FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Guedes, SD Vitorino, R Domingues, R Tomer, K Correia, AJF Amado, F Domingues, P AF Guedes, SD Vitorino, R Domingues, R Tomer, K Correia, AJF Amado, F Domingues, P TI Proteomics of immune-challenged Drosophila melanogaster larvae hemolymph SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE Drosophila; hemolymph larvae; immune response; MALDI-TOF/TOF ID HOST-DEFENSE; HEAT-SHOCK; INNATE IMMUNITY; PROTEIN; IMMUNOPHILINS; EXPRESSION; CYCLOPHILIN; TOLL; IDENTIFICATION; THIOREDOXIN AB In the last decade, the fruit fly Drosophila melanogaster has emerged as a promising invertebrate model for the investigation of innate immunity, in part because of its well characterised genetics. The information provided by the innumerous reports on Drosophila's immune response indicates that a large number of genes, in addition to the well-known antimicrobial peptide genes, are both up- and down-regulated upon immune challenge. Nevertheless, their contribution to fighting off infection has not been seriously addressed. With the application of recent advances in proteomics, the effects of an immune challenge in the overall modification of Drosophila 2-DE protein patterns were investigated. The aim of this study was to investigate hemolymph proteins differentially expressed between control and immunised larvae sets, which could be related solely to the Drosophila immune response. The list of immune-related protein spots included heat shock proteins and other proteins with chaperone properties, serine proteases, phenol oxidase, and Drosophila antioxidant system components, which accounted for 21% of the total of 70 identified proteins, metabolic enzymes implicated in pathways such as cellular respiration, fatty-acid oxidation, protein biosynthesis, and structural proteins. (C) 2005 Elsevier Inc. All rights reserved. C1 Univ Aveiro, Dept Chem, P-3800 Aveiro, Portugal. NIEHS, Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA. RP Domingues, P (reprint author), Univ Aveiro, Dept Chem, P-3800 Aveiro, Portugal. EM pedrom@dq.ua.pt RI Tomer, Kenneth/E-8018-2013; Domingues, Pedro/E-5202-2010; Vitorino, Rui/G-7356-2014; Domingues, Rosario/K-7444-2014; Amado, Francisco/M-5337-2015 OI Domingues, Pedro/0000-0002-8060-7675; Vitorino, Rui/0000-0003-3636-5805; Domingues, Rosario/0000-0001-5357-3601; Guedes, Sofia de Morais/0000-0001-9556-3639; Amado, Francisco/0000-0001-8256-1749 NR 45 TC 48 Z9 49 U1 0 U2 9 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X EI 1090-2104 J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 4 PY 2005 VL 328 IS 1 BP 106 EP 115 DI 10.1016/j.bbrc.2004.12.135 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 894NU UT WOS:000226799600017 PM 15670757 ER PT J AU Aldridge, JR Spolski, R Jeanette, MA Kuhn, RE AF Aldridge, JR Spolski, R Jeanette, MA Kuhn, RE TI CpG-ODN stimulates protective immunity against larval taenia crassiceps SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Wake Forest Univ, Dept Biol, Winston Salem, NC 27109 USA. NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. RI Aldridge, Jerry/B-4777-2013 OI Aldridge, Jerry/0000-0002-9653-1775 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A938 EP A938 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706508 ER PT J AU Amos, RN Macchiarini, F Fowlkes, BJ AF Amos, RN Macchiarini, F Fowlkes, BJ TI A dominant negative form of Presenilin blocks thymocytes at early stages but enhances development of other lineages SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Cellular & Mol Immunol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A921 EP A921 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706428 ER PT J AU Andersson, J Shevach, EM AF Andersson, J Shevach, EM TI IL-2 alone can activate the suppressor-effector function of CD4(+)CD25(+) T cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A909 EP A910 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706375 ER PT J AU Ansari, HR Teng, B Oldenberg, PJ Schnermann, JB Mustafa, SJ AF Ansari, HR Teng, B Oldenberg, PJ Schnermann, JB Mustafa, SJ TI Up-regulation of Protein Kinase C-isoforms in primary cultured coronary artery smooth muscle cells from A1-adenosine receptor-deficient mice (A1AR-/-) and respective Wild Type (WT) SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 E Carolina Univ, Greenville, NC 27834 USA. NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A725 EP A725 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705176 ER PT J AU Asiedu, C Le Bas-Bernardet, S Goodwin, K Hutchings, A Neville, D Thomas, J AF Asiedu, C Le Bas-Bernardet, S Goodwin, K Hutchings, A Neville, D Thomas, J TI Homeostatic expansion of memory cells and thymopoiesis contribute to T cell recovery following profound depletion in juvenile macaques SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Alabama, Birmingham, AL 35294 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A24 EP A25 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700115 ER PT J AU Awumey, EM Putney, JW Howlett, AC Bukoski, RD AF Awumey, EM Putney, JW Howlett, AC Bukoski, RD TI Desensitization of the sensory nerve Ca2+-sensing receptor stably expressed in HEK293 cells is mediated by protein kinase C SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 N Carolina Cent Univ, JLC Biomed Biotechnol Res Inst, Durham, NC 27707 USA. Natl Inst Environm Hlth Sci, Lab Signal Transduct, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A524 EP A525 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703501 ER PT J AU Bansal, G Gant, V Druey, KM AF Bansal, G Gant, V Druey, KM TI Regulation of G-protein-dependent mast cell responses by RGS13 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Mol Signal Transduct Sect, Lab Allerg Dis, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A957 EP A957 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706597 ER PT J AU Basu, NK Garza, A Banerjee, R Owens, IS AF Basu, NK Garza, A Banerjee, R Owens, IS TI PKC epsilon mediated phosphorylation of human UDP-glucuronosyltransferase (UGT) 1A7 regulates substrate specificity SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NICHD, HDB, SGDDM, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A846 EP A846 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706076 ER PT J AU Bazinet, RP Rosenberger, TA Rapoport, SI Weis, WT AF Bazinet, RP Rosenberger, TA Rapoport, SI Weis, WT TI Valproic acid inhibits brain microsomal fatty acyl-CoA synthetases at physiologically relevant concentrations SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIA, BPMS, NIH, Bethesda, MD 20892 USA. Univ N Dakota, Grand Forks, ND 58203 USA. Texas Tech Univ, Dept Pharmaceut Sci, Amarillo, TX 79106 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A843 EP A843 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706058 ER PT J AU Beaird, LC Woolf, K Mason, M Reese, C Vaughan, LA Salbe, A AF Beaird, LC Woolf, K Mason, M Reese, C Vaughan, LA Salbe, A TI Psychological correlates of eating behaviors between active and sedentary women throughout the adult lifecycle SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Arizona State Univ E, Dept Nutr, Mesa, AZ 85212 USA. NIDDK, NIH, Phoenix, AZ 85016 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A460 EP A460 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703202 ER PT J AU Benyajati, S Pritchard, JB AF Benyajati, S Pritchard, JB TI Taurine efflux is mediated by renal luminal organic anion transporter, hOAT4 (SLC22A11) SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK 73104 USA. NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A150 EP A150 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701052 ER PT J AU Bird, GS Putney, JW AF Bird, GS Putney, JW TI Capacitative calcium entry supports calcium oscillations in human embryonic kidney cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A678 EP A678 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610704598 ER PT J AU Bisht, H Roberts, A Vogel, L Bukreyev, A Lamirande, E Collins, P Murphy, B Subbarao, K Moss, B AF Bisht, H Roberts, A Vogel, L Bukreyev, A Lamirande, E Collins, P Murphy, B Subbarao, K Moss, B TI Spike protein of SARS coronavirus (SARS-CoV) induces protective immunity against subsequent SARS-CoV challenge in mice SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A894 EP A894 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706301 ER PT J AU Borrego, F Maasho, K Opoku-Anane, J Marusina, AI Valas, R Coligan, JE AF Borrego, F Maasho, K Opoku-Anane, J Marusina, AI Valas, R Coligan, JE TI NKG2D co-stimulation of human naive CD8+T cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Lab Allerg Dis, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A907 EP A907 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706363 ER PT J AU Borthakur, G Sprandel, K Hwang, ES Bowen, PE Stacewicz-Sapuntzakis, M Sharifi, R Wu, ZG Gustin, D Crowell, J Rodvold, K AF Borthakur, G Sprandel, K Hwang, ES Bowen, PE Stacewicz-Sapuntzakis, M Sharifi, R Wu, ZG Gustin, D Crowell, J Rodvold, K TI Effect of chronic dosing of lycopene as tomato based beverage on oxidative stress biomarkers SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Illinois, Chicago, IL 60612 USA. Univ Chicago, Chicago, IL 60615 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A472 EP A472 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703254 ER PT J AU Bow, DAJ Sweet, DH Grissom, SF Parker, J Pritchard, JB AF Bow, DAJ Sweet, DH Grissom, SF Parker, J Pritchard, JB TI Gene expression in liver and kidney of the wild-type and organic anion transporter 3 (OAT3) knockout mouse SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIEHS, NIEHS Microarray Grp, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. Med Univ S Carolina, Dept Pharmaceut Sci, Charleston, SC 29425 USA. Constella Grp Inc, Durham, NC 27713 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A151 EP A151 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701057 ER PT J AU Breslow, RA Guenther, PM Smothers, BA AF Breslow, RA Guenther, PM Smothers, BA TI Measures of alcohol intake and diet quality SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAAA, Bethesda, MD 20892 USA. USDA, Ctr Nutr Policy & Promot, Alexandria, VA 22302 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A63 EP A64 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700295 ER PT J AU Brinster, C Shevach, EM AF Brinster, C Shevach, EM TI Bone-marrow-derived dendritic cells (BMDC) reverse the "anergic" state of CD4(+)CD25(+) T cells without reversing their suppressive activity SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A912 EP A912 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706387 ER PT J AU Burgess, SJ Borrego, F Coligan, JE AF Burgess, SJ Borrego, F Coligan, JE TI Ligation of the NK cell inhibitory receptor CD94/NKG2A induces tyrosine phosphorylation of c-Cbl and Cbl-b and mediates the ubiquitination of ZAP-70 in NK cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Rockville, MD 20852 USA. NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A391 EP A391 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702527 ER PT J AU Butts, CL Duncan, KM Danoff, EJ Sternberg, EM AF Butts, CL Duncan, KM Danoff, EJ Sternberg, EM TI Comparison of Lewis and Fischer rat dendritic cell responses to progesterone SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIMH, NIH, Sect Neuroendocrine Immunol & Behav, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A412 EP A412 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702624 ER PT J AU Caspi, RR Tang, J Zhu, W Silver, PB So, SB Chan, CC AF Caspi, RR Tang, J Zhu, W Silver, PB So, SB Chan, CC TI FIt3L-elicited, in vitro-matured splenic dendritic cells (DC) induce autoimmune disease in the retina SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A345 EP A345 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702314 ER PT J AU Chaturvedi, A Pierce, S AF Chaturvedi, A Pierce, S TI B cell receptor signaling influences the response to CpG SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIH, Immunogenet Lab, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A951 EP A951 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706571 ER PT J AU Chiu, WK Fann, M Chrest, J Madara, K Wersto, R Weng, NP AF Chiu, WK Fann, M Chrest, J Madara, K Wersto, R Weng, NP TI Molecular and cellular characterization of CD28null CD8+memory phenotype T cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIA, Immunol Lab, Baltimore, MD 21224 USA. NIA, Flow Cytometry Unit, Baltimore, MD 21224 USA. NIA, Blood Phoresis Unit, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A26 EP A26 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700123 ER PT J AU Choi, YH Zmuda-Trzebiatowska, E Svennelid, F Tang, Y Gavrilova, O Haluzik, M Park, S Hockman, S Stenson-Holst, L Degerman, E Manganiello, V AF Choi, YH Zmuda-Trzebiatowska, E Svennelid, F Tang, Y Gavrilova, O Haluzik, M Park, S Hockman, S Stenson-Holst, L Degerman, E Manganiello, V TI Alterations in energy homeostasis in cyclic nucleotide phosphodiesterase 3B (PDE3B) knockout mice SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, PCCMB, NIH, Bethesda, MD 20892 USA. NIDDK, NIH, DB, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A826 EP A826 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705651 ER PT J AU Chou, CL Hoffert, JD Knepper, MA AF Chou, CL Hoffert, JD Knepper, MA TI Nonmuscle myosin II inhibitor blebbistatin inhibits AVP-stimulated water permeability but not urea permeability in rat IMCD SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 LKEM, NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A153 EP A153 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701066 ER PT J AU Citterio, C Pacheco-Rodriguez, G Moss, J Vaughan, M AF Citterio, C Pacheco-Rodriguez, G Moss, J Vaughan, M TI Intracellular translocation of BIG1 and ARF in response to cyclic AMP SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, NIH, P CCMB, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A824 EP A824 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705644 ER PT J AU Coleman, JW Gilfillan, AM Metcalfe, DD AF Coleman, JW Gilfillan, AM Metcalfe, DD TI Suppression of IgE-mediated mast cell cytokine production by nitric oxide is associated with impaired Fos and Jun induction SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A932 EP A932 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706480 ER PT J AU Conley, MP Jang, MK DeGiorgis, JA Bearer, EL AF Conley, MP Jang, MK DeGiorgis, JA Bearer, EL TI Zip code for the synapse: Do transport failures cause neurodegeneration? SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunologists, Amer Physiol Soc, Amer Soc Biochem & Mol Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Expt Therapeut, Int Union Physiol Sci C1 Brown Univ, Providence, RI 02912 USA. Marine Biol Lab, Woods Hole, MA 02543 USA. NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 EI 1530-6860 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A506 EP A506 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703412 ER PT J AU Cortes, LM Avichezer, D Silver, PB Chan, CC Caspi, RR AF Cortes, LM Avichezer, D Silver, PB Chan, CC Caspi, RR TI Altered peptide ligands derived from a major pathogenic epitope protect from anti-retinal autoimmunity SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A925 EP A925 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706450 ER PT J AU Davies, GE Locke, S Miller, JS Anderson, SK AF Davies, GE Locke, S Miller, JS Anderson, SK TI Identification of a novel KIR promoter that may represent a probabilistic switch SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, SAIC Frederick, Basic Res Program, Ft Detrick, MD 21702 USA. NCI, CCR, Expt Immunol Lab, Ft Detrick, MD 21702 USA. Univ Minnesota, Dept Med, Ctr Canc, Minneapolis, MN 55455 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A19 EP A20 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700091 ER PT J AU Dean, M Fojo, T Bates, S AF Dean, M Fojo, T Bates, S TI Tumor stem cells, drug transporters and cyclopamine SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Frederick, MD 21704 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A261 EP A261 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701575 ER PT J AU DeLozier, TC Lee, SC Coulter, SJ Cher, GB Goldstein, JA AF DeLozier, TC Lee, SC Coulter, SJ Cher, GB Goldstein, JA TI Catalytic activity of recently discovered allelic variants of CYP2C9 occurring in southeast Asians SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunologists, Amer Physiol Soc, Amer Soc Biochem & Mol Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Expt Therapeut, Int Union Physiol Sci C1 Natl Inst Environm Hlth Sci, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. Natl Univ Singapore Hosp, Dept Hematol Oncol, Singapore 119074, Singapore. Natl Univ Singapore Hosp, Dept Hematol Oncol, Singapore 119074, Singapore. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A541 EP A541 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703577 ER PT J AU Deng, GM Zheng, LX Lenardo, M AF Deng, GM Zheng, LX Lenardo, M TI A potential therapeutic molecule for inflammatory arthritis targeting pre-ligand assembly domain (PLAD) of TNF receptors SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A915 EP A915 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706400 ER PT J AU Fattakhova, GV Borrego, F Gilfillan, A Metcalfe, D Coligan, J AF Fattakhova, GV Borrego, F Gilfillan, A Metcalfe, D Coligan, J TI Endocytosis of Fc epsilon RI in RBL-2H3 cells does not require a clathrin-dependent mechanism SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A933 EP A933 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706486 ER PT J AU Feng, C Jankovic, D Kullberg, M Sher, A AF Feng, C Jankovic, D Kullberg, M Sher, A TI Maintenance of pulmonary Th1 effector function in chronic tuberculosis requires persistent IL-12 production SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A392 EP A392 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702529 ER PT J AU Fenton, JI Block, EM Laird, J Ustunol, Z Pestka, JJ Hord, NG AF Fenton, JI Block, EM Laird, J Ustunol, Z Pestka, JJ Hord, NG TI Modulation of Escherichia Coli O157 : H7-mediated production of proinflammatory mediators by Lactobacilli: role of p38 MAPK and JNK signaling SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Canc Prevent Fellowship Program, E Lansing, MI 48824 USA. Michigan State Univ, E Lansing, MI 48824 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A81 EP A81 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700373 ER PT J AU Fenton, RA Schnermann, J Flynn, A Smith, CP Shodiende, A Knepper, MA AF Fenton, RA Schnermann, J Flynn, A Smith, CP Shodiende, A Knepper, MA TI Role of urea in renal function: Studies using UT-A1/3 knockout mice SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, LKEM, NIH, Bethesda, MD 20892 USA. NIDDK, NIH, Bethesda, MD 20892 USA. Univ Manchester, Fac Life Sci, Manchester, Lancs, England. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A589 EP A589 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610704184 ER PT J AU Fiala, M Eshleman, A Lossinsky, A Arthos, J AF Fiala, M Eshleman, A Lossinsky, A Arthos, J TI Cocaine remodels and disrupts brain endothelial cells and enhances HIV-1 invasion SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunologists, Amer Physiol Soc, Amer Soc Biochem & Mol Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Expt Therapeut, Int Union Physiol Sci C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90095 USA. Vet Adm Med Ctr, Portland, OR 97239 USA. 3 Huntington Med Res Inst, Pasadena, CA 91105 USA. NIAID, Immunoregulat Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A502 EP A503 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703396 ER PT J AU Gentile, S Darden, T Russo, A Erxleben, C Rossie, S Armstrong, D AF Gentile, S Darden, T Russo, A Erxleben, C Rossie, S Armstrong, D TI Rac GTPase signaling through the S/T protein phosphatase, PP5 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIEHS, Res Triangle Pk, NC 27709 USA. Purdue Univ, W Lafayette, IN 47907 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A821 EP A821 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705629 ER PT J AU Golech, SA Lee, WH Huston, G Swain, S Weng, NP AF Golech, SA Lee, WH Huston, G Swain, S Weng, NP TI Multiple steps are associated with the transition of CD4+effector T cells to memory T cells as revealed by gene expression analysis SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIA, LI, NIH, Baltimore, MD 21224 USA. Trudeau Inst Inc, Saranac Lake, NY 12983 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A27 EP A27 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700127 ER PT J AU Green, ED AF Green, ED TI Decoding the human genome by multi-species sequence comparisons SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A810 EP A810 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705578 ER PT J AU Guenther, PM Dodd, KW Reedy, J Krebs-Smith, SM AF Guenther, PM Dodd, KW Reedy, J Krebs-Smith, SM TI Fifty-eight percent of Americans eat less than five servings of fruits and vegetables a day SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 USDA, Ctr Nutr Policy & Promot, Alexandria, VA 22302 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A91 EP A92 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700421 ER PT J AU Guo, LY Hu-Li, J Paul, W AF Guo, LY Hu-Li, J Paul, W TI Regulation of IL-4 and IL-13 expression in TH2 cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A902 EP A902 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706340 ER PT J AU Gupta, K Yu, ZY Restifo, NP Schneck, JP AF Gupta, K Yu, ZY Restifo, NP Schneck, JP TI Increased TCR cross-linking on high avidity CD8+ T cells generated by low antigenic stimulation: Potential application for tumor immunotherapy SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21218 USA. NIH, Surg Branch, Bethesda, MD 20892 USA. RI Restifo, Nicholas/A-5713-2008 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A365 EP A365 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702403 ER PT J AU Houghton, LA Sherwood, K Pawlosky, R Moser, R O'Connor, DL AF Houghton, LA Sherwood, K Pawlosky, R Moser, R O'Connor, DL TI Effect of folate supplementation on folate status and the distribution of the individual folate forms in red blood cells of lactating women SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Hosp Sick Children, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Nutr Sci, Toronto, ON M5S 3E2, Canada. NIH, Rockville, MD 20852 USA. Merck Eprova AG, CH-8200 Schaffhausen, Switzerland. RI Houghton, Lisa/F-5305-2011 OI Houghton, Lisa/0000-0002-2276-6205 NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A420 EP A420 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703017 ER PT J AU Hu, JY Li, GC Tong, YQ Li, YH Zhou, GH He, XJ Xie, PL Wang, JM Sun, QB AF Hu, JY Li, GC Tong, YQ Li, YH Zhou, GH He, XJ Xie, PL Wang, JM Sun, QB TI Transduction of the gene coding for a human G-protein coupled receptor FPRL1 in mouse tumor cells increases host anti-tumor immunity SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Mol Immunoregulat Lab, Frederick, MD 21702 USA. Cent S Univ, Xiang Ya Sch Med, Lab Tumor Immunobiol, Canc Res Inst, Changsha, Peoples R China. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A37 EP A37 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700175 ER PT J AU Inobe, M Schwartz, RH AF Inobe, M Schwartz, RH TI Profound down-modulation of adaptive tolerant CD4(+) T cell proliferation in the absence of CD28 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Hokkaido Univ, Div Mol Immunol, Inst Med Genet, Kita Ku, Sapporo, Hokkaido 0600815, Japan. NIAID, LCMI, NIH, DHHS, Bethesda, MD 20892 USA. RI INOBE, Manabu/D-8393-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A908 EP A908 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706370 ER PT J AU Islam, A Levine, SJ AF Islam, A Levine, SJ TI NEFA, an ARTS-1 interacting and calcium binding protein, that promotes the release of soluble TNFR1 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A310 EP A310 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702149 ER PT J AU Jayachandran, M Karnicki, K Miller, RS Owen, WG Korach, KS Miller, VM AF Jayachandran, M Karnicki, K Miller, RS Owen, WG Korach, KS Miller, VM TI Integrity of estrogen receptor beta affects platelet response to immunological challenge SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Mayo Clin, Coll Med, Rochester, MN 55905 USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A699 EP A699 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705054 ER PT J AU Jiang, YC Cheng, ML Liu, J Kang, YJ AF Jiang, YC Cheng, ML Liu, J Kang, YJ TI Retro-transdifferentiation of activated hepatic stellate cells leading to Han-Dan-Gan-Le resolution of advanced liver fibrosis SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Louisville, Louisville, KY 40202 USA. Guiyang Med Coll, Guiyang 550004, Peoples R China. NIEHS, NCI, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A499 EP A499 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703381 ER PT J AU Katz, JL Newman, AH AF Katz, JL Newman, AH TI Assessment of antimuscarinic behavioral effects of analogs of benztropine SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIDA, Psychobiol Sect, Intramural Res Program, Baltimore, MD 21224 USA. NIDA, Med Chem Sect, Intramural Res Program, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A513 EP A514 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703449 ER PT J AU Kelley, MW Montcouquiol, ME AF Kelley, MW Montcouquiol, ME TI Regulation of planar cell polarity in the mammalian cochlea SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIDCD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A791 EP A791 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705485 ER PT J AU Khan, AQ Chen, QY Wu, ZQ Paton, JC Snapper, CM AF Khan, AQ Chen, QY Wu, ZQ Paton, JC Snapper, CM TI Innate and type 1 humoral immunity to Streptococcus pneumoniae are both mediated by MyD88, but differ in their relative dependence on Toll-like receptor 2 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NIAMS, Autoimmun Branch, NIH, Bethesda, MD 20892 USA. Univ Adelaide, Sch Mol & Biomed Sci, Adelaide, SA 5005, Australia. RI Paton, James/A-9920-2008 NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A370 EP A370 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702427 ER PT J AU Kim, SJ Zhang, Z Lee, YC Ray, R Wang, JY Chowdhury, B Choi, MS Tsai, PC Mukherjee, AB AF Kim, SJ Zhang, Z Lee, YC Ray, R Wang, JY Chowdhury, B Choi, MS Tsai, PC Mukherjee, AB TI Interaction of uteroglobin with lipocalin-1 receptor suppresses cancer cell motility and invasion SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A817 EP A817 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705611 ER PT J AU Kim, SW Wang, WD Knepper, MA Frokiaer, J Nielsen, S AF Kim, SW Wang, WD Knepper, MA Frokiaer, J Nielsen, S TI Increased apical targeting of renal ENaC subunits and decreased abundance of 11 beta HSD2 in rats with CBL-induced liver cirrhosis SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Aarhus Univ, Inst Anat, Water & Salt Res Ctr, DK-8000 Aarhus, Denmark. NHLBI, LKEM, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A499 EP A499 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703380 ER PT J AU Kim, YS Kim, SC Kang, HS Yang, XP Joo, JH Jetten, A AF Kim, YS Kim, SC Kang, HS Yang, XP Joo, JH Jetten, A TI Identification and characterization of RORBP70: a novel protein modulating RORgamma transcriptional activity SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIEHS, LRB Cell Biol, NIH, Res Triangle Pk, NC 27709 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A298 EP A298 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702092 ER PT J AU Kirby, TW DeRose, EF London, RE AF Kirby, TW DeRose, EF London, RE TI The response of [methyl-C-13]methioinine-labeled DNA polymerase polymerase beta to double-hairpin DNA SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A308 EP A308 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702139 ER PT J AU Kirvan, CA Swedo, SE Heuser, JS Cunningham, MW AF Kirvan, CA Swedo, SE Heuser, JS Cunningham, MW TI Antibody mediated neuronal cell signaling in pediatric autoimmune neuropsychiatric disorders associated with streptococcus (PANDAS) SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Calif State Univ Sacramento, Sacramento, CA 95818 USA. NIMH, Pediat & Dev Neuropsychiat Branch, Bethesda, MD 20892 USA. Univ Oklahoma, Ctr Biomed Res, Oklahoma City, OK USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A889 EP A889 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706280 ER PT J AU Kole, HK Chi, AWS Bolland, S AF Kole, HK Chi, AWS Bolland, S TI SHIP1 modulates c-Cbl phosphorylation and its ubiquitin-ligase function SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Immunogenet Lab, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A391 EP A391 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702528 ER PT J AU Kudo-Saito, C Schlom, J Hodge, JW AF Kudo-Saito, C Schlom, J Hodge, JW TI The requirement of multimodal therapy (vaccine, local tumor radiation, and reduction of suppressor cells) to eliminate established tumors SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, NIH, Tumor Immunol & Biol Lab, Bethesda, MD 20892 USA. RI Hodge, James/D-5518-2015 OI Hodge, James/0000-0001-5282-3154 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A40 EP A41 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700190 ER PT J AU Laky, K Fowlkes, BJ AF Laky, K Fowlkes, BJ TI Presenilin-dependent Notch signals affect multiple stages of up thymocyte differentiation SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, LCMI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A359 EP A359 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702378 ER PT J AU Leak, LV Calvert, VS Wulkuhle, JD Liotta, LA Petricoin, EP AF Leak, LV Calvert, VS Wulkuhle, JD Liotta, LA Petricoin, EP TI The application of reverse protein microarrays for proteomic evaluation of signal pathway profiling during lymph angiogenesis SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Howard Univ, Washington, DC 20059 USA. NCI, FDA, Bethesda, MD 20892 USA. NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA. US FDA, CBER, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A168 EP A168 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701137 ER PT J AU Lee, JH Levine, M AF Lee, JH Levine, M TI Glucose inhibition of vitamin C recycling in activated human neutrophils SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIDDK, MCNS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A71 EP A71 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700329 ER PT J AU Lee, YC Zhang, ZJ Hitomi, E Mukherjee, A AF Lee, YC Zhang, ZJ Hitomi, E Mukherjee, A TI Protective role of uteroglobin against bleomycin-induced pulmonary fibrosis SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A279 EP A279 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702002 ER PT J AU Levin, D Mage, M Candon, S Natarajan, K Shevach, EM Margulies, DH AF Levin, D Mage, M Candon, S Natarajan, K Shevach, EM Margulies, DH TI TCR dependence of T-helper cell polarization in autoimmune gastritis (AIG) SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NCI, Lab Basic Res, NIH, Bethesda, MD 20892 USA. RI Margulies, David/H-7089-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A888 EP A888 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706273 ER PT J AU Lewis, JB Laiosa, MD Fowlkes, BJ AF Lewis, JB Laiosa, MD Fowlkes, BJ TI A role for the adapter protein numb in lymphocyte development SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A923 EP A923 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706439 ER PT J AU Li, CL Wang, WD Norregaard, R Knepper, MA Nielsen, S Frokiaer, J AF Li, CL Wang, WD Norregaard, R Knepper, MA Nielsen, S Frokiaer, J TI Dysregulation of ENaC subunit expression and targeting in rats with urinary tract obstruction SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, Lab Kidney & Electrolyte Metab, NIH, Bethesda, MD 20892 USA. Univ Aarhus, Water & Salt Res Ctr, DK-8000 Aarhus, Denmark. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A584 EP A584 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610704164 ER PT J AU Li, HF Wojciechowski, W Dell'Agnola, C Lopez, N Marshall, S Espinoza-Delgado, I AF Li, HF Wojciechowski, W Dell'Agnola, C Lopez, N Marshall, S Espinoza-Delgado, I TI Bryostatin-1 directly induces STAT-1 phosphorylation and IFN-g production by dendritic cells: Association with ERK1/2 phosphorylation SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIA, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A411 EP A412 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702623 ER PT J AU Li, TW Santockyte, R Shen, RF Tekle, E Wang, GH Yang, DCH Chock, PB AF Li, TW Santockyte, R Shen, RF Tekle, E Wang, GH Yang, DCH Chock, PB TI Identification of SUMO-2/3 target proteins via proteomic approaches SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Washington, DC 20057 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A852 EP A852 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706105 ER PT J AU Liang, W Wu, S Fishman, PH AF Liang, W Wu, S Fishman, PH TI Ubiquitination of lysines in the carboxyl tail of the human beta 2-adrenergic receptor directs lysosomal trafficking and degradation of the receptor SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NINDS, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A319 EP A319 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702195 ER PT J AU Lipsky, RH Jiang, XY Hoberman, J Xu, K Marko, A Waheed, J Harris, C Marini, AM Enoch, MA AF Lipsky, RH Jiang, XY Hoberman, J Xu, K Marko, A Waheed, J Harris, C Marini, AM Enoch, MA TI BDNF variation and mood disorders: A novel functional promoter polymorphism and Val66Met are associated with anxiety but have opposing effects SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAAA, Neurogenet, NIH, Rockville, MD 20852 USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A309 EP A309 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702145 ER PT J AU Liu, ZY Berman, D Fisher, RA AF Liu, ZY Berman, D Fisher, RA TI RGS6 promotes growth arrest, cell cycle arrest and apoptosis in U20S cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Iowa, Iowa City, IA 52242 USA. NCI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A850 EP A850 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706093 ER PT J AU Long, EO Bryceson, YT March, ME Barber, DF AF Long, EO Bryceson, YT March, ME Barber, DF TI Hierarchy and synergy of activation receptors on resting NK cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA. RI Barber, Domingo/G-1257-2010 OI Barber, Domingo/0000-0001-8824-5405 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A30 EP A30 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700142 ER PT J AU Lumsden, J McCarty, T Petiniot, L Shen, R Barlow, C Wynn, T Morse, H Gearhart, P Wynshaw-Boris, A Max, E Hodes, R AF Lumsden, J McCarty, T Petiniot, L Shen, R Barlow, C Wynn, T Morse, H Gearhart, P Wynshaw-Boris, A Max, E Hodes, R TI Immunoglobulin class switch recombination is impaired in Atm-deficient mice SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIH, Bethesda, MD 20892 USA. RI Lumsden, Joanne/B-6475-2009 NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A16 EP A16 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700075 ER PT J AU Lutsiak, C Semnani, RT De Pascalis, R Kashmiri, SVS Schlom, J Sabzevari, H AF Lutsiak, C Semnani, RT De Pascalis, R Kashmiri, SVS Schlom, J Sabzevari, H TI Inhibition of CD4(+)25(+) T regulatory cell function implicated in enhanced immune response by low dose cyclophosphamide SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Tumor Immunol & Biol Lab, Bethesda, MD 20892 USA. NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 1 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A32 EP A32 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700151 ER PT J AU Machado, FS Johndrow, J Bafica, A Dias, A Aliberti, J AF Machado, FS Johndrow, J Bafica, A Dias, A Aliberti, J TI SOCS-2 mediates LXA4 dependent inhibition of IL-12 production by dendritic cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Duke Univ, Durham, NC 27706 USA. NIAID, LPD, NIH, Bethesda, MD USA. RI Aliberti, Julio/I-7354-2013 OI Aliberti, Julio/0000-0003-3420-8478 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A372 EP A372 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702436 ER PT J AU Martin, A Norris, HH Wang, H Lybarger, L Chervenak, D Chervenak, R AF Martin, A Norris, HH Wang, H Lybarger, L Chervenak, D Chervenak, R TI Initiation of B-lineage differentiation in a novel subset of common lymphoid progenitors SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Louisiana State Univ, Hlth Sci Ctr, Res Core Facil, Shreveport, LA 71130 USA. NIAID, NIH, Rockville, MD 20852 USA. Univ Arizona, Tucson, AZ 85724 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A917 EP A917 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706408 ER PT J AU Marusina, AI Kim, DK Lieto, LD Borrego, F Coligan, JE AF Marusina, AI Kim, DK Lieto, LD Borrego, F Coligan, JE TI GATA-3 is an important transcription factor for regulating human NKG2A gene expression SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, RCBS, LAD, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A16 EP A17 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700077 ER PT J AU Moaddel, R Yamaguchi, R Patel, S Ho, P Wainer, IW AF Moaddel, R Yamaguchi, R Patel, S Ho, P Wainer, IW TI Development of an immobilized organic cation transporter column for on line screening using chromatographic SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIA, Ctr Gerontol Res, NIH, Baltimore, MD 21224 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A542 EP A542 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703579 ER PT J AU Mongini, P Kalled, S Inman, J AF Mongini, P Kalled, S Inman, J TI BAFF & IL4 exhibit synergy in promoting activation-associated replication & death of BCR: CD21-triggered human B cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NYU Med Ctr, Hosp Joint Dis, New York, NY 10003 USA. Biogen Idec, Cambridge, MA 02142 USA. NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A885 EP A886 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706263 ER PT J AU Mooney, JM Chan, A Schwartzberg, PL Wakeland, EK Schatzle, JD AF Mooney, JM Chan, A Schwartzberg, PL Wakeland, EK Schatzle, JD TI 2B4 (CD244) haplotype expression dictates cytotoxic function SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Texas, SW Med Ctr, Grad Program Immunol, Dallas, TX 75390 USA. Univ Texas, SW Med Ctr, Ctr Immunol, Dallas, TX 75390 USA. Natl Genome Res Inst, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A390 EP A390 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702522 ER PT J AU Morris, RG Knepper, MA AF Morris, RG Knepper, MA TI Water restriction increases WNK4 expression in mouse kidney SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, LKEM, Bethesda, MD 20892 USA. LKEM, NHLBI, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A152 EP A152 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701063 ER PT J AU Mostbock, S Schlom, J Sabzevari, H AF Mostbock, S Schlom, J Sabzevari, H TI Role of enhanced costimulation on functionality of CD8(+) T cells induced by altered peptide ligands SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Lab Tumor Immunol & Biol, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A906 EP A906 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706359 ER PT J AU Mueller, K Finkelstein, LD Schwartzberg, PL Shimizu, Y AF Mueller, K Finkelstein, LD Schwartzberg, PL Shimizu, Y TI The adapter protein ADAP is a critical regulator of antigen dependent T cell interactions with antigen presenting cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Minnesota, Ctr Immunol, Minneapolis, MN 55455 USA. NHGRI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A388 EP A388 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702512 ER PT J AU Nahirney, PC Wang, K AF Nahirney, PC Wang, K TI Myosin flares and actin leptomeres as myofibril assembly/disassembly intermediates in sonic muscle fiber SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAMS, Muscle Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A800 EP A800 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705528 ER PT J AU Nguyen, TT Shizukuda, Y Bolan, CD Sachdev, V Tripodi, D Yau, YY Leitman, SF Rosing, D AF Nguyen, TT Shizukuda, Y Bolan, CD Sachdev, V Tripodi, D Yau, YY Leitman, SF Rosing, D TI Correlation between reactive oxygen species and iron levels in NYHA class I hereditary hemochromatosis patients SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, Cardiovasc Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A700 EP A701 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705062 ER PT J AU Nielsen, J Kwon, TH Praetorius, J Frokiaer, J Knepper, MA Nielsen, S AF Nielsen, J Kwon, TH Praetorius, J Frokiaer, J Knepper, MA Nielsen, S TI Aldosterone decrease apical AQP2 expression in connecting tubule and cortical collecting duct and increase urine production in rats with lithium-induced diabetes insipidus SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Aarhus Univ, Inst Anat, Water & Salt Res Ctr, DK-8000 Aarhus, Denmark. NHLBI, Lab Kidney & Electrolyte Metab, NIH, Bethesda, MD 20992 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A151 EP A151 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701058 ER PT J AU Nijhara, R AF Nijhara, R TI Chemokine mediated cytoskeletal changes on T cells occur via Rac1-ERM signaling SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, NIH, Bethesda, MD 20896 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A928 EP A928 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706463 ER PT J AU O'Callaghan, MJ Xu, M Katz, JL AF O'Callaghan, MJ Xu, M Katz, JL TI Effects of dopamine D2/3 ligands on cocaine discrimination in dopamine D3 receptor KO and WT mice SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIDA, Psychobiol Lab, Intramural Res Program, Baltimore, MD 21224 USA. Univ Cincinnati, Med Ctr, Dept Cell Biol Neurobiol & Anat, Cincinnati, OH 45267 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A511 EP A511 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703439 ER PT J AU Oppermann, M Castrop, H Huang, YN Mizel, D Deng, CX Briggs, JP Schnermann, J AF Oppermann, M Castrop, H Huang, YN Mizel, D Deng, CX Briggs, JP Schnermann, J TI Macula densa regulation in mice lacking the B-isoform of the renal Na/K/2Cl Cotransporter NKCC2 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A151 EP A151 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701059 ER PT J AU Panyutin, I Sedelnikova, O Bonner, W Panyutin, I Neumann, R AF Panyutin, I Sedelnikova, O Bonner, W Panyutin, I Neumann, R TI DNA damage produced by I-125-triplex-forming oligonucleotides inside cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIH, CC, Bethesda, MD 20892 USA. NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A506 EP A506 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703413 ER PT J AU Park, IK Shultz, LD Letterio, JL Gorham, JD AF Park, IK Shultz, LD Letterio, JL Gorham, JD TI TGF-beta 1 inhibits IFN-gamma responses in T helper cells through the protein tyrosine phosphatase Shp-1 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Dartmouth Coll Sch Med, Lebanon, NH 03756 USA. Jackson Lab, Bar Harbor, ME 04609 USA. NIH, Lab Cell Regulat & Carcinogenesis, Ctr Canc Res, Bethesda, MD 20892 USA. NIH, Mol Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A382 EP A382 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702480 ER PT J AU Pascal, V Abshari, M Anderson, SK AF Pascal, V Abshari, M Anderson, SK TI NFkB affects Natural Killer cell development by regulating the Ly49 repertoire SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Expt Immunol Lab, Frederick, MD 21702 USA. SAIC Frederick, Expt Immunol Lab, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A918 EP A918 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706413 ER PT J AU Peng, Z Beaven, MA AF Peng, Z Beaven, MA TI An essential role for phospholipase D (PLD) in the activation of protein kinase C (PKC) and degranulation in mast cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, Lab Mol Immunol, Bethesda, MD 20892 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A933 EP A933 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706487 ER PT J AU Perry, JL Pritchard, JB AF Perry, JL Pritchard, JB TI Structure/Function insights into the renal human organic transporters SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIEHS, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A149 EP A149 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701050 ER PT J AU Poirier, L Ross, S Pogribna, M Wise, C James, SJ Dragan, Y Pogribny, I AF Poirier, L Ross, S Pogribna, M Wise, C James, SJ Dragan, Y Pogribny, I TI Irreversible global DNA hypomethylation during hepatocarcinogenesis induced by dietary methyl deficiency SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Natl Ctr Toxicol Res, Jefferson, AR 72079 USA. NCI, Bethesda, MD 20892 USA. UAMS, Little Rock, AR 72205 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A219 EP A219 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701375 ER PT J AU Puri, N Roche, PA AF Puri, N Roche, PA TI Ternary SNARE complexes are associated with lipid rafts in RBL mast cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A35 EP A36 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700167 ER PT J AU Qiao, M Shevach, EM AF Qiao, M Shevach, EM TI Conversion of naive CD4+CD25-T cells to anergic-suppressor T cells by co-culture with CD4+CD25+T cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Immunol Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A337 EP A337 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702276 ER PT J AU Rajagopalan, S Bryceson, YT Kuppusamy, SP Young, H Joosten, I van der Meer, A Long, EO AF Rajagopalan, S Bryceson, YT Kuppusamy, SP Young, H Joosten, I van der Meer, A Long, EO TI Regulation of vascularization during pregnancy by an NK receptor for soluble HLA-G SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, LIG, NIH, Rockville, MD 20852 USA. NCI, Frederick Canc Res & Dev Ctr, Expt Immunol Lab, Frederick, MD 21702 USA. UMC Nijmegen, Dept Blood Transfus & Transplantat Immunol, NL-6500 HB Nijmegen, Netherlands. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A330 EP A330 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702242 ER PT J AU Ray, R Choi, MS Zhang, ZJ Silverman, G Askew, D Mukherjee, A AF Ray, R Choi, MS Zhang, ZJ Silverman, G Askew, D Mukherjee, A TI Uteroglobin suppresses SCCA2 gene expression associated with allergic asthma SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIH, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A279 EP A279 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702003 ER PT J AU Reynolds, DM Rodriguez-Galan, MC Brooks, A Abshari, M Sayers, TJ Ortaldo, JR Young, HA AF Reynolds, DM Rodriguez-Galan, MC Brooks, A Abshari, M Sayers, TJ Ortaldo, JR Young, HA TI In vivo development of NK cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Expt Immunol Lab, Ft Detrick, MD 21702 USA. SAIC Frederick, Expt Immunol Lab, Ft Detrick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A921 EP A922 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706431 ER PT J AU Rieg, T Steigele, H Schnermann, J Richter, K Osswald, H Vallon, V AF Rieg, T Steigele, H Schnermann, J Richter, K Osswald, H Vallon, V TI Diuretic and natriuretic actions of the methylxanthines caffeine and theophylline depend on intact adenosine A1 receptor (A1AR): Evidence from knockout mice SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Tubingen, Dept Pharmacol & Toxicol, D-72074 Tubingen, Germany. NIDDK, NIH, Bethesda, MD 20892 USA. VASDHS, La Jolla, CA 92161 USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A109 EP A109 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700504 ER PT J AU Rochman, I Ben-Sasson, SZ Paul, W AF Rochman, I Ben-Sasson, SZ Paul, W TI Interleukin-6 promotes the survival of antigen-stimulated CD4+T cells in vivo SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Lautenberg Ctr Gen & Tumor Immunol, IL-91120 Jerusalem, Israel. NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A11 EP A11 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700051 ER PT J AU Roh, TY Cuddapah, S Zhao, KJ AF Roh, TY Cuddapah, S Zhao, KJ TI High-resolution genome-wide mapping of histone modification by GMAT SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 3 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A18 EP A18 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700083 ER PT J AU Romeo, E Dave, MH Kleta, R Ristic, Z Camargo, SMR Makrides, V Wagner, CA Verrey, F AF Romeo, E Dave, MH Kleta, R Ristic, Z Camargo, SMR Makrides, V Wagner, CA Verrey, F TI B(0)AT1 (SLC6A19) and other SLC6 orphan transporters: Hartnup disorder and beyond SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Zurich, Inst Physiol, CH-8057 Zurich, Switzerland. NHGRI, NIH, Med Genet Branch, Bethesda, MD 20892 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A747 EP A747 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705277 ER PT J AU Ross, SA Finley, JW Leary, P Gregoire, B Milner, J AF Ross, SA Finley, JW Leary, P Gregoire, B Milner, J TI Speciation effects of allyl sulfur compounds on aberrant crypt formation SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, DCP, NSRG, NIH, Bethesda, MD 20892 USA. USDA ARS, Grand Forks Human Nutr Res Ctr, Grand Forks, ND 58202 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A80 EP A80 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700366 ER PT J AU Salnikow, K Karaczyn, A Inanov, S Zhitkovich, A Donald, S Kasprzak, K AF Salnikow, K Karaczyn, A Inanov, S Zhitkovich, A Donald, S Kasprzak, K TI Mechanisms of HIF up regulation by metals SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Comparat Carcinogenesis Lab, Ft Detrick, MD 21702 USA. SAIC, Frederick, MD 21702 USA. Brown Univ, Providence, RI 02912 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A877 EP A877 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706223 ER PT J AU Santockyte, R Li, TW Shen, RF Tekle, E Wang, GH Chock, B Yang, DCH AF Santockyte, R Li, TW Shen, RF Tekle, E Wang, GH Chock, B Yang, DCH TI A proteomic analysis of NEDD8 conjugated proteins SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Georgetown Univ, Washington, DC 20057 USA. NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A852 EP A852 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706104 ER PT J AU Sarkar, K Weinberg, C Oddis, CV Medsger, TA Plotz, PH Reveille, JD Arnett, FC Targoff, IN Genth, E Love, LA Miller, FW AF Sarkar, K Weinberg, C Oddis, CV Medsger, TA Plotz, PH Reveille, JD Arnett, FC Targoff, IN Genth, E Love, LA Miller, FW TI Seasonal influences in the onset of serologic groups of idiopathic inflammatory myopathies SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIH, Bethesda, MD 20892 USA. Univ Pittsburgh, Pittsburgh, PA 15261 USA. Univ Texas, Houston, TX 77030 USA. OMRF, Oklahoma City, OK 73104 USA. Dept Rheumatol, D-52066 Aachen, Germany. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A890 EP A890 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706285 ER PT J AU Sassen, MC Kim, SW Knepper, MA Miller, RT Frokiaer, J Nielsen, S AF Sassen, MC Kim, SW Knepper, MA Miller, RT Frokiaer, J Nielsen, S TI Dysregulation of renal sodium transporters in gentamicin-treated rats SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Aarhus Univ, Water & Salt Res Ctr, DK-8000 Aarhus, Denmark. NHLBI, LKEM, NIH, Bethesda, MD 20892 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A153 EP A153 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701067 ER PT J AU Sato, N Dubois, S Waldmann, TA Tagaya, Y AF Sato, N Dubois, S Waldmann, TA Tagaya, Y TI IL-15R alpha mediates the long-term retention of IL-15 in microenvironments, which resulted in a persistent and sustained action of IL-15 in vivo SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A23 EP A23 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700108 ER PT J AU Shah, BH Catt, KJ AF Shah, BH Catt, KJ TI Role of EGF receptor transactivation in phosphoinositide 3-kinase-dependent activation of MAP kinase by GPCRs SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NICHD, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. NICHD, ERRB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A820 EP A820 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705625 ER PT J AU Sheng, Y Tsai-Morris, CH Dufau, ML AF Sheng, Y Tsai-Morris, CH Dufau, ML TI Gonadotropin-regulated testicular RNA helicase (GRTH/Ddx25) is a shuttling protein involved in mRNA export and protein translation SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NICHD, Sect Mol Endocrinol, Endocrinol & Reprod Res Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A318 EP A318 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702189 ER PT J AU Shieh, JJ Lin, CY AF Shieh, JJ Lin, CY TI Identification of novel splicing variants of the human Na+/Pi co-transporter 4 in human kidney SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK 73104 USA. Natl Inst Environm Hlth Sci, Lab Pharmacol & Chem, Res Triangle Pk, NC 27709 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A150 EP A150 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701053 ER PT J AU Shizukuda, Y Bolan, CD Nguyen, T Tripodi, DJ Smith, KP Vandana, S Birdsall, CW Yau, YY Leitman, SF Rosing, DR AF Shizukuda, Y Bolan, CD Nguyen, T Tripodi, DJ Smith, KP Vandana, S Birdsall, CW Yau, YY Leitman, SF Rosing, DR TI Preserved left ventricular systolic function during exercise in asymptomatic patients with iron overload secondary to hereditary hemochromatosis SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, Cardiovasc Branch, NIH, Bethesda, MD 20892 USA. NIH, Dept Transfus Med, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A127 EP A127 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700590 ER PT J AU Song, KM Zhang, HW Dale, J Dugan, F Straus, S Roederer, M Farber, J AF Song, KM Zhang, HW Dale, J Dugan, F Straus, S Roederer, M Farber, J TI Chemokine receptor expression in autoimmune lymphoproliferative syndrome(ALPS) SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, LMI, NIH, Bethesda, MD 20892 USA. NIAID, LCID, Bethesda, MD 20892 USA. NIAID, VRC, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A941 EP A941 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706524 ER PT J AU Spolski, R Ozaki, K Ettinger, R Kim, HP Roopenian, D Morse, HC Lipsky, PE Leonard, WJ AF Spolski, R Ozaki, K Ettinger, R Kim, HP Roopenian, D Morse, HC Lipsky, PE Leonard, WJ TI Regulation of B cell differentiation and plasma cell generation by interleukin-21 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, Lab Mol Immunol, NIH, LMI, Bethesda, MD 20892 USA. Univ Tokyo, Minato Ku, Tokyo, Japan. NIAID, NIH, Bethesda, MD 20892 USA. NIAMS, NIH, Bethesda, MD 20892 USA. NHLBI, LMI, NIH, Bethesda, MD 20892 USA. Jackson Lab, Bar Harbor, ME 04609 USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A358 EP A358 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702370 ER PT J AU Stephens, G Whitters, M Collins, M Collins, M Shevach, E AF Stephens, G Whitters, M Collins, M Collins, M Shevach, E TI GITR/GITR-L interactions promote the survival/expansion of antigen-activated T cells in vivo SO FASEB JOURNAL LA English Estonian DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Bethesda, MD 20892 USA. Wyeth, Cambridge, MA 02140 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A905 EP A905 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706354 ER PT J AU Su, SB Silver, PB Grajewski, RS Agarwal, RK Tang, J Chan, CC Caspi, RR AF Su, SB Silver, PB Grajewski, RS Agarwal, RK Tang, J Chan, CC Caspi, RR TI Essential role of the myeloid differentiation factor 88 pathway, but nonessential roles of Toll receptors 2, 4 and 9, in the adjuvant effect promoting Th1 mediated-autoimmunity SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A346 EP A346 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702317 ER PT J AU Swietnicki, W O'Brien, S Nystrom, S Dyas, B Ruthel, G Tropea, J Waugh, D Ulrich, R AF Swietnicki, W O'Brien, S Nystrom, S Dyas, B Ruthel, G Tropea, J Waugh, D Ulrich, R TI Intra- and inter-domain interactions between Yersinia pestis virulence proteins YopB, YopD, and the chaperone SycD SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 USA, Med Res Inst Infect Dis, Ft Detrick, MD 21702 USA. SAIC Frederick, Frederick, MD 21702 USA. NCI Frederick, Macromol Crystallog Lab, Frederick, MD 21702 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A314 EP A314 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702168 ER PT J AU Swindle, EJ Coleman, JW Metcalfe, DD AF Swindle, EJ Coleman, JW Metcalfe, DD TI Blockade of antigen induced reactive oxygen species generation in mast cells results in altered degranulation and cytokine production SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, Lab Allerg Dis, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A933 EP A933 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706488 ER PT J AU Tagaya, Y Sato, N Dubois, S Waldmann, TA Kobayashi, H AF Tagaya, Y Sato, N Dubois, S Waldmann, TA Kobayashi, H TI By presenting IL-15 in trans, APCs activate NK cells into effective killers of tumor cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Metab Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A940 EP A940 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706519 ER PT J AU Tarasenko, TN Lig, SB AF Tarasenko, TN Lig, SB TI SHIP-/- macrophages induce T cell activation in vivo and restore proliferation of anergic T cells in vitro SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A390 EP A390 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702520 ER PT J AU Teng, BY Ansari, HR Oldenburg, PJ Schnermann, JB Mustafa, SJ AF Teng, BY Ansari, HR Oldenburg, PJ Schnermann, JB Mustafa, SJ TI Expression of smoothelin in cultured coronary smooth muscle cells from wild type and A(1) adenosine receptor-deficient mice (A(1)AR-/-) SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 E Carolina Univ, Greenville, NC 27834 USA. NIDDK, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A685 EP A685 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610704629 ER PT J AU Tkaczyk, C Ali, K Vanhaesebroeck, B Beaven, MA Metcalfe, DD Gilfillan, AM AF Tkaczyk, C Ali, K Vanhaesebroeck, B Beaven, MA Metcalfe, DD Gilfillan, AM TI PI-3 kinase regulates an amplification pathway for mast cell (MC) activation SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Lab Allerg Dis, Bethesda, MD 20892 USA. Ludwig Inst Canc Res, London W1W 7BS, England. NHLBI, NIH, Lab Mol Immunol, Bethesda, MD 20892 USA. NIAID, NIH, Lab Allerg Dis, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A934 EP A934 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706490 ER PT J AU Vallon, V Volkl, H Grahammer, F Richter, K Gerlach, U Pfeifer, K AF Vallon, V Volkl, H Grahammer, F Richter, K Gerlach, U Pfeifer, K TI Role of K+ channel KCNQ1 in electrogenic glucose reabsorption of proximal tubule SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunologists, Amer Physiol Soc, Amer Soc Biochem & Mol Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Expt Therapeut, Int Union Physiol Sci C1 UCSD, Dept Med, La Jolla, CA 92161 USA. UCSD, Dept Pharmacol, La Jolla, CA 92161 USA. VASDHS, La Jolla, CA 92161 USA. Univ Innsbruck, Dept Physiol, A-6010 Innsbruck, Austria. Univ Tubingen, Dept Physiol, D-72076 Tubingen, Germany. Aventis, D-65926 Frankfurt, Germany. NICHHD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A155 EP A155 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610701077 ER PT J AU Wright, DG Elrod, JW Greer, JJM Noguchi, CT Lefer, DJ AF Wright, DG Elrod, JW Greer, JJM Noguchi, CT Lefer, DJ TI Acute erythropoietin therapy attenuates myocardial ischemia-reperfusion injury in a murine model SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 LSU, Hlth Sci Ctr, Dept Mol & Cellular Physiol, Shreveport, LA 71130 USA. NIDDK, Biol Chem Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A688 EP A688 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610705009 ER PT J AU Wu, Z Leonard, WJ AF Wu, Z Leonard, WJ TI Transcriptional regulation of human interleukin-21 receptor in T lymphocytes is mediated by Sp1 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A904 EP A904 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706349 ER PT J AU Yarovinsky, F Andersen, JF Khurana, S King, LR Aliberti, J Golding, H Sher, A AF Yarovinsky, F Andersen, JF Khurana, S King, LR Aliberti, J Golding, H Sher, A TI Structural determinants of the interaction between Toxoplasma gondii cyclophilin and the HIV-1 co-receptor CCR5 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 LPD, Bethesda, MD 20894 USA. NIAID, LMVR, NIH, Bethesda, MD 20894 USA. FDA, CBER, Bethesda, MD 20892 USA. RI Aliberti, Julio/G-4565-2012; Aliberti, Julio/I-7354-2013 OI Aliberti, Julio/0000-0003-3420-8478 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A939 EP A939 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706513 ER PT J AU Yasar, S Lee, SH Stefanski, R Justinova, Z Goldberg, S Tanda, G AF Yasar, S Lee, SH Stefanski, R Justinova, Z Goldberg, S Tanda, G TI Metabolic transformation plays a primary role in psychostimulant-like discriminative stimulus effects of selegiline in rats SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Johns Hopkins Univ, Sch Med, Div Geriatr Med & Gerontol, Baltimore, MD 21224 USA. NIDA, Behav Neurosci Branch, DHHS, NIH, Baltimore, MD 21224 USA. NIDA, Medicat Discovery Branch, DHHS, NIH, Baltimore, MD 21224 USA. Korea FDA, Seoul, South Korea. Inst Psychiat & Neurol, Warsaw, Poland. RI Tanda, Gianluigi/B-3318-2009 OI Tanda, Gianluigi/0000-0001-9526-9878 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A512 EP A513 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610703444 ER PT J AU Yoshimura, T Matsuyama, W Mizuta, H Matsukawa, A AF Yoshimura, T Matsuyama, W Mizuta, H Matsukawa, A TI Interferon-gamma and collagen synergistically induce monocyte chemoattractant protein-1 production in human polymorphonuclear leukocytes (PMN): Role of discoidin domain receptor 1 (DDR1) SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Lab Mol Immunoregulat, Frederick, MD 21702 USA. Kumamoto Univ, Dept Pathol & Expt Med, Kumamoto 8608556, Japan. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A10 EP A10 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700047 ER PT J AU Yu, CR Mahdi, R Takase, H Vistica, BP Song, KM Gery, I Egwuagu, CE AF Yu, CR Mahdi, R Takase, H Vistica, BP Song, KM Gery, I Egwuagu, CE TI Suppressor of cytokine signaling (SOCS) proteins regulate T cell activation and homeostasis SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NIAID, Clin Invest Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A23 EP A23 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700110 ER PT J AU Zhang, Y Fatima, N Dufau, ML AF Zhang, Y Fatima, N Dufau, ML TI PKC zeta-mediated Sp1 phosphorylation is essential for derepression of transcription of human luteinizing hormone receptor (hLHR) gene SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NICHD, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A877 EP A877 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706222 ER PT J AU Zhang, YH Wahl, LM AF Zhang, YH Wahl, LM TI C reactive protein and oxidized LDL enhance matrix metalloproteinase production by cytokine activated monocytes through monocyte chemotactic protein-1 and prostaglandin E2 SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIDCR, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A6 EP A6 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700028 ER PT J AU Zhao, DM Thornton, AM DiPaolo, RJ Shevach, EM AF Zhao, DM Thornton, AM DiPaolo, RJ Shevach, EM TI Activated CD4+CD25+T cells kill activated B cells via the perforin-granzyme pathway SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A31 EP A31 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610700147 ER PT J AU Zhou, J Tagaya, Y Semnani, RT Schlom, J Sabzevari, H AF Zhou, J Tagaya, Y Semnani, RT Schlom, J Sabzevari, H TI Physiological relevance of antigen presentosome (APS), an acquired MHC/costimulatory complex, in the sustained activation of CD4 T cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Lab Tumor Immunol & Biol, Bethesda, MD 20892 USA. NCI, Metab Branch, Bethesda, MD 20892 USA. NIAID, Parasit Dis Lab, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A414 EP A414 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702634 ER PT J AU Zhou, M Wahl, LM AF Zhou, M Wahl, LM TI Role of ADAM17 in LPS-induced human monocyte TNF-alpha release and matrix metalloproteinase production SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIDCR, Immunopathol Sect, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A864 EP A864 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706161 ER PT J AU Zhu, JF Hu-Li, J Guo, LY Paul, WE AF Zhu, JF Hu-Li, J Guo, LY Paul, WE TI The role of GATA-3 in promoting and maintaining the accessibility of Il4 locus in CD4(+) T cells SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NIAID, William E Paul Lab Immunol, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A902 EP A902 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706338 ER PT J AU Zhu, Q Belyakov, IM Berzofsky, JA AF Zhu, Q Belyakov, IM Berzofsky, JA TI Macrophage-activating lipoprotein (MALP)-2 can enhance DC costimulation and mucosal immunity to a peptide mucosal vaccine SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A947 EP A948 PN 1 PG 2 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610706553 ER PT J AU Zisman, P Ben Sasson, SZ Makedonski, K Nedvetzki, S Pikarsky, E Zhou, YJ Ben Sasson, SA AF Zisman, P Ben Sasson, SZ Makedonski, K Nedvetzki, S Pikarsky, E Zhou, YJ Ben Sasson, SA TI A specific designer inhibitor of Jak3 modulates T-cell activation in-vitro and in-vivo SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2005 Meeting/35th International Congress of Physiological Sciences CY MAR 31-APR 06, 2005 CL San Diego, CA SP Amer Assoc Anatomists, Amer Assoc Immunol, Amer Phtsiol Soc & Int Union Physiol Sci, Amer Soc Biochem & Mole Biol, Amer Soc Investigat Pathol, Amer Soc Nutr Sci, Amer Soc Pharmacol & Exptl Therapeut C1 Hebrew Univ Jerusalem, Hadassah Med Sch, Lautenberg Ctr Gen & Tumor Immunol, IL-91120 Jerusalem, Israel. Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Pathol, IL-91010 Jerusalem, Israel. Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA. Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Expt Med & Canc Res, IL-91120 Jerusalem, Israel. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 4 PY 2005 VL 19 IS 4 SU S BP A386 EP A386 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 905ZQ UT WOS:000227610702500 ER PT J AU Rose, JJ Janvier, K Chandrasekhar, S Sekaly, RP Bonifacino, JS Venkatesano, S AF Rose, JJ Janvier, K Chandrasekhar, S Sekaly, RP Bonifacino, JS Venkatesano, S TI CD4 down-regulation by HIV-1 and simian immunodeficiency virus (SIV) nef proteins involves both internalization and intracellular retention mechanisms SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYPE-1 ENVELOPE GLYCOPROTEIN; CYTOPLASMIC DOMAIN; DILEUCINE MOTIF; SORTING PATHWAYS; CLATHRIN ADAPTER; BINDING SURFACE; VACCINIA VIRUS; COATED PITS; IN-VITRO; BETA-COP AB Among the pleiotropic effects of Nef proteins of HIV and simian immunodeficiency virus ( SIV), down-modulation of cell surface expression of CD4 is a prominent phenotype. It has been presumed that Nef proteins accelerate endocytosis of CD4 by linking the receptor to the AP-2 clathrin adaptor. However, the related AP-1 and AP-3 adaptors have also been shown to interact with Nef, hinting at role( s) for these complexes in the intracellular retention of CD4. By using genetic inhibitors of endocytosis and small interfering RNA-induced knockdown of AP-2, we show that accelerated CD4 endocytosis is not a dominant mechanism of HIV-1( NL4-3 strain) Nef in epithelial cells, T lymphocyte cell lines, or peripheral blood lymphocytes. Furthermore, we show that both the CD4 recycling from the plasma membrane and the nascent CD4 in transit to the plasma membrane are susceptible to intracellular retention in HIV-1 Nef-expressing cells. In contrast, AP-2-mediated enhanced endocytosis constitutes the predominant mechanism for SIV ( MAC-239 strain) Nef-induced down-regulation of human CD4 in human cells. C1 NIAID, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NICHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA. Univ Montreal, Montreal, PQ H3C 3J7, Canada. RP Venkatesano, S (reprint author), NIAID, Mol Biol Lab, NIH, Bldg 10,Rm 6A05, Bethesda, MD 20892 USA. EM svls@nih.gov OI Bonifacino, Juan S./0000-0002-5673-6370 NR 62 TC 39 Z9 39 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 2005 VL 280 IS 9 BP 7413 EP 7426 DI 10.1074/jbc.M409420200 PG 14 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 902ZR UT WOS:000227395700002 PM 15611114 ER PT J AU Hong, S Choi, I Woo, JM Oh, J Kim, T Choi, E Kim, TW Jung, YK Kim, DH Sun, CH Yi, GS Eddy, EM Cho, CH AF Hong, S Choi, I Woo, JM Oh, J Kim, T Choi, E Kim, TW Jung, YK Kim, DH Sun, CH Yi, GS Eddy, EM Cho, CH TI Identification and integrative analysis of 28 novel genes specifically expressed and developmentally regulated in murine spermatogenic cells SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MALE GERM-CELLS; MOUSE SPERMATOGENESIS; MALE-INFERTILITY; FERTILIN-BETA; MICE LACKING; MUTANT MICE; SPERM; TESTIS; PROTEIN; MEIOSIS AB Mammalian spermatogenesis is a highly ordered process that occurs in mitotic, meiotic, and postmeiotic phases. The unique mechanisms responsible for this tightly regulated developmental process suggest the presence of an intrinsic genetic program composed of spermatogenic cell-specific genes. In this study, we analyzed the mouse round spermatid UniGene library currently containing 2124 gene-oriented transcript clusters, predicting that 467 of them are testis-specific genes, and systematically identified 28 novel genes with evident testis-specific expression by in silico and in vitro approaches. We analyzed these genes by Northern blot hybridization and cDNA cloning, demonstrating the presence of additional transcript sequences in five genes and multiple transcript isoforms in six genes. Genomic analysis revealed lack of human orthologues for 10 genes, implying a relationship between these genes and male reproduction unique to mouse. We found that all of the novel genes are expressed in developmentally regulated and stage-specific patterns, suggesting that they are primary regulators of male germ cell development. Using computational bioinformatics tools, we found that 20 gene products are potentially involved in various processes during spermatogenesis or fertilization. Taken together, we predict that over 20% of the genes from the round spermatid library are testis-specific, have discovered the 28 authentic, novel genes with probable spermatogenic cell-specific expression by the integrative approach, and provide new and thorough information about the novel genes by various in vitro and in silico analyses. Thus, the study establishes on a comprehensive scale a new basis for studies to uncover molecular mechanisms underlying the reproductive process. C1 Gwangju Inst Sci & Technol, Dept Life Sci, Kwangju 500712, South Korea. Informat & Commun Univ, Sch Engn, Taejon 305714, South Korea. NIEHS, Gamete Biol Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Cho, CH (reprint author), Gwangju Inst Sci & Technol, Dept Life Sci, Kwangju 500712, South Korea. EM choch@gist.ac.kr RI Kim, Taewan/M-5867-2013; Yi, Gwan-Su/A-7896-2011; OI Kim, Taewan/0000-0002-7202-009X; Yi, Gwan-Su/0000-0003-0012-6546; Choi, Inchul/0000-0001-5011-2658; Jung, Yong-Keun/0000-0002-9686-3120 NR 43 TC 39 Z9 43 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 2005 VL 280 IS 9 BP 7685 EP 7693 DI 10.1074/jbc.M412444200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 902ZR UT WOS:000227395700032 PM 15613475 ER PT J AU Williams, KL Zhang, YJ Shkriabai, N Karki, RG Nicklaus, MC Kotrikadze, N Hess, S Le Grice, SFJ Craigie, R Pathak, VK Kvaratskhelia, M AF Williams, KL Zhang, YJ Shkriabai, N Karki, RG Nicklaus, MC Kotrikadze, N Hess, S Le Grice, SFJ Craigie, R Pathak, VK Kvaratskhelia, M TI Mass spectrometric analysis of the HIV-1 integrase-pyridoxal 5 '-phosphate complex reveals a new binding site for a nucleotide inhibitor SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID VIRUS TYPE-1 INTEGRASE; PHOTO-CROSS-LINKING; DNA-BINDING; CRYSTAL-STRUCTURE; CATALYTIC DOMAIN; TERMINAL DOMAINS; STRAND TRANSFER; ACTIVE-SITE; IN-VIVO; PROTEIN AB HIV-1 integrase (IN) is an important target for designing new antiviral therapies. Screening of potential inhibitors using recombinant IN-based assays has revealed a number of promising leads including nucleotide analogs such as pyridoxal 5'-phosphate (PLP). Certain PLP derivatives were shown to also exhibit antiviral activities in cell-based assays. To identify an inhibitory binding site of PLP to IN, we used the intrinsic chemical property of this compound to form a Schiff base with a primary amine in the protein at the nucleotide binding site. The amino acid affected was then revealed by mass spectrometric analysis of the proteolytic peptide fragments of IN. We found that an IC50 concentration (15 muM) of PLP modified a single IN residue, Lys(244), located in the C-terminal domain. In fact, we observed a correlation between interaction of PLP with Lys(244) and the compound's ability to impair formation of the IN(.)DNA complex. Site-directed mutagenesis studies confirmed an essential role of Lys(244) for catalytic activities of recombinant IN and viral replication. Molecular modeling revealed that Lys(244) together with several other DNA binding residues provides a plausible pocket for a nucleotide inhibitor-binding site. To our knowledge, this is the first report indicating that a small molecule inhibitor can impair IN activity through its binding to the protein C terminus. At the same time, our findings highlight the importance of structural analysis of the full-length protein. C1 Ohio State Univ, Coll Pharm, Hlth Sci Ctr, Ctr Retrovirus Res, Columbus, OH 43210 USA. Ohio State Univ, Coll Pharm, Hlth Sci Ctr, Ctr Comprehens Canc, Columbus, OH 43210 USA. NCI Frederick, Lab Med Chem, Ft Detrick, MD 21702 USA. NCI Frederick, HIV Drug Resistance Program, Ft Detrick, MD 21702 USA. Tbilisi State Univ, Dept Cell & Mol Biol, GE-0128 Tbilisi, Rep of Georgia. NIDDK, NIH, Bethesda, MD 20892 USA. RP Kvaratskhelia, M (reprint author), Ohio State Univ, Coll Pharm, Hlth Sci Ctr, Ctr Retrovirus Res, 500 W 12th Ave, Columbus, OH 43210 USA. EM kvaratskhelia.1@osu.edu RI Hess, Sonja/K-4842-2013; Nicklaus, Marc/N-4183-2014; OI Hess, Sonja/0000-0002-5904-9816; Nicklaus, Marc/0000-0002-4775-7030 NR 45 TC 20 Z9 20 U1 1 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 2005 VL 280 IS 9 BP 7949 EP 7955 DI 10.1074/jbc.M413579200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 902ZR UT WOS:000227395700064 PM 15615720 ER PT J AU Baranova, IN Vishnyakova, TG Bocharov, AV Kurlander, R Chen, ZG Kimelman, ML Remaley, AT Csako, G Thomas, F Eggerman, TL Patterson, AP AF Baranova, IN Vishnyakova, TG Bocharov, AV Kurlander, R Chen, ZG Kimelman, ML Remaley, AT Csako, G Thomas, F Eggerman, TL Patterson, AP TI Serum amyloid a binding to CLA-1 (CD36 and LIMPII analogous-1) mediates serum amyloid A protein-induced activation of ERK1/2 and p38 mitogen-activated protein kinases SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HIGH-DENSITY-LIPOPROTEIN; SCAVENGER RECEPTOR-BI; ACUTE-PHASE RESPONSE; CELLULAR CHOLESTEROL EFFLUX; CASSETTE TRANSPORTER A1; NITRIC-OXIDE SYNTHASE; SMOOTH-MUSCLE CELLS; SR-BI; ATHEROSCLEROTIC LESIONS; COUPLED RECEPTOR AB Serum amyloid A protein (SAA) is an acute-phase reactant, known to mediate pro-inflammatory cellular responses. This study reports that CLA-1 ( CD36 and LIMPII Analogous-1; human orthologue of the Scavenger Receptor Class B Type I (SR-BI)) mediates SAA uptake and downstream SAA signaling. Flow cytometry experiments revealed more than a 5-fold increase of Alexa-488 SAA uptake in HeLa cells stably transfected with CLA-1. Alexa 488-HDL uptake directly correlated with SAA uptake when determined in several CLA-1 stably transfected HeLa cell clones expressing various levels of CLA-1. SAA directly binds to CLA-1 as determined by cross-linking and colocalization of anti-CLA-1 antibody with SAA. SAA was co-internalized with transferrin to the endocytic recycling compartment pointing to a potential site of SAA metabolism. Alexa-488 SAA uptake in the CLA-1-overexpressing HeLa cells, as well as in THP-1 monocyte cell line, can be efficiently blocked by unlabeled SAA, high density lipoprotein, and other CLA-1 ligands. At the same time, markedly enhanced levels of phosphorylation of the mitogen-activated protein kinases (MAPKs), ERK1/2, and p38, were observed in cells stably transfected with CLA-1 cells following SAA stimulation when compared with mock transfected cells. The levels of the SAA-induced interleukin-8 (IL-8) secretion by CLA-1-overexpressing cells also significantly exceeded (5- to 10-fold) those detected for control cells. Synthetic amphipathic peptides possessing a structural alpha-helical motif inhibited SAA-induced activation of both MAPKs and IL-8 secretion in THP-1 cells. The results of this study demonstrate for the first time that CLA-1 functions as an endocytic SAA receptor and is involved in SAA-mediated cell signaling events associated with the immune-related and inflammatory effects of SAA. C1 NHLBI, Div Diabet Endocrinol & Metab Dis, NIH, Bethesda, MD 20892 USA. RP Patterson, AP (reprint author), Off Sci, Off Biotechnol Activ, NIH, 6705 Rockledge Dr,St 750, Rockville, MD 20892 USA. EM abocharov@mail.cc.nih.gov; pattersa@od.nih.gov NR 69 TC 102 Z9 107 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 2005 VL 280 IS 9 BP 8031 EP 8040 DI 10.1074/jbc.M405009200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 902ZR UT WOS:000227395700073 PM 15576377 ER PT J AU Braun, DC Garfield, SH Blumberg, PM AF Braun, DC Garfield, SH Blumberg, PM TI Analysis by fluorescence resonance energy transfer of the interaction between ligands and protein kinase C delta in the intact cell SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NONPROMOTING 12-DEOXYPHORBOL 13-ESTERS; PHORBOL 12-MYRISTATE 13-ACETATE; CD-1 MOUSE SKIN; DOWN-REGULATION; BRYOSTATIN 1; GLUTAMINE-SYNTHETASE; LIVING CELLS; GLIAL-CELLS; IN-VIVO; PHOSPHORYLATION AB The role of the protein kinase C (PKC) family of serine/threonine kinases in cellular differentiation, proliferation, apoptosis, and other responses makes them attractive therapeutic targets. The activation of PKCs by ligands in vivo varies depending upon cell type; therefore, methods are needed to screen the potency of PKCs in this context. Here we describe a genetically encoded chimera of native PKCdelta fused to yellow- and cyan-shifted green fluorescent protein, which can be expressed in mammalian cells. This chimeric protein kinase, CY-PKCdelta, retains native or near-native activity in the several biological and biochemical parameters that we tested. Binding assays showed that CY-PKCdelta and native human PKCdelta have similar binding affinity for phorbol 12,13-dibutyrate. Analysis of translocation by Western blotting and confocal microscopy showed that CY-PKCdelta, translocates from the cytosol to the membrane upon treatment with ligand, that the translocation has similar dose dependence as that of endogenous PKCdelta, and that the pattern of translocation is indistinguishable from that of the green fluorescent protein-PKCdelta fusion well characterized from earlier studies. Treatment with phorbol ester of cells expressing CY-PKCdelta resulted in a dose-dependent increase in FRET that could be visualized in situ by confocal microscopy or measured fluorometrically. By using this construct, we were able to measure the kinetics and potencies of 12 known PKC ligands, with respect to CY-PKCdelta, in the intact cell. The CY-PKCdelta chimera and the in vivo assays described here therefore show potential for high throughput screening of prospective PKCdelta ligands within the context of cell type. C1 NCI, NIH, Lab Expt Carcinogenesis, Bethesda, MD 20892 USA. Gallaudet Univ, Dept Biol, Washington, DC 20002 USA. Cellular Carcinogenesis & Tumor Promot Lab, Washington, DC 20002 USA. RP Blumberg, PM (reprint author), NCI, NIH, Lab Expt Carcinogenesis, Bldg 37,Rm 4048,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA. EM blumberp@dc37a.nci.nih.gov NR 41 TC 26 Z9 29 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 2005 VL 280 IS 9 BP 8164 EP 8171 DI 10.1074/jbc.M413896200 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 902ZR UT WOS:000227395700089 PM 15611119 ER PT J AU Li, J O'Connor, KL Greeley, GH Blackshear, PJ Townsend, CM Evers, BM AF Li, J O'Connor, KL Greeley, GH Blackshear, PJ Townsend, CM Evers, BM TI Myristoylated alanine-rich C kinase substrate-mediated neurotensin release via protein kinase C-delta downstream of the Rho/ROK pathway SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INDUCED INSULIN-SECRETION; HUMAN NEURONAL CELLS; BOVINE LUTEAL CELLS; MARCKS PROTEIN; PHORBOL ESTERS; PKC-ALPHA; GASTROINTESTINAL HORMONES; ACTIN CYTOSKELETON; SEROTONIN RELEASE; CHROMAFFIN CELLS AB Myristoylated alanine- rich protein kinase C substrate (MARCKS) is a cellular substrate for protein kinase C (PKC). Recently, we have shown that PKC isoforms- alpha and - delta, as well as the Rho/ Rho kinase ( ROK) pathway, play a role in phorbol 12- myristate 13- acetate (PMA)mediated secretion of the gut peptide neurotensin (NT) in the BON human endocrine cell line. Here, we demonstrate that activation of MARCKS protein is important for PMA- and bombesin (BBS)- mediated NT secretion in BON cells. Small interfering RNA (siRNA) to MARCKS significantly inhibited, whereas overexpression of wildtype MARCKS significantly increased PMA- mediated NT secretion. Endogenous MARCKS and green fluorescent protein- tagged wild- type MARCKS were translocated from membrane to cytosol upon PMA treatment, further confirming MARCKS activation. MARCKS phosphorylation was inhibited by PKC- delta siRNA, ROK alpha siRNA, and C3 toxin (a Rho protein inhibitor), suggesting that the PKC- delta and the Rho/ ROK pathways are necessary for MARCKS activation. The phosphorylation of PKC- delta was inhibited by C3 toxin, demonstrating that the role of MARCKS in NT secretion was regulated by PKC- delta downstream of the Rho/ ROK pathway. BON cell clones stably transfected with the receptor for gastrin releasing peptide, a physiologic stimulant of NT, and treated with BBS, the amphibian equivalent of gastrin releasing peptide, demonstrated a similar MARCKS phosphorylation as noted with PMA. BBS- mediated NT secretion was attenuated by MARCKS siRNA. Collectively, these findings provide evidence for novel signaling pathways, including the sequential regulation of MARCKS activity by Rho/ ROK and PKC- delta proteins, in stimulated gut peptide secretion. C1 Univ Texas, Med Branch, Dept Surg, Galveston, TX 77555 USA. Univ Texas, Med Branch, Sealy Ctr Canc Cell Biol, Galveston, TX 77555 USA. NIEHS, Off Clin Res, Res Triangle Pk, NC 27709 USA. NIEHS, Neurobiol Lab, Res Triangle Pk, NC 27709 USA. RP Evers, BM (reprint author), Univ Texas, Med Branch, Dept Surg, 301 Univ Blvd, Galveston, TX 77555 USA. EM mevers@utmb.edu RI Li, Jing/B-7206-2011; O'Connor, Kathleen/H-2569-2013 FU NCI NIH HHS [R21 CA10212]; NIA NIH HHS [2R37 AG10885]; NIDDK NIH HHS [R01 DK48489, P01 DK35608] NR 63 TC 27 Z9 27 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 2005 VL 280 IS 9 BP 8351 EP 8357 DI 10.1074/jbc.M409431200 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 902ZR UT WOS:000227395700110 PM 15623535 ER PT J AU Ray, S Gao, C Wyatt, K Fariss, RN Bundek, A Zelenka, P Wistow, G AF Ray, S Gao, C Wyatt, K Fariss, RN Bundek, A Zelenka, P Wistow, G TI Platelet-derived growth factor D, tissue-specific expression in the eye, and a key role in control of lens epithelial cell proliferation SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEASE-ACTIVATED LIGAND; PDGF-BETA-RECEPTOR; DIFFERENTIATION; ALPHA; ORIENTATION; NEIBANK; PROJECT; BIOLOGY AB Platelet-derived growth factor D (PDGF-D), also known as Iris-expressed growth factor, is a member of the PDGF/vascular endothelial growth factor family. The expression of PDGF-D in the eye is tissue-specific. In the anterior segment, it is localized to iris and ciliary body, whereas in the retina, PDGF-D is restricted to the outer plexiform layer. PDGF-D is present in aqueous humor but is not detectable in mature lens or in mouse lens-derived alphaTN4-1 cells. However, it is expressed in rabbit lens-derived N/N1003A cells. N/N1003A cell-conditioned medium stimulates proliferation in rat lens explants, and this is blocked by immunodepletion of PDGF-D. Immunopurified PDGF-D also stimulates cell proliferation in rat lens explants and in NIH 3T3 cells. In organ culture of rat eye anterior segments, anti-PDGF-D strongly inhibits lens epithelial cell proliferation. This finding suggests a major in vivo role for PDGF-D in the mechanisms of coordinated growth of eye tissues. Intervention in the PDGF-D pathway in the eye, perhaps by antibody or blocking peptide, could be useful in the treatment of certain cataracts, including post-operative secondary cataract. C1 NEI, NIH, Sect Mol Struct & Funct Genom, Bethesda, MD 20892 USA. RP Wistow, G (reprint author), NEI, NIH, Sect Mol Struct & Funct Genom, Bldg 7,Rm 201, Bethesda, MD 20892 USA. EM graeme@helix.nih.gov NR 42 TC 22 Z9 26 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 2005 VL 280 IS 9 BP 8494 EP 8502 DI 10.1074/jbc.M413570200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 902ZR UT WOS:000227395700126 PM 15611105 ER PT J AU Krishnegowda, G Hajjar, AM Zhu, JZ Douglass, EJ Uematsu, S Akira, S Woods, AS Gowda, DC AF Krishnegowda, G Hajjar, AM Zhu, JZ Douglass, EJ Uematsu, S Akira, S Woods, AS Gowda, DC TI Induction of proinflammatory responses in macrophages by the Glycosylphosphatidylinositols of Plasmodium falciparum - Cell signaling receptors, glycosylphosphatidylinositol (GPI) structural requirement, and regulation of GPI activity SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TOLL-LIKE RECEPTORS; VASCULAR ENDOTHELIAL-CELLS; PROTEIN-KINASE-C; PARASITIC PROTOZOA; TRYPANOSOMA-CRUZI; NITRIC-OXIDE; ERYTHROCYTIC STAGES; CEREBRAL MALARIA; PHOSPHOLIPASE-D; ANCHORS AB The glycosylphosphatidylinositol (GPI) anchors of Plasmodium falciparum have been proposed to be the major factors that contribute to malaria pathogenesis through their ability to induce proinflammatory responses. In this study we identified the receptors for P. falciparum GPI-induced cell signaling that leads to proinflammatory responses and studied the GPI structure-activity relationship. The data show that GPI signaling is mediated mainly through recognition by TLR2 and to a lesser extent by TLR4. The activity of sn-2-lyso-GPIs is comparable with that of the intact GPIs, whereas the activity of Man(3)-GPIs is about 80% that of the intact GPIs. The GPIs with three ( intact GPIs and Man3-GPIs) and two fatty acids (sn-2-lyso-GPIs) appear to differ considerably in the requirement of the auxiliary receptor, TLR1 or TLR6, for recognition by TLR2. The former are preferentially recognized by TLR2/TLR1, whereas the latter are favored by TLR2/TLR6. However, the signaling pathways initiated by all three GPI types are similar, involving the MyD88-dependent activation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 and NF-kappaB-signaling pathways. The signaling molecules of these pathways differentially contribute to the production of various cytokines and nitric oxide (Zhu, J., Krishnegowda, G., and Gowda, D. C. ( 2004) J. Biol. Chem. 280, 8617-8627). Our data also show that GPIs are degraded by the macrophage surface phospholipases predominantly into inactive species, indicating that the host can regulate GPI activity at least in part by this mechanism. These results imply that macrophage surface phospholipases play important roles in the GPI-induced innate immune responses and malaria pathogenesis. C1 Univ Washington, Dept Immunol, Seattle, WA 98195 USA. Penn State Univ, Coll Med, Dept Biochem & Mol Biol, Hershey, PA 17033 USA. Osaka Univ, Dept Host Def, Res Inst Microbial Dis, Osaka 5650871, Japan. NIDA, NIH, Baltimore, MD 21224 USA. RP Hajjar, AM (reprint author), Univ Washington, Dept Immunol, Box 357650, Seattle, WA 98195 USA. EM hajjar@u.washington.edu; gowda@psu.edu RI Akira, Shizuo/C-3134-2009; OI GOWDA, KRISHNE/0000-0002-6042-0520 FU NHLBI NIH HHS [HL69503, R01 HL069503]; NIAID NIH HHS [AI41139, R01 AI041139] NR 63 TC 295 Z9 306 U1 4 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 4 PY 2005 VL 280 IS 9 BP 8606 EP 8616 DI 10.1074/jbc.M413541200 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 902ZR UT WOS:000227395700137 PM 15623512 ER PT J AU Schubot, FD Jackson, MW Penrose, KJ Cherry, S Tropea, JE Plano, GV Waugh, DS AF Schubot, FD Jackson, MW Penrose, KJ Cherry, S Tropea, JE Plano, GV Waugh, DS TI Three-dimensional structure of a macromolecular assembly that regulates type III secretion in yersinia pestis SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE type III secretion; Tye A; YopN; SycN; YscB ID MESSENGER-RNA SIGNAL; EUKARYOTIC CELLS; SHIGELLA-FLEXNERI; YOP PROTEINS; CHAPERONE; ENTEROCOLITICA; TYEA; COMPLEX; SYCN; PSEUDOTUBERCULOSIS AB Yersinia pestis, the causative agent of plague, utilizes a type III secretion system (T3SS) to inject effector proteins directly into the cytosol of mammalian cells where they interfere with signal transduction pathways that regulate actin cytoskeleton dynamics and inflammation, thereby enabling the bacterium to avoid engulfment and destruction by macrophages. Type III secretion normally does not occur in the absence of close contact with eukaryotic cells. Negative regulation is mediated in part by a multiprotein complex that has been proposed to act as a physical impediment to type III secretion by blocking the entrance to the secretion apparatus prior to contact with mammalian cells. This complex is composed of YopN, its heterodimeric secretion chaperone SycN-YscB, and TyeA. Here, we report two crystal structures of YopN in complex with its heterodimeric secretion chaperone SycN-YscB and the co-regulatory protein TyeA, respectively. By merging these two overlapping structures, it was possible to construct a credible theoretical model of the YopN-SycN-YscB-TyeA complex. The modeled assembly features the secretion signaling elements of YopN at one end of an elongated structure and the secretion regulating TyeA binding site at the other. A patch of highly conserved residues on the surface of the C-terminal alpha-helix of TyeA may mediate its interaction with structural components of the secretion apparatus. Conserved arginine residues that reside inside a prominent cavity at the dimer interface of SycN-YscB were mutated in order to investigate whether they play a role in targeting the YopN-chaperone complex to the type III secretion apparatus. One of the mutants exhibited a phenotype that is consistent with this hypothesis. Published by Elsevier Ltd. C1 NCI, Frederick Canc Res & Dev Ctr, Canc Res Ctr, Macromol Crystallog Lab, Frederick, MD 21702 USA. Univ Miami, Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA. RP Waugh, DS (reprint author), NCI, Frederick Canc Res & Dev Ctr, Canc Res Ctr, Macromol Crystallog Lab, POB B, Frederick, MD 21702 USA. EM waughd@ncifcrf.gov NR 55 TC 77 Z9 79 U1 2 U2 6 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD MAR 4 PY 2005 VL 346 IS 4 BP 1147 EP 1161 DI 10.1016/j.jmb.2004.12.036 PG 15 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 900AM UT WOS:000227187800016 PM 15701523 ER PT J AU Adams, S Robbins, FM Chen, D Wagage, D Holbeck, SL Morse, HC Stroncek, D Marincola, FM AF Adams, S Robbins, FM Chen, D Wagage, D Holbeck, SL Morse, HC Stroncek, D Marincola, FM TI HLA class I and II genotype of the NCI-60 cell lines SO JOURNAL OF TRANSLATIONAL MEDICINE LA English DT Article ID ANTICANCER DRUG SCREEN; NATIONAL-CANCER-INSTITUTE; GENE-EXPRESSION; MOLECULAR PHARMACOLOGY; DOWN-REGULATION; MELANOMA-CELLS; IMMUNOTHERAPY; ANTIGENS; IMMUNODOMINANCE; IDENTIFICATION AB Sixty cancer cell lines have been extensively characterized and used by the National Cancer Institute's Developmental Therapeutics Program (NCI-60) since the early 90's as screening tools for anti-cancer drug development. An extensive database has been accumulated that could be used to select individual cells lines for specific experimental designs based on their global genetic and biological profile. However, information on the human leukocyte antigen (HLA) genotype of these cell lines is scant and mostly antiquated since it was derived from serological typing. We, therefore, re-typed the NCI-60 panel of cell lines by high-resolution sequence-based typing. This information may be used to: 1) identify and verify the identity of the same cell lines at various institutions; 2) check for possible contaminant cell lines in culture; 3) adopt individual cell lines for experiments in which knowledge of HLA molecule expression is relevant. Since genome-based typing does not guarantee actual surface protein expression, further characterization of relevant cell lines should be entertained to verify surface expression in experiments requiring correct antigen presentation. C1 NIH, Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA. NCI, Dev Therapeut Program, Informat Technol Branch, Bethesda, MD 20892 USA. NIAID, Immunopathol Lab, Rockville, MD USA. RP Marincola, FM (reprint author), NIH, Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA. EM sadams1@mail.cc.nih.gov; FRobbins@mail.cc.nih.gov; dschen@mail.cc.nih.gov; DWagage@mail.cc.nih.gov; holbecks@mail.nih.gov; hmorse@niaid.nih.gov; DStroncek@mail.cc.nih.gov; fmarincola@mail.cc.nih.gov OI Morse, Herbert/0000-0002-9331-3705 NR 46 TC 1 Z9 1 U1 2 U2 2 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1479-5876 J9 J TRANSL MED JI J. Transl. Med. PD MAR 4 PY 2005 VL 3 DI 10.1186/1479-5876-3-11 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 968JX UT WOS:000232159900001 ER PT J AU Bustin, M Catez, F Lim, JH AF Bustin, M Catez, F Lim, JH TI The dynamics of histone H1 function in chromatin SO MOLECULAR CELL LA English DT Review ID LINKER-HISTONE; IN-VIVO; GENE-EXPRESSION; TRANSCRIPTION; PROTEINS; BINDING; CELLS AB Over 80% of the nucleosomes in chromatin contain histone H1, a protein family known to affect the structure and activity of chromatin. Genetic studies and in vivo imaging experiments are changing the traditional view of H1 function and mechanism of action. H1 variants are partially redundant, mobile molecules that interact with nucleosomes as members of a dynamic protein network and serve as fine tuners of chromatin function. C1 NCI, NIH, Prot Sect, Lab Metab, Bethesda, MD 20892 USA. RP Bustin, M (reprint author), NCI, NIH, Prot Sect, Lab Metab, Bethesda, MD 20892 USA. EM bustin@helix.nih.gov RI Bustin, Michael/G-6155-2015 NR 20 TC 156 Z9 161 U1 2 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1097-2765 J9 MOL CELL JI Mol. Cell PD MAR 4 PY 2005 VL 17 IS 5 BP 617 EP 620 DI 10.1016/j.molcel.2005.02.019 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 903TZ UT WOS:000227449800002 PM 15749012 ER PT J AU Su, H Bidere, N Zheng, LX Cubre, A Sakai, K Dale, J Salmena, L Hakem, R Straus, S Lenardo, M AF Su, H Bidere, N Zheng, LX Cubre, A Sakai, K Dale, J Salmena, L Hakem, R Straus, S Lenardo, M TI Requirement for caspase-8 in NF-kappa B activation by antigen receptor SO SCIENCE LA English DT Article ID T-CELL PROLIFERATION; LYMPHOCYTES; MALT1; BCL10; PATHWAY; THETA AB Caspase-8, a proapoptotic protease, has an essential role in lymphocyte activation and protective immunity. We show that caspase-8 deficiency (CED) in humans and mice specifically abolishes activation of the transcription factor nuclear factor kappaB (NF-kappaB) after stimulation through antigen receptors, Fc receptors, or Toll-like receptor 4 in T, B, and natural killer cells. Caspase-8 also causes the up complex of the inhibitor of NF-kappaB kinase (IKK) to associate with the upstream Bcl10-MALT1 (mucosa-associated lymphatic tissue) adapter complex. Recruitment of the IKKalpha,beta complex, its activation, and the nuclear translocation of NF-kappaB require enzyme activity of full-length caspase-8. These findings thus explain the paradoxical association of defective apoptosis and combined immunodeficiency in human CED. C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA. Univ Toronto, Ontario Canc Inst, Toronto, ON M5G 2C1, Canada. RP Lenardo, M (reprint author), NIAID, Immunol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA. EM lenardo@nih.gov RI sakai, Keiko/F-5807-2013; Su, Helen/H-9541-2015; bidere, nicolas/K-8887-2015 OI Su, Helen/0000-0002-5582-9110; bidere, nicolas/0000-0001-9177-0008 NR 21 TC 277 Z9 294 U1 0 U2 9 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD MAR 4 PY 2005 VL 307 IS 5714 BP 1465 EP 1468 DI 10.1126/science.1104765 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 904MT UT WOS:000227503100047 PM 15746428 ER PT J AU Stanley, RJ Hou, ZJ Yang, AP Hawkins, ME AF Stanley, RJ Hou, ZJ Yang, AP Hawkins, ME TI The two-photon excitation cross section of 6MAP, a fluorescent adenine analogue SO JOURNAL OF PHYSICAL CHEMISTRY B LA English DT Article ID ULTRAFAST INTERNAL-CONVERSION; BASE; 2-AMINOPURINE; NUCLEOTIDES; NUCLEOSIDES; DYNAMICS; PULSES AB 6MAP is a fluorescent analogue of adenine that undergoes Watson-Crick base pairing and base stacking in double-stranded DNA. The one-photon absorption spectrum of 6MAP is characterized by a maximum around 330 nm with moderate quantum yield fluorescence centered at about 420 nm. To take advantage of this probe for confocal and single-molecule microscopy, it would be advantageous to be able to excite the analogue via two photons. We report the first determination of the two-photon excitation cross section and spectrum for 6MAP from 614 to 700 nm. The power dependence of the fluorescence indicates that emission results from the absorption of two photons. The one-photon and two-photon emission line shapes are identical within experimental error. A study of the concentration dependence of the fluorescence yield for one-photon excitation shows no measurable quenching up to about 5 muM. The maximum in the two-photon excitation spectrum gives a two-photon cross section, delta(TPE), of 3.4 +/- 0.1 Goeppert-Mayer (G.M.) at 659 nm, which correlates well with the one-photon absorption maximum. This compares quite favorably with cross sections of various naturally fluorescent biological molecules such as flavins and nicotiamide. In addition, we have also obtained the two-photon-induced fluorescence emission spectrum of quinine sulfate. It is approximately the same as that for one-photon excitation, suggesting that two-photon excitation of quinine sulfate may be used for calibration purposes. C1 Temple Univ, Dept Chem, Philadelphia, PA 19122 USA. NCI, CRC, Bethesda, MD 20892 USA. RP Stanley, RJ (reprint author), Temple Univ, Dept Chem, 201 Beury Hall, Philadelphia, PA 19122 USA. EM robert.stanley@temple.edu NR 22 TC 12 Z9 12 U1 2 U2 10 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1520-6106 J9 J PHYS CHEM B JI J. Phys. Chem. B PD MAR 3 PY 2005 VL 109 IS 8 BP 3690 EP 3695 DI 10.1021/jp0455982 PG 6 WC Chemistry, Physical SC Chemistry GA 900XH UT WOS:000227247100084 PM 16851408 ER PT J AU Kalivas, PW Volkow, N Seamans, J AF Kalivas, PW Volkow, N Seamans, J TI Unmanageable motivation in addiction: A pathology in prefrontal-accumbens glutamate transmission SO NEURON LA English DT Review ID COCAINE-INDUCED REINSTATEMENT; NUCLEUS-ACCUMBENS; SEEKING BEHAVIOR/; DRUG-SEEKING; CORTEX; RECEPTORS; DOPAMINE; ACTIVATION; PLASTICITY; RELEASE C1 Med Univ S Carolina, Dept Neurosci, Charleston, SC 29465 USA. NIDA, Bethesda, MD 20892 USA. RP Kalivas, PW (reprint author), Med Univ S Carolina, Dept Neurosci, Charleston, SC 29465 USA. EM kalivasp@musc.edu NR 23 TC 349 Z9 359 U1 3 U2 27 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0896-6273 J9 NEURON JI Neuron PD MAR 3 PY 2005 VL 45 IS 5 BP 647 EP 650 DI 10.1016/j.neurons.2005.02.005 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 903SU UT WOS:000227446700004 PM 15748840 ER PT J AU Horstmann, E McCabe, MS Grochow, L Yamamoto, S Rubinstein, L Budd, T Shoemaker, D Emanuel, EJ Grady, C AF Horstmann, E McCabe, MS Grochow, L Yamamoto, S Rubinstein, L Budd, T Shoemaker, D Emanuel, EJ Grady, C TI Risks and benefits of phase 1 oncology trials, 1991 through 2002 SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID NATIONAL-CANCER-INSTITUTE; I CLINICAL-TRIALS; THERAPEUTIC RESPONSE; PROGNOSTIC-FACTORS; ANTICANCER AGENTS; DRUG DEVELOPMENT; ETHICS; DESIGN; SURVIVAL; RATES AB BACKGROUND Previous reviews of phase 1 oncology trials reported a rate of response to treatment of 4 to 6 percent and a toxicity-related death rate of 0.5 percent. These results may not reflect the rates in current phase 1 oncology trials. METHODS We reviewed all nonpediatric phase 1 oncology trials sponsored by the Cancer Therapy Evaluation Program at the National Cancer Institute between 1991 and 2002. We report the rates of response to treatment, of stable disease, of grade 4 toxic events, and of treatment-related deaths. RESULTS We analyzed 460 trials involving 11,935 participants, all of whom were assessed for toxicity and 10,402 of whom were assessed for a response to therapy. The overall response rate (i.e., for both complete and partial responses) was 10.6 percent, with considerable variation among trials. ``Classic'' phase 1 trials of single investigational chemotherapeutic agents represented only 20 percent of the trials and had a response rate of 4.4 percent. Studies that included at least one anticancer agent approved by the Food and Drug Administration constituted 46.3 percent of the trials and had a response rate of 17.8. An additional 34.1 percent of participants had stable disease or a less-than-partial response. The overall rate of death due to toxic events was 0.49 percent. Of 3465 participants for whom data on patient-specific grade 4 toxic events were available, 14.3 percent had had at least one episode of grade 4 toxic events. CONCLUSIONS Overall response rates among phase 1 oncology trials are higher than previously reported, although they have not changed for classic phase 1 trials, and toxicity-related death rates have remained stable. Rates of response and toxicity vary, however, among the various types of phase 1 oncology trials. C1 NIH, Dept Clin Bioeth, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA. NCI, Canc Therapy Evaluat Program, NIH, Rockville, MD USA. Natl Canc Ctr, Res Ctr Canc Prevent & Screening, Tokyo 104, Japan. RP Grady, C (reprint author), NIH, Dept Clin Bioeth, Warren G Magnuson Clin Ctr, Bldg 10,Rm 1C118, Bethesda, MD 20892 USA. EM cgrady@nih.gov NR 31 TC 245 Z9 248 U1 2 U2 13 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 3 PY 2005 VL 352 IS 9 BP 895 EP 904 DI 10.1056/NEJMsa042220 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA 901VQ UT WOS:000227310700008 PM 15745980 ER PT J AU Pfeffer, MA Domanski, MJ Braunwald, E AF Pfeffer, MA Domanski, MJ Braunwald, E TI ACE inhibition in stable coronary artery disease - The authors reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID LEFT-VENTRICULAR DYSFUNCTION C1 Brigham & Womens Hosp, Boston, MA 02115 USA. NHLBI, Bethesda, MD 20824 USA. RP Pfeffer, MA (reprint author), Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 3 PY 2005 VL 352 IS 9 BP 938 EP 939 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 901VQ UT WOS:000227310700024 ER PT J AU Sengupta, S Shimamoto, A Koshiji, M Pedeux, R Rusin, M Spillare, EA Shen, JC Huang, LE Lindor, NM Furuichi, Y Harris, CC AF Sengupta, S Shimamoto, A Koshiji, M Pedeux, R Rusin, M Spillare, EA Shen, JC Huang, LE Lindor, NM Furuichi, Y Harris, CC TI Tumor suppressor p53 represses transcription of RECQ4 helicase SO ONCOGENE LA English DT Article DE repression; histone deacetylases; trichostatin A; Rothmund-Thomson syndrome; SP1; promoter ID ROTHMUND-THOMSON-SYNDROME; WILD-TYPE P53; TATA-BINDING PROTEIN; CELL-CYCLE; FUNCTIONAL INTERACTION; HISTONE DEACETYLASE; REPLICATION FORKS; FAMILY HELICASES; GENE-EXPRESSION; BREAST-CANCER AB RECQ4 is a member of the RecQ helicase family, which has been implicated in the regulation of DNAreplication, recombination and repair. p53 modulates the functions of RecQ helicases including BLM and WRN. In this study, we demonstrate that p53 can regulate the transcription of RECQ4. Using nontransformed, immortalized normal human fibroblasts, we show that p53-dependent downregulation of RECQ4 expression occurred in G1-arrested cells, both in the absence or presence of exogenous DNA damage. Wild-type p53 ( but not the tumor-derived mutant forms) repressed RECQ4 promoter activity. The camptothecin or etoposide-dependent p53-mediated repression was attenuated by trichostatin A (TSA), an inhibitor of histone deacetylases (HDACs). Repression of the RECQ4 promoter was accompanied with an increased accumulation of HDAC1, and the loss of SP1 and p53 binding to the promoter. The simultaneous formation of a camptothecin-dependent p53-SP1 complex indicated its occurrence outside of the RECQ4 promoter. These data suggest that p53-mediated repression of RECQ4 transcription during DNA damage results from the modulation of the promoter occupancy of transcription activators and repressors. C1 NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA. Gene Care Res Inst, Kamakura, Kanagawa, Japan. Mayo Clin, Dept Med Genet, Rochester, MN 55905 USA. Marie Sklodowska Curie Mem Inst, Ctr Oncol, Dept Tumor Biol, PL-44101 Gliwice, Poland. 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 OI Sengupta, Sagar/0000-0002-6365-1770 NR 66 TC 51 Z9 53 U1 0 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR 3 PY 2005 VL 24 IS 10 BP 1738 EP 1748 DI 10.1038/sj.onc.1208380 PG 11 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA 902HI UT WOS:000227345100010 PM 15674334 ER PT J AU Weinstein, SJ Wright, ME Pietinen, P King, F Tan, C Taylor, PR Virtamo, J Albanes, D AF Weinstein, SJ Wright, ME Pietinen, P King, F Tan, C Taylor, PR Virtamo, J Albanes, D TI Serum alpha-tocopherol and gamma-tocopherol in relation to prostate cancer risk in a prospective study SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID VITAMIN-E; BETA-CAROTENE; FOLLOW-UP; ASSOCIATION; RETINOL; MICRONUTRIENTS; MEN; SUPPLEMENTATION; PREVENTION; MORTALITY AB The Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study demonstrated a 32% reduction in prostate cancer incidence in response to daily alpha-tocopherol supplementation. We examined baseline serum concentrations of alpha-tocopherol and gamma-tocopherol to compare their respective associations with prostate cancer risk. From the ATBC study cohort of 29 133 Finnish men, 50-69 years old, we randomly selected 100 incident prostate cancer case patients and matched 200 control subjects. Odds ratios and 95% confidence intervals (CIs) were estimated for the serum tocopherols (measured by high-performance liquid chromatography) using logistic regression models. All P values were two-sided. Odds ratios for the highest versus the lowest tertiles were 0.49 (95% CI = 0.24 to 1.01, P-trend =.05) for alpha-tocopherol and 0.57 (95% CI = 0.31 to 1.06, P-trend =.08) for gamma-tocopherol. Further analyses indicated that the association of high serum tocopherols with low prostate cancer risk was stronger in the alpha-tocopherol-supplemented group than in those not receiving alpha-tocopherol. Participants with higher circulating concentrations of the major vitamin E fractions, alpha-tocopherol and gamma-tocopherol, had similarly lower prostate cancer risk. C1 NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA. NCI, Ctr Canc Res, NIH, DHHS, Bethesda, MD 20892 USA. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Informat Management Serv Inc, Silver Spring, MD USA. RP Albanes, D (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, EPS-3044,9000 Rockville Pike, Bethesda, MD 20892 USA. EM daa@nih.gov RI Albanes, Demetrius/B-9749-2015 FU CCR NIH HHS [N01-RC-37004, N01-RC-45035]; NCI NIH HHS [N01-CN-45165] NR 27 TC 61 Z9 63 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 2 PY 2005 VL 97 IS 5 BP 396 EP 399 DI 10.1093/jnci/dji045 PG 4 WC Oncology SC Oncology GA 902JY UT WOS:000227352800015 PM 15741576 ER PT J AU Taplin, S Ulcikas-Yood, M Geiger, A Ichikawa, L Bischoff, K Barlow, W AF Taplin, S Ulcikas-Yood, M Geiger, A Ichikawa, L Bischoff, K Barlow, W TI Re: Reason for late-stage breast cancer: Absence of screening or detection, or breakdown in follow-up? Response SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter ID PROGRAM C1 NCI, Div Canc Control & Populat Sci, Appl Res Program, Rockville, MD 20852 USA. Henry Ford Hlth Syst, Detroit, MI USA. Kaiser Permanente So Calif, Pasadena, CA USA. Grp Hlth Cooperat Puget Sound, Seattle, WA USA. Kaiser Permanente Colorado, Denver, CO USA. RP Taplin, S (reprint author), NCI, Div Canc Control & Populat Sci, Appl Res Program, 6130 Execut Blvd,MSC 7344,EPN 4005, Rockville, MD 20852 USA. EM taplins@mail.nih.gov NR 7 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 2 PY 2005 VL 97 IS 5 BP 400 EP 401 DI 10.1093/jnci/dji063 PG 2 WC Oncology SC Oncology GA 902JY UT WOS:000227352800017 ER PT J AU Purdue, MP AF Purdue, MP TI Re: Determinants of BRAF mutations in primary melanomas SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Letter C1 NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Purdue, MP (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,MSC 7240,Execut Plaza S 8121, Bethesda, MD 20892 USA. EM purduem@mail.nih.gov RI Purdue, Mark/C-9228-2016 OI Purdue, Mark/0000-0003-1177-3108 NR 3 TC 1 Z9 1 U1 0 U2 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAR 2 PY 2005 VL 97 IS 5 BP 401 EP 402 DI 10.1093/jnci/dji074 PG 2 WC Oncology SC Oncology GA 902JY UT WOS:000227352800018 PM 15741578 ER PT J AU Jeang, KT AF Jeang, KT TI Retrovirology highlights a quarter century of HTLV-1 research SO RETROVIROLOGY LA English DT Editorial Material ID SARCOMA AB In 1977, Takatsuki and co-workers described in Japan a human malignant disease termed adult T-cell leukemia (ATL). Three years later, in 1980, Gallo and colleagues reported the identification of the first human retrovirus, human T-cell leukemia virus type I (HTLV-I), in a patient with cutaneous T-cell lymphoma. This month, Retrovirology commemorates these two land mark findings by publishing separate personal recollections by Takatsuki and Gallo respectively on the discovery of ATL and HTLV. C1 NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA. RP Jeang, KT (reprint author), NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA. EM kj7e@nih.gov RI Jeang, Kuan-Teh/A-2424-2008 NR 7 TC 2 Z9 2 U1 0 U2 0 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1742-4690 J9 RETROVIROLOGY JI Retrovirology PD MAR 2 PY 2005 VL 2 AR 15 DI 10.1186/1742-4690-2-15 PG 3 WC Virology SC Virology GA 032RD UT WOS:000236791200002 PM 15743525 ER PT J AU Chang, S Hursting, SD Perkins, SN Dores, GM Weed, DL AF Chang, S Hursting, SD Perkins, SN Dores, GM Weed, DL TI Adapting postdoctoral training to interdisciplinary science in the 21st century: The Cancer Prevention Fellowship Program at the National Cancer Institute SO ACADEMIC MEDICINE LA English DT Article AB Preparing junior scientists for careers in the health sciences has become an immense challenge for many reasons, including the emerging demand for multidisciplinary approaches to solving problems in the health Sciences. For those choosing careers in hybrid and interdisciplinary fields, the "traditional" postdoctoral training model may not perform well, particularly in light of other problems that plague postdoctoral success. New approaches are required. Using the interdisciplinary field of cancer prevention as an example, the authors describe the Cancer Prevention Fellowship Program (CPFP) of the National Cancer Institute, a three-year postdoctoral program of which the goal is to provide its fellows with a strong foundation in cancer prevention through education, mentored research, and structured professional development training activities that emphasize multidisciplinary approaches and leadership skills. Over time the CPFP has incorporated the best aspects of the traditional postdoctoral training model with newer training approaches in an effort to overcome existing problems in postdoctoral training and to address the additional complexities inherent in training those who seek careers in interdisciplinary science. Many aspects of the CPFP, including an efficient infrastructure, a dedicated staff, a capacity to provide educational activities, and the provision of rich research opportunities, may translate well to other postdoctoral programs that face similar issues. C1 NCI, Off Prevent Oncol, Div Canc Prevent, NIH,DHHS,Program Evaluat & Career Dev, Bethesda, MD 20892 USA. RP Chang, S (reprint author), NCI, Off Prevent Oncol, Div Canc Prevent, NIH,DHHS,Program Evaluat & Career Dev, 6120 Execut Blvd,Suite T-41 MSC 7361, Bethesda, MD 20892 USA. EM ChangSh@mail.nih.gov NR 20 TC 13 Z9 13 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1040-2446 J9 ACAD MED JI Acad. Med. PD MAR PY 2005 VL 80 IS 3 BP 261 EP 265 DI 10.1097/00001888-200503000-00011 PG 5 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA 902MV UT WOS:000227362100010 PM 15734808 ER PT J AU Kaptchuk, TJ Miller, FG AF Kaptchuk, TJ Miller, FG TI What is the best and most ethical model for the relationship between mainstream and alternative medicine: Opposition, integration, or pluralism? SO ACADEMIC MEDICINE LA English DT Article ID UNITED-STATES; COMPLEMENTARY; THERAPY; PLACEBO; MOVEMENT; TRIALS; AMA AB Despite radical improvements in medicine over the past 60 years, patients maintain multiple health care pathways that include high utilization of unconventional treatments. The authors examine three possible relationships between mainstream and alternative medicine: opposition, integration, and pluralism. Opposition, the traditional ethical position that the medical profession must eradicate unconventional medicine for the good of the patient, has withered away. Integration of mainstream and alternative medicine is increasingly advocated in tandem with hospital-based programs that amalgamate the use of conventional and alternative therapies. While advocates of integrative medicine often speak of "evidence-based" complementary and alternative medicine (CAM), integration fosters double standards for validating conventional and unconventional treatments. integration also ignores unbridgeable epistemological beliefs and practices between mainstream and alternative medicine. Pluralism, which has been relatively ignored, calls for cooperation between the different medical systems rather than their integration. By recognizing the value of freedom of choice in medical options, pluralism is compatible with the principle of patient autonomy. Nonetheless, the pluralistic model does not amount to a relativistic stance according in which there would be no objective standards for comparing the therapeutic merit of conventional and CAM treatments. As an ethical model, pluralism realizes that physicians must be prepared to disagree with patient choices to pursue alternative therapies, and urge patients not to forgo medically indicated treatment. Pluralism encourages cooperation, research, and open communication and respect between practitioners despite the possible existence of honest disagreement, and preserves the integrity of each of the treatment systems involved. C1 NIH, Dept Clin Bioeth, Unit Clin Res, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Boston, MA USA. RP Miller, FG (reprint author), NIH, Dept Clin Bioeth, Unit Clin Res, Bldg 10,Room 1C118, Bethesda, MD 20892 USA. EM FMiller@cc.nih.gov NR 29 TC 46 Z9 49 U1 0 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1040-2446 J9 ACAD MED JI Acad. Med. PD MAR PY 2005 VL 80 IS 3 BP 286 EP 290 DI 10.1097/00001888-200503000-00015 PG 5 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA 902MV UT WOS:000227362100013 PM 15734812 ER PT J AU Halpain, MC Jeste, DV Trinidad, GI Wetherell, JL Lebowitz, BD AF Halpain, MC Jeste, DV Trinidad, GI Wetherell, JL Lebowitz, BD TI Intensive short-term research training for undergraduate, graduate, and medical students: Early experience with a new national-level approach in geriatric mental health SO ACADEMIC PSYCHIATRY LA English DT Article ID SUMMER RESEARCH-INSTITUTE; PHYSICIAN-SCIENTISTS; CAREER-DEVELOPMENT; PSYCHIATRY AB Objective: There is an urgent need for research training in psychiatry at early career stages, especially in geriatric psychiatry. The authors describe their first-year experience with the Summer Training in Aging Research Topics-in Mental Health (START-MH), a new federally funded national-level training program intended to offer intensive short-term research training for undergraduate, graduate, and medical students. Methods: The funding was used primarily to pay stipends for trainees who spent 10 weeks during the Summer working on research projects under established research mentors. At the end, a workshop brought together all the trainees who presented research posters. Results: Thirty trainees were selected from among 85 applicants. They worked on projects including basic, translational, clinical, or services research. Evaluations from trainees and mentors were uniformly positive. All the trainees reported that the START-MH program enhanced their interest in pursuing a career in geriatric mental health research. Several trainees later submitted their work for presentation or publication. Conclusions: The initial data suggest that the START-MH program can be a potentially useful model for attracting talented early-career trainees into mental health research. C1 VA San Diego Healthcare Syst, Dept Psychiat, San Diego, CA 92161 USA. Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA. NIMH, Bethesda, MD 20892 USA. RP Jeste, DV (reprint author), VA San Diego Healthcare Syst, Dept Psychiat, 3350 La Jolla Village Dr, San Diego, CA 92161 USA. EM djeste@ucsd.edu FU NIMH NIH HHS [MH-019946, MH-019934, MH-066248] NR 19 TC 15 Z9 15 U1 0 U2 2 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1042-9670 J9 ACAD PSYCHIATR JI Acad. Psych. PD SPR PY 2005 VL 29 IS 1 BP 58 EP 65 DI 10.1176/appi.ap.29.1.58 PG 8 WC Education & Educational Research; Psychiatry SC Education & Educational Research; Psychiatry GA 902KS UT WOS:000227355600012 PM 15772406 ER PT J AU Morgan, NY English, S Chen, W Chernomordik, V Russo, A Smith, PD Gandjbakhche, A AF Morgan, NY English, S Chen, W Chernomordik, V Russo, A Smith, PD Gandjbakhche, A TI Real time in vivo non-invasive optical imaging using near-infrared fluorescent quantum dots SO ACADEMIC RADIOLOGY LA English DT Article DE nanocrystals; quantum dots; deep-tissue imaging; near-infrared ID NANOCRYSTALS; NANOPARTICLES; OXYGENATION; RESONANCE; LOCALIZATION; TEMPERATURE; MICROSCOPY; PROTEIN; TISSUE; TUMORS AB Rationale and Objective. Deep-tissue optical imaging is of particular interest, as the equipment costs are lower than for competing technologies such as MRI. For this purpose, the development of novel contrast agents with near-infrared (NIR) fluorescence is especially important. We report on the use of NIR semiconductor nanocrystals in deep-tissue in vivo optical imaging. Materials and Methods. Semiconductor nanocrystals of CdMnTe/Hg were grown in aqueous solution and then coated with bovine serum albumin (BSA). The nanocrystals were approximately 5 nm in diameter and have a broad fluorescence peak in the NIR (770 nm). Nanocrystals were injected either subcutaneously or intravenously into athymic NCR NU/NU and C3H/HENCR MTV mice and then excited with a spatially broad 633 nm source; the resulting fluorescence was captured with a sensitive CCD camera. Results. We have demonstrated that the nanocrystals are a useful angiographic contrast agent for vessels surrounding and penetrating a murine squamous cell carcinoma in a C3H mouse. Preliminary assessment of the depth of penetration for excitation and emission was done by imaging a beating mouse heart, both through an intact thorax and after a thoracotomy. The temporal resolution associated with imaging the nanocrystals in circulation has been addressed, and the blood clearance for this contrast agent has also been measured. Conclusions. There was no significant photobleaching or degradation of the nanocrystals after an hour of continuous excitation. The stability of the nanocrystals together with the time resolution of the optical detection makes them particularly attractive candidates for pharmacokinetic imaging studies. C1 NIH, Bethesda, MD 20892 USA. Nomad Inc, Stillwater, OK 74074 USA. RP Morgan, NY (reprint author), NIH, Bethesda, MD 20892 USA. EM morgann@mail.nih.gov FU NCI NIH HHS [1R43CA110091-01, CA112756-01] NR 44 TC 125 Z9 133 U1 2 U2 33 PU ASSOC UNIV RADIOLOGISTS PI OAK BROOK PA 820 JORIE BLVD, OAK BROOK, IL 60523-2251 USA SN 1076-6332 J9 ACAD RADIOL JI Acad. Radiol. PD MAR PY 2005 VL 12 IS 3 BP 313 EP 323 DI 10.1016/j.acra.2004.04.023 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 907GK UT WOS:000227703800009 PM 15766692 ER PT J AU Leiderman, DB Shoptaw, S Montgomery, A Bloch, DA Elkashef, A LoCastro, J Vocci, F AF Leiderman, DB Shoptaw, S Montgomery, A Bloch, DA Elkashef, A LoCastro, J Vocci, F TI Cocaine Rapid Efficacy Screening Trial (CREST): a paradigm for the controlled evaluation of candidate medications for cocaine dependence SO ADDICTION LA English DT Article DE clinical trials; cocaine; design; medications ID INTERVIEW AB Aim Development of effective medications for the treatment of cocaine dependence remains a major priority for the National Institute on Drug Abuse (NIDA) at the National Institutes of Health. The Cocaine Rapid Efficacy Screening Trial (CREST) paradigm was developed by the Division of Treatment Research and Development (DT RAD) at NIDA with the goal of enhancing pilot clinical trial validity when systematically assessing a range of medications and drug classes for potential utility in treatment of cocaine dependence. Design CREST utilizes a randomized, controlled, parallel group, blinded methodology for comparing one or more marketed medications against a standard, pharmaceutical grade placebo. The trial design is comprised of a flexible 2-4-week screening/baseline period followed by randomization to an 8-week treatment period. Measures Standard measures of outcomes for the CREST included urinary benzoylecgonine (primary metabolite of cocaine), retention, cocaine craving, depression, clinical global impression and HIV-risk behaviors. In order to facilitate comparisons of data from the CREST studies across sites, drug classes and time, standardized procedures, measures and psychosocial counseling were used. Results A total of 19 medications were evaluated in out-patient treatment research clinics in Boston, Cincinnati, Los Angeles, New York and Philadelphia. Conclusions Findings supported decisions to move forward three medications (cabergoline, reserpine, tiagabine) using full-scale, adequately powered, randomized placebo-controlled trial designs. Lessons learned from the CREST experience continue to shape cocaine pharmacotherapy trial design and execution. C1 US FDA, Ctr Drug Evaluat & Res, Controlled Subst Staff, Rockville, MD 20852 USA. Univ Calif Los Angeles, Integrated Subst Abuse Programs, Los Angeles, CA USA. Univ Calif Los Angeles, Friends Res Inst, Los Angeles, CA USA. NIDA, Div Treatment Res & Dev, Bethesda, MD USA. Stanford Univ, Sch Med, Dept Hlth Res & Policy, Div Biostat, Stanford, CA 94305 USA. Boston Univ, Sch Med, Div Psychiat, Boston, MA 02118 USA. VA Boston Healthcare Syst Medicat Dev Res Unit, Boston, MA USA. RP Leiderman, DB (reprint author), US FDA, Ctr Drug Evaluat & Res, Controlled Subst Staff, HFD 009,5515 Secur Lane 1201, Rockville, MD 20852 USA. EM leidermand@cder.fda.gov FU NIDA NIH HHS [Y01 DA 50038-05] NR 16 TC 27 Z9 28 U1 1 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 1 EP 11 DI 10.1111/j.1360-0443.2005.00988.x PG 11 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200001 PM 15773068 ER PT J AU Ciraulo, DA Sarid-Segal, O Knapp, CM Ciraulo, AM LoCastro, J Bloch, DA Montgomery, MA Leiderman, DB Elkashef, A AF Ciraulo, DA Sarid-Segal, O Knapp, CM Ciraulo, AM LoCastro, J Bloch, DA Montgomery, MA Leiderman, DB Elkashef, A TI Efficacy screening trials of paroxetine, pentoxifylline, riluzole, pramipexole and venlafaxine in cocaine dependence SO ADDICTION LA English DT Article DE antidepressant; cocaine dependence; dopamine agonist; glutamate inhibitor; phosphodiesterase inhibitor; SSRI ID D-3 DOPAMINE-RECEPTOR; SELECTIVE-INHIBITION; FLUOXETINE TREATMENT; NUCLEUS-ACCUMBENS; SEEKING BEHAVIOR; GLUTAMATE; ANTIDEPRESSANTS; ANTAGONIST; FATALITIES; RELEASE AB Aims The two studies presented here were conducted to assess the efficacy of paroxetine, pentoxifylline, riluzole, venlafaxine and pramipexole as medications for the treatment of cocaine dependence. Design A multi-arm, modified blinded, placebo-controlled design was used. Setting The studies were conducted at the Boston VA Healthcare System and the Boston University School of Medicine Medication Development Research Unit (MDRU). Participants Participants met criteria for cocaine dependence during a 2-week screening period. Intervention Following random assignment to one of the treatment groups, subjects received active medication or placebo for 8 weeks in combination with cognitive behavioral counseling. In the first study the efficacy of the antidepressant paroxetine (20 mg daily), the phosphodiesterase inhibitor pentoxifylline (1200 mg daily) and the glutamate release inhibitor riluzole (100 mg daily) was assessed. The antidepressant venlafaxine (15 0 mg daily) and the dopamine agonist pramipexole (1.5 mg daily) were evaluated in the second study. Measurements Urine benzoylecgonine (BE) concentrations, self-report of cocaine use and global impression scores served as primary outcome measures. Secondary measures included assessments of cocaine craving and psychiatric functioning. Adverse events were monitored during the treatment period. Findings None of the active medications produced greater reductions in urine BE concentrations over the treatment period than did placebo. There were trends for BE levels to become reduced in the pentoxifylline group during the first 4 weeks of treatment and for Addiction Severity Index (ASI) drug composite scores to be lower in the pentoxyfylline group at end-point compared to the placebo group. Significant within-group reductions in reported cocaine use and craving were found for all treatment groups, but none of the active medications were superior to placebo on these measures. The accuracy of self-reported cocaine use declined over the study period. Overall, the active medications were well tolerated. Conclusions This study does not support the use of paroxetine, pentoxifylline, riluzole, venlafaxine or pramipexole for the treatment of cocaine dependence. However, these results need to be interpreted with caution because of the small size and lack of homogeneity of the experimental groups. C1 Boston Univ, Sch Med, Div Psychiat, Boston, MA 02118 USA. VA Boston Healthcare Syst Medicat Dev Res Unit, Boston, MA USA. Stanford Univ, Sch Med, Dept Hlth & Res Policy, Div Biostat, Stanford, CA 94305 USA. US FDA, Ctr Drug Evaluat & Res, Rockville, MD 20857 USA. NIDA, Medicat Dev Div, Bethesda, MD 20892 USA. RP Ciraulo, DA (reprint author), Boston Univ, Sch Med, Div Psychiat, Doctors Off Bldg,Suite 914,720 Harrison Ave, Boston, MA 02118 USA. EM dciraulo@bu.edu FU NIDA NIH HHS [N01 DA 28837] NR 35 TC 30 Z9 30 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 12 EP 22 DI 10.1111/j.1360-0443.2005.00985.x PG 11 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200002 PM 15730346 ER PT J AU Reid, MS Angrist, B Baker, S Woo, C Schwartz, M Montgomery, A Majewska, D Robinson, J Rotrosen, J AF Reid, MS Angrist, B Baker, S Woo, C Schwartz, M Montgomery, A Majewska, D Robinson, J Rotrosen, J TI A placebo-controlled screening trial of celecoxib for the treatment of cocaine dependence SO ADDICTION LA English DT Article DE cocaine dependence; craving; celecoxib; COX-2; treatment ID ALZHEIMERS-DISEASE; INTERVIEW GUIDE; RATING-SCALE; CYCLOOXYGENASE-2; BRAIN; SENSITIZATION; CARBAMAZEPINE; RELIABILITY; INVOLVEMENT; EXPRESSION AB Aims To conduct a medication screening trial study on the efficacy of celecoxib versus placebo for the treatment of cocaine dependence. Design A modified blinded, parallel group study in an outpatient setting using the Cocaine Rapid Efficacy and Safety Trials (CREST) study design. Setting The study was performed at the New York Medications Development Research Unit (MDRU). Participants All participants met Diagnostic and Statistical Manual version IV (DSM-IV) criteria for cocaine dependence and provided at least two urine samples positive for benzoylecgonine (BE) during the 2-week screening period. Twenty-three participants were enrolled in the treatment phase of the study. Intervention After a 2-week screening period, subjects were assigned randomly to receive either celebrex (200 mg/day) or placebo for an 8-week treatment period. All subjects also received individual cognitive behavioral counseling during treatment. Measurements Primary outcome measures included quantitative urine benzoylecgonine (BE) levels, self-report of drug use and global impression scores. Secondary outcomes included cocaine craving, study retention and related psychosocial measures. Safety measures included adverse event monitoring, vital signs and extrapyramidal side-effects tests. Results Study retention was similar across both treatment groups and safety measures indicated that celecoxib was moderately tolerated. Cocaine use, as measured by self-report and urine BE levels at end of treatment, indicated weaker improvement in the celecoxib group. Reductions in the intensity of cocaine craving were also weaker in the celecoxib group. Cocaine abstinence rates, global impression scores and all other related psychometric measures did not differ significantly between treatment groups. Conclusion This study does not support the effectiveness of celecoxib for the treatment of cocaine dependence. C1 NYU, Sch Med, VA NYHHS, Dept Psychiat, New York, NY 10010 USA. VA New York Harbor Healthcare Syst, Dept Psychiat, New York, NY USA. NIDA, Medicat Dev Div, Bethesda, MD 20892 USA. Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA. RP Reid, MS (reprint author), NYU, Sch Med, VA NYHHS, Dept Psychiat, 116 A,423 E 23rd St, New York, NY 10010 USA. EM malcolm.reid@med.va.gov FU NIDA NIH HHS [Y01 DA 50038] NR 37 TC 5 Z9 5 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 32 EP 42 DI 10.1111/j.1360-0443.2005.00989.x PG 11 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200004 PM 15730348 ER PT J AU Reid, MS Casadonte, P Baker, S Sanfilipo, M Braunstein, D Hitzemann, R Montgomery, A Majewska, D Robinson, J Rotrosen, J AF Reid, MS Casadonte, P Baker, S Sanfilipo, M Braunstein, D Hitzemann, R Montgomery, A Majewska, D Robinson, J Rotrosen, J TI A placebo-controlled screening trial of olanzapine, valproate, and coenzyme Q10/L-carnitine for the treatment of cocaine dependence SO ADDICTION LA English DT Article DE cocaine dependence; coenzyme Q10; L-carnitine; olanzapine; treatment; valproate ID POSITRON-EMISSION-TOMOGRAPHY; ACETYL-L-CARNITINE; IN-VIVO; RECEPTOR-BINDING; RATS; METABOLISM; ABUSERS; BLIND; BRAIN; WITHDRAWAL AB Aims To conduct a medication screening trial on the efficacy of olanzapine, valproate or coenzyme Q10/L-carnitine combination versus placebo for the treatment of cocaine dependence. Design A four-arm, modified blinded, parallel group study in an out-patient setting using the Cocaine Rapid Efficacy and Safety Trials (CREST) study design. Setting The study was performed at the New York Medications Development Research Unit (MDRU). Participants All participants met Diagnostic and Statistical Manual version IV (DSM-IV) criteria for cocaine dependence and provided at least two urine samples positive for benzoylecgonine (BE) during the 2-week screening period. Sixty-eight participants were enrolled with 39 completing the study. Intervention After a 2-week screening period, 68 subjects were assigned randomly to receive either olanzapine (10 mg/day), valproate (1500 mg/day), coenzyme Q10 (200 mg/day) and L-carnitine (500 mg/day) combination or placebo for an 8-week treatment period. All subjects also received individual cognitive behavioral counseling during treatment. Measurements Primary outcome measures included quantitative urine benzoylecgonine (BE) levels, self-report of drug use, and global impression scores. Secondary outcomes included cocaine craving, study retention and related psychosocial measures. Safety measures included adverse event monitoring, vital signs, and extrapyramidal side-effects tests. Results Study retention was similar across all treatment groups, and all groups showed improvement across most measures of treatment efficacy over the duration of the study. None of the study medications, however, were superior to placebo on any of the primary or secondary outcome measures. Cocaine use, as measured by urine BE levels and self-report, was not significantly lower than placebo in any of the drug treatment groups. All study medications were equally well tolerated, and few medication side effects were observed. Conclusion This pilot study does not support the effectiveness of olanzapine, valproate or coenzyme Q10/L-carnitine combination for the treatment of cocaine dependence. C1 NYU, Sch Med, Dept Psychiat, VA NYHHS, New York, NY 10010 USA. Natl Inst Drug Abuse, Med Dev Div, Bethesda, MD USA. Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA. Oregon Hlth Sci Univ, Dept Behav Neurosci L470, Portland, OR 97201 USA. RP Reid, MS (reprint author), NYU, Sch Med, Dept Psychiat, VA NYHHS, 116A,423 E 23rd St, New York, NY 10010 USA. EM malcolm.reid@med.va.gov FU NIDA NIH HHS [Y01 DA 50038] NR 61 TC 35 Z9 35 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 43 EP 57 DI 10.1111/j.1360-0443.2005.00990.x PG 15 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200005 PM 15730349 ER PT J AU Berger, SP Winhusen, TM Somoza, EC Harrer, JM Mezinskis, JP Leiderman, DB Montgomery, MA Goldsmith, RJ Bloch, DA Singal, BM Elkashef, A AF Berger, SP Winhusen, TM Somoza, EC Harrer, JM Mezinskis, JP Leiderman, DB Montgomery, MA Goldsmith, RJ Bloch, DA Singal, BM Elkashef, A TI A medication screening trial evaluation of reserpine, gabapentin and lamotrigine pharmacotherapy of cocaine dependence SO ADDICTION LA English DT Article DE clinical trial; cocaine dependence; CREST; gabapentin; lamotrigine; reserpine ID DRUG; DEPRESSION; ABUSE; ADDICTION; RESPONSES; DOPAMINE; RECEPTOR AB Aims To conduct a preliminary evaluation of the safety and efficacy of reserpine, gabapentin or lamotrigine versus an,unmatched placebo control as a treatment for cocaine dependence. Design A 10-week out-patient study using the Cocaine Rapid Efficacy and Safety Trial (CREST) study design. Setting The study was conducted at the Cincinnati Medication Development Research Unit (MDRU). Participants Participants met Diagnostic and Statistical Manual version IV (DSM-IV) criteria for cocaine dependence. Sixty participants were enrolled, with 50 participants completing the final study measures. Intervention The targeted daily doses of medication were reserpine 0.5 mg, gabapentin 1800 mg and lamotrigine 150 mg. All participants received I hour of manualized individual cognitive behavioral therapy on a weekly basis. Measurements Primary outcome measures of efficacy included urine benzoylecgonine (BE) level, Cocaine Clinical Global Impression scale-observer and self-report of cocaine use. Safety measures included adverse events, electrocardiograms (ECGs), vital signs and laboratory tests. Findings Subjective measures of cocaine dependence indicated significant improvement for all study groups. Urine BE results indicated a significant improvement for the reserpine group (P < 0.05) and non-significant changes for the other study groups. No pattern of physical or laboratory abnormalities attributable to treatment with any of the medications was identified. There were three serious adverse events reported, none of which were related to study procedures. The medications appeared to be tolerated well. Conclusions The present findings suggest that reserpine maybe worthy of further study as a cocaine dependence treatment. C1 VA Med Ctr, Cincinnati VA UC NIDA MDRU, Cincinnati, OH USA. Univ Cincinnati, Coll Med, CinARC, Cincinnati, OH USA. Natl Inst Drug Abuse, Medicat Dev Div, Bethesda, MD USA. Stanford Univ, Sch Med, Dept Hlth Res, Stanford, CA 94305 USA. Stanford Univ, Sch Med, Policy Div Biostat, Stanford, CA 94305 USA. RP Berger, SP (reprint author), Dept Vet Affairs Med Ctr, Psychiat Serv, 3710 SW US Vet Hosp Rd, Portland, OR 97201 USA. EM bergerp@ohsu.edu OI Winhusen, Theresa/0000-0002-3364-0739 FU NIDA NIH HHS [N01DA-7-8074, Y01 DA 50038-00] NR 32 TC 44 Z9 44 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 58 EP 67 DI 10.1111/j.1360-0443.2005.00983.x PG 10 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200006 PM 15730350 ER PT J AU Winhusen, TM Somoza, EC Harrer, JM Mezinskis, JP Montgomery, MA Goldsmith, RJ Coleman, FS Bloch, DA Leiderman, DB Singal, BM Berger, P Elkashef, A AF Winhusen, TM Somoza, EC Harrer, JM Mezinskis, JP Montgomery, MA Goldsmith, RJ Coleman, FS Bloch, DA Leiderman, DB Singal, BM Berger, P Elkashef, A TI A placebo-controlled screening trial of tiagabine, sertraline and donepezil as cocaine dependence treatments SO ADDICTION LA English DT Article DE clinical trial; cocaine dependence; CREST; donepezil; sertraline; tiagabine ID NUCLEUS-ACCUMBENS DOPAMINE; GAMMA-VINYL-GABA; INTRAVENOUS COCAINE; INDUCED INCREASES; DRUG-ADDICTION; FLUOXETINE; WITHDRAWAL; RATS; SEROTONIN; ABUSERS AB Aims To conduct a preliminary evaluation of the safety and efficacy of tiagabine, sertraline or donepezil versus an unmatched placebo control as a treatment for cocaine dependence. Design A 10-week out-patient study was conducted using the Cocaine Rapid Efficacy and Safety Trial (CREST) study design. Setting This study was conducted at the Cincinnati Medication Development Research Unit (MDRU) and at an affiliated site in Dayton, Ohio. Participants Participants met Diagnostic and Statistical Manual version IV (DSM-IV) criteria for cocaine dependence. Sixty-seven participants were enrolled with 55 completing final study measures. Intervention The targeted daily doses of medication were tiagabine 20 mg, sertraline 100 mg and donepezil 10 mg. All participants received 1 hour of manualized individual cognitive behavioral therapy on a weekly basis. Measurements Primary outcome measures of efficacy included urine benzoylecgonine (BE) level, Cocaine Clinical Global Impression Scale-Observer and self-report of cocaine use. Safety measures included adverse events, ECGs, vital signs and laboratory tests. Findings Subjective measures of cocaine dependence indicated significant improvement for all study groups. Generalized estimating equations analysis indicated that the tiagabine group showed a trend toward a significant decrease in urine BE level from baseline to weeks 5-8 (P = 0.10) and non-significant changes for the other study groups. No pattern of physical or laboratory abnormalities attributable to treatment with any of the medications was identified. There were three serious adverse events reported, none of which were related to study procedures. Conclusions The present findings suggest that tiagabine maybe worthy of further study as a cocaine dependence treatment. C1 Univ Cincinnati, Coll Med, CinARC, Cincinnati, OH 45220 USA. Cincinnati VA UC NIDA MDRU, VA Med Ctr, Cincinnati, OH USA. Natl Inst Drug Abuse, Medicat Dev Div, Bethesda, MD USA. Dayton VA Med Ctr, Dayton, OH USA. Stanford Univ, Sch Med, Dept Hlth Res & Policy Div Biostat, Stanford, CA USA. RP Winhusen, TM (reprint author), Univ Cincinnati, Coll Med, CinARC, 3210 Jefferson Ave, Cincinnati, OH 45220 USA. EM winhusen@mdru.uc.edu OI Winhusen, Theresa/0000-0002-3364-0739 FU NIDA NIH HHS [Y01 DA50038-00, N01DA-7-8074] NR 45 TC 64 Z9 64 U1 1 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 68 EP 77 DI 10.1111/j.1360-0443.2005.00992.x PG 10 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200007 PM 15730351 ER PT J AU Shoptaw, S Watson, DW Reiber, C Rawson, RA Montgomery, MA Majewska, MD Ling, W AF Shoptaw, S Watson, DW Reiber, C Rawson, RA Montgomery, MA Majewska, MD Ling, W TI Randomized controlled pilot trial of cabergoline, hydergine and levodopa/carbidopa: Los Angeles Cocaine Rapid Efficacy Screening Trial (CREST) SO ADDICTION LA English DT Article DE cabergoline; cocaine; hydergine; levodopa/carbidopa; out-patient ID PLACEBO-CONTROLLED TRIAL; ERGOLOID MESYLATES HYDERGINE; VENTRAL TEGMENTAL AREA; NUCLEUS-ACCUMBENS; PARKINSONS-DISEASE; DOPAMINE RELEASE; DOUBLE-BLIND; TOLERABILITY; RECEPTORS; DEMENTIA AB Aim This study tested three dopaminergic medications against a common unmatched placebo condition: hydergine 1 mg three times daily (n = 15); levodopa/carbidopa 25/100 mg three times daily (n = 15); cabergoline 0.5 mg per week (n = 15); and placebo three times daily (n = 15) as potential pharmacotherapies for cocaine dependence. Design The four-parallel group, Cocaine Rapid Efficacy Screening Trial (CREST) design featured a 2-week baseline period followed by randomization to an 8-week medication condition that included I hour per week of cognitive behavioral drug counseling. A safety evaluation was conducted 4 weeks after termination. Measures Outcomes included cocaine metabolites measured in urine, retention and self-reports for drug use, cocaine craving, clinical improvement, mood and HIV risk behaviors. Results Participants assigned to receive cabergoline provided more urine samples negative for cocaine metabolites (42.4%) than those assigned to receive placebo (25.0%), a statistically. significant difference after controlling for baseline differences in self-reported cocaine use (F = 2.95, df = 3; P = 0.05). Cabergoline-treated participants demonstrated a significant improvement over placebo from baseline to week 8 when measured using the Addiction Severity Index (ASI) employment subscale (overall change = -0.09, SD = 0.10, t = 2.3 6, P < 0.05). Safety and adverse event measures showed similar rates and types of complaints by treatment condition. Conclusions These results, combined with the apparent safety of cabergoline when used with this population, provide empirical support for conducting a larger study of the medication. C1 Univ Calif Los Angeles, Integrated Substance Abuse Programs, Los Angeles, CA 90025 USA. Friends Res Inst Inc, Los Angeles, CA USA. Natl Inst Drug Abuse, Div Treatment Res & Dev, Bethesda, MD USA. RP Shoptaw, S (reprint author), Univ Calif Los Angeles, Integrated Substance Abuse Programs, 11075 Santa Monica Blvd,Suite 200, Los Angeles, CA 90025 USA. EM Sshoptaw@mednet.ucla.edu FU NIDA NIH HHS [1 Y01 DA 50038] NR 45 TC 23 Z9 24 U1 0 U2 2 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 78 EP 90 DI 10.1111/j.1360-0443.2005.00991.x PG 13 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200008 PM 15730352 ER PT J AU Elkashef, A Holmes, TH Bloch, DA Shoptaw, S Kampman, K Reid, MS Somoza, ER Ciraulo, D Rotrosen, J Leiderman, D Montgomery, A Vocci, F AF Elkashef, A Holmes, TH Bloch, DA Shoptaw, S Kampman, K Reid, MS Somoza, ER Ciraulo, D Rotrosen, J Leiderman, D Montgomery, A Vocci, F TI Retrospective analyses of pooled data from CREST I and CREST II trials for treatment of cocaine dependence SO ADDICTION LA English DT Article DE cocaine; pharmacotherapy; statistics ID INTERVIEW GUIDE; RATING-SCALE; SUCCESS; ABUSE AB Aim To analyze pooled data from the Cocaine Rapid Evaluation Screening Trial (CREST). Pooling data from these small pilot trials into four major drug classes permitted data exploration for treatment and covariate effects with increased sample size. Design Small pilot trials were conducted to screen fifteen medications as prospective treatments for cocaine dependence. Studies included a flexible 2-week to 4-week screening/baseline period followed by an 8-week randomized treatment condition. Participants were randomized equally to one of up to three active medications or placebo. Setting Five Medications Development Research Units at the five academic centers of University of Cincinnati, New York University, University of Pennsylvania, University of California Los Angeles and Boston University. Participants The pooled data set consisted of 3 5 7 total subjects. Standardized inclusion and exclusion criteria were employed in subject selection to enhance consistency of cocaine-dependent study participants across all sites (see reports on individual trials in this supplement for details). All participants provided at least two urine samples that were positive for cocaine metabolite during a two-week period prior to being randomized. Intervention All subjects in these trials, those randomized to placebo and active medications, received active treatment in the form of evidence-based cognitive behavioral therapy. Measures Quantitative urine benzoylecgonine (BE), self-report of cocaine use, and total Brief Substance Craving Scale (BSCS) scores were compared between each class of medication and its matched-placebo group. Findings Regression analysis of pooled data did not identify any statistically significant differences between treatment and matched-placebo for any of the four classes. Exploration of the effects of baseline covariates indicated that gender and African American status were associated significantly with outcome. Female gender was consistently associated with poorer outcomes for medication and placebo groups, while the direction of association between African American status and outcome differed by treatment groups. Retention was also examined: dropout rates may have been somewhat higher for placebo than treatment. groups during the early active-treatment period. Classification trees were used to identify characteristics of subjects who were abstinent for at least two weeks during the eight-week trial; only 4.0% of females while 17.9% of males achieved this criterion. Conclusions Results presented here may prove useful for planning future clinical trials for therapies targeting cocaine dependence. C1 Stanford Univ, Sch Med, Dept Hlth Res & Policy, Div Biostat, Stanford, CA 94305 USA. NIDA, Div Pharmacotherapies & Med Consequences Drug Abu, NIH, Dept Hlth & Human Serv, Bethesda, MD USA. US FDA, Ctr Drug Evaluat & Res, Rockville, MD 20857 USA. Univ Calif Los Angeles, Integrated Substance Abuse Programs, Los Angeles, CA USA. Friends Res Inst Inc, Los Angeles, CA USA. Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA. NYU, Sch Med, New York, NY USA. VA New York Harbor Healthcare Syst, Dept Psychiat, New York, NY USA. Cincinnati VA Med Ctr, Cincinnati, OH USA. Univ Cincinnati, Coll Med, CinARC, Cincinnati, OH USA. Boston Univ, Sch Med, Div Psychiat, Boston, MA 02118 USA. VA Boston Healthcare Syst, MDRU, Boston, MA 02118 USA. RP Holmes, TH (reprint author), Stanford Univ, Sch Med, Dept Hlth Res & Policy, Div Biostat, HRP Redwood Bldg, Stanford, CA 94305 USA. EM tholmes@stanford.edu FU NIDA NIH HHS [1 Y01 DA 50038] NR 19 TC 23 Z9 23 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 91 EP 101 DI 10.1111/j.1360-0443.2005.00986.x PG 11 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200009 PM 15730353 ER PT J AU Kampman, KM Leiderman, D Holmes, T LoCastro, J Bloch, DA Reid, MS Shoptaw, S Montgomery, MA Winhusen, TM Somoza, EC Ciraulo, DA Elkashef, A Vocci, F AF Kampman, KM Leiderman, D Holmes, T LoCastro, J Bloch, DA Reid, MS Shoptaw, S Montgomery, MA Winhusen, TM Somoza, EC Ciraulo, DA Elkashef, A Vocci, F TI Cocaine Rapid Efficacy Screening Trials (CREST): lessons learned SO ADDICTION LA English DT Article DE clinical trial; cocaine; pharmacotherapy ID DEPENDENCE; FLUOXETINE; THERAPY; ABUSERS AB Aims The Cocaine Rapid Efficacy Screening Trials (CREST) were designed by the National Institute on Drug Abuse Division of Treatment Research and Development (NIDA, DT RAD) to rapidly screen a number of medications potentially useful for the treatment of cocaine dependence. Design, Each CREST trial was designed to compare several medications in a single trial against an unmatched placebo. The placebo group was included in each trial to avoid the nearly universal positive response to medications seen in open-label trials. In addition, a common set of procedures and outcome measures were employed throughout to increase comparability of results obtained from different trials and from different times. Participants In all, 18 medications were screened in seven different trials, conducted in four different sites throughout the United States involving 398 cocaine-dependent patients. Findings Three medications were found to be promising enough to include in subsequent larger trials. Common statistical procedures for evaluating medications were developed to facilitate comparisons across sites and across time. A portion of the data were pooled and analyzed, which yielded some useful insights into cocaine dependence and its treatment. Finally, a review of individual trials together with the pooled analysis revealed several potential improvements for future screening trials. Conclusions Overall, the CREST trials proved to be useful for rapidly screening medications for treatment of cocaine dependence, but several modifications in design should be made before this framework is applied further. C1 Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA. Natl Inst Drug Abuse, Medicat Dev Div, Bethesda, MD USA. Boston Univ, Sch Med, Div Psychiat, Boston, MA 02118 USA. VA Boston Healthcare Syst, MDRU, Boston, MA USA. VA Med Ctr, Cincinnati VA UC NIDA MDRU, Cincinnati, OH USA. Univ Cincinnati, Coll Med, CinARC, Cincinnati, OH USA. NYU, Sch Med, New York, NY USA. VA New York Harbor Healthcare Syst, Dept Psychiat, New York, NY USA. Stanford Univ, Sch Med, Dept Hlth Res, Stanford, CA USA. Stanford Univ, Sch Med, Policy Div Biostat, Stanford, CA USA. Univ Calif Los Angeles, Integrated Substance Abuse Programs, Los Angeles, CA USA. Friends Res Inst Inc, Los Angeles, CA USA. RP Kampman, KM (reprint author), Univ Penn, Treatment Res Ctr, 3900 Chestnut St, Philadelphia, PA 19104 USA. EM kampman_k@mail.trc.upenn.edu OI Winhusen, Theresa/0000-0002-3364-0739 FU NIDA NIH HHS [Y01 DA 30012] NR 14 TC 13 Z9 13 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 SU 1 BP 102 EP 110 DI 10.1111/j.1360-0443.2005.00987.x PG 9 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 907PB UT WOS:000227729200010 PM 15730354 ER PT J AU Dawson, DA Grant, BF Stinson, FS Chou, PS Huang, B Ruan, WJ AF Dawson, DA Grant, BF Stinson, FS Chou, PS Huang, B Ruan, WJ TI Recovery from DSM-IV alcohol dependence: United States, 2001-2002 SO ADDICTION LA English DT Editorial Material DE dependence; natural recovery; remission; recovery; risk drinking ID NATIONAL EPIDEMIOLOGIC SURVEY; SUBSTANCE USE DISORDERS; 10-YEAR FOLLOW-UP; PERSONALITY-DISORDERS; OUTCOME PREDICTORS; NATURAL RECOVERY; PROBLEM DRINKERS; COLLEGE ALCOHOL; HARVARD-SCHOOL; AUDADIS-ADR AB Aims To investigate the prevalence and correlates of recovery from Diagnostic and Statistical Manual version IV (DSM-IV) alcohol dependence by examining the past-year status of individuals who met the criteria for prior-to-past-year (PPY) dependence. Design Cross-sectional, retrospective survey of a nationally representative sample of US adults 18 years of age and over (first wave of a planned longitudinal survey). Methods This analysis is based on data from the 2001-02 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), in which data were collected in personal interviews conducted with one randomly selected adult in each sample household. A subset of the NESARC sample (total n = 43 093), consisting of 4422 US adults 18 years of age and over classified with PPY DSM-IV alcohol dependence, were evaluated with respect to their past-year recovery status: past-year dependence, partial remission, full remission, asymptomatic risk drinking, abstinent recovery (AR) and non-abstinent recovery (NR). Correlates of past-year status were examined in bivariate analyses and using multivariate logistic regression models. Findings Of people classified with PPY alcohol dependence, 25.0% were still classified as dependent in the past year; 27.3% were classified as being in partial remission; 11.8% were asymptomatic risk drinkers who demonstrated a pattern of drinking that put them at risk of relapse; 17.7% were low-risk drinkers; and 18.2% were abstainers. Only 25.5% of people with PPY dependence ever received treatment. Being married was associated positively with the odds of both AR and NR, and ethanol intake was negatively associated with both. Severity of dependence increased the odds of AR but decreased the odds of NR. The odds of AR (but not NR) increased with age and female gender but were decreased by the presence of a personality disorder. Treatment history modified the effects of college attendance/graduation, age at onset and interval since onset on the odds of recovery. Conclusions There is a substantial level of recovery from alcohol dependence. Information on factors associated with recovery may be useful in targeting appropriate treatment modalities. C1 NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, NIH, Bethesda, MD 20892 USA. RP Dawson, DA (reprint author), NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, NIH, Room 3083,5635 Fishers Lane,MSC 9304, Bethesda, MD 20892 USA. EM ddawson@mail.nih.gov NR 45 TC 272 Z9 277 U1 2 U2 17 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 IS 3 BP 281 EP 292 DI 10.1111/j.1360-0443.2004.00964.x PG 12 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 902RJ UT WOS:000227373900005 PM 15733237 ER PT J AU Dawson, DA Grant, BF Stinson, FS Chou, PS Huang, BJ Ruan, WJ AF Dawson, DA Grant, BF Stinson, FS Chou, PS Huang, BJ Ruan, WJ TI Recovery from alcohol dependence: Response to commentaries SO ADDICTION LA English DT Editorial Material ID DSM-IV; SYMPTOMS; VALIDITY C1 NIAAA, LEB, Bethesda, MD 20892 USA. RP Dawson, DA (reprint author), NIAAA, LEB, Room 3083,5635 Fishers Lane,MSC 9304, Bethesda, MD 20892 USA. EM ddawson@willco.niaaa.nih.gov NR 9 TC 1 Z9 1 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0965-2140 J9 ADDICTION JI Addiction PD MAR PY 2005 VL 100 IS 3 BP 296 EP 298 DI 10.1111/j.1360-0443.2005.01042.x PG 3 WC Substance Abuse; Psychiatry SC Substance Abuse; Psychiatry GA 902RJ UT WOS:000227373900010 ER PT J AU Reimers, M AF Reimers, M TI Statistical analysis of microarray data SO ADDICTION BIOLOGY LA English DT Article ID ART. NO. E15; GENE-EXPRESSION; NORMALIZATION; VARIANCE; QUALITY; DESIGN AB Microarrays promise dynamic snapshots of cell activin but microarray results are unfortunately not straightforward to intepret. This article aims to distill the most useful practical results from the vast body of literature availalable on microarray data analysis. Topics covered include: experimental design issues, normalization, quality control, exploratory analysis, and tests for differential expression. Special attention is paid to the peculiarities of low-level analysis of Affymetrix chips, and the multiple testing problem in determining differential expression. The aim of this article is to provide useful answers to the most common practical issues in microarray data analysis. The main topics are preprocessing (normalization), and detecting differential expression. Subsidiary topics include experimental design, and exploratory analysis. Further discussion is found Lit the author's web page (http://discover.nci.nih.gov --> Notes on Microarray Data Analysis). C1 NIH, Bethesda, MD 20892 USA. RP Reimers, M (reprint author), NIH, 9000 Rockville Pike,Bldg 37,Room 5068, Bethesda, MD 20892 USA. EM reimersm@mail.nih.gov NR 22 TC 23 Z9 27 U1 2 U2 5 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1355-6215 J9 ADDICT BIOL JI Addict. Biol. PD MAR PY 2005 VL 10 IS 1 BP 23 EP 35 DI 10.1080/13556210412331327795 PG 13 WC Biochemistry & Molecular Biology; Substance Abuse SC Biochemistry & Molecular Biology; Substance Abuse GA 893WU UT WOS:000226752300004 PM 15849016 ER PT J AU Sommer, WH Arlinde, C Heilig, M AF Sommer, WH Arlinde, C Heilig, M TI The search for candidate genes of alcoholism: Evidence from expression profiling studies SO ADDICTION BIOLOGY LA English DT Article ID AVOIDING ANA RATS; FALSE DISCOVERY RATE; PREFERRING AA; DIFFERENTIAL EXPRESSION; MICROARRAY DATA; OLIGONUCLEOTIDE ARRAYS; ETHANOL-CONSUMPTION; BRAIN-REGIONS; PREFERENCE; DEPENDENCE AB Alcoholism is the outcome of complex interactions between the environment and multiple gene loci, which may encode pre-existing susceptibility, or contribute to the neuroadaptations underlying the process of developing dependence. Because of this, the prospect of simultaneous, genome wide, high-throughput analysis of gene expression allowed by microarray technology has met with great expectations. The hope has been that new insights into pathogenesis of substance disorders will rapidly be gained, leading to identification of novel treatment targets. The usefulness of this approach as a discovery tool in addiction research will be critically reviewed here. In this article, we describe the evolution of our experimental approaches, from first generation Affymetrix expression arrays to present high-density arrays, and from the use of original Affymetrix software to more advanced analysis of the probe signal, and different statistical approaches to creating candidate gene lists. Further, we address some methodological issues critical to the study of brain samples by microarray technology. We also summarize findings from several expression profiling experiments involving different animal models of alcoholism. The accumulation of expression data from different annual models allows mining the database for patterns of overlap. Such second level analysis depends on the generation of uniform and reliable datasets. C1 Huddinge Univ Hosp, Karolinska Inst, NEUROTEC Dept, Div Psychiat, S-14186 Huddinge, Sweden. NIAAA, Lab Translat & Clin Studies, NIH, Bethesda, MD USA. RP Sommer, WH (reprint author), Huddinge Univ Hosp, Karolinska Inst, NEUROTEC Dept, Div Psychiat, M57, S-14186 Huddinge, Sweden. EM wolfgang.sommer@neurotec.ki.se NR 52 TC 26 Z9 26 U1 0 U2 1 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1355-6215 J9 ADDICT BIOL JI Addict. Biol. PD MAR PY 2005 VL 10 IS 1 BP 71 EP 79 DI 10.1080/13556210412331327821 PG 9 WC Biochemistry & Molecular Biology; Substance Abuse SC Biochemistry & Molecular Biology; Substance Abuse GA 893WU UT WOS:000226752300009 PM 15849021 ER PT J AU Fagan, P Brook, JS Rubenstone, E Zhang, CS AF Fagan, P Brook, JS Rubenstone, E Zhang, CS TI Parental occupation, education, and smoking as predictors of offspring tobacco use in adulthood: A longitudinal study SO ADDICTIVE BEHAVIORS LA English DT Article DE blue-collar smoking; SES and smoking; offspring smoking; parental education; parental occupation ID CIGARETTE-SMOKING; ADOLESCENT SMOKING; SOCIOECONOMIC-STATUS; INTERGENERATIONAL TRANSMISSION; AFRICAN-AMERICAN; YOUNG ADULTHOOD; COLLAR WORKERS; FAMILY PROCESS; SUBSTANCE USE; HEALTH AB This study examined the interrelation of parental occupational status (blue-versus white-collar), parental education, parental smoking, parent-child relations, late adolescent tobacco use, and adult offspring smoking. A longitudinal data set was employed, composed of 603 participants who were first studied in childhood and then followed to mean age 27 years. Structural Equation Modeling (SEM) showed that the distal factors of parental blue-collar status, low parental educational achievement, and parental smoking were related to adult offspring smoking. Specifically, parental blue-collar status and parental smoking were mediated by the latent construct of the parent-child relationship, which in turn was mediated by smoking in late adolescence with respect to adult offspring smoking. Parental educational level was partially mediated by the parent-adolescent relationship but also had a direct path to adult offspring smoking. The most powerful predictor of offspring smoking in adulthood was smoking in late adolescence. Findings imply areas that may be targeted by intervention programs to decrease offspring tobacco use. (c) 2004 Elsevier Ltd. All rights reserved. C1 NYU, Sch Med, New York, NY 10016 USA. NCI, Tobacco Control Res Branch, Bethesda, MD 20892 USA. RP Brook, JS (reprint author), NYU, Sch Med, 215 Lexington Ave,15th Floor, New York, NY 10016 USA. EM judith.brook@med.nyu.edu OI Zhang, Chenshu/0000-0002-3233-3905 FU NCI NIH HHS [CA 84063, CA 94845]; NIDA NIH HHS [DA 00244, DA 03188] NR 58 TC 26 Z9 28 U1 2 U2 11 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0306-4603 J9 ADDICT BEHAV JI Addict. Behav. PD MAR PY 2005 VL 30 IS 3 BP 517 EP 529 DI 10.1016/j.addbeh.2004.08.002 PG 13 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA 904XT UT WOS:000227532600011 PM 15718068 ER PT J AU Brody, CL Hamer, DH Haaga, DAF AF Brody, CL Hamer, DH Haaga, DAF TI Depression vulnerability, cigarette smoking, and the serotonin transporter gene SO ADDICTIVE BEHAVIORS LA English DT Article DE depression vulnerability; cigarette smoking; serotonin transporter gene; behavioral genetics ID NICOTINE DEPENDENCE; ASSOCIATION; POLYMORPHISM; PERSONALITY; PERSPECTIVE; NEUROTICISM; POPULATION; DISORDER; BEHAVIOR; TRAITS AB People with current or past depression are more likely to have been smokers at some point in their lives. Smokers with depression histories are also less likely to quit. Attempts to understand this relationship are important insofar as they can help treatment efficacy for this group of smokers. Prior research indicates that different genetic variations affect the relationship between smoking and neuroticism. This study examined whether people with a short serotonin transporter genotype would likewise show a stronger relationship between depression vulnerability and smoking behavior than those with the long genotype. Although depression vulnerability was associated with smoking behaviors, genotype did not significantly affect this relationship. Discussion centered on possible reasons for varying results across conceptually similar studies. (c) 2004 Elsevier Ltd. All rights reserved. C1 American Univ, Dept Psychol, Washington, DC 20016 USA. NCI, Bethesda, MD 20892 USA. RP Haaga, DAF (reprint author), American Univ, Dept Psychol, Asbury Bldg, Washington, DC 20016 USA. EM dhaaga@american.edu NR 20 TC 19 Z9 20 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0306-4603 J9 ADDICT BEHAV JI Addict. Behav. PD MAR PY 2005 VL 30 IS 3 BP 557 EP 566 DI 10.1016/j.addbeh.2004.08.005 PG 10 WC Psychology, Clinical; Substance Abuse SC Psychology; Substance Abuse GA 904XT UT WOS:000227532600014 PM 15718071 ER PT J AU Anson, RM Jones, B de Cabo, R AF Anson, R. Michael Jones, Bruce de Cabo, Rafael TI The diet restriction paradigm: a brief review of the effects of every-other-day feeding SO AGE LA English DT Review DE aging; caloric restriction; dietary restriction; fasting; longevity ID LIFE-SPAN; FOOD RESTRICTION; CALORIC RESTRICTION; VOLUNTARY EXERCISE; BODY-WEIGHT; RATS; LONGEVITY; MICE; GROWTH; AGE AB It has been known since the early 1900s that restriction of dietary intake relative to the ad libitum (AL) level increases stress resistance, cancer resistance, and longevity in many species. Studies investigating these phenomena have used three paradigms for dietary restriction. In the first, the AL intake of a control group is measured, and an experimental group is fed less than that amount in a specified proportion, e. g., 40%. In the second, food is provided AL to both the control and experimental groups: however, the experimental group is subjected to periods of fasting. Recent studies using this paradigm provide food every other day (EOD). Both of these paradigms have been in use since the early 1900s. A third paradigm that combines them was developed in the early 1970s: one or more days of fasting separate the provision of a limited amount of food. It was assumed for many years that the physiological responses to these paradigms were due exclusively to a net decrease in energy intake. Recently, however, it was found that some species and strains of laboratory animals, when fed AL every other day, are capable of gorging so that their net weekly intake is not greatly decreased. Despite having only a small deficit in energy intake relative to control levels, however, these animals experience enhanced longevity and stress resistance in comparison to AL controls as much as in animals enduring daily restriction of diet. These observations warrant renewed interest in this paradigm and suggest that comparisons of the paradigms and their effects can be used to determine which factors are critical to the beneficial effects of caloric restriction. C1 NIA, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA. Ctr Gerontol Res, Lab Expt Gerontol, Baltimore, MD 21224 USA. RP de Cabo, R (reprint author), NIA, Lab Expt Gerontol, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA. EM decabora@gmail.com RI de Cabo, Rafael/E-7996-2010; de Cabo, Rafael/J-5230-2016; OI de Cabo, Rafael/0000-0002-3354-2442; , rafael/0000-0003-2830-5693 NR 31 TC 28 Z9 28 U1 1 U2 7 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0161-9152 J9 AGE JI Age PD MAR PY 2005 VL 27 IS 1 BP 17 EP 25 DI 10.1007/s11357-005-3286-2 PG 9 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 121FO UT WOS:000243143700004 PM 23598600 ER PT J AU Mattison, JA Croft, MA Dahl, DB Roth, GS Lane, MA Ingram, DK Kaufman, PL AF Mattison, J. A. Croft, M. A. Dahl, D. B. Roth, G. S. Lane, M. A. Ingram, D. K. Kaufman, P. L. TI Accommodative function in rhesus monkeys: effects of aging and calorie restriction SO AGE LA English DT Article DE accommodation; diet; Macaca mulatta; refraction; vision ID RETINAL GANGLION-CELLS; HUMAN CRYSTALLINE LENS; AGE-RELATED DECLINE; DIETARY RESTRICTION; CILIARY MUSCLE; DEPENDENT LOSS; PRESBYOPIA; RATS; PREVENTS; GLAUCOMA AB Numerous degenerative changes in the visual system occur with age, including a loss of accommodative function possibly related to hardening of the lens or loss of ciliary muscle mobility. The rhesus monkey is a reliable animal model for studying age-related changes in ocular function, including loss of accommodation. Calorie restriction (CR) is the only consistent intervention to slow aging and extend lifespan in rodents, and more recently the beneficial effects of CR have been reported in nonhuman primates. The goal of the present study was to evaluate age-related changes in ocular accommodation and the potential effect of long-term ( 98 years) CR on accommodation in male and female rhesus monkeys. Refraction, accommodation (Hartinger coincidence refractometer), and lens thickness (A-scan ultrasound) were measured in 97 male and female rhesus monkeys age 8-36 years under Telazol/acepromazine anesthesia. Refraction and accommodation measurements were taken before and after 40% carbachol corneal iontophoresis to induce maximum accommodation. Half the animals were in the control (CON) group and were fed approximately ad libitum. The CR group received 30% fewer calories than age- and weight-matched controls. Males were on CR for 12 years and females for 8 years. With increasing age, accommodative ability declined in both CON and CR monkeys by 1.03 +/- 0.12 ( P = 0.001) and 1.18 +/- 0.12 ( P = 0.001) diopters/year, respectively. The age- related decline did not differ significantly between the groups ( P = 0.374). Baseline lens thickness increased with age in both groups by 0.03 +/- 0.005 mm/ year ( P = 0.001) and 0.02 +/- 0.005 mm/year ( P = 0.001) for the CON and CR groups, respectively. The tendency for the lens to thicken with age occurred at a slower rate in the CR group vs. the CON group but the difference was not statistically significant ( P = 0.086). Baseline refraction was -2.8 +/- 0.55 and -3.0 +/- 0.62 diopters for CON and CR, respectively. Baseline refraction tended to become slightly more negative with age ( P = 0.070), but this trend did not differ significantly between the groups ( P = 0.587). In summary, there were no significant differences in the slope of the age- related changes in accommodation, lens thickness, or refraction in the carbachol-treated eyes due to diet. These data are consistent with previous findings of decreased accommodative ability in aging rhesus monkeys, comparable to the age- dependent decrease in accommodative ability in humans. This study is the first to indicate that the accommodative system may not benefit from CR. C1 NIA, Lab Expt Gerontol, Intramural Res Program, NIH, Baltimore, MD 21224 USA. Univ Wisconsin, Dept Ophthalmol & Visual Sci, Madison, WI 53792 USA. Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI 53792 USA. RP Mattison, JA (reprint author), NIA, Lab Expt Gerontol, Intramural Res Program, NIH, Baltimore, MD 21224 USA. EM mattisonj@mail.nih.gov NR 32 TC 2 Z9 3 U1 0 U2 4 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0161-9152 J9 AGE JI Age PD MAR PY 2005 VL 27 IS 1 BP 59 EP 67 DI 10.1007/s11357-005-4005-8 PG 9 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA 121FO UT WOS:000243143700008 PM 23598604 ER PT J AU Nilsson, LG Soderlund, H Berger, K Breteler, M de Ridder, M Dufouil, C Fuhrer, R Giampaoli, S Hofman, A Pajak, A Sans, S Schmidt, R Launer, LJ AF Nilsson, LG Soderlund, H Berger, K Breteler, M de Ridder, M Dufouil, C Fuhrer, R Giampaoli, S Hofman, A Pajak, A Sans, S Schmidt, R Launer, LJ TI Cognitive test battery of CASCADE: Tasks and data SO AGING NEUROPSYCHOLOGY AND COGNITION LA English DT Article ID MINI-MENTAL-STATE; WHITE-MATTER LESIONS; PROSPECTIVE MEMORY; EXAMINATION MMSE; COMPUTED-TOMOGRAPHY; ALZHEIMERS-DISEASE; CIGARETTE-SMOKING; PURDUE PEGBOARD; BRAIN-LESIONS; PERFORMANCE AB This paper presents the cognitive test battery used in the CASCADE Study (Cardiovascular Determinants of Dementia) for examining the consequences of cerebral white matter lesions and atrophy. The test battery includes nine different tasks assessing memory, executive function, and global cognitive function. Three episodic memory tasks were used in combinations to assess the role of attention and speed on encoding. Estimates of short- and long-term memory capacity were also derived front these three memory tasks. Semantic memory production / frontal lobe functions were assessed by means of a word fluency test. The Letter Digit Substitution test and the Stroop test were used to assess speed of processing and attention. Motor speed was measured with the Purdue Pegboard test, and global cognitive function was assessed by the Mini Mental State Examination. Overall performance data for the whole CASCADE sample and for each of eight study centers are presented for each test. Possible reasons for performance differences among study centers are discussed. C1 Stockholm Univ, Dept Psychol, S-10691 Stockholm, Sweden. Univ Munster, Inst Epidemiol & Social Med, Munster, Germany. Erasmus Univ, Sch Med, Dept Epidemiol & Biostat, NL-3000 DR Rotterdam, Netherlands. Hop La Pitie Salpetriere, Paris, France. UCL, London, England. Natl Inst Hlth, Rome, Italy. Jagiellonian Univ, Dept Clin Epidemiol & & Populat Studies, Coll Med, Krakow, Poland. Inst Hlth Studies, Dept Hlth & Social Secur, Barcelona, Spain. Karl Franzens Univ Graz, Dept Neurol, Graz, Austria. NIA, Epidemiol Demog Biometry Program, Bethesda, MD 20892 USA. RP Nilsson, LG (reprint author), Stockholm Univ, Dept Psychol, S-10691 Stockholm, Sweden. EM Inn@psychmax.psychology.su.se RI Dufouil, Carole/J-4968-2012; Soderlund, Hedvig/B-4060-2013; Breteler, Monique /J-5058-2014 NR 80 TC 8 Z9 8 U1 1 U2 3 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 1382-5585 J9 AGING NEUROPSYCHOL C JI Aging Neuropsychol. Cogn. PD MAR PY 2005 VL 12 IS 1 BP 32 EP 56 DI 10.1080/1.825580590925099 PG 25 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 915IZ UT WOS:000228299200002 ER PT J AU Oroszi, G Enoch, MA Chun, J Virkkunen, M Goldman, D AF Oroszi, G Enoch, MA Chun, J Virkkunen, M Goldman, D TI Thr105Ile, a functional polymorphism of histamine N-methyltransferase, is associated with alcoholism in two independent populations SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE HNMT; alcoholism; anxiety; genetics; histamine ID SINGLE NUCLEOTIDE POLYMORPHISM; BRAIN HISTAMINE; CONTAINING NEURONS; NERVOUS-SYSTEM; MOUSE-BRAIN; PHARMACOGENETICS; RECEPTORS; RELEASE; ANXIETY; MICE AB Background: Histamine is expressed in cortical and limbic areas that are involved in emotion and cognition and modulates these behaviors. H-1 receptor antagonists are sedative. Histamine N-methyltransferase (HNMT) catalyzes the N tau methylation of histamine, the sole pathway for termination of the neurotransmitter action of histamine in mammalian brain. A common and functionally significant polymorphism, a C314T transition in exon 4 of the HNMT gene results in a Thr105Ile substitution of the protein encoded. The Thr105 allele is associated with similar to 2-fold higher enzyme activity, leading to the prediction that it might be associated with diminished histamine levels, resulting in differences in anxiety, cognition, and sedation that play important roles in alcoholism. In two ethnically distinct populations, we tested whether the Thr105Ile polymorphism was associated with alcoholism and with harm avoidance, a dimensional measure of anxious personality. Methods: A 5' exonuclease assay (TaqMan) was used to genotype Thr105Ile in psychiatrically interviewed Finnish Caucasian (n = 218) and Plains American Indian (n = 186) alcoholics, along with ethnically matched, psychiatrically interviewed, controls (Finns: n = 313, Plains Indian: n = 140). Results: Ile105 allele frequencies were significantly lower in alcoholics compared with nonalcoholics in both populations (Finns: 0.12 vs. 0.17, chi(2) = 6, p = 0.015; Plains Indians: 0.03 vs. 0.08, chi(2) = 5, p = 0.023). Genotype distributions also differed significantly. In Finns, Ile105 showed borderline significance for an association with lower harm avoidance (p = 0.070) after correcting for alcoholism diagnosis. Conclusions: Decreased levels of brain histamine consequent to the Thr105 allele may result in higher levels of anxiety and, as a consequence, vulnerability to alcoholism. C1 NIAAA, Neurogenet Lab, NIH, Bethesda, MD USA. Univ Helsinki, Dept Psychiat, SF-00180 Helsinki, Finland. RP Oroszi, G (reprint author), 5625 Fishers Lane,Room 3532,MSC 9412, Rockville, MD 20852 USA. EM goroszi@mail.nih.gov RI Goldman, David/F-9772-2010 OI Goldman, David/0000-0002-1724-5405 NR 46 TC 26 Z9 26 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD MAR PY 2005 VL 29 IS 3 BP 303 EP 309 DI 10.1097/01.ALC.0000156128.28257.2E PG 7 WC Substance Abuse SC Substance Abuse GA 909VQ UT WOS:000227889200002 PM 15770103 ER PT J AU Wurst, FM Alling, C Araclottir, S Pragst, F Allen, JP Weinmann, W Marmillot, P Ghosh, P Lakshman, R Skipper, GE Neumann, T Spies, C Javors, M Johnson, BA Ait-Daoud, N Akhtar, F Roache, JD Litten, R AF Wurst, FM Alling, C Araclottir, S Pragst, F Allen, JP Weinmann, W Marmillot, P Ghosh, P Lakshman, R Skipper, GE Neumann, T Spies, C Javors, M Johnson, BA Ait-Daoud, N Akhtar, F Roache, JD Litten, R TI Emerging biomarkers: New directions and clinical applications SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE biomarkers; direct ethanol metabolites; apolipoprotein J; carbohydrate-deficient transferrin; gamma-glutamyl-transferase ID CARBOHYDRATE-DEFICIENT TRANSFERRIN; IONIZATION/TANDEM MASS-SPECTROMETRY; RANDOMIZED CONTROLLED-TRIAL; GAMMA-GLUTAMYL-TRANSFERASE; UPPER DIGESTIVE-TRACT; CARE-UNIT STAY; ETHYL GLUCURONIDE; ALCOHOL-CONSUMPTION; CONFIRMATORY ANALYSIS; APOLIPOPROTEIN-J AB This article summarizes content proceedings of a symposium held at the 2004 Research Society on Alcoholism Scientific Annual Meeting in Vancouver, Canada. The chairs were Friedrich M. Wurst and Raye Litten. The presentations were (1) Introduction, by Raye Litten; (2) Direct Ethanol Metabolites-On the Threshold From Science to Routine Use, by Friedrich M. Wurst; (3) Sialic Acid Index of Plasma Apolipoprotein J (SIJ) as a Viable Marker for Chronic Alcohol Consumption, by Philippe Marmillot; (4) The Emergence of Ethyl Glucuronide (EtG) Testing as a Tool in Monitoring Healthcare Professionals, by Gregory E. Skipper; (5) Application of Biomarkers for Alcohol Use Disorders in Clinical Practice, by Tim Neumann; (6) Utility of Biomarkers in Assessing the Efficacy of Medications for Treating Alcoholism, by Marty Javors; and (7) Discussion, by Raye, Litten. C1 Univ Basel, Psychiat Univ Hosp, CH-4025 Basel, Switzerland. Lund Univ, Dept Clin Neurochem, Lund, Sweden. Univ Berlin, Inst Med Legale, Freiburg, Germany. Pacific Inst Res & Evaluat, Calverton, MD USA. George Washington Univ, Med Ctr, Washington, DC 20037 USA. Vet Affairs Med Ctr, Dept Vet, Lipid Res Lab, Washington, DC USA. Bio Probes Inc, Gaithersburg, MD USA. Univ Alabama, Med Sch Birmingham, Montgomery, AL USA. Alabama Phys Hlth Program, Montgomery, AL USA. Univ Hosp Charite, Dept Anesthesiol & Intens Care Med, Berlin, Germany. Univ Texas, Hlth Sci Ctr, Dept Psychiat, San Antonio, TX USA. Univ Texas, Hlth Sci Ctr, Dept Pharmacol, San Antonio, TX USA. Univ Texas, Hlth Sci Ctr, START Ctr, San Antonio, TX USA. Univ Virginia, Sch Med, Dept Psychiat, Charlottesville, VA 22908 USA. NIAAA, NIH, Bethesda, MD USA. RP Wurst, FM (reprint author), Univ Basel, Psychiat Univ Hosp, Wilhelm Klein Str 27, CH-4025 Basel, Switzerland. EM ftiedrich.wurst@pukbasel.ch OI LAKSHMAN, RAJ/0000-0003-2415-4509 NR 43 TC 35 Z9 37 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD MAR PY 2005 VL 29 IS 3 BP 465 EP 473 DI 10.1097/01.ALC.0000156082.08248.AB PG 9 WC Substance Abuse SC Substance Abuse GA 909VQ UT WOS:000227889200022 PM 15770123 ER PT J AU Wilfond, BS Ravitsky, V AF Wilfond, BS Ravitsky, V TI On the proliferation of bioethics sub-disciplines: Do we really need "genethics" and "neuroethics"? SO AMERICAN JOURNAL OF BIOETHICS LA English DT Editorial Material C1 NHGRI, Warren G Magnuson Clin Ctr, NIH, Bethesda, MD 20892 USA. RP Wilfond, BS (reprint author), NHGRI, Warren G Magnuson Clin Ctr, NIH, Bethesda, MD 20892 USA. NR 5 TC 10 Z9 12 U1 0 U2 3 PU ROUTLEDGE TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1526-5161 J9 AM J BIOETHICS JI Am. J. Bioeth. PD MAR-APR PY 2005 VL 5 IS 2 BP 20 EP 21 DI 10.1080/15265'160590960924 PG 2 WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical SC Social Sciences - Other Topics; Medical Ethics; Social Issues; Biomedical Social Sciences GA 946OD UT WOS:000230580800005 PM 16036690 ER PT J AU O'Connor, CM Gottlieb, S Bourque, JM Krause-Steinrauf, H Anand, I Anderson, JL Plehn, JF Silver, MA White, M Carson, P AF O'Connor, CM Gottlieb, S Bourque, JM Krause-Steinrauf, H Anand, I Anderson, JL Plehn, JF Silver, MA White, M Carson, P CA BEST Invest TI Impact of nonfatal myocardial infarction on outcomes in patients with advanced heart failure and the effect of Bucindolol therapy SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID LEFT-VENTRICULAR DYSFUNCTION; CONVERTING-ENZYME-INHIBITOR; RANDOMIZED CONTROLLED-TRIAL; EJECTION FRACTIONS; UNSTABLE ANGINA; SURVIVAL TRIAL; CARVEDILOL; MORTALITY; METOPROLOL; MORBIDITY AB We sought to identify the clinical characteristics and outcomes of patients who had advanced heart failure and nonfatal myocardial infarction (MI) in the beta-Blocker Evaluation of Survival Trial (BEST) and to investigate whether bucindolol alters the risk of developing nonfatal MI. Of the 2,708 patients enrolled in the study, 142 had suspected MI and 69 had confirmed MI; there were 860 deaths overall. The rate of nonfatal MI in the BEST was low over the 4.1 years of follow-up (4.8% had suspected events and 2.4% had adjudicated events) and was similar to that in high-risk populations. Cox's proportional hazard model with 23 prespecified candidate variables associated advanced age, heart failure symptoms, male gender, ischemic etiology, diabetes, and hypertension with nonfatal MI or cardiovascular death. The 2-year mortality rate was 56% for the cohort that had suspected nonfatal MI versus 30% for the cohort that did not (p = 0.01). Likewise, the risk of hospitalization for congestive heart failure was twofold greater. Beta-blocker therapy with bucindolol resulted in a 52% decrease in suspected nonfatal MI (2.9% vs 5.5%, p = 0.001). In conclusion, nonfatal MI occurs at low rates but increases the risks for mortality and hospitalization in patients who have advanced heart failure. Beta-blocker therapy with bucindolol appears to attenuate the risk of nonfatal MI in this population. (C) 2005 by Excerpta Medica Inc. C1 Duke Univ, Med Ctr, Div Cardiol, Dept Med, Durham, NC 27710 USA. Baltimore VAMC, Baltimore, MD USA. NHLBI, Bethesda, MD 20892 USA. Minneapolis VAMC, Minneapolis, MN USA. Univ Utah, Hlth Sci Ctr, Salt Lake City, UT 84112 USA. Advocate Christ Med Ctr, Oak Lawn, IL USA. Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada. Washington DC VAMC, Washington, DC USA. RP O'Connor, CM (reprint author), Duke Univ, Med Ctr, Div Cardiol, Dept Med, Box 3356,Room 7401-A Duke N, Durham, NC 27710 USA. EM oconn002@mc.duke.edu NR 28 TC 8 Z9 8 U1 0 U2 2 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAR 1 PY 2005 VL 95 IS 5 BP 558 EP 564 DI 10.1016/j.amjcard.2004.11.001 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 899PH UT WOS:000227156400002 PM 15721091 ER PT J AU Gardin, JM Iribarren, C Detrano, RC Liu, K Schreiner, PJ Loria, CM Wong, ND AF Gardin, JM Iribarren, C Detrano, RC Liu, K Schreiner, PJ Loria, CM Wong, ND TI Relation of echocardiographic left ventricular mass, geometry and wall stress, and left atrial dimension to coronary calcium in young adults (The CARDIA Study) SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID BEAM COMPUTED-TOMOGRAPHY; RISK-FACTORS; PROGNOSTIC VALUE; HEART-DISEASE; EVENTS; ATHEROSCLEROSIS; PREVALENCE; MORTALITY; STROKE; WOMEN AB We examined the relation of measures of echocardiographic left ventricular mass and geometry with coronary artery calcium (CAC) in 2,724 young adults. After adjustment for other coronary risk factors, left atrial dimension remained associated with the presence of CAC, and among subjects positive for CAC, left ventricular mass, end-systolic stress, and septal and posterior wall thicknesses in diastole remained associated with an increased extent of CAC. (C)2005 by Excerpta Medica Inc. C1 Univ Calif Irvine, Heart Dis Prevent Program, Irvine, CA 92697 USA. Kaiser Permanente, Oakland, CA USA. St John Hosp & Med Ctr, Detroit, MI USA. Harbor UCLA Res & Educ Inst, Torrance, CA USA. Northwestern Univ, Chicago, IL 60611 USA. Univ Minnesota, Minneapolis, MN 55455 USA. NHLBI, NIH, Bethesda, MD 20892 USA. RP Gardin, JM (reprint author), Univ Calif Irvine, Heart Dis Prevent Program, C240 Med Sci, Irvine, CA 92697 USA. EM ndwong@uci.edu FU NHLBI NIH HHS [N01-HC-05187, N01-HC-48050, N01-HC-48048, N01-HC-95095, N01-HC-45134, N01-HC-48047, N01-HC-48049] NR 14 TC 12 Z9 12 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 USA SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAR 1 PY 2005 VL 95 IS 5 BP 626 EP 629 DI 10.1016/j.amjcard.2004.11.010 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 899PH UT WOS:000227156400016 PM 15721105 ER PT J AU Stark, KD Pawlosky, RJ Beblo, S Murthy, M Flanagan, VP Janisse, J Buda-Abela, M Rockett, H Whitty, JE Sokol, RJ Hannigan, JH Salem, N AF Stark, KD Pawlosky, RJ Beblo, S Murthy, M Flanagan, VP Janisse, J Buda-Abela, M Rockett, H Whitty, JE Sokol, RJ Hannigan, JH Salem, N TI Status of plasma folate after folic acid fortification of the food supply in pregnant African American women and the influences of diet, smoking, and alcohol consumption SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE 5-methyltetrahydrofolic acid; folate; folic acid; fortification; African American women; pregnancy; nutrition; smoking; alcohol; electrospray mass spectrometry; human plasma; polyunsaturated fatty acids ID NEURAL-TUBE DEFECTS; UNITED-STATES; HOMOCYSTEINE CONCENTRATIONS; SCREENING QUESTIONNAIRES; FREQUENCY; SERUM; SUPPLEMENTATION; VALIDATION; NUTRITION; KNOWLEDGE AB Background: African American women and socioeconomically challenged women are at risk of compromised folate status and, thus, of folate-related birth defects. Data are limited on circulating folate concentrations in pregnant African American women after folic acid fortification of the food supply was implemented. Objective: The objective was to determine the influence of smoking and alcohol consumption on plasma 5-methyltetrahydrofolic acid (5-MTHFA) concentrations in pregnant African American women. Design: Alcohol consumption, smoking exposure, and other characteristics of pregnant African American women reporting to an inner-city antenatal clinic were assessed. At 24 wk of gestation, blood samples and food-frequency intake data were collected. Plasma 5-MTHFA concentrations were determined by liquid chromatography-mass spectrometry for 116 subjects and examined in a correlational study design. Results: Dietary folate and markers of alcohol consumption were positively associated, whereas exposure to smoke was negatively associated with plasma 5-MTHFA. More than one-half of the participants in this population failed to meet the recommended dietary allowance for dietary folate equivalents of 600 mu g/d during pregnancy. Conclusions: Most inner-city African American women are not meeting the recommended dietary allowance for dietary folate during pregnancy, and smoking may further compromise their folate status. Programs to reduce smoking and raise awareness about the importance of folate and multivitamin supplementation during pregnancy need to target this population. C1 NIAAA, Div Intramural Clin & Biol Res, Lab Membrane Biochem & Biophys, NIH, Rockville, MD 20852 USA. USDA, Beltsville Human Nutr Res Ctr, Food Composit Lab, Beltsville, MD USA. Harvard Univ, Sch Med, Dept Med, Brigham & Womens Hosp, Boston, MA USA. Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA. RP Salem, N (reprint author), NIAAA, Div Intramural Clin & Biol Res, Lab Membrane Biochem & Biophys, NIH, 5625 Fishers Lane,Room 3N-07, Rockville, MD 20852 USA. EM nsalem@niaaa.nih.gov RI Stark, Ken/I-1347-2016 OI Stark, Ken/0000-0001-7828-4072 FU NIAAA NIH HHS [N01-AA83019] NR 41 TC 18 Z9 19 U1 0 U2 6 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998 USA SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAR PY 2005 VL 81 IS 3 BP 669 EP 677 PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 905KD UT WOS:000227566100020 PM 15755838 ER PT J AU Hampson, NB Hampson, LA AF Hampson, NB Hampson, LA TI Inducing high levels of carbon monoxide in a tent SO AMERICAN JOURNAL OF EMERGENCY MEDICINE LA English DT Letter C1 Virginia Mason Med Ctr, Ctr Hyperbar Med, Seattle, WA 98101 USA. NIH, Dept Clin Bioeth, Bethesda, MD 20892 USA. RP Hampson, NB (reprint author), Virginia Mason Med Ctr, Ctr Hyperbar Med, Seattle, WA 98101 USA. EM neil.hampson@vmmc.org NR 5 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0735-6757 J9 AM J EMERG MED JI Am. J. Emerg. Med. PD MAR PY 2005 VL 23 IS 2 BP 204 EP 204 DI 10.1016/j.ajem.2004.09.030 PG 1 WC Emergency Medicine SC Emergency Medicine GA 909HI UT WOS:000227850600027 PM 15765348 ER PT J AU Agrawal, S Bhupinderjit, A Bhutani, MS Boardman, L Nguyen, C Romero, Y Srinvasan, R Figueroa-Moseley, C AF Agrawal, S Bhupinderjit, A Bhutani, MS Boardman, L Nguyen, C Romero, Y Srinvasan, R Figueroa-Moseley, C TI Colorectal cancer in African Americans SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Review ID FECAL OCCULT BLOOD; COMPUTED TOMOGRAPHIC COLONOGRAPHY; BLACK-WHITE DIFFERENCES; COLON-CANCER; RACIAL-DIFFERENCES; UNITED-STATES; ADENOMATOUS POLYPS; SCREENING SIGMOIDOSCOPY; ANATOMICAL DISTRIBUTION; MEDICARE BENEFICIARIES AB Colorectal cancer in African Americans has an increased incidence and mortality relative to Whites. The mean age of CRC development in African Americans is younger than that of Whites. There is also evidence for a more proximal colonic distribution of cancers and adenomas in African Americans. African Americans are less likely to have undergone diagnostic testing and screening for colorectal cancer. Special efforts are needed to improve colorectal cancer screening participation rates in African Americans. Clinical gastroenterologists should play an active role in educating the public and primary care physicians about special issues surrounding colorectal cancer in African Americans. Community healthcare groups and gastrointestinal specialists should develop culturally sensitive health education programs for African Americans regarding colorectal cancer. The high incidence and younger age at presentation of colorectal cancer in African Americans warrant initiation of colorectal cancer screening at the age 45 yr rather than 50 yr. C1 NIDDK, NIH, Bethesda, MD 20892 USA. RP Agrawal, S (reprint author), NIDDK, NIH, 6707 Democracy Blvd,Democracy Z,Room 669, Bethesda, MD 20892 USA. NR 100 TC 151 Z9 152 U1 1 U2 3 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD MAR PY 2005 VL 100 IS 3 BP 515 EP 523 DI 10.1111/j.1572-0241.2005.41829.x PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 907EJ UT WOS:000227697900004 PM 15743345 ER PT J AU Schron, EB Jenkins, LS AF Schron, EB Jenkins, LS TI Quality of life in older patients with atrial fibrillation SO AMERICAN JOURNAL OF GERIATRIC CARDIOLOGY LA English DT Review ID LONGITUDINAL DATA; RANDOMIZED-TRIAL; CLINICAL-TRIALS; RHYTHM-CONTROL; IMPAIRMENT; MANAGEMENT; OUTCOMES; THERAPY; INDEX AB This review summarizes what is known about quality of life (QOL) in older patients with atrial fibrillation (AF). The studies reviewed in this paper represent an increasingly broad repertoire of therapies for the treatment of AF and suggest that QOL in older patients does improve with treatment. The most dramatic improvements in QOL are noted in patients who are highly symptomatic and have poorer QOL at baseline. The data from studies where ablation and pacing therapy is used for treatment in patients with refractory AF vividly demonstrate this statement. There is also evidence of improvement in QOL in those with less severe symptoms, though it is extremely challenging to measure improvements in older patients who are asymptomatic (e.g., silent AF) or mildly symptomatic. Recommendations about new knowledge needed to optimize outcomes, Particularly QOL, in patients with AF are based on these findings and the gaps in existing knowledge. C1 NHLBI, Clin Trials Sci Res Grp, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20817 USA. Univ Maryland, Sch Nursing, Baltimore, MD USA. RP Schron, EB (reprint author), NHLBI, Clin Trials Sci Res Grp, Div Epidemiol & Clin Applicat, NIH, 6701 Rockledge Dr,Room 8144,MSC 7936, Bethesda, MD 20817 USA. EM schrone@nih.gov NR 26 TC 2 Z9 2 U1 0 U2 0 PU LE JACQ LTD PI DARIEN PA 3 PARKLANDS DRIVE, DARIEN, CT 06820 USA SN 1076-7460 J9 AM J GERIATR CARDIOL JI Am. J. Geriatr. Cardiol. PD MAR-APR PY 2005 VL 14 IS 2 BP 87 EP 90 DI 10.1111/j.1076-7460.2005.02283.x PG 4 WC Cardiac & Cardiovascular Systems; Geriatrics & Gerontology SC Cardiovascular System & Cardiology; Geriatrics & Gerontology GA 010GN UT WOS:000235175400008 PM 15785150 ER PT J AU Voorhees, CC Murray, D Welk, G Birnbaum, A Ribisl, KM Johnson, CC Pfeiffer, KA Saksvig, B Jobe, JB AF Voorhees, CC Murray, D Welk, G Birnbaum, A Ribisl, KM Johnson, CC Pfeiffer, KA Saksvig, B Jobe, JB TI The role of peer social network factors and physical activity in adolescent girls SO AMERICAN JOURNAL OF HEALTH BEHAVIOR LA English DT Article DE social networks; social support; physical activity; adolescents; girls ID CIGARETTE-SMOKING; ACTIVITY QUESTIONNAIRE; OLDER CHILDREN; EXERCISE AB Objective: To study the relationship between peer-related physical activity (PA) social networks and the PA of adolescent girls. Methods: Cross-sectional, convenience sample of adolescent girls. Mixed-model linear regression analyses to identify significant correlates of self-reported PA while accounting for correlation of girls in the same school. Results: Younger girls were more active than older girls. Most activity-related Peer social network items were related to PA levels. More PA with friends was significantly related to self-reported PA in multivariate analyses. Conclusions: Frequency of PA with friends was an important correlate of PA among the peer network variables for adolescent girls. C1 Univ Maryland, Dept Publ & Community Hlth, College Pk, MD 20742 USA. Univ Maryland, Dept Kinesiol, College Pk, MD 20742 USA. Univ Memphis, Dept Psychol, Memphis, TN 38152 USA. Iowa State Univ, Dept Hlth & Human Performance, Ames, IA USA. Weill Cornell Med Ctr, Dept Publ Hlth, New York, NY USA. UNC, Sch Publ Hlth, Dept Hlth Behav & Hlth Educ, Chapel Hill, NC USA. Tulane Univ, Dept Community Hlth Sci, Sch Publ Hlth & Trop Med, New Orleans, LA 70118 USA. Univ Maryland, Dept Kinesiol, Baltimore, MD 21201 USA. NHLBI, Div Epidemiol & Clin Applicat, Behav Med Sci Res Grp, Bethesda, MD 20892 USA. RP Voorhees, CC (reprint author), Univ Maryland, Dept Publ & Community Hlth, 2358 HHP Bldg,Valley Dr, College Pk, MD 20742 USA. EM ccv@umd.edu RI Loureiro, Nuno/I-6400-2012; Ribisl, Kurt/C-4867-2015 OI Loureiro, Nuno/0000-0002-1166-3219; Ribisl, Kurt/0000-0003-3318-8524 FU NHLBI NIH HHS [U01 HL066857, U01 HL066845, U01 HL066845-01, U01 HL066852, U01 HL066852-01, U01 HL066853, U01 HL066853-01, U01 HL066855, U01 HL066855-01, U01 HL066856, U01 HL066856-01, U01 HL066857-01, U01 HL066858-01, U01HL-66845, U01HL-66852, U01HL-66856, U01HL-66857, U01HL-66858, U01HL-6853] NR 26 TC 90 Z9 92 U1 3 U2 11 PU PNG PUBLICATIONS PI STAR CITY PA PO BOX 4593, STAR CITY, WV 26504-4593 USA SN 1087-3244 J9 AM J HEALTH BEHAV JI Am. J. Health Behav. PD MAR-APR PY 2005 VL 29 IS 2 BP 183 EP 190 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 898WU UT WOS:000227107700009 PM 15698985 ER PT J AU Connor, TH Sessink, PJM Harrison, BR Pretty, JR Peters, BG Alfaro, RM Bilos, A Beckmann, G Bing, MR Anderson, LM DeChristoforo, R AF Connor, TH Sessink, PJM Harrison, BR Pretty, JR Peters, BG Alfaro, RM Bilos, A Beckmann, G Bing, MR Anderson, LM DeChristoforo, R TI Surface contamination of chemotherapy drug vials and evaluation of new vial-cleaning techniques: Results of three studies SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY LA English DT Article DE antineoplastic agents; cisplatin; contamination; cyclophosphamide; decontamination; fluorouracil; ifosfamide; injections; manufacturing; pharmacy; vials ID CHROMATOGRAPHY-MASS-SPECTROMETRY; ANTINEOPLASTIC AGENTS; CLOSED-SYSTEM; ENVIRONMENTAL CONTAMINATION; OCCUPATIONAL EXPOSURE; PHARMACY TECHNICIANS; HOSPITAL PERSONNEL; CYCLOPHOSPHAMIDE; URINE; IFOSFAMIDE AB Purpose. The results of three studies that describe the external contamination of chemotherapy drug vials are presented. New techniques for the improved decontamination of vials containing cisplatin are also described. Summary. Study 1 evaluated the external contamination of drug vials with cyclophosphamide and ifosfamide in a pharmacy setting. Widespread contamination of the outside of drug vials was found with each drug. Study 2 evaluated the surface contamination of drug vials with cyclophosphamide and fluorouracil in three pharmacies. Sporadic contamination with fluorouracil was detected, while cyclophosphamide was found on most vials. In study 3, investigators compared the decontamination abilities of a standard decontamination procedure at the manufacturer level with an improved decontamination procedure and the use of sleeves to further decrease contamination. Though the methods of each study reported herein differed, the outcomes were similar. All chemotherapy drug vials studied demonstrated levels of contamination with the drug well above the limit of detection. Improved decontamination procedures, combined with the use of protective sleeves, reduced the level of platinum contamination by 90%, suggesting that standard decontamination procedures should be reconsidered. Conclusion. The results of these studies are consistent with several others that have reported contamination of the outside surface of drug vials for a number of chemotherapy drugs. Contamination can be reduced by using decontamination equipment and protective sleeves during the manufacturing process. C1 NIOSH, Div Appl Res & Technol, Cincinnati, OH 45226 USA. Exposure Control BV, Wijchen, Netherlands. Vet Affairs Med Ctr, Hematol Oncol Sect, St Louis, MO USA. Washington Univ, Sch Med, Alvin J Siteman Canc Ctr, St Louis, MO USA. NIH, Clin Pharmacokinet Res Lab, Dept Pharm, Ctr Clin, Bethesda, MD 20892 USA. Univ Nijmegen, Med Ctr, Dept Epidemiol & Biostat, Res Lab Mol Epidemiol, Nijmegen, Netherlands. St Louis Univ, Ctr Canc, St Louis, MO 63103 USA. Univ Alabama, Dept Environm Hlth, Birmingham, AL USA. RP Connor, TH (reprint author), NIOSH, Div Appl Res & Technol, MS C-23,4676 Columbia Pkwy, Cincinnati, OH 45226 USA. EM tmc6@cdc.gov RI Connor, Thomas/B-7937-2011 NR 43 TC 46 Z9 53 U1 0 U2 3 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 USA SN 1079-2082 J9 AM J HEALTH-SYST PH JI Am. J. Health-Syst. Pharm. PD MAR 1 PY 2005 VL 62 IS 5 BP 475 EP 484 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 903UR UT WOS:000227451600013 PM 15745910 ER PT J AU Reiner, AP Ziv, E Lind, DL Nievergelt, CM Schork, NJ Cummings, SR Phong, A Burchard, EG Harris, TB Psaty, BM Kwok, PY AF Reiner, AP Ziv, E Lind, DL Nievergelt, CM Schork, NJ Cummings, SR Phong, A Burchard, EG Harris, TB Psaty, BM Kwok, PY TI Population structure, admixture, and aging-related phenotypes in African American adults: The cardiovascular health study SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID MULTILOCUS GENOTYPE DATA; DISEASE RISK-FACTORS; ADMIXED POPULATIONS; ALLELIC ASSOCIATION; RACIAL-DIFFERENCES; GENETIC ADMIXTURE; ATHEROSCLEROSIS; STRATIFICATION; PROPORTIONS; INFERENCE AB U.S. populations are genetically admixed, but surprisingly little empirical data exists documenting the impact of such heterogeneity on type I and type II error in genetic-association studies of unrelated individuals. By applying several complementary analytical techniques, we characterize genetic background heterogeneity among 810 self-identified African American subjects sampled as part of a multisite cohort study of cardiovascular disease in older adults. On the basis of the typing of 24 ancestry-informative biallelic single-nucleotide-polymorphism markers, there was evidence of substantial population substructure and admixture. We used an allele-sharing-based clustering algorithm to infer evidence for four genetically distinct subpopulations. Using multivariable regression models, we demonstrate the complex interplay of genetic and socioeconomic factors on quantitative phenotypes related to cardiovascular disease and aging. Blood glucose level correlated with individual African ancestry, whereas body mass index was associated more strongly with genetic similarity. Blood pressure, HDL cholesterol level, C-reactive protein level, and carotid wall thickness were not associated with genetic background. Blood pressure and HDL cholesterol level varied by geographic site, whereas C-reactive protein level differed by occupation. Both ancestry and genetic similarity predicted the number and quality of years lived during follow-up, but socioeconomic factors largely accounted for these associations. When the 24 genetic markers were tested individually, there were an excess number of marker-trait associations, most of which were attenuated by adjustment for genetic ancestry. We conclude that the genetic demography underlying older individuals who self identify as African American is complex, and that controlling for both genetic admixture and socioeconomic characteristics will be required in assessing genetic associations with chronic-disease-related traits in African Americans. Complementary methods that identify discrete subgroups on the basis of genetic similarity may help to further characterize the complex biodemographic structure of human populations. C1 Univ Washington, Cardiovasc Hlth Res Unit, Dept Epidemiol, Seattle, WA 98101 USA. Univ Washington, Dept Med, Seattle, WA 98101 USA. Univ Washington, Dept Lab Med, Seattle, WA 98101 USA. Univ Washington, Dept Hlth Serv, Seattle, WA 98101 USA. NIA, Geriatr Epidemiol Sect, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA. Univ Calif San Diego, Dept Psychiat, Polymorphism Res Lab, La Jolla, CA 92093 USA. Calif Pacific Med Ctr, San Francisco Coordinating Ctr, San Francisco, CA USA. Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA. Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Biostat, San Francisco, CA 94143 USA. RP Reiner, AP (reprint author), Univ Washington, Cardiovasc Hlth Res Unit, Dept Epidemiol, 1730 Minor Ave,Suite 1360, Seattle, WA 98101 USA. EM apreiner@u.washington.edu RI Kwok, Pui-Yan/F-7725-2014; Ziv, Elad/L-5396-2014; OI Kwok, Pui-Yan/0000-0002-5087-3059; Nievergelt, Caroline/0000-0001-5766-8923 FU NHLBI NIH HHS [N01-HC-85079, N01-HC-85080, N01 HC035129, N01 HC015103, N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084, N01-HC-85085, N01-HC-85086, N01HC85079, N01HC85086] NR 50 TC 107 Z9 108 U1 1 U2 3 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD MAR PY 2005 VL 76 IS 3 BP 463 EP 477 DI 10.1086/428654 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA 895HO UT WOS:000226851900009 PM 15660291 ER PT J AU Chiba-Falek, O Kowalak, JA Smulson, ME Nussbaum, RL AF Chiba-Falek, O Kowalak, JA Smulson, ME Nussbaum, RL TI Regulation of alpha-synuclein expression by poly (ADP ribose) polymerase-1 (PARP-1) binding to the NACP-Rep1 polymorphic site upstream of the SNCA gene SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID NF-KAPPA-B; FAMILIAL PARKINSONS-DISEASE; POLY(ADP-RIBOSE) POLYMERASE; TRANSCRIPTIONAL ACTIVATION; NACP/ALPHA-SYNUCLEIN; LOCUS TRIPLICATION; SEQUENCE-ANALYSIS; ALLELIC VARIATION; LEWY BODIES; COACTIVATOR AB Alleles at NACP-Rep1, the polymorphic microsatellite repeat located similar to 10 kb upstream of the alpha-synuclein gene ( SNCA), are associated, in some reports, with differing risks of sporadic Parkinson disease (PD). We showed previously that NACP-Rep1 acts as a negative modulator of SNCA transcription, with an effect that varied threefold among different NACP-Rep1 alleles. Given that duplications and triplications of SNCA have been implicated in familial Parkinson disease (PD), even a 1.5 - 2-fold increase in alpha-synuclein expression may, over many decades, contribute to PD. Thus, the association of different NACP-Rep1 alleles with PD may be a consequence of polymorphic differences in transcriptional regulation of SNCA. Here we aimed to identify the factor(s) that bind to NACP-Rep1 and potentially contribute to SNCA transcriptional modulation, by pulling down proteins that bind to NACP- Rep1 and identifying them by mass spectrometry. One of these proteins was poly-(ADP-ribose) transferase/ polymerase-1 (PARP-1), a DNA-binding protein and transcriptional regulator. Electrophoresis mobility shift and chromatin immunoprecipitation assays showed specific binding of PARP-1 to NACP- Rep1. Inhibition of PARP-1's catalytic domain increased the endogenous SNCA mRNA levels in cultured SH-SY5Y cells. Furthermore, PARP-1 binding to NACP- Rep1 specifically reduced the transcriptional activity of the SNCA promoter/enhancer in luciferase reporter assays. This down-regulation effect of PARP-1 depended on NACP- Rep1 being present in the construct and was abrogated by inhibiting PARP-1's catalytic activity with 3-aminobenzamide. The association of different NACP- Rep1 alleles with PD may be mediated, in part, by the effect of PARP-1, as well as other factors, on SNCA expression. C1 NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA. NIMH, Lab Neurotoxicol, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Med Ctr, Dept Biochem & Mol Biol, Washington, DC 20007 USA. RP Nussbaum, RL (reprint author), NHGRI, Genet Dis Res Branch, NIH, 49 Convent Dr,MSC 4472, Bethesda, MD 20892 USA. EM rlnuss@mail.nih.gov FU NCI NIH HHS [P01CA-74175, P01 CA074175] NR 49 TC 58 Z9 59 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD MAR PY 2005 VL 76 IS 3 BP 478 EP 492 DI 10.1086/428655 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA 895HO UT WOS:000226851900010 PM 15672325 ER PT J AU McInerney-Leo, A Biesecker, BB Hadley, DW Kase, RG Giambarresi, TR Johnson, E Lerman, C Struewing, JP AF McInerney-Leo, A Biesecker, BB Hadley, DW Kase, RG Giambarresi, TR Johnson, E Lerman, C Struewing, JP TI BRCA1/2 testing in hereditary breast and ovarian cancer families II: Impact on relationships SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE family cohesion; conflict; expressiveness; genetic counseling; cancer risk testing ID SOCIAL SUPPORT; PSYCHOLOGICAL DISTRESS; HUNTINGTONS-DISEASE; STRESS; SUSCEPTIBILITY; COMMUNICATION; ADJUSTMENT; MEMBERS AB Members of hereditary breast and ovarian cancer (HBOC) families often express concern during genetic counseling about the impact of BRCA1/2 testing on close relatives. Yet whether there are likely to be adverse effects of either the decision to undergo genetic testing or the results of testing on family relationships is unknown. One purpose of this study was to assess the impact on close family relationships. Within a randomized trial of breast cancer genetic counseling methods, members of 13 HBOC families were offered BRCA1/2 testing for a known family mutation. The Family Relationship Index (FRI) of the Family Environment Scale (FES) was used to measure perceived family cohesion, conflict, and expressiveness at baseline and again 6-9 months following the receipt of test results, or at the equivalent time for those who declined testing. Participants (n = 212) completed baseline and follow-up questionnaires. Comparisons were made between testers and non-testers as well as between those who tested positive and negative for the family mutation. One hundred eighty-one participants elected to undergo genetic testing (85%) and 47 (26%) were identified to have a mutation. After adjusting for baseline family relationship scores, counseling intervention, gender and marital status, non-testers reported a greater increase in expressiveness (P = 0.006) and cohesion (P = 0.04) than testers. Individuals who tested positive reported a decrease in expressiveness (P = 0.07), although as a trend. Regardless of test decision or test result, those who were randomized to a client-centered counseling intervention reported a decrease in conflict (P = 0.006). Overall, study results suggest that undergoing genetic testing and learning ones BRCA1/2 status may affect family relationships. Those individuals who declined testing reported feeling closer to family members and more encouraged to express emotions to other family members demonstrating potential benefit from the offer of testing. Since those who tested positive reported feeling less encouraged to express their emotions within the family, we recommend helping clients to identify others with whom they feel comfortable sharing their thoughts and feelings about their positive gene status and increased cancer risk. Published 2005 Wiley-Liss, Inc. C1 NHGRI, Med Genet Branch, Bethesda, MD 20892 USA. NCI, Genet Epidemiol Branch, Bethesda, MD 20892 USA. Westat Res, Rockville, MD USA. Johns Hopkins Biostat Ctr, Baltimore, MD USA. Univ Penn, Ctr Canc, Philadelphia, PA 19104 USA. NCI, Lab Populat Genet, Bethesda, MD 20892 USA. RP Biesecker, BB (reprint author), NHGRI, Med Genet Branch, Bldg 10,Room 10C101,10 Ctr Dr,MSC 1852, Bethesda, MD 20892 USA. EM barbarab@nhgri.nih.gov RI Struewing, Jeffery/C-3221-2008; Struewing, Jeffery/I-7502-2013 OI Struewing, Jeffery/0000-0002-4848-3334 NR 23 TC 26 Z9 27 U1 1 U2 2 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4825 J9 AM J MED GENET A JI Am. J. Med. Genet. A PD MAR 1 PY 2005 VL 133A IS 2 BP 165 EP 169 DI 10.1002/ajmg.a.30566 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 900CX UT WOS:000227194100009 PM 15633195 ER PT J AU Schellinger, PD Chalela, JA Kang, DW Latour, LL Warach, S AF Schellinger, PD Chalela, JA Kang, DW Latour, LL Warach, S TI Diagnostic and prognostic value of early MR imaging vessel signs in hyperacute stroke patients imaged < 3 hours and treated with recombinant tissue plasminogen activator SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article; Proceedings Paper CT 5th World Stroke Congress CY JUN 23-26, 2004 CL Vancouver, CANADA SP Int Stroke Soc, Canadian Stroke Consortium, Natl Stroke Assoc, Canadian Stroke Network ID INVERSION-RECOVERY IMAGES; ACUTE ISCHEMIC-STROKE; CEREBRAL-ARTERY; INTRACEREBRAL HEMORRHAGE; INTRAARTERIAL SIGNAL; MCA SIGN; EARLY CT; ANGIOGRAPHY; ENHANCEMENT; OCCLUSION AB BACKGROUND AND PURPOSE. Analogous to the CT hyperattenuated vessel sign (HMCAS), MR imaging may show hypo- or hyperintense vessels in acute ischemic stroke (AIS) patients. We assessed the diagnostic and prognostic strength of early MR imaging vessel signs in AIS patients treated with intravenous thrombolysis (IVT) within 3 hours of the onset of symptoms. METHODS: We studied AIS patients both treated with IVT and stroke MR imaged within 3 hours of the onset of symptoms and at 2 hours and 24 hours after treatment. We assessed the presence or absence of early vessel signs (hyperintense fluid-attenuated inversion recovery sign [FLAIR HVS]; gradient-echo susceptibility vessel sign [GRE SVS]) compared with a combined MR angiography/perfusion-weighted imaging reference and their strength for predicting clinical outcome (favorable vs. poor, independent vs. dependent, or dead, death), recanalization (by clot composition and flow), and hemorrhage in uni- and multivariate analysis. RESULTS: Fifty-six patients (age range, 76 years +/- 13 years; median National Institutes of Health stroke scale score [NIHSSS], 11) met the inclusion criteria. Forty-four patients (78.6%) had a vessel occlusion at baseline; 22 of them (50%) recanalized. Nineteen patients (33.9%) suffered some form of intracranial hemorrhage (ICH), 24 patients (42.9%) had an independent outcome, 18 patients (32.1%) a favorable outcome, and 14 patients died. Compared with our combined reference for vessel status PWI/MRA, the sensitivities of CT HMCAS, FLAIR HVS, and GRE SVS were 40%, 66%, and 34%, respectively, and improved during the hours that followed. Localization was accurately reflected by FLAIR HVS but not by GRE SVS. Only NIHSSS and age were independent predictors for recanalization and all clinical outcomes in multiple logistic regression analysis. CONCLUSION. Although early vessel signs can be helpful in the diagnosis of intravascular disease, they do not independently predict recanalization, ICH, or any of the three clinical outcomes in a multivariate logistic regression model. Thrombus composition as reflected by signal intensity characteristics on GRE and FLAIR does not predict the therapeutic effect of IVT. C1 NINDS, NIH, Bethesda, MD 20892 USA. Univ Heidelberg, Dept Neurol, Heidelberg, Germany. Univ Ulsan, Asan Med Ctr, Dept Neurol, Seoul, South Korea. RP Schellinger, PD (reprint author), Kopfklin, Dept Neurol, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany. NR 23 TC 87 Z9 94 U1 0 U2 1 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD MAR PY 2005 VL 26 IS 3 BP 618 EP 624 PG 7 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 906GK UT WOS:000227628500032 PM 15764589 ER PT J AU Gomez, R Romero, R Nien, JK Chaiworapongsa, T Medina, L Kim, YM Yoon, BH Carstens, M Espinoza, J Iams, JD Gonzalez, R AF Gomez, R Romero, R Nien, JK Chaiworapongsa, T Medina, L Kim, YM Yoon, BH Carstens, M Espinoza, J Iams, JD Gonzalez, R TI A short cervix in women with preterm labor and intact membranes: A risk factor for microbial invasion of the amniotic cavity SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE uterine cervix; ultrasound; chorioamnionitis; amniocentesis; preterm delivery ID BLOOD-CELL COUNT; FETAL INFLAMMATORY RESPONSE; POLYMERASE-CHAIN-REACTION; WHITE-MATTER LESIONS; IMMEDIATE POSTPARTUM TREATMENT; UMBILICAL-CORD PLASMA; C-REACTIVE PROTEIN; INTRAUTERINE INFECTION; INTRAAMNIOTIC INFECTION; UREAPLASMA-UREALYTICUM AB Objective: The purpose of this study was to determine whether there was a relationship between sonographic cervical length and the presence of culture-proven microbial invasion of the ammotic cavity in women with preterm labor and intact membranes. Study design: Ultrasonography and amniocentesis were performed in 401 patients admitted with preterm labor (22-35 weeks) and cervical dilatation of less than or equal to 3 cm. as assessed by digital examination. Cervical length was determined by transvaginal ultrasound at admission. Outcome variables were the presence of microbial invasion of the amniotic cavity (defined as a positive amniotic fluid culture) and the occurrence of preterm delivery before 35 weeks. Contingency tables x(2) test, receiver-operator characteristic (ROC) curves, and logistic regression were used for statistical analysis. Results: The prevalence of microbial invasion of the amniotic cavity was 7% (28/401). Spontaneous preterm delivery (less than or equal to 35 weeks) occurred in 21.4% (82/384) of patients. ROC curve analysis showed a significant relationship between the frequency of microbial invasion of the ammotic cavity and the length of the uterine cervix (area under the curve: 0.77; P <.005). Patients with a cervical length < 15 mm had a higher rate of a positive ammotic fluid culture than patients with a cervical length greater than or equal to 15 mm (26.3% [15/57] vs. 3.8% [13/344], respectively; P <.05). Moreover, patients with a short cervix (defined as < 15 mm) were more likely to deliver spontaneously before 35 weeks, 32 weeks, within 7 days, and within 48 hours of admission (P <.05 for all comparisons). Forty percent of patients (161/401) had a cervical length 30 mm. These patients had a very low risk of microbial invasion of the ammotic cavity (1.9% [3/161]), spontaneous delivery less than or equal to 35 weeks (4.5% [7/154]),less than or equal to 32 weeks (2.6% [2/76]), within 7 days (1.9% [3/154]), and within 48 hours (0% [0/154]) of admission. Conclusion: Endovaginal ultrasonographic examination of the uterine cervix in women with preterm labor identifies patients at increased risk for intrauterine infection. (C) 2005 Elsevier Inc. All rights reserved. C1 NICHD, Perinatol Res Branch, NIH, DHHS, Detroit, MI 48201 USA. Pontificia Univ Catolica Chile, Sotero Rio Hosp, Ctr Perinatal Diag & Res CEDIP, Puente Alto, Chile. Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA. Wayne State Univ, Sch Med, Dept Pathol, Detroit, MI 48201 USA. Seoul Natl Univ, Coll Med, Dept Obstet & Gynecol, Seoul, South Korea. Ohio State Univ, Dept Obstet & Gynecol, Columbus, OH 43210 USA. RP Romero, R (reprint author), NICHD, Perinatol Res Branch, NIH, DHHS, 3990 John R Blvd, Detroit, MI 48201 USA. EM warfiela@mail.nih.gov RI Yoon, Bo Hyun/H-6344-2011 NR 86 TC 68 Z9 70 U1 0 U2 2 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD MAR PY 2005 VL 192 IS 3 BP 678 EP 689 DI 10.1016/j.ajog.2004.10.624 PG 12 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 904DZ UT WOS:000227477600005 PM 15746658 ER PT J AU Poggi, SH Park, J Toso, L Abebe, D Roberson, R Woodard, JE Spong, CY AF Poggi, SH Park, J Toso, L Abebe, D Roberson, R Woodard, JE Spong, CY TI No phenotype associated with established lipopolysaccharide model for cerebral palsy SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 25th Annual Meeting of the Society-for-Maternal-Fetal-Medicine CY FEB 09-12, 2005 CL Reno, NV SP Soc Maternal Fetal Med DE cerebral palsy; periventricular leukomalacia; lipopolysaccharide rat ID WHITE-MATTER INJURY; INDUCED PRETERM BIRTH; INTRAUTERINE INFECTION; RAT-BRAIN; INFLAMMATION; PREGNANCY; LABOR; MICE; CYTOKINES; CHILDREN AB Objective: Cerebral palsy (CP) is associated with childhood spasticity, seizures, and paralysis. Oligodendrocyte damage resulting in periventicular leukomalacia (PVL) in the developing brain has been implicated. Animal models of CP have used prenatal hypoxia and infection with histopathology of PVL as the end point. To evaluate whether this histologic end point is associated with a CP phenotype, we reproduced a lipopolysaccharide (LPS) model for PVL, I and evaluated developmental, behavioral, and motor outcomes. Study design: On gestational day 15, Fischer 344 rats were intracervically injected with .1 mg/kg LPS (n = 5) or saline (n = 4). After delivery, evaluation for developmental milestones was performed on days I to 21 (LPS = 45; control = 30 pups). Males were also tested at 2.5 months using open-field, rotarod, and anxiety tests. On day 21, 2 pups/litter were perfused for immunohistochemistry, and stained with 2 oligodendrocyte antibodies: 2', d'-cyclic nucleotide phosphodiesterase (CNP), and myelin proteolipid protein (PLP) with relative densities of staining assessed using NIH Image software. Statistical analysis included Mann-Whitney U and analysis of variance (ANOVA). Results: LPS pups demonstrated decreased CNP (P =.04) and PLP (P =.06) staining, replicating the model. There was no difference seen in neonatal weight, righting, negative geotaxis, cliff aversion, rooting, forelimb grasp, audio startle, air righting, eye opening, and activity. Surprisingly, LPS-exposed neonatal rats mastered forelimb placement (P <.01) and surface righting (P =.02) earlier than control rats. There were no differences between adult groups in open field distance traveled (P =.8), open-field locomotion time (P =.6), rotarod (P =.6), or anxiety (P =.7). Conclusion: Histologic evidence of white matter damage can be replicated using an LPS model for intrauterine inflammation. Significant phenotypic differences consistent with the motor and cognitive damage sequelae of such lesions (ie, CP) were not demonstrated. When evaluating animal models, it is important to assess not only biochemical markers for human disease, but also clinically relevant phenotypes. (C) 2005 Elsevier Inc. All rights reserved. C1 NICHHD, NIH, Unit Perinatal & Dev Neurobiol, Bethesda, MD 20892 USA. Georgetown Univ Hosp, Dept Obstet & Gynecol, Washington, DC 20007 USA. NIAAA, NIH, Bethesda, MD USA. RP Poggi, SH (reprint author), INOVA Alexandria Hosp, Perinatal Diagnost Ctr, 4320 Seminary Rd, Alexandria, VA 22304 USA. EM sarah.poggi@inova.com NR 32 TC 30 Z9 36 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD MAR PY 2005 VL 192 IS 3 BP 727 EP 733 DI 10.1016/j.ajog.2004.12.053 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 904DZ UT WOS:000227477600011 PM 15746664 ER PT J AU Wren, PA Janz, NK Brubaker, L Fitzgerald, MP Weber, AM LaPorte, FB Wei, JT AF Wren, PA Janz, NK Brubaker, L Fitzgerald, MP Weber, AM LaPorte, FB Wei, JT CA Pelvic Floor Disorders Netork TI Reliability of health-related quality-of-life measures 1 year after surgical procedures for pelvic floor disorders SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT 70th Annual Meeting of the Central-Association-of-Obstetricians-and-Gynecologists CY OCT 01-04, 2003 CL La Jolla, CA SP Cent Assoc Obstet & Gynecol DE pelvic organ prolapse; urinary incontinence; quality of life ID URINARY-INCONTINENCE; SEVERITY INDEX; PATIENT; WOMEN; INSTRUMENT; SYMPTOMS; RECOVERY; OPTIMISM; OUTCOMES; SURGERY AB Objective: The purpose of this Study was to assess the reliability and validity of condition-specific health-related quality-of-life measures in women who are treated surgically for pelvic organ prolapse and urinary incontinence. Study design: The study used the cross-sectional telephone interview-based administration of a health-related quality-of-life measure, with a 2-week follow-up interview for test-retest reliability. Results: Initial and follow-up interviews were completed by 88 women (mean age, 65.7 +/- 11.6 years) approximately I year after surgical procedures. Condition-specific measures demonstrated acceptable reliability with test-retest correlation coefficients that approached or exceeded 0.6 and Cronbach's alpha that exceeded 0.8 in most domains. Validity was demonstrated with significant correlations of the urinary domains of the Pelvic Floor Distress Inventory and Pelvic Floor Impact Questionnaire, with continence defined by the medical, epidemiologic, and social aspects of aging and Hunskaar severity measures (all P <.001). Conclusion: The condition -specific health-related quality-of-life assessment is reliable and valid in women after Surgical procedures for pelvic floor disorders. These findings support the inclusion of condition-specific health-related quality-of-life measures in clinical trials for women with pelvic floor disorders. (C) 2005 Elsevier Inc. All rights reserved. C1 Univ Michigan, Dept Urol, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Hlth Behav & Hlth Educ, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA. Loyola Univ, Ctr Med, Dept Obstet & Gynecol, Maywood, IL 60153 USA. NICHHD, NIH, Bethesda, MD 20892 USA. RP Wei, JT (reprint author), Univ Michigan, Dept Urol, Room 1013,Womens Trailer,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. EM jtwei@umich.edu RI Wei, John/E-8967-2012 FU NICHD NIH HHS [U01 HD41249, U10 HD 41269, U10 HD41248, U10 HD41250, U10 HD41261, U10 HD41263, U10 HD41267, U10 HD41268] NR 28 TC 33 Z9 35 U1 0 U2 0 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD MAR PY 2005 VL 192 IS 3 BP 780 EP 788 DI 10.1016/j.ajog.2004.10.603 PG 9 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 904DZ UT WOS:000227477600019 PM 15746672 ER PT J AU Hendler, I Goldenberg, RL Mercer, BM Iams, JD Meis, PJ Moawad, AH MacPherson, CA Caritis, SN Miodovnik, M Menard, KM Thurnau, GR Sorokin, Y AF Hendler, I Goldenberg, RL Mercer, BM Iams, JD Meis, PJ Moawad, AH MacPherson, CA Caritis, SN Miodovnik, M Menard, KM Thurnau, GR Sorokin, Y TI The Preterm Prediction study: Association between maternal body mass index and spontaneous and indicated preterm birth SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the Society-for-Gynecologic-Investigation CY 2004 CL Houston, TX SP Soc Gynecolog Investigation DE maternal obesity; spontaneous preterm birth; body mass index ID ADVERSE PREGNANCY OUTCOMES; RISK-FACTORS; PREPREGNANCY WEIGHT; MORBID-OBESITY; WOMEN; POPULATION; DELIVERY; GAIN AB Objective: The purpose of this Study was to evaluate the relationship between prepregnancy maternal body mass index and spontaneous preterm birth and indicated preterm birth. Study design: This was a secondary analysis of the Maternal-Fetal Medicine Units Network, Preterm Prediction Study. Patients were classified into categories that were based on their body mass index. Rates of indicated and spontaneous preterm birth were compared. Results: Five hundred ninety-seven (20.5%) of 2910 women were obese. Obese women had fewer spontaneous preterm births at < 37 weeks of gestation (6.2% vs 11.2%: P < .001) and at < 34 weeks of gestation (1.5% vs 3.5%; P = .012). Women with a body mass index of < 19 kg/m(2) had 16.6% spontaneous preterm birth. with a body mass index of 19 to 24.9 kg/m(2) had 11.3% Spontaneous preterm birth, with a body mass index of 25 to 29.9 kg/m(2) had 8.1% spontaneous preterm birth with a body mass index of 30 to 34.9 kg/m(2) had 7.1% spontaneous preterm birth, and with a body mass index of greater than or equal to 35 kg/m(2) had 5.2% spontaneous preterm, birth (P < .0001). Indicated delivery was responsible for an increasing proportion of preterm births with increasing body mass index (P = .001). Obese women had lower rates of cervical length < 25 min (5% vs 8%: P = .012). Multivariable regression analysis confirmed a lower rate of spontaneous preterm birth in obese in-avid women (odds ratio, 0.57: 95% CI 0.39-0.83. P = .003). Conclusion: Obesity before pregnancy is associated with a lower rate of spontaneous preterm birth. (C) 2005 Elsevier Inc. All rights reserved. C1 NICHHD, Maternal Fetal Med Units Network, NIH, Bethesda, MD 20892 USA. RP Hendler, I (reprint author), Wayne State Univ, Hutzel Hosp, Dept Obstet & Gynecol, Div Maternal Fetal Med, 3990 John R Rd, Detroit, MI 48201 USA. EM ihendler@med.wayne.edu OI caritis, steve/0000-0002-2169-0712 FU NICHD NIH HHS [HD21410, HD19897, HD21414, HD27860, HD27861, HD27869, HD27889, HD27905, HD27915, HD27917, HD36801] NR 25 TC 128 Z9 133 U1 1 U2 14 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD MAR PY 2005 VL 192 IS 3 BP 882 EP 886 DI 10.1016/j.ajog.2004.09.021 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 904DZ UT WOS:000227477600033 PM 15746686 ER PT J AU Lim, WK Ursea, R Rao, K Buggage, RR Suhler, EB Dugan, F Chan, CC Straus, SE Nussenblatt, RB AF Lim, WK Ursea, R Rao, K Buggage, RR Suhler, EB Dugan, F Chan, CC Straus, SE Nussenblatt, RB TI Bilateral uveitis in a patient with autoimmune lymphoproliferative syndrome SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID EXPRESSION; TISSUE AB PURPOSE: We report a case of autoimmune lymphoproliferative syndrome (ALPS) presenting with bilateral uveitis. DESIGN: Observational case report. METHODS: Review of case record, serum and aqueous IL-10 and IL-6 cytokine results, and immunosuppressive treatment of a patient with a mutation in the gene encoding Fas. RESULTS: Control of the intermediate uveitis required sustained doses of topical and periocular corticosteroids as well as systemic cyclosporine. The serum IL-10 level was elevated, as commonly seen in ALPS, but the aqueous 11,10 was not. CONCLUSIONS: Despite a Th2 immune predominance in ALPS, uveitis, a Th1-mediated disease, may still manifest in these patients. The pathogenesis of uveitis in ALPS may differ from that of the systemic disease overall. Long,term follow-up is required for patients with uveitis associated with ALPS. (c) 2005 by Elsevier Inc. All rights reserved. C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. Singapore Natl Eye Ctr, Singapore, Singapore. NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA. RP Nussenblatt, RB (reprint author), NEI, Immunol Lab, NIH, Bldg 10,Room 10N112, Bethesda, MD 20892 USA. EM drbob@nei.nih.gov NR 5 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD MAR PY 2005 VL 139 IS 3 BP 562 EP 563 DI 10.1016/j.ajo.2004.09.017 PG 2 WC Ophthalmology SC Ophthalmology GA 907GO UT WOS:000227704200034 PM 15767081 ER PT J AU Arnold, JT Le, H McFann, KK Blackman, MR AF Arnold, JT Le, H McFann, KK Blackman, MR TI Comparative effects of DHEA vs. testosterone, dihydrotestosterone, and estradiol on proliferation and gene expression in human LNCaP prostate cancer cells SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE dehydroepiandrosterone; androgen receptor; prostate-specific antigen; insulin-like growth factor axis; estrogen receptor-beta; lymph nodederived cancer of prostate ID FACTOR-BINDING PROTEIN-3; ESTROGEN-RECEPTOR-BETA; 17-BETA-HYDROXYSTEROID DEHYDROGENASE TYPES; PERIPHERAL TARGET TISSUES; I IGF-I; ANDROGEN-RECEPTOR; ADRENAL ANDROGENS; 3-BETA-HYDROXYSTEROID DEHYDROGENASE; ADENOCARCINOMA CELLS; ER-ALPHA AB Serum levels of the adrenal androgen dehydroepiandrosterone (DHEA) peak in men and women in the third decade of life and decrease progressively with age. Increasing numbers of middle-aged and older individuals consume over-the-counter preparations of DHEA, hoping it will retard aging by increasing muscle and bone mass and strength, decreasing fat, and improving immunologic and neurobehavioral functions. Because DHEA can serve as a precursor to more potent androgens and estrogens, like testosterone (T), dihydrotestosterone (DHT), and 17beta-estradiol (E-2), supplemental DHEA use may pose a cancer risk in patients with nascent or occult prostate cancer. The steroid-responsive human LNCaP prostate cancer cells, containing a functional but mutated androgen receptor (AR), were used to compare effects of DHEA with those of T, DHT, and E-2 on cell proliferation and protein and/or gene expression of AR, prostate-specific antigen (PSA), IGF-I, IGF-I receptor (IGF-IR), IGF-II, IGF-binding proteins-2, -3, and -5, (IGFBPs-2, -3, and -5), and estrogen receptor-beta (ERbeta). Cell proliferation assays revealed significant stimulation by all four steroids. DHEA-and E-2-induced responses were similar but delayed and reduced compared with that of T and DHT. All four hormones increased gene and/or protein expression of PSA, IGF-IR, IGF-I, and IGFBP-2 and decreased that of AR, ERbeta, IGF-II, and IGFBP-3. There were no significant effects of hormone treatment on IGFBP-5 mRNA. DHEA and E-2 responses were similar, and distinct from those of DHT and T, in time- and dose-dependent studies. Further studies of the mechanisms of DHEA effects on prostate cancer epithelial cells of varying AR status, as well as on prostate stromal cells, will be required to discern the implications of DHEA supplementation on prostatic health. C1 NIH, Endocrine Sect, Clin Invest Lab, Div Intramural Res,LCI NCCAM, Bethesda, MD 20892 USA. NIH, Off Clin & Regulatory Affairs, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA. RP Arnold, JT (reprint author), NIH, Endocrine Sect, Clin Invest Lab, Div Intramural Res,LCI NCCAM, 9 Mem Dr,Rm 1N105, Bethesda, MD 20892 USA. EM jarnold@mail.nih.gov NR 60 TC 71 Z9 72 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD MAR PY 2005 VL 288 IS 3 BP E573 EP E584 DI 10.1152/ajpendo.00454.2004 PG 12 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA 894MD UT WOS:000226795000014 PM 15536203 ER PT J AU Alpert, NR Mohiddin, SA Tripodi, D Jacobson-Hatzell, J Vaughn-Whitley, K Brosseau, C Warshaw, DM Fananapazir, L AF Alpert, NR Mohiddin, SA Tripodi, D Jacobson-Hatzell, J Vaughn-Whitley, K Brosseau, C Warshaw, DM Fananapazir, L TI Molecular and phenotypic effects of heterozygous, homozygous, and compound heterozygote myosin heavy-chain mutations SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE hypertrophy; cardiomyopathy; motility assay; penetrance ID FAMILIAL HYPERTROPHIC CARDIOMYOPATHY; BETA-CARDIAC MYOSIN; DILATED CARDIOMYOPATHY; FUNCTIONAL CONSEQUENCES; MECHANICAL PERFORMANCE; GENES; ACTIN; EXPRESSION; MOTILITY; PARADIGM AB Autosomal dominant familial hypertrophic cardiomyopathy ( FHC) has variable penetrance and phenotype. Heterozygous mutations in MYH7 encoding beta-myosin heavy chain are the most common causes of FHC, and we proposed that "enhanced" mutant actin-myosin function is the causative molecular abnormality. We have studied individuals from families in which members have two, one, or no mutant MYH7 alleles to examine for dose effects. In one family, a member homozygous for Lys207Gln had cardiomyopathy complicated by left ventricular dilatation, systolic impairment, atrial fibrillation, and defibrillator interventions. Only one of five heterozygous relatives had FHC. Leu908Val and Asp906Gly mutations were detected in a second family in which penetrance for Leu908Val heterozygotes was 46% ( 21/46) and 25% ( 3/12) for Asp906Gly. Despite the low penetrance, hypertrophy was severe in several heterozygotes. Two individuals with both mutations developed severe FHC. The velocities of actin translocation ( V-actin) by mutant and wild-type ( WT) myosins were compared in the in vitro motility assay. Compared with WT/WT, V-actin was 34% faster for WT/D906G and 21% for WT/L908V. Surprisingly Vactin for Leu908Val/Asp906Gly and Lys207Gln/Lys207Gln mutants were similar to WT. The apparent enhancement of mechanical performance with mutant/WT myosin was not observed for mutant/mutant myosin. This suggests that Vactin may be a poor predictor of disease penetrance or severity and that power production may be more appropriate, or that the limited availability of double mutant patients prohibits any definitive conclusions. Finally, severe FHC in heterozygous individuals can occur despite very low penetrance, suggesting these mutations alone are insufficient to cause FHC and that uncharacterized modifying mechanisms exert powerful influences. C1 Univ Vermont, Dept Physiol & Mol Biophys, Burlington, VT USA. Dakota Cardiovasc Phys Corp, Rapid City, SD USA. NHLBI, NIH, Cardiovasc Branch, Bethesda, MD 20892 USA. RP Mohiddin, SA (reprint author), Rm 5-5330,Bldg 10 CRC,10 Ctr Dr, Bethesda, MD 20892 USA. EM mohiddis@nhlbi.nih.gov FU NHLBI NIH HHS [P01-HL-59408] NR 37 TC 36 Z9 37 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD MAR PY 2005 VL 288 IS 3 BP H1097 EP H1102 DI 10.1152/ajpheart.00650.2004 PG 6 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA 896CB UT WOS:000226911100017 PM 15528230 ER PT J AU Tawfik, HE Schnermann, J Oldenburg, PJ Mustafa, SJ AF Tawfik, HE Schnermann, J Oldenburg, PJ Mustafa, SJ TI Role of A(1) adenosine receptors in regulation of vascular tone SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE A(1) adenosine receptor; knockout mice; smooth muscle ID PORCINE CORONARY-ARTERY; MOUSE ISOLATED AORTA; SMOOTH-MUSCLE-CELLS; ADENOSINE RECEPTOR; MICE LACKING; A(1); SUBTYPES; VASODILATION; RELAXATION; ANALOGS AB The vascular response to adenosine and its analogs is mediated by four adenosine receptors (ARs), namely, A(1), A(2A), A(2B), and A(3). A(2A)ARs and/or A(2B)ARs are involved in adenosine-mediated vascular relaxation of coronary and aortic beds. However, the role of A(1)ARs in the regulation of vascular tone is less well substantiated. The aim of this study was to determine the role of A(1)ARs in adenosine-mediated regulation of vascular tone. A(1)AR-knockout [A(1)AR((-/-))] mice and available pharmacological tools were used to elucidate the function of A(1)ARs and the impact of these receptors on the regulation of vascular tone. Isolated aortic rings from A(1)AR((-/-)) and wild-type [A(1)AR((+/+))] mice were precontracted with phenylephrine, and concentration-response curves for adenosine and its analogs, 5'-N-ethyl-carboxamidoadenosine (NECA, nonselective), 2-chloro-N-6-cyclopentyladenosine (CCPA, A(1)AR selective), 2-(2-carboxyethyl) phenethyl amino-5'-N-ethylcarboxamido-adenosine (CGS-21680, A(2A) selective), and 2-chloro-N-6-3-iodobenzyladenosine-5'-N-methyluronamide (Cl-IBMECA, A(3) selective) were obtained to determine relaxation. Adenosine and NECA (0.1 muM) caused small contractions of 13.9 +/- 3.0 and 16.4 +/- 6.4%, respectively, and CCPA at 0.1 and 1.0 muM caused contractions of 30.8 +/- 4.3 and 28.1 +/- 3.9%, respectively, in A(1)AR((+/+)) rings. NECA- and CCPA-induced contractions were eliminated by 100 nM of 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, selective A(1)AR antagonist). Adenosine, NECA, and CGS-21680 produced an increase in maximal relaxation in A(1)AR((-/-)) compared with A(1)AR((+/+)) rings, whereas Cl-IBMECA did not produce contraction in either A(1)AR((+/+)) or A(1)AR((-/-)) rings. CCPA-induced contraction at 1.0 muM was eliminated by the PLC inhibitor U-73122. These data suggest that activation of A(1)ARs causes contraction of vascular smooth muscle through PLC pathways and negatively modulates the vascular relaxation mediated by other adenosine receptor subtypes. C1 E Carolina Univ, Brody Sch Med, Dept Pharmacol & Toxicol, Greenville, NC 27858 USA. Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD USA. RP Mustafa, SJ (reprint author), E Carolina Univ, Brody Sch Med, Dept Pharmacol & Toxicol, Greenville, NC 27858 USA. EM mustafas@mail.ecu.edu FU NHLBI NIH HHS [HL-27339] NR 24 TC 51 Z9 53 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD MAR PY 2005 VL 288 IS 3 BP H1411 EP H1416 DI 10.1152/ajpheart.00684.2004 PG 6 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA 896CB UT WOS:000226911100057 PM 15539423 ER PT J AU Hashimoto, S Adams, JW Bernstein, KE Schnermann, J AF Hashimoto, S Adams, JW Bernstein, KE Schnermann, J TI Micropuncture determination of nephron function in mice without tissue angiotensin-converting enzyme SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY LA English DT Article DE nephron filtration rate; proximal fluid reabsorption; tubuloglomerular feedback; angiotensin II kidney weight ID PROXIMAL TUBULE TRANSPORT; NORMAL BLOOD-PRESSURE; TUBULOGLOMERULAR FEEDBACK; TRANSGENIC MICE; DEFICIENT MICE; RENIN; GENE; RAT; LACKING; SYSTEM AB Micropuncture determination of nephron function in mice without tissue angiotensin-converting enzyme. Am J Physiol Renal Physiol 288: F445-F452, 2005. First published October 19, 2004; doi: 10.1152/ajprenal.00297.2004.-To determine the role of the local renin-angiotensin system in renal function, micropuncture was performed on two lines of mice in which genetic changes to the angiotensin-converting enzyme (ACE) gene markedly reduced or eliminated the expression of renal tissue ACE. Whereas blood pressure is low in one line (ACE 2/2), it is normal in the other (ACE 1/3) due to ectopic hepatic ACE expression. When normalized for renal size, levels of glomerular filtration rate [GFR; mul(.)min(-1.)g kidney wt(-1) (KW)] and single-nephron GFR (SNGFR; nl-min(-1.)g KW(-1)) were similar between wild-type (WT) and ACE 1/3 mice, while both measures were significantly reduced in ACE 2/2 mice (WT: 500 +/- 63 and 41.7 +/- 3.5; ACE 1/3: 515.8 +/- 71 and 44.3 +/- 3.3; ACE 2/2: 131.4 +/- 23 and 30.3 +/- 3.5). Proximal fractional reabsorption was not significantly different between WT and ACE 1/3 mice (51 +/- 3.5 and 49 +/- 2.3 %), and it was increased significantly in ACE 2/2 mice (74 +/- 3.5 %). Infusion of ANG 11 (50 ng(.)kg(-1.)min(-1)) increased mean arterial pressure by similar to7 mmHg in all groups of mice and reduced SNGFR in WT and ACE 1/3 mice (to 30.9 +/- 2.8 and 31.9 +/- 2.5 nl(.)min(-1.)g KW(-1)) while increasing it in ACE 2/2 mice (to 55.3 +/- 5.3 nl(.)min(-1.)g KW(-1)) despite an increase in total renal vascular resistance. The tubuloglomerular feedback (TGF) response was markedly reduced in ACE 1/3 mice (stop-flow pressure change -2.5 +/- 0.9 mmHg) compared with WT despite similar blood pressures (-8.3 +/- 0.6 mmHg). In ACE 2/2 mice, TGF was absent (-0.7 +/- 0.2 mmHg). We conclude that the chronic lack of ACE, and presumably ANG II generation, in the proximal tubule was not associated with sustained proximal fluid transport defects. However, renal tissue ACE is an important contributor to TGF. C1 NIDDK, NIH, Bethesda, MD 20892 USA. Emory Univ, Dept Pathol, Atlanta, GA 30322 USA. RP Schnermann, J (reprint author), NIDDK, NIH, Bldg 10,Rm 4 D51,10 Ctr Dr,MSC 1370, Bethesda, MD 20892 USA. EM jurgens@intra.niddk.nih.gov OI Bernstein, Kenneth/0000-0001-8097-3272 FU NIDDK NIH HHS [DK-39777, DK-51445, DK-55503] NR 42 TC 26 Z9 26 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 1931-857X J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Physiol. PD MAR PY 2005 VL 288 IS 3 BP F445 EP F452 DI 10.1152/ajprenal.00297.2004 PG 8 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA 898IK UT WOS:000227070300003 PM 15494545 ER PT J AU Andreasen, NC Carpenter, WT Kane, JM Lasser, RA Marder, SR Weinberger, DR AF Andreasen, NC Carpenter, WT Kane, JM Lasser, RA Marder, SR Weinberger, DR TI Remission in schizophrenia: Proposed criteria and rationale for consensus SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Review ID 1ST-EPISODE SCHIZOPHRENIA; PREMORBID ADJUSTMENT; SYMPTOM DIMENSIONS; POSITIVE SYMPTOMS; RATING-SCALE; RECOVERY; DISORDER; PSYCHOSIS; ANXIETY; DEPRESSION AB New advances in the understanding of schizophrenia etiology, course, and treatment have increased interest on the part of patients, families, advocates, and professionals in the development of consensus-defined standards for clinical status and improvement, including illness remission and recovery. As demonstrated in the area of mood disorders, such standards provide greater clarity around treatment goals, as well as an improved framework for the design and comparison of investigational trials and the subsequent evaluation of the effectiveness of interventions. Unlike the approach to mood disorders, however, the novel application of the concept of standard outcome criteria to schizophrenia must reflect the wide heterogeneity of its long-term course and outcome, as well as the variable effects of different treatments on schizophrenia symptoms. As an initial step in developing operational criteria, an expert working group reviewed available definitions and assessment instruments to provide a conceptual framework for symptomatic, functional, and cognitive domains in schizophrenia as they relate to remission of illness. The first consensus-based operational criteria for symptomatic remission in schizophrenia are based on distinct thresholds for reaching and maintaining improvement, as opposed to change criteria, allowing for alignment with traditional concepts of remission in both psychiatric and nonpsychiatric illness. This innovative approach for standardizing the definition for outcome in schizophrenia will require further examination of its validity and utility, as well as future refinement, particularly in relation to psychosocial and cognitive function and dysfunction. These criteria should facilitate research and support a positive, longer-term approach to studying outcome in patients with schizophrenia. C1 Univ Iowa, Dept Psychiat, Iowa City, IA 52242 USA. Univ New Mexico, MIND Inst, Albuquerque, NM 87131 USA. Univ New Mexico, Dept Psychiat, Albuquerque, NM 87131 USA. Univ New Mexico, Dept Neurol, Albuquerque, NM 87131 USA. Univ New Mexico, Dept Neurosci, Albuquerque, NM 87131 USA. Maryland Psychiat Res Ctr, Baltimore, MD 21228 USA. Zucker Hillside Hosp, Glen Oaks, NY USA. Univ Calif Los Angeles, Inst Neuropsychiat, Los Angeles, CA 90024 USA. NIMH, Bethesda, MD 20892 USA. RP Lasser, RA (reprint author), Janssen Pharmaceutica Prod LP, 1125 Trenton Harbourton Rd,Off A20904, Titusville, NJ 08560 USA. EM rlasser@janus.jnj.com NR 55 TC 871 Z9 925 U1 7 U2 59 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 2005 VL 162 IS 3 BP 441 EP 449 DI 10.1176/appi.ajp.162.3.441 PG 9 WC Psychiatry SC Psychiatry GA 904UP UT WOS:000227523500003 PM 15741458 ER PT J AU Simons-Morton, BG Hartos, JL Leaf, WA Preusser, DF AF Simons-Morton, BG Hartos, JL Leaf, WA Preusser, DF TI Persistence of effects of the checkpoints program on parental restrictions of teen driving privileges SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID MOTOR-VEHICLE CRASHES; DRIVER EDUCATION; PASSENGERS; RISKS AB Objectives. We describe intervention effects on parent limits on novice teenage driving. Methods. We recruited parents and their 16-year-old children (n=469) with learner's permits and randomized them from August 2000 to March 2003. Intervention families received persuasive newsletters related to high-risk teenage driving and a parent-teenager driving agreement; comparison families received standard information on driver safety. We conducted interviews when the adolescents obtained a learner's permit, upon licensure, and at 3, 6, and 12 months postlicensure. Results. Intervention parents and teenagers reported stricter limits on teen driving compared with the comparison group at 12 months, with direct effects through 3 months and indirect effects through 12 months postlicensure. Conclusions. A simple behavioral intervention was efficacious in increasing parental restriction of high-risk teen driving conditions among newly licensed drivers. C1 NICHHD, Prevent Res Branch, Dept Epidemiol Stat & Prevent Res,Div Epidemiol S, NIH, Bethesda, MD 20892 USA. RP Simons-Morton, BG (reprint author), NICHHD, Prevent Res Branch, Dept Epidemiol Stat & Prevent Res,Div Epidemiol S, NIH, 6100 Execut Blvd,Suite 7B13M, Bethesda, MD 20892 USA. EM mortonb@mail.nih.gov OI Simons-Morton, Bruce/0000-0003-1099-6617 FU NHGRI NIH HHS [300N1HG83285A]; NICHD NIH HHS [N01-HD-8-3285] NR 28 TC 30 Z9 30 U1 0 U2 2 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD MAR PY 2005 VL 95 IS 3 BP 447 EP 452 DI 10.2105/AJPH.2003.023127 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 918AR UT WOS:000228511100025 PM 15727975 ER PT J AU Levy, MM Baylor, MS Bernard, GR Fowler, R Franks, TJ Hayden, FG Helfand, R Lapinsky, SE Martin, TR Niederman, MS Rubenfeld, GD Slutsky, AS Stewart, TE Styrt, BA Thompson, BT Harabin, AL AF Levy, MM Baylor, MS Bernard, GR Fowler, R Franks, TJ Hayden, FG Helfand, R Lapinsky, SE Martin, TR Niederman, MS Rubenfeld, GD Slutsky, AS Stewart, TE Styrt, BA Thompson, BT Harabin, AL TI Clinical issues and research in respiratory failure from severe acute respiratory syndrome SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article DE acute lung injury; acute respiratory distress syndrome; infectious disease ID CRITICALLY-ILL PATIENTS; MECHANICALLY VENTILATED PATIENTS; INTENSIVE-CARE UNIT; SARS-ASSOCIATED CORONAVIRUS; COMMUNITY-ACQUIRED PNEUMONIA; ACUTE LUNG INJURY; DISTRESS-SYNDROME; INTERFERON-ALPHA; GASTROESOPHAGEAL-REFLUX; VENOUS THROMBOEMBOLISM AB The National Heart, Lung, and Blood Institute, along with the Centers for Disease Control and Prevention and the National Institute of Allergy and Infectious Diseases, convened a panel to develop recommendations for treatment, prevention, and research for respiratory failure from severe acute respiratory syndrome (SARS) and other newly emerging infections. The clinical and pathological features of acute lung injury (ALI) from SARS appear indistinguishable from ALI from other causes. The mainstay of treatments for ALI remains supportive. Patients with ALI from SARS who require mechanical ventilation should receive a lung protective, low tidal volume strategy. Adjuvant treatments recommended include prevention of venous thromboembolism, stress ulcer prophylaxis, and semirecumbent positioning during ventilation. Based on previous experience in Canada, infection control resources and protocols were recommended. Leadership structure, communication, training, and morale are an essential aspect of SAIRS management. A multicenter, placebo-controlled trial of corticosteroids for late SARS is justified because of widespread clinical use and uncertainties about relative risks and benefits. Studies of combined pathophysiologic endpoints were recommended, with mortality as a secondary endpoint. The group recommended preparation for studies, including protocols, ethical considerations, Web-based registries, and data entry systems. C1 NHLBI, Div Lung Dis, NIH, Bethesda, MD 20892 USA. Brown Univ, Rhode Isl Hosp, Dept Med, Providence, RI 02903 USA. US FDA, Div Antiviral Drug Prod, Rockville, MD 20857 USA. Vanderbilt Univ, Sch Med, Dept Med, Nashville, TN 37212 USA. Armed Forces Inst Pathol, Dept Pulm & Mediastinal Pathol, Washington, DC 20306 USA. Univ Virginia, Dept Internal Med, Charlottesville, VA USA. Ctr Dis Control & Prevent, Resp & Enter Viruses Branch, Atlanta, GA USA. VA Puget Sound Med Ctr, Div Pulm & Crit Care Med, Seattle, WA USA. Winthrop Univ Hosp, Dept Med, Mineola, NY 11501 USA. Univ Washington, Harborview Med Ctr, Dept Pulm & Crit Care Med, Seattle, WA 98195 USA. Massachusetts Gen Hosp, Dept Med, Pulm & Crit Care Unit, Boston, MA 02114 USA. Sunnybrook & Womens Coll Hlth Sci Ctr, Interdept Div Crit Care Med, Toronto, ON, Canada. Mt Sinai Hosp, Dept Med, Toronto, ON M5G 1X5, Canada. Mt Sinai Hosp, Dept Crit Care Med, Toronto, ON M5G 1X5, Canada. Univ Hlth Network, Toronto, ON, Canada. St Michaels Hosp, Dept Med, Toronto, ON M5B 1W8, Canada. St Michaels Hosp, Dept Crit Care, Toronto, ON M5B 1W8, Canada. RP Harabin, AL (reprint author), NHLBI, Div Lung Dis, NIH, 6,701 Rockledge Dr,Room 10018, Bethesda, MD 20892 USA. EM harabin@nih.gov RI Slutsky, Arthur/A-6013-2008; Lapinsky, Stephen/C-4624-2015 OI Slutsky, Arthur/0000-0002-6063-3876; Lapinsky, Stephen/0000-0002-6930-0306 NR 84 TC 25 Z9 26 U1 0 U2 0 PU AMER THORACIC SOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD MAR 1 PY 2005 VL 171 IS 5 BP 518 EP 526 DI 10.1164/rccm.200405-621WS PG 9 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA 900EF UT WOS:000227197500016 PM 15591472 ER PT J AU Granville, CA Dennis, PA AF Granville, CA Dennis, PA TI An overview of lung cancer genomics and proteomics SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Review DE lung cancer; genomics; proteomics ID DIFFERENTIALLY EXPRESSED GENES; LASER CAPTURE MICRODISSECTION; COMPLEMENTARY-DNA MICROARRAY; MOLECULAR CLASSIFICATION; PROTEIN IDENTIFICATION; SEQUENCE DATABASES; ADENOCARCINOMA; TUMORS; PROFILES; SURVIVAL AB Lung cancer is the cause of nearly 170,000 cancer deaths in the United States each year, accounting for nearly 25% of all deaths from cancer. The 5-yr survival rate for lung cancer is < 15% from the time of diagnosis. This is largely due to the late stage of diagnosis and the lack of effective treatments, reflecting the need for a better understanding of the mechanisms that underlie lung carcinogenesis. Unlike the study of a single gene, protein, or pathway, genomic and proteomic technologies enable a systematic overview that provides the potential to improve our understanding of this disease. Ultimately, this could improve the diagnosis, prognosis, and clinical management of patients with lung cancer. Here, we review studies that generated profiles of gene and protein expression in lung cancer specimens and relevant model systems, and make recommendations to facilitate the clinical application of these technologies. C1 NCI, Canc Therapeut Branch, Canc Res Ctr, Bethesda, MD 20889 USA. George Washington Univ, Genet Program, Washington, DC USA. RP Dennis, PA (reprint author), NCI, Canc Therapeut Branch, Canc Res Ctr, Bldg 8,Room 5101,8901 Wisconsin Ave, Bethesda, MD 20889 USA. EM pdennis@nih.gov NR 62 TC 94 Z9 110 U1 4 U2 11 PU AMER THORACIC SOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD MAR PY 2005 VL 32 IS 3 BP 169 EP 176 DI 10.1165/rcmb.F290 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA 900DS UT WOS:000227196200001 PM 15713815 ER PT J AU Pearl, JP Parris, J Hale, DA Hoffmann, SC Bernstein, WB McCoy, KL Swanson, SJ Mannon, RB Roederer, M Kirk, AD AF Pearl, JP Parris, J Hale, DA Hoffmann, SC Bernstein, WB McCoy, KL Swanson, SJ Mannon, RB Roederer, M Kirk, AD TI Immunocompetent T-cells with a memory-like phenotype are the dominant cell type following antibody-mediated T-cell depletion SO AMERICAN JOURNAL OF TRANSPLANTATION LA English DT Article DE depletion; immunosuppression; T cell; transplantation ID DOSE CYCLOSPORINE MONOTHERAPY; RENAL-ALLOGRAFT RECIPIENTS; TRANSPLANTATION TOLERANCE; HOMEOSTATIC PROLIFERATION; HEMATOPOIETIC CHIMERISM; HUMAN NAIVE; CAMPATH 1H; INDUCTION; IMMUNOTOXIN; REJECTION AB cell depletion facilitates reduced immunosuppression following organ transplantation and has been suggested to be pro-tolerant. However, the characteristics of post-depletional T cells have not been evaluated as they relate to tolerance induction. We therefore studied patients undergoing profound T-cell depletion with alemtuzumab or rabbit anti-thymocyte globulin following renal transplantation, evaluating the phenotype and functional characteristics of their residual cells. Naive T cells and T cells with potential regulatory function (CD4+CD25+) were not prevalent following aggressive depletion. Rather, post-depletion T cells were of a single phenotype (CD3+CD4+CD45RA-CD62L- CCR7-) consistent with depletion-resistant effector memory T cells that expanded in the first month and were uniquely prevalent at the time of rejection. These cells were resistant to steroids, deoxyspergualin or sirolimus in vitro, but were calcineurin-inhibitor sensitive. These data demonstrate that therapeutic depletion begets a limited population of functional memory-like T cells that are easily suppressed with certain immunosuppressants, but cannot be considered uniquely pro-tolerant. C1 NIDDKD, Transplant Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Natl Naval Med Res Inst, Dept Surg, Bethesda, MD USA. Walter Reed Army Med Ctr, Organ Transplant Serv, Washington, DC 20307 USA. Walter Reed Army Inst Res, Div Retrovirol, Rockville, MD USA. NIAID, Immunotechnol Sect, Vaccine Res Ctr, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Kirk, AD (reprint author), NIDDKD, Transplant Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. EM AllanK@intra.niddk.nih.gov RI Roederer, Mario/G-1887-2011; Kirk, Allan/B-6905-2012 NR 47 TC 309 Z9 316 U1 0 U2 4 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 1600-6135 J9 AM J TRANSPLANT JI Am. J. Transplant. PD MAR PY 2005 VL 5 IS 3 BP 465 EP 474 DI 10.1111/j.1600-6143.2005.00759.x PG 10 WC Surgery; Transplantation SC Surgery; Transplantation GA 896UB UT WOS:000226958200009 PM 15707400 ER PT J AU Hoffmann, SC Hale, DA Kleiner, DE Mannon, RB Kampen, RL Jacobson, LM Cendales, LC Swanson, SJ Becker, BN Kirk, AD AF Hoffmann, SC Hale, DA Kleiner, DE Mannon, RB Kampen, RL Jacobson, LM Cendales, LC Swanson, SJ Becker, BN Kirk, AD TI Functionally significant renal allograft rejection is defined by transcriptional criteria SO AMERICAN JOURNAL OF TRANSPLANTATION LA English DT Article DE acute rejection; real-time PCR; renal allotransplantation; sub-clinical rejection ID KIDNEY-TRANSPLANT RECIPIENTS; QUANTITATIVE RT-PCR; PROTOCOL BIOPSIES; COSTIMULATORY PATHWAY; MEDICAL PROGRESS; GENE-EXPRESSION; MESSENGER-RNA; GRANZYME-B; T-BET; ACTIVATION AB Renal allograft acute cellular rejection (ACR) is a T-cell mediated disease that is diagnosed histologically. However, many normally functioning allografts have T-cell infiltrates and histological ACR, and many nonimmune processes cause allograft dysfunction. Thus, neither histological nor functional criteria are sufficient to establish a significant rejection, and the fundamental features of clinical rejection remain undefined. To differentiate allograft lymphocyte infiltration from clinically significant ACR, we compared renal biopsies from patients with ACR to patients with: sub-clinical rejection (SCR, stable function with histological rejection); no rejection; and nontransplanted kidneys. Biopsies were compared histologically and transcriptionally by RT-PCR for 72 relevant immune function genes. Neither the degree nor the composition of the infiltrate defined ACR. However, transcripts up-regulated during effector T(H)1T-cell activation, most significantly the transcription factor T-bet, the effector receptor Fas ligand and the costimulation molecule CD152 clearly (p = 0.001) distinguished the patient categories. Transcripts from other genes were equivalently elevated in SCR and ACR, indicating their association with infiltration, not dysfunction. Clinically significant ACR is not defined solely by the magnitude nor composition of the infiltrate, but rather by the transcriptional activity of the infiltrating cells. Quantitative analysis of selected gene transcripts may enhance the clinical assessment of allografts. C1 NIDDK, Transplantat Branch, DHHS, NIH, Bethesda, MD 20892 USA. Walter Reed Army Med Ctr, Organ Transplant Serv, Washington, DC USA. NCI, Pathol Lab, DHHS, NIH, Bethesda, MD 20892 USA. Univ Wisconsin, Dept Med, Madison, WI 53706 USA. RP Kirk, AD (reprint author), NIDDK, Transplantat Branch, DHHS, NIH, Bethesda, MD 20892 USA. EM Allank@intra.niddk.nih.gov RI Kirk, Allan/B-6905-2012; OI Kleiner, David/0000-0003-3442-4453 FU NIAID NIH HHS [R01 AI49285-04]; NIDDK NIH HHS [1K24 DK616962-02] NR 38 TC 88 Z9 90 U1 0 U2 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 1600-6135 J9 AM J TRANSPLANT JI Am. J. Transplant. PD MAR PY 2005 VL 5 IS 3 BP 573 EP 581 DI 10.1111/j.1600-6143.2005.00719.x PG 9 WC Surgery; Transplantation SC Surgery; Transplantation GA 896UB UT WOS:000226958200022 PM 15707413 ER PT J AU Lipsky, RH Jiang, X Xu, K Marko, AJ Neyer, KM Anderson, TR Marini, AM AF Lipsky, RH Jiang, X Xu, K Marko, AJ Neyer, KM Anderson, TR Marini, AM TI Genomics and variation of ionotropic glutamate receptors: implications for neuroplasticity SO AMINO ACIDS LA English DT Article; Proceedings Paper CT 8th International Congress on Amino Acids and Proteins CY SEP 05-09, 2003 CL Rome, ITALY DE ionotropic glutamate receptor genes; sequence variant; genomics; polymorphism; neuroplasticity ID SINGLE-NUCLEOTIDE POLYMORPHISMS; NMDA RECEPTOR; BINDING-SITE; SUBUNITS; REGIONS; INJURY; GENE AB We used two approaches to identify sequence variants in ionotropic glutamate receptor (IGR) genes: high-throughput screening and resequencing techniques, and ''information mining'' of public ( e. g. dbSNP, ENSEMBL) and private (i.e. Celera Discovery System) sequence databases. Each of the 16 known IGRs is represented in these databases, their positions on a canonical physical map are established. Comparisons of mouse, rat, and human sequences revealed substantial conservation among these genes, which are located on different chromosomes but found within syntenic groups of genes. The IGRs are members of a phylogenetically ancient gene family, sharing similarities with glutamate-like receptors in plants. Parsimony analysis of amino acid sequences groups the IGRs into three distinct clades based on ligand-binding specificity and structural features, such as the channel pore and membrane spanning domains. A collection of 38 variants with amino acid changes was obtained by combining screening, resequencing, and informatics approaches for several of the IGR genes. This represents only a fraction of the sequence variation across these genes, but in fact these may constitute a large fraction of the common polymorphisms at these genes and these polymorphisms are a starting point for understanding the role of these variants in function. Genetically influenced human neurobehavioral phenotypes are likely to be linked to IGR genetic variants. Because ionotropic glutamate receptor activation leads to calcium entry, which is fundamental in brain development and in forms of synaptic plasticity essential for learning and memory and is essential for neuronal survival, it is likely that sequence variants in IGR genes may have profound functional roles in neuronal activation and survival mechanisms. C1 NIAAA, Sect Mol Genet, Lab Neurogenet, NIH, Bethesda, MD 20892 USA. Univ Hlth Sci, Neurosci Program Uniformed Serv, Dept Neurol, Bethesda, MD USA. RP Lipsky, RH (reprint author), NIAAA, Sect Mol Genet, Lab Neurogenet, NIH, 5625 Fishers Lane,Room 3S32,Room 3S32, Bethesda, MD 20892 USA. EM rlipsky@mail.nih.gov OI Lipsky, Robert/0000-0001-7753-1473 NR 18 TC 4 Z9 4 U1 0 U2 1 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0939-4451 J9 AMINO ACIDS JI Amino Acids PD MAR PY 2005 VL 28 IS 2 BP 169 EP 175 DI 10.1007/s00726-005-0164-2 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 907UP UT WOS:000227743800009 PM 15714255 ER PT J AU Westermark, P Benson, MD Buxbaum, JN Cohen, AS Frangione, B Ikeda, SI Masters, CL Merlini, G Saraiva, MJ Sipe, JD AF Westermark, P Benson, MD Buxbaum, JN Cohen, AS Frangione, B Ikeda, SI Masters, CL Merlini, G Saraiva, MJ Sipe, JD TI Amyloid: Toward terminology clarification - Report from the Nomenclature Committee of the International Society of Amyloidosis SO AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS LA English DT Article DE amyloidosis; amyloid protein; nomenclature; inclusion body ID PROTEIN; FIBRIL AB The modem nomenclature of amyloidosis now includes 25 human and 8 animal fibril proteins. To be included in the list, the protein has to be a major fibril protein in extracellular deposits, which have the characteristics of amyloid, including affinity for Congo red with resulting green birefringence. Synthetic fibrils with amyloid properties are best named 'amyloid-like'. With increasing knowledge, however, the borders between different protein aggregates tend to become less sharp. C1 Uppsala Univ, Rudbeck Lab, SE-75185 Uppsala, Sweden. Uppsala Univ, Dept Genet & Pathol, SE-75185 Uppsala, Sweden. Indiana Univ, Sch Med, Dept Pathol & Lab Med, Indianapolis, IN USA. Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA USA. Boston Univ, Sch Med, Boston, MA USA. NYU Sch Med, Dept Pathol, New York, NY USA. Shinshu Univ, Sch Med, Dept Med 3, Matsumoto, Nagano, Japan. Univ Melbourne, Dept Pathol, Parkville, Vic, Australia. Univ Hosp IRCCS Policlin, Biotechnol Res Labs, Amyloidosis Ctr, Pavia, Italy. Unidade Amiloide, Inst Biol Mol & Celular, Oporto, Portugal. NIH, Ctr Sci Review, Bethesda, MD USA. RP Westermark, P (reprint author), Uppsala Univ, Rudbeck Lab, C5, SE-75185 Uppsala, Sweden. EM Per.Westermark@genpat.uu.se RI Merlini, Giampaolo/A-3817-2008; Saraiva, Maria Joao/K-3907-2013 OI Merlini, Giampaolo/0000-0001-7680-3254; Saraiva, Maria Joao/0000-0002-3360-6899 NR 14 TC 189 Z9 197 U1 0 U2 13 PU PARTHENON PUBLISHING GROUP PI LANCASTER PA RICHMOND HOUSE, WHITE CROSS, SOUTH ROAD, LANCASTER LA1 4XQ, ENGLAND SN 1350-6129 J9 AMYLOID JI Amyloid-J. Protein Fold. Disord. PD MAR PY 2005 VL 12 IS 1 BP 1 EP 4 DI 10.1080/13506120500032196 PG 4 WC Biochemistry & Molecular Biology; Medicine, General & Internal; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; General & Internal Medicine; Research & Experimental Medicine GA 941YP UT WOS:000230250400001 PM 16076605 ER PT J AU Law, B Hsiao, JK Bugge, TH Weissleder, R Tung, CH AF Law, B Hsiao, JK Bugge, TH Weissleder, R Tung, CH TI Optical zymography for specific detection of urokinase plasminogen activator activity in biological samples SO ANALYTICAL BIOCHEMISTRY LA English DT Article DE optical zymography; urokinase; fluorescence; probe ID COLON-CARCINOMA CELLS; MATRIX METALLOPROTEINASES; PROTEOLYTIC ACTIVITY; POLYACRYLAMIDE GELS; PROTEASE ACTIVITY; CATHEPSIN-D; COLLAGENASE; INHIBITORS; INVASION; CHARACTERIZE AB Zymography techniques are routinely used to quantify proteolytic activity. In the current study, we describe an optical zymographic procedure that specifically detects urokinase-type plasminogen activator (uPA) activity in biological samples. The method employs a synthetic polymeric uPA fluorescent probe, which is copolymerized in sodium dodecyl sulfate (SDS)-polyacrylamide gel. Following electrophoresis and renaturation, enzymatic digestions of the substrate in 50 mM of Tris buffer at pH 7.4 generates fluorescence emission at 695 nm. The enzymatic activities can be analyzed directly by conventional gel imaging systems with a detection limit of 40 pg. This protocol is fast (hours) and does not require staining and destaining steps. The procedure is independent of plasminogen and, therefore, can efficiently distinguish the active two-chain uPA from its proenzyme. Densitometry analysis demonstrated a highly correlative relationship (r(2)=0.999) between the amount of uPA (over the range of 0.1-8.0 ng) and the average intensity of the fluorescent band. We were able to directly measure uPA activities in different cancer cell lines. This newly developed technique could be expanded to nearly all proteases, including the ones that cannot be analyzed by traditional zymography. (C) 2004 Elsevier Inc. All rights reserved. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Charlestown, MA 02129 USA. Natl Inst Dent & Craniofacial Res, Proteases Tissue Remodeling Unit, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA. RP Tung, CH (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, 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 [R01-CA99385, N01-CO17016, P50-CA86355] NR 36 TC 15 Z9 16 U1 0 U2 4 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD MAR 1 PY 2005 VL 338 IS 1 BP 151 EP 158 DI 10.1016/j.ab.2004.11.039 PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 900OA UT WOS:000227223000018 PM 15707946 ER PT J AU Melloy, PG Kusnierczyk, MK Meyer, RA Lo, CW Desmond, ME AF Melloy, PG Kusnierczyk, MK Meyer, RA Lo, CW Desmond, ME TI Overexpression of Connexin43 alters the mutant phenotype of midgestational Wnt-1 null mice resulting in recovery of the midbrain and cerebellum SO ANATOMICAL RECORD PART A-DISCOVERIES IN MOLECULAR CELLULAR AND EVOLUTIONARY BIOLOGY LA English DT Article DE midbrain-hindbrain junction; isthmus; embryonic neural tube; Chiari II malformations; neural tube defects ID GAP-JUNCTIONAL COMMUNICATION; GASTRULATING MOUSE EMBRYO; ZINC-FINGER GENE; ISTHMIC ORGANIZER; MID/HINDBRAIN ORGANIZER; INT-1 PROTOONCOGENE; SIGNALING PATHWAY; CAUDAL LIMIT; EXPRESSION; BRAIN AB The midbrain-hindbrain (MHB) junction plays a key role in the patterning of the embryonic neural tube and the formation of brain structures such as the cerebellum. The mitogen wnt-1 is critical for cerebellar development, as evidenced by the lack of MHB region and cerebellar formation in the wnt-1 null embryo. We have generated wnt-1 null embryos overexpressing the gap junction gene connexin43 by crossing wnt-1 null heterozygotes into the CMV43 mouse line. We have confirmed that these mice show an increase in gap junctional communication by dye coupling analysis. Two-thirds of wnt-1 null CMV43(+) mouse embryos at E18.5 have a cerebellum. In addition, changes in the wnt-1 null phenotype in mouse embryos overexpressing connexin43 are observed as early as E9.5. At this stage, one-quarter of wnt-1 null CMV43(+) embryos display extra or expanded tissue present at the MHB boundary (a wnt-1 null enlarged phenotype). In situ hybridization studies conducted on these embryos have indicated no changes in the expression of embryonic brain positional markers in this region. We conclude from these studies that overexpression of the connexin43 gap junction restores cerebellar formation by compensating for the loss of wnt-1. (C) 2005 Wiley-Liss, Inc. C1 Princeton Univ, Lewis Thomas Lab, Dept Mol Biol, Princeton, NJ 08544 USA. Villanova Univ, Dept Biol, Villanova, PA 19085 USA. Univ Penn, Dept Biol, Philadelphia, PA 19104 USA. Philadelphia Coll Osteopath Med, Philadelphia, PA USA. Creighton Univ, Dept Biomed Sci, Omaha, NE 68178 USA. NHLBI, Dev Biol Lab, NIH, Bethesda, MD 20892 USA. RP Melloy, PG (reprint author), Princeton Univ, Lewis Thomas Lab, Dept Mol Biol, Princeton, NJ 08544 USA. EM pmelloy@molbio.princeton.edu FU NHLBI NIH HHS [Z01-HL005701]; NICHD NIH HHS [HD 24710]; NINDS NIH HHS [NS 24136] NR 72 TC 8 Z9 9 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4884 J9 ANAT REC PART A JI Anat. Rec. Part A PD MAR PY 2005 VL 283A IS 1 BP 224 EP 238 DI 10.1002/ar.a.20158 PG 15 WC Anatomy & Morphology SC Anatomy & Morphology GA 903WD UT WOS:000227455400007 PM 15678491 ER PT J AU Brown, RH Hamilton, RG Mintz, M Jedlicka, AE Scott, AL Kleeberger, SR AF Brown, RH Hamilton, RG Mintz, M Jedlicka, AE Scott, AL Kleeberger, SR TI Genetic predisposition to latex allergy - Role of interleukin 13 and interleukin 18 SO ANESTHESIOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-of-Anesthesiologists CY OCT 23-27, 2004 CL Las Vegas, NV SP Amer Soc Anesthesiologists ID PROMOTER POLYMORPHISMS; ASTHMA; ATOPY; IL-18 AB Background. Occupational exposure of healthcare workers to natural rubber latex has led to sensitization and potentially life-threatening anaphylaxis. Although environmental exposure to natural rubber latex products is necessary for sensitization, it is not sufficient. A number of genetic factors also seem to contribute to the latex sensitization; however, the multigenic nature of the allergic phenotype has made the identification of susceptibility genes difficult. The current study tests the hypothesis that known functional polymorphisms in genes encoding interleukin 4, interleukin 13, and interleukin 18 occur in a higher frequency in healthcare workers with natural rubber latex allergy. Methods: Four hundred thirty-two healthcare workers with occupational exposure to natural rubber latex were screened using a clinical history questionnaire and latex-specific immunoglobulin E serology. Genomic DNA was extracted from peripheral blood lymphocytes and analyzed for single-nucleotide polymorphisms in candidate genes of interest. Data from cases and controls were analyzed by nominal logistic regression, with P < 0.05 considered significant. Results: The latex allergy phenotype was significantly associated with promoter polymorphisms in IL13 -1055 (P = 0.02), IL18 -607 (P = 0.02), and IL18 -656 (P = 0.02) compared with nonatopic controls. Conclusions: The significant association of IL13 and IL18 promoter polymorphisms with latex allergy suggests a potential location of,or genetic control in the induction of latex allergy in individuals and extends the understanding of the genetic basis for the induction of immediate-type hypersensitivity in healthcare workers occupationally exposed to natural rubber latex. C1 Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Med, Div Clin Immunol & Allergy, Baltimore, MD 21205 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA. NIEHS, NIH, Res Triangle Pk, NC 27709 USA. RP Brown, RH (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Room 7006,615 N Wolfe St, Baltimore, MD 21205 USA. EM rbrown2@jhem.jhmi.edu FU NIAID NIH HHS [AI43654] NR 20 TC 21 Z9 23 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAR PY 2005 VL 102 IS 3 BP 496 EP 502 DI 10.1097/00000542-200503000-00004 PG 7 WC Anesthesiology SC Anesthesiology GA 901IW UT WOS:000227277200003 PM 15731584 ER PT J AU Sambuughin, N Holley, H Muldoon, S Brandom, BW de Bantel, AM Tobin, JR Nelson, TE Goldfarb, LG AF Sambuughin, N Holley, H Muldoon, S Brandom, BW de Bantel, AM Tobin, JR Nelson, TE Goldfarb, LG TI Screening of the entire ryanodine receptor type 1 coding region for sequence variants associated with malignant hyperthermia susceptibility in the North American population SO ANESTHESIOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-of-Anesthesiologists CY OCT 23-27, 2004 CL Las Vegas, NV SP Amer Soc Anesthesiologists ID CENTRAL CORE DISEASE; RYR1 GENE; SKELETAL-MUSCLE; FUNCTIONAL-CHARACTERIZATION; CONGENITAL MYOPATHY; CONTRACTURE TEST; DENATURING HPLC; NEW-ZEALAND; MUTATIONS; IDENTIFICATION AB Background: Malignant hyperthermia (MH) is a life-threatening and frequently fatal disorder triggered by commonly used anesthetics. MH susceptibility is a genetically determined predisposition to the development of MH. Mutations in the ryanodine receptor type 1 (RYR1) gene are the major cause of MH susceptibility. The authors sought to develop a reliable genetic screening strategy based on efficient and relatively inexpensive mutation-detection procedures. Methods: A cohort (n = 30) of North American MH patients and MH-susceptible individuals was studied. RNA and DNA extracted from muscle tissue or blood lymphocytes were used for analysis. The entire RYR1 coding region was amplified in 57 overlapping fragments and subjected to denaturing high-performance liquid chromatography analysis followed by direct nucleotide sequencing to characterize RYR1 alterations. Results: Nine previously reported and nine unknown RYR1 mutations were identified in 21 of 30 studied patients (70%). Some of the new mutations were located outside of known mutational "hot spots," suggesting that RYR1 contains previously unknown mutation-prone areas requiring analysis. The North American MH/MH-susceptible population is characterized by a high RVR1 allelic heterogeneity. Conclusions: Denaturing high-performance liquid chromatography analysis of RNA samples extracted from the biopsied skeletal muscle followed by DNA sequencing is a highly efficient methodology for RYR1 mutation detection. This approach allows increasing the rate of mutation detection to 70% and identifying mutations in the entire RYR1 coding region. C1 NINDS, Clin Neurogenet Unit, NIH, Training Program, Bethesda, MD 20892 USA. Barrow Neurol Inst, Phoenix, AZ 85013 USA. Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA. Univ Pittsburgh, Pittsburgh, PA USA. Wake Forest Univ Med, Winston Salem, NC USA. RP Sambuughin, N (reprint author), NINDS, Clin Neurogenet Unit, NIH, Training Program, 5625 Fishers Lane,Rm 4S14, Bethesda, MD 20892 USA. EM sambuugn@ninds.nih.gov NR 36 TC 68 Z9 71 U1 1 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAR PY 2005 VL 102 IS 3 BP 515 EP 521 DI 10.1097/00000542-200503000-00007 PG 7 WC Anesthesiology SC Anesthesiology GA 901IW UT WOS:000227277200006 PM 15731587 ER PT J AU Sarnak, MJ Greene, T Wang, XL Beck, G Kusek, JW Collins, AJ Levey, AS AF Sarnak, MJ Greene, T Wang, XL Beck, G Kusek, JW Collins, AJ Levey, AS TI The effect of a lower target blood pressure on the progression of kidney disease: Long-term follow-up of the modification of diet in renal disease study SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID CONVERTING ENZYME-INHIBITION; PROTEIN RESTRICTION; METAANALYSIS; DESIGN; TRIAL AB Background: Hypertension is a risk factor for progression of chronic kidney disease. The optimal blood pressure to slow progression is unknown. Objective: To evaluate the effects of a low target blood pressure on kidney failure and all-cause mortality. Design: Long-term follow-up of the Modification of Diet in Renal Disease Study, a randomized, controlled trial conducted from 1989 to 1993. Setting: 15 outpatient nephrology practices. Participants: 840 persons with predominantly nondiabetic kidney disease and a glomerular filtration rate of 13 to 55 mL/min per 1.73 m(2). Intervention: A low target blood pressure (mean arterial pressure < 92 mm Hg) or a usual target blood pressure (mean arterial pressure < 107 mm Hg). Measurements: After the randomized trial was completed, kidney failure (defined as initiation of dialysis or kidney transplantation) and a composite outcome of kidney failure or all-cause mortality were ascertained through 31 December 2000. Results: Kidney failure occurred in 554 participants (66%), and the composite outcome occurred in 624 participants (74%). After Cox proportional hazards modeling and intention-to-treat analysis, the adjusted hazard ratios were 0.68 (95% Cl, 0.57 to 0.82; P < 0.001) for kidney failure and 0.77 (Cl, 0.65 to 0.91; P = 0.0024) for the composite outcome in the low target blood pressure group compared with the usual target blood pressure group. Evidence was insufficient to conclude that the benefit of a low target blood pressure differed according to the cause of kidney disease, baseline glomerular filtration rate, or degree of proteinuria. Limitations: The exact mechanism underlying the benefit of a low target blood pressure is unknown. Conclusions: Assignment to a low target blood pressure slowed the progression of nondiabetic kidney disease in patients with a moderately to severely decreased glomerular filtration rate. C1 Tufts New England Med Ctr, Div Nephrol, Boston, MA 02111 USA. Cleveland Clin Fdn, Cleveland, OH 44195 USA. NIH, Bethesda, MD 20892 USA. US Renal Data Syst, Minneapolis, MN USA. RP Sarnak, MJ (reprint author), Tufts New England Med Ctr, Div Nephrol, Box 391,750 Washington St, Boston, MA 02111 USA. EM msarnak@tufts-nemc.org FU NIDDK NIH HHS [UO1 DK 35073, K23 DK 02904] NR 13 TC 250 Z9 262 U1 1 U2 4 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 1 PY 2005 VL 142 IS 5 BP 342 EP 351 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA 902BB UT WOS:000227325100004 PM 15738453 ER PT J AU Dal Forno, G Palermo, MT Donohue, JE Karagiozis, H Zonderman, AB Kawas, CH AF Dal Forno, G Palermo, MT Donohue, JE Karagiozis, H Zonderman, AB Kawas, CH TI Depressive symptoms, sex, and risk for Alzheimer's disease SO ANNALS OF NEUROLOGY LA English DT Article ID ESTROGEN REPLACEMENT THERAPY; LATE-LIFE DEPRESSION; COGNITIVE DECLINE; GENDER-DIFFERENCES; MAJOR DEPRESSION; CES-D; REVERSIBLE DEMENTIA; PARKINSONS-DISEASE; HUMAN HYPOTHALAMUS; OLDER PERSONS AB Depression associates with increased risk for dementia and Alzheimer's disease (AD), although it is unclear whether it represents an actual risk factor or a prodrome. To determine the relative hazard of premorbid depressive symptomatology for development of dementia and AD, we studied risk for incident dementia and AD over a 14-year period in 1,357 community-dwelling men and women participating in the 40-year prospective Baltimore Longitudinal Study of Aging. Screening for depressive symptoms, comprehensive medical and neuropsychological evaluations were prospectively collected every 2 years. Time-dependent proportional hazards of development of AD or dementia were calculated separately for men and women, with symptoms of depression detected at 2-, 4-, and 6-year intervals before onset of dementia symptoms. Vascular risk factors were analyzed as covariates. Premorbid depressive symptoms significantly increased risk for dementia, particularly AD in men but not in women. Hazard ratios were approximately two times greater than for individuals without history of depressive symptoms, an effect independent of vascular disease. We conclude that the impact of depressive symptoms on risk for dementia and AD may vary with sex. Further studies assessing separately the role of depression as a risk factor in men and women are necessary. C1 AFaR, Rome, Italy. Ctr Med Parioli, Rome, Italy. NIA, Intramural Res Program, Lab Personal & Cognit, Baltimore, MD 21224 USA. Sinai Hosp, Ctr Canc Res, Baltimore, MD 21215 USA. Univ Calif Irvine, Gillespie Neurosci Res Facil, Dept Neurol, Irvine, CA USA. Univ Calif Irvine, Gillespie Neurosci Res Facil, Dept Neurobiol & Behav, Irvine, CA USA. RP Dal Forno, G (reprint author), Univ Campus BioMed,Via Compositori 130-132, I-00128 Rome, Italy. EM g.dalforno@unicampus.it OI Zonderman, Alan B/0000-0002-6523-4778 FU NCRR NIH HHS [M01 RR 02719]; NIA NIH HHS [AG 05146, AG 08325] NR 72 TC 79 Z9 81 U1 2 U2 5 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAR PY 2005 VL 57 IS 3 BP 381 EP 387 DI 10.1002/ana.20405 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 903CK UT WOS:000227402800010 PM 15732103 ER PT J AU Hernandez, DG Paisan-Ruiz, C McInerney-Leo, A Jain, S Meyer-Lindenberg, A Evans, EW Berman, KF Johnson, J Auburger, G Schaffer, AA Lopez, GJ Nussbaum, RL Singleton, AB AF Hernandez, DG Paisan-Ruiz, C McInerney-Leo, A Jain, S Meyer-Lindenberg, A Evans, EW Berman, KF Johnson, J Auburger, G Schaffer, AA Lopez, GJ Nussbaum, RL Singleton, AB TI Clinical and positron emission tomography of Parkinson's disease caused by LRRK2 SO ANNALS OF NEUROLOGY LA English DT Article ID GENE; MUTATIONS AB We have recently identified mutations in a gene leucine-rich repeat kinase-2 (LRRK2), which cause autosomal dominant Parkinson's disease. Here, we describe two families with autosomal dominant Parkinson's disease caused by a LRRK2 G2019S mutation. We present here a clinical description of patients, including 6-F-18-fluoro-L-dopa positron emission tomography and discuss the potential implications of this mutation, which alters a conserved residue in a domain required for kinase activation. C1 NIA, Neurogenet Lab, NIH, Mol Genet Unit,Dept Hlth & Human Serv,Porter Neur, Bethesda, MD 20892 USA. CSIC, Unitat Genet Mol, Dept Genomica & Prot, Inst Biomed Valencia, Valencia, Spain. NHGRI, Genet Dis Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Reta Lila Weston Inst Neurol Sci, London, England. Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England. NIMH, Unit Integrat Neuroimaging, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA. Univ Frankfurt, Mol Genet Sect, Neurol Clin, D-6000 Frankfurt, Germany. NIH, Natl Ctr Biotechnol Informat, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Singleton, AB (reprint author), NIA, Neurogenet Lab, NIH, Mol Genet Unit,Dept Hlth & Human Serv,Porter Neur, Bldg 10,Room 6C103,MSC 1589,9000 Rockville Pike, Bethesda, MD 20892 USA. EM singleta@mail.nih.gov RI Paisan-Ruiz, Coro/C-2912-2009; Johnson, Janel/A-7136-2010; Singleton, Andrew/C-3010-2009; Schaffer, Alejandro/F-2902-2012; OI Meyer-Lindenberg, Andreas/0000-0001-5619-1123 NR 9 TC 83 Z9 89 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAR PY 2005 VL 57 IS 3 BP 453 EP 456 DI 10.1002/ana.20401 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 903CK UT WOS:000227402800021 PM 15732108 ER PT J AU Floel, A Nagorsen, U Werhahn, KJ Ravindran, S Birbaumer, N Knecht, S Cohen, LG AF Floel, A Nagorsen, U Werhahn, KJ Ravindran, S Birbaumer, N Knecht, S Cohen, LG TI Influence of somatosensory input on motor function in patients with chronic stroke - Reply SO ANNALS OF NEUROLOGY LA English DT Letter ID DEAFFERENTATION; CORTEX; MODULATION; OUTPUTS C1 NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20892 USA. NINDS, Stroke Neurorehabil Clin, NIH, Bethesda, MD 20892 USA. RP Floel, A (reprint author), NINDS, Human Cort Physiol Sect, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA. RI Floel, Agnes/A-9426-2017 NR 13 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAR PY 2005 VL 57 IS 3 BP 466 EP 467 DI 10.1002/ana.20409 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 903CK UT WOS:000227402800028 ER PT J AU Van Mello, NM Pillemer, SR Tak, PP Sankar, V AF Van Mello, NM Pillemer, SR Tak, PP Sankar, V TI B cell MALT lymphoma diagnosed by labial minor salivary gland biopsy in patients screened for Sjogren's syndrome SO ANNALS OF THE RHEUMATIC DISEASES LA English DT Article ID CLASSIFICATION; APOPTOSIS; RISK AB Case report: Three patients presented to the Sjogren's syndrome ( SS) Clinic at the National Institute of Dental and Craniofacial Research for screening. The records of patients with SS with a diagnosis of lymphoma were examined to determine whether the diagnosis was made in any of the cases as a result of labial salivary gland (LSG) biopsies. All patients had typical features of primary SS according to the American-European Consensus Group criteria. B cell mucosa associated lymphoid tissue ( MALT) lymphoma was diagnosed based upon the LSG biopsy. Conclusion: This report underlines the advantages of performing LSG biopsies as a routine part of screening for SS, and shows that it may in some instances lead to early diagnosis of MALT lymphomas in patients who show no signs of pre-existing lymphoma. C1 Natl Inst Dent & Craniofacial Res, Gene Therapy & Therapeut Branch, NIH, DHHS, Bethesda, MD 20892 USA. Univ Amsterdam, Acad Med Ctr, Div Clin Immunol & Rheumatol, NL-1105 AZ Amsterdam, Netherlands. RP Tak, PP (reprint author), Univ Amsterdam, Acad Med Ctr, Div Clin Immunol & Rheumatol, F4-218,POB 22700, NL-1100 DE Amsterdam, Netherlands. EM P.P.Tak@amc.uva.nl NR 14 TC 18 Z9 18 U1 0 U2 1 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-4967 J9 ANN RHEUM DIS JI Ann. Rheum. Dis. PD MAR PY 2005 VL 64 IS 3 BP 471 EP 473 DI 10.1136/ard.2004.022707 PG 3 WC Rheumatology SC Rheumatology GA 897CD UT WOS:000226980700022 PM 15708896 ER PT J AU Lemaire, M Momparler, LF Bernstein, ML Marquez, VE Momparler, RL AF Lemaire, M Momparler, LF Bernstein, ML Marquez, VE Momparler, RL TI Enhancement of antineoplastic action of 5-aza-2'-deoxycytidine by zebularine on L1210 leukemia SO ANTI-CANCER DRUGS LA English DT Article DE 5-aza-2'-deoxycytidine; chemotherapy; cytidine deaminase; DNA methylation; leukemia; p57KIP2 expression; zebularine ID ABERRANT DNA METHYLATION; HUMAN CYTIDINE DEAMINASE; CYTOSINE-ARABINOSIDE; 5-AZA-2'-DEOXYCYTIDINE DECITABINE; CANCER EPIGENETICS; TRANSITION-STATE; CELLS; DEMETHYLATION; INHIBITION; MALIGNANCIES AB Tumor suppressor genes that have been silenced by aberrant DNA methylation are potential targets for reactivation by novel chemotherapeutic agents. The potent inhibitor of DNA methylation and antileukemic agent, 5-aza-2'-deoxycytidine (5-AZA-CdR, Decitabine), can reactivate silent tumor suppressor genes. One hindrance to the curative potential of 5-AZA-CdR is its rapid in vivo inactivation by cytidine deaminase (CD). An approach to overcome this obstacle is to use 5-AZA-CdR in combination with zebularine (Zeb), a potent inhibitor of CD. Zeb also possesses independent antineoplastic activity due to its inhibition of DNA methylation. We tested the capacity of 5-AZA-CdR and Zeb alone and in combination to inhibit growth and colony formation of different leukemic cell lines. 5-AZA-CdR and Zeb in combination produced a greater inhibition of growth against murine L1210 lymphoid leukemic cells, and a greater reduction in colony formation by L1210 and human HL-60 myeloid leukemic cells, than either agent alone. The ability of these agents to reactivate the tumor suppressor gene, p57KIP2, was also tested using RT-PCR. The combination produced a synergistic reactivation of p57KIP2 in HL-60 leukemic cells. A methylation-specific PCR assay showed that this combination also induced a significantly greater demethylation level of the p57KIP2 promoter than either drug alone. The in vivo antineoplastic activity of the agents was evaluated in mice with L1210 leukemia. A greater increase in survival time of mice with L1210 leukemia was observed with the combination than with either agent alone using three different dose schedules. The enhanced activity observed with 5-AZA-CdR plus Zeb in both murine and human leukemic cells lines provides a rationale for the clinical investigation of these drugs in patients with advanced leukemia. The probable mechanism of this drug interaction involves inhibition of CD by Zeb and the complementary inhibition of DNA methylation by both agents. (C) 2005 Lippincott Williams Wilkins. C1 Hop St Justine, Ctr Rech, Serv Hematol Oncol, Montreal, PQ H3T 1C5, Canada. Univ Montreal, Dept Pharmacol, Ctr Rech Pediatr, Montreal, PQ H3C 3J7, Canada. NCI, Med Chem Lab, Ctr Canc Res, NIH, Frederick, MD 21701 USA. RP Momparler, RL (reprint author), Hop St Justine, Ctr Rech, Serv Hematol Oncol, 3175 Cote St Catherine, Montreal, PQ H3T 1C5, Canada. EM richard.l.momparler@umontreal.ca NR 34 TC 42 Z9 44 U1 1 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4973 J9 ANTI-CANCER DRUG JI Anti-Cancer Drugs PD MAR PY 2005 VL 16 IS 3 BP 301 EP 308 DI 10.1097/00001813-200503000-00009 PG 8 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 902BM UT WOS:000227326200009 PM 15711182 ER PT J AU Lara, PN Law, LY Wright, JJ Frankel, P Twardowski, P Lenz, HJ Lau, DHM Kawaguchi, T Gumerlock, PH Doroshow, JH Gandara, DR AF Lara, PN Law, LY Wright, JJ Frankel, P Twardowski, P Lenz, HJ Lau, DHM Kawaguchi, T Gumerlock, PH Doroshow, JH Gandara, DR TI Intermittent dosing of the farnesyl transferase inhibitor tipifarnib (R115777) in advanced malignant solid tumors: a phase I California Cancer Consortium Trial SO ANTI-CANCER DRUGS LA English DT Article DE clinical trial; dose escalation; signal transduction ID FARNESYLTRANSFERASE; EFFICACY AB Tipifarnib (R115777) inhibits farnesylation of key proteins that modulate signaling pathways implicated in cell growth and proliferation, including members of the Ras and Rho families. It has broad-spectrum anti proliferative activity in vitro and in vivo. Clinical trials employing a continuous administration schedule have demonstrated dose-limiting neurotoxicity and myelosuppression. Preclinical studies have shown that intermittent oral administration can suppress tumor growth comparable to continuous administration. We conducted a National Cancer Institute-sponsored phase I trial to determine the feasibility of an intermittent dosing schedule of R115777 given orally twice daily on weeks 1 and 3 of a 28-day cycle in patients with malignant solid tumors. Starting dose was 300 mg twice daily (b.i.d.) with escalation by 300 mg b.i.d. increments over six dose levels to a maximum of 1800 mg b.i.d. Dose-limiting toxicity (DLT) was defined as any grade 3 or 4 non-hematologic toxicity, grade 4 thrombocytopenia, grade 4 neutropenia (ANC) with fever (38.3degreesC or above) or a documented infection. Twenty-one patients with advanced solid tumors, all of whom had prior systemic therapy, were accrued. Grade 3 fatigue was dose limiting for two of three patients at the 900 mg b.i.d. dose level. Although no responses were seen, four of six patients with stable disease remained on study for at least a year (16, 17, 13 and 12 months) before developing progressive disease. Three of these prolonged stable disease patients had non-small cell lung cancer. We conclude that intermittent dosing of R115777 is feasible and tolerable. The recommended phase II dose is 600 mg orally b.i.d. on alternate weeks. (C) 2005 Lippincott Williams Wilkins. C1 Univ Calif Davis, Ctr Canc, Sacramento, CA 95817 USA. City Hope Comprehens Canc Ctr, Duarte, CA USA. Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA. Vet Adm No Calif Hlth Care Syst, Martinez, CA USA. NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA. RP Lara, PN (reprint author), Univ Calif Davis, Ctr Canc, 4501 X St, Sacramento, CA 95817 USA. EM primo.lara@ucdmc.ucdavis.edu FU NCI NIH HHS [N01 CM17101, CA63265, CA62505] NR 14 TC 13 Z9 14 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4973 J9 ANTI-CANCER DRUG JI Anti-Cancer Drugs PD MAR PY 2005 VL 16 IS 3 BP 317 EP 321 DI 10.1097/00001813-200503000-00011 PG 5 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 902BM UT WOS:000227326200011 PM 15711184 ER PT J AU Akahane, M Akahane, T Shah, A Okajima, E Thorgeirsson, UP AF Akahane, M Akahane, T Shah, A Okajima, E Thorgeirsson, UP TI A potential role for vascular endothelial growth factor-D as an autocrine growth factor for human breast carcinoma cells SO ANTICANCER RESEARCH LA English DT Article DE VEGF-D; cell proliferation; breast cancer; cyclin; angiogenesis ID VEGF-D; TUMOR-CELLS; EXPRESSION; RECEPTORS; SURVIVAL; CANCER; LYMPHANGIOGENESIS; PROLIFERATION; ANGIOGENESIS; PROMOTES AB Background. Vascular endothelial growth factor-D (VEGF-D) binds and activates vascular endothelial growth factor receptor-2 (VEGFR-2), which signals for angiogenesis, and VEGFR-3, which signals for lymphangiogenesis. Besides endothelial cells, VEGFR-2 has been detected on malignant cells, including human breast carcinoma cells. Materials and Methods. It was examined if ectopic expression of human VEGF-D affected growth of breast carcinoma cell lines in vitro and in vivo. Results. VEGF-D overexpressing clonal MCF-7 and MDA-MB-231 cell lines displayed increased proliferative activities and upregulation of cyclins A, D1 and D3, compared to the vector control. Following subcutaneous inoculation of the MDA-MB-231 cells into nude mice, growth of the VEGF-D overexpressing cells was greatly accelerated. The tumor weight gain was accompanied by increased proliferative activity, cyclin A expression and microvascular density. Conclusions. These findings suggest that VEGF-D functions both as an autocrine growth factor and a stimulator of angiogenesis in breast cancer. C1 NCI, Cellular Carcinogenesis & Tumor Promot Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. Natl Canc Ctr, Chuo Ku, Tokyo 1040045, Japan. RP Thorgeirsson, UP (reprint author), NCI, Cellular Carcinogenesis & Tumor Promot Lab, Canc Res Ctr, NIH, Bldg 37,Room 4032A,Convent Dr, Bethesda, MD 20892 USA. EM thorgeiu@mail.nih.gov NR 35 TC 11 Z9 12 U1 0 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD MAR-APR PY 2005 VL 25 IS 2A BP 701 EP 707 PG 7 WC Oncology SC Oncology GA 919BT UT WOS:000228594000003 PM 15868899 ER PT J AU Perabo, FGE Demant, AW Wirger, A Schmidt, DH Sitia, M Wardelmann, E Muller, SC Kohn, EC AF Perabo, FGE Demant, AW Wirger, A Schmidt, DH Sitia, M Wardelmann, E Muller, SC Kohn, EC TI Carboxyamido-triazole (CAI) reverses the balance between proliferation and apoptosis in a rat bladder cancer model SO ANTICANCER RESEARCH LA English DT Article DE bladder cancer; carboxyamido-triazole; apoptosis; proliferation; animal model ID SIGNAL-TRANSDUCTION INHIBITOR; METHYL-N-NITROSOUREA; CALCIUM HOMEOSTASIS; SOLID TUMORS; CELL-LINES; PHASE-II; COMBINATION; CARCINOMA; EFFICACY; GROWTH AB Carboxyamido-triazole (CAI) is an orally bioavailable calcium influx and signal transduction inhibitor that has been shown to be anti-invasive, anti-angiogenic and anti-metastatic in v different human tumors including transitional cell carcinoma. This study was undertaken to further evaluate the activity of CAI in a rat bladder cancer model. A transitional cell carcinoma (TCC) was chemically induced by intravesical installation of methyl-nitrosurea (MNU) in the bladder of female Fischer 344 rats. First, a toxicity study was performed which revealed no side-effects of CAI in the animals up to a dose of 250 mg/kg CAI. For treatment, a dose of 100 mg/kg CAI dissolved in PEG-400 vehicle was chosen. Oral administration of CAI continuously daily for 4 weeks (group A), 3 days/week over 6 weeks (group B), or intravesically twice a week for 6 weeks (group C) caused a reduction of spontaneous development of TCC. Lower stage and grade of tumors were seen in all CAI-treated animals. Under CAI treatment, the apoptotic rate in tumors increased, whereas the proliferation rate decreased, as shown by TUNEL assay and KI-67-immunhistochemistry, respectively. The highest efficacy was seen in group B, with 5 out of 10 animals tumor free. Intravesical application (group C) resulted in 3 out of 10 animals tumor free. Normal urothelium was not affected by CAI. This animal model confirms the anti-tumor effect of CAI and shows induction of apoptosis and growth inhibition in bladder cancer by the drug. C1 Univ Bonn, Dept Urol, D-53105 Bonn, Germany. Med Univ Lubeck, Dept Urol, D-23562 Lubeck, Germany. Univ Bonn, Inst Pathol, D-53105 Bonn, Germany. NCI, Pathol Lab, Bethesda, MD 20892 USA. RP Perabo, FGE (reprint author), POB 1906, D-82309 Starnberg, Germany. EM perabo@lycos.com NR 23 TC 3 Z9 5 U1 3 U2 3 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD MAR-APR PY 2005 VL 25 IS 2A BP 725 EP 729 PG 5 WC Oncology SC Oncology GA 919BT UT WOS:000228594000006 PM 15868902 ER PT J AU Mogi, S Dang, DM Van Waes, C Ellis, D Atakilit, A Ramos, DM AF Mogi, S Dang, DM Van Waes, C Ellis, D Atakilit, A Ramos, DM TI The expression of integrin alpha v beta 6 promotes the epithelial cell morphology and suppresses invasive behavior in transformed oral keratinocytes SO ANTICANCER RESEARCH LA English DT Article DE oral keratinocyte; alpha v beta 6; squamous cell carcinoma; epithelial-mesenchymal transition (EMT) ID MURINE MODEL; TENASCIN-C; CARCINOMA; MIGRATION; LINES; CD80 AB The expression of the integrin av beta 6 has been correlated with oral SCC invasion. We evaluated its expression in three 4NQO transformed murine oral keratinocyte cell lines (B7E3, B7E11 and B4B8). The B7E3 cells were negative for beta 6, whereas the B7E11 and the B4B8 cells were both positive. The beta 6 negative B7E3 cells were fibroblast-like in appearance, whereas the B7E11 cells were more epithelial-like. The B4B8 cells were a mixture of the two cell types. Using immunofluorescent microscopy, we found that vimentin was highly expressed in the B7E3 cells, whereas the B7E11 cells keratin positive. The B4B8 cells expressed both filaments. The B7E3 cells formed large tumors when injected into nude mice, whereas the B4B8 cells formed small tumors and the B7E11 cells formed none. These results suggest that the expression of the av beta 6 integrin suppresses tumor formation and may promote the epithelial phenotype in 4NQO-transformed murine oral keratinocytes. C1 Univ Calif San Francisco, Dept Orofacial Sci, Ctr Comprehens Canc, San Francisco, CA 94143 USA. Univ Calif San Francisco, Lung Biol Ctr, San Francisco, CA 94143 USA. NIDOCD, Tumor Biol Sect, NIH, Bethesda, MD USA. RP Ramos, DM (reprint author), Univ Calif San Francisco, Dept Orofacial Sci, Ctr Comprehens Canc, 513 Parnassus Ave,C415 Box 0422, San Francisco, CA 94143 USA. NR 22 TC 6 Z9 6 U1 0 U2 0 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD MAR-APR PY 2005 VL 25 IS 2A BP 751 EP 755 PG 5 WC Oncology SC Oncology GA 919BT UT WOS:000228594000010 PM 15868906 ER PT J AU Shelton, MD Chock, PB Mieyal, JJ AF Shelton, MD Chock, PB Mieyal, JJ TI Glutaredoxin: Role in reversible protein S-glutathionylation and regulation of redox signal transduction and protein translocation SO ANTIOXIDANTS & REDOX SIGNALING LA English DT Review ID NF-KAPPA-B; METABOLIC OXIDATIVE STRESS; TYROSINE-PHOSPHATASE 1B; EPIDERMAL-GROWTH-FACTOR; CYSTEINE-SULFINIC ACID; KINASE-C; THIOLTRANSFERASE GLUTAREDOXIN; DNA-BINDING; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; NUCLEAR-LOCALIZATION AB Reversible posttranslational modifications on specific amino acid residues can efficiently regulate protein functions. O-Phosphorylation is the prototype and analogue to the rapidly emerging mechanism of regulation known as S-glutathionylation. The latter is being recognized as a potentially widespread form of modulation of the activities of redox-sensitive thiol proteins, especially those involved in signal transduction pathways and translocation. The abundance of reduced glutathione in cells and the ready conversion of sulfenic acids and S-nitroso derivatives to S-glutathione mixed disulfides support the notion that reversible S-glutathionylation is likely to be the preponderant mode of redox signal transduction. The glutaredoxin enzyme has served as a focal point and important tool for evolution of this regulatory mechanism because of its characterization as a specific and efficient catalyst of protein-SSG de-glutathionylation (akin to phosphatases). Identification of specific mechanisms and enzyme(s) that catalyze formation of protein-SSG intermediates, however, is largely unknown and represents a prime objective for furthering understanding of this evolving mechanism of cellular regulation. Several proteomic approaches, including the use of cysteine-reactive fluorescent and radiolabel probes, have been developed to detect arrays of proteins whose cysteine residues are modified in response to oxidants, thus identifying them as potential interconvertible proteins to be regulated by redox signaling (glutathionylation). Specific criteria were used to evaluate current data on cellular regulation via S-glutathionylation. Among many proteins under consideration, actin, protein tyrosine phosphatase-1B, and Ras stand out as the best current examples for establishing this regulatory mechanism. C1 Case Western Reserve Univ, Sch Med, Dept Pharmacol, Cleveland, OH 44106 USA. NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA. RP Case Western Reserve Univ, Sch Med, Dept Pharmacol, 2109 Adelbert Rd, Cleveland, OH 44106 USA. EM jjm5@cwru.edu FU NEI NIH HHS [5T32 EY07157]; NIA NIH HHS [1P01 AG 15885, 1R01 AG 024413] NR 119 TC 240 Z9 251 U1 0 U2 22 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1523-0864 EI 1557-7716 J9 ANTIOXID REDOX SIGN JI Antioxid. Redox Signal. PD MAR-APR PY 2005 VL 7 IS 3-4 BP 348 EP 366 DI 10.1089/ars.2005.7.348 PG 19 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 901YW UT WOS:000227319200006 PM 15706083 ER PT J AU Kurup, SK Yin, PD Wright, M Kump, L Moeller, K Clarke, GL Coleman, HR Smith, JA Fischer, SH Nussenblatt, RB AF Kurup, SK Yin, PD Wright, M Kump, L Moeller, K Clarke, GL Coleman, HR Smith, JA Fischer, SH Nussenblatt, RB TI Progressive outer retinal necrosis in an AIDS patient during the era of highly active anti-retroviral therapy (HAART): Successful outcome with intravitreal drugs and monitoring with quantitative PCR SO ANTIVIRAL RESEARCH LA English DT Meeting Abstract CT 18th International Conference on Antiviral Research CY APR 11-14, 2005 CL Barcelona, SPAIN SP Int Soc Antiviral Res C1 NEI, NIH, Bethesda, MD 20892 USA. NIAID, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD MAR PY 2005 VL 65 IS 3 BP A36 EP A36 PG 1 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA 911GF UT WOS:000227989900020 ER PT J AU Morrey, JD Kocisko, DA Race, RE Chen, JC Caughey, B AF Morrey, JD Kocisko, DA Race, RE Chen, JC Caughey, B TI Evaluation of new cell culture inhibitors of protease-resistant prion protein against scrapie infection in mice SO ANTIVIRAL RESEARCH LA English DT Meeting Abstract CT 18th International Conference on Antiviral Research CY APR 11-14, 2005 CL Barcelona, SPAIN SP Int Soc Antiviral Res C1 Utah State Univ, Inst Antiviral Res, Logan, UT 84322 USA. NIAID, NIH, Persistent Viral Dis Lab, Hamilton, MT USA. Food Bur Sichuan Prov, Chengdu Jinniu Inst, Chengdu, Sichuan, Peoples R China. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD MAR PY 2005 VL 65 IS 3 BP A84 EP A84 PG 1 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA 911GF UT WOS:000227989900130 ER PT J AU Ohrui, H Kohgo, S Kitano, K Ashida, N Hayakawa, H Kodama, E Matsuoka, M Mitsuya, H AF Ohrui, H Kohgo, S Kitano, K Ashida, N Hayakawa, H Kodama, E Matsuoka, M Mitsuya, H TI 4 '-C-ethynyl-2 '-deoxy-2-fluoroadenosine, a nucleoside derivative potent against HIV-1 with no acute mouse toxicity: Highlights of the role of 3 '-OH for biological activity SO ANTIVIRAL RESEARCH LA English DT Meeting Abstract CT 18th International Conference on Antiviral Research CY APR 11-14, 2005 CL Barcelona, SPAIN SP Int Soc Antiviral Res C1 Tohoku Univ, Grad Sch Life Sci, Sendai, Miyagi 980, Japan. Yamasa Corp, Choshi, Chiba, Japan. Kyoto Univ, Inst Virus Res, Kyoto 606, Japan. Kumamoto Univ, Sch Med, Kumamoto 860, Japan. NCI, NIH, Bethesda, MD 20892 USA. RI Kodama, Eiichi /C-4032-2009 OI Kodama, Eiichi /0000-0002-6622-2752 NR 1 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0166-3542 J9 ANTIVIR RES JI Antiviral Res. PD MAR PY 2005 VL 65 IS 3 BP A42 EP A42 PG 1 WC Pharmacology & Pharmacy; Virology SC Pharmacology & Pharmacy; Virology GA 911GF UT WOS:000227989900031 ER PT J AU Hintz, SR Poole, WK Wright, LL Fanaroff, AA Kendrick, DE Laptook, AR Goldberg, R Duara, S Stoll, BJ Oh, W AF Hintz, SR Poole, WK Wright, LL Fanaroff, AA Kendrick, DE Laptook, AR Goldberg, R Duara, S Stoll, BJ Oh, W TI Changes in mortality and morbidities among infants born at less than 25 weeks during the post-surfactant era SO ARCHIVES OF DISEASE IN CHILDHOOD-FETAL AND NEONATAL EDITION LA English DT Article ID LOW-BIRTH-WEIGHT; NEONATAL RESEARCH NETWORK; EXTREMELY PREMATURE-INFANTS; WEEKS GESTATIONAL-AGE; NATIONAL INSTITUTE; CHILD HEALTH; RISK-FACTORS; SURVIVAL; OUTCOMES; GRAMS AB Objectives: To compare mortality and death or major morbidity (DOMM) among infants < 25 weeks estimated gestational age (EGA) born during two post-surfactant era time periods. Study design and patients: Comparative cohort study of very low birthweight (501-1500 g) infants < 25 weeks EGA in the NICHD Neonatal Research Network born during two post-surfactant era time periods (group 1, 1991-1994, n = 1408; group II, 1995-1998, n = 1348). Perinatal and neonatal factors were compared, and group related mortality and DOMM risk were evaluated. Results: Mortality was higher for group 1 (63.1% v 56.7%; p = 0.0006). Antenatal steroids (ANS) and antenatal antibiotics (AABX), surfactant (p < 0.0001), and bronchopulmonary dysplasia (p = 0.0008) were more prevalent in group II. In a regression model that controlled for basic and delivery factors only, mortality risk was greater for group I than for group 11 (odds ratio (OR) 1.4, 95% confidence interval (CI) 1.2 to 1.7); the addition of AABX and surfactant, or ANS (OR 0.97, 95% CI 0.79 to 1.2) to the model appeared to account for this difference. There was no difference in DOMM (86.8% v 88.4%; p = 0.2), but risk was lower for group I in regression models that included ANS (OR 0.70, 95% Cl 0.52 to 0.94). Conclusion: Survival to discharge was more likely during the more recent period because of group differences in ANS, AABX, and surfactant. However, this treatment shift may reflect an overall more aggressive management approach. More consistent application of treatment has led to improving survival < 25 week EGA infants during the post-surfactant era, but possibly at the cost of greater risk of major Of in hospital morbidities. C1 Stanford Univ, Med Ctr, Div Neonatol, Palo Alto, CA 94304 USA. Res Triangle Inst, Res Triangle Pk, NC 27709 USA. NICHHD, Dept Pediat, Bethesda, MD 20892 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. Univ Texas, SW Med Ctr, Dept Pediat, Dallas, TX USA. Duke Univ, Durham, NC USA. Univ Miami, Dept Pediat, Miami, FL 33152 USA. Emory Univ, Sch Med, Dept Pediat, Atlanta, GA USA. Brown Univ, Dept Pediat, Providence, RI 02912 USA. RP Hintz, SR (reprint author), Stanford Univ, Dept Pediat, Div Neonatal & Dev Med, 750 Welch Rd,Suite 315, Palo Alto, CA 94304 USA. EM srhintz@stanford.edu NR 39 TC 11 Z9 15 U1 0 U2 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 1359-2998 J9 ARCH DIS CHILD-FETAL JI Arch. Dis. Child.-Fetal Neonatal Ed. PD MAR PY 2005 VL 90 IS 2 BP 128 EP 133 DI 10.1136/adc.2003.046268 PG 6 WC Pediatrics SC Pediatrics GA 943GE UT WOS:000230340700009 ER PT J AU van den Bree, MBM Pickworth, WB AF van den Bree, MBM Pickworth, WB TI Risk factors predicting changes in marijuana involvement in teenagers SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID HIGH-SCHOOL-STUDENTS; ADOLESCENT SUBSTANCE USE; DRUG-USE; CANNABIS USE; YOUNG ADULTHOOD; ENVIRONMENTAL-INFLUENCES; MENTAL-DISORDERS; DEVIANT-BEHAVIOR; COMMUNITY SAMPLE; PEER INFLUENCE AB Background: Marijuana use during adolescence has various adverse psychological and health outcomes. It is poorly understood whether the same risk factors influence different stages of marijuana involvement. Objective: To establish which risk factors best explain different stages of marijuana involvement. Design: Data were collected at 2 points using computer-assisted personal interview (wave I and wave 2 were separated by I year). Twenty-one well-established risk factors of adolescent substance use/abuse were used to predict 5 stages of marijuana involvement: (1) initiation of experimental use, (2) initiation of regular use, (3) progression to regular use, (4) failure to discontinue experimental use, and (5) failure to discontinue regular use. Data were analyzed- using logistic regression analysis. Participants: Middle school and high school students (N = 13 718, aged 11-21 years) participating in the National Longitudinal Study of Adolescent Health (Add Health). Results: Three risk factors (own and peer involvement with substances, delinquency, and school problems) Were the strongest predictors of all stages. Their combined presence greatly increased risk of initiation of experimental (odds ratio, 20) and regular (odds ratio, 87) marijuana use over the next year. Personality, family, religious, and pastime factors exerted stage-specific, sex-specific, and age-specific influences. Conclusions: Assessment of substance, school, and delinquency factors is important in identifying individuals at high risk for continued involvement with marijuana. Prevention and/or intervention efforts should focus on these areas of risk. C1 Univ Wales Coll Cardiff, Div Psychol Med, Coll Med, Cardiff CF14 4XN, S Glam, Wales. Natl Inst Drug Abuse, Intramural Res Program, NIH, Baltimore, MD 21224 USA. RP van den Bree, MBM (reprint author), Univ Wales Coll Cardiff, Div Psychol Med, Coll Med, Heat Pk, Cardiff CF14 4XN, S Glam, Wales. EM vandenbreemb@cardiff.ac.uk RI turton, miranda/F-4682-2011 FU NICHD NIH HHS [P01-HD31921] NR 84 TC 97 Z9 98 U1 4 U2 21 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD MAR PY 2005 VL 62 IS 3 BP 311 EP 319 DI 10.1001/archpsyc.62.3.311 PG 9 WC Psychiatry SC Psychiatry GA 902YC UT WOS:000227391600009 PM 15753244 ER PT J AU Chew, EY Clemons, T AF Chew, EY Clemons, T TI Vitamin E and the age-related eye disease study supplementation for age-related macular degeneration SO ARCHIVES OF OPHTHALMOLOGY LA English DT Editorial Material ID MORTALITY C1 Natl Inst Hlth, Div Epidemiol & Clin Res, Bethesda, MD 20892 USA. RP Chew, EY (reprint author), Natl Inst Hlth, Div Epidemiol & Clin Res, Bldg 10 CRC,Room 3-2531,10 Ctr Dr,MSC-1204, Bethesda, MD 20892 USA. EM echew@nei.nih.gov FU Intramural NIH HHS [Z99 EY999999] NR 4 TC 15 Z9 15 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAR PY 2005 VL 123 IS 3 BP 395 EP 396 DI 10.1001/archopht.123.3.395 PG 2 WC Ophthalmology SC Ophthalmology GA 903SV UT WOS:000227446800015 PM 15767485 ER PT J AU Corby, PMA Bretz, WA Hart, TC Melo, M Oliveira, B Vanyukov, M AF Corby, PMA Bretz, WA Hart, TC Melo, M Oliveira, B Vanyukov, M TI Mutans streptococci in preschool twins SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE mutans streptococci; twins; preschool children ID INITIAL ACQUISITION; DENTAL-CARIES; CHILDREN; INFANTS; DECAY AB Objective: The purpose of this study was to determine whether genetic factors influence variation in salivary levels of the mutans streptococci (MS) in preschool twins. Design: The study population consisted of 48 pairs of monozygotic (MZ) twins and 54 pairs of dizygotic (DZ) twins. Genotyping eight highly polymorphic DNA markers determined zygosity. Demographic data and antibiotic exposure as reported by mothers were obtained by a face-to-face interview. Salivary levels of MS were determined by the Stripmutans (TM) test. Test results are reported on a scale of 0-3. Regression analysis, two sample t-tests and structural equation modeling were applied to analyse the data. Results: Only 6 % of the participants ever visited a dentist (F component of the DMFS was 0 for this population). Average salivary scores for the mutans streptococci were significantly different between MZ (1.1 +/- 0.1) and DZ (0.8 +/- 0.1) twins (p = 0.021). High salivary levels of MS (scores 2 and 3) were observed in 42 % of MZ twins and in 26 % of DZ twins. Regression analysis on the MS salivary levels revealed no significant effects of age, gender and antibiotic intake for MZ or DZ twins. The heritability of mutans streptococci colonisation in 48 pairs MZ and in 26 pairs of DZ twins was estimated to be 52 %. The non-shared environment contribution was estimated to be 48 %. Conclusions: These results suggest that variation in the salivary levels of the mutans streptococci is significantly contributed by genetic factors. (c) 2004 Elsevier Ltd. All rights reserved. C1 Univ Pittsburgh, Sch Dent Med, Pittsburgh, PA 15261 USA. UNIMONTES, BR-39400 Momtes Claros, MG, Brazil. NIDCR, NIH, Div Intramural Clin Res, Bethesda, MD 20892 USA. Univ Pittsburgh, Sch Pharm, Pittsburgh, PA 15261 USA. RP Bretz, WA (reprint author), Univ Pittsburgh, Sch Dent Med, 380 Salk Hall,3501 Terrace St, Pittsburgh, PA 15261 USA. EM wab2@pitt.edu NR 18 TC 11 Z9 12 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0003-9969 J9 ARCH ORAL BIOL JI Arch. Oral Biol. PD MAR PY 2005 VL 50 IS 3 BP 347 EP 351 DI 10.1016/j.archoralbio.2004.08.010 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 909JO UT WOS:000227856400008 PM 15740714 ER PT J AU Duez, H Lefebvre, B Poulain, P Torra, IP Percevault, F Luc, G Peters, JM Gonzalez, FJ Gineste, R Helleboid, S Dzavik, V Fruchart, JC Fievet, C Lefebvre, P Staels, B AF Duez, H Lefebvre, B Poulain, P Torra, IP Percevault, F Luc, G Peters, JM Gonzalez, FJ Gineste, R Helleboid, S Dzavik, V Fruchart, JC Fievet, C Lefebvre, P Staels, B TI Regulation of human ApoA-I by gemfibrozil and fenofibrate through selective peroxisome proliferator-activated receptor alpha modulation SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY LA English DT Article DE apolipoprotein A-I; high-density lipoprotein; fibrates; peroxisome proliferator-activated receptor alpha; selective PPAR modulator ID APOLIPOPROTEIN-A-I; RANDOMIZED CONTROLLED-TRIAL; FIBRIC ACID-DERIVATIVES; TRANSGENIC MICE; IIB HYPERLIPOPROTEINEMIA; MICRONIZED FENOFIBRATE; ALLOSTERIC REGULATION; HDL CHOLESTEROL; GENE-EXPRESSION; LIPID-LEVELS AB Objective - The objective of this trial was to study the effects of fenofibrate (FF) and gemfibrozil (GF), the most commonly used fibrates, on high-density lipoprotein (HDL) and apolipoprotein (apo) A-I. Methods and Results - In a head-to-head double-blind clinical trial, both FF and GF decreased triglycerides and increased HDL cholesterol levels to a similar extent, whereas plasma apoA-I only increased after FF but not GF. Results in human ( h) apoA-Itransgenic (hA-ITg) peroxisome proliferator - activated receptor ( PPAR) alpha(-/-) mice demonstrated that PPARalpha mediates the effects of FF and GF on HDL in vivo. Although plasma and hepatic mRNA levels of hapoA-I increased more pronouncedly after FF than GF in hA-ITgPPARalpha(+/+) mice, both fibrates induced acylCoAoxidase mRNA similarly. FF and GF transactivated PPARalpha with similar activity and affinity on a DR-1 PPAR response element, but maximal activation on the hapoA-I DR-2 PPAR response element was significantly lower for GF than for FF. Moreover, GF induced recruitment of the coactivator DRIP205 on the DR-2 site less efficiently than did FF. Conclusion - Both GF and FF exert their effects on HDL through PPARalpha. Whereas FF behaves as a full agonist, GF appears to act as a partial agonist due to a differential recruitment of coactivators to the promoter. These observations provide an explanation for the differences in the activity of these fibrates on apoA-I. C1 Inst Pasteur, Dept Atherosclerose, INSERM, UR545, F-59019 Lille, France. Univ Lille 2, Fac Pharm, F-59800 Lille, France. Fac Med Lille, INSERM, UR459, Lille, France. Penn State Univ, Ctr Mol Toxicol, Dept Vet Sci, Hershey, PA USA. NCI, Lab Metab, NIH, Bethesda, MD 20892 USA. GENFIT SA, Loos, France. Univ Hlth Network, Cardiac Catheterizat Lab & Intervent Cardiol, Toronto, ON, Canada. RP Duez, H (reprint author), Inst Pasteur, Dept Atherosclerose, INSERM, UR545, 1 Rue Calmette, F-59019 Lille, France. EM helene.duez@pasteur-lille.fr; bart.staels@pasteur-lille.fr RI Peters, Jeffrey/D-8847-2011; percevault, frederic/K-1836-2015; Lefebvre, Philippe/F-2685-2010; OI Lefebvre, Philippe/0000-0002-9366-5129; Staels, Bart/0000-0002-3784-1503 NR 38 TC 73 Z9 80 U1 1 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1079-5642 J9 ARTERIOSCL THROM VAS JI Arterioscler. Thromb. Vasc. Biol. PD MAR PY 2005 VL 25 IS 3 BP 585 EP 591 DI 10.1161/01.ATV.0000154140.73570.00 PG 7 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA 900NL UT WOS:000227221500021 PM 15618549 ER PT J AU Stone, JH Rajapakse, VN Hoffman, GS Specks, U Merkel, PA Spiera, RF Davis, JC Clair, EWS McCune, J Ross, S Hitt, BA Veenstra, TD Conrads, TP Liotta, LA Petricoin, EF AF Stone, John H. Rajapakse, Vinodh N. Hoffman, Gary S. Specks, Ulrich Merkel, Peter A. Spiera, Robert F. Davis, John C. Clair, E. William St. McCune, Joseph Ross, Sally Hitt, Ben A. Veenstra, Timothy D. Conrads, Thomas P. Liotta, Lance A. Petricoin, Emanuel F., III CA Wegeners Granulomatosis Etanercept TI A Serum Proteomic Approach to Gauging the State of Remission in Wegener's Granulomatosis SO ARTHRITIS AND RHEUMATISM LA English DT Article ID OVARIAN-CANCER; ETANERCEPT TRIAL; PROSTATE-CANCER; METHOTREXATE; PREDNISONE; PATTERNS; ANTIBODY; BLOOD; CARE AB Objective. To identify serum ion patterns that distinguish remission from active disease in patients with Wegener's granulomatosis (WG). Methods. Using sera collected in the WG Etanercept Trial, we selected samples from patients who either were undergoing a period of extended disease remission or had recent flares of active WG. Unfractionated samples were randomized into sets for training and testing, such that remission sera and active disease sera could be analyzed without batch bias. Molecular species within the sera were ionized by high-resolution, matrix-assisted laser desorption ionization time-of-flight mass spectrometry. We then used a bioinformatics pattern-recognition tool to identify optimal combinations of ions. During the training stage, the clinical data (remission versus active disease) were provided in association with the spectral data from each sample. In the testing stage, we performed blinded testing on a previously unexamined set of samples. Results. The most robust model, trained on a total of 82 samples (42 remission, 40 active disease), included 7 key ions with mass:charge ratios of 803.239, 2,171.672, 2,790.574, 3,085.237, 5,051.726, 5,833.989, and 6,630.465. The combined relative amplitudes of these 7 ions identified 5 distinct clusters of either remission or active disease samples during the training stage. In the testing stage, this model segregated 72 samples into the same 5 clusters, including I large remission cluster (n = 28) and another large active disease cluster (n = 32). Three smaller clusters of active disease or remission samples were also identified, with remission clusters populated by 2 samples in one cluster and 8 in another, and an active disease cluster populated by 2 samples. The model categorized 35 of 37 remission samples correctly (sensitivity 95%, 95% confidence interval [95% CI] 82.1-99.4) and 32 of 35 active disease samples correctly (specificity 91%, 95% CI 78.1-98.1). Conclusion. This serum proteomic profiling approach appears to be useful in distinguishing between states of stable clinical remission and active disease. Further validation and refinement of this strategy may help clinicians apply immunosuppressive therapies more judiciously among their patients, thereby avoiding morbidity and mortality from excessive treatment. Identification of the most robust and clinically useful combinations of ions will permit the rational selection of molecules for sequencing and analysis. C1 [Stone, John H.] Johns Hopkins Univ, Johns Hopkins Vasculitis Ctr, Sch Med, Baltimore, MD 21224 USA. [Rajapakse, Vinodh N.; Ross, Sally; Liotta, Lance A.; Petricoin, Emanuel F., III] NCI, FDA Clin Proteom Program, Bethesda, MD 20892 USA. [Hoffman, Gary S.] Cleveland Clin Fdn, Lerner Coll Med, Cleveland, OH 44195 USA. [Specks, Ulrich] Mayo Clin, Rochester, MN USA. [Merkel, Peter A.] Boston Univ, Sch Med, Boston, MA 02118 USA. [Spiera, Robert F.] Beth Israel Deaconess Med Ctr, New York, NY 10003 USA. [Davis, John C.] Univ Calif San Francisco, San Francisco, CA 94143 USA. [Clair, E. William St.] Duke Univ, Durham, NC USA. [McCune, Joseph] Univ Michigan, Ann Arbor, MI 48109 USA. [Hitt, Ben A.] Correlogic Inc, Bethesda, MD USA. [Veenstra, Timothy D.; Conrads, Thomas P.] NCI, Biomed Proteom Program, Mass Spectrometry Ctr, Frederick, MD 21701 USA. RP Stone, JH (reprint author), Johns Hopkins Univ, Johns Hopkins Vasculitis Ctr, Sch Med, 5501 Hopkins Bayview Circle,JHAAC 1B23, Baltimore, MD 21224 USA. EM jstone@jhmi.edu FU FDA HHS [FD-R-001652-01]; NCRR NIH HHS [M01-RR0-0042, M01-RR0-00533, M01-RR-30, M01-RR0-2719]; NIAMS NIH HHS [K24-AR-049185-01, N01-AR-9-2240] NR 35 TC 29 Z9 30 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD MAR PY 2005 VL 52 IS 3 BP 902 EP 910 DI 10.1002/art.20938 PG 9 WC Rheumatology SC Rheumatology GA 905LU UT WOS:000227570600029 PM 15751091 ER PT J AU Skapenko, A Leipe, J Lipsky, PE Schulze-Koops, H AF Skapenko, A Leipe, J Lipsky, PE Schulze-Koops, H TI The role of the T cell in autoimmune inflammation SO ARTHRITIS RESEARCH & THERAPY LA English DT Review ID COLLAGEN-INDUCED ARTHRITIS; ACCESSORY MOLECULE CD28; RHEUMATOID-ARTHRITIS; MONOCLONAL-ANTIBODY; PERIPHERAL-BLOOD; SYNOVIAL-FLUID; IN-VITRO; MESSENGER-RNA; CUTTING EDGE; FUNCTIONAL-CHARACTERIZATION AB T cells, in particular CD4(+) T cells, have been implicated in mediating many aspects of autoimmune inflammation. However, current evidence suggests that the role played by CD4(+) T cells in the development of rheumatoid inflammation exceeds that of activated proinflammatory T-helper (Th)1 effector cells that drive the chronic autoimmune response. Subsets of CD4(+) T cells with regulatory capacity, such as CD25(+) regulatory T (Treg) cells and Th2 cells, have been identified, and recent observations suggest that in rheumatoid arthritis the function of these regulatory T cells is severely impaired. Thus, in rheumatoid arthritis, defective regulatory mechanisms might allow the breakdown of peripheral tolerance, after which the detrimental Th1-driven immune response evolves and proceeds to chronic inflammation. Here, we review the functional abnormalities and the contribution of different T cell subsets to rheumatoid inflammation. C1 Univ Erlangen Nuremberg, Dept Internal Med 3, Nikolaus Fiebiger Ctr Mol Med, Clin Res Grp 3, Erlangen, Germany. Univ Erlangen Nuremberg, Inst Clin Immunol, Erlangen, Germany. NIAMSD, Autoimmun Branch, Bethesda, MD 20892 USA. RP Schulze-Koops, H (reprint author), Univ Erlangen Nuremberg, Dept Internal Med 3, Nikolaus Fiebiger Ctr Mol Med, Clin Res Grp 3, Erlangen, Germany. EM Schulze-Koops@med3.imed.uni-erlangen.de NR 101 TC 89 Z9 96 U1 0 U2 3 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1478-6354 J9 ARTHRITIS RES THER JI Arthritis Res. Ther. PD MAR PY 2005 VL 7 SU 2 BP S4 EP S14 DI 10.1186/ar1505 PG 11 WC Rheumatology SC Rheumatology GA 955HB UT WOS:000231215400002 PM 15833146 ER PT J AU Cendoroglo, MS Lahoz, C Martinez, TLR Ordovas, JM Lamon-Fava, S Cupples, LA Wilson, PW Schaefer, EJ AF Cendoroglo, MS Lahoz, C Martinez, TLR Ordovas, JM Lamon-Fava, S Cupples, LA Wilson, PW Schaefer, EJ TI Association of apo A-IV 360 (Gln -> His) polymorphism with plasma lipids and lipoproteins: the Framingham Offspring Study SO ATHEROSCLEROSIS LA English DT Article DE apolipoprotein A-IV; triglycerides; cholesterol; lipoproteins; genetic polymorphism ID APOLIPOPROTEIN-A-IV; HIGH-DENSITY-LIPOPROTEIN; AORTIC ENDOTHELIAL-CELLS; CHOLESTEROL ACYLTRANSFERASE; GENETIC POLYMORPHISMS; MYOCARDIAL-INFARCTION; POPULATION-GENETICS; ACTIVATION; FREQUENCY; METABOLISM AB The effect of a common apolipoprotein (apo) A-IV polymorphism (substitution of histidine for glutamine at position 360) on plasma lipid, lipoprotein cholesterol and lipoprotein(a) (Lp(a)) levels, and on low-density lipoprotein (LDL) particle size was examined by genotyping in 2322 Caucasian men and women (mean age: 48.9 +/- 10.1 years) participating in the Framingham Offspring Study (FOS). The relative frequencies of the apo A-IV-Gln (apo A-IV-1) and the apo A-IV-His (apo A-IV-2) alleles were 0.932 and 0.068, respectively, and were in Hardy-Weinberg equilibrium. No effect of the apo A-IV-2 genotype was observed on plasma triglyceride, total and lipoprotein cholesterol, and LDL particle size in either men or women after adjustment for age and body mass index. To avoid a possible interaction between the apo E genotype and the apo A-IV genotype, subgroup analyses were undertaken in 1,414 male and female subjects with the apo E3/3 genotype. Among women in this group there was a significant effect of the apo A-IV-2 allele on triglyceride levels (p = 0.046). This effect was no longer significant after adjustment for age and BMI (p = 0.074). No significant allele effect on other lipoprotein levels, including Lp(a), was noted in apo E3/3 men or women. We have also conducted a meta-analysis of our own data and of other studies found in the literature, indicating a significant lowering effect of apo A-IV-2 on plasma triglycerides, but no effects on other parameters. In conclusion, the apo A-IV-2 allele is associated with a modest reduction in plasma triglyceride levels in the general population. (c) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Tufts Univ, Jean Mayer Human Nutr Res Ctr Aging, Lipid Metab Lab, Boston, MA 02111 USA. Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA. Boston Univ, Sch Med, Boston, MA 02215 USA. NHLBI, Framingham Heart Study, Framingham, MA USA. RP Schaefer, EJ (reprint author), Tufts Univ, Jean Mayer Human Nutr Res Ctr Aging, Lipid Metab Lab, 711 Washington St, Boston, MA 02111 USA. EM Ernst.Schaefer@Tufts.edu RI Cendoroglo, Maysa /A-7993-2010; OI Cupples, L. Adrienne/0000-0003-0273-7965; Ordovas, Jose/0000-0002-7581-5680 FU NHLBI NIH HHS [HL54776] NR 64 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0021-9150 J9 ATHEROSCLEROSIS JI Atherosclerosis PD MAR PY 2005 VL 179 IS 1 BP 169 EP 175 DI 10.1016/j.atherosclerosis.2004.09.020 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 905ME UT WOS:000227571700021 PM 15721024 ER PT J AU Schweizer, U Streckfuss, F Pelt, P Carlson, BA Hatfield, DL Kohrle, J Schomburg, L AF Schweizer, U Streckfuss, F Pelt, P Carlson, BA Hatfield, DL Kohrle, J Schomburg, L TI Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply SO BIOCHEMICAL JOURNAL LA English DT Article DE brain; glutathione peroxidase; selenium; selenocysteine; selenoprotein P; tRNA([Ser]Soc) ID GLUTATHIONE PEROXIDASES; TARGET TISSUES; HUMAN PLASMA; PROTEIN; MOUSE; SELENOCYSTEINE; EXPRESSION; GENE; MICE; RAT AB Liver-specific inactivation of Trsp, the gene for selenocysteine tRNA, removes SePP (selenoprotein P) from plasma, causing serum selenium levels to fall from 298 mu g/l to 50 mu g/l and kidney selenium to decrease to 36 % of wild-type levels. Likewise, glutathione peroxidase activities decreased in plasma and kidney to 43 % and 18 % respectively of wild-type levels. This agrees nicely with data from SePP knockout mice, supporting a selenium transport role for hepatically expressed SePP. However, brain selenium levels remain unaffected and neurological defects do not occur in the liver-specific Trsp knockout mice, while SePP knockout mice suffer from neurological defects. This indicates that a transport function in plasma is exerted by hepatically derived SePP, while in brain SePP fulfils a second, hitherto unexpected, essential role. C1 Neurowissenschaft Forschungszentrum, D-10117 Berlin, Germany. Univ Med Berlin, Inst Expt Endokrinol, D-10117 Berlin, Germany. NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Canc Ctr Res,NIH, Bethesda, MD 20892 USA. RP Schweizer, U (reprint author), Neurowissenschaft Forschungszentrum, Charite Univmed Berlin,Schumannstr 20-21, D-10117 Berlin, Germany. EM ulrich.schweizer@charite.de RI Schweizer, Ulrich/E-8105-2013; OI Kohrle, Josef/0000-0002-9187-9078 NR 35 TC 109 Z9 112 U1 1 U2 4 PU PORTLAND PRESS LTD PI LONDON PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAR 1 PY 2005 VL 386 BP 221 EP 226 PN 2 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 905NA UT WOS:000227574200003 PM 15638810 ER PT J AU Kumari, D Gabrielian, A Wheeler, D Usdin, K AF Kumari, D Gabrielian, A Wheeler, D Usdin, K TI The roles of Sp1, Sp3, USF1/USF2 and NRF-1 in the regulation and three-dimensional structure of the Fragile X mental retardation gene promoter SO BIOCHEMICAL JOURNAL LA English DT Article DE DNA bending; Fragile X mental retardation 1 (FMR1); promoter regulation; specificity protein 1 (Sp 1); upstream stimulatory factor 1 (USF1) ID PREMATURE OVARIAN FAILURE; FMR1 PROMOTER; TRANSCRIPTION FACTORS; CGG-REPEAT; LEUCINE-ZIPPER; BEND DNA; IN-VIVO; BINDING; USF; ACTIVATION AB Expansion of a CGG (.) CCG-repeat tract in the 5'-untranslated region of the FMR1 (Fragile X mental retardation 1) gene causes its aberrant transcription. This produces symptoms ranging from premature ovarian failure and Fragile X associated tremor and ataxia syndrome to FMR syndrome, depending on the size of the expansion. The promoter from normal alleles shows four protein-binding regions in vivo. We had previously shown that in mouse brain extracts two of these sites are bound by USF1/USF2 (upstream stimulatory factors 1 and 2) heterodimers and NRF-1 (nuclear respiratory factor-1). We also showed that these sites are involved in the positive regulation of FMR1 transcription in neuronally derived cells. In the present study, we show that Sp1 (specificity protein 1) and Sp3 are also strong positive regulators of FMR1 promoter activity. We also show that, like Sp1 and E-box-binding proteins such as USF1 and USF2, NRF-1 causes DNA bending, in this case producing a bend of 57 degrees towards the major groove. The combined effect of the four protein-induced bends on promoter geometry is the formation of a highly compact arch-like structure in which the 5' end of the promoter is brought in close proximity to the 3' end. We had previously shown that while point mutations in the GC-boxes decrease promoter activity, deletion of either one of them leads to an increase in promoter activity. We can reconcile these observations with the positive effect of Sp1 and Sp3 if protein-induced bending acts, at least in part, to bring together distally spaced factors important for transcription initiation. C1 NIDDKD, NIH, Bethesda, MD 20892 USA. Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20892 USA. RP Usdin, K (reprint author), NIDDKD, NIH, Bethesda, MD 20892 USA. EM ku@helix.nih.gov NR 47 TC 17 Z9 18 U1 1 U2 3 PU PORTLAND PRESS LTD PI LONDON PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAR 1 PY 2005 VL 386 BP 297 EP 303 DI 10.1042/BJ20041124 PN 2 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 905NA UT WOS:000227574200012 PM 15479157 ER PT J AU Minko, IG Kurtz, AJ Croteau, DL Van Houten, B Harris, TM Lloyd, RS AF Minko, IG Kurtz, AJ Croteau, DL Van Houten, B Harris, TM Lloyd, RS TI Initiation of repair of DNA-polypeptide cross-links by the UvrABC nuclease SO BIOCHEMISTRY LA English DT Article ID NUCLEOTIDE EXCISION-REPAIR; T4 ENDONUCLEASE-V; HUMAN-CELLS; ESCHERICHIA-COLI; MAMMALIAN-CELLS; ABASIC SITES; DEOXYGUANOSINE ADDUCT; DAMAGE RECOGNITION; TOPOISOMERASE-I; PROTEIN AB Although the biochemical pathways that repair DNA-protein cross-links have not been clearly elucidated, it has been proposed that the partial proteolysis of cross-linked proteins into smaller oligopeptides constitutes an initial step in removal of these lesions by nucleotide excision repair (NER). To test the validity of this repair model, several site-specific DNA-peptide and DNA-protein cross-links were engineered via linkage at (1) an acrolein-derived gamma-hydroxypropanodeoxyguanosine adduct and (2) an apurinic/apyrimidinic site, and the initiation of repair was examined in vitro using recombinant proteins UvrA and UvrB from Bacillus caldotenax and UvrC from Thermotoga maritima. The polypeptides crosslinked to DNA were Lys-Trp-Lys-Lys, Lys-Phe-His-Glu-Lys-His-His-Ser-His-Arg-Gly-Tyr, and the 16 kDa protein, T4 pyrimidine dimer glycosylase/apurinic/apyrimidinic site lyase. For the substrates examined, DNA incision required the coordinated action of all three proteins and occurred at the eighth phosphodiester bond 5' to the lesion. The incision rates for DNA-peptide cross-links were comparable to or greater than that measured on fluorescein-adducted DNA, an excellent substrate for UvrABC. Incision rates were dependent on both the site of covalent attachment on the DNA and the size of the bound peptide. Importantly, incision of a DNA-protein cross-link occurred at a rate approximately 3.5-8-fold slower than the rates observed for DNA-peptide cross-links. Thus, direct evidence has been obtained indicating that (1) DNA-peptide cross-links can be efficiently incised by the NER proteins and (2) DNA-peptide cross-links are preferable substrates for this system relative to DNA-protein cross-links. These data suggest that proteolytic degradation of DNA-protein cross-links may be an important processing step in facilitating NER. C1 Oregon Hlth Sci Univ, Ctr Res Occupat & Environm Toxicol, Portland, OR 97239 USA. Univ Texas, Med Branch, Dept Human Biol Chem & Genet, Galveston, TX 77555 USA. NIEHS, Genet Mol Lab, Res Triangle Pk, NC 27709 USA. Vanderbilt Univ, Ctr Mol Toxicol, Dept Chem, Nashville, TN 37235 USA. RP Lloyd, RS (reprint author), Oregon Hlth Sci Univ, Ctr Res Occupat & Environm Toxicol, Portland, OR 97239 USA. EM lloydst@ohsu.edu FU NCI NIH HHS [CA 106858]; NIEHS NIH HHS [ES 05355, T32 ES07254-10] NR 58 TC 45 Z9 45 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 1 PY 2005 VL 44 IS 8 BP 3000 EP 3009 DI 10.1021/bi0478805 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 900ZJ UT WOS:000227252500028 PM 15723543 ER PT J AU Zhou, LH Civitello, ER Gupta, N Silverman, RH Molinaro, RJ Anderson, DE Torrence, PF AF Zhou, LH Civitello, ER Gupta, N Silverman, RH Molinaro, RJ Anderson, DE Torrence, PF TI Endowing RNase H-inactive antisense with catalytic activity: 2-5A-morphants SO BIOCONJUGATE CHEMISTRY LA English DT Article; Proceedings Paper CT 227th National Meeting of the American-Chemical Society CY MAR 28-APR 01, 2004 CL Anaheim, CA SP Amer Chem Soc ID 2-5A ANTISENSE; VIRUS-REPLICATION; TARGETING RNA; MESSENGER-RNA; OLIGOMERS; CHIMERAS; CELLS; OLIGONUCLEOTIDE; DEGRADATION; INHIBITION AB A convergent synthetic approach was used to conjugate 2',5'-oligoadenylate (2-5A, p5'A2' [p5'A2'](n)p5A) to phosphorodiamidate morpholino oligomers (morphants). To provide requisite quantities of 2-5A starting material, commercially and readily available synthons for solid-phase synthesis were adapted for larger scale solution synthesis. Thus, the tetranucleotide 5'-phosphoryladenylyl(2'-> 5')adenylyl(2'-> 5')adenylyl(2'-> 5')adenosine (p5A2'p5A2'](2)p5A2', tetramer 2-5A, 9) was synthesized starting with 2',3'-O-dibenzoyl-N-6,N-6-dibenzoyl adenosine prepared from commercially available 5'-O-(4-monomethoxytrityl) adenosine. Coupling with N-6-benzoyl-5'-O-(4,4'-dimethoxytrityl)-3'-O-(tert-butyldimethylsilyl) adenosine-2'-(N,N-diisopropyl-2-cyanoethyl)phosphoramidite, followed by oxidization and deprotection, generated 5'-deprotected dimer 2-5A. Similar procedures lengthened the chain to form protected tetramer 2-5 A. The title product 9 p5'A(2'p5A)(3) (tetramer 2-5A) was obtained through phosphorylation of the terminal 5'-hydroxy of the protected tetramer and removal of remaining protecting groups using concentrated ammonium hydroxide-ethanol (3:1, v/v) at 55 degrees C and tetrabutylammonium fluoride (TBAF) in THF at room temperature, respectively. The 2-5A-phosphorodiamidate morpholino antisense chimera 11 (2-5A-morphant) was synthesized by covalently linking an aminolinker-functionalized phosphorodiamidate morpholino oligomer with periodate oxidized 2-5A tetramer (p5'A2'[p5'A2'](2)p5'A). The resulting Schiff base was reduced with cyanoborohydride thereby transforming the ribose of the T-terminal nucleotide of 2-5A N-substituted morpholine. RNase L assays demonstrated that this novel 2-5A-antisense chimera had significant biological activity, thereby providing another potential tool for RNA ablation. C1 No Arizona Univ, Dept Chem, Flagstaff, AZ 86011 USA. Cleveland Clin Fdn, Lerner Res Inst, Dept Canc Biol, Cleveland, OH 44195 USA. Cleveland State Univ, Dept Chem, Cleveland, OH 44115 USA. NIDDKD, Struct Mass Spectrometry Facil, Bethesda, MD 20892 USA. RP Torrence, PF (reprint author), No Arizona Univ, Dept Chem, Box 5698, Flagstaff, AZ 86011 USA. EM Paul.Torrence@nau.edu FU NCI NIH HHS [CA44059] NR 50 TC 7 Z9 7 U1 0 U2 8 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD MAR-APR PY 2005 VL 16 IS 2 BP 383 EP 390 DI 10.1021/bc049778q PG 8 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA 907QF UT WOS:000227732300019 PM 15769093 ER PT J AU Lissek, S Baas, JMP Pine, DS Orme, K Dvir, S Nugent, M Rosenberger, E Rawson, E Grillon, C AF Lissek, S Baas, JMP Pine, DS Orme, K Dvir, S Nugent, M Rosenberger, E Rawson, E Grillon, C TI Airpuff startle probes: an efficacious and less aversive alternative to white-noise SO BIOLOGICAL PSYCHOLOGY LA English DT Article DE startle; psychophysiology; anxiety; fear ID POSTTRAUMATIC-STRESS-DISORDER; FEAR-POTENTIATED STARTLE; ANXIETY DISORDERS; ACOUSTIC STARTLE; BLINK REFLEX; VIETNAM VETERANS; BRAIN MECHANISMS; ATTENTION; EMOTION; RESPONSES AB Fear-potentiated startle (FPS) is an increasingly popular psychophysiological method for the objective assessment of fear and anxiety. Studies applying this method often elicit the startle reflex with loud white-noise stimuli. Such intense stimuli may, however, alter psychological processes of interest by creating unintended emotional or attentional artifacts. Additionally, loud acoustic probes may be unsuitable for use with infants, children, the elderly, and those with hearing damage. Past studies have noted robust and reliable startle reflexes elicited by low intensity airpuffs. The current study compares the aversiveness of white-noise (102 dB) and airpuff (3 psi) probes and examines the sensitivity of each probe for the assessment of fear-potentiated startle. Results point to less physiological arousal and self-reported reactivity to airpuff versus white-noise probes. Additionally, both probes elicited equal startle magnitudes, response probabilities, and levels of fear-potentiated startle. Such results support the use of low intensity airpuffs as efficacious and relatively non-aversive startle probes. (C) 2004 Elsevier B.V. All rights reserved. C1 NIMH, Mood & Anxiety Disorders Program, NIH, DHHS, Bethesda, MD 20892 USA. Univ Utrecht, Psychol Lab, Helmholtz Inst, NL-3508 TB Utrecht, Netherlands. RP Lissek, S (reprint author), NIMH, Mood & Anxiety Disorders Program, NIH, DHHS, 15K N Dr,Bldg 15K,MSC 2670, Bethesda, MD 20892 USA. EM lisseks@intra.nimh.nih.gov RI Lissek, Shmuel/B-6577-2008; OI Baas, Johanna/0000-0001-6267-8712 NR 43 TC 19 Z9 19 U1 4 U2 16 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0301-0511 J9 BIOL PSYCHOL JI Biol. Psychol. PD MAR PY 2005 VL 68 IS 3 BP 283 EP 297 DI 10.1016/j.biopsycho.2004.07.007 PG 15 WC Psychology, Biological; Behavioral Sciences; Psychology; Psychology, Experimental SC Psychology; Behavioral Sciences GA 892RI UT WOS:000226667300007 PM 15620795 ER PT J AU Savani, BN Montero, A Wu, C Nlonda, N Read, E Dunbar, C Childs, R Solomon, S Barrett, AJ AF Savani, BN Montero, A Wu, C Nlonda, N Read, E Dunbar, C Childs, R Solomon, S Barrett, AJ TI Prediction and prevention of transplant-related mortality from pulmonary causes after total body irradiation and allogeneic stem cell transplantation SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION LA English DT Article DE pulmonary complications; stem cell transplantation ID BONE-MARROW-TRANSPLANTATION; IDIOPATHIC-PNEUMONIA-SYNDROME; VERSUS-HOST-DISEASE; SEVERE APLASTIC-ANEMIA; RISK-FACTORS; INTERSTITIAL PNEUMONITIS; FUNCTION TESTS; LUNG INJURY; COMPLICATIONS; RADIATION AB Between July 1997 and August 2004, 146 consecutive patients with hematologic malignancies received a T cell-depleted peripheral blood stem cell transplant from an HLA-identical sibling by using total body irradiation (TBI) and cyclophosphamide conditioning regimens. Eighty-five patients received 13.6 Gy of TBI with no lung shielding, and 61 received lung shielding (total lung dose, 6-12 Gy). Ninety-four patients (65.5%) had standard-risk disease; the remainder had more advanced disease or unfavorable diagnoses. Of the 21 transplant-related deaths, 14 were from pulmonary causes (10 idiopathic pulmonary syndromes and 4 from infection) that occurred at a median of 90 days (range, 23-238 days) after transplantation. Independent risk factors for pulmonary transplant-related mortality (PTRM) were pretransplantation diffusion capacity for carbon monoxide (relative risk, 5.7 for diffusion capacity for carbon monoxide < 85%), smoking (relative risk, 5.0), and CD34 cell dose (relative risk, 9.4 for a CD34 dose of < 5 x 10(6) cells per kilogram). Patients receiving lung shielding had significantly lower PTRM (3.3 % versus 14.1 %; P =.02) and better overall survival (70% +/- 6% versus 52% +/- 5%; P =.04), but lung shielding was not a significant independent factor for determining PTRM. These results suggest that pulmonary mortality after TBI-based preparative regimens is predictable and that higher CD34 cell doses can reduce the risk. (c) 2005 American Society for Blood and Marrow Transplantation. C1 NHLBI, Hematol Branch, Stem Cell Allotransplant Sect, NIH, Bethesda, MD 20892 USA. RP Barrett, AJ (reprint author), Bldg 10,Room 3-5330,9000 Rockville Pike, Bethesda, MD 20892 USA. EM barrettj@nhlbi.nih.gov NR 37 TC 32 Z9 33 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 USA SN 1083-8791 J9 BIOL BLOOD MARROW TR JI Biol. Blood Marrow Transplant. PD MAR PY 2005 VL 11 IS 3 BP 223 EP 230 DI 10.1016/j.bbmt.2004.12.328 PG 8 WC Hematology; Immunology; Transplantation SC Hematology; Immunology; Transplantation GA 910US UT WOS:000227958300008 PM 15744241 ER PT J AU Morasso, MI Tomic-Canic, M AF Morasso, MI Tomic-Canic, M TI Epidermal stem cells: the cradle of epidermal determination, differentiation and wound healing SO BIOLOGY OF THE CELL LA English DT Review DE differentiation; epidermis; hair follicle; stem cell; wound healing ID LABEL-RETAINING CELLS; HAIR FOLLICLE; C-MYC; P53 HOMOLOG; SIGNAL-TRANSDUCTION; HUMAN KERATINOCYTES; INTEGRIN RECEPTORS; CORNIFIED ENVELOPE; BARRIER FUNCTION; GROWTH-FACTOR AB The field of epidermal stem cells has dramatically advanced in the last decade, leading to a better understanding of the molecular factors, signalling pathways and cellular events that identify and characterize stem cells, thus revealing their immense potential for therapeutic use. Furthermore, multipotent epidermal stem cells present the major advantage of easy accessibility with the discovery of their specific location within the bulge of the hair follicle. This review focuses on the most recent findings on epidermal stem cells, and their potential role in initial epidermal commitment, differentiation and wound healing processes in the skin. C1 NIAMSD, Dev Skin Biol Unit, NIH, Bethesda, MD 20892 USA. NYU, Sch Med, Ronald O Perelman Dept Dermatol, New York, NY 10016 USA. Dept Microbiol, New York, NY 10016 USA. RP Morasso, MI (reprint author), NIAMSD, Dev Skin Biol Unit, NIH, Bethesda, MD 20892 USA. EM morassom@mail.nih.gov FU NIAMS NIH HHS [AR45974, R01 AR045974, Z01 AR041124-06]; NINR NIH HHS [R01 NR008029, NR08029] NR 92 TC 85 Z9 109 U1 2 U2 11 PU PORTLAND PRESS LTD PI LONDON PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND SN 0248-4900 J9 BIOL CELL JI Biol. Cell PD MAR PY 2005 VL 97 IS 3 BP 173 EP 183 PG 11 WC Cell Biology SC Cell Biology GA 907FV UT WOS:000227702100001 PM 15715523 ER PT J AU Horkay, F Horkayne-Szakaly, I Basser, PJ AF Horkay, F Horkayne-Szakaly, I Basser, PJ TI Measurement of the osmotic properties of thin polymer films and biological tissue samples SO BIOMACROMOLECULES LA English DT Article ID QUARTZ-CRYSTAL MICROBALANCE; ARTICULAR-CARTILAGE; POLY(VINYL ALCOHOL); SWELLING PRESSURE; HYDROGELS; NETWORK; ACID; POLYETHYLENE; RESONATORS; BEHAVIOR AB A new type of micro-osmometer is described in which water absorption of small tissue samples is measured by a quartz crystal microbalance (QCM). The swelling of the sample deposited on the surface of a quartz crystal is determined by monitoring the change in resonance frequency of the quartz sensor as a function of the vapor pressure in the surrounding environment. The measurement principle is verified by studying the water uptake of poly(vinyl alcohol) films. Reasonable agreement is found between the results obtained by the QCM-based osmometer and previous osmotic pressure measurements made on a similar poly(vinyl alcohol) sample. The feasibility of the new method is demonstrated by measuring the osmotic response of tissue-engineered cartilage samples. It is found that the osmotic pressure of cartilage substantially increases with culture time. The present result is consistent with cartilage models, suggesting that the proteoglycan content governs the compressive resistance of the tissue. C1 NICHD, Sect Tissue Biophys & Biomimet, Lab Integrat & Med Biophys, NIH, Bethesda, MD 20892 USA. RP Horkay, F (reprint author), NICHD, Sect Tissue Biophys & Biomimet, Lab Integrat & Med Biophys, NIH, 13 S Dr, Bethesda, MD 20892 USA. EM horkay@helix.nih.gov RI Basser, Peter/H-5477-2011 NR 35 TC 8 Z9 8 U1 0 U2 6 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 1525-7797 J9 BIOMACROMOLECULES JI Biomacromolecules PD MAR-APR PY 2005 VL 6 IS 2 BP 988 EP 993 DI 10.1021/bm049332c PG 6 WC Biochemistry & Molecular Biology; Chemistry, Organic; Polymer Science SC Biochemistry & Molecular Biology; Chemistry; Polymer Science GA 907AT UT WOS:000227687800062 PM 15762669 ER PT J AU Baker, SG Lichtenstein, P Kaprio, J Holm, N AF Baker, SG Lichtenstein, P Kaprio, J Holm, N TI Genetic susceptibility to prostate, breast, and colorectal cancer among Nordic twins SO BIOMETRICS LA English DT Article DE breast cancer; colorectal cancer; EM algorithm; genetics; Hardy-Weinberg; latent class; prostate cancer; twins ID REARED APART; EPIDEMIOLOGY; DENMARK AB To investigate the role of genetics in the development of cancer, we developed a new approach to analyze data on prostate, breast, and colorectal cancer from the Swedish, Danish, and Finnish twin registries on monozygotic (MZ) and same-sex dizygotic (DZ) twins. In the spirit of a sensitivity analysis, we modeled genetic inheritance as either an autosomal recessive or dominant cancer susceptibility (CS) genotype that involves either a single gene, many genes with equal allele frequencies, or three genes with a ninefold range of allele frequencies. We also modeled the joint probability of cancer incidence among five age categories, conditional on the presence or absence of the CS genotype. The main assumptions are: (1) The joint distribution of unobserved environmental effects in a twin pair conditional on the presence or absence of the CS genotype is the same for MZ and DZ twins, (2) the probability of cancer conditional on the presence or absence of the CS genotype and the unobserved environmental effects (i.e., the gene-environment interaction) is the same for MZ and DZ twins, and (3) the probability of cancer is independent between twins with the CS genotype. Estimation was maximum likelihood via a search over allele frequency and two levels of EM algorithms. Models had acceptable or good fits. Variability was estimated using a bootstrap approach, but only 50 replications were feasible. The 94th percentile of bootstrap replications for the estimated fraction of cancers with the CS genotype ranged, over the various genetic models, from 0.16 to 0.45 for prostate cancer, 0.12 to 0.30 for breast cancer, and 0.08 to 0.27 for colorectal cancer. We conclude that genetic susceptibility makes only a small to moderate contribution to the incidence of prostate, breast, and colorectal cancer. C1 NCI, Biometry Res Grp, Div Canc Prevent, Bethesda, MD 20892 USA. Karolinska Inst, Dep Med Epidemiol, S-17177 Stockholm, Sweden. Univ Helsinki, Dept Publ Hlth, FIN-00014 Helsinki, Finland. Univ So Denmark, Danish Twin Registry, Inst Publ Hlth, DK-5000 Odense, Denmark. Odense Univ Hosp, Dept Oncol, DK-5000 Odense, Denmark. 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 RI Kaprio, Jaakko/A-1820-2008; OI Kaprio, Jaakko/0000-0002-3716-2455 FU NCI NIH HHS [R35 CA 42581]; NIA NIH HHS [NIA-PO1-AG08761] NR 17 TC 29 Z9 30 U1 0 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 2005 VL 61 IS 1 BP 55 EP 63 DI 10.1111/j.0006-341X.2005.030924.x PG 9 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA 905NX UT WOS:000227576600007 PM 15737078 ER PT J AU Dunson, DB Stanford, JB AF Dunson, DB Stanford, JB TI Bayesian inferences on predictors of conception probabilities SO BIOMETRICS LA English DT Article DE aggregated Bernoulli; data augmentation algorithm; discrete event time; gamina frailty; human fertility; nonlinear mixed model; pregnancy; random effect ID MENSTRUAL-CYCLE; FERTILITY; FECUNDABILITY; INTERCOURSE; OVULATION; VIABILITY; MODEL; BABY; SEX AB Reproductive scientists and couples attempting pregnancy are interested in identifying predictors of the day-specific probabilities of conception in relation to the timing of a single intercourse act. Because most menstrual cycles have multiple days of intercourse, the occurrence of conception represents the aggregation across Bernoulli trials for each intercourse day. Because of this data structure and dependency among the multiple cycles from a woman, implementing analyses has proven challenging. This article proposes a Bayesian approach based on a generalization of the Barrett and Marshall model to incorporate a woman-specific frailty and day-specific covariates. The model results in a simple closed form expression for the marginal probability of conception, and has an auxiliary variables formulation that facilitates efficient posterior computation. Although motivated by fecundability studies, the approach can be used for efficient variable selection and model averaging in general applications with categorical or discrete event time data. C1 Natl Inst Environm Hlth Sci, Biostat Branch, Res Triangle Pk, NC 27709 USA. Univ Utah, Dept Family & Prevent Med, Salt Lake City, UT 84132 USA. RP Dunson, DB (reprint author), Natl Inst Environm Hlth Sci, Biostat Branch, MD A3-03,POB 12233, Res Triangle Pk, NC 27709 USA. EM dunsonl@niehs.nih.gov NR 30 TC 23 Z9 23 U1 0 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 2005 VL 61 IS 1 BP 126 EP 133 DI 10.1111/j.0006-341X.2005.031231.x PG 8 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA 905NX UT WOS:000227576600014 PM 15737085 ER PT J AU Zheng, G Freidlin, B Li, ZH Gastwirth, JL AF Zheng, G Freidlin, B Li, ZH Gastwirth, JL TI Genomic control for association studies under various genetic models SO BIOMETRICS LA English DT Article DE Cochran-Arinitage trend test; genetic model; optimal genornic control; variance inflation factor ID GENOTYPE RELATIVE RISKS; COMPLEX HUMAN-DISEASES; CANDIDATE-GENE; LINKAGE DISEQUILIBRIUM; TREND TESTS; SAMPLE-SIZE; POWER; FREQUENCIES; DESIGN AB Case-control studies are commonly used to study whether a candidate allele and a disease are associated. However. spurious association can arise due to population substructure or cryptic relatedness, which cause the variance of the trend test to increase. Devlin and Roeder derived the appropriate variance inflation factor (VIF) for the trend test and proposed a novel genomic control (GC) approach to estimate VIF and adjust the test statistic. Their results were derived assuming an additive genetic model and the corresponding VIF is independent of the candidate allele frequency. We determine the appropriate VIFs for recessive and dominant models. Unlike the additive test, the VIFs for the optimal tests for these two models depend on the candidate allele frequency. Simulation results show that, when the null loci used to estimate the VIF have allele frequencies similar to that of the candidate gene, the GC tests derived for recessive and dominant models remain optimal. When the underlying genetic model is unknown or the null loci and candidate gene have quite different allele frequencies, the GC tests derived for the recessive or dominant models cannot be used while the GC test derived for the additive model can be. C1 NHLBI, DECA, Off Biostat Res, Bethesda, MD 20892 USA. NCI, Div Canc Epidemiol & Genet, Biometr Res Branch, DCTD, Bethesda, MD 20892 USA. NCI, Div Canc Epidemiol & Genet, Biostat Branch, Bethesda, MD 20892 USA. George Washington Univ, Dept Stat, Washington, DC 20052 USA. RP Zheng, G (reprint author), NHLBI, DECA, Off Biostat Res, 6701 Rockledge Dr,MSC 7938, Bethesda, MD 20892 USA. EM zhengg@nhlbi.nih.gov; freidlinb@ctep.nci.nih.gov; zli@gwu.edu; jlgast@gwu.edu FU NEI NIH HHS [EY14478] NR 19 TC 31 Z9 31 U1 0 U2 5 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 2005 VL 61 IS 1 BP 186 EP 192 DI 10.1111/j.0006-341X.2005.t01-1-.x PG 7 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA 905NX UT WOS:000227576600021 PM 15737092 ER PT J AU Zheng, G Chen, ZH AF Zheng, G Chen, ZH TI Comparison of maximum statistics for hypothesis testing when a nuisance parameter is present only under the alternative SO BIOMETRICS LA English DT Article DE genetic analysis; maximum statistics; robustness; score test ID CANDIDATE-GENE ASSOCIATION; EFFICIENCY ROBUST-TESTS; LINKAGE TESTS; AFFECTED SIBS; SURVIVAL; DESIGN AB In many practical problems, a hypothesis testing involves a nuisance parameter which appears only under the alternative hypothesis. Davies (1977, Biometrika 64, 247-254) proposed the maximum of the score statistics over the whole range of the nuisance parameter as a test statistic for this type of hypothesis testing. Freidlin, Podgor, and Gastwirth (1999, Biometrics 55, 883-886) studied two other simpler maximum test statistics, the maximum of the score statistics at two extreme points of the nuisance parameter, and the maximum of the score statistics at three points of the nuisance parameter including the two extreme points. In this article, we compare the powers of these three maximum-type statistics in the context of three genetic problems. C1 NHLBI, DECA, Off Biostat Res, Bethesda, MD 20892 USA. Natl Univ Singapore, Dept Stat & Appl Probabil, Singapore 119260, Singapore. RP Zheng, G (reprint author), NHLBI, DECA, Off Biostat Res, 6701 Rockledge Dr,MSC 7938, Bethesda, MD 20892 USA. EM zhengg@nhlbi.nih.gov NR 15 TC 23 Z9 24 U1 1 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 2005 VL 61 IS 1 BP 254 EP 258 DI 10.1111/j.0006-341X.2005.030531.x PG 5 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA 905NX UT WOS:000227576600030 PM 15737101 ER PT J AU Yang, S Prentice, R AF Yang, S Prentice, R TI Semiparametric analysis of short-term and long-term hazard ratios with two-sample survival data SO BIOMETRIKA LA English DT Article DE clinical trial; crossing survival curves; martingale; pseudo maximum likelihood estimator; semiparametric inference; survival analysis; time-varying hazard ratio ID REGRESSION-MODELS; RESIDUALS; ESTIMATOR AB Standard approaches to semiparametric modelling of two-sample survival data are not appropriate when the two survival curves cross. We introduce a two-sample model that accommodates crossing survival curves. The two scalar parameters of the model have the interpretations of being the short-term and long-term hazard ratios respectively. The time-varying hazard ratio is expressed semiparametrically by the two scalar parameters and an unspecified baseline distribution. The new model includes the Cox model and the proportional odds model as submodels. For inference we use a pseudo maximum likelihood approach that can be expressed via some simple estimating equations, analogous to that for the maximum partial likelihood estimator of the Cox model, that provide consistent and asymptotically normal estimators. Simulation studies show that the estimators perform well for moderate sample sizes. We also illustrate the methods with a real-data example. The new model can be extended easily to the regression setting. C1 NHLBI, Off Biostat Res, Bethesda, MD 20892 USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA. RP Yang, S (reprint author), NHLBI, Off Biostat Res, 6701 Rockledge Dr,MSC 7938, Bethesda, MD 20892 USA. EM yangso@nhlbi.nih.gov; rprentic@whi.org NR 23 TC 29 Z9 29 U1 0 U2 7 PU BIOMETRIKA TRUST PI LONDON PA UNIV COLLEGE LONDON GOWER ST-BIOMETRIKA OFFICE, LONDON WC1E 6BT, ENGLAND SN 0006-3444 J9 BIOMETRIKA JI Biometrika PD MAR PY 2005 VL 92 IS 1 BP 1 EP 17 DI 10.1093/biomet/92.1.1 PG 17 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA 912SH UT WOS:000228099300001 ER PT J AU Kaur, G Narayanan, VL Risbood, PA Hollingshead, MG Stinson, SF Varma, RK Sausville, EA AF Kaur, G Narayanan, VL Risbood, PA Hollingshead, MG Stinson, SF Varma, RK Sausville, EA TI Synthesis, structure-activity relationship, and p210(bcr-abl) protein tyrosine kinase activity of novel AG 957 analogs SO BIOORGANIC & MEDICINAL CHEMISTRY LA English DT Article DE PTK; NSC680410; adaphostin; AG 957; p210(bcr-abl) ID CHRONIC MYELOGENOUS LEUKEMIA; CHRONIC MYELOID-LEUKEMIA; CELLS IN-VITRO; PHILADELPHIA-CHROMOSOME; TYRPHOSTIN AG957; LAVENDUSTIN-A; BLAST CRISIS; INHIBITOR; NSC-680410; INDUCTION AB A series of novel, sterically hindered lipophilic analogs of AG 957 was designed and synthesized as potential protein tyrosine kinase (PTK) inhibitors. The in vitro activity, in vivo anti-leukemia activity, and pharmacology of these PTK inhibitors were studied. Some aspects of the structure-activity relationship associated with the carboxylic acid, phenol ring, and linker modifications are discussed. We have demonstrated that the 1,4-hydroquinone moiety is essential for activity and that sterically hindered esters contribute to enhanced in vivo efficacy. Adaphostin (NSC 680410) has emerged as the improved compound with the maximum in vivo anti-leukemia hollow fiber activity, concordant with the original lead compound AG 957. Currently, adaphostin is undergoing preclinical toxicology studies. (C) 2004 Elsevier Ltd. All rights reserved. C1 NCI, Dev Therapeut Program, Div Canc Treatment & Diag, Bethesda, MD 20892 USA. Starks Associates Inc, Buffalo, NY 14213 USA. RP Sausville, EA (reprint author), Univ Maryland, Greenebaum Canc Ctr, 22,S Greene St, Baltimore, MD 21201 USA. EM esausville@umm.edu FU NCI NIH HHS [N01-CO-12400, N0-CM-47015] NR 30 TC 16 Z9 20 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0968-0896 J9 BIOORGAN MED CHEM JI Bioorg. Med. Chem. PD MAR 1 PY 2005 VL 13 IS 5 BP 1749 EP 1761 DI 10.1016/j.bmc.2004.12.003 PG 13 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry, Organic SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA 900YX UT WOS:000227251300034 PM 15698792 ER PT J AU Shi, ZD Karki, RG Oishi, S Worthy, KM Bindu, LK Dharmawardana, PG Nicklaus, MC Bottaro, DP Fisher, RJ Burke, TR AF Shi, ZD Karki, RG Oishi, S Worthy, KM Bindu, LK Dharmawardana, PG Nicklaus, MC Bottaro, DP Fisher, RJ Burke, TR TI Utilization of a nitrobenzoxadiazole (NBD) fluorophore in the design of a Grb2 SH2 domain-binding peptide mimetic SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS LA English DT Article ID HUMAN BREAST-CANCER; LIGANDS; INHIBITORS AB Fluorescence labeling has become a general technique for studying the intracellular accumulation and localization of exogenously administered materials. Reported herein is a low nanomolar affinity Grb2 SH2 domain-binding antagonist that utilizes the environmentally-sensitive nitrobenzoxadiazole (NBD) fluorophore as a naphthyl replacement. This novel agent should serve as a useful tool to visualize the actions of this class of Grb2 SH2 domain-binding antagonists in whole cell systems. (c) 2005 Elsevier Ltd. All rights reserved. C1 NCI, CCR, Med Chem Lab, NIH, Frederick, MD 21702 USA. SAIC Frederick, Prot Chem Lab, Frederick, MD 21702 USA. NCI, CCR, Urol Oncol Branch, NIH, Bethesda, MD 21702 USA. RP Burke, TR (reprint author), NCI, CCR, Med Chem Lab, NIH, Frederick, MD 21702 USA. EM tburke@helix.nih.gov RI Fisher, Robert/B-1431-2009; Bottaro, Donald/F-8550-2010; Nicklaus, Marc/N-4183-2014; Burke, Terrence/N-2601-2014; OI Bottaro, Donald/0000-0002-5057-5334; Nicklaus, Marc/0000-0002-4775-7030 NR 19 TC 10 Z9 10 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0960-894X J9 BIOORG MED CHEM LETT JI Bioorg. Med. Chem. Lett. PD MAR 1 PY 2005 VL 15 IS 5 BP 1385 EP 1388 DI 10.1016/j.bmcl.2005.01.017 PG 4 WC Chemistry, Medicinal; Chemistry, Organic SC Pharmacology & Pharmacy; Chemistry GA 902QG UT WOS:000227371000023 PM 15713392 ER PT J AU Haliloglu, T Keskin, O Ma, BY Nussinov, R AF Haliloglu, T Keskin, O Ma, BY Nussinov, R TI How similar are protein folding and protein binding nuclei? Examination of vibrational motions of energy hot spots and conserved residues SO BIOPHYSICAL JOURNAL LA English DT Article ID SINGLE-PARAMETER; INTERFACES; COMPLEXES; RECOGNITION; REFINEMENT; BEHAVIOR; MODEL AB The underlying physico-chemical principles of the interactions between domains in protein folding are similar to those between protein molecules in binding. Here we show that conserved residues and experimental hot spots at intermolecular binding interfaces overlap residues that vibrate with high frequencies. Similarly, conserved residues and hot spots are found in protein cores and are also observed to vibrate with high frequencies. In both cases, these residues contribute significantly to the stability. Hence, these observations validate the proposition that binding and folding are similar processes. In both packing plays a critical role, rationalizing the residue conservation and the experimental alanine scanning hot spots. We further show that high-frequency vibrating residues distinguish between protein binding sites and the remainder of the protein surface. C1 NCI, Basic Res Program, SAIC Frederick Inc, Lab Expt & Computat Biol, Ft Detrick, MD 21702 USA. Bogazici Univ, Ctr Polymer Res, TR-34342 Istanbul, Turkey. Bogazici Univ, Dept Chem Engn, TR-34342 Istanbul, Turkey. Koc Univ, Ctr Computat Biol & Bioinformat & Chem & Biol Eng, TR-34450 Istanbul, Turkey. Tel Aviv Univ, Sackler Sch Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel. RP Nussinov, R (reprint author), NCI, Basic Res Program, SAIC Frederick Inc, Lab Expt & Computat Biol, Bldg 468,Rm 151, Ft Detrick, MD 21702 USA. EM turkan@prc.bme.boun.edu.tr; ruthn@ncifcrf.gov RI Ma, Buyong/F-9491-2011 OI Ma, Buyong/0000-0002-7383-719X FU NCI NIH HHS [N01-CO-12400, N01CO12400] NR 39 TC 43 Z9 45 U1 1 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 MAR PY 2005 VL 88 IS 3 BP 1552 EP 1559 DI 10.1529/biophysj.104.051342 PG 8 WC Biophysics SC Biophysics GA 904JV UT WOS:000227494600007 PM 15596504 ER PT J AU Rothstein, EC Carroll, S Combs, CA Jobsis, PD Balaban, RS AF Rothstein, EC Carroll, S Combs, CA Jobsis, PD Balaban, RS TI Skeletal muscle NAD(P)H two-photon fluorescence microscopy in vivo: Topology and optical inner filters SO BIOPHYSICAL JOURNAL LA English DT Article ID REDUCED PYRIDINE NUCLEOTIDE; DENDRITIC CALCIUM DYNAMICS; LASER-SCANNING MICROSCOPY; OXIDATIVE-PHOSPHORYLATION; PYRAMIDAL NEURONS; RAT-HEART; TISSUE; MOUSE; EXCITATION; FIBERS AB Two-photon excitation fluorescence microscopy (TPEFM) permits the investigation of the topology of intercellular events within living animals. TPEFM was used to monitor the distribution of mitochondrial reduced nicotinamide adenine dinucleotide ( NAD(P) H) in murine skeletal muscle in vivo. NAD( P) H fluorescence emission was monitored (similar to460 nm) using 710 - 720 nm excitation. High-resolution TPEFM images were collected up to a depth of 150 mm from the surface of the tibialis anterior muscle. The NAD( P) H fluorescence images revealed subcellular structures consistent with subsarcolemmal, perivascular, intersarcomeric, and paranuclear mitochondria. In vivo fiber typing between IIB and IIA/D fibers was possible using the distribution and content of mitochondria from the NAD( P) H fluorescence signal. The intersarcomeric mitochondria concentrated at the Z-line in the IIB fiber types resulting in a periodic pattern with a spacing of one sarcomere (2.34 +/- 0.17 mum). The primary inner filter effects were nearly equivalent to water, however, the secondary inner filter effects were highly significant and dynamically affected the observed emission frequency and amplitude of the NAD( P) H fluorescence signal. These data demonstrate the feasibility, and highlight the complexity, of using NAD( P) H TPEFM in skeletal muscle to characterize the topology and metabolic function of mitochondria within the living mouse. C1 NHLBI, Cardiac Energet Lab, NIH, Dept Human Hlth Serv, Bethesda, MD 20892 USA. RP Rothstein, EC (reprint author), NHLBI, Cardiac Energet Lab, NIH, Dept Human Hlth Serv, Bldg 10,Rm B1D416,9000 Rockville Pike, Bethesda, MD 20892 USA. EM emilyr@nih.gov RI Balaban, Robert/A-7459-2009 OI Balaban, Robert/0000-0003-4086-0948 NR 58 TC 42 Z9 43 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 MAR PY 2005 VL 88 IS 3 BP 2165 EP 2176 DI 10.1529/biophysj.104.053165 PG 12 WC Biophysics SC Biophysics GA 904JV UT WOS:000227494600063 PM 15596503 ER PT J AU Berezhkovskii, AM Bezrukov, SM AF Berezhkovskii, AM Bezrukov, SM TI Optimizing transport of metabolites through large channels: Molecular sieves with and without binding SO BIOPHYSICAL JOURNAL LA English DT Letter ID FACILITATED MEMBRANE-TRANSPORT; TRANSLOCATION; MALTOPORIN AB Using a diffusion model of molecules moving through a pore, we rationalize why biological channels have an affinity for the molecules they have evolved to translocate. C1 NICHHD, Math & Stat Comp Lab, Div Biosci, Ctr Informat Technol,NIH, Bethesda, MD 20892 USA. NICHHD, Lab Phys & Struct Biol, NIH, Bethesda, MD 20892 USA. RP Bezrukov, SM (reprint author), NICHHD, Math & Stat Comp Lab, Div Biosci, Ctr Informat Technol,NIH, Bethesda, MD 20892 USA. EM bezrukov@helix.nih.gov NR 11 TC 100 Z9 101 U1 0 U2 6 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD MAR PY 2005 VL 88 IS 3 BP L17 EP L19 DI 10.1529/biophysj.104.057588 PG 3 WC Biophysics SC Biophysics GA 904JV UT WOS:000227494600001 PM 15626697 ER PT J AU Hong, KM Yang, SH Guo, MZ Herman, JG Jen, J AF Hong, KM Yang, SH Guo, MZ Herman, JG Jen, J TI Semiautomatic detection of DNA methylation at CpG islands SO BIOTECHNIQUES LA English DT Article ID EXTENSION MS-SNUPE; SITES; ASSAY; PCR C1 NCI, Lab Populat Genet, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. RP Jen, J (reprint author), NCI, Lab Populat Genet, Canc Res Ctr, NIH, Bldg 41,Room D702, Bethesda, MD 20892 USA. EM jenj@mail.nih.gov NR 6 TC 5 Z9 6 U1 0 U2 0 PU EATON PUBLISHING CO PI WESTBOROUGH PA ONE RESEARCH DRIVE, SUITE 400A, PO BOX 1070, WESTBOROUGH, MA 01581-6070 USA SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD MAR PY 2005 VL 38 IS 3 BP 354 EP + DI 10.2144/05383BM02 PG 3 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 907VK UT WOS:000227745900004 PM 15786801 ER PT J AU Bleckwenn, NA Bentley, WE Shiloach, J AF Bleckwenn, NA Bentley, WE Shiloach, J TI Evaluation of production parameters with the vaccinia virus expression system using microcarrier attached HeLa cells SO BIOTECHNOLOGY PROGRESS LA English DT Article ID GREEN FLUORESCENT PROTEIN; INFECTED INSECT CELLS; RECOMBINANT PROTEIN; DISSOLVED-OXYGEN; MAMMALIAN-CELLS; FUSION PROTEIN; ADENOVIRUS PRODUCTION; ADSORPTION-KINETICS; MONOCLONAL-ANTIBODY; RNA-POLYMERASE AB Parameters that affect production of the recombinant reporter protein, EGFP, in the T7 promoter based VOTE vaccinia virus-HeLa cell expression system were examined. Length of infection phase, inducer concentration, and timing of its addition relative to infection were evaluated in 6-well plate monolayer cultures. One hour infection with 1.0 mM IPTG added at the time of infection provided a robust process. For larger scale experiments, anchorage-dependent HeLa cells were grown on 5 g/L Cytodex 3 microcarriers. The change to this dynamic culture environment, with cell-covered microcarriers suspended in culture medium in spinner flasks, suggested a re-examination of the multiplicity of infection (MOI) for this culture type that indicated a need for an increase in the number of virus particles per cell to 5.0, higher than that needed for complete infection in monolayer tissue flask culture. Additionally, dissolved oxygen level and temperature during the protein production phase were evaluated for their effect on EGFP expression in microcarrier spinner flask culture. Both increased dissolved oxygen, based on surface area to volume (SA/V) adjustments, and decreased temperature from 37 to 31 degrees C showed increases in EGFP production over the course of the production phase. The level of production achieved with this system reached approximately 17 mu g EGFP/10(6) infected cells. C1 NIDDK, Biotechnol Unit, DHHS, NIH, Bethesda, MD 20892 USA. RP Shiloach, J (reprint author), NIDDK, Biotechnol Unit, DHHS, NIH, Bldg 14A Rm 176,9000 Rockville Pike, Bethesda, MD 20892 USA. EM yossi@nih.gov NR 50 TC 9 Z9 10 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 8756-7938 J9 BIOTECHNOL PROGR JI Biotechnol. Prog. PD MAR-APR PY 2005 VL 21 IS 2 BP 554 EP 561 DI 10.1021/bp0498443 PG 8 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA 913CF UT WOS:000228127200033 PM 15801798 ER PT J AU Solow, SP Sengbusch, J Laird, MW AF Solow, SP Sengbusch, J Laird, MW TI Heterologous protein production from the inducible MET25 promoter in Saccharomyces cerevisiae SO BIOTECHNOLOGY PROGRESS LA English DT Article ID GENE; EXPRESSION; ALBUMIN; YEAST AB Heterologous protein production late in Saccharomyces cerevisiae fermentations is often desirable because it may help avoid the unintentional selection of more rapidly growing, non-protein-expressing cells or allow for the expression of toxic proteins. Here, we describe the use of the MET25 promoter for the production of human serum albumin (HSA) and HSA-fusion proteins in S. cerevisiae. In media lacking methionine, the MET25 promoter yielded high expression levels of HSA and HSA fused to human glucagon, human growth hormone, human interferon a., and human interleukin-2. More importantly, we have shown that this system can be used to delay heterologous protein production until late log phase of the growth of the culture and does not require the addition of an exogenous inducer. C1 Human Genome Sci Inc, Rockville, MD 20850 USA. RP Solow, SP (reprint author), NIH, 45 Ctr Dr,MSC 6510,Bldg 45,Room 6AN-22N-26, Bethesda, MD 20892 USA. EM solow@ncbi.nlm.nih.gov NR 15 TC 16 Z9 16 U1 2 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 8756-7938 J9 BIOTECHNOL PROGR JI Biotechnol. Prog. PD MAR-APR PY 2005 VL 21 IS 2 BP 617 EP 620 DI 10.1021/bp049916q PG 4 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA 913CF UT WOS:000228127200043 PM 15801808 ER PT J AU Heindel, JJ AF Heindel, JJ TI The fetal basis of adult disease: Role of environmental exposures - Introduction SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY LA English DT Editorial Material C1 NIEHS, NIH, Div Extramural Res & Training, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. RP Heindel, JJ (reprint author), NIEHS, NIH, Div Extramural Res & Training, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA. EM heindelj@niehs.nih.gov NR 0 TC 34 Z9 36 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1542-0752 J9 BIRTH DEFECTS RES A JI Birth Defects Res. Part A-Clin. Mol. Teratol. PD MAR PY 2005 VL 73 IS 3 BP 131 EP 132 DI 10.1002/bdra.20119 PG 2 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA 912AJ UT WOS:000228049200001 PM 15751038 ER PT J AU Linehan, WM Grubb, RL Coleman, JA Zbar, B Walther, MM AF Linehan, WM Grubb, RL Coleman, JA Zbar, B Walther, MM TI The genetic basis of cancer of kidney cancer: implications for gene-specific clinical management SO BJU INTERNATIONAL LA English DT Article; Proceedings Paper CT 1st World Meeting on Kidney Surgery CY FEB 05-07, 2003 CL Cleveland Clin Fdn, Cleveland, OH HO Cleveland Clin Fdn DE kidney cancer; gene; VHL; Met ID RENAL-CELL CARCINOMA; HIPPEL-LINDAU-DISEASE; TUMOR-SUPPRESSOR GENE; HOGG-DUBE-SYNDROME; PARENCHYMAL SPARING SURGERY; SPONTANEOUS PNEUMOTHORAX; 10-YEAR EXPERIENCE; GERMLINE MUTATIONS; MET PROTOONCOGENE; SOMATIC MUTATIONS C1 NCI, Urol Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA. NCI, Immunobiol Lab, Ctr Canc Res, Bethesda, MD 20892 USA. RP Linehan, WM (reprint author), NCI, Urol Oncol Branch, Ctr Canc Res, Bldg 10,Rm 2B47, Bethesda, MD 20892 USA. EM uob@mail.nih.gov OI Coleman, Jonathan/0000-0002-6428-7835 NR 55 TC 25 Z9 26 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 1464-4096 J9 BJU INT JI BJU Int. PD MAR PY 2005 VL 95 SU 2 BP 2 EP 7 DI 10.1111/j.1464-410X.2005.05189.x PG 6 WC Urology & Nephrology SC Urology & Nephrology GA 906NP UT WOS:000227649200002 PM 15720328 ER PT J AU Wiestner, A AF Wiestner, A TI More ZAP for chronic lymphocytic leukemia (CLL) SO BLOOD LA English DT Editorial Material ID EXPRESSION; PHENOTYPE AB Antigen stimulation of the leukemic clone is increasingly implicated in the pathogenesis of CLL. Chen and colleagues provide evidence that expression of ZAP-70 in CLL B cells renders lgM signaling more effective and thereby could contribute to the more rapidly progressive clinical course of ZAP-70-positive CLL. C1 NHLBI, Bethesda, MD 20892 USA. RP Wiestner, A (reprint author), NHLBI, Bldg 10, Bethesda, MD 20892 USA. NR 5 TC 6 Z9 6 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 MAR 1 PY 2005 VL 105 IS 5 BP 1839 EP 1840 DI 10.1182/blood-2004-12-4758 PG 2 WC Hematology SC Hematology GA 901UU UT WOS:000227308400001 PM 15747395 ER PT J AU Aplan, PD AF Aplan, PD TI "You break it, you fix it" SO BLOOD LA English DT Editorial Material ID CLUSTER REGION; DNA CLEAVAGE AB Nonrandom chromosomal translocations are considered to be causal events leading to leukemic transformation. However, the mechanism(s) that cause these translocations are poorly understood. Libura and colleagues report exciting new findings on the mechanism(s) that lead to chromosomal translocation. C1 NCI, Bethesda, MD 20892 USA. RP Aplan, PD (reprint author), NCI, Bethesda, MD 20892 USA. RI Aplan, Peter/K-9064-2016 NR 6 TC 1 Z9 1 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 MAR 1 PY 2005 VL 105 IS 5 BP 1843 EP 1844 DI 10.1182/blood-2004-12-4760 PG 2 WC Hematology SC Hematology GA 901UU UT WOS:000227308400006 PM 15747400 ER PT J AU Sloand, EM AF Sloand, EM TI Soluble urokinase activator receptor (suPAR) in stem cell mobilization SO BLOOD LA English DT Editorial Material ID PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; EXPRESSION; PLASMA; UPAR AB Selleri et al demonstrate that healthy donors given granulocvte-colony-stimulating-factor (G-CSF) have increases in plasma soluble plasminogen activator receptor (suPAR) levels, which in turn induces chemotaxis of CD34 cells. Selleri et al's findings help better define the complicated mechanism of stem cell mobilization by G-CSF and point to a wide role for uPAR in cell surface adhesion and recognition. C1 NIH, Bethesda, MD 20892 USA. RP Sloand, EM (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA. NR 7 TC 2 Z9 2 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 MAR 1 PY 2005 VL 105 IS 5 BP 1847 EP 1848 DI 10.1182/blood-2004-12-4766 PG 2 WC Hematology SC Hematology GA 901UU UT WOS:000227308400010 PM 15747404 ER PT J AU Jelacic, T Linnekin, D AF Jelacic, T Linnekin, D TI PKC delta plays opposite roles in growth mediated by wild-type Kit and an oncogenic Kit mutant SO BLOOD LA English DT Article ID PROTEIN-KINASE-C; RECEPTOR TYROSINE KINASE; BLOOD MONONUCLEAR-CELLS; HUMAN LEUKEMIA-CELLS; PHASE-I; CATALYTIC DOMAIN; ACTIVATING MUTATIONS; POINT MUTATION; MAST-CELLS; W-LOCUS AB The Kit receptor tyrosine kinase is critical for normal hematopolesis. Mutation of the aspartic acid residue encoded by codon 816 of human c-kit or codon 814 of the murine gene results in an oncogenic form of Kit. Here we investigate the role of protein kinase Cdelta (PKCdelta) in responses mediated by wild-type murine Kit and the D814Y mutant in a murine mast cell-like line. PKCdelta is activated after wild-type (WT) Kit binds stem cell factor (SCF), is constitutively active in cells expressing the Kit catalytic domain mutant, and coprecipitates with both forms of Kit. Inhibition of PKCdelta had opposite effects on growth mediated by wild-type and mutant Kit. Both rottlerin and a dominant-negative PKCdelta construct inhibited the growth of cells expressing mutant Kit, while SCF-induced growth of cells expressing wildtype Kit was not inhibited. Further, overexpression of PKCdelta inhibited growth of cells expressing wild-type Kit and enhanced growth of cells expressing the Kit mutant. These data demonstrate that PKCdelta contributes to factor-independent growth of cells expressing the D814Y mutant, but negatively regulates SCF-induced growth of cells expressing wildtype Kit. This is the first demonstration that PKCdelta has different functions in cells expressing normal versus oncogenic forms of a receptor. C1 Natl Canc Inst Frederick, Ctr Canc Res, Basic Res Lab, Ft Detrick, MD 21702 USA. RP Jelacic, T (reprint author), Natl Canc Inst Frederick, Ctr Canc Res, Basic Res Lab, Bldg 469,Rm 205, Ft Detrick, MD 21702 USA. EM t_jelacic_obreiter@ncifcrf.gov FU NCI NIH HHS [N01-CO-12400] NR 67 TC 12 Z9 12 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 MAR 1 PY 2005 VL 105 IS 5 BP 1923 EP 1929 DI 10.1182/blood-2004-04-1450 PG 7 WC Hematology SC Hematology GA 901UU UT WOS:000227308400021 PM 15542581 ER PT J AU Murga, M Fernandez-Capetillo, O Tosato, G AF Murga, M Fernandez-Capetillo, O Tosato, G TI Neuropilin-1 regulates attachment in human endothelial cells independently of vascular endothelial growth factor receptor-2 SO BLOOD LA English DT Article ID TUMOR-CELLS; IN-VIVO; MONOCLONAL-ANTIBODY; TYROSINE KINASE; FACTOR VEGF; INTEGRIN ALPHA(V)BETA(3); DEVELOPING CHICK; CARCINOMA-CELLS; NERVOUS-SYSTEM; SEMAPHORIN-III AB Neuropilin-1 (NRP-1) is a type 1 membrane protein that binds the axon guidance factors belonging to the class-3 semaforin family. In endothelial cells, NRP-1 serves as a co-receptor for vascular endothelial growth factor (VEGF) and regulates VEGF receptor 2 (VEGFR-2)dependent angiogenesis. Although genetargeting studies documenting embryonic lethality in NRP-1 null mice have demonstrated a critical role for NRP-1 in vascular development, the activities of NRP-1 in mature endothelial cells have been incompletely defined. Using RNA interference-mediated silencing of NRP-1 or VEGFR-2 in primary human endothelial cells, we confirm that NRP-1 modulates VEGFR-2 signaling-dependent mitogenic functions of VEGF. Importantly, we now show that NRP-1 regulates endothelialcell adhesion to extracellular matrix proteins independently of VEGFR-2. Based on its dual role as an enhancer of VEGF activity and a mediator of endothelial cell adhesiveness described here, NRP-1 emerges as a promising molecular target for the development of antiangiogenic drugs. (C) 2005 by The American Society of Hematology. C1 NCI, Expt Transplantat & Immunol Branch, CCR, NIH, Bethesda, MD 20892 USA. NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. RP Tosato, G (reprint author), NCI, Expt Transplantat & Immunol Branch, CCR, NIH, Bldg 10-12C205,10 Ctr Dr, Bethesda, MD 20892 USA. EM tosatog@mail.nih.gov RI Fernandez-Capetillo, Oscar/H-3508-2015 OI Fernandez-Capetillo, Oscar/0000-0002-2690-6885 NR 80 TC 86 Z9 89 U1 0 U2 2 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 MAR 1 PY 2005 VL 105 IS 5 BP 1992 EP 1999 DI 10.1182/blood-2004-07-2598 PG 8 WC Hematology SC Hematology GA 901UU UT WOS:000227308400031 PM 15522955 ER PT J AU Shanafelt, TD Lee, YK Bone, ND Strege, AK Narayanan, VL Sausville, EA Geyer, SM Kaufmann, SH Kay, NE AF Shanafelt, TD Lee, YK Bone, ND Strege, AK Narayanan, VL Sausville, EA Geyer, SM Kaufmann, SH Kay, NE TI Adaphostin-induced apoptosis in CLL B cells is associated with induction of oxidative stress and exhibits synergy with fludarabine SO BLOOD LA English DT Article ID CHRONIC LYMPHOCYTIC-LEUKEMIA; DRUG-INDUCED APOPTOSIS; IN-SITU HYBRIDIZATION; P53 GENE MUTATION; PURINE ANALOGS; EXPRESSION; INHIBITORS; VITRO; RESISTANCE; NSC-680410 AB B-cell chronic lymphocytic leukemia (CLL) is characterized by accumulation of clonal lymphocytes resistant to apoptosis. We evaluated the ability of the investigational antileukemic agent adaphostin to induce apoptosis in CLL B cells and synergize with fludarabine in vitro. Analysis by annexin V/propidium iodide (PI) staining revealed that the concentration of adaphostin required to induce 50% cell death (IC50) at 24 hours was 4.2 muM (range, 1.10-11.25 muM; median, 4.25 muM; n = 29) for CLL isolates and more than 10 muM for B and T cells from healthy donors. Immunoblots demonstrated adaphostin induced poly(adenosine diphosphate-ribose) polymerase (PARP) cleavage and cleavage of caspase-3 substrates, suggesting that adaphostin induces apoptosis. Adaphostin increased the level of reactive oxygen species (ROS) within CLL B cells, and the antioxidant N-acetylcysteine blocked both adaphostin-induced ROS generation and apoptosis. Adaphostin also caused a decrease in the level of the antiapoptotic protein Bcl-2. When adaphostin was combined with fludarabine (F-ARA-AMP), a synergistic effect on cell death was observed in all 10 CLL samples. These findings not only indicate that adaphostin induces apoptosis selectively in CLL B cells through a mechanism that involves ROS generation but also demonstrate its ability to augment the effects of fludarabine. Further preclinical development of adaphostin as a novel agent for the treatment of CLL appears warranted. (C) 2005 by The American Society of Hematology. C1 Mayo Clin & Mayo Fdn, Dept Med, Div Hematol, Div Oncol Res, Rochester, MN 55905 USA. Mayo Clin & Mayo Fdn, Div Biostat, Dept Med, Rochester, MN 55905 USA. NCI, Dev Therapeut Program, Div Canc Treatment & Diagnosis, Bethesda, MD 20892 USA. Univ Maryland, Greenbaum Canc Ctr, Baltimore, MD 21201 USA. RP Shanafelt, TD (reprint author), Mayo Clin & Mayo Fdn, Dept Med, Div Hematol, Div Oncol Res, 200 1st St SW,Stabil 6-28, Rochester, MN 55905 USA. EM shanafelt.tait@mayo.edu RI Geyer, Susan/E-3112-2011 FU NCI NIH HHS [R01 CA85972, R01 CA91542] NR 65 TC 36 Z9 38 U1 0 U2 1 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 MAR 1 PY 2005 VL 105 IS 5 BP 2099 EP 2106 DI 10.1182/blood-2004-06-2205 PG 8 WC Hematology SC Hematology GA 901UU UT WOS:000227308400046 PM 15388586 ER PT J AU Zhu, D Qi, CF Morse, HC Janz, S Stevenson, FK AF Zhu, D Qi, CF Morse, HC Janz, S Stevenson, FK TI Deregulated expression of the Myc cellular oncogene drives development of mouse "Burkitt-like" lymphomas from naive B cells SO BLOOD LA English DT Article ID IMMUNOGLOBULIN VARIABLE REGION; CHRONIC LYMPHOCYTIC-LEUKEMIA; C-MYC; GLYCOSYLATION SITES; CLINICAL-FEATURES; GENE; TRANSLOCATIONS; PHENOTYPE; MUTATION; PROTEIN AB Chromosomal translocations juxtaposing immunoglobulin (Ig) and MYC genes are the hallmarks of human Burkitt lymphoma (BL), with deregulated MYC expression being a critical factor in pathogenesis. By inserting an intact mouse Myc gene into the mouse genome, proximal to the 19 enhancer Emu, the effect of a precise mimic of the major t(8;14) translocation of human endemic BIL (eBL) could be investigated. Knock-in mice developed IgM-positive B-cell tumors, with most being typical of eBL by histology and immunophenotype, including expression of the germinal center (GC)-associated protein, BCL6. Unlike eBL, however, analysis Of 19 V-H sequences revealed no significant level of somatic mutation. Thus, constitutive expression of Myc in the knock-in mice is apparently able to induce "Burkift-like" lymphomas before antigen stimulation and formation of a GC. In contrast, human eBL development occurs in a GC or post-GC site with a likely contribution to pathogenesis from Epstein-Barr virus (EBV) and other epigenetic factors. (C) 2005 by The American Society of Hematology C1 Southampton Univ Hosp Trust, Tenovus Lab, Mol Immunol Grp, Southampton SO16 6YD, Hants, England. NIAID, Immunopathol Lab, NIH, Bethesda, MD USA. NCI, Genet Lab, NIH, Bethesda, MD USA. RP Zhu, D (reprint author), Southampton Univ Hosp Trust, Tenovus Lab, Mol Immunol Grp, Southampton SO16 6YD, Hants, England. EM d.zhu@soton.ac.uk OI Morse, Herbert/0000-0002-9331-3705 NR 21 TC 25 Z9 27 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 MAR 1 PY 2005 VL 105 IS 5 BP 2135 EP 2137 DI 10.1182/blood-2004-07-2573 PG 3 WC Hematology SC Hematology GA 901UU UT WOS:000227308400051 PM 15522957 ER PT J AU Kim, A Zhao, H Dean, A AF Kim, A Zhao, H Dean, A TI RNA polymerase II elongation and histone acetylation in chromatin. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 NIDDKD, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 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 MAR-APR PY 2005 VL 34 IS 2 MA 19 BP 83 EP 83 PG 1 WC Hematology SC Hematology GA 907VH UT WOS:000227745600020 ER PT J AU Felsenfeld, G Burgess-Beusse, B Farrell, C Gaszner, M Ghirlando, R Huang, SM Jin, CY Nakatani, Y Litt, M Mutskov, V Tagami, H West, A Yusufzai, T AF Felsenfeld, G Burgess-Beusse, B Farrell, C Gaszner, M Ghirlando, R Huang, SM Jin, CY Nakatani, Y Litt, M Mutskov, V Tagami, H West, A Yusufzai, T TI A division of labor at the chicken beta-globin insulator. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. Dana Farber Canc Inst, Boston, MA 02115 USA. RI Ghirlando, Rodolfo/A-8880-2009 NR 0 TC 0 Z9 0 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 MAR-APR PY 2005 VL 34 IS 2 MA 26 BP 86 EP 86 PG 1 WC Hematology SC Hematology GA 907VH UT WOS:000227745600027 ER PT J AU Gallagher, PG Pilon, AM Nilson, DG Wong, E Bodine, DM AF Gallagher, PG Pilon, AM Nilson, DG Wong, E Bodine, DM TI Multiple defects in erythroid gene expression in erythroid krupple-like factor (EKLF) target genes in EKLF-deficient mice. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 Yale Univ, Dept Pediat, Sch Med, New Haven, CT 06520 USA. NHGRI, GMBB, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 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 MAR-APR PY 2005 VL 34 IS 2 MA 31 BP 87 EP 88 PG 2 WC Hematology SC Hematology GA 907VH UT WOS:000227745600032 ER PT J AU Sterner, L Miyazaki, T Swift, L Dean, A Little, J AF Sterner, L Miyazaki, T Swift, L Dean, A Little, J TI Endogenous elevations of short chain fatty acids up-regulate embryonic globin gene expression during primitive etythropoiesis. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD USA. Univ Texas, SW Med Ctr, Ctr Immunol, Dallas, TX USA. Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA. NR 0 TC 0 Z9 0 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 MAR-APR PY 2005 VL 34 IS 2 MA 63 BP 102 EP 103 PG 2 WC Hematology SC Hematology GA 907VH UT WOS:000227745600064 ER PT J AU Noguchi, CT Rogers, H AF Noguchi, CT Rogers, H TI Hypoxia and histone deacetylase inhibitors alter expression of transcription factors in erythroid progenitor cells and induces gamma-globin gene expression. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 NIDDK, Biol Chem Lab, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 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 MAR-APR PY 2005 VL 34 IS 2 MA 76 BP 109 EP 110 PG 2 WC Hematology SC Hematology GA 907VH UT WOS:000227745600077 ER PT J AU Shimizu, R Ohneda, K Nishikawa, K Trainor, CD Yamamoto, M AF Shimizu, R Ohneda, K Nishikawa, K Trainor, CD Yamamoto, M TI Self-association of GATA-1 is required for erythropoiesis in vivo. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 Univ Tsukuba, Grad Sch Comprehens Human Sci, Ctr Tsukuba Adv Res Alliance, Tsukuba, Ibaraki 3058577, Japan. Univ Tsukuba, ERATO, Environm Response Project, Tsukuba, Ibaraki 3058577, Japan. NIDDKD, Mol Biol Lab, Bethesda, MD 20892 USA. RI Yamamoto, Masayuki/A-4873-2010 NR 0 TC 0 Z9 0 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 MAR-APR PY 2005 VL 34 IS 2 BP 122 EP 122 PG 1 WC Hematology SC Hematology GA 907VH UT WOS:000227745600105 ER PT J AU Ghirlando, R Simpson, M Trainor, C AF Ghirlando, R Simpson, M Trainor, C TI Determinants of GATA-1 DNA binding and the regulation of the folate receptor gene. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 NIDDK, LMB, NIH, Bethesda, MD 20892 USA. RI Ghirlando, Rodolfo/A-8880-2009 NR 0 TC 0 Z9 0 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 MAR-APR PY 2005 VL 34 IS 2 MA 115 BP 126 EP 127 PG 2 WC Hematology SC Hematology GA 907VH UT WOS:000227745600116 ER PT J AU Wen, J Huang, SM Noguchi, CT AF Wen, J Huang, SM Noguchi, CT TI SATB1 differentially regulates globin gene transcription by interaction with the beta-globin cluster. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 NIDDK, Biol Chem Lab, NIH, Bethesda, MD 20892 USA. NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 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 1079-9796 J9 BLOOD CELL MOL DIS JI Blood Cells Mol. Dis. PD MAR-APR PY 2005 VL 34 IS 2 MA 121 BP 129 EP 130 PG 2 WC Hematology SC Hematology GA 907VH UT WOS:000227745600122 ER PT J AU Zhao, H Dean, A AF Zhao, H Dean, A TI Use of chromatin insulators to dissect enhancer function. SO BLOOD CELLS MOLECULES AND DISEASES LA English DT Meeting Abstract CT 14th Conference on Hemoglobin Switching CY SEP 10-14, 2004 CL Orcas Isl, WA C1 NIDDKD, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 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 MAR-APR PY 2005 VL 34 IS 2 MA 132 BP 134 EP 134 PG 1 WC Hematology SC Hematology GA 907VH UT WOS:000227745600133 ER PT J AU Bonds, DR AF Bonds, DR TI Three decades of innovation in the management of sickle cell disease: the road to understanding the sickle cell disease clinical phenotype SO BLOOD REVIEWS LA English DT Review DE sickle cell disease; clinical phenotype; severity; acute chest syndrome; leg ulcers; osteonecrosis of bones; stroke; attoimmunization; pneumococcal sepsis; hydroxyurea; blood transfusions ID ACUTE CHEST SYNDROME; DIAGNOSTIC ERROR RATES; RISK-FACTORS; LONGITUDINAL DATA; ANEMIA; CHILDREN; HYDROXYUREA; HEMOGLOBIN; TRIAL; OSTEONECROSIS AB In the United States, sickle cell disease affects approximately 1 in 350 African-American newborn infants each year, and approximately 72,000 individuals total. Sickle cell disease is the most prevalent genetic hematologic disorder in the US. In 1972, the National, Sickle Cell Disease Control Act was passed by Congress. This Landmark piece of legislation established the National Sickle Cell Disease Program which mandated that scientific research programs should be funded to improve the care and quality of life of patients with sickle cell disease. The National Heart, Lung, and Blood Institute has been responsible for the organization and funding of the extramural research programs in sickle cell disease since establishment of the National Sickle Cell Disease Program. This review will discuss the major prospective epidemiologic cohort study that described the prevalence and incidence of the major syndromes responsible for the morbidity and mortality in sickle cell disease, as welt as the major phase II and phase III clinical trials that have lead to the major therapeutic advances in the care of sickle cell disease patients. The clinical research conducted by the National Sickle Cell Disease Program has allowed the description of the major risk factors responsible for morbidity and mortatity in sickle cell disease. These clinical studies have paved the way to our understanding the severe phenotype that will ultimately allow aggressive therapies to be targeted to patients at high risk for a morbid outcome. (C) Published by Elsevier Ltd. C1 NHLBI, Blood Dis Program, Div Blood Dis & Resources, Bethesda, MD 20892 USA. RP Bonds, DR (reprint author), NHLBI, Blood Dis Program, Div Blood Dis & Resources, 6701 Rockledge Dr,MSC-7950, Bethesda, MD 20892 USA. EM db56g@nih.gov NR 50 TC 41 Z9 42 U1 0 U2 19 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0268-960X J9 BLOOD REV JI Blood Rev. PD MAR PY 2005 VL 19 IS 2 BP 99 EP 110 DI 10.1016/j.blre.2004.04.002 PG 12 WC Hematology SC Hematology GA 896LJ UT WOS:000226935300004 PM 15603913 ER PT J AU Calmels, B Ferguson, C Adler, R Sellers, S Dunbar, C AF Calmels, B Ferguson, C Adler, R Sellers, S Dunbar, C TI Recurrent retroviral vector integration at the MDS1-EVI1 locus in rhesus long-term repopulating haematopoietic stem cells SO BONE MARROW TRANSPLANTATION LA English DT Meeting Abstract CT 31st Annual Meeting of the European-Group-for-Blood-and-Marrow-Transplantation/21st Meeting of the EBMT-Nurses-Group/4th Meeting of the EBMT-Data-Management-Group CY MAR 20-23, 2005 CL Prague, CZECH REPUBLIC SP European Grp Blood & Marrow Transplantat, EBMT Nurses Grp, EBMT Data Management Grp C1 NHLBI, NIH, Bethesda, MD 20892 USA. RI calmels, boris/R-2538-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD MAR PY 2005 VL 35 SU 2 BP S17 EP S17 PG 1 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA 915UE UT WOS:000228336000040 ER PT J AU Fry, TJ Mackall, CL AF Fry, TJ Mackall, CL TI Immune reconstitution following hematopoietic progenitor cell transplantation: challenges for the future SO BONE MARROW TRANSPLANTATION LA English DT Article DE thymopoiesis; GVHD; IL-7; keratinocyte growth factor; homeostatic peripheral expansion ID BONE-MARROW-TRANSPLANTATION; VERSUS-HOST-DISEASE; T-CELLS; LATE INFECTIONS; B-CELL; REGENERATION; REPOPULATION; LYMPHOCYTE; LEUKEMIA; ADULTS AB Successful hematopoietic progenitor cell transplantation requires rapid and complete transfer of the donor hematopoietic and immune systems to the host. Whereas the uncontrolled transfer of a nontolerant donor immune system results in GVHD in many cases, strategies which diminish GVHD also diminish immune reconstitution. Thus, the reliable, rapid and safe transfer of immunity from donor to host remains a major challenge for the field. Advances in the understanding of the biology of immune reconstitution have elucidated that thymic-dependent immune reconstitution can restore global immunity, but is especially vulnerable to toxicities associated with transplant. Alternatively, homeostatic peripheral expansion can be exploited for targeted immunity toward pathogens and tumors, but is difficult to manipulate without exacerbating GVHD risk. New translatable strategies are needed to safely augment one or both of these pathways in the setting of allogeneic hematopoietic progenitor cell transplantation. C1 NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA. RP Mackall, CL (reprint author), NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA. EM cm35c@nih.gov NR 34 TC 34 Z9 35 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD MAR PY 2005 VL 35 SU 1 BP S53 EP S57 DI 10.1038/sj.bmt.1704848 PG 5 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA 913JC UT WOS:000228146700013 PM 15812532 ER PT J AU Risitano, A Young, N Maciejewski, J Wlodarski, M Pane, F Selleri, C Federico, BR AF Risitano, A Young, N Maciejewski, J Wlodarski, M Pane, F Selleri, C Federico, BR TI Clonal T-cell populations attacking the haematopoietic tissue are responsible for immune-mediated aplastic anaemia and pathogenically related marrow failure syndromes SO BONE MARROW TRANSPLANTATION LA English DT Meeting Abstract CT 31st Annual Meeting of the European-Group-for-Blood-and-Marrow-Transplantation/21st Meeting of the EBMT-Nurses-Group/4th Meeting of the EBMT-Data-Management-Group CY MAR 20-23, 2005 CL Prague, CZECH REPUBLIC SP European Grp Blood & Marrow Transplantat, EBMT Nurses Grp, EBMT Data Management Grp C1 Univ Naples Federico II, Naples, Italy. NHLBI, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD MAR PY 2005 VL 35 SU 2 BP S28 EP S28 PG 1 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA 915UE UT WOS:000228336000070 ER PT J AU Hummel, F Celnik, P Giraux, P Floel, A Wu, WH Gerloff, C Cohen, LG AF Hummel, F Celnik, P Giraux, P Floel, A Wu, WH Gerloff, C Cohen, LG TI Effects of non-invasive cortical stimulation on skilled motor function in chronic stroke SO BRAIN LA English DT Article DE cortical stimulation; motor control; rehabilitation; stroke ID TRANSCRANIAL MAGNETIC STIMULATION; HAND FUNCTION-TEST; CORTEX EXCITABILITY; CLINICAL-APPLICATION; SENSORIMOTOR CORTEX; PREFRONTAL CORTEX; ISCHEMIC INFARCT; PREMOTOR CORTEX; RECOVERY; HUMANS AB Stroke is a leading cause of adult motor disability. Despite recent progress, recovery of motor function after stroke is usually incomplete. This double blind, Sham-controlled, crossover study was designed to test the hypothesis that non-invasive stimulation of the motor cortex could improve motor function in the paretic hand of patients with chronic stroke. Hand function was measured using the Jebsen-Taylor Hand Function Test (JTT), a widely used, well validated test for functional motor assessment that reflects activities of daily living. JTT measured in the paretic hand improved significantly with non-invasive transcranial direct current stimulation (tDCS), but not with Sham, an effect that outlasted the stimulation period, was present in every single patient tested and that correlated with an increment in motor cortical excitability within the affected hemisphere, expressed as increased recruitment curves (RC) and reduced short-interval intracortical inhibition. These results document a beneficial effect of non-invasive cortical stimulation on a set of hand functions that mimic activities of daily living in the paretic hand of patients with chronic stroke, and suggest that this interventional strategy in combination with customary rehabilitative treatments may play an adjuvant role in neurorehabilitation. C1 NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20817 USA. Univ Tubingen, Cort Physiol Res Grp, Dept Neurol, D-72076 Tubingen, Germany. Univ Tubingen, Hertie Inst Clin Brain Res, D-72076 Tubingen, Germany. RP Cohen, LG (reprint author), NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20817 USA. EM cohenl@ninds.nih.gov RI Floel, Agnes/A-9426-2017 NR 78 TC 559 Z9 585 U1 5 U2 75 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD MAR PY 2005 VL 128 BP 490 EP 499 DI 10.1093/brain/awh369 PN 3 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 899EN UT WOS:000227127800009 PM 15634731 ER PT J AU Anderson, WF Jatoi, I Devesa, SS AF Anderson, WF Jatoi, I Devesa, SS TI Distinct breast cancer incidence and prognostic patterns in the NCI's SEER program: suggesting a possible link between etiology and outcome SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE actuarial survival; age frequency distribution; breast cancer age-specific incidence rates; etiology; hazard rates; prognosis ID GENE-EXPRESSION PROFILES; END RESULTS DATABASE; FEMALE BREAST; AGE DISTRIBUTION; CARCINOMA; EPIDEMIOLOGY; SURVEILLANCE; RATES AB Background. Breast cancer is a heterogeneous and chronic disease with relapses and death occurring 25 years or more after primary diagnosis. Standard tumor characteristics are used to predict initial relapse or death, but their ability to estimate long-term patterns of failure may be limited. Methods. To further evaluate the significance of standard tumor features, we compared incidence and prognostic patterns in the National Cancer Institutes (NCIs) large-scale population-based Surveillance, Epidemiology, and End Results (SEER) program for high-risk versus low-risk breast cancers, i.e., size > 2.0 versus <= 2.0 cm, lymph node positive versus negative, high versus low histologic grade, and hormone receptor negative versus positive expression, respectively. Data were stratified by age 50 years to approximate menopause. Results. High-risk versus low-risk breast cancers demonstrated two very different incidence and prognostic patterns. Age-specific incidence rates among women with high-risk tumors increased until age 50 years then flattened, whereas rates among women with low-risk tumors increased continuously with aging. Hazard rates for breast cancer death spiked sharply two years following primary breast cancer diagnosis among women with high-risk but not with low-risk tumors. Paradoxically, hazard function crossed over 6-8 years following breast cancer diagnosis, with hazard rates lower for high-risk than for low-risk breast cancers. Conclusion. Distinct incidence and prognostic patterns among high-risk and low-risk breast cancers suggest a possible link between breast cancer etiology and outcome. These epidemiologic results appear to complement emerging molecular genetic techniques, showing distinct genotypes for high-risk and low-risk breast cancer phenotypes. C1 NCI, DHHS, NIH, NCL,Div Canc Prevent,EPN, Bethesda, MD 20892 USA. Uniformed Serv Univ Hlth Sci, Dept Surg, Natl Naval Med Ctr, Bethesda, MD 20814 USA. NCI, DHHS, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Anderson, WF (reprint author), NCI, DHHS, NIH, NCL,Div Canc Prevent,EPN, EPN Suite 2144,6130 Execut Blvd, Bethesda, MD 20892 USA. EM wanderso@mail.nih.gov NR 44 TC 76 Z9 76 U1 0 U2 4 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. PD MAR PY 2005 VL 90 IS 2 BP 127 EP 137 DI 10.1007/s10549-004-3777-3 PG 11 WC Oncology SC Oncology GA 914DW UT WOS:000228206400004 PM 15803359 ER PT J AU Baccarelli, A Pesatori, AC Consonni, D Mocarelli, P Patterson, DG Caporaso, NE Bertazzi, PA Landi, MT AF Baccarelli, A Pesatori, AC Consonni, D Mocarelli, P Patterson, DG Caporaso, NE Bertazzi, PA Landi, MT TI Health status and plasma dioxin levels in chloracne cases 20 years after the Seveso, Italy accident SO BRITISH JOURNAL OF DERMATOLOGY LA English DT Article DE age; chloracne; dermatotoxicity; hair colour; tetrachlorodibenzodioxin ID OPERATION RANCH HAND; HALF-LIFE; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN; TCDD; VETERANS; DIBENZOFURANS; INTOXICATION; EMPHASIS; WORKERS; SERUM AB Background The Seveso, Italy accident of 1976 exposed a large population to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or simply dioxin). The accident resulted, mostly among children, in one of the largest ever-reported outbreaks of chloracne, the typical skin disorder due to halogenated-hydrocarbon compounds. Objectives Approximately 20 years after the accident, we conducted an epidemiological study in Seveso to investigate (a) the health status of chloracne cases; (b) TCDD-chloracne exposure-response relationship; and (c) factors modifying TCDD toxicity. Methods From 1993 to 1998, we recruited 101 chloracne cases and 211 controls. Trained interviewers administered a structured questionnaire assessing, among other epidemiological variables, information on an extensive list of diseases. During the interview, individual pigmentary characteristics were determined. We measured plasma TCDD levels using high-resolution gas chromatography/mass spectrometry. Results Plasma TCDD was still elevated (> 10 ppt) in 78 (26.6%) of the 293 subjects with adequate plasma samples, particularly in females, in subjects who had eaten home-grown animals, and in individuals with older age, higher body mass index and residence near the accident site. After 20 years, health conditions of chloracne cases were similar to those of controls from the Seveso area. Elevated plasma TCDD was associated with chloracne [odds ratio (OR) = 3.7, 95% confidence interval (CI) 1.6-8.8, adjusted for age, sex and residence]. Chloracne risk was higher in subjects younger than 8 years at the accident (OR = 7.4, 95% CI 1.8-30.3) and, contrary to previous hypotheses, did not increase at puberty onset or in teenage years. Subjects with elevated TCDD levels and light hair colour had higher relative odds of chloracne (OR = 9.2, 95% CI 2.6-32.5). Conclusions Dioxin toxicity in chloracne cases was confined to the acute dermatotoxic effects. Chloracne occurrence appeared related to younger age and light hair colour. Age-related dioxin elimination or dilution must be taken into account in interpreting these results. C1 NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA. Univ Milan, Dept Environm & Occupat Hlth, Res Ctr Occupat Clin & Environm Epidemiol, EPOCA, Milan, Italy. Univ Milano Bicocca, Dept Lab Med, Desio, Italy. Ctr Dis Control & Prevent, Div Environm Hlth Lab Sci, Natl Ctr Environm Hlth, Atlanta, GA USA. RP Landi, MT (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, 6120 Execut Blvd,EPS 7114, Bethesda, MD 20892 USA. EM landim@mail.nih.gov RI bertazzi, pietro alberto/D-5039-2017; OI bertazzi, pietro alberto/0000-0003-3475-2449; Baccarelli, Andrea/0000-0002-3436-0640; pesatori, angela/0000-0002-0261-3252 NR 34 TC 29 Z9 32 U1 2 U2 11 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0007-0963 J9 BRIT J DERMATOL JI Br. J. Dermatol. PD MAR PY 2005 VL 152 IS 3 BP 459 EP 465 DI 10.1111/J.1365-2133.2005.06444.X PG 7 WC Dermatology SC Dermatology GA 908FV UT WOS:000227773800008 PM 15787814 ER PT J AU Krauss, J Arndt, MAE Vu, BK Newton, DL Rybak, SM AF Krauss, J Arndt, MAE Vu, BK Newton, DL Rybak, SM TI Targeting malignant B-cell lymphoma with a humanized anti-CD22 scFv-angiogenin immunoenzyme SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article DE angiogenin; humanized single chain Fv; fusion protein; eukaryotic expression; cytotoxicity ID SINGLE-CHAIN FV; PHASE-I; PSEUDOMONAS EXOTOXIN; IMMUNOTOXIN; ANTIBODY; PROTEIN; RIBONUCLEASE; THERAPY; TRIAL; GENERATION AB We report on the generation and functional characterization of a humanized immunoenzyme comprising a stable humanized single chain Fv (scFv) with grafted specificity of the anti-CD22 murine monoclonal antibody RFB4 and the human ribonuclease angiogenin (ANG). The fusion protein produced from transiently transfected mammalian Chinese hamster ovary cells could easily be purified to homogeneity, retained full ribonucleolytic activity, and efficiently killed CD22(+) tumour cells with an IC50 of 56 nmol/l. In contrast, incubation of tumour cells with either ANG or scFv alone did not result in any cytotoxicity. Potent receptor-mediated killing of target cells, expected lack of extracellular toxicity, predictable low immunogenic potential, and ease of production, suggest that this novel immunoenzyme has potential for the immunotherapy of CD22(+) malignancies. C1 Natl Canc Inst, SAIC, Frederick, MD USA. Natl Canc Inst, Dev Therapeut Program, Frederick, MD 21702 USA. RP Krauss, J (reprint author), Univ Essen Gesamthsch, Dept Internal Med Canc Res, D-45122 Essen, Germany. EM juergen.krauss@uni-essen.de; rybak@ncifcrf.gov FU NCI NIH HHS [N01-CO-12400] NR 33 TC 20 Z9 21 U1 0 U2 2 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD MAR PY 2005 VL 128 IS 5 BP 602 EP 609 DI 10.1111/j.1365-2141.2005.05356.x PG 8 WC Hematology SC Hematology GA 899XE UT WOS:000227178300003 PM 15725080 ER PT J AU Griffith, LM McCoy, JP Bolan, CD Stroncek, DF Pickett, AC Linton, GF Lundqvist, A Srinivasan, R Leitman, SF Childs, RW AF Griffith, LM McCoy, JP Bolan, CD Stroncek, DF Pickett, AC Linton, GF Lundqvist, A Srinivasan, R Leitman, SF Childs, RW TI Persistence of recipient plasma cells and anti-donor isohaemagglutinins in patients with delayed donor erythropoiesis after major ABO incompatible non-myeloablative haematopoietic cell transplantation SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article DE plasma cells; chimaerism; major ABO incompatible transplantation; non-myeloablative allogeneic transplantation ID MULTIPLE-MYELOMA; RITUXIMAB; ENGRAFTMENT; CHIMERISM; RESPONSES; ANTIGENS; APLASIA; ANEMIA; GRAFT AB Delayed donor erythropoiesis and pure red-cell aplasia (PRCA) complicate major-ABO mismatched non-myeloablative allogeneic stem-cell transplantation. To characterize these events, we analysed red-cell serology and chimaerism in lymphohaematopoietic lineages, including plasma cells and B cells, in 12 consecutive major-ABO incompatible transplants following cyclophosphamide/fludarabine-based conditioning. Donor erythropoiesis was delayed to more than 100 days in nine (75%) patients including six (50%) who developed PRCA. During PRCA, all patients had persistent anti-donor isohaemagglutinins and recipient plasma cells (5-42%), while myeloid and T cells were completely donor in origin. In contrast, B-cell chimaerism was frequently full-donor when significant anti-donor isohaemagglutinins persisted. Four patients with early mixed haematopoietic chimaerism and the prolonged presence of anti-donor isohaemagglutinins and recipient plasma cells developed delayed-onset (>100 days post-transplant) red cell transfusion dependence and PRCA after myeloid chimaerism converted from mixed to full donor. These findings confirm that donor-erythropoiesis is impacted by temporal disparities in donor immune-mediated eradication of recipient lymphohaematopoietic cells during major-ABO incompatibility and suggest that plasma cells are relatively resistant to graft-versus-host haematopoietic effects. C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Dept Transfus Med, NIH, Bethesda, MD 20892 USA. NHLBI, Warren G Magnuson Clin Ctr, NIH, Core Flow Cytometry Facil, Bethesda, MD 20892 USA. NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA. RP Childs, RW (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10,Rm 7C103,MSC-1652,9000 Rockville Pike, Bethesda, MD 20892 USA. EM childsr@nih.gov NR 26 TC 49 Z9 51 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD MAR PY 2005 VL 128 IS 5 BP 668 EP 675 DI 10.1111/j.1365-2141.2005.05364.x PG 8 WC Hematology SC Hematology GA 899XE UT WOS:000227178300012 PM 15725089 ER PT J AU Katano, H Cohen, JI AF Katano, H Cohen, JI TI Perforin and lymphohistiocytic proliferative disorders SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Review DE perforin; familial haemophagocytic lymphohistiocytosis; haemophagocytosis; histiocytosis; Epstein-Barr virus ID EPSTEIN-BARR-VIRUS; FAMILIAL HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS; LINKED LYMPHOPROLIFERATIVE-DISEASE; CD8(+) T-CELLS; BONE-MARROW-TRANSPLANTATION; CHEDIAK-HIGASHI-SYNDROME; GRANULE-MEDIATED CYTOTOXICITY; CHRONIC VIRAL-INFECTION; VERSUS-HOST-DISEASE; GRANZYME-B AB Perforin is critical for cytotoxicity mediated by granules present in natural killer (NK) cells and cytotoxic T lymphocytes (CTLs). Perforin-deficient mice have impaired cytotoxicity by NK cells and CTLs, resulting in failure to control infections with certain viruses or bacteria. Infection of perforin-deficient mice with lymphocytic choriomeningitis virus results in haemophagocytic lymphohistiocytosis and elevated levels of pro-inflammatory cytokines. Mutations throughout the perforin gene have been identified in patients with familial haemophagocytic lymphohistiocytosis (FHL) type 2. These patients present with fever, hepatosplenomegaly, pancytopenia, have marked elevations of T-helper type 1 and type 2 cytokines, and have impaired NK cell and CTL cytotoxicity. A number of infectious pathogens have been implicated as triggering the onset of disease. Identification of mutations in perforin as the cause of FHL should allow prenatal diagnosis of the disorder. While stem cell transplantation is curative, gene therapy might be effective in the future. C1 NIH, Lab Clin Infect Dis, Med Virol Sect, Bethesda, MD 20892 USA. Natl Inst Infect Dis, Dept Pathol, Shinjuku Ku, Tokyo, Japan. RP Cohen, JI (reprint author), NIH, Lab Clin Infect Dis, Med Virol Sect, Bldg 10,Room 11N228,10 Ctr Dr, Bethesda, MD 20892 USA. EM jcohen@niaid.nih.gov NR 112 TC 36 Z9 42 U1 0 U2 3 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD MAR PY 2005 VL 128 IS 6 BP 739 EP 750 DI 10.1111/j.1365-2141.2004.05305.x PG 12 WC Hematology SC Hematology GA 904FA UT WOS:000227480300001 PM 15755277 ER PT J AU Schindler, CW Karcz-Kubicha, M Thorndike, EB Muller, CE Tella, SR Ferre, S Goldberg, SR AF Schindler, CW Karcz-Kubicha, M Thorndike, EB Muller, CE Tella, SR Ferre, S Goldberg, SR TI Role of central and peripheral adenosine receptors in the cardiovascular responses to intraperitoneal injections of adenosine A(1) and A(2A) subtype receptor agonists SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE CGS 21680; CPA; A(1) receptors; A(2A) receptors; blood pressure; heart rate ID CENTRAL-NERVOUS-SYSTEM; ANTAGONIST IN-VIVO; NORMOTENSIVE RATS; BLOOD-PRESSURE; NTS A(2A); PHARMACOLOGY; STIMULATION; MECHANISM; TELEMETRY; CAFFEINE AB 1 The cardiovascular effects of the adenosine A(1) receptor agonist N-6-cyclopentyladenosine (CPA) and the adenosine A(2A) receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680) were investigated in rats implanted with telemetry transmitters for the measurement of blood pressure and heart rate. 2 Intraperitoneal (i.p.) injections of the adenosine A(1) receptor agonist CPA led to dose-dependent decreases in both blood pressure and heart rate. These effects of 0.3 mg kg(-1) CPA were antagonized by i.p. injections of the adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dimethyl-xanthine (CPT), but not by i.p. injections of the adenosine A(2A) receptor antagonist 3-(3- hydroxypropyl)-8-(m-methoxystyryl)-7-methyl-1-propargylxanthine phosphate disodium salt (MSX-3). Injections (i.p.) of the peripherally acting nonselective adenosine antagonist 8-sulfophenyltheophylline (8-SPT) and the purported nonselective adenosine antagonist caffeine also antagonized the cardiovascular effects of CPA. 3 The adenosine A(2A) agonist CGS 21680 given i.p. produced a dose-dependent decrease in blood pressure and an increase in heart rate. These effects of 0.5 mg kg(-1) CGS 21680 were antagonized by i.p. injections of the adenosine A(2A) receptor antagonist MSX-3, but not by i.p. injections of the antagonists CPT, 8-SPT or caffeine. 4 Central administration (intracerebral ventricular) of CGS 21680 produced an increase in heart rate, but no change in blood pressure. MSX-3 given i.p. antagonized the effects of the central injection of CGS 21680. 5 These results suggest that adenosine A(1) receptor agonists produce decreases in blood pressure and heart rate that are mediated by A(1) receptors in the periphery, with little or no contribution of central adenosine A(1) receptors to those effects. 6 The heart rate increasing effect of adenosine A(2A) agonists appears to be mediated by adenosine A(2A) receptors in the central nervous system. The blood pressure decreasing effect of adenosine A(2A) agonists is most probably mediated in the periphery. C1 NIDA, Preclin Pharmacol Sect, Behav Neurosci Branch, Dept Hlth & Human Serv,NIH,Intramural Res Program, Baltimore, MD 21224 USA. Univ Bonn, Inst Pharmaceut, D-5300 Bonn, Germany. Drug Enforcement Adm, Drug & Chem Evaluat Sect, Off Divers Control, Washington, DC USA. RP Schindler, CW (reprint author), NIDA, Preclin Pharmacol Sect, Behav Neurosci Branch, Dept Hlth & Human Serv,NIH,Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA. EM cschindl@helix.nih.gov RI Ferre, Sergi/K-6115-2014; Muller, Christa/C-7748-2014 OI Ferre, Sergi/0000-0002-1747-1779; Muller, Christa/0000-0002-0013-6624 NR 36 TC 46 Z9 48 U1 1 U2 1 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD MAR PY 2005 VL 144 IS 5 BP 642 EP 650 DI 10.1038/sj.bjp.0706043 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 908ZF UT WOS:000227828000005 PM 15678095 ER PT J AU Wingo, PA Howe, HL Thun, MJ Ballard-Barbash, R Ward, E Brown, ML Sylvester, J Friedell, GH Alley, L Rowland, JH Edwards, BK AF Wingo, PA Howe, HL Thun, MJ Ballard-Barbash, R Ward, E Brown, ML Sylvester, J Friedell, GH Alley, L Rowland, JH Edwards, BK TI A national framework for cancer surveillance in the United States SO CANCER CAUSES & CONTROL LA English DT Review DE cancer surveillance; surveillance; incidence; mortality; survival; cancer control; survivorship; quality of care; quality of life ID QUALITY-OF-LIFE; PATIENT-CARE-EVALUATION; HEALTH INTERVIEW SURVEY; MEDICARE MANAGED CARE; RESULTS SEER PROGRAM; END RESULTS PROGRAM; COLORECTAL-CANCER; BREAST-CANCER; MAMMOGRAPHY FACILITIES; AMERICAN-COLLEGE AB Enhancements to cancer surveillance systems are needed for meeting increased demands for data and for developing effective program planning, evaluation, and research on cancer prevention and control. Representatives from the American Cancer Society, Centers for Disease Control and Prevention, National Cancer Institute, National Cancer Registrars Association, and North American Association of Central Cancer Registries have worked together on the National Coordinating Council for Cancer Surveillance to develop a national framework for cancer surveillance in the United States. The framework addresses a continuum of disease progression from a healthy state to the end of life and includes primary prevention (factors that increase or decrease cancer occurrence in healthy populations), secondary prevention (screening and diagnosis), and tertiary prevention (factors that affect treatment, survival, quality of life, and palliative care). The framework also addresses cross-cutting information needs, including better data to monitor disparities by measures of socioeconomic status, to assess economic costs and benefits of specific interventions for individuals and for society, and to study the relationship between disease and individual biologic factors, social policies, and the environment. Implementation of the framework will require long-term, extensive coordination and cooperation among these major cancer surveillance organizations. C1 Ctr Dis Control & Prevent, Atlanta, GA 30341 USA. N Amer Assoc Cent Canc Registries, Springfield, IL USA. Amer Canc Soc, Atlanta, GA 30329 USA. NCI, Bethesda, MD 20892 USA. Amer Coll Surg, Chicago, IL USA. Univ Kentucky, Lucille P Markey Canc Ctr, Lexington, KY USA. RP Wingo, PA (reprint author), Ctr Dis Control & Prevent, 4770 Buford Highway, Atlanta, GA 30341 USA. EM paw1@cdc.gov NR 135 TC 31 Z9 33 U1 1 U2 3 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD MAR PY 2005 VL 16 IS 2 BP 151 EP 170 DI 10.1007/s10552-004-3487-5 PG 20 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 923AZ UT WOS:000228882300008 PM 15868456 ER PT J AU Cooney, MM Tserng, KY Makar, V McPeak, RJ Ingalls, ST Dowlati, A Overmoyer, B McCrae, K Ksenich, P Lavertu, P Ivy, P Hoppel, CL Remick, S AF Cooney, MM Tserng, KY Makar, V McPeak, RJ Ingalls, ST Dowlati, A Overmoyer, B McCrae, K Ksenich, P Lavertu, P Ivy, P Hoppel, CL Remick, S TI A phase IB clinical and pharmacokinetic study of the angiogenesis inhibitor SU5416 and paclitaxel in recurrent or metastatic carcinoma of the head and neck SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE SU5416; paclitaxel; angiogenesis inhibitor; head and neck cancer; VEGF tyrosine kinase receptor ID ENDOTHELIAL GROWTH-FACTOR; SQUAMOUS-CELL CARCINOMA; TUMOR ANGIOGENESIS; SOLID TUMORS; HUMAN-PLASMA; CISPLATIN; CANCER; EXPRESSION; RECEPTOR; THERAPY AB Purpose: SU5416 is a novel small organic molecule that non-competitively inhibits the phosphorylation of the VEGF tyrosine kinase receptor, Flk-1. This phase IB study was performed to determine the safety, pharmacokinetics, and preliminary efficacy of the combination of SU5416 and paclitaxel in recurrent or metastatic carcinoma of the head and neck. Methods: Enrolled in the study were 12 patients with biopsy-proven recurrent or metastatic carcinoma of the head and neck. Six patients received intravenous SU5416 110 mg/m(2) on days 1, 15, 18, 22 and 25, and paclitaxel 70 mg/m(2) on days 8, 15 and 22. Since two patients experienced a dose-limiting toxicity (DLT) in cohort 1, the next six patients received identical treatment as above except the paclitaxel dose was reduced to 55 mg/ m 2 per week. Results: A total of 42 cycles at two different dose levels were given. In cohort 1 there were two deep venous thromboses that were DLTs. In the second cohort there was a DLT consisting of a transient ischemic attack after receiving SU5416. Most of the other toxicities seen were grade 1 or 2 in nature and consisted of headache, facial flushing, and fatigue. Two patients developed extensive ulcerative cavities at sites of prior radiation. There were no significant changes in the pharmacokinetic parameters of SU5416 given with paclitaxel. Four patients had prolonged freedom from progression of 18, 28, 42, and 60 weeks duration. Conclusions: The combination of SU5416 with paclitaxel had a higher than expected incidence of thromboembolic events and prophylactic anticoagulation should be considered for future trials that combine an angiogenesis inhibitor with cytotoxic chemotherapy. Although the future development of SU5416 as a chemotherapeutic agent is unclear, there was a clinical benefit seen with this combination in 36% of the patients. This trial supports the use of developing antiangiogenic combinations, using molecular targeted agents, in head and neck carcinoma. C1 Univ Hosp Cleveland, Dev Therapeut Program, CASE, Ctr Comprehens Canc, Cleveland, OH 44106 USA. Louis Stokes Cleveland Dept Vet Affairs Med Ctr, Cleveland, OH USA. Case Western Reserve Univ, Dept Nutr, Cleveland, OH 44106 USA. Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA. Case Western Reserve Univ, Dept Pharmacol, Cleveland, OH 44106 USA. Univ Hosp Cleveland, Dept Otolaryngol Head & Neck Surg, Cleveland, OH 44106 USA. NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA. RP Cooney, MM (reprint author), Univ Hosp Cleveland, Dev Therapeut Program, CASE, Ctr Comprehens Canc, 211100 Euclid Ave, Cleveland, OH 44106 USA. EM matthew.cooney@uhhs.com FU NCI NIH HHS [U01 CA62502, P30 CA 43703]; NCRR NIH HHS [M01 RR-00080-36] NR 42 TC 31 Z9 31 U1 0 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD MAR PY 2005 VL 55 IS 3 BP 295 EP 300 DI 10.1007/s00280-004-0871-5 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA 882BG UT WOS:000225912900012 PM 15538570 ER PT J AU Brown, EE Fallin, MD Goedert, JJ Chen, R Whitby, D Foster, CB Lauria, C Alberg, AJ Messina, A Montella, M Rezza, G Vitale, F Chanock, SJ AF Brown, EE Fallin, MD Goedert, JJ Chen, R Whitby, D Foster, CB Lauria, C Alberg, AJ Messina, A Montella, M Rezza, G Vitale, F Chanock, SJ CA Kaposi Sarcoma Genetics Working Gr TI A common genetic variant in FCGR3A-V158F and risk of Kaposi sarcoma herpesvirus infection and classic Kaposi sarcoma SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID NATURAL-KILLER-CELLS; FC-GAMMA RECEPTOR; ACTIVE ANTIRETROVIRAL THERAPY; SEX-DIFFERENCES; AUTOIMMUNE-DISEASE; GENERAL-POPULATION; PERIPHERAL-BLOOD; DNA-SEQUENCES; POLYMORPHISMS; RIIIA AB Associations of FCGR3A among men with HIV/acquired immunodeficiency syndrome suggest that host responses affect the pathogenesis of Kaposi sarcoma herpesvirus (KSHV) infection and risk of acquired immunodeficiency syndrome-associated Kaposi sarcoma. Using DNA from two HIV seronegative case-control populations in Italy, we examined whether the functional FCGR3A-VI58F variant was associated with risk of KSHV infection or classic Kaposi sarcoma (CKS). In population I, we examined FCGR3A variants and risk of KSHV infection in 34 KSHV latent nuclear antigen (LANA)-seropositive and 120 LANA-seronegative adults from Sardinia (52% male; median age, 45 years; range, 31-60), whereas in population II, we examined risk of CKS from 133 CKS cases and 172 KSHV LANA-seropositive controls from Sicily, Rome, and Naples (70% males; median age, 74 years; range, 29-91). FCGR3A variants were determined by direct sequence analysis of a nested PCR of genomic DNA assay using allele-specific primers. KSHV LANA was determined by immunofluorescence assay. Overall, compared with the 158F allele, 158V was overrepresented among controls from both Mediterranean populations (frequency = 0.52 and 0.51, respectively). After controlling for age, 158V homozygous women were at increased risk of KSHV infection and CKS compared with 158F homozygous women [odds ratio (OR), 8.7; 95% confidence interval (95% CI), 0.8-98 and OR, 3.8; 95% Cl, 1.0-14, respectively], whereas homozygous men were at decreased risk (OR, 0.4; 95% Cl, 0.1-2.3 and OR, 0.4; 95% CI, 0.2-0.8, respectively). Significant gene-dose effects were observed among men and women at risk for CKS (P-trend <= 0.05). Our findings suggest that gender differences could possibly modify the effect of FCGR3A on risk of KSHV infection and CKS. Additional studies are required to confirm these relationships and determine their etiologic significance. C1 NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA. Johns Hopkins Univ, Sch Med, Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD USA. NCI, Ctr Adv Technol, NIH, Dept Hlth & Human Serv, Gaithersburg, MD USA. NCI, Viral Epidemiol Sect, AIDS Vaccine Program, Sci Applicat Int Corp, Frederick, MD 21701 USA. Lega Italiana Lotta Contro Tumori, Sez Ragusa, Ragusa, Italy. Univ Catania, Dipartimento Sci Biomed, Catania, Italy. G Pascale Fdn, Natl Canc Inst, Dept Epidemiol, Naples, Italy. Ist Super Sanita, Epidemiol & Biostat Lab, I-00161 Rome, Italy. Univ Palermo, Dipartimento Igiene & Microbiol Giuseppe DAlessan, Palermo, Italy. RP Brown, EE (reprint author), NCI, Viral Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 6120 Execut Blvd,EPS 8003,MSC 7248, Rockville, MD 20852 USA. EM brownbe@mail.nih.gov RI REZZA, GIOVANNI/D-4393-2016 OI REZZA, GIOVANNI/0000-0003-0268-6790 FU NCI NIH HHS [CA-09314-23, N01-CO-12400, N01-CP-91027] NR 50 TC 11 Z9 12 U1 0 U2 0 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 MAR PY 2005 VL 14 IS 3 BP 633 EP 637 DI 10.1158/1055-9965.EPI-04-0598 PG 5 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 905CS UT WOS:000227545900017 PM 15767342 ER PT J AU Kristal, AR King, IB Albanes, D Pollak, MN Stanzyk, FZ Santella, RM Hoque, A AF Kristal, AR King, IB Albanes, D Pollak, MN Stanzyk, FZ Santella, RM Hoque, A TI Centralized blood processing for the Selenium and Vitamin E cancer prevention trial: Effects of delayed processing on carotenoids, tocopherols, insulin-like growth factor-I, insulin-like growth factor binding protein 3, steroid hormones, and lymphocyte viability SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID BARR-VIRUS TRANSFORMATION; CRYOPRESERVED LYMPHOCYTES; PLASMA; STABILITY; RETINOL; STORAGE; ASSAY; SERUM; RISK AB This experiment examined the effects of delays in separation and freezing of whole blood components on analytes of interest in studies of prostate cancer prevention, in order to evaluate the feasibility of centralized processing of blood for the multisite Selenium and Vitamin E Cancer Prevention Trial. Blood from 40 healthy men was subjected to four treatment protocols, allowing the contrast of immediate processing to delays of 32, 72, and 144 hours. At 32 hours, simulating refrigerated storage and overnight shipping, there was a 2.9% decrease (95% confidence interval, 0.7-5.1) in insulin-like growth factor-I (IGF-I) but no significant change in carotenoids, tocopherols, testosterone, 3 alpha-androstanediol glucuronide (AAG), sex hormone-binding globulin (SHBG) or insulin-like growth factor binding protein 3 (IGFBP3). A 144-hour processing delay, simulating weekend blood collection or shipping delay, resulted in significant changes in gamma-tocopherol (-1.5%), IGF-I (-5.7%), IGFBP3 (-2.9%), SHBG (-4.0%), testosterone (+4.7%), and AAG (+5.5%). The rank-order and intraclass correlations between analytes from blood processed immediately and those subjected to delayed processing were 0.96 or higher for carotenoids, tocopherols, AAG, and SHBG, and between 0.87 and 0.95 for IGF-I, IGFBP3, and testosterone. A 32-hour delay decreased lymphocyte viability from 82.5% to 75.0% (P = 0.45), but a 72-hour delay decreased viability to 36.8% (P < 0.001). Overnight shipping and centralized processing is an acceptable approach to blood collection in large multisite trials examining the cancer-related measures proposed in the Selenium and Vitamin E Cancer Prevention Trial. Longer processing delays, however, have small but statistically significant effects on many analytes and substantially decrease lymphocyte viability. C1 Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Canc Prevent Program, Seattle, WA 98109 USA. Fred Hutchinson Canc Res Ctr, Publ Hlth Sci Labs, Canc Prevent Program, Seattle, WA 98109 USA. Univ Texas, MD Anderson Canc Ctr, Dept Clin Canc Prevent, Houston, TX 77030 USA. Jewish Gen Hosp, Dept Oncol, Canc Prevent Res Unit, Montreal, PQ, Canada. McGill Univ, Montreal, PQ, Canada. Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA. Univ So Calif, Keck Sch Med, Dept Obstet & Gynecol, Los Angeles, CA USA. Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Kristal, AR (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Canc Prevent Program, POB 19024,M4-B402, Seattle, WA 98109 USA. EM akristal@fhcrc.org RI Kristal, Alan/A-8779-2008; Perez , Claudio Alejandro/F-8310-2010; Pollak, Michael/G-9094-2011; Albanes, Demetrius/B-9749-2015 OI Perez , Claudio Alejandro/0000-0001-9688-184X; Pollak, Michael/0000-0003-3047-0604; NR 15 TC 21 Z9 21 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 MAR PY 2005 VL 14 IS 3 BP 727 EP 730 DI 10.1158/1055-9965.EPI-04-0596 PG 4 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 905CS UT WOS:000227545900033 PM 15767358 ER PT J AU Terry, PD Umbach, DM Taylor, JA AF Terry, PD Umbach, DM Taylor, JA TI No association between SOD2 or NQ01 genotypes and risk of bladder cancer SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION LA English DT Article ID GENETIC POLYMORPHISMS; SMOKING; MNSOD; NQO1 C1 NIEHS, Epidemiol Branch, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA. NIEHS, Biostat Branch, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA. NIEHS, Mol Carcinogenesis Lab, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA. Emory Univ, Sch Publ Hlth, Dept Epidemiol, Atlanta, GA USA. RP Taylor, JA (reprint author), NIEHS, Epidemiol Branch, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA. EM taytor@niehs.nih.gov NR 9 TC 16 Z9 16 U1 0 U2 0 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 MAR PY 2005 VL 14 IS 3 BP 753 EP 754 DI 10.1158/1055-9965.EPI-04-0574 PG 2 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA 905CS UT WOS:000227545900039 PM 15767364 ER PT J AU Barenboim-Stapleton, L Yang, XZ Tsokos, M Wigginton, JM Padilla-Nash, H Ried, T Thiele, CJ AF Barenboim-Stapleton, L Yang, XZ Tsokos, M Wigginton, JM Padilla-Nash, H Ried, T Thiele, CJ TI Pediatric pancreatoblastoma: histopathologic and cytogenetic characterization of tumor and derived cell line SO CANCER GENETICS AND CYTOGENETICS LA English DT Article ID CHROMOSOMAL-ABERRATIONS; CYTOMETRIC ANALYSIS; DIFFERENTIATION; AMPLIFICATION; HYBRIDIZATION; CARCINOMAS; GENE AB Little is known of the molecular events underlying the genesis of pancreatoblastoma tumors in the pediatric population. Such studies have been limited by the rare nature of the disease, infrequent reports detailing cytogenetic alterations, and the lack of availability of cell lines for biologic studies. We present the isolation of a cell line from a 14-year-old boy with malignant pancreatoblastoma, and its cytogenetic characterization using spectral karyotyping and comparative genomic hybridization (CGH). The cytogenetic analysis revealed an exceedingly complex cytogenetic karyotype, with 33 aberrant chromosomes. CGH revealed multiple regions of chromosomal loss and gain, including a region on 8q gained in adult pancreatic cancers, one that frequently contains the MYC oncogene. (C) 2005 Elsevier Inc. All rights reserved. C1 NCI, Cell & Mol Biol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA. NCI, Genet Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. NCI, Pathol Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA. RP Thiele, CJ (reprint author), NCI, Cell & Mol Biol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA. EM ct47@nih.gov NR 18 TC 9 Z9 12 U1 0 U2 1 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 MAR PY 2005 VL 157 IS 2 BP 109 EP 117 DI 10.1016/j.cancergencyto.2004.05.017 PG 9 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA 903ZF UT WOS:000227463600003 PM 15721631 ER PT J AU Libutti, SK AF Libutti, SK TI Understanding the role of gender in the incidence of thyroid cancer SO CANCER JOURNAL LA English DT Editorial Material ID BENIGN; TUMORS 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 4W-5940, Bethesda, MD 20892 USA. NR 7 TC 9 Z9 10 U1 0 U2 2 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 MAR-APR PY 2005 VL 11 IS 2 BP 104 EP 105 DI 10.1097/00130404-200503000-00003 PG 2 WC Oncology SC Oncology GA 927DN UT WOS:000229172700003 PM 15969983 ER PT J AU Prasad, NB Biankin, AV Fukushima, N Maitra, A Dhara, S Elkahloun, AG Hruban, RH Goggins, N Leach, SD AF Prasad, NB Biankin, AV Fukushima, N Maitra, A Dhara, S Elkahloun, AG Hruban, RH Goggins, N Leach, SD TI Gene expression profiles in pancreatic intraepithelial neoplasia reflect the effects of hedgehog signaling on pancreatic ductal epithelial cells SO CANCER RESEARCH LA English DT Article ID PAPILLARY MUCINOUS NEOPLASMS; TRANSCRIPTION FACTORS; ECTOPIC EXPRESSION; CANCER; ADENOCARCINOMA; DIFFERENTIATION; PROGRESSION; OVEREXPRESSION; CDX2; GUT AB Invasive pancreatic cancer is thought to develop through a series of noninvasive duct lesions known as pancreatic intraepithelial neoplasia (PanIN). We used cDNA microarrays interrogating 15,000 transcripts to identify 49 genes that were differentially expressed in microdissected early PanIN lesions (PanIN-1B/2) compared with microdissected normal duct epithelium. In this analysis, a cluster of extrapancreatic foregut markers, including pepsinogen C, MUC6, KLF4, and TFF1, was found to be up-regulated in PanIN. Up-regulation of these genes was further validated using combinations of real-time reverse transcription-PCR, in situ hybridization, and immunohistochemistry in a total of 150 early PanIN lesions from 81 patients. Identification of these gastrointestinal transcripts in human PanIN prompted assessment of other foregut markers by both semiquantitative and realtime reverse transcription-PCR, revealing similar upregulation of Sox-2, Gastrin, HoxA5, GATA4/5/6, Villin and Forkbead 6 (FoxI1). In contrast to frequent expression of multiple gastric epithelial markers, the intestinal markers intestinal fatty acid binding protein, CDX1 and CDX2 were rarely expressed either in PanIN lesions or in invasive pancreatic cancer. Hedgehog pathway activation induced by transfection of immortalized human pancreatic ductal epithelial cells with Gli1 resulted in up-regulation of the majority of foregut markers seen in early PanIN lesions. These data show frequent up-regulation of foregut markers in early PanIN lesions and suggest that PanIN development may involve Hedgehog-mediated conversion to a gastric epithelial differentiation program. C1 Johns Hopkins Univ, Sch Med, Dept Surg, Baltimore, MD 21287 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21287 USA. Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21287 USA. NIH, Natl Human Genome Res Inst, Bethesda, MD 20892 USA. RP Leach, SD (reprint author), Johns Hopkins Univ, Sch Med, Dept Surg, 600 N Wolfe St,Osler 603, Baltimore, MD 21287 USA. EM stleach@jhmi.edu OI Biankin, Andrew/0000-0002-0362-5597 FU NIDDK NIH HHS [DK-56211] NR 43 TC 149 Z9 156 U1 0 U2 18 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 MAR 1 PY 2005 VL 65 IS 5 BP 1619 EP 1626 DI 10.1158/0008-5472.CAN-04-1413 PG 8 WC Oncology SC Oncology GA 901PO UT WOS:000227294600001 PM 15753353 ER PT J AU Zhang, Q Yang, XM Pins, M Javonovic, B Kuzel, T Kim, SJ Van Parijs, L Greenberg, NM Liu, V Guo, YL Lee, C AF Zhang, Q Yang, XM Pins, M Javonovic, B Kuzel, T Kim, SJ Van Parijs, L Greenberg, NM Liu, V Guo, YL Lee, C TI Adoptive transfer of tumor-reactive transforming growth factor-beta-insensitive CD8(+) T cells: Eradication of autologous mouse prostate cancer SO CANCER RESEARCH LA English DT Article ID TGF-BETA; RECOMBINANT INTERLEUKIN-2; INFILTRATING LYMPHOCYTES; METASTATIC MELANOMA; THERAPY; IMMUNOTHERAPY; MICE; COMBINATION; REGRESSION; CARCINOMA AB Transforming growth factor (TGF)-beta is a potent immunosuppressant. Overproduction of TGF-beta by tumor cells may lead to tumor evasion from the host immune surveillance and tumor progression. The present study was conducted to develop a treatment strategy through adoptive transfer of tumor-reactive TGF-beta-insensitive CD8(+) T cells. The mouse TRAMP-C2 prostate cancer cells produced large amounts of TGF-beta1 and were used as an experimental model. C57BL/6 mice were primed with irradiated TRAMP-C2 cells. CD8(+) T cells were isolated from the spleen of primed animals, were expanded ex vivo, and were rendered TGF-beta insensitive by infecting with a retrovirus containing dominant-negative TGF-beta type II receptor. Results of in vitro cytotoxic assay revealed that these CD8(+) T cells showed a specific and robust tumor-killing activity against TRAMP-C2 cells but were ineffective against an irrelevant tumor line, B16-F10. To determine the in vivo antitumor activity, recipient mice were challenged with a single injection of TRAMP-C2 cells for a period up to 21 days before adoptive transfer of CD8(+) T cells was done. Pulmonary metastasis was either eliminated or significantly reduced in the group receiving adoptive transfer of tumor-reactive TGF-beta-insensitive CD8(+) T cells. Results of immunofluorescent studies showed that only tumor-reactive TGF-beta-insensitive CD8(+) T cells were able to infiltrate into the tumor and mediate apoptosis in tumor cells. Furthermore, transferred tumor-reactive TGF-beta-insensitive CD8(+) T cells were able to persist in tumor-bearing hosts but declined in tumor-free animals. These results suggest that adoptive transfer of tumor-reactive TGF-beta-insensitive CD8(+) T cells may warrant consideration for cancer therapy. C1 Northwestern Univ, Feinberg Sch Med, Dept Urol, Chicago, IL 60611 USA. Northwestern Univ, Feinberg Sch Med, Dept Pathol, Chicago, IL 60611 USA. Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA. Northwestern Univ, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA. NCI, Lab Cell Regulat & Carcinogenesis, Bethesda, MD 20892 USA. MIT, Dept Biol, Cambridge, MA USA. Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA. Peking Univ, Inst Urol, Beijing 100871, Peoples R China. RP Lee, C (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Urol, 303 E Chicago Ave,Tarry 16-733, Chicago, IL 60611 USA. EM c-lee7@northwestern.edu FU NCI NIH HHS [CA107186, CA90036] NR 29 TC 89 Z9 99 U1 1 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 MAR 1 PY 2005 VL 65 IS 5 BP 1761 EP 1769 DI 10.1158/0008-5472.CAN-04-3169 PG 9 WC Oncology SC Oncology GA 901PO UT WOS:000227294600020 PM 15753372 ER PT J AU Charo, J Finkelstein, SE Grewal, N Restifo, NP Robbins, PF Rosenberg, SA AF Charo, J Finkelstein, SE Grewal, N Restifo, NP Robbins, PF Rosenberg, SA TI Bcl-2 overexpression enhances tumor-specific T-cell survival SO CANCER RESEARCH LA English DT Article ID PERIPHERAL-BLOOD LYMPHOCYTES; TRANSGENIC MICE; IMMUNE-SYSTEM; GENE-TRANSFER; INFILTRATING LYMPHOCYTES; GAMMA-CHAIN; MELANOMA; APOPTOSIS; CD8(+); IMMUNOTHERAPY AB Although immunotherapy based on the adoptive transfer of tumor-specific T lymphocytes has been shown to result in dramatic clinical responses in some patients, the relatively low levels of engraftment and persistence of the adoptively transferred cells may limit these responses in many patients. In an attempt to develop strategies for prolonging the survival of adoptively transferred T cells, we have carried out studies in which T cells obtained from healthy donors as well as tumor-specific T cells were transduced with a retrovirus expressing the human Bcl-2 gene. Our results indicate that these transduced T cells overexpress Bcl-2, are resistant to death, and have a survival advantage following interleukin-2 withdrawal compared with control T cells transduced with a retrovirus expressing green fluorescent protein. Tumor-specific T cells overexpressing Bcl-2 maintained their ability to specifically recognize and respond to target cells. Furthermore, we show that adoptive immunotherapy of an established B16 tumor can be significantly enhanced by overexpressing Bcl-2 in melanoma-specific T-cell receptor transgenic T cells. Our data suggest that adoptive immunotherapy approaches to the treatment of cancer patients may be enhanced using Bcl-2-modified tumorreactive T cells. C1 Natl Canc Inst, NIH, Surg Branch, Bethesda, MD 20892 USA. RP Charo, J (reprint author), Natl Canc Inst, NIH, Surg Branch, Bldg 10,Ctr Dr, Bethesda, MD 20892 USA. EM j.charo@mdc-berlin.de RI Restifo, Nicholas/A-5713-2008; Charo, Jehad/K-4433-2013; OI Charo, Jehad/0000-0002-5409-9160; Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z01 BC010763-01, Z01 SC003811-32, Z99 CA999999] NR 46 TC 75 Z9 87 U1 0 U2 2 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 MAR 1 PY 2005 VL 65 IS 5 BP 2001 EP 2008 DI 10.1158/0008-5472.CAN-04-2006 PG 8 WC Oncology SC Oncology GA 901PO UT WOS:000227294600048 PM 15753400 ER PT J AU Khanna, C Hunter, K AF Khanna, C Hunter, K TI Modeling metastasis in vivo SO CARCINOGENESIS LA English DT Review ID TRANSGENIC MOUSE MODEL; LEWIS LUNG-CARCINOMA; LARGE T-ANTIGEN; BREAST-CANCER; NUDE-MICE; PROSTATE-CANCER; MAMMARY-TUMOR; MURINE MODELS; CELL-LINES; SCID MICE AB Metastasis, the spread of a tumor from its primary site to other parts of the body, continues to be the most significant problem in the field of cancer. Patients who present with metastatic disease or those who develop metastases after successful management of the primary tumor carry a universally grave prognosis. To improve treatment outcomes for these patients a broader understanding of the biology of metastases is necessary. The biological complexity that characterizes metastasis requires complex experimental systems for its study. To a large extent the modeling of this biological complexity is only possible using animal models. The following review will summarize the strengths and weaknesses of available in vivo models of metastasis including transplantable syngeneic mouse and human-mouse xenografts, genetically engineered mice and naturally occurring cancers of companion animals (pet dogs and cats). No single metastasis model is sufficient to answer all questions. As such, the selection of the optimal model(s) for each biological or translational question is necessary. C1 NCI, Comparat Oncol Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NCI, Lab Populat Genet, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. RP Khanna, C (reprint author), NCI, Comparat Oncol Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. EM khannac@mail.nih.gov; hunterk@mail.nih.gov NR 126 TC 186 Z9 194 U1 4 U2 17 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD MAR PY 2005 VL 26 IS 3 BP 513 EP 523 DI 10.1093/carcin/bgh261 PG 11 WC Oncology SC Oncology GA 900VM UT WOS:000227242400001 PM 15358632 ER PT J AU Lubet, RA Huebner, K Fong, LYY Altieri, DC Steele, VE Kopelovich, L Kavanaugh, C Juliana, MM Soong, SJ Grubbs, CJ AF Lubet, RA Huebner, K Fong, LYY Altieri, DC Steele, VE Kopelovich, L Kavanaugh, C Juliana, MM Soong, SJ Grubbs, CJ TI 4-Hydroxybutyl(butyl)nitrosamine-induced urinary bladder cancers in mice: characterization of FHIT and survivin expression and chemopreventive effects of indomethacin SO CARCINOGENESIS LA English DT Article ID CYCLOOXYGENASE-2 INHIBITOR; GENE-EXPRESSION; DEFICIENT MICE; P53 MUTATIONS; LUNG-CANCER; N-BUTYL-N-(4-HYDROXYBUTYL)NITROSAMINE; CARCINOMAS; CELECOXIB; RATS; CARCINOGENESIS AB The administration of 4-hydroxybutyl(butyl)nitrosamine (OH-BBN) to male B6D2F1 mice yielded a high incidence of large palpable urinary bladder cancers. Since prior studies demonstrated chemopreventive effects of non-steroidal anti-inflammatory drugs (NSAIDs), we further explored the efficacy of the NSAID indomethacin using different treatment regimens. OH-BBN was administered twice per week for 12 weeks (the first week of treatment was designated week 1). In Experiment I continual indomethacin treatment (20 mg/kg diet) was initiated either prior to (week -1) or following (week 13) OH-BBN dosing. Palpable bladder masses (subsequently diagnosed as cancers) developed in 32% of carcinogen-treated only mice by 32 weeks, while mice administered indomethacin either prior to or after OH-BBN developed palpable masses in 3 and 6% of the animals, respectively. In Experiment II mice were treated with indomethacin beginning 1 week after OH-BBN for either 12 weeks (limited treatment, weeks 13-24) or for 30 weeks (weeks 13-42). Continual treatment resulted in a 77% decrease in palpable bladder masses and an 82% decrease in all cancers (palpable and microscopic), while limited treatment decreased palpable masses by 48% but failed to decrease the number of bladder cancers (palpable plus microscopic). In Experiment III OH-BBN-treated mice were followed for 61 weeks. Palpable masses developed in 66% of control mice, while 26% of mice treated with indomethacin continually from 1 week after OH-BBN (weeks 13-61) developed palpable masses. A separate group in this study treated with indomethacin beginning when 5% of the mice had palpable bladder masses continued to develop new masses for an additional 4 weeks. By 6 weeks after beginning indomethacin treatment, however, these animals showed a profound decrease in the development of additional cancers. The expressions of FHIT and survivin in normal urinary bladder epithelium and in bladder cancers were determined by immunohistochemical analysis. FHIT was expressed at high levels in normal epithelium, but was minimally expressed in cancers, and even showed decreased expression in papillomas. The anti-apoptotic protein survivin was not expressed in normal bladder epithelium, but was variably expressed in cancers. FHIT and survivin expressions were similar in cancers from indomethacin-treated and non-treated mice. C1 NCI, Div Canc Prevent, Bethesda, MD 20852 USA. Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA. Univ Massachusetts, Sch Med, Ctr Canc, Worcester, MA USA. Univ Alabama, Dept Surg, Birmingham, AL 35294 USA. Univ Alabama, Dept Genet & Med, Birmingham, AL 35294 USA. RP Lubet, RA (reprint author), NCI, Div Canc Prevent, Execut Plaza N,Suite 2110,6130 Execut Blvd, Bethesda, MD 20852 USA. EM rl57@nih.gov FU NCI NIH HHS [R01 CA96131] NR 28 TC 20 Z9 20 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD MAR PY 2005 VL 26 IS 3 BP 571 EP 578 DI 10.1093/carcin/bgh352 PG 8 WC Oncology SC Oncology GA 900VM UT WOS:000227242400008 PM 15591090 ER PT J AU Mechanic, LE Marrogi, AJ Welsh, JA Bowman, ED Khan, MA Enewold, L Zheng, YL Chanock, S Shields, PG Harris, CC AF Mechanic, LE Marrogi, AJ Welsh, JA Bowman, ED Khan, MA Enewold, L Zheng, YL Chanock, S Shields, PG Harris, CC TI Polymorphisms in XPD and TP53 and mutation in human lung cancer SO CARCINOGENESIS LA English DT Article ID REPAIR GENE XPD; P53 CODON-72 POLYMORPHISM; EXCISION-REPAIR; LYS751GLN POLYMORPHISM; CHINESE POPULATION; SEQUENCE-ANALYSIS; VARIANT ALLELES; DNA-DAMAGE; RISK; ASSOCIATION AB The pattern of somatic mutations in TP53 is distinct for particular cancers and carcinogenic exposures, providing clues to disease etiology, e.g. G:C-->T:A mutations in TP53 are more frequently observed in smoking-associated lung cancers. In order to investigate possible causes and mechanisms of lung cancer susceptibility differences, the TP53 gene was sequenced in a case-only study of lung cancers (206 men and 103 women). Our primary hypothesis was that the TP53 mutation spectrum is influenced by polymorphisms in genes involved in DNA repair and apoptosis. We observed a TP53 mutation frequency in exons 5-8 of 25%. Functional polymorphisms in XPD (Asp312Asn, rs1799793 and Lys751Gln, rs1052559), a protein required for nucleotide excision repair and with roles in p53-mediated apoptosis, were modestly associated with G:C-->T:A mutations in TP53 in lung tumors [Asp/Asn312 + Asn/Asn312 and/or Lys/Gln751 + Gln/Gln751 versus Asp/Asp312 + Lys/Lys751; odds ratio (OR) 2.73, 95% confidence interval (CI) 0.98-7.61], consistent with the role of this protein in repair of bulky carcinogen-DNA adducts. In addition, a TP53 polymorphism (Arg72Pro, rs1042522) with a known role in the efficiency of apoptosis was also associated with the presence of a TP53 mutation (Pro/Arg72 or Pro/Pro72 versus Arg/Arg72; OR 2.25, 95% CI 1.21-4.17) or a G:C-->T:A mutation in TP53 (Pro/Arg72 or Pro/Pro72 versus Arg/Arg72; OR 2.42, 95% CI 0.97-6.04). An interaction between the XPD variant alleles (Asn312 and Gln751) and the TP53 Pro72 allele was observed for TP53 mutations (any TP53 mutation P(int) = 0.027, G:C-->T:A TP53 mutation P(int) = 0.041). The statistical interaction observed in our study is consistent with the observed biological interaction for XPD and p53 in nucleotide excision repair and apoptosis. In conclusion, differences in TP53 mutation spectra in lung tumors are associated with several genetic factors and may reflect differences in lung cancer susceptibility and carcinogenesis. C1 NCI, Human Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA. USUHS, Lab Carcinogenesis & Biomarkers, CBCP IRC, Bethesda, MD USA. Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA. NCI, Ctr Adv Technol, Gaithersburg, MD 20892 USA. RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, Ctr Canc Res, 37 Convent Dr, Bethesda, MD 20892 USA. EM curtis_harris@nih.gov RI Shields, Peter/I-1644-2012 NR 66 TC 45 Z9 51 U1 0 U2 6 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD MAR PY 2005 VL 26 IS 3 BP 597 EP 604 DI 10.1093/carcin/bgh344 PG 8 WC Oncology SC Oncology GA 900VM UT WOS:000227242400011 PM 15564288 ER PT J AU Fiala, ES Sohn, OS Wang, CX Seibert, E Tsurutani, J Dennis, PA El-Bayoumy, K Sodum, RS Desai, D Reinhardt, J Aliaga, C AF Fiala, ES Sohn, OS Wang, CX Seibert, E Tsurutani, J Dennis, PA El-Bayoumy, K Sodum, RS Desai, D Reinhardt, J Aliaga, C TI Induction of preneoplastic lung lesions in guinea pigs by cigarette smoke inhalation and their exacerbation by high dietary levels of vitamins C and E SO CARCINOGENESIS LA English DT Article ID SYRIAN GOLDEN-HAMSTERS; CELL NUCLEAR ANTIGEN; BETA-CAROTENE; ASCORBIC-ACID; BRONCHIAL EPITHELIUM; OXIDATION-PRODUCTS; EXPOSED FERRETS; CANCER-CELLS; IN-VIVO; PLASMA AB The development of effective chemopreventive agents against cigarette smoke-induced lung cancer could be greatly facilitated by the availability of suitable laboratory animal models. Here we report that male Hartley guinea pigs treated with cigarette smoke by inhalation twice a day for 28 days developed preneoplastic lung lesions, including bronchial hyperplasia, dysplasia and squamous metaplasia, analogous to those found in human smokers. The lesions were accompanied by increased expression of proliferating cell nuclear antigen and activation of the serine/threonine kinase Akt in the bronchial epithelium. In contrast, no lung lesions were found in guinea pigs ('sham smoked') that were submitted to identical procedures but without cigarettes. Compared with a diet low in vitamin C (50 p.p.m.) and vitamin E (15 p.p.m.), a diet high in vitamin C (4000 p.p.m.) and vitamin E (40 p.p.m.) significantly increased the incidence of these lesions. The inclusion of 1,4-phenylenebis(methylene)selenocyanate (p-XSC), a synthetic chemopreventive organoselenium compound, in the high vitamin C-high vitamin E diet at a level of 15 p.p.m. as selenium appeared to decrease the lesion incidence. Administration of (-)-epigallocatechin gallate, a powerful green tea polyphenolic antioxidant, at 560 p.p.m. in the drinking water had no effect. As in human smokers, levels of ascorbate in blood plasma, lung, liver and the adrenal glands were significantly decreased by cigarette smoke inhalation. These results identify a relevant in vivo laboratory model of cigarette smoke-induced lung cancer, suggest that p-XSC may have activity as a chemopreventive agent against cigarette smoke-induced lung lesions and provide additional evidence that very high dietary levels of certain antioxidants can have co-carcinogenic activity in cigarette smoke-induced lung cancer. C1 Inst Canc Prevent, Valhalla, NY 10595 USA. NCI, Canc Therapeut Branch, Ctr Canc Res, Bethesda, MD 20892 USA. RP Fiala, ES (reprint author), Inst Canc Prevent, Valhalla, NY 10595 USA. EM efiala@att.net FU NCI NIH HHS [P01 CA 70972] NR 47 TC 24 Z9 27 U1 0 U2 1 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD MAR PY 2005 VL 26 IS 3 BP 605 EP 612 DI 10.1093/carcin/bgh341 PG 8 WC Oncology SC Oncology GA 900VM UT WOS:000227242400012 PM 15579485 ER PT J AU Gunter, MJ Probst-Hensch, NM Cortessis, VK Kulldorff, M Haile, RW Sinha, R AF Gunter, MJ Probst-Hensch, NM Cortessis, VK Kulldorff, M Haile, RW Sinha, R TI Meat intake, cooking-related mutagens and risk of colorectal adenoma in a sigmoidoscopy-based case-control study SO CARCINOGENESIS LA English DT Article ID HETEROCYCLIC AMINE CONTENT; VARYING DEGREES; N-NITROSATION; WELL-DONE; RED MEAT; CANCER; CONSUMPTION; DIET; CARCINOGEN; EXPOSURE AB Reported habits of red meat consumption, particularly red meat that has been cooked to the degree termed 'well-done', is a positive risk factor for colorectal cancer. Under high, pyrolytic temperatures, heterocyclic amines (HCA) and benzo[a]pyrene (BP) molecules can form inside and on the surface of red meat, respectively. These compounds are precursors that are metabolically converted to compounds known to act as mutagens and carcinogens in animal models, yet their role in human colorectal carcinogenesis remains to be clarified. We investigated whether intake of these compounds is associated with risk of colorectal adenoma in the context of a polyp-screening study conducted in Southern California. Using a database of individual HCAs and BP in meats of various types and subjected to specified methods and degrees of cooking, we estimated nanogram consumption of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, 2-amino-3,4,8-trimethylimidazo[4,5-f] quinoxaline, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline and benzo[a]pyrene (BP). We observed a 6% increased risk of large (>1 cm) adenoma per 10 ng/day consumption of BP [OR = 1.06 (95% CI, 1.00-1.12), P (trend) = 0.04]. A major source of BP is red meat exposed to a naked flame, as occurs during the barbecuing process. Consistent with this finding an incremental increase of 10 g of barbecued red meat per day was associated with a 29% increased risk of large adenoma [OR = 1.29 (95% CI, 1.02-1.63), P (trend) = 0.04]. Individuals in the top quintile of barbecued red meat intake were at increased risk of large adenoma [OR = 1.90 (95% CI, 1.04-3.45)], compared with never consuming barbecued red meat. The consumption of oven-broiled red meat was inversely related to adenoma risk compared with non-consumers [OR = 0.49 (95% CI, 0.28-0.85)]. We did not identify any association with consumption of individual HCAs and colorectal adenoma risk. These results support the hypothesis that BP contributes to colorectal carcinogenesis. C1 NCI, Div Canc Epidemiol & Genet, NIH, EPS, Rockville, MD 20852 USA. Univ Zurich, Canc Registry, Dept Mol Epidemiol, CH-8091 Zurich, Switzerland. Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA. Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, Boston, MA 02215 USA. Harvard Pilgrim Hlth Care, Boston, MA 02215 USA. RP Gunter, MJ (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, EPS, 6120 Execut Blvd, Rockville, MD 20852 USA. EM gunterm@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 22 TC 63 Z9 65 U1 1 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD MAR PY 2005 VL 26 IS 3 BP 637 EP 642 DI 10.1093/carcin/bgh350 PG 6 WC Oncology SC Oncology GA 900VM UT WOS:000227242400016 PM 15579480 ER PT J AU Iida, M Anna, CH Holliday, WM Collins, JB Cunningham, ML Sills, RC Devereux, TR AF Iida, M Anna, CH Holliday, WM Collins, JB Cunningham, ML Sills, RC Devereux, TR TI Unique patterns of gene expression changes in liver after treatment of mice for 2 weeks with different known carcinogens and non-carcinogens SO CARCINOGENESIS LA English DT Article ID GLAND CANCER-CELL; BETA STIMULATED CLONE-22; B6C3F1 MICE; IN-VIVO; APOPTOSIS; OXAZEPAM; ACTIVATION; CATENIN; PROTEIN; GROWTH AB Previously we demonstrated that the mouse liver tumor response to the non-genotoxic carcinogens oxazepam and Wyeth-14,643 involved more differences than similarities in changes in early gene expression. In this study we used quantitative real-time PCR and oligonucleotide microarray analysis to identify genes that were up- or down-regulated in mouse liver early after treatment with different known carcinogens, including oxazepam (125 and 2500 p.p.m.), o-nitrotoluene (1250 and 5000 p.p.m.) and methyleugenol (75 mg/kg/day), or the non-carcinogens p-nitrotoluene (5000 p.p.m.), eugenol (75 mg/kg/day) and acetaminophen (6000 p.p.m.). Starting at 6 weeks of age, mice were treated with the different compounds for 2 weeks in the diet, at which time the livers were collected. First, expression of 12 genes found previously to be altered in liver after 2 weeks treatment with oxazepam and/or Wyeth-14,643 was examined in livers from the various chemical treatment groups. These gene expression changes were confirmed for the livers from the oxazepam-treated mice in the present study, but were not good early markers for all the carcinogens in this study. In addition, expression of 20 842 genes was assessed by oligonucleotide microarray [n = 4 livers/group, 2 hybridizations/liver (with fluor reversals)] and the results were analyzed using the Rosetta Resolver System and GeneSpring software. The analyses revealed that several cancer-related genes, including Fhit, Wwox, Tsc-22 and Gadd45b, were induced or repressed in unique patterns for specific carcinogens and not altered by the non-carcinogens. The data indicate that even if the tumor response, including molecular alterations, is similar, such as for oxazepam and methyleugenol, early gene expression changes appear to be carcinogen specific and seem to involve apoptosis and cell cycle-related genes. C1 NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Natl Ctr Toxicogen, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. NIEHS, Lab Expt Pathol, NIH, Res Triangle Pk, NC 27709 USA. RP Devereux, TR (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, Mail Drop D4-04,POB 12233, Res Triangle Pk, NC 27709 USA. EM devereux@niehs.nih.gov NR 37 TC 33 Z9 36 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD MAR PY 2005 VL 26 IS 3 BP 689 EP 699 DI 10.1093/carcin/bgi005 PG 11 WC Oncology SC Oncology GA 900VM UT WOS:000227242400023 PM 15618236 ER PT J AU Dick, AJ Raman, VK Raval, AN Guttman, MA Thompson, RB Ozturk, C Peters, DC Stine, AM Wright, VJ Schenke, WH Lederman, RJ AF Dick, AJ Raman, VK Raval, AN Guttman, MA Thompson, RB Ozturk, C Peters, DC Stine, AM Wright, VJ Schenke, WH Lederman, RJ TI Invasive human magnetic resonance imaging: Feasibility during revascularization in a combined XMR suite SO CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS LA English DT Article DE interventional magnetic resonance imaging; angioplasty; invasive imaging; catheterization; peripheral artery disease ID IN-VIVO; CARDIAC-CATHETERIZATION; INTERVENTIONAL MRI; RF COIL; RESOLUTION; PLACEMENT; GUIDANCE; CLOSURE; DEVICE; SWINE AB We tested the feasibility and safety of invasive magnetic resonance imaging (MRI) during peripheral angioplasty. Real-time MRI can image soft tissue and may potentially guide therapeutic procedures without ionizing radiation or nephrotoxic contrast. MRI-guided diagnostic catheterization has been described recently, but safe and conspicuous catheter devices are not widely available. An active guidewire, which serves as an MRI receiver antenna, might be useful to guide catheterization or even to image atheroma. We describe a combined interventional suite offering both X-ray fluoroscopy and real-time MRI. We used a 0.030" active guidewire receiver coil for invasive MRI after X-ray lesion traversal in patients undergoing percutaneous iliofemoral artery revascularization. Intravascular MRI was compared with noninvasive MRI, X-ray angiography, and intravascular ultrasound (IVUS). Seven eligible patients consented to participate, but three were excluded because of lengthy revascularization procedures. Four remaining patients safely underwent combined X-ray fluoroscopy and real-time magnetic resonance imaging (XMR) transport, continuous monitoring, and all imaging modalities. There was no device dislodgment, contamination or evidence of heating. The intravascular MRI coil was well visualized except at the tip, but did not provide superior mural imaging compared with IVUS. Therefore, because an adequate safety and workflow experience was obtained, enrollment was terminated after only four subjects. Invasive MRI is feasible and apparently safe during peripheral angioplasty. Patients can safely be transported and monitored in an XMR interventional suite. An active quarter-wavelength guidewire coil does not provide superior imaging compared with IVUS, but provides satisfactory guidewire visualization. These tools may prove useful for advanced therapeutic procedures in the future. C1 NHLBI, Div Intramural Res, Cardiovasc Branch, NIH, Bethesda, MD 20892 USA. NHLBI, Cardiac Energet Lab, Bethesda, MD 20892 USA. RP Lederman, RJ (reprint author), NHLBI, Div Intramural Res, Cardiovasc Branch, NIH, Bldg 10,Room 2c713,MSC 1538, Bethesda, MD 20892 USA. EM lederman@nih.gov RI Thompson, Richard/E-9821-2011; Ozturk, Cengizhan/A-6177-2016; OI Ozturk, Cengizhan/0000-0002-6966-0774; lederman, robert/0000-0003-1202-6673 FU NHLBI NIH HHS [Z01 HL005062-03, HL005062-01, Z01 HL005062] NR 24 TC 38 Z9 38 U1 0 U2 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1522-1946 J9 CATHETER CARDIO INTE JI Catheter. Cardiovasc. Interv. PD MAR PY 2005 VL 64 IS 3 BP 265 EP 274 DI 10.1002/ccd.20302 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 902SC UT WOS:000227375800001 PM 15736247 ER PT J AU Gershengorn, MC Geras-Raaka, E Hardikar, AA Raaka, BM AF Gershengorn, MC Geras-Raaka, E Hardikar, AA Raaka, BM TI Are better islet cell precursors generated by epithelial-to-mesenchymal transition? SO CELL CYCLE LA English DT Article DE stem cells; beta cells; insulin; endocrine pancrease; islet transplantation; diabetes mellitus ID EMBRYONIC STEM-CELLS; BONE-MARROW; BETA-CELLS; DIFFERENTIATION; PANCREAS; TISSUES AB To generate cells for replacement therapy for patients with diabetes, preclinical research is being conducted to establish in vitro systems that generate large numbers of human islets of Langerhans ( or insulin-expressing beta cells). Based on the concept that undifferentiated precursor cells can expand exponentially and then be induced to differentiate into mature cells, researchers are using islet ( or beta cell) precursor cells for this purpose. The cells being used include embryonic stem cells, bone marrow-derived stem cells, pancreatic stem cells and cells derived from epithelial-to-mesenchymal transition of insulin-expressing cells. Transdifferentiation of another epithelial cell type is being studied also. Herein, we review our data of epithelial-to-mesenchymal-to-epithelial transition of human insulin-expressing cells and present our hypothesis that precursor cells obtained from insulin-expressing cells by epithelial-to-mesenchymal transition, after expansion, more easily differentiate into insulin-expressing cells ( by mesenchymal-to-epithelial transition) than other precursor cells or by transdifferentiation. C1 NIDDK, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Gershengorn, MC (reprint author), NIDDK, Clin Endocrinol Branch, NIH, 50 South Dr,Room 4134, Bethesda, MD 20892 USA. EM marving@intra.niddk.nih.gov NR 17 TC 22 Z9 22 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 MAR PY 2005 VL 4 IS 3 BP 380 EP 382 DI 10.4161/cc.4.3.1538 PG 3 WC Cell Biology SC Cell Biology GA 932FB UT WOS:000229538500010 PM 15711124 ER PT J AU Amano, T Kwak, O Fu, LZ Marshak, A Shi, YB AF Amano, T Kwak, O Fu, LZ Marshak, A Shi, YB TI The matrix metalloproteinase stromelysin-3 cleaves laminin receptor at two distinct sites between the transmembrane domain and laminin binding sequence within the extracellular domain SO CELL RESEARCH LA English DT Article DE stromelysin-3; laminin receptor; matrix metalloproteinase; extracellular matrix; Xenopus laevis; cell surface substrate ID THYROID-HORMONE REGULATION; XENOPUS-LAEVIS; BREAST-CANCER; PROGNOSTIC-SIGNIFICANCE; MOUSE STROMELYSIN-3; FROG METAMORPHOSIS; EXPRESSION PATTERN; RESPONSE GENES; MESSENGER-RNA; GELATINASE-A AB The matrix metalloproteinase (MMP) stromelysin-3 (ST3) has long been implicated to play an important role in extracellular matrix (ECM) remodeling and cell fate determination during normal and pathological processes. However, like other MMPs, the molecular basis of ST3 function in vivo remains unclear due to the lack of information on its physiological substrates. Furthermore, ST3 has only weak activities toward all tested ECM proteins. Using thyroid hormone-dependent Xenopus laevis metamorphosis as a model, we demonstrated previously that ST3 is important for apoptosis and tissue morphogenesis during intestinal remodeling. Here, we used yeast two-hybrid screen with mRNAs from metamorphosing tadpoles to identify potential substrate of ST3 during development. We thus isolated the 37 kd laminin receptor precursor (LR). We showed that LR binds to ST3 in vitro and can be cleaved by ST3 at two sites, distinct from where other MMPs cleave. Through peptide sequencing, we determined that the two cleavage sites are in the extracellular domain between the transmembrane domain and laminin binding sequence. Furthermore, we demonstrated that these cleavage sites are conserved in human LR. These results together with high levels of human LR and ST3 expression in carcinomas suggest that LR is a likely in vivo substrate of ST3 and that its cleavage by ST3 may alter cell-extracellular matrix interaction, thus, playing a role in mediating the effects of ST3 on cell fate and behavior observed during development and pathogenesis. C1 NICHHD, Lab Gene Regualt & Dev, NIH, Bethesda, MD 20892 USA. RP Shi, YB (reprint author), NICHHD, Lab Gene Regualt & Dev, NIH, Bethesda, MD 20892 USA. EM Shi@helix.nih.gov NR 45 TC 24 Z9 26 U1 0 U2 1 PU INST BIOCHEMISTRY & CELL BIOLOGY PI SHANGHAI PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA SN 1001-0602 J9 CELL RES JI Cell Res. PD MAR PY 2005 VL 15 IS 3 BP 150 EP 159 DI 10.1038/sj.cr.7290280 PG 10 WC Cell Biology SC Cell Biology GA 914XG UT WOS:000228260800002 PM 15780176 ER PT J AU Kunick, C Zeng, ZH Gussio, R Zaharevitz, D Leost, M Totzke, F Schachtele, C Kubbutat, MHG Meijer, L Lemcke, T AF Kunick, C Zeng, ZH Gussio, R Zaharevitz, D Leost, M Totzke, F Schachtele, C Kubbutat, MHG Meijer, L Lemcke, T TI Structure-aided optimization of kinase inhibitors derived from alsterpaullone SO CHEMBIOCHEM LA English DT Article DE enzymes; inhibitors; lactams; molecular modeling; paullones; proteins ID CYCLIN-DEPENDENT KINASES; GLYCOGEN-SYNTHASE KINASE-3-BETA; STRUCTURE-BASED DESIGN; ALZHEIMERS-DISEASE; PROTEIN-KINASES; FORCE-FIELD; PAULLONES; PHOSPHORYLATION; GSK-3-BETA; TARGETS AB In order to perform computer-aided design of novel alsterpaullone derivatives, the vicinity of the entrance to the ATP-binding site was scanned for areas that could be useful as anchoring points for additional protein-ligand interactions. Based on the alignment of alsterpaullone in a CDK1/cyclin B homology model, substituents were attached to the 2-position of the parent scaffold to enable contacts within the identified areas. Synthesis of the designed structures revealed three derivatives (3-5) with kinase-inhibitory activity similar to alsterpaullone. The novel 2-cyanoethylalsterpaullone (7) proved to be the most potent paullone described so for, exhibiting inhibitory concentrations for CDK1/ cyclin B and GSK-3 beta in the picomolar range. C1 Tech Univ Carolo Wilhelmina Braunschweig, Inst Pharmaceut Chem, D-38106 Braunschweig, Germany. Univ Hamburg, Inst Pharm, D-20146 Hamburg, Germany. NCI, Div Canc Treatment & Diagnosis, Dev Therapeut Program, Rockville, MD 20852 USA. CNRS, Biol Stn, F-29682 Roscoff, France. ProQinase GmbH, D-79106 Freiburg, Germany. RP Kunick, C (reprint author), Tech Univ Carolo Wilhelmina Braunschweig, Inst Pharmaceut Chem, Beethovenstr 55, D-38106 Braunschweig, Germany. EM c.kunick@tu-bs.de NR 34 TC 33 Z9 34 U1 0 U2 2 PU WILEY-V C H VERLAG GMBH PI WEINHEIM PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY SN 1439-4227 J9 CHEMBIOCHEM JI Chembiochem PD MAR PY 2005 VL 6 IS 3 BP 541 EP 549 DI 10.1002/cbic.200400099 PG 9 WC Biochemistry & Molecular Biology; Chemistry, Medicinal SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA 906JJ UT WOS:000227636700012 PM 15696597 ER PT J AU Dorner, T Lipsky, PE AF Dorner, T Lipsky, PE TI Molecular basis of immunoglobulin variable region gene usage in systemic autoimmunity SO CLINICAL AND EXPERIMENTAL MEDICINE LA English DT Article DE IgV gene usage; autoimmunity; autoantibody; systemic lupus erythematosus; Sjogren's syndrome ID ANTI-DNA ANTIBODIES; B-CELL REPERTOIRE; V-H GENES; ENHANCED MUTATIONAL ACTIVITY; PRIMARY SJOGRENS-SYNDROME; LIGHT-CHAIN PAIRINGS; J-LAMBDA REPERTOIRE; LUPUS-ERYTHEMATOSUS; PERIPHERAL-BLOOD; SOMATIC MUTATION AB This review focuses on the immunoglobulin variable region (IgV) chain gene usage in patients with systemic autoimmune diseases, with particular emphasis on systemic lupus erythematosus (SLE), a condition known to be associated with the production of a number of characteristic autoantibodies as an abnormality. The IgV repertoire is shaped by a variety of molecular and selective influences that are difficult to distinguish. Studies of IgV gene rearrangement by PCR of individual B cells permitted insight in the differential impact of these processes, including somatic hypermutation and indications of receptor editing/revision. Although the majority of current data indicate that there is no major molecular abnormality in V(D)J recombination in SLE patients, abnormalities in subsequent events, such as the degree of receptor editing and somatic hypermutation, and positive and negative selection fundamentally alter the composition of the peripheral B-cell repertoire. Identification of the mechanisms that influence the IgV gene and B-cell repertoire may allow new therapeutic approaches in autoimmunity. C1 Charite Univ Med, Dept Transfus Med, D-10098 Berlin, Germany. NIAMSD, NIH, Bethesda, MD 20892 USA. RP Dorner, T (reprint author), Charite Univ Med, Dept Transfus Med, Schumannstr 20-21, D-10098 Berlin, Germany. EM thomas.doerner@charite.de FU NIAID NIH HHS [AI 31229] NR 97 TC 23 Z9 23 U1 0 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 1591-8890 J9 CLIN EXP MED JI Clin. Exper. Med. PD MAR PY 2005 VL 4 IS 4 BP 159 EP 169 DI 10.1007/s10238-004-0051-2 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 903TT UT WOS:000227449200001 PM 15750762 ER PT J AU Petridou, E Mantzoros, CS Belechri, M Skalkidou, A Dessypris, N Papathoma, E Salvanos, H Lee, JH Kedikoglou, S Chrousos, G Trichopoulos, D AF Petridou, E Mantzoros, CS Belechri, M Skalkidou, A Dessypris, N Papathoma, E Salvanos, H Lee, JH Kedikoglou, S Chrousos, G Trichopoulos, D TI Neonatal leptin levels are strongly associated with female gender, birth length, IGF-I levels and formula feeding SO CLINICAL ENDOCRINOLOGY LA English DT Article ID GROWTH-FACTOR-I; ADIPOSE-SPECIFIC PROTEIN; CORD-BLOOD; SERUM LEPTIN; INSULIN-RESISTANCE; PLASMA LEPTIN; OBESE GENE; DIABETIC PREGNANCY; ADIPONECTIN LEVELS; BINDING-PROTEINS AB Objective To investigate predictors of circulating leptin in healthy full-term newborns and to explore the relationship with anthropometric variables, serum levels of adiponectin and the major components of the IGF system at birth. To explore whether leptin levels are regulated by breastfeeding vs. formula feeding. Design Observational cross-sectional study. Patients Three hundred and nineteen healthy full-term newborns delivered during 1999 in Athens, Greece. Measurements Anthropometric measurements, formula feeding information and blood samples were obtained. Leptin and adiponectin determinations were performed using a radioimmunoassay (RIA). Results Multivariate regression analyses showed that leptin levels were positively associated with female gender, newborn length, ponderal index and IGF-I levels, but not with adiponectin levels. Newborns who were fed exclusively with milk formulas had more than twice the leptin levels of those who were exclusively breastfed. Conclusions Leptin levels are positively related to female gender and anthropometric characteristics of neonates but, contrary to studies in adults, are not correlated with adiponectin levels. We also found evidence that formula feeding imparts a considerable increase in leptin levels in newborns. C1 Univ Athens, Sch Med, Dept Hyg & Epidemiol, GR-11527 Athens, Greece. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med,Dept Internal Med, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA. Alexandra Matern Hosp, Dept Neonatol, Athens, Greece. Elenas Venizelou Matern, Dept Neonatol, Athens, Greece. Univ Athens, Sch Med, Ag Sofia Childrens Hosp, Dept Paediat 1, GR-11527 Athens, Greece. NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Petridou, E (reprint author), Univ Athens, Sch Med, Dept Hyg & Epidemiol, 75 M Asias Str,Goudi,POB, GR-11527 Athens, Greece. EM epetrid@med.uoa.gr FU NIDDK NIH HHS [5T32DK07516-18, DK 58785] NR 66 TC 34 Z9 36 U1 0 U2 1 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0300-0664 J9 CLIN ENDOCRINOL JI Clin. Endocrinol. PD MAR PY 2005 VL 62 IS 3 BP 366 EP 371 DI 10.1111/j.1365-2265.2005.02225.x PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 900PF UT WOS:000227226100016 PM 15730421 ER PT J AU Trivers, KF De Roos, AJ Gammon, MD Vaughan, TL Risch, HA Olshan, AF Schoenberg, JB Mayne, ST Dubrow, R Stanford, JL Abrahamson, P Rotterdam, H West, AB Fraumeni, JF Chow, WH AF Trivers, KF De Roos, AJ Gammon, MD Vaughan, TL Risch, HA Olshan, AF Schoenberg, JB Mayne, ST Dubrow, R Stanford, JL Abrahamson, P Rotterdam, H West, AB Fraumeni, JF Chow, WH TI Demographic and lifestyle predictors of survival in patients with esophageal or gastric cancers SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY LA English DT Article ID BODY-MASS INDEX; SOCIOECONOMIC-STATUS; RISK; CARDIA; ADENOCARCINOMAS; CARCINOMA AB Background & Aims: Risk factors for subtypes of esophageal and gastric cancer recently have been identified, but their effect on survival is unknown. Methods: Incident cases (n = 1142) from a population-based case-control study were followed-up from diagnosis (19931995) until 2000. Cox regression models were used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for esophageal and gastric cancer in relation to prediagnostic factors. Results: Relative to distant stage, esophageal adenocarcinoma (EA) patients with localized disease had a decreased risk for death (HR, .22; 95% Cl, .15-31), followed by those with regional spread (HR,.32; 95% Cl, .23-.45). Similar patterns were seen for the other tumor types. Except for other (non-cardia) gastric adenocarcinomas (OGA), higher household income ( >= $15,000/y vs. <$15,000/y) was associated with a 33%-38% decrease in risk for death. Prediagnosis body mass index (BMI) between 25 and 29.9 kg/m(2) was associated with longer survival for EA and OGA patients (EA: HR, .67; 95% Cl, .51-.88) vs. BMI <25 kg/m(2). Women with esophageal squamous cell carcinoma (ES) and OGA experienced longer survival compared with men. Age, education, cigarette smoking, alcohol intake, gastroesophageal reflux disease, and nonsteroidal anti-inflammatory drug use did not consistently predict survival. Conclusions: Predictors of lengthened esophageal and gastric cancer survival included higher income (except in OGA), overweight (among EA and OGA patients), and female sex (among ES and OGA patients). C1 Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA. NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA. Yale Univ, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA. New Jersey State Dept Hlth & Senior Serv, Appl Canc Epidemiol Program, Trenton, NJ USA. Columbia Univ Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA. NYU, Sch Med, Dept Pathol, New York, NY USA. RP Trivers, KF (reprint author), Univ N Carolina, Dept Epidemiol, CB 7435, Chapel Hill, NC 27599 USA. EM trivers@unc.edu FU NCI NIH HHS [U01-CA57949, N01-CN05230, N02-CP40501, T32-CA09330, U01-CA57923, U01-CA57983]; NIEHS NIH HHS [P30ES10126] NR 24 TC 50 Z9 51 U1 0 U2 2 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 MAR PY 2005 VL 3 IS 3 BP 225 EP 230 DI 10.1053/S1542-3565(04)006:13-5 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 995MS UT WOS:000234105000006 PM 15765441 ER PT J AU Wong, LJC Lin, YH Suwannarat, P Hsu, CH Kwon, HY Mackowiak, S AF Wong, LJC Lin, YH Suwannarat, P Hsu, CH Kwon, HY Mackowiak, S TI Mitochondrial DNA mutations in a patient with sex reversal and clinical features consistent with Fraser syndrome SO CLINICAL GENETICS LA English DT Article DE Fraser syndrome; LHON and Fraser syndrome; mitochondrial disease; mitochondrial DNA mutation; T14484C ID HEREDITARY OPTIC NEUROPATHY; PERMEABILITY TRANSITION PORE; BLEBBED PHENOTYPE; CRYPTOPHTHALMOS; CELLS AB We describe a 20-year-old 46,XY woman, with clinical findings of Fraser syndrome and three mitochondrial DNA (mtDNA) mutations of Leber hereditary optic neuropathy. The patient had microphthalmia, blindness, widely spaced nipples, bifid ureter, syndactyly of the toes, and mental retardation. Sonography showed the presence of a uterus and intra-abdominal gonads. The proband was screened for mtDNA mutations because of chronic gastrointestinal pseudo-obstruction, urinary tract dysmotility, seizures, mental retardation and persistent macrocytosis, as well as the intermittent elevation of methylmalonic acid. Analysis of point mutations by multiplex polymerase chain reaction and allele-specific oligonucleotide dot-blot hybridization revealed three homoplasmic mtDNA mutations, T14484C, T4216C, and T3394C. This represents a unique case with sex reversal, Fraser-like syndrome, and mitochondrial disease. C1 Georgetown Univ, Med Ctr, Inst Mol & Human Genet, Washington, DC 20007 USA. NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH,DHHS, Bethesda, MD 20892 USA. SUNY Syracuse, Dept Pediat, Syracuse, NY USA. RP Wong, LJC (reprint author), Georgetown Univ, Med Ctr, Inst Mol & Human Genet, M4000,3800 Reservoir Rd NW, Washington, DC 20007 USA. EM wonglj@georgetown.edu NR 22 TC 1 Z9 2 U1 0 U2 0 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD MAR PY 2005 VL 67 IS 3 BP 252 EP 257 DI 10.1111/j.1399-0004.2004.00394.x PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 894EG UT WOS:000226772800009 PM 15691363 ER PT J AU McMaster, ML Giambarresi, T Vasquez, L Goldstein, AM Tucker, MA AF McMaster, ML Giambarresi, T Vasquez, L Goldstein, AM Tucker, MA TI Cytogenetics of familial Waldenstrom's macroglobulinemia: In pursuit of an understanding of genetic predisposition SO CLINICAL LYMPHOMA LA English DT Article; Proceedings Paper CT 3rd International Workshop on Waldenstroms Macroglobulinemia CY OCT 07-10, 2004 CL Paris, FRANCE SP Int Waldenstroms Macroglobulinemia Fdn, Dana Farber Canc Inst, Bing Program Waldenstroms Macroglobulinemia DE comparative genomic hybridization; family studies; lymphoproliferative disorder; spectral karyotyping ID IN-SITU HYBRIDIZATION; CLONAL CHROMOSOME-ABNORMALITIES; PLASMA-CELL LEUKEMIA; MULTIPLE-MYELOMA; KARYOTYPIC ABERRATIONS; TRANSLOCATIONS; DELETIONS; DISEASE; REGIONS; 6Q AB Despite recent identification of a recurrent chromosome 6q21 deletion in sporadic Waldenstrom's macroglobulinemia (WM), elucidation of the molecular pathogenesis of WM remains challenging. In contrast to the growing body of cytogenetic studies in sporadic WM, there have been virtually no informative studies of familial W The authors therefore undertook conventional and molecular cytogenetic evaluation of 18 patients with familial WM and 3 patients with immunoglobulin (Ig) M monoclonal gammopathy (IgM-MG) from 15 families to determine the nature and extent of chromosomal abnormalities associated with familial W The frequency and distribution of chromosomal changes in familial WM resembled those in sporadic WM, including lack of IgH rearrangements and t(9;14); however, we detected del6q21 in only 1 patient. Occasional findings appeared to be novel; however, none were recurrent, and their significance remains unclear. Only one abnormality found in bone marrow specimens was detected in parallel peripheral blood lymphocyte studies, suggesting that most abnormalities represented somatic changes. Although they must be viewed in light of the hypoproliferative nature of WM, our results suggest that further progress in delineating the genetic determinants of WM susceptibility might be gained from alternative approaches such as candidate gene or linkage analysis. C1 NCI, Genet Epidemiol Branch, DCEG, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Westat Res Inc, Rockville, MD USA. RP McMaster, ML (reprint author), NCI, Genet Epidemiol Branch, DCEG, NIH,Dept Hlth & Human Serv, 6120 Execut Blvd,MSC 7236, Bethesda, MD 20892 USA. EM mcmastem@mail.nih.gov RI Tucker, Margaret/B-4297-2015 NR 35 TC 7 Z9 7 U1 0 U2 1 PU CANCER INFORMATION GROUP, LP PI DALLAS PA 3535 WORTH ST, SAMMONS TOWER, STE 4802, DALLAS, TX 75246 USA SN 1526-9655 J9 CLIN LYMPHOMA JI Clin. Lymphoma PD MAR PY 2005 VL 5 IS 4 BP 230 EP 234 DI 10.3816/CLM.2005.n.005 PG 5 WC Oncology SC Oncology GA 981HK UT WOS:000233078100005 PM 15794854 ER PT J AU Kratochvil, CJ Simons, A Vitiello, B Walkup, J Emslie, G Rosenberg, D March, JS AF Kratochvil, CJ Simons, A Vitiello, B Walkup, J Emslie, G Rosenberg, D March, JS TI A multisite psychotherapy and medication trial for depressed adolescents: Background and benefits SO COGNITIVE AND BEHAVIORAL PRACTICE LA English DT Article ID COGNITIVE-BEHAVIORAL THERAPY; PLACEBO-CONTROLLED TRIAL; MAJOR DEPRESSION; CHILDREN; EFFICACY; DISORDER; COMBINATION; FLUOXETINE; SUICIDE; PHARMACOTHERAPY AB The Treatment for Adolescents With Depression Study (TADS) is an NIMH-supported multisite clinical trial that compares the effectiveness of a depression-specific cognitive behavioral therapy (CBT), medication management with fluoxetine (FLX), the combination of CBT and FLX (COMB), and medical management with pill placebo (PBO). TADS was specifically designed as a comprehensive effectiveness study, able to answer clinically meaningful questions by including a broad and representative sample of depressed teens, delivering treatment at both tertiary medical centers and community clinics, and assessing functional as well as symptomatic outcomes. This report supports the importance of conducting clinical trials in youth with depression to bridge the gap between science and practice. C1 Univ Nebraska, Med Ctr, Lincoln, NE 68583 USA. Univ Oregon, Eugene, OR 97403 USA. NIMH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Baltimore, MD 21218 USA. Univ Texas, SW Med Ctr, Dallas, TX 75230 USA. Wayne State Univ, Detroit, MI 48202 USA. Duke Univ, Med Ctr, Durham, NC 27706 USA. RP Kratochvil, CJ (reprint author), 985581 Nebraska Med Ctr, Omaha, NE 68198 USA. EM Ckratoch@unmc.edu NR 42 TC 4 Z9 4 U1 1 U2 2 PU ASSOC ADV BEHAVIOR THERAPY PI NEW YORK PA 305 7TH AVE #16A, NEW YORK, NY 10001-6008 USA SN 1077-7229 J9 COGN BEHAV PRACT JI Cogn. Behav. Pract. PD SPR PY 2005 VL 12 IS 2 BP 159 EP 165 DI 10.1016/S1077-7229(05)80021-5 PG 7 WC Psychology, Clinical SC Psychology GA 989OE UT WOS:000233682600003 ER PT J AU Long, LR Antani, SK Thoma, GR AF Long, LR Antani, SK Thoma, GR TI Image informatics at a national research center SO COMPUTERIZED MEDICAL IMAGING AND GRAPHICS LA English DT Article DE content-based image retrieval; document image; spine; X-ray; uterine cervix ID DOCUMENT IMAGES; X-RAYS; SEGMENTATION; SPINE; METHODOLOGY; RADIOGRAPHS; OSTEOPHYTES; ALGORITHMS; RETRIEVAL AB Image informatics at the Communications Engineering Branch of the Lister Hill National Center for Biomedical Communications (LHNCBC), an R&D division of the National Library of Medicine (NLM), includes document and biomedical images. In both domains, research into computer-assisted methods for information extraction, and the implementation of prototype systems incorporating such methods, is central to our mission. Current document image research focuses on extracting bibliographic data from scanned journal articles. Current biomedical imaging work focuses on content-based image retrieval (CBIR) and related problems in segmentation, indexing, and classifying collections of images of the spine and of the uterine cervix. (c) 2004 Elsevier Ltd. All rights reserved. C1 NIH, Dept Hlth & Human Serv, Commun Engn Branch, US Natl Lib Med,Lister Hill Natl Ctr Biomed Commu, Bethesda, MD 20894 USA. RP NIH, Dept Hlth & Human Serv, Commun Engn Branch, US Natl Lib Med,Lister Hill Natl Ctr Biomed Commu, 8600 Rockville Pike,Bldg 38A,MS 55, Bethesda, MD 20894 USA. EM rlong@mail.nih.gov; santani@mail.nih.gov; gthoma@mail.nih.gov OI Antani, Sameer/0000-0002-0040-1387 NR 80 TC 25 Z9 25 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0895-6111 EI 1879-0771 J9 COMPUT MED IMAG GRAP JI Comput. Med. Imaging Graph. PD MAR-APR PY 2005 VL 29 IS 2-3 BP 171 EP 193 DI 10.1016/j.compmedimag.2004.09.015 PG 23 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Radiology, Nuclear Medicine & Medical Imaging GA 910VZ UT WOS:000227961600009 PM 15755536 ER PT J AU Jo, JH Jang, HS Ko, HC Kim, MB Oh, CK Kwon, YW Kwon, KS AF Jo, JH Jang, HS Ko, HC Kim, MB Oh, CK Kwon, YW Kwon, KS TI Pustular psoriasis and the Kobner phenomenon caused by allergic contact dermatitis from zinc pyrithione-containing shampoo SO CONTACT DERMATITIS LA English DT Article DE cosmetics; Kobner phenomenon; psoriasis; shampoo; zinc pyrithione ID KOEBNER AB Zinc pyrithione is a shampoo ingredient that has been shown to be safe and effective for dandruff and scalp psoriasis. It is thought to decrease the cell turnover rate in hyperproliferative dermatoses such as psoriasis, and also has fungistatic and antimicrobial activity, although its exact mode of action is unknown. In psoriasis, external factors, such as trauma.. infection and drugs, may provoke aggravated manifestations of psoriatic skin lesions. Rarely, irritant or allergic mechanisms are likely causes of psoriatic flare and Kobnerization. A patient had had stable psoriasis for 25 years and no any other skin disease. Within 20 days, she developed an aggravated scaly erythematous patch on the scalp, where a shampoo had been applied, and simultaneously developed pustular psoriasis on both forearms. Patch testing showed a relevant sensitization to zinc pyrithione, and we observed symptomatic aggravation by provocation testing with zinc pyrithione shampoo. We report a rare case of psoriasis aggravated by the induction of allergic contact dermatitis from zinc pyrithione after using antidandruff shampoo. C1 Pusan Natl Univ, Dept Dermatol, Coll Med, Pusan 602739, South Korea. NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA. RP Jang, HS (reprint author), Pusan Natl Univ, Dept Dermatol, Coll Med, 1-10 Ami Dong, Pusan 602739, South Korea. EM hsjang@pusan.ac.kr NR 11 TC 9 Z9 10 U1 0 U2 0 PU BLACKWELL MUNKSGAARD PI FREDERIKSBERG C PA 1 ROSENORNS ALLE, DK-1970 FREDERIKSBERG C, DENMARK SN 0105-1873 J9 CONTACT DERMATITIS JI Contact Dermatitis PD MAR PY 2005 VL 52 IS 3 BP 142 EP 144 DI 10.1111/j.0105-1873.2005.00528.x PG 3 WC Allergy; Dermatology SC Allergy; Dermatology GA 918XL UT WOS:000228582800006 PM 15811028 ER PT J AU Hough, CL Kallet, RH Ranieri, VM Rubenfeld, GD Luce, JM Hudson, LD AF Hough, CL Kallet, RH Ranieri, VM Rubenfeld, GD Luce, JM Hudson, LD TI Intrinsic positive end-expiratory pressure in Acute Respiratory Distress Syndrome (ARDS) Network subjects SO CRITICAL CARE MEDICINE LA English DT Article DE acute lung injury; acute respiratory distress syndrome; intrinsic positive end expiratory pressure; lung-protective ventilation ID ACUTE LUNG INJURY; AIR-FLOW OBSTRUCTION; LOW TIDAL VOLUME; AUTO-PEEP; MECHANICAL VENTILATION AB Objective: We tested the hypothesis that subjects randomized to the 6 mL/kg predicted body weight tidal volume study group of the National Institutes of Health Acute Respiratory Distress Syndrome (ARDS) Network study had higher levels of intrinsic positive end-expiratory pressure (PEEP) than subjects randomized to the 12 mL/kg predicted body weight tidal volume study group. Design: Secondary analysis of a subgroup from a randomized controlled trial. Setting: Hospitals located in San Francisco, CA, and Seattle, WA. Patients: Eighty-four patients enrolled in the ARDS Network tidal volume trial in San Francisco, CA, and Seattle, WA, with records of measurement of intrinsic PEEP. Interventions: None. Measurements and Main Results: Intrinsic PEEP was assessed a median of six times over the first 48 hrs of ARDS Network protocol ventilation in study subjects, with no significant difference in number of measurements between subjects randomized to the tidal volume protocol of 6 mL/kg compared with 12 mL/kg. We found that intrinsic PEEP was higher among subjects randomized to the 6 mL/kg protocol, with a median intrinsic PEEP of 1.3 cm H2O (interquartile range, 0-3.1 cm H2O), compared with a median intrinsic PEEP of 0.5 cm H2O (interquartile range, 0-1.5 cm H2O) among subjects randomized to 12 mL/kg (p = .029). There was no difference in total PEEP between the study groups. Conclusions: In a subgroup of ARDS Network subjects, intrinsic PEEP was statistically significantly higher in subjects randomized to the 6 mL/kg protocol than those in the 12 mL/kg study group. The amount of intrinsic PEEP was very low in both study groups, and difference of median intrinsic PEEP between the groups was < 1 cm H2O. It is unlikely that the difference in intrinsic PEEP between the study groups was clinically important in the ARDS Network study of low tidal volume ventilation. C1 Univ Washington, Dept Med, Div Pulm & Crit Care Med, Seattle, WA 98195 USA. San Francisco Gen Hosp, Resp Care Serv, San Francisco, CA 94110 USA. NHLBI, ARDS Network, Bethesda, MD 20892 USA. Univ Turin, Osped S Giovanni Battista, Sez Antestesio & Rianimaz, Dipartimento Discipline Med Chirurg, I-10124 Turin, Italy. RP Hough, CL (reprint author), Univ Washington, Dept Med, Div Pulm & Crit Care Med, Seattle, WA 98195 USA. FU NHLBI NIH HHS [HL07287, P50 HL30452, N01 HR46055] NR 22 TC 17 Z9 18 U1 0 U2 3 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 MAR PY 2005 VL 33 IS 3 BP 527 EP 532 DI 10.1097/01.ccm.0000155782.86244.42 PG 6 WC Critical Care Medicine SC General & Internal Medicine GA 907CD UT WOS:000227691800008 PM 15753743 ER PT J AU Majdalani, N Vanderpool, CK Gottesman, S AF Majdalani, N Vanderpool, CK Gottesman, S TI Bacterial small RNA regulators SO CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Review DE CsrA; CsrB; DsrA; Hfq; RpoS ID CAROTOVORA SUBSP CAROTOVORA; SM-LIKE PROTEIN; PSEUDOMONAS-FLUORESCENS CHA0; CARBON STARVATION GENE; ACID RESISTANCE GENES; ESCHERICHIA-COLI; MESSENGER-RNA; DSRA-RNA; RPOS TRANSLATION; H-NS AB Small regulatory RNAs can modify the activity of proteins and the stability and translation of mRNAs. They have now been found in a wide range of organisms, and can play previously unsuspected critical regulatory roles. The bacterial small RNAs include two major classes. The largest family (with at least 20 members in Escherichia coli K12) acts by basepairing with target mRNAs to modify mRNA translation or stability; this class of RNAs also uses an RNA chaperone protein, Hfq. DsrA is the best-studied example of this family of RNAs. It has been shown to positively regulate translation of the transcription factor RpoS by opening an inhibitory hairpin in the mRNA, and to negatively regulate translation of hns by pairing Just beyond the translation initiation codon. The class of RNAs that modify activity of proteins is exemplified by CsrB and CsrC of E. coli, two RNAs that bind to and inhibit CsrA, a protein translational regulator. Homologs of CsrA and related regulatory RNAs have been implicated in the regulation of gluconeogenesis, biofilm formation, and virulence factor expression in plant and human pathogens. C1 NCI, Mol Biol Lab, Bethesda, MD 20892 USA. RP Gottesman, S (reprint author), NCI, Mol Biol Lab, Bldg 37,Rm 5132, Bethesda, MD 20892 USA. EM susang@helix.nih.gov NR 105 TC 182 Z9 194 U1 4 U2 23 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 1040-9238 J9 CRIT REV BIOCHEM MOL JI Crit. Rev. Biochem. Mol. Biol. PD MAR-APR PY 2005 VL 40 IS 2 BP 93 EP 113 DI 10.1080/10409230590918702 PG 21 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 923PU UT WOS:000228922600002 PM 15814430 ER PT J AU Noronha, V Shafi, NQ Obando, JA Kummar, S AF Noronha, V Shafi, NQ Obando, JA Kummar, S TI Primary non-Hodgkin's lymphoma of the liver SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY LA English DT Review DE non-Hodgkin's lymphoma; hepatic lymphoma; liver tumors ID PRIMARY HEPATIC LYMPHOMA; B-CELL LYMPHOMA; PRIMARY BILIARY-CIRRHOSIS; ACQUIRED-IMMUNODEFICIENCY-SYNDROME; C VIRUS-INFECTION; OF-THE-LITERATURE; TISSUE TYPE; PATIENT AB We review the literature on primary hepatic lymphoma (PHL). PHL is a rare malignancy, and constitutes about 0.016% of all cases of non-Hodgkin's lymphoma. It has been reported to occur with increased frequency in patients with chronic hepatitis C infection. Most patients with PHL present with abdominal pain, constitutional symptoms and have hepatomegaly on examination. Imaging studies reveal solitary, or less often, multiple masses in the liver. The predominant histology is B-cell lymphoma, most commonly diffuse large cell type. Most patients are treated with chemotherapy, with some physicians employing a multimodality approach incorporating surgery and radiotherapy with chemotherapy. The prognosis is variable, with good response to early aggressive combination chemotherapy. (c) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Yale Canc Ctr, New Haven, CT 06520 USA. VA Connecticut Healthcare Syst, Dept Pathol & Lab Med, West Haven, CT 06516 USA. Va Connecticut Healthcare Syst, Dept Radiol, West Haven, CT 06516 USA. VA Connecticut Canc Ctr, Yale Canc Ctr, Yale Sch Med, West Haven, CT 06516 USA. RP Kummar, S (reprint author), NCI, Natl Naval Med Ctr, Aerodigest Canc Clin Res Sect, Med Oncol Clin Res Unit,NIH, 8901 Wisconsin Ave,Bldg 8 Rm 5101, Bethesda, MD 20889 USA. EM sk157a@nih.gov NR 52 TC 67 Z9 76 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1040-8428 J9 CRIT REV ONCOL HEMAT JI Crit. Rev. Oncol./Hematol. PD MAR PY 2005 VL 53 IS 3 BP 199 EP 207 DI 10.1016/j.critrevonc.2004.10.010 PG 9 WC Oncology; Hematology SC Oncology; Hematology GA 905DQ UT WOS:000227548300003 PM 15718146 ER PT J AU Park, YS Jeong, HS Sung, HC Yun, CW AF Park, YS Jeong, HS Sung, HC Yun, CW TI Sed1p interacts with Arn3p physically and mediates ferrioxamine B uptake in Saccharomyces cerevisiae SO CURRENT GENETICS LA English DT Article DE Saccharomyces cerevisiae; iron; ferrioxamine B; FOB; cell wall protein; ARN3 ID CELL-WALL PROTEIN; SIDEROPHORE-IRON; FERRICHROME; GENES; YEAST AB Two-hybrid analysis can be used to study protein function and metabolic pathways. Using yeast two-hybrid analysis to identify a siderophore uptake pathway in the yeast Saccharomyces cerevisiae, we found that the C-terminal part of the cell-wall protein Sed1p interacts with the N-terminal region of Arn3p. To confirm the physical interaction between the Sed1p C-terminal fragment and the hydrophilic N-terminal fragment of Arn3p, we used an in vitro co-immunoprecipitation assay and a growth test of the strain with bait and SED1 plasmids in quadruple amino acid-depleted medium. The expression of SED1 was upregulated by overexpression of AFT1-1(up) under the control of the GAL promoter. This occurred despite the lack of an Aft1p-binding consensus region on the upstream region of SED1 or a high concentration of free iron. Although free-iron uptake activity in the Delta sed1 strain did not differ from that in the parental strain, ferrioxamine bound-iron uptake activity was reduced in the Dsed1 strain. Moreover, the Dsed1 strain showed low viability at high iron concentrations. Taken together, these results suggest that Sed1p mediates siderophore transport and confers iron resistance in S. cerevisiae. C1 Korea Univ, Coll Life Sci, Grad Sch Biotechnol, Seoul 136701, South Korea. NICHHD, Genet Mol Lab, NIH, Bethesda, MD 20892 USA. RP Yun, CW (reprint author), Korea Univ, Coll Life Sci, Grad Sch Biotechnol, Anam Dong, Seoul 136701, South Korea. EM cheolwony@korea.ac.kr NR 21 TC 5 Z9 5 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0172-8083 J9 CURR GENET JI Curr. Genet. PD MAR PY 2005 VL 47 IS 3 BP 150 EP 155 DI 10.1007/s00294-004-0554-0 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 905FX UT WOS:000227554900002 PM 15611868 ER PT J AU Kingston, DGI Newman, DJ AF Kingston, DGI Newman, DJ TI The search for novel drug leads for predominately antitumor therapies by utilizing mother nature's pharmacophoric libraries SO CURRENT OPINION IN DRUG DISCOVERY & DEVELOPMENT LA English DT Review DE combinatorial scaffolds; drug discovery; natural products ID HISTONE-DEACETYLASE INHIBITORS; ARYL-HYDROCARBON RECEPTOR; LACTACYSTIN BETA-LACTONE; THIOREDOXIN REDUCTASE SYSTEM; LEUKOTRIENE A(4) HYDROLASE; CYCLIN-DEPENDENT KINASES; SOLID-PHASE SYNTHESIS; COMBINATORIAL LIBRARIES; PROTEASOME INHIBITORS; SELECTIVE INHIBITORS AB Recent advances in the use of natural products and compounds derived from natural products as agents for the treatment of cancer and other diseases are reviewed. The antitumor agents discussed include tubulin interactive agents, inhibitors of topoisomerases I and II, caspase activators, proteasome inhibitors, histone deacetylase inhibitors, heat shock protein 90 inhibitors, protein kinase inhibitors, and inhibitors of hypoxia inducible factor 1. It can be concluded that, despite a perceived lack of popularity in recent years, the use of natural product scaffolds in searching for drug leads is still being practiced. C1 NCI, Frederick Nat Prod Branch, Dev Therapeut Program, Frederick, MD 21702 USA. Virginia Polytech Inst & State Univ, Dept Chem, Blacksburg, VA 24061 USA. RP Newman, DJ (reprint author), NCI, Frederick Nat Prod Branch, Dev Therapeut Program, Frederick, MD 21702 USA. EM dn22a@nih.gov OI Kingston, David/0000-0001-8944-246X NR 153 TC 25 Z9 25 U1 0 U2 5 PU THOMSON SCIENTIFIC PI LONDON PA 34-42 CLEVELAND STREET, LONDON, W1T 4JE, ENGLAND SN 1367-6733 J9 CURR OPIN DRUG DISC JI Curr. Opin. Drug Discov. Dev. PD MAR PY 2005 VL 8 IS 2 BP 207 EP 227 PG 21 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 903YZ UT WOS:000227463000007 PM 15782545 ER PT J AU Woodman, R Ferrucci, L Guralnik, J AF Woodman, R Ferrucci, L Guralnik, J TI Anemia in older adults SO CURRENT OPINION IN HEMATOLOGY LA English DT Article DE anemia; disability; elderly persons; outcomes ID IRON-DEFICIENCY ANEMIA; HEMOGLOBIN CONCENTRATION; GASTROINTESTINAL-TRACT; RHEUMATOID-ARTHRITIS; PHYSICAL PERFORMANCE; TRANSFERRIN RECEPTOR; RENAL-INSUFFICIENCY; UNEXPLAINED ANEMIA; POPULATION SAMPLES; UNITED-STATES AB Purpose of review Anemia is common in older adults and is an independent predictor for increased morbidity and mortality in several disease states. Older persons with anemia suffer hospitalization, physical decline, and disability at higher rates than those people without anemia. Recent findings The prevalence and causes of anemia in community-dwelling older persons in the US were evaluated in the third National Health and Nutrition Examination Survey (NHANES) 1988-1994. In persons 65 years and older, anemia was present in 11.0% of men and 10.2% of women, with the prevalence rising to over 20% in people 85 years and older. One third of the cases were due to nutritional deficiencies, and one third was due to chronic illness, including but not limited to chronic kidney disease. About one third of the cases of anemia remain unexplained. Anemia is also prognostic for diminished physical performance and loss of mobility in people 65 years and older. A recent report suggests that the prevalence of anemia is even higher in elderly persons living in nursing homes. The data suggest that the risk of mortality and loss of mobility even extends to levels of hemoglobin normally considered low normal by WHO criteria, raising the question about optimal hemoglobin levels in the elderly. Summary Anemia is a common modifiable predictor of poor medical outcome in older adults and, as such, should be actively managed. Clinical studies are necessary to assess the effect of treatment of anemia on outcomes specific to the elderly, like disability. C1 Ortho Biotech Clin Affairs, Bridgewater, NJ 08807 USA. Harbor Hosp, Baltimore Longitudinal Study Aging,NIH, Longitudinal Studies Sect,NIA, Clin Res Branch,Gerontol Res Ctr, Baltimore, MD USA. NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA. RP Woodman, R (reprint author), Ortho Biotech Clin Affairs, 430 Route 22 East, Bridgewater, NJ 08807 USA. EM rwoodman@obius.jnj.com NR 43 TC 68 Z9 73 U1 0 U2 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1065-6251 J9 CURR OPIN HEMATOL JI Curr. Opin. Hematol. PD MAR PY 2005 VL 12 IS 2 BP 123 EP 128 PG 6 WC Hematology SC Hematology GA 947PP UT WOS:000230658800004 PM 15725902 ER PT J AU Odutola, J Ward, MM AF Odutola, J Ward, MM TI Ethnic and socioeconomic disparities in health among patients with rheumatic disease SO CURRENT OPINION IN RHEUMATOLOGY LA English DT Review DE African America; health disparities; Hispanic; socioeconomic status ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; TOTAL HIP-REPLACEMENT; AFRICAN-AMERICAN; JOINT ARTHROPLASTY; UNITED-STATES; MEDICARE BENEFICIARIES; RACIAL-DIFFERENCES; CARE UTILIZATION; EDUCATION LEVEL; OLDER PATIENTS AB Purpose of review To describe recent studies of differences in the occurrence and outcomes of rheumatic diseases and differences in treatment by ethnic group or socioeconomic status. Recent findings African Americans and Hispanics in the United States have consistently been found to have higher prevalences of arthritis and other rheumatic conditions than whites and also generally have more activity limitations in the setting of rheumatic disease. Variations in disease occurrence by socioeconomic status have not been studies extensively. African Americans with osteoarthritis were less likely than whites to be treated with narcotic analgesics. Rates of total knee or hip arthroplasty were found to be substantially lower among African Americans and Hispanics than among whites in the United States, and lower among those of low socioeconomic status in the United Kingdom. Ethnic differences in use of arthroplasty have been associated with less willingness of African Americans to have surgery, which has been related to perceptions of uncertain benefits of surgery. Poverty and ethnicity had important associations with the activity of systemic lupus erythematosus, whereas socioeconomic status was a more important predictor of mortality in these patients. Treatment adherence was similar in African American and white patients with systemic lupus erythematosus, but barriers to adherence differed by ethnic group. Summary Ethnic disparities in health have been more extensively studied than socioeconomic disparities. Most studies only describe the disparities, but several studies have begun to investigate potential reasons for the disparities. C1 NIAMSD, Intramural Res Program, NIH, US Dept HHS, Bethesda, MD 20892 USA. RP Ward, MM (reprint author), NIAMS, NIH, Bldg 10,Room 9S205,10 Ctr Dr,MSC 1828, Bethesda, MD 20892 USA. EM wardm1@mail.nih.gov NR 44 TC 31 Z9 32 U1 2 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1040-8711 J9 CURR OPIN RHEUMATOL JI CURR. OPIN. RHEUMATOL. PD MAR PY 2005 VL 17 IS 2 BP 147 EP 152 DI 10.1097/01.bor.0000151403.18651.de PG 6 WC Rheumatology SC Rheumatology GA 912LH UT WOS:000228079200006 PM 15711226 ER PT J AU Khan, SS Solomon, MA McCoy, JP AF Khan, SS Solomon, MA McCoy, JP TI Detection of circulating endothelial cells and endothelial progenitor cells by flow cytometry SO CYTOMETRY PART B-CLINICAL CYTOMETRY LA English DT Review DE endothelial cells; rare events; CEC; endothelial progenitor ID ACUTE MYOCARDIAL-INFARCTION; PERIPHERAL-BLOOD; STEM-CELLS; PULMONARY-HYPERTENSION; PRECURSOR CELLS; CANCER-PATIENTS; GENE-THERAPY; IN-VITRO; ANGIOGENESIS; DISEASE AB The finding of angiogenic and vasculogenic cells in the peripheral circulation may have profound effects on the course of a variety of diseases ranging from cancer to cardiovascular disease. These cells are ascribed to be endothelial in nature and are generally referred to as circulating endothelial cells if mature or as endothelial progenitor cells if immature. Different approaches have been used to detect these cells, including in vitro culture, magnetic bead isolation, and flow cytometry. We review flow cytometric methods for the detection and enumeration of these cells and provide technical suggestions to promote the accurate enumeration of circulating endothelial cells and endothelial progenitor cells. Published 2005 Wiley-Liss, Inc.(dagger). C1 NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA. Warren G Magnuson Clin Ctr, Crit Care Med Dept, NIH, Bethesda, MD USA. NHLBI, Cardiol Branch, NIH, Bethesda, MD 20892 USA. RP McCoy, JP (reprint author), NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA. EM mccoyj@nhlbi.nih.gov NR 51 TC 213 Z9 228 U1 1 U2 12 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4949 J9 CYTOM PART B-CLIN CY JI Cytom. Part B-Clin. Cytom. PD MAR PY 2005 VL 64B IS 1 BP 1 EP 8 DI 10.1002/cyto.b.20040 PG 8 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA 899CM UT WOS:000227122500001 PM 15668988 ER PT J AU Orlic, D AF Orlic, D TI BM stem cells and cardiac repair: where do we stand in 2004? SO CYTOTHERAPY LA English DT Review DE infarction; ischemia; myocardial regeneration; plasticity; stem cell ID BONE-MARROW-CELLS; SKELETAL MYOBLAST TRANSPLANTATION; ENDOTHELIAL PROGENITOR CELLS; FUNCTIONAL HEMANGIOBLAST ACTIVITY; COLONY-STIMULATING FACTOR; NONHUMAN PRIMATE MODEL; C-KIT RECEPTOR; STROMAL CELLS; IN-VIVO; MYOCARDIAL-INFARCTION AB Adult BM stem cells are being investigated for their potential to regenerate injured tissues by a process referred to as plasticity or transdifferentiation. Although data supporting stem cell plasticity is extensive, a controversy has emerged based on findings that propose cell-cell fusion as a more appropriate interpretation for this phenomenon. A major focus of this controversy is the claim that acutely infarcted myocardium in adult hearts can be regenerated by BM stem cells. Many researchers consider the adult heart to be a post-mitotic organ, whereas others believe that a low level of cardiomyocyte renewal occurs throughout life. If renewal occurs, it may be in response to cardiac stem cell activity or to stem cells that migrate from distant tissues. Post-mortem microscopic analysis of experimentally induced myocardial infarctions in several rodent models suggests that cardiomyocyte renewal is achieved by stem cells that infiltrate the damaged tissue. For a better understanding of the possible involvement of stem cells in myocardial regeneration, it is important to develop appropriate technologies to monitor myocardial repair over time with an emphasis on large animal models. Studies on non-human primate, swine and canine models of acute myocardial infarctions would enable investigators to utilize clinical quality cell-delivery devices, track labeled donor cells after precision transplantation and utilize non-invasive imaging for functional assays over time with clinical accuracy. In addition, if stem cell plasticity is to reach the next level of acceptance, it is important to identify the environmental cues needed for stem cell trafficking and to define the genetic and cellular mechanisms that initiate transdifferentiation. Only then will it be possible to determine if, and to what extent, BM stem cells are involved in myocardial regeneration and to begin to regulate precisely tissue repair. C1 NHLBI, Cardiovasc Branch, NIH, Bethesda, MD 20892 USA. RP Orlic, D (reprint author), NHLBI, Cardiovasc Branch, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 126 TC 25 Z9 27 U1 1 U2 3 PU TAYLOR & FRANCIS AS PI OSLO PA PO BOX 12 POSTHUSET, NO-0051 OSLO, NORWAY SN 1465-3249 J9 CYTOTHERAPY JI Cytotherapy PD MAR PY 2005 VL 7 IS 1 BP 3 EP 15 DI 10.1080/14653240510018028 PG 13 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Cell Biology; Hematology; Medicine, Research & Experimental SC Cell Biology; Biotechnology & Applied Microbiology; Hematology; Research & Experimental Medicine GA 935OI UT WOS:000229791200003 PM 16040379 ER PT J AU Murali, D Yoshikawa, S Corrigan, RR Plas, DJ Crair, MC Oliver, G Lyons, KM Mishina, Y Furuta, Y AF Murali, D Yoshikawa, S Corrigan, RR Plas, DJ Crair, MC Oliver, G Lyons, KM Mishina, Y Furuta, Y TI Distinct developmental programs require different levels of Bmp signaling during mouse retinal development SO DEVELOPMENT LA English DT Article DE Bmpr1a; Bmpr1b; Bmp signaling; mutant mouse; retinal patterning; retinal growth; retinal neurogenesis ID BONE MORPHOGENETIC PROTEINS; DROSOPHILA EYE DEVELOPMENT; FIBROBLAST GROWTH-FACTORS; GANGLION-CELL; HOMEOBOX GENE; TRANSCRIPTION FACTORS; MUTANT MICE; NEURAL-TUBE; CHICK EYE; RECEPTOR AB The Bmp family of secreted signaling molecules is implicated in multiple aspects of embryonic development. However, the cell-type-specific requirements for this signaling pathway are often obscure in the context of complex embryonic tissue interactions. To define the cell-autonomous requirements for Bmp signaling, we have used a Cre-loxP strategy to delete Bmp receptor function specifically within the developing mouse retina. Disruption of a Bmp type I receptor gene, Bmpr1a, leads to no detectable eye abnormality. Further reduction of Bmp receptor activity by removing one functional copy of another Bmp type I receptor gene, Bmpr1b, in the retina-specific Bmpr1a mutant background, results in abnormal retinal dorsoventral patterning. Double mutants completely lacking both of these genes exhibit severe eye defects characterized by reduced growth of embryonic retina and failure of retinal neurogenesis. These studies provide direct genetic evidence that Bmpr1a and Bmpr1b play redundant roles during retinal development, and that different threshold levels of Bmp signaling regulate distinct developmental programs such as patterning, growth and differentiation of the retina. C1 Univ Texas, Hlth Sci Ctr, Grad Sch Biomed Sci, Houston, TX 77030 USA. Univ Texas, MD Anderson Canc Ctr, Dept Biochem & Mol Biol, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA. St Jude Childrens Res Hosp, Dept Genet, Memphis, TN 38105 USA. Univ Calif Los Angeles, Dept Mol Cell & Dev Biol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Orthoped Surg, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Biol Chem, Los Angeles, CA 90095 USA. Natl Inst Environm Hlth & Safety, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA. RP Furuta, Y (reprint author), Univ Texas, Hlth Sci Ctr, Grad Sch Biomed Sci, Houston, TX 77030 USA. EM yfuruta@mdanderson.org RI Lyons, Karen/P-1843-2014 OI Lyons, Karen/0000-0001-9420-5813 FU NCI NIH HHS [CA16672]; NEI NIH HHS [EY13128] NR 64 TC 80 Z9 84 U1 0 U2 3 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 MAR PY 2005 VL 132 IS 5 BP 913 EP 923 DI 10.1242/dev.01673 PG 11 WC Developmental Biology SC Developmental Biology GA 912QC UT WOS:000228093300006 PM 15673568 ER PT J AU Ting, CY Yonekura, S Chung, P Hsu, SN Robertson, HM Chiba, A Lee, CH AF Ting, CY Yonekura, S Chung, P Hsu, SN Robertson, HM Chiba, A Lee, CH TI Drosophila N-cadherin functions in the first stage of the two-stage layer-selection process of R7 photoreceptor afferents SO DEVELOPMENT LA English DT Article DE Drosophila; N-cadherin; R7 ID LAMINA-SPECIFIC CONNECTIVITY; SYNAPTIC ADHESION MOLECULES; VISUAL-SYSTEM; TARGET SPECIFICITY; CLASSIC CADHERIN; GENOME SEQUENCE; RETINAL AXONS; CELL-ADHESION; DN-CADHERIN; RECEPTOR AB Visual information received from the three types of photoreceptor neurons (R1-R6, R7 and R8) in the fly compound eyes converges to the external part of the medulla neuropil (M1-M6 layers) in a layer-specific fashion: R7 and R8 axons terminate at the M6 and M3 layers, respectively, whereas lamina neurons (L1-L5) relay R1-R6 to multiple medulla layers (M1-M5). Here, we show that during development, R7 and R8 neurons establish layer-specific projections in two separate stages: during the first stage, R7 and R8 axons sequentially target to the R7-and R8-temporary layers, respectively; and at the second stage, R7 and R8 growth cones progress synchronously to their destined layers. Using a set of mutations that delete different afferent subsets or alter R7 connectivity, we defined the mechanism of layer selection. We observed that R8, R7 and L1-L5 afferents target to their temporary layers independently, suggesting that afferent-target, but not afferent-afferent, interactions dictate the targeting specificity. N-cadherin is required in the first stage for R7 growth cones to reach and remain in the R7-temporary layer. The Ncad gene contains three pairs of alternatively spliced exons and encodes 12 isoforms. However, expressing a single Ncad isoform in Ncad mutant R7s is sufficient to rescue mistargeting phenotypes. Furthermore, Ncad isoforms mediate promiscuous heterophilic interactions in an in vitro cell-aggregation assay. We propose that Ncad isoforms do not form an adhesion code; rather, they provide permissive adhesion between R7 growth cones and their temporary targets. C1 NICHHD, Unit Neuronal Connectiv, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA. Univ Illinois, Dept Cell & Struct Biol, Urbana, IL 61801 USA. RP Lee, CH (reprint author), NICHHD, Unit Neuronal Connectiv, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA. EM leechih@mail.nih.gov RI Lee, Chi-Hon/G-9190-2012; Ting, chun-yuan/F-6448-2013 FU NICHD NIH HHS [HD008748-03] NR 40 TC 78 Z9 78 U1 0 U2 0 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 MAR PY 2005 VL 132 IS 5 BP 953 EP 963 DI 10.1242/dev.01661 PG 11 WC Developmental Biology SC Developmental Biology GA 912QC UT WOS:000228093300010 PM 15673571 ER PT J AU Steinberg, Z Myers, C Heim, VM Lathrop, CA Rebustini, IT Stewart, JS Larsen, M Hoffman, MP AF Steinberg, Z Myers, C Heim, VM Lathrop, CA Rebustini, IT Stewart, JS Larsen, M Hoffman, MP TI FGFR2b signaling regulates ex vivo submandibular gland epithelial cell proliferation and branching morphogenesis SO DEVELOPMENT LA English DT Article DE fibroblast growth factor receptors; FGF7; FGF10; signaling; salivary gland development; organ culture ID KERATINOCYTE GROWTH-FACTOR; GENE-EXPRESSION; URETERAL BUD; IN-VITRO; MATRIX METALLOPROTEINASES; SALIVARY-GLAND; LUNG; FGF10; MICE; RECEPTOR AB Branching morphogenesis of mouse submandibular glands is regulated by multiple growth factors. Here, we report that ex vivo branching of intact submandibular glands decreases when either FGFR2 expression is downregulated or soluble recombinant FGFR2b competes out the endogenous growth factors. However, a combination of neutralizing antibodies to FGF1, FGF7 and FGF10 is required to inhibit branching in the intact gland, suggesting that multiple FGF isoforms are required for branching. Exogenous FGFs added to submandibular epithelial rudiments cultured without mesenchyme induce distinct morphologies. FGF7 induces epithelial budding, whereas FGF10 induces duct elongation, and both are inhibited by FGFR or ERK1/2 signaling inhibitors. However, a PI3-kinase inhibitor also decreases FGF7-mediated epithelial budding, suggesting that multiple signaling pathways exist. We immunolocalized FGF receptors and analyzed changes in FGFR, FGF and MMP gene expression to identify the mechanisms of FGF-mediated morphogenesis. FGFR1b and FGFR2b are present throughout the epithelium, although FGFR1b is more highly expressed around the periphery of the buds and the duct tips. FGF7 signaling increases FGFR1b and FGF1 expression, and MMP2 activity, when compared with FGF10, resulting in increased cell proliferation and expansion of the epithelial bud, whereas FGF10 stimulates localized proliferation at the tip of the duct. FGF7- and FGF10-mediated morphogenesis is inhibited by an MMP inhibitor and a neutralizing antibody to FGF1, suggesting that both FGF1 and MMPs are essential downstream mediators of epithelial morphogenesis. Taken together, our data suggests that FGFR2b signaling involves a regulatory network of FGFR1b/FGF1/MMP2 expression that mediates budding and duct elongation during branching morphogenesis. C1 NIDCR, Craniofacial Dev Biol & Regenerat Branch, Matrix & Morphognesis Unit, NIH, Bethesda, MD 20892 USA. Natl Inst Dent & Craniofacial Res, Craniofacial Dev Biol & Regenerat Branch, Dev Mech Sect, Bethesda, MD 20892 USA. RP Hoffman, MP (reprint author), NIDCR, Craniofacial Dev Biol & Regenerat Branch, Matrix & Morphognesis Unit, NIH, 30 Convent Dr,MSC 4370, Bethesda, MD 20892 USA. EM mhoffman@mail.nih.gov NR 55 TC 120 Z9 123 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 MAR PY 2005 VL 132 IS 6 BP 1223 EP 1234 DI 10.1242/dev.01690 PG 12 WC Developmental Biology SC Developmental Biology GA 916IG UT WOS:000228378000006 PM 15716343 ER PT J AU Liu, W Sun, XX Braut, A Mishina, Y Behringer, RR Mina, M Martin, JF AF Liu, W Sun, XX Braut, A Mishina, Y Behringer, RR Mina, M Martin, JF TI Distinct functions for Bmp signaling in lip and palate fusion in mice SO DEVELOPMENT LA English DT Article DE Bmp; palate; morphogenesis ID SELECTIVE TOOTH AGENESIS; RETINOIC ACID; CLEFT-PALATE; OROFACIAL CLEFTS; BRANCHIAL-ARCH; EEC-SYNDROME; MORPHOGENESIS; MOUSE; MSX1; P63 AB Previous work suggested that cleft lip with or without cleft palate (CL/P) is genetically distinct from isolated cleft secondary palate (CP). Mutations in the Bmp target gene Msx1 in families with both forms of orofacial clefting has implicated Bmp signaling in both pathways. To dissect the function of Bmp signaling in orofacial clefting, we conditionally inactivated the type 1 Bmp receptor Bmpr1a in the facial primordia, using the Nestin cre transgenic line. Nestin cre; Bmpr1a mutants had completely penetrant, bilateral CUP with arrested tooth formation. The cleft secondary palate of Nestin cre; Bmprla mutant embryos was associated with diminished cell proliferation in maxillary process mesenchyme and defective anterior posterior patterning. By contrast, we observed elevated apoptosis in the fusing region of the Nestin cre; Bmprla mutant medial nasal process. Moreover, conditional inactivation of the Bmp4 gene using the Nestin cre transgenic line resulted in isolated cleft lip. Our data uncover a Bmp4-Bmpr1a genetic pathway that functions in lip fusion, and reveal that Bmp signaling has distinct roles in lip and palate fusion. C1 Texas A&M Univ, Ctr Hlth Sci, Alkek Inst Biosci & Technol, Houston, TX 77030 USA. Texas A&M Univ, MD Anderson Canc Ctr, Dept Mol Genet, Houston, TX 77030 USA. NIEHS, Lab Reprod & Dev Toxicol, Res Triangle Pk, NC 27709 USA. Univ Connecticut, Sch Dent Med, Ctr Hlth Sci, Dept Pediat Dent, Farmington, CT 06030 USA. RP Martin, JF (reprint author), Texas A&M Univ, Ctr Hlth Sci, Alkek Inst Biosci & Technol, 2121 Holcombe Blvd, Houston, TX 77030 USA. EM jmartin@ibt.tamhsc.edu FU NIAMS NIH HHS [AR42919]; NIDCR NIH HHS [2R01DE/HD12324-06, DE08682, R01DE013509] NR 42 TC 160 Z9 167 U1 1 U2 8 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 MAR PY 2005 VL 132 IS 6 BP 1453 EP 1461 DI 10.1242/dev.01676 PG 9 WC Developmental Biology SC Developmental Biology GA 916IG UT WOS:000228378000025 PM 15716346 ER PT J AU Youle, RJ AF Youle, RJ TI Morphology of mitochondria during apoptosis: Worms-to-beetles in worms SO DEVELOPMENTAL CELL LA English DT Editorial Material ID FISSION; DEATH AB Although mitochondria are crucial for most pathways of mammalian cell apoptosis, evidence for their role in classic invertebrate models of programmed cell death has been frustratingly scant. New work showing that inhibition of mitochondrial fragmentation during C. elegans development inhibits programmed cell death bridges this gap and should advance a more detailed understanding of the role of mitochondria in caspase activation. C1 NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20815 USA. RP Youle, RJ (reprint author), NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20815 USA. NR 8 TC 12 Z9 12 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1534-5807 J9 DEV CELL JI Dev. Cell PD MAR PY 2005 VL 8 IS 3 BP 298 EP 299 DI 10.1016/j.devcel.2005.02.003 PG 2 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA 906CK UT WOS:000227617900002 PM 15737923 ER PT J AU Belsky, J Booth-LaForce, CL Bradley, R Brownell, C Burchinal, M Campbell, SB Clarke-Stewart, KA Friedman, SL Hirsh-Pasek, K Knoke, B Marshall, N McCartney, K Morrison, FJ O'Brien, M Owen, MT Payne, CC Pianta, R Spieker, S Vandell, DL Weinraub, M Nicolopoulou, A AF Belsky, J Booth-LaForce, CL Bradley, R Brownell, C Burchinal, M Campbell, SB Clarke-Stewart, KA Friedman, SL Hirsh-Pasek, K Knoke, B Marshall, N McCartney, K Morrison, FJ O'Brien, M Owen, MT Payne, CC Pianta, R Spieker, S Vandell, DL Weinraub, M Nicolopoulou, A CA NICHD Early Child Care Res Network TI Pathways to reading: The role of oral language in the transition to reading SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID METALINGUISTIC AWARENESS; PHONOLOGICAL SENSITIVITY; EMERGENT LITERACY; CHILDREN; SKILLS; ABILITIES; IMPAIRMENT; DISABILITY; DEFICITS; MODEL AB What is the role of oral language in reading competence during the transition to school? Is oral language in preschool best conceptualized as vocabulary knowledge or as more comprehensive language including grammar, vocabulary, and semantics? These questions were examined longitudinally using 1,137 children from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development. Children were followed from age 3 through 3rd grade, and the results suggest that oral language conceptualized broadly plays both a direct and an indirect role in word recognition during the transition to school and serves as a better foundation for early reading skill than does vocabulary alone. Implications of these findings are discussed in terms of both theoretical models of early reading and practical implications for policy and assessment. C1 NICHD, Early Child Care Res Network, Rockville, MD 20852 USA. RP Belsky, J (reprint author), NICHD, Early Child Care Res Network, 6100 Execut Blvd,Room 4B05, Rockville, MD 20852 USA. RI Marshall, Nancy/C-3428-2012 NR 64 TC 209 Z9 210 U1 7 U2 22 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0012-1649 EI 1939-0599 J9 DEV PSYCHOL JI Dev. Psychol. PD MAR PY 2005 VL 41 IS 2 BP 428 EP 442 DI 10.1037/0012-1649.41.2.428 PG 15 WC Psychology, Developmental SC Psychology GA 908AD UT WOS:000227758600012 ER PT J AU Touger, L Looker, HC Krakoff, J Lindsay, RS Cook, V Knowler, WC AF Touger, L Looker, HC Krakoff, J Lindsay, RS Cook, V Knowler, WC TI Early growth in offspring of diabetic mothers SO DIABETES CARE LA English DT Article ID IMPAIRED GLUCOSE-TOLERANCE; PIMA INDIAN WOMEN; BIRTH-WEIGHT; INTRAUTERINE ENVIRONMENT; CHILDHOOD; CHILDREN; OBESITY; PREGNANCY; INFANTS; COMPLICATIONS AB OBJECTIVE - By age 5 years, offspring of diabetic mothers (ODMs) are heavier and have altered glucose metabolism compared with offspring of mothers without diabetes (non-DMs). This study evaluates the growth pattern of ODMs before the age of 5 years. RESEARCH DESIGN AND METHODS - Anthropometric measures (z scores) from birth, 1.5 years, and 7.7 years in Pima Indian children were compared by maternal diabetes status. RESULTS - After adjustment for earlier gestational age at delivery (37.8 vs. 39.3 weeks, P < 0.01), ODMs were heavier at birth (z score birth weight 0.49 vs. -0.04, P < 0.01) than non-DMs. At age 1.5 years, ODMs were shorter than the non-DMs (z score = -0.24 vs. 0.12, P < 0.01) but their weight and relative weight (RW; weight adjusted for age, sex, and length or height) were similar. From birth to 1.5 years, ODMs showed significant "catch down" of weight compared with non-DMs (change in weight z score from birth to 1.5 years of ODMs and non-DMs was -0.56 and 0.12, respectively, P < 0.01). By age 7.7 years, ODMs were heavier (weight z score 0.89 vs. -0.07, P < 0.01) but had similar height as non-DMs. Differences in glucose and insulin concentrations at age 7.7 years were dependent on RW. CONCLUSIONS - ODMs had a dramatically different growth pattern from that of nonDMs. Gestational age-adjusted birth weight was higher. During the first 1.5 postnatal years, the change in weight z score and attained height were reduced. Subsequently, height caught up to that of non-DMs, while weight gain greatly exceeded that of non-DMs. C1 NIDDK, Diabet Epidemiol & Clin Res Sect, Phoenix, AZ 85014 USA. RP Touger, L (reprint author), NIDDK, Diabet Epidemiol & Clin Res Sect, 1550 E Indian Sch Rd, Phoenix, AZ 85014 USA. EM ltouger@mail.nih.gov NR 31 TC 28 Z9 29 U1 0 U2 0 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 MAR PY 2005 VL 28 IS 3 BP 585 EP 589 DI 10.2337/diacare.28.3.585 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 903ME UT WOS:000227429200014 PM 15735192 ER PT J AU Cusick, M Meleth, AD Agron, E Fisher, MR Reed, GF Knatterud, GL Barton, FB Davis, MD Ferris, FL Chew, EY AF Cusick, M Meleth, AD Agron, E Fisher, MR Reed, GF Knatterud, GL Barton, FB Davis, MD Ferris, FL Chew, EY CA Early Treatment Diabetic Retinopat TI Associations of mortality and diabetes complications in patients with type 1 and type 2 diabetes - Early Treatment Diabetic Retinopathy Study Report no. 27 SO DIABETES CARE LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; CARDIOVASCULAR-DISEASE MORTALITY; CORONARY-HEART-DISEASE; VASCULAR-DISEASE; RISK-FACTORS; FOLLOW-UP; CLINICAL PROTEINURIA; NONDIABETIC SUBJECTS; MEXICAN-AMERICANS; MELLITUS AB OBJECTIVE - Diabetes is a leading cause of morbidity and mortality. The purpose of this study is to assess the associations between diabetes complications and mortality in the Early Treatment Diabetic Retinopathy Study (ETDRS). RESEARCH DESIGN AND METHODS - We examined demographic, clinical, and laboratory characteristics of the 3,711 subjects enrolled in the ETDRS, a randomized controlled clinical trial designed to evaluate the role of laser photocoagulation and aspirin therapy for diabetic retinopathy. The outcome assessed was all-cause mortality. Multivariable Cox proportional hazards regression was used to assess associations between diabetes complications and mortality for type 1 and type 2 diabetes separately. RESULTS - The 5-year estimates of all-cause mortality were 5.5 and 18.9% for patients with type 1 and type 2 diabetes, respectively. In patients with type 1 diabetes, amputation (hazard ratio [HR] 5.08 [95% CI 2.06-12.54]) and poor visual acuity (1.74 [1.10-2.75]) remained significantly associated with mortality, after adjusting for other diabetes complication's and baseline characteristics. In patients with type 2 diabetes, macrovascular disease and worsening levels of nephropathy, neuropathy, retinopathy, and visual acuity are associated with progressively increasing risks of mortality, after controlling for other baseline risk factors. CONCLUSIONS - Amputation is the strongest predictor for mortality in. patients. with type 1 diabetes. All complications independently predict mortality in patients with type 2 diabetes. There is an increased risk for mortality as the degree of each complication worsens. Additional studies are needed to investigate the effectiveness of tertiary prevention to decrease mortality in these patients. C1 NEI, NIH, Bethesda, MD 20892 USA. NIH, Howard Hughes Med Inst, Bethesda, MD 20892 USA. Univ Wisconsin, Dept Ophthalmol, Madison, WI USA. Maryland Med Res Inst, Baltimore, MD USA. EMMES, Rockville, MD USA. RP Chew, EY (reprint author), NEI, NIH, Bldg 10,CRC,Rm 3-2531,10 Ctr Dr,MSC 1204, Bethesda, MD 20892 USA. EM echew@nei.nih.gov FU Intramural NIH HHS [Z99 EY999999] NR 72 TC 61 Z9 64 U1 0 U2 5 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 MAR PY 2005 VL 28 IS 3 BP 617 EP 625 DI 10.2337/diacare.28.3.617 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 903ME UT WOS:000227429200020 PM 15735198 ER PT J AU Simons-Morton, DG Genuth, S Byington, RP Gerstein, HC Friedewald, WT AF Simons-Morton, DG Genuth, S Byington, RP Gerstein, HC Friedewald, WT TI The burden of treatment failure in type 2 diabetes - Response SO DIABETES CARE LA English DT Letter C1 NHLBI, NIH, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA. Case Western Reserve Univ, Div Clin & Mol Endocrinol, Cleveland, OH 44106 USA. Wake Forest Univ, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA. McMaster Univ, Dept Med, Hamilton, ON, Canada. Columbia Univ, Mailman Sch Publ Hlth, Dept Biostat, New York, NY USA. Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA. RP Simons-Morton, DG (reprint author), NHLBI, NIH, Div Epidemiol & Clin Applicat, 6701 Rockledge Dr,MSC 7936,Room 8130, Bethesda, MD 20892 USA. EM simonsd@nhlbi.nih.gov NR 1 TC 2 Z9 2 U1 0 U2 0 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 MAR PY 2005 VL 28 IS 3 BP 761 EP 762 DI 10.2337/diacare.28.3.761 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 903ME UT WOS:000227429200054 PM 15735233 ER PT J AU Basson, MD Bartoshuk, LM DiChello, SZ Panzini, L Weiffenbach, JM Duffy, VB AF Basson, MD Bartoshuk, LM DiChello, SZ Panzini, L Weiffenbach, JM Duffy, VB TI Association between 6-n-propylthiouracil (PROP) bitterness and colonic neoplasms SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE colon cancer; diet; vegetable intake; polyps; bitter taste; genetics ID GENETIC TASTE SENSITIVITY; CANCER RISK; ORAL SENSATION; DIETARY INTERVENTION; COLORECTAL ADENOMAS; FOOD ACCEPTANCE; ALCOHOL INTAKE; HIGH-FIBER; LOW-FAT; PERCEPTION AB Inadequate vegetable intake appears to increase colon cancer risk. Since genetic variation in taste influences vegetable preference, we tested associations between bitterness of 6-n-propylthiouracil (PROP), a measure of taste genetics, and number of colonic polyps, a measure of colon cancer risk, in 251 men who underwent screening lower endoscopy. Patients used the general Labeled Magnitude Scale to rate bitterness of 1.6 mg PROP delivered via filter paper. A subset of 86 patients reported weekly vegetable intakes, excluding salad or potatoes. PROP bitterness correlated significantly with polyp number, an effect separate from age-associated increases in polyp number. The PROP-polyp relationship was strongest in men over 66 years, and older men with polyps were most likely to be overweight or obese. In the subset reporting vegetable intake, men who tasted PROP as more bitter consumed fewer vegetables. These preliminary findings suggest that taste genetics may influence colon cancer risk, possibly through intake of vegetables. C1 Wayne State Univ, Dept Surg, Detroit, MI USA. John D Dingell VA Med Ctr, Dept Surg, Detroit, MI USA. Yale Univ, Sch Med, Dept Surg, New Haven, CT 06510 USA. Yale Univ, Sch Med, Dept Med, New Haven, CT 06510 USA. Vet Affairs Med Ctr, Vet Hlth Adm, Bay Pines, FL USA. Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA. RP Duffy, VB (reprint author), Univ Connecticut, Sch Allied Hlth, 358 Mansfield Rd,Box U-101, Storrs, CT 06269 USA. EM Valerie.duffy@uconn.edu FU NIDCD NIH HHS [DC00283] NR 62 TC 46 Z9 47 U1 2 U2 11 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD MAR PY 2005 VL 50 IS 3 BP 483 EP 489 DI 10.1007/s10620-005-2462-7 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 910PK UT WOS:000227943800012 PM 15810630 ER PT J AU Kuznetsov, A AF Kuznetsov, A TI Integer 64-bit optimizations SO DR DOBBS JOURNAL LA English DT Article C1 NIH, Bethesda, MD 20892 USA. EM kuznetsov@yahoo.com NR 0 TC 0 Z9 0 U1 0 U2 0 PU MILLER FREEMAN, INC PI SAN FRANCISCO PA 600 HARRISON ST,, SAN FRANCISCO, CA 94107 USA SN 1044-789X J9 DR DOBBS J JI Dr. Dobbs J. PD MAR PY 2005 VL 30 IS 3 BP 36 EP 38 PG 3 WC Computer Science, Software Engineering SC Computer Science GA 893BW UT WOS:000226695300008 ER PT J AU Lukashev, DE Ohta, A Sitkovsky, MV AF Lukashev, DE Ohta, A Sitkovsky, MV TI Physiological regulation of acute inflammation by A(2A) adenosine receptor SO DRUG DEVELOPMENT RESEARCH LA English DT Review DE adenosine; inflammation; tissue damage; A(2A) receptor ID LYMPHOCYTE-T ACTIVATION; PROTEIN-KINASE; PURINERGIC RECEPTOR; EXTRACELLULAR ATP; MAST-CELLS; RELEASE; INHIBITION; MICE; MECHANISMS; PROTECTION AB The activation of Gs-coupled A(2A) adenosine receptor on the surface of immune cells increases levels of immunosuppressive cyclic AMP and leads to inhibition of secretion of proinflammatory cytokines, which, in turn, results in downregulation of acute inflammation. The role of A(2A) receptors in the regulation of inflammation appears to be non-redundant. Small doses of inflammatory stimulus induce high levels of proinflammatory cytokines and extensive tissue injury in A2A receptor-deficient (Adora2a(-/-)) mice leading to death due to unregulated inflammatory damage. The gene-dose effect of A2A receptor expression in T cells suggests that there are no spare A2A receptors and that the final outcome of immune cell activation may be dependent on the number of these receptors on the individual immune cells. Heterozygous (Adora2a(+/-)) mice express decreased levels of A2A receptor on the surface and adenosine-induced cAMP-accumulation of immune cells was lower than in wild-type. Thus, the number of A2A receptors determines cAMP response to adenosine and may pre-determine the immunosuppressive role of adenosine. (c) 2005 Wiley-Liss, Inc. C1 NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Lukashev, DE (reprint author), NIAID, Immunol Lab, NIH, Bldg 10,Rm 11N311,10 Ctr Dr,MSC-1892, Bethesda, MD 20892 USA. EM dlukashev@niaid.nih.gov RI Lukashev, Dmitriy/F-8133-2010 NR 53 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 0272-4391 J9 DRUG DEVELOP RES JI Drug Dev. Res. PD MAR PY 2005 VL 64 IS 3 BP 172 EP 177 DI 10.1002/ddr.10428 PG 6 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 941ZX UT WOS:000230253800004 ER PT J AU Cheung, C Yu, AM Ward, JM Krausz, KW Akiyama, TE Feigenbaum, L Gonzalez, FJ AF Cheung, C Yu, AM Ward, JM Krausz, KW Akiyama, TE Feigenbaum, L Gonzalez, FJ TI The CYP2E1-humanized transgenic mouse: Role of CYP2E1 in acetaminophen hepatotoxicity SO DRUG METABOLISM AND DISPOSITION LA English DT Article ID RAT-LIVER CYTOCHROME-P-450; HUMAN CYP3A4 GENE; MONOCLONAL-ANTIBODIES; POSTTRANSCRIPTIONAL REGULATION; OXIDATIVE STRESS; INDUCIBLE RAT; HEPG2 CELLS; P450 2E1; IN-VITRO; CHLORZOXAZONE AB The cytochrome P450 (P450) CYP2E1 enzyme metabolizes and activates a wide array of toxicological substrates, including alcohols, the widely used analgesic acetaminophen, acetone, benzene, halothane, and carcinogens such as azoxymethane and dimethylhydrazine. Most studies on the biochemical and pharmacological actions of CYP2E1 are derived from studies with rodents, rabbits, and cultured hepatocytes; therefore, extrapolation of the results to humans can be difficult. Creating "humanized" mice by introducing the human CYP2E1 gene into Cyp2e1-null mice can circumvent this disadvantage. A transgenic mouse line expressing the human CYP2E1 gene was established. Western blot and high-performance liquid chromatography/ mass spectrometry analyses revealed human CYP2E1 protein expression and enzymatic activity in the liver of CYP2E1-humanized mice. Treatment of mice with the CYP2E1 inducer acetone demonstrated that human CYP2E1 was inducible in this transgenic model. The response to the CYP2E1 substrate acetaminophen was explored in the CYP2E1-humanized mice. Hepatotoxicity, resulting from the CYP2E1-mediated activation of acetaminophen, was demonstrated in the livers of CYP2E1-humanized mice by elevated serum alanine aminotransferase levels, increased hepatocyte necrosis, and decreased P450 levels. These data establish that in this humanized mouse model, human CYP2E1 is functional and can metabolize and activate different CYP2E1 substrates such as chlorzoxazone, p-nitrophenol, acetaminophen, and acetone. CYP2E1-humanized mice will be of great value for delineating the role of human CYP2E1 in ethanol-induced oxidative stress and alcoholic liver damage. They will also function as an important in vivo tool for predicting drug metabolism and disposition and drug-drug interactions of chemicals that are substrates for human CYP2E1. C1 NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NIAID, Comparat Med Branch, NIH, Bethesda, MD 20892 USA. SoBran Inc, Bethesda, MD USA. Sci Applicat Int Corp, Lab Anim Sci Program, NCI, Frederick, MD USA. RP Gonzalez, FJ (reprint author), NCI, Lab Metab, Ctr Canc Res, NIH, Bldg 37,Room 3106,9000 Rockville Pike, Bethesda, MD 20892 USA. EM fjgonz@helix.nih.gov NR 57 TC 79 Z9 84 U1 2 U2 8 PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA SN 0090-9556 J9 DRUG METAB DISPOS JI Drug Metab. Dispos. PD MAR PY 2005 VL 33 IS 3 BP 449 EP 457 DI 10.1124/dmd.104.002402 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 897NE UT WOS:000227010100021 PM 15576447 ER PT J AU Marsh, AA Ambady, N Kleck, RE AF Marsh, AA Ambady, N Kleck, RE TI The effects of fear and anger facial expressions on approach- and avoidance-related behaviors SO EMOTION LA English DT Article ID HUMAN AMYGDALA; ARM FLEXION; EXTENSION; DOMINANCE; ATTITUDES; RESPONSES; EMOTION; GENDER AB The facial expressions of fear and anger are universal social signals in humans. Both expressions have been frequently presumed to signify threat to perceivers and therefore are often used in studies investigating responses to threatening stimuli. Here the authors show that the anger expression facilitates avoidance-related behavior in participants, which supports the notion of this expression being a threatening stimulus. The fear expression, on the other hand, facilitates approach behaviors in perceivers. This contradicts the notion of the fear expression as predominantly threatening or aversive and suggests it may represent an affiliative stimulus. Although the fear expression may signal that a threat is present in the environment. the effect of the expression on conspecifics may be in part to elicit approach. C1 Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA. Tufts Univ, Dept Psychol, Medford, MA 02155 USA. Dartmouth Coll, Dept Psychol & Brain Sci, Hanover, NH 03755 USA. RP Marsh, AA (reprint author), NIMH, Mood & Anxiety Disorders Program, 15K N Dr,MSC 2670, Bethesda, MD 20892 USA. EM amarsh@post.harvard.edu NR 31 TC 182 Z9 187 U1 5 U2 48 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 1528-3542 J9 EMOTION JI Emotion PD MAR PY 2005 VL 5 IS 1 BP 119 EP 124 DI 10.1037/1528-3542.5.1.119 PG 6 WC Psychology, Experimental SC Psychology GA 908DS UT WOS:000227768200011 PM 15755225 ER PT J AU Mutsuga, N Shahar, T Verbalis, JG Xiang, CC Brownstein, MJ Gainer, H AF Mutsuga, N Shahar, T Verbalis, JG Xiang, CC Brownstein, MJ Gainer, H TI Regulation of gene expression in magnocellular neurons in rat supraoptic nucleus during sustained hypoosmolality SO ENDOCRINOLOGY LA English DT Article ID ZINC-FINGER GENE; LIM DOMAIN; HYPOTHALAMONEUROHYPOPHYSEAL SYSTEM; TYROSINE-HYDROXYLASE; ZEBRAFISH FOREBRAIN; OSMOTIC STIMULATION; MESSENGER-RNAS; PROTEIN LMO4; VASOPRESSIN; IDENTIFICATION AB Hypoosmolality produces a dramatic inhibition of vasopressin (VP) and oxytocin gene expression in the supraoptic nucleus ( SON). This study examines the effect of sustained hypoosmolality on global gene expression in the oxytocin and VP magnocellular neurons of the hypothalamo-neurohypophysial system, to identify genes associated with the magnocellular neuron's adaptation to this physiological condition. Using laser microdissection of the SON, T7-based linear amplification of its RNA, and a 35,319-element cDNA microarray, we compare gene expression profiles between SONs in normoosmolar ( control), 1-desamino-[8-D-arginine]-VP-treated normoosmolar, and hypoosmolar rats. We found 4959 genes with statistically significant differences in expression between normosmolar control and the hypoosmolar SONs, with 1564 of these differing in expression by more than 2-fold. These genes serve a wide variety of functions, and most were up-regulated in gene expression in hypoosmolar compared with control SONs. Of these, 90 were preferentially expressed in the SON, and 44 coded for transcription-related factors, of which 15 genes were down-regulated and 29 genes were up-regulated in the hypoosmolar rat SONs. None of these transcription-related factor genes significantly changed in expression after sustained 1-desamino-[8-D-arginine]-VP-treatment alone, indicating that these changes were associated with the hypoosmolar state and not due solely to a decreased activity in the SON. Quantitative in situ hybridization histochemistry was selectively used to confirm and extend these microarray observations. These results indicate that the hypoosmolar state is accompanied by a global, but selective, increase in expression of a wide variety of regulatory genes in the SON. C1 NINDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Dept Med, Div Endocrinol & Metab, Washington, DC 20007 USA. NIMH, Genet Lab, NIH, Bethesda, MD 20892 USA. RP Gainer, H (reprint author), NINDS, Neurochem Lab, NIH, Bethesda, MD 20892 USA. EM gainerh@ninds.nih.gov NR 80 TC 23 Z9 23 U1 1 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 2005 VL 146 IS 3 BP 1254 EP 1267 DI 10.1210/en.2004-1202 PG 14 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 897WC UT WOS:000227035400034 PM 15591143 ER PT J AU Zavacki, AM Ying, H Christoffolete, MA Aerts, G So, E Harney, JW Cheng, SY Larsen, PR Bianco, AC AF Zavacki, AM Ying, H Christoffolete, MA Aerts, G So, E Harney, JW Cheng, SY Larsen, PR Bianco, AC TI Type 1 iodothyronine deiodinase is a sensitive marker of peripheral thyroid status in the mouse SO ENDOCRINOLOGY LA English DT Article ID MESSENGER-RIBONUCLEIC-ACID; HORMONE RECEPTOR ISOFORMS; CENTRAL-NERVOUS-SYSTEM; GENE-EXPRESSION; BETA-RECEPTOR; GLYCEROL-3-PHOSPHATE DEHYDROGENASE; TARGETED MUTATION; RESPONSE ELEMENT; MICE; RAT AB Mice with one thyroid hormone receptor (TR) alpha-1 allele encoding a dominant negative mutant receptor (TRalpha1(PV/+)) have persistently elevated serum T-3 levels (1.9-fold above normal). They also have markedly increased hepatic type 1 iodothyronine deiodinase (D1) mRNA and enzyme activity (4- to 5-fold), whereas other hepatic T-3-responsive genes, such as Spot14 and mitochondrial alpha-glycerol phosphate dehydrogenase (alpha-GPD), are only 0.7-fold and 1.7-fold that of wild-type littermates (TRalpha1(+/+)). To determine the cause of the disproportionate elevation of D1, TRalpha1(+/+) and TRalpha1(PV/+) mice were rendered hypothyroid and then treated with T-3. Hypothyroidism decreased hepatic D1, Spot14, and alpha-GPD mRNA to similar levels in TRalpha1(+/+) and TRalpha1(PV/+) mice, whereas T-3 administration caused an approximately 175-fold elevation of D1 mRNA but only a 3- to 6-fold increases in Spot14 and alpha-GPD mRNAs. Interestingly, the hypothyroidism-induced increase in cerebrocortical type 2 iodothyronine deiodinase activity was 3 times greater in the TRalpha1(PV/+) mice, and these mice had no T-3-dependent induction of type 3 iodothyronine deiodinase. Thus, the marked responsiveness of hepatic D1 to T-3 relative to other genes, such as Spot14 and alpha-GPD, explains the relatively large effect of the modest increase in serum T-3 in the TRalpha1(PV/+) mice, and TRalpha plays a key role in T-3-dependent positive and negative regulation of the deiodinases in the cerebral cortex. C1 Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Thyroid Sect, Boston, MA 02115 USA. Katholieke Univ Leuven, Lab Comparat Endocrinol, B-3000 Louvain, Belgium. NCI, Gene Regulat Sect, Mol Biol Lab, Bethesda, MD 20892 USA. RP Zavacki, AM (reprint author), Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Thyroid Sect, 77 Ave Louis Pasteur,HIM 641, Boston, MA 02115 USA. EM azavacki@rics.bwh.harvard.edu RI Bianco, Antonio/A-4965-2008 OI Bianco, Antonio/0000-0001-7737-6813 FU NIDDK NIH HHS [DK44128, DK65765] NR 40 TC 80 Z9 80 U1 1 U2 9 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 2005 VL 146 IS 3 BP 1568 EP 1575 DI 10.1210/en.2004-1392 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 897WC UT WOS:000227035400069 PM 15591136 ER PT J AU Klauda, JB Sandler, SI AF Klauda, JB Sandler, SI TI Global distribution of methane hydrate in ocean sediment SO ENERGY & FUELS LA English DT Article ID GAS-HYDRATE; PHASE-EQUILIBRIA; BLAKE RIDGE; THERMODYNAMIC PROPERTIES; SOUTHERN-OCEAN; SEA-FLOOR; MARGIN; CONSTRAINTS; MUDSTONES; CYCLES AB In this paper, we present an equilibrium thermodynamic model to accurately predict the maximum depth of hydrate stability in the seafloor, including the effects of water salinity, hydrate confinement in pores, and the distribution of pore sizes in natural sediments. This model uses sediment type, geothermal gradient, and seafloor depth as input to predict the thickness of the hydrate zone. Using this hydrate model and a mass-transfer description for hydrate formation, we have also developed a predictive method for the occurrence of methane hydrates in the ocean. Based on this information, a prediction for the distribution of methane hydrate in ocean sediment is presented on a 1 degrees latitude by 1 degrees longitude (1 degrees x 1 degrees) global grid. From this detailed prediction, we estimate that there is a total volume of 1.2 x 10(17) m(3) of methane gas (expanded to atmospheric conditions), or, equivalently, 74 400 Gt of CH4 in ocean hydrates, which is 3 orders of magnitude larger than worldwide conventional natural gas reserves. Of this number, we estimate that 4.4 x 10(16) m(3) of methane expanded to standard temperature and pressure (STP) exists on the continental margins. C1 Univ Delaware, Dept Chem Engn, Ctr Mol & Engn Thermodynam, Newark, DE 19716 USA. RP Klauda, JB (reprint author), NHLBI, Lab Computat Biol, NIH, Bldg 50,Rm 3308,50 S Dr, Bethesda, MD 20892 USA. EM klauda@helix.nih.gov RI Klauda, Jeffery/A-4345-2008; Sandler, Stanley/A-8866-2009 NR 61 TC 183 Z9 210 U1 9 U2 72 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0887-0624 EI 1520-5029 J9 ENERG FUEL JI Energy Fuels PD MAR-APR PY 2005 VL 19 IS 2 BP 459 EP 470 DI 10.1021/ef049798o PG 12 WC Energy & Fuels; Engineering, Chemical SC Energy & Fuels; Engineering GA 908II UT WOS:000227780300018 ER PT J AU Bonassi, S Ugolini, D Kirsch-Volders, M Stromberg, U Vermeulen, R Tucker, JD AF Bonassi, S Ugolini, D Kirsch-Volders, M Stromberg, U Vermeulen, R Tucker, JD TI Human population studies with cytogenetic biomarkers: Review of the literature and future prospectives SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Review DE chromosomal aberrations; micronucleus test; molecular epidemiology; review; environmental exposure; risk assessment ID SISTER-CHROMATID EXCHANGES; CHROMOSOME-ABERRATION FREQUENCIES; EXPOSED GREENHOUSE WORKERS; PREDICT HUMAN CANCER; DNA-REPAIR GENES; S-TRANSFERASE M1; HUMAN-LYMPHOCYTES; PERIPHERAL-BLOOD; IN-VITRO; MOLECULAR EPIDEMIOLOGY AB Cytogenetic biomarkers are by far the most frequently used endpoints in human population studies. Their sensitivity for measuring exposure to genotoxic agents and their role as early predictors of cancer risk have contributed to this success. In this article, we present an overview of the last 25 years of population studies with cytogenetic biomarkers, describing the evolution of this research and addressing the most promising innovations for the future. The evaluation has been restricted to the most popular assays, i.e., chromosomal aberrations (CAs) and micronucleus (MN), which are considered to be causally related to early stages of chronic diseases, especially cancer, and may therefore play a major role in prevention. An extensive literature search covering the period 1 January 1980 to 31 December 2003 was performed using the Medline/PubMed database. A total of 833 population studies using CAs and 434 using matched MN inclusion criteria were included in the analysis. We report the distribution of selected papers by year of publication, country, language, agents investigated, and methods employed. The state of the art and future prospects regarding cytogenetic techniques and epidemiologic and statistical methods are discussed. The role of susceptibility and its potential impact on genotoxic damage are discussed with special attention to the effect of major genetic polymorphisms on the baseline frequency of CAs and micronuclei. Environ. Mol. Mutagen. 45:258-270, 2005. (c) 2005 Wiley-Liss, Inc. C1 Ist Nazl Ric Canc, Unit Environm Epidemiol & Biostat, I-16132 Genoa, Italy. Univ Genoa, Dipartimento Oncol Biol & Genet, I-16126 Genoa, Italy. Free Univ Brussels, Lab Cellulaire Genet, Brussels, Belgium. Lund Univ, Dept Occupat & Environm Med, S-22100 Lund, Sweden. NCI, Occupat & Environm Epidemiol Branch, Rockville, MD USA. Wayne State Univ, Dept Biol Sci, Detroit, MI 48202 USA. RP Bonassi, S (reprint author), Ist Nazl Ric Canc, Unit Environm Epidemiol & Biostat, Largo Rosanna Benzi 10, I-16132 Genoa, Italy. EM stefano.bonassi@istge.it RI Vermeulen, Roel/F-8037-2011; OI Vermeulen, Roel/0000-0003-4082-8163; bonassi, stefano/0000-0003-3833-6717 NR 86 TC 155 Z9 164 U1 1 U2 7 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. PD MAR-APR PY 2005 VL 45 IS 2-3 BP 258 EP 270 DI 10.1002/em.20115 PG 13 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 914XX UT WOS:000228262500016 PM 15688363 ER PT J AU Allegretta, M Ardell, SK Sullivan, LM Jacobson, S Mortreux, F Wattel, E Albertini, RJ AF Allegretta, M Ardell, SK Sullivan, LM Jacobson, S Mortreux, F Wattel, E Albertini, RJ TI HPRT mutations, TCR gene rearrangements, and HTLV-1 integration sites define in vivo T-cell clonal lineages SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS LA English DT Article DE HPRT mutations; T-lymphocytes; T-cell receptors; HTLV-1; HAM/TSP ID TROPICAL SPASTIC PARAPARESIS; VIRUS TYPE-I; SYSTEMIC LUPUS-ERYTHEMATOSUS; DEPENDENT DIABETES-MELLITUS; INFECTED CIRCULATING CELLS; PERIPHERAL-BLOOD; MUTANT FREQUENCY; MUTATOR PHENOTYPE; HUMAN-POPULATION; LYMPHOCYTES AB HPRT mutations in vivo in human T-lymphocytes are useful probes for mechanistic investigations. Molecular analyses of isolated mutants reveal their underlying mutational changes as well as the T-cell receptor (TCR) gene rearrangements present in the cells in question. The latter provide temporal reference points for other perturbations in the in vivo clones as well as evidence of clonal relationships among mutant isolates. Immunological studies and investigations of genomic instability have benefited from such analyses. A method is presented describing a T-cell lineage analysis in a patient with HTLV-1 infection. Lineage reconstruction of an in vivo proliferating HPRT mutant clone allows timing of the integration event to a postthymic differentiated cell prior to the occurrence of HPRT mutations. Environ. Mol. Mutagen. 45:326337,2005. (c) 2005 Wiley-Liss, Inc. C1 Univ Vermont, Dept Pathol, Burlington, VT 05405 USA. BioMosa, Burlington, VT USA. NINDS, Viral Immunol Sect, Neuroimmunol Branch, Bethesda, MD 20892 USA. Univ Lyon 1, CNRS, UMR5537, Ctr Leon Berard, F-69365 Lyon, France. Hop Edouard Herriot, Serv Hematol, Lyon, France. RP Albertini, RJ (reprint author), Univ Vermont, Dept Pathol, Burlington, VT 05405 USA. EM r.albertini@biomosaics.com RI mortreux, franck/M-5944-2014 FU NCI NIH HHS [1 R43 CA88587]; PHS HHS [1 R21A1056191] NR 54 TC 2 Z9 2 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. PD MAR-APR PY 2005 VL 45 IS 2-3 BP 326 EP 337 DI 10.1002/em.20120 PG 12 WC Environmental Sciences; Genetics & Heredity; Toxicology SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology GA 914XX UT WOS:000228262500020 PM 15744741 ER PT J AU Bonner, MR Lee, WJ Sandler, DA Hoppin, JA Dosemeci, M Alavanja, MCR AF Bonner, MR Lee, WJ Sandler, DA Hoppin, JA Dosemeci, M Alavanja, MCR TI Occupational exposure to carbofuran and the incidence of cancer in the Agricultural Health Study SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE agriculture; cancer incidence; carbofuran; lung cancer; pesticides ID LUNG-CANCER; ENDOTOXIN EXPOSURE; CARBAMATE PESTICIDES; UNITED-STATES; RISK; MORTALITY; MICE; INDUCTION; LYMPHOMA; FARMERS AB Carbofuran is a carbamate insecticide registered for use on a variety of food crops including corn, alfalfa, rice, and tobacco. An estimated 5 million pounds of carbofuran is used annually in the United States, and 45% of urban African-American women have detectable levels of carbofuran in their plasma. Nitrosated carbofuran has demonstrated mutagenic properties. We examined exposure to carbofuran and several tumor sites among 49,877 licensed pesticide applicators from Iowa and North Carolina enrolled in the Agricultural Health Study. We obtained information regarding years of use, frequency of use in an average year, and when use began for 22 pesticides using self-administered questionnaires. Poisson regression was used to calculate rate ratios (RR) and 95% confidence intervals (Cls) adjusting for potential confounders. Lung cancer risk was 3-fold higher for those with > 109 days of lifetime exposure to carbofuran (RR = 3.05; 95% Cl, 0.94-9.87) compared with those with < 9 lifetime exposure days, with a significant dose-response trend for both days of use per year and total years of use. However, carbofuran use was not associated with lung cancer risk when nonexposed persons were used as the referent. In addition, carbofuran exposure was not associated with any other cancer site examined. Although carbamate pesticides are suspected human carcinogens, these results should be interpreted cautiously because there was no a priori hypothesis specifically linking carbofuran to lung cancer. C1 NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Korea Univ, Coll Med, Dept Prevent Med, Seoul 136701, South Korea. Natl Inst Environm Hlth Sci, Epidemiol Branch, Res Triangle Pk, NC USA. RP Bonner, MR (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 8121,MSC 7240, Bethesda, MD 20892 USA. EM bonnerm@mail.nih.gov OI Sandler, Dale/0000-0002-6776-0018 NR 30 TC 33 Z9 42 U1 0 U2 7 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 MAR PY 2005 VL 113 IS 3 BP 285 EP 289 DI 10.1289/ehp.7451 PG 5 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 903MM UT WOS:000227430100036 PM 15743716 ER PT J AU Pi, JB Yamauchi, H Sun, GF Yoshida, T Aikawa, H Fujimoto, W Iso, H Cui, RZ Waalkes, MP Kumagai, Y AF Pi, JB Yamauchi, H Sun, GF Yoshida, T Aikawa, H Fujimoto, W Iso, H Cui, RZ Waalkes, MP Kumagai, Y TI Vascular dysfunction in patients with chronic arsenosis can be reversed by reduction of arsenic exposure SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE arsenic; cGMP; endothelial dysfunction; intervention study; nitric oxide ID NITRIC-OXIDE; OXIDATIVE STRESS; DRINKING-WATER; BANGLADESH; CHINESE AB Chronic arsenic exposure causes vascular diseases associated with systematic dysfunction of endogenous nitric oxide. Replacement of heavily arsenic-contaminated drinking water with low-arsenic water is a potential intervention strategy for arsenosis, although the reversibility of arsenic intoxication has not established. In the present study, we examined urinary excretion of cyclic guanosine 3',5'-monophosphate (cGMP), a second messenger of the vasoactive effects of nitric oxide, and signs and symptoms for peripheral vascular function in 54 arsenosis patients before and after they were supplied with low-arsenic drinking water in an endemic area of chronic arsenic poisoning in Inner Mongolia, China. The arsenosis patients showed a marked decrease in urinary excretion of cGMP (mean +/- SEM: male, 37.0 +/- 6.1; female, 37.2 +/- 5.4 nmol/mmol creatinine), and a 13-month period of consuming low-arsenic drinking water reversed this trend (male, 68.0 +/- 5.6; female, 70.6 +/- 3.0 nmol/mmol creatinine) and improved peripheral vascular response to cold stress. Our intervention study indicates that peripheral vascular disease in arsenosis patients can be reversed by exposure cessation and has important implications for the public health approach to arsenic exposure. C1 Univ Tsukuba, Grad Sch Comprehens Human Sci, Dept Environm Med, Doctoral Programs Med Sci, Tsukuba, Ibaraki 3058575, Japan. Univ Tsukuba, Grad Sch Comprehens Human Sci, Dept Publ Hlth, Doctoral Programs Med Sci, Tsukuba, Ibaraki 3058575, Japan. Univ Tsukuba, Grad Sch Med Sci, Tsukuba, Ibaraki 305, Japan. Natl Canc Inst, Comparat Carcinogenesis Lab, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA. St Marianna Univ, Sch Med, Dept Prevent Med, Kawasaki, Kanagawa, Japan. China Med Univ, Sch Publ Hlth, Dept Labor Hyg & Occupat Hlth, Shenyang, Peoples R China. Asahikawa Med Coll, Dept Publ Hlth, Asahikawa, Hokkaido 078, Japan. Tokai Univ, Sch Med, Dept Environm Hlth, Hiratsuka, Kanagawa 25912, Japan. Kawasaki Med Univ, Dept Dermatol, Kurashiki, Okayama, Japan. RP Kumagai, Y (reprint author), Univ Tsukuba, Grad Sch Comprehens Human Sci, Dept Environm Med, Doctoral Programs Med Sci, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. EM yk-em-tu@md.tsukuba.ac.jp NR 17 TC 18 Z9 20 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 MAR PY 2005 VL 113 IS 3 BP 339 EP 341 DI 10.1289/ehp.7471 PG 3 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 903MM UT WOS:000227430100045 PM 15743725 ER PT J AU Krewski, D Lubin, JH Zielinski, JM Alavanja, M Catalan, VS Field, RW Klotz, JB Letourneau, EG Lynch, CF Lyon, JI Sandler, DP Schoenberg, JB Steck, DJ Stolwijk, JA Weinberg, C Wilcox, HB AF Krewski, D Lubin, JH Zielinski, JM Alavanja, M Catalan, VS Field, RW Klotz, JB Letourneau, EG Lynch, CF Lyon, JI Sandler, DP Schoenberg, JB Steck, DJ Stolwijk, JA Weinberg, C Wilcox, HB TI Residential radon and risk of lung cancer - A combined analysis of 7 north American case-control studies SO EPIDEMIOLOGY LA English DT Article ID INDOOR RADON; EXPOSURE ASSESSMENT; NONSMOKING WOMEN; GAS EXPOSURE; SWEDEN; MINERS; CHINA; FINLAND; GERMANY; ERRORS AB Background: Underground miners exposed to high levels of radon have an excess risk of lung cancer. Residential exposure to radon is at much lower levels, and the risk of lung cancer with residential exposure is less clear. We conducted a systematic analysis of pooled data from all North American residential radon studies. Methods: The pooling project included original data from 7 North American case-control studies, all of which used long-term a-track detectors to assess residential radon concentrations. A total of 3662 cases and 4966 controls were retained for the analysis. We used conditional likelihood regression to estimate the excess risk of lung cancer. Results: Odds ratios (ORs) for lung cancer increased with residential radon concentration. The estimated OR after exposure to radon at a concentration of 100 Bq/m(3) in the exposure time window 5 to 30 years before the index date was 1.11 (95% confidence interval = 1.00-1.28). This estimate is compatible with the estimate of 1.12 (1.02-1.25) predicted by downward extrapolation of the miner data. There was no evidence of heterogeneity of radon effects across studies. There was no apparent heterogeneity in the association by sex, educational level, type of respondent (proxy or self), or cigarette smoking, although there was some evidence of a decreasing radon-associated lung cancer risk with age. Analyses restricted to subsets of the data with presumed more accurate radon dosimetry resulted in increased estimates of risk. Conclusions: These results provide direct evidence of an association between residential radon and lung cancer risk, a finding predicted using miner data and consistent with results from animal and in vitro studies. C1 Univ Ottawa, Inst Populat Hlth, McL Ctr Populat Hlth Risk Assessment, Ottawa, ON K1N 6N5, Canada. NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Hlth Canada, Healthy Environm & Consumer Safety Branch, Ottawa, ON K1A 0L2, Canada. NCI, Occupat Epidemiol Branch, Div Canc Epidemiol & Genet, Washington, DC USA. Lakehead Univ, Ctr Excellence Children & Adolescents Special Nee, Thunder Bay, ON P7B 5E1, Canada. Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA. Univ Iowa, Coll Publ Hlth, Dept Environm & Occupat Hlth, Iowa City, IA USA. Dept Hlth & Sr Serv, Trenton, NJ USA. Hlth Canada, Radiat Protect Bur, Hlth Protect Branch, Ottawa, ON K1A 0L2, Canada. Univ Utah, Dept Family & Prevent Med, Salt Lake City, UT 84112 USA. Natl Inst Environm Hlth Sci, Epidemiol Branch, Res Triangle Pk, NC USA. St Johns Univ, Dept Phys, Collegeville, MN 56321 USA. Yale Univ, Sch Med, New Haven, CT USA. Natl Inst Environm Hlth Sci, Biostat Branch, Res Triangle Pk, NC USA. RP Krewski, D (reprint author), Univ Ottawa, Inst Populat Hlth, McL Ctr Populat Hlth Risk Assessment, 1 Stewart St,Room 320, Ottawa, ON K1N 6N5, Canada. EM dkrewski@uottawa.ca OI Sandler, Dale/0000-0002-6776-0018 FU NCI NIH HHS [R01 CA85942]; NIEHS NIH HHS [P30 ES05695] NR 51 TC 258 Z9 282 U1 5 U2 35 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD MAR PY 2005 VL 16 IS 2 BP 137 EP 145 DI 10.1097/01.ede.0000152522.80261.e3 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 898MF UT WOS:000227080200001 PM 15703527 ER PT J AU Cooper, GS Klebanoff, MA Promislow, J Brock, JW Longnecker, MP AF Cooper, GS Klebanoff, MA Promislow, J Brock, JW Longnecker, MP TI Polychlorinated biphenyls and menstrual cycle characteristics SO EPIDEMIOLOGY LA English DT Article ID CHLORINATED HYDROCARBONS; POSTMENARCHEAL PERIOD; ETHNIC-DIFFERENCES; FISH CONSUMPTION; RHESUS-MONKEYS; SERUM; PCB; EXPOSURE; LENGTH; WOMEN AB Background: Experimental studies in nonhuman primates provide evidence that low-level exposure to persistent organochlorine pollutants such as polychlorinated biphenyls (PCBs) may affect aspects of their menstrual cycle, including cycle length, regularity, and bleeding duration. Few studies have examined these associations in humans. Methods: We used data from 2314 pregnant women who participated in the Collaborative Perinatal Project, a cohort study that enrolled pregnant women in the 1960s in 12 centers in the United States. Information about usual (prepregnancy) menstrual cycle length, regularity, bleeding duration, and dysmenorrhea was collected at enrollment, and 11 PCBs and p,p'-DDE (1,1-dichloro-2,2bis(p-chlorophenyl)ethylene) (DDE) were measured in stored blood samples collected during the third trimester of pregnancy. We used multivariate linear and logistic regression to examine the association between organochlorine levels and menstrual cycles, adjusting for demographic factors, cholesterol, and triglycerides. Results: Total PCBs were positively associated with increasing menstrual cycle length (adjusted difference across 5 categories of PCB exposure = 0.7 days, trend-test P value = 0.02). Irregular cycles were slightly more frequent among those in the 2 highest categories of PCB exposure (odds ratio for highest category = 1.5; 95% confidence interval = 0.70-3.3), and there also was some evidence of an association with DDE. The strengths of these associations increased with various exclusions made to decrease potential misclassification of the outcome and the exposures. There was little evidence for associations between DDE or PCBs and bleeding duration, heavy bleeding, or dysmenorrhea. Conclusions: This study supports experimental studies in monkeys showing an effect of low-dose PCB exposure on menstrual function. C1 NIEHS, Epidemiol Branch, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA. NICHHD, Div Epidemiol Stat & Prevent Res, Dept Hlth & Human Serv, NIH, Rockville, MD USA. Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Atlanta, GA 30341 USA. RP Cooper, GS (reprint author), NIEHS, Epidemiol Branch, Dept Hlth & Human Serv, NIH, MD A3-05,POB 12233, Res Triangle Pk, NC 27709 USA. EM cooper1@niehs.nih.gov OI Longnecker, Matthew/0000-0001-6073-5322 NR 40 TC 36 Z9 38 U1 1 U2 5 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD MAR PY 2005 VL 16 IS 2 BP 191 EP 200 DI 10.1097/01.ede.0000152913.12393.86 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 898MF UT WOS:000227080200007 PM 15703533 ER PT J AU Rauscher, GH Sandler, DP AF Rauscher, GH Sandler, DP TI Validating cancer histories in deceased relatives SO EPIDEMIOLOGY LA English DT Article ID REPORTED FAMILY-HISTORY; ACUTE-LEUKEMIA; ACCURACY; IDENTIFICATION; POPULATION; REGISTRY AB Background: A family history of cancer is a marker of familially shared genetic and environmental risk factors for cancer but is subject to inaccurate and biased reporting. Methods: In a case-control study of adult acute leukemia, we examined the accuracy of cancer reports in deceased first-degree relatives using death certificates and the National Death Index (NDI). We submitted information on 1058 deceased relatives to the NDI or civil vital statistics registries. Social security numbers were not available and identifying information was incomplete. Results: A death certificate was located for 70% of records sent to state registries but for only 32% of records submitted to the NDI. Death certificates confirmed 95% of relatives reported to be cancer-free and 83% of those reported to have any form of cancer. Confirmation of cancer of specific sites ranged from 50% for breast cancer and 54% for leukemia to 86% for prostate cancer. Conclusions: State searches may be preferable to the NDI when identifying information is incomplete. C1 Univ Illinois, Div Epidemiol & Biostat, Sch Publ Hlth, Chicago, IL 60612 USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. RP Rauscher, GH (reprint author), Univ Illinois, Div Epidemiol & Biostat, Sch Publ Hlth, SPHPI M-C 923,1603 W Taylor, Chicago, IL 60612 USA. EM garthr@uic.edu OI Rauscher, Garth/0000-0003-0374-944X; Sandler, Dale/0000-0002-6776-0018 FU NCI NIH HHS [CA09330-20, CA57699-06] NR 14 TC 8 Z9 8 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD MAR PY 2005 VL 16 IS 2 BP 262 EP 265 DI 10.1097/01.ede.0000152521.18215.eb PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 898MF UT WOS:000227080200018 PM 15703544 ER PT J AU Ward, MM AF Ward, MM TI Estimating rare disease prevalence from administrative hospitalization databases SO EPIDEMIOLOGY LA English DT Letter ID MULTIPLE-SCLEROSIS; SYSTEMIC-SCLEROSIS; OLMSTED COUNTY; CROHNS-DISEASE; UNITED-STATES; EPIDEMIOLOGY; POPULATION; MINNESOTA; SURVIVAL C1 NIAMS, NIH, Bethesda, MD USA. RP Ward, MM (reprint author), NIAMS, NIH, Bethesda, MD USA. EM wardm1@mail.nih.gov NR 14 TC 10 Z9 10 U1 1 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1044-3983 J9 EPIDEMIOLOGY JI Epidemiology PD MAR PY 2005 VL 16 IS 2 BP 270 EP 271 DI 10.1097/01.ede.0000153643.88019.92 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 898MF UT WOS:000227080200020 PM 15703546 ER PT J AU Rubovszky, B Hajdu, P Krasznai, Z Gaspar, R Waldmann, TA Damjanovich, N Bene, L AF Rubovszky, B Hajdu, P Krasznai, Z Gaspar, R Waldmann, TA Damjanovich, N Bene, L TI Detection of channel proximity by nanoparticle-assisted delaying of toxin binding; a combined patch-clamp and flow cytometric energy transfer study SO EUROPEAN BIOPHYSICS JOURNAL WITH BIOPHYSICS LETTERS LA English DT Article DE interleukin receptor; lipid raft; major histocompatibility complex glycoproteins; potassium channel; very late antigen integrin ID MHC CLASS-II; GATED POTASSIUM CHANNELS; HLA CLASS-I; LYMPHOCYTE KV1.3 CHANNELS; CELL-SURFACE RECEPTORS; LIPID RAFTS; PLASMA-MEMBRANE; K+ CHANNELS; T-CELLS; FUNCTIONAL ASSOCIATION AB Gold nanoparticles of 30 nm diameter bound to cell- surface receptor major histocompatibility complex glycoproteins (MHCI and MHCII), interleukin-2 receptor a subunit (IL-2R alpha), very late antigen-4 (VLA-4) integrin, transferrin receptor, and the receptor-type protein tyrosin phosphatase CD45 are shown by the patch- clamp technique to selectively modulate binding characteristics of Pi(2) toxin, an efficient blocker of K(v)1.3 channels. After correlating the electrophysiological data with those on the underlying receptor clusters obtained by simultaneously conducted flow cytometric energy transfer measurements, the modulation was proved to be sensitive to the density and size of the receptor clusters, and to the locations of the receptors as well. Based on the observation that engagement of MHCII by a monoclonal antibody down-regulates channel current and based on the close nanometer-scale proximity of the MHCI and MHCII glycoproteins, an analogous experiment was carried out when gold nanoparticles bound to MHCI delayed down-regulation of the Kv1.3 current initiated by ligation of MHCII. Localization of Kv1.3 channels in the nanometer-scale vicinity of the MHC-containing lipid rafts is demonstrated for the first time. A method is proposed for detecting receptor-channel or receptor-receptor proximity by observing nanoparticle-induced increase in relaxation times following concentration jumps of ligands binding to channels or to receptors capable of regulating channel currents. C1 Univ Debrecen, Med & Hlth Sci Ctr, Dept Biophys & Cell Biol, H-4012 Debrecen, Hungary. Hungarian Acad Sci, Cell Biophys Res Grp, H-4012 Debrecen, Hungary. NCI, Metab Branch, NIH, Bethesda, MD 20892 USA. RP Bene, L (reprint author), Univ Debrecen, Med & Hlth Sci Ctr, Dept Biophys & Cell Biol, H-4012 Debrecen, Hungary. EM bene@jaguar.dote.hu NR 83 TC 3 Z9 3 U1 1 U2 7 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0175-7571 EI 1432-1017 J9 EUR BIOPHYS J BIOPHY JI Eur. Biophys. J. Biophys. Lett. PD MAR PY 2005 VL 34 IS 2 BP 127 EP 143 DI 10.1007/s00249-004-0436-x PG 17 WC Biophysics SC Biophysics GA 952FG UT WOS:000230988600003 PM 15375639 ER PT J AU Ugolini, D Garrucciu, R AF Ugolini, D Garrucciu, R TI Low impact factor of Italian Journals: another aspect of the poor research funding? SO EUROPEAN JOURNAL OF CANCER LA English DT Editorial Material C1 Univ Genoa, Dept Oncol Biol & Genet, I-16132 Genoa, Italy. Natl Canc Inst, I-16132 Genoa, Italy. Univ Genoa, Dept Oncol Biol & Genet, I-16132 Genoa, Italy. RP Ugolini, D (reprint author), Univ Genoa, Dept Oncol Biol & Genet, Largo R Benzi 10, I-16132 Genoa, Italy. EM donatella.ugolini@istge.it NR 6 TC 3 Z9 3 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD MAR PY 2005 VL 41 IS 4 BP 485 EP 488 DI 10.1016/j.ejca.2004.11.008 PG 4 WC Oncology SC Oncology GA 910NG UT WOS:000227937800010 PM 15737550 ER PT J AU Kelloff, GJ Sigman, CC AF Kelloff, GJ Sigman, CC TI New science-based endpoints to accelerate oncology drug development SO EUROPEAN JOURNAL OF CANCER LA English DT Article DE drug development; oncology; surrogate endpoint; biomarker; genomics; proteomics; functional imaging; molecular imaging ID FAMILIAL ADENOMATOUS POLYPOSIS; CIRCULATING ENDOTHELIAL-CELLS; UNITED-STATES FOOD; BREAST-CANCER; PROSTATE-CANCER; COLORECTAL-CANCER; CLINICAL-TRIALS; OVARIAN-CANCER; CYCLOOXYGENASE-2 INHIBITOR; PROTEOMIC PATTERNS AB Although several new oncology drugs have reached the market, more than 80% of drugs for all indications entering clinical development do not get marketing approval, with many failing late in development often in Phase III trials, because of unexpected safety issues or difficulty determining efficacy, including confounded outcomes. These factors contribute to the high costs of oncology drug development and clearly show the need for faster, more cost-effective strategies for evaluating oncology drugs and better definition of patients who will benefit from treatment. Remarkable advances in the understanding of neoplastic progression at the cellular and molecular levels have spurred the discovery of molecularly targeted drugs. This progress along with advances in imaging and bio-assay technologies are the basis for describing and evaluating new biomarker endpoints as well as for defining other biomarkers for identifying patient populations, potential toxicity, and providing evidence of drug effect and efficacy. Definitions and classifications of these biomarkers for use in oncology drug development are presented in this paper. Science-based and practical criteria for validating biomarkers have been developed including considerations of mechanistic plausibility, available methods and technology, and clinical feasibility. New promising tools for measuring biomarkers have also been developed and are based on genomics and proteomics, direct visualisation by microscopy (e.g., confocal microscopy and computer-assisted image analysis of cellular features), nanotechnologies, and direct and remote imaging (e.g., fluorescence endoscopy and anatomical, functional and molecular imaging techniques). The identification and evaluation of potential surrogate endpoints and other biomarkers require access to and analysis of large amounts of data, new technologies and extensive research resources. Further, there is a requirement for a convergence of research, regulatory and drug developer thinking - an effort that will not be accomplished by individual scientists or research institutions. Research collaborations are needed to foster development of these new endpoints and other biomarkers and, in the United States (US), include ongoing efforts among the Food and Drug Administration (FDA), National Cancer Institute (NCI), academia, and industry. (c) 2004 Elsevier Ltd. All rights reserved. C1 NCI, Canc Imaging Program, Div Canc Treatment & Diagnosis, Bethesda, MD 20892 USA. CCS Assoc, Mountain View, CA USA. RP Kelloff, GJ (reprint author), NCI, Canc Imaging Program, Div Canc Treatment & Diagnosis, Execut Plaza N Room 6038,9000 Rockville Pike, Bethesda, MD 20892 USA. EM kelloffg@mail.nih.gov NR 87 TC 55 Z9 62 U1 2 U2 7 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD MAR PY 2005 VL 41 IS 4 BP 491 EP 501 DI 10.1016/j.ejca.2004.12.006 PG 11 WC Oncology SC Oncology GA 910NG UT WOS:000227937800012 PM 15737552 ER PT J AU Weber, A Liu, J Collins, I Levens, D AF Weber, A Liu, J Collins, I Levens, D TI TFIIH modulates the c-myc promoter configuration to fine-tune transcriptional activity SO EUROPEAN JOURNAL OF CELL BIOLOGY LA English DT Meeting Abstract CT Annual Meeting of the Deutsche-Gesellschaft-fur-Zellbiologie CY MAR 16-19, 2005 CL Heidelberg, GERMANY SP Deutsch Gesell Zellbiol C1 Univ Mainz, Inst Pathol, D-6500 Mainz, Germany. NCI, Gene Regulat Sect, Pathol Lab, NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU URBAN & FISCHER VERLAG PI JENA PA BRANCH OFFICE JENA, P O BOX 100537, D-07705 JENA, GERMANY SN 0171-9335 J9 EUR J CELL BIOL JI Eur. J. Cell Biol. PD MAR PY 2005 VL 84 SU 55 BP 17 EP 17 PG 1 WC Cell Biology SC Cell Biology GA 918FM UT WOS:000228527700011 ER PT J AU Huff, T Philp, D Gho, YS Hannappel, E Kleinman, HK AF Huff, T Philp, D Gho, YS Hannappel, E Kleinman, HK TI Beta-thymosins stimulate directional migration of human umbilical vein endothelial cells and promote angiogenesis. SO EUROPEAN JOURNAL OF CELL BIOLOGY LA English DT Meeting Abstract CT Annual Meeting of the Deutsche-Gesellschaft-fur-Zellbiologie CY MAR 16-19, 2005 CL Heidelberg, GERMANY SP Deutsch Gesell Zellbiol C1 Univ Erlangen Nurnberg, Fac Med, Inst Biochem, D-91054 Erlangen, Germany. NIH, CDBRB, NIDCR, Bethesda, MD 20892 USA. EM t.huff@biochem.uni-erlangen.de NR 0 TC 0 Z9 0 U1 0 U2 1 PU URBAN & FISCHER VERLAG PI JENA PA BRANCH OFFICE JENA, P O BOX 100537, D-07705 JENA, GERMANY SN 0171-9335 J9 EUR J CELL BIOL JI Eur. J. Cell Biol. PD MAR PY 2005 VL 84 SU 55 BP 55 EP 55 PG 1 WC Cell Biology SC Cell Biology GA 918FM UT WOS:000228527700105 ER PT J AU Kania, G Corbeil, D Fuchs, J Tarosov, KV Blyszczuk, P Huttner, WB Boheler, KR Wobus, AM AF Kania, G Corbeil, D Fuchs, J Tarosov, KV Blyszczuk, P Huttner, WB Boheler, KR Wobus, AM TI The somatic stem cell marker prominin-1/CD133 is expressed in embryonic stem cell-derived progenitors SO EUROPEAN JOURNAL OF CELL BIOLOGY LA English DT Meeting Abstract CT Annual Meeting of the Deutsche-Gesellschaft-fur-Zellbiologie CY MAR 16-19, 2005 CL Heidelberg, GERMANY SP Deutsch Gesell Zellbiol C1 IPK Gatersleben, D-06466 Gatersleben, Germany. Univ Dresden, Dresden, Germany. Max Planck Inst Mol Cell Biol & Genet, Dresden, Germany. NIH, Baltimore, MD USA. EM wobusam@ipk-gatersleben.de NR 0 TC 0 Z9 0 U1 0 U2 0 PU URBAN & FISCHER VERLAG PI JENA PA BRANCH OFFICE JENA, P O BOX 100537, D-07705 JENA, GERMANY SN 0171-9335 J9 EUR J CELL BIOL JI Eur. J. Cell Biol. PD MAR PY 2005 VL 84 SU 55 BP 76 EP 76 PG 1 WC Cell Biology SC Cell Biology GA 918FM UT WOS:000228527700159 ER PT J AU Kohl, S Varsanyi, B Antunes, GA Baumann, B Hoyng, CB Jagle, H Rosenberg, T Kellner, U Lorenz, B Salati, R Jurklies, B Farkas, A Andreasson, S Weleber, RG Jacobson, SG Rudolph, G Castellan, C Dollfus, H Legius, E Anastasi, M Bitoun, P Lev, D Sieving, PA Munier, FL Zrenner, E Sharpe, LT Cremers, FPM Wissinger, B AF Kohl, S Varsanyi, B Antunes, GA Baumann, B Hoyng, CB Jagle, H Rosenberg, T Kellner, U Lorenz, B Salati, R Jurklies, B Farkas, A Andreasson, S Weleber, RG Jacobson, SG Rudolph, G Castellan, C Dollfus, H Legius, E Anastasi, M Bitoun, P Lev, D Sieving, PA Munier, FL Zrenner, E Sharpe, LT Cremers, FPM Wissinger, B TI CNGB3 mutations account for 50% of all cases with autosomal recessive achromatopsia SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE CNGB3 mutations; ACHM3 locus; achromatopsia; rod monochromacy; total colorblindness; cyclic nucleotide-gated channel ID GATED CATION CHANNEL; ALPHA-SUBUNIT; CONE DEGENERATION; TOTAL COLOURBLINDNESS; GENE; GNAT2; PHOTORECEPTORS; DYSTROPHY; CLONING; LOCUS AB Achromatopsia is a congenital, autosomal recessively inherited disorder characterized by a lack of color discrimination, low visual acuity (<0.2), photophobia, and nystagmus. Mutations in the genes for CNGA3, CNGB3, and GNAT2 have been associated with this disorder. Here, we analyzed the spectrum and prevalence of CNGB3 gene mutations in a cohort of 341 independent patients with achromatopsia. In 163 patients, CNGB3 mutations could be identified. A total of 105 achromats carried apparent homozygous mutations, 44 were compound (double) heterozygotes, and 14 patients had only a single mutant allele. The derived CNGB3 mutation spectrum comprises 28 different mutations including 12 nonsense mutations, eight insertions and/or deletions, five putative splice site mutations, and three missense mutations. Thus, the majority of mutations in the CNGB3 gene result in significantly altered and/or truncated polypeptides. Several mutations were found recurrently, in particular a 1 bp deletion, c.1148delC, which accounts for over 70% of all CNGB3 mutant alleles. In conclusion, mutations in the CNGB3 gene are responsible for approximately 50% of all patients with achromatopsia. This indicates that the CNGB3/ACHM3 locus on chromosome 8q21 is the major locus for achromatopsia in patients of European origin or descent. C1 Univ Tubingen, Augenklin, Mol Genet Labor, Abt Pathophysiol Sehens & Neuroophthalmol, D-72076 Tubingen, Germany. Semmelweis Univ, Dept Ophthalmol 2, H-1085 Budapest, Hungary. Univ Med Ctr, Dept Human Genet, Nijmegen, Netherlands. Univ Tubingen, Augenklin, Psychophys Labor, Abt Pathophysiol Sehens & Neuroophthalmol, D-72076 Tubingen, Germany. Natl Eye Clin Visually Impaired, Gordon Norrie Ctr Genet Eye Dis, Hellerup, Denmark. Charite, Augenklin, Berlin, Germany. Univ Regensburg, Augenklin, Abt Kinderophthalmol Strabismol & Ophthalmogenet, D-8400 Regensburg, Germany. Univ Essen Gesamthsch, Augenklin, Essen, Germany. IRCCS Eugenio Medea, Bosisio Parini, Italy. Lund Univ, Hosp Eye, Lund, Sweden. Casey Eye Inst, Portland, OR USA. Scheie Eye Inst, Philadelphia, PA USA. Univ Munich, Augenklin, D-8000 Munich, Germany. Reg Hosp Bozen, Clin Genet Serv, Bolzano, Italy. Hop Hautepierre, Serv Genet Med, Strasbourg, France. Katholieke Univ Leuven, Ctr Human Genet, Louvain, Belgium. Univ Palermo, Clin Oculist, Palermo, Italy. Hop Jean Verdier, CHU Paris Nord, Bondy, France. Wolfson Med Ctr, Inst Med Genet, Holon, Israel. NEI, Bethesda, MD 20892 USA. Hop Jules Bonin, Unite Oculogenet, Lausanne, Switzerland. Univ Med Ctr, Dept Ophthalmol, Nijmegen, Netherlands. RP Kohl, S (reprint author), Univ Tubingen, Augenklin, Mol Genet Labor, Abt Pathophysiol Sehens & Neuroophthalmol, Rontgenweg 11, D-72076 Tubingen, Germany. EM susanne.kohl@uni-tuebingen.de; wissinger@uni-tuebingen.de RI Hoyng, C.B./H-8050-2014; Cremers, Frans/A-5625-2014 NR 28 TC 103 Z9 111 U1 1 U2 5 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PD MAR PY 2005 VL 13 IS 3 BP 302 EP 308 DI 10.1038/sj.ejhg.5201269 PG 7 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 899AK UT WOS:000227117100009 PM 15657609 ER PT J AU Belfer, I Buzas, B Evans, C Hipp, H Phillips, G Taubman, J Lorincz, I Lipsky, RH Enoch, MA Max, MB Goldman, D AF Belfer, I Buzas, B Evans, C Hipp, H Phillips, G Taubman, J Lorincz, I Lipsky, RH Enoch, MA Max, MB Goldman, D TI Haplotype structure of the beta adrenergic receptor genes in US Caucasians and African Americans SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE single-nucleotide polymorphism; linkage disequilibrium; haplotype; beta adrenergic receptors; ADRB1; ADRB2; ADRB3 ID BETA-2-ADRENERGIC RECEPTOR; BETA(2)-ADRENERGIC RECEPTOR; ARG16GLY POLYMORPHISM; DILATED CARDIOMYOPATHY; ASSOCIATION ANALYSIS; ASTHMATIC SUBJECTS; HEART-FAILURE; IN-VIVO; BETA(1)-ADRENOCEPTOR; OBESITY AB The beta-adrenergic receptors (beta-AR) are G protein-coupled receptors activated by epinephrine and norepinephrine and are involved in a variety of their physiological functions. Previously, three beta-AR genes (ADRB1, ADRB2 and ADRB3) were resequenced, identifying polymorphisms that were used in genetic association studies of cardiovascular and metabolic disorders. These studies have produced intriguing but inconsistent results, potentially because the known functional variants: ADRB1 Arg389Gly and Gly49Ser, ADRB2 Arg16Gly and Gln27Glu, and ADRB3 Arg64Trp provided an incomplete picture of the total functional diversity at these genes. Therefore, we created marker panels for each beta-AR gene that included the known functional markers and also other markers evenly spaced and with sufficient density to identify haplotype block structure and to maximize haplotype diversity. A total of 27 markers were genotyped in 96 US Caucasians and 96 African Americans. In both populations and for each gene, a single block with little evidence of historical recombination was observed. For each gene, haplotype captured most of the information content of each functional locus, even if that locus was not genotyped, and presumably haplotype would capture the signal from unknown functional loci whose alleles are of moderate abundance. This study demonstrates the utility of using beta-AR gene haplotype maps and marker panels as tools for linkage studies on beta-AR function. C1 Natl Inst Dent & Craniofacial Res, Pain & Neurosensory Mech Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA. NIAAA, Neurogenet Lab, NIH, US Dept HHS, Bethesda, MD 20892 USA. RP Belfer, I (reprint author), NIH, 12420 Parklawn Dr,Suite 451,MSC 8110, Rockville, MD 20852 USA. EM ibelfer@mail.nih.gov RI Goldman, David/F-9772-2010; OI Goldman, David/0000-0002-1724-5405; Lipsky, Robert/0000-0001-7753-1473; Hipp, Heather/0000-0002-1089-3928 FU NIAAA NIH HHS [Z01 AA000301]; NIDCR NIH HHS [Z01 DE00366] NR 41 TC 31 Z9 32 U1 0 U2 2 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1018-4813 J9 EUR J HUM GENET JI Eur. J. Hum. Genet. PD MAR PY 2005 VL 13 IS 3 BP 341 EP 351 DI 10.1038/sj.ejhg.5201313 PG 11 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 899AK UT WOS:000227117100015 PM 15523499 ER PT J AU Goldman, KP Park, CS Kim, M Matzinger, P Anderson, CC AF Goldman, KP Park, CS Kim, M Matzinger, P Anderson, CC TI Thymic cortical epithelium induces self tolerance SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE T lymphocytes; autoimmunity; central tolerance; tissue-specific tolerance; thymus ID T-CELL SELECTION; DIFFERENTIAL-AVIDITY MODEL; POSITIVE SELECTION; NUDE-MICE; INTERCELLULAR TRANSFER; MEDULLARY EPITHELIUM; NEGATIVE SELECTION; SKIN-GRAFTS; ANTIGEN; COMPLEX AB Because of its role in positive selection, the ability of cortical epithelium to induce tolerance is controversial. On the one hand, experiments with transplanted thymuses showed that the recipients were functionally tolerant of all the antigens expressed by the cells of those thymuses, including cells of the cortical epithelium. On the other, the keratin 14 (K14) transgenic mouse strain, which expresses MHC class II on cortical epithelium under the control of the K14 promoter, does not seem to be tolerant of the transgenic MHC molecule. Here we tested whether the lack of tolerance in the K14 mouse might be more apparent than real. We found that K14 mice are indeed completely tolerant of K14 cortical thymic epithelium, whereas they remain reactive to tissues that express the same MHC allele under normal genetic control. These results establish the ability of cortical epithelium to induce central tolerance, and impinge on several of the models concerning positive selection of newly developing T cells. C1 Univ Alberta, Surg Med Res Inst, Dept Surg, Dent Pharm Ctr 1074, Edmonton, AB T6G 2N8, Canada. Univ Alberta, Surg Med Res Inst, Dept Med Microbiol, Edmonton, AB T6G 2N8, Canada. NIAID, Ghost Lab, LCMI, NIH, Bethesda, MD 20892 USA. NIAID, Thym Mol Dev Unit, LCMI, NIH, Bethesda, MD 20892 USA. RP Anderson, CC (reprint author), Univ Alberta, Surg Med Res Inst, Dept Surg, Dent Pharm Ctr 1074, Edmonton, AB T6G 2N8, Canada. EM colinand@ualberta.ca NR 51 TC 19 Z9 19 U1 0 U2 2 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 MAR PY 2005 VL 35 IS 3 BP 709 EP 717 DI 10.1002/eji25675 PG 9 WC Immunology SC Immunology GA 906II UT WOS:000227633900005 PM 15719367 ER PT J AU Goldman, D AF Goldman, D TI Genetic approaches to psychiatric diseases SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Workshop on Neuropsychopharmacology for Young Scientists in Europe CY MAR 12-14, 2004 CL Nice, FRANCE SP European Coll Neuropsychopharmacol C1 NIAAA, Neurogenet Lab, NIH, Rockville, MD 20852 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD MAR PY 2005 VL 15 SU 1 BP S1 EP S2 DI 10.1016/S0924-977X(05)00021-0 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 902DN UT WOS:000227331900002 ER PT J AU Heilig, M AF Heilig, M TI NPY gene in anxiety-related phenotypes and alcohol dependence SO EUROPEAN PSYCHIATRY LA English DT Meeting Abstract C1 NIAAA, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0924-9338 J9 EUR PSYCHIAT JI Eur. Psychiat. PD MAR PY 2005 VL 20 SU 1 BP S17 EP S17 PG 1 WC Psychiatry SC Psychiatry GA 922WE UT WOS:000228869800055 ER PT J AU Lorman, V Podgornik, R Zeks, B AF Lorman, V Podgornik, R Zeks, B TI Correlated and decorrelated positional and orientational order in the nucleosomal core particle mesophases SO EUROPHYSICS LETTERS LA English DT Article ID LIPID-DNA COMPLEXES; COLUMNAR PHASE AB We investigate the orientational order of transverse-polarization vectors of long columns of nucleosomal core particles and their coupling to positional order in high-density mesophases discovered recently. Inhomogeneous polar ordering of these columns precipitates crystallization of the 2D sections with different orientations of the transverse-polarization vector on each column in the unit cell. We propose possible scenarios for going from the 2D hexagonal phase into distorted lamellar and related phases observed experimentally. C1 Univ Montpellier 2, Lab Phys Math & Theor, F-34095 Montpellier, France. Univ Ljubljana, Dept Phys, Fac Math & Phys, SI-1000 Ljubljana, Slovenia. Jozef Stefan Inst, Dept Theoret Phys, SI-1000 Ljubljana, Slovenia. NICHHD, LPSB, NIH, Bethesda, MD 20892 USA. Univ Ljubljana, Fac Med, Inst Biophys, SI-1000 Ljubljana, Slovenia. RP Lorman, V (reprint author), Univ Montpellier 2, Lab Phys Math & Theor, F-34095 Montpellier, France. RI Podgornik, Rudolf/C-6209-2008 OI Podgornik, Rudolf/0000-0002-3855-4637 NR 18 TC 9 Z9 9 U1 0 U2 0 PU E D P SCIENCES PI LES ULIS CEDEX A PA 17, AVE DU HOGGAR, PA COURTABOEUF, BP 112, F-91944 LES ULIS CEDEX A, FRANCE SN 0295-5075 J9 EUROPHYS LETT JI Europhys. Lett. PD MAR PY 2005 VL 69 IS 6 BP 1017 EP 1023 DI 10.1209/epl/i2004-10437-5 PG 7 WC Physics, Multidisciplinary SC Physics GA 917GX UT WOS:000228445900025 ER PT J AU Sohn, Y Kang, S Hallett, M AF Sohn, Y Kang, S Hallett, M TI Corticospinal disinhibition during dual action SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE transcranial magnetic stimulation; motor cortex; dual action; silent period ID TRANSCRANIAL MAGNETIC STIMULATION; SILENT PERIOD; FUNCTIONAL MRI; EXCITABILITY; CORTEX; FORCE; COORDINATION; POTENTIALS; DEFICIT AB When attempting to perform two tasks simultaneously, the human motor as well as the cognitive system shows interference. Such interference often causes altered activation of the cortical area representing each task compared to the single task condition. We investigated changes in corticospinal inhibition during dual action by transcranial magnetic stimulation (TMS). Single-pulse TMS was applied to the left motor cortex, triggered by right leg movement (tibialis anterior muscle) while the right abductor digiti minimi (ADM) muscle was moderately activated (10-20% of the maximal voluntary contraction). The background electromyography (EMG) activity of ADM was measured before and during the leg movement. The silent period (SP) and amplitude of motor evoked potential (MEP) following magnetic stimulation in active ADM were compared for the conditions with and without leg movement. The mean area of the rectified EMG activity of ADM did not alter, while the SP was significantly shortened during leg movement compared to that without leg movement. MEP amplitude was comparable between the two conditions. These results suggest that corticospinal inhibition tested by the SP duration is reduced during the movement of another body part, presumably in order to help maintain muscle force by compensating interference-related alteration in motor cortical activation. C1 NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA. Yonsei Univ, Coll Med, Dept Neurol, Brain Korea 21 Project Med Sci, Seoul, South Korea. Yonsei Univ, Brain Res Inst, Brain Korea 21 Project Med Sci, Seoul, South Korea. RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, NIH, Bldg 10-5n226,10 Ctr Dr, Bethesda, MD 20892 USA. EM hallettm@ninds.nih.gov NR 20 TC 14 Z9 14 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PD MAR PY 2005 VL 162 IS 1 BP 95 EP 99 DI 10.1007/s00221-004-2109-5 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 907TH UT WOS:000227740400011 PM 15502976 ER PT J AU Sinha, D Hose, S Zhang, C Neal, R Ghosh, M O'Brien, TP Sundin, O Goldberg, MF Robison, WG Russell, P Lo, WK Zigler, JS AF Sinha, D Hose, S Zhang, C Neal, R Ghosh, M O'Brien, TP Sundin, O Goldberg, MF Robison, WG Russell, P Lo, WK Zigler, JS TI A spontaneous mutation affects programmed cell death during development of the rat eye SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE apoptosis; eye development; lens denucleation; abnormal development of retina ID LENS FIBER DIFFERENTIATION; TERMINAL DIFFERENTIATION; TRANSCRIPTION FACTOR; TRANSGENIC MICE; BOVINE LENS; MOUSE EYE; DENUCLEATION; DEGRADATION; APOPTOSIS; CATARACT AB We have discovered a spontaneous mutation in the Sprague-Dawley rat with a novel eye phenotype that we have named Nuc1. The Nuc1 mutation behaves as a single semi-dominant locus with an intermediate phenotype in the heterozygotes. Heterozygotes exhibit nuclear cataracts. Homozygous Nucl rats are fully viable and have microphthalmia, retinal abnormalities and disruption of lens structure shortly before birth. The homozygous mutant shows no obvious pathology outside of the eye, indicating that the mutation is highly eye specific in its effects. An unusual feature of the mutation is that it prevents the normal programmed loss of nuclei from lens fiber cells, but does not affect the loss of other organelles. TUNEL, light, and electron microscopic studies show normal intact nuclei in lens fibers, in contrast to many other models with degenerate nuclei and unlike normal lenses where no such nuclei remain. The beaded filament protein, filensin, is down-regulated in fibers of Nuc1, while heat shock cognate 70 is up-regulated. Homozygous retinas are thicker than normal, and TUNEL labeling indicates roughly half the number of apoptotic cells compared to a wild-type retina. The transient layer of Chievitz persists in adult Nucl retina, indicative of delayed development. Hence, Nucl is a novel mutation that could be an eye-specific regulator of apoptosis. (c) 2004 Elsevier Ltd. All rights reserved. C1 Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Sch Med, Dept Ophthalmol, Baltimore, MD 21287 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21287 USA. NIH, NEI, Lab Mechan Ocular Dis, Bethesda, MD USA. Morehouse Sch Med, Dept Anat & Neurobiol, Atlanta, GA USA. RP Sinha, D (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Ophthalmol, Sch Med & Dent, 600 N Wolfe St, Baltimore, MD 21287 USA. EM debasish@jhmi.edu FU NEI NIH HHS [EY05314] NR 52 TC 16 Z9 16 U1 0 U2 2 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 MAR PY 2005 VL 80 IS 3 BP 323 EP 335 DI 10.1016/j.exer.2004.09.014 PG 13 WC Ophthalmology SC Ophthalmology GA 905QI UT WOS:000227584000004 PM 15721615 ER PT J AU Neal, RE Bettelheim, FA Lin, C Winn, KC Garland, DL Zigler, JS AF Neal, RE Bettelheim, FA Lin, C Winn, KC Garland, DL Zigler, JS TI Alterations in human vitreous humour following cataract extraction SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE phacoemulsification; proteome; vitreous; crystallin; dynamic light scattering; viscosity; cataract; surgery ID RETINAL-PIGMENT EPITHELIUM; DYNAMIC LIGHT-SCATTERING; SOLUBLE-PROTEINS; LENS; ACID; GEL; ELECTROPHORESIS; IDENTIFICATION; TRANSTHYRETIN; BIOSYNTHESIS AB Cataract extraction is associated with the risk of posterior vitreous detachment, macular edema and retinal detachment possibly as a result of a disturbance to the vitreous body during surgery. While it is common for lens cortical fiber debris to leak into the vitreous humour during cataract extraction, the extent to which the vitreous humour is altered post-surgery is unknown. The current study examines the integrity of the vitreous humour of pseudophakic and phakic human donor eyes by comparing the proteome, the viscosity and the size distribution of macromolecules in different regions of the vitreous humour from human pseudophakic and phakic donor eyes. Major differences between the proteomes of anterior and posterior vitreous humour were observed in phakic and pseudophakic donor eyes. Seventeen spots identified as complete, modified or cleaved forms of alpha A-, alpha B-, beta A(4)-, beta B-2, and gamma S-crystallins were present in the anterior vitreous humour of all pseudophakic eyes studied. Crystallins were not detected in the posterior vitreous humour of the pseudophakic eye or the vitreous humour of the phakic eye. Significant alterations in abundance and/or modification of transthyretim, alpha antitrypsin, and retinoic acid binding protein were observed in all locations of pseudophakic vitreous humour as compared to phakic samples. In addition, a significant decrease in the number and intensity of protein spots was observed for the posterior vitreous humour of pseudophakic eyes when compared to posterior vitreous humour of phakic eyes. Proteins which were affected include antioxidant proteins and enzymes such as carbonic anhydrase and trisephosphate isomerase. A reversal of the viscosity gradient, anterior to posterior, in the vitreous humour of pseudophakic eyes was observed concomitant with alterations in the distribution of 50 nm particles. These particles are likely primarily composed of hyaluronan. While varying degrees of vitreous degradation may have existed prior to surgery and may have contributed to the cataract formation, in no case did the phakic donor eyes exhibit the same alterations in the vitreous humour proteome, viscosity or particle sizes as did the pseudophakic donor eyes. The examination of phakic/pseudophakic donor eye pairs confirmed that the vitreous humour proteome and structural integrity were very similar in the matched phakic donor eye to eyes from donors with no history of cataract. Even though the number of samples for this study was limited, the observed changes support the hypothesis that alterations in the vitreous humour proteome occur in psuedophakic eyes with concurrent alterations in the structure of the vitreous humor. These modifications of the microenvironment of the retina may contribute to the development of retinal complications following cataract surgery. Published by Elsevier Ltd. C1 NEI, NIH, Bethesda, MD 20892 USA. RP Neal, RE (reprint author), NEI, NIH, 7 Mem Dr,MSC 0703, Bethesda, MD 20892 USA. EM nealr@nei.nih.gov NR 31 TC 47 Z9 48 U1 0 U2 5 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 MAR PY 2005 VL 80 IS 3 BP 337 EP 347 DI 10.1016/j.exer.2004.09.015 PG 11 WC Ophthalmology SC Ophthalmology GA 905QI UT WOS:000227584000005 PM 15721616 ER PT J AU Espinosa-Heidmann, DG Reinoso, MA Pina, Y Csaky, KG Caicedo, A Cousins, SW AF Espinosa-Heidmann, DG Reinoso, MA Pina, Y Csaky, KG Caicedo, A Cousins, SW TI Quantitative enumeration of vascular smooth muscle cells and endothelial cells derived from bone marrow precursors in experimental choroidal neovascularization SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE age-related macular degeneration (AMD); choroidal neovascularization (CNV); macrophages; bone marrow-derived vascular progenitor cells; RPE cells; laser photocoagulation; animal model; cellular composition ID MACULAR DEGENERATION; PHOTODYNAMIC THERAPY; PROGENITOR CELLS; STEM-CELLS; INTRAVITREAL TRIAMCINOLONE; POSTNATAL NEOVASCULARIZATION; GROWTH-FACTOR; UVEAL TRACT; RAT MODEL; AGE AB Choroidal neovascularization (CNV) is characterized by the subretinal invasion of a pathologic new vessel complex from the choriocapillaris. Although CNV is traditionally considered to consist of endothelial cells, the cellular population of CNV is likely more complex in nature, comprising several different cell types. In addition, recent studies suggest that the CNV cell population has a dual origin (circulating versus resident populations). In this study we sought to determine the contribution and origin of different cell types in experimental CNV. Laser-induced CNV was performed on chimeric mice generated by reconstituting C57BL/6 mice with bone marrow from green fluorescent protein (GFP)-transgenic mice. In these mice, bone marrow-derived cells are GFP-labeled. Immunofluorescence staining was used to examine both flatmount preparations of the choroid and cross sections of the posterior pole for macrophages, endothelial cells, vascular smooth muscle cells, retinal pigment epithelial (RPE) cells, lymphocytes, or neutrophils at day 3, 7, 14 and 28 post-laser (n = 5 per group). Cell types present in CNV included macrophages (20% of the cells in CNV), endothelial cells (25%), vascular smooth muscle cells (11%), RPE cells (12%) and non-labeled cells (32%). The macrophage population was mostly derived from circulating monocytes at all timepoints studied (70% were GFP labeled), while endothelial and vascular smooth muscle cells were partly bone marrow derived (50-60% were GFP labeled), and RPE cells appeared to be entirely derived from preexisting tissue resident cells. These results demonstrate that bone marrow-defived progenitor cells contribute significantly to the vascular and inflammatory components of CNV. Knowledge of the cellular composition and origin might help understand the pathogenic mechanisms controlling CNV severity as well as indicate potential targets for therapeutic intervention. (c) 2004 Elsevier Ltd. All rights reserved. C1 Univ Miami, Sch Med, Dept Ophthalmol, Bascom Palmer Eye Inst,William L McKnight Vis Res, Miami, FL 33136 USA. NEI, NIH, Bethesda, MD USA. RP Espinosa-Heidmann, DG (reprint author), Univ Miami, Sch Med, Dept Ophthalmol, Bascom Palmer Eye Inst,William L McKnight Vis Res, 1638 NW 10th Ave, Miami, FL 33136 USA. EM despinosa@med.miami.edu RI Caicedo, Alejandro/F-1202-2010 FU NEI NIH HHS [EY/AY 13318, R03 EY015292] NR 54 TC 45 Z9 52 U1 0 U2 2 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 MAR PY 2005 VL 80 IS 3 BP 369 EP 378 DI 10.1016/j.exer.2004.10.005 PG 10 WC Ophthalmology SC Ophthalmology GA 905QI UT WOS:000227584000008 PM 15721619 ER PT J AU Pereira, MA Tao, LH Wang, W Gunning, WT Lubet, R AF Pereira, MA Tao, LH Wang, W Gunning, WT Lubet, R TI Chemoprevention: Mouse colon and lung tumor bioassay and modulation of DNA methylation as a biomarker SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT 4th International Mouse Lung Tumorigenesis Symposium CY OCT 23-26, 2003 CL Jackson Lab, Bar Harbor, ME HO Jackson Lab DE chemoprevention; colon tumors; dexamethasone; DNA methylation; IGF-II; lung tumors; piroxicam ID FEMALE A/J MICE; NONSTEROIDAL ANTIINFLAMMATORY DRUG; DIFFERENT GENETIC SUSCEPTIBILITY; ABERRANT CRYPT FOCI; CLARA CELL ADENOMA; VINYL CARBAMATE; K-RAS; PULMONARY CARCINOGENESIS; ALLELIC METHYLATION; ETHYL CARBAMATE AB Lung and colon tumors were induced in A/J, C3H, and A/J x C3H (AC3) mice by administering 16 mg/kg vinyl carbamate followed by 6 weekly doses of 12 mg/kg azoxymethane (AOM). Beginning I week after carcinogen treatment, the mice received the chemopreventive agents, dexamethasone or piroxicam, at 0.1 and 75 mg/kg in the diet, respectively. Both AOM and vinyl carbamate induced lung tumors, but only AOM induced colon tumors. The strain sensitivity for both colon and lung tumors was A/J> AC3 > C3H mice. Dexamethasone and piroxicam reduced the multiplicity of colon and lung tumors in A/J and AC3 mice, demonstrating the advantage of a combined colon and lung bioassay. The ability of budesonide, a drug that prevents mouse lung tumors, to modulate DNA methylation in vinyl carbamate-induced lung tumors was also determined. Budesonide administered for only 7 days prior to sacrifice caused a dose-dependent (0.6 to 2.4 mg/kg diet) reversal in tumors of DNA hypomethylation and hypomethylation of the insulin-like growth factor (IGF)-II gene in the differentially methylated region (DMR) 2 region of exons 4 to 5. Longer treatment with budesonide reversed hypomethylation when administered up to the time of sacrifice. These results indicate that reversal of the hypomethylation of DNA and of specific genes in lung tumors may be applicable as a surrogate end-point biomarker for chemoprevention. C1 Med Coll Ohio, Dept Pathol, Toledo, OH 43699 USA. NCI, Chemoprevent Agent Dev Res Grp, Div Canc Chemoprevent, Bethesda, MD 20892 USA. RP Pereira, MA (reprint author), Ohio State Univ, Coll Med & Publ Hlth, Dept Internal Med, 300 W 10th Ave,1148B CHRI, Columbus, OH 43210 USA. EM pereira-1@medctr.osu.edu RI Gunning, William/E-4681-2010 NR 53 TC 6 Z9 6 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PD MAR PY 2005 VL 31 IS 2 BP 145 EP 163 DI 10.1080/01902140490495534 PG 19 WC Respiratory System SC Respiratory System GA 903PV UT WOS:000227439000001 PM 15824018 ER PT J AU Wang, M Wang, Y You, M Devereux, TR AF Wang, M Wang, Y You, M Devereux, TR TI Analysis of the Par2 modifier of pulmonary adenoma formation in mice SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT 4th International Mouse Lung Tumorigenesis Symposium CY OCT 23-26, 2003 CL Jackson Lab, Bar Harbor, ME HO Jackson Lab DE congenic mice; DNA polymerase iota; linkage mapping; mouse lung tumor susceptibility; Par2 ID LUNG-TUMOR SUSCEPTIBILITY; DNA-POLYMERASE-IOTA; SOMATIC HYPERMUTATION; URETHANE-INDUCTION; RESISTANCE LOCUS; BALB/CBYJ MICE; UNITED-STATES; MOUSE STRAINS; FAMILIAL RISK; POL-IOTA AB Inbred strains of mice show various susceptibilities to spontaneous and chemical-induced lung tumorigenesis. Genetic analyses have revealed that lung tumor susceptibilities of inbred mouse strains are governed by quantitative trait loci (QTLs) located on multiple chromosomes. A major lung tumor resistance QTL, designated pulmonary adenoma resistance 2 (Par2), was mapped to the mouse chromosome 18 independently by several groups and accounted for up to 60% phenotype variance between the susceptible A/J and more resistant BALB/c strains. The authors recently conducted studies to positionally clone the Par2 gene. This review summarizes the effort and progress towards the identification of Par2 candidates. C1 NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA. Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA. Washington Univ, Sch Med, Alvin J Siteman Canc Ctr, St Louis, MO USA. RP Devereux, TR (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, 111 Alexander Dr, Res Triangle Pk, NC 27709 USA. EM devereux@niehs.nih.gov FU NCI NIH HHS [R01CA58554, R01CA099147] NR 52 TC 1 Z9 1 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PD MAR PY 2005 VL 31 IS 2 BP 193 EP 204 DI 10.1080/01902140390116517 PG 12 WC Respiratory System SC Respiratory System GA 903PV UT WOS:000227439000004 PM 15828125 ER PT J AU Yao, RS Wang, Y D'Agostini, F Izzotti, A Lubet, RA You, M De Flora, S AF Yao, RS Wang, Y D'Agostini, F Izzotti, A Lubet, RA You, M De Flora, S TI K-ras mutations in lung tumors from p53 mutant mice exposed to cigarette smoke SO EXPERIMENTAL LUNG RESEARCH LA English DT Article; Proceedings Paper CT 4th International Mouse Lung Tumorigenesis Symposium CY OCT 23-26, 2003 CL Jackson Lab, Bar Harbor, ME HO Jackson Lab DE tobacco-smoke; lung tumorigenesis; K-ras mutation; p53 transgenic mice ID TOBACCO-SMOKE; PROTEIN ACCUMULATION; CANCER; GENE; CARCINOGENESIS; CHEMOPREVENTION; A/J AB In this study, we used p53 trangenic mice to investigate whether mice carrying this germline mutation would be susceptible to tobacco smoke-induced lung tumorigenesis. We subjected male transgenic mice and their wild-type littermates to whole-body exposure to environmental cigarette smoke (ECS) for up to 9.5 months. K-ras gene expression was significantly increased, 28 days after ECS exposure, in the apparently healthy lung of p53 mutant mice. An increase of lung tumor incidence and multiplicity was observed in P53 transgenic mice after exposure to ECS for either 5 months, followed by recovery in air for 4.5 months, or 9.5 continuative months of exposure. Conversely, no tumorigenic effect was observed in their wild-type littermates. Sequence analysis of the K-ras gene indicated that mutations had occurred at codon 12, 13 or codon 61 in tumors both from the air control group and tobacco smoke treatment groups. K-ras mutations were found in 100%, 100% and 77% of tumors from animals exposed to air, ECS for 5 months, followed by recovery in air for 4.5 months, and ECS for 9.5 continuative months, respectively. The K-ras mutations were seemingly not related to the p53 genotype of the animals or to ECS exposure. The mutation spectrum was similar in tumors from the different groups. An apparently higher incidence of K-ras codon 12 mutations in the 9.5-months ECS group was not statistically significant. These findings provide evidence that mice carrying a mutant P53 transgene appear to be more sensitive to ECS-induced lung tumors than the corresponding wild-type littermates. K-ras mutations seem to be independent of the p53 status but the early overexpression of this oncogene is related to the P53 status in ECS-exposed mice. These results suggest that tobacco smoke enhances lung tumorigensis primarily through promoting spontaneously occuring K-ras mutations. C1 Univ Genoa, Dept Hlth Sci, I-16132 Genoa, Italy. Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA. Washington Univ, Sch Med, Alvin J Siteman Canc Ctr, St Louis, MO USA. NCI, Chemoprevent Branch, Bethesda, MD 20892 USA. RP De Flora, S (reprint author), Univ Genoa, Dept Hlth Sci, Via A Pastore 1, I-16132 Genoa, Italy. EM sdf@unige.it OI izzotti, alberto/0000-0002-8588-0347 FU NCI NIH HHS [N01-CN-05122, N01-CN-75008] NR 31 TC 15 Z9 16 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0190-2148 J9 EXP LUNG RES JI Exp. Lung Res. PD MAR PY 2005 VL 31 IS 2 BP 271 EP 281 DI 10.1080/0190214059090386 PG 11 WC Respiratory System SC Respiratory System GA 903PV UT WOS:000227439000009 PM 15824025 ER PT J AU Talbott, JF Loy, DN Liu, Y Qiu, MS Bunge, MB Rao, MS Whittemore, SR AF Talbott, JF Loy, DN Liu, Y Qiu, MS Bunge, MB Rao, MS Whittemore, SR TI Endogenous Nkx2.2(+)/Olig2(+) oligodendrocyte precursor cells fail to remyelinate the demyelinated adult rat spinal cord in the absence of astrocytes SO EXPERIMENTAL NEUROLOGY LA English DT Article DE demyelination; remyelination; Nkx2.2; NG2; oligodendrocyte precursor cell; radial glia ID CENTRAL-NERVOUS-SYSTEM; NEURAL STEM-CELL; HOMEODOMAIN TRANSCRIPTION FACTOR; BROMIDE-INDUCED DEMYELINATION; TYPE-1 ASTROCYTES; PROGENITOR-CELL; SCHWANN-CELLS; GLIAL-CELLS; INTERMEDIATE FILAMENT; CNS DEMYELINATION AB Chronic demyelination is a pathophysiologic component of compressive spinal cord injury (SCI) and a characteristic finding in demyelinating diseases including multiple sclerosis (MS). A better characterization of endogenous cells responsible for successful remyelination is essential for designing therapeutic strategies aimed at restoring functional myelin. The present study examined the spatiotemporal response of endogenous oligodendrocyte precursor cells (OPCs) following ethidium. bromide (EB)-induced demyelination of the adult rat spinal cord. Beginning at 2 days post-EB injection (dpi), a robust mobilization of highly proliferative NG2(+) cells within the lesion was observed, none of which expressed the oligodendrocyte lineage-associated transcription factor Nkx2.2. At 7 dpi, a significant upregulation of Nkx2.2 by OPCs within the lesion was observed, 90% of which coexpressed NG2 and virtually all of which coexpressed the bHLH transcription factor Olig2. Despite successful recruitment of Nkx2.2(+)/Olig2(+) OPCs within the lesion, demyelinated axons were not remyelinated by these OPCs in regions lacking astrocytes. Rather, Schwann cell remyelination predominated throughout the central core of the lesion, particularly around blood vessels. Oligodendrocyte remyelination was observed in the astrogliotic perimeter, suggesting a necessary role for astrocytes in oligodendrocyte maturation. In addition, reexpression of the radial glial antigen, RC-I, by reactive astrocytes and ependymal cells was observed following injury. However, these cells did not express the neural stem cell (NSC)-associated transcription factors Sox1 or Sox2, suggesting that the endogenous response is primarily mediated by glial progenitors. In vivo electrophysiology demonstrated a limited and unsustained functional recovery concurrent with endogenous remyelination following EB-induced lesions. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Louisville, Sch Med, Dept Neurol Surg, Kentucky Spinal Cord Injury Res Ctr, Louisville, KY 40202 USA. Univ Louisville, MD PhD Program, Louisville, KY 40202 USA. Univ Louisville, Dept Anat Sci & Neurobiol, Louisville, KY 40202 USA. Univ Utah, Dept Anat Sci & Neurobiol, Salt Lake City, UT 84132 USA. NIA, Neurosci Lab, Baltimore, MD 21224 USA. Univ Miami, Sch Med, Miami Project Cure Paralysis, Miami, FL 33136 USA. Univ Miami, Sch Med, Dept Cell Biol & Anat, Miami, FL 33136 USA. Univ Miami, Sch Med, Dept Neurol Surg, Miami, FL 33136 USA. RP Whittemore, SR (reprint author), Univ Louisville, Sch Med, Dept Neurol Surg, Kentucky Spinal Cord Injury Res Ctr, MDR 616,511 S Floyd St, Louisville, KY 40202 USA. EM swhittemore@louisville.edu FU NCRR NIH HHS [P20 RR015576, P20 RR015576-04, RR15576]; NINDS NIH HHS [NS38665, P01 NS038665, P01 NS038665-040003] NR 71 TC 117 Z9 129 U1 0 U2 6 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD MAR PY 2005 VL 192 IS 1 BP 11 EP 24 DI 10.1016/j.expneurol.2004.05.038 PG 14 WC Neurosciences SC Neurosciences & Neurology GA 899LZ UT WOS:000227147200003 PM 15698615 ER PT J AU Bibbiani, F Costantini, LC Patel, R Chase, TN AF Bibbiani, F Costantini, LC Patel, R Chase, TN TI Continuous dopaminergic stimulation reduces risk of motor complications in parkinsonian primates SO EXPERIMENTAL NEUROLOGY LA English DT Article DE dopamine; Parkinson's disease; dyskinesia; striatum; nigra; implant; polymeric; subcutaneous; apomorphine; ethylene-vinyl acetate ID LEVODOPA THERAPY; DISEASE; APOMORPHINE; MECHANISMS; FLUCTUATIONS; MONKEYS; PATHOPHYSIOLOGY; DYSKINESIAS AB Levodopa or short-acting dopamine (DA) agonist treatment of advanced parkinsonian patients exposes striatal DA receptors to non-physiologic intermittent stimulation that contributes to the development of dyskinesias and other motor complications. To determine whether continuous dopaminergic stimulation can delay or prevent onset of motor complications, four MPTP-lesioned, levodopa-naive cynomolgus monkeys were implanted subcutaneously with apomorphine containing ethylene vinyl acetate rods. Three other MPTP-lesioned monkeys received daily injections of apomorphine. Animals receiving apomorphine rods showed improved motor function ('ON' state) within 1 day of implantation, and remained continually 'ON' for the duration of treatment (up to 6 months) without developing dyskinesias. Injected animals also showed similar improvement in motor function after each apomorphine injection. However, these primates remained 'ON' for only 90 min and within 7-10 days all developed severe dyskinesias. Implanted monkeys evidenced local irritation, which was alleviated by steroid co-therapy. (C) 2004 Elsevier Inc. All rights reserved. C1 NINDS, Expt Therapeut Branch, NIH, Bethesda, MD 20892 USA. Titan Pharmaceut Inc, San Francisco, CA USA. RP Chase, TN (reprint author), NINDS, Expt Therapeut Branch, NIH, Bldg 10,Room 5C103, Bethesda, MD 20892 USA. EM TChase@ninds.nih.gov NR 36 TC 71 Z9 76 U1 0 U2 2 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD MAR PY 2005 VL 192 IS 1 BP 73 EP 78 DI 10.1016/j.expneurol.2004.11.013 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 899LZ UT WOS:000227147200008 PM 15698620 ER PT J AU Dancey, JE AF Dancey, JE TI Inhibitors of the mammalian target of rapamycin SO EXPERT OPINION ON INVESTIGATIONAL DRUGS LA English DT Review DE AP-34573; everolimus; mammalian target of rapamycin; sirolimus; temsirolimus ID TUBEROUS SCLEROSIS COMPLEX; PROSTATE-CANCER CELLS; LYMPHOPROLIFERATIVE-DISEASE TREATMENT; ENDOTHELIAL GROWTH-FACTOR; INDUCIBLE FACTOR 1-ALPHA; CYCLIN D1 EXPRESSION; INDUCED G(1) ARREST; AMINO-ACID; IN-VITRO; PHOSPHATIDYLINOSITOL 3-KINASE AB The mammalian target of rapamycin (mTOR) is a downstream protein kinase of the phosphaticlylinositol 3'-kinase-Akt signalling pathway. As a result of its position within this pathway and its central role in controlling cellular growth, mTOR is viewed as an important target for anticancer therapeutics development. Currently, the mTOR inhibitor rapamycin (sirolimus, Wyeth) and its derivatives ternsirolimus (CCI-779, Wyeth), everolimus (RAD-001, Novartis Pharma AG) and AP-23573 (Ariad Pharmaceuticals) are being evaluated in cancer clinical trials. Preclinical studies suggest that sensitivity to mTOR inhibition may correlate with aberrant activation of the phosphaticlylinositol T-kinase pathway and/or with aberrant expression of cell-cycle regulatory or antiapoptotic proteins. Clinical trial results show that mTOR inhibitors are generally well tolerated and may induce prolonged stable disease and even tumour regressions in a subset of patients. Questions remain regarding optimal dose, schedule, patient selection and combination strategies for this novel class of agents. C1 NCI, DCTD, CTEP, Invest Drug Branch, Rockville, MD 20852 USA. RP Dancey, JE (reprint author), NCI, DCTD, CTEP, Invest Drug Branch, 6130 Execut Blvd,Room 7131, Rockville, MD 20852 USA. EM danceyj@crep.nci.nih.gov NR 115 TC 67 Z9 76 U1 0 U2 4 PU ASHLEY PUBLICATIONS LTD PI LONDON PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB, ENGLAND SN 1354-3784 J9 EXPERT OPIN INV DRUG JI Expert Opin. Investig. Drugs PD MAR PY 2005 VL 14 IS 3 BP 313 EP 328 DI 10.1517/13543784 PG 16 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 914VU UT WOS:000228256900008 PM 15833062 ER PT J AU Watanabe, A Cornelison, R Hostetter, G AF Watanabe, A Cornelison, R Hostetter, G TI Tissue microarrays: applications in genomic research SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS LA English DT Review DE high-throughput; IHC; ISH; standardization; TMA ID METHYLACYL-COA RACEMASE; IN-SITU HYBRIDIZATION; PROSTATE-CANCER PROGRESSION; INTRAEPITHELIAL NEOPLASIA; EXPRESSION ANALYSIS; BREAST-CARCINOMA; GENE-EXPRESSION; DRUG DISCOVERY; VALIDATION; SPECIMENS AB The widespread application of tissue microarrays in cancer research and the clinical pathology laboratory demonstrates a versatile and portable technology. The rapid integration of tissue microarrays into biomarker discovery and validation processes reflects the forward thinking of researchers who have pioneered the high-density tissue microarray. The precise arrangement of hundreds of archival clinical tissue samples into a composite tissue microarray block is now a proven method for the efficient and standardized analysis of molecular markers. With applications in cancer research, tissue microarrays are a valuable tool in validating candidate markers discovered in highly sensitive genome-wide microarray experiments. With applications in clinical pathology, tissue microarrays; are used widely in immunohistochemistry quality control and quality assurance. The timeline of a biomarker implicated in prostate neoplasia, which was identified by complementary DNA expression profiling, validated by tissue microarrays; and is now used as a prognostic immunohistochemistry marker, is reviewed. The tissue microarray format provides opportunities for digital imaging acquisition, image processing and database integration. Advances in digital imaging help to alleviate previous bottlenecks in the research pipeline, permit computer image scoring and convey telepathology opportunities for remote image analysis. The tissue microarray industry now includes public and private sectors with varying degrees of research utility and offers a range of potential tissue microarray applications in basic research, prognostic oncology and drug discovery. C1 Translat Genomics Res Inst, TMA Core Serv, Phoenix, AZ 85004 USA. George Washington Univ, Inst Biomed Sci, Mol & Cellular Oncol Program, Washington, DC 20037 USA. NHGRI, NIH, Canc Genet Branch, Bethesda, MD 20892 USA. RP Watanabe, A (reprint author), Translat Genomics Res Inst, TMA Core Serv, 445 N 5th St, Phoenix, AZ 85004 USA. EM ghostetter@tgen.org NR 67 TC 29 Z9 31 U1 0 U2 5 PU FUTURE DRUGS LTD PI LONDON PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEYY CENTRAL, LONDON N3 1QB, ENGLAND SN 1473-7159 J9 EXPERT REV MOL DIAGN JI Expert Rev. Mol. Diagn. PD MAR PY 2005 VL 5 IS 2 BP 171 EP 181 DI 10.1586/14737159.5.2.171 PG 11 WC Pathology SC Pathology GA 940SF UT WOS:000230163700005 PM 15833047 ER PT J AU Tong, H Bernstein, D Murphy, E Steenbergen, C AF Tong, H Bernstein, D Murphy, E Steenbergen, C TI The role of beta-adrenergic receptor signaling in cardioprotection SO FASEB JOURNAL LA English DT Article DE Gs protein; PKA; ischemic preconditioning ID PROTEIN-KINASE-A; BETA(2)-ADRENERGIC RECEPTOR; G(I) PROTEINS; HEART; PHOSPHORYLATION; REPERFUSION; INHIBITION; ISCHEMIA; SYSTEM; INJURY AB This study examines the role of the Beta2-adrenergic receptor (Beta2-AR) in cardioprotection. The Beta2-AR couples to Gs and Gi proteins. Gs activates PKA, which phosphorylates the receptor and switches Beta2-AR coupling from Gs to Gi. Prior to 20 min of global ischemia, mouse hearts were either perfused for 30 min without treatment (control), treated with 10 nmol/L of isoproterenol (ISO) for 5 min followed by 5 min washout, or preconditioned with 4 cycles of 5 min ischemia and 5 min reflow (PC). Recovery of left ventricular developed pressure (LVDP) and infarct size were measured. Intermittent ISO treatment improved post-ischemic recovery of LVDP (58.5+/-4.8% vs. 22.0+/-6.3% in control) and reduced infarct size (31.0+/-2.4% vs. 53.0+/-4.6% in control). The Gi inhibitor pertussis toxin blocked the ISO-induced improvement in postischemic LVDP and infarct size. To test the role of Beta2-AR in PC, we studied mice lacking Beta2-AR (Beta2-AR-/-) and found that PC had no effect on postischemic LVDP or infarct size in Beta2-AR-/-. To test whether PKA is required for the PC and ISO-induced protection, hearts were treated with the PKA inhibitors PKI and H-89. We found that PKI and H-89 blocked the PC- and ISO-induced improvement in postischemic LVDP and infarct size. These data show an important role for Beta2-AR in cardioprotection and support the novel hypothesis that preconditioning involves switching of Beta2-AR coupling from Gs to Gi. C1 Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA. Stanford Univ, Dept Pediat, Stanford, CA USA. NIEHS, Lab Signal Transduct, Res Triangle Pk, NC USA. RP Steenbergen, C (reprint author), Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA. EM steen001@mc.duke.edu FU NHLBI NIH HHS [HL-39752, HL-51535, R01 HL039752] NR 22 TC 47 Z9 50 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR PY 2005 VL 19 IS 3 BP 983 EP + DI 10.1096/fj.04-3067fje PG 14 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 910AH UT WOS:000227901300041 PM 15802488 ER PT J AU Yamagishi, H Fitzgerald, DH Sein, T Walsh, TJ O'Connell, BC AF Yamagishi, H Fitzgerald, DH Sein, T Walsh, TJ O'Connell, BC TI Saliva affects the antifungal activity of exogenously added histatin 3 towards Candida albicans SO FEMS MICROBIOLOGY LETTERS LA English DT Article DE antifungal; candida; histatin; saliva; histatin degradation; rabbit submandibular gland saliva ID HISTIDINE-RICH POLYPEPTIDES; RESISTANT DERIVATIVES; AMPHOTERICIN-B; AIDS PATIENTS; IN-VITRO; FLUCONAZOLE; HIV; BINDING; PROTEIN; INTERNALIZATION AB Antifungal activity of histatin 3 against two Candida albicans clinical isolates was determined in assays containing rabbit submandibular gland saliva. Histatin 3 inhibited the cell growth and germination of both isolates dose-dependently (10-100 mug ml(-1)) with maximum inhibition occurring after 60 min incubation. Adding fresh histatin 3 after 60 min caused further reduction in the viable cell count. Higher histatin 3 concentrations (50-100 mug ml(-1)) and prolonged exposure to peptide were required to inhibit germination. Histatin 3 was rapidly degraded in rabbit submandibular gland saliva and this may explain why fresh addition of histatin 3 increases candidacidal activity. (C) 2005 Published by Elsevier B.V. on behalf of the Federation of European Microbiological Societies. C1 Trinity Coll Dublin, Sch Dent Sci, Dept Restorat Dent & Periodontol, Dublin 2, Ireland. Natl Inst Dent & Craniofacial Res, Gene Therapy & Therapeut Branch, NIH, Bethesda, MD USA. Tokyo Dent Coll, Dept Pharmacol, Chiba, Japan. NCI, Pharmacokinet Sect, Pediat Branch, NIH, Bethesda, MD 20892 USA. RP Fitzgerald, DH (reprint author), Trinity Coll Dublin, Dublin Dent Sch & Hosp, Dept 2, Dublin 2, Ireland. EM deirdre.hughes@dental.tcd.ie OI O'Connell, Brian/0000-0003-4529-7664; Fitzgerald-Hughes, Deirdre/0000-0002-4843-3839 NR 28 TC 1 Z9 2 U1 2 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1097 J9 FEMS MICROBIOL LETT JI FEMS Microbiol. Lett. PD MAR 1 PY 2005 VL 244 IS 1 BP 207 EP 212 DI 10.1016/j.femsle.2005.01.045 PG 6 WC Microbiology SC Microbiology GA 903SY UT WOS:000227447100029 PM 15727842 ER PT J AU Neithardt, AB Segars, JH Hennessy, S James, AN McKeeby, JL AF Neithardt, AB Segars, JH Hennessy, S James, AN McKeeby, JL TI Embryo afterloading: a refinement in embryo transfer technique that may increase clinical pregnancy SO FERTILITY AND STERILITY LA English DT Article; Proceedings Paper CT 59th Annual Meeting of the American-Society-for-Reproductive-Medicine CY OCT 11-15, 2003 CL SAN ANTONIO, TX SP Amer Soc Reprod Med DE embryo transfer; technique; IVF-ET; pregnancy rate ID IN-VITRO FERTILIZATION; INVITRO FERTILIZATION; OVARIAN STIMULATION; TRANSFER CATHETER; LUTEAL-PHASE; RATES; IMPACT; RECOMBINANT; IMPROVES; CYCLE AB Objective: Given the importance of ET technique during assisted reproductive technology cycles, we evaluated the effect of embryo afterloading subsequent to placement of the ET catheter on pregnancy rates vs. a standard direct Et. Design: Retrospective cohort analysis. Setting: University-based assisted reproductive technology program. Patient(s): Patients undergoing a fresh nondonor day 3 ET by a single provider over a 1-year period. Intervention(s): None. Main Outcome Measure(s): Clinical pregnancy. Result(s): One hundred twenty-seven patients met inclusion criteria, and the overall pregnancy rate was 46.5%. There was no difference between the two groups with respect to age, basal FSH, or number of embryos transferred. The ET method used was at the discretion of the provider. There was no difference between the two groups in the presence of blood on the transfer catheter. However, there were significantly more transfer catheters with mucus contamination in the direct transfer group (25.58% vs. 5.95%). The clinical pregnancy rate in the group with ET using the afterloading technique was higher than in the direct ET group (52.4% vs. 34.9%). Conclusion(s): There was a trend toward an increase in pregnancy rate when an embryo afterloading technique was used. A prospective randomized trial is needed to examine this issue. (c) 2005 by American Society for Reproductive Medicine. C1 NICHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bethesda, MD 20814 USA. ATR Inst Washington, Washington, DC USA. Walter Reed Army Med Ctr, Dept Obstet & Gynecol, Washington, DC 20307 USA. Shady Grove Fertil Reprod Sci Ctr, Rockville, MD USA. RP Neithardt, AB (reprint author), NICHD, Pediat & Reprod Endocrinol Branch, NIH, Blgd 10,Room 9D-42,9000 Rockville Pike, Bethesda, MD 20892 USA. EM neithara@mail.nih.gov FU Intramural NIH HHS [Z99 HD999999] NR 26 TC 31 Z9 31 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 MAR PY 2005 VL 83 IS 3 BP 710 EP 714 DI 10.1016/j.fertnstert.2004.08.022 PG 5 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 906JS UT WOS:000227637600029 PM 15749502 ER PT J AU Shaib, YH El-Serag, HB Davila, JA Morgan, R McGlynn, KA AF Shaib, YH El-Serag, HB Davila, JA Morgan, R McGlynn, KA TI Risk factors of intrahepatic cholangiocarcinoma in the United States: A case-control study SO GASTROENTEROLOGY LA English DT Article ID HEPATITIS-C VIRUS; PRIMARY SCLEROSING CHOLANGITIS; DIABETES-MELLITUS; LIVER-CANCER; POPULATION; INFECTION; CARCINOMA; CIRRHOSIS; DENMARK; COHORT AB Background & Aims: The incidence of intrahepatic cholangiocarcinoma has been recently increasing in the United States. In this case-control study, we used the Surveillance, Epidemiology, and End Results-Medicare database to evaluate the prevalence of known risk factors for intrahepatic cholangiocarcinoma and explore other potential risk factors. Methods: We identified all patients with intrahepatic cholangiocarcinoma aged 65 years and older diagnosed between 1993 and 1999 in the population-based Surveillance, Epidemiology, and End Results registries (14% of the US population). Controls were randomly chosen from individuals without any cancer diagnosis in the underlying population of the Surveillance, Epidemiology, and End Results regions. We obtained information on risk factors from Medicare claims (parts A and 13) for all cases and controls with at least 2 years of continuous Medicare enrollment. Unadjusted and adjusted odds ratios were calculated in logistic regression analysis. Results: A total of 625 cases and 90,834 controls satisfied the inclusion and exclusion criteria. Cases were older than controls (78.7 vs. 76.5 years; P = .02) and were more likely to be male (48.3% vs. 36.8%; P < .0001). The racial composition was similar between cases and controls. Several risk factors were significantly more prevalent among cases. These included nonspecific cirrhosis (adjusted odds ratio, 27.2; P < .0001), alcoholic liver disease (adjusted odds ratio, 7.4; P < .0001), hepatitis C virus infection (adjusted odds ratio, 6.1; P < .0001), human immunodeficiency virus infection (adjusted odds ratio, 5.9; P = .003), diabetes (adjusted odds ratio, 2.0; P < .0001), and inflammatory bowel diseases (adjusted odds ratio, 2.3; P = .002). Conclusions: This population-based study shows that in addition to previously well described risk factors, several others could be associated with intrahepatic cholangiocarcinoma. These include hepatitis C virus, human immunodeficiency virus, liver cirrhosis, and diabetes. C1 Baylor Coll Med, Michael E Debakey Vet Affairs Med Ctr, Sect Hlth Serv Res, Houston, TX 77030 USA. Baylor Coll Med, Michael E Debakey Vet Affairs Med Ctr, Dept Gastroenterol, Houston, TX 77030 USA. NCI, NIH, Dept Human & Hlth Serv, Bethesda, MD 20892 USA. RP Shaib, YH (reprint author), Houston Vet Affairs Med Ctr, 2002 Holcombe Blvd,152, Houston, TX 77030 USA. EM yshalb@bcm.tmc.edu NR 18 TC 248 Z9 262 U1 1 U2 13 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD MAR PY 2005 VL 128 IS 3 BP 620 EP 626 DI 10.1053/j.gastro.2004.12.048 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 903SO UT WOS:000227446100015 PM 15765398 ER PT J AU Pabby, A Schoen, RE Weissfeld, JL Burt, R Kikendall, JW Lance, P Shike, M Lanza, E Schatzkin, A AF Pabby, A Schoen, RE Weissfeld, JL Burt, R Kikendall, JW Lance, P Shike, M Lanza, E Schatzkin, A TI Analysis of colorectal cancer occurrence during surveillance colonoscopy in the dietary Polyp Prevention Trial SO GASTROINTESTINAL ENDOSCOPY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-for-Gastrointestinal-Endoscopy CY MAY 18-21, 2004 CL New Orleans, LA SP Amer Soc Gastrointestinal Endoscopy ID ADENOMAS; RECURRENCE AB Background: Interval colorectal cancer (CRC) occasionally is detected in patients who have recently undergone colonoscopy. Systematic evaluation of CRC detected after colonoscopy could identify ways to improve the quality and the outcome of colonoscopy. Methods: This study examined cancer diagnoses in the course of the dietary Polyp Prevention Trial, a randomized study of a dietary intervention on recurrence of adenomatous polyps. An algorithm was developed to classify each cancer into one of 4 etiologies: (1) incomplete removal (cancer at the site of previous adenoma), (2) failed biopsy detection (cancer in an area of suspected neoplasia with negative biopsy specimens), (3) missed cancer (large, advanced stage cancer found at a short interval after colonoscopy), or (4) new cancer (small, early stage cancer after a longer time interval). Results: Of 2079 patients, 13 had cancer detected over 5810 person years of observation (PYO) (2.2 cases/1000 PYO); 7/13 or 53.8% of patients had either a potentially "avoidable" cancer or one detectable at an earlier time interval because of incomplete removal (4/13) or missed cancer (3/13). Conclusions: Interval cancer occurs despite colonoscopy. Improved quality of colonoscopy may have reduced cancer prevalence or resulted in earlier cancer detection in over 50% of prevalent cancers in the dietary Polyp Prevention Trial. C1 Univ Pittsburgh, Div Gastroenterol, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15260 USA. Univ Utah, Div Prevent & Outreach, Huntsman Canc Inst, Salt Lake City, UT 84112 USA. Univ Utah, Dept Gastroenterol, Salt Lake City, UT 84112 USA. Natl Navy Med Ctr, Div Gastroenterol, Washington, DC USA. Arizona Canc Ctr, Tucson, AZ USA. Mem Sloan Kettering Canc Ctr, Div Gastroenterol, New York, NY 10021 USA. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. RP Schoen, RE (reprint author), Div Gastroenterol Hepatol & Nutr, Mezzanine Level,C Wing,PUH,200 Lothrop St, Pittsburgh, PA 15213 USA. NR 23 TC 208 Z9 215 U1 0 U2 7 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD MAR PY 2005 VL 61 IS 3 BP 385 EP 391 AR PII S0016-5107(04)02765-8 DI 10.1016/S0016-5107(04)02765-8 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 909LL UT WOS:000227861300006 PM 15758908 ER PT J AU Makrigiannis, AP Patel, D Goulet, ML Dewar, K Anderson, SK AF Makrigiannis, AP Patel, D Goulet, ML Dewar, K Anderson, SK TI Direct sequence comparison of two divergent class I MHC natural killer cell receptor haplotypes SO GENES AND IMMUNITY LA English DT Article DE Ly49; natural killer cell; haplotype; comparative genomics; strain-129 ID LY49 GENE-CLUSTER; MAJOR HISTOCOMPATIBILITY COMPLEX; GENOMIC DNA; MULTIGENE FAMILY; C57BL/6 MICE; KIR GENES; REPERTOIRE; EVOLUTION; MOUSE; IDENTIFICATION AB The murine Ly49 gene family encoding natural killer cell receptors for class I MHC is an example of a rapidly evolving cluster of immune response genes. Determining the genomic sequence of the 129S6/SvEvTac (129S6) Ly49 cluster and comparing it to the known sequence of the C57BL/6 (B6) region provided insight into the mechanisms of Ly49 gene evolution. 129S6 contains 20 Ly49, many of which are pseudogenes and 40% of the genes have no counterpart in the B6 genome. The difference in gene content between these two strains is primarily the result of distinct patterns of gene duplication. Phylogenetic analyses of individual exons showed that Ly49 genes form distinct sub-families and an ancestral haplotype can be surmised. Dotplot analysis supports limited allelism in the two haplotypes; however, large regions of variation punctuate these islands of co-linearity. These variable regions contain a high concentration of repetitive elements that are predicted to contribute to the dynamic evolution of this cluster. The extreme variation in Ly49 haplotype content between mouse strains provides a genetic explanation for the documented differences in natural killer cell phenotype, and also indicates that differences in natural killer cell function observed between B6 and 129-derived gene-targeted mice should be interpreted with caution. C1 Inst Rech Clin Montreal, Lab Mol Immunol, Montreal, PQ H2W 1R7, Canada. Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada. McGill Univ, Dept Med, Div Expt Med, Montreal, PQ, Canada. McGill Univ, Dept Microbiol & Immunol, Montreal, PQ, Canada. McGill Univ, Dept Human Genet, Montreal, PQ, Canada. Genome Quebec Innovat Ctr, Montreal, PQ, Canada. NCI, Basic Res Program, SAIC Frederick, Frederick, MD 21701 USA. RP Makrigiannis, AP (reprint author), Inst Rech Clin Montreal, Lab Mol Immunol, Rm 1340,110 Ave Pns Ouest, Montreal, PQ H2W 1R7, Canada. EM makriga@ircm.qc.ca RI Anderson, Stephen/B-1727-2012 OI Anderson, Stephen/0000-0002-7856-4266 FU NCI NIH HHS [N01CO12400] NR 43 TC 35 Z9 35 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 1466-4879 J9 GENES IMMUN JI Genes Immun. PD MAR PY 2005 VL 6 IS 2 BP 71 EP 83 DI 10.1038/sj.gene.6364154 PG 13 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA 902CQ UT WOS:000227329400001 PM 15674375 ER PT J AU Roh, TY Cuddapah, S Zhao, K AF Roh, TY Cuddapah, S Zhao, K TI Active chromatin domains are defined by acetylation islands revealed by genome-wide mapping SO GENES & DEVELOPMENT LA English DT Article DE chromatin; epigenome; transcription ID HISTONE ACETYLATION; TRANSCRIPTION FACTOR; GENE-EXPRESSION; BAF COMPLEX; CPG ISLANDS; PROMOTER; IDENTIFICATION; NUCLEOSOME; SEQUENCES; BINDING AB The identity and developmental potential of a human cell is specified by its epigenome that is largely defined by patterns of chromatin modifications including histone acetylation. Here we report high-resolution genome-wide mapping of diacetylation of histone H3 at Lys 9 and Lys 14 in resting and activated human T cells by genome-wide mapping technique (GMAT). Our data show that high levels of the H3 acetylation are detected in gene-rich regions. The chromatin accessibility and gene expression of a genetic domain is correlated with hyperacetylation of promoters and other regulatory elements but not with generally elevated acetylation of the entire domain. Islands of acetylation are identified in the intergenic and transcribed regions. The locations of the 46,813 acetylation islands identified in this study are significantly correlated with conserved noncoding sequences (CNSs) and many of them are colocalized with known regulatory elements in T cells. TCR signaling induces 4045 new acetylation loci that may mediate the global chromatin remodeling and gene activation. We propose that the acetylation islands are epigenetic marks that allow prediction of functional regulatory elements. C1 NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. RP Zhao, K (reprint author), NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA. EM zhaok@nhlbi.nih.gov NR 52 TC 298 Z9 313 U1 3 U2 6 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR 1 PY 2005 VL 19 IS 5 BP 542 EP 552 DI 10.1101/gad.1272505 PG 11 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA 901OV UT WOS:000227292700004 PM 15706033 ER PT J AU Jessop, L Allers, T Lichten, M AF Jessop, L Allers, T Lichten, M TI Infrequent co-conversion of markers flanking a meiotic recombination initiation site in Saccharomyces cerevisiae SO GENETICS LA English DT Article ID DOUBLE-STRAND BREAKS; HETERODUPLEX DNA; MISMATCH REPAIR; HIS4 LOCUS; HOLLIDAY JUNCTIONS; GENE CONVERSION; YEAST MEIOSIS; INTERMEDIATE; CROSSOVERS; RESOLUTION AB To study the mechanism of meiotic recombination in Saccharomyces cerevisiae, we examined recombination in an interval where the majority of events are initiated at a single hotspot for DNA double-strand breaks (DSBs), with little or no expected contribution by outside initiation events. This interval contained infrequently corrected palindromic markers 300 bp to the left and 600 bp to the right of the DSB hotspot. Conversion of single markers occurred frequently, while conversion of both markers occurred rarely, and many of the tetrads in which both markers converted were the products of multiple events. These data indicate that most meiotic recombination intermediates are asymmetrically positioned around the initiating DSB, with a short (< 300 bp) tract of heteroduplex DNA (hDNA) to one side and hDNA on the other side frequently extending 600 bp or more. One consequence of this asymmetry is the preferential concentration of crossovers in the vicinity of the initiating DSB. C1 NCI, Canc Res Ctr, Bethesda, MD 20892 USA. Univ Nottingham, Queens Med Ctr, Genet Inst, Nottingham NG7 2UH, England. RP Lichten, M (reprint author), NCI, Bldg 37,Room 6124,37 Convent Dr,MSC 4255, Bethesda, MD 20829 USA. EM lichten@helix.nih.gov RI Allers, Thorsten/G-5503-2010; Lichten, Michael/C-5795-2013 OI Allers, Thorsten/0000-0002-7308-3332; Lichten, Michael/0000-0001-9707-2956 NR 48 TC 43 Z9 45 U1 0 U2 2 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 USA SN 0016-6731 J9 GENETICS JI Genetics PD MAR PY 2005 VL 169 IS 3 BP 1353 EP 1367 DI 10.1534/genetics.104.036509 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA 917HD UT WOS:000228450800014 PM 15654098 ER PT J AU de Serres, FJ Blanco, I Fernandez-Bustillo, E AF de Serres, FJ Blanco, I Fernandez-Bustillo, E TI Health implications of alpha(1)-antitrypsin deficiency in Sub-Sahara African countries and their emigrants in Europe and the New World SO GENETICS IN MEDICINE LA English DT Article DE alpha(1)-antitrypsin deficiency; PI subtypes; Sub-Sahara Africa; genetic epidemiology; indigenous populations; environmental health ID HETEROZYGOUS ALPHA-1-ANTITRYPSIN DEFICIENCY; OBSTRUCTIVE PULMONARY-DISEASE; CLINICAL-FEATURES; LIVER-DISEASE; LUNG-FUNCTION; ALPHA1-ANTITRYPSIN DEFICIENCY; ANTITRYPSIN DEFICIENCY; GENETIC EPIDEMIOLOGY; POPULATION-GENETICS; M SUBTYPES AB Purpose: To determine the frequencies of the protease inhibitor (PI) deficiency alleles of alpha(1)-antitrypsin deficiency (AAT Deficiency) in indigenous populations in 12 countries in Sub-Sahara Africa because of their potential impact on the health in these populations with regard to the high risk for development of liver and lung disease. In addition, to discuss the unique susceptibility of these populations and emigrants to Europe and the New World to the adverse health effects associated with exposure to environmental microbes, chemicals, and particulates. Methods: Detailed statistical analysis of the 24 control cohort databases from genetic epidemiological studies by others were used to estimate the allele frequencies and prevalence for the two most common deficiency alleles PIS and PIZ and to estimate the numbers at risk in each of the local Sub-Sahara populations as well as those who have emigrated from these countries to Europe and the New World. Results: The present study has provided evidence for the presence of both PIS and PIZ in the general populations of Nigeria, Republic of South Africa, and Somalia, the PIS allele in Angola, Botswana, Cameroon, Mozambique, Namibia, and the Republic of Congo, and only the PIZ allele in Mali. Conclusion: AAT Deficiency is found in both the Black and "Colored" populations in many of the Sub-Sahara countries in Africa, providing evidence for the presence of AAT Deficiency in such populations in Europe and in the New World. Such populations should be screened for AAT Deficiency and made aware of their unique susceptibility to exposure to chemical and particulate agents in the environment. C1 Natl Inst Environm Hlth Sci, Mol Toxicol Lab, Environm Toxicol Program, Res Triangle Pk, NC 27709 USA. Hosp Valle Nalon, Resp Dis Branch, Sama De Langreo, Spain. Hosp Cent Asturias, Biostat Unit, Oviedo, Spain. RP de Serres, FJ (reprint author), Natl Inst Environm Hlth Sci, Mol Toxicol Lab, Environm Toxicol Program, Box 12233, Res Triangle Pk, NC 27709 USA. NR 72 TC 9 Z9 9 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1098-3600 J9 GENET MED JI Genet. Med. PD MAR PY 2005 VL 7 IS 3 BP 175 EP 184 DI 10.1097/01.GIM.0000156533.06057.89 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 908BG UT WOS:000227761600004 PM 15775753 ER PT J AU Leib, JR Gollust, SE Hull, SC Wilfond, BS AF Leib, JR Gollust, SE Hull, SC Wilfond, BS TI Carrier screening panels for Ashkenazi Jews: Is more better? SO GENETICS IN MEDICINE LA English DT Article DE carrier screening; Ashkenazi Jews; guidelines; policy development; stigmatization ID TAY-SACHS-DISEASE; JEWISH POPULATION; CYSTIC-FIBROSIS; LESSONS; LEADERS; MODEL AB Purpose: To describe the characteristics of Ashkenazi Jewish carrier testing panels offered by US Laboratories, including what diseases are included, the labels used to describe the panels, and the prices of individual tests compared to the prices of panels for each laboratory. Methods: GeneTests (http://www.genetests.org) was searched for laboratories that offered Tay-Sachs disease testing. Information was obtained from laboratory web sites, printed brochures, and telephone calls about tests/panels. Results: Twenty-seven laboratories offered up to 10 tests. The tests included two diseases associated with death in childhood (Niemann-Pick type A and Tay-Sachs disease), five with moderate disability and a variably shortened life span (Bloom syndrome, Canavan disease, cystic fibrosis, familial dysautonomia, Fanconi anemia, and mucolipiclosis type IV), and two diseases that are not necessarily disabling or routinely shorten the lifespan (Gaucher disease type I and DFNB1 sensorineural hearing loss). Twenty laboratories offered a total of 27 panels of tests for three to nine diseases, ranging in price from $200 to $2082. Of these, 15 panels cost less than tests ordered individually. The panels were described by 24 different labels; eight included the phrase Ashkenazi Jewish Disease or disorder and six included the phrase Ashkenazi Jewish Carrier. Conclusion: There is considerable variability in the diseases, prices, and labels of panels. Policy guidance for establishing appropriate criteria for inclusion in panels may be useful to the Ashkenazi Jewish community, clinicians, and payers. Pricing strategies that offer financial incentives for the use of "more tests" should be reexamined. C1 NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA. NHGRI, Policy & Program Anal Branch, NIH, Bethesda, MD 20892 USA. NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA. NIH, Warren G Magnuson Clin Ctr, Dept Clin Bioeth, Bethesda, MD 20892 USA. RP Wilfond, BS (reprint author), Bldg 10,Room 1C 118 MSC 1156,9000 Rockville Pike, Bethesda, MD 20892 USA. NR 28 TC 25 Z9 27 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1098-3600 J9 GENET MED JI Genet. Med. PD MAR PY 2005 VL 7 IS 3 BP 185 EP 190 DI 10.1097/01.GIM.0000156527.87525.8F PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 908BG UT WOS:000227761600005 PM 15775754 ER PT J AU Son, CG Bilke, S Davis, S Greer, BT Wei, JS Whiteford, CC Chen, QR Cenacchi, N Khan, J AF Son, CG Bilke, S Davis, S Greer, BT Wei, JS Whiteford, CC Chen, QR Cenacchi, N Khan, J TI Database of mRNA gene expression profiles of multiple hunian organs SO GENOME RESEARCH LA English DT Article ID NORMAL HUMAN TISSUES; NEUROBLASTOMA; MOUSE; TRANSCRIPTOMES; MICROARRAYS; MUTATIONS; GENOME; PHOX2B AB Genome-wide expression profiling of normal tissue may facilitate Our Understanding of the etiology of diseased organs and augment the development of new targeted therapeutics. Here, we have developed a high-density gene expression database of 18,927 unique genes for 158 normal human samples from 19 different organs of 30 different individuals using DNA microarrays. We report four main findings. First, despite very diverse sample parameters (e.g., age, ethnicity, sex, and postmortem interval), the expression profiles belonging to the same organs cluster together, demonstrating internal stability of the database. Second, the gene expression profiles reflect major organ-specific functions oil the molecular level, indicating consistency Of our database with known biology. Third, we demonstrate that any small (i.e., n similar to 100), randomly selected subset of genes can approximately reproduce the hierarchical clustering of the full data set, suggesting that the observed differential expression of >90% of the probed genes is of biological origin. Fourth, we demonstrate a potential application of this database to cancer research by identifying 19 tumor-specific genes in neuroblastoma. The selected genes are relatively underexpressed in all of the organs examined and belong to therapeutically relevant pathways, making them potential novel diagnostic markers and targets for therapy. We expect this database will be Of utility for developing rationally designed molecularly targeted therapeutics in diseases Such as cancer, as well as for exploring the functions of genes. C1 NCI, Oncogenom Sect, Ctr Adv Technol, Pediat Oncol Branch,NIH, Gaithersburg, MD 20877 USA. Daejeon Univ, Coll Oriental Med, Dept Internal Med, Taejon 301724, South Korea. NHGRI, NIH, Bethesda, MD 20892 USA. RP Khan, J (reprint author), NCI, Oncogenom Sect, Ctr Adv Technol, Pediat Oncol Branch,NIH, Gaithersburg, MD 20877 USA. EM khanjav@mail.nih.gov RI Khan, Javed/P-9157-2014 OI Khan, Javed/0000-0002-5858-0488 FU NCI NIH HHS [Z01 BC010593-02] NR 30 TC 90 Z9 93 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 1088-9051 J9 GENOME RES JI Genome Res. PD MAR PY 2005 VL 15 IS 3 BP 443 EP 450 DI 10.1101/gr.3124505 PG 8 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 902CB UT WOS:000227327800012 PM 15741514 ER PT J AU Zhang, JH Finney, RP Clifford, RJ Derr, LK Buetow, KH AF Zhang, JH Finney, RP Clifford, RJ Derr, LK Buetow, KH TI Detecting false expression signals in high-density oligonucleotide arrays by an in silico approach SO GENOMICS LA English DT Article DE affymetrix; probe; cross-hybridization; mistargeted; mRNA; expression ID GENE-EXPRESSION; GLUTAMATE-DEHYDROGENASE; HUMAN GENOME; HYBRIDIZATION; TRANSCRIPTION; MICROARRAY; CANCER; NOMENCLATURE; PROBESETS; PATTERNS AB High-density oligonucleotide arrays have become a popular assay for concurrent measurement of mRNA expression at the genome scale. Much effort has been devoted to the development of statistical analysis tools aimed at reducing experimental noise and normalizing experimental variation in gene expression analysis. However, these investigations do not detect or catalog systematic problems associated with specific oligonucleotide probes. Here, we present an investigation of problematic probes that yield consistent but inaccurate signals across multiple experiments. By evaluating data integrity among gene, probe sequence, and genomic structure we identified a total of 20,696 (10.5%) nonspecific probes that could cross-hybridize to multiple genes and a total of 18,363 (9.3%) probes that miss the target transcript sequences on the Affymetrix GeneChip U95A/Av2 array. The numbers of nonspecific and mistargeted probes on the U133A array are 29,405 (12.1%) and 19,717 (8.0%), respectively. The poor performance of the mistargeted probes was confirmed in two GeneChip experiments, in which these probes showed a 20-30% decrease in detecting present signals compared with normal probes. Comparison of qualitative expression signals obtained from SAGE and EST data with those from GeneChip arrays showed that the consistency of the two platforms is 30% lower in problematic probes than in normal probes. A Web application was developed to apply our results for improving the accuracy of expression analysis. (c) 2004 Elsevier Inc. All rights reserved. C1 NCI, Lab Populat Genet, NIH, Bethesda, MD 20892 USA. RP Zhang, JH (reprint author), NCI, Lab Populat Genet, NIH, 8424 Helgerman Court,Room 101,MSC 8302, Bethesda, MD 20892 USA. EM jinghuiz@mail.nih.gov NR 36 TC 46 Z9 48 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD MAR PY 2005 VL 85 IS 3 BP 297 EP 308 DI 10.1016/j.ygeno.2004.11.004 PG 12 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 906OT UT WOS:000227652200002 PM 15718097 ER PT J AU Trimble, EL Harlan, LC Clegg, LMX Stevens, JL AF Trimble, EL Harlan, LC Clegg, LMX Stevens, JL TI Pre-operative imaging, surgery and adjuvant therapy for women diagnosed with cancer of the corpus uteri in community practice in the United States SO GYNECOLOGIC ONCOLOGY LA English DT Article DE surgery; adjuvant therapy; corpus uteri; SEER ID ENDOMETRIAL CARCINOMA; RANDOMIZED-TRIAL; SURVIVAL AB Introduction. Non-Hispanic black women are less often diagnosed with endometrial cancer than are non-Hispanic white women, but are more likely to die of their disease. Reasons for this disparity in outcome are not well understood. Methods. The Surveillance, Epidemiology, and End-Results Program data were used to sample women newly diagnosed in 1998 with cancer of the corpus uteri. A total of 711 women with no previous diagnosis of cancer were selected. Women with sarcoma were not eligible for the study. We then sought to verify the therapy provided each woman with her treating physician. Results. Non-Hispanic black women were diagnosed with higher stage, grade, poor histologic subtype, and greater extension of the tumor than were non-Hispanic white women. Hispanic women were diagnosed with more favorable tumor characteristics than non-Hispanic black women, but less favorable than non-Hispanic white women. The use of radiation and chemotherapy increased with stage. Conclusions. Our study did not show any difference in recommended therapy for women With uterine adenocarcinoma among NH black women, NH white women, and Hispanic women. We must look for other factors, therefore, to explain the disparities in cancer outcome observed among NH black women with endometrial cancer. (c) 2004 Elsevier Inc. All rights reserved. C1 NCI, Surg Sect, Bethesda, MD 20892 USA. Informat Management Serv Inc, Silver Spring, MD USA. RP Trimble, EL (reprint author), NCI, Surg Sect, 6130 Executive Blvd,Ste 741, Bethesda, MD 20892 USA. EM tt6m@nih.gov NR 15 TC 14 Z9 14 U1 0 U2 1 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD MAR PY 2005 VL 96 IS 3 BP 741 EP 748 DI 10.1016/j.ygyno.2004.11.041 PG 8 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA 906BN UT WOS:000227615600025 PM 15721420 ER PT J AU Geisler, SA Olshan, AF Cai, JW Weissler, M Smith, J Bell, D AF Geisler, SA Olshan, AF Cai, JW Weissler, M Smith, J Bell, D TI Glutathione S-transferase polymorphisms and survival from head and neck cancer SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK LA English DT Article DE longevity; cancer outcomes; genetics; squamous cell carcinoma ID SQUAMOUS-CELL CARCINOMA; AERODIGESTIVE TRACT CANCERS; GENETIC POLYMORPHISMS; DNA-REPAIR; CYTOCHROME-P450 CYP2D6; SUSCEPTIBILITY FACTOR; XRCC1 POLYMORPHISMS; COMORBIDITY INDEX; RISK-FACTORS; ORAL-CANCER AB Background. The purpose of this study was to evaluate the prognostic ability of polymorphisms of three genes involved in the metabolism of tobacco carcinogens (GSTT1, GSTM1, GSTP1) and one polymorphism of a DNA repair gene (XRCC1) for patients diagnosed with squamous cell carcinoma (SCC). Methods. Cox proportional hazard models were used to estimate risk of death for a prospective cohort of 190 patients. Results. Individuals with the GSTT1 functional genotype were twice as likely to die from any cause (hazard ratio [HR], 2.4; 95% confidence interval [CI], 1.13-4.97) and were three times as likely to die from SCC (HR, 3.4; 95% CI, 1.33-8.41) after adjustment for age, primary therapy, and stage of disease. The XRCC1 399 Gln genotype was predictive of disease recurrence. Conclusions. Our findings, from one of the first studies to examine this research question, suggest that genomic markers of carcinogen metabolism and DNA repair capability may serve as prognostic indicators of disease recurrence and death. (C) 2005 Wiley Periodicals, Inc. C1 Oregon Hlth Sci Univ, Sch Med & Dent, Dept Oral & Maxillofacial Surg, Portland, OR 97201 USA. Oregon Hlth Sci Univ, Dept Surg, Portland, OR 97201 USA. Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27515 USA. Univ N Carolina, Sch Med, Dept Otolaryngol Head & Neck Surg, Chapel Hill, NC 27515 USA. Univ N Carolina, Sch Publ Hlth, Dept Biostat, Chapel Hill, NC 27515 USA. Natl Inst Environm Hlth Sci, Lab Computat Biol & Risk Assessment, Res Triangle Pk, NC USA. RP Geisler, SA (reprint author), Oregon Hlth Sci Univ, Sch Med & Dent, Dept Oral & Maxillofacial Surg, 611 SW Campus Dr,Mailcode SD544, Portland, OR 97201 USA. EM geislest@ohsu.edu FU NCI NIH HHS [CA61188]; NIEHS NIH HHS [P30ES10126] NR 55 TC 21 Z9 23 U1 0 U2 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1043-3074 J9 HEAD NECK-J SCI SPEC JI Head Neck-J. Sci. Spec. Head Neck PD MAR PY 2005 VL 27 IS 3 BP 232 EP 242 DI 10.1002/hed.20141 PG 11 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA 902AW UT WOS:000227324600008 PM 15668931 ER PT J AU Barry, J Breen, N AF Barry, J Breen, N TI The importance of place of residence in predicting late-stage diagnosis of breast or cervical cancer SO HEALTH & PLACE LA English DT Article DE breast cancer; cervical cancer; poor neighborhoods; medically underserved areas ID SOCIOECONOMIC-STATUS; UNITED-STATES; MEDICAL-CARE; HEALTH; MAMMOGRAPHY; WOMEN; AREA; MORTALITY; INTERVENTIONS; UNDERCLASS AB Vie tested whether inner-city women were at significantly increased risk of late-stage cancer diagnosis because they resided in extremely poor and socially isolated neighborhoods or in neighborhoods meeting the federal definition of a medically underserved area (MUA). Cancer registry data on women in three American cities were matched to Census data. Using logistic regression we found that residence in economically and socially distressed or medically underserved neighborhoods tended to increase the likelihood of late-stage cancer diagnoses. Further, we found that not all areas that are economically and socially distressed receive the federal MUA designation. Consequently, we argue that economically and socially distressed neighborhoods should be automatically designated as MUA. Published by Elsevier Ltd. C1 Fordham Univ, Dept Econ, New York, NY 10023 USA. Lincoln Ctr, New York, NY 10023 USA. NCI, Appl Res Branch, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. RP Barry, J (reprint author), Fordham Univ, Dept Econ, 113 W 60th St, New York, NY 10023 USA. EM barryfiguero@fordham.edu NR 56 TC 56 Z9 60 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 1353-8292 J9 HEALTH PLACE JI Health Place PD MAR PY 2005 VL 11 IS 1 BP 15 EP 29 DI 10.1016/j.healthplace.2003.12.002 PG 15 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 878NU UT WOS:000225654300002 PM 15550353 ER PT J AU Newton-Cheh, C Larson, MG Corey, DC Benjamin, EJ Herbert, AG Levy, D D'Agostino, RB O'Donnell, CJ AF Newton-Cheh, C Larson, MG Corey, DC Benjamin, EJ Herbert, AG Levy, D D'Agostino, RB O'Donnell, CJ TI QT interval is a heritable quantitative trait with evidence of linkage to chromosome 3 in a genome-wide linkage analysis: The Framingham Heart Study SO HEART RHYTHM LA English DT Article; Proceedings Paper CT 54th Annual Fall Conference and Scientific Sessions of the American-Heart-Association Council for High Pressure Research CY OCT 24-27, 2000 CL WASHINGTON, D.C. SP Amer Heart Assoc DE genetics; QT interval; electrocardiography; long QT syndrome; arrthythmia; cohort study ID CARDIOVASCULAR MORTALITY; HYPERTENSIVE PATIENTS; CARDIAC-ARRHYTHMIA; TWINS; RISK; ELECTROCARDIOGRAM; POPULATION; DISEASE; REPOLARIZATION; VARIABILITY AB OBJECTIVES To identify genomic regions linked to QT interval duration in an unselected population. BACKGROUND QT interval prolongation is associated with increased risk of sudden cardiac death and coronary heart disease and may result from acquired conditions or inherited ion channel defects. The influence of genetic variants on QT interval length in apparently healthy individuals is uncertain. METHODS We studied subjects from the Framingham Heart Study in whom 12-lead ECGs were available from regular clinic examinations. QT, QT-peak, and RR intervals were measured using digital calipers. A 10-centiMorgan (cM) density genome-wide scan was performed in a subset of the largest families having at least two members with ECG phenotypes (326 families). Variance components methods (Genehunter) were used. RESULTS Evidence was observed for significant heritability of the QT interval (h(2) 0.35; 95% CI, 0.29-0.41), QT-peak interval (h(2) 0.37; 95% CI, 0.29-0.45), and calculated JT interval (h(2) 0.25; 95% CI, 0.19 - 0.31). In the genome-wide linkage analysis, we found suggestive evidence for linkage of the QT interval 19 to 48 cM from the tip of the short arm of chromosome 3 (maximum two-point LOD score 3.00, maximum multipoint LOD score 2.71). After fine-mapping with seven microsatellite markers, the peak multipoint LOD score rose to 2.84 at 24.4 cM. The region of linkage contains potassium and sodium channel genes, including the SCN5A gene, which has been implicated in one form of the long QT syndrome and in the Brugada syndrome. CONCLUSIONS QT and related ECG intervals are heritable traits in a large unselected population. We provide suggestive evidence for a quantitative trait locus on chromosome 3 influencing QT interval duration. Further studies are warranted to identify genes that influence QT interval variation and to determine the role of heritable factors in life-threatening QT prolongation. C1 NHLBI, Framinigham Heart Study, Framingham, MA 01702 USA. Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA. Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Beth Israel Deaconess Hosp, Boston, MA USA. Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Prevent Med, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Genet & Genom, Boston, MA 02118 USA. Boston Univ, Sch Med, Epidemiol & Prevent Med Sect, Boston, MA 02118 USA. Boston Univ, Dept Math, Boston, MA 02215 USA. NHLBI, Bethesda, MD 20892 USA. RP O'Donnell, CJ (reprint author), NHLBI, Framinigham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA. EM codonnell@nih.gov OI Larson, Martin/0000-0002-9631-1254; Benjamin, Emelia/0000-0003-4076-2336 FU NHLBI NIH HHS [1U01 HL 66582, HL07575] NR 41 TC 76 Z9 76 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 1547-5271 J9 HEART RHYTHM JI Heart Rhythm PD MAR PY 2005 VL 2 IS 3 BP 277 EP 284 DI 10.1016/j.hrthm.2004.11.009 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 904LQ UT WOS:000227500000012 PM 15851319 ER PT J AU Nakagawa-Goto, K Jung, MK Hamel, E Wu, CC Bastow, KF Brossi, A Ohta, S Lee, KH AF Nakagawa-Goto, K Jung, MK Hamel, E Wu, CC Bastow, KF Brossi, A Ohta, S Lee, KH TI Antitumor agents 238. Anti-tubulin and in vitro cytotoxic effects of N-substituted allocolchicinoids SO HETEROCYCLES LA English DT Article ID RING MODIFIED ALLOCOLCHICINOIDS; MODIFIED COLCHICINES; CONFIGURATION AB (-)-N-Substituted colchinol methyl ethers (6-10) and N-alkyl HCl salts (8a-10a) were synthesized from (-)-colchicine (1). The new compounds were evaluated for in vitro cytotoxic activity against five human tumor cell lines and for inhibition of tubulin polymerization. The new carbamate (6) and amide (7) showed 10-fold stronger activity against human tumor cell line replication than the amines (8-10). The corresponding HCl salts (8a-10a) generally showed decreased activity. Compounds (6) and (7) also exerted strong inhibitory effects on tubulin polymerization. All of the colchinol methyl ethers showed essentially equal cytotoxic effects against MDR-resistant (KB-V) and non-resistant (KB) cells, while the potency of colchicine was decreased 100-fold against KB-V cells. C1 Univ N Carolina, Sch Pharm, Nat Prod Lab, Chapel Hill, NC 27599 USA. SAIC Frederick Inc, Ft Detrick, MD 21702 USA. Natl Canc Inst, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diag,NIH, Ft Detrick, MD 21702 USA. Kyoto Pharmaceut Univ, Kyoto 6078414, Japan. RP Nakagawa-Goto, K (reprint author), Univ N Carolina, Sch Pharm, Nat Prod Lab, Chapel Hill, NC 27599 USA. RI GOTO, Kyoko/D-8389-2015 OI GOTO, Kyoko/0000-0002-1642-6538 NR 26 TC 19 Z9 19 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0385-5414 J9 HETEROCYCLES JI Heterocycles PD MAR 1 PY 2005 VL 65 IS 3 BP 541 EP 550 PG 10 WC Chemistry, Organic SC Chemistry GA 911VP UT WOS:000228034700004 ER PT J AU Olson, MOJ Dundr, M AF Olson, MOJ Dundr, M TI The moving parts of the nucleolus SO HISTOCHEMISTRY AND CELL BIOLOGY LA English DT Review DE nucleolus; ribosome assembly; mitosis; nucleolar assembly; macromolecular mobility ID RNA-POLYMERASE-I; TUMOR-SUPPRESSOR PROTEIN; PRE-RIBOSOMAL-RNA; NUCLEAR EXPORT; CELL-PROLIFERATION; RIBONUCLEOPROTEIN COMPLEX; HUMAN P14(ARF); MYOSIN-I; LOCALIZATION; P53 AB The cell nucleolus is the subnuclear body in which ribosomal subunits are assembled, and it is also the location of several processes not related to ribosome biogenesis. Recent studies have revealed that nucleolar components move about in a variety of ways. One class of movement is associated with ribosome assembly, which is a vectorial process originating at the sites of transcription in the border region between the fibrillar center and the dense fibrillar component. The nascent preribosomal particles move outwardly to become the granular components where further maturation takes place. These particles continue their travel through the nucleoplasm for eventual export to the cytoplasm to become functional ribosomes. In a second kind of motion, many nucleolar components rapidly exchange with the nucleoplasm. Thirdly, nucleolar components engage in very complex movements when the nucleolus disassembles at the beginning of mitosis and then reassembles at the end of mitosis. Finally, many other cellular and viral macromolecules, which are not related to ribosome assembly, also pass through or are retained by the nucleolus. These are involved in nontraditional roles of the nucleolus, including regulation of tumor suppressor and oncogene activities, signal recognition particle assembly, modification of small RNAs, control of aging, and modulating telomerase function. C1 Univ Mississippi, Med Ctr, Dept Biochem, Jackson, MS 39216 USA. NCI, NIH, Bethesda, MD 20892 USA. RP Olson, MOJ (reprint author), Univ Mississippi, Med Ctr, Dept Biochem, 2500 N State St, Jackson, MS 39216 USA. EM molson@biochem.umsmed.edu NR 91 TC 144 Z9 151 U1 0 U2 10 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0948-6143 J9 HISTOCHEM CELL BIOL JI Histochem. Cell Biol. PD MAR PY 2005 VL 123 IS 3 BP 203 EP 216 DI 10.1007/s00418-005-0754-9 PG 14 WC Cell Biology; Microscopy SC Cell Biology; Microscopy GA 920XN UT WOS:000228728900001 PM 15742198 ER PT J AU Buggage, RR Myers-Powell, B McManaway, J Shen, D Robinson, MR Chan, CC AF Buggage, RR Myers-Powell, B McManaway, J Shen, D Robinson, MR Chan, CC TI Detection of the Philadelphia chromosome in the iris of a child with acute lymphoblastic leukaemia SO HISTOPATHOLOGY LA English DT Letter ID TRANSCRIPTS; FUSION; BCR C1 NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA. NEI, Off Clin Director, NIH, Bethesda, MD 20892 USA. Retina & Macula Specialists, Renton, WA USA. Hershey Pediat Ophthalmol Associates, Hershey, PA USA. RP Buggage, RR (reprint author), NEI, Immunol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA. NR 6 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0309-0167 J9 HISTOPATHOLOGY JI Histopathology PD MAR PY 2005 VL 46 IS 3 BP 350 EP 352 DI 10.1111/j.1365-2559.2004.01993.x PG 4 WC Cell Biology; Pathology SC Cell Biology; Pathology GA 899GW UT WOS:000227133900016 PM 15720426 ER PT J AU Sorensen, DB Johnsen, PF Bibby, BM Bottner, A Bornstein, SR Eisenhofer, G Pacak, K Hansen, AK AF Sorensen, DB Johnsen, PF Bibby, BM Bottner, A Bornstein, SR Eisenhofer, G Pacak, K Hansen, AK TI PNMT transgenic mice have an aggressive phenotype SO HORMONE AND METABOLIC RESEARCH LA English DT Article DE epinephrine; mice; open field; behavior; C57B1/6 ID N-METHYLTRANSFERASE ACTIVITIES; MAINTAINING SOCIAL TOLERANCE; MUS-MUSCULUS-DOMESTICUS; MALE DBA/2J MICE; MALE HOUSE MICE; SUBSTRATE ODORS; BEHAVIOR; MOUSE; EPINEPHRINE; RESPONSES AB PNMT (phenylethanolamine-N-methyl-transferase) is the enzyme that catalyzes the formation of epinephrine from norepinephrine. In transgenic mice over-expressing PNMT, observations revealed a very high level of aggression compared to their background strain, C57BL/6J. To evaluate the influence of PNMT on aggression and emotionality in this transgenic line, single-sex male and female groups were independently established that consisted of either four wild-type mice or four transgenic mice overexpressing PNMT. The members of each group were littermates. Mixed single-sex groups consisting of two transgenic mice and two wild-type mice were also established. Almost no fights were observed within the female groups. in males, the transgenic line showed a significantly higher level of fighting than controls (p = 0.007) and mixed male groups (p = 0.02). Housing mice from the transgenic line in mixed groups with wild-type mice seems to decrease the level of aggression in the transgenic line. In conclusion, this is the first study to demonstrate a clear, significant increase in aggression arising from PNMT overexpression. This suggests an important role for central epinephrine levels in aggressive behavior. C1 Royal Vet & Agr Univ, Div Lab Anim Sci & Welf, Dept Vet Pathobiol, DK-1870 Copenhagen, Denmark. Royal Vet & Agr Univ, Dept Math & Phys, Frederiksberg, Denmark. Univ Leipzig, Univ Hosp Children & Adolescents, D-7010 Leipzig, Germany. Univ Dresden, Dept Med 3, Dresden, Germany. NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD USA. NICHHD, Pediat & Reprod Endocrinol Branch, NIH, Bethesda, MD 20892 USA. RP Sorensen, DB (reprint author), Royal Vet & Agr Univ, Div Lab Anim Sci & Welf, Dept Vet Pathobiol, Groennegaardsvej 15, DK-1870 Copenhagen, Denmark. EM dobj@kvl.dk RI Korner, Antje/B-3988-2015 OI Korner, Antje/0000-0001-6001-0356 NR 25 TC 7 Z9 7 U1 0 U2 2 PU GEORG THIEME VERLAG KG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0018-5043 J9 HORM METAB RES JI Horm. Metab. Res. PD MAR PY 2005 VL 37 IS 3 BP 159 EP 163 DI 10.1055/s-2005-861301 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 919JO UT WOS:000228614500006 PM 15824970 ER PT J AU Jansen, A Floel, A Van Randenborgh, J Konrad, C Rotte, M Forster, AF Deppe, M Knecht, S AF Jansen, A Floel, A Van Randenborgh, J Konrad, C Rotte, M Forster, AF Deppe, M Knecht, S TI Crossed cerebro-cerebellar language dominance SO HUMAN BRAIN MAPPING LA English DT Article DE cerebellum; language lateralization; motor theory of speech perception; fMRI ID TRANSCRANIAL DOPPLER SONOGRAPHY; COGNITIVE-AFFECTIVE SYNDROME; FUNCTIONAL MRI; SPEECH-PERCEPTION; VERBAL FLUENCY; BASAL GANGLIA; CEREBELLAR CONTRIBUTIONS; MOTOR THEORY; LATERALIZATION; APHASIA AB In addition to its traditional role in motor control, the cerebellum has been implicated in various cognitive and linguistic functions. Lesion, anatomic, and functional imaging studies indicate a link between left frontal language regions and the right cerebellum. To probe the specificity of this circuit, we examined the association between language-related lateralized activation of the frontal cortex with lateralized activation of the cerebellum. Functional magnetic resonance imaging (fMRI) was carried out during letter-cued word generation in 14 healthy subjects: 7 subjects displayed typical left-hemisphere and 7 subjects displayed atypical right-hemisphere language dominance. We found activation of the cerebellar hemisphere contralateral to the language-dominant cerebral hemisphere in each subject. The cerebellar activation was confined to the lateral posterior cerebellar hemisphere (lobule VI, VII B, Cr I, Cr II). This study demonstrates that crossed cerebral and cerebellar language dominance is a typical characteristic of brain organization. The functional significance of the reported activations can now be tested in patients with lesions of the lateral posterior cerebellum. (C) 2004 Wiley-Liss, Inc. C1 Univ Munster, Dept Neurol, D-48129 Munster, Germany. NINDS, Human Cort Physiol Sect, NIH, Bethesda, MD 20892 USA. Univ Magdeburg, Dept Neurol 2, D-39106 Magdeburg, Germany. Ruhr Univ Bochum, BG Kliniken Bergmannsheil, Dept Radiol, D-4630 Bochum, Germany. RP Jansen, A (reprint author), Univ Munster, Dept Neurol, Albert Schweitzer Str 33, D-48129 Munster, Germany. EM anjan@uni-muenster.de RI Floel, Agnes/A-9426-2017; Deppe, Michael/C-5780-2017; OI Deppe, Michael/0000-0002-8372-9678; Knecht, Stefan/0000-0003-1056-9228 NR 80 TC 69 Z9 71 U1 3 U2 5 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PD MAR PY 2005 VL 24 IS 3 BP 165 EP 172 DI 10.1002/hbm.20077 PG 8 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 900YQ UT WOS:000227250600002 PM 15486988 ER PT J AU Kemeny, S Ye, FQ Birn, R Braun, AR AF Kemeny, S Ye, FQ Birn, R Braun, AR TI Comparison of continuous overt speech fMRI using BOLD and arterial spin labeling SO HUMAN BRAIN MAPPING LA English DT Article DE magnetic resonance imaging; brain function; speech; artifacts; human brain mapping; motion artifact; spin tagging ID CEREBRAL-BLOOD-FLOW; EVENT-RELATED FMRI; BRAIN ACTIVATION; PERFUSION; IDENTIFICATION; INCREASES; ARTIFACTS; DISPLAY; MOTION; CORTEX AB Overt speech production in functional magnetic resonance imaging (fMRI) studies is often associated with imaging artifacts, attributable to both movement and susceptibility. Various image-processing methods have been proposed to remove these artifacts from the data but none of these methods has been shown to work with continuous overt speech, at least over periods greater than 3 s. In this study natural, continuous, overt sentence production was evaluated in normal volunteers using both arterial spin labeling (ASL) and conventional echoplanar blood oxygenation level-dependent (BOLD) imaging sequences on the same 1.5-T scanner. We found a high congruency between activation results obtained with ASL and the de facto gold standard in overt language production imaging, positron emission tomography (PET). No task-related artifacts were found in the ASL study. However, the BOLD data showed artifacts that appeared as large bilateral false-positive temporopolar activations; percent signal change estimated in these regions showed signal increases and temporal dynamics that were incongruent with typical BOLD activations. These artifacts were not distributed uniformly, but were aligned at the frontotemporal base, close to the oropharynx. The calculated head movement parameters for overt speech blocks were within the range of the rest blocks, indicating that head movement is unlikely the reason for the artifact. We conclude that ASL is not influenced by overt speech artifacts, whereas BOLD showed significant susceptibility artifacts, especially in the opercular and insular regions, where activation would be expected. ASL may prove to be the method of choice for fMRI investigations of continuous overt speech. Published 2004 Wiley-Liss, Inc.(dagger). C1 NIDCD, Language Sect, Voise Speech & Language Branch, NIH,Ckin Ctr, Bethesda, MD 20892 USA. NIMH, Funct Imaging Methods Unit, NIH, Bethesda, MD 20892 USA. RP Kemeny, S (reprint author), NIDCD, Language Sect, Voise Speech & Language Branch, NIH,Ckin Ctr, 9000 Rockville Pike Bld 10,Rm 3C716, Bethesda, MD 20892 USA. EM kemenys@nidcd.nih.gov NR 23 TC 56 Z9 56 U1 1 U2 5 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1065-9471 J9 HUM BRAIN MAPP JI Hum. Brain Mapp. PD MAR PY 2005 VL 24 IS 3 BP 173 EP 183 DI 10.1002/hbm.20078 PG 11 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 900YQ UT WOS:000227250600003 PM 15486986 ER PT J AU Huszthy, PC Svendsen, A Wilson, JM Kotin, RM Lonning, PE Bjerkvig, R Hoover, F AF Huszthy, PC Svendsen, A Wilson, JM Kotin, RM Lonning, PE Bjerkvig, R Hoover, F TI Widespread dispersion of adeno-associated virus serotype 1 and adeno-associated virus serotype 6 vectors in the rat central nervous system and in human glioblastoma multiforme xenografts SO HUMAN GENE THERAPY LA English DT Article ID GENE-THERAPY; VIRAL VECTORS; HEMOPHILIA-B; SIALIC-ACID; FACTOR-IX; IN-VIVO; INTRAMUSCULAR INJECTION; EFFICIENT TRANSDUCTION; CANINE MODEL; AAV VECTOR AB The transduction patterns of recombinant adeno-associated virus serotype 1 (AAV1) and serotype 6 (AAV6) vectors were assessed in human glioblastoma multiforme (GBM) cell lines, in human GBM biopsy spheroids, and in tumor xenografts growing in nude rat brains. All the cell lines tested (A172, D37, GaMg, HF66, and U373Mg) were found to be permissive to both AAV1 and AAV6 vectors, and thus displayed a transduction pattern similar to AAV2 vectors. For every cell line tested, the transduction efficiency displayed by AAV2 vectors was better than by isogenic and isopromoter AAV1 vectors. Transduction efficiency was dependent on the viral particle number used, suggesting that the receptors for these vectors are widely distributed in GBM tissues. Interestingly, AAV1, AAV2, and AAV6 vectors were able to infect and transduce the same cells when added simultaneously to monolayer cultures. Infection of human GBM biopsy spheroids with AAV1 and AAV6 vectors resulted in transgene expression both at the surface layers and in the core of the spheroids. Following injection of AAV1 and AAV6 vectors into human GBM biopsy xenografts growing in nude rat brains, reporter gene expression was seen both in the periphery as well as in the central regions of the tumors. When injected into the normal rat brain, both AAV1 and AAV6 vectors were found to transduce several central nervous system (CNS) regions. The presented results suggest a potential therapeutic role for AAV1 and AAV6 vectors in gene therapy for GBM and also for other CNS malignancies. C1 Haukeland Hosp, Dept Oncol & Med Phys, Gene Therapy Program, N-5021 Bergen, Norway. Ctr Rech Publ Sante, NorlUx Neurosci Labs, L-1417 Luxembourg, Luxembourg. Univ Penn, Wistar Inst, Philadelphia, PA 19104 USA. NHLBI, NIH, Bethesda, MD 20892 USA. RP Huszthy, PC (reprint author), Haukeland Hosp, Dept Oncol & Med Phys, Gene Therapy Program, N-5021 Bergen, Norway. EM Peter.Huszthy@helse-bergen.no RI kotin, robert/B-8954-2008; Wilson, James/F-9220-2011; Huszthy, Peter Csaba/H-1414-2016 OI Wilson, James/0000-0002-9630-3131; Huszthy, Peter Csaba/0000-0003-0184-8989 NR 52 TC 18 Z9 18 U1 0 U2 5 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1043-0342 J9 HUM GENE THER JI Hum. Gene Ther. PD MAR PY 2005 VL 16 IS 3 BP 381 EP 392 DI 10.1089/hum.2005.16.381 PG 12 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA 915CX UT WOS:000228276300011 PM 15812233 ER PT J AU Mustanski, BS DuPree, MG Nievergelt, CM Bocklandt, S Schork, NJ Hamer, DH AF Mustanski, BS DuPree, MG Nievergelt, CM Bocklandt, S Schork, NJ Hamer, DH TI A genomewide scan of male sexual orientation SO HUMAN GENETICS LA English DT Article ID HOMOSEXUAL-MEN; LINKAGE; GENE; RECEPTOR; POPULATIONS; CHROMOSOME; EXPRESSION; RELEASE; MARKERS; NUCLEI AB This is the first report of a full genome scan of sexual orientation in men. A sample of 456 individuals from 146 families with two or more gay brothers was genotyped with 403 microsatellite markers at 10-cM intervals. Given that previously reported evidence of maternal loading of transmission of sexual orientation could indicate epigenetic factors acting on autosomal genes, maximum likelihood estimations (mlod) scores were calculated separated for maternal, paternal, and combined transmission. The highest mlod score was 3.45 at a position near D7S798 in 7q36 with approximately equivalent maternal and paternal contributions. The second highest mlod score of 1.96 was located near D8S505 in 8p12, again with equal maternal and paternal contributions. A maternal origin effect was found near marker D10S217 in 10q26, with a mlod score of 1.81 for maternal meioses and no paternal contribution. We did not find linkage to Xq28 in the full sample, but given the previously reported evidence of linkage in this region, we conducted supplemental analyses to clarify these findings. First, we re-analyzed our previously reported data and found a mlod of 6.47. We then re-analyzed our current data, after limiting the sample to those families previously reported, and found a mlod of 1.99. These Xq28 findings are discussed in detail. The results of this first genome screen for normal variation in the behavioral trait of sexual orientation in males should encourage efforts to replicate these findings in new samples with denser linkage maps in the suggested regions. C1 Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60608 USA. NCI, NIH, Biochem Lab, Bethesda, MD USA. Penn State Univ, Dept Anthropol, University Pk, PA 16802 USA. Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA USA. RP Mustanski, BS (reprint author), Univ Illinois, Dept Psychiat, Inst Juvenile Res, M-C 747,1747 W Roosevelt Rd, Chicago, IL 60608 USA. EM bmustanski@psych.uic.edu OI Nievergelt, Caroline/0000-0001-5766-8923 FU NHLBI NIH HHS [HL64777-01] NR 40 TC 79 Z9 84 U1 3 U2 64 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD MAR PY 2005 VL 116 IS 4 BP 272 EP 278 DI 10.1007/s00439-004-1241-4 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 898AD UT WOS:000227047100005 PM 15645181 ER PT J AU Ouyang, XM Yan, D Du, LL Hejtmancik, JF Jacobson, SG Nance, WE Li, AR Angeli, S Kaiser, M Newton, V Brown, SDM Balkany, T Liu, XZ AF Ouyang, XM Yan, D Du, LL Hejtmancik, JF Jacobson, SG Nance, WE Li, AR Angeli, S Kaiser, M Newton, V Brown, SDM Balkany, T Liu, XZ TI Characterization of Usher syndrome type I gene mutations in an Usher syndrome patient population SO HUMAN GENETICS LA English DT Article ID MYOSIN VIIA GENE; SYNDROME TYPE 1D; RECESSIVE DEAFNESS; HAPLOTYPE ANALYSIS; ALLELIC MUTATIONS; HETEROGENEITY; FAMILIES; CDH23; USH1C; PROTEIN AB Usher syndrome type I (USH1), the most severe form of this syndrome, is characterized by profound congenital sensorineural deafness, vestibular dysfunction, and retinitis pigmentosa. At least seven USH1 loci, USH1A-G, have been mapped to the chromosome regions 14q32, 11q13.5, 11p15, 10q21-q22, 21q21, 10q21-q22, and 17q24-25, respectively. Mutations in five genes, including MYO7A, USH1C, CDH23, PCDH15 and SANS, have been shown to be the cause of Usher syndrome type 1B, type 1C, type 1D, type 1F and type 1G, respectively. In the present study, we carried out a systematic mutation screening of these genes in USH1 patients from USA and from UK. We identified a total of 27 different mutations; of these, 19 are novel, including nine missense, two nonsense, four deletions, one insertion and three splicing defects. Approximatelly 35-39% of the observed mutations involved the USH1B and USH1D genes, followed by 11% for USH1F and 7% for USH1C in non-Acadian alleles and 7% for USH1G. Two of the 12 MYO7A mutations, R666X and IVS40-1G>T accounted for 38% of the mutations at that locus. A 193delC mutation accounted for 26% of CDH23 (USH1D) mutations, confirming its high frequency. The most common PCDH15 (USH1F) mutation in this study, 5601-5603delAAC, accounts for 33% of mutant alleles. Interestingly, a novel SANS mutation, W38X, was observed only in the USA cohort. The present study suggests that mutations in MYO7A and CDH23 are the two major components of causes for USH1, while PCDH15, USH1C, and SANS are less frequent causes. C1 Univ Miami, Dept Otolaryngol, Miami, FL 33136 USA. NEI, NIH, Bethesda, MD 20892 USA. Univ Penn, Scheie Eye Inst, Philadelphia, PA 19104 USA. Virginia Commonwealth Univ, Dept Human Genet, Richmond, VA USA. Univ Manchester, Ctr Audiol, Manchester, Lancs, England. MRC, Mouse Genome Ctr, Harwell OX11 ORD, Oxon, England. MRC, Mammalian Genet Unit, Harwell OX11 ORD, Oxon, England. RP Liu, XZ (reprint author), Univ Miami, Dept Otolaryngol, 1666 NW 12th Ave, Miami, FL 33136 USA. EM xliu@med.miami.edu FU NEI NIH HHS [EY-13385]; NIDCD NIH HHS [DC05575] NR 35 TC 62 Z9 66 U1 0 U2 4 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD MAR PY 2005 VL 116 IS 4 BP 292 EP 299 DI 10.1007/s00439-004-1227-2 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 898AD UT WOS:000227047100007 PM 15660226 ER PT J AU Arcury, TA Quandt, SA Rao, P Doran, AM Snively, BM Barr, DB Davis, SW AF Arcury, TA Quandt, SA Rao, P Doran, AM Snively, BM Barr, DB Davis, SW TI Organophosphate pesticide exposure in farmworker family members in Western North Carolina and Virginia: Case comparisons SO HUMAN ORGANIZATION LA English DT Article DE migrant and seasonal farmworkers; farinworker families; pesticides; organophosphate pesticide metabolites ID AGRICULTURAL COMMUNITY; CHILDREN; PERCEPTIONS; SAFETY; URBAN AB Farmworkers and their family members are exposed to pesticides in their homes as well as at work. Using a sample of nine farmworker households in western North Carolina and Virginia, this analysis describes the organophosphate (OP) pesticide urinary metabolite levels of adults and children in these households, and compares these farmworker household OP metabolite levels to the national reference data. Data from survey and in-depth interviews are analyzed to find dwelling, household, and work characteristics related to OP metabolite levels. All participants had measurable OP metabolites. Every household had a high level of OP metabolites when compared to national reference data. There were common factors among the households that could cause the high household OP exposure, including farm employment and living adjacent to agricultural fields. Factors associated with household variability in OP exposure included having a non-nuclear family structure, and, therefore, having more adult males who were employed doing farm work, living in rental housing, not owning a vacuum cleaner, residing in a dwelling that is difficult to clean, and the season (spring versus summer) in which urine samples were collected. These results indicate that regulatory changes that improve low income housing, improve industrial hygiene standards, and provide farmworkers information about their pesticide exposure are needed to protect farmworkers and their families. C1 Wake Forest Univ, Dept Family & Community Med, Sch Med, Winston Salem, NC 27109 USA. Univ N Carolina, Chapel Hill, NC USA. Wake Forest Univ, Dept Publ Hlth Sci, Epidemiol Sect, Sch Med, Winston Salem, NC 27109 USA. Ctr Dis Control & Prevent, Pesticide Lab, Atlanta, GA USA. NIEHS, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA. Wake Forest Univ, Dept Psychol, Winston Salem, NC 27109 USA. RP Arcury, TA (reprint author), Wake Forest Univ, Dept Family & Community Med, Sch Med, Winston Salem, NC 27109 USA. EM tarcury@wfubmc.edu RI Barr, Dana/E-6369-2011; Barr, Dana/E-2276-2013 NR 33 TC 25 Z9 25 U1 1 U2 6 PU SOC APPLIED ANTHROPOLOGY PI OKLAHOMA CITY PA 3000 UNITED FOUNDERS BLVD, STE 148, OKLAHOMA CITY, OK 73112 USA SN 0018-7259 J9 HUM ORGAN JI Hum. Organ. PD SPR PY 2005 VL 64 IS 1 BP 40 EP 51 PG 12 WC Anthropology; Social Sciences, Interdisciplinary SC Anthropology; Social Sciences - Other Topics GA 908OQ UT WOS:000227797000005 ER PT J AU Hernandez, BY Frierson, HF Moskaluk, CA Li, YJ Clegg, L Cote, TR McCusker, ME Hankey, BF Edwards, BK Goodman, MT AF Hernandez, BY Frierson, HF Moskaluk, CA Li, YJ Clegg, L Cote, TR McCusker, ME Hankey, BF Edwards, BK Goodman, MT TI CK20 and CK7 protein expression in colorectal cancer: Demonstration of the utility of a population-based tissue microarray SO HUMAN PATHOLOGY LA English DT Article DE colorectal cancer; tissue microarray; cytokeratin ID VALIDATION; TECHNOLOGY; CARCINOMA; TUMORS; P53 AB The ability to use archival tissue to test externally valid hypotheses of carcinogenesis is dependent on the availability of population-based samples of cancer tissue. Tissue microarrays (TMAs) provide an efficient format for developing population-based samples of tissue. A TMA was constructed consisting of archival tissue from patients diagnosed with invasive colorectal cancer in the state of Hawaii in 1995. The population representativeness of the TMA was evaluated by comparing patient and clinical characteristics of TMA cases to that of all cases of colorectal carcinoma diagnosed statewide in 1995. Cytokeratin 20 (CK20) and cytokeratin 7 (CK7) immunohistochemistry was used to validate the utility of the TMA, and the expression of these proteins was correlated with patient and tumor characteristics. The TMA comprised tissue specimens from 286 patients representing 47% of all invasive cases diagnosed statewide in 1995. TMA cases were comparable to all invasive colorectal cases statewide with respect to age, sex, race/ethnicity, anatomic site, and survival. There were some differences between TMA cases and all cases With respect to tumor stage, histological classification, and treatment. There were significant differences in the relative expression of CK20 and CK7 proteins between malignant and normal tissues and by tumor stage. Advanced cancers were more likely to have CK20+/cytokeratin 7+ (CK7+) profiles than early-stage cancers, which were predominantly CK20+/cytokeratin 7- (CK7-). CK7+ expression was not correlated with anatomic location of carcinomas. This well-characterized TMA offers a powerful tool for testing hypotheses regarding colorectal carcinogenesis, including the identification of potential markers of neoplastic development and progression. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ Hawaii, Canc Res Ctr Hawaii, Hawaii Tumor Reg, Etiol Program, Honolulu, HI 96813 USA. Univ Virginia, Med Ctr, Dept Pathol, Charlottesville, VA 22908 USA. NCI, Surveillance Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. Univ Maryland, Sch Med, Dept Epidemiol & Prevent Med, Baltimore, MD 21201 USA. RP Hernandez, BY (reprint author), Univ Hawaii, Canc Res Ctr Hawaii, Hawaii Tumor Reg, Etiol Program, Honolulu, HI 96813 USA. EM brenda@crch.hawaii.edu FU NCI NIH HHS [N01-CN-67001, N01-PC-35137, N01-CN-25403] NR 12 TC 37 Z9 42 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD MAR PY 2005 VL 36 IS 3 BP 275 EP 281 DI 10.1016/j.humpath.2005.01.013 PG 7 WC Pathology SC Pathology GA 915DR UT WOS:000228278400008 PM 15791572 ER PT J AU Waldstein, SR Giggey, PP Thayer, JF Zonderman, AB AF Waldstein, SR Giggey, PP Thayer, JF Zonderman, AB TI Nonlinear relations of blood pressure to cognitive function - The Baltimore Longitudinal Study of Aging SO HYPERTENSION LA English DT Article DE blood pressure; hypertension; cognitive function; neuropsychology ID ALZHEIMERS-DISEASE; RISK-FACTORS; PERFORMANCE; DEMENTIA; AGE AB This investigation examined cross- sectional and longitudinal relations, both linear and nonlinear, of blood pressure ( BP) and its interaction with demographic and lifestyle variables to a broad spectrum of cognitive functions. Eight hundred forty- seven participants ( 503 men and 344 women) from the Baltimore Longitudinal Study of Aging completed tests of verbal and nonverbal memory, attention, perceptuo- motor speed, executive functions, and confrontation naming, and clinical assessment of BP on 1 to 7 occasions over 11 years. Mixed- effects regression models, adjusted for age, education, gender, alcohol consumption, smoking status, depression scores, and use of antihypertensive medications, revealed nonlinear relations of systolic BP with longitudinal change on tests of nonverbal memory and confrontation naming; cognitive decline was apparent among older ( 80 years) individuals with higher systolic BP. Cross- sectional findings, across testing sessions, indicated moderated U- and J- shaped relations between BP and cognitive function. Both high and low diastolic BP were associated with poorer performance on tests of executive function and confrontation naming among less- educated persons; with tests of perceptuo- motor speed and confrontation naming among nonmedicated ( antihypertensives) individuals; and with executive function among older individuals. Cross- sectional linear relations included higher systolic BP and poorer nonverbal memory in nondrinkers, and higher diastolic BP and poorer working memory among less- educated individuals. Results indicate that cross- sectional and longitudinal relations of BP to cognitive function are predominantly nonlinear and moderated by age, education, and antihypertensive medications. Careful monitoring and treatment of both high and low BP levels may be critical to the preservation of cognitive function. C1 Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21250 USA. NIA, Lab Personal & Cognit, Gerontol Res Ctr, Baltimore, MD 21224 USA. RP Waldstein, SR (reprint author), Univ Maryland Baltimore Cty, Dept Psychol, 1000 Hilltop Cir, Baltimore, MD 21250 USA. EM waldstei@umbc.edu OI Zonderman, Alan B/0000-0002-6523-4778 NR 23 TC 130 Z9 133 U1 0 U2 8 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD MAR PY 2005 VL 45 IS 3 BP 374 EP 379 DI 10.1161/01.HYP.0000156744.44218.74 PG 6 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 900NF UT WOS:000227220900014 PM 15699446 ER PT J AU Mitchell, GF Warner, E Parise, H Vita, JA Keaney, JF Keyes, MJ Levy, D Larson, MG Vasan, RS Benjamin, EJ AF Mitchell, GF Warner, E Parise, H Vita, JA Keaney, JF Keyes, MJ Levy, D Larson, MG Vasan, RS Benjamin, EJ TI Flow-mediated dilation: Just a marker of local shear stress? Response SO HYPERTENSION LA English DT Letter C1 Cardiovasc Engn Inc, Holliston, MA USA. Boston Univ, Sch Med, Boston, MA 02118 USA. NHLBI, Framingham Study, Framingham, MA USA. RP Mitchell, GF (reprint author), Cardiovasc Engn Inc, Holliston, MA USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0194-911X J9 HYPERTENSION JI Hypertension PD MAR PY 2005 VL 45 IS 3 BP E11 EP E12 DI 10.1161/01.HYP.0000154362.35209.b9 PG 2 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA 900NF UT WOS:000227220900030 ER PT J AU Zhou, QF Cannata, JM Meyer, RJ Van Tol, DJ Tadigadapa, S Hughes, WJ Shung, KK Trolier-McKinstry, S AF Zhou, QF Cannata, JM Meyer, RJ Van Tol, DJ Tadigadapa, S Hughes, WJ Shung, KK Trolier-McKinstry, S TI Fabrication and characterization of micromachined high-frequency tonpilz transducers derived by PZT thick films SO IEEE TRANSACTIONS ON ULTRASONICS FERROELECTRICS AND FREQUENCY CONTROL LA English DT Article AB Miniaturized tonpilz transducers are potentially useful for ultrasonic imaging in the 10 to 100 MHz frequency range due to their higher efficiency and output capabilities. In this work, 4 to 10-mu m thick piezoelectric thin films were used as the active element in the construction of miniaturized tonpilz structures. The tonpilz stack consisted of silver/lead zirconate titanate (PZT)/lanthanum nickelate (LaNiO3)/silicon on insulator (SOI) substrates. First, conductive LaNiO3 thin films, approximately 300 nm in thickness, were grown on SOI substrates by a metal-organic decomposition (MOD) method. The room temperature resistivity of the LaNiO3 was 6.5 X 10(-6) Omega circle m. Randomly oriented PZT (52/48) films up to 7-mu m thick were then deposited using a sol-gel process on the LaNiO3-coated SOI substrates. The PZT films with LaNiO3 bottom electrodes showed good dielectric and ferroelectric properties. The relative dielectric permittivity (at 1 kHz) was about 1030. The remanent polarization of PZT films was larger than 26 mu C/cm(2). The effective transverse piezoelectric e(31,f) coefficient of PZT thick films was about -6.5 C/m(2) when poled at -75 kV/cm for 15 minutes at room temperature. Enhanced piezoelectric properties were obtained on poling the PZT films at higher temperatures. A silver layer about 40-mu m thick was prepared by silver powder dispersed in epoxy and deposited onto the PZT film to form the tail mass of the tonpilz structure. The top layers of this wafer were subsequently diced with a saw, and the structure was bonded to a second wafer. The original silicon carrier wafer was polished and etched using a Xenon difluoride (XeF2) etching system. The resulting structures showed good piezoelectric activity. This process flow should enable integration of the piezoelectric elements with drive/receive electronics. C1 Penn State Univ, University Pk, PA 16802 USA. Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA. Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA. RP Zhou, QF (reprint author), Penn State Univ, University Pk, PA 16802 USA. EM qifazhou@usc.edu OI Trolier-McKinstry, Susan/0000-0002-7267-9281; Tadigadapa, Srinivas/0000-0002-8700-2476 NR 20 TC 19 Z9 19 U1 3 U2 13 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA SN 0885-3010 J9 IEEE T ULTRASON FERR JI IEEE Trans. Ultrason. Ferroelectr. Freq. Control PD MAR PY 2005 VL 52 IS 3 BP 350 EP 357 DI 10.1109/TUFFC.2005.1417256 PG 8 WC Acoustics; Engineering, Electrical & Electronic SC Acoustics; Engineering GA 911VA UT WOS:000228032800001 PM 15857042 ER PT J AU Williams, MS Henkart, PA AF Williams, MS Henkart, PA TI Do cytotoxic lymphocytes kill via reactive oxygen species? SO IMMUNITY LA English DT Editorial Material ID CELL-DEATH; GRANZYME-B; APOPTOSIS AB A paper by Martinvalet et al. (2005) in this issue of Immunity examines the mechanisms used by granzyme A to kill target cells after its cytoplasmic injection by cytotoxic lymphocytes. They show that this protease induces mitochondrial damage and generation of reactive oxygen species that are necessary for cell death. C1 Univ Maryland, Sch Med, Dept Microbiol & Immunol, Rockville, MD 20855 USA. NCI, Expt Immunol Branch, Bethesda, MD 20892 USA. RP Williams, MS (reprint author), Univ Maryland, Sch Med, Dept Microbiol & Immunol, Rockville, MD 20855 USA. NR 12 TC 1 Z9 1 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD MAR PY 2005 VL 22 IS 3 BP 272 EP 274 DI 10.1016/j.immuni.2005.03.003 PG 3 WC Immunology SC Immunology GA 912UP UT WOS:000228105700002 PM 15780984 ER PT J AU Han, SB Moratz, C Huang, NN Kelsall, B Cho, H Shi, CS Schwartz, O Kehrl, JH AF Han, SB Moratz, C Huang, NN Kelsall, B Cho, H Shi, CS Schwartz, O Kehrl, JH TI Rgs1 and Gnai2 regulate the entrance of B lymphocytes into lymph nodes and B cell motility within lymph node follicles SO IMMUNITY LA English DT Article ID PROTEIN-COUPLED RECEPTOR; SPHINGOSINE 1-PHOSPHATE; DENDRITIC CELLS; VASCULAR ADDRESSIN; T-LYMPHOCYTE; L-SELECTIN; MICE; CHEMOTAXIS; EXPRESSION; MIGRATION AB Signaling by G protein-coupled receptors coupled to G alpha(i) assists in triggering lymphocyte movement into and out of lymph nodes. Here, we show that modulating the signaling output from these receptors dramatically alters B cell trafficking. Intravital microscopy of adoptively transferred B cells from wild-type and Rgs1(-/-) mice revealed that Rgs1(-/-) B cells stick better to lymph node high endothelial venules, home better to lymph nodes, and move more rapidly within lymph node follicles than do wild-type B cells. In contrast, B cells from Gnai2(-/-) mice enter lymph nodes poorly and move more slowly than do wild-type B cells. The Gnai2(-/-) mice often lack multiple peripheral lymph nodes, and their B cells respond poorly to chemokines, indicating that G alpha(i1) and G alpha(i3) poorly compensate for the loss of G alpha(i2). These results demonstrate opposing roles for Rgs1 and Gnai2 in B cell trafficking into and within lymph nodes. C1 NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. NIAID, Clin Invest Lab, NIH, Bethesda, MD 20892 USA. NIAID, Res Technol Branch, NIH, Bethesda, MD 20892 USA. RP Kehrl, JH (reprint author), NIAID, Immunoregulat Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM jkehrl@niaid.nih.gov OI Kehrl, John/0000-0002-6526-159X NR 45 TC 111 Z9 116 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1100 MASSACHUSETTS AVE, CAMBRIDGE, MA 02138 USA SN 1074-7613 J9 IMMUNITY JI Immunity PD MAR PY 2005 VL 22 IS 3 BP 343 EP 354 DI 10.1016/j.immuni.2005.01.017 PG 12 WC Immunology SC Immunology GA 912UP UT WOS:000228105700009 PM 15780991 ER PT J AU Koya, V Leppla, SH Daniell, H AF Koya, Vijay Leppla, Stephen H. Daniell, Henry TI Efficacy and functionality of chloroplast-derived anthrax protective antigen SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL LA English DT Meeting Abstract C1 Univ Cent Florida, Dept Mol Biol & Microbiol, Orlando, FL 32816 USA. NIAID, Microbial Pathogenesis Sect, NIH, Bethesda, MD 20892 USA. EM daniell@mail.ucf.edu 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 1071-2690 J9 IN VITRO CELL DEV-AN JI In Vitro Cell. Dev. Biol.-Anim. PD SPR PY 2005 VL 41 BP 24A EP 24A PG 1 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA V44IC UT WOS:000202995400087 ER PT J AU Cho, H Lasco, TM Allen, SS Yoshimura, T McMurray, DN AF Cho, H Lasco, TM Allen, SS Yoshimura, T McMurray, DN TI Recombinant guinea pig tumor necrosis factor alpha stimulates the expression of interleukin-12 and the inhibition of Mycobacterium tuberculosis growth in macrophages SO INFECTION AND IMMUNITY LA English DT Article ID BOVIS BCG VACCINATION; HUMAN ALVEOLAR MACROPHAGES; MESSENGER-RNA EXPRESSION; IFN-GAMMA PRODUCTION; TNF-ALPHA; INTERFERON-GAMMA; PULMONARY TUBERCULOSIS; DIFFERENTIAL REGULATION; PERITONEAL-MACROPHAGES; LATENT TUBERCULOSIS AB Tumor necrosis factor alpha (TNF-alpha) plays an important role in the host immune response to infection with the intracellular pathogen Mycobacterium tuberculosis. It is essential for the formation of protective tuberculous granulomas and regulates the expression of other cytokines which contribute to a protective immune response. Interleukin-12 (IL-12) is known to promote a Th1 response, which is essential for antimycobacterial resistance. Recombinant guinea pig TNF-alpha (rgpTNF-alpha) protein (17 kDa) was purified, and its bioactivity was confirmed by its cytotoxicity for L929 fibroblasts. High titers of polyclonal anti-gpTNF-alpha antibody were obtained by immunization of rabbits. Resident alveolar and peritoneal macrophages were isolated from guinea pigs and infected with either the H37Ra or H37Rv strain of M. tuberculosis. The mRNA levels for TNF-alpha and IL-12 p40 were measured using real-time PCR. IL-12 p40 mRNA was up-regulated in a dose-dependent manner by rgpTNF-alpha alone. In infected macrophages, a lower dose of rgpTNF-alpha intensified the mRNA levels of TNF-alpha and IL-12 p40. However, higher doses of rgpTNF-alpha suppressed TNF-a and IL-12 p40 mRNA. The antimycobacterial activity of macrophages was assessed by metabolic labeling of M. tuberculosis with [H-3] uracil. Resident alveolar and peritoneal macrophages treated with anti-gpTNF-alpha antibody to block endogenous TNF-alpha exhibited increased intracellular mycobacterial growth. These data suggest that the dose of TNF-alpha is crucial to the stimulation of optimal expression of protective cytokines and that TNF-alpha contributes to the control of mycobacterial replication to promote host resistance against M. tuberculosis. C1 Texas A&M Univ Syst, Hlth Sci Ctr, Dept Med Microbiol & Immunol, College Stn, TX 77843 USA. Natl Canc Inst, Canc Res & Dev Ctr, Mol Immunoregulat Lab, Frederick, MD USA. RP Cho, H (reprint author), Texas A&M Univ Syst, Hlth Sci Ctr, Dept Med Microbiol & Immunol, 407 Reynolds Med Bldg, College Stn, TX 77843 USA. EM HScho@medicine.tamu.edu FU NIAID NIH HHS [R01 AI015495, R01 AI15495] NR 53 TC 46 Z9 48 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD MAR PY 2005 VL 73 IS 3 BP 1367 EP 1376 DI 10.1128/IAI.73.3.1367-1376.2005 PG 10 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 902RD UT WOS:000227373300012 PM 15731034 ER PT J AU Yao, YF Sturdevant, DE Villaruz, A Xu, L Gao, Q Otto, M AF Yao, YF Sturdevant, DE Villaruz, A Xu, L Gao, Q Otto, M TI Factors characterizing Staphylococcus epidermidis invasiveness determined by comparative genomics SO INFECTION AND IMMUNITY LA English DT Article ID POLYSACCHARIDE INTERCELLULAR ADHESIN; FIBRINOGEN-BINDING PROTEIN; SEQUENCE ELEMENT IS256; SURFACE-PROTEINS; VIRULENCE GENES; AUREUS; EXPRESSION; RESISTANCE; INSERTION; IDENTIFICATION AB Virulence mechanisms of the leading nosocomial pathogen Staphylococcus epidermidis are poorly understood. We used microarray-based genome-wide comparison of clinical and commensal S. epidermidis strains to identify putative virulence determinants. Our study revealed high genetic variability of the S. epidermidis genome, new markers for invasiveness of S. epidermidis, and potential targets for drug development against S. epidermidis infections. C1 NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT USA. Fudan Univ, Shanghai Med Coll, Key Lab Med Mol Virol, Shanghai, Peoples R China. RP Otto, M (reprint author), 903 S 4th St, Hamilton, MT 59840 USA. EM motto@niaid.nih.gov OI Otto, Michael/0000-0002-2222-4115 NR 23 TC 54 Z9 58 U1 0 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD MAR PY 2005 VL 73 IS 3 BP 1856 EP 1860 DI 10.1128/IAI.73.3.1856-1860.2005 PG 5 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 902RD UT WOS:000227373300066 PM 15731088 ER PT J AU Gutmann, R Czermak, G Dumfort, A van der Veer, WE Hong, B Kopacka, H Ongania, KH Bechtold, T Bruggeller, P AF Gutmann, R Czermak, G Dumfort, A van der Veer, WE Hong, B Kopacka, H Ongania, KH Bechtold, T Bruggeller, P TI Unprecedented conformational modulation of the efficiency of luminescence in Ru(II) bipyridyl complexes containing a bis(bidentate) phosphine SO INORGANIC CHEMISTRY COMMUNICATIONS LA English DT Article DE mono- and dinuclear Ru complexes; crystal structures; bis(bidentate) phosphine; luminescence; metal-to-ligand charge-transfer; steric effects ID RIGID MOLECULAR RODS; MLCT EXCITED-STATES; DIIMINE COMPLEXES; RUTHENIUM(II); LIGAND; PHOTOCHEMISTRY; POLYPHOSPHINE; PHOTOPHYSICS; REACTIVITY; METAL AB We report the first observation of conformational modulation of the efficiency of luminescence of a chelating phosphine containing a saturated backbone and combined with [Ru(bpy)(2)](2+). The observed luminescent lifetimes are very long: 910(20) ns in CD(3)CN and 794(20) ns in CH(3)CN at 298 K. The bimetallic structure of rac-(DeltaDelta/LambdaLambda)-[Ru(2)(dppcb)(bpy)(4)](PF(6))(4) (1) and meso-(DeltaLambda/LambdaDelta)-[Ru(2)(dppcb)(bpy)(4)](PF(6))(4) (2), where dppcb is cis, trans, cis-1,2,3,4-tetrakis(diphenylphosphino)cyclobutane, is responsible for this dramatic effect. An enhanced folding of the cyclobutane rings drastically reduces the efficiency of luminescence as observed in the new monometallic complexes [Ru(dppcb)(bpy)(2)](PF(6))(2) (3) and [Ru(dppcbO(2))(bpy)(2)](PF(6))(2) (4), where dppcbO(2) is cis, trans, cis-1,2-bis(diphenylphosphinoyl)-3,4-bis(diphenylphosphino)cyclobutane. (C) 2005 Elsevier B.V. All rights reserved. C1 Univ Innsbruck, Inst Gen Inorgan & Theoret Chem, A-6020 Innsbruck, Austria. Univ Calif Irvine, Dept Chem, Irvine, CA 92697 USA. NIH, Bethesda, MD 20817 USA. Univ Innsbruck, Inst Organ Chem, A-6020 Innsbruck, Austria. Univ Innsbruck, Inst Text Chem & Text Phys, A-6020 Innsbruck, Austria. RP Bruggeller, P (reprint author), Univ Innsbruck, Inst Gen Inorgan & Theoret Chem, Innrain 52A, A-6020 Innsbruck, Austria. EM Peter.Bruegeller@uibk.ac.at OI Bruggeller, Peter/0000-0001-9411-6554; Bechtold, Thomas/0000-0002-9222-9755 NR 18 TC 8 Z9 8 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1387-7003 J9 INORG CHEM COMMUN JI Inorg. Chem. Commun. PD MAR PY 2005 VL 8 IS 3 BP 319 EP 322 DI 10.1016/j.inoche.2005.01.009 PG 4 WC Chemistry, Inorganic & Nuclear SC Chemistry GA 900OE UT WOS:000227223400023 ER PT J AU Bergmann-Leitner, ES Scheiblhofer, S Duncan, EH Leitner, WW Chen, D Angov, E Khan, F Williams, JL Winter, DB Thalhamer, J Lyon, JA Tsokos, GC AF Bergmann-Leitner, ES Scheiblhofer, S Duncan, EH Leitner, WW Chen, D Angov, E Khan, F Williams, JL Winter, DB Thalhamer, J Lyon, JA Tsokos, GC TI C3d binding to the circumsporozoite protein carboxy-terminus deviates immunity against malaria SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE complement; host defense; malaria; T lymphocytes ID B-CELL RESPONSE; PLASMODIUM-BERGHEI; MOLECULAR ADJUVANT; PROTECTIVE IMMUNITY; FUSION PROTEINS; COMPLEMENT; ANTIBODY; DNA; SPOROZOITES; EXPRESSION AB The immunogenicity of recombinant protein or anti-viral DNA vaccines can be significantly improved by the addition of tandem copies of the complement fragment C3d. We sought to determine if the efficacy of a circumsporozoite protein (CSP)-based DNA vaccine delivered to mouse skin by gene gun was improved by using this strategy. Instead, we found that C3d suppressed the protective immunity against Plasmodium berghei malaria infection and deviated immunity, most notably by suppressing the induction of antibodies specific for the CSP C-terminal flanking sequence and by suppressing the induction of CSP-specific IL-4-producing spleen cells. We further showed that C3d bound to the C-terminal flanking sequence of the CSP, which may explain the immune deviation observed in CS/C3d chimeric antigen. We have thus identified C3d-mediated epitope masking and shifting of both the humoral and cellular immune responses as a potential novel escape mechanism, which plasmodia may use to divert the induction of protective immunity. C1 Walter Reed Army Inst Res, Dept Cellular Injury, Silver Spring, MD 20910 USA. Walter Reed Army Inst Res, Dept Entomol, Silver Spring, MD 20910 USA. Salzburg Univ, Inst Chem & Biochem, Immunol Grp, A-5020 Salzburg, Austria. NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA. RP Tsokos, GC (reprint author), Walter Reed Army Inst Res, Dept Cellular Injury, Silver Spring, MD 20910 USA. EM gtsokos@usuhs.mil RI Bergmann-Leitner, Elke/B-3548-2011; Leitner, Wolfgang/F-5741-2011; Weiss, Richard/N-7279-2013; Thalhamer, Josef/E-5787-2011 OI Bergmann-Leitner, Elke/0000-0002-8571-8956; Leitner, Wolfgang/0000-0003-3125-5922; Weiss, Richard/0000-0003-3185-7253; Thalhamer, Josef/0000-0003-2285-6400 FU NIAID NIH HHS [R03 AI053463] NR 42 TC 27 Z9 28 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD MAR PY 2005 VL 17 IS 3 BP 245 EP 255 DI 10.1093/intimm/dxh205 PG 11 WC Immunology SC Immunology GA 900WB UT WOS:000227243900004 PM 15710912 ER PT J AU Chau, KY Keane-Myers, AM Fedele, M Ikeda, Y Creusot, RJ Menozzi, L Cousins, DJ Manfioletti, G Feigenbaum, L Fusco, A Ono, SJ AF Chau, KY Keane-Myers, AM Fedele, M Ikeda, Y Creusot, RJ Menozzi, L Cousins, DJ Manfioletti, G Feigenbaum, L Fusco, A Ono, SJ TI IFN-gamma gene expression is controlled by the architectural transcription factor HMGA1 SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE gene regulation; HMGA1; IFN-gamma ID T-CELL DIFFERENTIATION; INTERFERON-GAMMA; NUCLEAR FACTOR; SELECTIVE EXPRESSION; REGULATORY ELEMENTS; CHROMATIN-STRUCTURE; PROMOTER ELEMENTS; DNA-BINDING; ACTIVATION; PROTEINS AB We report for the first time that IFNG gene expression requires high mobility group (HMG)A1, the architectural transcription factor mediating enhanceosome formation. This finding is supported by our direct studies of T cells isolated from the HMGA1-transgenic mice displaying an up-regulation of IFN-gamma production and of HMGA1-deficient mice exhibited a decreased IFN-gamma induction. In parallel transfection studies in EL4 cells, we observed elevated IFNG gene promoter activity in cells stably over-expressing HMGA1 and a reduction of such activity in cells expressing dominant-negative HMGA1. In vitro binding assays further demonstrated a specific interaction of HMGA1 to defined regions of the IFNG gene proximal promoter. C1 UCL, Inst Ophthalmol, Dept Immunol, London EC1V 9EL, England. Moorfields Eye Hosp, NHS Fdn Trust, London EC1V 9EL, England. NIAID, Lab Allerg Dis, Eosinophil Biol Sect, NIH, Rockville, MD USA. Univ Naples Federico 2, CNR, Ist Endocrinol & Oncol Sperimentale, Dipartimento Biol & Patol Cellulare & Mol, Naples, Italy. UCL, Windeyer Inst Med Sci, Dept Immunol & Mol Pathol, London WC1E 6BT, England. Kings Coll London, GKT Sch Med, Dept Asthma Allergy & Resp Sci, London WC2R 2LS, England. Univ Trieste, Dipartimento Biochim Biofis & Chim Macromol, I-34127 Trieste, Italy. NCI, Sci Applicat Int Corp, Frederick, MD 21701 USA. RP Ono, SJ (reprint author), UCL, Inst Ophthalmol, Dept Immunol, 11-43 Bath St, London EC1V 9EL, England. EM santa.ono@ucl.ac.uk RI Chau, Kai-Yin (David)/C-2845-2011; Fedele, Monica/C-1417-2015; OI Fusco, Alfredo/0000-0003-3332-5197; Fedele, Monica/0000-0002-9171-1312 FU NIGMS NIH HHS [R01 GM49661] NR 44 TC 9 Z9 9 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD MAR PY 2005 VL 17 IS 3 BP 297 EP 306 DI 10.1093/intimm/dxh209 PG 10 WC Immunology SC Immunology GA 900WB UT WOS:000227243900009 PM 15710911 ER PT J AU Stein, WD Litman, T Fojo, T Bates, SE AF Stein, WD Litman, T Fojo, T Bates, SE TI Differential expression of cell adhesion genes: Implications for drug resistance SO INTERNATIONAL JOURNAL OF CANCER LA English DT Review DE cell adhesion; drug resistance; database mining; gene expression; metastasis; Surveillance; Epidemiology and End Results data ID SNAKE-VENOM DISINTEGRIN; IN-VIVO; CLINICAL-APPLICATIONS; INDUCED APOPTOSIS; SOLID TUMORS; CANCER; GROWTH; DISRUPTION; CONTORTROSTATIN; CHEMORESISTANCE AB It is well known that tumors arising from tissues such as kidney, pancreas, liver and stomach are particularly refractory to treatment. Searching for new anticancer drugs using cells in culture has yielded some effective therapies, but these refractory tumors remain intractable. Studies that compare cells grown in suspension to similar cells grown attached to one another as aggregates have suggested that it is adhesion to the extracellular matrix of the basal membrane that confers resistance to apoptosis and, hence, resistance to cytotoxins. The genes whose expression correlates with poor survival might, therefore, act through such a matrix-to-cell suppression of apoptosis. Indeed, correlative mining of gene expression and patient survival databases suggests that poor survival in patients with metastatic cancer correlates highly with tumor expression of a common theme: the genes involved in cell adhesion and the cytoskeleton. If the proteins involved in tethering cells to the extracellular matrix are important in conferring drug resistance, it may be possible to improve chemotherapy by designing drugs that target these proteins. (C) 2004 Wiley-Liss, Inc. C1 Hebrew Univ Jerusalem, Silberman Inst Life Sci, Jerusalem, Israel. Univ Copenhagen, Bioinformat Ctr, Copenhagen, Denmark. Natl Canc Inst, Canc Therapeut Branch, Bethesda, MD USA. RP Stein, WD (reprint author), Hebrew Univ Jerusalem, Silberman Inst Life Sci, Jerusalem, Israel. EM wdstein@vms.huji.ac.il NR 46 TC 10 Z9 10 U1 1 U2 3 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD MAR 1 PY 2005 VL 113 IS 6 BP 861 EP 865 DI 10.1002/ijc.20671 PG 5 WC Oncology SC Oncology GA 888BD UT WOS:000226348300001 PM 15514970 ER PT J AU Nilsen, TIL Romundstad, PR Troisi, R Vatten, LJ AF Nilsen, TIL Romundstad, PR Troisi, R Vatten, LJ TI Birth size and subsequent risk for prostate cancer: A prospective population-based study in Norway SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article DE prostate cancer; metastasis; birth weight; birth length; head circumference ID BREAST-CANCER; FOLLOW-UP; WEIGHT; COHORT; PREDICTOR; GROWTH AB Studies on birth size characteristics and adult risk for prostate cancer have been few and inconclusive. We prospectively examined the association between birth size and risk for prostate cancer with particular emphasis on metastatic disease. A total of 19,681 singleton males born between 1920 and 1958, whose birth records were kept at St. Olav's University Hospital (Trondheim, Norway), were followed up for prostate cancer by linkage to the Norwegian Cancer Registry. A total of 159 cases of prostate cancer were diagnosed during follow-up; 33 had metastases at diagnosis. Overall, there was little evidence for any association between birth size and prostate cancer risk; however, there was a positive association for birth size and metastatic disease. Men in the highest quartile of birth length ( greater than or equal to 53 cm) had a relative risk of 2.5 (95% CI 1.0-6.3) compared to men in the lowest quartile ( < 51 cm). Further, men in the highest quartile of both birth weight and birth length had a relative risk of 3.8 (95% CI 1.2-12.0) for metastatic prostate cancer compared to men in the lowest category of both factors. These results support the hypothesis that factors that determine intrauterine growth could be important for aggressive forms of prostate cancer in adulthood. (C) 2004 Wiley-Liss, Inc. C1 Norwegian Univ Sci & Technol, Dept Publ Hlth & Gen Practice, NO-7489 Trondheim, Norway. Natl Canc Inst, Div Epidemiol & Genet, Bethesda, MD USA. RP Vatten, LJ (reprint author), Norwegian Univ Sci & Technol, Dept Publ Hlth & Gen Practice, NO-7489 Trondheim, Norway. EM lars.vatten@medisin.ntnu.no OI Romundstad, Pal Richard/0000-0003-2061-4336 NR 14 TC 25 Z9 25 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD MAR 1 PY 2005 VL 113 IS 6 BP 1002 EP 1004 DI 10.1002/ijc.20674 PG 3 WC Oncology SC Oncology GA 888BD UT WOS:000226348300018 PM 15514943 ER PT J AU Nunez, JT Gomez, G AF Nunez, JT Gomez, G TI Low-dose secnidazole in the treatment of bacterial vaginosis SO INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS LA English DT Article DE secnidazole; bacterial vaginosis; Gardnerella vaginalis ID NONSPECIFIC VAGINITIS; METRONIDAZOLE; INFECTIONS; ASSOCIATIONS; CLINDAMYCIN; MANAGEMENT; TINIDAZOLE; THERAPY AB Objective: To determine whether bacterial, vaginosis could be cured with a single 1-g oral dose of secnidazole. Material and methods: A total of 80 women were recruited at the outpatient gynecologic clinic of Manuel Noriega Hospital, Maracaibo, Venezuela. Diagnosis and patient enrollment were based on the Amsel criteria. The participants were randomized to 2 groups. In group 1 (n=44) participants received a single 1-g oral dose and in group 2 (n=32) participants received a single 2-g oral dose of secnidazole. Clinical cure was defined as the absence of the characteristic symptoms (a bad odor and a grossly abnormal discharge) and at least 2 of the following: vaginal pH less than 4.5, no fish odor on addition of KOH, and no Gardnerella vaginalis or clue cells on wet-mount examination. Cytologic cure was defined as an absence of G. vaginalis on a Papanicolaou (Pap) smear. Results: Clinical cure was experienced by 95.5% of the women who received the 1-g oral dose and by 97.4% of the women who received the 2-g oral dose,of secnidazole. There was no significant difference between the groups in the clinical resolution of bacterial. vaginosis. Following treatment, results were negative for G. vaginalis in 94.7% of the women. In group 1, 41 women (93.2%), and in group 2, 31 women (96.9%) had cytologic cure. The Pap smear revealed G. vaginalis in 3 of the women in group 1 and 1 of the women in group 2 (P=0.47). Twenty-seven women (35.5%) reported mild side effects. More women had adverse effects in group 1 (n=16) than in group 2 (n=11) but this difference was not statistically significant. Conclusion: This clinical study showed that a single 1-g oral dose of secnidazole is effective to cure bacterial. vaginosis associated with G. vaginalis. (c) 2005 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved. C1 Univ Zulia, Hosp Manuel Noruega Trigo, Fac Med, Maracaibo 4011, Venezuela. Hosp Manuel Noriega Trigo, Maracaibo, Venezuela. RP Nunez, JT (reprint author), Natl Canc Inst, Lab Mol Technol, 915 Tollouse Ave,Suite 211, Frederick, MD 21701 USA. EM jnunez@ncifcrf.gov NR 21 TC 8 Z9 13 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0020-7292 J9 INT J GYNECOL OBSTET JI Int. J. Gynecol. Obstet. PD MAR PY 2005 VL 88 IS 3 BP 281 EP 285 DI 10.1016/j.ijgo.2004.11.028 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA 909BK UT WOS:000227833700008 PM 15733882 ER PT J AU Smego, RA Sebanego, P AF Smego, RA Sebanego, P TI Treatment options for hepatic cystic echinococcosis SO INTERNATIONAL JOURNAL OF INFECTIOUS DISEASES LA English DT Review DE cystic hepatic echinococcosis; hepatic hydatid cyst; PAIR; atbendazole; mebendazole ID HYDATID LIVER CYSTS; PERCUTANEOUS TREATMENT; SURGICAL-TREATMENT; PHARMACOKINETIC INTERACTION; ALBENDAZOLE SULFOXIDE; SONOGRAPHIC GUIDANCE; THERAPEUTIC APPROACH; HYPERTONIC SALINE; ALCOHOL INJECTION; DISEASE AB A number of surgical and non-surgical options exist to treat cystic echinococcosis of the liver. For decades, surgical excision via a conservative or radical approach was the recommended approach for hepatic hydatid cysts. The availability of chemotherapeutic agents with significant activity against Echinococcus granulosis has made it possible to undertake ultrasound- or computed tomography-guided transhepatic percutaneous drainage (termed puncture, aspiration, injection, and re-aspiration (PAIR)) of hydatid cysts. Pre- and post-intervention chemotherapy with albendazote or mebendazole offers the advantage of reducing the risk of disease recurrence and intraperitoneal seeding of infection that may develop via cyst rupture and spillage occurring spontaneously or during surgery or needle drainage. PAIR appears to have greater clinical efficacy (i.e. a higher incidence of cure), tower rates of major and minor complications, mortality, and disease recurrence, and fewer days of hospitalization compared to patients treated surgically. For patients who fait drug therapy atone, PAIR is a safe and effective procedure of choice for patients with hepatic echinococcosis, and perhaps other anatomic sites of infection such as lung, peritoneum, kidney, and other viscera. Surgery should be reserved for patients with hydatid cysts refractory to PAIR because of secondary bacterial. infection or for those with difficult-to-manage cyst-biliary communication or obstruction. Published by Elsevier Ltd on behalf of International Society for Infectious Diseases. C1 Univ N Dakota, Dept Med, Sch Med & Hlth Sci, Fargo, ND USA. RP Smego, RA (reprint author), NIAID, Tuberculosis Res Sect, Immunogenet Lab, NIH, Twinbrook 2,Room 236,MSC 8180,12441 Parklawn Dri, Rockville, MD 20852 USA. EM rsmego@niaid.nih.gov RI ozerhan, ismail hakki/H-8689-2012 OI ozerhan, ismail hakki/0000-0001-5777-8671 NR 87 TC 74 Z9 79 U1 2 U2 7 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1201-9712 J9 INT J INFECT DIS JI Int. J. Infect. Dis. PD MAR PY 2005 VL 9 IS 2 BP 69 EP 76 DI 10.1016/j.ijid.2004.08.001 PG 8 WC Infectious Diseases SC Infectious Diseases GA 908CJ UT WOS:000227764600004 PM 15708321 ER PT J AU Hristovski, D Peterlin, B Mitchell, JA Humphrey, SM AF Hristovski, D Peterlin, B Mitchell, JA Humphrey, SM TI Using literature-based discovery to identify disease candidate genes SO INTERNATIONAL JOURNAL OF MEDICAL INFORMATICS LA English DT Article DE medical informatics; knowledge discovery; data mining; MEDLINE; discovery support; genes; diseases ID FISH-OIL; GENERATING HYPOTHESES; RESOURCES; RAYNAUDS AB We present BITOLA, an interactive titerature-based biomedical discovery support system. The goal of this system is to discover new, potentially meaningful relations between a given starting concept of interest and other concepts, by mining the bibliographic database MEDLINE(R). To make the system more suitable for disease candidate gene discovery and to decrease the number of candidate relations, we integrate background knowledge about the chromosomal location of the starting disease as well as the chromosomal location of the candidate genes from resources such as LocusLink and Human Genome Organization (HUGO). BITOLA can also be used as an alternative way of searching the MEDLINE database. The system is available at http://www.mf.uni-lj.si/bitola/. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Univ Ljubljana, Fac Med, Inst Biomed Informat, Ljubljana 1104, Slovenia. Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Bethesda, MD USA. Univ Ljubljana, Med Ctr, Div Med Genet, Ljubljana 1104, Slovenia. Univ Missouri, Sch Med, Dept Hlth Management & Informat, Columbia, MO 65211 USA. RP Hristovski, D (reprint author), Univ Ljubljana, Fac Med, Inst Biomed Informat, Vrazov Trg 2-2, Ljubljana 1104, Slovenia. EM dimitar.hristovski@mf.uni-lj.si RI Hristovski, Dimitar/A-6288-2009; peterlin, borut/C-6086-2011; OI peterlin, borut/0000-0001-7824-4978; Hristovski, Dimitar/0000-0001-6908-0246 NR 24 TC 116 Z9 122 U1 0 U2 9 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 1386-5056 J9 INT J MED INFORM JI Int. J. Med. Inform. PD MAR PY 2005 VL 74 IS 2-4 BP 289 EP 298 DI 10.1016/j.ijmedinf.2004.04.024 PG 10 WC Computer Science, Information Systems; Health Care Sciences & Services; Medical Informatics SC Computer Science; Health Care Sciences & Services; Medical Informatics GA 903DW UT WOS:000227406700024 PM 15694635 ER PT J AU Chen, G Adeyemo, AA Johnson, T Zhou, J Amoah, A Owusu, S Acheampong, J Agyenim-Boateng, K Eghan, BA Oli, J Okafor, G Abbiyesuku, F Dunston, GM Chen, Y Collins, F Rotimi, C AF Chen, G Adeyemo, AA Johnson, T Zhou, J Amoah, A Owusu, S Acheampong, J Agyenim-Boateng, K Eghan, BA Oli, J Okafor, G Abbiyesuku, F Dunston, GM Chen, Y Collins, F Rotimi, C TI A genome-wide scan for quantitative trait loci linked to obesity phenotypes among West Africans SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE genome scan; type 2 diabetes; genetics; West Africa ID RESTING METABOLIC-RATE; SERUM LEPTIN LEVELS; BODY-MASS INDEX; LINKAGE ANALYSIS; RESPIRATORY QUOTIENT; SUSCEPTIBILITY GENES; SEARCH; FAT; TRIPHOSPHATASE; HYPERTENSION AB OBJECTIVE: To identify quantitative trait loci (QTL) for three obesity phenotypes: body mass index (BMI), fat mass (FM) and percent body fat (PBF) in West Africans with type 2 diabetes (T2DM). DESIGN: An affected sibling pair (ASP) design, in which both siblings had T2DM. Obesity was analyzed as a quantitative trait using a variance components approach. SUBJECTS: Sib-pairs affected with T2DM from the Africa America Diabetes Mellitus (AADM) study, comprising 321 sibling pairs and 36 half-sibling pairs. MEASUREMENTS: Weight was measured on an electronic scale to the nearest 0.1 kg, and height was measured with a stadiometer to the nearest 0.1 cm. Body composition was estimated using bioelectric impedance analysis (BIA). Genotyping was carried out at the Center for Inherited Disease Research (CIDR) with a panel of 390 trinucleotide and tetranucleotide repeats. RESULTS: The obesity-related phenotype showing the strongest linkage evidence was PBF on chromosome 2 (LOD 3.30 at 72.6 cM, marker D2S739). Suggestive linkage to FM was found on chromosomes 2 (LOD 2.56 at 80.4 cM) and 5 (LOD 2.25 at 98 cM, marker D5S1725). The highest LOD score for BMI was 1.68 (chromosome 4, 113.8 cM). The areas of linkage for the three phenotypes showed some clustering as all three phenotypes were linked to the same regions of 2p13 and 5q14, and our study replicated linkage evidence for several regions previously reported in other studies. CONCLUSION: We obtained evidence for several QTLs on chromosome 2, 4 and 5 to three obesity phenotypes. This study provides data on the genetics of obesity in populations that are currently under represented in the global effort directed at understanding the pathophysiology of excess adiposity in free living individuals. C1 Howard Univ, Coll Med, Natl Human Genome Ctr, Genet Epidemiol Unit, Washington, DC 20059 USA. Univ Ibadan, Coll Med, Ibadan, Nigeria. Univ Lagos, Coll Med, Endocrine & Metab Unit, Lagos, Nigeria. Univ Ghana, Sch Med, Dept Med, Accra, Ghana. Univ Sci & Technol, Dept Med, Kumasi, Ghana. Univ Nigeria, Teaching Hosp, Dept Med, Enugu, Nigeria. NHGRI, NIH, Bethesda, MD 20892 USA. RP Rotimi, C (reprint author), Howard Univ, Coll Med, Natl Human Genome Ctr, Genet Epidemiol Unit, 2216 6th St NW, Washington, DC 20059 USA. EM crotimi@howard.edu OI Adeyemo, Adebowale/0000-0002-3105-3231 FU FIC NIH HHS [3T37TW00041-03S2]; NCRR NIH HHS [RR03655]; NIDDK NIH HHS [DK-54001] NR 25 TC 24 Z9 24 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD MAR PY 2005 VL 29 IS 3 BP 255 EP 259 DI 10.1038/sj.ijo.0802873 PG 5 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA 897CK UT WOS:000226981400001 PM 15611782 ER PT J AU Koltay, A Daly, NL Gustafson, KR Craik, DJ AF Koltay, A Daly, NL Gustafson, KR Craik, DJ TI Structure of circulin B and implications for antimicrobial activity of the cyclotides SO INTERNATIONAL JOURNAL OF PEPTIDE RESEARCH AND THERAPEUTICS LA English DT Article DE circular proteins; cyclotides; cystine knot; NMR; protein structure ID CYCLIC CYSTINE-KNOT; INHIBITORY MACROCYCLIC PEPTIDES; NUCLEAR MAGNETIC-RESONANCE; SPIN COUPLING-CONSTANTS; POLYPEPTIDE KALATA B1; PLANT CYCLOTIDES; CHASSALIA-PARVIFOLIA; TRYPSIN-INHIBITOR; NMR-SPECTROSCOPY; DRUG DESIGN AB The solution structure of one of the first members of the cyclotide family of macrocyclic peptides to be discovered, circulin B has been determined and compared with that of circulin A and related cyclotides. Cyclotides are mini-proteins derived from plants that have the characteristic features of a head-to-tail cyclised peptide backbone and a knotted arrangement of their three disulfide bonds. First discovered because of their uterotonic or anti-HIV activity, they have also been reported to have activity against a range of Gram positive and Gram negative bacteria as well as fungi. The aim of the current study was to develop structure-activity relationships to rationalise this antimicrobial activity. Comparison of cyclotide structures and activities suggests that the presence and location of cationic residues may be a requirement for activity against Gram negative bacteria. Understanding the topological differences associated with the antimicrobial activity of the cyclotides is of significant interest and potentially may be harnessed for pharmaceutical applications. C1 Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia. NCI, Mol Targets Dev Program, Ctr Canc Res, Frederick, MD 21701 USA. RP Craik, DJ (reprint author), Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia. EM d.craik@imb.uq.edu.au RI Daly, Norelle/D-4302-2013; Craik, David/B-1695-2010 OI Craik, David/0000-0003-0007-6796 NR 49 TC 18 Z9 19 U1 0 U2 5 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 1573-3149 J9 INT J PEPT RES THER JI Int. J. Pept. Res. Ther. PD MAR PY 2005 VL 11 IS 1 BP 99 EP 106 DI 10.1007/s10989-004-1722-2 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 933MM UT WOS:000229632900007 ER PT J AU Carr, ZA Land, CE Kleinerman, RA Weinstock, RW Stovall, M Griem, ML Mabuchi, K AF Carr, ZA Land, CE Kleinerman, RA Weinstock, RW Stovall, M Griem, ML Mabuchi, K TI Coronary heart disease after radiotherapy for peptic ulcer disease SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE coronary heart disease; peptic ulcer disease; cerebrovascular disease; radiotherapy; smoking ID BREAST-CANCER PATIENTS; ATOMIC-BOMB SURVIVORS; MYOCARDIAL-INFARCTION; HODGKINS-DISEASE; RADIATION-THERAPY; CARDIOVASCULAR-DISEASE; ADJUVANT RADIOTHERAPY; MORTALITY; IRRADIATION; RISK AB Purpose: To evaluate the risk of coronary heart disease (CHD) and cerebrovascular disease after radiotherapy (RT) for peptic ulcer disease. Methods and Materials: Peptic ulcer disease patients treated with RT (n = 1859) or by other means (n 1860) at the University of Chicago Medical Center between 1936 and 1965, were followed through 1997. The observed numbers of cause-specific deaths were compared with the expected numbers from the general population rates. During RT, 5% of the heart was in the treatment field and the remainder of the heart mostly received scattered radiation. A volume-weighted cardiac dose was computed to describe the average tissue dose to the entire organ. We used Cox proportional hazards regression analysis to analyze the CHD and cerebrovascular disease risk associated with RT, adjusting for confounding factors. Results: Greater than expected CHD mortality was observed among the irradiated patients. The irradiated patients received volume-weighted cardiac doses ranging from 1.6 to 3.9 Gy and the portion of the heart directly in the field received doses of 7.6-18.4 Gy. The CHD risk increased with the cardiac dose (p trend = 0.01). The cerebrovascular disease risk was not associated with the surrogate carotid dose. Conclusion: The excess CHD risk in patients undergoing RT for peptic ulcer disease decades previously indicates the need for long-term follow-up for cardiovascular disease after chest RT. (C) 2005 Elsevier Inc. C1 NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept HHS, Rockville, MD 20852 USA. WHO, Dept Protect Human Environm, Radiat & Environm Hlth Unit, CH-1211 Geneva, Switzerland. Univ Texas, MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA. Univ Chicago, Med Ctr, Dept Radiat & Cellular Oncol, Chicago, IL 60637 USA. RP Mabuchi, K (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept HHS, 6120 Execut Blvd,EPS 7038, Rockville, MD 20852 USA. EM mabuchik@mail.nih.gov OI Kleinerman, Ruth/0000-0001-7415-2478 NR 53 TC 108 Z9 116 U1 1 U2 7 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAR 1 PY 2005 VL 61 IS 3 BP 842 EP 850 DI 10.1016/j.ijrobp.2004.07.708 PG 9 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA 898CG UT WOS:000227052900027 PM 15708264 ER PT J AU Salicrup, LA Rohrbaugh, ML AF Salicrup, LA Rohrbaugh, ML TI Partnerships in technology transfer. An innovative program to enhance biomedical research and global health SO INTERNATIONAL MICROBIOLOGY LA English DT Editorial Material C1 NIH, Off Director, Off Technol Transfer, Rockville, MD 20852 USA. RP Salicrup, LA (reprint author), NIH, Off Director, Off Technol Transfer, 6011 Execut Blvd Suite 325, Rockville, MD 20852 USA. EM salicru@mail.nih.gov OI Rohrbaugh, Mark/0000-0002-6136-3337 NR 0 TC 5 Z9 5 U1 0 U2 1 PU SPANISH SOCIETY MICROBIOLOGY PI MADRID PA VITRUBIO, 8, MADRID, 28006, SPAIN SN 1139-6709 J9 INT MICROBIOL JI Int. Microbiol. PD MAR PY 2005 VL 8 IS 1 BP 1 EP 3 PG 3 WC Biotechnology & Applied Microbiology; Microbiology SC Biotechnology & Applied Microbiology; Microbiology GA 006KS UT WOS:000234897000001 PM 15906255 ER PT J AU Solheim, K AF Solheim, K TI Patterns of community relationship: nurses, non-governmental organizations and internally displaced persons SO INTERNATIONAL NURSING REVIEW LA English DT Article DE community; internally displaced persons; non governmental organization; nursing; relationship ID PRIMARY HEALTH-CARE; PROJECT AB Background: Internally displaced persons (IDPs) are one of the largest at-risk populations in the world. Nurses provide health services to IDPs as staff of non-governmental organizations (NGO). IDPs are also employed to deliver NGO services. The way that NGOs and field staff (nurses and others) interact with employed IDPs can enhance or diminish IDP quality of life. Aim: This report describes patterns of relationships in a community formed by an American NGO, its field staff and IDPs as they worked together in a refugee camp at the Thai-Cambodian border over 13 years. Methods: This qualitative case study describes relational patterns from the NGO perspective. Content analysis was used to process data from in-depth interviews with organizational leaders (n = 4) and organizational documents (n = 234). Findings: A health care training and service mission, carried out between an NGO, its field staff and IDPs, was based on a philosophy that turned programme activity and authority over to IDP staff. Over 400 IDPs, assisted by 235 field staff, delivered effective health care to 85 000 people over 13 years. Conclusions: Work-centred relationships between NGOs, field staff and IDPs are significant; they can be consciously created to promote effective, autonomous IDP management of health care. C1 Univ Illinois, Coll Nursing MC 802, NIH, Chicago, IL 60612 USA. RP Solheim, K (reprint author), Univ Illinois, Coll Nursing MC 802, NIH, 845 S Damen Ave, Chicago, IL 60612 USA. EM ksolheim@uic.edu FU PHS HHS [T32 NPO 7079] NR 38 TC 1 Z9 1 U1 1 U2 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0020-8132 J9 INT NURS REV JI Int. Nurs. Rev. PD MAR PY 2005 VL 52 IS 1 BP 60 EP 67 DI 10.1111/j.1466-7657.2004.00265.x PG 8 WC Nursing SC Nursing GA 048WV UT WOS:000237978100022 PM 15725278 ER PT J AU Djalilian, AR Mahesh, SP Koch, CA Nussenblatt, RB Shen, DF Zhuang, ZP Holland, EJ Chan, CC AF Djalilian, AR Mahesh, SP Koch, CA Nussenblatt, RB Shen, DF Zhuang, ZP Holland, EJ Chan, CC TI Survival of donor epithelial cells after limbal stem cell transplantation SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article ID POLYMERASE-CHAIN-REACTION; SINGLE CORNEAL CELLS; LONG-TERM SURVIVAL; ALLOGRAFT; ORIGIN AB PURPOSE To determine the long-term fate of donor epithelial cells after limbal allograft transplantation. METHODS. Corneal buttons and peripheral blood leukocytes were obtained at the time of penetrating keratoplasty from three patients who had undergone a successful limbal allograft transplantation. Microdissection was used to remove the corneal epithelial cells from the button. The presence of donor and recipient epithelial cells in each sample was determined by using PCR for DNA microsatellites. Phenotypic analysis of the epithelium was performed by immunohistochemistry. RESULTS. Various patterns of DNA microsatellites were observed. Nonrecipient cells (presumed to be donor) were consistently detected in all three corneal buttons. In two of the three cases, recipient cells were also detected, whereas in the third case, exclusively donor epithelial cells were found at 3.5 years after limbal allograft transplantation. Mild T-lymphocytes and macrophages were observed in one of the corneal buttons. CONCLUSIONS. This study provides evidence for the persistence of donor epithelial cells up to 3.5 years after limbal allograft transplantation and supports the use of systemic immunosuppressive therapy. C1 NEI, NIH, Bethesda, MD 20892 USA. NICHHD, NIH, Bethesda, MD 20892 USA. Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD USA. Univ Cincinnati, Cincinnati Eye Inst, Cincinnati, OH USA. RP Djalilian, AR (reprint author), NEI, NIH, Bldg 10,Room 10N112,10 Ctr Dr, Bethesda, MD 20892 USA. EM djaliliana@nei.nih.gov RI Koch, Christian/A-4699-2008; OI Koch, Christian/0000-0003-3127-5739; Koch, Christian/0000-0003-0678-1242 NR 17 TC 28 Z9 29 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR PY 2005 VL 46 IS 3 BP 803 EP 807 DI 10.1167/iovs.04-0575 PG 5 WC Ophthalmology SC Ophthalmology GA 900LR UT WOS:000227216900006 PM 15728534 ER PT J AU Laeyendecker, O Zhang, GW Quinn, TC Garten, R Ray, SC Lai, SG Liu, W Chen, X Yu, XF AF Laeyendecker, O Zhang, GW Quinn, TC Garten, R Ray, SC Lai, SG Liu, W Chen, X Yu, XF TI Molecular epidemiology of HIV-1 subtypes in southern China SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Article DE HIV-1; CRF01_AE; CRF08_BC; China ID IMMUNODEFICIENCY-VIRUS TYPE-1; INJECTION-DRUG USERS; NORTHERN VIETNAM; GUANGXI PROVINCE; B/C RECOMBINANT; RECENT OUTBREAK; INFECTION; SEQUENCES; INDIA; STRAINS AB The driving forces of the HIV-1 epidemic in Guangxi, China were assessed by investigating virologic and epidemiologic data from a cohort of longitudinally followed injection drug users (IDUs) in Binyang and Pingxiang, major urban areas along 2 separate drug routes in the province. Sera and interview data were obtained in September and October of 2000. Sequence analysis of HIV-1 was per-formed on the gag-pol region (HXB2 nt 1850-3005) and C2 to V4 env (HXB2 nt 6704-7626). Sequence data demonstrated that 88% of the infections in Pingxiang were CRF01_AE, whereas 96% in Binyang were CRF08_BC. Three recently infected subjects in Pingxiang were infected with CRFOS_BC, and 1 chronically infected subject had evidence of a recombinant virus. Intersubject distances were statistically greater for CRF01_AE-infected subjects than CRF08_BC-infected subjects for all regions except V4. The epidemic in Binyang is similar to previously described IDU-based epidemics, with a strong founder effect with little variation in V3. The epidemic in Pingxiang may have had multiple introductions of the CRF01_AE epidemic into the city and greater spread through sexual transmission, resulting in greater variation in V3 than typically seen in purely parenterally based epidemics. C1 NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Mol & Microbiol & Immunol, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD USA. Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol, Baltimore, MD USA. Guangxi Hlth & Anti Epidem Ctr, Guangxi, Peoples R China. RP Quinn, TC (reprint author), 1159,720 Rutland Ave, Baltimore, MD 21205 USA. EM tquinn@jhmi.edu RI Laeyendecker, Oliver/B-9331-2009; Ray, Stuart/B-7527-2008; OI Ray, Stuart/0000-0002-1051-7260; Laeyendecker, Oliver/0000-0002-6429-4760 FU NIDA NIH HHS [DA13918, DA12327]; NIDDK NIH HHS [R01 DK057998, R01 DK57998] NR 25 TC 42 Z9 50 U1 1 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 JAIDS-J ACQ IMM DEF JI JAIDS PD MAR 1 PY 2005 VL 38 IS 3 BP 356 EP 362 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 903EK UT WOS:000227408100018 PM 15735457 ER PT J AU Newcomer, S AF Newcomer, S TI Fertility Regulation and Systemic Hormones in HIV-Infected and At-Risk Women - Conference Proceedings - Welcoming remarks SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Editorial Material C1 NICHHD, NIH, DHHS, Bethesda, MD 20892 USA. RP Newcomer, S (reprint author), NICHHD, NIH, DHHS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 JAIDS-J ACQ IMM DEF JI JAIDS PD MAR PY 2005 VL 38 SU 1 BP S1 EP S1 DI 10.1097/01.qai.0000167018.98384.3b PG 1 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 927YO UT WOS:000229238500002 ER PT J AU Reichelderfer, P AF Reichelderfer, P TI Fertility Regulation and Systemic Hormones in HIV-Infected and At-Risk Women - Conference Proceedings - Closing remarks: NIH research prospective SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Article; Proceedings Paper CT Conference on Fertility Regulation and Systemic Hormones in HIV-infected and At-Risk Women CY JAN 13-15, 2003 CL McLean, VA SP NIH, Off AIDS Res, NICHD C1 NICHHD, NIH, DHHS, Bethesda, MD 20892 USA. RP Reichelderfer, P (reprint author), NICHHD, NIH, DHHS, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 JAIDS-J ACQ IMM DEF JI JAIDS PD MAR PY 2005 VL 38 SU 1 BP S51 EP S52 DI 10.1097/01.qai.0000167054.42041.6b PG 2 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 927YO UT WOS:000229238500030 PM 15867629 ER PT J AU Watts, DH AF Watts, DH TI Topic V: Hormonal influence on changes in genital tract virological/immunological parameters and implications for transmission - Effect of pregnancy SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES LA English DT Article; Proceedings Paper CT Conference on Fertility Regulation and Systemic Hormones in HIV-infected and At-Risk Women CY JAN 13-15, 2003 CL McLean, VA SP NIH, Off AIDS Res, NICHD ID IMMUNODEFICIENCY-VIRUS TYPE-1; HIV-INFECTED WOMEN; CERVICOVAGINAL SECRETIONS; VERTICAL TRANSMISSION; VIRAL LOAD; DNA; ASSOCIATION; INFLAMMATION; LYMPHOCYTES; PROGRESSION C1 NICHHD, NIH, DHHS, Bethesda, MD 20892 USA. RP Watts, DH (reprint author), NICHHD, NIH, DHHS, Bethesda, MD 20892 USA. NR 20 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1525-4135 J9 JAIDS-J ACQ IMM DEF JI JAIDS PD MAR PY 2005 VL 38 SU 1 BP S36 EP S38 DI 10.1097/01.qai.0000167041.35311.be PG 3 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA 927YO UT WOS:000229238500024 PM 15867616 ER PT J AU Morris, KA Snir, E Pompeia, C Koroleva, IV Kachar, B Hayashizaki, Y Carninci, P Soares, MB Beisel, KW AF Morris, KA Snir, E Pompeia, C Koroleva, IV Kachar, B Hayashizaki, Y Carninci, P Soares, MB Beisel, KW TI Differential expression of genes within the cochlea as defined by a custom mouse inner ear microarray SO JARO-JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY LA English DT Article DE differential expression; cochlea; organ of Corti; spiral ganglion; lateral wall; deafness genes ID AUTOSOMAL RECESSIVE DEAFNESS; P2X(2) RECEPTOR SUBUNIT; GATED ION CHANNELS; RAT COCHLEA; HAIR-CELL; FULL-LENGTH; SENSORY EPITHELIA; PROTEIN; CDNA; MUTATIONS AB Microarray analyses have contributed greatly to the rapid understanding of functional genomics through the identification of gene networks as well as gene discovery. To facilitate functional genomics of the inner ear, we have developed a mouse inner-ear-pertinent custom microarray chip (CTMA-IE1). Non-redundant cDNA clones were obtained from two cDNA library resources: the RIKEN subtracted inner car set and the NIH organ of Corti library. At least 2000 cDNAs unique to the inner ear were present on the chip. Comparisons were performed to examine the relative expression levels of these unique cDNAs within the organ of Corti, lateral wall, and spiral ganglion. Total RNA samples were obtained from the three cochlear-dissected fractions from adult CF-1 mice. The total RNA was linearly amplified, and a dendrimer-based system was utilized to enhance the hybridization signal. Differentially expressed genes were verified by comparison to known gene expression patterns in the cochlea or by correlation with genes and gene families deduced to be present in the three tissue types. Approximately 22-25% of the genes on the array had significant levels of expression. A number of differentially expressed genes were detected in each tissue fraction. These included genes with known functional roles, hypothetical genes, and various unknown or uncharacterized genes. Four of the differentially expressed genes found in the organ of Corti are linked to deafness loci. None of these are hypothetical or unknown genes. C1 Creighton Univ, Dept Biomed Sci, Omaha, NE 68178 USA. Univ Iowa, Iowa City, IA 52242 USA. NIDCD, Sect Struct Cell Biol, NIH, Bethesda, MD 20892 USA. RIKEN, Lab Genome Explorat Res Grp, Genom Sci Ctr, Tsukuba, Ibaraki, Japan. RP Beisel, KW (reprint author), Creighton Univ, Dept Biomed Sci, 2500 Calif Plaza, Omaha, NE 68178 USA. EM beisel@creighton.edu RI Carninci, Piero/K-1568-2014 OI Carninci, Piero/0000-0001-7202-7243 FU NIDCD NIH HHS [R01 DC05009, DC04279, R01 DC004279, R01 DC005009] NR 79 TC 26 Z9 32 U1 0 U2 7 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 1525-3961 J9 JARO-J ASSOC RES OTO JI JARO PD MAR PY 2005 VL 6 IS 1 BP 75 EP 89 DI 10.1007/s10162-004-5046-x PG 15 WC Neurosciences; Otorhinolaryngology SC Neurosciences & Neurology; Otorhinolaryngology GA 932VP UT WOS:000229582900008 PM 15735932 ER PT J AU Gruchalla, RS Pongracic, J Plaut, M Evans, R Visness, CM Walter, M Crain, EF Kattan, M Morgan, WJ Steinbach, S Stout, J Malindzak, G Smartt, E Mitchell, H AF Gruchalla, RS Pongracic, J Plaut, M Evans, R Visness, CM Walter, M Crain, EF Kattan, M Morgan, WJ Steinbach, S Stout, J Malindzak, G Smartt, E Mitchell, H TI Inner City Asthma Study: Relationships among sensitivity, allergen exposure, and asthma morbidity SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article DE asthma; allergen exposure; allergen sensitivity; morbidity; allergens; cockroach; dust mite; cat; dog ID RISK-FACTORS; CHILDHOOD ASTHMA; INDOOR ALLERGENS; COCKROACH ALLERGEN; MANAGEMENT PROGRAM; CAT ALLERGEN; CHILDREN; SENSITIZATION; SEVERITY; MITE AB Background: Asthma-associated morbidity is rising, especially in inner city children. Objective: We evaluated the allergen sensitivities, allergen exposures, and associated morbidity for participants in the Inner City Asthma Study. We also determined geographic variations of indoor allergen levels. Methods: Nine hundred thirty-seven inner city children 5 to 11 years old with moderate to severe asthma underwent allergen skin testing. Bedroom dust samples were evaluated for Der p 1, Der f 1, Bla g 1, Fel d 1, and Can f 1. Results: Skin test sensitivities to cockroach (69%), dust mites (62%), and molds (50%) predominated, with marked study site-specific differences. Cockroach sensitivity was highest in the Bronx, New York, and Dallas (81.2%, 78.7%, and 78.5%, respectively), and dust mite sensitivity was highest in Dallas and Seattle (83.7% and 78.0%, respectively). A majority of homes in Chicago, New York, and the Bronx had cockroach allergen levels greater than 2 U/g, and a majority of those in Dallas and Seattle had dust mite allergen levels greater than 2 mu g/g. Levels of both of these allergens were influenced by housing type. Cockroach allergen levels were highest in high-rise apartments, whereas dust mite allergen levels were highest in detached homes. Children who were both sensitive and exposed to cockroach allergen had significantly more asthma symptom days, more caretaker interrupted sleep, and more school days missed than children who were not sensitive or exposed. Conclusion: Geographic differences in allergen exposure and sensitivity exist among inner city children. Cockroach exposure and sensitivity predominate in the Northeast, whereas dust mite exposure and sensitivity are highest in the South and Northwest. Cockroach allergen appears to have a greater effect on asthma morbidity than dust mite or pet allergen in these children. C1 Univ Texas, SW Med Ctr, Dallas, TX 75390 USA. Childrens Mem Hosp, Chicago, IL 60614 USA. NIAID, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Rho Inc, Chapel Hill, NC USA. Albert Einstein Coll Med, Jacobi Med Ctr, Bronx, NY 10467 USA. Mt Sinai Sch Med, New York, NY USA. Univ Arizona, Coll Med, Tucson, AZ 85721 USA. Boston Univ, Sch Med, Boston, MA 02215 USA. Univ Washington, Sch Med & Publ Hlth, Seattle, WA 98195 USA. Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA. RP Gruchalla, RS (reprint author), Univ Texas, SW Med Ctr, 5323 Harry Hines Blvd, Dallas, TX 75390 USA. EM Rebecca.Gruchalla@utsouthwestern.edu FU NCRR NIH HHS [M01 RR00533]; NIAID NIH HHS [AI-39761, AI-39769, AI-39776, AI-39785, AI-39789, AI-39900, AI-39901, AI-39902] NR 22 TC 232 Z9 242 U1 0 U2 10 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD MAR PY 2005 VL 115 IS 3 BP 478 EP 485 DI 10.1016/j.jaci.2004.12.006 PG 8 WC Allergy; Immunology SC Allergy; Immunology GA 907AN UT WOS:000227687000007 PM 15753892 ER PT J AU Sampson, HA Munoz-Furlong, A Bock, A Schmitt, M Bass, R Chowdhury, BA Decker, WW Furlong, TJ Galli, SJ Golden, DB Gruchalla, RS Harlor, AD Hepner, DL Howarth, M Kaplan, AP Levy, JH Lewis, LM Lieberman, PL Metcalfe, DD Murphy, R Pollart, SM Pumphrey, RS Rosenwasser, LJ Simons, FE Wood, JP Camargo, CA AF Sampson, HA Munoz-Furlong, A Bock, A Schmitt, M Bass, R Chowdhury, BA Decker, WW Furlong, TJ Galli, SJ Golden, DB Gruchalla, RS Harlor, AD Hepner, DL Howarth, M Kaplan, AP Levy, JH Lewis, LM Lieberman, PL Metcalfe, DD Murphy, R Pollart, SM Pumphrey, RS Rosenwasser, LJ Simons, FE Wood, JP Camargo, CA TI Symposium on the definition and management of anaphylaxis: Summary report SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Editorial Material DE anaphylaxis; hypersensitivity; allergy; allergic reaction; insect sting; food allergy ID EXERCISE-INDUCED ANAPHYLAXIS; ALLERGIC REACTIONS; EPINEPHRINE ABSORPTION; VENOM IMMUNOTHERAPY; INSECT STINGS; CHILDREN; EMERGENCY; FOOD; EPIDEMIOLOGY; ADOLESCENTS C1 Mt Sinai Sch Med, Dept Pediat, New York, NY 10029 USA. Food Allergy& Anaphylaxis Network, Fairfax, VA USA. Stanford Univ, Sch Med, Stanford, CA 94305 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Univ Texas, SW Med Ctr, Dallas, TX 75230 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA. Univ Penn, Med Ctr, Philadelphia, PA 19104 USA. Med Univ S Carolina, Charleston, SC 29425 USA. NIAID, NIH, Bethesda, MD 20892 USA. Univ Virginia, Charlottesville, VA USA. Cent Manchester Healthcare Natl Hlth Serv Trust H, Manchester, Lancs, England. Univ Manitoba, Winnipeg, MB R3T 2N2, Canada. Massachusetts Gen Hosp, Boston, MA 02114 USA. RP Sampson, HA (reprint author), Mt Sinai Sch Med, Dept Pediat, Box 1198,1 Gustave L Levy Pl, New York, NY 10029 USA. EM hugh.sampson@mssm.edu NR 55 TC 218 Z9 226 U1 0 U2 5 PU MOSBY, INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 USA SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD MAR PY 2005 VL 115 IS 3 BP 584 EP 591 DI 10.1016/j.jaci.2005.01.008 PG 8 WC Allergy; Immunology SC Allergy; Immunology GA 907AN UT WOS:000227687000023 PM 15753908 ER PT J AU Netzel-Arnett, S Bugge, TH Antalis, TM AF Netzel-Arnett, S Bugge, TH Antalis, TM TI Role of testisin (PRSS21) in male fertility SO JOURNAL OF ANDROLOGY LA English DT Meeting Abstract CT 30th Annual Meeting of the American-Society-of-Andrology CY MAR 30-APR 05, 2005 CL Seattle, WA SP Amer Soc Androl C1 Univ Maryland, Sch Med, Dept Physiol & Surg, Rockville, MD USA. Natl Inst Dent & Craniofacial Res, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU AMER SOC ANDROLOGY, INC PI LAWRENCE PA C/O ALLEN PRESS, INC PO BOX 368, LAWRENCE, KS 66044 USA SN 0196-3635 J9 J ANDROL JI J. Androl. PD MAR-APR PY 2005 SU S MA 15 BP 42 EP 42 PG 1 WC Andrology SC Endocrinology & Metabolism GA 902CK UT WOS:000227328700016 ER PT J AU Miclet, E Boisbouvier, J Bax, A AF Miclet, E Boisbouvier, J Bax, A TI Measurement of eight scalar and dipolar couplings for methine-methylene pairs in proteins and nucleic acids SO JOURNAL OF BIOMOLECULAR NMR LA English DT Article DE alignment; dipolar coupling; E.COSY; liquid crystal; methylene; scalar coupling; side chain conformation ID E.COSY-TYPE MEASUREMENT; ONE-BOND COUPLINGS; NMR-SPECTROSCOPY; ORIENTED MACROMOLECULES; ACCURATE MEASUREMENTS; IMPROVED SENSITIVITY; RNA BACKBONE; CONSTANTS; ALIGNMENT; DYNAMICS AB A new 3D, spin-state-selective coherence transfer NMR experiment is described that yields accurate measurements for eight scalar or dipolar couplings within a spin system composed of a methylene adjacent to a methine group. Implementations of the experiment have been optimized for proteins and for nucleic acids. The experiments are demonstrated for C-β-C-α moieties of the third IgG-binding domain from Streptococcal Protein G (GB3) and for C5'-C4' groups in a 24-nt RNA oligomer. Chemical shifts of C-α, C-β and H-β (respectively C4', C5' and H5') are dispersed in the three orthogonal dimensions, and the absence of heteronuclear decoupling leads to distinct and well-resolved E.COSY multiplet patterns. In an isotropic sample, the E.COSY displacements correspond to (1)J(Cα Hα), (2)J(Cα Hα) + (2)J(Cα Hβ 3), (2)J(Cβ Hα), (1)J(Cβ Hβ 2) + (1)JC(β Hβ 3), (1)J(Cβ Hβ 2)-(2)J(Hβ 2Hβ 3,) (1)J(Cβ Hβ 3)-(2)J(Hβ 2Hβ 3), (3)J(Hα Hβ 2) and (3)J(Hα Hβ 3) for proteins, and (1)J(C4'H4'), (2)JC(4'H5')+2J(C4'H5'), (2)J(C5'H4'), (1)J(C5'H5')+(1)J(C5'H5"), (1)J(C5'H5')-(2)J(H5'H5'), (1)J(C5'H5')-(2)J(H5'H5'), (3)J(H4'H5'), and (3)J(H4'H5") in nucleic acids. The experiment, based on relaxation-optimized spectroscopy, yields best results when applied to residues where the methine-methylene group corresponds to a reasonably isolated spin system, as applies for C, F, Y, W, D, N and H residues in proteins, or the C5'-C4' groups in nucleic acids. Splittings can be measured under either isotropic or weakly aligned conditions, yielding valuable structural information both through the (3)J couplings and the one-, two- and three-bond dipolar interactions. Dipolar couplings for 10 out of 13 sidechains in GB3 are found to be in excellent agreement with its X-ray structure, whereas one residue adopts a different backbone geometry, and two residues are subject to extensive x(1) rotamer averaging. The abundance of dipolar couplings can also yield stereospecific assignments of the non-equivalent methylene protons. For the RNA oligomer, dipolar data yielded stereospecific assignments for six out of the eight C5'H-2 groups in the loop region of the oligomer, in all cases confirmed by (1)J(C5'H5')>(1)J(C5'H5"), and H-5' resonating downfield of H-5". C1 Univ Paris 06, UMR 7613, Lab Struct & Fonct Mol Bioact, F-75252 Paris, France. NIDDK, Phys Chem Lab, NIH, Bethesda, MD 20892 USA. RP Miclet, E (reprint author), Univ Paris 06, UMR 7613, Lab Struct & Fonct Mol Bioact, 4 Pl Jussieu, F-75252 Paris, France. NR 63 TC 30 Z9 30 U1 1 U2 7 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0925-2738 J9 J BIOMOL NMR JI J. Biomol. NMR PD MAR PY 2005 VL 31 IS 3 BP 201 EP 216 DI 10.1007/s10858-005-0175-z PG 16 WC Biochemistry & Molecular Biology; Spectroscopy SC Biochemistry & Molecular Biology; Spectroscopy GA 924KS UT WOS:000228978300002 PM 15803394 ER PT J AU Morcombe, CR Paulson, EK Gaponenko, V Byrd, RA Zilm, KW AF Morcombe, CR Paulson, EK Gaponenko, V Byrd, RA Zilm, KW TI H-1-N-15 correlation spectroscopy of nanocrystalline proteins SO JOURNAL OF BIOMOLECULAR NMR LA English DT Article DE FSLG decoupling; high resolution solid state H-1 NMR; Lee-Goldburg decoupling; magnetic dilution; MAS H-1 NMR; solid state protein NMR ID SOLID-STATE NMR; MULTIPLE-PULSE NMR; NUCLEAR-MAGNETIC-RESONANCE; ANGLE-SPINNING NMR; ROTATING SOLIDS; INVERSE DETECTION; CHEMICAL-SHIFTS; HIGH-FIELD; MAS; RESOLUTION AB The limits of resolution that can be obtained in H-1-N-15 2D NMR spectroscopy of isotopically enriched nanocrystalline proteins are explored. Combinations of frequency switched Lee-Goldburg (FSLG) decoupling, fast magic angle sample spinning (MAS), and isotopic dilution via deuteration are investigated as methods for narrowing the amide H-1 resonances. Heteronuclear decoupling of N-15 from the H-1 resonances is also studied. Using human ubiquitin as a model system, the best resolution is most easily obtained with uniformly H-2 and N-15 enriched protein where the amides have been exchanged in normal water, MAS at &SIM; 20 kHz, and WALTZ-16 decoupling of the N-15 nuclei. The combination of these techniques results in average 1H lines of only &SIM; 0.26 ppm full width at half maximum. Techniques for optimizing instrument stability and N-15 decoupling are described for achieving the best possible performance in these experiments. C1 Yale Univ, Dept Chem, New Haven, CT 06520 USA. Natl Canc Inst, Struct Biophys Lab, Ft Detrick, MD 21702 USA. RP Zilm, KW (reprint author), Yale Univ, Dept Chem, POB 208107, New Haven, CT 06520 USA. EM kurt.zilm@yale.edu RI Paulson, Eric/I-1816-2012; Byrd, R. Andrew/F-8042-2015 OI Byrd, R. Andrew/0000-0003-3625-4232 NR 36 TC 29 Z9 29 U1 0 U2 10 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0925-2738 J9 J BIOMOL NMR JI J. Biomol. NMR PD MAR PY 2005 VL 31 IS 3 BP 217 EP 230 DI 10.1007/s10858-005-0527-8 PG 14 WC Biochemistry & Molecular Biology; Spectroscopy SC Biochemistry & Molecular Biology; Spectroscopy GA 924KS UT WOS:000228978300003 PM 15803395 ER PT J AU Jaroniec, CP Boisbouvier, J Tworowska, I Nikonowicz, EP Bax, A AF Jaroniec, CP Boisbouvier, J Tworowska, I Nikonowicz, EP Bax, A TI Accurate measurement of N-15-C-13 residual dipolar couplings in nucleic acids SO JOURNAL OF BIOMOLECULAR NMR LA English DT Article DE DNA; heteronuclear NMR; liquid crystal; multiple quantum coherence; RDC; RNA; TROSY ID MULTIDIMENSIONAL NMR EXPERIMENTS; MULTIPLE-QUANTUM COHERENCE; QUANTITATIVE J-CORRELATION; TRIPLE-RESONANCE NMR; BIOLOGICAL MACROMOLECULES; DNA OLIGONUCLEOTIDES; IMPROVED SENSITIVITY; SPIN SYSTEMS; ONE-BOND; RNA AB New 3D HCN quantitative J (QJ) pulse schemes are presented for the precise and accurate measurement of one-bond N-15(1/9)-C-13(1), N-15(1/9)-C-13(6/8), and N-15(1/9)-C-13(2/4) residual dipolar couplings (RDCs) in weakly aligned nucleic acids. The methods employ H-1-C-13 multiple quantum (MQ) coherence or TROSY-type pulse sequences for optimal resolution and sensitivity. RDCs are obtained from the intensity ratio of H-1,-C-1'-N-1/9 (MQ-HCN-QJ) or H-6/8-C-6/8-N-1/9 (TROSY-HCN-QJ) correlations in two interleaved 3D NMR spectra, with dephasing intervals of zero (reference spectrum) and &SIM; 1/(2J(NC)) (attenuated spectrum). The different types of N-15-C-13 couplings can be obtained by using either the 3D MQ-HCN-QJ or TROSY-HCN-QJ pulse scheme, with the appropriate setting of the duration of the constant-time N-15 evolution period and the offset of two frequency-selective C-13 pulses. The methods are demonstrated for a uniformly C-13, N-15-enriched 24-nucleotide stem-loop RNA sequence, helix-35ψ, aligned in the magnetic field using phage Pf1. For measurements of RDCs systematic errors are found to be negligible, and experiments performed on a 1.5 mM helix-35ψ sample result in an estimated precision of ca. 0.07 Hz for D-1(NC), indicating the utility of the measured RDCs in structure validation and refinement. Indeed, for a complete set of N-15(1/9)-C-13(1'), N-15(1/9)-C-13(6/8), and N-15(1/9)-C-13(2/4) dipolar couplings obtained for the stem nucleotides, the measured RDCs are in excellent agreement with those predicted for an NMR structure of helix-35ψ, refined using independently measured observables, including C-13-H-1, C-13-C-13 and H-1-H-1 dipolar couplings. C1 NIDDK, Phys Chem Lab, NIH, Bethesda, MD 20892 USA. UJF, CEA, CNRS,Inst Biol Struct, UMR 5075,Lab RMN, F-38027 Grenoble, France. Rice Univ, Dept Biochem & Cell Biol, Houston, TX 77251 USA. RP Jaroniec, CP (reprint author), NIDDK, Phys Chem Lab, NIH, Bethesda, MD 20892 USA. RI Jaroniec, Christopher/A-4948-2008; OI Tworowska, Izabela/0000-0002-1461-1801; Jaroniec, Christopher/0000-0003-0364-2888 NR 64 TC 26 Z9 26 U1 1 U2 11 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0925-2738 J9 J BIOMOL NMR JI J. Biomol. NMR PD MAR PY 2005 VL 31 IS 3 BP 231 EP 241 DI 10.1007/s10858-005-0646-2 PG 11 WC Biochemistry & Molecular Biology; Spectroscopy SC Biochemistry & Molecular Biology; Spectroscopy GA 924KS UT WOS:000228978300004 PM 15803396 ER PT J AU Hu, JS Plaksin, D Margulies, DH AF Hu, JS Plaksin, D Margulies, DH TI Backbone and side chain resonance assignments of a TRAV14-3 mouse T cell receptor domain SO JOURNAL OF BIOMOLECULAR NMR LA English DT Letter DE NMR assignments; T cell receptor; TRAV14-3*02 ; TRAJ38*01 domain ID ISOTOPICALLY ENRICHED PROTEINS; NMR EXPERIMENT; J-COUPLINGS; CARBONYL; ANGLES C1 Univ Maryland, Dept Chem & Biochem, College Pk, MD 20742 USA. Univ Maryland, Ctr Biomol Struct & Org, College Pk, MD 20742 USA. NIAID, Mol Biol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Hu, JS (reprint author), Univ Maryland, Dept Chem & Biochem, College Pk, MD 20742 USA. EM jh336@umail.umd.edu RI Margulies, David/H-7089-2013 NR 10 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0925-2738 J9 J BIOMOL NMR JI J. Biomol. NMR PD MAR PY 2005 VL 31 IS 3 BP 271 EP 272 DI 10.1007/s10858-005-0524-y PG 2 WC Biochemistry & Molecular Biology; Spectroscopy SC Biochemistry & Molecular Biology; Spectroscopy GA 924KS UT WOS:000228978300015 PM 15803407 ER PT J AU Sharp, PC Michielutte, R Spangler, JG Cunningham, L Freimanis, R AF Sharp, PC Michielutte, R Spangler, JG Cunningham, L Freimanis, R TI Primary care providers' concerns and recommendations regarding mammography screening for older women SO JOURNAL OF CANCER EDUCATION LA English DT Article; Proceedings Paper CT Annual Spring Conference of the Society-of-Teachers-of-Family-Medicine CY MAY, 2001 CL DENVER, CO SP Soc Teachers Family Med ID BREAST-CANCER; ELDERLY-WOMEN; AGE AB Background. Morbidity and mortality from breast cancer increase with age; however, mammography screening does not reflect this increased risk for older women. Lack of provider recommendation is a major barrier to screening. Methods. This is a descriptive study of mammography screening recommendations of community primary care providers in North Carolina (N = 96) participating in a National Cancer Institute funded research project. Providers self-reported screening recommendations for typical patients of different ages and issues and concerns that might influence the decision. Chart reviews compared actual practices with policies stated. Results. Of the providers, 51% recommended biannual, 45% annual for women ages 50 through 74; 4% recommended biannual, 80% annual, 5% did not recommend screening, and 10% had no general policy for women over 75. Cost, inconsistent guidelines, comorbidity, functional status, value of mammography, and patient resistance influenced screening recommendations. Chart review showed even lower rates of recommendation than self-reported figures. Conclusions. Although the use of screening mammography has increased over the past decade, older women are one of the last subgroups to derive benefit from this screening test. Our survey revealed lower rates for mammography referral in older women. The primary care provider appears to be essential to increasing participation for these older women in breast cancer screening. C1 Wake Forest Univ, Sch Med, Dept Family & Community Med, Winston Salem, NC 27157 USA. Wake Forest Univ, Sch Med, Dept Radiol, Winston Salem, NC 27157 USA. Wake Forest Univ, Sch Med, Natl Canc Inst, Winston Salem, NC 27157 USA. RP Sharp, PC (reprint author), Wake Forest Univ, Sch Med, Dept Family & Community Med, Med Ctr Blvd, Winston Salem, NC 27157 USA. EM psharp@yadtel.net FU NCI NIH HHS [5 R01 CA79746-03] NR 31 TC 10 Z9 10 U1 0 U2 0 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA SN 0885-8195 J9 J CANCER EDUC JI J. Cancer Educ. PD SPR PY 2005 VL 20 IS 1 BP 34 EP 38 DI 10.1207/s15430154jce2001_11 PG 5 WC Oncology; Education, Scientific Disciplines; Public, Environmental & Occupational Health SC Oncology; Education & Educational Research; Public, Environmental & Occupational Health GA 928AV UT WOS:000229244400010 PM 15876180 ER PT J AU Petereit, DG Rogers, D Burhansstipanov, L Kaur, J Govern, F Howard, SP Osburn, CH Coleman, N Fowler, JE Chappell, R Mehta, MP AF Petereit, DG Rogers, D Burhansstipanov, L Kaur, J Govern, F Howard, SP Osburn, CH Coleman, N Fowler, JE Chappell, R Mehta, MP TI Walking Forward: The South Dakota Native American project SO JOURNAL OF CANCER EDUCATION LA English DT Article ID DOSE-RATE BRACHYTHERAPY; PROSTATE-CANCER; RADIATION-THERAPY; BREAST-CANCER; CARCINOMA; RADIOTHERAPY; PROLONGATION; DISPARITIES; TRIALS AB Background. The "Walking Forward" program is a scientific collaborative program between Rapid City Regional Hospital, the University of Wisconsin, the Mayo Clinic, and partnerships with the American Indian community in western South Dakota-3 reservations and I urban population. The purpose is to increase participation of health disparities populations on National Cancer Institute clinical trials as part of the Cancer Disparities Research Partnership program. Clinical practice suggests that Native American cancer patients present with more advanced stages of cancer and hence have lower cure rates and higher treatment-related morbidities. It is hypothesized that a conventional course of cancer treatment lasting 6 to 8 weeks may be a barrier. Methods. Innovative clinical trials have been developed to shorten the course of treatment. A molecular predisposition to treatment side effects is also explored. These clinical endeavors will be performed in conjunction with a patient navigator research program. Results and Conclusions. Research metrics include analysis of process, clinical trials participation, treatment outcome, and assessment of access to cancer care at an early stage of disease. C1 John T Vucurevich Canc Care Inst, Rapid City, SD 57701 USA. Univ Wisconsin, Ctr Comprehens Canc, Dept Human Oncol, Madison, WI USA. Native Amer Canc Res Corp, Pine, CO USA. Mayo Clin, Comprehens Canc Ctr, Rochester, MN USA. NCI, Radiat Res Program, Bethesda, MD 20892 USA. Univ Wisconsin, Ctr Comprehens Canc, Dept Biostat & Med Informat, Madison, WI USA. RP Petereit, DG (reprint author), John T Vucurevich Canc Care Inst, 353 Fairmont Blvd, Rapid City, SD 57701 USA. EM dpetereit@rcrh.org OI mehta, minesh/0000-0002-4812-5713 FU NCI NIH HHS [N01-CO-12400, RFA 1U56CA99010-01] NR 29 TC 12 Z9 12 U1 0 U2 6 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA SN 0885-8195 J9 J CANCER EDUC JI J. Cancer Educ. PD SPR PY 2005 VL 20 IS 1 SU S BP 65 EP 70 DI 10.1207/s15430154jce2001s_14 PG 6 WC Oncology; Education, Scientific Disciplines; Public, Environmental & Occupational Health SC Oncology; Education & Educational Research; Public, Environmental & Occupational Health GA 929WK UT WOS:000229377100014 PM 15916524 ER PT J AU Gamito, EJ Burhansstipanov, L Krebs, LU Bemis, L Bradley, A AF Gamito, EJ Burhansstipanov, L Krebs, LU Bemis, L Bradley, A TI The use of an electronic audience response system for data collection SO JOURNAL OF CANCER EDUCATION LA English DT Article AB Background. Gathering complete and accurate data from community groups, particularly medically underserved populations, is challenging. Methods. An electronic audience response system (ARS) is a novel method for the efficient collection of data while maintaining participant confidentiality in group settings. Results. Because data are captured electronically, an ARS eliminates the need to transfer data from paper forms, reducing errors and the amount of time required for data management. Conclusions. ARS is a useful data collection tool that works well with diverse populations and greatly increases data accuracy and completeness while maintaining participant confidentiality. C1 Univ Colorado, Hlth Sci Ctr, Denver, CO 80202 USA. Native Amer Canc Res, Pine, CO 80470 USA. Univ Colorado, Sch Nursing, Denver, CO 80202 USA. Natl Canc Inst, Canc Informat Serv, Colorado Springs, CO USA. RP Burhansstipanov, L (reprint author), Native Amer Canc Res, 3022 S Nova Rd, Pine, CO 80470 USA. EM LindaB@NatAmCancer.org FU AHRQ HHS [P01 HS010854]; NCHS CDC HHS [P01SH010854]; NCI NIH HHS [R25 CA81714, U01 CA86098]; NHGRI NIH HHS [R25 HG01866] NR 10 TC 14 Z9 14 U1 1 U2 4 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA SN 0885-8195 J9 J CANCER EDUC JI J. Cancer Educ. PD SPR PY 2005 VL 20 IS 1 SU S BP 80 EP 86 DI 10.1207/s15430154jce2001s_16 PG 7 WC Oncology; Education, Scientific Disciplines; Public, Environmental & Occupational Health SC Oncology; Education & Educational Research; Public, Environmental & Occupational Health GA 929WK UT WOS:000229377100016 PM 15916526 ER PT J AU Domanski, M Fleg, J Bristow, M Knox, S AF Domanski, M Fleg, J Bristow, M Knox, S TI The effect of gender on outcome in digitalis-treated heart failure patients SO JOURNAL OF CARDIAC FAILURE LA English DT Article DE heart failure; left ventricular dysfunction; digitalis ID VENTRICULAR EJECTION FRACTIONS; SURVIVAL; GUIDELINES; MANAGEMENT; ENALAPRIL; MORTALITY; DIGOXIN AB Background: The use of digitalis is recommended for the treatment of heart failure to reduce hospitalization. Recent data suggest that digitalis treatment may adversely affect survival in women but not in men. We studied patients with left ventricular dysfunction enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) to determine whether there was a gender-based survival difference in patients treated with digitalis. Methods and Results: Symptomatic (n = 2569) and asymptomatic (n = 4228) patients with left ventricular ejection fraction <= 0.35 were studied. Digitalis use was assessed at baseline and baseline demographic variables were catalogued and compared. A multivariate analysis, incorporating known covariates of risk for adverse cardiovascular events, was used to examine the association of digitalis with all-cause mortality, cardiovascular death, death from heart failure, and arrhythinic death, with, or without, worsening heart failure in women compared with men. Analysis for an interaction between digitalis and gender on mortality was also performed. No interaction between gender and digitalis treatment on survival was found, and there was no significant difference in the hazard ratios for men and women on digitalis either with respect to all-cause mortality, cardiovascular mortality, heart failure mortality, or arrhythmic death with worsening heart failure. When mortality for arrhythinic death without worsening heart failure was adjusted for the probability of being treated with digitalis (propensity analysis), women fared better than men. Conclusion: Data from the SOLVD trials suggest that digitalis treatment of heart failure does not result in a difference in survival between men and women. Because a randomized trial to definitively answer the question is unlikely, and perhaps inappropriate, examination of other heart failure populations for a gender-digitalis interaction is indicated. C1 NHLBI, Clin Trials Grp, Bethesda, MD 20892 USA. Univ Colorado, Sch Med, Div Cardiol, Denver, CO 80202 USA. NICHHD, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA. RP Domanski, M (reprint author), NHLBI, Clin Trials Grp, Bldg 10, Bethesda, MD 20892 USA. RI bristow, michael/G-7850-2011 NR 11 TC 21 Z9 22 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI PHILADELPHIA PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA SN 1071-9164 J9 J CARD FAIL JI J. Card. Fail. PD MAR PY 2005 VL 11 IS 2 BP 83 EP 86 DI 10.1016/j.cardfail.2004.07.002 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA 907AW UT WOS:000227688100001 PM 15732025 ER PT J AU Sarikkola, AU Sen, HN Uusitalo, RJ Laatikainen, L AF Sarikkola, AU Sen, HN Uusitalo, RJ Laatikainen, L TI Traumatic cataract and other adverse events with the implantable contact lens SO JOURNAL OF CATARACT AND REFRACTIVE SURGERY LA English DT Article; Proceedings Paper CT 21st Congress of the European-Society-of-Cataract-and-Refractive-Surgeons CY SEP, 2003 CL Munich, GERMANY SP European Soc Cataract & Refract Surg ID PHAKIC INTRAOCULAR-LENS; CORRECT HIGH MYOPIA; FLARE-CELL METER; FOLLOW-UP; CHAMBER LENSES; MODERATE; HYPEROPIA; EXTRACTION; OPACITIES; DIOPTERS AB Purpose: To evaluate the surgical outcome and adverse events associated with implantation of the implantable contact lens (ICL) for the correction of high myopia or high hyperopia. Setting: Helsinki University Eye Hospital, Helsinki, Finland. Methods: In this nonrandomized prospective clinical trial, the ICL V4 was implanted in 26 eyes of 13 patients with normal enrollment criteria (younger than 45 years, a clinically clear crystalline lens) (Group 1) and the V2, V3, or V4 were implanted in 38 eyes of 22 patients with heterogeneous criteria (older than 45 years or opacities in the crystalline lens) (Group 2). The main outcome measures were lens opacity classification system (LOCS II) assessment and transparency analysis of the lens. Results: In Group 1, microdensitometric assessment showed no decrease in crystalline lens transparency and no statistically significant increase in crystalline lens density at any follow-up examination (P > .05). The incidence of anterior subcapsular (AS) opacities was 7.7%, and no eye developed clinically significant cataract during the mean follow-up of 13.2 months +/- 12.3 (SD). No myopic eye lost a line of best corrected visual acuity (BCVA); 50.0% of hyperopic eyes lost 1 line of BCVA. Sixty-eight percent of myopic eyes and 75.0% of hyperopic eyes were within +/- 1.0 diopter of the predicted refraction. In Group 2, the incidence of AS opacities was 47.4% and 10 eyes (26.3%) developed clinically significant cataract during the mean follow-up of 30.9 +/- 18.0 months. The visual and refractive results were similar to those in Group 1 at 1 month, but due to progressive AS opacities in the crystalline lens, 23.4% of eyes lost BCVA lines during the follow-up. Intraoperative complications were few and insignificant. Conclusions: Implantation of the ICL for correction of high myopia or high hyperopia appears to be a safe procedure with good visual and refractive results immediately. There was no decrease in the transparency or increase in the density of the crystalline lens with the latest generation of the ICL device in the normal group, indicating enhanced safety. Progressive lens opacification in the heterogeneous group shows there are risk factors for cataract formation; ie, type V3 ICL, preexisting lens opacities, and older patient age. Anterior subcapsular opacities are most likely the result of trauma. (c) 2005 ASCRS and ESCRS. C1 Univ Helsinki, Hosp Eye, HUS 00029, Finland. NEI, NIH, Bethesda, MD USA. RP Uusitalo, RJ (reprint author), Univ Helsinki, Hosp Eye, POB 220, HUS 00029, Finland. EM risto.uusitalo@hus.fi NR 40 TC 30 Z9 30 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0886-3350 J9 J CATARACT REFR SURG JI J. Cataract. Refract. Surg. PD MAR PY 2005 VL 31 IS 3 BP 511 EP 524 DI 10.1016/j.jcrs.2004.06.084 PG 14 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA 917VD UT WOS:000228496400017 PM 15811739 ER PT J AU Tokumasu, F Fairhurst, RM Ostera, GR Brittain, NJ Hwang, J Wellems, TE Dvorak, JA AF Tokumasu, F Fairhurst, RM Ostera, GR Brittain, NJ Hwang, J Wellems, TE Dvorak, JA TI Band 3 modifications in Plasmodium falciparum-infected AA and CC erythrocytes assayed by autocorrelation analysis using quantum dots SO JOURNAL OF CELL SCIENCE LA English DT Article DE hemoglobin C; malaria; band 3 clustering; quantum dots; power spectrum; autocorrelation; membrane modification ID HEINZ BODY FORMATION; RED-BLOOD-CELL; HEMOGLOBIN DENATURATION; MONOCLONAL-ANTIBODIES; UNSTABLE HEMOGLOBINS; IGG-BINDING; MALARIA; PHAGOCYTOSIS; MEMBRANE; AUTOANTIBODIES AB The molecular stability of hemoglobin is critical for normal erythrocyte functions, including oxygen transport. Hemoglobin C (HbC) is a mutant hemoglobin that has increased oxidative susceptibility due to an amino acid substitution (beta 6: Glu to Lys). The growth of Plasmodium falciparuin is abnormal in homozygous CC erythrocytes in vitro, and CC individuals show innate protection against severe P falciparuin malaria. We investigated one possible mechanism of innate protection using a quantum dot technique to compare the distribution of host membrane band 3 molecules in genotypically normal (AA) to CC erythrocytes. The high photostability of quantum dots facilitated the construction of 3D cell images and the quantification of fluorescent signal intensity. Power spectra and 1D autocorrelation analyses showed band 3 clusters on the surface of infected AA and CC erythrocytes. These clusters became larger as the parasites matured and were more abundant in CC erythrocytes. Further, average cluster size (500 nm) in uninfected (native) CC erythrocytes was comparable with that of parasitized AA erythrocytes but was significantly larger (1 mu m) in parasitized CC erythrocytes. Increased band 3 clustering may enhance recognition sites for autoantibodies, which could contribute to the protective effect of hemoglobin C against malaria. C1 NIAID, Viochem & Biophys Parasitol Sect, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA. NIAID, Malaria Genet Sect, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA. Natl Inst Stand & Technol, Opt Technol Div, Phys Lab, Gaithersburg, MD 20899 USA. RP Dvorak, JA (reprint author), NIAID, Viochem & Biophys Parasitol Sect, Lab Malaria & Vector Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA. EM jdvorak@niaid.nih.gov OI Tokumasu, Fuyuki/0000-0003-2790-1071 NR 42 TC 53 Z9 55 U1 0 U2 5 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD MAR 1 PY 2005 VL 118 IS 5 BP 1091 EP 1098 DI 10.1242/jcs.01662 PG 8 WC Cell Biology SC Cell Biology GA 916IK UT WOS:000228378400023 PM 15731014 ER PT J AU Liang, XJ Shen, DW Chen, KG Wincovitch, SM Garfield, SH Gottesman, MM AF Liang, XJ Shen, DW Chen, KG Wincovitch, SM Garfield, SH Gottesman, MM TI Trafficking and localization of platinum complexes in cisplatin-resistant cell lines monitored by fluorescence-labeled platinum SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID OVARIAN ADENOCARCINOMA CELLS; CROSS-RESISTANCE; CARCINOMA-CELLS; MULTIDRUG-RESISTANCE; CANCER; COPPER; ACCUMULATION; EXPRESSION; PROTEINS; BINDING AB Cisplatin is a chemotherapeuttic agent commonly used in the treatment of a wide variety of malignant tumors. Resistance to cisplatin represents a major obstacle to effective cancer therapy because clinically significant levels of resistance quickly emerge after treatment. Based on previous Studies indicating abnormal plasma membrane protein trafficking in cisplatin-resistant (CP-r) cells, Fluorescence (Alexa fluor)-labeled cisplatin was used to determine whether this defect altered the trafficking and localization of cisplatin by comparing drug sensitive KB-3-1 and KB-CP-r cells. Alexa Fluor-cisplatin was readily internalized and localized throughout the KB-3-1 cells, but overall fluorescence decreased in KB-CP-r cells, as detected by flow cytometry(FACS) and coniocal microscopy. Only punctate cytoplasmic staining was observed in KB-CP-r cells with less fluorescence observed in the nucleus. Colocalization experiments with a Golgi-selective stain indicate the involvement of Golgi-like vesicles in initial intracellular processing of Alexa Fluor Conjugated cisplatin complexes. As detected using an antibody to Alexa Fluor-cisplatin, cisplatin complex-binding proteins (CCBPs) were reduced in membrane fractions of single-step cisplatin-resistant KB-CP.5 cells and increased in the cytoplasm of KB-CP.5 cells compared to KB-3-1 cells. CCBPs localized to lower density fractions in KB-CP.5 cells than in KB-3-1 cells as determined by iodixanol gradient centrifugation. In summary inappropriate trafficking of CCBPs might explain resistance to cisplatin in Cultured cancer cells, presumably because membrane binding proteins for cisplatin are not properly located on the cell Surface in these cells, but are instead trapped in low density vesicles within the cytoplasm. J. Cell. Physiol. (C) Wiley-Liss, Inc. C1 NCI, Cell Biol Lab,Dept Hlth & Human Serv, NIH, Canc Res Ctr, Bethesda, MD 20892 USA. NCI, Lab Expt Carcinogenesis,Dept Hlth & Human Serv, NIH, Canc Res Ctr, Bethesda, MD 20892 USA. RP Gottesman, MM (reprint author), NCI, Cell Biol Lab,Dept Hlth & Human Serv, NIH, Canc Res Ctr, 37 Convent Dr,Room 2108, Bethesda, MD 20892 USA. EM mgottesman@nih.gov RI Chen, Kevin/D-6769-2011 OI Chen, Kevin/0000-0003-2983-6330 FU Intramural NIH HHS [Z99 NS999999] NR 29 TC 38 Z9 38 U1 0 U2 14 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD MAR PY 2005 VL 202 IS 3 BP 635 EP 641 DI 10.1002/jcp.20253 PG 7 WC Cell Biology; Physiology SC Cell Biology; Physiology GA 892WT UT WOS:000226681400001 PM 15546142 ER PT J AU Ramasamy, S Venkateshrao, S Rifkind, JM Manoharan, PT AF Ramasamy, S Venkateshrao, S Rifkind, JM Manoharan, PT TI Metal ion coordination in 'R' and 'T' state hybrid hemoglobins as revealed by optical, EPR and sulphhydryl reactivity studies SO JOURNAL OF CHEMICAL SCIENCES LA English DT Article DE hybrid hemoglobin; -SH reactivity study; EPR; subunit heterogeneity ID NUCLEAR-MAGNETIC-RESONANCE; ELECTRON-PARAMAGNETIC-RESONANCE; HEME-HEME INTERACTION; QUATERNARY STRUCTURES; OXYGEN EQUILIBRIUM; PROXIMAL HISTIDINE; PROTOPORPHYRIN-IX; COBALT MYOGLOBINS; BETA-CHAINS; MODEL AB The sulphhydryl environment in various mixed-metal hybrid hemoglobins, viz. alpha(2)(Cu)beta(2)(FeCO), alpha(2)(FeCO)-beta(2)(Cu), alpha(2)(Cu)-beta(2)(Ni), alpha(2)(Ni)-beta(2)(Cu), was studied by reacting them with the sulphhydryl reagent, 4,4'-dithiodipyridine (4-PDS). The reactivity was compared with that of HbCO, NiHb and CuHb. It is found that there exists a correlation between conformational change and metal ion environment, not only at the extreme R and T states but also the intermediate conformations. EPR examinations of these hybrids show that both in R state- [Cu(II)-Fe(II)] and T state- [Cu(II)-Ni(II)] hybrids at neutral pH and in the absence of IHP, CuPPIX, irrespective of the subunit in which it is present, has a mixed-metal ion environment: Species 1, a five-coordinated Cu2+, complex with strong proximal histidine bond and species 2, a four-coordinated complex without any covalent linkage with N epsilon F8-histidine. C1 Indian Inst Technol, Dept Chem, Madras 600036, Tamil Nadu, India. Indian Inst Technol, Reg Sophisticated Instrumentat Ctr, Madras 600036, Tamil Nadu, India. NIA, Mol Dynam Sect, NIH, Baltimore, MD 21224 USA. RP Manoharan, PT (reprint author), Indian Inst Technol, Dept Chem, Madras 600036, Tamil Nadu, India. EM ptm@rsic.iitm.ernet.in NR 30 TC 1 Z9 1 U1 0 U2 1 PU INDIAN ACADEMY SCIENCES PI BANGALORE PA C V RAMAN AVENUE, SADASHIVANAGAR, P B #8005, BANGALORE 560 080, INDIA SN 0253-4134 J9 J CHEM SCI JI J. Chem. Sci. PD MAR PY 2005 VL 117 IS 2 BP 85 EP 97 PG 13 WC Chemistry, Multidisciplinary SC Chemistry GA 914NB UT WOS:000228233400003 ER PT J AU Swedo, SE Grant, PJ AF Swedo, SE Grant, PJ TI Annotation: PANDAS: a model for human autoimmune disease SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE PANDAS; Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infections; Sydenham's chorea; streptococcal infection; autoimmunity; tics ID OBSESSIVE-COMPULSIVE DISORDER; A STREPTOCOCCAL INFECTIONS; SYDENHAMS-CHOREA; TOURETTES-SYNDROME; NEUROPSYCHIATRIC DISORDERS; RHEUMATIC-FEVER; BASAL GANGLIA; ANTINEURONAL ANTIBODIES; MOVEMENT-DISORDERS; TIC DISORDERS AB Background: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infections (PANDAS) is a recently recognized syndrome in which pre-adolescent children have abrupt onsets of tics and/or obsessive-compulsive symptoms, a recurring and remitting course of illness temporally related to streptococcal infections, and associated neurologic findings including adventitious movements, hyperactivity and emotional lability. Methods: Inspired by observations of similar symptoms in children with Sydenham's chorea, a search was undertaken for clinical and laboratory evidence in support of the new syndrome. Results: Consistent and predictable clinical findings have been described in a large case series. Magnetic resonance imaging has supported the postulated pathobiology of the syndrome with evidence of inflammatory changes in basal ganglia. Antibasal ganglia antibodies have been found in some acute cases, mimicking streptococcal antigen epitopes. Conclusions: While PANDAS remains a controversial diagnostic concept, it has stimulated new research endeavors into the possible links between bacterial pathogens, autoimmune reactions, and neuropsychiatric symptoms. C1 NIH, Pediat & Dev Neuropsychiat Branch, NIMH, Bethesda, MD 20892 USA. RP Grant, PJ (reprint author), NIH, Pediat & Dev Neuropsychiat Branch, NIMH, 10 Ctr Dr MSC 1255,Bldg 10,Room 4N208, Bethesda, MD 20892 USA. EM paul.grant@nih.gov NR 51 TC 47 Z9 50 U1 4 U2 5 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD MAR PY 2005 VL 46 IS 3 BP 227 EP 234 DI 10.1111/j.1469-7610.2004.00386.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 910SR UT WOS:000227953000002 PM 15755299 ER PT J AU Blair, RJR Budhani, S Colledge, E Scott, S AF Blair, RJR Budhani, S Colledge, E Scott, S TI Deafness to fear in boys with psychopathic tendencies SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE amygdala; psychopathic tendencies; psychopathy; integrated emotion systems ID ORBITOFRONTAL CORTEX DYSFUNCTION; FACIAL EXPRESSIONS; RESPONSE REVERSAL; NEURAL RESPONSES; CONDUCT PROBLEMS; AMYGDALA LESIONS; STARTLE REFLEX; CHILDREN; EMOTION; RECOGNITION AB The processing of the emotional signals of others is fundamental for normal socialization and interaction. Reduced responsiveness to the expressions of sadness and fear has been implicated in the development of psychopathy (Blair, 1995). The current study investigates the ability of boys with psychopathic tendencies to process auditory affect information. Boys with psychopathic tendencies and a comparison group, as defined by the Antisocial Process Screening Device (APSD: Frick & Hare, 2001), were presented with neutral words spoken with intonations conveying happiness, disgust, anger, sadness and fear and were asked to identify the emotion of the speaker based on prosody. The boys with psychopathic tendencies presented with a selective impairment for the recognition of fearful vocal affect. These results are interpreted with reference to amygdala dysfunction and components of the Integrated Emotion Systems model. C1 NIMH, Unit Affect Cognit Neurosci, Mood & Anxiety Disorders Program, NIH,US Dept HHS, Bethesda, MD 20892 USA. UCL, Dept Psychol, London, England. UCL, Inst Cognit Neurosci, London, England. Kings Coll London, Inst Psychiat, London WC2R 2LS, England. UCL, Dept Linguist, London, England. RP Blair, RJR (reprint author), NIMH, Unit Affect Cognit Neurosci, Mood & Anxiety Disorders Program, NIH,US Dept HHS, 15K North Dr,Room 206,MSC 2670, Bethesda, MD 20892 USA. EM blairj@intra.nimh.nih.gov RI Scott, Sophie/A-1843-2010 OI Scott, Sophie/0000-0001-7510-6297 FU Wellcome Trust [090961] NR 56 TC 80 Z9 80 U1 3 U2 15 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD MAR PY 2005 VL 46 IS 3 BP 327 EP 336 DI 10.1111/j.1469-7610.2004.00356.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 910SR UT WOS:000227953000011 PM 15755308 ER PT J AU Prinstein, MJ Cheah, CSL Guyer, AE AF Prinstein, MJ Cheah, CSL Guyer, AE TI Peer victimization, cue interpretation, and internalizing symptoms: Preliminary concurrent and longitudinal findings for children and adolescents SO JOURNAL OF CLINICAL CHILD AND ADOLESCENT PSYCHOLOGY LA English DT Article ID INFORMATION-PROCESSING FACTORS; AGGRESSIVE-BEHAVIOR; DEPRESSIVE SYMPTOMS; SOCIAL-ANXIETY; HOSTILE ATTRIBUTION; LONELINESS; REJECTION; PREDICTORS; ADJUSTMENT; CHILDHOOD AB This study examined hostile intent and causal, critical self-referent attributions for ambiguous peer cues to examine the hypothesis that these latter interpretations would be uniquely associated with symptoms of depression, social anxiety, and loneliness. Critical self-referent attributions were assessed in 116 kindergarteners (Study 1) and 159 adolescents (Study 2) using a hypothetical vignette procedure, replicating past work on social information processing. In both samples, critical self-referent attributions were concurrently associated with depressive symptoms as reported by teacher (Study 1), peer and self-report (Study 2). Critical self-referent attributions also were concurrently associated with loneliness and with actual peer experiences, including peer rejection in both studies. Results from both studies support a cognitive vulnerability-stress model, suggesting that the tendency to derive critical self-referent attributions from ambiguous peer experiences is most closely associated with depressive symptoms when accompanied by high levels of peer victimization. Longitudinal findings (Study 2) offers preliminary evidence for this cognitive vulnerability-stress model as a predictor of adolescents' depressive symptoms over a 17-month interval. C1 Univ N Carolina, Dept Psychol, Chapel Hill, NC 27599 USA. Univ Maryland Baltimore Cty, Dept Psychol, Baltimore, MD 21228 USA. NIMH, Mood & Anxiety Disorders Program, Bethesda, MD USA. RP Prinstein, MJ (reprint author), Univ N Carolina, Dept Psychol, Davie Hall,Campus Box 3270, Chapel Hill, NC 27599 USA. EM mitch.prinstein@unc.edu RI Prinstein, Mitchell/F-7955-2013 FU NIMH NIH HHS [R01 MH59766] NR 68 TC 99 Z9 102 U1 0 U2 15 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 USA SN 1537-4416 J9 J CLIN CHILD ADOLESC JI J. Clin. Child Adolesc. Psychol. PD MAR PY 2005 VL 34 IS 1 BP 11 EP 24 DI 10.1207/s15374424jccp3401_2 PG 14 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 893XQ UT WOS:000226754800003 PM 15677277 ER PT J AU D'Amico, R Yang, YJ Mildvan, D Evans, SR Schnizlein-Bick, CT Hafner, R Webb, N Basar, M Zackin, R Jacobson, MA AF D'Amico, R Yang, YJ Mildvan, D Evans, SR Schnizlein-Bick, CT Hafner, R Webb, N Basar, M Zackin, R Jacobson, MA TI Lower CD4+ T lymphocyte nadirs may indicate limited immune reconstitution in HIV-1 infected individuals on potent antiretroviral therapy: Analysis of immunophenotypic marker results of AACTG 5067 SO JOURNAL OF CLINICAL IMMUNOLOGY LA English DT Article DE immune reconstitution; CD4 nadir; opportunistic infection; antiretroviral therapy ID PNEUMOCYSTIS-CARINII PNEUMONIA; IMMUNODEFICIENCY-VIRUS TYPE-1; HIV-INFECTED PERSONS; CELL COUNT INCREASE; PROTEASE INHIBITOR; LOAD REDUCTION; RESTORATION; DISEASE; MORTALITY; SUBSETS AB Background: Although initiation of potent antiretroviral therapy (ART) has significantly improved immune perturbations in individuals with AIDS, it is unclear which factors are most important in determining the degree of immune reconstitution. Methods: Whole blood was analyzed at baseline and week 12 in six groups of subjects (n = 81): those with acute or following immune reconstitution after Pneumocystis jirovecii (previously known as Pneumocystis carinii) pneumonia (PcP) (two groups) and cytomegalovirus (CMV) retinitis (two groups), HIV-infection without AIDS (one group), and healthy volunteers (one group). Absolute CD4+ and CD8+ T lymphocytes, naive (CD45RA+) and memory (CD45RO+) CD4+ T lymphocytes and percentages of activated CD8+ T lymphocytes (CD8+/CD38+/HLA-DR), and CD28 expression on CD4+ and CD8+ T lymphocytes were enumerated. Results: The reconstituted CMV group, which had a history of a lower CD4+ T lymphocyte nadir compared to the reconstituted PcP group (15 cells/mm(3) versus 48 cells/mm(3); p = .013), had significantly lower absolute CD4+, CD8+ and naive CD4+ T lymphocytes and a trend toward lower memory CD4+ T lymphocytes compared to the reconstituted PcP group. Moreover, no difference was noted between the reconstituted groups in the proportion of subjects with undetected HIV-1 RNA. The reconstituted subjects had significantly lower absolute CD4+, memory CD4+ and naive CD4+ T lymphocytes than the HIV-positive controls and a significantly higher percentage of activated CD8+ T lymphocytes with a lower percentage of CD8+CD28 expression than the HIV-negative controls. Conclusion: The association of CD4+ T lymphocyte nadir with the extent of immune reconstitution in HIV-infected individuals suggests that HIV-1 may cause irreparable immune system damage despite potent ART. C1 Beth Israel Med Ctr, New York, NY 10003 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Indiana Univ, Sch Med, Indianapolis, IN USA. NIH, Div Aids, Bethesda, MD 20892 USA. Frontier Sci & Technol Res Fdn Inc, Amherst, NY USA. Univ Calif San Francisco, Dept Med, Posit Hlth Program, San Francisco, CA USA. San Francisco Gen Hosp, Med Serv, San Francisco, CA 94110 USA. RP D'Amico, R (reprint author), Beth Israel Med Ctr, 350 E 17th St, New York, NY 10003 USA. EM RonDDAmico@aol.com FU NIAID NIH HHS [5U01AI038855-08, 1U01AI46370] NR 40 TC 26 Z9 27 U1 0 U2 1 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0271-9142 J9 J CLIN IMMUNOL JI J. Clin. Immunol. PD MAR PY 2005 VL 25 IS 2 BP 106 EP 115 DI 10.1007/s10875-005-2816-0 PG 10 WC Immunology SC Immunology GA 915EJ UT WOS:000228280400003 PM 15821887 ER PT J AU Cohen, JI AF Cohen, JI TI Licking latency with licorice SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Editorial Material ID PRIMARY EFFUSION LYMPHOMA; EPSTEIN-BARR-VIRUS; MULTICENTRIC CASTLEMANS-DISEASE; KAPOSIS-SARCOMA; GROWTH; EXPRESSION; THERAPY; CELLS; PHARMACOKINETICS; INHIBITION AB Numerous viruses cause latent infections in humans, and reactivation often results in pain and suffering. While vaccines for several of these viruses are available or currently being studied in clinical trials, and antiviral therapies have been successful in preventing or treating active infection, therapy to eradicate latent infection has lagged behind. A new study reported in this issue of the JCI shows that treatment of cells latently infected with Kaposi sarcoma-associated herpesvirus (KSHV) with glycyrrhizic acid, a component of licorice, reduces synthesis of a viral latency protein and induces apoptosis of infected cells (see the related article beginning on page 642). This finding suggests a novel way to interrupt latency. C1 Med Virol Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA. RP Cohen, JI (reprint author), Med Virol Sect, Lab Clin Infect Dis, NIH, Bldg 10,Room 11N228,10 Ctr Dr,MSC 1888, Bethesda, MD 20892 USA. EM jcohen@niaid.nih.gov NR 20 TC 9 Z9 15 U1 0 U2 1 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAR PY 2005 VL 115 IS 3 BP 591 EP 593 DI 10.1172/JCI200524507 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 902YN UT WOS:000227392700020 PM 15765143 ER PT J AU Rhee, DK Marcelino, J Baker, MA Gong, YQ Smits, P Lefebvre, V Jay, GD Stewart, M Wang, HW Warman, ML Carpten, JD AF Rhee, DK Marcelino, J Baker, MA Gong, YQ Smits, P Lefebvre, V Jay, GD Stewart, M Wang, HW Warman, ML Carpten, JD TI The secreted glycoprotein lubricin protects cartilage surfaces and inhibits synovial cell overgrowth SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article ID SUPERFICIAL ZONE PROTEIN; ARTICULAR-CARTILAGE; RHEUMATOID-ARTHRITIS; LUBRICATING ACTIVITY; FLUID; ADHESION; BOVINE; VITRONECTIN; GENE; PROTEOGLYCAN AB The long-term integrity of an articulating joint is dependent upon the nourishment of its cartilage component and the protection of the cartilage surface from friction-induced wear. Loss-of-function mutations in lubricin (a secreted glycoprotein encoded by the gene PRG4) cause the human autosomal recessive disorder camptodactyly-arthropathy-coxa vara-pericarditis syndrome (CACP). A major feature of CACP is precocious joint failure. In order to delineate the mechanism by which lubricin protects joints, we studied the expression of Prg4 mRNA during mouse joint development, and we created lubricin-mutant mice. Prg4 began to be expressed in surface chondrocytes and synoviocytes after joint cavitation had occurred and remained strongly expressed by these cells postnatally. Mice lacking lubricin were viable and fertile. In the newborn period, their joints appeared normal. As the mice aged, we observed abnormal protein deposits on the cartilage surface and disappearance of underlying superficial zone chondrocytes. In addition to cartilage surface changes and subsequent cartilage deterioration, intimal cells in the synovium surrounding the joint space became hyperplastic, which further contributed to joint failure. Purified or recombinant lubricin inhibited the growth of these synoviocytes in vitro. Tendon and tendon sheath involvement was present in the ankle joints, where morphologic changes and abnormal calcification of these structures were observed. We conclude that lubricin has multiple functions in articulating joints and tendons that include the protection of surfaces and the control of synovial cell growth. C1 Case Western Reserve Univ, Sch Med, Dept Genet, Cleveland, OH 44106 USA. Case Western Reserve Univ, Sch Med, Ctr Human Genet, Cleveland, OH 44106 USA. Univ Hosp Cleveland, Cleveland, OH 44106 USA. NHGRI, Canc Genet Branch, Bethesda, MD 20892 USA. Cleveland Clin Fdn, Lerner Res Inst, Dept Biomed Engn, Cleveland, OH 44195 USA. Cleveland Clin Fdn, Lerner Res Inst, Orthopaed Res Ctr, Cleveland, OH 44195 USA. Rhode Isl Hosp, Dept Med, Providence, RI 02903 USA. Brown Univ, Providence, RI 02903 USA. Case Western Reserve Univ, Sch Med, Dept Orthopaed, Cleveland, OH 44106 USA. RP Carpten, JD (reprint author), Case Western Reserve Univ, Sch Med, Dept Genet, 2109 Adelbert Rd,BRB 719, Cleveland, OH 44106 USA. EM jcarpten@tgen.org RI Jay, Gregory/C-6346-2013 FU NIA NIH HHS [K08AG/AR01008]; NIAMS NIH HHS [AR050180, AR46249, R01 AR046249, R01 AR050180]; NICHD NIH HHS [HD07104, HD07518, T32 HD007104, T32 HD007518]; NIGMS NIH HHS [GM07250, GM08613, T32 GM007250, T32 GM008613] NR 37 TC 252 Z9 260 U1 6 U2 38 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAR PY 2005 VL 115 IS 3 BP 622 EP 631 DI 10.1172/JCI200522263 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 902YN UT WOS:000227392700025 PM 15719068 ER PT J AU Kocianova, S Vuong, C Yao, YF Voyich, JM Fischer, ER DeLeo, FR Otto, M AF Kocianova, S Vuong, C Yao, YF Voyich, JM Fischer, ER DeLeo, FR Otto, M TI Key role of poly-gamma-DL-glutamic acid in immune evasion and virulence of Staphylococcus epidermidis SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article ID POLYSACCHARIDE INTERCELLULAR ADHESIN; BACILLUS-ANTHRACIS; JOINT PROSTHESES; INFECTIONS; BIOFILMS; VACCINE; INNATE; IDENTIFICATION; EXPRESSION; MUTANTS AB Coagulase-negative staphylococci, with the leading species Stapbylococcus epidermidis, are the predominant cause of hospital-acquired infections. Treatment is especially difficult owing to biofilm formation and frequent antibiotic resistance. However, virulence mechanisms of these important opportunistic pathogens have remained poorly characterized. Here we demonstrate that S. epidermidis secretes poly-gamma-DL-glutamic acid (PGA) to facilitate growth and survival in the human host. Importantly, PGA efficiently sheltered S. epidermidis from key components of innate host defense, namely antimicrobial peptides and neutrophil phagocytosis, and was indispensable for persistence during device-related infection. Furthermore, PGA protected S. epidermidis from high salt concentration, a key feature of its natural environment, the! human skin. Notably, PGA was synthesized by all tested strains of S. epidermidis and a series of closely related coagulase-negative staphylococci, most of which are opportunistic pathogens. Our study presents important: novel biological functions for PGA and indicates that PGA represents an excellent target for therapeutic maneuvers aimed at treating disease caused by S. epidermidis and related staphylococci. C1 NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. NIAID, Microscopy Core Facil, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA. RP Otto, M (reprint author), NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, 903 S 4th St, Hamilton, MT 59840 USA. EM motto@niaid.nih.gov NR 33 TC 113 Z9 122 U1 2 U2 13 PU AMER SOC CLINICAL INVESTIGATION INC PI ANN ARBOR PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAR PY 2005 VL 115 IS 3 BP 688 EP 694 DI 10.1172/JCI200523523 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 902YN UT WOS:000227392700032 PM 15696197 ER PT J AU Zelazny, AM Calhoun, LB Li, L Shea, YR Fischer, SH AF Zelazny, AM Calhoun, LB Li, L Shea, YR Fischer, SH TI Identification of Mycobacterium species by secA1 sequences SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID SLOWLY GROWING MYCOBACTERIA; RIBOSOMAL-RNA GENE; TUBERCULOSIS SECA; DNA; DIFFERENTIATION; ATPASE; HSP65; TAXONOMY; ENZYME AB We describe a novel molecular method for the differentiation and identification of 29 mycobacterial species. The target is the secA1 gene that codes for the essential protein SecA1, a key component of the major pathway of protein secretion across the cytoplasmic membrane. A 700-bp region of the secA1 gene was amplified and sequenced from 47 American Type Culture Collection strains of 29 Mycobacterium species as well as from 59 clinical isolates. Sequence variability in the amplified segment of the secA1 gene allowed the differentiation of all species except for the members of the Mycobacterium tuberculosis (MTB) complex, which had identical sequences. A range of 83.3 to 100% interspecies similarity was observed. All species could also be differentiated by their amino acid sequences as deduced from the sequenced region of the secA1 gene, with the exception of the MTB complex. Partial sequences of secA1 from clinical isolates belonging to nine frequently isolated species of mycobacteria revealed a very high intraspecies similarity at the DNA level (typically > 99%; range, 96.0 to 100%); all clinical isolates were correctly identified. Comparison of the deduced 233-amino-acid sequences among clinical isolates of the same species showed between 99.6 and 100% similarity. To our knowledge, this is the first time a secretion-related gene has been used for the identification of the species within a bacterial genus. C1 Warren G Magnuson Clin Ctr, Microbiol Serv, Dept Lab Med, Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA. RP Fischer, SH (reprint author), Warren G Magnuson Clin Ctr, Microbiol Serv, Dept Lab Med, Dept Hlth & Human Serv,NIH, 10 Ctr Dr,MSC 1508,Bldg,10,Rm 2C-385, Bethesda, MD 20892 USA. EM sfischer@cc.nih.gov NR 41 TC 39 Z9 41 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD MAR PY 2005 VL 43 IS 3 BP 1051 EP 1058 DI 10.1128/JCM.43.3.1051-1058.2005 PG 8 WC Microbiology SC Microbiology GA 905AD UT WOS:000227538900006 PM 15750059 ER PT J AU Galsky, MD Small, EJ Oh, WK Chen, I Smith, DC Colevas, AD Martone, L Curley, T DeLaCruz, A Scher, HI Kelly, WK AF Galsky, MD Small, EJ Oh, WK Chen, I Smith, DC Colevas, AD Martone, L Curley, T DeLaCruz, A Scher, HI Kelly, WK TI Multi-institutional randomized phase II trial of the epothilone B analog ixabepilone (BMS-247550) with or without estramustine phosphate in patients with progressive castrate metastatic prostate cancer SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article; Proceedings Paper CT 40th Annual Meeting of the American-Society-of-Clinical-Oncology CY JUN 05-08, 2004 CL New Orleans, LA SP Amer Soc Clin Oncol ID MICROTUBULE-STABILIZING AGENTS; MITOXANTRONE PLUS PREDNISONE; ANTITUMOR EFFICACY; CLINICAL-TRIALS; CELL-LINES; DOCETAXEL; HYDROCORTISONE; GUIDELINES; TAXOL; MEN AB Purpose To evaluate the antitumor activity and safety of the epothilone B analog, ixabepilone, with or without estramustine phosphate (EMP), in chemotherapy-naive patients with progressive castrate metastatic prostate cancer. Patients and Methods Patients were randomly assigned to receive ixabepilone (35 mg/m(2)) by intravenous infusion every 3 weeks with or without EMP 280 mg orally three times daily on days 1 to 5. Results Between December 2001 and October 2003, 92 patients were enrolled and randomly assigned to treatment with ixabepilone alone (45 patients) or in combination with EMP (47 patients). Grades 3 and 4 toxicities experienced by more than 5% of patients included neutropenia (22%), fatigue (9%), and neuropathy (13%) on the ixabepilone arm, and neutropenia (29%), febrile neutropenia (9%), fatigue (9%), neuropathy (7%), and thrombosis (6%) on the ixabepilone + EMP arm. Post-treatment declines in prostate-specific antigen of greater than or equal to 50% were achieved in 21 of 44 patients (48%; 95% Cl, 33% to 64%) on the ixabepilone arm, and 31 of 45 patients (69%, 95% Cl, 55% to 82%) on the ixabepilone + EMP arm. In patients with measurable disease, partial responses were observed in eight of 25 patients (32%; 95% Cl, 14% to 50%) on the ixabepilone arm, and 11 of 23 (48%; 95% Cl, 27% to 68%) on the ixabepilone + EMP arm. Time to prostate-specific antigen progression was 4.4 months (95% Cl, 3.1 to 6.9 months) on the ixabepilone-alone arm and 5.2 months (95% Cl, 4.5 to 6.8 months) on the combination arm. Conclusion Ixabepilone, with or without estramustine phosphate, is well tolerated and has antitumor activity in patients with castrate metastatic prostate cancer. C1 Mem Sloan Kettering Canc Ctr, Dept Nursing, Dept Med, Div Solid Tumor Oncol,Genitourinary Oncol Serv, New York, NY 10021 USA. Cornell Univ, Joan & Sanford I Weill Med Coll, Dept Med, New York, NY USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. Dana Farber Partners Canc Care, Boston, MA USA. Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA. Univ Michigan, Ann Arbor, MI 48109 USA. Natl Canc Inst, Bethesda, MD USA. RP Galsky, MD (reprint author), Mem Sloan Kettering Canc Ctr, Dept Nursing, Dept Med, Div Solid Tumor Oncol,Genitourinary Oncol Serv, 1275 York Ave, New York, NY 10021 USA. EM galskym@mskcc.org RI Oh, William/B-9163-2012 OI Oh, William/0000-0001-5113-8147 FU NCI NIH HHS [CM17105] NR 30 TC 137 Z9 140 U1 1 U2 2 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 330 JOHN CARLYLE ST, STE 300, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR 1 PY 2005 VL 23 IS 7 BP 1439 EP 1446 DI 10.1200/JCO.2005.09.042 PG 8 WC Oncology SC Oncology GA 902PB UT WOS:000227367900015 PM 15735119 ER PT J AU Blaney, SM Balis, FM Berg, S Arndt, CAS Heideman, R Geyer, JR Packer, R Adamson, PC Jaeckle, K Klenke, R Aikin, A Murphy, R McCully, C Poplack, DG AF Blaney, SM Balis, FM Berg, S Arndt, CAS Heideman, R Geyer, JR Packer, R Adamson, PC Jaeckle, K Klenke, R Aikin, A Murphy, R McCully, C Poplack, DG TI Intrathecal mafosfamide: A preclinical pharmacology and phase I trial SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID NONHUMAN-PRIMATES; PHARMACOKINETICS; TOPOTECAN; TUMORS; DRUGS AB Purpose Preclinical studies of mafosfamide, a preactivated cyclophosphamide analog, were performed to define a tolerable and potentially active target concentration for intrathecal (IT) administration. A phase I and pharmacokinetic study of IT mafosfamide was performed to determine a dose for subsequent phase II trials. Patients and Methods In vitro cytotoxicity studies were performed in MCF-7, Molt-4, and rhabdomyosarcoma cell lines. Feasibility and pharmacokinetic studies were performed in nonhuman primates. These preclinical studies were followed by a phase I trial in patients with neoplastic meningitis. There were five dose levels ranging from 1 mg to 6.5 mg. Serial CSF samples were obtained for pharmacokinetic studies in a subset of patients with Ommaya reservoirs. Results The cytotoxic target exposure for mafosfamide was 10 mumol/L. Preclinical studies demonstrated that this concentration could be easily achieved in ventricular CSF after intraventricular dosing. In the phase I clinical trial, headache was the dose-limiting toxicity. Headache was ameliorated at 5 mg by prolonging the infusion rate to 20 minutes, but dose-limiting headache occurred at 6.5 mg dose with prolonged infusion. Ventricular CSF mafosfamide concentrations at 5 mg exceeded target cytotoxic concentrations after an intraventricular dose, but lumbar CSF concentrations 2 hours after the dose were less than 10 mumol/L. Therefore, a strategy to alternate dosing between the intralumbar and intraventricular routes was tested. Seven of 30 registrants who were assessable for response had a partial response, and six had stable disease. Conclusion The recommended phase II dose for IT mafosfamide, administered without concomitant analgesia, is 5 mg over 20 minutes. C1 Baylor Coll Med, Texas Childrens Canc Ctr, Dept Pediat, Houston, TX 77030 USA. NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA. Mayo Clin, Rochester, MI USA. St Jude Childrens Res Hosp, Memphis, TN 38105 USA. Childrens Hosp & Med Ctr, Seattle, WA 98105 USA. Childrens Hosp, Natl Med Ctr, Washington, DC 20010 USA. MD Anderson Canc Ctr, Houston, TX USA. RP Blaney, SM (reprint author), Baylor Coll Med, Texas Childrens Canc Ctr, Dept Pediat, 6621 Fannin St,CC 1410 00, Houston, TX 77030 USA. EM sblaney@txccc.org FU NCRR NIH HHS [M01RR00188] NR 24 TC 37 Z9 39 U1 0 U2 2 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAR 1 PY 2005 VL 23 IS 7 BP 1555 EP 1563 DI 10.1200/JCO.2005.06.053 PG 9 WC Oncology SC Oncology GA 902PB UT WOS:000227367900029 PM 15735131 ER PT J AU Post, RM Altshuler, LL Frye, MA Suppes, T McElroy, SL Keck, PE Leverich, GS Kupka, R Nolen, WA Luckenbaugh, DA Walden, J Grunze, H AF Post, RM Altshuler, LL Frye, MA Suppes, T McElroy, SL Keck, PE Leverich, GS Kupka, R Nolen, WA Luckenbaugh, DA Walden, J Grunze, H TI Preliminary observations on the effectiveness of levetiracetam in the open adjunctive treatment of refractory bipolar disorder SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID ANTIEPILEPTIC DRUG LEVETIRACETAM; DEPRESSIVE SYMPTOMATOLOGY IDS; ADD-ON THERAPY; DOUBLE-BLIND; PARTIAL SEIZURES; ACUTE MANIA; UCB L059; EPILEPSY; ILLNESS; PROFILE AB Objective: Levetiracetam is a recently approved, well-tolerated anticonvulsant with a unique mechanism of action yielding efficacy in treatment-refractory seizure disorders and positive effects in an animal model of mania. Given the effectiveness of a range of other anticonvulsants in bipolar disorder, we sought to evaluate levetiracetam in patients with treatment-resistant illness. Method: Thirty-four patients received 500 to 1000 mg of levetiracetam titrated to a target dose of 2000 mg/day (maximum dose = 3000 mg/day) as open, adjunctive treatment for clinically significant symptoms of depression (N = 13), mania (N = 7), or cycling (N = 14) despite ongoing treatment with mood stabilizers. Inventory for Depressive Symptomatology-Clinician version (IDS-C), Young Mania Rating Scale (YMRS), and Clinical Global Impressions scale for use in Bipolar Illness ratings were completed at each visit for 8 weeks, and partial responders were offered continuation treatment. Data were collected from July 2001 to December 2002. Results: Five of 16 (31%; 13 depressed, 3 cycling) patients with initial depressive symptoms met the criterion for remission (IDS-C score of: 13) at last observation. All of these patients were less severely ill at baseline, whereas none of those more severely depressed at baseline responded. The majority of the 16 patients (7 manic, 9 cycling) with manic symptoms at baseline showed improvement in the YMRS in the first 2 weeks. While 7 of the 16 (44%) patients met the criterion for manic response and remission at last observation, 4 showed intervening periods of moderate to marked exacerbation. Levetiracetam was weight neutral. Conclusion: Other pilot trials should explore possible areas of psychotropic action of levetiracetam prior to the conduct of more controlled clinical trials. C1 NIMH, Biol Psychiat Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NIMH, Mood & Anxiety Disorders Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Ambulatory Clin Res Ctr, Los Angeles, CA 90024 USA. VA Med Ctr, Los Angeles, CA USA. Univ Texas, SW Med Ctr, Dallas, TX USA. Univ Cincinnati, Coll Med, Dept Psychiat, Psychopharmacol Res Program, Cincinnati, OH 45221 USA. Cincinnati Vet Affairs Med Ctr, Mental Hlth Care Line & Gen Clin Res Ctr, Cincinnati, OH USA. Univ Utrecht, NL-3508 TC Utrecht, Netherlands. Univ Groningen Hosp, Dept Psychiat, Groningen, Netherlands. Univ Freiburg Klinikum, Zentrum Innovat Therapie Bipolarer Storungen, Freiburg, Germany. Univ Munich, Psychiat Klin, Hosp Psychiat, Munich, Germany. RP Post, RM (reprint author), Bldg 10,Room 3S239,10 Ctr Dr,MSC 1272, Bethesda, MD 20892 USA. EM Robert.Post@nih.gov RI Nolen, Willem/E-9006-2014 NR 38 TC 37 Z9 39 U1 0 U2 2 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD MAR PY 2005 VL 66 IS 3 BP 370 EP 374 PG 5 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 907UY UT WOS:000227744700013 PM 15766304 ER PT J AU Lauronen, E Koskinen, J Veijola, J Miettunen, J Jones, PB Fenton, WS Isohanni, M AF Lauronen, E Koskinen, J Veijola, J Miettunen, J Jones, PB Fenton, WS Isohanni, M TI Recovery from schizophrenic psychoses within the Northern Finland 1966 Birth Cohort SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID LONG-TERM COURSE; FOLLOW-UP; NATURAL COURSE; ILLNESS; DISORDERS AB Background: Because of widely disparate findings from follow-up studies, the likelihood of recovery from schizophrenia remains controversial. We report the extent of recovery from schizophrenia in a population-based cohort. Method: Subjects with psychotic disorders were recruited from the Northern Finland 1966 Birth Cohort. Of the 91 subjects who agreed to participate, 59 were diagnosed with schizophrenia and 12 were diagnosed with schizophrenia spectrum disorders (schizophreniform psychosis, schizoaffective or delusional disorder) by DSM-III-R criteria. Diagnoses were established by interviewing the subjects, checking the Finnish Hospital Discharge Register, and reviewing their medical records. To assess recovery, we used the Clinical Global Impressions; the Positive and Negative Syndrome Scale; the Social and Occupational Functioning Assessment Scale; and information about psychiatric hospitalizations, use of antipsychotic medication, and occupational status. Results: Only 1 subject (1.7%) with DSM-III-R schizophrenia and 3 subjects (25%) with schizophrenia spectrum disorders fully recovered; 1 schizophrenia subject (1.7%) and 2 schizophrenia spectrum subjects (16.7%) experienced partial recovery. Conclusion: The data indicate that, at least until age 35, complete recovery from schizophrenia is rare, and the prognosis for the disorder is far more serious than suggested by some follow-up studies. C1 Oulu Univ, Dept Psychiat, FIN-90014 Oulu, Finland. Oulu Univ, Dept Publ Hlth & Gen Practice, FIN-90014 Oulu, Finland. Muurola Hosp, Totonvaara, Finland. Univ Cambridge, Dept Psychiat, Cambridge CB2 1TN, England. NIMH, Bethesda, MD 20892 USA. RP Lauronen, E (reprint author), Oulu Univ, Dept Psychiat, POB 5000, FIN-90014 Oulu, Finland. EM llaurone@paju.oulu.fi OI Jones, Peter/0000-0002-0387-880X NR 39 TC 24 Z9 24 U1 1 U2 1 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD MAR PY 2005 VL 66 IS 3 BP 375 EP 383 PG 9 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 907UY UT WOS:000227744700014 PM 15766305 ER PT J AU Cohen, JH Piatigorsky, J Ding, LL Colley, NJ Ward, R Horwitz, J AF Cohen, JH Piatigorsky, J Ding, LL Colley, NJ Ward, R Horwitz, J TI Vertebrate-like beta gamma-crystallins in the ocular lenses of a copepod SO JOURNAL OF COMPARATIVE PHYSIOLOGY A-NEUROETHOLOGY SENSORY NEURAL AND BEHAVIORAL PHYSIOLOGY LA English DT Article; Proceedings Paper CT Symposium on Mechanisms of Behavioral Switching CY JUL, 2003 CL Boise, ID SP Anim Behav Soc DE copepod; lens; crystallin; vision; Anomalocera ornata ID GLUTATHIONE S-TRANSFERASES; SPONGE GEODIA-CYDONIUM; ALPHA-CRYSTALLIN; EYE LENS; CUBOMEDUSAN JELLYFISH; CONVERGENT EVOLUTION; OMEGA-CRYSTALLIN; GENE-EXPRESSION; NONLENS MEMBER; PROTEINS AB The diverse crystallins are water-soluble proteins that are responsible for the optical properties of cellular lenses of animal eyes. While all vertebrate lenses contain physiological stress-related alpha- and beta gamma-crystallins, some also contain taxon-specific, often enzyme-related crystallins. To date, the alpha- and beta gamma-crystallins have been found only in vertebrate lenses. Here we report lenses from an invertebrate, the pontellid copepod Anomalocera ornata, accumulate beta gamma-crystallin family members as judged by immunocytochemistry, western immunoblotting and microsequencing. Our data provide the first example of beta gamma-crystallin members in an invertebrate lens, establishing that the use of this protein family as lens crystallins is not confined to vertebrates. C1 Duke Univ, Marine Lab, Beaufort, NC 28516 USA. Duke Univ, Dept Biol, Beaufort, NC 28516 USA. NEI, Mol & Dev Biol Lab, NIH, Bethesda, MD 20892 USA. Univ Calif Los Angeles, Sch Med, Jules Stein Eye Inst, Los Angeles, CA 90095 USA. Univ Wisconsin, Dept Ophthalmol & Visual Sci, Madison, WI 53706 USA. Univ Wisconsin, Dept Genet, Madison, WI 53706 USA. Oceanog Inst, Dept Visual Ecol, Marine Sci Div, Harbor Branch, Ft Pierce, FL 34946 USA. RP Cohen, JH (reprint author), Duke Univ, Marine Lab, Beaufort, NC 28516 USA. EM jcohen@hboi.edu FU NEI NIH HHS [EY014378, EY08768, EY03897, R01 EY008768] NR 52 TC 3 Z9 3 U1 0 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0340-7594 J9 J COMP PHYSIOL A JI J. Comp. Physiol. A -Neuroethol. Sens. Neural Behav. Physiol. PD MAR PY 2005 VL 191 IS 3 BP 291 EP 298 DI 10.1007/s00359-004-0594-4 PG 8 WC Behavioral Sciences; Neurosciences; Physiology; Zoology SC Behavioral Sciences; Neurosciences & Neurology; Physiology; Zoology GA 905FR UT WOS:000227554100009 PM 15702356 ER PT J AU Rossier, J Dahourou, D McCrae, RR AF Rossier, J Dahourou, D McCrae, RR TI Structural and mean-level analyses of the five-factor model and locus of control - Further evidence from Africa SO JOURNAL OF CROSS-CULTURAL PSYCHOLOGY LA English DT Article DE Five-Factor Model; locus of control; cross-cultural research; personality; Africa ID NEO-PI-R; POWERFUL OTHERS; PERSONALITY-INVENTORY; CONTROL SCALE; PROCRUSTES ROTATION; EXTERNAL CONTROL; CULTURES; CHANCE; VALIDATION; TRAITS AB This study examines the Five-Factor Model of personality and locus of control in French-speaking samples in Burkina Faso (N = 470) and Switzerland (Ns = 1,090,361), using the Revised NEO Personality Inventory (NEO-PI-R) and Levenson's Internality, Powerful others, and Chance (IPC) scales. Alpha reliabilities were consistently lower in Burkina Faso, but the factor structure of the NEO-PI-R was replicated in both cultures. The intended three-factor structure of the IPC could not be replicated, although a two-factor solution was replicable across the two samples. Although scalar equivalence has not been demonstrated, mean-level comparisons showed the hypothesized effects for most of the five factors and locus of control; Burkinabe scored higher in Neuroticism than anticipated. Findings from this African sample generally replicate earlier results from Asian and Western cultures and are consistent with a biologically based theory of personality. C1 Univ Lausanne, Inst Psychol, CH-1015 Lausanne, Switzerland. Univ Ouagadougou, Ouagadougou, Burkina Faso. NIA, DHHS, NIH, Bethesda, MD 20892 USA. RP Rossier, J (reprint author), Univ Lausanne, Inst Psychol, BFSH 2 Dorigny, CH-1015 Lausanne, Switzerland. EM Jerome.Rossier@unil.ch RI Rossier, Jerome/A-3494-2009 OI Rossier, Jerome/0000-0002-9924-3672 NR 65 TC 36 Z9 36 U1 1 U2 10 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0022-0221 J9 J CROSS CULT PSYCHOL JI J. Cross-Cult. Psychol. PD MAR PY 2005 VL 36 IS 2 BP 227 EP 246 DI 10.1177/0022022104272903 PG 20 WC Psychology, Social SC Psychology GA 898AR UT WOS:000227048600004 ER PT J AU Martin, S White, HR AF Martin, S White, HR TI Still at risk for substance abuse: Transitions, risks, and opportunities for prevention of drug abused during emerging adulthood SO JOURNAL OF DRUG ISSUES LA English DT Editorial Material C1 Natl Inst Drug Abuse, Lexington, KY 40583 USA. Rutgers State Univ, Ctr Alcohol Studies, Piscataway, NJ 08855 USA. Rutgers State Univ, Dept Sociol, Piscataway, NJ 08855 USA. RP Martin, S (reprint author), Natl Inst Drug Abuse, Lexington, KY 40583 USA. NR 2 TC 5 Z9 5 U1 0 U2 1 PU J DRUG ISSUES INC PI TALLAHASSEE PA FLORIDA STATE UNIV, SCHOOL CRIMINOLOGY CRIMINAL JUSTICE, PO BOX 66696, TALLAHASSEE, FL 32313-6696 USA SN 0022-0426 J9 J DRUG ISSUES JI J. Drug Issues PD SPR PY 2005 VL 35 IS 2 BP 229 EP 234 PG 6 WC Substance Abuse SC Substance Abuse GA 940XM UT WOS:000230179200001 ER PT J AU La Rooy, D Pipe, ME Murray, JE AF La Rooy, D Pipe, ME Murray, JE TI Reminiscence and hypermnesia in children's eyewitness memory SO JOURNAL OF EXPERIMENTAL CHILD PSYCHOLOGY LA English DT Article DE memory; eyewitness testimony; reminiscence; hypermnesia; repeated interviewing ID EVENT REPORTS; REPEATED RECALL; DELAY; TIME; EXPERIENCE; FORGOTTEN; PARADIGM; PICTURES; REMEMBER; DETAILS AB Three experiments examined reminiscence and hypermnesia in 5- and 6-year-olds' memory for an event across repeated interviews that occurred either immediately afterward (Experiment 1) or after a 6-month delay (Experiments 2 and 3). Reminiscence (recall of new information) was reliably obtained in all of the experiments, although the numbers of new items recalled were fewer after a delay than when the interviews occurred immediately afterward. Hypermnesia (increasing total recall over repeated recall attempts) was obtained only in Experiment 1 when interviews occurred immediately and 24 h after the event. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Otago, Dept Psychol, Dunedin, New Zealand. NICHD, Sect Social & Emot Dev, Bethesda, MD 20892 USA. RP La Rooy, D (reprint author), Univ Otago, Dept Psychol, Dunedin, New Zealand. EM larooyd@mail.nih.gov RI la rooy, david/A-2104-2009 NR 41 TC 37 Z9 38 U1 2 U2 8 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0022-0965 J9 J EXP CHILD PSYCHOL JI J. Exp. Child Psychol. PD MAR PY 2005 VL 90 IS 3 BP 235 EP 254 DI 10.1016/j.jecp.2004.11.002 PG 20 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 900YZ UT WOS:000227251500003 PM 15707861 ER PT J AU Margulies, DH AF Margulies, DH TI Monoclonal antibodies: Producing magic bullets by somatic cell hybridization SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MOUSE C1 NIAID, Mol Biol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Margulies, DH (reprint author), NIAID, Mol Biol Sect, Immunol Lab, NIH, 10 Ctr Dr,MSC 1892,Bldg 10,Room 11N311, Bethesda, MD 20892 USA. EM dhm@nih.gov RI Margulies, David/H-7089-2013; OI Margulies, David/0000-0001-8530-7375 NR 13 TC 14 Z9 15 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 2005 VL 174 IS 5 BP 2451 EP 2452 PG 2 WC Immunology SC Immunology GA 899UX UT WOS:000227172100001 PM 15728445 ER PT J AU Wolfraim, LA Letterio, JJ AF Wolfraim, LA Letterio, JJ TI Cutting edge: p27(Kip1) deficiency reduces the require,ment for CD28-mediated costimulation in naive CD8+ but not CD4+ T lymphocytes SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL PROLIFERATION; MICE LACKING; PROMOTES APOPTOSIS; CDK INHIBITORS; EXPRESSION; HYPERPLASIA; PROGRESSION AB Cell cycle re-en try of quiescent T cells is dependent upon cyclin-dependent kinase 2. Inhibition of cyclin-dependent kinase 2 by p27(Kip1) is believed to be the principal constraint on S-phase entry in T cells. We report that deficiency for p27(Kip1) has a more pronounced effect on the expansion of murine naive CD8(+) T cells and that this disparity is due to a reduced requirement for CD28-mediaited costimulation in CD8(+) but not CD4(+) T cells lacking p27(Kip1). These data highlight a previously unappreciated difference in the way CD28 signaling is coupled to the core cell cycle machinery in these two T cell subsets. C1 NCI, Lab Cell Regulat & Carcinogenesis, NIH, Bethesda, MD 20892 USA. RP Wolfraim, LA (reprint author), TolerGen, 9610 Med Ctr Dr,Suite 230, Rockville, MD 20850 USA. EM wolfraim@tolergenics.com NR 24 TC 15 Z9 16 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 2005 VL 174 IS 5 BP 2481 EP 2484 PG 4 WC Immunology SC Immunology GA 899UX UT WOS:000227172100007 PM 15728451 ER PT J AU Tamura, T Tailor, P Yamaoka, K Kong, HJ Tsujimura, H O'Shea, JJ Singh, H Ozato, K AF Tamura, T Tailor, P Yamaoka, K Kong, HJ Tsujimura, H O'Shea, JJ Singh, H Ozato, K TI IFN regulatory factor-4 and-8 govern dendritic cell subset development and their functional diversity SO JOURNAL OF IMMUNOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; SEQUENCE BINDING-PROTEIN; MYELOID PROGENITOR CELLS; BONE-MARROW CULTURES; TRANSCRIPTION FACTOR; GENE-EXPRESSION; IN-VIVO; IMMATURE APCS; FACTOR PU.1; KAPPA-B AB Dendritic cells (DCs) are bone marrow (BM)-derived APCs central to both innate and adaptive immunity. DCs are a heterogeneous cell population composed of multiple subsets with diverse functions. The mechanism governing the generation of multiple DC subsets is, however, poorly understood. In this study we investigated the roles of closely related transcription factors, IFN regulatory factor (IRF)-4 and IRF-8, in DC development by analyzing IRF-4(-/-), IRF-8(-/-), and IRF-4(-/-)IRF-8(-/-) (double-knockout) mice. We found that IRF-4 is required for the generation of CD4(+) DCs, whereas IRF-8 is, as reported previously, essential for CD8alpha(+) DCs. Both IRFs support the development of CD4(-)CD8alpha(-) DCs. IRF-8 and, to a lesser degree, IRF-4 contribute to plasmacytoid DC (PDC) development. Thus, the two IRFs together regulate the development of all conventional DCs as well as PDCs. Consistent with these findings, IRF-4, but not IRF-8, was expressed in CD4(+) DCs, whereas only IRF-8 was expressed in CD8alpha(+) DCs. CD4(-)CD8alpha(-) DCs and PDCs expressed both IRFs. We also demonstrate in vitro that GM-CSF-mediated DC differentiation depends on IRF-4, whereas Fms-like tyrosine kinase 3 ligand-mediated differentiation depends mainly on IRF-8. Gene transfer experiments with double-knockout BM cells showed that both IRFs have an overlapping activity and stimulate a common process of DC development. Nonetheless, each IRF also possesses a distinct activity to stimulate subset-specific gene expression, leading to the generation of functionally divergent DCs. Together, IRF-4 and IRF-8 serve as a backbone of the molecular program regulating DC subset development and their functional diversity. C1 NICHHD, Lab Mol Growth Regulat, NIH, Bethesda, MD 20892 USA. NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA. Univ Chicago, Howard Hughes Med Inst, Chicago, IL 60637 USA. Univ Chicago, Dept Mol Genet & Cell Biol, Chicago, IL 60637 USA. RP Ozato, K (reprint author), NICHHD, Lab Mol Growth Regulat, NIH, Bldg 6,Room 2A05,6 Ctr Dr,MSC 2426, Bethesda, MD 20892 USA. EM ozatok@mail.nih.gov NR 59 TC 222 Z9 226 U1 0 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 2005 VL 174 IS 5 BP 2573 EP 2581 PG 9 WC Immunology SC Immunology GA 899UX UT WOS:000227172100019 PM 15728463 ER PT J AU Antony, PA Piccirillo, CA Akpinarli, A Finkelstein, SE Speiss, PJ Surman, DR Palmer, DC Chan, CC Klebanoff, CA Overwijk, WW Rosenberg, SA Restifo, NP AF Antony, PA Piccirillo, CA Akpinarli, A Finkelstein, SE Speiss, PJ Surman, DR Palmer, DC Chan, CC Klebanoff, CA Overwijk, WW Rosenberg, SA Restifo, NP TI CD8+T cell immunity against a tumor/self-antigen is augmented by CD4(+) T helper cells and hindered by naturally occurring T regulatory cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INTERLEUKIN-2 DEFICIENT MICE; IMMUNOLOGICAL SELF-TOLERANCE; CUTTING EDGE; HOMEOSTATIC PROLIFERATION; ESTABLISHED TUMORS; AUTOIMMUNE-DISEASE; ACUTE INFECTION; IN-VITRO; IL-2; IMMUNOTHERAPY AB CD4(+) T cells control the effector function, memory, and maintenance of CD8(+) T cells. Paradoxically, we found that absence of CD4(+) T cells enhanced adoptive immunotherapy of cancer when using CD8(+) T cells directed against a persisting tumor/self-Ag. However, adoptive transfer of CD4(+)CD25(-) Th cells (Th cells) with tumor/self-reactive CD8(+) T cells and vaccination into CD4(+) T cell-deficient hosts induced autoimmunity and regression of established melanoma. Transfer of CD4(+) T cells that contained a mixture of Th and CD4(+)CD25(+) T regulatory cells (T-reg cells) or T-reg cells alone prevented effective adoptive immunotherapy. Maintenance of CD8(+) T cell numbers and function was dependent on Th cells that were capable of IL-2 production because therapy failed when Th cells were derived from IL-2(-/-) mice. These findings reveal that Th cells can help break tolerance to a persisting self-Ag and treat established tumors through an IL-2-dependent mechanism, but requires simultaneous absence of naturally occurring T-reg cells to be effective. C1 NCI, Div Surg, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. NIAID, Ghost Lab, Bethesda, MD 20892 USA. NEI, Immunol Lab, NIH, Bethesda, MD USA. NIH, Howard Hughes Med Inst, Res Scholars Program, Bethesda, MD 20892 USA. McGill Univ, Montreal, PQ, Canada. Netherlands Canc Inst, Amsterdam, Netherlands. RP Antony, PA (reprint author), NCI, Div Surg, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. EM Paul_Antony@nih.gov RI Restifo, Nicholas/A-5713-2008; Klebanoff, Christopher/B-8088-2008; Palmer, Douglas/B-9454-2008; Klebanoff, Christopher/D-9581-2011; OI Palmer, Douglas/0000-0001-5018-5734; Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z01 SC003811-32, Z01 BC010763-01, Z99 CA999999] NR 62 TC 424 Z9 451 U1 0 U2 14 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 2005 VL 174 IS 5 BP 2591 EP 2601 PG 11 WC Immunology SC Immunology GA 899UX UT WOS:000227172100021 PM 15728465 ER PT J AU Wang, HY Peng, GY Guo, Z Shevach, EM Wang, RF AF Wang, HY Peng, GY Guo, Z Shevach, EM Wang, RF TI Recognition of a new ARTC1 peptide ligand uniquely expressed in tumor cells by antigen-specific CD4(+) regulatory T cells SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TRANSCRIPTION FACTOR FOXP3; CONTROLLING AUTOIMMUNITY; CD8-T-CELL MEMORY; CD4-T-CELL HELP; CANCER-PATIENTS; SELF-TOLERANCE; CUTTING EDGE; TGF-BETA; MELANOMA; IMMUNITY AB CD4(+) regulatory T (Treg) cells play an important role in the maintenance of immunological self-tolerance by suppressing immune responses against autoimmune diseases and cancer. Yet very little is known about the natural antigenic ligands that preferentially activate CD4(+) Treg cells. Here we report the establishment of tumor-specific CD4(+) Treg cell clones from tumor-infiltrating lymphocytes (TILs) of cancer patients, and the identification of an Ag recognized by Treg cells (ARTC1) gene encoding a peptide ligand recognized by tumor-specific TIL164 CD4(+) Treg cells. The mutations in a gene encoding an ARTC1 in 164mel tumor cells resulted in the translation of a gene product containing the peptide ligand recognized by CD4(+) Treg cells. ARM peptide-activated CD4(+) Treg cells suppress the physiological function (proliferation and IL-2 secretion) of melanoma-reactive T cells. Furthermore, 164mel tumor cells, but not tumor lysates pulsed on B cells, were capable of activating TIL164 CD4(+) Treg cells. These results suggest that tumor cells may uniquely present an array of peptide ligands that preferentially recruit and activate CD4(+) Treg cells in sites where tumor-specific self-peptide is expressed, leading to the induction of local and tumor-specific immune suppression. C1 Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA. Baylor Coll Med, Dept Immunol, Houston, TX 77030 USA. NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. RP Wang, RF (reprint author), Baylor Coll Med, Ctr Cell & Gene Therapy, ALKEK Bldg,N1120, Houston, TX 77030 USA. EM Rongfuw@bcm.tmc.edu FU NCI NIH HHS [CA093459, CA90327] NR 51 TC 113 Z9 121 U1 0 U2 3 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 2005 VL 174 IS 5 BP 2661 EP 2670 PG 10 WC Immunology SC Immunology GA 899UX UT WOS:000227172100029 PM 15728473 ER PT J AU Rodriguez-Galan, MC Bream, JH Farr, A Young, HA AF Rodriguez-Galan, MC Bream, JH Farr, A Young, HA TI Synergistic effect of IL-2, IL-12, and IL-18 on thymocyte apoptosis and Th1/Th2 cytokine expression SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL DEVELOPMENT; THYMIC EPITHELIAL-CELLS; INTERFERON-GAMMA; GENE-EXPRESSION; IFN-GAMMA; IMMATURE THYMOCYTES; CHEMOKINE RECEPTORS; NEGATIVE SELECTION; STROMAL CELLS; PROLIFERATION AB In the periphery, IL-18 synergistically induces the expression of the Th1 cytokine IFN-gamma in the presence of IL-12 and the Th2 cytokines IL-5 and IL-13 in the presence of IL-2. Although the expression of these cytokines has been described in the thymus, their role in thymic development and function remains uncertain. We report here that freshly isolated thymocytes from C57BL/6 and BALB/c mice stimulated in vitro with IL-2-plus-IL-18 or IL-12-plus-IL-18 produce large amounts of IFN-gamma and IL-13. Analysis of the thymic subsets, CD4(-)CD8(-) (DN), CD4(+)CD8(+), CD4(+)CD8(-), and CD4(-)CD8(-) revealed that IL-18 in combination with IL-2 or IL-12 induces IFN-gamma and IL-13 preferentially from DN cells. Moreover, DN2 and DN3 thymocytes contained more IFN-y(+) cells than cells in the later stage of maturation. Additionally, IL-18 in combination with IL-2 induces CCR4 (Th2-associated) and CCR5 (Th1-associated) gene expression. In contrast, IL-18-plus-IL-12 specifically induced CCR5 expression. The IL-2-plus-IL-18 or IL-12-plus-IL-18 effect on IFN-gamma and IL-13 expression is dependent on Stat4 and NF-kappaB but independent of Stat6, T-bet, or NFAT. Furthermore, IL-12-plus-IL-18 induces significant thymocyte apoptosis when expressed in vivo or in vitro, and this effect is exacerbated in the absence of IFN-gamma. IL-12-plus-IL-18-stimulated thymocytes can also induce IA-IE expression on cortical and medullary thymic epithelial cells in an IFN-gamma-dependent manner. Thus, the combination of IL-2, IL-12, and IL-18 can induce phenotypic and functional changes in thymocytes that may alter migration, differentiation, and cell death of immature T cells inside the thymus and potentially affect the Th1/Th2 bias in peripheral immune compartments. C1 NCI, Canc Res Ctr, Expt Immunol Lab, Frederick, MD 21702 USA. Natl Inst Musculoskeletal Dis, Mol Immunol & Inflammat Branch, Lymphocyte & Cell Biol Sect, Bethesda, MD 20892 USA. Univ Washington, Dept Biol Struct, Seattle, WA 98195 USA. Univ Washington, Dept Immunol, Seattle, WA 98195 USA. RP Young, HA (reprint author), NCI, Canc Res Ctr, Expt Immunol Lab, Bldg 560,Room 31-23, Frederick, MD 21702 USA. EM youngh@nciferf.gov RI Young, Howard/A-6350-2008 OI Young, Howard/0000-0002-3118-5111 FU NCI NIH HHS [N01-CO-12400]; NIAID NIH HHS [AI 59575, AI 24137] NR 48 TC 33 Z9 37 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 2005 VL 174 IS 5 BP 2796 EP 2804 PG 9 WC Immunology SC Immunology GA 899UX UT WOS:000227172100045 PM 15728489 ER PT J AU Anderson, CF Mendez, S Sacks, DL AF Anderson, CF Mendez, S Sacks, DL TI Nonhealing infection despite Th1 polarization produced by a strain of Leishmania major in C57BL/6 mice SO JOURNAL OF IMMUNOLOGY LA English DT Article ID AZAR DERMAL LEISHMANIASIS; REGULATORY T-CELLS; KALA-AZAR; CUTANEOUS LEISHMANIASIS; INTERFERON-GAMMA; TRANSCRIPTION FACTOR; CYTOKINE PROFILE; RESISTANT MICE; BONE-MARROW; INTERLEUKIN-10 AB Experimental Leishmania major infection in mice has been of immense interest because it was among the first models to demonstrate the importance of the Th1/Th2 balance to infection outcome in vivo. However, the Th2 polarization that promotes the development of nonhealing cutaneous lesions in BALB/c mice has failed to adequately explain the mechanisms underlying nonhealing forms of leishmaniasis in humans. We have studied a L. major strain from a patient with northealing lesions that also produces nonhealing lesions with ulcerations and high parasite burden in conventionally resistant C57BL/6 mice. Surprisingly, these mice develop a strong, polarized, and sustained Th1 response, as evidenced by high levels of IFN-gamma, produced by Leishmania-specific cells in the draining lymph node and in the ear lesion, and an absence of IL-4 or IL-13. The parasites fail to be effectively cleared despite high level induction of inducible NO synthase in the lesion, and despite their sensitivity to killing by IFN-gamma-activated macrophages in vitro. Infection of IL-10(-/-) mice, blockade of the IL-10R, or depletion of CD25(+) cells during the chronic phase promotes parasite killing, indicating that IL-10 and regulatory T cells play a role in rendering the Th1 responses ineffective at controlling infection in the skin. Mice with nonhealing primary lesions are nonetheless resistant to reinfection in the other ear. We suggest that nonhealing infections in animal models that are explained not by aberrant Th2 development, but by overactivation of homeostatic pathways designed to control inflammation, provide better models to understand northealing or reactivation forms of leishmaniasis in humans. C1 NIAID, NIH, Parasit Dis Lab, Bethesda, MD 20892 USA. RP Sacks, DL (reprint author), NIAID, NIH, Parasit Dis Lab, Bldg 4,Room 126,4 Ctr Dr MSC 0425, Bethesda, MD 20892 USA. EM dsacks@nih.gov NR 38 TC 83 Z9 83 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 2005 VL 174 IS 5 BP 2934 EP 2941 PG 8 WC Immunology SC Immunology GA 899UX UT WOS:000227172100061 PM 15728505 ER PT J AU Skokowa, J Ali, SR Felda, O Kumar, V Konrad, S Shushakova, N Schmidt, RE Piekorz, RP Nurnberg, B Spicher, K Birnbaumer, L Zwirner, J Claassens, JWC Verbeek, JS van Rooijen, N Kohl, J Gessner, JE AF Skokowa, J Ali, SR Felda, O Kumar, V Konrad, S Shushakova, N Schmidt, RE Piekorz, RP Nurnberg, B Spicher, K Birnbaumer, L Zwirner, J Claassens, JWC Verbeek, JS van Rooijen, N Kohl, J Gessner, JE TI Macrophages induce the inflammatory response in the pulmonary Arthus reaction through G alpha(i2) activation that controls C5aR and Fc receptor cooperation SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAST-CELLS; GAMMA-RIII; DEFICIENT MICE; G-PROTEINS; ADENYLYL-CYCLASE; IMMUNOGLOBULIN-G; DISEASE; COMPLEMENT; INHIBITION; EXPRESSION AB Complement and FcgammaR effector pathways are central triggers of immune inflammation; however, the exact mechanisms for their cooperation with effector cells and their nature remain elusive. In this study we show that in the lung Arthus reaction, the initial contact between immune complexes and alveolar macrophages (AM) results in plasma complement-independent C5a production that causes decreased levels of inhibitory FcgammaRIIB, increased levels of activating FcgammaRIII, and highly induced FcgammaR-mediated TNF-alpha and CXCR2 ligand production. Blockade of C5aR completely reversed such changes. Strikingly, studies of pertussis toxin inhibition show the essential role of G(1)-type G protein signaling in C5aR-mediated control of the regulatory FcgammaR system in vitro, and analysis of the various C5aR-, FcgammaR-, and G(1)-deficient mice verifies the importance of Galpha(12)-associated C5aR and the FcgammaRIII-FcgammaRIIB receptor pair in lung inflammation in vivo. Moreover, adoptive transfer experiments of C5aR- and FcgammaRIII-positive cells into C5aR- and FegammaRIII-deficient mice establish AM as responsible effector cells. AM lacking either C5aR or FcgammaRIII do not possess any such inducibility of immune complex disease, whereas reconstitution with FcgammaRIIB-negative AM results in an enhanced pathology. These data suggest that AM function as a cellular link of C5a production and C5aR activation that uses a Galpha(12)-dependent signal for modulating the two opposing FcgammaR, FcgammaRIIB and FcgammaRIII, in the initiation of the inflammatory cascade in the lung Arthus reaction. C1 Hannover Med Sch, Abt Klin Immunol, Dept Clin Immunol, D-30625 Hannover, Germany. Hannover Med Sch, Inst Med Microbiol, Hannover, Germany. Univ Dusseldorf, Dept Biochem & Mol Biol 2, Dusseldorf, Germany. Free Univ Berlin, Inst Pharmacol, Berlin, Germany. NIEHS, Lab Signal Transduct, Dept Hlth & Human Sci, NIH, Res Triangle Pk, NC 27709 USA. Univ Gottingen, Dept Immunol, D-3400 Gottingen, Germany. Leiden Univ, Dept Genet, Leiden, Netherlands. Vrije Univ Amsterdam, Dept Mol Cell Biol, Amsterdam, Netherlands. RP Gessner, JE (reprint author), Hannover Med Sch, Abt Klin Immunol, Dept Clin Immunol, D-30625 Hannover, Germany. EM gessner.johannes@mh-hannover.de RI Ali, Syed/M-7418-2013; ali, syed/J-6124-2014; Koehl, Joerg/C-8531-2011 OI Koehl, Joerg/0000-0003-1121-3178 NR 47 TC 79 Z9 82 U1 0 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAR 1 PY 2005 VL 174 IS 5 BP 3041 EP 3050 PG 10 WC Immunology SC Immunology GA 899UX UT WOS:000227172100074 PM 15728518 ER PT J AU Antony, PA Restifo, NP AF Antony, PA Restifo, NP TI CD4(+)CD25(+) T regulatory cells, immunotherapy of cancer, and interleukin-2 SO JOURNAL OF IMMUNOTHERAPY LA English DT Review DE interleukin-2; T regulatory cell; T helper cell; immunetherapy; melanoma; autoimmunity; IL-2 receptor; interleukin-15 ID IMMUNOLOGICALLY MEDIATED REGRESSION; TUMOR-INFILTRATING LYMPHOCYTES; HUMAN DENDRITIC CELLS; GROWTH-FACTOR BETA-1; CUTTING EDGE; SELF-TOLERANCE; ADOPTIVE IMMUNOTHERAPY; SUPPRESSOR FUNCTION; ESTABLISHED TUMOR; IN-VIVO AB CD4(+)CD25(+) T regulatory (T-reg) cells control immunologic tolerance to self-antigens and play a role in suppressing antitumor immune responses, but the mechanism of suppression in vivo remains uncertain. Recently, signaling through the high-affinity interleukin-2 (IL-2) receptor has been shown to be critical for T-reg cell differentiation and survival in vivo. Mice deficient in IL-2 or its receptor (CD25 or CD122) or deficient in downstream signaling molecules, including JAK-3 and STAT-5, do not develop a stable population of T,,g cells and subsequently acquire lymphoproliferative disease and autoimmunity. in vitro, IL-2 is required to expand T-reg cells and to induce their suppressive characteristics. Conversely, IL-2based regimens can activate Cellular antitumor immunity and are the mainstay of immunotherapies directed against melanoma and kidney cancers. Given the seemingly disparate effects of IL-2, the authors discuss the possibility that IL-2 may not be the optimal T-cell growth factor in vivo, but rather an inducer of self-tolerance. The authors propose that other gamma(c)-signaling cytokines, including IL-15, may be alternative choices for the immunotherapy of cancer. genotypes is not cell autonomous but is due to a deficiency in naturally occurring T regulatory (T-reg) cells.(3) It is well established that naturally occurring T-reg Cells control immunologic tolerance to self-antigens and represent 5% to 10% of the CD4(+) T cells in rodents and 5% to 15% in humans.(4-9) T-reg cells constitutively express high levels of the cell surface molecules CD25 (IL-2Ralpha), GITR (glucocorticoidinduced TNF receptor), and CTLA-4. They also express a unique intracellular protein, Foxp3, which acts as a master regulator gene for inducing a T-reg phenotype and lineage. T-reg cells are either abnormally regulated or nonexistent in mice with genotypes that are Il2(-/-), 112ralpha(-/-), 112rbeta(-/-), stat5(-/-), jcik3(-/-) andfbxp3(-/-), which all develop some form of fatal lymphoproliferative disease, suggesting a critical role for IL-2 signaling and Foxp3 in the development of self-tolerance mediated through T-reg cells. (10-13) Interestingly, IL-2 signaling is not related to the expression of Foxp3 in T-reg cells,(14) but Foxp3 can negatively regulate the Il2 gene by blocking an NFAT (nuclear factor of activated T cells) binding site in the IL-2 promoter.(15),(16). C1 NCI, NIH, Ctr Canc Res, Surg Branch,Mark O Hatfield Clin Res Ctr, Bethesda, MD 20892 USA. RP Antony, PA (reprint author), NCI, NIH, Ctr Canc Res, Surg Branch,Mark O Hatfield Clin Res Ctr, 10 Ctr Dr, Bethesda, MD 20892 USA. EM Paul_Antony@nih.gov RI Restifo, Nicholas/A-5713-2008; OI Restifo, Nicholas P./0000-0003-4229-4580 FU Intramural NIH HHS [Z99 CA999999, Z01 BC010763-01] NR 105 TC 129 Z9 151 U1 1 U2 14 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 1524-9557 J9 J IMMUNOTHER JI J. Immunother. PD MAR-APR PY 2005 VL 28 IS 2 BP 120 EP 128 DI 10.1097/01.cji.0000155049.26787.45 PG 9 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA 902YG UT WOS:000227392000001 PM 15725955 ER PT J AU Graham, BS Mascola, JR AF Graham, BS Mascola, JR TI Lessons from failure - Preparing for future HIV-1 vaccine efficacy trials SO JOURNAL OF INFECTIOUS DISEASES LA English DT Editorial Material C1 NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA. RP Graham, BS (reprint author), NIAID, Vaccine Res Ctr, NIH, Bldg 40,Room 2502, Bethesda, MD 20892 USA. EM bgraham@mail.nih.gov NR 5 TC 38 Z9 41 U1 0 U2 4 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAR 1 PY 2005 VL 191 IS 5 BP 647 EP 649 DI 10.1086/428406 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 895LA UT WOS:000226862400001 PM 15688276 ER PT J AU Gilbert, PB Peterson, ML Follmann, D Hudgens, MG Francis, DP Gurwith, M Heyward, WL Jobes, DV Popovic, V Self, SG Sinangil, F Burke, D Berman, PW AF Gilbert, PB Peterson, ML Follmann, D Hudgens, MG Francis, DP Gurwith, M Heyward, WL Jobes, DV Popovic, V Self, SG Sinangil, F Burke, D Berman, PW TI Correlation between immunologic responses to a recombinant glycoprotein 120 vaccine and incidence of HIV-1 infection in a phase 3 HIV-1 preventive vaccine trial SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT AIDS Vaccine 2003 Conference CY SEP 18-21, 2003 CL New York, NY ID ANTIBODY-DEPENDENT ENHANCEMENT; ENVELOPE GLYCOPROTEIN; TYPE-1 INFECTION; VIRUS; DISEASE; IMMUNOGENICITY; PROSTITUTES; NAIROBI; SAFETY; RISK AB Background. An objective of the first efficacy trial of a candidate vaccine containing recombinant human immunodeficiency virus (HIV) type 1 envelope glycoprotein 120 (rgp120) antigens was to assess correlations between antibody responses to rgp120 and the incidence of HIV-1 infection. Methods. Within the randomized trial (for vaccinees, n = 3598; for placebo recipients, n = 1805), binding and neutralizing antibody responses to rgp120 were quantitated. A case- cohort design was used to study correlations between antibody levels and HIV-1 incidence. Results. Peak antibody levels were significantly inversely correlated with HIV-1 incidence. The relative risk (RR) of infection was 0.63 (95% confidence interval, 0.45-0.89) per log(10) higher neutralization titer against HIV-1 MN, and the RRs of infection for second-, third-, and fourth-quartile responses of antibody blocking of gp120 binding to soluble CD4 versus first-quartile responses (the lowest responses) were 0.35, 0.28, and 0.22, respectively. Conclusions. Despite inducing a complex, robust immune response, the vaccine was unable to reduce the incidence of HIV-1. Two interpretations of the correlative results are that the levels of antibodies (i) caused both an increased (low responders) and decreased (high responders) risk of HIV-1 acquisition or (ii) represented a correlate of susceptibility to HIV-1 but had no causal effect on susceptibility. Although the data cannot definitively discriminate between these 2 explanations, (ii) appears to be more likely. C1 VaxGen, Brisbane, CA 94005 USA. Global Solut Infect Dis, Brisbane, CA USA. Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA. NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA. Johns Hopkins Bloomberg Univ Sch Publ Hlth, Baltimore, MD USA. Univ N Carolina, Dept Biostat, Chapel Hill, NC USA. RP Gurwith, M (reprint author), VaxGen, 1000 Marina Blvd, Brisbane, CA 94005 USA. EM mgurwith@vaxgen.com OI /0000-0002-5704-8094 NR 38 TC 220 Z9 222 U1 0 U2 8 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAR 1 PY 2005 VL 191 IS 5 BP 666 EP 677 DI 10.1086/428405 PG 12 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 895LA UT WOS:000226862400004 PM 15688279 ER PT J AU Glesby, MJ Bassett, R Alston-Smith, B Fichtenbaum, C Jacobson, EL Brass, C Owens, S Sulkowski, M Race, EM Sherman, KE AF Glesby, MJ Bassett, R Alston-Smith, B Fichtenbaum, C Jacobson, EL Brass, C Owens, S Sulkowski, M Race, EM Sherman, KE CA AIDS Clin Trials Grp A5088 TI Pilot study of low-dose interleukin-2, pegylated interferon-alpha 2b, and ribavirin for the treatment of hepatitis C virus infection in patients with HIV infection SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 11th Conference on Retroviruses and Opportunistic Infections CY FEB 08-11, 2004 CL San Francisco, CA ID HUMAN-IMMUNODEFICIENCY-VIRUS; ALPHA-2A PLUS RIBAVIRIN; RANDOMIZED CONTROLLED-TRIAL; SUBCUTANEOUS INTERLEUKIN-2; RECOMBINANT INTERLEUKIN-2; ANTIRETROVIRAL THERAPY; IMMUNE FUNCTION; CLINICAL-TRIAL; VIRAL LOAD; RNA LEVELS AB Background. Patients infected with hepatitis C virus (HCV) and human immunodeficiency virus have a diminished HCV virologic response to standard interferon (IFN)-based therapies. We explored the strategy of initial immunostimulatory therapy with interleukin (IL)-2, followed by the addition of specific anti-HCV therapy, as a possible synergistic approach to treatment. Methods. Coinfected subjects (n = 23) with CD4 cell counts 1300 cells/muL received low-dose IL-2 daily for 12 weeks, followed by pegylated IFN-alpha2b and ribavirin for an additional 48 weeks. The primary end point was permanent discontinuation of treatment before week 24 due to toxicity or intolerance. Results. Six subjects (26.1%) discontinued treatment before week 24, and 11 (47.8%) discontinued treatment before week 60. Overall, 4 subjects discontinued because of adverse events. Four of 23 (17%; 95% confidence interval [CI], 5%-39%) had sustained virologic responses. Of 17 subjects with increased levels of alanine aminotransferase at baseline, 13 had follow-up measurements at week 60, of which 6 (46%) were normal. Conclusions. Low-dose IL-2 plus PEG-IFN and ribavirin was associated with a high discontinuation rate. Although the study was not powered for efficacy, CIs surrounding the treatment response rate suggest that this strategy should not be pursued in larger trials. C1 Cornell Univ, Weill Med Coll, New York, NY 10021 USA. Frontier Sci & Technol Res Fdn Inc, Buffalo, NY USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Univ Cincinnati, Cincinnati, OH USA. Schering Plough Corp, Res Inst, Kenilworth, NJ 07033 USA. NIAID, Div AIDS, NIH, Bethesda, MD 20892 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Univ Texas, SW Med Ctr, Dallas, TX USA. RP Glesby, MJ (reprint author), Cornell Univ, Weill Med Coll, 525 E 69th St,Box 566, New York, NY 10021 USA. EM mag2005@med.cornell.edu NR 28 TC 9 Z9 10 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAR 1 PY 2005 VL 191 IS 5 BP 686 EP 693 DI 10.1086/427812 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 895LA UT WOS:000226862400006 PM 15688281 ER PT J AU Durbin, AP Whitehead, SS McArthur, J Perreault, JR Blaney, JE Thumar, B Murphy, BR Karron, RA AF Durbin, AP Whitehead, SS McArthur, J Perreault, JR Blaney, JE Thumar, B Murphy, BR Karron, RA TI rDEN4 Delta 30, a live attenuated dengue virus type 4 vaccine candidate, is safe, immunogenic, and highly infectious in healthy adult volunteers SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Society-of-Tropical-Medicine-and-Hygiene CY DEC 03-06, 2003 CL Philadelphia, PA SP Amer Soc Trop Med Hygiene ID RHESUS-MONKEYS; BLOOD MONOCYTES; CELLS; SUBSTITUTION; LEUKOCYTES; MONOVALENT; MOSQUITOS; DELETION; PATTERN; PROTEIN AB Background. The live attenuated dengue virus type 4 (DEN-4) vaccine candidate virus rDEN4Delta30 was previously found to be safe and immunogenic at a dose of 10(5) plaque-forming units (pfu). Methods. In a follow-up placebo-controlled phase 2 clinical trial, rDEN4Delta30 was administered as a single inoculation to 3 separate dose cohorts (10(3) pfu, 10(2) pfu, or 10(1) pfu), for further evaluation. Each dose cohort consisted of 20 vaccinees and 4 placebo recipients. Volunteers were monitored closely for adverse events, and serum was collected on study days 28 and 42 for determination of neutralizing antibody titer. Results. The vaccine was well tolerated at all doses studied. The most common adverse events observed were a transient asymptomatic rash in >50% of vaccinees and a mild neutropenia in similar to20% of vaccinees. No vaccinee developed a dengue-like illness. The vaccine was highly infectious and immunogenic, with 95%-100% of vaccinees in each dose cohort developing a greater than or equal to4-fold increase in titers of serum neutralizing antibodies against DEN-4. Conclusions. The rDEN4Delta30 vaccine is safe and induced an antibody response that was broadly neutralizing against genotypically diverse DEN-4 viruses. It is a promising vaccine candidate for inclusion in a tetravalent dengue vaccine formulation. C1 Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Ctr Immunizat Res, Baltimore, MD 21205 USA. NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA. RP Durbin, AP (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Ctr Immunizat Res, Baltimore, MD 21205 USA. EM adurbin@jhsph.edu FU PHS HHS [N01A115444] NR 46 TC 87 Z9 89 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD MAR 1 PY 2005 VL 191 IS 5 BP 710 EP 718 DI 10.1086/427780 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 895LA UT WOS:000226862400009 PM 15688284 ER PT J AU Kaczmarek, P Jezowska-Bojczuk, M Bal, W Kasprzak, KS AF Kaczmarek, P Jezowska-Bojczuk, M Bal, W Kasprzak, KS TI Determination of the stability constants and oxidation susceptibility of nickel(II) complexes with 2 '-de oxyguano sine 5 '-triphosphate and L-histidine SO JOURNAL OF INORGANIC BIOCHEMISTRY LA English DT Article DE dGTP; 8-Oxo-dGTP; Ni(II); binary complexes; ternary complexes; reactive oxygen species ID METAL-BINDING SEQUENCE; ACID-BASE PROPERTIES; TERNARY COMPLEXES; AQUEOUS-SOLUTION; 2'-DEOXYGUANOSINE 5'-MONOPHOSPHATE; ISOMERIC EQUILIBRIA; DNA-SYNTHESIS; INDUCED CARCINOGENESIS; MUTAGENIC SUBSTRATE; ION COORDINATION AB The formation of binary Ni(II) complexes with 2'-deoxyguanosine 5'-triphosphate (dGTP (1), L) as well as ternary complexes thereof with L-histidine (His, A) was studied with the use of potentiometry and electronic absorption spectroscopy. In the binary and ternary systems, the complexes with stoichiometries NiH(2)L(-), NiHL(2-), NiL(3-) and NiHLA'-, NiH(2)LA(2-), NiLA(4-) respectively, were detected. The ternary complexes are very stable at pH 7.4 and thus may constitute biologically relevant Ni(II) carriers in the cell. In the presence of hydrogen peroxide, the binary and ternary systems both generate hydroxyl radical-like species and undergo dGTP degradation with the formation of the 8-oxo-dGTP intermediate. The latter, along with dGTP complexation and degradation, may lead to mutagenesis and carcinogenesis due to base-mispairing properties of 8-oxoguanine and the disturbance in the physiological balance among the four canonical triphosphodeoxynucleotide substrates for DNA synthesis. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Wroclaw, Fac Chem, PL-50383 Wroclaw, Poland. Polish Acad Sci, Inst Biochem & Biophys, PL-02106 Warsaw, Poland. NCI, Frederick Canc Res & Dev Ctr, Canc Res Ctr, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA. RP Jezowska-Bojczuk, M (reprint author), Univ Wroclaw, Fac Chem, F Joliot Curie 14, PL-50383 Wroclaw, Poland. EM mjb@wchuwr.chem.uni.wroc.pl NR 63 TC 17 Z9 17 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0162-0134 J9 J INORG BIOCHEM JI J. Inorg. Biochem. PD MAR PY 2005 VL 99 IS 3 BP 737 EP 746 DI 10.1016/j.jinorgbio.2004.12.006 PG 10 WC Biochemistry & Molecular Biology; Chemistry, Inorganic & Nuclear SC Biochemistry & Molecular Biology; Chemistry GA 902RT UT WOS:000227374900008 PM 15708794 ER PT J AU Klein, HG AF Klein, HG TI Pathogen inactivation technology: cleansing the blood supply SO JOURNAL OF INTERNAL MEDICINE LA English DT Review DE blood safety; pathogen reduction; transfusion ID VERSUS-HOST DISEASE; FACTOR-VIII CONCENTRATE; FRESH-FROZEN PLASMA; NON-B HEPATITIS; HUMAN-IMMUNODEFICIENCY-VIRUS; WEST-NILE VIRUS; PEN110 CHEMISTRY; PHOTOCHEMICAL INACTIVATION; INFECTIOUS PATHOGENS; INACTINE PEN110 AB The calculated residual infectious risk of HIV, hepatitis B virus (HBV) and hepatitis C virus (HCV) from blood transfusion is extremely low. However, the risk of bacterial contamination remains and a variety of other agents including emerging viruses, protozoa and tick-borne agents threaten blood supplies and undermine public confidence in blood safety. Traditional methods of donor screening and testing have limited ability to further reduce disease transmission and cannot prevent an emerging infectious agent from entering the blood supply. Pathogen inactivation technologies have all but eliminated the infectious risks of plasma-derived protein fractions, but as yet no technique has proved sufficiently safe and effective for traditional blood components. Half-way technologies can reduce the risk of pathogen transmission from fresh frozen plasma and cryoprecipitate. Traditional methods of mechanical removal such as washing and filtration have limited success in reducing the risk of cell-associated agents, but methods aimed at sterilizing blood have either proved toxic to the cells or to the recipients of blood components. Several promising methods that target pathogen nucleic acid have recently entered clinical testing. C1 NIH, Dept Transfus Med, Off Chief, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA. Johns Hopkins Sch Med, Dept Pathol & Med, Baltimore, MD USA. RP Klein, HG (reprint author), NIH, Dept Transfus Med, Off Chief, Warren G Magnuson Clin Ctr, 10 Ctr Dr,MSC-1184,Bldg 10,Room 1C711, Bethesda, MD 20892 USA. EM hklein@cc.nih.gov NR 79 TC 62 Z9 74 U1 1 U2 2 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0954-6820 J9 J INTERN MED JI J. Intern. Med. PD MAR PY 2005 VL 257 IS 3 BP 224 EP 237 DI 10.1111/j.1365-2796.2005.01451.x PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA 905GL UT WOS:000227556500002 PM 15715679 ER PT J AU Goldstein, DS Moak, J Eldadah, B AF Goldstein, DS Moak, J Eldadah, B TI Distinctive patterns of central and peripheral catecholamine lesions in primary chronic autonomic failure. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Joint Annual Meeting of the Central-Society-for-Clinical-Research/Midwestern American-Federation-for-Medical-Research CY APR, 2005 CL Chicago, IL SP Cent Soc Clin Res, Midwestern Amer Federat Med Res C1 NINDS, Clin Neurocardiol Sect, NIH, Bethesda, MD USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD MAR PY 2005 VL 53 IS 2 BP S397 EP S398 PG 2 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 909FU UT WOS:000227846600152 ER PT J AU Mirza, NM Rhee, L Carreiro, FP Palmer, M Davis, D Yanovski, L AF Mirza, NM Rhee, L Carreiro, FP Palmer, M Davis, D Yanovski, L TI Risk of type 2 diabetes and metabolic syndrome among Latino children and adolescents presenting to a weight loss program. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Joint Annual Meeting of the Central-Society-for-Clinical-Research/Midwestern American-Federation-for-Medical-Research CY APR, 2005 CL Chicago, IL SP Cent Soc Clin Res, Midwestern Amer Federat Med Res C1 Childrens Natl Med Ctr, Washington, DC 20010 USA. NIH, Unti Growth & Obes, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD MAR PY 2005 VL 53 IS 2 BP S399 EP S399 PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 909FU UT WOS:000227846600163 ER PT J AU Francis, DJ Fletcher, JM Stuebing, KK Lyon, GR Shaywitz, BA Shaywitz, SE AF Francis, DJ Fletcher, JM Stuebing, KK Lyon, GR Shaywitz, BA Shaywitz, SE TI Psychometric approaches to the identification of LD: IQ and achievement scores are not sufficient SO JOURNAL OF LEARNING DISABILITIES LA English DT Article ID LEARNING-DISABILITIES; READING-DISABILITY; SEVERE DISCREPANCY; DYSLEXIA; DEFINITIONS; RETARDATION; CHILDREN; PREVALENCE; PROFILE; ISSUES AB Simulated data were used to demonstrate that groups formed by imposing cut-points based on either discrepancy or low-achievement definitions of learning disabilities (LD) are unstable over time. Similar problems were demonstrated in longitudinal data from the Connecticut Longitudinal Study, where 39% of the children designated as having LD in Grade 3 changed group placement with repeated testing in Grade 5. These results show that the practice of subdividing a normal distribution with arbitrary cut-points leads to instability in group membership. Approaches to the identification of children as having LID based solely on individual test scores not linked to specific behavioral criteria lead to invalid decisions about individual children. Low-achievement definitions are not a viable alternative to IQ-discrepancy definitions in the absence of other criteria, such as the traditional exclusions and response to quality intervention. If we accept the premise of multiple classes of low achievers, then we must develop identification systems that are valid and abandon systems whose only merits are their historical precedence and convenience. C1 Univ Houston, Texas Inst Measurement Evaluat & Stat, Chair Psychol & Director, Houston, TX 77204 USA. Univ Texas, Ctr Hlth Sci, Houston, TX USA. NICHHD, Child Dev & Behav Branch, NIH, Bethesda, MD USA. Yale Univ, Ctr Study Learning & Attent, New Haven, CT 06520 USA. RP Francis, DJ (reprint author), Univ Houston, Texas Inst Measurement Evaluat & Stat, Chair Psychol & Director, 100 TLCC Annex, Houston, TX 77204 USA. EM dfrancis@uh.edu OI Francis, David/0000-0003-3944-3274 FU NICHD NIH HHS [HD21888, HD28172, HD30995, P50 HD 25802, R01 HD028172] NR 50 TC 104 Z9 105 U1 3 U2 8 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0022-2194 J9 J LEARN DISABIL-US JI J. Learn. Disabil. PD MAR-APR PY 2005 VL 38 IS 2 BP 98 EP 108 DI 10.1177/00222194050380020101 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 904EC UT WOS:000227477900001 PM 15813593 ER PT J AU Stark, KD Beblo, S Murthy, M Buda-Abela, M Janisse, J Rockett, H Whitty, JE Martier, SS Sokol, RJ Hannigan, JH Salem, N AF Stark, KD Beblo, S Murthy, M Buda-Abela, M Janisse, J Rockett, H Whitty, JE Martier, SS Sokol, RJ Hannigan, JH Salem, N TI Comparison of bloodstream fatty acid composition from African-American women at gestation, delivery, and postpartum SO JOURNAL OF LIPID RESEARCH LA English DT Article DE 3 fatty acids; omega-3; docosahexaenoic acid; arachidonic acid; pregnancy; dietary intake; maternal nutrition ID HORMONE REPLACEMENT THERAPY; DOCOSAHEXAENOIC ACID; NORMAL-PREGNANCY; TERM INFANTS; RISK-FACTOR; ARACHIDONIC-ACID; MATERNAL PLASMA; VISUAL-ACUITY; KOREAN WOMEN; DIET AB Our aim was to examine the docosahexaenoic acid (DHA; 22: 6n- 3) status of pregnant African-American women reporting to the antenatal clinic at Wayne State University in a longitudinal study design. Fatty acid compositions of plasma and erythrocyte total lipid extracts were determined and food frequency surveys were administered at 24 weeks of gestation, delivery, and 3 months postpartum for participants ( n = 157). DHA ( mean +/- SD) in the estimated total circulating plasma was similar at gestation ( 384 +/- 162 mg) and delivery ( 372 +/- 155 mg) but was significantly lower at 3 months postpartum ( 178 +/- 81 mg). The relative weight percentage of DHA and docosapentaenoic acid n- 6 ( DPAn- 6; 22: 5n- 6) decreased postpartum, whereas their respective metabolic precursors, eicosapentaenoic acid ( EPA; 20: 5n- 3) and arachidonic acid ( AA; 20: 4n- 6), increased. Similar results were found in erythrocytes. Dietary intake of DHA throughout the study was estimated at 68 +/- 75 mg/day. The relative amounts of circulating DHA and DPAn- 6 were increased during pregnancy compared with 3 months postpartum, possibly via increased synthesis from EPA and AA. The low dietary intake and blood levels of DHA in this population compared with others may not support optimal fetal DHA accretion and subsequent neural development. C1 NIAAA, Lab Membrane Biochem & Biophys, Div Intramural Clin & Biol Res, NIH, Rockville, MD 20852 USA. Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA. Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA. Wayne State Univ, Dept Psychol, Detroit, MI 48202 USA. RP Salem, N (reprint author), NIAAA, Lab Membrane Biochem & Biophys, Div Intramural Clin & Biol Res, NIH, Rockville, MD 20852 USA. EM nsalem@niaaa.nih.gov RI Stark, Ken/I-1347-2016 OI Stark, Ken/0000-0001-7828-4072 FU NIAAA NIH HHS [N01-AA-83019] NR 69 TC 63 Z9 64 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0022-2275 J9 J LIPID RES JI J. Lipid Res. PD MAR PY 2005 VL 46 IS 3 BP 516 EP 525 DI 10.1194/jlr.M400394-JLR200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 903UK UT WOS:000227450900015 PM 15604519 ER PT J AU Kim, JW Simmer, JP Hart, TC Hart, PS Ramaswami, MD Bartlett, JD Hu, JCC AF Kim, JW Simmer, JP Hart, TC Hart, PS Ramaswami, MD Bartlett, JD Hu, JCC TI MMP-20 mutation in autosomal recessive pigmented hypomaturation amelogenesis imperfecta SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID MATRIX METALLOPROTEINASE-20; MOUSE ENAMELYSIN; EXPRESSION; NOMENCLATURE; GENE; PROTEINASES; HYDROLYSIS; ACTIVATION; MATURATION; CLONING C1 Seoul Natl Univ, Coll Dent, Dept Pediat Dent, Seoul, South Korea. Seoul Natl Univ, Dent Res Inst, Seoul, South Korea. Univ Michigan, Sch Dent, Dept Biol & Mat Sci, Ann Arbor, MI 48109 USA. NIDCR, NIH, Bethesda, MD USA. Forsyth Inst, Harvard Forsyth Dept Cytokine Biol, Boston, MA USA. Forsyth Inst, Harvard Forsyth Dept Cytokine Biol, Boston, MA USA. Univ Michigan, Sch Dent, Dept Pediat Dent, Ann Arbor, MI 48109 USA. RP Hu, JCC (reprint author), Univ Michigan, Dent Res Lab, Dept Orthodont & Pediat Dent, 1210 Eisenhower Pl, Ann Arbor, MI 48108 USA. EM janhu@umich.edu RI KIM, JUNG-WOOK/G-8992-2012 FU NIDCR NIH HHS [DE11301, DE12769, DE15846, R01 DE014084] NR 37 TC 131 Z9 135 U1 0 U2 4 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD MAR PY 2005 VL 42 IS 3 BP 271 EP 275 DI 10.1136/jmg.2004.024505 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 904BO UT WOS:000227470300013 PM 15744043 ER PT J AU Feng, GH Sharp, CC Zhou, QF Pang, W Kim, ES Shung, KK AF Feng, GH Sharp, CC Zhou, QF Pang, W Kim, ES Shung, KK TI Fabrication of MEMS ZnO domeshaped-diaphragm transducers for high-frequency ultrasonic imaging SO JOURNAL OF MICROMECHANICS AND MICROENGINEERING LA English DT Article AB This paper presents the microfabrication technique for a dome-shaped-diaphragm transducer (DSDT) for 200 MHz cellular microstructure imaging. The DSDT uses piezoelectric ZnO film to generate acoustic waves, and is fabricated on a silicon substrate. The fabricated DSDTs have been tested with a pulse-echo method using a quartz target, and shown to produce an echo signal at 210 MHz with 20% bandwidth. The DSDT fabrication uses spherical balls to precisely shape wax molds, onto which parylene is deposited as a support layer for the DSDT. The wax molds are removed by toluene to release the parylene dome diaphragms. Piezoelectric ZnO film is sputter deposited on the parylene dome diaphragm. E-Solder silver epoxy is placed and cured on the back surface to function both as an acoustic backing and as structural support. Quarter wavelength thick parylene is deposited on the front side of the wafer for acoustic matching. The fabrication technique for the DSDTs is meant for low-cost mass production of the devices for high-frequency biomedical imaging. Moreover, the technique allows the precise control of the radius and curvature of the dome-shaped diaphragm through adjusting the size of the front-to-backside thru holes using different radii of the spherical balls. C1 Univ So Calif, Dept Elect Engn, Los Angeles, CA 90089 USA. Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA. Univ So Calif, NIH, Transducer Resource Ctr, Los Angeles, CA 90089 USA. RP Feng, GH (reprint author), Univ So Calif, Dept Elect Engn, Los Angeles, CA 90089 USA. EM guohuafe@usc.edu NR 11 TC 24 Z9 24 U1 1 U2 10 PU IOP PUBLISHING LTD PI BRISTOL PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND SN 0960-1317 J9 J MICROMECH MICROENG JI J. Micromech. Microeng. PD MAR PY 2005 VL 15 IS 3 BP 586 EP 590 DI 10.1088/0960-1317/15/3/021 PG 5 WC Engineering, Electrical & Electronic; Nanoscience & Nanotechnology; Instruments & Instrumentation; Physics, Applied SC Engineering; Science & Technology - Other Topics; Instruments & Instrumentation; Physics GA 923NQ UT WOS:000228917000021 ER PT J AU Jobsis, PD Combs, CA Balaban, RS AF Jobsis, PD Combs, CA Balaban, RS TI Two-photon excitation fluorescence pH detection using 2,3-dicyanohydroquinone: a spectral ratiometric approach SO JOURNAL OF MICROSCOPY-OXFORD LA English DT Article DE cellular pH; dicyanohydroquinone; dihydroxyphthalonitrile; spectral calibration; spectral imaging; two-photon AB The use of 2,3-dicyanohydroquinone (DCHQ) as an emission ratiometric probe of pH in vitro and in fibroblast cells was evaluated using two-photon excitation fluorescence microscopy (TPEFM). In addition, methods for spectrally calibrating the Zeiss LSM510 META spectroscopy system for TPEFM were also developed. The emissions of both the acid and base forms of DCHQ were detectable when using an 800-nm excitation in TPEFM, thereby allowing ratiometric determination of pH. These data suggest that, in contrast to most other emission ratiometric probes, both acid and base forms of DCHQ have similar two-photon cross-sectional areas at 800 nm. Acid (maximum at similar to457 nm) and base (maximum at similar to489 nm) DCHQ TPEFM emission spectra were similar to previously reported one-photon excitation emission spectra. Calibration curves for pH were successfully constructed using the ratio of DCHQ emission difference maxima at 460 nm and 512 nm in vitro and in cells. To our knowledge, DCHQ is currently the only effective emission ratiometric pH indicator for two-photon microscopy and may serve as a useful starting point for the development of other TPEFM ratiometric dyes for quantitative measurement of other cell parameters such as Ca2+, Mg2+ or Na+. C1 NHLBI, Cardiac Energet Lab, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. NHLBI, Light Microscopy Core, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Jobsis, PD (reprint author), NHLBI, Cardiac Energet Lab, NIH, Dept Hlth & Human Serv, Bldg 10, Bethesda, MD 20892 USA. EM Jobsisp@nhlbi.nih.gov NR 7 TC 9 Z9 9 U1 1 U2 8 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0022-2720 J9 J MICROSC-OXFORD JI J. Microsc.-Oxf. PD MAR PY 2005 VL 217 BP 260 EP 264 DI 10.1111/j.1365-2818.2005.01442.x PG 5 WC Microscopy SC Microscopy GA 899WF UT WOS:000227175800011 PM 15725129 ER PT J AU Tang, JH Naitow, H Gardner, NA Kolesar, A Tang, L Wickner, RB Johnson, JE AF Tang, JH Naitow, H Gardner, NA Kolesar, A Tang, L Wickner, RB Johnson, JE TI The structural basis of recognition and removal of cellular mRNA 7-methyl G 'caps' by a viral capsid protein: a unique viral response to host defense SO JOURNAL OF MOLECULAR RECOGNITION LA English DT Article DE dsRNA virus structure; RNA-protein interaction; mRNA decapping; L-A virus; cap binding protein; quasiequivalence ID DOUBLE-STRANDED-RNA; POL FUSION PROTEIN; L-A-VIRUS; RICE-DWARF-VIRUS; SACCHAROMYCES-CEREVISIAE; ELECTRON CRYOMICROSCOPY; ANGSTROM RESOLUTION; ANTIVIRAL SYSTEM; DECAPPING ENZYME; ATOMIC-STRUCTURE AB The single segment, double-stranded RNA genome of the L-A virus (L-A) of yeast encodes two proteins: the major coat protein Gag (76 kDa) and the Gag-Poll fusion protein (180 kDa). The icosahedral L-A capsid is formed by 120 copies of Gag and has architecture similar to that seen in the reovirus, blue tongue virus and rice dwarf virus inner protein shells. Gag chemically removes the m(7)GMP caps from host cellular mRNAs. Previously we identified a trench on the outer surface of Gag that included His154, to which caps are covalently attached. Here we report the refined L-A coordinates at 3.4 angstrom resolution with additional structural features and the structure of L-A with bound m(7)GDP at 6.5 angstrom resolution, which shows the conformational change of the virus upon ligand binding. Based on site-directed mutations, residues in or adjacent to the trench that are essential (or dispensable) for the decapping reaction are described here. Along with His154, the reaction requires a cluster of positive charge adjoining the trench and residues Tyr 452, Tyr150 and either Tyr or Phe at position 538. A tentative mechanism for decapping is proposed. Copyright (c) 2004 John Wiley T Sons, Ltd. C1 Scripps Res Inst, Dept Mol Biol, La Jolla, CA 92037 USA. NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA. RP Johnson, JE (reprint author), Scripps Res Inst, Dept Mol Biol, 10550 N Torrey Pines Rd, La Jolla, CA 92037 USA. EM jack@scripps.edu FU NCRR NIH HHS [RR-07707]; NIGMS NIH HHS [GM54076] NR 55 TC 19 Z9 21 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0952-3499 J9 J MOL RECOGNIT JI J. Mol. Recognit. PD MAR-APR PY 2005 VL 18 IS 2 BP 158 EP 168 DI 10.1002/jmr.724 PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 907GQ UT WOS:000227704400004 PM 15597333 ER PT J AU Deng, JZ Newman, DJ Hecht, SM AF Deng, JZ Newman, DJ Hecht, SM TI Umbelactonyl cinnamate derivatives from Crypteronia paniculata that mediate DNA strand scission SO JOURNAL OF NATURAL PRODUCTS LA English DT Article ID CLEAVE DNA; BLEOMYCIN; 5-ALKYLRESORCINOLS AB As part of an initiative to discover functional natural product analogues of bleomycin guided by the use of the COMPARE algorithm, a CH2Cl2-MeOH extract prepared from Crypteronia paniculata was found to exhibit relaxation of supercoiled pSP64 DNA in the presence of Cu2+. Bioassay-guided fractionation employing a DNA strand scission assay resulted in the isolation of three novel DNA cleavage agents. Their structures were elucidated as umbelactonyl cinnamate derivatives 1-3 through their NMR and MS spectral data analyses. This is the first example of the isolation and structural characterization of naturally occurring umbelactonyl cinnamate derivatives. Compound 1 exhibited strong Cu2+-dependent relaxation of supercoiled pSP64 DNA, while compounds 2 and 3 had only weak DNA cleavage activity. C1 Univ Virginia, Dept Chem, Charlottesville, VA 22901 USA. Univ Virginia, Dept Biol, Charlottesville, VA 22901 USA. Frederick Canc Res & Dev Ctr, Nat Prod Branch, Natl Canc Inst, Ft Detrick, MD 21702 USA. RP Hecht, SM (reprint author), Univ Virginia, Dept Chem, Charlottesville, VA 22901 USA. EM sidhecht@virginia.edu FU NCI NIH HHS [CA50771] NR 22 TC 5 Z9 5 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0163-3864 J9 J NAT PROD JI J. Nat. Prod. PD MAR PY 2005 VL 68 IS 3 BP 465 EP 467 DI 10.1021/np0401112 PG 3 WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy SC Plant Sciences; Pharmacology & Pharmacy GA 910JP UT WOS:000227927700037 PM 15787463 ER PT J AU Li, FQ Wang, T Pei, Z Liu, B Hong, JS AF Li, FQ Wang, T Pei, Z Liu, B Hong, JS TI Inhibition of microglial activation by the herbal flavonoid baicalein attenuates inflammation-mediated degeneration of dopaminergic neurons SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article; Proceedings Paper CT 11th IWCN Congress CY SEP 14-16, 2003 CL Campbell River, CANADA SP IWCN DE baicalein; neuroprotection; neurodegeneration; inflammation; microglia; dopaminergic neuron ID NITRIC-OXIDE SYNTHASE; PARKINSONS-DISEASE; SCUTELLARIA-BAICALENSIS; GLIAL-CELLS; NEURODEGENERATIVE DISEASES; ALZHEIMERS-DISEASE; REACTIVE OXYGEN; LIPOPOLYSACCHARIDE; BRAIN; NEUROTOXICITY AB Accumulating evidence has suggested that inflammation in the brain participates in the pathogenesis of Parkinson's disease (PD). Therefore, anti-inflammatory therapy has attracted much attention as novel interference to neurodegenerative diseases. Baicalein, a major flavonoid extracted from a traditional Chinese herb Scutellaria baicalensis Georgi (Huangqin), possesses potent anti-inflammatory and antioxidant properties. To test the potential neuroprotective effect of baicalein on dopaminergic neurons, primary midbrain neuron-glia cultures from E-14 rat embryos were used. Cultures were pretreated with baicalein for 30 min prior to stimulation with lipopolysaccharide (LPS, 10 ng/ml). LPS leads to massive activation of microglial cells revealed by OX-42 immunostaining, and produced excessive quantities of NO. Excessive elevation of superoxide level was also observed in enriched-microglia after stimulating with LPS. LPS-induced damage to dopaminergic neurons was evaluated by uptake capacity for [H-3] ]dopamine and tyrosine hydroxylase (TH)-immunocytochemistry. Pretreatment with baicalein concentration-dependently attenuated LPS-induced decrease in [H-3] stopH]dopamine uptake and loss of TH-immunoreactive (TH-ir) neurons, which the maximum protective effect was observed at the concentration of 5muM. Post-treatment with baicalein (5 muM) was also shown to be effective even if baicalein administered up to 2 h later than LPS application. Morphological study shows that baicalein (5 muM) almost completely blocked LPS-induced activation of microglia. Excessive production of TNFalpha and free radicals such as NO and superoxide by LPS stimulation were also attenuated by baicalein at a concentration-dependent pattern. The present study indicates that baicalein exerts potent neuroprotective effect on LPS-induced injury of dopaminergic neurons. We hypothesize that the inhibition of LPS-induced production of NO and free radicals from microglia may underlie the mechanism of baicalein's neuroprotection. C1 NIEHS, Neuropharmacol Sect, Lab Pharmacol & Chem, NIH, Res Triangle Pk, NC 27709 USA. RP Li, FQ (reprint author), NIEHS, Neuropharmacol Sect, Lab Pharmacol & Chem, NIH, POB 12233, Res Triangle Pk, NC 27709 USA. EM hong3@niehs.nih.gov RI liu, Bin/A-7695-2009 NR 65 TC 68 Z9 81 U1 2 U2 7 PU SPRINGER WIEN PI VIENNA PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 VIENNA, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PD MAR PY 2005 VL 112 IS 3 BP 331 EP 347 DI 10.1007/s00702-004-0213-0 PG 17 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 899ML UT WOS:000227148400002 PM 15503194 ER PT J AU Santi, M Quezado, M Ronchetti, R Rushing, EJ AF Santi, M Quezado, M Ronchetti, R Rushing, EJ TI Analysis of chromosome 7 in adult and pediatric ependymomas using chromogenic in situ hybridization SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE chromosome 7; CISH; ependymoma; myxopapillary; polysomy ID NERVOUS-SYSTEM TUMORS; ABNORMALITIES; ARCHIVAL; TISSUE AB Few studies have yielded reliable data that distinguish between ependymal neoplasms based on molecular genetic attributes. The present study utilizes chromogenic in situ hybridization (CISH), a relatively recent hybridization technique, to retrospectively examine chromosome 7-copy number in pediatric and adult ependymomas. Of the 27 hybridizations, polysomy of chromosome 7 was detected in 10 out of 15 (66%) adult ependymomas, and in only three out of 12 (25%) pediatric lesions. All myxopapillary ependymomas showed polysomy. The remaining tumors were diploid. The authors conclude that (1) there are distinct genetic subsets of ependymoma, in particular, increases in copy number of chromosome 7 are almost exclusively found in myxopapillary ependymoma, and that (2) CISH is a rapid and sensitive method of stratifying morphological variants of ependymoma and potentially other central nervous system (CNS) tumors. These results encourage further investigations with CISH on a larger scale to determine its merit as an ancillary diagnostic and prognostic tool. C1 Armed Forces Inst Pathol, Dept Neuropathol & Ophthalm Pathol, Washington, DC 20306 USA. Childrens Hosp, Natl Med Ctr, Dept Pathol, Washington, DC 20010 USA. Natl Canc Inst, NIH, Pathol Lab, Bethesda, MD USA. RP Rushing, EJ (reprint author), Armed Forces Inst Pathol, Dept Neuropathol & Ophthalm Pathol, Washington, DC 20306 USA. EM rushinge@afip.osd.mil NR 20 TC 7 Z9 8 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD MAR PY 2005 VL 72 IS 1 BP 25 EP 28 DI 10.1007/s11060-004-3117-9 PG 4 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA 914BW UT WOS:000228200600004 PM 15803371 ER PT J AU Han, J Yang, LM Puri, RK AF Han, J Yang, LM Puri, RK TI Analysis of target genes induced by IL-13 cytotoxin in human glioblastoma cells SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE cDNA microarray; gene expression profiles; IL-13 cytotoxin; IL-13R alpha 2 receptor ID INTERLEUKIN-13 RECEPTOR-ALPHA; PSEUDOMONAS EXOTOXIN; CHIMERIC PROTEIN; THYMIDYLATE SYNTHASE; EXPRESSION PROFILES; SIGNAL-TRANSDUCTION; CYTOKINE RECEPTOR; MALIGNANT GLIOMAS; FUSION CYTOTOXIN; CARCINOMA-CELLS AB IL-13 cytotoxin comprised of IL-13 and a mutated form of Pseudomonas exotoxin (fusion protein termed IL-13-PE38QQR) has been shown to inhibit protein synthesis leading to necrotic and apoptotic cell death in glioblastoma cells that express high levels of interleukin-13 receptors (IL-13R). To identify target genes of cell death and other cellular genes with IL-13 receptors in glioblastoma cells, we utilized the cDNA microarrays to analyze global gene expression profiles after IL-13 cytotoxin and IL-13 treatment. IL-13 cytotoxin mediated cytotoxicity to U251 cells in a dose-dependant manner. Hierarchical cluster analysis of differentially expressed genes in U251 glioma cells at different time points after IL-13 cytotoxin treatment showed three major groups, each representing a specific expression pattern. Randomly selected differentially expressed genes from each group were confirmed by RT-PCR analysis. Most down-regulated genes belong to cell adhesion, motility, angiogenesis, DNA repair, and metabolic pathways. While up-regulated genes belong to cell cycle arrest, apoptosis, signaling and various metabolic pathways. Unexpectedly, at early time points, both IL-13 and IL-13 cytotoxin induced several genes belonging to different pathways most notably IL-8, DIO2, END1, and ALDH1A3 indicating that these genes are early response genes and their products may be associated with IL-13R. In addition, IL-13 cytotoxin induced IL-13R alpha 2 mRNA expression during the treatment in glioma cells. Our results indicate that novel cellular genes are involved with IL-13 receptors and that IL-13 cytotoxin induced cell death involves various target genes in human glioblastoma cells. On going studies will determine the role of associated genes and their products in the IL-13R functions in glioma cells. C1 NIH, CBER, FDA, Ctr Informat Technol,Bioinformat & Mol Anal Sect, Bethesda, MD 20892 USA. US FDA, Ctr Biol Evaluat & Res, Lab Mol Tumor Biol, CBER,NCI Genom Program,Div Cellular & Gene Therap, Bethesda, MD USA. RP Puri, RK (reprint author), NIH, CBER, FDA, Ctr Informat Technol,Bioinformat & Mol Anal Sect, Bldg 29B,Rm 2NN10,29 Lincoln Dr, Bethesda, MD 20892 USA. EM puri@cber.fda.gov NR 60 TC 9 Z9 11 U1 0 U2 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD MAR PY 2005 VL 72 IS 1 BP 35 EP 46 DI 10.1007/s11060-004-3119-7 PG 12 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA 914BW UT WOS:000228200600006 PM 15803373 ER PT J AU Truckenmiller, ME Princiotta, MF Norbury, CC Bonneau, RH AF Truckenmiller, ME Princiotta, MF Norbury, CC Bonneau, RH TI Corticosterone impairs MHC class I antigen presentation by dendritic cells via reduction of peptide generation SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE antigen processing/presentation; glucocorticoid; dendritic cells; virus ID NEWLY SYNTHESIZED PROTEINS; CD8(+) T-CELLS; ENDOPLASMIC-RETICULUM; PROTEASOMAL DEGRADATION; MONOCLONAL-ANTIBODY; VIRAL-INFECTION; 26S PROTEASOME; ACUTE STRESSOR; CTL RESPONSES; VIVO AB The presentation of viral peptide-MHC class I complexes by antigen presenting cells, such as dendritic cells (DCs), is obligatory for the generation of antiviral effector and memory CD8(+) cytotoxic T lymphocyte (CTL) responses. Prolonged psychological stress is immunosuppressive and undermines primary and memory CTL-mediated antiviral immunity; however, the mechanisms involved are unknown. Using a panel of novel reagents and techniques, we quantitatively measured the effect of the stress-induced hormone corticosterone (CORT) on the efficiency of DCs to process and present virally expressed antigen, characterized the conditions for this CORT-inediated effect, and delineated the components of the MHC class I pathway that were affected. We found that physiologically relevant levels of CORT, prior to infection and acting via the glucocorticoid receptor, suppressed the formation of peptide-MHC class I complexes on the Surface of infected DCs. We further showed that this suppression of peptide-MHC class I complexes is via the action of CORT on elements of the class I pathway upstream from TAP that are involved in the generation of antigenic peptides. This CORT-mediated suppression of peptide-class I complexes on DCs also resulted in a marked reduction of their ability to activate a specific T cell hybridoma. These findings offer a mechanism contributing to the stress-induced suppression of host defenses against viral diseases and have implications for the efficacy of antiviral vaccines. At the most fundamental cellular level, this impairment of antigen processing has implications for the regulation of protein degradation in all cells, which is critical to many aspects of immune function. (c) 2004 Elsevier B.V. All rights reserved. C1 Penn State Univ, Coll Med, Dept Microbiol & Immunol, Milton S Hershey Med Ctr, Hershey, PA 17033 USA. NIAID, Viral Dis Lab, Bethesda, MD 20892 USA. RP Truckenmiller, ME (reprint author), Penn State Univ, Coll Med, Dept Microbiol & Immunol, Milton S Hershey Med Ctr, Hershey, PA 17033 USA. EM met11@psu.edu NR 58 TC 32 Z9 34 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD MAR PY 2005 VL 160 IS 1-2 BP 48 EP 60 DI 10.1016/j.jneuroim.2004.10.024 PG 13 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 906IE UT WOS:000227633500007 PM 15710457 ER PT J AU Blohm, G Missal, M Lefevre, P AF Blohm, G Missal, M Lefevre, P TI Processing of retinal and extraretinal signals for memory-guided saccades during smooth pursuit SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID FRONTAL EYE FIELD; DOUBLE-STEP SACCADES; SUPERIOR COLLICULUS; QUANTITATIVE-ANALYSIS; COROLLARY DISCHARGE; COLLIDING SACCADES; EXPRESS SACCADES; SPATIAL LOCATION; CORTICAL CONTROL; PARIETAL CORTEX AB It is an essential feature for the visual system to keep track of self-motion to maintain space constancy. Therefore the saccadic system uses extraretinal information about previous saccades to update the internal representation of memorized targets, an ability that has been identified in behavioral and electrophysiological studies. However, a smooth eye movement induced in the latency period of a memory-guided saccade yielded contradictory results. Indeed some studies described spatially accurate saccades, whereas others reported retinal coding of saccades. Today, it is still unclear how the saccadic system keeps track of smooth eye movements in the absence of vision. Here, we developed an original two-dimensional behavioral paradigm to further investigate how smooth eye displacements could be compensated to ensure space constancy. Human subjects were required to pursue a moving target and to orient their eyes toward the memorized position of. a briefly presented second target (flash) once it appeared. The analysis of the first orientation saccade revealed a bimodal latency distribution related to two different saccade programming strategies. Short-latency (<175 ms) saccades were coded using the only available retinal information, i.e., position error. In addition to position error, longer-latency (>175 ms) saccades used extraretinal information about the smooth eye displacement during the latency period to program spatially more accurate saccades. Sensory parameters at the moment of the flash (retinal position error and eye velocity) influenced the choice between both strategies. We hypothesize that this tradeoff between speed and accuracy of the saccadic response reveals the presence of two coupled neural pathways for saccadic programming. A fast striatal-collicular pathway might only use retinal information about the flash location to program the first saccade. The slower pathway could involve the posterior parietal cortex to update the internal representation of the flash once extraretinal smooth eye displacement information becomes available to the system. C1 Univ Catholique Louvain, Ctr Syst Engn & Appl Mech, B-1348 Louvain, Belgium. Univ Catholique Louvain, Neurophysiol Lab, B-1200 Brussels, Belgium. NEI, NIH, Bethesda, MD 20892 USA. RP Lefevre, P (reprint author), Univ Catholique Louvain, Ctr Syst Engn & Appl Mech, 4 Ave G Lemaitre, B-1348 Louvain, Belgium. EM lefevre@csam.ucl.ac.be NR 79 TC 38 Z9 39 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD MAR PY 2005 VL 93 IS 3 BP 1510 EP 1522 DI 10.1152/jn.00543.2004 PG 13 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 901AX UT WOS:000227256500037 PM 15483070 ER PT J AU Zhu, L Lovinger, D Delpire, E AF Zhu, L Lovinger, D Delpire, E TI Cortical neurons lacking KCC2 expression show impaired regulation of intracellular chloride SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID K-CL COTRANSPORTER; DEVELOPING RABBIT HIPPOCAMPUS; POSTNATAL RAT BRAINS; GABA(A) RECEPTOR; POSTSYNAPTIC INHIBITION; NA-K-2CL COTRANSPORTER; PYRAMIDAL CELLS; UP-REGULATION; I NEURONS; GENE AB As excitable cells, neurons experience constant changes in their membrane potential due to ion flux through plasma membrane channels. They maintain their transmembrane cation concentrations through robust Na+/K+-ATPase pump activity. During synaptic transmission and spread of action potentials, the concentration of the major anion, Cl-, is also under constant challenge from membrane potential changes. Moreover, intracellular Cl- is also affected by ligand-gated Cl- channels such as GABA, and glycine receptors. To regulate intracellular Cl- in an electrically silent manner, neurons couple the movement of Cl- with K+. In this study, we have used gene-targeted KCC2(-/-) mice to provide strong evidence that KCC2, the neuronal-specific K-Cl co-transporter, drives neuronal Cl- to low concentrations, shifting the GABA reversal potential toward more negative potentials, thus promoting hyperpolarizing GABA responses. Cortical neurons lacking KCC2, not only fail to show a developmental decrease in [Cl-](i), but also are unable to regulate [Cl-](i) on Cl- loading or maintain [Cl](i) during membrane depolarization. These data are consistent with the central role of KCC2 in promoting inhibition and preventing hyperexcitability. C1 Vanderbilt Univ, Med Ctr, Dept Anesthesiol, Nashville, TN 37232 USA. NIAAA, Lab Integrat Neurosci, Rockville, MD 20852 USA. RP Delpire, E (reprint author), Vanderbilt Univ, Med Ctr, Dept Anesthesiol, T-4202 Med Ctr N, Nashville, TN 37232 USA. EM eric.delpire@vanderbilt.edu RI Zhu, Lei /J-7210-2013 OI Zhu, Lei /0000-0002-0898-8602 FU NINDS NIH HHS [NS-36758] NR 56 TC 78 Z9 80 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD MAR PY 2005 VL 93 IS 3 BP 1557 EP 1568 DI 10.1152/jn.00616.2004 PG 12 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 901AX UT WOS:000227256500039 PM 15469961 ER PT J AU Bradley, DC Troyk, PR Berg, JA Bak, M Cogan, S Erickson, R Kufta, C Mascaro, M McCreery, D Schmidt, EM Towle, VL Xu, H AF Bradley, DC Troyk, PR Berg, JA Bak, M Cogan, S Erickson, R Kufta, C Mascaro, M McCreery, D Schmidt, EM Towle, VL Xu, H TI Visuotopic mapping through a multichannel stimulating implant in primate V1 SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID HUMAN OCCIPITAL CORTEX; VISUAL-CORTEX; ELECTRICAL-STIMULATION; INTRACORTICAL MICROSTIMULATION; SUPERIOR COLLICULUS; ARTIFICIAL VISION; STRIATE CORTEX; BLIND; PROSTHESIS; MONKEY AB We report on our efforts to establish an animal model for the development and testing of a cortical visual prostheses. One-hundred-fifty-two electrodes were implanted in the primary Visual cortex of a rhesus monkey. The electrodes were made from iridium with an activated iridium oxide film, which has a large charge capacity for a given surface area, and insulated with parylene-C. One-hundred-fourteen electrodes were functional after implantation. The activity of small (2-3) neuronal clusters was first recorded to map the visually responsive region corresponding to each electrode. The animal was then trained in a memory (delayed) saccade task. first with a visual target, then to a target defined by direct cortical stimulation with coordinates specified by the stimulating electrode's mapped receptive field. The SD of saccade endpoints was similar to2.5 larger for electrically stimulated versus visual saccades; nevertheless, when trial-to-trial scatter was averaged out. the correlation between saccade end points and receptive field locations was highly significant and approached unity after several months of training. Five electrodes were left unused until the monkey was fully trained when these were introduced, the receptive field-saccade correlations were high oil the first day of use (R = 0.85. P = 0.03 for angle, R = 0.98, P < 0,001 for eccentricity), indicating that the monkey had not learned to perform the task empirically by memorizing reward zones. The results of this experiment suggest the potential for rigorous behavioral testing of cortical visual prostheses in the macaque. C1 Univ Chicago, Dept Psychol, Chicago, IL 60637 USA. Univ Chicago, Dept Neurol, Chicago, IL 60637 USA. Univ Chicago, Dept Neurosurg, Chicago, IL 60637 USA. Univ Chicago, Dept Stat, Chicago, IL 60637 USA. IIT, Pritzker Inst Biomed Sci & Engn, Chicago, IL 60616 USA. Huntington Med Res Inst, Pasadena, CA USA. NIH, Neural Control Lab, Bethesda, MD 20892 USA. EIC Labs, Norwood, MA USA. RP Bradley, DC (reprint author), Univ Chicago, Dept Psychol, 5848 S Univ Ave,Green 314, Chicago, IL 60637 USA. EM bradley@uchicago.edu FU NINDS NIH HHS [NS-40690-01A1] NR 26 TC 88 Z9 88 U1 1 U2 5 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD MAR PY 2005 VL 93 IS 3 BP 1659 EP 1670 DI 10.1152/jn.01213.2003 PG 12 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 901AX UT WOS:000227256500047 PM 15342724 ER PT J AU Bonnot, AS Mentis, GZ Skoch, J O'Donovan, MJ AF Bonnot, AS Mentis, GZ Skoch, J O'Donovan, MJ TI Electroporation loading of calcium-sensitive dyes into the CNS SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID IN-VIVO ELECTROPORATION; LOCOMOTOR-LIKE ACTIVITY; LEFT-RIGHT COORDINATION; MOUSE SPINAL-CORD; NEONATAL MOUSE; RHYTHMIC ACTIVITY; NETWORK ACTIVITY; GENE-EXPRESSION; NERVOUS-SYSTEM; CHICK-EMBRYO AB Calcium imaging of neural network function has been limited by the extent Of tissue labeled or the time taken for labeling. We now describe the use of electroporation-an established technique for transfecting cells with genes-to load neurons with calcium-sensitive dyes in the isolated spinal cord of the neonatal mouse in vitro. The dyes were injected subdurally. intravascularly. or into the central canal. This technique results in rapid and extensive labeling of neurons and their processes at all depths of the spinal cord. over a rostrocaudal extent determined by the position and size of the electrodes. Our results suggest that vascular distribution of the dye is involved in all three types of injections. Electroporation disrupts local reflex and network function only transiently (similar to1 h), after which time they recover. We describe applications of the method to image activity of neuronal populations and individual neurons during antidromic, reflex, and locomotor-like behaviors. We show that these different motor behaviors are characterized by distinct patterns of activation among the labeled populations of cells. C1 NINDS, Lab Neural Control, Sect Dev Neurobiol, NIH, Bethesda, MD 20892 USA. RP Bonnot, AS (reprint author), NINDS, Lab Neural Control, Sect Dev Neurobiol, NIH, 35 Convent Dr,Rm 3C1010, Bethesda, MD 20892 USA. EM bonnota@ninds.nih.gov RI o'donovan, michael/A-2357-2015 OI o'donovan, michael/0000-0003-2487-7547 NR 35 TC 31 Z9 31 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD MAR PY 2005 VL 93 IS 3 BP 1793 EP 1808 DI 10.1152/jn.00923.2004 PG 16 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 901AX UT WOS:000227256500056 PM 15509647 ER PT J AU Nesic-Taylor, O Cittelly, D Ye, Z Xu, GY Unabia, G Lee, JC Svrakic, NM Liu, XH Youle, RJ Wood, TG McAdoo, D Westlund, KN Hulsebosch, CE Perez-Polo, JR AF Nesic-Taylor, O Cittelly, D Ye, Z Xu, GY Unabia, G Lee, JC Svrakic, NM Liu, XH Youle, RJ Wood, TG McAdoo, D Westlund, KN Hulsebosch, CE Perez-Polo, JR TI Exogenous Bcl-X-L fusion protein spares neurons after spinal cord injury SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE spinal cord injury; Bcl-X-L; Bcl-X-L fusion protein; neurons ID APOPTOTIC CELL-DEATH; NECROSIS-FACTOR-ALPHA; CYTOCHROME-C; CONTUSION INJURY; NERVOUS-SYSTEM; MESSENGER-RNA; BRAIN-INJURY; RAT; MITOCHONDRIA; EXPRESSION AB Spinal cord injury (SCI) induces neuronal death, including apoptosis, which is completed within 24 hr at and around the impact site. We identified early proapoptotic transcriptional changes, including upregulation of proapoptotic Bax and downregulation of antiapoptotic Bcl-X-L, Bcl-2, and Bcl-w, using Affymetrix DNA microarrays. Because Bcl-X-L is the most robustly expressed antiapoptotic Bcl-2 molecule in adult central nervous system, we decided to characterize better the effect of SCI on Bcl-X-L expression. We found Bcl-X-L expressed robustly throughout uninjured spinal cord in both neurons and glia cells. We also found Bcl-XL localized in different cellular compartments: cytoplasmic, mitochondrial, and nuclear. Bcl-X-L protein levels decreased in the cytoplasm and mitochondria 2 hr after SCI and persisted for 24 hr. To test the contribution of proapoptotic decreases in Bcl-X-L to neuronal death, we augmented endogenous Bcl-X-L levels by administering Bcl-X-L fusion protein (Bcl-X-L FP) into injured spinal cords. Bcl-X-L FP significantly increased neuronal survival, suggesting that SCI-induced changes in Bcl-X-L contribute considerably to neuronal death. Because Bcl-X-L FP increases survival of dorsal horn neurons and ventral horn motoneurons, it could become clinically relevant in preserving sensory and motor functions after SCI. (C) 2005 Wiley-Liss, Inc. C1 Univ Texas, Med Branch, Dept Human Biol Chem & Genet, Galveston, TX 77555 USA. Univ Texas, Med Branch, Dept Neurosci & Cell Biol, Galveston, TX 77555 USA. Univ Texas, Med Branch, Mol Genom Core Lab, Galveston, TX 77555 USA. Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA. RP Nesic-Taylor, O (reprint author), Univ Texas, Med Branch, Dept Human Biol Chem & Genet, 7-138G Med Res Bldg,301 Univ Blvd, Galveston, TX 77555 USA. EM Olnesic@utmb.edu RI Wood, Thomas/B-6172-2012; Perez-Polo, Jose/B-6250-2009; nesic, olivera/C-6456-2012 NR 40 TC 55 Z9 57 U1 0 U2 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0360-4012 J9 J NEUROSCI RES JI J. Neurosci. Res. PD MAR 1 PY 2005 VL 79 IS 5 BP 628 EP 637 DI 10.1002/jnr.20400 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 902NS UT WOS:000227364400006 PM 15668909 ER PT J AU Kim, HJ Butman, JA Brewer, C Zalewski, C Vortmeyer, AO Glenn, G Oldfield, EH Lonser, RR AF Kim, HJ Butman, JA Brewer, C Zalewski, C Vortmeyer, AO Glenn, G Oldfield, EH Lonser, RR TI Tumors of the endolymphatic sac in patients with von Hippel-Lindau disease: implications for their natural history, diagnosis, and treatment SO JOURNAL OF NEUROSURGERY LA English DT Article DE anatomy; endolymphatic sac tumor; pathophysiology; von Hippel-Lindau disease; neurosurgery ID SURGICAL-MANAGEMENT; HEMANGIOBLASTOMAS; ADENOCARCINOMA AB Object. Endolymphatic sac tumors (ELSTs), which often are associated with von Hippel-Lindau (VHL) disease, cause irreversible hearing loss and vestibulopathy. Clinical and imaging surveillance protocols provide new insights into the natural history, mechanisms of symptom formation, and indications for the treatment of ELSTs. To clarify the uncertainties associated with the pathophysiology and treatment of ELSTs, the authors describe a series of patients with VHL disease in whom serial examinations recorded the development of ELSTs. Methods. Patients with VHL disease were included if serial clinical and imaging studies captured the development of ELSTs, and the patients underwent tumor resection. The patients' clinical, audiological, and imaging characteristics as well as their operative results were analyzed. Five consecutive patients (three men and two women) with a mean age at surgery of 34.8 years and a follow-up period of 6 to 18 months were included in this study. Audiovestibular symptoms were present in three patients before a tumor was evident on neuroimaging. Imaging evidence of an intralabyrinthine hemorrhage coincided with a loss of hearing in three patients. Successful resection of the ELSTs was accomplished by performing a retrolabyrinthine posterior petrosectomy (RLPP). Hearing stabilized and vestibular symptoms resolved after surgery in all patients. No patient has experienced a recurrence. Conclusions. Audiovestibular symptoms, including hearing loss, in patients with,VHL disease can be the result of microscopic ELSTs. Once an ELST has been detected, it can be completely resected via an RLPP with preservation of hearing and amelioration of vestibular symptoms. Early detection and surgical treatment of small ELSTs, when hearing is still present, should reduce the incidence and severity of hearing loss, tinnitus, vertigo, and cranial nerve dysfunction, which are associated with these tumors. C1 NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA. NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. Georgetown Univ, Med Ctr, Dept Otolaryngol Head & Neck Surg, Washington, DC 20007 USA. Natl Inst Deafness & Other Commun Disorders, Neurootol Branch, Dept Diagnost Radiol, Warren G Magnuson Clin Ctr, Bethesda, MD USA. RP Lonser, RR (reprint author), NINDS, Surg Neurol Branch, NIH, Bldg 10,Room 5D37, Bethesda, MD 20892 USA. EM lonserr@ninds.nih.gov RI Butman, John/A-2694-2008; OI Butman, John/0000-0002-1547-9195 NR 17 TC 32 Z9 34 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 USA SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD MAR PY 2005 VL 102 IS 3 BP 503 EP 512 DI 10.3171/jns.2005.102.3.0503 PG 10 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA 911PR UT WOS:000228017200016 PM 15796386 ER PT J AU Tender, GC Walbridge, S Olah, Z Karai, L Iadarola, M Oldfield, EH Lonser, RR AF Tender, GC Walbridge, S Olah, Z Karai, L Iadarola, M Oldfield, EH Lonser, RR TI Selective ablation of nociceptive neurons for elimination of hyperalgesia and neurogenic inflammation SO JOURNAL OF NEUROSURGERY LA English DT Article DE neuropathic pain; pain; trigeminal neuralgia; resiniferatoxin; trigeminal ganglion; treatment; macaca mulatta ID CAPSAICIN RECEPTOR; DELETION AB Object. Neuropathic pain is mediated by nociceptive neurons that selectively express the vanilloid receptor 1 (VR1). Resiniferatoxin (RTX) is an excitotoxic VR1 agonist that causes destruction of VR1-positive neurons. To determine whether RTX can be used to ablate VR1-positive neurons selectively and to eliminate hyperalgesia and neurogenic inflammation without affecting tactile sensation and motor function, the authors infused it unilaterally into the trigeminal ganglia in Rhesus monkeys. Methods. Either RTX (three animals) or vehicle (one animal) was directly infused (20 mu 1) into the right trigeminal ganglion in Rhesus monkeys. Animals were tested postoperatively at 1, 4, and 7 weeks thereafter for touch and pain perception in the trigeminal distribution (application of saline and capsaicin to the cornea). The number of eye blinks, eye wipes, and duration of squinting were recorded. Neurogenic inflammation was tested using capsaicin cream. Animals were killed 4 (one monkey) and 12 (three monkeys) weeks postinfusion. Histological and immunohistochemical analyses were performed. Throughout the duration of the study, response to high-intensity pain stimulation (capsaicin) was selectively and significantly reduced (p < 0.001, RTX-treated compared with vehicle-treated eye [mean +/- standard deviation]): blinks, 25.7 +/- 4.4 compared with 106.6 +/- 20.8; eye wipes, 1.4 +/- 0.8 compared with 19.3 +/- 2.5; and squinting, 1.4 +/- 0.6 seconds compared with 11.4 +/- 1.6 seconds. Normal response to sensation was maintained. Animals showed no neurological deficit or sign of toxicity. Neurogenic inflammation was blocked on the RTX-treated side. Inummohistochemical analysis of the RTX-treated ganglia showed selective elimination of VR1-positive neurons. Conclusions. Nociceptive neurons can be selectively ablated by intraganglionic RTX infusion, resulting in the elimination of high-intensity pain perception and neurogenic inflammation while maintaining normal sensation and motor function. Analysis of these findings indicated that intraganglionic RTX infusion may provide a new treatment for pain syndromes such as trigeminal neuralgia as well as others. C1 NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA. Natl Inst Dent & Craniofacial Res, Pain Neurosensory Mech Branch, NIH, Bethesda, MD USA. Louisiana State Univ, Dept Neurosurg, New Orleans, LA USA. RP Lonser, RR (reprint author), NINDS, Surg Neurol Branch, NIH, 10 Ctr Dr,Bldg 10,Room 5D37, Bethesda, MD 20892 USA. EM lonserr@ninds.nih.gov NR 8 TC 37 Z9 38 U1 0 U2 4 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 USA SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD MAR PY 2005 VL 102 IS 3 BP 522 EP 525 DI 10.3171/jns.2005.102.3.0522 PG 4 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA 911PR UT WOS:000228017200018 PM 15796388 ER PT J AU Tucker, KL Hallfrisch, J Qiao, N Muller, D Andres, R Fleg, JL AF Tucker, KL Hallfrisch, J Qiao, N Muller, D Andres, R Fleg, JL TI The combination of high fruit and vegetable and low saturated fat intakes is more protective against mortality in aging men than is either alone: The Baltimore longitudinal study of aging SO JOURNAL OF NUTRITION LA English DT Article DE fruit and vegetables; saturated fat; coronary heart disease; mortality; men ID CORONARY-HEART-DISEASE; CARDIOVASCULAR-DISEASE; DIETARY PATTERNS; US ADULTS; RISK; PREVENTION; WOMEN; TRENDS; TRIAL AB Saturated fat (SF) intake contributes to the risk of coronary heart disease (CHD) mortality. Recently, the protective effects of fruit and vegetable (FV) intake on both CHD and all-cause mortality were documented. However, individuals consuming more FV may be displacing higher-fat foods. Therefore, we investigated the individual and combined effects of FV and SF consumption on total and CHD mortality among 501 initially healthy men in the Baltimore Longitudinal Study of Aging (BLSA). Over a mean 18 y of follow-up, 7-d diet records were taken at 1-7 visits. Cause of death was ascertained from death certificates, hospital records, and autopsy data. After adjustment for age, total energy intake, BMI, smoking, alcohol use, dietary supplements, and physical activity score, FV and SF intakes were individually associated with lower all-cause and CHD mortality (P < 0.05). When both FV and SF were included in the same model, associations of each were attenuated with CHD mortality, and no longer significant for all-cause mortality. Men consuming the combination of 5 servings of FV/d and less than or equal to 12% energy from SF were 31% less likely to die of any cause (P < 0.05), and 76% less likely to die from CHD (P < 0.001), relative to those consuming < 5 FV and > 12% SF Men consuming either low SF or high FV, but not both, did not have a significantly lower risk of total mortality; but did have 64-67% lower risk of CHD mortality (P < 0.05) relative to those doing neither. These results confirm the protective effects of low SF and high FV intake against CHD mortality. In addition, they extend these findings by demonstrating that the combination of both behaviors is more protective than either alone, suggesting that their beneficial effects are mediated by different mechanisms. C1 Tufts Univ, Jean Mayer US Dept Agr, Human Nutr Res Ctr Aging, Boston, MA 02111 USA. NIA, Intramural Program, NIH, Bethesda, MD 20892 USA. RP Tucker, KL (reprint author), Tufts Univ, Jean Mayer US Dept Agr, Human Nutr Res Ctr Aging, Boston, MA 02111 USA. EM katherine.tucker@tufts.edu RI Tucker, Katherine/A-4545-2010; OI Tucker, Katherine/0000-0001-7640-662X NR 30 TC 53 Z9 55 U1 1 U2 2 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-3166 J9 J NUTR JI J. Nutr. PD MAR PY 2005 VL 135 IS 3 BP 556 EP 561 PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 904PF UT WOS:000227509500031 PM 15735093 ER PT J AU Mattson, MP Wan, RQ AF Mattson, MP Wan, RQ TI Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems SO JOURNAL OF NUTRITIONAL BIOCHEMISTRY LA English DT Article DE heart rate variability; ischemia; insulin sensitivity; oxidative stress; stroke ID ENDOTHELIAL GROWTH-FACTOR; ISCHEMIC BRAIN-DAMAGE; DIETARY RESTRICTION; NEUROTROPHIC FACTOR; OXIDATIVE STRESS; RAT-HEART; NEURODEGENERATIVE DISORDERS; INSULIN-RESISTANCE; GENE-EXPRESSION; LIFE-SPAN AB Intermittent fasting (IF; reduced meal frequency) and caloric restriction (CR) extend lifespan and increase resistance to age-related diseases in rodents and monkeys and improve the health of overweight humans. Both IF and CR enhance cardiovascular and brain functions and improve several risk factors for coronary artery disease and stroke including a reduction in blood pressure and increased insulin sensitivity. Cardiovascular stress adaptation is improved and heart rate variability is increased in rodents maintained on an IF or a CR diet. Moreover, rodents maintained on an IF regimen exhibit increased resistance of heart and brain cells to ischemic injury in experimental models of myocardial infarction and stroke. The beneficial effects of IF and CR result from at least two mechanisms reduced oxidative damage and increased cellular stress resistance. Recent findings suggest that some of the beneficial effects of IF on both the cardiovascular system and the brain are mediated by brain-derived neurotrophic factor signaling in the brain. Interestingly, cellular and molecular effects of IF and CR on the cardiovascular system and the brain are similar to those of regular physical exercise, suggesting shared mechanisms. A better understanding of the cellular and molecular mechanisms by which IF and CR affect the blood vessels and heart and brain cells will likely lead to novel preventative and therapeutic strategies for extending health span. (c) 2005 Elsevier Inc. All rights reserved. C1 NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA. RP Mattson, MP (reprint author), NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD 21224 USA. EM mausonm@grc.nia.nih.gov RI Mattson, Mark/F-6038-2012 NR 80 TC 194 Z9 201 U1 10 U2 62 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0955-2863 J9 J NUTR BIOCHEM JI J. Nutr. Biochem. PD MAR PY 2005 VL 16 IS 3 BP 129 EP 137 DI 10.1016/j.jnutbio.2004.12.007 PG 9 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA 908TL UT WOS:000227813000001 PM 15741046 ER PT J AU Coble, J Arbuckle, T Lee, WJ Alavanja, M Doserneci, M AF Coble, J Arbuckle, T Lee, WJ Alavanja, M Doserneci, M TI The validation of a pesticide exposure algorithm using biological monitoring results SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL HYGIENE LA English DT Article DE exposure; pesticides; ppe; questionnaires ID AGRICULTURAL HEALTH; 2,4-DICHLOROPHENOXYACETIC ACID; 2,4-D DIMETHYLAMINE; APPLICATORS AB A pesticide exposure algorithm was developed to calculate pesticide exposure intensity scores based on responses to questions about pesticide handling procedures and application methods in a self-administered questionnaire. The validity of the algorithm was evaluated through comparison of the algorithm scores with biological monitoring data from a study of 126 pesticide applicators who applied the herbicdes MCPA or 2,4-D. The variability in the algorithm scores calculated for these applicators was due primarily to differences in their use of personal protective equipment (PPE). Rubber gloves were worn by 75% of applicators when mixing and 22% when applying pesticides, rubber boots were worn by 33% when mixing and 23% when applying, and goggles were worn by 33% and 17% of applicators when mixing and when applying, respectively. Only 2% of applicators wore all three types of PPE when both mixing and applying, and 15% wore none of these three types of PPE when either mixing or applying. Substantial variability was also observed in the concentrations of pesticides detected in the post application urine samples. The concentration of MCPA detected in urine samples collected on the second day after the application ranged from less than < 1.0 to 610 mu g/L among 84 of the applicators who applied MCPA. The concentrations of 2,4-D detected in the urine samples ranged from less than < 1.0 to 514 mu g/L among 41 of the applicators who applied 2,4-D. When categorized into three groups based on the algorithm scores, the geometric mean in the highest exposure group was 20 mu g/L compared with 5 mu g/L in the lowest exposure group for the MCPA applicators, and 29 mu g/L in highest exposure group compared with 2 mu g/L in the low exposure group for the 2,4-D applicators. A regression analysis detected statistically significant trends in the geometric mean of the urine concentrations across the exposure categories for both the 2,4-D and the MCPA applicators. The algorithm scores, based primarily on the use of PPE, appear to provide a reasonably valid measure of exposure intensity for these applicators, however further studies art needed to generalize these results to other types of pesticides and application methods. C1 Natl Canc Inst Occupat & Environm Epidemiol Branc, DHHS, Dept Canc Epidemiol & Genet, NIH, Rockville, MD USA. Korea Univ, Coll Med, Dept Prevent Med, Seoul, South Korea. RP Coble, J (reprint author), Natl Canc Inst Occupat & Environm Epidemiol Branc, DHHS, Dept Canc Epidemiol & Genet, NIH, Rockville, MD USA. EM jcoble@mail.nih.gov NR 14 TC 36 Z9 37 U1 0 U2 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1545-9624 J9 J OCCUP ENVIRON HYG JI J. Occup. Environ. Hyg. PD MAR PY 2005 VL 2 IS 3 BP 194 EP 201 DI 10.1080/15459620590923343 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA 910JM UT WOS:000227927400011 PM 15764542 ER EF