immunol Lab, NIH, 5 Res Ct,2A31, Rockville, MD 20850 USA. EM guxx@nidcd.nih.gov NR 25 TC 11 Z9 11 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 1071-412X J9 CLIN DIAGN LAB IMMUN JI Clin. Diagn. Lab. Immunol. PD JAN PY 1999 VL 6 IS 1 BP 96 EP 100 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 156BE UT WOS:000077980900017 PM 9874671 ER PT J AU Hornick, JL Khawli, LA Hu, PS Sharifi, J Khanna, C Epstein, AL AF Hornick, JL Khawli, LA Hu, PS Sharifi, J Khanna, C Epstein, AL TI Pretreatment with a monoclonal antibody/interleukin-2 fusion protein directed against DNA enhances the delivery of therapeutic molecules to solid tumors SO CLINICAL CANCER RESEARCH LA English DT Article ID TARGETED INTERLEUKIN-2 THERAPY; VASCULAR-PERMEABILITY; NECROSIS-FACTOR; ANTIBODY UPTAKE; NITRIC-OXIDE; RECOMBINANT INTERLEUKIN-2; MEMBRANE ANTIGEN; NUDE-MICE; TOXICITY; CANCER AB The efficacy of molecular therapies for human malignancies is limited by inadequate accumulation within solid tumors. Our laboratory has developed a novel approach that uses monoclonal antibodies (MAbs) to direct vasoactive proteins to tumor sites to increase local vascular permeability and, in turn, improve the delivery of therapeutic reagents. previously, we demonstrated that pretreatment with immunoconjugates containing interleukin-2 (IL-2) enhances specific tumor uptake of radiolabeled MAbs without affecting normal tissues. In the present study, we describe a fusion protein consisting of a chimeric antinuclear antibody and IL-2 (chTNT-3/IL-2) and illustrate its potential for improving the delivery of both MAbs and drugs. The ability of pretreatment with chTNT-3/IL-2 to increase specific tumor uptake of the MAb B72.3 was demonstrated in LS174T colon tumor-bearing mice. Tumor accretion of B72.3 increased nearly 3-fold, with no changes in normal tissues. Abrogation of this effect,vith N-G-methyl-l-arginine, a chemical inhibitor of nitric oxide synthase, suggests that rapid generation of nitric oxide in the tumor is responsible for the enhanced uptake. To demonstrate that pretreatment with chTNT-3/IL-2 can improve the uptake of other clinically relevant MAbs in different tumor models, additional studies were performed in both lung and prostate xenograft models. Pretreatment with the fusion protein increased specific tumor uptake of the MAb NR-LU-10 in A427 lung tumor-bearing mice and enhanced tumor uptake of the MAb CYT-351 in LNCaP prostate tumor-bearing mice, 2.1-fold and 1.7-fold, respectively. Finally, tumor uptake of the radiolabeled thymidine analogue (125)IUdR also increased similar to 3-fold after pretreatment, indicating that this approach can be extended to small molecules such as chemotherapeutic drugs. Because TNT-3 recognizes a universal nuclear antigen accessible in degenerating and necrotic cells within all solid tumors, this strategy may be applicable to the majority of human cancers. C1 Univ So Calif, Sch Med, Dept Pathol, Los Angeles, CA 90033 USA. NCI, Pediat Branch, NIH, Bethesda, MD 20892 USA. RP Epstein, AL (reprint author), Univ So Calif, Sch Med, Dept Pathol, 2011 Zonal Ave,HMR 210, Los Angeles, CA 90033 USA. NR 63 TC 45 Z9 48 U1 1 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN PY 1999 VL 5 IS 1 BP 51 EP 60 PG 10 WC Oncology SC Oncology GA 157AX UT WOS:000078037600009 PM 9918202 ER PT J AU Stearns, ME Rhim, J Wang, M AF Stearns, ME Rhim, J Wang, M TI Interleukin 10 (IL-10) inhibition of primary human prostate cell-induced angiogenesis: IL-10 stimulation of tissue inhibitor of metalloproteinase-1 and inhibition of matrix metalloproteinase (MMP)-2/MMP-9 secretion SO CLINICAL CANCER RESEARCH LA English DT Article ID ENDOTHELIAL-CELLS; HUMAN-MELANOMA; TUMOR-GROWTH; IN-VITRO; INVITRO; CULTURE; DENSITY; CANCER; LINES AB In in vitro angiogenesis assays, aggregates of human papilloma virus (HPV)-18-immortalized primary human prostate cancer cells (HPCA-5aHPV-18 or HPCA-10aHPV-18 cells) induced human bone marrow endothelial cells (HBMCE-1 cells) to form microvessels in three-dimensional collagen I gels after 1-2 days incubation at 37 degrees C. The microvessels aligned perpendicular to the tumor aggregates and abutted on the edges of the aggregates. The number and length of the microvessels increased significantly from day 1 to 2 (i.e., by similar to 30%). ELISAs showed that the HPCA-5aHPV-18 cells normally secreted low levels of tissue inhibitor of metalloproteinase (TIMP)-2, matrix metalloproteinase (MMP)-2, and MMP-9 but relatively high levels of TIMP-1. In contrast, HPCA-10aHPV-18 cells secreted high levels of MMP-2 and MMP-9 (>40 pg/mu g protein) but low levels of TIMP-1 and TIMP-2 (<5 pg/mu g protein). Interleukin 10 (IL-10) (15 ng/ml) induced TIMP-1 production (>15 pg/mu g protein) but reduced MMP-2 and MMP-9 secretion (<5 pg/mu g protein) by the HPCA-10aHPV-18 and HPCA-10aHPV-18 cells. IL-10 (15 ng/ml) and MMP-9/MMP-2 antibodies all blocked induction of microvessel formation in the coculture experiments, In contrast, IL-10 receptor antibodies and TIMP-1 antibodies countered IL-10's effects and promoted angiogenesis, The data demonstrated that IL-10 stimulation of TIMP-1 and inhibition of MMP-2 and MMP-9 secretion by prostate tumor cells can control induction of angiogenesis in vitro. C1 Med Coll Penn & Hahnemann Univ, Dept Pathol & Lab Sci, Philadelphia, PA 19102 USA. NCI, NIH, Bethesda, MD 20892 USA. RP Stearns, ME (reprint author), Med Coll Penn & Hahnemann Univ, Dept Pathol & Lab Sci, 15th & Vine St,Mail Stop 435, Philadelphia, PA 19102 USA. NR 24 TC 106 Z9 112 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI BIRMINGHAM PA PO BOX 11806, BIRMINGHAM, AL 35202 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN PY 1999 VL 5 IS 1 BP 189 EP 196 PG 8 WC Oncology SC Oncology GA 157AX UT WOS:000078037600025 PM 9918218 ER PT J AU March, KL Woody, M Mehdi, K Zipes, DP Brantly, M Trapnell, BC AF March, KL Woody, M Mehdi, K Zipes, DP Brantly, M Trapnell, BC TI Efficient in vivo catheter-based pericardial gene transfer mediated by adenoviral vectors SO CLINICAL CARDIOLOGY LA English DT Article; Proceedings Paper CT Intrapericardial Therapeutic and Diagnostics Workshop CY JUL 28, 1998 CL CHICAGO, ILLINOIS ID IN-VIVO; GROWTH-FACTOR; CYSTIC-FIBROSIS; MYOCARDIUM; DISEASE; THERAPY; FLUID; DOGS; POLOXAMER-407; DELIVERY AB Adenoviral vectors are promising agents for a number of in vivo gene therapy applications including diseases of the heart and coronary vessels. Efficient intravascular gene transfer to specific sites has been achieved in occluded vessels, but otherwise is hampered by the effect of blood flow on localized vector uptake in the vessel wall. An alternative delivery approach to coronary arteries is the expression of diffusible gene products into the pericardial space surrounding the heart and coronary arteries. However, in vivo pericardial access is comparatively difficult and has been limited to surgical approaches. We hypothesized that efficient adenovirus-mediated gene expression in pericardial lining mesothelium could be achieved by transmyocardial vector delivery to the pericardium. To evaluate this concept, a hollow, helical-tipped penetrating catheter was used to deliver vector-containing fluid directly into the intrapericardial space. The catheter was introduced percutaneously in anesthetized mongrel dogs, advanced into the right ventricle, and the tip passed through the apical right ventricular myocardium under direct radiographic visualization until the open end of the catheter tip resided in the intrapericardial space. Adenoviral vectors expressing either nuclear-localizing beta-galactosidase, cytoplasmic luciferase, or secreted human alpha 1AT reporters (Av1nBg, Av1Lu, or Av1Aa, respectively) were instilled through the catheter into the intrapericardial space. Three days later the animals were sacrificed and reporter gene expression was evaluated in pericardium, epicardium, and multiple other tissues. In animals receiving AvlnBg, beta-galactosidase activity was evident in most of the pericardial lining endothelium, up to 100% in many areas. In animals receiving Av1Lu, luciferase reporter activity was abundant in pericardial tissues, but near-background levels were observed in other organs. In animals receiving Av1Aa, human alpha 1AT was abundant (16-29 mg/ml) in pericardial fluid, but was undetectable in serum. All animals tolerated the procedure well with no electrocardiographic changes and no clinical sequelae. These observations demonstrate highly efficient adenovirus vector delivery and gene transfer and expression in the pericardium and support the feasibility of localized gene therapy via catheter-based pericardial approaches. We suggest that the pericardial sac may serve as a sustained-release protein delivery system for the generation of desired gene products or their metabolites for diffusion into the epicardial region. C1 Indiana Univ, Sch Med, Krannert Inst Cardiol, Indianapolis, IN 46202 USA. Richard L Roudebush Vet Adm Med Ctr, Indianapolis, IN 46202 USA. NIH, Pulm Branch, Bethesda, MD 20892 USA. Childrens Hosp, Med Ctr, Div Pulm Biol, Cincinnati, OH 45229 USA. RP March, KL (reprint author), Indiana Univ, Sch Med, Krannert Inst Cardiol, 1111 W 10th St, Indianapolis, IN 46202 USA. FU NHLBI NIH HHS [HL52323] NR 45 TC 14 Z9 14 U1 0 U2 2 PU CLINICAL CARDIOLOGY PUBL CO PI MAHWAH PA PO BOX 832, MAHWAH, NJ 07430-0832 USA SN 0160-9289 J9 CLIN CARDIOL JI Clin. Cardiol. PD JAN PY 1999 VL 22 IS 1 SU 1 BP I23 EP I29 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 159AN UT WOS:000078149800007 PM 9929764 ER PT J AU Stoll, HP Carlson, K Keefer, LK Hrabie, JA March, KL AF Stoll, HP Carlson, K Keefer, LK Hrabie, JA March, KL TI Pharmacokinetics and consistency of pericardial delivery directed to coronary arteries: Direct comparison with endoluminal delivery SO CLINICAL CARDIOLOGY LA English DT Article; Proceedings Paper CT Intrapericardial Therapeutic and Diagnostics Workshop CY JUL 28, 1998 CL CHICAGO, ILLINOIS DE pericardium; coronary disease; local drug delivery; restenosis; angiogenesis ID LOCAL-DRUG DELIVERY; BALLOON ANGIOPLASTY; CATHETER; MICROPARTICLES; LOCALIZATION; HEPARIN; WALL AB Background and hypothesis: Pharmacologic modulation of the contents of the pericardial space has been shown to influence the response of coronary arteries to balloon injury. Endoluminal (EL) local delivery of various drugs into coronaries has been found to be limited by short residence time, as well as by highly variable deposited agent concentration. We hypothesized that compounds placed into the pericardial space (P) would penetrate into coronary tissue with greater consistency than seen after EL delivery and provide for prolonged coronary exposure to agents. Methods and Results: I-125-labeled basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), albumin, or I-131-labeled diazeniumdiolated albumin (NONO-albumin) were delivered as model/therapeutic proteins into the porcine pericardial space (n = 15 pigs) or into coronaries using an EL delivery catheter (n = 48 arteries). In subjects receiving I-125-labeled proteins, the delivery target or mid-regions of the left anterior descending (LAD) and left circumflex (LCx) arteries were harvested at 1 h or 24 h for gamma-counting and autoradiography, and fractional intramural delivery (FID) or retention measured as percent agent in 100 mg artery/agent in infusate for both time points. In the animals receiving I-131-labeled NONO-albumin, serial gamma imaging was employed to evaluate the rate of redistribution in individual animals following either pericardial or endoluminal delivery. At 1 h, FID values ranged from 0.00064 to 0.0052% for P delivery (median 0.0022%), and from 0.00021 to 6.7 for EL delivery (median 0.27%). At 23 h, FID values ranged from 0.00011 to 0.003 for P delivery (median 0.0013), and from 0.0002 to 1,4 for EL delivery. The estimated T1/2 for bFGF redistribution from the vascular tissue was 22 h (P) and 7 h (EL), respectively, while the directly determined T1/2 values fur NONO-albumin redistribution from the delivery region were 22.2 h (P) and 2.5 h (EL). Conclusions: These data show that pericardial fluid contents can access coronary arteries with intramural concentrations which typically vary by 10-15-fold, while EL delivery results in a remarkably wide intramural concentration range with up to 33,000-fold variability The apparent redistribution rate is more rapid following EL delivery, possibly clue to sustained diffusive tissue loading from the pericardial space. Pericardial delivery appears to offer substantial advantages over EL administration with respect to residence lime and reproducibility. C1 Indiana Univ, Med Ctr, Sch Med, Krannert Inst Cardiol, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Radiol, Indianapolis, IN 46202 USA. NCI, Chem Sect, Comparat Carcinogenesis Lab, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. NCI, Chem Synth & Anal Lab, SAIC Frederick, FCRDC, Frederick, MD 21701 USA. Richard L Roudebush Vet Adm Med Ctr, Indianapolis, IN 46202 USA. RP March, KL (reprint author), Indiana Univ, Med Ctr, Sch Med, Krannert Inst Cardiol, 1111 W 10th St, Indianapolis, IN 46202 USA. RI Keefer, Larry/N-3247-2014 OI Keefer, Larry/0000-0001-7489-9555 NR 23 TC 1 Z9 1 U1 0 U2 1 PU CLINICAL CARDIOLOGY PUBL CO PI MAHWAH PA PO BOX 832, MAHWAH, NJ 07430-0832 USA SN 0160-9289 J9 CLIN CARDIOL JI Clin. Cardiol. PD JAN PY 1999 VL 22 IS 1 SU 1 BP I10 EP I16 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 159AN UT WOS:000078149800005 PM 9929762 ER PT J AU Murphy, WJ Funakoshi, S Fanslow, WC Rager, HC Taub, DD Longo, DL AF Murphy, WJ Funakoshi, S Fanslow, WC Rager, HC Taub, DD Longo, DL TI CD40 stimulation promotes human secondary immunoglobulin responses in HuPBL-SCID chimeras SO CLINICAL IMMUNOLOGY LA English DT Article DE CD40; SCID; antigen-specific; xenogenic chimera; adjuvant; humoral response; human/mouse chimera; B cell ID PERIPHERAL-BLOOD LYMPHOCYTES; VIVO CD40-GP39 INTERACTIONS; DEPENDENT HUMORAL IMMUNITY; ANTIBODY-PRODUCTION; FACTOR RECEPTOR; LIGAND; MICE; ACTIVATION; CELLS; CYTOKINES AB Antibodies to CD40 have been demonstrated to promote B-cell, growth and differentiation in vitro. In order to determine if CD40 stimulation could promote antigen-specific human immunoglobulin (Ig) production in vivo we examined the effects of anti-human CD40 MoAb in an in vivo system where human peripheral blood lymphocytes (huPBL) were engrafted into mice with severe combined immune deficiency (SCID). The huPBL-SCID mice were then given various doses of diphtheria-tetanus toroid (DT) vaccine and were examined for the presence of human DT-specific antibodies by ELISA. Surprisingly treatment with anti-CD40 significantly lowered background DT responses versus untreated chimeras in unimmunized huPBL-SCID mice. However, after immunization, huPBL-SCID mice treated with anti-CDBO MoAb responded to a significantly greater extent in response 60 the vaccine compared with control huPBL-SCID mice, although total Ig levels were sometimes lower in anti-CD40-treated mice. The predominant Ig isotype induced after immunization was IgG. Thus, CD40 stimulation promotes human secondary IgG responses in huPBL-SCID mice. These data demonstrate that CD40 stimulation is capable of promoting antigen-specific human B-cell responses in vice. (C) 1999 Academic Press. C1 NCI, Lab Leukocyte Biol, Div Basic Sci, SAIC Frederick,Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. NCI, Intramural Res Support Program, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. NCI, Clin Serv Program, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA. Immunex Corp, Seattle, WA USA. NIA, Baltimore, MD 21224 USA. RP Murphy, WJ (reprint author), NCI, Lab Leukocyte Biol, Div Basic Sci, SAIC Frederick,Frederick Canc Res & Dev Ctr, Bldg 567,Room 210, Frederick, MD 21702 USA. EM murphyw@ncifcrf.gov FU NCI NIH HHS [N01-CO-56000] NR 21 TC 8 Z9 7 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PD JAN PY 1999 VL 90 IS 1 BP 22 EP 27 DI 10.1006/clim.1998.4632 PG 6 WC Immunology SC Immunology GA 176NT UT WOS:000079158600004 PM 9884349 ER PT B AU Hallett, M AF Hallett, M BE Comi, G Lucking, CH Kimura, J Rossini, PM TI Motor cortex plasticity SO CLINICAL NEUROPHYSIOLOGY: FROM RECEPTORS TO PERCEPTION SE ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY SUPPLEMENT LA English DT Proceedings Paper CT 14th International Congress of EEG and Clinical Neurophysiology CY AUG 24-29, 1997 CL FLORENCE, ITALY SP Palazzo Congressi ID TRANSCRANIAL MAGNETIC STIMULATION; HUMAN CEREBRAL-CORTEX; FUNCTIONAL REORGANIZATION; CORTICAL OUTPUTS; BRAILLE READERS; READING HAND; ACUTE STROKE; BLOOD-FLOW; RECOVERY; MODULATION C1 NINDS, NIH, Human Motor Control Sect, Med Neurol Branch, Bethesda, MD 20892 USA. RP Hallett, M (reprint author), NINDS, NIH, Human Motor Control Sect, Med Neurol Branch, Bldg 10,Room 5N226, Bethesda, MD 20892 USA. NR 40 TC 14 Z9 14 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-50048-0 J9 EEG CL N SU PY 1999 VL 50 BP 85 EP 91 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA BP61N UT WOS:000085689700009 PM 10689449 ER PT J AU Jonas, WB AF Jonas, WB TI Complementary and alternative medicine and the NIH SO CLINICS IN DERMATOLOGY LA English DT Article ID RHEUMATOID-ARTHRITIS; OSTEOARTHRITIS; EFFICACY; THERAPY; TRIAL C1 Uniformed Serv Univ Hlth Sci, Dept Family Med, Bethesda, MD 20814 USA. RP Jonas, WB (reprint author), NIH, Off Alternat Med, Room Bldg 5B37-31, Bethesda, MD 20892 USA. NR 29 TC 4 Z9 4 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0738-081X J9 CLIN DERMATOL JI Clin. Dermatol. PD JAN-FEB PY 1999 VL 17 IS 1 BP 99 EP 103 DI 10.1016/S0738-081X(98)00055-8 PG 5 WC Dermatology SC Dermatology GA 173RG UT WOS:000078993100014 PM 10089592 ER PT J AU Alizadeh, A Eisen, M Davis, RE Ma, C Sabet, H Tran, T Powell, JI Yang, L Marti, GE Moore, DT Hudson, JR Chan, WC Greiner, T Weisenburger, D Armitage, JO Lossos, I Levy, R Botstein, D Brown, PO Staudt, LM AF Alizadeh, A Eisen, M Davis, RE Ma, C Sabet, H Tran, T Powell, JI Yang, L Marti, GE Moore, DT Hudson, JR Chan, WC Greiner, T Weisenburger, D Armitage, JO Lossos, I Levy, R Botstein, D Brown, PO Staudt, LM TI The lymphochip: A specialized cDNA microarray for the genomic-scale analysis of gene expression in normal and malignant lymphocytes SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 64th Symposia: Signaling and Gene Expression in the Immune System CY JUN 02-07, 1999 CL NEW YORK, NEW YORK SP Alafi Capital Co, Amgen Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med, Diagnost Prod Corp, Du Pont Pharmaceut Co, Forest Labs, Genentech Inc, Genet Inst, Glaxo Wellcome Inc, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Eli Lilly & Co, Merck Res Labs, New England BioLabs Inc, Novartis Pharma Res, OSI Pharmaceut Inc, Pall Corp, Parke Davis Pharmaceut Res, PE Biosyst, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Schering Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC ID B-CELL LINE; OLIGONUCLEOTIDE ARRAYS; GERMINAL-CENTERS; DNA MICROARRAY; PATTERNS; MUTATION; HYPERMUTATION; HYBRIDIZATION; LYMPHOMAS; EXPANSION C1 NCI, Metab Branch, Div Clin Sci, NIH, Bethesda, MD 20892 USA. Stanford Univ, Sch Med, Dept Biochem, Stanford, CA 94035 USA. Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94035 USA. Stanford Univ, Sch Med, Dept Med, Stanford, CA 94035 USA. Stanford Univ, Sch Med, Howard Hughes Med Inst, Stanford, CA 94035 USA. NIH, Bioinformat & Mol Anal Sect, CBEL, CTT, Bethesda, MD 20892 USA. US FDA, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA. Res Genet Inc, Huntsville, AL 35801 USA. Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA. Univ Nebraska, Med Ctr, Dept Med, Omaha, NE 68198 USA. RP Alizadeh, A (reprint author), NCI, Metab Branch, Div Clin Sci, NIH, Bethesda, MD 20892 USA. OI Eisen, Michael/0000-0002-7528-738X; Alizadeh, Arash Ash/0000-0002-5153-5625 NR 32 TC 182 Z9 187 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1999 VL 64 BP 71 EP 78 DI 10.1101/sqb.1999.64.71 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 317KW UT WOS:000087225400011 PM 11232339 ER PT J AU Gellert, M Hesse, JE Hiom, K Melek, M Modesti, M Paull, TT Ramsden, DA van Gent, DC AF Gellert, M Hesse, JE Hiom, K Melek, M Modesti, M Paull, TT Ramsden, DA van Gent, DC TI V(D)J recombination: Links to transposition and double-strand break repair SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 64th Symposia: Signaling and Gene Expression in the Immune System CY JUN 02-07, 1999 CL NEW YORK, NEW YORK SP Alafi Capital Co, Amgen Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med, Diagnost Prod Corp, Du Pont Pharmaceut Co, Forest Labs, Genentech Inc, Genet Inst, Glaxo Wellcome Inc, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Eli Lilly & Co, Merck Res Labs, New England BioLabs Inc, Novartis Pharma Res, OSI Pharmaceut Inc, Pall Corp, Parke Davis Pharmaceut Res, PE Biosyst, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Schering Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC ID DEPENDENT PROTEIN-KINASE; DNA-LIGASE-IV; RAG2 PROTEINS; CHROMOSOMAL TRANSLOCATIONS; JOINT FORMATION; IMMUNE-SYSTEM; MECHANISM; INTEGRATION; COMPLEX; SIMILARITIES C1 NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. Erasmus Univ, Dept Cell Biol & Genet, Rotterdam, Netherlands. RP Gellert, M (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RI Hiom, Kevin/B-4374-2009 NR 43 TC 18 Z9 18 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1999 VL 64 BP 161 EP 167 DI 10.1101/sqb.1999.64.161 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 317KW UT WOS:000087225400020 PM 11232281 ER PT J AU Baker, BM Ding, YH Garboczi, DN Biddison, WE Wiley, DC AF Baker, BM Ding, YH Garboczi, DN Biddison, WE Wiley, DC TI Structural, biochemical, and biophysical studies of HLA-A2/altered peptide ligands binding to viral-peptide-specific human T-cell receptors SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 64th Symposia: Signaling and Gene Expression in the Immune System CY JUN 02-07, 1999 CL NEW YORK, NEW YORK SP Alafi Capital Co, Amgen Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med, Diagnost Prod Corp, Du Pont Pharmaceut Co, Forest Labs, Genentech Inc, Genet Inst, Glaxo Wellcome Inc, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Eli Lilly & Co, Merck Res Labs, New England BioLabs Inc, Novartis Pharma Res, OSI Pharmaceut Inc, Pall Corp, Parke Davis Pharmaceut Res, PE Biosyst, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Schering Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC ID PROTEIN-PROTEIN RECOGNITION; COMPLEX; TCR; ACTIVATION; REPERTOIRE; INTERFACES; AFFINITY; KINETICS; ANTIGEN; CLONES C1 Harvard Univ, Dept Cellular & Mol Biol, Cambridge, MA 02138 USA. Howard Hughes Med Inst, Cambridge, MA 02138 USA. NIAID, Struct Biol Sect, NIH, Rockville, MD 20852 USA. NINDS, Mol Immunol Sect, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA. RP Baker, BM (reprint author), Harvard Univ, Dept Cellular & Mol Biol, Cambridge, MA 02138 USA. RI Baker, Brian/B-4584-2009 OI Baker, Brian/0000-0002-0864-0964 FU NIAID NIH HHS [AI-39619] NR 30 TC 11 Z9 11 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1999 VL 64 BP 235 EP 241 DI 10.1101/sqb.1999.64.235 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 317KW UT WOS:000087225400029 PM 11232291 ER PT J AU Samelson, LE Bunnell, SC Trible, RP Yamazaki, T Zhang, W AF Samelson, LE Bunnell, SC Trible, RP Yamazaki, T Zhang, W TI Studies on the adapter molecule LAT SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 64th Symposia: Signaling and Gene Expression in the Immune System CY JUN 02-07, 1999 CL NEW YORK, NEW YORK SP Alafi Capital Co, Amgen Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med, Diagnost Prod Corp, Du Pont Pharmaceut Co, Forest Labs, Genentech Inc, Genet Inst, Glaxo Wellcome Inc, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Eli Lilly & Co, Merck Res Labs, New England BioLabs Inc, Novartis Pharma Res, OSI Pharmaceut Inc, Pall Corp, Parke Davis Pharmaceut Res, PE Biosyst, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Schering Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC ID CELL ANTIGEN RECEPTOR; SIGNAL-TRANSDUCTION; TYROSINE PHOSPHORYLATION; PROTEIN SLP-76; T-CELLS; ACTIVATION; ZAP-70; TCR; STIMULATION; KINASES C1 NCI, Lab Cellular & Mol Biol, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP Samelson, LE (reprint author), NCI, Lab Cellular & Mol Biol, Div Basic Sci, NIH, Bethesda, MD 20892 USA. NR 32 TC 4 Z9 4 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1999 VL 64 BP 259 EP 263 DI 10.1101/sqb.1999.64.259 PG 5 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 317KW UT WOS:000087225400032 PM 11232294 ER PT J AU Leonard, WJ Imada, K Nakajima, H Puel, A Soldaini, E John, S AF Leonard, WJ Imada, K Nakajima, H Puel, A Soldaini, E John, S TI Signaling via the IL-2 and IL-7 receptors from the membrane to the nucleus SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 64th Symposia: Signaling and Gene Expression in the Immune System CY JUN 02-07, 1999 CL NEW YORK, NEW YORK SP Alafi Capital Co, Amgen Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med, Diagnost Prod Corp, Du Pont Pharmaceut Co, Forest Labs, Genentech Inc, Genet Inst, Glaxo Wellcome Inc, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Eli Lilly & Co, Merck Res Labs, New England BioLabs Inc, Novartis Pharma Res, OSI Pharmaceut Inc, Pall Corp, Parke Davis Pharmaceut Res, PE Biosyst, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Schering Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC ID SEVERE COMBINED IMMUNODEFICIENCY; DEFECTIVE LYMPHOID DEVELOPMENT; RESCUES T-LYMPHOPOIESIS; COMMON GAMMA-CHAIN; MICE LACKING JAK3; INTERLEUKIN-2 RECEPTOR; BETA-CHAIN; ALPHA-CHAIN; GENE-EXPRESSION; DEFICIENT MICE C1 NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. RP Leonard, WJ (reprint author), NHLBI, Lab Mol Immunol, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 62 TC 11 Z9 12 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1999 VL 64 BP 417 EP 424 DI 10.1101/sqb.1999.64.417 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 317KW UT WOS:000087225400051 PM 11232316 ER PT J AU Baer, M Nedospasov, S Johnson, PF AF Baer, M Nedospasov, S Johnson, PF TI Attenuation of tumor necrosis factor alpha gene transcription in macrophages by an autocrine factor SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 64th Symposia: Signaling and Gene Expression in the Immune System CY JUN 02-07, 1999 CL NEW YORK, NEW YORK SP Alafi Capital Co, Amgen Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med, Diagnost Prod Corp, Du Pont Pharmaceut Co, Forest Labs, Genentech Inc, Genet Inst, Glaxo Wellcome Inc, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Eli Lilly & Co, Merck Res Labs, New England BioLabs Inc, Novartis Pharma Res, OSI Pharmaceut Inc, Pall Corp, Parke Davis Pharmaceut Res, PE Biosyst, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Schering Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC ID NF-KAPPA-B; PROTOONCOGENE BCL-3 ENCODES; CYTOKINE PRODUCTION; P50 HOMODIMERS; NUCLEAR FACTOR; CELL-LINE; LIPOPOLYSACCHARIDE; EXPRESSION; BETA; PROSTAGLANDIN-E2 C1 NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Intramural Res Support Program, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Div Basic Sci, Frederick, MD 21702 USA. Russian Acad Sci, Engelhardt Inst Mol Biol, Moscow 119899, Russia. Moscow State Univ, Belozersky Inst Phys Chem Biol, Moscow 119899, Russia. RP Baer, M (reprint author), NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Frederick, MD 21702 USA. RI Johnson, Peter/A-1940-2012; Nedospasov, Sergei/J-5936-2013; Nedospasov, Sergei/L-1990-2015; Nedospasov, Sergei/Q-7319-2016 OI Johnson, Peter/0000-0002-4145-4725; FU NCI NIH HHS [N01-CO-56000] NR 38 TC 1 Z9 1 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1999 VL 64 BP 437 EP 444 DI 10.1101/sqb.1999.64.437 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 317KW UT WOS:000087225400054 PM 11232319 ER PT J AU Lopez-Rodriguez, C Aramburu, J Rakeman, AS Copeland, NG Gilbert, DJ Thomas, S Disteche, C Jenkins, NA Rao, A AF Lopez-Rodriguez, C Aramburu, J Rakeman, AS Copeland, NG Gilbert, DJ Thomas, S Disteche, C Jenkins, NA Rao, A TI NF-AT5: The NF-AT family of transcription factors expands in a new direction SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 64th Symposia: Signaling and Gene Expression in the Immune System CY JUN 02-07, 1999 CL NEW YORK, NEW YORK SP Alafi Capital Co, Amgen Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med, Diagnost Prod Corp, Du Pont Pharmaceut Co, Forest Labs, Genentech Inc, Genet Inst, Glaxo Wellcome Inc, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Eli Lilly & Co, Merck Res Labs, New England BioLabs Inc, Novartis Pharma Res, OSI Pharmaceut Inc, Pall Corp, Parke Davis Pharmaceut Res, PE Biosyst, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Schering Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC ID ACTIVATED T-CELLS; KAPPA-B SITE; NUCLEAR FACTOR; FACTOR NFAT1; FUNCTIONAL-CHARACTERIZATION; GENE-EXPRESSION; BINDING PROTEIN; CYCLOSPORINE-A; MICE LACKING; CALCINEURIN C1 Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Mammalian Genet Lab, Frederick, MD 21702 USA. Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA. RP Lopez-Rodriguez, C (reprint author), Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA. RI Lopez-Rodriguez, C/G-4482-2014; Aramburu, J/G-8991-2014 OI Lopez-Rodriguez, C/0000-0002-2311-2406; Aramburu, J/0000-0001-9279-9523 FU NCI NIH HHS [CA-42471]; NIAID NIH HHS [AI-40127] NR 53 TC 24 Z9 26 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1999 VL 64 BP 517 EP 526 DI 10.1101/sqb.1999.64.517 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 317KW UT WOS:000087225400062 PM 11233530 ER PT J AU Pannetier, C Hu-Li, J Paul, WE AF Pannetier, C Hu-Li, J Paul, WE TI Bias in the expression of IL-4 alleles: The use of T cells from a GFP knock-in mouse SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 64th Symposia: Signaling and Gene Expression in the Immune System CY JUN 02-07, 1999 CL NEW YORK, NEW YORK SP Alafi Capital Co, Amgen Inc, BASF Biores Corp, Bayer Corp, Bristol Myers Squibb Co, Chiron Corp, Chugai Res Inst Molec Med, Diagnost Prod Corp, Du Pont Pharmaceut Co, Forest Labs, Genentech Inc, Genet Inst, Glaxo Wellcome Inc, Hoechst Marion Roussel, Hoffmann La Roche Inc, Johnson & Johnson, Eli Lilly & Co, Merck Res Labs, New England BioLabs Inc, Novartis Pharma Res, OSI Pharmaceut Inc, Pall Corp, Parke Davis Pharmaceut Res, PE Biosyst, Pfizer Inc, Pharmacia & Upjohn Inc, Res Genet Inc, Schering Plough Corp, SmithKline Beecham Pharmaceut, Wyeth Ayerst Res, Zeneca Grp PLC ID STIMULATORY FACTOR-I; GENE-EXPRESSION; DIFFERENTIATION; ACTIVATION; RECEPTOR C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Pannetier, C (reprint author), NIAID, Immunol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 16 TC 7 Z9 7 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1999 VL 64 BP 599 EP 602 DI 10.1101/sqb.1999.64.599 PG 4 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 317KW UT WOS:000087225400071 PM 11232337 ER PT S AU Schatzkin, A AF Schatzkin, A GP KLUWER ACADEMIC TI Dietary intervention studies of colorectal cancer SO COLON CANCER PREVENTION: DIETARY MODULATION OF CELLULAR AND MOLECULAR MECHANISMS SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 8th Annual Research Conference of the American-Institute-for-Cancer-Research CY SEP 03-04, 1998 CL WASHINGTON, D.C. SP Amer Inst Canc Res ID FAMILIAL ADENOMATOUS POLYPOSIS; LARGE-BOWEL CANCER; RANDOMIZED TRIAL; ANTIOXIDANT VITAMINS; PREVENTION; FIBER; RECURRENCE; FAT; CARCINOMA; DESIGN C1 NCI, Div Can Etiol & Genet, Bethesda, MD 20892 USA. RP Schatzkin, A (reprint author), NCI, Div Can Etiol & Genet, 9000 rockville Pike,EPN 211, Bethesda, MD 20892 USA. NR 21 TC 0 Z9 0 U1 1 U2 1 PU KLUWER ACADEMIC / PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46207-9 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1999 VL 470 BP 85 EP 93 PG 9 WC Oncology; Medicine, Research & Experimental; Nutrition & Dietetics SC Oncology; Research & Experimental Medicine; Nutrition & Dietetics GA BP75W UT WOS:000086075300009 PM 10709677 ER PT S AU Bogardus, C Baier, L Pratley, R Prochazka, M Hanson, R AF Bogardus, C Baier, L Pratley, R Prochazka, M Hanson, R BE Imura, H Kasuga, M Nakao, K TI Studies of the etiology of type 2 diabetes mellitus in Pima Indians SO COMMON DISEASE: GENETIC AND PATHOGENETIC ASPECTS OF MULTIFACTORIAL DISEASES SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 6th Uehara-Memorial-Foundation International Symposium on Common Disease CY JUN 30-JUL 02, 1999 CL TOKYO, JAPAN SP Uehara Mem Fdn ID AUTOSOMAL GENOMIC SCAN; INSULIN-RESISTANCE; LINKAGE ANALYSIS; GENE AB The Pima Indians of Arizona have the world's highest reported prevalence of type 2 diabetes mellitus. Prospective studies indicate that obesity, insulin resistance and decreased insulin secretory function are found in Pimas with normal glucose tolerance and are predictive of the disease. These risk factors appear to be genetically determined and diabetes itself appears to be oligogenic in nature. To identify the genes which contribute to the development of the disease, we have recently completed a genomic scan of microsatellite markers on more than 1300 Pima DNA samples. Sib-pair linkage analyses identified regions on chromosomes one, seven and II which are potentially linked to diabetes. The same region on chromosome 11 also was linked to measures of adiposity, which may indicate that this region contains a gene (or genes) which contribute to both diabetes and obesity. The genetic linkage to diabetes on chromosome seven appears to result, in part, from a functional polymorphism altering a mRNA destablizing element in the gene encoding the glycogen targeting subunit of protein phosphatase 1. To identify the genetic basis for the linkage to diabetes on chromosome one and diabetes and obesity on chromosome II, evenly spaced, single nucleotide polymorphisms are being identified across these regions and analyzed for linkage disequilibrium with these phenotypes. C1 NIDDKD, Clin Diabet & Nutr Sect, NIH, Phoenix, AZ 85016 USA. RP Bogardus, C (reprint author), NIDDKD, Clin Diabet & Nutr Sect, NIH, 4212 N 16Th St,Room 541, Phoenix, AZ 85016 USA. NR 13 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-50200-9 J9 INT CONGR SER PY 1999 VL 1181 BP 101 EP 106 PG 6 WC Genetics & Heredity; Medicine, General & Internal SC Genetics & Heredity; General & Internal Medicine GA BP49E UT WOS:000085307700012 ER PT J AU Turkheimer, F Pettigrew, K Sokoloff, L Schmidt, K AF Turkheimer, F Pettigrew, K Sokoloff, L Schmidt, K TI A minimum variance adaptive technique for parameter estimation and hypothesis testing SO COMMUNICATIONS IN STATISTICS-SIMULATION AND COMPUTATION LA English DT Article DE robust statistics; bootstrap; permutation tests ID LEAST-SQUARES; ROBUST; REGRESSION; LECTURE AB This report presents numerical results of an approach for parameter estimation and hypothesis testing that does not rely on specific assumptions about the underlying distribution of errors in the measured data. This approach combines robust estimation procedures, the bootstrap method for estimation of parameter uncertainties, permutation techniques for hypothesis testing, and adaptive approaches to estimation in order to obtain the minimum variance estimator or test statistic (within a predefined class) for-the data under consideration. The technique produces efficient estimators of central tendency and powerful test statistics, even for small sample sizes. (Portions of this work have been presented in preliminary form (Turkheimer et al., 1996)). C1 NIMH, Cerebral Metab Lab, Bethesda, MD 20892 USA. NIMH, Div Epidemiol & Serv Res, Bethesda, MD 20892 USA. RI Turkheimer, Federico/B-9485-2012 OI Turkheimer, Federico/0000-0002-3766-3815 NR 28 TC 2 Z9 2 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0361-0918 J9 COMMUN STAT-SIMUL C JI Commun. Stat.-Simul. Comput. PY 1999 VL 28 IS 4 BP 931 EP 956 DI 10.1080/03610919908813586 PG 26 WC Statistics & Probability SC Mathematics GA 254YC UT WOS:000083641000004 ER PT J AU Troendle, JF Yu, KF AF Troendle, JF Yu, KF TI Conditional estimation following a group sequential clinical trial SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE bias adjustment; conditional bias; simulation; stopping time ID CONFIDENCE-INTERVALS; BIAS AB Recently, an unbiased estimator (Emerson and Kittelson, 1997) and an essentially unbiased estimator (Todd, Whitehead, and Facey, 1996) have been developed to analyze a group sequential clinical trial after it has stopped. However, for these methods, the expectation of the estimator is not close to the parameter value when conditioned on the stopping time. We propose an approach conditioned on the stopping time, which reduces the discrepancy. The result leads to a group of estimators with less discrepancy and sometimes less mean squared error as well. The new estimators are compared by simulation to five existing methods in the case of a two-armed clinical trial with normal response. C1 NICHHD, Biometry & Math Stat Branch, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA. NR 12 TC 9 Z9 9 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0361-0926 J9 COMMUN STAT-THEOR M JI Commun. Stat.-Theory Methods PY 1999 VL 28 IS 7 BP 1617 EP 1634 DI 10.1080/03610929908832376 PG 18 WC Statistics & Probability SC Mathematics GA 204RJ UT WOS:000080777700007 ER PT J AU Fay, MP AF Fay, MP TI Approximate confidence intervals for rate ratios from directly standardized rates with sparse data SO COMMUNICATIONS IN STATISTICS-THEORY AND METHODS LA English DT Article DE exact test; epidemiologic method; relative risk; stratification ID PARAMETER; COHORT AB We consider a class of exact confidence intervals for rate ratio (or relative risk) estimators calculated with directly standardized rates (DSRs) assuming a multiplicative Poisson model, which we call "exact DSR intervals". These intervals relate more closely to some standard rate ratio estimators than standard exact intervals, yet they are more difficult to calculate. We introduce an approximation to estimate these intervals using the inverse F distribution. We show that the approximation is equivalent to both types of exact intervals when the standard is proportional to both populations and is asymptotically equivalent to the log transformed normal method as the counts and person-years increase at the same rate. We compare our approximation to the exact DSR intervals and show by simulating some cases with non-proportional populations that the approximation is usually slightly more conservative than the exact DSR intervals. Comparing other known approximations in the same manner, we show that these other intervals are often more liberal than the exact DSR intervals. C1 NCI, Bethesda, MD 20892 USA. RI Fay, Michael/A-2974-2008; OI Fay, Michael P./0000-0002-8643-9625 NR 20 TC 23 Z9 23 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0361-0926 J9 COMMUN STAT-THEOR M JI Commun. Stat.-Theory Methods PY 1999 VL 28 IS 9 BP 2141 EP 2160 DI 10.1080/03610929908832411 PG 20 WC Statistics & Probability SC Mathematics GA 228GF UT WOS:000082128200009 ER PT B AU Richmond, BJ Hertz, JA Gawne, TJ AF Richmond, BJ Hertz, JA Gawne, TJ BE Bower, JM TI The relation between V1 neuronal responses and eye movement-like stimulus presentations SO COMPUTATIONA L NEUROSCIENCE: TRENDS IN RESEARCH 1999 LA English DT Proceedings Paper CT 7th Annual Computational Neuroscience Meeting (CNS 98) CY JUL, 1998 CL SANTA BARBARA, CA AB Primates normally make 2-3 saccadic eye movements/s to explore the environment. To investigate how these eye movements might influence visual responses, we compared the dynamics of stimuli arriving on V1 complex cell receptive fields by switching stimuli in sequence while a monkey fixated to the responses occurring when the stimulus appears due to saccadic eye movements. During the image sequences, information was greater when each image remained on the receptive fields longer, up to 200 ms; information was greatest when there was a gap of 50 ms between images. Responses were more variable when the image appeared due to a saccadic eye movement. The amount of stimulus-related information was lower in the early phase of the post-saccadic time, but increased during the post-saccadic fixation, so that after 400 ms there was almost as much stimulus-related information available as during the image switching. Eye position showed much larger variability after saccades, with the variability decreasing over 350-400 ms to reach the level seen during long fixations. The dynamics of information accumulation in V1 complex cells appear to be well matched to the manner in which the environment is normally viewed, (C) 1999 Elsevier Science B.V. All rights reserved. C1 NIMH, Neuropsychol Lab, Bethesda, MD 20892 USA. RP Richmond, BJ (reprint author), NIMH, Neuropsychol Lab, Bldg 49,Room 1B80, Bethesda, MD 20892 USA. EM bjr@ln.nimh.nih.gov; hertz@nordita.dk; tgawne@icare.opt.uab.edu NR 4 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-50307-2 PY 1999 BP 247 EP 254 PG 8 WC Neurosciences SC Neurosciences & Neurology GA BN90A UT WOS:000083408000032 ER PT B AU Tabak, J Senn, W O'Donovan, MJ Rinzel, J AF Tabak, J Senn, W O'Donovan, MJ Rinzel, J BE Bower, JM TI Comparison of two models for pattern generation based on synaptic depression SO COMPUTATIONA L NEUROSCIENCE: TRENDS IN RESEARCH 1999 LA English DT Proceedings Paper CT 7th Annual Computational Neuroscience Meeting (CNS 98) CY JUL, 1998 CL SANTA BARBARA, CA DE spontaneous activity; synaptic depression; excitatory network; connectivity ID ANTAGONISTS AB Previously, we developed two similar 3-variable models to explain the pattern of spontaneous rhythmic activity generated by the spinal cord of chick embryo. The models differ in the implementation of a slow depression variable, but each produces patterns of activity that qualitatively resemble experimental recordings. For both models, the ratio inter-episode interval/episode duration (i/d ratio) was too small compared to experiments. The introduction of a parameter representing the connectivity of the network has different effects on each model, therefore allowing them to be distinguished experimentally. Also, the model that seems to better satisfy experimental constraints is able to generate a large i/d ratio. (C) 1999 Elsevier Science B.V. All rights reserved. C1 NINCDS, Neural Control Lab, Bethesda, MD 20892 USA. RP Tabak, J (reprint author), NINCDS, Neural Control Lab, Bldg 49,Rm 3A50,NIH Campus, Bethesda, MD 20892 USA. EM joel@spine.ninds.nih.gov RI tabak, joel/K-1549-2013; Senn, Walter/D-6308-2014 OI Senn, Walter/0000-0003-3622-0497 NR 5 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS BN 0-444-50307-2 PY 1999 BP 551 EP 556 PG 6 WC Neurosciences SC Neurosciences & Neurology GA BN90A UT WOS:000083408000072 ER PT J AU Kloczkowski, A Jernigan, RL AF Kloczkowski, A Jernigan, RL TI Contacts between segments in the random-flight model of polymer chains SO COMPUTATIONAL AND THEORETICAL POLYMER SCIENCE LA English DT Article DE random-flight model; Gaussian approximation; polymer chain ID SELF-AVOIDING WALKS; FOLDED PROTEINS; ENUMERATION; CONFORMATIONS; COPOLYMERS; GENERATION; SEQUENCE; LATTICES; MOTIONS AB The probabilities of single and double contacts, and correlations among contacts were calculated for the random-flight model of a polymer chain. The problem was studied earlier by various authors using the Gaussian statistics of the random-flight chain, which is applicable only for long chains, and for contacts which are formed by pair of residues (i,j) which are far from each other (i.e. /i - j/ much greater than 1). We used the exact (non-Gaussian) solution of the random flight model, so that our results are applicable also for residues which are relatively close to each other. We applied the results to close contacts of the beta-sheet type and alpha-helix type in proteins, and compared the exact solutions of the problem with Gaussian approximations. Published by Elsevier Science Ltd. C1 NCI, Mol Struct Sect, Lab Expt & Computat Biol, NIH, Bethesda, MD 20892 USA. RI Jernigan, Robert/A-5421-2012; Kloczkowski, Andrzej/B-9868-2012 NR 21 TC 5 Z9 5 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1089-3156 J9 COMPUT THEOR POLYM S JI Comput. Theor. Polym. Sci. PY 1999 VL 9 IS 3-4 BP 285 EP 294 DI 10.1016/S1089-3156(99)00016-1 PG 10 WC Polymer Science SC Polymer Science GA 230TM UT WOS:000082266500012 ER PT J AU Klein, SL AF Klein, SL TI Guest Editor's Introduction to the Special Issue - The need for computers in the study of embryonic and fetal development SO COMPUTERIZED MEDICAL IMAGING AND GRAPHICS LA English DT Editorial Material C1 NICHHD, Dev Biol Genet & Teratol Branch, NIH, Bethesda, MD 20892 USA. RP Klein, SL (reprint author), NICHHD, Dev Biol Genet & Teratol Branch, NIH, 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 OX5 1GB, ENGLAND SN 0895-6111 J9 COMPUT MED IMAG GRAP JI Comput. Med. Imaging Graph. PD JAN-FEB PY 1999 VL 23 IS 1 BP 1 EP 2 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 173LB UT WOS:000078981100001 ER PT J AU Ramakrishna, R Srinivasan, R AF Ramakrishna, R Srinivasan, R TI Gene identification in bacterial and organellar genomes using GeneScan SO COMPUTERS & CHEMISTRY LA English DT Article DE GeneScan; mycoplasma; plasmodium; Haemophilus; Fourier ID HAEMOPHILUS-INFLUENZAE; MYCOPLASMA-GENITALIUM; DNA; RECOGNITION; SEQUENCES AB The performance of the GeneScan algorithm for gene identification has been improved by incorporation of a directed iterative scanning procedure. Application is made here to the cases of bacterial and organnellar genomes. The sensitivity of gene identification was 100% in Plasmodium falciparum plastid-like genome (35 kb) and in 98% in the Mycoplasma genitalium genome (similar to 580 kb) and the Haemophilus influenzae Rd genome (similar to 1.8 Mb). Sensitivity was found to improve in both the Open Reading Frames (ORFs) which have been identified as genes (by homology or by other methods) and those that are classified as hypothetical. False positive assignments (at the nucleotide level) were 0.25% in H. influenzae genome and 0.3% in M. genitalium. There were no false positive assignments in the plastid-like genome. The agreement between the GeneScan predictions and GeneMark predictions of putative ORFs was 97% in M. genitalium genome and 86% in H. influenzae genome. In terms of an exact match between predicted genes/ORFs and the annotation in the databank, GeneScan performance was evaluated to be between 72% and 90% in different genomes. We predict five putative ORFs that were not annotated earlier in the GenBank files for both M. genitalium and H. influenzae genomes. Our preliminary analysis of the newly sequenced G + C rich genome of Mycobacterium tuberculosis H37Rv also shows comparable sensitivity (99%). (C) 1999 Elsevier Science Ltd. All rights reserved. C1 NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA. Jawaharlal Nehru Univ, Sch Phys Sci, New Delhi 110067, India. RP Ramakrishna, R (reprint author), NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA. OI Ramaswamy, Ramakrishna/0000-0002-9085-8224 NR 17 TC 14 Z9 14 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PY 1999 VL 23 IS 2 BP 165 EP 174 DI 10.1016/S0097-8485(98)00034-5 PG 10 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA 197YV UT WOS:000080395100007 PM 10353188 ER PT J AU Gabrielian, A Bolshoy, A AF Gabrielian, A Bolshoy, A TI Sequence complexity and DNA curvature SO COMPUTERS & CHEMISTRY LA English DT Article DE complexity; DNA curvature; nucleotide composition; linguistic analysis ID CURVED DNA; NUCLEOTIDE-SEQUENCES; BENDING PROPENSITY; KINETOPLAST DNA; B-DNA; COMPONENTS; CHICKEN; ANGLES AB A linguistic complexity measure was applied to the complete genomes of HIV-1, Escherichia coli, Bacillus subtilis, Haemophilus influenzae, Mycoplasma genitalium, and to long human and yeast genomic fragments. Complexity values averaged over entire genomic sequences were compared, as were predicted average values of intrinsic DNA curvature. We found that both the most curved and the least complex fragments are located preferentially in noncoding parts of the genome. Analysis of location of the most curved and the simplest regions in bacteria showed that the low-complexity segments are preferentially located in close proximity to the highly curved sequences, which are, in turn, placed from 100 to 200 bases upstream to the start of the nearest coding sequence. We conclude that the parallel analysis of sequence complexity and: DNA curvature might provide important information about sequence-structure-function relationship in genomes. (C) 1999 Elsevier Science Ltd. All rights reserved. C1 Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RP Bolshoy, A (reprint author), Univ Haifa, Inst Evolut, Mt Carmel, IL-31905 Haifa, Israel. NR 29 TC 26 Z9 29 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0097-8485 J9 COMPUT CHEM JI Comput. Chem. PY 1999 VL 23 IS 3-4 BP 263 EP 274 DI 10.1016/S0097-8485(99)00007-8 PG 12 WC Chemistry, Multidisciplinary; Computer Science, Interdisciplinary Applications SC Chemistry; Computer Science GA 209VC UT WOS:000081068900007 PM 10404619 ER PT J AU Xiang, BS AF Xiang, BS TI Coherence-transfer table: A convenient method for deriving coherence-transfer pathways of an NMR pulse sequence. I. Coherence-transfer table in I-x, I-y, and I-z system SO CONCEPTS IN MAGNETIC RESONANCE LA English DT Article DE spectroscopy; magnetic resonance; nuclear magnetic resonance; coherence-transfer pathway; coherence-transfer table ID PRODUCT OPERATOR-FORMALISM; FIELD GRADIENTS; PICTORIAL REPRESENTATION; MULTIPULSE NMR; SPIN SYSTEMS; SPECTROSCOPY; HAMILTONIANS; SELECTION AB A method for deriving coherence-transfer pathways of a nuclear magnetic resonance (NMR) pulse sequence in a table format, called a coherence-transfer table, has been developed. This method provides a convenient and easy-to-understand means to describe coherence transfers. In a coherence-transfer table, coherence at any time point, all the coherence-transfer pathways, and their NMR signals can be easily found. The coherence-transfer table method helps in understanding the effects of phase cycling. It is very useful in analyzing various multidimensional NMR pulse sequences. (C) 1999 John Wiley & Sons, Inc. C1 NHLBI, Biophys Chem Lab, NIH, Bethesda, MD 20892 USA. RP Xiang, BS (reprint author), Cornell Univ, Dept Chem & Chem Biol, Ithaca, NY 14853 USA. NR 29 TC 3 Z9 3 U1 0 U2 4 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1043-7347 J9 CONCEPT MAGNETIC RES JI Concepts Magn. Resonance PY 1999 VL 11 IS 6 BP 393 EP 408 DI 10.1002/(SICI)1099-0534(1999)11:6<393::AID-CMR4>3.0.CO;2-1 PG 16 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Chemistry; Physics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA 245XG UT WOS:000083133000004 ER PT J AU Harris, BD Segal, JA Kustova, Y Basile, A Skolnick, P AF Harris, BD Segal, JA Kustova, Y Basile, A Skolnick, P TI Aminoglycoside neurotoxicity involves N-methyl-D-aspartate receptor activation SO CRITICAL CARE MEDICINE LA English DT Meeting Abstract C1 NIDDKD, Neurosci Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1999 VL 27 IS 1 SU S MA 224 BP A104 EP A104 DI 10.1097/00003246-199901001-00264 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA 160NN UT WOS:000078236900267 ER PT J AU Marrison, AM Bonville, CA Rosenberg, HF Domachowske, JB AF Marrison, AM Bonville, CA Rosenberg, HF Domachowske, JB TI Eosinophil granule proteins are present in the lower respiratory tract of children with RSV bronchiolitis SO CRITICAL CARE MEDICINE LA English DT Meeting Abstract C1 SUNY Hlth Sci Ctr, Dept Pediat, Syracuse, NY 13210 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1999 VL 27 IS 1 SU S MA 432 BP A161 EP A161 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA 160NN UT WOS:000078236900477 ER PT J AU O'Grady, NP Tropea, M Preas, HL Reda, D Suffredini, AF AF O'Grady, NP Tropea, M Preas, HL Reda, D Suffredini, AF TI Factors delaying apoptosis of elicited neutrophils in humans challenged with endobronchial endotoxin. SO CRITICAL CARE MEDICINE LA English DT Meeting Abstract C1 NIH, Dept Crit Care Med, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1999 VL 27 IS 1 SU S MA 10 BP A41 EP A41 DI 10.1097/00003246-199901001-00050 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA 160NN UT WOS:000078236900051 ER PT J AU Stratakis, CA Rennert, OM AF Stratakis, CA Rennert, OM TI Congenital adrenal hyperplasia: Molecular genetics and alternative approaches to treatment SO CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES LA English DT Review DE adrenal gland; hyperplasia; adrenal cortex; genetics; gonads; differentiation ID ACUTE REGULATORY PROTEIN; STEROID 21-HYDROXYLASE DEFICIENCY; 3-BETA-HYDROXYSTEROID DEHYDROGENASE GENE; 17-ALPHA-HYDROXYLASE 17,20-LYASE DEFICIENCY; CLASSIC 11-BETA-HYDROXYLASE DEFICIENCY; GLUCOCORTICOID REPLACEMENT THERAPY; STRAND CONFORMATION POLYMORPHISM; COMPOUND HETEROZYGOUS MUTATIONS; HOMOZYGOUS FRAMESHIFT MUTATION; FIELD GEL-ELECTROPHORESIS AB Several autosomal recessive disorders affecting the adrenal cortex and its development and leading to defective cortisol biosynthesis are known under the collective term "congenital adrenal hyperplasia" (CAH). Over the last two decades, the genes causing most of these disorders have been identified and molecular genetics may supplement their clinical and biochemical diagnosis. In addition, new treatments have emerged; although gene therapy has yet to be applied in humans, studies are ongoing in gene transfer in adrenocortical cell lines and animal models. In this review, after a brief introduction on the developmental biology and biochemistry of the adrenal cortex and its enzymes, we will list the new developments in the genetics and treatment of diseases causing CAH, starting with the most recent findings. This order happens to follow adrenal steroidogenesis from the mitochondrial entry of cholesterol to cortisol synthesis; it is unlike other presentations of CAH syndromes that start with the most frequently seen syndromes, because the latter were also the first to be investigated at the genetic level and have been extensively reviewed elsewhere. We will start with the latest syndrome to be molecularly investigated, congenital lipoid adrenal hyperplasia (CLAH), which is caused by mutations in the gene coding for the steroidogenic acute regulatory (StAR) protein. We will then present new developments in the genetics of 3-beta-hydroxysteroid dehydrogenase (3 beta HSD), 17 hydroxylase and 17,20-lyase (P450c17), 11 hydroxylase (P450c11 beta), and 21 hydroxylase (P450c21) deficiencies. Alternative treatment approaches and gene therapy experiments are reviewed collectively in the last section, because they are still in their infantile stages. C1 NICHD, Unit Genet & Endocrinol, SPE, DEB,NIH, Bethesda, MD 20892 USA. Georgetown Univ, Dept Pediat, Div Pediat Endocrinol & Genet, Washington, DC 20007 USA. RP Stratakis, CA (reprint author), NICHD, Unit Genet & Endocrinol, SPE, DEB,NIH, Bldg 10,Room 10N262,10 Ctr Dr,MSC 1862, Bethesda, MD 20892 USA. NR 201 TC 15 Z9 15 U1 0 U2 1 PU CRC PRESS INC PI BOCA RATON PA 2000 CORPORATE BLVD NW, JOURNALS CUSTOMER SERVICE, BOCA RATON, FL 33431 USA SN 1040-8363 J9 CRIT REV CL LAB SCI JI Crit. Rev. Clin. Lab. Sci. PY 1999 VL 36 IS 4 BP 329 EP 363 DI 10.1080/10408369991239222 PG 35 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 231YK UT WOS:000082338800002 PM 10486704 ER PT J AU Bianco, P Riminucci, N Kuznetsov, S Robey, PG AF Bianco, P Riminucci, N Kuznetsov, S Robey, PG TI Multipotential cells in the bone marrow stroma: Regulation in the context of organ physiology SO CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION LA English DT Article DE marrow stromal cells; stem cells; osteogenesis; commitment; adipogenesis; development ID ACTIVATED RECEPTOR-GAMMA; MESENCHYMAL PROGENITOR CELLS; OSTEOBLAST-LIKE CELLS; FORMATION IN-VITRO; ALKALINE-PHOSPHATASE; PRECURSOR CELLS; HYPERTROPHIC CHONDROCYTES; ADIPOCYTE DIFFERENTIATION; GENE-EXPRESSION; STEM-CELLS AB Multipotential (osteogenic, adipogenic, chondrogenic, and myelosupportive) cells associated with the bone marrow stroma are revealed by in vitro or in vivo differentiation assays. If considered in the context of development, growth, and adaptive changes of bone as an organ, the hierarchical organization, histophysiology, and biological significance of the so-called "stromal system" appear distinct from those predicted from the commonly used analogy with the hematopoietic system, with which the stromal system and its putative "stem" cell. are usually compared. The plasticity of differentiated phenotypes and the emergence of individual lineages in a defined temporal succession throughout development and postnatal life reflect the role of the multipotential cells in the stromal system in tissue adaptation and growth, rather than in cell consumption and replacement. This makes the stromal system and its progenitors an interesting paradigm of the biology of an individual cell's flexibility in complex organisms. C1 Univ Aquila, Dipartimento Med Sperimentale, I-67100 Laquila, Italy. Natl Inst Dent & Craniofacial Res, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA. RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 89 TC 87 Z9 90 U1 0 U2 1 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 USA SN 1045-4403 J9 CRIT REV EUKAR GENE JI Crit. Rev. Eukaryot. Gene Expr. PY 1999 VL 9 IS 2 BP 159 EP 173 PG 15 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 222EW UT WOS:000081771300003 PM 10445154 ER PT J AU Zlatanova, J Leuba, SH van Holde, K AF Zlatanova, J Leuba, SH van Holde, K TI Chromatin structure revisited SO CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION LA English DT Article DE core particle; chromatosome; linker histone; HMG1; extended chromatin fiber; condensed chromatin fiber ID SCANNING FORCE MICROSCOPY; HIGHER-ORDER STRUCTURE; LINKER HISTONES B4; GLOBULAR DOMAIN; NUCLEOSOME STRUCTURE; BINDING-SITE; DNA; H1; MODEL; FIBER AB Independently of the enormous progress in our understanding of the structure of the core particle, then remain a multitude of structural questions still to be answered. The main points discussed here can be summarized as follows: (1) The meaning of the term 'core particle' should be widened to reflect the fact that the actual length of DNA wrapped around the histone octamer in the context of the chromatin fiber may vary between similar to 100 and similar to 170 bp. (2) In the chromatosome, the Linker histone forms a bridge between one terminus of the chromatosomal DNA and a point close to the dyad axis, (3) The particle that contains one molecule of HMG 1 may be classified as a bonafide chromatosome. (4) In the extended fiber, the partition of the nucleosomal DNA into core and linker is a dynamic feature, responding to environmental influences; fiber structure-related constraints demand that linker length be beyond a certain minimal value. (5) The compact fiber structure seems to be rather irregular; the precise nature of this structure is still to be determined. Finally, the term 30-nm fiber should be dropped as a designator of the compact or condensed chromatin fiber structure. C1 Agronne Natl Lab, Biochip Technol Ctr, Argonne, IL 60439 USA. Natl Canc Inst, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20896 USA. Oregon State Univ, Dept Biochem & Biophys, Corvallis, OR 97331 USA. RI Zlatanova, Jordanka/B-3273-2009 FU FIC NIH HHS [TW00568] NR 51 TC 34 Z9 35 U1 1 U2 4 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 USA SN 1045-4403 J9 CRIT REV EUKAR GENE JI Crit. Rev. Eukaryot. Gene Expr. PY 1999 VL 9 IS 3-4 BP 245 EP + PG 13 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 275HT UT WOS:000084815300009 PM 10651241 ER PT J AU Kirk, AD AF Kirk, AD TI Transplantation tolerance: A look at the nonhuman primate literature in the light of modern tolerance theories SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Review DE costimulation; immunosuppression; primate; review; transplantation; tolerance ID MAJOR HISTOCOMPATIBILITY COMPLEX; CARDIAC-ALLOGRAFT SURVIVAL; TOTAL LYMPHOID IRRADIATION; DONOR BONE-MARROW; T-CELL SUBSETS; INTERCELLULAR-ADHESION MOLECULE-1; OKT4A MONOCLONAL-ANTIBODY; NF-KAPPA-B; MIXED ALLOGENEIC CHIMERISM; HUMAN LYMPHOCYTES-T AB Ever since the beginning of clinical transplantation, investigators have searched for a way to transplant tissues from one person to another without chronic immunosuppression. That goal, known as allograft tolerance, has remained clinically elusive. In the past decade, however, many of the fundamental principles of tolerance have been redefined, and biological agents capable of exploiting them in vivo have been developed. Accordingly, experimental methods for tolerance induction have rapidly evolved in concert with a growing understanding of physiological tolerance to self and the development of novel immunoreactive reagents. In general, old world monkeys have become the pre-clinical testing ground for methods that have shown reasonable promise for clinical application, particularly antibodies or other biological agents with limited cross-species reactivity. As such, a survey of the nonhuman primate experience in transplantation is representative of all reasonably successful experimental attempts to develop clinically applicable tolerance regimens. This article summarizes many of the concepts currently unfolding in the tolerance literature. It also reviews the techniques for tolerance induction that have been and are currently being investigated in nonhuman primates. The validity of these models is summarized, and the older literature is reinterpreted in light of recent changes in our understanding of tolerance. C1 NIDDK, Navy Transplant & Autoimmun Branch, Bethesda, MD 20892 USA. RP Kirk, AD (reprint author), NIDDK, Navy Transplant & Autoimmun Branch, 10 Ctr Dr,Bldg 10,Room 11S219, Bethesda, MD 20892 USA. RI Kirk, Allan/B-6905-2012 NR 325 TC 76 Z9 77 U1 0 U2 0 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 USA SN 1040-8401 J9 CRIT REV IMMUNOL JI Crit. Rev. Immunol. PY 1999 VL 19 IS 5-6 BP 349 EP 388 PG 40 WC Immunology SC Immunology GA 274NG UT WOS:000084771500001 PM 10647743 ER PT J AU Vacchio, MS Jiang, SP AF Vacchio, MS Jiang, SP TI The fetus and the maternal immune system: Pregnancy as a model to study peripheral T-cell tolerance SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Article DE clonal deletion; receptor downregulation; immune deviation; immune privilege; placenta; trophoblast ID RECEPTOR TRANSGENIC MICE; RESTRICTED CROSS-PRESENTATION; MHC CLASS-I; INDUCED APOPTOSIS; CLONAL DELETION; SELF-ANTIGENS; FAS LIGAND; LYMPHOCYTE SUBSETS; LEISHMANIA-MAJOR; DENDRITIC CELLS AB In this article, we discuss recent findings that describe how maternal T cells respond upon encountering fetal antigens. Many earlier studies have characterized changes in the maternal T-cell repertoire of both humans and mice, yet it has been difficult to understand the significance of these findings since there has been no way to decipher if the alterations were the result of encounters with fetal antigens or were nonspecific changes related to pregnancy itself. Now, in the mouse, the availability of TCR transgenic mice and other technological advances allow direct visualization of the fate of maternal T cells that are reactive to the fetus and provide a means to probe the mechanisms by which tolerance to the fetus is maintained. This article focuses on how the fetus more closely resembles "developmental self" than a true allograft and how the study of maternal T-cell interactions with fetally derived antigens can be useful as a model for the study of peripheral T-cell tolerance. C1 NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. Univ Oklahoma, Oklahoma Hlth Sci Ctr, Dept Pathol, Oklahoma City, OK USA. RP Vacchio, MS (reprint author), NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. NR 99 TC 31 Z9 33 U1 1 U2 1 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 USA SN 1040-8401 J9 CRIT REV IMMUNOL JI Crit. Rev. Immunol. PY 1999 VL 19 IS 5-6 BP 461 EP 480 PG 20 WC Immunology SC Immunology GA 274NG UT WOS:000084771500004 PM 10647746 ER PT J AU London, ED Bonson, KR Ernst, M Grant, S AF London, ED Bonson, KR Ernst, M Grant, S TI Brain imaging studies of cocaine abuse: Implications for medication development SO CRITICAL REVIEWS IN NEUROBIOLOGY LA English DT Article DE positron emission tomography; magnetic resonance imaging; drug abuse; cocaine; treatment ID POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL BLOOD-FLOW; DOPAMINE TRANSPORTER OCCUPANCY; GLUCOSE-METABOLISM; RECEPTOR-BINDING; POLYDRUG ABUSERS; NEUROCHEMICAL CHANGES; RHESUS-MONKEYS; IN-VIVO; WITHDRAWAL AB Contemporary in vivo brain imaging techniques confer the ability to assess brain function and structure noninvasively, and thereby can yield information to help guide the development of new treatments for substance abuse. The advantages and limitations of the major imaging modalities (positron emission tomography [PET], single photon emission computed tomography [SPECT], structural and functional magnetic resonance imaging [MRI, fMRI, respectively]) are discussed with respect to their applicability to research on cocaine abuse. The effects of acute administration of cocaine have been studied using PET and fMRI, with PET manifesting decreases in cerebral glucose metabolism and blood flow, and fMRI revealing regional effects that are correlated temporally with subjective responses. In addition, studies of drug abusers, abstinent from cocaine for various lengths of time, have revealed persistent differences in brain function and structure, especially in the frontal cortex, when compared with parameters in the brains of subjects who do not use illicit drugs of abuse. PET studies also have revealed abnormalities in markers for dopaminergic and opioid systems during withdrawal from cocaine. Moreover, studies of cue-elicited craving for cocaine demonstrate a connection between the response to drug related stimuli and neural elements of cognition and emotion. The future directions of in vivo brain imaging to identify functional and structural alterations in the brains of cocaine abusers are discussed in relation to the development of medications to treat cocaine dependence. C1 NIDA, Brain Imaging Ctr, Baltimore, MD 21224 USA. RP London, ED (reprint author), NIDA, Brain Imaging Ctr, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 74 TC 38 Z9 41 U1 1 U2 4 PU BEGELL HOUSE INC PI NEW YORK PA 79 MADISON AVE, SUITE 1205, NEW YORK, NY 10016-7892 USA SN 0892-0915 J9 CRIT REV NEUROBIOL JI Crit. Rev. Neurobiol. PY 1999 VL 13 IS 3 BP 227 EP 242 PG 16 WC Neurosciences SC Neurosciences & Neurology GA 307YD UT WOS:000086681000001 PM 10803636 ER PT B AU Powell, KD Colby, CL Gottlieb, J Kusunoki, M Goldberg, ME AF Powell, KD Colby, CL Gottlieb, J Kusunoki, M Goldberg, ME BE Becker, W Deubel, H Mergner, T TI Space and salience in parietal cortex SO CURRENT OCULOMOTOR RESEARCH: PHYSIOLOGICAL AND PSYCHOLOGICAL ASPECTS LA English DT Proceedings Paper CT 9th European Conference on Eye Movements (ECEM 9) CY SEP 23-26, 1997 CL ULM, GERMANY ID FRONTAL EYE FIELDS; LATERAL INTRAPARIETAL AREA; MONKEY CEREBRAL-CORTEX; SUPERIOR COLLICULUS; VISUAL RESPONSES; BEHAVIORAL ENHANCEMENT; SELECTIVE ATTENTION; CORTICAL AFFERENTS; NEURONAL RESPONSES; MACAQUE MONKEY C1 NEI, Sensorimotor Res Lab, Bethesda, MD 20892 USA. RP Powell, KD (reprint author), NEI, Sensorimotor Res Lab, Bethesda, MD 20892 USA. NR 31 TC 4 Z9 4 U1 0 U2 0 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA BN 0-306-46049-1 PY 1999 BP 25 EP 35 PG 5 WC Behavioral Sciences; Clinical Neurology; Neurosciences; Ophthalmology SC Behavioral Sciences; Neurosciences & Neurology; Ophthalmology GA BP40H UT WOS:000085046500004 ER PT B AU Gahl, WA AF Gahl, WA BE Broyer, M TI Cysteamine: from in vitro efficacy to effectiveness in patients SO CYSTINOSIS LA English DT Proceedings Paper CT Symposium on Cystinosis a Rare Disease CY JAN 17, 1998 CL PARIS, FRANCE ID LEUKOCYTE GRANULAR FRACTIONS; CYSTINE COUNTER-TRANSPORT; NEPHROPATHIC CYSTINOSIS; RENAL-FUNCTION; THERAPY; LYSOSOMES; DEPLETION; CHILDREN; INSUFFICIENCY; MYOPATHY C1 NICHHD, Sect Human Biochem Genet, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. RP Gahl, WA (reprint author), NICHHD, Sect Human Biochem Genet, Heritable Disorders Branch, NIH, 10 Ctr Dr,MSC 1830,Bldg 10,Room 9S-241, Bethesda, MD 20892 USA. NR 35 TC 1 Z9 1 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ET MEDICALES ELSEVIER PI PARIS PA 23, RUE LINOIS, 75724 PARIS, FRANCE BN 2-84299-116-8 PY 1999 BP 111 EP 120 PG 10 WC Endocrinology & Metabolism; Pediatrics; Urology & Nephrology SC Endocrinology & Metabolism; Pediatrics; Urology & Nephrology GA BM98S UT WOS:000080351800017 ER PT J AU Nakatsu, F Kadohira, T Gilbert, DJ Jenkins, NA Kakuta, H Copeland, NG Saito, T Ohno, H AF Nakatsu, F Kadohira, T Gilbert, DJ Jenkins, NA Kakuta, H Copeland, NG Saito, T Ohno, H TI Genomic structure and chromosome mapping of the genes encoding clathrin-associated adaptor medium chains mu 1A (Ap1m1) and mu 1B (Ap1m2) SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID INSITU HYBRIDIZATION; SORTING SIGNALS; PROTEINS; SEQUENCES; ORGANIZATION; VESICLES; CLONING AB The protein mu 1B is a member of the medium chain family of the clathrin-associated adaptor complex and is expressed exclusively in epithelial cells. We determined the genomic structure of previously cloned murine genes for mu 1B (Ap1m2) and its closely related homolog, mu 1A (Ap1m1). Comparison of their genomic structures revealed that the positions of introns are identical between these two genes, except for the insertion of an additional intron in Ap1m1 (intron 4). By contrast, these structures are different from that of the more distantly related Ap2m1 gene encoding mu 2. Taken together with the similarity of amino acid sequences among these genes, the data presented in this study suggest that Ap1m1/2 and Ap2m1 diverged long before the separation of Ap1m1 and Ap1m2, which most likely resulted from a relatively recent gene duplication. We also mapped AP1M2 to human chromosome 19p13.2 and Ap1m2 to the proximal region of mouse chromosome 9. The results are consistent with the fact that these regions are syntenic. Copyright (C) 1999 S. Karger AG, Basel. C1 Kanazawa Univ, Inst Canc Res, Div Mol Membrane Biol, Kanazawa, Ishikawa 9200934, Japan. Chiba Univ, Grad Sch Med, Dept Mol Genet, Chiba, Japan. NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Mammalian Genet Lab, Frederick, MD USA. RP Kanazawa Univ, Inst Canc Res, Div Mol Membrane Biol, 13-1 Takaramachi, Kanazawa, Ishikawa 9200934, Japan. EM hohno@kenroku.kanazawa-u.ac.jp RI Saito, Takashi/C-9684-2009 OI Saito, Takashi/0000-0001-9495-3547 NR 27 TC 2 Z9 4 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 87 IS 1-2 BP 53 EP 58 DI 10.1159/000015391 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 271XF UT WOS:000084619600011 PM 10640811 ER PT J AU Yuan, BZ Yang, Y Keck-Waggoner, CL Zimonjic, DB Thorgeirsson, SS Popescu, NC AF Yuan, BZ Yang, Y Keck-Waggoner, CL Zimonjic, DB Thorgeirsson, SS Popescu, NC TI Assignment and cloning of mouse Arhgap7 to chromosome 8A4-B2, a conserved syntenic region of human chromosome 8p22 -> p21 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID LOCALIZATION C1 NCI, Expt Carcinogenesis Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP Popescu, NC (reprint author), NCI, Expt Carcinogenesis Lab, Div Basic Sci, NIH, 37 Convent Dr,MSC 4255,Bldg 37,Room 3C28, Bethesda, MD 20892 USA. NR 5 TC 7 Z9 8 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 87 IS 3-4 BP 189 EP 190 DI 10.1159/000015462 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 288PT UT WOS:000085572800006 PM 10702663 ER PT J AU Leach, R Ko, M Krawetz, SA AF Leach, R Ko, M Krawetz, SA TI Assignment of amyloid-precursor-like protein 2 gene (APLP2) to 11q24 by fluorescent in situ hybridization SO CYTOGENETICS AND CELL GENETICS LA English DT Article C1 Wayne State Univ, Sch Med, CS Mott Ctr Human Growth & Dev, Dept Obstet & Gynecol, Detroit, MI 48201 USA. Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI 48201 USA. NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. RP Leach, R (reprint author), Wayne State Univ, Sch Med, CS Mott Ctr Human Growth & Dev, Dept Obstet & Gynecol, 275 E Hancock, Detroit, MI 48201 USA. RI Ko, Minoru/B-7969-2009 OI Ko, Minoru/0000-0002-3530-3015 FU NICHD NIH HHS [HD-98-004] NR 5 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 87 IS 3-4 BP 215 EP 216 DI 10.1159/000015472 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 288PT UT WOS:000085572800016 PM 10702673 ER PT J AU Pinhasov, A Giliadi, E Zamostiano, R Steingart, RA Busciglio, J Brenneman, DE Gozes, I AF Pinhasov, A Giliadi, E Zamostiano, R Steingart, RA Busciglio, J Brenneman, DE Gozes, I TI Activity-dependent neuroprotective protein (ADNP): gene expression in Down syndrome SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 Tel Aviv Univ, Sackler Fac Med, Dept Clin Biochem, IL-69978 Tel Aviv, Israel. Univ Connecticut, Ctr Hlth, Storrs, CT 06269 USA. NICHD, SMDP, LDN, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 86 IS 1 BP 7 EP 7 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 234AW UT WOS:000082462300018 ER PT J AU Deng, X Copeland, NG Gilbert, DJ Jenkins, NA Martin-DeLeon, PA AF Deng, X Copeland, NG Gilbert, DJ Jenkins, NA Martin-DeLeon, PA TI Assignment of the zona pellucida 3 receptor (Zp3r) gene to mouse chromosome 1E-F by fluorescence in situ hybridization and confirmation by genetic mapping SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID PROTEIN; EXPRESSION; SPERM C1 Univ Delaware, Dept Biol, Newark, DE 19716 USA. NCI, Mammalian Genet Lab, ABL Basic Res Program, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. RP Martin-DeLeon, PA (reprint author), Univ Delaware, Dept Biol, Newark, DE 19716 USA. FU NICHD NIH HHS [HD35158] NR 7 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 86 IS 3-4 BP 235 EP 236 DI 10.1159/000015346 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 260LC UT WOS:000083951300010 PM 10575213 ER PT J AU Schrock, E Ghadimi, BM Hilgenfeld, E Padilla-Nash, H Heselmeyer, K Wangsa, D McNeil, N Difilippantonio, M Yonescu, R Haas, OA Berdel, W Weaver, Z Ried, T AF Schrock, E Ghadimi, BM Hilgenfeld, E Padilla-Nash, H Heselmeyer, K Wangsa, D McNeil, N Difilippantonio, M Yonescu, R Haas, OA Berdel, W Weaver, Z Ried, T TI Spectral karyotyping (SKY) reveals new specific chromosomal aberrations in human tumors and mouse models of human disease SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 NCI, NIH, Bethesda, MD 20892 USA. Univ Munster, D-4400 Munster, Germany. St Anna Kinderspital, Vienna, Austria. Inst Mol Biotechnol, Jena, Germany. NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 85 IS 1-2 MA O016 BP 9 EP 10 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 214NW UT WOS:000081334900017 ER PT J AU Sauter, G Kononen, J Kallioniemi, OP AF Sauter, G Kononen, J Kallioniemi, OP TI Tissue chips for high throughput molecular analysis of tumors SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 Univ Basel, Inst Pathol, Basel, Switzerland. Natl Inst Hlth, Canc Genet Branch, Bethesda, MD USA. RI Kallioniemi, Olli/H-4738-2012; Kallioniemi, Olli/H-5111-2011 OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 85 IS 1-2 MA O056 BP 19 EP 19 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 214NW UT WOS:000081334900057 ER PT J AU Wienberg, J Stanyon, R Finelli, P Archidiacono, N Muller, S AF Wienberg, J Stanyon, R Finelli, P Archidiacono, N Muller, S TI Molecular cytogenetic dissection of human chromosome evolution SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 Univ Munich, Inst Anthropol & Human Genet, D-8000 Munich, Germany. Natl Canc Inst, Lab Genom Divers, Frederick, MD USA. Univ Bari, Ist Genet, Bari, Italy. RI Finelli, Palma/A-3578-2016 OI Finelli, Palma/0000-0001-8464-6906 NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 85 IS 1-2 MA O106 BP 31 EP 31 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 214NW UT WOS:000081334900107 ER PT J AU Neusser, M Muller, S Stanyon, R Wienberg, J AF Neusser, M Muller, S Stanyon, R Wienberg, J TI Chromosomal homologies between human, Callitrix jacchus, Saimiri sciureus, Sagiunus nigricollis and Cebuella pygmaea revealed by comparative chromosome painting SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 LMU Munchen, Inst Anthropol & Human Genet, Munich, Germany. NCI, FCRDC, Lab Genom Divers, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 85 IS 1-2 MA O109 BP 32 EP 32 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 214NW UT WOS:000081334900110 ER PT J AU Volleth, M Muller, S Wienberg, J Pfeiffer, RA AF Volleth, M Muller, S Wienberg, J Pfeiffer, RA TI Patterns of mammalian chromosomal evolution traced by comparative chromosome painting between Tupaia, Eulemur, flying foxes and microbats SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 Univ Erlangen Nurnberg, Inst Humangenet, D-8520 Erlangen, Germany. Univ Magdeburg, Inst Humangenet, D-39106 Magdeburg, Germany. Univ Munich, Inst Anthropol & Humangenet, Munich, Germany. NCI, Lab Genomic Divers, Frederick, MD 21701 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 85 IS 1-2 MA P768 BP 181 EP 181 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 214NW UT WOS:000081334900768 ER PT J AU Wienberg, J Stanyon, R O'Brien, PCM Ferguson-Smith, MA Plesker, R Muller, S AF Wienberg, J Stanyon, R O'Brien, PCM Ferguson-Smith, MA Plesker, R Muller, S TI Defining the ancestral karyotype for all primates by multidirectional chromosome painting between tree shrews, lemurs and humans SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 LMU Munchen, Inst Anthropol & Humangenet, Munich, Germany. Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England. NCI, Lab Genomic Divers, Frederick, MD 21701 USA. Paul Ehrlich Inst, Frankfurt, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 85 IS 1-2 MA P770 BP 181 EP 181 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 214NW UT WOS:000081334900770 ER PT J AU Woitach, JT Hong, R Keck, CL Zimonjic, DB Popescu, NC Thorgeirsson, SS AF Woitach, JT Hong, R Keck, CL Zimonjic, DB Popescu, NC Thorgeirsson, SS TI Assignment of the Bog gene (RBBP9) to syntenic regions of mouse chromosome 2G1-H1 and human chromosome 20p11.2 by fluorescence in situ hybridization SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID COMPARATIVE GENOMIC HYBRIDIZATION C1 NCI, Expt Carcinogenesis Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP Thorgeirsson, SS (reprint author), NCI, Expt Carcinogenesis Lab, Div Basic Sci, NIH, Bldg 37,Room 3C28,37 Convent Dr MSC4255, Bethesda, MD 20892 USA. NR 4 TC 1 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 85 IS 3-4 BP 252 EP 253 DI 10.1159/000015304 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 227QB UT WOS:000082090200014 PM 10449909 ER PT J AU Wagner, KU Dierisseau, P Hennighausen, L AF Wagner, KU Dierisseau, P Hennighausen, L TI Assignment of the murine tumor susceptibility gene 101 (tsg101) and a processed tsg101 pseudogene (tsg101-ps1) to mouse chromosome 7 band B5 and chromosome 15 band D1 by in situ hybridization SO CYTOGENETICS AND CELL GENETICS LA English DT Article C1 NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA. RP Wagner, KU (reprint author), NIDDK, Lab Genet & Physiol, NIH, Bldg 8,Rm 107, Bethesda, MD 20892 USA. RI Wagner, Kay-Uwe/B-6044-2009 NR 6 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 84 IS 1-2 BP 87 EP 88 DI 10.1159/000015221 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 195RY UT WOS:000080266200018 PM 10343110 ER PT J AU Lee, JH Cho, KW AF Lee, JH Cho, KW TI Assignment of TCRB encoding the T-cell receptor beta chain gene to cat chromosome A2q25-q26 by fluorescence in situ hybridization SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID IMMUNOGLOBULIN; DETERMINANTS; TUMORS; MYC C1 Gyeongsang Natl Univ, Dept Pathol, Coll Med, Chinju 660280, South Korea. NCI, Lab Genom Divers, Frederick, MD 21701 USA. RP Lee, JH (reprint author), Gyeongsang Natl Univ, Dept Pathol, Coll Med, 92 Chilamdong, Chinju 660280, South Korea. NR 8 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 84 IS 1-2 BP 109 EP 110 DI 10.1159/000015232 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 195RY UT WOS:000080266200029 PM 10343121 ER PT J AU Stanyon, R Yang, F Cavagna, P O'Brien, PCM Bagga, M Ferguson-Smith, MA Wienberg, J AF Stanyon, R Yang, F Cavagna, P O'Brien, PCM Bagga, M Ferguson-Smith, MA Wienberg, J TI Reciprocal chromosome painting shows that genomic rearrangement between rat and mouse proceeds ten times faster than between humans and cats SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID INSITU SUPPRESSION HYBRIDIZATION; IN-SITU HYBRIDIZATION; GENETIC-LINKAGE MAP; CYTOGENETIC ANALYSIS; MAMMALS; HOMOLOGIES; KARYOTYPE; SEGMENTS; FISH; PCR AB Reciprocal chromosome painting between mouse and rat using complete chromosome probe sets of both species permitted us to assign the chromosomal homology between these rodents. The comparative gene mapping data and chromosome painting have a better than 90% correspondence. The reciprocal painting results graphically show that mouse and rat have strikingly different karyotypes. At least 14 translocations have occurred in the 10-20 million years of evolution that separates these two species. The evolutionary rate of chromosome translocations between these two rodents appears to be up to 10 times greater than that found between humans and cats, or between humans and chimpanzees, where over the last 5-6 million years just one translocation has occurred. Outgroup comparison shows that the mouse genome has incorporated at least three times the amount of interchromosomal rearrangements compared to the rat genome. The utility of chromosome painting was also illustrated by the assignment of two new chromosome homologies between rat and mouse unsuspected by gene mapping: between mouse 11 and rat 20 and between mouse 17 and rat 6. We conclude that reciprocal chromosome painting is a powerful method, which can be used with confidence to chart the genome and predict the chromosome location of genes. Reciprocal painting combined with gene mapping data will allow the construction of large-scale comparative chromosome maps between placental mammals and perhaps other animals. C1 Natl Canc Inst, Lab Genomic Divers, Frederick, MD 21702 USA. Univ Cambridge, Dept Pathol, Cambridge CB2 1QP, England. Univ Genoa, Inst Comparat Anat, Genoa, Italy. RP Wienberg, J (reprint author), Natl Canc Inst, Lab Genomic Divers, Frederick, MD 21702 USA. OI Stanyon, Roscoe/0000-0002-7229-1092 NR 29 TC 78 Z9 79 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1999 VL 84 IS 3-4 BP 150 EP 155 DI 10.1159/000015244 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 212AX UT WOS:000081195000003 PM 10393417 ER PT J AU Raupach, B Mecsas, J Heczko, U Falkow, S Finlay, BB AF Raupach, B Mecsas, J Heczko, U Falkow, S Finlay, BB TI Bacterial epithelial cell cross talk SO DEFENSE OF MUCOSAL SURFACES: PATHOGENESIS, IMMUNITY AND VACCINES SE CURRENT TOPICS IN MICROBIOLOGY AND IMMUNOLOGY LA English DT Review ID ENTEROPATHOGENIC ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM MUTANTS; MEDIATES SPECIFIC BINDING; CULTURED-MAMMALIAN-CELLS; GROWTH-FACTOR-RECEPTOR; MEMBRANE PROTEIN YADA; YERSINIA-PSEUDOTUBERCULOSIS; SHIGELLA-FLEXNERI; TYROSINE PHOSPHORYLATION; SIGNAL-TRANSDUCTION C1 Stanford Univ, Dept Microbiol & Immunol, Stanford, CA 94305 USA. Max Planck Inst Infekt Biol, D-10117 Berlin, Germany. Univ British Columbia, Biotechnol Lab, Vancouver, BC V6T 1Z3, Canada. NIAID, Rocky Mt Lab, Hamilton, MT 59840 USA. RP Raupach, B (reprint author), Stanford Univ, Dept Microbiol & Immunol, Stanford, CA 94305 USA. NR 82 TC 17 Z9 17 U1 0 U2 2 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0070-217X J9 CURR TOP MICROBIOL JI Curr.Top.Microbiol.Immunol. PY 1999 VL 236 BP 137 EP 161 PG 25 WC Immunology; Microbiology SC Immunology; Microbiology GA BM10J UT WOS:000077639500008 PM 9893359 ER PT J AU Lorberbaum, JP Newman, JD Dubno, JR Horwitz, AR Nahas, Z Teneback, CC Bloomer, CW Bohning, DE Vincent, D Johnson, MR Emmanuel, N Brawman-Mintzer, O Book, SW Lydiard, RB Ballenger, JC George, MS AF Lorberbaum, JP Newman, JD Dubno, JR Horwitz, AR Nahas, Z Teneback, CC Bloomer, CW Bohning, DE Vincent, D Johnson, MR Emmanuel, N Brawman-Mintzer, O Book, SW Lydiard, RB Ballenger, JC George, MS TI Feasibility of using fMRI to study mothers responding to infant cries SO DEPRESSION AND ANXIETY LA English DT Article DE maternal behavior; social bonding; attachment; infant crying; fMRI; MRI; imaging; anterior cingulate ID RIGHT-HEMISPHERE; BEHAVIOR; CORTEX; BRAIN; CALL AB While parenting is a universal human behavior, its neuroanatomic basis is currently unknown. Animal data suggest that the cingulate may play an important function in mammalian parenting behavior For example, in rodents cingulate lesions impair maternal behavior Here, in an attempt to understand the brain basis of human maternal behavior, we had mothers listen to recorded infant cries and white noise control sounds while they underwent functional MRI (fMRI) of the brain. We hypothesized that mothers would show significantly greater cingulate activity during the cries compared to the control sounds. Of 7 subjects scanned 4 had fMRI data suitable for analysis. When fMRI data were averaged for these 4 subjects, the anterior cingulate and right medial prefrontal cortex were the only brairn regions showing statistically increased activity with the cries compared to white noise control sounds (cluster analysis with one-tailed z-map threshold of P < 0.001 and spatial extent threshold of P < 0.05). These results demonstrate the feasibility of using fMRI to study brain activity in mothers listening to infant cries and that the anterior cingulate may be involved in mothers listening to crying babies. We are currently replicating this study in a larger group of mothers. Future work in this area may help (1) unravel the functional neuroanatomy of the parent-infant bond and (2) examine whether markers of this bond, such as maternal brain response to infant crying, can predict maternal style (i.e., child neglect), offspring temperament, or offspring depression or anxiety. (C) 1999 Wiley-Liss, Inc. C1 Med Univ S Carolina, Dept Psychiat, Charleston, SC 29425 USA. NICHHD, NIH, Bethesda, MD 20892 USA. RP Lorberbaum, JP (reprint author), Med Univ S Carolina, Dept Psychiat, Charleston, SC 29425 USA. NR 34 TC 64 Z9 67 U1 0 U2 12 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1091-4269 J9 DEPRESS ANXIETY JI Depress. Anxiety PY 1999 VL 10 IS 3 BP 99 EP 104 DI 10.1002/(SICI)1520-6394(1999)10:3<99::AID-DA2>3.0.CO;2-# PG 6 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 283JC UT WOS:000085271800002 PM 10604082 ER PT J AU Chiang, C Swan, RZ Grachtchouk, M Bolinger, M Ying, LTT Robertson, EK Cooper, MK Gaffield, W Westphal, H Beachy, PA Dlugosz, AA AF Chiang, C Swan, RZ Grachtchouk, M Bolinger, M Ying, LTT Robertson, EK Cooper, MK Gaffield, W Westphal, H Beachy, PA Dlugosz, AA TI Essential role for Sonic hedgehog during hair follicle morphogenesis SO DEVELOPMENTAL BIOLOGY LA English DT Article DE hair follicle; Sonic hedgehog; morphogenesis; cyclopamine; vibrissae ID GENE-EXPRESSION; STEM-CELLS; TRANSCRIPTION FACTOR; HUMAN HOMOLOG; NEURAL-TUBE; MOUSE; SKIN; KERATINS; GROWTH; CYCLE AB The hair follicle is a source of epithelial stem cells and site of origin for several types of skin tumors. Although it is clear that follicles arise by way of a series of inductive tissue interactions, identification of the signaling molecules driving this process remains a major challenge in skin biology. In this study we report an obligatory role for the secreted morphogen Sonic hedgehog (Shh) during hair follicle development. Hair germs comprising epidermal placodes and associated dermal condensates were detected in both control and Shh -/- embryos, but progression through subsequent stages of follicle development was blocked in mutant skin. The expression of Gli1 and Ptc1 was reduced in Shh -/- dermal condensates and they failed to evolve into hair follicle papillae, suggesting that the adjacent mesenchyme is a critical target for placode-derived Shh. Despite the profound inhibition of hair follicle morphogenesis, late-stage follicle differentiation markers were detected in Shh -/- skin grafts, as well as cultured vibrissa explants treated with cyclopamine to block Shh signaling. Our findings reveal an essential role for Shh during hair follicle morphogenesis, where it is required for normal advancement beyond the hair germ stage of development. (C) 1999 Academic Press. C1 NIH, Lab Mammalian Genes & Dev, Bethesda, MD 20892 USA. Univ Michigan, Dept Dermatol, Ann Arbor, MI 48109 USA. Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA. NIH, Basic Res Lab, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Dept Mol Biol & Genet, Baltimore, MD 21205 USA. USDA ARS, Western Reg Res Ctr, Albany, CA 94710 USA. RP Dlugosz, AA (reprint author), 3310 CCGC,Box 0932,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. EM dlugosza@umich.edu NR 50 TC 343 Z9 347 U1 4 U2 14 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN 1 PY 1999 VL 205 IS 1 BP 1 EP 9 DI 10.1006/dbio.1998.9103 PG 9 WC Developmental Biology SC Developmental Biology GA 162VN UT WOS:000078367800001 PM 9882493 ER PT J AU Arend, LJ Smart, A Briggs, JP AF Arend, LJ Smart, A Briggs, JP TI Metanephric rat-mouse chimeras to study cell lineage of the nephron SO DEVELOPMENTAL GENETICS LA English DT Article DE kidney; development; vasopressin receptor; Tamm-Horsfall protein; renin; oxytocin receptor ID HUMAN-KIDNEY; V2 RECEPTOR; CLONING; RENIN; MESENCHYME; EXPRESSION; LIVER; CDNA; GENE AB The nephron is derived from the ureteric bud and metanephric mesenchyme and develops into a complex epithelial structure with a wide variety of phenotypes along iis length. This segmental variation in expression of molecules provides an approach to understand the lineage of unique segments. present study evaluated the expression of four relatively well-localized molecules - renin, Tamm-Horsfall protein (THP), oxytocin receptor (OTR), and the vasopressin type 2 receptor (V2R) - in cultured mouse-rat chimeric metanephric kidneys using reverse transcription-polymerase chain reaction (RT-PCR). Chimeric kidneys were formed by 1) separating the ureteric bud (U) from the metanephric mesenchyme (M) of mouse (m) at E11 and rat (r) at E13 days of gestation and 2) recombining the ureteric bud of one species with the metanephric mesenchyme of the other species (i.e., UrMm and UmMr), followed by filter culture until differentiated. Species-specific restriction enzymes for all four genes were chosen to digest the PCR product from either rat or mouse. RT-PCR was performed for each mRNA species and the products digested. The V2R product from the UrMm chimera was cleaved by a restriction enzyme known to digest only rat product, suggesting the PCR product was produced predominantly by cells derived from the ureteric bud. The renin, OTR, and THP products from both chimeras were cleaved equally well by species-specific restriction enzymes, suggesting the products were made by cells originating from both the ureteric bud and the metanephric mesenchyme. These studies demonstrate that the cultured chimeric metanephric model is useful to study segment lineage. The results suggest that the lineage of at least ceria in portions of the nephron is heterogenous. (C) 1999 Wiley-Liss, Inc. C1 Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA. NIDDK, NIH, Bethesda, MD USA. RP Arend, LJ (reprint author), Univ Michigan, Dept Pathol, 1150 W Med Ctr Dr,1560 MSRB 2, Ann Arbor, MI 48109 USA. RI Briggs, Josephine/B-9394-2009 OI Briggs, Josephine/0000-0003-0798-1190 FU NIDDK NIH HHS [DK09325, DK37448, DK39255] NR 22 TC 7 Z9 7 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 0192-253X J9 DEV GENET JI Dev. Genet. PY 1999 VL 24 IS 3-4 BP 230 EP 240 DI 10.1002/(SICI)1520-6408(1999)24:3/4<230::AID-DVG6>3.0.CO;2-Y PG 11 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA 194JL UT WOS:000080189000006 PM 10322631 ER PT J AU Nitkin, RM AF Nitkin, RM TI Dendritic mechanisms in mental retardation and developmental disabilities: An overview SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article AB The following brief articles are derived from a meeting sponsored by the National Institute of Child Health and Human Development held at the National Institutes of Health from April 30 to May 1, 1998. The meeting brought together researchers from neurobiological and behavioral fields to discuss how synaptic abnormalities impact on brain function. This builds on a broad foundation of research in synaptic development, brain organization, behavioral assessment, and more recent attempts to define the structural basis of learning, memory, and cognition. Over the last 2 decades, researchers have described dendritic abnormalities associated with Down Syndrome, Fragile X Syndrome, Rett Syndrome, autism, and other brain disorders. It is hoped that consideration of developmental disorders in the context of dendritic abnormalities will improve our understanding of the underlying deficits and enhance therapeutic strategies. C1 NICHHD, NIH, Mental Retardat & Dev Disabil Branch, Bethesda, MD 20892 USA. RP Nitkin, RM (reprint author), NICHHD, NIH, Mental Retardat & Dev Disabil Branch, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA SN 8756-5641 J9 DEV NEUROPSYCHOL JI Dev. Neuropsychol. PY 1999 VL 16 IS 3 BP 299 EP 303 DI 10.1207/S15326942DN1603_1A PG 5 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 275DB UT WOS:000084803200001 ER PT J AU Segal, M Murphy, DD Korkotian, E AF Segal, M Murphy, DD Korkotian, E TI Activity-dependent morphological plasticity of dendritic spines in cultured hippocampal neurons SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article C1 Weizmann Inst Sci, IL-76100 Rehovot, Israel. NINDS, NIH, Bethesda, MD 20892 USA. RP Segal, M (reprint author), Weizmann Inst Sci, IL-76100 Rehovot, Israel. OI Korkotian, Eduard/0000-0001-5515-3387 NR 6 TC 0 Z9 0 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA SN 8756-5641 J9 DEV NEUROPSYCHOL JI Dev. Neuropsychol. PY 1999 VL 16 IS 3 BP 329 EP 330 DI 10.1207/S15326942DN1603_7 PG 2 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 275DB UT WOS:000084803200009 ER PT J AU Schrauwen, P Xia, J Bogardus, C Pratley, RE Ravussin, E AF Schrauwen, P Xia, J Bogardus, C Pratley, RE Ravussin, E TI Skeletal muscle uncoupling protein 3 expression is a determinant of energy expenditure in Pima Indians SO DIABETES LA English DT Article ID RESTING METABOLIC-RATE; GENE; THERMOGENESIS; MEDIATOR; HOMOLOG; TISSUE AB The recent discovery of uncoupling protein (UCP)-2 and UCP-3? and their high expression in skeletal muscle, has renewed interest in a possible role for these proteins in underlying the variability in energy expenditure and therefore metabolic efficiency. Using reverse transcription-polymerase chain reaction, levels of expression of UCP-2 and long and short forms of UCP-3 were measured in skeletal muscle of 19 nondiabetic, male Pima Indians covering a wide range of body weight. Twenty-four-hour energy expenditure was measured ill a respiratory chamber in IG of these indi viduals. BMI was negatively correlated with the expression levels of the long (r = -0.53, P = 0.025) and short (r = -0.46, P = 0.047) forms of UCP-3. BMI was not correlated with UCP-2 expression. Metabolic rate during sleep, adjusted for fat-free mass and fat mass, was positively correlated with the long form of UCP-3 (r = 0.69, P = 0.006). These results indicate that UCP-3 may be a determinant of energy expenditure and metabolic efficiency in Pima Indians. C1 NIDDKD, Clin Diabet & Nutr Sect, NIH, Phoenix, AZ 85016 USA. Maastricht Univ, Dept Human Biol, Maastricht, Netherlands. RP Lilly Corp Ctr, Drop Code 0545, Indianapolis, IN 46285 USA. EM eric_ravussin@lilly.com NR 22 TC 106 Z9 109 U1 0 U2 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0012-1797 EI 1939-327X J9 DIABETES JI Diabetes PD JAN PY 1999 VL 48 IS 1 BP 146 EP 149 DI 10.2337/diabetes.48.1.146 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 151VT UT WOS:000077741900022 PM 9892236 ER PT J AU Sumner, AE Kushner, H Sherif, KD Tulenko, TN Falkner, B Marsh, JB AF Sumner, AE Kushner, H Sherif, KD Tulenko, TN Falkner, B Marsh, JB TI Sex differences in African-Americans regarding sensitivity to insulin's glucoregulatory and antilipolytic actions SO DIABETES CARE LA English DT Article ID NONESTERIFIED FATTY-ACIDS; MEDIATED SUPPRESSION; PLASMA TRIGLYCERIDE; BODY-FAT; GLUCOSE; METABOLISM; POPULATIONS; OVERWEIGHT; OBESITY; GENDER AB OBJECTIVE - The purpose of this study was to determine if there are sex differences in African-Americans regarding the effect of obesity on sensitivity to insulin as a glucoregulatory and antilipolytic hormone. RESEARCH DESIGN AND METHODS - Data from study participants, 127 nondiabetic African-Americans (mean age 32 +/- 4 years), included anthropometric measurements, an oral glucose tolerance test (OGTT), a 2-h euglycemic-hyperinsulinemic clamp, and a fasting triglyceride level. Sensitivity to insulin as a glucoregulatory hormone was determined by M/FFM, where M is the mean glucose infusion rate during the second hour of the clamp and FFM is fat-free mass. Sensitivity to insulin's antilipolytic action was assessed during the OGTT by the percent suppression of free fatty acid (FFA) concentrations between 0 and 120 min. The higher the suppression of FFAs, the greater the sensitivity to insulin's antilipolytic action. RESULTS - The participants were classified by BMI into three groups: nonobese (31 men, 24 women), obese (17 men, 14 women), and severely obese (12 men, 29 women). The women had higher percentages of body fat (P < 0.001), and the men had greater FFM (P < 0.001). The M/FFM values for men versus women in each BMI group were nonobese, 8.8 +/- 2.8 vs. 10.8 +/- 4.4; obese, 7.2 +/- 3.4 vs. 8.5 +/- 3.4; and severely obese, 4.7 +/- 2.1 vs. 6.1 +/- 2.2. The difference between the BMI groups was significant (P < 0.001), as was the difference between men and women (P < 0.01). In addition, there was a significant sex difference in percent suppression of FFAs (P < 0.001). The men and women had similar fasting insulin and FFA concentrations; however, in the men only, the percent suppression of FFA declined with increasing obesity (nonobese, 83 +/- 15%; obese, 73 +/- 18%; and severely obese, 69 +/- 19%; P = 0.02). The women in all three BMI groups had lower FFA levels of 86-88%. CONCLUSIONS - Obese African-American men and women are resistant to insulin as a glucoregulatory hormone, but only obese men are resistant to insulin's antilipolytic action; obese African-American women are sensitive to insulin's antilipolytic action. The combined presence of sensitivity to insulin's antilipolytic action with resistance to insulin's glucoregulatory action in obese African-American women may contribute to their high prevalence of obesity and type 2 diabetes. C1 Allegheny Univ Hlth Sci, Inst Womens Hlth, Philadelphia, PA 19102 USA. Allegheny Univ Hlth Sci, Dept Biostat, Philadelphia, PA 19102 USA. Allegheny Univ Hlth Sci, Dept Physiol, Philadelphia, PA 19102 USA. Allegheny Univ Hlth Sci, Dept Biochem, Philadelphia, PA 19102 USA. RP Sumner, AE (reprint author), NIDDK, Diabet Branch, NIH, Bldg 10,Room 8S235D, Bethesda, MD 20892 USA. EM annes@intra.niddk.nih.gov FU NHLBI NIH HHS [HL-51536, HL-51547] NR 27 TC 32 Z9 33 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 USA SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JAN PY 1999 VL 22 IS 1 BP 71 EP 77 DI 10.2337/diacare.22.1.71 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150WT UT WOS:000077689400012 PM 10333906 ER PT J AU Genuth, S Nathan, D Shamoon, H Duffy, H Dahms, B Mayer, L Brillion, D Lackaye, M Whitehouse, F Kruger, D Bergenstal, R Johnson, M Jacobson, A Doyle, J Waters, M Nathan, D Crowell, S Godine, J McKitrick, C Service, J Ziegler, G Colwell, J Wood, D Maytield, R Molitch, M Schaefer, B Kolterman, O Lorenzi, G Sivitz, M Bayless, M Counts, D Kowarski, A Ostrowski, D Greene, D Martin, C Bantle, J Rogness, B Goldstein, D Smith, A Schade, D Johannes, C Schwartz, S Maschak-Carey, BJ Orchard, T Silvers, N Malone, J Mangione, A Kitabchi, A Murphy, MB Raskin, P Strowig, S Zinman, B Barnie, A Palmer, J Ginsberg, J Dupre, J Harth, J Lorenz, R Lipps, J White, N Santiago, J Levandoski, L Tamborlane, W Gatcomb, P Dahms, B Corcoran, P Quin, J Lachin, J Cleary, P Kenny, D Diminick, L Lamas, D Cowie, C Eastman, R Davis, M Hubbard, L Geithman, P Brickbauer, J Kastorff, L Neider, M Steffes, M Bucksa, J Chavers, B O'Leary, D Crow, R O'Donnell, C Weir, G Clark, C D'Agostino, R Espeland, M Klein, B Jacobson, H Manolio, T Rand, L Singer, D Stern, M Cleary, P Barnie, A Genuth, S Maffin, C Tamborlane, W Wesche, J Nathan, D AF Genuth, S Nathan, D Shamoon, H Duffy, H Dahms, B Mayer, L Brillion, D Lackaye, M Whitehouse, F Kruger, D Bergenstal, R Johnson, M Jacobson, A Doyle, J Waters, M Nathan, D Crowell, S Godine, J McKitrick, C Service, J Ziegler, G Colwell, J Wood, D Maytield, R Molitch, M Schaefer, B Kolterman, O Lorenzi, G Sivitz, M Bayless, M Counts, D Kowarski, A Ostrowski, D Greene, D Martin, C Bantle, J Rogness, B Goldstein, D Smith, A Schade, D Johannes, C Schwartz, S Maschak-Carey, BJ Orchard, T Silvers, N Malone, J Mangione, A Kitabchi, A Murphy, MB Raskin, P Strowig, S Zinman, B Barnie, A Palmer, J Ginsberg, J Dupre, J Harth, J Lorenz, R Lipps, J White, N Santiago, J Levandoski, L Tamborlane, W Gatcomb, P Dahms, B Corcoran, P Quin, J Lachin, J Cleary, P Kenny, D Diminick, L Lamas, D Cowie, C Eastman, R Davis, M Hubbard, L Geithman, P Brickbauer, J Kastorff, L Neider, M Steffes, M Bucksa, J Chavers, B O'Leary, D Crow, R O'Donnell, C Weir, G Clark, C D'Agostino, R Espeland, M Klein, B Jacobson, H Manolio, T Rand, L Singer, D Stern, M Cleary, P Barnie, A Genuth, S Maffin, C Tamborlane, W Wesche, J Nathan, D CA Epidemiology Diabetes Intervention Complication TI Epidemiology of Diabetes Interventions and Complications (EDIC): Design, implementation, and preliminary results of a long-term follow-up of the Diabetes Control and Complications Trial cohort SO DIABETES CARE LA English DT Article ID CORONARY-ARTERY DISEASE; LONGITUDINAL DATA; JUVENILE-ONSET; RISK-FACTORS; RETINOPATHY; IDDM; NEPHROPATHY; PROGRESSION; NEUROPATHY; PREDICTION AB OBJECTIVE - The Diabetes Control and Complications Trial (DCCT) demonstrated the powerful impact of glycemic control on the early manifestations of microvascular complications. Contemporary prospective data on the evolution of macrovascular and late microvascular complications of type 1 diabetes are limited. The Epidemiology of Diabetes Interventions and Complications (EDIC) study is a multicenter, longitudinal, observational study designed to use the well-characterized DCCT cohort of >1,400 patients to determine the long-term effects of prior separation of glycemic levels on micro- and macrovascular outcomes. RESEARCH DESIGN AND METHODS - Using a standardized annual history and physical examination, 28 EDIC clinical centers that were DCCT clinics will follow the EDIC cohort for 10 years. Annual evaluation also includes resting electrocardiogram, Doppler ultrasound measurements of ankle/arm blood pressure, and screening for nephropathy At regular intervals, a timed 4-h urine is collected, lipid profiles are obtained, and stereoscopic fundus photographs are taken. In addition, dual B-mode Doppler ultrasound scans of the common and internal carotid arteries will be performed at years 1 and 6 and at study end. RESULTS - Written informed consent was obtained from 96% of the DCCT subjects. The participants, compared with nonparticipants, tended to have better glycemic control at the completion of the DCCT and were more likely to have their diabetes care provided by DCCT personnel. The EDIC baseline measurement stratified by sex delineates multiple cardiovascular disease risk factor differences such as age (older in men), waist-to-hip ratio (higher in men), HDL cholesterol (lower in men), hypertension (more prevalent in men), and maximum intimal-medial thickness of common and internal carotid arteries (thicker in men). Of the original conventional treatment group, 69% have changed to continuous subcutaneous insulin infusion or multiple daily injections. Although the mean HbA(1c) difference between the intensive and conventional treatment groups narrowed at EDIC years 1 and 2, HbA(1c) remained significantly lower in the intensive group. Of all expected clinic visits, 95% were completed, and the quality of EDIC data is very similar to that observed in the DCCT. CONCLUSIONS - Although obvious problems exist in extended follow-up studies of completed clinical trials, these are balanced by the value of continued systematic observation of the DCCT cohort. In contrast to other epidemiologic studies, EDIC will provide 1) definitive data on type 1 as distinct from type 2 diabetes; 2) reliance on prospective rather than on cross-sectional analysis; 3) long-term followup in a large population; 4) consistent use of objective, reliable measures of outcomes and glycemia; and 5) observation of patients from before the onset of complications. C1 Albert Einstein Coll Med, Bronx, NY 10461 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. Cornell Univ, Med Ctr, Ithaca, NY 14853 USA. Henry Ford Hlth Syst, Detroit, MI USA. Int Diabet Ctr, Minneapolis, MN USA. Joslin Diabet Ctr, Boston, MA USA. Massachusetts Gen Hosp, Boston, MA 02114 USA. Mayo Clin & Mayo Fdn, Rochester, MN USA. Med Univ S Carolina, Charleston, SC USA. Northwestern Univ, Evanston, IL 60208 USA. Univ Calif San Diego, San Diego, CA 92103 USA. Univ Iowa, Iowa City, IA 52242 USA. Univ Maryland, Sch Med, Baltimore, MD 21201 USA. Univ Michigan, Ann Arbor, MI 48109 USA. Univ Minnesota, Minneapolis, MN 55455 USA. Univ Missouri, Columbia, MO 65211 USA. Univ New Mexico, Albuquerque, NM 87131 USA. Univ Penn, Philadelphia, PA 19104 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. Univ S Florida, Tampa, FL 33620 USA. Univ Tennessee, Knoxville, TN 37996 USA. Univ Texas, SW Univ Med Ctr, Houston, TX USA. Univ Toronto, Toronto, ON, Canada. Univ Washington, Seattle, WA 98195 USA. Univ Western Ontario, London, ON N6A 3K7, Canada. Vanderbilt Univ, Nashville, TN USA. Washington Univ, St Louis, MO 63130 USA. Yale Univ, Sch Med, New Haven, CT 06520 USA. George Washington Univ, Ctr Biostat, Washington, DC 20052 USA. NIDDKD, Program Off, Bethesda, MD USA. Univ Wisconsin, Madison, WI 53706 USA. Tufts Univ New England Med Ctr, Boston, MA USA. RP Genuth, S (reprint author), EDIC Res Grp, Box NDIC-DCCT, Bethesda, MD 20892 USA. RI Zinman, Bernard/E-7266-2013; OI Shamoon, Harry/0000-0002-5014-5211 NR 50 TC 252 Z9 254 U1 1 U2 6 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 EI 1935-5548 J9 DIABETES CARE JI Diabetes Care PD JAN PY 1999 VL 22 IS 1 BP 99 EP 111 PG 13 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 150WT UT WOS:000077689400016 ER PT J AU Leslie, RDG Atkinson, MA Notkins, AL AF Leslie, RDG Atkinson, MA Notkins, AL TI Antoantigens IA-2 and GAD in type I (insulin-dependent) diabetes SO DIABETOLOGIA LA English DT Review DE diabetes; IA-2; GAD; pathogenesis; immune response; prediction ID GLUTAMIC-ACID DECARBOXYLASE; PROTEIN-TYROSINE-PHOSPHATASE; STIFF-MAN SYNDROME; T-CELL EPITOPES; FIRST-DEGREE RELATIVES; ONSET IDDM PATIENTS; TRANSMEMBRANE PROTEIN; MOLECULAR-CLONING; NOD MICE; ANTIGENIC DETERMINANTS C1 St Bartholomews Hosp, Dept Diabet & Metab, London EC1A 7BE, England. Univ Florida, Coll Med, Dept Pathol & Lab Med, Gainesville, FL 32610 USA. NIDR, Oral Infect & Immun Branch, Expt Med Sect, NIH, Bethesda, MD USA. RP Leslie, RDG (reprint author), St Bartholomews Hosp, Dept Diabet & Metab, London EC1A 7BE, England. NR 104 TC 155 Z9 162 U1 0 U2 5 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JAN PY 1999 VL 42 IS 1 BP 3 EP 14 DI 10.1007/s001250051105 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 160YQ UT WOS:000078261300002 PM 10027571 ER PT J AU Gautier, JF Milner, MR Elam, E Chen, K Ravussin, E Pratley, RE AF Gautier, JF Milner, MR Elam, E Chen, K Ravussin, E Pratley, RE TI Visceral adipose tissue is not increased in Pima Indians compared with equally obese Caucasians and is not related to insulin action or secretion SO DIABETOLOGIA LA English DT Article DE abdominal obesity; insulin resistance; insulin secretion; Pima Indians ID BODY-FAT DISTRIBUTION; DEPENDENT DIABETES-MELLITUS; ABDOMINAL FAT; COMPUTED-TOMOGRAPHY; REGIONAL ADIPOSITY; GLUCOSE-TOLERANCE; MEN; SENSITIVITY; RESISTANCE; NIDDM AB Pima Indians are insulin resistant and hyperinsulinaemic compared with Caucasians. We investigated whether abdominal fat distribution was different between Pimas and Caucasians and whether differences in the amount of visceral fat explained metabolic differences between the groups. Total body fat (absorptiometry) and abdominal fat distribution at L4-L5 (magnetic resonance imaging) were compared in 20 Pima Indians (10 men/10 women) and 20 age-, sex- and BMI-matched Caucasians. Insulin action was measured as glucose disposal during a two-step hyperinsulinaemic-euglycaemic glucose clamp and insulin secretion was assessed in response to oral and intravenous glucose tolerance tests. By design, percent body fat was similar in Pimas and Caucasians. Abdominal visceral and subcutaneous adipose tissue areas were also similar in the two groups (151 +/- 16 vs 139 +/- 15 cm(2) and 489 +/- 61 vs 441 +/- 57 cm(2) respectively). Plasma insulin concentrations were higher in Pimas than Caucasians in the fasting state (27 +/- 6 vs 11 +/- 2 mU/ml; p < 0.01) and after a 75-g oral glucose load (area under the curve 19975 +/- 2626 vs 9293 +/- 1847 mU.l(-1) 180 min(-1); p < 0.005). Glucose disposal was lower in Pimas than Caucasians during both steps of the clamp and negatively correlated (after adjustment for percent body fat and sex) with visceral adipose tissue in Caucasians (partial r = -0.51, p = 0.03), but not in Pima Indians (r = -0.03, p = 0.92). Insulin secretion was not related to visceral fat independently of percent body fat in either group. We conclude that a relative increase in visceral fat does not explain insulin resistance and hyperinsulinaemia in Pima Indians. C1 NIDDKD, Clin Diabet & Nutr Sect, NIH, Phoenix, AZ 85016 USA. Good Samaritan Reg Med Ctr, Dept Radiol, Phoenix, AZ USA. RP Gautier, JF (reprint author), NIDDKD, Clin Diabet & Nutr Sect, NIH, 4212 N 16Th St, Phoenix, AZ 85016 USA. RI Chen, kewei/P-6304-2015 OI Chen, kewei/0000-0001-8497-3069 NR 29 TC 35 Z9 35 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JAN PY 1999 VL 42 IS 1 BP 28 EP 34 DI 10.1007/s001250051108 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 160YQ UT WOS:000078261300005 PM 10027574 ER PT J AU Greig, NH Holloway, HW De Ore, KA Jani, D Wang, Y Zhou, J Garant, MJ Egan, JM AF Greig, NH Holloway, HW De Ore, KA Jani, D Wang, Y Zhou, J Garant, MJ Egan, JM TI Once daily injection of exendin-4 to diabetic mice achieves long-term beneficial effects on blood glucose concentrations SO DIABETOLOGIA LA English DT Article DE exendin-LC; glucose; GLP-1; db/db mice; Wistar rats ID GLUCAGON-LIKE PEPTIDE-1; RECEPTOR; ANTAGONIST; GLP-1; AMIDE; RATS; EXPRESSION; TOLERANCE; AGONIST AB Glucagon-like peptide-1 is the main hormonal mediator of the enteroinsular axis. Recently, it has additionally received considerable attention as a possible new treatment for Type II (non-insulin-dependent) diabetes mellitus. Its major disadvantage is that its duration of action is too short to achieve good 24-h metabolic control. Exendin-4, which is produced in the salivary glands of Gila monster lizards, is structurally similar to glucagon-like peptide-1 and shares several useful biological properties with glucagon-like peptide-1. It binds the glucagon-like peptide-1 receptor, stimulates insulin release and increases the cAMP production in beta cells. We report that exendin-4 is a more potent insulinotropic agent when given intravenously to rats than is glucagonlike peptide-1 (ED50 0.19 nmol/kg for glucagon-like peptide-1 vs 0.0143 nmol/kg for exendin-4) and causes a greater elevation in cAMP concentrations in isolated islets. Of even greater interest we found that when given intraperitoneally only once daily to diabetic mice it had a prolonged effect of lowering blood glucose. After 1 week of treatment blood glucoses were 5.0 +/- 2.6 mmol/l compared to diabetic concentrations of 13.2 +/- 2.5 mmol/l. After 13 weeks of daily treatment HbA(1c) was 8.8 +/- 0.4% in non-treated diabetic animals compared with 4.7 +/- 0.25% in treated diabetic animals. Blood glucoses also were lower (p < 0.005) and insulin concentrations higher (p < 0.02) in the treated animals. Exendin-4 could therefore be preferable to glucagon-like peptide-1 as a long-term treatment of Type II diabetes. C1 NIA, Gerontol Res Ctr, Diabet Sect, NIH, Baltimore, MD 21224 USA. NIA, Drug Design & Dev Sect, NIH, Baltimore, MD 21224 USA. Howard Univ, Sch Med, Washington, DC 20059 USA. RP Egan, JM (reprint author), NIA, Gerontol Res Ctr, Diabet Sect, NIH, Box 23,5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 19 TC 168 Z9 177 U1 2 U2 13 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JAN PY 1999 VL 42 IS 1 BP 45 EP 50 DI 10.1007/s001250051111 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 160YQ UT WOS:000078261300008 PM 10027577 ER PT J AU Nelson, RG Tan, M Beck, GJ Bennett, PH Knowler, WC Mitch, WE Blouch, K Myers, BD AF Nelson, RG Tan, M Beck, GJ Bennett, PH Knowler, WC Mitch, WE Blouch, K Myers, BD TI Changing glomerular filtration with progression from impaired glucose tolerance to Type II diabetes mellitus SO DIABETOLOGIA LA English DT Article DE Diabetic Renal Disease Study; glomerular filtration rate; impaired glucose tolerance; Type II diabetes; Pima Indians ID PIMA-INDIANS; KIDNEY-FUNCTION AB Glomerular filtration rate (iothalamate clearance) was measured serially for 48 months in 26 Pima Indians with impaired glucose tolerance and 27 with normal glucose tolerance. At baseline, the mean glomerular filtration rate (SEM) was 133 +/- 8 ml/min in subjects with impaired glucose tolerance and 123 +/- 5 ml/min in those with normal glucose tolerance (p = 0.12). In the 12 subjects with impaired glucose tolerance who progressed to Type II (non-insulin-dependent) diabetes during follow-up, mean glomerular filtration rate increased by 30% (p = 0.011). Among the remaining 14 subjects with impaired glucose tolerance, 12 reverted to normoglycaemia. The glomerular filtration rate both at baseline and after 48 months in this subgroup exceeded the values of subjects with normal glucose tolerance by 20% (p = 0.008) and 14% (p = 0.013), respectively. A pronounced rise in the glomerular filtration rate occurs at the onset of Type II diabetes but a trend to hyperfiltration is also present in these with impaired glucose tolerance. C1 NIDDKD, Phoenix Epidemiol & Clin Res Branch, Phoenix, AZ 85014 USA. Cleveland Clin Fdn, Dept Biostat & Epidemiol, Cleveland, OH 44195 USA. Emory Univ, Sch Med, Div Renal, Atlanta, GA 30322 USA. Stanford Univ, Sch Med, Div Nephrol, Stanford, CA 94305 USA. RP Nelson, RG (reprint author), NIDDKD, Phoenix Epidemiol & Clin Res Branch, 1550 E Indian Sch Rd, Phoenix, AZ 85014 USA. RI Nelson, Robert/B-1470-2012 FU NIDDK NIH HHS [N01-DK-6-2285, N01-DK-7-2291] NR 10 TC 16 Z9 17 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JAN PY 1999 VL 42 IS 1 BP 90 EP 93 DI 10.1007/s001250051118 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 160YQ UT WOS:000078261300015 PM 10027584 ER PT J AU Lindblad, P Chow, WH Chan, J Bergstrom, A Wolk, A Gridley, G McLaughlin, JK Nyren, O Adami, HO AF Lindblad, P Chow, WH Chan, J Bergstrom, A Wolk, A Gridley, G McLaughlin, JK Nyren, O Adami, HO TI The role of diabetes mellitus in the aetiology of renal cell cancer SO DIABETOLOGIA LA English DT Article DE kidney neoplasms; diabetes mellitus; cohort study; risk factors; Sweden ID POPULATION-BASED COHORT; CYSTIC KIDNEY-DISEASE; RISK-FACTORS; GLUCOSE-TOLERANCE; MEDICAL HISTORY; CARCINOMA; INSULIN; WEIGHT; OBESITY; DENMARK AB To investigate the relation between diabetes mellitus and the risk of renal cell cancer we carried out a population-based retrospective cohort study. Patients identified in the Swedish Inpatient Register who were discharged from hospitals with a diagnosis of diabetes mellitus between 1965 and 1983 formed a cohort of 153852 patients (80005 women and 73 847 men). The cohort members were followed up to 1989 by record linkage to three nation-wide registries. Standardized incidence ratios (SIRs) and standardized mortality ratios (SMRs) were computed using age-specific sex-specific and period-specific incidence and mortality rates derived from the entire Swedish population. After exclusion of the first year of observation, a total of 267 incidences of renal cell cancer (ICD-7:180.0) occurred in diabetic patients compared with the 182.4 that had been expected. Increased risks were observed in both women (SIR = 1.7, 95% confidence interval, CI = 1.4-2.0) and men (SIR = 1.3; 95% CI = 1.1-1.6) throughout the duration of follow-up (1-25 years). A higher risk was seen for kidney cancer (ICD-7:180) mortality (SMR = 1.9; 95% CI = 1.7-2.2, women; SMR 1.7, 95% CI = 1.4-1.9, men). In comparison with the general population, patients with diabetes mellitus have an increased risk of renal cell cancer. C1 Karolinska Inst, Dept Med Epidemiol, S-17177 Stockholm, Sweden. NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Int Epidemiol Inst, Rockville, MD USA. RP Lindblad, P (reprint author), Karolinska Inst, Dept Med Epidemiol, S-17177 Stockholm, Sweden. FU NCI NIH HHS [N01CP-60538] NR 48 TC 140 Z9 145 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JAN PY 1999 VL 42 IS 1 BP 107 EP 112 DI 10.1007/s001250051122 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 160YQ UT WOS:000078261300019 PM 10027588 ER PT J AU Schrump, DS Nguyen, DM AF Schrump, DS Nguyen, DM TI Strategies for molecular intervention in esophageal cancers and their precursor lesions SO DISEASES OF THE ESOPHAGUS LA English DT Article ID DEPENDENT KINASE INHIBITOR; CYCLIN-D GENE; BARRETTS-ESOPHAGUS; CELL-CYCLE; NEOPLASTIC PROGRESSION; SUPPRESSOR GENES; ALLELIC LOSSES; CDK INHIBITORS; FREQUENT LOSS; EXPRESSION AB Molecular analysis of malignant transformation in Barrett's epithelium provides insight into the temporal nature and significance of individual genetic events during multistep esophageal carcinogenesis. Potential targets for intervention in esophageal neoplasms include mutations involving retinoblastoma (Rb) and p53 tumor-suppressor pathways as well as tyrosine kinase cascades, which are known to promote cell cycle progression. Data from recent experiments provide the preclinical rationale for novel: pharmacologic interventions in established esophageal cancers, and suggest strategies for chemoprevention in patients at risk for the development of these neoplasms. C1 NCI, Surg Branch, Thorac Oncol Sect, NIH, Bethesda, MD 20892 USA. RP Schrump, DS (reprint author), NCI, Surg Branch, Thorac Oncol Sect, NIH, Room 2B-07,10 Ctr Dr, Bethesda, MD 20892 USA. NR 47 TC 12 Z9 12 U1 0 U2 1 PU BLACKWELL SCIENCE ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 1120-8694 J9 DIS ESOPHAGUS JI Dis. Esophagus PY 1999 VL 12 IS 3 BP 181 EP 185 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 268UN UT WOS:000084434100006 PM 10631909 ER PT J AU Buesing, MA McSweegan, E AF Buesing, MA McSweegan, E TI Submitting biologics applications to the Center for Biologics Evaluation and Research electronically SO DRUG INFORMATION JOURNAL LA English DT Article DE Investigational New Drug; biologic product license; electronic; guidance; CBER AB The Food and Drug Administration (FDA) has gained significant experience with computer-assisted licensing applications, and has concluded that continued reliance on customized formats is a burden for the FDA and industry. As a result, the FDA is working to standardize the content and format of electronically submitted applications, and to establish procedures for electronic applications that will: create minimal additional work for industry and reviewers, establish consistency across the FDA's centers, and expedite the review process. The FDA is proposing to move to a paperless regulatory process by the year 2002. Toward that goal, the FDA's Center for Biologics Evaluation and Research (CBER) has released new guidance for the electronic submission of biologic and product license applications; case report forms, tabulations, and statistical data; and lot release protocols. A pilot program for Investigational New Drug applications also has been initiated. C1 US FDA, Ctr Biol Evaluat & Res, Rockville, MD 20857 USA. RP McSweegan, E (reprint author), NIAID, DMID, NIH, Solar Bldg,Rm 3A34, Bethesda, MD 20892 USA. NR 8 TC 2 Z9 2 U1 0 U2 0 PU DRUG INFORMATION ASSOCIATION PI FORT WASHINGTON PA 501 OFFICE CENTER DR, STE 450, FORT WASHINGTON, PA 19034-3212 USA SN 0092-8615 J9 DRUG INF J JI Drug Inf. J. PD JAN-MAR PY 1999 VL 33 IS 1 BP 1 EP 15 PG 15 WC Health Care Sciences & Services; Pharmacology & Pharmacy SC Health Care Sciences & Services; Pharmacology & Pharmacy GA 192WJ UT WOS:000080102400001 ER PT J AU Ripp, SL Itagaki, K Philpot, RM Elfarra, AA AF Ripp, SL Itagaki, K Philpot, RM Elfarra, AA TI Species and sex differences in expression of flavin-containing monooxygenase form 3 in liver and kidney microsomes SO DRUG METABOLISM AND DISPOSITION LA English DT Article ID CONTAINING MONO-OXYGENASES; ADULT HUMAN LIVER; S-OXIDASE; S-(1,2-DICHLOROVINYL)-L-CYSTEINE SULFOXIDE; ESCHERICHIA-COLI; RABBIT LIVER; FMO3; CYSTEINE; MOUSE; RAT AB Flavin-containing monooxygenase (FMO) 3 is the predominant FMO isoform in adult human liver; however, little is known about its expression in common laboratory species. Studies have shown FMO3 levels to be sex-dependent in mouse liver, but not in human liver. The current study was undertaken to determine the expression of FMO3 in liver and kidney microsomes from multiple species, and to determine whether the sex dependence seen in mouse liver extends to other species and/or tissues. FMO3 had previously been shown to be the major FMO involved in methionine S-oxidation in rat and rabbit liver microsomes, In this study, species differences in FMO3 levels were assessed in liver microsomes from humans, rats, dogs, mice, and rabbits, and in kidney microsomes from rats, dogs, mice, and rabbits, by comparing methionine S-oxidase activities. Species differences were noted in male liver microsomes, with rabbits having 3-fold higher methionine S-oxidase activity than mice and dogs and 1.5-fold higher activity than humans and rats. Species differences were also noted in male and female kidney microsomes, with rats exhibiting 2- to 6-fold higher methionine S-oxidase activity than the other species. Sex differences in FMO3 levels were assessed using methionine S-oxidase activity and immunoblotting, and were noted only in liver microsomes from mice and dogs, with females having higher levels than males. Results also show that FMO3 orthologs from multiple species are catalytically similar with regard to methionine, S-allyl-L-cysteine, and S-(1,2-dichlorovinyl)-L-cysteine S-oxidations. C1 Univ Wisconsin, Sch Vet Med, Dept Comparat Biosci, Madison, WI 53706 USA. Univ Wisconsin, Ctr Environm Toxicol, Madison, WI 53706 USA. NIEHS, Res Triangle Pk, NC 27709 USA. RP Elfarra, AA (reprint author), Univ Wisconsin, Sch Vet Med, Dept Comparat Biosci, 2015 Linden Dr W, Madison, WI 53706 USA. FU NIDDK NIH HHS [DK44295] NR 27 TC 52 Z9 52 U1 0 U2 0 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0090-9556 J9 DRUG METAB DISPOS JI Drug Metab. Dispos. PD JAN PY 1999 VL 27 IS 1 BP 46 EP 52 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 156WH UT WOS:000078024900007 PM 9884308 ER PT J AU Sugiyama, K Wang, TCL Simpson, JT Rodriguez, L Kador, PF Sato, S AF Sugiyama, K Wang, TCL Simpson, JT Rodriguez, L Kador, PF Sato, S TI Aldose reductase catalyzes the oxidation of naphthalene-1,2-dihydrodiol for the formation of ortho-naphthoquinone SO DRUG METABOLISM AND DISPOSITION LA English DT Article ID POLYCYCLIC AROMATIC-HYDROCARBONS; NAPHTHALENE CATARACT; DIHYDRODIOL DEHYDROGENASE; RAT LENS; ESCHERICHIA-COLI; SENILE CATARACT; STEREOSELECTIVITY; PURIFICATION; METABOLISM; TISSUES C1 NEI, Lab Ocular Therapeut, NIH, Bethesda, MD 20892 USA. NIMH, Lab Neurotoxicol, NIH, Bethesda, MD 20892 USA. RP Sato, S (reprint author), NEI, Lab Ocular Therapeut, NIH, Bldg 10,Rm 10B09,10 Ctr Dr,MSC 1850, Bethesda, MD 20892 USA. EM sanai@helix.nih.gov NR 28 TC 12 Z9 12 U1 0 U2 2 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0090-9556 J9 DRUG METAB DISPOS JI Drug Metab. Dispos. PD JAN PY 1999 VL 27 IS 1 BP 60 EP 67 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 156WH UT WOS:000078024900009 PM 9884310 ER PT J AU Yang, TJ Krausz, KW Sai, Y Gonzalez, FJ Gelboin, HV AF Yang, TJ Krausz, KW Sai, Y Gonzalez, FJ Gelboin, HV TI Eight inhibitory monoclonal antibodies define the role of individual P-450S in human liver microsomal diazepam, 7-ethoxycoumarin, and imipramine metabolism SO DRUG METABOLISM AND DISPOSITION LA English DT Article ID CYTOCHROME P450S; RAT; DEMETHYLATION; CYP3A4; 2E1 AB Eight inhibitory monoclonal antibodies (MAbs) individually specific to human cytochrome P-450 (P-450) 1A1, 1A2, 2A6, 2B6, 2C subfamily (2C8, 2C9, 2C18 and 2C19), 2D6, 2E1, and 3A4/5 were used to define the role of single P-450s in the metabolism of diazepam (DZ), 7-ethoxycoumarin (7-EC), and imipramine (IMI) in human liver microsomes (HLM). The MAbs were added combinatorially to six HLM samples. With DZ as a substrate, more than 80% of temazepam (TMZ) formation was inhibited in all six samples by the addition of MAb to 3A4/5, indicating an 80% contribution of 3A4/5 to TMZ formation. Nordiazepam formation was inhibited with MAbs to 2B6 (6-23%), 2C subfamily (12-61%) and 3A4/5 (14-45%). The MAbs to 1A1, 1A2, 2A6, 2D6, and 2E1 did not inhibit TMZ or nordiazepam formation; this indicates their noninvolvement in DZ metabolism. The MAb-defined P-450 contribution to 7-EC O-deethylation in six HLM samples was 17 to 60% for 2E1, 15 to 46% for 2A6, and 5 to 22% for 1A2, reflecting the role and variation of each P-450 in this activity. MAbs to 1A1,the 2C subfamily, 2D6, and 3A4/5 did not affect 7-EC metabolism in the HLM samples. IMI is metabolized mainly to 2-hydroxyimipramine by expressed 2C19 and 2D6, and desipramine (DIM) by expressed 1A2, 2C18, 2C19 and 2D6. Expressed 1A1, 2C9, and 3A4 showed low activities for the formation of DIM. Of six HLM samples, five showed IMI hydroxylation activity (0.35-2.6 nmol/min/nmol P-450) while one (HL43) lacked hydroxylation activity. All six HLM samples showed N-deethylation activity (0.74-1.4 nmol/min/nmol P-450). The MAb-determined contribution of 2D6 and 2C19 to 2-hydroxyimipramine formation ranged from 47 to 90% and from 0 to 49%, respectively, while HL43 did not show P-hydroxylation. The role of P-450s involved in DIM formation varied for 2C19 (13-50%), 1A2 (23-41%), and 3A4 (8-26%). These studies demonstrate a system for identifying the quantitative metabolic role of single P-450s and their interindividual variability in a tissue containing multiple P-450s. The system using inhibitory MAbs is simple, precise, and applicable to any P-450-mediated catalytic activity including that for drugs, carcinogens, mutagens, toxic chemicals and endobiotics. C1 NCI, Mol Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. NCI, Lab Metab, NIH, Bethesda, MD 20892 USA. RP Gelboin, HV (reprint author), NCI, Mol Carcinogenesis Lab, NIH, Bldg 37,Rm 3E24,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 28 TC 44 Z9 44 U1 0 U2 4 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0090-9556 J9 DRUG METAB DISPOS JI Drug Metab. Dispos. PD JAN PY 1999 VL 27 IS 1 BP 102 EP 109 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 156WH UT WOS:000078024900016 PM 9884317 ER PT J AU Rose, ML Rusyn, I Bojes, HK Germolec, DR Luster, M Thurman, RG AF Rose, ML Rusyn, I Bojes, HK Germolec, DR Luster, M Thurman, RG TI Role of Kupffer cells in peroxisome proliferator-induced hepatocyte proliferation SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Symposium on Enzymatic Transformation of Xenobiotic Chemicals Celebrating 30 Years of Environmental and Molecular Toxicology at Vanderbilt University CY APR 18-19, 1997 CL VANDERBILT UNIV, NASHVILLE, TENNESSEE HO VANDERBILT UNIV ID TUMOR-NECROSIS-FACTOR; PROTEIN-KINASE-C; NF-KAPPA-B; ACYL-COA SYNTHETASE; PERFUSED-RAT-LIVER; REPLICATIVE DNA-SYNTHESIS; FACTOR-ALPHA; ACTIVATED RECEPTOR; H2O2 PRODUCTION; CLOFIBRIC ACID C1 Univ N Carolina, Dept Pharmacol, Hepatobiol & Toxicol Lab, Chapel Hill, NC 27599 USA. Univ N Carolina, Curriculum Toxicol, Chapel Hill, NC 27599 USA. NIEHS, Res Triangle Pk, NC 27709 USA. RP Thurman, RG (reprint author), Univ N Carolina, Dept Pharmacol, Hepatobiol & Toxicol Lab, CB 7365,Mary Ellen Jones Bldg, Chapel Hill, NC 27599 USA. EM thurman@med.unc.edu RI Rusyn, Ivan/S-2426-2016 FU NIEHS NIH HHS [ES-04325] NR 81 TC 33 Z9 35 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1999 VL 31 IS 1 BP 87 EP 116 DI 10.1081/DMR-100101909 PG 30 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 170VW UT WOS:000078828600006 PM 10065367 ER PT J AU Scarborough, PE Ma, JX Qu, W Zeldin, DC AF Scarborough, PE Ma, JX Qu, W Zeldin, DC TI P450 subfamily CYP2J and their role in the bioactivation of arachidonic acid in extrahepatic tissues SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Symposium on Enzymatic Transformation of Xenobiotic Chemicals Celebrating 30 Years of Environmental and Molecular Toxicology at Vanderbilt University CY APR 18-19, 1997 CL VANDERBILT UNIV, NASHVILLE, TN HO VANDERBILT UNIV ID POTENTIAL FUNCTIONAL-SIGNIFICANCE; CYTOSOLIC EPOXIDE HYDROLASE; EPOXYEICOSATRIENOIC ACIDS; CYTOCHROME-P-450 ENZYMES; MOLECULAR-CLONING; CRYSTAL-STRUCTURE; MICROSOMAL CYTOCHROME-P450; ENANTIOFACIAL SELECTIVITY; PROXIMAL TUBULE; CDNA CLONING AB Historically, there has been intense interest in P450 metabolic oxidation, peroxidation, and reduction of xenobiotics. More recently, there has been a growing appreciation for the role of P450s in the oxidation of lipophilic endobiotics, such as bile acids, fat-soluble vitamins, and eicosanoids. This review details the emerging CYP2J subfamily of P450s and their role as catalysts of arachidonic acid metabolism. C1 NIEHS, Pulm Pathobiol Lab, NIH, Res Triangle Pk, NC 27709 USA. RP NIEHS, Pulm Pathobiol Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. EM zeldin@niehs.nih.gov NR 87 TC 87 Z9 92 U1 0 U2 1 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND SN 0360-2532 EI 1097-9883 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1999 VL 31 IS 1 BP 205 EP 234 DI 10.1081/DMR-100101915 PG 30 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 170VW UT WOS:000078828600012 PM 10065373 ER PT J AU Buters, JTM Doehmer, J Gonzalez, FJ AF Buters, JTM Doehmer, J Gonzalez, FJ TI Cytochrome P450-null mice SO DRUG METABOLISM REVIEWS LA English DT Article; Proceedings Paper CT Satellite Symposium on Microsomes, Drug Oxidation, and Clinical Pharmacology CY SEP 20-21, 1997 CL BERLIN, GERMANY DE null mice; cytochrome P450; CYP1A1; CYP1A2; CYP1B1; CYP2E1; caffeine; acetaminophen; dimethylbenzo[a]anthracene ID AH RECEPTOR; C/EBP-ALPHA; NULL ALLELE; METABOLISM; GENE; EXPRESSION; MOUSE; ACTIVATION; DEFICIENT; SEQUENCE C1 Tech Univ Munich, Inst Toxicol & Environm Hlth, D-80636 Munich, Germany. NCI, Metab Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP Buters, JTM (reprint author), Tech Univ Munich, Inst Toxicol & Environm Hlth, D-80636 Munich, Germany. RI Buters, Jeroen/G-5070-2011 NR 32 TC 27 Z9 28 U1 0 U2 2 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0360-2532 J9 DRUG METAB REV JI Drug Metab. Rev. PY 1999 VL 31 IS 2 BP 437 EP 447 DI 10.1081/DMR-100101929 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 197KU UT WOS:000080364600012 PM 10335446 ER PT J AU Neckers, L Mimnaugh, E Schulte, TW AF Neckers, L Mimnaugh, E Schulte, TW TI Hsp90 as an anti-cancer target SO DRUG RESISTANCE UPDATES LA English DT Review ID HEAT-SHOCK PROTEIN; ROUS-SARCOMA VIRUS; ATP-BINDING-PROPERTIES; 2 CELLULAR PROTEINS; N-TERMINAL DOMAIN; CASEIN KINASE-II; MOLECULAR CHAPERONE; TYROSINE KINASE; SIGNAL-TRANSDUCTION; STEROID-RECEPTOR AB Heat shock protein 90 is one of the most abundant cellular proteins. Although its functions are still being characterized, it appears to serve as a chaperone for a growing list of cell signaling proteins, including many tyrosine and serine/threonine kinases, involved in cell proliferation and/or survival. The recent discovery of natural products which are able to inhibit Hsp90 function have allowed for both identification of its client proteins and for a better understanding of its role in their activity. Accumulating data have suggested that targeting Hsp90 in cancer cells may be of clinical benefit. C1 NCI, Med Branch, Dept Cell & Canc Biol, NIH, Rockville, MD 20850 USA. RP Neckers, L (reprint author), NCI, Med Branch, Dept Cell & Canc Biol, NIH, 9610 Med Ctr Dr,Suite 300, Rockville, MD 20850 USA. NR 97 TC 54 Z9 54 U1 1 U2 5 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 1368-7646 J9 DRUG RESIST UPDATE JI Drug Resist. Update PY 1999 VL 2 IS 3 BP 165 EP 172 DI 10.1054/drup.1999.0082 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 227WY UT WOS:000082104000005 ER PT J AU Pommier, Y Pourquier, P Urasaki, Y Wu, JX Laco, GS AF Pommier, Y Pourquier, P Urasaki, Y Wu, JX Laco, GS TI Topoisomerase I inhibitors: selectivity and cellular resistance SO DRUG RESISTANCE UPDATES LA English DT Review ID ACTIVE METABOLITE SN-38; HUMAN LIVER-MICROSOMES; CROSS-LINKING AGENTS; CAMPTOTHECIN RESISTANCE; IRINOTECAN CPT-11; LUNG-CANCER; ATAXIA-TELANGIECTASIA; CLEAVABLE COMPLEXES; COVALENT COMPLEXES; DNA TOPOISOMERASES AB Topoisomerase I (top I)inhibitors (camptothecins and other structurally diverse compounds) are effective and promising anticancer agents. Determinants of selectivity toward cancer cells and resistance are multifactorial. These factors can be separated in three groups. The first is related to alterations in drug distribution and metabolism. The second group includes both quantitative and qualitative (mutations) differences in top I. The third group includes resistance and sensitivity factors downstream from the cleavage complexes. They include DNA repair, cell cycle checkpoints and apoptosis, and are probably key to the relative selectivity of camptothecins toward cancer cells and to clinical resistance. C1 NCI, Mol Pharmacol Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RP Pommier, Y (reprint author), NCI, Mol Pharmacol Lab, Div Basic Sci, NIH, Bldg 37,Rm 5D02, Bethesda, MD 20892 USA. NR 119 TC 144 Z9 145 U1 1 U2 13 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 1368-7646 J9 DRUG RESIST UPDATE JI Drug Resist. Update PY 1999 VL 2 IS 5 BP 307 EP 318 DI 10.1054/drup.1999.0102 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 279AM UT WOS:000085021200005 ER PT J AU Saxman, S AF Saxman, S TI Oral etoposide in germ cell tumours SO DRUGS LA English DT Article; Proceedings Paper CT Conference on Oral Chemotherapy - Past, Present and Future Directions CY FEB 26-28, 1998 CL CANCUN, MEXICO SP Sarah Cannon Canc Ctr ID TESTICULAR CANCER; SALVAGE THERAPY; PHASE-II; TUMORS; CHEMOTHERAPY AB Patients with germ cell tumours who relapse or fail to achieve disease-free status after first-line chemotherapy have a poor prognosis. When administered orally, etoposide produces responses in approximately 25% of patients whose disease is refractory to therapy and is a reasonable choice for palliative treatment in patients who are otherwise incurable. Oral etoposide has also been studied as maintenance therapy in patients who have been treated with salvage chemotherapy or surgery, with results that compare favourably with historical data. We recommend 3 months of maintenance oral etoposide for patients who achieve a complete response to any type of salvage therapy. C1 Indiana Univ, Sch Med, Dept Med, Div Hematol Oncol, Indianapolis, IN USA. RP Saxman, S (reprint author), NCI, Canc Therapy Evaluat Program, 6130 Execut Blvd,Room 741, Bethesda, MD 20892 USA. NR 11 TC 2 Z9 2 U1 0 U2 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 0012-6667 J9 DRUGS JI Drugs PY 1999 VL 58 SU 3 BP 31 EP 34 DI 10.2165/00003495-199958003-00005 PG 4 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 279XY UT WOS:000085071400006 PM 10711839 ER PT B AU Hunt, WA Liu, Y AF Hunt, WA Liu, Y BE Liu, Y Hunt, WA TI Overview of the symposium SO "DRUNKEN" SYNAPSE: STUDIES OF ALCOHOL-RELATED DISORDERS LA English DT Proceedings Paper CT Symposium on the Drunken Synapse - Studies of Alcohol-Related Disorders, Held in Conjunction with the Annual Meeting of the Society-for-Neuroscience CY OCT 25, 1997 CL NEW ORLEANS, LA SP Soc Neurosci ID HIPPOCAMPAL SYNAPSES; ALCOHOL RESEARCH; ANIMALS; VESICLES; POOL C1 NIAAA, Neurosci & Behav Res Branch, Bethesda, MD 20892 USA. RP Hunt, WA (reprint author), NIAAA, Neurosci & Behav Res Branch, Bethesda, MD 20892 USA. NR 16 TC 0 Z9 0 U1 0 U2 0 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA BN 0-306-46111-0 PY 1999 BP 1 EP 15 PG 15 WC Substance Abuse; Neurosciences SC Substance Abuse; Neurosciences & Neurology GA BN44D UT WOS:000081933600001 ER PT S AU Potter, M AF Potter, M BE Honn, KV Marnett, LJ Nigam, S Dennis, EA TI Indomethacin inhibition of pristane plasmacytomagenesis in genetically susceptible inbred mice SO EICOSANOIDS AND OTHER BIOACTIVE LIPIDS IN CANCER, IMFLAMMATION AND RADIATION INJURY, 4 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 5th International Conference on Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Related Diseases CY SEP 17-20, 1997 CL LA JOLLA, CALIFORNIA ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ANTI-INFLAMMATORY DRUGS; COLON-CANCER; POTENTIAL ROLE; BALB/C MICE; DNA DAMAGE; CELLS; INDUCTION; PROSTAGLANDINS; PROLIFERATION C1 NCI, Genet Lab, NIH, Bethesda, MD 20892 USA. RP Potter, M (reprint author), NCI, Genet Lab, NIH, Bldg 37, Bethesda, MD 20892 USA. NR 34 TC 5 Z9 5 U1 0 U2 0 PU KLUWER ACADEMIC / PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46138-2 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1999 VL 469 BP 151 EP 156 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA BP58H UT WOS:000085570100023 PM 10667324 ER PT S AU Glasgow, WC Hui, RT Jayawickreme, S Angerman-Stewart, J Han, BB Eling, TE AF Glasgow, WC Hui, RT Jayawickreme, S Angerman-Stewart, J Han, BB Eling, TE BE Honn, KV Marnett, LJ Nigam, S Dennis, EA TI 13(S)-HpODE augments epidermal growth factor signal transduction by attentuating EGF receptor dephosphorylation SO EICOSANOIDS AND OTHER BIOACTIVE LIPIDS IN CANCER, IMFLAMMATION AND RADIATION INJURY, 4 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 5th International Conference on Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Related Diseases CY SEP 17-20, 1997 CL LA JOLLA, CALIFORNIA ID HAMSTER EMBRYO FIBROBLASTS; TYROSINE KINASE; LINOLEIC-ACID; METABOLITES; PHENOTYPES; CELLS C1 Mercer Univ, Sch Med, Div Basic Med Sci, Macon, GA 31207 USA. NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Glasgow, WC (reprint author), Mercer Univ, Sch Med, Div Basic Med Sci, Macon, GA 31207 USA. NR 8 TC 0 Z9 0 U1 0 U2 2 PU KLUWER ACADEMIC / PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46138-2 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1999 VL 469 BP 371 EP 375 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA BP58H UT WOS:000085570100054 PM 10667355 ER PT S AU Anderson, KM Ondrey, FG Harris, JE AF Anderson, KM Ondrey, FG Harris, JE BE Honn, KV Marnett, LJ Nigam, S Dennis, EA TI Modulation of cellular proliferation and induction of apoptosis in a human lymphoma cell line after treatment with selective lipoxygenase inhibitors SO EICOSANOIDS AND OTHER BIOACTIVE LIPIDS IN CANCER, IMFLAMMATION AND RADIATION INJURY, 4 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 5th International Conference on Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Related Diseases CY SEP 17-20, 1997 CL LA JOLLA, CALIFORNIA ID ARACHIDONIC-ACID METABOLISM; 5,8,11,14-EICOSATETRAYNOIC ACID; DNA-SYNTHESIS; 5-LIPOXYGENASE; MEMBRANE; GROWTH; U937 C1 Rush Med Coll, Dept Med Oncol, Chicago, IL 60612 USA. NIH, Natl Inst Deafness & Other Commun Disorders, Head & Neck Surg Branch, Tumor Cell Biol Div, Bethesda, MD 20892 USA. RP Anderson, KM (reprint author), Rush Med Coll, Dept Med Oncol, Chicago, IL 60612 USA. NR 14 TC 1 Z9 1 U1 0 U2 1 PU KLUWER ACADEMIC / PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46138-2 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1999 VL 469 BP 563 EP 568 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA BP58H UT WOS:000085570100082 PM 10667383 ER PT S AU Kamitani, H Geller, M Eling, T AF Kamitani, H Geller, M Eling, T BE Honn, KV Marnett, LJ Nigam, S Dennis, EA TI The possible involvement of 15-lipoxygenase/leukocyte type 12-lipoxygenase in colorectal carcinogenesis SO EICOSANOIDS AND OTHER BIOACTIVE LIPIDS IN CANCER, IMFLAMMATION AND RADIATION INJURY, 4 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 5th International Conference on Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Related Diseases CY SEP 17-20, 1997 CL LA JOLLA, CALIFORNIA ID APOPTOSIS; EXPRESSION; CLONING; PATHWAY; LIPOXYGENASES; PHENOTYPES; ADENOMAS; CANCER; CELLS; CDNA C1 NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Kamitani, H (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. NR 17 TC 17 Z9 17 U1 0 U2 0 PU KLUWER ACADEMIC / PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46138-2 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1999 VL 469 BP 593 EP 598 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA BP58H UT WOS:000085570100086 PM 10667387 ER PT J AU Takeuchi, Y Konishi, M Hori, H Takahashi, T Kirk, KL AF Takeuchi, Y Konishi, M Hori, H Takahashi, T Kirk, KL TI Simple synthesis of alpha-cyano-alpha-fluoro-p-tolylacetic acid (CFTA), a new efficient chiral derivatizing agent SO ENANTIOMER LA English DT Article DE alpha-cyano-alpha-fluoro-p-tolylacetic acid; Candida rugosa; chiral derivatizing agent; Delta delta(F); enantioselective resolution; lipase ID ENANTIOMERIC EXCESS DETERMINATION; CANDIDA-RUGOSA LIPASE; CARBOXYLIC-ACIDS; ENANTIOSELECTIVITY; ESTERS AB The new chiral derivatizing agent, alpha-cyano-alpha-fluoro-p-tolylacetic acid (CFTA) (2) was prepared in optically pure form by Candida rugosa lipase (CRL)-mediated kinetic resolution of racemic CFTA ethyl ester (CFTA Et ester) (1). The ester was obtained by fluorination of ethyl alpha-cyano-p-tolylacetate with FClO3. The CFTA method has proven to be significantly superior for enantiomeric excess (e.e.) determinations when compared to the MTPA method, particularly in those compounds that have a remotely disposed chiral center. C1 Toyama Med & Pharmaceut Univ, Toyama 9300194, Japan. NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA. RP Takeuchi, Y (reprint author), Toyama Med & Pharmaceut Univ, Sugitani 2630, Toyama 9300194, Japan. EM takeuchi@ms.toyama-mpu.ac.jp NR 15 TC 19 Z9 19 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1024-2430 J9 ENANTIOMER JI Enantiomer PY 1999 VL 4 IS 3-4 BP 339 EP 344 PG 6 WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA 249FR UT WOS:000083322900018 PM 10550891 ER PT J AU Deak, T Nguyen, KT Ehrlich, AL Watkins, LR Spencer, RL Maier, SF Licinio, J Wong, ML Chrousos, GP Webster, E Gold, PW AF Deak, T Nguyen, KT Ehrlich, AL Watkins, LR Spencer, RL Maier, SF Licinio, J Wong, ML Chrousos, GP Webster, E Gold, PW TI The impact of the nonpeptide corticotropin-releasing hormone antagonist antalarmin on behavioral and endocrine responses to stress SO ENDOCRINOLOGY LA English DT Article ID FEAR-POTENTIATED STARTLE; RECEPTOR MESSENGER-RNA; CENTRAL-NERVOUS-SYSTEM; RAT-BRAIN; EXPLORATORY-BEHAVIOR; INESCAPABLE SHOCK; LOCUS COERULEUS; CENTRAL NUCLEUS; AMYGDALA; ACTIVATION AB The nonpeptide CRH antagonist antalarmin has been shown to block both behavioral and endocrine responses to CRH. However, it's potential activity in blunting behavioral and endocrine sequelae of stressor exposure has not been assessed. Because antagonism of central CRH by alpha-helical CRH attenuates conditioned fear responses, we sought to test antalarmin in this regard. In addition, it remains unclear as to whether this is a result of receptor blockade during conditioning or during testing. Thus, we explored whether CRH mediates the induction or expression of conditioned fear (freezing in a context previously associated with 2 footshocks; 1.0 mA, 5 sec each). Furthermore, because rats previously exposed to inescapable shock (IS; 100 shocks, 1.6 mA, 5 sec each), demonstrate enhanced fear conditioning, we investigated whether this effect would be blocked by antalarmin. Antalarmin (20 mg/kg.2 mi ip) impaired both the induction and expression of conditioned fear. In addition, antalarmin blocked the enhancement of fear conditioning produced by prior exposure to IS. Despite the marked behavioral effects observed in antalarmin-treated rats, antalarmin had no effect on IS-induced rises in ACTH or corticosterone. However, antalarmin did block the ACTH response produced by exposure to 2 footshocks. C1 Univ Colorado, Dept Psychol, Boulder, CO 80309 USA. NIMH, Clin Neuroendocrinol Branch, NIH, Bethesda, MD 20892 USA. NICHHD, Dev Neuroendocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Deak, T (reprint author), Univ Colorado, Dept Psychol, Campus Box 345, Boulder, CO 80309 USA. EM tdeak@clipr.colorado.edu RI Wong, Ma-Li/D-7903-2011; Licinio, Julio/L-4244-2013 OI Licinio, Julio/0000-0001-6905-5884 NR 58 TC 187 Z9 191 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1999 VL 140 IS 1 BP 79 EP 86 DI 10.1210/en.140.1.79 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 149VH UT WOS:000077626500012 PM 9886810 ER PT J AU Marmary, Y Parlow, AF Goldsmith, CM He, XJ Wellner, RB Satomura, K Kriete, MF Robey, PG Nieman, LK Bruce, BJ AF Marmary, Y Parlow, AF Goldsmith, CM He, XJ Wellner, RB Satomura, K Kriete, MF Robey, PG Nieman, LK Bruce, BJ TI Construction and in vivo efficacy of a replication-deficient recombinant adenovirus encoding murine growth hormone SO ENDOCRINOLOGY LA English DT Article ID MEDIATED GENE-TRANSFER; RAT SALIVARY-GLANDS; SNELL DWARF MICE; INTRAMUSCULAR INJECTION; EXPRESSION; THERAPY; TRANSGENE; VECTOR; ERYTHROPOIETIN; THYROXINE AB We have constructed a recombinant, replication-deficient, first-generation adenovirus-encoding mouse GH (mGH), AdCMVmGH. This virus directed mGH production from an epithelial cell line in vitro in a dose-dependent manner. When injected into the quadriceps muscle or submandibular ducts of mGH-deficient Snell dwarf mice, AdCMVmGH resulted in the production of significantly elevated serum mGH levels. Furthermore, after im injection, dwarf mice increased in weight by 8% over 4 days and close to 100% by 30 days. When AdCMVmGH was administered to 3- to 4-week-old rats by iv injection to assess general metabolic responses, serum mGH, insulinlike growth factor 1, triglycerides and cholesterol levels were significantly elevated. AdCMVmGH should be a valuable experimental tool for the controlled, directed expression of mGH in preclinical mouse model studies. C1 Natl Inst Dent & Craniofacial Res, Gene Therapy & Therapeut Branch, NIH, Bethesda, MD 20892 USA. Harbor UCLA Med Ctr, Natl Hormone & Pituitary Program, Torrance, CA 90509 USA. Natl Inst Dent & Craniofacial Res, Craniofacial & Skeletal Dis Branch, Bethesda, MD 20892 USA. Natl Inst Dent & Craniofacial Res, Anim Care Unit, Bethesda, MD 20892 USA. NICHHD, Dev Endocrinol Branch, Bethesda, MD 20892 USA. RP Bruce, BJ (reprint author), Natl Inst Dent & Craniofacial Res, Gene Therapy & Therapeut Branch, NIH, 10 Ctr Dr,MSC-1190,Bldg 10,Room 1N-113, Bethesda, MD 20892 USA. EM bruce_j_baum@nih.gov RI Robey, Pamela/H-1429-2011 OI Robey, Pamela/0000-0002-5316-5576 NR 28 TC 16 Z9 16 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1999 VL 140 IS 1 BP 260 EP 265 DI 10.1210/en.140.1.260 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 149VH UT WOS:000077626500035 PM 9886833 ER PT J AU Erexson, GL Watson, DE Tindall, KR AF Erexson, GL Watson, DE Tindall, KR TI Characterization of new transgenic Big Blue((R)) mouse and rat primary fibroblast cell strains for use in molecular toxicology studies SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE Big Blue((R)); transgenic lacl; cll; primary cell strains ID SISTER-CHROMATID EXCHANGE; LIVER EPITHELIAL-CELLS; IN-VIVO MUTATIONS; BLUE(R) RAT2; SHUTTLE VECTORS; RISK ASSESSMENT; GENETIC RISK; GERM-CELLS; LUNG-CELLS; MICE AB We have established and characterized primary mouse and rat cell strains for studies designed to complement in vivo gene mutation assays using the Big Blue(R) mouse or rat. Primary fibroblast cell strains, designated BBM1 and BBR1,were derived from a transgenic male Big Blue(R) B6C3F1 mouse and from a male Big Blue(R) fischer-344 rat, respectively. Both BBM1 and BBR1 are genetically stable and mostly diploid. Both cell strains have low spontaneous frequencies of mutation at the lad and cll loci as well as low Frequencies of sister chromatid exchange and micronuclei formation. In addition, N-ethyl-N-nitrosourea (ENU) induces mutations at the cll locus in both BBM1 and BBR1 cells. These new primary Big Blue(R) mouse (BBM1) and rat (BBR1) fibroblast cell strains represent useful new models For molecular toxicology studies. Published 1999 Wiley-Liss, Inc. C1 NIEHS, Mol Mutagenesis Grp, Lab Environm Carcinogenesis & Mutagenesis, Res Triangle Pk, NC 27709 USA. N Carolina State Univ, Coll Vet Med, Dept Anat Physiol Sci & Radiol, Comparat Biomed Sci Program, Raleigh, NC 27606 USA. RP Tindall, KR (reprint author), NIEHS, Mol Mutagenesis Grp, Lab Environm Carcinogenesis & Mutagenesis, POB 12233, Res Triangle Pk, NC 27709 USA. NR 63 TC 10 Z9 10 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1999 VL 34 IS 2-3 BP 90 EP 96 DI 10.1002/(SICI)1098-2280(1999)34:2/3<90::AID-EM6>3.0.CO;2-W PG 7 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 249UZ UT WOS:000083352800005 PM 10529731 ER PT J AU Johnson, FM AF Johnson, FM TI Carcinogenic chemical-response "fingerprint" for male F344 rats exposed to a series of 195 chemicals: Implications for predicting carcinogens with transgenic models SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material DE chemical carcinogens; rodent carcinogens; carcinogen testing; alternative models; transgenic models; National Toxicology Program ID NATIONAL-TOXICOLOGY-PROGRAM; MOUSE; PERSPECTIVE; BIOASSAYS; SYSTEM; CANCER; ASSAYS; MICE; GENE; NTP AB Transgenic model systems have recently been advocated as replacements For traditional methods of testing chemicals for carcinogenicity in rodents. To shed light on the diversity of responses induced by chemicals in natural whole animal systems, a type of "fingerprint" is devised and, in turn, applied to describe the results of testing approximately 200 chemicals in male F344 rats. Such focus helps develop an appreciation of the complexity involved in the chemical carcinogenic response. When we ask transgenic systems to serve as replacements for natural whole animals, for predicting the risk of chemically induced cancer, we are asking them somehow to reflect or express this complexity so that the effects of exposure in humans can be realistically appraised. For the fingerprint, a graphic data display is used to represent the different tissues and organs that show statistically significant, chemically related tumor increases. Chemicals vary extensively according to the particular sites and the array of sites that display a carcinogenic response; but any given site may also show a carcinogenic response to a variety of different chemicals. The data suggest that a large number of different genetic factors may underlie the determination of the chemical carcinogenic response. This apparent genotypic variability and complexity in phenotypic expression would seem to make it quite difficult, if not impossible, to decide on the specific performance requirements of transgenic systems for detecting carcinogens. Unless this and other obstacles can be overcome, the transgenic approach to identifying carcinogenic chemicals for regulatory purposes may best be abandoned. Published 1999 Wiley-Liss, Inc. C1 NIEHS, Environm Toxicol Program, Toxicol Operat Branch, Res Triangle Pk, NC 27709 USA. RP Johnson, FM (reprint author), NIEHS, Environm Toxicol Program, Toxicol Operat Branch, EC-14, Res Triangle Pk, NC 27709 USA. NR 34 TC 11 Z9 11 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1999 VL 34 IS 4 BP 234 EP 245 DI 10.1002/(SICI)1098-2280(1999)34:4<234::AID-EM3>3.3.CO;2-U PG 12 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 275EE UT WOS:000084805800003 PM 10618171 ER PT J AU Zhang, LP Rothman, N Wang, YX Hayes, RB Yin, SN Titenko-Holland, N Dosemeci, M Wang, YZ Kolachana, P Lu, W Xi, LQ Li, GL Smith, MT AF Zhang, LP Rothman, N Wang, YX Hayes, RB Yin, SN Titenko-Holland, N Dosemeci, M Wang, YZ Kolachana, P Lu, W Xi, LQ Li, GL Smith, MT TI Benzene increases aneuploidy in the lymphocytes of exposed workers: A comparison of data obtained by fluorescence in situ hybridization in interphase and metaphase cells SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE benzene; biomarkers; chromosomal aberrations; epidemiology ID LONG ARM DELETION; CHROMOSOMAL-ABERRATIONS; INSITU HYBRIDIZATION; DNA PROBES; CYTOGENETICS; MONOSOMY-7; DISORDERS; ANEUSOMY; AGENTS; CANCER AB Benzene is an established human leukemogen that increases the level of chromosome aberrations in lymphocytes of exposed workers. Numerical aberrations (aneusomy) can be observed by fluorescence in situ hybridization (FISH) in both interphase and metaphase cells. Whereas interphase FISH allows nondividing cells to be analyzed, one advantage of metaphase FISH is that it can also detect structural changes. The present study compares the abilities of metaphase and interphase FISH to detect aneusomy of chromosomes 7 and 8 in healthy benzene-exposed human subjects. Metaphase and interphase cells from the peripheral blood of 43 workers exposed to benzene (median = 31 ppm, 8-hr TWA) and 44 frequency-matched controls were analyzed by FISH. Normal diploid cells contained two hybridization signals, whereas those that were potentially monosomic contained one, trisomic 3 and tetrasomic 4. The frequency of cells with one hybridization signal For chromosome 7 in metaphase spreads rose from 2.72 +/- 0.19 (%, mean +/- SE) in controls to 3.79 +/- 0.63 workers exposed to 31 or Fewer ppm benzene and 5.9 +/- 0.85 in those exposed to more than 31 ppm (P-trend < 0.0001). No similar dose-dependent increase in the Frequency of cells with one hybridization signal was observed by interphase FISH, probably because of probe overlap artifact. Although significant dose-dependent increases in the frequency of cells with three hybridization signals for chromosome 7 were detected by both methods in the higher-exposed group, a larger, more significant difference was detected by metaphase FISH between controls and workers exposed to 31 or fewer ppm. Similar data were obtained For chromosome 8. Interphase and metaphase FISH were moderately correlated for three hybridization signals but not for one hybridization signal in chromosome 7 or 8. In general, metaphase FISH was more sensitive in detecting both monosomy and trisomy in the lymphocytes of exposed workers. (C) 1999 Wiley-Liss, Inc. C1 Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA. Natl Canc Inst, Div Canc Epidemiol & Genet, Bethesda, MD USA. Chinese Acad Prevent Med, Inst Occupat Med, Beijing 100050, Peoples R China. Shanghai Hyg & Aniti Epidem Ctr, Dept Occupat Hlth, Shanghai, Peoples R China. RP Smith, MT (reprint author), Univ Calif Berkeley, Sch Publ Hlth, 140 Warren Hall, Berkeley, CA 94720 USA. FU NIEHS NIH HHS [P30 ES01896, R01 ES06721, P42 ES04705] NR 30 TC 43 Z9 47 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1999 VL 34 IS 4 BP 260 EP 268 DI 10.1002/(SICI)1098-2280(1999)34:4<260::AID-EM6>3.0.CO;2-P PG 9 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 275EE UT WOS:000084805800006 PM 10618174 ER PT J AU Dunkel, VC San, RHC Seifried, HE Whittaker, P AF Dunkel, VC San, RHC Seifried, HE Whittaker, P TI Genotoxicity of iron compounds in Salmonella typhimurium and L5178Y mouse lymphoma cells SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE iron; mutagenicity; Salmonella; mouse lymphoma ID METAL-COMPOUNDS; MUTAGENICITY; TOXICOLOGY; TRANSPORT; RADICALS; SYSTEM; DAMAGE; CANCER; ASSAY; RISK AB The mutagenic activity of elemental and salt forms of iron (Fe), including compounds currently being used in dietary supplements and for food fortification, were evaluated for mutagenicity in Salmonella typhimurium and L5178Y mouse lymphoma cells. Except for the weak response obtained with ferrous fumarate, none of the compounds induced a mutagenic response in Salmonella. In the mouse lymphoma assay, responses were related to the Fe compound and/or reduction of ferric (Fe+3) to ferrous (Fe+2). Responses with the elemental forms of Fe were divergent. Electrolytic Fe with a relatively larger particle size and irregular shape was negative. The smaller-sized carbonyl Fe, which after 4 hr attached to and was taken up by the cells, induced mutagenic responses both with and without S9. With ferric chloride (FeCl3) and ferric phosphate (FePO4), there was an increase in mutant frequency only with S9. With the Fe+2 compounds, ferrous sulfate (FeSO4) and ferrous fumarate (FeC4H2O4), positive responses were observed without S9. The Fe chelate, sodium Fe(III)EDTA was positive in both the presence and absence of S9. The lowest effective doses (LED) for induction of mutagenicity were identified for these compounds and an LED ratio calculated. The LED ratio ranges from 1 for FeSO4 to 30 for carbonyl Fe, which are similar to oral ID50 values obtained in animal studies. (C) 1999 Wiley Liss, Inc. C1 US FDA, Ctr Food Safety & Appl Nutr, Washington, DC 20204 USA. Bio Reliance Corp Inc, Rockville, MD USA. NCI, NIH, Bethesda, MD 20892 USA. RP Dunkel, VC (reprint author), US FDA, Ctr Food Safety & Appl Nutr, 200 C St SW, Washington, DC 20204 USA. EM VCD@CFSAN.FDA.GOV FU NCI NIH HHS [N01-CB-40509] NR 35 TC 24 Z9 24 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1999 VL 33 IS 1 BP 28 EP 41 DI 10.1002/(SICI)1098-2280(1999)33:1<28::AID-EM4>3.0.CO;2-S PG 14 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 163YF UT WOS:000078433900004 PM 10037321 ER PT J AU Schildcrout, JS Margolin, BH Zeiger, E AF Schildcrout, JS Margolin, BH Zeiger, E TI Predicting rodent carcinogenicity using potency measures of the in vitro sister chromatid exchange and chromosome aberration assays SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE CHO cells; sister chromatid exchanges; chromosome aberrations; potency estimations; carcinogenicity prediction ID HAMSTER OVARY CELLS; INVITRO CYTOGENETIC ASSAYS; GENETIC TOXICITY ASSAYS; TOX PROGRAM; CHEMICALS; TESTS AB In vitro sister chromatid exchange (SCE) and chromosome aberration (ABS) tests have been extensively used to identify potential rodent carcinogens. A number of measures of potency were developed to describe in vitro SCE and ABS test results: the dose needed to induce a unit increase over the control; the lowest effective dose; the slope of the ordinary linear regression; the maximum observed slope; and the maximum fold increase over background. The ability of these potency measures to predict the qualitative and quantitative carcinogenicity of chemicals was compared to the predictivity of the qualitative in vitro responses. The results of the analyses showed that the quantitative measures of the SCE or ABS responses only minimally increased the predictivity of carcinogenesis when compared to the predictivity using the qualitative responses. (C) 1999 Wiley-Liss, Inc. C1 Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA. Natl Inst Environm Hlth Sci, Environm Toxicol Program, Res Triangle Pk, NC USA. RP Margolin, BH (reprint author), Univ N Carolina, Dept Biostat, CB 7400 McGavran Greenberg, Chapel Hill, NC 27599 USA. NR 16 TC 6 Z9 6 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1999 VL 33 IS 1 BP 59 EP 64 DI 10.1002/(SICI)1098-2280(1999)33:1<59::AID-EM7>3.0.CO;2-9 PG 6 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 163YF UT WOS:000078433900007 PM 10037324 ER PT J AU Witt, KL Tice, RR Shelby, MD Chhabra, RS Zeiger, E AF Witt, KL Tice, RR Shelby, MD Chhabra, RS Zeiger, E TI Induction of micronucleated erythrocytes in rodents by diisopropylcarbodiimide and dicyclohexylcarbodiimide: Dependence on exposure protocol SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE micronuclei; chromosome damage; skin painting; peripheral blood; bone marrow; genotoxicity; PCE; NCE; mice; rats ID MICE AB The induction of micronucleated erythrocytes by diisopropylcarbodiimide (DIC) and dicyclohexylcarbodiimide (DCC) was investigated as part of a U.S. National Toxicology Program (NTP) evalvation of the subchronic toxicity of these chemicals. Analysis of peripheral blood smears from male and Female B6C3F(1) mice exposed to 17.5-140.0 mg DIC/kg/day by skin painting for 13 weeks revealed dose-related increases in the frequency of micronucleated normochromatic erythrocytes (MN-NCE) in both sexes. Results of a similar 13-week peripheral blood micronucleus (MN) test with DCC (1.5-12.0 mg/kg/day) were also positive, although the increases in MN-NCE were not as great as those observed with DIG. In contrast to the positive results of the subchronic skin-pointing studies in mice, acute bone marrow MN studies with DIC and DCC in male F344 rats, using intraperitoneal (i.p.) injection, yielded negative results. Both the acute and the subchronic exposures included doses that produced clinical signs of toxicity. Acute mouse bone marrow MN tests with DIC administered in single or triple i.p. injection protocols were subsequently conducted to determine if the differing responses between mice and rats were due to species or protocol differences. The results of these acute tests were negative or equivocal. Because the subchronic studies produced positive results, it was hypothesized that these carbodiimides required multiple treatments over an extended period of time to produce an increase in MN-erythrocytes. To confirm the original response, a second dermal subchronic study was conducted with DIG; the protocol was modified to include sequential blood samplings to permit monitoring MN Frequencies over time. The data demonstrated a small but consistent induction of micronucleated erythrocytes in mice treated with DIC by skin painting. (C) 1999 Wiley-Liss, Inc. C1 Integrated Syst Lab, Res Triangle Pk, NC 27709 USA. NIEHS, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA. RP Witt, KL (reprint author), Integrated Syst Lab, POB 13501, Res Triangle Pk, NC 27709 USA. NR 13 TC 7 Z9 8 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1999 VL 33 IS 1 BP 65 EP 74 DI 10.1002/(SICI)1098-2280(1999)33:1<65::AID-EM8>3.0.CO;2-7 PG 10 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 163YF UT WOS:000078433900008 PM 10037325 ER PT J AU Taningher, M Malacarne, D Perrotta, A Parodi, S AF Taningher, M Malacarne, D Perrotta, A Parodi, S TI Computer-aided analysis of mutagenicity and cell transformation data for assessing their relationship with carcinogenicity SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE short-term tests; SAR analysis; molecular connectivity; carcinogenicity predictions ID BALB/C 3T3 CELLS; NATIONAL-TOXICOLOGY-PROGRAM; GENE-TOX PROGRAM; IN-VITRO; CHEMICAL-STRUCTURE; GRAPH-THEORY; NONGENOTOXIC CARCINOGENS; RODENT CARCINOGENS; 42 CHEMICALS; SALMONELLA AB Using a computer-aided approach, the tests for Salmonella mutagenicity and transformation in established cell lines were compared for the qualitative bases of their carcinogenicity predictions. For this purpose, a database of 145 chemicals was prepared in which rodent carcinogenicity data and results of the Ames' and transformation tests were available. Using a software program for connectivity analysis (previously developed and validated by vs), we assayed the molecular structures of these chemicals for the presence of fragments relatable to their positive (i.e., biophores) or negative (i.e., biophobes) response to the tests in question. These Fragments were then studied For their association with genotoxic and nongenotoxic carcinogenicity. The philosophy adopted was that the type and number of molecular fragments chosen by the software to describe the chemicals correctly predicted by the tests could be related to the type carcinogenic effects to which the tests themselves were sensitive. The classifications made by the software were interpreted by human expertise and the biophores found were compared with the acknowledged structural alerts to DNA reactivity as formalized by Ashby and co-workers [(1991). Mutat Res 257:229-306; (1993). Mutat Res 286. 3-74]. The results show that, in quantitative terms, the overall ability to predict carcinogenicity is about the same for both the Salmonella and transformation tests. However, in qualitative terms the transformation test appears to be sensitive to effects that are more heterogeneous than those inducing mutation, some of which are presumably related to nongenotoxic carcinogenic activities. This study illustrates a possible, innovative model of analysis of chemical structures that, using an automated approach along with the biologist's judgment, could contribute to the detection of complementarities among short-term test endpoints. (C) 1999 Wiley-Liss, Inc. C1 Natl Canc Inst, I-16132 Genoa, Italy. Univ Genoa, Dept Clin & Expt Oncol, Genoa, Italy. RP Parodi, S (reprint author), Natl Canc Inst, Largo R Benzi 10, I-16132 Genoa, Italy. NR 53 TC 4 Z9 4 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 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1999 VL 33 IS 3 BP 226 EP 239 DI 10.1002/(SICI)1098-2280(1999)33:3<226::AID-EM7>3.0.CO;2-U PG 14 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 192YY UT WOS:000080108400007 PM 10334625 ER PT J AU Bolognesi, C Landini, E Roggieri, P Fabbri, R Viarengo, A AF Bolognesi, C Landini, E Roggieri, P Fabbri, R Viarengo, A TI Genotoxicity biomarkers in the assessment of heavy metal effects in mussels: Experimental studies SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE heavy metals; genotoxicity; alkaline elution; micronucleus test; biomarkers; mussel ID AQUATIC ORGANISMS; MERCURY-COMPOUNDS; MAMMALIAN-CELLS; CADMIUM; DNA; MICRONUCLEI; INDICATORS; RESPONSES; POLLUTION; MOLLUSKS AB Heavy metals are stable and persistent environmental contaminants. The range of metal concentrations is generally below acute thresholds in coastal areas, where recognition of chronic sublethal effects is more relevant. Evidence of long-term adverse effects, such as cancer, due to heavy metals in marine animals comes from a number of field and experimental studies. The mechanism of metal carcinogenicity remains largely unknown, although several lines of experimental evidence suggest that a genotoxic effect may be involved. The aim of our study was to evaluate the sensitivity of genotoxicity tests, alkaline elution and micronucleus test, as biomarkers for the detection of heavy metals in mussels as the sentinel species. Experimental studies were carried out on Mytilus galloprovincialis exposed in aquarium (5 days) to different concentrations of three selected metal salts, CuCl2 (5, 10, 20, 40, 80 mu g/l/a), CdCl2 (1.84, 18.4, 184 mu g/l/a), and HgCl2 (32 mu g/l/a), and to a mixture of equimolar doses of the three metals to study the results of their ioini action. Metallothionein quantitation was used as a marker of metal exposure. Lysosomal membrane stability was applied to evaluate the influence of physiological status on genotoxic damage. The ranking of genotoxic potential was in decreasing order: Hg > Cu > Cd. Cu and Hg caused an increase of DNA single-strand breaks and micronuclei frequency. Cd induced a statistical increase of DNA damage, but gave negative results with the micronucleus test. A relationship between genotoxic effects and metallothionein content was observed. Reduction in lysosomal membrane stability with the increasing concentration of heavy metals was also evident. Environ. Mol. Mutagen. 33:287-292, 1999 (C) 1999 Wiley-Liss, Inc. C1 Natl Canc Inst, Toxicol Evaluat Unit, I-16132 Genoa, Italy. Univ Genoa, Inst Gen Physiol, Genoa, Italy. Univ Piemonte Orientale, Dept Sci & Adv Technol, Alessandria, Italy. RP Bolognesi, C (reprint author), Natl Canc Inst, Toxicol Evaluat Unit, Largo Rosanna Benzi 10, I-16132 Genoa, Italy. OI Viarengo, Aldo/0000-0002-1557-6526 NR 39 TC 110 Z9 115 U1 1 U2 26 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 1999 VL 33 IS 4 BP 287 EP 292 DI 10.1002/(SICI)1098-2280(1999)33:4<287::AID-EM5>3.0.CO;2-G PG 6 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 212ZU UT WOS:000081248200005 PM 10398376 ER PT S AU Sato, S Kawamura, M Eisenhofer, G Kopin, IJ Fujisawa, S Kador, PF AF Sato, S Kawamura, M Eisenhofer, G Kopin, IJ Fujisawa, S Kador, PF BE Weiner, H Maser, E Crabb, DW Lindahl, R TI Aldo-keto reductases in norepinephrine metabolism SO ENZYMOLOGY AND MOLECULAR BIOLOGY OF CARBONYL METABOLISM 7 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 9th International Symposium on Enzymology and Molecular Biology of Carbonyl Metabolism CY JUN 20-24, 1998 CL VARALLO SESIA, ITALY ID INHIBITION C1 NEI, Lab Ocular Therapeut, NIH, Bethesda, MD 20892 USA. NINDS, Clin Neurosci Branch, NIH, Bethesda, MD 20892 USA. Nippon Zoki Pharmaceut Co Ltd, Inst Bioact Sci, Hyogo 67314, Japan. RP Sato, S (reprint author), NEI, Lab Ocular Therapeut, NIH, Bethesda, MD 20892 USA. NR 10 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC / PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46113-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1999 VL 463 BP 459 EP 463 PG 5 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA BN44B UT WOS:000081933300057 PM 10352719 ER PT S AU Lee, YS Sugiyama, K Kador, PF AF Lee, YS Sugiyama, K Kador, PF BE Weiner, H Maser, E Crabb, DW Lindahl, R TI Rotamers of tolrestat and their binding mode to aldose reductase SO ENZYMOLOGY AND MOLECULAR BIOLOGY OF CARBONYL METABOLISM 7 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 9th International Symposium on Enzymology and Molecular Biology of Carbonyl Metabolism CY JUN 20-24, 1998 CL VARALLO SESIA, ITALY ID INHIBITOR C1 NEI, NIH, Bethesda, MD 20892 USA. RP Lee, YS (reprint author), NEI, NIH, Bldg 10,Room 10B11,10 Ctr Dr MSC 1850, Bethesda, MD 20892 USA. NR 15 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC / PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46113-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1999 VL 463 BP 465 EP 472 PG 8 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA BN44B UT WOS:000081933300058 PM 10352720 ER PT S AU Mizoguchi, T Maeda, I Yagi, K Kador, PF AF Mizoguchi, T Maeda, I Yagi, K Kador, PF BE Weiner, H Maser, E Crabb, DW Lindahl, R TI Formation of lens aldose reductase mixed disulfides with GSH by UV irradiation and its proteolysis by lens calpain SO ENZYMOLOGY AND MOLECULAR BIOLOGY OF CARBONYL METABOLISM 7 SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT 9th International Symposium on Enzymology and Molecular Biology of Carbonyl Metabolism CY JUN 20-24, 1998 CL VARALLO SESIA, ITALY ID BOVINE LENS; THIOLTRANSFERASE; CATARACT; CELLS; RADIATION C1 Osaka Univ, Grad Sch Pharmaceut Sci, Suita, Osaka 5650871, Japan. NEI, NIH, Bethesda, MD 20892 USA. RP Mizoguchi, T (reprint author), Osaka Univ, Grad Sch Pharmaceut Sci, Suita, Osaka 5650871, Japan. NR 18 TC 2 Z9 2 U1 0 U2 1 PU KLUWER ACADEMIC / PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0065-2598 BN 0-306-46113-7 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 1999 VL 463 BP 481 EP 486 PG 6 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA BN44B UT WOS:000081933300060 PM 10352722 ER PT J AU Rabinovich, NR Orenstein, WA AF Rabinovich, NR Orenstein, WA TI Vaccines - Overview SO EPIDEMIOLOGIC REVIEWS LA English DT Editorial Material ID GUILLAIN-BARRE-SYNDROME; COST-EFFECTIVENESS; UNITED-STATES; ADULT IMMUNIZATION; VACCINATION; INFLUENZA; EFFICACY; CHILDREN; POLIOMYELITIS; STRATEGIES C1 NIAID, Clin & Regulatory Affairs Branch, Div Microbiol & Infect Dis, Rockville, MD 20852 USA. Ctr Dis Control & Prevent, Natl Immunizat Program, Atlanta, GA USA. RP Rabinovich, NR (reprint author), NIAID, Clin & Regulatory Affairs Branch, Div Microbiol & Infect Dis, 6019 Neilwood Dr, Rockville, MD 20852 USA. NR 48 TC 4 Z9 4 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 USA SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1999 VL 21 IS 1 BP 1 EP 6 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 235QX UT WOS:000082555000001 PM 10520469 ER PT J AU Clemens, J Keckich, N Naficy, A Glass, R Rao, M AF Clemens, J Keckich, N Naficy, A Glass, R Rao, M TI Public health considerations for the introduction of new rotavirus vaccines for infants: A case study of tetravalent rhesus rotavirus-based reassortant vaccine SO EPIDEMIOLOGIC REVIEWS LA English DT Review ID COST-EFFECTIVENESS ANALYSIS; PLACEBO-CONTROLLED TRIAL; YOUNG-CHILDREN; PROTECTIVE EFFICACY; UNITED-STATES; DEVELOPING-COUNTRIES; DIARRHEAL DISEASE; VIRAL GASTROENTERITIS; BANGLADESHI CHILDREN; IMMUNIZATION PROGRAM C1 Int Vaccine Inst, Seoul 151600, South Korea. NICHHD, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA. NICHHD, World Hlth Org, Collaborating Ctr Clin Evaluat Vaccines Dev Count, Bethesda, MD 20892 USA. Ctr Dis Control & Prevent, Atlanta, GA USA. RP Clemens, J (reprint author), Int Vaccine Inst, POB 14, Seoul 151600, South Korea. NR 116 TC 12 Z9 12 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 USA SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1999 VL 21 IS 1 BP 24 EP 42 PG 19 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 235QX UT WOS:000082555000003 PM 10520471 ER PT J AU Sorkin, JD Muller, DC Andres, R AF Sorkin, JD Muller, DC Andres, R TI Longitudinal change in the heights of men and women: Consequential effects on body mass index SO EPIDEMIOLOGIC REVIEWS LA English DT Article ID POPULATION; STATURE; AGE; TREND C1 NIA, Metab Sect, Intramural Res Program, Gerontol Res Ctr, Baltimore, MD 21224 USA. Univ Maryland, Sch Med, Vet Affairs Med Ctr, Div Gerontol, Baltimore, MD 21201 USA. RP Sorkin, JD (reprint author), NIA, Metab Sect, Intramural Res Program, Gerontol Res Ctr, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 29 TC 73 Z9 73 U1 1 U2 2 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 USA SN 0193-936X J9 EPIDEMIOL REV JI Epidemiol. Rev. PY 1999 VL 21 IS 2 BP 247 EP 260 PG 14 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 283LA UT WOS:000085276000008 PM 10682261 ER PT J AU Potischman, N Gail, MH Troisi, R Wacholder, S Hoover, RN AF Potischman, N Gail, MH Troisi, R Wacholder, S Hoover, RN TI Measurement error does not explain the persistence of a body mass index association with endometrial cancer after adjustment for endogenous hormones SO EPIDEMIOLOGY LA English DT Article DE regression calibration; errors in variables; measurement error correction; hormones; endometrial cancer ID POST-MENOPAUSAL WOMEN; POSTMENOPAUSAL WOMEN; RISK; ESTROGENS; OBESITY AB Identified risk factors for endometrial cancer are accepted as operating through estrogen exposure. In a recent analysis, the effect of risk factors such as body mass index (BMI) was not explained by circulating estrogen concentrations. In the present analysis, we correct for measurement error associated with obtaining only one blood sample per subject. Applying regression calibration ideas, we found that error correction of log estrone had little impact on estimates of the BMI effect, suggesting that hormone measurement error does not account for the residual importance of BMI. The biologic mechanism for the increased risk associated with BMI remains to be explained. C1 NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Potischman, N (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Execut Plaza N,Suite 430, Bethesda, MD 20892 USA. NR 17 TC 8 Z9 8 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD JAN PY 1999 VL 10 IS 1 BP 76 EP 79 DI 10.1097/00001648-199901000-00014 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 151HR UT WOS:000077715100014 PM 9888284 ER PT J AU McBain, CJ Suares, G Fleck, MW Phillips-Tansey, E Hirotsune, S Gambello, M Wynshaw-Boris, A AF McBain, CJ Suares, G Fleck, MW Phillips-Tansey, E Hirotsune, S Gambello, M Wynshaw-Boris, A TI Dendritic atrophy and a reduced electrographic seizure threshold following abnormal neuronal migration in a mouse model of lissencephaly. SO EPILEPSIA LA English DT Meeting Abstract C1 NICHD, NIH, Bethesda, MD USA. NHGRI, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 7 BP 8 EP 8 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 242NR UT WOS:000082947600031 ER PT J AU Theodore, WH AF Theodore, WH TI Measurements of CNS GABA using MRS. SO EPILEPSIA LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 2 BP 79 EP 79 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 225BU UT WOS:000081936800316 ER PT J AU Wise, MS Mizrahi, EM Hrachovy, RA Clancy, RR Dunn, JK Lane, J McGaurn, SA Hirtz, DG AF Wise, MS Mizrahi, EM Hrachovy, RA Clancy, RR Dunn, JK Lane, J McGaurn, SA Hirtz, DG TI Seizures in very low birthweight (VLBW) infants: Seizure characterization using bedside EEG/video/polygraphic monitoring SO EPILEPSIA LA English DT Meeting Abstract C1 Baylor Coll Med, Houston, TX 77030 USA. Univ Penn, Philadelphia, PA 19104 USA. Univ Alabama, Birmingham, AL USA. NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 7 BP 161 EP 161 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 242NR UT WOS:000082947600647 ER PT J AU Vega-Bermundez, F Graham, B Theodore, W Sato, S AF Vega-Bermundez, F Graham, B Theodore, W Sato, S TI Sawtooth waves and REM sleep in patients with epilepsy SO EPILEPSIA LA English DT Meeting Abstract C1 NINDS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 7 BP 176 EP 177 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 242NR UT WOS:000082947600709 ER PT J AU Theodore, WH Gaillard, WD DeCarli, C Bhatia, S Hatta, J AF Theodore, WH Gaillard, WD DeCarli, C Bhatia, S Hatta, J TI Hippocampal volume and glucose metabolism in temporal lobe epileptic foci. SO EPILEPSIA LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. RI DeCarli, Charles/B-5541-2009 NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 7 BP 184 EP 184 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 242NR UT WOS:000082947600740 ER PT J AU Spanaki, MV Kopylev, L Liow, K Gaillard, WD Theodore, WH AF Spanaki, MV Kopylev, L Liow, K Gaillard, WD Theodore, WH TI Relationship of seizure frequency to hippocampus volume in temporal lobe epilepsy SO EPILEPSIA LA English DT Meeting Abstract C1 NINDS, NIH, CES, ERB, Bethesda, MD 20892 USA. NINDS, NIH, Biometry & Field Studies Branch, Bethesda, MD USA. Childrens Natl Med Ctr, Washington, DC 20010 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 7 BP 194 EP 194 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 242NR UT WOS:000082947600779 ER PT J AU Spanaki, MV Liow, K Siegel, H Fazilat, S Dean, A Hunter, K Gaillard, WD Menachem, EB Theodore, WH AF Spanaki, MV Liow, K Siegel, H Fazilat, S Dean, A Hunter, K Gaillard, WD Menachem, EB Theodore, WH TI The relation between CSF GABA, cerebral blood flow and metabolism. SO EPILEPSIA LA English DT Meeting Abstract C1 NINDS, Clin Epilepsy Sect, Bethesda, MD 20892 USA. Univ Gothenburg, Gothenburg, Sweden. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 2 BP 209 EP 210 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 225BU UT WOS:000081936800866 ER PT J AU Gaillard, WD Conry, JA Weinstein, S Pearl, PL Fazilat, S Kolodgie, MJ Dubovsky, EC Vezina, LG Theodore, WH AF Gaillard, WD Conry, JA Weinstein, S Pearl, PL Fazilat, S Kolodgie, MJ Dubovsky, EC Vezina, LG Theodore, WH TI Metabolic abnormalities in children with recent onset partial epilepsy determined by FDG-PET. SO EPILEPSIA LA English DT Meeting Abstract C1 Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA. Childrens Natl Med Ctr, Dept Neuroradiol, Washington, DC 20010 USA. NINDS, Epilepsy Res Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 2 BP 220 EP 221 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 225BU UT WOS:000081936800914 ER PT J AU Liow, K Liow, M Spanaki, MV Biesecker, LG Sato, S AF Liow, K Liow, M Spanaki, MV Biesecker, LG Sato, S TI Polysyndactyly and bifid epiglottis in gelastic seizures with hypothalamic hamartoma SO EPILEPSIA LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 7 BP 234 EP 234 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 242NR UT WOS:000082947600941 ER PT J AU Liow, K Spanaki, M Vega, F Durrani, S Peters, K Sato, S Biesecker, LG Theodore, W AF Liow, K Spanaki, M Vega, F Durrani, S Peters, K Sato, S Biesecker, LG Theodore, W TI Gelastic seizure as a manifestation of an autosomal-dominant genetic syndrome. SO EPILEPSIA LA English DT Meeting Abstract C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 2 BP 240 EP 240 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 225BU UT WOS:000081936800999 ER PT J AU Zhu, WJ Rogawski, MA AF Zhu, WJ Rogawski, MA TI Zonisamide depresses excitatory synaptic transmission by a presynaptic action SO EPILEPSIA LA English DT Meeting Abstract C1 NINDS, NIH, Bethesda, MD 20892 USA. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 0 TC 13 Z9 13 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 1999 VL 40 SU 7 BP 245 EP 245 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 242NR UT WOS:000082947600983 ER PT J AU Locatis, C Al-Nuaim, H AF Locatis, C Al-Nuaim, H TI Interactive technology and authoring tools: A historical review and analysis SO ETR&D-EDUCATIONAL TECHNOLOGY RESEARCH AND DEVELOPMENT LA English DT Article ID SYSTEMS; PERFORMANCE AB Computer systems, interactive technologies, and the software tools for authoring multimedia programs have evolved over the past several decades. The evolution of multimedia technology is discussed and current alternatives for authoring multimedia programs are described. Issues related to analyzing authoring tool requirements and selecting software are presented and trends in the evolution of authoring tools are identified. Many factors affecting the selection and use of authoring software are exogenous to the technology itself. Both technological trends and market forces must be considered. C1 Natl Lib Med, Bethesda, MD 20209 USA. George Washington Univ, Washington, DC 20052 USA. RP Locatis, C (reprint author), Natl Lib Med, Bethesda, MD 20209 USA. NR 42 TC 2 Z9 2 U1 0 U2 0 PU ASSOC EDUC COMMUNICATIONS & TECHNOLOGY PI WASHINGTON PA 1025 VERMONT AVE NW, SUITE 820, WASHINGTON, DC 20005 USA SN 1042-1629 J9 ETR&D-EDUC TECH RES JI ETR&D-Educ. Tech. Res. Dev. PY 1999 VL 47 IS 3 BP 63 EP 75 DI 10.1007/BF02299634 PG 13 WC Education & Educational Research SC Education & Educational Research GA 248CE UT WOS:000083257100005 ER PT J AU Rapoport, SI AF Rapoport, SI TI In vivo PET imaging and postmortem studies suggest potentially reversible and irreversible stages of brain metabolic failure in Alzheimer's disease SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE LA English DT Article DE Alzheimer's disease; positron emission tomography; brain; energy; metabolism; oxidative phosphorylation; mitochondria; cytochrome oxidase; activation; glucose; blood flow ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL GLUCOSE-METABOLISM; OXIDASE COX ACTIVITY; CYTOCHROME-OXIDASE; OXIDATIVE-PHOSPHORYLATION; MESSENGER-RNA; NEURONAL-ACTIVITY; GENE-EXPRESSION; NEUROFIBRILLARY TANGLES; QUANTITATIVE ASSESSMENT AB In vivo brain imaging of patients with Alzheimer's disease (AD) using positron emission tomography (PET) demonstrates progressive reductions in resting-state brain glucose metabolism and blood now (markers of synaptic activity) in relation to dementia severity, more so in association than primary cortical regions. During cognitive or psychophysical stimulation, however, blood flow and metabolism in the affected brain regions can increase to the same extent in mildly demented AD patients as in age-matched controls, despite reduced resting state values. The extent of activation declines with dementia severity and is markedly reduced in severely demented patients. Thus, there appears to be an initial functionally-responsive stage in AD, which direct brain analysis suggests is accompanied by reversible down-regulation because of reduced synaptic energy demand of enzymes mediating mitochondrial oxidative-phosphorylation. A later irreversible stage of AD is accompanied by marked synaptic loss, accumulation of intracellular neurofibrillary tangles, reduced general transcriptional capacity, and death of neurons. C1 NIA, Neurosci Lab, NIH, Bethesda, MD 20892 USA. RP Rapoport, SI (reprint author), NIA, Neurosci Lab, NIH, Bldg 10,Rm 6C103, Bethesda, MD 20892 USA. EM sir@helix.nih.gov NR 70 TC 51 Z9 51 U1 4 U2 4 PU SPRINGER HEIDELBERG PI HEIDELBERG PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY SN 0940-1334 J9 EUR ARCH PSY CLIN N JI Eur. Arch. Psych. Clin. Neurosci. PY 1999 VL 249 SU 3 BP 46 EP 55 PG 10 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 273KU UT WOS:000084707500009 PM 10654100 ER PT J AU Jin, AJ Huster, D Gawrisch, K Nossal, R AF Jin, AJ Huster, D Gawrisch, K Nossal, R TI Light scattering characterization of extruded lipid vesicles SO EUROPEAN BIOPHYSICS JOURNAL WITH BIOPHYSICS LETTERS LA English DT Article DE membrane; liposome; morphology; elongation; osmotic effect ID LARGE UNILAMELLAR VESICLES; RAPID EXTRUSION PROCEDURE; SIZE DISTRIBUTION; MECHANICAL-PROPERTIES; LIPOSOMES; STABILITY; MEMBRANES; DELIVERY; CURVATURE; SYSTEM AB By modeling extruded unilamellar lipid vesicles as thin-walled ellipsoidal shells, mathematical analysis provides simple equations which relate the mean elongation and other morphological characteristics of a vesicle population to quantities readily obtained from combined static and dynamic light scattering measurements. For SOPC vesicles extruded through a 100 nm pore-size filter into a 72.9 mM NaCl solution, the inferred elongation ratio (vesicle long axis to short axis) is approximately 3.7+/-0.6. When these vesicles were dialyzed into hypertonic or hypotonic solutions, this elongation ratio varied from 1 (for spherical liposomes) in strongly hypotonic solutions to greater than 6 in increasingly hypertonic solutions, beyond which abrupt morphological transformations appear. These results are quantitatively consistent with a mechanism of vesicle formation by extrusion and with the expectation that vesicle volumes change to equalize internal and external osmolarity via water flow, subject to the constraint of constant bilayer area. Our analysis also provides simplified equations to assess the effects of vesicle elongation and polydispersity on liposome parameters that are commonly required to characterize vesicle preparations for diverse applications. The implications of this study for routine light scattering characterization of extruded vesicles are discussed. C1 NIAMS, Phys Biol Lab, NIH, Bethesda, MD 20892 USA. NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. Univ Leipzig, Inst Med Phys & Biophys, D-04103 Leipzig, Germany. NICHD, Lab Integrat & Med Biophys, NIH, Bethesda, MD 20892 USA. RP Jin, AJ (reprint author), NIAMS, Phys Biol Lab, NIH, Bldg 6 Rm 408, Bethesda, MD 20892 USA. EM ajjin@helix.nih.gov OI Jin, Albert/0000-0003-3826-1081 NR 50 TC 43 Z9 44 U1 2 U2 20 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0175-7571 J9 EUR BIOPHYS J BIOPHY JI Eur. Biophys. J. Biophys. Lett. PY 1999 VL 28 IS 3 BP 187 EP 199 DI 10.1007/s002490050199 PG 13 WC Biophysics SC Biophysics GA 178PK UT WOS:000079274900002 PM 10192934 ER PT J AU Schonherr, E O'Connell, BC Schittny, J Robenek, H Fastermann, D Fisher, LW Plenz, G Vischer, P Young, MF Kresse, H AF Schonherr, E O'Connell, BC Schittny, J Robenek, H Fastermann, D Fisher, LW Plenz, G Vischer, P Young, MF Kresse, H TI Paracrine or virus-mediated induction of decorin expression by endothelial cells contributes to tube formation and prevention of apoptosis in collagen lattices SO EUROPEAN JOURNAL OF CELL BIOLOGY LA English DT Article DE adenovirus; angiogenesis; EAhy 926; extracellular matrix; sprouting ID DERMATAN SULFATE PROTEOGLYCAN; GROWTH-FACTOR-BETA; TRANSFORMING GROWTH-FACTOR-BETA-1; DIFFERENTIAL EXPRESSION; ANGIOGENESIS INVITRO; BASEMENT-MEMBRANE; GENE-EXPRESSION; GEL CONTRACTION; CANCER CELLS; FIBRONECTIN AB Resting endothelial cells express the small proteoglycan biglycan, whereas sprouting endothelial cells also synthesize decorin, a related proteoglycan, Here we show that decorin is expressed in endothelial cells in human granulomatous tissue. For in vitro investigations, the human endothelium-derived cell line, EA.hy 926, was cultured for 6 or more days in the presence of 1% fetal calf serum on top of or within floating collagen lattices which were also populated by a small number of rat fibroblasts. Endothelial cells aligned in cord-like structures and developed cavities that were surrounded by human decorin, About 14% and 20 % of endothelial cells became apoptotic after 6 and 12 days of co-culture, respectively. In the absence of fibroblasts, however, the extent of apoptosis was about 60 % after 12 days, and cord-like structures were not formed nor could decorin production be induced. This was also the case when lattices populated by EA.hy 926 cells were maintained under one of the Following conditions: 1) 10 % fetal calf serum; 2) fibroblast-conditioned media; 3) exogenous decorin; or 4) treatment with individual growth factors known to be involved in angiogenesis. The mechanism(s) by which fibroblasts induce an angiogenic phenotype in EA.hy 926 cells is (are) not known, but a causal relationship between decorin expression and endothelial cell phenotype was suggested by transducing human decorin cDNA into EA.hy 926 cells using a replication-deficient adenovirus. When the transduced cells were cultured in collagen lattices, there was no requirement of fibroblasts for the formation of capillary-like structures and apoptosis was reduced. Thus. decorin expression seems to be of special importance for the survival of EA.hy 926 cells as well as for cord and tube formation in this angiogenesis model. C1 Univ Munster, Dept Physiol Chem & Pathobiochem, D-48149 Munster, Germany. NIDR, NIH, Bethesda, MD 20892 USA. Univ Bern, Dept Anat, CH-3000 Bern, Switzerland. Univ Munster, Dept Atheriosclerosis Res, D-4400 Munster, Germany. RP Schonherr, E (reprint author), Univ Munster, Dept Physiol Chem & Pathobiochem, Waldeyerstr 15, D-48149 Munster, Germany. EM schonhe@uni-muenster.de OI O'Connell, Brian/0000-0003-4529-7664 NR 49 TC 66 Z9 66 U1 0 U2 1 PU URBAN & FISCHER VERLAG PI JENA PA BRANCH OFFICE JENA, P O BOX NO.100 537, D-07705 JENA, GERMANY SN 0171-9335 J9 EUR J CELL BIOL JI Eur. J. Cell Biol. PD JAN PY 1999 VL 78 IS 1 BP 44 EP 55 PG 12 WC Cell Biology SC Cell Biology GA 169XZ UT WOS:000078776100005 PM 10082423 ER PT J AU Lopes, MF Nunes, MP Henriques-Pons, A Giese, N Morse, HC Davidson, WF Araujo-Jorge, TC DosReis, GA AF Lopes, MF Nunes, MP Henriques-Pons, A Giese, N Morse, HC Davidson, WF Araujo-Jorge, TC DosReis, GA TI Increased susceptibility of Fas ligand-deficient gld mice to Trypanosoma cruzi infection due to a Th2-biased host immune response SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE CD4(+) T cell; apoptosis; Trypanosoma cruzi; Fas ligand; Chagas' disease ID INDUCED CELL-DEATH; EXPERIMENTAL CHAGAS-DISEASE; MEDIATED CYTOTOXICITY; T-LYMPHOCYTES; ACTIVATION; APOPTOSIS; INVOLVEMENT; INTERFERON; EXPRESSION; ANTIGEN AB Infection of BALB/c mice with Trypanosoma cruzi resulted in up-regulated expression of Fas and Fas ligand (FasL) mRNA by splenic CD4(+) T cells, activation-induced CD4(+) T cell death (AICD), and in Fas:FasL-mediated cytotoxicity. When CD4(+) T cells from infected mice were co-cultured with T. cruzi-infected macrophages, onset of AICD exacerbated parasite replication. CD4(+) T cells from T. cruzi-infected FasL-deficient BALB gld/gld mice had no detectable AICD in vitro and their activation with anti-TCR did not exacerbate T. cruzi replication in macrophages. However, infection of BALE gld/gld mice with T. cruzi resulted in higher and more prolonged parasitemia, compared to wild-type mice. Secretion of Th2 cytokines IL-10 and IL-4 by CD4(+) T cells from infected gld mice was markedly increased, compared to controls. In addition, in vivo injection of anti-IL-4 mAb, but not of an isotype control mAb, reduced parasitemia in both gld and wild-type mice. These results indicate that, besides controlling CD4(+) T cell AICD and parasite replication in vitro, an intact Fas:FasL pathway also controls the host cytokine response to T. cruzi infection in vivo, being required to prevent an exacerbated Th2-type immune response to the parasite. C1 Fed Univ Rio De Janeiro, Inst Biofis Carlos Chagas Filho, Programa Imunobiol, Ctr Ciencias Saude, BR-21944970 Rio De Janeiro, Brazil. FIOCRUZ, Inst Oswaldo Cruz, BR-21045900 Rio De Janeiro, Brazil. NIAID, Immunopathol Lab, NIH, Bethesda, MD 20892 USA. NCI, Genet Lab, NIH, Bethesda, MD 20892 USA. RP Lopes, MF (reprint author), Fed Univ Rio De Janeiro, Inst Biofis Carlos Chagas Filho, Programa Imunobiol, Ctr Ciencias Saude, Bloco,G,Ilha Fundao, BR-21944970 Rio De Janeiro, Brazil. RI lopes, marcela/E-2201-2012; Henriques-Pons, Andrea/J-4030-2014; OI lopes, marcela/0000-0002-4508-0505; Morse, Herbert/0000-0002-9331-3705 FU NIAID NIH HHS [N0I-AI-45203] NR 40 TC 48 Z9 48 U1 0 U2 0 PU WILEY-V C H VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 1999 VL 29 IS 1 BP 81 EP 89 DI 10.1002/(SICI)1521-4141(199901)29:01<81::AID-IMMU81>3.3.CO;2-P PG 9 WC Immunology SC Immunology GA 160DM UT WOS:000078215200010 PM 9933089 ER PT J AU Trobst, KK AF Trobst, KK TI Social support as an interpersonal construct SO EUROPEAN JOURNAL OF PSYCHOLOGICAL ASSESSMENT LA English DT Article DE social support; interpersonal theory; interpersonal circumplex model; resource exchange; agency and communion ID BIG 5; BEHAVIOR; CIRCUMPLEX; TAXONOMY; HELPFUL; EMOTION; SCALE AB The present article relied upon interpersonal theory (Sullivan, 1953), the interpersonal circumplex model (Leary, 1957), resource exchange theory (Foa & Foa, 1974), and the meta-constructs of agency and communion (Bakan, 1966; Wiggins. 1991) in the attempt to explicate a theoretical and measurement model of social support. The Support Actions Scale - Circumplex (SAS-C: Trobst, in press) provides a circumplex measure of social support whose psychometric characteristics are comparable to the best circumplexes repot ted In the literature. Empirical findings using this recent measure are summarized and interpreted with respect to an interpersonal theory perspective. C1 NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. RP Trobst, KK (reprint author), York Univ, Dept Psychol, 4700 Keele St, Toronto, ON M3J 1P3, Canada. NR 54 TC 8 Z9 8 U1 0 U2 1 PU HOGREFE & HUBER PUBLISHERS PI GOTTINGEN PA ROHNSWEG 25, D-37085 GOTTINGEN, GERMANY SN 1015-5759 J9 EUR J PSYCHOL ASSESS JI Eur. J. Psychol. Assess. PY 1999 VL 15 IS 3 BP 246 EP 255 DI 10.1027//1015-5759.15.3.246 PG 10 WC Psychology, Applied SC Psychology GA 277CD UT WOS:000084914400007 ER PT J AU Deterding, LJ Tomer, KB Wellemans, JMY Cerny, RL Gross, ML AF Deterding, LJ Tomer, KB Wellemans, JMY Cerny, RL Gross, ML TI Capillary electrophoresis tandem mass spectrometry with array detection SO EUROPEAN MASS SPECTROMETRY LA English DT Article DE capillary electrophoresis; tandem mass spectrometry; array detection; coaxial continuous flow FAB; peptides ID HIGH-SENSITIVITY ANALYSIS; MPC-CE-MS/MS; ZONE-ELECTROPHORESIS; MEMBRANE PRECONCENTRATION; PROTEIN IDENTIFICATION; PEPTIDES; LEVEL AB Mixtures of standard compounds of biological interest were analyzed by capillary electrophoresis in conjunction with tandem four-sector mass spectrometry (MS/MS) using an array detector. Capillary electrophoresis offers extremely high separation efficiencies while array detection allows for the simultaneous acquisition of a large fraction of a tandem mass spectrum and high utilization of the sample ions produced. Consequently, improvements in sensitivity and structural information were observed for the combined techniques in comparison to similar measurements with a four-sector and a single-point detector. Coaxial continuous-flow fast atom bombardment was used to create (M + H)(+) precursor ions of the separated analytes and their product ion spectra were acquired from femtomole levels in electrophoretic real-time, The limit-of-detection for the acquisition of MS/MS data from electrophoretically-separated peptides was 35-100 fmol, The MS/MS data acquired at these levels showed cleavages of the peptide backbone (i.e. to give a and y ions) and production of immonium ions from the constituent amino acids. Acquisition of the spectra via the array detector is more routine acid, at the 100 femtomole level, provides more structurally informative ions and yields better ion statistics than comparable spectra acquired with a point detector. C1 NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. Univ Nebraska, Dept Chem, Lincoln, NE 68588 USA. RP Deterding, LJ (reprint author), NIEHS, Struct Biol Lab, POB 12233,MD FO-03, Res Triangle Pk, NC 27709 USA. RI Tomer, Kenneth/E-8018-2013 NR 32 TC 1 Z9 1 U1 0 U2 0 PU IM PUBLICATIONS PI W SUSSEX PA 6 CHARLTON MILL, CHARLTON, CHICHESTER,, W SUSSEX, ENGLAND PO18 0HY SN 1356-1049 J9 EUR MASS SPECTROM JI Eur. Mass Spectrom. PY 1999 VL 5 IS 1 BP 33 EP 40 DI 10.1255/ejms.247 PG 8 WC Physics, Atomic, Molecular & Chemical; Spectroscopy SC Physics; Spectroscopy GA 201LA UT WOS:000080595200007 ER PT J AU Koch, CA AF Koch, CA TI Papilledema and proteinuria in cerebral venous thrombosis SO EUROPEAN NEUROLOGY LA English DT Letter C1 NIH, Bethesda, MD 20892 USA. RP Koch, CA (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. RI Koch, Christian/A-4699-2008 OI Koch, Christian/0000-0003-3127-5739 NR 2 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0014-3022 J9 EUR NEUROL JI Eur. Neurol. PY 1999 VL 42 IS 2 BP 118 EP 118 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 233YL UT WOS:000082454700010 PM 10755856 ER PT J AU Applegren, LE Arnold, D Boisseau, J Boobis, AR Ellis, RL Livingston, RC McLean, JG MacNeil, JD Miller, MA Miterna, ES Palermo-Neto Pinter, A Martinez, JLR Sinhaseni, P Soback, S Wells, R Cernigilia, CE Chamberlain, P Chernausek, SD Fuchs, R Good, EAM Hansen, MK Heitzman, RJ Herrman, JL Mitsumori, K Nord, CE Olsen, P Paakkanen, J Pronk, MEJ Ritter, L Roberts, G Roestal, B Sills, RC Sundlof, S Ungemach, FR Weber, N AF Applegren, LE Arnold, D Boisseau, J Boobis, AR Ellis, RL Livingston, RC McLean, JG MacNeil, JD Miller, MA Miterna, ES Palermo-Neto Pinter, A Martinez, JLR Sinhaseni, P Soback, S Wells, R Cernigilia, CE Chamberlain, P Chernausek, SD Fuchs, R Good, EAM Hansen, MK Heitzman, RJ Herrman, JL Mitsumori, K Nord, CE Olsen, P Paakkanen, J Pronk, MEJ Ritter, L Roberts, G Roestal, B Sills, RC Sundlof, S Ungemach, FR Weber, N CA Joint FAO WHO Expert Comm Food Additives TI Evaluation of certain veterinary drug residues in food - Fiftieth report of the Joint FAO/WHO Expert Committee on Food Additives SO EVALUATION OF CERTAIN VETERINARY DRUG RESIDUES IN FOOD SE WHO TECHNICAL REPORT SERIES LA English DT Article C1 Swedish Univ Agr Sci, Fac Vet Med, Biomed Ctr, Dept Pharmacol & Toxicol, Uppsala, Sweden. Fed Inst Hlth Protect Consumers & Vet Med, Berlin, Germany. Natl Agcy Vet Med, Nalt Ctr Vet & Food Studies, Fougeres, France. Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Sch Med, Div Med,Sect Clin Pharmacol, London, England. Dept Agr, Off Publ Hlth & Sci, Sci Res & Oversight Staff, Washington, DC USA. US FDA, Ctr Vet Med, Off New Anim Drug Evaluat, Rockville, MD 20857 USA. Canadian Food Inspect Agcy, Hlth Anim Lab, Ctr Vet Drug Residues, Saskatoon, SK, Canada. Univ Nairobi, Coll Agr & Vet Sci, Fac Vet Med, Dept Publ Hlth Pharmacol & Toxicol, Kabete, Kenya. Univ Sao Paulo, Fac Vet Med & Anim Husb, Dept Pathol, Sao Paulo, Brazil. Natl Inst Environm Hlth, Budapest, Hungary. Minist Agr & Anim Husb, Nalt Lab Vet Sci, Toxicol & Residues Sect, San Jose, Costa Rica. Chulalongkorn Univ, Inst Hlth Res, Bangkok, Thailand. Minist Agr, Kimron Vet Inst, Natl Residue Lab, Beit Dagan, Israel. US FDA, Natl Ctr Toxicol Res, Dept Microbiol & Chem, Jefferson, AR 72079 USA. US FDA, Ctr Vet Med, Off New Anim Drug Evaluat, Div Human Food Safety, Rockville, MD 20857 USA. Childrens Hosp, Med Ctr, Div Endocrinol, Cincinnati, OH 45229 USA. Inst Med Res & Occupat Hlth, Dept Expt Toxicol & Ecotoxicol, Zagreb, Croatia. Minist Agr Fisheries & Food, Vet Med Directorate, Surrey, England. Consumers Union, Consumer Policy Inst, Yonkers, NY USA. WHO, Int Programme Chem Safety, CH-1211 Geneva, Switzerland. Natl Inst Hlth Sci, Biol Safety Res Ctr, Div Pathol, Tokyo 158, Japan. Huddinge Univ Hosp, Karolinska Inst, Dept Immunol Microbiol Pathol & Infect Dis, S-14186 Huddinge, Sweden. Danish Vet & Food Adm, Inst Food Safety & Toxicol, Pathol Sect, Soborg, Denmark. FAO, Div Food & Nutr, Food Qual & Stand Serv, Food Qual Liaison Grp, I-00100 Rome, Italy. Natl Inst Publ Hlth & Environm, Ctr Subst & Risk Assessment, Bilthoven, Netherlands. Univ Guelph, Canadian Network Toxicol Ctr, Guelph, ON, Canada. Commonwealth Dept Hlth & Family Serv, Therapeut Goods Adm, Chem Prod Assessment Sect, Woden, ACT, Australia. NIEHS, Res Triangle Pk, NC 27709 USA. Univ Leipzig, Fac Vet Med, Inst Pharmacol Pharm & Toxicol, Leipzig, Germany. RP Applegren, LE (reprint author), Swedish Univ Agr Sci, Fac Vet Med, Biomed Ctr, Dept Pharmacol & Toxicol, Uppsala, Sweden. NR 8 TC 3 Z9 3 U1 0 U2 4 PU WORLD HEALTH ORGANIZATION PI GENEVA PA 1211 27 GENEVA, SWITZERLAND SN 0512-3054 J9 WHO TECH REP SER PY 1999 VL 888 BP 1 EP 95 PG 95 WC Food Science & Technology; Toxicology SC Food Science & Technology; Toxicology GA BN61F UT WOS:000082354800001 ER PT J AU Simon-Stoos, KL Bloom, ML AF Simon-Stoos, KL Bloom, ML TI The hemoglobin-deficit mouse: Cure of the anemia following bone marrow transplantation with normal marrow SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE bone marrow transplantation; hemoglobin deficit; anemia; mice; congenic strains ID CELLS; MICE AB The hemoglobin-deficit mouse mutant (hbd) is characterized by a severe microcytic anemia that is inherited in an autosomal-recessive manner, Previous results from our laboratory indicated that normal mice develop anemia if they are transplanted with bone marrow from mutant animals. Furthermore, we demonstrated a delay in erythroid reconstitution from hbd marrow compared to normal marrow, Although these experiments show a defect that is intrinsic to hbd marrow, it is unclear if the hbd phenotype is solely the result of a bone marrow-derived defect. To exclude an environmental influence on hbn anemia, we attempted to cure the defect by transplanting normal marrow into the hbd mouse. We observed that the transplanted animals converted to a normal phenotype, These results indicated that the defect is bone marrow derived, In contrast to the microcytosis mutant whose defective gene is ubiquitiously expressed, our data suggest that the defective gene product is specific to hematopoietic cells. (C) 1999 International Society for Experimental Hematology. Published by Elsevier Science Inc. C1 NHLBI, NIH, Bethesda, MD 20892 USA. RP Bloom, ML (reprint author), NHLBI, NIH, Bldg 10,Room 7C 118, Bethesda, MD 20892 USA. NR 17 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JAN PY 1999 VL 27 IS 1 BP 162 EP 168 DI 10.1016/S0301-472X(98)00011-3 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA 157TV UT WOS:000078078500018 PM 9923455 ER PT B AU Hussain, SP Harris, CC AF Hussain, SP Harris, CC BE Utsunomiya, J Mulvihill, JJ Weber, W TI Molecular epidemiology of human cancer SO FAMILIAL CANCER AND PREVENTION: MOLECULAR EPIDEMIOLOGY - A NEW STRATEGY TOWARD CANCER CONTROL LA English DT Proceedings Paper CT UICC Symposium on Familial Cancer and Prevention CY MAY 14-16, 1997 CL KOBE, JAPAN SP UICC Int Union Against Canc ID TUMOR-SUPPRESSOR GENE; HUMAN P53 GENE; WILD-TYPE P53; SKIN-CANCER; HEPATOCELLULAR CARCINOMAS; CHEMICAL CARCINOGENS; MUTATIONAL HOTSPOTS; HUMAN HEPATOCYTES; ESCHERICHIA-COLI; EPITHELIAL-CELLS C1 NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA. RP Hussain, SP (reprint author), NCI, Human Carcinogenesis Lab, Bldg 37, Bethesda, MD 20892 USA. NR 56 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS, INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA BN 0-471-24937-8 PY 1999 BP 7 EP 18 PG 12 WC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; Medicine, General & Internal SC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; General & Internal Medicine GA BM95P UT WOS:000080246400003 ER PT B AU Fraser, MC AF Fraser, MC BE Utsunomiya, J Mulvihill, JJ Weber, W TI Familial cancer: New and evolving challenges for oncology nurses and their patients SO FAMILIAL CANCER AND PREVENTION: MOLECULAR EPIDEMIOLOGY - A NEW STRATEGY TOWARD CANCER CONTROL LA English DT Proceedings Paper CT UICC Symposium on Familial Cancer and Prevention CY MAY 14-16, 1997 CL KOBE, JAPAN SP UICC Int Union Against Canc AB Recent advances in molecular biology have led to the identification of several inherited cancer susceptibility genes that markedly increase cancer risk. These advances have had a major impact on nursing management of familial cancer. Advanced practice nurses are assuming greater roles in performing familial cancer risk assessments, implementing comprehensive cancer risk management plans, and providing genetic education and services. Predisposition testing for mutations in selected cancer susceptibility genes is moving rapidly from the research setting into the general oncology and primary care communities. Ethical, legal, and psychosocial issues associated with predisposition testing for cancer susceptibility are quite complex. Oncology nurses must become knowledgeable about concepts in cancer genetics to be able to translate research findings and implement the appropriate clinical implications for nursing practice. Education in genetics is a priority for several organizations; major initiatives to educate professionals and lay persons about cancer genetics are being implemented. The essence of nursing is caring for patients and their families. Thus, oncology nurses are in a strategic position to address the emerging clinical challenges related to cancer genetics. C1 NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. RP Fraser, MC (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS, INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA BN 0-471-24937-8 PY 1999 BP 117 EP 120 PG 4 WC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; Medicine, General & Internal SC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; General & Internal Medicine GA BM95P UT WOS:000080246400019 ER PT B AU Schatzkin, A Goldstein, A Hawk, E AF Schatzkin, A Goldstein, A Hawk, E BE Utsunomiya, J Mulvihill, JJ Weber, W TI Chemo- and dietary prevention of familial cancer: From theory to practice SO FAMILIAL CANCER AND PREVENTION: MOLECULAR EPIDEMIOLOGY - A NEW STRATEGY TOWARD CANCER CONTROL LA English DT Proceedings Paper CT UICC Symposium on Familial Cancer and Prevention CY MAY 14-16, 1997 CL KOBE, JAPAN SP UICC Int Union Against Canc ID ADENOMATOUS POLYPOSIS; APC AB This paper discusses the theoretical and practical possibilities of preventing the development of familial, or hereditary, cancer through dietary modification or use of a chemopreventive agent. We focus on hereditary cancers associated with so-called "major cancer genes" such as BRCA1 and BRCA2 for breast cancer and APC for familial adenomatous polyposis. C1 NCI, NIH, Bethesda, MD 20892 USA. RP Schatzkin, A (reprint author), NCI, NIH, Bethesda, MD 20892 USA. NR 12 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS, INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA BN 0-471-24937-8 PY 1999 BP 295 EP 301 PG 7 WC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; Medicine, General & Internal SC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; General & Internal Medicine GA BM95P UT WOS:000080246400045 ER PT B AU Miller, RW AF Miller, RW BE Utsunomiya, J Mulvihill, JJ Weber, W TI Diverse cancers in genetic disorders: Case series compared SO FAMILIAL CANCER AND PREVENTION: MOLECULAR EPIDEMIOLOGY - A NEW STRATEGY TOWARD CANCER CONTROL LA English DT Proceedings Paper CT UICC Symposium on Familial Cancer and Prevention CY MAY 14-16, 1997 CL KOBE, JAPAN SP UICC Int Union Against Canc AB The arrays of neoplasms in six genetic syndromes differ from one another, although there is some overlap. Soft tissue sarcomas and osteosarcomas occur excessively, but not in the same ratio in Werner (premature aging) syndrome (WS), Li-Fraumeni syndrome (LFS), and Rothmund-Thomson syndrome. Excesses of leukemia of dissimilar types occur in the chromosome instability syndrome: Bloom syndrome (BS), Fanconi anemia (FA), and ataxia-telangiectasia (A-T). BS and A-T have excesses of lymphoma. In adulthood, carcinomas occur excessively in BS and FA. Japanese with WS have marked increases in three rare cancers; persons with LFS are predisposed to four others under the age of 45. Laboratory research should provide explanations for such peculiarities of cancer occurrence in genetic disorders. C1 NCI, NIH, Bethesda, MD 20892 USA. RP Miller, RW (reprint author), NCI, NIH, Bethesda, MD 20892 USA. NR 11 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS, INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA BN 0-471-24937-8 PY 1999 BP 449 EP 453 PG 5 WC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; Medicine, General & Internal SC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; General & Internal Medicine GA BM95P UT WOS:000080246400067 ER PT B AU Kraemer, KH AF Kraemer, KH BE Utsunomiya, J Mulvihill, JJ Weber, W TI Xeroderma pigmentosum: Diagnosis, registration, and skin cancer prevention SO FAMILIAL CANCER AND PREVENTION: MOLECULAR EPIDEMIOLOGY - A NEW STRATEGY TOWARD CANCER CONTROL LA English DT Proceedings Paper CT UICC Symposium on Familial Cancer and Prevention CY MAY 14-16, 1997 CL KOBE, JAPAN SP UICC Int Union Against Canc ID DNA-REPAIR; EXCISION-REPAIR; SUNLIGHT; MELANOMA; PATIENT; DISEASE; VECTOR; GENE AB Patients with xeroderma pigmentosum (XP) are at greater than 1,000-fold increased risk of developing skin cancer on sunlight-exposed portions of the body. These tumors include cutaneous basal cell carcinomas, squamous cell carcinomas (SCC), and melanomas, as well as cancers of the anterior eye and SCC of the tip of the tongue. XP patients have a 50-year reduction in age of onset of skin cancer compared with the general population in the United States. These abnormalities are caused by defective DNA excision repair. XP cells are hypersensitive to killing by ultraviolet (UV) radiation and are UV-hypermutable. Early diagnosis of XP is based on a clinical suspicion and laboratory confirmation by measurement of post-UV cell survival or post-UV unscheduled DNA synthesis (UDS). There are seven XP UDS complementation groups with different defective DNA repair genes and varying clinical features. Molecular diagnosis is possible in some cases. Skin cancer prevention depends on early diagnosis and rigorous sun protection. Oral isotretinoin was found to be effective in prevention of new cancers in XP patients with a history of numerous cutaneous neoplasms but had numerous side effects. C1 NCI, Mol Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. RP Kraemer, KH (reprint author), NCI, Mol Carcinogenesis Lab, NIH, Bldg 37, Bethesda, MD 20892 USA. NR 18 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS, INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA BN 0-471-24937-8 PY 1999 BP 501 EP 506 PG 6 WC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; Medicine, General & Internal SC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; General & Internal Medicine GA BM95P UT WOS:000080246400075 ER PT B AU Harris, CC AF Harris, CC BE Utsunomiya, J Mulvihill, JJ Weber, W TI Workshop report 1 SO FAMILIAL CANCER AND PREVENTION: MOLECULAR EPIDEMIOLOGY - A NEW STRATEGY TOWARD CANCER CONTROL LA English DT Proceedings Paper CT UICC Symposium on Familial Cancer and Prevention CY MAY 14-16, 1997 CL KOBE, JAPAN SP UICC Int Union Against Canc C1 NCI, NIH, Bethesda, MD 20892 USA. RP Harris, CC (reprint author), NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS, INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA BN 0-471-24937-8 PY 1999 BP 531 EP 532 PG 2 WC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; Medicine, General & Internal SC Oncology; Genetics & Heredity; Public, Environmental & Occupational Health; General & Internal Medicine GA BM95P UT WOS:000080246400079 ER PT J AU Miller, HG Cain, VS Rogers, SM Gribble, JN Turner, CF AF Miller, HG Cain, VS Rogers, SM Gribble, JN Turner, CF TI Correlates of sexually transmitted bacterial infections among US women in 1995 SO FAMILY PLANNING PERSPECTIVES LA English DT Article ID PELVIC INFLAMMATORY DISEASE; RISK-FACTORS; FERTILITY; COHORT; AGE AB Context: Sexually transmitted diseases (STDs) of bacterial origin such as gonorrhea and chlamydial infection can lead to pelvic inflammatory disease (PID) and infertility. identifying behaviors and characteristics associated with infection may assist in preventing these often asymptomatic diseases and their sequelae. Methods: Data from 9,882 sexually active women who participated in the 1995 National Survey of Family Growth describe the characteristics of women who report a history of infection with a bacterial STD or of treatment for PID. Multivariate analysis is used to determine which demographic characteristics and sexual and health-related behaviors affect the likelihood of infection or the occurrence of complications. Results: Overall, 6% of sexually active women reported a history of a bacterial STD, and 8% reported a history of PID. Women who first had sexual intercourse before age 15 were nearly four times as likely to report a bacterial STD, and more than twice as likely to report PID, as were women who first had sex after age 18. Having more than five lifetime sexual partners also was associated with both having an STD and having PID. PID was more common among women reporting a history of a bacterial STD (23%) than among women who reported no such history (7%). In multivariate analyses, age, race, age at first intercourse and lifetime number of sexual partners had a significant effect on the risk of a bacterial STD. Education, age, a history of IUD use, douching and a history of a bacterial STD had a significant impact on the risk of PID, but early onset of intercourse did not, and lifetime number of partners had only a marginal effect. Conclusions: The pattern of characteristics and behaviors that place women at risk of infection with bacterial STDs is not uniform among groups of women. Further the level of self-reported PID would suggest higher rates of gonorrhea and chlamydial infection than reported. C1 Res Triangle Inst, Program Hlth & Behav Measurement, Washington, DC USA. NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA. RP Miller, HG (reprint author), Res Triangle Inst, Program Hlth & Behav Measurement, Washington, DC USA. NR 30 TC 52 Z9 52 U1 0 U2 0 PU ALAN GUTTMACHER INST PI NEW YORK PA 125 MAIDEN LANE, 7TH FLOOR, NEW YORK, NY 10038 USA SN 0014-7354 J9 FAM PLANN PERSPECT JI Fam. Plann. Perspect. PD JAN-FEB PY 1999 VL 31 IS 1 BP 4 EP + DI 10.2307/2991550 PG 7 WC Demography; Family Studies SC Demography; Family Studies GA 165NC UT WOS:000078526700001 PM 10029926 ER PT J AU Malinda, KM Nomizu, M Chung, M Delgado, M Kuratomi, Y Yamada, Y Kleinman, HK Ponce, ML AF Malinda, KM Nomizu, M Chung, M Delgado, M Kuratomi, Y Yamada, Y Kleinman, HK Ponce, ML TI Identification of laminin alpha 1 and beta 1 chain peptides active for endothelial cell adhesion, tube formation, and aortic sprouting SO FASEB JOURNAL LA English DT Article DE angiogenesis; basement membrane; synthetic peptides ID EXPERIMENTAL METASTASIS FORMATION; AMINO-ACID-SEQUENCE; A-CHAIN; TUMOR-GROWTH; ANGIOGENESIS; MATRIGEL; DIFFERENTIATION; INHIBITION; ATTACHMENT; BINDING AB Laminin-1 is a basement membrane glycoprotein that promotes several biological activities including cell attachment, tumor metastasis, and angiogenesis. Angiogenesis plays an important role in tissue formation, reproduction, wound healing,;md several pathological conditions. In this study, we screened 405 synthetic peptides from the al and pi chains to identify potential sites on laminin-l active with endothelial cells, Peptides were initially screened by testing both endothelial cell adhesion to peptide-coated wells and tube formation on Matrigel in the presence of soluble peptide. Twenty active peptides were identified in these screens, A secondary screen using the rat aortic ring sprouting assay identified 13 of the 20 peptides that stimulated endothelial sprouting, Several of these active peptides were also found to stimulate human umbilical vein endothelial cell migration in Boyden chamber assays. Differences in the amount of peptide needed for the response and in the resultant morphologies/responses were observed between the peptides in all of the assays. Our results suggest that several active domains on laminin-1 may play important roles in stimulating different steps in angiogenesis. C1 NIDR, Craniofacial Dev Biol & Regenerat Branch, NIH, Bethesda, MD 20892 USA. RP Kleinman, HK (reprint author), NIDR, Craniofacial Dev Biol & Regenerat Branch, NIH, Bldg 30,Room 433, Bethesda, MD 20892 USA. NR 26 TC 131 Z9 135 U1 0 U2 4 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN PY 1999 VL 13 IS 1 BP 53 EP 62 PG 10 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 156YB UT WOS:000078029500006 PM 9872929 ER PT B AU Grossenbacher, PG AF Grossenbacher, PG BE Killeen, PR Uttal, WR TI Correspondence between tactile temporal frequency and visual spatial frequency SO FECHNER DAY 99: THE END OF 20TH CENTURY PSYCHOPHYSICS, PROCEEDINGS LA English DT Proceedings Paper CT 15th Annual Meeting of the International-Society-for-Psychophysics CY OCT 21-24, 1999 CL ARIZONA STATE UNIV, TEMPE, AZ SP Int Soc Psychophys, Arizona State Univ, Coll Engn & Appl Sci, Arizona State Univ, Coll Liberal Arts & Sci, Arizona State Univ, Dept Psychol HO ARIZONA STATE UNIV ID TEXTURE-PERCEPTION; GROOVED SURFACES; ROUGHNESS; TOUCH AB This study attempted to simulate seen and felt surface roughness with visual spatial frequency and vibrotactile frequency in order to determine whether visual stimulation can influence perception of mechanical stimulation of the skin. A filtering experiment required speeded discrimination of fingertip vibrations during irrelevant visual stimulation. Despite zero correlation between visual and tactile frequencies, the irrelevant visual stimuli influenced tactile discrimination performance. Responses to slow (or fast) fingertip vibrations were quicker and more accurate when they were accompanied by low (or high) visual spatial frequency. In other words, discrimination performance was better under conditions of corresponding visual and tactile stimulation compared to non-corresponding conditions. Participants also reported subjective phenomena that revealed psychological correspondence between visual and tactile frequency dimensions. This visuotactile frequency correspondence is discussed in relation to multisensory perception of objects having visible and tangible attributes. C1 NIMH, Lab Brain & Cognit, Sect Clin & Expt Neuropsychol, Bethesda, MD 20892 USA. NR 22 TC 0 Z9 0 U1 0 U2 0 PU ARIZONA STAT UNIV, DEPT PSYCHOLOGY PI TEMPE PA TEMPE, AZ 85287 USA PY 1999 BP 55 EP 61 PG 7 WC Psychology, Biological; Psychology, Applied; Psychology, Multidisciplinary; Psychology, Mathematical; Psychology, Social SC Psychology GA BP33R UT WOS:000084731400010 ER PT J AU Tasaki, I AF Tasaki, I TI Evidence for phase transition in nerve fibers, cells and synapses SO FERROELECTRICS LA English DT Article DE nerve excitation; phase transition ID DISCONTINUOUS VOLUME TRANSITIONS; PROPAGATED IMPULSE; MECHANICAL CHANGES; ACTION-POTENTIALS; THERMAL-CHANGES; EXCITATION; CALCIUM; SODIUM; GELS AB By examining rapid changes in the volume and temperature during excitation of a large number of excitable cells and tissues, we have shown that the excitation process is invariably accompanied by swelling and heat production in the superficial protoplasmic layer. By comparing the behavior of a model system (synthetic anionic gels containing both Ca- and Na- ions) with that of nerve fibers under comparable environmental conditions, we have demonstrated that the onset of an action potential is a reflection of a discontinuous volume transition in the superficial layer of nerve cells and fibers. Evidence for the existence of a first-order phase transition (involving volume and temperature changes) in nerve cells, fibers and synapses is presented. C1 NIMH, Bethesda, MD 20892 USA. RP Tasaki, I (reprint author), NIMH, Bethesda, MD 20892 USA. NR 44 TC 18 Z9 20 U1 0 U2 3 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD, PO BOX 90, READING RG1 8JL, BERKS, ENGLAND SN 0015-0193 J9 FERROELECTRICS JI Ferroelectrics PY 1999 VL 220 IS 3-4 BP 305 EP 316 DI 10.1080/00150199908216221 PG 12 WC Materials Science, Multidisciplinary; Physics, Condensed Matter SC Materials Science; Physics GA 193ZP UT WOS:000080167900010 ER PT J AU Baird, DD Weinberg, CR Zhou, HB Kamel, F McConnaughey, DR Kesner, JS Wilcox, AJ AF Baird, DD Weinberg, CR Zhou, HB Kamel, F McConnaughey, DR Kesner, JS Wilcox, AJ TI Preimplantation urinary hormone profiles and the probability of conception in healthy women SO FERTILITY AND STERILITY LA English DT Article DE conception; estrogen; progesterone; LH; epidemiology ID FOLLICLE-STIMULATING-HORMONE; HUMAN MENSTRUAL-CYCLE; LUTEINIZING-HORMONE; PROGESTERONE METABOLITES; INVITRO FERTILIZATION; LEUPROLIDE ACETATE; SERUM PROGESTERONE; EMBRYO TRANSFER; PREGNANCY; OVULATION AB Objective: To examine hormonal predictors of conception in menstrual cycles from normal women. Design: Longitudinal study. Setting: Community. Patient(s): Two hundred fifteen healthy female volunteers with no known fertility problems who were trying to conceive. Intervention(s): Participants recorded menstrual bleeding, sexual intercourse, and collected first morning urine specimens daily from when they stopped contraception until they became pregnant or for 6 months if no clinical pregnancy was achieved. Measurements were made of urinary LH and urinary metabolites of estrogen and progesterone. Main Outcome Measure(s): Conception was identified by a sensitive and specific immunoradiometric assay for urinary hCG. Result(s): Statistical analyses of 189 conception and 409 nonconception cycles controlled for sexual intercourse and interdependence of cycles from the same woman. Conception was more likely in cycles with lower baseline progesterone metabolite levels, higher ovulatory LH, and higher midluteal progesterone. Midluteal estrogen also was elevated in conception cycles when examined without adjusting for other hormone levels, but this finding did not persist after multivariate adjustment. Conclusions: Menstrual cycles in normal women vary in their hormonal quality in ways that are predictive of cycle fertility. American Society for Reproductive Medicine. C1 NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. RP Baird, DD (reprint author), NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA. OI Kamel, Freya/0000-0001-5052-6615; Wilcox, Allen/0000-0002-3376-1311; Baird, Donna/0000-0002-5544-2653 NR 39 TC 57 Z9 58 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD JAN PY 1999 VL 71 IS 1 BP 40 EP 49 DI 10.1016/S0015-0282(98)00419-1 PG 10 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 157MD UT WOS:000078065500009 PM 9935114 ER PT J AU Hovest, AS Horne, MK AF Hovest, AS Horne, MK TI The effect of arginine on coagulation and fibrinolysis in vitro SO FIBRINOLYSIS & PROTEOLYSIS LA English DT Article ID PLASMINOGEN AB Arginine is added to commercially-available recombinant tissue plasminogen activator (rtPA) to promote its solubility. However, arginine is also known to inhibit certain proteases. To explore the possibility that arginine inhibits the highly concentrated rtPA in commercial formulations, we tested the amino acid in assays of rtPA function. Although arginine was found to inhibit rtPA cleavage of a chromogenic substrate, it did not interfere with rtPA-mediated fibrinolysis. However, whole-blood clotting time and thrombin clotting time of purified fibrinogen were prolonged by arginine. Therefore, the concentration of arginine in commercial preparations of rtPA appears to have an anticoagulant effect but does not retard fibrinolysis. C1 NIH, Warren G Magnuson Clin Ctr, Dept Clin Pathol, Hematol Serv, Bethesda, MD 20892 USA. RP Horne, MK (reprint author), NIH, Warren G Magnuson Clin Ctr, Dept Clin Pathol, Hematol Serv, Rm 2C306,Bldg 10, Bethesda, MD 20892 USA. NR 5 TC 1 Z9 1 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 0268-9499 J9 FIBRINOLYSIS PROTEOL JI Fibrinolysis Proteolysis PD JAN PY 1999 VL 13 IS 1 BP 31 EP 34 DI 10.1016/S0268-9499(99)90013-9 PG 4 WC Biochemistry & Molecular Biology; Hematology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Hematology; Research & Experimental Medicine GA 192LP UT WOS:000080080500005 ER PT S AU Wilson, P AF Wilson, P BE Plutzky, J Libby, P Nakamura, H TI Emerging risk factors for coronary artery disease SO FIRST US-JAPANESE DIALOGUE ON LIPID DISORDERS AND CORONARY ARTERY DISEASE: NEW ISSUES FOR THE NEXT MILLENNIUM SE ROYAL SOCIETY OF MEDICINE INTERNATIONAL CONGRESS AND SYMPOSIUM SERIES LA English DT Proceedings Paper CT 1st US-Japanese Dialogue on Lipid Disorders and Coronary Artery Disease Symposium CY NOV 12, 1998 CL BRIGHAM & WOMENS HOSP, BOSTON, MA SP Parke Davis Pharmaceut HO BRIGHAM & WOMENS HOSP ID APOLIPOPROTEIN-E ALLELES; HEART-DISEASE; PLASMA HOMOCYSTEINE; LIPOPROTEIN; POPULATION; ASSOCIATION; BENEFITS; TRIAL; MEN C1 NHLBI, Framingham, MA USA. RP Wilson, P (reprint author), NHLBI, Framingham, MA USA. NR 20 TC 0 Z9 0 U1 0 U2 0 PU ROYAL SOC MEDICINE PRESS LTD PI LONDON PA 1 WIMPOLE STREET, LONDON W1M 8AE, ENGLAND SN 0142-2367 BN 1-85315-445-8 J9 ROY SOC MED INT CONG PY 1999 IS 238 BP 17 EP 25 PG 9 WC Cardiac & Cardiovascular Systems; Medicine, General & Internal; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; General & Internal Medicine GA BN39Z UT WOS:000081802200003 ER PT J AU Lands, WEM AF Lands, WEM TI Balancing fatty acids SO FOOD TECHNOLOGY LA English DT Editorial Material C1 NIAAA, NIH, Bethesda, MD 20992 USA. RP Lands, WEM (reprint author), NIAAA, NIH, Bethesda, MD 20992 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU INST FOOD TECHNOLOGISTS PI CHICAGO PA SUITE 300 221 N LASALLE ST, CHICAGO, IL 60601-1291 USA SN 0015-6639 J9 FOOD TECHNOL-CHICAGO JI Food Technol. PD JAN PY 1999 VL 53 IS 1 BP 120 EP 120 PG 1 WC Food Science & Technology SC Food Science & Technology GA 159JP UT WOS:000078169200019 ER PT J AU Cadet, JL Ordonez, S Burrell, S AF Cadet, JL Ordonez, S Burrell, S TI Toxic effects of methamphetamine and dopamine in cell culture SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIDA, Mol Neuropsychiat Sect, Intramural Res Program, NIH, Baltimore, MD 21224 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 418 BP S138 EP S138 DI 10.1016/S0891-5849(99)90954-1 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900443 ER PT J AU Cardozo-Pelaez, F Stedeford, T Brooks, PJ Song, SJ Sanchez-Ramos, J AF Cardozo-Pelaez, F Stedeford, T Brooks, PJ Song, SJ Sanchez-Ramos, J TI Diethylmaleate (DEM) upregulates brain capacity to excise 8-hydroxy-2'-deoxyguanosine (oxo(8)DG) in a region specific manner SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 James Haley Vet Affairs Res Serv, Tampa, FL USA. Univ S Florida, Coll Med, Dept Neurol, Tampa, FL 33620 USA. NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. RI Sanchez-Ramos, Juan/A-1188-2009 OI Sanchez-Ramos, Juan/0000-0002-3391-7857 NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 277 BP S92 EP S92 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900301 ER PT J AU Chen, YR Deterding, LJ Tomer, KB Mason, RP AF Chen, YR Deterding, LJ Tomer, KB Mason, RP TI The nature of the inhibition of horseradish peroxidase and mitochondrial cytochrome C oxidase by cyanyl radical SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 15 BP S18 EP S18 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900039 ER PT J AU Daruwala, R Koh, WS Park, JB Levine, M AF Daruwala, R Koh, WS Park, JB Levine, M TI The dietary flavone quercetin is a potential inhibitor of glucose transporter glut1, glut2 and glut3 SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 70 BP S34 EP S34 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900094 ER PT J AU Dikalov, SJ Mason, RP AF Dikalov, SJ Mason, RP TI Reassignment of organic peroxyl radical adducts SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 1 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 404 BP S131 EP S131 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900429 ER PT J AU Dikalov, SJ Mason, RP AF Dikalov, SJ Mason, RP TI Spin trapping of lipid peroxyl radical reassignment of secondary alkoxyl radical adducts SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 405 BP S132 EP S132 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900430 ER PT J AU Eck, P Daruwala, R Levine, M AF Eck, P Daruwala, R Levine, M TI Mechanism of dehydroascorbic acid reduction by glutaredoxin (thioltransferase) SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIDDK, NIH, 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 73 BP S35 EP S35 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900099 ER PT J AU Finkelstein, EJ Chanock, SJ van der Vliet, A AF Finkelstein, EJ Chanock, SJ van der Vliet, A TI Effect of myeloperoxidase promoter polymorphism on enzyme activity in human moncytes SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 Univ Calif Davis, Dept Internal Med, Davis, CA 95616 USA. NCI, NIH, 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 127 BP S50 EP S50 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900151 ER PT J AU Gilbert, DL AF Gilbert, DL TI Sulfur is an ideal redox regulator SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NINDS, BNP, NIH, 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 2 BP S14 EP S14 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900028 ER PT J AU Komarov, AM Wink, DA Feelisch, M Schmidt, HHHW AF Komarov, AM Wink, DA Feelisch, M Schmidt, HHHW TI NO or not NO? SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 George Washington Univ, Med Ctr, Washington, DC 20037 USA. NCI, Bethesda, MD 20892 USA. UCL, London, England. Univ Wurzburg, Wurzburg, Germany. RI Schmidt, Harald H. H. W./B-1549-2008 OI Schmidt, Harald H. H. W./0000-0003-0419-5549 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 231 BP S79 EP S79 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900257 ER PT J AU Krishna, MC Afeworki, M Devasahayam, N Cook, J Subramanian, S Mitchell, JB AF Krishna, MC Afeworki, M Devasahayam, N Cook, J Subramanian, S Mitchell, JB TI In vivo free radical detection and imaging by EPR: Non-invasive mapping of tissue oxygen status. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 468 BP S154 EP S154 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900493 ER PT J AU Levine, M Daruwala, R Song, J Rumsey, SC Koh, WS Eck, P AF Levine, M Daruwala, R Song, J Rumsey, SC Koh, WS Eck, P TI Ascorbate transport and recycling in human neutrophils: Potential roles in oxidant defense SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIDDK, Mol & Clin Nutr Sect, NIH, 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA P9 BP S6 EP S6 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900011 ER PT J AU Levine, RL AF Levine, RL TI Protein oxidation in aging and disease SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NHLBI, Biochem Lab, Bethesda, MD 20892 USA. RI Levine, Rodney/D-9885-2011 NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA P5 BP S4 EP S4 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900007 ER PT J AU Mason, RP Marchesi, E Rota, C Fann, YC Chignell, C AF Mason, RP Marchesi, E Rota, C Fann, YC Chignell, C TI ESR and spin-trapping study of the free radical formation by 2',7'-dichlorofluorescein and its implications for oxidative stress measurements. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 409 BP S133 EP S133 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900434 ER PT J AU McCullough, KD Martindale, JL Klotz, LO Aw, TY Holbrook, NJ AF McCullough, KD Martindale, JL Klotz, LO Aw, TY Holbrook, NJ TI GADD153 sensitizes cells to ER stress by down regulating bcl2 and perturbing the cellular redox state. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIA, Biol Chem Lab, Baltimore, MD 21224 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 173 BP S63 EP S63 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900199 ER PT J AU Mukhopadhyay, P Storz, G AF Mukhopadhyay, P Storz, G TI The mechanism of redox sensing by the OxyR transcription factor SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NICHD, CBMB, NIH, 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 177 BP S64 EP S64 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900203 ER PT J AU Reszka, KJ Matuszak, Z McCormick, ML Britigan, BE Chignell, CF AF Reszka, KJ Matuszak, Z McCormick, ML Britigan, BE Chignell, CF TI Nitrite is the catalyst in the metabolic activation of quinonoid anticancer agents SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 Vet Adm Med Ctr, Res Serv, Iowa City, IA 52240 USA. NIEHS, Chem Pharmacol Lab, NIH, Res Triangle Pk, NC 27709 USA. Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 452 BP S148 EP S148 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900478 ER PT J AU Rusyn, I Kadiiska, MB Dikalova, A Kono, H Mason, RP Thurman, RG AF Rusyn, I Kadiiska, MB Dikalova, A Kono, H Mason, RP Thurman, RG TI Phthalates rapidly increase reactive oxygen species in vivo SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 Univ N Carolina, Dept Pharmacol, Hepatobiol & Toxicol Lab, Chapel Hill, NC 27599 USA. Univ N Carolina, Curriculum Toxicol, Chapel Hill, NC 27599 USA. NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. RI Rusyn, Ivan/S-2426-2016 NR 0 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 453 BP S148 EP S148 DI 10.1016/S0891-5849(99)90989-9 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900477 ER PT J AU Shacka, JJ Kim, ES Roberts, AB Flanders, KC AF Shacka, JJ Kim, ES Roberts, AB Flanders, KC TI Transforming growth factor beta (TGF-beta) is a survival factor in the oxidative stress response SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIGMS, Bethesda, MD USA. NCI, Lab Cell Regulat & Carcinogenesis, NIH, 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 437 BP S142 EP S142 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900462 ER PT J AU Sturgeon, BE Glover, RE Chen, YR Mason, RP AF Sturgeon, BE Glover, RE Chen, YR Mason, RP TI Direct ESR detection of the enzyme-generated, solution-phase, tyrosine imminoxyl radical SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 263 BP S87 EP S87 DI 10.1016/S0891-5849(99)90799-2 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900289 ER PT J AU Tsuchiya, K Mason, RP AF Tsuchiya, K Mason, RP TI NO-forming reactions between the iron-N-methyl-D-glucamine dithiocarbamate complex and nitrite SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract C1 NIEHS, NIH, Res Triangle Pk, NC 27709 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 OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PY 1999 VL 27 SU 1 MA 266 BP S88 EP S88 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 254EL UT WOS:000083598900291 ER PT J AU Marchesi, E Rota, C Fann, YC Chignell, CF Mason, RP AF Marchesi, E Rota, C Fann, YC Chignell, CF Mason, RP TI Photoreduction of the fluorescent dye 2 '-7 '-dichlorofluorescein: A spin trapping and direct electron spin resonance study with implications for oxidative stress measurements SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Article DE 2 '-7 '-dichlorofluorescein; photoreduction; free radical; superoxide; spin-trapping ID FREE-RADICAL FORMATION; REACTIVE OXYGEN; HYDROGEN-PEROXIDE; PROBE 2',7'-DICHLOROFLUORESCIN; ENDOTHELIAL-CELLS; CRYSTAL VIOLET; NITRIC-OXIDE; IN-VITRO; SUPEROXIDE; STIMULATION AB The photoreduction of 2'-7'-dichlorofluorescein (DCF) was investigated in buffer solution using direct electron spin resonance (ESR) and the ESR spin-trapping technique. Anaerobic studies of the reaction of DCF in the presence of reducing agents demonstrated that during visible irradiation (lambda > 300 nm) 2'-7'-dichlorofluorescein undergoes one-electron reduction to produce a semiquinone-type free radical as demonstrated by direct ESR. Spin-trapping studies of incubations containing DCF, 5,5-dimethyl-1-pyrroline N-oxide (DMPO) and either reduced glutathione (GSH) or reduced NADH demonstrate, under irradiation with visible light, the production of the superoxide dismutase-sensitive DMPO/-OOH adduct. In the absence of DMPO, measurements with a Clark-type oxygen electrode show that molecular oxygen is consumed in a light-dependent process. The semiquinone radical of DCF, when formed in an aerobic system, is immediately oxidized by oxygen, which regenerates the dye and forms superoxide. (C) 1998 Elsevier Science Inc. C1 NIEHS, NIH, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. Univ Bologna, Dipartimento Chim Organ A Mangini, I-40126 Bologna, Italy. NIEHS, NIH, Informat Technol Support Serv, Res Triangle Pk, NC 27709 USA. RP Rota, C (reprint author), NIEHS, NIH, Lab Pharmacol & Chem, MD F0-02,POB 12233, Res Triangle Pk, NC 27709 USA. NR 49 TC 110 Z9 114 U1 1 U2 22 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-5849 J9 FREE RADICAL BIO MED JI Free Radic. Biol. Med. PD JAN PY 1999 VL 26 IS 1-2 BP 148 EP 161 DI 10.1016/S0891-5849(98)00174-9 PG 14 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 147PB UT WOS:000077574700017 PM 9890650 ER PT J AU Van Bergen, P Rauhala, P Spooner, CM Chiueh, CC AF Van Bergen, P Rauhala, P Spooner, CM Chiueh, CC TI Hemoglobin and iron-evoked oxidative stress in the brain: Protection by bile pigments, manganese and S-nitrosoglutathione SO FREE RADICAL RESEARCH LA English DT Article; Proceedings Paper CT International Conference on Nitric Oxide CY APR 05-09, 1999 CL NATL UNIV SINGAPORE, SINGAPORE, SINGAPORE HO NATL UNIV SINGAPORE DE hemoglobin; bile pigments/biliverdin/bilirubin; manganese; S-nitrosoglutathione/GSNO; brain lipid peroxidation; dopamine ID LIPID-PEROXIDATION; NITRIC-OXIDE; DOPAMINE NEURONS; FENTON REACTION; HEME OXYGENASE; RAT-BRAIN; ANTIOXIDANT; BILIRUBIN; NEUROPROTECTION; NEUROTOXICITY AB In the present in vitro and in vivo study we investigated the pro-oxidant effects of hemoglobin, as well as the antioxidant effects of its metabolites, in the brain. Incubation of rat brain homogenates with hemoglobin (0-10 mu M) but not hemin induced lipid peroxidation up to 24 h (EC50 = 1.2 mu M). Hemoglobin's effects were similar to ferrous ion (EC50 = 1.7 mu M) and were blocked by the chelating agent deferoxamine (IC50 = 0.5 mu M) and a nitric oxide-releasing compound S-nitrosoglutathione (IC50 = 40 mu M). However, metabolites of hemoglobin - biliverdin and bilirubin - inhibited brain lipid peroxidation induced by cell disruption and hemoglobin (biliverdin IC50 = 12-30 and bilirubin IC50 = 75-170 mu M). Biliverdin's antioxidative effects in spontaneous and iron-evoked lipid peroxidation were further augmented by manganese (2 mu M?) since manganese is an antioxidative transition metal and conjugates with bile pigments. Intrastriatal infusion of hemoglobin (0-24 nmol) produced slight, but significant 20-22% decreases in striatal dopamine levels. Whereas, intrastriatal infusion of ferrous citrate (0-24 nmol) dose-dependently induced a greater 66% depletion of striatal dopamine which was preceded by an acute increase of lipid peroxidation. In conclusion, contrary to the in with results hemoglobin is far less neurotoxic than ferrous ions in the brain. It is speculated that hemoglobin may be partially detoxified by heme oxygenase and biliverdin reductase to its antioxidative metabolites in the brain. However, in head trauma and stroke, massive bleeding could significantly produce iron-mediated oxidative stress and neurodegeneration which could be minimized by endogenous antioxidants such as biliverdin, bilirubin, manganese and S-nitrosoglutathione. C1 NIMH, Univ Neurodegenerat & Neuroprotect, Clin Sci Lab, NIH,Clin Ctr, Bethesda, MD 20892 USA. RP Chiueh, CC (reprint author), NIMH, Univ Neurodegenerat & Neuroprotect, Clin Sci Lab, NIH,Clin Ctr, Bldg 10,Room 3D-41, Bethesda, MD 20892 USA. OI Rauhala, Pekka/0000-0003-2036-3522 NR 36 TC 30 Z9 30 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 1999 VL 31 IS 6 BP 631 EP 640 DI 10.1080/10715769900301201 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 263ZF UT WOS:000084154600018 PM 10630686 ER PT J AU Chiueh, CC Rauhala, P AF Chiueh, CC Rauhala, P TI The redox pathway of S-nitrosoglutathione, glutathione and nitric oxide in cell to neuron communications SO FREE RADICAL RESEARCH LA English DT Article; Proceedings Paper CT International Conference on Nitric Oxide CY APR 05-09, 1999 CL NATL UNIV SINGAPORE, SINGAPORE, SINGAPORE HO NATL UNIV SINGAPORE DE apoptosis; brain dopamine neurons; caspases; GSNO/GSH; HIV-1 protease; nitrosylation by nitric oxide ID CARDIOPLEGIC ISCHEMIC ARREST; SODIUM-NITROPRUSSIDE; NITROSO-GLUTATHIONE; LIPID-PEROXIDATION; HYDROXYL RADICALS; PEROXYL RADICALS; DOPAMINE NEURONS; OXIDATIVE STRESS; RAT CEREBELLUM; IN-VITRO AB Recent results demonstrated that S-nitrosoglutathione (GSNO) and nitric oxide ((NO)-N-.) protect brain dopamine neurons from hydroxyl radical ((OH)-O-.)-induced oxidative stress in vivo because they are potent antioxidants. GSNO and (NO)-N-. terminate oxidant stress in the brain by (i) inhibiting iron-stimulated hydroxyl radicals formation or the Fenton reaction, (ii) terminating lipid peroxidation, (iii) augmenting the antioxidative potency of glutathione (GSH), (iv) mediating neuroprotective action of brain-derived neurotrophin (BDNF), and (v) inhibiting cysteinyl proteases. In fact, GSNO - S-nitrosylated GSH - is approximately 100 times more potent than the classical antioxidant GSH. In addition, S-nitrosylation of cysteine residues by GSNO inactivates caspase-3 and HIV-I protease, and prevents apoptosis and neurotoxicity. GSNO-induced antiplatelet aggregation is also mediated by S-nitrosylation of clotting factor XIII. Thus the elucidation of chemical reactions involved in this GSNO pathway (GSH --> GS(.) + (NO)-N-. --> [GSNO] --> GSSG + (NO)-N-. --> GSH) is necessary for understanding the biology of (NO)-N-., especially its beneficial antioxidative and neuroprotective effects in the CNS. GSNO is most likely generated in the endothelial and astroglial cells during oxidative stress because these cells contain mM GSH and nitric oxide synthase. Furthermore, the transfer of GSH and (NO)-N-. to neurons via this GSNO pathway may facilitate cell to neuron communications, including not only the activation of guanylyl cyclase, but also the nitrosylation of iron complexes, iron containing enzymes, and cysteinyl proteases. GSNO annihilates free radicals and promotes neuroprotection via its c-GMP-independent nitrosylation actions. This putative pathway of GSNO/GSH/(NO)-N-. may provide new molecular insights for the redox cycling of GSH and GSSG in the CNS. C1 NIMH, Unit Neurodegenerat & Neuroprotect, Clin Sci Lab, NIH, Bethesda, MD 20892 USA. Univ Helsinki, Dept Pharmacol & Toxicol, FIN-00170 Helsinki, Finland. RP Chiueh, CC (reprint author), NIMH, Unit Neurodegenerat & Neuroprotect, Clin Sci Lab, NIH, Bldg 10,Room 3D41, Bethesda, MD 20892 USA. OI Rauhala, Pekka/0000-0003-2036-3522 NR 56 TC 73 Z9 75 U1 0 U2 5 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1071-5762 J9 FREE RADICAL RES JI Free Radic. Res. PY 1999 VL 31 IS 6 BP 641 EP 650 DI 10.1080/10715769900301211 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 263ZF UT WOS:000084154600019 PM 10630687 ER PT B AU Johnson, CA Sofer, A AF Johnson, CA Sofer, A GP IEEE COMP SOC IEEE COMP SOC TI A data-parallel algorithm for iterative tomographic image reconstruction SO FRONTIERS '99 - THE SEVENTH SYMPOSIUM ON THE FRONTIERS OF MASSIVELY PARALLEL COMPUTATION, PROCEEDINGS LA English DT Proceedings Paper CT 7th Symposium on the Frontiers of Massively Parallel Computation (Frontiers 99) CY FEB 21-25, 1999 CL ANNAPOLIS, MD SP IEEE Comp Soc Tech Comm Comp Architecture, USRA, CESDIS, NASA Goddard Space Flight Ctr ID EMISSION COMPUTED-TOMOGRAPHY; EM ALGORITHM; TRANSMISSION TOMOGRAPHY; OPTIMIZATION AB In the tomographic imaging problem, images are reconstructed from a set of measured projections. Iterative reconstruction methods are computationally intensive alternatives to the more traditional Fourier-based methods. Despite their high cost, the popularity of these methods is increasing because of the advantages they pose. Although numerous iterative methods have been proposed over the years, all of these methods can be shown to have a similar computational structure. This paper presents a parallel algorithm that we originally developed for performing the expectation maximization algorithm in emission tomography. This algorithm is capable of exploiting the sparsity and symmetries of the model in a computationally efficient manner Our parallelization scheme is based upon decomposition of the measurement-space vectors. We demonstrate that such a parallelization scheme is applicable to the vast majority of iterative reconstruction algorithms proposed to date. C1 NIH, Ctr Informat Technol, Bethesda, MD 20892 USA. RP Johnson, CA (reprint author), NIH, Ctr Informat Technol, Bldg 10, Bethesda, MD 20892 USA. NR 30 TC 7 Z9 9 U1 0 U2 0 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 USA BN 0-7695-0087-0 PY 1999 BP 126 EP 137 DI 10.1109/FMPC.1999.750592 PG 12 WC Computer Science, Hardware & Architecture; Computer Science, Theory & Methods SC Computer Science GA BM59P UT WOS:000079197000014 ER PT J AU Gorospe, M Wang, XT Holbrook, NJ AF Gorospe, M Wang, XT Holbrook, NJ TI Functional role of p21 during the cellular response to stress SO GENE EXPRESSION LA English DT Article DE Cip1; Waf1; Sdi1; cyclin-dependent kinase inhibitor; stress response; genotoxic stress; p53; growth arrest; apoptosis; gene induction ID CYCLIN-DEPENDENT KINASES; MESSENGER-RNA DEGRADATION; HUMAN CANCER-CELLS; P21(WAF1/CIP1) EXPRESSION; TRANSCRIPTIONAL ACTIVATION; P53-INDEPENDENT INDUCTION; LEUKEMIC-CELLS; GROWTH ARREST; APOPTOSIS; PROTEIN AB A wide range of stress stimuli, including oxidants, genotoxins, metabolic deficiencies, and irradiation, have been shown to induce expression of the cyclin-dependent kinase inhibitor p21. Among the best characterized media tors of p21 induction by stress is the tumor suppressor gene p53, which acts as a transcriptional activator to enhance the expression of the p21 gene. However, many other mechanisms involving transcriptional and posttranscriptional events have been found to participate in the elevation of p21 levels by stressful agents. The significance of the stress-mediated elevation in p21 expression is not fully understood, but it is clear that alterations in p21 expression impact on the ability of the cell to survive the insult. Although a large number of reports have demonstrated correlations between the expression of p21 and cellular outcome, this review will focus only on those reports where the role of p21 in a given stress paradigm has been investigated directly, through use of different strategies to manipulate p21 expression followed by assessment of the consequences of altered p21 expression on cell survival. The majority of such studies have revealed that p21 exerts a protective function against stress, and this property appears to rely, at least in part, on the ability of p21 to suppress cell proliferation. A few exceptions to this universal protective influence of p21 have also been observed and will be discussed. C1 NIA, Gerontol Res Ctr, Biol Chem Lab, NIH, Baltimore, MD 21224 USA. RP Holbrook, NJ (reprint author), NIA, Gerontol Res Ctr, Biol Chem Lab, NIH, Box 12,5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 61 TC 69 Z9 70 U1 0 U2 0 PU COGNIZANT COMMUNICATION CORP PI ELMSFORD PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA SN 1052-2166 J9 GENE EXPRESSION JI Gene Expr. PY 1999 VL 7 IS 4-6 BP 377 EP 385 PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 219XY UT WOS:000081634900017 PM 10440238 ER PT J AU Fornace, AJ Amundson, SA Bittner, M Myers, TG Meltzer, P Weinsten, JN Trent, J AF Fornace, AJ Amundson, SA Bittner, M Myers, TG Meltzer, P Weinsten, JN Trent, J TI The complexity of radiation stress responses: Analysis by informatics and functional genomics approaches SO GENE EXPRESSION LA English DT Article DE ionizing radiation; p53; microarray; genotoxic stress ID TUMOR-CELL-LINES; ANTICANCER DRUG SCREEN; NATIONAL-CANCER-INSTITUTE; CYCLE CHECKPOINT PATHWAY; GENE-EXPRESSION PATTERNS; DNA-DAMAGING AGENTS; GAMMA-RAY RESPONSE; INDUCED APOPTOSIS; MOLECULAR PHARMACOLOGY; IONIZING-RADIATION AB Molecular responses to genotoxic stress are complex and are mediated by a variety of regulatory pathways. One key element in cellular response is the stress gene transcription factor p53, which can regulate nearly 100 genes that have already been identified. Although p53 plays a central role in the cellular response to DNA-damaging agents such as ionizing radiation (IR), other pathways can also have important roles. One example is the transcriptional responses associated with IR-induced apoptosis, where induction of some genes is limited to p53 wild-type (wt) cells that also have the ability to undergo rapid apoptosis after irradiation. In contrast, other genes are triggered after IR in lines undergoing rapid apoptosis regardless of p53 status. From this and other examples, it is apparent that the pattern of stress gene expression is cell type specific in both primary and transformed lines. The premise will be developed that such differences in stress gene responsiveness can be employed as molecular markers using a combination of informatics and functional genomics approaches. An example is given using the panel of lines of the NCI anticancer drug screen where both the p53 status and sensitivity to a large collection of cytotoxic agents have been determined. The utility of cDNA microarray hybridization to measure IR-stress gene responses has recently been demonstrated and a large number of additional IR-stress genes have been identified. The responses of some of these genes to IR and other DNA-damaging agents varied widely in cell lines from different tissues of origin and different genetic backgrounds, highlighting the importance of cellular context to genotoxic stress responses; this also highlights the need for informatics approaches to discover and prioritize hypotheses regarding the importance of particular cellular factors. The aim of this review is to demonstrate the utility of combining an informatics approach with functional genomics in the study of stress responses. C1 NCI, Div Basic Sci, NIH, Bethesda, MD 20892 USA. NCI, Dev Therapeut Program, Bethesda, MD 20892 USA. NHGRI, NIH, Bethesda, MD USA. RP Fornace, AJ (reprint author), NCI, Div Basic Sci, NIH, Bldg 37,Room SC09,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA. RI Fornace, Albert/A-7407-2008 OI Fornace, Albert/0000-0001-9695-085X NR 74 TC 78 Z9 84 U1 0 U2 2 PU COGNIZANT COMMUNICATION CORP PI ELMSFORD PA 3 HARTSDALE ROAD, ELMSFORD, NY 10523-3701 USA SN 1052-2166 J9 GENE EXPRESSION JI Gene Expr. PY 1999 VL 7 IS 4-6 BP 387 EP 400 PG 14 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 219XY UT WOS:000081634900018 PM 10440239 ER PT J AU Bunnell, BA Kluge, KA Lee-Lin, SQ Byrne, ER Orlic, D Metzger, ME Agricola, BA Wersto, RP Bodine, DM Morgan, RA Donahue, RE AF Bunnell, BA Kluge, KA Lee-Lin, SQ Byrne, ER Orlic, D Metzger, ME Agricola, BA Wersto, RP Bodine, DM Morgan, RA Donahue, RE TI Transplantation of transduced nonhuman primate CD34(+) cells using a gibbon ape leukemia virus vector: restricted expression of the gibbon ape leukemia virus receptor to a subset of CD34(+) cells SO GENE THERAPY LA English DT Article DE hematopoietic cells; retroviral vector; retrovirus receptor; restricted expression ID HEMATOPOIETIC PROGENITOR CELLS; MEDIATED GENE-TRANSFER; HUMAN GLUCOCEREBROSIDASE GENE; PERIPHERAL-BLOOD LYMPHOCYTES; MARROW REPOPULATING CELLS; COLONY-STIMULATING FACTOR; CD4(+) T-LYMPHOCYTES; IN-VIVO EXPRESSION; BONE-MARROW; STEM-CELL AB The transduction efficiencies of immunoselected rhesus macaque (Macaca mulatta) CD34(+) cells and colony-forming progenitor cells based on polymerase chain reaction (PCR) analysis were comparable for an amphotropic Moloney murine leukemia virus (MLV) retroviral vector and a retroviral vector derived from the gibbon ape leukemia virus (GaLV) packaging cell line, PG13. On performing autologous transplantation studies using immunoselected CD34(+) cells transduced with the GaLV envelope (env) retroviral vector, less than 1% of peripheral blood (PB) contained provirus. This was true whether bone marrow (BM) or cytokine-mobilized PB immunoselected CD34(+) cells were reinfused. This level of marking was evident in two animals whose platelet counts never fell below 50 000/mu l and whose leukocyte counts had recovered by days 8 and 10 after having received 1.7 x 10(7) or greater of cytokine-mobilized CD34(+) PB cells/kg. Reverse transcriptase(RT)PCR analysis of CD34(+) subsets for both the GaLV and amphotropic receptor were performed. The expression of the GaLV receptor was determined to be restricted to CD34(+) Thy-1(+) cells, and both CD34(+) CD38(+) and CD34(+) CD38dim cells, while the amphotropic receptor was present on all CD34(+) cell subsets examined. Our findings suggest that, in rhesus macaques, PG13-derived retroviral vectors may only be able to transduce a subset of CD34(+) cells as only CD34(+) Thy-1(+) cells express the GaLV receptor. C1 NHLBI, Hematol Branch, NIH, Rockville, MD 20850 USA. NIH, Natl Human Genome Res Inst, Clin Gene Therapy Branch, Bethesda, MD 20892 USA. NIH, Natl Human Genome Res Inst, Lab Gene Transfer, Hematopoiesis Sect, Bethesda, MD 20892 USA. RP Donahue, RE (reprint author), NHLBI, Hematol Branch, NIH, 5 Res Court, Rockville, MD 20850 USA. NR 40 TC 11 Z9 11 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0969-7128 J9 GENE THER JI Gene Ther. PD JAN PY 1999 VL 6 IS 1 BP 48 EP 56 DI 10.1038/sj.gt.3300808 PG 9 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 159JQ UT WOS:000078169300021 PM 10341875 ER PT J AU Wildner, O Morris, JC Vahanian, NN Ford, H Ramsey, WJ Blaese, RM AF Wildner, O Morris, JC Vahanian, NN Ford, H Ramsey, WJ Blaese, RM TI Adenoviral vectors capable of replication improve the efficacy of HSVtk/GCV suicide gene therapy of cancer SO GENE THERAPY LA English DT Article DE gene therapy; replication-competent adenovirus; thymidine kinase; gancliclovir; melanoma; cervical cancer ID VIRUS-THYMIDINE KINASE; B SURFACE-ANTIGEN; RETROVIRAL VECTORS; HUMAN-MELANOMA; MOLT-4 CELLS; E1A ONCOGENE; BRAIN-TUMORS; IN-VIVO; DNA; EXPRESSION AB A major obstacle to the success of gene therapy strategies that directly target cancer cells is the poor vector distribution within solid tumors. To address this problem, we developed an Elb 55 kDa attenuated, replication-competent adenovirus (Ad.TKRC) which expresses the herpes simplex-l thymidine kinase (HSVtk) gene to sensitize tumors to ganciclovir (GCV). Efficacy of this combined strategy was tested in nude mice with subcutaneous human A375 melanoma and ME180 cervical carcinomas. Intratumoral injection of a replication-defective adenoviral vector expressing HSVtk (Ad.TK) followed by GCV treatment resulted in doubling of the survival time of mice bearing A375 tumors and 20% long-term survival of mice with ME180 tumors. Treatment of tumors with Ad.TKRC without GCV resulted in a similar antitumor effect, confirming that the replicating vector has an oncolytic effect. When GCV was initiated 3 days after Ad.TKRC injection, survival of mice with each tumor type was greatly prolonged, with 60% of animals with ME180 tumors surviving for over 160 days. These results confirm that both the oncolysis caused by a replicating virus and suicide/prodrug gene therapy with HSVtk/GCV have potent antitumor effects. When combined, these two approaches are complementary resulting in a significantly improved treatment outcome. C1 NIH, Natl Human Genome Res Inst, Clin Gene Therapy Branch, Natl Canc Inst, Bethesda, MD 20892 USA. NIH, Lab Med Chem, Div Bas Sci, Natl Canc Inst, Bethesda, MD USA. RP Wildner, O (reprint author), NIH, Natl Human Genome Res Inst, Clin Gene Therapy Branch, Natl Canc Inst, 10 Ctr Dr,Bldg 10,Room 10C103, Bethesda, MD 20892 USA. NR 43 TC 138 Z9 140 U1 0 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE RG21 6XS, HAMPSHIRE, ENGLAND SN 0969-7128 J9 GENE THER JI Gene Ther. PD JAN PY 1999 VL 6 IS 1 BP 57 EP 62 DI 10.1038/sj.gt.3300810 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 159JQ UT WOS:000078169300008 PM 10341876 ER PT J AU Nihei, N Ohta, S Kuramochi, H Kugoh, H Oshimura, M Barrett, JC Isaacs, JT Igarashi, T Ito, H Masai, M Ichikawa, Y Ichikawa, T AF Nihei, N Ohta, S Kuramochi, H Kugoh, H Oshimura, M Barrett, JC Isaacs, JT Igarashi, T Ito, H Masai, M Ichikawa, Y Ichikawa, T TI Metastasis suppressor gene(s) for rat prostate cancer on the long arm of human chromosome 7 SO GENES CHROMOSOMES & CANCER LA English DT Article ID PRIMARY BREAST-CANCER; MAMMARY-CANCER; FREQUENT LOSS; ALLELIC LOSS; HETEROZYGOSITY; PROGRESSION; KAI1; HUMAN-CHROMOSOME-8; LOCALIZATION; EXPRESSION AB Allelotype analyses of human prostate cancer indicate that allelic losses on human chromosome arms 7q, 8p, 10q, 13q, 16q, 17q, and 18q are observed frequently. For the study of the possible biological significance of the frequently observed deletions on chromosome arm 7q in human prostate cancer, human chromosome 7 was introduced into highly metastatic rat prostate cancer cells by use of a microcell-mediated chromosome transfer technique. The introduction of human chromosome 7 resulted in the suppression of metastatic ability of the microcell hybrids, whereas no suppression of tumorigenicity was observed. To identify the portion of chromosome 7 containing the metastasis-suppressive function gene, the derivative chromosome 7 that was generated with the initial transfer was retransferred into rat prostate cancer cells. Human chromosome 7-containing rat prostate cancer cells could be used as the donor cells, because rodent cells produced a sufficient number of microcells with colchicine treatment. Cytogenetic and molecular analyses of these clones demonstrated that loss of segments on 7q was related to the reexpression of the metastatic phenotype. These results show that human 7q contains a metastasis suppressor gene or genes for rat prostate cancer. The findings also suggest that this gene may play an important role in the progression of human prostate cancer. Genes Chromosomes Cancer 24:1-8, 1999. (C) 1999 Wiley-Liss, Inc. C1 Teikyo Univ, Sch Med, Dept Urol, Ichihara, Chiba 2990111, Japan. Tottori Univ, Sch Med, Dept Mol & Cell Genet, Tottori, Japan. NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. Johns Hopkins Univ, Sch Med, Dept Urol, Ctr Oncol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, James Buchanan Brady Urol Inst, Baltimore, MD USA. Teikyo Univ, Ichihara Hosp, Sch Med, Dept Urol, Chiba, Japan. RP Ichikawa, T (reprint author), Teikyo Univ, Sch Med, Dept Urol, 3426-3 Anesaki, Ichihara, Chiba 2990111, Japan. NR 28 TC 22 Z9 22 U1 0 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD JAN PY 1999 VL 24 IS 1 BP 1 EP 8 DI 10.1002/(SICI)1098-2264(199901)24:1<1::AID-GCC1>3.0.CO;2-A PG 8 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA 142UN UT WOS:000077218900001 PM 9892102 ER PT J AU Vidgren, V Varis, A Kokkola, A Monni, O Puolakkainen, P Nordling, S Forozan, F Kallioniemi, A Vakkari, ML Kivilaakso, E Knuutila, S AF Vidgren, V Varis, A Kokkola, A Monni, O Puolakkainen, P Nordling, S Forozan, F Kallioniemi, A Vakkari, ML Kivilaakso, E Knuutila, S TI Concomitant gastrin and ERBB2 gene amplifications at 7q12-q21 in the intestinal type of gastric cancer SO GENES CHROMOSOMES & CANCER LA English DT Article ID HYBRIDIZATION; CARCINOMA; OVEREXPRESSION; SURVIVAL; AMPLICON AB Our recent studies using comparative genomic hybridization showed that gain or amplification at the 17q12-q21 region is very common in the intestinal type of gastric cancer. Here, we describe a fluorescence in situ hybridization study with gastrin (GAS)-specific and ERBB2-specific probes on ten specimens of gastric carcinoma that, by using comparative genomic hybridization, showed I) DNA copy number gain or amplification at 17q12-q21,a region known to harbor the GAS and ERBB2 genes (four cases); 2) gain of the entire chromosome 17 (three cases); or 3) normal copy number of chromosome 17 (three cases). GAS and ERBB2 protein expression was studied by Western immunoblotting from gastric canter cell lines with or without gain at 17q12-q21 as well as a breast cancer cell line with ERBB2 amplification. Our results showed that simultaneous amplification of both GAS and ERBB2 was four- to ninefold in the tumors with the 17q12-q21 amplification. Both genes were amplified in the same nuclei, and the hybridization signals were localized to the same region of the nucleus. Overexpression of GAS and ERBB2 was observed by Western immunoblotting only in the gastric cancer cell line with gain at 17q12-q21. The ERBB2 amplification is also a recurrent change in breast cancer. To investigate whether the GAS amplification is unique in gastric cancer, Fluorescence in situ hybridization analysis was performed on 40 breast cancer cell lines. The ERBB2 amplification was observed in 11 cell lines, but none of the lines showed the GAS amplification. This indicates that the formation of an amplicon, in which both the GAS and the ERBB2 genes are amplified, might be unique in gastric cancer, especially in its intestinal type, and that simultaneous amplification of both genes is important to the tumorigenesis of intestinal gastric cancer. We demonstrate here for the first time that a gene of a physiological hormone is amplified in tumors that originate from cells that normally secrete the hormone. Genes Chromosomes Cancer 24:24-29, 1999. (C) 1999 Wiley-Liss, Inc. C1 Univ Helsinki, Cent Hosp, Mol Genet Lab, FIN-00029 Helsinki, Finland. Univ Helsinki, Dept Med Genet, Haartman Inst, Helsinki, Finland. Univ Helsinki, Cent Hosp, Dept Surg 2, FIN-00029 Helsinki, Finland. Univ Helsinki, Haartman Inst, Dept Pathol, Helsinki, Finland. NIH, Natl Human Genome Res Inst, Canc Genet Lab, Bethesda, MD USA. RP Knuutila, S (reprint author), Univ Helsinki, Cent Hosp, Mol Genet Lab, POB 404 Haartmaninkatu 3, FIN-00029 Helsinki, Finland. OI Kallioniemi, Anne/0000-0003-3552-8158 NR 18 TC 36 Z9 37 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 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD JAN PY 1999 VL 24 IS 1 BP 24 EP 29 DI 10.1002/(SICI)1098-2264(199901)24:1<24::AID-GCC4>3.0.CO;2-H PG 6 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA 142UN UT WOS:000077218900004 PM 9892105 ER PT J AU Tirkkonen, M Kainu, T Loman, N Johannsson, OT Olsson, H Barkardottir, RB Kallioniemi, OP Borg, A AF Tirkkonen, M Kainu, T Loman, N Johannsson, OT Olsson, H Barkardottir, RB Kallioniemi, OP Borg, A TI Somatic genetic alterations in BRCA2-associated and sporadic male breast cancer SO GENES CHROMOSOMES & CANCER LA English DT Article ID COMPARATIVE GENOMIC HYBRIDIZATION; SOLID TUMORS; RISK-FACTORS; BRCA2; MUTATIONS; FAMILIES; LINE AB The genetic changes underlying the development and progression of male breast cancer are poorly understood. Germline BRCA2 mutations account: for a significant pan of male breast cancer, but the majority of patients lack a known inherited predisposition, We recently demonstrated that the progression of breast cancer in female carriers of a germline BRCA1 or BRCA2 mutation follows specific genetic pathways, distinct from each other and from sporadic breast cancer. In the present study, we performed a genome-wide survey by comparative genomic hybridization (CGH) of somatic generic aberrations in 26 male breast cancers, including five tumors from BRCA2 mutation carriers. BRCA2 tumors exhibited a significantly higher number of chromosomal aberrations than sporadic tumors. The most common alterations in sporadic male breast cancer were +1q (38%), +8q (33%), + 17q (33%), -13q (29%), and -8p (24%). In tumors from BRCA2 mutation carriers. the five most common genetic changes were +8q (100%), +20q (100%), +17q +80%), -13q (80%), and -6q (60%). The CGH results in these two groups of male breast cancers are almost identical to those identified in the corresponding sporadic and BRCA2-associated female breast cancers, The results suggest that despite substantial hormonal differences between females and males, similar genetic changes are selected For during tumor progression. Furthermore, the presence of a highly penetrant germline BRCA2 mutation apparently leads to a characteristic somatic tumor progression pathway, again shared between affected male and female mutation carriers. Genes Chromosomes Cancer 24:56-61, 1999. (C) 1999 Wiley-Liss, Inc C1 Univ Lund Hosp, Dept Oncol, S-22185 Lund, Sweden. Tampere Univ, FIN-33101 Tampere, Finland. Tampere Univ Hosp, Inst Med Technol, Canc Genet Lab, Tampere, Finland. NIH, Natl Human Genome Res Inst, Canc Genet Lab, Bethesda, MD USA. Univ Hosp, Dept Pathol, Cell Biol Lab, Reykjavik, Iceland. RP Borg, A (reprint author), Univ Lund Hosp, Dept Oncol, S-22185 Lund, Sweden. EM ake.borg@onk.lu.se 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 26 TC 45 Z9 45 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 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD JAN PY 1999 VL 24 IS 1 BP 56 EP 61 DI 10.1002/(SICI)1098-2264(199901)24:1<56::AID-GCC8>3.0.CO;2-X PG 6 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA 142UN UT WOS:000077218900008 PM 9892109 ER PT J AU Vermeesch, JR Petit, P Dutra, A Schrock, E Ried, T Fryns, JP AF Vermeesch, JR Petit, P Dutra, A Schrock, E Ried, T Fryns, JP TI A mosaic extra ring chromosome 4 in a female patient with postnatal overgrowth SO GENETIC COUNSELING LA English DT Letter ID MARKER CHROMOSOMES; FISH C1 Katholieke Univ Leuven VIB, Ctr Human Genet, Louvain, Belgium. Katholieke Univ Leuven Hosp, Ctr Human Genet, Louvain, Belgium. Natl Human Genome Res Inst, NIH, Bethesda, MD USA. NR 6 TC 4 Z9 4 U1 0 U2 0 PU MEDECINE ET HYGIENE PI GENEVA 4 PA 78 AVE ROSERALE, 1211 GENEVA 4, SWITZERLAND SN 1015-8146 J9 GENET COUNSEL JI Genet. Couns. PY 1999 VL 10 IS 2 BP 195 EP 196 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medical Ethics; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Medical Ethics; Research & Experimental Medicine GA 214NY UT WOS:000081335100014 PM 10422016 ER PT J AU Bensen, JT Liese, AD Rushing, JT Province, M Folsom, AR Rich, SS Higgins, M AF Bensen, JT Liese, AD Rushing, JT Province, M Folsom, AR Rich, SS Higgins, M TI Accuracy of proband reported family history: The NHLBI Family Heart Study (FHS) SO GENETIC EPIDEMIOLOGY LA English DT Article DE coronary heart disease; family history; diabetes; hypertension; asthma; sensitivity; specificity ID INFORMATION; RESPONDENTS; DISEASE; HEALTH AB Proband-reported family histories are widely used in research and counseling, yet little is known about the validity of family history reporting. The Family Heart Study (FHS), a population-based study of familial cardiovascular disease, gathered family history information from 3,020 middle-aged probands in four U.S. communities. Probands reported on the history of coronary heart disease (CHD), diabetes, hypertension, and asthma among a total of 10,316 living relatives (9,186 siblings, 1,130 parents) and 2,685 spouses. Questionnaires were returned by 6,672 siblings, 901 parents, and 2,347 spouses, yielding response rates of 73, 79, and 87%, respectively. Utilizing the relatives' self-report as the standard, sensitivity of the proband report on their spouse, parent, and sibling was 87, 85, and 81% for CHD, 83, 87, and 72% for diabetes, 77, 76, and 56% for hypertension, and 66, 53, and 39% for asthma, respectively. Most specificity values were above 90%. Analyses using generalized estimating equations (GEE) were performed to evaluate differences in proband accuracy based on the proband's age, gender, disease state, center, and ethnicity. In multi-variate models, age, gender, and disease status were significantly associated with the accuracy of proband's report of sibling disease history, but had little effect on the accuracy of their report on spouses or parents. In general, older probands were significantly less accurate reporters of disease than younger probands. These results demonstrate that CHD family history can be captured effectively based on proband reports, but suggest that additional family contacts may be helpful when working with older probands or with chronic diseases that have few recognized medical events or procedures. (C) 1999 Wiley-Liss, Inc. C1 Wake Forest Univ, Bowman Gray Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27157 USA. Univ Muenster, Inst Epidemiol & Social Med, Munster, Germany. Washington Univ, Dept Biostat, St Louis, MO 63130 USA. Univ Minnesota, Div Epidemiol, Minneapolis, MN 55455 USA. NHLBI, NIH, Bethesda, MD 20892 USA. RP Bensen, JT (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Dept Publ Hlth Sci, Med Ctr Blvd, Winston Salem, NC 27157 USA. FU NHLBI NIH HHS [N01-HC-25104, N01-HC-25105, N01-HC-25106] NR 20 TC 112 Z9 112 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 IS 2 BP 141 EP 150 DI 10.1002/(SICI)1098-2272(1999)17:2<141::AID-GEPI4>3.0.CO;2-Q PG 10 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 211XD UT WOS:000081186400004 PM 10414557 ER PT J AU Goldin, LR Chase, GA Wilson, AF AF Goldin, LR Chase, GA Wilson, AF TI Regional inference with averaged P values increases the power to detect linkage SO GENETIC EPIDEMIOLOGY LA English DT Article DE regional inference; linkage detection; genome screening; sib-pair tests ID TRAITS; DISEASE; GENES; SCANS AB Controversy exists with respect to the choice of an appropriate critical value when testing for linkage in a genomic screen. A number of critical values have been proposed for single-locus and multi-locus linkage analyses. In this study, criteria based on multiple single-locus analyses (i.e., regional test criteria) are evaluated using simulation methods for three different map densities. Tests based on single loci, multiple consecutive single loci, and moving averages of consecutive single loci are considered. Appropriate critical values are determined based on results from simulations under the null hypothesis of no linkage. The power of each "regional test" was compared to the power of a single-locus test. Results suggest that the best power was found when averaging P values over an interval size of 9-15 cM, and that testing the average of P values from two consecutive loci is superior to testing each single locus separately. The increase in power ranged from 7-29% over the simulations considered. Genet. Epidemiol. 17:157-164, 1999. (C) 1999 Wiley-Liss, Inc. C1 NCI, Genet Epidemiol Branch, DCEG, NIH, Bethesda, MD 20892 USA. Henry Ford Hlth Syst, Dept Biostat & Res Epidemiol, Detroit, MI USA. Natl Human Genome Res Inst, Inherited Dis Res Branch, Genometr Sect, NIH, Baltimore, MD USA. RP Goldin, LR (reprint author), NCI, Genet Epidemiol Branch, DCEG, NIH, 6120 Execut Blvd,MSC 7236, Bethesda, MD 20892 USA. RI Wilson, Alexander/C-2320-2009 FU NCRR NIH HHS [1P41 RR03655] NR 12 TC 13 Z9 14 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 IS 3 BP 157 EP 164 DI 10.1002/(SICI)1098-2272(1999)17:3<157::AID-GEPI1>3.0.CO;2-P PG 8 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 226XT UT WOS:000082049000001 PM 10446463 ER PT J AU Anderson, JL Hauser, ER Martin, ER Scott, WK Ashley-Koch, A Kim, KJ Monks, SA Haynes, CS Speer, MC Pericak-Vance, MA AF Anderson, JL Hauser, ER Martin, ER Scott, WK Ashley-Koch, A Kim, KJ Monks, SA Haynes, CS Speer, MC Pericak-Vance, MA TI Complete genomic screen for disease susceptibility loci in nuclear families SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE genexenvironment interaction; linkage disequilibrium; maximum lod score; sibship disequilibrium test; T-sp ID AFFECTED RELATIVE PAIRS; LINKAGE STRATEGIES; TRAITS AB We performed genome-wide model dependent and independent analyses on a simulated data set of 400 families segregating for a rare disorder. Regions on chromosomes 1, 3, and 5 were consistently indicated across the various analyses performed. Follow-up analyses included stratification for locus heterogeneity and clinical phenotype and studies of gene x gene and gene x environment interaction. The region around D1G024 was most notable, showing strong association and linkage with the trait. We also identified regions D3G043-46 and D5G037-39 by strong linkage and association findings and region DIG001-09 by linkage analysis. A complex statistical interaction was suggested between D1G024, D3G046 and environmental factor 1. This report suggests that traditional methods of analysis can be implemented to analyze and describe the mechanisms that may underlie the more complex genetic disorders. (C) 1999 Wiley-Liss, Inc. C1 Duke Univ, Med Ctr, Dept Med, Med Genet Sect,Ctr Human Genet, Durham, NC 27707 USA. NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. N Carolina State Univ, Dept Stat, Program Stat Genet, Raleigh, NC 27695 USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Dept Med, Med Genet Sect,Ctr Human Genet, Box 3445, Durham, NC 27707 USA. RI Scott, William/A-7593-2009 FU NICHD NIH HHS [HD33400]; NINDS NIH HHS [NS26630, NS36768] NR 12 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S473 EP S478 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800074 PM 10597478 ER PT J AU Badner, JA Goldin, LR AF Badner, JA Goldin, LR TI Meta-analysis of linkage studies SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE genome-wide probabilities; linkage analysis ID TRAITS AB Lander and Kruglyak [1995] gave guidelines for interpreting linkage results based on estimating how often a particular threshold for significance would be exceeded by chance in a single genome scan. What is unknown is how often two or more genome scans would exceed a particular threshold within the same region. We develop theoretical estimates of these values and compare these with the empirical estimates derived from the GAW11 data. For single-point analysis, the theoretical estimates predict the empirical estimates. For multipoint analysis, the theoretical values overestimate what is observed. For both single point and multipoint, modest p-values within a single genome scan may give highly significant results when replicated in the same region in other scans. (C) 1999 Wiley-Liss, Inc. C1 NIMH, NIH, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. RP Badner, JA (reprint author), Univ Chicago, Dept Psychiat, 5841 S Maryland Ave,MC3077, Chicago, IL 60637 USA. FU NCRR NIH HHS [RR03655] NR 3 TC 7 Z9 7 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S485 EP S490 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800076 PM 10597480 ER PT J AU Bergen, AW Korczak, JF Weissbecker, KA Goldstein, AM AF Bergen, AW Korczak, JF Weissbecker, KA Goldstein, AM TI A genome-wide search for loci contributing to smoking and alcoholism SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE genome scan ID DEPRESSION AB Using the Collaborative Study on the Genetics of Alcoholism (COGA) data, we performed a sib-pair linkage analysis of two smoking-related traits and one alcoholism phenotype. The first trait, EVRNVR, was a dichotomous one we constructed based on epidemiological definitions of smoking. The second trait, PKYRS, used the quantitative pack-year history provided, and the third trait was the COGA alcoholism classification, ALDX1. There was some evidence for linkage of the EVRNVR trait to regions on chromosomes 6, 9, and 14. Smaller numbers of loci provided nominal evidence for linkage to PKYRS, although some candidate gene regions were identified. The number of loci identified using EVRNVR suggests that a threshold-based phenotype may better identify loci affecting smoking history. Approximately one-third of the loci that showed evidence for linkage to EVRNVR at a nominal significance level (p < 0.01) also showed evidence for linkage to ALDX1. Some of these regions may represent loci increasing vulnerability to both smoking and alcoholism. (C) 1999 Wiley-Liss, Inc. C1 Natl Canc Inst, GEB, DCEG, Rockville, MD 20852 USA. Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, Washington, DC 20007 USA. Tulane Univ, Med Ctr, Dept Psychiat & Neurol, New Orleans, LA USA. Tulane Univ, Med Ctr, Hayward Genet Program, New Orleans, LA USA. RP Bergen, AW (reprint author), Natl Canc Inst, GEB, DCEG, 6120 Execut Blvd, Rockville, MD 20852 USA. FU NCRR NIH HHS [RR03655] NR 10 TC 76 Z9 77 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S55 EP S60 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800008 PM 10597412 ER PT J AU Chase, GA King, TM Oja-Tebbe, N Rybicki, BA Goldin, LR AF Chase, GA King, TM Oja-Tebbe, N Rybicki, BA Goldin, LR TI Assessment of estimation procedures for risk and onset hazard with dependent data SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE candidate genes; robustness; survival analysis ID SURVIVAL ANALYSIS AB Analysis of the role of candidate genes its risk factors for age-dependent hereditary conditions often ignores the importance of dependence among sibships or other family clusters for age of onset. We examined the performance of several methods of survival analysis with dependent data using Collaborative Study on the Genetics of Alcoholism families as submitted for GAW 11. Additionally, an arbitrary truncation of cluster size was performed to explore the potential impact of heterogeneity of family size on the resulting inferences concerning the role of candidate genes. Our results showed substantial differences in attribution of risk to candidate genes according to whether the method utilized allowed for dependence in onset age and according to whether the sample was truncated or arbitrarily stratified. Further work needs to be done to clarify the importance of properly accounting for dependent data in age-dependent phenotypes and in integrating these methods into widely used genetic analysis computer programs. (C) 1999 Wiley-Liss, Inc. C1 Henry Ford Hlth Sci Ctr, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USA. Univ Texas, MD Anderson Canc Inst, Dept Epidemiol, Houston, TX 77030 USA. NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Chase, GA (reprint author), Henry Ford Hlth Sci Ctr, Dept Biostat & Res Epidemiol, 1 Ford Pl,Suite 3E, Detroit, MI 48202 USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S97 EP S102 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800015 PM 10597419 ER PT J AU Goldin, LR Chase, GA AF Goldin, LR Chase, GA TI Comparison of two linkage inference procedures for genes related to the P300 component of the event related potential SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE alcoholism; regional inference; sib-pair linkage ID QUANTITATIVE TRAIT AB Our goal was to detect genes contributing to the P300 component of the event related potential (ERP). We found that all of the ERP traits were highly correlated. Most of them distinguished alcoholics from nonalcoholics. To have one summary variable for the ERP traits, we calculated the first principal component(PRIN1). After adjusting for age and sex, we screened for linkage of PRIN1 to all of the markers using the two-point Haseman-Elston sib-pair test. We compared results obtained from computing a moving average of two-point p-values ("regional" inference) in an approximately 10 cM region with those obtained from single, two-point tests. Different "suggestive" and "significant" linkage regions were found using the two methods. Based on the regional method, areas on chromosomes 2 and 5 should be followed up in future studies. (C) 1999 Wiley-Liss, Inc. C1 NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA. Henry Ford Hlth Syst, Dept Biostat & Res Epidemiol, Detroit, MI USA. RP Goldin, LR (reprint author), DCEG, Genet Epidemiol Branch, NCI, 6120 Execut Blvd,Room 7008,MSC 7236, Bethesda, MD 20892 USA. FU NCRR NIH HHS [1 P41 RR03655] NR 9 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S163 EP S167 PG 5 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800026 PM 10597430 ER PT J AU Juo, SHH Pugh, EW Baffoe-Bonnie, A Kingman, A Sorant, AJM Klein, AP O'Neill, J Mathias, RA Wilson, AF Bailey-Wilson, JE AF Juo, SHH Pugh, EW Baffoe-Bonnie, A Kingman, A Sorant, AJM Klein, AP O'Neill, J Mathias, RA Wilson, AF Bailey-Wilson, JE TI Possible linkage of alcoholism, monoamine oxidase activity and p300 amplitude to markers on chromosome 12q24 SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE association; genetics; MAO ID RISK; ALLELE; TRAITS; GENES; LOCUS AB Multipoint linkage analysis was used to screen for evidence of linkage between alcoholism and five alcoholism-related quantitative traits. The results suggest that a susceptibility locus that influences monoamine oxidase activity and P300 amplitude at the Pt lead, and increases the risk of alcohol dependence may be linked to markers in the 12q24 region. Furthermore, the susceptibility for alcoholism may be associated with allele 3 (allele size 144) of D12S392. (C) 1999 Wiley-Liss, Inc. C1 Natl Human Genome Res Inst, Triad Technol Ctr, NIH, Baltimore, MD 21224 USA. Rockefeller Univ, New York, NY 10021 USA. Johns Hopkins Univ, Sch Med, Ctr Inherited Dis Res, Baltimore, MD USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. NIDR, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Baltimore, MD USA. RP Bailey-Wilson, JE (reprint author), Natl Human Genome Res Inst, Triad Technol Ctr, NIH, Suite 2000,333 Cassell Dr, Baltimore, MD 21224 USA. RI Juo, Suh-Hang/A-1765-2010; Wilson, Alexander/C-2320-2009; Juo, Suh-Hang/C-9545-2009 FU NCRR NIH HHS [RR03655] NR 15 TC 2 Z9 2 U1 2 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S193 EP S198 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800031 PM 10597435 ER PT J AU Korczak, JF Bergen, AW Goldstein, AM Weissbecker, KA AF Korczak, JF Bergen, AW Goldstein, AM Weissbecker, KA TI Sib-pair linkage analyses of alcoholism: Dichotomous and quantitative measures SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE COGA; genome scan; nonparametric linkage analysis ID DEPENDENCE; FAMILY AB We hypothesized that a quantitative alcoholism trait would have greater power than the Collaborative Study on the Genetics of Alcoholism (COGA) dichotomous alcoholism traits, ALDX1 and ALDX2, to detect putative alcoholism loci. To test this, we performed nonparametric sib-pair linkage analysis to screen 285 polymorphic autosomal markers for evidence of linkage to ALDX1, ALDX2, and a quantitative trait, QUANT, defined from the 11 COGA latent class variables. We also examined the effects on the analyses of including covariates (sex, age, and pack-years of smoking) and of transforming QUANT (log and square root). ALDX1 and ALDX2 showed the greatest evidence for linkage to markers on chromosome 1, by both the affected sib-pair and the Haseman-Elston tests. Regions of interest were also identified on chromosomes 4, 8, 16, and 17. QUANT showed little evidence for linkage to any chromosomal region, having no more significant results than were expected by chance. Including covariates or transforming QUANT had little effect on the analyses. A quantitative trait based on all 37 latent class variables, with each variable appropriately weighted, may have had more power than QUANT to detect genomic regions of relevance to alcoholism. (C) 1999 Wiley-Liss, Inc. C1 Georgetown Univ, Med Ctr, Lombardi Canc Ctr, Washington, DC 20007 USA. NCI, Genet Epidemiol Branch, Bethesda, MD 20892 USA. Tulane Univ, Med Ctr, Dept Psychiat & Neurol, New Orleans, LA USA. Tulane Univ, Med Ctr, Hayward Gent Program, New Orleans, LA USA. RP Korczak, JF (reprint author), Georgetown Univ, Med Ctr, Lombardi Canc Ctr, 2233 Wisconsin Ave NW,Suite 317, Washington, DC 20007 USA. FU NCRR NIH HHS [RR03655] NR 8 TC 0 Z9 0 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S205 EP S210 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800033 PM 10597437 ER PT J AU Mandal, DM Sorant, AJM Pugh, EW Marcus, SE Klein, AP Mathias, RA O'Neill, J Temiyakarn, LF Wilson, AF Bailey-Wilson, JE AF Mandal, DM Sorant, AJM Pugh, EW Marcus, SE Klein, AP Mathias, RA O'Neill, J Temiyakarn, LF Wilson, AF Bailey-Wilson, JE TI Environmental covariates: Effects on the power of sib-pair linkage methods SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE affected-sib-pair test; complex traits; sib-pair linkage test AB The effect of inclusion of environmental risk factors on the power of sib-pair linkage methods was tested for a qualitative trait. It was found that inclusion of an environmental variable did not increase the power of the Haseman-Elston (H-E) sib-pair nonparametric linkage analysis test. However, a significant increase in power was observed for both the H-E and affected-sib-pair tests, even in small samples, when persons unexposed to the environmental risk factor were coded as unknown. (C) 1999 Wiley-Liss, Inc. C1 NHGRI, NIH, Trad Technol Ctr, Baltimore, MD 21224 USA. Louisiana State Univ, Med Ctr, Dept Med, Sect Genet & Geriatr, New Orleans, LA 70112 USA. Johns Hopkins Univ, Sch Med, Ctr Inherited Dis Res, Baltimore, MD USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Baltimore, MD USA. RP Bailey-Wilson, JE (reprint author), NHGRI, NIH, Trad Technol Ctr, Suite 2000,333 Cassell Dr, Baltimore, MD 21224 USA. RI Wilson, Alexander/C-2320-2009 FU NCRR NIH HHS [RR03655] NR 8 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S643 EP S648 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800103 PM 10597507 ER PT J AU Mitchell, BD Ghosh, S Watanabe, RM Slifer, SH Hsueh, WC Birznieks, G AF Mitchell, BD Ghosh, S Watanabe, RM Slifer, SH Hsueh, WC Birznieks, G TI Identifying influential individuals in linkage analysis: Application to a quantitative trait locus detected in the COGA data SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE alcoholism; influence plot; outliers AB Once linkage is detected to a quantitative trait locus (QTL), the next step towards localizing the gene involved may be to identify those families, or individuals, in whom the putative mutations are segregating. In this paper, we describe a jackknife procedure for identifying individuals (and families) who contribute disproportionately to the linkage. Following initial detection of linkage to a QTL, the strategy involves sequentially removing each individual (or each family) from the analysis and recomputing the lod score associated with the linked region using data from all remaining subjects (or families). This procedure can be used to determine if particular observations have substantial impact on evidence for linkage. Identification of such observations may provide insights for further efforts to localize the QTL. (C) 1999 Wiley-Liss, Inc. C1 SW Fdn Biomed Res, Dept Genet, San Antonio, TX USA. Natl Human Genome Res Inst, Bethesda, MD USA. Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA. RP Mitchell, BD (reprint author), SW Fdn Biomed Res, Dept Genet, POB 760549, San Antonio, TX USA. FU NHLBI NIH HHS [P01-HL45522]; NIAMS NIH HHS [R01-AR43351] NR 2 TC 2 Z9 2 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S259 EP S264 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800042 PM 10597446 ER PT J AU Monks, SA Martin, ER Umbach, DM Kaplan, NL AF Monks, SA Martin, ER Umbach, DM Kaplan, NL TI Two tests of association for a susceptibility locus for families of variable size: An example using two sampling strategies SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE family based; linkage disequilibrium; sibship; transmission/disequilibrium ID TRANSMISSION/DISEQUILIBRIUM TEST; NUCLEAR FAMILIES; LINKAGE; TDT AB A two-stage approach was used to analyze Problem 2 simulated data from Genetic Analysis Workshop 11. In the first stage, we tested for linkage with the Haseman-Elston test in SIBPAL. Markers that were significant in the first stage were followed up with two types of association tests. These association tests differ in the type of family information used: 1) parental transmissions to affected children or 2) differences in marker allele frequencies between affected and unaffected siblings. We also explored how the conclusions changed when different sampling strategies were used. Of particular interest was whether the entire data set should be used to test for both linkage and association or whether the data set should be halved to allow for replication of the initial association results. (C) 1999 Wiley-Liss, Inc. C1 NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA. N Carolina State Univ, Dept Stat, Program Stat Genet, Raleigh, NC 27695 USA. Duke Univ, Med Ctr, Dept Med, Med Genet Sect, Durham, NC 27710 USA. RP Monks, SA (reprint author), NIEHS, Biostat Branch, POB 12233, Res Triangle Pk, NC 27709 USA. FU NCRR NIH HHS [1 P41 RR03655]; NIGMS NIH HHS [GM45344] NR 9 TC 1 Z9 1 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S655 EP S660 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800105 PM 10597509 ER PT J AU Watanabe, RM Ghosh, S Birznieks, G Duren, WL Mitchell, BD AF Watanabe, RM Ghosh, S Birznieks, G Duren, WL Mitchell, BD TI Application of an ordered subset analysis approach to the genetics of alcoholism SO GENETIC EPIDEMIOLOGY LA English DT Article; Proceedings Paper CT 11th Genetic Analysis Workshop on Analysis of Genetic and Environmental Factors in Common Diseases CY SEP 08-10, 1998 CL ARCACHON, FRANCE SP INSERM, Commiss Europeenne, Assoc Francaise Myopathiers, Inst Rhone Poulence Rorer France, Conseil Reg Aquitaine DE linkage analysis; permutation tests; quantitative traits; subsetting ID TRAITS; MODELS; GENES AB For complex diseases, underlying etiologic heterogeneity may reduce power to detect linkage. Thus, methods to identify more homogeneous subgroups within a given sample in a linkage study may improve detection of putative susceptibility loci. In this study we describe an ordered subsetting approach that utilizes disease-related quantitative trait data to complement traditional linkage analysis. This approach uses family-based lod scores derived from the initial genome screen and a family-based descriptor of the trait of interest. The goal of the approach is to identify more homogeneous subgroups of the data by ranking families based on their quantitative trait data. Permutation testing is used to assess statistical significance. This approach can be adapted to a variety of linkage methods and may provide a means to dissect some of the underlying heterogeneity in complex disease genetics. (C) 1999 Wiley-Liss, Inc. C1 Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA. Natl Human Genome Res Inst, Genet & Mol Biol Branch, NIH, Bethesda, MD USA. SW Fdn Biomed Res, Dept Genet, San Antonio, TX USA. RP Watanabe, RM (reprint author), Univ Michigan, Sch Publ Hlth, Dept Biostat, 1420 Washington Hts, Ann Arbor, MI 48109 USA. FU NHGRI NIH HHS [HG-00376]; NHLBI NIH HHS [P01-HL45522]; NIAMS NIH HHS [R01-AR43351] NR 7 TC 5 Z9 5 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 17 SU 1 BP S385 EP S390 PG 6 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 260JM UT WOS:000083945800063 PM 10597467 ER PT J AU Gail, MH Pee, D Benichou, J Carroll, R AF Gail, MH Pee, D Benichou, J Carroll, R TI Designing studies to estimate the penetrance of an identified autosomal dominant mutation: Cohort, case-control, and genotyped-proband designs SO GENETIC EPIDEMIOLOGY LA English DT Article DE bias; dichotomous phenotypes; family study; kin-cohort design; sample sizes for estimating penetrance; survival data ID OVARIAN-CANCER; BREAST-CANCER; BRCA1 AB One can obtain population-based estimates of the penetrance of a measurable mutation from cohort studies, from population-based case-control studies, and from genotyped-proband designs (GPD). In a GPD, we assume that representative individuals (probands) agree to be genotyped, and one then obtains information on the phenotypes of first-degree relatives. We also consider an extension of the GPD in which a relative is genotyped (GPDR design). In this paper, we give methods and tables for determining sample sizes needed to achieve desired precision for penetrance estimates from such studies. We emphasize dichotomous phenotypes, but methods for survival data are also given. In an example based on the BRCA1 gene and parameters given by Claus et al. [(1991) Am J Hum Genet 48:232-242], we find that similar large numbers of families need to be studied using the cohort, case-control, and GPD designs if the allele frequency is known, though the GPDR design requires fewer families, and, if one can study mainly probands with disease, the GPD design also requires fewer families. If the allele frequency is not known, somewhat larger sample sizes are required. Surprisingly, studies with mixtures of families of affected and non-affected probands can sometimes be more efficient than studies based exclusively on affected probands when the allele frequency is unknown. We discuss the feasibility and validity of these designs and point out that GPD and GPDR designs are more susceptible to a bias that results when the tendency for an individual to volunteer to be a proband or to be a subject in a cohort or case-control study depends on the phenotypes of his or her relatives. Published 1999 by Wiley-Liss. C1 Informat Management Serv, Rockville, MD USA. Univ Rouen, Sch Med, Biostat Unit, Rouen, France. Texas A&M Univ, Dept Stat, College Stn, TX 77843 USA. RP Gail, MH (reprint author), NCI, Biostat Branch, Div Canc Epidemiol & Genet, 6130 Execut Blvd,EPN-431, Bethesda, MD 20892 USA. FU NCI NIH HHS [CA-57030] NR 10 TC 38 Z9 39 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 16 IS 1 BP 15 EP 39 DI 10.1002/(SICI)1098-2272(1999)16:1<15::AID-GEPI3>3.3.CO;2-# PG 25 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 154GF UT WOS:000077880100003 PM 9915565 ER PT J AU Schaffer, AA AF Schaffer, AA TI Computing probabilities of homozygosity by descent SO GENETIC EPIDEMIOLOGY LA English DT Article DE genetics; algorithms; homozygosity; autozygosity; identity by descent; recessive diseases; dynamic programming AB A person is autozygous at a locus if the person inherits the same allele twice identical by descent along two distinct paths from the same ancestor. Autozygosity is a common cause of recessive diseases in inbred populations. Homozygosity mapping uses this fact to locate the genes that cause recessive diseases. The probability of autozygosity can be used to estimate the probability of a true positive and of a false positive in homozygosity mapping. Thompson [1994] and Cuo [1997] therefore studied the problem of computing the prior, unconditional (multilocus) probability of autozygosity (MPA). I consider a different quantity: the interval probability of autozygosity (IPA). The two measures are identical in the single-locus case. IPA has two notable advantages over MPA: 1. IPA does not include the possibility of heterozygous regions between the homozygous markers. 2. IPA can be computed in time that is polynomial in the pedigree size. My polynomial-time algorithm for the single-locus case solves a problem mentioned by Guo. I implemented a program to compute the IPA. The contribution of this work is the application of basic, abstract methods from computer science to address a problem in genetics. Genet. Epidemiol. (C) 1999 Wiley-Liss, Inc. C1 NHGRI, NIH, Baltimore, MD 21224 USA. Natl Human Genome Res Inst, NIH, Bethesda, MD USA. RP Schaffer, AA (reprint author), NHGRI, NIH, Suite 2000,333 Cassell Dr, Baltimore, MD 21224 USA. RI Schaffer, Alejandro/F-2902-2012 NR 12 TC 5 Z9 5 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1999 VL 16 IS 2 BP 135 EP 149 DI 10.1002/(SICI)1098-2272(1999)16:2<135::AID-GEPI2>3.0.CO;2-W PG 15 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA 163YX UT WOS:000078435500002 PM 10030397 ER PT J AU Fanos, JH AF Fanos, JH TI The missing link in linkage analysis: The well sibling revisited SO GENETIC TESTING LA English DT Article ID ATAXIA-TELANGIECTASIA GENE; POLYMORPHIC DNA MARKER; CYSTIC-FIBROSIS; FAMILIES; CANCER; CHILDREN; DISEASE; NEUROFIBROMATOSIS; HETEROZYGOTES; DIAGNOSIS AB Linkage analysis is a powerful tool for gene localization. Although the impact of genetic testing of miners has been debated, the impact of genetic sampling of miners has been ignored. Inclusion of the well sibling in linkage analysis represents a unique situation in that the sibling has not sought testing and therefore encounters genetic possibilities without the offer of genetic counseling. Thirty-five siblings of individuals with ataxia-telangiectasia (A-T), including 26 adults and 9 adolescents, drawn from the University of California, Los Angeles, The A-T Clinical Center at the Johns Hopkins University School of Medicine, and the A-T Children's Project, were interviewed; 27 reported having given blood sometime before the age of 18, They reported that sampling during their childhood or adolescence stimulated fears of the procedure itself, apprehension concerning follow-up reporting of carrier results, and confusion about the possibility of having A-T, The investigator's direct encounter with minor siblings of persons affected with genetic disorders represented a highly charged event in the lives of these individuals, Although the visit may increase anxiety, this intervention may in fact be a healthy change, offering permission to speak of difficult concerns, as well as serving as a powerful vehicle of conveying important information of a medical and genetic nature. C1 Calif Pacific Med Ctr, Res Inst, Dept Pediat, San Francisco, CA 94115 USA. Calif Pacific Med Ctr, Res Inst, Dept Med, San Francisco, CA 94115 USA. Calif Pacific Med Ctr, Res Inst, Dept Psychiat, San Francisco, CA 94115 USA. NIH, Med Genet Branch, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. RP Fanos, JH (reprint author), Calif Pacific Med Ctr, Res Inst, Dept Pediat, 2340 Clay St, San Francisco, CA 94115 USA. NR 40 TC 13 Z9 13 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1090-6576 J9 GENET TEST JI Genet. Test. PY 1999 VL 3 IS 3 BP 273 EP 278 DI 10.1089/109065799316581 PG 6 WC Genetics & Heredity; Medicine, Research & Experimental SC Genetics & Heredity; Research & Experimental Medicine GA 238XK UT WOS:000082739900004 PM 10495926 ER PT J AU Battaile, KP Maslen, CL Wassif, CA Krakowiak, P Porter, FD Steiner, RD AF Battaile, KP Maslen, CL Wassif, CA Krakowiak, P Porter, FD Steiner, RD TI A simple PCR-based assay allows detection of a common mutation, IVS8-1G -> C, in DHCR7 in Smith-Lemli-Opitz syndrome SO GENETIC TESTING LA English DT Article ID DEFECTIVE CHOLESTEROL-BIOSYNTHESIS; DELTA-7-STEROL REDUCTASE; GENE; 7-DEHYDROCHOLESTEROL; METABOLISM AB Smith-Lemli-Opitz syndrome (SLOS) is an autosomal recessive multiple malformation disorder, A deficiency of the enzyme 7-dehydrocholesterol Delta(7)-reductase (DHCR7) is the primary abnormality in SLOS, The gene encoding DHCR7 has been cloned, and we have identified a mutation affecting the splice acceptor site 5' of exon 9 that occurs frequently in affected individuals. We developed a novel PCR-based assay to detect this common mutation in DHCR7, Using this assay, heterozygosity was detected for this mutation in 18 of 26 and homozygosity in 1 of 26 unrelated affected individuals. The high frequency of this mutation is suggestive of either a founder effect in our group of patients or a mutational hotspot. The simplicity and reliability of this assay will allow it to be used as a clinical test to aid in diagnosis of atypical cases, in carrier testing, in prediction of prognosis based on genotype, and in prenatal molecular genetic diagnostic testing. C1 Oregon Hlth Sci Univ, Dept Pediat, CDRCF, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Dept Mol & Med Genet, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Dept Med, Portland, OR 97201 USA. NICHHD, Unit Mol Dysmorphol, Heritable Disorders Branch, NIH, Bethesda, MD 20892 USA. RP Steiner, RD (reprint author), Oregon Hlth Sci Univ, Dept Pediat, CDRCF, 3181 SW Sam Jackson Pk Rd, Portland, OR 97201 USA. OI Battaile, Kevin/0000-0003-0833-3259; Steiner, Robert/0000-0003-4177-4590; Wassif, Christopher/0000-0002-2524-1420 FU NCRR NIH HHS [M01 RR00334-33S3]; NICHD NIH HHS [HD 33703-03] NR 24 TC 13 Z9 13 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1090-6576 J9 GENET TEST JI Genet. Test. PY 1999 VL 3 IS 4 BP 361 EP 363 DI 10.1089/gte.1999.3.361 PG 3 WC Genetics & Heredity; Medicine, Research & Experimental SC Genetics & Heredity; Research & Experimental Medicine GA 267UT UT WOS:000084378200007 PM 10627944 ER PT J AU Jordan, IK McDonald, JF AF Jordan, IK McDonald, JF TI Comparative genomics and evolutionary dynamics of Saccharomyces cerevisiae Ty elements SO GENETICA LA English DT Article DE genomics; molecular evolution; retrotransposons; selection; Ty elements ID DNA LOSS; RETROTRANSPOSONS; DROSOPHILA; SEQUENCE; PERSPECTIVE; EXPRESSION; MECHANISM; GENES; LIFE AB The availability of the complete genome sequence of cerevisiae provides the unique opportunity to study an entire genomic complement of retrotransposons from an evolutionary perspective. There are five families of yeast retrotransposons, Ty1-Ty5. We have conducted a series of comparative sequence analyses within and among S. cerevisiae Ty families in an effort to document the evolutionary forces that have shaped element variation. Our results indicate that within families Ty elements vary little in terms of both size and sequence. Furthermore, intra-element 5'-3' long terminal repeat (LTR) sequence comparisons indicate that almost all Ty elements in the genome have recently transposed. For each family, solo LTR sequences generated by intra-element recombination far outnumber full length insertions. Taken together, these results suggest a rapid genomic turnover of S. cerevisiae Ty elements. The closely related Ty1 and Ty2 are the most numerous elements in the genome. Phylogenetic analysis of full length insertions reveals that reverse transcriptase mediated recombination between Ty1 and Ty2 elements has generated a number of hybrid Ty1/2 elements. These hybrid Ty1/2 elements have similar genomic structures with chimeric LTRs and chimeric TYB (pol) genes. Analysis of the levels of nonsynonymous (Ka) and synonymous (Ks) nucleotide variation indicates that Ty1 and Ty2 coding regions have been subject to strong negative (purifying) selection. Distribution of Ka and Ks on Ty1, Ty2 and Ty1/2 phylogenies reveals evidence of negative selection on both internal and external branches. This pattern of variation suggests that the majority of full length Ty1, Ty2 and Ty1/2 insertions represent active or recently active element lineages and is consistent with a high level of genomic turnover. The evolutionary dynamics of S. cerevisae Ty elements uncovered by our analyses are discussed with respect to selection among elements and the interaction between the elements and their host genome. C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. Univ Georgia, Dept Genet, Athens, GA 30602 USA. RP Jordan, IK (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 38A, Bethesda, MD 20894 USA. NR 32 TC 18 Z9 19 U1 0 U2 3 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0016-6707 J9 GENETICA JI Genetica PY 1999 VL 107 IS 1-3 BP 3 EP 13 DI 10.1023/A:1004022704701 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 331QK UT WOS:000088029600002 PM 10952193 ER PT J AU Felsenfeld, A Peterson, J Schloss, J Guyer, M AF Felsenfeld, A Peterson, J Schloss, J Guyer, M TI Assessing the quality of the DNA sequence from the human genome project SO GENOME RESEARCH LA English DT Article C1 NIH, NHGRI, Bethesda, MD 20892 USA. RP NIH, NHGRI, Bldg 10, Bethesda, MD 20892 USA. EM adam_felsenfeld@nih.gov NR 9 TC 36 Z9 37 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 1088-9051 EI 1549-5469 J9 GENOME RES JI Genome Res. PD JAN PY 1999 VL 9 IS 1 BP 1 EP 4 PG 4 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 165NB UT WOS:000078526500001 PM 9927479 ER PT J AU Wolf, YI Brenner, SE Bash, PA Koonin, EV AF Wolf, YI Brenner, SE Bash, PA Koonin, EV TI Distribution of protein folds in the three superkingdoms of life SO GENOME RESEARCH LA English DT Article ID COMPLETE GENOME SEQUENCE; STRUCTURAL CLASSIFICATION; MYCOPLASMA-GENITALIUM; DATABASE; ARCHAEON; UNIVERSE; GENES; SCOP AB A sensitive protein-fold recognition procedure was developed on the basis of iterative database search using the PSI-BLAST program. A collection of 1193 position-dependent weight matrices that can be used as fold identifiers was produced. In the completely sequenced genomes, folds could be automatically identified for 20%-30% of the proteins, with 3%-6% more detectable by additional analysis of conserved motifs. The distribution of the most common folds is very similar in bacteria and archaea but distinct in eukaryotes. Within the bacteria, this distribution differs between parasitic and free-living species. In all analyzed genomes, the P-loop NTPases are the most abundant fold. In bacteria and archaea, the next most common folds are ferredoxin-like domains, TIM-barrels, and methyltransferases, whereas in eukaryotes, the second to fourth places belong to protein kinases, beta-propellers and TIM-barrels. The observed diversity of protein folds in different proteomes is approximately twice as high as it would be expected from a simple stochastic model describing a proteome as a finite sample from an infinite pool of proteins with an exponential distribution of the fold fractions. Distribution of the number of domains with different folds in one protein fits the geometric model, which is compatible with the evolution of multidomain proteins by random combination of domains. C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. Stanford Univ, Dept Biol Struct, Stanford, CA 94305 USA. Northwestern Univ, Dept Mol Pharmacol & Biol Chem, Chicago, IL 60611 USA. Russian Acad Sci, Inst Cytol & Genet, Novosibirsk 630090, Russia. RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. EM koonin@ncbi.nlm.nih.gov RI Brenner, Steven/A-8729-2008 OI Brenner, Steven/0000-0001-7559-6185 NR 49 TC 142 Z9 145 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD JAN PY 1999 VL 9 IS 1 BP 17 EP 26 PG 10 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 165NB UT WOS:000078526500003 PM 9927481 ER PT J AU Neuwald, AF Aravind, L Spouge, JL Koonin, EV AF Neuwald, AF Aravind, L Spouge, JL Koonin, EV TI AAA(+): A class of chaperone-like ATPases associated with the assembly, operation, and disassembly of protein complexes SO GENOME RESEARCH LA English DT Review ID RESTRICTION-ENDONUCLEASE MCRBC; DNA-POLYMERASE-III; CELL-CYCLE CONTROL; ESCHERICHIA-COLI; BINDING-PROTEIN; CRYSTAL-STRUCTURE; ATP-BINDING; SACCHAROMYCES-CEREVISIAE; PEROXISOME BIOGENESIS; MOLECULAR CHAPERONES AB Using a combination of computer methods for iterative database searches and multiple sequence alignment, we show that protein sequences related to the AAA family of ATPases are far more prevalent than reported previously. Among these are regulatory components of Lon and Clp proteases, proteins involved in DNA replication, recombination, and restriction (including subunits of the origin recognition complex, replication factor C proteins, MCM DNA-licensing factors and the bacterial DnaA, RuvB, and McrB proteins) prokaryotic NtrC-related transcription regulators, the Bacillus sporulation protein SpoVJ, M2+, and Co2+ Chelatases, the Halobacterium GvpN gas Vesicle synthesis protein, dynein motor proteins, TorsinA, and Rubisco activase. Alignment of these sequences, in light of the structures of the clamp loader delta' subunit of Escherichia coli DNA polymerase III and the hexamerization component of N-ethylmaleimide-sensitive fusion protein, provides structural and mechanistic insights into these proteins, collectively designated the AAA(+) class. Whole-genome analysis indicates that this class is ancient and has undergone considerable functional divergence prior to the emergence of the major divisions of life. These proteins often perform chaperone-like functions that assist in the assembly, operation, or disassembly of protein complexes. The hexameric architecture often associated with this class can provide a hole through which DNA or RNA can be thread; this may be important for assembly or remodeling of DNA-protein complexes. C1 Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. RP Neuwald, AF (reprint author), Cold Spring Harbor Lab, POB 100, Cold Spring Harbor, NY 11724 USA. FU NCI NIH HHS [5 P30 CA45508-11]; NLM NIH HHS [1R01 LM06747-01, R01 LM006747] NR 110 TC 1290 Z9 1316 U1 7 U2 72 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD JAN PY 1999 VL 9 IS 1 BP 27 EP 43 PG 17 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 165NB UT WOS:000078526500004 PM 9927482 ER PT J AU Zhang, JH Shen-Ong, G Ostell, J AF Zhang, JH Shen-Ong, G Ostell, J TI "KARIBIN," an information resource for obtaining genomic information in a cytogenetic band SO GENOME RESEARCH LA English DT Article ID MAP; INTEGRATION; SEQUENCE; CLONES; GENE AB KARIBIN [http://sgiweb.ncbi.nlm.nih.gov:80/Zjing/yac.html] is a karyotypic region-based integrated information resource that provides a comprehensive view of the integrated mapping and sequencing data for the human genome. A cytogenetic band is linked to a genetic or physical location using fluorescence in situ hybridization (FISH) mapping data. The genetic, physical mapping data and the sequencing data are integrated using STS markers positioned on multiple maps. For each cytogenetic band, the user can obtain the most up-to-date information that includes genetic and physical maps, human transcript gene map, YAC and PAC/BAC clone coverage, disease gene phenotype, and high throughput genomic sequences from the major human genome sequencing centers. This information provides a framework for future experiments and may accelerate the process of disease gene hunting. It is envisioned that other cytogenetic-based information such as chromosome aberrations can be linked to this framework. C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. Glaxo Wellcome Inc, Res Triangle Pk, NC 27709 USA. NCI, Rockville, MD 20892 USA. RP Zhang, JH (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA. RI Shen-Ong, Grace/C-8327-2014 NR 16 TC 4 Z9 4 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD JAN PY 1999 VL 9 IS 1 BP 91 EP 98 PG 8 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 165NB UT WOS:000078526500010 PM 9927488 ER PT J AU Song, HJ Poy, G Darwiche, N Lichti, U Kuroki, T Steinert, PM Kartasova, T AF Song, HJ Poy, G Darwiche, N Lichti, U Kuroki, T Steinert, PM Kartasova, T TI Mouse Sprr2 genes: A clustered family of genes showing differential expression in epithelial tissues SO GENOMICS LA English DT Article ID CORNIFIED CELL-ENVELOPE; PROLINE-RICH PROTEIN; HUMAN EPIDERMAL-KERATINOCYTES; CROSS-LINKED ENVELOPE; HUMAN-CHROMOSOME 1Q21; RETINOIC ACID; TERMINAL DIFFERENTIATION; HUMAN LORICRIN; PHORBOL ESTER; INVOLUCRIN AB Small proline-rich (SPR) proteins are structural components of the cornified cell envelope of stratified squamous epithelia, They are subdivided into three families, i.e., SPR1, SPR2, and SPR3, of which the SPR2 family is the most complex. To understand the significance of this complexity, we have isolated 11 mouse Sprr2 genes, constructed a provisional physical map of the Sprr2 locus on mouse Chromosome 3, and examined the expression patterns of the Sprr2 genes in mouse epithelial tissues. The 11 Sprr2 sequences are highly conserved with a central domain containing a variable number of repeats. lit situ hybridization showed the Sprr2 expression to be confined to epithelia. RT-PCR using primers specific for each of the 11 Sprr2 members demonstrated varying degrees of expression among the individual Sprr2 members in different tissues. The correlation between the physical location of the genes in the Sprr2 locus and their expression patterns suggests multiple levels of controlled expression. (C) 1999 Academic Press. C1 NIAMSD, Skin Biol Lab, NIH, Bethesda, MD 20892 USA. NIDDKD, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA. NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bethesda, MD 20892 USA. Univ Tokyo, Inst Med Sci, Dept Canc Cell Res, Tokyo, Japan. RP Kartasova, T (reprint author), NIAMSD, Skin Biol Lab, NIH, Bldg 6 Room 425, Bethesda, MD 20892 USA. RI Kuroki, Toshio/A-9500-2011; OI Kuroki, Toshio/0000-0001-6369-4351; Darwiche, Nadine/0000-0002-1862-5426 NR 83 TC 58 Z9 68 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD JAN 1 PY 1999 VL 55 IS 1 BP 28 EP 42 DI 10.1006/geno.1998.5607 PG 15 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 158YX UT WOS:000078146000004 PM 9888996 ER PT J AU Collins, FS AF Collins, FS TI Genetics: An explosion of knowledge is transforming clinical practice SO GERIATRICS LA English DT Article AB Genetics is considered by many to be the field in which the next revolution in medicine will occur. The Human Genome Project, which is an effort to map the entire sequence of human DNA, is already leading to better diagnostics and therapeutics for clinical medicine. The ultimate goal of genetic medicine is to learn how to prevent disease or to treat it with gene therapy or a drug developed specifically for the underlying defect. Other applications include pharmacogenomics and patient counseling about individual health risks, which will be facilitated by new DNA chip technology. Concerns include how to integrate genetic technology into clinical practice and how to prevent genetic-based discrimination. A new coalition is being developed to educate health professionals about genetic medicine. C1 NIH, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. RP Collins, FS (reprint author), NIH, Natl Human Genome Res Inst, Bldg 10, Bethesda, MD 20892 USA. NR 8 TC 26 Z9 30 U1 0 U2 1 PU ADVANSTAR COMMUNICATIONS PI DULUTH PA 131 W FIRST ST, DULUTH, MN 55802 USA SN 0016-867X J9 GERIATRICS JI Geriatrics PD JAN PY 1999 VL 54 IS 1 BP 41 EP 47 PG 7 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 160CJ UT WOS:000078212500009 PM 9934355 ER PT S AU Collins, FS AF Collins, FS BE Grossman, DC Valtin, H TI The human Genome Project and the future of medicine SO GREAT ISSUES FOR MEDICINE IN THE TWENTY-FIRST CENTURY: ETHICAL AND SOCIAL ISSUES ARISING OUT OF ADVANCES IN THE BIOMEDICAL SCIENCES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Great Issues for Medicine in the 21st Century CY SEP 05-07, 1997 CL HANOVER, NEW HAMPSHIRE SP Glaxo Wellcome Inc, Kettering Family Fdn, Off President Dartmouth Coll, Off Provost Dartmouth Coll C1 Natl Human Genome Res Inst, Bethesda, MD 20892 USA. RP Collins, FS (reprint author), Natl Human Genome Res Inst, Bethesda, MD 20892 USA. NR 6 TC 39 Z9 39 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 1-57331-143-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 882 BP 42 EP 55 DI 10.1111/j.1749-6632.1999.tb08532.x PG 14 WC Health Care Sciences & Services; History & Philosophy Of Science; Multidisciplinary Sciences SC Health Care Sciences & Services; History & Philosophy of Science; Science & Technology - Other Topics GA BN33K UT WOS:000081643900007 PM 10415885 ER PT J AU Hager, GL AF Hager, GL TI Studying nuclear receptors with green fluorescent protein fusions SO GREEN FLUORESCENT PROTEIN SE METHODS IN ENZYMOLOGY LA English DT Review ID LIVING CELLS; GLUCOCORTICOID RECEPTOR; PROGESTERONE-RECEPTOR; MINERALOCORTICOID RECEPTOR; ESTROGEN-RECEPTOR; HORMONE RECEPTORS; IN-VIVO; LOCALIZATION; TRAFFICKING; CHIMERA C1 NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA. RP Hager, GL (reprint author), NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA. NR 35 TC 7 Z9 7 U1 0 U2 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 302 BP 73 EP 84 PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12W UT WOS:000087254200009 PM 12876764 ER PT J AU Webb, CD Resnekov, O AF Webb, CD Resnekov, O TI Use of green fluorescent protein for visualization of cell-specific gene expression and subcellular protein localization in Bacillus subtilis SO GREEN FLUORESCENT PROTEIN SE METHODS IN ENZYMOLOGY LA English DT Review ID DEVELOPMENTAL TRANSCRIPTION FACTOR; BIPOLAR LOCALIZATION; PROTEOLYTIC ACTIVATION; SPORULATION; CHROMOSOME; MICROSCOPY; IMMUNOFLUORESCENCE; DIVISION; SITES; CYCLE C1 Def Adv Res Project Agcy, Informat Technol Off, Arlington, VA 22203 USA. NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA. RP Webb, CD (reprint author), Def Adv Res Project Agcy, Informat Technol Off, Arlington, VA 22203 USA. FU NIGMS NIH HHS [GM18568] NR 32 TC 5 Z9 5 U1 1 U2 2 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 302 BP 136 EP 153 PG 18 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12W UT WOS:000087254200013 PM 12876768 ER PT J AU Palm, GJ Wlodawer, A AF Palm, GJ Wlodawer, A TI Spectral variants of green fluorescent protein SO GREEN FLUORESCENT PROTEIN SE METHODS IN ENZYMOLOGY LA English DT Review ID CRYSTAL-STRUCTURE; EXPRESSION; CELLS; RED; CHROMOPHORE; GENE; PHOTOACTIVATION; EXCITATION; INDICATORS; CALMODULIN C1 Inst Mol Biotechnol, Dept Struct Biol & Crystallog, D-07745 Jena, Germany. NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, Macromol Struct Lab, Frederick, MD 21702 USA. RP Palm, GJ (reprint author), Inst Mol Biotechnol, Dept Struct Biol & Crystallog, D-07745 Jena, Germany. NR 39 TC 39 Z9 39 U1 2 U2 6 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 J9 METHOD ENZYMOL JI Methods Enzymol. PY 1999 VL 302 BP 378 EP 394 PG 17 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BQ12W UT WOS:000087254200032 PM 12876787 ER PT J AU Diaugustine, RP Henry, R Sewall, CH Suarez-Quian, CA Walker, MP AF Diaugustine, RP Henry, R Sewall, CH Suarez-Quian, CA Walker, MP TI Synthesis and properties of an EGF-like domain (residues 361-406) in the extreme N-terminal region of the mouse EGF precursor SO GROWTH FACTORS LA English DT Article DE epidermal growth factor; EGF precursor (361-406); cystine disulfide bonds; putative calcium binding motifs; gel filtration; immunolocalization ID EPIDERMAL GROWTH-FACTOR; LACTATING MAMMARY-GLAND; FACTOR-ALPHA; CALCIUM-BINDING; FACTOR-IX; PROTEIN; KIDNEY; DIFFERENTIATION; EXPRESSION; RECEPTOR AB Various proteins contain EGF-like domains that are not ligands for the EGF receptor. In the present study a cognate polypeptide for residues 361-406 of the mouse EGF precursor was synthesized by the solid-phase method. The product was renatured under oxidative conditions since it probably has an EGF-like array of three cystine disulfide bonds in its native state. HPLC analysis of the renaturation reaction revealed formation of a peak material with no apparent free-SH groups. Accordingly, the HPLC retention time of this product was readily increased by treatment (reduction of disulfides) with dithiothreitol, The renatured 46-mer (PEGF-1) did not displace I-125-EGF bound to rat liver membranes and I-125-PEGF-1 did not exhibit specific binding to membrane preparations from the mouse liver, mammary gland, or kidney, with or without Ca2+ in the binding medium. Although PEGF-1 contains a putative Ca2+ binding motif, specific binding of this cation by the polypeptide could not be demonstrated by electromobility shiff or incubation with Ca-45(2+), Immunoassay of PEGF-1 and EGF in fractions obtained following gel filtration of mouse urine revealed multiple peaks of PEGF-1 immunoreactivity with the major peaks eluting at an Mr > 30 kDa, In contrast, virtually all the EGF immunoreactivity eluted at a volume similar to that of I-125-EGF. These data suggest that selective cleavage of the PEGF-1 domain from the precursor does not occur with the proclivity known for that of EGF, Instead, the PEGF-1 probably functions coordinately with other EGF-like domains while tethered to the precursor backbone. Finally, localization of PEGF-1 immunoreactivity occurred only in cell populations of the mouse previously demonstrated as sites for EGF/EGF precursor, which suggests that PEGF-1 is exclusively a domain of the EGF precursor. C1 NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Biochem Risk Anal Lab, NIH, Res Triangle Pk, NC 27709 USA. Univ N Carolina, Dept Chem, Chapel Hill, NC 27514 USA. Georgetown Univ, Sch Med, Dept Cell Biol, Washington, DC 20007 USA. RP Diaugustine, RP (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, Mail Drop D4-04,POB 12233, Res Triangle Pk, NC 27709 USA. NR 41 TC 2 Z9 2 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 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1999 VL 17 IS 1 BP 37 EP 48 DI 10.3109/08977199909001061 PG 12 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA 234RJ UT WOS:000082497900004 PM 10495961 ER PT J AU Ishimura, A Princler, GL Lin, JJ Kung, HF Maeno, M AF Ishimura, A Princler, GL Lin, JJ Kung, HF Maeno, M TI Immunodetection of Xenopus bone morphogenetic protein-1 in adult and embryonic cells SO GROWTH FACTORS LA English DT Article DE tolloid; dorso-ventral axis; BMP-1; processing ID C-PROTEINASE; DROSOPHILA; GENE; EXPRESSION; HOMOLOG AB In order to analyze biochemical properties of Xenopus bone morphogenetic protein-1 (XBMP-1), rabbit antiserum (alpha-B1) was raised against a synthetic peptide (P1) corresponding to a hydrophilic N-terminal region. XBMP-1B (Xtld) synthesized in the reticulocyte lysate was successfully immunoprecipitated by this antiserum. This precipitation was completely blocked when Pi was added to the reaction, indicating that alpha-B1 recognized XBMP-1B specifically. In Western blot analysis, two distinct sizes of protein (107 and 34 kD) were detected in hind limbs in metamorphosing animals. Both proteins were detected in various adult tissues such as lung, liver, kidney, heart, muscle, intestine, brain, and testis, The mixing of the liver and muscle extracts, and the following detection of immunoreactive proteins suggested that the 34 kD band was a proteolytic product of the 107 kD protein. In the embryonic extracts from the unfertilized egg (stage 0) to swimming tadpoles (stage 40), a 63 kD protein was detected in addition to the 107 kD protein. We also showed that the 107 kD protein was much more expressed in the animal half of the unfertilized eggs than in the vegetal half, but that it was ubiquitously expressed in the gastrula embryos. We suggest that the 63 and 107 kD proteins correspond to full-length proteins encoded by XBMP-1A and XBMP-1B genes, and these proteins are expressed in embryo and in various adult tissues. C1 Niigata Univ, Fac Sci, Dept Biol, Niigata 9502181, Japan. NCI, Frederick Canc Res & Dev Ctr, Div Basic Sci, Lab Biochem Physiol, Frederick, MD 21702 USA. RP Maeno, M (reprint author), Niigata Univ, Fac Sci, Dept Biol, Niigata 9502181, Japan. NR 13 TC 1 Z9 1 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 0897-7194 J9 GROWTH FACTORS JI Growth Factors PY 1999 VL 16 IS 3 BP 171 EP 177 DI 10.3109/08977199909002127 PG 7 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA 195EZ UT WOS:000080237500002 PM 10372958 ER PT S AU Slavkin, HC AF Slavkin, HC BE McNamara, JA TI Possibilities of growth modification: Nature versus nurture SO GROWTH MODIFICATION: WHAT WORKS, WHAT DOESN'T, AND WHY SE CRANIOFACIAL GROWTH SERIES, MONOGRAPH LA English DT Proceedings Paper CT 25th Annual Moyers Symposium CY FEB 28-MAR 01, 1998 CL ANN ARBOR, MI SP Sch Dent Dept Orthodont & Pediat Dent, Univ Michigan Ctr Human Growth & Dev ID BONE MORPHOGENETIC PROTEINS; TOOTH DEVELOPMENT; GENOME-PROJECT; CARTILAGE; EXPRESSION; TISSUES; MODEL; CELLS C1 NIDR, NIH, Bethesda, MD 20892 USA. RP Slavkin, HC (reprint author), NIDR, NIH, Bethesda, MD 20892 USA. NR 48 TC 0 Z9 0 U1 0 U2 0 PU UNIV MICHIGAN PI ANN ARBOR PA CENTER HUMAN GROWTH & DEVELOPM ENT, ANN ARBOR, MI 48109 USA SN 0162-7279 BN 0-929921-31-3 J9 CRANIO GROW PY 1999 VL 35 BP 1 EP 15 PG 15 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA BM93U UT WOS:000080192300001 ER PT J AU Sabol, SZ Nelson, ML Fisher, C Gunzerath, L Brody, CL Hu, S Sirota, LA Marcus, SE Greenberg, BD Lucas, FR Benjamin, J Murphy, DL Hamer, DH AF Sabol, SZ Nelson, ML Fisher, C Gunzerath, L Brody, CL Hu, S Sirota, LA Marcus, SE Greenberg, BD Lucas, FR Benjamin, J Murphy, DL Hamer, DH TI A genetic association for cigarette smoking behavior SO HEALTH PSYCHOLOGY LA English DT Article DE smoking; SLC6A3 gene; dopamine; personality ID DOPAMINE TRANSPORTER GENE; SEXUAL ORIENTATION; PARKINSONS-DISEASE; NOVELTY SEEKING; PERSONALITY; TEMPERAMENT; DRUGS; DAT1; POLYMORPHISM; PERSPECTIVE AB Dopaminergic genes are likely candidates for heritable influences on cigarette smoking. In an accompanying article, Lerman et al. (1999) report associations between allele 9 of a dopamine transporter gene polymorphism (SLC6A3-9) and lack of smoking, late initiation of smoking, and length of quitting attempts. The present investigation extended their study by examining both smoking behavior and personality traits in a diverse population of nonsmokers, current smokers, and former smokers (N = 1,107). A significant association between SLC6A3-9 and smoking status was confirmed and was due to an effect on cessation rather than initiation. The SLC6A3-9 polymorphism was also associated with low scores for novelty seeking, which was the most significant personality correlate of smoking cessation. It is hypothesized that individuals carrying the SLC6A3-9 polymorphism have altered dopamine transmission, which reduces their need for novelty and reward by external stimuli, including cigarettes. C1 NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. NIDR, Bethesda, MD 20892 USA. NIMH, Clin Sci Lab, Bethesda, MD 20892 USA. RP Hamer, DH (reprint author), NCI, Biochem Lab, NIH, Bldg 37,Room 4A13,37 Convent Dr, Bethesda, MD 20892 USA. NR 40 TC 200 Z9 204 U1 3 U2 4 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0278-6133 J9 HEALTH PSYCHOL JI Health Psychol. PD JAN PY 1999 VL 18 IS 1 BP 7 EP 13 DI 10.1037//0278-6133.18.1.7 PG 7 WC Psychology, Clinical; Psychology SC Psychology GA 158EX UT WOS:000078104000002 PM 9925040 ER PT J AU Lerman, C Caporaso, NE Audrain, J Main, D Bowman, ED Lockshin, B Boyd, NR Shields, PG AF Lerman, C Caporaso, NE Audrain, J Main, D Bowman, ED Lockshin, B Boyd, NR Shields, PG TI Evidence suggesting the role of specific genetic factors in cigarette smoking SO HEALTH PSYCHOLOGY LA English DT Article DE dopamine; genetics; smoking ID DOPAMINE-D2 RECEPTOR GENE; ALLELIC ASSOCIATION; TRANSPORTER GENE; NICOTINE; ALCOHOLISM; HYPERACTIVITY; POPULATION; CESSATION; BUPROPION; DISORDER AB Twin studies suggest that propensity to smoke and ability to quit smoking are influenced by genetic factors. As a means of investigating the risk of smoking associated with genetic polymorphisms in the dopamine transporter (SLC6A3) and the D-2 dopamine receptor (DRD2) genes, a case-control study of 289 smokers and 233 nonsmoking controls and a case series analysis of smokers were conducted. A significant effect for SLC6A3 and a significant gene-gene interaction were found in a logistic regression model, indicating that individuals with SLC6A3-9 genotypes were significantly less likely to be smokers, especially if they also had DRD2-A2 genotypes. Smokers with SLC6A3-9 genotypes were also significantly less likely to have started smoking before 16 years of age and had prior smoking histories indicating a longer period of prior smoking cessation. This study provides preliminary evidence that the SLC6A3 gene may influence smoking initiation and nicotine dependence. C1 Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, Washington, DC 20007 USA. NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. RP Lerman, C (reprint author), Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, 2233 Wisconsin Ave NW,Suite 317, Washington, DC 20007 USA. FU NCI NIH HHS [R01 CA63562] NR 35 TC 229 Z9 236 U1 3 U2 10 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0278-6133 J9 HEALTH PSYCHOL JI Health Psychol. PD JAN PY 1999 VL 18 IS 1 BP 14 EP 20 DI 10.1037/0278-6133.18.1.14 PG 7 WC Psychology, Clinical; Psychology SC Psychology GA 158EX UT WOS:000078104000003 PM 9925041 ER PT J AU Brossi, A Lee, HH Yeh, HJC AF Brossi, A Lee, HH Yeh, HJC TI Axial configuration of optically active colchicinoids and allocolchicinoids: A correction SO HELVETICA CHIMICA ACTA LA English DT Article ID ANTITUMOR AGENTS; ANTITUBULIN ACTIVITY; ESTER ANALOGS; ALLOTHIOCOLCHICINOIDS AB Correction of the axial configuration of (-)-rotating colchicinoids and allocolchicinoids from (aS) to (aR) is reported. C1 Univ N Carolina, Sch Pharm, Div Med Chem & Nat Prod, Nat Prod Lab, Chapel Hill, NC 27599 USA. NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD USA. RP Brossi, A (reprint author), Univ N Carolina, Sch Pharm, Div Med Chem & Nat Prod, Nat Prod Lab, Chapel Hill, NC 27599 USA. NR 12 TC 11 Z9 11 U1 0 U2 0 PU WILEY-V C H VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0018-019X J9 HELV CHIM ACTA JI Helv. Chim. Acta PY 1999 VL 82 IS 8 BP 1223 EP 1224 DI 10.1002/(SICI)1522-2675(19990804)82:8<1223::AID-HLCA1223>3.0.CO;2-6 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA 227KA UT WOS:000082078500008 ER PT J AU Marquez, VE Russ, P Alonso, R Siddiqui, MA Hernandez, S George, C Nicklaus, MC Dai, F Ford, H AF Marquez, VE Russ, P Alonso, R Siddiqui, MA Hernandez, S George, C Nicklaus, MC Dai, F Ford, H TI Synthesis of conformationally restricted carbocyclic nucleosides: The role of the O(4 ')-atom in the key hydration step of adenosine deaminase SO HELVETICA CHIMICA ACTA LA English DT Article ID TRANSITION-STATE ANALOG; INHIBITORS; COFORMYCIN; CATALYSIS; BINDING; PH AB Conformationally restricted carbocyclic nucleosides with either a northern(N)-type conformation. i.e., N-type 2'-deoxy-methanocarba-adenosine 8 ((N)MCdAdo), or a southern(S)-type conformation, i.e. S-type 2'-deoxy-methanocarba-adenosine 9, ((S)MCdAdo), were used as substrates for adenosine deaminase (ADA) to assess the enzyme's preference for a fixed conformation relative to the flexible conformation represented by the carbocyclic nucleoside aristeromycin (10). Further comparison between the rates of deamination of these compounds with those of the two natural substrates adenosine (Ado; 1) and 2'-deoxyadenosine (dAdo; 2), as well as with that of the conformationally locked nucleoside LNA-Ado (11), which, like the natural substrates, has a furanose O(4') atom, helped differentiate between the roles of the O(4') anomeric effect and sugar conformation in controlling the rates of deamination by ADA. Differences in rates of deamination as large as 10000 can be attributed to the combined effect of the O(4') atom and the enzyme's preference for an N-type conformation. The hypothesis proposed is that ADA's preference For N-type substrates is not arbitrary; it is rather the direct consequence of the conformationally dependent O(4') anomeric effect, which is more efficient in N-type conformers in promoting the formation of a covalent hydrate at the active site of the enzyme. The formation of a covalent hydrate at the active site of ADA precedes deamination. A new and efficient synthesis of the important carbobicyclic template 14a, a useful intermediate for the synthesis of (N)MCdAdo (8) and other conformationally restricted nucleosides, is also reported. C1 NCI, Med Chem Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. USN, Struct Matter Lab, Res Lab, Washington, DC 20375 USA. RP Marquez, VE (reprint author), NCI, Med Chem Lab, Div Basic Sci, NIH, Bethesda, MD 20892 USA. RI Nicklaus, Marc/N-4183-2014 NR 28 TC 70 Z9 70 U1 0 U2 1 PU WILEY-V C H VERLAG GMBH PI BERLIN PA MUHLENSTRASSE 33-34, D-13187 BERLIN, GERMANY SN 0018-019X J9 HELV CHIM ACTA JI Helv. Chim. Acta PY 1999 VL 82 IS 12 BP 2119 EP 2129 PG 11 WC Chemistry, Multidisciplinary SC Chemistry GA 270VG UT WOS:000084557400005 ER PT S AU Orlic, D Girard, LJ Anderson, SM Barrette, S Broxmeyer, HE Bodine, DH AF Orlic, D Girard, LJ Anderson, SM Barrette, S Broxmeyer, HE Bodine, DH BE Orlic, D Bock, TA Kanz, L TI Amphotropic retrovirus transduction of hematopoietic stem cells SO HEMATOPOIETIC STEM CELLS: BIOLOGY AND TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 2nd International Symposium and Workshop on Hematopoietic Stem Cells CY JUL 01-04, 1998 CL UNIV TUBINGEN, MEERSBURG, GERMANY SP AMGEN, Germany, AMGEN, Europe, KIRIN, Japan HO UNIV TUBINGEN ID APE LEUKEMIA-VIRUS; COLONY-STIMULATING FACTOR; EXPRESSING HIGH-LEVELS; UMBILICAL-CORD BLOOD; PROGENITOR CELLS; BONE-MARROW; MESSENGER-RNA; ADENOSINE-DEAMINASE; PERIPHERAL-BLOOD; GENE-TRANSFER AB Mice treated with cytokines for 5 days have large numbers of hematopoietic stem cells (HSCs) in their peripheral blood and bone marrow at 1 and 14 days after the last injection. We fractionated the HSCs from the bone marrow of these mice using elutriation at flow rates of 25, 30 and 35 ml/min. The subpopulations of HSCs from cytokine-treated mice show a 3- to 8-fold higher level of mRNA encoding the amphotropic retrovirus receptor (amphoR) compared with the corresponding HSC subpopulation from untreated mouse bone marrow, In an earlier study with mouse HSCs we showed a direct correlation between high levels of amphoR mRNA and efficient retrovirus transduction. We have now utilized our gene transfer protocol to assay amphotropic retrovirus transduction efficiency using HSCs from the bone marrow of mice treated with granulocyte-colony stimulating factor/stem cell factor (GCSF/SCF), To extend these findings to a more clinically relevant protocol we analyzed the amphoR mRNA levels in HSCs from human cord blood and adult bone marrow, The amphoR mRNA level in HSCs from human bone marrow and fresh cord blood was detectable at an extremely low level compared with the HSC population in cryopreserved cord blood samples. The 12- to 22-fold increase in amphoR mRNA in HSCs from cryopreserved cord blood renders these HSCs likely candidates for high efficiency, gene transfer. C1 NIH, Hematopoiesis Sect, Genet & Mol Biol Branch, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. Indiana Univ, Sch Med, Dept Microbiol Immunol, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Med, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Walther Oncol Ctr, Indianapolis, IN 46202 USA. RP Orlic, D (reprint author), NIH, Hematopoiesis Sect, Genet & Mol Biol Branch, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. FU NHLBI NIH HHS [P01 HL 53586, R01 HL 54037, R01 HL 46416] NR 25 TC 10 Z9 12 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 1-57331-188-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 872 BP 115 EP 124 DI 10.1111/j.1749-6632.1999.tb08458.x PG 10 WC Cell Biology; Hematology; Multidisciplinary Sciences; Transplantation SC Cell Biology; Hematology; Science & Technology - Other Topics; Transplantation GA BN24X UT WOS:000081273400012 PM 10372116 ER PT S AU Orlic, D Laprise, SL Cline, AP Anderson, SM Bodine, DM AF Orlic, D Laprise, SL Cline, AP Anderson, SM Bodine, DM BE Orlic, D Bock, TA Kanz, L TI Isolation of stem cell-specific cDNAs from hematopoietic stem cell populations SO HEMATOPOIETIC STEM CELLS: BIOLOGY AND TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 2nd International Symposium and Workshop on Hematopoietic Stem Cells CY JUL 01-04, 1998 CL UNIV TUBINGEN, MEERSBURG, GERMANY SP AMGEN, Germany, AMGEN, Europe, KIRIN, Japan HO UNIV TUBINGEN ID EXPRESSING HIGH-LEVELS; MESSENGER-RNA; C-KIT; MOUSE; RECEPTOR; PURIFICATION; PROTEIN; LIN AB We have begun to isolate gene sequences that are specifically expressed in hematopoietic stem cells (HSCs). There are at least three fundamental requirements for the isolation of HSC-specific transcripts. First, highly enriched populations of HSCs, and an HSC-depleted cell population for comparison must be isolated. Secondly, the gene isolation procedures must be adapted to accommodate the small amounts of RNA obtained from purified HSCs. Finally, a defined screening strategy must be developed to focus on sequences to be examined in more detail. In this report, we describe the characterization of populations of HSCs that are highly enriched (Lin(-) c-kit(HI)) or depleted (Lin(-) c.kit(NEG)) of HSCs. We compared two methods for gene isolation, differential display polymerase chain reaction (DD-PCR) and subtractive hybridization (SH), and found that the latter was more powerful and efficient in our hands. Lastly we describe the strategy that we have developed to screen clones for further study. C1 NIH, Hematopoiesis Sect, Genet & Mol Biol Branch, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. RP Bodine, DM (reprint author), NIH, Hematopoiesis Sect, Genet & Mol Biol Branch, Natl Human Genome Res Inst, 49 Convent Dr,Rm 3A14,MSC-4442, Bethesda, MD 20892 USA. NR 32 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 1-57331-188-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 872 BP 243 EP 255 DI 10.1111/j.1749-6632.1999.tb08469.x PG 13 WC Cell Biology; Hematology; Multidisciplinary Sciences; Transplantation SC Cell Biology; Hematology; Science & Technology - Other Topics; Transplantation GA BN24X UT WOS:000081273400023 PM 10372127 ER PT S AU Whitwam, T Haskins, ME Henthorn, PS Bodine, DM Puck, JM AF Whitwam, T Haskins, ME Henthorn, PS Bodine, DM Puck, JM BE Orlic, D Bock, TA Kanz, L TI Canine lymphocyte expression of retrovirally transferred human common gamma chain SO HEMATOPOIETIC STEM CELLS: BIOLOGY AND TRANSPLANTATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 2nd International Symposium and Workshop on Hematopoietic Stem Cells CY JUL 01-04, 1998 CL UNIV TUBINGEN, MEERSBURG, GERMANY SP AMGEN, Germany, AMGEN, Europe, KIRIN, Japan HO UNIV TUBINGEN ID SEVERE COMBINED IMMUNODEFICIENCY; GENE-TRANSFER; REPOPULATING CELLS; PERIPHERAL-BLOOD; STEM-CELLS; PROGENITORS; POPULATIONS C1 NIH, Genet & Mol Biol Branch, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. Univ Penn, Sch Vet Med, Dept Genet, Philadelphia, PA 19104 USA. RP Puck, JM (reprint author), NIH, Genet & Mol Biol Branch, Natl Human Genome Res Inst, Bldg 49,Rm 3A14,49 Convent Dr, Bethesda, MD 20892 USA. FU NIAID NIH HHS [AI3317]; NIDDK NIH HHS [DK54481]; NINDS NIH HHS [NS33526] NR 19 TC 0 Z9 0 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 1-57331-188-X J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 872 BP 387 EP 390 DI 10.1111/j.1749-6632.1999.tb08483.x PG 4 WC Cell Biology; Hematology; Multidisciplinary Sciences; Transplantation SC Cell Biology; Hematology; Science & Technology - Other Topics; Transplantation GA BN24X UT WOS:000081273400037 PM 10372141 ER PT J AU Coop, A Rice, KC AF Coop, A Rice, KC TI Direct and simple conversion of codeine to thebainone-A and dihydrothebainone SO HETEROCYCLES LA English DT Article AB Codeine can be rearranged directly to thebainone-A in 74% yield by treatment with BuLi. Hydrogenation of the crude material followed by crystallization as the hydrochloride salt leads to dihydrothebainone in 78% yield. C1 NIDDKD, Med Chem Lab, Bethesda, MD 20892 USA. RP Coop, A (reprint author), NIDDKD, Med Chem Lab, Bldg 8,Rm B1-23, Bethesda, MD 20892 USA. NR 9 TC 6 Z9 6 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0385-5414 J9 HETEROCYCLES JI Heterocycles PD JAN 1 PY 1999 VL 50 IS 1 BP 39 EP 42 PG 4 WC Chemistry, Organic SC Chemistry GA 169YR UT WOS:000078778100012 ER PT J AU Yu, QS Greig, NH Holloway, HW Brossi, A AF Yu, QS Greig, NH Holloway, HW Brossi, A TI 4 '-hydroxyphenylcarbamates of (3aS)-eseroline and (3aS)-N(1)-noreseroline: Potential metabolites of the Alzheimer's anticholinesterase drug phenserine SO HETEROCYCLES LA English DT Article ID CARBAMATE ANALOGS; BUTYRYLCHOLINESTERASE; PHYSOSTIGMINE; (-)-ESEROLINE; INHIBITORS AB 4'-Hydroxyphenylcarbamates of (3aS)-eseroline (3) and (3aS)-N(1)-noreseroline (4), as predicted metabolites of phenserine (1), were synthesized. Biological evaluation showed that 3 and 4 possessed potent activities for inhibition of acetylcholinesterase and butyrylcholinesterase in vitro. In contrast the intermediates, 4'-benzyloxyphenserine (8) and 4'-benzyloxy N(1)-benzylphenserine (12), demonstrated unusually potent and selective activities against butyrylcholinesterase. C1 NIA, Cellular & Mol Biol Lab, Intramural Program, NIH, Baltimore, MD 21224 USA. Univ N Carolina, Sch Pharm, Chapel Hill, NC 27599 USA. RP Yu, QS (reprint author), NIA, Cellular & Mol Biol Lab, Intramural Program, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 15 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0385-5414 J9 HETEROCYCLES JI Heterocycles PD JAN 1 PY 1999 VL 50 IS 1 BP 95 EP 102 PG 8 WC Chemistry, Organic SC Chemistry GA 169YR UT WOS:000078778100024 ER PT J AU Martin, A AF Martin, A TI Automatic activation of the medial temporal lobe during encoding: Lateralized influences of meaning and novelty SO HIPPOCAMPUS LA English DT Article DE memory; hippocampus; medial temporal lobe; positron emission tomography (PET) ID POSITRON EMISSION TOMOGRAPHY; EPISODIC MEMORY; HIPPOCAMPAL-FORMATION; BRAIN ACTIVITY; RETRIEVAL; HUMANS; PET; ORGANIZATION; NEUROANATOMY; LOBECTOMY AB In contrast to early failures, recent functional brain imaging studies have shown that medial temporal lobe (MTL) structures are active during performance of a variety of tasks. These studies have revealed three properties of the MTL that are consistent with its critical role in establishing new declarative memories. First, the MTL is automatically engaged whenever an event is experienced, with the side of activation (left, right) dependent on the nature of the material presented (verbal, nonverbal). Second, the strength or amount of activity depends on how well the material is encoded. Deep encoding will produce more MTL activity than shallow encoding. Depth of encoding-related increases in activity are more commonly seen on the left, because deep encoding is nearly always synonymous with encoding for meaning, and, therefore, depends on left-lateralized language mechanisms. Third, the amount of MTL activity depends on novelty. Unfamiliar events and contexts will produce more MTL activity than familiar events and contexts. Novelty-related increases are more commonly seen on the right, perhaps reflecting the greater role of the right hemisphere in maintaining tonic attention and arousal. These findings suggest a hemispheric division of labor involving encoding for meaning (left) and novelty detection (right), both of which lead to better remembering. Hippocampus 1999; 9:62-70. Published 1999 Wiley-Liss, Inc.dagger C1 NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA. RP Martin, A (reprint author), NIMH, Lab Brain & Cognit, Bldg 10,Room 4c-104,10 Ctr Dr MSC 1366, Bethesda, MD 20892 USA. EM alex@codon.nih.gov RI martin, alex/B-6176-2009 NR 57 TC 111 Z9 112 U1 1 U2 6 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1050-9631 J9 HIPPOCAMPUS JI Hippocampus PY 1999 VL 9 IS 1 BP 62 EP 70 DI 10.1002/(SICI)1098-1063(1999)9:1<62::AID-HIPO7>3.0.CO;2-K PG 9 WC Neurosciences SC Neurosciences & Neurology GA 173WD UT WOS:000079002000007 PM 10088901 ER PT J AU Wise, SP Murray, EA AF Wise, SP Murray, EA TI Role of the hippocampal system in conditional motor learning: Mapping antecedents to action SO HIPPOCAMPUS LA English DT Editorial Material DE mapping; procedural memory; declarative memory; nonhuman primates; visuomotor behavior; archicortex ID MEDIAL TEMPORAL-LOBE; INFEROTEMPORAL-FRONTAL DISCONNECTION; CONFIGURAL ASSOCIATION THEORY; MONKEYS MACACA-FASCICULARIS; FIMBRIA-FORNIX LESIONS; SHORT-TERM-MEMORY; RHESUS-MONKEYS; PATH INTEGRATION; RECOGNITION MEMORY; OBJECT-RECOGNITION AB Macaque monkeys can learn arbitrary mappings between stimuli and spatially directed actions (often termed conditional motor learning), and, after the development of a strong learning set, can do so in just a few trials. Ablation studies have shown that the hippocampus plus subjacent cortex is necessary for this rapid and highly flexible type of learning. We consider evidence that the arbitrary mapping function of the hippocampal system may be more general and fundamental than currently accepted and what limitations there may be, if any, on the information that it can map. Removal of the hippocampal system yields a pattern of deficits and preserved abilities that correlates remarkably closely with that found in human global amnesics, such as patient H.M., on a variety of declarative memory tasks. Thus, the rapid acquisition of arbitrary visuomotor mappings may represent an example of declarative memory in nonhuman primates. Hippocampos 1999;9:101-117. Published 1999 Wiley-Liss, Inc. C1 NIMH, Neuropsychol Lab, Bethesda, MD 20892 USA. NIMH, Lab Syst Neurosci, Poolesville, MD USA. RP Murray, EA (reprint author), NIMH, Neuropsychol Lab, Bldg 49,Room 1B80,49 Convent Dr, Bethesda, MD 20892 USA. EM eam@ln.nimh.nih.gov OI Murray, Elisabeth/0000-0003-1450-1642 NR 111 TC 82 Z9 82 U1 0 U2 4 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1050-9631 J9 HIPPOCAMPUS JI Hippocampus PY 1999 VL 9 IS 2 BP 101 EP 117 DI 10.1002/(SICI)1098-1063(1999)9:2<101::AID-HIPO3>3.0.CO;2-L PG 17 WC Neurosciences SC Neurosciences & Neurology GA 190JQ UT WOS:000079959700003 PM 10226772 ER PT J AU Su, Y Damjanovski, S Shi, Y Shi, YB AF Su, Y Damjanovski, S Shi, Y Shi, YB TI Molecular and cellular basis of tissue remodeling during amphibian metamorphosis SO HISTOLOGY AND HISTOPATHOLOGY LA English DT Review DE apoptosis; thyroid hormone; amphibian metamorphosis; transcriptional regulation; development ID THYROID-HORMONE-RECEPTOR; RETINOIC ACID RECEPTORS; GENE-EXPRESSION PROGRAM; XENOPUS-LAEVIS; SMALL-INTESTINE; TRANSCRIPTIONAL ACTIVATION; TADPOLE TAIL; POSTEMBRYONIC DEVELOPMENT; MESSENGER-RNA; CO-REPRESSOR AB Amphibian metamorphosis involves systematic transformations of various tadpole organs/ tissues. Three major types of changes take place during this process. These are remodeling, resorption, and de novo development, all of which appear to involve both cell proliferation and apoptosis (programmed cell death). All metamorphic changes are controlled by thyroid hormone (T-3) and are organ-autonomous. Recent studies using primary cell cultures and a stably transformed cell line from tadpole tissues have implicated that T-3 induces apoptosis cell-autonomously. This T-3-induced, metamorphosis-associated apoptosis is similar to cell death in other animal species and involves similar cell death executioners. Both the activation of these executioners and the pathways leading to cell proliferation and differentiation are believed to be through transcriptional regulation by T-3 receptors (TRs). TRs can activate or repress target gene transcription depending upon the presence or absence of T-3, respectively. Many direct T-3-response genes have been isolated and found to encode a variety of proteins that can affect both intra- and extra-cellular events. The determinations of the identities of these response genes through sequence analyses and studies on their expression profiles during development have provided strong clues toward their roles in metamorphosis. However, future studies using organ and cell culture systems and/or transient or stable transgenic technologies are required to understand how these genes transduce the T-3 signal to activate the downstream cell death and proliferation/differentiation pathways. C1 NICHD, Mol Embryol Lab, NIH, Bethesda, MD 20892 USA. Amer Red Cross, Holland Lab, Dept Immunol, Rockville, MD 20814 USA. RP Shi, YB (reprint author), NICHD, Mol Embryol Lab, NIH, Bldg 18T,Rm 106, Bethesda, MD 20892 USA. EM Shi@helix.nih.gov RI Damjanovski, Sashko/N-8728-2015 NR 83 TC 19 Z9 19 U1 0 U2 0 PU F HERNANDEZ PI MURCIA PA PLAZA FUENSANTA 2-7 C, 30008 MURCIA, SPAIN SN 0213-3911 J9 HISTOL HISTOPATHOL JI Histol. Histopath. PD JAN PY 1999 VL 14 IS 1 BP 175 EP 183 PG 9 WC Cell Biology; Pathology SC Cell Biology; Pathology GA 156TC UT WOS:000078017300020 PM 9987663 ER PT J AU Horwitz, B Tagamets, MA AF Horwitz, B Tagamets, MA TI Predicting human functional maps with neural net modeling SO HUMAN BRAIN MAPPING LA English DT Article DE brain; positron emission tomography; functional magnetic resonance imaging; computational neuroscience; cognition ID WORKING-MEMORY; HUMAN BRAIN; FMRI; PET AB Formidable difficulties exist in interpreting positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) hemodynamic signals in terms of the underlying neural activity. These include issues of spatial and temporal resolution and problems relating neuronal activity (i.e., action potentials) measured in nonhuman studies by single unit electrodes to hemodynamic measurements reflecting synaptic activity. Also, regional hemodynamic measurements correspond to a mixture of local and afferent synaptic activity. To surmount these difficulties, we propose using large-scale neurobiologically realistic models in which data at various spatial and temporal levels can be simulated and cross-validated by multiple disciplines, including functional neuroimaging. A delayed match-to-sample visual task is used to illustrate this approach. (C) 1999 Wiley-Liss, Inc. C1 NIDCD, Language Sect, VSL Branch, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Sch Med, Georgetown Inst Cognit & Computat Sci, Washington, DC 20057 USA. RP Horwitz, B (reprint author), NIDCD, Language Sect, VSL Branch, NIH, Bldg 10,Rm 6C414,MSC 1588,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 14 TC 39 Z9 41 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PY 1999 VL 8 IS 2-3 BP 137 EP 142 DI 10.1002/(SICI)1097-0193(1999)8:2/3<137::AID-HBM11>3.0.CO;2-B PG 6 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 242TM UT WOS:000082957800011 PM 10524605 ER PT J AU Chiang, GG Rubin, HL Cherington, V Wang, T Sobolewski, J McGrath, CA Gaffney, A Emami, S Sarver, N Levine, PH Greenberger, JS Hurwitz, DR AF Chiang, GG Rubin, HL Cherington, V Wang, T Sobolewski, J McGrath, CA Gaffney, A Emami, S Sarver, N Levine, PH Greenberger, JS Hurwitz, DR TI Bone marrow stromal cell-mediated gene therapy for hemophilia A: In vitro expression of human factor VIII with high biological activity requires the inclusion of the proteolytic site at amino acid 1648 SO HUMAN GENE THERAPY LA English DT Article ID RECOMBINANT FACTOR-VIII; HUMAN FACTOR-IX; B-DOMAIN; IN-VIVO; PROTEIN; MICE; CONSTRUCTION; TRANSLATION; MECHANISM; MOLECULES AB To evaluate the potential of the ex vivo bone marrow stromal cell. (BMSC) system as a gene therapy for hemophilia A, we studied the irt vitro expression of human factor VIII (hFVIII) in canine BMSCs following transfection with plasmid vectors and transduction with retroviral vectors. Vectors were composed of B domain-deleted forms of hFVIII that either retain or delete the proteolytic site at amino acid 1648, On transfection of BMSCs, vectors supported expression and secretion of similar levels of up to 386 mU/10(6) cells/24 hr, even though only 3-9% of the cells expressed hFVIII while 42-48% of transfected cells harbored plasmid vector, Much higher percentages (similar to 70%) of cells expressing hFVIII were achieved when BMSCs were transduced by retroviral vectors, resulting in expression and secretion as high as 1000-4000 mU/10(6) cells/24 hr, Western analysis demonstrated that the B domain-deleted forms possessing the proteolytic site were secreted predominantly as heavy and light chain heterodimers that resemble native forms found in plasma. In contrast, the hFVIII lacking the proteolytic site was expressed mostly as unprocessed, single heavy-light chains. Both hFVIII forms were correctly cleaved and activated by thrombin, The proteolyzed hFVIII form possessed greater than or equal to 93% normal biological activity while the unproteolyzed form possessed consistently less than 55% normal biological activity and was therefore considered less suitable for therapeutic application. These results demonstrate that the BMSC system has potential utility in gene therapy for hemophilia A and stress the importance of selecting the appropriate hFVIII structure for prospective clinical use. C1 ALG Co, Marlborough, MA 01752 USA. NIAID, Div Aids, Bethesda, MD 20892 USA. Mem Hlth Care, Worcester, MA 01605 USA. RP Chiang, GG (reprint author), ALG Co, 734 Forest St, Marlborough, MA 01752 USA. NR 48 TC 21 Z9 24 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD JAN 1 PY 1999 VL 10 IS 1 BP 61 EP 76 DI 10.1089/10430349950019192 PG 16 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 155RU UT WOS:000077960800007 PM 10022531 ER PT J AU Ragheb, JA Couture, L Mullen, C Ridgway, A Morgan, RA AF Ragheb, JA Couture, L Mullen, C Ridgway, A Morgan, RA TI Inhibition of human immunodeficiency virus type I by Tat/Rev-regulated expression of cytosine deaminase, interferon alpha 2, or diphtheria toxin compared with inhibition by transdominant Rev SO HUMAN GENE THERAPY LA English DT Article ID A CHAIN GENE; ACTIVE ANTIRETROVIRAL THERAPY; THYMIDINE KINASE GENE; HUMAN T-CELLS; HIV TYPE-1; HAIRPIN RIBOZYME; PROTECTIVE GENE; ANTISENSE-TAR; SUICIDE GENE; REPLICATION AB A retroviral vector was designed to express toxic proteins only in the presence of the HIV-1 Rev and/or Tat protein(s). The design of this vector incorporates an HIV-specific expression cassette that consists of three elements: the U3R region of the HIV-1 IIIB LTR provides the promoter and Tat-responsive element, a modified intron derived from the human c-src gene facilitates the splicing of inserted genes, and the HIV-1 RRE region enhances the transport of unspliced mRNAs. To further limit potential readthrough transcription, the expression cassette was inserted in the reverse transcriptional orientation relative to the retroviral vector LTR. Three different genes, interferon alpha 2, diphtheria toxin (DT-A), and cytosine deaminase, were inserted into this vector. Tat and Rev inducibility was demonstrated directly by a >300-fold induction of interferon production and functionally by a decrease in colony-forming units when a Tat and Rev expression vector was titered on HeLa cells harboring the inducible DT-A cassette. The Tat-inducible cytosine deaminase gene was tested in the Sup-T1 T cell line and shown to inhibit HIV-1 production only when engineered cells were grown in the presence of 5-fluorocytosine. To test the ability of this system to inhibit HIV-1 infection in bulk PBL cultures, a series of transduction and challenge experiments was initiated with both the interferon and DT-A vectors. Protection against infection was documented against three HIV strains in PBLs. Last, the interferon and DT-A vectors were compared with a vector encoding a transdominant Rev protein and were shown to mediate equal or greater inhibition of HIV-1. C1 Natl Human Genome Res Inst, Clin Gene Therapy Branch, NIH, Bethesda, MD 20892 USA. NIAID, NIH, Bethesda, MD 20892 USA. Hlth Canada, Bur Biol & Radiopharmaceut, Ottawa, ON K1A 0L2, Canada. RP Morgan, RA (reprint author), Natl Human Genome Res Inst, Clin Gene Therapy Branch, NIH, Bldg 10,Room 10C103, Bethesda, MD 20892 USA. NR 50 TC 13 Z9 13 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD JAN 1 PY 1999 VL 10 IS 1 BP 103 EP 112 DI 10.1089/10430349950019237 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 155RU UT WOS:000077960800011 PM 10022535 ER PT J AU Li, Y Millikan, RC Newman, B Conway, K Tse, CKJ Liu, ET AF Li, Y Millikan, RC Newman, B Conway, K Tse, CKJ Liu, ET TI P57 (KIP2) polymorphisms and breast cancer risk SO HUMAN GENETICS LA English DT Article ID BECKWITH-WIEDEMANN-SYNDROME; DEPENDENT KINASE INHIBITOR; HUMAN P57(KIP2) GENE; WILMS-TUMORS; CHROMOSOME AB A previous report in this journal has suggested that germline deletions in the proline-alanine-rich (PAPA-repeat) region of P57 (KIP2) are associated with increased risk of a variety of cancers, including breast cancer. We have analyzed the association of P57 PAPA-repeat deletion polymorphisms and breast cancer risk as part of a population-based case-control study of breast cancer. We have not observed an association between the presence of one or two copies of deletion polymorphisms in P57 and breast cancer risk (adjusted odds ratio: 1.1, 95% confidence interval: 0.6-2.0), Further investigation is necessary to determine the functional significance of P57 deletion polymorphisms and their potential relationship with disease. C1 Univ N Carolina, Dept Epidemiol, Sch Publ Hlth, Chapel Hill, NC 27599 USA. Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA. NCI, Div Clin Sci, Bethesda, MD 20892 USA. RP Millikan, RC (reprint author), Univ N Carolina, Dept Epidemiol, Sch Publ Hlth, CB 7400, Chapel Hill, NC 27599 USA. RI Liu, Edison/C-4141-2008 FU NCI NIH HHS [P50-CA58223] NR 25 TC 10 Z9 11 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD JAN PY 1999 VL 104 IS 1 BP 83 EP 88 DI 10.1007/s004390050914 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 167QX UT WOS:000078645700013 PM 10071197 ER PT J AU Tsai-Morris, C Geng, Y Buczko, E Dehejia, A Dufau, ML AF Tsai-Morris, C Geng, Y Buczko, E Dehejia, A Dufau, ML TI Genomic distribution and gonadal mRNA expression of two human luteinizing hormone receptor exon 1 sequences in random populations SO HUMAN HEREDITY LA English DT Article DE luteinizing hormone receptor; polymorphism; mRNA; ovary; testis; signal peptide AB Exon 1 of the human luteinizing hormone receptor (LHR) gene coding region exhibits at least two forms of sequence heterogeneity between 37 and 60 bp, spanning the junction of the signal peptide and the amino terminus of the mature protein. The LHR 1 differs from the LHR 2 by the insertion of 6 bp in exon 1 but is of identical sequence in the 5' flanking region. RFLP analysis of the two haplotypes within a random population of 63 individuals revealed allele frequencies of 0.37 and 0.63 for LHR 1 and LHR 2, respectively. 94% of the samples contained at least one LHR 2 allele, whereas only 68% contained the LHR 1 allele. No gender differences were observed, and both homozygotes and heterozygotes displayed apparently normal reproduction. Reverse-transcriptase polymerase chain-reaction analyses of LHR mRNA from testes and ovaries revealed that both haplotypes are transcribed in normal individuals, with no difference in tissue specific distribution, Thus, at least two functional polymorphic forms of exon 1 coding region of the same LHR gene are present in a random human population. C1 NICHHD, Sect Mol Endocrinol, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. Natl Human Genome Res Inst, Genet Dis Res Branch, NIH, Bethesda, MD USA. RP Dufau, ML (reprint author), NICHHD, Sect Mol Endocrinol, Endocrinol & Reprod Res Branch, NIH, Bldg 49,Rm 6A36,49 Convent Dr,MSC4510, Bethesda, MD 20892 USA. NR 4 TC 9 Z9 10 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0001-5652 J9 HUM HERED JI Hum. Hered. PY 1999 VL 49 IS 1 BP 48 EP 51 DI 10.1159/000022840 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 161WU UT WOS:000078313300010 PM 9858858 ER PT J AU Watanabe, RM Valle, T Hauser, ER Ghosh, S Eriksson, J Kohtamaki, K Ehnholm, C Tuomilehto, J Collins, FS Bergman, RN Boehnke, M AF Watanabe, RM Valle, T Hauser, ER Ghosh, S Eriksson, J Kohtamaki, K Ehnholm, C Tuomilehto, J Collins, FS Bergman, RN Boehnke, M CA Study Investigators TI Familiality of quantitative metabolic traits in Finnish families with non-insulin-dependent diabetes mellitus SO HUMAN HEREDITY LA English DT Article DE heritability; variance components; pedigree analysis; genetics glucose tolerance ID CARDIOVASCULAR RISK-FACTORS; BETA-CELL FUNCTION; PIMA-INDIANS; GLUCOSE-TOLERANCE; PEDIGREE ANALYSIS; INTRAVENOUS GLUCOSE; MAPPING GENES; SENSITIVITY; RESISTANCE; FINLAND AB Type 2 mellitus (NIDDM) is a complex disorder encompassing multiple metabolic defects. There exists strong evidence for a genetic component to NIDDM; however, to date there have been few reports of linkage between genetic markers along the genome and NIDDM or NIDDM-related quantitative traits. We sought to determine whether individual quantitative traits which determine glucose tolerance exhibit familiarity in Finnish families with at least one NIDDM-affected sibling pair. Tolbutamide-modified frequently sampled intravenous glucose tolerance tests (FSIGT) were performed on unaffected offspring (n = 431) and spouses (n = 154) of affected sibling pairs sampled for the Finland-United States Investigation of NIDDM Genetics (FUSION) study. FSIGT data were analyzed using the Minimal Model to obtain quantitative measures of insulin sensitivity (S-I), glucose effectiveness (S-G), and insulin secretion assessed as the acute insulin response to glucose (AIR). The disposition index (DI), a measure of insulin resistance-corrected beta-cell function, was also derived as the product of S-I and AIR. Variance components analysis was used to determine for each trait, the heritability (h(2)), the proportion of the total trait variance accounted for by additive genes. After adjustment for age, gender, and body mass index, h(2) estimates were: S-G: 18 +/- 9%, S-I: 28 +/- 8%, AIR: 35 +/- 8%, and DI: 23 +/- 8%. We conclude that there is strong evidence for modest heritability of Minimal-Model-derived NIDDM-related quantitative traits in unaffected spouses and offspring of Finnish affected sibling pairs. C1 Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Diabetes & Genet Epidemiol Unit, Helsinki, Finland. Natl Publ Hlth Inst, Dept Biochem, Helsinki, Finland. Natl Human Genome Res Inst, Genet & Mol Biol Branch, Lab Gene Transfer, Bethesda, MD USA. Univ So Calif, Sch Med, Dept Physiol & Biophys, Los Angeles, CA 90033 USA. RP Watanabe, RM (reprint author), Univ Michigan, Sch Publ Hlth, Dept Biostat, 1420 Washington Heights, Ann Arbor, MI 48109 USA. OI Hauser, Elizabeth/0000-0003-0367-9189 NR 40 TC 88 Z9 88 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0001-5652 J9 HUM HERED JI Hum. Hered. PY 1999 VL 49 IS 3 BP 159 EP 168 DI 10.1159/000022865 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 204YB UT WOS:000080792600008 PM 10364681 ER PT J AU Li, CL Chen, L Iwata, T Kitagawa, M Fu, XY Deng, CX AF Li, CL Chen, L Iwata, T Kitagawa, M Fu, XY Deng, CX TI A Lys644Glu substitution in fibroblast growth factor receptor 3 (FGFR3) causes dwarfism in mice by activation of STATs and ink4 cell cycle inhibitors SO HUMAN MOLECULAR GENETICS LA English DT Article ID HORMONE-RELATED PEPTIDE; ENDOCHONDRAL BONE-FORMATION; LETHAL SKELETAL DYSPLASIA; THANATOPHORIC DYSPLASIA; TRANSMEMBRANE DOMAIN; TRANSCRIPTION FACTOR; ACHONDROPLASIA; MUTATIONS; GENE; CARTILAGE AB Missense mutations of human fibroblast growth factor receptor 3 (FGFR3) result in several skeletal dysplasias, including hypochondroplasia, achondroplasia and thanatophoric dysplasia. To study the function of FGFR3 in bone growth and to create animal models for the FGFR3-related inherited skeletal disorders, we introduced a point mutation (Lys644Glu) into the murine FGFR3 genome using a knock-in approach. We found that the Lys644Glu mutation resulted in retarded endochondral bone growth with severity directly linked to the expression level of the mutated Fgfr3, Mice heterozygous for the mutation (Fgfr3(TD/+)) expressed the mutant allele at similar to 20% of the wild-type level and exhibited a mild bone dysplasia, However, when the copy number of the mutant allele increased from one (Fgfr3(TD/+)) to two (Fgfr3(TD/TD)), the retardation of bone growth became more severe and showed phenotypes resembling those of achondroplasia patients, characterized by a dramatically reduced proliferation of growth plate cartilage, macrocephaly and shortening of the long bones, which was most pronounced in the femur. Molecular analysis revealed that expression of the mutant receptor caused the activation of Stat1, Stat5a and Stat5b, and the up-regulation of p16, p18 and p19 cell cycle inhibitors, leading to dramatic expansion of the resting zone of chondrocytes at the expense of the proliferating chondrocytes. The mutant growth plates consequently were in a less active state and generated fewer maturing and hypertrophic chondrocytes. These data provide direct genetic evidence that the point mutations in FGFR3 cause human skeletal dysplasias and uncover a mechanism through which the FGFR3 signals regulate bone growth by modulating expression of Stats and ink4 cell cycle inhibitors. C1 NIDDKD, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA. Natl Human Genome Res Inst, Med Genet Branch, NIH, Bethesda, MD 20892 USA. Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA. RP Deng, CX (reprint author), NIDDKD, Genet Dev & Dis Branch, NIH, 10-9N105,10 Ctr Dr, Bethesda, MD 20892 USA. RI deng, chuxia/N-6713-2016 NR 50 TC 162 Z9 167 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD JAN PY 1999 VL 8 IS 1 BP 35 EP 44 DI 10.1093/hmg/8.1.35 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 162ZF UT WOS:000078377200004 PM 9887329 ER PT J AU Everett, LA Green, ED AF Everett, LA Green, ED TI A family of mammalian anion transporters and their involvement in human genetic diseases SO HUMAN MOLECULAR GENETICS LA English DT Review ID CONGENITAL CHLORIDE DIARRHEA; DYSPLASIA SULFATE-TRANSPORTER; ADENOMA DRA GENE; SENSORINEURAL HEARING-LOSS; ACHONDROGENESIS TYPE 1B; DIASTROPHIC DYSPLASIA; PENDRED-SYNDROME; ATELOSTEOGENESIS TYPE-2; LINKAGE DISEQUILIBRIUM; POSITIONAL CLONING AB Tremendous advances in human genetics have been made in recent years, as the fruits of the Human Genome Project are facilitating the identification of genes associated with myriad genetic diseases. Among the many triumphs in positional (and positional candidate) cloning are a number of cases where apparently unrelated diseases have been found to share common genetic origins. A vivid example of this has unfolded in the past few years with the identification of the genes causing diastrophic dysplasia, congenital chloride diarrhoea and Pendred syndrome. While these three disorders are clinically distinct, the associated genes (DTDST, CLD and PDS, respectively) emanate from a well conserved family of genes that all encode anion transporters. Our current knowledge of these diseases coupled with new insights about the implicated genes and proteins illustrates the complex nature of mammalian genomes, especially with respect to the evolutionary subtleties of protein families and tissue-specific gene expression. C1 Natl Human Genome Res Inst, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. RP Green, ED (reprint author), Natl Human Genome Res Inst, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. NR 101 TC 98 Z9 100 U1 1 U2 4 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PY 1999 VL 8 IS 10 SI SI BP 1883 EP 1891 DI 10.1093/hmg/8.10.1883 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 242QN UT WOS:000082952800009 PM 10469841 ER PT J AU Fletcher, CF Frankel, WN AF Fletcher, CF Frankel, WN TI Ataxic mouse mutants and molecular mechanisms of absence epilepsy SO HUMAN MOLECULAR GENETICS LA English DT Review ID POTASSIUM CHANNEL GENE; MICE LACKING; NEUROTROPHIC FACTOR; INHERITED EPILEPSY; WAVE EPILEPSY; SPIKE-WAVE; MUTATION; SEIZURES; SUBUNIT; EXPRESSION AB Mouse genetic models for common human diseases have been studied for most of the 20th century. Although many polygenic strain differences and spontaneous single gene mutants have been extensively characterized over the years, knowing their innermost secrets ultimately requires the identity of the mutated genes. One group of neurological mutants, detected initially clue to cerebellar dysfunction, was identified as models for epilepsy when they were unexpectedly found to have spike-wave seizures associated with behavioral arrest, a central feature of absence or petit-mal epilepsy. A further surprise was that recently identified defective genes encode different subunits of voltage-gated Ca2+ channels (VGCCs), implying common seizure mechanisms. In this review we first consider these spontaneous mutants with VGCC defects in the context of other mouse models for epilepsy. Then, from the new wave of genetic and functional studies of these mutants we discuss their prospects for yielding insight into the molecular mechanisms of epilepsy. C1 Jackson Lab, Bar Harbor, ME 04609 USA. NCI, Frederick Canc Res & Dev Ctr, ABL Basic Res Program, MGL, Frederick, MD USA. RP Frankel, WN (reprint author), Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA. NR 57 TC 38 Z9 38 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PY 1999 VL 8 IS 10 SI SI BP 1907 EP 1912 DI 10.1093/hmg/8.10.1907 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 242QN UT WOS:000082952800012 PM 10469844 ER PT J AU Carrington, M Dean, M Martin, MP O'Brien, SJ AF Carrington, M Dean, M Martin, MP O'Brien, SJ TI Genetics of HIV-1 infection: chemokine receptor CCR5 polymorphism and its consequences SO HUMAN MOLECULAR GENETICS LA English DT Review ID MACROPHAGE-TROPIC HIV-1; DISEASE PROGRESSION; FUNCTIONAL EXPRESSION; CO-RECEPTORS; CCR5-DELTA-32; CORECEPTOR; RESISTANCE; CLONING; ALLELE; AIDS AB The chemokine receptor gene, CCR5, has become a central theme in studies of host genetic effects on HIV-1 pathogenesis ever since the discovery that the CCR5 molecule serves as a major cell surface co-receptor for the virus. A growing number of genetic variants within the coding and 5' regulatory region of CCR5 have been identified, several of which have functional consequences for HIV-1 pathogenesis. Here we review the CCR5 literature describing CCR5 polymorphism and the functional ramifications that several of these variants have on HIV-1 infection and progression to AIDS. The multiplicity of CCR5 genetic effects on HIV-1 disease underscores the critical importance of this gene in controlling AIDS pathogenesis and provides the logic for development of therapeutic strategies that target the interaction of HIV-1 envelope and CCR5 in HIV-1 associated disease. C1 NCI, Lab Gen Divers, Frederick, MD 21702 USA. SAIC, Intramural Res Support Program, Frederick, MD 21702 USA. RP O'Brien, SJ (reprint author), NCI, Lab Gen Divers, Frederick, MD 21702 USA. RI Dean, Michael/G-8172-2012 OI Dean, Michael/0000-0003-2234-0631 NR 60 TC 141 Z9 149 U1 0 U2 10 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PY 1999 VL 8 IS 10 SI SI BP 1939 EP 1945 DI 10.1093/hmg/8.10.1939 PG 7 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 242QN UT WOS:000082952800015 PM 10469847 ER PT J AU Banerjee-Basu, S Baxevanis, AD AF Banerjee-Basu, S Baxevanis, AD TI Threading analysis of the Pitx2 homeodomain: Predicted structural effects of mutations causing Rieger syndrome and iridogoniodysgenesis SO HUMAN MUTATION LA English DT Article DE PITX2; Rieger syndrome; RIEG1; iridogoniodysgenesis type 2; IRID2; threading analysis; protein structure; folding; homeodomain ID DNA-BINDING; ANTENNAPEDIA HOMEODOMAIN; ENGRAILED HOMEODOMAIN; CRYSTAL-STRUCTURE; COMPLEX; GENE; SPECTROSCOPY; SPECIFICITY AB Mutations in the homeobox gene PITX2 are responsible for a range of clinical phenotypes involving ocular and craniofacial development. Several mutations within the Pitx2 homeodomain region are specifically responsible for the development of the related autosomal-dominant disorders Rieger syndrome and iridogoniodysgenesis,To address the question of the structural effect of disease causing mutations on the Pitx2 homeodomain, we used threading techniques to examine the tertiary structure of the Pitx2 wild-type and mutant homeodomain, using the crystal structure of Drosophila engrailed homeodomain bound with DNA as a template [Kissinger et al., 1990], The threading analysis reveals that the wild-type Pitx2 homeodomain is indeed capable of forming the typical three-helical bundle-fold characteristic of homeodomain proteins. Energy calculations indicate that the homeodomain structure is stabilized primarily by hydrophobic interactions between residues at the helical interface. Point mutations responsible for the development of these genetic disorders were also examined; the results suggest that these mutations lead to the inability of Pitx2 to adopt its proper structure and bind to the regulatory sequences of its target gene(s), which in turn affects its metabolic role in the cell, Hum Mutat 14:312-319, 1999. Published 1999 Wiley-Liss, Inc.dagger C1 Natl Human Genome Res Inst, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. RP Baxevanis, AD (reprint author), Natl Human Genome Res Inst, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. NR 22 TC 10 Z9 11 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 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1999 VL 14 IS 4 BP 312 EP 319 DI 10.1002/(SICI)1098-1004(199910)14:4<312::AID-HUMU6>3.0.CO;2-S PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 242TC UT WOS:000082956900006 PM 10502778 ER PT J AU Anikster, Y Shotelersuk, V Gahl, WA AF Anikster, Y Shotelersuk, V Gahl, WA TI CTNS mutations in patients with cystinosis SO HUMAN MUTATION LA English DT Article DE cystinosis; lysosomal storage disease; transport; deletions; variants ID NEPHROPATHIC CYSTINOSIS; ESCHERICHIA-COLI; BINDING-PROTEIN; CYSTEAMINE; FRACTIONS; CHILDREN AB Cystinosis is an autosomal recessive lysosomal storage disease caused by mutations in the gene CTNS, The CTNS gene product, cystinosin, has 367 amino acids and seven transmembrane domains and is thought to transport cystine out of lysosomes. The most common form of cystinosis, the nephropathic or infantile type, is characterized by renal failure at 10 years of age and other systemic complications. To date, 32 different CTNS mutations have been described in nephropathic cystinosis patients. Intermediate cystinosis, with later onset of renal disease, has been associated with three different CTNS mutations. Benign or nonnephropathic cystinosis, with symptoms related only to corneal crystals and photophobia, has been associated with two other CTNS mutations. In general, only certain splicing or missense mutations are associated with milder cystinosis phenotypes. Hum Mutat 14:454-458, 1999. Published 1999 Wiley-Liss, Inc.dagger. C1 NICHHD, Sect Human Biochem Genet, Heritable Disorders Branch, Bethesda, MD 20892 USA. RP Gahl, WA (reprint author), NICHD, NIH, 10 Ctr Dr,MSC 1830,Bldg 10,Room 9S-241, Bethesda, MD 20892 USA. NR 24 TC 36 Z9 38 U1 1 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1999 VL 14 IS 6 BP 454 EP 458 DI 10.1002/(SICI)1098-1004(199912)14:6<454::AID-HUMU2>3.0.CO;2-H PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 263AR UT WOS:000084100900001 PM 10571941 ER PT J AU Heino, M Scott, HS Chen, QY Peterson, P Maenpaa, U Papasavvas, MP Mittaz, L Barras, C Rossier, C Chrousos, GP Stratakis, CA Nagamine, K Kudoh, J Shimizu, N Maclaren, N Antonarakis, SE Krohn, K AF Heino, M Scott, HS Chen, QY Peterson, P Maenpaa, U Papasavvas, MP Mittaz, L Barras, C Rossier, C Chrousos, GP Stratakis, CA Nagamine, K Kudoh, J Shimizu, N Maclaren, N Antonarakis, SE Krohn, K TI Mutation analyses of North American APS-1 patients SO HUMAN MUTATION LA English DT Article DE autoimmunity; polyendocrinopathies; chromosome 21 ID DISEASE TYPE-I; AUTOIMMUNE-DISEASE; SERIES; GENE AB Autoimmune polyendocrinopathy syndrome type 1 (APS-1; MIM# 240300) is a rare autosomal recessively inherited disease characterised by destructive autoimmune diseases of endocrine glands. The gene responsible for APS-1, known as AIRE (for autoimmune regulator), was recently identified and contains motifs suggestive of a transcription regulator, To date, nine APS-1-associated mutations have been identified in the AIRE gene, including two common mutations R257X and 1094-1106del. In addition to these two mutations, we report seven novel mutations in 16 APS-1 patients from North America, We found that 1094-1106del and R257X were the most common mutations in this population of mixed geoethnic origin, accounting for 17/32 and 4/32 alleles, respectively, Haplotype analyses suggest that both are recurrent mutations, occurring on several different haplotypes with closely linked markers. All the novel mutations appear to be rare, occur ring in only single APS 1 families. After examining all coding sequences and exon/intron boundaries of the AIRE gene, the other APS 1 allele remained unidentified in three patients, Genotype phenotype correlations for APS-1 remain difficult, suggesting that other genetic or environmental factors, or both, influence the clinical presentation and disease progression in individual APS 1 patients. Hum Mutat 13:69-74, 1999. (C) 1999 Wiley-Liss, Inc. C1 Univ Tampere, Inst Med Technol, Dept Pathol, FIN-33101 Tampere, Finland. Tampere Univ Hosp, Tampere, Finland. Hop Cantonal Geneva, Div Med Genet, CH-1211 Geneva, Switzerland. Res Inst Children, Harahan, LA USA. NICHD, DEB, Sect Pediat Endocrinol, Unit Genet & Endocrinol,NIH, Bethesda, MD USA. Keio Univ, Sch Med, Dept Mol Biol, Tokyo, Japan. RP Heino, M (reprint author), Univ Tampere, Inst Med Technol, Dept Pathol, FIN-33101 Tampere, Finland. EM mh55012@uta.fi RI Peterson, Part/A-5788-2009; Scott, Hamish/B-2122-2009; Antonarakis, Stylianos/N-8866-2014 OI Peterson, Part/0000-0001-6755-791X; Scott, Hamish/0000-0002-5813-631X; Antonarakis, Stylianos/0000-0001-8907-5823 NR 20 TC 76 Z9 79 U1 1 U2 2 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PY 1999 VL 13 IS 1 BP 69 EP 74 DI 10.1002/(SICI)1098-1004(1999)13:1<69::AID-HUMU8>3.0.CO;2-6 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 151BA UT WOS:000077700000008 PM 9888391 ER PT J AU Fidelia-Lambert, MN Zhuang, ZP Tsokos, M AF Fidelia-Lambert, MN Zhuang, ZP Tsokos, M TI Sensitive detection of rare Ewing's sarcoma cells in peripheral blood by reverse transcriptase polymerase chain reaction SO HUMAN PATHOLOGY LA English DT Article DE ewing's; peripheral blood; RT-PCR ID CIRCULATING TUMOR-CELLS; CHROMOSOMAL TRANSLOCATIONS; EWS GENE; FAMILY; FUSION; MICROMETASTASES; FUSES; BONE AB Disseminated disease is very important in the clinical assessment of pediatric sarcomas. Several reports suggest that reverse transcriptase polymerase chain reaction (RT-PCR) holds great promise in the early staging of cancer patients in general. However, the complexities of these protocols hamper adequate standardization, and their application as routine diagnostic tools has been difficult. The aim of this study is to assess the actual minimal number of tumor cells that may be detected by RT-PCR in a blood sample. Specific tumor cell dilutions from a Ewing's sarcoma cell line reconstituted in peripheral blood from healthy individuals were "ficolled" and submitted to RNA extraction for cDNA preparation and PCR amplification of the t(11-22) (q24;q12) fusion transcript. After PCR amplification, we were able to detect the EWS/FLI-1 chimeric gene product at a dilution of 10 tumor cells per 1 or 2 mt of blood. Our simple method supports a role for routine clinical use of RT-PCR in the detection of circulating Ewing's sarcoma cells. C1 NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA. RP Tsokos, M (reprint author), NCI, Pathol Lab, NIH, Bldg 10,Rm 2A10,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 21 TC 3 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1999 VL 30 IS 1 BP 78 EP 80 DI 10.1016/S0046-8177(99)90304-0 PG 3 WC Pathology SC Pathology GA 158DY UT WOS:000078101800013 PM 9923931 ER PT J AU Rugge, M Shiao, YH Guido, M Bovo, D AF Rugge, M Shiao, YH Guido, M Bovo, D TI Microsatellite instability and gastric cancer subtypes SO HUMAN PATHOLOGY LA English DT Letter ID HIGH-RISK POPULATION; CARCINOMAS C1 Univ Padua, Cattedra Istochim & Immunoistochim Patol, Padua, Italy. NCI, Frederick Canc Res & Dev Ctr, Comparat Carcinogenesis Lab, NIH, Frederick, MD 21702 USA. Univ Padua, Dept Pediat, Padua, Italy. RP Rugge, M (reprint author), Univ Padua, Cattedra Istochim & Immunoistochim Patol, Padua, Italy. RI Rugge, Massimo/K-7525-2016; Fiocca, Roberto/K-9705-2016 OI Fiocca, Roberto/0000-0002-8856-6185 NR 8 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1999 VL 30 IS 1 BP 108 EP 109 DI 10.1016/S0046-8177(99)90310-6 PG 2 WC Pathology SC Pathology GA 158DY UT WOS:000078101800019 PM 9923937 ER PT S AU Leikin, S AF Leikin, S BE BellissentFunel, MC TI Hydration forces between biological macromolecules: Measurements, speculations and established facts SO HYDRATION PROCESSES IN BIOLOGY: THEORETICAL AND EXPERIMENTAL APPROACHES SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES A, LIFE SCIENCES LA English DT Proceedings Paper CT Conference on the Nato Advanced Study Institute on Hydration Processes in Biology - Theoretical and Experimental Approaches CY MAY 04-05, 1998 CL LES HOUCHES, FRANCE SP Nato Sci Comm, CEA, CNRS ID COLLAGEN TRIPLE HELICES; DNA DOUBLE HELICES; GUANOSINE 4-STRANDED HELICES; PHOSPHOLIPID-BILAYERS; INTERMOLECULAR FORCES; COLLOIDAL FORCES; OSMOTIC-STRESS; SURFACE FORCES; WATER; TEMPERATURE AB The existence of short-range forces between polar surfaces resulting from interaction between structured surface water lavers has been debated for most of this century. Starting from the pioneering work of Langmuir [1], it was often assumed that they may contribute significantly to colloid stability. However, experimental techniques achieved enough sophistication for their direct measurement only in the last two decades. The measurements, indeed, revealed strong exponential interactions of unknown nature in the last several nanometers of separation between a variety of surfaces. Still, the puzzle persists. Are these hydration forces? This interpretation seems to be natural, but it is difficult to exclude interpretations based on other interactions including, e.g., electrostatic and steric forces. There seem to be almost as many opinions as there are researchers studying these phenomena. (For several recent reviews see, e.g., [2-4]). Here I summarize the latest developments in understanding of short-range forces between biological macromolecules. I briefly review experimental techniques of force measurement, the existing data and interpretations. This analysis is far from exhaustive. Instead, I describe only those results which, in my opinion, are most interesting and revealing. Specifically, I focus on interactions between collagen helices because recent evidence overwhelmingly favors the hydration interpretation. C1 NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA. RP Leikin, S (reprint author), NICHD, Lab Phys & Struct Biol, NIH, Bldg 12A,Rm 2041, Bethesda, MD 20892 USA. NR 58 TC 2 Z9 2 U1 0 U2 0 PU I O S PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0258-1213 BN 90-5199-439-7 J9 NATO ADV SCI I A-LIF PY 1999 VL 305 BP 313 EP 321 PG 9 WC Biophysics SC Biophysics GA BP30C UT WOS:000084623300018 ER PT S AU Leikin, S AF Leikin, S BE BellissentFunel, MC TI Theory of electrostatic and hydration interactions between helical macromolecules SO HYDRATION PROCESSES IN BIOLOGY: THEORETICAL AND EXPERIMENTAL APPROACHES SE NATO ADVANCED SCIENCE INSTITUTES SERIES, SERIES A, LIFE SCIENCES LA English DT Proceedings Paper CT Conference on the Nato Advanced Study Institute on Hydration Processes in Biology - Theoretical and Experimental Approaches CY MAY 04-05, 1998 CL LES HOUCHES, FRANCE SP Nato Sci Comm, CEA, CNRS ID GUANOSINE 4-STRANDED HELICES; COLLAGEN TRIPLE HELICES; DEBYE-HUCKEL THEORY; DNA DOUBLE HELICES; RAMAN-SPECTROSCOPY; B-DNA; FORCES; WATER; CONDENSATION; RESOLUTION AB Helices are common structural blocks of all living organisms. Their interactions play a crucial role in biology. Measurements have revealed unexpectedly strong repulsive and attractive forces at biologically relevant surface separations (0 to 20 Angstrom) between a variety of helical molecules [1-9]. These forces do not conform to the Derjaguin-Landau-Verwey-Overbeek (DLVO) theory. In the preceding lecture we discussed these force measurements and their qualitative interpretations. In this lecture I describe the theoretical foundation behind some of these hypotheses and focus on the analysis of possible roles of these forces in various observed phenomena. C1 NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA. RP Leikin, S (reprint author), NICHD, Lab Phys & Struct Biol, NIH, Bldg 12A,Rm 2041, Bethesda, MD 20892 USA. NR 38 TC 0 Z9 0 U1 0 U2 0 PU I O S PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0258-1213 BN 90-5199-439-7 J9 NATO ADV SCI I A-LIF PY 1999 VL 305 BP 323 EP 332 PG 10 WC Biophysics SC Biophysics GA BP30C UT WOS:000084623300019 ER PT J AU Goldstein, DS Golczynska, A Stuhlmuller, J Holmes, C Rea, RF Grossman, E Lenders, J AF Goldstein, DS Golczynska, A Stuhlmuller, J Holmes, C Rea, RF Grossman, E Lenders, J TI A test of the "epinephrine hypothesis" in humans SO HYPERTENSION LA English DT Article DE epinephrine; norepinephrine; nervous system, sympathetic; yohimbine; nitroprusside ID SYMPATHETIC-NERVE ACTIVITY; HUMAN FOREARM; NOREPINEPHRINE; RELEASE; STIMULATION; REMOVAL; PLASMA; HYPERTENSION; ACTIVATION; INFUSION AB According to the "epinephrine hypothesis," circulating epinephrine taken up by sympathetic nerves is coreleased with norepinephrine during sympathetic stimulation and binding of coreleased epinephrine to presynaptic beta-adrenoceptors augments exocytotic release of norepinephrine, contributing to high blood pressure. This study examined whether infusion of a physiologically active amount of epinephrine affects subsequent vascular responses and the estimated rate of entry of norepinephrine into regional venous plasma (norepinephrine spillover). Each of 3 experiments included intravenous infusion of H-3-norepinephrine, measurements of forearm vascular resistance, and intra-arterial infusion of epinephrine (3 ng/min per deciliter forearm volume). In experiment I, subjects underwent lower body negative pressure (LBNP-25 mm Hg) before and after intra-arterial epinephrine; in experiment 2, LBNP and intra-arterial yohimbine before and after intra-arterial epinephrine; and in experiment 3, intravenous nitroprusside before and after intra-arterial epinephrine. In all subjects, intra-arterial epinephrine produced ipsilateral pallor and decreased forearm vascular resistance. Ipsilateral venous epinephrine increased by 10-fold. Epinephrine did not affect forearm vasoconstrictor responses to LBNP or vasodilator responses to intra-arterial yohimbine or intravenous nitroprusside; did not affect venous norepinephrine levels or norepinephrine spillover during LBNP, yohimbine, LBNP during yohimbine, or nitroprusside; and did not increase venous epinephrine levels during any of these manipulations. Loading of forearm sympathetic terminals with epinephrine therefore does not augment subsequent neurogenic vasoconstriction or norepinephrine release in the human forearm in response to sympathetic stimulation. The findings are inconsistent with the epinephrine hypothesis. C1 NINDS, Clin Neurosci Branch, NIH, Bethesda, MD 20892 USA. US FDA, Dept Hlth & Human Serv, Rockville, MD USA. Mayo Clin, Rochester, MN USA. Chaim Sheba Med Ctr, Dept Internal Med D, IL-52621 Tel Hashomer, Israel. Univ Nijmegen St Radboud Hosp, Dept Internal Med, NL-6500 HB Nijmegen, Netherlands. RP Goldstein, DS (reprint author), NINDS, Clin Neurosci Branch, NIH, Bldg 10,Room 6N252,10 Ctr Dr MSC 1620, Bethesda, MD 20892 USA. NR 24 TC 17 Z9 17 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1999 VL 33 IS 1 BP 36 EP 43 PG 8 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 161JM UT WOS:000078285500008 PM 9931079 ER PT J AU Li, ZH Froehlich, J Galis, ZS Lakatta, EG AF Li, ZH Froehlich, J Galis, ZS Lakatta, EG TI Increased expression of matrix metalloproteinase-2 in the thickened intima of aged rats SO HYPERTENSION LA English DT Article DE intimal thickening; aging; matrix metalloproteinase-2; cytokines; cells, vascular smooth muscle ID SMOOTH-MUSCLE CELLS; GROWTH-FACTOR-BETA; IV COLLAGENASE; TISSUE INHIBITOR; ARTERIAL INJURY; VASCULAR CELLS; DIFFERENTIATION; MIGRATION; PROLIFERATION; LOCALIZATION AB To characterize remodeling of elastic arteries with aging and to investigate its potential mechanisms, matrix metalloproteinase-2 (MMP-2), intracellular adhesive molecule-1 (ICAM-1), transforming growth factor-beta (TGF-beta), and fibronectin protein levels were measured in the aortas of young adult (6 months) and aged (30 months) Fischer 344XBN rats. At 30 versus 6 months, the thickness of the intima was 5-fold greater and contained marked increases in TGF-beta and ICAM-1, and fibronectin expression was enhanced throughout the aortic wall. Total MMP-2 protein (Western blot) of 30-month-old rats was increased 8-fold over that of 6-month-old rats (0.166+/-0.032 versus 0.020+/-0.006; P<0.01), and staining and activity were regionally localized to the intima, often near breaks in the internal elastic membrane and lamellae. Early passage, explanted smooth muscle cells (SMC) from aged aorta secreted more MMP-2 than those from young aorta; while basal MMP-2 production did not differ with age, after stimulation with cytokines (interleukin-1, tumor necrosis factor-alpha, or TGF-beta, 10 ng/mL each for 24 hours), MMP-2 production in SMC from 30-month-old rats increased to levels greater than those in 6-month-old rats. Thus, enhanced expression of TGF-beta, MMP-2, and ICAM-1 in the thickened vascular intima of aged rats may in part be produced by exaggerated SMC responses to cytokines and may have potential roles in intimal remodeling with aging. C1 NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Emory Univ, Sch Med, Div Cardiol, Atlanta, GA 30322 USA. RP Lakatta, EG (reprint author), NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. NR 32 TC 108 Z9 116 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD JAN PY 1999 VL 33 IS 1 BP 116 EP 123 PG 8 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 161JM UT WOS:000078285500020 PM 9931091 ER PT S AU McCray, AT Gallagher, ME Flannick, MA AF McCray, AT Gallagher, ME Flannick, MA GP IEEE COMP SOC IEEE COMP SOC TI Extending the role of metadata in a digital library system SO IEEE FORUM ON RESEARCH AND TECHNOLOGY ADVANCES IN DIGITAL LIBRARIES, PROCEEDINGS SE PROCEEDINGS - IEEE INTERNATIONAL FORUM ON RESEARCH AND TECHNOLOGY ADVANCES IN DIGITAL LIBRARIES LA English DT Proceedings Paper CT IEEE Forum on Research and Technology Advances in Digital Libraries CY MAY 19-21, 1999 CL BALTIMORE, MD SP IEEE Comp Soc, Tech Comm Digital Lib, Rutgers, CIMIC, Forsch Zentrum Informat Technik GmbH, Natl Lib Med, NASA, CESDIS, GTE Labs, Oracle Corp, Sun Microsyst, Silicon Graph AB We describe an approach to the development of a digital library system that is founded on a number of basic principles. In particular, we discuss the critical role of metadata in all aspects of the system design. We begin by describing how the notion of metadata is sometimes interpreted and go on to discuss some of our early experiences in a digital conversion project. We report on the Profiles in Science project, which is making the archival collections of prominent biomedical scientists available on the World Wide Web. We discuss the principles that are used in our system design, illustrating these throughout the discussion. Our approach has involved interpreting metadata in its broadest sense. We capture data about the items in our digital collection for a a variety of purposes and use those data to drive the entire system. Further, we have designed our overall system architecture such that it can accommodate changes while still ensuring the persistence of the underlying data. C1 Natl Lib Med, Bethesda, MD 20894 USA. RP McCray, AT (reprint author), Natl Lib Med, Bethesda, MD 20894 USA. NR 16 TC 6 Z9 6 U1 0 U2 2 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 USA SN 1092-9959 BN 0-7695-0219-9 J9 P IEEE INT FORUM RES PY 1999 BP 190 EP 199 DI 10.1109/ADL.1999.777714 PG 10 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications SC Computer Science GA BN77E UT WOS:000082879600026 ER PT S AU McCray, AT AF McCray, AT GP IEEE COMP SOC IEEE COMP SOC TI Digital libraries initiative, phase 2 SO IEEE FORUM ON RESEARCH AND TECHNOLOGY ADVANCES IN DIGITAL LIBRARIES, PROCEEDINGS SE PROCEEDINGS - IEEE INTERNATIONAL FORUM ON RESEARCH AND TECHNOLOGY ADVANCES IN DIGITAL LIBRARIES LA English DT Proceedings Paper CT IEEE Forum on Research and Technology Advances in Digital Libraries CY MAY 19-21, 1999 CL BALTIMORE, MD SP IEEE Comp Soc, Tech Comm Digital Lib, Rutgers, CIMIC, Forsch Zentrum Informat Technik GmbH, Natl Lib Med, NASA, CESDIS, GTE Labs, Oracle Corp, Sun Microsyst, Silicon Graph C1 Natl Lib Med, Bethesda, MD 20894 USA. RP McCray, AT (reprint author), Natl Lib Med, 8600 Rockville Pike, Bethesda, MD 20894 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU IEEE COMPUTER SOC PI LOS ALAMITOS PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 USA SN 1092-9959 BN 0-7695-0219-9 J9 P IEEE INT FORUM RES PY 1999 BP 216 EP 216 DI 10.1109/ADL.1999.777716 PG 1 WC Computer Science, Information Systems; Computer Science, Interdisciplinary Applications SC Computer Science GA BN77E UT WOS:000082879600028 ER PT J AU Garboczi, DN Biddison, WE AF Garboczi, DN Biddison, WE TI Shapes of MHC restriction SO IMMUNITY LA English DT Review ID T-CELL RECEPTOR; ANTIGEN RECEPTOR; VIRAL PEPTIDES; ALPHA-BETA; NEGATIVE SELECTION; VIRUS TYPE-1; PROTEIN; SPECIFICITY; TCR; CRYSTALLIZATION C1 NIAID, Struct Biol Sect, NIH, Rockville, MD 20852 USA. NINDS, Mol Immunol Sect, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA. RP Garboczi, DN (reprint author), NIAID, Struct Biol Sect, NIH, Rockville, MD 20852 USA. NR 44 TC 67 Z9 69 U1 2 U2 3 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD JAN PY 1999 VL 10 IS 1 BP 1 EP 7 DI 10.1016/S1074-7613(00)80001-1 PG 7 WC Immunology SC Immunology GA 163WE UT WOS:000078428700001 PM 10023765 ER PT J AU Boyington, JC Riaz, AN Patamawenu, A Coligan, JE Brooks, AG Sun, PD AF Boyington, JC Riaz, AN Patamawenu, A Coligan, JE Brooks, AG Sun, PD TI Structure of CD94 reveals a novel C-type lectin fold: Implications for the NK cell-associated CD94/NKG2 receptors SO IMMUNITY LA English DT Article ID MANNOSE-BINDING PROTEIN; NATURAL-KILLER-CELLS; HELICAL COILED-COIL; CRYSTAL-STRUCTURE; INHIBITORY RECEPTOR; RECOGNITION; DOMAIN; COMPLEX; MOLECULES AB The crystal structure of the extracellular domain of CD94, a component of the CD94/NKG2 NK cell receptor, has been determined to 2.6 Angstrom resolution, revealing a unique variation of the C-type lectin fold. In this variation, the second cu helix, corresponding to residues 102-112, is replaced by a loop, the putative carbohydrate-binding site is significantly altered, and the Ca2+-binding site appears nonfunctional. This structure may serve as a prototype for other NK cell receptors such as Ly-49, NKR-P1, and CD69. The CD94 dimer observed in the crystal has an extensive hydrophobic interface that stabilizes the loop conformation of residues 102-112. The formation of this dimer reveals a putative ligand-binding region for HLA-E and suggests how NKG2 interacts with CD94. C1 NIAID, Struct Biol Sect, Off Sci Director, NIH, Rockville, MD 20852 USA. NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA. RP Sun, PD (reprint author), NIAID, Struct Biol Sect, Off Sci Director, NIH, 12441 Parklawn Dr, Rockville, MD 20852 USA. EM sun@magenta.niaid.nih.gov NR 43 TC 115 Z9 117 U1 0 U2 7 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD JAN PY 1999 VL 10 IS 1 BP 75 EP 82 DI 10.1016/S1074-7613(00)80008-4 PG 8 WC Immunology SC Immunology GA 163WE UT WOS:000078428700008 PM 10023772 ER PT J AU Rosenberg, HF Domachowske, JB AF Rosenberg, HF Domachowske, JB TI Eosinophils, ribonucleases and host defense: Solving the puzzle SO IMMUNOLOGIC RESEARCH LA English DT Article DE eosinophilis; ribonucleases; antiviral agents; host defense ID RESPIRATORY SYNCYTIAL VIRUS; INTERCELLULAR-ADHESION MOLECULE-1; GROWTH FACTOR-ALPHA; A GENE SUPERFAMILY; CATIONIC PROTEIN; SCHISTOSOMA-MANSONI; ANTIVIRAL ACTIVITY; EPITHELIAL-CELLS; HLA-DR; NEUROTOXIN AB The eosinophil ribonucleases eosinophil-derived neurotoxin (EDN/RNase 2) and eosinophil cationic protein (ECP/RNase 3) are among the major secretory effector proteins of human eosinophilic leukocytes, cells whose role in host defense remains controversial and poorly understood. We have recently described the unusual manner in which this ribonuclease lineage has evolved, with extraordinary diversification observed in primate as well as in rodent EDNs and ECPs. The results of our evolutionary studies suggest that the EDN/ECP ribonucleases are in the process of being tailored for a specific, ribonuclease-related goal. With this in mind, we have begun to look carefully at some of the intriguing associations that link eosinophils and their ribonucleases to disease caused by the single-stranded RNA viral pathogen, respiratory syncytial virus (RSV). Recent work in our laboratory has demonstrated that eosinophils can mediate a direct, ribonuclease-dependent reduction in infectivity of RSV in vitro, and that EDN can function alone as an independent antiviral agent. The results of this work have led us to consider the possibility that the EDN/ECP ribonucleases represent a heretofore unrecognized element of innate and specific antiviral host defense. C1 NIAID, LHD, NIH, Bethesda, MD 20892 USA. SUNY Hlth Sci Ctr, Dept Pediat, Syracuse, NY 13210 USA. RP Rosenberg, HF (reprint author), NIAID, LHD, NIH, Bldg 10,Room 11N104,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 66 TC 45 Z9 45 U1 1 U2 1 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1999 VL 20 IS 3 BP 261 EP 274 DI 10.1007/BF02790409 PG 14 WC Immunology SC Immunology GA 284XL UT WOS:000085358100008 PM 10741866 ER PT J AU Slavik, JM Hutchcroft, JE Bierer, BE AF Slavik, JM Hutchcroft, JE Bierer, BE TI CD28/CTLA-4 and CD80/CD86 families - Signaling and function SO IMMUNOLOGIC RESEARCH LA English DT Review DE T lymphocytes; signal transduction; cell-surface molecules; costimulatory molecules ID T-CELL RECEPTOR; PROTEIN-KINASE-C; PHOSPHATIDYLINOSITOL 3-KINASE ASSOCIATION; MULTIORGAN TISSUE DESTRUCTION; LYMPHOCYTE ANTIGEN RECEPTORS; CD28 COSTIMULATORY PATHWAY; CTLA-4 COUNTER-RECEPTOR; P70 S6 KINASE; TYROSINE KINASE; CTLA-4-DEFICIENT MICE AB T cell stimulation in the absence of a second, costimulatory signal can lead to anergy or the induction of cell death. CD28 is a major T cell costimulatory receptor, the coengagement of which can prevent anergy and cell death. The CD28 receptor is a member of a complex family of polypeptides that includes at least two receptors and two ligands. Cytotoxic lymphocyte-associated molecule-4 (CTLA-4, CD152) is the second member of the CD28 receptor family. The ligands or counterreceptors for these two proteins are the B7 family members, CD80 (B7-1) and CD86 (B7-2). This article reviews the CD28/CTLA4 and CD80/CD86 families, and outlines the functional outcomes an biochemical signaling pathways recruited after CD28 ligation. C1 NHLBI, NIH, Bethesda, MD 20892 USA. Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA. Purdue Univ, Dept Biochem, W Lafayette, IN 47907 USA. RP Bierer, BE (reprint author), NHLBI, NIH, Bldg 10,Room 5D49,10 Ctr Dr, Bethesda, MD 20892 USA. NR 199 TC 112 Z9 126 U1 0 U2 8 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA SN 0257-277X J9 IMMUNOL RES JI Immunol. Res. PY 1999 VL 19 IS 1 BP 1 EP 24 DI 10.1007/BF02786473 PG 24 WC Immunology SC Immunology GA 193CN UT WOS:000080118400001 PM 10374692 ER PT J AU Wojda, U Njoroge, J Miller, J AF Wojda, U Njoroge, J Miller, J TI Protection of cells from complement-mediated attack: CD59 receptor clustering for the entry of macromolecules into hematopoietic cells SO IMMUNOLOGICAL INVESTIGATIONS LA English DT Article ID GPI-ANCHORED PROTEINS; CROSS-LINKING; TYROSINE KINASE; FOLATE; CHOLESTEROL; ENDOCYTOSIS; CAVEOLAE; SURFACE; LYMPHOCYTES; ASSOCIATION AB CD59 is a glycosylphosphatidylinositol anchored protein (GPI-protein) that is expressed on surface membranes to protect host cells from complement-mediated attack. CD59 may also serve as a receptor for the endocytosis of macromolecules into nucleated cells. Here we investigate the effects of primary clustering of CD59 with anti-CD59 monoclonal antibody and the secondary clustering of biotinylated anti-CD59 with avidin on red blood cells and erythroleukemic K562 cells. On red blood cells, CD59-targeted antibodies remained evenly distributed on the external membranes. In contrast, clustering, capping and endocytosis of the CD59-targeted complexes was detected on K562 cells. Secondary clustering appeared more efficient and resulted in endosomal localization of the fluorescently labeled complexes within 2 hours. The endocytosis of CD59-bound complexes did not affect K562 cell viability or growth and the surface level of CD59 was constant during the process. These result suggest clustering and subsequent endocytosis of CD59 may enable the entry of macromolecules to the endosomal compartments of hematopoietic cells. C1 NIDDKD, Biol Chem Lab, NIH, Bethesda, MD 20892 USA. RP Miller, J (reprint author), NIDDKD, Biol Chem Lab, NIH, Bldg 10,Room 9N308, Bethesda, MD 20892 USA. RI Wojda, Urszula/M-6079-2015 OI Wojda, Urszula/0000-0002-4525-2004 NR 27 TC 6 Z9 6 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0882-0139 J9 IMMUNOL INVEST JI Immunol. Invest. PY 1999 VL 28 IS 2-3 BP 127 EP 135 DI 10.3109/08820139909061142 PG 9 WC Immunology SC Immunology GA 204FZ UT WOS:000080754600004 PM 10484678 ER PT S AU Srinivasan, A King, RD Bristol, DW AF Srinivasan, A King, RD Bristol, DW BE Dzeroski, S Flach, P TI An assessment of ILP-assisted models for toxicology and the PTE-3 experiment SO INDUCTIVE LOGIC PROGRAMMING SE LECTURE NOTES IN ARTIFICIAL INTELLIGENCE LA English DT Article; Proceedings Paper CT 9th International Workshop on Inductive Logic Programming (ILP-99) CY JUN 24-27, 1999 CL BLED, SLOVENIA SP ILPNet 2, Network Excellence Induct Log Programming, COMPULOG Net, European Network Excellence Computat Log, Jozef Stefan Inst, LPA Software Inc, Univ Bristol ID CHEMICALS; CARCINOGENICITY AB The Predictive Toxicology Evaluation (or PTE) Challenge provided Machine Learning techniques with the opportunity to compete against specialised techniques for toxicology prediction. Toxicity models that used findings from ILP programs have performed creditably in the PTE-2 experiment proposed under this challenge. We report here on an assessment of such models along scales of: (1) quantitative performance, in comparison to models developed with expert collaboration; and (2) potential explanatory value for toxicology. Results appear to suggest the following: (a) across of range of class distributions and error costs, some explicit models constructed with ILP-assistance appear closer to optimal than most expert-assisted ones. Given the paucity of test-data, this is to be interpreted cautiously; (b) a combined use of propositional and ILP techniques appears to yield models that contain unusual combinations of structural and biological features; and (c) significant effort was required to interpret the output, strongly indicating the need to invest greater effort in transforming the output into a "toxicologist-friendly" form. Based on the lessons learnt from these results, we propose a new predictive toxicology evaluation experiment - PTE-3 - which will address some important shortcomings of the previous study. C1 Univ Oxford, Comp Lab, Oxford OX1 3QD, England. Univ Wales, Dept Comp Sci, Aberystwyth, Ceredigion, Wales. NIEHS, Lab Carcinogenesis & Mutagenesis, Res Triangle Pk, NC 27709 USA. RP Srinivasan, A (reprint author), Univ Oxford, Comp Lab, Wolfson Bldg,Parks Rd, Oxford OX1 3QD, England. OI King, Ross/0000-0001-7208-4387 NR 20 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-66109-3 J9 LECT NOTES ARTIF INT PY 1999 VL 1634 BP 291 EP 302 PG 12 WC Computer Science, Artificial Intelligence SC Computer Science GA BR08D UT WOS:000165602200027 ER PT J AU Bornstein, MH Tamis-LeMonda, CS Haynes, OM AF Bornstein, MH Tamis-LeMonda, CS Haynes, OM TI First words in the second year: Continuity, stability, and models of concurrent and predictive correspondence in vocabulary and verbal responsiveness across age and context SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE child language; mother language; methodology; developmental models ID CHILDRENS LANGUAGE-DEVELOPMENT; EARLY LEXICAL ACQUISITION; COGNITIVE COMPETENCE; INFANT; SPEECH; ENVIRONMENT; MOTHERS; INPUT; PLAY; INTELLIGENCE AB This prospective longitudinal study assessed children's and mothers' productive vocabulary and mothers' verbal responses to children's exploratory and vocal behavior in spontaneous speech, and evaluated multiple relations in those measures in two Contexts (play and mealtimes) at two child ages (13 and 20 months). Continuity, stability, and several models of concurrent and lagged child-mother correspondences were evaluated. Child and mother vocabulary increased across the second year, but did so differently in the two contexts; vocabulary of both showed significant stability of individual variation across context and age. Developmental change in maternal verbal responses predicted child vocabulary (maternal vocabulary did not), and developmental change in child vocabulary predicted maternal responses. The results support a model of specificity in mother-child language exchange and child vocabulary growth. C1 NICHHD, Bethesda, MD 20892 USA. NYU, New York, NY USA. RP Bornstein, MH (reprint author), NICHHD, Bldg 31,Room B2B15,9000 Rockville Pike, Bethesda, MD 20892 USA. EM Marc_H_Bornstein@nih.gov NR 69 TC 74 Z9 74 U1 2 U2 13 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0163-6383 J9 INFANT BEHAV DEV JI Infant Behav. Dev. PY 1999 VL 22 IS 1 BP 65 EP 85 DI 10.1016/S0163-6383(99)80006-X PG 21 WC Psychology, Developmental SC Psychology GA 203PQ UT WOS:000080716400006 ER PT J AU Nicely, P Tamis-LeMonda, CS Bornstein, MH AF Nicely, P Tamis-LeMonda, CS Bornstein, MH TI Mothers' attuned responses to infant affect expressivity promote earlier achievement of language milestones SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE mother-infant interaction; affect; maternal responsiveness; child language ID 2ND YEAR; CHILD; WORD; COMPREHENSION; COMPETENCE AB To investigate infants' affective expressivity and maternal attuned responsiveness to infant expressivity in relation to early language achievement, 77 dyads were visited in their homes at 9 and 13 months, and mothers were interviewed about their children's language between 9 and 21 months. Maternal responses that were attuned to infant affect, by selectively matching either the gradient features or the valence of infants' affective expressions, were more predictive of children's language achievement than maternal nonmatching responses; and maternal matching responses at 9 months were more predictive of children's language achievements than maternal responses at 13 months. Moreover, maternal matching responses at 9 months predicted second-year language achievements over and above infant affect expressivity at 9 and 13 months, and over and above maternal matching responses at 13 months. Infants' affective expressivity per se was not predictive. C1 NYU, New York, NY 10012 USA. NICHHD, Bethesda, MD 20892 USA. RP Nicely, P (reprint author), 3839 Mound View Ave, Studio City, CA 91604 USA. EM pnicely@aol.com NR 33 TC 27 Z9 29 U1 2 U2 10 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0163-6383 J9 INFANT BEHAV DEV JI Infant Behav. Dev. PY 1999 VL 22 IS 4 BP 557 EP 568 DI 10.1016/S0163-6383(00)00023-0 PG 12 WC Psychology, Developmental SC Psychology GA 335AC UT WOS:000088218500011 ER PT J AU Manca, C Paul, S Barry, CE Freedman, VH Kaplan, G AF Manca, C Paul, S Barry, CE Freedman, VH Kaplan, G TI Mycobacterium tuberculosis catalase and peroxidase activities and resistance to oxidative killing in human monocytes in vitro SO INFECTION AND IMMUNITY LA English DT Article ID BACILLUS-CALMETTE-GUERIN; ISONIAZID RESISTANCE; INTERFERON-GAMMA; MURINE MACROPHAGES; RESPIRATORY BURST; GENE; REDUCTASE; AVIUM; KATG; IDENTIFICATION AB Mycobacterium tuberculosis has a relatively high resistance to killing by hydrogen peroxide and organic peroxides, Resistance map be mediated by mycobacterial catalase-peroxidase (KatG) and possibly by alkyl hydroperoxide reductase (AhpC), To determine the interrelationship between sensitivity to H2O2, catalase and peroxidase activities, and bacillary growth rates measured bath intracellularly in human monocytes and in culture medium, we examined one laboratory strain, two clinical isolates, and three recombinant strains of M. tuberculosis with differing levels of KatG and AhpC. Five of the mycobacterial strains had intracellular doubting times of 27 to 32 h, while one KatG-deficient clinical isolate (ATCC 35825) doubled in similar to 76 h, Killing of mycobacteria by exogenously added H2O2 was more pronounced for intracellular bacilli than for those bacilli derived from disrupted monocytes, Strains,vith no detectable KatG expression or catalase activity were relatively sensitive to killing (43 to 67% killing) by exogenous H2O2. However, once even minimal catalase activity was present, mycobacterial catalase activity over a 10-fold range (0.56 to 6.2 U/mg) was associated with survival of 85% of the bacilli. Peroxidase activity levels correlated significantly with resistance of the mycobacterial strains to H2O2-mediated killing. An endogenous oxidative burst induction by 4 beta-phorbol 12 beta-myristate 13 alpha-acetate treatment of infected monocytes reduced the viability of the KatG null strain (H37Rv Inh(r)) but not the KatG-overespressing strain [H37Rv(pMH59)]. These results suggest that mycobacterial resistance to oxidative metabolites (including H2O2 and other peroxides) may be an important mechanism of bacillary survival within the host phagocyte. C1 Rockefeller Univ, Cellular Physiol & Immunol Lab, New York, NY 10021 USA. NIAID, Rocky Mt Lab, TB Res Unit, Intracellular Parasites Lab, Hamilton, MT 59840 USA. RP Kaplan, G (reprint author), Rockefeller Univ, Cellular Physiol & Immunol Lab, 1230 York Ave, New York, NY 10021 USA. RI Barry, III, Clifton/H-3839-2012 FU Intramural NIH HHS [Z01 AI000783-11]; NIAID NIH HHS [AI 22616, AI 42056] NR 40 TC 144 Z9 154 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1999 VL 67 IS 1 BP 74 EP 79 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 152EV UT WOS:000077764000011 PM 9864198 ER PT J AU Stevens, LA Moss, J Vaughan, M Pizza, M Rappuoli, R AF Stevens, LA Moss, J Vaughan, M Pizza, M Rappuoli, R TI Effects of site-directed mutagenesis of Escherichia coli heat-labile enterotoxin on ADP-ribosyltransferase activity and interaction with ADP-ribosylation factors SO INFECTION AND IMMUNITY LA English DT Article ID NAD-BINDING-SITE; CHOLERA-TOXIN; A-SUBUNIT; NONTOXIC DERIVATIVES; CRYSTAL-STRUCTURE; DIPHTHERIA-TOXIN; NITRIC-OXIDE; PROTEINS; TRANSPORT; IDENTIFICATION AB Escherichia coli heat-labile enterotoxin (LT), an oligomeric protein with one A subunit (LTA) and five B subunits, exerts its effects via the ADP-ribosylation of G(s alpha), a guanine nucleotide-binding (G) protein that activates adenylyl cyclase. LTA also ADP-ribosylates simple guanidino compounds (e.g., arginine) and catalyzes its own auto-ADP-ribosylation. All LTA-catalyzed reactions are enhanced by ADP-ribosylation factors (ARFs), 20-kDa guanine nucleotide-binding proteins. Replacement of arginine-7 (R7R), valine-53 (V53D), serine-63 (S63K), valine 97 (V97K), or tyrosine-104 (Y104K) in LTA resulted in fully assembled but nontoxic proteins. S63K, V53D, and R7K are catalytic-site mutations, whereas V97K and Y104K are amino acid replacements adjacent to and outside of the catalytic site, respectively. The effects of mutagenesis were quantified by measuring ADP-ribosyltransferase activity (i.e., auto-ADP-ribosylation and ADP-ribosylagmatine synthesis) and interaction with ARF (i.e., inhibition of ARF-stimulated cholera toxin ADP-ribosyltransferase activity and effects of ARF on mutant auto-ADP-ribosylation). All mutants were inactive in the ADP-ribosyltransferase assay; however, auto-ADP-ribosylation in the presence of recombinant human ARF6 was detected, albeit much less than that of native LT (Y104K > V53D > V97K > R7K, S63K). Based on the lack of inhibition by free ADP-ribose, the observed auto-ADP-ribosylation activity was enzymatic and not due to the nonenzymatic addition of free ADP-ribose. V53D, S63K, and R7K were more effective than Y104K or V97K in blocking ARF stimulation of cholera toxin ADP-ribosyltransferase. Based on these data, it appears that ARF-binding and catalytic sites are not identical and that a region outside the NAD cleft may participate in the LTA-ARF interaction. C1 NHLBI, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA. Chiron SPA, IRIS, I-53100 Siena, Italy. RP NHLBI, Pulm Crit Care Med Branch, NIH, Room 6D-03,Bldg 10,10 Ctr Dr,MSC 1590, Bethesda, MD 20892 USA. EM mossj@fido.nhlbi.nih.gov NR 36 TC 16 Z9 16 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 EI 1098-5522 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1999 VL 67 IS 1 BP 259 EP 265 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 152EV UT WOS:000077764000037 PM 9864224 ER PT J AU Yang, CF Collins, WE Sullivan, JS Kaslow, DC Xiao, LH Lal, AA AF Yang, CF Collins, WE Sullivan, JS Kaslow, DC Xiao, LH Lal, AA TI Partial protection against Plasmodium vivax blood-stage infection in Saimiri monkeys by immunization with a recombinant C-terminal fragment of merozoite surface protein 1 in block copolymer adjuvant SO INFECTION AND IMMUNITY LA English DT Article ID T-CELL EPITOPES; CIRCUMSPOROZOITE PROTEIN; MONOCLONAL-ANTIBODIES; IMMUNE-RESPONSE; MURINE MALARIA; AOTUS MONKEYS; TETANUS TOXIN; YOELII; ANTIGEN; ISOTYPE AB Merozoite surface protein 1 is a candidate for blood-stage vaccines against malaria parasites. Ne report here an immunization study of Saimiri monkeys with a yeast-expressed recombinant protein containing the C terminus of Plasmodium vivax merozoite surface protein 1 and two T-helper epitopes of tetanus toxin (yP(2)P(30)Pv200(19)), formulated in aluminum hydroxide (alum) and block copolymer P1005. Monkeys immunized three times with yP(2)P(30)Pv200(19) in block copolymer P1005 had significantly higher prechallenge titers of immunoglobulin G (IgG) antibodies against the immunogen and asexual blood-stage parasites than those immunized with yP(2)P(30)Pv200(19) in alum, antigen alone, or phosphate-buffered saline (PBS) (P < 0.05). Their peripheral blood mononuclear cell proliferative responses to immunogen stimulation 4 weeks after the second immunization were also significantly higher than those from the PBS control group (P < 0.05). Upon challenge with 100,000 asexual blood-stage parasites 5 weeks after the last immunization, monkeys immunized with YP(2)P(30)PV200(19) in block copolymer P1005 had prepatent periods longer than those for the control alone group (P > 0.05). Three of the five animals in this group also had low parasitemia (peak parasitemia, less than or equal to 20 parasites/mu l of blood). Partially protected monkeys had significantly higher levels of prechallenge antibodies against the immunogen than those unprotected (P < 0.05). There was also a positive correlation between the prepatent period and titers of IgG antibodies against the immunogen and asexual blood-stage parasites end a negative correlation between accumulated parasitemia and titers of IgG antibodies against the immunogen (P < 0.05). These results indicate that when combined with block copolymer and potent T-helper epitopes, the yeast-expressed P(2)P(30)Pv200(19) recombinant protein may offer some protection against malaria. C1 Ctr Dis Control & Prevent, Immunol Branch, Div Parasit Dis,US Dept Hlth & Human Serv, Natl Ctr Infect Dis,Publ Hlth Serv, Atlanta, GA 30341 USA. NIAID, Malaria Res Lab, NIH, Bethesda, MD 20892 USA. RP Lal, AA (reprint author), Ctr Dis Control & Prevent, Immunol Branch, Div Parasit Dis,US Dept Hlth & Human Serv, Natl Ctr Infect Dis,Publ Hlth Serv, Mail Stop F-12,4770 Buford Highway, Atlanta, GA 30341 USA. RI Xiao, Lihua/B-1704-2013; Yang, Chunfu/G-6890-2013 OI Xiao, Lihua/0000-0001-8532-2727; NR 47 TC 37 Z9 39 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JAN PY 1999 VL 67 IS 1 BP 342 EP 349 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 152EV UT WOS:000077764000048 PM 9864235 ER PT S AU Pham, DL Prince, JL AF Pham, DL Prince, JL BE Kuba, A Samal, M ToddPokropek, A TI An adaptive fuzzy segmentation algorithm for three-dimensional magnetic resonance images SO INFORMATION PROCESSING IN MEDICAL IMAGING, PROCEEDINGS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 16th International Conference on Information Processing in Medical Imaging (IPMI 99) CY JUN 28-JUL 02, 1999 CL VISEGRAD, HUNGARY SP Jozsef Attila Univ, Inst Informat, Charles Univ, 1st Fac Med, Hungarian Natl Comm Technol Dev, Philips Med Syst Nederland BV, Czech Soc Nucl Med, Czech Med Assoc, Leapfrog Technol Ltd, London ID C-MEANS ALGORITHM; MR-IMAGES; INTENSITY INHOMOGENEITIES; NONUNIFORMITY AB An algorithm is proposed for the fuzzy segmentation of two and three-dimensional multispectral magnetic resonance (MR) images that have been corrupted by intensity inhomogeneities, also known as shading artifacts. The algorithm is an extension of the two-dimensional adaptive fuzzy C-means algorithm (2-D AFCM) presented in previous work by the authors. This algorithm models the intensity inhomogeneities as a gain field that causes image intensities to smoothly and slowly vary through the image space. It iteratively adapts to the intensity inhomogeneities and is completely automated. In this paper, we fully generalize 2-D AFCM to three-dimensional (3-D) multispectral images. Because of the potential size of 3-D image data, we also describe a new, faster multigrid-based algorithm for its implementation. We show using simulated MR data that 3-D AFCM yields significantly lower error rates than both the standard fuzzy C-means algorithm and several other competing methods when segmenting corrupted images. Its efficacy is further demonstrated using real 3-D scalar and multispectral MR brain images. C1 Johns Hopkins Univ, Dept Elect & Comp Engn, Ctr Imaging Sci, Baltimore, MD 21218 USA. NIA, Ctr Gerontol Res, Lab Personal & Cognit, Baltimore, MD 21224 USA. RP Pham, DL (reprint author), Johns Hopkins Univ, Dept Elect & Comp Engn, Ctr Imaging Sci, Baltimore, MD 21218 USA. RI Prince, Jerry/A-3281-2010; Samal, Martin/I-7868-2016 OI Prince, Jerry/0000-0002-6553-0876; NR 19 TC 15 Z9 15 U1 0 U2 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-66167-0 J9 LECT NOTES COMPUT SC PY 1999 VL 1613 BP 140 EP 153 PG 14 WC Computer Science, Theory & Methods; Radiology, Nuclear Medicine & Medical Imaging SC Computer Science; Radiology, Nuclear Medicine & Medical Imaging GA BS60G UT WOS:000170515200011 ER PT S AU Williams, S Barnes, J Wakisaka, A Ogasa, H Liang, CT AF Williams, S Barnes, J Wakisaka, A Ogasa, H Liang, CT BE Greenwald, RA Zucker, S Golub, LM TI Treatment of osteoporosis with MMP inhibitors SO INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC APPLICATIONS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Inhibition of Matrix Metalloproteinases - Therapeutic Applications CY OCT 21-24, 1998 CL TAMPA, FLORIDA SP Long Isl Jewish Med Ctr, NY Acad Sci, NIH, Collagenex Pharmaceut Inc, Amersham Pharmacia Biotech, Block Drug Co inc, Bristol-Meyers Squibb Pharmaceut Res Inst, Glaxo Wellcome Inc, Novartis, Parke-Davis, TNO Pharma, Pharmaceut Res Div, Warner Lambert Inc ID OSTEOPONTIN MESSENGER-RNA; GROWTH-FACTOR-I; AGED RATS; BONE-RESORPTION; OLD RATS; IGF-I; EXPRESSION; CELLS; PREVENTS; CAPACITY AB In the current study, we examined the effects of minocycline on the osteopenia of ovariectomized (OVX) aged rats using the marrow ablation model, This injury induces rapid bone formation followed by bone resorption in the marrow cavity. Old female rats were randomly divided into five groups: sham, OVX, OVX+minocycline (5-15 mg/day, orally), OVX+17 beta-estradiol (25 mu g/day, subcutaneously), and OVX+both agents. Rats were OVX, treated with minocycline and/or estrogen, followed by marrow ablation, Bone samples were collected 16 days post-marrow ablation, X-ray radiography of bones operated on showed that treatment of OVX old rats with minocycline increased bone mass in diaphyseal region. Diaphyseal bone mineral density (BMD) was measured by DEXA scan. Diaphyseal BMD of OVX rats was increased 17-25% by treatment with 5-15 mg of minocycline or 17 beta-estradiol. The effects of minocycline and estrogen treatments on the expression of osteoblast and osteoclast markers were also examined, Northern and dot blot analysis of RNA samples showed that treatment of OVX aged rats with minocycline increased the expression of type I collagen (COL I) (49%) and decreased that of interleukin-6 (IL-6) (31%). In contrast, estrogen treatment decreased the expression of interleukin-6 (IL-6) (39%), carbonic anhydrase II (CA II) (36%), and osteopontin (OP) (37%). Neither minocycline nor 17 beta-estradiol had an effect on the expression of osteocalcin (OC) and alkaline phosphatase (AP), To elucidate the mechanism by which minocycline prevented the loss of bone in OVX aged rats, we examined the colony-formation potential of bone marrow stromal cells in ex vivo cultures. Minocycline stimulated the colony-forming efficiency of marrow stromal cells derived from old animals, We have therefore concluded that the modest increase in BMD noted in OVX aged rats, in response to minocycline treatment, may be due to a change in bone remodeling that favors bone formation; and the anabolic effect of minocycline is likely due to its effect on the expression of COL I and/or the metabolism of osteoprogenitor cells. C1 NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA. RP Liang, CT (reprint author), NIA, Gerontol Res Ctr, NIH, 4940 Easterns Ave, Baltimore, MD 21224 USA. NR 21 TC 21 Z9 22 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 1-57331-180-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 878 BP 191 EP 200 DI 10.1111/j.1749-6632.1999.tb07684.x PG 10 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Research & Experimental Medicine; Science & Technology - Other Topics GA BN31Z UT WOS:000081587000015 PM 10415730 ER PT S AU Lim, MS Guedez, L Stetler-Stevenson, WG Stetler-Stevenson, M AF Lim, MS Guedez, L Stetler-Stevenson, WG Stetler-Stevenson, M BE Greenwald, RA Zucker, S Golub, LM TI Tissue inhibitor of metalloproteinase-2 induces apoptosis in human T lymphocytes SO INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC APPLICATIONS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Inhibition of Matrix Metalloproteinases - Therapeutic Applications CY OCT 21-24, 1998 CL TAMPA, FLORIDA SP Long Isl Jewish Med Ctr, NY Acad Sci, NIH, Collagenex Pharmaceut Inc, Amersham Pharmacia Biotech, Block Drug Co inc, Bristol-Meyers Squibb Pharmaceut Res Inst, Glaxo Wellcome Inc, Novartis, Parke-Davis, TNO Pharma, Pharmaceut Res Div, Warner Lambert Inc C1 Univ Toronto, Sunnybrook & Womens Coll Hlth Sci Ctr, Dept Lab Med, Toronto, ON M4N 3M5, Canada. NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA. RP Lim, MS (reprint author), Univ Toronto, Sunnybrook & Womens Coll Hlth Sci Ctr, Dept Lab Med, 2075 Bayview Ave, Toronto, ON M4N 3M5, Canada. RI Stetler-Stevenson, William/H-6956-2012; Guedez, Liliana/H-4951-2012 OI Stetler-Stevenson, William/0000-0002-5500-5808; NR 4 TC 29 Z9 33 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 1-57331-180-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 878 BP 522 EP 523 DI 10.1111/j.1749-6632.1999.tb07715.x PG 2 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Research & Experimental Medicine; Science & Technology - Other Topics GA BN31Z UT WOS:000081587000046 PM 10415761 ER PT S AU Caterina, J Caterina, N Yamada, S Holmback, K Longenecker, G Shi, J Netzel-Arnett, S Engler, J Yermovski, A Windsor, J Birkedal-Hansen, H AF Caterina, J Caterina, N Yamada, S Holmback, K Longenecker, G Shi, J Netzel-Arnett, S Engler, J Yermovski, A Windsor, J Birkedal-Hansen, H BE Greenwald, RA Zucker, S Golub, LM TI Murine TIMP-2 gene-targeted mutation SO INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC APPLICATIONS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Inhibition of Matrix Metalloproteinases - Therapeutic Applications CY OCT 21-24, 1998 CL TAMPA, FLORIDA SP Long Isl Jewish Med Ctr, NY Acad Sci, NIH, Collagenex Pharmaceut Inc, Amersham Pharmacia Biotech, Block Drug Co inc, Bristol-Meyers Squibb Pharmaceut Res Inst, Glaxo Wellcome Inc, Novartis, Parke-Davis, TNO Pharma, Pharmaceut Res Div, Warner Lambert Inc C1 Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD 20892 USA. Univ Alabama, Birmingham, AL 35294 USA. RP Caterina, J (reprint author), Natl Inst Dent & Craniofacial Res, NIH, 9000 Rockville Pike,Bldg 30,Room 4A400, Bethesda, MD 20892 USA. NR 2 TC 9 Z9 9 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 1-57331-180-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 878 BP 528 EP 530 DI 10.1111/j.1749-6632.1999.tb07717.x PG 3 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Research & Experimental Medicine; Science & Technology - Other Topics GA BN31Z UT WOS:000081587000048 PM 10415763 ER PT S AU Buck, TB Yoshiji, H Harris, SR Bunce, OR Thorgeirsson, UP AF Buck, TB Yoshiji, H Harris, SR Bunce, OR Thorgeirsson, UP BE Greenwald, RA Zucker, S Golub, LM TI The effects of sustained elevated levels of circulating tissue inhibitor of metalloproteinases-1 on the development of breast cancer in mice SO INHIBITION OF MATRIX METALLOPROTEINASES: THERAPEUTIC APPLICATIONS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Inhibition of Matrix Metalloproteinases - Therapeutic Applications CY OCT 21-24, 1998 CL TAMPA, FLORIDA SP Long Isl Jewish Med Ctr, NY Acad Sci, NIH, Collagenex Pharmaceut Inc, Amersham Pharmacia Biotech, Block Drug Co inc, Bristol-Meyers Squibb Pharmaceut Res Inst, Glaxo Wellcome Inc, Novartis, Parke-Davis, TNO Pharma, Pharmaceut Res Div, Warner Lambert Inc C1 NCI, Tumor Biol & Carcinogenesis Sect, Cellular Carcinogenesis & Tumor Promot Lab, Div Basic Sci,NIH, Bethesda, MD 20892 USA. Nara Med Univ, Dept Internal Med 3, Nara, Japan. Pikeville Coll Sch Osteopath Med, Dept Pharmacol, Pikeville, KY USA. Univ Georgia, Coll Pharm, Dept Pharmaceut & Biomed Sci, Athens, GA 30602 USA. RP Thorgeirsson, UP (reprint author), NCI, Tumor Biol & Carcinogenesis Sect, Cellular Carcinogenesis & Tumor Promot Lab, Div Basic Sci,NIH, Bldg 37,Room 2D02, Bethesda, MD 20892 USA. NR 5 TC 13 Z9 14 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 1-57331-180-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1999 VL 878 BP 732 EP 735 DI 10.1111/j.1749-6632.1999.tb07775.x PG 4 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Research & Experimental Medicine; Science & Technology - Other Topics GA BN31Z UT WOS:000081587000106 PM 10415821 ER PT S AU Hauser, SE Sabir, TF Thoma, GR AF Hauser, SE Sabir, TF Thoma, GR BE Gopalakrishnan, B Murugesan, S TI Speech recognition for program control and data entry in a production environment SO INTELLIGENT SYSTEMS IN DESIGN AND MANUFACTURING II SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Intelligent Systems in Design and Manufacturing II CY SEP 21-22, 1999 CL BOSTON, MA SP SPIE DE speech recognition; software evaluation; process control; National Library of Medicine ID VOICE AB The Lister Hill National Center for Biomedical Communications, an R&D division of the National Library of Medicine, has developed a PC-based system for semi-automated entry of journal citation data into MEDLINE(R). The system, called MARS for Medical Article Records System, includes many automated features but requires a few manual tasks such as scanning and the entry of certain data that are not located on the scanned page. Now that considerable computing power and speed are routinely available on desktop PCs, we think it may be possible to include speech recognition as an optional user interface to reduce operator burden and to improve speed and quality for document scanning and data entry. We undertook a study to determine if speech recognition was sufficiently accurate, reliable and immune to noise to warrant integration with MARS workstations. The study focussed on the suitability of both continuous and discrete speech recognition for computer program control and for data entry in a production environment. Following a carefully structured format, 20 participants tested continuous speech recognition and 20 participants tested discrete speech recognition in both a quiet and a noisy environment. Performance measures were accuracy and speed. Both continuous and discrete recognition were very accurate, fast and immune to noise when used for program control. For data entry, though discrete speech recognition was about 90% accurate, it was very slow. Continuous speech recognition was faster for data entry, but was only about 76% accurate. As a result of the study, speech recognition has been integrated into the MARS scan workstation for program control. C1 Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD 20894 USA. RP Hauser, SE (reprint author), Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD 20894 USA. NR 8 TC 3 Z9 3 U1 0 U2 0 PU SPIE-INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA SN 0277-786X BN 0-8194-3426-4 J9 P SOC PHOTO-OPT INS PY 1999 VL 3833 BP 24 EP 34 DI 10.1117/12.359522 PG 11 WC Automation & Control Systems; Engineering, Industrial; Engineering, Manufacturing; Optics SC Automation & Control Systems; Engineering; Optics GA BN92K UT WOS:000083488200003 ER PT J AU Samaan, A Thibodeau, J Mahana, W Castellino, F Cazenave, PA Kindt, TJ AF Samaan, A Thibodeau, J Mahana, W Castellino, F Cazenave, PA Kindt, TJ TI Cellular distribution of a mixed MHC class II heterodimer between DR alpha and a chimeric DO beta chain SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE class II; DR alpha; DO beta; MHC ID B-LYMPHOBLASTOID CELLS; INVARIANT CHAIN; HLA-DM; MONOCLONAL-ANTIBODIES; INTRACELLULAR-TRANSPORT; ENDOCYTIC COMPARTMENTS; ANTIGEN PRESENTATION; CYTOSOLIC TAIL; T-CELLS; EXPRESSION AB Human MHC class II antigens include HLA-DR, -DQ, and -DP molecules that present antigens to CD4(+) T cells, as well as the non-classical molecules HLA-DM and -DO. HLA-DM promotes peptide binding to class II molecules in endocytic compartments and HLA-DO, which is physically associated with HLA-DM in B lymphocytes, regulates HLA-DM function. Antibodies specific for the DO beta chain were obtained by immunization of mice with a heterodimer consisting of a chimeric DO beta chain (DR/DO beta), containing 18 N-terminal residues of DR beta, paired with the DR alpha chain and isolated from transfected murine fibroblasts. The specificity of this serum for the DO beta chain and the lysosomal expression of the HLA-DO protein was confirmed using mutant human B cell lines lacking DR or DO molecules. The lysosomal localization of HLA-DO in human B cells contrasts with the cell surface expression of the mixed pair in transfected murine fibroblasts and raises questions concerning the role of the putative targeting motifs in HLA-DO. Transfection of the chimeric DR/DO beta chain along with DR alpha into human epithelial HeLa cells resulted in high levels of expression of the mixed isotypic pair at the surface of transfectants as well as in lysosomes, The same pattern was observed in HeLa cells transfected with the DO beta chimera and a DR alpha chain lacking the cytoplasmic tail. Taken together, these results suggest that functional sorting motifs exist in the DO beta chain but that the tight compartmentalization of HLA-DO observed inside B lymphocytes is controlled by the HLA-DO alpha chain and HLA-DM. C1 NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA. NIAID, Immunol Lab, NIH, Rockville, MD 20852 USA. Inst Pasteur, Lab Analyt Immunochem, F-75724 Paris, France. RP Thibodeau, J (reprint author), Univ Montreal, Dept Microbiol & Immunol, Lab Mol Immunol, CP 6128,Succ Ctr Ville, Montreal, PQ H3C 3J7, Canada. NR 56 TC 10 Z9 10 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD JAN PY 1999 VL 11 IS 1 BP 99 EP 111 DI 10.1093/intimm/11.1.99 PG 13 WC Immunology SC Immunology GA 161LB UT WOS:000078289300011 PM 10050678 ER PT J AU Spencer, R AF Spencer, R TI Guest Editorial: Advanced signal processing in MRI. Part I SO INTERNATIONAL JOURNAL OF IMAGING SYSTEMS AND TECHNOLOGY LA English DT Editorial Material C1 NIA, Nucl Magnet Resonance Unit, Baltimore, MD 21224 USA. RP Spencer, R (reprint author), NIA, Nucl Magnet Resonance Unit, Baltimore, MD 21224 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 USA SN 0899-9457 J9 INT J IMAG SYST TECH JI Int. J. Imaging Syst. Technol. PY 1999 VL 10 IS 2 BP 107 EP 108 PG 2 WC Engineering, Electrical & Electronic; Optics; Imaging Science & Photographic Technology SC Engineering; Optics; Imaging Science & Photographic Technology GA 173VV UT WOS:000079001200001 ER PT J AU Spencer, RGS AF Spencer, RGS TI Advanced Signal Processing in MRI. Part II SO INTERNATIONAL JOURNAL OF IMAGING SYSTEMS AND TECHNOLOGY LA English DT Editorial Material C1 Johns Hopkins Univ, Sch Med, Baltimore, MD 21224 USA. NIA, NIH, Intramural Res Program, Baltimore, MD 21224 USA. RP Spencer, RGS (reprint author), Johns Hopkins Univ, Sch Med, GRC 4D-08,5600 Nathan Shock Dr, Baltimore, MD 21224 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 USA SN 0899-9457 J9 INT J IMAG SYST TECH JI Int. J. Imaging Syst. Technol. PY 1999 VL 10 IS 3 BP 207 EP 208 DI 10.1002/(SICI)1098-1098(1999)10:3<207::AID-IMA1>3.0.CO;2-U PG 2 WC Engineering, Electrical & Electronic; Optics; Imaging Science & Photographic Technology SC Engineering; Optics; Imaging Science & Photographic Technology GA 192WZ UT WOS:000080103900001 ER PT J AU Borbely, K Brooks, RA Jacob, P Miletich, RS AF Borbely, K Brooks, RA Jacob, P Miletich, RS TI Positron emission tomography F-18-deoxyglucose studies of cerebral metabolism in asymmetric parkinsonism SO INTERNATIONAL JOURNAL OF NEURORADIOLOGY LA English DT Article DE F-18-deoxyglucose; glucose metabolism; hemiparkinson; Parkinson disease; positron emission tomography ID NIGROSTRIATAL DOPAMINERGIC PATHWAYS; GLUCOSE-UTILIZATION; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE-INDUCED PARKINSONISM; F-18 FLUORODEOXYGLUCOSE; DISEASE; THALAMUS; MONKEYS; 2-DEOXYGLUCOSE; INVOLVEMENT; DISORDERS AB Purpose: To obtain quantitative information on regional cerebral metabolic dysfunction in early Parkinson disease (PD). Methods: Twenty-two patients with PD who displayed predominantly or exclusively unilateral symptoms and 13 age-matched control subjects were studied with positron emission tomography (PET) using F-18-deoxyglucose (FDC). Results: Metabolic asymmetry in the lenticular nucleus was 7.8%: the nucleus contralateral to the more affected side was hypermetabolic compared with the other side and compared with the normal lenticular nucleus. The caudate was unaffected. Thalamic metabolism was bilaterally elevated by 13% compared with the control subjects. The cortex generally showed a small metabolic asymmetry in the opposite direction (contralateral hypometabolism). The lenticular asymmetry decreased with disease duration, whereas the cortical asymmetry increased (became more negative). Conclusion: These results support current theories of the effects of PD on neural pathways. The changes with disease duration help to bridge the gap between differing reports in early and advanced PB. C1 NINDS, Neuroimaging Branch, NIH, Bethesda, MD 20892 USA. NR 29 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1079-8110 J9 INT J NEURORADIOL JI Int. J. Neuroradiol. PD JAN-FEB PY 1999 VL 5 IS 1 BP 38 EP 42 PG 5 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 235DR UT WOS:000082525200007 ER PT J AU Dipple, A Khan, QA Page, JE Ponten, I Szeliga, J AF Dipple, A Khan, QA Page, JE Ponten, I Szeliga, J TI DNA reactions, mutagenic action and stealth properties of polycyclic aromatic hydrocarbon carcinogens (Review) SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE DNA adduct; dihydrodiol epoxide; stealth properties; p53; p21(waf1/eip1); site-specific mutagenesis; sequence context effects ID BENZOPHENANTHRENE DIHYDRODIOL EPOXIDES; DOSE-DEPENDENT DIFFERENCES; SITE-SPECIFIC MUTAGENESIS; SINGLE-STRANDED VECTOR; REGION DIOL-EPOXIDES; MOUSE SKIN; SUPF GENE; 11,12-DIHYDRODIOL 13,14-EPOXIDE; 3,4-DIHYDRODIOL 1,2-EPOXIDES; POLY(ADP-RIBOSE) POLYMERASE AB A brief summary of recent research, primarily from the authors' laboratory, on polycyclic aromatic hydrocarbon carcinogens with respect to their DNA adduct formation, the mutational properties of these adducts and the effects of hydrocarbon dihydrodiol epoxide metabolites on the passage of cells through the cell cycle is presented. The concept of stealth properties of potent carcinogens, i.e. their ability to damage DNA without inducing a G1 arrest, is discussed. Also, mutation studies with dihydrodiol epoxide metabolites, the sequence-dependence of site-specific mutation, as well as the selectivity of hydrocarbon-DNA adduct formation are summarized. C1 NCI, Frederick Canc Res & Dev Ctr, Chem Carcinogenesis Lab, ABL Basic Res Program, Frederick, MD 21702 USA. RP Dipple, A (reprint author), NCI, Frederick Canc Res & Dev Ctr, Chem Carcinogenesis Lab, ABL Basic Res Program, POB B, Frederick, MD 21702 USA. NR 81 TC 93 Z9 94 U1 0 U2 5 PU PROFESSOR D A SPANDIDOS PI ATHENS PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD JAN PY 1999 VL 14 IS 1 BP 103 EP 111 PG 9 WC Oncology SC Oncology GA 150NF UT WOS:000077670500013 PM 9863015 ER PT J AU Gutierrez, MI Hamdy, N Bhatia, K Bornkamm, G Lenoir, G Epelman, S Magrath, I AF Gutierrez, MI Hamdy, N Bhatia, K Bornkamm, G Lenoir, G Epelman, S Magrath, I TI Geographic variation in t(8;14) chromosomal breakpoint locations and EBV association in Burkitt's lymphoma SO INTERNATIONAL JOURNAL OF PEDIATRIC HEMATOLOGY/ONCOLOGY LA English DT Article DE neoplasia; non-Hodgkin's lymphomas; c-myc; oncogenes; immunoglobulin genes; molecular epidemiology ID EPSTEIN-BARR-VIRUS AB We have extended our analysis of the geographical variation in the pattern of t(8; 14) chromosomal breakpoint locations and EBV association in Burkitt's lymphoma and conducted a more detailed analysis of the geography of the molecular subtypes of BL based on 120 tumors. Our data, overall, suggest that chromosomal breakpoint locations on chromosome 8 fall into three main groups, and that each of these groups is variably represented in the countries studied so far. In Equatorial Africa (Ghana) and Brazil, the predominant breakpoint location is outside the HindIII fragment encompassing c-myc (74% and 50% respectively). In temperate South American tumors (from Argentina and Chile) breakpoints most often (48%) occur in the c-myc regulatory region immediately upstream of the major promoters, P1 and P2. In tumors from the USA and North Africa (Algeria), most breakpoints are downstream of the major promoters and result in truncation of c-myc (60% and 43% respectively). Ghanaian and North American tumors differ most dramatically from each other. Most breakpoints in Ghanaian tumors are outside HindIII (74%), while most of those in North American tumors are within HindIII (91%). EBV association also differs, being highest in Ghanaian and Algerian tumors (both 100%) lowest in US tumors (38%) and intermediate in South American countries. Our results suggest that environmental factors or lifestyle influence the molecular subtype, in Burkitt's lymphoma, but do not support a relationship between the presence of EBV and breakpoint locations - at least, as determined by Southern blotting. C1 NCI, Lymphoma Biol Sect, Pediat Oncol Branch, Bethesda, MD 20892 USA. Inst Hematol, Munich, Germany. Natl Canc Inst, Cairo, Egypt. Univ Lyon, Lyon, France. Pediat Canc Hosp, Campinas, Brazil. RP Magrath, I (reprint author), NCI, Lymphoma Biol Sect, Pediat Oncol Branch, Bldg 10,Room 13N240,10 Ctr Dr,MSC 1928, Bethesda, MD 20892 USA. NR 17 TC 4 Z9 4 U1 0 U2 1 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1070-2903 J9 INT J PEDIAT HEM ONC JI Int. J. Pediatr. Hematol-Oncol. PY 1999 VL 6 IS 3 BP 161 EP 168 PG 8 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA 218AU UT WOS:000081531800002 ER PT B AU Strober, W Fuss, IJ AF Strober, W Fuss, IJ BE Domschke, W Stoll, R Brasitus, TA Kagnoff, MF TI Experimental models of inflammation and their relation to human inflammatory bowel disease SO INTESTINAL MUCOSA AND ITS DISEASES: PATHOPHYSIOLOGY AND CLINICS SE FALK SYMPOSIUM LA English DT Proceedings Paper CT International Symposium on Intestinal Mucosa and Its Diseases - Pathophysiology and Clinics CY OCT 16-17, 1998 CL TITISEE, GERMANY SP Falk Fdn ID CD4(+) T-CELLS; ALPHA MUTANT MICE; MUCOSAL IMMUNE-RESPONSES; ANTIGEN-PRESENTING CELLS; TUMOR-NECROSIS-FACTOR; HAPTEN-INDUCED MODEL; CROHNS-DISEASE; IFN-GAMMA; INTERLEUKIN-10-DEFICIENT MICE; EXPERIMENTAL COLITIS C1 NIAID, NIH, Bethesda, MD 20892 USA. RP Strober, W (reprint author), NIAID, NIH, Bldg 10,Room 11N238,10 Ctr Dr,MSC 1888, Bethesda, MD 20892 USA. NR 52 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS BN 0-7923-8754-6 J9 FALK SYMP PY 1999 VL 110 BP 457 EP 470 PG 14 WC Gastroenterology & Hepatology; Medicine, General & Internal SC Gastroenterology & Hepatology; General & Internal Medicine GA BP01D UT WOS:000083828400039 ER PT J AU Neckers, L Schulte, TW Mimnaugh, E AF Neckers, L Schulte, TW Mimnaugh, E TI Geldanamycin as a potential anti-cancer agent: Its molecular target and biochemical activity SO INVESTIGATIONAL NEW DRUGS LA English DT Review DE Hsp90; chaperone; geldanamycin; benzoquinone ansamycin ID HEAT-SHOCK PROTEIN; ROUS-SARCOMA VIRUS; IMPORTANT BIOLOGIC ACTIVITIES; ATP-BINDING-PROPERTIES; 2 CELLULAR PROTEINS; HUMAN BREAST-CANCER; N-TERMINAL DOMAIN; CASEIN KINASE-II; IN-VIVO; TYROSINE KINASE AB Heat shock protein 90 is one of the most abundant cellular proteins. Although its functions are still being characterized, it appears to serve as a chaperone for a growing list of cell signaling proteins, including many tyrosine and serine/threonine kinases, involved in proliferation and/or survival. The benzoquinone ansamycin geldanamycin has been shown to bind to Hsp90 and to specifically inhibit this chaperone's function, resulting in client protein destabilization. Its ability to simultaneously stimulate depletion of multiple oncogenic proteins suggests that geldanamycin, or other molecules capable of targeting Hsp90 in cancer cells, may be of clinical benefit. C1 NCI, Dept Cell & Canc Biol, Med Branch, Rockville, MD USA. RP Neckers, L (reprint author), 9610 Med Ctr Dr,Suite 300, Rockville, MD 20850 USA. NR 115 TC 251 Z9 262 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1999 VL 17 IS 4 BP 361 EP 373 DI 10.1023/A:1006382320697 PG 13 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 283QA UT WOS:000085285400004 PM 10759403 ER PT J AU Pazdur, R Medgyesy, DC Winn, RJ Dakhil, SR Moore, DF Scalzo, A Hoff, PM Arbuck, SG Abbruzzese, JL AF Pazdur, R Medgyesy, DC Winn, RJ Dakhil, SR Moore, DF Scalzo, A Hoff, PM Arbuck, SG Abbruzzese, JL TI Phase II trial of 9-aminocamptothecin (NSC 603071) administered as a 120-hour continuous infusion weekly for three weeks in metastatic colorectal carcinoma SO INVESTIGATIONAL NEW DRUGS LA English DT Article DE 9-AC; 9-aminocamptothecin; camptothecin; colorectal cancer; phase II ID CAMPTOTHECIN NSC-100880; CANCER; IRINOTECAN; ANALOGS AB 9-Aminocamptothecin (9-AC) is a camptothecin derivative with broad antitumor activity in preclinical studies. Prior investigations suggested that prolonged maintenance of 9-AC lactone plasma concentrations above 10 nmol/l and frequent administration of the drug are important determinants of antitumor activity. Our phase II study, therefore, examined a 5-day continuous infusion of 9-AC weekly for 3 weeks in patients with advanced colorectal cancer. Eighteen patients previously untreated for metastatic disease received 480 mu g/m(2)/day of 9-AC. No responses were observed in 17 evaluable patients. Severe toxicities included granulocytopenia, nausea, vomiting and diarrhea. The median absolute granulocyte count (AGC) nadir was 2,300/mu l (range 0-9,000/mu l) and occurred on day 10. Eight patients received an escalated dose of 600 mu g/m(2)/day. The median AGC nadir at the escalated dose was 1,500/mu l (range: 300-2,700/mu l) and occurred on day 22. The median number of courses given was 2 (range: 1-8); and the median time to disease progression was 8 weeks (range: 1-40 weeks). 9-AC administered by this schedule lacked antitumor activity in patients with advanced colorectal carcinomas. C1 Univ Texas, MD Anderson Canc Ctr, Div Med, Houston, TX 77030 USA. Wichita CCOP, Wichita, KS USA. Syracuse CCOP, Syracuse, NY USA. NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. RP Pazdur, R (reprint author), Univ Texas, MD Anderson Canc Ctr, Div Med, Box 92,1515 Holcombe Blvd, Houston, TX 77030 USA. NR 26 TC 1 Z9 1 U1 0 U2 2 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PY 1999 VL 16 IS 4 BP 341 EP 346 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 206FJ UT WOS:000080866400010 ER PT B AU Thoma, GR Le, DX AF Thoma, GR Le, DX BE Cibbarelli, PR Nixon, C TI Automating data entry for online biomedical databases SO IOLS'99: INTEGRATED ONLINE LIBRARY SYSTEMS, PROCEEDING-1999: PREPARED FOR THE FUTURE LA English DT Proceedings Paper CT 14th National Conference on Integrated Online Library Systems (IOLS 99) CY MAY 19-20, 1999 CL NEW YORK, NY SP Informat Today Inc DE automated data entry; document image analysis; image understanding; OCR; biomedical databases; classifier; syntax reformatting; National Library of Medicine AB The Lister Hill National Center for Biomedical Communications, an R&D division of the National Library of Medicine (NLM), is engaged in developing systems for automating the extraction of information from biomedical journals to create bibliographic records in MEDLINE(R), NLM's premier online database used worldwide. The first phase of this project has resulted in a system that involves scanning and converting (by OCR) the abstracts that appear in journal articles, while keyboarding the remaining fields. A second generation system is being designed to automate the entry of other fields such as author names, institutional affiliations, page numbers, article titles and others. This system will employ scanning and OCR as well as document image analysis techniques that will automatically zone the scanned pages, identify the zones as particular fields, and reformat the field syntax to adhere To conventional practice in MEDLINE. This paper describes the first generation system currently used for production, and the work toward the design of the second generation system. C1 Natl Lib Med, Bethesda, MD 20894 USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU INFORMATION TODAY INC PI MEDFORD PA 143 OLD MARLTON PIKE, MEDFORD, NJ 08055 USA BN 1-57387-085-4 PY 1999 BP 121 EP 128 PG 8 WC Information Science & Library Science SC Information Science & Library Science GA BP67V UT WOS:000085841600012 ER PT B AU Walker, FL Thoma, GR AF Walker, FL Thoma, GR BE Cibbarelli, PR Nixon, C TI Multimode delivery of multimedia information SO IOLS'99: INTEGRATED ONLINE LIBRARY SYSTEMS, PROCEEDING-1999: PREPARED FOR THE FUTURE LA English DT Proceedings Paper CT 14th National Conference on Integrated Online Library Systems (IOLS 99) CY MAY 19-20, 1999 CL NEW YORK, NY SP Informat Today Inc DE HotMed; MedJava; Internet; Java; document delivery; email; MIME; Ariel; DocView; World Wide Web; FTP; interlibrary loan; PDF; NLM AB Increasing numbers of libraries are using the Internet for document delivery, not only for interlibrary loan but for delivering documents directly to the patron's desktop computer. The widespread adoption of software such as Ariel and DocView is making this possible. Ariel, a product of the Research Libraries Group, converts paper-based documents to monochrome (black and white) bitmapped images, and delivers them over the Internet. The National Library of Medicine's DocView is primarily designed for library patrons to receive, display and manage documents received from Ariel systems. While libraries and their patrons are beginning to reap the benefits of this new technology, there still are areas where improvements can be made. The Communications Engineering Branch of the Lister Hill National Center for Biomedical Communications, an R&D division of NLM, is developing software code-named HotMed to increase the options for delivering library information over the Internet. For instance, HotMed adds a third method for one-time information delivery, via the World Wide Web (WWW), to the two methods already used by Ariel and DocView: File Transfer Protocol (FTP) and Multipurpose Internet Mail Extensions (MIME) Email. HotMed also permits delivery of multiple files to multiple recipients, and goes beyond monochrome bitmapped images to deliver any multimedia file type, such as color and grayscale images, audio and video information, and word processing documents. Finally, by incorporating a Java applet (MedJava) for delivering documents via the WWW, the HotMed software gives the librarian a new option that potentially solves several problems commonly associated with Internet document delivery. This paper describes the design of the prototype HotMed software and shows how it can aid the librarian in delivering many types of library information over the Internet to the patron's desktop. C1 Natl Lib Med, Bethesda, MD 20894 USA. NR 10 TC 2 Z9 2 U1 0 U2 0 PU INFORMATION TODAY INC PI MEDFORD PA 143 OLD MARLTON PIKE, MEDFORD, NJ 08055 USA BN 1-57387-085-4 PY 1999 BP 141 EP 152 PG 12 WC Information Science & Library Science SC Information Science & Library Science GA BP67V UT WOS:000085841600014 ER PT J AU Humphrey, JH Quinn, T Fine, D Lederman, H Yamini-Roodsari, S Wu, LSF Moeller, S Ruff, AJ AF Humphrey, JH Quinn, T Fine, D Lederman, H Yamini-Roodsari, S Wu, LSF Moeller, S Ruff, AJ TI Short-term effects of large-dose vitamin a supplementation on viral load and immune response in HIV-infected women SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE vitamin A; viral load; women; HIV/AIDS ID A-DEFICIENCY; IMMUNODEFICIENCY; CELLS; MORTALITY; EXPRESSION; RETINOL; PLASMA; INFANT; MOTHER AB Vitamin A supplementation has been suggested for treatment and prevention of HIV infection. However, some in vitro data indicate that vitamin A may activate HIV. Randomly, 40 HIV-seropositive women of reproductive age were allocated to receive a single oral dose of 9900 mu mol (300,000 IU) vitamin A or placebo. Plasma HIV-1 RNA concentration, total lymphocytes, selected lymphocyte subsets and activation markers, and in vitro lymphocyte proliferation to phytohemagglutinin (PKA) and Candida were measured before dosing and at various lime points over an 8-week follow-up period. No differences were found between treatment groups in the frequency of signs or symptoms of acute vitamin A toxicity, nor were differences evident in any lymphocyte subset or activation marker at any time during follow-up. Mean and median viral load concentration at each time point and change in viral load from baseline to each follow-up point did not differ between treatment,groups. No difference was measured between treatment groups in the proportion of women who responded to PHA or Candida. This study provides no evidence that high dose vitamin A supplementation of HIV-infected women is associated with significant clinical or immunologic adverse effects. C1 Johns Hopkins Sch Hyg & Publ Hlth, Dept Int Hlth, Div Human Nutr, Baltimore, MD 21205 USA. Johns Hopkins Sch Hyg & Publ Hlth, Dept Int Hlth, Div Dis Control, Baltimore, MD 21205 USA. Johns Hopkins Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Johns Hopkins Sch Med, Dept Med, Baltimore, MD 21205 USA. NIAID, Immunoregulat Lab, Bethesda, MD 20892 USA. RP Humphrey, JH (reprint author), Johns Hopkins Sch Hyg & Publ Hlth, Dept Int Hlth, Div Human Nutr, 615 N Wolfe St,Room 2041, Baltimore, MD 21205 USA. FU NCRR NIH HHS [RROO722, S10-RR04060] NR 33 TC 24 Z9 26 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN 1 PY 1999 VL 20 IS 1 BP 44 EP 51 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 157UA UT WOS:000078079000007 PM 9928729 ER PT J AU Arango, C Maloney, E Rugeles, MT Bernal, E Bernal, C Borrero, I Herrera, S Restrepo, M Espinal, A Blattner, WA AF Arango, C Maloney, E Rugeles, MT Bernal, E Bernal, C Borrero, I Herrera, S Restrepo, M Espinal, A Blattner, WA TI HTLV-I and HTLV-II coexist among the Embera and Inga Amerindians of Colombia SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Letter ID INFECTION; INDIANS; REGION; ANDES C1 Univ Valle, Fac Salud, Cali, Colombia. NCI, Viral Epidemiol Branch, Rockville, MD USA. Univ Antioquia, Fac Med, Medellin, Colombia. Univ Miami, Sch Med, Miami, FL 33152 USA. Washington Univ, St Louis, MO USA. Inst Trop Med, Medellin, Colombia. Univ Los Andes, Bogota, Colombia. Univ Maryland, Inst Human Virol, Baltimore, MD USA. RP Arango, C (reprint author), Univ Valle, Fac Salud, Cali, Colombia. NR 9 TC 7 Z9 8 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN 1 PY 1999 VL 20 IS 1 BP 102 EP 103 PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 157UA UT WOS:000078079000021 PM 9928743 ER PT J AU Allen, JP AF Allen, JP TI Carbohydrate deficient transferrin as a marker of relapse to drinking SO JOURNAL OF ADDICTIVE DISEASES LA English DT Meeting Abstract C1 NIAAA, NIH, DCPR, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1999 VL 18 IS 2 MA 2A BP 106 EP 106 PG 1 WC Substance Abuse SC Substance Abuse GA 189VR UT WOS:000079927300012 ER PT J AU Gorelick, DA Sacks, N Nelson, R Bencherif, B Frost, JJ AF Gorelick, DA Sacks, N Nelson, R Bencherif, B Frost, JJ TI Influence of enforced abstinence on cocaine use by research subjects SO JOURNAL OF ADDICTIVE DISEASES LA English DT Meeting Abstract C1 NIDA, Intramural Res Program, Baltimore, MD 21224 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1999 VL 18 IS 2 MA 11A BP 115 EP 115 PG 1 WC Substance Abuse SC Substance Abuse GA 189VR UT WOS:000079927300021 ER PT J AU Gorelick, DA Soderstrom, CA Carriero, NJ Smith, GS Dischinger, PC McDuff, DR Hebel, JR Kerns, TJ Ho, SM Read, KM AF Gorelick, DA Soderstrom, CA Carriero, NJ Smith, GS Dischinger, PC McDuff, DR Hebel, JR Kerns, TJ Ho, SM Read, KM TI Relative drug dependence liability among trauma center inpatients SO JOURNAL OF ADDICTIVE DISEASES LA English DT Meeting Abstract C1 NIDA, Intramural Res Program, Baltimore, MD 21224 USA. Univ Maryland, Baltimore, MD 21201 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 1055-0887 J9 J ADDICT DIS JI J. Addict. Dis. PY 1999 VL 18 IS 2 MA 12A BP 116 EP 116 PG 1 WC Substance Abuse SC Substance Abuse GA 189VR UT WOS:000079927300022 ER PT J AU Akin, C Kirshenbaum, A Scott, LM Semere, T Metcalfe, DD AF Akin, C Kirshenbaum, A Scott, LM Semere, T Metcalfe, DD TI The Asp816Val C-kit mutation is present in the peripheral blood of adult patients with urticaria pigmentosa. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA. 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 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1999 VL 103 IS 1 SU S MA 898 BP S233 EP S233 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 165FC UT WOS:000078509000900 ER PT J AU Bhattacharyya, SP Bianchine, PJ Mekori, YA Metcalfe, DD AF Bhattacharyya, SP Bianchine, PJ Mekori, YA Metcalfe, DD TI Enhanced focal adhesion kinase (FAK) phosphorylation in mast cells induced by vitronectin (VN) is dependent on protein kinase C (PKC) and calcium. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA. 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 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1999 VL 103 IS 1 SU S MA 876 BP S227 EP S227 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 165FC UT WOS:000078509000878 ER PT J AU Blumenthal, M Bleecker, ER Barnes, K Cox, N Beaty, T Banks-Schlegal, S Ober, C Rich, S Meyers, DA AF Blumenthal, M Bleecker, ER Barnes, K Cox, N Beaty, T Banks-Schlegal, S Ober, C Rich, S Meyers, DA CA Collaborative Studies Genetics Asthma TI Genome screen for atopy and skin test responsiveness (STR) susceptibility loci in US populations. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Univ Minnesota, Minneapolis, MN 55455 USA. Univ Maryland, College Pk, MD 20742 USA. Bowman Gray Sch Med, Winston Salem, NC 27103 USA. Univ Chicago, Chicago, IL 60637 USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. NHLBI, Bethesda, MD 20892 USA. 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 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1999 VL 103 IS 1 SU S MA 665 BP S174 EP S174 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 165FC UT WOS:000078509000668 ER PT J AU Devouassoux, G Foster, B Scott, LM Metcalfe, DD Prussin, C AF Devouassoux, G Foster, B Scott, LM Metcalfe, DD Prussin, C TI Frequency and characterization of antigen-specific IL-4 and IL-13 producing basophils and T cells in peripheral blood of normals and asthmatics. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA. 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 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1999 VL 103 IS 1 SU S MA 747 BP S194 EP S194 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 165FC UT WOS:000078509000749 ER PT J AU Kirshenbaum, AS Goff, JP Semere, T Scott, LM Metcalfe, DD AF Kirshenbaum, AS Goff, JP Semere, T Scott, LM Metcalfe, DD TI Demonstration that human mast cells arise from a bipotential progenitor cell that is CD34+, c-kit+, and expresses aminopeptidase N (CD13). SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA. NIAID, LAD, NIH, Bethesda, MD 20892 USA. 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 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1999 VL 103 IS 1 SU S MA 652 BP S170 EP S170 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 165FC UT WOS:000078509000655 ER PT J AU Lantz, AB Wray, BB Cuccherini, B AF Lantz, AB Wray, BB Cuccherini, B TI Idiopathic lower extremity "wooden leg" syndrome in two patients with X-linked agammaglobulinemia. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Med Coll Georgia, Augusta, GA 30912 USA. Natl Inst Hlth, Bethesda, MD USA. 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 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1999 VL 103 IS 1 SU S MA 548 BP S144 EP S144 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 165FC UT WOS:000078509000554 ER PT J AU Nickel, R Barnes, KC Sengler, CA Casolaro, V Freidhoff, LR Weber, P Naidu, RP Caraballo, L Ehrlich, E Plitt, J Schleimer, RP Huang, SK Beaty, T AF Nickel, R Barnes, KC Sengler, CA Casolaro, V Freidhoff, LR Weber, P Naidu, RP Caraballo, L Ehrlich, E Plitt, J Schleimer, RP Huang, SK Beaty, T CA CSGA TI Evidence for linkage of chemokine polymorphisms to asthma in populations of African descent. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 JHU, Baltimore, MD USA. NHLBI, Bethesda, MD USA. Univ Cartagena, Cartagena, Colombia. Univ W Indies, Bridgetown, Barbados. RI Casolaro, Vincenzo/E-9144-2010 OI Casolaro, Vincenzo/0000-0001-9810-0488 NR 0 TC 8 Z9 8 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1999 VL 103 IS 1 SU S MA 667 BP S174 EP S174 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 165FC UT WOS:000078509000670 ER PT J AU Saini, S MacGlashan, D Klion, A Holland, S Hamilton, R Bochner, B AF Saini, S MacGlashan, D Klion, A Holland, S Hamilton, R Bochner, B TI Relationship between serum IgE and Fc epsilon RI levels on human basophils, monocytes, and eosinophils. SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Meeting Abstract C1 Johns Hopkins Univ, Sch Med, Johns Hopkins Asthma & Allergy Ctr, Baltimore, MD USA. NIH, Bethesda, MD USA. 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 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JAN PY 1999 VL 103 IS 1 SU S MA 643 BP S168 EP S168 PN 2 PG 1 WC Allergy; Immunology SC Allergy; Immunology GA 165FC UT WOS:000078509000646 ER PT J AU Groll, AH Gonzalez, CE Giri, N Kligys, K Love, W Peter, J Feuerstein, E Bacher, J Piscitelli, SC Walsh, TJ AF Groll, AH Gonzalez, CE Giri, N Kligys, K Love, W Peter, J Feuerstein, E Bacher, J Piscitelli, SC Walsh, TJ TI Liposomal nystatin against experimental pulmonary aspergillosis in persistently neutropenic rabbits: efficacy, safety and non-compartmental pharmacokinetics SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID AMPHOTERICIN-B; ENCAPSULATED NYSTATIN; ANTIFUNGAL ACTIVITY; FUNGAL-INFECTIONS; TOXICITY; MICE AB The activity of liposomal nystatin against invasive pulmonary aspergillosis was investigated in persistently neutropenic rabbits. Treatment groups included liposomal nystatin at dosages of 1,2 and 4 mg/kg/day intravenously, or amphotericin B deoxycholate 1 mg/kg/day administered intravenously after normal saline loading. As compared with untreated controls, liposomal nystatin administered at 2 and 4 mg/kg/day prolonged survival and reduced fungus-mediated tissue injury and excess lung weight at post-mortem in a similar manner to amphotericin B. Although amphotericin B was superior in clearing infected lung tissue, treatment with all regimens of liposomal nystatin led to a significant reduction in pulmonary fungal tissue burden. During treatment, ultrafast CT-scan demonstrated ongoing resolution of pulmonary lesions at 2 and 4 mg/kg/day, but not at 1 mg/kg/day. With the exception of mild increases in blood urea nitrogen (BUN) and serum creatinine values during treatment at 2 and 4 mg/kg/day, which were similar to those found in amphotericin B-treated rabbits, liposomal nystatin was well tolerated. Preliminary pharmacokinetic studies in non-infected animals established linear drug disposition of liposomal nystatin in plasma over the investigated dosage range and peak plasma levels above the MIC for the test strain after multiple daily dosing for 7 days. Liposomal nystatin increased survival and provided reduced tissue injury, effective microbiological clearance and tolerable side effects in experimental pulmonary aspergillosis in persistently neutropenic rabbits, thus providing a rational basis for further investigations in clinical trials. C1 NCI, Immunocompromised Host Sect, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA. NIH, Warren Grant Magnuson Clin Ctr, Dept Radiol, Bethesda, MD 20892 USA. NIH, Natl Ctr Res Resources, Surg Serv, Vet Resources Program, Bethesda, MD 20892 USA. NIH, Pharmacokinet Res Lab, Dept Pharm, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA. RP Walsh, TJ (reprint author), NCI, Immunocompromised Host Sect, Pediat Oncol Branch, NIH, Bldg 10,Room 13N240,10 Ctr Dr, Bethesda, MD 20892 USA. NR 31 TC 21 Z9 24 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD JAN PY 1999 VL 43 IS 1 BP 95 EP 103 DI 10.1093/jac/43.1.95 PG 9 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA 162NY UT WOS:000078354400013 PM 10381106 ER PT J AU Lynch, NA Metter, EJ Lindle, RS Fozard, JL Tobin, JD Roy, TA Fleg, JL Hurley, BF AF Lynch, NA Metter, EJ Lindle, RS Fozard, JL Tobin, JD Roy, TA Fleg, JL Hurley, BF TI Muscle quality. I. Age-associated differences between arm and leg muscle groups SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE concentric and eccentric peak torque; muscle strength; appendicular skeletal muscle mass; gender differences ID SKELETAL-MUSCLE; QUADRICEPS MUSCLES; STRENGTH; MEN; WOMEN; YOUNG; MASS; OLD; ENDURANCE; POWER AB To determine the differences between arm and leg muscle quality (MQ) across the adult life span in men and women, concentric (Con) and eccentric (Ecc) peak torque (PT) were measured in 703 subjects (364 men and 339 women, age range 19-93 yr) and appendicular skeletal muscle mass (MM, was determined in the arm and leg in a subgroup of 502 of these subjects (224 men and 278 women). Regression analysis showed that MQ, defined as PT per unit of MM, was significantly higher in the arm (similar to 30%) than in the leg across age in both genders (P < 0.01). Arm and leg MQ declined at a similar rate with age in men, whereas leg MQ declined similar to 20% more than arm MQ with increasing age in women (P less than or equal to 0.01 and P < 0.05 for Con and Ecc PT, respectively). Moreover, the age-associated decrease in arm MQ was steeper in men than in women whether Con or Ecc PT was used (both P < 0.05). Arm MQ as determined by Con PT showed a linear age-related decline in men and women (28 and 20%, respectively, P < 0.001), whereas arm MIQ as determined by Ecc PT showed a Linear age-related decline in men (25%, P < 0.001) but not in women (not significant). In contrast, both genders exhibited an age-related quadratic decline in leg MQ as determined by Con PT (similar to 40%) and Ecc PT (similar to 25%; both P < 0.001), and the rate of decline was similar for men and women. Thus MQ is affected by age and gender, but the magnitude of this effect depends on the muscle group studied and the type of muscle action (Con vs. Ecc) used to assess strength. C1 Univ Maryland, Coll Hlth & Human Performance, Dept Kinesiol, College Pk, MD 20742 USA. NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. RP Hurley, BF (reprint author), Univ Maryland, Coll Hlth & Human Performance, Dept Kinesiol, College Pk, MD 20742 USA. RI Fozard, James Leonard/B-3660-2009 NR 34 TC 282 Z9 296 U1 1 U2 13 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JAN PY 1999 VL 86 IS 1 BP 188 EP 194 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA 191EN UT WOS:000080009600026 PM 9887130 ER PT J AU Tracy, BL Ivey, FM Hurlbut, D Martel, GF Lemmer, JT Siegel, EL Metter, EJ Fozard, JL Fleg, JL Hurley, BF AF Tracy, BL Ivey, FM Hurlbut, D Martel, GF Lemmer, JT Siegel, EL Metter, EJ Fozard, JL Fleg, JL Hurley, BF TI Muscle quality. II. Effects of strength training in 65- to 75-yr-old men and women SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE knee extension; muscle mass; muscle strength; sarcopenia; muscle hypertrophy ID CROSS-SECTIONAL AREA; SKELETAL-MUSCLE; OLDER MEN; QUADRICEPS MUSCLES; NEURAL ACTIVATION; ELDERLY PEOPLE; YOUNG-WOMEN; HYPERTROPHY; AGE; ADAPTATIONS AB To determine the effects of strength training (ST) on muscle quality (MQ, strength/muscle volume of the trained muscle group), 12 healthy older men (69 +/- 3 yr, range 65-75 yr) and 11 healthy older women (68 +/- 3 yr, range 65-73 yr) were studied before and after a unilateral leg ST program. After a warm-up set, four sets of heavy-resistance knee extensor ST exercise were performed 3 days/wk for 9 wk on the Keiser K-300 leg extension machine. The men exhibited greater absolute increases in the knee extension one-repetition maximum (1-RM) strength test (75 +/- 2 and 94 +/- 3 kg before and after training, respectively) and in quadriceps muscle volume measured by magnetic resonance imaging (1,753 +/- 44 and 1,955 +/- 43 cm(3)) than the women (42 +/- 2 and 55 +/- 3 kg for the 1-RM test and 1,125 +/- 53 vs. 1,261 +/- 65 cm(3) for quadriceps muscle volume before and after training, respectively, in women; both P < 0.05). However, percent increases were similar for men and women in the 1-RM test (27 and 29% for men and women, respectively), muscle volume (12% for both), and MQ (14 and 16% for men and women, respectively). Significant increases in MQ were observed in both groups in the trained leg (both P < 0.05) and in the 1-RM test for the untrained leg (both P < 0.05), but no significant differences were observed between groups, suggesting neuromuscular adaptations in both gender groups. Thus, although older men appear to have a greater capacity for absolute strength and muscle mass gains than older women in response to ST, the relative contribution of neuromuscular and hypertrophic factors to the increase in strength appears to be similar between genders. C1 Univ Maryland, Coll Hlth & Human Performance, Dept Kinesiol, College Pk, MD 20742 USA. Baltimore Vet Affairs Med Ctr, Dept Radiol, Baltimore, MD 21201 USA. NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. RP Hurley, BF (reprint author), Univ Maryland, Coll Hlth & Human Performance, Dept Kinesiol, College Pk, MD 20742 USA. RI Fozard, James Leonard/B-3660-2009 FU NIA NIH HHS [1-AG-4-2148] NR 34 TC 193 Z9 201 U1 2 U2 16 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JAN PY 1999 VL 86 IS 1 BP 195 EP 201 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA 191EN UT WOS:000080009600027 PM 9887131 ER PT J AU Martin, DEK Troendle, JF AF Martin, DEK Troendle, JF TI Paired comparison models applied to the design of the Major League baseball play-offs SO JOURNAL OF APPLIED STATISTICS LA English DT Article AB This paper presents an analysis of the effect of various baseball play-off configurations on the probability of advancing to the Would Series. Play-off games are assumed to be independent. Several paired comparisons models are considered for modeling the probability of a home team winning a single game as a function of the winning percentages of the contestants over the course of the season. The uniform and logistic regression models are both adequate, whereas the Bradley-Terry model (modified for within-pair order effects, i. e. the home field advantage) is not. The single-game probabilities are then used to compute the probability of winning the play-offs under various structures. The extra round of play-offs, instituted in 1994, significantly lowers the probability of the team with the best record advancing to the World Series, whereas home field advantage and the different possible play-off draws have a minimal effect. C1 Howard Univ, Dept Math, Washington, DC 20059 USA. NIH, Bethesda, MD 20892 USA. NR 16 TC 3 Z9 3 U1 0 U2 0 PU CARFAX PUBLISHING PI BASINGSTOKE PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND SN 0266-4763 J9 J APPL STAT JI J. Appl. Stat. PD JAN PY 1999 VL 26 IS 1 BP 69 EP 80 DI 10.1080/02664769922665 PG 12 WC Statistics & Probability SC Mathematics GA 182EM UT WOS:000079485800006 ER PT J AU Wall, D Kolenbrander, PE Kaiser, D AF Wall, D Kolenbrander, PE Kaiser, D TI The Myxococcus xanthus pilQ (sglA) gene encodes a secretin homolog required for type IV pilus biogenesis, social motility, and development SO JOURNAL OF BACTERIOLOGY LA English DT Article ID GRAM-NEGATIVE BACTERIA; OUTER-MEMBRANE PROTEIN; PSEUDOMONAS-AERUGINOSA; GLIDING MOTILITY; FILAMENTOUS PHAGE; NEISSERIA-GONORRHOEAE; TWITCHING MOTILITY; TERMINAL DOMAIN; FIMBRIAE; MUTANTS AB The Myxococcus xanthus sglA1 spontaneous mutation was originally isolated because it allowed dispersed cell growth in liquid yet retained the ability. to form fruiting bodies. Consequently, most of today's laboratory strains either contain the sglA1 mutation or were derived from strains that carry it. Subsequent work showed that sglA was a gene for social gliding motility, a process which is mediated by type IV pill. Here sglA is shown to map to the major pil cluster and to encode a 901-amino-acid open reading frame (ORF) that is homologous to the secretin superfamily of proteins. Secretins form a channel in the outer membrane for the transport of macromolecules. The closest homologs found were PilQ proteins from Pseudomonas aeruginosa and Neisseria gonorrhoeae, which are required for type IV pill biogenesis and twitching motility. To signify these molecular and functional similarities, we have changed the name of sglA to pilQ. The hypomorphic pilQ1 (sglA1) allele was sequenced and found to contain two missense mutations at residues 741 (G --> S) and 762 (N --> G). In addition, 19 independent social (S)-motility mutations are shown to map to the pilQ locus. In-frame deletions of pile and its downstream gene, orfL, were constructed. pilQ is shown to be essential for pilus biogenesis, S-motility, rippling, and fruiting body formation, while orfL is dispensable for these processes. The pilQ1 allele, but not the Delta pilQ allele, was found to render cells hypersensitive to vancomycin, suggesting that PilQ1 alters the permeability properties of the outer membrane. Many differences between pilQ1 and pilQ(+) strains have been noted in the literature. We discuss some of these observations and how they may be rationalized in the context of our molecular and functional findings. C1 Stanford Univ, Dept Biochem, Stanford, CA 94305 USA. Stanford Univ, Dept Dev Biol, Stanford, CA 94305 USA. Natl Inst Dent & Craniofacial Res, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA. RP Wall, D (reprint author), Stanford Univ, Dept Biochem, Stanford, CA 94305 USA. NR 65 TC 97 Z9 98 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1999 VL 181 IS 1 BP 24 EP 33 PG 10 WC Microbiology SC Microbiology GA 151HX UT WOS:000077715600005 PM 9864308 ER PT J AU Weisberg, RA Gottesman, ME AF Weisberg, RA Gottesman, ME TI Processive antitermination SO JOURNAL OF BACTERIOLOGY LA English DT Review ID TRANSCRIPTION TERMINATION FACTOR; RIBOSOMAL-RNA TRANSCRIPTION; HK022 NUN PROTEIN; RHO-DEPENDENT TERMINATION; LAMBDA-PR PROMOTER; COLI NUSG PROTEIN; N-GENE-PRODUCT; ESCHERICHIA-COLI; PHAGE-LAMBDA; BACTERIOPHAGE-LAMBDA C1 NICHHD, Sect Microbial Genet, Genet Mol Lab, NIH, Bethesda, MD 20892 USA. Columbia Univ, Inst Canc Res, New York, NY 10032 USA. RP Weisberg, RA (reprint author), NICHHD, Sect Microbial Genet, Genet Mol Lab, NIH, Bethesda, MD 20892 USA. NR 112 TC 86 Z9 86 U1 1 U2 7 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JAN PY 1999 VL 181 IS 2 BP 359 EP 367 PG 9 WC Microbiology SC Microbiology GA 157BX UT WOS:000078040200002 PM 9882646 ER PT J AU Crotti, LB Jabor, VAP Chellegatti, MAD Fonseca, MJV Said, S AF Crotti, LB Jabor, VAP Chellegatti, MAD Fonseca, MJV Said, S TI Studies of pectic enzymes produced by Talaromyces flavus in submerged and solid substrate cultures SO JOURNAL OF BASIC MICROBIOLOGY LA English DT Article ID EXO-1 MUTANT STRAIN; PENICILLIUM-FREQUENTANS; VERTICILLIUM-DAHLIAE; PECTOLYTIC ENZYMES; GALACTURONIC ACID; NEUROSPORA-CRASSA; GLUCOSE-OXIDASE; ASPERGILLUS SP; POLYGALACTURONASES; BIOCONTROL AB Tons of peel and rag are generated each year by industries of citrus fruit juices. These by-products are used either for the elaboration of pectin or as substrate for enzyme production. Talaromyces flavus produces extracellular pectinesterase and polygalacturonase after 24 h in submerged culture supplemented with 0.5-0.8% citrus pectin preceded by preculture for 24 h in 2% (w/v) sucrose or in solid substrate culture on passion fruit peel, lemon or orange pulp pellets after 3-6 days of incubation. Chromatographic profiles in a CM-Sepharose column of liquid and solid cultures were very similar, consisting of one endopolygalacturonase (endo-PG I) and one pectinolytic complex constituted by an endopoligalacturonase (endo-PG II) and pectinesterase. Pectin and pectate lyases were undetectable in both media. In Talaromyces flavus the synthesis of pectinases was repressed by glucose and finally controlled by the concentration of products from pectic enzymes degradation. C1 Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Ciencias Farmaceut, BR-14040903 Ribeirao Preto, Brazil. RP NIH, Bldg 8,Room 403,8 Ctr Dr MSC 0851, Bethesda, MD 20892 USA. EM lucianae@intra.niddk.nih.gov RI Fonseca, Maria Jose Vieira/H-7881-2013 OI Fonseca, Maria Jose Vieira/0000-0002-7123-4838 NR 25 TC 11 Z9 11 U1 0 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0233-111X EI 1521-4028 J9 J BASIC MICROB JI J. Basic Microbiol. PY 1999 VL 39 IS 4 BP 227 EP 235 PG 9 WC Microbiology SC Microbiology GA 239GG UT WOS:000082760000002 PM 10520268 ER PT J AU Klose, TS Blaisdell, JA Goldstein, JA AF Klose, TS Blaisdell, JA Goldstein, JA TI Gene structure of CYP2C8 and extrahepatic distribution of the human CYP2Cs SO JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY LA English DT Article DE CYP2C8 gene structure; human CYP2C mRNA expression; extrahepatic tissues ID CYTOCHROME-P450 GENES; MOLECULAR-CLONING; MESSENGER-RNA; EXPRESSION; SUBFAMILY; ENZYMES; FORMS; P450S; IDENTIFICATION; TRANSCRIPTS AB Extrahepatic tissue distribution of the mRNAs for the four human CYP2Cs (2C8, 2C9, 2C18, and 2C19) was examined in kidney, testes, adrenal gland, prostate, brain, uterus, mammary gland, ovary, lung, and duodenum. CYP2C mRNAs were detected by RT-PCR using specific primers for each individual CYP2C. CYF2C8 mRNA was detected in the kidney, adrenal gland, brain, uterus, mammary gland, ovary, and duodenum. CYP2C9 mRNA was detected in the kidney, testes, adrenal gland, prostate, ovary, and duodenum. CYP2C18 mRNA was found only in the brain, uterus, mammary gland, kidney, and duodenum and CYP2C19 mRNA was found only in the duodenum. Immunoblot analysis of small intestinal microsomes detected both 2C9 and 2C19 proteins. In addition, genomic clones for CYP2C8 were sequenced, and long-distance PCR was performed to determine the complete gene structure. CYP2C8 spanned a 31 kb region. Comparative analysis of the 2.4 kb upstream region of CYP2C8 with CYP2C9 revealed two previously unidentified transcription factors sites, C/EBP and HPF-1, and the latter might be involved in hepatic expression. Although CYP2C8 has been shown to be phenobarbital inducible, neither a barbiturate-responsive regulatory sequence (a Barbie box) nor a phenobarbital-responsive enhancer module (PBREM) was found within the upstream region analyzed. (C) 1999 John Wiley & Sons, Inc. C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. N Carolina State Univ, Dept Toxicol, Raleigh, NC 27695 USA. RP Goldstein, JA (reprint author), NIEHS, Lab Pharmacol & Chem, POB 12233, Res Triangle Pk, NC 27709 USA. NR 42 TC 118 Z9 125 U1 0 U2 4 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1095-6670 J9 J BIOCHEM MOL TOXIC JI J. Biochem. Mol. Toxicol. PY 1999 VL 13 IS 6 BP 289 EP 295 DI 10.1002/(SICI)1099-0461(1999)13:6<289::AID-JBT1>3.0.CO;2-N PG 7 WC Biochemistry & Molecular Biology; Toxicology SC Biochemistry & Molecular Biology; Toxicology GA 232QN UT WOS:000082381600001 PM 10487415 ER PT J AU Tabor, H AF Tabor, H TI Prions of mammals and fungi minireview series SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review C1 NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. RP Tabor, H (reprint author), NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 1 PY 1999 VL 274 IS 1 BP 1 EP 1 DI 10.1074/jbc.274.1.1 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 154QP UT WOS:000077900200001 PM 9867801 ER PT J AU Huh, KH Wenthold, RJ AF Huh, KH Wenthold, RJ TI Turnover analysis of glutamate receptors identifies a rapidly degraded pool of the N-methyl-D-aspartate receptor subunit, NR1, in cultured cerebellar granule cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HETEROMERIC NMDA RECEPTORS; K+-INDUCED DEPOLARIZATION; LONG-TERM POTENTIATION; CENTRAL-NERVOUS-SYSTEM; PROTEIN-KINASE-C; RAT-BRAIN; ACETYLCHOLINE-RECEPTOR; SURFACE EXPRESSION; FUNCTIONAL EXPRESSION; ENDOPLASMIC-RETICULUM AB The Plumber, composition, and location of receptors in neurons are critically important factors in determining the neuron's response to neurotransmitters. The functional expression of receptors appears to be regulated both generally, at the level of transcription or translation, and locally, at the level of the individual synapse, A key component in the regulation of any protein is its turnover rate, which, measured in half-lives, ranges from a few minutes to several days. In the present study, we measured the turnover rates of subunits of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors, the two major ionotropic glutamate receptors, using cultured cerebellar granule cells. Turnover rates for NR1, NR2A/B, GluR2/3, and GluR4 subunits were determined by pulse-chase labeling of cells with [S-35]methionine. Half-lives were found to be 18 +/- 5 h and 23 +/- 8 h for the AMPA receptor subunits GluR2/3 and GluR4, respectively, and 16 +/- 5 h for NR2A. The NR1 subunit showed a biphasic decay with half-lives of 2 and 34 h for the rapidly and slowly degraded populations, respectively, Splice variants of the NR1 subunit with different carboxyl-terminal cassettes, C2 and C2', showed similar biphasic degradation patterns, To further characterize the rapidly degraded pool of NR1, surface receptors were labeled by biotinylation, and half-lives of the biotinylated proteins were determined, All surface NR1 was slowly degraded with a pattern similar to that of NR2A, GluR2/3, and GluR4, suggesting that the rapidly degraded pool is confined to the cytoplasm and not assembled with NR2 subunits, A significant amount of NR1 was not immunoprecipitated by NR2 subunit-specific antibodies after solubilization with deoxycholate. This unassembled pool, but not the assembled one, was greatly diminished following treatment of cycloheximide for 5 h, indicating that the rapidly degraded pool of NR1 is not assembled with NR2, These results show that MMDA and AMPA receptors have similar turnover rates, but NMDA receptors have a separate pool of NR1 subunits that is rapidly degraded and accounts for most of the intracellular pool. C1 NIDCD, Neurochem Lab, NIH, Bethesda, MD 20892 USA. RP Huh, KH (reprint author), NIDCD, Neurochem Lab, NIH, Bldg 36,Rm 5D08, Bethesda, MD 20892 USA. NR 71 TC 191 Z9 197 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 1 PY 1999 VL 274 IS 1 BP 151 EP 157 DI 10.1074/jbc.274.1.151 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 154QP UT WOS:000077900200023 PM 9867823 ER PT J AU Park, EA Song, S Vinson, C Roesler, WJ AF Park, EA Song, S Vinson, C Roesler, WJ TI Role of CCAAT enhancer-binding protein beta in the thyroid hormone and cAMP induction of phosphoenollolpyruvate carboxykinase gene transcription SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TISSUE-SPECIFIC EXPRESSION; GTP GENE; C/EBP-ALPHA; ORPHAN RECEPTORS; RESPONSE ELEMENT; DNA-BINDING; COUP-TF; PHOSPHOENOLPYRUVATE; PROMOTER; ACTIVATION AB Transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK) is stimulated by thyroid hormone (T-3) and cAMP. Two DNA elements in the PEPCK promoter are required for T-3 responsiveness including a thyroid hormone response element and a binding site called P3(I) for the CCAAT enhancer-binding protein (C/EBP). Both the alpha and beta isoforms of C/EBP are highly expressed in the liver. C/EBP alpha contributes to the liver-specific expression and cAMP responsiveness of the PEPCK gene. In this study, we examined the ability of C/EBP beta when bound to the P3(I) site to regulate PEPCK gene expression. We report that C/EBP beta can stimulate basal expression and participate in the induction of PEPCK gene transcription by T-3 and cAMP. The cAMP-responsive element-binding protein and API proteins that contribute to the induction by cAMP are not involved in the stimulation by T-3. A small region of the transactivation domain of C/EBP beta is sufficient for the stimulation of basal expression and cAMP responsiveness. Our results suggest that C/EBP alpha and C/EBP beta are functionally interchangeable when bound to the P3(I) site of the PEPCK promoter. C1 Univ Tennessee, Ctr Hlth Sci, Coll Med, Dept Pharmacol, Memphis, TN 38163 USA. Univ Saskatchewan, Dept Biochem, Saskatoon, SK S7N 5E5, Canada. NCI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Park, EA (reprint author), Univ Tennessee, Ctr Hlth Sci, Coll Med, Dept Pharmacol, 874 Unioin Ave, Memphis, TN 38163 USA. EM epark@utmem1.utmem.edu FU NIDDK NIH HHS [DK-46399] NR 50 TC 38 Z9 38 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JAN 1 PY 1999 VL 274 IS 1 BP 211 EP 217 DI 10.1074/jbc.274.1.211 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 154QP UT WOS:000077900200032 PM 9867832 ER PT J AU Delfino, L Longo, A Morabito, A Parodi, A Pera, C Pozzi, S Ferrara, GB AF Delfino, L Longo, A Morabito, A Parodi, A Pera, C Pozzi, S Ferrara, GB TI HLA class I sequence-based typing for high resolution matching in bone marrow transplantation SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS LA English DT Article ID UNRELATED DONORS; HEART-TRANSPLANTATION; ALLELES; AMPLIFICATION; POLYMORPHISM; GRAFT; LOCUS; DNA; MOLECULES; LEUKEMIA C1 Adv Biotechnol Ctr, Natl Canc Inst, Immunogenet Lab, Genoa, Italy. RP Ferrara, GB (reprint author), Ist Nazl Ric Canc, Immunogenet Lab, Lgo R Benzi 10, I-16132 Genoa, Italy. NR 32 TC 3 Z9 3 U1 0 U2 0 PU WICHTIG EDITORE PI MILAN PA 72/74 VIA FRIULI, 20135 MILAN, ITALY SN 0393-974X J9 J BIOL REG HOMEOS AG JI J. Biol. Regul. Homeost. Agents PD JAN-MAR PY 1999 VL 13 IS 1 BP 42 EP 46 PG 5 WC Endocrinology & Metabolism; Immunology; Medicine, Research & Experimental; Physiology SC Endocrinology & Metabolism; Immunology; Research & Experimental Medicine; Physiology GA 214GZ UT WOS:000081321400008 PM 10432441 ER PT J AU Kidder, LH Colarusso, P Stewart, SA Levin, IW Appel, NM Lester, DS Pentchev, PG Lewis, EN AF Kidder, LH Colarusso, P Stewart, SA Levin, IW Appel, NM Lester, DS Pentchev, PG Lewis, EN TI Infrared spectroscopic imaging of the biochemical modifications induced in the cerebellum of the Niemann-Pick type C mouse SO JOURNAL OF BIOMEDICAL OPTICS LA English DT Article DE infrared spectroscopic imaging; FTIR spectroscopy; Niemann-Pick type C; neuropathology; cerebellum ID DISEASE TYPE-C; MURINE MODEL; TISSUE; STORAGE; CLASSIFICATION; CARCINOMA; SECTIONS; MUTATION; SYSTEMS; SPECTRA AB We have applied Fourier transform infrared (IR) spectroscopic imaging to the investigation of the neuropathologic effects of a genetic lipid storage disease, Niemann-Pick type C (NPC). Tissue sections both from the cerebella of a strain of BALB/c mice that demonstrated morphology and pathology of the human disease and from control animals were used. These samples were analyzed by standard histopathological procedures as well as this new IR imaging approach. The IR absorbance images exhibit contrast based on biochemical variations and allow for the identification of the cellular layers within the tissue samples. Furthermore, these images provide a qualitative description of the localized biochemical differences existing between the diseased and control tissue in the absence of histological staining. Statistical analyses of the IR spectra extracted from individual cell layers of the imaging data sets provide concise quantitative descriptions of these biochemical changes. The results indicate that lipid is depleted specifically in the white matter of the NPC mouse in comparison to the control samples. Minor differences were noted for the granular layers, but no significant differences were observed in the molecular layers of the cerebellar tissue. These changes are consistent with significant demyelination within the cerebellum of the NPC mouse. (C) 1999 Society of Photo-Optical Instrumentation Engineers. [S1083-3668(99)00401-3]. C1 NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. US FDA, Ctr Drug Evaluat & Res, Div Appl Pharmacol Res, Laurel, MD 20708 USA. NINDS, NIH, Dev & Metab Neurol Branch, Mol & Cellular Pathol Sect, Bethesda, MD 20892 USA. RP Lewis, EN (reprint author), 9000 Rockville Pike,Bldg 5,Room B1-38, Bethesda, MD 20892 USA. NR 29 TC 21 Z9 22 U1 0 U2 2 PU SPIE-INT SOCIETY OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA SN 1083-3668 J9 J BIOMED OPT JI J. Biomed. Opt. PD JAN PY 1999 VL 4 IS 1 BP 7 EP 13 DI 10.1117/1.429915 PG 7 WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine & Medical Imaging SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine & Medical Imaging GA 229FY UT WOS:000082183900002 PM 23015163 ER PT J AU Zhang, J Kovac, P AF Zhang, J Kovac, P TI An alternative method for regioselective, anomeric deacylation of fully acylated carbohydrates SO JOURNAL OF CARBOHYDRATE CHEMISTRY LA English DT Article ID DERIVATIVES; GLYCOSIDES; FRAGMENTS; HYDRAZINE; RESIDUES; ANTIGEN AB Ethylenediamine in admixture with acetic acid has been found useful to selectively effect the title conversion and can be of general utility. Reaction rates anomeric deacylations effected with this reagent are slower than with reagents introduced earlier, resulting in easier control and greater selectivity of deprotection. C1 NIH, Bethesda, MD 20892 USA. RP Kovac, P (reprint author), NIH, Bldg 8, Bethesda, MD 20892 USA. NR 16 TC 39 Z9 39 U1 2 U2 17 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0732-8303 J9 J CARBOHYD CHEM JI J. Carbohydr. Chem. PY 1999 VL 18 IS 4 BP 461 EP 469 DI 10.1080/07328309908544010 PG 9 WC Biochemistry & Molecular Biology; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA 199WB UT WOS:000080506100009 ER PT J AU Lenfant, C AF Lenfant, C TI The Journal of Cardiovascular Magnetic Resonance: Yet another new journal SO JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE LA English DT Editorial Material C1 NHLBI, Bethesda, MD 20892 USA. RP Lenfant, C (reprint author), NHLBI, Bldg 10, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 1097-6647 J9 J CARDIOV MAGN RESON JI J. Cardiov. Magn. Reson. PY 1999 VL 1 IS 1 BP XIII EP XIII PG 1 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA 278CQ UT WOS:000084970700002 ER PT J AU Budinger, T Berson, A McVeigh, E Pettigrew, R Pohost, G Watson, J Wickline, S AF Budinger, T Berson, A McVeigh, E Pettigrew, R Pohost, G Watson, J Wickline, S TI Magnetic resonance imaging of the cardiovascular system (Reprinted from Radiology, vol 208, pg 573-576, 1998) SO JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE LA English DT Reprint C1 NHLBI, NIH, Bethesda, MD 20892 USA. Univ Calif Berkeley, Lawrence Natl Berkeley Lab, Berkeley, CA 94720 USA. Johns Hopkins Univ, Baltimore, MD USA. Emory Univ, Atlanta, GA 30322 USA. Univ Alabama, Birmingham, AL USA. Jewish Hosp, St Louis, MO USA. RP Berson, A (reprint author), NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 1 TC 8 Z9 8 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 1097-6647 J9 J CARDIOV MAGN RESON JI J. Cardiov. Magn. Reson. PY 1999 VL 1 IS 1 BP 53 EP 58 DI 10.3109/10976649909080834 PG 6 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA 278CQ UT WOS:000084970700009 ER PT J AU Danielpour, D AF Danielpour, D TI Transdifferentiation of NRP-152 rat prostatic basal epithelial cells toward a luminal phenotype: regulation by glucocorticoid, insulin-like growth factor-I and transforming growth factor-beta SO JOURNAL OF CELL SCIENCE LA English DT Article DE Lobund-Wistar rat; dorsal-lateral prostate; cytokeratin; tight junction; cell growth ID ANDROGEN-REPRESSED GENES; VENTRAL PROSTATE; DIFFERENTIAL EXPRESSION; REGIONAL VARIATION; STROMAL CELLS; DUCTAL SYSTEM; TGF-BETA; FACTOR-BETA-1; ACTIVATION; DEATH AB The role of basal epithelial cells in prostatic function, development and carcinogenesis is unknown, The ability of basal prostatic epithelial cells to acquire a luminal phenotype was explored in vitro using the NRP-152 rat dorsal-lateral prostate epithelial cell line as a model system, NRP-152, which was spontaneously immortalized and clonally derived, is an androgen-responsive and nontumorigenic cell line that has a basal cell phenotype under normal growth conditions. However, when placed in mitogen-deficient media, these cells undergo a dramatic morphological change to a luminal phenotype, Under these growth-restrictive conditions, immunocytochemical analysis shows that NRP-152 cells acquire the luminal markers Z0-1 (a tight-junction associated protein), occludin (integral tight-junction protein), and cytokeratin 18, and lose the basal markers cytokeratins 5 and 14, Total protein and mRNA levels of cytokeratins 8, 18, c-CAM 105 (the calcium-independent cell adhesion molecule) and Z0-1, as detected by western and/or northern blot analyses, respectively, are induced, while cytokeratin 5 and 15 are lost, and occludin is unchanged, Concomitant with this differentiation, expression of transforming growth factor-beta 2 (TGF-beta 2), TGF-beta 3, and TGF-beta receptor type II (T beta RII) is induced, while those of TGF-beta 1 and T beta RI remain essentially unchanged. Mitogens, such as insulinlike growth factor-I and dexamethasone inhibit luminal differentiation, while exogenous TGF-beta induces such differentiation. These data together with TGF-beta neutralization experiments using pan-specific antibody implicate an important role for autocrine TGF-beta in the induction of the luminal differentiation. C1 NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. Case Western Reserve Univ, Ireland Canc Ctr, Cleveland, OH 44106 USA. Univ Hosp Cleveland, Ireland Canc Ctr, Dept Pharmacol, Cleveland, OH 44106 USA. RP Danielpour, D (reprint author), Case Western Reserve Univ, Ireland Canc Ctr, UCRC 2,Room 200,Lab 3,11001 Cedar Ave, Cleveland, OH 44106 USA. NR 57 TC 61 Z9 62 U1 0 U2 0 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 1999 VL 112 IS 2 BP 169 EP 179 PG 11 WC Cell Biology SC Cell Biology GA 166NM UT WOS:000078583200003 PM 9858470 ER PT J AU Feuillan, PP Jones, JV Barnes, K Oerter-Klein, K Cutler, GB AF Feuillan, PP Jones, JV Barnes, K Oerter-Klein, K Cutler, GB TI Reproductive axis after discontinuation of gonadotropin-releasing hormone analog treatment of girls with precocious puberty: Long term follow-up comparing girls with hypothalamic hamartoma to those with idiopathic precocious puberty SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID AGONIST TREATMENT; CHILDREN; GROWTH; ADOLESCENTS; THERAPY; OVARIES; BOYS AB Although the GnRH agonist analogs have become an established treatment for precocious puberty, there have been few long term studies of reproductive function and general health after discontinuation of therapy. To this end, we compared peak LH and FSH after 100 mu g sc GnRH, estradiol, mean ovarian volume (MOV), age of onset and frequency of menses, body mass (BMT), and incidence of neurological and psychiatric problems in 2 groups of girls: those with precocious puberty due to hypothalamic hamartoma (HH; n = 18) and those with idiopathic precocious puberty (IPP; n = 32) who had been treated with deslorelin (4-8 mu g/kg.day, sc) or histrelin (10 mu g/kg.day, SC) for 3.1-10.3 yr and were observed at 1, 2, 3, and 4-5 yr after discontinuation of treatment. The endocrine findings were also compared to those in 14 normal perimenarcheal girls. There were no differences between the HH and IPP groups in age or bone age at the start of treatment, at the end of treatment, or during GnRH analog therapy. We found that whereas the peak LH level was higher in HH than in IPP girls before (165.5 +/- 129 os. 97.5 +/- 55.7; P < 0.02) and at the end (6.8 +/- 6.0 vs. 3.9 +/- 1.8 mIU/mL; P < 0.05) of therapy, this difference did not persist at any of the posttherapy time points. LH, FSH, and estradiol rose into the pubertal range by 1 yr posttherapy in both HH and IPP. However, the mean posttherapy peak LH levels in both HH and IPP groups tended to be lower than normal, whereas the peak FSH levels were not different from normal, so that the overall posttherapy LH/FSH ratio was decreased compared to that in the normal girls (HH, 2.1 +/- 0.3; TPP, 2.6 +/- 0.1; normal, 5.2 +/- 4.8; P < 0.05). The MOV was larger in HH than IPP at the end of treatment (3.7 +/- 3.5 vs. 2.0 +/- 1.2 mL; P < 0.05) and tended to increase in both groups over time to become larger than that in normal girls by 4-5 yr posttherapy(HH, 14.9 +/- 12.9: IPP 7.6 +/- 2.2; normal, 5.4 +/- 2.5 mL; P < 0.05). Whereas the onset of spontaneous menses varied widely in both groups, once menses had started, the HH group had a higher incidence of oligomenorrhea. Pelvic ultrasonography revealed more than 10-mm hypoechoic regions in 4 HH patients, 15 IPP patients, and 3 normal girls, all of whom were reporting regular menses. Live births of normal infants were reported by 2 HH and 2 IPP patients, and elective terminations of pregnancy were reported by 1 HH and 2 IPP patients. BMI was greater than normal in HH and IPP both before treatment and at all posttherapy time points and tended to be higher in the HH patients. Marked obesity (BMT, +2 to +5.2 SD score) was observed in 5 HH and 6 IPP patients, 1 of whom had a BMI of +2.5 so score and developed acanthosis nigricans, insulin resistance, and hyperglycemia. Seizure disorders developed during GnRH analog therapy in 5 HH and 1 IPP patient, and 2 additional HH girls developed severe depression and emotional lability posttherapy. Although the mean anterior-posterior dimension of the hamartoma was larger in the KH patients with seizure than in those who were seizure free (1.7 +/- 1.2 vs. 0.9 +/- 0.4 cm; P < 0.05), no change in hamartoma size was observed either during or after therapy, and no patient has reported the onset of a seizure disorder posttherapy. Other than a tendency toward a larger MOV, a higher incidence of oligomenorrhea, obesity, and frequency of neurological disorders, recovery of the reproductive iuds after GnRH analog therapy was not markedly different in HH compared to IPP. Continued follow-up of these patients may determine whether the decreased LH responses and increased BMI in both groups compared to those in normal girls remain clinically significant problems. C1 NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Feuillan, PP (reprint author), NICHHD, Dev Endocrinol Branch, NIH, Bldg 10,Room 10N 262, Bethesda, MD 20892 USA. NR 27 TC 72 Z9 78 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1999 VL 84 IS 1 BP 44 EP 49 DI 10.1210/jc.84.1.44 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 155VN UT WOS:000077967200009 PM 9920060 ER PT J AU Leschek, EW Jones, J Barnes, KM Hill, SC Cutler, GB AF Leschek, EW Jones, J Barnes, KM Hill, SC Cutler, GB TI Six-year results of spironolactone and testolactone treatment of familial male-limited precocious puberty with addition of deslorelin after central puberty onset SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID SEXUAL PRECOCITY; LUTEINIZING-HORMONE; KETOCONAZOLE THERAPY; HEPATIC-INJURY; TESTOTOXICOSIS; MUTATION; LEYDIG; RADIOIMMUNOASSAY; BIOSYNTHESIS; GENERATIONS AB Short term treatment with spironolactone, testolactone, and, after the onset of central puberty, deslorelin can normalize the rate of growth and bone maturation in boys with familial male-limited precocious puberty. To test the hypothesis that this treatment can achieve long term normalization of the growth and development of these children, are examined the growth rate, bone maturation rate (change in bone age/change in chronological age), and predicted adult height of 10 boys who were treated with spironolactone (5.7 mg/ kg day) and testolactone (40 mg/kg day) for at least 6 yr. Deslorelin (4 mu g/kg.day) treatment was initiated 2.6 +/- 1.3 yr after beginning spironolactone and testolactone treatment. The growth rate normalized within 1 yr of starting treatment and remained normal during the next 5 yr of treatment (P < 0.001). The rate of bone maturation normalized during the second year of treatment and remained normal thereafter (P < 0.001). Predicted height increased from 160.7 +/- 14.7 centimeters at baseline to 173.6 +/- 10.1 centimeters after 6 yr of treatment (P < 0.05 during the fourth through the sixth year of treatment compared to baseline). We conclude that long term treatment with spironolactone, testolactone, and, after central puberty, deslorelin normalizes the growth rate and bone maturation and improves the predicted height in boys with familial male-limited precocious puberty. The ultimate effect of this approach on adult height will require further study. C1 NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. NIH, Dept Radiol, Bethesda, MD 20892 USA. RP Leschek, EW (reprint author), NICHHD, Dev Endocrinol Branch, NIH, Bldg 10,Room 10N262,10 Ctr Dr,MSC 1862, Bethesda, MD 20892 USA. EM ellen_leschek@nih.gov NR 26 TC 49 Z9 53 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1999 VL 84 IS 1 BP 175 EP 178 DI 10.1210/jc.84.1.175 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 155VN UT WOS:000077967200028 PM 9920079 ER PT J AU Heppner, C Reincke, M Agarwal, SK Mora, P Allolio, B Burns, AL Spiegel, AM Marx, SJ AF Heppner, C Reincke, M Agarwal, SK Mora, P Allolio, B Burns, AL Spiegel, AM Marx, SJ TI MEN1 gene analysis in sporadic adrenocortical neoplasms SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID TUMOR-SUPPRESSOR GENE; CHROMOSOME 11Q13; TYPE-1; MUTATIONS; CARCINOMA; PART; DNA AB Adrenocortical tumors occur as sporadic tumors, as part of the multiple endocrine neoplasia type 1 (MEN1) syndrome or as part of other hereditary disorders. We recently cloned the MEN1 gene, a tumor-suppressor gene located on chromosome 11q13. Subsequently, we showed that sequential somatic inactivation of both alleles of the MEN1 gene contributes to the development of some sporadic endocrine neoplasms (parathyroid, enteropancreatic neuroendocrine, branchial carcinoid, and pituitary tumors). We now studied whether somatic inactivation of the MEN1 gene contributes to the pathogenesis of sporadic adrenocortical neoplasms. Seven adrenocortical carcinomas, 2 adrenocortical carcinoma cell Lines, and 11 aldosterone-secreting, 8 cortisol-secreting, and 5 nonsecreting benign adrenocortical tumors were studied. Seven tumors (5 of 5 carcinomas, 2 of 21 nonsecreting benign adenomas; P < 0.001) exhibited loss of heterozygosity on 11q13. All 33 tumors and cell lines were screened for mutation throughout the MEN1 open-reading frame and adjacent splice junctions. None exhibited a mutation within the MEN1-coding region. We conclude that somatic MEN1 mutation within the MEN1-coding region does not occur commonly in sporadic adrenocortical tumors, although the majority of adrenocortical carcinomas exhibit 11q13 loss of heterozygosity. C1 NIDDK, Metab Dis Branch, NIH, Bethesda, MD 20892 USA. Univ Klin Freiburg, Innere Med Abt 2, Freiburg, Germany. Univ Klin Wurzburg, Med Klin, Wurzburg, Germany. RP Heppner, C (reprint author), NIDDK, Metab Dis Branch, NIH, Bldg 10,Room 9C101,10 Ctr Dr, Bethesda, MD 20892 USA. EM christinah@bdg10.niddk.nih.gov RI Agarwal, Sunita/D-1428-2016 OI Agarwal, Sunita/0000-0002-7557-3191 NR 26 TC 76 Z9 78 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JAN PY 1999 VL 84 IS 1 BP 216 EP 219 DI 10.1210/jc.84.1.216 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 155VN UT WOS:000077967200036 PM 9920087 ER PT J AU Fried, LP Bandeen-Roche, K Kaser, JD Guralnik, JM AF Fried, LP Bandeen-Roche, K Kaser, JD Guralnik, JM CA Women's Hlth Aging Study Collaborative Res Grp TI Association of comorbidity with disability in older women: The Women's Health and Aging Study SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE aging; comorbidity; disability; chronic disease; physical function; geriatrics ID PHYSICAL-DISABILITY; ADULTS; ARTHRITIS; ELDERS; RISK AB There is substantial evidence that physical disability results from chronic diseases and that the number of chronic diseases is associated with the presence and severity of disability. There is some evidence that interactions between specific diseases are of import in causing disability. Beyond arthritis, however, little is known of the disease pairs that may be important to focus on in future research. This study explores the associations between multiple disease pairs and different types of physical disability, with the objective of hypothesis;development regarding the importance of disease interactions. The study population comprised a representative sample of 3841 women 65 years and older living in Baltimore, screened for participation in the Women's Health and Aging Study. The study design was cross-sectional. An interviewer-administered screening questionnaire was administered regarding self-reported physical disability in 15 tasks of daily life, history of physician diagnosis of 14 chronic diseases, and MiniMental State examination. Task difficulty was empirically grouped into six subsets of minimally overlapping disabilities, with a comparison group consisting of those with no difficulty in any task subset. Multiple logistic regression models were fit assessing the relationship of major chronic diseases and of interactions of disease pairs with each disability subtype and with any disability, adjusting for confounders. Fourteen percent of the population reported mobility difficulty only; 5%, upper extremity difficulty only; 9%, both of these difficulties but no others; 7%, difficulty in higher function but not self-care tasks; 7%, self-care task difficulty but not higher function tasks; and 15%, difficulty in both higher function and self-care (weighted data). Almost all in the latter three groups had difficulty, as well, in mobility or upper extremity tasks. In regression models, specific disease pairs were synergistically associated with different types of disability. For example, important disease pairs that recurred in their associations with different disability types were the presence of arthritis and visual impairments, arthritis and high blood pressure, heart disease and cancer, lung disease and cancer, and stroke and high blood pressure. In addition, the type of disability that a disease was associated with varied, depending on the other disease that was present. Finally, when interactions were accounted for, many diseases were no longer, in themselves, independently associated with a given type of disability. Partitioning disability into six subtypes was more informative in terms of associations than was evaluating a summary category of "any disability." These findings provide a basis for further hypothesis development and testing of synergistic relationships of specific diseases with disabilities. If testing confirms these observations, these findings could provide a basis for new strategies for prevention of disability by minimizing comorbid interactions. J CLIN EPIDEMIOL 52;1:27-37, 1999. (C) 1999 Elsevier Science Inc. C1 Johns Hopkins Med Inst, Baltimore, MD 21205 USA. NIA, Epidemiol Demog & Biometry Program, Bethesda, MD 20892 USA. RP Fried, LP (reprint author), Welch Ctr Prevent Epidemiol & Clin Res, Suite 2-600,2024 E Monument St, Baltimore, MD 21205 USA. FU NIA NIH HHS [AG11703-05, N01AG12112] NR 17 TC 289 Z9 293 U1 1 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD JAN PY 1999 VL 52 IS 1 BP 27 EP 37 DI 10.1016/S0895-4356(98)00124-3 PG 11 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA 159TC UT WOS:000078189600005 PM 9973071 ER PT J AU Fahle, GA Gill, VJ Fischer, SH AF Fahle, GA Gill, VJ Fischer, SH TI Optimal activation of isopsoralen to prevent amplicon carryover SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; FALSE POSITIVES; STERILIZATION; CONTAMINATION; INACTIVATION; PROTOCOLS; PCR AB We compared the efficiencies of activation of the photochemical isopsoralen compound 10 and its resulting amplicon neutralizations under conditions with a UV transilluminator box at room temperature (RT) and a HRI-300 UV photothermal reaction chamber at RT and at 5 degrees C. Our data suggest that use of the HRI-300 reaction chamber at 5 degrees C results in a statistically significantly higher degree of amplicon neutralization. C1 NIH, Warren G Magnuson Clin Ctr, Microbiol Serv, Dept Clin Pathol, Bethesda, MD 20892 USA. RP Fahle, GA (reprint author), NIH, Warren G Magnuson Clin Ctr, Microbiol Serv, Dept Clin Pathol, Bldg 10,Room 2C-385, Bethesda, MD 20892 USA. EM gfahle@nih.gov NR 13 TC 7 Z9 8 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 USA SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JAN PY 1999 VL 37 IS 1 BP 261 EP 262 PG 2 WC Microbiology SC Microbiology GA 149CQ UT WOS:000077587900056 PM 9854109 ER PT J AU Coleman, CN Mitchell, JB AF Coleman, CN Mitchell, JB TI Clinical radiosensitization: Why it does and does not work SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material ID CANCER; RADIOTHERAPY; CHEMOTHERAPY; RADIATION C1 Harvard Univ, Sch Med, Joint Ctr Radiat Therapy, Boston, MA 02115 USA. NCI, Radiat Biol Branch, Bethesda, MD 20892 USA. RP Coleman, CN (reprint author), Harvard Univ, Sch Med, Joint Ctr Radiat Therapy, Boston, MA 02115 USA. NR 14 TC 19 Z9 19 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1999 VL 17 IS 1 BP 1 EP 3 PG 3 WC Oncology SC Oncology GA 155CB UT WOS:000077927400001 PM 10458210 ER PT J AU Abrams, J Aisner, J Cirrincione, C Berry, DA Muss, HB Cooper, MR Henderson, IC Panasci, L Kirshner, J Ellerton, J Norton, L AF Abrams, J Aisner, J Cirrincione, C Berry, DA Muss, HB Cooper, MR Henderson, IC Panasci, L Kirshner, J Ellerton, J Norton, L TI Dose-response trial of megestrol acetate in advanced breast cancer: Cancer and leukemia group B phase III study 8741 SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID QUALITY-OF-LIFE; MEDROXYPROGESTERONE ACETATE; PROGESTATIONAL AGENTS; POSTMENOPAUSAL WOMEN; RANDOMIZED TRIAL; RECEPTOR LEVELS; ANOREXIA; PROGESTINS; INDUCTION; APPETITE AB Purpose: To investigate whether dose escalation of megestrol acetate (MA) improves response rate and survival in comparison with standard doses of MA. Patients and Methods: Three hundred sixty-eight patients with metastatic breast cancer, positive and/or unknown estrogen and progesterone receptors, zero or one prior trial of hormonal therapy and no prior chemotherapy for metastatic disease were prospectively randomized into three groups. The groups of patients received either MA 160 mg/d (one tablet per day), MA 800 mg/d (five tablets per day), or MA 1,600 mg/d (10 tablets per day). Results: patient characteristics were well balanced in the three treatment groups. Three hundred sixty-six patients received treatment and were included in the analyses. The response rates were 23%, 27%, and 27% For the 160-mg, 800-mg, and 1,600-mg arms, respectively. Response duration correlated inversely with dose, Median durations of response were 17 months, 14 months, and 8 months for the 160-mg, 800-mg, and 1,600-mg arms, respectively No significant differences in the treatment arms were noted for time to disease progression or for survival; survival medians were 28 months (low dose), 24 months (mid dose) and 29 months (high dose). The mast frequent and troublesome toxicity, weight gain, was dose-related, with approximately 20% of patients on the two higher-dose arms reporting weight gain of more than 20% of their prestudy weight, compared with only 2% in the 160-mg dose arm. Conclusion: With a median follow-up of 8 years, these results demonstrate no advantage for dose escalation of MA in the treatment of metastatic breast cancer. J Clin Oncol 17:64-73, (C) 1999 by American Society of Clinical Oncology. C1 Univ Maryland, Ctr Canc, Baltimore, MD 21201 USA. Stat Off, Leukemia Grp B, Durham, NC USA. Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA. Dana Farber Canc Inst, Boston, MA 02115 USA. McGill Canc Ctr, Montreal, PQ, Canada. SUNY Syracuse, Syracuse, NY USA. Univ Calif San Diego, San Diego, CA 92103 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. RP Abrams, J (reprint author), NCI, 6130 Execut Blvd,EPN 741, Bethesda, MD 20892 USA. NR 30 TC 24 Z9 24 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1999 VL 17 IS 1 BP 64 EP 73 PG 10 WC Oncology SC Oncology GA 155CB UT WOS:000077927400010 PM 10458219 ER PT J AU Marshall, JL Hawkins, MJ Tsang, KY Richmond, E Pedicano, JE Zhu, MZ Schlom, J AF Marshall, JL Hawkins, MJ Tsang, KY Richmond, E Pedicano, JE Zhu, MZ Schlom, J TI Phase I study in cancer patients of a replication-defective avipox recombinant vaccine that expresses human carcinoembryonic antigen SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID VIRUS-VACCINE; CEA; IMMUNOGENICITY; EPITOPES; SAFETY; VECTOR; CELLS; GENE AB Purpose: A phase I clinical trial in patients with advanced carcinoma was conducted, using a replication-defective avipox vaccine containing the gene for the human carcinoembryonic antigen (CEA). The canarypox vector, designated ALVAC, has the ability to infect human cells but cannot replicate, Patients and Methods: The recombinant vaccine, designated ALVAC-CEA, was administered intramuscularly three times a, 28-day intervals. Each cohort of six patients received three doses of either 2.5 x 10(5), 2.5 x 10(6), Or 2.5 x 10(7) plaque-forming units of vaccine. Results: The vaccine was well tolerated at all dose levels and no significant toxicity was attributed to the treatment, No objective antitumor response was observed during the trial in patients with measurable disease. Studies were conducted to assess whether ALVAC-CEA had the ability to induce cytolytic T-lymphocyte (CTL) responses in patients with advanced cancer, Peripheral blood mononuclear cells (PBMCs) from patients with the MHC class I A2 allele were obtained before vaccine administration and 1 month after the third vaccination. Peripheral blood mononuclear cells were incubated with the CEA immunodominant CTL epitope carcinoembryonic antigen peptide-1 and interleukin 2 and quantitated using CTL precursor frequency analysis. In seven of nine patients evaluated, statistically significant increases in CTL precursors specific for CEA were observed in PBMCs after vaccination, compared with before vaccination. Conclusion: These studies constitute the first phase I trial of an avipox recombinant in cancer patients, The recombinant vaccine ALVAC-CEA seems ta be safe and has been demonstrated to elicit CEA-specific CTL responses, These studies thus form the basis for the further clinical exploration of the ALVAC-CEA recombinant vaccine in phase I/II studies in protocols designed to enhance the generation of human T-cell responses to CEA. J Clin Oncol 17:332-337. (C) 1999 by American Society of Clinical Oncology. C1 Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, Washington, DC 20007 USA. NCI, Tumor Immunol & Biol Lab, Div Basic Sci, NIH, Bethesda, MD USA. RP Marshall, JL (reprint author), Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, 3800 Resvoir Rd NW, Washington, DC 20007 USA. FU NCI NIH HHS [2 P30 CA51008, U01 CA62500] NR 27 TC 150 Z9 152 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1999 VL 17 IS 1 BP 332 EP 337 PG 6 WC Oncology SC Oncology GA 155CB UT WOS:000077927400042 PM 10458251 ER PT J AU Roy, A Nielsen, D Rylander, G Sarchiapone, M Segal, N AF Roy, A Nielsen, D Rylander, G Sarchiapone, M Segal, N TI Genetics of suicide in depression SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on the Effects of Medical Interventions on Suicidal Behavior CY FEB 26-28, 1998 CL MIAMI, FLORIDA SP Amer Fdn Suicide Prevent, Johns Hopkins Univ Sch Med, Long Island Jewish Med Ctr, Suicide Prevent Advocacy Network, Solvay Pharmaceut Inc ID SEROTONIN TRANSPORTER GENE; TRYPTOPHAN-HYDROXYLASE GENE; FAMILY HISTORY; CEREBROSPINAL-FLUID; AFFECTIVE-DISORDERS; MAJOR DEPRESSION; BEHAVIOR; POLYMORPHISM; PLATELET; RISK AB Evidence is mounting that genetic factors may be included in the many determinants of suicide. Clinical studies of psychiatric patients have suggested that risk of suicidal behavior is increased by the presence of family history of suicidality, a claim that is also supported by findings of twin and adoption studies. In addition, molecular genetic studies have reported polymorphisms in the tryptophan hydroxylase gene that is involved in the synthesis of serotonin. The genetic susceptibility to suicide, however, tends to affect individuals only in association with stress or psychiatric illness. C1 Med Ctr, Psychiat Serv 116A, New Jersey Hlth Care Syst, Dept Vet Affairs, E Orange, NJ 07018 USA. Karolinska Inst, S-10401 Stockholm, Sweden. Catholic Univ, Rome, Italy. NIAAA, Neurogenet Lab, Bethesda, MD USA. Calif State Univ Fullerton, Dept Psychol, Fullerton, CA 92634 USA. RP Roy, A (reprint author), Med Ctr, Psychiat Serv 116A, New Jersey Hlth Care Syst, Dept Vet Affairs, 385 Tremont Ave, E Orange, NJ 07018 USA. RI Nielsen, David/B-4655-2009; OI Sarchiapone, Marco/0000-0001-9583-3117 NR 43 TC 49 Z9 51 U1 3 U2 4 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 1999 VL 60 SU 2 BP 12 EP 17 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 171JZ UT WOS:000078861300003 PM 10073383 ER PT J AU Dodge, MR Goldberg, TE AF Dodge, MR Goldberg, TE TI Associations between cognitive impairment and tardive dyskinesia: Another perspective SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on the Use of Newer Antipsychotic Medications in the Elderly CY JUL 11, 1997 CL TORONTO, CANADA ID BASAL GANGLIA; RISK-FACTORS; OLDER PATIENTS; HUMAN BRAIN; SCHIZOPHRENIA; CLOZAPINE; RECEPTORS; MEMORY; RISPERIDONE; PREVALENCE AB The extended administration of neuroleptics, especially those of high potency, is the essential etiologic factor in the development of tardive dyskinesia (TD). Schizophrenic patients, almost all of whom receive neuroleptics to reduce psychotic symptoms, are therefore at risk for the development of TD Tn this review of the literature, we propose that neuroleptic use is not the sole risk factor for the emergence of TD. Rather, we attempt to demonstrate that impairments of cognitive function play a role in the development of TD. Furthermore, we show that this idea has explanatory value for understanding higher rates of TD in the elderly. C1 NIMH, Ctr Neurosci, Clin Brain Disorders Branch, Intramural Res Program, Washington, DC 20032 USA. RP Goldberg, TE (reprint author), NIMH, Ctr Neurosci, Clin Brain Disorders Branch, Intramural Res Program, Washington, DC 20032 USA. NR 35 TC 2 Z9 2 U1 0 U2 0 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 1999 VL 60 SU 13 BP 17 EP 21 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 214BJ UT WOS:000081307500004 ER PT J AU McNamara, RK Hyde, TM Kleinman, JE Lenox, RH AF McNamara, RK Hyde, TM Kleinman, JE Lenox, RH TI Expression of the myristoylated alanine-rich C kinase substrate (MARCKS) and MARCKS-related protein (MRP) in the prefrontal cortex and hippocampus of suicide victims SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on the Effects of Medical Interventions on Suicidal Behavior CY FEB 26-28, 1998 CL MIAMI, FLORIDA SP Amer Fdn Suicide Prevent, Johns Hopkins Univ Sch Med, Long Island Jewish Med Ctr, Suicide Prevent Advocacy Network, Solvay Pharmaceut Inc ID ABNORMAL BRAIN-DEVELOPMENT; LITHIUM; FAMILY; DISORDERS; RISK; MICE AB Background: Although suicide is a leading cause of death in the United States and represents a significant public health threat, little is known about the neurobiological or molecular factors that contribute to its pathophysiology. A number of studies now indicate that lithium has considerable efficacy in the prevention of suicide in patients with affective disorders, and accumulating evidence indicates that protein kinase C (PKC) and its substrates, in particular the myristoylated alanine-rich C kinase substrate (MARCKS), are primary targets of chronic lithium treatment. We therefore hypothesized that a dysregulation in MARCKS expression in key brain regions could contribute to the pathophysiology associated with suicide. To address this, we examined MARCKS, as well as the closely related MARCKS-related protein (MRP), mRNA expression in the hippocampus and dorsolateral prefrontal cortex of suicide victims and normal controls. Method: MARCKS and MRP mRNA expression was assessed by quantitative in situ hybridization histochemistry performed on postmortem hippocampal and dorsolateral prefrontal cortex sections from suicide (N = 9) and normal control (N = 10) brains. Results: In the normal hippocampus, both MARCKS and MRP mRNA expression were highest in the granule cell layer and low-moderate in CA1, CA3, and hilus. A high level of MRP mRNA expression was also observed in the white matter of the fimbria/fornix. Neither MARCKS nor MRP mRNA expression levels differed significantly in the granule cell layer, CA3, hilus, or CAI in suicide victims relative to normal controls (I-way ANOVA, p > .05). In the normal prefrontal cortex, MARCKS was expressed exclusively in gray matter (layers I-VI), whereas MRP was expressed in both gray and white matter. Neither MARCKS nor MRP mRNA expression levels in the gray and white matter regions of the dorsal prefrontal cortex differed between suicides and normal controls (l-way ANOVA, p >.05). Conclusion: The present findings are the first to demonstrate the expression and distribution of MARCKS and MRP in the human hippocampus and dorsolateral prefrontal cortex, and their expression pattern within these regions bears strong resemblance to those observed in the adult rat brain. Comparison of MARCKS and MRP mRNA expression in the hippocampus and prefrontal cortex of suicide victims and normal controls indicates that these 2 mRNAs are not differentially regulated in these regions. However, differences in MARCKS and MRP protein expression and function cannot be ruled out by the present findings. C1 Univ Penn, Sch Med, Dept Psychiat, Abramson Res Ctr, Philadelphia, PA 19104 USA. NIMH, Neuropathol Sect, Clin Brain Disorders Branch, IRP,NIH, Bethesda, MD 20892 USA. RP Lenox, RH (reprint author), Univ Penn, Sch Med, Dept Psychiat, Abramson Res Ctr, Rm 802,34th & Civ & Ctr Blvd, Philadelphia, PA 19104 USA. EM rlenox@mail.med.upenn.edu RI McNamara, Robert/J-4309-2014 NR 31 TC 15 Z9 15 U1 0 U2 1 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 1999 VL 60 SU 2 BP 21 EP 26 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 171JZ UT WOS:000078861300005 PM 10073384 ER PT J AU Magruder, KM Norquist, GS AF Magruder, KM Norquist, GS TI Structural issues and policy in the primary care management of depression SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT 3rd Meeting of the International-Consensus-Group on Depression and Anxiety - Focus on Primary Care Management of Depression CY OCT 15-16, 1998 CL CHARLESTON, SOUTH CAROLINA SP Int Consensus Grp ID PREVALENCE AB This article reviews problems in the primary care management of depression at the patient, provider, and practice levels. These problems make it difficult for physicians to deliver proven treatments optimally and for patients to adhere optimally. Potential structural and policy solutions are proposed, suggesting that modifications addressed at multiple levels will make it possible to deliver existing treatments more effectively in primary care settings. C1 Med Univ S Carolina, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA. NIMH, Div Serv & Intervent Res, Rockville, MD 20857 USA. RP Magruder, KM (reprint author), Med Univ S Carolina, Dept Psychiat & Behav Sci, 67 President St, Charleston, SC 29425 USA. NR 23 TC 6 Z9 6 U1 1 U2 1 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 1999 VL 60 SU 7 BP 45 EP 51 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 195NF UT WOS:000080256900012 PM 10326874 ER PT J AU Palmer, DD Henter, ID Wyatt, RJ AF Palmer, DD Henter, ID Wyatt, RJ TI Do antipsychotic medications decrease the risk of suicide in patients with schizophrenia? SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on the Effects of Medical Interventions on Suicidal Behavior CY FEB 26-28, 1998 CL MIAMI, FLORIDA SP Amer Fdn Suicide Prevent, Johns Hopkins Univ Sch Med, Long Island Jewish Med Ctr, Suicide Prevent Advocacy Network, Solvay Pharmaceut Inc ID HOSPITALIZED SCHIZOPHRENICS; AKATHISIA; DEPRESSION; INPATIENTS; REDUCTION; CLOZAPINE; MORTALITY; BEHAVIOR AB The lifetime risk of suicide in persons with schizophrenia is much greater than that in the general population. The role of antipsychotic medications is decreasing suicide risk in schizophrenia has been little studied, and results often appear inconclusive and even confusing when issues such as dose-response effect are examined. Yet, evidence exists that both the traditional and newer antipsychotic medications reduce the risk of suicide and suicide attempts in schizophrenia. Because side effects are potentially significant risk factors in suicide, considerable incentive exists to examine whether newer antipsychotic agents that have a lower incidence of extrapyramidal side effects offer greater safety for this population. C1 NIMH, Neuropsychiat Branch, Dept Hlth & Human Serv, Neurosci Res Ctr St Elizabeths,NIH, Washington, DC 20032 USA. RP Wyatt, RJ (reprint author), NIMH, Neuropsychiat Branch, Dept Hlth & Human Serv, Neurosci Res Ctr St Elizabeths,NIH, 2700 Martin Luther King Jr Ave, Washington, DC 20032 USA. NR 43 TC 28 Z9 28 U1 1 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 1999 VL 60 SU 2 BP 100 EP 103 PG 4 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 171JZ UT WOS:000078861300020 PM 10073396 ER PT J AU Chao, LL Martin, A AF Chao, LL Martin, A TI Cortical regions associated with perceiving, naming, and knowing about colors SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID CEREBRAL BLOOD-FLOW; POSITRON-EMISSION-TOMOGRAPHY; PRIMARY VISUAL-CORTEX; MENTAL-IMAGERY; OBJECT RECOGNITION; PET IMAGES; ACTIVATION; BRAIN; ATTENTION; KNOWLEDGE AB Positron emission tomography (PET) was used to investigate whether retrieving information about a specific object attribute requires reactivation of brain areas that mediate perception of that attribute. During separate PET scans, subjects passively viewed colored and equiluminant gray-scale Mondrians, named colored and achromatic objects, named the color of colored objects, and generated color names associated with achromatic objects. Color perception was associated with activations in the lingual and fusiform gyri of the occipital lobes, consistent with previous neuroimaging and human lesion studies. Retrieving information about object color (generating color names for achromatic objects relative to naming achromatic objects) activated the left inferior temporal, left frontal, and left posterior parietal cortices, replicating previous findings from this laboratory. When subjects generated color names for achromatic objects relative to the low-level baseline of viewing gray-scale Mondrians, additional activations in the left fusiform/lateral occipital region were detected. However, these activations were lateral to the occipital regions associated with color perception and identical to occipital regions activated when subjects simply named achromatic objects relative to the same low-level baseline. This suggests that the occipital activations associated with retrieving color information were due to the perception of object form rather than to the top-down influence of brain areas that mediate color perception. Taken together, these results indicate that retrieving previously acquired information about an object's typical color does not require reactivation of brain regions that subserve color perception. C1 NIH, Bethesda, MD 20892 USA. RP Chao, LL (reprint author), Bldg 10,Room 4C104, Bethesda, MD 20892 USA. RI martin, alex/B-6176-2009 NR 48 TC 144 Z9 148 U1 1 U2 5 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD JAN PY 1999 VL 11 IS 1 BP 25 EP 35 DI 10.1162/089892999563229 PG 11 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 197LG UT WOS:000080365800003 PM 9950712 ER PT J AU Grafman, J AF Grafman, J TI The use of transcranial magnetic stimulation in the study of learning and memory. SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract C1 Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 1999 SU S BP 8 EP 9 PG 2 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 238FJ UT WOS:000082700000007 ER PT J AU Leland, DS Richardson, JS Vankov, A Grant, SJ Pineda, JA AF Leland, DS Richardson, JS Vankov, A Grant, SJ Pineda, JA TI P300 and the Iowa Gambling Task: Neural basis of decision-making and addiction. SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract C1 UC San Diego, Dept Cognit Sci, La Jolla, CA USA. NIDA, Addict Res Ctr, Neurosci Branch, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 1999 SU S BP 13 EP 13 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 238FJ UT WOS:000082700000029 ER PT J AU Neumann, E Johnson, M AF Neumann, E Johnson, M TI Hyperspecific preservation of ignored novel information: Long-term negative priming for possible and impossible 3-d objects. SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract C1 NIMH, Bethesda, MD 20205 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 1999 SU S BP 20 EP 21 PG 2 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 238FJ UT WOS:000082700000056 ER EF