FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Lu, S Carroll, S Herrera, AH Ozanne, B Horowits, R AF Lu, S Carroll, S Herrera, AH Ozanne, B Horowits, R TI New N-RAP binding partners alpha-actinin, filamin, and Krp1 detected by yeast two-hybrid screening: Implications for myofibril assembly SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Beatson Inst Canc Res, Glasgow G61 1BD, Lanark, Scotland. 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 2004 VL 86 IS 1 SU S BP 70A EP 70A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200361 ER PT J AU Luca, S White, JF Sohal, AK Filippov, DV van Boom, JH Grisshammer, R Baldus, M AF Luca, S White, JF Sohal, AK Filippov, DV van Boom, JH Grisshammer, R Baldus, M TI Characterizing structural heterogeneity in peptides by solid-state NMR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Max Planck Inst, Solid State NMR, Gottingen, Germany. NIDDKD, Mol Biol Lab, Bethesda, MD 20892 USA. MRC, Mol Biol Lab, Cambridge CB2 2QH, England. Leiden Univ, Leiden Inst Chem, NL-2300 RA Leiden, Netherlands. NR 3 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 2004 VL 86 IS 1 SU S BP 74A EP 74A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200384 ER PT J AU Misra, S Shi, D Milne, JLS Khan, S Subramaniam, S AF Misra, S Shi, D Milne, JLS Khan, S Subramaniam, S TI Electron microscopic analysis of rotor complexes formed by assemblies of recombinant Salmonella typhimurium FliF-FliG fusion proteins SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA. Univ Illinois, Dept Bioengn, Chicago, IL 60680 USA. Univ Illinois, Dept Microbiol, Chicago, IL 60680 USA. Univ Illinois, Dept Immunol, Chicago, IL 60680 USA. Mol Biol Consortium, Chicago, IL USA. 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 2004 VL 86 IS 1 SU S BP 79A EP 79A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200407 ER PT J AU Borgnia, MJ Shi, D Zhang, PJ Milne, JLS AF Borgnia, MJ Shi, D Zhang, PJ Milne, JLS TI Improved single particle reconstructions by stringent sorting of molecular images obtained using electron cryo-microscopy. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, 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 2004 VL 86 IS 1 SU S BP 80A EP 80A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200416 ER PT J AU Lee, S Subramaniam, S AF Lee, S Subramaniam, S TI Use of cylindrically symmetric specimen chambers for full tilt electron tomography SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Bethesda, MD 20892 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 2004 VL 86 IS 1 SU S BP 80A EP 80A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200412 ER PT J AU Morrison, R Subramaniam, S AF Morrison, R Subramaniam, S TI Development of an automated, multi-specimen, cartridge-based loading system for transmission electron microscopy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 GATAN Inc, Oxford, England. NCI, 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 2004 VL 86 IS 1 SU S BP 80A EP 80A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200413 ER PT J AU Lefman, J Zhang, PJ Hirai, T Weis, RM Juliani, J Bliss, D Kessel, M Bos, E Peters, PJ Subramaniam, S AF Lefman, J Zhang, PJ Hirai, T Weis, RM Juliani, J Bliss, D Kessel, M Bos, E Peters, PJ Subramaniam, S TI Analysis of the spatial arrangement of bacterial chemotaxis receptors in E-coli using three-dimensional electron microscopy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Biochem Lab, Bethesda, MD 20892 USA. Univ Massachusetts, Dept Chem, Amherst, MA 01003 USA. Netherlands Canc Inst, Div Tumor Biol, Amsterdam, Netherlands. RI Hirai, Teruhisa/G-2105-2015 OI Hirai, Teruhisa/0000-0002-2114-8149 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 2004 VL 86 IS 1 SU S BP 81A EP 81A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200421 ER PT J AU Ni, YS Minton, AP McPhie, P AF Ni, YS Minton, AP McPhie, P TI Macromolecular crowding stabilizes the molten globule conformation of apomyoglobin with respect to cold- and heat- induced unfolding SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc ID STATES C1 NIDDK, Lbg, NIH, Bethesda, MD USA. NR 2 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 2004 VL 86 IS 1 SU S BP 85A EP 86A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200444 ER PT J AU Gruschus, JM Greene, LE Eisenberg, E Ferretti, JA AF Gruschus, JM Greene, LE Eisenberg, E Ferretti, JA TI Model structure of the Hsp70/Hsp40 chaperone system complex SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, NHIBI, 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 2004 VL 86 IS 1 SU S BP 88A EP 89A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200460 ER PT J AU Sharma, S Hoskins, JR Wickner, SH AF Sharma, S Hoskins, JR Wickner, SH TI Substrate recognition by the ClpA chaperone SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, NCI, 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 2004 VL 86 IS 1 SU S BP 88A EP 88A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200459 ER PT J AU Stan, G Thirumalai, D Brooks, BR AF Stan, G Thirumalai, D Brooks, BR TI Annealing action of the GroEL-GroES chaperonin system SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, NHLBI, Bethesda, MD 20892 USA. Univ Maryland, Inst Phys Sci & Technol, College Pk, MD 20742 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 2004 VL 86 IS 1 SU S BP 89A EP 89A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200464 ER PT J AU Hoskins, JR Awai, H Pluckthun, A Wickner, S AF Hoskins, JR Awai, H Pluckthun, A Wickner, S TI Mechanism of action of E. coli Clp/hsp100 chaperones SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Mol Biol Lab, Bethesda, MD 20892 USA. Univ Zurich, Inst Biochem, CH-8057 Zurich, Switzerland. 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 2004 VL 86 IS 1 SU S BP 90A EP 91A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200470 ER PT J AU Piszczek, G Rozycki, J Singh, SK Maurizi, MR Ginsburg, A AF Piszczek, G Rozycki, J Singh, SK Maurizi, MR Ginsburg, A TI Substrate peptide interactions with the ClpA hexamer: Isothermal titration calorimetry SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, 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 2004 VL 86 IS 1 SU S BP 90A EP 90A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200467 ER PT J AU Preusch, PC Chin, J Norvell, J AF Preusch, PC Chin, J Norvell, J TI Structural biology: Centers for membrane protein production. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Natl Inst Gen Med Sci, 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 2004 VL 86 IS 1 SU S BP 97A EP 97A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200504 ER PT J AU Woo, SH Soldatov, NM Morad, M AF Woo, SH Soldatov, NM Morad, M TI Modulation of Ca2+ signalling in rat atrial myocytes: possible role of alpha(1C) carboxyl terminal SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Georgetown Univ, Dept Pharmacol, Washington, DC USA. NIA, Natl Inst Hlth, Baltimore, MD 21224 USA. NR 0 TC 0 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 2004 VL 86 IS 1 SU S BP 107A EP 108A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200558 ER PT J AU Brochet, DXP Yang, DM Cheng, HP AF Brochet, DXP Yang, DM Cheng, HP TI Visualization of calcium release waves in the sarcoplamic reticulum in rabbit ventricular myocytes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Cardiovasc Sci Lab, Gerontol Res Ctr, Natl Inst Aging, 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 2004 VL 86 IS 1 SU S BP 111A EP 111A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200575 ER PT J AU Rohacs, T Lopes, CMB Czirjak, GB Craciun, L Ma, T Balla, T AF Rohacs, T Lopes, CMB Czirjak, GB Craciun, L Ma, T Balla, T TI Phosphoinositide regulation of 2-P domain potassium channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical-Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Mt Sinai Sch Med, New York, NY USA. Semmelweis Univ, H-1085 Budapest, Hungary. Natl Inst Hlth, Bethesda, MD 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 2004 VL 86 IS 1 SU S BP 127A EP 127A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200655 ER PT J AU Tarasov, S Nelson, C Lipchock, J Cholody, WM Hariprakasha, H Kosakowska-Cholody, T Gryczynski, ZK Casas-Finet, J Michejda, C AF Tarasov, S Nelson, C Lipchock, J Cholody, WM Hariprakasha, H Kosakowska-Cholody, T Gryczynski, ZK Casas-Finet, J Michejda, C TI Physico-chemical study of DNA binding properties of the naphthylimido-imidazoacridone WMC79 and related compounds SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Frederick, MD 21701 USA. Univ Maryland, Ctr Fluorescence Spect, Baltimore, MD 21201 USA. Medimmune Inc, Gaithersburg, MD 20878 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 2004 VL 86 IS 1 SU S BP 138A EP 138A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200710 ER PT J AU Rothstein, EC Jobsis, PD Combs, CA Balaban, RS AF Rothstein, EC Jobsis, PD Combs, CA Balaban, RS TI Two-photon imaging of the tibialis cranilias muscle in the living mouse SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc 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 2004 VL 86 IS 1 SU S BP 149A EP 150A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200772 ER PT J AU Jobsis, PD Rothstein, EC Combs, CA Balaban, RS AF Jobsis, PD Rothstein, EC Combs, CA Balaban, RS TI Tissue absorbance and heating in two-photon microscopy of the heart SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc 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 2004 VL 86 IS 1 SU S BP 150A EP 150A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200774 ER PT J AU Gaede, HC Luckett, K Polozov, IV Gawrisch, K AF Gaede, HC Luckett, K Polozov, IV Gawrisch, K TI Multinuclear, solid-state NMR studies of a single lipid bilayer on a porous aluminum oxide support SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD USA. RI Gaede, Holly/B-7392-2015 OI Gaede, Holly/0000-0003-4444-4394 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 2004 VL 86 IS 1 SU S BP 163A EP 163A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200845 ER PT J AU Ishikawa, T Maurizi, MR Steven, AC AF Ishikawa, T Maurizi, MR Steven, AC TI Three-dimensional reconstruction of ClpA unfoldase by cryo-electron microscopy: the N-terminal substrate-binding domain is highly mobile SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAMS, LSBR, NIH, Bethesda, MD USA. NCI, LCB, NIH, Bethesda, MD 20892 USA. RI Ishikawa, Takashi/E-5023-2017 OI Ishikawa, Takashi/0000-0002-1976-7477 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 2004 VL 86 IS 1 SU S BP 175A EP 175A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200905 ER PT J AU Shen, JX Wang, SQ Song, LS Han, TZ Cheng, HP AF Shen, JX Wang, SQ Song, LS Han, TZ Cheng, HP TI Polymorphism of Ca2+ sparks evoked from in-focus Ca2+ release units in cardiac myocytes SO BIOPHYSICAL JOURNAL LA English DT Article ID CHANNELS RYANODINE RECEPTORS; CALCIUM-RELEASE; SKELETAL-MUSCLE; SARCOPLASMIC-RETICULUM; AMPLITUDE DISTRIBUTION; VENTRICULAR MYOCYTES; ELEMENTARY EVENTS; HEART-MUSCLE; CONTRACTION; CELLS AB Ca2+ sparks are the elementary release events in many types of cells. Here we present a morphometric analysis of Ca2+ sparks (i.e., amplitude and kinetic parameters) using an approach that minimizes the confounding factor of the detection of out-of-focus events. By activation and visualization of Ca2+ sparks from Ca2+ release units under loose-seal patch-clamp conditions, we found that the amplitude and rising rate of in-focus sparks exhibited a broad modal distribution, whereas spark rise time and spatial width appeared to be stereotyped. Spark morphometrics were constant irrespective of the latency of spark production and the time-dependent L-type Ca2+ channel activation. Polymorphism of Ca2+ sparks in terms of variable amplitude and rising rate was evident for events from the same release units, and intra- and interrelease unit variability contributed equally to the overall variability. The rising rate, a reporter of the underlying Ca2+ release flux, displayed a strong positive correlation with spark amplitude, but a negative correlation with spark rise time, an index of Ca2+ release duration. On the basis of Ca2+ spark morphometrics measured here, we suggested a model in which cohorts of variable number of ryanodine receptors are activated in the genesis of Ca2+ sparks, and the ensuing negative feedback overrides the regenerative Ca2+-induced Ca2+ release to extinguish the ongoing Ca2+ spark. C1 NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA. Xian Jiaotong Univ, Sch Med, Dept Physiol, Xian 710061, Peoples R China. Peking Univ, Coll Life Sci, Natl Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China. RP Cheng, HP (reprint author), NIA, Cardiovasc Sci Lab, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. RI Song, Long-Sheng/D-5899-2012 NR 38 TC 27 Z9 34 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 2004 VL 86 IS 1 BP 182 EP 190 DI 10.1016/S0006-3495(04)74095-3 PN 1 PG 9 WC Biophysics SC Biophysics GA 757MA UT WOS:000187565000019 PM 14695261 ER PT J AU Song, LS Balke, CW Cheng, HP AF Song, LS Balke, CW Cheng, HP TI Defective local excitation-contraction coupling in failing spontaneously hypertensive rats SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIA, Gerontol Res Ctr, Cardiovasc Sci Lab, Baltimore, MD 21224 USA. Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA. Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 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 2004 VL 86 IS 1 SU S BP 182A EP 182A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200940 ER PT J AU Forbes, JG Wang, K AF Forbes, JG Wang, K TI Elasticity of muscle proteins SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAMS, DHHS, Lab Muscle Biol, 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 2004 VL 86 IS 1 SU S BP 183A EP 183A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200946 ER PT J AU Kobrinsky, E Kepplinger, KJF Yu, A Harry, JB Kahr, H Romanin, C Soldatov, NM AF Kobrinsky, E Kepplinger, KJF Yu, A Harry, JB Kahr, H Romanin, C Soldatov, NM TI Voltage-gated rearrangements associated with beta subunit modulation of the L-type calcium channel inactivation SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIA, Clin Invest Lab, NIH, Baltimore, MD 21224 USA. Univ Linz, Inst Biophys, A-4040 Linz, Austria. 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 2004 VL 86 IS 1 SU S BP 186A EP 186A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200959 ER PT J AU Davis, JS Epstein, ND AF Davis, JS Epstein, ND TI Tension generation can be approximated by a two-state transition from attached preforce generating (moderate stiffness) to attached force generating (high stiffness) states SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc 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 2004 VL 86 IS 1 SU S BP 187A EP 187A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200967 ER PT J AU Maderia, M Shenoy, S O'Keefe, B Wu, J Bax, A Marquez, V Barchi, JJ AF Maderia, M Shenoy, S O'Keefe, B Wu, J Bax, A Marquez, V Barchi, JJ TI Manipulating DNA structure with "locked" nucleosides SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, NIH, Frederick, MD USA. NIDDK, NIH, Bethesda, MD USA. RI Barchi Jr., Joseph/N-3784-2014 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 2004 VL 86 IS 1 SU S BP 188A EP 189A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971200973 ER PT J AU Teague, WE Petrache, HI Fuller, N Rand, RP Gawrisch, K AF Teague, WE Petrache, HI Fuller, N Rand, RP Gawrisch, K TI Membrane curvature elasticity of polyunsaturated phosphatidylethanolamine monolayers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD USA. Brock Univ, St Catharines, ON L2S 3A1, Canada. NR 0 TC 1 Z9 1 U1 1 U2 5 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 2004 VL 86 IS 1 SU S BP 198A EP 198A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201021 ER PT J AU Dustman, J Gaede, HC Gawrisch, K Feller, SE AF Dustman, J Gaede, HC Gawrisch, K Feller, SE TI Interaction of a series of aromatic solutes with a phospholipid bilayer SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Wabash Coll, Crawfordsville, IN 47933 USA. NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. RI Gaede, Holly/B-7392-2015 OI Gaede, Holly/0000-0003-4444-4394 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 2004 VL 86 IS 1 SU S BP 200A EP 200A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201033 ER PT J AU Martinez, GV Dykstra, EM Lope-Piedrafita, S Petrache, HI Brown, MF AF Martinez, GV Dykstra, EM Lope-Piedrafita, S Petrache, HI Brown, MF TI Lanosterol and cholesterol-induced variations in bilayer elasticity studied by deuterium NMR and X-ray diffraction SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical-Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Arizona, Dept Chem, Tucson, AZ 85721 USA. Univ Arizona, Dept Phys, Tucson, AZ 85721 USA. NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD USA. RI Lope-Piedrafita, Silvia/I-4808-2012 NR 1 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 2004 VL 86 IS 1 SU S BP 200A EP 200A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201031 ER PT J AU Polozov, IV Gawrisch, K AF Polozov, IV Gawrisch, K TI Quantitative studies of lipid phase transitions by H-1 MAS NMR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. 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 2004 VL 86 IS 1 SU S BP 200A EP 200A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201032 ER PT J AU Veatch, SL Polozov, IV Gawrisch, K Keller, SL AF Veatch, SL Polozov, IV Gawrisch, K Keller, SL TI NMR and fluorescence microscopy reveal tie-lines and low temperature transition in membranes containing DOPC, DPPC, and cholesterol. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Washington, Seattle, WA 98195 USA. NIAAA, NIH, Rockville, MD 20852 USA. NR 0 TC 10 Z9 10 U1 0 U2 4 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 2004 VL 86 IS 1 SU S BP 201A EP 201A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201038 ER PT J AU Forbes, JG Morris, HD Wang, F AF Forbes, JG Morris, HD Wang, F TI Structural organization of the sonic organ of the midshipman fish via high-resolution MRI SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 DHHS, NIAMS, Lab Muscle Biol, NIH, Bethesda, MD USA. DHHS, NINDS, 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 2004 VL 86 IS 1 SU S BP 212A EP 213A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201095 ER PT J AU Xu, SG Gu, J Yu, LP White, H AF Xu, SG Gu, J Yu, LP White, H TI BDM promotes the disorder to order transition in thick filaments. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Niams, NIH, Bethesda, MD USA. Eastern Virginia Med Sch, Norfolk, VA 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 2004 VL 86 IS 1 SU S BP 213A EP 213A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201096 ER PT J AU Ferguson, M Boukari, H Sackett, D Nossal, R AF Ferguson, M Boukari, H Sackett, D Nossal, R TI Solution conformations of clathrin triskelions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Bethesda, MD 20892 USA. NR 4 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 2004 VL 86 IS 1 SU S BP 234A EP 235A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201206 ER PT J AU Chen, YJ Zhang, PJ Moon, KH Egelman, EH Hinshaw, JE AF Chen, YJ Zhang, PJ Moon, KH Egelman, EH Hinshaw, JE TI Electron microscopic studies of dynamin in the non-constricted state SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Virginia, Dept Biochem & Mol Genet, Charlottesville, VA USA. NIDDKD, Lab Cell Biochem & Biol, NIH, Bethesda, MD 20892 USA. RI Egelman, Edward/A-2488-2009 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 2004 VL 86 IS 1 SU S BP 236A EP 236A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201215 ER PT J AU Froehlich, JP Fedorova, O Bagrov, A Mahmmoud, YA Cornelius, F AF Froehlich, JP Fedorova, O Bagrov, A Mahmmoud, YA Cornelius, F TI The PLMS-truncated Na,K-ATPase from shark rectal gland exhibits increased ADP-sensitive phosphoenzyme (E1P) formation and higher ouabain affinity compared to the PLMS-regulated enzyme. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Maryland, Sch Med, Baltimore, MD 21201 USA. NIA, NIH, Baltimore, MD 21224 USA. Univ Aarhus, Aarhus, Denmark. 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 2004 VL 86 IS 1 SU S BP 244A EP 244A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201254 ER PT J AU Ramasamy, S Nagababu, E Rifkind, JM AF Ramasamy, S Nagababu, E Rifkind, JM TI The role of the beta-93 cysteine residue in the formation of labile NO by nitrite reduction of deoxyhemoglobin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIA, NIH, 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 2004 VL 86 IS 1 SU S BP 246A EP 246A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201264 ER PT J AU Huang, K Xu, XL Shields, H Jeffers, A Cho, M Huang, JM King, B Gladwin, M Patel, R Kim-Shapiro, D AF Huang, K Xu, XL Shields, H Jeffers, A Cho, M Huang, JM King, B Gladwin, M Patel, R Kim-Shapiro, D TI Nitrite and deoxygenated hemoglobin: A source of nitric oxide SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Wake Forest Univ, Sch Med, Winston Salem, NC USA. NIH, Bethesda, MD USA. Univ Alabama, Birmingham, AL USA. NR 2 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 2004 VL 86 IS 1 SU S BP 249A EP 249A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201280 ER PT J AU Xu, XL Patel, RP Gladwin, MT Kim-Shapiro, DD AF Xu, XL Patel, RP Gladwin, MT Kim-Shapiro, DD TI Simulation of the diffusion and reaction of nitric oxide produced within erythrocytes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Wake Forest Univ, Dept Phys, Winston Salem, NC 27109 USA. Univ Alabama, Dept Pathol, Ctr Free Rad Biol, Birmingham, AL USA. Ctr Clin, Dept Crit Care Med, NIH, Bethesda, MD USA. NR 1 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 2004 VL 86 IS 1 SU S BP 249A EP 249A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201279 ER PT J AU Bailey, BW Lewis, J Mitchell, DC AF Bailey, BW Lewis, J Mitchell, DC TI Impact of membrane cholesterol on binding properties of benzodiazepine and convulsant site ligands to the GABA(A) receptor: A discrete binding site? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAAA, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD USA. RI Bailey, Brian/B-1732-2009 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 2004 VL 86 IS 1 SU S BP 253A EP 253A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201300 ER PT J AU Keskin, O Haliloglu, T Ma, BY Nussinov, R AF Keskin, O Haliloglu, T Ma, BY Nussinov, R TI Protein-protein interactions: Structurally conserved residues at protein-protein interfaces SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Koc Univ, Istanbul, Turkey. Bogazici Univ, Istanbul, Turkey. NCI, NIH, Frederick, MD 21701 USA. Tel Aviv Univ, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel. 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 2004 VL 86 IS 1 SU S BP 267A EP 267A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201376 ER PT J AU Lengyel, JS Borgnia, MJ Shi, D Subramaniam, S Perham, RN Milne, JLS AF Lengyel, JS Borgnia, MJ Shi, D Subramaniam, S Perham, RN Milne, JLS TI Molecular structures of icosahedral pyruvate dehydrogenase complexes from B-stearothermophilus determined by cryo electron microscopy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Cambridge, Cambridge, England. NCI, 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 2004 VL 86 IS 1 SU S BP 268A EP 269A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201382 ER PT J AU Josephson, I Guia, A Lakatta, E Lederer, J Stern, M AF Josephson, I Guia, A Lakatta, E Lederer, J Stern, M TI Elementary events in calcium-dependent inactivation of unitary L-type Ca channel currents SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Maryland, Inst Biotechnol, Ctr Med Biotechnol, Baltimore, MD USA. NIH, Cardiovasc Sci Lab, 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 2004 VL 86 IS 1 SU S BP 275A EP 275A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201417 ER PT J AU Zhang, M Liu, J Sonawane, K Jiang, M Guy, HR Tseng, GN AF Zhang, M Liu, J Sonawane, K Jiang, M Guy, HR Tseng, GN TI Interactions between charged residues in the transmembrane helices of Herg's voltage-sensing domain SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Virginia Commonwealth Univ, Dept Physiol, Richmond, VA USA. NIH, Bethesda, MD 20892 USA. 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 2004 VL 86 IS 1 SU S BP 277A EP 277A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201426 ER PT J AU Jiang, M Zhang, M Liu, J Maslennikov, I Korolkova, YV Arseniev, AS Grishin, EV Sonawane, K Guy, HR Tseng, GN AF Jiang, M Zhang, M Liu, J Maslennikov, I Korolkova, YV Arseniev, AS Grishin, EV Sonawane, K Guy, HR Tseng, GN TI Probing dynamic interactions between extracellular S5-p linker and other domains of the Herg channel using disulfide formation SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Virginia Commonwealth Univ, Dept Physiol, Richmond, VA USA. Russian Acad Sci, Moscow, Russia. 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 2004 VL 86 IS 1 SU S BP 278A EP 278A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201428 ER PT J AU Maltsev, VA Vinogradova, TM Bogdanov, KY Lakatta, EG Stern, MD AF Maltsev, VA Vinogradova, TM Bogdanov, KY Lakatta, EG Stern, MD TI Numerical modeling of diastolic calcium release and its effect on action potentials in rabbit sinoatrial node cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIA, Gerontol Res Ctr, 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 2004 VL 86 IS 1 SU S BP 299A EP 299A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201537 ER PT J AU Li, X Keskin, O Ma, BY Nussinov, R Liang, J AF Li, X Keskin, O Ma, BY Nussinov, R Liang, J TI Interfacial pockets, structurally conserved residues, and energetic hot spots in protein-protein interactions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Illinois, Dept Bioengn, Chicago, IL USA. Bogazici Univ, Dept Chem Engn, Istanbul, Turkey. Bogazici Univ, Ctr Polymer Res, Istanbul, Turkey. NCI, FCRDC, Lab Expt & Computat Biol, Frederick, MD 21701 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 2004 VL 86 IS 1 SU S BP 301A EP 301A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201544 ER PT J AU Kinde, I Tang, C Loeliger, E Kyere, S AF Kinde, I Tang, C Loeliger, E Kyere, S TI Antiviral inhibition of the HIV-1 capsid protein SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 UMBC, Baltimore, MD USA. NIH, Bethesda, MD 20892 USA. Univ Maryland, Baltimore, MD 21201 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. Achill Pharmaceut, New Haven, CT USA. NR 0 TC 0 Z9 0 U1 2 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 2004 VL 86 IS 1 SU S BP 307A EP 308A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201579 ER PT J AU Yeh, IC Hummer, G AF Yeh, IC Hummer, G TI Hydrodynamic and electrophoretic properties of small nucleic acids from molecular dynamics simulations SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RI Hummer, Gerhard/A-2546-2013 OI Hummer, Gerhard/0000-0001-7768-746X 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 2004 VL 86 IS 1 SU S BP 311A EP 311A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201600 ER PT J AU Selmane, T Schofield, MJ Nayak, S Du, CW Hsieh, P AF Selmane, T Schofield, MJ Nayak, S Du, CW Hsieh, P TI Formation of a DNA mismatch repair complex mediated by ATP SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIDDK, NIH, Bethesda, MD 20892 USA. Invitrogen, Carlsbad, CA USA. NIAID, 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 2004 VL 86 IS 1 SU S BP 314A EP 314A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201617 ER PT J AU Yoshioka, K Yumoto-Yoshioka, Y Hsieh, P AF Yoshioka, K Yumoto-Yoshioka, Y Hsieh, P TI Mismatch repair proteins are differentially modulated by nucleotide co-factor SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc 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 2004 VL 86 IS 1 SU S BP 314A EP 314A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201618 ER PT J AU Blinova, K Combs, C Mejia, R Balaban, RS AF Blinova, K Combs, C Mejia, R Balaban, RS TI Long distance intracellular diffusion measurements of calcein AM using FLIP. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NHLBI, Bethesda, MD 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 2004 VL 86 IS 1 SU S BP 320A EP 321A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201652 ER PT J AU Hwang, J Krogmeier, JR Giulian, GG Goldner, LS Merril, CR AF Hwang, J Krogmeier, JR Giulian, GG Goldner, LS Merril, CR TI Real-time fluorescence polarization modulation microscopy of the dynamic boundary in SDS-PAGE and the interfaces of lipid fusion and diffusion. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIST, Opt Technol Div, Gaithersburg, MD 20899 USA. NIMH, Lab Biochem Genet, 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 2004 VL 86 IS 1 SU S BP 320A EP 320A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201650 ER PT J AU Yang, J Cai, XE Harries, D Rau, DC Parsegian, VA Cheley, S Bayley, H AF Yang, J Cai, XE Harries, D Rau, DC Parsegian, VA Cheley, S Bayley, H TI The intepaction between alpha-hemolysin and egg-PC bilayers SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Vermont, Dept Phys, Burlington, VT 05405 USA. NICHD, Lab Phys & Struct Biuol, NIH, Bethesda, MD USA. Texas A&M Univ, Dept Med Biochem & Genet, College Stn, TX USA. Univ Oxford, Dept Chem, Oxford OX1 2JD, England. 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 2004 VL 86 IS 1 SU S BP 322A EP 323A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201663 ER PT J AU Sanabia, JE Goldner, LS Lacaze, PA Hawkins, ME AF Sanabia, JE Goldner, LS Lacaze, PA Hawkins, ME TI Single molecule detection of 3-MI SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIST, Phys Lab, Opt Technol Div, Gaithersburg, MD 20899 USA. NCI, Pediat Oncol 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 2004 VL 86 IS 1 SU S BP 327A EP 327A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201684 ER PT J AU Krasilnikov, OV Merzlyak, PG Yuldasheva, LN Rodrigues, CG Bezrukov, SM AF Krasilnikov, OV Merzlyak, PG Yuldasheva, LN Rodrigues, CG Bezrukov, SM TI Interaction of 18crown6 with the aqueous pore of staphylococcal alpha-hemolysin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Fed Pernambuco, Dept Biophys Radiobiol, Recife, PE, Brazil. NICHD, Lab Phys Struct Biol, 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 2004 VL 86 IS 1 SU S BP 338A EP 338A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201739 ER PT J AU Sharpe, S Tycko, R AF Sharpe, S Tycko, R TI Structural studies of uniformly labelled peptides in macromolecular assemblies by solid-state NMR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIDDKD, 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 2004 VL 86 IS 1 SU S BP 340A EP 340A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201749 ER PT J AU Boukari, H Schuck, P Sackett, D Nossal, R AF Boukari, H Schuck, P Sackett, D Nossal, R TI Hydrodynamics of drug-induced tubulin rings in dilute solutions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc 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 2004 VL 86 IS 1 SU S BP 341A EP 341A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201753 ER PT J AU Vinogradova, TM Zhou, YY Layshkov, AE Lakatta, EG AF Vinogradova, TM Zhou, YY Layshkov, AE Lakatta, EG TI beta-adrenergic receptor stimulation initiated, cAMP mediated, augmentation of localized rhythmic subsarcolemmal Ca2+ releases in sino-atrial nodal cells in the absence of a voltage activated trigger SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 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 2004 VL 86 IS 1 SU S BP 344A EP 344A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201769 ER PT J AU Liu, YF Kucerka, N Chu, NJ Tristram-Nagle, S Petrache, HI Feller, SE Nagle, JF AF Liu, YF Kucerka, N Chu, NJ Tristram-Nagle, S Petrache, HI Feller, SE Nagle, JF TI Structure and interactions of biomembranes using diffuse X-ray scattering on fully hydrated oriented systems SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Carnegie Mellon Univ, Pittsburgh, PA 15213 USA. NIH, Lab Phys & Struct Biol, Bethesda, MD 20892 USA. Wabash Coll, Crawfordsville, IN 47933 USA. RI Nagle, John/B-1917-2015 OI Nagle, John/0000-0002-9844-5934 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 2004 VL 86 IS 1 SU S BP 349A EP 349A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201796 ER PT J AU Klosek, M Durell, SR Guy, HR AF Klosek, M Durell, SR Guy, HR TI A new profile/profile alignment method and its appication to transmembrane segments ofdistantly related 6TM channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Lab Expt & Computat Biol, 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 2004 VL 86 IS 1 SU S BP 351A EP 351A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201807 ER PT J AU Lee, YS Krauss, N AF Lee, YS Krauss, N TI Dynamics of proton transfer in bacteriorhodopsin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Ctr Mol Modeling, Ctr Informat Technol, Bethesda, MD 20892 USA. Ctr Adv Res Biotechnol, Rockville, MD 20850 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 2004 VL 86 IS 1 SU S BP 351A EP 351A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201805 ER PT J AU Silberberg, SD Swartz, KJ AF Silberberg, SD Swartz, KJ TI Probing the structure of P2X receptor channels with ivermectin SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NINDS, 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 2004 VL 86 IS 1 SU S BP 356A EP 356A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201833 ER PT J AU Adhikari, BB Wang, K AF Adhikari, BB Wang, K TI Interplay of troponin- and myosin-based pathways of calcium activation in skeletal and cardiac muscle: The use of W7 as an inhibitor of thin filament activation SO BIOPHYSICAL JOURNAL LA English DT Article ID RABBIT PSOAS FIBERS; CROSS-BRIDGES; ACTIN-TROPOMYOSIN; 2,3-BUTANEDIONE MONOXIME; COOPERATIVE REGULATION; FORCE GENERATION; CA2+ ACTIVATION; PEPTIDE COMPLEX; SMOOTH-MUSCLE; RATE-CONSTANT AB To investigate the interplay between the thin and thick. laments during calcium activation in striated muscle, we employed n-(6-aminohexyl)5-chloro-1-napthalenesulfonamide(W7) as an inhibitor of troponin C and compared its effects with that of the myosin-specific inhibitor, 2,3-butanedione 2-monoxime (BDM). In both skeletal and cardiac fibers, W7 reversibly inhibited ATPase and tension over the full range of calcium activation between pCa 8.0 and 4.5, resulting in reduced calcium sensitivity and cooperativity of ATPase and tension activations. At maximal activation in skeletal fibers, the W7 concentrations for half-maximal inhibition (K-I) were 70-80 muM for ATPase and 20-30 muM for tension, nearly >200-fold lower than BDM (20 mM and 5-8 mM, respectively). When W7 (50 muM) and BDM (20 mM) were combined in skeletal fibers, the ATPase and tension-pCa curves exhibited lower apparent cooperativity and maxima and higher calcium sensitivity than expected from two independent activation pathways, suggesting that the interplay between the thin and thick. laments varies with the level of activation. Significantly, the inhibition of W7 increased the ATPase/tension ratio during activation in both muscle types. W7 holds much promise as a potent and reversible inhibitor of thin. lament-mediated calcium activation of skeletal and cardiac muscle contraction. C1 NIAMSD, Muscle Proteom & Nanotechnol Sect, Muscle Biol Lab, NIH, Bethesda, MD 20892 USA. RP Wang, K (reprint author), NIAMS, Muscle Biol Lab, NIH, Bldg 50,Rm 1140,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 57 TC 20 Z9 20 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 2004 VL 86 IS 1 BP 359 EP 370 DI 10.1016/S0006-3495(04)74112-0 PN 1 PG 12 WC Biophysics SC Biophysics GA 757MA UT WOS:000187565000036 PM 14695278 ER PT J AU Nanda, H Sachs, JN Petrache, HI Woolf, TB AF Nanda, H Sachs, JN Petrache, HI Woolf, TB TI The critical role of the membrane interface in stabilizing the GpA transmembrane domain. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Johns Hopkins Univ, Sch Med, Program Mol Biophys, Baltimore, MD 21218 USA. NIH, Lab Phys & Struct Biol, 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 2004 VL 86 IS 1 SU S BP 362A EP 362A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201860 ER PT J AU Gawrisch, K Eldho, NV Polozov, IV AF Gawrisch, K Eldho, NV Polozov, IV TI Order parameter profiles, correlation time gradients, and lateral diffusion in polyunsaturated membranes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc 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 2004 VL 86 IS 1 SU S BP 366A EP 367A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201885 ER PT J AU Salem, N AF Salem, N TI Evidence for a high degree of structural specificity for docosahexaenoic acid (C22 : 6n3) function in the nervous system SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc 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 2004 VL 86 IS 1 SU S BP 366A EP 366A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201883 ER PT J AU Brown, MF Botelho, AV Huber, T Petrache, HI AF Brown, MF Botelho, AV Huber, T Petrache, HI TI Polyunsaturated bilayers: What's the difference? SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Arizona, Tucson, AZ 85721 USA. Rockefeller Univ, New York, NY 10021 USA. NIH, Bethesda, MD 20892 USA. NR 2 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 2004 VL 86 IS 1 SU S BP 367A EP 367A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201886 ER PT J AU Hall, T Vargason, J Szittya, G Burgyan, J AF Hall, T Vargason, J Szittya, G Burgyan, J TI Crystal structure and binding specificity of an RNA silencing suppressor SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Ctr Agr Biotechnol, Godollo, Hungary. RI Szittya, Gyorgy/A-2905-2012; Burgyan, Jozsef/C-7511-2012 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 2004 VL 86 IS 1 SU S BP 367A EP 367A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201889 ER PT J AU Ma, BY Nussinov, R AF Ma, BY Nussinov, R TI Interpreting the toxicity of amyloid beta-peptide fragments (A beta 25-35, A beta 25-35 amide and A beta 25-36): examination of ion-chanel model SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, SAIC Frederick, NIH, Frederick, MD 21701 USA. RI Ma, Buyong/F-9491-2011 OI Ma, Buyong/0000-0002-7383-719X 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 2004 VL 86 IS 1 SU S BP 373A EP 373A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201923 ER PT J AU Petrache, HI Kimchi, I Harries, D Tristram-Nagle, S Podgornik, R Parsegian, VA AF Petrache, HI Kimchi, I Harries, D Tristram-Nagle, S Podgornik, R Parsegian, VA TI Forces measured between neutral lipid bilayers swollen by mononvalent salt SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NICHD, Lab Phys Struct Biol, NIH, Bethesda, MD USA. Carnegie Mellon Univ, Dept Biol Sci, Pittsburgh, PA 15213 USA. RI Podgornik, Rudolf/C-6209-2008 OI Podgornik, Rudolf/0000-0002-3855-4637 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 2004 VL 86 IS 1 SU S BP 379A EP 379A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201953 ER PT J AU Kim, DH Bezrukov, S Dathe, M Przybylo, M Kloesgen, B AF Kim, DH Bezrukov, S Dathe, M Przybylo, M Kloesgen, B TI Effect of the synthetic antimicrobial peptide KLA1 on the mechanical stability of giant vesicles SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ So Denmark, Odense M, Denmark. NICHD, Sect Mol Transport, LPSB, SMT, Bethesda, MD USA. Inst Mol Pharmacol, Berlin, Germany. 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 2004 VL 86 IS 1 SU S BP 380A EP 381A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201964 ER PT J AU Huffman, SW Li, Q Schlucker, S Levin, IW AF Huffman, SW Li, Q Schlucker, S Levin, IW TI Reorganizational dynamics monitoring using continuously scanning Fourier transform infrared spectroscopic imaging of model multilamellar lipid bilayer assemblies SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RI Schlucker, Sebastian/D-1031-2010 OI Schlucker, Sebastian/0000-0003-4790-4616 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 2004 VL 86 IS 1 SU S BP 381A EP 381A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201967 ER PT J AU Mason, JT Batenjany, MM Levin, IW O'Leary, TJ AF Mason, JT Batenjany, MM Levin, IW O'Leary, TJ TI The Raman terminal methyl symmetric deformation mode as a probe of bilayer structure SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Armed Forces Inst Pathol, Rockville, MD USA. NIDDK, 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 2004 VL 86 IS 1 SU S BP 382A EP 382A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971201970 ER PT J AU Kovacs, M Toth, J Sellers, JR AF Kovacs, M Toth, J Sellers, JR TI Blebbistatin alters actin and nucleotide interaction of myosin II in a unique manner SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NHLBI, Mol Cardiol Lab, Bethesda, MD 20892 USA. RI Kovacs, Mihaly/A-6841-2011 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 2004 VL 86 IS 1 SU S BP 406A EP 406A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202090 ER PT J AU Bao, JJ Adelstein, RS AF Bao, JJ Adelstein, RS TI RNAi-mediated decrease in nonmuscle myosin heavy chain II-B protein inhibits proliferation and induces multi-nucleation of COS-7 cells SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Mol Cardiol 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 2004 VL 86 IS 1 SU S BP 407A EP 407A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202097 ER PT J AU Jana, SS Kawamoto, S Adelstein, RS AF Jana, SS Kawamoto, S Adelstein, RS TI Tissue and cellular distribution of an inserted isoform of nonmuscle myosin II-C SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Mol Cardiol 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 2004 VL 86 IS 1 SU S BP 407A EP 407A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202099 ER PT J AU Ma, XF Kawamoto, S Liu, CY Adelstein, RS AF Ma, XF Kawamoto, S Liu, CY Adelstein, RS TI Mice with a point mutation in nonmuscle myosin heavy chain II-B show defects in ventral wall closure SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Mol Cardiol Lab, Bethesda, MD 20892 USA. NIH, Transgen Mouse Core Facil, 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 2004 VL 86 IS 1 SU S BP 407A EP 407A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202096 ER PT J AU Tsai, HHG Tsai, CJ Ma, B Gunasekaran, K Zanuy, D Nussinov, R AF Tsai, HHG Tsai, CJ Ma, B Gunasekaran, K Zanuy, D Nussinov, R TI The stability and free energy landscape of an amyloid-forming peptide DFNKF from the human calcitonin in explicit water SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, SAIC Frederick, NIH, Lab Expt & Computat Biol, Frederick, MD 21701 USA. Tel Aviv Univ, Dept Human Genet, IL-69978 Tel Aviv, Israel. RI Zanuy, David/G-3930-2014 OI Zanuy, David/0000-0001-7704-2178 NR 0 TC 2 Z9 2 U1 0 U2 5 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 2004 VL 86 IS 1 SU S BP 412A EP 412A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202125 ER PT J AU Gordon, DJ Balbach, JJ Tycko, R Meredith, SC AF Gordon, DJ Balbach, JJ Tycko, R Meredith, SC TI Increasing the amphiphilicity of an amyloidogenic peptide changes the beta-sheet structure in the fibrils from antiparallel to parallel SO BIOPHYSICAL JOURNAL LA English DT Article ID SOLID-STATE NMR; NUCLEAR-MAGNETIC-RESONANCE; AIR-WATER-INTERFACE; APOLIPOPROTEIN-A-I; PECTATE LYASE-C; ROTATIONAL-ECHO; CHEMICAL-SHIFTS; ALPHA-HELIX; SECONDARY STRUCTURE; CONFORMATION AB Solid-state NMR measurements have been reported for four peptides derived from beta-amyloid peptide Abeta(1-42): Abeta(1-40), Abeta(10-35), Abeta(16-22), and Abeta(34-42). Of these, the first two are predicted to be amphiphilic and were reported to form parallel beta-sheets, whereas the latter two peptides appear nonamphiphilic and adopt an antiparallel beta-sheet organization. These results suggest that amphiphilicity may be significant in determining fibril structure. Here, we demonstrate that acylation of Abeta(16-22) with octanoic acid increases its amphiphilicity and changes the organization of fibrillar beta-sheet from antiparallel to parallel. Electron microscopy, Congo Red binding, and one-dimensional C-13 NMR measurements demonstrate that octanoyl-Abeta(16-22) forms typical amyloid fibrils. Based on the stability of monolayers at the air-water interface, octanoyl-Abeta(16-22) is more amphiphilic than Abeta(16-22). Measurements of C-13-C-13 and N-15-C-3 nuclear magnetic dipole-dipole couplings in isotopically labeled fibril samples, using the constant-time finite-pulse radiofrequency-driven recoupling (fpRFDR-CT) and rotational echo double resonance (REDOR) solid-state NMR techniques, demonstrate that octanoyl-Abeta(16-22) fibrils are composed of parallel beta-sheets, whereas Abeta(16-22) fibrils are composed of antiparallel beta-sheets. These data demonstrate that amphiphilicity is critical in determining the structural organization of beta-sheets in the amyloid fibril. This work also shows that all amyloid fibrils do not share a common supramolecular structure, and suggests a method for controlling the structure of amyloid fibrils. C1 Univ Chicago, Dept Pathol, Chicago, IL 60637 USA. Univ Chicago, Dept Biochem & Mol Biol, Chicago, IL 60637 USA. NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA. RP Meredith, SC (reprint author), Univ Chicago, Dept Pathol, 5841 S Maryland Ave, Chicago, IL 60637 USA. FU NIGMS NIH HHS [5 T32 GM07281, T32 GM007281]; NINDS NIH HHS [1 R01 NS042852, R01 NS042852] NR 36 TC 103 Z9 104 U1 1 U2 11 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 2004 VL 86 IS 1 BP 428 EP 434 DI 10.1016/S0006-3495(04)74119-3 PN 1 PG 7 WC Biophysics SC Biophysics GA 757MA UT WOS:000187565000043 PM 14695285 ER PT J AU Kitaguchi, T Sukhareva, M Swartz, KJ AF Kitaguchi, T Sukhareva, M Swartz, KJ TI Stabilizing the closed gate of the Shaker Kv channel with a hydrophobic seal SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NINDS, Mol Physiol & Biophys Sect, NIH, Bethesda, MD 20892 USA. RI Kitaguchi, Tetsuya/F-5260-2017 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 2004 VL 86 IS 1 SU S BP 433A EP 433A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202232 ER PT J AU Lee, HC Swartz, KJ AF Lee, HC Swartz, KJ TI Gating of the Shaker Kv channel with hanatoxin bound to the voltage-sensors SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NINDS, Mol Physiol & Biophys 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 2004 VL 86 IS 1 SU S BP 434A EP 434A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202238 ER PT J AU Wang, JM Roh, SH Kim, S Lee, CW Il Kim, J Swartz, KJ AF Wang, JM Roh, SH Kim, S Lee, CW Il Kim, J Swartz, KJ TI The surface of tarantula toxins interacting with the voltage-sensor paddle in Kv channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NINDS, Mol Physiol & Biophys Sect, NIH, Bethesda, MD 20892 USA. Kwangju Inst Sci & Technol, Dept Life Sci, Kwangju, South Korea. 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 2004 VL 86 IS 1 SU S BP 434A EP 434A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202239 ER PT J AU Shrivastava, IR Durell, SR Guy, HR AF Shrivastava, IR Durell, SR Guy, HR TI Models of the structure and gating mechanism of the KvAP channel developed using the KvAP K+ channel crystal structures SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Lab Expt & Computat Biol, 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 2004 VL 86 IS 1 SU S BP 436A EP 437A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202251 ER PT J AU Guy, HR Shrivastava, IR Durell, SR AF Guy, HR Shrivastava, IR Durell, SR TI Models of the structure and gating mechanism of the Shaker channel developed from models of the KvAP channel SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Lab Expt & Computat Biol, 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 2004 VL 86 IS 1 SU S BP 437A EP 437A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202252 ER PT J AU Sonawane, K Tseng, GN Guy, HR AF Sonawane, K Tseng, GN Guy, HR TI Models of the structure and gating mechanism of the Herg K+ channel developed from models of KvAP SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Lab Expt & Computat Biol, NIH, Bethesda, MD USA. Virginia Commonwealth Univ, Dept Physiol, Richmond, VA 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 2004 VL 86 IS 1 SU S BP 437A EP 437A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202253 ER PT J AU Niu, SL Mitchell, DC Lim, SY Wen, ZM Kim, HY Salem, N Litman, BJ AF Niu, SL Mitchell, DC Lim, SY Wen, ZM Kim, HY Salem, N Litman, BJ TI N-3 fatty acid deficiency produces reduced G protein-coupled signaling efficiency in retinal rod outer segments SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Rockville, 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 2004 VL 86 IS 1 SU S BP 448A EP 448A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202305 ER PT J AU Pacifico, AM Hayakawa, E Mitchell, DC Litman, BJ AF Pacifico, AM Hayakawa, E Mitchell, DC Litman, BJ TI Effect of the phosphatidylethanolamine (PE) headgroup on rhodopsin activation and acyl chain packing SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAAA, Lab Mem Biochem & Biophys, Bethesda, MD 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 2004 VL 86 IS 1 SU S BP 448A EP 448A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202306 ER PT J AU Altan-Bonnet, G Stefanova, I Germain, RN AF Altan-Bonnet, G Stefanova, I Germain, RN TI The elusive first moments of T lymphocyte activation SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAID, LBS, LI, NIH, Bethesda, MD 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 2004 VL 86 IS 1 SU S BP 449A EP 449A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202312 ER PT J AU Skupsky, R AF Skupsky, R TI Distinguishing modes of eukaryotic gradient sensing SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NICHD, NIH, LIMB, UMD, 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 2004 VL 86 IS 1 SU S BP 450A EP 450A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202317 ER PT J AU Weerth, S Holtzclaw, L Russell, JT AF Weerth, S Holtzclaw, L Russell, JT TI Glial cell calcium signaling proteins segregate into caveolin containing lipid rafts. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NICHD, 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 2004 VL 86 IS 1 SU S BP 452A EP 453A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202329 ER PT J AU Yang, DM Zhu, WZ Xiao, RP Cheng, HP AF Yang, DM Zhu, WZ Xiao, RP Cheng, HP TI Ca2+/calmodin-dependent kinase II regulation of ryanodine receptor/Ca2+ release channelin intact cardiac myocytes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 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 2004 VL 86 IS 1 SU S BP 452A EP 452A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202326 ER PT J AU Toews, JC Russell, JT AF Toews, JC Russell, JT TI Signaling proteins in the axoglial apparatus around the nodes of Ranvier SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NICHD, 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 2004 VL 86 IS 1 SU S BP 455A EP 455A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202341 ER PT J AU Liu, XB Groschner, K Ambudkar, I AF Liu, XB Groschner, K Ambudkar, I TI Distinct Ca2+ selective and non-selective channels cation channels are activated by internal Ca2+ store depletion in human salivary gland and rat basophilic leukemia cells. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Graz Univ, Dept Pharmacol & Toxicol, A-8010 Graz, Austria. NIDCR, Physiol Sect, GTTB, 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 2004 VL 86 IS 1 SU S BP 459A EP 459A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202364 ER PT J AU Lin, X Varnai, P Csordas, G Balla, T Hajnoczky, G AF Lin, X Varnai, P Csordas, G Balla, T Hajnoczky, G TI Control of global and local Ca2+ signals by IP3-binding proteins SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical-Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Thomas Jefferson Univ, Philadelphia, PA 19107 USA. Semmelweis Univ, Dept Physiol, H-1085 Budapest, Hungary. Semmelweis Univ, Lab Cellular & Mol Physiol, H-1085 Budapest, Hungary. NICHHD, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 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 2004 VL 86 IS 1 SU S BP 463A EP 463A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202380 ER PT J AU Rostovtseva, TK Antonsson, B AF Rostovtseva, TK Antonsson, B TI Formation and regulation of Bax channels SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD USA. Serono Pharmaceut Res Inst, Geneva, Switzerland. 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 2004 VL 86 IS 1 SU S BP 464A EP 464A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202385 ER PT J AU Alcaraz, A Aguilella-Arzo, M Nestorovich, E Aguilella, VM Bezrukov, SM AF Alcaraz, A Aguilella-Arzo, M Nestorovich, E Aguilella, VM Bezrukov, SM TI Asymmetry of OmpF probed by reversal potential measurements SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Jaume 1, Castellon, Spain. NICHD, LPSB, NIH, Bethesda, MD USA. RI Aguilella, Vicente/B-7592-2008; Alcaraz, Antonio/F-8498-2016 OI Aguilella, Vicente/0000-0002-2420-2649; 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 2004 VL 86 IS 1 SU S BP 466A EP 466A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202396 ER PT J AU Nestorovich, EM Bezrukov, SM AF Nestorovich, EM Bezrukov, SM TI Cation-dependent stability of proteins studied as "voltage gating" of general bacterial porin OmpF SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Lab Phys & Struct Biol, NICHD, Bethesda, MD 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 2004 VL 86 IS 1 SU S BP 466A EP 466A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202397 ER PT J AU Blinova, K Carroll, S Bose, SK Smirnov, AV Harvey, JJ Knutson, JR Balaban, RS AF Blinova, K Carroll, S Bose, SK Smirnov, AV Harvey, JJ Knutson, JR Balaban, RS TI Steady state kinetic properties of NADH binding and utilization in the mitochondrial matrix. A NADH fluorescence lifetime study. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NHLBI, Bethesda, MD 20892 USA. Nanyang Technol Univ, Singapore 2263, Singapore. 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 2004 VL 86 IS 1 SU S BP 469A EP 469A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202412 ER PT J AU Horkay, F Horkayne-Szakaly, I Basser, PJ AF Horkay, F Horkayne-Szakaly, I Basser, PJ TI Osmotic investigations on cartilage biopolymers and tissue engineered cartilage samples using a new tissue microosmometer SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Bethesda, MD 20892 USA. RI Basser, Peter/H-5477-2011 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 2004 VL 86 IS 1 SU S BP 480A EP 480A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202476 ER PT J AU Hwang, JS Krogmeier, JR Tokumasu, F Briggman, KA Dvorak, JA AF Hwang, JS Krogmeier, JR Tokumasu, F Briggman, KA Dvorak, JA TI Photoluminescence studies of CdSe nanocrystals conjugated with biomolecules. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIST, Opt Technol Div, Gaithersburg, MD 20899 USA. NIAID, Malaria Res 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 2004 VL 86 IS 1 SU S BP 481A EP 482A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202483 ER PT J AU Cho, HS Smirnov, A Anfinrud, PA AF Cho, HS Smirnov, A Anfinrud, PA TI Development of a femtosecond time-resolved microfocusing absorption spectrometer for studying dynamics of proteins in solution and in single crystals SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 1 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 2004 VL 86 IS 1 SU S BP 485A EP 485A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202503 ER PT J AU Gomara, DZ Nussinov, R AF Gomara, DZ Nussinov, R TI Exploration of structural models of highly repetitive PolyGlutamine sequences: beta-helix like organization and possible pathological implications in Huntington Disease. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 LECB, NCI, NIH, Frederick, MD USA. SAIC Frederick, Basic Res Program, Frederick, 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 2004 VL 86 IS 1 SU S BP 505A EP 505A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202612 ER PT J AU Petkova, AT Leapman, RD Yau, WM Tycko, R AF Petkova, AT Leapman, RD Yau, WM Tycko, R TI Structural investigations of Alzheimer's beta-amyloid fibrils by solid state NMR SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIDDK, Lab Chem Phys, NIH, Bethesda, MD USA. Off Res Serv, Div Bioengn & Phys Sci, NIH, Bethesda, MD USA. NR 0 TC 5 Z9 5 U1 1 U2 5 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 2004 VL 86 IS 1 SU S BP 506A EP 506A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202615 ER PT J AU Buchete, NV Tycko, R Hummer, G AF Buchete, NV Tycko, R Hummer, G TI Exploring the sequence space of beta-amyloid fibril forming peptides using threading and molecular dynamics SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIDDK, Lab Chem Phys, NIH, Bethesda, MD USA. RI Hummer, Gerhard/A-2546-2013 OI Hummer, Gerhard/0000-0001-7768-746X 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 2004 VL 86 IS 1 SU S BP 507A EP 507A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202622 ER PT J AU Jozwiak, K Ravichandran, S Wainer, IW Collins, JR AF Jozwiak, K Ravichandran, S Wainer, IW Collins, JR TI The analysis of interactions of some non-competitive inhibitors with the nicotinic acetylcholine receptor. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Natl Inst Hlth, Gerontol Res Ctr, Baltimore, MD USA. Frederick SAIC, Natl Canc Inst, Adv Biomed Comp Ctr, Frederick, 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 2004 VL 86 IS 1 SU S BP 511A EP 511A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202641 ER PT J AU Moaddel, R Jozwiak, K Wainer, IW AF Moaddel, R Jozwiak, K Wainer, IW TI Conformational mobility of immobilized neuronal nicotinic receptors: demonstrated by bioaffinity chromatography SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Natl Inst Hlth, Gerontol Res Ctr, Baltimore, MD 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 2004 VL 86 IS 1 SU S BP 511A EP 511A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202642 ER PT J AU Grunewald, K Desai, P Winkler, DC Heymann, B Belnap, DM Baumeister, W Steven, AC AF Grunewald, K Desai, P Winkler, DC Heymann, B Belnap, DM Baumeister, W Steven, AC TI Thinking outside the box: Nonicosahedral virus structure in three dimensions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical-Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAMS, Struct Biol Lab, NIH, Bethesda, MD USA. Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA. Max Planck Inst Biochem, D-82152 Martinsried, Germany. 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 2004 VL 86 IS 1 SU S BP 523A EP 523A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202702 ER PT J AU Schotte, F Anfinrud, PA Hummer, G Wulff, M AF Schotte, F Anfinrud, PA Hummer, G Wulff, M TI Picosecond crystallography: Snapshots of a protein at work SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIDDK, LCP, NIH, Bethesda, MD USA. European Synchrotron Radiat Facil, Experiments Div, F-38043 Grenoble, France. RI Hummer, Gerhard/A-2546-2013 OI Hummer, Gerhard/0000-0001-7768-746X NR 0 TC 9 Z9 9 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 2004 VL 86 IS 1 SU S BP 525A EP 525A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202711 ER PT J AU Gunasekaran, K Nussinov, R AF Gunasekaran, K Nussinov, R TI Economy of enzyme mechanism: Triggering loops as an evolving common mechanism SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, SAIC Frederick, LECB, Basic Res Lab, Frederick, MD 21701 USA. Tel Aviv Univ, Frederick, 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 2004 VL 86 IS 1 SU S BP 526A EP 526A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202715 ER PT J AU Choi, EJ Niu, SL Smith, PD Jin, AJ Litman, BJ AF Choi, EJ Niu, SL Smith, PD Jin, AJ Litman, BJ TI Molecular organization of bovine rhodopsin in vision membranes studied via atomic force microscopy SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Natl Inst Hlth, Ors, Dbeps, Irdr, Bethesda, MD USA. NIAAA, DICBR, Imbb, Sfs,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 2004 VL 86 IS 1 SU S BP 529A EP 529A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202731 ER PT J AU Sirenko, SG Casimiro, M Pfeifer, K Katchman, A Ebert, SN Knollmann, BC AF Sirenko, SG Casimiro, M Pfeifer, K Katchman, A Ebert, SN Knollmann, BC TI Isoform 1 of the murine Kcnq1 gene is essential for IKs in the neonatal mouse heart SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Georgetown Univ, Ctr Med, Washington, DC USA. NIH, Bethesda, MD 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 2004 VL 86 IS 1 SU S BP 531A EP 531A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202743 ER PT J AU Pereira, EFR Alkondon, M Arruda, EZ Almeida, LEF Fawcett, WP Randall, WR Guidetti, P Sapko, MT Yu, P Tagle, DA Schwarcz, R Albuquerque, EX AF Pereira, EFR Alkondon, M Arruda, EZ Almeida, LEF Fawcett, WP Randall, WR Guidetti, P Sapko, MT Yu, P Tagle, DA Schwarcz, R Albuquerque, EX TI Endogenous kynurenic acid regulates alpha 7 nicotinic receptor activity and gabaergic synaptic transmission in the hippocampus SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Maryland, Sch Med, Dept Pharmacol Exp Ther, Baltimore, MD 21201 USA. Univ Fed Rio de Janeiro, Dept Farmacol Bas Clin, ICB, CCS, Rio De Janeiro, Brazil. Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Baltimore, MD 21201 USA. 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 2004 VL 86 IS 1 SU S BP 541A EP 541A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202793 ER PT J AU Iwasa, KH AF Iwasa, KH TI Gating compliance revisited SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc 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 2004 VL 86 IS 1 SU S BP 547A EP 547A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202821 ER PT J AU Kinzer, CA Schwartz, JW Ikeda, SR DeFelice, LJ AF Kinzer, CA Schwartz, JW Ikeda, SR DeFelice, LJ TI Ion dependence of substrate binding in norepinephrine transporters SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN USA. NIAID, Lab Mol Physiol, NIH, Rockville, 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 2004 VL 86 IS 1 SU S BP 555A EP 556A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202866 ER PT J AU Sauna, ZE Nandigama, KN Ambudkar, SV AF Sauna, ZE Nandigama, KN Ambudkar, SV TI Characterization of ATP hydrolysis by the multidrug resistance-associated protein 4 (MRP4, ABCC4) SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Bethesda, MD 20892 USA. RI Ambudkar, Suresh/B-5964-2008 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 2004 VL 86 IS 1 SU S BP 557A EP 557A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202873 ER PT J AU Melikov, K Chernomordik, LV AF Melikov, K Chernomordik, LV TI Lipid bilayer destabilization by TAT48-60 peptide and its implication for transducing activity of the peptide. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NICHD, Bethesda, MD USA. RI Melikov, Kamran/A-6604-2009 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 2004 VL 86 IS 1 SU S BP 561A EP 561A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202895 ER PT J AU Li, Q Huffman, SW Levin, IW AF Li, Q Huffman, SW Levin, IW TI Effects of lipid Microdomain formation on membrane protein reorganizations in model membrane assemblies: Infrared spectroscopic studies of bacteriorhodopsin in aqueous binary phosphatidylcholine dispersions SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIDDK, NIH, Bethesda, MD 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 2004 VL 86 IS 1 SU S BP 562A EP 562A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202897 ER PT J AU Niu, SL Litman, BJ AF Niu, SL Litman, BJ TI Effect of trans fatty acids on membrane cholesterol and receptor function SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAAA, NIH, Rockville, 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 2004 VL 86 IS 1 SU S BP 562A EP 562A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202901 ER PT J AU Gu, J Xu, SG Belknap, B White, H Yu, LC AF Gu, J Xu, SG Belknap, B White, H Yu, LC TI Binding of myosin.ADP.P-i to actin improves the regularity of the thick filament helix SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAMS, NIH, Bethesda, MD USA. E Virginia Med Sch, Norfolk, VA 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 2004 VL 86 IS 1 SU S BP 567A EP 567A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202925 ER PT J AU Jiang, GY Giannone, G Critchley, DR Fukumoto, E Sheetz, MP AF Jiang, GY Giannone, G Critchley, DR Fukumoto, E Sheetz, MP TI Minimal connections between fibronectin trimers and the cytoskeleton mediated by Talin-1 SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Columbia Univ, New York, NY USA. Univ Leicester, Dept Biochem, Leicester, Leics, England. Natl Inst Dent & Craniofacial Res, 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 2004 VL 86 IS 1 SU S BP 570A EP 570A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202941 ER PT J AU Ma, K Gutierrez-Curz, G Wang, K AF Ma, K Gutierrez-Curz, G Wang, K TI Titin as a giant signaling molecule in the SH3 pathway: Interaction of SH3 domain with the proline-rich titin PEVK segment SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAMS, LMB, 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 2004 VL 86 IS 1 SU S BP 570A EP 571A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202944 ER PT J AU Tsai, WL Forbes, JG Wang, K AF Tsai, WL Forbes, JG Wang, K TI Modular proteins and bioengineering of polyproteins SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 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 2004 VL 86 IS 1 SU S BP 570A EP 570A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202943 ER PT J AU Snyder, GE Sakamoto, T Hammer, JA Sellers, JR Selvin, PR AF Snyder, GE Sakamoto, T Hammer, JA Sellers, JR Selvin, PR TI Nanometer localization of single green fluorescent proteins: Evidence that myosin V walks hand-over-hand via telemark configuration SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ Illinois, Dept Phys, Urbana, IL USA. Univ Illinois, Ctr Biophys, Urbana, IL USA. NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA. 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 2004 VL 86 IS 1 SU S BP 572A EP 572A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971202950 ER PT J AU Tokumasu, F Dvorak, JA AF Tokumasu, F Dvorak, JA TI The application of quantum dots for immunocytochemical studies of normal and malaria-infected erythrocytes SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NIAID, Lab Malaria & Vector Res, 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 2004 VL 86 IS 1 SU S BP 581A EP 581A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203002 ER PT J AU Sass, LE Chapados, BR Prasad, R Tainer, JA Wilson, SH Erie, DA AF Sass, LE Chapados, BR Prasad, R Tainer, JA Wilson, SH Erie, DA TI Atomic force microscopy studies of the oligomerization states of human PCNA and its interactions with fenl in the presence and absence of DNA SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ N Carolina, Dept Chem, Chapel Hill, NC USA. Scripps Res Inst, Dept Mol Biol, La Jolla, CA 92037 USA. NIEHS, Struct Biol Lab, 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 2004 VL 86 IS 1 SU S BP 589A EP 589A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203040 ER PT J AU Yang, Y Du, CW Hsieh, P Erie, DA AF Yang, Y Du, CW Hsieh, P Erie, DA TI A novel single-molecule method for measuring protein-DNA binding constants and specificity SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Univ N Carolina, Curriculum Appl & Mat Sci, Chapel Hill, NC USA. NIDDKD, Genet & Biochem Branch, 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 2004 VL 86 IS 1 SU S BP 589A EP 589A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203038 ER PT J AU Fodor, E Mack, JW Ferretti, JA Ginsburg, A AF Fodor, E Mack, JW Ferretti, JA Ginsburg, A TI Conformational stability and DNA binding of the NKx-2.5(C56S) cardiac-specific homeodomain SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NHLBI, 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 2004 VL 86 IS 1 SU S BP 592A EP 592A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203054 ER PT J AU Sidorova, N Muradymov, S Rau, DC AF Sidorova, N Muradymov, S Rau, DC TI Water release accompanying specific versus nonspecific BamHI-DNA binding. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NICHD, LPSB, NIH, Bethesda, MD 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 2004 VL 86 IS 1 SU S BP 594A EP 594A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203066 ER PT J AU Tcherkasskaya, O Gronenborn, AM AF Tcherkasskaya, O Gronenborn, AM TI Effects of molecular distributions on the fluorescence energy transfer SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Georgetown Univ, Sch Med, Washington, DC 20057 USA. NIDDK, Chem Phys Lab, 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 2004 VL 86 IS 1 SU S BP 603A EP 604A PN 2 PG 2 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203118 ER PT J AU Hawkins, M Wojtuszewski, K Knutson, JR Balis, FM AF Hawkins, M Wojtuszewski, K Knutson, JR Balis, FM TI A comparison of time resolved anisotropies of 3-MI and 6-MI in single and double stranded oligonucleotides SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NCI, Pediat Oncol Branch, Bethesda, MD 20892 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 2004 VL 86 IS 1 SU S BP 606A EP 606A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203131 ER PT J AU Hirai, T Heymann, JAW Shi, D Subramaniam, S AF Hirai, T Heymann, JAW Shi, D Subramaniam, S TI Comparative structural analysis of the "symmetric", substrate-bound state of the oxalate transporter OxlT with the "cytoplasmically-open" state of the MFS transporters GlpT and LacY SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc ID ESCHERICHIA-COLI; MECHANISM C1 NCI, NIH, Bethesda, MD 20892 USA. RI Hirai, Teruhisa/G-2105-2015 OI Hirai, Teruhisa/0000-0002-2114-8149 NR 2 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 2004 VL 86 IS 1 SU S BP 611A EP 611A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203160 ER PT J AU Tran, T Mittal, A Bentz, J AF Tran, T Mittal, A Bentz, J TI The elementary mass action rate constants of P-gp transport across a confluent MDCKH-hMDR1 cell monolayer obtained by exhaustive fitting. SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Drexel Univ, Philadelphia, PA 19104 USA. NIH, Bethesda, MD 20892 USA. RI Mittal, Aditya/E-3087-2010 OI Mittal, Aditya/0000-0002-4030-0951 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 2004 VL 86 IS 1 SU S BP 612A EP 612A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203163 ER PT J AU Barsky, D Kim, KS Beernink, PT Hadi, MZ Wilson, DM AF Barsky, D Kim, KS Beernink, PT Hadi, MZ Wilson, DM TI Mutations that affect protein stability: An experimental and computational approach applied to cancer-associated variants of a DNA repair enzyme, APEI SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 Lawrence Livermore Natl Lab, Biol & Biotechnol Res Program, Livermore, CA USA. Sandia Natl Labs, Biosyst Res Dept, Livermore, CA USA. NIA, Lab Mol Gerontol, GRC, IRP,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 2004 VL 86 IS 1 SU S BP 620A EP 620A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203208 ER PT J AU Harries, D Rau, DC Parsegian, VA AF Harries, D Rau, DC Parsegian, VA TI Using cosolutes to probe the specific association of cyclodextrin and adamantane SO BIOPHYSICAL JOURNAL LA English DT Meeting Abstract CT 48th Annual Meeting of the Biophysical Society CY FEB 14-18, 2004 CL Baltimore, MD SP Biophys Soc C1 NICHD, Lab Phys & Struct Biol, 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 2004 VL 86 IS 1 SU S BP 625A EP 625A PN 2 PG 1 WC Biophysics SC Biophysics GA 762KQ UT WOS:000187971203234 ER PT J AU Joubert, F Fales, HM Wen, H Combs, CA Balaban, RS AF Joubert, F Fales, HM Wen, H Combs, CA Balaban, RS TI NADH enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP): Applications to enzyme and mitochondrial reaction kinetics, in vitro SO BIOPHYSICAL JOURNAL LA English DT Article ID NICOTINAMIDE-ADENINE-DINUCLEOTIDE; GLUTAMATE-DEHYDROGENASE SYSTEM; REDUCED PYRIDINE NUCLEOTIDE; OXIDATIVE-PHOSPHORYLATION; REDOX STATE; RAT-HEART; MAGNETIC RESONANCE; CYTOCHROME-C; CONFORMATION; CALCIUM AB NADH enzyme-dependent fluorescence recovery after photobleaching (ED-FRAP) was evaluated for studying enzyme kinetics in vitro and in isolated mitochondria. Mass, optical, and nuclear magnetic resonance spectroscopy data were consistent with the UV NADH photolysis reaction being NADH-->NAD(circle)-->H+ + e(-). The overall net reaction was O-2+2NADH+2H(+)-->2NAD(+) + 2H(2)O, or in the presence of other competing electron acceptors such as cytochrome c, NADH+2Cyt(ox)-->NAD(+) + H+ + 2Cyt(red). Solution pH could differentiate between these free-radical scavenging pathways. These net reactions represent the photooxidation of NADH to NAD(+). Kinetic models and acquisition schemes were developed, varying [NADH] and [NAD] by altering NADH photolysis levels, for extracting kinetic parameters. UV irradiation levels used did not damage mitochondrial function or enzymatic activity. In mitochondria, [NADH] is a high affinity product inhibitor that significantly reduced the NADH regeneration rate. Matrix NADH regeneration only slightly exceeded the net rate of NADH consumption, suggesting that the NADH regeneration process is far from equilibrium. Evaluation of NADH regeneration in active mitochondria, in comparison to rotenone-treated preparations, revealed other regulatory elements in addition to matrix [NADH] and [NAD] that have yet to be fully characterized. These studies demonstrate that the rapid UV photolysis of NADH to NAD is an effective tool in evaluating the steady-state kinetic properties of enzyme systems. Initial data support the notion that the NADH regeneration process is far from equilibrium in mitochondria and is potentially controlled by NADH levels as well as several other matrix factors. C1 NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA. RP Balaban, RS (reprint author), NHLBI, Cardiac Energet Lab, NIH, Bldg 10,Rm B1D-161, Bethesda, MD 20892 USA. RI Balaban, Robert/A-7459-2009; Wen, Han/G-3081-2010 OI Balaban, Robert/0000-0003-4086-0948; Wen, Han/0000-0001-6844-2997 NR 33 TC 25 Z9 25 U1 0 U2 7 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 2004 VL 86 IS 1 BP 629 EP 645 DI 10.1016/S0006-3495(04)74141-7 PN 1 PG 17 WC Biophysics SC Biophysics GA 757MA UT WOS:000187565000065 PM 14695307 ER PT J AU Vives, M Eritja, R Tauler, R Marquez, VE Gargallo, R AF Vives, M Eritja, R Tauler, R Marquez, VE Gargallo, R TI Synthesis, stability, and protonation studies of a self-complementary dodecamer containing the modified nucleoside 2 '-deoxyzebularine SO BIOPOLYMERS LA English DT Article DE 2'-deoxyzebularine; spectroscopy; DNA structure; multivariate curve resolution; factor analysis ID MULTIVARIATE CURVE RESOLUTION; ACID-BASE; SPECTROPHOTOMETRIC TITRATIONS; NUCLEIC BASES; ZEBULARINE; RANK; OLIGODEOXYNUCLEOTIDES; MALONDIALDEHYDE; DECOMPOSITION; EQUILIBRIUM AB The nucleoside 2'-deoxyzebularine (K) was incorporated into the self-complementary dodecamer 5'-CGTACGKGTACG-3' by solid-phase 2-cyanoethylphosphoramidite chemistry using dimethoxytrityl (DMT) as the 5'-hydroxyl protecting group. Standard synthesis cycles using trichloroacetic acid and short ammonia treatment (50degreesC for 30 min) were found to be the optimal conditions to obtain the desired dodecamer with minimum acid and basic degradation of the acid- and base-sensitive 2-pyrimidinone residue. The protonation equilibria of the K nucleoside and of the dodecamer at 37degreesC were studied by means of spectroscopically monitored titrations. For the K nucleoside, a pK(a) value of 3.13 +/- 0.09 was obtained. For the dodecamer, four acid-base species were found in the pH range 2-12, with pK(a) values of 9.60 +/- 0.07, 4.46 +/- 0.16, and 2.87 +/- 0.19. Melting experiments were carried out to confirm the proposed acid-base concentration profiles. Finally, kinetic experiments were also carried out at several pH values to evaluate the stability of the K nucleoside and of the dodecamer. An increased stability was shown by the K nucleoside when incorporated into the dodecamer. Multivariate methods based on both hard- and soft-modeling were applied for the analysis of spectroscopic data, allowing the estimation of concentration profiles and pure spectra. (C) 2003 Wiley Periodicals, Inc. C1 Univ Barcelona, Dept Analyt Chem, E-08028 Barcelona, Spain. CSIC, Inst Mol Biol, E-08034 Barcelona, Spain. Natl Canc Inst, Canc Res Ctr, Med Chem Lab, Frederick, MD 21702 USA. RP Gargallo, R (reprint author), Univ Barcelona, Dept Analyt Chem, Marti & Franques,1-11, E-08028 Barcelona, Spain. RI eritja, ramon/B-5613-2008; Gargallo, Raimundo/A-6084-2017 OI eritja, ramon/0000-0001-5383-9334; Gargallo, Raimundo/0000-0001-8716-8356 NR 29 TC 8 Z9 8 U1 0 U2 3 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0006-3525 J9 BIOPOLYMERS JI Biopolymers PD JAN PY 2004 VL 73 IS 1 BP 27 EP 43 DI 10.1002/bip.10515 PG 17 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 759VP UT WOS:000187757800003 PM 14691937 ER PT J AU Satten, GA Kong, FH Wright, DJ Glynn, SA Schreiber, GB AF Satten, GA Kong, FH Wright, DJ Glynn, SA Schreiber, GB TI How special is a 'special' interval: modeling departure from length-biased sampling in renewal processes SO BIOSTATISTICS LA English DT Article DE human immunodeficiency virus; infinite-dimensional nuisance parameter; length-biased sampling; renewal process ID SCREENED BLOOD; DONORS; RISK AB Length-biased sampling occurs in renewal processes when the probability that an interval is selected is proportional to the length of the interval. This can occur when intervals are selected because they contain an event that is independent of the renewal process and occurs with constant hazard. For example, if the times between donations for repeat blood donors are independent and identically distributed, and if the donor seroconverts to HIV (develops antibodies that indicate infection with human immunodeficiency virus), then the interval between the last HIV seronegative and first HIV seropositive test is expected to be longer than that donor's previous time intervals between donations. We develop hypothesis tests to determine if the relationship between the typical and length-biased intervals is as expected, or if there is departure from length-biased sampling. We further develop a regression method to determine if there are covariates that explain the departure from length-biased sampling. Our approach is motivated by the question of whether there is evidence that repeat blood donors who develop antibodies to HIV or other viral infections change their donation pattern in some way because of seroconversion. C1 Ctr Dis Control & Prevent, Atlanta, GA 30333 USA. WESTAT Corp, Natl Heart Lung & Blood Inst, Retrovirus Epidemiol Donor Study Coordinating Ctr, Rockville, MD 20850 USA. RP Satten, GA (reprint author), Ctr Dis Control & Prevent, Atlanta, GA 30333 USA. EM GSatten@cdc.gov NR 10 TC 5 Z9 5 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1465-4644 J9 BIOSTATISTICS JI Biostatistics PD JAN PY 2004 VL 5 IS 1 BP 145 EP 151 DI 10.1093/biostatistics/5.1.145 PG 7 WC Mathematical & Computational Biology; Statistics & Probability SC Mathematical & Computational Biology; Mathematics GA 771QG UT WOS:000188797100010 PM 14744833 ER PT J AU Aerts, JL Gonzales, MI Topalian, SL AF Aerts, JL Gonzales, MI Topalian, SL TI Selection of appropriate control genes to assess expression of tumor antigens using real-time RT-PCR SO BIOTECHNIQUES LA English DT Article ID POLYMERASE CHAIN-REACTION; RNA-PROCESSING ENZYME; HOUSEKEEPING GENES AB Real-time reverse transcription PCR (RT-PCR) is a sensitive and accurate method to monitor gene expression and is often used to profile the expression of putative tumor antigens in the context of immunotherapy. However, this technique consists of several steps, including cell processing, RNA extraction, RNA storage, assessment of RNA concentration, and cDNA synthesis prior to PCR. To compensate for potential variability introduced in this procedure, the expression of housekeeping genes is commonly assessed in parallel with the expression of the gene of interest. In this study, the expression of a variety of housekeeping genes in a panel of 26 different human tumor and embryonal cell lines was assessed using real-time RT-PCR. For some control genes, the variability in expression was significant between different cell lines, despite the equalization of quantities of input RNA. The greatest variability was found for GAPDH. The lowest variability was found for beta-glucuronidase (GUS) and 18S rRNA. While real-time RT-PCR is a powerful tool for gene expression analysis, these results suggest that the choice of control genes to normalize the expression of the gene of interest is critical to the interpretation of experimental results and should be tailored to the nature of the study. C1 NCI, Surg Branch, NIH, Bethesda, MD 20892 USA. RP Topalian, SL (reprint author), NCI, Surg Branch, NIH, 10-2B47, Bethesda, MD 20892 USA. EM suzanne_topalian@nih.gov RI Aerts, Joeri/J-6957-2014 OI Aerts, Joeri/0000-0002-9902-3696 NR 13 TC 124 Z9 129 U1 0 U2 6 PU BIOTECHNIQUES OFFICE PI NEW YORK PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD JAN PY 2004 VL 36 IS 1 BP 84 EP + PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 763KF UT WOS:000188083600013 PM 14740490 ER PT J AU Arthur, DC AF Arthur, DC TI MLL - a gene of interest SO BLOOD LA English DT Editorial Material ID ACUTE LEUKEMIAS; DIMERIZATION C1 NCI, Bethesda, MD 20892 USA. RP Arthur, DC (reprint author), NCI, Bethesda, MD 20892 USA. NR 5 TC 0 Z9 0 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 2004 VL 103 IS 1 BP 6 EP 7 DI 10.1182/blood-2003-10-3567 PG 2 WC Hematology SC Hematology GA 757QM UT WOS:000187573000008 ER PT J AU Hans, CP Weisenburger, DD Greiner, TC Gascoyne, RD Delabie, J Ott, G Muller-Hermelink, HK Campo, E Braziel, RM Jaffe, ES Pan, ZG Farinha, P Smith, LM Falini, B Banham, AH Rosenwald, A Staudt, LM Connors, JM Armitage, JO Chan, WC AF Hans, CP Weisenburger, DD Greiner, TC Gascoyne, RD Delabie, J Ott, G Muller-Hermelink, HK Campo, E Braziel, RM Jaffe, ES Pan, ZG Farinha, P Smith, LM Falini, B Banham, AH Rosenwald, A Staudt, LM Connors, JM Armitage, JO Chan, WC TI Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray SO BLOOD LA English DT Article ID NON-HODGKINS-LYMPHOMA; BCL-2 PROTEIN EXPRESSION; PROGNOSTIC-SIGNIFICANCE; GERMINAL-CENTER; CLINICAL-SIGNIFICANCE; NEGATIVE AUTOREGULATION; GENE REARRANGEMENT; CD10 EXPRESSION; C-MYC; SURVIVAL AB Diffuse large B-cell lymphoma (DLBCL) can be divided into prognostically important subgroups with germinal center B-cell-like (GCB), activated B-cell-like (ABC), and type 3 gene expression profiles using a cDNA microarray. Tissue microarray (TMA) blocks were created from 152 cases of DLBCL, 142 of which had been successfully evaluated by cDNA microarray (75 GCB, 41 ABC, and 26 type 3). Sections were stained with antibodies to CD10, bcl-6, MUM1, FOXP1, cyclin D2, and bcl-2. Expression of bcl-6 (P <.001) or CD10 (P =.019) was associated with better overall survival (OS), whereas expression of MUM1 (P =.009) or cyclin D2 (P <.001) was associated with worse OS. Cases were subclassified using CD10, bcl-6, and MUM1 expression, and 64 cases (42%) were considered GCB and 88 cases (58%) non-GCB. The 5-year OS for the GCB group was 76% compared with only 34% for the non-GCB group (P <.001), which is similar to that reported using the cDNA microarray. Bcl-2 and cyclin D2 were adverse predictors in the non-GCB group. In multivariate analysis, a high International Prognostic Index score (3-5) and the non-GCB phenotype were independent adverse predictors (P <.0001). In summary, immunostains can be used to determine the GCB and non-GCB subtypes of DLBCL and predict survival similar to the cDNA microarray. C1 Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA. Univ Nebraska, Med Ctr, Dept Internal Med, Omaha, NE 68198 USA. Univ Nebraska, Med Ctr, Dept Prevent & Soc Med, Omaha, NE 68198 USA. British Columbia Canc Agcy, Dept Pathol, Vancouver, BC V5Z 4E6, Canada. British Columbia Canc Agcy, Dept Med Oncol, Vancouver, BC V5Z 4E6, Canada. Norwegian Radium Hosp, Dept Pathol, Oslo, Norway. Univ Wurzburg, Dept Pathol, D-97070 Wurzburg, Germany. Univ Barcelona, Hosp Clin, Dept Pathol, E-08007 Barcelona, Spain. Univ Oregon, Hlth Sci Ctr, Dept Pathol, Portland, OR USA. Univ Oregon, Hlth Sci Ctr, SW Oncol Grp, Portland, OR USA. NCI, Hematopathol Sect, NIH, Bethesda, MD 20892 USA. NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. Univ Perugia, Inst Hematol, I-06100 Perugia, Italy. Univ Oxford, Dept Clin Lab Sci, Oxford OX1 2JD, England. RP Weisenburger, DD (reprint author), Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, 983135 Nebraska Med Ctr, Omaha, NE 68198 USA. RI Banham, Alison/B-2966-2009; OI Banham, Alison/0000-0002-3197-273X; Delabie, Jan/0000-0001-5023-0689; Farinha, Pedro/0000-0001-9364-9391; Campo, elias/0000-0001-9850-9793 FU NCI NIH HHS [CA36727, CA84967] NR 69 TC 1607 Z9 1801 U1 7 U2 41 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 2004 VL 103 IS 1 BP 275 EP 282 DI 10.1182/blood-2003-05-1545 PG 8 WC Hematology SC Hematology GA 757QM UT WOS:000187573000049 PM 14504078 ER PT J AU Qiang, YW Yao, L Tosato, G Rudikoff, S AF Qiang, YW Yao, L Tosato, G Rudikoff, S TI Insulin-like growth factor I induces migration and invasion of human multiple myeloma cells SO BLOOD LA English DT Article ID FOCAL ADHESION KINASE; ACTIVATED PROTEIN-KINASE; MARROW STROMAL CELLS; ACTIN STRESS FIBERS; SMOOTH-MUSCLE-CELLS; RHO FAMILY GTPASES; PHOSPHATIDYLINOSITOL 3-KINASE; TYROSINE PHOSPHORYLATION; FACTOR RECEPTOR; PHORBOL ESTERS AB Multiple myeloma (MM) is an incurable form of cancer characterized by accumulation of malignant plasma cells in the bone marrow. During the course of this disease, tumor cells cross endothelial barriers and home to the bone marrow. In latter stages, myeloma cells extravasate through blood vessels and may seed a variety of organs. Insulin-like growth factor I (IGF-I) is one of several growth factors shown to promote the growth of MM cells. In the current study, we have assessed the ability of IGF-I to serve additionally as a chemotactic factor affecting the mobility and invasive properties of these cells. Results indicate that IGF-l promotes transmigration through vascular endothelial cells and bone marrow stromal cell lines. Analysis of endogenous signaling pathways revealed that protein kinase D/protein kinase Cmu (PKD/ PKCmu) and RhoA were both activated in a phosphatidylinositol 3-kinase (PI-3K)dependent manner. Inhibition of PI-3K, PKCs, or Rho-associated kinase by pharmacologic inhibitors abrogated migration, whereas mitogen-activated protein kinase (MAPK), Akt, and p70S6 kinase inhibitors had no effect. These results suggest that IGF-I promotes myeloma cell migration by activation of PI-3K/PKCmu and PI-3K/RhoA pathways independent of Akt. The identification of IGF-I as both a proliferative and migratory factor provides a rational basis for the development of targeted therapeutic strategies directed at IGF-I in the treatment of MM. C1 NCI, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA. RP Rudikoff, S (reprint author), NCI, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NR 54 TC 92 Z9 95 U1 1 U2 4 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 2004 VL 103 IS 1 BP 301 EP 308 DI 10.1182/blood-2003-06-2066 PG 8 WC Hematology SC Hematology GA 757QM UT WOS:000187573000052 PM 14504085 ER PT J AU Zeng, WH Chen, GB Kajigaya, S Nunez, O Charrow, A Billings, EM Young, NS AF Zeng, WH Chen, GB Kajigaya, S Nunez, O Charrow, A Billings, EM Young, NS TI Gene expression profiling in CD34 cells to identify differences between aplastic anemia patients and healthy volunteers SO BLOOD LA English DT Article ID HEMATOPOIETIC STEM-CELLS; BONE-MARROW; INTERFERON-GAMMA; ANTITHYMOCYTE GLOBULIN; FLOW-CYTOMETRY; T-LYMPHOCYTES; FLT3 LIGAND; CYCLOSPORINE; RECEPTOR; BETA AB An Immune pathophysiology for acquired aplastic anemia (AA) has been inferred from the responsiveness of the patients to immunosuppressive therapies and experimental laboratory data. To address the transcriptome of hematopoietic cells in AA, we undertook GeneChip analysis of the extremely limited numbers of progenitor and stem cells in the marrow of patients with this disease. We pooled total RNA from highly enriched bone marrow CD34 cells of 36 patients with newly diagnosed AA and 12 healthy volunteers for analysis on oligonucleotide chips. A large number of genes implicated in apoptosis and cell death showed markedly increased expression in AA CD34 cells, and negative proliferation control genes also had increased activity. Conversely, cell cycle progress-enhancing genes showed low expression in AA. Cytokine/ chemokine signal transducer genes, stress response genes, and defense/ immune response genes were up-regulated, as anticipated from other evidence of the heightened immune activity in AA patients' marrow. In summary, detailed genetic analysis of small numbers of hematopoietic progenitor cells is feasible even in marrow failure states where such cells are present in very small numbers. The gene expression profile of primary human CD34 hematopoietic stem cells from AA was consistent with a stressed, dying, and immunologically activated target cell population. Many of the genes showing differential expression in AA deserve further detailed analysis, including comparison with other marrow failure states and autoimmune disease. C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. RP Zeng, WH (reprint author), NHLBI, Hematol Branch, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 38 TC 50 Z9 60 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 2004 VL 103 IS 1 BP 325 EP 332 DI 10.1182/blood-2003-02-0490 PG 8 WC Hematology SC Hematology GA 757QM UT WOS:000187573000056 PM 14504100 ER PT J AU Asefa, B Klarmann, KD Copeland, NG Gilbert, DJ Jenkins, NA Keller, JR AF Asefa, B Klarmann, KD Copeland, NG Gilbert, DJ Jenkins, NA Keller, JR TI The interferon-inducible p200 family of proteins: a perspective on their roles in cell cycle regulation and differentiation SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Article; Proceedings Paper CT 5th International Workshop on Molecular Aspects of Myeloid Stem Cell Development and Leukemia CY MAY 04-07, 2003 CL ANNAPOLIS, MARYLAND SP Leukemia & Lymphoma Soc DE interferon-inducible p200; IFN; cell cycle regulation ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; PROSTATE-CANCER CELLS; NECROSIS-FACTOR-ALPHA; DNA-BINDING DOMAIN; GENE 200 CLUSTER; NF-KAPPA-B; TRANSCRIPTIONAL ACTIVATION; MYOBLAST DIFFERENTIATION; RETINOBLASTOMA PROTEIN; NEGATIVE REGULATOR AB The interferon-inducible p200 (IFI-200) family of proteins is among the numerous gene products induced by interferons (IFNs), which are important regulators of cell growth, immunomodulation and host resistance to tumors and viral infections. The members of this family of proteins are highly homologous to one another and consist of five murine proteins including p202, p203, p204 and p205 as well as three human homologues; IFI-16, myeloid cell nuclear differentiation antigen (MNDA) and absent in melanoma (AIM) 2. They possess at least one copy of a conserved 200 amino-acid motif which exists in two types; the a and b domains. Most of the IFI-200 proteins also possess a domain in apoptosis and interferon response (DAPIN)/PYRIN domain, which is a conserved motif associated with protein-protein interactions in the regulation of apoptotic and inflammatory signaling pathways. The p200 proteins have been implicated in cell cycle regulation and differentiation based on their ability to interact with and modulate the activities of multiple transcriptional factors such as Rb and p53, and there are significant findings that link mutations in their genetic loci to the incidence of cancer. Here, we describe the structure and biological activities of these proteins, and discuss recent studies that describe their relevant roles in processes regulating cell proliferation and differentiation. Published by Elsevier Inc. C1 NCI, Mol Immunoregulat Lab, Frederick, MD 21702 USA. NCI, Canc Res Ctr, Mouse Canc Genet Program, Frederick, MD 21702 USA. NCI, SAIC Frederick Inc, Basic Res Program, Frederick, MD 21702 USA. RP Asefa, B (reprint author), NCI, Mol Immunoregulat Lab, Bldg 560,Room 12-3, Frederick, MD 21702 USA. EM basefa@mail.ncifcrf.gov; kellerj@mail.ncifcrf.gov FU NCI NIH HHS [N01-CO-12400] NR 101 TC 85 Z9 89 U1 1 U2 5 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1079-9796 J9 BLOOD CELL MOL DIS JI Blood Cells Mol. Dis. PD JAN-FEB PY 2004 VL 32 IS 1 BP 155 EP 167 DI 10.1016/j.bcmd.2003.10.002 PG 13 WC Hematology SC Hematology GA 773DT UT WOS:000188883000028 PM 14757431 ER PT J AU Wolff, L Garin, MT Koller, R Bies, J Tessarollo, L Anver, MR Powell, D Perella, C AF Wolff, L Garin, MT Koller, R Bies, J Tessarollo, L Anver, MR Powell, D Perella, C TI A novel retrovirus provides the cooperating oncogenic event(s) required to demonstrate the tumor suppressor activity of p15(Ink4b) in myeloid cells in vivo SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Article; Proceedings Paper CT 5th International Workshop on Molecular Aspects of Myeloid Stem Cell Development and Leukemia CY MAY 04-07, 2003 CL ANNAPOLIS, MARYLAND SP Leukemia & Lymphoma Soc DE tumor suppressor; myeloid leukemia; hypermethylation; retrovirus; Ink4b ID MURINE LEUKEMIA-VIRUS; FUSION GENE CBFB-MYH11; PIM-1 TRANSGENIC MICE; C-MYC; CANCER; IDENTIFICATION; EXPRESSION; DIFFERENTIATION; HEMATOPOIESIS; LYMPHOMAS AB Cancer is a multistep process resulting from an accumulation of several genetic changes. The determination of cooperating events in experimental models can help scientists decipher specific neoplastic pathways and place genes with similar functions in complementation groups. In leukemia models, retrovirus tagging is a powerful approach to determine genes that cooperate with oncogenic transgenes or tumor suppressors that have undergone targeted deletion. Experimental models for B and T cell leukemias involving transgenic c-myc were the first to show the utility of retroviral tagging. Here we review these experiments and present examples of new models of myeloid leukemia where retroviruses have collaborated with a transgene [Cbfbeta-MYH111 from Inv(16)] and with loss of a tumor suppressor (Ink4b) mice to induce disease. (C) 2003 Elsevier Inc. All rights reserved. C1 NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NCI, SAIC Frederick, Frederick, MD 21702 USA. NCI, Frederick Canc Res & Dev Ctr, Data Management Serv, Frederick, MD 21702 USA. RP Wolff, L (reprint author), NCI, Ctr Canc Res, NIH, Bldg 37,Room 4124,37 Convent Dr,MSC4255, Bethesda, MD 20892 USA. EM lwolff@helix.nih.gov FU NCI NIH HHS [N01-CO-12400] NR 29 TC 3 Z9 3 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1079-9796 J9 BLOOD CELL MOL DIS JI Blood Cells Mol. Dis. PD JAN-FEB PY 2004 VL 32 IS 1 BP 226 EP 231 DI 10.1016/j.bcmd.2003.09.006 PG 6 WC Hematology SC Hematology GA 773DT UT WOS:000188883000036 PM 14757439 ER PT J AU Pavlov, YI Maki, S Maki, H Kunkel, TA AF Pavlov, Youri I. Maki, Satoko Maki, Hisaji Kunkel, Thomas A. TI Evidence for interplay among yeast replicative DNA polymerases alpha, delta and epsilon from studies of exonuclease and polymerase active site mutations SO BMC BIOLOGY LA English DT Article AB Background: DNA polymerase epsilon (Pol epsilon) is essential for S-phase replication, DNA damage repair and checkpoint control in yeast. A pol2-Y831A mutation leading to a tyrosine to alanine change in the Pol epsilon active site does not cause growth defects and confers a mutator phenotype that is normally subtle but strong in a mismatch repair-deficient strain. Here we investigate the mechanism responsible for the mutator effect. Results: Purified four-subunit Y831A Pol epsilon turns over more deoxynucleoside triphosphates to deoxynucleoside monophosphates than does wild-type Pol epsilon, suggesting altered coordination between the polymerase and exonuclease active sites. The pol2-Y831A mutation suppresses the mutator effect of the pol2-4 mutation in the exonuclease active site that abolishes proofreading by Pol epsilon, as measured in haploid strain with the pol2-Y831A, 4 double mutation. Analysis of mutation rates in diploid strains reveals that the pol2-Y831A allele is recessive to pol2-4. In addition, the mutation rates of strains with the pol2-4 mutation in combination with active site mutator mutations in Pol delta and Pol alpha suggest that Pol epsilon may proofread certain errors made by Pol alpha and Pol delta during replication in vivo. Conclusions: Our data suggest that Y831A replacement in Pol epsilon reduces replication fidelity and its participation in chromosomal replication, but without eliminating an additional function that is essential for viability. This suggests that other polymerases can substitute for certain functions of polymerase epsilon. C1 [Pavlov, Youri I.; Kunkel, Thomas A.] NIEHS, Genet Mol Lab, DHHS, NIH, Res Triangle Pk, NC 27709 USA. [Pavlov, Youri I.] Univ Nebraska, Med Ctr, Eppley Inst Res Canc, Omaha, NE 68198 USA. [Pavlov, Youri I.] Univ Nebraska, Med Ctr, Dept Biochem & Mol Biol, Omaha, NE 68198 USA. [Maki, Satoko; Maki, Hisaji] Nara Inst Sci & Technol, Grad Sch Biol Sci, Lab Microbial Mol Genet, Nara 63001, Japan. [Kunkel, Thomas A.] NIEHS, Struct Biol Lab, DHHS, NIH, Res Triangle Pk, NC 27709 USA. RP Pavlov, YI (reprint author), NIEHS, Genet Mol Lab, DHHS, NIH, 3OB 12233, Res Triangle Pk, NC 27709 USA. EM ypavlov@unmc.edu; smaki@bs.naist.jp; maki@bs.naist.jp; kunkel@niehs.nih.gov NR 47 TC 30 Z9 31 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1741-7007 J9 BMC BIOL JI BMC Biol. PY 2004 VL 2 AR 11 DI 10.1186/1741-7007-2-11 PG 13 WC Biology SC Life Sciences & Biomedicine - Other Topics GA V40AM UT WOS:000209451500011 PM 15163346 ER PT J AU Wangemann, P Itza, EM Albrecht, B Wu, T Jabba, SV Maganti, RJ Lee, JH Everett, LA Wall, SM Royaux, IE Green, ED Marcus, DC AF Wangemann, Philine Itza, Erin M. Albrecht, Beatrice Wu, Tao Jabba, Sairam V. Maganti, Rajanikanth J. Lee, Jun Ho Everett, Lorraine A. Wall, Susan M. Royaux, Ines E. Green, Eric D. Marcus, Daniel C. TI Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model SO BMC MEDICINE LA English DT Article AB Background: Pendred syndrome, a common autosomal-recessive disorder characterized by congenital deafness and goiter, is caused by mutations of SLC26A4, which codes for pendrin. We investigated the relationship between pendrin and deafness using mice that have (Slc26a4(+/+)) or lack a complete Slc26a4 gene (Slc26a4(-/-)). Methods: Expression of pendrin and other proteins was determined by confocal immunocytochemistry. Expression of mRNA was determined by quantitative RT-PCR. The endocochlear potential and the endolymphatic K+ concentration were measured with double-barreled microelectrodes. Currents generated by the stria marginal cells were recorded with a vibrating probe. Tissue masses were evaluated by morphometric distance measurements and pigmentation was quantified by densitometry. Results: Pendrin was found in the cochlea in apical membranes of spiral prominence cells and spindle-shaped cells of stria vascularis, in outer sulcus and root cells. Endolymph volume in Slc26a4(-/-) mice was increased and tissue masses in areas normally occupied by type I and II fibrocytes were reduced. Slc26a4(-/-) mice lacked the endocochlear potential, which is generated across the basal cell barrier by the K+ channel KCNJ10 localized in intermediate cells. Stria vascularis was hyperpigmented, suggesting unalleviated free radical damage. The basal cell barrier appeared intact; intermediate cells and KCNJ10 mRNA were present but KCNJ10 protein was absent. Endolymphatic K+ concentrations were normal and membrane proteins necessary for K+ secretion were present, including the K+ channel KCNQ1 and KCNE1, Na+/2Cl(-)/K+ cotransporter SLC12A2 and the gap junction GJB2. Conclusions: These observations demonstrate that pendrin dysfunction leads to a loss of KCNJ10 protein expression and a loss of the endocochlear potential, which may be the direct cause of deafness in Pendred syndrome. C1 [Wangemann, Philine; Itza, Erin M.; Albrecht, Beatrice; Wu, Tao; Jabba, Sairam V.; Maganti, Rajanikanth J.; Lee, Jun Ho; Marcus, Daniel C.] Kansas State Univ, Dept Anat & Physiol, Manhattan, KS 66506 USA. [Everett, Lorraine A.; Royaux, Ines E.; Green, Eric D.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA. [Wall, Susan M.] Emory Univ, Sch Med, Div Renal, Dept Med, Atlanta, GA 30322 USA. RP Wangemann, P (reprint author), Kansas State Univ, Dept Anat & Physiol, Manhattan, KS 66506 USA. EM wange@vet.k-state.edu; erin.itza@imperial.edu; albrecht_B@klinik.uni-wuerzburg.de; wutao@vet.k-state.edu; sjabba@vet.k-state.edu; rmaganti@vet.k-state.edu; jlee@brm.co.kr; lae@sanger.ac.uk; smwall@emory.edu; iroyaux@prdbe.jnj.com; egreen@nhgri.nih.gov; marcus@k-state.edu RI Wangemann, Philine/N-2826-2013; Jabba, Sairam/B-5790-2015 FU [NIH-R01-DC01098]; [NIH-R01-DC00212]; [NIH-R01-DK52935]; [NIH-P20-RR017686] FX This work was supported by NIH-R01-DC01098 (PW), NIH-R01-DC00212 (DCM), NIH-R01-DK52935 (SMW) and Core facilities funded by NIH-P20-RR017686 (Confocal Microfluorometry and Microscopy Core, Molecular Biology Core) are gratefully acknowledged. NR 39 TC 129 Z9 138 U1 0 U2 5 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1741-7015 J9 BMC MED JI BMC Med. PY 2004 VL 2 AR 30 DI 10.1186/1741-7015-2-30 PG 15 WC Medicine, General & Internal SC General & Internal Medicine GA V22MX UT WOS:000208280400030 PM 15320950 ER PT J AU Yoon, SS Dambrosia, J Chalela, J Ezzeddine, M Warach, S Haymore, J Davis, L Baird, AE AF Yoon, Sung Sug Dambrosia, James Chalela, Julio Ezzeddine, Mustapha Warach, Steven Haymore, Joseph Davis, Lisa Baird, Alison E. TI Rising statin use and effect on ischemic stroke outcome SO BMC MEDICINE LA English DT Article AB Background: Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) have neuroprotective effects in experimental stroke models and are commonly prescribed in clinical practice. The aim of this study was to determine if patients taking statins before hospital admission for stroke had an improved clinical outcome. Methods: This was an observational study of 436 patients admitted to the National Institutes of Health Suburban Hospital Stroke Program between July 2000 and December 2002. Self-reported risk factors for stroke were obtained on admission. Stroke severity was determined by the admission National Institutes of Health Stroke Scale score. Good outcome was defined as a Rankin score < 2 at discharge. Statistical analyses used univariate and multivariate logistic regression models. Results: There were 436 patients with a final diagnosis of ischemic stroke; statin data were available for 433 of them. A total of 95/433 (22%) of patients were taking a statin when they were admitted, rising from 16% in 2000 to 26% in 2002. Fifty-one percent of patients taking statins had a good outcome compared to 38% of patients not taking statins (p = 0.03). After adjustment for confounding factors, statin pretreatment was associated with a 2.9 odds (95% CI: 1.2-6.7) of a good outcome at the time of hospital discharge. Conclusions: The proportion of patients taking statins when they are admitted with stroke is rising rapidly. Statin pretreatment was significantly associated with an improved functional outcome at discharge. This finding could support the early initiation of statin therapy after stroke. C1 [Yoon, Sung Sug; Baird, Alison E.] NINDS, Stroke Neurosci Unit, NIH, Bethesda, MD 20892 USA. [Dambrosia, James] NINDS, Biostat Branch, NIH, Bethesda, MD 20892 USA. [Chalela, Julio; Warach, Steven; Davis, Lisa] NINDS, Sect Stroke Diagnost & Therapeut, NIH, Bethesda, MD 20892 USA. [Ezzeddine, Mustapha] Emory Univ, Atlanta, GA 30322 USA. [Haymore, Joseph] Washington Adventist Hosp, Ctr Neuro Serv CNS, Takoma Pk, MD 20912 USA. RP Baird, AE (reprint author), NINDS, Stroke Neurosci Unit, NIH, Bethesda, MD 20892 USA. EM sungsyoon@yahoo.com; dambrosj@ninds.nih.gov; chalelaj@ninds.nih.gov; Mustapha_Ezzeddine@emoryhealthcare.org; warachs@ninds.nih.gov; jhaymore@ahm.com; davisl@ninds.nih.gov; bairda@ninds.nih.gov NR 33 TC 46 Z9 48 U1 0 U2 1 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1741-7015 J9 BMC MED JI BMC Med. PY 2004 VL 2 AR 4 DI 10.1186/1741-7015-2-4 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA V22MX UT WOS:000208280400004 PM 15035663 ER PT J AU Smith, CJ Emsley, HCA Gavin, CM Georgiou, RF Vail, A Barberan, EM del Zoppo, GJ Hallenbeck, JM Rothwell, NJ Hopkins, SJ Tyrrell, PJ AF Smith, Craig J. Emsley, Hedley C. A. Gavin, Carole M. Georgiou, Rachel F. Vail, Andy Barberan, Elisa M. del Zoppo, Gregory J. Hallenbeck, John M. Rothwell, Nancy J. Hopkins, Stephen J. Tyrrell, Pippa J. TI Peak plasma interleukin-6 and other peripheral markers of inflammation in the first week of ischaemic stroke correlate with brain infarct volume, stroke severity and long-term outcome SO BMC NEUROLOGY LA English DT Article AB Background: Cerebral ischaemia initiates an inflammatory response in the brain and periphery. We assessed the relationship between peak values of plasma interleukin-6 (IL-6) in the first week after ischaemic stroke, with measures of stroke severity and outcome. Methods: Thirty-seven patients with ischaemic stroke were prospectively recruited. Plasma IL-6, and other markers of peripheral inflammation, were measured at pre-determined timepoints in the first week after stroke onset. Primary analyses were the association between peak plasma IL-6 concentration with both modified Rankin score (mRS) at 3 months and computed tomography (CT) brain infarct volume. Results: Peak plasma IL-6 concentration correlated significantly (p < 0.001) with CT brain infarct volume (r = 0.75) and mRS at 3 months (r = 0.72). It correlated similarly with clinical outcome at 12 months or stroke severity. Strong associations were also noted between either peak plasma C-reactive protein (CRP) concentration or white blood cell (WBC) count, and all outcome measures. Conclusions: These data provide evidence that the magnitude of the peripheral inflammatory response is related to the severity of acute ischaemic stroke, and clinical outcome. C1 [Smith, Craig J.; Rothwell, Nancy J.] Univ Manchester, Sch Biol Sci, Manchester M13 9PT, Lancs, England. [Smith, Craig J.; Emsley, Hedley C. A.; Georgiou, Rachel F.; Barberan, Elisa M.; Tyrrell, Pippa J.] Hope Hosp, Stroke Serv, Salford M6 8HD, Lancs, England. [Vail, Andy] Univ Manchester, Hope Hosp, Biostat Grp, Salford M6 8HD, Lancs, England. [del Zoppo, Gregory J.] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA. [Hallenbeck, John M.] NINDS, Stroke Branch, NIH, Bethesda, MD 20892 USA. [Hopkins, Stephen J.] Hope Hosp, NWIRC, Salford M6 8HD, Lancs, England. RP Smith, CJ (reprint author), Univ Manchester, Sch Biol Sci, Manchester M13 9PT, Lancs, England. EM csmith@fs1.ho.man.ac.uk; hemsley@fs1.ho.man.ac.uk; Carole.Gavin@srht.nhs.uk; rdrennan@fs1.ho.man.ac.uk; avail@fs1.ho.man.ac.uk; elisa.barberan@man.ac.uk; grgdlzop@scripps.edu; hallenbj@ninds.nih.gov; Nancy.Rothwell@man.ac.uk; shopkins@fs1.ho.man.ac.uk; ptyrrell@fs1.ho.man.ac.uk RI Hopkins, Stephen/I-7363-2015; OI Hopkins, Stephen/0000-0001-7644-2823; Smith, Craig/0000-0002-9078-9919 FU Research into Ageing; UK Community Fund; Salford Royal Hospitals NHS Trust Research and Development Directorate; North Manchester Healthcare NHS Trust; Salford Royal Hospitals NHS Trust; NIH [NS26945, NS38710]; National Institute of Neurological Disorders and Stroke; Medical Research Council; University of Manchester, UK FX This study was funded by a grant from Research into Ageing, provided by the UK Community Fund, and supported by Salford Royal Hospitals NHS Trust Research and Development Directorate. CJS, HCAE and RFG are funded by Research into Ageing; EMB is funded by North Manchester Healthcare NHS Trust; CMG, AV and SJH are funded by Salford Royal Hospitals NHS Trust. GJDZ is supported by grants NS26945 and NS38710 of the NIH; JMH is supported by the National Institute of Neurological Disorders and Stroke; NJR is supported by the Medical Research Council; PJT is funded by the University of Manchester, UK. NR 45 TC 248 Z9 261 U1 2 U2 16 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1471-2377 J9 BMC NEUROL JI BMC Neurol. PY 2004 VL 4 AR 2 DI 10.1186/1471-2377-4-2 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA V22HA UT WOS:000208265100002 PM 14725719 ER PT J AU Longo, M Brama, M Marino, M Bernardini, S Korach, KS Wetsel, WC Scandurra, R Faraggiana, T Spera, G Baron, R Teti, A Migliaccio, S AF Longo, M Brama, M Marino, M Bernardini, S Korach, KS Wetsel, WC Scandurra, R Faraggiana, T Spera, G Baron, R Teti, A Migliaccio, S TI Interaction of estrogen receptor a with protein kinase C alpha and c-Src in osteoblasts during differentiation SO BONE LA English DT Article DE osteoblast; differentiation; estrogen receptor alpha; PKC; c-Src ID EPIDERMAL-GROWTH-FACTOR; PHORBOL ESTER; SIGNALING PATHWAYS; DOWN-REGULATION; BREAST-CANCER; MCF-7 CELLS; BETA-II; ACTIVATION; EXPRESSION; ISOENZYMES AB In cultured osteoblasts, protein kinase C (PKC) activity increases and estrogen receptor alpha (ERalpha) binding capacity decreases upon confluence. We investigated potential interactions between ERalpha and PKC isoforms and their confluence-induced modulations in clonal ROS. SMER#14 cells and primary osteoblasts. In sub-confluent ROS.SMER#14 cells, which express an exogenous plus small amounts of the endogenous ERalpha gene, the receptor appeared as two main bands of approximate to 66 and approximate to 46 kDa. In over-confluent, more differentiated cells, the cytosolic approximate to 66 kDa ERa appeared decreased and the approximate to 46 kDa variant increased. Enhanced expression and/or membrane translocation of PKCalpha and PKCepsilon, but not PKCzeta, was evidenced at over-confluence, along with transient increases in expression and kinase activity of c-Src, accompanied by membrane translocation of the kinase-activated enzyme. In contrast, negligible membrane translocation of PKCa and/or activated c-Src was observed in parental ROS 17/2.8 cells, which express low levels of full-length ERalpha. PKCa from over-confluent cells phosphorylated p60(c-Src) in vitro, suggesting functional interaction between the two kinases. ERalpha co-immunoprecipitated c-Src and PKCalpha, mostly in its cleaved form (PKMalpha). An analogous interaction was observed in primary osteoblasts. However, in these cells, much more PKCalpha/ PKMa was ERalpha-co-immunoprecipitated at over-confluence, a condition in which the shorter, approximate to 46 kDa ERalpha variant is increased. This interaction was enhanced by estradiol treatment or PKC down-regulation, but was unaffected by c-Src inhibition. These data highlight direct PKCalpha-c-Src-ERalpha interactions, which may be crucial in the modulation of estrogen responsiveness and the differentiation process in osteoblasts. (C) 2003 Published by Elsevier Inc. C1 Univ Aquila, Dept Expt Med, I-67100 Laquila, Italy. Univ Roma La Sapienza, Dept Histol & Med Embryol, I-00185 Rome, Italy. Univ Roma 3, Dept Biol, Rome, Italy. Ist Dermopat Immacolata, Rome, Italy. Natl Inst Environm Hlth Sci, Reprod & Dev Toxicol Lab, Res Triangle Pk, NC USA. Duke Univ, Med Ctr, Dept Psychiat & Behav Sci Med Endocrinol & Cell B, Durham, NC 27705 USA. Univ Roma La Sapienza, Dept Biochem, Rome, Italy. Univ Roma La Sapienza, Dept Expt Med, Rome, Italy. Univ Roma La Sapienza, Dept Med Physiopathol, Rome, Italy. Yale Univ, Dept Orthopaed & Cell Biol, New Haven, CT USA. RP Migliaccio, S (reprint author), Univ Aquila, Dept Expt Med, Via Vetoio Coppito 2, I-67100 Laquila, Italy. EM silvia.migliaccio@uniroma1.it FU NICHD NIH HHS [HD36015]; Telethon [E.0831] NR 49 TC 35 Z9 35 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 8756-3282 J9 BONE JI Bone PD JAN PY 2004 VL 34 IS 1 BP 100 EP 111 DI 10.1016/j.bone.2003.09.007 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 772UX UT WOS:000188861100010 PM 14751567 ER PT J AU Bellahcene, A Chaplet, M Detry, C Deroanne, C Fisher, LW Castronovo, V AF Bellahcene, A Chaplet, M Detry, C Deroanne, C Fisher, LW Castronovo, V TI Zoledronate up-regulates bone sialoprotein expression in Saos-2 cells through RhoA inhibition SO BONE LA English DT Meeting Abstract CT Workshop on What is New in Bisphosphonates CY MAR 24-26, 2004 CL Davos, SWITZERLAND C1 Univ Liege, Metastasis Res Lab, B-4000 Liege, Belgium. Univ Liege, Expt Canc Res Ctr, B-4000 Liege, Belgium. NIDCR, Craniofacial & Skeletal Dis Branch, NIH, HHS, Bethesda, MD USA. 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 8756-3282 J9 BONE JI Bone PY 2004 VL 34 SU 1 BP S48 EP S49 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 808HK UT WOS:000220560000096 ER PT J AU Wuerfel, J Bellmann-Strobl, J Brunecker, P Aktas, O McFarland, H Villringer, A Zipp, F AF Wuerfel, J Bellmann-Strobl, J Brunecker, P Aktas, O McFarland, H Villringer, A Zipp, F TI Changes in cerebral perfusion precede plaque formation in multiple sclerosis: a longitudinal perfusion MRI study SO BRAIN LA English DT Article DE diffusion; longitudinal; MRI; multiple sclerosis; perfusion ID APPEARING WHITE-MATTER; APPARENT DIFFUSION-COEFFICIENT; MAGNETIC-RESONANCE; BLOOD-FLOW; STATUS EPILEPTICUS; WATER DIFFUSION; LESIONS; BRAIN; MS; ISCHEMIA AB New MRI techniques such as the analysis of magnetization transfer or diffusion have provided evidence for subtle progressive alterations in tissue integrity prior to focal leakage of the blood-brain barrier (BBB) as part of plaque formation in multiple sclerosis. Since inflammation is capable of modulating the microcirculation, we investigated the hypothesis that changes in the local perfusion might be one of the earliest signs of lesion development. 20 patients with definite relapsing-remitting multiple sclerosis were analysed with regard to cerebral blood volume, cerebral blood flow, mean transit time and apparent diffusion coefficient (ADC), as well as conventional MRI parameters, on monthly follow-up scans. Among 89 gadolinium-enhancing lesions, we selected 18 that developed during the study and met strict inclusion criteria. In these, changes of perfusion parameters were detectable not only prior to the BBB breakdown, but also prior to increases in the ADC. Our data indicate that inflammation is accompanied by altered local perfusion, which can be detected prior to permeability of the BBB. C1 Charite, Inst Neuroimmunol, Berlin, Germany. Charite, Dept Neurol, Berlin Neuro Imaging Ctr, Berlin, Germany. NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA. RP Zipp, F (reprint author), Charite Univ Hosp, Neurosci Res Ctr, Inst Neuroimmunol, NWFZ 2680, D-10098 Berlin, Germany. RI Zipp, Frauke/C-9968-2015; Aktas, Orhan/B-7623-2009 OI Zipp, Frauke/0000-0002-1231-1928; Aktas, Orhan/0000-0002-2020-9210 NR 48 TC 103 Z9 107 U1 1 U2 7 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD JAN PY 2004 VL 127 BP 111 EP 119 DI 10.1093/brain/awh007 PN 1 PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 756LK UT WOS:000187466400010 PM 14570816 ER PT J AU Robinson, GW AF Robinson, GW TI Identification of signaling pathways in early mammary gland development by mouse genetics SO BREAST CANCER RESEARCH LA English DT Review DE ectodysplasin; fibroblast growth factor; parathyroid hormone-related protein; Tbx3; tissue interaction; wnt ID HORMONE-RELATED PROTEIN; HAIR FOLLICLE DEVELOPMENT; BREAST DEVELOPMENT; LIMB; P63; ECTODYSPLASIN; EXPRESSION; MUTATIONS; EDAR; MICE AB The mammary gland develops as an appendage of the ectoderm. The prenatal stage of mammary development is hormone independent and is regulated by sequential and reciprocal signaling between the epithelium and the mesenchyme. A number of recent studies using human and mouse genetics, in particular targeted gene deletion and transgenic expression, have identified some of the signals that control specific steps in development. This process involves cell specification and proliferation, reciprocal tissue interactions and cell migration. Since some of these events are recapitulated during tumorigenesis, an understanding of these signaling pathways may contribute to the development of targeted therapies and novel drugs. C1 NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA. RP Robinson, GW (reprint author), NIDDK, Lab Genet & Physiol, NIH, Bldg 8,Room 101, Bethesda, MD 20892 USA. EM traudl@nih.gov RI Robinson, Gertraud/I-2136-2012 NR 21 TC 10 Z9 10 U1 1 U2 7 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-542X J9 BREAST CANCER RES JI Breast Cancer Res. PY 2004 VL 6 IS 3 BP 105 EP 108 DI 10.1186/bcr776 PG 4 WC Oncology SC Oncology GA 815UZ UT WOS:000221068500001 PM 15084230 ER PT J AU John, EM Hopper, JL Beck, JC Knight, JA Neuhausen, SL Senie, RT Ziogas, A Andrulis, IL Anton-Culver, H Boyd, N Buys, SS Daly, MB O'Malley, FP Santella, RM Southey, MC Venne, VL Venter, DJ West, DW Whittemore, AS Seminara, D AF John, EM Hopper, JL Beck, JC Knight, JA Neuhausen, SL Senie, RT Ziogas, A Andrulis, IL Anton-Culver, H Boyd, N Buys, SS Daly, MB O'Malley, FP Santella, RM Southey, MC Venne, VL Venter, DJ West, DW Whittemore, AS Seminara, D CA Breast Canc Family Registry TI The Breast Cancer Family Registry: an infrastructure for cooperative multinational, interdisciplinary and translational studies of the genetic epidemiology of breast cancer SO BREAST CANCER RESEARCH LA English DT Review DE biospecimen repository; breast cancer; familial aggregation; genetic epidemiology ID SUSCEPTIBILITY GENE; BRCA1; MUTATIONS; PARTICIPATION; CANDIDATE; RELATIVES; DESIGNS; HISTORY; TWINS; RISK AB Introduction The etiology of familial breast cancer is complex and involves genetic and environmental factors such as hormonal and lifestyle factors. Understanding familial aggregation is a key to understanding the causes of breast cancer and to facilitating the development of effective prevention and therapy. To address urgent research questions and to expedite the translation of research results to the clinical setting, the National Cancer Institute ( USA) supported in 1995 the establishment of a novel research infrastructure, the Breast Cancer Family Registry, a collaboration of six academic and research institutions and their medical affiliates in the USA, Canada, and Australia. Methods The sites have developed core family history and epidemiology questionnaires, data dictionaries, and common protocols for biospecimen collection and processing and pathology review. An Informatics Center has been established to collate, manage, and distribute core data. Results As of September 2003, 9116 population-based and 2834 clinic-based families have been enrolled, including 2346 families from minority populations. Epidemiology questionnaire data are available for 6779 affected probands (with a personal history of breast cancer), 4116 unaffected probands, and 16,526 relatives with or without a personal history of breast or ovarian cancer. The biospecimen repository contains blood or mouthwash samples for 6316 affected probands, 2966 unaffected probands, and 10,763 relatives, and tumor tissue samples for 4293 individuals. Conclusion This resource is available to internal and external researchers for collaborative, interdisciplinary, and translational studies of the genetic epidemiology of breast cancer. Detailed information can be found at the URL http://www.cfr.epi.uci.edu/. C1 NCI, Clin & Genet Epidemiol Res Branch, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. No Calif Canc Ctr, Union City, CA USA. Univ Melbourne, Ctr Genet Epidemiol, Parkville, Vic 3052, Australia. Coriell Inst Med Res, Camden, NJ USA. Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Div Epidemiol & Biostat, Toronto, ON M5G 1X5, Canada. Univ Calif Irvine, Dept Med, Div Epidemiol, Irvine, CA 92717 USA. Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA. Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Fred A Litwin Ctr Canc Genet, Toronto, ON M5G 1X5, Canada. Ontario Canc Inst, Univ Hlth Network, Div Epidemiol & Stat, Toronto, ON M4X 1K9, Canada. Univ Utah, Huntsman Canc Inst, Salt Lake City, UT USA. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON M5G 1X5, Canada. Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia. Stanford Univ, Sch Med, Dept Hlth Res & Policy, Stanford, CA 94305 USA. RP Seminara, D (reprint author), NCI, Clin & Genet Epidemiol Res Branch, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. EM seminard@epndce.nci.nih.gov RI Knight, Julia/A-6843-2012; Andrulis, Irene/E-7267-2013 FU NCI NIH HHS [CA-95-003, CA13696, P30 CA013696, U01 CA069417, U01 CA069417-10, U01CA 71966]; NCRR NIH HHS [M01 RR000064, M01-RR00064]; NIEHS NIH HHS [ES09089, P30 ES009089] NR 34 TC 171 Z9 171 U1 2 U2 9 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2004 VL 6 IS 4 BP R375 EP R389 DI 10.1186/bcr801 PG 15 WC Oncology SC Oncology GA 840AA UT WOS:000222828200022 PM 15217505 ER PT J AU Li, Y Millikan, RC Bell, DA Cui, L Tse, CKJ Newman, B Conway, K AF Li, Y Millikan, RC Bell, DA Cui, L Tse, CKJ Newman, B Conway, K TI Cigarette smoking, cytochrome P4501A1 polymorphisms, and breast cancer among African-American and white women SO BREAST CANCER RESEARCH LA English DT Review DE African Americans; breast cancer; cytochrome P4501A1 ID ARYL-HYDROCARBON HYDROXYLASE; LUNG-CANCER; HUMAN CYP1A1; RISK; GENE; ASSOCIATION; GENOTYPE; IMPACT AB Introduction Previous epidemiologic studies suggest that women with variant cytochrome P4501A1 (CYP1A1) genotypes who smoke cigarettes are at increased risk for breast cancer. Methods We evaluated the association of breast cancer with CYP1A1 polymorphisms and cigarette smoking in a population-based, case-control study of invasive breast cancer in North Carolina. The study population consisted of 688 cases ( 271 African Americans and 417 whites) and 702 controls ( 285 African Americans and 417 whites). Four polymorphisms in CYP1A1 were genotyped using PCR/restriction fragment length polymorphism analysis: M1 ( also known as CYP1A1*2A), M2 (CYP1A1*2C), M3 (CYP1A1*3), and M4 (CYP1A1*4) Results No associations were observed for CYP1A1 variant alleles and breast cancer, ignoring smoking. Among women who smoked for longer than 20 years, a modest positive association was found among women with one or more M1 alleles (odds ratio [OR] = 2.1, 95% confidence interval [CI] = 1.2-3.5) but not among women with non-M1 alleles (OR = 1.2, 95% Cl = 0.9-1.6). Odds ratios for smoking longer than 20 years were higher among African-American women with one or more M3 alleles (OR = 2.5, 95% CI = 0.9-7.1) compared with women with non-M3 alleles (OR = 1.3, 95% Cl = 0.8-2.2). ORs for smoking in white women did not differ appreciably based upon M2 or M4 genotypes. Conclusions Cigarette smoking increases breast cancer risk in women with CYP1A1 M1 variant genotypes and in African-American women with CYP1A1 M3 variant genotypes, but the modifying effects of the CYP1A1 genotype are quite weak. C1 Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27514 USA. Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA. NIEHS, Res Triangle Pk, NC 27709 USA. Queensland Univ Technol, Sch Publ Hlth, Kelvin Grove, Qld, Australia. RP Millikan, RC (reprint author), Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27514 USA. EM bob_millikan@unc.edu FU NCI NIH HHS [P50 CA058223]; NIEHS NIH HHS [P30 ES010126, P42 ES005948] NR 28 TC 48 Z9 48 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2004 VL 6 IS 4 BP R460 EP R473 DI 10.1186/bcr814 PG 14 WC Oncology SC Oncology GA 840AA UT WOS:000222828200031 PM 15217514 ER PT J AU Millikan, RC Player, J de Cotret, AR Moorman, P Pittman, G Vannappagari, V Tse, CKJ Keku, T AF Millikan, RC Player, J de Cotret, AR Moorman, P Pittman, G Vannappagari, V Tse, CKJ Keku, T TI Manganese superoxide dismutase Ala-9Val polymorphism and risk of breast cancer in a population-based case-control study of African Americans and whites SO BREAST CANCER RESEARCH LA English DT Review DE African Americans; breast cancer; manganese superoxide dismutase polymorphism ID MITOCHONDRIAL TARGETING SEQUENCE; GENETIC ASSOCIATIONS; MNSOD POLYMORPHISM; IN-SITU; CELLS; DISEASES; OVEREXPRESSION; EPIDEMIOLOGY; EXPRESSION; DIMORPHISM AB Introduction: A polymorphism in the manganese superoxide dismutase (MnSOD) gene, Ala-9Val, has been examined in association with breast cancer risk in several epidemiologic studies. Results suggest that the Ala allele increases the risk of breast cancer and modifies the effects of environmental exposures that produce oxidative damage to DNA. Methods: We examined the role of the MnSOD Ala-9Val polymorphism in a population-based case-control study of invasive and in situ breast cancer in North Carolina. Genotypes were evaluated for 2025 cases ( 760 African Americans and 1265 whites) and for 1812 controls ( 677 African Americans and 1135 whites). Results: The odds ratio for MnSOD Ala/Ala versus any MnSOD Val genotypes was not elevated in African Americans (odds ratio = 0.9, 95% confidence interval = 0.7-1.2) or in whites (odds ratio = 1.0, 95% confidence interval = 0.8-1.2). Greater than additive joint effects were observed for the Ala/Ala genotype and smoking, radiation to the chest, and occupational exposure to ionizing radiation. Antagonism was observed between the Ala/Ala genotype and the use of nonsteroidal anti-inflammatory drugs. Conclusions: The MnSOD genotype may contribute to an increased risk of breast cancer in the presence of specific environmental exposures. These results provide further evidence for the importance of reactive oxygen species and of oxidative DNA damage in the etiology of breast cancer. C1 Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA. Duke Univ, Med Ctr, Dept Community & Family Med, Durham, NC 27710 USA. NIEHS, Res Triangle Pk, NC 27709 USA. Univ N Carolina, Sch Med, Ctr Gastrointestinal Biol & Dis, Chapel Hill, NC USA. RP Millikan, RC (reprint author), Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, CB 7435, Chapel Hill, NC 27599 USA. EM bob_millikan@unc.edu FU NCI NIH HHS [P50 CA058223, P50-CA58223]; NIEHS NIH HHS [P30 ES010126, P30-ES10126, P42 ES005948, P42-ES05948] NR 44 TC 45 Z9 46 U1 2 U2 4 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2004 VL 6 IS 4 BP R264 EP R274 DI 10.1186/bcr786 PG 11 WC Oncology SC Oncology GA 840AA UT WOS:000222828200009 PM 15217492 ER PT J AU Sparks, R Ulrich, CM Bigler, J Tworoger, SS Yasui, Y Rajan, KB Porter, P Stanczyk, FZ Ballard-Barbash, R Yuan, XP Lin, MG McVarish, L Aiello, EJ McTiernan, A AF Sparks, R Ulrich, CM Bigler, J Tworoger, SS Yasui, Y Rajan, KB Porter, P Stanczyk, FZ Ballard-Barbash, R Yuan, XP Lin, MG McVarish, L Aiello, EJ McTiernan, A TI UDP-glucuronosyltransferase and sulfotransferase polymorphisms, sex hormone concentrations, and tumor receptor status in breast cancer patients SO BREAST CANCER RESEARCH LA English DT Review DE breast cancer; estrogen; glucuronosyltransferase; polymorphism; sulfotransferase; testosterone ID HUMAN LIVER; PHENOL SULFOTRANSFERASE; ESTROGEN-RECEPTOR; GENETIC POLYMORPHISMS; KI-67 ANTIGEN; PROGESTERONE-RECEPTOR; POSTMENOPAUSAL WOMEN; ALLELE FREQUENCIES; ANDROGEN RECEPTOR; PARAFFIN SECTIONS AB Introduction UDP-glucuronosyltransferase (UGT) and sulfotransferase (SULT) enzymes are involved in removing sex hormones from circulation. Polymorphic variation in five UGT and SULT genes - UGT1A1 ((TA)(6)/(TA)(7)), UGT2B4 (Asp(458)Glu), UGT2B7 (His(268)Tyr), UGT2B15 (Asp(85)Tyr), and SULT1A1 (Arg(213)His) - may be associated with circulating sex hormone concentrations, or the risk of an estrogen receptor-negative (ER-) or progesterone receptor-negative (PR-) tumor. Methods Logistic regression analysis was used to estimate the odds ratios of an ER- or PR- tumor associated with polymorphisms in the genes listed above for 163 breast cancer patients from a population-based cohort study of women in western Washington. Adjusted geometric mean estradiol, estrone, and testosterone concentrations were calculated within each UGT and SULT genotype for a subpopulation of postmenopausal breast cancer patients not on hormone therapy 2 - 3 years after diagnosis (n = 89). Results The variant allele of UGT1A1 was associated with reduced risk of an ER- tumor (P for trend = 0.03), and variants of UGT2B15 and SULT1A1 were associated with non-statistically significant risk reductions. There was some indication that plasma estradiol and testosterone concentrations varied by UGT2B15 and SULT1A1 genotypes; women with the UGT2B15 Asp/Tyr and Tyr/Tyr genotypes had higher concentrations of estradiol than women with the Asp/Asp genotype (P = 0.004). Compared with women with the SULT1A1 Arg/Arg and Arg/His genotypes, women with the His/His genotype had elevated concentrations of testosterone (P = 0.003). Conclusions The risk of ER- breast cancer tumors may vary by UGT or SULT genotype. Further, plasma estradiol and testosterone concentrations in breast cancer patients may differ depending on some UGT and SULT genotypes. C1 Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA. Univ So Calif, Los Angeles, CA USA. NCI, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. Grp Hlth Cooperat Puget Sound, Ctr Hlth Studies, Seattle, WA 98101 USA. RP Ulrich, CM (reprint author), Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA. EM nulrich@fhcrc.org RI Yasui, Yutaka/E-2564-2015; OI Yasui, Yutaka/0000-0002-7717-8638; Rajan, Kumar/0000-0003-1268-4617 FU NCI NIH HHS [N01 PC-67009, 5 P30 CA15704, N01 PC067009, P30 CA015704] NR 58 TC 62 Z9 63 U1 0 U2 3 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1465-5411 J9 BREAST CANCER RES JI Breast Cancer Res. PY 2004 VL 6 IS 5 BP R488 EP R498 DI 10.1186/bcr818 PG 11 WC Oncology SC Oncology GA 853YH UT WOS:000223866400010 PM 15318931 ER PT J AU Anderson, WF Jatoi, I Devesa, SS AF Anderson, WF Jatoi, I Devesa, SS TI Distinct breast cancer incidence and prognostic factor patterns in the SEER database, a possible link between etiology and outcome? SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S120 EP S121 PG 2 WC Oncology SC Oncology GA 877SE UT WOS:000225589600341 ER PT J AU Arun, B Lammey, J Broglio, K Valero, V Babiera, G Browne, D Hortobagyi, GN Sneige, A AF Arun, B Lammey, J Broglio, K Valero, V Babiera, G Browne, D Hortobagyi, GN Sneige, A TI Downregulation of estrogen receptor expression with celecoxib in breast tissue of women at increased risk for developing breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Natl Canc Inst, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S157 EP S158 PG 2 WC Oncology SC Oncology GA 877SE UT WOS:000225589600445 ER PT J AU Baumgartner, KB Baumgartner, RN Wayne, S Hunt, WC Joste, N Royce, M Ballard-Barbash, R AF Baumgartner, KB Baumgartner, RN Wayne, S Hunt, WC Joste, N Royce, M Ballard-Barbash, R TI Hispanic ethnicity is associated with increased recurrence and death in women with breast cancer in New Mexico: the Health, Eating, Activity and Lifestyle Study. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ New Mexico, Albuquerque, NM 87131 USA. NCI, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 1 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S98 EP S99 PG 2 WC Oncology SC Oncology GA 877SE UT WOS:000225589600279 ER PT J AU Baumgartner, RN Baumgartner, KB Wayne, S Hunt, WC Royce, ME Ballard-Barbash, R AF Baumgartner, RN Baumgartner, KB Wayne, S Hunt, WC Royce, ME Ballard-Barbash, R TI High C-peptide is associated with increased recurrence and death in women with breast cancer independent of ethnicity - The Health, Eating, Activity and Lifestyle Study. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ New Mexico, Albuquerque, NM USA. NCI, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S99 EP S99 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600280 ER PT J AU Bear, HD Anderson, S Smith, RE Robidoux, A Kahlenberg, MS Margolese, RG Dakhil, SR Pajon, ER Hoehn, JL Mamounas, EP Geyer, CE Julian, TB Wolmark, N AF Bear, HD Anderson, S Smith, RE Robidoux, A Kahlenberg, MS Margolese, RG Dakhil, SR Pajon, ER Hoehn, JL Mamounas, EP Geyer, CE Julian, TB Wolmark, N TI A randomized trial comparing preoperative (preop) doxorubicin/cyclophosphamide (AC) to preop AC followed by preop docetaxel (T) and to preop AC followed by postoperative (postop) T in patients (pts) with operable carcinoma of the breast: results of NSABP B-27 SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NSABP, Pittsburgh, PA USA. NR 0 TC 31 Z9 31 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S16 EP S16 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600042 ER PT J AU Beattie, MS Costantino, JP Vogel, V Wickerham, DL Wolmark, N Dowsett, M Folkerd, LJ Hankinson, SE Cummings, SR AF Beattie, MS Costantino, JP Vogel, V Wickerham, DL Wolmark, N Dowsett, M Folkerd, LJ Hankinson, SE Cummings, SR TI Endogenous sex hormones and response to tamoxifen: an ancillary study in the breast cancer prevention trial (P-01) SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ Calif San Francisco, San Francisco, CA 94143 USA. Univ Pittsburgh, Pittsburgh, PA USA. Harvard Univ, Boston, MA 02115 USA. Londons Royal Marsden Hosp, London, England. Natl Surg Adjuvant Breast & Bowel Project, Pittsburgh, PA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S14 EP S14 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600037 ER PT J AU Grubbs, CJ Steele, VE Lubet, RA AF Grubbs, CJ Steele, VE Lubet, RA TI Limited preventive efficacy of standard NSAIDS and specific COX-2 inhibitors in ER+ rat mammary cancers. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ Alabama, Birmingham, AL USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S158 EP S158 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600446 ER PT J AU Jones, LP Li, M Halama, ED Ma, YX Lubet, R Grubbs, C Deng, C Rosen, E Furth, PA Lombardi, CCC AF Jones, LP Li, M Halama, ED Ma, YX Lubet, R Grubbs, C Deng, C Rosen, E Furth, PA Lombardi, CCC TI Promotion of mammary cancer development by tamoxifen in a mouse model of Brca1-mutation related breast cancere SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Georgetown Univ, Washington, DC USA. NCI, NIH, Bethesda, MD 20892 USA. Univ Alabama, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S10 EP S10 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600027 ER PT J AU Korde, L Fears, T Wu, A Nomura, A West, D Pike, M Hoover, R Ziegler, R AF Korde, L Fears, T Wu, A Nomura, A West, D Pike, M Hoover, R Ziegler, R TI Adolescent and childhood soy intake and breast cancer risk in Asian-American women. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NCI, Bethesda, MD 20892 USA. Univ So Calif, Sch Med, Los Angeles, CA USA. Univ Hawaii, Honolulu, HI 96822 USA. No Calif Canc Ctr, Union City, CA USA. NR 0 TC 0 Z9 0 U1 2 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S149 EP S149 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600420 ER PT J AU Leighl, NB Warr, D Vandenberg, T Dent, S Tannock, IF Crump, M Tozer, R Dancey, J Moore, MJ AF Leighl, NB Warr, D Vandenberg, T Dent, S Tannock, IF Crump, M Tozer, R Dancey, J Moore, MJ TI Phase II study of perifosine in metastatic or advanced breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S67 EP S68 PG 2 WC Oncology SC Oncology GA 877SE UT WOS:000225589600185 ER PT J AU Lubet, RA Wang, Y Yao, R Grubbs, CJ Muccio, D You, M AF Lubet, RA Wang, Y Yao, R Grubbs, CJ Muccio, D You, M TI Effects of various doses of targretin or other RXR analogues on RNA expression following treatment of ER plus rat mammary cancers. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Natl Canc Inst, Bethesda, MD USA. Washington Univ, Sch Med, St Louis, MO USA. Univ Alabama, Birmingham, AL USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S158 EP S158 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600448 ER PT J AU Michalowska, AM Qiu, T Lee, E Medina, D Powell, JI Shih, JH Green, JE AF Michalowska, AM Qiu, T Lee, E Medina, D Powell, JI Shih, JH Green, JE TI Common mouse and human breast tumor signatures: microarray comparison between p53 knockout mouse tumors and human breast cancer SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NCI, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. UC Irvine, Irvine, CA USA. BCM, Houston, TX USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S25 EP S25 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600069 ER PT J AU Orzano, JA Prindiville, S Zujewski, J Eng-Wong, J Venzon, DJ Galbo, C Yao, J Korde, L Catherine, CK Bethesda, MD AF Orzano, JA Prindiville, S Zujewski, J Eng-Wong, J Venzon, DJ Galbo, C Yao, J Korde, L Catherine, CK Bethesda, MD TI Mammographic density is not modulated by raloxifene in pre-menopausal women at high-risk for invasive breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NCI, Bethesda, MD 20892 USA. Natl Naval Med Res Inst, Bethesda, MD USA. RI Venzon, David/B-3078-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S160 EP S160 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600453 ER PT J AU Overmoyer, B Silverman, P Leeming, R Shenk, R Dumadag, L Beman, M Chen, H Boothman, D AF Overmoyer, B Silverman, P Leeming, R Shenk, R Dumadag, L Beman, M Chen, H Boothman, D TI Induction of the prosurvival secretory clusterin protein as a marker of response after neoadjuvant docetaxel, with or without bevacizumab in patients with locally advanced breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ Hosp Cleveland, Cleveland, OH 44106 USA. NCI, CTEP, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S253 EP S253 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600720 ER PT J AU Overmoyer, B Silverman, P Leeming, R Shenk, R Lyons, J Jesberger, J Hartman, P Dumadag, L Chen, H AF Overmoyer, B Silverman, P Leeming, R Shenk, R Lyons, J Jesberger, J Hartman, P Dumadag, L Chen, H TI Phase II trial of neoadjuvant docetaxel with or without bevacizumab in patients with locally advanced breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ Hosp Cleveland, Cleveland, OH 44106 USA. NCI, CTEP, Bethesda, MD 20892 USA. NR 0 TC 13 Z9 14 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S106 EP S106 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600300 ER PT J AU Paik, S Shak, S Tang, G Kim, C Kim, W Baker, J Cronin, M Walker, M Watson, D Bryant, J Wolmark, N AF Paik, S Shak, S Tang, G Kim, C Kim, W Baker, J Cronin, M Walker, M Watson, D Bryant, J Wolmark, N TI Risk classification of breast cancer patients by the Recurrence Score assay: comparison to guidelines based on patient age, tumor size, and tumor grade SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NSABP, Pittsburgh, PA USA. Genom Hlth Inc, Redwood City, CA USA. NR 0 TC 1 Z9 2 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S21 EP S21 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600056 ER PT J AU Paik, S Shak, S Tang, G Kim, C Joo, H Baker, J Cronin, M Watson, D Braynt, J Costantino, J Wolmark, N AF Paik, S Shak, S Tang, G Kim, C Joo, H Baker, J Cronin, M Watson, D Braynt, J Costantino, J Wolmark, N TI Expression of the 21 genes in the Recurrence Score assay and prediction of clinical benefit from tamoxifen in NSABP study B-14 and chemotherapy in NSABP study B-20 SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NSABP, Pittsburgh, PA USA. Genom Hlth Inc, Redwood City, CA USA. NR 0 TC 23 Z9 24 U1 1 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S15 EP S15 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600040 ER PT J AU Royce, ME Baumgartner, KB Baumgartner, RN Wayne, S Hunt, WC Joste, N Ballard-Barbash, R AF Royce, ME Baumgartner, KB Baumgartner, RN Wayne, S Hunt, WC Joste, N Ballard-Barbash, R TI Factors influencing breast cancer prognosis: divergent patterns for Hispanic and non-Hispanic White women in New Mexico - the Health, Eating, Activity and Lifestyle (HEAL) Study. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ New Mexico, Albuquerque, NM 87131 USA. NCI, Bethesda, MD USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S99 EP S99 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600281 ER PT J AU Rugo, HS Yardley, D Tan-Chiu, E Brufsky, A Kaufman, P Paik, S Ulcickas-Yood, M Mayer, M Tripathy, D AF Rugo, HS Yardley, D Tan-Chiu, E Brufsky, A Kaufman, P Paik, S Ulcickas-Yood, M Mayer, M Tripathy, D TI registHER: Results from a prospective, longitudinal cohort study of women with HER2 positive metastatic breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 UCSF, Ctr Comprehens Canc, San Francisco, CA USA. Sarah Cannon Canc Ctr, Nashville, TN USA. Canc Res Network, Plantation, FL USA. Univ Pittsburgh, Ctr Canc, Pittsburgh, PA USA. Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA. Galt Associates, Sterling, VA USA. Univ Texas, SW Med Ctr, Dallas, TX USA. NSABP, Pittsburgh, PA USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S90 EP S90 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600254 ER PT J AU Uray, IP Seo, HS Kim, H William, L Johnson, K Brown, P AF Uray, IP Seo, HS Kim, H William, L Johnson, K Brown, P TI IGFBP6: an RXR-induced mediator of breast cancer chemoprevention. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Baylor Coll Med, Houston, TX 77030 USA. Ligand Pharmaceut Inc, San Diego, CA USA. NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S158 EP S158 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600447 ER PT J AU Wedam, SB Yang, X Low, JA Berman, A Choyke, P McCarthy, N Chow, C Steinberg, SM Swain, SM AF Wedam, SB Yang, X Low, JA Berman, A Choyke, P McCarthy, N Chow, C Steinberg, SM Swain, SM TI Effects of bevacizumab and chemotherapy on markers of angiogenesis in previously untreated patients with locally advanced or inflammatory breast cancer SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 NCI, NIH, Bethesda, MD 20892 USA. Univ Auckland, Auckland 1, New Zealand. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S142 EP S142 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600401 ER PT J AU Xu, L Wang, G Tang, N Nikolovska-Coleska, Z Wang, R Demchik, L Liu, M Zhang, M Roller, P Tomita, Y Yang, D Rae, J Lippman, ME Wang, S AF Xu, L Wang, G Tang, N Nikolovska-Coleska, Z Wang, R Demchik, L Liu, M Zhang, M Roller, P Tomita, Y Yang, D Rae, J Lippman, ME Wang, S TI Discovery and therapeutic potential of novel Bcl-2/Bcl-xL small-molecule inhibitors in human breast cancer. SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Meeting Abstract CT 27th Annual Charles A Colman San Antonio Breast Cancer Symposium CY DEC 08-11, 2004 CL San Antonio, TX C1 Univ Michigan, Ann Arbor, MI 48109 USA. NIH, Frederick, MD USA. George Washington Univ, Washington, DC USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PY 2004 VL 88 SU 1 BP S66 EP S66 PG 1 WC Oncology SC Oncology GA 877SE UT WOS:000225589600181 ER PT J AU Anderson, WF Althuis, MD Brinton, LA Devesa, SS AF Anderson, WF Althuis, MD Brinton, LA Devesa, SS TI Is male breast cancer similar or different than female breast cancer? SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE age-frequency distribution; estrogen receptor expression; incidence rates; male breast cancer ID END RESULTS DATABASE; UNITED-STATES; RISK-FACTORS; AGE-INCIDENCE; EPIDEMIOLOGY; CARCINOMA; SUSCEPTIBILITY; SURVEILLANCE; SURVIVAL; BRCA2 AB Objective. To determine if male breast carcinogenesis was similar to its more common female counterpart, we compared incidence patterns among men and women with breast cancer. Methods. Breast cancer records were obtained from the SEER database. Women were stratified by age < 50 and &GE; 50 years to simulate premenopausal and postmenopausal breast cancer. Results. Age-adjusted incidence trends were stable among men but increased among women. Male to female breast cancer ratio was higher for blacks than for whites. Favorable prognostic factors reflective of tumor biology ( nuclear grade and hormone receptor expression) were more common for men and postmenopausal women than for premenopausal women. For example, low nuclear grade, estrogen and progesterone receptor-positive expression were more common among men and postmenopausal women than among premenopausal women. The age-specific incidence rate curve for men increased steadily for all ages with a constant slope. On the other hand, age-specific rates for women increased rapidly until age 50 years then rose at a slower rate for postmenopausal women. Age-frequency distribution for male breast cancer was unimodal, with peak incidence at age 71 years. Age-frequency distribution for women was bimodal with early-onset and late-onset incidence at 52 and 71 years, respectively. Conclusions. Gender-specific incidence trends differed, most likely reflective of female-related changes in surveillance and/or reproductive risk factors. On the other hand, similar prognostic factor profiles reflective of tumor biology, age-specific incidence rate patterns, and age-frequency distributions suggested that male breast cancer was more like postmenopausal than premenopausal female breast cancer. C1 NCI, Div Canc Prevent, EPN, Bethesda, MD 20892 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Anderson, WF (reprint author), NCI, Div Canc Prevent, EPN, Room 2144,6130 Execut Blvd, Bethesda, MD 20892 USA. RI Brinton, Louise/G-7486-2015 OI Brinton, Louise/0000-0003-3853-8562 NR 33 TC 119 Z9 141 U1 1 U2 5 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD JAN PY 2004 VL 83 IS 1 BP 77 EP 86 DI 10.1023/B:BREA.0000010701.08825.2d PG 10 WC Oncology SC Oncology GA 760AN UT WOS:000187788200009 PM 14997057 ER PT J AU Shields, TS Falk, RT Herrero, R Schiffman, M Weiss, NS Bratti, C Rodriguez, AC Sherman, ME Burk, RD Hildesheim, A AF Shields, TS Falk, RT Herrero, R Schiffman, M Weiss, NS Bratti, C Rodriguez, AC Sherman, ME Burk, RD Hildesheim, A TI A case-control study of endogenous hormones and cervical cancer SO BRITISH JOURNAL OF CANCER LA English DT Article DE DHEAS; oestradiol; oestrone; oestrone sulphate; progesterone; SHBG; cervical neoplasia; case-control study ID HUMAN-PAPILLOMAVIRUS TYPE-16; MULTICENTRIC CASE-CONTROL; SQUAMOUS CARCINOGENESIS; COSTA-RICA; CONTRACEPTIVES; TRANSFORMATION; TESTOSTERONE; INFECTION; CELLS; RISK AB Both parity and oral contraceptive use are associated with elevated circulating levels of sex hormones, at least transiently, and with increased risk of cervical cancer in human papillomavirus (HPV)-infected women. We directly evaluated whether elevations in the physiologic levels of these hormones predispose to the development of cervical neoplasia. We identified 67 premenopausal and 43 postmenopausal women with cervical intraepithelial neoplasia 2, 3, or cervical cancer (greater than or equal toCIN2) diagnosed during enrollment of a population-based cohort of 10 077 women. Four controls, two chosen randomly and two chosen from women testing positive for cancer-associated HPV, were matched to each case on menopausal status, age, days since last menses (pre), or years since menopause (post). Sex hormone-binding globulin, oestradiol, oestrone, oestrone-sulphate, dehydroepiandrosterone sulphate, and progesterone were measured in enrollment plasma. There was no consistent association between the sex hormones and risk of greater than or equal toCIN2. Excluding cases with invasive disease had a minimal impact on results. Though this case-control study was based on a well-defined population, it was limited by reliance on a single measure of hormone levels taken at the time of diagnosis. Nonetheless, our results do not support the hypothesis that plasma levels of sex hormones have an important bearing on the risk of cervical neoplasia in HPV-infected women. C1 NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Rockville, MD 20852 USA. Fdn Costarricense Docencia Ciencias Salud, Proyecto Epidemiol Guanacaste, San Jose, Costa Rica. Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98195 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA. Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA. RP Shields, TS (reprint author), NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, 6120 Execut Blvd,MSC 7234, Rockville, MD 20852 USA. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X NR 19 TC 8 Z9 12 U1 0 U2 3 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD JAN 1 PY 2004 VL 90 IS 1 BP 146 EP 152 DI 10.1038/sj.bjc.66015 PG 7 WC Oncology SC Oncology GA 763PY UT WOS:000188096500026 PM 14710222 ER PT J AU Jemal, A Tiwari, RC Murray, T Ghafoor, A Samuels, A Ward, E Feuer, EJ Thun, MJ AF Jemal, A Tiwari, RC Murray, T Ghafoor, A Samuels, A Ward, E Feuer, EJ Thun, MJ TI Cancer statistics, 2004 SO CA-A CANCER JOURNAL FOR CLINICIANS LA English DT Article ID TRENDS; SURVEILLANCE; SURVIVAL; WHITES AB Each year, the American Cancer Society estimates the number of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival rates based on incidence data from the National Cancer Institute and mortality data from the National Center for Health Statistics. Incidence and mortality rates are age standardized to the 2000 US standard million population. A total of 1,368,030 new cancer cases and 563,700 deaths are expected in the United States in 2004. Incidence rates stabilized among men from 1995 through 2000 but continued to increase among females by 0.4% per year from 1987 through 2000. Mortality rates have decreased by 1.5% per year since 1992 among men, but have stabilized from 1998 through 2000 among women. Cancer death rates continued to decrease from the three major cancer sites in men (lung and bronchus, colon and rectum, and prostate) and from female breast and colorectal cancers in women. In analyses by race and ethnicity, African-American men and women have 40% and 20% higher death rates from all cancers combined compared with White men and women, respectively. Cancer incidence and mortality rates are lower in other racial and ethnic groups than in Whites and African Americans for all sites combined and for the four major cancer sites. However, these groups generally have higher rates for stomach, liver, and cervical cancers than do Whites. Furthermore, minority populations are more likely to be diagnosed with advanced stage disease than are Whites. Progress in reducing the burden from cancer can be accelerated by applying existing cancer control knowledge into practice among all segments of the population. C1 Amer Canc Soc, Dept Epidemiol & Surveillance Res, Atlanta, GA 30329 USA. NCI, Math Stat Stat Res & Applicat Branch, Div Canc Control & Populat Sci, Rockville, MD USA. RP Jemal, A (reprint author), Amer Canc Soc, Dept Epidemiol & Surveillance Res, Atlanta, GA 30329 USA. NR 15 TC 2741 Z9 2888 U1 4 U2 84 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0007-9235 J9 CA-CANCER J CLIN JI CA-Cancer J. Clin. PD JAN-FEB PY 2004 VL 54 IS 1 BP 8 EP 29 PG 22 WC Oncology SC Oncology GA 958XW UT WOS:000231482500005 PM 14974761 ER PT J AU Tiwari, RC Ghosh, K Jemal, A Hachey, M Ward, E Thun, MJ Feuer, EJ AF Tiwari, RC Ghosh, K Jemal, A Hachey, M Ward, E Thun, MJ Feuer, EJ TI A new method of predicting US and state-level cancer mortality counts for the current calendar year SO CA-A CANCER JOURNAL FOR CLINICIANS LA English DT Article AB Every January for more than 40 years, the American Cancer Society (ACS) has estimated the total number of cancer deaths that are expected to occur in the United States and individual states in the upcoming year. In a collaborative effort to improve the accuracy of the predictions, investigators from the National Cancer Institute and the ACS have developed and tested a new prediction method. The new method was used to create the mortality predictions for the first time in Cancer Statistics, 2004 and Cancer Facts & Figures 2004. The authors present a conceptual overview of the previous ACS method and the new state-space method (SSM), and they review the results of rigorous testing to determine which method provides more accurate predictions of the observed number of cancer deaths from the years 1997 to 1999. The accuracy of the methods was compared using squared deviations (the square of the predicted minus observed values) for each of the cancer sites for which predictions are published as well as for all cancer sites combined. At the national level, the squared deviations were not consistently lower for every cancer site for either method, but the average squared deviations (averaged across cancer sites, years, and sex) was substantially lower for the SSM than for the ACS method. During the period 1997 to 1999, the ACS estimates of deaths were usually greater than the observed numbers for all cancer sites combined and for several major individual cancer sites, probably because the ACS method was less sensitive to recent changes in cancer mortality rates (and associated counts) that occurred for several major cancer sites in the early and mid 1990s. The improved accuracy of the new method was particularly evident for prostate cancer, for which mortality rates changed dramatically in the late 1980s and early 1990s. At the state level, the accuracy of the two methods was comparable. Based on these results, the ACS has elected to use the new method for the annual prediction of the number of cancer deaths at the national and state levels. C1 NCI, Statist Res & Applicat Branch, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. George Washington Univ, Dept Stat, Washington, DC USA. Informat Management Serv Inc, Silver Spring, MD USA. Amer Canc Soc, Dept Epidemiol & Surveillance Res, Atlanta, GA 30329 USA. RP Tiwari, RC (reprint author), NCI, Statist Res & Applicat Branch, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. NR 16 TC 42 Z9 46 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0007-9235 J9 CA-CANCER J CLIN JI CA-Cancer J. Clin. PD JAN-FEB PY 2004 VL 54 IS 1 BP 30 EP 40 PG 11 WC Oncology SC Oncology GA 958XW UT WOS:000231482500006 PM 14974762 ER PT J AU Chaplet, N Detry, C Deroanne, C Fisher, LW Castronovo, V Bellahcene, A AF Chaplet, N. Detry, C. Deroanne, C. Fisher, L. W. Castronovo, V. Bellahcene, A. TI ZOLEDRONATE UP-REGULATES BONE SIALOPROTEIN EXPRESSION IN SAOS-2 CELLS THROUGH RHOA INHIBITION SO CALCIFIED TISSUE INTERNATIONAL LA English DT Meeting Abstract C1 [Chaplet, N.; Detry, C.; Castronovo, V.; Bellahcene, A.] Univ Liege, Metastasis Res Lab, Expt Canc Res Ctr, Liege, Belgium. [Fisher, L. W.] NIDCR, Craniofacial & Skeletal Dis Branch, NIH, HHS, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 2004 VL 74 BP S31 EP S31 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 460TI UT WOS:000267211300041 ER PT J AU Elefteriou, F Takeda, S Ebihara, K Magre, J Patano, N Kim, CA Ogawa, Y Liu, X Craigen, W Robert, J Vinson, C Nakao, K Capeau, J Karsenty, G AF Elefteriou, F. Takeda, S. Ebihara, K. Magre, J. Patano, N. Kim, C. Ae Ogawa, Y. Liu, X. Craigen, W. Robert, J. Vinson, C. Nakao, K. Capeau, J. Karsenty, G. TI BONE MASS VARIES IN MAMMALS ACCORDING TO SERUM LEPTIN LEVELS. SO CALCIFIED TISSUE INTERNATIONAL LA English DT Meeting Abstract C1 [Elefteriou, F.; Patano, N.; Liu, X.; Craigen, W.; Karsenty, G.] Baylor Coll Med, Houston, TX 77030 USA. [Takeda, S.; Ebihara, K.; Nakao, K.] Kyoto Univ, Grad Sch Med, Dept Med & Clin Sci, Kyoto, Japan. [Magre, J.; Robert, J.; Capeau, J.] Univ Paris 06, INSERM, U402, Paris, France. [Kim, C. Ae] Genet Inst Crianea, Sao Paulo, Brazil. [Ogawa, Y.] Tokyo Med & Dent Univ, Ctr Excellence, Program Frontier Res, Tokyo, Japan. [Vinson, C.] NCI, Biochem Lab, Bethesda, MD 20892 USA. RI MAGRE, Jocelyne/D-4788-2015 NR 0 TC 0 Z9 0 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PY 2004 VL 74 BP S106 EP S106 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 460TI UT WOS:000267211300323 ER PT J AU Lin, YW Aplan, PD AF Lin, YW Aplan, PD TI Leukemic transformation SO CANCER BIOLOGY & THERAPY LA English DT Review DE leukemia; mutation; proliferation; differentiation; leukemic transformation; genomic instability; enhanced proliferation; disrupted differentiation; molecular target ID BINDING-PROTEIN-ALPHA; ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; ACUTE PROMYELOCYTIC LEUKEMIA; STIMULATING FACTOR-RECEPTOR; PARTIAL-TANDEM DUPLICATION; BREAKPOINT CLUSTER REGION; RETINOIC ACID RECEPTOR; ABL TYROSINE KINASE; C/EBP-ALPHA AB Leukemia results from the uncontrolled accumulation of primitive, poorly differentiated blood cells, and is a consequence of the accumulation of mutations in hematopoietic precursor cells. These mutations include point mutations (single base pair insertions, deletions, or substitutions), gross chromosomal rearrangements such as deletions, insertions, amplifications, and translocations, and epigenetic changes. It seems likely that mutations affecting at least two pathways are required for the development of leukemia. One of these pathways regulates cell accumulation; the second regulates hematopoietic differentiation. Molecularly targeted therapy, which interrupts functions of the leukemogenic proteins generated by mutations, has been developed and shown to be effective for several forms of malignancy. Therefore, it is our hope and belief that a clearer understanding of the mechanism(s) that underlie leukemic transformation will lead to effective new therapies for this dreaded disease. C1 NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20889 USA. Kyoto Univ, Grad Sch Med, Dept Pediat, Sakyo Ku, Kyoto, Japan. RP Aplan, PD (reprint author), NCI, Genet Branch, Ctr Canc Res, NIH, Navy 8,Room 5105,8901 Wisconsin Ave, Bethesda, MD 20889 USA. EM aplanp@mail.nih.gov RI Aplan, Peter/K-9064-2016 NR 109 TC 13 Z9 13 U1 0 U2 0 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4047 J9 CANCER BIOL THER JI Cancer Biol. Ther. PD JAN PY 2004 VL 3 IS 1 BP 13 EP 20 DI 10.4161/cbt.3.1.537 PG 8 WC Oncology SC Oncology GA 805QF UT WOS:000220380100002 PM 14726677 ER PT J AU Fearnhead, HO AF Fearnhead, HO TI Getting back on track, or what to do when apoptosis is de-railed - Recoupling oncogenes to the apoptotic machinery SO CANCER BIOLOGY & THERAPY LA English DT Review DE tumorigenesis; oncogenes; apoptosis; caspase; therapy ID CYTOCHROME-C RELEASE; BCL-2 ANTISENSE OLIGONUCLEOTIDE; CANCER CELL-LINES; NF-KAPPA-B; DEPENDENT CASPASE ACTIVATION; ENDOPLASMIC-RETICULUM CA2+; STRESS-INDUCED APOPTOSIS; MYC-INDUCED APOPTOSIS; WD-40 REPEAT REGION; STRUCTURAL BASIS AB Programmed cell death or apoptosis is of fundamental importance to cancer as it both limits tumorigenesis and is also triggered by many cancer chemotherapeutics. Many oncogenes that deregulate the cell cycle also trigger apoptosis, so eliminating cells that are proliferating inappropriately. To acquire a complete neoplastic phenotype, cancer cells often acquire mutations that compromise the apoptotic process, allowing these cells to escape both normal growth constraints but to also become resistant to many anti-cancer drugs and leading to the emergence of drug-resistant malignancies. Thus discovering how oncogenes are coupled to apoptosis and how these links are compromised in cancer is central to both understanding cancer progression and developing new therapies to counter chemo-resistant cancers. This review will consider how oncogenes activate apoptosis and how this response is subverted in cancer cells with a focus on the proposed therapeutic strategies that exploit these changes. C1 NCI, Apoptosis Sect, Regulat Cell Growth Lab, Frederick, MD 21702 USA. RP Fearnhead, HO (reprint author), NCI, Apoptosis Sect, Regulat Cell Growth Lab, Bldg 560,Room 22-90C, Frederick, MD 21702 USA. EM hfearnhead@ncifcrf.gov RI Fearnhead, Howard/D-4826-2012; OI Fearnhead, Howard/0000-0002-8054-9794 NR 157 TC 2 Z9 3 U1 0 U2 3 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4047 J9 CANCER BIOL THER JI Cancer Biol. Ther. PD JAN PY 2004 VL 3 IS 1 BP 21 EP 28 DI 10.4161/cbt.3.1.538 PG 8 WC Oncology SC Oncology GA 805QF UT WOS:000220380100003 PM 14726669 ER PT J AU Maxwell, P Salnikow, K AF Maxwell, P Salnikow, K TI HIF-1 - An oxygen and metal responsive transcription factor SO CANCER BIOLOGY & THERAPY LA English DT Review DE HIF-1 transcription factor; VHL; nickel; cobalt; hypoxia ID HYPOXIA-INDUCIBLE FACTOR; FACTOR-STIMULATED TRANSCRIPTION; NICKEL-INDUCED TRANSFORMATION; ENDOTHELIAL GROWTH-FACTOR; HIPPEL-LINDAU PROTEIN; FACTOR-I; GENE-EXPRESSION; ERYTHROPOIETIN GENE; EPITHELIAL-CELLS; PROLYL HYDROXYLATION/ AB Normal development and function of metazoan organisms depend on oxygen availability. The level of oxygen can be sensed by individual cells, which respond to reduced oxygenation (hypoxia) largely through activation of hypoxia-inducible factor-1 (HIF-1). At the organism level the response to hypoxia involves an increase in red blood cell production. Within tissues, HIF activation increases the blood supply and blood vessel growth. At the individual cell level it is manifested as an increase in anaerobic metabolism in order to sustain basic cellular functions. Iron is central to the oxygen sensing mechanism, and sensitivity to other metals, namely cobalt and nickel, is a distinctive feature of the HIF system; in fact, this is often used as an initial way of implicating HIF-1 in a biological response. Historically, the fact that nickel or cobalt mimicked hypoxia provided an important clue as to the nature of the oxygen sensing mechanism. It also raises the possibility that nickel or cobalt exposure may have important toxic and pathological effects mediated by HIF activation. Here we review the implications of the metal sensitivity of the HIF-1 system, and examine the hypothesis that HIF-1 activation may play an important role in metal induced carcinogenesis. C1 NCI, Frederick, MD 21701 USA. Univ London Imperial Coll Sci Technol & Med, London, England. RP Salnikow, K (reprint author), NCI, Bldg 538,Room 205 E, Frederick, MD 21701 USA. EM salnikow@ncifcrf.gov RI Maxwell, Patrick/C-5557-2008 OI Maxwell, Patrick/0000-0002-0338-2679 NR 100 TC 127 Z9 133 U1 1 U2 12 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4047 J9 CANCER BIOL THER JI Cancer Biol. Ther. PD JAN PY 2004 VL 3 IS 1 BP 29 EP 35 DI 10.4161/cbt.3.1.547 PG 7 WC Oncology SC Oncology GA 805QF UT WOS:000220380100004 PM 14726713 ER PT J AU Smith, AP Weeraratna, AT Spears, JR Meltzer, PS Becker, D AF Smith, AP Weeraratna, AT Spears, JR Meltzer, PS Becker, D TI SAGE identification and fluorescence imaging analysis of genes and transcripts in melanomas and precursor lesions SO CANCER BIOLOGY & THERAPY LA English DT Article DE SAGE; fluorescence imaging; nevi; melanomas ID FIBROBLAST GROWTH-FACTOR; MALIGNANT MELANOMAS; HUMAN MELANOCYTES; TUMOR-GROWTH; EXPRESSION; CELLS; PROLIFERATION; PROGRESSION; ASSOCIATION; INHIBITION AB Melanomas of sporadic and familial origin develop in a stepwise fashion in approximately 40-80% of all cases; yet, the genetic events governing the progression from nevocytic precursor lesions to early and advanced-stage melanomas remain largely unknown. In the present study, we provide an analysis of genes that were identified in four recently generated primary and metastatic melanoma Serial Analysis of Gene Expression (SAGE) libraries. In addition to SAGE tags corresponding to transcripts with unknown function, or to unidentified transcripts, known genes were identified that hitherto have not been shown to be expressed or have a function in early and advanced-stage melanomas and/or melanoma precursor lesions. Conducting fluorescence imaging analysis with cyanine dye-conjugated antibodies and oligonucleotides, we established the expression pattern of ATM, HEl10, PKD1, KAl11, IL-10R, and hypothetical protein FLA 1151 in nevus and melanoma specimens. C1 Univ Pittsburgh, Dept Pathol, Pittsburgh, PA 15213 USA. NIH, Immunol Lab, Baltimore, MD USA. NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA. RP Becker, D (reprint author), Univ Pittsburgh, Dept Pathol, HCC Res Pavil,Suite 1-46A,5117 Ctr Ave, Pittsburgh, PA 15213 USA. EM dbecker@pitt.edu NR 23 TC 18 Z9 18 U1 0 U2 1 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4047 J9 CANCER BIOL THER JI Cancer Biol. Ther. PD JAN PY 2004 VL 3 IS 1 BP 104 EP 109 DI 10.4161/cbt.3.1.661 PG 6 WC Oncology SC Oncology GA 805QF UT WOS:000220380100022 PM 14726694 ER PT J AU Schimmer, AD Welsh, K Pinilla, C Wang, ZL Krajewska, M Bonneau, MJ Pedersen, IM Kitada, S Scott, FL Bailly-Maitre, B Glinsky, G Scudiero, D Sausville, E Salvesen, G Nefzi, A Ostresh, JM Houghten, RA Reed, JC AF Schimmer, AD Welsh, K Pinilla, C Wang, ZL Krajewska, M Bonneau, MJ Pedersen, IM Kitada, S Scott, FL Bailly-Maitre, B Glinsky, G Scudiero, D Sausville, E Salvesen, G Nefzi, A Ostresh, JM Houghten, RA Reed, JC TI Small-molecule antagonists of apoptosis suppressor XIAP exhibit broad antitumor activity SO CANCER CELL LA English DT Article ID STRUCTURAL BASIS; LUNG-CANCER; COMBINATORIAL LIBRARIES; CASPASE ACTIVATION; PROTEIN XIAP; INHIBITOR; IAP; SMAC/DIABLO; EXPRESSION; CELLS AB Apoptosis resistance commonly occurs in cancers, preventing activation of Caspase family cell death proteases. XIAP is an endogenous inhibitor of Caspases overexpressed in many cancers. We developed an enzyme derepression assay, based on overcoming XIAP-mediated suppression of Caspase-3, and screened mixture-based combinatorial chemical libraries for compounds that reversed XIAP-mediated inhibition of Caspase-3, identifying a class of polyphenylureas with XIAP-inhibitory activity. These compounds, but not inactive structural analogs, stimulated increases in Caspase activity, directly induced apoptosis of many types of tumor cell lines in culture, and sensitized cancer cells to chemotherapeutic drugs. Active compounds also suppressed growth of established tumors in xenograft models in mice, while displaying little toxicity to normal tissues. These findings validate IAPs as targets for cancer drug discovery. C1 Torres Pines Inst Mol Studies, San Diego, CA 92121 USA. Burnham Inst, La Jolla, CA 92037 USA. Sidney Kimmel Canc Ctr, La Jolla, CA 92037 USA. NCI, Bethesda, MD 20817 USA. RP Reed, JC (reprint author), Torres Pines Inst Mol Studies, San Diego, CA 92121 USA. EM jreed@burnham.org FU NCI NIH HHS [CA78040, CA89827]; NIA NIH HHS [AG15402] NR 45 TC 324 Z9 337 U1 2 U2 13 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1535-6108 J9 CANCER CELL JI Cancer Cell PD JAN PY 2004 VL 5 IS 1 BP 25 EP 35 DI 10.1016/S1535-6108(03)00332-5 PG 11 WC Oncology; Cell Biology SC Oncology; Cell Biology GA 766XH UT WOS:000188400300007 PM 14749124 ER PT J AU Alberg, AJ Daudt, A Huang, HY Hoffman, SC Comstock, GW Helzlsouer, KJ Strickland, PT Bell, DA AF Alberg, AJ Daudt, A Huang, HY Hoffman, SC Comstock, GW Helzlsouer, KJ Strickland, PT Bell, DA TI N-acetyltransferase 2 (NAT2) genotypes, cigarette smoking, and the risk of breast cancer SO CANCER DETECTION AND PREVENTION LA English DT Article DE breast cancer; neoplasms; epidemiology; N-acetyltransferase 2; cigarette smoking; acetylation ID DNA-ADDUCTS; GENETIC POLYMORPHISMS; HETEROCYCLIC AMINES; ACETYLATOR GENOTYPE; ASSOCIATION; WOMEN; CARCINOGENESIS; POPULATION; INCREASE; TISSUE AB N-acetyltransferases (NATs) are important catalytic enzymes that metabolize carcinogenic arylamines. NAT2 genotype might modify the role of cigarette smoking, a source of arylamine exposure, in breast cancer. We conducted a nested case-control study to investigate the association between NAT2 genotype, smoking and breast cancer risk among women (I 10 cases, 113 matched controls) from the CLUE II cohort in Washington County, MD. Compared to women with the slow acetylator genotype, the main effects odds ratios (OR) for NAT2 were 1.4 for the intermediate acetylator genotype (95% confidence limits (CL) 0.7, 2.7) and 3.6 for the homozygous rapid acetylator genotype (95% CL 1.1, 11.4) (P for trend = 0.05). Smoking was associated in the direction of increased breast cancer risk in slow acetylators (e.g., >15 pack-years versus never smokers OR 2.0; 95% CL 0.7, 5.8) but not in rapid acetylators. These associations were not statistically significant in the total study population, but a statistically significant interaction between smoking and NAT2 acetylator status was present in postmenopausal women. The main effect of NAT2 in the direction of increased risk suggests that exposures to NAT2-activated carcinogens other than cigarette smoke may be important in this study population. The results for smoking were consistent with an inactivation role for NAT2 in breast cancer. (C) 2004 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved. C1 Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA. Johns Hopkins Bloombreg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. RP Alberg, AJ (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Room E6132B,615 N Wolfe St, Baltimore, MD 21205 USA. EM aalberg@jhsph.edu FU NCI NIH HHS [CA62988, CA73790, U01 CA86308]; NHLBI NIH HHS [HL21670]; NIEHS NIH HHS [ES06052, P30 ES03819] NR 26 TC 23 Z9 24 U1 0 U2 1 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0361-090X J9 CANCER DETECT PREV JI Cancer Detect. Prev. PY 2004 VL 28 IS 3 BP 187 EP 193 DI 10.1016/j.cdp.2004.04.001 PG 7 WC Oncology SC Oncology GA 839GZ UT WOS:000222773100004 PM 15225898 ER PT J AU Gammon, MD Terry, MB Arber, N Chow, WH Risch, HA Vaughan, TL Schoenberg, JB Mayne, ST Stanford, JL Dubrow, R Rotterdam, H West, AB Fraumeni, JF Weinstein, IB Hibshoosh, H AF Gammon, MD Terry, MB Arber, N Chow, WH Risch, HA Vaughan, TL Schoenberg, JB Mayne, ST Stanford, JL Dubrow, R Rotterdam, H West, AB Fraumeni, JF Weinstein, IB Hibshoosh, H TI Nonsteroidal anti-inflammatory drug use associated with reduced incidence of adenocarcinomas of the esophagus and gastric cardia that overexpress cyclin D1: A population-based study SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID BODY-MASS INDEX; BARRETTS-ESOPHAGUS; BREAST-CANCER; GASTROESOPHAGEAL-REFLUX; SULINDAC SULFIDE; CELL-LINES; RISK; PROLIFERATION; EXPRESSION; PROTEINS AB This study was undertaken to determine whether selected risk factors for esophageal and gastric cancer are associated with tumors that overexpress cyclin D1. Archived tumor tissue was available for 630 esophageal and gastric cancer patients who participated in a population-based case-control study. Patients were categorized into case groups based on whether protein overexpression of the cyclin D1 gene, as assessed by immunohistochemistry, was present (cyclin D1+, n=285) or not (cyclin D1-, n=345) in the tumor. The distribution of risk factors in each of these case groups was then compared with the distribution among the 695 controls. Multivariate-adjusted odds ratios (OR) for esophageal adenocarcinoma were reduced in relation to use of aspirin and other nonsteroidal anti-inflammatory drug (NSAID) use but only among patients with cyclin D1+ tumors (0.45, 95% confidence interval [C1]=0.26, 0.79) and not among those with cyclin D1- tumors (1.12, 95% CI=0.67, 1.86). A similar pattern was observed for gastric cardia adenocarcinomas. In contrast, ORs for esophageal squamous cell carcinoma and noncardia gastric adenocarcinomas in relation to NSAID use were reduced, regardless of cyclin D1 status. ORs did not vary with cyclin D1 status in relation to alcohol, body size, or cigarette smoking, with the following exception; for noncardia gastric adenocarcinomas the cyclin D1-tumors showed a 2-fold elevation in the OR with ever smoking. These data suggest that the reduction in risk associated with NSAID use may be restricted to those esophageal and gastric cardia adenocarcinomas that overexpress cyclin D1. C1 Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA. Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10027 USA. Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10027 USA. Columbia Univ, Herbert Irving Canc Ctr, New York, NY 10027 USA. Tel Aviv Sourasky Med Ctr, Dept Gastroenterol, IL-69978 Tel Aviv, Israel. NCI, Div Epidemiol & Genet, Bethesda, MD 20892 USA. Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA. Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA. Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98195 USA. New Jersey Dept Hlth & Senior Serv, Appl Canc Epidemiol Program, Trenton, NJ USA. NYU, Dept Pathol, New York, NY 10016 USA. RP Gammon, MD (reprint author), Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, CB 7435 McGavran Greenberg Hall, Chapel Hill, NC 27599 USA. EM gammon@unc.edu FU NIEHS NIH HHS [P30ES10126] NR 27 TC 26 Z9 28 U1 0 U2 2 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 2004 VL 13 IS 1 BP 34 EP 39 DI 10.1158/1055-9965.EPI-03-0198 PG 6 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 767KG UT WOS:000188438300008 PM 14744730 ER PT J AU Mannisto, S Smith-Warner, SA Spiegelman, D Albanes, D Anderson, K van den Brandt, PA Cerhan, JR Colditz, G Feskanich, D Freudenheim, JL Giovannucci, E Goldbohm, RA Graham, S Miller, AB Rohan, TE Virtamo, J Willett, WC Hunter, DJ AF Mannisto, S Smith-Warner, SA Spiegelman, D Albanes, D Anderson, K van den Brandt, PA Cerhan, JR Colditz, G Feskanich, D Freudenheim, JL Giovannucci, E Goldbohm, RA Graham, S Miller, AB Rohan, TE Virtamo, J Willett, WC Hunter, DJ TI Dietary carotenoids and risk of lung cancer in a pooled analysis of seven cohort studies SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID FOOD-FREQUENCY QUESTIONNAIRE; YORK-STATE COHORT; BETA-CAROTENE; BREAST-CANCER; CARDIOVASCULAR-DISEASE; WOMENS-HEALTH; VITAMIN-A; ASSESSMENT INSTRUMENTS; SERUM MICRONUTRIENTS; COMPOSITION DATABASE AB Intervention trials with supplemental beta-carotene have observed either no effect or a harmful effect on lung cancer risk. Because food composition databases for specific carotenoids have only become available recently, epidemiological evidence relating usual dietary levels of these carotenoids with lung cancer risk is limited. We analyzed the association between lung cancer risk and intakes of specific carotenoids using the primary data from seven cohort studies in North America and Europe. Carotenoid intakes were estimated from dietary questionnaires administered at baseline in each study. We calculated study-specific multivariate relative risks (RRs) and combined these using a random-effects model. The multivariate models included smoking history and other potential risk factors. During follow-up of up to 7-16 years across studies, 3,155 incident lung cancer cases were diagnosed among 399,765 participants. beta-Carotene intake was not associated with lung cancer risk (pooled multivariate RR = 0.98; 95% confidence interval, 0.87-1.11; highest versus lowest quintile). The RRs for alpha-carotene, lutein/zeaxanthin, and lycopene were also close to unity. beta-Cryptoxanthin intake was inversely associated with lung cancer risk (RR = 0.76; 95% confidence interval, 0.67-0.86; highest versus lowest quintile). These results did not change after adjustment for intakes of vitamin C (with or without supplements), folate (with or without supplements), and other carotenoids and multivitamin use. The associations generally were similar among never, past, or current smokers and by histological type. Although smoking is the strongest risk factor for lung cancer, greater intake of foods high in P-cryptoxanthin, such as citrus fruit, may modestly lower the risk. C1 Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland. NCI, Div Clin Sci, Canc Prevent Studies Branch, Bethesda, MD 20892 USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. Maastricht Univ, Dept Epidemiol, Maastricht, Netherlands. Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA. Harvard Univ, Ctr Canc Prevent, Boston, MA 02115 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Channing Lab, Cambridge, MA 02138 USA. SUNY Buffalo, Univ Buffalo, Dept Social & Prevent Med, Buffalo, NY 14222 USA. TNO, Nutr & Food Res Inst, Dept Epidemiol, NL-3700 AJ Zeist, Netherlands. Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada. Deutsch Krebsforschungszentrum, Div Clin Epidemiol, D-6900 Heidelberg, Germany. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. RP Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave, Boston, MA 02115 USA. RI Albanes, Demetrius/B-9749-2015; Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NCI NIH HHS [CA55075, CA78548] NR 75 TC 105 Z9 109 U1 0 U2 9 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1055-9965 EI 1538-7755 J9 CANCER EPIDEM BIOMAR JI Cancer Epidemiol. Biomarkers Prev. PD JAN PY 2004 VL 13 IS 1 BP 40 EP 48 DI 10.1158/1055-9965.EPI-038-3 PG 9 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 767KG UT WOS:000188438300009 PM 14744731 ER PT J AU Alguacil, J Silverman, DT AF Alguacil, J Silverman, DT TI Smokeless and other noncigarette tobacco use and pancreatic cancer: A case-control study based on direct interviews SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID CIGAR SMOKING; DIAGNOSTIC CERTAINTY; MEDICAL HISTORY; RISK; MEN; COFFEE; 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE; CONSUMPTION; INDUCTION; ALCOHOL AB Cigarette smoking is an important and well-established cause of pancreatic cancer. In contrast, little is known about the effects of smoking cigars, pipes, and use of smokeless tobacco on pancreatic cancer risk. The objective of the present study was to examine the association between noncigarette tobacco use (i.e., Cigars, pipes, smokeless tobacco) and pancreatic cancer risk among nonsmokers of cigarettes. A population-based case-control study of pancreatic cancer was conducted during 1986-1989 among residents of Atlanta, Georgia, Detroit, Michigan, and 10 counties in New Jersey. Direct interviews were successfully completed with 526 newly diagnosed pancreatic cancer patients and 2153 controls ages 30-79 years. This analysis was restricted to lifelong nonsmokers of cigarettes and based on interviews with 154 cases newly diagnosed with carcinoma of the exocrine pancreas and 844 population controls who reported no history of cigarette smoking. We observed a consistent pattern of increased risk associated with cigar smoking, although these elevations were not statistically significant. Participants who smoked cigars regularly (i.e., at least one cigar/week for greater than or equal to 6 months) experienced a 70% increased risk [95% confidence interval (Cl): 0.9-3.3], and those who never used other form of tobacco had a 90% increased risk (95% CI: 0.8-4.3). Risk was elevated among those who smoked more than one cigar/day [odds ratio (OR) = 1.8; 95% CI: 0.8-4.2) and among those who smoked cigars > 20 years (OR = 1.9; 95% CI: 0.9-3.9). Trends in risk with increasing amount and duration smoked were consistent but not statistically significant (P = 0.17 and P = 0.16, respectively). Subjects who used smokeless tobacco regularly had a 40% increased risk of pancreatic cancer (95% CI: 0.5-3.6) compared with nonusers of tobacco. We observed a marginally significant increasing risk with increased use of smokeless tobacco (P = 0.04); participants who used >2.5 oz of smokeless tobacco a week had an OR of 3.5 (95% CI: Long-term use of smokeless tobacco (i.e., >20 years) was also associated with a nonsignificant increased risk (OR = 1.5; 95% CI: 0.6-4.0). In contrast, pipe smokers experienced no increased risk (OR = 0.6; 95% CI: 0.1-2.8). Our results suggest that heavy use of smokeless tobacco, and to a lesser extent, cigar smoking may increase the risk of pancreatic cancer among nonsmokers of cigarettes. C1 NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA. RP Silverman, DT (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 6120 Execut Blvd,EPS 8108, Rockville, MD 20852 USA. EM silvermd@mail.nih.gov FU NCI NIH HHS [N01-CP-51090, N01-CN-31022, N01-CN-05225, N01-CN-05227, N01-CP51089, N01-CP51092] NR 26 TC 43 Z9 46 U1 0 U2 4 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 2004 VL 13 IS 1 BP 55 EP 58 DI 10.1158/1055-9965.EPI-03-0033 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 767KG UT WOS:000188438300011 PM 14744733 ER PT J AU Tseng, M Breslow, RA DeVellis, RF Ziegler, RG AF Tseng, M Breslow, RA DeVellis, RF Ziegler, RG TI Dietary patterns and prostate cancer risk in the national health and nutrition examination survey epidemiological follow-up study cohort SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID VITAMIN-D; ULTRAVIOLET-RADIATION; COLON-CANCER; BREAST; HYPOTHESIS; MORTALITY; PRODUCTS; CALCIUM; ALCOHOL; FAT AB Ecological studies implicate a "Western" diet in prostate cancer development, but whether dietary patterns measured in individuals are associated with risk has not been studied previously. We examined this issue using prospective data from the nationally representative United States Health Examination Epidemiological Follow-up Study. Among 3,779 men followed from 1982-84 to 1992, 136 incident cases were identified. Using principal component analysis on responses to a 105-item dietary questionnaire, the following three distinct patterns were identified: a vegetable-fruit pattern; a red meat-starch pattern characterized by red meats, potatoes, cheese, salty snacks, and desserts; and a Southern pattern characterized by such foods as cornbread, grits, sweet potatoes, okra, beans, and rice. In adjusted proportional hazards models, prostate cancer risk was not associated with the vegetable-fruit or red meat-starch pattern, but higher intake of the Southern pattern showed a reduction in risk (3rd versus 1st tertile relative risk, 0.6; 95% confidence interval, 0.4-1.1; trend P = 0.08) that approached statistical significance. The inverse association was observed in black and non-black men and was not attributable to intake of any individual foods or nutrients. A Southern dietary pattern may reflect a history of living in the South and serve as an integrative marker of sunlight exposure and protection through 1,25-dihydroxyvitamin D production. Further evaluation and better characterization of the pattern would offer more information on potentially beneficial features of the diet or its associated lifestyle. C1 Fox Chase Canc Ctr, Div Populat Sci, Philadelphia, PA 19111 USA. NIAAA, Bethesda, MD USA. Univ N Carolina, Dept Hlth Behav & Hlth Educ, Chapel Hill, NC USA. NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Tseng, M (reprint author), Fox Chase Canc Ctr, Div Populat Sci, 333 Cottman Ave, Philadelphia, PA 19111 USA. EM m_tseng@fccc.edu RI Tseng, Marilyn/B-9334-2016 OI Tseng, Marilyn/0000-0002-9969-9055 FU NCI NIH HHS [CA-06927] NR 53 TC 51 Z9 53 U1 0 U2 2 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 2004 VL 13 IS 1 BP 71 EP 77 DI 10.1158/1055-9965.EPI-03-0076 PG 7 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 767KG UT WOS:000188438300014 PM 14744736 ER PT J AU Habermann, JK Hellman, K Freitag, S Heselmeyer-Haddad, K Hellstrom, AC Shah, K Auer, G Ried, T AF Habermann, JK Hellman, K Freitag, S Heselmeyer-Haddad, K Hellstrom, AC Shah, K Auer, G Ried, T TI A recurrent gain of chromosome arm 3q in primary squamous carcinoma of the vagina SO CANCER GENETICS AND CYTOGENETICS LA English DT Article ID COMPARATIVE-GENOMIC-HYBRIDIZATION; HIGH GENETIC INSTABILITY; INVASIVE-CARCINOMA; CERVICAL-CARCINOMA; CANCER; ABERRATIONS; NEOPLASMS; REVEALS; PATTERN; TUMORS AB Primary carcinomas of the vagina are rare tumors, accounting for 2%-3% of all gynecologic malignancies. Only a few karyotypes based on chromosome banding techniques have been reported. We have, therefore, used comparative genomic hybridization to establish a pattern of genomic imbalances in vaginal squamous cell carcinomas. Analysis of 16 formalin-fixed and paraffin-embedded tumors revealed that 70% of vaginal carcinomas carry relative copy number increases that map to chromosome arm 3q. Other recurring gains were observed on chromosome arms 5p and 19p. Chromosomal losses were infrequent. Most tumors were aneuploid, as measured by image cytometry on Feulgen-stained tissue sections. The cytogenetic data were related to the presence of human papillomavirus genomes, expression of laminin-5 as a marker for invasiveness, and expression levels of markers for proliferative activity and mutated TP53. All relevant clinical data were recorded. The results suggest that vaginal carcinomas are defined by a specific distribution of chromosomal aneuploidies and that the pattern of genomic imbalances is strikingly similar to that observed in squamous cell carcinomas of the uterine cervix. Age at diagnosis (P = 0.031), tumor size (P = 0.025), and increased laminin-5 expression (P = 0.006) have a significant influence on the survival time. (C) 2004 Elsevier Inc. All rights reserved. C1 NCI, Genet Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. Karolinska Inst, Ctr Canc, Stockholm, Sweden. Karolinska Hosp, Radiumhemmet, Dept Gynecol Oncol, S-10401 Stockholm, Sweden. Univ Hosp Schleswig Holstein, Inst Med Informat & Stat, Kiel, Germany. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Baltimore, MD USA. RP Ried, T (reprint author), NCI, Genet Lab, Ctr Canc Res, NIH, Bldg 50,Room 1408,50 South Dr, Bethesda, MD 20892 USA. RI Habermann, Jens/E-2968-2010; Hellman, Kristina/Q-2154-2015; OI Hellstrom, Ann/0000-0002-9259-1244 NR 28 TC 15 Z9 15 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0165-4608 J9 CANCER GENET CYTOGEN JI Cancer Genet. Cytogenet. PD JAN 1 PY 2004 VL 148 IS 1 BP 7 EP 13 DI 10.1016/S0165-4608(03)00245-0 PG 7 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA 760HD UT WOS:000187804800002 PM 14697635 ER PT J AU Thomas, GR Chen, Z Leukinova, E Van Waes, C Wen, J AF Thomas, GR Chen, Z Leukinova, E Van Waes, C Wen, J TI Cytokines IL-1 alpha, IL-6, and GM-CSF constitutively secreted by oral squamous carcinoma induce down-regulation of CD80 costimulatory molecule expression: restoration by interferon gamma SO CANCER IMMUNOLOGY IMMUNOTHERAPY LA English DT Article DE cytokines; IFN-gamma; CD80; squamous cell carcinoma; regulation ID COLONY-STIMULATING FACTOR; CELL CARCINOMAS; NECK-CANCER; T-CELLS; DENDRITIC CELLS; CO-STIMULATION; MURINE MODEL; B-CELLS; HEAD; PROMOTES AB We previously characterized the expression of CD80 in different murine head and neck squamous cell carcinoma (HNSCC) clones derived following tumor progression in the absence of T cell-mediated immunity in severe combined immunodeficient (SCID) mice. We found that HNSCCs that did not express CD80 grew as progressors, while those that expressed CD80 were regressors when grown in immune-competent animals. In the present study, we characterized expression of a repertoire of immunoregulatory cytokines in these HNSCC lines, and found that HNSCCs that express cytokines IL-1alpha, IL-6, and GM-CSF do not express CD80, suggesting the hypothesis that these cytokines may down-modulate expression of CD80. Cytokine-conditioned medium from progressor HNSCC and recombinant IL-1alpha, IL-6, and GM-CSF caused a reduction of CD80 expression in regressor HNSCCs without affecting proliferation. Conversely, the decrease in CD80 expression in progressor HNSCCs could be restored by IFN-gamma, a known inducer of CD80 expression. These data strongly suggest that high levels of cytokines IL-1alpha, IL-6, and GM-CSF expressed by tumor cells can down-regulate CD80 expression in HNSCC, and that IFN-gamma can independently stimulate expression. These data provide evidence for a novel mechanism of cytokine-mediated down-modulation of CD80 during malignant progression of HNSCC that can be restored by IFN-gamma. C1 Univ Miami, Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA. NIDCD, Tumor Biol Sect, NIH, Bethesda, MD USA. RP Thomas, GR (reprint author), Univ Miami, Sch Med, Sylvester Comprehens Canc Ctr, Papanicolau Bldg,1550 NW 10th Ave,Room 214, Miami, FL 33136 USA. NR 33 TC 28 Z9 29 U1 0 U2 4 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0340-7004 J9 CANCER IMMUNOL IMMUN JI Cancer Immunol. Immunother. PD JAN PY 2004 VL 53 IS 1 BP 33 EP 40 DI 10.1007/s00262-003-0433-4 PG 8 WC Oncology; Immunology SC Oncology; Immunology GA 752BD UT WOS:000187125800004 PM 14551747 ER PT J AU Buetow, KH AF Buetow, KH TI The NCI Center for Bioinformatics (NCICB): Building a foundation for in silico biomedical research SO CANCER INVESTIGATION LA English DT Article DE NCICB; bioinformatics; cancer C1 NCI, Ctr Bioinformat, Bethesda, MD 20892 USA. RP Buetow, KH (reprint author), NCI, Ctr Bioinformat, 6116 Execut Blvd, Bethesda, MD 20892 USA. EM buetowk@nih.gov NR 0 TC 2 Z9 2 U1 0 U2 0 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 2004 VL 22 IS 1 BP 117 EP 122 DI 10.1081/CNV-120027586 PG 6 WC Oncology SC Oncology GA 807DZ UT WOS:000220483500012 PM 15069769 ER PT J AU Sparber, A Ford, D Kvochak, PA AF Sparber, A Ford, D Kvochak, PA TI National Institutes of Health's Clinical Center sets new policy on use of herbal and other alternative supplements by patients enrolled in clinical trials SO CANCER INVESTIGATION LA English DT Article DE herbal; alternative; supplements ID ST JOHNS WORT; MEDICINE; THERAPIES; ADULTS; CANCER AB The nationwide concern over the escalating use of herbal and other alternative dietary supplements is prompting a call for action in health care organizations. Not only is there mounting evidence to support a strong concern for patient safety, but the use of these products by people participating in biomedical research protocols has an added impact on the integrity of the research design and data gathering. These issues are of increasing concern to the National Institutes of Health's hospital for. biomedical research, the Warren Grant Magnuson Clinical Center. Surveys completed in 2000 showed that 25-45% of Clinical Center patients reported taking herbal and other alternative dietary supplements. In 2001, the Clinical Center moved forward to develop and implement a policy to guide hospital staff in the management of patient use of herbal and alternative supplements. The policy established the requirement for all patients to be screened for supplement use upon admission or outpatient visit. Continued use of supplement products during hospitalization and/or outpatient enrollment on protocol require a physician's authorizing order. The implementation of this policy has increased awareness and provided an important step forward in protecting patient safety and preserving the scientific. integrity of the research at the NIH's Clinical Center. C1 NIH, Ctr Clin, Bethesda, MD 20892 USA. RP Ford, D (reprint author), NIH, Ctr Clin, Bethesda, MD 20892 USA. EM dford@mail.cc.nih.gov NR 20 TC 4 Z9 4 U1 3 U2 4 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 2004 VL 22 IS 1 BP 132 EP 137 DI 10.1081/CNV-120027588 PG 6 WC Oncology SC Oncology GA 807DZ UT WOS:000220483500014 PM 15069771 ER PT J AU Purow, B Fine, HA AF Purow, B Fine, HA TI Progress report on the potential of angiogenesis inhibitors for neuro-oncology SO CANCER INVESTIGATION LA English DT Article DE brain tumor; glioma; meningioma; primitive neuroectodermal tumor (PNET); angiogenesis; anti-angiogenic; antivascular ID ENDOTHELIAL GROWTH-FACTOR; PHASE-I TRIAL; INDEPENDENT PROSTATE-CANCER; MATRIX-METALLOPROTEINASE INHIBITOR; ADENOVIRUS-MEDIATED DELIVERY; HUMAN BRAIN-TUMORS; SOLID TUMORS; ANTIANGIOGENIC THERAPY; CORNEAL ANGIOGENESIS; MONOCLONAL-ANTIBODY AB New therapies for brain tumors are urgently needed. Brain tumors are highly vascularized, supporting the potential of anti-angiogenic therapies in their treatment. The promise of blocking tumor growth through inhibiting new blood vessel formation with anti-angiogenic agents has been heralded as a therapeutic breakthrough, and preclinical data supported this enthusiasm. However, early clinical trials in humans have been somewhat disappointing. Nonetheless, great optimism for these agents remains, and many new anti-angiogenic agents and strategies are being evaluated pre-clinically and in clinical trials. A number of issues need to be considered in the application of these agents to neuro-oncology. In this review, we discuss the biology of blood vessel formation in the brain and brain tumors as it relates to anti-angiogenic therapies. The difficulties inherent in performing clinical trials of anti-angiogenic therapies in patients with brain tumors are outlined. Finally, we consider numerous individual anti-angiogenic and antivascular therapies now in pre-clinical testing or in clinical trials. C1 NINDS, Neurooncol Branch, NCI, NIH, Bethesda, MD 20892 USA. RP Fine, HA (reprint author), NINDS, Neurooncol Branch, NCI, NIH, Bethesda, MD 20892 USA. EM hfine@mail.nih.gov NR 81 TC 15 Z9 15 U1 0 U2 0 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 2004 VL 22 IS 4 BP 577 EP 587 DI 10.1081/CNV-200027141 PG 11 WC Oncology SC Oncology GA 870TB UT WOS:000225079900013 PM 15565816 ER PT J AU Sigurdson, AJ Ron, E AF Sigurdson, AJ Ron, E TI Cosmic radiation exposure and cancer risk among flight crew SO CANCER INVESTIGATION LA English DT Article DE cancer; cosmic radiation; epidemiology; review; occupation; air crew; pilots; flight attendants; chromosomal aberrations ID AIRLINE CABIN ATTENDANTS; CHROMOSOME-ABERRATION ANALYSIS; ATOMIC-BOMB SURVIVORS; IN-SITU HYBRIDIZATION; NESTED CASE-CONTROL; LONG-HAUL FLIGHTS; BREAST-CANCER; COCKPIT CREW; UNITED-STATES; AIR CREW AB Nearly 20 epidemiologic or related studies of cancer incidence and mortality have been published during or since 2000, with several reporting increased risks of female breast cancer among flight attendants and melanoma among both pilots and cabin crew. Occasionally, excesses of other cancers have been observed, but not consistently. Although the real causes of these excess cancer risks are not known, there is concern that they may be related to occupational exposures to ionizing radiation of cosmic origin. It is possible that confounding risk factors may partially or totally explain the observed relationships, but several investigations are beginning to address lack of past adjustment for reproductive factors and suit exposure with improved study designs. With progress in aviation technology, planes will fly longer and at higher altitudes, and presumably the number of flights and passengers will increase. To respond responsibly to the real and perceived risks associated with flying, more extensive data are needed, but special efforts should be considered to ensure new projects can genuinely add to our current knowledge. C1 NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, DHHS, Bethesda, MD 20892 USA. RP Sigurdson, AJ (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, DHHS, 6120 Execut Blvd,EPS 7092,MSC 7238, Bethesda, MD 20892 USA. EM sigurdsa@mail.nih.gov NR 83 TC 42 Z9 42 U1 3 U2 16 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 0735-7907 EI 1532-4192 J9 CANCER INVEST JI Cancer Invest. PY 2004 VL 22 IS 5 BP 743 EP 761 DI 10.1081/CNV-200032767 PG 19 WC Oncology SC Oncology GA 873AG UT WOS:000225250400012 PM 15581056 ER PT J AU Ramanathan, RK Hwang, JJ Zmaboni, WC Sinicrope, FA Safran, H Wong, MK Earle, M Brufsky, A Evans, T Troetschel, M Walko, C Day, R Chen, HX Finkelstein, S AF Ramanathan, RK Hwang, JJ Zmaboni, WC Sinicrope, FA Safran, H Wong, MK Earle, M Brufsky, A Evans, T Troetschel, M Walko, C Day, R Chen, HX Finkelstein, S TI Low overexpression of HER-2/PPPNeu in advanced colorectal cancer limits the usefulness of trastuzumab (herceptin (R)) and irinotecan as therapy. A phase II trial SO CANCER INVESTIGATION LA English DT Article; Proceedings Paper CT 37th Annual Meeting of the American-Society-of-Clinical-Oncology CY MAY 12-15, 2001 CL SAN FRANCISCO, CA SP Amer Soc Clin Oncol DE clinical trial; colorectal cancer; HER-2/neu; irinotecan; trastuzumab ID METASTATIC BREAST-CANCER; MONOCLONAL-ANTIBODY; RANDOMIZED-TRIAL; C-ERBB-2 PROTEIN; FLUOROURACIL; SURVIVAL; PLUS; EXPRESSION; LEUCOVORIN; CARCINOMA AB Background: To determine the response rate of trastuzumab and irinotecan in HER-2/neu overexpressing advanced colorectal cancer (CRC), determine the frequency of HER-2/neu expression in CRC, and evaluate the pharmacokinetics of trastuzumab in a phase II study. Patients and Methods: Patients were screened for HER-2/neu by immunohistochemistry (DAKO HercepTest(TM)). Prior chemotherapy was limited to one regimen. Trastuzumab was administered weekly (loading dose of 4 mg/ka IV and 2 mg/kg thereafter). Irinotecan 125 mg/m(2), IV was administered weekly for 4 weeks with a 2-week rest period. Results: HER-2/neu overexpression was detected in 11 of 138 (8.0%) of screened tumors (2+ in 5 and 3+ in 6 patients). Nine patients were entered in the study; 6 had received prior chemotherapy. Partial responses were seen in 5 of 7 evaluable patients. Grade 3-4 toxicities in 31 cycles of therapy included diarrhea (19%), nausea (10%), and vomiting (6%). Leukopenia occurred in 6%, and congestive heart failure and acute renal failure (secondary to diarrhea and dehydration) were seen in 3% of cycles. The study was prematurely closed due to low accrual. Conclusions: The low overexpression rate of HER-2/neu (8.0%) in advanced CRC limits the potential for further investigation of regimens involving trastuzumab, despite evidence Suggestive of activity. Irinotecan did not alter the pharmacokinetic disposition of trastuzumab. C1 Univ Pittsburgh, Inst Canc, Pittsburgh, PA 15232 USA. Univ Pittsburgh, Sch Pharm, Dept Pharmaceut Sci, Pittsburgh, PA USA. MD Anderson Canc Ctr, Houston, TX USA. Brown Univ, Bio Med Med, Providence, RI USA. NCI, Canc Therapy & Evaluat Program, Rockville, MD USA. Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA USA. RP Ramanathan, RK (reprint author), Univ Pittsburgh, Inst Canc, UPMC Canc Pavil,5150 Ctr Ave,562, Pittsburgh, PA 15232 USA. EM ramanathanrk@msx.upmc.edu FU NCI NIH HHS [2P30 CA 479004]; NCRR NIH HHS [5M01 RR00056] NR 25 TC 56 Z9 58 U1 2 U2 2 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 2004 VL 22 IS 6 BP 858 EP 865 DI 10.1081/CNV-200039645 PG 8 WC Oncology SC Oncology GA 882AN UT WOS:000225910900005 PM 15641483 ER PT J AU Williams, ML Torres-Duarte, A Brant, LJ Bhargava, P Marshall, J Wainer, IW AF Williams, ML Torres-Duarte, A Brant, LJ Bhargava, P Marshall, J Wainer, IW TI The relationship between a urinary cachectic factor and weight loss in advanced cancer patients SO CANCER INVESTIGATION LA English DT Article DE proteolysis-inducing factor; longitudinal study; weight loss; cachexia ID MUSCLE PROTEIN-DEGRADATION; CACHEXIA; INDUCTION; PRODUCT; TUMORS; MICE AB A 24K glycoprotein, the proteolysis-inducing factor (PIF), has been identified in mice and humans with cancer cachexia. Clinical cross-sectional studies found an association between the presence of PIF in urine and tumors of patients and weight loss. For the first time, we report results from a longitudinal Study establishing the relationship between a urinary PIF pattern and persistent weight loss. Over time, cancer patients positive for the PIF pattern experienced weight loss, whereas those with a negative test gained weight. C1 NIA, Gerontol Res Ctr, Bioanalyt & Drug Discovery Unit, NIH, Baltimore, MD 21224 USA. Georgetown Univ, Dept Pharmacol, Washington, DC USA. Univ Massachusetts, Ctr Med, Div Hematol, Worcester, MA USA. Georgetown Univ, Ctr Med, Lombardi Canc Ctr, Washington, DC USA. RP Wainer, IW (reprint author), NIA, Gerontol Res Ctr, Bioanalyt & Drug Discovery Unit, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM Wainerir@grc.nia.nih.gov NR 13 TC 18 Z9 19 U1 0 U2 4 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 2004 VL 22 IS 6 BP 866 EP 870 DI 10.1081/CNV-200039649 PG 5 WC Oncology SC Oncology GA 882AN UT WOS:000225910900006 PM 15641484 ER PT J AU Widemann, BC AF Widemann, BC TI Merlin PAKs a punch SO CANCER JOURNAL LA English DT Editorial Material ID FARNESYL-PROTEIN TRANSFERASE; HUMAN SCHWANNOMA CELLS; NF1 TUMOR-SUPPRESSOR; TYPE-2 GENE-PRODUCT; RAS-INDUCED CANCERS; INHIBITOR R115777; MOUSE MODELS; DRUG MKT-077; FARNESYLTRANSFERASE; NEUROFIBROMATOSIS C1 NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA. RP Widemann, BC (reprint author), NCI, Pediat Oncol Branch, 10 Ctr Dr,Bldg10,Room 13C103, Bethesda, MD 20892 USA. EM Widemanb@mail.nih.gov NR 42 TC 1 Z9 1 U1 0 U2 0 PU JONES AND BARTLETT PUBLISHERS PI SUDBURY PA 40 TALL PINE DR, SUDBURY, MA 01776 USA SN 1528-9117 J9 CANCER J JI Cancer J. PD JAN-FEB PY 2004 VL 10 IS 1 BP 8 EP 11 DI 10.1097/00130404-200401000-00002 PG 4 WC Oncology SC Oncology GA 775KG UT WOS:000189038900002 PM 15000489 ER PT J AU Libutti, SK AF Libutti, SK TI Do angiogenesis inhibitors perform a physiologic gatekeeper role in cancer prevention? SO CANCER JOURNAL LA English DT Editorial Material ID SERUM ENDOSTATIN LEVELS; ENDOTHELIAL GROWTH-FACTOR; TUMOR ANGIOGENESIS; COLLAGEN; INTEGRIN; ANGIOSTATIN; CARCINOMA; TUMSTATIN; MEMBRANE; TARGET C1 NCI, Ctr Canc Res, Surg Branch, Bethesda, MD 20892 USA. RP Libutti, SK (reprint author), NCI, Ctr Canc Res, Surg Branch, 10 Ctr Dr,Room 2B07, Bethesda, MD 20892 USA. EM slibutti@nih.gov NR 30 TC 1 Z9 1 U1 0 U2 0 PU JONES AND BARTLETT PUBLISHERS PI SUDBURY PA 40 TALL PINE DR, SUDBURY, MA 01776 USA SN 1528-9117 J9 CANCER J JI Cancer J. PD JAN-FEB PY 2004 VL 10 IS 1 BP 12 EP 14 DI 10.1097/00130404-200401000-00003 PG 3 WC Oncology SC Oncology GA 775KG UT WOS:000189038900003 PM 15000490 ER PT J AU Nielsen, TO Andrews, HN Cheang, M Kucab, JE Hsu, FD Ragaz, J Gilks, CB Makretsov, N Bajdik, CD Brookes, C Neckers, LM Evdokimova, V Huntsman, DG Dunn, SE AF Nielsen, TO Andrews, HN Cheang, M Kucab, JE Hsu, FD Ragaz, J Gilks, CB Makretsov, N Bajdik, CD Brookes, C Neckers, LM Evdokimova, V Huntsman, DG Dunn, SE TI Expression of the insulin-like growth factor I receptor and urokinase plasminogen activator in breast cancer is associated with poor survival: Potential for intervention with 17-allylamino geldanamycin SO CANCER RESEARCH LA English DT Article ID TISSUE MICROARRAYS; TYROSINE KINASES; UP-REGULATION; THERAPY; PEPTIDE; CELLS; AMPLIFICATION; DEGRADATION; SENSITIVITY; METASTASIS AB Urokinase plasminogen activator (uPA) expression in breast cancer is associated with relapse and a reduction in disease-specific survival. Thus, efforts are under way to identify uPA inhibitors. By screening a chemical library of >1000 compounds, 17-allyaminogeldanamycin (17AAG) was identified as a potent inhibitor of uPA by the National Cancer Institute and is now in Phase I clinical trials. At this time, it remains unclear how 17AAG blocks uPA; one possibility is through disruption of the insulin-like growth factor I receptor (IGF-IR) pathway. This would be consistent with studies from our laboratory showing that activation of IGF-IR results in the induction of uPA protein. In the study described herein, we observed that IGF-IR and uPA were highly expressed in 87 and 55% of breast cancer by screening tumor tissue microarrays representing 930 cases. A significant proportion (52.1 % = 354 of 680 cases, P < 0.0001) of the patients had tumors expressing both proteins. uPA alone (P = 0.033) or in combination with IGF-IR (P = 0.0104) was indicative of decreased disease-specific survival. Next, we demonstrated that treating MDA-MB-231 cells with increasing concentrations of 17AAG resulted in IGF-IR degradation (IC50 = 1.0 muM) and blocked signal transduction through the Akt and mitogen-activated protein kinase pathways. Finally, we found that 17AAG had a robust inhibitory effect on the production of uPA mRNA and protein in the presence of IGF-I. Thus, our study raises the possibility that 17AAG could prove to be an effective therapeutic agent for a large number of breast cancer patients by inhibiting the IGF-IR and ultimately uPA. C1 Univ British Columbia, Dept Pediat, Lab Oncogenom Res, British Columbia Inst Childrens & Womens Hlth, Vancouver, BC V5Z 4H4, Canada. Vancouver Gen Hosp, Genet Pathol Evaluat Ctr, Vancouver, BC, Canada. Hlth Sci Ctr, Vancouver, BC, Canada. British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada. NCI, Tumor Cell Biol Sect, Clin Pharmacol Branch, Bethesda, MD 20892 USA. RP Dunn, SE (reprint author), Univ British Columbia, Dept Pediat, Lab Oncogenom Res, British Columbia Inst Childrens & Womens Hlth, 950 W 28th Ave, Vancouver, BC V5Z 4H4, Canada. EM sedunn@interchange.ubc.ca NR 30 TC 64 Z9 71 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 2004 VL 64 IS 1 BP 286 EP 291 DI 10.1158/0008-5472.CAN-03-1242 PG 6 WC Oncology SC Oncology GA 765QA UT WOS:000188293900039 PM 14729636 ER PT J AU Camphausen, K Burgan, W Cerra, M Oswald, KA Trepel, JB Lee, MJ Tofilon, PJ AF Camphausen, K Burgan, W Cerra, M Oswald, KA Trepel, JB Lee, MJ Tofilon, PJ TI Enhanced radiation-induced cell killing and prolongation of gamma H2AX foci expression by the histone deacetylase inhibitor MS-275 SO CANCER RESEARCH LA English DT Article ID VIVO ANTITUMOR-ACTIVITY; DOUBLE-STRAND BREAKS; SODIUM-BUTYRATE; REPAIR; H2AX; PHOSPHORYLATION; ACETYLATION; LEUKEMIA; TUMORS; CYCLE AB Histone deacetylase (HDAC) inhibitors are undergoing clinical evaluation for cancer therapy. Because HDAC modulates chromatin structure and gene expression, parameters considered to influence radioresponse, we have investigated the effects of the HDAC inhibitor MS-275 on the radiosensitivity of two human tumor cell lines (DU145 prostate carcinoma and U251 glioma). Acetylation status of histones H3 and H4 was determined as a function of time after MS-275 addition to and removal from culture medium. Histone acetylation increased by 6 h after MS-275 addition, reaching a maximum between 24 and 48 h of exposure; providing fresh drug-free medium then resulted in a decrease in histone acetylation that began by 6 h and approached untreated levels by 16 It. Treatment of cells with MS-275 for 48 h followed by irradiation had little or no effect on radiation-induced cell death. However, exposure to MS-275 before and after irradiation resulted in an increase in radiosensitivity with dose enhancement factors of 1.9 and 1.3 for DU145 and U251 cells, respectively. This MS-275 treatment protocol did not result in a redistribution of the cells into a more radiosensitive phase of the cell cycle or in an increase in apoptosis. However, MS-275 did modify the time course of gammaH2AX expression in irradiated cells. Whereas there was no significant difference in radiation-induced gammaH2AX foci at 6 It, the number of cells expressing gammaH2AX foci was significantly greater in the MS-275-treated cells at 24 h after irradiation. These results indicate that MS-275 can enhance radiosensitivity and suggest that this effect may involve an inhibition of DNA repair. C1 NCI, Radiat Oncol Branch, Bethesda, MD 20892 USA. NCI, Mol Radiat Therapeut Branch, Radiat Oncol Sci Program, Bethesda, MD 20892 USA. NCI, Med Branch, Bethesda, MD 20892 USA. RP Tofilon, PJ (reprint author), Mol Radiat Therapeut Branch, Radiat Oncol Sci Program, EPN-6015A,6130 Execut Blvd,MSC 7440, Rockville, MD 20892 USA. EM tofilonp@mail.nih.gov NR 26 TC 168 Z9 177 U1 0 U2 7 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 2004 VL 64 IS 1 BP 316 EP 321 DI 10.1158/0008-5472.CAN-03-2630 PG 6 WC Oncology SC Oncology GA 765QA UT WOS:000188293900043 PM 14729640 ER PT J AU MacDonald, CJ Ciolino, HP Yeh, GC AF MacDonald, CJ Ciolino, HP Yeh, GC TI The drug salicylamide is an antagonist of the aryl hydrocarbon receptor that inhibits signal transduction induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin SO CANCER RESEARCH LA English DT Article ID DIBENZO-P-DIOXINS; AH RECEPTOR; CYP1A1 GENE; CYTOCHROME-P450 1A1; OXIDATIVE STRESS; ANIMAL-MODELS; ASPIRIN USE; EXPOSURE; TOXICITY; TCDD AB 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminant, that has been linked with a variety of deleterious effects on human health, including increased cancer rates and reproductive anomalies. The detrimental effects of TCDD are mediated via the aryl hydrocarbon receptor (AhR), a transcription factor that regulates the expression of the carcinogen-activating enzymes cytochromes P-450 (CYP) 1A1, 1A2, and 1B1. In the present study, we examined the ability of synthetic derivatives of salicylic acid to affect TCDD-stimulated AhR-mediated signal transduction in human hepatoma HepG2 cells. Salicylamide (SAL), an analgesic drug, caused a potent and long-lasting inhibition of TCDD-induced CYP enzyme activity. Acetylsalicylic acid (aspirin) and the naturally occurring phytochemical salicylic acid had no effect on CYP activity. SAL inhibited the increase in CYP1A1, -1A2, and -1B1 mRNA levels that occurs on exposure to TCDD. TCDD-induced transcription of these genes was also inhibited by SAL, but not by aspirin or salicylic acid, as demonstrated by luciferase reporter assays. The transcription of the CYP1 family of genes is regulated by the interaction of TCDD-activated AhR with the xenobiotic-responsive element present in the promoter regions of these genes. As shown by electrophoretic mobility shift assay, SAL completely blocked the binding of TCDD-activated AhR to the xenobiotic responsive element. Also, SAL substantially blocked the binding of TCDD to the cytosolic AhR. These results demonstrate that SAL, a commonly used analgesic, is a potent inhibitor of AhR-mediated signal transduction, and may be an effective agent in the prevention of TCDD-associated disease. C1 Natl Canc Inst, Basic Res Lab, Ctr Canc Res, Cellular Def & Carcinogenesis Sect, Frederick, MD 21702 USA. RP Yeh, GC (reprint author), Natl Canc Inst, Basic Res Lab, Ctr Canc Res, Cellular Def & Carcinogenesis Sect, Bldg 538-Room 141, Frederick, MD 21702 USA. EM yeh@ncifcrf.gov NR 46 TC 33 Z9 34 U1 0 U2 5 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JAN 1 PY 2004 VL 64 IS 1 BP 429 EP 434 DI 10.1158/0008-5472.CAN-03-0974 PG 6 WC Oncology SC Oncology GA 765QA UT WOS:000188293900058 PM 14729655 ER PT J AU Zurer, I Hofseth, LJ Cohen, Y Xu-Welliver, M Hussain, SP Harris, CC Rotter, V AF Zurer, I Hofseth, LJ Cohen, Y Xu-Welliver, M Hussain, SP Harris, CC Rotter, V TI The role of p53 in base excision repair following genotoxic stress SO CARCINOGENESIS LA English DT Article ID WILD-TYPE P53; NITRIC-OXIDE SYNTHASE; C-TERMINAL DOMAIN; DNA-DAMAGE; P53-MEDIATED APOPTOSIS; SPONTANEOUS MUTATION; HUMAN FIBROBLASTS; MOUSE CELLS; IN-VITRO; INVOLVEMENT AB The p53 tumor suppressor protein is involved in apoptosis and cell cycle checkpoints. We have shown recently that p53 also facilitates base excision repair (BER). To further examine p53 involvement in the regulation of BER we chose to focus on 3-methyladenine DNA glycosylase (3-MeAde DNA glycosylase), the first enzyme acting in the BER pathway. 3-MeAde DNA glycosylase activity was found to be modulated by the p53 protein. This modulation was dependent on the type of genotoxic stress used. gamma-Irradiation damage resulted in activation of glycosylase, which was enhanced by p53. Doxorubicin and hydrogen peroxide (H2O2) treatment, although inducing p53 stabilization, did not cause the activation of glycosylase. Nitric oxide (NO) resulted in activation of 3-MeAde DNA glycosylase. Surprisingly this activation was down regulated by wild-type p53. The down regulation of 3-MeAde DNA glycosylase activity was due to trans repression of glycosylase mRNA by p53. Furthermore, we found that AP endonuclease (APE) activity was not altered by NO. Our study provides evidence for a possible antimutagenic role for p53 following exposure of cells to NO species. In the absence of p53, NO exposure results in elevation of 3-MeAde DNA glycosylase activity that results in elevation in the number of AP sites in DNA. At the same time, APE activity does not rise and removal of the AP sites is not further processed resulting in a mutator phenotype. When p53 is present, it down regulates the transcription of 3-MeAde DNA glycosylase. This provides a new model by which p53 prevents the creation of a mutator phenotype. C1 Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel. NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. RP Rotter, V (reprint author), Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel. EM varda.rotter@weizmann.ac.il NR 58 TC 41 Z9 42 U1 0 U2 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 2004 VL 25 IS 1 BP 11 EP 19 DI 10.1093/carcin/bgg186 PG 9 WC Oncology SC Oncology GA 762MG UT WOS:000187975700002 PM 14555612 ER PT J AU Hou, DX Kai, K Li, JJ Lin, SG Terahara, N Wakamatsu, M Fujii, M Young, MR Colburn, N AF Hou, DX Kai, K Li, JJ Lin, SG Terahara, N Wakamatsu, M Fujii, M Young, MR Colburn, N TI Anthocyanidins inhibit activator protein 1 activity and cell transformation: structure-activity relationship and molecular mechanisms SO CARCINOGENESIS LA English DT Article ID NF-KAPPA-B; MULTISTAGE SKIN CARCINOGENESIS; NEOPLASTIC TRANSFORMATION; IN-VITRO; AP-1 TRANSACTIVATION; TUMOR PROMOTION; C-JUN; CYANIDIN 3-O-BETA-D-GLUCOSIDE; QUINONE OXIDOREDUCTASE; HUMAN KERATINOCYTES AB Anthocyanins are the chemical components that give the intense color to many fruits and vegetables, such as blueberries, red cabbages and purple sweet potatoes. Extensive studies have indicated that anthocyanins have strong antioxidant activities. To investigate the mechanism of anthocyanidins as an anticancer food source, six kinds of anthocyanidins representing the aglycons of most anthocyanins, were used to examine their effects on tumor promotion in mouse JB6 cells, a validated model for screening cancer chemopreventive agents and elucidating the molecular mechanisms. Of the six anthocyanins tested, only those with an ortho-dihydroxyphenyl structure on the B-ring suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell transformation and activator protein-1 transactivation, suggesting that the ortho-dihydroxyphenyl may contribute to the inhibitory action. Delphinidin, but not peonidin, blocked the phosphorylation of protein kinases in the extracellular signal-regulated protein kinase (ERK) pathway at early times and the c-Jun N-terminal kinase (JNK) signaling pathway at later times. p38 kinase was not inhibited by delphinidin. Furthermore, two mitogen-activated protein kinase (MAPK) specific inhibitors (SP600125 for JNK and UO126 for ERK) could specifically block the activation of JNK and ERK and cell transformation. Those results demonstrate that anthocyanidins contribute to the inhibition of tumorigenesis by blocking activation of the MAPK pathway. These findings provide the first molecular basis for the anticarcinogenic action of anthocyanidins. C1 Kagoshima Univ, Fac Agr, Dept Biochem Sci & Technol, Kagoshima 8900065, Japan. City Hope Natl Med Ctr, Beckman Res Inst, Dept Radiat Res, Duarte, CA 91010 USA. Minami Kyushu Univ, Dept Food Sci & Technol, Miyazaki 8840003, Japan. NCI, Gene Regulat Sect, Basic Res Lab, Frederick, MD 21702 USA. RP Hou, DX (reprint author), Kagoshima Univ, Fac Agr, Dept Biochem Sci & Technol, Kagoshima 8900065, Japan. EM hou@chem.agri.kagoshima-u.ac.jp RI Hou, De-Xing/C-9296-2011 NR 70 TC 125 Z9 135 U1 1 U2 14 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 EI 1460-2180 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 2004 VL 25 IS 1 BP 29 EP 36 DI 10.1093/carcin/bgg184 PG 8 WC Oncology SC Oncology GA 762MG UT WOS:000187975700004 PM 14514663 ER PT J AU Waalkes, MP Ward, JM Diwan, BA AF Waalkes, MP Ward, JM Diwan, BA TI Induction of tumors of the liver, lung, ovary and adrenal in adult mice after brief maternal gestational exposure to inorganic arsenic: promotional effects of postnatal phorbol ester exposure on hepatic and pulmonary, but not dermal cancers SO CARCINOGENESIS LA English DT Article ID INDUCED MALIGNANT-TRANSFORMATION; MALE F344 RATS; DIMETHYLARSINIC ACID; DRINKING-WATER; TRANSPLACENTAL CARCINOGENICITY; DIAPLACENTAL INITIATION; CHRONIC STIMULATION; SKIN TUMORIGENESIS; INTERNAL CANCERS; TRANSGENIC MICE AB Arsenic is a recognized human carcinogen and development of rodent models remains a critically important research objective. Since gestation can be a period of high sensitivity to chemical carcinogenesis, we have performed a series of transplacental carcinogenicity studies in mice with inorganic arsenic. In this study, groups of pregnant C3H mice received drinking water containing sodium arsenite (NaAsO2) at 0, 42.5 and 85 p.p.m. arsenic ad libitum from days 8 to 18 of gestation. These doses of arsenic were well tolerated. Dams delivered normally and at weaning (4 weeks) offspring were randomly put into groups (n = 25) of males or females according to maternal dose. In an attempt to promote skin cancers initiated by transplacental arsenic, duplicate groups of control or arsenic exposed offspring were topically exposed to 12-O-tetradecanoyl phorbol-13-acetate (TPA; 2 mug/0.1 ml acetone, twice/week) from 4 to 25 weeks of age. Irrespective of TPA exposure, male offspring showed arsenic-induced dose-related increases in hepatocellular carcinoma incidence and multiplicity, as well as increases in adrenal tumor incidence and multiplicity. In female offspring, an increase in epithelial ovarian tumors occurred with arsenic exposure regardless of TPA exposure. Females also showed pre-neoplastic lesions of the reproductive tract, including hyperplasia of the uterus and oviduct, after arsenic but independent of TPA exposure. Although TPA had no effect on skin tumors, it promoted arsenic initiated liver tumors in females and lung tumors in both sexes. Thus, inorganic arsenic, as a single agent, can consistently act as a complete transplacental carcinogen in mice, inducing tumors at multiple sites, and as a tumor initiator in some tissues. Skin tumors were not initiated by arsenic in mouse fetuses possibly indicating tissue-specific mechanisms of action. This study indicates that gestation is a period of high sensitivity to arsenic carcinogenesis. C1 NIEHS, Inorgan Carcinogenesis Sect, Comparat Carcinogenesis Lab, NCI, Res Triangle Pk, NC 27709 USA. NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA. RP Waalkes, MP (reprint author), NIEHS, Inorgan Carcinogenesis Sect, Comparat Carcinogenesis Lab, NCI, POB 12233, Res Triangle Pk, NC 27709 USA. EM waalkes@niehs.nih.gov FU NCI NIH HHS [N01-CO-12400] NR 49 TC 93 Z9 95 U1 0 U2 10 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JAN PY 2004 VL 25 IS 1 BP 133 EP 141 DI 10.1093/carcin/bgg181 PG 9 WC Oncology SC Oncology GA 762MG UT WOS:000187975700016 PM 14514661 ER PT S AU Oh, H Chi, X Bradfute, SB Mishina, Y Pocius, J Michael, LH Behringer, RR Schwartz, RJ Entman, ML Schneider, MD AF Oh, H Chi, X Bradfute, SB Mishina, Y Pocius, J Michael, LH Behringer, RR Schwartz, RJ Entman, ML Schneider, MD BE Sideman, S Beyar, R TI Cardiac muscle plasticity in adult and embryo by heart-derived progenitor cells SO CARDIAC ENGINEERING: FROM GENES AND CELLS TO STRUCTURE AND FUNCTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 2nd Larry and Horti Fairberg Cardiac Workshop CY SEP 20-24, 2003 CL Erice, ITALY SP Technion Israel Inst Technol, Ettore Majorana Fdn & Ctr Sci Culture DE myocardial regeneration; cardiac embryogenesis; cell fusion ID HEMATOPOIETIC STEM-CELLS; SIDE POPULATION CELLS; BONE-MARROW; INFARCTED MYOCARDIUM; IN-VIVO; SKELETAL-MUSCLE; TRANSPLANTATION; FUSION; CARDIOMYOCYTES; REGENERATION AB The evidence of cardiomyocyte proliferation in damaged heart implied cardiac regeneration might occur by resident or extra cardiac stem cells. However, the specification and origin of these cells remain unknown. Here, we report using fluorescence-activated cell sorting that cardiac progenitor cells resided in adult heart and colocalized with small capillary vessels, within the stem cell antigen (Sca-1) population expressing high telomerase activity. Notably, hematopoietic stem cells capable of efflux Hoechst 33342, termed side-population cells, also were identified within the heart-derived cells. The cardiac progenitor cells (CD45(-)/CD34(-)) express neither cardiac muscle nor endothelial cell markers at an undifferentiated stage. The exposure of 5-azacytidine induced cardiac differentiation, which depends, in part, on Bmpr1a, a type IA receptor for bone morphogenetic protein (BMP). The capability of adult Sca1(+) cells to adopt a cardiac muscle in embryogenesis was substantiated by blastocyst injection, using progenitors from the adult hearts of transgenic mice that harbor a bacterial artificial chromosome expressing GFP via the Nkx-2.5 locus. Intravenously injected progenitors, shortly after ischemic/reperfusion, homed and functionally differentiated 3.5% of total left ventricle in the host myocardium. Differentiation included both fusion-independent and fusion-associated components, proved by the Cre/loxP donor/recipient system. Our studies suggest that endogenous cardiac progenitors reside in the adult heart, regenerate cardiomyocytes functionally, and integrate into the existing heart circuitry. C1 Baylor Coll Med, Ctr Cardiovasc Dev, Houston, TX 77030 USA. Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA. Baylor Coll Med, DeBakey Heart Ctr, Houston, TX 77030 USA. Baylor Coll Med, Dept Med, Houston, TX 77030 USA. Baylor Coll Med, Dept Immunol, Houston, TX 77030 USA. Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA. Baylor Coll Med, Dept Mol Physiol & Biophys, Houston, TX 77030 USA. NIEHS, Res Triangle Pk, NC 27709 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. RP Oh, H (reprint author), Kyoto Univ Hosp, Translatat Res Ctr, Dept Expt Therapeut, Sajti Ku, 54 Shogoin Kawahara Cho, Kyoto 6068507, Japan. EM hidemasa@kuhp.kyoto-u.ac.jp OI Schneider, Michael/0000-0001-9645-1938 NR 47 TC 94 Z9 98 U1 0 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-480-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1015 BP 182 EP 189 DI 10.1196/annals.1302.015 PG 8 WC Biotechnology & Applied Microbiology; Cardiac & Cardiovascular Systems; Multidisciplinary Sciences SC Biotechnology & Applied Microbiology; Cardiovascular System & Cardiology; Science & Technology - Other Topics GA BAN56 UT WOS:000222976600016 PM 15201159 ER PT S AU Manoli, I De Martino, MU Kino, T Alesci, S AF Manoli, I De Martino, MU Kino, T Alesci, S BE Alesci, S Manoli, I Costello, R Coates, P Gold, PW Chrousos, GP Blackman, MR TI Modulatory effects of L-carnitine on glucocorticoid receptor activity SO CARNITINE: THE SCIENCE BEHIND A CONDITIONALLY ESSENTIAL NUTRIENT SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Carnitine - Science Behind a Conditionally Esseential Nutrient CY MAR 25-26, 2004 CL Natl Inst Hlth Campus, Bethesda, MD SP Natl Inst Child Hlth & Human Dev, Natl Ctr Complementary & Alterat Med, Natl Inst Ment Hlth, Off Dietary Supplements HO Natl Inst Hlth Campus DE carnitine; glucocorticoids; glucocorticoid receptor; cytokines; inflammation ID ACETYL-L-CARNITINE; PHOSPHATIDYLCHOLINE CONTENT; RAT LUNG; METABOLISM; HORMONE; ADULTS; FETAL; BETAMETHASONE; DETERMINANTS; ANTAGONIST AB L-Carnitine (3-hydroxy-4-NNN-trimethylaminobuty rate i is a conditionally essential nutrient with a major role in cellular energy metabolism. It is available in the United States as both a prescription drug and an over-the-counter nutritional supplement. Accumulating evidence from both animal and human studies indicates that pharmacologic doses of L-carnitine LCAR) have immunomodulatory effects resembling those or glucocorticoids i (GC). On the other hand. in contrast to GC. which cause bone loss. LCAR seems to have positive effects on bone metabolism. To explore the molecular bases of this GC-like activity of I-CAR. we inestigated its effects on glucocorticoid receptor (GR-modlulated cytokine release ex viro. and on the transcriptional activity. intracellular trafficking. and binding of GR in vitro. At high monocytotoxic doses. I-CAR (a) suppressed the lipopolysaccharide-stimulated release of tumor necrosis factor alpha and interleukin-12 from primary human monocytes in a GC-like fashion. (b)stimulated the transcriptional activity of(;R on the GC-responsive promoters. (c) triggered nuclear translocation of green fluorescent protein (GFP)-fused GR. and (d) reduced the whole cell binding of [H-3]-dexamethasone to GR. These results suggest that LCAR is a "nutritional modulator" of the GR. by acting as an agonist-like compound. Since LCAR appears to have positive effects on bone metabolism. in contrast to GC, LCAR may share some of the therapeutic properties of GC. particularly on the immune system. but not their deleterious side effects on some of other organs tissues. Thus. LCAR is potentially. a useful alternative compound of GC in particular therapeutic situations. The clinical and therapeutic implications or these findings, as well as a better understanding of their mechanisms. warrant further research. C1 NIH, Endocrine Sect, Clin Invest Lab, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA. Univ Athens, Dept Pediat 1, Metab Unit, Athens 11527, Greece. NIMH, Clin Neuroendocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Alesci, S (reprint author), NIMH, Clin Neuroendocrinol Branch, NIH, Bldg 10,Room 2D46,10 Ctr Dr,MSC 1284, Bethesda, MD 20892 USA. EM alescisa@mail.nih.gov OI Manoli, Irini/0000-0003-1543-2941 NR 51 TC 17 Z9 18 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-555-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1033 BP 147 EP 157 DI 10.1196/annals.1320.014 PG 11 WC Multidisciplinary Sciences; Nutrition & Dietetics; Pharmacology & Pharmacy; Physiology SC Science & Technology - Other Topics; Nutrition & Dietetics; Pharmacology & Pharmacy; Physiology GA BBO92 UT WOS:000226783500014 PM 15591012 ER PT S AU Ng, CM Blackman, MR Wang, C Swerdloff, S AF Ng, CM Blackman, MR Wang, C Swerdloff, S BE Alesci, S Manoli, I Costello, R Coates, P Gold, PW Chrousos, GP Blackman, MR TI The role of carnitine in the male reproductive system SO CARNITINE: THE SCIENCE BEHIND A CONDITIONALLY ESSENTIAL NUTRIENT SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Carnitine - Science Behind a Conditionally Esseential Nutrient CY MAR 25-26, 2004 CL Natl Inst Hlth Campus, Bethesda, MD SP Natl Inst Child Hlth & Human Dev, Natl Ctr Complementary & Alterat Med, Natl Inst Ment Hlth, Off Dietary Supplements HO Natl Inst Hlth Campus DE apoptosis; spermatogenesis; testis; epididymis; infertility ID ACETYL-L-CARNITINE; GERM-CELL APOPTOSIS; HIV-1-INFECTED SUBJECTS; LYMPHOCYTE APOPTOSIS; CERAMIDE GENERATION; L-ACETYLCARNITINE; DOUBLE-BLIND; SUPPLEMENTATION; EXPOSURE; DEATH AB Carnitine is highly concentrated in the epididymis and spermatozoa. where it may serve as an intramitochondrial vehicle for the acyl group. which in the form of acyl CoA acts as a substrate for the oxidation process producing energy for sperm respiration and motility. To date. studies in rodents and humans suggest that sperm count. motility. and maturation are related to epididymal free carnitine concentrations. Moreover. supplementation with carnitine improves sperm quality and/or quantity in testes of mice exposed to physical insults. such as heat and X-irradiation. and in men with idiopathic oligoasthenospermia. These benefits may be due to increased mitochondrial fatty acid oxidation resulting in improvement in motility or epididymal sperm. The antiapoptotic effect(s) or carnitine in the testes may also contribute, but this remains speculative and requires further investigation. Research to uncover the many characteristics and mechanisms of action of carnitine in somatic and germ cells may provide insights into the pathophysiology or germ cell apoptosis. the prevention or germ cell death, and possibly specific therapy of some forms of infertility. Further well-controlled. carefully designed. larger-scale studies are necessary and desirable before widespread clinical use as an infertility therapy can be contemplated. C1 NIH, Endocrine Sect, Clin Invest Lab, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Harbor Med Ctr, Dept Med, Torrance, CA 90509 USA. Res Educ Inst, Torrance, CA 90509 USA. RP Blackman, MR (reprint author), NIH, Endocrine Sect, Clin Invest Lab, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA. EM blackman@mail.nih.gov FU NIDDK NIH HHS [T32DK7571-16] NR 36 TC 39 Z9 48 U1 0 U2 9 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-555-9 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1033 BP 177 EP 188 DI 10.1196/annals.1320.017 PG 12 WC Multidisciplinary Sciences; Nutrition & Dietetics; Pharmacology & Pharmacy; Physiology SC Science & Technology - Other Topics; Nutrition & Dietetics; Pharmacology & Pharmacy; Physiology GA BBO92 UT WOS:000226783500017 PM 15591015 ER PT S AU Campbell, SR Summers, RM AF Campbell, SR Summers, RM BE Lemke, HU Inamura, K Doi, K Vannier, MW Farman, AG Reiber, JHC TI Analysis of kernel method for surface curvature estimation SO CARS 2004: COMPUTER ASSISTED RADIOLOGY AND SURGERY, PROCEEDINGS SE INTERNATIONAL CONGRESS SERIES LA English DT Proceedings Paper CT 18th International Congress and Exhibition on Computer Assisted Radiology and Surgery (CARS 2004) CY JUN 23-26, 2004 CL Chicago, IL DE curvature estimation; volume data; medical image processing ID COMPUTER-AIDED DIAGNOSIS; COLONIC POLYPS; IMAGES AB We examine a method of curvature estimation that computes the curvature directly from three dimensional data. We refer to this as the kernel method of curvature estimation and our experiments indicate that several parameters be modified from those originally suggested to achieve more accurate and reliable results. This improved performance is essential for analysis of medical volume data by computer aided diagnosis algorithms, many of which use curvature estimation for shape computations and pattern recognition. We also examine cases in which the kernel method yields inaccurate responses based on specific topologies. (C) 2004 CARS and Elsevier B.V. All rights reserved. C1 NIH, Dept Diagnost Radiol, Ctr Clin, Bethesda, MD 20892 USA. RP Summers, RM (reprint author), NIH, Dept Diagnost Radiol, Ctr Clin, Bldg 10 Room 1C660,10 Ctr Dr MSC 1182, Bethesda, MD 20892 USA. EM rms@cc.nih.gov NR 11 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA SARA BURGERHARTSTRAAT 25, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0531-5131 BN 0-444-51731-6 J9 INT CONGR SER JI Int. Congr. Ser. PY 2004 VL 1268 BP 999 EP 1003 DI 10.1016/j.ics.2004.03.319 PG 5 WC Computer Science, Interdisciplinary Applications; Radiology, Nuclear Medicine & Medical Imaging; Surgery SC Computer Science; Radiology, Nuclear Medicine & Medical Imaging; Surgery GA BAV01 UT WOS:000223659100179 ER PT J AU Close, N Anand, R Hering, B Eggerman, T AF Close, N Anand, R Hering, B Eggerman, T TI NIH-supported national islet transplantation registry SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article; Proceedings Paper CT 3rd Annual Rachmiel Levine Diabetes and Obesity Symposium CY OCT, 2002 CL Anaheim, CA DE islet; transplantation; registry; multicenter; type 1; diabetes mellitus AB An estimated 300,000 to 500,000 cases of type 1 diabetes exist today in the United States. Despite strict monitoring and attempts at control, people with type 1 diabetes still face the prospect of diminished health and earlier death than the general population. Islet transplantation offers an alternative to insulin usage and a potential treatment for type 1 diabetes mellitus. There are more than 30 islet transplant centers in the world focusing their efforts on the challenges and methods of this procedure. As the field of islet transplantation matures and the number of islet transplants performed increases, detailed analyses on factors that predict patient and graft survival are needed. This increased amount of data will allow for a better understanding of the safety and efficacy of islet transplantation. In response to the need for more complete information in the field, the National Institute of Diabetes and Digestive and Kidney Diseases is sponsoring the North American Collaborative Islet Transplant Registry (CITR). The mission of CITR is to expedite progress and promote safety in islet/beta-cell transplantation through the collection, analysis, and communication of comprehensive and current data on all islet/beta-cell transplants performed in North America. Compiling and analyzing data from all transplant centers in North America will accelerate the identification of both critical risk factors and key determinants of success, and thereby guide transplant centers in developing and refining islet/beta-cell transplant protocols, leading to an advancement in the field of islet transplantation. Participation in CITR is voluntary, and more than 22 transplant centers have been invited to join. Seven centers are actively participating in CITR, with an additional 11 centers in the process of joining. Both an executive committee and a scientific advisory committee guide CITR. All islet transplants performed in North America since January 1, 1996, are captured by the CITR database. Through an electronic, Internet-based data capture system, quality control procedures, and minimization of duplicate efforts at the transplant center, the most relevant and succinct information are entered. From these data a comprehensive report will be published annually. In addition, special analyses will be performed and published periodically. C1 EMMES Corp, Rockville, MD USA. Univ Minnesota, Minneapolis, MN USA. NIDDKD, NIH, Rockville, MD USA. RP Close, N (reprint author), EMMES Corp, Rockville, MD USA. EM nclose@emmes.com NR 4 TC 1 Z9 1 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 2004 SU S BP 9 EP 17 PG 9 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 853SC UT WOS:000223846900002 ER PT J AU Bernier, M AF Bernier, M TI Protein tyrosine phosphatases - Potential role in beta-cell insulin signal transduction SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Article; Proceedings Paper CT 3rd Annual Rachmiel Levine Diabetes and Obesity Symposium CY OCT, 2002 CL Anaheim, CA DE insulin receptor; tyrosine kinase; protein tyrosine phosphatase; beta-cells; knockout mice; antisense oligonucleotides ID SUBSTRATE-TRAPPING MUTANTS; MICE LACKING; GLUCOSE-HOMEOSTASIS; GENE-TRANSCRIPTION; PANCREATIC-ISLETS; GLUCOKINASE GENE; SKELETAL-MUSCLE; DIABETIC MICE; IN-VIVO; RECEPTOR AB Insulin receptor signal transduction plays a critical role in regulating pancreatic beta-cell function, notably the acute first-phase insulin release in response to glucose. The basis for insulin resistance in pancreatic beta-cells is not well understood but may be related to abnormal regulation of tyrosine phosphorylation events, which, in turn, may alter organization of insulin-signaling molecules in space and time. Members of the protein tyrosine phosphatase (PTPase) family are both functionally and structurally diverse; and within the past few years data have emerged from many laboratories that suggest selectivity of the PTPase catalytic domains toward cellular substrates. Of significance, a subset of PTPases has been implicated in the regulation of insulin signaling in a number of insulin-sensitive tissues. Alteration in PTPase expression or activity has been associated with abnormal regulation of tyrosine phosphorylation events and is accompanied by modulation of insulin sensitivity in vivo. Manipulations aimed at reducing expression of physiologically relevant PTPases acting at a step proximal to the insulin receptor are accompanied by normalization of blood glucose levels and improved insulin sensitivity in both normal and diabetic animals. Hence, the development of tissue-specific gene inactivation strategies should facilitate the study of the potential role of PTPases in beta-cell insulin signaling transduction. C1 NIA, Diabet Sect, Clin Invest Lab, NIH, Baltimore, MD USA. RP Bernier, M (reprint author), NIA, Diabet Sect, Clin Invest Lab, NIH, Baltimore, MD USA. EM Bernierm@grc.nia.nih.gov OI Bernier, Michel/0000-0002-5948-368X NR 57 TC 0 Z9 0 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 2004 SU S BP 209 EP 217 PG 9 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 853SC UT WOS:000223846900020 ER PT J AU [Anonymous] AF [Anonymous] TI Role of NCRR-supported Islet Resource Centers in advancing islet transplantation SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Meeting Abstract RP NIH, Natl Ctr Res Resources, Div Clin Res, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 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 2004 SU S BP 235 EP 236 PG 2 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 853SC UT WOS:000223846900050 ER PT J AU [Anonymous] AF [Anonymous] TI NIH-supported national islet transplantation registry SO CELL BIOCHEMISTRY AND BIOPHYSICS LA English DT Meeting Abstract RP NIH, NIDDK, Bldg 10, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 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 2004 SU S BP 235 EP 235 PG 1 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 853SC UT WOS:000223846900049 ER PT J AU Aleem, E Berthet, C Kaldis, P AF Aleem, E Berthet, C Kaldis, P TI Cdk2 as a master of S phase entry - Fact or fake? SO CELL CYCLE LA English DT Article DE Cdk2; Cdk4; cyclin E; cyclin A; p27(Kip1); S phase ID CYCLIN-DEPENDENT KINASES; TARGETED DISRUPTION; MICE LACKING; P27(KIP1); HYPERPLASIA; INHIBITOR; MOUSE; DEFICIENT; MEIOSIS; GROWTH AB It has long been believed that Cdk2 and its activator cyclin E play essential roles in the progression of the mitotic cell cycle. However, recent studies using knockout mouse models revealed that neither Cdk2 nor cyclin E are essential in vivo. The purpose of this Perspective is to compare both Cdk2 and cyclin E knockout mice models and to discuss potential mechanisms driving the cell cycle in the absence of Cdk2 or cyclin E. Particular emphasis is placed on possible non-catalytic roles of cyclin E, the expression and activity of the second cyclin binding partner of Cdk2, cyclin A, as well as on the expression and degradation of the Cdk2 inhibitor p27(Kip1) in the absence of Cdk2. C1 NCI, Regulat Cell Growth Lab, NIH, Frederick, MD 21702 USA. RP Kaldis, P (reprint author), NCI, Regulat Cell Growth Lab, NIH, Bldg 560-22-56,1050 Boyles St, Frederick, MD 21702 USA. EM kaldis@ncifcrf.gov RI Kaldis, Philipp/G-2714-2010; OI Kaldis, Philipp/0000-0002-7247-7591; Aleem, Eiman/0000-0002-9215-8213 NR 25 TC 29 Z9 32 U1 0 U2 0 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4101 J9 CELL CYCLE JI Cell Cycle PD JAN PY 2004 VL 3 IS 1 BP 35 EP 37 PG 3 WC Cell Biology SC Cell Biology GA 833RB UT WOS:000222354900012 PM 14657662 ER PT J AU Woodhouse, EC Liotta, LA AF Woodhouse, EC Liotta, LA TI Drosophila invasive tumors - A model for understanding metastasis SO CELL CYCLE LA English DT Article DE Drosophila; neoplastic growth; metastasis; genetic screen; tumor supressor gene ID HUMAN HOMOLOG; TGF-BETA; CELL POLARITY; GROWTH; PROTEIN; CANCER; PROLIFERATION; SUPPRESSORS; EXPRESSION; APOPTOSIS AB Inactivation of Drosophila tumor suppressor genes can cause excessive proliferation and, in some cases, neoplastic growth. Neoplastic growth in Drosophila tissues can also be followed by metastasis upon transplantation into hosts or in vivo. Recently, we have shown that metastatic tumors of Drosophila can provide a model in which to identify genes that are involved in the metastatic process. C1 NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA. RP Woodhouse, EC (reprint author), NCI, Pathol Lab, NIH, 9000 Rockville Pike,Bldh 10,Rm 2A33, Bethesda, MD 20892 USA. EM elisa@mail.nih.gov NR 23 TC 8 Z9 9 U1 0 U2 1 PU LANDES BIOSCIENCE PI GEORGETOWN PA 810 SOUTH CHURCH STREET, GEORGETOWN, TX 78626 USA SN 1538-4101 J9 CELL CYCLE JI Cell Cycle PD JAN PY 2004 VL 3 IS 1 BP 38 EP 40 PG 3 WC Cell Biology SC Cell Biology GA 833RB UT WOS:000222354900013 PM 14657663 ER PT J AU Yu, P Neamati, N Tarasov, S He, Q Sheikh, MS Wang, YX AF Yu, P Neamati, N Tarasov, S He, Q Sheikh, MS Wang, YX TI Codon-optimized cloning, expression and characterization of the C-terminal region of human apoptotic protein GADD34 in Escherichia coli SO CELL CYCLE LA English DT Article DE GADD34; synthetic gene; expression; purification; apoptotic protein ID HERPES-SIMPLEX-VIRUS; DNA-DAMAGE; GROWTH ARREST; GENE; CELLS; DIFFERENTIATION; POLYMERASE; SIMILARITY; LYSOZYME; SEQUENCE AB The human GADD34 (Growth Arrest and DNA Damage-inducible 34) is the product of an apoptosis- and DNA-damage-inducible gene. The C-terminus domain of GADD34 is highly homologous to HSV-1.1 34.5, HSV-2 and the African swine fever virus virulence-associated factor NL-S. Among these viral proteins, HSV-gamma(1). 34.5 protein is known to prevent apoptosis of viral-infected cells. Because of the difficulty in expressing GADD34 protein or any of its fragments, including the C-terminus ( amino acids 533-632) in E. coli, partially due to sub-optimal expression of eukaryotic codons in prokaryotic E. coli, we used a codon-optimized cloning scheme to construct the eukaryotic gene that codes for GADD34(533-632). We derived a novel PCR protocol to assemble 20 oligonucleotides into the synthetic GADD34(533-632) gene. The clear advantage of using this protocol is that the assembled gene is without the mutation and deletion that are usually of a major problem in constructing synthetic genes. The synthetic GADD34(533-632) gene was cloned, expressed, and purified in large quantity. We obtained approximately 50 mg of GADD34(533-632) protein per liter minimum-medium culture. To our knowledge, this is the first report of a large-scale production of the C-terminus of GADD34. The production and purification of GADD34(533-632) in large quantity are essential for structure determination as well as for understanding its interactions with other proteins such as phosphatase 1-alpha using NMR spectroscopy and other biophysical methods. C1 NCI, Prot Nucleic Acid Interact Sect, Struct Biophys Lab, Frederick, MD 21702 USA. Univ So Calif, Sch Pharm, Dept Pharmaceut Sci, Los Angeles, CA 90033 USA. NCI, Biophys Resource, Struct Biophys Lab, Frederick, MD 21701 USA. SUNY Upstate Med Univ, Dept Pharmacol, Syracuse, NY USA. RP Wang, YX (reprint author), NCI, Prot Nucleic Acid Interact Sect, Struct Biophys Lab, Bldg 538,Room 133, Frederick, MD 21702 USA. EM wangyu@ncifcrf.gov NR 21 TC 5 Z9 5 U1 0 U2 0 PU LANDES BIOSCIENCE PI AUSTIN PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA SN 1538-4101 J9 CELL CYCLE JI Cell Cycle PD JAN PY 2004 VL 3 IS 1 BP 75 EP 79 PG 5 WC Cell Biology SC Cell Biology GA 833RB UT WOS:000222354900021 PM 14657671 ER PT J AU Freed, WJ AF Freed, WJ TI A perspective on transplantation therapy and stem cells for Parkinson's disease SO CELL TRANSPLANTATION LA English DT Editorial Material ID ADRENAL-MEDULLA GRAFTS; UNILATERAL DOPAMINE DEPLETION; BRAIN-TISSUE TRANSPLANTATION; EMBRYONIC NIGRAL NEURONS; MEDIATED GENE-TRANSFER; SUBSTANTIA-NIGRA; RAT MODEL; NIGROSTRIATAL PATHWAY; NEUROTROPHIC FACTOR; ANIMAL-MODEL C1 NIDA, Cellular Neurobiol Res Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Baltimore, MD 21224 USA. RP Freed, WJ (reprint author), NIDA, Cellular Neurobiol Res Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, 333 Cassell Dr,Triad Bldg,Room 3501, Baltimore, MD 21224 USA. EM wfreed@intra.nida.nih.gov NR 66 TC 18 Z9 21 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. PY 2004 VL 13 IS 3 BP 319 EP 327 DI 10.3727/000000004783984025 PG 9 WC Cell & Tissue Engineering; Medicine, Research & Experimental; Transplantation SC Cell Biology; Research & Experimental Medicine; Transplantation GA 821XY UT WOS:000221497900013 PM 15191169 ER PT S AU Heimlich, G Bortner, CD Cidlowski, JA AF Heimlich, G Bortner, CD Cidlowski, JA BE Lauf, PK Adragna, NC TI Apoptosis and cell volume regulation - The importance of ions and ion channels SO CELL VOLUME AND SIGNALING SE ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY LA English DT Article; Proceedings Paper CT International Symposium on Cell Volume and Signaling CY SEP 20-24, 2003 CL Wright State Univ, Dayton, OH SP Natl Inst Hlth, Natl Inst Diabetes Digest & Kidney Dis HO Wright State Univ ID PLASMA-MEMBRANE DEPOLARIZATION; TUMOR-NECROSIS-FACTOR; T-LYMPHOCYTES; CD95-INDUCED APOPTOSIS; THYMOCYTE APOPTOSIS; CORTICAL-NEURONS; SMOOTH-MUSCLE; K+ CHANNEL; IN-VITRO; DEATH C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. RP Heimlich, G (reprint author), NIEHS, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. EM bortner@niehs.nih.gov; cidlows1@niehs.nih.gov NR 59 TC 14 Z9 16 U1 1 U2 6 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES SN 0065-2598 BN 0-387-23299-0 J9 ADV EXP MED BIOL JI Adv.Exp.Med.Biol. PY 2004 VL 559 BP 189 EP 203 PG 15 WC Cell Biology; Medicine, Research & Experimental SC Cell Biology; Research & Experimental Medicine GA BDB39 UT WOS:000232359300018 PM 18727240 ER PT J AU Panelli, MC Martin, B Nagorsen, D Wang, E Smith, K Monsurro, V Marincola, FM AF Panelli, MC Martin, B Nagorsen, D Wang, E Smith, K Monsurro, V Marincola, FM TI A genomic- and proteomic-based hypothesis on the eclectic effects of systemic interleukin-2 administration in the context of melanoma-specific immunization SO CELLS TISSUES ORGANS LA English DT Article; Proceedings Paper CT 2nd International Workshop on Space Radiation Research CY MAR 11-15, 2002 CL NARA, JAPAN DE chemokines; cytokines; immunization; interleukin-2; melanoma ID HIGH-DOSE INTERLEUKIN-2; RECEPTOR GENES; T-CELLS; CYTOKINE; CANCER; IMMUNOTHERAPY; IL-2; IDENTIFICATION; POLYMORPHISMS; MACROPHAGES AB Among human cancers, melanoma is characterized by an almost unique predisposition to regress in response to immune therapy. Recent clinical studies suggest that the frequency of this favorable event is enhanced by combining T-cell-directed active specific immunization with the systemic administration of interleukin (IL)-2. While waiting for additional clinical experience to confirm this observation, we embraced the working hypothesis that this combination provides superior response rates than either treatment alone. In particular, we have focused our interest on the paradoxical observation that active specific immunization consistently induces circulating CD8+ T cells capable of recognizing in ex vivo assays tumor cells, but cannot induce tumor regression alone. In these settings, it appears that combining the systemic administration of IL-2 is almost an absolute requirement for the induction of clinical responses. Here, we will expand on previous speculations on the postulated mechanism(s) of action of systemic IL-2 administration and, based on original data recently derived through high-throughput transcriptional and post-translational analysis, we will suggest an explanation for the eclectic effects of IL-2 administration in the context of active specific immunization. Copyright (C) 2004 S. Karger AG, Basel. C1 NIH, Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA. NIMH, NIH, Bethesda, MD 20892 USA. RP Marincola, FM (reprint author), NIH, Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bldg 10,Room 1C-711,10 Ctr Dr MSC 1502, Bethesda, MD 20892 USA. EM FMarincola@mail.cc.nih.gov NR 23 TC 6 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1422-6405 J9 CELLS TISSUES ORGANS JI Cells Tissues Organs PY 2004 VL 177 IS 3 BP 124 EP 131 DI 10.1159/000079986 PG 8 WC Anatomy & Morphology; Cell Biology; Developmental Biology SC Anatomy & Morphology; Cell Biology; Developmental Biology GA 852LM UT WOS:000223756800003 PM 15388986 ER PT J AU Pfutzner, W Vogel, JC AF Pfutzner, W Vogel, JC TI Topical colchicine selection of keratinocytes transduced with the multidrug resistance gene (MDR1) can sustain and enhance transgene expression in vivo SO CELLS TISSUES ORGANS LA English DT Article; Proceedings Paper CT 2nd International Workshop on Space Radiation Research CY MAR 11-15, 2002 CL NARA, JAPAN DE keratinocytes; MDR; retroviral vector; selection ID PRODUCT P-GLYCOPROTEIN; LONG-TERM EXPRESSION; HEMATOPOIETIC-CELLS; EPIDERMAL-KERATINOCYTES; DRUG SELECTION; BONE-MARROW; STEM-CELLS; SKIN; THERAPY; MICE AB In gene therapy, a clinically relevant therapeutic effect requires long-term expression of the desired gene at a level sufficient to correct or at least alleviate the underlying gene defect. One approach to achieve persistent as well as high-level transgene expression in a significant percentage of target cells would be to select cells expressing both the desired transgene and a linked selectable gene such as the human multi-drug resistance (MDR1) gene-in a bicistronic vector. Because of its accessibility, the skin is a very attractive target tissue to select genetically modified cells, allowing topical application of a selecting agent, thus minimizing potential toxic side effects. Among the potential selecting drugs, agents that block cell division, such as colchicine, are of particular interest because the use of anti-mitotic drugs takes advantage of the rapid keratinocyte ( KC) turnover in the epidermis and the need for continued proliferation to substitute the KC lost due to selection. Before assessing the therapeutic benefit of such an approach, several key questions need to be answered in preclinical models: ( 1) Does topical colchicine application achieve the desired in vivo effect by blocking KC mitosis without eliciting unwanted toxic side effects? ( 2) Are MDR-transduced (MDR+) human KC still able to proliferate and differentiate when treated with colchicine? ( 3) Can MDR+ KC be enriched by topical selection? ( 4) Does topical selection result in persistent transgene expression by selecting KC stem cells expressing MDR? To answer these questions and to test the feasibility of such an approach both an in vitro skin equivalent and an in vivo human skin graft model were developed in which MDR+ KC were treated with different dosages of colchicine. Quantitative and qualitative analyses of MDR expression in human KC showed that topical colchicine treatment selects high-level transgene expression in a high percentage of KC. Moreover, determination of transgene copy numbers demonstrated that MDR+ KC progenitor cells were enriched by topical selection resulting in long-term expression of the transgene in the skin. Thus, in summary, these models demonstrate that topical selection of MDR+ KC is a safe approach to efficiently enhance long-term gene expression in the skin and holds future promise for clinical gene therapy applications. Copyright (C) 2004 S. Karger AG, Basel. C1 Univ Munich, Dermatol Klin, Dept Dermatol, DE-80337 Munich, Germany. NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA. RP Pfutzner, W (reprint author), Univ Munich, Dermatol Klin, Dept Dermatol, Frauenlobstr 9-11, DE-80337 Munich, Germany. EM Wolfgang_Pfutzner@web.de NR 47 TC 2 Z9 2 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1422-6405 J9 CELLS TISSUES ORGANS JI Cells Tissues Organs PY 2004 VL 177 IS 3 BP 151 EP 159 DI 10.1159/000079989 PG 9 WC Anatomy & Morphology; Cell Biology; Developmental Biology SC Anatomy & Morphology; Cell Biology; Developmental Biology GA 852LM UT WOS:000223756800006 PM 15388989 ER PT J AU Holland, AL Ramage, AE AF Holland, Audrey L. Ramage, Amy E. BE Duchan, JF Byng, S TI Learning from Roger Ross: A clinical journey SO CHALLENGING APHASIA THERAPIES: BROADENING THE DISCOURSE AND EXTENDING THE BOUNDARIES LA English DT Article; Book Chapter C1 [Holland, Audrey L.] Univ Arizona, Tucson, AZ 85721 USA. [Holland, Audrey L.] US Natl Inst Deafness & Other Commun Disorders, Advisory Council, NIH, Bethesda, MD USA. [Ramage, Amy E.] San Diego State Univ, San Diego, CA 92182 USA. RP Holland, AL (reprint author), Univ Arizona, Tucson, AZ 85721 USA. NR 12 TC 3 Z9 3 U1 0 U2 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH ROAD, HOVE BN3 2FA, E SUSSEX, ENGLAND BN 978-0-20346-270-6 PY 2004 BP 118 EP 129 DI 10.4324/9780203462706_chapter_7 D2 10.4324/9780203462706 PG 12 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA BUJ51 UT WOS:000289513000008 ER PT J AU Berezhkovskii, AM Barzykin, A AF Berezhkovskii, AM Barzykin, A TI Diffusive escape and reentry through a channel in the cavity wall SO CHEMICAL PHYSICS LETTERS LA English DT Article ID FACILITATED MEMBRANE-TRANSPORT; PARTICLE; HOLE AB We show that the kinetics of diffusive escape from a cavity through a narrow channel in the cavity wall and successive reentry can be described by a formal kinetic scheme for reversible dissociation of a spherical binding site with appropriately defined effective association and dissociation rate constants. Initially the population of the cavity decays exponentially, with the rate constant determined by the cavity volume and the channel length and radius. A crossover to the universal inverse power law behavior, which does not depend on the channel geometry, occurs at long times. These simple predictions are in excellent agreement with the results of Brownian dynamics simulations. (C) 2003 Elsevier B.V. All rights reserved. C1 Natl Inst AIST, PCRC, Tsukuba, Ibaraki 3058565, Japan. NIH, Ctr Informat Technol, Bethesda, MD 20892 USA. RP Berezhkovskii, AM (reprint author), Natl Inst AIST, PCRC, Higashi 1-1, Tsukuba, Ibaraki 3058565, Japan. NR 9 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-2614 J9 CHEM PHYS LETT JI Chem. Phys. Lett. PD JAN 1 PY 2004 VL 383 IS 1-2 BP 6 EP 10 DI 10.1016/j.cplett.2003.10.128 PG 5 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical SC Chemistry; Physics GA 759TL UT WOS:000187752900002 ER PT J AU Inbaraj, JJ Chignell, CF AF Inbaraj, JJ Chignell, CF TI Cytotoxic action of juglone and plumbagin: A mechanistic study using HaCaT keratinocytes SO CHEMICAL RESEARCH IN TOXICOLOGY LA English DT Article ID ISOLATED RAT HEPATOCYTES; ELECTRON-SPIN-RESONANCE; OXIDATIVE STRESS; SUBSTITUTED 1,4-NAPHTHOQUINONES; ENDOTHELIAL DYSFUNCTION; RELATIVE IMPORTANCE; THIOL HOMEOSTASIS; MENADIONE; GLUTATHIONE; REDUCTASE AB Juglone (5-hydroxy-1,4-naphthoquinone) and plumbagin (5-hydroxy-3-methyl-1,4-naphthoquinone) are yellow pigments found in black walnut (Juglans regia). Herbal preparations derived from black walnut have been used as hair dyes and skin colorants in addition to being applied topically for the treatment of acne, inflammatory diseases, ringworm, and fungal, bacterial, or viral infections. We have studied the cytotoxicity of these quinones to HaCaT keratinocytes. Exposure to juglone or plumbagin (1-20 muM) resulted in a concentration-dependent decrease in cell viability. The cytotoxicity of these quinones is due to two different mechanisms, namely, redox cycling and reaction with glutathione (GSH). Redox cycling results in the generation of the corresponding semiquinone radicals, which were detected by electron paramagnetic resonance. Incubation of keratinocytes with the quinones generated hydrogen peroxide (H2O2) and resulted in the oxidation of GSH to GSSG. Depletion of GSH by buthionine sulfoximine enhanced semiquinone radical production, increased H2O2 generation, and produced greater cytotoxicity, suggesting that GSH plays an important protective role. Both quinones decreased the intracellular levels of GSH. However, plumbagin stoichiometrically converted GSH to GSSG, indicating that redox cycling is its main metabolic pathway. In contrast, much of the GSH lost during juglone exposure, especially at the higher concentrations (10 and 20 muM), did not appear as GSSG, suggesting that the cytotoxicity of this quinone may also involve nucleophilic addition to GSH. Our findings indicate that topical preparations containing juglone and plumbagin should be used with care as their use may damage the skin. However, it is probable that the antifungal, antiviral, and antibacterial properties of these quinones are the result of redox cycling. C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. RP Chignell, CF (reprint author), NIEHS, Lab Pharmacol & Chem, POB 12233, Res Triangle Pk, NC 27709 USA. EM chignell@niehs.nih.gov NR 29 TC 166 Z9 181 U1 4 U2 45 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 2004 VL 17 IS 1 BP 55 EP 62 DI 10.1021/tx034132s PG 8 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA 766XF UT WOS:000188400100007 PM 14727919 ER PT J AU Kovac, P AF Kovac, P TI Quantity over quality? An open letter to the community of chemists SO CHEMISTRY & BIODIVERSITY LA English DT Editorial Material C1 NIDDK, LMC, NIH, Bethesda, MD 20892 USA. RP Kovac, P (reprint author), NIDDK, LMC, NIH, Bldg 8,Rm B1A25,8 Ctr Dr, Bethesda, MD 20892 USA. EM kpn@helix.nih.gov NR 0 TC 3 Z9 4 U1 0 U2 1 PU VERLAG HELVETICA CHIMICA ACTA AG PI ZURICH PA HOFWIESENSTRASSE 26, POSTFACH, CH-8042 ZURICH, SWITZERLAND SN 1612-1872 J9 CHEM BIODIVERS JI Chem. Biodivers. PY 2004 VL 1 IS 4 BP 606 EP 608 DI 10.1002/cbdv.200490051 PG 3 WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary SC Biochemistry & Molecular Biology; Chemistry GA 852OH UT WOS:000223765700004 PM 17191871 ER PT J AU Kang, SU Yang, G Li, W Zhang, ZY Burke, TR AF Kang, SU Yang, G Li, W Zhang, ZY Burke, TR TI Enantioselective synthesis of (S)-3-carboxy-4-((carboxy)difluoromethyl)phenylalanine in protected form and its incorporation into a PTP-1B-directed tripeptide SO CHEMISTRY & BIODIVERSITY LA English DT Article ID SIGNAL-TRANSDUCTION INHIBITORS; PROTEIN-TYROSINE PHOSPHATASE-1B; SOLID-PHASE SYNTHESIS; PHOSPHOTYROSYL MIMETICS; POTENT INHIBITION; AMINO-ACIDS; PEPTIDES; DESIGN; ESTERS; ETHERS AB Recent findings have shown that, when expressed in the tripeptide platform, 'Fmoc-Glu-Xxx-Leu-amide', the phosphotyrosyl mimetic (pTyr), Xxx=(S)-3-carboxy-4-(carboxymethyl)-Phe, provides higher PTP-1B affinity than that obtained with Xxx=(S)-difluorophosphonomethyl-Phe (F2PMP). This was of note, since difluorophosphonomethyl-containing pTyr mimetics have typically exhibited higher PTP-inhibitory potencies than carboxy-based mimetics, indicating the potential value of 3-carboxy-4-(carboxymethyl)-Phe as a starting point for further analogue development. Therefore, relying on precedence that alpha-fluorination often enhances PTP-1B affinity, (S)-3-carboxy-4-((carboxy)difluoromethyl)-Phe was designed as a PTP-1B-directed pTyr mimetic. Reported herein is the synthesis of this new amino acid analogue through application of commercially available Williams chiral auxiliary. The target was prepared in an orthogonally protected form suitable for peptide synthesis according to Fmoc chemistries and utilization for the synthesis of a PTP-1B-directed tripeptide bearing the sequence indicated above. Biological evaluation with in vitro PTP-1B assays indicated nearly total loss of affinity for this peptide. Evidence is provided that the unexpected deleterious effect of fluorination is probably not related to pK(a) effects. C1 NCI, Canc Res Ctr, Med Chem Lab, NIH, Frederick, MD 21702 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10461 USA. RP Burke, TR (reprint author), NCI, Canc Res Ctr, Med Chem Lab, NIH, POB B,Bldg 376 Boyles St, Frederick, MD 21702 USA. EM tburke@helix.nih.gov RI Burke, Terrence/N-2601-2014 FU NIAID NIH HHS [1U54 AI057158] NR 25 TC 4 Z9 4 U1 0 U2 4 PU VERLAG HELVETICA CHIMICA ACTA AG PI ZURICH PA HOFWIESENSTRASSE 26, POSTFACH, CH-8042 ZURICH, SWITZERLAND SN 1612-1872 J9 CHEM BIODIVERS JI Chem. Biodivers. PY 2004 VL 1 IS 4 BP 626 EP 633 DI 10.1002/cbdv.200490053 PG 8 WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary SC Biochemistry & Molecular Biology; Chemistry GA 852OH UT WOS:000223765700006 PM 17191873 ER PT J AU Taylor, RK Kim, TJ Bose, N Stonehouse, E Tripathi, SA Kovac, P Wade, WE AF Taylor, RK Kim, TJ Bose, N Stonehouse, E Tripathi, SA Kovac, P Wade, WE TI Progress towards development of a cholera subunit vaccine SO CHEMISTRY & BIODIVERSITY LA English DT Review ID TOXIN-COREGULATED PILUS; VIRULENCE FACTOR EXPRESSION; VIBRIO-CHOLERAE; MONOCLONAL-ANTIBODIES; INTESTINAL COLONIZATION; SEROTYPE INABA; PROTECTIVE IMMUNITY; O-PS; LIPOPOLYSACCHARIDE; OGAWA AB Cholera, an enteric disease that can reach pandemic proportions, remains a world-wide problem that is positioned to increase in incidence as changes in global climate or armed conflict spawn the conditions that enhance transmission to humans and, thus, precipitate epidemic cholera. An effective subunit cholera vaccine that can provide protective immunity with one parenteral immunization would be a major advantage over the existing oral vaccines that can require two doses for optimal protection. The existing vaccines are clearly effective in some settings, but are less so in others, especially with respect to specific groups such as young (2 - 5 years) children. In our efforts to develop a cholera subunit vaccine, we focused on two Vibrio cholerae antigens, LPS (lipopolysaccharide) and TCP (toxin co-regulated pilus). that are known to induce protective antibodies in animal models and, in the case of anti-LPS antibodies, to be associated with clinical protection of V cholerae exposed or vaccinated individuals. This review discusses the current cholera vaccines and compares the advantages of a cholera subunit vaccine to that of the whole cell vaccines. We discuss the possible subunit antigens and prospective targeted use of a subunit cholera vaccine. C1 Dartmouth Coll Sch Med, Dept Microbiol & Immunol, Lebanon, NH 03756 USA. NIDDKD, Med Chem Lab, NIH, Bethesda, MD 20892 USA. RP Taylor, RK (reprint author), Dartmouth Coll Sch Med, Dept Microbiol & Immunol, Lebanon, NH 03756 USA. FU Intramural NIH HHS; NIAID NIH HHS [AI25096, AI47373] NR 68 TC 15 Z9 16 U1 0 U2 0 PU VERLAG HELVETICA CHIMICA ACTA AG PI ZURICH PA HOFWIESENSTRASSE 26, POSTFACH, CH-8042 ZURICH, SWITZERLAND SN 1612-1872 J9 CHEM BIODIVERS JI Chem. Biodivers. PY 2004 VL 1 IS 7 BP 1036 EP 1057 DI 10.1002/cbdv.200490078 PG 22 WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary SC Biochemistry & Molecular Biology; Chemistry GA 855FD UT WOS:000223957700004 PM 17191897 ER PT J AU Law, B Curino, A Bugge, TH Weissleder, R Tung, CH AF Law, B Curino, A Bugge, TH Weissleder, R Tung, CH TI Design, synthesis, and characterization of urokinase plasminogen-activator-sensitive near-infrared reporter SO CHEMISTRY & BIOLOGY LA English DT Article ID BREAST-CANCER; TUMOR INVASION; SYSTEM; METASTASIS; INHIBITOR; MICE; ANGIOGENESIS; PROTEASES; RECEPTOR; TISSUE AB The urokinase-type plasminogen activator (uPA) plays a critical role in malignancies, and its overexpression has been linked to poor clinical prognosis in breast cancer. The ability to noninvasively and serially map uPA expression as a biomarker would thus have significant potential in improving novel cancer therapies. Here, we describe the development of a selective uPA activatable near-infrared (NIR) fluorescent imaging probe. The probe consists of multiple peptide motifs, GGSGRSANAKC-NH2, terminally capped with different NIR fluorochromes (Cy5.5 or Cy7) and a pegylated poly-L-lysine graft copolymer. Upon addition of recombinant human uPA to the probe, significant fluorescence amplification was observed, up to 680% with the optimized preparation. No activation with negative control compounds and uPA inhibitors could be measured. These data indicate that the optimized preparation should be useful for imaging uPA in cancer. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02129 USA. NIDCR, Proteases & Tissue Remodeling Unit, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA. RP Tung, CH (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02129 USA. EM tung@helix.mgh.harvard.edu OI Tung, Ching-Hsuan/0000-0001-6648-6195 FU NCI NIH HHS [N01-CO17016, P50-CA86355, R01 CA99385] NR 31 TC 64 Z9 68 U1 2 U2 18 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1074-5521 J9 CHEM BIOL JI Chem. Biol. PD JAN PY 2004 VL 11 IS 1 BP 99 EP 106 DI 10.1016/j.chembiol.2003.12.017 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 768NQ UT WOS:000188549400017 PM 15112999 ER PT J AU Shorr, AF Susla, GM O'Grady, NP AF Shorr, AF Susla, GM O'Grady, NP TI Pulmonary infiltrates in the non-HIV-infected immunocompromised patient - Etiologies, diagnostic strategies, and outcomes SO CHEST LA English DT Review DE bronchoscopy; complications; fungus; immunocompromised; infection; infiltrates; malignancy; outcomes; transplant ID STEM-CELL TRANSPLANT; PNEUMOCYSTIS-CARINII PNEUMONIA; FEBRILE NEUTROPENIC PATIENTS; BONE-MARROW-TRANSPLANTATION; ACUTE RESPIRATORY-FAILURE; OPEN LUNG-BIOPSY; INVASIVE ASPERGILLOSIS; SOLID-ORGAN; NONINVASIVE VENTILATION; BRONCHOALVEOLAR LAVAGE AB Pulmonary complications remain a major cause of both morbidity and mortality in immunocompromised patients. When such individuals present with radiographic infiltrates, the clinician faces a diagnostic challenge. The differential diagnosis in this setting is broad and includes both infectious and noninfectious processes. Rarely are the radiographic findings classic for one disease, and most potential etiologies have overlapping clinical and radiographic appearances. In recent years, several themes have emerged in the literature on this topic. First, an aggressive approach to identifying a specific etiology is necessary; as a corollary, diagnostic delay increases the risk for mortality. Second, the evaluation of these infiltrates nearly always entails bronchoscopy. Bronchoscopy allows identification of some etiologies with certainty, and often allows for the exclusion of infectious agents even if the procedure is otherwise unrevealing. Third, early use of CT scanning regularly demonstrates lesions missed by plain radiography. Despite these advances, initial therapeutic interventions include the use of broad-spectrum antibiotics and other anti-infectives in order to ensure that the patients is receiving appropriate therapy. With the results of invasive testing, these treatments are then narrowed. Frustratingly, outcomes for immunocompromised patients with infiltrates remain poor. C1 Walter Reed Army Med Ctr, Pulm & Crit Care Med Serv, Washington, DC 20307 USA. NIH, Dept Crit Care Med, Clin Ctr, Bethesda, MD 20892 USA. RP Shorr, AF (reprint author), Walter Reed Army Med Ctr, Pulm & Crit Care Med Serv, 6900 Georgia Ave NW, Washington, DC 20307 USA. EM afshorr@dnamail.com NR 58 TC 64 Z9 74 U1 0 U2 2 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 2004 VL 125 IS 1 BP 260 EP 271 DI 10.1378/chest.125.1.260 PG 12 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 764QN UT WOS:000188217700042 PM 14718449 ER PT J AU Bornstein, MH Cote, LR AF Bornstein, MH Cote, LR TI Mothers' parenting cognitions in cultures of origin, acculturating cultures, and cultures of destination SO CHILD DEVELOPMENT LA English DT Article ID UNITED-STATES; SELF-CONCEPT; MIDDLE-CLASS; BEHAVIOR; INDIVIDUALISM; ATTRIBUTIONS; COLLECTIVISM; METAANALYSIS; PARENTHOOD; COMPETENCE AB Japanese and South American immigrant mothers' parenting cognitions (attributions and self-perceptions) were compared with mothers from their country of origin (Japan and Argentina, respectively) and European American mothers in the United States. Participants were 231 mothers of 20-month-old children. Generally, South American immigrant mothers' parenting cognitions more closely resembled those of mothers in the United States, whereas Japanese immigrant mothers' cognitions tended to be similar to those of Japanese mothers or intermediate between Japanese and U.S. mothers. This study provides insight into the nature of parenting cognitions generally and those of immigrant mothers specifically and therefore the parenting climate in which immigrant children are reared. C1 NICHHD, NIH, US Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Bornstein, MH (reprint author), NICHHD, NIH, US Dept Hlth & Human Serv, Suite 8030,6705 Rockledge Dr, Bethesda, MD 20892 USA. EM Marc_H_Bornstein@nih.gov NR 98 TC 58 Z9 59 U1 0 U2 8 PU BLACKWELL PUBLISHERS PI MALDEN PA 350 MAIN STREET, STE 6, MALDEN, MA 02148 USA SN 0009-3920 J9 CHILD DEV JI Child Dev. PD JAN-FEB PY 2004 VL 75 IS 1 BP 221 EP 235 DI 10.1111/j.1467-8624.2004.00665.x PG 15 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 776YF UT WOS:000189146400015 PM 15015686 ER PT J AU Allhusen, V Belsky, J Booth-LaForce, C Bradley, RH Brownell, CA Burchinal, M Campbell, SB Clarke-Stewart, A Cox, M Friedman, SL Hirsh-Pasek, K Huston, A Jaeger, E Kelly, JF Knoke, B Marshall, NL McCartney, K O'Brien, M Owen, MT Parke, R Payne, CC Pierce, KM Phillips, D Pianta, R Spieker, S Vandell, DL Weinraub, M AF Allhusen, V Belsky, J Booth-LaForce, C Bradley, RH Brownell, CA Burchinal, M Campbell, SB Clarke-Stewart, A Cox, M Friedman, SL Hirsh-Pasek, K Huston, A Jaeger, E Kelly, JF Knoke, B Marshall, NL McCartney, K O'Brien, M Owen, MT Parke, R Payne, CC Pierce, KM Phillips, D Pianta, R Spieker, S Vandell, DL Weinraub, M CA Natl Inst Child Hlth & Human Dev TI Are child developmental outcomes related to before- and after-school care arrangements? Results from the NICHD Study of Early Child Care SO CHILD DEVELOPMENT LA English DT Article ID BEHAVIORAL-ADJUSTMENT; ACADEMIC-ACHIEVEMENT; INCOME; PROGRAMS; EXPERIENCES; CONTINUITY; YOUTH; RISK AB Data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care, a prospective, longitudinal study involving 933 children, were used to examine relations between cumulative participation in 5 types of out-of-school care (before- and after-school programs, extracurricular activities, sitters, fathers, and nonadult care) and child developmental outcomes in the latter part of first grade (approximately age 7 years). Children who consistently participated in extracurricular activities during kindergarten and first grade obtained higher standardized test scores than children who did not consistently participate in these activities, controlling for child and family factors and children's prior functioning. Participation in other types of out-of-school care was not associated with child functioning in first grade when background factors were controlled. C1 Univ Calif Irvine, Irvine, CA USA. Univ London, London WC1E 7HU, England. Univ Washington, Seattle, WA 98195 USA. Univ Arkansas, Little Rock, AR 72204 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. Univ N Carolina, Chapel Hill, NC USA. NICHD, Bethesda, MD USA. Temple Univ, Philadelphia, PA 19122 USA. Univ Texas, Austin, TX 78712 USA. St Josephs Univ, Philadelphia, PA 19131 USA. Res Triangle Inst, Res Triangle Pk, NC 27709 USA. Wellesley Coll, Wellesley, MA 02181 USA. Harvard Univ, Cambridge, MA 02138 USA. Univ N Carolina, Greensboro, NC 27412 USA. Univ Texas, Dallas, TX 75230 USA. Univ Calif Riverside, Riverside, CA 92521 USA. Univ Wisconsin, Madison, WI USA. Georgetown Univ, Washington, DC 20057 USA. Univ Virginia, Charlottesville, VA 22903 USA. RP Allhusen, V (reprint author), NICHD, Early Child Care & Youth Dev Res Network, CRMC, 6100 Execut Blvd,4B05, Rockville, MD 20852 USA. RI Marshall, Nancy/C-3428-2012 NR 39 TC 30 Z9 30 U1 3 U2 12 PU BLACKWELL PUBLISHERS PI MALDEN PA 350 MAIN STREET, STE 6, MALDEN, MA 02148 USA SN 0009-3920 J9 CHILD DEV JI Child Dev. PD JAN-FEB PY 2004 VL 75 IS 1 BP 280 EP 295 PG 16 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 776YF UT WOS:000189146400019 ER PT J AU Sullivan, SA Landsman, D AF Sullivan, SA Landsman, D TI Mining core historic sequences from public protein databases SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID CHROMATIN; VARIANTS; H2A; HISTONES; H3 C1 Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RP Sullivan, SA (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA. RI Landsman, David/C-5923-2009 FU Intramural NIH HHS [Z01 LM000071-13, ZIA LM000071-15, ZIA LM000071-16] NR 22 TC 1 Z9 1 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 2004 VL 375 BP 3 EP 20 PG 18 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY51R UT WOS:000189397900001 PM 14870656 ER PT J AU Pilch, DR Redon, C Sedelnikova, OA Bonner, WM AF Pilch, DR Redon, C Sedelnikova, OA Bonner, WM TI Two-dimensional gel analysis of histones and other H2AX-related methods SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID DISC ELECTROPHORESIS; DNA; PROTEINS; CELLS C1 NCI, Mol Pharmacol Lab, Bethesda, MD 20892 USA. RP Pilch, DR (reprint author), NCI, Mol Pharmacol Lab, Bethesda, MD 20892 USA. NR 15 TC 10 Z9 12 U1 1 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 2004 VL 375 BP 76 EP 88 PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY51R UT WOS:000189397900005 PM 14870660 ER PT J AU Lim, JH Catez, F Birger, Y Postnikov, YV Bustin, M AF Lim, JH Catez, F Birger, Y Postnikov, YV Bustin, M TI Preparation and functional analysis of HMGN proteins SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID HIGH-MOBILITY; CHROMOSOMAL-PROTEINS; CHROMATIN; HMG-17; NUCLEUS; DNA; NUCLEOSOMES C1 NCI, NIH, Bethesda, MD 20892 USA. RP Lim, JH (reprint author), NCI, NIH, Bethesda, MD 20892 USA. RI Bustin, Michael/G-6155-2015 NR 23 TC 13 Z9 13 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 2004 VL 375 BP 323 EP 342 PG 20 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY51R UT WOS:000189397900021 PM 14870676 ER PT J AU Phair, RD Gorski, SA Misteli, T AF Phair, RD Gorski, SA Misteli, T TI Measurement of dynamic protein binding to chromatin in vivo, using photobleaching microscopy SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID LIVING HUMAN-CELLS; RAPID EXCHANGE; SAAM-II; MOBILITY; DIFFUSION; SOFTWARE; KINETICS; RECEPTOR; NUCLEUS; FIBERS C1 BioInformat Serv, Rockville, MD 20854 USA. NCI, NIH, Bethesda, MD 20892 USA. RP Phair, RD (reprint author), BioInformat Serv, Rockville, MD 20854 USA. NR 26 TC 184 Z9 188 U1 0 U2 9 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 2004 VL 375 BP 393 EP 414 PG 22 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY51R UT WOS:000189397900025 PM 14870680 ER PT J AU Stavreva, DA McNally, JG AF Stavreva, DA McNally, JG TI Fluorescence recovery after photobleaching (FRAP) methods for visualizing protein dynamics in living mammalian cell nuclei SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT A SE METHODS IN ENZYMOLOGY LA English DT Review ID LATERAL DIFFUSION; MEMBRANES; MOBILITY C1 NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA. RP Stavreva, DA (reprint author), NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA. NR 11 TC 26 Z9 27 U1 1 U2 4 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 2004 VL 375 BP 443 EP 455 PG 13 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY51R UT WOS:000189397900027 PM 14870682 ER PT J AU Bustin, M Robinson, RC Friedman, FK AF Bustin, M Robinson, RC Friedman, FK TI Immunochemical analysis of chromatin SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT B SE METHODS IN ENZYMOLOGY LA English DT Review ID ANTIGENIC DETERMINANTS; CHROMOSOMAL-PROTEINS; ANTIBODIES; HISTONE; NUCLEOSOMES; HETEROCHROMATIN; AUTOANTIBODIES; TRANSCRIPTION; CELLS C1 NCI, Prot Sect, NIH, Lab Metab, Bethesda, MD 20892 USA. RP Bustin, M (reprint author), NCI, Prot Sect, NIH, Lab Metab, Bethesda, MD 20892 USA. RI Friedman, Fred/D-4208-2016; Bustin, Michael/G-6155-2015 NR 24 TC 1 Z9 1 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 2004 VL 376 BP 209 EP + PG 14 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY68Z UT WOS:000189439600014 PM 14975308 ER PT J AU Kennison, JA AF Kennison, JA TI Introduction to Trx-G and Pc-G genes SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID DOSAGE-DEPENDENT MODIFIERS; DROSOPHILA HOMEOTIC GENES; BITHORAX COMPLEX; POLYCOMB GROUP; ANTENNAPEDIA GENE; DEFORMED FUNCTION; BINDING-PROTEIN; MELANOGASTER; MUTATIONS; ENCODES C1 NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA. RP Kennison, JA (reprint author), NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA. NR 37 TC 17 Z9 18 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 2004 VL 377 BP 61 EP 70 PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY57W UT WOS:000189412900003 PM 14979018 ER PT S AU Gangadharan, S Ghidelli, S Kamakaka, RT AF Gangadharan, S Ghidelli, S Kamakaka, RT BE Allis, CD Wu, C TI Purification of Sir2 proteins from yeast SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT C SE Methods in Enzymology LA English DT Review ID SACCHAROMYCES-CEREVISIAE; TELOMERIC HETEROCHROMATIN; HISTONE DEACETYLASE; COMPLEX INCLUDES; ACETYLATION; LOCUS; REPRESSOR; TERMINUS; BINDING; FAMILY C1 NICHHD, Unit Chromatin & Transcript, Bethesda, MD 20892 USA. RP NICHHD, Unit Chromatin & Transcript, Bethesda, MD 20892 USA. NR 32 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0076-6879 BN 0-12-182781-X J9 METHOD ENZYMOL JI Methods Enzymol. PY 2004 VL 377 BP 234 EP 254 PG 21 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY57W UT WOS:000189412900014 PM 14979029 ER PT J AU Chi, TH Yan, ZJ Xue, YT Wang, WD AF Chi, TH Yan, ZJ Xue, YT Wang, WD TI Purification and functional analysis of the mammalian SWI/SNF-family of chromatin-remodeling complexes SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID TRANSCRIPTION; BINDING C1 Stanford Univ, Howard Hughes Med Inst, Stanford, CA 94305 USA. NIA, Genet Lab, NIH, Baltimore, MD 21224 USA. RP Chi, TH (reprint author), Stanford Univ, Howard Hughes Med Inst, Stanford, CA 94305 USA. NR 13 TC 10 Z9 10 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 2004 VL 377 BP 299 EP 316 PG 18 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY57W UT WOS:000189412900018 PM 14979033 ER PT J AU Hamiche, A Xiao, H AF Hamiche, A Xiao, H TI Methods for analysis of nucleosome sliding by Drosophila NURF SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID CHROMATIN-REMODELING COMPLEX; HISTONE OCTAMER; ISWI; BINDING; MOBILIZATION; PROTEINS; SUBUNIT C1 Inst Andre Lwoff, F-94800 Villejuif, France. NIH, Mol Cell Biol Lab, Bethesda, MD 20892 USA. RP Hamiche, A (reprint author), Inst Andre Lwoff, F-94800 Villejuif, France. NR 20 TC 6 Z9 6 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 2004 VL 377 BP 353 EP 363 PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY57W UT WOS:000189412900022 PM 14979037 ER PT J AU Liu, H Zhao, KJ AF Liu, H Zhao, KJ TI Assay of Z-DNA induction by chromatin remodeling factors SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID PROMOTER; COMPLEX C1 NIH, Lab Mol Immunol, Bethesda, MD 20892 USA. RP Liu, H (reprint author), NIH, Lab Mol Immunol, Bldg 10, Bethesda, MD 20892 USA. NR 13 TC 2 Z9 2 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 2004 VL 377 BP 412 EP 420 PG 9 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY57W UT WOS:000189412900027 PM 14979042 ER PT J AU Walter, W Kashlev, M Studitsky, VM AF Walter, W Kashlev, M Studitsky, VM TI Transcription through the nucleosome by mRNA-producing RNA polymerases SO CHROMATIN AND CHROMATIN REMODELING ENZYMES, PT C SE METHODS IN ENZYMOLOGY LA English DT Review ID POSITIONED NUCLEOSOMES; DNA HYBRID; TRANSCRIBING POLYMERASE; II ELONGATION; TEMPLATES; PROCESSIVITY; INITIATION; MECHANISM; MOBILITY; BARRIER C1 Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Dept Biochem & Mol Biol, Detroit, MI 48201 USA. NCI, Frederick Canc Res & Dev Ctr, Ctr Canc Res, Frederick, MD 21702 USA. RP Walter, W (reprint author), Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Dept Biochem & Mol Biol, Detroit, MI 48201 USA. RI Studitsky, Vasily/A-9382-2014 FU NIGMS NIH HHS [GM58650] NR 29 TC 5 Z9 6 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 2004 VL 377 BP 445 EP 460 PG 16 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY57W UT WOS:000189412900029 PM 14979044 ER PT J AU Svartman, M Stone, G Page, JE Stanyon, R AF Svartman, M Stone, G Page, JE Stanyon, R TI A chromosome painting test of the basal Eutherian karyotype SO CHROMOSOME RESEARCH LA English DT Article DE Afrotheria; comparative genomics; phylogeny ID PLACENTAL MAMMAL RADIATION; ANCESTRAL KARYOTYPE; TREE; PHYLOGENY; EVOLUTION; REVEALS; HUMANS AB We studied the chromosomes of an Afrotherian species, the short-eared elephant shrew Macroscelides proboscideus with traditional banding techniques and mapped the homology to human chromosomes by in-situ hybridization of human chromosome paints. Here we present for the first time the karyotype of this species, including banding patterns. The chromosome painting allowed us to test various hypotheses of the ancestral Eutherian karyotype, the validity of the radical taxonomic assemblage known as Afrotheria and the phylogenetic position of the elephant shrew within the Afrotheria. Current hypotheses concerning the Eutherian ancestral karyotype include diploid numbers ranging from 2n = 44 to 50 while molecular studies have proposed a new superordinal grouping of extant Eutherians. In particular, the Afrotheria is hotly debated, as it appears to be an odd mixture of species from Ungulata, Tubulidentata, Macroscelidea and Lipotyphla, which have no apparent morphological traits to unite them. The hybridization pattern delimited a total of 37 segments in the elephant shrew genome and revealed 21 different associations of human chromosome segments. Associations 1/19 and 5/21 link all Afrotheria so far studied and support the Afrotheria assemblage. Associations 2/8, 3/20, and 10/17 strongly link aardvarks and elephant shrews after the divergence of the line leading to elephants. The most likely ancestral Eutherian karyotype would be 2n = 48 chromosomes. However, the lack of comparative chromosome painting data between Eutherians and an appropriate outgroup is a severe limitation on attempts to delineate the ancestral genome of Eutherians. Current attempts lack legitimacy until this situation is corrected. C1 NCI, Genet Branch, Frederick, MD 21702 USA. NCI, Lab Genom Divers, Frederick, MD 21702 USA. RP Stanyon, R (reprint author), NCI, Genet Branch, Frederick, MD 21702 USA. RI Svartman, Marta/B-4528-2008; OI Svartman, Marta/0000-0003-3239-1862; Stanyon, Roscoe/0000-0002-7229-1092 NR 27 TC 41 Z9 42 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0967-3849 J9 CHROMOSOME RES JI Chromosome Res. PY 2004 VL 12 IS 1 BP 45 EP 53 DI 10.1023/B:CHRO.0000009294.18760.e4 PG 9 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 754VN UT WOS:000187353000006 PM 14984101 ER PT J AU Masumoto, H Nakano, M Ohzeki, J AF Masumoto, H Nakano, M Ohzeki, J TI The role of CENP-B and alpha-satellite DNA: de novo assembly and epigenetic maintenance of human centromeres SO CHROMOSOME RESEARCH LA English DT Article DE alphoid DNA; CENP-A; CENP-B; centromere; epigenetics; human artificial chromosome ID ARTIFICIAL CHROMOSOME FORMATION; INNER KINETOCHORE PLATE; HUMAN NEOCENTROMERE; FISSION YEAST; HISTONE H3; NULL MICE; CHROMATIN; PROTEIN; COMPLEX; CONSTRUCTION AB The centromere is an essential functional domain responsible for the correct inheritance of eukaryotic chromosomes during cell division. Eukaryotic centromeres include the highly conserved centromere-specific histone H3 variant, CENP-A, which has provided a powerful tool for investigating the recruitment of centromere components. However, the trigger that targets CENP-A to a specific genomic locus during centromere assembly remains unknown. Although, on rare occasions, CENP-A chromatin may assemble at non-centromeric DNA, all normal human centromeres are assembled and maintained on alpha-satellite (alphoid) DNA. The importance of alphoid DNA and CENP-B binding sites (CENP-B boxes), typical of normal human centromere DNA configurations, has been demonstrated through their requirement in de novo centromere assembly and Human Artificial Chromosome ( HAC) assays. Mechanisms to link the centromere tightly to specific genomic sequences exist in humans and the two yeast species. C1 NCI, Lab Biosyst & Canc, NIH, Bethesda, MD 20892 USA. RP Masumoto, H (reprint author), NCI, Lab Biosyst & Canc, NIH, Bldg 37,Rm 5040,9000 Rockville Pike, Bethesda, MD 20892 USA. EM masumoth@mail.nih.gov NR 61 TC 51 Z9 55 U1 3 U2 9 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0967-3849 J9 CHROMOSOME RES JI Chromosome Res. PY 2004 VL 12 IS 6 BP 543 EP 556 DI 10.1023/B:CHRO.0000036593.72788.99 PG 14 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 843AA UT WOS:000223044600004 PM 15289662 ER PT J AU Ruiz-Herrera, A Garcia, F Fronicke, L Ponsa, M Egozcue, J Caldes, MG Stanyon, R AF Ruiz-Herrera, A Garcia, F Fronicke, L Ponsa, M Egozcue, J Caldes, MG Stanyon, R TI Conservation of aphidicolin-induced fragile sites in Papionini (Primates) species and humans SO CHROMOSOME RESEARCH LA English DT Article DE artificial chromosome; cytogenetics; evolution; fluorescence in-situ hybridization; fragile site; primate ID CHROMOSOME EVOLUTION; MACACA-FASCICULARIS; MOLECULAR CHARACTERIZATION; BREAKPOINTS; CERCOPITHECIDAE; EXPRESSION; SEQUENCES; NEOPLASIA; FRA3B AB Fragile sites are considered structural features of mammalian chromosomes and a commonly repeated hypothesis is that they are evolutionarily conserved. We tested this hypothesis by establishing the subchromosomal homology of regions harbouring fragile sites in the chromosomes of humans, Macaca fascicularis (MFA) and Mandrillus sphinx (MSP). We delineated the interspecific homology of chromosome bands expressing aphidicolin-induced fragile sites of homologues to human chromosomes 1, 3, 5, 7, 18 and X by the comparative FISH of human BAC and YAC clones. Notably, two YAC clones known to span human chromosome regions containing fragile sites were shown to also span fragile sites in macaques and mandrills. The present comparative BAC/YAC mapping data represent, up to now, the most precise evidence of fragile site conservation during primate evolution. C1 Univ Autonoma Barcelona, IBB, E-08193 Barcelona, Spain. Univ Autonoma Barcelona, Dept Biol Cellular Fisiol & Immunol, E-08193 Barcelona, Spain. NCI, Comparat Mol Cytogenet Core, Frederick, MD 21701 USA. Univ Autonoma Barcelona, Fac Med, Unitat Biol, E-08193 Barcelona, Spain. RP Caldes, MG (reprint author), Univ Autonoma Barcelona, IBB, E-08193 Barcelona, Spain. EM Montserrat.Garcia.Caldes@uab.es RI Ponsa, Montse/B-9504-2008; Ruiz-Herrera, Aurora/K-3728-2012; OI Ruiz-Herrera, Aurora/0000-0003-3868-6151; Stanyon, Roscoe/0000-0002-7229-1092 NR 27 TC 26 Z9 27 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0967-3849 J9 CHROMOSOME RES JI Chromosome Res. PY 2004 VL 12 IS 7 BP 683 EP 690 DI 10.1023/B:CHRO.0000045753.88789.ea PG 8 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 865KO UT WOS:000224701800002 PM 15505403 ER PT S AU Wagner, PD Verma, M Srivastava, S AF Wagner, PD Verma, M Srivastava, S BE Hoon, DSB Taback, B TI Challenges for biomarkers in cancer detection SO CIRCULATING NUCLEIC ACIDS IN PLASMA/SERUM III AND SERUM PROTEOMICS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 3rd International Symposium on Circulating Nucleic Acids in Plasma/Serum (CNAPS III) and Serum Proteomics CY NOV 09-12, 2003 CL Santa Monica, CA SP John Wayne Canc Inst, Dept Mol Oncol DE cancer detection; biomarkers ID OVARIAN-CANCER; SERUM; IDENTIFICATION AB Cancer remains the leading cause of death in the United States. Biomarkers can be used to detect cancer in different stages, initiation, development, and progression. The desirable property and utility of a biomarker lie in its ability to provide an early indication of disease progression. Biomarkers should be easy to detect, measurable across populations, and useful for detection of cancer at an early stage, identification of high-risk individuals, detection of recurrence, or monitoring endpoints in intervention studies. Recent technological advances have helped develop noninvasive, sensitive, and specific biomarkers to detect cancer at early stages of the disease. C1 NCI, Div Canc Prevent, Canc Biomarkers Res Grp, NIH, Bethesda, MD USA. RP Srivastava, S (reprint author), NCI, Div Canc Prevent, Canc Biomarkers Res Grp, NIH, MSC 7346,Execut Plaza N,Room 3142,6130 Execut Blv, Bethesda, MD USA. EM ssla@nih.gov NR 18 TC 54 Z9 56 U1 0 U2 7 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-551-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1022 BP 9 EP 16 DI 10.1196/annals.1318.003 PG 8 WC Biochemistry & Molecular Biology; Oncology; Medical Laboratory Technology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Oncology; Medical Laboratory Technology; Research & Experimental Medicine; Science & Technology - Other Topics GA BAN78 UT WOS:000223005300002 PM 15251933 ER PT S AU Johann, DJ McGuigan, MD Patel, AR Tomov, S Ross, S Conrads, TP Veenstra, TD Fishman, DA Whiteley, GR Petricoin, EF Liotta, LA AF Johann, DJ McGuigan, MD Patel, AR Tomov, S Ross, S Conrads, TP Veenstra, TD Fishman, DA Whiteley, GR Petricoin, EF Liotta, LA BE Hoon, DSB Taback, B TI Clinical proteomics and biomarker discovery SO CIRCULATING NUCLEIC ACIDS IN PLASMA/SERUM III AND SERUM PROTEOMICS SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT 3rd International Symposium on Circulating Nucleic Acids in Plasma/Serum (CNAPS III) and Serum Proteomics CY NOV 09-12, 2003 CL Santa Monica, CA SP John Wayne Canc Inst, Dept Mol Oncol DE proteomics; bioinformatics; mass spectroscopy ID PROSTATE-CANCER; SERUM; PATTERNS AB Early detection of disease generally provides much-improved outcomes by a definitive medical procedure or through lifestyle modification along with specific medical management strategies. For serum biomarkers, which are central to the diagnosis of many diseases, to become truly useful sentinels of pathogenesis, their sensitivity and specificity in both early detection and recurrence monitoring must be improved. Currently, the detection and monitoring of disease markers is based on solitary proteins, and this approach is not always reliable. New classes of biomarkers derived from mass spectroscopy analysis of the low molecular weight proteome have shown improved abilities in the early detection of disease and hence in patient risk stratification and outcome. The development of a modular platform technology with sufficient flexibility and design abstractions allowing for concurrent experimentation, test, and refinement will help speed the progress of mass spectroscopy-derived proteomic pattern-based diagnostics from the scientific laboratory to the medical clinic. For acceptance by scientists, physicians, and regulatory personnel, new bioinformatic tools are essential system components for data management, analysis, and intuitive display of these new and complex data. Clinically engineered mass spectroscopy systems are essential for the further development and validation of multiplexed biomarkers that have shown tremendous promise for the early detection of disease. C1 NCI, NIH, Pathol Lab,Ctr Canc Res, FDA Clin Proteom Program, Bethesda, MD 20892 USA. Brookhaven Natl Lab, Div Informat Technol, Upton, NY 11973 USA. NCI, NIH,Summer Student Program, Pathol Lab, FDA Clin Proteom Program, Bethesda, MD 20892 USA. SAIC Frederick Inc, Natl Canc Inst, Biomed Proteom Program, Analyt Chem Lab,Mass Spectrometry Ctr, Frederick, MD 21702 USA. Northwestern Univ, Sch Med, Natl Ovarian Canc Early Detect Program, Chicago, IL 60611 USA. SAIC Frederick, NCI, FDA Clin Proteom Program, Clin Proteom Reference Lab, Gaithersburg, MD USA. NCI, FDA Clin Proteom Program, Off Director, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA. RP Johann, DJ (reprint author), NCI, NIH, Pathol Lab,Ctr Canc Res, FDA Clin Proteom Program, 8800 Rockville Pike,Bldg 29A,Room 2A21, Bethesda, MD 20892 USA. EM johannd@mail.nih.gov NR 17 TC 57 Z9 57 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 1-57331-551-6 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1022 BP 295 EP 305 DI 10.1196/annals.1318.045 PG 11 WC Biochemistry & Molecular Biology; Oncology; Medical Laboratory Technology; Medicine, Research & Experimental; Multidisciplinary Sciences SC Biochemistry & Molecular Biology; Oncology; Medical Laboratory Technology; Research & Experimental Medicine; Science & Technology - Other Topics GA BAN78 UT WOS:000223005300044 PM 15251975 ER PT J AU Hassan, R Williams-Gould, J Watson, T Pai-Scherf, L Pastan, I AF Hassan, R Williams-Gould, J Watson, T Pai-Scherf, L Pastan, I TI Pretreatment with rituximab does not inhibit the human immune response against the immunogenic protein LMB-1 SO CLINICAL CANCER RESEARCH LA English DT Article ID MONOCLONAL-ANTIBODY THERAPY; B-CELLS; PHASE-I; DEPLETION; RICIN; IMMUNOTOXIN; IDEC-C2B8; INFUSION; TRIAL AB Purpose: Rituximab, a humanized monoclonal antibody directed to the CD20 antigen present on B lymphocytes, could potentially abrogate the humoral immune response to murine monoclonal antibodies or immunotoxins by depleting antibody-producing B cells. Experimental Design: A Phase II study of LMB-1, an immunotoxin targeting the Lewis Y tumor antigen, in combination with rituximab was conducted to test the hypothesis that rituximab could abolish or diminish the development of human antibodies to LMB-1. Five patients were treated in this study and received 375 mg/m(2) rituximab on days 1 and 7 followed by 45 mug/kg/day LMB-1 on days 10, 12, and 14. The development of human antibodies against LMB-1 was detected using a serum neutralization and ELISA. Results: All five of the patients had a total suppression of circulating CD20/CD19 B-cell population before the administration of the first dose of the immunotoxin. Before rituximab treatment, the mean percentage of CD20/CD19-positive B cells in the five treated patients was 19.8% (range, 4.5-29.8%) of the total peripheral lymphocytes. After two doses of rituximab, CD20/CD19-positive B lymphocytes constituted less than or equal to0.1% of the total peripheral lymphocytes. Despite absent circulating antibody-producing B cells, before and during LMB-1 treatment, all of the patients developed neutralizing antibodies to the immunotoxin by day 21 of drug administration, which prevented retreatment. Conclusions: Even though rituximah caused complete depletion of circulating CD20/CD19-positive B cells, it had no effect in suppressing the human antibody response to LMB-1 and may be of limited utility in suppressing human antibody responses to other immunogenic proteins. C1 NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NCI, Med Oncol Clin Res Unit, NIH, Bethesda, MD 20892 USA. US FDA, Ctr Drug Evaluat & Res, Rockville, MD 20857 USA. RP Hassan, R (reprint author), NCI, Mol Biol Lab, NIH, 37 Convent Dr,Room 5116, Bethesda, MD 20892 USA. EM hassanr@mail.nih.gov NR 16 TC 28 Z9 29 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN 1 PY 2004 VL 10 IS 1 BP 16 EP 18 DI 10.1158/1078-0432.CCR-1160-3 PN 1 PG 3 WC Oncology SC Oncology GA 765YM UT WOS:000188318700004 PM 14734446 ER PT J AU Come, SE Buzdar, AU Arteaga, CL Bissell, MJ Brown, MA Ellis, MJ Goss, PE Green, JE Ingle, JN Lee, AV Medina, D Nicholson, RI Santen, RJ Schiff, R Hart, CS AF Come, SE Buzdar, AU Arteaga, CL Bissell, MJ Brown, MA Ellis, MJ Goss, PE Green, JE Ingle, JN Lee, AV Medina, D Nicholson, RI Santen, RJ Schiff, R Hart, CS TI Proceedings of the Third International Conference on Recent Advances and Future Directions in Endocrine Manipulation of Breast Cancer: Conference summary statement SO CLINICAL CANCER RESEARCH LA English DT Editorial Material C1 Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Breast Canc Program, Boston, MA 02215 USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA. Vanderbilt Univ, Sch Med, Dept Canc Biol, Nashville, TN 37212 USA. Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA. Washington Univ, Sch Med, St Louis, MO USA. Princess Margaret Hosp, Breast Canc Prevent Program, Toronto, ON M4X 1K9, Canada. NIH, Transgen Oncogenes Grp, Bethesda, MD 20892 USA. Mayo Clin & Mayo Fdn, Rochester, MN 55905 USA. Baylor Coll Med, Baylor Breast Canc, Houston, TX 77030 USA. Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA. Univ Wales Coll Cardiff, Welsh Sch Pharm, Tenovus Ctr Canc Res, Cardiff CF1 3XF, S Glam, Wales. Univ Virginia, Hlth Sci Syst, Dept Med, Charlottesville, VA USA. InforMED, Narberth, PA USA. RP Come, SE (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Breast Canc Program, 330 Brookline Ave, Boston, MA 02215 USA. EM scome@bidmc.harvard.edu NR 0 TC 5 Z9 5 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN 1 PY 2004 VL 10 IS 1 SU S BP 327S EP 330S DI 10.1158/1078-0432.CCR-031213 PN 2 PG 4 WC Oncology SC Oncology GA 767DB UT WOS:000188424000001 PM 14734487 ER PT J AU Green, JE Desai, K Ye, YM Kavanaugh, C Calvo, A Huh, JI AF Green, JE Desai, K Ye, YM Kavanaugh, C Calvo, A Huh, JI TI Genomic approaches to understanding mammary tumor progression in transgenic mice and responses to therapy SO CLINICAL CANCER RESEARCH LA English DT Article; Proceedings Paper CT 3rd International Conference on Recent Advances and Future Directions in Endocrine Manipulation of Breast Cancer CY JUL 21-22, 2003 CL CAMBRIDGE, MASSACHUSETTS ID GENE-EXPRESSION PATTERNS; BREAST-CANCER; MOUSE MODELS; HA-RAS; INDUCTION; GLAND; ONCOGENE; MILK; ADENOCARCINOMA; APOPTOSIS AB Scores of genetically engineered mice have been generated in the quest to understand mechanisms of breast cancer development and progression. More recently, there has been a growing trend for using such models for testing various therapeutic strategies and agents. The application of these mouse models for these purposes requires that they be characterized in ways that demonstrate they possess important similarities to human breast cancer. In particular, detailed comparisons of the features of the models to human breast cancer must include attention to the histological phenotypes, chromosomal and molecular alterations, and the predictive value of the models for preclinical testing. Whereas these models have become important tools for the study of breast cancer, the great majority of existing mouse mammary cancer models develop tumors that are estrogen receptor negative, with relatively few models demonstrating metastatic spread to the lungs, and none developing metastases to bone. This review focuses on recent studies using genomic approaches to further understand the oncogenic processes occurring in mouse models of mammary cancer and to compare these changes with those identified in human breast cancer. Gene expression profiling is being applied to help define pharmacological responses that occur in vivo. Detailed genomic analyses will provide important information for selecting models for specific experimental purposes, contribute to the understanding of oncogene-specific expression signatures and potential therapeutic targets, and further define mechanisms of chemoprevention and chemotherapy. C1 NCI, Lab Cell Regulat & Carcinogenesis, Transgen Oncogenesis Grp, Bethesda, MD 20892 USA. RP Green, JE (reprint author), NCI, Lab Cell Regulat & Carcinogenesis, Transgen Oncogenesis Grp, Bldg 41,Room C629,41 Medlars Dr, Bethesda, MD 20892 USA. EM JEGreen@nih.gov NR 22 TC 8 Z9 9 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD JAN 1 PY 2004 VL 10 IS 1 SU S BP 385S EP 390S DI 10.1158/1078-0432.CCR-031201 PN 2 PG 6 WC Oncology SC Oncology GA 767DB UT WOS:000188424000010 PM 14734496 ER PT J AU Hortin, GL Meilinger, B Drake, SK AF Hortin, GL Meilinger, B Drake, SK TI Size-selective extraction of peptides from urine for mass spectrometric analysis SO CLINICAL CHEMISTRY LA English DT Letter ID LASER-DESORPTION/IONIZATION-TIME; PROTEINURIA C1 NIH, Dept Lab Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. NIH, Dept Crit Care Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. RP Hortin, GL (reprint author), NIH, Dept Lab Med, Warren G Magnuson Clin Ctr, Bldg 10,Room 2C-407, Bethesda, MD 20892 USA. EM ghortin@mail.cc.nih.gov NR 15 TC 16 Z9 16 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PY 2004 VL 50 IS 6 BP 1092 EP 1095 DI 10.1373/clinchem.2003.030 PG 4 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 827BR UT WOS:000221873800025 PM 15161733 ER PT J AU Choo, RE Huestis, MA AF Choo, RE Huestis, MA TI Oral fluid as a diagnostic tool SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE LA English DT Review DE illicit drugs; oral fluid; saliva; therapeutic drug monitoring ID EPSTEIN-BARR-VIRUS; SALIVARY FLOW-RATE; HEPATITIS-C VIRUS; BREAST-CARCINOMA; CELIAC-DISEASE; PARACETAMOL CONCENTRATIONS; CODEINE CONCENTRATIONS; PLASMA-CONCENTRATIONS; N-DESMETHYLDIAZEPAM; DRUG CONCENTRATIONS AB Technological advances over the past decades have enabled oral fluid to expand its usefulness in the diagnosis of disease, prediction of disease progression, monitoring of therapeutic drug levels and detection of illicit drugs. The easy non-invasive nature of collection and the relationship between oral fluid and plasma levels make oral fluid a valuable clinical tool. This review describes advances over the past 5 years in the area of oral fluid as a diagnostic tool, its use in therapeutic and illicit drug monitoring, including proposed guidelines for cut-off values, and methods of collection. C1 NIDA, Chem & Drug Metab Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA. RP Huestis, MA (reprint author), NIDA, Chem & Drug Metab Sect, Intramural Res Program, NIH, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM mhuestis@intra.nida.nih.gov NR 137 TC 86 Z9 86 U1 0 U2 9 PU WALTER DE GRUYTER & CO PI BERLIN PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY SN 1434-6621 J9 CLIN CHEM LAB MED JI Clin. Chem. Lab. Med. PY 2004 VL 42 IS 11 BP 1273 EP 1287 DI 10.1515/CCLM.2004.248 PG 15 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 875QZ UT WOS:000225438100008 PM 15576290 ER PT J AU Post, RM Weiss, SRB AF Post, RM Weiss, SRB TI Convergences in course of illness and treatments of the epilepsies and recurrent affective disorders SO CLINICAL EEG AND NEUROSCIENCE LA English DT Article DE affective disorders; amygdala kindling; anticonvulsants; depression; mania; mood stabilizers; seizures; tolerance ID VAGUS NERVE-STIMULATION; REFRACTORY AFFECTIVE-DISORDERS; AMYGDALA-KINDLED SEIZURES; MANIC-DEPRESSIVE ILLNESS; STRESSFUL LIFE EVENTS; BIPOLAR DISORDER; CONTINGENT TOLERANCE; MAJOR DEPRESSION; CROSS-TOLERANCE; FOLLOW-UP AB The failure to achieve and maintain remission is a critical problem for a high percentage of patients with epilepsy and the primary affective disorders. Early illness onset and delayed initiation of treatment may contribute to primary treatment resistance or that associated with loss of efficacy (tolerance phenomenon). Neurobiological data and principles drawn from the amygdala kindling model of seizure progression are reviewed for their heuristic value in conceptualizing molecular mechanisms of illness progression and its prevention with pharmacological agents in the epilepsies and, indirectly, the recurrent affective disorders. Caveats in the use of this model and convergences and divergences in its predictive validity for seizures and affective disorders are noted. C1 NIMH, Biol Psychiat Branch, NIH, DHHS, Bethesda, MD 20892 USA. NIDA, NIH, DHHS, Bethesda, MD 20892 USA. RP Post, RM (reprint author), NIMH, Biol Psychiat Branch, NIH, DHHS, Bldg 10,Room 3S239,10 Ctr Dr,MSC-1272, Bethesda, MD 20892 USA. EM Robert.Post@NIH.gov NR 44 TC 15 Z9 18 U1 0 U2 0 PU EEG & CLINICAL NEUROSCIENCE SOC (E C N S) PI WHEATON PA 805 W LIBERTY DR, PO BOX 725, WHEATON, IL 60187 USA SN 1550-0594 J9 CLIN EEG NEUROSCI JI Clin. EEG Neurosci. PD JAN PY 2004 VL 35 IS 1 BP 14 EP 24 PG 11 WC Clinical Neurology; Neurosciences; Neuroimaging; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA 852NY UT WOS:000223764000003 PM 15112460 ER PT J AU Theodore, WH AF Theodore, WH TI Epilepsy and depression: Imaging potential common factors SO CLINICAL EEG AND NEUROSCIENCE LA English DT Review DE cerebral glucose metabolism; complex partial seizures; depression; epilepsy; magnetic resonance imaging; neuroimaging; positron emission tomography; serotonin receptor ID TEMPORAL-LOBE EPILEPSY; POSITRON-EMISSION-TOMOGRAPHY; SEROTONIN TRANSPORTER AVAILABILITY; TRANSCRANIAL MAGNETIC STIMULATION; COMPLEX PARTIAL SEIZURES; 5-HT1A RECEPTOR-BINDING; CEREBRAL BLOOD-FLOW; METHYL-L-TRYPTOPHAN; OBSESSIVE-COMPULSIVE DISORDER; TUBEROUS SCLEROSIS COMPLEX AB Patients with seizure disorders have an increased incidence of depression. This may be due in part to psychosocial factors, or side effects of antiepileptic drugs. However, there may be underlying physiologic mechanisms for the relationship. Neuroimaging studies, including structural magnetic resonance imaging, positron emission tomography measurements of cerebral glucose metabolism, and, more recently, imaging of serotonin 1 A receptors, may provide additional data to explain overlapping clinical manifestations of epilepsy and depression. C1 NINDS, Clin Epilepsy Sect, NIH, Bethesda, MD 20892 USA. RP Theodore, WH (reprint author), NINDS, Clin Epilepsy Sect, NIH, Bldg 10 Room 5N-250, Bethesda, MD 20892 USA. EM theodorw@ninds.nih.gov NR 119 TC 4 Z9 4 U1 2 U2 2 PU EEG & CLINICAL NEUROSCIENCE SOC (E C N S) PI WHEATON PA 805 W LIBERTY DR, PO BOX 725, WHEATON, IL 60187 USA SN 1550-0594 J9 CLIN EEG NEUROSCI JI Clin. EEG Neurosci. PD JAN PY 2004 VL 35 IS 1 BP 38 EP 45 PG 8 WC Clinical Neurology; Neurosciences; Neuroimaging; Psychiatry; Psychology SC Neurosciences & Neurology; Psychiatry; Psychology GA 852NY UT WOS:000223764000005 PM 15112462 ER PT J AU Davidson, B Goldberg, I Tell, L Vigdorchik, S Baekelandt, M Berner, A Kristensen, GB Reich, R Kopolovic, J AF Davidson, B Goldberg, I Tell, L Vigdorchik, S Baekelandt, M Berner, A Kristensen, GB Reich, R Kopolovic, J TI The clinical role of the PEA3 transcription factor in ovarian and breast carcinoma in effusions SO CLINICAL & EXPERIMENTAL METASTASIS LA English DT Article DE Ets transcription factors; mRNA in situ hybridization; serous effusions; metastasis ID MESSENGER-RNA EXPRESSION; ETS ONCOGENE FAMILY; ALPHA-V-INTEGRIN; SEROUS EFFUSIONS; GENE-EXPRESSION; MATRIX METALLOPROTEINASES; PLASMINOGEN-ACTIVATOR; MOLECULAR-CLONING; SIGNALING PATHWAY; CANCER-CELLS AB Ets transcription factors play a central role in invasion and metastasis through regulation of synthesis of proteolytic enzymes and angiogenic molecules. The objective of this study was to investigate the role of PEA3 in tumor progression of ovarian and breast carcinoma metastatic to effusions, and to evaluate the expression of Ets-2 and Erg in ovarian carcinoma. Ovarian (83 malignant effusions, 102 corresponding solid lesions) and breast (33 malignant effusions, 40 corresponding solid lesions) carcinomas were evaluated for expression of PEA3 using mRNA in situ Hybridization (ISH). Expression of Ets-2 and Erg mRNA was analyzed in 50 ovarian carcinoma effusions using the same method. PEA3 mRNA expression was comparable at all sites in ovarian carcinoma (44 out of 83; 53% of effusions, 48 out of 102; 47% of solid tumors). PEA3 mRNA expression in effusions correlated with mRNA expression of the previously studied alphaV (P=0.022), alpha6 (P<0.001) and β1 (P<0.001) integrin subunits, the matrix metalloproteinase (MMP) inducer EMMPRIN (P=0.015) and interleukin-8 (IL-8) ( P=0.033). Erg and Ets-2 mRNA was expressed in 15 out of 50 (30%) and 18 out of 50 (36%) effusions, respectively, and co-localized with PEA3 (P=0.017 for Erg, P=0.004 for Ets-2). In breast carcinoma, PEA3 expression was seen in 19/40 (48%) of solid lesions, with a significant upregulation in corresponding effusions compared to primary tumors (24 out of 33; 73%, P=0.038). PEA3 mRNA expression in effusions obtained prior to the institution of chemotherapy predicted significantly shorter overall survival in univariate analysis (24 vs 37 months, P=0.03), with a similar trend for Erg (13 vs 30 months, P=0.1). In conclusion, PEA3 is expressed at all anatomic sites in serous ovarian cancer and co-localizes with Erg, Ets-2 and several metastasis-associated molecules. PEA3 mRNA expression is a novel marker for tumor progression to malignant effusion in breast carcinoma, and predicts poor outcome in effusions sampled prior to therapeutic intervention in ovarian carcinoma. These findings support a biological role for Ets transcription factors in these malignancies and suggests that they may be targets for therapeutic intervention. C1 Univ Oslo, Dept Pathol, Norwegian Radium Hosp, Oslo, Norway. Sheba Med Ctr, Dept Pathol, Tel Hashomer, Israel. Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel. Hebrew Univ Jerusalem, Fac Med, Dept Pharmacol & Expt Therapeut, Jerusalem, Israel. Norwegian Radium Hosp, Dept Gynecol Oncol, Oslo, Norway. Hebrew Univ Jerusalem, David R Bloom Ctr Pharm, IL-91905 Jerusalem, Israel. RP Davidson, B (reprint author), NIH, Pathol Lab, Bldg 10,Room 2A33,9000 Rockville Pike, Bethesda, MD 20892 USA. EM davidsob@mail.nih.gov NR 54 TC 23 Z9 24 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0262-0898 J9 CLIN EXP METASTAS JI Clin. Exp. Metastasis PY 2004 VL 21 IS 3 BP 191 EP 199 DI 10.1023/B:CLIN.0000037703.37275.35 PG 9 WC Oncology SC Oncology GA 845NO UT WOS:000223251800002 PM 15387369 ER PT J AU Fu, YM Zhang, H Ding, MJ Li, YQ Fu, X Yu, ZX Meadows, GG AF Fu, YM Zhang, H Ding, MJ Li, YQ Fu, X Yu, ZX Meadows, GG TI Specific amino acid restriction inhibits attachment and spreading of human melanoma via modulation of the integrin/focal adhesion kinase pathway and actin cytoskeleton remodeling SO CLINICAL & EXPERIMENTAL METASTASIS LA English DT Article DE adhesion; amino acid; cytoskeleton; integrin; melanoma; nutrition ID PHENYLALANINE RESTRICTION; SIGNAL-TRANSDUCTION; MALIGNANT-MELANOMA; CELL-MIGRATION; RHO GTPASES; TYROSINE; INVASION; ACTIVATION; PHOSPHORYLATION; METASTASIS AB We had previously found that selective restriction of amino acids inhibits invasion of human A375 melanoma. Integrins, cell surface receptors for the components of extracellular matrix (ECM), are activated during cell adhesion and spreading, and initiate signaling pathways that control growth and invasion of tumor cells. We examined the effect of tyrosine (Tyr) and phenylalanine (Phe), methionine (Met) or glutamine (Gln) restriction on attachment and spreading of A375 and MeWo melanoma cell lines on fibronectin and laminin. In A375 cells, restriction of Tyr/Phe or Met inhibited attachment to and spreading on laminin and fibronectin, inhibited alpha 3 and alpha 4 integrin expression, and inhibited accumulation of FAK-Tyr(397) and F-actin at leading edges of cell protrusions. Tyr/Phe restriction also inhibited attachment-induced autophosphorylation of FAK-Tyr(397). In MeWo cells, the order of inhibition by amino acid restriction on cell attachment and spreading was as follows: Gln > Tyr/Phe > Met. Restriction of Gin reduced alpha 5 integrin expression. All amino acid restrictions similarly inhibited phosphorylation of FAK-Tyr(397), FAK-Tyr(577), FAK-Tyr(861) and paxillin-Tyr(31). Gln restriction exhibited the strongest inhibition of actin cytoskeleton remodeling during the cell spreading. The present study reveals that specific amino acid restriction inhibits attachment and spreading of melanoma via inhibition of specific integrin expression, inhibition of integrin-mediated FAK phosphorylation, and modulation of actin cytoskeleton remodeling. These data provide additional understanding of the mechanism by which specific amino acid restriction controls invasion and migration of melanoma. C1 Washington State Univ, Coll Pharm, Canc Prevent & Res Ctr, Dept Pharmaceut Sci,Pharmacol & Toxicol Grad Prog, Pullman, WA 99164 USA. NHLBI, Pathol Sect, Bethesda, MD 20892 USA. RP Meadows, GG (reprint author), Washington State Univ, Coll Pharm, Canc Prevent & Res Ctr, Dept Pharmaceut Sci,Pharmacol & Toxicol Grad Prog, Pullman, WA 99164 USA. EM meadows@wsu.edu FU NCI NIH HHS [CA 77604, CA 101035] NR 40 TC 15 Z9 17 U1 0 U2 2 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0262-0898 J9 CLIN EXP METASTAS JI Clin. Exp. Metastasis PY 2004 VL 21 IS 7 BP 587 EP 598 PG 12 WC Oncology SC Oncology GA 907NM UT WOS:000227724800003 PM 15787096 ER PT J AU Yang, HY Rouse, J Lukes, L Lancaster, M Veenstra, T Zhou, M Shi, Y Park, YG Hunter, K AF Yang, HY Rouse, J Lukes, L Lancaster, M Veenstra, T Zhou, M Shi, Y Park, YG Hunter, K TI Caffeine suppresses metastasis in a transgenic mouse model: a prototype molecule for prophylaxis of metastasis SO CLINICAL & EXPERIMENTAL METASTASIS LA English DT Article DE caffeine; 2-D gel analysis; metastasis; microarray; transgenic ID BREAST DUCTAL CARCINOMA; PRIMARY MAMMARY-TUMORS; EXTRACELLULAR-MATRIX; CYCLIC-NUCLEOTIDES; TYROSINE KINASE; GENE-EXPRESSION; CELL-ADHESION; C-MYC; CANCER; PROTEIN AB A significant fraction of cancer patients have occult disseminated tumors at the time of primary diagnosis, which usually progress to become clinically relevant lesions. Since the majority of cancer mortality is associated with metastatic disease, the ability to inhibit the growth of the secondary tumors would significantly reduce cancer-related morbidity and mortality. We have investigated whether caffeine, which has been shown to suppress tumor cell invasiveness and experimental metastasis, can suppress metastasis in a spontaneous transgene-induced mammary tumor model. Chronic exposure to caffeine prior to the appearance of palpable mammary tumors significantly reduced both tumor burden and metastatic colonization. However, when caffeine exposure began after the appearance of frank tumors, caffeine suppressed metastasis without changing primary tumor burden. The means by which caffeine suppressed metastatic activity may be associated with inhibition of malignant transformation of mammary epithelial cells, inhibition of conversion of dormant tumor cells to micrometastases, micrometastases to macrometastases, or inhibition of tumor cell adhesion and motility. Gene and protein expression patterns resulting from caffeine treatment showed that metastasis suppression may be associated with up-regulation the mRNA expression of multiple extracellular matrix genes, including Fbln1, Bgn, Sparc, Fbn1, Loxl1, Col1a1, Col3a1, Col5a1, Col5a2, Col5a3, Col6a1, Col6a2, and Col6a3. These data suggested that caffeine or other methyl xanthine derivatives may improve the clinical outcome in patients prior to and following the diagnosis of metastatic disease, and could potentially reduce the morbidity and mortality associated with disseminated tumors. C1 NCI, Lab Populat Genet, Ctr Canc Res, Bethesda, MD 20892 USA. NCI, Lab Prote & Analyt Technol, SAIC Frederick, Frederick, MD 21701 USA. NIDDKD, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA. RP Hunter, K (reprint author), NCI, Lab Populat Genet, Ctr Canc Res, 41 Lib Dr, Bethesda, MD 20892 USA. EM hunterk@mail.nih.gov NR 49 TC 42 Z9 44 U1 1 U2 4 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0262-0898 J9 CLIN EXP METASTAS JI Clin. Exp. Metastasis PY 2004 VL 21 IS 8 BP 719 EP 735 DI 10.1007/s10585-004-8251-4 PG 17 WC Oncology SC Oncology GA 927ZJ UT WOS:000229240600006 PM 16035617 ER PT J AU Furuta, T Shirai, N Xiao, F El-omar, EM Rabkin, CS Sugimura, H Ishizaki, T Ohashi, K AF Furuta, Takahisa Shirai, Naohito Xiao, Fang El-omar, Emad M. Rabkin, Charles S. Sugimura, Haruhiko Ishizaki, Takashi Ohashi, Kyoichi TI Polymorphism of Interleukin-1 beta Affects the Eradication Rates of Helicobacter pylori by Triple Therapy SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY LA English DT Article ID GASTRIC-ACID-SECRETION; PEPTIC-ULCER PATIENTS; PROTEIN-KINASE-C; GENOTYPIC DIFFERENCES; CYP2C19 GENOTYPE; INTRAGASTRIC PH; INCREASED RISK; CURE RATES; EXTENSIVE METABOLIZERS; OMEPRAZOLE METABOLISM AB Background & Aims: Polymorphism in interleukin-1 beta (IL-1 beta) is associated with intragastric pH levels in Helicobacter pylori-positive subjects. Intragastric pH levels affect the activity of antibiotics against H. pylori in the stomach. The aim of this study was to investigate whether IL-1 beta polymorphism is associated with eradication rates of H. pylori by triple therapy with a proton pump inhibitor (PPI), amoxicillin, and clarithromycin. Methods: Three hundred thirty-six patients infected with H. pylori completed treatment with omeprazole, 20 mg, or lansoprazole, 30 mg twice daily; clarithromycin, 200 mg 3 times daily; and amoxicillin, 500 mg 3 times daily, for 1 week. IL-1 beta-511 and CYP2C19 genotypes of patients and sensitivity of H. pylori to clarithromycin and amoxicillin were determined. Results: Logistic regression analysis showed that the IL-1 beta-511 polymorphism, as well as CYP2C19 genotype of patients and clarithromycin-resistance of H. pylori, was associated with successful eradication. Eradication rates for H. pylori were 77.3% (75 of 97; 95% confidence interval, 67.5-84.6), 89.6% (147 of 164; 95% confidence interval, 83.9-93.1), and 94.7% (95% confidence interval, 86.9-98.5) in patients with the C/C, C/T, and T/T genotypes of IL-1 beta-511, respectively (P = 0.0014). Conclusions: IL-1 beta-511 polymorphism is one of the determinants of successful eradication of H. pylori using triple therapy with a PPI, amoxicillin, and clarithromycin, together with CYP2C19 genotype and bacterial resistance to clarithromycin. C1 [Furuta, Takahisa; Shirai, Naohito; Xiao, Fang] Hamamatsu Univ Sch Med, Dept Med 1, Hamamatsu, Shizuoka 4313192, Japan. [Ishizaki, Takashi] Hamamatsu Univ Sch Med, Dept Pathol 1, Hamamatsu, Shizuoka 4313192, Japan. [Ohashi, Kyoichi] Hamamatsu Univ Sch Med, Dept Clin Pharmacol & Therapeut, Hamamatsu, Shizuoka 4313192, Japan. [Sugimura, Haruhiko] Kumamoto Univ, Dept Pharmacol & Therapeut, Grad Sch Med & Pharmaceut Sci, Kumamoto, Japan. [El-omar, Emad M.] Univ Aberdeen, Dept Med & Therapeut, Aberdeen, Scotland. [Rabkin, Charles S.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Furuta, T (reprint author), Hamamatsu Univ Sch Med, Dept Med 1, 1-20-1 Handa Yama, Hamamatsu, Shizuoka 4313192, Japan. EM furuta@hama-med.ac.jp FU Yokoyama Rinshoyakuri Zaidan; Center of Excellence (COE) from the Ministry of Education, Culture, Sports, Science and Technology, Japan; Ministry of Health, Labour, and Welfare, Japan FX Supported in part by grants-in-aid for Scientific Research from Yokoyama Rinshoyakuri Zaidan, and by a grant-in-aid for the Center of Excellence (COE) from the Ministry of Education, Culture, Sports, Science and Technology, Japan, and from the Ministry of Health, Labour, and Welfare, Japan. NR 59 TC 39 Z9 41 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1542-3565 J9 CLIN GASTROENTEROL H JI Clin. Gastroenterol. Hepatol. PD JAN PY 2004 VL 2 IS 1 BP 22 EP 30 DI 10.1053/S1542-3565(04)00288-X PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA V19KM UT WOS:000208071300005 PM 15017629 ER PT J AU Hale, LP Buckley, RH Puck, JM Patel, DD AF Hale, LP Buckley, RH Puck, JM Patel, DD TI Abnormal development of thymic dendritic and epithelial cells in human X-linked severe combined immunodeficiency SO CLINICAL IMMUNOLOGY LA English DT Article DE development; X-SCID; epithelial cells ID HEMATOPOIETIC STEM-CELLS; MONOCLONAL-ANTIBODIES; TRANSPLANTATION; MICROENVIRONMENT; MUTATION; EXPRESSION; EPIDERMIS; PATHOLOGY; ANTIGENS; SURVIVAL AB The X-linked form of severe combined immunodeficiency (X-SCID) is caused by mutations in the common cytokine receptor gamma chain and results in lack of T and NK cells and defective B cells. Without immune reconstitution, X-SCID patients typically die from infection during infancy. This report describes thymic epithelial (TE), lymphocyte, and dendritic cell (DC) differentiation in the thymic microenvironment of seven X-SCID patients who died before or after treatment for their immunodeficiency. X-SCID thymus consisted predominately of TE cells without grossly evident corticomedullary distinction. CD3(+) and CD1a(+) developing T cells and CD83(+) thymic DC were reduced >50-fold when compared to age- and gender-matched control thymus (P < 0.001). TE expression of epithelial differentiation markers CK14, involucrin, and high molecular weight cytokeratins also differed in X-SCID versus normal thymus. These histopathologic findings indicate that in addition to T cells, thymic DC development and differentiation of TE cells are also abnormal in X-SCID. (C) 2003 Elsevier Inc. All rights reserved. C1 Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA. NHGRI, Bethesda, MD 20892 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. RP Hale, LP (reprint author), Duke Univ, Med Ctr, Dept Pathol, DUMC 3712, Durham, NC 27710 USA. EM laura.hale@duke.edu FU NCRR NIH HHS [M01-RR-30]; NIAID NIH HHS [AI47604, AI47605, AI142951] NR 40 TC 15 Z9 15 U1 1 U2 4 PU ACADEMIC PRESS INC ELSEVIER SCIENCE 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 2004 VL 110 IS 1 BP 63 EP 70 DI 10.1016/j.clin.2003.09.002 PG 8 WC Immunology SC Immunology GA 775XF UT WOS:000189085400008 PM 14962797 ER PT J AU Giordano, TP Soini, H Teeter, LD Adams, GJ Musser, JM Graviss, EA AF Giordano, TP Soini, H Teeter, LD Adams, GJ Musser, JM Graviss, EA TI Relating the size of molecularly defined clusters of tuberculosis to the duration of symptoms SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 38th Annual Meeting of the Infectious-Diseases-Society-of-America CY SEP 06-11, 2000 CL NEW ORLEANS, LOUISIANA SP Infect Dis Soc Amer ID NEW-YORK-CITY; DRUG-RESISTANT TUBERCULOSIS; MYCOBACTERIUM-TUBERCULOSIS; NOSOCOMIAL TRANSMISSION; SAN-FRANCISCO; OUTBREAK; EPIDEMIOLOGY; STRAIN; POPULATION; VIRULENT AB Molecular profiling of Mycobacterium tuberculosis isolates has improved recognition of tuberculosis case clusters, but the determinants of cluster size are unknown. We hypothesized that longer duration of symptoms prior to initiation of tuberculosis therapy would be associated with increased cluster size. All patients with tuberculosis in Harris County, Texas, identified between 10/1/95 and 12/31/97 through a prospective population-based project were interviewed, had their medical records reviewed, and had M. tuberculosis isolates molecularly characterized. There were 506 symptomatic, evaluable patients in 74 clusters, ranging in size from 2 patients (32 clusters) to 61 patients (1 cluster). The median duration of symptoms was 46 days (range, 1-471 days). There was no association between the log-transformed duration of symptoms and cluster size in univariate or multivariate analysis. In multivariate analysis, age and HIV coinfection were inversely related to cluster size, but only weakly. The size of molecularly defined clusters of tuberculosis was not related to the duration of symptoms of most patients who belonged to clusters. C1 Baylor Coll Med, Dept Med, Houston, TX 77030 USA. Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA. Baylor Coll Med, Dept Psychiat, Houston, TX 77030 USA. NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. RP Giordano, TP (reprint author), Houston VA Med Ctr, Houston Ctr Qual Care & Utilizat Studies, 2002 Holcombe Blvd 152, Houston, TX 77030 USA. FU NIAID NIH HHS [N01-AO-02738, 5T32AI07456-10]; NIMH NIH HHS [1K23MH67505-01] NR 35 TC 7 Z9 7 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN 1 PY 2004 VL 38 IS 1 BP 10 EP 16 DI 10.1086/380454 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 754PF UT WOS:000187325000002 PM 14679442 ER PT J AU Bray, M AF Bray, M TI New data in a 200-year investigation SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material ID SMALLPOX VACCINATION; CELL MEMORY; RESPONSES C1 NIAID, Biodef Clin Res Branch, Off Clin Res,Off Director, NIH, Bethesda, MD 20892 USA. RP Bray, M (reprint author), NIAID, Biodef Clin Res Branch, Off Clin Res,Off Director, NIH, Bethesda, MD 20892 USA. NR 11 TC 2 Z9 2 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN 1 PY 2004 VL 38 IS 1 BP 90 EP 91 DI 10.1086/380467 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 754PF UT WOS:000187325000013 PM 14679453 ER PT J AU Robinson, MR Csaky, KG Lee, SS Masur, H Polis, MA AF Robinson, MR Csaky, KG Lee, SS Masur, H Polis, MA TI Fibrovascular changes misdiagnosed as cytomegalovirus retinitis reactivation in a patient with immune recovery SO CLINICAL INFECTIOUS DISEASES LA English DT Editorial Material ID ACTIVE ANTIRETROVIRAL THERAPY; UVEITIS; NEOVASCULARIZATION; AIDS AB A patient with human immunodeficiency virus infection and cytomegalovirus ( CMV) retinitis developed immune recovery uveitis as a result of receipt of highly active antiretroviral therapy. Fibrovascular changes occurred in the CMV retinitis scar, were misdiagnosed as CMV retinitis reactivation, and were treated with anti- CMV medication. Fibrovascular membranes can be misdiagnosed as reactivated CMV retinitis, and a proper diagnosis is essential to avoid unnecessary therapy with potentially toxic antiviral medications. C1 NEI, NIH, Bethesda, MD 20892 USA. NIAID, NIH, Bethesda, MD 20892 USA. RP Robinson, MR (reprint author), NEI, NIH, 10-10S229,10 Ctr Dr,MSC 1863, Bethesda, MD 20892 USA. OI Polis, Michael/0000-0002-9151-2268 NR 13 TC 3 Z9 4 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN 1 PY 2004 VL 38 IS 1 BP 139 EP 141 DI 10.1086/380127 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 754PF UT WOS:000187325000020 PM 14679460 ER PT J AU Smith, WB AF Smith, WB TI Research methodology: Implications for CAM pain research SO CLINICAL JOURNAL OF PAIN LA English DT Article DE CAM; research methodology; homeopathy; Traditional Chinese Medicine AB The National Cancer Institute's Office of Cancer Complementary and Alternative Medicine established a series of expert panels to develop the state of the science in research methodologies in CAM cancer research. Panelists from both conventiona an CAM research draw on their expertise in their relative fields to apply their knowledge and expertise to specific topic areas within cancer CAM. The first panel is focused on cancer symptom research. The discussion and conclusions raised by this panel primarily address pain research but are applicable to other symptoms as well. This article will focus on the panel presentations that are most applicable to CAM pain research in both cancer and noncareer pain populations, identifying the major challenges and conclusions offered by the panelists. C1 NCI, Res Dev & Support Program, Off Canc Complementary & Alternat Med, NIH, Bethesda, MD 20892 USA. RP Smith, WB (reprint author), NCI, Res Dev & Support Program, Off Canc Complementary & Alternat Med, NIH, 6130 Execut Blvd,Execut Plaza N Suite 102,MSC 730, Bethesda, MD 20892 USA. NR 0 TC 27 Z9 27 U1 0 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0749-8047 J9 CLIN J PAIN JI Clin. J. Pain PD JAN-FEB PY 2004 VL 20 IS 1 BP 3 EP 7 DI 10.1097/00002508-200401000-00002 PG 5 WC Anesthesiology; Clinical Neurology SC Anesthesiology; Neurosciences & Neurology GA 758KN UT WOS:000187633700002 PM 14668649 ER PT J AU Keiser, PB Nutman, TB AF Keiser, PB Nutman, TB TI Strongyloides stercoralis in the immunocompromised population SO CLINICAL MICROBIOLOGY REVIEWS LA English DT Review ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; RENAL-TRANSPLANT RECIPIENTS; LYMPHOTROPIC VIRUS TYPE-1; HYPERINFECTION SYNDROME; OVERWHELMING STRONGYLOIDIASIS; SYSTEMIC STRONGYLOIDIASIS; NEPHROTIC SYNDROME; PULMONARY STRONGYLOIDIASIS; IMMUNOCOMPETENT PATIENT; CORTICOSTEROID-THERAPY AB Strongyloides stercoralis is an intestinal nematode of humans that infects tens of millions of people worldwide. S. stercoralis is unique among intestinal nematodes in its ability to complete its life cycle within the host through an asexual autoinfective cycle, allowing the infection to persist in the host indefinitely. Under some conditions associated with immuno-compromise, this autoinfective cycle can become amplified into a potentially fatal hyperinfection syndrome, characterized by increased numbers of infective filariform larvae in stool and sputum and clinical manifestations of the increased parasite burden and migration, such as gastrointestinal bleeding and respiratory distress. S. stercoralis hyperinfection is often accompanied by sepsis or meningitis with enteric organisms. Glucocorticoid treatment and human T-lymphotropic virus type 1 infection are the two conditions most specifically associated with triggering hyperinfection, but cases have been reported in association with hematologic malignancy, malnutrition, and AIDS. Anthelmintic agents such as ivermectin have been used successfully in treating the hyperinfection syndrome as well as for primary and secondary prevention of hyperinfection in patients whose exposure history and underlying condition put them at increased risk. C1 NIAID, LPD, NIH, Helminth Immunol Sect, Bethesda, MD 20892 USA. RP Nutman, TB (reprint author), NIAID, LPD, NIH, Helminth Immunol Sect, 4 Ctr Dr,Room 4-126, Bethesda, MD 20892 USA. EM tnutman@niaid.nih.gov NR 135 TC 359 Z9 382 U1 1 U2 8 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0893-8512 J9 CLIN MICROBIOL REV JI Clin. Microbiol. Rev. PD JAN PY 2004 VL 17 IS 1 BP 208 EP + DI 10.1128/CMR.17.1.208-217.2004 PG 11 WC Microbiology SC Microbiology GA 769FX UT WOS:000188616800009 PM 14726461 ER PT J AU Nguyen, JD Dunleavy, K Carrasquillo, JA Chen, CC AF Nguyen, JD Dunleavy, K Carrasquillo, JA Chen, CC TI F-18 fluorodeoxyglucose positron emission tomographic imaging in a patient with persistent hiccups SO CLINICAL NUCLEAR MEDICINE LA English DT Editorial Material DE positron emission tomography (PET); F-18 fluorodeoxyglucose (FDG); hiccups C1 NIH, Dept Nucl Med, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA. NCI, Med Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Chen, CC (reprint author), NIH, Dept Nucl Med, Warren Grant Magnuson Clin Ctr, Bldg 10, Bethesda, MD 20892 USA. RI Carrasquillo, Jorge/E-7120-2010; OI Carrasquillo, Jorge/0000-0002-8513-5734 NR 8 TC 4 Z9 4 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0363-9762 J9 CLIN NUCL MED JI Clin. Nucl. Med. PD JAN PY 2004 VL 29 IS 1 BP 35 EP 36 DI 10.1097/01.rlu.0000102762.66515.67 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 757VV UT WOS:000187582900006 PM 14688595 ER PT J AU Huang, SM Hall, SD Watkins, P Love, LA Serabjit-Singh, C Betz, JM Hoffman, FA Honig, P Coates, PM Bull, J Chen, ST Kearns, GL Murray, MD AF Huang, SM Hall, SD Watkins, P Love, LA Serabjit-Singh, C Betz, JM Hoffman, FA Honig, P Coates, PM Bull, J Chen, ST Kearns, GL Murray, MD TI Drug interactions with herbal products and grapefruit juice: A conference report SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Editorial Material ID ST-JOHNS-WORT; ALTERNATIVE MEDICINE USE; HYPERICUM-PERFORATUM; ORAL AVAILABILITY; UNITED-STATES; DIETARY-SUPPLEMENTS; BRUSSELS-SPROUTS; PHARMACOKINETICS; COMPLEMENTARY; CYP3A4 C1 Purdue Univ, Regenstrief Inst, Indianapolis, IN 46202 USA. US FDA, Ctr Drug Evaluat & Res, Rockville, MD 20857 USA. US FDA, Off Regulatory Affairs, Rockville, MD 20857 USA. Indiana Univ, Sch Med, Indianapolis, IN USA. Univ N Carolina, Ctr Med, Chapel Hill, NC USA. GlaxoSmithKline, Res Triangle Pk, NC USA. NIH, Off Dietary Supplements, Bethesda, MD 20892 USA. Pfizer Inc, Pfizer Consumer Hlth Care, Morris Plains, NJ USA. Merck Res Labs, W Point, PA USA. Childrens Mercy Hosp & Clin, Kansas City, MO USA. RP Murray, MD (reprint author), Purdue Univ, Regenstrief Inst, 1050 Wishard Blvd,RG-6, Indianapolis, IN 46202 USA. EM mmurray@regenstrief.org NR 55 TC 54 Z9 58 U1 3 U2 7 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2004 VL 75 IS 1 BP 1 EP 12 DI 10.1016/j.clpt.2003.07.002 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 765YJ UT WOS:000188318400001 PM 14749688 ER PT J AU Montoya, ID Gorelick, DA Preston, KL Schroeder, JR Umbricht, A Cheskin, LJ Lange, R Contoreggi, C Johnson, RE Fudala, PJ AF Montoya, ID Gorelick, DA Preston, KL Schroeder, JR Umbricht, A Cheskin, LJ Lange, R Contoreggi, C Johnson, RE Fudala, PJ TI Randomized trial of buprenorphine for treatment of concurrent opiate and cocaine dependence SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Article ID METHADONE-MAINTENANCE TREATMENT; OPIOID DEPENDENCE; RHESUS-MONKEYS; CLINICAL-TRIAL; INTRAVENOUS COCAINE; MAINTAINED PATIENTS; ABUSE; USERS; IMPACT; HUMANS AB Background: Buprenorphine is a partial mu-opiate agonist and kappa-opiate antagonist with established efficacy in the treatment of opiate dependence. Its efficacy for cocaine dependence is uncertain. This study evaluated buprenorphine for the treatment of concomitant cocaine and opiate dependence. Methods: Two hundred outpatients currently dependent on both cocaine and opiates were randomly assigned to double-blind groups receiving a sublingual solution of buprenorphine (2, 8, or 16 mg daily, or 16 mg on alternate days, or placebo), plus weekly individual drug abuse counseling, for 13 weeks. The chief outcome measures were urine concentrations of opiate and cocaine metabolites (quantitative) and proportion of urine samples positive for opiates or cocaine (qualitative). Group differences were assessed by use of mixed regression modeling. Results: The target dose of buprenorphine was achieved in 179 subjects. Subjects receiving 8 or 16 mg buprenorphine daily showed statistically significant decreases in urine morphine levels (P = .0135 for 8 mg and P < .001 for 16 mg) or benzoylecgonine concentrations (P = .0277 for 8 mg and P = .006 for 16 mg) during the maintenance phase of the study. For the 16-mg group, mean benzoylecgonine concentrations fell from 3715 ng/mL during baseline to 186 ng/mL during the withdrawal phase; mean morphine concentrations fell from 3311 ng/mL during baseline to 263 ng/mL during withdrawal. For the 8-mg group, mean benzoylecgonine concentrations fell from 6761 ng/mL during baseline to 676 ng/mL during withdrawal; mean morphine concentrations fell from 3890 ng/mL during baseline to 661 ng/mL during withdrawal. Qualitative urinalysis showed a similar pattern of results. Subjects receiving the highest dose showed concomitant decreases in both urine morphine and benzoylecgonine concentrations. There were no significant group differences in treatment retention or adverse events. Conclusions: A sublingual buprenorphine solution at 16 mg daily is well tolerated and effective in reducing concomitant opiate and cocaine use. The therapeutic effect on cocaine use appears independent of that on opiate use. C1 NIDA, Intramural Res Program, NIH, Dept Hlth & Human Serv, Baltimore, MD 21224 USA. NIDA, Div Treatment Res & Dev, NIH, Dept Hlth & Human Serv, Baltimore, MD 21224 USA. Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA. Dept Vet Affairs Med Ctr, Philadelphia, PA USA. RP Gorelick, DA (reprint author), NIDA, Intramural Res Program, NIH, Dept Hlth & Human Serv, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM dgorelic@intra.nida.nih.gov RI Preston, Kenzie/J-5830-2013 OI Preston, Kenzie/0000-0003-0603-2479 FU Intramural NIH HHS [Z99 DA999999] NR 51 TC 80 Z9 81 U1 1 U2 4 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2004 VL 75 IS 1 BP 34 EP 48 DI 10.1016/j.clpt.2003.09.004 PG 15 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 765YJ UT WOS:000188318400003 PM 14749690 ER PT J AU Urquidi-Macdonald, M Mager, DE Mascelli, MA Frederick, B Freedman, J Fitzgerald, DJ Kleiman, NS Abernethy, DR AF Urquidi-Macdonald, M Mager, DE Mascelli, MA Frederick, B Freedman, J Fitzgerald, DJ Kleiman, NS Abernethy, DR TI Abciximab pharmacodynamic model with neural networks used to integrate sources of patient variability SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Article ID FEEDFORWARD NETWORKS; CORONARY ANGIOPLASTY; MONOCLONAL-ANTIBODY; PLATELET ACTIVATION; HEALTHY-SUBJECTS; PHARMACOKINETICS; AGGREGATION; RECEPTOR AB Objective: Our objective was to develop a computational model for predicting abciximab-induced inhibition of ex vivo platelet aggregation from the administered dose and readily available patient clinical characteristics by use of a neural network approach. Methods: A back-propagation neural network was designed to establish the relationship between abciximab dosing, patient clinical history, and effect (inhibition of 20 mumol/L adenosine diphosphate-induced ex vivo platelet aggregation). The neural network was trained by use of data from 8 (out of 47) patients undergoing coronary angioplasty and 30 healthy individuals. Final neuron connection weights were used to evaluate significant patient covariates. The final neural network was validated via (1) predicting the effects of the validation database (remaining 39 patients) and (2) predicting the individual patient doses to achieve 20% of baseline platelet aggregation. Results: The trained neural network successfully captured the complex pharmacodynamic profiles of abciximab without specifying a structural model and identified several patient covariates that significantly contribute to establishing the abciximab dose-effect relationship, including stable angina with nitrate treatment, previous myocardial infarction, and smoking. A wide distribution of individual bolus doses of abciximab was predicted, suggesting the potential for dosing individualization while improving the risk of adverse drug events. The mean predicted dose (16.9 mg) was in agreement with the results from a previously published concentration-effect relationship for abciximab (18.9 +/- 2.0 mg). Conclusions: These findings suggest the usefulness of neural network methods to individualize dosing for drugs with a narrow therapeutic index when real-time measures of drug concentration and effect are unavailable, but future clinical studies are required for prospective validation. C1 NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA. Penn State Univ, Dept Engn Sci & Mech, University Pk, PA 16802 USA. Centocor Inc, Malvern, PA USA. Boston Univ, Sch Med, Div Cardiol, Boston, MA 02215 USA. Royal Coll Surgeons Ireland, Ctr Cardiovasc Sci, Dublin 2, Ireland. Baylor Coll Med, Div Cardiol, Houston, TX 77030 USA. RP Abernethy, DR (reprint author), NIA, Gerontol Res Ctr, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM abernethyd@grc.nia.nih.gov NR 41 TC 4 Z9 4 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD JAN PY 2004 VL 75 IS 1 BP 60 EP 69 DI 10.1016/j.clpt.2003.09.008 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 765YJ UT WOS:000188318400005 PM 14749692 ER PT J AU Takahashi, K Reynolds, M Ogawa, N Longo, DL Burdick, J AF Takahashi, K Reynolds, M Ogawa, N Longo, DL Burdick, J TI Augmentation of T-cell apoptosis by immunosuppressive agents SO CLINICAL TRANSPLANTATION LA English DT Article DE activation-induced cell death; cyclosporine; immunosupression; mycophenolate mofetil; rapamycin; tacrolimus; T lympocytes ID CYCLOSPORINE-A; ACTIVATION; INDUCTION; RAPAMYCIN AB The regulatory benefit of apoptosis (activation-induced cell death, AICD) in T cells can be influenced by immunosupressive agents. We examined this for mycophenolate mofetile (MMF, using it's active metabolite, mycophenolate (MPA)) compared with rapamycin (RAPA) and the calcineurin inhibitors (CI) cyclosporin (CYA) and FK506 (FK). Pure T cells from peripheral blood leucocytes (PBL) were stimulated by anti-CD3 plus anti-CD28. Cell division (sequential cohort reduction in carboxyflourescein diacetate succinimidyl ester, CFSE) was used to measure proliferation and determine status of different cell generations without or with added drug at 4 d. Apoptosis was measured by Annexin V staining of activated cells using flow cytometry. We confirmed in this stringent system the inhibition of AICD by CI and showed that RAPA is intermediate and MPA most effective in this potentiation of AICD. C1 Johns Hopkins Med Inst, Baltimore, MD 21205 USA. Saitama Med Sch, Baltimore, MD USA. NIA, Immunol Lab, NIH, Baltimore, MD 21224 USA. RP Burdick, J (reprint author), Johns Hopkins Univ Hosp, Harvey 611,600 N Wolfe St, Baltimore, MD 21287 USA. EM jburdick@att.net NR 14 TC 17 Z9 18 U1 0 U2 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0063 J9 CLIN TRANSPLANT JI Clin. Transplant. PY 2004 VL 18 SU 12 BP 72 EP 75 DI 10.1111/j.1399-0012.2004.00222.x PG 4 WC Surgery; Transplantation SC Surgery; Transplantation GA 833SU UT WOS:000222360000014 PM 15217412 ER PT J AU Hayashi, T Su, TP AF Hayashi, T Su, TP TI sigma-1 receptor ligands - Potential in the treatment of neuropsychiatric disorders SO CNS DRUGS LA English DT Review ID METHYL-D-ASPARTATE; INDUCED BEHAVIORAL SENSITIZATION; COCAINE-INDUCED TOXICITY; ION-CHANNEL COMPLEX; OPEN CLINICAL-TRIAL; GUINEA-PIG BRAIN; RAT-BRAIN; BINDING-SITES; NUCLEUS-ACCUMBENS; AUTORADIOGRAPHIC LOCALIZATION AB The sigma receptor was originally proposed to be a subtype of the opioid receptor. However, it is now clear that a receptors are unique non-opioid, non-phencyclidine brain proteins. Two types of sigma receptor exist, the (sigma-1 receptor and the sigma-2 receptor. sigma- 1 receptors have been cloned and their distribution, physiological functions and roles in signal transduction were recently characterised. Certain sex hormones in the brain (neurosteroids) are known to interact with sigma- 1 receptors. sigma- 1 receptors regulate glutamate NMDA receptor function and the release of neurotransmitters such as dopamine. They are thus proposed to be involved in learning and memory as well as in certain neuropsychiatric disorders. Selective sigma- I receptor ligands have been suggested to represent a new class of therapeutic agents for neuropsychiatric disorders, although none have yet been introduced into therapeutic use. Early studies showed that psychotomimetic benzomorphans, as well as several antipsychotics, can bind to sigma-1 receptors. As a result of these findings, sigma-1 receptor ligands have been proposed as being of potential use in the treatment of schizophrenia. Nevertheless, the relationship of sigma-1 receptors to the underlying pathogenesis of schizophrenia is still unclear. sigma-1 receptor ligands have failed to improve acute psychotic symptoms of schizophrenia in clinical trials, but, interestingly, a few studies have shown an improvement in negative symptoms in schizophrenic patients. A number of preclinical studies have shown that selective agonists of sigma-1 receptors affect higher-ordered brain functions such as learning and memory, cognition and mood. These studies indicate that sigma-l receptor agonists may exert therapeutic effects in depression and senile dementia. Indeed, the sigma-1 receptor agonist igmesine, has been shown to improve depression in a clinical trial. The most distinctive feature of the action of sigma-1 receptor ligands is their 'modulatory' role. In behavioural studies of depression and memory, they exert beneficial effects only when brain functions are perturbed. Given the recently accumulated preclinical and clinical data, it is time to reconstruct the concept of sigma-1 receptors and the associated pathophysiological conditions that ligands of these receptors target. This would allow clinical trials to be performed more efficiently, and the results may confirm a long-speculated possibility that sigma- 1 receptor ligands represent a new class of therapeutic agents for neuropsychiatric disorders. C1 Natl Inst Drug Abuse, Cellular Pathobiol Unit, Cellular Neurobiol Res Branch, Intramural Res Program,Dept Hlth & Human Serv,NIH, Baltimore, MD 21209 USA. RP Hayashi, T (reprint author), Natl Inst Drug Abuse, Cellular Pathobiol Unit, Cellular Neurobiol Res Branch, Intramural Res Program,Dept Hlth & Human Serv,NIH, 5500 Nathan Shock Dr, Baltimore, MD 21209 USA. EM THAYASHI@intra.nida.nih.gov RI Hayashi, Teruo/A-9690-2008 NR 135 TC 177 Z9 186 U1 3 U2 15 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PY 2004 VL 18 IS 5 BP 269 EP 284 DI 10.2165/00023210-200418050-00001 PG 16 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 814PD UT WOS:000220985700001 PM 15089113 ER PT J AU Vitiello, B Wagner, A AF Vitiello, B Wagner, A TI Government initiatives in autism clinical trials SO CNS SPECTRUMS LA English DT Review ID RISPERIDONE AB Randomized clinical trials remain the most valid method of testing the efficacy and safety of treatments. While efforts to elucidate the genetic and neurodevelopmental bases of autism are underway, clinicians and families are in need of scientifically valid information on how to best treat patients with autism. The effectiveness of many interventions currently used in communities has not been adequately tested. Given the high public health relevance of autism treatment research and the low interest of the pharmaceutical industry in autism, the role of the National Institutes of Health in supporting this research is paramount. Among recently launched initiatives in autism clinical trials, there are the Research Units on Pediatric Psychopharmacology Autism Network and the network of centers for Studies to Advance Autism Research and Treatment. These and other government activities in the area of autism clinical trials are here briefly reviewed. C1 Natl Inst Mental Hlth, Div Serv & Intervent Res, Bethesda, MD 20892 USA. RP Vitiello, B (reprint author), Natl Inst Mental Hlth, Div Serv & Intervent Res, Room 7147,6001 Execut Blvd,MSC 9633, Bethesda, MD 20892 USA. EM bvitiell@mail.nih.gov NR 11 TC 3 Z9 3 U1 1 U2 1 PU M B L COMMUNICATIONS, INC PI NEW YORK PA 333 HUDSON ST, 7TH FLOOR, NEW YORK, NY 10013 USA SN 1092-8529 J9 CNS SPECTRUMS JI CNS Spectr. PD JAN PY 2004 VL 9 IS 1 BP 66 EP 70 PG 5 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895UY UT WOS:000226890500007 PM 14999177 ER PT J AU Felsenfeld, G Burgess-Beusse, B Farrell, C Gaszner, M Ghirlando, R Huang, S Jin, C Litt, M Magdinier, F Mutskov, V Nakatani, Y Tagami, H West, A Yusufzai, T AF Felsenfeld, G Burgess-Beusse, B Farrell, C Gaszner, M Ghirlando, R Huang, S Jin, C Litt, M Magdinier, F Mutskov, V Nakatani, Y Tagami, H West, A Yusufzai, T TI Chromatin boundaries and chromatin domains SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 69th Cold Spring Harbor Symsposium on Quantitative Biology CY JUN 02-07, 2004 CL Cold Spring Harbor, NY SP NCI, Natl Inst Environm Hlth Sci, Amgen Inc, Aventis Pharma AG, Bristol Myers Squibb Co, Eli Lilly, GlaxoSmithKline, Novartis Inst BioMed Res, Pfizer, Appl Biosyst, AstraZeneca, BioVentures, Cogene BioTech Ventures, Diagnost Prod Corp, Forest Labs, Genentech Inc, Hoffmann La Roche, Johnson & Johnson Pharmaceut Res & Dev LLC, Kyowa Hakko Kogyo Co Ltd, Lexicon Genet Inc, Merck Res Labs, New England BioLabs, OSI Pharmaceut, Pall Corp, Schering Plough Res Inst, Wyeth Genet Inst ID ENHANCER-BLOCKING ACTIVITY; BETA-GLOBIN LOCUS; PROMOTER DNA; DAD1 GENES; CTCF; INSULATOR; METHYLATION; REGION; MOUSE; MECHANISMS C1 NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RP Felsenfeld, G (reprint author), NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. RI Ghirlando, Rodolfo/A-8880-2009; Magdinier, Frederique/I-4735-2016; OI Magdinier, Frederique/0000-0002-0159-9559; West, Adam/0000-0003-3502-7804 NR 28 TC 66 Z9 70 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI WOODBURY PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 2004 VL 69 BP 245 EP 250 DI 10.1101/sqb.2004.69.245 PG 6 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 969IG UT WOS:000232227200030 PM 16117655 ER PT J AU Cam, H Grewal, SIS AF Cam, H Grewal, SIS TI RNA interference and epigenetic control of heterochromatin assembly in fission yeast SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 69th Cold Spring Harbor Symsposium on Quantitative Biology CY JUN 02-07, 2004 CL Cold Spring Harbor, NY SP NCI, Natl Inst Environm Hlth Sci, Amgen Inc, Aventis Pharma AG, Bristol Myers Squibb Co, Eli Lilly, GlaxoSmithKline, Novartis Inst BioMed Res, Pfizer, Appl Biosyst, AstraZeneca, BioVentures, Cogene BioTech Ventures, Diagnost Prod Corp, Forest Labs, Genentech Inc, Hoffmann La Roche, Johnson & Johnson Pharmaceut Res & Dev LLC, Kyowa Hakko Kogyo Co Ltd, Lexicon Genet Inc, Merck Res Labs, New England BioLabs, OSI Pharmaceut, Pall Corp, Schering Plough Res Inst, Wyeth Genet Inst ID H3 LYSINE-9 METHYLATION; HISTONE H3; SCHIZOSACCHAROMYCES-POMBE; CHROMODOMAIN PROTEIN; CHROMATIN-STRUCTURE; DNA-POLYMERASE; HP1 PROTEINS; DOMAIN; CENTROMERE; INHERITANCE C1 NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. RP Cam, H (reprint author), NCI, Mol Cell Biol Lab, NIH, Bethesda, MD 20892 USA. NR 62 TC 15 Z9 15 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI WOODBURY PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 2004 VL 69 BP 419 EP 427 DI 10.1101/sqb.2004.69.419 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 969IG UT WOS:000232227200051 PM 16117676 ER PT J AU Bjornsson, HT Cui, H Gius, D Fallin, MD Feinberg, AP AF Bjornsson, HT Cui, H Gius, D Fallin, MD Feinberg, AP TI The new field of epigenomics: Implications for cancer and other common disease research SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 69th Cold Spring Harbor Symsposium on Quantitative Biology CY JUN 02-07, 2004 CL Cold Spring Harbor, NY SP NCI, Natl Inst Environm Hlth Sci, Amgen Inc, Aventis Pharma AG, Bristol Myers Squibb Co, Eli Lilly, GlaxoSmithKline, Novartis Inst BioMed Res, Pfizer, Appl Biosyst, AstraZeneca, BioVentures, Cogene BioTech Ventures, Diagnost Prod Corp, Forest Labs, Genentech Inc, Hoffmann La Roche, Johnson & Johnson Pharmaceut Res & Dev LLC, Kyowa Hakko Kogyo Co Ltd, Lexicon Genet Inc, Merck Res Labs, New England BioLabs, OSI Pharmaceut, Pall Corp, Schering Plough Res Inst, Wyeth Genet Inst ID DNA METHYLATION; HETEROCHROMATIN FORMATION; MAMMALIAN DEVELOPMENT; HISTONE MODIFICATIONS; ABNORMAL METHYLATION; DIABETES-MELLITUS; IMPRINTED GENES; SOMATIC-CELLS; WILMS-TUMOR; H19 LOCUS C1 Johns Hopkins Univ, Sch Med, Predoctoral Program Human Genet, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Genet & Mol Biol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA. NCI, Radiat Oncol Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. RP Bjornsson, HT (reprint author), Johns Hopkins Univ, Sch Med, Predoctoral Program Human Genet, Baltimore, MD 21205 USA. RI Cui, Hengmi/A-2598-2008; Bjornsson, Hans/A-2964-2013 OI Bjornsson, Hans/0000-0001-6635-6753 FU NCI NIH HHS [CA65145, R37 CA054358, R37 CA054358-14]; NHGRI NIH HHS [HG003233]; NIGMS NIH HHS [T32 GM007471] NR 63 TC 17 Z9 17 U1 0 U2 3 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI WOODBURY PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 2004 VL 69 BP 447 EP 456 DI 10.1101/sqb.2004.69.447 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 969IG UT WOS:000232227200055 PM 16117680 ER PT J AU Wickner, RB Edskes, HK Ross, ED Pierce, MM Shewmaker, F Baxa, U Brachmann, A AF Wickner, RB Edskes, HK Ross, ED Pierce, MM Shewmaker, F Baxa, U Brachmann, A TI Prions of yeast are genes made of protein: Amyloids and enzymes SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 69th Cold Spring Harbor Symsposium on Quantitative Biology CY JUN 02-07, 2004 CL Cold Spring Harbor, NY SP NCI, Natl Inst Environm Hlth Sci, Amgen Inc, Aventis Pharma AG, Bristol Myers Squibb Co, Eli Lilly, GlaxoSmithKline, Novartis Inst BioMed Res, Pfizer, Appl Biosyst, AstraZeneca, BioVentures, Cogene BioTech Ventures, Diagnost Prod Corp, Forest Labs, Genentech Inc, Hoffmann La Roche, Johnson & Johnson Pharmaceut Res & Dev LLC, Kyowa Hakko Kogyo Co Ltd, Lexicon Genet Inc, Merck Res Labs, New England BioLabs, OSI Pharmaceut, Pall Corp, Schering Plough Res Inst, Wyeth Genet Inst ID UREIDOSUCCINIC ACID UPTAKE; CHAIN RELEASE FACTOR; DE-NOVO APPEARANCE; SOLID-STATE NMR; SACCHAROMYCES-CEREVISIAE; GUANIDINE-HYDROCHLORIDE; PSI+ PRION; ANTAGONISTIC INTERACTIONS; PODOSPORA-ANSERINA; FILAMENTOUS FUNGI C1 NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. RP Wickner, RB (reprint author), NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. RI Brachmann, Andreas/I-2241-2013; OI Brachmann, Andreas/0000-0001-7980-8173; Ross, Eric/0000-0002-6473-9977 NR 78 TC 5 Z9 5 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI WOODBURY PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 2004 VL 69 BP 489 EP 496 DI 10.1101/sqb.2004.69.489 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 969IG UT WOS:000232227200060 PM 16117685 ER PT J AU Klar, AJS AF Klar, AJS TI An epigenetic hypothesis for human brain laterality, handedness, and psychosis development SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article; Proceedings Paper CT 69th Cold Spring Harbor Symposium on Quantitative Biology CY JUN 02-07, 2004 CL Cold Spring Harbor, NY SP NCI, Natl Inst Environm Hlth Sci, Amgen Inc, Aventis Pharma AG, Bristol Myers Squibb Co, Eli Lilly, GlaxoSmithKline, Novartis Inst BioMed Res, Pfizer, Appl Biosyst, AstraZeneca, BioVentures, Cogene BioTech Ventures, Diagnost Prod Corp, Forest Labs, Genentech Inc, Hoffmann La Roche, Johnson & Johnson Pharmaceut Res & Dev LLC, Kyowa Hakko Kogyo Co Ltd, Lexicon Genet Inc, Merck Res Labs, New England BioLabs, OSI Pharmaceut, Pall Corp, Schering Plough Res Inst, Wyeth Genet Inst ID GENOME SCAN METAANALYSIS; FISSION YEAST; SCHIZOSACCHAROMYCES-POMBE; CHROMOSOMAL TRANSLOCATION; GENETIC MECHANISM; BIPOLAR DISORDER; DNA STRANDS; SCHIZOPHRENIA; ASYMMETRY; CELLS C1 NCI, Gene Regulat & Chromosome Biol Lab, Frederick, MD 21702 USA. RP Klar, AJS (reprint author), NCI, Gene Regulat & Chromosome Biol Lab, Frederick, MD 21702 USA. NR 39 TC 14 Z9 14 U1 1 U2 5 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 2004 VL 69 BP 499 EP 506 DI 10.1101/sqb.2004.69.499 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 969IG UT WOS:000232227200062 PM 16117687 ER PT S AU Agnati, LF Santarossa, L Genedani, S Canela, EI Leo, G Franco, R Woods, A Lluis, C Ferre, S Fuxe, K AF Agnati, LF Santarossa, L Genedani, S Canela, EI Leo, G Franco, R Woods, A Lluis, C Ferre, S Fuxe, K BE Erdi, P Esposito, A Marinaro, M Scarpetta, S TI On the nested hierarchical organization of CNS: Basic characteristics of neuronal molecular networks SO COMPUTATIONAL NEUROSCIENCE: CORTICAL DYNAMICS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT International Summer School on Neural Nets CY OCT 31-NOV 06, 2003 CL Erice, ITALY SP Italian Neural Networks Soc, Minist Italiano Istruz Univ & Ricerca, Univ Salerno, Dipartimento Fis ER Caianiello, Univ Salerno, Reg Campania, Int Inst Adv Sci Studies ID CENTRAL-NERVOUS-SYSTEM; PROTEIN-COUPLED RECEPTORS/; VOLUME TRANSMISSION; HEPTAHELICAL RECEPTORS; SIGNALING PATHWAYS; COMPLEXITY; BRAIN; HYPOTHESIS; MODULES; COMMUNICATION AB It has been suggested that the Central Nervous System (CNS) is built as a "nested system of networks of networks" structured according to hierarchical principles. Thus, it is possible to recognize networks at multiple scales (miniaturisation principle) moving top-down from neuronal to molecular networks. Such a nested organization of the CNS leads to the problem how circulation and integration of information at different levels of miniaturisation (i.e., macro-scale, meso-scale and micro-scale) take place. We suggest that local circuits are the highly specialised meso-scale level capable of functionally interconnecting macro-with micro-scale level. Furthermore, it is suggested that the same modes for communication (Wiring and Volume Transmission) are in operation at various miniaturisation levels. This indicates a sort of "fractal organization" of the CNS. Detailed analysis of molecular networks is discussed. In particular, receptor-receptor interactions are examined as an important input to horizontal molecular networks located at plasma membrane level. C1 Univ Modena & Reggio Emilia, Dept Biomed Sci, Physiol Sect, I-41100 Modena, Italy. Univ Modena & Reggio Emilia, Dept Biomed Sci, Pharmacol Sect, I-41100 Modena, Italy. Univ Barcelona, Dept Biochem & Mol Biol, E-08028 Barcelona, Spain. NIDA, Dept Hlth & Human Serv, Intramural Res Program, Baltimore, MD 21224 USA. Karolinska Inst, Dept Neurosci, Stockholm, Sweden. RP Agnati, LF (reprint author), Univ Modena & Reggio Emilia, Dept Biomed Sci, Physiol Sect, Via Campi 287, I-41100 Modena, Italy. EM luigiagnati@tin.it RI Ferre, Sergi/K-6115-2014; Franco, Rafael/C-3694-2015; Genedani, Susanna/K-4370-2016 OI Fuxe, Kjell/0000-0001-8491-4288; Canela, Enric I./0000-0003-4992-7440; Ferre, Sergi/0000-0002-1747-1779; Franco, Rafael/0000-0003-2549-4919; Genedani, Susanna/0000-0003-1526-153X NR 62 TC 19 Z9 19 U1 0 U2 3 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-22566-8 J9 LECT NOTES COMPUT SC PY 2004 VL 3146 BP 24 EP 54 PG 31 WC Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Neurosciences SC Computer Science; Neurosciences & Neurology GA BAT53 UT WOS:000223462900002 ER PT J AU Borkowf, CB AF Borkowf, CB TI An efficient algorithm for generating two-way contingency tables with fixed marginal totals and arbitrary mean proportions, with applications to permutation tests SO COMPUTATIONAL STATISTICS & DATA ANALYSIS LA English DT Article DE copula; enumeration; exact inference; iterative proportion fitting (IPF); multivariate extended hypergeometric (MXH) distribution; simulation AB In this paper, we present an algorithm for generating two-way contingency tables with fixed marginal totals and arbitrary mean proportions. These tables have exactly the multivariate extended hypergeometric (MXH) distribution in special cases where certain local independence conditions hold, and approximately that distribution otherwise. One can simulate MXH tables to approximate the results of permutation tests under null and alternative hypotheses. We also consider appropriate classes of models for the mean proportions of MXH tables. Finally, we illustrate the use of the methods developed in this paper on two medical applications. Published by Elsevier B.V. C1 NCI, Canc Res Ctr, Canc Prevent Studies Branch, Bethesda, MD 20892 USA. RP Borkowf, CB (reprint author), CDCP, NCID, DVRD, Influenza Branch,Epidemiol Sect, Mail Stop A32,1600 Clifton Rd NE, Atlanta, GA 30333 USA. EM cborkowf@cdc.gov NR 14 TC 1 Z9 1 U1 1 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-9473 J9 COMPUT STAT DATA AN JI Comput. Stat. Data Anal. PD JAN 1 PY 2004 VL 44 IS 3 BP 431 EP 449 AR PII S0167-9473(02)00253-0 DI 10.1016/S0167-9473(02)00253-0 PG 19 WC Computer Science, Interdisciplinary Applications; Statistics & Probability SC Computer Science; Mathematics GA 760WW UT WOS:000187859100001 ER PT J AU Chamarthy, P Stanley, RJ Cizek, G Long, R Antani, S Thoma, G AF Chamarthy, P Stanley, RJ Cizek, G Long, R Antani, S Thoma, G TI Image analysis techniques for characterizing disc space narrowing in cervical vertebrae interfaces SO COMPUTERIZED MEDICAL IMAGING AND GRAPHICS LA English DT Article DE degenerative disk disease; disc space narrowing; image processing; cervical spine disorders; K-means; self-organizing maps ID SPINE DEFORMITY; FRACTURES; DEGENERATION; MORPHOMETRY; DIAGNOSIS; ABILITY AB Image analysis techniques are introduced for evaluating disc space narrowing of cervical vertebrae interfaces from X-ray images. Four scale-invariant, distance transforrn-based features are presented for characterizing the spacing between adjacent vertebrae. K-means and self-organizing map clustering techniques are applied to estimate the degree of disc space narrowing using a four grade (0-3) scoring system, where 0 and 3 represent normal spacing and significant narrowing, respectively. For a data set of 294 vertebrae interfaces, experimental results yield average correct grade assignment of greater than 82.10% for each of the four grades using a one grade window around the correct grade. (C) 2003 Elsevier Ltd. All rights reserved. C1 Univ Missouri, Dept Elect & Comp Engn, Rolla, MO 65409 USA. Excel Imaging, St Louis, MO USA. Natl Lib Med, Commun Engn Branch, Bethesda, MD USA. RP Stanley, RJ (reprint author), Univ Missouri, Dept Elect & Comp Engn, Rolla, MO 65409 USA. OI Antani, Sameer/0000-0002-0040-1387 NR 36 TC 13 Z9 13 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-MAR PY 2004 VL 28 IS 1-2 BP 39 EP 50 DI 10.1016/j.compmedimag.2003.10.001 PG 12 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 774JT UT WOS:000188976900006 PM 15127748 ER PT J AU Cherukuri, M Stanley, RJ Long, R Antani, S Thoma, G AF Cherukuri, M Stanley, RJ Long, R Antani, S Thoma, G TI Anterior osteophyte discrimination in lumbar vertebrae using size-invariant features SO COMPUTERIZED MEDICAL IMAGING AND GRAPHICS LA English DT Article DE osteoarthritis; osteophyte; neural networks; image processing; lumbar spine; X-ray ID SPINE DEFORMITY; FRACTURES; POSTMENOPAUSAL; MORPHOMETRY; ABILITY; WOMEN AB Radiologists often examine X-rays of cervical, thoracic and lumbar vertebrae for determining the presence of osteoarthritis and osteoporosis. For individual vertebra assessment, the boundary increasingly digresses from the general rectangular shape as the vertebra becomes less normal in appearance. For an abnormal vertebra, bony growths ('osteophytes') may appear at the vertebral corners, resulting in a change in the vertebra's shape. Image processing techniques are presented for computing size-invariant, convex hull-based features to highlight anterior osteophytes. Feature evaluation of 714 lumbar spine vertebrae using a multi-layer perceptron yielded normal and abnormal average correct discrimination of 90.5 and 86.6%, respectively. (C) 2003 Elsevier Ltd. All rights reserved. C1 Univ Missouri, Dept Elect & Comp Engn, Rolla, MO 65409 USA. Natl Lib Med, Commun Engn Branch, Bethesda, MD USA. RP Stanley, RJ (reprint author), Univ Missouri, Dept Elect & Comp Engn, 127 Emerson Elect Co Hall,1870 Miner Circle, Rolla, MO 65409 USA. EM stanleyr@umr.edu OI Antani, Sameer/0000-0002-0040-1387 NR 25 TC 13 Z9 13 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-MAR PY 2004 VL 28 IS 1-2 BP 99 EP 108 DI 10.1016/j.compmedimag.2003.09.002 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 774JT UT WOS:000188976900012 PM 15127754 ER PT J AU Sarno, RJ Villalba, L Bonacic, C Gonzalez, B Zapata, B Mac Donald, DW O'Brien, SJ Johnson, WE AF Sarno, RJ Villalba, L Bonacic, C Gonzalez, B Zapata, B Mac Donald, DW O'Brien, SJ Johnson, WE TI Phylogeography and subspecies assessment of vicunas in Chile and Bolivia utilizing mtDNA and microsatellite markers: implications for vicuna conservation and management SO CONSERVATION GENETICS LA English DT Article DE camelid; microsatellites; mtDNA sequences; ungulate; Vicugna vicugna ID REDUCE FEEDING DAMAGE; GEOGRAPHICAL-DISTRIBUTION; POPULATION SUBDIVISION; CLADISTIC-ANALYSIS; PREDATOR ODORS; DNA HAPLOTYPES; BIGHORN SHEEP; EVOLUTION; ALLELES; AMPLIFICATION AB The rearing and maintenance of wild vicunas in semi-captivity for economic utilization is practiced mainly in Peru, but Argentina, Bolivia, and Chile are quickly developing their own programs of economic use. Large scale rearing practices will likely isolate populations and may foster selective breeding. In addition to these concerns, there are also uncertainties about the distribution and validity of the currently recognized subspecies. To better understand the potential impact that economic utilization will have on the vicuna, we describe the molecular genetic variation among four populations and both described subspecies. An analysis of 794 bp of mitochondrial DNA sequences (16s, cytochrome b genes, and mtDNA control region) revealed appreciable genetic diversity, low to moderate levels of genetic differentiation, and restricted gene flow with isolation by distance among populations. Analysis of microsatellite data also indicated genetic differentiation among populations. Past climatic and geologic events, coupled with human history, have likely subjected the vicuna to various episodes of population isolation and admixture. Therefore, we suggest that managers aim to ensure gene flow among adjoining populations, as observed at mtDNA and microsatellite loci, as well as maintaining apparent restricted gene flow with isolation by distance among populations separated by great distances. Intensive rearing procedures like those being practiced in Peru will ultimately disrupt movements and migration among wild populations. Furthermore, animals that are not exposed to predation by remaining inside fences, may overtime, lose portions of their behavioral repertoire that enable them to recognize potentially dangerous sounds associated with the presence of predators. Therefore, we do not recommend that animals be placed behind fences as this could lead to a loss of genetic and behavioral diversity as well as halting natural ecological processes. If, however, vicunas are placed behind fences for commercial purposes ( with little or no regard for the retention of genetic, and/or behavioral diversity as well as natural population processes) then we suggest close genetic monitoring of animals that are (will be) maintained in captivity. C1 NCI, Lab Genom Divers, Frederick, MD 21702 USA. Colecc Boliviana Fauna, La Paz, Bolivia. Univ Oxford, Conservat Unit, Oxford OX1 3PS, England. Pontificia Univ Catolica Chile, Fac Agron & Ingn Forestal, Santiago, Chile. Univ Oxford Wolfson Coll, Wildlife Conservat Res Unit, Oxford OX2 6UD, England. RP Sarno, RJ (reprint author), Univ S Florida, Dept Biol, 4202 E Fowler Ave, Tampa, FL 33620 USA. EM rsarno@chuma1.cas.usf.edu RI Gonzalez, Benito/I-9570-2014; Johnson, Warren/D-4149-2016 OI Gonzalez, Benito/0000-0001-8201-8789; Johnson, Warren/0000-0002-5954-186X NR 78 TC 16 Z9 17 U1 1 U2 9 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 1566-0621 J9 CONSERV GENET JI Conserv. Genet. PY 2004 VL 5 IS 1 BP 89 EP 102 DI 10.1023/B:COGE.0000014014.01531.b6 PG 14 WC Biodiversity Conservation; Genetics & Heredity SC Biodiversity & Conservation; Genetics & Heredity GA 769UF UT WOS:000188667600008 ER PT J AU Memarzadeh, F Harrison, PC Riskowski, GL Henze, T AF Memarzadeh, F Harrison, PC Riskowski, GL Henze, T TI Comparison of environment and mice in static and mechanically ventilated isolator cages with different air velocities and ventilation designs SO CONTEMPORARY TOPICS IN LABORATORY ANIMAL SCIENCE LA English DT Article AB The purpose of this study was to compare environmental conditions and mice in cages with four different mechanical ventilation designs and a static isolator cage. Environmental conditions (air velocity, temperature, relative humidity, bedding weight change, airborne dust, NH3' and CO2) were compared for each cage type (n = 5 per cage). Bedding type was chipped hardwood. Mouse response in each cage type was evaluated by body weight, feed consumption, water intake, location of specific behaviors, and budding of bedding mounds. Commercial polycarbonate mouse caging units (29.2 x 19.1 x 12.7 cm shoebox style, stainless-steel round wire bar lids, and 7-cm-deep isolator cage filter tops) were modified to fit the mechanical ventilation cage types and were used for the static isolator cages. Mechanically ventilated cages were fitted with forced air inlets centered 5 cm above the cage floor on the 19.1 cm-side of the cage. Inlet air velocity was either 40 or 200 feet/min (n = 10 cages each), and the air volume exchange rate was 9.3 L/min. In half of the mechanically ventilated cages, the exhaust air was forced through a filter in the isolator cage top, whereas in the remaining mechanically ventilated cages, the air was forced through a single exhaust port fixed in the narrow side of the cage top directly above the air inlet. Inlet air velocity but not exhaust design affected intracage air velocity distribution. Other environmental conditions were similar between the four mechanical ventilation designs. Relative to the mechanically ventilated cages, the static isolator cages had lower air velocities, higher relative humidities, higher NH3 levels, higher CO2 levels, lower body weight gain, and lower water consumption; temperatures, particulate levels, and feed consumption rates did not differ significantly between cage types. Locations of bedding mounds and behaviors were similar in all cage treatments. C1 Texas A&M Univ, Dept Anim Sci, College Stn, TX 77843 USA. NIH, Div Policy & Program Assessment, Off Res Facil, Bethesda, MD 20892 USA. Univ Illinois, Coll Agr Consumer & Environm Sci, Chicago, IL 60680 USA. RP Harrison, PC (reprint author), Texas A&M Univ, Dept Anim Sci, College Stn, TX 77843 USA. NR 12 TC 24 Z9 24 U1 0 U2 2 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI MEMPHIS PA 9190 CRESTWYN HILLS DR, MEMPHIS, TN 38125 USA SN 1060-0558 J9 CONTEMP TOP LAB ANIM JI Contemp. Top. Lab. Anim. Sci. PD JAN PY 2004 VL 43 IS 1 BP 14 EP 20 PG 7 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA 766XK UT WOS:000188400500003 PM 14984284 ER PT J AU Dorman, T Angood, PB Angus, DC Clemmer, TP Cohen, NH Durbin, CG Falk, JL Helfaer, MA Haupt, MT Horst, HM Ivy, ME Ognibene, FP Sladen, RN Grenvik, ANA Napolitano, LM AF Dorman, T Angood, PB Angus, DC Clemmer, TP Cohen, NH Durbin, CG Falk, JL Helfaer, MA Haupt, MT Horst, HM Ivy, ME Ognibene, FP Sladen, RN Grenvik, ANA Napolitano, LM TI Guidelines for critical care medicine training and continuing medical education SO CRITICAL CARE MEDICINE LA English DT Article DE critical care medicine; patient outcomes; intensive care unit utilization; continuing medical education; ethics AB Objective. Critical care medicine trainees and faculty must acquire and maintain the skills necessary to provide state-of-the art clinical care to critically ill patients, to improve patient outcomes, optimize intensive care unit utilization, and continue to advance the theory and practice of critical care medicine. This should be accomplished in an environment dedicated to compassionate and ethical care. Participants: A multidisciplinary panel of professionals with expertise in critical care education and the practice of critical care medicine under the direction of the American College of Critical Care Medicine. Scope. Physician education in critical care medicine in the United States should encompass all disciplines that provide care in the intensive care unit and all levels of training: from medical students through all levels of postgraduate training and continuing medical education for all providers of clinical critical care. The scope of this guideline includes physician education in the United States from residency through ongoing practice after subspecialization. Data Sources and Synthesis. Relevant literature was accessed via a systematic Medline search as well as by requesting references from all panel members. Subsequently, the bibliographies of obtained literature were reviewed for additional references. In addition, a search of organization-based published material was conducted via the Internet. This included but was not limited to material published by the American College of Critical Care Medicine, Accreditation Council for Graduate Medical Education, Accreditation Council for Continuing Medical Education, and other primary and specialty organizations. Collaboratively and iteratively, the task force met, by conference call and in person, to construct the tenets and ultimately the substance of this guideline. Conclusions: Guidelines for the continuum of education in critical care medicine from residency through specialty training and ongoing throughout practice will facilitate standardization of physician education in critical care medicine. C1 Johns Hopkins Univ Hosp, Dept Anesthesia & Crit Care Med, Baltimore, MD 21287 USA. Univ Massachusetts, Sch Med, Div Trauma & Crit Care Med, Worcester, MA 01605 USA. Univ Pittsburgh, Dept Crit Care Med, Pittsburgh, PA USA. LDS Hosp, Dept Crit Care Med, Salt Lake City, UT USA. Univ Calif San Francisco, Dept Crit Care Med, San Francisco, CA 94143 USA. Univ Virginia, Hlth Syst, Dept Anesthesiol, Charlottesville, VA USA. Orlando Reg Med Ctr Inc, Dept Emergency Med, Orlando, FL USA. Childrens Hosp Philadelphia, Pediat Intens Care Unit, Philadelphia, PA 19104 USA. Oregon Hlth Sci Univ, Adult Crit Care Serv, Portland, OR 97201 USA. Henry Ford Hosp, Div Trauma Surg, Detroit, MI 48202 USA. Bridgeport Hosp, Dept Surg, Bridgeport, CT USA. NIH, Ctr Clin, Dept Crit Care Med, Bethesda, MD 20892 USA. Columbia Univ Coll Phys & Surg, Columbia Presbyterian Med Ctr, New York, NY 10032 USA. Univ Maryland, Med Syst, Dept Surg, Baltimore, MD 21201 USA. RP Dorman, T (reprint author), Johns Hopkins Univ Hosp, Dept Anesthesia & Crit Care Med, Baltimore, MD 21287 USA. RI Angus, Derek/E-9671-2012 NR 0 TC 51 Z9 58 U1 0 U2 2 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 2004 VL 32 IS 1 BP 263 EP 272 DI 10.1097/01.CCM.000104916.33769.9A PG 10 WC Critical Care Medicine SC General & Internal Medicine GA 765YN UT WOS:000188318800037 PM 14707590 ER PT J AU Holt, AE Slonim, AD AF Holt, AE Slonim, AD TI Linezolid for treatment of ventilator-associated pneumonia: A cost-effective alternative to vancomycin - Caveats of evaluating costs in critical care SO CRITICAL CARE MEDICINE LA English DT Editorial Material DE cost; intensive care; healthcare economics; resource consumption; quality; outcome ID DESCRIPTIVE ANALYSIS; UNITS C1 NIH, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. George Washington Univ, Sch Med, Childrens Natl Med Ctr Pediat & Internal Med, Washington, DC USA. RP Holt, AE (reprint author), NIH, Warren G Magnuson Clin Ctr, Bldg 10, Bethesda, MD 20892 USA. NR 11 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 2004 VL 32 IS 1 BP 299 EP 300 DI 10.1097/01.CCM.0000104928.95675.4C PG 2 WC Critical Care Medicine SC General & Internal Medicine GA 765YN UT WOS:000188318800049 PM 14707602 ER PT J AU Verma, M Maruvada, P Srivastava, S AF Verma, M Maruvada, P Srivastava, S TI Epigenetics and cancer SO CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES LA English DT Review DE acetylation; biomarkers; chromatin; early detection; epigenetics; epigenome; methylation; prevention; risk assessment ID CPG-ISLAND METHYLATION; HISTONE DEACETYLASE INHIBITORS; ABERRANT PROMOTER METHYLATION; HUMAN PROSTATE-CANCER; CELL LUNG-CANCER; ACUTE PROMYELOCYTIC LEUKEMIA; INFLAMMATORY-BOWEL-DISEASE; TUMOR-SUPPRESSOR GENES; DNA METHYLATION; COLORECTAL-CANCER AB Both genetics and epigenetics regulate gene expression in cancer. Regulation by genetics involves a change in the DNA sequence, whereas epigenetic regulation involves alteration in chromatin structure and methylation of the promoter region. During the initiation, development, and progression of cancer, a number of genes undergo epigenetic changes. Some of these changes can be used as biomarkers for early detection of cancer as well as to follow treatment. A panel of epigenetic biomarkers is preferred to a single biomarker in clinical assays. Changes in gene expression due to epigenetic regulation can be reversed by chemicals, and this approach opens up a novel approach in cancer prevention and treatment. C1 NCI, Canc Biomarkers Res Grp, Div Canc Prevent, Bethesda, MD 20892 USA. RP Verma, M (reprint author), NCI, Analyt Epidemiol Res Branch, Epidemiol & Genet Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. EM vermam@mail.nih.gov NR 171 TC 35 Z9 38 U1 2 U2 6 PU CRC PRESS LLC 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 2004 VL 41 IS 5-6 BP 585 EP 607 DI 10.1080/10408360490516922 PG 23 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 870RK UT WOS:000225075400004 PM 15603512 ER PT J AU Wadhwa, S Embree, MC Bi, YM Young, MF AF Wadhwa, S Embree, MC Bi, YM Young, MF TI Regulation, regulatory activities, and function of biglycan SO CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION LA English DT Review DE proteoglycans; extracellular matrix; skeleton; biglycan; gene regulation ID LEUCINE-RICH REPEAT; HUMAN ARTICULAR-CARTILAGE; SMOOTH-MUSCLE CELLS; GROWTH-FACTOR-BETA; CHONDROITIN SULFATE PROTEOGLYCAN; HUMAN INTERVERTEBRAL DISC; NECROSIS-FACTOR-ALPHA; EXTRACELLULAR-MATRIX; GENE-EXPRESSION; DEFICIENT MICE AB Biglycan is a member of the small leucine repeat proteoglycan family (SLRP). The biglycan gene is located on the X chromosome. Based on the amino acid sequence, the protein core of biglycan can be divided into six distinct domains: (1) a signal sequence, (2) a propeptide region, (3) a N-terminal glycosaminoglycan attachment region, (4) a cysteine loop, followed by (5) a leucine-rich repeat region domain (that makes up over 66% of the core protein), and (6) a final cysteine loop. Biglycan has been found in almost every organ within our body, but it is not uniformly distributed within an organ. Biglycan has been shown to be expressed on the cell surface, pericellularly, and sometimes within the extracellular matrices of a range of specialized cell types within the organ. Its expression pattern has been shown to be altered by growth factors and certain pathologic conditions. The regulation of biglycan expression occurs by both transcriptional and nontranscriptional mechanisms. The currently proposed biglycan functions appear to be dependent on the particular microenvironment and on the organ in question. In this review, we will focus on gene and protein structure, localization, expression, regulation, and function. C1 NIDCR, CSDB, NIH, Bethesda, MD 20892 USA. RP Young, MF (reprint author), NIDCR, CSDB, NIH, Bldg 30 Room 225,MSC 4320, Bethesda, MD 20892 USA. EM myoung@dir.nidcr.nih.gov NR 112 TC 29 Z9 31 U1 0 U2 4 PU BEGELL HOUSE INC PI NEW YORK PA 145 MADISON AVE, NEW YORK, NY 10016 USA SN 1045-4403 J9 CRIT REV EUKAR GENE JI Crit. Rev. Eukaryot. Gene Expr. PY 2004 VL 14 IS 4 BP 301 EP 315 DI 10.1615/CritRevEukaryotGeneExpr.v14.i4.50 PG 15 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 887TC UT WOS:000226327400005 PM 15663360 ER PT J AU Kehrl, JH AF Kehrl, JH TI G-protein-coupled receptor signaling, RGS proteins, and lymphocyte function SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Review DE GPCRs; RGS proteins; G-proteins; lymphocytes; cell migration; gene targeting ID HETEROTRIMERIC G-PROTEINS; GTPASE-ACTIVATING PROTEINS; B-CELL DIFFERENTIATION; N-TERMINAL KINASE; ALPHA-SUBUNIT; T-CELL; MICE LACKING; PLATELET ACTIVATION; TYROSINE KINASE; TRANSITION-STATE AB The positioning of lymphocytes in immune organs and the migration of lymphocytes that occurs during normal immune surveillance and following immune activation depends on appropriate signaling through receptors that couple to heterotrimeric G-proteins. In addition other mediators that affect lymphocyte function, such as histamine, purine nucleosides, C5A, prostaglandins, leukotrienes, serotonin, epinephrine, opioids, and certain phospholipids, also signal through G-protein-coupled receptors (GPCRs). Downstream of heterotrimeric G-proteins are a limited number of downstream effectors, which, in turn, activate a large number of other signaling molecules, many of which are shared with other signaling pathways, such as those activated by antigen receptors, coreceptors, and adhesion receptors. Crucial to signaling through GPCRs are finely developed regulatory systems, which control the activation of heterotrimeric G-proteins and their interactions with their immediate downstream effectors. This review will focus on the overall importance of GPCR signaling in lymphocyte function and an upstream regulatory system present in lymphocytes, which fine tunes heterotrimeric G-protein signaling. C1 NIAID, Immunoregulat Lab, Cell Mol Immunol Sect B, NIH, Bethesda, MD 20892 USA. RP Kehrl, JH (reprint author), NIAID, Immunoregulat Lab, Cell Mol Immunol Sect B, NIH, Bethesda, MD 20892 USA. EM jkehrl@niaid.nih.gov OI Kehrl, John/0000-0002-6526-159X NR 124 TC 22 Z9 23 U1 0 U2 0 PU BEGELL HOUSE INC PI NEW YORK PA 145 MADISON AVE, NEW YORK, NY 10016 USA SN 1040-8401 J9 CRIT REV IMMUNOL JI Crit. Rev. Immunol. PY 2004 VL 24 IS 6 BP 409 EP 423 PG 15 WC Immunology SC Immunology GA 910LF UT WOS:000227932200002 PM 15777161 ER PT J AU Olden, K AF Olden, K TI Use of 'omic' approaches in unraveling mechanisms of gene-environment interactions SO CURRENT GENOMICS LA English DT Article DE toxicogenomics; environmental genome project; gene-environment interactions; comparative toxicogenomics database ID EXPRESSION; GENOME AB The genocentric view of disease that has dominated biomedical science for the past 25 years has proven insufficient for determining causation of most diseases. The technology arising from genomic efforts, however, provides powerful tools for developing the more meaningful cellular and molecular understanding of disease causation, particularly as it is affected by environmental and behavioral parameters. The Environmental Genome Project, the Mouse Genetic Variation Mappinp Initiative, and the Comparative Toxicogenomics Initiative are discussed as projects that aim to capitalize on genomic technology in ways that better define the environmental and genetic underpinnings of chronic diseases and disorders. C1 NIEHS, Res Triangle Pk, NC 27709 USA. Natl Toxicol Program, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. RP Olden, K (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA. EM olden@niehs.nih.gov NR 12 TC 5 Z9 5 U1 0 U2 0 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1389-2029 J9 CURR GENOMICS JI Curr. Genomics PD JAN PY 2004 VL 5 IS 1 BP 1 EP 6 DI 10.2174/1389202043489980 PG 6 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 818JP UT WOS:000221241700001 ER PT J AU Stevceva, L Strober, W AF Stevceva, L Strober, W TI Mucosal HIV vaccines: Where are we now? SO CURRENT HIV RESEARCH LA English DT Article DE HIV; vaccine; mucosal; CTL; immunoglobulin ID SIMIAN IMMUNODEFICIENCY VIRUS; CYTOTOXIC T-LYMPHOCYTE; IMMUNE-RESPONSES; DENDRITIC CELLS; DNA VACCINE; RHESUS MACAQUES; INTRANASAL IMMUNIZATION; SECRETORY IGA; DC-SIGN; INTRAVAGINAL CHALLENGE AB Around the world, approximately 5 million people became infected with HIV in 2001, an estimated 70% via sexual transmission. Numerous studies have demonstrated that it is difficult to achieve total protection from vaginally or rectally acquired HIV/SIV when using parenteral immunization. Mucosal immunization was seen as the best approach to achieve sustainable immune responses at mucosal sites of viral entry. This was further emphasized when several studies implicated rectal and vaginal mucosa as latent reservoirs for the HIV virus and virus-specific CD8+ T cell immune responses in gastrointestinal mucosa were shown to be less efficient than in systemic tissues. Mucosal vaccines utilizing various routes of immunization including intranasal, intrarectal, intravaginal and oral immunization have been tested for their potency to induce virus-specific immune responses systemically but especially at mucosal sites of viral entry. The unsatisfactory results in initiating simultaneously sufficient immune responses at mucosal and systemic sites are being overcomed by use of appropriate and novel adjuvants such as Cholera toxin, Escherichia coli heat-labile toxin, immunostimulatory CpG motifs, coinjection of cytokines and others. Various routes of immunization are now being compared and combinations of mucosal immunization and parenteral boost and vice versa have also been tested. Generations of new vaccines, such as DNA-based vaccines, multipeptide, lipopeptide and alphavirus replicon particles-based vaccines have been created and studied for their efficiency. C1 Thomas Jefferson Med Coll, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA. NIAID, Clin Invest Lab, Bethesda, MD 20892 USA. RP Stevceva, L (reprint author), Thomas Jefferson Med Coll, Dept Pathol Anat & Cell Biol, Jefferson Alumni Hall,Room 219,1020 Locust St, Philadelphia, PA 19107 USA. EM Liljana.Stevceva@mail.tju.edu NR 73 TC 40 Z9 42 U1 0 U2 0 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1570-162X J9 CURR HIV RES JI Curr. HIV Res. PD JAN PY 2004 VL 2 IS 1 BP 1 EP 10 DI 10.2174/1570162043485004 PG 10 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA 779HN UT WOS:000189289400002 PM 15053336 ER PT J AU Dror, O Shulman-Peleg, A Nussinov, R Wolfson, HJ AF Dror, O Shulman-Peleg, A Nussinov, R Wolfson, HJ TI Predicting molecular interactions in silico: I. A guide to pharmacophore identification and its applications to drug design SO CURRENT MEDICINAL CHEMISTRY LA English DT Review DE pharmacophore mapping; pharmacophore modeling; receptor-based pharmacophore; pharmacophore fingerprints; virtual screening; pharmacophore searching; docking; de-novo design; lead generation; computer-aided drug design ID 3-DIMENSIONAL CHEMICAL STRUCTURES; FAVORABLE BINDING-SITES; HYDROGEN-BOND FUNCTIONS; LIGAND PROBE GROUPS; COMBINATORIAL LIBRARIES; LEAD GENERATION; SEARCHING ALGORITHMS; GENETIC ALGORITHM; FLEXIBLE DOCKING; PROTEIN AB A major goal in contemporary drug design is to develop new ligands with high affinity of binding toward a given protein receptor. Pharmacophore, which is the three-dimensional arrangement of essential features that enable a molecule to exert a particular biological effect, is a very useful model for achieving this goal. If the three-dimensional structure of the receptor is known, pharmacophore is a complementary tool to standard techniques, such as docking. However, frequently the,structure of the receptor protein is unknown and only a set of ligands together with their measured binding affinities towards the receptor is available. In such a case, a pharmacophore-based strategy is one of the few applicable tools. Here we present a broad, yet concise guide to pharmacophore identification and review a sample of applications for drug design. In particular, we present the framework of the algorithms, classify their modules and point out their advantages and challenges. C1 Tel Aviv Univ, Sch Comp Sci, IL-69978 Tel Aviv, Israel. Tel Aviv Univ, Sackler Fac Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel. NCI, Basic Res Program, SAIC Frederick Inc, Lab Expt & Computat Biol, Frederick, MD 21702 USA. RP Tel Aviv Univ, Sch Comp Sci, IL-69978 Tel Aviv, Israel. EM oranit@tau.ac.il; shulmana@tau.ac.il RI Wolfson, Haim/A-1837-2011 FU NCI NIH HHS [N01-CO-12400] NR 143 TC 83 Z9 87 U1 1 U2 14 PU BENTHAM SCIENCE PUBL LTD PI SHARJAH PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB EMIRATES SN 0929-8673 EI 1875-533X J9 CURR MED CHEM JI Curr. Med. Chem. PD JAN PY 2004 VL 11 IS 1 BP 71 EP 90 DI 10.2174/0929867043456287 PG 20 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA 761HQ UT WOS:000187895800007 PM 14754427 ER PT J AU Schneidman-Duhovny, D Nussinov, R Wolfson, HJ AF Schneidman-Duhovny, D Nussinov, R Wolfson, HJ TI Predicting molecular interactions in silico: II. Protein-protein and protein-drug docking SO CURRENT MEDICINAL CHEMISTRY LA English DT Review DE biomolecular recognition; computer-aided drug design; protein-protein docking; protein-ligand docking; active site detection; flexibility ID FLEXIBLE LIGAND DOCKING; QUADRATIC SHAPE DESCRIPTORS; SIDE-CHAIN FLEXIBILITY; AUTOMATED DOCKING; GENETIC ALGORITHM; SURFACE RECOGNITION; COMPUTER-PROGRAM; GEOMETRIC FIT; SOFT DOCKING; HOT-SPOTS AB This article reviews the docking field starting from basic docking algorithms and describing the latest advances. We present the algorithmic framework and classify the state of-the-art methods. We point out the bottlenecks of the methods, like flexibility, absence of absolute scoring functions and explain what types of information can potentially be added to improve the results. C1 Tel Aviv Univ, Sch Comp Sci, IL-69978 Tel Aviv, Israel. Tel Aviv Univ, Sackler Fac Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel. SAIC Frederick Inc, Basic Res Program, Lab Expt & Computat Biol, NCI, Frederick, MD 21702 USA. RP Schneidman-Duhovny, D (reprint author), Tel Aviv Univ, Sch Comp Sci, IL-69978 Tel Aviv, Israel. EM duhovka@tau.ac.it RI Wolfson, Haim/A-1837-2011 FU NCI NIH HHS [N01-CO-12400] NR 106 TC 57 Z9 57 U1 0 U2 8 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 0929-8673 J9 CURR MED CHEM JI Curr. Med. Chem. PD JAN PY 2004 VL 11 IS 1 BP 91 EP 107 DI 10.2174/0929867043456223 PG 17 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA 761HQ UT WOS:000187895800008 PM 14754428 ER PT J AU Kiyatkin, EA AF Kiyatkin, EA TI Brain hyperthermia during physiological and pathological conditions: Causes, mechanisms, and functional implications SO CURRENT NEUROVASCULAR RESEARCH LA English DT Review DE brain; metabolism; cerebral blood flow; hyperthermia; metabolic neural activation; addictive drugs; emotional and physical activation; neurotoxicity ID CEREBRAL-BLOOD-FLOW; PROLONGED EXERCISE; 3,4-METHYLENEDIOXYMETHAMPHETAMINE MDMA; METHAMPHETAMINE NEUROTOXICITY; DOPAMINERGIC NEUROTOXICITY; HYPOTHALAMIC TEMPERATURE; HUMAN THERMOREGULATION; UNRESTRAINED RATS; NEURONAL-ACTIVITY; BODY-TEMPERATURE AB Although brain metabolism consumes high amounts of energy and is accompanied by intense heat production, brain temperature is usually considered a stable, tightly regulated homeostatic parameter. Current animal research, however, has shown that different forms of functional neural activation are accompanied by relatively large brain hyperthermia (2-3degreesC), which has an intra-brain origin; cerebral circulation plays a crucial role in dissipating this potentially dangerous metabolic heat from brain tissue. Brain hyperthermia, therefore, reflects enhanced brain metabolism and is a normal physiological phenomenon that can be enhanced by interaction with common elements of an organism's environment. There are, however, instances when brain hyperthermia becomes pathological. Both exposure to extreme environmental heat and intense physical activity in a hot, humid environment restrict heat dissipation from the brain and may push brain temperatures to the limits of physiological functions, resulting in acute life-threatening complications and destructive effects on neural cells and functions of the brain as a whole. Brain hyperthermia may also result from metabolic activation induced by various addictive drugs, such as heroin, cocaine, and meth-amphetamine (METH). In contrast to heroin and cocaine, whose stimulatory effects on brain metabolism invert with increases in dose, METH increases brain metabolism dose-dependently and diminishes heat dissipation because of peripheral vasoconstriction. The thermogenic effects of this drug, moreover, are enhanced during physiological activation, resulting in pathological brain hyperthermia. Since brain hyperthermia exacerbates drug-induced toxicity and is destructive to neural cells, uncontrollable use of amphetamine-like drugs under conditions restricting heat dissipation from the brain may result both in acute life-threatening complications and clinically latent but dangerous morphological and functional brain destruction. C1 NIDA, Behav Neurosci Branch, Intramural Res Program, NIH,DHHS, Baltimore, MD 21224 USA. RP NIDA, Behav Neurosci Branch, Intramural Res Program, NIH,DHHS, 5500 Nathan Shock, Baltimore, MD 21224 USA. EM ekiyatki@intra.nida.nih.gov NR 112 TC 23 Z9 25 U1 0 U2 7 PU BENTHAM SCIENCE PUBL LTD PI SHARJAH PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB EMIRATES SN 1567-2026 EI 1875-5739 J9 CURR NEUROVASC RES JI Curr. Neurovasc. Res. PD JAN PY 2004 VL 1 IS 1 BP 77 EP 90 DI 10.2174/1567202043480233 PG 14 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 902LB UT WOS:000227357500009 PM 16181068 ER PT J AU Nanda, A St Croix, B AF Nanda, A St Croix, B TI Tumor endothelial markers: new targets for cancer therapy SO CURRENT OPINION IN ONCOLOGY LA English DT Review DE angiogenesis; tumor endothelial markers (TEMs); gene expression ID PROTEIN-COUPLED RECEPTORS; ANTHRAX TOXIN RECEPTOR; ED-B DOMAIN; GROWTH-FACTOR; TISSUE FACTOR; SOLID TUMORS; ANGIOGENESIS INHIBITORS; ANTITUMOR-ACTIVITY; LETHAL FACTOR; IN-VITRO AB Purpose of review: Targeting the endothelial cells that line tumor infiltrating blood vessels is a new anticancer strategy that has gained widespread support from biologists and clinicians. Here we highlight different approaches currently being used to target tumor endothelium and discuss new avenues for intervention that have been opened through the recent identification of tumor endothelial markers (TEMs). Recent findings: The ability of Avastin to prolong survival in a Phase III clinical trial of human colorectal cancer has established the validity of the anti-angiogenic approach. However, realization of the full potential of a vascular targeting strategy may require the exploitation of molecules which are highly restricted in expression to tumor endothelium. Here we explore the potential of TEMs as new targets for cancer therapy. Current knowledge of these markers and their relation to other family members in the context of tumor angiogenesis is discussed. In particular, we highlight those molecules which, by virtue of their structure, cell-surface location and expression pattern, appear to hold promise as targets for future drug development. The identification of TEM8 as the anthrax toxin receptor and the successful targeting of this receptor in preclinical tumor models make this molecule a particularly attractive candidate for future vascular targeting studies. Summary: Technological advances in cellular fractionation and genomics enabled the identification of several markers preferentially expressed on human tumor endothelium. Studies of these TEMs are expected to aid in our understanding of angiogenesis and could lead to the development of new imaging and diagnostic agents for cancer. C1 Natl Canc Inst, Mouse Canc Genet Program, Tumor Angiogenesis Sect, Frederick, MD 21702 USA. Johns Hopkins Sch Med, Program Human Genet & Mol Biol, Baltimore, MD USA. Johns Hopkins Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA. RP Nanda, A (reprint author), Natl Canc Inst, Mouse Canc Genet Program, Tumor Angiogenesis Sect, Bldg 560,POB B, Frederick, MD 21702 USA. EM stcroix@ncifcrf.gov NR 59 TC 98 Z9 107 U1 1 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1040-8746 J9 CURR OPIN ONCOL JI Curr. Opin. Oncol. PD JAN PY 2004 VL 16 IS 1 BP 44 EP 49 DI 10.1097/00001622-200401000-00009 PG 6 WC Oncology SC Oncology GA 879ND UT WOS:000225723600008 PM 14685092 ER PT J AU Piekarz, R Bates, S AF Piekarz, R Bates, S TI A review of depsipeptide and other histone deacetylase inhibitors in clinical trials SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE histone deacetylase inhibitors ID ACUTE PROMYELOCYTIC LEUKEMIA; ACUTE MYELOID-LEUKEMIA; HYDROXAMIC ACID SAHA; DNA TOPOISOMERASE-II; TRANS-RETINOIC ACID; CHROMOBACTERIUM-VIOLACEUM NO-968; AGENT SODIUM PHENYLBUTYRATE; T-CELL LYMPHOMA; PHASE-I; MYELODYSPLASTIC SYNDROMES AB The historic deacetylase inhibitors (HDIs) are a new class of antineoplastic agents currently being evaluated in clinical trials. While these agents have been Studied extensively in the laboratory, only recently has their mechanism of action begun to be elucidated. Several structural classes of compounds have been shown to exert histone deacetylase inhibition, including sodium n-butyrate, suberoylanilide hydroxamic acid, LAQ824, CI-994, MS-275, and depsipeptide. The HDIs have been shown to induce differentiation. to decrease cell proliferation, and to induce cell death. HDIs are thought to exert their anti-neoplastic effects by altering the expression of genes that play a role in the control of cell growth, and transformation. The HDIs have specific and well-defined effects on cancer cell,. Preliminary results from clinical trials suggest that these agents are very promising. While there were sporadic case reports of activity using the early generation HDIs, dramatic responses have recently been observed in patients with T-cell lymphomas treated with depsipeptide. one of the never agents. With the well-defined molecular effects on cancer cells, surrogate markers can be analyzed for evidence of activity and efficacy using either tumor samples or normal tissue. presented in this review are details from clinical trials with both earlier and newer generations of HDIs. Toxicities specific to this class of agents are outlined and possibilities tor rational combination therapies are discussed. C1 NCI, Canc Therapeut Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. RP Bates, S (reprint author), Bldg 10,Room 12N226,9000 Rockville Pike, Bethesda, MD 20892 USA. EM sebates@helix.nih.gov NR 104 TC 151 Z9 158 U1 0 U2 4 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 19 BP 2289 EP 2298 DI 10.2174/1381612043383980 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 831LL UT WOS:000222195800002 PM 15279609 ER PT J AU Dyba, M Tarasova, NI Michejda, CJ AF Dyba, M Tarasova, NI Michejda, CJ TI Small molecule toxins targeting tumor receptors SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE peptide therapeutics; anti-cancer drugs; lysosomal cleavage; drug delivery ID ACUTE MYELOID-LEUKEMIA; ENZYMATICALLY DEGRADABLE BONDS; IN-VITRO EFFICACY; CELL LUNG-CANCER; HORMONE-RELATED PROTEIN; CARBOXYMETHYL DEXTRAN CONJUGATE; GROWTH-FACTOR RECEPTORS; N-(2-HYDROXYPROPYL)METHACRYLAMIDE CO-POLYMERS; ANTIBODY-CALICHEAMICIN CONJUGATE; ANTICANCER DRUG CHLORAMBUCIL AB Targeting toxic therapeutics to tumors through receptors Over expressed on file Surface of cancer cells can reduce systemic toxicity and increase the effectiveness of the targeted compounds. Small Molecule targeted therapeutics have a number of advantages over toxic immunoconjugates including, better tumor penetration, lack Of neutralizing host immune response and superior flexibility in selection of drug components with optimal specificity. potency and stability in circulation. Three major components of the targeted drug, the toxic warhead, tumor-specific ligand and the linker can influence the properties of each other and thus have to be optimized for each system. All receptor-targeted drugs are delivered inside the cells through endocytosis and undergo processing liberating the toxins in endosomes and lysosomes. Common delivery route defines a number of general requirements for each drug component. The review addresses currently known possible receptor targets and their ligands along with toxins that have been used and that have a potential to be successfully applied in tumor targeting. Linkers that are stable in Circulation, but efficiently cleaved in lysosomes constitute all essential component of receptor-targeted drugs and are evaluated in greater detail. C1 NCI, Mol Aspects Drug Design Sect, Struct Biophys Lab, Frederick, MD 21702 USA. RP Michejda, CJ (reprint author), POB B, Frederick, MD 21702 USA. EM michejda@ncifcrf.gov OI Dyba, Marcin/0000-0001-6311-6877 NR 249 TC 31 Z9 33 U1 0 U2 6 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 19 BP 2311 EP 2334 DI 10.2174/1381612043384024 PG 24 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 831LL UT WOS:000222195800004 PM 15279611 ER PT J AU Mori, T AF Mori, T TI Cancer-specific ligands identified from screening of peptide-display libraries SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE peptide; phage display; library; cancer; targeting; diagnostics; therapeutics ID VIVO PHAGE DISPLAY; VASCULAR ENDOTHELIAL-CELLS; INHIBITS TUMOR-GROWTH; TARGETING IN-VIVO; BINDING PEPTIDES; COMBINATORIAL LIBRARIES; GENE-TRANSFER; EX-VIVO; PARAMAGNETIC PROTEOLIPOSOMES; SYNTHETIC PEPTIDE AB Although monoclonal antibodies have demonstrated clinical potentials as tumor targeting agents, poor tumor penetration of the antibodies due to the size of molecules and liver/bone marrow toxicity by non-specific uptake of the antibodies are the two major limitations of antibody therapy. Peptidic targeting agents may ease the problems associated with antibody cancer therapy. Combinatorial libraries displayed on microorganisms have successfully been utilized to discover cell surface-binding peptides, which can be tumor-targeting agents. Among many molecular display techniques. phage display has been the most Popular approach. Peptides can be used as targeting molecules of receptor-targeted toxins and gene therapy, imaging and/or therapeutic agents, and nano-medical technologies. Recent results from preclinical studies with various peptides support their targeting potential and Suggest that the role of peptides as targeting molecules in drug developruent should be further exploited. C1 NCI, Mol Targets Dev Program, Canc Res Ctr, Frederick, MD 21702 USA. RP Mori, T (reprint author), NCI, Mol Targets Dev Program, Canc Res Ctr, Bldg 1052,Rm 121, Frederick, MD 21702 USA. EM mori@ncifcrf.gov NR 103 TC 60 Z9 64 U1 4 U2 16 PU BENTHAM SCIENCE PUBL LTD PI SHARJAH PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB EMIRATES SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 19 BP 2335 EP 2343 DI 10.2174/1381612043383944 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 831LL UT WOS:000222195800005 PM 15279612 ER PT J AU Howard, OMZ Galligan, CL AF Howard, OMZ Galligan, CL TI An expanding appreciation of the role chemokine receptors play in cancer progression SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review ID NEUTROPHIL CHEMOTACTIC FACTOR; HUMAN ENDOTHELIAL-CELLS; HUMAN BREAST-CARCINOMA; LYMPH-NODE METASTASIS; CHRONIC LYMPHOCYTIC-LEUKEMIA; PROTEIN-COUPLED RECEPTOR; HUMAN MULTIPLE-MYELOMA; HUMAN-MELANOMA CELLS; MALIGNANT B-CELLS; CC-CHEMOKINE AB The contribution of small molecular weight chemoattractant cytokines (chemokines) and their receptors in the trafficking of tumor, immune and vascular cells pertaining to the development and progression of cancer has begun to be investigated. The current literature indicates that interactions between the immune network, angiogenic and cell survival cascades are important for the trafficking and progression of human cancer and that chemokines and chemokine receptors play a central role in these complex inter-related pathways. Several therapeutic approaches have been reviewed and Suggest that the most promising arise from the development of combinations of chemokine receptor antagonists. C1 NCI, CCR, LMI, Frederick, MD 21702 USA. RP Howard, OMZ (reprint author), NCI, CCR, LMI, Frederick, MD 21702 USA. EM howardz@mail.ncifcrf.gov RI Howard, O M Zack/B-6117-2012 OI Howard, O M Zack/0000-0002-0505-7052 NR 140 TC 11 Z9 11 U1 0 U2 0 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 19 BP 2377 EP 2389 DI 10.2174/1381612043383935 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 831LL UT WOS:000222195800008 PM 15279615 ER PT J AU Pacher, P Kecskemeti, V AF Pacher, P Kecskemeti, V TI Cardiovascular side effects of new antidepressants and antipsychotics: New drugs, old concerns? SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE antidepressants; neuroleptics; antipsychotics; QT prolongation; arrhythmia; cardiac ion channels; repolarization ID SEROTONIN-REUPTAKE INHIBITOR; RECTIFIER POTASSIUM CURRENT; TORSADES-DE-POINTES; FLUOXETINE-INDUCED BRADYCARDIA; QT-INTERVAL PROLONGATION; PIG VENTRICULAR MYOCYTES; ELECTRO-PHYSIOLOGICAL PROPERTIES; TRANSIENT OUTWARD CURRENT; INTENSIVE-CARE-UNIT; SUDDEN-DEATH AB The cardiovascular toxicity of older generation of tricyclic anti depressants (e.g. imipramine, desipramine, amitriptyline, clomipramine) and neuroleptics (e.g. haloperidol, droperidol, thioridazine, pimozide) is well established. These drugs inhibit cardiovascular Na+, Ca2+ and K+ channels often leading to life-threatening arrhythmia. To overcome the toxicity of old generation of antidepressants and antipsychotics, selective serotonin reuptake inhibitor antidepressants (SSRIs: fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, venlafaxin) and several new antipsychotics (e.g. clozapine, olanzapine, risperidone, sertindole, aripiprazole, ziprasidone, quetiapine) were introduced during the past decade. Although these new compounds are not more effective in treating psychiatric disorders than older medications, they gained incredible popularity since they have been reported to have fewer and more benign side effect profile (including cardiovascular) than predecessors. Surprisingly, an increasing number of case reports have demonstrated that the use of SSRIs and new antipsychotics (e.g. clozapine, olanzapine, risperidone, sertindole, aripiprazole, ziprasidone, quetiapine) is associated with cases of arrhythmias, prolonged QTc interval on electrocardiogram (ECG) and orthostatic hypotension in patients lacking cardiovascular disorders. raising new concerns about the putative cardiovascular safety of these compounds. In agreement with these clinical reports these new compounds indeed show marked cardiovascular depressant effects in different mammalian and human cardiovascular preparations by inhibiting cardiac and vascular Na+, Ca2+ and K+ channels. Taken together, these results suggest that the new generation of antidepressants and antipsychotics also have clinically important cardiac as well as vascular effects. Clinicians should be more vigilant about these potential adverse reactions and ECG control may be suggested during therapy, especially in patients with cardiovascular disorders. The primary goal of this review is to shed light on the recently observed clinically important cardiovascular effects of new antidepressants and antipsychotics and discuss the mechanism beyond this phenomenon. C1 Semmelweis Univ, Fac Med, Dept Pharmacol & Pharmacotherapy, H-1445 Budapest, Hungary. NIAAA, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA. RP Kecskemeti, V (reprint author), Semmelweis Univ, Fac Med, Dept Pharmacol & Pharmacotherapy, Nagyvarad Ter 4,POB 370, H-1445 Budapest, Hungary. EM ppacher@lycos.com; kecsval@pharma.sote.hu RI Pacher, Pal/B-6378-2008 OI Pacher, Pal/0000-0001-7036-8108 FU Intramural NIH HHS [Z99 AA999999] NR 173 TC 151 Z9 158 U1 5 U2 30 PU BENTHAM SCIENCE PUBL LTD PI SHARJAH PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB EMIRATES SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 20 BP 2463 EP 2475 DI 10.2174/1381612043383872 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 836EX UT WOS:000222539500005 PM 15320756 ER PT J AU Lahiri, DK Rogers, JT Greig, NH Sambamurti, K AF Lahiri, DK Rogers, JT Greig, NH Sambamurti, K TI Rationale for the development of cholinesterase inhibitors as anti-Alzheimer agents SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE Alzheimer's disease; acetylcholine; anticholinesterase; ApoE; APP gene; BACE; beta-amyloid; butyrylcholine; cholinesterase; cholinergic agents; cholinomimetic drugs; dementia; oxidative stress; phenserine; secretase; tau protein ID AMYLOID PRECURSOR PROTEIN; BETA-PEPTIDE; GAMMA-SECRETASE; MESSENGER-RNA; MOUSE MODEL; A-BETA; ACETYLCHOLINESTERASE PROMOTES; NEUROBLASTOMA-CELLS; CHOLINERGIC NEURONS; DISEASE TREATMENT AB Alzheimer's disease (AD) is characterized by progressive dementia caused by the loss of the presynaptic markers of the cholinergic system in the brain areas related to memory and learning and brain deposits of amyloid beta peptide (Abeta) and neurofibrillary tangles (NFT). A small fraction of early onset familial AD (FAD) is caused by mutations in genes, such as the beta-amyloid precursor protein (APP) and presenilins that increase the load of Abeta in the brain. These studies together with findings that Abeta is neurotoxic in vitro, provide evidence that some aggregates of this peptide are the key to the pathogenesis of AD. The yield of Abeta and the processing and turnover of APP are regulated by a number of pathways including apolipoprotein E, cholesterol and cholinergic agonists. Early studies showed that muscarinic agonists increased APP processing within the Abeta sequence (sAPPalpha). More recently, we have presented evidence showing that some, but not all, anticholinesterases reduce secretion of sAPPalpha as well as Abeta into the media suggesting that cholinergic agonists modulate Abeta levels by multiple mechanisms. Herein we review the recent advances in understanding the function of cholinesterase (ChE) in the brain and the use of ChE-inhibitors in AD. We propose and support the position that the influence of cholinergic stimulation on amyloid formation is critical in light of the early targeting of the cholinergic basal forebrain in AD and the possibility that maintenance of this cholinergic tone might slow amyloid deposition. In this context, the dual action of certain cholinesterase inhibitors on their ability to increase acetylcholine levels and decrease amyloid burden assumes significance as it may identify a single drug to both arrest the progression of the disease as well as treat its symptoms. A new generation of acetyl- and butyryl cholinesterase inhibitors is being studied and tested in human clinical trials for AD. We critically discuss recent trends in AD research, from molecular and genetic to clinical areas, as it relates to the effects of cholinergic agents and their secondary effects on Abeta. Finally, we examine different neurobiological mechanisms that provide the basis of new targets for AD drug development. C1 Indiana Univ, Sch Med, Dept Psychiat, Inst Psychiat Res, Indianapolis, IN 46202 USA. Harvard Univ, Sch Med, Charlestown, MA USA. NIA, NIH, Baltimore, MD USA. Med Univ S Carolina, Charlestown, MA USA. RP Lahiri, DK (reprint author), Indiana Univ, Sch Med, Dept Psychiat, Inst Psychiat Res, 791 Union Dr, Indianapolis, IN 46202 USA. EM dlahiri@iupui.edu NR 82 TC 6 Z9 6 U1 0 U2 2 PU BENTHAM SCIENCE PUBL LTD PI SHARJAH PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB EMIRATES SN 1381-6128 EI 1873-4286 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 25 BP 3113 EP 3121 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 853QF UT WOS:000223841500008 ER PT J AU Barry, CE Boshoff, HIM Dowd, CS AF Barry, CE Boshoff, HIM Dowd, CS TI Prospects for clinical introduction of nitroimidazole antibiotics for the treatment of tuberculosis SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE mycobacterium tuberculosis; nitroimidazole; bioreduction; nitroreductase; persistence; anaerobic metabolism; metronidazole; mutagenicity ID MYCOBACTERIUM-BOVIS BCG; MICROBIAL ENUMERATION TECHNIQUE; SINGLE-STRAND BREAKS; HELICOBACTER-PYLORI; METRONIDAZOLE-RESISTANCE; TRICHOMONAS-VAGINALIS; BACTERICIDAL ACTIVITY; CHAGAS-DISEASE; MURINE TUBERCULOSIS; ANAEROBIC-BACTERIA AB Nitroaromatic antibiotics have a long and controversial history in human and veterinary medicine. This controversy lies behind the presumption of many pharmaceutical companies that nitroaromatic compounds should be filtered from the list of drug-like compounds but stands at odds with the remarkably safe clinical record of use of such compounds. In this review, we will describe the whole-cell structure-activity relationships that have been reported for anti mycobacterial nitroimidazoles as well as the available in vivo data supporting efficacy with a particular emphasis on nitroimidazo[2,1-b]oxazines such as PA-824. We will also explore the unique potential of such compounds to shorten the course of tuberculosis therapy by exerting a bactericidal effect on non-replicating bacilli. We will consider the mode of action of such compounds in sensitive organisms and discuss the mechanisms by which resistance may emerge. Finally, we will review the pharmacokinetics, toxicology and laboratory and animal studies linking nitroimidazoles with carcinogenicity and mutagenicity and assess the prospects for the clinical introduction of nitroimidazoles for the treatment of tuberculosis. C1 NIAID, TB Res Sect, NIH, Rockville, MD 20852 USA. RP Barry, CE (reprint author), NIAID, TB Res Sect, NIH, Rm 239 Twinbrook 2,12441 Parklawn Dr, Rockville, MD 20852 USA. EM clifton_barry@nih.gov RI Barry, III, Clifton/H-3839-2012 FU Intramural NIH HHS [Z01 AI000693-15] NR 178 TC 91 Z9 94 U1 0 U2 14 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 26 BP 3239 EP 3262 DI 10.2174/1381612043383214 PG 24 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 853UI UT WOS:000223854000007 PM 15544513 ER PT J AU Patton, JT Carpi, RVD Spencer, E AF Patton, JT Carpi, RVD Spencer, E TI Replication and transcription of the rotavirus genome SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review ID MINUS-STRAND SYNTHESIS; TEMPERATURE-SENSITIVE MUTANTS; NONSTRUCTURAL PROTEIN NSP2; SINGLE-SHELLED PARTICLES; MESSENGER-RNA; BOVINE ROTAVIRUS; 3-DIMENSIONAL STRUCTURE; VACCINE CANDIDATES; CONSENSUS SEQUENCE; INFECTED-CELLS AB Rotaviruses are an important cause of human morbidity and mortality, representing the primary pathogens responsible for acute dehydrating diarrhea in children under the age of 3. The infectious rotavirus particle is made up of three concentric layers of protein, and contains a genome consisting of eleven segments of double-stranded (ds)RNA. Upon infection.. RNA polymerases associated with double-layered virus particles are activated, resulting in genome transcription and extrusion of the eleven viral mRNAs from such particles. The mRNAs not only direct protein synthesis, but also serve as templates for minus-strand synthesis to yield dsRNAs. Synthesis of the dsRNAs is an event that occurs following the gene-specific packaging of viral mRNAs into core-like assembly intermediates. Electron-dense cytoplasmic inclusions, termed viroplasms, function as sites of genome packaging and replication in the infected cell. On understanding of key events in the viral life cycle has been advanced considerably by the development of cell-free systems that support mRNA synthesis from virion-derived double-layered particles and dsRNA synthesis from virion-derived cort: particles. The recent expression and purification of rotavirus recombinant proteins have also allowed progress to be made in defining the roles of viral proteins in genome replication and viroplasm formation. However, our efforts towards a ful description of the viral life cycle, most notably an understanding of the events occurring during gene-specific packaging remain hampered by the lack of a cell-free packaging system and a reverse genetics systems. The lack of a reverse genetics systems also confounds efforts towards the generation of molecular engineered second-generation vaccines. C1 Univ Santiago Chile, Fac Quim & Biol, Dept Ciencias Biol, Virol Lab, Santiago 3363, Chile. NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA. Univ Santiago Chile, Fac Quim & Biol, Virol Lab, Dept Ciencias Biol, Santiago, Chile. RP Spencer, E (reprint author), Univ Santiago Chile, Fac Quim & Biol, Dept Ciencias Biol, Virol Lab, Casilla 33 Correo 40, Santiago 3363, Chile. EM espencer@lauca.usach.cl RI Patton, John/P-1390-2014 NR 102 TC 16 Z9 17 U1 1 U2 10 PU BENTHAM SCIENCE PUBL LTD PI SHARJAH PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB EMIRATES SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 30 BP 3769 EP 3777 DI 10.2174/1381612043382620 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 863DZ UT WOS:000224542300007 PM 15579070 ER PT J AU Zdanov, A AF Zdanov, A TI Structural features of the interleukin-10 family of cytokines SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE cytokines; interleukin-10; ligand/receptor interactions; helix bundle; signal transduction ID X-RAY CRYSTALLOGRAPHY; VIRUS PROTEIN BCRF1; CRYSTAL-STRUCTURE; RECEPTOR COMPLEX; SOLUBLE RECEPTOR; INDUCIBLE FACTOR; FUNCTIONAL-CHARACTERIZATION; ERYTHROPOIETIN RECEPTOR; CELLULAR INTERLEUKIN-10; EXTRACELLULAR DOMAIN AB The interleukin-10 (IL-10) family of cytokines includes IL-10, a number of its viral gene homologs, and eight recently discovered cellular cytokines (IL-19, IL-20, IL-22, IL-24, IL-26, IFN-lambda1, IFN-lambda2, IFN-lambda3). IL-10 is an intercalated dimer consisting of two six-helix bundle domains. Signal transduction occurs when each domain of IL-10 binds to two receptor chains, IL-10R1 and IL-10R2. Viral homologs use the same IL-10 receptor system, while cellular homologs use their own receptors: three long receptor chains (IL-20R1, IL-22R1 and IFN-lambda1R1) and two short receptor chains (IL-20R2 and IL-10R2). Most of the cellular homologs belong to the IL-19 subfamily of cytokines including IL-19, IL-20, IL-22 and IL-24. It is likely that IFN-lambda1, IFN-lambda2, and IFN-lambda3 also belong to the same subfamily. All these proteins are monomers in solution. Crystal structures of IL-19 and IL-22 show that the molecules consist of seven helices (A-G) forming a seven-helix bundle with compact hydrophobic core inside. Structures of complexes of IL-10 and CMVIL-10 with an extracellular domain of high affinity receptor IL-10R1 (sIL-10R1) showed that ligand/receptor interactions are of mostly polar nature, with two hydrophobic patches around receptor residues Tyr43 and Phe143 at the top and bottom of the interface. The location and structure of the binding site for the second receptor chain are still unknown. It has also been shown that in the case of IL-19 and IL-20, IL-20R2 rather than IL-20R1 is a high-affinity receptor chain. This review summarizes all published three-dimensional structures of the cytokines representing the IL-10 family of homologs, including the IL-19 subfamily and their interaction with appropriate receptors. C1 NCI, Macromol Crystallog Lab, Canc Res Ctr, Frederick, MD 21702 USA. RP Zdanov, A (reprint author), NCI, Macromol Crystallog Lab, Canc Res Ctr, Frederick, MD 21702 USA. EM zdanov@ncifcrf.gov NR 87 TC 42 Z9 49 U1 1 U2 10 PU BENTHAM SCIENCE PUBL LTD PI SHARJAH PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB EMIRATES SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 31 BP 3873 EP 3884 DI 10.2174/1381612043382602 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 874ZO UT WOS:000225389400003 PM 15579076 ER PT J AU Imamichi, T AF Imamichi, T TI Action of Anti-HIV drugs and resistance: Reverse transcriptase inhibitors and protease inhibitors SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE HIV-1; RT; PR; RT inhibitors; PR inhibitors; mutations; drug-resistance ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIGH-LEVEL RESISTANCE; STRAND TRANSFER-REACTIONS; RELEVANT MUTANT VARIANTS; IN-VITRO SELECTION; STRUCTURE-BASED DESIGN; RAY CRYSTAL-STRUCTURE; AMINO-ACID DELETION; TYPE-1 PROTEASE; VIRAL FITNESS AB Currently, 20 drugs have been approved for Human Immunodeficiency Virus type-1 (HIV-1) clinical therapy. These drugs inhibit HIV-1 reverse transcriptase, protease, or virus entry. Introduction of a combination therapy with reverse transcriptase inhibitors and protease inhibitors has resulted in a drastic decrease in HIV-1 related mortality. Although the combination therapy can suppress viral replication below detection levels in current available assays, low levels of on-going viral replication still persist in some patients; Long-term administration of the combination therapy may increase selective pressure against viruses, and subsequently induce emergence of multiple drug-resistant HIV-1 variants. Attempts have been made to design novel antiretroviral drugs that would be able to suppress replication of the resistant variants. At present, several investigational drugs are being tested in clinical trials. These drugs target not only the resistant variants, but also improvement in oral bioavilability or other viral proteins such as HIV-1 integrase, ribonuclease H, and HIV-1 entry (CD4 attachment inhibitors, chemokine receptors antagonists, and fusion inhibitors). Understanding mechanism(s) of action of the drugs and mechanisms of drug resistance is necessary for successful designs in the next generation of anti-HIV-1 drugs. In this review, the mechanisms of action of reverse transcriptase- and protease-inhibitors, and the mechanism of resistance to these inhibitors, are described. C1 Sci Applicat Int Corp Frederick Inc, Natl Inst Allergy & Infect Dis, Appl & Dev Res Program, Lab Human Retrovirol, Frederick, MD 21702 USA. RP Imamichi, T (reprint author), Sci Applicat Int Corp Frederick Inc, Natl Inst Allergy & Infect Dis, Appl & Dev Res Program, Lab Human Retrovirol, Bldg 550,Room 126,POB 8, Frederick, MD 21702 USA. EM timamichi@niaid.nih.gov FU NCPDCID CDC HHS [NCI-CO-12400] NR 206 TC 67 Z9 74 U1 1 U2 12 PU BENTHAM SCIENCE PUBL LTD PI SHARJAH PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB EMIRATES SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 32 BP 4039 EP 4053 DI 10.2174/1381612043382440 PG 15 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 875UR UT WOS:000225447900003 PM 15579086 ER PT J AU Tarasova, NI AF Tarasova, NI TI Peptides and peptidomimeties as anti-cancer therapeutics - Preface SO CURRENT PHARMACEUTICAL DESIGN LA English DT Editorial Material ID RECEPTOR FUNCTION; CANCER-CELLS; THERAPY; DOMAIN; INHIBITOR; DIAGNOSIS; ANALOGS; BINDING; TUMORS; POTENT C1 NCI, Canc Res Ctr, Mol Aspects Drug Design Sect, Frederick, MD 21702 USA. RP Tarasova, NI (reprint author), NCI, Canc Res Ctr, Mol Aspects Drug Design Sect, Frederick, MD 21702 USA. EM tarasova@ncifcrf.gov NR 30 TC 0 Z9 0 U1 0 U2 0 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1381-6128 J9 CURR PHARM DESIGN JI Curr. Pharm. Design PY 2004 VL 10 IS 19 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 831LL UT WOS:000222195800001 ER PT S AU Uhl, GR AF Uhl, GR BE Ali, SF Nabeshima, T Yanagita, T TI Molecular genetics of substance abuse vulnerability: Remarkable recent convergence of genome scan results SO CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Current Status of Depedence and Abuse Studies CY JUL 30-AUG 01, 2003 CL Kyoto, JAPAN SP Int Soc Neurochem, Japanese Pharmacol Soc, Japanese Med Soc Alcohol& Drug Studies, Japanese Soc Neurochem, Japanese Soc Neuropsychopharmocol, Minist Educ, Culture, Sports, Sci & Technol, Nagoya Univ Fdn, Uehara Memorial Fdn, Sigma-Tau Hlth Sci, Natl Inst Drug Abuse, Natl Ctr Toxicol Res, US FDA DE substance abuse; loci; genome scan; convergence; addiction ID ALCOHOL DEPENDENCE; POLYSUBSTANCE ABUSERS; DRUG-ABUSE; ENVIRONMENTAL-INFLUENCES; COGNITIVE PERFORMANCE; FEMALE TWINS; WIDE SEARCH; RECEPTOR; SAMPLE; LOCI AB Classical genetic studies document strong complex genetic contributions to abuse of multiple addictive substances. Goals of molecular genetic studies of addiction include: (1) locating chromosomal regions that contain allelic gene variants that contribute to vulnerability to drug dependence and (2) discovering which alleles of which gene markers and which genes provide these enhanced vulnerabilities. Genome scanning provides an approach to these goals. Until recently, data from genome scanning studies did not convincingly identify chromosomal positions for allelic variants predisposing to substance dependence. Nominal results of initial genome scans for alcohol and nicotine dependence failed to display much agreement; no two studies' results seemed to identify the same chromosomal regions for addiction vulnerability alleles. However, recent data from our association-based genome scans for illegal addictions, reanalyses of prior linkage-based results, and data from even newer linkage-based genome scans now provide a striking body of converging results. Sixteen chromosomal regions are identified by reproducible positive results obtained in multiple populations. These 16 regions are thus good candidates to harbor common allelic variants that confer human vulnerability to addiction to several classes of substances. Genomic markers that identify allelic variants that reproducibly alter addiction vulnerability in studies in several populations provide powerful tools for clinical research in addictions and addiction treatments. C1 NIDA, Mol Neurobiol Branch, IRP, NIH, Baltimore, MD 21224 USA. RP Uhl, GR (reprint author), NIDA, Mol Neurobiol Branch, IRP, NIH, Box 5180, Baltimore, MD 21224 USA. EM guhl@intra.nida.nih.gov NR 40 TC 49 Z9 52 U1 6 U2 14 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-522-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1025 BP 1 EP 13 DI 10.1196/annals.1316.001 PG 13 WC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Science & Technology - Other Topics; Neurosciences & Neurology GA BBP90 UT WOS:000226975200001 PM 15542694 ER PT S AU Hall, FS Sora, I Drgonova, J Li, XF Goeb, M Uhl, GR AF Hall, FS Sora, I Drgonova, J Li, XF Goeb, M Uhl, GR BE Ali, SF Nabeshima, T Yanagita, T TI Molecular mechanisms underlying the rewarding effects of cocaine SO CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Current Status of Depedence and Abuse Studies CY JUL 30-AUG 01, 2003 CL Kyoto, JAPAN SP Int Soc Neurochem, Japanese Pharmacol Soc, Japanese Med Soc Alcohol& Drug Studies, Japanese Soc Neurochem, Japanese Soc Neuropsychopharmocol, Minist Educ, Culture, Sports, Sci & Technol, Nagoya Univ Fdn, Uehara Memorial Fdn, Sigma-Tau Hlth Sci, Natl Inst Drug Abuse, Natl Ctr Toxicol Res, US FDA DE cocaine reward; transporters; dopamine; serotonin; norepinephrine ID CONDITIONED PLACE PREFERENCE; TRANSPORTER KNOCKOUT MICE; NEUROTROPHIC FACTOR; NEURONAL DIFFERENTIATION; DOPAMINE-TRANSPORTER; NUCLEUS-ACCUMBENS; SUBSTANTIA-NIGRA; SELF-STIMULATION; RHESUS-MONKEYS; MEDIAN RAPHE AB The initially surprising observation that cocaine retains its rewarding effects in dopamine transporter (DAT) knockout (KO) mice led our laboratory to examine the effects of deletion of other monoaminergic genes on cocaine reward. Our initial approach to this problem was to combine DAT KO mice with serotonin transporter (SERT) KO mice to make combined DAT/ SERT KO mice. The combination of these knockouts eliminates cocaine reward as assessed in the conditioned place preference (CPP) paradigm. We have also identified evidence that, in the absence of DAT, there is greater participation in cocaine reward by serotonin (SERT) and norepinephrine (NET) transporters. Both NET and SERT blockers (nisoxetine and fluoxetine) produced significant CPPs in DAT KO mice, but not in wild-type (WT) mice. The striking elimination of cocaine CPP in combined DAT/SERT KO mice contrasts with effects that we have identified in combined NET/SERT knockout mice, which display increases in cocaine reward, and with recent reports that suggest that DAT/NET combined KOs retain substantial cocaine CPP. Overall, these studies indicate important requirements for several monoaminergic system genes to fully explain cocaine reward, in particular those expressed by dopamine and serotonin systems. C1 NIDA, Mol Neurobiol Branch, IRP, NIH,DHHS, Baltimore, MD 21224 USA. Tohoku Univ, Sch Med, Dept Neurosci, Sendai, Miyagi 980, Japan. RP Hall, FS (reprint author), NIDA, Mol Neurobiol Branch, IRP, NIH,DHHS, Box 5180, Baltimore, MD 21224 USA. EM shall@intra.nida.nih.gov RI Drgonova, Jana/B-2903-2008; Hall, Frank/C-3036-2013; OI Hall, Frank/0000-0002-0822-4063; Drgonova, Jana/0000-0002-4623-8466 NR 43 TC 58 Z9 60 U1 2 U2 4 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-522-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1025 BP 47 EP 56 DI 10.1196/annals.1316.006 PG 10 WC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Science & Technology - Other Topics; Neurosciences & Neurology GA BBP90 UT WOS:000226975200006 PM 15542699 ER PT S AU Hironaka, N Ikeda, K Sora, I Uhl, GR Niki, H AF Hironaka, N Ikeda, K Sora, I Uhl, GR Niki, H BE Ali, SF Nabeshima, T Yanagita, T TI Food-reinforced operant behavior in dopamine transporter knockout mice - Enhanced resistance to extinction SO CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Current Status of Depedence and Abuse Studies CY JUL 30-AUG 01, 2003 CL Kyoto, JAPAN SP Int Soc Neurochem, Japanese Pharmacol Soc, Japanese Med Soc Alcohol& Drug Studies, Japanese Soc Neurochem, Japanese Soc Neuropsychopharmocol, Minist Educ, Culture, Sports, Sci & Technol, Nagoya Univ Fdn, Uehara Memorial Fdn, Sigma-Tau Hlth Sci, Natl Inst Drug Abuse, Natl Ctr Toxicol Res, US FDA ID COCAINE-SEEKING BEHAVIOR AB Dopamine (DA) plays roles in circuits that are important for brain reward and in striatal brain regions that are important for certain types of habit learning. These processes in wildtype, heterozygous, and homozygous dopamine transporter knockout (DAT-KO) mice, which were mildly food deprived and allowed to make nose-poke responses for food reinforcement, were studied. The mice were given 20-min sessions of daily (a) baseline exposure to the operant chambers, (b) acquisition of nose-poke responses in which responses were reinforced under a fixed ratio (FR5) schedule, (c) a progressive ratio schedule in which the number of responses required to obtain food was gradually increased, and (d) extinction of responses in which nose pokes were not followed by food. Neither heterozygous nor homozygous DAT-KO mice differed from their wildtype litter mates in the number of nose pokes displayed during baseline exposures to the chambers, the number of sessions required for acquisition, the number of responses under the FR5 schedule, or the number of responses under the progressive ratio schedule. Interestingly, however, in the five extinction sessions in which food was no longer delivered by nose poking, homozygous DAT-KO mice exerted significantly more responses than mice of either of the other two genotypes. These lines of evidence suggest a greater resistance of DAT-KO mice to the elimination of the response and support roles of dopaminergic systems in habit memory. C1 Ishinomaki Senshu Univ, Dept Psychol, Tama Ku, Kawasaki, Kanagawa 2148580, Japan. RIKEN, Brain Sci Inst, Lab Neurobiol Emot, Wako, Saitama 3510198, Japan. Tokyo Inst Psychiat, Dept Mol Psychiat, Tokyo 1568585, Japan. Tohoku Univ, Grad Sch Med, Dept Neurosci, Sendai, Miyagi 9808574, Japan. NIDA, Mol Biol Branch, Div Intramural Res, Baltimore, MD 21224 USA. Saitama Inst Technol, Dept Psychol, Okabe, Saitama 3690293, Japan. RP Hironaka, N (reprint author), Ishinomaki Senshu Univ, Dept Psychol, Tama Ku, 2-1-1 Higashi Mita, Kawasaki, Kanagawa 2148580, Japan. EM hironaka@psy.senshu-u.ac.jp RI Ikeda, Kazutaka/I-4694-2013 OI Ikeda, Kazutaka/0000-0001-8342-0278 NR 7 TC 33 Z9 33 U1 0 U2 7 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-522-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1025 BP 140 EP 145 DI 10.1196/annals.1316.018 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Science & Technology - Other Topics; Neurosciences & Neurology GA BBP90 UT WOS:000226975200018 PM 15542711 ER PT S AU Rothman, RB Jayanthi, S Cadet, JL Wang, XY Dersch, CM Baumann, MH AF Rothman, RB Jayanthi, S Cadet, JL Wang, XY Dersch, CM Baumann, MH BE Ali, SF Nabeshima, T Yanagita, T TI Substituted amphetamines that produce long-term serotonin depletion in rat brain ("neurotoxicity") do not decrease serotonin transporter protein expression SO CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Current Status of Depedence and Abuse Studies CY JUL 30-AUG 01, 2003 CL Kyoto, JAPAN SP Int Soc Neurochem, Japanese Pharmacol Soc, Japanese Med Soc Alcohol& Drug Studies, Japanese Soc Neurochem, Japanese Soc Neuropsychopharmocol, Minist Educ, Culture, Sports, Sci & Technol, Nagoya Univ Fdn, Uehara Memorial Fdn, Sigma-Tau Hlth Sci, Natl Inst Drug Abuse, Natl Ctr Toxicol Res, US FDA DE serotonin transporter; fenfluramine; parachloroamphetamine; neurotoxicity; amphetamine ID BIOGENIC-AMINE TRANSPORTERS; P-CHLOROAMPHETAMINE; UPTAKE SITES; FENFLURAMINE; BINDING; INNERVATION; DEXFENFLURAMINE; HIPPOCAMPUS; COCAINE AB Administration of high-dose D-fenfluramine (D-FEN) or parachloroamphetamine (PCA) produces long-lasting decreases in serotonin transporter (SERT) binding and tissue levels of serotonin (5-HT) in rat forebrain. These changes have been viewed as evidence for 5-HT neurotoxicity, but few studies have measured SERT protein levels. Thus, in the present study we determined the effect of high-dose D-FEN or PCA, administered according to a "neurotoxic" dosing regimen, on the density of SERT sites using ligand binding methods and on SERT protein levels using Western blots. Rats were sacrificed 2 days and 2 weeks after administration of drug or saline. The density of SERT was determined in homogenates of caudate and whole brain minus caudate. D-FEN and PCA decreased SERT binding by 30 to 60 % in both tissues and at both time points. Similarly, D-FEN and PCA administration profoundly decreased tissue 5-HT and 5-HIAA in frontal cortex. Despite the large decreases in SERT binding and depletion of tissue 5-HT that occurred with D-FEN administration, SERT protein expression, as determined by Western blot analysis, did not change in either tissue or time point. PCA administration decreased SERT protein by about 20 % only at the 2-day point in the caudate. Drug treatments did not change expression of glial fibrillary acidic protein (GFAP), a hallmark indicator of neuronal damage, in whole brain minus caudate in the 2-week group. These results support the hypothesis that D-FEN- and PCA-induced decreases in tissue 5-HT and SERT binding sites reflect neuroadaptive changes rather than neurotoxic effects. C1 NIDA, Intramural Res Program, Clin Psychopharmacol Sect, NIH, Baltimore, MD 21224 USA. NIDA, Intramural Res Program, Mol Neuropsychiat Branch, NIH, Baltimore, MD 21224 USA. RP Rothman, RB (reprint author), NIDA, Intramural Res Program, Clin Psychopharmacol Sect, NIH, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM rrothman@intra.nida.nih.gov NR 24 TC 9 Z9 9 U1 1 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-522-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1025 BP 151 EP 161 DI 10.1196/annals.1316.020 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Science & Technology - Other Topics; Neurosciences & Neurology GA BBP90 UT WOS:000226975200020 PM 15542713 ER PT S AU Baumann, MH Clark, RD Budzynski, AG Partilla, JS Blough, BE Rothman, RB AF Baumann, MH Clark, RD Budzynski, AG Partilla, JS Blough, BE Rothman, RB BE Ali, SF Nabeshima, T Yanagita, T TI Effects of "Legal X" piperazine analogs on dopamine and serotonin release in rat brain SO CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Current Status of Depedence and Abuse Studies CY JUL 30-AUG 01, 2003 CL Kyoto, JAPAN SP Int Soc Neurochem, Japanese Pharmacol Soc, Japanese Med Soc Alcohol& Drug Studies, Japanese Soc Neurochem, Japanese Soc Neuropsychopharmocol, Minist Educ, Culture, Sports, Sci & Technol, Nagoya Univ Fdn, Uehara Memorial Fdn, Sigma-Tau Hlth Sci, Natl Inst Drug Abuse, Natl Ctr Toxicol Res, US FDA DE 3,4-methylenedioxymethamphetamine (MDMA); serotonin (5HT); dopamine (DA); piperazine analog; 1-benzylpiperazine (BZP); 1-(m-trifluoromethylphenyl)piperazine (TFMPP) ID 3,4-METHYLENEDIOXYMETHAMPHETAMINE MDMA; EXTRACELLULAR SEROTONIN; H-3 DOPAMINE; ECSTASY; 5-HYDROXYTRYPTAMINE; MICRODIALYSIS; DIENCEPHALON; COCAINE; NAIVE; MDA AB 3,4-Methylenedioxymethamphetamine (MDMA) is a popular illicit drug that evokes transporter-mediated release of serotonin (5-HT) and dopamine (DA) from nerve cells. Recently, drug users have ingested combinations of the piperazine analogs, 1-benzylpiperazine (BZP) and 1-(m-trifluoromethylphenyl)piperazine (TFMPP), in an attempt to mimic the subjective effects of MDMA. In the present study, we compared neurochemical effects of MDMA, BZP, and TFMPP in rat brain. The ability of MDMA, BZP, and TFMPP to stimulate efflux of [H-3]5-11T and [H-3]MPP+ (a DA transporter substrate) was determined in vitro using release assays in synaptosomes. The ability of these drugs to increase extracellular 5-HT and DA in vivo was assessed using intracranial microdialysis in nucleus accumbens. MDMA stimulated transporter-mediated release of 5-HT (EC50 = 58 nM) and MPP+ (EC50 = 119 nM). BZP was a selective releaser of MPP+ (EC50 = 175 nM), whereas TFMPP was a selective releaser of 5-HT (EC50 = 121 nM). MDMA injections (1 and 3 mg/kg, i.v.) increased dialysate 5-HT and DA in a dose-related manner, but actions on 5-HT were predominant. BZP (3 and 10 mg/kg, i.v.) elevated dialysate DA and 5-11T, while TFMPP (3 and 10 mg/kg, i.v.) elevated only 5-11T. The coadministration of BZP plus TFMPP (BZP/TFMPP) produced marked elevations in extracellular 5-11T and DA that mirrored the effects of MDMA. At the high dose of BZP/TFMPP (10 mg/kg, i.v.). the rise in dialysate DA exceeded the summed effects of the drugs alone. Our results support the hypothesis that the BZP/TFMPP combination mimics the neurochemical mechanism of MDMA, providing a basis for recreational use of these agents. Additionally, the findings suggest possible drug-drug synergism when piperazine drugs are coadministered at high doses. C1 NIDA, IRP, Clin Psychopharmacol Sect, NIH, Baltimore, MD 21224 USA. RTI Int, Chem & Life Sci Grp, Res Triangle Pk, NC 27709 USA. RP Baumann, MH (reprint author), NIDA, IRP, Clin Psychopharmacol Sect, NIH, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM mbaumann@intra.nida.nih.gov NR 25 TC 40 Z9 42 U1 0 U2 5 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-522-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1025 BP 189 EP 197 DI 10.1196/annals.1316.024 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Science & Technology - Other Topics; Neurosciences & Neurology GA BBP90 UT WOS:000226975200024 PM 15542717 ER PT S AU Okada, M Goldman, D Linnoila, M Iwata, N Ozaki, N Northup, JK AF Okada, M Goldman, D Linnoila, M Iwata, N Ozaki, N Northup, JK BE Ali, SF Nabeshima, T Yanagita, T TI Comparison of G-protein selectivity of human 5-HT2C and 5-HT1A receptors SO CURRENT STATUS OF DRUG DEPENDENCE / ABUSE STUDIES: CELLULAR AND MOLECULAR MECHANISMS OF DRUGS OF ABUSE AND NEUROTOXICITY SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Current Status of Depedence and Abuse Studies CY JUL 30-AUG 01, 2003 CL Kyoto, JAPAN SP Int Soc Neurochem, Japanese Pharmacol Soc, Japanese Med Soc Alcohol& Drug Studies, Japanese Soc Neurochem, Japanese Soc Neuropsychopharmocol, Minist Educ, Culture, Sports, Sci & Technol, Nagoya Univ Fdn, Uehara Memorial Fdn, Sigma-Tau Hlth Sci, Natl Inst Drug Abuse, Natl Ctr Toxicol Res, US FDA ID SF9 CELLS; GAMMA-SUBUNIT; RECONSTITUTION; ACTIVATION; INVOLVEMENT AB We compared the ability of human 5-HT2C and 5-HT1A receptors to couple to selected G proteins expressed in insect Sf9 cells through simultaneous infection with recombinant baculoviruses. We also examined the coupling of G proteins to these same receptors in membranes derived from the Sf9 cells using in situ reconstitution with purified G proteins. Our data show that unoccupied 5-HT2C and 5-HT1A receptors can attain an activated conformation that is stabilized by interaction with specific G proteins. While high-affinity agonist binding to the 5-HT2C receptor was increased to a greater extent by Galpha(q) than by Galpha(i2), the high-affinity agonist binding to the 5-HT1A receptor was preferentially enhanced by Galpha(i2) coexpression. When the two 5-HT receptors were expressed in cells also expressing G proteins, both 5-HT2C and 5-HT1A receptors appear to activate Gai2 in preference to Gaq. In contrast, in situ reconstitution data show that 5-HT2C receptors robustly activate Get 9 and marginally activate Galpha(0) or Galpha(j), whereas 5-HT1A receptors only marginally activate Galpha(q) and robustly activate Galpha(0) and Galpha(i). These results suggest that the overexpression of receptor and potential G-protein coupling partners is Sf9 cells may lead to erroneous conclusions as to the signaling selectivity of receptors. C1 Osaka City Univ, Fac Med, Dept Publ Hlth, Abeno Ku, Osaka 5458585, Japan. NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. NIAAA, Clin Studies Lab, NIH, Rockville, MD 20852 USA. Nagoya Univ, Grad Sch Med, Dept Psychiat, Nagoya, Aichi 4668550, Japan. NIDCD, Biol Cellulaire Lab, NIH, Rockville, MD 20850 USA. RP Okada, M (reprint author), Osaka City Univ, Fac Med, Dept Publ Hlth, Abeno Ku, 1-4-3 Asahi Machi, Osaka 5458585, Japan. EM mokada@med.osaka-cu.ac.jp RI Ozaki, Norio/M-8908-2014; Goldman, David/F-9772-2010 OI Ozaki, Norio/0000-0002-7360-4898; Goldman, David/0000-0002-1724-5405 NR 20 TC 4 Z9 5 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 EAST 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 BN 1-57331-522-2 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 2004 VL 1025 BP 570 EP 577 DI 10.1196/annals.1316.070 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Multidisciplinary Sciences; Neurosciences SC Biochemistry & Molecular Biology; Cell Biology; Substance Abuse; Science & Technology - Other Topics; Neurosciences & Neurology GA BBP90 UT WOS:000226975200071 PM 15542764 ER PT J AU Novak, MFSX AF Novak, MFSX TI Fetal-maternal interactions: Prenatal psychobiological precursors to adaptive infant development SO CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY, VOL 59 SE CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY LA English DT Review ID PREGNANT RHESUS-MONKEYS; MACACA-MULATTA; MYOMETRIAL CONTRACTIONS; CONDITIONED-RESPONSE; NONHUMAN-PRIMATES; NEURAL MECHANISMS; EARLY EXPERIENCE; GRAVID BABOON; BLOOD-FLOW; RAT FETUS C1 NICHHD, Sect Comparat Behav Genet, Lab Comparat Ecol, NIH, Bethesda, MD 20892 USA. RP Novak, MFSX (reprint author), NIH, Anim Ctr, POB 539, Poolesville, MD 20837 USA. NR 111 TC 10 Z9 10 U1 2 U2 3 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0070-2153 J9 CURR TOP DEV BIOL PY 2004 VL 59 BP 37 EP 60 DI 10.1016/S0070-2153(04)59002-6 PG 24 WC Developmental Biology SC Developmental Biology GA BY84Z UT WOS:000189478000002 PM 14975246 ER PT J AU Mounkes, L Stewart, CL AF Mounkes, L Stewart, CL TI Structural organization and functions of the nucleus in development, aging, and disease SO CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY, VOL. 61 SE CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY LA English DT Review ID DREIFUSS MUSCULAR-DYSTROPHY; LAMIN A/C GENE; A-TYPE LAMINS; HUTCHINSON-GILFORD PROGERIA; CHARCOT-MARIE-TOOTH; GERM CELL-LESS; FAMILIAL PARTIAL LIPODYSTROPHY; WERNER-SYNDROME PROTEIN; B RECEPTOR GENE; MEMBRANE-PROTEIN AB In the past four years at least ten different diseases have been shown to be associated with mutations in genes whose products are associated with the nuclear envelope. Seven of these diseases, including muscular dystrophies, cardiomyopathies, lipodystrophies, and most intriguingly, Progeria, or premature aging, are caused by mutations in gene encoding the A-type lamins. The A-type lamins are the principle components that make up the nuclear lamina, a thin proteinaceous layer underlying the nuclear envelope. How different tissue specific diseases arise from unique mutations in the LMNA gene, encoding almost ubiquitously expressed nuclear proteins, are providing tantalizing insights into the structural and functional organization of the importance of nuclear architecture in embryonic development, disease, and aging. (C) 2004, Elsevier Inc. C1 NCI, Canc & Dev Biol Lab, Ctr Canc Res, Frederick, MD 21702 USA. RP Mounkes, L (reprint author), NCI, Canc & Dev Biol Lab, Ctr Canc Res, Frederick, MD 21702 USA. NR 210 TC 11 Z9 12 U1 1 U2 2 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0070-2153 J9 CURR TOP DEV BIOL PY 2004 VL 61 BP 191 EP + DI 10.1016/S0070-2153(04)61008-8 PG 40 WC Developmental Biology SC Developmental Biology GA BBF69 UT WOS:000225259200008 PM 15350402 ER PT J AU Jacobson, KA Costanzi, S Ohno, M Joshi, BV Besada, P Xu, B Tchilibon, S AF Jacobson, KA Costanzi, S Ohno, M Joshi, BV Besada, P Xu, B Tchilibon, S TI Molecular recognition at purine and pyrimidine nucleotide (P2) receptors SO CURRENT TOPICS IN MEDICINAL CHEMISTRY LA English DT Review ID HUMAN P2Y(1) RECEPTOR; SITE-DIRECTED MUTAGENESIS; PHARMACOLOGICAL CHARACTERIZATION; P-2Y-PURINOCEPTOR AGONISTS; PLATELET-AGGREGATION; EXTRACELLULAR LOOPS; BIOLOGICAL-ACTIVITY; LIGAND RECOGNITION; ACTIVE METABOLITE; P2X(1) RECEPTORS AB In comparison to other classes of cell surface receptors, the medicinal chemistry at P2X (ligand-gated ion channels) and P2Y (G protein-coupled) nucleotide receptors has been relatively slow to develop. Recent effort to design selective agonists and antagonists based on a combination of library screening, empirical modification of known ligands, and rational design have led to the introduction of potent antagonists of the P2X(1) (derivatives of pyridoxal phosphates and suramin), P2X(3) (A-317491), P2X(7) (derivatives of the isoquinoline KN-62), P2Y, (nucleotide analogues MRS 2179 and MRS 2279), P2Y, (thiouracil derivatives such as AR-C126313), and P2Y(12) (nucleotide/nucleoside analogues AR-C69931X and AZD6140) receptors. A variety of native agonist ligands (ATP, ADP, UTP, UDP, and UDP-glucose) are currently the subject of structural modification efforts to improve selectivity. MRS2365 is a selective agonist for P2Y, receptors. The dinucleotide INS 37217 potently activates the P2Y(2) receptor. UTP-gamma-S and UDP-beta-S are selective agonists for P2Y(2)/P2Y(4) and P2Y(6) receptors, respectively. The current knowledge of the structures of P2X and P2Y receptors, is derived mainly from mutagenesis studies. Site-directed mutagenesis has shown that ligand recognition in the human P2Y, receptor involves individual residues of both the TMs (3, 5, 6, and 7), as well as EL 2 and 3. The binding of the negatively-charged phosphate moiety is dependent on positively charged lysine and arginine residues near the exofacial side of TMs 3 and 7. C1 NIDDK, Mol Recognit Sect, NIH, LBC, Bethesda, MD 20892 USA. RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, NIH, LBC, Bldg 8A,Rm B1A-19, Bethesda, MD 20892 USA. EM kajacobs@helix.nih.gov RI Jacobson, Kenneth/A-1530-2009; Besada Pereira, Pedro/E-6051-2012; Costanzi, Stefano/G-8990-2013; OI Jacobson, Kenneth/0000-0001-8104-1493; Besada Pereira, Pedro/0000-0002-9985-9063; Costanzi, Stefano/0000-0003-3183-7332 FU Intramural NIH HHS [Z01 DK031116-20] NR 76 TC 31 Z9 32 U1 0 U2 7 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1568-0266 J9 CURR TOP MED CHEM JI Curr. Top. Med. Chem. PY 2004 VL 4 IS 8 BP 805 EP 819 DI 10.2174/1568026043450961 PG 15 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 810BZ UT WOS:000220681100003 PM 15078212 ER PT J AU Gao, ZG Jacobson, KA AF Gao, ZG Jacobson, KA TI Partial agonists for A(3) adenosine receptors SO CURRENT TOPICS IN MEDICINAL CHEMISTRY LA English DT Review ID A(1) RECEPTOR; STRUCTURAL DETERMINANTS; SELECTIVE LIGANDS; IN-VIVO; DERIVATIVES; ANALOGS; RAT; N-6-CYCLOPENTYLADENOSINE; AFFINITY; EFFICACY AB Selective agonists for A(3) adenosine receptors (ARs) could potentially be therapeutic agents for a variety of disorders, including brain and heart ischemic conditions, while partial agonists may have: advantages over full agonists as a result of an increased selectivity of action. A number of structural determinants for A(3)AR activation have recently been identified, including the N-6-benzyl group, methanocarba substitution of ribose, 2-chloro and 2-fluoro substituents, various 2'- and 3'-substitutions and 4'-thio substitution of oxygen. The 2-chloro substitution of CPA and R-PIA led to A; antagonism (CCPA) and partial agonism (Cl-R-PIA). 2-Chloroadenosine was a full agonist, while 2-fluoroadenosine was a partial, agonist. Both 2'- and 3'- substitutions have a pronounced effect on its efficacy, although the effect of 2'-substitution was more dramatic. The 4-thio substitution of oxygen may also diminish efficacy, depending on other substitutions. Both N-6-methyl and N-6-benzyl groups may contribute to the A(3) affinity and selectivity; however, an N-6-benzyl group but not an N-6-methyl group diminishes A(3)AR efficacy. N-6-benzyl substituted adenosine derivatives have similar potency for human and rat A(3)ARs while N-6-methyl substitution was preferable for the human A(3)AR. The combination of 2-chloro and N-6-benzyl substitutions appeared to reduce efficacy further than either modification alone. The A(2A)AAR agonist DPMA was shown to be an antagonist for the human A(3)AR. Thus, the efficacy of adenosine derivatives at the A(3)AR appears to be more sensitive to small structural changes than at other subtypes. Potent and selective partial agonists for the A(3)AR could be identified by screening known adenosine derivatives and by modifying adenosine and the adenosine derivatives. C1 NIDDK, Mol Recognit Sect, LBC, NIH, Bethesda, MD 20892 USA. RP Gao, ZG (reprint author), NIDDK, Mol Recognit Sect, LBC, NIH, Bldg 8A,Rm B1A-23, Bethesda, MD 20892 USA. EM zhanguog@intra.niddk.nih.gov RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 FU Intramural NIH HHS [Z01 DK031117-20] NR 33 TC 13 Z9 14 U1 0 U2 1 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1568-0266 J9 CURR TOP MED CHEM JI Curr. Top. Med. Chem. PY 2004 VL 4 IS 8 BP 855 EP 862 DI 10.2174/1568026043450989 PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 810BZ UT WOS:000220681100007 PM 15078216 ER PT J AU Chiu, TK Davies, DR AF Chiu, TK Davies, DR TI Structure and function of HIV-1 integrase SO CURRENT TOPICS IN MEDICINAL CHEMISTRY LA English DT Review ID IMMUNODEFICIENCY-VIRUS TYPE-1; PHOTO-CROSS-LINKING; DNA-BINDING DOMAIN; TETRAD-FORMING OLIGONUCLEOTIDES; SEQUENCE-SPECIFIC RECOGNITION; CARBOXYL-TERMINAL DOMAINS; TARGET SITE SELECTION; CATALYTIC DOMAIN; ACTIVE-SITE; MINOR-GROOVE AB HIV-1 integrase is a multidomain enzyme which is required for the integration of viral DNA into the host genome. it is one of three enzymes of HIV, the others being the Reverse Transcriptase and the Protease. It is an attractive target for therapeutic drug design. The enzyme consists of three domains. The N-terminal domain has a His(2)Cys(2) motif which chelates zinc, the core domain has the catalytic DDE motif which is required for its enzymatic activity, and the C-terminal domain has an SH3-like fold which binds DNA nonspecifically. We review the structures of various integrase fragments, the core domain with inhibitors bound, and propose a model for DNA binding. C1 NIDDKD, NIH, Mol Biol Lab, Bethesda, MD 20892 USA. RP Davies, DR (reprint author), NIDDKD, NIH, Mol Biol Lab, Bldg 5,Room 338, Bethesda, MD 20892 USA. EM david.davies@nih.gov NR 113 TC 155 Z9 171 U1 2 U2 24 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1568-0266 J9 CURR TOP MED CHEM JI Curr. Top. Med. Chem. PY 2004 VL 4 IS 9 BP 965 EP 977 DI 10.2174/1568026043388547 PG 13 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 817KN UT WOS:000221176500007 PM 15134551 ER PT J AU Johnson, AA Marchand, C Pommier, Y AF Johnson, AA Marchand, C Pommier, Y TI HIV-1 integrase inhibitors: A decade of research and two drugs in clinical trial SO CURRENT TOPICS IN MEDICINAL CHEMISTRY LA English DT Review DE HIV-1 integrase; diketo acids; HIV inhibitors; AIDS; integrase inhibitors ID HUMAN-IMMUNODEFICIENCY-VIRUS; CHAIN VARIABLE FRAGMENT; PHOTO-CROSS-LINKING; METAL-DEPENDENT INHIBITION; DNA-BINDING DOMAIN; N-TERMINAL DOMAIN; BETA-DIKETO ACIDS; TYPE-1 INTEGRASE; IN-VITRO; ACTIVE-SITE AB AIDS is currently treated with a combination therapy of reverse transcriptase and protease inhibitors. Recently, the FDA approved a drug targeting HIV-1 entry into cells. There are currently no FDA approved drugs targeting HIV-1 integrase, though many scientists and drug companies are actively in pursuit of clinically useful integrase inhibitors. The objective of this review is to provide an update on integrase inhibitors reported in the last two years, including two novel inhibitors in early clinical trials, recently developed hydroxylated aromatics, natural products, peptide, antibody and oligonucleotide inhibitors. Additionally, the proposed mechanism of diketo acid inhibition is reviewed. C1 NCI, Mol Pharmacol Lab, CCR, NIH, Bethesda, MD 20892 USA. RP Pommier, Y (reprint author), NCI, Mol Pharmacol Lab, CCR, NIH, Bldg 37,Room 5068, Bethesda, MD 20892 USA. EM pommier@nih.gov RI Marchand, Christophe/D-8559-2016 NR 103 TC 102 Z9 107 U1 2 U2 5 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1568-0266 J9 CURR TOP MED CHEM JI Curr. Top. Med. Chem. PY 2004 VL 4 IS 10 BP 1059 EP 1077 DI 10.2174/1568026043388394 PG 19 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 835BP UT WOS:000222455200005 PM 15193139 ER PT J AU Jacobson, KA AF Jacobson, KA TI Receptors for extracellular nucleosides and nucleotides - Preface SO CURRENT TOPICS IN MEDICINAL CHEMISTRY LA English DT Editorial Material C1 NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA. RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA. EM kajacobs@helix.nih.gov RI Jacobson, Kenneth/A-1530-2009 OI Jacobson, Kenneth/0000-0001-8104-1493 NR 1 TC 0 Z9 0 U1 0 U2 1 PU BENTHAM SCIENCE PUBL LTD PI HILVERSUM PA PO BOX 1673, 1200 BR HILVERSUM, NETHERLANDS SN 1568-0266 J9 CURR TOP MED CHEM JI Curr. Top. Med. Chem. PY 2004 VL 4 IS 8 PG 1 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 810BZ UT WOS:000220681100001 ER PT J AU Sood, R Bader, PI Speer, MC Edwards, YH Eddings, EM Blair, RT Hu, P Faruque, MU Robbins, CM Zhang, H Leuders, J Morrison, K Thompson, D Schwartzberg, PL Meltzer, PS Trent, JM AF Sood, R Bader, PI Speer, MC Edwards, YH Eddings, EM Blair, RT Hu, P Faruque, MU Robbins, CM Zhang, H Leuders, J Morrison, K Thompson, D Schwartzberg, PL Meltzer, PS Trent, JM TI Cloning and characterization of an inversion breakpoint at 6q23.3 suggests a role for Map7 in sacral dysgenesis SO CYTOGENETIC AND GENOME RESEARCH LA English DT Article ID MICROTUBULE-ASSOCIATED PROTEIN; CURRARINO-SYNDROME; HOMEOBOX GENE; EPITHELIAL-CELLS; AGENESIS; E-MAP-115; HLXB9; DIFFERENTIATION; IDENTIFICATION; TRANSLOCATION AB Here we report on a male patient with sacral dysgenesis (SD) and constitutional pericentric inversion of chromosome 6 (p11.2; q23.3). SD is a heterogeneous group of congenital anomalies with complex genetic etiology. Previously, a patient with sacral abnormalities and an interstitial deletion of 6q23. q25 region has been described. We speculated that a susceptibility gene for SD lies in 6q23.3 region ( disrupted in both patients), and therefore, cloning of the breakpoint in our patient would lead to the identification of the disrupted gene. We performed FISH analysis followed by Southern blot analysis and inverse PCR to clone the breakpoint. The 6p11.2 breakpoint mapped very close to the centromere, and the 6q23.3 breakpoint localized in the ninth intron of the MAP7 gene. We then evaluated the involvement of MAP7 in SD by further screening of the gene in several patients with a similar phenotype. Two nucleotide changes causing Ile257Asn and Glu571Ala substitutions in the protein, both affecting amino acid residues conserved in the mouse homolog, were identified in two patients. Both changes are either very rare polymorphisms or true mutations, since they were not detected in 167 normal individuals nor found in the SNP database. Therefore, our study suggests MAP7 as a candidate gene for SD. However, we were unable to detect any sacral defects in the MAP7 knockout mice. Copyright (C) 2004 S. Karger AG, Basel. C1 NHGRI, NIH, Canc Genet Branch, Bethesda, MD 20892 USA. NE Indiana Genet Counseling Ctr, Ft Wayne, IN USA. Duke Univ, Med Ctr, Durham, NC USA. UCL, MRC Human Biochem Genet Unit, Dept Biol, London, England. NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA. Great Ormond St Hosp Sick Children, London WC1N 3JH, England. RP Sood, R (reprint author), NHGRI, NIH, Canc Genet Branch, Bldg 49,Room 3A30,9000 Rockville Pike, Bethesda, MD 20892 USA. EM rsood@nhgri.nih.gov FU NICHD NIH HHS [HD33400]; NINDS NIH HHS [NS39818] NR 38 TC 3 Z9 4 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1424-8581 J9 CYTOGENET GENOME RES JI Cytogenet. Genome Res. PY 2004 VL 106 IS 1 BP 61 EP 67 DI 10.1159/000078563 PG 7 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 859DU UT WOS:000224243600086 PM 15218243 ER PT J AU Moore, CM Dunn, BG McMahan, CA Dunne, CL Mattison, JA Lane, MA Roth, GS Ingram, DK AF Moore, CM Dunn, BG McMahan, CA Dunne, CL Mattison, JA Lane, MA Roth, GS Ingram, DK TI Does calorie restriction reduce age-related chromosome breakage? SO CYTOGENETIC AND GENOME RESEARCH LA English DT Meeting Abstract CT 16th European Colloquium on Animal Cytogenetics and Gene Mapping (16th ECACGM) CY JUL 06-09, 2004 CL Jouy en Josas, FRANCE SP Natl Inst Agron Res C1 Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Dept Clin Lab Sci, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Dept Pathol, San Antonio, TX 78229 USA. NIA, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1424-8581 J9 CYTOGENET GENOME RES JI Cytogenet. Genome Res. PY 2004 VL 106 IS 1 MA 7 BP 126 EP 127 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 859DU UT WOS:000224243600101 ER PT J AU Svartman, M Stone, G Page, J Stanyon, R AF Svartman, M Stone, G Page, J Stanyon, R TI Chromosome painting applied to testing the basal Eutherian karyotype SO CYTOGENETIC AND GENOME RESEARCH LA English DT Meeting Abstract CT 16th European Colloquium on Animal Cytogenetics and Gene Mapping (16th ECACGM) CY JUL 06-09, 2004 CL Jouy en Josas, FRANCE SP Natl Inst Agron Res C1 NCI, Lab Genom Divers, Ft Detrick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1424-8581 J9 CYTOGENET GENOME RES JI Cytogenet. Genome Res. PY 2004 VL 106 IS 1 MA 28 BP 132 EP 133 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 859DU UT WOS:000224243600122 ER PT J AU Olson, SB Akkari, YMN Brown, MG Alter, BP Young, N Magenis, E AF Olson, SB Akkari, YMN Brown, MG Alter, BP Young, N Magenis, E TI The cytogenetic aspect of Fanconi anemia diagnosis SO CYTOGENETIC AND GENOME RESEARCH LA English DT Meeting Abstract CT 16th European Colloquium on Animal Cytogenetics and Gene Mapping (16th ECACGM) CY JUL 06-09, 2004 CL Jouy en Josas, FRANCE SP Natl Inst Agron Res C1 Oregon Hlth & Sci Univ, Clin Cytogenet Lab, Portland, OR 97239 USA. NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. NHLBI, Hematol Branch, NIH, 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 1424-8581 J9 CYTOGENET GENOME RES JI Cytogenet. Genome Res. PY 2004 VL 106 IS 1 MA 34 BP 134 EP 134 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 859DU UT WOS:000224243600128 ER PT J AU Kim, SH McQueen, PG Lichtman, MK Shevach, EM Parada, LA Misteli, T AF Kim, SH McQueen, PG Lichtman, MK Shevach, EM Parada, LA Misteli, T TI Spatial genome organization during T-cell differentiation SO CYTOGENETIC AND GENOME RESEARCH LA English DT Article ID CHROMOSOME TERRITORIES; NUCLEAR ARCHITECTURE; INTERPHASE NUCLEI; MAMMALIAN-CELLS; INACTIVE GENES; IN-VITRO; LOCALIZATION; CHROMATIN; HETEROCHROMATIN; COMPARTMENTALIZATION AB The spatial organization of genomes within the mammalian cell nucleus is non-random. The functional relevance of spatial genome organization might be in influencing gene expression programs as cells undergo changes during development and differentiation. To gain insight into the plasticity of genomes in space and time and to correlate the activity of specific genes with their nuclear position, we systematically analyzed the spatial genome organization in differentiating mouse T-cells. We find significant global reorganization of centromeres, chromosomes and gene loci during the differentiation process. Centromeres were repositioned from a preferentially internal distribution in undifferentiated cells to a preferentially peripheral position in differentiated CD4+ and CD8+ cells. Chromosome 6, containing the differentially expressed T-cell markers CD4 and CD8, underwent differential changes in position depending on whether cells differentiated into CD4+ or CD8+ thymocytes. Similarly, the two marker loci CD4 and CD8 showed distinct behavior in their position relative to the chromosome 6 centromere at various stages of differentiation. Our results demonstrate that significant spatial genome reorganization occurs during differentiation and indicate that the relationship between dynamic genome topology and single gene regulation is highly complex. Copyright (C) 2004 S. Karger AG, Basel. C1 NCI, NIH, Bethesda, MD 20892 USA. NIH, Math & Stat Lab, DCB, CIT, Bethesda, MD 20892 USA. NIAID, Immunol Lab, Bethesda, MD 20892 USA. RP Misteli, T (reprint author), NCI, NIH, 41 Lib Rd,Bldg 41,B610, Bethesda, MD 20892 USA. EM mistelit@mail.nih.gov NR 52 TC 71 Z9 74 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1424-8581 J9 CYTOGENET GENOME RES JI Cytogenet. Genome Res. PY 2004 VL 105 IS 2-4 BP 292 EP 301 DI 10.1159/000078201 PG 10 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 857YW UT WOS:000224158000017 PM 15237218 ER PT J AU Stanyon, R Yang, F Morescalchi, AM Galleni, L AF Stanyon, R Yang, F Morescalchi, AM Galleni, L TI Chromosome painting in the long-tailed field mouse provides insights into the ancestral murid karyotype SO CYTOGENETIC AND GENOME RESEARCH LA English DT Article ID ZOO-FISH; GENOME ORGANIZATION; LABORATORY MOUSE; RAT; GENE; EVOLUTION; APODEMUS; SEGMENTS; RODENTS; MAPS AB We report on the hybridization of mouse chromosomal paints to Apodemus sylvaticus, the long-tailed field mouse. The mouse paints detected 38 conserved segments in the Apodemus karyotype. Together with the species reported here there are now six species of rodents mapped with Mus musculus painting probes. A parsimony analysis indicated that the syntenies of nine M. musculus chromosomes were most likely already formed in the muroid ancestor: 3, 4, 7, 9, 14, 18, 19, X and Y. The widespread occurrence of syntenic segment associations of mouse chromosomes 1/17, 2/13, 7/19, 10/17, 11/16, 12/17 and 13/15 suggests that these associations were ancestral syntenies for muroid rodents. The muroid ancestral karyotype probably had a diploid number of about 2n = 54. It would be desirable to have a richer phylogenetic array of species before any final conclusions are drawn about the Muridae ancestral karyotype. The ancestral karyotype presented here should be considered as a working hypothesis. Copyright (C) 2004 S. Karger AG, Basel. C1 NCI, Comparat Mol Cytogenet Core Genet Branch, Frederick, MD 21702 USA. Univ Cambridge, Ctr Vet Sci, Cambridge, England. Chinese Acad Sci, Kunming Inst Zool, Key Lab Cellular & Mol Evolut, Kunming, Yunnan, Peoples R China. Seconda Univ Studi Napoli, Dipartimento Sci Vita, Caserta, Italy. Univ Pisa, Dipartimento Chim & Biotecnol Agr, Pisa, Italy. RP Stanyon, R (reprint author), NCI, Comparat Mol Cytogenet Core Genet Branch, Bldg 560,Room 11-74A, Frederick, MD 21702 USA. EM stanyonr@ncifcrf.gov OI Stanyon, Roscoe/0000-0002-7229-1092 NR 40 TC 26 Z9 26 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1424-8581 J9 CYTOGENET GENOME RES JI Cytogenet. Genome Res. PY 2004 VL 105 IS 2-4 BP 406 EP 411 DI 10.1159/000078213 PG 6 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 857YW UT WOS:000224158000029 PM 15237228 ER PT J AU Schmid, I Roederer, M Koup, RA Ambrozak, D Perfetto, SP AF Schmid, I Roederer, M Koup, RA Ambrozak, D Perfetto, SP TI Biohazard sorting SO CYTOMETRY, 4TH EDITION: NEW DEVELOPMENTS SE METHODS IN CELL BIOLOGY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; FLOW-CYTOMETRY; POSTEXPOSURE PROPHYLAXIS; HEALTH-CARE; INFECTIONS; EXPOSURES; CONTAINMENT; GUIDELINES; PARTICLES; SORTERS C1 Univ Calif Los Angeles, David Geffen Sch Med, Dept Hematol Oncol, Los Angeles, CA 90095 USA. NIAID, Immunol Lab, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA. RP Schmid, I (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Hematol Oncol, Los Angeles, CA 90095 USA. RI Roederer, Mario/G-1887-2011 FU NCI NIH HHS [CA 16042]; NIAID NIH HHS [AI 28697] NR 31 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X J9 METHOD CELL BIOL PY 2004 VL 75 BP 221 EP 240 PG 20 WC Cell Biology SC Cell Biology GA BBS31 UT WOS:000227570400009 PM 15603428 ER PT J AU Roederer, M Darzynkiewicz, Z Parks, DR AF Roederer, M Darzynkiewicz, Z Parks, DR TI Guidelines for the presentation of flow cytometric data SO CYTOMETRY, 4TH EDITION: NEW DEVELOPMENTS SE METHODS IN CELL BIOLOGY LA English DT Review C1 NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA. New York Med Coll, Braner Canc Res Inst, Hawthorne, NY 10532 USA. Stanford Univ, Dept Genet, Stanford, CA 94305 USA. RP Roederer, M (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. RI Roederer, Mario/G-1887-2011; OI Darzynkiewicz, Zbigniew/0000-0002-2040-7081 FU NCI NIH HHS [R01 CA028704, R01 CA028704-26] NR 5 TC 13 Z9 13 U1 1 U2 3 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X J9 METHOD CELL BIOL PY 2004 VL 75 BP 241 EP 256 PG 16 WC Cell Biology SC Cell Biology GA BBS31 UT WOS:000227570400010 PM 15603429 ER PT J AU Brenchley, JM Douek, DC AF Brenchley, JM Douek, DC TI Flow cytometnic analysis of human antigen-specific T-cell proliferation SO CYTOMETRY, 4TH EDITION: NEW DEVELOPMENTS SE METHODS IN CELL BIOLOGY LA English DT Review ID LONG-TERM NONPROGRESSORS; HIV-1 INFECTION; RHEUMATOID-ARTHRITIS; LYMPHOCYTE ACTIVITY; MULTIPLE-SCLEROSIS; SUCCINIMIDYL ESTER; HUMAN NAIVE; IN-VIVO; VACCINE; RESPONSES C1 NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20874 USA. RP Brenchley, JM (reprint author), NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20874 USA. NR 69 TC 9 Z9 9 U1 0 U2 5 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X J9 METHOD CELL BIOL PY 2004 VL 75 BP 481 EP 496 PG 16 WC Cell Biology SC Cell Biology GA BBS31 UT WOS:000227570400019 PM 15603438 ER PT J AU Betts, MR Koup, RA AF Betts, MR Koup, RA TI Detection of T-cell degranulation: CD107a and b SO CYTOMETRY, 4TH EDITION: NEW DEVELOPMENTS SE METHODS IN CELL BIOLOGY LA English DT Review ID FLOW-CYTOMETRIC ASSAY; MEDIATED CYTOTOXICITY; LYMPHOCYTE ACTIVITY; MEMBRANE-PROTEINS; TARGET-CELLS; SURFACE; IDENTIFICATION; DEATH; IMMUNODEFICIENCY; GLYCOPROTEINS C1 NIAID, Immunol Lab, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA. RP Betts, MR (reprint author), NIAID, Immunol Lab, Vaccine Res Ctr, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 39 TC 84 Z9 88 U1 0 U2 6 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X J9 METHOD CELL BIOL PY 2004 VL 75 BP 497 EP 512 PG 16 WC Cell Biology SC Cell Biology GA BBS31 UT WOS:000227570400020 PM 15603439 ER PT J AU Lore, K AF Lore, K TI Isolation and immunophenotyping of human and rhesus macaque dendritic cells SO CYTOMETRY, 4TH EDITION: NEW DEVELOPMENTS SE METHODS IN CELL BIOLOGY LA English DT Review ID TOLL-LIKE RECEPTORS; HUMAN PERIPHERAL-BLOOD; CLASS-II COMPARTMENT; CORD BLOOD; HIV-1 INFECTION; INFLAMMATORY RESPONSE; LYMPHOID-TISSUE; FLOW-CYTOMETRY; MESSENGER-RNA; NORMAL DONORS C1 NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA. RP Lore, K (reprint author), NIH, Vaccine Res Ctr, Bldg 10, Bethesda, MD 20892 USA. NR 83 TC 12 Z9 12 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X J9 METHOD CELL BIOL PY 2004 VL 75 BP 623 EP 642 PG 20 WC Cell Biology SC Cell Biology GA BBS31 UT WOS:000227570400026 PM 15603445 ER PT J AU Mascola, JR AF Mascola, JR TI Neutralizing antibody quantification by flow cytometry SO CYTOMETRY, 4TH EDITION: NEW DEVELOPMENTS SE METHODS IN CELL BIOLOGY LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-INFECTION; P24 ANTIGEN; T-CELLS; TYPE-1; LYMPHOCYTES; QUANTITATION; DETECT C1 NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA. RP Mascola, JR (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. NR 19 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0091-679X J9 METHOD CELL BIOL PY 2004 VL 75 BP 709 EP 716 PG 8 WC Cell Biology SC Cell Biology GA BBS31 UT WOS:000227570400030 PM 15603449 ER PT J AU Telford, WG Frolova, EG AF Telford, WG Frolova, EG TI Discrimination of the Hoechst side population in mouse bone marrow with violet and near-ultraviolet laser diodes SO CYTOMETRY PART A LA English DT Article DE stem cell; Hoechst 33342; side population; near-ultraviolet laser diode ID HEMATOPOIETIC STEM-CELLS; TRANSPORTER; ABCG2; CYTOMETRY; EFFLUX AB Background: Discrimination of stem cells with flow cytometric analysis of Hoechst 33342 efflux by the ABCG2 transporter (termed the Hoechst side population, or SP technique) is a valuable methodology for identifying bone marrow progenitors enriched with stem cells. Unfortunately, it requires a ultraviolet (UV) laser source, usually necessitating an expensive and maintenance-intensive argon- or krypton-ion gas laser on a large-scale cell sorter. In this study, we evaluated the ability of recently available violet and near-UV laser diodes to discriminate Hoechst SP on smaller cuvette-based flow cytometers. Methods: Violet laser diodes (emitting at 408 and 401 nm) and a near-UV laser diode (emitting at 370 nm) were mounted on a BD Biosciences LSR 11 and evaluated for their ability to discriminate Hoechst SP in murine bone marrow. Results: The violet laser diodes discriminated the Hoechst SP, but with poorer resolution than with the standard UV gas laser on a large-scale cell sorter. The near-UV laser diode, in contrast, gave excellent Hoechst SP resolution. Conclusions: These evaluations indicated that near-UV laser diodes give excellent Hoechst SP resolution on cuvette-based instruments. As the next generation of cell sorters integrate cuvette-based cell interrogation into conventional jet-in-air cell separation, these laser sources should become applicable for analysis and physical separation of Hoechst SP cells. (C) 2003 Wiley-Liss, Inc. C1 NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NICHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD USA. RP Telford, WG (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bldg 10,Room 12C121,9000 Rockville Pike, Bethesda, MD 20892 USA. EM telfordw@mail.nih.gov NR 15 TC 13 Z9 14 U1 1 U2 6 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0196-4763 J9 CYTOM PART A JI Cytom. Part A PD JAN PY 2004 VL 57A IS 1 BP 45 EP 52 DI 10.1002/cyto.a.10109 PG 8 WC Biochemical Research Methods; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 765JK UT WOS:000188263200006 PM 14699605 ER PT J AU Lunning, MA Zenger, VE Dreyfuss, R Stetler-Stevenson, M Rick, ME White, TA Wilson, WH Marti, GE AF Lunning, MA Zenger, VE Dreyfuss, R Stetler-Stevenson, M Rick, ME White, TA Wilson, WH Marti, GE TI Albumin enhanced morphometric image analysis in CLL SO CYTOMETRY PART B-CLINICAL CYTOMETRY LA English DT Article DE chronic lymphocytic leukemia; morphology; atypical morphology; atypical chronic lymphocytic leukemia; morphometric analysis ID CHRONIC LYMPHOCYTIC-LEUKEMIA; IN-SITU HYBRIDIZATION; B-CELL DISORDERS; PROLYMPHOCYTIC LEUKEMIA; PROGNOSTIC-SIGNIFICANCE; SCORING SYSTEM; NUCLEAR CLEFTS; LABORATORY FEATURES; LYMPHOID LEUKEMIAS; MORPHOLOGY AB Background: The heterogeneity of lymphocytes from patients with chronic lymphocytic leukemia (CLL) and blood film artifacts make morphologic subclassification of this disease difficult. Methods: We reviewed paired blood films prepared from ethylene-diamine-tetraacetic acid (ETDA) samples with and without bovine serum albumin (BSA) from 82 CLL patients. Group 1 adhered to NCCLS specifications for the preparations of EDTA blood films. Group 2 consisted of blood films containing EDTA and a 1:12 dilution of 22% BSA. Eight patients were selected for digital photomicroscopy and statistical analysis. Approximately 100 lymphocytes from each slide were digitally captured. Results: The mean cell area +/- standard error was 127.8 muM(2) +/- 1.42 for (n = 793) for group 1 versus 100.7 muM(2) +/- 1.39 (n = 831) for group 2. The nuclear area was 88.9 muM(2) +/- 0.85 for group 1 versus 76.4 muM(2) 0.83 for group 2. For the nuclear transmittance, the values were 97.6 +/- 0.85 for group 1 and 104.1 +/- 0.83 for group 2. The nuclear:cytoplasmic ratios were 0.71 +/- 0.003 for group 1 and 0.78 +/- 0.003 for group 2. All differences were statistically significant (P < 0.001). Conclusions: BSA addition results in the reduction of atypical lymphocytes and a decrease in smudge cells. BSA also decreases the lymphocyte area and nuclear area, whereas nuclear transmittance and nuclear:cytoplasmic ratio are increased. A standardized method of slide preparation would allow accurate interlaboratory comparison. The use of BSA may permit better implementation of the blood film-based subclassification of CLL and lead to a better correlation of morphology with cytogenetics and immunophenotyping. Published 2003 Wiley-Liss, Inc(dagger). C1 US FDA, Flow & Image Cytometry Sect, Lab Stem Biol, DCGT,CBER, Bethesda, MD 20892 USA. NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA. NCI, Med Oncol Clin Res Unit, NIH, Bethesda, MD 20892 USA. NIH, Hematol Serv, Ctr Clin, Bethesda, MD 20892 USA. NIH, Clin Flow Cytometry Sect, Pathol Lab, Div Clin Sci, Bethesda, MD 20892 USA. NIH, Med Arts Photog Branch, Bethesda, MD 20892 USA. RP Marti, GE (reprint author), US FDA, Flow & Image Cytometry Sect, Lab Stem Biol, DCGT,CBER, NIH Bldg 29B,Room 2NN08,8800 Rockville Pike, Bethesda, MD 20892 USA. EM gemarti@helix.nih.gov NR 40 TC 6 Z9 6 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 0196-4763 J9 CYTOM PART B-CLIN CY JI Cytom. Part B-Clin. Cytom. PD JAN PY 2004 VL 57B IS 1 BP 7 EP 14 DI 10.1002/cyto.b.10059 PG 8 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA 760XQ UT WOS:000187860900002 PM 14696058 ER PT J AU Horikawa, I Michishita, E Barrett, JC AF Horikawa, I Michishita, E Barrett, JC TI Regulation of hTERT transcription: a target of cellular and viral mechanisms for immortalization and carcinogenesis SO CYTOTECHNOLOGY LA English DT Article DE c-Myc; human telomerase reverse transcriptase; immortalization; oncogenes; telomerase; transcriptional regulation; tumor suppressor genes ID TELOMERASE-REVERSE-TRANSCRIPTASE; PAPILLOMAVIRUS TYPE-16 E6; HUMAN CANCER-CELLS; C-MYC; CATALYTIC SUBUNIT; DIRECT ACTIVATION; EPITHELIAL-CELLS; PROMOTER REGION; DOWN-REGULATION; GENE PROMOTER AB A hallmark of human cancer cells is immortal cell growth, which is associated with telomere maintenance by telomerase. The transcriptional regulation of the human telomerase reverse transcriptase (hTERT) gene is a major mechanism that negatively and positively controls telomerase activity in normal and cancer cells, respectively. A growing body of data suggests that various cellular and viral factors and pathways involved in cell senescence, immortalization and carcinogenesis act on the hTERT promoter. The activity of the hTERT promoter is regulated, either directly or through signaling pathways, by oncogene products (e.g., Myc and Ets families) and tumor suppressor proteins (e.g., BRCA1). Endogenous factors involved in the physiological repression of the hTERT gene have also been revealed by chromosome transfer experiments. The integration of viral genomes in the hTERT locus can lead to hTERT activation and telomerase induction. Here, we summarize these findings and pay special attention to recent findings with relevance to the endogenous regulatory mechanisms of hTERT transcription. C1 NCI, Lab Biosyst & Canc, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Horikawa, I (reprint author), NCI, Lab Biosyst & Canc, Ctr Canc Res, NIH, 9000 Rockville Pike,Bldg 37,Room 5046, Bethesda, MD 20892 USA. EM horikawi@mail.nih.gov NR 65 TC 6 Z9 6 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0920-9069 J9 CYTOTECHNOLOGY JI Cytotechnology PD JAN PY 2004 VL 45 IS 1-2 BP 23 EP 32 DI 10.1007/s10616-004-5122-4 PG 10 WC Biotechnology & Applied Microbiology; Cell Biology SC Biotechnology & Applied Microbiology; Cell Biology GA 907GA UT WOS:000227702700004 PM 19003240 ER PT S AU Aberer, K Cudre-Mauroux, P Ouksel, AM Catarci, T Hacid, MS Illarramendi, A Kashyap, V Mecella, M Mena, E Neuhold, EJ De Troyer, O Risse, T Scannapieco, M Saltor, F de Santis, L Spaccapietra, S Staab, S Studer, R AF Aberer, K Cudre-Mauroux, P Ouksel, AM Catarci, T Hacid, MS Illarramendi, A Kashyap, V Mecella, M Mena, E Neuhold, EJ De Troyer, O Risse, T Scannapieco, M Saltor, F de Santis, L Spaccapietra, S Staab, S Studer, R BE Lee, YJ Li, JH Whang, KY Lee, D TI Emergent semantics principles and issues SO DATABASE SYSTEMS FOR ADVANCED APPLICATIONS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 9th International Conference on Database Systems for Advanced Applications (DASFAA 2004) CY MAR 17-19, 2004 CL Jeju Isl, SOUTH KOREA SP Adv Informat Technol Res Ctr, SIGDB, Korea Informat Sci Soc, Asian Off Aerosp Res & Div, Korea Adv Inst Sci & Technol, AF Off Sci Res, Army Res Off Far E, ORACLE, SAMSUNG SDS, Korea TeleCom Data Inc, Korea Informat Sci Soc, Informat Proc Soc Japan, Database Soc, China Comp Fdn, Data Soc Japan, ACM SIGMOD ID ONTOLOGIES AB Information and communication infrastructures underwent a rapid and extreme decentralization process over the past decade: From a world of statically and partially connected central servers rose an intricate web of millions of information sources loosely connecting one to another. Today, we expect to witness the extension of this revolution with the wide adoption of meta-data standards like RDF or OWL underpinning the creation of a semantic web. Again, we hope for global properties to emerge from a multiplicity of pair-wise, local interactions, resulting eventually in a self-stabilizing semantic infrastructure. This paper represents an effort to summarize the conditions under which this revolution would take place as well as an attempt to underline its main properties, limitations and possible applications. C1 Swiss Fed Inst Technol, EPFL, Lausanne, Switzerland. Univ Illinois, Chicago, IL USA. Univ Rome 1, I-00185 Rome, Italy. Univ Lyon 1, F-69365 Lyon, France. Natl Lib Med, Bethesda, MD 20894 USA. Univ Zaragoza, E-50009 Zaragoza, Spain. Free Univ Brussels, Brussels, Belgium. Univ Politecn Catalunya, E-08028 Barcelona, Spain. Univ Karlsruhe, Karlsruhe, Germany. RP Aberer, K (reprint author), Swiss Fed Inst Technol, EPFL, Lausanne, Switzerland. RI Mecella, Massimo/F-7106-2011; Aberer, Karl/G-6336-2011; ILLARRAMENDI, ARANTZA/E-3466-2016; OI ILLARRAMENDI, ARANTZA/0000-0001-9567-6326; Mecella, Massimo/0000-0002-9730-8882; Mena Nieto, Eduardo/0000-0002-7462-0080; Risse, Thomas/0000-0001-6248-1709 NR 58 TC 22 Z9 23 U1 0 U2 2 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-21047-4 J9 LECT NOTES COMPUT SC PY 2004 VL 2973 BP 25 EP 38 PG 14 WC Computer Science, Artificial Intelligence; Computer Science, Information Systems; Computer Science, Theory & Methods SC Computer Science GA BY72A UT WOS:000189446900002 ER PT J AU Lough, S Treise, C Blair, J Watson, P Hodges, JR AF Lough, S Treise, C Blair, J Watson, P Hodges, JR TI Social cognition in frontal variant frontotemporal dementia SO DEMENTIA AND GERIATRIC COGNITIVE DISORDERS LA English DT Meeting Abstract CT 4th International Conference on Frontotemporal Dementia CY APR 24-26, 2003 CL Lund, SWEDEN SP Alzheimer Fdn, Crafoord Fdn, Ellen & Henrik Sjobring Fdn, Konsul Thure Carlssons Minne, Jansen Cilag AB, Ratiopharm AB, William & Py Gibson Fdn, H Lundbeck AB, Merk, Sharp & Dome, Novartis Sweden AB, Pfizer AB, ADERMA C1 Fulbourne Hosp, Dept Clin Psychol, Cambridge CB1 5EF, England. NIMH, Washington, DC USA. MRC CBU, Cambridge, England. NR 1 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1420-8008 J9 DEMENT GERIATR COGN JI Dement. Geriatr. Cogn. Disord. PY 2004 VL 17 IS 4 MA 12 BP 373 EP 373 PG 1 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA 825XV UT WOS:000221793000040 ER PT J AU Bienvenu, OJ Samuels, JF Costa, PT Reti, IM Eaton, WW Nestadt, G AF Bienvenu, OJ Samuels, JF Costa, PT Reti, IM Eaton, WW Nestadt, G TI Anxiety and depressive disorders and the five-factor model of personality: A higher- and lower-order personality trait investigation in a community sample SO DEPRESSION AND ANXIETY LA English DT Article DE anxiety; anxiety disorders; depression; depressive disorder; neurotic disorders; personality; personality inventory AB We describe in detail normal personality traits in persons with psychiatrist-ascertained anxiety and depressive disorders in a general population sample. We investigated Revised NEO Personality Inventory traits in 731 community subjects examined by psychiatrists with the Schedules for Clinical Assessment in Neuropsychiatry. All of the lifetime disorders of interest (simple phobia, social phobia, agoraphobia, panic disorder, obsessive-compulsive disorder (OCD), generalized anxiety disorder, major depressive disorder (MDD), and dysthymia) were associated with high neuroticism. Social phobia, agoraphobia, and dysthymia were associated with low extraversion, and OCD was associated with high openness to experience. In addition, lower-order facets of extraversion (E), openness (O), agreeableness (A), and conscientiousness (C) were associated with certain disorders (specifically, low assertiveness (E) and high openness to feelings (O) with MDD, low trust (A) with social phobia and agoraphobia, low self-discipline (C) with several of the disorders, and low competence and achievement striving (C) with social phobia). Neuroticism in particular was related to acuity of disorder. Longitudinal study is necessary to differentiate state versus pathoplastic effects. (C) 2004 Wiley-Liss, Inc. C1 Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. NIA, NIH, Baltimore, MD 21224 USA. Johns Hopkins Univ, Bloomberg Sch Hyg & Publ Hlth, Dept Mental Hyg, Baltimore, MD USA. RP Bienvenu, OJ (reprint author), 600 N Wolfe St,Meyer 125, Baltimore, MD 21287 USA. EM jbienven@mail.jhmi.edu OI Samuels, Jack/0000-0002-6715-7905; Costa, Paul/0000-0003-4375-1712 FU NIMH NIH HHS [R01-MH47447, K23-MH64543, R01-MH50616] NR 12 TC 147 Z9 149 U1 16 U2 50 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1091-4269 J9 DEPRESS ANXIETY JI Depress. Anxiety PY 2004 VL 20 IS 2 BP 92 EP 97 DI 10.1002/da.20026 PG 6 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 865ZF UT WOS:000224742000006 PM 15390211 ER PT J AU Bann, CM Parker, CB Bradwejn, J Davidson, JRT Vitiello, B Gadde, KM AF Bann, CM Parker, CB Bradwejn, J Davidson, JRT Vitiello, B Gadde, KM TI Assessing patient beliefs in a clinical trial of Hypericum perforatum in major depression SO DEPRESSION AND ANXIETY LA English DT Article DE depression; alternative medicine; complementary therapies; psychometrics ID ANTIDEPRESSANT TREATMENT; MHLC SCALES; LOCUS; ADHERENCE; SYMPTOMS; ANXIETY AB Little is known about the beliefs of patients suffering from major depression as to the causes of their illness and effective treatments. This study introduces a new instrument for capturing these beliefs, the Explanatory Model for Depression (EMD) Questionnaire, and explores the beliefs of patients participating in a clinical trial of an alternative medicine, Hypericum perforatum. Although the EMD was originally conceptualized as having five factors pertaining to models of the illness and treatment approaches, the data suggest that patient beliefs are aligned on two factors pertaining to internal and external locus of control. Strong beliefs on either of the EMD locus of control subscales are associated with more severe depression. More importantly, strong beliefs on the external locus of control subscale are associated with less improvement over the 8-week period of observation. These results support the role of patients' beliefs in their recovery from depression and suggest that patients who believe the causes of their depression are outside of their control are less likely to improve over time. It is important to note that beliefs did not mediate the effect of treatment on depression in this study, perhaps because patients were blinded to their treatment condition. Future studies should explore whether patient beliefs have an even greater impact when patients are aware of the treatment they are receiving and can determine whether that treatment is consistent with their beliefs. (C) 2004 Wiley-Liss, Inc. C1 RTI Int, Div Stat Res, Res Triangle Pk, NC 27709 USA. Univ Ottawa, Ottawa, ON K1N 6N5, Canada. Duke Univ, Med Ctr, Durham, NC 27706 USA. NIMH, Bethesda, MD 20892 USA. RP Bann, CM (reprint author), RTI Int, Div Stat Res, POB 12194, Res Triangle Pk, NC 27709 USA. EM cmb@rti.org FU NIMH NIH HHS [N01MH70007] NR 35 TC 17 Z9 17 U1 0 U2 4 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1091-4269 J9 DEPRESS ANXIETY JI Depress. Anxiety PY 2004 VL 20 IS 3 BP 114 EP 122 DI 10.1002/da.20036 PG 9 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 876BV UT WOS:000225471500003 PM 15549690 ER PT J AU Coupland, NJ Sustrik, RA Ting, P Li, D Hartfeil, M Singh, AJ Blair, RJ AF Coupland, NJ Sustrik, RA Ting, P Li, D Hartfeil, M Singh, AJ Blair, RJ TI Positive and negative affect differentially influence identification of facial emotions SO DEPRESSION AND ANXIETY LA English DT Article DE facial expression; emotion; depression; anxiety; social perception ID DSM-IV ANXIETY; TRIPARTITE MODEL; MOOD DISORDERS; DEPRESSION; DISCRIMINANT; EXPRESSIONS; RECOGNITION; CONVERGENT; VOLUNTEERS; AMYGDALA AB Positive and negative affects may bias behavior toward approach to rewards and withdrawal from threat, particularly when the contingencies are ambiguous. The hypothesis was that positive and negative affects would associate predictably with identification of happy, disgusted, or angry expressions that may signal potentially rewarding or aversive social interactions. Healthy volunteers (n = 86) completed affect ratings and a facial emotion task that employed morphed continua in which emotional expressions gradually decreased in ambiguity. Relations between mood and intensity thresholds for emotion identification were computed. Anhedonia (low positive affect) predicted thresholds for happy expressions (r = 0.24; P = .026) whereas negative affect predicted thresholds for disgust (r = -0.25; P = .022). Even within a normal range of mood, mood predicted emotion identification, supporting constructs of positive and negative affect derived originally from self-report measures. (C) 2004 Wiley-Liss, Inc. C1 Univ Alberta, Psychopharmacol Res Unit, Dept Psychiat, Edmonton, AB T6G 2B7, Canada. St Georges Univ, Fac Med, St Georges, Grenada. NIMH, Unit Cognit Affect Neurosci, Div Mood & Anxiety Disorders, Bethesda, MD 20892 USA. RP Coupland, NJ (reprint author), Univ Alberta, Psychopharmacol Res Unit, Dept Psychiat, 1E7-16 WMC,8440-112 St, Edmonton, AB T6G 2B7, Canada. EM nc2@ualberta.ca NR 17 TC 22 Z9 22 U1 2 U2 14 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 2004 VL 19 IS 1 BP 31 EP 34 DI 10.1002/da.10136 PG 4 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 775LJ UT WOS:000189041700005 PM 14978783 ER PT J AU LaSalle, VH Cromer, KR Nelson, KN Kazuba, D Justement, L Murphy, DL AF LaSalle, VH Cromer, KR Nelson, KN Kazuba, D Justement, L Murphy, DL TI Diagnostic interview assessed neuropsychiatric disorder comorbidity in 334 individuals with obsessive-compulsive disorder SO DEPRESSION AND ANXIETY LA English DT Article; Proceedings Paper CT 111th Annual Convention of the American-Psychological-Association CY AUG, 2003 CL TORONTO, CANADA SP Amer Psychol Assoc DE obsessions; compulsions; depression; mood disorders; anxiety disorders ID STRUCTURED CLINICAL INTERVIEW; DSM-III-R; MGH HAIRPULLING SCALE; LA-TOURETTE-SYNDROME; ANXIETY DISORDERS; EATING-DISORDERS; ANOREXIA-NERVOSA; PERSONALITY-DISORDER; PSYCHIATRIC-DISORDERS; 1ST-DEGREE RELATIVES AB Is obsessive-compulsive disorder (OCD) a discrete disorder? Three hundred thirty-four individuals with OCD were interviewed using the Structured Clinical Interview for DSM (SCID). Results demonstrate that OCD is highly comorbid with, other neuropsychiatric disorders, with 92% of OCD study participants receiving one or more additional Axis I DSM diagnoses. Among these additional diagnoses, lifetime mood disorders (81%) and anxiety disorders (53%) were the most prevalent. With, the exception of substance-related disorders and specific phobias, all disorders assessed were found in considerably higher frequency than in the general population, indicating that OCD is associated with highly complex comorbidity. These data have implications for genetic studies of OCD and disorders related to OCD, as well as for specific psychotherapeutic and psychopharmacologic interventions. (C) Published 2004 Wiley-Liss, Inc. C1 NIMH, Clin Sci Lab, Bethesda, MD 20892 USA. Catholic Univ Amer, Dept Psychol, Washington, DC 20064 USA. RP LaSalle, VH (reprint author), NIMH, Clin Sci Lab, 10-3D41,10 Ctr Dr,MSC 1264, Bethesda, MD 20892 USA. EM lasallev@intra.nimh.nih.gov RI Timpano, Kiara/C-8760-2012 NR 84 TC 69 Z9 70 U1 4 U2 8 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1091-4269 J9 DEPRESS ANXIETY JI Depress. Anxiety PY 2004 VL 19 IS 3 BP 163 EP 173 DI 10.1002/da.20009 PG 11 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 824DJ UT WOS:000221664200004 PM 15129418 ER PT J AU Sharan, SK Pyle, A Coppola, V Babus, J Swaminathan, S Benedict, J Swing, D Martin, BK Tessarollo, L Evans, JP Flaws, JA Handel, MA AF Sharan, SK Pyle, A Coppola, V Babus, J Swaminathan, S Benedict, J Swing, D Martin, BK Tessarollo, L Evans, JP Flaws, JA Handel, MA TI BRCA2 deficiency in mice leads to meiotic impairment and infertility SO DEVELOPMENT LA English DT Article DE BRCA2; spermatogenesis; oogenesis; meiosis; DNA repair ID BREAST-CANCER SUSCEPTIBILITY; DOUBLE-STRAND BREAKS; CHROMOSOME SYNAPSIS; DNA-REPAIR; EMBRYONIC LETHALITY; MOUSE OOCYTES; RAD51 RECOMBINATION; GENE BRCA2; MEIOSIS; PROTEIN AB The role of Brca2 in gametogenesis has been obscure because of embryonic lethality of the knockout mice. We generated Brca2-null mice carrying a human BAC with the BRCA2 gene. This construct rescues embryonic lethality and the mice develop normally. However, there is poor expression of the transgene in the gonads and the mice are infertile, allowing examination of the function of BRCA2 in gametogenesis. BRCA2-deficient spermatocytes fail to progress beyond the early prophase I stage of meiosis. Observations on localization of recombination-related and spermatogenic-related proteins suggest that the spermatocytes undergo early steps of recombination (DNA double strand break formation), but fail to complete recombination or initiate spermiogenic development. In contrast to the early meiotic prophase arrest of spermatocytes, some mutant oocytes can progress through meiotic prophase I, albeit with a high frequency of nuclear abnormalities, and can be fertilized and produce embryos. Nonetheless, there is marked depletion of germ cells in adult females. These studies provide evidence for key roles of the BRCA2 protein in mammalian gametogenesis and meiotic success. C1 NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA. Univ Tennessee, Dept Biochem & Cellular & Mol Biol, Knoxville, TN 37996 USA. Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA. Johns Hopkins Univ, Bllomberg Sch Publ Hlth, Dept Biochem & Mol Biol, Div Reprod Biol, Baltimore, MD 21205 USA. RP Sharan, SK (reprint author), NCI, Mouse Canc Genet Program, Ctr Canc Res, 1050 Boyles St, Frederick, MD 21702 USA. EM ssharan@mail.ncifcrf.gov RI Coppola, Vincenzo/E-2917-2011 OI Coppola, Vincenzo/0000-0001-6163-1779 FU NICHD NIH HHS [HD 37696, HD 33816, HD 38955] NR 52 TC 82 Z9 87 U1 0 U2 6 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0950-1991 J9 DEVELOPMENT JI Development PD JAN PY 2004 VL 131 IS 1 BP 131 EP 142 DI 10.1242/dev.00888 PG 12 WC Developmental Biology SC Developmental Biology GA 768UR UT WOS:000188553900013 PM 14660434 ER PT J AU Martin, CM Meeson, AP Robertson, SM Hawke, TJ Richardson, JA Bates, S Goetsch, SC Gallardo, TD Garry, DJ AF Martin, CM Meeson, AP Robertson, SM Hawke, TJ Richardson, JA Bates, S Goetsch, SC Gallardo, TD Garry, DJ TI Persistent expression of the ATP-binding cassette transporter, Abcg2, identifies cardiac SP cells in the developing and adult heart SO DEVELOPMENTAL BIOLOGY LA English DT Article DE ATP-binding cassette transporter; Abcg2; cardiac SP cells ID TRANSPLANTED HUMAN HEARTS; HEMATOPOIETIC STEM-CELLS; TRANSCRIPTION FACTOR; SMOOTH-MUSCLE; IN-VIVO; REGENERATION; PROGENITORS; MOUSE; MICE; HOECHST-33342 AB Stem cells are important in the maintenance and repair of adult tissues. A population of cells, termed side population (SP) cells, has stem cell characteristics as they have been shown to contribute to diverse lineages. In this study, we confirm that Abcg2 is a determinant of the SP cell phenotype. Therefore, we examined Abcg2 expression during murine embryogenesis and observed robust expression in the blood islands of the E8.5 yolk sac and in developing tissues including the heart. During the latter stages of embryogenesis, Abcg2 identifies a rare cell population in the developing organs. We further establish that the adult heart contains an Abcg2 expressing SP cell population and these progenitor cells are capable of proliferation and differentiation. We define the molecular signature of cardiac SP cells and compare it to embryonic stem cells and adult cardiomyocytes using emerging technologies. We propose that the cardiac SP cell population functions as a progenitor cell population for the development, maintenance, and repair of the heart. (C) 2003 Elsevier Inc. All rights reserved. C1 Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75390 USA. Univ Texas, SW Med Ctr, Dept Mol Biol, Dallas, TX 75390 USA. Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX 75390 USA. NIH, Bethesda, MD 20892 USA. RP Garry, DJ (reprint author), Univ Texas, SW Med Ctr, Dept Internal Med, NB11-118A,5323 Harry Hines Blvd, Dallas, TX 75390 USA. EM daniel.garry@utsouthwestern.edu OI Hawke, Thomas/0000-0003-4974-4820 FU NIAMS NIH HHS [AR47850] NR 44 TC 416 Z9 436 U1 2 U2 15 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0012-1606 EI 1095-564X J9 DEV BIOL JI Dev. Biol. PD JAN 1 PY 2004 VL 265 IS 1 BP 262 EP 275 DI 10.1016/j.ydbio.2003.09.028 PG 14 WC Developmental Biology SC Developmental Biology GA 758UW UT WOS:000187669700021 PM 14697368 ER PT J AU Moore, KB Mood, K Daar, IO Moody, SA AF Moore, KB Mood, K Daar, IO Moody, SA TI Morphogenetic movements underlying eye field formation require interactions between the FGF and ephrinB1 signaling pathways SO DEVELOPMENTAL CELL LA English DT Article ID GROWTH-FACTOR RECEPTOR-2; CENTRAL-NERVOUS-SYSTEM; XENOPUS-LAEVIS; EPH RECEPTORS; MESODERM INDUCTION; DEVELOPMENTAL EXPRESSION; TYROSINE PHOSPHORYLATION; TRANSMEMBRANE LIGANDS; CYTOPLASMIC DOMAIN; COMMISSURAL AXONS AB The definitive retinal progenitors of the eye field are specified by transcription factors that both promote a retinal fate and control cell movements that are critical for eye field formation. However, the molecular signaling pathways that regulate these movements are largely undefined. We demonstrate that both the FGF and ephrin pathways impact eye field formation. Activating the FGF pathway before gastrulation represses cellular movements in the presumptive anterior neural plate and prevents cells from expressing a retinal fate, independent of mesoderm induction or anterior-posterior patterning. Inhibiting the FGF pathway promotes cell dispersal and significantly increases eye field contribution. ephrinB1 reverse signaling is required to promote cellular movements into the eye field, and can rescue the FGF receptor-induced repression of retinal fate. These results indicate that FGF modulation of ephrin signaling regulates the positioning of retinal progenitor cells within the definitive eye field. C1 George Washington Univ, Med Ctr, Dept Anat & Cell Biol, Washington, DC 20037 USA. George Washington Univ, Med Ctr, Inst Biomed Sci, Washington, DC 20037 USA. NCI, Frederick Canc Res & Dev Ctr, Regulat & Cell Growth Lab, Frederick, MD 21702 USA. RP Moody, SA (reprint author), George Washington Univ, Med Ctr, Dept Anat & Cell Biol, Washington, DC 20037 USA. EM anasam@gwumc.edu OI Daar, Ira/0000-0003-2657-526X FU NEI NIH HHS [EY10096] NR 70 TC 67 Z9 67 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1534-5807 J9 DEV CELL JI Dev. Cell PD JAN PY 2004 VL 6 IS 1 BP 55 EP 67 DI 10.1016/S1534-5807(03)00395-2 PG 13 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA 834WX UT WOS:000222442700007 PM 14723847 ER PT J AU Hamatani, T Carter, MG Sharov, AA Ko, MSH AF Hamatani, T Carter, MG Sharov, AA Ko, MSH TI Dynamics of global gene expression changes during mouse preimplantation development SO DEVELOPMENTAL CELL LA English DT Article ID EARLY EMBRYONIC-DEVELOPMENT; GENOME ACTIVATION; DNA-REPLICATION; MICROARRAY DATA; BLASTOCYST FORMATION; PROTEIN-SYNTHESIS; ALPHA-AMANITIN; CELL; RNA; OOCYTE AB Understanding preimplantation development is important both for basic reproductive biology and for practical applications including regenerative medicine and livestock breeding. Global expression profiles revealed and characterized the distinctive patterns of maternal RNA degradation and zygotic gene activation, including two major transient waves of de novo transcription. The first wave corresponds to zygotic genome activation (ZGA); the second wave, named mid-preimplantation gene activation (MGA), precedes the dynamic morphological and functional changes from the morula to blastocyst stage. Further expression profiling of embryos treated with inhibitors of transcription, translation, and DNA replication revealed that the translation of maternal RNAs is required for the initiation of ZGA. We propose a cascade of gene activation from maternal RNA/protein sets to ZGA gene sets and thence to MGA gene sets. The large number of genes identified as involved in each phase is a first step toward analysis of the complex gene regulatory networks. C1 NIA, Genet Lab, Dev Genom & Aging Sect, NIH, Baltimore, MD 21224 USA. RP Ko, MSH (reprint author), NIA, Genet Lab, Dev Genom & Aging Sect, NIH, 333 Cassell Dr,Suite 3000, Baltimore, MD 21224 USA. EM kom@grc.nia.nih.gov RI Carter, Mark/B-5089-2010; Ko, Minoru/B-7969-2009 OI Ko, Minoru/0000-0002-3530-3015 NR 60 TC 489 Z9 506 U1 9 U2 31 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1534-5807 J9 DEV CELL JI Dev. Cell PD JAN PY 2004 VL 6 IS 1 BP 117 EP 131 DI 10.1016/S1534-5807(03)00373-3 PG 15 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA 834WX UT WOS:000222442700012 PM 14723852 ER PT J AU Hou, L Loftus, SK Incao, A Chen, A Pavan, WJ AF Hou, L Loftus, SK Incao, A Chen, A Pavan, WJ TI Complementation of melanocyte development in SOX10 mutant neural crest using lineage-directed gene transfer SO DEVELOPMENTAL DYNAMICS LA English DT Article; Proceedings Paper CT Meeting on the Neural Crest CY 2003 CL TIMBERLINE LODGE, OREGON DE transcription factor; Pax3; neurocristopathies; Waardenburg syndrome; RCAS virus; tv-a; Gateway; Sox10 ID TRANSCRIPTION FACTOR SOX10; SITE-SPECIFIC RECOMBINATION; RETROVIRAL VECTORS; HIRSCHSPRUNG-DISEASE; TRANSGENIC MICE; MOUSE MODEL; CELLS; EXPRESSION; PAX3; DIFFERENTIATION AB An in vitro gene complementation approach has been developed to dissect gene function and regulation in neural crest (NC) development and disease. The approach uses the avian RCAS virus to express genes in NC cells derived from transgenic mice expressing the RCAS receptor TVA, under the control of defined promoter elements. Constructs for creating TVA transgenic mice were developed using site-specific recombination GATEWAY (GW), compatible vectors that can also be used to facilitate analysis of genomic fragments for transcriptional regulatory elements. By using these GW vectors to facilitate cloning, transgenic mouse lines were generated that express TVA in SOX10-expressing NC stem cells under the control of the Pax3 promoter. The Pax3-tv-a transgene was bred onto a Sox10-deficient background, and the feasibility of complementing genetic NC defects was demonstrated by infecting the Pax3-tv-a cells with an RCAS-Sox10 expression virus, thereby rescuing melanocyte development of Sox10-deficient NC cells. This system will be useful for assessing genetic hierarchies in NC development. (C) 2003 Wiley-Liss, Inc. C1 NHGRI, NIH, Mouse Embryol Sect, Genet Dis Res Branch, Bethesda, MD 20892 USA. RP Pavan, WJ (reprint author), NHGRI, NIH, Mouse Embryol Sect, Genet Dis Res Branch, Room 4A82,Bldg 49,49 Convent Dr, Bethesda, MD 20892 USA. OI Hou, Ling/0000-0003-0705-8099 NR 40 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 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD JAN PY 2004 VL 229 IS 1 BP 54 EP 62 DI 10.1002/dvdy.10468 PG 9 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA 760FD UT WOS:000187800200007 PM 14699577 ER PT J AU Chapman, S Raible, D Henken, D Tosney, K AF Chapman, S Raible, D Henken, D Tosney, K TI Neural crest as a way of knowing: New perspectives on lineage and morphogenesis SO DEVELOPMENTAL DYNAMICS LA English DT Editorial Material ID CELLS C1 Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA. Univ Utah, Sch Med, Dept Neurobiol & Anat, Salt Lake City, UT USA. Univ Washington, Dept Biol Struct, Seattle, WA 98195 USA. NICHHD, NIH, Bethesda, MD 20892 USA. RP Tosney, K (reprint author), Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA. NR 5 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD JAN PY 2004 VL 229 IS 1 BP 140 EP 142 DI 10.1002/dvdy.10476 PG 3 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA 760FD UT WOS:000187800200016 PM 14699586 ER PT J AU Barlow, BK Richfield, EK Cory-Slechta, DA Thiruchelvam, M AF Barlow, BK Richfield, EK Cory-Slechta, DA Thiruchelvam, M TI A fetal risk factor for Parkinson's disease SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE maneb; paraquat; Parkinson's disease ID DOPAMINERGIC NIGROSTRIATAL SYSTEM; ETHYLENE-BIS-DITHIOCARBAMATE; TYROSINE-HYDROXYLASE; MESENCEPHALIC NEURONS; MPTP NEUROTOXICITY; PESTICIDE EXPOSURE; PRENATAL EXPOSURE; COMBINED PARAQUAT; FUNGICIDE MANEB; MARMOSET BRAIN AB A lack of strong evidence for genetic heritability of idiopathic Parkinson's disease (PD) has focused attention on environmental toxicants in the disease etiology, particularly agrichemicals. PD is associated with advanced age, but it is unclear whether specific neuronal damage could result from insults during development. This study hypothesized that prenatal exposure to pesticides would disrupt the development of the nigrostriatal dopamine (DA) system and enhance its vulnerability to dopaminergic neurotoxicant exposures later in life. Pregnant C57BL/6J mice were treated on gestational days 10-17 with saline or the pesticides maneb (MB, 1 mg/kg) or paraquat (PQ, 0.3 mg/kg). When offspring were evaluated in adulthood, there were no significant effects of prenatal MB or PQ exposure on locomotor activity. Subsequently, offspring were treated for 8 consecutive days with saline, MB (30 mg/kg), or PQ (5 mg/kg). One week after the last exposure, only males exposed to prenatal MB and adulthood PQ showed significant reductions in locomotor activity (95%) and changes in striatal neurochemistry. Stereological assessment of the substantia nigra pars compacta (SNpc) and ventral tegmental area correspondingly confirmed selective dopaminergic-neuron loss in SNpc. The lack of changes in other exposure groups suggests a specificity to the sequence of exposures as well as gender specificity. These results suggest that prenatal exposure to MB produces selective, permanent alterations of the nigrostriatal dopaminergic system and enhances adult susceptibility to PQ exposure. This study implicates a role for developmental neurotoxicant exposure in the induction of neurodegenerative disorders such as PD. Copyright (C) 2004 S. Karger AG, Basel. C1 Univ Rochester, Sch Med & Dent, Dept Pathol & Lab Med, Rochester, NY USA. Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY USA. Univ Rochester, Sch Med & Dent, NIEHS, Environm Hlth Sci Ctr, Rochester, NY USA. RP Thiruchelvam, M (reprint author), UMDNJ, Robert Wood Johnson Med Sch, Environm & Occupat Hlth Sci Inst, Dept Environm & Community Med, 170 Frelinghuysen Rd, Piscataway, NJ 08854 USA. EM mjt@eohsi.rutgers.edu FU NIEHS NIH HHS [ES11839, ES01247, ES10791] NR 86 TC 52 Z9 55 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PY 2004 VL 26 IS 1 BP 11 EP 23 DI 10.1159/000080707 PG 13 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 866BW UT WOS:000224748900002 PM 15509894 ER PT J AU Cai, JL Xue, HP Zhan, M Rao, MS AF Cai, JL Xue, HP Zhan, M Rao, MS TI Characterization of progenitor-cell-specific genes identified by subtractive suppression hybridization SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE neuroepithelial cells; stem cell; A2B5; neuroblast; glioblast; astrocyte; oligodendrocyte; bromodeoxyuridine (BrdU) ID CENTRAL-NERVOUS-SYSTEM; CHONDROITIN SULFATE PROTEOGLYCANS; NEUROEPITHELIAL STEM-CELLS; FIBRILLARY ACIDIC PROTEIN; POLYMERASE CHAIN-REACTION; MESSENGER-RNA EXPRESSION; MOLECULE TENASCIN-C; MOUSE EMBRYO CELLS; SPINAL-CORD; CYSTATIN-C AB We have utilized subtractive suppression hybridization (SSH) to identify differentially expressed genes present in either neuroepithelial (NEP) cells or glial restricted precursor (GRP) cells. Eighteen clones enriched in GRP cells and 28 in NEP cells were identified. Five of the GRP-specific clones ( tenascin C, cystatin C, GABA transporter 3, extracellular matrix molecule 2 and H2 - 4) were characterized further, and their glial specificity was confirmed by RT-PCR, in situ hybridization and immunocytochemistry. H2 - 4 ( an expressed sequence tag) was shown to be part of chondroitin sulfate proteoglycan 3. Overall, our results show that SSH can be used to identify lineage- and stage-specific markers and that extracellular matrix molecules likely play important roles in the migration and differentiation of GRPs. Copyright (C) 2004 S. Karger AG, Basel. C1 NIA, Neurosci Lab, Baltimore, MD 21224 USA. NIA, Res Resources Branch, Baltimore, MD 21224 USA. Univ Utah, Dept Neurobiol & Anat, Salt Lake City, UT USA. RP Rao, MS (reprint author), NIA, Neurosci Lab, 333 Cassell Dr,Room 406A, Baltimore, MD 21224 USA. EM raomah@grc.nia.nih.gov NR 90 TC 4 Z9 6 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PY 2004 VL 26 IS 2-4 BP 131 EP 147 DI 10.1159/000082133 PG 17 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 897BH UT WOS:000226978500006 PM 15711056 ER PT J AU Ellis, P Fagan, BM Magness, ST Hutton, S Taranova, O Hayashi, S McMahon, A Rao, M Pevny, L AF Ellis, P Fagan, BM Magness, ST Hutton, S Taranova, O Hayashi, S McMahon, A Rao, M Pevny, L TI SOX2, a persistent marker for multipotential neural stem cells derived from embryonic stem cells, the embryo or the adult SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE Sox2 gene; enhanced green fluorescent protein; neural stem cells; neurospheres ID CENTRAL-NERVOUS-SYSTEM; MAMMALIAN SPINAL-CORD; SUBVENTRICULAR ZONE; DENTATE GYRUS; TRANSCRIPTION FACTORS; NEURONAL PRECURSORS; BINDING PROTEINS; GROWTH-FACTOR; CHICKEN SOX2; IN-VIVO AB Multipotent neural stem cells are present throughout the development of the central nervous system (CNS), persist into adulthood in defined locations and can be derived from more primitive embryonic stem cells. We show that SOX2, an HMG box transcription factor, is expressed in multipotent neural stem cells at all stages of mouse ontogeny. We have generated transgenic mice expressing enhanced green fluorescent protein (EGFP) under the control of the endogenous locus-regulatory regions of the Sox2 gene to prospectively identify neural stem/progenitor cells in vivo and in vitro. Fluorescent cells coexpress SOX2 protein, and EGFP fluorescence is detected in proliferating neural progenitor cells of the entire anterior-posterior axis of the CNS from neural plate stages to adulthood. SOX2-EGFP cells can form neurospheres that can be passaged repeatedly and can differentiate into neurons, astrocytes and oligodendrocytes. Moreover, prospective clonal analysis of SOX2-EGFP-positive cells shows that all neurospheres, whether isolated from the embryonic CNS or the adult CNS, express SOX2-EGFP. In contrast, the pattern of SOX2-EGFP expression using randomly integrated Sox2 promoter/ reporter construct differs, and neurospheres are heterogeneous for EGFP expression. These studies demonstrate that SOX2 may meet the requirements of a universal neural stem cell marker and provides a means to identify cells which fulfill the basic criteria of a stem cell: self-renewal and multipotent differentiation. Copyright (C) 2004 S. Karger AG, Basel. C1 Univ N Carolina, Dept Genet, Ctr Neurosci, Chapel Hill, NC 27599 USA. Harvard Univ, Biolabs, Cambridge, MA 02138 USA. NIA, LNS, GRC, Baltimore, MD 21224 USA. Univ Sheffield, Dev Genet Program, Sheffield S10 2TN, S Yorkshire, England. RP Pevny, L (reprint author), Univ N Carolina, Dept Genet, Ctr Neurosci, 103 Mason Farm Rd, Chapel Hill, NC 27599 USA. EM larysa_pevny@med.unc.edu FU NIMH NIH HHS [MH64798-01]; NINDS NIH HHS [NS33642] NR 70 TC 329 Z9 350 U1 0 U2 17 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PY 2004 VL 26 IS 2-4 BP 148 EP 165 DI 10.1159/000082134 PG 18 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 897BH UT WOS:000226978500007 PM 15711057 ER PT J AU Brazel, CY Rosti, RT Boyce, S Rothstein, RP Levison, SW AF Brazel, CY Rosti, RT Boyce, S Rothstein, RP Levison, SW TI Perinatal hypoxia/ischemia damages and depletes progenitors from the mouse subventricular zone SO DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE caspase 3; apoptosis; stem cells; neonate brain injury; asphyxia ID HYPOXIC-ISCHEMIC INJURY; NEONATAL MICE; BRAIN-DAMAGE; CELL-DEATH; RAT AB Hypoxia-ischemia (H/I) as a result of asphyxia at term remains a major cause of neurologic disability. Our previous studies in the P7 rat model of perinatal H/I have shown that progenitors within the subventricular zone (SVZ) are vulnerable to this insult. Since many investigators are using transgenic and knockout mice to determine the importance of specific molecules in the evolution of damage after a stroke, there is a need to perform comparative studies on the relative vulnerability of the mouse SVZ. Here we assess damage to the SVZ of 5-, 7- and 10-day- old C57BL/6 mice after unilateral common carotid artery cauterization followed by 70 min of H/I (10% O-2). Whereas 5- and 7-day-old mice sustained little SVZ damage as assessed by hematoxylin and eosin staining, there was a 16% reduction of cellularity in 10-day-old animals by 18 h of recovery. Additionally, swollen cells were observed in the medial region of the SVZ of 10-day-old mice. However, few caspase-3+ and TUNEL+ cells were observed in this region, which contains the putative neural stem cells. Rather, the majority of the dying cells were situated in the mediolateral and lateral tail of the SVZ. At 18 h of recovery, there was a 2-fold increase in the frequency of TUNEL+ cells in the ipsilateral SVZ as well as a 3-fold increase in the frequency of active-caspase-3+ cells. We conclude that progenitors within the neonatal mouse SVZ are vulnerable to hypoxic/ischemic insult. The demise of these early progenitors likely leads to depletion of neuronal and late oligodendrocyte progenitors, contributing to cerebral dysgenesis. Copyright (C) 2004 S. Karger AG, Basel. C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurol & Neurosci, Newark, NJ 07103 USA. NIA, Stem Cell Biol Unit, Neurosci Lab, Gerontol Res Ctr, Baltimore, MD 21224 USA. Penn State Univ, Coll Med, Dept Neural & Behav Sci, Hershey, PA USA. Messiah Coll, Dept Biol, Grantham, PA USA. RP Levison, SW (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurol & Neurosci, 185 S Orange Ave,H-506, Newark, NJ 07103 USA. EM levisosw@umdnj.edu OI Levison, Steven/0000-0002-1264-7309 FU NIMH NIH HHS [R01 MH059950] NR 18 TC 35 Z9 37 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0378-5866 J9 DEV NEUROSCI-BASEL JI Dev. Neurosci. PY 2004 VL 26 IS 2-4 BP 266 EP 274 DI 10.1159/000082143 PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 897BH UT WOS:000226978500016 PM 15711066 ER PT J AU Nadler, JL AF Nadler, JL TI A now dietary approach, to reduce the risk of type 2 diabetes? SO DIABETES CARE LA English DT Editorial Material ID MAGNESIUM SUPPLEMENTATION; INSULIN-RESISTANCE; CARDIOVASCULAR-DISEASE; HYPERTENSION; DEFICIENCY; SERUM; RATS C1 Univ Virginia Hlth Syst, Div Endocrinol & Metab, Charlottesville, VA 22908 USA. NIH, DK 63609, Diabet & Endocrinol Res Ctr, Charlottesville, VA USA. RP Nadler, JL (reprint author), Univ Virginia Hlth Syst, Div Endocrinol & Metab, POB 801405,450 Ray C Hunt dr, Charlottesville, VA 22908 USA. NR 21 TC 3 Z9 3 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JAN PY 2004 VL 27 IS 1 BP 270 EP 271 DI 10.2337/diacare.27.1.270 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 758JX UT WOS:000187632200045 PM 14694000 ER PT J AU Sanchez-Corona, J Flores-Martinez, SE Machorro-Lazo, MV Galaviz-Hernandez, C Moran-Moguel, MC Perea, FJ Mujica-Lopez, KI Vargas-Ancona, L Laviada-Molina, HA Fernandez, V Pardio, J Arroyo, P Barrera, H Hanson, RL AF Sanchez-Corona, J Flores-Martinez, SE Machorro-Lazo, MV Galaviz-Hernandez, C Moran-Moguel, MC Perea, FJ Mujica-Lopez, KI Vargas-Ancona, L Laviada-Molina, HA Fernandez, V Pardio, J Arroyo, P Barrera, H Hanson, RL TI Polymorphisms in candidate genes for type 2 diabetes mellitus in a Mexican population with metabolic syndrome findings SO DIABETES RESEARCH AND CLINICAL PRACTICE LA English DT Article DE metabolic syndrome; genetics; type 2 diabetes mellitus; candidate genes; insulin ID INSULIN-RECEPTOR SUBSTRATE-1; 5' FLANKING REGION; RESISTANCE; OBESITY; NIDDM; VARIANTS; LOCUS; SUSCEPTIBILITY; HYPERTENSION; ASSOCIATION AB The metabolic or insulin resistance syndrome, characterized by hypertension, dyslipidemia, glucose intolerance and hyperinsulinemia, may have genetic determinants. The insulin gene (INS), insulin receptor gene (INSR) and insulin receptor substrate 1 gene (IRS1) have been proposed as candidate genes. We examined eight polymorphisms in these genes in 163 individuals from Yucatan, Mexico; this population has a high prevalence of obesity, type 2 diabetes mellitus and dyslipidemia. Subjects were evaluated for body mass index (BMI) and blood pressure. Blood samples were collected to determine glucose, insulin, triglycerides and cholesterol levels, as well as for DNA isolation. Restriction fragment length polymorphisms in INS, INSR and IRS1 were identified by polymerase chain reaction and digestion with selected restriction enzymes. Among the eight polymorphisms analyzed, the PstI polymorphism in INS was significantly associated with hypertriglyceridemia and with the presence of at least one abnormality related to the metabolic syndrome (P = 0.007 and 0.004, respectively). The MaeIII polymorphism in INS was associated with fasting hyperinsulinemia (P = 0.045). In multilocus analyses including both INS polymorphisms, significant associations were seen with hypertriglyceridemia (P = 0.006), hypercholesterolemia (P = 0.031) and with presence of at least one metabolic abnormality (P = 0.009). None of the polymorphisms in INSR or IRS1 was associated with any of these traits. These findings suggest that the insulin gene may be an important determinant of metabolic syndrome, and particularly of dyslipidemia, in this population. (C) 2003 Elsevier Ireland Ltd. All rights reserved. C1 IMSS, Ctr Invest Biomed Occidente, Div Mol Med, Guadalajara 44340, Jalisco, Mexico. Fdn Mexicana Salud, Mexico City, DF, Mexico. Univ Autonoma Nuevo Leon, Fac Med, Monterrey, Nuevo Leon, Mexico. NIDDKD, Diabet & Arthrit Epidemiol Sect, Phoenix, AZ 85016 USA. RP Sanchez-Corona, J (reprint author), IMSS, Ctr Invest Biomed Occidente, Div Mol Med, Sierra Mojada 800,Col Independencia, Guadalajara 44340, Jalisco, Mexico. EM josancomx@yahoo.com.mx NR 51 TC 21 Z9 23 U1 0 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0168-8227 J9 DIABETES RES CLIN PR JI Diabetes Res. Clin. Pract. PD JAN PY 2004 VL 63 IS 1 BP 47 EP 55 DI 10.1016/j.diabres.2003.08.004 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 764QW UT WOS:000188218400006 PM 14693412 ER PT J AU Kubosaki, A Miura, J Notkins, AL AF Kubosaki, A Miura, J Notkins, AL TI IA-2 is not required for the development of diabetes in NOD mice SO DIABETOLOGIA LA English DT Letter ID PROTEIN-TYROSINE-PHOSPHATASE; INSULIN; DECARBOXYLASE; AUTOANTIGENS; LESSONS C1 NIDCR, Expt Med Sect, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA. RP Notkins, AL (reprint author), NIDCR, Expt Med Sect, Oral Infect & Immun Branch, NIH, Bldg 30,Room 121,30 Convent Dr,MSC 4322, Bethesda, MD 20892 USA. EM anotkins@mail.nih.gov NR 9 TC 28 Z9 29 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 2004 VL 47 IS 1 BP 149 EP 150 DI 10.1007/s00125-003-1252-z PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 770WA UT WOS:000188753300025 PM 14614561 ER PT J AU Layfield, LJ Elsheikh, TM Fili, A Nayar, R Shidham, V AF Layfield, LJ Elsheikh, TM Fili, A Nayar, R Shidham, V TI Review of the State of the Art and Recommendations of the Papanicolaou Society of Cytopathology for Urinary Cytology Procedures and Reporting - The Papanicolaou Society of Cytopathology Practice Guidelines Task Force SO DIAGNOSTIC CYTOPATHOLOGY LA English DT Article ID IN-SITU HYBRIDIZATION; WORLD-HEALTH-ORGANIZATION; TRANSITIONAL-CELL CARCINOMA; SUPERFICIAL BLADDER-CANCER; COMPLEMENT FACTOR-H; INTERNATIONAL-SOCIETY; UROTHELIAL CARCINOMA; VOIDED URINE; FOLLOW-UP; BTA TEST C1 Univ Utah, Sch Med, Salt Lake City, UT 84132 USA. Ball Mem Hosp Pathologists Associated, Dept Pathol, Muncie, IN USA. NIH, Ctr Clin, Bethesda, MD 20892 USA. Northwestern Univ, Feinberg Sch Med, Dept Pathol, Chicago, IL 60611 USA. Med Coll Wisconsin, Dept Pathol, Milwaukee, WI 53226 USA. RP Layfield, LJ (reprint author), Univ Utah, Sch Med, 50 N Med Dr, Salt Lake City, UT 84132 USA. NR 63 TC 40 Z9 42 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 8755-1039 J9 DIAGN CYTOPATHOL JI Diagn. Cytopathol. PD JAN PY 2004 VL 30 IS 1 BP 24 EP 30 DI 10.1002/dc.10401 PG 7 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA 760FB UT WOS:000187800000005 PM 14696141 ER PT J AU Husgafvel-Pursiainen, K Hayes, RB Vainio, H AF Husgafvel-Pursiainen, K Hayes, RB Vainio, H TI ICT X Satellite Meeting on Molecular Epidemiology - Linking Toxicology to Epidemiology - Biomarkers and New Technologies - Haikko, Porvoo, Finland, 8-10 July 2004 - Foreword SO DISEASE MARKERS LA English DT Editorial Material C1 Finnish Inst Occupat Hlth, Dept Ind Hyg & Toxicol, Helsinki, Finland. NCI, Div Canc Epidemiol & Genet, Occupat & Environm Epidemiol Branch, NIH, Bethesda, MD 20892 USA. RP Husgafvel-Pursiainen, K (reprint author), Finnish Inst Occupat Hlth, Dept Ind Hyg & Toxicol, Helsinki, Finland. NR 0 TC 0 Z9 0 U1 0 U2 0 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0278-0240 J9 DIS MARKERS JI Dis. Markers PY 2004 VL 20 IS 1 BP 1 EP 2 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental; Pathology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine; Pathology GA 837UH UT WOS:000222665900001 ER PT J AU Conley, BA Taube, SE AF Conley, BA Taube, SE TI Prognostic and predictive markers in cancer SO DISEASE MARKERS LA English DT Article ID NEGATIVE BREAST-CANCER; ADJUVANT CHEMOTHERAPY TRIAL; ENDOTHELIAL GROWTH-FACTOR; COLON-CANCER; MICROSATELLITE-INSTABILITY; COLORECTAL-CANCER; CLINICALLY USEFUL; UROKINASE-TYPE; RECTAL-CANCER; TUMOR-MARKER AB The elucidation of the human genome and advances in knowledge about molecular abnormalities, signaling pathways, influence of the local tissue milieu and the relevance of genetic polymorphisms offer hope of designing more effective, individualized cancer treatment plans. Although the scientific and medical literature is replete with reports of putative prognostic or predictive markers for cancer, few new diagnostics have been incorporated into routine clinical practice. Criteria are needed to a) identify markers that have the promise to be clinically useful; b) assess the best methodology for clinical evaluation of the markers in question and c) confirm or validate that using the marker adds useful information compared to using standard prognostic factors alone. This review presents a methodology for the clinical evaluation of putative prognostic and predictive markers in cancer, with considerations of pitfalls in the early evaluation, rationale for development and optimization of assay methodology, and examples of possible clinical trials for assessing the clinical utility of putative markers. C1 NCI, Aerodigest Canc Clin Res Sect, Med Oncol Clin Res Unit, Canc Res Ctr,DHHS,NIH, Bethesda, MD 20892 USA. NCI, Canc Diagnosis Program, Div Canc Treatment & Diagnosis, DHHS,NIH, Bethesda, MD 20892 USA. RP Conley, BA (reprint author), NCI, Aerodigest Canc Clin Res Sect, Med Oncol Clin Res Unit, Canc Res Ctr,DHHS,NIH, 10 Ctr Dr,Room 12C103A, Bethesda, MD 20892 USA. EM conleyb@mail.nih.gov NR 39 TC 31 Z9 32 U1 0 U2 1 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0278-0240 J9 DIS MARKERS JI Dis. Markers PY 2004 VL 20 IS 2 BP 35 EP 43 PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental; Pathology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine; Pathology GA 852EW UT WOS:000223739000001 PM 15322312 ER PT J AU Vourlekis, JS Szabo, E AF Vourlekis, JS Szabo, E TI Use of markers for the detection and treatment of lung cancer SO DISEASE MARKERS LA English DT Review ID GROWTH-FACTOR RECEPTOR; CARCINOMA IN-SITU; ABERRANT PROMOTER METHYLATION; HOGG1 SER326CYS POLYMORPHISM; ARYL-HYDROCARBON HYDROXYLASE; SQUAMOUS-CELL CARCINOMA; IGF-BINDING PROTEIN-3; DNA-REPAIR CAPACITY; LONG-TERM SURVIVAL; OF-THE-LITERATURE AB The unacceptably high morbidity and mortality associated with the diagnosis of lung cancer mandates new approaches toward the early detection and treatment of this disease. Enhanced understanding of the molecular biology of the carcinogenic process is identifying many potential markers of risk of lung cancer occurrence as well as of poor prognosis. Identification of high risk populations who are at greatest risk of being diagnosed with and dying from lung cancer would allow delivery of more intensive screening and interventions to the individuals who are most likely to benefit from such strategies. This review examines the current status of markers of lung cancer risk, early detection, and prognosis, and their applicability to current standards of clinical care. C1 NCI, Lung & Upper Aerodigest Canc Res Grp, Div Canc Prevent, Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA. RP Szabo, E (reprint author), NCI, Lung & Upper Aerodigest Canc Res Grp, Div Canc Prevent, Dept Hlth & Human Serv,NIH, 6130 Execut Blvd,Rm 2132, Bethesda, MD 20892 USA. EM szaboe@mail.nih.gov NR 154 TC 3 Z9 3 U1 0 U2 0 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0278-0240 J9 DIS MARKERS JI Dis. Markers PY 2004 VL 20 IS 2 BP 71 EP 85 PG 15 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental; Pathology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine; Pathology GA 852EW UT WOS:000223739000004 PM 15322315 ER PT J AU Umar, A Srivastava, S AF Umar, A Srivastava, S TI The promise of biomarkers in colorectal cancer detection SO DISEASE MARKERS LA English DT Article ID MISMATCH REPAIR; MICROSATELLITE INSTABILITY; HYPERPLASTIC POLYPS; DNA-REPLICATION; OVARIAN-CANCER; COLON-CANCER; LUNG-CANCER; CARCINOMA; CHEMOPREVENTION; MARKERS C1 NCI, Div Canc Prevent, Gastrointestinal & Other Canc Res Grp, Rockville, MD 20852 USA. NCI, Div Canc Prevent, Canc Biomarkers Res Grp, Rockville, MD 20852 USA. RP Umar, A (reprint author), NCI, Div Canc Prevent, Gastrointestinal & Other Canc Res Grp, 6130 Execut Blvd,EPN 2143, Rockville, MD 20852 USA. NR 65 TC 9 Z9 9 U1 0 U2 0 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0278-0240 J9 DIS MARKERS JI Dis. Markers PY 2004 VL 20 IS 2 BP 87 EP 96 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental; Pathology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine; Pathology GA 852EW UT WOS:000223739000005 PM 15322316 ER PT J AU Baker, SG Kramer, BS Prorok, PC AF Baker, SG Kramer, BS Prorok, PC TI Development tracks for cancer prevention markers SO DISEASE MARKERS LA English DT Article ID SURROGATE END-POINTS; EARLY INTERVENTION; BREAST-CANCER; MORTALITY; TRIALS; VALIDATION; IMPACT AB We provide a general framework for describing various roles for biomarkers in cancer prevention research (early detection, surrogate endpoint, and cohort identification for primary prevention) and the phases in their evaluation. C1 NCI, Biometry Res Grp, Div Canc Prevent, Bethesda, MD 20892 USA. NIH, Off Dis Prevent, Bethesda, MD 20892 USA. RP Baker, SG (reprint author), NCI, Biometry Res Grp, Div Canc Prevent, EPN 3131,6130 Execut Blvd,MSC 7354, Bethesda, MD 20892 USA. EM sb16i@nih.gov NR 25 TC 10 Z9 10 U1 0 U2 0 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0278-0240 J9 DIS MARKERS JI Dis. Markers PY 2004 VL 20 IS 2 BP 97 EP 102 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental; Pathology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine; Pathology GA 852EW UT WOS:000223739000006 PM 15322317 ER PT J AU Umar, A AF Umar, A TI Lynch syndrome (HNPCC) and microsatellite instability SO DISEASE MARKERS LA English DT Editorial Material ID NONPOLYPOSIS COLORECTAL-CANCER; BETHESDA GUIDELINES; MISMATCH REPAIR; CARCINOMA; CLUES C1 NCI, Gastrointestinal & Other Canc Res Grp, Div Canc Prevent, EPN, Bethesda, MD 20892 USA. RP Umar, A (reprint author), NCI, Gastrointestinal & Other Canc Res Grp, Div Canc Prevent, EPN, Suite 2141,6130 Execut Blvd, Bethesda, MD 20892 USA. NR 18 TC 11 Z9 13 U1 0 U2 0 PU IOS PRESS PI AMSTERDAM PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS SN 0278-0240 J9 DIS MARKERS JI Dis. Markers PY 2004 VL 20 IS 4-5 BP 179 EP 180 PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental; Pathology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine; Pathology GA 893XZ UT WOS:000226755700001 PM 15528783 ER PT S AU Bebenek, K Kunkel, TA AF Bebenek, K Kunkel, TA BE Yang, W TI Functions of DNA polymerases SO DNA REPAIR AND REPLICATION SE ADVANCES IN PROTEIN CHEMISTRY LA English DT Review ID STRAND BREAK REPAIR; BASE EXCISION-REPAIR; PHOSPHATE LYASE ACTIVITY; SYN THYMINE DIMER; MU POL-MU; SACCHAROMYCES-CEREVISIAE; ERROR-PRONE; CRYSTAL-STRUCTURE; ESCHERICHIA-COLI; IN-VITRO C1 NIEHS, Genet Mol Lab, Res Triangle Pk, NC 27709 USA. NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. RP Bebenek, K (reprint author), NIEHS, Genet Mol Lab, POB 12233, Res Triangle Pk, NC 27709 USA. NR 110 TC 179 Z9 181 U1 0 U2 7 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0065-3233 BN 0-12-034269-3 J9 ADV PROTEIN CHEM JI Adv.Protein Chem. PY 2004 VL 69 BP 137 EP 165 PG 29 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BBU72 UT WOS:000227918600005 PM 15588842 ER PT J AU Vaisman, A Lehmann, AR Woodgate, R AF Vaisman, A Lehmann, AR Woodgate, R TI DNA polymerases eta and iota SO DNA REPAIR AND REPLICATION SE ADVANCES IN PROTEIN CHEMISTRY LA English DT Review ID PIGMENTOSUM VARIANT CELLS; THYMINE-THYMINE DIMER; ESCHERICHIA-COLI DINB; XERODERMA-PIGMENTOSUM; ERROR-PRONE; SACCHAROMYCES-CEREVISIAE; TRANSLESION SYNTHESIS; LESION-BYPASS; Y-FAMILY; LOW-FIDELITY C1 NICHHD, Lab Genom Integr, NIH, Bethesda, MD 20892 USA. Univ Sussex, Genome Damage & Stabil Ctr, Brighton BN1 9RQ, E Sussex, England. RP Vaisman, A (reprint author), NICHHD, Lab Genom Integr, NIH, Bethesda, MD 20892 USA. NR 103 TC 26 Z9 27 U1 0 U2 1 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0065-3233 J9 ADV PROTEIN CHEM JI Adv.Protein Chem. PY 2004 VL 69 BP 205 EP 228 PG 24 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BBU72 UT WOS:000227918600007 PM 15588844 ER PT S AU Mao, S Kim, JW Thoma, GR AF Mao, S Kim, JW Thoma, GR BE Smith, EHB Hu, J Allan, J TI Style-independent document labeling: Design and performance evaluation SO DOCUMENT REGOGNITION AND RETRIEVAL XI SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Document Recognition and Retrieval XI CY JAN 21-22, 2004 CL San Jose, CA SP Soc Imaging Sci & Technol, SPIE DE style independent labeling; string matching; clustering; quantitative performance evaluation; metric; geometric and non-geometric features AB The Medical Article Records System or MARS has been developed at the U.S. National Library of Medicine (NLM) for automated data entry of bibliographical information from medical journals into MEDLINE(R), the premier bibliographic citation database at NLM. Currently, a rule-based algorithm (called ZoneCzar) is used for labeling important bibliographical fields (title, author, affiliation, and abstract) on medical journal article page images. While rules have been created for medical journals with regular layout types, new rules have to be manually created for any input journals with arbitrary or new layout types. Therefore, it is of interest to label any journal articles independent of their layout styles. In this paper, we first describe a system (called ZoneMatch) for automated generation of crucial geometric and non-geometric features of important bibliographical fields based on string-matching and clustering techniques. The rule-based algorithm is then modified to use these features to perform style-independent labeling. We then describe a performance evaluation method for quantitatively evaluating our algorithm and characterizing its error distributions. Experimental results show that the labeling performance of the rule-based algorithm is significantly improved when the generated features are used. C1 Natl Lib Med, Bethesda, MD 20894 USA. RP Mao, S (reprint author), Natl Lib Med, Bethesda, MD 20894 USA. NR 10 TC 0 Z9 0 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 0-8194-5199-1 J9 P SOC PHOTO-OPT INS PY 2004 VL 5296 BP 14 EP 22 PG 9 WC Computer Science, Artificial Intelligence; Imaging Science & Photographic Technology SC Computer Science; Imaging Science & Photographic Technology GA BY62S UT WOS:000189424500003 ER PT J AU Berger, VW AF Berger, VW TI Selection bias and baseline imbalances in randomized trials SO DRUG INFORMATION JOURNAL LA English DT Letter ID BALANCE C1 NCI, EPN, Bethesda, MD 20892 USA. Univ Maryland Baltimore Cty, Dept Math & Stat, Baltimore, MD 21228 USA. RP Berger, VW (reprint author), NCI, EPN, Suite 3131,6130 Execut Blvd,MSC-7354, Bethesda, MD 20892 USA. EM vb78c@nih.gov NR 4 TC 11 Z9 11 U1 0 U2 2 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. PY 2004 VL 38 IS 1 BP 1 EP 2 PG 2 WC Health Care Sciences & Services; Pharmacology & Pharmacy SC Health Care Sciences & Services; Pharmacology & Pharmacy GA 774CD UT WOS:000188961400001 ER PT J AU Knoben, JE Phillips, SJ Szczur, MR AF Knoben, JE Phillips, SJ Szczur, MR TI The National Library of Medicine and drug information. Part 1: Present resources SO DRUG INFORMATION JOURNAL LA English DT Article DE drug information; National Library of Medicine; Internet AB The National Library of Medicine began in 1836 as a small collection of books in the office of the Army Surgeon General. Today, the National Library of Medicine is the world's largest medical library, providing access to its vast collection of seven million items onsite and through the World Wide Web. Historical interest in drug information dates to 1967, when Congress provided funds for a Drug Literature Program at the National Library of Medicine. Drug information is now dispersed among a number of National Library of Medicine bibliographic and factual databases that offer an array of clinical, research, and toxicological drug data. Target audiences for drug information include consumers, patients, healthcare practitioners, clinical researchers and scientists. Drug development and medical publishing have both accelerated to such an extent that it is virtually impossible for healthcare practitioners and researchers to keep apprised of current information. Due to wide utilization for posting medically-related data, the Internet is discussed in terms of its impact on medical library responsibilities, the need to preserve clinical and scientific information in the public domain, and how such imperatives indicate a need to create new drug-related databases, including an Internet portal to drug information. C1 NIH, Specialized Informat Serv, Natl Lib Med, Bethesda, MD 20892 USA. RP Knoben, JE (reprint author), NIH, Specialized Informat Serv, Natl Lib Med, 6707 Democracy Blvd,Suite 510, Bethesda, MD 20892 USA. EM knobenj@mail.nlm.nih.gov NR 7 TC 4 Z9 4 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. PY 2004 VL 38 IS 1 BP 69 EP 81 PG 13 WC Health Care Sciences & Services; Pharmacology & Pharmacy SC Health Care Sciences & Services; Pharmacology & Pharmacy GA 774CD UT WOS:000188961400010 ER PT J AU Knoben, JE Phillips, SJ Snyder, JW Szczur, MR AF Knoben, JE Phillips, SJ Snyder, JW Szczur, MR TI The national library of medicine and drug information. Part 2: An evolving future SO DRUG INFORMATION JOURNAL LA English DT Article DE drug information; National Library of Medicine; Internet ID HEALTH INFORMATION; QUALITY ISSUES; WEB SITES; INTERNET AB The National Library of Medicine (NLM) began in 1836 as a small collection of books in the office of the Army Surgeon General. Today, the NLM is the world's largest medical library, providing access to its vast collection of seven million items onsite and through the World Wide Web. Historical interest in drug information dates to 1967, when Congress provided funds for a Drug Literature Program at the NLM. Drug information is now dispersed among a number of NLM bibliographic and factual databases that offer an array of clinical, research, and toxicological drug data. Target audiences for drug information include consumers, patients, healthcare practitioners, clinical researchers, and scientists. Drug development and medical publishing have both accelerated to such an extent that it is virtually impossible for healthcare practitioners and researchers to keep apprised of cut-rent information. Due to wide utilization for posting medically-related data, the Internet is discussed in terms of its impact on medical library responsibilities, drug information and efforts to evaluate Web-based health information, and how resultant imperatives indicate a need to create new drug-related databases including an Internet portal to drug information. C1 NIH, Natl Lib Med, Specialized Informat Serv, Bethesda, MD 20892 USA. RP Knoben, JE (reprint author), NIH, Natl Lib Med, Specialized Informat Serv, 6707 Democracy Blvd,Suite 510, Bethesda, MD 20892 USA. EM knobenj@mail.nlm.nih.gov NR 32 TC 5 Z9 5 U1 1 U2 1 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. PY 2004 VL 38 IS 2 BP 171 EP 180 PG 10 WC Health Care Sciences & Services; Pharmacology & Pharmacy SC Health Care Sciences & Services; Pharmacology & Pharmacy GA 819WU UT WOS:000221347700010 ER PT J AU Frattarelli, DAC Reed, MD Giacoia, GP Aranda, JV AF Frattarelli, DAC Reed, MD Giacoia, GP Aranda, JV TI Antifungals in systemic neonatal candidiasis SO DRUGS LA English DT Review ID LOW-BIRTH-WEIGHT; LIPOSOMAL AMPHOTERICIN-B; INTENSIVE-CARE-UNIT; DISSEMINATED FUNGAL-INFECTIONS; INVASIVE CANDIDIASIS; RISK-FACTORS; CLINICAL MANIFESTATIONS; PEDIATRIC-PATIENTS; PREMATURE NEONATE; ORAL FLUCONAZOLE AB Fungal infections are common in the newborn period, especially among premature neonates, and are responsible for considerable morbidity and mortality. Currently, three classes of antifungals are commonly used in the treatment of systemic fungal infections in neonates: the polyene macrolides (e.g. amphotericin B [deoxycholate and lipid preparations]); the azoles (e.g. fluconazole); and the fluorinated pyrimidines (e.g. flucytosine). The echinocandins (e.g. caspofungin and micafungin) are a newer class of antifungals which shows promise in this population. The available kinetic data on amphotericin B deoxycholate in neonates are derived from very small studies and exhibit considerable variability. There are no kinetic data available for the use of lipid preparations in this population and, again, much has been inferred from adult studies. The information available for flucytosine is also limited but appears similar to what is observed in adults. Fluconazole has the most neonatal pharmacokinetic data, which show slightly less variability than the other antifungals. Genomic factors which affect the metabolism of amphotericin B and fluconazole may explain some of the observed variability. Most of the data for the efficacy of antifungal drugs in neonates are derived from retrospective studies and case reports. The data for amphotericin B deoxycholate and flucytosine are limited. There are more data for the liposomal and lipid complex preparations of amphotericin B and for fluconazole in this population. These support the use of these drugs in neonates, but because of their largely noncomparative nature they can not define the optimal dosage or duration of therapy. Amphotericin B deoxycholate is primarily nephrotoxic. It also induces electrolyte abnormalities and is to a lesser degree cardiotoxic. This toxicity in neonates appears similar to published data in older children and adults. While the lipid preparations of amphotericin B owe their existence to a presumed decrease in toxicity, the observed toxicity in neonates appears to be equal to that seen with the deoxycholate, although it should be noted that the lipid preparations are usually given at much higher dosages. Fluconazole toxicity appears to be milder and less frequent in this population than is seen with amphotericin B. In the final analysis, we do not have sufficient data to define the pharmacokinetic profiles, optimal dose or duration of therapy, or toxicity for any of these compounds in neonates. Further studies are necessary if the optimisation of antifungal therapy in this population is to continue. C1 Wayne State Univ, Childrens Hosp Michigan, Sch Med, Div Clin Pharmacol, Detroit, MI 48201 USA. Rainbow Babies & Childrens Hosp, Div Pediat Pharmacol & Crit Care, Cleveland, OH 44106 USA. NICHD, Dev Pediat Pharmacol Program, Pediat Pharmacol Res Unit Network, NIH, Rockville, MD USA. RP Frattarelli, DAC (reprint author), Wayne State Univ, Childrens Hosp Michigan, Sch Med, Div Clin Pharmacol, 3901 Beaubien, Detroit, MI 48201 USA. EM dfrattar@med.wayne.edu NR 127 TC 48 Z9 52 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 2004 VL 64 IS 9 BP 949 EP 968 DI 10.2165/00003495-200464090-00003 PG 20 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 820MJ UT WOS:000221393100003 PM 15101785 ER PT J AU Gorelick, DA Gardner, EL Xi, ZX AF Gorelick, DA Gardner, EL Xi, ZX TI Agents in development for the management of cocaine abuse SO DRUGS LA English DT Review ID CONDITIONED PLACE PREFERENCE; CORTICOTROPIN-RELEASING-FACTOR; GAMMA-VINYL-GABA; DOPAMINE TRANSPORTER OCCUPANCY; PROGRESSIVE RATIO SCHEDULE; RECEPTOR AGONIST LY379268; BRAIN-STIMULATION REWARD; STRESS-INDUCED RELAPSE; DRUG-SEEKING BEHAVIOR; CCK-B RECEPTOR AB Cocaine abuse is a serious health problem in many areas of the world, yet there are no proven effective medications for the treatment of cocaine dependence. Preclinical studies suggest that the reinforcing effect of cocaine that promotes its abuse is mediated by blockade of the presynaptic dopamine transporter. This results in increased dopamine activity in the mesolimbic or meso-accumbens dopamine reward system of brain. Development of new medications to treat cocaine dependence has focused on manipulation of this dopamine system, either by direct action on dopamine binding sites (transporter or receptors) or indirectly by affecting other neurotransmitter systems that modulate the dopamine system. In principle, a medication could act via one of three mechanisms: (i) as a substitute for cocaine by producing similar dopamine effects; (ii) as a cocaine antagonist by blocking the binding of cocaine to the dopamine transporter; or (iii) as a modulator of cocaine effects by acting at other than the cocaine binding site. The US National Institute on Drug Abuse has a Clinical Research Efficacy Screening Trial (CREST) programme to rapidly screen existing medications. CREST identified four medications warranting phase II controlled clinical trials: cabergoline, reserpine, sertraline and tiagabine. In addition, disulfiram and selegiline (deprenyl) have been effective and well tolerated in phase II trials. However, selegiline was found ineffective in a recent phase III trial. Promising existing medications probably act via the first or third aforementioned mechanisms. Sustained-release formulations of stimulants such as methylphenidate and amfetamine (amphetamine) have shown promise in a stimulant substitution approach. Disulfiram and selegiline increase brain dopamine concentrations by inhibition of dopamine-catabolising enzymes (dopamine-p-hydroxylase and monoamine oxidase B, respectively). Cabergoline is a direct dopamine receptor agonist, while reserpine depletes presynaptic stores of dopamine (as well as norepinephrine and serotonin). Sertraline, baclofen and vigabatrin indirectly reduce dopamine activity by increasing activity of neurotransmitters (serotonin and GABA) that inhibit dopamine activity. Promising new medications act via the second or third aforementioned mechanisms. Vanoxerine is a long-acting inhibitor of the dopamine transporter which blocks cocaine binding and reduces cocaine self-administration in animals. Two dopamine receptor ligands that reduce cocaine self-administration in animals are also undergoing phase I human safety trials. Adrogolide is a selective dopamine D(1) receptor agonist; BP 897 is a D(3) receptor partial agonist. A pharmacokinetic approach to treatment would block the entry of cocaine into the brain or enhance its catabolism so that less cocaine reached its site of action. This is being explored in animals using the natural cocaine-metabolising enzyme butyrylcholinesterase (or recombinant versions with enhanced capabilities), catalytic antibodies, and passive or active immunisation to produce anti-cocaine binding antibodies. A recent phase I trial of a 'cocaine vaccine' found it to be well tolerated and producing detectable levels of anti-cocaine antibodies for up to 9 months after immunisation. C1 NIDA, Intramural Res Program, NIH, Dept Hlth & Human Serv, Baltimore, MD USA. RP Gorelick, DA (reprint author), 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM dgorelic@intra.nida.nih.gov NR 252 TC 128 Z9 129 U1 1 U2 9 PU ADIS INT LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 1311, NEW ZEALAND SN 0012-6667 J9 DRUGS JI Drugs PY 2004 VL 64 IS 14 BP 1547 EP 1573 DI 10.2165/00003495-200464140-00004 PG 27 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 841MA UT WOS:000222933000004 PM 15233592 ER PT J AU Boucher, HW Groll, AH Chiou, CC Walsh, TJ AF Boucher, HW Groll, AH Chiou, CC Walsh, TJ TI Newer systemic antifungal agents - Pharmacokinetics, safety and efficacy SO DRUGS LA English DT Review ID IN-VITRO ACTIVITIES; EXPERIMENTAL PULMONARY ASPERGILLOSIS; INVASIVE FUNGAL-INFECTIONS; LIPOSOMAL AMPHOTERICIN-B; GUINEA-PIG MODEL; PERSISTENTLY NEUTROPENIC RABBITS; ANTIMICROBIAL SURVEILLANCE PROGRAM; CLINICALLY IMPORTANT MOLDS; SCEDOSPORIUM-APIOSPERMUM; VORICONAZOLE UK-109,496 AB The past few years have seen the advent of several new antifungal agents, including those of a new class and a new generation of an existing class. Caspofungin, the first available echinocandin, has greatly expanded the antifungal armamentarium by providing a cell wall-active agent with candidacidal activity as well as demonstrated clinical efficacy in the therapy of aspergillosis refractory to available therapy. In addition, in clinical trials, caspofungin had comparable efficacy to amphotericin B for candidaemia and invasive Candida infections. Caspofungin and two more recently introduced echinocandins, micafungin and anidulafungin, are available as intravenous formulations only and characterised by potent anti-candidal activity, as well as few adverse events and drug interactions. Voriconazole, the first available second-generation triazole, available in both intravenous and oral formulations, has added a new and improved therapeutic option for primary therapy of invasive aspergillosis and salvage therapy for yeasts and other moulds. In a randomised trial, voriconazole demonstrated superior efficacy and a survival benefit compared with amphotericin B followed by other licensed antifungal therapy. This and data from a noncomparative study led to voriconazole becoming a new standard of therapy for invasive aspergillosis. Voriconazole has several important safety issues, including visual adverse events, hepatic enzyme elevation and skin reactions, as well as a number of drug interactions. Posaconazoie, only available orally and requiring dose administration four times daily, shows encouraging efficacy in difficult to treat infections due to zygomycetes. Ravuconazole, available in both intravenous and oral formulations, has broad-spectrum in vitro potency and in vivo efficacy against a wide range of fungal pathogens. Clinical studies are underway. Despite the advances offered with each of these drugs, the morbidity and mortality associated with invasive fungal infections remains unacceptable, especially for the most at-risk patients. For individuals with severe immunosuppression as a result of chemotherapy, graft-versus-host disease and its therapy, or transplantation, new drugs and strategies are greatly needed. C1 NCI, Immunocompromised Host Sect, Pediat Oncol Branch, Bethesda, MD 20892 USA. Tufts Univ, New England Med Ctr, Div Geog Med & Infect Dis, Boston, MA 02111 USA. RP Walsh, TJ (reprint author), NCI, Immunocompromised Host Sect, Pediat Oncol Branch, Bldg 10,Room 13N-240, Bethesda, MD 20892 USA. NR 198 TC 174 Z9 196 U1 2 U2 17 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 2004 VL 64 IS 18 BP 1997 EP 2020 DI 10.2165/00003495-200464180-00001 PG 24 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA 858CB UT WOS:000224166700001 PM 15341494 ER PT J CA NICHD Early Child Care Res Network TI Type of child care and children's development at 54 months SO EARLY CHILDHOOD RESEARCH QUARTERLY LA English DT Article DE child care; development; care setting ID NONMATERNAL CARE; FAMILY SELECTION; TIME SPENT; HOME CARE; EXPERIENCES; OUTCOMES; QUALITY; INCOME; CHOICE; AGE AB The types of non-maternal child care received by more than 1000 U.S. children were examined from birth to 54 months and related to family selection factors and to child outcomes. Individual children tended to experience a variety of different types of care and not to fit into clear patterns of either stable care types or progressive patterns of movement from less structured to more highly structured care settings. Across the entire sample, however, hours in center care were higher in the preschool period than earlier, whereas hours in relative care remained stable and hours in child care homes decreased. Mothers who were single, those with more education and less traditional beliefs about child rearing, and families with higher incomes and fewer children in the household were more likely to use more hours of center care than other families; single mothers and those with fewer children also used more hours of care in child care homes. Minority families, those with low incomes, and mothers with less education and fewer children used more hours of relative care. With family selection factors and quality of child care controlled, only hours in center care across the time period from 3 to 54 months were related to child outcomes. Children who experienced more center care were reported by caregivers at 54 months to have somewhat higher externalizing behavior problem scores than other children, although these scores were not in the clinical or at-risk range. Center care hours were also related to cognitive and language outcomes, with more hours in infancy associated with lower preacademic test scores and more hours in the toddler period with higher language scores. (C) 2004 Elsevier Inc. All rights reserved. C1 NICHD, Early Child Care Res Network, CRMC, Rockville, MD 20852 USA. RP NICHD, Early Child Care Res Network, CRMC, 6100 Execut Blvd,4B05, Rockville, MD 20852 USA. NR 67 TC 0 Z9 0 U1 6 U2 12 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0885-2006 J9 EARLY CHILD RES Q JI Early Childhood Res. Q. PY 2004 VL 19 IS 2 BP 203 EP 230 DI 10.1016/j.ecresq.2004.04.002 PG 28 WC Education & Educational Research; Psychology, Developmental SC Education & Educational Research; Psychology GA 841WM UT WOS:000222962600002 ER PT J AU Cabanes-Macheteau, M Chrambach, A Taverna, M Buzas, Z Berna, P AF Cabanes-Macheteau, M Chrambach, A Taverna, M Buzas, Z Berna, P TI Resolution of 8-aminonaphthalene-1,3,6-trisulfonic acid-labeled glucose oligomers in polyacrylamide gel electrophoresis at low gel concentration SO ELECTROPHORESIS LA English DT Article DE 8-aminonaphthalene-1,3,6-trisulfonic acid-labeled glucose oligomers; discontinuous buffer system; gel electrophoresis ID ASSISTED CARBOHYDRATE ELECTROPHORESIS; CHARGE-COUPLED-DEVICE; OLIGOSACCHARIDES; SEPARATION; SYSTEM; PROTEINS AB A discontinuous Tris-Cl/acetate (OAc) buffer system, unprecedently containing OAc as the trailing constituent, and operative in polyacrylamide gel electrophoresis (PAGE) at low polyacrylamide concentration (T = 4.8%) is described in the paper. The characteristics of the electrophoretic system are illustrated by the resolution of fluorescent 8-aminonaphthalene-1,3,6-trisulfonic acid (ANTS)-labeled malto-oligosaccharides and dextran homopolymers. In this buffer system, the resolving phase is constituted by Tris-OAc behind a moving boundary formed between the leading chloride ion of Tris-HCl gel buffer and the trailing OAc ion provided by a catholyte of NH4OAc. In contrast with the results obtained with Tris-Cl/glycinate buffer commonly used in electrophoresis, or with Tris-Cl/borate, the best resolution of the glucose oligomers containing 1-4 glucose units in Tris-OAc, pH 8.8, ionic strength of 0.08, was obtained at 4.8% polyacrylamide concentration, using 0.5 m NH4OAc, pH 9.5 as the catholyte. Under those conditions, the ANTS-glucose oligomers were separated with mobilities decreasing from glucose to maltohexaose. The linear Ferguson plots (log relative mobility, R-f, vs.%T) of the glucose oligomers show that the surface net charge of those oligomers is inversely related to their sizes, given by the slopes, K-R, of the plots. The molecular weight of the oligomers is directly but nonlinearly related to K-R. The novel electrophoretic system illustrated here for separation of short ANTS-saccharides can be potentially applied to the resolution of other biomolecules such as rapidly migrating DNA, peptides or proteins. C1 Fac Pharm Chatenay Malabry, Chim Analyt Lab, Chatenay Malabry, France. NICHHD, Macromol Anal Sect, Lab Cellular & Mol Biophys, NIH, Bethesda, MD 20892 USA. Pfizer Globabl Res & Dev, Res Technol Dept, Prot Generat Lab, Fresnes, France. RP Cabanes-Macheteau, M (reprint author), 49 Ave Bois de Verrieres, F-92160 Antony, France. EM jpmachet@club-internet.fr NR 19 TC 1 Z9 1 U1 0 U2 3 PU WILEY-V C H VERLAG GMBH PI WEINHEIM PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD JAN PY 2004 VL 25 IS 1 BP 8 EP 13 DI 10.1002/elps.200305689 PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 767AU UT WOS:000188417100002 PM 14730562 ER PT J AU Xiao, Z Conrads, TP Lucas, DA Janini, GM Schaefer, CF Buetow, KH Issaq, HJ Veenstra, TD AF Xiao, Z Conrads, TP Lucas, DA Janini, GM Schaefer, CF Buetow, KH Issaq, HJ Veenstra, TD TI Direct ampholyte-free liquid-phase isoelectric peptide focusing: Application to the human serum proteome SO ELECTROPHORESIS LA English DT Article DE ampholyte-free isoelectric focusing; microcapillary liquid chromatography; proteome; serum; tandem mass spectrometry ID CAPILLARY-ELECTROPHORESIS; MASS-SPECTROMETRY; PROSTATE-CANCER; SEPARATION; IDENTIFICATION; PATTERNS; PROTEINS; HPLC; MEN AB In this study, we utilized a multidimensional peptide separation strategy combined with tandem mass spectrometry (MS/MS) for the identification of proteins in human serum. After enzymatically digesting serum with trypsin, the peptides were fractionated using liquid-phase isoelectric focusing (IEF) in a novel ampholyte-free format. Twenty IEF fractions were collected and analyzed by reversed-phase microcapillary liquid chromatography (muLC)-MS/MS. Bioinformatic analysis of the raw MS/MS spectra resulted in the identification of 844 unique peptides, corresponding to 437 proteins. This study demonstrates the efficacy of ampholyte-free peptide autofocusing, which alleviates peptide losses in ampholyte removal strategies. The results show that the separation strategy is effective for high-throughput characterization of proteins from complex proteomic mixtures. C1 NCI, Lab Prote & Analyt Technol, SAIC Frederick Inc, Frederick, MD 21702 USA. NCI, Ctr Bioinformat, Frederick, MD 21702 USA. RP Veenstra, TD (reprint author), NCI, Lab Prote & Analyt Technol, SAIC Frederick Inc, Bldg 469,POB B, Frederick, MD 21702 USA. EM veenstra@ncifcrf.gov FU NCI NIH HHS [N01-CO-12400] NR 17 TC 59 Z9 64 U1 0 U2 1 PU WILEY-V C H VERLAG GMBH PI WEINHEIM PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY SN 0173-0835 J9 ELECTROPHORESIS JI Electrophoresis PD JAN PY 2004 VL 25 IS 1 BP 128 EP 133 DI 10.1002/elps.200305700 PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 767AU UT WOS:000188417100017 PM 14730577 ER PT J AU Viboud, C Boelle, PY Pakdaman, K Carrat, F Valleron, AJ Flahault, A AF Viboud, C Boelle, PY Pakdaman, K Carrat, F Valleron, AJ Flahault, A TI Influenza epidemics in the United States, France, and Australia, 1972-1997 SO EMERGING INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 3rd International Conference on Emerging Infectious Diseases CY MAR 24-27, 2002 CL ATLANTA, GEORGIA ID DISEASE SURVEILLANCE; POPULATION-DYNAMICS; MORTALITY; IMPACT; SYNCHRONY; DEATHS; VACCINATION; PNEUMONIA; EVOLUTION; ENGLAND AB Influenza epidemics occur once a year during the winter in temperate areas. Little is known about the similarities between epidemics at different locations. We have analyzed pneumonia and influenza deaths from 1972 to 1997 in the United States, France, and Australia to examine the correlation over space and time between the three countries. We found a high correlation in both areas between France and the United States (correlation in impact, Spearman's rho = 0.76, p < 0.001, and test for synchrony in timing of epidemics, p < 0.001). We did not find a similar correlation between the United States and Australia or between France and Australia, when considering a systematic half-year lead or delay of influenza epidemics in Australia as compared with those in the United States or France. These results support a high correlation at the hemisphere level and suggest that the global interhemispheric circulation of epidemics follows an irregular pathway with recurrent changes in the leading hemisphere. C1 Inst Natl Sante & Rech Med, Paris, France. WHO, Collaborat Ctr Elect Dis Surveillance, Paris, France. CHU St Antoine, Hop Paris, Paris, France. RP Viboud, C (reprint author), NIH, Fogarty Int Ctr, 16 Ctr Dr, Bethesda, MD 20892 USA. EM viboudc@mail.nih.gov NR 45 TC 77 Z9 81 U1 0 U2 1 PU CENTER DISEASE CONTROL PI ATLANTA PA ATLANTA, GA 30333 USA SN 1080-6040 J9 EMERG INFECT DIS JI Emerg. Infect. Dis PD JAN PY 2004 VL 10 IS 1 BP 32 EP 39 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 762GD UT WOS:000187962800006 PM 15078594 ER PT J AU Hao, YL Basile, AS Chen, G Zhang, L AF Hao, YL Basile, AS Chen, G Zhang, L TI Glutamate-induced over-expression of GAD is down-regulated by acetyl-L-carnitine in rat islet cells SO ENDOCRINE RESEARCH LA English DT Article DE acetyl-L-carnitine; GAD; glutamate; insulin-dependent diabetes mellitus; IDDM; islet cells ID DEPENDENT DIABETES-MELLITUS; PANCREATIC BETA-CELLS; ACID DECARBOXYLASE; FOLLOW-UP; T-CELLS; AUTOANTIBODIES; ANTIBODIES; ISOFORM; STATE; MOUSE AB Glutamic acid decarboxylase (GAD65 and GAD67) in pancreatic beta cells is the target of autoantibodies and autoreactive T cells in insulin-dependent diabetes mellitus (IDDM). Regulating expression of GAD perhaps is a practical approach to treat IDDM. In this study, we established an in vitro system, in which GAD was expressed and glutamate treatment produced over-expression of GAD67 and GAD65 in rat islet cells. By using the system we were able to demonstrate basal level of expression of GAD and effects of glutamate and the antioxidant, acetyl-L-carnitine (ALC) on expression of GAD. We found that GAD67 expressed in 10% of islets cells, whereas GAD65 was localized in only 4% of the cells. Glutamate treatment resulted in significant over-expression of GAD67, but not GAD65. Such glutamate-induced overexpression of GAD67 was attenuated by pretreatment with ALC (100 muM). These findings suggest that the over-expression of GAD67 induced by glutamate in islet cells of rat may act as a suitable cellular model to study GAD autoreactivity during the development of IDDM. Meanwhile, it indicates that ALC, an ester of the trimethylated amino acid, can block glutamate-induced over-expression of GAD67, a key beta-cell autoantigen, suggesting a therapeutic potential of ALC in IDDM. C1 NIMH, Mol Pathophysiol Lab, NIH, Bethesda, MD 20892 USA. Alkermes Inc, Cambridge, MA USA. RP Zhang, L (reprint author), NIMH, Mol Pathophysiol Lab, NIH, Bldg 49,B1EE16, Bethesda, MD 20892 USA. EM 123g@nih.gov RI Chen, Guang/A-2570-2017 NR 35 TC 4 Z9 5 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 2004 VL 30 IS 1 BP 107 EP 116 DI 10.1081/ERC-120029890 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 812IU UT WOS:000220834000010 PM 15098924 ER PT J AU Hoffman, WH Litaker, MS Pluta, RM Camens, ML AF Hoffman, WH Litaker, MS Pluta, RM Camens, ML TI Cerebral vasoreactivity in children and adolescents with type 1 diabetes mellitus SO ENDOCRINE RESEARCH LA English DT Article DE cerebral vasoreactivity; transcranial Doppler; type 1 diabetes mellitus ID BLOOD-FLOW; NITRIC-OXIDE; CEREBROVASCULAR REACTIVITY; YOUNG-ADULTS; GLUCOSE; INSULIN; DOPPLER; COMPLICATIONS; ULTRASOUND; ARTERY AB It is well established in clinical and experimental settings that diabetes mellitus, especially if long lasting, impairs autoregulation of cerebral blood flow (CBF). However, the onset and the course of development of this dysfunction remain unknown. We hypothesized that assessment of autoregulatory functions of cerebral arteries in children with relatively short duration of type 1 diabetes mellitus may provide an insight into the pathophysiology of the development of impaired autoregulation of CBF. Such a dysfunction of vasodilation of cerebral arteries can be assessed by transcranial Doppler. Therefore, to examine whether and when autoregulation of CBF becomes affected by diabetes, we used transcranial Doppler and a pCO(2) challenge in 17 males between the ages of 12-20 years with type I diabetes mellitus of 0.2-16 years duration and with varying degrees of glucose control. The results were compared with age-matched, healthy, nondiabetic controls. The CO2 challenge increased cerebral blood-flow velocities and decreased the pulsatility index. These changes were not influenced by the presence or duration of diabetes, insulin dose, or degree of diabetic control. C1 Med Coll Georgia, Dept Pediat, Sect Pediat Endocrinol, Augusta, GA 30912 USA. Med Coll Georgia, Off Biostat, Augusta, GA USA. NINDS, NIH, Bethesda, MD USA. Henry Ford Hosp, Dept Radiol, Detroit, MI 48202 USA. RP Hoffman, WH (reprint author), Med Coll Georgia, Dept Pediat, Sect Pediat Endocrinol, BG-1012, Augusta, GA 30912 USA. EM whoffman@mail.mcg.edu NR 38 TC 5 Z9 6 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 2004 VL 30 IS 3 BP 315 EP 325 DI 10.1081/ERC-200033190 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 869GL UT WOS:000224971300002 PM 15554347 ER PT J AU Griffin, KJ Kirschner, LS Matyakhina, L Stergiopoulos, S Robinson-White, A Weinberg, F Meoli, E Bornstein, SR Stratakis, CA AF Griffin, KJ Kirschner, LS Matyakhina, L Stergiopoulos, S Robinson-White, A Weinberg, F Meoli, E Bornstein, SR Stratakis, CA TI A mouse model for carney complex SO ENDOCRINE RESEARCH LA English DT Article; Proceedings Paper CT 11th Conference on Adrenal Cortex CY JUN 12-15, 2004 CL New Orleans, LA DE protein kinase A; PRKAR1A; mouse model; carney complex; adrenal tumors; thyroid tumors; mesenchymal tumors ID PROTEIN-KINASE-A; RII(BETA) REGULATORY SUBUNIT; RI-ALPHA; PRKAR1A GENE; CYCLIC-AMP; I-ALPHA; MUTATIONS; GROWTH; TUMORS; SITE AB Mice with complete inactivation of the type lot regulatory subunit (RIalpha) of cyclic (c) AMP-dependent protein kinase (PKA) (coded by the Prkar1a gene) die early in embryonic life. To bypass the early embryonic lethality of Prkar1a(-/-) mice, we established transgenic mice carrying an antisense transgene for Prkar1a exon 2 (X2AS) under the control of a tetracycline-responsive promoter. Mice developed thyroid follicular hyperplasia and adenomas, adrenocortical hyperplasia, and other features reminiscent of PPNAD, and histiocytic and epithelial hyperplasias, lymphomas, and other mesenchymal tumors. This mouse provides a useful tool for the investigation of cAMP, R1alpha, and PKA functions and confirms Prkar1a's critical role in tumorigenesis in endocrine and other tissues. C1 NICHHD, Sect Genet & Endocrinol, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA. Univ Dusseldorf, D-4000 Dusseldorf, Germany. Ohio State Univ, Dept Internal Med, Div Human Canc Genet, Columbus, OH 43210 USA. Ohio State Univ, Dept Internal Med, Div Endocrinol, Columbus, OH 43210 USA. RP Stratakis, CA (reprint author), NICHHD, Sect Genet & Endocrinol, Dev Endocrinol Branch, NIH, Bldg 10,Room 10N262,MSC1862,10 Ctr Dr, Bethesda, MD 20892 USA. EM Stratakc@mail.nih.gov NR 24 TC 11 Z9 12 U1 0 U2 0 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 0743-5800 J9 ENDOCR RES JI Endocr. Res. PY 2004 VL 30 IS 4 BP 903 EP 911 DI 10.1081/ERC-20044145 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 887GQ UT WOS:000226294200079 PM 15666843 ER PT J AU Chen, YD AF Chen, YD TI Multiple binding of ligands to a linear biopolymer SO ENERGETICS OF BIOLOGICAL MACROMOLECULES, PT D SE METHODS IN ENZYMOLOGY LA English DT Review ID TROPONIN-TROPOMYOSIN COMPLEX; MYOSIN SUBFRAGMENT-1; COOPERATIVE BINDING; PIGGYBACK BINDING; MODEL; ACTIN; DNA; EQUILIBRIUM; CALDESMON; LATTICE C1 NIDDKD, Lab Biol Medeling, NIH, Bethesda, MD 20892 USA. RP Chen, YD (reprint author), NIDDKD, Lab Biol Medeling, NIH, Bethesda, MD 20892 USA. NR 15 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 2004 VL 379 BP 145 EP 152 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BY88J UT WOS:000189486200008 PM 15051356 ER PT J AU Veigl, ML Harris, CC AF Veigl, ML Harris, CC TI Special section: Impact of the environment on colon cancer - Introduction SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material C1 Case Western Reserve Univ, Case Comprehens Canc Ctr, Dept Environm Hlth Sci, Cleveland, OH 44106 USA. NCI, Human Carcinogenesis Lab, Bethesda, MD 20892 USA. RP Veigl, ML (reprint author), Case Western Reserve Univ, Case Comprehens Canc Ctr, Dept Environm Hlth Sci, Cleveland, OH 44106 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 1 BP 1 EP 2 DI 10.1002/em.20035 PG 2 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 841JM UT WOS:000222926100001 ER PT J AU Goodman, JE Hofseth, LJ Hussain, SP Harris, CC AF Goodman, JE Hofseth, LJ Hussain, SP Harris, CC TI Nitric oxide and p53 in cancer-prone chronic inflammation and oxyradical overload disease SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article; Proceedings Paper CT Conference on the Impact of the Environment on Colon Cancer CY MAY 14-16, 2003 CL Miami Beach, FL DE nitric oxide; p53; iNOS; ulcerative colitis ID TUMOR-SUPPRESSOR GENE; ULCERATIVE-COLITIS; SYNTHASE EXPRESSION; COLORECTAL-CANCER; INDUCED APOPTOSIS; CROHNS-DISEASE; BOWEL-DISEASE; MUTATIONS; CARCINOGENESIS; PHOSPHORYLATION AB Nitric oxide (NOcircle), which is generated under chronic inflammatory conditions that predispose individuals to cancer, has paradoxical effects. NOcircle can activate p53, which can result in anti-carcinogenic effects, or it can be mutagenic and increase cancer risk. We explored the mechanisms by which NOcircle induced p53 activation in vitro and found that NOcircle induced p53 accumulation and phosphorylation, particularly at ser-15, via ATM and ATR kinases, which then led to cell cycle arrest at G(2)/M. We next examined proteins in these pathways in both inflamed and normal human colon tissue. Inducible nitric oxide synthase (iNOS) levels and p53-P-ser 15 levels were positively correlated with the degree of inflammation and with each other. Additionally, the p53 targets, HDM-2 and p21 (WAF1), were present in ulcerative colitis (UC) colon, but undetectable in normal colon, consistent with activated p53. We also found higher p53 mutant frequencies of both G:C-->A:T transitions at the CpG site of codon 248 and C:G-->T:A transitions at codon 247 in lesional colon tissue from UC cases versus nonlesional tissue from these cases or colon tissue from normal adult controls. Consistent with nitrosative stress and the deamination of 5-methylcytosine, p53 mutations were also detected in sporadic colon cancer tissue and were associated with iNOS activity in these tissues. These studies identified a potential mechanistic link between NOcircle and p53 in UC and sporadic colon cancer. C1 NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. NCI, Canc Prevent Fellowship Program, Div Canc Prevent, NIH, Bethesda, MD 20892 USA. RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, NIH, 37 Convent Dr,Bldg 37,Room 3068, Bethesda, MD 20892 USA. EM curtis_harris@nih.gov NR 42 TC 65 Z9 69 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 1 BP 3 EP 9 DI 10.1002/em.20024 PG 7 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 841JM UT WOS:000222926100002 PM 15199542 ER PT J AU Cross, AJ Sinha, R AF Cross, AJ Sinha, R TI Meat-related mutagens/carcinogens in the etiology of colorectal cancer SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article; Proceedings Paper CT Conference on the Impact of the Environment on Colon Cancer CY MAY 14-16, 2003 CL Miami Beach, FL DE heterocyclic amines; polycyclic aromatic hydrocarbons; N-nitroso compounds; meat and colorectal cancer ID N-NITROSO COMPOUNDS; HETEROCYCLIC AROMATIC-AMINES; HYDROCARBON-DNA ADDUCTS; FRIED BEEF PATTIES; WHITE BLOOD-CELLS; DONE RED MEAT; URINARY MUTAGENICITY; COLON-CANCER; CYTOCHROME P4501A2; WELL-DONE AB Diets containing substantial amounts of red or preserved meats may increase the risk of various cancers, including colorectal cancer. This association may be due to a combination of factors such as the content of fat, protein, iron, and/or meat preparation (e.g., cooking or preserving methods). Red meat may be associated with colorectal cancer by contributing to N-nitroso compound (NOC) exposure. Humans can be exposed to NOCs by exogenous routes (from processed meats in particular) and by endogenous routes. Endogenous exposure to NOCs is dose-dependently related to the amount of red meat in the diet. Laboratory results have shown that meats cooked at high temperatures contain other potential mutagens in the form of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHS). To investigate the role of these compounds, we have created separate databases for HCAs and PAHs, which we have used in conjunction with a validated meat-cooking food frequency questionnaire. The role of meat type, cooking methods, doneness levels, and meat-cooking mutagens has been examined in both case-control studies and prospective cohort studies, with mixed results. Here, we review the current epidemiologic knowledge of meat-related mutagens, and evaluate the types of studies that may be required in the future to clarify the association between meat consumption and colorectal cancer. C1 NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA. RP Cross, AJ (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 6120 Execut Plaza, Rockville, MD 20852 USA. EM crossa@mail.nih.gov RI Sinha, Rashmi/G-7446-2015 OI Sinha, Rashmi/0000-0002-2466-7462 NR 121 TC 164 Z9 169 U1 9 U2 45 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 1 BP 44 EP 55 DI 10.1002/em.20030 PG 12 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 841JM UT WOS:000222926100006 PM 15199546 ER PT J AU Borts, RH Hoffmann, ER Cotton, VE Abdullah, MFF Kunkel, TA AF Borts, RH Hoffmann, ER Cotton, VE Abdullah, MFF Kunkel, TA TI A structural and functional analysis of the meiotic activities of mismatch repair proteins SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 Univ Leicester, Dept Genet, Leicester LE1 7RH, Leics, England. Univ Teknol MARA, Fac Sci Appl, Shah Alam 40450, Malaysia. NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA. Univ Nebraska, Eppley Inst Canc Res, Nebraska Med Ctr 986805, Omaha, NE 68198 USA. RI Abdullah, Mohamad Faiz/A-2328-2012 NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 15 BP 189 EP 189 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700017 ER PT J AU Cabelof, DC Ikeno, Y Sobol, RW Tucker, JD Wilson, SH Richardson, A Heydari, AR AF Cabelof, DC Ikeno, Y Sobol, RW Tucker, JD Wilson, SH Richardson, A Heydari, AR TI Induction of chromosomal instability and tumors in beta-pol haploinsufficient mice SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 Wayne State Univ, Dept Nutr & Food Sci, Detroit, MI 48202 USA. Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78284 USA. Univ Pittsburgh, Inst Canc, Hillman Canc Ctr, Pittsburgh, PA 15213 USA. Wayne State Univ, Dept Biol Sci, Detroit, MI 48202 USA. NIEHS, Res Triangle Pk, NC 27709 USA. RI Sobol, Robert/E-4125-2013 OI Sobol, Robert/0000-0001-7385-3563 NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 18 BP 190 EP 190 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700020 ER PT J AU Chan, S Naviaux, R Copeland, W AF Chan, S Naviaux, R Copeland, W TI A new form of RNA editing found in a childhood disease corrects a lethal stop codon SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 Univ Calif San Diego, Sch Med, Dept Med & Pediat, San Diego, CA 92103 USA. NIEHS, Genet Mol Lab, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 22 BP 191 EP 191 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700024 ER PT J AU Copeland, WC AF Copeland, WC TI Consequences of mutations in DNA polymerase gamma SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIEHS, Genet Mol Lab, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 1 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 32 BP 193 EP 193 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700034 ER PT J AU Divi, RL Leonard, SL Nagashima, K Harbaugh, SW Harbaugh, JW St Claire, MC Poirier, MC AF Divi, RL Leonard, SL Nagashima, K Harbaugh, SW Harbaugh, JW St Claire, MC Poirier, MC TI Post-birth mitochondrial toxicity of in utero nucleoside reverse transcriptase inhibitor (NRTI) exposures in a primate model SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, NIH, Bethesda, MD 20892 USA. NCI, Frederick Canc Res & Dev Ctr, SAIC, Frederick, MD 21702 USA. Bioqual Inc, Rockville, MD 20850 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 38 BP 195 EP 195 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700041 ER PT J AU Graziewicz, MA Longley, MJ Bienstock, RJ Zeviani, M Copeland, WC AF Graziewicz, MA Longley, MJ Bienstock, RJ Zeviani, M Copeland, WC TI Structure-function defects of human mitochondrial DNA polymerase in autosomal dominant progressive external ophthalmoplegia SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIEHS, Genet Mol Lab, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Comp Sci Lab, NIH, Res Triangle Pk, NC 27709 USA. Natl Neurol Inst Carlo Besta, Unit Mol Neurogenet, Milan, Italy. NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 64 BP 202 EP 202 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700067 ER PT J AU Haugen, AC Karthikeyan, G Collins, JB Tucker, CJ Resnick, MA Van Houten, B AF Haugen, AC Karthikeyan, G Collins, JB Tucker, CJ Resnick, MA Van Houten, B TI A yeast model of Friedreich's Ataxia: Genotoxicity of mitochondrial iron accumulation SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIEHS, Genet Mol Lab, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Natl Ctr Toxicogenom, Microarray Ctr, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 74 BP 204 EP 204 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700077 ER PT J AU Kaufmann, WK Heffernan, T Unsal-Kacmaz, K Heinloth, A Sancar, A Paules, RS Cordeiro-Stone, M AF Kaufmann, WK Heffernan, T Unsal-Kacmaz, K Heinloth, A Sancar, A Paules, RS Cordeiro-Stone, M TI Human S checkpoints: Multiple mechanisms inhibit replicon initiation after DNA damage SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Biochem & Biophys, Chapel Hill, NC 27599 USA. NIEHS, Res Triangle Pk, NC 27705 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 75 BP 204 EP 204 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700078 ER PT J AU Hofseth, LJ Khan, MA Ambrose, M Kartalou, M Hussain, SP Samson, LD Harris, CC AF Hofseth, LJ Khan, MA Ambrose, M Kartalou, M Hussain, SP Samson, LD Harris, CC TI Induction of a mutator phenotype in inflamed tissues SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. Univ S Carolina, Coll Pharm, Columbia, SC 29208 USA. MIT, Biol Engn Div, Cambridge, MA 02139 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 79 BP 205 EP 205 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700082 ER PT J AU Hussain, SP Hofseth, LJ Wogan, G Wang, XW Harris, CC AF Hussain, SP Hofseth, LJ Wogan, G Wang, XW Harris, CC TI Radical causes of human cancer SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, Human Carcinogenesis Lab, CCR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 82 BP 207 EP 207 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700087 ER PT J AU John, K Keshava, C Divi, RL Whipkey, DL Poirier, MC Weston, A Nath, J AF John, K Keshava, C Divi, RL Whipkey, DL Poirier, MC Weston, A Nath, J TI Modulation of CYP1A1 and CYP1B1 expression by chlorophyllin in normal human mammary epithelial cells exposed to benzo(a)pyrene SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 W Virginia Univ, Genet & Dev Biol Program, Morgantown, WV 26506 USA. CDC, Toxicol & Mol Biol Lab, NIOSH, Morgantown, WV 26505 USA. NCI, Carcinogen DNA Interact Sect, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 86 BP 208 EP 208 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700091 ER PT J AU Kasprzak, KS AF Kasprzak, KS TI Nickel-induced chromatin damage SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 90 BP 209 EP 209 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700095 ER PT J AU Keohavong, P Lan, Q Gao, WM Zheng, KC Mady, H Melhem, M Mumford, JL AF Keohavong, P Lan, Q Gao, WM Zheng, KC Mady, H Melhem, M Mumford, JL TI Detection of p53 and K-ras mutations in sputum of nonsmoking women exposed to smoky coal combustion emissions in Xuan Wei County, China SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 Univ Pittsburgh, Pittsburgh, PA 15260 USA. NCI, Bethesda, MD 20892 USA. US EPA, Res Triangle Pk, NC 27711 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 91 BP 209 EP 209 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700096 ER PT J AU Mahadevan, B Arora, V Schild, LJ Keshava, C Cate, ML Iversen, PL Poirer, MC Weston, A Pereira, C Baird, WM AF Mahadevan, B Arora, V Schild, LJ Keshava, C Cate, ML Iversen, PL Poirer, MC Weston, A Pereira, C Baird, WM TI Reduction in tamoxifen metabolic activation and genotoxicity by antisense technology SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, NIH, Bethesda, MD 20829 USA. NIOSH, CDC, Morgantown, WV 26505 USA. Oregon State Univ, Dept Stat, Corvallis, OR 97331 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 109 BP 213 EP 213 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700114 ER PT J AU Meyer, JN Boyd, WA Haugen, AC Freedman, JH Van Houten, B AF Meyer, JN Boyd, WA Haugen, AC Freedman, JH Van Houten, B TI A caenorhabditis elegans model of Friedreich's ataxia shows iron sensitivity, mitochondrial DNA damage, and altered gene expression. SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIEHS, Genet Mol Lab, Res Triangle Pk, NC 27709 USA. Duke Univ, Nicholas Sch Environm & Earth Sci, Durham, NC 27708 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 115 BP 215 EP 215 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700120 ER PT J AU Olivero, OA Tejera, AM Das, SA Divi, RL Poirier, MC AF Olivero, OA Tejera, AM Das, SA Divi, RL Poirier, MC TI Genotoxicity and cell cycle gene expression changes induced by nucleoside reverse transcriptase inhibitors (NRTIs) SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, Carcinogen DNA Interact, NIH, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 131 BP 219 EP 219 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700137 ER PT J AU Opresko, PL Otterlei, M Fan, J Kolvraa, S Wilson, DM Seidman, MM Bohr, VA AF Opresko, PL Otterlei, M Fan, J Kolvraa, S Wilson, DM Seidman, MM Bohr, VA TI The Werner syndrome protein and DNA repair pathways at telomeric DNA. SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA. Norwegian Univ Sci & Technol, Dept Canc Res & Mol Med, N-7489 Trondheim, Norway. Aarhus Univ, Inst Human Genet, DK-8000 Aarhus, Denmark. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 132 BP 219 EP 219 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700138 ER PT J AU Pratt, MM Castle, PE Schiffman, M Glass, AG Scott, DR Rush, BB Olivero, OA Poirier, MC AF Pratt, MM Castle, PE Schiffman, M Glass, AG Scott, DR Rush, BB Olivero, OA Poirier, MC TI Semi-quantitation of polycyclic aromatic hydrocarbon (PAH)-DNA adducts in human cervix by immunohistochemistry and the automated cellular imaging system (ACIS). SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, Canc Res Ctr, Carcinogen DNA Interact Sect, NIH, Bethesda, MD 20892 USA. NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA. NW Kaiser Permanente, Portland, OR USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 138 BP 221 EP 221 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700144 ER PT J AU Shaughnessy, DS Taylor, JA AF Shaughnessy, DS Taylor, JA TI Inhibition of PhIP-induced damage by chlorophyllin in human lymphoblastoid cells in the alkaline single-cell gel electrophoresis (Comet) assay. SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIEHS, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 158 BP 226 EP 226 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700165 ER PT J AU Theruvathu, JA Nath, RG Brooks, PJ AF Theruvathu, JA Nath, RG Brooks, PJ TI Polyamines facilitate the formation of the mutagenic DNA adduct 1,N-2-PropanodG from acetaldehyde and DNA: Implications for the mechanism of alcohol-related carcinogenesis SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 175 BP 231 EP 231 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700184 ER PT J AU Torres, SM Walker, VE Olivero, OA Carter, M Cook, D Poirier, M Walker, DM AF Torres, SM Walker, VE Olivero, OA Carter, M Cook, D Poirier, M Walker, DM TI Relationships between exposure concentration, exposure duration, levels of DNA incorporation of drugs and mutagenic effects in human lymphoblastoid TK6 cells exposed in vitro to AZT, 3TC, and AZT-3TC SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 Univ New Mexico, Hlth Sci Ctr, Albuquerque, NM 87131 USA. Lovelace Resp Res Inst, Albuquerque, NM USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 180 BP 232 EP 232 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700189 ER PT J AU Van Houten, B Santos, JH Haugen, AC Meyer, J Karthikeyan, G Resnick, MA AF Van Houten, B Santos, JH Haugen, AC Meyer, J Karthikeyan, G Resnick, MA TI Consequences of iron-mediated mitochondrial DNA damage SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIEHS, Mol Genet Lab, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 185 BP 234 EP 234 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700195 ER PT J AU Vazquez, IL Olivero, O Poirier, M AF Vazquez, IL Olivero, O Poirier, M TI Altered AZT metabolism may induce cellular drug resistance in human cells SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, Cellular Carcinogenesis & Tumor Promot Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 186 BP 234 EP 234 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700196 ER PT J AU Wang, XW Kim, JW Ye, QH Forgues, M Budhu, A Qin, LX Tang, ZY AF Wang, XW Kim, JW Ye, QH Forgues, M Budhu, A Qin, LX Tang, ZY TI Lessons learned from molecular profiling of human hepatocellular cancer SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NCI, Liver Carcinogenesis Grp, LHC, CCR,NIH, Bethesda, MD 20892 USA. Fudan Univ, Liver Canc Inst, Shanghai 200032, Peoples R China. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 191 BP 235 EP 235 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700201 ER PT J AU Witt, KL Tice, RR Wolfe, GW Bishop, JB AF Witt, KL Tice, RR Wolfe, GW Bishop, JB TI Zidovudine is the mutagenic component of combination antiretroviral drug therapy administered to CD-1 mouse pups in a treatment regimen similar to that used in humans for prevention of mother-to-child transmission of HIV SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Meeting Abstract CT 35th Annual Meeting of the Environmental-Mutagen-Society CY OCT 02-06, 2004 CL Pittsburgh, PA SP Environm Mutagen Soc C1 NIEHS, Res Triangle Pk, NC 27709 USA. Integrated Lab Syst Inc, Res Triangle Pk, NC 27709 USA. Gene Log Inc, Gaithersburg, MD 20879 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 3 MA 197 BP 237 EP 237 PG 1 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 852MF UT WOS:000223758700207 ER PT J AU Witt, KL Tice, RR Wolfe, GW Bishop, JB AF Witt, KL Tice, RR Wolfe, GW Bishop, JB TI Genetic damage detected in CD-1 mouse pups exposed perinatally to 3'-azido-3'-deoxythymidine or dideoxyinosine via maternal dosing, nursing, and direct gavage: II. Effects of the individual agents compared to combination treatment SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE HIV; nucleoside analogues; AZT; chromosome damage; transplacental exposures; micronuclei ID HUMAN-IMMUNODEFICIENCY-VIRUS; PERSISTENT MITOCHONDRIAL DYSFUNCTION; HIV-INFECTED WOMEN; MICRONUCLEUS TEST; ZIDOVUDINE TREATMENT; INFANT TRANSMISSION; UNINFECTED INFANTS; PERIPHERAL-BLOOD; PREVENTION; CHILDREN AB We previously reported extraordinary increases in micronucleated erythrocytes in CD-1 mouse pups exposed to 3'-aziclo-3'-deoxythymidine (AZT) and dideoxyinosine (ddl; 50/250, 75/375, 150/750 mg/kg/day AZT/ddl) by gavage throughout gestation and lactation, followed by direct pup dosing beginning postnatal day (PND) 4 (Bishop et al. [2004]: Environ Mal Mutagen 43: 3-9). That study was conducted to explore the potential for genetic damage in newborns exposed perinatally to antiretrovirals in order to reduce maternal-infant transmission of HIV-1 Because dramatic increases in frequencies of micronucleated erythrocytes were seen in exposed pups, additional studies were conducted to clarify the relative contribution of each drug to the observed damage. Pregnant CD-1 mice were administered AZT (50, 75, 150 mg/kg/day) or ddl (250, 375, 750 mg/kg/day) by gavage twice daily in equal fractions beginning prior to mating and continuing throughout gestation and lactation. Direct pup dosing (same regimens) began on PND 4. Peripheral blood erythrocytes of male pups were screened for micronuclei on PNDs 1, 4, 8, and 21. Significant increases in micronucleated erythrocytes were observed in pups and dams exposed to AZT at all doses and sampling times. The highest micronucleus levels were observed in pups on PND 8 after the initiation of direct dosing. In contrast, effects seen in pups and dams treated with ddl were minimal. These results demonstrate that AZT, a component of many anti-HIV combination therapies, induces chromosomal damage in perinatally exposed neonatal mice. Comparison of micronucleated cell frequencies induced by AZT alone or in combination with ddl suggests that ddl potentiates AZT-induced chromosomal damage following direct exposure. Published 2004 Wiley-Liss, Inc.(dagger) C1 Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC 27709 USA. Integrated Syst Lab, Res Triangle Pk, NC USA. Gene Log Labs, Gaithersburg, MD USA. RP Witt, KL (reprint author), Natl Inst Environm Hlth Sci, NIH, MD EC-32,POB 12233, Res Triangle Pk, NC 27709 USA. EM witt@niehs.nih.gov FU NIEHS NIH HHS [N01-ES-35514, N01-ES-1-75412, N01-ES-05455, N01-ES-75409] NR 31 TC 19 Z9 19 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 4 BP 321 EP 328 DI 10.1002/em.20048 PG 8 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 867LY UT WOS:000224845300008 PM 15476197 ER PT J AU Malling, HV AF Malling, HV TI History of the science of mutagenesis from a personal perspective SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Editorial Material DE mutagenesis; mutation research; Environmental Mutagen Society; history of science; metabolic activation; mutagen assays ID CHINESE HAMSTER CELLS; LACTATE DEHYDROGENASE-X; INDUCED AD-3B MUTANTS; NEUROSPORA-CRASSA; ESCHERICHIA-COLI; IN-VIVO; GENE-A; MICE; MUTATION; MOUSE AB A career in the study of mutagenesis spanning 50 years is a gift few scientists have been bestowed. My tenure in the field started in 1953, the year the structure of DNA became known (Watson and Crick [19531: Nature 171:737). Before that time, it was suspected that DNA was the genetic material based on the research of Oswald T. Avery (Avery et al. [ 1944]: J Exp Med 79:137), but many scientists still believed that proteins or polysaccharicles could be the genetic material. The present article describes a lifetime of personal experience in the field of chemical mutagenesis. The methods used to treat viruses with chemical mutagens were well developed in the 1950s. Here I review the early use of nitrous acid and hydroxylamine as mutagens in eukaryotes, the development of methods for the metabolic activation of mutagens by microsomal preparations, and the selection of a mutant tester set for the qualitative characterization of the mutagenic activity of chemicals. These studies provided critical background information that was used by Bruce Ames in the development of his Salmonella/microsome assay, widely known as the Ames test (Ames et al. [ 1973]: Proc Nat Acad Sci USA 70:2281-2285). This article also describes how a set of diagnostic chemical mutagens was selected and used to identify the molecular nature of gene mutations. Today, DNA sequencing has replaced the use of diagnostic mutagens, but studies of this kind formed the foundation of modern mutation research. They also helped set the stage for the organization of the Environmental Mutagen Society and the Environmental Mutagen Information Center, which are described. The article ends with the development of mammalian single-cell mutation assays, the first system for studying in vivo mutagenesis using recoverable vectors in transgenic animals, other mutation assays in intact mammals, and my thoughts on the critically important area of germ cell mutagenesis. This narrative is not a complete autobiographical account, in that I have selected only those experiences that I feel are important for the history of the field and the edification of today's students. I hope I have shown that science not only is a valuable pursuit but can also be fun, stimulating, and satisfying. A good sense of humor and the knowledge that many discoveries come by serendipity are essential. Published 2004 WileyLiss, Inc. C1 NIEHS, NIH, Dept HHS,Mammalian Mutagenesis Grp, Environm Toxicol Program,Lab Toxicol, Res Triangle Pk, NC 27709 USA. RP Malling, HV (reprint author), NIEHS, NIH, Dept HHS,Mammalian Mutagenesis Grp, Environm Toxicol Program,Lab Toxicol, POB 12233, Res Triangle Pk, NC 27709 USA. EM malling@niehs.nih.gov NR 86 TC 9 Z9 11 U1 0 U2 7 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 5 BP 372 EP 386 DI 10.1002/em.20064 PG 15 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 886MN UT WOS:000226231600004 PM 15529325 ER PT J AU Dertinger, SD Camphausen, K MacGregor, JI Bishop, ME Torous, DK Avlasevich, S Cairns, S Tometsko, CR Menard, C Muanza, T Chen, YY Miller, RK Cederbrant, K Sandelin, K Ponten, I Bolcsfoldi, G AF Dertinger, SD Camphausen, K MacGregor, JI Bishop, ME Torous, DK Avlasevich, S Cairns, S Tometsko, CR Menard, C Muanza, T Chen, YY Miller, RK Cederbrant, K Sandelin, K Ponten, I Bolcsfoldi, G TI Three-color labeling method for flow cytometric measurement of cytogenetic damage in rodent and human blood SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE micronuclei; cytogenetic damage; DNA damage; reticulocytes; CD71 antigen ID RAT PERIPHERAL-BLOOD; MICRONUCLEUS ASSAY; BONE-MARROW; RETICULOCYTES; ERYTHROCYTES; ENUMERATION; CYCLOPHOSPHAMIDE; SUITABILITY AB Experiments described herein were designed to evaluate the performance characteristics of a flow cytometry-based system that scores the incidence of peripheral blood micronucleated reticulocytes IMN-RETs). These procedures represent the continued refinement of a previously reported anti-CD71-based method (Dertinger et al. [1996]: Mutat Res 371:283-292), with the following modifications: incorporation of a third fluorescent label to exclude platelets from the MN-RET region, and use of a CD71 -associated fluorescence thresholding technique to increase data acquisition rates. Mouse, rat, and human blood samples were analyzed using both the previously described two-color procedure (anti-CD71-FITC and propidium iodide) and a newly developed three-color technique (which adds an antiplatelet-PE antibody). The rodent specimens were also evaluated by standard microscopy procedures (acridine orange staining). Mouse blood was collected via heart puncture of vehicle- and 5-fluorouracil-treated CD-1 mice; blood samples from saline-treated Sprague-Dawley rats were collected from the tail vein and via heart puncture. Rodent blood samples were analyzed by both the two- and three-color methods. Human blood specimens, obtained via arm venipuncture from cancer patients undergoing radiation therapy, were analyzed for MNRETs using the two-color method. Subsequently, blood samples from a single chemotherapy patient were analyzed by both the two- and three-color methods. Finally, the chemotherapy patient blood samples and blood samples from 15 healthy volunteers were evaluated at very high densities in conjunction with a CD71-associated fluorescence thresholding technique. Results of these investigations showed that data from mouse blood analyzed by the two- and threecolor procedures correlated well with microscopy data (r values = 0.917 and 0.937 for the two- and three-color methods, respectively); all three methods confirmed the genotoxicity of 5-FU. Data from rat tail vein samples showed improved reproducibility with the three-color technique, but no significant difference between the two techniques was seen with the heart puncture specimens. Human blood analyzed according to the two-color procedure produced unreliable results, as platelets and platelet aggregates impacted the rare MN-RET scoring region. The three-color technique effectively overcome this problem and produced reproducible measurements that fell within expected ranges. For human blood analyses, the high cell density/CD71 -thresholding technique provided significant improvements over the low-density technique, as it allowed data acquisition to occur approximately six times faster with no loss of sensitivity. (C) 2004 Wiley-Liss, Inc. C1 Litron Labs, Rochester, NY 14620 USA. NCI, Radiat Oncol Branch, Bethesda, MD 20892 USA. US FDA, Natl Ctr Toxicol Res, Rockville, MD 20857 USA. US FDA, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA. Univ Rochester, Dept Radiat Oncol, James P Wilmot Canc Ctr, Rochester, NY USA. Univ Rochester, Med Ctr, Dept Obstet & Gynecol, Rochester, NY 14642 USA. AstraZeneca Res & Dev, Sodertalje, Sweden. RP Dertinger, SD (reprint author), Litron Labs, 1351 Mt Hope Ave, Rochester, NY 14620 USA. EM sdertinger@litronlabs.com OI Cederbrant, Karin/0000-0003-3341-5416 FU NIEHS NIH HHS [R44ES011244-03, R44ES010752-02] NR 21 TC 47 Z9 50 U1 0 U2 6 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0893-6692 J9 ENVIRON MOL MUTAGEN JI Environ. Mol. Mutagen. PY 2004 VL 44 IS 5 BP 427 EP 435 DI 10.1002/em.20075 PG 9 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 886MN UT WOS:000226231600009 PM 15517570 ER PT J AU Bishop, JB Witt, KL Tice, RR Wolfe, GW AF Bishop, JB Witt, KL Tice, RR Wolfe, GW TI Genetic damage detected in CD-1 mouse pups exposed perinatally to 3 '-azido-3 '-deoxythymidine and dideoxyinosine via maternal dosing, nursing, and direct gavage SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE antiretroviral drugs; nucleoside analogues; AZT; chromosome damage; transplacental exposures; micronuclei ID PERSISTENT MITOCHONDRIAL DYSFUNCTION; IMMUNODEFICIENCY-VIRUS TYPE-1; MICRONUCLEUS TEST; BONE-MARROW; CHROMOSOMAL-ABERRATIONS; ZIDOVUDINE TREATMENT; INFANT TRANSMISSION; NUCLEOSIDE ANALOGS; DNA INCORPORATION; PERIPHERAL-BLOOD AB Human immunodeficiency virus (HIV)-infected pregnant women are administered nucleoside-analogue antiretrovirals to reduce maternal-infant viral transmission. The current protocol recommends treating newborns for 6 additional weeks postpartum. The treatment is effective, but the risk of drug-induced chromosomal damage in neonates remains undefined. We used a mouse model to investigate this concern. In a multigeneration reproductive toxicity study, female CD-1 mice received 3'-azido-3'-deoxythymidine (AZT) and dideoxyinosine (ddl) (50/250, 75/375, 150/750 mg/ kg/day AZT/ddl) by gavage twice daily in equal fractions beginning prior to mating and continuing throughout gestation and lactation. Direct pup dosing (same regimen) began on postnatal day (PND) 4. Peripheral blood erythrocytes of male pups were screened for micronuclei, markers of chromosomal damage, on PNDs 1, 4, 8, and 21. Extraordinary increases in micronucleated cells were noted in pups for each treatment group at each sampling time; treated dams exhibited smaller yet significant increases in micronucleated erythrocytes. The frequencies of micronucleated cells in untreated pups were higher than in the untreated dams, and all pups had markedly elevated levels of circulating reticulocytes compared to dams. These observations suggest that fetal and neonatal mouse hematopoietic precursor cells have heightened sensitivity to genotoxic agents, perhaps due to rapid cell proliferation during the perinatal period of development. The amount of genetic damage observed in treated pups raises concern for the potential of similar damage in humans. Investigations of chromosomal integrity in exposed newborns and children are recommended. (C) 2004 Wiley-Liss, Inc. C1 NIEHS, NIH, Res Triangle Pk, NC 27709 USA. Integrated Lab Syst Inc, Res Triangle Pk, NC USA. TherImmune Inc, Gaithersburg, MD USA. RP Bishop, JB (reprint author), NIEHS, NIH, MD EC-01,POB 12233, Res Triangle Pk, NC 27709 USA. EM bishop@niehs.nih.gov FU NIEHS NIH HHS [N01-ES-1-75412, N01-ES-75409] NR 35 TC 25 Z9 25 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 2004 VL 43 IS 1 BP 3 EP 9 DI 10.1002/em.10210 PG 7 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 772JD UT WOS:000188838100001 PM 14743340 ER PT J AU Peters, U Sinha, R Bell, DA Rothman, N Grant, DJ Watson, MA Kulldorff, M Brooks, LR Warren, SH DeMarini, DM AF Peters, U Sinha, R Bell, DA Rothman, N Grant, DJ Watson, MA Kulldorff, M Brooks, LR Warren, SH DeMarini, DM TI Urinary mutagenesis and fried red meat intake: Influence of cooking temperature, phenotype, and genotype of metabolizing enzymes in a controlled feeding study SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article; Proceedings Paper CT Conference on Impact of the Environment on Colon Cancer CY MAY 14-16, 2003 CL MIAMI BEACH, FLORIDA DE fried red meat; urinary mutagenicity; heterocyclic amines; genotype; phenotype ID HETEROCYCLIC AMINE CONTENT; ARYLAMINE N-ACETYLTRANSFERASE; GROUND-BEEF; AROMATIC-AMINES; COLORECTAL ADENOMAS; CYTOCHROME P4501A2; GILBERTS-SYNDROME; VARYING DEGREES; HAMBURGER MEAL; BACON MEALS AB Meat cooked at high temperatures contains potential carcinogenic compounds, such as heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Samples from a 2-week controlled feeding study were used to examine the relationship between the intake of mutagenicity from meat fried at different temperatures and the levels of mutagenicity subsequently detected in urine, as well as the influence of the genotype of drug metabolizing enzymes on urinary mutagenicity. Sixty subjects consumed ground beef patties fried at low temperature (100degreesC) for 1 week, followed by ground beef patties fried at high temperature (250degreesC) the second week. Mutagenicity in the meat was assayed in Salmonella typhimurium TA98 (+S9), and urinary mutagenicity was determined using Salmonella YG1024 (+ S9). Genotypes for NAT1, NAT2, GSTM1, and UGT1A1 were analyzed using blood samples from the subjects. Meat fried at 100degreesC was not mutagenic, whereas meat hied at 250degreesC was mutagenic (1023 rev/g). Unhydrolyzed and hydrolyzed urine samples were 22 x and 131 X more mutagenic, respectively, when subjects consumed red meat fried at 250degreesC compared with red meat fried at 100degreesC. We found that hydrolyzed urine was similar to8X more mutagenic than unhydrolyzed urine, likely due to the deconjugation of mutagens from glucuronide. The intake of meat cooked at high temperature correlated with the mutagenicity of unhydrolyzed urine (r = 0.32, P = 0.01) and hydrolyzed urine (r = 0.34, P = 0.008). Mutagenicity in unhydrolyzed urine was not influenced by NAT1, NAT2, or GSTM1 genotypes. However, a UGT1A1*28 polymorphism that reduced UGT1A1 expression and conjugation modified the effect of intake of meat cooked at high temperature on mutagenicity of unhydrolyzed urine (P for interaction = 0.04). These mutagenicity data were also compared with previously determined levels of HCAs (measured as MelQx, DiMelQx, and PhIP) and polycyclic aromatic hydrocarbons (PAHs) in the meat, levels of HCAs in the urine, and CYP1A2 and NAT2 phenotypes. The levels of mutagenicity in the meat fried at low and high temperatures correlated with levels of HCAs, but not levels of PAHs, in the meat. Also, levels of mutagenicity in unhydrolyzed urine correlated with levels of MelQx in unhydrolyzed urine (r = 0.36; P = 0.01), and the levels of mutagenicity of hydrolyzed urine correlated with levels of MelQx (r = 0.34; P 0.01) and PhlP (r = 0.43; P = 0.001) of hydrolyzed urine. Mutagenicity in unhydrolyzed urine was not influenced by either the CYP1A2 or NAT2 phenotype. The data from this study indicate that urinary mutagenicity correlates with mutagenic exposure from cooked meat and can potentially be used as a marker in etiological studies on cancer. Published 2004 Wiley-Liss, Inc. C1 NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Rockville, MD 20892 USA. NIEHS, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA. Univ Connecticut, Sch Med, Farmington, CT USA. US EPA, Div Environm Carcinogenesis, Res Triangle Pk, NC 27711 USA. RP Peters, U (reprint author), NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, 6120 Execut Blvd,EPS 3024, Rockville, MD 20892 USA. EM petersu@mail.nih.gov RI Kulldorff, Martin/H-4282-2011; Sinha, Rashmi/G-7446-2015; OI Sinha, Rashmi/0000-0002-2466-7462; Kulldorff, Martin/0000-0002-5284-2993 NR 47 TC 26 Z9 27 U1 1 U2 4 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 2004 VL 43 IS 1 BP 53 EP 74 DI 10.1002/em.10205 PG 22 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 772JD UT WOS:000188838100007 PM 14743346 ER PT J AU Lasky, T Sun, WY Kadry, A Hoffman, MK AF Lasky, T Sun, WY Kadry, A Hoffman, MK TI Mean total arsenic concentrations in chicken 1989-2000 and estimated exposures for consumers of chicken SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE arsenic; chicken; dose; drug residue; exposure; food safety; risk assessment ID TOTAL DIET; FOLLOW-UP; KIDNEY; CANCER; LIVER; RISK; MORTALITY; COHORT; WATER; FEED AB The purpose of this study was to estimate mean concentrations of total arsenic in chicken liver tissue and then estimate total and inorganic arsenic ingested by humans through chicken consumption. We used national monitoring data from the Food Safety and Inspection Service National Residue Program to estimate mean arsenic concentrations for 1994-2000. Incorporating assumptions about the concentrations of arsenic in liver and muscle tissues as well as the proportions of inorganic and organic arsenic, we then applied the estimates to national chicken consumption data to calculate inorganic, organic, and total arsenic ingested by eating chicken. The mean concentration of total arsenic in young chickens was 0.39 ppm, 3- to 4-fold higher than in other poultry and meat. At mean levels of chicken consumption (60 g/person/day), people may ingest 1.38-5.24 mug/day of inorganic arsenic from chicken alone. At the 99th percentile of chicken consumption (350 g chicken/day), people may ingest 21.13-30.59 mug inorganic arsenic/day and 32.50-47.07 mug total arsenic/day from chicken. These concentrations are higher than previously recognized in chicken, which may necessitate adjustments to estimates of arsenic ingested through diet and may need to be considered when estimating overall exposure to arsenic. C1 USDA, Food Safety & Inspect Serv, Off Publ Hlth & Sci, Washington, DC 20250 USA. RP Lasky, T (reprint author), NICHD, MSC 7510,6100 Execut blvd, Bethesda, MD 20892 USA. EM TL177G@nih.gov NR 23 TC 67 Z9 74 U1 1 U2 19 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2004 VL 112 IS 1 BP 18 EP 21 DI 10.1289/ehp.6407 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 761NH UT WOS:000187914500034 PM 14698925 ER PT J AU Chapin, RE Buck, GM AF Chapin, RE Buck, GM TI Our once-in-a-lifetime opportunity SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE editorial material; National Children's Study; reproductive epidemiology ID CORONARY-HEART-DISEASE; FETAL ORIGINS AB Longitudinal studies of the determinants of children's health are complex, costly, infrequent, and incredibly valuable. It has become clear in recent years that the periconceptional environment plays a surprisingly large role in the health of the resulting child. This short introduction to this mini-monograph briefly recaps the articles included herein and reminds us that adequate forethought and planning will result in a study that could shed new light on the earliest determinants of children's health and thereby fill critical data gaps. C1 Pfizer Global R&D, Reprod & Dev Toxicol Grp, Groton, CT 06340 USA. NICHHD, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Rockville, MD USA. RP Chapin, RE (reprint author), Pfizer Global R&D, Reprod & Dev Toxicol Grp, Eastern Point Rd,MS 8274-1336, Groton, CT 06340 USA. EM robert_e_chapin@groton.pfizer.com OI Chapin, Robert/0000-0002-5997-1261; Buck Louis, Germaine/0000-0002-1774-4490 NR 10 TC 9 Z9 9 U1 0 U2 0 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2004 VL 112 IS 1 BP 67 EP 68 DI 10.1289/ehp.6733 PG 2 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 761NH UT WOS:000187914500042 PM 14698933 ER PT J AU Buck, GM Lynch, CD Stanford, JB Sweeney, AM Schieve, LA Rockett, JC Selevan, SG Schrader, SM AF Buck, GM Lynch, CD Stanford, JB Sweeney, AM Schieve, LA Rockett, JC Selevan, SG Schrader, SM TI Prospective pregnancy study designs for assessing reproductive and developmental toxicants SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE design; development; fetal; preconception; pregnancy; prospective; reproduction; toxicity ID IN-VITRO FERTILIZATION; BIRTH CERTIFICATE DATA; TIMING INTERCOURSE; HUMAN-FERTILITY; SEMINAL PLASMA; UNITED-STATES; OVULATION; WOMEN; EXPOSURE; COUPLES AB The determinants of successful human reproduction and development may act as early as periconceptionally, underscoring the need to capture exposures during these critical windows when assessing potential toxicants. To identify such toxicants, couples must be studied longitudinally prior to conception without regard to a couple's ability to ascertain a clinically recognized pregnancy. We examined the utility and feasibility of prospective pregnancy study designs by conducting a systematic review of the literature to summarize relevant information regarding the planning, implementation, and success of previously published prospective pregnancy studies. Information concerning design elements and participation was abstracted from 15 eligible studies (from a total of 20 identified studies) using a standardized form. The primary author of each study was contacted to review our summary of their work and obtain missing information. Our findings confirm the ability to recruit women/couples from diverse populations using a variety of recruitment strategies. Among the studies we reviewed, 4-97% of eligible individuals were successfully contacted, with enrollment rates ranging from 42 to 100%. Length of follow-up varied from 3 to 12 months. A high percentage of women provided urine (57-98%) and blood (86-91%) specimens and most male partners (94-100%) provided semen samples. These data support the feasibility of this design. C1 NICHD, Epidemiol Branch, NIH, DHHS, Rockville, MD 20852 USA. Univ Utah, Dept Family Prevent Med, Hlth Res Ctr, Salt Lake City, UT USA. Texas A&M Univ, Hlth Sci Ctr, Dept Epidemiol, Sch Rural Publ Hlth, Bryan, TX USA. Ctr Dis Control & Prevent, Div Reprod Hlth, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA. US EPA, Gamete & Early Embryo Res Branch, Reprod Toxicol Div, Natl Hlth & Environm Effects Res Lab,Off Res & De, Res Triangle Pk, NC 27711 USA. US EPA, Natl Ctr Environm Assessment, Off Res & Dev, Washington, DC 20460 USA. Ctr Dis Control & Prevent, Reprod Hlth Assessment Sect, Div Appl Res & Technol, NIOSH, Cincinnati, OH USA. RP Buck, GM (reprint author), NICHD, Epidemiol Branch, NIH, DHHS, 6100 Execut Blvd,Rm 7B03, Rockville, MD 20852 USA. EM gb156i@nih.gov RI Schrader, Steven/E-8120-2011; OI Buck Louis, Germaine/0000-0002-1774-4490 NR 77 TC 53 Z9 54 U1 0 U2 5 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2004 VL 112 IS 1 BP 79 EP 86 DI 10.1289/ehp.6262 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 761NH UT WOS:000187914500044 PM 14698935 ER PT J AU Tingen, C Stanford, JB Dunson, DB AF Tingen, C Stanford, JB Dunson, DB TI Methodologic and statistical approaches to studying human fertility and environmental exposure SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Review DE conception; fecundability; menstrual cycle; ovulation; reproductive epidemiology; statistical methods; study design; time to pregnancy ID EARLY-PREGNANCY LOSS; TIME-TO-PREGNANCY; MENSTRUAL-CYCLE; UNITED-STATES; CAFFEINE CONSUMPTION; DECREASED FERTILITY; DAILY PROBABILITIES; PESTICIDE EXPOSURE; CIGARETTE-SMOKING; FEMALE FECUNDITY AB Although there has been growing concern about the effects of environmental exposures on human fertility, standard epidemiologic study designs may not collect sufficient data to identify subtle effects while property adjusting for confounding. In particular, results from conventional time to pregnancy studies can be driven by the many sources of bias inherent in these studies. By prospectively collecting detailed records of menstrual bleeding, occurrences of intercourse, and a marker of ovulation day in each menstrual cycle, precise information on exposure effects can be obtained, adjusting for many of the primary sources of bias. This article provides an overview of the different types of study designs, focusing on the data required, the practical advantages and disadvantages of each design, and the statistical methods required to take fall advantage of the available data. We conclude that detailed prospective studies allowing inferences on day specific probabilities of conception should be considered as the gold standard for studying the effects of environmental exposures on fertility. C1 NIEHS, Biostat Branch, NIH, DHHS, Res Triangle Pk, NC 27709 USA. Univ Utah, Hlth Res Ctr, Dept Family & Prevent Med, Salt Lake City, UT USA. RP Dunson, DB (reprint author), NIEHS, Biostat Branch, NIH, DHHS, POB 12233,MD A3-03, Res Triangle Pk, NC 27709 USA. EM dunson1@niehs.nih.gov NR 109 TC 32 Z9 35 U1 1 U2 8 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2004 VL 112 IS 1 BP 87 EP 93 DI 10.1289/ehp.6263 PG 7 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 761NH UT WOS:000187914500045 PM 14698936 ER PT J AU Rockett, JC Buck, GM Lynch, CD Perreault, SD AF Rockett, JC Buck, GM Lynch, CD Perreault, SD TI The value of home-based collection of biospecimens in reproductive epidemiology SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Review DE biospecimen; blood; breast milk; buccal cells; hair; home collection; nail; reproduction; saliva; semen; tissue collection; urine ID IN-VITRO FERTILIZATION; HUMAN HAIR-FOLLICLES; SAMPLE COLLECTION; FILTER-PAPER; OCCUPATIONAL EXPOSURE; BACTERIAL VAGINOSIS; GREENHOUSE WORKERS; PESTICIDE EXPOSURE; URINE SAMPLES; BIRTH-DEFECTS AB Detection, quantification, and prognosis of environmental exposures in humans has been vastly enhanced by the ability of epidemiologists to collect biospecimens for toxicologic or other laboratory evaluation. Ease of collection and level of invasiveness are commonly cited reasons why study participants fail to provide biospecimens for research purposes. The use of methodologies for the collection of biospecimens in the home offers promise for improving the validity of health effects linked to environmental exposures while maximizing the number and type of specimens capable of being collected in a timely and cost-effective manner. In this review we examine biospecimens (urine and blood) that have been successfully collected from the home environment. Related issues such as storage and transportation will also be examined as well as promising new approaches for collecting less frequently studied biospecimens (including hair follicles, breast milk, semen, and others). Such biospecimens are useful in the monitoring of reproductive development and function. C1 US EPA, Reprod Toxicol Div, NHEERL, Off Res & Dev, Res Triangle Pk, NC 27711 USA. NICHHD, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Rockville, MD USA. RP Rockett, JC (reprint author), US EPA, Reprod Toxicol Div, NHEERL, Off Res & Dev, MD-72, Res Triangle Pk, NC 27711 USA. EM rockett.john@epa.gov OI Buck Louis, Germaine/0000-0002-1774-4490 NR 125 TC 26 Z9 27 U1 0 U2 4 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2004 VL 112 IS 1 BP 94 EP 104 DI 10.1289/ehp.6264 PG 11 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 761NH UT WOS:000187914500046 PM 14698937 ER PT J AU Rockett, JC Lynch, CD Buck, GM AF Rockett, JC Lynch, CD Buck, GM TI Biomarkers for assessing reproductive development and health: Part 1 - Pubertal develonment SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE biomarker; development; human; longitudinal cohort study; puberty ID NUTRITION EXAMINATION SURVEY; 3RD NATIONAL-HEALTH; SECONDARY SEXUAL CHARACTERISTICS; MULLERIAN-INHIBITING SUBSTANCE; ADOLESCENT SELF-ASSESSMENT; ANTISPERM ANTIBODIES; LUTEINIZING-HORMONE; PREPUBERTAL BOYS; SERUM INHIBIN; PRECOCIOUS PUBERTY AB The proposed National Children's Study has helped raise awareness of the issues related to children's health and the importance of monitoring die growth and development of children from preconception through adulthood. Many genetic predispositions can adversely impact the normal development process, and various environmental exposures have been linked to adverse reproductive health in rodent models and a small number of accidental human exposures. To monitor reproductive health and identify adverse effects at the earliest possible juncture, investigators must develop a network of biomarkers covering all stages and aspects of reproductive development and function. Biomarkers are biological indicators that can be measured repeatedly and are informative on one or more aspects of biological development or friction. They can range from the anatomical level down to the molecular level and may provide information on the nature of an exposure, the effect of an exposure, or the susceptibility of individuals or populations to the toxic effects of an exposure. In theory, biomarkers can be used to monitor a wide variety of conditions and responses ranging from abnormal development to early indicators of late-onset disease. The main stumbling block with this theory has been finding appropriate biomarkers for particular conditions and exposures. Such biomarkers must be easily accessible, robust, and sensitive. Ideally, they will be expressed across a large section of the population, and can be monitored quickly, easily, conveniently, and with minimal cost. In this review, we discuss some of the current and emerging biomarkers of human pubertal development. C1 US EPA, Reprod Toxicol Dic, NHEERL, Off Res & Dev,Gamete & Early Embryo Biol Branch, Res Triangle Pk, NC 27711 USA. NICHHD, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Rockville, MD USA. RP Rockett, JC (reprint author), US EPA, Reprod Toxicol Dic, NHEERL, Off Res & Dev,Gamete & Early Embryo Biol Branch, MD-72, Res Triangle Pk, NC 27711 USA. EM rockett.john@epa.gov NR 93 TC 28 Z9 30 U1 1 U2 6 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2004 VL 112 IS 1 BP 105 EP 112 DI 10.1289/ehp.6265 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 761NH UT WOS:000187914500047 PM 14698938 ER PT J AU Olden, K Goehl, TJ AF Olden, K Goehl, TJ TI EHP moves to open access SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Editorial Material C1 NIEHS, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA. RP Olden, K (reprint author), NIEHS, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA. EM olden@niehs.nih.gov; goehl@niehs.nih.gov NR 0 TC 1 Z9 1 U1 0 U2 2 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JAN PY 2004 VL 112 IS 1 BP A13 EP A14 PG 2 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 761NH UT WOS:000187914500002 ER PT J AU Ben-Ari, Y Hablitz, JJ Rogawski, MA AF Ben-Ari, Y Hablitz, JJ Rogawski, MA TI The role of kainate receptors in epilepsy SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 INSERM, INMED, U29, Marseille, France. Univ Alabama, Dept Neurobiol, Chicago, IL USA. Univ Alabama, Dept Neurobiol, Birmingham, AL USA. NINDS, Epilepsy Res Sect, Washington, DC USA. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 2 EP 2 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100009 ER PT J AU Jacobs, MP Moshe, SL Nehlig, A Schwartzkroin, PA Swann, JW AF Jacobs, MP Moshe, SL Nehlig, A Schwartzkroin, PA Swann, JW TI Creating new animal models of the childhood epilepsies SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 NINDS, DHHS, NIH, Bethesda, MD 20892 USA. Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10467 USA. Univ Louis Pasteur Strasbourg 1, INSERM, Fac Med, Strasbourg, France. Univ Calif Davis, Dept Neurol Surg, Davis, CA 95616 USA. Baylor Coll Med, Dept Pediat, Houston, TX USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 2 EP 2 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100008 ER PT J AU Post, RM AF Post, RM TI Neurobiology of seizures and behavioral abnormalities SO EPILEPSIA LA English DT Article DE kindling; seizures; antiepileptic drugs; tolerance ID AMYGDALA-KINDLED SEIZURES; THYROTROPIN-RELEASING-HORMONE; REFRACTORY AFFECTIVE-DISORDERS; CONTINGENT TOLERANCE; ELECTRICAL STIMULATION; MESSENGER-RNA; AFFECTIVE-ILLNESS; BIPOLAR DISORDER; CROSS-TOLERANCE; CARBAMAZEPINE AB Seizures are both caused by and induce a complex set of neurobiological alterations and adaptations. The animal model of amygdala kindling provides insight into the spatiotemporal evolution of these changes as a function of seizure development and progression. Intracellular, synaptic, and microstructural changes are revealed as related to both the primary pathophysiology of kindled seizure evolution and compensatory secondary, or endogenous anticonvulsant adaptations. At the level of gene expression, the balance of these pathological and adaptive processes (as augmented by exogenous medications) probably determines whether seizures will be manifest or suppressed and could account for aspects of their intermittency. As anxiety and emotion modulation are subserved by many of the same neuroanatomic substrates involved in the evolution of complex partial seizures, particularly those of the medial temporal lobe, it is readily conceptualized how vulnerability to a range of psychiatric disorders could be related to the primary or secondary neurochemical alterations associated with seizure disorders. The discrete and methodologically controlled elucidation of the cascades and spatiotemporal distributions of neurobiological alterations that accompany seizure evolution in the kindling model may help resolve some of the difficulty and complexity of elucidating these biobehavioral relationships in the clinic. C1 NIMH, Biol Psychiat Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Post, RM (reprint author), NIMH, Biol Psychiat Branch, NIH, Dept Hlth & Human Serv, Bldg 10,Room 3S239,MSC-1272, Bethesda, MD 20892 USA. EM Robert.Post@NIH.gov NR 51 TC 42 Z9 43 U1 0 U2 2 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 2 BP 5 EP 14 DI 10.1111/j.0013-9580.2004.452001.x PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA 829WS UT WOS:000222082400002 PM 15186339 ER PT J AU Bonwetsch, R Fotheringham, J Donati, D Akhyani, N Vortmeyer, A Heiss, JD Gaillard, WD Theodore, WH Jacobson, S AF Bonwetsch, R Fotheringham, J Donati, D Akhyani, N Vortmeyer, A Heiss, JD Gaillard, WD Theodore, WH Jacobson, S TI Detection of human herpesvirus-6 in primary adult astrocyte cultures from epilepsy patients with mesial temporal sclerosis SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 NINDS, Clin Epilepsy Sect, Bethesda, MD 20892 USA. NINDS, Viral Immunol Sect, Bethesda, MD 20892 USA. Policlin Le Scott V Siena, Dipartimento Biol Mol, Siena, Italy. NINDS, Surg Neurol Branch, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 30 EP 30 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100089 ER PT J AU Gasior, M White, N Tang, R Rogawski, MA AF Gasior, M White, N Tang, R Rogawski, MA TI Attenuation of amygdala-kindled seziures in rats by convection-enhanced delivery of omega-conotoxins GVIA and MVIIA SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 NIND, Epilepsy Res Stn, NIH, Bethesda, MD USA. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 42 EP 42 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100122 ER PT J AU Bagic, A Balish, M Bonwetsch, R Theodore, WH Sato, S AF Bagic, A Balish, M Bonwetsch, R Theodore, WH Sato, S TI Restricted high-frequency coherent neural activity revealed by wide-band magnetoencephalography (MEG) in epilepsia partialis continua (EPC) SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 NIH, EEG Sect, Bethesda, MD 20892 USA. NINDS, CES, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 64 EP 64 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100188 ER PT J AU Pearl, PL Acosta, MT Gasior, M Theodore, WH Rogawski, MA Gibson, M AF Pearl, PL Acosta, MT Gasior, M Theodore, WH Rogawski, MA Gibson, M TI Epilepsy and movement disorders in succinate semialdehyde dehydrogenase (SSADH) deficiency: Relevance to human gamma-hydroxybutyrate (GHB) toxicity SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 Childrens Natl Med Ctr, Washington, DC USA. NINDS, NIH, Bethesda, MD 20892 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 94 EP 94 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100280 ER PT J AU Danielsson, I Su, KG Kauer, L Barnette, L Reeves-Tyer, P Kelley, K Theodore, WH Wassermann, E Rogawski, MA AF Danielsson, I Su, KG Kauer, L Barnette, L Reeves-Tyer, P Kelley, K Theodore, WH Wassermann, E Rogawski, MA TI Talampanel and human cortical excitability: EEG and TMS SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 NINDS, Epilepsy Res Sect, Bethesda, MD 20892 USA. NINDS, Clin Epilepsy Sect, Bethesda, MD 20892 USA. NINDS, NIH, Off Director, Bethesda, MD 20892 USA. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 0 TC 4 Z9 6 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 120 EP 121 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100355 ER PT J AU Kaminski, LM Marini, H Kim, LJ Rogawski, MA AF Kaminski, LM Marini, H Kim, LJ Rogawski, MA TI Androsterone, a metabolite of testosterone that positively modulates GABA(A) receptors, protects against seizures in animal models: In vivo and in vitro studies SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 NINDS, Epilepsy Res Sect, NIH, Bethesda, MD 20892 USA. Univ Messina, Fac Med & Surg, AOU G Martino, I-98100 Messina, Italy. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 209 EP 209 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100613 ER PT J AU Banerjee, M Munasinghe, J Despres, D Anstadt, M Lizak, M Silva, A Rogawski, M Koretsky, A Theodore, WH AF Banerjee, M Munasinghe, J Despres, D Anstadt, M Lizak, M Silva, A Rogawski, M Koretsky, A Theodore, WH TI Focal amygdalar glutamatergic agonist infusion leads to rapid diffuse cerebral activation SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 NINDS, NIH, Bethesda, MD 20892 USA. RI Rogawski, Michael/B-6353-2009 OI Rogawski, Michael/0000-0002-3296-8193 NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 216 EP 216 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100635 ER PT J AU Bagic, A Bagic, D Balish, M Sato, S AF Bagic, A Bagic, D Balish, M Sato, S TI Public awareness and perception of epilepsy in Bosnia and Herzegovina (B&H) SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 NIH, EEG Sect, Bethesda, MD 20892 USA. PULS, Zagreb, Croatia. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 234 EP 234 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100688 ER PT J AU Dickens, D Gaillard, WD Martinez-Castillo, E Ritter, FJ Frost, MD Penovich, P Risse, G Gates, J AF Dickens, D Gaillard, WD Martinez-Castillo, E Ritter, FJ Frost, MD Penovich, P Risse, G Gates, J TI Presurgical localization of language: A preliminary comparison of multiple techniques SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 Minnesota Epilepsy Grp PA, NP EP, St Paul, MN USA. Univ Minnesota, Minneapolis, MN USA. Univ Texas, Houston, TX USA. NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 336 EP 336 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420100988 ER PT J AU Berl, MM Moore, E Xu, B Pearl, PL Conry, JA Weinstein, SL Ritter, FJ Theodore, WH Gaillard, WD AF Berl, MM Moore, E Xu, B Pearl, PL Conry, JA Weinstein, SL Ritter, FJ Theodore, WH Gaillard, WD TI Atypical language dominance and patterns of reorganization in epilepsy as assessed by a panel of fMRI tasks SO EPILEPSIA LA English DT Meeting Abstract CT Annual Meeting of the American-Epilepsy-Society CY DEC 03-07, 2004 CL New Orlands, LA SP Amer Epilepsy Soc C1 Childrens Natl Med Ctr, Dept Neurosci, Washington, DC 20010 USA. NINDS, Clin Epilepsy Sect, NIH, Bethesda, MD 20892 USA. Minnesota Epilepsy Grp, St Paul, MN USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 7 BP 366 EP 366 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 861MG UT WOS:000224420101080 ER PT J AU Kino, T Chrousos, GP AF Kino, T Chrousos, GP TI Glucocorticoid and mineralocorticoid receptors and associated diseases SO ESSAYS IN BIOCHEMISTRY: NUCLEAR RECEPTOR SUPERFAMILY SE ESSAYS IN BIOCHEMISTRY LA English DT Review ID PSEUDOHYPOALDOSTERONISM TYPE-1; CORTISOL RESISTANCE; MISSENSE MUTATION; BINDING DOMAIN; GENE; HYPERTENSION; MICE; GR; DETERMINANTS; DISRUPTION AB Adrenal corticosteroids, le. glucocorticoids and mineralocorticoids, play important physiological roles in humans. Their actions are mediated by intracellular receptor molecules, the glucocorticold receptor (GR) and mineral ocorticold receptor (MR), which function as hormone-dependent transcription factors. Ligand-activated receptors modulate the transcription rates of responsive genes by interacting with responsive elements in the promoters of these genes or by influencing the activities of other transcription factors, via protein-protein interactions. Natural inactivating mutations of the GR or MR genes have been reported in humans with significant clinical phenotypes. The former causes sporadic or familial glucocorticold resistance characterized by generalized partial insensitivity of tissues to glucocorticolds and subsequent activation of the hypothalamic/pitultary/adrenal axis with resultant hyperandrogenism in children and women and/or mineralocorticold excess symptoms in both sexes. The latter develop pseudohypoaldosteronism type 1, i.e. hypotension and hyperkalaemic acidosis, as a result of reduced aldosterone actions in the kidney. An activating mutation in the MR gene causing early-onset, periodic hypertension was reported recently. The biological relevance of the GR and MR receptors was also addressed in mice whose GR or MR genes were inactivated or modified by gene targeting. The results were generally confirmatory of the concepts obtained by the human studies. Similarly, natural, compensated glucocorticold and/or mineralocorticold 'resistance' were described in several mammalian species, including non-human primates and rodents. Here we discuss the actions of GR and MR and the molecular defects of naturally occuring mutations in these receptors with associated pathophysiological changes. C1 NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Kino, T (reprint author), NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. EM kinot@mail.nih.gov NR 37 TC 40 Z9 41 U1 0 U2 4 PU PORTLAND PRESS LTD PI LONDON PA 59 PORTLAND PL, LONDON W1N 3AJ, ENGLAND SN 0071-1365 J9 ESSAYS BIOCHEM PY 2004 VL 40 BP 137 EP 155 PG 19 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BAR67 UT WOS:000223268600010 PM 15242344 ER PT B AU Brock, DW AF Brock, DW BE Gutmann, T Daar, AS Sells, RA Land, W TI The misplaced role of urgency in allocation of persistently scarce life-saving organs SO ETHICAL, LEGAL, AND SOCIAL ISSUES IN ORGAN TRANSPLANTATION LA English DT Proceedings Paper CT 1st International Congress of the German-Academy-of-Transplantation-Medicine on Ethics in Organ Transplantation CY DEC 10-13, 2002 CL Munich, GERMANY SP German Acad Transplatat Med C1 NIH, Warren G Magnuson Clin Ctr, Dept Clin Bioeth, Bethesda, MD 20892 USA. RP Brock, DW (reprint author), NIH, Warren G Magnuson Clin Ctr, Dept Clin Bioeth, Bldg 10,Room 1C118, Bethesda, MD 20892 USA. NR 10 TC 1 Z9 1 U1 0 U2 1 PU PABST SCIENCE PUBLISHERS PI D-49525 LENGERICH PA EICHENGRUND 28, D-49525 LENGERICH, GERMANY BN 1-59326-063-6 PY 2004 BP 41 EP 48 PG 8 WC Medical Ethics; Transplantation SC Medical Ethics; Transplantation GA BBP81 UT WOS:000226965300003 ER PT J AU Wang, XD Dougherty, ER Chen, YD Peterson, CO AF Wang, XD Dougherty, ER Chen, YD Peterson, CO TI Genomic signal processing - Editorial SO EURASIP JOURNAL ON APPLIED SIGNAL PROCESSING LA English DT Editorial Material C1 Columbia Univ, Dept Elect Engn, New York, NY 10027 USA. Texas A&M Univ, Dept Elect Engn, College Stn, TX 77843 USA. Natl Human Genome Res Inst, NIH, Bethesda, MD 20892 USA. Lund Univ, Dept Theoret Phys, SE-22362 Lund, Sweden. RP Wang, XD (reprint author), Columbia Univ, Dept Elect Engn, New York, NY 10027 USA. EM wangx@ee.columbia.edu; e-dougherty@tamu.edu; yidong@nhgri.nih.gov; carsten@thep.lu.se NR 0 TC 30 Z9 32 U1 0 U2 2 PU HINDAWI PUBLISHING CORPORATION PI SYLVANIA PA PO BOX 1210, SYLVANIA, OH 43560 USA SN 1110-8657 J9 EURASIP J APPL SIG P JI EURASIP J Appl. Signal Process. PD JAN 1 PY 2004 VL 2004 IS 1 BP 3 EP 4 DI 10.1155/S1110865704002756 PG 2 WC Engineering, Electrical & Electronic SC Engineering GA 817PN UT WOS:000221189500001 ER PT J AU Wu, XW Chen, YD Brooks, BR Su, YA AF Wu, XW Chen, YD Brooks, BR Su, YA TI The local maximum clustering method and its application in microarray gene expression data analysis SO EURASIP JOURNAL ON APPLIED SIGNAL PROCESSING LA English DT Article DE data cluster; clustering method; microarray; gene expression; classification; model data sets ID SELF-ORGANIZING MAPS; PATTERNS AB An unsupervised data clustering method, called the local maximum clustering (LMC) method, is proposed for identifying clusters in experiment data sets based on research interest. A magnitude property is defined according to research purposes, and data sets are clustered around each local maximum of the magnitude property. By properly defining a magnitude property, this method can overcome many difficulties in microarray data clustering such as reduced projection in similarities, noises, and arbitrary gene distribution. To critically evaluate the performance of this clustering method in comparison with other methods, we designed three model data sets with known cluster distributions and applied the LMC method as well as the hierarchic clustering method, the K-mean clustering method, and the self-organized map method to these model data sets. The results show that the LMC method produces the most accurate clustering results. As an example of application, we applied the method to cluster the leukemia samples reported in the microarray study of Golub et al. (1999). C1 Natl Heart Lung & Blood Inst, Lab Biophys Chem, NIH, Bethesda, MD 20892 USA. Natl Human Genome Res Inst, NIH, Bethesda, MD 20892 USA. Loyola Univ, Ctr Med, Dept Pathol, Maywood, IL 60153 USA. RP Wu, XW (reprint author), Natl Heart Lung & Blood Inst, Lab Biophys Chem, NIH, Bethesda, MD 20892 USA. EM wuxw@nhlbi.nih.gov; yidong@nhgri.nih.gov; brb@nih.gov; ysu2@lumc.edu NR 13 TC 16 Z9 16 U1 0 U2 1 PU HINDAWI PUBLISHING CORPORATION PI SYLVANIA PA PO BOX 1210, SYLVANIA, OH 43560 USA SN 1110-8657 J9 EURASIP J APPL SIG P JI EURASIP J Appl. Signal Process. PD JAN 1 PY 2004 VL 2004 IS 1 BP 53 EP 63 DI 10.1155/S1110865704309145 PG 11 WC Engineering, Electrical & Electronic SC Engineering GA 817PN UT WOS:000221189500006 ER PT J AU Iribarren, C Markovitz, JH Jacobs, DR Schreiner, PJ Daviglus, M Hibbeln, JR AF Iribarren, C Markovitz, JH Jacobs, DR Schreiner, PJ Daviglus, M Hibbeln, JR TI Dietary intake of n-3, n-6 fatty acids and fish: Relationship with hostility in young adults - the CARDIA study SO EUROPEAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE dietary n-3 fatty acids; dietary n-6 fatty acids; fish consumption; hostility; young adults ID ACUTE MYOCARDIAL-INFARCTION; CORONARY-ARTERY DISEASE; ISCHEMIC-HEART-DISEASE; DOCOSAHEXAENOIC ACID; ADIPOSE-TISSUE; RISK FACTOR; MEN; CONSUMPTION; MORTALITY; PLASMA AB Background: Hostility has been shown to predict both the development and manifestation of coronary disease. Examining the inter-relation of dietary intake of fish and of polyunsaturated (n-3 and n-6) essential fatty acids with hostility may provide additional insights into the cardioprotective effect of dietary fish and polyunsaturated fatty acids. Objective: To examine the association of dietary n-3, n-6 fatty acids and fish with level of hostility in a sample of 3581 urban white and black young adults. Design: Cross-sectional observational study as part of an ongoing cohort study. A dietary assessment in 1992-1993 and measurement of hostility and other covariates in 1990-1991 were used in the analysis. Results: The multivariate odds ratios of scoring in the upper quartile of hostility (adjusting for age, sex, race, field center, educational attainment, marital status, body mass index, smoking, alcohol consumption and physical activity) associated with one standard deviation increase in docosahexaenoic acid (DHA, 22: 6) intake was 0.90 (95% CI = 0.82-0.98; P = 0.02). Consumption of any fish rich in n-3 fatty acids, compared to no consumption, was also independently associated with lower odds of high hostility (OR = 0.82; 95% CI = 0.69-0.97; P = 0.02). Conclusions: These results suggest that high dietary intake of DHA and consumption of fish rich in n-3 fatty acids may be related to lower likelihood of high hostility in young adulthood. The association between dietary n-3 fatty acids and hostile personality merits further research. C1 Kaiser Permanente, Div Res, Oakland, CA 94611 USA. Univ Alabama, Div Prevent Med, Birmingham, AL 35294 USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. Northwestern Univ, Sch Med, Dept Prevent Med, Chicago, IL 60611 USA. NIAAA, Lab Membrane Biophys & Biochem, NIH, Rockville, MD 20852 USA. RP Iribarren, C (reprint author), Kaiser Permanente, Div Res, 2000 Broadway, Oakland, CA 94611 USA. FU NHLBI NIH HHS [N01-HC-48047, N01-HC-48048, N01-HC-48050]; NIA NIH HHS [R01-AG12264-01A1] NR 58 TC 70 Z9 83 U1 0 U2 7 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0954-3007 J9 EUR J CLIN NUTR JI Eur. J. Clin. Nutr. PD JAN PY 2004 VL 58 IS 1 BP 24 EP 31 DI 10.1038/sj.ejcn.1601739 PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 754DF UT WOS:000187286900004 PM 14679363 ER PT J AU Chen, WS Masterman, KA Basta, S Haeryfar, SMM Dimopoulos, N Knowles, B Bennink, JR Yewdell, JW AF Chen, WS Masterman, KA Basta, S Haeryfar, SMM Dimopoulos, N Knowles, B Bennink, JR Yewdell, JW TI Cross-priming of CD8(+) T cells by viral and tumor antigens is a robust phenomenon SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE CTL; cross-priming; MHC; virus; tumor ID IMMUNODOMINANCE HIERARCHIES; MEDIATED CYTOTOXICITY; INFLUENZA-VIRUS; RESPONSES; INDUCTION; EPITOPE; CTL AB "Cross-priming" refers to the activation of naive CD8(+) T cells by antigen-presenting cells that have acquired nominal antigens from another cell. The biological relevance of cross-priming of CD8(+)T cells has recently been challenged (Zinkernagel, R. M., Eur J. Immunol. 2002. 32: 2385-2392), on the basis that responses are weak or poorly quantitated, and the determinants recognized are undefined. Here we show that cross-priming is a robust process that elicits vigorous primary responses to multiple pepticles in two well-defined systems. Our findings support the relevance of cross-priming in CD8(+) T cell responses to viruses and tumor cells, and demonstrate that cross-priming elicits CD8(+) T cells to determinants generated by the endogenous processing pathway. C1 Austin & Repatriat Med Ctr, Ludwig Inst Canc Res, Canc Vaccine Unit, T Cell Lab, Heidelberg, Vic, Australia. NIAID, Viral Dis Lab, Bethesda, MD 20892 USA. Jackson Lab, Bar Harbor, ME 04609 USA. RP Yewdell, JW (reprint author), Room 211 Bldg 4,4 Ctr Dr, Bethesda, MD 20892 USA. EM jyewdell@nih.gov RI yewdell, jyewdell@nih.gov/A-1702-2012; Chen, Weisan/E-7828-2012 NR 17 TC 55 Z9 59 U1 0 U2 0 PU WILEY-V C H VERLAG GMBH PI WEINHEIM PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 2004 VL 34 IS 1 BP 194 EP 199 DI 10.1002/eji.200324257 PG 6 WC Immunology SC Immunology GA 766YY UT WOS:000188412400021 PM 14971045 ER PT J AU Vashishtha, SC Zello, GA Nienaber, KH Balzarini, J De Clercq, E Stables, JP Dimmock, JR AF Vashishtha, SC Zello, GA Nienaber, KH Balzarini, J De Clercq, E Stables, JP Dimmock, JR TI Cytotoxic and anticonvulsant aryloxyaryl Mannich bases and related compounds SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article DE Mannich bases; cytotoxicity; molecular modelling; structure-activity relationships; murine toxicity; anticonvulsant activity ID ARYLIDENE KETONES; ANTICANCER; ARYL AB A series of 1-(4-aryloxyphenyl)-3-diethylamino-1-propanone hydrochlorides 3a-3e and related compounds 3f, 3g and 4a-4d were synthesised. In addition, a group of 4-(4-aryloxyphenyl)-3-(4-aryloxyphenylcarbonyl)-1-ethyl-4-piperidinol hydrochlorides 6a-6e were prepared which incorporated most of the structural features of 3a-3e. All of these compounds displayed cytotoxic properties towards murine L1210 cells as well as human Molt 4/C8 and CEM T-lymphocytes. A number of these compounds possessed noteworthy potencies towards seven human colon cancer cell lines. Some correlations were noted between the IC50 values generated in the different screens and the sigma, pi and molar refractivity constants of the aryl substituents as well as with the volumes and solvent accessible surface areas of various basic groups. Molecular modelling of representative compounds revealed structural features, which may have contributed to the varying potencies noted. In general, the compounds in series 6 were well tolerated when administered to mice. Anticonvulsant properties were demonstrated by a number of compounds in the maximal electroshock (MES) screen when administered intraperitoneally to mice while 4c and 6e afforded protection in the MES test when given orally to rats. (C) 2003 Elsevier SAS. All rights reserved. C1 Univ Saskatchewan, Coll Pharm & Nutr, Saskatoon, SK S7N 5C9, Canada. Univ Saskatchewan, Dept Biochem, Saskatoon, SK S7N 5E5, Canada. Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium. NINDS, NIH, Bethesda, MD 20892 USA. RP Dimmock, JR (reprint author), Univ Saskatchewan, Coll Pharm & Nutr, 110 Sci Pl, Saskatoon, SK S7N 5C9, Canada. EM dimmock@skyway.usask.ca NR 26 TC 14 Z9 15 U1 0 U2 3 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0223-5234 J9 EUR J MED CHEM JI Eur. J. Med. Chem. PD JAN PY 2004 VL 39 IS 1 BP 27 EP 35 DI 10.1016/j.ejmech.2003.09.011 PG 9 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 807MY UT WOS:000220506800003 PM 14987831 ER PT J AU Lee, J Kim, SY Kang, JH Acs, G Acs, P Blumberg, PM Marquez, VE AF Lee, J Kim, SY Kang, JH Acs, G Acs, P Blumberg, PM Marquez, VE TI Conformationally constrained diacylglycerol (DAG) analogs: 4-C-hydroxyethyl-5-O-acyl-2,3-dideoxy-D-glyceropentono-1,4-lactone analogs as protein kinase C (PKC) ligands SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article DE protein kinase C; DAG-lactone; diacylglycerol; phorbol ester ID PHORBOL ESTER; BINDING-AFFINITY; STRUCTURAL BASIS; TUMOR PROMOTERS; SN-2 CARBONYLS; ACTIVATION; LACTONES; RECEPTOR AB The (R)-DAG-lactones (5 and 7E/Z) are conformationally constrained diacylglycerol (DAG) analogs with high potency as protein kinase C (PKC) ligands. Here, we have prepared and characterized their one-carbon lengthened analogs (6 and 8E/Z). The target compounds were synthesized from 1,2-O-isopropylidene D-xylose through a key intermediate, 4-C-hydroxyethyl-2,3-dideoxy-D-glyceropentono-1,4-lactone (13); they were evaluated as competitive ligands to displace bound [H-3]phorbol 12,13-dibutyrate (PDBU) from a recombinant single isozyme (PKC-alpha). The binding affinities of the synthesized compounds were K-i = 2.623 muM for 6, K-i = 1.080 muM for 8Z and K-i = 0.92 muM for 8E, which were ca. 27, 90, and 70 times less potent than the corresponding parent compounds (5, 7Z and 7E). Molecular modeling indicated that the reduced binding affinity of the representative 3-alkylidene lactone 8Z, as compared to 7Z, may be explained by its poor fit in the sn-1 binding mode as well as by its entropic loss due to the relatively flexible hydroxyethyl group. (C) 2003 Elsevier SAS. All rights reserved. C1 Seoul Natl Univ, Coll Pharm, Pharmaceut Sci Res Inst, Med Chem Lab, Seoul 151742, South Korea. NCI, Ctr Canc Res, Cellular Carcinogenesis & Tumor Promot Lab, Bethesda, MD 20892 USA. NCI, Med Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21701 USA. RP Marquez, VE (reprint author), Seoul Natl Univ, Coll Pharm, Pharmaceut Sci Res Inst, Med Chem Lab, Seoul 151742, South Korea. EM jeewoo@snu.ac.kr; marquez@dc37a.nci.nih.gov NR 18 TC 2 Z9 2 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0223-5234 J9 EUR J MED CHEM JI Eur. J. Med. Chem. PD JAN PY 2004 VL 39 IS 1 BP 69 EP 77 DI 10.1016/j.ejmech.2003.10.006 PG 9 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA 807MY UT WOS:000220506800007 PM 14987835 ER PT J AU Garvey, MA Gilbert, DL AF Garvey, MA Gilbert, DL TI Transcranial magnetic stimulation in children SO EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY LA English DT Review DE cortical maturation; motor evoked potential; silent period; interhemispheric interactions ID CENTRAL MOTOR REORGANIZATION; HEMIPLEGIC CEREBRAL-PALSY; DEFICIT-HYPERACTIVITY DISORDER; PELIZAEUS-MERZBACHER DISEASE; CENTRAL CONDUCTION DELAYS; HUMAN CORPUS-CALLOSUM; EVOKED-POTENTIALS; CORTICOSPINAL PROJECTIONS; TRANSCALLOSAL INHIBITION; HUMAN HANDEDNESS AB Single and paired pulse transcranial magnetic stimulation (TMS) provide a non-invasive, painless method of probing the motor system. These techniques are of particular interest for studying maturation of the motor system and may provide insights into those developmental disabilities strongly associated with specific delays of motor development. This article will review studies using single pulse and paired pulse TMS in children, with particular reference to insights into neurodevelopment in children. It will also briefly touch on the potential of TMS as a diagnostic tool in neurological disorders. It will not address the use of repetitive TMS in children. (C) 2003 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved. C1 NINDS, Pediat Movement Disorders Unit, Human Motor Control Sect, MNB, Bethesda, MD 20892 USA. Cincinnati Childrens Hosp, Med Ctr, Movement Disorders Clin, Cincinnati, OH USA. RP Garvey, MA (reprint author), NINDS, Pediat Movement Disorders Unit, Human Motor Control Sect, MNB, 10 Ctr Dr,Room 5N226,MSC 1428, Bethesda, MD 20892 USA. EM mg202m@nih.gov RI Gilbert, Donald/D-6443-2016 OI Gilbert, Donald/0000-0002-9245-6878 NR 92 TC 42 Z9 44 U1 0 U2 6 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1090-3798 J9 EUR J PAEDIATR NEURO JI Eur. J. Paediatr. Neurol. PY 2004 VL 8 IS 1 BP 7 EP 19 DI 10.1016/j.ejpn.2003.11.002 PG 13 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 778WH UT WOS:000189264000002 PM 15023371 ER PT J AU Chan, LMS Lowes, S Hirst, BH AF Chan, LMS Lowes, S Hirst, BH TI The ABCs of drug transport in intestine and liver: efflux proteins limiting drug absorption and bioavailability SO EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES LA English DT Review DE ABC efflux transporters; intestinal clearance; MDR1 P-glycoprotein; MRP; regulation ID MULTIDRUG-RESISTANCE PROTEIN; ORGANIC ANION TRANSPORTER; HUMAN P-GLYCOPROTEIN; CONJUGATE EXPORT PUMP; PREGNANE-X-RECEPTOR; ATP-DEPENDENT TRANSPORT; BLOOD-BRAIN-BARRIER; CONSTITUTIVE ANDROSTANE RECEPTOR; GLUTATHIONE-S-TRANSFERASE; KIDNEY PROXIMAL TUBULES AB Many orally administered drugs must overcome several barriers before reaching their target site. The first major obstacle to cross is the intestinal epithelium. Although lipophilic compounds may readily diffuse across the apical plasma membrane, their subsequent passage across the basolateral membrane and into blood is by no means guaranteed. Efflux proteins located at the apical membrane, which include P-glycoprotein (Pgp; MDR1) and MRP2, may drive compounds from inside the cell back into the intestinal lumen, preventing their absorption into blood. Drugs may also be modified by intracellular phase I and phase II metabolising enzymes. This process may not only render the drug ineffective, but it may also produce metabolites that are themselves substrates for Pgp and/or MRP2. Drugs that reach the blood are then passed to the liver, where they are subject to further metabolism and biliary excretion, often by a similar system of ATP-binding cassette (ABC) transporters and enzymes to that present in the intestine. Thus a synergistic relationship exists between intestinal drug metabolising enzymes and apical efflux transporters, a partnership that proves to be a critical determinant of oral bioavailability. The effectiveness of this system is optimised through dynamic regulation of transporter and enzyme expression; tissues have a remarkable capacity to regulate the amounts of protein both at transcriptional and post-transcriptional levels in order to maintain homeostasis. This review addresses the progress to date on what is known about the role and regulation of drug efflux mechanisms in the intestine and liver. (C) 2003 Elsevier B.V. All rights reserved. C1 Univ Newcastle Upon Tyne, Sch Med, Sch Cell & Mol Biosci, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England. NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. RP Hirst, BH (reprint author), Univ Newcastle Upon Tyne, Sch Med, Sch Cell & Mol Biosci, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England. EM barry.hirst@ncl.ac.uk NR 270 TC 367 Z9 385 U1 4 U2 42 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0928-0987 J9 EUR J PHARM SCI JI Eur. J. Pharm. Sci. PD JAN PY 2004 VL 21 IS 1 BP 25 EP 51 DI 10.1016/j.ejps.2003.07.003 PG 27 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 767AF UT WOS:000188415600004 PM 14706810 ER PT J AU Wang, CK Wu, YR Hwu, WL Chen, CM Ro, LS Chen, ST Gwinn-Hardy, K Yang, CC Wu, RM Chen, TF Wang, HC Chao, MC Chiu, MJ Lu, CJ Lee-Chen, GJ AF Wang, CK Wu, YR Hwu, WL Chen, CM Ro, LS Chen, ST Gwinn-Hardy, K Yang, CC Wu, RM Chen, TF Wang, HC Chao, MC Chiu, MJ Lu, CJ Lee-Chen, GJ TI DNA haplotype analysis of CAG repeat in Taiwanese Huntington's disease patients SO EUROPEAN NEUROLOGY LA English DT Article DE Huntington's disease; genotyping; CAG repeat; CCG repeat; dinucleotide repeat markers; haplotype analysis ID AGE-OF-ONSET; GENE; TRINUCLEOTIDE; POLYMORPHISM; CHROMOSOMES; ADJACENT; REVEALS; CHOREA; INDIA AB We studied the expanded CAG repeat and adjacent CCG repeat in 53 Huntington's disease (HD) patients and 172 unrelated normal subjects matched to the patients for ethnic origin. The range of the CAG repeat varied from 38 to 109 in the HD patients and from 10 to 29 in the control group. A significant negative correlation was found between the age at onset and the CAG expansion, with no significant influence of the adjacent CCG repeat on the age at onset by multiple regression analysis. Allelic association using CCG repeat and 2 flanking dinucleotide repeat markers within 150 kb of the HD gene revealed linkage disequilibrium for 2 of 3 markers. Haplotype analysis of 24 HD families using these markers identified 3 major haplotypes underlying 87.5% of HD chromosomes. The data suggested frequent haplotypes in the Taiwanese population on which one or more mutational events leading to the disease occurred. Copyright (C) 2004 S. Karger AG, Basel. C1 Natl Taiwan Normal Univ, Dept Life Sci, Taipei 116, Taiwan. Chang Gung Mem Hosp, Taipei 10591, Taiwan. Natl Taiwan Univ Hosp, Taipei, Taiwan. Shin Kong Wu Ho Su Mem Hosp, Taipei, Taiwan. Jen Teh Jr Coll Med Nursing & Management, Miaoli, Taiwan. Kaohsiung Med Univ, Chang Ho Mem Hosp, Kaohsiung, Taiwan. NIH, Bethesda, MD 20892 USA. RP Lee-Chen, GJ (reprint author), Natl Taiwan Normal Univ, Dept Life Sci, 88 Ting Chou Rd,Sect 4, Taipei 116, Taiwan. EM t43019@cc.ntnu.edu.tw RI Gwinn, Katrina/C-2508-2009; OI HWU, WUH-LIANG/0000-0001-6690-4879; Yang, Chih-Chao/0000-0002-0352-3144; Wu, Ruey-Meei/0000-0002-4947-5467; Chen, Ta-Fu/0000-0003-1988-6924; Chiu, Ming-Jang/0000-0002-4158-4423; Gwinn, Katrina/0000-0002-8277-651X NR 17 TC 12 Z9 12 U1 1 U2 4 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0014-3022 J9 EUR NEUROL JI Eur. Neurol. PY 2004 VL 52 IS 2 BP 96 EP 100 DI 10.1159/000079938 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 869MP UT WOS:000224988600007 PM 15273431 ER PT J AU Chu, K Jung, KH Kim, HJ Jeong, SW Kang, DW Roh, JK AF Chu, K Jung, KH Kim, HJ Jeong, SW Kang, DW Roh, JK TI Diffusion-weighted MRI and Tc-99m-HMPAO SPECT in delayed relapsing type of carbon monoxide poisoning: Evidence of delayed cytotoxic edema SO EUROPEAN NEUROLOGY LA English DT Article DE carbon monoxide; diffusion-weighted MRI; delayed cytotoxic edema; SPECT ID MAGNETIC-RESONANCE; INTERVAL FORM; APPARENT DIFFUSION; NEURONAL DAMAGE; HUMAN STROKE; RAT-BRAIN; ENCEPHALOPATHY; SPECTROSCOPY; HYPERGLYCEMIA; INFARCTION AB Background: Carbon monoxide (CO) is a common cause of poisoning, and its sequelae include a progressive (25%) and a delayed relapsing form (75%). We report the diffusion-weighted MRI (DWI) findings in the delayed relapsing form of CO poisoning and characterize the types of edema. Methods: From November 1, 2000 to June 1, 2003, 5 consecutive patients (2 men, 3 women, range of age: 54-67 years), who had the delayed relapsing type of CO poisoning, underwent DWI, conventional MRI, MR angiography and SPECT. CO poisoning was diagnosed by the presence of a typical clinical history, an abnormally increased level of serum carboxyhemoglobin and MRI findings. Apparent diffusion coefficient (ADC) values were measured in all of the abnormal lesions with visual inspection of DWI and T-2-weighted echo-planar imaging. Results: DWI showed high signal intensities in bilateral periventricular white matter, in the splenium of the corpus callosum, in internal capsules, and brainstem showing moderately decreased ADC values. In the globus pallidus, the ADC values were rather increased with low signal intensities on DWI. Brain SPECT showed decreased perfusion in bilateral white matter and some parts of the cerebral cortex, which correlated well with the DWI findings. Conclusions: We suggest that prominent, symmetric restricted diffusion can occur in periventricular white matter, brainstem, and corpus callosum after the delayed relapsing type of CO poisoning. Delayed cytotoxic edema can occur in this setting, which provides a new guidance for the pathogenesis of CO poisoning and the differential diagnosis of white matter diseases. Copyright (C) 2004 S. Karger AG, Basel. C1 Seoul Natl Univ, Dept Neurol, Seoul Natl Univ Hosp, Seoul 110744, South Korea. Seoul Natl Univ, Stroke & Neural Stem Cell Lab, Seoul Natl Univ Hosp, Clin Res Inst, Seoul 110744, South Korea. Seoul Natl Hosp, Dept Neurol & Geriatr Psychiat, Seoul, South Korea. Inje Univ, Dept Neurol, Ilsan Pk Hosp, Goyang, South Korea. Ulsan Med Sch, Dept Neurol, Asan Med Ctr, Seoul, South Korea. NINDS, Sect Stroke Diagnost & Therapeut, Bethesda, MD 20892 USA. RP Roh, JK (reprint author), Seoul Natl Univ, Dept Neurol, Seoul Natl Univ Hosp, 28 Yongon Dong, Seoul 110744, South Korea. EM rohjk@snu.ac.kr RI Roh, Jae Kyu/J-5459-2012 NR 36 TC 24 Z9 31 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 2004 VL 51 IS 2 BP 98 EP 103 DI 10.1159/000076536 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 800KL UT WOS:000220027100007 PM 14752216 ER PT J AU Helip-Wooley, A Thoene, JG AF Helip-Wooley, A Thoene, JG TI Sucrose-induced vacuolation results in increased expression of cholesterol biosynthesis and lysosomal genes SO EXPERIMENTAL CELL RESEARCH LA English DT Article DE sucrose-induced vacuolation; cholesterol biosynthesis; lysosomal genes ID LOW-DENSITY-LIPOPROTEIN; REGULATORY ELEMENT; HUMAN FIBROBLASTS; MEMBRANE-PROTEIN; BINDING PROTEINS; STORAGE; DISEASE; CELL; IDENTIFICATION; PATHWAY AB Mammalian cells cultured in the presence of high concentrations of sucrose demonstrate large, phase-lucent, osmotically swollen vacuoles. Three normal human fibroblast cell lines exposed to 100 mM of sucrose for 24 h demonstrated increased expression of lysosomal, intracellular vesicle trafficking, cholesterol biosynthesis, and fatty acid metabolism genes. Most steps of the cholesterol biosynthesis pathway were upregulated including HMG CoA reductase, which catalyzes the rate-limiting step of cholesterol biosynthesis. The lysosomal genes neuraminidase, CLN3, and CLCN5 and the small GTP-binding proteins Rab7L1 and Ar17 were also increased. A Rab7L1-GFP fusion protein was overexpressed in human fibroblasts and was demonstrated to localize primarily to the Golgi apparatus, and in some cells to the membranes bounding vesicles in the perinuclear region. Increased levels of the transcription factor C/EBP were found in nuclear extracts from cells exposed to sucrose for 12 h, relative to matched controls suggesting regulation of gene expression following sucrose-induced vacuolation may be coordinated, at least in part, by the transcription factor C/EBP. Sucrose-induced vacuolation is a useful model in which to study the regulation of lysosomal gene expression and biogenesis. (C) 2003 Elsevier Inc. All rights reserved. C1 Tulane Univ, Sch Med, Hayward Human Genet Ctr, New Orleans, LA 70112 USA. RP Helip-Wooley, A (reprint author), NHGRI, NIH, Bldg 10,Room 10C107,MSC1851,10 Ctr Dr, Bethesda, MD 20892 USA. NR 29 TC 17 Z9 18 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4827 J9 EXP CELL RES JI Exp. Cell Res. PD JAN 1 PY 2004 VL 292 IS 1 BP 89 EP 100 DI 10.1016/j.yexcr.2003.09.003 PG 12 WC Oncology; Cell Biology SC Oncology; Cell Biology GA 759XD UT WOS:000187777800009 PM 14720509 ER PT J AU Chen, ZG John, M Subramanian, S Chen, H Carper, D AF Chen, ZG John, M Subramanian, S Chen, H Carper, D TI 17Beta-estradiol confers a protective effect against transforming growth factor-beta2-induced cataracts in female but not male lenses SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE alpha-smooth muscle actin; anterior subcapsular cataract; gene expression; lens; 17beta-estradiol; transforming growth factor-beta ID POSTERIOR CAPSULAR OPACIFICATION; HORMONE REPLACEMENT THERAPY; BEAVER DAM EYE; BETA TGF-BETA; EPITHELIAL-CELLS; SUBCAPSULAR CATARACTS; ESTROGEN USE; OPACITIES; RAT; AGE AB Transforming growth factor-beta2 (TGF-beta2) induces anterior subcapsular cataracts, with a marked increase in cytoskeletal and extracellular matrix proteins, such as alpha-smooth muscle actin (alphaSMA). It has been shown that 17beta-estradiol (E2) can prevent TGF-beta2-induced cataracts in lenses from ovariectomized female rats. The purpose of the current study was to extend this finding by testing whether E2 can prevent TGF-beta2-induced cataracts and inhibit the induction of aSMA gene expression in normal male and normal, nonovariectomized female rats. Sex-specific differences were observed in 17-week-old rat lenses incubated in 0.15 ng ml(-1) TGF-beta2 and in 10(-8) M E2 plus TGF-beta2. TGF-beta2 induced approximately twice as many anterior subcapsular plaques and 1.5 times the level of alphaSMA transcripts in male lenses compared to female lenses. Notably, E2 inhibited plaque formation and the induction of alphaSMA transcripts in female rat lenses but not in male rat lenses. E2 also inhibited the induction of aSMA in TGF-beta2-incubated lenses from ovariectomized female rats. E2 prevented lens opacification and the induction of alphaSMA gene expression in female, but not male, lenses. This sex-specific difference may have implications for studies on the therapeutic use of estradiol for treatment of secondary cataract. (C) 2004 Elsevier Ltd. All rights reserved. C1 NEI, Sect Mol Therapeut, NIH, Bethesda, MD 20892 USA. RP Carper, D (reprint author), NEI, Sect Mol Therapeut, NIH, 9000 Rockville Pike,Bldg 6,Room 232, Bethesda, MD 20892 USA. NR 31 TC 9 Z9 10 U1 0 U2 0 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JAN PY 2004 VL 78 IS 1 BP 67 EP 74 DI 10.1016/j.exer.2003.09.015 PG 8 WC Ophthalmology SC Ophthalmology GA 756HZ UT WOS:000187460800006 PM 14667828 ER PT J AU Albright, JW Bream, JH Bere, EW Young, HA Winkler-Pickett, R Ortaldo, JR AF Albright, JW Bream, JH Bere, EW Young, HA Winkler-Pickett, R Ortaldo, JR TI Aging of innate immunity: functional comparisons of NK/LAK cells obtained from bulk cultures of young and aged mouse spleen cells in high concentrations of interleukin-2 SO EXPERIMENTAL GERONTOLOGY LA English DT Article DE NK cells; chemokines; aging; rodent ID NATURAL-KILLER-CELLS; PERIPHERAL T-CELLS; NK CELLS; IFN-GAMMA; INTERFERON-GAMMA; GENE-EXPRESSION; NO SYNTHASE; OLD MICE; CYTOKINE; PRECURSOR AB The technique of bulk cultivation of aged mouse spleen cells in high concentration of IL-2 was employed to obtain NK/LAK cells in sufficient number and enrichment for studies on the effects of aging on their functions. The yield and enrichment were equivalent to that of young mouse spleen cells. The aged and young mouse NK/LAK cells were equivalent also in their functional competence to proliferate, kill target cells and produce IFN-gamma; i.e. they did not display age-associated defects typical of freshly-isolated NK/LAK cells. In two respects, however, the NK/LAK cells derived from aged mouse spleen were altered: (a) in the efficiency of nuclear translocation of transcription factors STAT 5A and 5B, and (b) in the deficiency in production of mRNA transcripts representing several chemokines. We recommend caution in the use of bulk cultivation in IL-2 to obtain NK/LAK cells for studies on aging. However, it does appear from this study that aging may severely affect chemokine production, at least in the case of NK/LAK cells. (C) 2003 Elsevier Inc. All rights reserved. C1 George Washington Univ, Sch Med, Dept Microbiol & Trop Med, Washington, DC 20037 USA. NCI, Frederick Canc Res & Dev Ctr, Div Basic Sci, Lab Expt Immunol, Frederick, MD 21702 USA. RP Albright, JW (reprint author), George Washington Univ, Sch Med, Dept Microbiol & Trop Med, 2300 1 St,NW, Washington, DC 20037 USA. EM mbijwa@gwumc.edu RI Young, Howard/A-6350-2008 OI Young, Howard/0000-0002-3118-5111 FU NIA NIH HHS [AG 17351] NR 56 TC 14 Z9 16 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0531-5565 J9 EXP GERONTOL JI Exp. Gerontol. PD JAN PY 2004 VL 39 IS 1 BP 73 EP 82 DI 10.1016/j.exger.2003.09.017 PG 10 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 766ZF UT WOS:000188413100011 PM 14724067 ER PT J AU Bailey, DP Kashyap, M Mirmonsef, P Bouton, LA Domen, J Zhu, JF Dessypris, EN Ryan, JJ AF Bailey, DP Kashyap, M Mirmonsef, P Bouton, LA Domen, J Zhu, JF Dessypris, EN Ryan, JJ TI Interleukin-4 elicits apoptosis of developing mast cells via a Stat6-dependent mitochondrial pathway SO EXPERIMENTAL HEMATOLOGY LA English DT Article ID MESSENGER-RNA; IL-4; STAT6; EXPRESSION; MICE; IDENTIFICATION; STIMULATION; RESPONSES; DISEASE; KIT AB Objective. The aim of this study was to assess the effects of interleukin-4 and signal transducer and activator of transcription (Stat)-6 on IL-3 + SCF-induced mast cell development. Materials and Methods. Unseparated mouse bone marrow cells were cultured in IL-3 + SCF, giving rise to mast cells and monocytes/macrophages. The addition of IL-4, the use of Stat6-deficient bone marrow cells, and expression of a constitutively active Stat6 mutant were employed to assess the effects of IL-4 and Stat6 on cell viability, proliferation, and differentiation. Bax-deficient and bcl-2 transgenic bone marrow cells were used to assess the importance of the mitochondria in IL-4-mediated effects. Results. IL-4 elicited apoptosis and limited the cell cycle progression of developing bone marrow cells, without affecting cell differentiation. Apoptosis required that IL-4 be present during the first 8 days of the 21-day culture period. Cell death correlated with loss of mitochondrial membrane potential. Accordingly, IL-4-mediated apoptosis was inhibited by Bax deletion or bcl-2 overexpression. Lastly, Stat6 activation was both necessary and sufficient to inhibit cell survival. Conclusion. IL-4 exerts potent apoptotic effects on developing mast cells and monocyte/ macrophages through mitochondrial damage and Stat6 activation. (C) 2004 International Society for Experimental Hematology. Published by Elsevier Inc. C1 Virginia Commonwealth Univ, Dept Biol, Richmond, VA 23284 USA. Duke Univ, Ctr Med, Dept Med, Durham, NC USA. Duke Univ, Ctr Med, Dept Immunol, Durham, NC USA. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. HH McGuire VA Med Ctr, Richmond, VA USA. RP Ryan, JJ (reprint author), Virginia Commonwealth Univ, Dept Biol, Box 842012, Richmond, VA 23284 USA. EM jjryan@saturn.vcu.edu RI Kashyap, Mohit/F-4534-2011; Zhu, Jinfang/B-7574-2012 FU NCI NIH HHS [1R01CA91839]; NIAID NIH HHS [1R01 AI43433] NR 28 TC 19 Z9 20 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JAN PY 2004 VL 32 IS 1 BP 52 EP 59 DI 10.1016/j.exphem.2003.10.011 PG 8 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA 814HH UT WOS:000220965300007 PM 14725901 ER PT J AU Ravi, V Kubofcik, J Bandopathyaya, S Geetha, M Narayanan, RB Nutman, TB Kaliraj, P AF Ravi, V Kubofcik, J Bandopathyaya, S Geetha, M Narayanan, RB Nutman, TB Kaliraj, P TI Wuchereria bancrofti: cloning and characterization of heat shock protein 70 from the human lymphatic filarial parasite SO EXPERIMENTAL PARASITOLOGY LA English DT Article DE nematode; parasite-host relationship; heterologous protein expression; Wuchereria bancrofti; heat shock protein; tropical pulmonary eosinophilia; chronic pathology; microfilariae; endemic normal; polymerase chain reaction; splice leader sequence1; sodium dodyecyl sulfate-polyacrylamide gel electrophoresis; tris-buffered saline; immunoglobulinG; amino acid; nitric oxide; isopropyl-1-thio-beta-D-galactopyranoside; open reading frame; expressed sequence tag; enzyme-linked immunosorbent assay; Brugia malayi adult ID HEAT-SHOCK-PROTEIN; GONDII-INFECTED MICE; HSP70 GENE; PLASMODIUM-FALCIPARUM; SCHISTOSOMA-MANSONI; TOXOPLASMA-GONDII; ANTIBODY-LEVELS; BRUGIA-MALAYI; 70 KDA; ONCHOCERCA-VOLVULUS AB Heat shock protein 70 (HSP70) was identified as an immunodominant antigen by screening a Wuchereria bancrofti (Wb) microfilarial cDNA library with pooled Wb-infected sera, with 28% of the immunopositive clones coding for Wb-HSP70. The deduced amino acid sequence showed greater than 97 and 85% identity with HSP70 from filarial nematodes and humans, respectively. Recombinant HSP70 (74 kDa) and a recombinant protein from the C-terminal portion (43 kDa) also reacted with pooled Wb-infected sera, suggesting that the C-terminal region of HSP70 contains at least one antibody epitope. Brugia malayi L3 larvae showed increasing levels of HSP70 with increasing temperatures. Further, a polyclonal mouse anti-Wb-HSP70 antibody had reactivity to the HSP70 of cattle filarial parasite Settaria digitata and to human HSP70 derived from a Hep-2 cell line. Immune reactivity to Wb-HSP70 was strong, with uninfected non-endemic normal sera showing significantly greater reactions than sera from filaria-infected individuals. Both immunodominant self-HSP70 and HSP70 from other microbial infections may be primary targets for developing autoantibodies naturally. (C) 2004 Elsevier Inc. All rights reserved. C1 Anna Univ, Ctr Biotechnol, Madras 600025, Tamil Nadu, India. NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. RP Kaliraj, P (reprint author), Anna Univ, Ctr Biotechnol, Madras 600025, Tamil Nadu, India. EM pkaliraj@annauniv.edu OI Varatharajalu, Ravi/0000-0001-6773-1922 NR 61 TC 19 Z9 25 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4894 J9 EXP PARASITOL JI Exp. Parasitol. PD JAN-FEB PY 2004 VL 106 IS 1-2 BP 1 EP 10 DI 10.1016/j.exppara.2004.01.001 PG 10 WC Parasitology SC Parasitology GA 804IG UT WOS:000220291800001 PM 15013783 ER PT J AU Espina, V Dettloff, KA Cowherd, S Petricoin, EF Lotta, LA AF Espina, V Dettloff, KA Cowherd, S Petricoin, EF Lotta, LA TI Use of proteomic analysis to monitor responses to biological therapies SO EXPERT OPINION ON BIOLOGICAL THERAPY LA English DT Review DE biomarker; cancer; individualised therapy; laser capture nucrodissection; mass spectrometry; protein microarray; proteomics; SELDI-TOF ID LASER CAPTURE MICRODISSECTION; CATALYZED REPORTER DEPOSITION; SIGNAL AMPLIFICATION; PROTEIN MICROARRAYS; CLINICAL PROTEOMICS; MASS-SPECTROMETRY; PROSTATE-CANCER; SELDI-TOF; EXPRESSION; PATTERNS AB Proteomics has the potential to revolutionise diagnosis and disease management. Serum protein pattern profiling by surface-enhanced laser desorption/ionisation time of flight (SELDI-TOF) mass spectrometry is emerging as a novel approach to discover protein patterns capable of distinguishing disease and disease-free states with high sensitivity and specificity. This method has shown great promise for early diagnosis of ovarian cancer and is being applied to a range of pathological states. Protein microarray technology is being evaluated as a new means to track biological responses to therapy. Through the measurement of key protein phosphorylation sites at different stages of disease progression or before and after treatment, protein signal pathways can be mapped and thus become the starting point for individualised therapy. Laser capture microdissection (LCM) coupled with immunostaining of protein microarrays allows isolation of pure cell populations and relative quantitation of phosphorylated and non-phosphorylated forms of the cell's key signalling proteins. This technology is currently in use at the National Institutes of Health in Phase 11 clinical trials of metastatic breast and ovarian cancer. Cell survival and apoptotic protein pathways are monitored as biological markers of disease progression in these clinical trials. Proteomic technologies, such as serum protein pattern profiling, combined with protein microarray technologies, constitute a new paradigm for detecting disease and monitoring disease response to therapy. Ultimately, proteomics and genomics will become integrated into cancer patient management through the design and tracking of individualised therapy. C1 NCI, Canc Res Ctr, Pathol Lab, Bethesda, MD 20892 USA. RP Espina, V (reprint author), NCI, Canc Res Ctr, Pathol Lab, Bethesda, MD 20892 USA. OI Espina, Virginia/0000-0001-5080-5972 NR 96 TC 71 Z9 77 U1 0 U2 0 PU ASHLEY PUBLICATIONS LTD PI LONDON PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB, ENGLAND SN 1471-2598 J9 EXPERT OPIN BIOL TH JI Expert Opin. Biol. Ther. PD JAN PY 2004 VL 4 IS 1 BP 83 EP 93 DI 10.1517/eobt.4.1.83.25248 PG 11 WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Research & Experimental Medicine GA 759YF UT WOS:000187781900008 PM 14680471 ER PT J AU Boyiadzis, M Pavletic, S AF Boyiadzis, M Pavletic, S TI Haematopoietic stem cell transplantation: indications, clinical developments and future directions SO EXPERT OPINION ON PHARMACOTHERAPY LA English DT Review DE allogeneic; autologous; bone marrow transplantation; haematopoietic stem cell transplantation; indications ID BONE-MARROW-TRANSPLANTATION; VERSUS-HOST-DISEASE; CHRONIC LYMPHOCYTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; HIGH-DOSE CHEMOTHERAPY; NON-HODGKINS-LYMPHOMA; UMBILICAL-CORD BLOOD; PREVENT CYTOMEGALOVIRUS DISEASE; TERM-FOLLOW-UP; PERIPHERAL-BLOOD AB Haematopoietic stem cell transplantation (HSCT) is an established curative treatment for many malignant and non-malignant diseases. Over the last two decades, novel approaches have resulted in significant reductions in the morbidity and mortality associated with HSCT. These include the utilisation of reduced intensity regimens, more effective graft versus host disease prophylaxis, exploration of new sources of progenitor haematopoietic stem cells and better prophylaxis and treatment of infections. Despite current advances, new strategies are needed to further reduce the complications associated with HSCT. This article reviews the current indications for HSCT and the recent progress in the field of both allogeneic- and autologous HSCT. C1 NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA. RP Boyiadzis, M (reprint author), NCI, Expt Transplantat & Immunol Branch, Bldg 10,Room 12N226,10 Ctr Dr, Bethesda, MD 20892 USA. NR 72 TC 8 Z9 8 U1 0 U2 0 PU ASHLEY PUBLICATIONS LTD PI LONDON PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB, ENGLAND SN 1465-6566 J9 EXPERT OPIN PHARMACO JI Expert Opin. Pharmacother. PD JAN PY 2004 VL 5 IS 1 BP 97 EP 108 DI 10.1517/eoph.5.1.97.25505 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 759YG UT WOS:000187782000011 PM 14680439 ER PT J AU Wallace, BA Wien, F Miles, AJ Lees, JG Hoffmann, SV Evans, P Wistow, GJ Slingsby, C AF Wallace, BA Wien, F Miles, AJ Lees, JG Hoffmann, SV Evans, P Wistow, GJ Slingsby, C TI Biomedical applications of synchrotron radiation circular dichroism spectroscopy: Identification of mutant proteins associated with disease and development of a reference database for fold motifs SO FARADAY DISCUSSIONS LA English DT Article ID VACUUM-ULTRAVIOLET; SECONDARY STRUCTURE; CATARACTS AB Synchrotron radiation circular dichroism (SRCD) spectroscopy is an emerging technique in structural biology with particular value for accurate secondary structure determination, monitoring protein folding and kinetics, and drug discovery. This paper discusses new biomedical applications of SRCD, notably the identification of conformational changes associated with a mutant protein that causes disease, and the development of methods for identification of fold motifs in the context of structural genomics programmes. In addition, it presents for the first time, very low wavelength ( below 154 nm) data for a protein in aqueous solution, demonstrating the presence of heretofore-unseen electronic transitions. C1 Univ London Birkbeck Coll, Dept Crystallog, London WC1E 7HX, England. NEI, NIH, Bethesda, MD 20892 USA. Univ Aarhus, Inst Storage Ring Facil, DK-8000 Aarhus, Denmark. RP Wallace, BA (reprint author), Univ London Birkbeck Coll, Dept Crystallog, Malet St, London WC1E 7HX, England. RI Miles, Andrew/A-5414-2010; Wien, Frank/B-7846-2012; Wallace, B. A./C-3753-2008 OI Wien, Frank/0000-0002-0752-8735; Wallace, B. A./0000-0001-9649-5092 NR 20 TC 26 Z9 26 U1 0 U2 2 PU ROYAL SOC CHEMISTRY PI CAMBRIDGE PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS, ENGLAND SN 1364-5498 J9 FARADAY DISCUSS JI Faraday Discuss. PY 2004 VL 126 BP 237 EP 243 DI 10.1039/b306055c PG 7 WC Chemistry, Physical SC Chemistry GA 755HN UT WOS:000187397600017 PM 14992410 ER PT J AU Ermak, G Cheadle, C Becker, KG Harris, CD Davies, KJA AF Ermak, G Cheadle, C Becker, KG Harris, CD Davies, KJA TI DSCR1 (Adapt78) modulates expression of SOD1 SO FASEB JOURNAL LA English DT Article DE calcipressin 1; sod 1; oxidative stress; Down's syndrome ID CU/ZN-SUPEROXIDE DISMUTASE; SYNDROME CRITICAL REGION; CALCINEURIN A-ALPHA; DOWN-SYNDROME; GENE-EXPRESSION; GLUTATHIONE-PEROXIDASE; OXIDATIVE STRESS; MESSENGER-RNA; SACCHAROMYCES-CEREVISIAE; INHIBITS CALCINEURIN AB DSCR1(Adapt78) is a stress responsive gene that can be induced by multiple stresses. We have previously demonstrated that acute DSCR1(Adapt78) overexpression can transiently protect cells against oxidative stress and calcium-mediated stresses, while its chronic overexpression is associated with neurofibrillary tangles, Alzheimer disease, and Down's syndrome. It seems that a delicate balance of DSCR1(Adapt78) expression is maintained in cells, and this gene can have either protective or damaging effects, depending on both its level and duration of expression. The mechanisms by which DSCR1(Adapt78) can protect or harm cells are poorly understood. Here, we tried to identify pathways and targets affected by the DSCR1(Adapt78) gene using regulated expression of DSCR1(Adapt78) in PC-12 cells, followed by microarray analysis of mRNAs from these cells. We found that DSCR1(Adapt78) expression stimulates SOD1 (intracellular Cu,Zn superoxide dismutase) gene expression and increased sod 1 enzyme activity. Previous studies have indicated that sod 1 can either protect or damage cells, depending on its levels. Our findings suggest that sod 1 may also be involved in both the acute protective and the chronic damaging effects of DSCR1(Adapt78) expression. These data also have importance for our understanding of Down's syndrome, Alzheimer's disease, and other human pathologies. C1 Univ So Calif, Ethel Percy Andrus Gerontol Ctr, Los Angeles, CA 90089 USA. Univ So Calif, Div Mol & Computat Biol, Los Angeles, CA 90089 USA. NIA, DNA Array Unit, Res Resources Branch, NIH, Baltimore, MD 21224 USA. RP Davies, KJA (reprint author), Univ So Calif, Ethel Percy Andrus Gerontol Ctr, 3715 McClintock Ave, Los Angeles, CA 90089 USA. EM kelvin@usc.edu OI Becker, Kevin/0000-0002-6794-6656 FU NIA NIH HHS [AG16256] NR 43 TC 23 Z9 25 U1 0 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 EI 1530-6860 J9 FASEB J JI Faseb J. PD JAN PY 2004 VL 18 IS 1 BP 62 EP 69 DI 10.1096/fj.03-0451com PG 8 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 772EX UT WOS:000188829300040 PM 14718387 ER PT J AU Akunda, JK Lao, HC Lee, CA Sessoms, AR Slade, RM Langenbach, R AF Akunda, JK Lao, HC Lee, CA Sessoms, AR Slade, RM Langenbach, R TI Genetic deficiency or pharmacological inhibition of cyclooxygenase-1 or-2 induces mouse keratinocyte differentiation in vitro and in vivo SO FASEB JOURNAL LA English DT Article DE knockout; celecoxib; SC-560; terminal differentiation ID COLON-CANCER CELLS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; H SYNTHASE ISOENZYMES; EPIDERMAL DIFFERENTIATION; ADENOCARCINOMA CELLS; GROWTH-INHIBITION; TUMOR-GROWTH; SKIN; APOPTOSIS; EXPRESSION AB Previously we demonstrated that genetic deficiency of the cyclooxygenases (COX-1 or COX-2) altered keratinocyte differentiation in mouse skin [Tiano et. al. (2002) Cancer Res. 62, 3395-3401]. In this study, we show that topical application of SC-560 (a COX-1 selective inhibitor) or celecoxib (COX-2 selective) to TPA-treated wild-type skin caused fivefold increases in the number of basal keratinocytes expressing the early differentiation marker keratin 1 (K1). In contrast to skin, COX-2 not COX-1 was the major isoform expressed in cultured primary keratinocytes. COX-1 was predominantly expressed in detached, differentiated cells, whereas COX-2 was found in the attached, proliferating cells. High Ca++ medium induced K1 and COX-1 in wild-type keratinocytes but did not change COX-2 expression. As observed in skin, COX-1(-/-) and COX-2(-/-) primary keratinocytes expressed fivefold more K1 than wild-type cells. K1 levels in cultured wild-type keratinocytes were also increased by treatment with celecoxib and indomethacin. However, unlike its in vivo effect, SC-560, possibly due to low COX-1 expression in cultured mouse keratinocytes, did not increase K1 levels. Furthermore, no increases in apoptotic cell numbers were observed in COX-deficient keratinocytes or COX-inhibitor treated wild-type cells. Thus, a major effect of COX inhibitors and COX-deficiency is the induction of keratinocyte differentiation. C1 NIEHS, NIH, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA. Myriad Pharmaceut Inc, Salt Lake City, UT USA. RP Langenbach, R (reprint author), NIEHS, MD C4-09,POB 12233, Res Triangle Pk, NC 27709 USA. EM langenb1@niehs.nih.gov FX The authors wish to thank Carl Bortner (NIEHS) for help with the FACS analysis, Kevin Trouba (NIEHS) for helping with human keratinocyte cultures, Robert Smart (North Carolina State University), Thomas Eling, Carol Trempus, and Thomas Gray (All at NIEHS) for the critical review of this manuscript. NR 40 TC 17 Z9 18 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 EI 1530-6860 J9 FASEB J JI Faseb J. PD JAN PY 2004 VL 18 IS 1 BP 185 EP 187 DI 10.1096/fj.02-1192fje PG 3 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 772EX UT WOS:000188829300068 PM 14630706 ER PT J AU Marquez, S Crespo, P Carlini, V Garbarino-Pico, E Baler, R Caputto, BL Guido, ME AF Marquez, S Crespo, P Carlini, V Garbarino-Pico, E Baler, R Caputto, BL Guido, ME TI The metabolism of phospholipids oscillates rhythmically in cultures of fibroblasts and is regulated by the clock protein PERIOD 1 SO FASEB JOURNAL LA English DT Article DE circadian rhythms; phospholipid synthesis; cell cultures; Per1; CLOCK/CLOCK mutants ID CIRCADIAN GENE-EXPRESSION; NIH 3T3 FIBROBLASTS; SUPRACHIASMATIC NUCLEUS; PERIPHERAL-TISSUES; RAT-1 FIBROBLASTS; MESSENGER-RNA; BIOLOGICAL CLOCK; GANGLION-CELLS; LIGHT; RHYTHMS AB The mammalian circadian timing system is composed of countless cell oscillators distributed throughout the body and central pacemakers regulating temporal physiology and behavior. Peripheral clocks display circadian rhythms in gene expression both in vivo and in culture. We examined the biosynthesis of phospholipids as well as the expression of the clock gene period 1 (Per1) and its potential involvement in the regulation of the phospholipid metabolism in cultured quiescent NIH 3T3 cells synchronized by a 2 h serum shock. A 30 min pulse of radiolabeled precursor was given at phases ranging from 0.5 to 62 h after serum treatment. We observed a daily rhythm in the phospholipid labeling that persisted at least for two cycles, with levels significantly decreasing 29 and 58 h after treatment. Per1 expression exhibited a rapid and transient induction and a daily rhythmicity in antiphase to the lipid labeling. After Per1 expression knockdown, the rhythm of phospholipid labeling was lost. Furthermore, in cultures of CLOCK mutant fibroblasts-cells with a clock mechanism impairment-PERI was equally expressed at all times examined and the phospholipid labeling did not oscillate. The results demonstrate that the biosynthesis of phospholipids oscillates daily in cultured fibroblasts by an endogenous clock mechanism involving Per1 expression. C1 Univ Nacl Cordoba, Fac Ciencias Quim, Dept Quim Biol, CIQUIBIC,CONICET, RA-5000 Cordoba, Argentina. NIMH, Unit Temporal Gene Express, Lab Cellular & Mol Regulat, NIH, Bethesda, MD 20892 USA. RP Guido, ME (reprint author), Univ Nacl Cordoba, Fac Ciencias Quim, Dept Quim Biol, CIQUIBIC,CONICET, Ciudad Univ, RA-5000 Cordoba, Argentina. EM mguido@dqb.fcq.unc.edu.ar OI Garbarino Pico, Eduardo/0000-0002-2931-2038 NR 56 TC 24 Z9 24 U1 2 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 EI 1530-6860 J9 FASEB J JI Faseb J. PD JAN PY 2004 VL 18 IS 1 BP 519 EP + DI 10.1096/fj.03-0417fje PG 20 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 772EX UT WOS:000188829300021 PM 14715703 ER PT J AU Zhang, W Wang, TG Qin, LY Gao, HM Wilson, B Ali, SF Zhang, WQ Hong, JS Liu, B AF Zhang, W Wang, TG Qin, LY Gao, HM Wilson, B Ali, SF Zhang, WQ Hong, JS Liu, B TI Neuroprotective effect of dextromethorphan in the MPTP Parkinson's disease model: role of NADPH oxidase SO FASEB JOURNAL LA English DT Article DE reactive oxygen species; microglia; dopamine; substantia nigra; morphinan ID INJURY FOLLOWING TRANSIENT; DOPAMINERGIC-NEURONS; FOCAL ISCHEMIA; NITRIC-OXIDE; MICROGLIAL ACTIVATION; SUPEROXIDE PRODUCTION; GLUTAMATE TOXICITY; TETRAZOLIUM SALT; MOUSE MODEL; PROTECTS AB Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra and depletion of the neurotransmitter dopamine in the striatum. Progress in the search for effective therapeutic strategies that can halt this degenerative process remains limited. Mechanistic studies using animal systems such as the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) rodent PD model have revealed the involvement of the brain's immune cells and free radical-generating processes. We recently reported that dextromethorphan (DM), a widely used anti-tussive agent, attenuated endotoxin-induced dopaminergic neurodegeneration in vitro. In the current study, we investigated the potential neuroprotective effect of DM and the underlying mechanism of action in the MPTP rodent PD model. Mice (C57BL/6J) that received daily MPTP injections (15 mg free base/kg body weight, s.c.) for 6 consecutive days exhibited significant degeneration of the nigrostriatal dopaminergic pathway. However, the MPTP-induced loss of nigral dopaminergic neurons was significantly attenuated in those mice receiving DM (10 mg/kg body weight, s.c.). In mesencephalic neuron-glia cultures, DM significantly reduced the MPTP-induced production of both extracellular superoxide free radicals and intracellular reactive oxygen species (ROS). Because NADPH oxidase is the primary source of extracellular superoxide and intracellular ROS, we investigated the involvement of NADPH oxidase in the neuroprotective effect of DM. Indeed, the neuroprotective effect of DM was only observed in the wild-type but not in the NADPH oxidase-deficient mice, indicating that NADPH oxidase is a critical mediator of the neuroprotective activity of DM. More importantly, due to its proven safety record of long-term clinical use in humans, DM may be a promising agent for the treatment of degenerative neurological disorders such as PD. C1 Univ Florida, Coll Pharm, Dept Pharmacodynam, Gainesville, FL 32610 USA. NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. First Clin Hosp, Dept Neurol, Dalian, Peoples R China. Dalian Med Univ, Dept Physiol, Dalian, Peoples R China. US FDA, Neurochem Lab, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA. RP Liu, B (reprint author), Univ Florida, Coll Pharm, Dept Pharmacodynam, Box 100487 HSC, Gainesville, FL 32610 USA. EM liu@cop.ufl.edu RI gao, huiming/C-8454-2012; liu, Bin/A-7695-2009 NR 47 TC 116 Z9 120 U1 0 U2 8 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 EI 1530-6860 J9 FASEB J JI Faseb J. PD JAN PY 2004 VL 18 IS 1 BP 589 EP + DI 10.0983/fj.03-0983fje PG 21 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 772EX UT WOS:000188829300001 PM 14734632 ER PT J AU Stuart, JA Karahalil, B Hogue, BA Souza-Pinto, NC Bohr, VA AF Stuart, JA Karahalil, B Hogue, BA Souza-Pinto, NC Bohr, VA TI Mitochondrial and nuclear DNA base excision repair are affected differently by caloric restriction SO FASEB JOURNAL LA English DT Article DE OGG1; UDG; AP endonuclease; dietary restriction; aging; mitochondria ID RAT-LIVER MITOCHONDRIA; OXIDATIVE DAMAGE; DIETARY RESTRICTION; POLYMERASE-GAMMA; LIFE-SPAN; AGE; STRESS; BRAIN; MUSCLE; MODEL AB Aging is strongly correlated with the accumulation of oxidative damage in DNA, particularly in mitochondria. Oxidative damage to both mitochondrial and nuclear DNA is repaired by the base excision repair (BER) pathway. The "mitochondrial theory of aging" suggests that aging results from declining mitochondrial function, due to high loads of damage and mutation in mitochondrial DNA (mtDNA). Restriction of caloric intake is the only intervention so far proven to slow the aging rate. However, the molecular mechanisms underlying such effects are still unclear. We used caloric-restricted (CR) mice to investigate whether lifespan extension is associated with changes in mitochondrial BER activities. Mice were divided into two groups, receiving 100% (PF) or 60% (CR) of normal caloric intake, a regime that extends mean lifespan by similar to40% in CR mice. Mitochondria isolated from CR mice had slightly higher uracil (UDG) and oxoguanine DNA glycosylase (OGGI) activities but marginally lower abasic endonuclease and polymerase gamma gap-filling activities, although these differences were tissue-specific. Uracil-initiated BER synthesis incorporation activities were significantly lower in brain and kidney from CR mice but marginally enhanced in liver. However, nuclear repair synthesis activities were increased by CR, indicating differential regulation of BER in the two compartments. The results indicate that a general up-regulation of mitochondrial BER does not occur in CR. C1 NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA. RP Bohr, VA (reprint author), 5600 Nathan Shock Dr,Box 1, Baltimore, MD 21224 USA. EM vbohr@nih.gov RI Souza-Pinto, Nadja/C-3462-2013 OI Souza-Pinto, Nadja/0000-0003-4206-964X NR 34 TC 70 Z9 75 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 EI 1530-6860 J9 FASEB J JI Faseb J. PD JAN PY 2004 VL 18 IS 1 BP 595 EP + DI 10.1096/fj.03-0890fje PG 21 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 772EX UT WOS:000188829300012 PM 14734635 ER PT J AU Mills, JL England, LJ Granath, F Cnattingius, S AF Mills, JL England, LJ Granath, F Cnattingius, S TI Sex ratio associations: opinions, theories, and facts - Reply SO FERTILITY AND STERILITY LA English DT Letter C1 NICHHD, Div Epidemiol Stat & Prevent Res, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Karolinska Inst, Dept Med Epidemiol, S-10401 Stockholm, Sweden. RP Mills, JL (reprint author), NICHHD, Div Epidemiol Stat & Prevent Res, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NR 2 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 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD JAN PY 2004 VL 81 IS 1 BP 225 EP 226 DI 10.1016/j.fertnstert.2003.09.020 PG 2 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 762JY UT WOS:000187969500048 ER PT J AU Thomas, JW AF Thomas, JW TI Cell sources and support programs for stem cell research and cell-based therapy in the USA SO FETAL DIAGNOSIS AND THERAPY LA English DT Article; Proceedings Paper CT 6th International Symposium on In Utero Stem Cell Transplantation and Gene Therapy CY MAR 13-14, 2003 CL LYON, FRANCE SP Merieux Fdn DE stem cell; embryonic stem cell; human embryonic stem cell line; cell-based therapy; cellular therapy AB In August 2002, the Health & Human Services Secretary Tommy Thompson and National Institutes of Health (NIH) Director Elias Zerhouni announced the creation of a new NIH Task Force to advance stem cell research. The National Heart, Lung, and Blood Institute (NHLBI), with a long history of sponsored research programs for stem cell biology, is participating in the NIH Stem Cell Task Force to facilitate stem cell and embryonic stem (ES) cell research including programs to improve access to cell sources. Programs being implemented include infrastructure enhancement awards to develop eligible human ES cell lines into distribution-quality cell lines, grant supplements for human ES cell line research, an educational program to provide laboratory courses on human ES cell culture techniques, and a new training program to assist investigators wishing to re-direct their laboratories into stem cell research. Copyright (C) 2004 S. Karger AG, Basel. C1 NHLBI, Div Blood Dis & Resources, Bethesda, MD 20892 USA. RP Thomas, JW (reprint author), NHLBI, Div Blood Dis & Resources, Rockledge 2 Ctr,Room 10154,6701 Rockledge Dr,Mail, Bethesda, MD 20892 USA. EM ThomasJ@nhlbi.nih.gov NR 0 TC 1 Z9 2 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-3837 J9 FETAL DIAGN THER JI Fetal Diagn. Ther. PY 2004 VL 19 IS 3 BP 212 EP 217 DI 10.1159/000076700 PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 809QD UT WOS:000220650300002 PM 15067229 ER PT B AU Mao, S Kim, JW Thoma, GR AF Mao, S Kim, JW Thoma, GR BE Werner, B TI A dynamic feature generation system for automated metadata extraction in preservation of digital materials SO FIRST INTERNATIONAL WORKSHOP ON DOCUMENT IMAGE ANALYSIS FOR LIBRARIES, PROCEEDINGS LA English DT Proceedings Paper CT 1st International Workshop on Document Image Analysis for Libraries (DIAL 2004) CY JAN 23-24, 2004 CL PALO ALTO, CA SP IAPR, SEIMENSDEMATIC, NSF, Palo Alto Res Ctr AB Obsolescence in storage media and the hardware and software for access and use can render old electronic files inaccessible and unusable. Therefore, the long-term preservation of digital materials has become an active area of research. At the U.S. National Library of Medicine (NLM), we are investigating the preservation of scanned and online medical journal articles, though other data types (e.g., video sequences) are also of interest. Metadata of different types have been proposed to save the information needed to preserve digital materials. Given the ever-increasing volume of medical journals and high labor cost of manual data entry, automated metadata extraction is crucial. A system has been developed at NLM to automatically generate descriptive metadata that includes title, author, affiliation, and abstract from scanned medical journals. A module called ZoneMatch is used to generate geometric and contextual features from a set of issues of each journal. A rule-based labeling module (called ZoneCzar) then uses these features to perform labeling independent of journal layout styles. However, if there are significant style variations among the issues of a same journal, the features generated from one set of journal issues may not be very useful to label a different set. In this paper, we describe a dynamic feature updating system in which the features used for labeling a current journal issue are generated from previous issues with similar layout style. This new system can adapt to possible style variations among different issues of the same journal. Experimental results presented show that the new system delivers improved labeling performance accuracy. C1 Natl Lib Med, Bethesda, MD 20894 USA. NR 9 TC 12 Z9 12 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 BN 0-7695-2088-X PY 2004 BP 225 EP 232 PG 8 WC Computer Science, Information Systems; Information Science & Library Science; Imaging Science & Photographic Technology SC Computer Science; Information Science & Library Science; Imaging Science & Photographic Technology GA BY43N UT WOS:000189234500016 ER PT S AU Nestorovich, EM Bezrukov, SM AF Nestorovich, EM Bezrukov, SM BE Abbott, D Bezrukov, SM Der, A Sanchez, A TI Voltage-induced "Gating" of bacterial porin as reversible protein denaturation SO FLUCTUATIONS AND NOISE IN BIOLOGICAL, BIOPHYSICAL, AND BIOMEDICAL SYSTEMS II SE PROCEEDINGS OF THE SOCIETY OF PHOTO-OPTICAL INSTRUMENTATION ENGINEERS (SPIE) LA English DT Proceedings Paper CT Conference on Fluctuations and Noise in Biological, Biophysical and Biomedical Systems II CY MAY 26-28, 2004 CL Maspalomas, SPAIN SP SPIE DE channel reconstitution; conductance fluctuations; hysteresis; Hofmeister series; single-molecule experiments ID PLANAR LIPID BILAYERS; AUREUS ALPHA-TOXIN; ESCHERICHIA-COLI; OUTER-MEMBRANE; OMPF PORIN; ION-CHANNEL; CHARGED RESIDUES; MOLECULAR-BASIS; MATRIX PROTEIN; K+ CHANNELS AB General porin OmpF forms water-filled channels in the outer membrane of E. coli bacteria. When reconstituted into planar bilayer lipid membranes, these channels can be closed (or "gated") by high electric fields. We discover that: (i) channel gating is sensitive to the type of cations in the membrane-bathing solution according to their position in the Hofmeister series; (ii) channel gates to a "closed" state that is represented by a set of multiple sub-conformations with at least three distinctly different conformations contributing to the closed-state conductance histogram. Taken together with the nearly symmetric response to the applied voltage of changing polarity and the hysteresis phenomena reported previously by others and reproduced here, these findings suggest that the voltage-induced closure of the OmpF channel is a consequence of reversible denaturation of the protein by the high electric field. If so, the voltage-induced gating of bacterial porins can serve as an instructive model to study the physics of protein folding at the single-molecule level. C1 NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA. RP Nestorovich, EM (reprint author), NICHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA. NR 49 TC 0 Z9 0 U1 0 U2 1 PU SPIE-INT SOC OPTICAL ENGINEERING PI BELLINGHAM PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98227-0010 USA SN 0277-786X BN 0-8194-5390-0 J9 P SOC PHOTO-OPT INS PY 2004 VL 5467 BP 42 EP 53 DI 10.1117/12.548223 PG 12 WC Biophysics; Medicine, Research & Experimental; Physics, Applied SC Biophysics; Research & Experimental Medicine; Physics GA BAQ26 UT WOS:000223199800006 ER PT J AU Hughes, SH AF Hughes, SH TI The RCAS vector system SO FOLIA BIOLOGICA LA English DT Article ID ROUS-SARCOMA-VIRUS; CHICKEN-EMBRYO FIBROBLASTS; AVIAN RETROVIRAL VECTORS; MURINE LEUKEMIA-VIRUS; TRANSGENIC CHICKENS; LOW PH; P21(WAF1/CIP1) ARRESTS; ENVELOPE GLYCOPROTEIN; LEUKOSIS VIRUSES; GENE-TRANSFER C1 Natl Canc Inst, HIV Drug Resistance Program, Frederick, MD USA. RP Hughes, SH (reprint author), POB B,Bldg 539,Room 130A, Ft Detrick, MD 21702 USA. EM hughes@ncifcrf.gov NR 45 TC 66 Z9 67 U1 0 U2 2 PU INST MOLECULAR GENETICS PI PRAGUE 6 PA FOLIA BIOLOGICA(PRAHA) FLEMINGOVO N.2, PRAGUE 6 166 37, CZECH REPUBLIC SN 0015-5500 J9 FOLIA BIOL-PRAGUE JI Folia Biol.-Prague PY 2004 VL 50 IS 3-4 BP 107 EP 119 PG 13 WC Biochemistry & Molecular Biology; Biology; Oncology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Oncology; Cell Biology GA 842UH UT WOS:000223029300006 PM 15373344 ER PT J AU Sikorska, B Walis, A Bratoslewicz-Wasik, J Brown, P Liberski, PP AF Sikorska, B Walis, A Bratoslewicz-Wasik, J Brown, P Liberski, PP TI Fate of myelinated fibres in the optic nerves in experimental Creutzfeldt-Jakob disease in rodents: An ultrastructural study SO FOLIA NEUROPATHOLOGICA LA English DT Article DE prions; Creutzfeldt Jakob disease; myelin ID SCRAPIE AB We report the ultrastructural appearances of myelinated fibres of the optic nerves from mice infected with the Fujisakistrain of Gerstmann-Straussler-Scheinker (GSS) disease and from Echigo-1 strain of Creutzfeldt-Jakob disease (CJD). Optic nerves from CJD- and GSS-infected rodents showed severe pathological changes. Theses changes were qualitatively indistinguishable from each other but were more robust in the Fujisaki GSS model than in the hamsters inoculated with Echigo-1. The most characteristic finding was the distension with the attenuation of the myelin sheath forming a vacuole while shrunken axon was attached to the innermost layer of the myelin. With high power electron microscopy, we could observe the splitting of the myelin lamellae at the major dense or intraperiod lines to form complex openings that extended to line the vacuole. This finding suggests that myelin lamellae participate in the formation of vacuoles. C1 Med Univ Lodz, Chair Oncol, Dept Mol Pathol & Neuropathol, PL-92216 Lodz, Poland. Med Univ Silesia Katowice, Dept Virol Diagnost, Chair Mol Biol Biochem & Biopharm, Katowice, Poland. NINDS, NIH, Bethesda, MD 20892 USA. RP Liberski, PP (reprint author), Med Univ Lodz, Chair Oncol, Dept Mol Pathol & Neuropathol, Czechoslowacka 8-10, PL-92216 Lodz, Poland. EM ppliber@csk.am.lodz.pl NR 11 TC 2 Z9 2 U1 0 U2 0 PU VIA MEDICA PI GDANSK PA UL SWIETOKRZYSKA 73, 80-180 GDANSK, POLAND SN 1641-4640 J9 FOLIA NEUROPATHOL JI Folia Neuropathol. PY 2004 VL 42 IS 2 BP 101 EP 105 PG 5 WC Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 836IR UT WOS:000222549600006 PM 15266784 ER PT J AU Sineo, L Romagno, D Stanyon, R AF Sineo, L. Romagno, D. Stanyon, R. TI Primate cytogenetics and comparative Genomics SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract C1 [Sineo, L.] Univ Palermo, DBA, Palermo, Italy. [Romagno, D.] Univ Florence, Dipartimento Biol Anim & Genet, Lab Antropol, I-50125 Florence, Italy. [Stanyon, R.] NCI, Frederick, MD 21701 USA. EM llsineo@unipa.it NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 5 BP 4 EP 4 PG 1 WC Zoology SC Zoology GA V50KS UT WOS:000203407800007 ER PT J AU Stanyon, R AF Stanyon, R. TI The last fifty years of primate cytogenetics SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract C1 [Stanyon, R.] NCI, Frederick, MD 21701 USA. EM stanyonr@ncifcrf.gov NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 6 BP 4 EP 4 PG 1 WC Zoology SC Zoology GA V50KS UT WOS:000203407800008 ER PT J AU Dumas, F Bigoni, F Stone, G Stanyon, R Sineo, L AF Dumas, F. Bigoni, F. Stone, G. Stanyon, R. Sineo, L. TI Chromosome sorting and multi-directional painting in new world primates SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract C1 [Dumas, F.; Sineo, L.] Univ Palermo, Dipartimento Biol Anim, I-90133 Palermo, Italy. [Dumas, F.; Bigoni, F.; Stone, G.; Stanyon, R.] NCI, Frederick, MD 21701 USA. EM francescadumas@hotmail.com NR 0 TC 0 Z9 0 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 11 BP 7 EP 7 PG 1 WC Zoology SC Zoology GA V50KS UT WOS:000203407800013 ER PT J AU Leighty, KA Byrne, G Fragaszya, DM Visalberghi, E Welker, C Lussier, I AF Leighty, KA Byrne, G Fragaszya, DM Visalberghi, E Welker, C Lussier, I TI Twinning in tufted capuchins (Cebus apella): Rate, survivorship, and weight gain SO FOLIA PRIMATOLOGICA LA English DT Article DE twins; twinning; capuchin; Cebus apella; multiple births; reproduction AB We calculated the rate of twinning across four captive collections of tufted capuchins (Cebus apella) to be 2.4%. This rate contrast with previous reports that twinning in tufted capuchins is rare. Additionally, we present data on the survival and weight gain of twins in this species as compared to singletons. Twins face their greatest risk of mortality on or before the first day of life, when 45% will die compared to 16% of singletons. After the first day of life, twins and singletons demonstrate comparable survival rates. This, in conjunction with the finding that at no time during the first year of life do twins and singletons differ significantly in their weights, suggests that twinning is a viable reproductive form for these animals, especially in the captive setting where nutritional demands are met. Copyright (C) 2004 S. Karger AG, Basel. C1 Univ Georgia, Dept Psychol, Athens, GA 30602 USA. NICHD, Comparat Ethol Lab, Poolesville, MD USA. CNR, Inst Psicol, Rome, Italy. Univ Kassel, D-3500 Kassel, Germany. LABS Virginia, Hampton, SC USA. RP Leighty, KA (reprint author), Univ Georgia, Dept Psychol, Athens, GA 30602 USA. EM kleighty@arches.uga.edu OI Visalberghi, Elisabetta/0000-0001-7407-5468 NR 14 TC 8 Z9 8 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 IS 1 BP 14 EP 18 DI 10.1159/000073425 PG 5 WC Zoology SC Zoology GA 762QA UT WOS:000187992600002 PM 14716148 ER PT J AU Higley, D Schwandt, M Barr, C AF Higley, D. Schwandt, M. Barr, C. TI HPA and CNS serotonin correlates of female maternal behaviour and outcomes SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE maternal behaviour; macaques; serotonin; cortisol C1 [Higley, D.; Schwandt, M.; Barr, C.] NIAAA, Clin Studies Lab, Primate Unit, Poolesville, MD USA. EM higleyd@exchange.nih.gov NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 95 BP 54 EP 54 PG 1 WC Zoology SC Zoology GA V50KS UT WOS:000203407800097 ER PT J AU Newman, TK Babb, PL Higley, DJ Goldman, D AF Newman, T. K. Babb, P. L. Higley, D. J. Goldman, D. TI Monoamine Oxidase A gene variation in Papio: Behaviour, evolution and phylogeny SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE Papio; phylogeny; monoamine oxidase A; evolution C1 [Newman, T. K.; Babb, P. L.; Higley, D. J.; Goldman, D.] NIAAA, NIH, Rockville, MD 20852 USA. EM tknewman@mail.nih.gov RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 0 TC 0 Z9 0 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 103 BP 58 EP 59 PG 2 WC Zoology SC Zoology GA V50KS UT WOS:000203407800105 ER PT J AU Dvoskin, R Juarez, CP Fernandez-Duque, E AF Dvoskin, R Juarez, CP Fernandez-Duque, E TI Population density of black howlers (Alouatta caraya) in the gallery forests of the Argentinean Chaco: a preliminary assessment SO FOLIA PRIMATOLOGICA LA English DT Article DE Allouatta caraya; black howler; population density; Argentinean Chaco ID NORTHERN ARGENTINA C1 NYU, Dept Anthropol, New York, NY 10003 USA. Zool Soc San Diego, Ctr Reprod Endangered Species, San Diego, CA 92112 USA. Ctr Ecol Aplicada Litoral, Corrientes, Argentina. RP Dvoskin, R (reprint author), NIH, 12420 Parklawn Dr, Rockville, MD 20852 USA. EM rlk208@nyu.edu NR 12 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 IS 2 BP 93 EP 96 DI 10.1159/000076267 PG 4 WC Zoology SC Zoology GA 801KP UT WOS:000220095100004 PM 15010581 ER PT J AU Becker, ML Newman, JD AF Becker, M. L. Newman, J. D. TI Comparative primate bioacoustics: Convergent and divergent themes of vocal behaviour SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE vocal communication; bioacoustics C1 [Becker, M. L.; Newman, J. D.] NICHD, Natl Inst Hlth, Poolesville, MD USA. EM mbecker@mail.nih.gov NR 0 TC 0 Z9 0 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 339 BP 195 EP 195 PG 1 WC Zoology SC Zoology GA V50KS UT WOS:000203407800338 ER PT J AU Becker, ML Buder, EH AF Becker, M. L. Buder, E. H. TI Function of close contact vocalisations in a nocturnal and non-gregarious prosimian primate SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE vocal communication; prosimian; Otolemur garnettii C1 [Becker, M. L.] NICHD, Natl Inst Hlth, Poolesville, MD USA. [Buder, E. H.] Univ Memphis, Sch Audiol & Speech Language Pathol, Memphis, TN 38105 USA. EM mbecker@mail.nih.gov NR 0 TC 0 Z9 0 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 341 BP 196 EP 196 PG 1 WC Zoology SC Zoology GA V50KS UT WOS:000203407800340 ER PT J AU Newman, JD Becker, ML AF Newman, J. D. Becker, M. L. TI Comparative primate bioacoustics: Development of the isolation call in squirrel monkeys and common marmosets SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE vocal communication; new world primates; isolation call C1 [Newman, J. D.; Becker, M. L.] NICHD, Natl Inst Hlth, Poolesville, MD USA. EM tknewman@mail.nih.gov NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 344 BP 198 EP 198 PG 1 WC Zoology SC Zoology GA V50KS UT WOS:000203407800343 ER PT J AU Carosi, M Visalberghi, E Suomi, SJ AF Carosi, M. Visalberghi, E. Suomi, S. J. TI What is urine washing for? The case of the tufted Capuchin monkey (Cebus apella) SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE urine washing; thermoregulation; scent marking; Cebus apella C1 [Carosi, M.; Suomi, S. J.] NICHD, Comparat Ethol Lab, NIH, Poolesville, MD USA. [Carosi, M.; Visalberghi, E.] Inst Cognit Sci & Technol, Lab Comparat Primatol, Rome, Italy. [Carosi, M.; Visalberghi, E.] Inst Cognit Sci & Technol, Ctr Primate, Rome, Italy. EM monica_carosi@hotmail.com RI Carosi, Monica/C-9683-2014 NR 0 TC 1 Z9 1 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 419 BP 242 EP 243 PG 2 WC Zoology SC Zoology GA V50KS UT WOS:000203407800418 ER PT J AU Higley, DJ Schwandt, M Barr, C AF Higley, D. J. Schwandt, M. Barr, C. TI HPA and CNS serotonin correlates of maternal behaviour and outcomes SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE maternal behaviour; aggression; macaque; serotonin C1 [Higley, D. J.; Schwandt, M.; Barr, C.] NIAAA, Clin Studies Lab, Primate Unit, Poolesville, MD USA. EM higley@mail.nih.gov NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 473 BP 273 EP 273 PG 1 WC Zoology SC Zoology GA V50KS UT WOS:000203407800472 ER PT J AU Carosi, M Gerald, MS Suomi, SJ AF Carosi, M. Gerald, M. S. Suomi, S. J. TI Female tufted capuchin (Cebus apella) have male-like external genitalia SO FOLIA PRIMATOLOGICA LA English DT Meeting Abstract DE Cebus apella; clitoris; baubellum; androgens C1 [Carosi, M.; Suomi, S. J.] NICHD, Comparat Ethol Lab, NIH, Poolesville, MD USA. Inst Cognit Sci & Technol, Unit Cognit Primatol, Rome, Italy. Inst Cognit Sci & Technol, Ctr Primate, Rome, Italy. [Gerald, M. S.] Univ Puerto Rico, Dept Med, Caribbean Primate Res Ctr, San Juan, PR 00936 USA. EM monica_carosi@hotmail.com RI Carosi, Monica/C-9683-2014 NR 0 TC 0 Z9 0 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0015-5713 J9 FOLIA PRIMATOL JI Folia Primatol. PY 2004 VL 75 SU 1 MA 630 BP 362 EP 363 PG 2 WC Zoology SC Zoology GA V50KS UT WOS:000203407800629 ER PT J AU Arai, H Berlett, BS Chock, PB Stadtman, ER AF Arai, H Berlett, BS Chock, PB Stadtman, ER TI Effect of bicarbonate on iron-mediated oxidation of LDL SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NHLBI, Biochem Lab, 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 2004 VL 37 SU 1 BP S19 EP S19 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900037 ER PT J AU Azarov, I Cass, MA Huang, KT Maree, RD Nichols, JS Gladwin, MT Hogg, N Kim-Shapiro, DB AF Azarov, I Cass, MA Huang, KT Maree, RD Nichols, JS Gladwin, MT Hogg, N Kim-Shapiro, DB TI NO uptake by normal and sickle red blood cells SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 Wake Forest Univ, Winston Salem, NC 27109 USA. NIH, Bethesda, MD 20892 USA. Med Coll Wisconsin, Milwaukee, WI 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 2004 VL 37 SU 1 BP S79 EP S79 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900231 ER PT J AU Batthyany, C Boggia, J Noboa, O Castellanos, R Cassina, P Mason, R Barbeito, L Radi, R Rubbo, H AF Batthyany, C Boggia, J Noboa, O Castellanos, R Cassina, P Mason, R Barbeito, L Radi, R Rubbo, H TI Immunological in vivo detection of DMPO-radical adducts in angiotensin II-induced tissue damage SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NIEHS, NIH, LPC, Res Triangle Pk, NC 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 2004 VL 37 SU 1 BP S48 EP S49 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900129 ER PT J AU Bonini, M Myamoto, S Di Mascio, P Augusto, O AF Bonini, M Myamoto, S Di Mascio, P Augusto, O TI Production of the carbonate radical anion during xanthine oxidase turnover in the presence of bicarbonate. SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 Univ Sao Paulo, Inst Quim, Sao Paulo, Brazil. NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC USA. RI Augusto, Ohara/D-3839-2012; Di Mascio, Paolo/D-1264-2014 OI Augusto, Ohara/0000-0002-7220-4286; Di Mascio, Paolo/0000-0003-4125-8350 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 2004 VL 37 SU 1 BP S25 EP S25 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900054 ER PT J AU Chignell, C Kukielczak, B Sik, R Bilski, P AF Chignell, C Kukielczak, B Sik, R Bilski, P TI Uva sensitivity in Smith-Lemli-Opitz syndrome: Possible involvement of cholesta-5,7,9(11)-trien-3 beta-ol SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 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 2004 VL 37 SU 1 BP S147 EP S147 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900453 ER PT J AU Corpe, C Levine, M AF Corpe, C Levine, M TI Intracellular accumulation of vitamin C: Halo ascorbate analogs as tools to study vitamin C transport pathways and function in vivo SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NIDDK, NIH, MCNS, Bethesda, MD 20892 USA. NIDDK, Mol & Clin Nutr Sect, NIH, Bethesda, MD USA. EM christopherc@intra.niddk.nih.gov 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 2004 VL 37 SU 1 BP S32 EP S33 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900076 ER PT J AU Dejam, A Duranski, M Greer, JM Oldfield, EH Lefer, DJ Pluto, RM Schechter, AN Gladwin, MT AF Dejam, A Duranski, M Greer, JM Oldfield, EH Lefer, DJ Pluto, RM Schechter, AN Gladwin, MT TI Bioactivation of nitrite involves transition to nitros(yl)ative NO adducts SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NIDDK, Biol Chem Lab, Bethesda, MD 20892 USA. NIH, Bethesda, MD 20892 USA. HSU, Shreveport, LA USA. NIH, Surg Neurol Branch, Bethesda, MD USA. NIH, CCMD, Bethesda, MD 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 2004 VL 37 SU 1 BP S95 EP S95 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900285 ER PT J AU Dejam, A Gladwin, MT Hunter, CJ Hsu, L Shiva, S Kelm, M Schechter, AN AF Dejam, A Gladwin, MT Hunter, CJ Hsu, L Shiva, S Kelm, M Schechter, AN TI Red blood cells as a reservoir for nitrite SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NIDDK, Biol Chem Lab, Bethesda, MD 20892 USA. NIH, CCMD, Bethesda, MD USA. HHU Duesseldorf, Div Cardiol, Dept Med, Dusseldorf, Germany. NIH, Bethesda, MD 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 2004 VL 37 SU 1 BP S80 EP S80 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900235 ER PT J AU Di Noto, L Whitson, LJ Hart, PJ Levine, RL AF Di Noto, L Whitson, LJ Hart, PJ Levine, RL TI Susceptibility of mutant superoxide dismutase to degradation by the proteasome correlates with the clinical severity of amyotrophic lateral sclerosis SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 Univ Texas, Hlth Sci Ctr, Houston, TX USA. NIH, 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 2004 VL 37 SU 1 BP S133 EP S133 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900410 ER PT J AU Donzelli, S AF Donzelli, S TI Identification of a novel adduct from HNO/NO- and glutathione reaction SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NCI, NIH, Bethesda, MD 20892 USA. Univ Arizona, Tucson, AZ 85721 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 2004 VL 37 SU 1 BP S95 EP S96 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900288 ER PT J AU Ehrenshaft, M AF Ehrenshaft, M TI Thyroid peroxidase radical formation and its potential role in Hashimoto's disease SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med 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 2004 VL 37 SU 1 BP S15 EP S15 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900028 ER PT J AU Huang, KP Huang, F AF Huang, KP Huang, F TI Thionylation of proteins by disulfide oxides SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 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 2004 VL 37 SU 1 BP S108 EP S108 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900332 ER PT J AU Huang, KT Keszler, A Huang, Z Patel, NK Patel, RP Gladwin, MT Kim-Shapiro, DB Hogg, N AF Huang, KT Keszler, A Huang, Z Patel, NK Patel, RP Gladwin, MT Kim-Shapiro, DB Hogg, N TI Mechanistic re-examination of the reaction between nitrite and hemoglobin SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 Med Coll Wisconsin, Milwaukee, WI USA. NIH, Bethesda, MD 20892 USA. Univ Alabama, Tuscaloosa, AL 35487 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 2004 VL 37 SU 1 BP S82 EP S82 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900244 ER PT J AU Huang, Z Shiva, S Schechter, A Ringwood, L Irby, C Cushenberry, C Grand, P Patel, R Kim-Shapiro, D Hogg, N Gladwin, M AF Huang, Z Shiva, S Schechter, A Ringwood, L Irby, C Cushenberry, C Grand, P Patel, R Kim-Shapiro, D Hogg, N Gladwin, M TI Electronic and allosteric regulation of nitrite reduction and NO generation by deoxyhemoglobin SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NHLBI, NIH, Bethesda, MD 20892 USA. NIDDK, 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 2004 VL 37 SU 1 BP S20 EP S21 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900043 ER PT J AU Hunter, C Dejam, A Lin, E Pelletier, M Machado, R Schechter, A Power, G Gladwin, M AF Hunter, C Dejam, A Lin, E Pelletier, M Machado, R Schechter, A Power, G Gladwin, M TI Hypoxia potentiates nitrite mediated vasodilatation in newborn lamb circulation SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NIH, Bethesda, MD 20892 USA. Loma Linda Univ, Sch Med, Loma Linda, CA 92350 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 2004 VL 37 SU 1 BP S82 EP S83 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900245 ER PT J AU Hussain, SP Trivers, G Hofseth, L He, PJ Shaikh, I Mechanic, L Doja, S Jiang, WD Subleski, J Shorts, L Haines, D Laubach, V Wiltrout, R Djurickovic, D Harris, C AF Hussain, SP Trivers, G Hofseth, L He, PJ Shaikh, I Mechanic, L Doja, S Jiang, WD Subleski, J Shorts, L Haines, D Laubach, V Wiltrout, R Djurickovic, D Harris, C TI Nitric oxide, a mediator of inflammation, suppresses tumorigenesis SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NCI, FCRDC, SAIC, Bethesda, MD 20892 USA. Univ Virginia, Ctr Hlth Sci, Charlottesville, VA 22903 USA. RI Laubach, Victor/E-8818-2015 OI Laubach, Victor/0000-0001-9673-5383 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 2004 VL 37 SU 1 BP S173 EP S173 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900529 ER PT J AU Ikeno, YJ Lew, C Cortez, L Chaudhuri, A Ran, QT Qi, WB Levine, R Yodoi, JJ Richardson, A AF Ikeno, YJ Lew, C Cortez, L Chaudhuri, A Ran, QT Qi, WB Levine, R Yodoi, JJ Richardson, A TI Does overexpression of thioredoxin 1 increase resistance to oxidative stress and alter aging? SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NIH, Bethesda, MD 20892 USA. Kyoto Univ, Kyoto, Japan. 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 2004 VL 37 SU 1 BP S108 EP S108 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900333 ER PT J AU Isbell, TS Crawford, JH Shiva, S Chacko, BK Lang, JD Ho, C Gladwin, MT Patel, RP AF Isbell, TS Crawford, JH Shiva, S Chacko, BK Lang, JD Ho, C Gladwin, MT Patel, RP TI Coordinated regulation of hypoxic vasodilation by the red blood cell: Role of nitrite and ATP derived nitric oxide SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NHLBI, Vasc Therapeut Sect, Bethesda, MD USA. Carnegie Mellon Univ, Dept Biol Sci, Pittsburgh, PA 15213 USA. RI Ho, Chien/O-6112-2016 OI Ho, Chien/0000-0002-4094-9232 NR 0 TC 0 Z9 0 U1 0 U2 3 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 2004 VL 37 SU 1 BP S83 EP S84 PG 2 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900249 ER PT J AU Isenberg, J Ridnour, L Espey, M Wink, D Roberts, D AF Isenberg, J Ridnour, L Espey, M Wink, D Roberts, D TI Nitric oxide modulation of angiogenic phenotypic responses in vascular cells is context dependent SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 NCI, Dept Pathol, Bethesda, MD 20892 USA. NCI, Sect Radiat Biol, 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 2004 VL 37 SU 1 BP S84 EP S84 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900250 ER PT J AU Jeffers, A Xu, XL Huang, KT King, SB Hogg, N Gladwin, MT Patel, RP Kim-Shapiro, DB AF Jeffers, A Xu, XL Huang, KT King, SB Hogg, N Gladwin, MT Patel, RP Kim-Shapiro, DB TI Nitrite activation of sGC in blood SO FREE RADICAL BIOLOGY AND MEDICINE LA English DT Meeting Abstract CT 11th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine CY NOV 17-21, 2004 CL St Thomas, VI SP Soc Free Rad Biol & Med C1 Wake Forest Univ, Winston Salem, NC 27109 USA. NIH, Bethesda, MD 20892 USA. Med Coll Wisconsin, Milwaukee, WI 53226 USA. Univ Alabama, Tuscaloosa, AL 35487 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 2004 VL 37 SU 1 BP S84 EP S84 PG 1 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 875YK UT WOS:000225458900251 ER EF